Hormone Replacement Therapy Market Outlook 2021

Hormone Replacement Therapy market report is the major research for those who look for an entire analysis of markets. The report covers all information on the Global and regional markets, including old and future trends for market demand, size, trading, supply, competitors, prices, and globalpredominant vendors information. We have provided CAGR, value, volume, sales, production, revenue, and other estimations for the global as well as regional markets.

The market is designed to serve as a ready-to-use guide for developing accurate pandemic management programs allowing market players to successfully emerge from the crisis and retract numerous gains and profits. The SMI analyzes recent strategic activities, such as partnerships, acquisitions, mergers, collaborations, and joint ventures. The report analyzes the demographics, growth potential, and capability of the market through the forecast period 2021 to 2027. The players included in this report are chosen in terms of their product portfolio, market share, brand value, and the well-being of the organizations. Our report is based on current situations across the globe.

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Top players listed in Hormone Replacement Therapy report:

Novartis AG, Abbott Laboratories, Mylan NV, Merck KgaA, Bayer AG, Pfizer Inc., Novo Nordisk A/S, QuatRx Pharmaceuticals, Teva Pharmaceutical Industries Ltd., Amgen Inc., Eli Lilly and Company

Hormone Replacement Therapy Market Segmentation

Global Hormone Replacement Therapy Market,By Type

Oral, Parenteral, Others

Global Hormone Replacement Therapy Market,By Applications:

Hypothyroidism, Male Hypogonadism, Growth Hormone Deficiency, Menopause, Others

If you are part of the Hormone Replacement Therapy industry or intend to be, then study would provide you comprehensive outlook. It is vital to keep your market knowledge up to date analysed by major players and high growth emerging players. If a different set of players need to be analysed as per geography or regional target then enquire us with your customized requirements.

The report forecasts revenue growth at all geographic levels and provides an in-depth analysis of the latest industry trends and development patterns from 2020 to 2027 in each of the segments and sub-segments.

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This report also offers specific consumer preferences and expectations to gain insights into changing needs and behavior of the consumer. Thus, we offer more reliable, accurate, and actionable information specifically tailored to suit your business needs. If you have any special requirements, please let us know and we will offer you the report as you want.

Some of the important Key Questions ones are:

Research Methodology:

TheHormone Replacement Therapy market research follows a four-step methodology: primary research, secondary research, market estimation, and final presentations. Data is collected through self-conducted research methods in the primary research, whereas in secondary research, data is collected from previously conducted studies.The market estimation involves data processed in primary and secondary research. The final step is a holistic representation of the data and analysis made to make the report highly comprehensible for the reader.

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**NOTE: Our analysts monitoring the situation across the globe explains that the market will generate remunerative prospects for producers to post the COVID-19 crisis.

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Our strength lies in the unrivaled diversity of our people, methodologies, specialisms, and points of view. This market has a significant impact on the COVID-19 pandemic. Our experts are closely monitoring the industry to capture and analyze appropriate indicators.

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Hormone Replacement Therapy Market by 2027 Worldwide Growth Opportunities Recent Trends Forecast by Types and Application to 2027 The Manomet Current...

Recommendation and review posted by Bethany Smith

What makes a man? This question has been a subject of great argument for many centuries. However, the thing that leaps to the mind first is, undeniably, testosterone. Testosterone is the most vital male sex hormone that is a critical factor in mens adolescence.

An optimal proportion of testosterone maintains high energy levels as well as enhances body strength and masculinity. Besides, it is a crucial aspect regarding physical changes in boys.

But, what course of action should you adopt if you have lower testosterone levels? You will find a vast chain of treatments and procedures in this regard, but it is hard to access an authentic one.

In that sense, you have landed on the right platform. With enough research on this significant health affair, we will introduce you to the precious nine ways that will help you increase testosterone naturally. And, the good news is these will bring beneficial changes to your overall health and well-being.

So, keep scrolling down.

Your diet has a significant impact on your testosterone levels. Recent studies have found that men who consume a low-fat diet face testosterone deficiency. Therefore, always be mindful of your diet routine and stay away from prolonged dieting strategies.

Eating bulked-up ingredients fuels your masculinity. Therefore, following a rich diet plan and the intake of the best testosterone booster supplements might boost up your testosterone levels effectively.

You might be missing some essential nutrients in your daily diet that may boost your T levels.

We have discussed their importance and how you can have all of them at once below in detail:

D-Aspartic acid is a natural amino acid that can increase your testosterone levels effectively. Colossal research has been done on D-Aspartic acid, which shows it is bound to many fruitful outcomes regarding the whole male reproductive system.

Recent studies have revealed D-Aspartic acid works on some critical testosterone-stimulating hormones like follicle-stimulating hormones and luteinizing hormones, which increases your testosterone levels.

Adding D-Aspartic acid into your diet for 12 days may help enhance testosterone levels and other hormones. Additionally, it may also elevate their production and transportation around the body.

Many studies have also shown that such amino acids may be helpful in sperm production and quality. So, overall, it can be a significant step towards better testosterone levels.

Magnesium is a critical mineral deeply associated with the vital processes in our body, like cellular processes, bone formation, and muscle functions.

A couple of researches revealed magnesium supplementation for four weeks increases testosterone levels in athletic and sedentary individuals.

A magnesium-rich diet can, directly and indirectly, translate it into an increased T level (since magnesium is also responsible for converting Vitamin D into an active form).

Although magnesium deficiency is more common in old age, many younger people, like athletes, may also suffer from it, as many minerals like Zinc, magnesium, etc., may be lost in sweat. Therefore, make sure you consume a proper intake of magnesium.

Though many competitive supplements include magnesium as an ingredient, dietary magnesium always comes first, so try to reach out to the magnesium-rich foods that are abundant, such as greens, nuts, seeds, dry beans, whole grains, and wheat and oat bran.

Try to stay away from magnesium oxide, as it may cause some significant health issues like intestinal discomfort or diarrhea.

Zinc is found to be the second most abundant element in humans. Apart from having countless benefits in other health regards, researchers have found Zinc may play a tremendous role in mens masculinity, fertilization, sperm quality, and hormonal secretion.

Some researchers have also witnessed that an average Zinc concentration in the body is required for the normal functioning of the pituitary gland, which is highlighted in male reproductive potential.

Zinc is found to affect mens fertility in numerous ways. In addition, low zinc levels in the body have a highlighted negative effect on testosterone concentrations.

So, keeping all of this in mind, try to incorporate zinc supplements in your diet, which include oysters, beef, nuts, chicken, beans, and many more.

TestoPrime is the answer, as it is an effective testosterone-boosting supplement. With TestoPrime, you can get all of the essential nutrients in a single package.

You can get all of these benefits by using this natural testosterone booster. The influential testosterone support can help you maintain your pubescent liveliness with new and fresh testosterone.

TestoPrime is a cost-friendly and 100% dependent combination of natural ingredients, like vitamins and fruit extracts, mainly created to give the best results and promote your overall health.

Men who have entered their 40s or are near to it are advised to purchase it. It may not only bring a flood of testosterone into your body, but it may also help you get rid of tiredness, low energy levels, loss of focus, decreased sexual desires, and a bad memory.

So, if you want all these in a short time, grab this fantastic T-boosting supplement.

Modern studies have shown testosterone makes you manly, and vitamin D supports your bones and muscles. However, recently, it has been concluded these two biomarkers are associated with many other body functions and may affect each others levels.

Vitamin D is an essential nutrient that is achieved via sun exposure and many diet supplements. The essential vitamin crucially influences the proper growth and functioning of bones, muscles, nerves, and numerous body organs.

Various researches have been performed on discovering the role of vitamin D in testosterone boosting. It has been found that low vitamin D levels can drop your testosterone levels theoretically. Additionally, it can lead to improper working of the testes.

A few years ago, it was concluded that men with lower Vitamin D and T levels might have more cardiovascular diseases. In addition, people with low T levels may experience some other sexual problems like erectile dysfunction and lower sexual drives. These can be treated with Vitamin D.

Always make sure to have enough Vitamin D included in your diet. There are various supplements available in the market. Another option is to go out in the sunshine, as it is the most reliable and productive way of consuming vitamin D.

Therefore, the sun is the best way to get vitamin D. When you take some Vitamin D-rich supplements or expose your skin to sun rays, your body absorbs it. Your liver will then translate it into its active form called 25(OH) D, which your doctor looks for when he suggests a Vitamin D blood test.

The active form of Vitamin D is then transported throughout your body for different functions. It is now proven the male reproductive system is one of its receivers.

Apart from that, there are some other ways to consume vitamin D like:

Exercises tend to be the most crucial factor in preventing many health diseases. Surprisingly, this can also be the best alternative to increase your testosterone levels. You can increase your testosterone levels on your own by adopting some essential pieces of training and workouts.

Low testosterone levels are nearly bound to lowered energy levels, decreased muscle mass, and inadequate mental health. Exercises can be the best in this regard.

Exercises increase testosterone in two ways:

Research has found that heavy training like weight lifting may be the best way to boost testosterone. Lifting heavy weights may help gain muscle mass and, likewise, higher T levels. If you are new to this, opt for a trainer to get basic knowhow of it.

High-intensity interval exercises, if done along with weight lifting, may be the best combination that will not only elevate your T levels but may also help promote heart health.

High-intensity training is also found to have positive effects on testosterone levels. Research revealed that resting for a couple of minutes between intervals is more advantageous.

Moderate cardio exercises also contribute to some extent, as they protect your heart and inhibit extra cortisol productions, which can negatively impact your muscle mass and T levels.

Make sure to stay away from chronic and prolonged exercises like cycling, running, and swimming for a long time, as these may cause problems regarding your testosterone production.

Follow a reliable diet plan that includes the intake of all of the necessary nutrients in the proper proportions. A balanced diet is a crucial factor in elevating T levels. Hundreds of researches show that low testosterone levels and poor diet patterns are strongly interrelated.

A balanced diet not only enhances your T levels, but it has countless health benefits. Many studies show that alterations in dietary plans may lead to hypogonadism. Consuming a balanced diet enriched in proteins, carbs, and healthy fats can go longer toward normal T levels as you age.

Many essential nutrients like proteins, carbs, and healthy fats may bring noticeable benefits to your health and hormonal secretions.

According to recent health researchers, a diet rich in proteins may aid a lot in testosterone boosting. However, another study has revealed low protein levels may damage the Leyden cells assigned to testosterone production.

Therefore, try to increase your protein intake. This will help you in fat loss which, likewise, is linked with your testosterone. Moreover, it will support your muscle development, which may be essential in testosterone boosting.

Carbs may bring out a rapid increase in your T levels. According to the latest research, eating a carbohydrate-rich diet may be harmful to diabetic people, but it is associated with a high testosterone level in the average person. Instead, try to consume carbs from starchy tubers such as potatoes, yams, pumpkins, etc.

When it comes to fats, many of you may think it has nothing to do with testosterone levels, but it is essential to take a sufficient amount of healthy fats to produce testosterone effectively. In this regard, saturated fats are beneficial.

It would be best if you add the following foods to your daily routine:

In short, we would say a healthier diet will result in a healthier weight that may boost your T levels even if you age.

The pressures you are dealing with in your life may reveal several ways. Lower T levels are one of these. Stress may affect some essential hormones like testosterone responsible for pubescence in boys. However, the clear physiological linkage between stress and low testosterone is not known.

Many researchers and physicians have shown some brain chemicals released in response to stress and anxiety, and then they might be transferred to the testosterone-controlling sites in the brain.

Other research shows stress elevates the cortisol levels in the body. Cortisol is a stress hormone released by adrenal glands in the kidneys when you are under stress. It is assigned with the management of numerous processes in the body like metabolism and immune system. Therefore, increased cortisol impacts testosterone productions negatively.

In this regard, meditation may be the best option to get rid of stress. Researchers have found that at least 20-30 minutes of meditation per day will indirectly lower cortisol and increase your testosterone and growth hormone levels.

Always try to manage yourself in stressful situations. This will preserve your sanity and promote your health in many ways.

Lack of sleep can adversely affect the secretions and levels of many essential hormones and chemicals in the body, including testosterone. Simply speaking, your testosterone levels are directly linked with your sleep. So, the longer you sleep, the higher your T levels will be.

Recent studies have disclosed that testosterone production is at its peak during the REM stage of your sleep. Many physicians also suggest that for a healthy testosterone level, around seven to nine hours of sleep are required.

People who have problems regarding their sleep should consult a doctor, as they unconsciously face a significant problem.

Your T levels are also affected by many other factors. For example, healthier life is based upon the regulation of your sex hormones like testosterone.

Always try to stay away from some chemicals like endocrine disruptors, as they can spoil your hormones badly. Some of them are estrogens compounds that can adversely affect your T levels. So, try to maintain a distance from BPA, Parabens, and other chemicals.

They act as estrogen-rich elements, and your body may make mistakes in recognizing them due to their similar composition. They create disturbances in normal body functions. So, choose the products which do not have them.

It is a common fact that excessive alcohol and drug consumption may have several adverse effects on your health and, particularly, on your liver. But, does alcohol affect your T levels?

The answer is yes. When you consume alcohol and other similar drugs, your body requires a lot of time to break and process the alcohol. In this way, your system focuses mainly on this task ,which in turn, causes your liver to work more.

During this process, your liver does not get time to perform its other functions, like breaking down some hormones, including estrogen and testosterone. In other words, when you consume alcohol regularly, your testosterone levels are not the same as they are when you avoid alcohol.

Some men are still having a proper T level while consuming alcohol, but that is rare. If you want a normal and healthy T level, it should be your top concern to avoid alcohol and other drug supplements.

Even in just 30 days, you can get an average level of testosterone after quitting your alcohol and drug consumption. Proper T levels are an essential part of your health and well-being. Therefore, staying away from alcohol and drug consumption can be the easiest step to achieve such goals.

Mental health is something that should never be ignored. Talking about how it affects testosterone levels in the body, you might not believe us. But, if you are stressed out and mentally upset, your T-levels drop significantly low.

Do not hesitate to consult a psychiatrist whenever you feel like there is something troubling you and making you depressed. Always talk about your mental health with professionals, as it is not a thing to be ignored.

More to keep in mind is to constantly check the medications you are taking for other health problems. This is because they might contain any ingredient that promotes low T levels. This might not happen, but you should be careful and talk to your online therapist if you feel anything like that.

Testosterone is an important male sex hormone that promotes masculinity. It also facilitates many other body functions.

A lot of options are available in the market to boost your T levels, including many therapies, treatments, artificial supplements, and pills. But, the best way to do so is to follow or implement something natural.

In addition to following the simple tips we mentioned above, TestoPrime might help you a lot with getting your testosterone levels boosted up. It is associated with many extra health benefits regarding your heart, brain, and weight balance in addition to boosting T-levels.

However, if you are already on some kind of medication, or have a particular medical condition, make sure to consult your doctor before opting for any supplement.

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More:
9 Ways to Increase Testosterone Naturally in 2021 - Men's Journal

Recommendation and review posted by Bethany Smith

Its safe to say that before the development of the Pfizer-BioNTech and Moderna COVID-19 vaccines, most people hadnt thought about messenger RNA, or mRNA, since high school science classif ever. The molecule plays a pivotal role in the body, carrying the recipes for making various proteins to the parts of cells that produce them. But mRNA wasnt exactly a common phrase until Pfizer-BioNTech and Moderna harnessed the genetic materials power to teach the body to make a piece of a protein found on the COVID-19 virus surface, thus training it to fight the real thing, were it to attack.

The tremendous efficacy of mRNA-based COVID-19 vaccines has generated plenty of excitement about its potential use in vaccines for other diseases. And vaccines may be just the beginning. Last month, researchers used mRNA to deliver CRISPR gene-editing technology that could permanently treat a rare genetic disease in humansan advance that experts say has implications far beyond the treatment of a single condition.

Medical science research utilizing CRISPRa system that allows scientists to add, remove or change specific genetic information within the bodyhad already been advancing rapidly in recent years. Researchers have shown its potential for reversing blindness and sickle cell anemia, and to treat genetic diseases in animals. But new work described in the New England Journal of Medicine in June marks what researchers are calling the first time CRISPR has been shown to treat a genetic disorder when directly administered to human patients.

In this case, the technology was applied towards a therapy for transthyretin amyloidosis, a genetic disease that causes sufferers livers to produce a protein that eventually builds up to toxic levels. The diseases prevalence varies depending on patient demographicsit affects about one in 100,000 Americans of European descent, but as many as one in every 538 people in northern Portugal, for exampleand can be passed down to future generations. While there are drugs that can help patients manage the disease, the goal of the new research was to stop the problem at its source.

To imagine using [CRISPR] as a therapy for people, you need to figure out how to get these editing tools into the cells youre trying to fix. Thats where messenger RNA comes in, explains Daniel Anderson, a professor of chemical engineering at the Massachusetts Institute of Technology and a co-founder of CRISPR Therapeutics, which uses CRISPR technology to develop medications. Anderson was not involved in the research.

The research team, led by Dr. Julian Gillmore, an amyloidosis expert at the U.K.s Royal Free Hospital, programmed mRNA to deliver gene-editing instructions to the liver, shutting down the part responsible for producing the toxic protein. After a one-time injection of the drug, three of the six people in the trial saw an almost complete drop-off in protein production; the remaining three, who received a smaller dose, saw less dramatic results. It will take a few months to see if that accomplishment translates to symptom relief, but the early findings are promising. (The work was funded by pharmaceutical companies Intellia Therapeutics and Regeneron, which produce the injectable CRISPR drug.)

As Dr. John Leonard, Intellias president and CEO, puts it: mRNA is a way to make CRISPR gene editing come alive. CRISPR is the workhorse; mRNA encodes it.

In theory, the same general technology could be used to treat conditions beyond transthyretin amyloidosis. There are a host of diseases in the liver where this might work in an analogous manner, says Dr. Kenneth Chien, a senior professor of cardiology research at Swedens Karolinska Institutet and a co-founder of Moderna Therapeutics, who was not involved in the research. The most important aspect of this is the implications that the technology can be repurposed.

Chien has believed in mRNAs drug-development potential for more than a decade. When Moderna was founded in 2010, in fact, its chief goal was to develop mRNA-based drugs, not vaccines. (Chien no longer works at Moderna and is now an advisor to the pharmaceutical giant AstraZeneca.) He continues to work on an mRNA-based drug he hopes could eventually treat heart conditions.

The tricky part, Leonard says, is figuring out how to get a drug into different tissues, since the strategy for delivering CRISPR-based therapeutics varies depending on its target. The new research offers a blueprint for liver-based conditions, and Leonard believes similar approaches could be used in the near-term for bone-marrow, nervous-system and muscle diseases. The list theoretically grows from there, so long as researchers can fine-tune delivery.

COVID [vaccines are] a big success for mRNA, and if it does nothing else, its been great, Chien says. However, I think youre going to see the next chapter of mRNA is going to be as exciting, if not more so, than the story of mRNA vaccines.

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Write to Jamie Ducharme at jamie.ducharme@time.com.

More:
MRNA's Next Chapter Has Nothing to Do With COVID-19 Vaccines - TIME

Recommendation and review posted by Bethany Smith

- More than 45 patients have been dosed with CTX001 across CLIMB-Thal-111 and CLIMB-SCD-121 to date; completion of enrollment in both trials is expected in 2021-

-Received Orphan Drug Designation (ODD) for Phase 1 clinical trial of CTX130 for the treatment of T-cell lymphoma-

-Enrollment ongoing in CTX110, CTX120 and CTX130 clinical trials-

ZUG, Switzerland and CAMBRIDGE, Mass., July 29, 2021 (GLOBE NEWSWIRE) -- CRISPR Therapeutics(Nasdaq: CRSP), a biopharmaceutical company focused on creating transformative gene-based medicines for serious diseases, today reported financial results for the second quarter ended June 30, 2021.

We concluded an important quarter in which we reported notable data from our hemoglobinopathies program while rapidly advancing our entire clinical and pre-clinical portfolio and our capabilities, said Samarth Kulkarni, Ph.D., Chief Executive Officer of CRISPR Therapeutics. Updated clinical data on CTX001 presented at EHA demonstrate consistency and durability, further validating the promise of a functional cure for sickle cell disease and beta thalassemia. We expect to report clinical data from our immuno-oncology programs later this year, and to file multiple INDs for our regenerative medicine and in vivo programs in the next 18 to 24 months.In addition, we continue to expand our portfolio and access best-in-class capabilities through collaborations, such as those recently announced with Capsida Biotherapeutics and Nkarta Therapeutics.

Recent Highlights and Outlook

Second Quarter 2021 Financial Results

About CTX001CTX001 is an investigational, autologous, ex vivo CRISPR/Cas9 gene-edited therapy that is being evaluated for patients suffering from TDT or severe SCD, in which a patients hematopoietic stem cells are edited to produce high levels of fetal hemoglobin (HbF; hemoglobin F) in red blood cells. HbF is a form of the oxygen-carrying hemoglobin that is naturally present at birth, which then switches to the adult form of hemoglobin. The elevation of HbF by CTX001 has the potential to alleviate or eliminate transfusion requirements for patients with TDT and reduce or eliminate painful and debilitating sickle crises for patients with SCD. Earlier results from these ongoing trials were published as a Brief Report in The New England Journal of Medicine in January of 2021.

