The Food and Drug Administration is cracking down on "unscrupulous" clinics selling unproven and potentially dangerous treatments involving stem cells.

Hundreds of clinics around the country have started selling stem cell therapies that supposedly use stem cells but have not been approved as safe and effective by the FDA, according to the agency.

"There are a small number of unscrupulous actors who have seized on the clinical promise of regenerative medicine, while exploiting the uncertainty, in order to make deceptive, and sometimes corrupt assurances to patients based on unproven and, in some cases, dangerously dubious products," FDA Commissioner Scott Gottlieb said in a statement Monday.

The FDA has taken action against clinics in California and Florida.

The agency sent a warning letter to the US Stem Cell Clinic of Sunrise, Fla., and its chief scientific officer, Kristin Comella, for "marketing stem cell products without FDA approval and significant deviations from current good manufacturing practice requirements."

The clinic is one of many around the country that claim to use stem cells derived from a person's own fat to treat a variety of conditions, including Parkinson's disease, amyotrophic lateral sclerosis (ALS), and lung and heart diseases, the FDA says.

The Florida clinic had been previously linked to several cases of blindness caused by attempts to use fat stem cells to treat macular degeneration.

The FDA also said it has taken "decisive action" to "prevent the use of a potentially dangerous and unproven treatment" offered by StemImmune Inc. of San Diego, Calif., and administered to patients at California Stem Cell Treatment Centers in Rancho Mirage and Beverly Hills, Calif.

As part of that action, the U.S. Marshals Service seized five vials of live vaccinia virus vaccine that is supposed to be reserved for people at high risk for smallpox but was being used as part of a stem-cell treatment for cancer, according to the FDA. "The unproven and potentially dangerous treatment was being injected intravenously and directly into patients' tumors," according to an FDA statement.

Smallpox essentially has been eradicated from the planet, but samples are kept in reserve in the U.S. and Russia, and vaccines are kept on hand as a result.

But Elliot Lander, medical director of the California Stem Cell Treatment Centers, denounced the FDA's actions in an interview with Shots.

"I think it's egregious," Lander says. "I think they made a mistake. I'm really baffled by this."

While his clinics do charge some patients for treatments that use stem cells derived from fat, Lander says, none of the cancer patients were charged and the treatments were administered as part of a carefully designed research study.

"Nobody was charged a single penny," Lander says. "We're just trying to move the field forward."

In a written statement, U.S. Stem Cell also defended its activities.

"The safety and health of our patients are our number one priority and the strict standards that we have in place follow the laws of the Food and Drug Administration," according to the statement.

"We have helped thousands of patients harness their own healing potential," the statement says. "It would be a mistake to limit these therapies from patients who need them when we are adhering to top industry standards."

But stem-cell researchers praised the FDA's actions.

"This is spectacular," says George Daley, dean of the Harvard Medical School and a leading stem-cell researcher. "This is the right thing to do."

Daley praised the FDA's promise to provide clear guidance soon for vetting legitimate stem-cell therapies while cracking down on "snake-oil salesmen" marketing unproven treatments.

Stem-cell research is "a major revolution in medicine. It's bound to ultimately deliver cures," Daley says. "But it's so early in the field," he adds. "Unfortunately, there are unscrupulous practitioners and clinics that are marketing therapies to patients, often at great expense, that haven't been proven to work and may be unsafe."

Others agreed.

"I see this is a major, positive step by the FDA," says Paul Knoepfler, a professor of cell biology at the University of of California, Davis, who has documented the proliferation of stem-cell clinics.

"I'm hoping that this signals a historic shift by the FDA to tackle the big problem of stem-cell clinics selling unapproved and sometimes dangerous stem cell "treatments" that may not be real treatments," Knoepfler says.

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FDA cracks down on stem-cell clinics selling unapproved treatments - 89.3 KPCC

Researchers at the University of California San Diego and at the San Diego Veterans Administration Medical Center have shown that human neural stem cells (NSCs) grafted onto the spinal cord injuries of mice produced a functional recovery after one year. The team has shown that the NSCs continue to grow slowly and steadily even18 months after implantation.

The study is published in the Journal of Clinical Investigation and set out to answer how long it would take for the cells to mature inside the rodents. Mice and humans have a very different pace when it comes to cell biology.

"The NSCs retained an intrinsic human rate of maturation despite being placed in a traumatic rodent environment," lead author Professor Paul Lu said in a statement. "That's a finding of great importance in planning for human clinical trials."

The researchers were worried that the animal model would not reflect the how this approach might in the future work in humans. For example, pregnancies last 21 days in mice and 280 days in humans. And the weight of a toddlers brain is comparable with that of a 20-day-old mouse.

"Most NSC grafting studies have been short-term, measuring survival times in weeks to a few months," added co-author Professor Mark Tuszynski. "That's not enough time to fully measure the growth and maturation rate of human NSCs or what changes might occur farther out from the original grafting. These are important considerations, not just for the basic science of stem cell biology, but for the practical design of translational human trials using NSCs for spinal cord injuries."

