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Stem Cell Research in Cardiology – Video


Stem Cell Research in Cardiology
Bharat Book Bureau provides the report, on Stem Cell Research in Cardiology. The study is segmented by Source (Allogenic and Autogenic) and by Type (Bone Marrow Stem Cells, Embryonic...

By: Bharat Book

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Stem Cell Research in Cardiology - Video

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Telomeres and cancer mortality: The long and the short of it

Telomeres are short stretches of repeated nucleotides that protect the ends of chromosomes. In somatic cells, these protective sequences become shorter with each cellular replication until a critical length is reached, which can trigger cell death.

In actively replicating cells such as germ cells, embryonic stem cells, and blood stem cells of the bone marrow, the enzyme telomerase replenishes these protective caps to ensure adequate replication. Cancer cells also seem to have the ability to activate telomerase, which allows them to keep dividing indefinitely, with dire consequences for the patient. However, according to a study published April 10 in the JNCI: Journal of the National Cancer Institute, the extent to which cancer cells can utilize telomerase may depend on which variants of the genes related to telomerase activity are expressed in an individual's cells.

Telomere shortening is an inevitable, age-related process, but it can also be exacerbated by lifestyle factors such as obesity and smoking. Thus, some previous studies have found an association between short telomeres and high mortality, including cancer mortality, while others have not. A possible explanation for the conflicting evidence may be that the association found between short telomeres and increased cancer mortality was correlational but other factors (age and lifestyle), not adjusted for in previous studies, were the real causes. Genetic variation in several genes associated with telomere length (TERC, TERT, OBFC1) is independent of age and lifestyle. Thus, a genetic analysis called a Mendelian randomization could eliminate some of the confounding and allow the presumably causal association of telomere length and cancer mortality to be studied.

To perform this analysis, Line Rode, M.D., Ph.D., of the Department of Clinical Biochemistry and The Copenhagen General Population Study, Herlev Hospital, Copenhagen University Hospital, Herlev, Denmark, and colleagues, used data from two prospective cohort studies, the Copenhagen City Heart Study and the Copenhagen General Population Study, including 64,637 individuals followed from 1991-2011. Participants completed a questionnaire and had a physical examination and blood drawn for biochemistry, genotyping, and telomere length assays.

For each subject, the authors had information on physical characteristics such as body mass index, blood pressure, and cholesterol measurements, as well as smoking status, alcohol consumption, physical activity, and socioeconomic variables. In addition to the measure of telomere length for each subject, three single nucleotide polymorphisms of TERC, TERT, and OBFC1 were used to construct a score for the presence of telomere shortening alleles.

A total of 7607 individuals died during the study, 2420 of cancer. Overall, as expected, decreasing telomere length as measured in leukocytes was associated with age and other variables such as BMI and smoking and with death from all causes, including cancer. Surprisingly, and in contrast, a higher genetic score for telomere shortening was associated specifically with decreased cancer mortality, but not with any other causes of death, suggesting that the slightly shorter telomeres in the cancer patients with the higher genetic score for telomere shortening might be beneficial because the uncontrolled cancer cell replication that leads to tumor progression and death is reduced.

The authors conclude, "We speculate that long telomeres may represent a survival advantage for cancer cells, allowing multiple cell divisions leading to high cancer mortality."

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Contact info:

Stig E. Bojesen, M.D., D.M.Sc., stig.egil.bojesen@regionh.dk

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Telomeres and cancer mortality: The long and the short of it

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RoosterBio Inc. launches new stem cell product format enabling rapid, scalable cell manufacturing and 3D bioprinting

Frederick, MD (PRWEB) April 09, 2015

Based upon strong market demand, RoosterBio Inc has announced the commercial launch of RoosterVial-hBM-50M MSC, a single vial containing 50 million human bone-marrow derived mesenchymal stem/stromal cells. This unprecedented, ultra-high cell number product configuration enables Regenerative Medicine organizations to accelerate scale-up and product development activities. RoosterBios core technology, which includes cell and media systems, allows tissue engineers, biofabricators, 3D bioprinters and cell therapy developers to instantly scale up, using simplified and standardized methods.

The 50 million hMSC vial delivers immediate cell biomass without the need for prior expansion. This results in saving significant time, resources and expense during bioprocess scale-up optimization. Since the system contains the most well-characterized hMSCs available on the market, the industry is assured robust and reproducible results. As with other RoosterBio products, this 50 million cell product is capable of greater than 100-fold expansion (>5 billion cells) within two weeks when cultured in RoosterBio medium. Prior to this technology, obtaining such cell numbers so rapidly was virtually impossible.

RoosterBio continues to broaden their portfolio of product formats, providing solutions for an extensive range of Regenerative Medicine therapeutic categories. The evolving product portfolio enables researchers and product developers to perform small scale screening studies, large scale development studies, and now, scale-up manufacturing bioprocess experiments using the 50 million cell product. Rapid prototyping of 3D bioprinted tissues utilizing hMSCs as the primary component of the cellular bioink is also now achievable. The Company offers various product configurations including 1 million cell vials, 10 million cell vials, and high performance media systems, as well as pre-assembled working cell banks and kits for rapidly achieving stem cell biomass. Jon Rowley, CEO of RoosterBio stated: "The Industry has published a technology roadmap for scalable cell manufacturing and 3D bioprinting, yet the materials needed to test and implement these technologies are not readily available. RoosterBio is addressing this major roadblock with innovative product formats that enable users to do more work, faster, and with much less out-of-pocket expense."

