TORONTO--(BUSINESS WIRE)--Acerus Pharmaceuticals Corporation (TSX:ASP) today announced the signing of an agreement granting medac Gesellschaft fr klinische Spezialprparate mbH (medac) the exclusive right to market NATESTO in 15 European countries (Germany, United Kingdom, France, Italy, Czech Republic, Slovakia, Spain, Sweden, Finland, Denmark, Norway, Poland, Austria, Netherland and Belgium). medac is a German pharmaceutical company with business in 80 countries and more than 1,200 employees worldwide.

We are delighted to be partnering with medac for the commercialization of NATESTO in Europe, said Tom Rossi, President and Chief Executive Officer of Acerus. Their extensive reach and commercial expertise within the speciality pharmaceutical sector will be a key advantage as we aim to maximize the full potential of NATESTO. This agreement represents a significant milestone for Acerus as we continue to execute on our strategy of expanding the brands reach on a global scale.

We are very pleased to announce this partnership with Acerus as it enables us to provide patients in Europe with an innovative product and address a medical need, said Dr. Ulrich Kosciessa, Managing Director of medac. NATESTO is an important advance for patients suffering from hypogonadism. Its novel nasal administration and unique safety and efficacy profile represent a clear opportunity to improve patient quality of life and represents a perfect fit to our current portfolio. We look forward to working closely with Acerus as we prepare to file NATESTO for European marketing approval.

Under the terms of the agreement, Acerus will receive a non-refundable upfront fee and regulatory milestone payments upon medac receiving marketing approval in certain countries as well as milestone payments based on achieving sales targets. In total, Acerus is eligible to receive up to 11,500,000 in upfront and milestone payments. Acerus will oversee the manufacturing of NATESTO and, in addition, will receive a supply price for the product. If approved, NATESTO will be the first and only testosterone nasal gel for androgen replacement therapy in adult males for conditions associated with a deficiency or absence of endogenous testosterone (hypogonadism) in Europe.1

About NATESTO(Testosterone) Nasal Gel

NATESTO is approved and available in Canada for replacement therapy in adult males for conditions associated with a deficiency or absence of endogenous testosterone (hypogonadism). NATESTO is a testosterone nasal gel available in a no-touch dispenser with a metered dose pump for reduced transference risk. The recommended starting dose of NATESTO in Canada is 11 mg of testosterone (one actuation per nostril) administered twice daily for a total daily dose of 22 mg, the lowest topical gel testosterone dose approved in Canada. A copy of the NATESTO product monograph can be found at: http://www.aceruspharma.com/English/products-and-pipeline/natesto/default.aspx.

NATESTO is also approved and available in the United States. For further information, specific to the U.S. product dosing and administration, please visit: http://www.NATESTO.com.

About Acerus

Acerus Pharmaceuticals Corporation is a fully-integrated, Canadian specialty pharmaceutical company engaged in the development, manufacture, marketing and distribution of innovative, branded products in Mens and Womens Health. Acerus shares trade on TSX under the symbol ASP. For more information, visit http://www.aceruspharma.com and follow us on Twitter and LinkedIn.

About medac

medac is a privately held, global pharmaceutical company based in Hamburg, Germany, specialising in the diagnosis and treatment of oncological, urological and autoimmune diseases since 1970. Besides an already established product portfolio medac is dedicated to the refining of existing and the development of new therapeutic products providing patients with ground-breaking individualized treatments. medac prides itself in taking a personalized approach to medicine by supporting doctors and patients as they seek to overcome acute and persistent diseases.

Notice regarding forward-looking statements

Information in this press release that is not current or historical factual information may constitute forward-looking information within the meaning of securities laws. Implicit in this information are assumptions regarding our future operational results. These assumptions, although considered reasonable by the company at the time of preparation, may prove to be incorrect. Readers are cautioned that actual performance of the company is subject to a number of risks and uncertainties, including with respect to the regulatory approval of NATESTO in Europe and the achievement of the milestone payments by Acerus, and could differ materially from what is currently expected as set out above. For more exhaustive information on these risks and uncertainties you should refer to our annual information form dated March 7, 2017 that is available at http://www.sedar.com. Forward-looking information contained in this press release is based on our current estimates, expectations and projections, which we believe are reasonable as of the current date. You should not place undue importance on forward-looking information and should not rely upon this information as of any other date. While we may elect to, we are under no obligation and do not undertake to update this information at any particular time, whether as a result of new information, future events or otherwise, except as required by applicable securities law.

References

1. NATESTO Product Monograph, October 25th, 2016 and Rogol et al. J Andrology 2015, 4(1), 46.

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Acerus Announces Licensing of NATESTO - Business Wire (press release)

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Domainex will expand its two-year-old collaboration with Imperial College London to discover new therapies that reduce heart muscle damage during heart attacks, the partners said today.

Domainex and Imperial aim to discover a treatment that inhibits the enzyme MAP4K4, which is linked to cell death following heart attacks. Since the collaboration was launched in 2015, the partners said, they have discovered novel, potent, and selective MAP4K4 inhibitors using human cardiac muscle grown from human induced pluripotent stem cells (iPSCs).

The inhibitors have shown promise in protecting these cells against oxidative stress, a trigger for cell death during heart attacks, Domainex and Imperial said.

As a result of the progress, Imperial College London said, its Professor Michael Schneider, Ph.D., has secured a follow-on award of 4.5 million (nearly $5.8 million) from the Wellcome Trusts Seeding Drug Discovery initiative to continue the research.

From its Medicines Research Centre near Cambridge, U.K., Domainex said, its researchers will continue to provide integrated drug discovery servicesincluding further biochemical, cellular and biophysical assay screening, and structure-guided medicinal chemistry coupled with drug metabolism, safety, and pharmacokinetic assessment of promising candidates.

Domainex and Imperial said they aim to advance potential treatments into preclinical development and ultimately to clinical evaluation.

"We have already identified a number of very exciting, novel inhibitors through structure-based drug design," Domainex CSO Trevor Perrior said in a statement. The innovative cardiac muscle assay developed by the team here at Domainex working in partnership with Imperial College London, is enabling early testing on human cardiac muscle cells, which will make cardiac drug discovery more efficient and effective in identifying efficacious candidate drugs.

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Domainex, Imperial College London Extend Cardiac Therapy Collaboration - Genetic Engineering & Biotechnology News

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If youre having a heart attack, your life might someday be saved by pond scum.

Thats because these lowly bacteria are capable of producing something a stricken heart desperately needs: oxygen.

In fact, when Stanford scientists injected massive doses of cyanobacteria into the hearts of rats who suffered the equivalent of a widow-maker heart attack, oxygen levels ballooned by a factor of 25.

The results, published Wednesday in the journal Science Advances, suggest a truly original approach to reducing the damage done to heart muscle when it is suddenly deprived of oxygen.

When blood flow to the heart is interrupted by a clot or the narrowing of vessels, the effect can be deadly, either now or later. Its not uncommon for a heart attack victim to survive his or her immediate ordeal, only to succumb to heart failure the effects of heart muscle weakened by its brush with oxygen deprivation months or years after the event.

Physicians have long sought to avert that lingering damage by restoring the flow of oxygenated blood to the heart muscle as quickly as possible. Wielding an arsenal of drugs, stents, grasping devices, saws, scalpels and long, threaded catheters, cardiac surgeons try to isolate, remove or dissolve clots in the arteries feeding the heart before cells start to die off and lasting damage is done. More recently, stem cells have shown great promise in restoring damaged heart muscle.

But this new approach to rescuing living tissue from so-called ischemic damage proceeds from the observation that oxygen abounds in our atmosphere as a result of photosynthesis the fuel-making industry of green plants all around us.

If a lack of oxygen is the problem when living tissue is deprived of blood flow, perhaps we should invite into our bodies the forests genius for manufacturing the gas our cells depend on to survive.

Every day we walk around and see trees, said Dr. Joseph Woo, chair of Stanford School of Medicines department of cardiothoracic surgery and the papers senior author. We wondered, would there be any possibility of taking plants and putting them next to the heart and getting them to work together?

Several years ago, researchers in Woos Stanford lab started by grinding spinach, and then kale, with mortar and pestle. When they introduced the green slurry to living tissue in Petri dishes and set them in the sun, nothing happened.

But when they tried a more primitive practitioner of photosynthesis pond scum the oxygenation effect was clear to see.

The scientists used cyanobacteria, the blue-green algae that often blooms on the surface of still waters, to supply life-giving oxygen to the stricken hearts of rats. After clamping off the largest of three arteries feeding blood to the heart the left anterior descending coronary artery the researchers injected those hearts with tens of millions of the single-celled organisms.

For two full hours one hour while the clamp remained in place and a second hour after it was removed the animals incisions remained open. During that time, the hearts of the treated rats were exposed to strong light, which jump-started the photosynthetic process.

Just as they would on the surface of a pond, the cyanobacteria used the pigment chlorophyll to combine water, carbon dioxide and light to produce glucose. The incidental byproduct of that process oxygen kept cells deprived of oxygenated blood from dying off in droves.

A day later, the damage to the hearts of treated rats was less than half as severe as that seen in rats that got an inactive treatment, according to the study.

And four weeks after the ischemic crisis, the hearts of rats that got the photosynthesis treatment performed dramatically better than the hearts of rats that did not.

In humans, an improvement in heart function of the magnitude shown in treated rats would have profound clinical implications, the Stanford team wrote. If humans were to reap benefits as great as those seen in the lab rats, they added, such a treatment probably would spell the difference between a healthy patient and one suffering from heart failure.

Woo sees the new research as a proof of principle that photosynthesis, in some form, might someday be used as a bridge treatment for patients who have had blood flow cut off to any organ. It might be useful in sustaining organs harvested for transplant during their long journey to a new owner, Woo said, and in preventing the death of brain cells during a stroke. It may even one day improve the treatment of malignant tumors that thrive in oxygen-deprived environments, he added.

But in its current form, a photosynthetic bridge treatment is far from ready for use in clinical settings.

It would be very suboptimal to have to crack someones chest open and shine the light on them to begin the oxygenation process, Woo said. To work around that impracticality, a team at Stanford is already working on supercharged versions of the cyanobacteria that rescued rats hearts in his teams new paper.

Researchers may have to engineer ways other than direct exposure to visible light to jump-start the photosynthesis process, he said. Plants or cyanobacteria may be amenable to genetic engineering that would allow them to produce oxygen more copiously, or to initiate photosynthesis in response to energy at wavelengths that can penetrate skin and other tissue.

Remarkably, the direct injection into the heart of millions of cyanobacteria did not cause any infection. Nor did it prompt the rats immune systems to mount a defensive response a reaction that can be just as deadly as infection.

Virtually all of the millions of single-celled organisms injected into the rats hearts were gone 24 hours after the experiment. And in a more thorough search four weeks later, the researchers could find no sign of infection or of lingering bacterial cells anywhere near the hearts of rats who got the treatment.

If cyanobacteria were someday to play a key role in the treatment of human disease, it would be a nice footnote to an already striking record of accomplishment. Thats because cyanobacteria one of the largest, oldest and most important groups of bacteria on Earth are already pretty much responsible for life as we know it.

In the Archaean and Proterozoic eons 2.5 billion years ago, cyanobacteria flourished by using light and carbon dioxide for nourishment. The oxygen given off by this photosynthesis created Earths oxygen-rich atmosphere, making the evolution of ever more complex life forms possible.

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How oxygen-producing pond scum could save your life after a heart attack - Los Angeles Times

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Release from the University of Virginia Health System:

CHARLOTTESVILLE, Va., June 14, 2017 - University of Virginia Cancer Center has earned recognition as a national center of excellence for its care of patients with myelodysplastic syndrome (MDS), a cancer of the bone marrow that often leads to leukemia.

UVA is the only center in Virginia to receive this designation from the MDS Foundation for the treatment of this condition, which UVA hematologist Michael Keng, MD, said is often referred to as a bone marrow failure disorder.

Bone marrow produces stem cells that make white blood cells, red blood cells and platelets. In patients with MDS, the marrow does not produce enough healthy cells. When there are not enough healthy cells, there is an increased risk of infection, bleeding, easy bruising and anemia. Approximately 30 percent of patients diagnosed with MDS will progress to a diagnosis of acute myeloid leukemia.

According to the MDS Foundation website, centers of excellence have:

UVA provides tailored care for each MDS patient through a multidisciplinary team. UVAs care team includes medical oncologists/hematologists, pharmacists, care coordinators, nurses, infectious diseases specialists, clinical trial coordinators, and support services such as social workers, case workers, and therapists.

UVA is devoted to providing support, research, treatment and education around MDS to all patients, caregivers, physicians, nurses and other healthcare providers, Keng said.

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UVA Honored as Center of Excellence for Bone Marrow Cancer - NBC 29 News

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Dr. Keith Roach, Syndicated Columnist

DEAR DR. ROACH: I hope you can answer some questions about myelodysplastic syndrome. What does it do to your body? Is there a known cause or cure? What is the prognosis? P.B. ANSWER: The myelodysplastic syndromes are a group of similar diseases, specific types of blood cancers, that prevent your bone marrow from working properly. They also can transform into acute leukemia. These are uncommon cancers, with perhaps 30,000 cases per year in the U.S. The specific myelodysplastic syndromes are now categorized by appearance, genetic abnormalities of the cells, and condition of the bone marrow.

MDS may arise from damage to DNA, such as from radiation or other toxic exposures. However, many cases have no known cause, and its likely that these are spontaneous mutations in the bone marrow cells.

Because MDS is a group of related diseases, the treatment and prognosis vary among the different subtypes. However, supporting the bone marrow with transfusions of red blood cells and platelets often is necessary. Medications to stimulate both red and white blood cell production can be used. A few people will be recommended for bone marrow (stem cell) transplant, but the decision to consider this treatment must be made cautiously, as many people who get MDS will not benefit from this treatment due to age or other medical conditions.

The prognosis depends on the age of the person affected and their specific MDS. A person younger than 60 with a low-risk MDS has a median survival (based on data published in 1997) of about 12 years. However, high-risk MDS has a much worse outcome: Half of people succumb within six months. Advances in treatment since these data were published have improved these results, but not as much as hoped.

DEAR DR. ROACH: My 89-year-old mother suffers from fluttering in her heart. She saw an expert in cardiac arrhythmias, who diagnosed her with tachy-brady syndrome and sick sinus syndrome. A nurse also said she has PVCs. She is taking metoprolol, but still has episodes of fluttering. What are these conditions? Are there other medications she could take to correct this heart condition? M.D.P.

ANSWER: Tachy-brady syndrome (from the Greek roots for fast and slow) and sick sinus syndrome are the same thing. The sinus in sick sinus syndrome refers to the sino-atrial node of the heart, which is the hearts natural pacemaker. It is where every beat normally starts. This part of the heart can become diseased, and the heart can beat both too quickly (tachycardia) and, at other times, too slowly (bradycardia). Sick sinus syndrome can come from many different conditions and, rarely, from medications.

Medications are sometimes used for sick sinus syndrome. Beta blockers, like the metoprolol your mother is taking, are given to slow down the tachycardic component of sick sinus, but it can make the bradycardia worse. Most often, the treatment for sick sinus syndrome is a permanent pacemaker. Not everyone needs it, but Im sure your mothers cardiologist is monitoring her and will recommend a pacemaker if needed. If one is necessary, 89 years old is not too old to put in a pacemaker.

PVCs are very common and do not usually indicate disease in the heart, although they are more common in people with heart disease, especially poor blood flow to the heart. Premature ventricular contractions themselves seldom need treatment.

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TO YOUR GOOD HEALTH: 'Myelodysplastic syndrome' covers a range of diseases - Prescott Daily Courier

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AUSTIN, Texas -- Gov. Greg Abbott has signed a new law that allows terminally ill or those which chronic diseases receive stem cell treatments in Texas.

