Stem Cell Clinic

Cancer – Wikipedia, the free encyclopedia

By adminJune 27, 2015Uncategorized

Cancer i, also known as a malignant tumor or malignant neoplasm, is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] Not all tumors are cancerous; benign tumors do not spread to other parts of the body.[2] Possible signs and symptoms include: a new lump, abnormal bleeding, a prolonged cough, unexplained weight loss, and a change in bowel movements among others.[3] While these symptoms may indicate cancer, they may also occur due to other issues.[3] There are over 100 different known cancers that affect humans.[2]

Tobacco use is the cause of about 22% of cancer deaths.[1] Another 10% is due to obesity, a poor diet, lack of physical activity, and consumption of ethanol (alcohol).[1] Other factors include certain infections, exposure to ionizing radiation, and environmental pollutants.[4] In the developing world nearly 20% of cancers are due to infections such as hepatitis B, hepatitis C, and human papillomavirus.[1] These factors act, at least partly, by changing the genes of a cell.[5] Typically many such genetic changes are required before cancer develops.[5] Approximately 510% of cancers are due to genetic defects inherited from a person's parents.[6] Cancer can be detected by certain signs and symptoms or screening tests.[1] It is then typically further investigated by medical imaging and confirmed by biopsy.[7]

Many cancers can be prevented by not smoking, maintaining a healthy weight, not drinking too much alcohol, eating plenty of vegetables, fruits and whole grains, being vaccinated against certain infectious diseases, not eating too much red meat, and avoiding too much exposure to sunlight.[8][9] Early detection through screening is useful for cervical and colorectal cancer.[10] The benefits of screening in breast cancer are controversial.[10][11] Cancer is often treated with some combination of radiation therapy, surgery, chemotherapy, and targeted therapy.[1][12] Pain and symptom management are an important part of care. Palliative care is particularly important in those with advanced disease.[1] The chance of survival depends on the type of cancer and extent of disease at the start of treatment.[5] In children under 15 at diagnosis the five year survival rate in the developed world is on average 80%.[13] For cancer in the United States the average five year survival rate is 66%.[14]

In 2012 about 14.1 million new cases of cancer occurred globally (not including skin cancer other than melanoma).[5] It caused about 8.2 million deaths or 14.6% of all human deaths.[5][15] The most common types of cancer in males are lung cancer, prostate cancer, colorectal cancer, and stomach cancer, and in females, the most common types are breast cancer, colorectal cancer, lung cancer, and cervical cancer.[5] If skin cancer other than melanoma were included in total new cancers each year it would account for around 40% of cases.[16][17] In children, acute lymphoblastic leukaemia and brain tumors are most common except in Africa where non-Hodgkin lymphoma occurs more often.[13] In 2012, about 165,000 children under 15 years of age were diagnosed with cancer. The risk of cancer increases significantly with age and many cancers occur more commonly in developed countries.[5] Rates are increasing as more people live to an old age and as lifestyle changes occur in the developing world.[18] The financial costs of cancer have been estimated at $1.16 trillion US dollars per year as of 2010.[19]

Cancers are a large family of diseases that involve abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] They form a subset of neoplasms. A neoplasm or tumor is a group of cells that have undergone unregulated growth, and will often form a mass or lump, but may be distributed diffusely.[20][21]

Six characteristics of cancer have been proposed:

The progression from normal cells to cells that can form a discernible mass to outright cancer involves multiple steps known as malignant progression.[22][23]

When cancer begins, it invariably produces no symptoms. Signs and symptoms only appear as the mass continues to grow or ulcerates. The findings that result depend on the type and location of the cancer. Few symptoms are specific, with many of them also frequently occurring in individuals who have other conditions. Cancer is the new "great imitator". Thus, it is not uncommon for people diagnosed with cancer to have been treated for other diseases, which were assumed to be causing their symptoms.[24]

Local symptoms may occur due to the mass of the tumor or its ulceration. For example, mass effects from lung cancer can cause blockage of the bronchus resulting in cough or pneumonia; esophageal cancer can cause narrowing of the esophagus, making it difficult or painful to swallow; and colorectal cancer may lead to narrowing or blockages in the bowel, resulting in changes in bowel habits. Masses in breasts or testicles may be easily felt. Ulceration can cause bleeding that, if it occurs in the lung, will lead to coughing up blood, in the bowels to anemia or rectal bleeding, in the bladder to blood in the urine, and in the uterus to vaginal bleeding. Although localized pain may occur in advanced cancer, the initial swelling is usually painless. Some cancers can cause a buildup of fluid within the chest or abdomen.[24]