RoosterBios mission is to accelerate the development and commercialization of Regenerative Medicine products, by providing standardized stem cell product platforms that enable rapid translation of discoveries into product development. For more information, please email Priya Baraniak at priya@roosterbio.com or phone 1-412-606-1160.

About RoosterBio

RoosterBio is a privately held biofabrication tools company focused on accelerating the development of a sustainable regenerative medicine industry, one customer at a time. RoosterBios products are high volume, affordable, and well-characterized adult human mesenchymal stem/stromal cells (hMSCs) paired with highly engineered media systems. RoosterBio has simplified and standardized how stem cells are purchased, expanded, and used in development, leading to marked time and costs savings for customers. RoosterBios innovative products are ushering in a new era of productivity and standardization into the field, where researchers spend newly found time and money performing more high-value experiments, accelerating the road to discovery in Regenerative Medicine. For more information on RoosterBio and adult stem cells, you can visit http://www.roosterbio.com, follow on twitter (@RoosterBio), or read the highly-acclaimed blog Democratizing Cell Technologies (http://www.roosterbio.blogspot.com).

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RoosterBio Inc. launches new stem cell product format enabling rapid, scalable cell manufacturing and 3D bioprinting

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Amniotic stem cells demonstrate healing potential

Rice University and Texas Children's Hospital scientists are using stem cells from amniotic fluid to promote the growth of robust, functional blood vessels in healing hydrogels.

In new experiments, the lab of bioengineer Jeffrey Jacot combined versatile amniotic stem cells with injectable hydrogels used as scaffolds in regenerative medicine and proved they enhance the development of vessels needed to bring blood to new tissue and carry waste products away.

The results appear in the Journal of Biomedical Materials Research Part A.

Jacot and his colleagues study the use of amniotic fluid cells from pregnant women to help heal infants born with congenital heart defects. Such fluids, drawn during standard tests, are generally discarded but show promise for implants made from a baby's own genetically matched material.

He contends amniotic stem cells are valuable for their ability to differentiate into many other types of cells, including endothelial cells that form blood vessels.

"The main thing we've figured out is how to get a vascularized device: laboratory-grown tissue that is made entirely from amniotic fluid cells," Jacot said. "We showed it's possible to use only cells derived from amniotic fluid."

In the lab, researchers from Rice, Texas Children's Hospital and Baylor College of Medicine combined amniotic fluid stem cells with a hydrogel made from polyethylene glycol and fibrin. Fibrin is a biopolymer critical to blood clotting, cellular-matrix interactions, wound healing and angiogenesis, the process by which new vessels branch off from existing ones. Fibrin is widely used as a bioscaffold but suffers from low mechanical stiffness and rapid degradation. Combining fibrin and polyethylene glycol made the hydrogel much more robust, Jacot said.

The lab used vascular endothelial growth factor to prompt stem cells to turn into endothelial cells, while the presence of fibrin encouraged the infiltration of native vasculature from neighboring tissue.

Mice injected with fibrin-only hydrogels showed the development of thin fibril structures, while those infused with the amniotic cell/fibrin hydrogel showed far more robust vasculature, according to the researchers.

Similar experiments using hydrogel seeded with bone marrow-derived mesenchymal cells also showed vascular growth, but without the guarantee of a tissue match, Jacot said. Seeding with endothelial cells didn't work as well as the researchers expected, he said.

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Amniotic stem cells demonstrate healing potential

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Pause Hydra Creme for dry skin – Video


Pause Hydra Creme for dry skin
http://www.phytomone.com Pause Hydra Crme -Menopause Skin Repair System Designed by skin therapists, clinical nutritionists and cosmetic scientists, to address the specific needs of hormonally...

By: Phytomone Ltd

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Pause Hydra Creme for dry skin - Video

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Stem Cells, Fecal Transplants Show Promise for Crohn's Disease

By Amy Norton HealthDay Reporter

FRIDAY, April 10, 2015 (HealthDay News) -- Two experimental therapies might help manage the inflammatory bowel disorder Crohn's disease, if this early research pans out.

In one study, researchers found that a fecal transplant -- stool samples taken from a healthy donor -- seemed to send Crohn's symptoms into remission in seven of nine children treated.

In another, a separate research team showed that stem cells can have lasting benefits for a serious Crohn's complication called fistula.

According to the Crohn's & Colitis Foundation, up to 700,000 Americans have Crohn's -- a chronic inflammatory disease that causes abdominal cramps, diarrhea, constipation and rectal bleeding. It arises when the immune system mistakenly attacks the lining of the digestive tract.

A number of drugs are available to treat Crohn's, including drugs called biologics, which block certain immune-system proteins.

But fecal transplants take a different approach, explained Dr. David Suskind, a gastroenterologist at Seattle Children's Hospital who led the new study.

Instead of suppressing the immune system, he said, the transplants alter the environment that the immune system is reacting against: the "microbiome," which refers to the trillions of bacteria that dwell in the gut.

Like the name implies, a fecal transplant involves transferring stool from a donor into a Crohn's patient's digestive tract. The idea is to change the bacterial composition of the gut, and hopefully quiet the inflammation that causes symptoms.

