In a groundbreaking study that provides scientists with a critical new understanding of stem cell development and its role in disease, UCLA researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research led by Dr. Kathrin Plath, professor of biological chemistry, have established a first-of-its-kind methodology that defines the unique stages by which specialized cells are reprogrammed into stem cells that resemble those found in the embryo.

The study was published online ahead of print in the journal Cell.

Induced pluripotent stem cells (known as iPSCs) are similar to human embryonic stem cells in that both cell types have the unique ability to self-renew and have the flexibility to become any cell in the human body. iPSC cells, however, are generated by reprogramming skin or blood cells and do not require an embryo.

Reprogramming is a long process (about one to two weeks) and largely inefficient, with typically less than one percent of the primary skin or blood cells successfully completing the journey to becoming an iPSC. The exact stages a cell goes through during the reprogramming process are also not well understood. This knowledge is important, as iPSCs hold great promise in the field of regenerative medicine, as they can provide a single source of patient-specific cells to replace those lost to injury or disease. They can also be used to create novel disease models from which new drugs and therapies can be developed.

"This research has broad impact, because by deepening our understanding of cell reprogramming we have the potential to improve disease modeling and the generation of better sources of patient-specific specialized cells suitable for replacement therapy," said Plath. "This can ultimately benefit patients with new and better treatments for a wide range of diseases.

Drs. Vincent Pasque and Jason Tchieu, postdoctoral fellows in the lab of Dr. Plath and co-first authors of the study, developed a roadmap of the reprogramming process using detailed time-course analyses. They induced the reprogramming of skin cells into iPSC, then observed and analyzed on a daily basis or every other day the process of transformation at the single-cell level. The data were collected and recorded over a period of up to two weeks.

Plath's team found that the changes that happen in cells during reprogramming occur in a sequential stage-by-stage manner, and that importantly, the stages were the same across all the different reprogramming systems and different cell types analyzed.

"The exact stage of reprogramming of any cell can now be determined," said Pasque. "This study signals a big change in thinking, because it provides simple and efficient tools for scientists to study stem cell creation in a stage-by-stage manner. Most studies to date ignore the stages of reprogramming, but we can now seek to better understand the entire process on both a macro and micro level."

Plath's team further discovered that the stages of reprogramming to iPSC are different from what was expected. They found that it is not simply the reversed sequence of stages of embryo development. Some steps are reversed in the expected order; others do not actually happen in the exact reverse order and resist a change until late during reprogramming to iPSCs.

"This reflects how cells do not like to change from one specialized cell type to another and resist a change in cell identity," said Pasque. "Resistance to reprogramming also helps to explain why reprogramming takes place only in a very small proportion of the starting cells."

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SAN FRANCISCO -

Mike Hinshaw and Katie Jackson have been a couple since college, but they've known each other much longer.

"We've been together forever. I've actually known Mike since I was five years old," Jackson said.

A marriage and three kids later, they've been through good times and bad. The worst came nine years ago when Hinshaw found out he had Huntington's disease.

"My father had it. He died from it," Hinshaw explained.

Huntington's causes uncontrollable movements and mental decline. There's no cure.

"Unfortunately, it ends in death. It's a fatal disease," said Dr. Vicki Wheelock, neurologist, health sciences clinical professor of neurology and director of HDSA Center of Excellence at UC Davis.

Now, researchers are gearing up for a new trial in humans. Patients will have special bone marrow stem cells injected directly into their brains.

"We've engineered them to make a growth factor that's like a fertilizer for the neurons," said Dr. Jan Nolta, professor and director of the Institute for Regenerative Cures at UC Davis.

That growth factor, BDNF, restored healthy brain cells and reduced behavior deficits in mice. Researchers hope the stem cells will also be the answer to slowing the disease in humans.

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A powerful "genome editing" technology known as CRISPR has been used by researchers since 2012 to trim, disrupt, replace or add to sequences of an organism's DNA. Now, scientists at Johns Hopkins Medicine have shown that the system also precisely and efficiently alters human stem cells.

In a recent online report on the work in Molecular Therapy, the Johns Hopkins team says the findings could streamline and speed efforts to modify and tailor human-induced pluripotent stem cells (iPSCs) for use as treatments or in the development of model systems to study diseases and test drugs.

"Stem cell technology is quickly advancing, and we think that the days when we can use iPSCs for human therapy aren't that far away," says Zhaohui Ye, Ph.D., an instructor of medicine at the Johns Hopkins University School of Medicine. "This is one of the first studies to detail the use of CRISPR in human iPSCs, showcasing its potential in these cells."

CRISPR originated from a microbial immune system that contains DNA segments known as clustered regularly interspaced short palindromic repeats. The engineered editing system makes use of an enzyme that nicks together DNA with a piece of small RNA that guides the tool to where researchers want to introduce cuts or other changes in the genome.

Previous research has shown that CRISPR can generate genomic changes or mutations through these interventions far more efficiently than other gene editing techniques, such as TALEN, short for transcription activator-like effector nuclease.

