Posts Tagged ‘research’

AMD Research - The Foundation Fighting Blindness

Stell Cell Research | Posted by admin
Jul 18 2015

New research is underway to develop additional treatments for both dry AMD and wet AMD.Several pharmaceutical companies are currently conducting trials of new drugs, while non-profitfunders like the FFB and the Canadian Institutes of Health Research are working together to speed the translation of treatments from animal studies to human trials.

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The Foundation Fighting Blindness supports scientists who are making incredible advances in understanding and treating age-related macular degeneration. For example in 2009, Dr. Gilbert Bernier identified a genethat helps to control the aging of cells in the eyes and brain. This discovery may one day help us prevent conditions of aging like AMD, Alzheimers and Parkinsons. Learn more about this discovery.

Until that day, research on age-related macular degeneration continues, with the support of donors like you.FFB projects and partnerships help fund pre-clinical studies that make the development of new therapies possible.Here are three ongoing projects that your donations will help to support:

Preventing the Death of Vision Cells in the Eye The FFB has also partnered with the Canadian Institutes of Health Research to support a team of researchers led by Dr. Catherine Tsilfidis at the Ottawa Health Research Institute. This team is exploring ways to slow or stop the death ofphotoreceptors (cells that capture light and allow us to see)in the retina of the eye.While such treatment would not correct the underlying problemthat leads to vision loss, it might preserve sight for many years. The Tsilfidis team has already shown that this approach works to protect the vision of blinded mice. This teamhopes to be ready for human clinical trialstesting this treatmentwithin five years. Learn more about therapies designed to slow cell death.

Producing New Cells to Restore Sight in Failing Eyes Dr. Gilbert Bernier at the Maisonneuve-Rosemont Hospital is receiving FFB funding to explore the use of stem cells as AMD treatment. Stem cells are very simple cells that can become other, more complex, cells to replace photoreceptors damaged by AMD. He recently patented a process that is effective fortransforming stem cells into adult eye cells. His current studies are using mice to test whether these newly created cells will be an effective treatment for AMD. He and his partners hope to begin clinical trials in the next few years.

Identifying the Factors that Cause Abnormal Blood Vessel Growth Wet AMD occurs when the blood vessels beneath the retina grow abnormally and begin leaking blood and fluid. This can cause rapid vision loss. In the past 10 years, factors within the body have been identified which promote rapid blood vessel group, and drugs which block these factors have been shown to protect the vision of people with wet AMD. The currently available drugs target one set of factors, called VEGF (vascular endothelial growth factors) however other potential factors and treatments are being identified. New drugs targetting these factors might be even more effective atcontrolling wet AMD. The Foundation Fighting Blindness funds several Canadian teams working to understand and control these blood vessel growth factors included Dr. Bob Gendron and Helene Paradis in St. John’s Newfoundland, and Dr. Mike Sapieha and Dr. Bruno Larrivee, both based in Montreal.

Clinical Trials of Emerging Treatments for AMD

Link:
AMD Research – The Foundation Fighting Blindness

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Stem Cell Center

Stem Cell Medical Center | Posted by admin
Jul 17 2015

Stem cells are fast becoming relevant to all aspects of our society, with medical, scientific, ethical, political, and economic implications. Therefore it is important that scientists and non-scientists alike be provided with accurate information about stem cell biology. The goals of the UCR Stem Cell Center is to provide the members of the community with a better understanding of the science of stem cells so that they have the necessary tools to make reasoned decisions about the related society issues.

UCR has a strong history in training undergraduate and graduate students and is developing a complete training program in stem cell biology.

Stem cell biology is currently one of the most exciting fields in science with the potential not only to answer basic biological questions but also to provide new therapies and treatments for debilitating diseases. Some of the most important biomedical breakthroughs of this century are likely to come through the use of stem cell technology.

Diseases that could in the future be treated by stem cell biology include (but are not limited to) diabetes, Parkinsons disease, spinal cord injury, Alzheimers disease, aging, heart disease, stroke, burns, amputations, and osteoarthritis.

Stem cell biology will form an important component in both the UCR Health Sciences Research Institute and future Medical School, which will work to facilitate translational research.

Web link to UCR Health Sciences Research Initiative: http://www.hsri.ucr.edu/ Web link to Medical School: http://www.medschool.ucr.edu/

Basic research is needed to understand, control, and use stem cells safely and effectively for therapeutic and environmental purposes.

The UCR Stem Cell Center is making major contributions to stem cell biology by attacking basic biological problems at an interdisciplinary level, enabling translation to the clinical level, and by using stem cells to monitor the effects of the environment on human health.

The Center has faculty working with various types of stem cells including human embryonic, mouse embryonic, hematopoietic, and human umbilical cord stem cells.

Stem cells are valuable tools that have the potential not only to treat numerous diseases, but also to study development and evaluate the toxicity of chemicals and drugs.

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Stem Cell Center

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Regenerating heart tissue through stem cell … - Mayo Clinic

Stem Cell Clinic | Posted by admin
Jul 16 2015

Volume 9, Issue 1 Summary

A groundbreaking study on repairing damaged heart tissue through stem cell therapy has given patients hope that they may again live active lives. An international team of Mayo Clinic researchers and collaborators has done it by discovering a way to regenerate heart tissue.

Clinical trial participant Miroslav Dlacic near his home in Belgrade.

Andre Terzic, M.D., Ph.D., is the Michael S. and Mary Sue Shannon Family Director, Center for Regenerative Medicine, and the Marriott Family Professor of Cardiovascular Diseases Research at Mayo Clinic in Minnesota.

Miroslav Dlacic’s heart attack changed his life drastically and seemingly forever. His damaged heart made him too tired to work in his garden or to spend much time at his leather-accessories workshop in Belgrade, Serbia. Like many patients with heart problems, Dlacic, who is 71, thought he would live his remaining years in a weakened condition.

Then, a groundbreaking Mayo Clinic trial of stem cell therapy to repair damaged heart tissue changed his life again this time for the better.

Dlacic agreed to participate in the Mayo Clinic stem cell trial through the hospital in Serbia where he is treated. Two years later, Dlacic is able to walk again without becoming worn out.

“I am more active, more peppy,” he says. “I feel quite well.”

“It’s a paradigm shift,” says Andre Terzic, M.D., Ph.D., director of Mayo Clinic’s Center for Regenerative Medicine and senior investigator of the stem cell trial. “We are moving from traditional medicine, which addresses the symptoms of disease, to being legitimately able to cure disease.”

For decades, treating patients with cardiac disease has typically involved managing heart damage with medication. It’s a bit like driving a car without fixing a sluggish engine you manage the consequences as best you can and learn to live with them.

