Pressure Ulcers and Spinal Cord Injury
Presented by: Laura Teague, Rn, MN, NP-Adult. Topics: What is a pressure ulcer; Stages of pressure ulcers; Why pressure ulcers are so common in people with spinal cord injuries; Psycho-social issues; Prevention and treatment; Pressure relief practices.

By: Thomson Rogers

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How to understand stem cells - regenerative medicine
http://www.12hourmba.com 12 Hour MBA in Stem Cells The 12 Hour MBA in Stem Cells is an introductory level course designed to bridge gaps in your knowledge. It is most useful to new entrants, senior managers needing a big picture refresher, professional advisors and suppliers to the industry. We make it all easy -- leading you through the dynamics of stem cells, the main business drivers, giving you precious insight into where the money is made, stem cell development, commercialisation and ethics. In less than 12 hours you #39;ll: - Understand stem cells from bench to bedside - Discover where the money is made with stem cells - Understand risk and project management techniques for stem cells - Explore practices for stem cell product commercialisation - Learn about regulations, the government and the impact they can have - Consider the ethics of stem cells - Discover what the future holds for stem cells For more information, contact us at: http://www.terrapinntraining.com/contact-us.aspx

By: TerrapinnTraining

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GE Free NZ is calling for intervention by the new Minister of Food Safety, Nikki Kaye, to direct the Food Standards Authority (FSANZ) to halt its assessment of a new GE soybean resistant to three herbicides, RoundUp, glufosinate and 2,4-D.

The latest scientific discovery of possible unexpected genetic consequences in GE crops being sold already has cast an even darker shadow over the flawed approval process for GE foods. The new 2,4-D-resistant crop (application A1073), must be kept out of the food chain.

The new research just published has detected an overlap of the introduced transgenic gene construct into an active viral region (Gene VI). This has the potential to seriously harm those who eat the foods containing this engineered event. Viral genes invade their host by disabling the protective defence of a cell to incorporate their infectious genes, and some plant viruses have similarities to those that affect humans)

The European Food Safety Authority has been alerted to the viral gene overlap that is a product of the genetic engineering process. Gene VI was found to be in 54 of the 86 GE/transgenic crops, which also contain a gene from the Cauliflower Mosaic virus (CaMV35S) gene to make a crop resistant to the RoundUp herbicide.

The call for intervention by the new Minister follows the failure to act by former Minister Kate Wilkinson when she held the food safety portfolio in cabinet.

"This is extremely concerning as the public rely on the purported expertise of food regulatory bodies," said Claire Bleakley president of GE Free NZ.

In September 2012, a paper by Professor Seralini and colleagues reported that there were serious deleterious effects including organ damage and tumour development in rats fed on GE corn that contained the CaMV 35S gene (Monsantos NK603).

There are few studies to monitor the effects of GE food when eaten. There are no diagnostic tools for health practitioners, no post-monitoring has ever been done and labelling of products is inadequate. This is in the context of a rising epidemic of digestive related cancers and illnesses with no as-yet identified cause.

"It is no good relying on industry studies: science must be unbiased and on the side of the public health. Those who are assessing GE food must be trained on the complex risks of GE/transgenic food and must stop dismissing all studies that go against the data supplied by industry," said Claire Bleakley.

"It is time that our Food Standards Authority (FSANZ) required rigorous long term feeding studies and assessed applications using independent published science rather than unpublished industry opinions," said Jon Carapiet, national spokesman for GE-Free NZ in food and environment.

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Intervention urged after viral gene found in GE crops

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Newswise ANN ARBOR, Mich. University of Michigan research sheds new light on why certain people are more likely to suffer from rheumatoid arthritis paving the way to explore new treatments for both arthritis and other autoimmune diseases.

The new UMHS research in mice identifies how a specific group of genes works behind the scenes to activate the bone-destroying cells that cause severe rheumatoid arthritis, a debilitating health issue for millions of Americans.

We believe this could be a significant breakthrough in our understanding of why certain genes are associated with higher risk of rheumatoid arthritis and other autoimmune diseases a link that has been a mystery in the field for decades, says lead author Joseph Holoshitz, M.D., professor of internal medicine and associate chief of research in the division of rheumatology at the U-M School of Medicine.

We hope that this improved understanding will open the door to future design of drugs to treat this crippling disease and autoimmune disease in general.

The research appeared in The Journal of Immunology and was highlighted by Nature Reviews Rheumatology.

Rheumatoid arthritis is a chronic inflammatory disorder that damages the lining of joints and causes bone erosion, joint deformity and disability. The disease is an autoimmune disorder, characterized by the bodys immune system mistakenly attacking the body's tissues.

Researchers have long studied the phenomenon of why certain versions of an inherited group of genes known as human leukocyte antigen (HLA) are associated with autoimmune disorders. One subset of these HLA genes that codes a protein sequence called shared epitope represents the most significant genetic risk factor for rheumatoid arthritis, affecting disease susceptibility and severity. However, until now, the reason for this strong link has been unclear.