Despite CRISPR's advantages, a recent study suggested that it might also produce a large number of "off-target" effects in human cancer cell lines, specifically modification of genes that researchers didn't mean to change.

To see if this unwanted effect occurred in other human cell types, Ye; Linzhao Cheng, Ph.D., a professor of medicine and oncology in the Johns Hopkins University School of Medicine; and their colleagues pitted CRISPR against TALEN in human iPSCs, adult cells reprogrammed to act like embryonic stem cells. Human iPSCs have already shown enormous promise for treating and studying disease.

The researchers compared the ability of both genome editing systems to either cut out pieces of known genes in iPSCs or cut out a piece of these genes and replace it with another. As model genes, the researchers used JAK2, a gene that when mutated causes a bone marrow disorder known as polycythemia vera; SERPINA1, a gene that when mutated causes alpha1-antitrypsin deficiency, an inherited disorder that may cause lung and liver disease; and AAVS1, a gene that's been recently discovered to be a "safe harbor" in the human genome for inserting foreign genes.

Their comparison found that when simply cutting out portions of genes, the CRISPR system was significantly more efficient than TALEN in all three gene systems, inducing up to 100 times more cuts. However, when using these genome editing tools for replacing portions of the genes, such as the disease-causing mutations in JAK2 and SERPINA1 genes, CRISPR and TALEN showed about the same efficiency in patient-derived iPSCs, the researchers report.

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'CRISPR' science: Newer genome editing tool shows promise in engineering human stem cells

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Vanderbilt University researcher William Mitchell, M.D., Ph.D., and colleagues in Germany and Canada have demonstrated a method for detecting "cell-free" tumor DNA in the bloodstream.

Mitchell believes the technique will be transformative in providing improved cancer diagnostics that can both predict treatment outcomes and monitor patient responses to therapy.

In a large retrospective study of blood samples, the researchers showed that the method, called a "liquid biopsy," could accurately distinguish prostate cancer from normal controls without prior knowledge of the genetic "signature" of the tumors, and with over three times the sensitivity of current prostate-specific antigen (PSA) screening.

The study appears in the January issue of Clinical Chemistry (volume 61, page 239), which is dedicated to "Molecular Diagnostics: A Revolution in Progress."

"Based on the reported data and work in progress, I believe the 'liquid biopsy' will revolutionize cancer diagnostics, not only before a patient begins therapy but also following patient responses to therapy," said Mitchell, the paper's corresponding author and professor of Pathology, Microbiology and Immunology.

The study collected serum from more than 200 patients with prostate cancer and more than 200 controls. The samples included PSA levels and prostate tissue biopsy grading, called the Gleason score.

The researchers reported that the technique distinguished prostate cancer from normal controls with 84-percent accuracy, and cancer from benign hyperplasia and prostatitis with an accuracy of 91 percent.

Because the method quantifies the inherent chromosomal instability of cancer and can be followed as a function of time without having to do an invasive tissue biopsy, it is called a "liquid biopsy."

It's been known for many years that dying cells, including tumor cells, shed DNA into the bloodstream.

But only recently has technology, notably "next-generation sequencing," made it possible to reliably distinguish and quantify cancer-specific DNA from normal controls by the identification and chromosomal location of billions of specific DNA fragments present in blood as cell-free DNA.

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Blood test for prostate cancer investigated

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THE WOODLANDS VGXI Inc., a Woodlands-based manufacturer of plasmid DNA used in vaccine and gene therapy clinical trials announced an expansion that will double its capacity and likely create jobs, according to VGXI Inc. Business Development Manager Christy Franco.

The expansion will add 3,000 square feet to the building, located at 2700 Research Forest Drive, and will include a small-scale cGMP (compliant with the U.S. Food and Drug Administrations current Good Manufacturing Practice regulations) production plant.

The expansion is in response to recent growth in the market for DNA-based pharmaceuticals.

Weve been seeing it coming, Franco said of the need to expand facilities. Clients need quality DNA for clinical trials.

This is an exciting time for the field of gene therapy and DNA vaccines, Franco state d in a press release. As these technologies mature, more and more companies are moving their products into clinical trials and closer to regulatory approval.

Franco said VGXI is contracted at capacity and the expansion will allow the company to perform multiple client campaigns simultaneously.

VGXI Inc., which employees 40-50 people in The Woodlands, has manufactured plasmid products for clinical trials in the U.S., EU, Asia and Australia over the past 15 years using a patented manufacturing process.

VGXI is a wholly owned subsidiary contract manufacturing organization of GeneOne Life Science Inc. and received the Vaccine Industry Excellence Award for best CMO in 2013 and 2014.

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Woodlands-based DNA manufacturer expands facilities

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Up to a quarter of patients with bowel cancer who have a family history of the disease could have the causes of their cancer identified through gene testing, a new study reports.

Wider testing for known cancer genes in patients with bowel cancer could help in their diagnosis and treatment, and in the early detection or prevention of cancers in their relatives, the researchers said.

Scientists at The Institute of Cancer Research, London, sequenced genes in more than 600 patients with a family history of bowel cancer - and found known mutations could be identified in 'a high proportion'.