Based on progress in this program to date, CTX001 has been granted Regenerative Medicine Advanced Therapy (RMAT), Fast Track, Orphan Drug, and Rare Pediatric Disease designations from the U.S. Food and Drug Administration (FDA) for both TDT and SCD. CTX001 has also been granted Orphan Drug Designation from the European Commission, as well as Priority Medicines (PRIME) designation from the European Medicines Agency (EMA), for both TDT and SCD.

Among gene-editing approaches being investigated/evaluated for TDT and SCD, CTX001 is the furthest advanced in clinical development.

About the CRISPR-Vertex CollaborationVertex and CRISPR Therapeutics entered into a strategic research collaboration in 2015 focused on the use of CRISPR/Cas9 to discover and develop potential new treatments aimed at the underlying genetic causes of human disease. CTX001 represents the first potential treatment to emerge from the joint research program. Under a recently amended collaboration agreement, Vertex will lead global development, manufacturing and commercialization of CTX001 and split program costs and profits worldwide 60/40 with CRISPR Therapeutics.

About CLIMB-111The ongoing Phase 1/2 open-label trial, CLIMB-Thal-111, is designed to assess the safety and efficacy of a single dose of CTX001 in patients ages 12 to 35 with TDT. The trial will enroll up to 45 patients and follow patients for approximately two years after infusion. Each patient will be asked to participate in a long-term follow-up trial.

About CLIMB-121The ongoing Phase 1/2 open-label trial, CLIMB-SCD-121, is designed to assess the safety and efficacy of a single dose of CTX001 in patients ages 12 to 35 with severe SCD. The trial will enroll up to 45 patients and follow patients for approximately two years after infusion. Each patient will be asked to participate in a long-term follow-up trial.

About CLIMB-131This is a long-term, open-label trial to evaluate the safety and efficacy of CTX001 in patients who received CTX001 in CLIMB-111 or CLIMB-121. The trial is designed to follow participants for up to 15 years after CTX001 infusion.

About CTX110CTX110, a wholly owned program of CRISPR Therapeutics, is a healthy donor-derived gene-edited allogeneic CAR-T investigational therapy targeting cluster of differentiation 19, or CD19. CTX110 is being investigated in the ongoing CARBON trial.

About CARBONThe ongoing Phase 1 single-arm, multi-center, open label clinical trial, CARBON, is designed to assess the safety and efficacy of several dose levels of CTX110 for the treatment of relapsed or refractory B-cell malignancies.

About CTX120CTX120, a wholly-owned program of CRISPR Therapeutics, is a healthy donor-derived gene-edited allogeneic CAR-T investigational therapy targeting B-cell maturation antigen, or BCMA. CTX120 is being investigated in an ongoing Phase 1 single-arm, multi-center, open-label clinical trial designed to assess the safety and efficacy of several dose levels of CTX120 for the treatment of relapsed or refractory multiple myeloma. CTX120 has been granted Orphan Drug designation from the FDA.

About CTX130CTX130, a wholly-owned program of CRISPR Therapeutics, is a healthy donor-derived gene-edited allogeneic CAR-T investigational therapy targeting cluster of differentiation 70, or CD70, an antigen expressed on various solid tumors and hematologic malignancies. CTX130 is being developed for the treatment of both solid tumors, such as renal cell carcinoma, and T-cell and B-cell hematologic malignancies. CTX130 is being investigated in two ongoing independent Phase 1, single-arm, multi-center, open-label clinical trials that are designed to assess the safety and efficacy of several dose levels of CTX130 for the treatment of relapsed or refractory renal cell carcinoma and various subtypes of lymphoma, respectively.

About CRISPR TherapeuticsCRISPR Therapeutics is a leading gene editing company focused on developing transformative gene-based medicines for serious diseases using its proprietary CRISPR/Cas9 platform. CRISPR/Cas9 is a revolutionary gene editing technology that allows for precise, directed changes to genomic DNA. CRISPR Therapeutics has established a portfolio of therapeutic programs across a broad range of disease areas including hemoglobinopathies, oncology, regenerative medicine and rare diseases. To accelerate and expand its efforts, CRISPR Therapeutics has established strategic collaborations with leading companies including Bayer, Vertex Pharmaceuticals and ViaCyte, Inc. CRISPR Therapeutics AG is headquartered in Zug, Switzerland, with its wholly-owned U.S. subsidiary, CRISPR Therapeutics, Inc., and R&D operations based in Cambridge, Massachusetts, and business offices in San Francisco, California and London, United Kingdom. For more information, please visit http://www.crisprtx.com.

CRISPR THERAPEUTICS word mark and design logo, CTX001, CTX110, CTX120, and CTX130 are trademarks and registered trademarks of CRISPR Therapeutics AG. All other trademarks and registered trademarks are the property of their respective owners.

CRISPR Therapeutics Forward-Looking StatementThis press release may contain a number of forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, including statements made by Dr. Kulkarni in this press release, as well as statements regarding CRISPR Therapeutics expectations about any or all of the following: (i) the safety, efficacy and clinical progress of CRISPR Therapeutics various clinical programs, including CTX001, CTX110, CTX120 and CTX130; (ii) the status of clinical trials and preclinical studies (including, without limitation, the expected timing of data releases and development, as well as initiation and completion of clinical trials) and development timelines for CRISPR Therapeutics product candidates; (iii) the data that will be generated by ongoing and planned clinical trials, and the ability to use that data for the design and initiation of further clinical trials or to support regulatory filings, including expectations regarding the CTX001 data; (iv) the actual or potential benefits of regulatory designations; (v) the potential benefits of CRISPR Therapeutics collaborations and strategic partnerships; (vi) the intellectual property coverage and positions of CRISPR Therapeutics, its licensors and third parties as well as the status and potential outcome of proceedings involving any such intellectual property; (vii) the sufficiency of CRISPR Therapeutics cash resources; and (viii) the therapeutic value, development, and commercial potential of CRISPR/Cas9 gene editing technologies and therapies. Without limiting the foregoing, the words believes, anticipates, plans, expects and similar expressions are intended to identify forward-looking statements. You are cautioned that forward-looking statements are inherently uncertain. Although CRISPR Therapeutics believes that such statements are based on reasonable assumptions within the bounds of its knowledge of its business and operations, forward-looking statements are neither promises nor guarantees and they are necessarily subject to a high degree of uncertainty and risk. Actual performance and results may differ materially from those projected or suggested in the forward-looking statements due to various risks and uncertainties. These risks and uncertainties include, among others: the potential for initial and preliminary data from any clinical trial and initial data from a limited number of patients not to be indicative of final trial results; the potential that clinical trial results may not be favorable; that one or more of CRISPR Therapeutics internal or external product candidate programs will not proceed as planned for technical, scientific or commercial reasons; that future competitive or other market factors may adversely affect the commercial potential for CRISPR Therapeutics product candidates; uncertainties inherent in the initiation and completion of preclinical studies for CRISPR Therapeutics product candidates (including, without limitation, availability and timing of results and whether such results will be predictive of future results of the future trials); uncertainties about regulatory approvals to conduct trials or to market products; the potential impacts due to the coronavirus pandemic such as (x) delays in regulatory review, manufacturing and supply chain interruptions, adverse effects on healthcare systems and disruption of the global economy; (y) the timing and progress of clinical trials, preclinical studies and other research and development activities; and (z) the overall impact of the coronavirus pandemic on its business, financial condition and results of operations; uncertainties regarding the intellectual property protection for CRISPR Therapeutics technology and intellectual property belonging to third parties, and the outcome of proceedings (such as an interference, an opposition or a similar proceeding) involving all or any portion of such intellectual property; and those risks and uncertainties described under the heading "Risk Factors" in CRISPR Therapeutics most recent annual report on Form 10-K, quarterly report on Form 10-Q, and in any other subsequent filings made by CRISPR Therapeutics with the U.S. Securities and Exchange Commission, which are available on the SEC's website at http://www.sec.gov. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date they are made. CRISPR Therapeutics disclaims any obligation or undertaking to update or revise any forward-looking statements contained in this press release, other than to the extent required by law.

Investor Contact:Susan Kim+1-617-307-7503susan.kim@crisprtx.com

Media Contact:Rachel Eides+1-617-315-4493rachel.eides@crisprtx.com

CRISPR Therapeutics AGCondensed Consolidated Statements of Operations(Unaudited, In thousands except share data and per share data)

CRISPR Therapeutics AGCondensed Consolidated Balance Sheets Data(Unaudited, in thousands)

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CRISPR Therapeutics Provides Business Update and Reports - GlobeNewswire

Recommendation and review posted by Bethany Smith

CRISPR Therapeutics AG (CRSP) came out with quarterly earnings of $9.44 per share, beating the Zacks Consensus Estimate of $4.19 per share. This compares to loss of $1.30 per share a year ago. These figures are adjusted for non-recurring items.

This quarterly report represents an earnings surprise of 125.30%. A quarter ago, it was expected that this company would post a loss of $1.45 per share when it actually produced a loss of $1.51, delivering a surprise of -4.14%.

Over the last four quarters, the company has surpassed consensus EPS estimates just once.

CRISPR Therapeutics AG, which belongs to the Zacks Medical - Biomedical and Genetics industry, posted revenues of $900.7 million for the quarter ended June 2021, surpassing the Zacks Consensus Estimate by 32.84%. This compares to year-ago revenues of $0.04 million. The company has topped consensus revenue estimates just once over the last four quarters.

The sustainability of the stock's immediate price movement based on the recently-released numbers and future earnings expectations will mostly depend on management's commentary on the earnings call.

CRISPR Therapeutics AG shares have lost about 21.8% since the beginning of the year versus the S&P 500's gain of 17.2%.

What's Next for CRISPR Therapeutics AG?

While CRISPR Therapeutics AG has underperformed the market so far this year, the question that comes to investors' minds is: what's next for the stock?

There are no easy answers to this key question, but one reliable measure that can help investors address this is the company's earnings outlook. Not only does this include current consensus earnings expectations for the coming quarter(s), but also how these expectations have changed lately.

Empirical research shows a strong correlation between near-term stock movements and trends in earnings estimate revisions. Investors can track such revisions by themselves or rely on a tried-and-tested rating tool like the Zacks Rank, which has an impressive track record of harnessing the power of earnings estimate revisions.

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Ahead of this earnings release, the estimate revisions trend for CRISPR Therapeutics AG was unfavorable. While the magnitude and direction of estimate revisions could change following the company's just-released earnings report, the current status translates into a Zacks Rank #4 (Sell) for the stock. So, the shares are expected to underperform the market in the near future. You can see the complete list of today's Zacks #1 Rank (Strong Buy) stocks here.

It will be interesting to see how estimates for the coming quarters and current fiscal year change in the days ahead. The current consensus EPS estimate is -$0.38 on $4.29 million in revenues for the coming quarter and $0.66 on $457.55 million in revenues for the current fiscal year.

Investors should be mindful of the fact that the outlook for the industry can have a material impact on the performance of the stock as well. In terms of the Zacks Industry Rank, Medical - Biomedical and Genetics is currently in the bottom 21% of the 250 plus Zacks industries. Our research shows that the top 50% of the Zacks-ranked industries outperform the bottom 50% by a factor of more than 2 to 1.

Want the latest recommendations from Zacks Investment Research? Today, you can download 7 Best Stocks for the Next 30 Days. Click to get this free reportCRISPR Therapeutics AG (CRSP) : Free Stock Analysis ReportTo read this article on Zacks.com click here.Zacks Investment Research

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CRISPR Therapeutics AG (CRSP) Tops Q2 Earnings and Revenue Estimates - Yahoo Finance

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COLLEGE PARK, Md. -- With two new funding sources, Yiping Qi, associate professor in the Department of Plant Science & Landscape Architecture (PSLA) at the University of Maryland (UMD), continues his work to expand the reach and utility of CRISPR gene editing technologies. Funded by the United States Department of Agricultures National Institute of Food and Agriculture (USDA-NIFA), Qi and his team will be testing new delivery technologies for CRISPR-Cas12a to develop a pipeline for genome editing in carrots. This could lead to the production of more nutritious and hypoallergenic carrot varieties that can be quickly introduced into the marketplace. Additionally, Qi will continue his search for novel CRISPR-Cas12a variants with funding from the Maryland Innovation Initiative (MII), with the ultimate goal of finding more CRISPR tools that are optimized for crop production.

With this new USDA funding, we are excited to showcase CRISPR-Cas12a gene editing technologies that my lab has been working on in carrots as an important vegetable, says Qi. The major innovations in this work are really in the delivery mechanisms that can make targeted and precise edits without the production of a highly regulated GMO [genetically modified organism]. But we also want to explore more CRISPR-Cas12a variants that can be useful for crop production, so the MII grant provides that support.

As Qi explains, most current methods for targeted mutations or precise genome edits rely on the use of transgenes (transferring a gene from one organism to another) that would then be regulated as GMOs. This is typically done by delivering genetic material with agrobacteria used to infect the plants and transfer the desired trait. However, for carrots, Qi is testing different delivery methods that use readily available proteins and guiding molecules to deliver the same material without using agrobacteria and transgenes. This method is new to carrots, and would allow new varieties to make it to market much faster without the need for GMO regulations.

Hopefully, we can take advantage of these technologies to develop some interesting and useful plants that have consumer benefits, says Qi. For example, we are targeting a gene to help the carrot accumulate more beta carotene, which can boost nutritional value. We are also targeting two genes that can potentially be knocked out to create a hypoallergenic carrot that could be eaten by those with certain allergies.

These varieties could not only be useful in and of themselves, but the work will establish a process for genome editing in carrots that hasnt been previously developed. This will save substantial time over traditional breeding, and Qi hopes will inspire many researchers and breeders to consider the possibilities of this technology in crops like carrots.

The whole project is to develop new technology for genome editing in more niche or minor crops that can have major impacts, stresses Qi. Not much work has been previously done in carrots, and I hope this will open up a lot of doors for gene editing in other root vegetables and more.

In addition to this work with the known variants of CRISPR-Cas12a, Qi is continuing his search for novel variants that are optimal for crop genome editing. Qis recent work contributing six novel variants of CRISPR-Cas12a (never before proven in plants) was named UMD Life Sciences Innovation of the Year. These patent-pending tools widen the scope of what CRISPR-Cas12a can do in plants, which can help to produce food more effectively to fight hunger.

With new funding from MII, Qi will continue to explore new patentable CRISPR variants, hoping to find more tools that work efficiently at lower temperatures. For work in human cells, gene editing is happening at the temperature of the human body, which is almost 100 degrees Fahrenheit, says Qi. This is the optimal temperature for most CRISPR systems, but this isnt the best temperature for doing work in plants. All that work needs to be done around room temperature where plants can comfortably grow. So finding tools that are optimized for this lower temperature application is important for advancing genome editing in crops.

Qis team has established a proprietary pipeline for identifying new candidate CRISPR variants, and he will first test these candidates in rice and tomatoes to expand the scope of gene editing in crops.

This work is funded by the United States Department of Agricultures National Institute of Food and Agriculture (USDA-NIFA), Award #2021-67013-34554, and the Maryland Innovation Initiative (MII).

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UMD Research Aims To Develop A Genome Editing Pipeline In Carrots, Optimize Crop Production - Bay Net

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COLLEGE PARK, Md. (WJZ) A professor at the University of Maryland in College Park has received new funding from two sources to continue research into CRISPRgenomeeditingtechnologies, withthegoal of enhancing crop productionand feeding a growing global population, according to a university statement.

Yiping Qi, associate professor in the Department of Plant Science & Landscape Architecture, received the funds from the U.S. Department of Agricultures National Institute of Food and Agriculture to develop a pipelineforgenomeediting in carrots that could lead to more nutritious and hypoallergenic carrot varieties in stores. He also received funding from theMaryland Innovation Initiative to continue his search for novel CRISPR-Cas12 variants. That goal is to find more CRISPR tools that are optimized for crop production.

Qi is testing delivery methods that use readily available proteins and guiding molecules to deliver the same material most current methods for targeted mutations use, transferring a gene from organisms to another that would then be regulated as genetically modified organisms.

This method is new to carrots and would allow new varieties to make it to market more quickly without the need for GMO regulations, according to the statement.

With the MII funding, he will continue exploring new patentable CRISPR variants, hoping to find more tools that work efficiently at lower temperatures.

Qis team has established a proprietary pipeline for identifying new candidate CRISPR variants, and he will first test these candidates in rice and tomatoes to expand the scope of gene editing in crops.

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University Of Maryland Professor Gets New Funds To Continue Research To Enhance Crop Production - CBS Baltimore

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Its hard to put just one label on Aaron Ciechanover. He was awarded the Nobel Prize in Chemistry for characterizing the method that cells use to degrade and recycle proteins usingubiquitin, but his background stems from biology, and he was also trained as a medical doctor and a surgeon. When it comes to understanding the intricacies around human health, few people on Earth can claim the broad view that Ciechanover has.

Which is why, when he says hes excited about whats to come in medicine, its hard not to share his excitement.

The future of medicine is going to be revolutionary, Ciechanover said at the 2021 Lindau Nobel meeting, which took place online this year due to the pandemic. The meetings bring together Nobel laureates and young scientists to foster scientific exchange.

Back in the days when Ciechanover was studying medicine, he recalls, things were very different.

Lets say, if a patient had a tumor, we were not interested in the molecular mechanism that underlies the tumor development, because we did not have the tools to study it, he says.

The procedure was simplistic and straightforward. Doctors would look at the imaging facilities they had access to at the time (either X-ray, CT Scan, or MRI) and decide whether the tumor could be operated on. Surgery was generally the preferred procedure because the tumor mass could be extracted. If the tumor was too big or was touching essential organs, then doctors would try to decrease its size using chemotherapy or radiation, and then try surgery.

But these were (and still are) very harsh measures, with harsh side effects.

They are like shooting a fly with a cannon. They are not discriminating between the healthy tissue and the sick tissue, they are very difficult to direct, Ciechanover explains.

Then, at the turn of the century, a revolution started unfolding. In 2000, a landmark paper published in the journal Nature opened the floodgates of genetic discovery.

I remember it very well, this exciting day when Nature magazine came out with the first human genome. The first human genome gave us the information, the library of what we are made of. This was really the very beginning, but the last 20 years have seen enormous progress. We are now able to diagnose the disease much better [..] and we are able to analyze tumors or any other disease at the molecular level.

Heres a sense of how much things have progressed. The price of whole human genome sequencing was around $2.7 billion in 2003. Today, its under $100. Advancements in technology and decrease in price has made genetic and molecular analyses more widely available, and its not about to stop.

We are developing dedicated tools to stop the tumor or the disease at large, with a very gentle tool directing a bullet direction at the underlying mechanism, Ciechanover adds.

Even with conventional medicine, healthcare has benefited tremendously. Things like imaging, antibiotics, vaccines, operating procedures, and so on, have made a tremendous difference in how we treat patients. But now we are into a much bigger revolution, Ciechanover believes. He foresees a future where the very definition of medicine will change. Finally, we will start treating patients, not diseases, and patients will receive individualized treatments.

Tasuku Honjo is also optimistic. He believes that while cancer wont be eradicated anytime soon, theres a good chance well be able to keep most cancers in check.

Honjo should know. He and his colleagues discovered a molecule called programmed cell death protein 1 (PD-1). They also showed that this molecule functions as a sort of braking system for acquired immunity making sure that your immune system doesnt go into overdrive and cause autoimmune disease. But too much PD-1, and the immune system would not do its job properly.

For instance, several tumors produce something similar to PD-1, which helps the tumors escape the immune system. But if PD-1 could be suppressed in cancer patients, then we could use peoples own immune systems to fight cancer. This is exactly what Honjo says can help keep cancers in check.

Honjo and colleagues found that blocking PD-1 in mice can cure tumors by reactivating acquired immunity in 2002. Then, in a landmark moment in 2014, the treatment of cancer in humans by PD-1 blockade was approved by regulatory bodies in Japan and the USA. Now, there are over 1,000 clinical trials happening in the world, and PD-1 treatments seem to be effective against a wide variety of cancers, with long-lasting positive effects.

Another Nobel-winning discovery that could help our fight against cancer is CRISPR/Cas9.

CRISPR is becoming a mainstream methodology used in many cancer biology studies because of the convenience of the technique, says Jerry Li of NCIsDivision of Cancer Biology.

CRISPR is a relatively simple but very powerful and accurate way to edit genes. It was inspired by nature, from a defense mechanism some bacteria use to protect themselves against viral invasions. The bacterium captures snippets of any virus intruders DNA and stores it as segments called CRISPRs. If the same virus returns and tries to attack again, the bacterium searches its DNA library and releases an enzyme called Cas to slice up the invaders DNA.

Gene editing is not new, ProfessorEmmanuelle Charpentier, one of the pioneers behind CRISPR explained at the Lindau Nobel meeting. But thanks to the work of Charpentier and Jennifer Doudna, who were awarded the 2020 Nobel Prize, we have access to unprecedented tools.