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Regenerating heart tissue through stem cell … – Mayo Clinic

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The Case for Adult Stem Cell Research

Adult Stem Cells | Posted by admin
Jul 03 2015

For more articles on biology and medicine, see Biology and Medicine categories in index.

BIOLOGY & MEDICINE

The Case for Adult Stem Cell Research

by Wolfgang Lillge, M.D.

(Full text of article from Winter 2001-2002 21st Century)

Problems of Therapeutic Cloning

Whoever Would Cure, Must Use Adult Stem Cells

Human Treatments

For more articles on biology and medicine, check the subject index

The question of stem cells is currently the dominant subject in the debate over biotechnology and human genetics: Should we use embryonic stem cells or adult stem cells for future medical therapies? Embryonic stem cells are taken from a developing embryo at the blastocyst stage, destroying the embryo, a developing human life. Adult stem cells, on the other hand, are found in all tissues of the growing human being and, according to latest reports, also have the potential to transform themselves into practically all other cell types, or revert to being stem cells with greater reproductive capacity. Embryonic stem cells have not yet been used for even one therapy, while adult stem cells have already been successfully used in numerous patients, including for cardiac infarction (death of some of the heart tissue).

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The Case for Adult Stem Cell Research

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Embryonic Stem Cell Research Pros and Cons | HRF

Embryonic Stem Cells | Posted by admin
Jul 02 2015

There may not be a greater debate in the medical community right now than that of embryonic stem cell research. Initially banned by the Federal government, these stem cells often originate from human embryos that were created for couples with reproductive issues and would be discarded. These stem cells are thought to be the key that will unlock the cure to many diseases, from Alzheimers to rare immune and even genetic disorders. On the other side of the issue, some see the destruction of an embryo as the murder of an unborn child.

The primary benefit of this research is the enormous amount of potential that it holds. Embryonic stem cells have the ability to create new organs, tissues, and systems within the human body. With a little guidance from scientists, these stem cells have shown that they can become new organs, new blood vessels, and even new ligaments for those with ACL tears. By culturing stem cells and them implanting them, recovery times could be halved for many serious injuries, illnesses, and diseases.

Because nearly one-third of the population could benefit from treatments and therapies that could originate from embryonic stem cell research, many scientists believe that this field could alleviate as much human suffering as the development of antibiotics was able to do. Because funding was restricted on embryonic stem cell lines for several years, however, the chances of any therapies being viable in the near future are slim.

The primary argument against this research is a moral one. Some people see the creation of an embryo as the creation of life, so to terminate that life would equate to murder. This primarily originates from a point of view where life as we define it begins at conception, which would mean that any medical advancement from this research would be at best unethical.

Those against this research argue that since the creation of this research field in the early 1980s, there have been no advancements in it whatsoever. Because of this lack of advancement, it could mean decades of additional research, thousands of embryos destroyed to further that research, and that is morally unacceptable for some.

The debate about embryonic stem cell research isnt in the potential benefits that this field of study could produce. It is in the ethics and morality of how embryonic stem cells are created. There often is no in-between view in this area: you either define life at some part of the physical development of the human body during the pregnancy or you define it at conception. This view then tends to lead each person to one side of this debate. Where do you stand?

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Embryonic Stem Cell Research Pros and Cons | HRF

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NIH Human Embryonic Stem Cell Registry - Research Using …