The researchers, who received funding from Cancer Research UK and the European Union, said their findings suggested patients with bowel cancer and a family history should routinely be tested for a range of known cancer genes.

But they stressed there was also a need for further research to identify new cancer genes that could be involved in the three quarters of cases where no mutations in known cancer genes could be detected.

Scientists at The Institute of Cancer Research (ICR) sequenced the DNA of 626 patients with bowel cancer and a family history of early-onset disease from 140 clinical centres across the UK.

Their study, published in the Journal of Clinical Oncology today (Monday), found that inherited susceptibility to bowel cancer was common among patients with a family history of the disease.

Inherited mutations in a well-known group of genes called the mismatch repair genes alone accounted for 11% of familial bowel cancers. Genetic screening to detect defects in these genes has previously been shown to reduce bowel cancer death rates.

Professor Richard Houlston, Professor of Molecular and Population Genetics at The Institute of Cancer Research, London, said:

"Knowing which cancer gene has caused bowel cancer isn't just important for researchers - it's crucial for the treatment, counselling and surveillance of patients and their relatives.

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Insight into regulation of the genes that allow the immune system to recognize pathogens will help scientists rationally design new vaccines and prevent autoimmunity

WORCESTER, MA - UMass Medical School scientists Jeremy Luban, MD, and Manuel Garber, PhD, will be principal investigators on a 3-year, $6.1 million grant to develop a model for predicting whether a given gene will be turned on or off under specific conditions. Funding for the grant comes from the recently launched Genomics of Gene Regulation (GGR) program at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health. In total, $28 million in new grants aimed at deciphering the language of gene expression were awarded.

"Why a certain gene is expressed in a specific cell at a given time is an essential biological question that is fundamental to our understanding of life and disease," said Dr. Luban, MD, the David J. Freelander Professor in AIDS Research and professor of molecular medicine. "This grant will help us decipher the rules that govern gene expression. Ultimately, such information will help explain why one person survives a viral infection and another person does not."

Dr. Garber, PhD, director of the Bioinformatics Core and associate professor of molecular medicine said "Understanding of the regulatory code network - the DNA elements that control when and for how long a gene is expressed - has been elusive. The work we'll carry out in this project will allow us to model and test the regulatory code of dendritic cells. As a result, we would be able to predict the impact of mutations that do not directly affect the gene product but that affect how and when the gene is made."

Over the past decade, new scientific evidence suggests that genomic regions outside of the primary protein-coding regions of our DNA harbor variations that play an important role in disease. These regions contain elements that control gene expression and, when altered, can increase the risk for a disease.

The GGR grants will allow researchers to study complex gene networks and pathways in different cells types and systems. The resulting insight into the mechanisms controlling gene expression may ultimately lead to new avenues for developing treatments for diseases affected by faulty gene regulation, such as cancer, diabetes and Parkinson's disease.

"There is a growing realization that the ways genes are regulated to work together can be important for understanding disease," said Mike Pazin, PhD, a program director in the Functional Analysis Program in NHGRI's Division of Genome Sciences. "The Genomics of Gene Regulation program aims to develop new ways for understanding how the genes and switches in the genome fit together as networks. Such knowledge is important for defining the role of genomic differences in human health and disease."

Luban and Garber will be working with UMMS colleagues Job Dekker, PhD, co-director of the Program in Systems Biology and professor of biochemistry & molecular pharmacology; Oliver Rando, PhD, MD, professor of biochemistry & molecular pharmacology, and Scot Wolfe, associate professor of biochemistry & molecular pharmacology, to develop a model system for exploring gene regulation using human dendritic cells.

The dendritic cell is a key part of the innate immune system that distinguishes self from non-self and, when appropriate, directs the body to attack invading pathogens. In its immature state dendritic cells help prevent autoimmunity by keeping the immune system's T-cells from attacking the body's own cells. When an immature dendritic cell encounters a pathogen, though, a developmental switch is activated and the cell undergoes profound changes in gene expression as it matures. In contrast to immature dendritic cells, these mature cells elicit a potent immune response from T-cells that targets the pathogen.

Luban, Garber and colleagues will examine the changes that the dendritic cell undergoes when it encounters a pathogen and moves from the immature to the mature state. Among the factors they will look at are the genes that are turned on and off during this process. They will examine changes in transcription factors, chromatin modifying enzymes and the cis-acting DNA elements. Linking these elements to specific changes in gene expression should provide a model for predicting the expression of specific genes in dendritic and other cells.

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IMAGE:New grants fund research on how the genes and switches in the genome fit together as networks. view more

Credit: Darryl Leja, NHGRI

The National Institutes of Health has awarded grants of more than $28 million aimed at deciphering the language of how and when genes are turned on and off. These awards emanate from the recently launched Genomics of Gene Regulation (GGR) program of the National Human Genome Research Institute (NHGRI), part of NIH.

