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fertility

Scientists say it may be possible to restore sperm production in boys who are left infertile by childhood cancer treatments, BBC News reported.

One of the harmful side effects of chemotherapy and radiotherapy is that the treatments also kill cells which make sperm.  However, in a new study on monkeys, researchers from the University of Pittsburgh and the Magee-Womens Research Institute extracted sperm-producing stem cells before cancer treatment and later restored the cells.

Nine out of 12 adult monkeys and three out of five prepubescent monkeys were later able to produce healthy sperm again – meaning the sperm was capable of fertilizing female eggs.

While male cancer patients have the option of freezing sperm before treatment, this is not an option for patients who have not yet goon through puberty.

"This report is a very useful step forward and clearly shows that the science of spermatogonial stem cells transplantation might one day work for humans,” Dr. Allan Pacey, senior lecturer in andrology at the University of Sheffield, told BBC News. “And, although the authors report relatively low efficiency so far, in the context of someone who does not have any banked sperm to fall back on, these odds are probably very encouraging to make this kind of approach worthwhile."

Pacey added a main concern of the treatment was that cancer could be lurking in the stem cells, raising the possibility of re-implanting cancer cells into a healthy patient.
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Stem Cell Therapy Key for the Treatment of Diabetes


 St. Petersburg, FL, April 09, 2014 --(PR.com)-- Diabetes is the 7th leading cause of death according to the Center for Disease Control and the number of people diagnosed each year continues to increase at epidemic proportions. Recent studies show that stem cells may be a very real answer to the treatment of diabetes; perhaps even a cure. Stemedix™ (stemedix.com) is a Florida based Autologous Adipose Stem Cell treatment organization offering cutting-edge stem cell therapy and expertise to patients who suffer from Type 1 and Type 2 Diabetes.

Time Magazine referenced a study where stem cells were being used to treat type 1 Diabetes. “The findings, published in the Journal of the American Medical Association, showed remarkable gains made by diabetes researchers, who are battling a continuously spreading disease that now affects nearly 8% of adults and children.”

The results of the study led by Dr. Julio Voltarelli and his research team were cited in the Time Magazine piece. Since Type I Diabetes patients are locked in a constant struggle to maintain their body’s insulin levels, because their own beta cells can no longer produce the hormone, they must constantly inject insulin. Sometimes patients may even become dependent on an automatic insulin pump. Voltarelli’s research is compelling because it proposes stem cells to be a less invasive, natural treatment alternative.

Another recent study out of Alberta, Canada noted seven out of seven patients who received stem cell therapy no longer needed to take insulin and their blood glucose concentrations were normal a year later. While there isn’t cure for Diabetes at the present time, ongoing and extensive research is indicating the key to a cure will be found through the application of stem cells.

Stemedix™ stem cell treatment sets the body into repair mode by using its own natural mechanisms. Once harvested, a process called “activation” uses a special laser to stimulate the stem cells. They are then transplanted back to the body, via the bloodstream; to target areas of the body to begin repairing and recreating damaged tissue. The process is minimally invasive and patients are able to leave the facility within hours of the procedure. Improvement in the following symptoms associated with Diabetes have been observed: enhanced mood, increased energy, increased ability to perform daily exercises, reduction in the required amount of insulin, improved urine function and improved gastrointestinal function.

In addition to Type 1 and Type 2 Diabetes, advancements in stem cell research are allowing patients suffering with the symptoms of diseases such as Muscular Sclerosis, Rheumatoid Arthritis, Osteoarthritis, Pulmonary Fibrosis, Lupus, Alzheimer’s and Parkinson’s to fight back against these ailments and begin the journey to healing. Stemedix™ stem cell therapy treatment is the product of these advancements.

For more information about Adipose Stem Cell Therapy visit Stemedix online at http://stemedix.com or call us at 800-531-0831.
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Type 1 Diabetes Reversed With Stem Cells From Cord Blood

Wednesday 11 January 2012 - 2am PST
 
DiabetesStem Cell ResearchImmune System / Vaccinesadd your opinionemailMNT FeaturedAcademic Journal

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Type 1 Diabetes Reversed With Stem Cells From Cord Blood
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Stem cells from cord blood "re-educated" the immune system T cells of people with type 1 diabetes so their pancreas started producing insulin again, thereby reducing the amount of insulin they needed to inject. These are the findings of a study led by Dr Yong Zhao, from University of Illinois at Chicago that were published online on Tuesday in the open access journal BMC Medicine.

