It was Aubrey Reinhardts last year at Texas Tech University. So when things started getting serious with her boyfriend, she decided it was time to look into birth control.

Reinhardt knew that abortion foes had been trying to strip Planned Parenthood of every penny it receives from government sources. But until that moment two years ago, Reinhardt recalled, she didnt appreciate what that could mean for a person like her who just needed somewhere to go for affordable contraception without feeling she was being judged.

Planned Parenthood had to close its two health centers in Lubbock, where Reinhardt was studying, so she turned to the campus clinic. But the doctor there told her she might have a blood clotting problem, and said Reinhardt would need to get approvals from three other doctors and a hormone specialist before she would prescribe contraception.

Reinhardt, now a 22-year-old law student in Dallas, was stunned. None of her previous physicians had suggested she might have such a problem. Could the doctor be using it as an excuse? She could feel herself tearing up.

Why are you crying? she recalled the doctor asking. Are you really in that big of a hurry to become sexually active?

Humiliated, Reinhardt hurried out of the office.

In the annals of the abortion wars, the call to defund Planned Parenthood has become one of the most potent and contentious rallying cries. The organization is the largest single provider of abortions in the country and has used its political clout to protect access to the procedure.

Now with President Trump in the White House and Republicans in control of Congress and statehouses across the nation, those seeking to curtail public funding for Planned Parenthood see opportunities to achieve their long-sought goal and they see Texas as a model to follow. But as Reinhardts experience shows, the effects of a successful defunding campaign can be far more extensive and potentially damaging than intended.

In 2011, Texas lawmakers slashed funding for family planning clinics rather than allow any of the money to go to Planned Parenthood. Because of the cuts, a quarter of the states clinics closed, making it harder for women of limited means to get a range of other basic health services, including contraception, breast and cervical cancer screenings, and testing for sexually transmitted infections.

Lawmakers have since attempted to repair the damage by directing more money to facilities not tied to abortion providers. But there isnt always a facility that can readily fill the void when women are denied access to Planned Parenthood, which serves about 2.4 million patients nationally each year.

Federally funded community health centers, which provide a range of low-cost primary care to poor families, are stretched thin. And family planning is not routinely offered at 40% of these facilities, according to a study by the Guttmacher Institute, which advocates for reproductive rights, including abortion.

After Reinhardts upsetting visit to the campus clinic, she called one such center in Lubbock. The soonest she could get an appointment was in April. It was January. She then tried facilities operated by Christian nonprofits. They didnt offer contraception.

So she called what was left of Planned Parenthood. They could see her right away, but their nearest locations were in El Paso and Fort Worth, both four-hour drives away.

Over spring vacation, Reinhardt drove to Fort Worth and received an implant that prevents pregnancies for up to four years. But she wondered, What about the mother that has two children, that works two jobs, that cant take off two days to drive four hours away to a clinic and come back?

It is already illegal to use federal dollars for abortions, except in cases of rape, incest or when the mothers life is in danger. And Planned Parenthood says about half of its health centers dont offer the procedure.

But the groups opponents argue that giving Planned Parenthood public funds for non-abortion-related care allows it to spend more of its private funds on abortions. In 2016, the group received $554.6 million from government sources, about 40% of its budget.

The Republican bill to replace Obamacare, which narrowly cleared the House on May 4, would prevent Planned Parenthood from receiving reimbursements from Medicaid for a year.

That would be a big hit. Medicaid, the federal-state program that insures more than 70 million poor Americans, accounts for the majority of Planned Parenthoods public funding, according to Congressional Budget Office estimates. Federal Title X family planning grants make up most of the rest.

The House bill, the American Health Care Act, faces an uncertain future in the Senate. And states have faced pushback from federal officials and the courts when they try to withhold federal money from Planned Parenthood themselves.

Texas, however, has found roundabout ways to chip away at the groups funding.

Texas Republicans scored their first big win in 2011 when the Legislature reduced the two-year budget for the states Family Planning Program to $38 million from $111 million. It also approved a new way to allocate the funds that prioritized community health centers and county health departments over specialized family planning clinics like those affiliated with Planned Parenthood.

The argument was that women would be better served if they had their reproductive health needs addressed at facilities that could provide more comprehensive care; critics contend it was a way to squeeze out Planned Parenthood.

Texas also wanted to exclude Planned Parenthood from a separate Medicaid-funded program that offered family planning coverage for certain women who didnt qualify for full healthcare benefits. But the Obama administration wouldnt allow that because of a federal law guaranteeing Medicaid clients their choice of providers.

The Legislatures solution: Forgo federal funding that had paid for 90% of the program and set up an entirely state-financed version called the Texas Womens Health Program. That effort, launched in 2013, does not contract with clinics affiliated with abortion providers.

Texas actions have provided a road map for other states to follow. In May, Planned Parenthood announced it was closing four of its 12 clinics in Iowa after lawmakers there decided to set up a state-run family planning program that can legally exclude the group.

Planned Parenthood wasnt the only organization hurt by such decisions. By 2013, 82 Texas clinics a third of them Planned Parenthood affiliates had closed or stopped offering family planning services, said Kari White of the Texas Policy Evaluation Project, which studied the defunding effort. None of the clinics performed abortions.

Of those that remained open, researchers found, many had to reduce hours or begin charging for services previously offered for free.

Even when there were other clinics nearby where women could use their state benefits, White said, women would often find that they did not stock the more expensive, long-acting birth control methods available at Planned Parenthood. So women switched to less effective methods, and a few years later, some had become pregnant.

State officials take issue with some of the conclusions because they are based on a study that sampled only patients enrolled in the Texas Womens Health Program expanded and rebranded last year as Healthy Texas Women and not those who received family planning care through other programs.

Now that Trump is in the White House, the state is applying to get its Medicaid funding back for Healthy Texas Women. Since 2013, the Legislature has also committed more than $150 million in additional state funds to rebuilding the network of family planning providers and improving care for poor women more than making up for the clinic closures, according to officials.

Although participation in the states womens health programs plunged from around 359,000 in 2011 to 201,000 two years later, state figures show, the number of clients enrolled has increased since then and in 2015 was approaching 364,000.

"Texas is committed to women's health, Republican state Sen. Jane Nelson, who heads the Senate Finance Committee, said in an email. The number of providers has tripled, and we are making sure that women throughout the state can access these vital services."

Kelly Hart, a spokeswoman for Planned Parenthood of Greater Texas, acknowledged the states efforts to improve family planning. But she said a question lingers: Can [those efforts] be as good as the citizens of this state deserve if you deny a major player in womens healthcare a seat in your program?

Planned Parenthood has 34 health centers left in Texas, four of which perform abortions.

Community health centers will try to fill the gap, but many will need to hire and train staff, reconfigure space and purchase equipment, said Jose Camacho, who heads an association of such facilities in Texas.

In the meantime, women who rely on publicly funded healthcare are still having trouble finding providers who will accept new patients and can see them in a timely manner, Planned Parenthood clinicians say. That can be critical for some patients.

Four years ago, Dayna Farris-Fisher, a mother of three from Plano, discovered a lump in her breast. She didnt have insurance, because her husband had been laid off. None of the low-cost clinics she tried could see her for at least four months.

In a panic, she called Planned Parenthood. Vivian Bigelow, a nurse practitioner at the groups local health center, saw her the next day.

But if a patient like Farris-Fisher, now 50, walked into her exam room today, Bigelow said, she would have to refer her somewhere else. The breast and cervical cancer screening program that paid for the diagnostic testing no longer accepts claims from Planned Parenthood, another casualty of the states defunding efforts.

That terrifies Farris-Fisher. In the five weeks that it took to confirm a diagnosis and begin treatment, her tumor doubled in size.

If I had had to wait for one of those other clinics, she said, I literally am convinced that I would be dead.

alexandra.zavis@latimes.com

Twitter: @alexzavis

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Link:
'Defund Planned Parenthood' has gained momentum. Texas shows the effects can go far beyond just clinics - Los Angeles Times

Recommendation and review posted by simmons

Dani Castro had developed a UTI, but was afraid to go to the doctor due to her track record of bad experiences. She collapsed and became unresponsive, so a friend drove her to the ER. (Content warning.)

I was hospitalized, and my gender marker was listed as male, she said. I had to push back and say something. They changed it, but before I was discharged the medical provider did a pelvic exam.

During the pelvic exam, the physician moved his fingers around inside of her vagina and told her he was impressed with the results of her surgery. Dani didnt have the energy or resources to file a lawsuit and dealt with the inappropriate, traumatizing eventthrough therapy, family and friends.

Today, Castro is a project director at the University of California, San Francisco Center of Excellence for Transgender Health. The UCSF center serves to offer comprehensive care to the trans community, and offers guidelines and resources for primary care providers treating transgender and gender non-binary people.

Castro says shes spoken to folks who have had disrespectful doctors and traumatizing experiences in the emergency room, and during the far more frequent routine visits. Often, Castro says, physicians just use trans patients to answer questions theyre curious about.

Madeline Deutsch, director of UCSF Transgender Care said that specific exams should only happen if its necessary, relevant and based on evidence. In her professional opinion, asking someone for a genital exam because, oh, well theyre taking hormones, maybe they have testicular cancermaybe first make sure theres evidence. Such a relationship between hormones and cancer has not been shown.

Patients already need to travel all over the country for gender-affirming surgery, and the waiting list could be over a year. Despite broader coverage for transgender services under the Affordable Care Act, some state health insurance plans still exclude them, and who knows what will happen with the outcome of the Affordable Care Act vote. Its no surprise that simply receiving preventative care is an ordeal for trans and gender non-binary folks.

Most of us dont go for prevention, said Castro. We go when its an emergency.

The situation is miserable. In 2015, 28,000 transgender people from all fifty states took the National Center for Transgender Equalitys United States Transgender Survey, the largest of its kind. A third had a discriminatory experience at the doctors office. A quarter of the respondents did not see a doctor when they needed to because of fear of being mistreated as a transgender person. A National LGBTQ Task Force survey of 6,450 transgender and gender non-binary people from 2011 documents cases of patients concealing their identities from their doctor, and what appears to be a general lack of sensitivityin the medical fieldwhen dealing with trans issues, including using the incorrect gender pronouns and even mocking patients. Around 20 percent of the participants of that study were flat-out denied care.

Theyre afraid to go to the doctor because of discrimination, and data shows that the fear is justified, said Deutsch. When patients arrive, theyre finding doctors who arent properly trained on how to care for them.

One 2011 survey completed by 132 American and Canadian medical school deans found that undergraduates received a median of just five hours of training in lesbian, gay, bisexual and transgender-related content. Of those schools, 44 had zero hours of LGBT content in their clinical studies.

As a result, trans folks might face what some have dubbed trans broken arm syndrome, where doctors blame whatever health ailment simply on the patient being trans. Malcolm Maune, who works for Trans Lifeline, a hotline staffed by transgender people for struggling transgender people, has lupus and has frequent interactions with doctors he trusts. But hes gone to new doctors whove assumed his troubles simply stem from taking testosterone. They think thats optional, somehow, he said. Theyll just attribute all kinds of things to it that have nothing to do with it.

Sure, a few studies have shown that some men receiving testosterone for other ailments have an increased risk of heart disease. But several studies comparing transgender men with cisgender women specifically havent found an increase in cardiovascular problems. And Maunes doctors ensure he has the same amount of testosterone as any cisgendered manand cisgendered men are more likely to suffer heart attacks younger, regardless! If people assigned male at birth are happy living with that heart disease risk, then Im happy being trans living with that heart disease risk, please and thank you very much.

Not all transgender or gender non-binary folks take hormones, but it is an important way for many trans people to match their physical appearance with their identity. And for them, hormone therapy isnt optional.

Uninformed medical advice could have devastating consequences. Taking someone off of their hormones is a good way to precipitate a suicide attempt, said Maune, adding that somewhere around 40 percent of trans people attempt suicide during their lifetime. This is a matter of life and death.

Somehow, even the endocrinologists who specialize in hormones arent knowledgeable in sex hormone treatment, Joshua Safer, Medical Director of the Transgender Center at Boston University, told me. Given the increasing number of folks who identify as transgender, possibly 1 in 137 teenagers, according to a recent New York Times report, It would be hard to have an endocrine practice without seeing some [trans people], he said. A 2017 study found that of 411 practicing endocrinologists, 80 percent had treated a transgender patient, but 80 percent never received training on how to care for them.