"There is a growing realization that the ways genes are regulated to work together can be important for understanding disease," said Mike Pazin, Ph.D., a program director in the Functional Analysis Program in NHGRI's Division of Genome Sciences. "The GGR program aims to develop new ways for understanding how the genes and switches in the genome fit together as networks. Such knowledge is important for defining the role of genomic differences in human health and disease."

With these new grants, researchers will study gene networks and pathways in different systems in the body, such as skin, immune cells and lung. The resulting insights into the mechanisms controlling gene expression may ultimately lead to new avenues for developing treatments for diseases affected by faulty gene regulation, such as cancer, diabetes and Parkinson's disease.

Over the past decade, numerous studies have suggested that genomic regions outside of protein-coding regions harbor variants that play a role in disease. Such regions likely contain gene-control elements that are altered by these variants, which increase the risk for a disease.

"Knowing the interconnections of these regulatory elements is critical for understanding the genomic basis of disease," Dr. Pazin said. "We do not have a good way to predict whether particular regulatory elements are turning genes off or activating them, or whether these elements make genes responsive to a condition, such as infection. We expect these new projects will develop better methods to answer these types of questions using genomic data."

Recipients of the new GGR three-year grants (pending available funds) are:

The body's immune system can cause inflammation, which plays a central role in some diseases. The investigators will use a mouse model to study genomic mechanisms underlying immune system activity during inflammation. They will determine what and when genes are turned on and off, and how they are controlled, in the development and activation of two different types of immune cells with opposite functions. One cell type promotes the immune system's response and inflammation; the other dampens these functions.

Researchers will characterize how human lung epithelial cells respond to anti-inflammatory drugs called glucocorticoids (a type of steroid hormone). They will determine what and when genes are turned on and off, and how this process is controlled. They hope to create a model for this type of response, and detail the gene regulation patterns involved. This may allow the researchers to understand how glucocorticoids control both anti-inflammatory and metabolic responses.

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NIH grants aim to decipher the language of gene regulation

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A new study of twins suggests that insomnia in childhood and adolescence is partially explained by genetic factors.

Results show that clinically significant insomnia was moderately heritable at all stages of the longitudinal study. Genetic factors contributed to 33 to 38 percent of the insomnia ratings at the first two stages of the study, when participants had an average age of 8 to 10 years. The heritability of insomnia was 14 to 24 percent at the third and fourth follow-up points, when the average age of participants was 14 to 15 years. The remaining source of variance in the insomnia ratings was the non-shared environment, with no influence of shared, family-wide factors. Further analysis found that genetic influences around age 8 contributed to insomnia at all subsequent stages of development, and that new genetic influences came into play around the age of 10 years.

"Insomnia in youth is moderately related to genetic factors, but the specific genetic factors may change with age," said study author Philip Gehrman, PhD, assistant professor in the Department of Psychology at the University of Pennsylvania in Philadelphia. "We were most surprised by the fact that the genetic factors were not stable over time, so the influence of genes depends on the developmental stage of the child."

Study results are published in the January issue of the journal Sleep.

Insomnia involves difficulty initiating or maintaining sleep, or waking up earlier than desired, according to the American Academy of Sleep Medicine. Children with insomnia may resist going to bed on an appropriate schedule or have difficulty sleeping without intervention by a parent or caregiver. An insomnia disorder results in daytime symptoms such as fatigue, irritability or behavioral problems.

According to the authors, the results suggest that genes controlling the sleep-wake system play a role in childhood insomnia. Therefore, molecular genetic studies are needed to identify this genetic mechanism, which could facilitate the development of targeted treatments.

"These results are important because the causes of insomnia may be different in teens and children, so they may need different treatment approaches," said Gehrman.

The study group comprised 1,412 twin pairs who were between the ages of 8 and 18 years: 739 monozygotic pairs, 672 dizygotic pairs and one pair with unknown zygosity. Participants were followed up at three additional time points. Average ages at each of the four waves of the study were 8, 10, 14 and 15 years. Results were interpreted in terms of the progression across time, rather than differences between discrete age groups. Clinical ratings of insomnia symptoms were assessed by trained clinicians using the Child and Adolescent Psychiatric Assessment and rated according to the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition.

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The above story is based on materials provided by American Academy of Sleep Medicine. Note: Materials may be edited for content and length.

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Genetic factors contribute to insomnia in children, teens, twin study suggests

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Snail Genetics - Counter-Strike: Global Offensive
Competitive CSGO I #39;m really good 😉

By: Who Is Deuce Fold

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Snail Genetics - Counter-Strike: Global Offensive - Video

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History explains why people with the malady, and their physicians, are cautious to believe that a cure is in sight

In 2011, a remarkable study in the New England Journal of Medicine detailed the successful treatment of six adults with haemophilia B, which is caused by a deficiency in the coagulation protein known as factor IX. All of the participants were able to eliminate or reduce the frequency of clotting-factor-replacement injections the current standard treatment for the disease after their livers began producing functional levels of factor IX. The experimental therapy came in the form of an adeno-associated virus (AAV) carrying a gene that encodes instructions for production of normal levels of human factor IX. Three trials of AAV-mediated gene transfer in patients with haemophilia B are ongoing, with high expectations.

