Minecraft - HERMITCRAFT ModSauce: Ep 11 "MAD SCIENCE WITH GENETICS" Part 4 w/BaconDonutTV
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Minecraft - HERMITCRAFT ModSauce: Ep 11 "MAD SCIENCE WITH GENETICS" Part 4 w/BaconDonutTV - Video

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Gage green genetics week 1
MMMP patient and caregiver in full compliance. 18 over channel. This strain seems like a nice indica so far, we have female pistils forming so i am stoked, ...

By: BolagnaSheetsMD .

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Gage green genetics week 1 - Video

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Anna David (Prenatal Cell and Gene Therapy, IfWH) UCLTEDx
Anna David (Prenatal Cell and Gene Therapy, Research Department of Maternal and Fetal Medicine, IfWH) gives UCLTEDx Women talk.

By: UCL EGA Institute for Women #39;s Health

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Anna David (Prenatal Cell and Gene Therapy, IfWH) UCLTEDx - Video

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PUBLIC RELEASE DATE:

1-Oct-2014

Contact: Nick Miller nicholas.miller@cchmc.org 513-803-6035 Cincinnati Children's Hospital Medical Center @CincyChildrens

CINCINNATI Researchers developed a new type of cell transplantation to treat mice mimicking a rare lung disease that one day could be used to treat this and other human lung diseases caused by dysfunctional immune cells.

Scientists at Cincinnati Children's Hospital Medical Center report their findings in a study posted online Oct. 1 by Nature. In the study, the authors used macrophages, a type of immune cell that helps collect and remove used molecules and cell debris from the body.

They transplanted either normal or gene-corrected macrophages into the respiratory tracts of mice, which were bred to mimic the hereditary form of a human disease called hereditary pulmonary alveolar proteinosis (hPAP). Treatment with both normal and gene-corrected macrophages corrected the disease in the mice.

"These are significant findings with potential implications beyond the treatment of a rare lung disease," said Bruce Trapnell, MD, senior author and a physician in the Division of Neonatology and Pulmonary Biology at Cincinnati Children's. "Our findings support the concept of pulmonary macrophage transplantation (PMT) as the first specific therapy for children with hPAP"

"Results also identified mechanisms regulating the numbers and phenotype of macrophages in the tiny air sacs of the lungs (called alveoli) in health and disease," said Takuji Suzuki, MD, PhD, the study's first author and a scientist in the Division of Neonatology and Pulmonary Biology at Cincinnati Children's.

Suzuki and Trapnell discovered hPAP at Cincinnati Children's and first reported it in 2008. In hPAP, the air sacs become filled with surfactant, a substance the lungs produce to reduce surface tension and keep the air sacs open. Children with hPAP have mutations in the genes of GM-CSF receptor alpha or beta (CSFR2RA or CSFR2RB). These mutations reduce the ability of alveolar macrophages to remove used surfactant from the lungs of these children.

The used surfactant builds up in the lungs, filling the alveoli and causing difficult breathing or respiratory failure. The only current treatment for these children is whole-lung lavage, an invasive lung-washing procedure performed under general anesthesia. Although the procedure works, it is temporary, must be repeated frequently, and creates quality of life issues for affected children.

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Researchers develop novel gene/cell therapy approach for lung disease

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Stem Cell Therapy The Aspen Institute for Anti Aging Regenerative Medicine

By: Cupio Media

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Stem Cell Therapy The Aspen Institute for Anti Aging & Regenerative Medicine - Video

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China tests stem cell therapy for heart disease
Monday marks World Heart Day. One of the most serious conditions is Chronic Heart Disease. It has no cure to date, but in China, scientists are hoping to find one, using stem-cell technology.

By: CCTV America

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China tests stem cell therapy for heart disease - Video

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About cell therapy

Cell therapy is a new official direction in medicine, based on the use of regenerative potential of the adult stem cells, aimed at the treatment of a variety of serious diseases, rehabilitation of patients after injuries and fighting with the premature signs of aging. Stem cells are also considered to be the promising biological material for the creation of the prosthetic heart valves, blood vessels, trachea, they are also used as the unique biofiller for the reconstitution of bone defects and other purposes of the plastic and reconstructive surgery.