A common theory in the field has been that the association between particular HLA genes and autoimmune diseases is a result of mistakenly identifying body tissues as foreign making the body the target of the immune system and setting off an attack on self-tissues, which results in disease.

The UMHS research challenges this long-held theory. The study shows, for the first time, how this subset of HLA genes causes arthritis by activating inflammation-causing cells, as well as bone-destroying cells (known as osteoclasts). This leads to severe arthritis and bone erosion.

We showed how the shared epitope is directly triggering osteoclasts, the very cells that are responsible for joint destruction in people with the disease, says Holoshitz.

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Researchers Uncover Gene's Role in Rheumatoid Arthritis, Findings Pave Way for New Treatments

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St. Jude Childrens Research Hospital Washington University Pediatric Cancer Genome Project takes new approach to measuring the repetitive DNA at the end of chromosomes and opens new window on mechanisms fueling cancer

Newswise (MEMPHIS, Tenn. January 24, 2013) Genome sequencing data once regarded as junk is now being used to gain important clues to help understand disease. The latest example comes from the St. Jude Childrens Research Hospital Washington University Pediatric Cancer Genome Project, where scientists have developed an approach to mine the repetitive segments of DNA at the ends of chromosomes for insights into cancer.

These segments, known as telomeres, had previously been ignored in next-generation sequencing efforts. That is because their repetitive nature meant that the resulting information had defied analysis and the data were labeled as junk. But researchers have now traced changes in the volume of telomeric DNA to particular types of cancer and their underlying genetic mistakes. Investigators found that 32 percent of pediatric solid tumors carried extra DNA for telomeres, compared to just 4 percent of brain tumors and none of the leukemia samples studied. The findings were published recently in the journal Genome Biology.

Using this new approach, the investigators have linked changes in telomeric DNA to mutations in the ATRX gene and to longer telomeres in patients with a subtype of neuroblastoma, a cancer of the sympathetic nervous system. Telomere length limits how many times cells can divide. Mechanisms that maintain or lengthen telomeres contribute to the unchecked cell division that is a hallmark of cancer.

This paper shows how measuring the DNA content of telomeres can enhance the value of whole- genome sequencing, said Matthew Parker, Ph.D., the papers first author and a St. Jude postdoctoral fellow. In the case of the ATRX mutation, the telomere findings gave us information about the mutations impact that would have been hard to get through other means.

The results stem from the largest study yet of whole-genome sequencing to measure the content of telomeric DNA. The effort involved whole-genome sequencing of normal and tumor DNA from 235 pediatric patients battling 13 different cancers. For comparison, normal DNA from 13 adult cancer patients was included in the research.

Theres been a lot of interest among cancer researchers into telomere length, said Richard Wilson, Ph.D., director of The Genome Institute at Washington University School of Medicine in St. Louis. While more research remains, we think its important to begin to characterize the genetic sequences that make up the telomeres. Thats a crucial first step to understanding more precisely any role they may play in cancer.

The Pediatric Cancer Genome Project sequenced the complete normal and cancer genomes of more than 600 children and adolescents with some of the most aggressive and least understood cancers. Investigators believe the projects findings will lay the foundation for a new generation of clinical tools. Despite advances, cancer remains the leading cause of death by disease of U.S. children age 1 and older.

The human genome is stored in the four-letter chemical alphabet of DNA, a molecule that stretches more than 3 billion characters in length and provides the instructions for building and sustaining life. Those instructions are the genes that are organized into the 46 chromosomes found in almost every cell.

Each chromosome ends with the same six-letter DNA sequence that is associated exclusively with telomeres. The DNA sequence does not vary, but the number of times it is repeated does, affecting the length of the telomeres. Telomeres shorten each time cells divide, which explains why their length declines naturally with age.

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Public release date: 25-Jan-2013 [ | E-mail | Share ]

Contact: Sibylle Kohlstdt s.kohlstaedt@dkfz.de Helmholtz Association of German Research Centres

About ten percent of all cases of malignant melanoma are familial cases. The genome of affected families tells scientists a lot about how the disease develops. Prof. Dr. Rajiv Kumar of the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) together with Prof. Dr. Dirk Schadendorf from Essen University Hospital studied a family where 14 family members were affected by malignant melanoma.

The scientists analyzed the genomes of family members and found an identical mutation in the gene for telomerase, an enzyme often called 'immortality enzyme', in all persons studied. Telomerase protects the ends of chromosomes from being lost in the process of cell division and, thus, prevents that the cell ages and dies. The inherited gene mutation leads to the formation of a binding site for protein factors in the controlling region of the telomerase gene, causing it to become overactive. As a result, mutated cells overproduce telomerase and hence become virtually immortal.