After more than 20 years of research on gene transfer, it is a promising time for haemophilia therapies. It now seems likely that a single-dose treatment for haemophilia B using an AAV or another gene-transfer technique will be a viable option for many people in the next decade or two.

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Gene Therapys Hemophilia Promise Is Tempered by Memories of Past Tragedies

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History explains why people with the malady, and their physicians, are cautious to believe that a cure is in sight

In 2011, a remarkable study in the New England Journal of Medicine detailed the successful treatment of six adults with haemophilia B, which is caused by a deficiency in the coagulation protein known as factor IX. All of the participants were able to eliminate or reduce the frequency of clotting-factor-replacement injections the current standard treatment for the disease after their livers began producing functional levels of factor IX. The experimental therapy came in the form of an adeno-associated virus (AAV) carrying a gene that encodes instructions for production of normal levels of human factor IX. Three trials of AAV-mediated gene transfer in patients with haemophilia B are ongoing, with high expectations.

After more than 20 years of research on gene transfer, it is a promising time for haemophilia therapies. It now seems likely that a single-dose treatment for haemophilia B using an AAV or another gene-transfer technique will be a viable option for many people in the next decade or two.

*You must have purchased this issue or have a qualifying subscription to access this content

2015 Scientific American, a Division of Nature America, Inc.

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Gene Therapys Haemophilia Promise Is Tempered by Memories of Past Tragedies

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Overcoming the Shock of a Spinal Cord Injury (Part 1)
Overcoming the Emotional Shock of a SCI. This video deals with issues I personally ran into in the acute stages of my injury and rehab. Please comment and le...

By: Blake Perkins

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Overcoming the Shock of a Spinal Cord Injury (Part 1) - Video

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NEW Treatments for Crohn #39;s Disease Ulcerative Colitis
Comprised of parts of my September 15, 2014 interview with Dr. Mark L. Chapman of the Mt. Sinai Center for Inflammatory Bowel Disease (IBD) in New York City, this short Video explores the IBD...

By: Michael Weiss

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Radiation therapy uses high-energy rays (such as x-rays) or particles to kill cancer cells. There are 2 main types of radiation therapy external beam radiation therapy and brachytherapy (internal radiation therapy).

External beam radiation therapy (EBRT) focuses radiation from outside the body on the cancer. This is the type of radiation therapy most often used to treat a primary lung cancer or its spread to other organs.

Before your treatments start, the radiation team will take careful measurements to determine the correct angles for aiming the radiation beams and the proper dose of radiation. Treatment is much like getting an x-ray, but the radiation dose is stronger. The procedure itself is painless. Each treatment lasts only a few minutes, although the setup time getting you into place for treatment usually takes longer. Most often, radiation treatments to the lungs are given 5 days a week for 5 to 7 weeks, but this can vary based on the type of EBRT and the reason its being given.

Standard (conventional) EBRT is used much less often than in the past. Newer techniques help doctors treat lung cancers more accurately while lowering the radiation exposure to nearby healthy tissues. These techniques may offer better success rates and fewer side effects. Most doctors now recommend using these newer techniques when they are available.

Three-dimensional conformal radiation therapy (3D-CRT): 3D-CRT uses special computers to precisely map the location of the tumor(s). Radiation beams are shaped and aimed at the tumor(s) from several directions, which makes it less likely to damage normal tissues.

Intensity modulated radiation therapy (IMRT): IMRT is an advanced form of 3D therapy. It uses a computer-driven machine that moves around you as it delivers radiation. Along with shaping the beams and aiming them at the tumor from several angles, the intensity (strength) of the beams can be adjusted to limit the dose reaching the most sensitive normal tissues. This technique is used most often if tumors are near important structures such as the spinal cord. Many major hospitals and cancer centers now use IMRT.

Stereotactic body radiation therapy (SBRT): SBRT, also known as stereotactic ablative radiotherapy (SABR), is sometimes used to treat very early stage lung cancers when surgery isnt an option due to issues with a patients health or in people who do not want surgery.

Instead of giving small doses of radiation each day for several weeks, SBRT uses very focused beams of high-dose radiation given in fewer (usually 1 to 5) treatments. Several beams are aimed at the tumor from different angles. To target the radiation precisely, you are put in a specially designed body frame for each treatment. This reduces the movement of the lung tumor during breathing. Like other forms of external radiation, the treatment itself is painless.

Early results with SBRT for smaller lung tumors have been very promising, and it seems to have a low risk of complications. It is also being studied for tumors that have spread to other parts of the body, such as the bones or liver.

Stereotactic radiosurgery (SRS): SRS is a type of stereotactic radiation therapy that is given in only one session. It can sometimes be used instead of or along with surgery for single tumors that have spread to the brain. In one version of this treatment, a machine called a Gamma Knife focuses about 200 beams of radiation on the tumor from different angles over a few minutes to hours. Your head is kept in the same position by placing it in a rigid frame. In another version, a linear accelerator (a machine that creates radiation) that is controlled by a computer moves around your head to deliver radiation to the tumor from many different angles. These treatments can be repeated if needed.