General symptoms occur due to distant effects of the cancer that are not related to direct or metastatic spread. These may include: unintentional weight loss, fever, being excessively tired, and changes to the skin.[25]Hodgkin disease, leukemias, and cancers of the liver or kidney can cause a persistent fever of unknown origin.[24]

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Cancer - Wikipedia, the free encyclopedia

Basal Cell Carcinoma Symptoms and Treatment. Patient | Patient

By adminJune 27, 2015Uncategorized

Basal cell carcinomas (BCCs) are slow-growing, locally invasive malignant epidermal skin tumours which are thought to arise from hair follicles. The tumour infiltrates local tissues through the slow irregular growth of subclinical finger-like outgrowths and morbidity results from local tissue invasion and destruction, especially on areas of chronic sun exposure, such as the face, head and neck.[1]

Metastasis is relatively rare with a metastasis rate of 0.0028% to 0.5%. However, there is a 2% incidence of metastasis for tumours larger than 3 cm in diameter, 25% for tumours larger than 5 cm and 50% for tumours larger than 10 cm in diameter.[2]

There are good photographs of basal cell carcinomas (BCCs) on the Dermatology Information System (DermIS) website.[6]

There is a good photograph of a superficial BCC on the DermIS website.[7]

The National Institute for Health and Clinical Excellence (NICE) recommends that low-risk BCCs be managed in primary care as long as the GP meets the requirements to perform skin surgery within the framework of the Direct Enhanced Services and Local Enhanced Services. There should be no diagnostic uncertainty that the lesion is a primary nodular low-risk BCC and meets the following criteria:

If the BCC does not meet the above criteria, or there is any diagnostic doubt, following discussion with the patient they should be referred to a member of the local hospital skin cancer multidisciplinary team (LSMDT).

If the lesion is thought to be a superficial BCC, the GP should ensure that the patient is offered the full range of medical treatments (eg photodynamic therapy (PDT)) and this may require referral to a member of the LSMDT. Incompletely excised BCCs should be discussed with a member of the LSMDT.

Surgery and radiotherapy appear to be the most effective treatments, with surgery showing the lowest failure rates. There is only limited evidence of the effectiveness of other treatment modalities compared with surgery.[11] Recurrent BCC is more difficult to cure than primary lesions.[1]

Sometimes, especially in the very elderly and debilitated, it may be appropriate to provide no treatment (given the slow growth and low risk of many superficial BCCs) or palliative (debulking or radiotherapy) treatment if the tumour is symptomatic.

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Basal Cell Carcinoma Symptoms and Treatment. Patient | Patient

Platelet Rich Plasma (PRP) Injections | Scottsdale, Tempe …

By adminJune 22, 2015Platelet Rich Plasma Injections

One of the most exciting emerging forms of regenerative medicine for soft tissue injuries is Platelet Rich Plasma (PRP) therapy. PRP injections are an increasingly popular alternative to surgery and are getting great results for patients of all ages. The physicians at Southwest Spine & Sports have been practicing regenerative medicine for decades and together have helped Arizona patients live pain-free. Whether you are an elite athlete or a Weekend Warrior if youre looking for a nonsurgical way to manage and eliminate your back, neck, joint or other pain, call Southwest Spine & Sports at (480) 860-8998 today!

No matter your age, activity level or condition, no one should have to live with pain. At Southwest Spine & Sports, weve used PRP to treat people in all phases of life, including:

PRP therapy can be used to treat a variety of acute and chronic injuries, including but not limited to:

Find out if PRP is right for you call today (480) 860-8998!

When tissue injury occurs, platelets collect at the site and begin to repair it. By concentrating these platelets and administering them straight into the injury site, we can deliver a powerful mixture of growth factors exactly where you need it, dramatically enhancing your bodys natural healing process. This treatment may lead to a more rapid, more efficient, and more thorough restoration of the tissue to a healthy state.

The PRP injection is very safe at most, you may experience very mild pain, stiffness or swelling. While any medical procedure carries a small risk of infection, since youre using your own blood this risk is minimal.

At Southwest Spine & Sports, we always start our PRP treatment with a musculoskeletal ultrasound. Ultrasound helps us pinpoint the exact location of the pain site, making the treatment much more effective for healing and pain relief. Because ultrasound is performed in real-time, our physician or physicians assistant has the ability to watch on a monitor as the needle is placed precisely in the correct position for the injection. A local anesthetic will be applied to the area followed by PRP injection with ultrasound guidance to ensure that the appropriate target is reached.

Musculoskeletal ultrasound is an invaluable part of our regenerative medicine procedures and allows us to deliver the most effective treatment right where it hurts eliminating the guesswork and helping us provide the best care possible.

