Source: Johns Hopkins Medicine
Date: July 17, 2012
Summary:
Using adult stem cells, Johns Hopkins researchers and a consortium of colleagues nationwide say they have generated the type of human neuron specifically damaged by Parkinson’s disease (PD) and used various drugs to stop the damage. Their experiments on cells in the laboratory, reported in the July 4 issue of the journal Science Translational Medicine, could speed the search for new drugs to treat the incurable neurodegenerative disease, but also, they say, may lead them back to better ways of using medications that previously failed in clinical trials.
Tuesday, July 17, 2012
StemCells, Inc. Announces Its Human Neural Stem Cells Restore Memory in Models of Alzheimer's Disease
Source: StemCells, Inc.
Date: July 17, 2012
Summary:
StemCells, Inc. today announced preclinical data demonstrating that its proprietary human neural stem cells restored memory and enhanced synaptic function in two animal models relevant to Alzheimer's disease (AD). The data was presented today at the Alzheimer's Association International Conference 2012 in Vancouver, Canada.
The study results showed that transplanting the cells into a specific region of the brain, the hippocampus, statistically increased memory in two different animal models. The hippocampus is critically important to the control of memory and is severely impacted by the pathology of AD. Specifically, hippocampal synaptic density is reduced in AD and correlates with memory loss. The researchers observed increased synaptic density and improved memory post transplantation. Importantly, these results did not require reduction in beta amyloid or tau that accumulate in the brains of patients with AD and account for the pathological hallmarks of the disease.
Date: July 17, 2012
Summary:
StemCells, Inc. today announced preclinical data demonstrating that its proprietary human neural stem cells restored memory and enhanced synaptic function in two animal models relevant to Alzheimer's disease (AD). The data was presented today at the Alzheimer's Association International Conference 2012 in Vancouver, Canada.
The study results showed that transplanting the cells into a specific region of the brain, the hippocampus, statistically increased memory in two different animal models. The hippocampus is critically important to the control of memory and is severely impacted by the pathology of AD. Specifically, hippocampal synaptic density is reduced in AD and correlates with memory loss. The researchers observed increased synaptic density and improved memory post transplantation. Importantly, these results did not require reduction in beta amyloid or tau that accumulate in the brains of patients with AD and account for the pathological hallmarks of the disease.
Monday, July 16, 2012
Scientists Discover Key Pathway For Development of Insulin-producing Cells
Source: Stanford University School of Medicine
Date: July 16, 2012
Summary:
Researchers at the Stanford University School of Medicine have identified a molecular signaling pathway that drives the growth and maturation of young human beta cells — the insulin-producing cell type in the pancreas that malfunctions in diabetes — in mice and humans. The pathway, called the Cn/NFAT pathway, has been shown to be important in the growth and development of many cell types, including immune cells and neurons. But this is the first time it’s been shown to be involved in the development of human beta cells. The research is published July 17 in Developmental Cell.
Date: July 16, 2012
Summary:
Researchers at the Stanford University School of Medicine have identified a molecular signaling pathway that drives the growth and maturation of young human beta cells — the insulin-producing cell type in the pancreas that malfunctions in diabetes — in mice and humans. The pathway, called the Cn/NFAT pathway, has been shown to be important in the growth and development of many cell types, including immune cells and neurons. But this is the first time it’s been shown to be involved in the development of human beta cells. The research is published July 17 in Developmental Cell.
Lab-Engineered Muscle Implants Restore Function in Animal Studies
Source: Wake Forest Baptist Medical Center
Date: July 16, 2012
Summary:
WINSTON-SALEM, N.C. -- New research shows that exercise is a key step in building a muscle-like implant in the lab with the potential to repair muscle damage from injury or disease. In mice, these implants successfully prompt the regeneration and repair of damaged or lost muscle tissue, resulting in significant functional improvement.
In the current issue of Tissue Engineering Part A, scientists at Wake Forest Baptist Medical Center build on their prior work and report their second round of experiments showing that placing cells derived from muscle tissue on a strip of biocompatible material - and then "exercising" the strip in the lab - results in a muscle-like implant that can prompt muscle regeneration and significant functional recovery. The researchers hope the treatment can one day help patients with muscle defects ranging from cleft lip and palate to those caused by traumatic injuries or surgery.