The researchers report that the cells maintained their natural maturation pace even though they were in a foreign environment. Thats why it took several months for the lesions to begin healing. The scientists noted that improvement in the mice mobility only happened after more mature nerve cells formed. As the grafts aged, they displayed the expected pruning and cell redistribution activities that help the development of fewer but more mature cells.

"The bottom line is that clinical outcome measures for future trials need to be focused on long time points after grafting," said Tuszynski. "We need to take into account the prolonged developmental biology of neural stem cells. Success, it would seem, will take time."

The team noticed that none of the implanted NSCs migrated from the graft but some supportive astrocytes cells did, which could be a potential safety concern. No tumors or anomalous formation were created by these cells and modified grafting should fix the problem. A better understanding of this approach, so that the results can be carefully assessed, is required before we can even think to try it on humans.

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Human Stem Cells Repair Spinal Cord Injuries In Mice At Human Biological Rate - IFLScience

A researcher pulls a frozen vial of human embryonic stem cells at the University of Michigan Center for Human Embryonic Stem Cell Research Laboratory in Ann Arbor, Mich., in this Oct. 22, 2008 file photo. The face of science, writes Kristin Baetz, should be changing, and here's how to do it. Paul Sancya, THE ASSOCIATED PRESSPaul Sancya / THE ASSOCIATED PRESS

At science meetings, women need to grab the mic and not let go.

As the director of the Ottawa Institute of Systems Biology at uOttawa and as past-president of the Canadian Society for Molecular Biosciences, I get a lot of emails asking me to attend or help advertise science conferences.

Most of these emails end up in my delete file.

Why? I am no longer going to promote, sponsor or attend meetings that do not have a significant number of female speakers.

If accomplished female scientists are not asked to present at meetings, by default it suggests their research is not as exciting or as good as that of their male colleagues.

This matters both financially and professionally your speaking portfolio contributes to the success of grant applications and whether one receives tenure or becomes a full professor.

Canada needs equity in science, technology, engineering and mathematics (STEM). As Imogen Coe, dean of science at Ryerson University and a leading expert in the barriers of women in STEMs, states, If we are to solve or even address the complex problems that we face, we need all hands on deck, we need everyone at the table, we need to leverage all the human potential and intellectual capacity that is available to us.

With women comprising more than 50 per cent of trainees and early-career researchers in biomedical fields, how is it that that the problem of #YAMMM (yet another mostly-male meeting) still exists?

The answer is this: Scientists let it happen.

Consider how science conferences are run. For a number of reasons, largely mid- or late-career scientists organize meetings, and they are often men. Only established researchers, who are no longer struggling to build their research programs, build new courses or possibly to raise young families, have the time to organize meetings.

Its only human that when they solicit speakers, its colleagues they know, or want to collaborate with. If you are an early-career researcher, especially female, many meeting organizers might not have you on their radar.

This will change when organizers of meetings including scientific societies and funders start demanding that equity is a fundamental requirement of meetings.

Coe recently challenged me to ensure that the speakers at our 2017 Canadian Society for Molecular Biosciences meeting reflected our attendees. I am both proud and ashamed to announce that at our 60th annual science meeting, 50 per cent of our speakers were female.

I insisted that our organizers seek out exceptional female speakers to give plenary talks.

While this was embraced by many of my colleagues, it was strongly resisted by others. Some refused to even consider equity issues when selecting speakers. Why? One often-made excuse is that there are no excellent females in a field to invite.

Jodi Nunnari, president-elect of the American Society for Cell Biology, calls this a poor excuse, which justifies the same old status quo. To counter this argument, her society established a speaker referral list to identify outstanding women scientists across the field of cell biology.

Heres what happened at our meeting. Many back-handed comments were made about how different the speaker lineup was. I got upset emails over not being asked to give a talk. One said, I guess I didnt tick-off the right boxes.

These reactions consistently originated from mid- and late-career male scientists.

However, for every negative comment, I received tenfold more positive comments from across the research spectrum, from trainees to retired professors, both male and female.

While I am hopeful that our government will one day tackle the equity issues in STEM by directly tying it to funding, scientists cannot just wait. As individuals and as institutions we have the ability to literally change the face of conferences and success in Canadian science.

Lets commit to ending the #YAMMM.

Kristin Baetz is the director of the Ottawa Institute of Systems Biology and professor at uOttawa.

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Baetz: Standing up for female scientists and researchers - Ottawa Citizen

The force gravity and physical activity put on our bones causes tiny tears in the membranes of the tiny cells that enable us to make or break down bone, scientists say. Pictured are Drs. Meghan E. McGee-Lawrence and Paul McNeil. Credit: Phil Jones, Senior Photographer, Augusta University

The force gravity and physical activity put on our bones causes tiny tears in the membranes of the tiny cells that enable us to make or break down bone, scientists say.

While that may sound bad, it's actually a key piece of how the force we put on our bones helps keep them strong, they report in the Journal of Orthopaedic Research.

"The bone has to constantly adapt and make sure that is has the right design to withstand the loads you are going to put it through," says Dr. Meghan E. McGee-Lawrence, biomedical engineer in the Department of Cellular Biology and Anatomy at the Medical College of Georgia at Augusta University.