Embryonic Stem Cells | Posted by admin
Jun 22 2015

CHB-1 (see details) 0001 On Hold ** George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-2 (see details) 0002 On Hold ** George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-3 (see details) 0003 On Hold ** George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-4 (see details) 0004 George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-5 (see details) 0005 George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-6 (see details) 0006 George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-8 (see details) 0007 George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-9 (see details) 0008 George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-10 (see details) 0009 George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-11 (see details) 0010 George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 CHB-12 (see details) 0011 George Q. Daley, M.D., Ph.D. Children’s Hospital Corporation 12/02/2009 RUES1 (see details) 0012 The Rockefeller University, Ali Brivanlou The Rockefeller University 12/02/2009 RUES2 (see details) 0013 The Rockefeller University, Ali Brivanlou The Rockefeller University 12/02/2009 HUES 1 (see details) 0014 HSCI iPS Core Harvard University 12/14/2009 HUES 2 (see details) 0015 HSCI iPS Core Harvard University 12/14/2009 HUES 3 (see details) 0016 HSCI iPS Core Harvard University 12/14/2009 HUES 4 (see details) 0017 HSCI iPS Core Harvard University 12/14/2009 HUES 5 (see details) 0018 HSCI iPS Core Harvard University 12/14/2009 HUES 6 (see details) 0019 HSCI iPS Core Harvard University 12/14/2009 HUES 7 (see details) 0020 HSCI iPS Core Harvard University 12/14/2009 HUES 8 (see details) 0021 HSCI iPS Core Harvard University 12/14/2009 HUES 9 (see details) 0022 HSCI iPS Core Harvard University 12/14/2009 HUES 10 (see details) 0023 HSCI iPS Core Harvard University 12/14/2009 HUES 11 (see details) 0024 HSCI iPS Core Harvard University 12/14/2009 HUES 12 (see details) 0025 HSCI iPS Core Harvard University 12/14/2009 HUES 13 (see details) 0026 HSCI iPS Core Harvard University 12/14/2009 HUES 14 (see details) 0027 HSCI iPS Core Harvard University 12/14/2009 HUES 15 (see details) 0028 HSCI iPS Core Harvard University 12/14/2009 HUES 16 (see details) 0029 HSCI iPS Core Harvard University 12/14/2009 HUES 17 (see details) 0030 HSCI iPS Core Harvard University 12/14/2009 HUES 18 (see details) 0031 HSCI iPS Core Harvard University 12/14/2009 HUES 19 (see details) 0032 HSCI iPS Core Harvard University 12/14/2009 HUES 20 (see details) 0033 HSCI iPS Core Harvard University 12/14/2009 HUES 21 (see details) 0034 HSCI iPS Core Harvard University 12/14/2009 HUES 22 (see details) 0035 HSCI iPS Core Harvard University 12/14/2009 HUES 23 (see details) 0036 HSCI iPS Core Harvard University 12/14/2009 HUES 24 (see details) 0037 HSCI iPS Core Harvard University 12/14/2009 HUES 26 (see details) 0038 HSCI iPS Core Harvard University 12/14/2009 HUES 27 (see details) 0039 HSCI iPS Core Harvard University 12/14/2009 HUES 28 (see details) 0040 HSCI iPS Core Harvard University 12/14/2009 CyT49 (see details) 0041 ViaCyte, Inc. 01/19/2010 RUES3 (see details) 0042 The Rockefeller University, Ali Brivanlou The Rockefeller University 01/19/2010 WA01 (H1) (see details) 0043 WiCell Research Institute WiCell Research Institute 01/29/2010 UCSF4 (see details) 0044 Susan Fisher University of California San Francisco 03/12/2010 NYUES1 (see details) 0045 Christoph Hansis, MD, PhD New York University School of Medicine 03/29/2010 NYUES2 (see details) 0046 Christoph Hansis, MD, PhD New York University School of Medicine 03/29/2010 NYUES3 (see details) 0047 Christoph Hansis, MD, PhD New York University School of Medicine 03/29/2010 NYUES4 (see details) 0048 Christoph Hansis, MD, PhD New York University School of Medicine 03/29/2010 NYUES5 (see details) 0049 Christoph Hansis, MD, PhD New York University School of Medicine 03/29/2010 NYUES6 (see details) 0050 Christoph Hansis, MD, PhD New York University School of Medicine 03/29/2010 NYUES7 (see details) 0051 Christoph Hansis, MD, PhD New York University School of Medicine 03/29/2010 MFS5; disease-specific mutation (see details) 0052 Eric Chiao Stanford University 04/27/2010 HUES 48 (see details) 0053 HSCI iPS Core Harvard University 04/27/2010 HUES 49 (see details) 0054 HSCI iPS Core Harvard University 04/27/2010 HUES 53 (see details) 0055 HSCI iPS Core Harvard University 04/27/2010 HUES 65 (see details) 0056 HSCI iPS Core Harvard University 04/27/2010 HUES 66 (see details) 0057 HSCI iPS Core Harvard University 04/27/2010 UCLA 1 (see details) 0058 Steven Peckman University of California, Los Angeles 04/27/2010 UCLA 2 (see details) 0059 Steven Peckman University of California, Los Angeles 04/27/2010 UCLA 3 (see details) 0060 Steven Peckman University of California, Los Angeles 04/27/2010 WA07 (H7) (see details) 0061 WiCell Research Institute WiCell Research Institute 04/27/2010 WA09 (H9) (see details) 0062 WiCell Research Institute WiCell Research Institute 04/27/2010 WA13 (H13) (see details) 0063 WiCell Research Institute WiCell Research Institute 04/27/2010 WA14 (H14) (see details) 0064 WiCell Research Institute WiCell Research Institute 04/27/2010 HUES 62 (see details) 0065 HSCI iPS Core Harvard University 06/03/2010 HUES 63 (see details) 0066 HSCI iPS Core Harvard University 06/03/2010 HUES 64 (see details) 0067 HSCI iPS Core Harvard University 06/03/2010 CT1 (see details) 0068 University of Connecticut Stem Cell Core UNIVERSITY OF CONNECTICUT SCH OF MED/DNT 06/21/2010 CT2 (see details) 0069 University of Connecticut Stem Cell Core UNIVERSITY OF CONNECTICUT SCH OF MED/DNT 06/21/2010 CT3 (see details) 0070 University of Connecticut Stem Cell Core UNIVERSITY OF CONNECTICUT SCH OF MED/DNT 06/21/2010 CT4 (see details) 0071 University of Connecticut Stem Cell Core UNIVERSITY OF CONNECTICUT SCH OF MED/DNT 06/21/2010 MA135 (see details) 0072 Advanced Cell Technology, Inc. Advanced Cell Technology, Inc. 06/21/2010 Endeavour-2 (see details) 0073 Kuldip Sidhu Stem Cell Laboratory, Faculty of medicine, University of New South Wales 06/21/2010 WIBR1 (see details) 0074 Whitehead Institute for Biomedical Research/Maya Mitalipova Whitehead Institute for Biomedical Research 06/21/2010 WIBR2 (see details) 0075 Whitehead Institute for Biomedical Research/Maya Mitalipova Whitehead Institute for Biomedical Research 06/21/2010 HUES 45 (see details) 0076 HSCI iPS Core Harvard University 09/28/2010 Shef 3 (see details) 0077 Centre for Stem Cell Biology University of Sheffield 11/17/2010 Shef 6 (see details) 0078 Centre for Stem Cell Biology University of Sheffield 11/17/2010 WIBR3 (see details) 0079 Whitehead Institute for Biomedical Research/Maya Mitalipova Whitehead Institute for Biomedical Research 11/17/2010 WIBR4 (see details) 0080 Whitehead Institute for Biomedical Research/Maya Mitalipova Whitehead Institute for Biomedical Research 11/17/2010 WIBR5 (see details) 0081 Whitehead Institute for Biomedical Research/Maya Mitalipova Whitehead Institute for Biomedical Research 11/17/2010 WIBR6 (see details) 0082 Whitehead Institute for Biomedical Research/Maya Mitalipova Whitehead Institute for Biomedical Research 11/17/2010 