And for most kids in the new study, it seemed to work. Within two weeks, seven of nine children were showing few to no Crohn's symptoms. Five were still in remission after 12 weeks, with no additional therapy, the researchers reported in a recent issue of the journal Inflammatory Bowel Diseases.

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Stem Cells, Fecal Transplants Show Promise for Crohn's Disease

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Stem cell disease model clarifies bone cancer trigger

Using induced pluripotent stem cells (iPSCs), a team led by Mount Sinai researchers has gained new insight into genetic changes that may turn a well known anti-cancer signaling gene into a driver of risk for bone cancers, where the survival rate has not improved in 40 years despite treatment advances.

The study results, published today in the journal Cell, revolve around iPSCs, which since their 2006 discovery have enabled researchers to coax mature (fully differentiated) bodily cells (e.g. skin cells) to become like embryonic stem cells. Such cells are pluripotent, able to become many cell types as they multiply and differentiate to form tissues. The iPSCs can then be converted again as needed into differentiated cells such as heart muscle, nerve cells, bone, etc.

While some seek to use iPSCs as replacements for cells compromised by disease, the new Mount Sinai study sought to determine if they could serve as an accurate model of genetic disease "in a dish." In this context, the dish stands for a self-renewing, unlimited supply of iPSCs or a cell line - which enables in-depth study of disease versions driven by each person's genetic differences. When matched with patient records, iPSCs and iPSC-derived target cells may be able to predict a patient's prognosis and whether or not a given drug will be effective for him or her.

In the current study, skin cells from patient with and without disease were turned into patient-specific iPSC lines, and then differentiated into bone-making cells where both rare and common bone cancers start. This new bone cancer model does a better job than previously used mouse or cellular models of "recapitulating" the features of bone cancer cells driven by key genetic changes.

"Our study is among the first to use induced pluripotent stem cells as the foundation of a model for cancer," said lead author Dung-Fang Lee, PhD, a postdoctoral fellow in the Department of Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai. "This model, when combined with a rare genetic disease, revealed for the first time how a protein known to prevent tumor growth in most cases, p53, may instead drive bone cancer when genetic changes cause too much of it to be made in the wrong place."

Rare Disease Sheds Light on Common Disease

The Mount Sinai disease model research is based on the fact that human genes, the DNA chains that encode instructions for building the body's structures and signals, randomly change all the time. As part of evolution, some code changes, or mutations, make no difference, some confer advantages, and others cause disease. Beyond inherited mutations that contribute to cancer risk, the wrong mix of random, accumulated DNA changes in bodily (somatic) cells as we age also contributes to cancer risk.

The current study focused on the genetic pathways that cause a rare genetic disease called Li-Fraumeni Syndrome or LFS, which comes with high risk for many cancers in affected families. A common LFS cancer type is osteosarcoma (bone cancer), with many diagnosed before the age of 30. Beyond LFS, osteosarcoma is the most common type of bone cancer in all children, and after leukemia, the second leading cause of cancer death for them.

Importantly, about 70 percent of LFS families have a mutation in their version of the gene TP53, which is the blueprint for protein p53, well known by the nickname "the tumor suppressor." Common forms of osteosarcoma, driven by somatic versus inherited mutations, have also been closely linked by past studies to p53 when mutations interfere with its function.

Rare genetic diseases like LFS are good study models because they tend to proceed from a change in a single gene, as opposed to many, overlapping changes seen in more related common diseases, in this case more common, non-inherited bone cancers. The LFS-iPSC based modeling highlights the contribution of p53 alone to osteosarcoma.

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Stem cell disease model clarifies bone cancer trigger

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Fecal transplant, stem cells may help Crohn's disease

Two experimental therapies might help manage the inflammatory bowel disorder Crohn's disease, if this early research pans out.

In one study, researchers found that a fecal transplant -- stool samples taken from a healthy donor -- seemed to send Crohn's symptoms into remission in seven of nine children treated.

In another, a separate research team showed that stem cells can have lasting benefits for a serious Crohn's complication called fistula.

According to the Crohn's & Colitis Foundation, up to 700,000 Americans have Crohn's -- a chronic inflammatory disease that causes abdominal cramps, diarrhea, constipation and rectal bleeding. It arises when the immune system mistakenly attacks the lining of the digestive tract.

Play Video

Hundreds of thousands of people suffer from the potentially life threatening C. difficile bacterial infection in their intestines. CBS News' Marl...

A number of drugs are available to treat Crohn's, including drugs called biologics, which block certain immune-system proteins.

But fecal transplants take a different approach, explained Dr. David Suskind, a gastroenterologist at Seattle Children's Hospital who led the new study.

Instead of suppressing the immune system, he said, the transplants alter the environment that the immune system is reacting against: the "microbiome," which refers to the trillions of bacteria that dwell in the gut.

Like the name implies, a fecal transplant involves transferring stool from a donor into a Crohn's patient's digestive tract. The idea is to change the bacterial composition of the gut, and hopefully quiet the inflammation that causes symptoms.

More:
Fecal transplant, stem cells may help Crohn's disease

Recommendation and review posted by Bethany Smith

MaryannAstle published Tried & Tested: Best beauty products new to the market

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From cleansers and toners to salt scrubs and perfumes there's plenty of beauty treats that have just been released. Mary-ann Astle puts forward some of the best new releases on the beauty market....