Stem cell therapy is the use of stem cells to treat or prevent a disease or condition, and is often patient's last hope for improvement.

Bone marrow transplant is the most widely used stem-cell therapy, and can often help those with multiple sclerosis and other diseases.

House Bill 810, which was introduced by Rep. Tan Parker, R-Flower Mound, passed in both the Texas House and Senate.

"It is easy to fall into the trap of viewing legislation as just words on a piece of paper," said Sen. Paul Bettencourt, R-Houston, the bill's sponsor in the Senate. "But for the many people who are ill with multiple sclerosis and other diseases that stem cell therapy has the hope of solving in our lifetime, I look at this bill, I look at the possibility of what can happen in the 21st Century, with Texas taking the lead on adult stem cell treatments and this bill has the potential to extend lives and make a difference for these patients."

The Texas Medical Board will be responsible for writing the rules for the treatment.

"Everyone has a zest for life. This adult stem cell treatment possibility gets government out of the way to let these new therapies flourish and give these patients hope for a future good quality of life," Bettencourt added.

The legislation takes effect Sept. 1.

-- Value of Stem Cell Therapy --

According to the National Institues of Health, stem cellshave the remarkable potential to develop into many different cell types in the body during early life and growth.

In addition, in many tissues they serve as a sort of internal repair system, dividing essentially without limit to replenish other cells as long as the person or animal is still alive.

When a stem cell divides, each new cell has the potential either to remain a stem cell or become another type of cell with a more specialized function, such as a muscle cell, a red blood cell, or a brain cell.

Doctors say stem cells are important for living organisms for many reasons.

In the 3- to 5-day-old embryo, called ablastocyst, the inner cells give rise to the entire body of the organism, including all of the many specialized cell types and organs such as the heart, lungs, skin, sperm, eggs and other tissues.

In some adult tissues, such as bone marrow, muscle, and brain, discrete populations of adult stem cells generate replacements for cells that are lost through normal wear and tear, injury, or disease.

---

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Governor Signs Law to Allow Chronic, Terminally Ill in Texas to Get Stem Cell Treatments - Spectrum News

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Dr. Jacob Hanna believes stem-cell treatments hold promise for restoring fertility to cancer survivors whose chemotherapy has rendered them infertile. (Weizmann Institute)

This article issponsoredby theIsrael Cancer Research Fund.

Cancer is the second-leading cause of death in the United States, responsible for 22.5 percent of American fatalities. Only heart disease is more deadly.

In Israel, cancer is the No. 1 killer. Thats partly why Israel has become a research leader in the fight against the disease.

Many of the worlds most effective cancer treatments have roots in Israeli research, sometimes going back decades. The work taking place in Israeli labs today may lead to lifesaving treatments years in the future.

Here are five promising areas Israeli researchers are studying in their quest for better cancer detection and treatment. Together they provide a glimpse into the remarkable scope of cancer research being conducted by internationally renowned scientists across Israeli institutions.

Mutant reeducation camp and the fight against ovarian cancer

Mutant reeducation may sound like the plot of the next X-Men movie, but for a team of Israeli researchers it could be central to finding new treatments for ovarian cancer, an especially deadly disease because of the difficulties of early detection. This year, 22,440 women in America will be diagnosed with ovarian cancer and 14,080 will die from it, according to American Cancer Society estimates.

In a program at Israels Weizmann Institute of Science financed in part by the Israel Cancer Research Fund, Dr. Varda Rotter is looking for ways to fight the disease on the molecular level using a protein known as the king of tumor suppressors.

The protein, p53, stops the formation of tumors. But when p53 mutates, it makes cancer cells more malignant and boosts their resistance to drugs.

Rotter and her team have identified a small number of molecules that are able to reeducate mutant p53 and restore it to its role scanning for damaged DNA and stopping the development of tumors. They are also looking for methods to reeducate the mutant p53 to fight and eradicate mutant cells.

We are trying to find a way to convert or reeducate the mutant p53 to its role as the guardian of the genome, Rotter said. It will reeducate the p53 into the right type of p53 and will show that under such circumstances there is a reduction of cell death in treated cells.

Rotter hopes her teams research will result in methods that can be applied along with immunotherapy to give women with ovarian cancer a better chance of beating the disease.

Restoring infertility? Hit the restart button.

For many cancer patients, surviving is just the first part of the battle. They often face serious lifelong problems, such as infertility or the loss of healthy tissue that is highly difficult to regrow.

How do you replace damaged body parts? asked Dr. Jacob Hanna of the Weizmann Institute.

The key, Hanna and many others believe, lies in stem cells.Stem cells are early-stage cells that are capable of dividing into infinitely more cells and have the potential to become different cell types, such as bone, skin or muscle. Stem cells can help repair damaged tissue.

Hanna is using ICRF funding to research ways to take cells from healthy areas of the patients body and turn them back into induced embryonic stem cells the equivalent of the first cells with which each human body begins. Because the stem cells in Hannas model would come directly from the patients DNA rather than from a donor, the tissue would not face rejection.

Reverting the cells to their beginning state would be like hitting the restart button of your computer, Hanna said.

The treatment would be unique. Currently the only proven stem-cell therapy in use is centered on transplanting bone marrow. There are no stem-cell-based treatments for replacing organs or tissue other than blood. But Hanna believes stem-cell treatments are going to become reality in the next 20 years, and restoring fertility to infertile cancer survivors could be one major benefit.

We want to make mature human cells in the Petri dish, Hanna said. If this is successful, it could be a major breakthrough for solving infertility problems in general, not only for women who underwent chemotherapy.

For example, scientists could make an unlimited supply of female eggs by growing stem cells in a dish and freezing them.

This could stop doctors from avoiding doing chemotherapy because theyre worried about damaging the patients fertility, Hanna said. It would allow them to give longer treatment or stronger regiments.

To fight brain cancer, think small. Very, very small.

Glioblastoma, a particularly aggressive and deadly form of brain cancer, carries a very grim prognosis: Patients have a median survival time of about 15 months from the day of discovery.

Tel Aviv University researcher Dr. Dan Peer is seeking ways to fight brain tumors using a targeted nanoparticle platform to transport drugs directly to the sites that need treatment rather than a more general chemotherapy or surgery. Targeted treatments the size of a nanometer a millionth of a millimeter would minimize the effects on the rest of the body by targeting only the cancer cells and avoiding healthy cells nearby.

The delivery vehicle would be RNA ribonucleic acid, whose main role is to carry instructions from DNA. It is one of the three major biological macromolecules essential for all forms of life, along with DNA and proteins. By binding the RNA to a nanoparticle platform, researchers hope to bypass the hurdles that usually thwart drug delivery by specifically targeting the problem areas of the tumor.

The fact that nanomedicine can get around many of the obstacles that hinder drug delivery could mean a greater quality of life and life expectancy for patients suffering from highly deadly forms of cancer like glioblastoma, Peer said.

He and his colleagues are also using their ICRF research grant to examine ways to design drugs suited to a patients specific genetic profile and then develop appropriate nanoparticle delivery vehicles.

By carrying the drugs specifically to the cancer cells and not to the healthy ones, the treatment will have fewer adverse effects and toxicities for the patient while maximizing the drugs therapeutic effect.

If we can somehow diminish the spreading of the tumor and improve diagnosis and therapeutic effect, Peer said, that will be beneficial for the patient.

Dr. Ruth Scherz-Shouval is studying how tumors metastasize by recruiting non-malignant cells to help them overcome the human immune system. (Weizmann Institute)

Fighting carcinomas: Rehab for non-malignant cells

Weve all had moments in life that spark our survival instincts under stress. Humans arent the only ones that use chemical processes to survive stressful situations.

To survive high fevers, for example, organisms as small as cells deploy the heat-shock response activating proteins called chaperones that help cells maintain their structure and not melt down in the event of high temperatures. Tumors, too, use the heat-shock response to increase their odds of survival and grow ever-more malignant.

For tumors to expand and metastasize, they recruit non-malignant cells in the tumor microenvironment and get them to work for them and help them evade the immune system.Dr. RuthScherz-Shouvalof the Weizmann Institute is studying the tumor microenvironment to determine how the non-cancerous cells get reprogrammed to act against the body and support the tumor rather than defend the body against the tumorous growth.

The cells of the microenvironment dont have the mutation that causes cancer cells to become cancer cells yet they do things they are not supposed to do, she said. We are interested in understanding how this happens.

Scherz-Shouvalcompared treatment in the microenvironment to rehabilitating a nonviolent offender who can still be put on the right path unlike a hardened felon (the tumorous cell) who is too far gone to save. Think rehab for non-malignant cells.

Theresearch is relevant to solid tumorsand specifically to carcinomas a cancer arising in skin tissue or the lining of internal organs. Scherz-Shouval has found a correlation between the heat-shock response and poor patient survival in late-stage breast and lung cancer.

She hopes her research, backed by the ICRF, will lead to a more generalized way to target cells in the microenvironment that will complement current cancer treatments and give patients a better chance at recovery.

Wanted: A better way to fight leukemia

Israel has the fourth-highest per capita rate of leukemia deaths worldwide. In America, leukemia kills more than 24,000 people per year.

Most leukemia treatments today focus on chemotherapy, steroid drugs and stem-cell transplants.But Ben-Gurion University of the Negev researcher RoiGazitis on the hunt for more effective, targeted treatments.

Immune therapies and stem-cells treatments offer great advantages but too many options to choose from, Gazit said. Our models will help to better specify which treatment may suit a specific type, and even sub-type, of the disease. Unfortunately, there is no one-size-fits-all treatment for leukemia. Thats why we need tailor-made models to fit the treatment to the disease.

Gazit is focusing on how to develop targeted treatment of cancer cells using hematopoietic stem cells stem cells used in cancer treatment because of their ability to divide and form new and different kinds of blood cells.

The research involvestaking primary cells cells cultured directly from a subject and turning them into malignant leukemia growth inside mice. By examining how the leukemia develops, Gazit is exploring ways that hematopoietic stem cells may be deployed to arrest the leukemia.

The research models his lab is using, part of a project supported by the Israel Cancer Research Fund, could help scientists develop more types of immunotherapy and more ways to use stem cells to combat leukemia.

With any new information we can gain better understanding, which translates into better treatment, Gazit said.

(This article wassponsoredby and produced in partnership with theIsrael Cancer Research Fund, whose ongoing support of these and other Israeli scientists work goes a long way toward ensuring that their efforts will have important and lasting impact in the global fight against cancer. This article was produced by JTAs native content team.)

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These 5 Israeli advances could transform cancer treatment - Jewish Telegraphic Agency

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On a November evening last year, Jennifer Doudna put on a stylish black evening gown and headed to Hangar One, a building at NASAs Ames Research Center that was constructed in 1932 to house dirigibles. Under the looming arches of the hangar, Doudna mingled with celebrities like Benedict Cumberbatch, Cameron Diaz and Jon Hamm before receiving the 2015 Breakthrough Prize in life sciences, an award sponsored by Mark Zuckerberg and other tech billionaires. Doudna, a biochemist at the University of California, Berkeley, and her collaborator, Emmanuelle Charpentier of the Helmholtz Centre for Infection Research in Germany, each received $3 million for their invention of a potentially revolutionary tool for editing DNA known as CRISPR.

Doudna was not a gray-haired emerita being celebrated for work she did back when dirigibles ruled the sky. It was only in 2012 that Doudna, Charpentier and their colleagues offered the first demonstration of CRISPRs potential. They crafted molecules that could enter a microbe and precisely snip its DNA at a location of the researchers choosing. In January 2013, the scientists went one step further: They cut out a particular piece of DNA in human cells and replaced it with another one.

In the same month, separate teams of scientists at Harvard University and the Broad Institutereported similar success with the gene-editing tool. A scientific stampede commenced, and in just the past two years, researchers have performed hundreds of experiments on CRISPR. Their results hint that the technique may fundamentally change both medicine and agriculture.

Some scientists have repaired defective DNA in mice, for example, curing them of genetic disorders. Plant scientists have used CRISPR to edit genes in crops, raising hopes that they can engineer a better food supply. Some researchers are trying to rewrite the genomes of elephants, with the ultimate goal of re-creating a woolly mammoth. Writing last year in the journal Reproductive Biology and Endocrinology, Motoko Araki and Tetsuya Ishii of Hokkaido University in Japan predicted that doctors will be able to use CRISPR to alter the genes of human embryos in the immediate future.

Thanks to the speed of CRISPR research, the accolades have come quickly. Last year MIT Technology Review called CRISPR the biggest biotech discovery of the century. The Breakthrough Prize is just one of several prominent awards Doudna has won in recent months for her work on CRISPR; National Public Radio recently reported whispers of a possible Nobel in her future.

Even the pharmaceutical industry, which is often slow to embrace new scientific advances, is rushing to get in on the act. New companies developing CRISPR-based medicine are opening their doors. In January, the pharmaceutical giant Novartis announced that it would be using Doudnas CRISPR technology for its research into cancer treatments. It plans to edit the genes of immune cells so that they will attack tumors.

But amid all the black-tie galas and patent filings, its easy to overlook the most important fact about CRISPR: Nobody actually invented it.

Doudna and other researchers did not pluck the molecules they use for gene editing from thin air. In fact, they stumbled across the CRISPR molecules in nature. Microbes have been using them to edit their own DNA for millions of years, and today they continue to do so all over the planet, from the bottom of the sea to the recesses of our own bodies.

Weve barely begun to understand how CRISPR works in the natural world. Microbes use it as a sophisticated immune system, allowing them to learn to recognize their enemies. Now scientists are discovering that microbes use CRISPR for other jobs as well. The natural history of CRISPR poses many questions to scientists, for which they dont have very good answers yet. But it also holds great promise. Doudna and her colleagues harnessed one type of CRISPR, but scientists are finding a vast menagerie of different types. Tapping that diversity could lead to more effective gene editing technology, or open the way to applications no one has thought of yet.

You can imagine that many labs including our own are busily looking at other variants and how they work, Doudna said. So stay tuned.

The scientists who discovered CRISPR had no way of knowing that they had discovered something so revolutionary. They didnt even understand what they had found. In 1987, Yoshizumi Ishino and colleagues at Osaka University in Japan published the sequence of a gene called iap belonging to the gut microbe E. coli. To better understand how the gene worked, the scientists also sequenced some of the DNA surrounding it. They hoped to find spots where proteins landed, turning iap on and off. But instead of a switch, the scientists found something incomprehensible.

Near the iap gene lay five identical segments of DNA. DNA is made up of building blocks called bases, and the five segments were each composed of the same 29 bases. These repeat sequences were separated from each other by 32-base blocks of DNA, called spacers. Unlike the repeat sequences, each of the spacers had a unique sequence.

This peculiar genetic sandwich didnt look like anything biologists had found before. When the Japanese researchers published their results, they could only shrug. The biological significance of these sequences is not known, they wrote.

It was hard to know at the time if the sequences were unique to E. coli, because microbiologists only had crude techniques for deciphering DNA. But in the 1990s, technological advances allowed them to speed up their sequencing. By the end of the decade, microbiologists could scoop up seawater or soil and quickly sequence much of the DNA in the sample. This technique called metagenomics revealed those strange genetic sandwiches in a staggering number of species of microbes. They became so common that scientists needed a name to talk about them, even if they still didnt know what the sequences were for. In 2002, Ruud Jansen of Utrecht University in the Netherlands and colleagues dubbed these sandwiches clustered regularly interspaced short palindromic repeats CRISPR for short.

Jansens team noticed something else about CRISPR sequences: They were always accompanied by a collection of genes nearby. They called these genes Cas genes, for CRISPR-associated genes. The genes encoded enzymes that could cut DNA, but no one could say why they did so, or why they always sat next to the CRISPR sequence.