BJNhem19 (see details) 0083 Jawaharlal Nehru Centre for Advanced Scientific Research Jawaharlal Nehru Centre for Advanced Scientific Research 12/17/2010 BJNhem20 (see details) 0084 Jawaharlal Nehru Centre for Advanced Scientific Research Jawaharlal Nehru Centre for Advanced Scientific Research 12/17/2010 SA001 (see details) 0085 Cellartis AB Cellartis AB 12/17/2010 SA002; abnormal karyotype (see details) 0086 Cellartis AB Cellartis AB 12/17/2010 UCLA 4 (see details) 0087 Steven Peckman University of California Los Angeles 02/03/2011 UCLA 5 (see details) 0088 Steven Peckman University of California Los Angeles 02/03/2011 UCLA 6 (see details) 0089 Steven Peckman University of California Los Angeles 02/03/2011 HUES PGD 13; disease-specific mutation (see details) 0090 Eggan Lab Harvard University 03/15/2011 HUES PGD 3; disease-specific mutation (see details) 0091 Eggan Lab Harvard University 03/15/2011 ESI-014 (see details) 0092 BioTime, Inc. 06/02/2011 ESI-017 (see details) 0093 BioTime, Inc. BioTime, Inc. 06/02/2011 HUES PGD 11; disease-specific mutation (see details) 0094 Eggan Lab Harvard University 06/07/2011 HUES PGD 12; disease-specific mutation (see details) 0095 Eggan Lab Harvard University 06/07/2011 WA15 (see details) 0096 WiCell Research Institute WiCell Research Institute 06/09/2011 WA16; disease-specific mutation/abnormal karyotype (see details) 0097 WiCell Research Institute WiCell Research Institute 06/09/2011 WA17 (see details) 0098 WiCell Research Institute WiCell Research Institute 06/09/2011 WA18 (see details) 0099 WiCell Research Institute WiCell Research Institute 06/09/2011 WA19 (see details) 0100 WiCell Research Institute WiCell Research Institute 06/09/2011 WA20 (see details) 0101 WiCell Research Institute WiCell Research Institute 06/09/2011 WA21 (see details) 0102 WiCell Research Institute WiCell Research Institute 06/09/2011 WA22 (see details) 0103 WiCell Research Institute WiCell Research Institute 06/09/2011 WA23 (see details) 0104 WiCell Research Institute WiCell Research Institute 06/09/2011 WA24 (see details) 0105 WiCell Research Institute WiCell Research Institute 06/09/2011 CSES2 (see details) 0106 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES4 (see details) 0107 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES7 (see details) 0108 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES8; abnormal karyotype (see details) 0109 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES11; abnormal karyotype (see details) 0110 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES12; abnormal karyotype (see details) 0111 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES13; abnormal karyotype (see details) 0112 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES14; abnormal karyotype (see details) 0113 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES15 (see details) 0114 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES17 (see details) 0115 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES19 (see details) 0116 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES20; abnormal karyotype (see details) 0117 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES21; abnormal karyotype (see details) 0118 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES22; abnormal karyotype (see details) 0119 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES23; abnormal karyotype (see details) 0120 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES24; abnormal karyotype (see details) 0121 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 CSES25 (see details) 0122 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 06/10/2011 HAD-C 100 (see details) 0123 Benjamin E. Reubinoff Hadassah Hebrew University Medical Center 06/16/2011 HAD-C 102 (see details) 0124 Benjamin E. Reubinoff Hadassah Hebrew University Medical Center 06/16/2011 HAD-C 106 (see details) 0125 Benjamin E. Reubinoff Hadassah Hebrew University Medical Center 06/16/2011 RNJ19; disease-specific mutation (see details) 0126 Reprogenetics, LLC Reprogenetics, LLC 06/16/2011 RNJ20; disease-specific mutation (see details) 0127 Reprogenetics, LLC Reprogenetics, LLC 06/16/2011 RNJ18; disease-specific mutation (see details) 0128 Reprogenetics, LLC Reprogenetics, LLC 06/16/2011 ESI-035 (see details) 0129 BioTime, Inc. BioTime, Inc. 08/18/2011 ESI-049 (see details) 0130 BioTime, Inc. BioTime, Inc. 08/18/2011 ESI-051 (see details) 0131 BioTime, Inc. BioTime, Inc. 08/18/2011 ESI-053 (see details) 0132 BioTime, Inc. BioTime, Inc. 08/18/2011 CSES5; abnormal karyotype (see details) 0133 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 09/27/2011 CSES6; abnormal karyotype (see details) 0134 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 09/27/2011 CSES18 (see details) 0135 Dhruv Sareen, Ph.D. Cedars-Sinai Medical Center 09/27/2011 HUES PGD 14; disease-specific mutation (see details) 0136 Eggan Lab Harvard University 10/11/2011 CA1 (see details) 0137 Andras Nagy Mt Sinai Hosp-Samuel Lunenfeld Research Institute 12/12/2011 CA2 (see details) 0138 Andras Nagy Mt Sinai Hosp-Samuel Lunenfeld Research Institute 12/12/2011 MEL-1 (see details) 0139 StemCore, Stem Cells Ltd University of Queensland 12/22/2011 MEL-2 (see details) 0140 StemCore, Stem Cells Ltd University of Queensland 12/22/2011 MEL-3 (see details) 0141 StemCore, Stem Cells Ltd University of Queensland 12/22/2011 MEL-4 (see details) 0142 StemCore, Stem Cells Ltd University of Queensland 12/22/2011 UCLA 7; disease-specific mutation/abnormal karyotype (see details) 0143 Steven Peckman University of California, Los Angeles 01/12/2012 UCLA 8 (see details) 0144 Steven Peckman University of California, Los Angeles 01/12/2012 UCLA 9 (see details) 0145 Steven Peckman University of California, Los Angeles 01/12/2012 UCLA 10 (see details) 0146 Steven Peckman University of California, Los Angeles 01/12/2012 UM4-6 (see details) 0147 Gary D. Smith, University of Michigan University of Michigan 02/02/2012 HUES PGD 1; disease-specific mutation (see details) 0148 Eggan Lab Harvard University 02/24/2012 HUES PGD 15; possible disease-specific mutation (see details) 0149 Eggan Lab Harvard University 02/24/2012 HUES PGD 16; disease-specific mutation (see details) 0150 Eggan Lab Harvard University 02/24/2012 GENEA002 (see details) 0151 Genea Biocells Genea Biocells 03/20/2012 GENEA048; abnormal karyotype (see details) 0152 Genea Biocells Genea Biocells 03/20/2012 UM11-1PGD; disease-specific mutation (see details) 0153 Gary D. Smith, University of Michigan University of Michigan 04/12/2012 UM9-1PGD; disease-specific mutation (see details) 0154 Gary D. Smith, University of Michigan University of Michigan 05/14/2012 UM38-2 PGD; disease-specific mutation (see details) 0155 Gary D. Smith, University of Michigan University of Michigan 05/14/2012 Elf1 (see details) 0156 University of Washington 05/15/2012 HUES 42 (see details) 0157 HSCI iPS Core Harvard University 05/31/2012 HUES 44 (see details) 0158 HSCI iPS Core Harvard University 05/31/2012 NMR-1 (see details) 0159 Rick A. Wetsel, Ph.D. University of Texas Hlth Sci Ctr Houston 05/31/2012 UM17-1 PGD; disease-specific mutation (see details) 0160 Gary D. Smith/University of Michigan University of