Type 1 diabetes develops when the body's own immune system attacks and destroys the insulin-producing islet beta cells in the pancreas. As a result, the body can't make insulin, causing blood glucose to reach dangerous levels and damage all the organs in the body.

In their background information, the researchers note that tests on mice and cells of patients with diabetes have shown that multipotent cells derived from cord blood "can control autoimmune responses by altering regulatory T cells (Tregs) and human islet beta cell-specific T cell clones".

Cord blood is blood that is collected from the placenta and umbilical cord after childbirth. It is a rich source of stem cells that can treat a range of blood and genetic disorders.

In their paper the researchers describe how they developed a procedure they called "Stem Cell Educator therapy" where the diabetic patient's blood is circulated through a closed-loop system that separates lymphocytes (a class of immune cell that includes T cells) from the whole blood and co-cultures them with cord blood stem cells from healthy donors for two to three hours before returning the "re-educated lymphocytes" to the patient's circulation.

For this small, open-label, phase1/phase 2 study they recruited 15 patients with type 1 diabetes aged from 15 to 41 years (median 29) with a diabetic history ranging from 1 to 21 years (median 8).

All but three of the patients (the controls) underwent Stem Cell Educator therapy once. The controls underwent a sham treatment where they received no educated cells. 

The researchers checked the patients' progress 4, 12, 24 and 40 weeks after therapy. Six of the patients who had the therapy had some residual beta cell function (moderate type 1 diabetes) and the other six had no residual beta cell function (severe type 1 diabetes).

The results showed that the median daily dose of required insulin was down by 38% at week 12 for the six patients with moderate diabetes and by 25% for the patients with severe diabetes. There was no change in required insulin dose for the controls.

All the patients who had received the Stem Cell Educator therapy also showed improved levels of C-peptide, a biomarker used to measure how well beta cells are working (it is a protein fragment that is left behind when insulin is made in the pancreas).

Levels of C-peptide continued to improve at 24 weeks and was maintained to the end of the study (at 40 weeks).

Zhao told the press:

"We also saw an improved autoimmune control in these patients. Stem Cell Educator therapy increased the percentage of regulatory T lymphocytes in the blood of people in the treatment group. Other markers of immune function, such as TGF-beta1 also improved."

The researchers detail the improvements in immune function in their paper:

"Individuals who received Stem Cell Educator therapy exhibited increased expression of costimulating molecules (specifically, CD28 and ICOS), increases in the number of CD4+CD25+Foxp3+ Tregs, and restoration of Th1/Th2/Th3 cytokine balance." 

Zhao suggests the autoimmune regulator AIRE in the cord blood stem cells mediated these changes which in turn allowed the pancreatic islet beta cells to recover.
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Cancer stem cells tracked
Cancer researchers can sequence tumour cells’ genomes, scan them for strange gene activity, profile their contents for telltale proteins and study their growth in laboratory dishes. What they have not been able to do is track errant cells doing what is more relevant to patients: forming tumours. Now three groups studying tumours in mice have done exactly that1–3. Their results support the ideas that a small subset of cells drives tumour growth and that curing cancer may require those cells to be eliminated.

It is too soon to know whether these results — obtained for tumours of the brain, the gut and the skin — will apply to other cancers, says Luis Parada at the University of Texas Southwestern Medical Center in Dallas, who led the brain study2. But if they do, he says, “there is going to be a paradigm shift in the way that chemotherapy efficacy is evaluated and how therapeutics are developed”. Instead of testing whether a therapy shrinks a tumour, for instance, researchers would assess whether it kills the right sorts of cell.

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Underlying this scenario is the compelling but controversial hypothesis that many tumours are fuelled by ‘cancer stem cells’ that produce the other types of cancer cell, just as ordinary stem cells produce normal tissues. Previous studies have tested this idea by sorting cells from a cancer biopsy into subsets on the basis of factors such as cell-surface markers, and injecting them into laboratory mice. In principle, those cells that generate new tumours are the cancer stem cells. But sceptics point out that transplantation removes cells from their natural environment and may change their behaviour. “You can see what a cell can do, but not what cells actually do,” says Cédric Blanpain of the Free University of Brussels, who co-led the skin study1.