The first CRISPR cancer therapy was launched in 2019. The goal of the study is to edit patients own immune cells to better detect and kill cancer. The treatment is safe, and early results are encouraging but CRISPR is still just getting warmed up.

This [trial] was really a proof-of-principle, feasibility, and safety thing that now opens up the whole world of CRISPR editing and other techniques of [gene] editing to hopefully make the next generation of therapies, said Edward Stadtmauer, M.D., of the University of Pennsylvania, who is involved with the research.

Weve come a long way in our fight against cancer in the past half-century, but despite improving diagnosis and treatments, theres still more work to be done if we want to keep cancer in check. But the tools we need to do so are now coming in.

With approaches like CRISPR or PD-1, researchers can develop customized, efficient treatments with few side effects. Thanks to the likes of Honjo, Charpentier, and Ciechanover, we are witnessing a new revolution of medicine, and its hard not to share their enthusiasm for whats to come.

Its still early days and there are plenty of hurdles to be overcome, but the science is progressing in leaps and bounds. It may not be today or tomorrow, but were gathering the weapons to fight cancer and its shaping up to be a big arsenal.

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A revolution against cancer is unfolding and were just getting started - ZME Science

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August2, 20215 min read

Opinions expressed by Entrepreneur contributors are their own.

A healthy spine must be strong enough to support your entire body, yet flexible enough to allow you to move your limbs. Thats why your spine isnt just one bone, but an intricately designed set of smaller bones called vertebrae each separated by a disc of cartilage.

These discs cushion each vertebra, so they dont grind against each other and cause pain. When degenerative disc disorders set in, however, these cushions wear out. But patients can now take advantage of advanced stem-cell therapy that can heal disc tissue and reduce inflammation, alleviate chronic pain and restore flexibility and range of motion.

While surgery and medications may be treatment options, surgical procedures can be risky and many patients cannot tolerate the side effects of many medications.

Related:This Is HowStem-CellTherapy Treats Serious Brain Injuries

Thats why more patients choose stem-cell therapy a procedure that takes advantage of the bodys natural healing processes. Discover how stem-cell therapy can help you heal more quickly and enjoy a more active lifestylewith less pain.

Advanced stem-cell treatments can help a range of issues:

Another remarkable aspect of the human body is that it actually knows how to heal itself, which is why the latest advancements in stem-cell therapy offerhope to more patients to relieve pain without the need for surgery or medications that can lead to serious side effects.

Because stem cells that come from your bone marrow have the potential to become any type of cell, the body turns those stem cells into specific cells needed to heal various tissues. If you burn your skin, for example, stem cells are turned into new skin cells. If youve injured a muscle, your body uses stem cells to regenerate muscle tissue. And as discs deteriorate, your body can use stem cells to create new disc tissue to rehydrate those discs and return them to a normal shape easing pain and inflammation.

Unfortunately, stem-cell production begins to decline as we age. But with an infusion of millions of fresh new stem cells, the body can use those cells to quickly stimulate healing without the need to go under the knife or risk serious side effects from steroids or the consequences of using addictive pain killers.

Related:Former Quarterback Jim McMahon Calls AdvancedStem-CellTreatment 'Truly Miraculous'

At BioXcellerator, we treat many patients for conditions like these with exceptional results often within days and even more ongoing improvement in the months and years following treatment.

For example, we treated Superbowl champion Mark May, who told us that he noticed improvement in just one day. I feel better. My neck feels a lot better and thats only after 24 hours, May said. Im shockingly surprised about how well its gone so far.

He also said that the first night after his treatment was the first he'd slept in once place in many years.

And army veteran and WWF Hall of Famer Kevin Nash let us know that his stem-cell therapy was a life-changing experience. He said that hes suffered from chronic pain for many years, but the very day after treatment said that when he was walking, I probably passed 300 people. Its the fastest Ive probably walked since I was 30 and that was 30 years ago.

Not only that, butafter two months of stem-cell therapy, he also reported the alleviation of his 24/7 pain.

These are only a few examples of the exceptional results stem cells can offer patients with disorders and injuries in the back and the neck. But its important to realize that the stem cells that various clinics offer can vary widely in quantity and potency. Stem cells derived from the placenta or umbilical cord are considered the gold standard and are rarely available in clinics located in the United States.

Our research team has developed a proprietary protocol for harvesting and reproducing only the most potent stem cells possible. Starting with a specific type of stem cell mesenchymal stem cells (MSCs) from donated umbilical cordswe then test these cells for specific proteins and genes that indicate the highest potential to reduce inflammation and stimulate healing. Then, those cells are reproduced into formulations of millions of high-potency stem cells called Golden Cells for infusion into patients during treatment.

Related:High-Potency 'Golden Cells' Offer Hope to Those With Severe Brain Injuries

In addition to promoting healing of damaged discs, stem-cell therapy can also be an effective treatment for other spinal injuries and diseases, brain injuriesand many other conditions. And one common treatment benefit is that because stem cells help the body better modulate the immune system and have powerful anti-inflammatory properties, stem-cell therapy helps improve immunity, performance and longevity.

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High-Potency 'Golden Cells' Offer Hope to Those With Severe Chronic Back and Neck Pain - Entrepreneur

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Colin Ray Jackson, CBE, 54, is a Welsh former sprinter and hurdling Olympic silver medal champion. Colins world record for his 60 metres hurdles stood for an incredible 27 years. As with most athletes of his calibre, Colin suffers with ongoing injuries from his sports days and will be undergoing a treatment to reduce the pain which Mike Tyson recently underwent too.

In recent years, stem cell therapy has been hailed as a miracle cure for many conditions, from wrinkles to spinal repair.

A stem cell is an immature, basic cell that has not yet developed to become, say, a skin cell or a muscle cell or a nerve cell.

There are different types of stem cells that the body can use for different purposes.

There is evidence that stem cell treatments work by triggering damaged tissues in the body to repair themselves, often referred to as regenerative therapy.

In animal studies, stem cell treatments have shown promise for various diseases, including heart disease, Parkinsons disease and muscular dystrophy.

A study undertaken by Dr Timothy McGuine found that 34 percent of athletes involved in the one-year study were more likely to report a history of knee and hip injuries.

Additionally, he found that specialised athletes, such as those competing in the Olympic games, were twice as likely to sustain a gradual onset or repetitive use injuries than athletes who did not specialise.

Dr McGuine also found that these athletes who find themselves competing year-round, stressing the same muscles and movements, and predisposed to the symptoms of burnout are at higher risk of long-term injuries.

Many doctors and athletes use stem cell therapy to treat sports injuries, such as Achilles tendinopathy or damaged knee ligaments, said Sports Health.

The site continued: While increasing in popularity, stem cell therapy is not considered standard practice by sports medicine doctors and not covered by most insurance companies.

The process of collecting stem cells is often called harvesting. Physicians usually harvest stem cells from the patients fat, blood, or bone marrow.

Many physicians who use stem cell therapy hypothesize that, when placed into a certain environment, stem cells can transform to meet a certain need.

Other sports stars who underwent stem cell therapy for long-term injuries included Cristiano Ronaldo, Rafael Nadal and most recently Mike Tyson.

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Colin Jackson health: Im in constant pain Athlete to undergo stem cell therapy to help - Express

Recommendation and review posted by Bethany Smith

SOUTH SAN FRANCISCO, Calif.--(BUSINESS WIRE)--Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY), today announced that the U.S. Food and Drug Administration (FDA) has accepted the companys supplemental Biologics License Application (sBLA) and granted Priority Review for Tecentriq (atezolizumab) as adjuvant treatment following surgery and platinum-based chemotherapy for people with non-small cell lung cancer (NSCLC) whose tumors express PD-L11%, as determined by an FDA-approved test. The FDA is reviewing the application under the Real-Time Oncology Review pilot program, which aims to explore a more efficient review process to ensure safe and effective treatments are available to patients as early as possible. The FDA is expected to make a decision on approval by December 1, 2021.

New treatment options are urgently needed in early-stage non-small cell lung cancer to help the nearly 50% of people who currently experience a recurrence following surgery, said Levi Garraway, M.D., Ph.D., chief medical officer and head of Global Product Development. Tecentriq is the first cancer immunotherapy to show a clinically meaningful benefit in the adjuvant lung cancer setting, and were working closely with the FDA to bring this significant advancement to patients as quickly as possible.

This application is based on disease-free survival (DFS) results from an interim analysis of the Phase III IMpower010 study, the first and only Phase III study of a cancer immunotherapy to demonstrate positive results in the adjuvant lung cancer setting. The study showed that treatment with Tecentriq following surgery and platinum-based chemotherapy reduced the risk of disease recurrence or death (DFS) by 34% (hazard ratio [HR]=0.66, 95% CI: 0.50-0.88) in people with Stage II-IIIA NSCLC whose tumors express PD-L11%, compared with best supportive care (BSC). In this population, median DFS was not yet reached for Tecentriq compared with 35.3 months for BSC. Follow-up on the IMpower010 trial will continue with planned analyses of DFS in the overall intent-to-treat (ITT) population, including Stage IB patients, which at the time of analysis did not cross the threshold, and overall survival (OS) data, which were immature at the time of interim analysis. Safety data for Tecentriq were consistent with its known safety profile and no new safety signals were identified. Results from the IMpower010 trial were presented at the 2021 ASCO Annual Meeting.

About the IMpower010 study

IMpower010 is a Phase III, global, multicenter, open-label, randomized study evaluating the efficacy and safety of Tecentriq compared with BSC, in participants with Stage IB-IIIA NSCLC (UICC 7th edition), following surgical resection and up to 4 cycles of adjuvant cisplatin-based chemotherapy. The study randomized 1,005 people with a ratio of 1:1 to receive either Tecentriq (up to 16 cycles) or BSC. The primary endpoint is investigator-determined DFS in the PD-L1-positive Stage II-IIIA, all randomized Stage II-IIIA and ITT Stage IB-IIIA populations. Key secondary endpoints include OS in the overall study population, ITT Stage IB-IIIA NSCLC.

About lung cancer

According to the American Cancer Society, it is estimated that more than 235,000 Americans will be diagnosed with lung cancer in 2021, and NSCLC accounts for 80-85% of all lung cancers. Today, about half of all people with early lung cancer still experience a cancer recurrence following surgery, but treating lung cancer early, before it has spread, may help prevent the disease from returning and provide people with the best opportunity for a cure.

About Tecentriq (atezolizumab)

Tecentriq is a monoclonal antibody designed to bind with a protein called PD-L1. Tecentriq is designed to bind to PD-L1 expressed on tumor cells and tumor-infiltrating immune cells, blocking its interactions with both PD-1 and B7.1 receptors. By inhibiting PD-L1, Tecentriq may enable the re-activation of T cells. Tecentriq may also affect normal cells.

Tecentriq U.S. Indications

Tecentriq is a prescription medicine used to treat adults with:

A type of lung cancer called non-small cell lung cancer (NSCLC).

A type of lung cancer called small cell lung cancer (SCLC).

It is not known if Tecentriq is safe and effective in children.

Important Safety Information

What is the most important information about Tecentriq?

Tecentriq can cause the immune system to attack normal organs and tissues in any area of the body and can affect the way they work. These problems can sometimes become severe or life threatening and can lead to death. Patients can have more than one of these problems at the same time. These problems may happen anytime during their treatment or even after their treatment has ended.

Patients should call or see their healthcare provider right away if they develop any new or worse signs or symptoms, including:

Lung problems

Intestinal problems

Liver problems

Hormone gland problems

Kidney problems

Skin problems

Problems can also happen in other organs.

These are not all of the signs and symptoms of immune system problems that can happen with Tecentriq. Patients should call or see their healthcare provider right away for any new or worse signs or symptoms, including:

Infusion reactions that can sometimes be severe or life-threatening. Signs and symptoms of infusion reactions may include:

Complications, including graft-versus-host disease (GVHD), in people who have received a bone marrow (stem cell) transplant that uses donor stem cells (allogeneic). These complications can be serious and can lead to death. These complications may happen if patients undergo transplantation either before or after being treated with Tecentriq. A healthcare provider will monitor for these complications.

Getting medical treatment right away may help keep these problems from becoming more serious. A healthcare provider will check patients for these problems during their treatment with Tecentriq. A healthcare provider may treat patients with corticosteroid or hormone replacement medicines. A healthcare provider may also need to delay or completely stop treatment with Tecentriq if patients have severe side effects.

Before receiving Tecentriq, patients should tell their healthcare provider about all of their medical conditions, including if they:

Patients should tell their healthcare provider about all the medicines they take, including prescription and over-the-counter medicines, vitamins, and herbal supplements.

The most common side effects of Tecentriq when used alone include:

The most common side effects of Tecentriq when used in lung cancer with other anti-cancer medicines include:

Tecentriq may cause fertility problems in females, which may affect the ability to have children. Patients should talk to their healthcare provider if they have concerns about fertility.

These are not all the possible side effects of Tecentriq. Patients should ask their healthcare provider or pharmacist for more information about the benefits and side effects of Tecentriq.

Report side effects to the FDA at 1-800-FDA-1088 or http://www.fda.gov/medwatch.

Report side effects to Genentech at 1-888-835-2555.

Please see http://www.Tecentriq.com for full Prescribing Information and additional Important Safety Information.

About Genentech in cancer immunotherapy

Genentech has been developing medicines to redefine treatment in oncology for more than 35 years, and today, realizing the full potential of cancer immunotherapy is a major area of focus. With more than 20 immunotherapy molecules in development, Genentech is investigating the potential benefits of immunotherapy alone, and in combination with various chemotherapies, targeted therapies and other immunotherapies with the goal of providing each person with a treatment tailored to harness their own unique immune system.

In addition to Genentechs approved PD-L1 checkpoint inhibitor, the companys broad cancer immunotherapy pipeline includes other checkpoint inhibitors, individualized neoantigen therapies and T cell bispecific antibodies. For more information visit http://www.gene.com/cancer-immunotherapy.

About Genentech in lung cancer

Lung cancer is a major area of focus and investment for Genentech, and we are committed to developing new approaches, medicines and tests that can help people with this deadly disease. Our goal is to provide an effective treatment option for every person diagnosed with lung cancer. We currently have five approved medicines to treat certain kinds of lung cancer and more than 10 medicines being developed to target the most common genetic drivers of lung cancer or to boost the immune system to combat the disease.

About Genentech

Founded more than 40 years ago, Genentech is a leading biotechnology company that discovers, develops, manufactures and commercializes medicines to treat patients with serious and life-threatening medical conditions. The company, a member of the Roche Group, has headquarters in South San Francisco, California. For additional information about the company, please visit http://www.gene.com.

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FDA Grants Priority Review to Genentech's Tecentriq as Adjuvant Treatment for Certain People With Early Non-small Cell Lung Cancer - Business Wire

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The day before he was euthanized by veterinarians in March of 2018, Sudan collapsed in the dirt at the Ol Pejeta Conservancy in Kenya, where he had lived since 2009. He was worn out and in pain.

At age 45, Sudan was the final progenitor of the earths most endangered animal species: the northern white rhinoceros. As the last male northern white in the world, he was both a global icon for conservation and a two-and-a-half-ton targetbecause the horn of even the most precious rhino is not safe from poachers. He lived out his final years under 24/7 armed protection at the conservancy, along with two of his female relatives.

Half a world away, Barbara Durrant felt it. She had never met Sudan, but she knew Nola. Most people in San Diego knew Nola, though not the way Durrant did. Nola was a northern white rhinoceros, one of only four that remained by the middle of the last decade, along with Sudan and his kin. She lived at the Nikita Kahn Rhino Rescue Center, located at the San Diego Zoo Safari Park, about 30 miles north of the city, and not far from where Durrant reports to work every day at the zoos Wildlife Biodiversity Bank.

Nola had also been euthanized, after age and infection caught up with her, in 2015. She was 41.

She was just the most amazing animal, says Durrant, recalling Nolas wide mouth, her skin the color of clay stone, and her distinctive horn, which curved toward the ground. Its not only losing that animal that you know personally and you love; its another step in losing the whole species.

Damon Casarez

Durrant is director of reproductive sciences at the San Diego Zoo Wildlife Alliance and one of a handful of scientists around the world who are trying to save the northern white rhino. In Europe, another group, under the direction of wildlife researcher Thomas Hildebrandt, is also working on the problem. And while their scientific approaches may be slightly divergent, the scientists end goal is the same: to rescue the northern white rhino before the bell of extinction rings.

Hildebrandt is the project head for BioRescue, an international consortium of scientists and conservationists. His group is harvesting eggs from female rhinos in Kenya; eventually the team hopes to create embryos using the frozen sperm of long-deceased northern white rhino males.

Meanwhile, Durrants team in San Diego is undertaking an ambitious bioengineering challenge. Inside the Wildlife Biodiversity Bank is the Frozen Zoo, a cryopreserve where 10,000 still-living skin cells from 1,100 different animal species are stored in tanks of liquid nitrogen at extremely low temperatures. Among them are 12 cell lines taken from 12 different northern white rhinos, dating back to 1979.

The Frozen Zoo is a cryopreserve where 10,000 still-living skin cells from 1,100 different animal species are stored in tanks of liquid nitrogen.

As recently as two decades ago, the next step amounted to the stuff of science fiction: taking those skin cells, reprogramming them into sperm and egg, combining them in a test tube, and then implanting that embryo into a surrogate host. Recreating a whole new northern white rhino. And then another, and another, and then, once nature took its course, dozens more. Breathing life back into that which is dead. De-extinction, in other words, the purposeful resurrection of animals that have died off. Animals like Sudan.

People are seeing a species go extinct right before their eyes, says Durrant. Can we really even make a dent? The answer is, well, we have to. We have to do this.

Astronomical costs and enormous risks stand in the way. An investment of at least $20 million is required to realize the ultimate goal of reconstituting a population of wild northern white rhinoceroses. Retrieving oocytes (eggs) is a delicate endeavor, because if scientists puncture blood vessels near the uterus, the animal will bleed to death. And preserving a species through bioengineering is a fraught, messy process, one that calls into question the sophistication of current reproduction techniques and the merits of meddling with nature.

If the project succeeds, it would be a scientific breakthrough like no other. What was once outside the realm of possibility is almost within our grasp. At some point in the not-too-distant future, a rhinoceros calfa cultivated northern whitemay very well take its first steps.

Ann and Steve Toon / Alamy Stock Photo

Of the worlds five rhino species, the northern whiteone of two subspecies of white rhinosdrew the short straw. Northern whites once roamed East and Central Africa, enjoying an herbivorous lifestyle with few natural predators. Humans prized them for their horns, which can grow over four feet. In Europe circa 1900, rhino horn was fashioned into ornamental accoutrements, like walking sticks and pistol grips. It remains a common ingredient in traditional Chinese medicine, which prescribes powdered rhino horn mixed with boiling water as a cure for fever, gout, and rheumatism.

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Poaching and war rapidly thinned their numbers, from the thousands to the hundreds to the tens. Nola arrived in San Diego in 1989; by the end of that decade, fewer than 40 northern whites remained in the northeast corner of what is today the Democratic Republic of the Congo. The last northern white was spotted in the wild in 2006. By then, the only survivors were those that had been relocated to zoos in the 1970s. They included Sudan, his daughter, Najin, her daughter, Fatu, and another bull, Suni, who were all taken to Kenyas Ol Pejeta Conservancy in 2009. They were the eligible breeders, yet no calves were born. Suni died four years before Sudan.

Four became three, then three became two, and now only Najin and Fatu remain. They are old and getting older, and even if they could mate, veterinarians have determined that neither is capable of carrying a pregnancy to term. Its a foregone conclusion then, yes? The line of northern white rhinos dies with Najin and Fatu.

TONY KARUMBAGetty Images

Sometimes we feel kind of helpless, says Durrant. Were battling such a huge wave of extinction.

Southern white rhinos, on the other hand, largely escaped their cousins misfortune. There were fewer than 100 remaining in the late 1800s, but a tenacious conservation effort followed and continues today. More than 20,000 of these rhinos currently roam the earth, mostly in South Africa. The San Diego Zoo Wildlife Alliance has six females, which will play a crucial role in its effort to produce a pure northern white rhino. Summarizing the idea is easy enough: An embryo made of northern white sperm and egg is implanted into a surrogatea female southern white rhino. Sixteen months later, a northern white calf is born.

I can say pretty clearly that this would be the first time a robot has ever been used in animals like this.

Durrant and her colleagues have already cleared several hurdles in the past five years. Using ultrasound technology, the team deciphered the inner workings of the rhinos reproductive system. Mapping the cervix was a key first step. A rhino cervix is a tight, convoluted maze of rings, a foot of anatomy thats fairly common to the two subspecies. Navigating it can be tricky. To practice, the zoo artificially inseminated two southern white females in 2018 using preserved southern white male sperm. Two healthy calves, Edward and Future, were born in 2019.

Damon Casarez

When female rhinos are ovulating, circulating estrogen helps relax the rings of the cervical tissue. For that reason, Durrant and her team were able to inseminate the zoos rhinos by hand. The future embryo transfer, however, will be much tougher. Once the team has produced a viable pure northern white rhino embryo, they will stimulate ovulation in one of the southern white rhinos residing at the Safari Park. Then theyll have to wait another 10 days to let the embryo mature in vitro before implantation. But the surrogates estrogen levels will have decreased by then, causing her cervix to tighten once more. Navigating it by hand will be impossible, because the risk of severely damaging cervical tissue is too great. Instead, Durrant and her team are currently collaborating with roboticists at the University of California San Diego to develop a workaround.