Michigan 05/31/2012 UM15-4 PGD; disease-specific mutation (see details) 0161 University of Michigan, Gary D. Smith University of Michigan 05/31/2012 UM14-1 (see details) 0162 Gary D. Smith/University of Michigan University of Michigan 05/31/2012 UM14-2 (see details) 0163 Gary D. Smith/University of Michigan University of Michigan 05/31/2012 UM29-2 PGD; disease-specific mutation (see details) 0164 Gary D. Smith/University of Michigan University of Michigan 06/18/2012 UM29-3 PGD; disease-specific mutation (see details) 0165 Gary D. Smith/University of Michigan University of Michigan 06/18/2012 GENEA017; disease-specific mutation (see details) 0166 Genea Biocells Genea Biocells 06/20/2012 GENEA041; disease-specific mutation (see details) 0167 Genea Biocells Genea Biocells 06/20/2012 GENEA068; disease-specific mutation (see details) 0168 Genea Biocells Genea Biocells 06/20/2012 GENEA018; disease-specific mutation (see details) 0169 Genea Biocells Genea Biocells 06/20/2012 GENEA024; disease-specific mutation (see details) 0170 Genea Biocells Genea Biocells 06/20/2012 GENEA040; disease-specific mutation (see details) 0171 Genea Biocells Genea Biocells 06/20/2012 GENEA060; disease-specific mutation (see details) 0172 Genea Biocells Genea Biocells 06/20/2012 GENEA061; disease-specific mutation (see details) 0173 Genea Biocells Genea Biocells 06/20/2012 GENEA064; disease-specific mutation (see details) 0174 Genea Biocells Genea Biocells 06/20/2012 GENEA059; disease-specific mutation (see details) 0175 Genea Biocells Genea Biocells 07/09/2012 HUES 68 (see details) 0176 HSCI iPS Core Harvard University 07/09/2012 HUES 70 (see details) 0177 HSCI iPS Core Harvard University 07/09/2012 HUES 69 (see details) 0178 HSCI iPS Core Harvard University 08/07/2012 HUES PGD 10 (see details) 0179 Eggan Lab Harvard University 09/24/2012 GENEA046; disease-specific mutation (see details) 0180 Genea Biocells Genea Biocells 10/05/2012 GENEA069; disease-specific mutation (see details) 0181 Genea Biocells Genea Biocells 10/05/2012 GENEA070; disease-specific mutation (see details) 0182 Genea Biocells Genea Biocells 10/05/2012 GENEA049; disease-specific mutation (see details) 0183 Genea Biocells Genea Biocells 11/02/2012 GENEA050; disease-specific mutation (see details) 0184 Genea Biocells Genea Biocells 11/02/2012 UCLA 11 (see details) 0185 Steven Peckman University of California, Los Angeles 11/20/2012 UCLA 12 (see details) 0186 Steven Peckman University of California, Los Angeles 11/20/2012 GENEA062; disease-specific mutation (see details) 0187 Genea Biocells Genea Biocells 12/14/2012 GENEA063; disease-specific mutation (see details) 0188 Genea Biocells Genea Biocells 12/14/2012 GENEA066; disease-specific mutation (see details) 0189 Genea Biocells Genea Biocells 12/14/2012 GENEA067; disease-specific mutation (see details) 0190 Genea Biocells Genea Biocells 12/14/2012 GENEA071; disease-specific mutation (see details) 0191 Genea Biocells Genea Biocells 12/14/2012 GENEA072; disease-specific mutation (see details) 0192 Genea Biocells Genea Biocells 12/14/2012 GENEA073; disease-specific mutation (see details) 0193 Genea Biocells Genea Biocells 12/14/2012 GENEA074; disease-specific mutation (see details) 0194 Genea Biocells Genea Biocells 12/14/2012 HUES PGD 2; possible disease-specific mutation (see details) 0195 Eggan Lab Harvard University 12/14/2012 WA25 (see details) 0196 WiCell Research Institute WiCell Research Institute 12/14/2012 WA26 (see details) 0197 WiCell Research Institute WiCell Research Institute 12/14/2012 WA27 (see details) 0198 WiCell Research Institute WiCell Research Institute 12/14/2012 GENEA058; Disease-specific mutation (see details) 0199 Genea Biocells Genea Biocells 01/08/2013 GENEA065; Disease-specific mutation (see details) 0200 Genea Biocells Genea Biocells 01/08/2013 HS346 (see details) 0201 Karolinska Institute Karolinska Institute 03/18/2013 HS401 (see details) 0202 Karolinska Institute Karolinska Institute 03/18/2013 HS420 (see details) 0203 Karolinska Institute Karolinska Institute 03/18/2013 I3 (TE03) (see details) 0204 Technion R&D foundation Technion R&D Foundation 03/18/2013 I4 (TE04) (see details) 0205 Technion R&D foundation Technion R&D Foundation 03/18/2013 I6 (TE06) (see details) 0206 Technion R&D foundation Technion R&D Foundation 03/18/2013 HS799; disease-specific mutation (see details) 0207 Karolinska Institute Karolinska Institute 03/18/2013 UM57-1 PGD; disease-specific mutation (see details) 0208 Gary D. Smith/University of Michigan University of Michigan 03/26/2013 UM22-2 (see details) 0209 Gary D. Smith/University of Michigan University of Michigan 03/26/2013 CR-4 (see details) 0210 Rick A. Wetsel, Ph.D. University of Texas Hlth Sci Ctr at Houston 05/29/2013 WCMC-37; disease-specific mutation (see details) 0211 Weill Cornell Medical College- Nikica Zaninovic, PhD and Zev Rosenwaks, MD Joan & Sanford I. Weill Medical College of Cornell University 06/27/2013 KCL011 (see details) 0212 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL012; disease-specific mutation (see details) 0213 Dusko Ilic, King’s College London King’s College London 09/19/2013 KC013; disease-specific mutation (see details) 0214 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL015; disease-specific mutation (see details) 0215 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL016; disease-specific mutation (see details) 0216 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL017; disease-specific mutation (see details) 0217 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL018; disease-specific mutation (see details) 0218 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL021; disease-specific mutation (see details) 0219 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL024; disease-specific mutation (see details) 0220 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL025; disease-specific mutation (see details) 0221 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL026; disease-specific mutation (see details) 0222 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL027; disease-specific mutation (see details) 0223 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL028; disease-specific mutation (see details) 0224 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL029; disease-specific mutation (see details) 0225 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL030; disease-specific mutation (see details) 0226 Dusko Ilic, King’s College London King’s College London 09/19/2013 KCL035; disease-specific mutation (see details) 0227 Dusko Ilic, King’s College London King’s College London 09/19/2013 GENEA015 (see details) 0228 Genea Biocells Genea Biocells 09/30/2013 GENEA016 (see details) 0229 Genea Biocells Genea Biocells 09/30/2013 GENEA047 (see details) 0230 Genea Biocells Genea Biocells 09/30/2013 GENEA042 (see details) 0231 Genea Biocells Genea Biocells 09/30/2013 GENEA043 (see details) 0232 Genea Biocells Genea Biocells 09/30/2013 GENEA057 (see details) 0233 Genea Biocells Genea Biocells 09/30/2013 GENEA052 (see details) 0234 Genea Biocells Genea Biocells 09/30/2013 NYUES12 (see details) 0235 Christoph Hansis, MD, PhD New York University School of Medicine 12/23/2013 NYUES11; abnormal