NURISS Swiss Apple Stem Cell Rejuvenator Serum

Skincare and wellness brand Nuriss has a new star product in the making. The Swiss Apple Stem Cell Rejuvenator Serum (30ml, 120) uses the longevity found in stem cells of the rare species of Swiss apple (the Uttwiler Sptlauber) to repair and rejuvenate your skin. When applied to the skin it can help with wrinkle reduction and increase collagen production.

Without wanting to blind you with science the serum is created by cultivating the apple's stem cells which are rich in phytonutrients and proteins which are beneficial to human skin. You don't need to use a lot to see the benefits after cleansing and toning, smooth one or two drops over your face and neck. Use morning and night to get the best results.

Click here to go to Nuriss

LouLouBelle Skincare of London

LouLouBelle has a new range of skincare products that will not only pamper you but which also smell absolutely gorgeous.

With tantalising blends like Geranium and Tea Tree, Lavender and Cypress and Palmarosa and Patchouli, LouLouBelle London is a boutique aromatherapy brand that uses natural ingredients to help make your skin feel great and smell delightful. It's also reasonably priced with cleansers (200ml, 19.95), toners (150ml, 17.95) and moisturisers (50ml, 24.95).

Every product is formulated from its own unique recipe that is created by selecting essential oils, plant essences and floral waters to match the specific requirements of a given skin type. The result is a refreshing range of cleansers, toners and moisturisers that are available in a different blend for each of the three main categories of skin dry skin, combination skin and problem/oily skin.

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MaryannAstle published Tried & Tested: Best beauty products new to the market

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Duke Medicine Profiles: Stefanie Sarantopoulos, MD, PhD – Video


Duke Medicine Profiles: Stefanie Sarantopoulos, MD, PhD
Get to know Stefanie Sarantopoulos, MD, PhD, a cell therapy hematologic malignancies specialist. Learn more at: ...

By: Duke Medicine

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Duke Medicine Profiles: Stefanie Sarantopoulos, MD, PhD - Video

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CryoStor Cell Preservation Selected For Phase III Clinical Trials of C-Cure Cell Therapy for Congestive Heart Failure

BioLife Solutions, Inc. (NASDAQ: BLFS), a leading developer, manufacturer and marketer of proprietary clinical grade hypothermic storage and cryopreservation freeze media and precision thermal shipping products for cells and tissues (BioLife or the Company), today announced that Cardio3 BioSciences, a leader in engineered cell therapy with clinical programs initially targeting indications in cardiovascular disease and oncology, has embedded the Companys clinical grade CryoStor cryopreservation freeze media in its ongoing Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART-1) phase III clinical trial in Europe and Israel and the pending CHART-2 phase III clinical trial to be conducted in the United States.

CHART-1 (Congestive Heart Failure Cardiopoietic Regenerative Therapy) is a patient prospective, controlled multi-centre, randomized, double-blinded Phase III clinical trial comparing treatment with C-Cure to a sham treatment. The trial has recruited 240 patients with chronic advanced symptomatic heart failure. The primary endpoint of the trial is a composite endpoint including mortality, morbidity, quality of life, Six Minute Walk Test and left ventricular structure and function at nine months post-procedure.

Dr. Christian Homsy, CEO of Cardio3 BioSciences, commented on the selection of CryoStor by stating, We evaluated several possible freeze media formulations for our clinical cell therapy product development and manufacturing. CryoStor and BioLife best met our preservation efficacy, product and supplier quality, and customer support requirements.

As of January 2015, BioLife management estimates that the Companys CryoStor freeze media and HypoThermosol cell and tissue storage/shipping media have been incorporated into at least 175 customer clinical trials of novel cellular immunotherapies and other cell-based approaches for treating and possibly curing the leading causes of death and disorders throughout the world. Within the cellular immunotherapy segment of the regenerative medicine market, BioLife's products are embedded in the manufacturing, storage, and delivery processes of at least 75 clinical trials of chimeric antigen receptor T cells (CAR-T), T cell receptor (TCR), dendritic cell (DC), tumor infiltrating lymphocytes (TIL), and other T cell-based cellular therapeutics targeting solid tumors, hematologic malignancies, and other diseases and disorders. A large majority of the currently active private and publicly traded cellular immunotherapy companies are BioLife customers.

Mike Rice, BioLife Solutions CEO, remarked; We are honored to be able to supply our clinical grade CryoStor cell freeze media for Cardio3 Biosciences phase III clinical trials. Congestive heart failure is a leading cause of death and C-Cure is a novel and potentially life-saving, cell-based therapy that offers hope to millions of patients throughout the world. We are very well positioned to participate in the growth of the regenerative medicine market, with our products being used in at least 75 phase II and over 20 phase III clinical trials of new cell and tissue based products and therapies.