I can say pretty clearly that this would be the first time a robot has ever really been used in animals in any kind of major computation effort like this, says Michael Yip, a professor of electrical and computer engineering at UCSD and director of the Advanced Robotics and Controls Laboratory.

Courtesy UCSD Jacobs School of Engineering

Yips lab is outfitting a noodlelike catheter with miniaturized robotic controls. Imagine a tiny metal cylinder, thinner than the circumference of a headphone jack and sheathed in a flexible filament. A camera on one end will give zoo workers a view of where theyre going, while a PlayStation-like controller will bend the catheter with sub-millimeter precisionenough to ensure that they can navigate the rings without scraping tissue or puncturing blood vessels.

Well do very little, if any, tissue damage, but well be able to get through that tightened-down cervix, Durrant says.

In March 2020, Durrant completed the zoos first oocyte pickups. Because the scientists had already done the ultrasound mapping, they had a clear idea of where the ovaries and follicles were located.

Eggs were collected from each of their six southern white females using a four-foot-long double-lumen (two channeled) needle, which is capable of flushing out the follicles and sucking out the oocytes. They collected a total of 22; in the lab, each oocyte was fertilized with a single sperm. In the end, while half of the fertilized oocytes matured, none developed into blastocysts, the final stage of embryo growth. But the effort allowed the researchers to start piecing together some novel rhino science: What nutrients do rhino embryos need, in vitro, to mature?

This was a critical juncture in the teams de-extinction work, as valuable practice for the fertilization procedure to come. You dont transfer an embryo on the initial try. Fail to navigate the cervical maze, and you might damage tissue, imperiling the pregnancy. Fail to mature a reprogrammed egg into a blastocyst, and theres no embryo to even transfer. Everything Durrants team has done with southern whites is a dress rehearsal for the premiere event, when it finally comes time to make a southern white female the surrogate mother of the main character: a northern white rhino embryo.

Damon Casarez

Damon Casarez

The task of generating the sperm and egg falls to the San Diego Zoo Wildlife Alliances Marisa Korody, a conservation geneticist who is trying to create stem cells from the functionally extinct northern white rhinos. She starts with cryopreserved fibroblasts, cells that compose the connective structural tissue of all animals. The Frozen Zoo has fibroblasts generated from skin samples of 12 different northern whiteseight of which are unrelatedthat contain enough genetic diversity to save the species. These fibroblasts are then reprogrammed into induced pluripotent stem cellsthat is, cells that can turn into any cell type in the body. By directing these stem cells to specific developmental paths, the researchers can generate primordial germ cells, precursors to what eventually become sperm and eggs.

This is as far as the science goesat least for now, and at least with rhinos. Korody is optimistic shes managed to generate the germ cells. Generating northern white rhino sperm and northern white rhino egg, though, is a long-term process, one that involves figuring out the hormones and growth signals needed to get the germ cells to differentiate further.

Maybe in 10 years or so, well be close, she says.

Damon Casarez

Its a different strategy from the one Thomas Hildebrandt and BioRescue are focused on right now. While the team in San Diego is trying to generate northern white rhino embryos from cells, BioRescue is attempting to fertilize eggs collected from Fatu and Najin with cryopreserved northern white rhino sperm.

We can use this approach to transfer the embryos into a southern white rhino surrogate, and then let the calf grow up with Najin and Fatu, says Hildebrandt, who also leads the department of reproduction management at the Leibniz Institute for Zoo and Wildlife Research in Germany.

In 2019, Hildebrandts team accomplished a scientific first: It transferred a rhino embryo fertilized in vitro into the uterus of a female rhino. In this case, it was a southern white. As of July 2021, BioRescue has completed seven southern white rhino embryo transfers.

In the next few years, Hildebrandt says, BioRescue will be ready to transfer a northern white rhino embryo into a surrogate southern white female.

In the 55-million-year evolutionary history of the rhino, 10 years is nothing but a heartbeat. In the here and now, however, a decade is enough time to exacerbate an annihilation crisis thats already underway.

In 2019, a landmark report from the United Nations revealed that a million animal and plant species are careening toward extinction. A subsequent report issued by the World Wildlife Fund in 2020 indicated that wildlife populations have declined by two-thirds in the past half century due to human activities; deforestation, insecticides, and poaching are all complicit. Various species we hardly think of but are nonetheless important for humans and ecosystems to thrive are in the crosshairs.

If we can think of this as a leaky bucket right now, the bucket is pouring out water and more and more species are falling out, says Tierra Curry, a senior scientist with the nonprofit Center for Biological Diversity, based in Arizona. Trying to put a couple more species back in the bucket isnt going to fix the problem.

Criticism of de-extinction efforts often begins with something like Currys premise. Her preference would be to fight like hell for everything still alive. After all, the natural world is at the brink, but animals arent the problem.

Instead, the ultimate problem is uniquely and definitely humans, says Ross MacPhee, a curator in the mammalogy department of the American Museum of Natural History in New York City. Theres no way to guarantee that a population of northern white rhinos wouldnt need around-the-clock protection the way Najin and Fatu do today. Southern white rhinos, despite their resurgence, are already considered a species on the way to endangered, as lust for rhino horn continues unabated. Some horns fetch a purse of $300,000. How much might a rare northern white rhino horn go for?

While the San Diego Zoo Wildlife Alliance hopes to generate a self-sustaining population of northern white rhinos back in part of their native range, Durrant says that would only happen if its safe to put the animals there. But not making the effort isnt an option, she says.

Everything is connected, says Durrant. When you take any species, plant or animal, out of an ecosystem, it starts to unravel.

As it stands now, most of the African species of rhinosthe southern white and black rhinosare concentrated mainly in southern Africa. Very few black rhinos are roaming around central Africa where northern white rhinos once predominated: The pointed mouth of the black rhino is good for eating branches and leaves, while the wide mouth of the white rhino is better adapted for grazing on grass.

Scientists keenly interested in saving the northern white rhino often cite the good that such a keystone species provides. A megafauna creature like the white rhino directly and indirectly affects the well-being of dozens of other creatures. By eating long grass, they help keep vegetation at a reasonable level so predators can see their prey. Their feet carve avenues in the grass so prey can escape. Their droppings fertilize the grass and provide nutrients for insects. Its a tiny biosphere where nonhuman life thrives. Upset the balance, and that life has to migrate elsewhere. Maybe to urban ecosystems. Maybe carrying disease.

Damon Casarez

Under any other circumstances, a group of people kneeling around Fatu inside the Ol Pejeta Conservancy would be a cause for concern. But on this Sunday in December 2020, the scientists and veterinarians in attendance were monitoring Fatu as she lay under general anesthesia. Near her backside was Hildebrandt. He was collecting eggs.

Over the past two years, with the permission of the Kenyan government, Hildebrandt and BioRescue have performed six separate egg pickups on Najin and Fatu. The latest one, in December 2020, yielded 14 oocytes from Fatu. Collection is done by anesthetizing the rhino and then inserting an ultrasound wand into the rectum. The wand is there only to provide a picture, a way to guide the needle that flushes out the rhinos follicles and grabs the eggs. Both times the eggs were rapidly transported to Avantea, an advanced biotechnology lab in Italy. There they were fertilized with frozen semen that had been extracted from Suni before he died. To date, BioRescue has cryopreserved nine embryos that combine northern white sperm and northern white egg.

The rhino hasnt failed in evolution. Its at the brink of extinction because humans have poached it and killed it.

Its a monumental step, one that represents the closest any group of scientists has come to bringing a northern white rhino calf into the world. Hildebrandt doesnt just consider it fascinating science; he likens it to a moral imperative. Picking and choosing which animals to de-extinct is easy when nature hasnt selected against them.

The rhino hasnt failed in evolution. Its at the brink of extinction because humans have poached it and killed it, he says. So it is actually our human responsibility to fix this problem, because we have caused it.

Courtesy Leibniz Institute for Zoo and Wildlife Research

While BioRescues current endeavor is separate from the work being conducted by Durrant, Korody, and others at the San Diego Zoo Wildlife Alliance, the two groups are working toward common goals. Hildebrandt and his counterparts in San Diego held the first international conference on rescuing the northern white rhino in 2015 in Vienna. He says the work being conducted on pluripotent stem cells in San Diego is an important component of the overall effort. BioRescue has created embryos made with eggs from Najin and Fatu and sperm from Suni; the embryos the San Diego team hopes to create will come from multiple other northern white rhinos, which will increase the genetic diversity of a future population. In turn, that should help improve the animals overall health by serving as a safeguard against disease.

Yet Hildebrandt wants to bring a baby northern white rhino into the world as quickly as possible. While the two subspecies are related, northern white rhinos are wider, with straighter backs, flatter skulls, and a different neck structure. The differences are stark enough that a baby northern white rhino might not learn how to graze properly if it comes up in a herd of its southern white cousins. Hildebrandt wants the animal to socialize with Najin and Fatu before they, too, die. Sudans granddaughter is only in her early 20s and still playful. Najin, on the other hand, is in her early 30s, and lives with a large tumor on her abdomen.

Theres a lot of things morphologically which are links to behaviors, says Hildebrandt. The social knowledge, how to behave as a northern white rhino, is something we can preserve. But there is no way to do that unless we produce a calf very soon.

Still, a de-extinction project inevitably requires two finite resources: time and money. Hildebrandt thinks it will take about 20 years to reintroduce a healthy population of the animals back to Africa, at a cost of approximately $1 million per calf. But how much is one northern white rhino worth to the world?

Damon Casarez

Damon Casarez

Depending on BioRescues progress this year, there might be a baby northern white rhino walking with Najin and Fatu within two years. The bioengineering tools required to accomplish the incredibleresurrecting a herd of 6,000-pound animalsare here, in the hands of Durrant, Korody, Hildebrandt, and their respective teams of researchers.

We have the technology. We can rebuild them. Now comes the hardest question of all: Should we?

Its perhaps too soon to tell if a new birth in a species that is on the brink of extinction would be heralded as a success. After all, humans nearly killed off every northern white rhino in existence. Whats to say that people wont poach the animals for their horns, and do it flippantly, openly, even expectantly? You created a bunch of northern white rhinos before, we may cry out. Just do it again. This, we might incorrectly believe, is the promise of something like the Frozen Zoo. We preserve natural history, only to reanimate it according to our whims.

Yes, science can save species. But dont rely on science to save species, says Durrant. We cant do this for every species. We dont want to do this for every species. We want species to be preserved in their native habitats before they go extinct.

Cryopreservation and embryo transfers arent blueprints for managing the planet. But they might preserve a legacy that the death of Sudan left behind. If were paying attention, maybe one new rhino will wake us up.

View post:
The Bioengineering Gambit to Save the Northern White Rhino - Popular Mechanics

Recommendation and review posted by Bethany Smith

July13, 20216 min read

Opinions expressed by Entrepreneur contributors are their own.

On June 13, Laura Wilkinson did not qualify in her attempt to join this years U.S. Olympic Diving Team finishing inonly 10th place at the final qualifying event in Indianapolis.

But Lauras performance was so inspiring that she received a standing ovation from everyone who attended. Why? Because at age 43, Laura is now more than twice as old as she was when she won her gold medal at the 2000 Olympics in Sydney.

While it may not be surprising that she didnt qualify for this years team, the very idea that she was in shape to compete at all clearly shows how much progress weve made in not only extending longevity, but also living healthier as we age. In the last century alone, average life expectancy in the U.S. has increased from around 60 to nearly 80 years.

At this rate, it wont be long before 100 years old becomes "the new 60."

Indeed, new scientific discoveries and innovative research into health and medicine continueto reveal new insights into how the human body works and how we can delay the impact of aging many that we couldnt even imagine only a few short years ago.

Related:Former Quarterback Jim McMahon Calls AdvancedStem-Cell Therapy 'Truly Miraculous'

As the CEO of BioXcellerator, a leading stem-cell treatment and research center, Ive made it my mission to work with a team of talented scientists and physicians to further progress to help everyone worldwide live longer and enjoy better health.

Weve long known about the benefits of a healthy lifestyle and diet. And physicians now have access to more advanced surgical procedures and new medications. But as it turns out, the secret to maintaining excellent health and vitality isnt so secretive at least at the cellular level.

You see, your body already knows how to heal itself, through a natural process based on stem cells. Youre not aware of it, of course, but all of the cells in your body neurons in your brain, cardiac cells in your heart, immune cells that circulate through your bloodand all other cells are constantly being replaced with new cells.

Yet even though each type of cell functions differently, they all begin as stem cells created in your bone marrow, then differentiated to become a specific type of cell.

As we age, however, stem-cell production declines. Thats why stem-cell therapy is such an exciting frontier in medicine today:After an infusion of millions of high-potency stem cells, your body goes right to workusingthose cells to heal damaged tissue, reduce inflammation, improve immunity, and boost vitality and performance.

Even damage from injuries sustained many years ago can be healed from an infusion of stem cells.

Related:This Is HowStem-CellTherapy Treats Serious Brain Injuries

Although more effective medical treatments for various diseases and disorders certainly benefits humanity, heres a better approach: Prevent disease in the first place. Yes, nutrition and exercise make a big difference, but recent studies clearly show how enhancing immunity and reducing chronic inflammation can add even more years to our lives and improve our health.

Yet, while were aware of what we eat and our level of physical activity, we dont fully appreciate the battle our immune cells fight every minute of every day 24/7. Theyre constantly on patrol throughout your body, seeking out and destroying various viruses and other microbes that threaten our health and lives. That may seem overly dramatic, but one things for sure:Without immunity, there would be no humanity. Our species couldnt exist.

Another battle that rages inside us comes in the form of inflammation. Although inflammation is the bodys natural signaling system that various tissues need repair and healing, when continued ongoing inflammation becomes chronic, it can actually cause even more serious damage throughout the entire body. Recent studies suggest that while an anti-inflammatory diet and other lifestyle choices (for example, getting enough sleep) can reduce excess inflammation, stem cells also provide anti-inflammatory benefits and boost immunity too.

At BioXcellerator, we offer stem-cell therapy to treat a wide range of diseases and injuries, but regardless of what patients get treated for, one common resultrings loud and clear:Patients report that they feel better. They have more vitality, moreenergy, enhanced cognitive function and a greater overall sense of well-being.

After all, the body doesnt know why its receiving new stem cells, so it uses those cells to both heal specific damage and better modulate the immune system and regulate inflammation.

Related:High-Potency 'GoldenCells' Offer Hope to Those With Severe Brain Injuries

With even more advanced testing now available, such as whole-body and brain MRIs, genome sequencing andliquid biopsy using cell-free DNA, we can detect the onset of many serious diseases and disorders far earlier, including heart disease, cancer, and autoimmune and degenerative conditions.

Theres overwhelming evidence that many cancers and heart disease can be treated more effectively when detected at an early stage. These more accurate and precise tests also enable us to provide personalized recommendations forchanges in diet and lifestyle that can help prevent or delay the onset of many diseases and conditions altogether.

Many athletes turn to stem cells to maintain peak performance duringtheir careers, and to extend them;they also receive treatment after they retire to alleviate chronic pain from injuries suffered over many years.

No, its not so miraculous. Its all based on science. As we learn more about extending longevity, immunityand performance, Im more convinced than ever that age 100 will become the new 60.

Excerpt from:
The Future of Health: Why Age 100 Will Soon Become 'the New 60' - Entrepreneur

Recommendation and review posted by Bethany Smith

Introduction

Profilin 1 (PFN1) is a ubiquitous small-molecule protein that exists in all eukaryotes.1 PFN1 was first identified as a G-actin sequestering molecule,2 and subsequently, its true functions in actin polymerization and F-actin dynamics were revealed.3 In the following decades, the structure of PFN1 was recognized to have 3 domains: an actin-binding domain,4 a poly-L-proline (PLP)-binding domain,5 and a phosphoinositide-binding domain.6

PFN1 plays a vital role in many cell functions, including membrane trafficking, endocytosis, cell cycle, motility, proliferation, cell survival, transcription, stemness, and autophagy (Figure 1). Abnormal expression or deletion of PFN1 can affect the normal physiological activity of cells and lead to disease development. PFN1 has been deeply studied in a variety of diseases, some genetic (eg, amyotrophic lateral sclerosis)7 and some chronic (eg, hypertension).8

In the past 10 years, PFN1s role in cancer has received increasing attention. In this review, we summarize the studies of PFN1 in cancer that have been completed in recent years, discuss the roles of PFN1 in cancer, and discuss the implications for tumor diagnosis and therapy in the future.

Early diagnosis of cancers is still a major challenge worldwide, and early detection can notably reduce their associated morbidity and mortality.9 PFN1, a critical actin-binding protein, is found to be dysregulated in many cancers, which makes it possible to use it as a biomarker for diagnosis and prognosis. PFN1 mainly plays a role in the cytoplasm, but it can also be found in the nucleus and can even be secreted into the extracellular space. The rich knowledge in the proteomics field makes the detection of proteins for new diagnostic markers and targets for therapy possible.10

In some tumor types (such as renal cell carcinoma [RCC], gastric cancer, and others), high expression of PFN1 indicates later stage and worse prognosis. Via differential proteomics, PFN1 has been identified in metastatic and primary RCC, and further analysis indicated that high PFN1 expression was associated with poor outcome and that PFN1 could be used as a potential prognostic marker in RCC.11 In clear-cell RCC (ccRCC), the expression of PFN1 was decreased in early-stage tumors compared with normal tissues. However, its expression in stage IV ccRCC was significantly increased. PFN1 was selected as a candidate marker of late-stage ccRCC.12 Results of a recent study determined that the vast majority of ccRCC tumors tend to be selectively PFN1-positive in stromal cells only; dramatic transcriptional upregulation of PFN1 was found in tumor-associated vascular endothelial cells in clinical specimens of ccRCC.13 Tissue microarray results also showed that PFN1 was increased in metastatic ccRCC compared with primary tumors. Univariate analysis suggested that higher PFN1 expression was associated with shorter disease-free survival (HR, 7.36; P = .047) and lower overall survival.14

In gastric cancer, Tanaka et al found that PFN1 was highly expressed in fetal rat stomach. Additionally, PFN1 was overexpressed in some human and rat gastric cancers.15 The results of later studies indicated that PFN1 expression was higher in gastric cancer tissues than in adjacent normal tissues. High PFN1 expression was correlated with tumor infiltration, lymph node metastasis, and tumor-node-metastases (TNM) stage. Functional assays confirmed that silencing PFN1 could inhibit the invasion and migration of gastric cancer cell lines.16

In addition, PFN1 expression was higher in nonsmall cell lung cancer (NSCLC). Lower expression of PFN1 was associated with better prognosis and a higher survival rate in NSCLC.17 Proteomic analysis revealed that PFN1 was differentially expressed in laryngeal carcinoma tissues compared with adjacent normal tissues. Further study results revealed that PFN1 was increased in laryngeal carcinoma tissues compared with adjacent normal tissues, indicating that PFN1 was a novel potential biomarker for the diagnosis of laryngeal carcinoma.18

However, in some other tumors (such as colorectal cancer [CRC], oral carcinoma, and others), the opposite is true. PFN1 was downregulated in pancreatic cancer.19-20 Lower expression of PFN1 was significantly associated with a shorter survival period.20 In late-stage oral squamous cell carcinoma, PFN1 expression was lower than that in normal oral epithelium, and loss of PFN1 expression was related to invasion into and metastasis of lymph nodes.21 PFN1 was also decreased in late advanced hepatocellular carcinoma (HCC) and was associated with a poor survival rate of patients.22-23 In addition, PFN1 was found to be downregulated in nasopharyngeal carcinoma24 and breast cancer.25 Combined with another 4 actin-binding proteins, PFN1 could be used to construct a model for predicting poor prognosis of esophageal squamous cell carcinoma.26

Under normal physiological conditions, PFN1 is involved in multiple cellular functions, such as cell motility, migration, adhesion, and transduction signaling pathways.27 PFN1 is differentially expressed in various types of tissues and cells, which may explain its variable tumorigenic mechanisms in different tumors, even in different stages of the same cancer (Figure 2). Because PFN1 plays important roles in tumorigenesis and progression, targeting PFN1 dysregulation could to some extent influence the prognosis of patients with cancer. Determining the expression of PFN1 could thus be used to distinguish high-risk disease from lower-risk disease. Combination with other indices could further improve the diagnostic and prognostic value of PFN1.

In addition to dysregulation in tumor tissues, PFN1 was also found to bedifferentially expressed in the serum, urine, and extracellular vesicles of patients with cancer, which makes it possible to utilize PFN1 in liquid biopsy analysis of tumors. Compared with tumor tissue biopsy, liquid biopsy is a more practical method for real-time monitoring of patients with cancer.28 In addition, PFN1 was detected in the supernatants of cultured cells.