For the study, small samples of muscle tissue from rats and mice were processed to extract cells, which were then multiplied in the lab. The cells, at a rate of 1 million per square centimeter, were placed onto strips of a natural biological material. The material, derived from pig bladder with all cells removed, is known to be compatible with the body.
Next, the strips were placed in a computer-controlled device that slowly expands and contracts - essentially "educating" the implants on how to perform in the body. This cyclic stretching and relaxation occurred three times per minute for the first five minutes of each hour for about a week. In the current study, the scientists tried several different protocols, such as adding more cells to the strips during the exercise process.
The next step was implanting the strips in mice with about half of a large muscle in the back (latissimus dorsi) removed to create functional impairment. While the strips are "muscle-like" at the time of implantation, they are not yet functional. Implantation in the body - sometimes referred to as "nature's incubator" - prompts further development.
The goal of the project was to speed up the body's natural recovery process as well as prompt the development of new muscle tissue. The scientists compared four groups of mice. One group received no surgical repair. The other groups received implants prepared in one of three ways: one was not exercised before implantation, one was exercised for five to seven days, and one had extra cells added midway through the exercise process. The results showed that exercising the implants made a significant difference in both muscle development and function.
Date: July 16, 2012
Summary:
WINSTON-SALEM, N.C. -- New research shows that exercise is a key step in building a muscle-like implant in the lab with the potential to repair muscle damage from injury or disease. In mice, these implants successfully prompt the regeneration and repair of damaged or lost muscle tissue, resulting in significant functional improvement.
In the current issue of Tissue Engineering Part A, scientists at Wake Forest Baptist Medical Center build on their prior work and report their second round of experiments showing that placing cells derived from muscle tissue on a strip of biocompatible material - and then "exercising" the strip in the lab - results in a muscle-like implant that can prompt muscle regeneration and significant functional recovery. The researchers hope the treatment can one day help patients with muscle defects ranging from cleft lip and palate to those caused by traumatic injuries or surgery.
For the study, small samples of muscle tissue from rats and mice were processed to extract cells, which were then multiplied in the lab. The cells, at a rate of 1 million per square centimeter, were placed onto strips of a natural biological material. The material, derived from pig bladder with all cells removed, is known to be compatible with the body.
Next, the strips were placed in a computer-controlled device that slowly expands and contracts - essentially "educating" the implants on how to perform in the body. This cyclic stretching and relaxation occurred three times per minute for the first five minutes of each hour for about a week. In the current study, the scientists tried several different protocols, such as adding more cells to the strips during the exercise process.
The next step was implanting the strips in mice with about half of a large muscle in the back (latissimus dorsi) removed to create functional impairment. While the strips are "muscle-like" at the time of implantation, they are not yet functional. Implantation in the body - sometimes referred to as "nature's incubator" - prompts further development.
The goal of the project was to speed up the body's natural recovery process as well as prompt the development of new muscle tissue. The scientists compared four groups of mice. One group received no surgical repair. The other groups received implants prepared in one of three ways: one was not exercised before implantation, one was exercised for five to seven days, and one had extra cells added midway through the exercise process. The results showed that exercising the implants made a significant difference in both muscle development and function.
Thursday, July 05, 2012
Common Diabetes Drug Promotes Development of Brain Stem Cells
Source: The Hospital for Sick Children (SickKids)
Date: July 5, 2012
Summary:
TORONTO – Researchers at The Hospital for Sick Children (SickKids) have found that metformin, a drug commonly used to treat Type II diabetes, can help trigger the pathway used to instruct stem cells in the brain to become neural (nerve) cells. Brain stem cells and the neural cells they generate play a role in the repair of the injured or degenerating brain. This study suggests a novel therapeutic approach to treating people with brain injuries or potentially even neurodegenerative diseases. The study – led by Dr. Freda Miller, Senior Scientist at SickKids and Professor in the Department of Molecular Genetics at the University of Toronto – is published in the July 5 advance online edition of Cell Stem Cell.