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Radiation therapy for non-small cell lung cancer

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Some people say that osteoarthritis, cartilage degradation, and chronic joint pains degenerative diseases associated with agingare conditions with no cure, but Dr. Charlie Poblete and Dr. Jae Pak say otherwise.

It is a new era of medicine, opens Dr. Jae Pak, one of Koreas premier orthopedic stem cell surgeons and a visiting expert consultant of the Stem Care Orthopedics Department under Aivee Institute (AI). He was recently in the country to shed light on stem cell therapy and how it offers more accessible treament options for patients suffering from degenerative orthopedic conditions.

Dr. Pak was joined by Dr. Charlie Poblete, one of the countrys leading orthopedic surgeon who has a special interest on regenerative medicine and stem cells. Incidentally, Dr. Poblete is the head of the Stem Care Orthopedic Department of AI. Stem cells are not really part of alternative medicine. Its part of a modern medicine because we are talking about the biochemistry that goes on in the body with stem cell treatment, Dr. Charlie relates while adding, the good thing about medicine nowadays is its starting to look at the molecular aspect of the body, the molecular and cellular side of medicine.

Over the years, stem cell therapy has been touted as one procedure that can heal multitude of bone, cartilage, and joint ailments. Stem cells are the bodys natural healing cells. They are recruited by chemical signals emitted by damaged tissues to repair and regenerate the damaged cells. Stem cells derived from an individuals tissues may well be the next major development in medicine. In the right environment, these stem cells can change into bone, cartilage, muscle, fat, collagen, neural tissue, blood vessels, and even some organs. Stem cells may also effect healing by secreting special chemical messengers that repair damaged tissue.

There are many clinical conditions that benefits from stem cell therapy: heart attack patients have shown quicker healing period, improved condition for patients with multiple sclerosis, muscular dystrophy, Parkinsons disease, ALS, and stroke. Stem cells may also be effective in the treatment of macular degeneration, Crohns disease, and numerous pulmonary conditions. Also, stem cells are now used for patients with kidney failure and in the treatment of critical limb ischemia.

Stem Cell therapy is a simple procedure. Fat is aspirated from the tummy or the thighs, and then we separate the stem cells from them. It is then activated and injected into joints to restore and regenerate, explains Dr. Jae.

Stem Care by The Aivee Group is the countrys pioneer in advanced Autologous Stem Cell Therapy with an esteemed orthopedic team of doctors and surgeons regarded with international qualifications. The institute, with its CEO and medical director Dr. Z. Teo, together with his wife dermatologist Dr. Aivee Teo, now features a stronger multifaceted protocol in treating orthopedic ailments with a faster rate of positive patient response. They are also adept in complimentary therapies to further intensify the restorative powers of stem cells through the effective use of Growth Factors, Shockwave, Radio Frequency, and Electro Magnetic Therapies. 4033245, 4031982, 09209665613, 09175210222. http://www.stemcareinstitute.com

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Restore and Regenerate

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(CNN)-- Ever marvel at someone who smoked and still lived to be 90? Just plain good luck, researchers say. And those who live like Puritans and get cancer anyway?

That's bad luck -- and it's the primary cause of most cancer cases, says a Johns Hopkins Medicine research study.

Roughly two-thirds of cancers in adults can be attributed to random mutations in genes capable of driving cancer growth, said two scientists who ran statistics on cancer cases.

That may sound jaw-dropping. And Johns Hopkins anticipates that the study will change the way people think about cancer risk factors.

They also believe it could lead to changes in the funding of cancer studies, with a greater focus on finding ways to detect those cancers attributed to random mutations in genes at early, curable stages.

Smoking can still kill you

But, no, that's not permission to smoke or to not use sunblock.

Some forms of cancer are exceptions, where lifestyle and environment play a big role. Lung cancer is one of them. So is skin cancer.

And, if cancer runs in your family, this unfortunately doesn't mean you're in the clear. Some cancers are more strongly influenced by genetic heritage than others.

"The remaining third (of cancer cases) are due to environmental factors and inherited genes," the Kimmel Cancer Center said in a statement on the study published Friday in the magazine Science.

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Random Gene Mutations Primary Cause Of Most Cancer

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(CNN) - Ever marvel at someone who smoked and still lived to be 90? Just plain good luck, researchers say. And those who live like Puritans and get cancer anyway?

That's bad luck -- and it's the primary cause of most cancer, says a Johns Hopkins Medicine research study.

Roughly "two-thirds of cancer incidence" in adults can be attributed to random mutations in genes capable of driving cancer growth, said two scientists who ran statistics on cancer cases.

That may sound jaw-dropping. And Johns Hopkins anticipates that the study will change the way people think about cancer risk factors.

They also believe it could lead to changes in the funding of cancer studies, with a greater focus on finding ways to detect those cancers attributed to random mutations in genes at early, curable stages.

But, no, that's not permission to smoke or to not use sunblock.