The Endocrine Society has a set of guidelines on treating transgender patients for endocrinologists, said Safer, but theyre not up-to-date. Today, they are literally called Endocrine Treatment of Transsexual Patients, transexual being a term no longer considered to be an umbrella term for transgender people. Theyre in serious need of being revised, said Safer. Weve been working at the revisions and are sorry theyve taken us until 2017.

These oversights lead to glaring omissions in even the most basic care, like advice on maintaining a healthy lifestyle. Trans folks already suffer from higher rates of diet pill use and eating disorders than other patients. Hormone therapy can lead to weight gain or weight loss, according to UCSF Transgender Care, which could exacerbate these issues. And yet, the folks undergoing hormone treatment that I talked to have had little dietary or nutrition advice from their doctors.

When my friend Mattie White chose to start taking hormones, she had questions. How should she eat? Should she alter her behavior or lifestyle? I would even ask, Are there any vitamins I should make sure I get enough of, things I should avoid? My doctors would just say, Take whatever you want. I asked my doctor if I should eat less protein so I dont have too much muscle mass. They said, If you want to, you can eat less. I want a more specific answer than that! This ambivalenceseems to be a repeating theme.

Sadly, much of the missing guidance is supplemented through message boards and testimonials shared online, like the common tip to decrease muscle mass by avoiding protein altogether. One person I spoke with, Sarah Garland, told me that she had found this posted on blogs, Reddits r/asktransgender board, or the Susans Place forum. I know that is not healthy, said Garland, but some people do it out of desperation.

Deutsch says its unacceptable that trans folks are not provided the same kind of health advice and basic care that many take for granted. I see fear and hesitation from medical providers on providing gender-affirming care, then walk around the clinic and see the curveballs other patients throw providers, she said. They take care of patients with far more complicated and rare situations that involve more complex and costly treatment that may have more side effects of risk.

Deutsch commented that yes, there is a lack of research studying transgender people specifically. But many providers are already treating patients who take hormones, and some of the ailments theyre blaming on hormones are just common ailments that people always have that doctors already know how to treat. High blood pressure is high blood pressure and high cholesterol is high cholesterol, said Deutsch.

If medical providers are unsure about how to treat a patient, there are guidelines that can help them not be shitty about it.

The Center of Excellence for Transgender Health offers some incredibly detailed guidelines that are readily available for a minimal amount of searching consistent with the degree of searching providers do on a daily basis for other uncommon symptoms, said Deutsch. These include ailments reasonlessly blamed on hormones like cardiovascular disease and testicular cancer.

Possibly most importantly, these guidelines provide instructions on how to perform an appropriate physical exam in a way that wont drive a patient away from seeing a doctor again. Things can get better.

Trans Lifeline is a hotline staffed by and for transgender people, with experts ready to chat to folks in distress or in need of support. Its numbers are (877) 565-8860 for the US and (877) 330-6366 in Canada.

Follow this link:
How American Healthcare Is Failing Transgender Patients - Gizmodo

Recommendation and review posted by Bethany Smith

More than 95% of testicular cancer are cured but they are at increased long-term risk of cardiovascular disease. The risk of cardiovascular disease and treatment intensity was reported, but it is unknown whether this effect of cancer therapy is direct or indirect, mediated through androgen deficiency. Our aim was, therefore, to evaluate whether testicular cancer patients have increased the prevalence of risk factors of cardiovascular disease and if these risk factors are associated with hypogonadism and/or the cancer treatment given. In 92 testicular cancer patients (mean 9.2years follow-up) and age-matched controls, blood samples were analysed for lipids, total testosterone, luteinizing hormone (LH), glucose and insulin. An estimate of insulin resistance, HOMAir was calculated. Hypogonadism was defined as total testosterone<10nmol/L and/or LH>10IU/L and/or androgen replacement. In testicular cancer men with hypogonadism, compared with eugonadal patients, higher insulin (mean difference: 3.10mIU/L; p=0.002) and HOMAir (mean difference: 0.792; p=0.007) were detected. Hypogonadism group presented with increased risk (OR=4.4; p=0.01) of metabolic syndrome. Most associations between the treatment given and the metabolic parameters became statistically non-significant after adjustment for hypogonadism. In conclusion, testicular cancer patients with signs of hypogonadism presented with significantly increased risk of metabolic syndrome and investigation of endocrine and metabolic parameters is warranted in these patients.

Andrology. 2017 May 23 [Epub ahead of print]

C Bogefors, S Isaksson, J Bobjer, M Kitlinski, I Leijonhufvud, K Link, A Giwercman

Molecular Reproductive Medicine Unit, Department of Translational Medicine, Lund University, Malm, Sweden., Department of Cardiology, Skane University Hospital, Malm, Sweden., Reproductive Medicine Centre, Skane University Hospital, Malm, Sweden.

PubMed http://www.ncbi.nlm.nih.gov/pubmed/28544654

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Hypogonadism in testicular cancer patients is associated with risk factors of cardiovascular disease and the ... - UroToday

Recommendation and review posted by simmons

Previous studies have examined testosterone levels after external beam radiation (EBRT) monotherapy, but since 2002 only sparse contemporary data have been reported.

To examine testosterone kinetics in a large series of contemporary patients after EBRT.

The study was conducted in 425 patients who underwent definitive EBRT for localized prostate cancer from 2002 through 2014. Patients were enrolled in several phase II and III trials. Exclusion criteria were neoadjuvant or adjuvant androgen-deprivation therapy or missing data. Testosterone was recorded at baseline and then according to each study protocol (not mandatory in all protocols). Statistical analyses consisted of means and proportions, Kaplan-Meier plots, and logistic and Cox regression analyses.

Testosterone kinetics after EBRT monotherapy and their influence on biochemical recurrence.

Median follow-up of 248 assessable patients was 72 months. One hundred eighty-six patients (75.0%) showed a decrease in testosterone. Median time to first decrease was 6.4 months. Median percentage of decrease to the nadir was 30% and 112 (45.2%) developed biochemical hypogonadism (serum testosterone < 8 nmol/L). Of all patients with testosterone decrease, 117 (62.9%) recovered to at least 90% of baseline levels. Advanced age, increased body mass index, higher baseline testosterone level, and lower nadir level were associated with a lower chance of testosterone recovery. Subgroup analyses of 166 patients treated with intensity-modulated radiotherapy confirmed the results recorded for the entire cohort. In survival analyses, neither testosterone decrease nor recovery was predictive for biochemical recurrence.

EBRT monotherapy influences testosterone kinetics, and although most patients will recover, approximately 45% will have biochemical hypogonadism.

We report on the largest contemporary series of patients treated with EBRT monotherapy in whom testosterone kinetics were ascertained. Limitations are that testosterone follow-up was not uniform and the study lacked information on health-related quality-of-life data.

Our findings indicate that up to 75% of patients will have a profound testosterone decrease, with up to a 40% increase in rates of biochemical hypogonadism, although the latter events will leave biochemical recurrence unaffected. Pompe RS, Karakrewicz PI, Zaffuto E, etal. External Beam Radiotherapy Affects Serum Testosterone in Patients With Localized Prostate Cancer. J Sex Med 2017;XX:XXX-XXX.

The journal of sexual medicine. 2017 May 22 [Epub ahead of print]

Raisa S Pompe, Pierre I Karakiewicz, Emanuele Zaffuto, Ariane Smith, Marco Bandini, Michele Marchioni, Zhe Tian, Sami-Ramzi Leyh-Bannurah, Jonas Schiffmann, Guila Delouya, Carole Lambert, Jean-Paul Bahary, Marie Claude Beauchemin, Maroie Barkati, Cynthia Mnard, Markus Graefen, Fred Saad, Derya Tilki, Daniel Taussky

Cancer Prognostics and Health Outcomes Unit, University of Montreal Health Center, Montreal, Canada; Martini Clinic, Prostate Cancer Center, University Hospital Hamburg-Eppendorf, Hamburg, Germany. Electronic address: ., Cancer Prognostics and Health Outcomes Unit, University of Montreal Health Center, Montreal, Canada; Department of Urology, University of Montreal Health Center, Montreal, Canada., Cancer Prognostics and Health Outcomes Unit, University of Montreal Health Center, Montreal, Canada; Department of Urology and Division of Experimental Oncology, Urological Research Institute, IRCCS San Raffaele Scientific Institute, Milan, Italy., Department of Urology, University of Montreal Health Center, Montreal, Canada., Cancer Prognostics and Health Outcomes Unit, University of Montreal Health Center, Montreal, Canada; Department of Urology, SS Annunziata Hospital, G.D. Annunzio University of Chieti, Chieti, Italy., Cancer Prognostics and Health Outcomes Unit, University of Montreal Health Center, Montreal, Canada., Cancer Prognostics and Health Outcomes Unit, University of Montreal Health Center, Montreal, Canada; Martini Clinic, Prostate Cancer Center, University Hospital Hamburg-Eppendorf, Hamburg, Germany; Department of Urology, University Hospital Hamburg-Eppendorf, Hamburg, Germany., Department of Urology, Academic Hospital Braunschweig, Braunschweig, Germany., Department of Radiation Oncology, University of Montreal Health Center, Montreal, Canada., Martini Clinic, Prostate Cancer Center, University Hospital Hamburg-Eppendorf, Hamburg, Germany., Martini Clinic, Prostate Cancer Center, University Hospital Hamburg-Eppendorf, Hamburg, Germany; Department of Urology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.

PubMed http://www.ncbi.nlm.nih.gov/pubmed/28546065

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External Beam Radiotherapy Affects Serum Testosterone in Patients ... - UroToday

Recommendation and review posted by Bethany Smith

A SpaceX rocket is slated to launch two University of Colorado Boulder-built payloads to the International Space Station (ISS) from Florida Thursday, including oneto look at changes in cardiovascular stem cells in microgravity that may someday help combat heart disease on Earth.

The Dragon spacecraft

The second payload will be used for rodent studies testing a novel treatment for bone loss in space, which has been documented in both astronauts and mice. The two payloads were developed by BioServe Space Technologies, a research center within the Ann and H.J Smead Department of Aerospace Engineering,

We have a solid relationship with SpaceX and NASA that allows us to regularly fly our flight hardware to the International Space Station, said BioServe Director Louis Stodieck. The low gravity of space provides a unique environment for biomedical experiments that cannot be reproduced on Earth, and our faculty, staff and students are very experienced in designing and building custom payloads for our academic, commercial and government partners.

The experiments will be launched on a SpaceX Falcon 9 rocket from Cape Canaveral, Florida and carried to the ISS on the companys Dragon spacecraft. The SpaceX-CRS-11 mission launching Thursday marks BioServes 55th mission to space.

The cardiovascular cell experiments, designed by Associate Professor Mary Kearns-Jonker of the Loma Linda University School of Medicine in Loma Linda, California, will investigate how low gravity affects stem cells, including physical and molecular changes. While spaceflight is known to affect cardiac cell structure and function, the biological basis for such impacts is not clearly understood, said BioServe Associate director Stefanie Countryman.

As part of the study, the researchers will be comparing changes in heart muscle stem cells in space with similar cells simultaneously cultured on Earth, said Countryman. Researchers are hopeful the findings could help lead to stem cell therapies to repair damaged cardiac tissue. The findings also could confirm suspicions by scientists that microgravity speeds up the aging process, Countryman said.

For the heart cell experiments, BioServe is providing high-tech, cell-culture hardware known as BioCells that will be loaded into shoebox-sized habitats on ISS. The experiments will be housed in BioServes Space Automated Bioproduct Lab (SABL), a newly updated smart incubator that will reduce the time astronauts spend manipulating the experiments.

The second experiment, created by Dr. Chia Soo of the UCLA School of Medicine, will test a new drug designed to not only block loss of bone but also to rebuild it.

The mice will ride in a NASA habitat designed for spaceflight to the ISS. Once on board, some mice will undergo injections with the new drug while others will be given a placebo. At the end of the experiments half of the mice will be returned to Earth in SpaceXs Dragon spacecraft and transported to UCLA for further study, said Stodieck, a scientific co-investigator on the experiment.

BioServes Space Automated Byproduct Lab

In addition to the two science experiments, BioServe is launching its third SABL unit to the ISS. Two SABL units are currently onboard ISS supporting multiple research experiments, including three previous stem cell experiments conducted by BioServe in collaboration with Stanford University, the Mayo Clinic and the University of Minnesota.

The addition of the third SABL unit will expand BioServes capabilities in an era of high-volume science on board the ISS, said Countryman.

BioServe researchers and students have flown hardware and experiments on missions aboard NASA space shuttles, the ISS and on Russian and Japanese government cargo rockets. BioServe previously has flown payloads on commercial cargo rockets developed by both SpaceX, headquartered in Hawthorne, California, and Orbital ATK, Inc. headquartered in Dulles, Virginia.