The scientists explain the regenerative mechanism of action of stem cells both by their ability to transform into the cells of blood, liver, myocardium, bone, cartilage or nervous tissue and thus restore damaged organs and also by the reovery of the functional activity of the other cells (through the so-called paracrine type) by means of the production of a variety of growth factors.

For clinical purposes, in most cases stem cells are obtained from the bone marrow and cord blood, it is also known that the amount of stem cells, sufficient for treatment, can be isolated from the peripheral blood of an adult person, but after pre-stimulation of hematopoiesis. In recent years there is an increasing number of reports worldwide on the clinical application of stem cells, derived from the placenta, adipose tissue, umbilical cord tissue, amniotic fluid, and even pulp of the milk teeth. Depending on the disease, age and condition of the patient, one or another source of stem cells may be preferred. Hematopoietic (blood-forming) stem cells are used for more than 50 years in the treatment of leukemia and lymphomas, and this treatment is commonly known as the bone marrow transplantation, but today hematopoietic stem cells, derived from umbilical cord blood and peripheral blood are more often used in the hematologic clinics of the world. At the same time, for the treatment of traumatic brain and spinal cord injuries, the stimulation of fractures and chronic wounds healing the mesenchymal stem cells are more preferred, being the precursors of the connective tissue. Mesenchymal stem cells are found in big quantity in fatty tissue, placenta, umbilical cord blood, amniotic fluid. Due to the immunosuppressive effects of mesenchymal stem cells, they are also used in the treatment of a variety of autoimmune diseases (multiple sclerosis, ulcerative colitis, Crohns disease, etc.), as well as post-transplantation complications (to prevent the rejection of the transplanted donor organ). For the treatment of cardiovascular diseases, including lower limbs ischemia, the umbilical cord blood is considered to be the most promising, as it contains a special kind of the endothelial progenitor stem cells, which can not be found in any other human tissue.

Cell therapy may be autologous (own cells are used) and allogeneic (donor cells are used). However, it is known that every nucleated cell in the human body has certain immunological characteristics (HLA-phenotype or immune passport), that is why the use of donor stem cells requires immunological compatibility. This fact determines the appropriateness of the banking of the own stem cells, frozen until the person is still young and healthy. In this aspect the human umbilical cord blood has undisputed medical and biological value as the source of several unique lines of stem cells. Collected in the first minutes of life, umbilical cord blood stem cells have the highest potential for proliferation (growth) and directed differentiation.

Stem cell therapy can be applied both intravenously like a drug, and directly into the damaged tissue. In recent years the method of intraosseous transplantation of cord blood stem cells is more widely used, contributing to the more rapid engraftment. Also a method of introducing stem cells directly into the coronary arteries (coronary heart disease, myocardial infarction) was introduced and it is called cellular cardiomyoplasty.

Cell therapy can be carried out both in monotherapy and complementary to the surgical or drug treatment.

Currently stem cells are successfully used in the treatment of about 100 serious diseases, and in some cases this is the only effective treatment.

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Cell therapy - Institute of Cell Therapy - ...

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Because heart cells cannot multiply and cardiac muscles contain few stem cells, heart tissue is unable to repair itself after a heart attack. Now Tel Aviv University researchers are literally setting a new gold standard in cardiac tissue engineering.

Dr. Tal Dvir and his graduate student Michal Shevach of TAU's Department of Biotechnology, Department of Materials Science and Engineering, and Center for Nanoscience and Nanotechnology, have been developing sophisticated micro- and nanotechnological tools -- ranging in size from one millionth to one billionth of a meter -- to develop functional substitutes for damaged heart tissues. Searching for innovative methods to restore heart function, especially cardiac "patches" that could be transplanted into the body to replace damaged heart tissue, Dr. Dvir literally struck gold. He and his team discovered that gold particles are able to increase the conductivity of biomaterials.

In a study published by Nano Letters, Dr. Dvir's team presented their model for a superior hybrid cardiac patch, which incorporates biomaterial harvested from patients and gold nanoparticles. "Our goal was twofold," said Dr. Dvir. "To engineer tissue that would not trigger an immune response in the patient, and to fabricate a functional patch not beset by signalling or conductivity problems."

A scaffold for heart cells

Cardiac tissue is engineered by allowing cells, taken from the patient or other sources, to grow on a three-dimensional scaffold, similar to the collagen grid that naturally supports the cells in the heart. Over time, the cells come together to form a tissue that generates its own electrical impulses and expands and contracts spontaneously. The tissue can then be surgically implanted as a patch to replace damaged tissue and improve heart function in patients.