About Cardio3 Biosciences Cardio3 BioSciences is a leader in engineered cell therapy with clinical programs initially targeting indications in cardiovascular disease and oncology. Founded in 2007 and based in the Walloon region of Belgium, Cardio3 BioSciences leverages research collaborations in the USA with the Mayo Clinic (MN, USA) and Dartmouth College (NH, USA). The Companys lead product candidate in cardiology is C-Cure, an autologous stem cell therapy for the treatment of ischemic heart failure. The Companys lead product candidate in oncology is CAR- NKG2D, an autologous CAR T-cell product candidate using NKG2D, a natural killer cell receptor designed to target ligands present on multiple tumor types, including ovarian, bladder, breast, lung and liver cancers, as well as leukemia, lymphoma and myeloma. Cardio3 BioSciences is also developing medical devices for enhancing the delivery of diagnostic and therapeutic agents into the heart (CCath) and potentially for the treatment of mitral valve defects. Cardio3 BioSciences shares are listed on Euronext Brussels and Euronext Paris under the ticker symbol CARD. To learn more about Cardio3 BioSciences, please visit c3bs.com

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CryoStor Cell Preservation Selected For Phase III Clinical Trials of C-Cure Cell Therapy for Congestive Heart Failure

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Research Team from Penn Receives Vaccine Industry Excellence Award

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Newswise PHILADELPHIA The laboratory of David Weiner, PhD, a professor of Pathology and Laboratory Medicine at the Perelman School of Medicine at the University of Pennsylvania, received the 2015 Vaccine Industry Excellence Award for Best Academic Research Team, at the World Vaccine Congress in Washington, DC this week. The Congress is an annual meeting of vaccine professionals from industry, academia, and non-profit organizations.

It is a great honor to receive this important award, especially with such an exceptional field of deserving finalists, says Weiner. This award is testimony to the many wonderful scientists who I have been lucky to have had pass through my laboratory, as well as those that I have been fortunate to collaborate with from academia or industry, and to the exceptional research environment present at Penn.

The Weiner lab's DNA vaccines program was chosen over other finalists from Duke University, Harvard Medical School, and the Memorial Sloan-Kettering Cancer Center by hundreds of vaccine stakeholders who voted for those most deserving of recognition for their work across 14 vaccine-related categories.

This award, given annually to the research group that has produced products with a novel mode of action, seen them progress into human trials, and can demonstrate significant supportive research grants, was given to Weiner and his lab for making significant contributions to the field of DNA vaccines.

Weiner is also chair of the Gene Therapy and Vaccine Program and co-leader of Tumor Virology Program in the Abramson Cancer Center.

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Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.9 billion enterprise.

The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 17 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $409 million awarded in the 2014 fiscal year.

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Leptin Gene research – Video


Leptin Gene research
risk assessment of the effects of leptin in the human body as well as its functions in the body and why is important to develop further studies on the effects of leptin.

By: Santiago Arango Garces

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Leptin Gene research - Video

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Advocate uses genetic history to increase knowledge of hereditary cancer risk

Rachel Koszegi is on a mission to fight cancer, and she's not alone.

The 33-year-old mother who has tested positive for the BRCA2 cancer gene is one of 12 people in her family over three generations linked to the gene or diagnosed with cancer.

Now Koszegi is using her family's genetic history to contribute to cancer research, prevention and treatment -- with the aim of improving the quality of life for those facing hereditary risk.

"Cancer has always been part of my life," said Koszegi, owner of Brushed Inc., a professional makeup, hair and wardrobe styling business. "Even though it has always been there, I want to aggressively monitor and protect my health and be my own advocate, and I want the same for my family members."

Koszegi's efforts began with enrolling herself and her cousins in the Gilda Radner Hereditary Cancer Program, part of the Women's Cancer Program at the Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute.

Founded in 1991, the program consists of several research studies for women at higher risk for breast and ovarian cancer.

Led by Beth Y. Karlan, MD, the program works to gain a better understanding of the relationship of genes to the growth of specific cancers, and to understand why some mutation carriers develop breast, ovarian and other types of cancer, while other mutation carriers do not.

"Family is an essential part of our program," said Karlan, director of the Women's Cancer Program.

Koszegi traces her family's history of cancer to her maternal grandfather and his siblings. In all, five of the seven siblings were diagnosed with breast or prostate cancer.

Prostate cancer claimed the life of Koszegi's grandfather. Two of his daughters -- including Koszegi's mother and aunt -- were diagnosed with breast cancer. Her mother died from the disease at 58 and her aunt is in remission.

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Advocate uses genetic history to increase knowledge of hereditary cancer risk

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A mother's genes can influence the bacteria in her baby's gut

(SACRAMENTO, Calif.) -- Researchers at UC Davis have found that a gene, which is not active in some mothers, produces a breast milk sugar that influences the development of the community of gut bacteria in her infant. The sugars produced by these mothers, called "secretors," are not digested by the infant, but instead nourish specific bacteria that colonize the babies' guts soon after birth.

Mothers known as "non-secretors" have a non-functional fucosyltransferase 2 (FUT2) gene, which alters the composition of their breast milk sugars and changes how the microbial community, or microbiota, of their infants' guts develop.

The research may have applications in a clinical setting for protecting premature infants from a range of intestinal diseases including necrotizing enterocolitis (NEC), a condition that is the second most common cause of death among premature infants in the United States.

The researchers emphasized that the finding does not suggest that breast milk from mothers without an active copy of the gene is less nourishing or healthy. Rather, it conveys the subtle and elegant choreography of one part of the human microbiome: The relationships between the mothers' genetics, the composition of her breast milk and the development of her infant's gut microbiota. It also reveals clues for enriching desirable bacteria in populations at risk of intestinal diseases -- such as preemies.