Some forms of cancer are exceptions, where lifestyle and environment play a big role. Lung cancer is one of them. So is skin cancer.

And, if cancer runs in your family, this unfortunately doesn't mean you're in the clear. Some cancers are more strongly influenced by genetic heritage than others.

"The remaining third (of cancer incidences) are due to environmental factors and inherited genes," the Kimmel Cancer Center said in a statement on the study published Friday in the magazine Science.

In fact, all three factors work together.

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Scientists: Random gene mutations -- 'bad luck' -- primary cause of most cancer

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Genetic Engineering+long one lives;Donna Douglas
What agency has power to control when one born+dies? As in Donna Douglas, She plays Ellie Mae ClampettBeverly Hillbillies.

By: Peggy Ann Childers

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'Genetic engineering' or genetic manipulation as it should properly be called, relies essentially on the ability to manipulate molecules in vitro. Most biomolecules exist in low concentrations & as complex, mixed populations which it is not possible to work with effectively. This problem was solved in 1970 using the molecular biologist's favourite bug, Escherichia coli , a normally innocuous commensal occupant of the human gut. By inserting a piece of DNA of interest into a vector molecule, i.e. a molecule with a bacterial origin of replication, when the whole recombinant construction is introduced into a bacterial host cell, a large number of identical copies is produced. Together with the rapid growth of bacterial colonies all derived from a single original cell bearing the recombinant vector, in a short time (e.g. a few hours) a large amount of the DNA of interest is produced. This can be purified from contaminating bacterial DNA easily & the resulting product is said to have been 'cloned'.

Most vector molecules were originally derived from one of two sources:

Vector molecules & cloning are not the only contribution which microorganisms have made to genetic manipulation. The actual task of altering the DNA at a molecular level is carried out by the use of naturally-occurring enzymes - most of which are derived from bacteria or viruses:

EcoRI from Escherichia coli BamHI from Bacillus amyloliquefaciens

These systems operate by enzymes which recognise specific short regions of DNA sequence, which are usually palindromic ('Able was I ere I saw Elba'), e.g:

5' GGATCC 3' 3' CCTAGG 5'

Recently, thermostable polymerases have become important, e.g. Taq DNA polymerase from Thermus aquaticus. This bacterium has evolved to grow in hot springs at temperatures which kill most other species. These enzymes allow the amplification of as little as one molecule of DNA into a large amount by means of repeated cycles of melting, primer annealing & extension by the enzyme which is not destroyed by the high temperatures used in this process. This is known as the polymerase chain reaction:

The utility of cloning is partly analytical, i.e it provides the ability to determine the genetic organization of particular regions or whole genomes (the human genome will soon be underway). However, it also facilitates the production of naturally-occurring & artificially-modifed biological products by the expression of cloned genes. The ability to take a gene from one organism (e.g. man or a tree), clone it in E. coli & express it in another (e.g. a yeast) is dependent on the universality of the genetic code, i.e. the triplets of bases which encode amino acids in proteins:

Link:
The Role of Microorganisms in Genetic Engineering

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Its first attempt to develop genetically engineered grass ended disastrously for Scotts Miracle-Gro Co. The grass escaped into the wild from test plots in Oregon in 2003, dooming the chances that the government would approve the product for commercial use.

Yet Scotts is once again developing genetically modified grass that would need less mowing, be a deeper green and be resistant to damage from the popular weedkiller Roundup. But this time the grass will not need federal approval before it can be field-tested and marketed.

Scotts and several other companies are developing genetically modified crops using techniques that either are outside the jurisdiction of the Agriculture Department or use new methods like genome editing that were not envisioned when the regulations were created.

The department has said, for example, that it has no authority over a new herbicide-resistant canola, or over a corn that would create less pollution from livestock waste, or switch grass tailored for biofuel production, or an ornamental plant that glows in the dark.

The trend alarms critics of biotech crops, who say there can be unintended effects of genetic modification, regardless of the process.

"They are using a technical loophole so that what are clearly genetically engineered crops and organisms are escaping regulation," said Michael Hansen, a senior scientist at Consumers Union. He said the grass "can have all sorts of ecological impact, and no one is required to look at it."

'Obsolete' regulation

Even some people who say the crops are safe and the regulations overly burdensome have expressed concern that because some crops can be left unregulated, the whole oversight process is confusing and illogical, in some cases doing more harm than good.

In November's Nature Biotechnology, plant researchers at the University of California, Davis wrote that the regulatory framework had become "obsolete and an obstacle to the development of new agricultural products."

But companies using the new techniques say that if the methods were not labeled genetic engineering, novel crops could be marketed or grown in Europe and other countries that do not readily accept genetically modified crops.

Link:
A gray area in regulation of genetically modified crops

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DARIEN, IL - A new study of twins suggests that insomnia in childhood and adolescence is partially explained by genetic factors.