karyotype (see details) 0236 Christoph Hansis, MD, PhD New York University School of Medicine 12/23/2013 NYUES13 (see details) 0237 Christoph Hansis, MD, PhD New York University School of Medicine 12/23/2013 NYUES8 (see details) 0238 Christoph Hansis, MD, PhD New York University School of Medicine 12/23/2013 NYUES9 (see details) 0239 Christoph Hansis, MD, PhD New York University School of Medicine 12/23/2013 NYUES10 (see details) 0240 Christoph Hansis, MD, PhD New York University School of Medicine 12/23/2013 KCL036; disease-specific mutation (see details) 0241 Dusko Ilic, King’s College London King’s College London 12/23/2013 KCL042; disease-specific mutation (see details) 0242 Dusko Ilic, King’s College London King’s College London 12/23/2013 KCL043; disease-specific mutation (see details) 0243 Dusko Ilic, King’s College London King’s College London 12/23/2013 GENEA096; disease-specific mutations (see details) 0244 Genea Biocells Genea Biocells 01/29/2014 GENEA090; disease-specific mutations (see details) 0245 Genea Biocells Genea Biocells 01/29/2014 GENEA091; disease-specific mutations (see details) 0246 Genea Biocells Genea Biocells 01/29/2014 GENEA089; disease-specific mutations (see details) 0247 Genea Biocells Genea Biocells 01/29/2014 GENEA097; disease-specific mutations (see details) 0248 Genea Biocells Genea Biocells 01/29/2014 GENEA098; disease-specific mutations (see details) 0249 Genea Biocells Genea Biocells 01/29/2014 GENEA085 ; disease-specific mutation (see details) 0250 Genea Biocells Genea Biocells 01/29/2014 GENEA082 ; disease-specific mutation, abnormal karyotype (see details) 0251 Genea Biocells Genea Biocells 01/29/2014 GENEA078 ; disease-specific mutation (see details) 0252 Genea Biocells Genea Biocells 01/29/2014 GENEA079 ; disease-specific mutation (see details) 0253 Genea Biocells Genea Biocells 01/29/2014 GENEA080 ; disease-specific mutation (see details) 0254 Genea Biocells Genea Biocells 01/29/2014 GENEA081 ; disease-specific mutation (see details) 0255 Genea Biocells Genea Biocells 01/29/2014 GENEA083; disease-specific mutations, abnormal karyotype (see details) 0256 Genea Biocells Genea Biocells 01/29/2014 GENEA084 ; disease-specific mutation (see details) 0257 Genea Biocells Genea Biocells 01/29/2014 GENEA086 ; disease-specific mutation (see details) 0258 Genea Biocells Genea Biocells 01/29/2014 GENEA087 ; disease-specific mutation (see details) 0259 Genea Biocells Genea Biocells 01/29/2014 GENEA088 ; disease-specific mutation (see details) 0260 Genea Biocells Genea Biocells 01/29/2014 GENEA077; disease-specific mutation (see details) 0261 Genea Biocells Genea Biocells 01/29/2014 KCL023 (see details) 0262 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL031 (see details) 0263 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL022 (see details) 0264 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL038 (see details) 0265 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL032 (see details) 0266 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL033 (see details) 0267 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL034 (see details) 0268 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL037 (see details) 0269 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL019 (see details) 0270 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL020 (see details) 0271 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL040 (see details) 0272 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL041; abnormal karyotype/disease-specific mutation (see details) 0273 Dusko Ilic, King’s College London King’s College London 03/25/2014 KCL039 (see details) 0274 Dusko Ilic, King’s College London King’s College London 03/25/2014 UM59-2 PGD; disease-specific mutation (see details) 0275 Gary D. Smith/University of Michigan University of Michigan 04/09/2014 UM89-1 PGD; disease-specific mutation (see details) 0276 Gary D. Smith/University of Michigan University Of Michigan 04/09/2014 UM63-1 (see details) 0277 Gary D. Smith/University of Michigan University of Michigan 04/09/2014 UM77-2 (see details) 0278 Gary D. Smith / University of Michigan University of Michigan 04/09/2014 UM33-4 (see details) 0279 Gary D. Smith / University of Michigan University of Michigan 04/09/2014 HUES 75 (see details) 0280 Eggan Lab Harvard University 07/31/2014 HUES 71 (see details) 0281 Eggan Lab Harvard University 07/31/2014 HUES 72 (see details) 0282 Eggan Lab Harvard University 07/31/2014 HUES 73 (see details) 0283 Eggan Lab Harvard University 07/31/2014 CSC14 (see details) 0284 NeoStem, Inc. (Irvine) NeoStem, Inc. 09/18/2014 UM112-1 PGD; disease-specific mutation (see details) 0285 Gary D. Smith / University of Michigan University of Michigan 09/29/2014 UM134-1 PGD; disease-specific mutation (see details) 0286 Gary D. Smith / University of Michigan University of Michigan 09/29/2014 UM90-12 PGS; abnormal karyotype (see details) 0287 Gary D. Smith / University of Michigan University of Michigan 09/29/2014 UM78-2 (see details) 0288 Gary D. Smith / University of Michigan University of Michigan 09/29/2014 UM76-1 PGS; abnormal karyotype (see details) 0289 Gary D. Smith / University of Michigan University of Michigan 09/29/2014 UM114-10 (see details) 0290 Gary D. Smith / University of Michigan University of Michigan 09/29/2014 UM121-7 (see details) 0291 Gary D. Smith / University of Michigan University of Michigan 09/29/2014 UM139-2 PGD; disease-specific mutation (see details) 0292 Gary D. Smith / University of Michigan University of Michigan 09/29/2014 UCLA 13 (see details) 0293 Steven Peckman University of California, Los Angeles 10/16/2014 UCLA 14 (see details) 0294 Steven Peckman University of California, Los Angeles 10/16/2014 UCLA 15 (see details) 0295 Steven Peckman University of California, Los Angeles 10/16/2014 UCLA 16 (see details) 0296 Steven Peckman University of California, Los Angeles 10/16/2014 UCLA 17 (see details) 0297 Steven Peckman University of California, Los Angeles 10/16/2014 UCLA 18 (see details) 0298 Steven Peckman University of California, Los Angeles 10/16/2014 WIN-1 (see details) 0299 Whitehead Institute for Biomedical Research/Maisam Mitalipova Whitehead Institute for Biomedical Research 10/16/2014 WIN-2 (see details) 0300 Whitehead Institute for Biomedical Research/Maisam Mitalipova Whitehead Institute for Biomedical Research 10/16/2014 WIN-3 (see details) 0301 Whitehead Institute for Biomedical Research/Maisam Mitalipova Whitehead Institute for Biomedical Research 10/16/2014 WIN-4 (see details) 0302 Whitehead Institute for Biomedical Research/Maisam Mitalipova Whitehead Institute for Biomedical Research 10/16/2014 WIN-5 (see details) 0303 Whitehead Institute for Biomedical Research/Maisam Whitehead Institute for Biomedical Research 10/16/2014 HUES 74 (see details) 0304 Eggan Lab Harvard University 04/02/2015 UM25-2 (see details) 0305 Gary D. Smith / University of Michigan University of Michigan 04/02/2015 UM90-14 PGD; disease-specific mutation (see details) 0306 Gary D. Smith/ University of Michigan University of Michigan 04/02/2015 UM112-2 PGD; disease-specific mutation (see details) 0307 Gary D. Smith/ University of Michigan University of Michigan 04/02/2015