"In no way is the nonsecretor mother's milk less healthy, and their babies are at no greater risk," said David Mills, Peter J. Shields Endowed Chair in Dairy Food Science at UC Davis and senior study author. "What this work does show us is that the mother's genotype matters, and that it influences the breast milk, which clearly drives the establishment of microbes in the intestines of their babies."

The research examining the differences in infant gut microbial populations arising from differences in human milk oligosaccharides (sugars), "Maternal Fucosyltransferase 2 Status Affects the Gut Bifidobacterial Communities of Breastfed Infants," is published online today in the journal Microbiome, a BioMedCentral journal.

Varieties of Bifidobacterium inhabit the gastrointestinal tracts and mouths of mammals and are one of the major genera of bacteria that make up the microbial community of the infant colon. The relationship between human genetics, breast milk and Bifidobacterium appears to have developed throughout mammalian evolution.

Development of a healthy gut microbiota can have a lifelong effect on health, and early intervention in the establishment of that microbiota could have lifelong positive effects: The early establishment of bifidobacteria has been shown to be associated with improved immune response to vaccines, development of the infants' immature immune system, and protection against pathogens.

Bifidobacterium are known to consume the 2'-fucosylated glycans (sugars) found in the breast milk of women with the fucosyltransferase 2 mammary gene. The study found that, on average, Bifidobacterium were established earlier and more frequently in infants fed by women with an active copy of the gene, the secretors, than without one, the non-secretors.

The authors found that the intestinal tracts of infants fed by non-secretor mothers are delayed in establishing a bifidobacteria-dominated microbiota. The delay, the authors said, may be due to difficulties in the infant acquiring a species of bifidobacteria that is geared toward consuming the specific milk sugar delivered by the mother.

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A mother's genes can influence the bacteria in her baby's gut

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Genetic engineering and biotecnology – Video


Genetic engineering and biotecnology
http://gebri.usc.edu.eg.

By: GEBRI usc

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Genetic engineering and biotecnology - Video

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How can we improve plant growth?

Supercomputers and genetic engineering could help boost crops ability to convert sunlight into energy and tackle looming food shortages, according to a team of researchers.

Photosynthesis is far from its theoretical maximum efficiency, say the authors of a paper in Cell, published on 26 March. They say that supercomputing advances could allow scientists to model every stage in the process and identify bottlenecks in improving plant growth.

But the authors add that far more science spending is needed to increase yields through these sophisticated genetic manipulations, which include refining the photosynthesis process.

Anything we discover in the lab now wont be in a farmers field for 20 to 30 years, says lead author Stephen Long, a plant biologist at the University of Illinois at Urbana-Champaign (UIUC) in the United States. If we discover we have a crisis then, its already too late.

The paper says that, by 2050, the world is predicted to require 85 per cent more staple food crops than were produced in 2013. It warns that yield gains from last centurys Green Revolution are stagnating as traditional approaches to genetic improvement reach biological limits.

Instead, the group says crops such as rice and wheat, which evolved the more common C3 method of photosynthesis, could be upgraded to the more efficient C4 process found in crops such as maize, sorghum and sugar cane.

This could be done by transplanting genes from C4 plants to widen the spectrum of light the receiving plants can process and improve their growth, the scientists say.

Longs lab has demonstrated in a soon-to-be-published paper that inserting genes from cyanobacteria, a type of photosynthetic bacteria, into crop plants can make photosynthesis 30 per cent more efficient. A project backed by the philanthropic Bill & Melinda Gates Foundation is now attempting to convert rice from C3 to C4

The paper identifies two steps necessary to achieve these gains. First, techniques that allow researchers to insert genes into targeted parts of the genome must be translated from microbe biotechnology into plant biotechnology. Second, existing partial computer models of crop plants must be combined into a complete simulation.

Genetic improvements will also have to work alongside improved farming practices, the authors say. Long says that only half of the yield gains from the Green Revolution were the result of improving crops genetic potential. Another large chunk was getting the agronomy right for those genetic improvements, he says.

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How can we improve plant growth?

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The Guardian view on the latest genetic engineering techniques: we need to talk about this, Professor

Genetic engineering of blood cells could help cure widespread and crippling diseases such as sickle cell anaemia. Above, blood samples collected during a conference on sickle cell anaemia in Senegal. Photograph: Pierre Holtz/EPA

The last time thoughtful and well-informed scientists demanded a moratorium on the use of genetic engineering techniques was in 1975, when it had just become obvious that DNA from one species could be spliced into entirely different organisms and still function there. This is now so commonplace that we take it for granted but at the time it seemed to open up terrible risks. So a conference, convened at Asilomar in California by the man who had come furthest in the world at the technique, drew up very clear safeguards and made them public.

The next stage could be to apply the technique to make modifications in the human genome that can be passed on

The transplantation of genes from one organism to another is now widespread in science and often extremely beneficial. No one doubts that it could be used in wicked and dangerous ways, but with the right safeguards it has an immense power for good. This does not mean that the fears expressed, and acted on, at Asilomar were ridiculous.

Now there are calls for a fresh moratorium on some techniques of genetic engineering. They are worth taking seriously. The demand has been prompted by the spread and incipient commercialisation of a new technique for editing single genes, called Crispr-Cas. This may not be more effective than some of its predecessors, but it is very much simpler to use, which means that far more labs can use it, and for many more purposes. They will be operating in very different political, ethical and regulatory frameworks. We can no longer assume that the exploitation of scientific discoveries will be controlled and directed from the US and Europe. But that does not relieve us of the responsibility of keeping our own housesinorder.