Three years later, three teams of scientists independently noticed something odd about CRISPR spacers. They looked a lot like the DNA of viruses.

And then the whole thing clicked, said Eugene Koonin.

At the time, Koonin, an evolutionary biologist at the National Center for Biotechnology Information in Bethesda, Md., had been puzzling over CRISPR and Cas genes for a few years. As soon as he learned of the discovery of bits of virus DNA in CRISPR spacers, he realized that microbes were using CRISPR as a weapon against viruses.

Koonin knew that microbes are not passive victims of virus attacks. They have several lines of defense. Koonin thought that CRISPR and Casenzymes provide one more. In Koonins hypothesis, bacteria use Casenzymes to grab fragments of viral DNA. They then insert the virus fragments into their own CRISPR sequences. Later, when another virus comes along, the bacteria can use the CRISPR sequence as a cheat sheet to recognize the invader.

Scientists didnt know enough about the function of CRISPR and Cas enzymes for Koonin to make a detailed hypothesis. But his thinking was provocative enough for a microbiologist named Rodolphe Barrangou to test it. To Barrangou, Koonins idea was not just fascinating, but potentially a huge deal for his employer at the time, the yogurt maker Danisco. Danisco depended on bacteria to convert milk into yogurt, and sometimes entire cultures would be lost to outbreaks of bacteria-killing viruses. Now Koonin was suggesting that bacteria could use CRISPR as a weapon against these enemies.

To test Koonins hypothesis, Barrangou and his colleagues infected the milk-fermenting microbe Streptococcus thermophilus with two strains of viruses. The viruses killed many of the bacteria, but some survived. When those resistant bacteria multiplied, their descendants turned out to be resistant too. Some genetic change had occurred. Barrangou and his colleagues found that the bacteria had stuffed DNA fragments from the two viruses into their spacers. When the scientists chopped out the new spacers, the bacteria lost their resistance.

Barrangou, now an associate professor at North Carolina State University, said that this discovery led many manufacturers to select for customized CRISPR sequences in their cultures, so that the bacteria could withstand virus outbreaks. If youve eaten yogurt or cheese, chances are youve eaten CRISPR-ized cells, he said.

As CRISPR started to give up its secrets, Doudna got curious. She had already made a name for herself as an expert on RNA, a single-stranded cousin to DNA. Originally, scientists had seen RNAs main job as a messenger. Cells would make a copy of a gene using RNA, and then use that messenger RNA as a template for building a protein. But Doudna and other scientists illuminated many other jobs that RNA can do, such as acting as sensors or controlling the activity of genes.

In 2007, Blake Wiedenheft joined Doudnas lab as a postdoctoral researcher, eager to study the structure of Cas enzymes to understand how they worked. Doudna agreed to the plan not because she thought CRISPR had any practical value, but just because she thought the chemistry might be cool. Youre not trying to get to a particular goal, except understanding, she said.

As Wiedenheft, Doudna and their colleagues figured out the structure of Cas enzymes, they began to see how the molecules worked together as a system. When a virus invades a microbe, the host cell grabs a little of the viruss genetic material, cuts open its own DNA, and inserts the piece of virus DNA into a spacer.

As the CRISPR region fills with virus DNA, it becomes a molecular most-wanted gallery, representing the enemies the microbe has encountered. The microbe can then use this viral DNA to turn Cas enzymes into precision-guided weapons. The microbe copies the genetic material in each spacer into an RNA molecule. Cas enzymes then take up one of the RNA molecules and cradle it. Together, the viral RNA and the Cas enzymes drift through the cell. If they encounter genetic material from a virus that matches the CRISPR RNA, the RNA latches on tightly. The Cas enzymes then chop the DNA in two, preventing the virus from replicating.

As CRISPRs biology emerged, it began to make other microbial defenses look downright primitive. Using CRISPR, microbes could, in effect, program their enzymes to seek out any short sequence of DNA and attack it exclusively.

Once we understood it as a programmable DNA-cutting enzyme, there was an interesting transition, Doudna said. She and her colleagues realized there might be a very practical use for CRISPR. Doudna recalls thinking, Oh my gosh, this could be a tool.

It wasnt the first time a scientist had borrowed a trick from microbes to build a tool. Some microbes defend themselves from invasion by using molecules known as restriction enzymes. The enzymes chop up any DNA that isnt protected by molecular shields. The microbes shield their own genes, and then attack the naked DNA of viruses and other parasites. In the 1970s, molecular biologists figured out how to use restriction enzymes to cut DNA, giving birth to the modern biotechnology industry.

In the decades that followed, genetic engineering improved tremendously, but it couldnt escape a fundamental shortcoming: Restriction enzymes did not evolve to make precise cuts only to shred foreign DNA. As a result, scientists who used restriction enzymes for biotechnology had little control over where their enzymes cut open DNA.

The CRISPR-Cas system, Doudna and her colleagues realized, had already evolved to exert just that sort of control.

To create a DNA-cutting tool, Doudna and her colleagues picked out the CRISPR-Cas system from Streptococcus pyogenes, the bacteria that cause strep throat. It was a system they already understood fairly well, having worked out the function of its main enzyme, called Cas9. Doudna and her colleagues figured out how to supply Cas9 with an RNA molecule that matched a sequence of DNA they wanted to cut. The RNA molecule then guided Cas9 along the DNA to the target site, and then the enzyme made its incision.

Using two Cas9 enzymes, the scientists could make a pair of snips, chopping out any segment of DNA they wanted. They could then coax a cell to stitch a new gene into the open space. Doudna and her colleagues thus invented a biological version of find-and-replace one that could work in virtually any species they chose to work on.

As important as these results were, microbiologists were also grappling with even more profound implications of CRISPR. It showed them that microbes had capabilities no one had imagined before.

Before the discovery of CRISPR, all the defenses that microbes were known to use against viruses were simple, one-size-fits-all strategies. Restriction enzymes, for example, will destroy any piece of unprotected DNA. Scientists refer to this style of defense as innate immunity. We have innate immunity, too, but on top of that, we also use an entirely different immune system to fight pathogens: one that learns about our enemies.

This so-called adaptive immune system is organized around a special set of immune cells that swallow up pathogens and then present fragments of them, called antigens, to other immune cells. If an immune cell binds tightly to an antigen, the cell multiplies. The process of division adds some random changes to the cells antigen receptor genes. In a few cases, the changes alter the receptor in a way that lets it grab the antigen even more tightly. Immune cells with the improved receptor then multiply even more.

This cycle results in an army of immune cells with receptors that can bind quickly and tightly to a particular type of pathogen, making them into precise assassins. Other immune cells produce antibodies that can also grab onto the antigens and help kill the pathogen. It takes a few days for the adaptive immune system to learn to recognize the measles virus, for instance, and wipe it out. But once the infection is over, we can hold onto these immunological memories. A few immune cells tailored to measlesstay with us for our lifetime, ready to attack again.

CRISPR, microbiologists realized, is also an adaptive immune system. It lets microbes learn the signatures of new viruses and remember them. And while we need a complex network of different cell types and signals to learn to recognize pathogens, a single-celled microbe has all the equipment necessary to learn the same lesson on its own.

CRISPR is an impressive adaptive immune system for another reason: Its lessons can be inherited. People cant pass down genes for antibodies to their children because only immune cells develop them. Theres no way for that information to get into eggs or sperm. As a result, children have to start learning about their invisible enemies pretty much from scratch.

CRISPR is different. Since microbes are single-celled organisms, the DNA they alter to fight viruses is the same DNA they pass down to their descendants. In other words, the experiences that these organisms have alter their genes, and that change is inherited by future generations.

For students of the history of biology, this kind of heredity echoes a largely discredited theory promoted by the naturalist Jean-Baptiste Lamarck in the early 19th century. Lamarck argued for the inheritance of acquired traits. To illustrate his theory, he had readers imagine a giraffe gaining a long neck by striving to reach high branches to feed on. A nervous fluid, he believed, stretched out its neck, making it easier for the giraffe to reach the branches. It then passed down its lengthened neck to its descendants.

The advent of genetics seemed to crush this idea. There didnt appear to be any way for experiences to alter the genes that organisms passed down to their offspring. But CRISPR revealed that microbes rewrite their DNA with information about their enemies information that Barrangou showed could make the difference between life and death for their descendants.

Did this mean that CRISPR meets the requirements for Lamarckian inheritance? In my humble opinion, it does, said Koonin.

But how did microbes develop these abilities? Ever since microbiologists began discovering CRISPR-Cas systems in different species, Koonin and his colleagues have been reconstructing the systems evolution. CRISPR-Cas systems use a huge number of different enzymes, but all of them have one enzyme in common, called Cas1. The job of this universal enzyme is to grab incoming virus DNA and insert it in CRISPR spacers. Recently, Koonin and his colleagues discovered what may be the origin of Cas1 enzymes.

Along with their own genes, microbes carry stretches of DNA called mobile elements that act like parasites. The mobile elements contain genes for enzymes that exist solely to make new copies of their own DNA, cut open their hosts genome, and insert the new copy. Sometimes mobile elements can jump from one host to another, either by hitching a ride with a virus or by other means, and spread through their new hosts genome.

Koonin and his colleagues discovered that one group of mobile elements, called casposons, makes enzymes that are pretty much identical to Cas1. In a new paper in Nature Reviews Genetics, Koonin and Mart Krupovic of the Pasteur Institute in Paris argue that the CRISPR-Cas system got its start when mutations transformed casposons from enemies into friends. Their DNA-cutting enzymes became domesticated, taking on a new function: to store captured virus DNA as part of an immune defense.

While CRISPR may have had a single origin, it has blossomed into a tremendous diversity of molecules. Koonin is convinced that viruses are responsible for this. Once they faced CRISPRs powerful, precise defense, the viruses evolved evasions. Their genes changed sequence so that CRISPR couldnt latch onto them easily. And the viruses also evolved molecules that could block the Cas enzymes. The microbes responded by evolving in their turn. They acquired new strategies for using CRISPR that the viruses couldnt fight. Over many thousandsof years, in other words, evolution behaved like a natural laboratory, coming up with new recipes for altering DNA.

To Konstantin Severinov, who holds joint appointments at Rutgers University and the Skolkovo Institute of Science and Technology in Russia, these explanations for CRISPR may turn out to be true, but they barely begin to account for its full mystery. In fact, Severinov questions whether fighting viruses is the chief function of CRISPR. The immune function may be a red herring, he said.

Severinovs doubts stem from his research on the spacers of E. coli. He and other researchers have amassed a database of tens of thousands of E. coli spacers, but only a handful of them match any virus known to infect E. coli. You cant blame this dearth on our ignorance of E. coli or its viruses, Severinov argues, because theyve been the workhorses of molecular biology for a century. Thats kind of mind-boggling, he said.

Its possible that the spacers came from viruses, but viruses that disappeared thousands of years ago. The microbes kept holding onto the spacers even when they no longer had to face these enemies. Instead, they used CRISPR for other tasks. Severinov speculates that a CRISPR sequence might act as a kind of genetic bar code. Bacteria that shared the same bar code could recognize each other as relatives and cooperate, while fighting off unrelated populations of bacteria.

But Severinov wouldnt be surprised if CRISPR also carries out other jobs. Recent experiments have shown that some bacteria use CRISPR to silence their own genes, instead of seeking out the genes of enemies. By silencing their genes, the bacteria stop making molecules on their surface that are easily detected by our immune system. Without this CRISPR cloaking system, the bacteria would blow their cover and get killed.

This is a fairly versatile system that can be used for different things, Severinov said, and the balance of all those things may differ from system to system and from species to species.

If scientists can get a better understanding of how CRISPR works in nature, they may gather more of the raw ingredients for technological innovations. To create a new way to edit DNA, Doudna and her colleagues exploited the CRISPR-Cas system from a single species of bacteria, Streptococcus pyogenes. Theres no reason to assume that its the best system for that application. At Editas, a company based in Cambridge, Massachusetts, scientists have been investigating the Cas9 enzyme made by another species of bacteria, Staphylococcus aureus. In January, Editas scientists reported that its about as efficient at cutting DNA as Cas9 from Streptococcus pyogenes. But it also has some potential advantages, including its small size, which may make it easier to deliver into cells.

To Koonin, these discoveries are just baby steps into the ocean of CRISPR diversity. Scientists are now working out the structure of distantly related versions of Cas9 that seem to behave very differently from the ones were now familiar with. Who knows whether this thing could become even a better tool? Koonin said.

And as scientists discover more tasks that CRISPR accomplishes in nature, they may be able to mimic those functions, too. Doudna is curious about using CRISPR as a diagnostic tool, searching cells for cancerous mutations, for example. Its seek and detect, not seek and destroy, she said. But having been surprised by CRISPR before, Doudna expects the biggest benefits from these molecules to surprise us yet again. It makes you wonder what else is out there, she said.

This article was reprinted on BusinessInsider.com.

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CRISPR Natural History in Bacteria | Quanta Magazine

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The CRISPR-Cas9 Technology Developed by Doudna and Charpentier

In June 2012, University of California, Berkeley professor and Howard Hughes Medical Institute investigator Jennifer Doudna and Umea University professor Emmanuelle Charpentier (now at the Max Planck Institute for Infection Biology) and their research team, which included Martin Jinek from UC and Krzysztof Chylinski from the University of Vienna, published an article in the journal Science that first revealed what has been described as the scientific breakthrough of the century. This international team of researchers determined how a bacterial immune system known as CRISPR-Cas9 is able to cut DNA, and then engineered CRISPR-Cas9 to be used as a powerful gene editing technology.

To understand this powerful new technology, think of the CRISPR-Cas9 system as special scissors that cut DNA threads. In nature, bacteria use these scissors to cut the DNA threads of invading viruses. The Doudna/Charpentier team figured out how to engineer and use these scissors to cut any DNA thread of their choosing, thereby allowing the system to be used to make repairs or modifications to the intricate, multicolored tapestry that is the human genome.

Additionally, the natural CRISPR-Cas9 system has three separate parts the scissors portion, which actually cuts the DNA thread, and a two-piece homing beacon portion that directs the scissors to the DNA thread. The two pieces of the homing beacon must find eachother and come together before the natural CRISPR-Cas9 system can home in on and cut a targeted thread. The Doudna/Charpentier team devised a way to make a one-piece homing beacon, thus simplifying the system and vastly increasing the ease of use of this technology.

The Doudna/Charpentier groups Science publication immediately ushered in a new and revolutionary era of gene editing. Within six months of the Doudna/Charpentier teams Science publication describing the engineering and use of the CRISPR-Cas9 system, many research groups successfully applied the CRISPR-Cas9 technology as originally described in that landmark publication, further verifying how readily the Doudna/Charpentier teams engineered CRISPR-Cas9 system can be used for gene editing in any cell type.

Since publication of the Doudna/Charpentier teams seminal paper, CRISPR-Cas9 gene editing has transformed biological research across the globe. CRISPR-Cas9 allows scientists to permanently edit the genetic information of any organism including human cells with unprecedented ease, accuracy and efficiency. CRISPR-Cas9s power and versatility has opened up new and wide-ranging uses across biology, including medicine and agriculture. The foundational research of the Doudna/Charpentier research team enabled subsequent work by many laboratories throughout the world that used CRISPR-Cas9 to treat and cure disease in animal models and to create pathways to sustainable biofuels, to more robust crops and to countless other applications that will continue to dramatically advance human health and well-being (for example, therapies for sickle cell disease).

The University of California has a rich history of scientific discovery and development. Our researchers have introduced many of the most significant technologies that have bettered our world and vastly improved the lives of its people. The ongoing work of Doudna and her team is another example of the universitys commitment to pursuing basic and applied research that is in the public interest, which is consistent with UCs standing as the worlds leading public research university system.