Date: July 5, 2012
Summary:
TORONTO – Researchers at The Hospital for Sick Children (SickKids) have found that metformin, a drug commonly used to treat Type II diabetes, can help trigger the pathway used to instruct stem cells in the brain to become neural (nerve) cells. Brain stem cells and the neural cells they generate play a role in the repair of the injured or degenerating brain. This study suggests a novel therapeutic approach to treating people with brain injuries or potentially even neurodegenerative diseases. The study – led by Dr. Freda Miller, Senior Scientist at SickKids and Professor in the Department of Molecular Genetics at the University of Toronto – is published in the July 5 advance online edition of Cell Stem Cell.
Critical Process in Stem Cell Development Identified
Source: Gladstone Institutes
Date: July 5, 2012
Summary:
Scientists at the Gladstone Institutes have discovered that environmental factors critically influence the growth of a type of stem cell -- called an iPS cell -- that is derived from adult skin cells. This discovery offers newfound understanding of how these cells form, while also advancing science closer to stem cell-based therapies to combat disease.
Researchers have for the first time shown that protein factors released by other cells affect the "reprogramming" of adult cells into stem cells known as induced pluripotent stem cells, or iPS cells. The scientists -- who collaborated on this research with colleagues from the University of California, San Francisco (UCSF) -- announce their findings July 5 online in Cell Stem Cell.
Date: July 5, 2012
Summary:
Scientists at the Gladstone Institutes have discovered that environmental factors critically influence the growth of a type of stem cell -- called an iPS cell -- that is derived from adult skin cells. This discovery offers newfound understanding of how these cells form, while also advancing science closer to stem cell-based therapies to combat disease.
Researchers have for the first time shown that protein factors released by other cells affect the "reprogramming" of adult cells into stem cells known as induced pluripotent stem cells, or iPS cells. The scientists -- who collaborated on this research with colleagues from the University of California, San Francisco (UCSF) -- announce their findings July 5 online in Cell Stem Cell.
Wednesday, July 04, 2012
Patient-derived Stem Cells Could Improve Drug Research for Parkinson's
Source: National Institute of Neurological Disorders and Stroke
Date: July 4, 2012
Summary:
Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.
The researchers collected skin cells from patients with genetically inherited forms of Parkinson’s and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability – in particular, abnormalities in the cellular energy factories known as mitochondria. At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.
The results were published in Science Translational Medicine.
Date: July 4, 2012
Summary:
Researchers have taken a step toward personalized medicine for Parkinson's disease, by investigating signs of the disease in patient-derived cells and testing how the cells respond to drug treatments. The study was funded by the National Institutes of Health.
The researchers collected skin cells from patients with genetically inherited forms of Parkinson’s and reprogrammed those cells into neurons. They found that neurons derived from individuals with distinct types of Parkinson's showed common signs of distress and vulnerability – in particular, abnormalities in the cellular energy factories known as mitochondria. At the same time, the cells' responses to different treatments depended on the type of Parkinson's each patient had.
The results were published in Science Translational Medicine.
Tuesday, July 03, 2012
Adult Stem Cells from Bone Marrow: Cell Replacement/Tissue Repair Potential in Adult Bone Marrow Stem Cells in Animal Model
Source: University of Maryland Medical Center
Date: July 3, 2012
Summary:
Baltimore, MD – Researchers from the University of Maryland School of Medicine report promising results from using adult stem cells from bone marrow in mice to help create tissue cells of other organs, such as the heart, brain and pancreas -- a scientific step they hope may lead to potential new ways to replace cells lost in diseases such as diabetes, Parkinson's or Alzheimer's. The research in collaboration with the University of Paris Descartes is published online in the June 29, 2012 edition of Comptes Rendus Biologies, a publication of the French Academy of Sciences.
Date: July 3, 2012
Summary:
Baltimore, MD – Researchers from the University of Maryland School of Medicine report promising results from using adult stem cells from bone marrow in mice to help create tissue cells of other organs, such as the heart, brain and pancreas -- a scientific step they hope may lead to potential new ways to replace cells lost in diseases such as diabetes, Parkinson's or Alzheimer's. The research in collaboration with the University of Paris Descartes is published online in the June 29, 2012 edition of Comptes Rendus Biologies, a publication of the French Academy of Sciences.