All three research groups tried to address this knowledge gap by using genetic techniques to track cells. Parada and his co-workers began by testing whether a genetic marker that labels healthy adult neural stem cells but not their more specialized descendents might also label cancer stem cells in glioblastoma, a type of brain cancer. When they did so, they found that all tumours contained at least a few labelled cells — presumably stem cells. Tumours also contained many unlabelled cells2. The unlabelled cells could be killed with standard chemotherapy, but the tumours quickly returned. Further experiments showed that the unlabelled cells originated from labelled predecessors. When chemotherapy was paired with a genetic trick to suppress the labelled cells, Parada says, the tumours shrank back into “residual vestiges” that did not resemble glioblastoma.

Meanwhile, Hans Clevers, a stem-cell biologist at the Hubrecht Institute in Utrecht, the Netherlands, and his colleagues focused on the gut. They had previously shown that a genetic marker that labels healthy gut stem cells also labels stem cells in benign intestinal tumours, which are precursors of cancer4. In their latest study3, he and his team engineered mice to carry a gene for a drug-inducible marker that, when activated, causes labelled cells to make molecules that fluoresce one of four colours. This experiment yielded single-colour tumours consisting of several cell types, suggesting that each tumour arose from a single stem cell. To check that stem cells continued to fuel the tumours, Clevers added a second, low dose of the drug, triggering a few of the stem cells to change colour. This produced streams of cells in the new colour, showing that stem cells were consistently producing the other cell types.

For the skin study, Blanpain and his group labelled individual tumour cells, without targeting stem cells specifically1. They found that cells showed two distinct patterns of division: they either produced a handful of cells before petering out, or went on to produce many cells. Once again, the results pointed to a distinct subset of cells as the engine of tumour growth. What’s more, as tumours became more aggressive, they were more likely to produce new stem cells — which can divide indefinitely — and less likely to produce differentiated cells, which can divide only a limited number of times. That could be a key to halting tumour development early, says Blanpain. Rather than eradicating cancer stem cells, for example, therapies could try to coax them to differentiate into non-dividing cells.

The papers provide clear experimental evidence that cancer stem cells exist, says Robert Weinberg, a cancer researcher at the Whitehead Institute in Cambridge, Massachusetts. “They have made a major contribution to validating the concept of cancer stem cells,” he says. But cancer cells probably also act in more complex ways than those observed, he warns. For example, non-stem cells within the tumour might de-differentiate into stem cells.

The next step, the three groups say, is figuring out how the cells tracked in these experiments relate to putative cancer stem cells identified by years of transplantation studies. Researchers are already busy hunting for ways to kill these cells; now they have more tools to tell whether such a strategy will work.
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Patient stem cells help identify common problem in ALS
Date:
April 3, 2014
Source:
Harvard University
Summary:
A recently approved medication for epilepsy may possibly be a meaningful treatment for amyotrophic lateral sclerosis -- Lou Gehrig's disease, a uniformly fatal neurodegenerative disorder, new stem cell research has shown. The researchers are now designing an initial clinical trial testing the safety of the treatment in ALS patients.
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B. D. Colen/Harvard Staff In 2008, Harvard Stem Cell Institute principal faculty member Kevin Eggan first raised the possibility of using ALS patient-derived stem cells to better understand the disease and identify therapeutic targets for new drugs. Based on those findings, Eggan and other Harvard stem cell scientists have discovered that a newly approved medication for epilepsy may offer meaningful treatment for ALS.
Credit: B. D. Colen/Harvard Staff
[Click to enlarge image]
Harvard stem cell scientists have discovered that a recently approved medication for epilepsy may possibly be a meaningful treatment for amyotrophic lateral sclerosis (ALS) -- Lou Gehrig's disease, a uniformly fatal neurodegenerative disorder. The researchers are now collaborating with Massachusetts General Hospital to design an initial clinical trial testing the safety of the treatment in ALS patients.