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Autism - Wu Medical Center - A Leading Medical Center for …

Stem Cell Medical Center | Posted by admin
Jun 11 2015

Stem Cell Therapy for AutismMay 25th, 2015

Like Wu, Xiaojuan Wang, Freda Peng, Bo Cheng, Susan Chu

Wu Medical Center

The patient is 8-year-old boy. He was presented with language, mental, behavioral and human communication disorders for the past 5 years. He was diagnosed as Autism. He was born full-term with normal delivery. He was hyperactive, upset, agitated, impaired language development and was unable to communicate with others when he was 2 years old.

Physical examination: he was stable, Skin and mucous membrane were with no yellow stain or petechia. His heart and lung were normal. He was alert, his comprehension, judgment, attention and adaptability were bad. He was hyperactive, upset, unquiet, soliloquize and he couldnt answer questions. He could count from 1-10. He couldnt cooperate with the memory, calculation ability, or orientation examinations. He seldom had eye contact with others. He couldnt cooperate with the cranial nerves, sensation and coordinated movement during examinations. The muscle power of four limbs was at level 5, his muscle tension was normal. The tendon reflex decreased. The pathological sign was negative. All of the laboratory examination and accessory examinations were normal. He was diagnosed as Autism.

Treatment target: increase the number of normal neural stem cells (NSCs) in the brain, switch on neural development, repair and regenerate the nerves. Increase the brain function, improve the patients cognitive function and communication skills.

Treatment procedure and results: We gave the patient 4 times neural stem cells (NSCs) and 4 times mesenchymal stem cells (MSCs) implantation treatment. The stem cells were activated in the patients body to repair the damaged nerves. Together with nourishment of the neurons, improve circulation, regulating the immune, daily rehabilitation training was incorporated. After the treatment, the patient was stable, developed a good spirit and mood. He seldom gets upset and he developed more concentration. He could see movies or listen to music by himself, and the duration was increased to between 30-40 minutes than before. He speaks more with family members. He could answer questions and gained more vocabulary. He could say a sentence which is made up of 6 words. His learning skill was better. The memory, calculation ability, orientation, comprehension and attention were better. He had more eye contact with others. His nerves, sensation, coordinated movement examinations and meningeal irritation sign examination cooperation degree was better.

Case analysis: Autism is also called autistic disorder, it is one subtype of the catholicity eccyliosis. Male patients were more than female as observed. This disease onset at early infancy. The cardinal symptoms: various degrees of speech disturbance, human communication disorders, less interesting or mechanic behavior. Around 3/4 young patients accompanied with visible mental retardation. The main pathogen was unclear, it may be: heredity, perinatal period factors, abnormal immune system or imbalance of various neuroendocrine and neurotransmitter function. The patient had this disease from very young, the pathogen was unclear, and his symptoms were: abnormal mind and behaviors, cognitive disorder, bad communication skills and excitement.

There are a lot of methods to treat autism, but most of them lack medical evidences and there is no best treatment plan. Our center uses advanced NSCs transplantation technique to treats patients with autism. The NSCs is used together with MSCs to make the imbedded NSCs increase the number of brain and spinal cord nerve cells, promotes nerve differentiation and growth to improve his cognition and mental. This technique was used in this patient and he recovered well and not only his cognition and mental, his self-care ability and social skills were improved also. This provided relief of mental stress and daily burden to his relatives. This brings hope to patients with this disease.

Research under our direction, the treatment result was satisfactory. During retrospective experiment on animals, we found the same program had made great advances in nerve precursor cells structure, migration, cortical tissue, neuron differentiation and connection. For example: a small group of neurons migration lag in specific area or appear in ectopia area of the patient, could result in mental hypoevolutism, epilepsy or speech impediment. This can be fixed with implantation of nerve precursor cell. The shape and structure of cortex can be normal. The safety of this treatment was confirmed in many medical literatures. But each patient need complicated clinical technology supporting, because the brain was controlled by gene in the development process, for example: when we use the NSCs to correct neuron developmental deviation and abnormality, neuron development need growth factors participation. It also need immunological surveillance. Over growth nerve will be controlled by immune system, only in that way can we get good result. All the processes need to be controlled by experienced clinician and complicated clinical technology.

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Stem Cell Therapy | Cellular Prolotherapy | Caring Medical

Stem Cell Medical Center | Posted by admin
Jun 08 2015

Home Stem Cell Therapy | Cellular Prolotherapy

Ross Hauser, MD

Ross Hauser, MD: the use of Stem Cell Therapy in the treatment of joint and spine degeneration.

Stem cell therapy is exploding in the medical field, and for good reason. Stem cells have the potential to regenerate into any type of body tissue. The amazing thing about stem cells is that when you inject them into the body, they know what kinds of cells your body needs for example, meniscus cells or cartilage cells. It is a very exciting time for medicine, especially in the field of regenerative medicine. In our office we often refer to this as Cellular Prolotherapy.

In Stem Cell Therapy we use a persons own healing cells from bone marrow, fat, and blood (alone or in various combinations) and inject them straight to the area which has a cellular deficiency.

The goal is the same: to stimulate the repair of injured tissues. Stem cells aid in fibroblastic proliferation where cell growth, proteosynthesis, reparation, the remodeling of tissues, and chondrocyte proliferation occurs. Our bone marrow contains stem cells,also termed mesenchymal stem cells and progenitor cells, among other names. These immature cells have the ability to become tissues like cartilage, bone, and ligaments.

Consequently, researchers and clinicians are focusing on alternative methods for cartilage preservation and repair. Recently,cell-basedtherapyhas become a key focus of tissue engineering research to achieve functional replacement of articular cartilage.1

Not all injuries require stem cells to heal. For many patients the success rate with traditionalProlotherapyin this office is in the 90%+ range for all patients. However, for those cases of advanced arthritis, meniscus tears, labral tears, bone-on-bone, or aggressive injuries, our Prolotherapy practitioners may choose to use stem cell injections to enhance the healing, in combination with dextrose Prolotherapy to strengthen and stabilize the surrounding support structures formeniscus repair.

In our research published inThe Open Stem Cell Journal,Rationale for Using Direct Bone Marrow Aspirate as a Proliferant for Regenerative Injection Therapy(Prolotherapy). We not only showed the benefit of bone marrow derived stem cells as a Prolotherapy proliferant solution, but also that this exciting field of medicine needs doctors and scientisists working together to expand research and technique guidelines.

Typically the tissue that we are trying to stimulate to repair with Stem Cell Therapy or Cellular Prolotherapy is articular cartilage, but we can also proliferate soft tissues structures such as ligament and tendons. This is new technology so we are studying it as we use it to treat patients.