It has been shown that PFN1 gene expression is increased in peripheral blood cells of patients with HCC compared with healthy controls.29 A 9-gene expression system (including PFN1) was used to discriminate patients with HCC from healthy people.30 Proteomic analysis of serum proteins showed that PFN1 was increased in patients with gallbladder cancer. The expression difference between these patients and healthy controls was more than 2-fold.31 PFN1 was differentially expressed in the urine of patients with invasive and noninvasive bladder cancer. Further studies confirmed that PFN1 was notably decreased in the epithelium of invasive bladder tumors compared with noninvasive tumors, which was associated with the clinical outcomes of bladder cancer.32 In in vitro pancreatic cancer cell lines, PFN1 was downregulated in secretomes compared with nonneoplastic pancreatic ductal cells.33 In invitro cultured RCC cell lines, PFN1 was differentially regulated in the supernatant. Further studies revealed that PFN1 was upregulated in RCC tissues.34 Apart from its dysregulation in serum and urine, PFN1 was found to be downregulated in the circulating leukocytes of patients with breast cancer compared with healthy controls, which provides a new paradigm for highly sensitive and less invasive approaches for the diagnosis of breast cancer.35 Studies have already revealed that PFN1 can be secreted via exosomes or other secretory pathways.36-38

Extracellular PFN1 in the tumor microenvironment can be taken up by recipient cells and execute its function in recipient cells, which in turn may influence the biological behavior of cells in the microenvironment, ultimately affecting tumorigenesis and progression of cancers. As mentioned above, PFN1 is expressed differentially in the serum and urine of patients with cancer, which enables its application as a biomarker for diagnosis and prognosis in liquid biopsy (Table 1).

Cell motility involves membrane protrusion, cell matrix adhesion, cell body translocation, and rear detachment. Many of these processes require the actin cytoskeleton and its regulators. By facilitating the exchange of ATP for ADP on G-actin, PFN1 plays a major role in actin polymerization, thus influencing motility in numerous cells.39 PFN1 also participates in cell motility by regulating actin polymerization and interactions with other regulators of actin cytoskeletons, such as ARP3, VASP, and proteins of cell signaling pathways. Cell-cell adhesion and cell-matrix adhesion are critical contributors to maintaining tissue architecture. Dysregulation of cell-cell adhesion is an important sign in tumor initiation and progression of malignancy. PFN1 can modulate cell adhesion and epithelial-to-mesenchymal transition (EMT) in cancer cells. However, the mechanisms by which PFN1 regulates cell adhesion are still not very clear. Undoubtedly, learning more about the roles of PFN1 in cell adhesion and motility will help us better understand its roles in modulating tumor invasion and migration.

Since PFN1 plays a critical role in actin polymerization, it is an indispensable regulator of cell motility. PFN1 participates in the invasion and metastasis of multiple cancers. However, the roles of PFN1 in regulating cell motility are context specific.27 Exogenous PFN1 with intact actin-binding abilities can ameliorate the adherence and spreading capabilities of cancer cells and exert tumor-suppressive effects in breast cancer.40 Consistent with the results of the study by Wittenmayer et al, Zou et al found that PFN1 overexpression could revert MDA MB-231 cells to an epithelioid phenotype, with restored adherence junctions.41 In addition, PFN1 overexpression could promote AMPK activation and p27 phosphorylation, which in turn induces epithelial morphological reversion of mesenchymal breast cancer through restoration of adherens junctions.42 These studies highlighted the involvement of PFN1 in epithelial adhesion and differentiation, which helped us better understand its roles in cancer cell motility.

Invadopodia are actin-driven membrane protrusions that can deliver matrix metalloproteinases to degrade the matrix and support invasion and dissemination of tumor cells. Any dysregulation of the actin cytoskeleton can impair the formation and maturation of invadopodia.43-46 PFN1 can regulate PI(3,4)P2, which in turn negatively regulates lamellipodin at the leading edge of breast cancer cells and thus inhibits those cells motility.47 The depletion of PFN1 leads to an increase in the level of PI(3,4)P2 in invadopodia and its interacting adaptor Tks5. The interaction of PI(3,4)P2-Tks5 has been shown to promote the anchorage, maturation, and turnover of invadopodia, which in turn enhances the invasiveness and motility of breast cancer.48 Breast cancer is an invasive adenocarcinoma, and numerous studies have found that PFN1 is downregulated in breast cancer tissues.49-54 Overexpression of PFN1 reduces the invasion and migration of breast cancer cells, while loss of PFN1 significantly enhances breast cancer cell motility and invasion. Mechanisms involved in PFN1s negative roles in breast cancer metastasis include Enabled (Ena)/vasodilator stimulated phosphoprotein (VASP)-dependent lamellipodial protrusion,51 miRNA-182 regulation,52 and regulation of PFN1 degradation.53 Mouneimne et al found that PFN1 knockdown (KD) could increase F-actin bundles and enhance stress fiber formation. In that study, the numbers of protrusions in PFN1-KD cells were markedly decreased, and PFN1-KD could inhibit the motility of breast cancer.55 Moreover, Liu et al indicated that the interaction of LMO2-PFN1 and LMO2-ARP3 could promote the formation of lamellipodia/filopodia in basal-type breast cancer cells.56 Ena/VASP is a critical regulator of the actin cytoskeleton at the leading edge of cells, which controls membrane protrusions and cell motility. Cell-substrate adhesion and downregulation of Protein Kinase A (PKA) promote interactions of PFN1 with VASP, which is another mechanism by which PFN1 regulates cell motility.57-58 Knockdown of PFN-1 has been shown to abrogate the inhibitory effect of tyrphostin A9, suggesting that modulating PFN1 expression could have therapeutic potential in the treatment of metastatic breast cancer.59

As in breast cancer, PFN1 was found to be a suppressor of migration in HCC.22,23,60 All-trans retinoic acid60 and guttiferone K22 could inhibit hepatocellular cell migration and proliferation by upregulating the expression of PFN1. In prostate cancer, cathepsin X can inactivate PFN1, thus promoting adhesion, invasion, and migration of cancer cells.61 In CRC, elevated expression of PFN1 obviously inhibited invasion and migration. PFN1 was suppressed by the HLA-F-AS1/miRNA-330-3p/PFN1 or HCP5/miRNA-299-3p/PFN1/AKT axis.62-63

Interestingly, Ding et al showed that in the early stages of metastasis, breast cancer cells exhibit a hyperinvasive phenotype characterized by upregulation of MMP-9 and by faster invasion when PFN1 expression is downregulated. However, in the late stages of metastasis, loss of PFN1 markedly inhibits the growth of metastatic colonies of breast cancer cells.54 Rizwani et al reported that PFN1 expression was elevated in breast cancer tissues and that overexpression of PFN1 could inhibit the migration of breast cancer cells. The phosphorylation of S137 mutants abrogated PFN1s promotion of migration. These studies provided a different vision of PFN1s role in breast cancer metastasis.64

In gastric cancer, silencing PFN1 inhibited the invasion and migration of cells, and the PFN1 expression level in cancer tissue was positively correlated with tumor infiltration and lymph node metastasis.16 However, different conclusions were drawn from the study of Ma et al. The authors found that PFN1 expression was inversely correlated with lymph node metastasis.65 In the lung cancer cell line A549, downregulation of PFN1 inhibited migration.17 In addition, in vitro studies support the importance of PFN1 in the proliferation and migration of RCC cells, and treatment with a novel computationally designed PFN1-actin interaction inhibitor reduced the proliferation and migration of RCC cells in vitro and RCC tumor growth in vivo.13 Additional studies have demonstrated that downregulation of PFN1 can also suppress the migration of laryngeal cancer18 and bladder cancer.66

Although more studies on PFN1 have been completed recently, its roles in cancer metastasis are still unclear. The concentrations of actin and PFN1 are time- and space-specific, and so is the regulation of the actin cytoskeleton (Table 2). Additional thorough studies are needed to comprehend the mechanisms and laws regulating the actin cytoskeleton. More importantly, in addition to actin dependence, PFN1 affects cell migration in an actin-independent manner by interacting with proteins with PIP2 or PLP domains. Furthermore, lncRNAs and microRNAs also modulate the functions of PFN1. All of these proteins and RNAs interact with PFN1 and indirectly influence the functions of cancer cells, which makes understanding the roles of PFN1 in cancer metastasis and other functions more complicated (Table 3).

In yeast, the gene encoding PFN1 is essential for cytokinesis.67 Early studies revealed that PFN1/ embryos died as early as the 2-cell stage, while PFN1/+ embryos displayed reduced survival during embryogenesis compared with wild-type embryos; this indicates that PFN1 is essential for cell division and survival during embryogenesis.68 PFN1 silencing in endothelial cells inhibits proliferation.69 In addition, homozygous deletion of PFN1 in chondrocytes failed to complete abscission at late-stage cytokinesis.70 The results of all these studies imply that PFN1 plays a role in cell proliferation. In breast cancer, PFN1 overexpression (PFN1-OE) has been shown to inhibit cell growth and exert an inhibitory effect on tumorigenesis,25,40,52,71-75 and PFN1-OE suppresses the activation of AKT, which in turn inhibits the growth of tumor cells.71 PFN1-OE cells arrested at the G1 phase, which was partly attributed to the upregulation of P27kip1.72 miRNA-182 could downregulate PFN1 expression and promote triple-negative breast cancer cell proliferation.52 However, Yap et al put forward opposite views. The authors research results revealed that silencing PFN1 resulted in a multinucleation phenotype of breast cancer cells, thus inhibiting proliferation.76 Recent studies from Chakraborty et al also reported that PFN1 knockdown could upregulate SMAD3 and inhibit the proliferation of breast cancer.77 Results of single-cell studies on the extracellular matrix revealed that stiff extracellular matrix led to upregulation of PFN1, possibly promoting the proliferation of breast cancer.78 Apart from breast cancer, PFN1 was also found to suppress proliferation in pancreatic adenocarcinoma,20 endometrial cancer,79 and HCC.23,60 In gastric cancer, silencing PFN1 caused cell cycle arrest at G0/G1 phase, thus restraining cell proliferation.16 Knockdown of PFN1 could also inhibit the proliferation of laryngeal cancer.18 Our previous studies found that overexpression of PFN1 could promote the proliferation of multiple myeloma cells by accelerating the cell cycle from G1 to S phase.80 PFN1 is indispensable for cytokinesis. Nevertheless, PFN1 is involved in regulating cell proliferation not only by impacting cytokinesis but also by modulating cell cyclerelated proteins. Otherwise, PFN1 could also interact with cell signaling pathways and indirectly influence cell proliferation.

Tumor growth is not only about uncontrolled proliferation but also resistance to apoptosis.81 Actin dynamics have notable impacts on multiple stages of apoptosis.82 PFN1, as a critical actin-binding protein, is an indispensable regulator of actin dynamics, through which PFN1 participates in regulating apoptosis. PFN1 overexpression could upregulate the most common tumor-associated hotspot mutation of p53p53R273Hthus sensitizing cancer cells to apoptosis via the intrinsic apoptotic pathway.83 PFN1 has been shown to facilitate apoptosis of breast cancer cells, thus exerting a suppressive effect on tumorigenesis.73,75,83,84 By inducing apoptosis and reducing autophagy, PFN1 has also been shown to sensitize pancreatic cancer cells to irradiation. Additionally, overexpression of PFN1 can significantly elevate apoptotic markers such as cleaved caspase-3 and cleaved PARP after irradiation, suggesting that PFN1 can modulate radiosensitivity partly by regulating apoptosis.85

Given that PFN1 is involved in cell proliferation and apoptosis, it is not difficult to understand its roles in the drug resistance of tumor cells. PFN1 was found to be downregulated in butyrate-treated CRC cells,86 and proteomics studies revealed that PFN1 was differentially expressed in erinacine Atreated CRC cells,87 which suggested the roles of PFN1 in drug-mediated cell death and inhibition of proliferation. In addition, proteomics showed that PFN1 was differentially expressed in mitotane-treated adrenocortical carcinoma,88 and PFN1 was found to be increased in tocotrienol-treated MDA-MB-231 cells,89 indicating its roles in predicting the response to anticancer therapies. Compared with temozolomide (TMZ)-treated glioblastoma cells, PFN1 was downregulated in OKN-007 combined with TMZ-treated glioblastoma cells. Further study results revealed that PFN1 is involved in TMZ resistance.90 Results of our previous studies showed that PFN1 could interact with the Beclin 1 complex and participate in bortezomib resistance in multiple myeloma.80 Since PFN1 is involved in multiple cell processes, including proliferation, apoptosis, and proteomics, it was recognized as a biomarker for therapy sensitivity, and it is worth further exploring its roles in drug resistance. In addition, PFN1 was found to participate in angiogenesis,91-92 initiation of tumors,93 and autophagy.80 Loss of PFN1 in A549 cell lines resulted in fewer early apoptotic cells after treatment with piperlongumine, and PFN1 sensitized A549 cells to anticancer agents.17 PFN1 serves as a bridge for actin-cytoskeleton and cell signaling pathways and is involved in multiple biological and physiological processes. Dysregulation of PFN1 in cancer cells has a notable impact on sensitivity to chemotherapy or radiotherapy and may be a new target for the treatment of drug-resistant or radioresistant patients.

Studies have already confirmed that PFN1 is essential for cell survival in early embryos, as PFN1-KN could induce Drosophila embryos to die at the 2-cell stage.94 For further investigation of PFN1s roles in tissue-specific stem cells, Zheng et al established PFN1flox/flox mice that inducibly delete PFN1 in HSCs. Results showed that PFN1 was essential for the retention and metabolism of mouse hematopoietic stem cells in bone marrow partially through the axis of PFN1/G13/EGR1.95 These study results implied important roles of PFN1 in stem cell function, which were still unclear and deserved further research. Later study results have found that both overexpression and depletion of PFN1 could reduce the stem-like phenotype of MDA-MB-231 (MDA-231) triple-negative breast cancer cells, suggesting that a balanced expression of PFN1 was required for maintenance of optimal stemness and tumor-initiating ability of breast cancer cells.93 Considering that tumor heterogeneity is still an ongoing challenge for cancer treatment and that cancer stem cells (CSC) are considered to be a determining factor of tumor heterogeneity,96 intensive studies on PFN1s roles in CSC may provide us new insight into tumor initiation.

As mentioned above, PFN1 has been shown to be a critical participator of actin dynamics and to play important roles in cell migration. For cytotoxic T lymphocytes (CTLs), migration abilities are essential for patrolling tissues and locating targeted cells.97-98 Schoppmeyer et al thus studied PFN1s roles in CTL functions. The authors found that PFN1 negatively regulated CTL-mediated elimination of target cells and that PFN1 downregulation promoted CTL invasion into a 3D matrix in vitro. In patients with pancreatic cancer, PFN1 expression was substantially decreased in peripheral CD8+ T cells.99 However, considering the complexity of immune responses in vivo, the exact roles of PFN1 in tumor immunity remain unclear and need to be further explored.

Based on previous studies, we found that PFN1participates in multiple biological processes of tumor development and progression. Meanwhile, it is noteworthy that PFN1 plays opposite roles in different tumors and at different periods of tumor, potentially leading to the conclusion that PFN1s function in tumor has spatial and temporal specificity. Future studies on PFN1 should take this into account. PFN1 was shown to be of great significance for diagnosis and prognosis prediction and for monitoring the therapeutic effect of anticancer drugs, and PFN1s roles in tumor stemness and immunity may provide a new avenue for cancer therapy. Although much research has been done on PFN1 and cancer, puzzles still need to be solved. With deepening research, the function of PFN1 in cancer would be further clarified and its clinical value would be more prominent.

Financial Disclosure: The authors have no significant financial interest in or other relationship with the manufacturer of any product or provider of any service mentioned in this article.

Conflicts of Interest: Authors declare no conflicts of interest for this article.

Acknowledgment: The authors are thankful for financial support from the Doctoral Fund Project of Hunan Provincial Peoples Hospital (program number BSJJ201812).

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Profilin 1 Protein and Its Implications for Cancers - Cancer Network

Recommendation and review posted by Bethany Smith

After closing a merger with GX Acquisition Corp., Celularity Inc., a clinical-stage cellular medicine company, is taking the next step in its evolution to enable further development of novel, off-the-shelf allogeneic placentaderived cellular therapies.1

Celularity aims to transform the way we approach the treatment of cancer and other diseases by harnessing the versatility, unique immune biology, and innate stemness of placental-derived cells, Robert J. Hariri, MD, PhD, found, chairperson, and chief executive officer of Celularity, stated in a press release. We are immensely proud of our clinical development results so far as well as the state-of-the-art manufacturing capabilities we built to support rapid scaling and a competitive cost structure for our placental-derived cell therapeutics. We believe off-the-shelf, allogeneic cell therapies will drive a paradigm shift in how clinicians approach the treatment of cancer and other serious diseases.

CYNK-001, the companys lead product candidate, is the only cryopreserved, allogeneic, off-the-shelf natural killer (NK) cell therapy to be developed from placental hematopoietic stem cells. The agent expresses perforin and granzyme B, has showcased cytotoxic activity against hematological tumors and solid tumor cell lines, and can secrete immunomodulatory cytokines in the presence of tumor cells.

The novel therapy is under investigation as a potential option in multiple myeloma, acute myeloid leukemia (AML), and glioblastoma multiforme; it is also being evaluated in infectious diseases like COVID-19 (NCT04365101).

An ongoing, open-label, multi-dose, phase 1 trial (NCT04310592) is examining the maximum-tolerated dose (MTD) or maximum planned dose of CYNK-001 in an estimated 22 patients with acute myeloid leukemia (AML).2 To participate, patients need to have primary or secondary AML and be in first or second morphological clinical response (CR), morphological CR with incomplete hematologic recovery, or a morphologic leukemia-free state per European LeukemiaNet recommendations for AML Response Criteria.

Patients also need to have MRD positivity, be aged between 18 and 80 years old, have an ECOG performance status of 0 to 2, and be able to be off immunosuppressive therapy for at least 3 days before infusion with the therapy. Patients who previously had central nervous system involvement are allowed to enroll if they had been treated and their cerebral spinal fluid is clear for at least 2 weeks before undergoing lymphodepletion.

Exclusion criteria include significant medical conditions, laboratory abnormalities, bi-phenotypic acute leukemia, acute promyelocytic leukemia, unacceptable organ function, autoimmune disease, uncontrolled graft-vs-host disease (GVHD), and GVHD that requires corticosteroids.

Participants are first given cyclophosphamide plus fludarabine. Then, they are administered CYNK-001 at 3 varying dose levels1.8 billion, 3.6 billion, and 5.4 billion CYNK-001 cellson days 0, 7, and 14. The primary objectives of the research include dose-limiting toxicity (DLT), maximum-tolerated dose (MTD), and frequency and severity of adverse effects. Important secondary objectives include the number of patients who convert from MRD-positive to -negative status; time to, and duration of, MRD response; progression-free survival; time to progression; duration of morphologic complete remission; and overall survival.

In June 2021, the study was expanded to include patients with relapsed/refractory AML following a case of conversion to MRD negativity, when the therapy was delivered at its highest dose level.3

The decision to expand the trial followed observations of a patient with NPM-1positive, FLT3-negative AML and good-risk cytogenetics who had been administered 5.4 billion CYNK-001 cells. The patient converted from MRD-positive to -negative status, without experiencing any DLTs.

For this patient, primary induction treatment with 7+3 chemotherapy had failed, and so they had gone on to receive second induction therapy followed by high-dose cytarabine consolidation. At this time point, the patient achieved a complete CR, but MRD was found to be persistent; it did not clear following 4 months of treatment with azacitidine. MRD positivity was confirmed on a marrow biopsy.

The patient went on to enter the phase 1 trial, where they received lymphodepletion, and then received 1.8 billion CYNK-001 cells on days 0, 7, and 14 in the outpatient setting, which totaled to 5.4 billion CYNK-001 cells. On day 28, the patient had converted from MRD positivity to negativity. CYNK-001 cells were present in both the peripheral blood and bone marrow.

Notably, no DLTs have been observed with the therapy at any of the dose levels examined thus far.

The company also shared plans to continue dose escalation with the therapy in the MRD indication up to 9.0 billion CYNK-001 cells. To strengthen the persistence of the treatment, the expansion arms of MRD and relapsed/refractory AML will include an augmented lymphodepletion protocol comprised of cyclophosphamide at 3600 mg and fludarabine at 120 mg over 4 days vs cyclophosphamide at 900 mg plus fludarabine at 75 mg over 3 days.

In April 2021, the FDA granted an orphan drug designation to CYNK-001 as a potential therapeutic option for patients with malignant gliomas.4 As such, the therapy is also under investigation in patients with glioblastoma multiforme as part of another phase 1 trial (NCT04489420).5

To be eligible for enrollment, patients need to have historically confirmed disease at first or second relapse, measurable disease, a Karnofsky performance status of 60 or higher, and acceptable organ function, among other criteria.

Patients who previously received radiation within 12 weeks of their screening MRI; those who were on growth factors with less than 4 weeks of a washout period; those treated with radiotherapy, chemotherapy, or other investigational drugs within 4 weeks; those who received prior cellular or gene therapy; and those with active autoimmune disease, were excluded.