The investigators all caution that a great deal needs to be done to assure the safety and efficacy of the treatment in ALS patients, before physicians should start offering it.
The work, laid out in two related papers in the April 3 online editions of Cell Stem Cell and Cell Reports, is the long-term fruition of studies by Harvard Stem Cell Institute (HSCI) Principal Faculty member Cell Stem Cell, PhD, who, in a 2008 Science paper, first raised the possibility of using ALS patient-derived stem cells to better understand the disease and identify therapeutic targets for new drugs.
Now Eggan and HSCI colleague Clifford Woolf, MD, PhD, have found that the many independent mutations that cause ALS may be linked by their ability to trigger abnormally high activity in motor neurons. Using neurons derived from stem cells made from ALS patient skin cells, the two research teams conducted clinical trials of the anti-epilepsy medication on neurons in laboratory dishes, finding that it reduced the hyperexcitability of the cells.
ALS is a devastating and currently untreatable degradation of motor neurons, the long nerve cells that connect the spinal cord to the muscles of the body. While several potential treatments have looked promising in mice, all proved disappointing in the clinic.
"The big problem in ALS is that there are more than a hundred mutations in dozens of genes that all cause the disease, but almost all of the therapeutics that have gone forward in the clinic have done so for just one of those mutations, SOD1, which almost everyone studies in mice," said Eggan, a professor in Harvard's Department of Stem and Regenerative Biology.
"And so," he continued, "the key question that we really wanted to address was -- are clinical efforts failing because the mouse is taking us on a wild goose chase, or is it simply that people haven't had the opportunity to pre-test whether their ideas are true across lots of forms of ALS?"
In the Cell Stem Cell study, Eggan and postdoctoral fellow Evangelos Kiskinis, PhD, led an effort to make stem cell lines from two women with ALS who have SOD1 mutations to compare human biology and mouse biology. Using a technology called RNA sequencing to look at how the mutation changes gene expression in these lines, the researchers then traced the changes to their impact on biological pathways.
"We found thhttps://old.sciencedaily.com/cms/at the mutation makes changes in the motor neurons, which aren't so different from the changes that you see in the mice," Eggan said. "I think our paper says that while there are definitely some human-specific biology, the mice weren't totally misleading."
Eggan's lab then created more stem cell-derived motor neurons from patients with another form of ALS, as well as people without the disease, to see what changes occur in ALS cells and if these were present across independent genetic mutations.
The surprising result, reported in the Cell Reports study, was that the motor neurons that possessed ALS mutations had a sporadic increase in motor neuron firing while the healthy neurons were quiet unless stimulated in some way.
The ALS hyperexcitability was further examined by Woolf's team, led by Harvard Medical School neurologist Brian Wainger, MD, PhD. Working with Eggan and Kiskinis collectively, they found a cyclical relationship between the increased neuron activity and abnormal protein folding. In the two papers, they describe how the overexcitable ALS neurons generate more abnormally folded proteins, further increasing their excitability. The strain of this cycle seems to put the neurons in a vulnerable state where they are more likely to die.
"The convergence on a single mechanism offered a very attractive place to intervene therapeutically," said Woolf, a Harvard Medical School professor in neurology and neurobiology at Boston Children's Hospital, who also co-leads HSCI's Nervous System Diseases Program.
"It looked like there's a deficit in potassium channels in the ALS motor neurons and that led us to then test whether drugs that open the potassium channels may reduce this hyperexcitability -- and indeed that's exactly what we found," he said. "We found that retigabine, which has recently been approved as an anticonvulsive, normalized this activity; so now we can formally go from the dish to the patient and actually explore whether the drug might have any beneficial effect."
Massachusetts General Hospital neurologist Merit Cudkowicz, MD, with Wainger, will be running the clinical trials, which will first test for side effects when giving the drug to ALS patients. The researchers caution against calling this work a breakthrough or having doctors prescribe this drug to patients immediately. Clinical trials are necessary to determine whether there are any unusual interactions between the drug and having ALS, as having a particular disease can make someone more sensitive to certain types of drugs.
"The whole intact nervous system is more complicated than the cells that we have in the dish at the moment," Eggan said. "And now the next step is to say whether or not the drug will be helpful in that context, and it's too early to say for sure."
The scientists credit emerging technologies and the unique collaboration between a stem cell lab and a neuron physiology lab as an essential part of making this research clinically relevant for ALS patients.
"I think it's the beginning of a complete change in the way we do medicine for serious diseases like this," Woolf said. "In a traditional clinical trial, you give the patient the placebo or an active ingredient to see the effects they have and it's over. Here we can take the same stem cell lines and have an infinite capacity to do clinical trials in a dish."
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