Osteocytes manage the osteoblasts that make bone as well as the osteoclasts that break bone down and were known to sense mechanical loading, but just how they sensed load was unknown.

McGee-Lawrence and MCG cell biologist Dr. Paul McNeil are the first to find the small tears in response to force exacted by walking up the stairs or lifting weights.

Not only do the cells experience membrane tears but it's the highest number McNeil, an expert in cell membrane repair, has seen in a variety of cell types. "It's remarkable," says the study coauthor. And, the heavier the mechanical load, the more tears; for example the mice walking on a treadmill versus just moving about in their cage.

Better understanding the specific mechanism by which these cells sense then respond to mechanical load should enable identification of logical targets for improving the strength and health of aging bones as well as bones challenged by diseases like diabetes, says McGee-Lawrence the study's corresponding author.

Osteocytes are plentiful in bone and each has hundreds of tiny processes reaching out in every direction that help secure them to the bone matrix. McGee-Lawrence likens their look to a sweetgum ball. She and McNeil have early evidence the diminutive cells and their projections are both very vulnerable to tearing and that vulnerability appears to make them a natural for responding to mechanical load.

Once tears happen to cell membranes, more calcium rushes inside the cells. This mineral closely associated with bone health and present outside the cell at concentrations 10,000 times higher than inside the cell, was known to be an initiating signal, McNeil says. His work has shown how in many cell types including now osteocytes, the load causes the tears which allows calcium to rush in to both rapidly heal tears and to set in motion inside a host of actions that, in this case, remodels bone.

In cell cultures, they watched as increased calcium levels inside osteocytes triggered an increase in the production of the protein c-fos. The protein also is well-studied and known to be involved in the signaling pathways that lead to stronger bones in response to exercise, but c-fos' connection with membrane tearing was another unknown.

Osteocytes use their micron-thin tentacles to communicate with each other and the scientists also learned that when one osteocyte gets tears, it appears to communicate its load to neighboring osteocytes so the calcium level goes up in those as well even without a tear. The message the torn osteocyte shares it to tell osteoblasts to make the bones stronger and the osteoclasts to quit breaking bone down.

The idea of further shoring up bone is likely to be better prepared for whatever mechanical load comes next, McGee-Lawrence says.

Conversely, the lack of loading and subsequent tearing may be why astronauts' bone and muscle weaken in zero gravity, McNeil says.

McGee-Lawrence is principal investigator on a new $450,000 National Science Foundation grant that will help them further parse this important puzzle and the potential for enabling better bone health with age and disease.

"We are wondering if bone loss with aging is due to osteocytes becoming more fragile or less able to repair as we age," say McNeil, co-investigator on the ongoing studies. "If they do, you would lose them over time and, in fact, we know you do lose them."

Part of what they are doing with the new grant includes looking at mice with a genetic deficiency in cell membrane repair. They want to see if the 50-year-old drug poloxamer 188, which was designed to reduce the thickness of blood, is found in products like toothpaste and has been shown to repair other cell membranes, might help osteocytes remain proficient at responding to mechanical load. Like many of our senses that dull with age, aging osteocytes don't sense critical mechanical loads as well.

"It's a way you can influence membrane repair rates so if we speed up how fast that tear repairs, is that going to influence the osteocytes?" McGee-Lawrence says. They'll also look at the impact of slowing repair down.

No drug on the market for osteoporosis is known to enhance osteocyte sensitivity.

"We are starting to understand why calcium signaling gets initiated in wounded cells and then that gives us a mechanism we can target to try to influence how well bone detects mechanical loading," McGee-Lawrence says.

Disease may also complicate the common action of cell membrane tear and repair. For example, McNeil has shown diabetes, which is associated with bone loss, can lead to problems with membrane repair of other cell types. Now the MCG scientists are looking at whether it similarly affects osteocytes.

Bone and muscle health are inextricably connected and McNeil has done pioneering work that shows one way we keep our muscles strong and even increase their size is through this process of tear and repair in the membrane of muscle cells.

"If you go to the gym and exercise your muscles, they are going to get bigger and stronger and at the same time if you sit around all day your muscles are going to get weaker," McGee-Lawrence says. "Bone does the same thing." McNeil notes the difference between the right and left hands and arms of a right-handed tennis player.

"This bone is full of cells. Some are building new bone, some are breaking down bone and it is constantly being remodeled," McNeil adds, holding up a large muskox bone.

People hit their peak bone mass in the late 20s or early 30s. After that, the percentage of osteoblasts to osteoclasts starts to shift so that you are slowly losing rather than building bones. Active youth, they note, tend to build a better bone mass that should comfortably see them into old age, particularly if they remain active.

Failure of rapid membrane repair is associated with weaker muscles even muscle disease, they note, and the scientists expect the same also holds true in bone. Future studies include exploring whether repair failure contributes to common problems like osteoporosis.

Explore further: Research identifies how master regulator, bone-building protein can be used for therapy

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Tears in tiny bone cells called osteocytes appear an important step to better bones - Medical Xpress