As part of that focus on, and commitment to, the greater good, the University of California, along with the University of Vienna, has reserved the right to allow educational and other nonprofit institutions to use the CRISPR-Cas9 related intellectual property for educational and research purposes.

How was CRISPR-Cas9 gene editing developed?

The invention of CRISPR-Cas9 gene editing technology was the result of basic research science at its best. More than 10 years ago, Jillian Banfield, UC Berkeley professor of earth and planetary sciences and of environmental science, policy and management, asked Doudna to analyze a genetic peculiarity of bacteria known generally as CRISPR. At that time, CRISPRs function in bacterial cells was only beginning to be understood. After several years of research by Doudna and her team into various proteins that make up bacterial CRISPR systems, Doudna began collaborating with Charpentier and her team, who had also been researching CRISPR systems, including the identification of tracrRNA.

Their research teams collaborated on studies to determine how the CRISPR-Cas9 system acts like a pair of molecular scissors to cleave the DNA of invading viruses. Through their scientific collaboration, the Doudna/Charpentier research team determined exactly what components were responsible for this DNA cleavage and the team engineered those components to modify target DNA outside of bacterial cells. The studies included making various modifications to the natural components of the system, and even included studies where two separate RNA components from the natural system were combined into a single molecule, thereby simplifying the system and making it easier to employ. This work demonstrated that engineered CRISPR-Cas9 can be used for gene editing. The Doudna/Charpentier research teams seminal 2012 publication of these results in Science is widely seen as the event that launched a new era of progress in genome editing.

What are the applications for CRISPR-Cas9?

With its vast potential for drug discovery and development, human applications are of particular interest to CRISPR-Cas9 researchers. On a new front in the battle against cancer, scientists are already working to use CRISPR-Cas9 as a means to edit a patients T-cells (immune cells) so that they have the capability to target particular types of tumors. Within the next 10 years it is likely that we will see CRISPR-Cas9-based therapies for blood disorders such as sickle cell disease, as well as other genetic diseases. For non-human applications, researchers are applying the CRISPR-Cas9 technology to engineer pest and disease-resistant crops and protect trees from bark beetles, as well as exploring the technologys ability to control mosquito populations and reduce their ability to spread Zika virus and malaria.

Excerpt from:

How CRISPR works | Berkeley News

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MilliporeSigma, the life science business of Merck KGaA, said today it has been awarded its first patent for CRISPR technologyan Australian patent relating to the use of CRISPR in a genomic integration method for eukaryotic cells.

The patent issued by the Australian Patent Office covers chromosomal integration or cutting of the chromosomal sequence of eukaryotic cells, and insertion of an external or donor DNA sequence into those cells using CRISPR.

Patent Application No. 2013355214 was filed December 5, 2013, and accepted on May 22, according to an online search of the Australian Patent Offices online database AusPat. The patent consists of 14 method claims.

MilliporeSigma says the CRISPR genomic integration technology is designed to enable researchers to replace a disease-associated mutation with a beneficial or functional sequence, a method important for creation of disease models and gene therapy. Researchers can also use the method to insert transgenes that label endogenous proteins for visual tracking within cells.

This patent decision recognizes our expertise in CRISPR technologya body of knowledge that we are committed to grow, MilliporeSigma CEO Udit Batra said in a statement.

MilliporeSigma has filed for patents covering its insertion CRISPR method in the U.S., as well as in Europe, Brazil, Canada, China, India, Israel, Japan, Singapore, and South Korea.

The Australian Patent Office website also lists six applications covering CRISPR claims, by applicants that include Cellectis, CRISPR Therapeutics, The Johns Hopkins University, MIT and the Broad Institute, Moderna Therapeutics, and the Regents of the University of Colorado.

MilliporeSigma said in May that it had developed the alternative CRISPR genome-editing method, called proxy-CRISPR, a month after publishing the results of its research in Nature Communications. According to the company, proxy-CRISPR differs from other genome editing systems in its ability to cut previously unreachable cell locations, making CRISPR more efficient, flexible, and specific, and giving researchers more experimental options.

Since 2012, MilliporeSigma has filed multiple CRISPR patent filings, including its filings related to proxy-CRISPR technology.

The company has been involved in genome editing for 14 years, having been the first company to offer custom biomolecules for genome editing globally (TargeTron RNA-guided group II introns and CompoZr zinc finger nucleases). MilliporeSigma was also first to manufacture arrayed CRISPR libraries covering the entire human genome.

Later this year, MilliporeSigma is expected to launch its next suite of genome editing tools for the research community, to include novel and modified versions of Cas and Cas-like proteins.

MilliporeSigma is the combined life sciences tools and technologies company formed in 2015 when Merck KGaA completed its $17 billion acquisition of Sigma-Aldrich.

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MilliporeSigma Wins Its First CRISPR Patent in Australia - Genetic Engineering & Biotechnology News

Recommendation and review posted by Bethany Smith

JOHNSTON, Iowa Green stalks have only just begun to sprout in the test fields where biotech giant DuPont Pioneer is planting rows of a new genetically edited corn. But across the street, in the companys sprawling research campus, executives are already fretting about how to sell it to the world.

On one hand, this corn is a revolution: It will probably be the first plant to market developed through the cutting-edge genome-editing technique called CRISPR-Cas.

On the other, the industrys last big breakthrough of this kind genetically modified organisms, or GMOs was an unqualified public-relations disaster, even according to its progenitor, Monsanto.

[We're having the wrong argument about GMOs]

Wary of that, DuPont Pioneer, which is developing a strain of drought-resistant waxy corn, is proactively neutralizing skeptical consumers years before these crops will even be available. The company recently began hosting CRISPR focus groups and launched a website on the technique, complete with animated videos.

The goal is to avoid the sort of public backlash that rocked Monsanto in the late 1990s and still plagues agriculture two decades later. In the United States,consumerskepticism of genetically modifiedcrops has forced biotech companies into long, costly battles over issues such as whether thesefoods should be labeled; elsewhere in the world, the public outcry has prevented seeds from winning government approval.

Its more about social science than science, said Neal Gutterson, the vice president of research and development at DuPont Pioneer. [Its] ultimately about getting social license for this technology.

Odes to plant technology are ubiquitous in DuPont Pioneers Iowa offices, where even the conference space boasts glossy, museum-like exhibits devoted to genetically modified foods. Plus-sized photos show farmers standing idly in golden corn fields, and mystery hands reaching into overflowing bowls.

But the problem for DuPont Pioneer, and agribusiness generally, is that large swaths of the public do not share this sunny vision of biotech. Since the late '90s, when Monsanto botched the introduction of genetically modified crops in Europe, consumers have treated the term GMO as if it were a dirty word.

According to the Pew Research Center, nearly 40 percent of Americans believe GMOs are bad for their health. This assertion is not supported by science, which has concluded that the genetically modified crops on the market are safe for consumption.

But science has made little headway in a fierce debate that hasoften focused on the perceived values of the companies developing these products.Each year, activists in hundreds of cities worldwide march against Monsanto and millions of consumers buy "Non-GMO Project Verified" products.

The biotech industry has taken strides to clean up its image in recent years: In 2013, Monsanto shook up its public-relations team, and the industry has banded behind a consumer education effort called GMO Answers.

But with CRISPR a breakthrough gene-editing tool the field gets a chance at its first real do-over.

Unlike conventional genetic modification, CRISPR works directly on the DNA of the plant or animal being bred. While GMOs, as we have traditionally known them, involve inserting target DNA from a different species, CRISPR can directly edit an organisms DNA for a result that falls within the genetic diversity of that animal or plant.

The technique was discovered almost simultaneously at several research universities and has since been licensed out to a number of bothnoncommercial researchers and private companies. Outside of agriculture, CRISPRhas diverse applications in medicine, where it's currently being used to develop everything from cancer therapies to noveldisease models.

In agriculture, scientists say it takes far less time, and is more precise, than both traditional and genetically modified breeding techniques.DuPont Pioneer expects its CRISPR-edited waxy corn to be on the market withinthree years.The Agriculture Departmenthas indicated that it does not intend to regulate the CRISPR-edited corn because its creation does not involve any plant pests' genetic materials.

That comes with a lot of responsibility, said Kerrey Kerr-Enskat, the publicist who handles DuPonts CRISPR outreach efforts. Its not just about row crops we dont want to waste that opportunity [to engage with the public].

Accordingly, DuPont Pioneer has spent the past several months convening regular focus groups with leaders from government, agriculture and environmental organizations, Kerr-Enskat said. The goal is to learn more about the publics CRISPR concerns and use them to inform future messaging efforts.

In April, the company launched a website that it calls the first step in a larger campaign to win consumers trust for the technology. Its an unusual move for a company that sees farmers, not food consumers, as its direct customers. Its product is, after all, seeds and its first CRISPR product, waxy corn, is for industrial use, not human consumption.

The homepage shows a stock photo of a smilingfamilyeating corn on the cob behind a green banner that calls CRISPR-Cas one of the greatest breakthroughs in biology. A guiding principles page promises the company's commitment to safety and open, transparent and timely communications. In a slick animated video, a measured female narrator claims that CRISPR is not so different from traditional plant breeding techniques deployed at the dawn of agriculture.

Ironically, the video is also not so different from the marketing that DuPont used 100 years ago: It was among the first companies to use silent film to advertise to consumers. In fact, DuPont which sold explosives and plastics, long before it bought Pioneer and got into seeds built interest in novel products such as nylon through what it called educational advertising.

Since then, of course, the atmosphere has changed. Its not clear if consumers see DuPont Pioneer as a scientific authority or if the company hurts its own position by wading into the debate.

Already, the controversy over GMOs has become so fractious, said Glenn Davis Stone, a professor of anthropology and environmental studies at Washington University, that even independent scientists havelet their role in educating be trampled by their interest in convincing. Many are so frustrated by the impasse, he added, that they'll gloss over questions such as regulation, rather than risk giving the other side anti-GMO ammunition.

Meanwhile, two decades of sociological research have shown that skepticism of genetic modification is largely fueled not by ignorance or technophobia but by a lack of trust in large companies, some of which is arguably well-deserved.Before they sold seeds, for instance, both Monsanto and DuPontmanufactured Agent Orange, a defoliant used extensively during the Vietnam War, and DDT, an insecticide that caused widespread environmental damage.

Even pro-GMO advocates, such as Sarah Davidson Evanega of the Cornell Alliance for Science, say that public-sector scientists may be best positioned to deliver messages about CRISPR.

Theres great optimism that this time well do communications better, Evanega said. The great hope is that CRISPR is going to be different.

Whether consumers will eventually embrace CRISPR is still, of course, anybodys guess. As with GMOs, there is compelling science here. There are also, particularly when it comes to human genome editing, worrying potential drawbacks.

But Kerr-Enskat, of DuPont Pioneer, is quick to emphasize that her company wont be the only or the loudest voice, no matter how the debate evolves.In fact, if you click the contact link on the new CRISPR site, your email will eventually make its way to her inbox.

For GMOs, they waited until the product hit the market before there was a lot of communication, she said. But this is a two-way engagement.

Read more:

The government is going to counter 'misinformation' about GMO foods

The apple that never browns wants to change your mind about genetically modified foods

Industry is counting on Trump to back off rules that tell you what's in your food

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Forget GMOs. The next big battle is over genetically 'edited' foods - Washington Post

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GenSight has announced Phase I/II data revealing that its gene therapy technology can restore sight in patients suffering from a rare mitochondrial disease.

GenSight Biologics develops gene therapies targeting degenerative diseases that cause blindness. The French biotech has now announced very promising results from its lead candidate, GS010, after 2 years of following patients treated with the gene therapy in an ongoing Phase I/II trial. Thetreatment targets Leber hereditaryoptic neuropathy (LHON), a rare genetic disease for which there is no curative treatment.

Patients sight was evaluated using the ETDRS test, the one consisting on recognizing increasingly smaller letters that most of us have done at some point in our life. Those patients treated with GS010 showed a statistically significant improvement in the number of letters they were able to recognize over time, especially in those that were treated within two years after their diagnosis. Detailed results after 96 weeks of follow-upare now pending publication in a peer-reviewed journal.

TE: treated eye; UTE: untreated eye

According to GenSight, 95% of LHON cases are caused by mutations in the genes that encodes the NADH dehydrogenase complex, which is involved in ATP metabolism within mitochondria. Since it affects amitochondrial gene, the disease is maternally inherited. GenSight is particularly focusing on patients with a mutation in the ND4 gene, which accounts for 70% of LHON cases in Europe and North America and up to 85% in Asia.

GenSight is already running two Phase III studies in Europe and the US evaluating GS010 in patients with the ND4 mutation that have been affected by LHON for a year or less.We are now less than a year away from Phase III efficacy data, and more than ever committed to find a cure for patients and their families affected by this devastating condition, said Bernard Gilly, CEO and co-founder of Gensight, in a statement. Philip recently interviewed him regarding his impressive track in biotech as both a serial entrepreneur and a partner at the VC firm Sofinnova.

So far, GenSight seems to be the only biotech developing a gene therapy for this disease. Ocular disorders are often rare,which leads most companies in the field to focus on age-related macular degeneration instead, which has a significantly higher prevalence. The French biotechs pipeline also includes GS011, a gene therapy to treat the ND1 mutation in LHON, still in the early research stage. The company is also working in GS030, an optogenetic gene therapyto introduce a protein that can respond to light with the aim of restoring sight in patients with retinitis pigmentosa, currently undergoing preclinical investigation.

Images via HQuality / Shutterstock; GenSight

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French Biotech Reports Sight Restoration thanks to Gene Therapy - Labiotech.eu (blog)

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Dr. Stephen Eulau speaks with cancer patient Michael Pastula (KOMO-TV)

A year ago, Michael Pastula felt perfectly healthy. His only indication that something might be wrong was a blood test that showed elevated levels of a protein, indicating possible prostate cancer.

"You'll never know unless you're looking for it. And you need to look for it. You need to look for it," Pastula said.

The prostate-specific antigen -- or PSA -- test is a simple blood draw with quick results. Eight years ago, a government task force recommended against it, saying it led to unnecessary treatment.

In new draft recommendations, the U.S. Preventive Services Task Force say men 55 to 69 years old should talk to their doctors to decide if PSA screening is right for them.

They still warn that screening could lead to potential misdiagnosis and treatment that could cause impotence and urinary incontinence.

But the panel also says new evidence supports the benefits of screening, including reducing the chance of dying from prostate cancer and catching it before cancer spreads to other parts of the body.

Dr. Stephen Eulau, a radiation oncology specialist in Seattle, said he is happy to see the more open-minded approach.

"It's really, really important that the patient and the doctor have a conversation in a collaborative way so they can form a partnership in making this decision. It's very important to recognize that we're not just looking at a blood test. We're looking at a patient," Eulau said.

Pastula's cancer was aggressive, spreading to his lymph nodes and bladder.

"If you don't have something like a PSA test to give you at least an indication that something's going on, then people are going to die from this," Pastula said.

Pastula had surgery and was undergoing radiation.

"I think you have an excellent opportunity to cure this cancer," Eulau said.

"I'd be happy about that," Pastula responded.

Read the rest here:
Sinclair Cares: New recommendations about PSA test - Turn to 10

Recommendation and review posted by sam

You know what its like.

Your breasts are so tender, the slightest touch brings you a surge of discomfort.

You cant enjoy sex like you usually do because, well, easy on the nipples, please.

To say the least, theres a lot going on during your menstrual cycle. Your uterus is shedding its wall, your hormone levels are unpredictably rising and falling, and your body is literally preparing for fertilization (honestly, the female anatomy sounds like a heroic machine).