According to Dr. Dvir, recent efforts in the scientific world focus on the use of scaffolds from pig hearts to supply the collagen grid, called the extracellular matrix, with the goal of implanting them in human patients. However, due to residual remnants of antigens such as sugar or other molecules, the human patients' immune cells are likely to attack the animal matrix.

In order to address this immunogenic response, Dr. Dvir's group suggested a new approach. Fatty tissue from a patient's own stomach could be easily and quickly harvested, its cells efficiently removed, and the remaining matrix preserved. This scaffold does not provoke an immune response.

Using gold to create a cardiac network

The second dilemma, to establish functional network signals, was complicated by the use of the human extracellular matrix. "Engineered patches do not establish connections immediately," said Dr. Dvir. "Biomaterial harvested for a matrix tends to be insulating and thus disruptive to network signals."

At his Laboratory for Tissue Engineering and Regenerative Medicine, Dr. Dvir explored the integration of gold nanoparticles into cardiac tissue to optimize electrical signaling between cells. "To address our electrical signalling problem, we deposited gold nanoparticles on the surface of our patient-harvested matrix, 'decorating' the biomaterial with conductors," said Dr. Dvir. "The result was that the nonimmunogenic hybrid patch contracted nicely due to the nanoparticles, transferring electrical signals much faster and more efficiently than non-modified scaffolds."

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A heartbeat away? Hybrid 'patch' could replace transplants

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PUBLIC RELEASE DATE:

30-Sep-2014

Contact: Laura Bailey baileylm@umich.edu 734-647-1848 University of Michigan @umich

ANN ARBORThe discovery of a gene mutation that causes a rare premature aging disease could lead to the development of drugs that block the rapid, unstoppable cell division that makes cancer so deadly.

Scientists at the University of Michigan and the U-M Health System recently discovered a protein mutation that causes the devastating disease dyskeratosis congenita, in which precious hematopoietic stem cells can't regenerate and make new blood. People with DC age prematurely and are prone to cancer and bone marrow failure.

But the study findings reach far beyond the roughly one in 1 million known DC patients, and could ultimately lead to developing new drugs that prevent cancer from spreading, said Jayakrishnan Nandakumar, assistant professor in the U-M Department of Molecular, Cellular, and Developmental Biology.

The DC-causing mutation occurs in a protein called TPP1. The mutation inhibits TPP1's ability to bind the enzyme telomerase to the ends of chromosomes, which ultimately results in reduced hematopoietic stem cell division. While telomerase is underproduced in DC patients, the opposite is true for cells in cancer patients.

"Telomerase overproduction in cancer cells helps them divide uncontrollably, which is a hallmark of all cancers," Nandakumar said. "Inhibiting telomerase will be an effective way to kill cancer cells."

The findings could lead to the development of gene therapies to repair the mutation and start cell division in DC patients, or drugs to inhibit telomerase and cell division in cancer patients. Both would amount to huge treatment breakthroughs for DC and cancer patients, Nandakumar said.

Nandakumar said that a major step moving forward is to culture DC patient-derived cells and try to repair the TPP1 mutation to see if telomerase function can be restored. Ultimately, the U-M scientist hopes that fixing the TPP1 mutation repairs telomerase function and fuels cell division in the stem cells of DC patients.

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Disease decoded: Gene mutation may lead to development of new cancer drugs

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PUBLIC RELEASE DATE:

30-Sep-2014

Contact: Emily Head emily.head@cancer.org.uk 44-203-469-6189 Cancer Research UK @CR_UK

A drug which targets a key gene fault could halt an aggressive womb cancer and shrink tumours, according to research published in the British Journal of Cancer*.

The scientists, from the Division of Gynaecologic Oncology at Yale School of Medicine funded by the National Institutes of Health, showed that the drug afatinib not only killed off uterine serous cancer cells after stopping their growth but also caused tumours to shrink.

The drug, a type of personalised medicine, attacks faults in the HER2 gene which lie at the heart of the cancer cells. This stops the disease in its tracks. Drugs which target HER2 are already used to treat breast cancer.

Uterine serous carcinoma is a fast-growing type of womb cancer. It is more likely than other womb cancers to come back after treatment, returning in one in two patients* even if it is caught early.