Since it was founded by NASA in 1987, BioServe has partnered with more than 100 companies and performed dozens of NASA-sponsored investigations. Itspartners include large and small pharmaceutical and biotechnology companies, universities and NASA-funded researchers, and investigations sponsored by the Center for the Advancement of Science in Space, which manages the ISS U.S. National Laboratory. CU-Boulder students are involved in all aspects of BioServe research efforts, said Stodieck.

Original post:
SpaceX to launch heart, bone health experiments to space station Thursday - CU Boulder Today

Recommendation and review posted by simmons

One of the experiments involves cardiovascular stem cells, investigating how gravity affects stem cells.

Jaime Berg, KUSA 4:47 PM. MDT May 31, 2017

Source: University of Colorado

KUSA - A SpaceX rocket is scheduled to launch Thursday -- and on board will be two payloads built by researchers at the University of Colorado in Boulder. The payloads include studies that could be life-changing for people on earth.

One of the experiments involves cardiovascular stem cells. The work is with some researchers in California.

Theyre investigating how gravity affects stem cells, including physical and molecular changes. The information, could help lead to stem cell therapies to repair damaged cardiac tissue.

One of the experiments has to do with rodents.

Mice are actually being sent to the international space station, in a NASA habitat, designed for spaceflight.

The mice will be going through a series of experiments to study bone loss in space.

The experiments will be sent in shoebox sized habitats.

Both undergrad and graduate students at CU are involved in the research efforts.

2017 KUSA-TV

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SpaceX rocket will be carrying CU experiments - 9NEWS.com

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Two separate research teams have succeeded in generating blood stem cells using completely different procedures. One team was led by stem cell biologist Dr. George Q. Daley of Harvard Medical School and Boston Childrens Hospital. The other team was spearheaded by Dr. Shahin Rafii of the Weill Cornell Medicines Ansary Stem Cell Institute in New York.

In both cases, reprogrammed blood stem cells were able to successfully produce blood cells when implanted into mice. And if either or both procedures turn out to be viable for humans, a future where blood donors will no longer be needed may soon be in the horizon because science has provided us with a way to produce unlimited blood supply.

Stem cells are specially programmed cells that are responsible for creating all of the bodys other cells. There are two types of stem cells embryonic and adult. Embryonic stem cells are located you guessed it in the embryo where they stay before they start to specialise. Adult stem cells are the ones used to repair and replace worn out or old cells.

Those are the natural types. Theres another type, though. Theyre called induced pluripotent stem cells (iPS cells for short). Unlike the first two types, iPS cells arent naturally present. Theyre actually adult stem cells that were converted back to their primitive state, which means they can be coaxed to turn into any type of cell.

Dr. Daley and his team chose to use both embryonic stem cells and iPS cells for their research. Using a combination of proteins, they coaxed the cells to turn into hemogenic endothelium a kind of embryonic tissue that eventually turns into blood stem cells. Next, they tested several transcription factors genes that tell other genes what to do until they came up with the combination (specifically: ERG, HOXA5, HOXA9, HOXA10, LCOR, RUNX1, and SPI1) that pushed the hemogenic endothelium into a blood-forming or blood stem cell state. They then injected those modified cells into the bone marrow of their mice subjects. After several weeks, portions of the mices blood and bone marrow developed different types of blood cells, including red blood cells, white blood cells, and even immune cells.

As Daley described the feat: Were tantalizingly close to generating bona fide human blood stem cells in a dish.

On the other hand, Rafii and his team chose a different route. They didnt make use of iPS cells. Instead, they created true blood stem cells, starting off by extracting stem cells from the blood vessel lining of mature mice. Next, they inserted transcription factors (Fosb, Gfi1, Runx1, and Spi1) into the genomes of the extracted cells, then kept these cells in Petri dishes designed to replicate the environment within human blood vessels.

Over time, the cells turned into blood stem cells and multiplied. They then injected those stem cells into mice treated with radiation (which meant most of their blood and immune cells were gone). The stem cells regenerated not just the blood, but the immune cells too. Consequently, the mice recovered and went on to live for over 1.5 years in the lab.

As described by Rafii, the procedure they used is similar to a direct aeroplane flight, while Daleys is like a flight that took a detour prior to reaching its ultimate destination. Doing away with the iPS part kind of makes Rafiis method slightly better than Daleys because it minimizes the threat of tumors forming or the body rejecting the stem cells, which is a typical reaction that iPS cells might cause. But if Daleys team is able to refine their process to eliminate this risk, then that will level the playing field, so to speak.

Whatever happens from here on, both procedures are nonetheless considered significant breakthroughs. And even though its not yet certain which method will turn out to be the better one for humans, whats clear is that both methods have the potential to be game-changers when it comes to any kind of treatment involving blood infusion and transfusion.

Both studies have been published in the journal Nature, with Daleys under the title Haematopoietic stem and progenitor cells from human pluripotent stem cells and Rafiis under the title Conversion of adult endothelium to immunocompetent haematopoietic stem cells.

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Scientists Close to Generating Unlimited Blood Supply from Stem Cells - Wall Street Pit

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The Hindu

Unrelated donor transplants to aid thalassemics The Hindu Transplantation of a special kind of stem cells found in the bone marrow has been the only curative option for patients with thalassemia major (genetic inability to produce normal, adult haemoglobin leading to severe anaemia). Since only 30-35% of such ...

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Unrelated donor transplants to aid thalassemics - The Hindu

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Physicist Stephen Hawking is perhaps the most famous sufferer of motor neuron disease, a crippling degenerative condition that affects an estimated 150,00 people around the world.

Karwai Tang / Getty

In news that may bring hope to Stephen Hawking and hundreds of thousands of others around the world, British scientists have used reprogrammed skin cells to study the development of motor neuron disease.

Its like changing the postcode of a house without actually moving it, explains neuroscientist Rickie Patani, referring to research offering startling new insights into the progress and treatment of the crippling degenerative condition, also known as amyotrophic lateral sclerosis (ALS).

Patani, together with colleague Sonia Gandhi, both from the Francis Crick Institute and University College London, in the UK, led a team of researchers investigating how the disease destroys the nerve cells that govern muscle movement.

The results, published in the journal Cell Reports, comprise the most fine-grained work to date on how ALS operates on a molecular level and suggest powerful new treatment methods based on stem cells.

Indeed, so exciting are the implications of the research that Ghandi and Patani are already working with pharmaceutical companies to develop their discoveries.

The neurologists uncovered two key interlinked interactions in the development of motor neuron disease, the first concerning a particular protein, and the second concerning an auxiliary nerve cell type called astrocytes.

To make their findings, the team developed stem cells from the skin of healthy volunteers and a cohort carrying a genetic mutation that leads to ALS. The stem cells were then guided into becoming motor neurons and astrocytes.

We manipulated the cells using insights from developmental biology, so that they closely resembled a specific part of the spinal cord from which motor neurons arise, says Patani.

We were able to create pure, high-quality samples of motor neurons and astrocytes which accurately represent the cells affected in patients with ALS."

The scientists then closely monitored the two sets of cells healthy and mutated to see how their functioning differed over time.

The first thing they noted was that a particular protein TDP-43 behaved differently. In the patient-derived samples TDP-43 leaked out of the cell nucleus, catalysing a damaging chain of events inside the cell and causing it to die.

The observation provided a powerful insight into the molecular mechanics of motor neuron disease.

Knowing when things go wrong inside a cell, and in what sequence, is a useful approach to define the critical molecular event in disease, says Ghandi.

One therapeutic approach to stop sick motor neurons from dying could be to prevent proteins like TDP-43 from leaving the nucleus, or try to move them back.

The second critical insight was derived from the behaviour of astrocytes, which turned out to function as a kind of nursemaid, supporting motor neuron cells when they began to lose function because of protein leakage.

During the progression of motor neuron disease, however, the astrocytes like nurses during an Ebola outbreak eventually fell ill themselves and died, hastening the death of the neurons.

To test this, the team did a type of mix and match exercise, concocting various combinations of neurons and astrocytes from healthy and diseased tissue.

They discovered that healthy astrocytes could prolong the functional life of ALS-affected motor neurons, but damaged astrocytes struggled to keep even healthy motor neurons functioning.

The research reveals both TDP-43 and astrocytes as key therapeutic targets, raising the possibility that the progress of ALS might be significantly slowed, or perhaps even halted.

Our work, along with other studies of ageing and neurodegeneration, would suggest that the cross-talk between neurons and their supporting cells is crucial in the development and progression of ALS, says Patani.

Read more here:
Patients' stem cells point to potential treatments for motor | Cosmos - Cosmos

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Stem Cell Research is an amazing field right now, and promises to be a powerful and potent tool to help us live longer and healthier lives. Just last month, for example, Stem Cell Therapy was used to restore sight in patients with severe retinal deterioration, allowing them to see clearer than they had in years, or even decades.

Now, there is another form of Stem Cell Treatment on the horizonthis one of a very different form. Stem Cells have now been used as a mechanism to deliver medical treatment designed to eliminate cancer cells, even in hard to reach places. One issue with current cancer treatments is that, treatments that are effective at treating tumors on the surface of the brain cannot be performed safely when the tumor is deeper within the brains tissues.

Stem Cells have the fantastic ability to transform into any other kind of cell within the human body, given the appropriate stimulation. As of today, most of these cells come from Embryonic Lines, but researchers are learning how to backwards engineer cells in the human body, reverting them back to their embryonic state. These cells are known as Induced Pluripotent Stem Cells.

How Does This Stem Cell Cancer Treatment Work?

Using genetic engineering, it is possible to create stem cells that are designed to release a chemical known as Pseudomonas Exotoxin, which has the ability to destroy certain tumor cells in the human brain.

What is Pseudomonas Exotoxin?

Pseudomonas Exotoxin is a compound that is naturally released by a form of bacteria known as Pseudomonas Aeruginosa. This chemical is toxic to brain tumor cells because it prevents polypeptides from growing longer, essentially preventing the polypeptides from growing and reproducing. When used in a specific manner, this toxin has the ability to destroy cancerous and malignant tissue without negatively impacting healthy tissue. In addition to its potential as a cancer treatment, there is also evidence that the therapy could be used for the treatment of Hepatitis B.

PE and Similar Toxins Have been Used Therapeutically in the Past

As of now, this chemical, which we will refer to for the rest of the article as PE, has been used as a cancer treatment before, but there are major limitations regarding the use of PE for particular cancers, not because of the risks of the treatment, but because of the lack of an effective method to deliver the medication to where it is needed.

For example, similar chemicals have been highly effective in the treatment of a large number of blood cancers, but havent been nearly as effective in larger, more inaccessible tumors. The chemicals break down or become metabolized before they can fully do their job.

How do Stem Cells Increase the Effectiveness of PE Cancer Treatment

Right now, PE has to be created in a laboratory before it is administered, which is not very effective for these embedded cancers. By using Stem Cells as an intermediary, it is possible to deliver the medication to deeper areas of the brain more effectively, theoretically highly increasing the efficacy of the treatment.

The leader of this Stem Cell Research is Harvard researcher Dr. Khalis Shah. His goal was to find an effective means to treat these deep brain tumors which are not easily treated by methods available today. In utilizing Stem Cells, Dr. Shah has potentially found a means by which the stem cells can constantly deliver this Cancer Toxin to the tumor area. The cells remain active and are fed by the body, which allows them to provide a steady stream of treatment that is impossible to provide via any other known method.

This research is still in its early stages, and has not yet reached human trials, but in mice, the PE Toxin worked exactly as hypothesized and was able to starve out tumors by preventing them from replicating effectively.

Perhaps this might seem a bit less complicated than it actually is. One of the major hurdles that had to be overcome was that this Toxin would normally be strong enough to kill the cell that hosted it. In order for the Stem Cells to release the cancer, they had to be able to withstand the effects of PE, themselves. Using genetic engineering, Dr. Shah and his associates were able to create a cell that is capable of both producing and withstanding the effects of the toxin.

Stem Cell delivered medical therapy is a 21st century form of medical treatment that researchers are just beginning to learn how to effectively utilize. Essentially, this treatment takes a stem cell and converts it into a unique symbiotic tool capable of feeding off of the host for energy in order to perform a potentially life-saving function. Its really quite fascinating.

How Does PE Not Damage or Kill Brain Cells Indiscriminately?

You might be concerned about the idea of a patient having a toxin injected into the brain to cure a disease. It sounds almost like a dangerous, tribal, homeopathic remedy. In reality, the researchers have been able to harness the destructive power of the toxin and re-engineer it so that it directly targets cancer cells while having limited negative effects on healthy, non-cancerous tissue.