The procedure takes approximately one to two hours, including preparation and recovery time. Performed safely in a medical office, PRP therapy relieves pain without the risks of surgery, general anesthesia, or hospital stays and without a prolonged recovery. In fact, most people return to their jobs or usual activities right after the procedure.

Some patients report swelling and stiffness or mild to moderate discomfort lasting a few hours after the injection. This is a normal response and is a sign that the treatment is working. Over time, the affected area will begin to heal and strengthen and you will experience considerably less pain.

NIH Human Embryonic Stem Cell Registry – Research Using …

By adminJune 22, 2015Embryonic Stem Cells

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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NIH Human Embryonic Stem Cell Registry - Research Using ...

Prostate Cancer Treatment – National Cancer Institute

By adminJune 22, 2015Uncategorized

General Information About Prostate Cancer Key Points Prostate cancer is a disease in which malignant (cancer) cells form in the tissues of the prostate. Signs of prostate cancer include a weak flow of urine or frequent urination. Tests that examine the prostate and blood are used to detect (find) and diagnose prostate cancer. Certain factors affect prognosis (chance of recovery) and treatment options. Prostate cancer is a disease in which malignant (cancer) cells form in the tissues of the prostate.

The prostate is a gland in the male reproductive system. It lies just below the bladder (the organ that collects and empties urine) and in front of the rectum (the lower part of the intestine). It is about the size of a walnut and surrounds part of the urethra (the tube that empties urine from the bladder). The prostate gland makes fluid that is part of the semen.Enlarge

Anatomy of the male reproductive and urinary systems, showing the prostate, testicles, bladder, and other organs.

Prostate cancer is found mainly in older men. In the U.S., about 1 out of 5 men will be diagnosed with prostate cancer.

These and other signs and symptoms may be caused by prostate cancer or by other conditions. Check with your doctor if you have any of the following:

Other conditions may cause the same symptoms. As men age, the prostate may get bigger and block the urethra or bladder. This may cause trouble urinating or sexual problems. The condition is called benign prostatic hyperplasia (BPH), and although it is not cancer, surgery may be needed. The symptoms of benign prostatic hyperplasia or of other problems in the prostate may be like symptoms of prostate cancer.

Normal prostate and benign prostatic hyperplasia (BPH). A normal prostate does not block the flow of urine from the bladder. An enlarged prostate presses on the bladder and urethra and blocks the flow of urine.

The following tests and procedures may be used:

Digital rectal exam (DRE). The doctor inserts a gloved, lubricated finger into the rectum and feels the prostate to check for anything abnormal.

Transrectal ultrasound. An ultrasound probe is inserted into the rectum to check the prostate. The probe bounces sound waves off body tissues to make echoes that form a sonogram (computer picture) of the prostate.

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Prostate Cancer Treatment - National Cancer Institute

Banner Cancer Center Adult Stem Cell Transplant Cellular …

By adminJune 20, 2015Stem Cell Medical Center

Banner Cancer Center Adult Stem Cell Transplant Cellular Therapy Apply Now Company: Banner Health System Location: Gilbert, AZ Date Posted: June 13, 2015 Source: ZipRecruiter Job Description: Oncology Job in Gilbert, AZ BANNER MD ANDERSON CANCER CENTER: Adult Stem Cell Transplant/Cellular TherapyBanner Health. Gilbert, AZ85284. Accepts J1s:No Job ID:292371. Loan Assistance:No Practice Type:Employee. Apply Now. Save JobShare with a FriendPrint. PracticeLink Login. Have an account? Email Address* Required. Password* Required. Log InForgot your password?Keep me Logged In New to PracticeLink? With PracticeLink you can manage your full CV, get updates on new jobs that interest you, respond to jobs across the country & more! Get Started. Banner MD Anderson Cancer Center seeks Hematology/Oncology experienced board-certified physicians (M.D. or D.O.) to join its adult stem cell transplantation and cellular therapy program. The SCT/CT Program expects to perform transplants using all donor types. Qualified candidates should have excellent clinical training in stem cell transplantation and cellular therapy and an interest in clinical research. Banner MD Anderson Cancer Center is a full clinical extension of The University of Texas M. D. Anderson Cancer in Houston. M. D. Anderson is ranked as the number one cancer center by U.S. News & World Report, is the worlds largest treatment facility for oncologic diseases including stem cell transplantation and cellular therapy. Banner MD Anderson Cancer Center is located in Gilbert, Arizona on the campus of Banner Gateway Medical Center. The Cancer Center is a new, state-of-the art facility that provides access to a world-renowned medical community and the splendid cultural and recreational diversity of the sophisticated, metropolitan Phoenix area. SUBMIT YOUR CV FOR IMMEDIATE CONSIDERATION. Banner MD Anderson Cancer Center is an equal opportunity employer and does not discriminate on the basis of race, color, national origin, gender, sexual orientation, age, religion, disability or veteran status except where such distinction is required by law. All positions at Banner MD Anderson Cancer Center are security sensitive and subject to examination of criminal history record information. Smoke-free and drug-free environment. Saudi Aramco - Phoenix, AZ

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Banner Cancer Center Adult Stem Cell Transplant Cellular ...