Although the cancer causes less than one in 10 womb cancers**, it accounts for 40 per cent of all deaths from womb cancer* which is around 800 deaths every year in the UK***.

The researchers looked at uterine serous carcinoma cell lines with normal and increased levels of the HER2 protein to see how afatinib affected the cancer. They found that the drug had a big impact on cancer cells with this gene fault, and could stop them growing and kill them. They also found that the drug shrank the size of uterine serous tumours when given to mice.

Afatinib works by targeting receptors that respond to growth signals. Cancers with high levels of the HER2 protein have too many of these receptors, allowing them to grow out of control. The drug is an example of personalised or tailored treatment, which works by specifically targeting the faulty genes and molecules in an individual's cancer. Afatinib is being tested in clinical trials for a number of cancers including bowel cancer and certain types of lung and breast cancer.

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Targeted treatment could halt womb cancer growth

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PUBLIC RELEASE DATE:

30-Sep-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, September 30, 2014Levothyroxine (L-T4), long the standard of care for treating hypothyroidism, is effective in most patients, but some individuals do not regain optimal health on L-T4 monotherapy. New knowledge about thyroid physiology may help to explain these differences. An expert task force of the American Thyroid Association on thyroid hormone replacement reviewed the latest studies on L-T4 therapy and on alternative treatments to determine whether a change to the current standard of care is appropriate, and they present their recommendations in the article "Guidelines for the Treatment of Hypothyroidism," published in Thyroid, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers and the official journal of the American Thyroid Association (ATA). The Guidelines are available free on the Thyroid website.

Task force co-chairs J. Jonklaas and A.C. Bianco, with colleagues from the Clinical and Translational Science sub-committees, coauthored the Guidelines on behalf of the American Thyroid Association Task Force on Thyroid Hormone Replacement. The authors reviewed the clinical literature related to three main therapeutic categories: levothyroxine therapy; non-levothyroxine-based thyroid hormone therapies (including thyroid extracts, synthetic combination therapy, triiodothyronine therapy, and compounded thyroid hormones); and use of thyroid hormone analogues.

The task force concluded that levothyroxine should remain the standard of care for treating hypothyroidism, noting that no consistently strong evidence supports the superiority of alternative therapies. They emphasize that the recommendations are intended to guide physicians' clinical decision-making on thyroid hormone replacement therapy for individual patients.

"These very comprehensive guidelines provide a superb overview on the current evidence about treatment modalities for patients with hypothyroidism," says Peter A. Kopp, MD, Editor-in-Chief of Thyroid and Associate Professor of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois. "In addition, the document highlights gaps in our knowledge and indicates which topics are in need of future research, for example the need for long-term outcome clinical trials testing combination therapies and continuing research on thyroid hormone analogs."

"These ATA guidelines, developed by an expert team, provide useful, up-to-date information on why to treat, including subclinical disease, who to treat, and how to treat hypothyroidism. Information is evidence-based and recommendations are graded. I think they will be used extensively by all clinical endocrinologists, especially by our members," says Hossein Gharib, MD, President of the ATA, Professor of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota.

###

About the Journal

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New hypothyroidism treatment guidelines from American Thyroid Association

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Pittsburgh, Pennsylvania (PRWEB) September 30, 2014

Researchers at the University of Pittsburgh School of Dental Medicine have been awarded a $11.8 million, five-year grant from the National Institute of Dental and Craniofacial Research, part of the National Institutes of Health, to continue their exploration of the genetic roots of cleft lip and cleft palate and to expand the effort to include populations in Colombia, Nigeria, the Philippines and Pennsylvania.

Orofacial clefts (OFCs), which are small gaps in the lip or palate that can form when a babys mouth doesnt develop properly during pregnancy, occurs in 1 out of 700 live births worldwide, said Mary L. Marazita, Ph.D., professor and vice chair, Department of Oral Biology, and director of the Center for Craniofacial and Dental Genetics (CCDG).

Orofacial clefts present a significant public health challenge as these patients typically require surgical, nutritional, dental, speech and behavioral treatments for years, Dr. Marazita said. We hope to build on the progress weve made in our previous studies by identifying genetic susceptibility not only for the overt defects, but also for more subtle features such as changes in facial structure that we have found in relatives of participants with OFCs.

