Cryoport - World Stem Cells Regenerative Medicine Congress 2013
We spoke with some of the sponsors at Europe #39;s largest stem cells and regenerative medicine industry conference. This is a three day congress that stages a s...

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Cryoport - World Stem Cells Regenerative Medicine Congress 2013 - Video

Public release date: 28-Jun-2013 [ | E-mail | Share ]

Contact: Robert Miranda cogcomm@aol.com Cell Transplantation Center of Excellence for Aging and Brain Repair

Putnam Valley, NY. (June 28 2013) A study carried out in India examining the safety and efficacy of self-donated (autologous), transplanted bone marrow stem cells in patients with type 2 diabetes (TD2M), has found that patients receiving the transplants, when compared to a control group of TD2M patients who did not receive transplantation, required less insulin post-transplantation.

The study appears as an early e-publication for the journal Cell Transplantation, and is now freely available on-line at http://www.ingentaconnect.com/content/cog/ct/pre-prints/ct0920bhansali.

"There is growing interest in the scientific community for cellular therapies that use bone marrow-derived cells for the treatment of type 2 diabetes mellitus and its complications," said study corresponding author Anil Bhansali, PhD professor and head of the Endocrinology Department at the Post Graduate Institute of Medical Education in Chandrigarh, India. "But the potential of stem cell therapy for this disease is yet to be fully explored."

While there is growing interest in using stem cell transplantation to treat TD2M, few studies have examined the utility of bone marrow-derived stem cells. By experimenting with bone marrow-derived stem cells, the researchers sought to exploit the rich source of stem cells in bone marrow.

Their study aimed at evaluating the efficacy and safety of autologous bone marrow-derived stem cell transplantation in patients with T2DM and who also had good glycemic control. Good glycemic control emerged as an important factor in the transplantation group and in the non-transplanted control group.

Cell transplantation had a significant impact on the patients in this study as those administered cells demonstrated a significant reduction in insulin requirement. A significantly smaller reduction in the insulin requirement of the control group was also observed but a "repeated emphasis on life style modification" was believed to be a contributing factor in this effect.

According to Dr. Bhansali, the strength of their study included the inclusion of a homogenous patient population with T2DM which exhibited good glycemic control, and the presence of a similar control group that did not get cell transplants.

"The efficacy and safety of stem cell therapy needs to be established in a greater number of patients and with a longer duration follow-up," concluded Bhansali and his co-authors. "The data available so far from animal and human studies is encouraging, however, it has enormous limitations."

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Type 2 diabetes patients transplanted with own bone marrow stem cells reduces insulin use

June 27, 2013 A chemical code scrawled on histones -- the protein husks that coat DNA in every animal or plant cell -- determines which genes in that cell are turned on and which are turned off. Now, Stanford University School of Medicine researchers have taken a new step in the deciphering of that histone code.

In a study published June 27 in Cell Reports, a team led by Thomas Rando, MD, PhD, professor of neurology and neurological sciences and chief of the Veterans Affairs Palo Alto Health Care System's neurology service, has identified characteristic differences in "histone signatures" between stem cells from the muscles of young mice and old mice. The team also distinguished histone-signature differences between quiescent and active stem cells in the muscles of young mice.

"We've been trying to understand both how the different states a cell finds itself in can be defined by the markings on the histones surrounding its DNA, and to find an objective way to define the 'age' of a cell," said Rando, who is also director of Stanford's Glenn Laboratories for the Biology of Aging and deputy director of the Stanford Center on Longevity.

While all cells in a person's body share virtually the same genes, these cells can be as different from one another as a nerve cell is from a fat cell. This is because only a fraction of a cell's genes are actually "turned on" -- actively involved in the production of one or another protein. A muscle cell produces the proteins it uses to be a muscle cell, a liver cell produces those it needs in order to be a liver cell and so forth. Rando's team thinks the same kinds of on/off differences may distinguish old stem cells from young stem cells.

In human cells, the DNA in which genes are found doesn't float loose inside the cell nucleus but is, rather, packaged inside protein "husks" called histones. Chemical marks on the histones, which sheathe our chromosomal DNA in each cell's nucleus, act as "stop" and "go" traffic signals. These signals tell the complex molecular machinery that translates genes' instructions into newly produced proteins which genes to read and which ones to skip.

In 2005, Rando and his colleagues published a study in Nature showing that stem cells in several tissues of older mice, including muscle, seemed to act younger after continued exposure to younger mice's blood. Their capacity to divide, differentiate and repopulate tissues, which typically declines with an organism's advancing age, resembled those of their stem-cell counterparts in younger animals.

This naturally led to curiosity about exactly what is happening inside a cell to rejuvenate it, said Rando. One likely place to look for an answer was histones, to see if changes in the patterns of the chemical marks on them might reveal any secrets, at the cellular level, of the aging process we all experience -- and, perhaps, whether there might be anything we can do about it. Rando and his colleagues also wanted to learn more about what kinds of difference in these patterns accompany a cell's transition from one level of activity to another.

To do that, Rando and his team looked at satellite cells, an important class of stem cells that serve as a reserve army of potential new muscle tissue. Under normal circumstances, these rather rare stem cells sit quietly adjacent to muscle fibers. But some signal provided by muscular injury or degeneration prompts satellite cells to start dividing and then to integrate themselves into damaged fibers, repairing the muscle tissue. The investigators profiled the histone markings of mice that are as old, in mouse years, as young human adults, as well as mice whose human counterparts would be 70 to 80 years old.

The researchers harvested satellite cells from both healthy and injured muscle tissue of young mice and from healthy tissue of old mice; extracted these cells' DNA with the histone coatings intact; and used tagged antibodies targeting the different kinds of marks to find which spots on those histones were flagged with either "stop" or "go" signals.

"Satellite cells can sit around for practically a lifetime in a quiescent state, not doing much of anything. But they're ready to transform to an activated state as soon as they get word that the tissue needs repair," Rando said. "So, you might think that satellite cells would be already programmed in a way that commits them solely to the 'mature muscle cell' state." The researchers expected that in these quiescent stem cells, the genes specific for other tissues like skin and brain would be marked by "stop" signals.

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Scientists discern signatures of old versus young stem cells