Cohort 1A of the trial will enroll up to 6 patients with recurrent glioblastoma multiforme who will receive intravenous CYNK-001 at a dose of 1.2 x 109 cells on days 0, 7, and 14. From the initial infusion of therapy, patients will be followed for a 42-day DLT period. No other interventions are planned between the last day of treatment.

If DLTs are experienced, cohort 1C, the de-escalation cohort, will include up to 6 patients with recurrent glioblastoma multiforme who will receive the therapy at a dose of 600 x 106 cells on days 0, 7, and 14. These patients will also be followed for DLTs for 42 days post infusion. Cohort 1B, the surgical cohort, will also enroll up to 6 patients, who will be given CYNK-001 at a maximum safe dose of either 1.2 x 109 cells or 600 x 106 cells at days 0, 7, and 14. Patients in this cohort will undergo resection following the last dose of the therapy in the DLT period.

Treatment of cohorts 2A or 2C will only begin after the safety data from cohorts 1A or 1C are determined to be acceptable. Here, patients will first have the Ommaya catheter placement in accordance with institutional policy within 1 week before CYNK-001 infusion on day 0. Cohort 2A will enroll up to 6 patients with recurrent glioblastoma multiforme who will be given the therapy at a dose of 200 x 106 cells +/- 50 x 106 cells intratumorally on day 0, 7, and 14.

Cohort 2C will also include up to 6 patients with recurrent disease who will receive the product at a dose of 200 x 106 cells +/- 50 x 106 cells intratumorally on day 0 and day 7. Lastly, cohort 2B, the surgical intratumoral cohort, will include 6 patients with glioblastoma multiforme who will receive the cellular therapy at a maximum safe dose of either 200 x 106 cells +/- 50 x 106 cells on day 0 and 7.

The primary objectives of the trial are to examine the number of patients who report DLTs with the therapy and toxicities. Important secondary objectives are to evaluate the overall response rate, duration of response, progression-free survival, time to progression, and overall survival.

The safety and efficacy of the cell therapy is also being explored in newly diagnosed patients with multiple myeloma after autologous stem cell transplant, as part of another phase 1 trial (NCT04309084).6 The objective of the program is to achieve durable responses with the therapy in these patients with multiple myeloma who are eligible for transplant in the first-line setting.

Another novel agent in the pipeline is CYNK-101, which is manufactured from NK cells extracted from postpartum placentas. The cells are then genetically engineered to boost cell-killing activity when given with a monoclonal antibody.7 Preclinical data with the product in combination with an antibody showed that the regimen resulted in cell-killing activity when administered to lymphoma cells in vitro.

Additionally, CYNK-CAR products are being developed as allogeneic, off-the-shelf strategies by modifying genes of the human placental hematopoietic stem cellderived NK cells. Several CAR constructs that are designed to target hematologic and solid tumor indications are currently under investigation.

Read more:
Developmental Interest in Allogeneic PlacentaDerived Cell Therapies Expands - OncLive

Recommendation and review posted by Bethany Smith

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The word Pandemic instantly takes me to the days of medical school, where we studied it as if it was a fictional entity, while never expecting to implement the knowledge in practice. Metaphors sound frivolous the way things have unfurled over past couple of months.

Everyone has been affected. With so many lives lost and many families left in despair and misery, this is perhaps the most shocking crisis of many peoples lives.

While for the larger population, this disease is all about lockdowns, keeping safe, protecting families and making ends meet; its implication for doctors is multifaceted. Without any immunity from the disease and with constant threat of violence, doctors bracedfor the unseen enemy since the beginning. As our country catapulted into the deadly second wave this summer, the challenges became even more stark. What they were dealing with was a mutant virus with high infective potential, failing health infrastructure and a billion plus unvaccinated population.

But this became the period when complacence overtook good sense, thirst for power overlooked greater good and the concept of shared responsibility was binned. Conveniently ignored was the fact that we had never touched baseline of normalcy and many places in world were still battling with subsequent waves. Poor planning and unscientific outlook were recipe for disaster.

A plethora of treatment options started being circulated amongst general population on social media platforms. Where a person with no medical background is free to administer treatment, doctors are being questioned over injudicious of some drugs. Where faltering oxygen supply and drug shortage is taking lives, doctors are harassed for loss of lives due to known complications of diseases. Where propaganda alternative medicine is portrayed as a panacea for COVID, doctors are asked to prove beyond doubt the rationale behind use of experimental drugs! Doctors have been facing this disease in its most horrendous forms. They have lost loved ones too. The plight of dying patients and distraught families has left their psyches scarred. Notwithstanding all this, their hope thrives on recovery of patients. Those who serve you do not yearn to be called Warriors or God; we just want patients to understand that our every effort we make is for your well-being. Every doctor believes in Do No Harm. The disbelief towards our intent is disconcerting. And when fear rather than care and compassion becomes our guiding principle, it is death knell for the medical system.

There are thousands of diseases in the world, but Medical Science only has an empirical cure for twenty-six of them. The rest is. guesswork. These words of Erich Segal in his famous novel Doctors so aptly described the state of medical science way back in 1988. We have come a long way since then. There has been phenomenal advancement in diagnostics and therapeutics in all specialities. It is for these advances in medicine, today we have options to treat COVID patients and save lives. Researchers came up with effective vaccines in unprecedented time. Modern medicine is evidence based.

A medical practitioner selects treatment options for specific cases based on the best research, patient preferences, and individual patient characteristics. But it is not an absolute science. Drugs that are effective in some patients might be ineffective in others; treatment of choice for diseases change as more insight into pathophysiology and imaging is attained. Hundreds of hours of scientific researches and deliberations are needed to develop a drug molecule and still more to prove its safety and efficacy. It took years of massive outreach programmes to eradicate few viral diseases. And despite every effort, there are still diseases that leave us intrigued and crippled. We too look forward to the day when gene therapy would eradicate blindness in young retinitis pigmentosa patients and new treatment options will likewise emerge for diseases that are still untreatable.

We doctors have been trained on ethical and humanitarian grounds. Hippocrates never prepared us for war-like situations, but that didnt deter any doctor in these perilous times. It is ironical that anything that is on social media is accepted to be the truth, whereas every word of doctors is scrutinized. The blabbering of self-promoting, fame mongers against the noble profession is an affront to our dedication and service. The development of alternate forms of medicine doesnt mandate disregard of the existing, proven and life saving modern medicine. The myopic policies for health and collective consciousness against doctors are corrosive to the future of this nation already compromised by the wrath of COVID19. If this catastrophic period doesnt change anything, nothing ever will.History will repeat with this denial of culpability and inaction at the highest level. The blind spots in sight must not taint ones vision. Its time to prioritize health and be prepared for any incipient third wave.

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Recommendation and review posted by Bethany Smith

Amidst a global push for mass vaccination as the battle against COVID-19 rages on many people are still afraid to be vaccinated.

People remain concerned about the perceived experimental nature of vaccines, whether they should be worried about short term risks such as blood clotting and myocarditis; and long term risks including side effects relating to DNA changes, fertility and reproduction, and other unknown long term chronic illnesses and side effects further down the track.

A lot of people continue to wonder whether the risks of vaccination outweigh the benefits.

Greek City Times spoke to trained scientist and medical professional Dr. Nicholas Lelos in our search for answers to some of the questions currently circulating around the controversial topic of vaccination, and here is what he had to say.

The science is constantly changing and there are multiple new sources of information. I think the most important thing to establish is that people need to be wary of sources, as there is a lot of anecdotal evidence and misinformation.

The most rife one, unfortunately, is that provided by several individuals that are prefaced by Dr. when this could be a PhD of certain institutions, a higher degree into a non-medical specialty (such as a nutritionist), or from institutions that have lax criteria in awarding the title. These individuals go on and publish their opinions and evidence that they highly cherry-pick on their own website, or some other sites of little to no accreditation or peer-reviewing, whereupon they then reference and draw whatever conclusions they wish.

Even a fully trained medical doctor, however, is not immune to various influences, and of having an agenda.

This is particularly evident in the United States, where a lot of authoritative narratives come with sponsoring from either competing pharma companies, anti-vaxxer sites or organisations, or even religious bodies that are trying to alter the narrative.

My personal advice, as a trained scientist before doing medicine just because it is published, available online, or even appears in a Journal, do not ever take anything as established fact: the key skill here is critical appraisal. This involves finding many different sources, checking their credentials and biases/conflicts of interests, then assessing the quality and level of evidence they furnish.

Critical appraisal is a difficult and lengthy task and a lot of people have confirmation bias, where if they see something that vaguely echoes their existing beliefs or ideas they are most likely to jump on it and not question it. It is important to look at patterns and identify various factors that can impact the question studied.

My own personal declaration is that I have no vested interests in the writing of this article, I receive no money or endorsement from institutions or of big pharma.

I only offer my experience and knowledge as someone who is a front-line clinician, and I am at the very forefront of the pandemic since the very beginning a protected population is everyones priority, from my patients to my friends and family.

Let us move with the questions.

Some have suggested that safe and effective early treatment alternatives exist such as hydroxychloroquine and ivermectinin place of vaccination. Is it true that the refusal of health authorities to issue early treatment guidance has contributed to the mortality rate of the disease?

To paraphrase another colleague there is a difference for clinical care involving individual patients, where you can see a lot of horrible side effects and consequences, and public health or epidemiology, which is the study of entire populations.

Public health is about finding solutions for multiple populations, whilst also looking into environmental impacts on health, genetics, historical cultural effects and even governmental.

The individual effect of a single drug can do miracles for an individual, or even 10 or 100, or your relatives, or even work well for one doctor or a group of doctors using it at a specific location with certain groups of patients this will not, however, mean that it will work across the entire population. And this is what the policy is made of, and what the World Health Organisation (WHO) are basing their decisions from.

The refusal of these health authorities basically entailed not using their population as test subjects for medications that have never been tested for this purpose. It would have been acceptable in Victorian times but there was also a really high accepted death risk which most people may struggle with nowadays.

So to answer your question there is currently no evidence that these medications work in severe or life threatening COVID.

Dexamethasone, a steroid, works when patients are gravely ill and about to be mechanically ventilated this has been studied, reduces mortality and ventilation needs.

Supplements and vitamins boost the immune system, so they help generally in health- but they do not treat COVID. And you need to have deficiencies of vitamins to benefit from supplementation anyway.

Hydroxychloroquine is a hideously potent medication used for malaria and immunosuppression, and has a relatively narrow window for it to do its effects before becoming toxic. A single tablet can kill children below 6 years of age. Definitely not a good option to have lying around the household. Here is a summary of the current state of these so-called remedies https://www.bmj.com/content/370/bmj.m3379

Here is an excellent live article that is getting constantly updated as new information gets out with other treatments for COVID and the evidence https://www.bmj.com/content/370/bmj.m2980

If it is true that there are safe and effective early treatment alternatives such as hydroxychloroquine and ivermectin, why the push for global vaccination?

So as stated above there are no other effective early treatment alternatives. Even steroids that work for severe COVID, when studied for mild cases, did not have a benefit.

Vaccinations, on the other hand, have worked time and time again small pox and polio have been eradicated, and measles was almost controlled until the rise of vaccination hesitancy when people did not have the stark reminders of their children dying on them or having life-long disabilities (such as with polio).

Global vaccination has worked in the past.

What is herd immunity and how does it relate to the COVID vaccine?

Herd immunity is a principle where a certain amount of the population needs to be immune in order for the disease to not be able to spread. As it requires hosts to go and infect more people, if enough people have immunity then the disease can not make the jump to infect new hosts and thus protect even people with no immunity, such as the newborn, the immunocompromised or people who develop allergies to the vaccine.

The problem that has come up with this pandemic, is that the different strains of the virus, and individuals immune systems, can elicit a different response in people studies have shown that even getting the virus and having a small course of illness means that you do not generate enough antibodies to protect yourself for long.

Meaning that you can get re-infected, or hit with a different strain.

The concept of vaccination is that it causes a sufficiently strong immune reaction that not only stays for longer but is also more effective against multiple strains. So just getting COVID may not protect someone enough, compared to getting a vaccination or boosters.

This is an approach that has been used very effectively for hepatitis B as well.

The vaccine has been referred to as experimental is this true and should we be concerned?

The technology has actually been around for 40 years. So I would hardly call it new.

Experimental would be accurate in the sense that the vaccines that we use did not have a large period of time to be tested, compared to other medications or treatments but this is usually how any medication or treatment made its debut.

Usually wars and pandemics lead to rapid progress of medical sciences because there is more of a drive to not let people die. Penicillin started in a similar fashion and it is one of our most effective and life saving medications. One of my friends was actually in the Oxford drug trials now she is fully protected.

I have to say, the difference though in this scenario and the past is stark big pharma drug and medication research and development, because of our extremely tight regulatory environment, used to take a long time to assess for safety, but also a lot of the data was not made public. So that the companies could make money.

Now, entire countries are being exposed, but the data is transparent and available to all, an extraordinary achievement in the sense that they are not allowed now to sweep mishaps or issues under the carpet anymore.

Also, external agents and scientists are able to look at the effectiveness data and how well vaccines work without interference from the parent company.

In the push for vaccination the government mentions informed consent. Informed consent must be given prior to administration of the vaccine. Is this a way for the government to avoid responsibility for any future side effects down the track considering that there is not enough data for anyone to ascertain long term effects on the body of vaccination?

Informed consent is one of the linchpins of medical practice you need to let people know about ALL the possible side effects before administering a treatment or procedure, no matter how exceedingly rare they can be. This has always been the case, and is not new.

We have been using vaccination as a principle for nearly 100 years the side-effects of getting COVID, on the other hand, are pretty immediate and quite dramatic.

Which groups should not be vaccinated? (For example those who have recovered from COVID-19 and many groups have no possibility of benefiting from the vaccine, including younger individuals, pregnant women, women of childbearing potential, and those with immunodeficiencies) and why?

So as for who should get it, this is where we are still learning Israel has managed to vaccinate its entire adult population and will be proceeding to reduce the age to include children so more information will be available.

So the very young will probably not be vaccinated at this point, the elderly definitely, emphatically should, as they are the population with the highest complications.

Pregnancy and being of childbearing potential has not shown any impacts at this stage. The numbers that we have for clots are extremely small from the vaccines whereas pregnancy and cancer, or even COVID, increases your risk several orders of magnitude up.

Immunodeficiencies such as HIV or immunocompromised patients due to organ transplants or renal dialysis, however, are still at the forefront of research because they do not seem to generate the immune response that the vaccine requires to provide protection. There is a recent initiative to see whether 3 doses are required for these patients. More information coming soon!

What do you think about claims that the global push towards vaccination is a strategy aimed at securing emergency use authorization (EUA) for COVID gene therapies? Why are some people referring to the vaccines as COVID gene therapies? Is this what they are?

I believe this is the usual rhetoric to trigger people, such as GMO food it does not mean what people think.

Gene therapy has a very specific goal replacing the patients genes, who are usually having defects causing diseases such as cystic fibrosis, with the gene sequences that aims to correct the areas that cause the diseases. Or to enhance the gene structure to provide protection against diseases, such as the recent case with the scientist in China who was aiming for producing resistance to HIV. All of them rely on being able to affect directly the patients DNA structure.

To date, this approach has not been successful the closest we have come is to identify what is missing from the body (proteins) and to provide them to the patient.

These vaccines are definitely not gene therapies they do not affect the DNA.

They work by providing mRNA, which is the blueprints that our cells in our body use to make proteins we are using it ourselves for our own proteins. So vaccinating provides our body with the ability to produce, from ourselves, a component of the virus, which on its own can not infect you.

This is in contrast with previous vaccines, such as the tetanus one, which used to give chopped components of the organisms, or of the live attenuated vaccines, which use the actual virus but weaken it so it does not have the strength to infect the host.

Those have been used extensively over the decades, but have inherently more risk for allergic reactions, or of reactivation.

This mRNA delivery is far more elegant, and far more efficient in providing to the body what it needs to mount an efficient immune response without putting it at risk of getting the infection in the first place.

What is mean by a toxin spike protein factory? Do you think that this what is happening to the bodies of those being vaccinated? Do the vaccines coat our DNA or change our DNA?

So this is complete balderdash the mRNA from the vaccines would need to penetrate the core of our cells, and be transcribed into our DNA which is impossible on its own without several other components.

mRNA is what comes from the DNA being read in order to synthesize proteins. Once it is read, it produces the spike proteins that are coating the outside of the virus it is what it needs to hook into our cells and infect them.

So it is both a key component of the virus, and hence important for our immune system to recognise quickly and efficiently, but also quite useless on its own it is like having a key without a hand behind it to insert it into the lock.

This is what the spike protein factory refers to our own cells have protein factories, this is how our DNA is used we are just borrowing our manufacturing ability to give us copies of these keys to prime our own immune system.

HIV, on the other hand, has got a reverse transcriptase that integrates it into our own DNA which is why no vaccines have been able to be made for it all these years.

Do the COVID vaccines trick the body into making the spike protein of the virus? Is it true that the vaccine is distributed in an uncontrolled way throughout the body and can potentially affect different organs of the individuals depending on where their body makes the spike protein? Could this potentially effect the reproductive organs?

I would like to highlight something interesting here the words used. Tricked. There is no tricking the body gets given blueprints to make the same components as the virus to identify it and use it for a better immune response before getting infected.

It is the virus way into the hosts cell it is not, by itself, causing the disease. Otherwise everyone who got a vaccine would be getting COVID. And this is the problem that we highlighted earlier the single case by case scenario can be different between patients or a group of patients, but when we are talking about populations you look at the big picture.

The disease control centre in the US is currently reviewing evidence about whether the vaccine is causing neurological conditions, such as Guillain-Barre Syndrome. My last reading of the data was about 100 cases reported in 12.5 million vaccines. The average background rates in the US are 10 in 1 million of population, because this condition is usually caused by viral infections.

The direct consequences of COVID are much, much higher and can cause direct neurological damage because you dont just get the spike protein but the whole package.

https://jamanetwork.com/journals/jamanetworkopen/article-abstract/2779759

No correlation has been found so far with the reproductive organs, and pregnant women have been vaccinated without any different effects to the ones that are not pregnant.

This is really important, as the initial trials did not include pregnant or lactating women so this is real world data with about 30000 vaccinated pregnant women that were studied and are being followed up.

Should we be worried about other long term health effects of being vaccinated?

It is only sensible to worry about the unknown or new treatments that have not been around for long enough on the other hand COVID poses a very real and documented risk both for short term and long term consequences.

Long COVID has been found to be quite devastating as it affects the heart, the lungs as well as possibly the brain.

Should we be Worried about DNA Changes, Cancer and Chronic Illness as Possible Side Effects?

Of course we should be worried, and of course big pharmaceutical companies pumping the entire population full of substances that are potentially harmful should make us cautious.

All our cells have a place in how they operate reverse transcription would indeed make it possible to get components integrated into our DNA. There are cells that need to do partially such operations, like the cells of our immune system in order to store the memory of this information so it can recall it when the body gets infected with COVID.

For the entire DNA of every single cell of our body to be changed, or at least the stem cells or germ cells that turn into sperm and eggs, to cause a permanent DNA mutation, would involve a level of technology or exposure of something that currently is only present in science fiction movies.

As highlighted before, this would be gene therapy. And the argument is vacuous the body generates the spike proteins. The virus also has these proteins.

So whether you are getting them from the vaccine or the virus the vaccine does not cause the infective consequences of the virus. These proteins can not be incorporated into the DNA.

Also any cell that has a deviation from the original program gets identified and destroyed by the body anyway this is the whole reason why we do not have more cancer or immune diseases.

Should we be concerned about our children being vaccinated and damaging long term effects on their health or for example reproduction or passing on DNA changes to babies?

For the reason mentioned above, as the vaccine has no ability to affect the germ cells, the answer is currently no.

But everyone is exerting the highest amount of caution before wanting to try it with children the current variants up until now seem to not cause them much distress but reports have been coming of some new strains that have been infectious and cause injury to younger age groups too Watch this space!

Should we be concerned about the vaccine ingredients? Some theories include that the ingredients include fetal cells can you please explain this further and should we be concerned about this?

No concerns about the vaccine ingredients now more than ever. Even the minute concentrations of metals that were used in vaccines decades ago have all been switched to inactive inert substances (see table I below).

Fetal cell lines have been used since the 1960s to trial many of our established treatments and vaccines in the past such as rabies and hepatitis A no parts of the cells or the DNA is in the vaccine, but they have been used to trial whether they worked or not. They were not used to produce the vaccines.

The fetal cell line usage, incidentally, has even been accepted by the Catholic church as able to be used for the common good and re-ratified in 2017. The benefits from these cells have saved millions of lives.

Does the Oxford/AstraZeneca vaccine contain animal/ chimpanzee DNA?

No this is patently false.

It uses an adenovirus (common cold virus) that has its ability to replicate snipped and replaced with the instructions for our body on how to make the spike proteins. So similar outcome to Pfizer or Moderna, but by using a carrier instead.

There have been videos circulating showing metal such as spoons and coins sticking to the injection site on the arm as if magnetised. Why is this happening? Do the vaccines contain any ingredients that would cause this? Is this cause for concern?