The toxin does its damage after it has been absorbed by a cell. By retooling the toxin so that it does not readily absorb into healthy cells, the dangers associated with having such a potentially dangerous toxin in the brain are seriously and significantly mitigated.

Beyond that, Dr. Shah and his associates have been able to take steps to effectively turn off PE while it is inside the host stem cell, and only activates when it has entered the cancerous tissue. Dr. Shah explains that, although this research has only been conducted in animal subjects, there is no known reason why the effectiveness and safety of the treatment would not be applicable to human patients.

In this treatment, surgeons remove as much of the tumor as possible from the brain, and insert the engineered Stem Cells submerged in a sterile gel in the area where the tumor was removed or partially still exists. Researchers found that, when they used this treatment on laboratory rats, they could tell through imaging and analysis that the modified PE toxin effectively killed the cancer cells, and that this cancer treatment effectively lengthened the life of the rat, as compared to control subjects.

Whats the Next Step?

Of course, cancer treatment is far more complex than a single treatment, no matter how effective that treatment may be. Because human cancer treatment is a comprehensive therapy approach, the end goal of this research is to create a form of therapy in which the method used in animal subjects is combined with other existing approaches, increasing and maximizing the effectiveness of the comprehensive treatment.

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A recent change in how well we understand stem cells may make it easier for scientists and researchers to gather stem cells for use in scientific research as well as medical application. A new study was released in the research publication, Cell, which was performed by representatives from the University of California San Francisco.

One of the issues which hinder the use of stem cells as a more widespread treatment or field of research is that researchers and patients have a bottleneck of available healthy stem cell lines which can be used for research. Researchers hope that this new discovery will allow future scientific discoveries and applications in the areas of creating new and healthy tissue for patients with kidney failure or any other form of organ tissue failure. The future of medical therapy lies with Stem Cell Research, but many other forms of treatment, including Hormone Replacement Therapy, are already in practice today.

Researchers have discovered that it is possible to essentially flip a switch in an adult cell, reverting it back to the preliminary state at which cells existed in one of the earliest stages of developmentthe embryonic stem cell. Medical researchers hypothesize that Stem Cell treatments could be used for a variety of medical health issues which plague the world today, including kidney failure, liver disease, and Type-1 and Type-2 Diabetes.

Use of Embryonic Stem Cells Contentious

There is an ethical issue in Stem Cell Research today. Many Pro-Life Advocates are vociferously against the use of Embryonic Stem Cells harvested from procedures such as fertility treatments designed for conception. They believe that the use of embryonic stem cells harvested from donors and couples looking to conceive is unethical.

Using current research, it may be possible to bypass this ethical quandary completely by using adult cells and converting them into embryonic stem cells. Furthermore, because these stem cells are genetic derivatives of the patient from which the adult cells were harvested, this potentially paves the way for patient-specific medical treatments using stem cells.

After adult cells have been converted back into Embryonic Stem Cells, it will be possible to convert them into any possible cell that the patient needs or would benefit from.

Hijacking the Blueprint of the Cell Allows Scientists to Revert Adult Cells to their Earliest State

Researchers have increased the capacity to produce Embryonic Stem Cells by identifying previously unrecognized biochemical processes which tell human cells how to develop. In essence, researchers have discovered how the body blueprints cells, and can change the blueprints so that a new cell is made.

By utilizing these newly recognized pathways, it is possible to create new stem cells more quickly than ever before. One of the researchers explains the implications of this research. Dr. Miguel Ramalho-Santos is an associate professor of obstetrics, medicine, and cancer research at the University of California San Francisco. Dr. Ramalho-Santos is also a member of the Broad Center of Regenerative Medicine and Stem Cell Research.

He explains that these stem cell discoveries have the ability to alter the way that the medical sciences can take advantage of stem cells with regard to both cancer research and regenerative medicine. Dr. Ramalho-Santos was the lead researcher for this study, and the research was largely funded by the Director of the National Institutes of Health New Innovator Award, granted to promising young researchers which are leading highly innovative and promising medical research studies.

Dr. Ramalho-Santos research builds off of earlier research which discovered that it was possible to take adult cells and turn them back into embryonic stem cells. These stem cells dont have any inherent aging processes, and they can be turned into any other kind of tissue. In the process of this conversion, the adult cells lose all of their unique characteristics, leaving them in an ultimately immature and malleable state.

This earlier research was conducted by researchers from UC San Francisco in partnership with Dr. Shinya Yamanaka from Kyoto University and Gladstone Institutes. These entities all gained a piece of the Nobel Prize in Physiology or Medicine from their part in the study.

Pluripotent Stem Cells vs. Embryonic Stem Cells

Thus far, weve described these cells as Embryonic Stem Cells, but in fact, the more accurate term for these cells are Induced Pluripotent Stem Cells (IPS). These cells are biologically and functionally similar to Embryonic Stem Cells, but have a different name because they are sourced from adult cells. The difference between Induced Pluripotent Stem Cells and Embryonic Stem Cells is that Induced Pluripotent Stem Cells do seem to retain some of the characteristics of their previous state, which appears to limit their ability to convert into any other type of cell. This new research identifies new pathways by which it may be possible to increase the number of cells that an individual IPS Cell can turn into, perhaps allowing them to convert into any other kind of human cell.

Induced Pluripotent Stem Cells are not explicitly considered an alternative to Embryonic Stem Cells, but are considered a different approach to produce similar cells. If researchers fully uncover the mechanisms of how to reprogram these cells, it will lower many barriers to stem cell research and the availability of stem cell treatments.

As of today, researchers have figured out how to make these Induced Pluripotent Stem Cells, but the percentage of adult cells which are reverted successfully is quite low, and frequently, these cells still show some aspects of specialization, which limits their use.

How Do Scientists Make Stem Cells From Adult Cells?

There are genes within every cell which have the ability to induce pluripotency, reverting the cell to an earlier stage of specialization. The initial stage of this process is the result of activating Yamanaka Factors, specific genes that initiate this reversion process.

As of today, this process of de-maturation is not completely understood, and researchers realized from the start that the cells they created were not truly identical to Embryonic Stem Cells, because they still showed signs of their former lives, which often prevented them from being successfully reprogrammed.

The new research conducted by Dr. Ramalho-Santos appears to increase our knowledge regarding how these cells work, and how to program them more effectively. Dr. Ramalho-Santos and his team discovered more genes associated with these programming/reprogramming processes, and by manipulating them, they have increased the viability and range of particular stem cells.

It appears that these genetic impulses are constantly at play to maintain the structure and function of a cell, and that by systematically removing these safeguards, it is possible to increase the ability to alter these cells.

This research increases researchers ability to produce these stem cells, by increasing the ability of medical scientists to produce adequate numbers of stem cells, while also increasing the range of potential treatment options by more effectively inducing the total pluripotency which is available in Embryonic Stem Cells. This research may also help scientists treat certain forms of cancer which are the result of malfunctions of these genes.

Dr. Patrick W. Thomas Published 7:00 p.m. ET May 30, 2017 | Updated 9 hours ago

Dr. Patrick W. Thomas, chief of cardiology at New York-Presbyterian Hudson Valley Hospital, supports state legislation to raise the age for tobacco sales to 21. Dr. Thomas is also president of the Board of Directors for the Putnam County Division of the American Heart Association. Video by Nancy Cutler/lohud Wochit

Those who seek support to stop smoking are more likely to succeed.(Photo: AndreyPopov, Getty Images/iStockphoto)

I see it in my cardiology practice each day the deadly effects of smoking: The obvious health implications, the attempts to quitand the resignation that comes when those quitting attempts fail. Tobacco addiction causes heart disease, damage to arteries throughout the body, chronic and debilitating breathing issues, stroke, aneurysms, cancer. The list goes on.

I prescribe medications (such as nicotine replacement therapies) and offer information for group or individual counseling. Most patients who smoke want to quit but the addiction is just too strong.

As a health-care provider, it is my job to speak out to break the cycle of tobacco addiction, and thats exactly what legislation thats been proposed to raise the age of sale for tobacco products in New York would do and our lawmakers have just a few weeks to move on it.

WESTCHESTER: County mulls age change for tobacco sales

TOMPKINS COUNTY: Legislators raise tobacco age to 21

Sponsored in the Senate by Sen. Diane Savino (S03978) and in the Assembly by Assemblywoman Linda Rosenthal (A0273), the legislation will raise the legal sale age for tobacco products from 18 to 21 statewide.

I know that not one of my patients who smokes would say he or she is glad to have started smoking. Some admit they wont live their lives without it, and some have paid a high price for their addiction but its too hard for them to quit.

And any of those smokers, most of whom started when they were young, would say they dont want to see future generations become addicted to deadly tobacco. Not their kids, grandkids or neighbors. We know that 95 percent of smokers started before age 21. Young people are warned of the reality of tobaccos addiction, but thats not enough we need to do all that is possible to keep these deadly products away from our children.

New York state lawmakers are considering an increase in the age to legally buy tobacco products from age 18 to 21. Joseph Spector, Albany Bureau

The Tobacco 21 bill, as it is known, will not totally prevent smoking. It will not help those who already have started smoking their addiction is likely already too strong. But it can help prevent others from starting. It is another tool for helping keep tobacco out of the hands of high school kids.

Kids tell us that its easy to get tobacco from older kids. Preventing the flow of products from older kids to younger kids is critical. Not many 21-year-olds are still in high school social circles, but plenty of 18- and 19-year-olds are and they supply the cigarettes, chew, and other products to those younger than them.

And the tobacco industry knows it. Theyve been on the record for years saying that laws such as this would gut their next generation of smokers.

As doctors, parents, lawmakers, isnt that exactly what we should be doing? Doing everything we can to prevent unnecessary deaths and illness caused by tobacco?

I commend the work thats been done across all corners of our state to drive this sort of regulation on the local level. From Tompkins County to New York City, and in nearby Orange and Sullivan counties, local leaders have taken this issue head on and have seen widespread support. In fact, to date, more than 55 percent of New Yorkers already livein an area covered by Tobacco 21 legislation. Its a good start, but a mishmash of town and county laws wont get the job done. We need statewide action on this public health crisis.

I urge the New York State Legislature to work to pass Tobacco 21 legislation this session.

The writer is chief of cardiology at New York-Presbyterian Hudson Valley Hospital and president of the Board of Directors for the Putnam County Division of the American Heart Association.

Dr. Patrick W. Thomas(Photo: SUBMITTED/Howard Copeland of Scotts Camera in Peekskill)

Read or Share this story: http://www.lohud.com/story/opinion/contributors/2017/05/30/cardiologist-tobacco-sales-21/354055001/

Original post: Take it from a cardiologist: Tobacco sales should be restricted to 21 and over The Journal News | LoHud.com

TAIPEI, Taiwan, May 30, 2017 /PRNewswire/ TaiGen Biotechnology Company, Limited (TaiGen) today announced that it has submitted a New Drug Application (NDA) for the intravenous formulation of Taigexyn (Nemonoxacin) to the China Food and Drug Administration (CFDA). Taigexyn is a novel non-fluorinated quinolone antibiotic.The NDA submission is supported by a pivotal Phase 3 trial comparing intravenous formulations of Taigexyn 500 mg to levofloxacin 500 mg in 518 patients with moderate to severe community-acquired pneumonia. The clinical success rates were 91.8% for Taigexyn vs. 85.7% for levofloxacin and Taigexyn was shown to be non-inferior to levofloxacin meeting the primary endpoint of the pivotal trial.

About Taigexyn Taigexyn is a novel broad spectrum antibiotic with excellent efficacy against drug-resistant bacteria available in both oral and intravenous formulations. The oral formulation is already approved for marketing and launched in Taiwan and mainland China. In addition, Taigexyn is also partnered in Russia, Commonwealth Independent States, Turkey, Mexico, Brazil and the Latin American territory for a total 32 countries worldwide.

Link: TaiGen Biotechnology Announces Submission of New Drug Application for Taigexyn Intravenous Formulation to the PR Newswire (press release)

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UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

WASHINGTON, DC 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section13 or 15(d)

of the Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): May30, 2017 (May 24, 2017)

PUMA BIOTECHNOLOGY, INC.

(Exact Name of Registrant as Specified in its Charter)

10880 Wilshire Boulevard, Suite 2150

Los Angeles, California 90024

(Address of principal executive offices) (Zip Code)

(424) 248-6500

(Registrants telephone number, including area code)

N/A

(Former name or former address, if changed since last report)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (240.12b-2 of this chapter).