Dr. Marazita and Seth M. Weinberg, Ph.D., assistant professor of oral biology, and director of the CCDG Imaging and Morphometrics Lab, lead the coordinating center for the project, which includes researchers from the University of Iowa, the Newborn Screening Foundation in the Philippines, the Lancaster Cleft Palate Clinic, Nigerias University of Lagos, Colombias Foundation Clinica Noel, and KU Leuven University in Belgium.

For the works next phase, the team will recruit for genetic studies about 6,100 individuals from more than 1,500 families with a history of cleft lip with or without cleft palate, or cleft palate alone, from a low-risk population in Nigeria; high-risk populations in the Philippines and Colombia; and mid-risk populations in Pittsburgh and Lancaster, Pa., as well as 2,000 unrelated individuals with no history of OFC.

Recent studies indicate different genes seem to be involved in different ethnic groups, so we must broaden our perspective to understand the factors that lead to clefts, Dr. Weinberg said. We have limited information about the development of cleft palate alone, for example. This research effort will greatly add to our knowledge.

The team also will assess participants for subclinical manifestations of genetic predisposition for OFCs with high-resolution ultrasound scanning of mouth muscles, lip print patterns, 3-D imaging of facial surfaces and more. Their previously published studies have shown that relatives of OFC patients are more likely to have subtle defects in the orbicularis oris muscle around the mouth, and facial differences such as mid-face retrusion and wider faces. OFC patients also report a family history of cancer more often than unaffected individuals, noted Dr. Marazita.

Minor dental abnormalities, facial shape differences, altered speech patterns and other less obvious changes in the mouth could all be part of a spectrum of defects that have the same genetic causes as cleft lip and palate, she said. If we can unravel those relationships and identify the biological pathways that cause them, we will gain insights that may lead to better treatments and better long-term outcomes for affected individuals.

# # # About the University of Pittsburgh School of Dental Medicine

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Pitt Researchers Search for Genetic Roots of Cleft Lip, Palate with Help from NIH Grant

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PUBLIC RELEASE DATE:

30-Sep-2014

Contact: Chris Jones jonesc83@cardiff.ac.uk Cardiff University @cardiffuni

Screening families of patients with bowel cancer for a genetic condition would cut their risk of developing bowel, womb, and ovarian cancers, new research has found.

In a major study, Dr Ian Frayling from Cardiff University's School of Medicine and researchers from the University of Exeter's Medical School assessed the effectiveness of introducing a UK-wide screening programme for a genetic condition known as Lynch Syndrome.

Lynch syndrome is a caused by changes in genes which check the spelling in DNA. The condition increases the risk of people developing cancer, particularly bowel cancer and cancers of the womb and ovaries later in life. Without testing cancers, it is not obvious that they are caused by Lynch syndrome, and so it is often not diagnosed.

It is responsible for around one in 12 cases of people aged under 50 and around a third of people with the disease develop bowel cancer by the time they are 70, if no action is taken.

"If Lynch Syndrome is identified as the cause of bowel cancer, patients can be offered risk-reducing measures such as more intensive post-operative colonoscopy surveillance to spot recurrences and new cancers early," according to Cardiff University's Dr Ian Frayling, the clinical adviser to the study.

"As close relatives have a 50 per cent chance of sharing the gene, screening would provide a valuable opportunity to detect the condition in children, siblings, parents and more distant relatives.

"It would mean measures could be taken to reduce the risk of cancers developing," he added.

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Genetic test would help 'cut bowel cancer spread'

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PUBLIC RELEASE DATE:

30-Sep-2014

Contact: Anita Srikameswaran SrikamAV@upmc.edu 412-578-9193 University of Pittsburgh Schools of the Health Sciences @UPMCnews

Researchers at the University of Pittsburgh School of Dental Medicine have been awarded a $11.8 million, five-year grant from the National Institute of Dental and Craniofacial Research, part of the National Institutes of Health, to continue their exploration of the genetic roots of cleft lip and cleft palate and to expand the effort to include populations in Colombia, Nigeria, the Philippines and Pennsylvania.

Orofacial clefts (OFCs), which are small gaps in the lip or palate that can form when a baby's mouth doesn't develop properly during pregnancy, occurs in 1 out of 700 live births worldwide, said Mary L. Marazita, Ph.D., professor and vice chair, Department of Oral Biology, and director of the Center for Craniofacial and Dental Genetics (CCDG).