The democratic control of science was an idea much more alive in the 1970s than it is today, when we are numbed by the assumption that all knowledge will be appropriated by the people who paid for its discovery. Shameless attempts to privatise knowledge essential to a technological civilisation, from software patents to the human genome, have flourished in ways thatwere almost unimaginable at the time ofthe Asilomar conference.

Crispr has already been shown capable of some astonishing feats when used on animals. It will undoubtedly lead to more precise genetic engineering in plants. There are clear therapeutic prospects for humans. Aspects of this future are exhilarating. To be able to re-engineer blood cells and cure the widespread and crippling diseases such as thalassaemia and sickle cell anaemia, is an exciting prospect. But pause, and consider the long-term implications. The next stage could be to apply the technique to make modifications in the human genome that can be passed on. It could wipe out some inherited disease. It could also be used to create a world in which the rich were different from you and me not because they have more money but because theyd spent some of it on better genes. It poses grave ethical questions that risk a public backlash against a technique that, properly directed, offers great potential. It is time for another Asilomar, and a global conversation about theproper limits ofscience.

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The Guardian view on the latest genetic engineering techniques: we need to talk about this, Professor

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This Craigslist Ad for a Genetic Engineer Is Pure Wonderful Madness

I have loved a lot of Craigslist ads in my time, but I truly love this one the most. It sounds like a plot ripped from The Avengers or Fantastic Four, crossed with VC-funded biotech startup madness.

Heres what the ad says:

I am a billionaire who needs help creating a mouth wash.solution.gum with CRISPR-Cas9 containing viruses that will change specific genetic loci in my cheek epithelial cells to prevent a positive match against DNA found at the scene of a crime (my DNA was planted by a Doctor who is Doomed).

Skills Required

*CRISPR-Cas9 engineering of mammalian epithelial cells

*Experience in DNA forensics

*Experience with Robotics

*Between 59 and 60 in height and medium build in case I need you to wear a custom built suit

*Must code in Python, Haha, joking, we will write everything in C and Assembly

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This Craigslist Ad for a Genetic Engineer Is Pure Wonderful Madness

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Microbe Produces Ethanol From Switchgrass Without Pretreatment

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The Science

The conventional strategy for producing ethanol from plant biomass requires costly pretreatment and enzyme-driven reactions. Refining another strategy known as consolidated bioprocessing (CPB) could reduce costs. In second-generation CPB, a microorganism splits of water and ferments the products to ethanol, reducing the cost. Now, scientists engineered a strain of a CBP bacterium called Caldicellulosiruptor bescii that efficiently breaks down biomass without pretreatment. The microbe produces ethanol, demonstrating the successful conversion of switchgrass cellulosic biomass.

The Impact

Direct conversion of biomass to ethanol without pretreatment represents a new paradigm for CPB, offering the potential for carbon-neutral, cost-effective, and sustainable biofuel production.

Summary

Producing ethanol from plant biomass typically requires three major steps: physicochemical pretreatment, enzymatic breakdown of biomass into its constituent sugars, and fermentation. Pretreatment and enzymatic hydrolysis are costly steps in the process. CBP could reduce costs. In CBP, unpretreated cellulosic biomass is converted to a biofuel in a single process by a microbe that breaks down the biomass and ferments the resulting sugars. Caldicellulosiruptor bescii had been shown to ferment untreated switchgrass, but it lacked the genes to make ethanol. Because C. bescii is a thermophile (heat loving) and CBP is carried out at elevated temperatures, a gene for a heat-stable enzyme enabling ethanol synthesis was needed. Researchers identified a candidate gene in Clostridium thermocellum and cloned it into C. bescii. The engineered strain of C. bescii was then able to produce ethanol from cellobiose, Avicel, and switchgrass. To optimize ethanol fermentation, two genes were deleted that would otherwise divert fermentation products. In this new C. bescii strain, roughly 30% of biomass was fermented, and 1.7 moles of ethanol were produced for each mole of glucose, an amount close to the theoretical 2.0 moles of ethanol per mole of glucose. Although efficiencies can be further improved, this study is an important step in realizing the potential of CBP and provides a platform for engineering the production of advanced biofuels and other bioproducts directly from cellulosic biomass without harsh and expensive pretreatment.

Funding

This research was conducted by the BioEnergy Science Center, a U.S. Department of Energy (DOE) Bioenergy Research Center supported by the Office of Biological and Environmental Research within DOE's Office of Science.

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Microbe Produces Ethanol From Switchgrass Without Pretreatment

Recommendation and review posted by Bethany Smith

TGen finds likely genetic source of muscle weakness in 6 previously undiagnosed children

Simple genetic test by TGen reveals likely causes of disease, after other extensive testing failed; 1 child's case produces discovery

PHOENIX, Ariz. -- April 9, 2015 -- Scientists at the Translational Genomics Research Institute (TGen), using state-of-the-art genetic technology, have discovered the likely cause of a child's rare type of severe muscle weakness.

The child was one of six cases in which TGen sequenced -- or decoded -- the genes of patients with Neuromuscular Disease (NMD) and was then able to identify the genetic source, or likely genetic source, of each child's symptoms, according to a study published April 8 in the journal Molecular Genetics & Genomic Medicine.