But the sore boob situation, which 72 percent of women deal with every month, is just too much for this heroic machine to handle. I need some answers, and I need them now.

If you and your sore boobs are also in need of some answers, heres why your chesticles are aching so much when youre on your period.

It really is as simple as that.

In the beginning of your cycle, estrogen increases and then peaksright before your mid-cycle, which causes your breast ducts to enlarge.

Couple that with your bodys production of progesterone, which leads toswollen milk glands, and voil, youre sore AF.

Fibrocystic breast condition (FBC) essentially causes your breasts feel so tender and lumpy thatit hurts to hug someone.

But, dont worry, theres no need to freak out if you have FBC. Those lumps may be large and super uncomfortable, but theyre completely benign, and theyllshrink once youre done menstruating.

Plus, youre not alone.According to Mayo Clinic, more than half of women will experience these types of changes in their breastsat some point in their lives.

For women with simple hormone fluctuations, feel free to tell people to kindly stay away from your chesticles until the soreness goes away.

However, for more advanced relief, over-the-counter medicine can be a great option. In an interview with Elite Daily, Dr. Jennifer Wider, M.D., author ofThe Savvy Woman Patient,provides somekey tips on what to look for in your medication.

Dr. Wider suggests,

You can do a non-steroidal anti-inflammatory medication, which is a non-prescription medication like acetaminophen [Tylenol] or ibuprofen.

Dr. Wider also recommendstaking the medication even before it starts, and that will help prevent the pain, especially if women are joggers, or have large breasts, or the pain gets in the way of their daily functioning.

Magnesium supplements, which can be purchased over the counter as well, can also help relieve cyclic breast pain by lowering inflammation and reducing tenderness, says Dr. Wider.

Dr. Wider explains,

For some women, birth control pills can reduce breast pain and swelling before a period. The synthetic hormones get in the way of the bodys natural hormonal fluctuations. This may help reduce pain for some women.

However, she says, birth control is kind of a weird thing.

She continues,

Some women would say that birth control actually increases the breast pain. What birth control does and the symptoms it can alleviate, may vary by person.

According to Dr. Wider, many women simply arent wearing the right bra for the size of their breasts.

She stresses the importance of payingattention to how a bra feels on your body. Do the straps feel uncomfortably tight? Are you getting enough support from your cup size?

She says,

You may want to wear a sports bra or something that allows the breasts to swell without confining them, and that may help alleviate the pain a little bit.

Ultimately, Dr. Wider says its extremely important toknow the state of your breasts:

Its so important to do the proper exams. This way, if anything changes, youre a patient that can bring any change to the attention of a health care practitioner.

Dont be afraid to approach your doctor regarding pain relief options.

Remember, your body is heroic.If your body deserves anything, it deserves relief.

Subscribe to Elite Daily's official newsletter, The Edge, for more stories you don't want to miss.

Imani Brammer is a writer, on-air talent and YouTuber, where she produces videos on how to navigate the nuances of adulthood. Subscribe to her channel at YouTube.com/ImaniBrammer.

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This Is Why Your Boobs Get Sore When You're On Your Period - Elite Daily

Recommendation and review posted by sam

Viet Nam News

Gia Lc

HCM CITY Eight years ago, a 24-year-old man from the Mekong Delta Province of ng Thp, who identified as gay at the time, decided he wanted to change his gender.

But he didnt know where to turn for advice.

I felt like a girl inside. Psychologically, thats how I felt, he said last Sunday during an interview at a signing ceremony for a new health clinic for the LGBT community in HCM City.

I could easily buy hormones from people who had visited Thailand for sex-change surgery. Hormones and that kind of surgery are still not available in Vit Nam, he said.

Changes in the national law, however, are expected to occur within several years, as the Ministry of Healths legal affairs department is working with several government agencies to compile a Law on Gender Transition.

The law is expected to allow sex-change surgery under certain criteria and include more detailed provisions about transgender people than what is in the current civil code. It will be submitted to the National Assembly next year, but may not take effect for another two to five years.

In 2015, the 24-year-old from ng Thp, who now identifies as a transgender woman, chose to have cosmetic surgery on her face, nose and breasts at a private beauty salon in Vit Nam.

Prior to the surgery, she began injecting hormones from a 0.5-millilitre tube every week for one year to help develop breasts, shrink muscle mass and reduce body hair.

After the cosmetic surgery, I continued to inject hormones, but only one tube every two weeks. I did not have any health problems from the injections.

However, my friends, who had gone through gender transition, had problems from overdoses because they did not go to a doctor, but just listened to advice from friends, she said.

They had vomiting and spinal pain, and at times felt dizzy. Others even had bleeding after returning to Vit Nam from Thailand where they had sex-change surgery.

Many of her friends did not want to go to Vietnamese health facilities because they felt uncomfortable, facing inquisitive eyes, she said.

Dr Tr Anh Duy of Bnh Dn Hospital in HCM City said that such unsupervised practices by people who fear discrimination are dangerous.

They can overdose or use substandard hormones, or those without clear origin. They also may not be using hormones in a hygienic way, he added.

Safe place

However, with a new dedicated centre for LGBT (lesbian, gay, bisexual and transgender) community, people who need counselling now have a place to go.

Though based in HCM City, the new centre will offer counselling to anyone in the country.

Patients in the LGBT community and those who have HIV can call the centre to receive counselling and monitoring of their health while taking hormones or after sex-change surgery performed outside the country.

The agreement to co-operate to provide counselling services was signed last Sunday between the Mens Health Center and G-Link, a social enterprise providing comprehensive health care and communication to improve societys awareness about transgender women and men who have sex with men.

The clinic will offer free counselling abouttherapy, examinations and treatments, all of which will be offered at low cost, to the LGBT community and people diagnosed with HIV. Foreigners who live and work in the country can also access the services.

The Mens Health Center will provide free HIV tests and free screening for sexually transmitted diseases such as gonorrhoea and syphilis. For those who test positive for HIV, G-Link will offer treatment assistance by connecting them with public health facilities which provide antiretroviral therapy.

Many people in the LGBT community have already called the centre and contacted staff via its website at http://www.menhealth.vn, and its Facebook fanpage at http://www.facebook.com/trungtamsuckhoenamgioi/

A 23-year-old man, who identified as MSM (men who have sex with men), said the clinic will be very useful and convenient for us.

According to the UK National Health Services guide to hormone therapy for trans people, blood tests must be taken to assess a patients health before hormone therapy. Doctors regularly test patients to see if they are absorbing the medicine and monitor any health problems. Hormone treatment can be adjusted or additional medication may be prescribed.

The Ministry of Health estimates that Vit Nam has 270,000 to 300,000 people who want to have transition to another gender.

As part of the countrys Civil Code issued in 2015, the Law on Civil Status addresses gender transition rights and the definition of transgender people.

Accordingly, individuals who have gone through gender transition have rights and responsibility to register their gender change. They have the right to redefine gender in case of congenital defects or indeterminate sex at birth and have medical intervention, according to a provision in the current Law on Civil Status.

The proposed Law on Gender Transition, however, is expected to extend those rights and will contain detailed provisions about citizens access to hormonal treatment and sex-change surgery.VNS

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A new safe place for the LGBT community - Viet Nam News

Recommendation and review posted by Bethany Smith

Testosterone (T) is a steroid hormone modulating multiple physiological functions and regulating carbohydrates, proteins,1-10 and lipid metabolism. Testosterone is a critical physiologic modulator for muscle structure and function and regulates the process of adipogenesis.1,3 T is a metabolic and vascular hormone required for maintaining overall physiological function in mens health.1-11

Testosterone deficiency (TD) contributes to a host of pathophysiological processes and affects mens overall health and quality of life.2,12,13 TD adversely reduces bone mineral density and muscle mass and increases fat mass contributing to larger body mass index (BMI). TD contributes to anemia, frailty, fatigue, and insulin resistance (IR). Other adverse effects of TD include altered mood, diminished vitality, and reduced level of energy and sense of well-being coupled with impaired memory and reduced cognition. TD is also associated with reduced libido, increased erectile, and orgasmic dysfunction. TD correlates with poor physical and social function and decline in overall health.2,12,13 TD predicts metabolic syndrome (MetS), diabetes, and obesity.2,12,13

Since MetS, obesity, and diabetes are risk factors for cardiovascular disease (CVD), it is likely that TD increases CVD risk as a result of potentiating such risk factors. Antonio et al and Laaksonen et al14,15 have shown that reduced T levels are independent predictors of MetS. Furthermore, in a large, well-executed epidemiological study with a long follow-up period, it was demonstrated that higher endogenous T levels are protective and associated with a reduced risk of CVD, whereas reduced T levels are associated with an increased risk of cardiovascular (CV) events, coronary heart disease, and cerebrovascular (CBV) disease.16

Recent reviews12,13 suggested that T therapy (TTh) in men with TD is not associated with increased CV risk. On the contrary, TTh appears to be protective. It should be pointed out that TTh has been used for over 70 years16-22 with little or no demonstrable risk. In fact, recent studies suggested that TTh does not increase CV risk or mortality and is thought to be beneficial.23-30 Of 9 meta-analyses published to date, all but 1 demonstrated that no serious harm is incurred from TTh; on the contrary, TTh is associated with significant overall health benefits.12,13 It is important to point out that since obesity, diabetes, IR, dyslipidemia, MetS, hypertension, and hyperglycemia are considered CV risk factors, any therapeutic modality that ameliorates these components is expected to reduce CV risk. Thus, it is not surprising that as published reports demonstrate that TTh ameliorates MetS; improves lipid profile, hyperglycemia, blood pressure, inflammation, and IR; increases lean body mass; improves bone mineral density; reduces waist circumference (WC); and improves vigor and vitality, TTh is also likely to reduce the risk of CVD and mortality.12,13

Over the past several years, 4 reports appeared in the clinical literature purporting increased CV risk and death attributed to TTh.31-34 A thorough analysis of these studies has been undertaken by several investigators12,13 as well as the Food and DrugAdministration (FDA),35 all arriving at the conclusion that such studies are neither credible nor convincing with regard to the purported CV risk, due to methodological flaws, data contamination, and use of unvalidated statistical methods. Seven recent studies23-30 did not confirm the findings of these purported studies.31-34 On the contrary, none reported an association with TTh and increased CV risk or increased mortality. A recent randomized controlled trial of 790 men treated or untreated withT for 1 year confirmed no increase in the risk of CVD.30 On thecontrary, in the second year of follow-up, the study showed more CV events in the placebo arm than in the T-treated group.30

We have undertaken this study to investigate the risks and benefits of TTh in men with TD treated for up to 8 years and compare these benefits with those in men with TD who remained untreated for the same length of time in a clinical setting that represents what is observed in real life. Our findings are summarized in this report.

Patients and Methods

This was an observational, prospective, cumulative registry study in 656 men (age: 60.72 + 7.15 years) with total T levels 12.1 nmol/L and symptoms of hypogonadism. Ethical guidelines as formulated by the German A rztekammer (the German Medical Association) for observational studies in patients receiving standard treatment were followed. After receiving an explanation regarding the nature and the purpose of the study, all participants consented to be included in the registry and have their data analyzed. Measurements of the parameters assessed in this study were carried out as previously described.36,37

Men seeking medical treatment for urological complaints were enrolled. In the T-treated group, 360 men received parenteral T undecanoate (TU) 1000 mg/12 weeks following an initial 6-week interval for up to 10 years. Men (n 14 296) who had opted against TTh, primarily due to financial reasons but also due to a negative perception of TTh as a risky treatment, served as controls. Median follow-up in both groups was 7 years.

Assessment and Follow-Up

Measurements were taken at least twice a year, and 8-year data were analyzed. We measured or calculated the following parameterstotal plasma T levels, weight, WC, BMI, hemoglobin, hematocrit, fasting glucose levels and glycated hemoglobin (HbA1c), systolic blood pressure (SBP) and diastolic blood pressure (DBP), heart rate, pulse pressure, rate pressure product, lipid profile (total cholesterol [TC], low-density lipoprotein [LDL]-cholesterol, high-density lipoprotein [HDL]-cholesterol, triglycerides [TGs]), C-reactive protein, and liver transaminases. We also assessed prostate volume and prostate-specific antigen and questionnaires including the International Prostate Symptom Score (IPSS), Aging Males Symptoms (AMS), and International Index of Erectile Function, Erectile Function domain (IIEF-EF). Measures were taken between 2 and 4 times per year and annual average was calculated.

Statistical Methods

In the treated group, patients returned quarterly for TU injections, whereas in the control group, patients returned biannually for a routine visit. Data in both treated groups have been averaged across each year of patients participating in the study. Thus, obtained yearly data were used to assess differences between the 2 groups while adjusting for possible confounding. Adjusted multivariable analyses and the propensity score matching approaches were used to compare the 2 groups across time while adjusting for baseline differences.

Adjusted Multivariable Analyses

In adjusted multivariable analyses, changes from baseline in parameters (weight, WC, etc) were analyzed using a mixed model for repeated measures in terms of treatment, visit, and treatment-by-visit interaction as fixed factors and age, WC, weight, systolic and DBP, TC, HDL, LDL, TG, AMS, glucose, and baseline values of the analysis parameter as covariates. Baseline parameter values are the values recorded prior to TU injection. A random effect was included in the model for the intercept. Adjusted mean differences between treatment groups at each time point and across time within each treatment group were estimated using estimate statements in SAS PROC MIXED, Version 9.3 (2011) provided by SAS Institute Inc, Cary, North Carolina.

Propensity Matching Analyses

Our general strategy for propensity matching of those on active treatment to those who remained untreated included calculating propensity score based on logistic regression model and selecting matching pairs (or one to many) based on the score. The matching was performed by nearest neighbor selection with caliper set to a fraction of standard deviation (SD) of the propensity score. Several scenarios were considered. We first attempted to create propensity score based on following variablesage, WC, weight, SBP and DBP, TC, HDL, LDL, TG, AMS, and glucose. That model discriminated between active drug and those who remained untreated too well, resulting in a very small overlap of propensity score distributions. We then created propensity score based on the following variables age, BMI, and WC. The 1:1 matching was done choosing nearest neighbor match with caliper set to 0.2 SD of the propensity score. Additionally, we explored 1:1 matching setting caliper to 0.5 SD and 1:2 matching with 0.2 SD and 0.5 SD calipers. These additional scenarios did not result in noticeable gain of the matched sample. Analyses were performed using SAS 9.3 software (SAS Institute, Cary, North Carolina).

Results

Baseline characteristics and comorbidities of the patients included in this registry and reported in this article are shown in Table 1. A total of 656 patients were included in the study and were followed up for up to 8 years. In the group that optedagainst TTh (henceforth referred to as untreated, control group), a total of 296 patients were followed up. The mean baseline age was 64.8 + 4.3 years, with a mean follow-up of 6.5 + 1.2 years and a median follow-up of 7 years. The T-treated group consists of a total of 360 patients with a mean baseline age of 57.4 + 7.3 years, with a mean follow-up of 6.5 + 2.4 years and a median follow-up of 7 years. In the control group, there were 12 men who were diagnosed with prostate cancer during the follow-up period. In the T-group, there were 7 men who were diagnosed with prostate cancer during the follow-up period. Furthermore, in the control group, there were 21 deaths, 19 of which were attributed to CVD. In the T-group, 2 deaths occurred, none was attributed to CVD. We should emphasize that the 2 groups are compared in terms of changes from baseline rather than the absolute values. This was done, in part, to ensure that differences between the 2 groups at baseline do not contribute to the observed differences between the groups. The data presented here reflect the estimated adjusted mean difference between the 2 groups.