"Orofacial clefts present a significant public health challenge as these patients typically require surgical, nutritional, dental, speech and behavioral treatments for years," Dr. Marazita said. "We hope to build on the progress we've made in our previous studies by identifying genetic susceptibility not only for the overt defects, but also for more subtle features such as changes in facial structure that we have found in relatives of participants with OFCs."

Dr. Marazita and Seth M. Weinberg, Ph.D., assistant professor of oral biology, and director of the CCDG Imaging and Morphometrics Lab, lead the coordinating center for the project, which includes researchers from the University of Iowa, the Newborn Screening Foundation in the Philippines, the Lancaster Cleft Palate Clinic, Nigeria's University of Lagos, Colombia's Foundation Clinica Noel, and KU Leuven University in Belgium.

For the work's next phase, the team will recruit for genetic studies about 6,100 individuals from more than 1,500 families with a history of cleft lip with or without cleft palate, or cleft palate alone, from a low-risk population in Nigeria; high-risk populations in the Philippines and Colombia; and mid-risk populations in Pittsburgh and Lancaster, Pa., as well as 2,000 unrelated individuals with no history of OFC.

"Recent studies indicate different genes seem to be involved in different ethnic groups, so we must broaden our perspective to understand the factors that lead to clefts," Dr. Weinberg said. "We have limited information about the development of cleft palate alone, for example. This research effort will greatly add to our knowledge."

The team also will assess participants for subclinical manifestations of genetic predisposition for OFCs with high-resolution ultrasound scanning of mouth muscles, lip print patterns, 3-D imaging of facial surfaces and more. Their previously published studies have shown that relatives of OFC patients are more likely to have subtle defects in the orbicularis oris muscle around the mouth, and facial differences such as mid-face retrusion and wider faces. OFC patients also report a family history of cancer more often than unaffected individuals, noted Dr. Marazita.

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Pitt team searches for genetic roots of cleft lip, palate

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Interviews, Annual Conference 2014: #39;Genetics, Genomics and Global Health
Annual Conference 2014: #39;Genetics, Genomics and Global Health -- Inequalities, Identities and Insecurities #39; 19th July 2014 University of Sussex Conference Ce...

By: Global Health Policy

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Interviews, Annual Conference 2014: 'Genetics, Genomics and Global Health - Video

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Minecraft - HERMITCRAFT ModSauce: Ep 8 "MAD SCIENCE WITH GENETICS" w/BaconDonutTV
JOIN CYANIDEEPIC BACONDONUT ON A NEW ADVENTURE PLAYING HERMITCRAFT MODSAUCE PACK! 😀 Don #39;t forget to give a like share, Thank you! Check out bacon here...

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Minecraft - HERMITCRAFT ModSauce: Ep 8 "MAD SCIENCE WITH GENETICS" w/BaconDonutTV - Video

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Genetics - The Fountain Of Salmacis - Teatro Rival - RJ - 26/09/2014
Descrio.

By: Nelson Santos

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Genetics - The Fountain Of Salmacis - Teatro Rival - RJ - 26/09/2014 - Video

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Genetics - The Knife - Teatro Rival - RJ - 26/09/2014
Descrio.

By: Nelson Santos

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Genetics in the Bible: Part 1
Paul Sandhu guests on The Curtner-Kerr radio show to discuss the central doctrine of the Bible of the reproduction of God for which purpose all things have been created. http://www.candkshow.com.

By: Paul Sandhu

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Genetics in the Bible: Part 1 - Video

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GENETICS - THE FOUNTAIN OF SALMACIS - TEATRO RIVAL - 26/09/2014 - video by Rogerio Favilla
GENETICS - THE FOUNTAIN OF SALMACIS - TEATRO RIVAL - RIO DE JANEIRO - 26/09/2014 Hermaphrodite: a flower containing both male and female organs; a person or animal of both sexes. The child...

By: Lakranya1

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GENETICS - THE FOUNTAIN OF SALMACIS - TEATRO RIVAL - 26/09/2014 - video by Rogerio Favilla - Video

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Muir-Torre Syndrome and Medical Genetics at Mayo Clinic
Dr. Jennifer Hand a dermatologist and specialist in the medical genetics clinic at Mayo Clinic provides an overview of Muir-Torre Syndrome and explains how a...