Unfortunately, as someone who is working in the front lines as an essential worker, therefore receiving both shots as a priority, and surrounded by colleagues, I have to report that neither myself nor any of my thousand colleagues that I worked with have developed super powers or magnetic abilities.

I would love to see such feats in person.

Why are some people still vulnerable to the virus even after vaccination?

Because the vaccination does not make you immune it does however decrease your risk of dying or being hospitalised from it by 100%.

The problem is when you have only received one shot and your immunity is not fully primed or immunocompromised.

The current scientific theory is about a partially vaccinated person with HIV being the source of one of the current strains in the UK as the virus has more chances to evolve in a partially protected individual and get more ways to infect us.

And people on dialysis or with solid organ transplants are always at risk because of the immune system deficiencies they have or acquire.

Visit link:
The Search For Answers In The Global Push For Mass Vaccination - Greek City Times - GreekCityTimes.com

Recommendation and review posted by Bethany Smith

In the past 18 months, there is one thought that has crossed the mind of nearly everyone in the world: if I get sick, whats the best way to get help? Medical care, unfortunately, is not evenly distributed, but there are a handful of companies that are making improvements to various processes within healthcare.

Singapore is home to more than 60 multinational medtech firms. The city-state is one of the leaders in medtech R&D in the Asia Pacific region, which is the worlds second largest medtech market with a compound annual growth rate of 9%.

Here are a few medtech companies rooted in Singapore that have caught our eye.

Biofourmis was founded by Kuldeep Singh Rajput in Singapore in 2015 before the company shifted its headquarters to Boston in 2019. The firm mines patient physiology data to provide insights for healthcare providers and pharmaceutical companiesand provides predictive suggestions for optimized personalized care regimens.

Heres how Rajput described Biofourmis work to KrASIA: In the most basic terms, Biofourmis enables clinicians to better manage patients at home by predicting bad outcomes before they happen.

The founder referenced heart disease, the leading cause of death in the world, and said less than 1% of heart failure patients are on the optimal dose of their medication and less than 25% of eligible patients receive all of their goal-directed medical therapy. To address this issue, Biofourmis BiovitalsHF platform uses wearable sensors that monitor patients vital signs at home and feeds data to an AI-powered algorithm, which in turn reports symptoms and other information through an app that can be accessed by patients. This also makes it possible for clinicians to address symptoms even before they manifest.

Another useful platform is Biovitals [emailprotected], which was co-developed by Biofourmis and Brigham and Womens Hospital, a Harvard teaching hospital, for use in Brighams Home Hospital Program. Patients that are part of this initiative had 70% lower readmission rates, a 32% increase in physical activity, and 38% lower costs than patients admitted to hospital facilities, according to a study published in the Annals of Internal Medicine.

With a flexible R&D process, Biofourmis was able to adapt to changing conditions in the past year and a half. At the onset of the pandemic, the company was contacted by a research partner at Queen Mary Hospital in Hong Kong who inquired about a remote patient monitoring solution. The goal was to help clinicians safely mange patients who had contracted the coronavirus. Biofourmis didnt have such a product at the time, but its team of engineers was able to develop its Biovitals Sentinel system, which uses machine learning to create a correlation between multiple vital signs during the patients daily activity and build an individualized biometric signature. The system was added onto the modular Biovitals platform, and then the Singapore Ministry of Health and Australian government also deployed it to monitor and manage COVID-19 patients.

Biofourmis counts a handful of notable investors as stakeholders, including SoftBank, Sequoia Capital, Openspace Ventures, SGInnovate, and EDBI, the private equity and venture capital arm of Singapore Economic Development Board.

Think of Doctor Anywhere as a virtual clinic. The company makes telehealth possible thanks to a team of online licensed medical professionals ready to attend to patients online within minutes. The service keeps people with medical conditions in contact with medical care providers at a time when it is crucial to hunker down and prevent community transmission of COVID-19. Founder and CEO Wai Mun Lim told KrASIA that Doctor Anywhere had around 50,000 cumulative users in January 2019, and that count is now 1.5 million in July 2021.

The company went from having a network of 1,000 medical providersgeneral practitioners, psychologists, psychiatrists, nutritionists, physiotherapists, chiropractors, specialists, and moreat the start of 2020 to nearly 2,500 now.

Lim cites EDBI as a helpful ally in its quest to expand across the region. As a Singapore-based company, the endorsement from the Singapore governments investment arm EDBI is especially meaningful. Their vote of confidence sends a very clear message to the public that Doctor Anywhere has a strong and trusted service. Their in-depth experience within the healthcare and tech space is especially valuable too, as they provide guidance on how to navigate the space to growing companies like ours. The EDBI network is also a very good way for the company to connect the dots within the healthcare and tech sectors across Southeast Asia, the founder said.

Beyond Singapore, Doctor Anywhere already operates in Thailand, Vietnam, Malaysia, and the Philippines. The company has tech hubs in India and Vietnam.

Originally a business that served cleanroom operations, Esco Lifesciences shifted direction around two decades ago. It now designs and makes a range of equipment used for scientific research, medical testing, and healthcare in areas such as fertility, cancer research, genomics, COVID-19 diagnostics, and more. Its machinery and equipment have been sold to medical, testing, and research facilities in more than 100 countries, and is a testament to the companys ingenuity and go-getter attitude.

Escos tools and services are in demand at a critical time when medical research will determine how all nations can move past the pandemic.

CEO XQ Lin describes the current era as the century of biology. He told KrASIA that Esco represents a proxy for growth for the Asian biopharma sector and the company supplies essential tools to major biotech and pharmaceutical companies for research and manufacturing.

Esco has a new facility in Singapore for its contract development manufacturing organization line of business that focuses on gene therapies and cultured meat. The company has production capabilities for established equipment lines in the United States, Europe, and China.

To meet overall demand, Esco raised a record-setting USD 200 million in May from Vivo Capital, Novo Holdings A/S, China Investment Corporation, EDBI, and other investors. The global nature of our investor syndicate also reflects our global ambitions, Lin said.

Hummingbird Bioscience is creating new therapies against cancer and autoimmune diseases by using data-driven methods to identify antibodies. The goal is to create treatment regimens for patients who are not served by current approaches. All of this depends on Hummingbirds proprietary discovery platform, which utilizes computational biology to generate fresh insights about serious diseases.

One landmark discovery made by Hummingbird was a new understanding of HER3, a well-known drug target involved in cancer that was difficult to inhibit, Ingram said. Hummingbirds researchers were able to generate a general solution to finding antibodies that bind specific regions of target proteins, making it possible to develop new drugs that hit hard targets with key roles in diseases.

Hummingbird started with two employees in 2015 and now has a team of 70, of which 90% are in Singapore, co-founder and CEO Piers Ingram said to KrASIA. He cited Singapores pool of highly skilled professionals and a high degree of internationalism in the labor market as core reasons behind establishing the company in the city-state.

Few domains are as international as science. Drug discovery and development is a perfect example of thiswith a need to attract and retain colleagues with both deep technical expertise, insights into disease biology, as well as the processes of taking a drug from concept to the clinic. Singapore fortunately established itself over many years as a highly attractive place to live and do great work, which makes it easy for us build an exceptionally strong team, Ingram said.

In particular, EDBI, the CEO said, has an unparalleled global network in the broader biotech ecosystem, making it possible for Hummingbird to enmesh itself with other stakeholders in the sector.The company has operations in the United States too, and may reshape medical professionals understanding of how to manage previously untreatable diseases.

More:
These 4 Singaporean companies are changing healthcare as we know it - KrASIA

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Special patient population needs special attention, especially those who undergo HCT

Patients with cancer have been particularly hard hit by the Covid-19 pandemic, both clinically with a higher infection risk and logistically with delays in care delivery. Several recent studies have taken a closer look at how SARS-CoV-2, and the vaccines against the virus, have impacted patients with cancer, particularly those with hematologic malignancies who underwent transplant therapy.

As more transplant physicians are now resuming normal functioning of their transplant units, possibilities of absolute increase in the number of transplant patients getting infected with Covid-19 is expected to rise, cautioned Kamal Kant Sahu, MD, and Ahmad Daniyal Siddiqui, MBBS, both of Saint Vincent Hospital in Worcester, Massachusetts, in a 2021 review. While our understanding about Covid-19 has improved dramatically, a special population such as [hematopoietic stem cell transplant] patients remains at high risk and needs special attention.

HCT and Covid-19

Patients who had hematogenic/hematopoietic stem cell transplant (HCT) or cellular therapy were at significant risk of increased mortality and morbidity due to Covid-19, according to Sibgha Gull Chaudhary, MD, of University of Kansas Medical Center in Kansas City, and co-authors in a publication-only study at the 2021 American Society of Clinical Oncology (ASCO) virtual meeting.

They conducted a systematic review and meta-analysis evaluating the outcomes of Covid-19 in HCT patients, settling on six studies with 1,619 patients (median age 63; 59% men), 646 of whom underwent HCT.

The authors reported that the median days for autologous HCT (autoHCT) was 690 days while it was 450 days for allogeneic HCT (alloHCT). The average follow-up duration after Covid-19 was 24 days.

Gull Chaudharys group found that Covid-19 mortality in HCT patients was 20% (95% CI 0.17-0.23) in a pooled analysis, with a 19% (95% CI 0.15-0.24) mortality rate among those who received autoHCT and 21% (95% CI 0.17-0.25) in those who got alloHCT.

There is a need to prioritize HCT patients for Covid-19 vaccination, close surveillance, and aggressive management, they concluded.

In another ASCO study, the same authors reported that patients who received HCT and CAR-T cell therapy were at an increased risk of moderate-to-severe Covid-19-related pneumonia, and a higher mortality rate with Covid-19.

Muhammad Umair Mushtaq, MD, from the Division of Hematologic Malignancies and Cellular Therapeutics, University of Kansas Medical Center, Kansas City, and co-authors conducted a prospective study of 40 patients (median age 58; 67.5% male) at their institution who were diagnosed with Covid-19 from April 2020 to January 2021. Of those, 25 underwent alloHCT with a median time since treatment of 12.4 months.

While the authors found that >42% of the patients in the study had mild-to-moderate Covid-19, nearly 63% had pneumonia, and that the mortality rate was 12.5% in all patients and 20% in alloHCT patients. They also reported that significant predictors of Covid-19 severity included alloHCT, concurrent immune suppression (65% of those with severe disease received this), and elevated inflammatory markers, such as a mean neutrophil-lymphocyte ratio of 19.7 in those with moderate-to-severe Covid-19.

Mushtaq and co-authors concluded that the findings confirm the need for continuing vigilance with social distancing and masks, and the results join data from other groups that offer similar conclusions: patients with hematologic malignancies undergoing HCT need special handling.

Researchers from the University of Michigan Rogel Cancer Center in Ann Arbor conducted a retrospective study of adult patients who received alloHCT or autoHCT and were subsequently diagnosed with moderate-to-severe Covid-19 infection between March and December 2020.

They found that the majority were either on immunosuppression or had significant comorbiditiesmost commonly diabetes and hypertension, according to a separate study from Braziland that all patients with chronic graft-versus-host disease (GVHD) required hospitalization. They advised that the potential relationship between Covid-19 infection and GVHD development or exacerbation needed more clarity.

A group from the Dana Farber Cancer Center in Boston reported that they had no cases of nosocomial Covid-19 infections in HCT or CAR-T patients at their single center, indicating that these therapies can be safely administered during this [pandemic] period. They also found that in alloHCT patients, cryopreservation of unrelated donor products does not appear to negatively affect early clinical outcomes.

However, they did have one patient with myelodysplastic syndrome (MDS) whose transplant was deferred and whose disease transformed to acute myeloid leukemia, highlight[ing] the risk associated with delaying treatment of hematologic malignancies and the benefit of proceeding with definitive therapy during the pandemic, as long as appropriate safeguards are implemented.

Akshay Sharma, MBBS, of St. Jude Childrens Research Hospital in Memphis, Tennessee, and co-authors conducted an observational study of cases reported to the Center for International Blood and Marrow Transplant Research, and found that recipients of autoHCT and alloHCT with Covid-19 had poor overall survival. We found that in [alloHCT] recipients, age >50 years, male gender, and having received their transplantation within the last 12 months were all associated with worse survival, Sharma explained to VJHemOnc at the 2021 Transplantation & Cellular Therapy (TCT) meeting.

Vaccine Safety

The two-dose mRNA-based Covid-19 vaccine BNT162b2 was deemed to be safe and achieve satisfactory serologic status in patients with cancer, although the study authors noted that there was a pronounced lag in antibody production compared with the rate in noncancer controls; however, the second dose did lead to seroconversion.

The prospective-study cohort consisted of 232 patients (median age 68; 57% male) with solid tumors (27% gastrointestinal; 21% genitourinary; 18% breast) who got IV treatment administered at the infusional ambulatory unit of the oncology center, or inpatient service, at the Rambam Health Care Campus (RHCC) in Haifa, Israel. Nearly three-fourths of the patients had metastatic disease and >70% received immunotherapy or a biological agent. Hematologic malignant neoplasms are treated in a different institution so these patients were not included in the study, explained Irit Ben-Aharon, MD, PhD, of RHCC, and co-authors in JAMA Oncology.Study enrollment and follow-up took place from January to March 2021. All patients were on active treatment and received both doses of the vaccine. They were age-matched with healthy healthcare workers (n=261) who formed the control group.

Serum samples were collected after each vaccine dose and in cases of seronegativity, and electronic health records were reviewed for documentation of Covid-19 infection and results of blood cell counts, liver enzyme levels, and imaging studies, according to Ben-Aharons group.

They reported that after the first dose of 29% of the patients were seropositive versus 84% of the controls (P<0.001), while after the second dose, the seropositive rate reached 86% in the patients.

Testing rate ratios/1,000 person-days after the first dose were 12.5 (95% CI 3.4-45.7) for the patients and 48.5 (95% CI 37.2-63.2) for the controls. The authors also found that patients getting chemotherapy showed reduced immunogenicity (odds ratio 0.41, 95% CI 0.17-0.98). Additionally, the rate of documented absolute leukopenia in seronegative patients reached 39%.

No Covid-19 cases were documented throughout the study period, but there were two cases in the patients immediately after the first dose. In the general U.S. population, a little over 10,000 post-vaccine breakthrough infections were reported by April 2021, according to the CDC.

For adverse events (AEs), 69% of the patients reported injection-site pain, followed by fatigue (24%). Also, elevation of liver enzyme levels >1.5 times from baseline levels was documented in 24 patients up to 6 weeks after the first vaccine dose, the authors reported, but the AE spontaneously resolved in 37% of those patients.

As to whether the specific type of cancer treatment had any role in seroconversion, Ben-Aharons group explained that patients with breast cancer comprised 29% of the seronegative group, and 74% of these patients were treated with chemotherapy, and the treatments were diverse. Hence, we cannot assume that a specific class of drugs may hamper immunogenicity but rather that lymphosuppressive agents may induce a lack of effective seroconversion.

Study limitations included the older population and the fact that cancer patients are generally more adherent to public health and safety measures. Finally, the study lacked a control group of unvaccinated patients.

During a January 2021 European Society of Medical Oncology (ESMO) roundtable, Ravindran Kanesvaran, MRCP, MD, of the National Cancer Centre Singapore, noted that both the mRNA and adenoviral vaccines induce both humoral and cellular immunity, which might be a good thing thinking about this population of patients that is often older or has comorbidities. The immunogenicity data that weve seen on older trial participants is promising and it might also work on the slightly immunocompromised population. We dont know the correlate of protection yet, so its hard for us to predict what type of immunosuppressive therapy would impact the vaccine efficacy.

Ben-Aharon and co-authors pointed out that [a]lthough the immunogenicity pattern was gradual and slower than in the noncancer population, after the second dose most patients were seropositive Our study lends credence to the widely adopted recommendation to prioritize patients with cancer for SARS-CoV-2 vaccination.

But many cancer patients have expressed vaccine hesitancy. For instance, a June 2021 survey-based study in Mexican breast cancer patients reported that over a third were uncertain about vaccination, while more than a fourth said they wanted to see the vaccines AEs in others, and 4% said they would only take the jab if it became mandatory. The study authors called for the active participation of oncologiststo educate cancer patients on the benefits of Covid-19 immunization and to endorse vaccination.

Its a message that cancer care specialists have been driving home. Health experts and federal agencies like the CDC all agree Covid vaccination is especially important for people with cancer. Even if the vaccine might be a little bit less effective in someone who is undergoing cancer treatment its actually even more important to take that vaccine, noted Welela Tereffe, MD, chief medical executive, of the MD Anderson Cancer Center in Houston.

In the same YouTube video, David Tweardy, MD, also of MD Anderson, emphasized that itll be important for cancer patients to work with your doctors to decide when to receive the vaccine in relation to when youre receiving chemotherapy or other treatments for your cancer.

ESMO President Solange Peters, MD, PhD, of the Centre Hospitalier Universitaire Vaudois in Lausanne, Switzerland, suggested that all patients under chemo, under immuno-oncology, under hormone therapy, under antibody therapy should be vaccinated. Some of my colleagues would say, If you can avoid giving the vaccine on the day of high-dose cancer therapy, it might be preferable but even if you have to do thatdo that. That is my main message, for the time being we shouldnt compromise this [Covid-19] protection.

Shalmali Pal, Contributing Writer, BreakingMED

Gull Chaudhary and Mushtaq reported no relationships relevant to the contents of this paper to disclose. Co-authors reported relationships with, and/or support from, TherapeuticsMD, Incyte, Seattle Genetics, AbbVie, Acetylon Pharmaceuticals, Astellas Pharma, Celgene, Millennium, Therakos, AlloVir, Juno Therapeutics, Kite/Gilead, Magenta Therapeutics, EcoR1 Capital, Fresenius Biotech, Gamida Cell, Novartis, and Pluristem Therapeutics.

The study by Ben-Aharons group was supported by the Israel Cancer Research Fund.

Ben-Aharon reported no relationships relevant to the contents of this paper to disclose. A co-author reported a relationship with Pfizer.

Cat ID: 118

Topic ID: 78,118,570,633,730,933,118,125,190,926,192,927,151,928,925,934,172

See more here:
Blood Cancer Patients and Covid-19: Higher Risks but Vaccine Ready - Physician's Weekly

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Gail Devers is best known as an American track-and-field star who won a gold medal in the 1992 Summer Olympics and two more in 1996. Competing in the 100 meters, 100 meter hurdles, and 100 meter relay, Devers wowed the crowds with her speed, strength, and agility, not to mention her signature long, colorful fingernails.

But her first Olympics, in Seoul, South Korea, in 1988, didnt go so well. In fact, it almost didnt happen, even though just months earlier, Devers had broken the American record in the 100 meter hurdles with a time of 12.61.

Soon after setting that record, Devers began feeling tired and had trouble training. Every time I stepped on the track, she says, every race that I ran, every practice, every time I warmed up was just taking more and more out of me.

Devers managed to qualify for the U.S. Olympic track-and-field team in the hurdles, but not for the 100 meter race, as she had hoped, and she was eliminated in the semifinals.

Things just got worse from there: Her hair starting falling out, her fingernails became brittle, she lost weight, she developed sores on her skin, she started having trouble sleeping, she had headaches and tremors, and she started having memory problems. On top of that, her eyes were bulging and irritated.

To say these symptoms were upsetting would be an understatement. I actually covered my mirrors, because I couldn't stand looking at that person. That image was not me, says Devers.

But even while she and those around her could clearly see that something was very wrong, the doctors she consulted had no answers.

It wasnt until Devers visited her old team physician at the University of California in Los Angeles, where she attended college, that anyone mentioned the word thyroid or suggested she get a thyroid-stimulating hormone (TSH) test.

Two days later she had a doctors appointment, but given how many doctors had already told her nothing was wrong, Devers was nervous.

This time was different: The doctor looked at me and he said, I can tell you're a walking thyroid disorder.

And not surprisingly, The tears just started flowing. I was like, Oh, my gosh. After two and a half years, somebody finally, finally, finally, finally saw what was going on!

Devers was diagnosed with Graves disease, an autoimmune disease thats the most common cause of hyperthyroidism.

In Graves disease, the immune system produces an antibody that stimulates the thyroid gland to produce more thyroid hormone than the body needs.

When this happens, the thyroid gland enlarges an enlarged thyroid gland is called a goiter and makes excessive amounts of thyroid hormone, leading to the symptoms of hyperthyroidism.

RELATED: Treatments for Hyperthyroidism: Medications, Surgery, and Other Therapies

Once Devers started treatment for Graves disease, she was able to start training and competing again, and in some respects, the rest is a gold-medal studded history of Olympic wins and World Championships.

But something still wasnt right.

Devers still had eye pain and cloudy vision, and she was constantly needing to use eye drops. The blurriness was so bad that when she was racing she couldnt even see the hurdles.

How did she make it through an event? I know its eight steps from the blocks to the first hurdle, three steps in between, five steps off the last hurdle to the finish line, Devers recounts.

It took Devers 30 years to find out she had a second condition in addition to Graves disease: Graves ophthalmology, also known as thyroid eye disease.

Thyroid eye disease is caused by inflammation in the tissues surrounding the eyes.

The disease typically occurs along with Graves disease, although it can occur on its own.