Impact of TTh on Mortality and Nonfatal Myocardial Infarction and Stroke

In this registry, the follow-up time for the total group (in months) was 73.29 + 22.9 (minimum: 9; maximum: 111) and in the control group was 74.37 + 13.60 (minimum: 24; maximum: 90). In the T-treated group, the follow-up time was 72.4 + 28.35 (minimum: 9; maximum: 111). As shown in Table 2, there were 2 deaths in the T-treated group, none was related to CV events. One was attributed to postsurgical thromboembolism and 1 due to traffic accident. In the nontreated control group, there were 21 deaths, 19 of which were related to CV events. Five were attributed to myocardial infarction (MI), 4 were attributed to stroke, 7 were attributed to heart failure, 2 to thromboembolism, 1 to lung embolism, and 1 to pneumonia and lung failure (Table 2). The incidence of death in 10 years was 0.1145 in the control group (95% confidence interval [CI]: 0.0746-0.1756; P < .000) and 0.0092 in the T-treated group (95% CI: 0.0023-0.0368; P < .000); the estimated difference between the groups was 0.0804 (95% CI: 0.0189-0.3431; P < .001). The estimated reduction in mortality for the T-group was between 66% and 92%. There were 26 nonfatal MIs (Table 3) and 30 nonfatal strokes (Table 4) in the control group and none in the T-treated group.

Impact of TTh on Hyperglycemia and HbA1c Levels in Men with Hypogonadism Treated or Untreated With TTh for up to 8 Years

TTh reduced blood glucose levels significantly in men with hypogonadism (5.7 + 0.7 to 5.2 + 0.1 mmol/L). When data were adjusted for baseline differences, the adjusted difference between the treated and untreated control groups showed a progressive decrease in glucose levels from baseline (Figure 1A). The estimated change from baseline was 0.4 mmol/L (P < .0001). In contrast, blood glucose levelsin untreated men did not show demonstrable changes (5.6 + 0.4-5.6 + 0.3 mmol/L). The change from baseline was 0.002 mmol/L (not significant [NS]). The most profound observation is the noted change in HbA1c levels in men treated with T when compared to the untreated group (Tables 5 and 6). As shown in Figure 1B, HbA1c levels were significantly reduced in the T-group, and the reduced values were maintained with TTh over the course of follow-up. Glycated hemoglobin was recorded from 6.9% + 1.4% to 5.6% + 0.4%, with an estimated change from baseline of 1.7% (P < .0001). After adjustment for baseline differences, the adjusted difference between the treated and untreated control groups showed a progressive decrease in HbA1c from baseline (Figure 1B). In contrast, HbA1c increased in the untreated group from baseline 6.1% + 1.2% to 6.4% + 1.4%, with an estimated change from baseline of 0.3% (P < .0001).

Subgroup analysis comparing the effects of TTh in diabetic men showed considerable and significant reductions in HbA1c values compared to diabetic men who remained untreated (control group; data not shown). This is consistent with observations reported previously by others.38-43 The reductions in HbA1c by TTh have important implications in reducing the IR burden in diabetic men and also in reducing the risk of CVD. Impact of TTh on SBP and DBP in Men with Hypogonadism Treated or Untreated With TTh for up to 8 Years

Systolic blood pressure decreased from 151.3 + 17.0 mm Hg to 130.0 + 6.6 mm Hg in the T-group (P < .0001) and increased slightly but significantly from 139.5 + 15 mm Hg to 140.3 + 13.3 mm Hg in the control group (P < .0005). Diastolic blood pressure decreased from 90.6 + 11.6 mm Hg to 74.4 + 4.6 mm Hg in the T-group (P < .0001) and increased slightly but significantly from 79.6 + 9.2 mm Hg to 81.1 + 8.4 mm Hg in the control group (P < .005). After adjustment for baseline differences, the adjusted difference between the treated and untreated control groups showed a progressive decrease in SBP and DBP from baseline (Figure 2A and B). Pulse pressure, a marker of arterial stiffness, decreased in the T-group from 60.7 + 7.7 mmHg to 55.6 + 4.9 mmHg (P < .0001) and remained unchanged in the control group. Heart rate (beats per minute) decreased in the T-group from 77.5 + 3.7 to 72.4 + 2.1 (P < .0001) and increased slightly but significantly in the control group from 76.2 + 5.0 to 77.6 + 4.0 (P < .01). Rate pressure product decreased from 11 751 + 1610 to 9421 + 617 in the T-group (P < .0001) and increased from 10 623 + 1347 to 10 890 + 1106 in the control group (P < .0005), withan estimated difference between groups of 2656 (Tables 5 and 6). These findings suggest that long-term TTh in men with hypogonadism resulted in significant reductions in both SBP and DBP as reported previously.36,37,44,45-53

Impact of TTh on Lipid Profiles in Men with Hypogonadism Treated or Untreated With TTh for up to 8 Years

As shown in Figure 3A-D and Tables 5 and 6, TTh produced significant decrease in TC (mmol/L) from 7.2 + 1.1 to 4.8 + 0.2 (P < .0001), whereas in the control group, TC increased from 6.3 + 1.2 to 6.8 + 1.1 (P < .0001). After adjustment for baseline differences, the difference between the treated and untreated control groups showed a progressive decrease in TC from baseline (Figure 3A). In the control group, LDL increased from 3.5 + 1.5 to 4.0 + 1.5 (P < .0001) but was significantly reduced in the T-group. After adjustment for baseline differences, the difference between the treated and untreated control groups showed a progressive decrease inLDL-cholesterol from baseline (Figure 3B). TTh increased HDL levels (mmol/L) from 1.4 + 0.5 to 1.9 + 0.5 (P < .0001). We also noted an increase in the control group (untreated) from 1.3 + 0.5 to 1.6 + 0.7 (P < .0001). This increase in HDL levels in the T-group is accompanied by significant reductions in LDL levels (mmol/L) from 4.2 + 1.1 to 2.7 + 0.8 (P < .0001). After adjustment for baseline differences, the difference between the treated and untreated control groups showed a progressive increase in HDL-cholesterol from baseline (Figure 3C). Triglyceride levels (mmol/L) decreased in the T-group from 3.1 + 0.6 to 2.1 + 0.1 (P < .0001) and increased in the control group from 2.9 + 0.6 to 3.1 + 0.6 (P < .0001). After adjustment for baseline differences, the difference between the treated and untreated control groups showed a progressive decrease in TG levels from baseline (Figure 3D). Most importantly, the TC/HDL ratio was reduced in both groups but did not reach statistical significance in the untreated (control) group. As shown in Figure 4A, the difference between the treated and untreated groups showed a progressive decrease in theTC/HDL ratio from 5.6 + 1.9 to 2.6 + 0.7 in the T-group (P < .0001) and from 6.2 + 3.5 to 5.6 + 3.5 in the control group (NS). Since TC/HDL ratio is considered as an important parameter for CV risk assessment, this observation is of considerable significance to the role of TTh and CV risk. Finally, non-HDL cholesterol (mmol/L) decreased in the T-group from 5.8 + 0.9 to 2.8 + 0.5 (P < .0001) and increased in the control group from 5.0 + 1.3 to 5.2 + 1.4 (P < .0001). After adjustment for baseline differences, the difference between the treated and untreated control groups showed a progressive decrease in non-HDL cholesterol from baseline (Figure 4B). Figure 1. Changes in fasting blood glucose and glycated Hemoglobin (HbA1C) in the testosterone (T)-treated and untreated (control) groups. A, Changes in glucose levels (yellow bars) were adjusted for baseline differences between the T-treated (green bars) and untreated (red bars) control groups. B, Changes in HbA1c (yellow bars) were adjusted for baseline differences between the T-treated (green bars) and untreated (red bars) control groups.

Impact of TTh on Liver Function Enzymes in Men with Hypogonadism Treated or Untreated With TThfor up to 8 Years

Testosterone therapy produced a gradual and progressive decrease in liver transaminases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]), suggesting potential reduction in liver fat content and inflammatory activity. In contrast, an increase in liver transaminases is noted in the untreated (control) group. In the T-group, AST decreased from 39.6 + 15.8 to 16.1 + 2.4 U/L (P < .0001). In the control group, AST increased from 23.4 + 4.8 to 40.3 + 7.7 U/L (P < .0001). ALT decreased from 41.7 + 15.9 to 16.1 + 3.0 in the T group (P < 0.0001) and increased from 27.4 +4.9 to 44.4 +7.8 in the control group (P < .0001; Tables 5 and 6).

Figure 2. Changes in systolic and diastolic blood pressure in the testosterone (T)-treated and untreated (control) groups. A, Changes in systolic blood pressure (yellow bars) were adjusted for baseline differences between the T-treated (green bars) and untreated (red bars) control groups. B, Changes in diastolic blood pressure (yellow bars) were adjusted for baseline differences between the T-treated (green bars) and untreated (red bars) control groups. Figure 3. Changes in lipid profile in the testosterone (T)-treated and untreated (control) groups. Changes in total cholesterol (A), low-density lipoprotein (LDL) cholesterol (B), high-density lipoprotein (HDL) cholesterol (C), and triglycerides (D; yellow bars) were adjusted for baseline differences between the T-treated (green bars) and untreated (red bars) control groups. Figure 4. Changes in total cholesterol (TC)/high-density lipoprotein (HDL) ratio and non-HDL cholesterol in the testosterone-treated and untreated (control) groups. Changes in TC/HDL ratio (A) and non-HDL cholesterol (B; yellow bars) were adjusted for baseline differences between the T-treated (green bars) and untreated (red bars) control groups.

Impact of TTh on Anthropometric Parameters in Men with Hypogonadism Treated or Untreated With TTh for up to 8 Years

TTh in men with hypogonadism produced significant and sustained weight loss (WL) over the course of the treatment period (mean weight decreased from 103.9 + 16.5 kg to 86.9 + 8.9 kg); the changes in weight were statistically significant for all 8 years versus the previous year (P < .0001). The estimated mean change from baseline was 19.3 kg and the mean percent change from baseline 17.0% + 7.8%. In contrast, there was a slight but significant weight gain in the control group (mean weight increased from 91.8 + 10.6 kg to 92.4 + 9.0 kg; P < .0005). The estimated mean change from baseline was 1.6 kg and the percent mean change from baseline 1.5% + 2.4% (Tables 5 and 6). The WL noted in the T-group appears to translate into a marked reduction in WC. Waist circumference in the T-group decreased from 105.8 + 8.6 cm to 97.2 + 6.5 cm (P < .0001). The changes were statistically significant for 8 years versus the previous year (P < .0001). The estimated mean change from baseline was 10.0 cm. When the data were adjusted for baseline differences, the adjusted difference between the treated and untreated control groups showed a progressive decrease in WC from baseline (Figure 5). A slight increase in WC was observed in the untreated group. Waist circumference in this group increased from 106.7 + 7.5 cm to 107.9 + 6.4 cm (P < .0001). The observed WL and reduction in WC in the T-group are also reflected in reduced BMI values (BMI decreased from 33.1 + 5.4 to 28.0+3.0, estimated mean change from baseline 6.2 kg/m2). A slight but significant increase in BMI was noted in the untreated group where BMI increased from 29.3 + 3.5 to 29.7 + 3.1 by an estimated 0.5 kg/m2 (P < .0005). Figure 5. Changes in waist circumference (WC) in the testosterone (T)-treated and untreated (control) groups. Changes (yellow bars) were adjusted for baseline differences between the T-treated (green bars) and untreated (red bars) control groups.

Effects of Long-Term TTh on Safety Parameters in Men with Hypogonadism

In this comparison registry study, long-term TTh in men with hypogonadism increased hemoglobin concentrations and hematocrit, but the levels remained within the physiological ranges.36,37,44 Seven patients were diagnosed with low-grade prostate cancer in the T-group (1.9%) and 12 patients were diagnosed with prostate cancer in the untreated (control) group (4.1%).

Epidemiological studies demonstrated that reduced circulating T levels are associated with greater CVD risk and physiological T levels are associated with a protective effect on the vascular system.16 However, to date, there are no published large, prospective, placebo-controlled studies of sufficient duration that investigated the effects of TTh, especially with regard to CVD, in men with hypogonadism and assessed the benefits and risks of TTh. A number of observational studies have demonstrated that TTh reduced mortality and produced improvements in CV risk factors, such as reduced fat mass, obesity, WC, blood pressure, and improvement in glycemic control.36,37,44

TD (hypogonadism), MetS, type 2 diabetes, and other known risk factors for CVD are chronic diseases requiring chronic, lifelong treatment. Indeed, assessment of TTh on these chronic conditions requires long-term randomized, controlled trials (RCTs) with long durations approaching a decade in order to truly assess what happens in real-life settings. Unfortunately, this is not feasible and most of the RCTs are of short duration. It is unlikely that we will be able to observe real-life changes in response to therapy in studies with short duration. Therefore, registry studies represent a bridge between RCTs and real life.54,55

In this report, we present data from an observational registry study on TTh in 360 men with hypogonadism who were followed up for a period of 8 years while on continuous TTh and compared these findings to data from 296 men with hypogonadism who remained untreated for the same follow-up period, approaching 8 years. Of particular interest is that there were only 2 deaths in the T-treated group and none was related to CV events. Interestingly, in the nontreated control group, there were 21 deaths, 19 of which were related to CV events. Furthermore, there were 26 nonfatal MIs and 30 nonfatal strokes in the control group but none in the T-treated group. These findings are in agreement with prior observational studies.24-30,56-58

TTh has been shown to reduce the risk of incidence of MI, stroke, and mortality in men with hypogonadism.24-30,56-58 These reports, together with the meta-analysis published by Corona et al59 and the FDA response to the petition to place a black box on T products,35 suggest that no credible or substantial evidence exists for increased CV risk with TTh. Our findings which span more than 8 years with a large number ofpatients also confirm this premise. Thus, we point out that the earlier reports that purported increased CV risk with TTh are confounded by methodological flaws and without adequate clinical acumen that makes them inconclusive, and at best suspect, in their conclusions. Considerable clinical benefits of TTh cannot be denied such as improvement in sexual desire and erectile function,59-62 increased energy, mood, and vitality,62-66 increased lean body mass67-71 reduction in total body fat mass,63-66,72-74 and reduction in WC.3,36,37,45,75

Epidemiological studies identified TD as a risk factor for CVD.88 Furthermore, TTh improves CBV perfusion and improves mood in men with TD and low T levels predict a poor CV risk profile.89,90 We should point out that we made no attempts to monitor changes in lifestyle, simply because when this registry study was initiated, there was no expectation that men would lose weight, lose WC, and experience improvement in lifestyle. For this reason, there were no plans to investigate the effects on changes in lifestyle, which is very important. However, placebo-controlled studies showed that obese men on a hypocaloric diet receiving T had a significant increase versus baseline in step count per day and activity, assessed by accelerometry.91 The patients in this registry also reported anecdotally that they had increased their level of physical activity. Future study should account for improvements in mood and quality of life in response to TTh.