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.

On May24, 2017, Puma Biotechnology, Inc. (the Company) announced that the U.S. Food and Drug Administrations (FDA) Oncologic Drugs Advisory Committee (ODAC) voted 12 to 4 to recommend approval of PB272 (neratinib) for the extended adjuvant treatment of HER2-positive early stage breast cancer based on finding that the risk-benefit profile of neratinib is favorable. Neratinib is an investigational therapy for the extended adjuvant treatment of early stage HER2-positive breast cancer that has previously been treated with a trastuzumab containing regimen.

ODAC is an independent panel of experts that evaluates data concerning the efficacy and safety of marketed and investigational products for use in the treatment of cancer and makes appropriate recommendations to the FDA. Although the FDA will consider the recommendation of the panel, the final decision regarding the approval of the product is made by the FDA solely, and the recommendations by the panel are non-binding.

SIGNATURE

See original here:
IPS Cell Therapy - Page 5423 IPS Cell Therapy

Recommendation and review posted by simmons

Laboratory mice are among the first animals to have their diseases treated by CRISPR.

A new research paper is stirring up controversy among scientists interested in using DNA editing to treat disease.

In a two-page article published in the journal Nature Methods on May 30, a group of six scientists report an alarming number of so-called off-target mutations in mice that underwent an experimental gene repair therapy.

CRISPR, the hot new gene-editing technique thats taken biology by storm, is no stranger to headlines. What is unusual, however, is a scientific article so clearly describing a potentially fatal shortcoming of this promising technology.

The research community is digesting this news with many experts suggesting flaws with the experiment, not the revolutionary technique.

The research team sought to repair a genetic mutation known to cause a form of blindness in mice. This could be accomplished, they showed, by changing just one DNA letter in the mouse genome.

They were able to successfully correct the targeted mutation in each of the two mice they treated. But they also observed an alarming number of additional DNA changes more than 1,600 per mouse in areas of the genome they did not intend to modify.

The authors attribute these unintended mutations to the experimental CRISPR-based gene editing therapy they used.

A central promise of CRISPR-based gene editing is its ability to pinpoint particular genes. But if this technology produces dangerous side effects by creating unexpected and unwanted mutations across the genome, that could hamper or even derail many of its applications.

Several previous research articles have reported off-target effects of CRISPR, but far fewer than this group found.

The publicly traded biotech companies seeking to commercialize CRISPR-based gene therapies Editas Medicine, Intellia Therapeutics and Crispr Therapeutics all took immediate stock market hits based on the news.

Experts in the field quickly responded.

Either the enzyme is acting at near optimal efficiency or something fishy is going on here, tweeted Matthew Taliaferro, a postdoctoral fellow at MIT who studies gene expression and genetic disease.

The Cas9 enzyme in the CRISPR system is what actually cuts DNA, leading to genetic changes. Unusually high levels of enzyme activity could account for the observed off-target mutations more cutting equals more chances for the cell to mutate its DNA. Different labs use slightly different methods to try to ensure the right amount of cuts happen only where intended.

Unusual methods were used, tweeted Lluis Montoliu, who runs a lab at the Spanish National Centre for Biotechnology that specializes in editing mice genes using CRISPR. He believes the authors used suboptimal molecular components in their injected CRISPR therapies specifically a plasmid that causes cells to produce too much Cas9 enzyme likely leading to the off-target effects they observed.

Gatan Burgio, whose laboratory at the Australian National University is working to understand the role that cellular context plays on CRISPR efficiency, believes the papers central claim that CRISPR caused such an alarming number of off-target mutations is not substantiated.

Burgio says there could be a range of reasons for seeing so many unexpected changes in the mice, including problems with accurately detecting DNA variation, the extremely small number of mice used, random events happening after Cas9 acted or, he concedes, problems with CRISPR itself.

Burgio has been editing the DNA of mice using CRISPR since 2014 and has never seen a comparable level of off-target mutation. He says hes confident that additional research will refute these recent findings.

Although the news of this two-mouse experiment fired up the science-focused parts of the Twittersphere, the issue it raises is not new to the field.

Researchers have known for a few years now that off-target mutations are likely given certain CRISPR protocols. More precise variants of the Cas9 enzyme have been shown to improve targeting in human tissue the lab.

Researchers have also focused on developing methods to more efficiently locate off-target mutations in the animals they study.

As scientists continue to hone the gene-editing technique, we recognize theres still a way to go before CRISPR will be ready for safe and effective gene therapy in humans.

See more here:

CRISPR controversy raises questions about gene-editing technique - The Conversation US

Recommendation and review posted by sam

Jennifer A. Doudna & Samuel H. Sternberg Houghton Mifflin: 2017. ISBN: 9780544716940

Buy this book: US UK Japan

Graeme Mitchell/Redux/Eyevine

Jennifer Doudna helped to uncover the CRISPRCas gene-editing system.

The prospect of a memoir from Jennifer Doudna, a key player in the CRISPR story, quickens the pulse. And A Crack in Creation does indeed deliver a welcome perspective on the revolutionary genome-editing technique that puts the power of evolution into human hands, with many anecdotes and details that only those close to her may have known. Yet it does not provide the probing introspection, the nuanced ethical analysis, the moral counterpoint that we CRISPR junkies crave.

After the race for discovery comes the battle for control of the discovery narrative. The stakes for the CRISPRCas system are extraordinarily high. In February, the US Patent and Trademark Office ruled against Doudna and the University of California, Berkeley. It found that a patent on the application of CRISPR to eukaryotic cells filed by Feng Zhang of the Broad Institute of MIT and Harvard in Cambridge, Massachusetts did not interfere with Berkeley's more sweeping patent on genetic engineering with CRISPR.

Although that battle is over, the war rages on. Berkeley has already appealed against the decision; meanwhile, the European Patent Office has ruled in favour of Doudna and Berkeley. Doubtless there are many more patents to milk out of this versatile system. And then there's the fistful of 66-millimetre gold medals they give out in Stockholm each year.

So far, the Broad Institute has controlled the CRISPR narrative. Rich in funds and talent, the Broad melds sleek, high-tech sexiness with a sense of East Coast, old-money privilege. Last year, institute director Eric Lander published a now-infamous piece entitled 'The heroes of CRISPR' (E.Lander Cell 164, 1828; 2016). It adopted a tone of magnanimity, crediting Lithuanian biochemist Virginijus Siksnys with observing early on that his findings pave the way for engineering of universal programmable RNA-guided DNA endonucleases, and Doudna and her CRISPR co-discoverer Emmanuelle Charpentier with noting the potential to exploit the system for RNA-programmable genome editing.

Lander's clear implication was that they were laying the groundwork; Zhang's group got CRISPR over the finish line. To many of us, such tactics made Team Broad look like the villains of CRISPR.

Doudna's book was a chance to deliver a righteous knockout blow. Instead, we get a counter-narrative just as constructed as Lander's article. It is written entirely in the first person; co-author Samuel Sternberg, a former student in the Doudna lab, barely surfaces.

In that counter-narrative, Doudna had always been interested in gene editing. Her early work was on RNA enzymes, or ribozymes. She developed an impeccable pedigree, doing her PhD with Jack Szostak at Harvard and a postdoc with Tom Cech at the University of Colorado Boulder, before joining the faculty at Yale University in New Haven, Connecticut. From the mid-1990s, she writes, she was exploring the basic molecular mechanisms that would be able to unlock the full potential of gene editing.

Her work on CRISPR dates to 2006 six years before the key papers were published and a call from Berkeley geomicrobiologist Jillian Banfield. Over coffee, Banfield described the clustered, regularly interspaced, short palindromic repeats that kept popping up in her DNA databases of bacteria and archaea. The sequences were ubiquitous among these prokaryotes, but unique to each species. This realization sent a little shiver of intrigue down my spine, Doudna writes. If CRISPR was so widespread, there was a good chance that nature was using it to do something important. By 2012, she and her co-workers had characterized the natural CRISPR system, harnessed it as a laboratory tool and developed a modified system that was programmable, cheap and easy to use.

The middle of the book reels off the obligatory breathless list of potential uses, generating everything from malaria-free mosquitoes and police dogs with muscles like Vin Diesel to the canonical cure for cancer. Thankfully, Doudna counterweights sensationalism with a sober accounting of the risks and responsibilities of applications such as altering the genomes of entire populations of organisms with 'gene drives'. In 2015, she sustained doubts about CRISPR ever being safe enough for clinical trials, but she has come to embrace editing of the human germ line inheritable DNA modification once it is proved safe.

But the discussion is ultimately unsatisfying. When it is time to grapple with tricky ethical issues, such as human experimentation, she baulks, unspooling instead a series of rhetorical questions. Rather than guiding us through the ethical thickets of precision genetic engineering, or providing a candid, warts-and-all look at one of the great scientists of our time, the book mainly polishes her 'good scientist' image and rationalizes the unfettered self-direction of human evolution, within liberal bounds of safety, efficacy and individual choice.

Rather than dispel the cartoon-character feel of this epic battle, Doudna elaborates on it. She presents us with a persona so flawless that it seems more concealing than revealing. She waves away the bloody patent fight as a disheartening twist in the story, but the entire biomedical world knows that it was much more. As I read A Crack in Creation, I was reminded of Benjamin Franklin's benevolent man, who, he wrote, should allow a few faults in himself, to keep his friends in countenance and, I would add, to give him- or herself more depth.

The narrative often substitutes melodrama for dramatic tension. A conference in Puerto Rico sees Charpentier and Doudna strolling the cobbles of Old San Juan, with Charpentier saying earnestly, I'm sure that by working together we can figure out the activity of what became the Cas enzyme. I felt a shiver of excitement as I contemplated the possibilities of this project, Doudna writes. When first wrestling with the ethical dilemmas of gene editing, she dreams of meeting Adolf Hitler, who demands to know the secrets of her technique. She wakes, of course, freshly determined to ensure that CRISPR is not put to nefarious use.

The larger purpose of A Crack in Creation, clearly, is to show that Doudna is the true hero of CRISPR. And ultimately, despite the book's flaws, I'm convinced. Nominators and the Nobel Committee will need to read this book. But CRISPR binge-watchers like me still await a truly satisfying account one that is insightful, candid and contextualized.

Link:

That's the way the CRISPR crumbles - Nature.com

Recommendation and review posted by sam

While were most enamored with CRISPRs ability to edit human genomes, the powerful tool is not selectiveit can edit other genomes as well. In one such study, researchers are using CRISPR to expand the size and weight of wheat kernels in the hope of increasing overall wheat yield.

Although humans consume more than 500 million tons of wheat per year, overall production is decreasing as farmers continue to move toward crops that are more profitable. Increasing yield is one way to ensure wheat becomes a desirable, profitable crop again. But, that takes some genetic manipulation.

Fundamentally, this can be achieved by improving wheats photosynthesis. For example, wheat uses less than 1 percent of sunlight to produce the parts we eat, compared to maizes 4 percent efficiency and sugarcanes 8 percent efficiency. Even increasing wheats photosynthetic efficiency from 1 percent to 1.5 percent would allow farmers to increase their yields on the same amount of land, using no more water, fertilizer or other inputs.

Through a new Department of Agriculture grant and working with the International Wheat Yield Partnership Program, South Dakota State Universitys Wanlong Li and Iowa States Bing Yang seek to apply CRISPR to wheats photosynthesis problem.

First, the researchers will identify the genes that control grain size and weight in bread wheat using a rice genome model. Then, they will use CRISPR to edit out each negatively regulating genewhich will serve the two-fold purpose of removing it from the genome, as well as having it available to study.

Li and Yang will create 30 constructs that target 20 negative genes. Partners from the University of California Davis Plant Transformation Facility will then produce 150 first-generation plants for the researchers to study. When all is said and done, the researchers should be able to identify which mutations yield larger seedsand thus, increased yields.

One of the benefits of this process is the end product will not be considered genetically modified organisms.

When we transfer one of the CRISPR genes to wheat, its transgenic. That then produces a mutation in a different genomic region. When the plants are then self-pollinated or backcrossed, the transgene and the mutation are separated, Li explained. This is null transgenic.

In fact, the USDA has approved this technique in other organisms, and Yang has already utilized it in unrelated research to develop bacterial blight-resistant rice.

Ultimately, these yield-increasing mutations, along with the markers to identify the traits, can be transferred to other varieties of wheat, such as durum, spring and winter wheat.