Stem cell expert: Bart Starr treatment shows need for …

By adminJune 19, 2015Stem Cell Medicine

The news that legendary Green Bay Packer quarterback Bart Starr has undergone stem cell therapy to recover from a stroke has raised the profile for a promising but unproven regenerative treatment intended to replace dead neurons with live ones.

The University of Wisconsin-Madison's Su-Chun Zhang was the first scientist to isolate neural stem cells from embryonic stem cells and then from other types of all-purpose stem cells. He says medical researchers and the federal government have a responsibility to forge ahead with clinical trials to prove whether and how these flexible cells can replace damaged or dead neural cells caused by spinal cord injury, stroke and Lou Gehrig's disease (ALS).

Su-Chun Zhang

"We have no effective treatment for stroke," says Zhang, a medical doctor and Ph.D. researcher at the UW's Waisman Center. "After a couple of hours, the cells are dead if they don't have a blood supply. And the brain has a very limited capacity to regenerate, particularly in older patients."

Embryonic stem cells the cells that give rise to all body tissues were first cultured by James Thomson at UW-Madison in 1998. Just three years later in 2001 Zhang discovered how to grow neural cells from embryonic stem cells.

Since then, he has been instrumental in differentiating these neural cells into neurons, which carry nerve signals, and glial cells, which keep neurons healthy. UW-Madison currently has more than 90 faculty working on the basic science and regenerative potential of stem cells. UW scientists publish more than 500 research articles each year on stem cells.

Zhang expressed hope that Starr will recover, but says there are plenty of question marks, such as what type of cells were used, and how they were inserted into the body.

In a statement Wednesday, Starr's family announced he was participating in a stem-cell trial but gave no details of how or where he was being treated. Published reports have said that the family received information about stem-cell treatment in Tijuana, Mexico, undergone by hockey Hall-of-Famer Gordie Howe.

The Food and Drug Administration has been more conservative than some foreign regulators, Zhang says, but science has advanced to the point where human trials are justified, especially for untreatable conditions.

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Stem cell expert: Bart Starr treatment shows need for ...

Stem Cell Institute Los Angeles Chronic Pain Treatments

By adminJune 17, 2015Stem Cell Doctors

Dr. Marc Darrow

Stroma cells are connective tissue cells found in body organs and in bone marrow.Fibroblasts(cells that make collagen) andpericytes( facilitating new blood vessel formation to bring circulation to the area) are the most common stroma cells. In our practice we use bone marrow derived stem cells to regenerate damaged joints.

Doctors at the University of Iowa are experimenting with stroma cells. This is from the University: Knee injuries are the bane of athletes everywhere, from professionals and college stars to weekend warriors.

Current surgical options for repairing damaged cartilage caused by knee injuries are costly, can have complications, and often are not very effective in the long run. Even after surgery, cartilage degeneration can progress leading to painful arthritis.

But a University of Iowa orthopedics research team is working on a solution with hopes it will result in a minimally invasive, practical, and inexpensive approach for repairing cartilage and preventing osteoarthritis.

We are creating an [injectable, bioactive] hydrogel that can repair cartilage damage, regenerate stronger cartilage, and hopefully delay or eliminate the development of osteoarthritis and eliminate the need for total knee replacement, says Yin Yu, a graduate student in the lab of James Martin, PhD, UI assistant professor of orthopedics and rehabilitation. Yu is first author of the study, which is featured on the cover of the May issue of the journalArthritis and Rheumatology.

Martins team had previously identified precursor cells within normal cartilage that can mature into new cartilage tissue. This was a surprising discovery because of the long-held assumption that cartilage is one of the few tissues in the body that cannot repair itself. (Note: Prolotgerapy doctors have often documented cartilage regrowth.)

The team also identified molecular signaling factors that attract these precursor cells, known as chondrogenic progenitor cells (CPC), out of the surrounding healthy tissue into the damaged area and cause them to develop into new, normal cartilage. One of the signals, called stromal cell-derived factor 1 (SDF1), acts like a homing beacon for the precursor cells.