"In all six cases of myopathy, or muscle weakness, these children had undergone extensive, expensive and invasive testing -- often over many years -- without a successful diagnosis, until they enrolled in our study," said Dr. Lisa Baumbach-Reardon, an Associate Professor of TGen's Integrated Cancer Genomics Division and the study's senior author.

This is a prime example of the type of "personalized medicine" TGen uses to zero in on diagnoses for patients, and to help their physicians find the best possible treatments.

"Our results demonstrate the diagnostic value of a comprehensive approach to genetic sequencing," said Dr. Baumbach-Reardon. "This type of next-generation sequencing can greatly improve the ability to identify pathogenic, or disease-causing, genetic variants with a single, timely, affordable test."

In one of the six cases, TGen researchers found a unique disease-causing variant, or mutation, in the CACNA1S gene for a child with severe muscle weakness in addition to ophthalmoplegia, or the inability to move his eyes. Properly functioning CACNA1S is essential for muscle movement. More specifically, CACNA1S senses electrical signals from the brain and enables muscles to contract.

"To our knowledge, this is the first reported case of severe congenital myopathy with ophthalmoplegia resulting from pathogenic variants in CACNA1S," said Dr. Jesse Hunter, a TGen Senior Post-Doctoral Fellow, and the study's lead author.

Learning the specific genetic cause of symptoms is a key step in finding new therapeutic drugs that could treat the patient's disease.

In another closely related case, TGen's genetic testing found a pathogenic variant in the RYR1 gene in a case of calcium channel myopathy. When the brain sends an electrical signal, CACNA1S opens the RYR1 calcium channel flooding muscles with calcium and causing them to contract. When either partner of this duo doesn't function correctly, devastating muscle weakness results.

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TGen finds likely genetic source of muscle weakness in 6 previously undiagnosed children

Recommendation and review posted by Bethany Smith

Likely genetic source of muscle weakness found in six previously undiagnosed children

Scientists at the Translational Genomics Research Institute (TGen), using state-of-the-art genetic technology, have discovered the likely cause of a child's rare type of severe muscle weakness.

The child was one of six cases in which TGen sequenced -- or decoded -- the genes of patients with Neuromuscular Disease (NMD) and was then able to identify the genetic source, or likely genetic source, of each child's symptoms, according to a study published April 8 in the journal Molecular Genetics & Genomic Medicine.

"In all six cases of myopathy, or muscle weakness, these children had undergone extensive, expensive and invasive testing -- often over many years -- without a successful diagnosis, until they enrolled in our study," said Dr. Lisa Baumbach-Reardon, an Associate Professor of TGen's Integrated Cancer Genomics Division and the study's senior author.

This is a prime example of the type of "personalized medicine" TGen uses to zero in on diagnoses for patients, and to help their physicians find the best possible treatments.

"Our results demonstrate the diagnostic value of a comprehensive approach to genetic sequencing," said Dr. Baumbach-Reardon. "This type of next-generation sequencing can greatly improve the ability to identify pathogenic, or disease-causing, genetic variants with a single, timely, affordable test."

In one of the six cases, TGen researchers found a unique disease-causing variant, or mutation, in the CACNA1S gene for a child with severe muscle weakness in addition to ophthalmoplegia, or the inability to move his eyes. Properly functioning CACNA1S is essential for muscle movement. More specifically, CACNA1S senses electrical signals from the brain and enables muscles to contract.

"To our knowledge, this is the first reported case of severe congenital myopathy with ophthalmoplegia resulting from pathogenic variants in CACNA1S," said Dr. Jesse Hunter, a TGen Senior Post-Doctoral Fellow, and the study's lead author.

Learning the specific genetic cause of symptoms is a key step in finding new therapeutic drugs that could treat the patient's disease.

In another closely related case, TGen's genetic testing found a pathogenic variant in the RYR1 gene in a case of calcium channel myopathy. When the brain sends an electrical signal, CACNA1S opens the RYR1 calcium channel flooding muscles with calcium and causing them to contract. When either partner of this duo doesn't function correctly, devastating muscle weakness results.

Five of the six cases involved patients under the care of Dr. Saunder Bernes, a neurologist at Barrow Neurological Institute at Phoenix Children's Hospital. Dr. Bernes referred all five cases to TGen for genetic sequencing in an effort to find the causes of the children's muscle weakness.

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Likely genetic source of muscle weakness found in six previously undiagnosed children

Recommendation and review posted by Bethany Smith

Genetics II Notes Bio – Video


Genetics II Notes Bio
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By: Kirsten Lindsay-Hudak

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Genetics II Notes Bio - Video

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Spring Fling Genetics Conference Dr. Dan Weigel Speaking – Video


Spring Fling Genetics Conference Dr. Dan Weigel Speaking
Spring Fling Genetics Conference Dr. Dan Weigel Speaking.

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Spring Fling Genetics Conference Dr. Dan Weigel Speaking - Video

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#35 Smartheads – Spannabis 2015 DNA Genetics – Video


#35 Smartheads - Spannabis 2015 DNA Genetics
Am having a talk with the guys from DNA Genetics. Have a look! Like Smartheads on Facebook! http://www.facebook.com/smartheadstv Chek out the channel: Smartheads TV Follow me on Instagram:...

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#35 Smartheads - Spannabis 2015 DNA Genetics - Video

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