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Induced Pluripotent Stem Cells (iPS) | UCLA Broad Stem …

Induced Pluripotent Stem Cells | Posted by admin
May 27 2015

iPSC are derived from skin or blood cells that have been reprogrammed back into an embryonic-like pluripotent state that enables the development of an unlimited source of any type of human cell needed for therapeutic purposes. For example, iPSC can be prodded into becoming beta islet cells to treat diabetes, blood cells to create new blood free of cancer cells for a leukemia patient, or neurons to treat neurological disorders.

In late 2007, a BSCRC team of faculty, Drs. Kathrin Plath, William Lowry, Amander Clark, and April Pyle were among the first in the world to create human iPSC. At that time, science had long understood that tissue specific cells, such as skin cells or blood cells, could only create other like cells. With this groundbreaking discovery, iPSC research has quickly become the foundation for a new regenerative medicine.

Using iPSC technology our faculty have reprogrammed skin cells into active motor neurons, egg and sperm precursors, liver cells, bone precursors, and blood cells. In addition, patients with untreatable diseases such as, ALS, Rett Syndrome, Lesch-Nyhan Disease, and Duchenne’s Muscular Dystrophy donate skin cells to BSCRC scientists for iPSC reprogramming research. The generous participation of patients and their families in this research enables BSCRC scientists to study these diseases in the laboratory in the hope of developing new treatment technologies.

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What is Wrong With Embryonic Stem Cell Research?

Embryonic Stem Cells | Posted by admin
May 22 2015

Introduction

Are conservatives more concerned about a tiny clump of cells than the suffering of their fellow human beings? Is embryonic stem cell research (ESCR) really the cure-all for countless diseases? If you haven’t kept up with the science involved in ESCR, this paper will jump-start your knowledge of the issues.

Embryonic stem cell research is a hot topic that seems to pit anti-abortion conservatives against pro-abortion liberals. The conservatives claim that there are better alternatives to embryonic stem cells, while the liberals claim that conservatives are blocking research that will provide cures to many tragic diseases. Much of the rhetoric is designed to muddy the waters to invoke emotional responses of those within each camp. This paper is designed to break through sound-bites and go the heart of the matter – what are the scientific issues that impact the question of stem cell research.

Much of what is promoted as being news is actually an oversimplification of the issues. Many news articles about stem cell research never distinguish between the kind of stem cell research that is being promoted. For example, the media often reports of breakthrough treatment for patients without mentioning that, in all cases, the source of stem cells is adult tissues. We know this to be true, because embryonic stem cells have never been used in human patients, and won’t likely be used in the near future (see reasons, below).

Stem cells are classified as being pluripotent or multipotent. Stem cells that are pluripotent are capable of forming virtually all of the possible tissue types found in human beings. These stem cells can only be found in a certain stage (a blastocyst) in human embryos. Multipotent stem cells are partially differentiated, so that they can form a limited number of tissue types. Multipotent stem cells can be found in the fetus, in umbilical cord blood, and numerous adult tissues. A summary of this information can be found in the Table 1.

A list of the sources of stem cells, along with their advantages and disadvantages can be found in Table 2.

Although the controversy of stem cell research is only recent, research first began in the 1960’s. The primary source of early human stem cells was adult bone marrow, the tissue that makes red and white blood cells. Since scientists realized that bone marrow was a good source of stem cells, early transplants were initiated in the early 1970’s to treat diseases that involved the immune system (genetic immunodeficiencies and cancers of the immune system). Bone marrow-derived stem cell therapy has been extremely successful, with dozens of diseases being treated and cured through the use of these adult stem cells. However, because the donor tissue type must be closely matched to the patient, finding a compatible donor can be problematic. If you haven’t already done so, you should become part of the Bone Marrow Registry.

With the advent of animal cloning, scientists had thought that patient-specific human cloning might provide cures without the tissue incompatibility problems usually associated with transplants. Specific stem cells, developed using clones genetically identical to the patient, would integrate optimally into the patient’s body. Although ideal in theory, problems associated with human cloning have been quite formidable. After many years of trying to produce human clones, a South Korean group claimed to have done so in 2004,2 followed by a claim that they had produced patient-specific clones. However, subsequent questions revealed that all the research was fraudulent. Contrary to the original claims, the researchers failed to produce even one clone after over 2,000 attempts. Although a number of labs are working on producing human clones, none have succeeded – even after several years of additional attempts. At a cost of $1,000-$2,000 just to produce each human egg,3 therapeutic cloning would easily cost hundreds of thousands of dollars, if not more, for each patient. Therefore, these kinds of therapies would only be available to the wealthy, assuming the technical difficulties will eventually be eliminated.

Three separate groups of researchers showed recently that normal skin cells can be reprogrammed to an embryonic state in mice.4 The fact that these iPS cells were pluripotent was proved by producing fetuses derived entirely from these transformed skin cells. Just five months after the mouse study was published, the feat was repeated by two separate laboratories using human skin cells.5 The ability to produce embryonic stem cell-like lines from individual patients removes the possibility of tissues rejection and avoids the high costs and moral problems associated with cloned embryos. Dr. Shinya Yamanaka, one of the study leaders later commented, “When I saw the embryo, I suddenly realized there was such a small difference between it and my daughters… I thought, we cant keep destroying embryos for our research. There must be another way.” The moral problem of destroying a human embryo encouraged Dr. Yamanaka to pursue a more ethical way to generate human stem cell lines. See the full report.

Stem cells have been promoted as a cure for numerous diseases in the popular press, although the reality of the science suggests otherwise. For example, claims that stem cells might cure Alzheimers disease are certainly untrue. According to Michael Shelanski, Taub Institute for Research on Alzheimer’s Disease and the Aging Brain (Columbia University Medical Center), I think the chance of doing repairs to Alzheimer’s brains by putting in stem cells is small. Ronald D.G. McKay, National Institute of Neurological Disorders and Stroke says, To start with, people need a fairy tale.6 Stem cell research is widely promoted as a possible cure for type I and type II diabetes. However, these diseases involve the destruction of islet pancreatic cells by the patient’s immune system. Even if tissue-compatible islet cells can be produced, transplanting them into a patient will be a very temporary cure, since the patient’s immune system will attack the transplant in short order. So, a total cure for diabetes might have to involve a total immune compartment replacement (with its risks), in addition to an islet cell transplant. Parkinsons disease is another disease that is often mentioned as potentially curable through stem cell research. Proponents of ESCR cite studies in which embryonic stem cells produce dopamine in the brain of rats. However, only 50% of the rats had improvement of function and 25% developed brain tumors and died!7 A main problem for ESCR is that these stem cells spontaneously form tumors in virtually all studies that have been conducted to date. In addition, it seems that the number of dopamine-producing neurons declined over time, suggesting that the cure might be just temporary.8

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What is Wrong With Embryonic Stem Cell Research?

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