In an experimental model of cartilage injury, Yu loaded the custom-made hydrogel with SDF1 and injected it into holes punched into the model cartilage. The precursor cells migrated toward the SDF1 signal and filled in the injury site. Subsequent application of a growth factor caused the cells to mature into normal cartilage that repaired the injury.

This process gives us a great result, Yu says. The new cartilage integrates seamlessly with the undamaged tissue, it has normal concentrations of proteoglycans, good structural properties, and looks like normal cartilage.

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Stem Cell Institute Los Angeles Chronic Pain Treatments

The Cell Cycle – CELLS alive

By adminJune 15, 2015Uncategorized

During development from stem to fully differentiated, cells in the body alternately divide (mitosis) and "appear" to be resting (interphase). This sequence of activities exhibited by cells is called the cell cycle. Follow the events in the entire cell cycle with the following animation.

Interphase: Interphase, which appears to the eye to be a resting stage between cell divisions, is actually a period of diverse activities. Those interphase activities are indispensible in making the next mitosis possible. Interphase generally lasts at least 12 to 24 hours in mammalian tissue. During this period, the cell is constantly synthesizing RNA, producing protein and growing in size. By studying molecular events in cells, scientists have determined that interphase can be divided into 4 steps: Gap 0 (G0), Gap 1 (G1), S (synthesis) phase, Gap 2 (G2).

Gap 0(G0): There are times when a cell will leave the cycle and quit dividing. This may be a temporary resting period or more permanent. An example of the latter is a cell that has reached an end stage of development and will no longer divide (e.g. neuron).

Gap 1(G1): Cells increase in size in Gap 1, produce RNA and synthesize protein. An important cell cycle control mechanism activated during this period (G1 Checkpoint) ensures that everything is ready for DNA synthesis. (Click on the Checkpoints animation, above.)

S Phase: To produce two similar daughter cells, the complete DNA instructions in the cell must be duplicated. DNA replication occurs during this S (synthesis) phase.

Gap 2(G2): During the gap between DNA synthesis and mitosis, the cell will continue to grow and produce new proteins. At the end of this gap is another control checkpoint (G2 Checkpoint) to determine if the cell can now proceed to enter M (mitosis) and divide.

MitosisorM Phase:Cell growth and protein production stop at this stage in the cell cycle. All of the cell's energy is focused on the complex and orderly division into two similar daughter cells. Mitosis is much shorter than interphase, lasting perhaps only one to two hours. As in both G1 and G2, there is a Checkpoint in the middle of mitosis (Metaphase Checkpoint) that ensures the cell is ready to complete cell division. Actual stages of mitosis can be viewed atAnimal Cell Mitosis.

Cancer cells reproduce relatively quickly in culture. In theCancer Cell CAMcompare the length of time these cells spend in interphase to that formitosisto occur.

Adult Stem Cells’ Role in Disease Management and Anti-Aging

By adminJune 13, 2015Adult Stem Cells

By Dr. Mercola

Since time immemorial, man has searched for the Fountain of Youth. Nothing has changed in that regard, but the methods of inquiry and discovery have certainly progressed.

Some of these ideas rival even the most outlandish sci-fi scenarios imaginable, up to and including the transfer of your consciousness into a bionic body.1 Personally, I dont want to veer too far from the natural order of things.

But the technology and science enthusiast in me cant help but be intrigued by the ideas and radical advances in the field of extreme life extension. One of the most promising techniques in this field, from my perspective, revolves around the use of adult stem cells.

Adult stem cells are undifferentiated cells found throughout your body. They multiply and replace cells as needed, in order to regenerate damaged tissues. Their value, in terms of anti-aging and life extension, centers around their ability to self-renew indefinitely, and their ability to generate every type of cell needed for the organ from which it originates.

Dr. Bryant Villeponteau, author of Decoding Longevity, is a leading researcher in novel anti-aging therapies involving stem cells. Hes been a pioneer in this area for over three decades.

Personally, I believe that stem cell technology could have a dramatic influence on our ability to live longer and replace some of our failing parts, which is the inevitable result of the aging process. With an interest in aging and longevity, Dr. Villeponteau started out by studying developmental biology.

If we could understand development, we could understand aging, he says.

Later, his interest turned more toward the gene regulation aspects. While working as a professor at the University of Michigan at the Institute of Gerontology, he received, and accepted, a job offer from Geron Corporationa Bay Area startup, in the early 90s.

They were working on telomerase, which I was pretty excited about at the time. I joined them when they first started, he says. We had an all-out engagement there to clone human telomerase. It had been cloned in other animals but not in humans or mammals.

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Adult Stem Cells' Role in Disease Management and Anti-Aging