Amniotic Fluid Yields Alternatives to Embryonic Stem Cells
Source: Imperial College London
Date: 3 July 2012
Summary:
Stem cells found in amniotic fluid can be transformed into a more versatile state similar to embryonic stem cells, according to a study published July 3 in the journal Molecular Therapy. Scientists from Imperial College London and the UCL Institute of Child Health succeeded in reprogramming amniotic fluid cells without having to introduce extra genes. The findings raise the possibility that stem cells derived from donated amniotic fluid could be stored in banks and used for therapies and in research, providing a viable alternative to the limited embryonic stem cells currently available.
Date: 3 July 2012
Summary:
Stem cells found in amniotic fluid can be transformed into a more versatile state similar to embryonic stem cells, according to a study published July 3 in the journal Molecular Therapy. Scientists from Imperial College London and the UCL Institute of Child Health succeeded in reprogramming amniotic fluid cells without having to introduce extra genes. The findings raise the possibility that stem cells derived from donated amniotic fluid could be stored in banks and used for therapies and in research, providing a viable alternative to the limited embryonic stem cells currently available.
Monday, July 02, 2012
Researchers Block Pathway to Cancer Cell Replication NOTCH1 Signaling Promotes T-Cell Acute Lymphoblastic Leukemia-Initiating Cell Regeneration
Source: University of California - San Diego
Date: July 2, 2012
Summary:
Research suggests that patients with leukemia sometimes relapse because standard chemotherapy fails to kill the self-renewing leukemia initiating cells, often referred to as cancer stem cells. In such cancers, the cells lie dormant for a time, only to later begin cloning, resulting in a return and metastasis of the disease.
One such type of cancer is called pediatric T cell acute lymphoblastic leukemia, or T-ALL, often found in children, who have few treatment options beyond chemotherapy. A team of researchers at the University of California, San Diego School of Medicine studied these cells in mouse models that had been transplanted with human leukemia cells. They discovered that the leukemia initiating cells which clone, or replicate, themselves most robustly activate the NOTCH1 pathway, usually in the context of a mutation.
Earlier studies showed that as many as half of patients with T-ALL have mutations in the NOTCH1 pathway – an evolutionarily conserved developmental pathway used during differentiation of many cell and tissue types. The new study shows that when NOTCH1 activation was inhibited in animal models using a monoclonal antibody, the leukemia initiating cells did not survive. In addition, the antibody treatment significantly reduced a subset of these cancer stem cells (identified by the presence of specific markers, CD2 and CD7, on the cell surface).
The study results suggest that such therapy would also be effective in other types of cancer stem cells, such as those that cause breast cancer, that also rely on NOTCH1 for self-renewal.
Date: July 2, 2012
Summary:
Research suggests that patients with leukemia sometimes relapse because standard chemotherapy fails to kill the self-renewing leukemia initiating cells, often referred to as cancer stem cells. In such cancers, the cells lie dormant for a time, only to later begin cloning, resulting in a return and metastasis of the disease.
One such type of cancer is called pediatric T cell acute lymphoblastic leukemia, or T-ALL, often found in children, who have few treatment options beyond chemotherapy. A team of researchers at the University of California, San Diego School of Medicine studied these cells in mouse models that had been transplanted with human leukemia cells. They discovered that the leukemia initiating cells which clone, or replicate, themselves most robustly activate the NOTCH1 pathway, usually in the context of a mutation.
Earlier studies showed that as many as half of patients with T-ALL have mutations in the NOTCH1 pathway – an evolutionarily conserved developmental pathway used during differentiation of many cell and tissue types. The new study shows that when NOTCH1 activation was inhibited in animal models using a monoclonal antibody, the leukemia initiating cells did not survive. In addition, the antibody treatment significantly reduced a subset of these cancer stem cells (identified by the presence of specific markers, CD2 and CD7, on the cell surface).
The study results suggest that such therapy would also be effective in other types of cancer stem cells, such as those that cause breast cancer, that also rely on NOTCH1 for self-renewal.
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