South Dakota State University is one of seven universities nationwide to receive funding to develop new wheat varieties as part of the National Institute of Food and Agricultures International Wheat Yield Partnership Program. Lis focus on CRISPR and photosynthesis efficiency is just one approach to the problem. Other research projects from the organization include: testing genes to boost spike development; optimizing canopy architecture to increase carbon capture and conserve nitrogen; and using selected genes from other species to increase biomass and yield, among others.

A distinguishing feature of the International Wheat Yield Partnership Program is its huba massive parcel of land in Mexico that is used for the evaluation of innovations, and subsequent development pipeline.

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CRISPR's Next Target: Wheat Kernels - Laboratory Equipment - Laboratory Equipment

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Xconomy Texas

San Antonio Most diabetes treatments work by giving the body the insulin it needs to break down sugar. But that approach deals with the symptoms of diabetes. In recent years, scientists and companies have taken aim at the root cause of the condition by attempting to stimulate or replace the cells in the pancreas responsible for producing insulin in the first place. One of them is a San Antonio researcher hoping to use gene therapya potentially one-time, long lasting treatmentto do the trick.

When cells in the pancreas, known as beta cells, either get destroyed by the immune system or stop producing enough insulin, the result is type 1 or type 2 diabetes. Companies large and small-from European diabetes drug giant Novo Nordisk to privately held startups ViaCyte, of San Diego, and Semma Therapeutics, of Cambridge, MAwant to engineer stem cells that develop into pancreatic beta cells to help a patient produce insulin.

Other researchers, such as Bruno Doiron, a scientist and assistant professor at the University of Texas Health Science Center at San Antonio, have different ideas. Doiron has developed an injectible treatment consisting of three molecules glucokinase, a second that targets a protein known as PTP1B, and a third that targets a protein called Pdx-1, a so-called transcription factor that regulates genesthat, when infused into the body, are meant to help stimulate the formation of new beta cells. Doiron has tried the method on mice, and based on some encouraging early results, intends to move the work forward through a startup company.

You have to prove you can translate that to a large animal model, he says.

The San Antonio company, Syner-III, got its name because of the synergistic use of three molecules to generate the beta cells, he says. Those molecules are administered via a gene therapy procedure: theyre stuffed into a modified virus and injected directly into the pancreas in a one-time treatment, where they are meant to stimulate beta cell production. The work was published in the peer-reviewed journal Current Pharmaceutical Biotechnology in 2016.

Doiron hopes to raise as much as $10 million to complete preclinical testing.

Others, including Novartis, are considering different ways of boosting beta cell production. Researchers from the Swiss company published findings in Nature Communications that showed a group of compounds called aminopyrazines could be packed into a pill and similarly lead to more beta cells, and more insulin, in mice. Such attempts are fraught with failure, however. In an article on its own website, Novartis notes that researchers have succeeded in producing beta cells in mice many times, but havent been able to reproduce those results in humans.

The potential payoff, however, is huge. Some 29.1 million Americans have diabetes, and 1.25 million of them have type 1 diabetes, according to the American Diabetes Association. Doiron believes the therapy may be able to help both types. While stem cell research has had its share of failures and competition continues to increase in insulin therapysuch as pumps that automatically deliver the treatmentDoiron says a gene therapy, if successful, could result in a longer-lasting, more effective treatment.

When I use your own body to produce medicine, that drastically changes the field, he says.

David Holley is Xconomy's national correspondent based in Austin, TX. You can reach him at dholley@xconomy.com

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(THE CONVERSATION) A new research paper is stirring up controversy among scientists interested in using DNA editing to treat disease.

In a two-page article published in the journal Nature Methods on May 30, a group of six scientists report an alarming number of so-called off-target mutations in mice that underwent an experimental gene repair therapy.

CRISPR, the hot new gene-editing technique thats taken biology by storm, is no stranger to headlines. What is unusual, however, is a scientific article so clearly describing a potentially fatal shortcoming of this promising technology.

The research community is digesting this news with many experts suggesting flaws with the experiment, not the revolutionary technique.

The research team sought to repair a genetic mutation known to cause a form of blindness in mice. This could be accomplished, they showed, by changing just one DNA letter in the mouse genome.

They were able to successfully correct the targeted mutation in each of the two mice they treated. But they also observed an alarming number of additional DNA changes more than 1,600 per mouse in areas of the genome they did not intend to modify.

The authors attribute these unintended mutations to the experimental CRISPR-based gene editing therapy they used.

A central promise of CRISPR-based gene editing is its ability to pinpoint particular genes. But if this technology produces dangerous side effects by creating unexpected and unwanted mutations across the genome, that could hamper or even derail many of its applications.

Several previous research articles have reported off-target effects of CRISPR, but far fewer than this group found.

The publicly traded biotech companies seeking to commercialize CRISPR-based gene therapies Editas Medicine, Intellia Therapeutics and Crispr Therapeutics all took immediate stock market hits based on the news.

Experts in the field quickly responded.

Either the enzyme is acting at near optimal efficiency or something fishy is going on here, tweeted Matthew Taliaferro, a postdoctoral fellow at MIT who studies gene expression and genetic disease.

The Cas9 enzyme in the CRISPR system is what actually cuts DNA, leading to genetic changes. Unusually high levels of enzyme activity could account for the observed off-target mutations more cutting equals more chances for the cell to mutate its DNA. Different labs use slightly different methods to try to ensure the right amount of cuts happen only where intended.

Unusual methods were used, tweeted Lluis Montoliu, who runs a lab at the Spanish National Centre for Biotechnology that specializes in editing mice genes using CRISPR. He believes the authors used suboptimal molecular components in their injected CRISPR therapies specifically a plasmid that causes cells to produce too much Cas9 enzyme likely leading to the off-target effects they observed.

Gatan Burgio, whose laboratory at the Australian National University is working to understand the role that cellular context plays on CRISPR efficiency, believes the papers central claim that CRISPR caused such an alarming number of off-target mutations is not substantiated.

Burgio says there could be a range of reasons for seeing so many unexpected changes in the mice, including problems with accurately detecting DNA variation, the extremely small number of mice used, random events happening after Cas9 acted or, he concedes, problems with CRISPR itself.

Burgio has been editing the DNA of mice using CRISPR since 2014 and has never seen a comparable level of off-target mutation. He says hes confident that additional research will refute these recent findings.

Although the news of this two-mouse experiment fired up the science-focused parts of the Twittersphere, the issue it raises is not new to the field.

Researchers have known for a few years now that off-target mutations are likely given certain CRISPR protocols. More precise variants of the Cas9 enzyme have been shown to improve targeting in human tissue the lab.

Researchers have also focused on developing methods to more efficiently locate off-target mutations in the animals they study.

As scientists continue to hone the gene-editing technique, we recognize theres still a way to go before CRISPR will be ready for safe and effective gene therapy in humans.

This article was originally published on The Conversation. Read the original article here: http://theconversation.com/crispr-controversy-raises-questions-about-gene-editing-technique-78638.

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CRISPR controversy raises questions about gene-editing technique - San Francisco Chronicle

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Researchers are working to determine why the aortic valve doesnt form correctly in patients with the most common congenital heart defect: bicuspid aortic valve.

In a new Nature Communications study, the Michigan Medicine-led group found two genetic variants associated with the condition.

Bicuspid aortic valve is moderately heritable, yet experts are still figuring out which part of our DNA code explains why some BAV patients inherit the disease.

Weve completed the first successful genomewide study of bicuspid aortic valve, by studying subjects at U-Ms Frankel Cardiovascular Center, says first author Bo Yang, M.D., Ph.D., a Michigan Medicine cardiac surgeon. We are using state-of-the-art technology of induced stem cell and gene editing to dissect the genomic region we found to be associated with BAV. Its a great collaboration that will accelerate our scientific understanding of this disease.

BAV patients have aortic valves with only two leaflets, rather than three, limiting the valves function as the heart pumps oxygen-rich blood toward the aorta to enrich the body. The condition is associated with various complications, including a narrowed valve (aortic stenosis), a leaky valve (aortic insufficiency or regurgitation), an infection of the valve or an aortic aneurysm.

"This finding gives us a great head start toward understanding the mechanism of how a genetic change outside the protein-coding part of the genome can lead to disease."Cristen Willer, Ph.D.

A great head start

The researchers performed genomewide association scans of 466 BAV cases from the Frankel Cardiovascular Center and 4,660 controls from the Michigan Genomics Initiative, with replication on 1,326 cases and 8,103 controls from collaborators at other leading institutions. They also reprogrammed the matured white blood cells to change them back into immortal cells (stem cells) and changed the genetic code of those cells to study the function of the variants they identified through the genomewide association study.

The team reports two genetic variants, both affecting a key cardiac transcription factor called GATA4, reached or nearly reached genomewide significance in BAV. GATA4 is a protein important to cardiovascular development in the womb, and GATA4 mutations have been associated with other cardiovascular defects.

One of the regions we identify actually changes the protein coded by the gene, and the other likely changes expression levels of GATA4 during valve formation, says senior author Cristen Willer, Ph.D., professor of internal medicine, human genetics and computational medicine and bioinformatics. Because most genetic variants associated with human disease are in the 99 percent of the genome that doesnt code for proteins, this finding gives us a great head start toward understanding the mechanism of how a genetic change outside the protein-coding part of the genome can lead to disease.

Specifically, the authors point to a disruption during the endothelial-mesenchymal transition, which is a critical step in the development of the aortic valve. Willer and Yang say this study, with support from the Frankel CVC and the Bob and Ann Aikens Aortic Program, adds new knowledge about the mechanism of BAV formation. They plan to continue to study the biological effect of both variants associated BAV in cells and animal models.

Reference

Yang, B., Zhou, W., Jiao, J., Nielsen, J. B., Mathis, M. R., Heydarpour, M., ... & Fritsche, L. (2017). Protein-altering and regulatory genetic variants near GATA4 implicated in bicuspid aortic valve. Nature Communications, 8, 15481.

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2 Gene Variants Linked to Most Common Congenital Heart Defect - Technology Networks

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A Devon family are swimming to Great Ormond Street Hospital to help a mum whose 15-month-old son has been diagnosed with very rare syndrome called Diskeratosis Congenita. Little Max Hilton's treatment is reliant on a steady supply of stem cell donors and after being around children with similar conditions Max's mum, Becca, is determined to encourage donors to come forward.

Through a touching Facebook group called Be There For Buzz Man Becca, has charted her son's journey and the difficulty they both face.

Becca's North Devon family have sprung into action to help spread the message that the UK needs more Stem Cell donors and to raise funds for the Antony Nolan Register, an organisation dedicated to researching stem cells and matching donors to those in need of help.

"We're delighted with the support we have received by so many people in aid of raising money for Anthony Nolan, including Reef, Tace and Aimee who are based in North Devon, have organised a charity swim called Swimming to Max; swimming 250 miles from Barnstaple to Romford, the distance between them and Max, over 20 weeks to raise as much as they can for the charity," said Becca.

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"Nobody ever expects their newborn child to be diagnosed with such a rare condition, to see him fighting every day is extremely painful, and to see so many brave children in the same ward really does showcase the need of more stem cell and bone marrow donors. Great Ormond Street Hospital are doing all they can, and we'd like to thank the staff for providing invaluable support to both Max and our family.

"For us, converting the negativity we have experienced with Max into making a positive impact for other patients in the same position will make our day.

"If just one person who reads our story decides to see if they're eligible, that could then continue to save a life. Please don't let it affect someone you love to then decide to register. There are so many patients waiting for suitable donors."

For Becca, telling Max's story is not just important for friends and family, but primarily to raise awareness of the desperate need for donors.

To see if you're eligible to donate stem cells, you must be 16 or over, and it is as easy as spitting in a cup to provide a saliva sample for Anthony Nolan to then assess eligibility to then donate - all done through a free sample kit sent via post, from their website.

Donating bone marrow and stem cells is not invasive at all; 9 out of 10 people donate stem cells via the bloodstream, in a procedure called peripheral blood stem cell collection. One in 10 people will have stem cells taken from the bone marrow itself, whilst under general anaesthetic.

Neither procedure hurts, and it's time more is done to increase the people on the register so patients, similar to Max, have a chance in recovering from their rare conditions with the help of those that are genetically matched to their blood type.

The Be There For Buzz Man Facebook page can be found at http://www.facebook.com/buzzman11, and to find out how to donate stem cells visit http://www.anthonynolan.org.

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Baby Max can only survive with a constant supply of stem cells - Devon Live

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Kansas City Star

Sickle cell cure is real, as this Kansas patient proves Kansas City Star Intense pain. Fatigue. Repeated infections, emergency room visits and hospitalizations. Desiree Ramirez endured them often until she became the first adult cured at a Kansas hospital of sickle cell disease. Bone marrow stem cells donated by a ...