Symptoms of thyroid eye disease can include redness, a feeling of grittiness in the eyes or constant eye watering, sensitivity to light, swelling or puffiness, bulging eyes, difficulty closing the eyes fully, double vision, and vision loss.

Several forms of treatment can help to relieve symptoms and treat the inflammation in the eyes.

Generally, treatment of thyroid eye disease includes:

On a Mission to Educate

Now that Devers knows whats going on with her health, she wants to make sure it doesnt take other people with Graves disease as long as it took her to find out about thyroid eye disease.

I feel like I've suffered for everyone in the world, she says. No one should have to go through what I went through. And the way to alleviate that suffering is education.

As the onetime relay runner says, You pass the baton from one person to the other. So what we can do as a community is to pass that baton of knowledge and education.

Devers is a strong believer in writing things down symptoms, questions, concerns and bringing those notes to doctor appointments so you can have a conversation and help your doctor help you. If you don't tell them everything, how can they make a proper diagnosis? she asks.

Deverss running goals helped her push through the challenges that Graves disease and thyroid eye disease put in her path. As she says, I'm a very goal oriented person.

Now that she's 53, Deverss goals have changed, but shes still up for a challenge. Right before the COVID-19 pandemic, somebody suggested she train for a half-marathon to coincide with the Olympic marathon trials in Atlanta, where she lives.

Her first response was, You do know I'm a sprinter. Distance for me is anything over 105 meters. But she trained for it and ran 13.1 miles in 1 hour and 53 minutes.

When shes not running, Devers can be found bicycling, dancing, skating, walking, or volunteering at her kids school. I love to stay fit, she says, and I think my life is about service.

Read the rest here:
Why Gail Devers Is on a Mission to Educate About Graves' Disease and Thyroid Eye Disease - Everyday Health

Recommendation and review posted by Bethany Smith

Living with ADHD while going through menopause can be challenging, but there are ways to manage both.

What do ADHD and menopause have in common other than mood changes and inattention?

Though some symptoms are observable on the outside, folks around you may not understand even half of what youre handling internally, let alone that youre managing both at the same time.

Living with attention deficit hyperactivity disorder (ADHD) comes with its own challenges. And if youre going through perimenopause or menopause, you may face more difficulties.

ADHD is a neurocognitive disorder that has three presentations:

People can receive a diagnosis early in childhood as well as late in life.

Dr. Ellen Littman, a clinical psychologist in New York state, explains that estrogen has powerful effects on brain chemistry throughout your lifetime.

Menopause is among the top biggest events to change estrogen in your body, among starting your period and becoming pregnant.

Estrogen is considered neuroprotective, in that high levels increase the availability of neurotransmitters (brain messengers) like dopamine and serotonin, which enhance cognition, mood, sleep, verbal memory, and even ADHD symptoms, Littman says, who is publishing an upcoming review article about the female hormonal effects on ADHD.

However, your levels of estrogen decline beginning in perimenopause and are spent during menopause.

While people face some symptoms off and on during menopause, Littman says those who also have ADHD experience intensified symptoms.

By understanding the relationship between menopause and increased ADHD symptoms, they are less likely to be ambushed by the amplified difficulties they experience, she says.

Both ADHD and menopause are known for patternless shifts in brain activity and hormone changes.

So, you might begin to see how overlapping symptoms happening concurrently or one after the other can worsen the experience of both conditions and make them difficult to manage.

A 2016 study even looks at the effectiveness of using ADHD medication to treat people experiencing executive function issues during menopause.

While going through menopause when you have ADHD can feel overwhelming, there are ways you can manage both conditions.

Finding a psychiatrist whos well versed and experienced in treating ADHD in people going through menopause can help you get the care you deserve.

While it might not be easy to find a psychiatrist with experience in this area, start by asking your current mental health professional or gynecologist for recommendations.

If you cant find a psychiatrist whos familiar with research demonstrating hormone involvement in ADHD symptoms, Littman suggests sharing information or articles (like this one) with them.

If you feel that your credibility is being questioned, its important to feel entitled to finding the clinician who best fits your needs, she says.

Littman suggests finding a gynecologist whos experienced in treating people going through menopause, and who will also work with the doctor who treats your ADHD.

Since women now spend about a third of their lives in menopause, it is critical to find a treatment regimen tailored to your specific needs, she says.

According to a 2019 survey of postgraduate resident trainees in family medicine, internal medicine, and obstetrics and gynecology in U.S. residency programs, only 6.8% of them reported feeling just adequately prepared to manage women experiencing menopause.

No one clinician is knowledgeable about all aspects of each individual experience, but Littman says finding doctors who will collaborate and communicate with your gynecologist can help tailor treatment.

For instance, if your ADHD medications need adjusting, as well as your decreasing estrogen levels, having both your gynecologist and doctor who treats your ADHD collaborate could help.

While pharmacologists often adjust the dosage to meet the new challenges, increased estrogen could address both menopausal and ADHD symptoms. Bioidentical hormone replacement therapy (HRT) is one route to increased estrogen for many women, Littman says.

Although your doctors may be hesitant to communicate with each other, being assertive and informing them of your conditions, as well as bringing information from each doctor to your appointments, can help ensure theyre in tune with whats going on with your body.

While theres a wide range of menopausal symptoms that occur on a continuum, Littman points out that ADHD can worsen symptoms like impaired cognition and mood.

In fact, a 2019 research paper suggests that ADHD symptoms, and even concurrent symptoms from other conditions, are also vulnerable to the hormonal changes experienced during menopause, says Littman.

Both conditions can muddle with your executive functions, a clinical term for your:

If you find that these areas of your life are becoming more difficult to manage, coming up with a plan to help navigate them can make your days easier.

For instance, if keeping and organizing appointments and commitments is difficult, setting an email calendar reminder so you get notifications on your phone, tablet, and desktop can help you stay on track.

If self-monitoring is a blind spot as of late, you could try leaning on your inner circle to gently give you a signal if agitation or strong emotions are coming off more than intended.

You might also look into present moment awareness to reconnect with mindfulness and strengthen your self-awareness.

In addition to seeing a professional, Littman suggests pursuing your own psychoeducation. Consider bookmarking the following resources:

The more you can understand about the relationship between your [brains response to ADHD] and your body in menopause, the more you can be an active participant in your treatment. And the more your support network understands about your challenges, the more supportive and compassionate they can be, Littman says.

While managing your ADHD while going through menopause can be challenging at times, there are ways to make the process easier.

Littman says that on the clinical front, new research brings hope for better treatments ahead.

Were on the brink of an exciting new understanding of the experience of women with ADHD, she says. As new studies continue to implicate the powerful role of hormones in womens experience of ADHD, the potential for more comprehensive and successful treatments may be on the horizon.

You can stay tuned for Littman and teams upcoming study on ADHD and estrogen, titled: ADHD in Females Across the Lifespan and the Role of Estrogen. It publishes August 2021 in The ADHD Report.

Original post:
Tips to Manage when You're in Menopause with ADHD - PsychCentral.com

Recommendation and review posted by Bethany Smith

Local health-care providers are being asked to fill out a survey to help make it easier for people who are transgender to access care in Hamilton.

The Hamilton Trans Health Coalition is calling on primary care providers to explain what barriers they face in providing gender-affirming care for patients who are trans.

Gender-affirming care includes things that are related to transitioning, like HRT (hormone replacement therapy) or surgery, but also includes doctors recognizing their patients pronouns and chosen names, and not making assumptions about their sexual history or sexual orientation.

Cole Gately, chair of the coalition, said the goal of the survey is to determine what kind of barriers and motivators are impacting Hamiltons health-care providers when they have a patient who is trans.

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We just want to know what are the barriers, whats getting in the way? Why arent you doing it and how can we help? There are lots of resources out there. Maybe youre not aware of them.

Since introducing a project co-ordinator earlier this year, the coalition has heard from some doctors, but its also heard from many trans Hamiltonians who are travelling outside of the city to get basic health care that their own doctors are capable of providing.

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Gately said some people are being told by their doctors to seek out specific care on their own and then theyll write a referral, but he said that burden shouldnt be on the patient if providing that care is well within the doctors own abilities.

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What I said to somebody yesterday was, imagine if you broke your wrist and you went into the doctor and the doctor said, Well, you find an orthopedic surgeon and then Ill make the referral. That doesnt happen. The doctor finds the orthopedic surgeon for you and makes the referral because the doctor is the expert.

The survey is open until July 28 and the coalition is urging any and all primary care providers in Hamilton including family doctors, registered nurses, nurse practitioners and physician assistants to fill it out.

2021 Global News, a division of Corus Entertainment Inc.

Link:
Primary care providers called on to respond to survey to improve trans health care in Hamilton - Global News

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Arianna Sholes-Douglas remembers the moment her body was in the grips of perimenopause though she didnt recognize it for what it was at the time, despite being an OB-GYN and integrative health physician focusing on womens health. Sholes-Douglas was performing a C-section, a surgery she estimates she had done over a thousand times, and her brain just blanked.

I had a total brain freeze. I couldnt remember what to do, she recalled. It was very scary, and I didnt know who to talk to or what to do.

At first, she worried it was early-onset Alzheimers. But the big changes shed been experiencing in cognitive function were hormonal. She was going through perimenopause, the transitional period before menopause when a womans body starts making less estrogen until eventually her ovaries stop releasing eggs.

And shes not alone about being in the dark. Many Gen X women and cusp millennials who are at the age range when perimenopause has begun or could soon start have far too little support and information.

We havent been educated. Patients havent been educated. Doctors havent been educated. There really hasnt been a resource thats been reliable for women, so they are caught off-guard, said Sholes-Douglas, who went on to write the book The Menopause Myth: What Your Mother, Doctor, and Friends Havent Told You About Life After 35.

Because in their minds, theyre thinking menopause is an old lady issue, she added. They think its only relevant when they stop having a period.

But thats not true. So here are three important things Xennial women should know about perimenopause:

It can start in your 30s or 40s.

There arent lines around when perimenopause begins, in part because it varies by individual and also because the types of symptoms are so broad. The term perimenopause really just means around menopause.

Its also a stretch of time that can drag on for a while. Many women start to experience symptoms five or even 10 years before they stop having a period (though the average is about four years). And given that full menopause can happen when women are in their 40s or 50s, perimenopause can begin when theyre in their early 40s or even mid-30s.

Since 5% to 7% of women are fully menopausal by age 45 (theyve gone that magical full year without a period), they could be experiencing these symptoms at age 40, not thinking a thing about menopause because these symptoms can be very vague and dont come with a big sign You are entering perimenopause, said Mary Jane Minkin, an OB-GYN with Yale University and founder of the informational website Madame Ovary.

Youre still able to get pregnant during perimenopause.

If youre a woman in your 30s or 40s who is planning to have children (and many women are) and youre fretting that you might instead enter perimenopause, dont freak out. Its very much still possible for women to get pregnant during this phase, though its definitely worth bringing up with your doctor if you have concerns.

The symptoms go way beyond hot flashes.

When most people think menopause, they think of hot flashes. And many (if not most) women getting closer to menopause will experience hot flashes, or brief feelings of being overheated, at some point ranging from pretty mild to really severe.

But there are so many other symptoms that can come along with perimenopause, including missed periods or periods that are heavier or lighter than usual, mood swings, changes in cholesterol levels and bone density, urinary incontinence and cognitive fuzziness.

Many [women] get disrupted sleep usually falling asleep quickly as they are exhausted, but are then up at 1 a.m., sometimes with a hot flash, sometimes without. They may have headaches, they may be achy, they may have some vaginal dryness or urinary leakage (although that usually comes later), Minkin said.

Perimenopause can affect your sexual health and well-being, as well. The sexual aspect part of perimenopause is something I deal with a lot, Sholes-Douglas said. Women are very much caught off-guard when they experience a decline in libido, vaginal pain, vaginal dryness and they dont know why.

But while the possible symptoms associated with perimenopause are wide-ranging, they all really come back to the hormonal changes women go through in the run-up to menopause, as estrogen and progesterone levels fall or rise and fall in uneven spikes.

The Good Brigade via Getty Images

Finding adequate care and support can still be difficult.

Though theres far more information available to women and health care providers now than had been the case a few decades ago, and many active support communities have flourished, perimenopause is still something women arent adequately educated about, according to experts.

Minkin said Gen X women are probably slightly better prepared, but not dramatically so. Sholes-Douglas was more emphatic: Most women are just not prepared.

There are a few reasons for this, one of which is that there simply isnt a test doctors can perform to see if women have entered perimenopause.

Hormone levels may not show much, Minkin said. For example, a doctor might do an estradiol test to check your estrogen levels, but since normal levels during a menstrual cycle range wildly (from 45 to 350 picograms per milliliter), its hard to know where your level should be.

Lets say we draw a blood level of 50. Well, is that normal? It may be. But if your level should be 300, thats low, Minkin explained.

Its a tough diagnosis to make at the time, she added. When the patient goes that year without the period, you can then say, Well, hey that was all perimenopausal!

On top of which there is a lack of consensus about how to treat symptoms of perimenopause even if it is clear thats the issue. Hormone therapy, which involves taking supplemental hormones, is one option, but some past studies have indicated it can come with other health risks. Some doctors might recommend lifestyle changes to help manage symptoms; in other cases, women might take medications to more directly address such symptoms as vaginal dryness or mental health changes.

Unfortunately, a lot of this ends up falling on women. They end up needing to connect the dots in their own symptoms and find health care providers who have experience dealing with perimenopause. Which is why it is so important for Xennial women to be aware of whats happening in their bodies now, or what lies just ahead.

Ive had countless patients tell me they went to the doctor and told them they suspected they were perimenopausal, and the doctor said: Oh, youre too young for that. Youre too young for that, Sholes-Douglas said.

You should not assume that your doctor is going to know more about this than you do, she added. On some level, obviously they will. But dont underestimate the power you have.

More:
Perimenopause: The Women's Health Issue No One's Talking About Enough - HuffPost

Recommendation and review posted by Bethany Smith

I am a 77-year-old woman. I am 5 feet, 2 inches tall and weigh 107 pounds. I take no medication. When I went to the doctor last week, he found that my alkaline phosphatase was 176, my ALT 10, and my AST 11. He told me I had fatty liver and to get a scan, but I had no way to get to the place to have it done. He did not say anything else about it. I have no symptoms. Does this sound like fatty liver to you? I did not really like my doctor, but with my insurance it is hard to change doctors. If I do have fatty liver, is there anything I can do for it?

Fatty liver is an increasingly common problem. Risk factors include being overweight and having diabetes, high blood pressure and abnormal blood cholesterol levels.

Alcohol use is also a cause of fatty liver, and all people with fatty liver are strongly recommended to abstain from alcohol entirely. The primary treatment is diet and weight loss.

It sounds like there was some missed communication between you and your doctor. Fatty liver is a possibility; however, it does not seem likely to me, as you have not identified any of the risk factors, and you are certainly not overweight if anything, you are a bit underweight.

Further, although the alkaline phosphatase can be elevated in fatty liver yours is just a bit high it is more common for AST and ALT to be elevated, which yours are not.

An ultrasound scan is a good, but not definitive, way of looking for fatty liver. A liver biopsy is still the definitive test, but its often not done in people whose history, physical exam and ultrasound are all suggestive.

A slightly abnormal alkaline phosphatase does not necessarily mean you have a liver problem. Bone issues fractures, Pagets disease of bone, high thyroid and parathyroid hormone levels can cause a high alkaline phosphatase, too.

Additional liver tests checking the GGT level or specifically what kind of alkaline phosphatase you have, by isoenzyme analysis can make the source of the elevated alkaline phosphatase clearer.

Getting an ultrasound scan and additional blood tests is a reasonable place to start. Unfortunately, lack of confidence in your physician is a different problem.

If you really cant get a new doctor, then you need to have a conversation about proceeding with evaluation in such a way that you can do so while being confident that you are getting good advice.

A few years ago, I read that the herbal supplement feverfew may help with some migraines. Having suffered with severe migraine for over 50 years, I decided to try it. I take one capsule four times a day, and it has completely rid me of my migraines. Would you please mention it again?

Feverfew is a common herbal remedy to prevent migraine, and although not all trials have shown benefit, the majority of studies I have read showed that it is more effective than a placebo and the side effect risk is very small.

Other nonprescription treatments that have been shown in most studies to be beneficial include magnesium, riboflavin and coenzyme Q10. They are generally safe and well-tolerated, and I hope others may get the same relief you have found.

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To Your Good Health: What is treatment for a fatty liver? - Agri News

Recommendation and review posted by Bethany Smith

Delayed mammograms and breast cancer diagnoses during the COVID-19 pandemic may have a small long-term impact on breast cancer mortality rates up to 2030, according to results of a study with simulation modeling.

Findings from this study published in the Journal of the National Cancer Institute highlight the importance of continuing breast cancer screenings and evaluations in symptomatic women.

Some women simply skipped their mammogram if they were scheduled to undergo a mammogram during the pandemic, said Oguzhan Alagoz, who holds a PhD in industrial engineering and is a professor of industrial and systems engineering at University of Wisconsin-Madison, in an interview with CURE. What we are suggesting is rather than skipping the mammogram and waiting for your next mammogram whether it is in two years or next year this suggests you need to make up that missed mammography exam as soon as possible. Thats the primary means of undoing the impact of the pandemic.

When the COVID-19 pandemic first started, screening mammography and diagnostic mammography declined up to 80%, according to the studys introduction. There were also changes in breast cancer treatment protocols, which led to treatment delays and lower rates of chemotherapy administration.

In this short term, there was a huge reduction in the number of screenings (and) diagnoses, Alagoz said. The concern is if we have these short-term declines in breast cancer control activities, what will be the impact in the long term? Breast cancer is an interesting disease, where if you delay mammography, youre not going to see the full effect of it in six months or 12 months. Sometimes, some of these effects are seen in five years, 10 years.

To assess the potential long-term impact of breast cancer control disruptions during the COVID-19 pandemic, researchers used three established breast cancer models to simulate reductions in mammogram screenings, delays in the diagnosis of cancer in symptomatic patients and reductions in chemotherapy treatments for women with early-stage breast cancer. These scenarios were assessed within the first six months of the pandemic, when reduced screening rates were observed, following a return to patterns similar to before the pandemic.

Alagoz provided the reason as to why researchers only focused on the first six months of the pandemic rather than the entire pandemic.

By the end of the summer of 2020, many practices, clinics and health systems actually made up all of the missed mammography exams, Alagoz said. We have seen the screening volumes basically reach almost 100% capacity back in the summer. I (spoke) with our radiologist collaborators, (who) are telling me that they scheduled additional weekend and weeknight mammographic screenings.

Based on the model projections, researchers found that by 2030, there could be 950 cumulative excess breast cancer deaths related to reduced screenings during the COVID-19 pandemic. In addition, there could be 1,314 deaths from the delayed diagnosis of symptomatic patients and 151 deaths linked with reduced chemotherapy in women with hormone-positive, early-stage cancer. Collectively, there may be an estimated 2,487 excess breast cancer deaths, which represents a 0.52% increase in deaths by 2030 compared with models indicating breast cancer deaths without the effect of the COVID-19 pandemic.

Although any increase in mortality rates isnt ideal, Alagoz mentioned that these results were a pleasant surprise for his research team.

Before I started this study, I was really expecting a significant number of breast cancer mortality over the next 10 years due to the pandemic, Alagoz said. Fortunately, the impact is actually relatively small (in magnitude). I was expecting maybe 10,000 additional deaths, 15,000 additional (deaths), but our modeling suggests that we are going to see an additional 2,500 deaths over the next 10 years due to the pandemic.

He mentioned that these lower-than-expected increases in mortality rates are a somewhat positive finding of the study.

I think the silver lining in this unfortunate paper is that the impact is not as high as I was scared it would be, which is good news, Alagoz said. Primarily, that is because many practices after the initial shock of the pandemic and many patients were able to actually make up the exams and did resume the normal operations within a six-month period.

Alagoz added that delays during the COVID-19 pandemic did not greatly affect women who were already diagnosed with breast cancer.

Our findings show that disruptions didnt affect (these women) too much, Alagoz said. In other words, anybody who was supposed to get surgery, radiotherapy or chemotherapy, they already got the treatment. Oncologists aware of the really terrible potential effect of delaying the treatment or stopping the treatment didnt really change treatment practices very much. The patients who were already diagnosed with breast cancer prior to the pandemic, the effect of the pandemic on their care or mortality, we found, is limited.

Although there are some effects of the COVID-19 pandemic that can be undone, such as making up missed mammograms sooner rather than later, Alagoz said there are some consequences that cannot.

For example, many women during their self-exam (or) during their annual physician visit, they observe a palpable lump in their breast and then they go and visit the clinic, Alagoz said. And those cases dropped significantly during the pandemic. There is very little we can do to undo those effects. Those women already came for a delayed diagnosis, maybe like three months (or) six months later, and, unfortunately, there is not much we can do to undo that. But at least for the screening mammography exams that women (missed), we can certainly mitigate the impacts of the pandemic.

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Disruption in Breast Cancer Care During COVID-19 Pandemic May Slightly Increase Long-Term Mortality - Curetoday.com

Recommendation and review posted by Bethany Smith