Results show that clinically significant insomnia was moderately heritable at all stages of the longitudinal study. Genetic factors contributed to 33 to 38 percent of the insomnia ratings at the first two stages of the study, when participants had an average age of 8 to 10 years. The heritability of insomnia was 14 to 24 percent at the third and fourth follow-up points, when the average age of participants was 14 to 15 years. The remaining source of variance in the insomnia ratings was the non-shared environment, with no influence of shared, family-wide factors. Further analysis found that genetic influences around age 8 contributed to insomnia at all subsequent stages of development, and that new genetic influences came into play around the age of 10 years.

"Insomnia in youth is moderately related to genetic factors, but the specific genetic factors may change with age," said study author Philip Gehrman, PhD, assistant professor in the Department of Psychology at the University of Pennsylvania in Philadelphia. "We were most surprised by the fact that the genetic factors were not stable over time, so the influence of genes depends on the developmental stage of the child."

Study results are published in the January issue of the journal Sleep.

Insomnia involves difficulty initiating or maintaining sleep, or waking up earlier than desired, according to the American Academy of Sleep Medicine. Children with insomnia may resist going to bed on an appropriate schedule or have difficulty sleeping without intervention by a parent or caregiver. An insomnia disorder results in daytime symptoms such as fatigue, irritability or behavioral problems.

According to the authors, the results suggest that genes controlling the sleep-wake system play a role in childhood insomnia. Therefore, molecular genetic studies are needed to identify this genetic mechanism, which could facilitate the development of targeted treatments.

"These results are important because the causes of insomnia may be different in teens and children, so they may need different treatment approaches," said Gehrman.

The study group comprised 1,412 twin pairs who were between the ages of 8 and 18 years: 739 monozygotic pairs, 672 dizygotic pairs and one pair with unknown zygosity. Participants were followed up at three additional time points. Average ages at each of the four waves of the study were 8, 10, 14 and 15 years. Results were interpreted in terms of the progression across time, rather than differences between discrete age groups. Clinical ratings of insomnia symptoms were assessed by trained clinicians using the Child and Adolescent Psychiatric Assessment and rated according to the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition.

###

The study was supported by funding from the Mid-Atlantic Twin Registry and the National Center for Advancing Translational Sciences of the National Institutes of Health. Additional support was provided by the Virginia Retirement System and the U.S. Department of Social Security. Data analyses were performed at Northumbria University in the U.K., and data were collected at the Virginia Commonwealth University School of Medicine in Richmond.

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Twin study suggests genetic factors contribute to insomnia in children, teens

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TIME Health Infectious Disease Health Workers See Promise in Software to Tackle Drug-Resistant Bacteria Getty Images New software may predict genetic changes in bacteria before they occur

Researchers have developed a new software that predicts changes in bacteria that can make them drug-resistant.

Drug resistance happens when disease-causing bacteria adapts to antibiotics and becomes less responsive to treatment. Antibiotic-resistant bacteria cause at least 2 million infections and 23,000 deaths in the United States each year, but because the bacteria are constantly reproducing, its hard to determine what changes and mutations will occur.

Concern about drug resistance has caused doctors to prescribe bacteria-killing drugs more sparingly.

Now a team of researchers at Duke University may have alighted on a solution. In a recently published study in the journal Proceedings of the National Academy of Sciences, the researchers software, OSPREY, was able to predict the most likely mutations to come out of certain bacteria.

Researchers were able to then test treatment with drugs that are still in the experimental phase. Identifying the most likely mutations while drugs are still under development, the team believes, means the medicine is better positioned for success when it hits the market.

If we can somehow predict how bacteria might respond to a particular drug ahead of time, we can change the drug, or plan for the next one, or rule out therapies that are unlikely to remain effective for long, said study co-author Pablo Gainza-Cirauqui in a statement.

The scientists looked specifically at a common drug-resistant bacteria called methicillin-resistant Staphylococcus aureus, or MRSAa common cause of infections in health care settings like hospitals. They used their software to successfully predict that genetic changes that would occur in the bacteria when treated with drugs.

The researchers are now testing their software on other bacteria, but have made the software open for use by any researcher. The hope is that with time and practice the software algorithm will be able to predict genetic changes more than one mutation ahead.

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Health Workers See Promise in Software to Tackle Drug-Resistant Bacteria

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Minecraft 1.7.10 - Hermitcraft Modsauce fr - Ep 9 "Jabba (barrel) Advanced genetics"
Episode 9 de se let #39;s play sur minecraft avec le modpack Hermicraft Modsauce du launcher ATL les liens si cela vous intresse son plus bas. Merci de d #39;avoir regarder cette pisode on se retrouve...

By: Warlyk

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Minecraft 1.7.10 - Hermitcraft Modsauce fr - Ep 9 "Jabba (barrel) & Advanced genetics" - Video

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The Sims 4: Perfect Genetics Legacy [Part 15] Our First Baby!
You guys, the time has finally come!! The 1st Legacy baby is here and its a....... Don #39;t forget to LIKE and SUBSCRIBE! Main Channel: youtube.com/HeyItsConnorK Twitter: twitter.com/HeyItsConnorK...

By: Connor K Games

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The Sims 4: Perfect Genetics Legacy [Part 15] Our First Baby! - Video

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