We should also point out that several studies showed reduced carotid intimamedial thickness in response to TTh, suggesting that normalizing serum T may prevent or reverse atherosclerosis. In addition, TTh reduced mortality by approximately 50% in men with hypogonadism57 and diabetic men.58 A recent large observational study by Wallis et al92 demonstrated that in long-term TTh, an inverse relationship between TTh and CVD risk and mortality was observed. It is our view that such important findings provide support for the premise that TTh reduces mortality associated with CVD and TD increases mortality among men with hypogonadism.11,76-81

We also investigated the changes in blood glucose levels and the levels of the surrogate marker for hyperglycemia, HbA1c. Most importantly, we noted that TTh in men with hypogonadism resulted in significant and sustained reductions in blood glucose throughout the observation period. Interestingly, however, this was not the case in men with hypogonadism who remained untreated for the same observational period. The reduction in blood glucose may be explained by improved glucose uptake, utilization, and disposal in response to T action and in overall improvement in fuel metabolism. This finding is of importance, since hyperglycemia is a component of the MetS and a contributor to IR and onset of diabetes, thus contributing to increased CVD risk. The marked improvement in glucose metabolism resulting from TTh is also reflected in the reduction in the fraction of HbA1c. This observation is consistent with previous studies.36,37,42-44 We did not observe, however, any significant decrease in HbA1c levels in the untreated (control) group, confirming a role of T action in glucose utilization and disposal.93,94 This finding has relevant clinical implication for regulating hyperglycemia in men with hypogonadism. Since hyperglycemia, IR, and diabetes are considered as risk factors for CVD, therefore, TTh ameliorates hyperglycemia and IR and reduces the risk of CVD. Intensive glucoselowering therapy by various therapeutic modalities has been the mainstay of treating hyperglycemia. However, many of such therapeutic agents are associated with adverse side effects and poor compliance, and initial improvements cannot be maintained. T is a physiological hormone and, when administered in physiological levels, it produces marked reductions in glucose and HbA1c levels without serious side effects.36,37,42-44,63 Thus, this therapy may serve as a novel approach to augment treating hyperglycemia in men with hypogonadism. These findings further support the notion that TTh contributes to a reduction in CV risk and an improvement in cardiometabolic function.

One of the critical findings of this long-term study is the improvements and normalization of the lipid profile only in men with hypogonadism treated with T. Pronounced and significant decreases in TC, LDL, and TGs were observed in response to TTh over the course of the treatment period. In contrast, no significant changes were noted in the untreated (control) group. Since dyslipidemia is one of the components of the MetS and a risk factor for CVD, any normalization in the lipid profile would be considered a benefit since it reduces the risk of MetS and CVD. It is worth noting that the observed decreases in TC, LDL, and TGs in response to TTh are significant and parallel those values observed in men treated with statins to prevent CVD. More importantly, the TC/HDL ratio in the T-treated men was lowered significantly compared to untreated men. Since this ratio is thought to predict the risk of CVD, in particular, ischemic heart disease, such decreases in this ratio noted in this study support the notion that TTh reduces the risk of CVD.95

In this study, we also compare the changes in SBP and DBP in the T-group with that of the untreated group. Our findings showed a significant and gradual decrease in both SBP and DBP in patients treated with T but no significant decreases in blood pressures in the untreated patients (control group). The decrease in blood pressure in the T-group was maintained over the entire course of the 8 years of continuous therapy. The link between TD and risk of hypertension and the improvement in blood pressure with TTh has been proposed previously.44,96

Several studies have suggested that T modulates arterial blood pressure via a host of biochemical and physiological mechanisms,47,48 and low circulating T levels may contribute to hypertension. Systolic blood pressure is inversely associatedwith T levels,47,48 suggesting that hypogonadism contributes to higher blood pressure. Men with hypogonadism treated with TTh were shown to exhibit reduced blood pressure.47,48 Of interest is the improvement in pulse pressure, a surrogate marker for arterial stiffness, in the T-treated but not in the untreated group. It should be noted that pulse pressure is considered a marker of vascular stiffness and any reduction in this parameter is considered favorable for reducing CVD risk.97,98 This observation is congruent with data from a recent placebo-controlled study in which reduction in arterial stiffness was reported following TTh.99 The reduction in rate pressure product in the T-group reflects a decrease in the myocardial workload.

Although a considerable body of evidence accumulated to suggest that TTh does not increase the risk of CVD, a recent review by Huo et al102 tabulated studies on TTh in men with hypogonadism and suggested that studies that examined clinical CV end points have not favored TTh over placebo. It appears that since the purported risks of TTh regarding prostate cancer and CVD risk have been debunked, the authors attempted to downplay the benefits of TTh, especially with regard to the CV physiology. It should be pointed out that this review made a large tabulation of methods and end points of studies reported in the literature but failed to perform appropriate analyses, such as Forest plots or any other form of analyses to account for difference among studies in baseline characteristics, comorbidities, differing end points, varying degrees of clinical assessment, differing T formulations and route of administration, different durations of treatments, or adjusting for variables among the tabulated studies. Interestingly, the authors of this review102 formulated their own conclusions based not on actual data presented in such studies but rather on preconceived ideology. This review either ignored or overlooked the findings of many studies that demonstrated significant benefits of TTh.11-16,24-30,36-46,57-59,62-69

We wish to emphasize that in addition to the adjusted multivariable analyses used in this study, we have also utilized the propensity score matching approaches to compare the 2 groups across time while adjusting for baseline differences. The propensity matching analysis of men on active TTh with those untreated men, calculating propensity score based on logistic regression model and selecting matching pairs based on the score (see Methods section), was carried out to verify that the data obtained with the regression model were meaningful. We must point out that all additional analyses using various scenarios did not result in any noticeable gain of the matched sample and were congruent with data from the adjusted multivariable analysis model.

Study Limitations

The present study was not designed or powered to address the effects of TTh on mortality in men with hypogonadism. There was no adjudication of previous CV events that were reported by the patients as part of their anamnesis. Since patients were treated for their underlying diseases by other specialists than the urologist performing TTh, there was no precise monitoring of concomitant medications, so that changes cannot be excluded.

We do not have any information on medication adherence with regard to any of the concomitant medications that patients had been prescribed. Treatment decisions were made by the same single urologist (A.H.), and the same laboratory was used at all times. We wish to note that the majority of patients whether in the TTh group or in the control group were receiving the standard-of-care treatment in a limited number of general clinical practice or internist offices in and around the city of Bremerhaven, Germany. Thus, we believe that there were minimal variations in the overall management of these patients. For these reasons, it is unlikely that patients in one group received different treatment for their comorbidities from patients in the other group.

Another limitation is that patients were not randomized: The decision for or against TTh, however, was not possible for all patients. Patients with Klinefelter syndrome and other forms of primary hypogonadism had no choice and invariably received TTh, and so did patients with inflammatory bowel diseases who were specifically referred to be treated with T. The fact that these 3 subgroups were considerably younger explains the age gap between the T-group and the control group. We should also point out that potential selection bias may exist based on socioeconomic statusa factor well known to influence the overall health and CV health. Since patients opting not to receive TTh due to financial reasons are part of the control group, it is possible that patients who decided against T treatment for financial reasons did so because of their lower income.

Conclusion

In the absence of long-term prospective, placebo-controlled trials to investigate the risks and benefits of TTh in men with hypogonadism, observational registry studies that include acontrol group, such as reported herein, provide critical information on the long-term safety and effectiveness in clinical practice, especially relevant information regarding adherence and health outcomes in the general population.54,55,92,103,104 In contrast to the majority of studies, patients in the T-group achieved a 100% medication adherence, as T injections were performed in the doctors office and documented. This aspect of treatment is of paramount importance and is considered to be a strength of this study. Thus, long-term TTh in men with hypogonadism appears to be an effective approach to achieve sustained improvements in anthropometric parameters, cardiometabolic function, and risk of CVD events. The low number of CV events observed in the T-group compared with the untreated (control) group strongly suggest that TTh is protective. We believe that the protective effect of T on the CV system provides clinicians with the opportunity to utilize this approach for secondary prevention for men with hypogonadism with a history of CV events.

Written By:Abdulmaged M. Traish, PhD, MBA, Departments of Biochemistry and Urology, Boston University School of Medicine, Boston, MA, USA; Ahmad Haider, MD, Private Urology Practice, Bremerhaven, Germany; Karim Sultan Haider, MD, Private Urology Practice, Bremerhaven, Germany; Gheorghe Doros, PhD, Department of Epidemiology and Statistics, Boston University School of Public Health, Boston, MA, USA; Farid Saad, DVM, PhD, Global Medical Affairs Andrology, Bayer AG, Berlin, Germany & Gulf Medical University, Ajman, United Arab Emirates

Declaration of Conflicting Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Dr. Farid Saad is a full-time employee of Bayer. Dr. Ahmad Haider has received partial compensation for data entry. Dr. Gheorghe Doros has received payment for statistical analysis.

Funding: The author(s) disclosed receipt of the following financial support for the research, authorship and/or publication of this article: Data entry and statistical analyses were supported by Bayer Pharma.

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Long-Term Testosterone Therapy Improves Cardiometabolic Function and Reduces Risk of Cardiovascular Disease in ... - UroToday

Recommendation and review posted by sam

Drug discovery sleuths at Domainex in Cambridge have expanded a partnership with Imperial College London to find novel therapies that reduce heart muscle damage during heart attacks.

The aim is to discover a drug that inhibits the enzyme MAP4K4, which plays a key role in triggering cell death following cardiac arrest.

Significant progress made in the first two years of the collaboration has enabled Imperials Professor Michael Schneider to secure a follow-on award of 4.5 million from Wellcomes Seeding Drug Discovery scheme, to continue the pioneering research.

Since initiating the project in 2015, Domainex and Imperial College London have worked closely together to advance promising therapeutic candidates. Novel, potent, and selective MAP4K4 inhibitors have already been discovered. Using human cardiac muscle grown from human induced pluripotent stem cells, these inhibitors have shown efficacy in protecting these cells against oxidative stress, a known trigger for cell death during heart attacks.

Trevor Perrior (pictured), chief scientific officer at Domainex, said: We have already identified a number of very exciting, novel inhibitors through structure-based drug design.

We look forward to continuing our strong partnership with Professor Schneider and his team and to building on the excellent progress made to date. The innovative cardiac muscle assay developed by the team here at Domainex working in partnership with Imperial College London is enabling early testing on human cardiac muscle cells, which will make cardiac drug discovery more efficient and effective in identifying efficacious candidate drugs.

The Domainex team will continue to provide integrated drug discovery services from its Medicines Research Centre at Chesterford Research Park near Cambridge UK including further biochemical, cellular and biophysical assay screening, structure-guided medicinal chemistry, coupled with drug metabolism, safety and pharmacokinetic assessment of promising candidates. The goal is to advance the project efficiently into pre-clinical development and ultimately to clinical evaluation.

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Domainex and Imperial step up cardiac research - Business Weekly

Recommendation and review posted by Bethany Smith

Dear Dr. Roach: I hope you can answer some questions about myelodysplastic syndrome. What does it do to your body? Is there a known cause or cure? What is the prognosis? P.B.

Dear P.B.: The myelodysplastic syndromes are a group of similar diseases, specific types of blood cancers, that prevent your bone marrow from working properly. They also can transform into acute leukemia. These are uncommon cancers, with perhaps 30,000 cases per year in the U.S. The specific myelodysplastic syndromes are now categorized by appearance, genetic abnormalities of the cells, and condition of the bone marrow.

MDS may arise from damage to DNA, such as from radiation or other toxic exposures. However, many cases have no known cause, and it's likely that these are spontaneous mutations in the bone marrow cells.

Because MDS is a group of related diseases, the treatment and prognosis vary among the different subtypes. However, supporting the bone marrow with transfusions of red blood cells and platelets often is necessary. Medications to stimulate both red and white blood cell production can be used. A few people will be recommended for bone marrow (stem cell) transplant, but the decision to consider this treatment must be made cautiously, as many people who get MDS will not benefit from this treatment due to age or other medical conditions.

Dear Dr. Roach:My 89-year-old mother suffers from ''fluttering'' in her heart. She saw an expert in cardiac arrhythmias, who diagnosed her with ''tachy-brady syndrome'' and ''sick sinus syndrome.'' A nurse also said she has PVCs. She is taking metoprolol, but still has episodes of fluttering. What are these conditions? Are there other medications she could take to correct this heart condition? M.D.P.

Dear M.D.P.:Tachy-brady syndrome (from the Greek roots for ''fast'' and ''slow'') and sick sinus syndrome are the same thing. The ''sinus'' in ''sick sinus syndrome'' refers to the sino-atrial node of the heart, which is the heart's natural pacemaker. It is where every beat normally starts. This part of the heart can become diseased, and the heart can beat both too quickly (tachycardia) and, at other times, too slowly (bradycardia).

Medications are sometimes used for sick sinus syndrome. Beta blockers, like the metoprolol your mother is taking, are given to slow down the tachycardic component of sick sinus, but it can make the bradycardia worse. Most often, the treatment for sick sinus syndrome is a permanent pacemaker.

Readers may email questions to ToYourGoodHealth@med.cornell.edu.

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'Myelodysplastic syndrome' covers a range of diseases - Sarasota Herald-Tribune

Recommendation and review posted by sam

Fat doesn't just sit on top of your bones according to recent research it can also be found inside of your bone marrow too, and running can help shrink it.

According to Dr. Maya Styner, the study's lead researcher and an assistant professor of endocrinology and metabolism at the University of North Carolina at Chapel Hill, exercise has the ability to improve bone quality, particularly in obese mice.

Though the research on mice is not directly translated to human results, Styner says, "The kinds of stem cells that produce bone and fat in mice are the same kind that produce bone and fat in humans."

Marrow is the spongy tissue found inside some of your bones and is comprised of stem cells, nerves, blood vessels and fat. In healthy adults, bone marrow is half red and half yellow.

The yellow portion of bone marrow is used to store fats and provide sustenance required for bone function. In the event of severe blood loss or fever, yellow marrow can turn red.

Styner's study suggests that, like other types of body fat, marrow fat can be used as a source of energy.

"There's been intense interest in marrow fat because it's highly associated with states of low bone density, but scientists still haven't understood its physiologic purpose," said Styner. "We know that exercise has a profound effect on fat elsewhere in the body, and we wanted to use exercise as a tool to understand the fat in the marrow."

The study, which looked at the marrow fat in mice, found after six weeks obese mice who ran on a wheel had a significant reduction in the size of their fat cells, and in some cases appeared identical to lean mice.

"One of the main clinical implications of this research is that exercise is not just good, but amazing for bone health," said Styner. "With obesity, it seems that you get even more bone formation from exercise. Our studies of bone biomechanics show that the quality and the strength of the bone is significantly increased with exercise and even more so in the obese exercisers."

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Exercise Can Help Reduce Fat Found In Bone Marrow - Huffington Post Canada

Recommendation and review posted by Bethany Smith

Stem cells might not be a good option for your kid's sports injury Miami Herald They are seen as the body's master cells, and studies have shown these cells have the capacity to differentiate into bone, cartilage, muscle and ligament tissues. MSC cells are usually harvested from bone marrow or fat cells. Evidence from laboratory ...

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Stem cells might not be a good option for your kid's sports injury - Miami Herald

Recommendation and review posted by Bethany Smith

In 15 years, LifeCell is the second stem cell bank to present its innovation (concept of 'Community Stem Cell Banking') at the 15th International Cord Blood Symposium scheduled to be held at San Diego, USA between 8th - 10th June, 2017.

Singapore - LifeCell International (India's first and the largest stem cell bank)has made an entry into global platform with their recently launched concept of 'Community Stem Cell Banking'. It is believed to be a general practice that technological advancements and new concepts from the western world and other countries percolate into the Indian market. In 15 years, LifeCell is the second stem cell bank to present its innovation at such a prestigious global platform.

Acknowledging the merit of this concept, LifeCell has been invited by AABB (formerly known as American Association of Blood Banks) to portray its recently launched concept of 'Community Stem Cell Banking' at the 15th International Cord Blood Symposium scheduled to be held at San Diego, USA between 8th - 10th June, 2017.

The International Cord Blood Symposium (ICBS) brings all the umbilical cord blood related fields of hematopoietic stem cell transplantation, banking and potential in regenerative medicine together in one interactive three-day conference where world-renowned experts in the field of cord blood will present their new innovations on advancements in the industry.