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By By Elianna Novitch, The Gazette

May 29, 2017 at 5:00 am | Print View

IOWA CITY More than 20 million people are registered as bone marrow donors in the Be the Match registry, the largest and most diverse donor registry in the world.

But none can help Calder Wills, a 12-year-old Iowa City boy battling stage 4 T-cell lymphoma, or cancer of the blood.

Only one person has been identified as a 100-percent match for Calder, but that person was deemed medically unable to donate bone marrow.

This has left the Wills family with few options.

And so, friends of the family are hosting a donor registry drive on Tuesday to raise awareness about the need for more marrow donors and to perhaps find a match for Calder and others like him.

The event takes place from 3 to 8 p.m. inside the gym at Hoover Elementary School, 2200 E. Court St., Iowa City. Those who attend can join the Be The Match registry. Those who are unable to attend can register online at bethematch.org.

Calder was diagnosed with lymphoma in February 2016. He went into remission within the first 30 days but found out on April 11 the day after his 12th birthday that he had relapsed and would need a bone-marrow transplant. He is one of thousands searching for a match.

He is among the 70 percent of patients who surprisingly dont have a match in their own family, explained Colleen Reardon, manager of the Iowa Marrow Donor Program at the University of Iowa Hospitals & Clinics. We are looking for a tissue type match and each sibling has about a 25 percent chance of being a match.

Calder has three siblings, a twin brother Grayson and sisters Charlotte, 7, and Arden, 5, all of whom were not matches. The next best chance a patient has, statistically, is to find an unrelated donor that is a 100-percent match.

Calders mother Brianna Wills described it as devastating when the family found out that the 58-year-old woman who matched with Calder was deemed medically unable to donate.

That left us with no match, no options, she said. Weve decided to pursue cord blood for his transplant, Wills said. He is going to have a cord blood transplant at the University of Minnesota because a bone marrow match wasnt available and he couldnt wait until one became available.

According to the Be The Match website, cord blood is one of three sources of blood-forming cells used in transplant. The others are bone marrow and peripheral blood stem cells. Cord blood can be used to treat more than 80 diseases, including blood cancers like leukemia and lymphoma. Cord blood comes from a babys umbilical cord.

Wills said that even though Calder is receiving a different type of transplant, she does not want people to not register as a marrow donor.

I dont want that to dissuade people from continuing to do it because he has about a two out of three chance that this transplant will fail because he has T-cell lymphoma that is very aggressive and very hard to treat, Wills said. Realistically, statistically, we are looking at him needing a second transplant down the road and thats when we hope that well find a donor and we can use a bone marrow match then.

Please still do it and not just for Calder, do it for the thousands of people who also dont have a match.

According to Reardon, of every 540 people who register as a donor, only one will be identified as that perfect match for someone and be asked to donate.

Were not realistically hoping to find Calders donor, I mean that would be amazing, but really were hoping to expand the database. Were just hoping that some family in Texas or somewhere else in the world is also doing this and maybe theyll find Calders donor, Wills said. If were all doing it, were going to expand the database for everyones benefit.

Wills recognizes that even though the drive is in Calders honor, it is truly to the benefit of thousands of other people who dont have donors.

There are other ethnic groups that have very little participation and to be a match you need to be matched with donors that have similar ethnic background as you do, Wills said. So African Americans, Hispanics, people that have mixed races, or Asian background wed love to have them come because there are people waiting for donors of all kinds of backgrounds.

What: Bone Marrow Donor Drive

When: 3 to 8 p.m. Tuesday

Where: Hoover Elementary School, 2200 E. Court St., Iowa City

Details: Join the Iowa Marrow Donor Program and Be The Match Registry using a simple cheek swab.

Info: join.bethematch.org/CalderStrong or call the Iowa Marrow Donor Program at (319) 356-3337.

l Comments: (319) 368-8538; elianna.novitch@thegazette.com

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For the first time, scientists have discovered that a common type of immune cell directly triggers stem cells in the skin that are responsible for hair growth in mice. Without this trigger, hair follicles just don't do their job -even if they have the stem cells necessary to proceed.

As the mechanisms for hair growth in mice are similar in humans, the researchers hope their newly uncovered mechanism could lead to a better understanding of conditions like alopecia, and other types of baldness.

Among the various immune system players we have in the body, there's a subclass of immune cells called regulatory T cells, or Tregs for short.

The vast majority of Tregs live in our lymph nodes, where they help to control inflammation throughout the body. But we also have subsets of Tregs that reside in other body parts, such as muscle or lung tissue.

And studies are starting to show that these 'tissue-resident' Tregs may be performing unique roles specific to the part of body they're in.

Researchers know that both mice and humans have a lot of Tregs in the skin, but so far we know very little about their function there.

Seeing that skin-specific Tregs tend to sit around hair follicles, a team led by researchers from the University of California San Francisco (UCSF) investigated the hypothesis that these immune cells were somehow involved in hair growth.

What they discovered is not just involvement, but a direct trigger - making Tregs a super-important part of the hair growth process.

"Our hair follicles are constantly recycling: when a hair falls out, a portion of the hair follicle has to grow back," senior researcher Michael Rosenblum said in a press statement.

"This has been thought to be an entirely stem cell-dependent process, but it turns out Tregs are essential."

In mammals, hair follicles regenerate in a specific pattern, cycling between growth phases (known as anagen) and rest phases (telogen).

The team tracked the amount of Tregs in the skin of mice during these different phases of hair growth, and found a tight correlation - in the telogen phase these immune cells were much more abundant.

What's more, highly active Tregs were crowding around hair follicles at three times the normal rate, right towards the end of the hair growth rest phase.

Intrigued by this correlation, the scientists took a step further to uncover the biological mechanism involved in the relationship between Tregs and the stem cells that make hair follicles do their job.

To do this, they took genetically modified mice whose Treg cells could be 'knocked out' with a simple intervention.

The researchers clipped the hair on the mice's backs and then applied a depilatory cream for 30 seconds - when you depilate the skin, hair follicles kick into the active hair growth phase.

They monitored the hair regrowth for 14 days, comparing the regrowth between control mice and the ones whose Tregs they had tampered with.

In mice whose Tregs were knocked out in the first three days after depilation, the hair just didn't grow back, leaving them with a bald patch on their backs.

A closer look revealed that Tregs directly trigger the activation of stem cells in the hair follicle through a well-known cell communication mechanism called the Notch signalling pathway, which involves a specific protein called Jag1.

They even found that when they replaced Tregs with microscopic beads covered in Jag1, it triggered the activity in the hair follicles just like Tregs would.

"It's as if the skin stem cells and Tregs have co-evolved, so that the Tregs not only guard the stem cells against inflammation but also take part in their regenerative work," Rosenblum said.

"Now the stem cells rely on the Tregs completely to know when it's time to start regenerating."

It's a really elegant demonstration of a previously unknown mechanism for hair growth in mice, but there's a lot more work to be done before we can tell whether defective skin Tregs could be the culprits behind hair loss in humans.

But there's at least one tantalising clue that the study is onto something here. In genome-wide association studies of alopecia areata, a condition characterised by 'patchy' hair loss, researchers have found mutations on genes that are involved in Treg function.

Next up, the researchers are hoping to expand their results and investigate how Tregs in the skin could be involved in wound healing, and also various hair loss conditions in humans.

"It will be important to determine whether this principle extends to human diseases of epithelial dysfunction and whether Tregs can be exploited to develop new therapies for stem-cell-mediated tissue regenerative disorders," they write in the study.

These new results are also an exciting addition to the growing body of knowledge scientists have about hair growth. Earlier this month, researchers reported the discovery of a protein that causes skin stem cells to develop into hair cells in mice. They are now investigating whether this protein is involved in hair loss in people.

The research has been published in Cell.

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We now have the first evidence that immune cells in the skin directly ... - ScienceAlert

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In experiments in mice, UC San Francisco researchers have discovered that regulatory T cells (Tregs; pronounced tee-regs), a type of immune cell generally associated with controlling inflammation, directly trigger stem cells in the skin to promote healthy hair growth. Without these immune cells as partners, the researchers found, the stem cells cannot regenerate hair follicles, leading to baldness.

"Our hair follicles are constantly recycling: when a hair falls out, the whole hair follicle has to grow back, said Michael Rosenblum, MD, PhD, an assistant professor of dermatology at UCSF and senior author on the new paper. This has been thought to be an entirely stem cell-dependent process, but it turns out Tregs are essential. If you knock out this one immune cell type, hair just doesnt grow.

The new study published online May 26 in Cell suggests that defects in Tregs could be responsible for alopecia areata, a common autoimmune disorder that causes hair loss, and could potentially play a role in other forms of baldness, including male pattern baldness, Rosenblum said. Since the same stem cells are responsible for helping heal the skin after injury, the study raises the possibility that Tregs may play a key role in wound repair as well.

Anti-Inflammatory Immune Cells Activate Skin Stem Cells

Normally Tregs act as peacekeepers and diplomats, informing the rest of the immune system of the difference between friend and foe. When Tregs dont function properly, we may develop allergies to harmless substances like peanut protein or cat dander, or suffer from autoimmune disorders in which the immune system turns on the bodys own tissues.

Like other immune cells, most Tregs reside in the bodys lymph nodes, but some live permanently in other tissues, where they seem to have evolved to assist with local metabolic functions as well as playing their normal anti-inflammatory role. In the skin, for example, Rosenblum and colleagues have previously shown that Tregs help establish immune tolerance to healthy skin microbes in newborn mice, and these cells also secrete molecules that help with wound healing into adulthood.

Rosenblum, who is both an immunologist and a dermatologist, wanted to better understand the role of these resident immune cells in skin health. To do this, he and his team developed a technique for temporarily removing Tregs from the skin. But when they shaved patches of hair from these mice to make observations of the affected skin, they made a surprising discovery. We quickly noticed that the shaved patches of hair never grew back, and we thought, Hmm, now thats interesting, Rosenblum said. We realized we had to delve into this further.

In the new research, led by UCSF postdoctoral fellow and first author Niwa Ali, PhD, several lines of evidence suggested that Tregs play a role in triggering hair follicle regeneration.

First, imaging experiments revealed that Tregs have a close relationship with the stem cells that reside within hair follicles and allow them to regenerate: the number of active Tregs clustering around follicle stem cells typically swells by three-fold as follicles enter the growth phase of their regular cycle of rest and regeneration. Also, removing Tregs from the skin blocked hair regrowth only if this was done within the first three days after shaving a patch of skin, when follicle regeneration would normally be activated. Getting rid of Tregs later on, once the regeneration had already begun, had no effect on hair regrowth.

Tregs role in triggering hair growth did not appear related to their normal ability to tamp down tissue inflammation, the researchers found. Instead, they discovered that Tregs trigger stem cell activation directly through a common cell-cell communication system known as the Notch pathway. First, the team demonstrated that Tregs in the skin express unusually high levels of a Notch signaling protein called Jagged 1 (Jag1), compared to Tregs elsewhere in the body. They then showed that removing Tregs from the skin significantly reduced Notch signaling in follicle stem cells, and that replacing Tregs with microscopic beads covered in Jag1 protein restored Notch signaling in the stem cells and successfully activated follicle regeneration.

Its as if the skin stem cells and Tregs have co-evolved, so that the Tregs not only guard the stem cells against inflammation but also take part in their regenerative work, Rosenblum said. Now the stem cells rely on the Tregs completely to know when its time to start regenerating.

Relevance to Autoimmune Hair Loss Rosenblum said the findings may have implications for alopecia areata, an autoimmune disease that interferes with hair follicle regeneration and causes patients to lose hair in patches from their scalp, eyebrows, and faces. Alopecia is among the most common human autoimmune diseases its as common as rheumatoid arthritis, and more common than type 1 diabetes but scientists have little idea what causes it.

After his team first observed hair loss in Treg-deficient mice, Rosenblum learned that the genes associated with alopecia in previous studies are almost all related to Tregs, and treatments that boost Treg function have been shown to be an effective treatment for the disease. Rosenblum speculates that better understanding Tregs critical role in hair growth could lead to improved treatments for hair loss more generally.

The study also adds to a growing sense that immune cells play much broader roles in tissue biology than had previously been appreciated, said Rosenblum, who plans to explore whether Tregs in the skin also play a role in wound healing, since the same follicle stem cells are involved in regenerating skin following injury.

We think of immune cells as coming into a tissue to fight infection, while stem cells are there to regenerate the tissue after its damaged, he said. But what we found here is that stem cells and immune cells have to work together to make regeneration possible.