By: Mayo Clinic

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Muir-Torre Syndrome and Medical Genetics at Mayo Clinic - Video

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Part Two (11) - Via: Genetics 101
I created this video with the YouTube Video Editor (http://www.youtube.com/editor)

By: FJH 7th ELA

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Part Two (11) - Via: Genetics 101 - Video

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Let #39;s Play Minecraft Episode 8- Advanced Genetics Pt. 2
Hello and welcome back for another episode! Mod spotlight/tutorial: https://www.youtube.com/watch?v=BZhgmR5q8vY Here are the mods I #39;m using in this Let #39;s Play. FYI this is in no way an organized...

By: SamiBlocks

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Let's Play Minecraft Episode 8- Advanced Genetics Pt. 2 - Video

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Gene therapy information

By: Alexandra Cook

Originally posted here:
Gene therapy information - Video

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PHILADELPHIA In the second of two papers outlining new gene-therapy approaches to treat a rare disease called MPS I, researchers from Perelman School of Medicine at the University of Pennsylvania examined systemic delivery of a vector to replace the enzyme IDUA, which is deficient in patients with this disorder. The second paper, which is published online in the Proceedings of the National Academy of Sciences this week, describes how an injection of a vector expressing the IDUA enzyme to the liver can prevent most of the systemic manifestations of the disease, including those found in the heart.

The first paper, published in Molecular Therapy, describes the use of an adeno-associated viral (AAV) vector to introduce normal IDUA to glial and neuronal cells in the brain and spinal cord in a feline model. The aim of that study was to directly treat the central nervous system manifestations of MPS while the more recent study aims to treat all other manifestations of the disease outside of the nervous system.

This family of diseases comprises about 50 rare inherited disorders marked by defects in the lysosomes, compartments within cells filled with enzymes to digest large molecules. If one of these enzymes is mutated, molecules that would normally be degraded by the lysosome accumulate within the cell and their fragments are not recycled. Many of the MPS disorders can share symptoms, such as speech and hearing problems, hernias, and heart problems. Patient groups estimate that in the United States 1 in 25,000 births will result in some form of MPS. Life expectancy varies significantly for people with MPS I.

The two main treatments for MPS I are bone marrow transplantation and intravenous enzyme replacement therapy (ERT), but these are only marginally effective or clinically impractical, and have significant drawbacks for patient safety and quality of life and do not effectively address some of the most critical clinical symptoms, such as life-threatening cardiac valve impairments.

Both of these papers are the first proof-of-principle demonstrations for the efficacy and practicality for gene therapies to be translated into the clinic for lysosomal storage diseases, says lead author James M. Wilson, MD, PhD, professor of Pathology and Laboratory Medicine and director of the Penn Gene Therapy Program. This approach may likely turn out to be better than ERT and compete with or replace ERT. We are especially excited about the use of this approach in treating the many MPS I patients who do not have access to ERT due to cost or inadequate health delivery systems to support repeated protein infusions, such as in China, Eastern Europe, India, and parts of South America.

Patients with mucopolysaccharidosis type I (MPS I), accumulate compounds called glycosaminoglycans in tissues, with resulting diverse clinical symptoms, including neurological, eye, skeletal, and cardiac disease.

Using a naturally occurring feline model of MPS I, the team tested liver-directed gene therapy via a single intravenous infusion as a means of establishing long-term systemic IDUA presence throughout the body.

The team treated four MPS I cats at three to five months of age with an AAV serotype 8 vector expressing feline IDUA. We observed sustained serum enzyme activity for six months at approximately 30 percent of normal levels in one animal and in excess of normal levels in the other three animals, says Wilson.

Remarkably, treated animals not only demonstrated reductions in glycosaminoglycans storage in most tissues, but most also exhibited complete resolution of aortic valve lesions, an effect which has not been previously observed in this animal model or in MPS I patients treated with current therapies.

Critical to the evaluation of these novel therapies is the feline model of MPS I, which was provided through coauthor Mark E. Haskins, School of Veterinary Medicine at Penn. Haskins and his colleagues maintain a variety of canine and feline models of human genetic diseases that have been instrumental in establishing proof of concept for a number of novel therapeutics, including the current enzyme replacement therapy.

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Gene Therapy Targeting Liver Corrects Cardiovascular Symptoms in Animal Model of Rare Enzyme Deficiency Disease

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