LifeCell has continuously been adding new innovations to its services. The innovative concept of 'Community Stem Cell Banking' allows access to donor stem cells within the community, thereby extending the protection of stem cells to all conditions treatable by stem cells. In addition to the child, its siblings, parents and grandparents too can access the community pool of preserved stem cells for treatments when required thereby extending the protection of stem cells to the entire family. Also, there is no limit on number of withdrawals of stem cell units from the community providing a comprehensive protection.

Mr Mayur Abhaya, CEO & Managing Director, LifeCell International said, "We are delighted with this acknowledgment for our innovations in stem cell industry. It is a prestigious moment for us being given an opportunity to present Community Stem Cell Banking in a global platform of industry leaders."

Community Stem Cell Banking will be the future of umbilical cord stem cell banking especially in a country like India where the inventory of donor stem cells or bone marrow registries of Indian ethnicity is very low at less than 1% of global inventory and hence the availability of matching donor stem cells is very low. LifeCell, with this new concept, aims to create a huge inventory of donor stem cells within the next few years, which could even exceed the global standards and this will pave way for the highest probability of finding a matching stem cell unit. Mr Vinesh Mandot, Technical Lead at LifeCell, would be presenting this innovative model in a session chaired by Dr. Frances Verter, Director of Parent's Guide to Cord Blood Foundation at the international symposium.

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LifeCell's Community Stem Cell Banking Receives Global Recognition - BSA bureau (press release)

Recommendation and review posted by Bethany Smith

Dear Dr. Roach: I hope you can answer some questions about myelodysplastic syndrome. What does it do to your body? Is there a known cause or cure? What is the prognosis?

A: The myelodysplastic syndromes are a group of similar diseases, specific types of blood cancers, that prevent your bone marrow from working properly. They also can transform into acute leukemia. These are uncommon cancers, with perhaps 30,000 cases per year in the U.S. The specific myelodysplastic syndromes are now categorized by appearance, genetic abnormalities of the cells and condition of the bone marrow.

MDS may arise from damage to DNA, such as from radiation or other toxic exposures. However, many cases have no known cause, and it's likely that these are spontaneous mutations in the bone marrow cells.

Because MDS is a group of related diseases, the treatment and prognosis vary among the different subtypes. However, supporting the bone marrow with transfusions of red blood cells and platelets often is necessary. Medications to stimulate both red and white blood cell production can be used. A few people will be recommended for bone marrow (stem cell) transplant, but the decision to consider this treatment must be made cautiously, as many people who get MDS will not benefit from this treatment due to age or other medical conditions.

The prognosis depends on the age of the person affected and their specific MDS. A person younger than 60 with a low-risk MDS has a median survival (based on data published in 1997) of about 12 years. However, high-risk MDS has a much worse outcome: Half of people succumb within six months. Advances in treatment since these data were published have improved these results, but not as much as hoped.

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Dear Dr. Roach: Myelodysplastic syndromes rare - Herald & Review

Recommendation and review posted by sam

Scholar finds that many citizens are comfortable with providing financial incentives to living organ donors.

Every year, the United States receives 35,000 new requests for kidney transplants. Kidney reserves, however, can supply only 17,000 procedures per year. Over time, this difference between need and supply has produced a wait list including roughly 100,000 patients hoping to receive kidneys, many of whom will die on the wait list. As a result, the time a patient is expected to remain on the wait list is less than the life expectancy of someone with kidney failure. What would it take for you to agree to donate a kidney? Direct payment? A tax incentive? Free health care coverage? A club membership guarantee that you would be the first to receive an organ if you needed it?

Nicola Lacetera, a professor at the University of Torontos Institute for Management and Innovation, has found that U.S. residents are likely to support the provision of governmental incentives directed toward living donors.

Specifically, Lacetera found that 50 percent of the over 3,000 people surveyed supported providing incentives to donors. In addition, 70 percent of participants surveyed agreed that the government should pay living donors if it were certain that doing so would increase the supply of organs.

Providing incentives would not just increase access to organs by a marginal percentage. It would eliminate the kidney transplant wait list. Economists estimate that paying donors $15,000 to $30,000 for their organs would eliminate the 100,000-person wait list within a few years.

Providing incentives to living organ donors has become a pressing policy question, with recent scientific developments rendering donation less invasive. Some countries have chosen to provide incentives to live organ donors. In Israel, for example, a live organ donor not only receives a refund for lost earnings from the time necessary for the procedure and recovery, but also receives refunds on medical and life insurance, and does not have to pay the national health tax for three years. Lacetera states that, in the United States, a federal appeals court recently concluded that it was not illegal to pay blood stem cell donors, although payment for organ donation is criminalized.

Why has the United States not adopted a new policy, like Israel?

Lacetera argues that, despite the support indicated in the survey, people are generally opposed to providing incentives to living organ donors for two reasons. First, we may be concerned with the implementation of any donation incentive program. Second, although we might support the program in theory, the thought of actually adopting one is a repugnant transaction.

In a case recently before the U.S. Court of Appeals for the Ninth Circuit, parents of children who had leukemia and other diseases that can be alleviated with bone marrow transplants sued Eric Holder, the then-U.S. Attorney General, arguing that the National Organ Transplant Act was unconstitutional in its denial of payments for bone marrow transplants.

A nonprofit organization, More Marrow Donors (MMD), which aims to pay donors for their bone marrow, joined the lawsuit. MMD proposed a program in which, through a new extraction operation, removal of the complete fatty substance of the bone marrow would not be necessary. Instead, the valuable blood stem cells from the bone marrow could be collected and separated from the rest of the blood stream. MMD sought to provide donation incentives by awarding donors $3,000 in the form of scholarships, housing allowances, or gifts to charities. In other words, the donor would not receive the funding directly. The National Organ Transplant Act, however, criminalized payment for organ donations, which included bone marrow. MMD argued that prohibiting such payments is unconstitutional.

Furthermore, Lacetera argues that we might be concerned with adverse selection in the donor incentive program. As Lacetera explains, the people who might benefit most from the incentives may also be those who would be more likely to carry transmissible diseases such as hepatitis. A system of in-kind rewards and delayed compensation, however, like MMDs proposed housing allowances, would address these concerns.

In considering whether an organ incentive program could be coercive, the court explained that Congress may have been concerned that if donors could be paid, rich patients or the medical industry might induce poor people to sell their organs, even when the transplant would create excessive medical risk, pain, or disability for the donor.

Still, effective policy and regulation could address these concerns. Lacetera argues these concerns are amenable to tradeoff thinking, in which the downsides could be weighed against the potential efficiency gains that payments may cause, such as an increase in organ supply. Lacetera found that the average respondent supported a policy in which a public agency controls payment for donations and allocation of organs if the end result is a six percent increase in the organ supply. If we such a system were unregulated, then the average respondent would want a 20 percent increase in organ supply to justify the potential downsides of such a program.

Lacetera argues the there may be deeper concerns, however. Providing financial incentives to organ donors may violate our sacred values, which Lacetera defines as principles that individuals and societies are not willing to compromise against any other form of potential gain.

The Ninth Circuit anticipated this moral revulsion. As the court observed, [p]eople tend to have an instinctive revulsion at denial of bodily integrity, particularly removal of flesh from a human being for us by another, and this revulsion is most acute with commodification of such conduct, that is, the sale of ones bodily tissue.

In the end, the court did not need to decide the broad policy questions of the legality of organ donation incentives. Instead, the court held that blood stem cells, which are extracted through the blood stream rather than the bone marrow, were not considered organs. Compensating individuals for donating their bone marrow was legal.

The Department of Health and Human Services responded to the case by announcing that it would undertake a regulatory proceeding to redefine bone marrow to include the kinds of extraction methods discussed in that case, essentially overruling the appellate courts decision.

Originally posted here:
Regulating the Kidney Club - The Regulatory Review

Recommendation and review posted by simmons

BURR RIDGE, Ill., June 13, 2017 /PRNewswire/ -- Dr. Win L. Chiou, a world-renowned authority in pharmacokinetics, an expert in dermatology and a former FDA consultant, has recently published a commentary questioning some widely accepted aging and anti-aging theories in the last century and postulated his new aging theories and anti-aging strategies in The Scientific Pages of Dermatology (TSPD). Chiou said this may have many very important implications and applications in future aging and anti-aging research. This and his other recent breakthroughs are disclosed.

Classical Cumulative Oxidative Stress/Accelerated Aging Theories QuestionedSurprisingly, these important classical theories were not supported by results from his critical analyses of reported aging data of human hearts and skin from a large number of normal subjects over many decades of lifespan. Some implications are: Generally, our skin and heart actually don't age faster as we get older as predicted from these accelerated aging theories. Also, we may have over-emphasized the use of purified anti-oxidants in dietary supplements to combat aging. This is because oxidative stress has been traditionally regarded as the culprit of our aging.

Classical Photoaging Theory Questioned: Intrinsic Aging as Root CauseThe photoaging theory claims that exposure to sunlight contributes about 80% of our skin aging. Chiou astoundingly found that sun exposure had no noticeable effects on the aging of skin collagen and superficial capillaries in their lifetime. Furthermore, age spots, commonly assumed to result from photoaging, were frequently found to occur on thighs, forearms and backs in seniors that were rarely exposed to sunlight. Chiou asked: Do we need to re-evaluate general recommendations that we should wear sunscreens as a daily ritual when we go outdoors? How much SPF number do we really need? This is especially significant because exposure to sunlight has many important health benefits such as reducing blood pressure, heart attacks and strokes, and increasing the immune system and vitamin D synthesis. These benefits are known to far outweigh the risks such as skin cancer.

New Cardiac-Output-Reduction Aging Theory: Utmost Importance of Cellular Nutrients in Determining Cellular/Tissue Aging

Chiou postulated a new theory that since our heart pumps nutrient-carrying blood to various organs/tissues to sustain their vitality, therefore, cardiac output should be closely related to our life expectancy and general health. Chiou said that we age mainly because our cardiac output decreases and cellular levels of nutrients in peripheral tissues also decrease with age. Cardiac output peaks at about age 12. By age 40 and 80, it can decrease very significantly by 30% and 49% respectively. Hence, Chiou postulated that one effective approach to combat body aging and to increase longevity is to increase cardiac output through stem-cell rejuvenation and to increase tissue nutrients. In other words, aging is reversible!!

New Theories for Formation of Wrinkles and Age Spots: Intrinsic Aging as Root CausesFor the first time, Chiou theorized that formation of wrinkles in aged adults results from body's defense mechanism in order to reduce effective surface area for minimizing environmental assaults. And the formation of age spots mainly results from birth defects and later acquired injuries in superficial capillaries that nourish the skin. Hence these disorders are generally first initiated by intrinsic aging. Sunlight may hasten the above problems. Chiou noted that young children and youths with healthy skin may stay outdoors unprotected daily for months or years without developing age spots or wrinkles.

New Strategy to Combat and Reverse Skin Aging: Stem-Cell RejuvenationJust as water can revitalize a dry wilted flower, an aging-reversing phenomenon, Chiou has developed a unique proprietary body-natural (ingredients being natural in our body) nutritional serum, Eternal Spring Serum (ESS), to be topically applied daily to rejuvenate our skin. Surprisingly, the firming and tightening effects are almost universally observed in all users. A stunning example is shown in his wife, Linda Chiou, who has used the product for more than 10 years and rarely used sunscreens. At age 75, her skin seems much better than many others 25 to 35 years younger (Figure 1). Many friends noticed her skin-age-reversing phenomenon. It is reasoned that the ESS must work via rejuvenation of stem or progenitor cells in the skin. Currently, skin reversal is considered by dermatologists as impossible to achieve. Therefore, the ESS represents a historical breakthrough in combating skin aging.

Growth Acceleration and Regeneration of Human Nails: Stem-Cell RejuvenationLiquid preparations containing body-natural nutrients have been shown to quickly accelerate nail growth or to regenerate new nails after nail injury in numerous subjects. This may be the first of its kind ever reported (patent pending). Such effects are also postulated to be due to stem-cell/progenitor cell rejuvenation. Interestingly, this approach also helps grow new hair on Dr. Chiou's decades-old baldhead.

Dr. Chiou is an editor for TSPD, and is organizing a Special Issue on "Aging and Anti-Aging". He was a former university professor for 36 years. Dr. Chiou is currently President of Winlind Skincare LLC and Chiou Consulting Inc. His detailed biography is available at the TSPD website. For inquiries or licensing, Dr. Chiou can be reached at 163879@email4pr.com.

Media Contact: Win Chiou163879@email4pr.com 630-861-0433

To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/major-breakthroughs-in-aging-theories-and-anti-aging-strategies-via-stem-cell-rejuvenation-in-humans-300472905.html

SOURCE Dr. Win L. Chiou

Read more:
Major Breakthroughs in Aging Theories and Anti-Aging Strategies via Stem-Cell Rejuvenation in Humans - PR Newswire (press release)

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Oper Technology, a Hong Kong biotechnology start-up, has pioneered what it claims is a world first in stem cell treatment that it says could potentially help millions of patients suffering from Alzheimers and Parkinsons diseases.

The business was co-founded by Hong Kong Baptist Universitys Professor Ken Yung, who specialises in neurobiology and neurological diseases in the universitys biology department.

He and his team has now developed a method of harvesting neural stem cells from the brains of live subjects using specially developed nanoparticles.

The exploration of using stem cells to repair damaged neural cells is not a new concept. Scientists in the US and elsewhere have experimented using stem cells from fat and skin, developing them into neural cells.

But Yung claims his team is the first to successfully harvest stem cells directly from the brain and re-inject the developed neural cells back into a live subject, thereby artificially regenerating any cells which have died off, due to neurological diseases from neural stem cells themselves.

Stem cells have the potential to develop into different types of cells with specialised functions.

The nanoparticles which are made of a type of iron oxide work like magnets to attract the stem cells within the brain.

Yung said these can then be developed into more specific neural cells and re-injected into the brain to replace damaged cells caused by diseases such as Alzheimers and Parkinsons, where neurons in the patients brains progressively die off with time.

He suggests the treatment could benefit almost 100 million patients around the world, who suffer from neurodegenerative diseases, including strokes.

China alone has the largest population of people with dementia, with an estimated 23.3 million now projected to suffer from the condition by 2030, according to the World Health Organisation.

Yung co-founded Oper Technology and serves as its chairman.

The company is being developed under Hong Kong Science and Technology Parks Incu-Bio programme, which provides select biotechnology start-ups with laboratory and support services, and ultimately it aims to commercialise its medical technology.

If you put the [developed] cells in a different environment from where the [stem cells are harvested], there might be [misdirected] growth in an uncontrolled environment, said Yung.

We want to use neural cells to repair neural cells, and since the stem cells and re-injected neural cells are from the same micro-environment, there will not be uncontrollable growth.

The method has proven to be very successful when tested on rats, especially in cases of Parkinsons, according to Yung, who suggested the method could eventually become an ultimate treatment for the disease.

Furthermore, the risks of this treatment are similar to what is currently on the market today, he added.

The treatment could also help to treat early-stage Alzheimers patients, slowing down or even halting the degeneration process, although Yung acknowledged that its effectiveness in treating terminal stage patients may be limited since it would be difficult to regenerate enough neural cells when patients brains have shrunk due to the condition.

While animals subjected to the treatment displayed an improvement in neural function following the re-injection, the team has yet to start on clinical trials as such cell therapy is still nascent and largely unregulated in Hong Kong.

Oper Technology is currently seeking investment and often sets up booths at conferences such as last weeks EmTech Hong Kong conference, which focuses on innovation and emerging technologies.

Yung hopes to raise enough funds to begin clinical trials in Australia in the near future, where autologous cell therapies are legal and thus provides an ideal environment for clinical trials.

Read more:
Hong Kong biotech start-up claims world first in stem cell treatment of Alzheimer's and Parkinson's diseases - South China Morning Post

Recommendation and review posted by simmons