This article has been republished frommaterialsprovided byUCSF. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference:

Ali, N., Zirak, B., Rodriguez, R. S., Pauli, M. L., Truong, H., Lai, K., . . . Rosenblum, M. D. (2017). Regulatory T Cells in Skin Facilitate Epithelial Stem Cell Differentiation. Cell. doi:10.1016/j.cell.2017.05.002

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Regulatory T Cells Play Essential Role in Hair Growth - Technology Networks

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One giant photo looks like a cocoon enmeshed in strands of silk. Another, like a distant nebula as seen by the Hubble Space Telescope. A third brings to mind rivulets of lava pouring down the sides of a volcano atnight.

Yet all of the images in Toronto artist Radha Chaddahs latest exhibition show the same thing: adult-human stem cells that have been reprogrammed to change from skin into neural tissue. The overall effect is similar to taking a voyage through a world that is both utterly exotic yet intimately related to thevoyager.

These are the most striking pictures for me, said Ms. Chaddah, directing attention to a photo in which a cell has been carefully prepared to reveal its cytoskeleton a network of protein fibres that helps maintain shape and function. People dont generally think of cells as having an internalarchitecture.

The Fall.

Courtesy of ArtaGallery

This is not the classic microscope view of the cell, familiar to anyone who has cracked open a high-school biology textbook. Often, the images do not show cell membranes or other recognizable components. Instead, they highlight the hidden structures within cells, which Ms. Chaddah tags with fluorescent antibodies and then blasts with a laser so they glow with vivid colour at the moment she captures the photo. Once the photo is taken, Ms. Chaddah can never go back. So intense are the exposures she requires, that her tiny subjects are destroyed in the act of imagingthem.

Researchers are keen to exploit the potential of stem cells because they can be induced to switch identity. This property holds tremendous promise for regenerative medicine. For example, in the future, a patients skin cells may be reprogrammed and used to help restore ailing vision due to a deterioratingretina.

This is the kind of possibility that Ms. Chaddah was helping to explore when she was a graduate student in cell and molecular biology a decade ago, eventually publishing her work on stem cells in the Journal ofNeuroscience.

Exodus.

courtesy of ArtaGallery

But, like the cells that fascinate her, Ms. Chaddah found herself changing identities. She had started off with training in fine arts and art conservation before going back to school to become a stem-cell researcher. After completing her masters degree, she turned to the arts again, this time with science as herinspiration.

Her current exhibition, which has been on display in Toronto as part of the annual Contact photography festival, is the product of a meeting of those two worlds. As a graduate student, she needed to repeatedly image the cells she was working with a laborious and frequently frustrating process that could sometimes produce results that were beautiful to look at even when they werent scientificallyusable.

I would go into that little microscope room and be lost in there for five or six hours, she said. Then Id come out with zero data, a major headache and a few amazingpictures.

Regents.

Courtesy of ArtaGallery

Recognizing the visual potential of the technique, Ms. Chaddah made a deal with her supervisor, University of Toronto stem-cell scientist Derek van der Kooy: In exchange for some additional research she conducted in the lab, she was given access to the microscope to pursue herart.

I think its a great idea because we look at these cells under the microscope and they look fantastic to us, but they should be fantastic to everyone, Dr. van der Kooysaid.

He added that while he was delighted to see Ms. Chaddahs images appreciated as art, he wished there was more about the science behind them in the exhibition. Ms. Chaddah has taken a less direct route, sparking the viewers curiosity by giving the images biblical titles a choice that is also meant to draw attention to the way medical discoveries can be viewed with something approaching religious reverence. While stem cells are the subject of legitimate research, they have also spurred the desperate to seek miracle treatments based on questionableevidence.

Genesis.

Courtesy of ArtaGallery

Yet, there is also plenty to feed a sense of wonder at the machinery of life. In a piece called Exodus, which is also the name of the exhibition, Ms. Chaddah has captured a neural cell in the act of migration a reminder, she said, that when human cells are cultured in a Petri dish they can revert to acting as individuals rather than as part of a larger organism. On another level, it also refers to the new world of medical benefits and risks that the manipulation of cells is leading us to as asociety.

But even without such layers of meaning, Ms. Chaddah said she is often surprised by the sense of connection her images seem to evoke, even when visitors are not entirely sure what they are looking at as they wander into thegallery.

Its interesting how many people stand amazed in front of these things and they have some feeling that it has something to do with them even before they read that it came from human skin, she said. I want to draw people in with beauty but I would love it if people would think beyond thebeauty.

Covenant.

Courtesy of ArtaGallery.

Exodus is on display until May 31 at the Arta Gallery, 14 Distillery Lane, Toronto, as part of the Scotiabank Contact PhotographyFestival.

Link:
Toronto artist exposes the hidden architecture of cells - The Globe ... - The Globe and Mail

Recommendation and review posted by sam

It's been hailed as one of the most potentially transformative inventions in modern medicine, bringing the prospect of designer babies closer than any other technology to date, but CRISPR-Cas9 could be riskier than we thought.

The technology that could spark a gene-editing revolution has been caught introducing hundreds of unintended mutations into the genome, and with scientistsalready testing it in humans, it's set off some serious alarm bells.

"We feel it's critical that the scientific community consider the potential hazards of all off-target mutations caused by CRISPR, including single nucleotide mutations and mutations in non-coding regions of the genome," says Stephen Tsang from the Columbia University Medical Centre.

Tsang and his team have conducted the first whole-genome screening of a living organism that's undergone CRISPR gene-editing to discover that unwanted mutations can crop up in areas that are totally unrelated to the targeted genes.

These mutations have likely been missed by previous studies because they've been using computer algorithms that are designed to identify and scan areas on the genome that are most likely to be affected, based on what's been edited.

"These predictive algorithms seem to do a good job when CRISPR is performed in cells or tissues in a dish, but whole genome sequencing has not been employed to look for all off-target effects in living animals," says one of the team, Alexander Bassuk from the University of Iowa.

If you've somehow missed the CRISPR-Cas9 hype train, we started hearing about it a few years ago, when the technology was already being touted as a"revolution", based on its ability to make specific edits to the DNA of humans, other animals, and plants.

The technique workslike a biological 'cut and paste' tool, where researchers use a protein to seek out a particular gene and cut it out of the genome, replacing it with DNA of their choice - for example, they could swap a defective gene for a healthy one.

And unlike many promising medical inventions, CRISPR has continued to live up to its potential.

In recent years, it's been used to tap into cancer's 'control centre', repair a mutation that causes blindness, treat genetic disease in living animals, and even modify human embryos to figure out what causes infertility and miscarriage.

While there have been signs of 'off-target' mutations occurring in preliminary trials, that hasn't stopped the technology from making its way to humans.

The first clinical trial to use CRISPR in actual subjects now underway in China, and the US and the UK are not far behind.

In fact, some researchers are predicting that it could soon trigger some serious competition between China and the US - a kind of biomedical equivalent of the original Space Race.

"I think this is going to trigger 'Sputnik 2.0', a biomedical duel on progress between China and the United States," Carl June, an immunotherapist from the University of Pennsylvania and a scientific adviser on next year's US CRISPR trial, told Nature late last year.

Now researchers have found evidence that the unwanted mutations brought on by CRISPR in living animals could be a more widespread than we thought.

Tsang and his team sequenced the entire genome of two mice that had undergone CRISPR gene-editing in a previous study, and one healthy control.

They were looking for any mutations linked to the technology, including those that only altered a single nucleotide - molecules that serve as the building blocks of DNA and RNA.

They found that the technique had successfully corrected a gene that causes blindness in the mice, but the two mice that had undergone CRISPR gene-editing had sustained more than 1,500 unintended single-nucleotide mutations, and more than 100 larger deletions and insertions.

"None of these DNA mutations were predicted by computer algorithms that are widely used by researchers to look for off-target effects," the team reports.

You can see the results for the two gene-edited mice below, including the unintended single-nucleotide mutations and larger deletions and insertions in the first two rows:

T. Tsang et. al./Nature Methods

To be clear, the find doesn't necessarily mean that CRISPR is unsuitable for use in humans going forward - more research is now needed to see if these results can be replicated in larger samples, and in humans, rather than mice.

But it's like discovering that a medical treatment could be having potentially serious and long-term side effects - and our tests aren't picking them up.

The researchers are now urging for better screening tests for off-target mutations to be applied to CRISPR research immediately.

"We're still upbeat about CRISPR," says one of the team, Vinit Mahajan from Stanford University.

"We're physicians, and we know that every new therapy has some potential side effects - but we need to be aware of what they are."

The research has been accepted for an upcoming edition ofNature Methods.

Excerpt from:

CRISPR Gene-Editing Can Cause Hundreds of Unexpected ... - ScienceAlert

Recommendation and review posted by simmons

It has been hailed as a cure for cancer and all forms of inherited disease.

But scientists have now discovered that a system for editing the genes of living creatures can have a potentially dangerous side-effect causing unintended mutations.

Human trials of the Crispr-Cas9 gene-editing technique are already underway in China and are due to start in the US next year.

One of the supposed strengths of the system is that it allows specific sections of the genome to be targeted.

This prompted one expert, Dr Edze Westra, to predict earlier this year that it would be used to cure all inherited diseases, to cure cancers, to restore sight to people by adding, deleting or repairing genes.

Writing in the journal Nature Methods, researchers in the US described how they had used Crispr-Cas9 to restore sight to blind mice.

However, when they then sequenced the entire genome of the animals, they found two had more than 1,500 small mutations and more than 100 larger deletions and insertions of genetic material.

One of the researchers, Professor Stephen Tsang, of Columbia University, said: We feel its critical that the scientific community consider the potential hazards of all off-target mutations caused by Crispr.

Researchers who arent using whole genome sequencing to find off-target effects may be missing potentially important mutations.

We hope our findings will encourage others to use whole-genome sequencing as a method to determine all the off-target effects of their Crispr techniques and study different versions for the safest, most accurate editing.

He added that even a small change even affecting a single nucleotide, the basic building block of DNA could have a huge impact.

Previously, scientists have used a computer algorithm to highlight areas of the genome most likely to have been damaged inadvertently and then examine those sections of DNA alone.

The researchers said these algorithms seem to do a good job when Crispr was used on tissues in the laboratory, but full genome sequencing was required when dealing with live animals.

The mice used in the study had a gene that causes blindness and Crispr was used to correct this.

While hundreds of mutations were discovered none of which were predicted by the algorithms the mice themselves did not appear to be any worse for wear.

And the researchers said they were still confident that gene-editing would be medically useful.

Professor Vinit Mahajan, of Stanford University, who also took part in the research, said: Were still upbeat about Crispr.

Were physicians, and we know that every new therapy has some potential side effects but we need to be aware of what they are.

They are now trying to improve the targeting and cutting techniques used by the Crispr system.

See the original post here:

Gene-editing technique scientists hope will cure cancer and all ... - The Independent

Recommendation and review posted by Bethany Smith

CRISPR.National Human Genome Research Institute (NHGRI)/Wikimedia

Science regularly goes through cycles of fads that regularly embodies particular generations. In the 80s, its climate change and in the 90s, it was the internet. This time, it seems the gene-editing tool CRISPR is starting to steal the spotlight from other sectors in the scientific community and its not exactly hard to see why. It holds the potential to allow for major transformations on the genetic level.

As Futurism notes, CRISPR is basically causing a revolution within the scientific community, particularly in Biology. Being the single most powerful tool for manipulating organisms at a genetic level, it can be used to change the properties of absolutely anything. Little wonder why so many fear the method, with some imagining a future where people walk around with tails and horns.

In any case, CRISPR was awarded the 2015 Breakthrough of the Year award by Science magazine. It also found a cozy home on the pages of numerous prestigious publications, including the New Yorker and even entertainment media like The Hollywood Reporter are getting in on the game. There is even a TV series planned by NBC, which will feature CRISPR and have Jennifer Lopez as the lead.

The revolutionary technique is also starting to make its way outside of laboratories and to middle schools, NPR reports. There are numerous special sessions all over the country where students of all ages are introduced to the wondrous world of genetic manipulation.

This is made possible because, despite its highly effective nature in editing genes, CRISPR is also incredibly cheap. Students can get a kit for only $150 and with that, they can do things like creating a naturally spicy mango or a gerbil that changes colors.

Whats more, scientists are only beginning to scratch the full potential of the tool. In the coming years, biologists will be unleashing CRISPR on some of the worlds deadliest diseases, with some touching on the matter of immortality.

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Recommendation and review posted by Bethany Smith