This spectacular finding of the family analysis prompted the scientists to also look for mutated telomerase genes in non-inherited (sporadic) melanoma, which is much more common than the familial variant. In most of the tissue samples of melanomas of all stages they found alterations in the telomerase gene switch, which the researchers clearly identified as typical consequences of sun exposure. Even though these mutations were not identical to those found in the melanoma family, they had the same effect: overactive telomerase.

"We don't believe that the telomerase gene in melanoma is mutated by pure chance, but that it is a so-called driver mutation that drives carcinogenesis," says Rajiv Kumar. This is also confirmed by the surprising incidence of this alteration: The telomerase gene is the most frequently mutated gene in melanoma. "This is something we hadn't expected, because malignant melanoma has been genetically analyzed thoroughly. But this mutation always seems to have been overlooked," says Kumar.

Rajiv Kumar, Dirk Schadendorf and their teams are hoping that the alterations in the telomerase gene may be a starting point for developing novel treatment methods for malignant melanoma. A very recent development targeting a specific alteration in the B-RAF gene, which characterizes about half of all melanomas, has shown that this is possible. The mutation gave rise to the development of a targeted drug that can arrest cancer growth. "Substances inhibiting telomerase have already been developed and some of them have even been tested in phase III clinical trials," said Rajiv Kumar. Inhibition of the immortality enzyme might also be able to arrest growth in melanoma.

###

Susanne Horn, Adina Figl, P. Sivaramakrishna Rachakonda, Christine Fischer, Antje Sucker, Andreas Gast, Stephanie Kadel, Iris Moll, Eduardo Nagore, Kari Hemminki, Dirk Schadendorf and Rajiv Kumar: TERT Promoter Mutations in Familial and Sporadic Melanoma. Science 2013, DOI: 10.1126/science.1230062

The German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) with its more than 2,500 employees is the largest biomedical research institute in Germany. At DKFZ, more than 1,000 scientists investigate how cancer develops, identify cancer risk factors and endeavor to find new strategies to prevent people from getting cancer. They develop novel approaches to make tumor diagnosis more precise and treatment of cancer patients more successful. The staff of the Cancer Information Service (KID) offers information about the widespread disease of cancer for patients, their families, and the general public. Jointly with Heidelberg University Hospital, DKFZ has established the National Center for Tumor Diseases (NCT) Heidelberg, where promising approaches from cancer research are translated into the clinic. In the German Consortium for Translational Cancer Research (DKTK), one of six German Centers for Health Research, DKFZ maintains translational centers at seven university partnering sites. Combining excellent university hospitals with high-profile research at a Helmholtz Center is an important contribution to improving the chances of cancer patients. DKFZ is a member of the Helmholtz Association of National Research Centers, with ninety percent of its funding coming from the German Federal Ministry of Education and Research and the remaining ten percent from the State of Baden-Wrttemberg.

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BioTalk Episode 2: Three Parent Embryos and the Brave New United States
In October of last year, scientists in Oregon made embryos with genes from one man and two women: lacrossetribune.com Rebecca and I discuss this kind of genetic engineering and the "Brave New" United States where there are no restrictions on this or other once unthinkable kinds of human experimentation currently in practice. We also discuss the impact this kind of experimentation has on women. Please leave us feedback at http://www.BioTalkBlog.com Chelsea #39;s website http://www.ReflectionsofaParalytic.com Rebecca #39;s website http://www.MaryMeetsDolly.com

By: Chelsea Zimmerman

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By Arthur Caplan, Special to CNN

updated 12:54 PM EST, Thu January 24, 2013

A display of a reconstruction of a Neanderthal man and boy at the Museum for Prehistory in Eyzies-de-Tayac, France.

STORY HIGHLIGHTS

Editor's note: Arthur Caplan is the Drs. William F and Virginia Connolly Mitty professor and director of the Division of Bioethics at New York University Langone Medical Center.

(CNN) -- So now we know -- there won't be a Neanderthal moving into your neighborhood.

Despite a lot of frenzied attention to the intentionally provocative suggestion by a renowned Harvard scientist that new genetic technology makes it possible to splice together a complete set of Neanderthal genes, find an adventurous surrogate mother and use cloning to gin up a Neanderthal baby -- it ain't gonna happen anytime soon.

Nor should it. But there are plenty of other things in the works involving genetic engineering that do merit serious ethical discussion at the national and international levels.

Arthur Caplan

Some thought that the Harvard scientist, George Church, was getting ready to put out an ad seeking volunteer surrogate moms to bear a 35,000-year-old, long-extinct Neanderthal baby. Church had to walk his comments back and note that he was just speculating, not incubating.

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Opinion: Don't clone a Neanderthal baby

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By Arthur Caplan, Special to CNN

updated 12:54 PM EST, Thu January 24, 2013

A display of a reconstruction of a Neanderthal man and boy at the Museum for Prehistory in Eyzies-de-Tayac, France.

STORY HIGHLIGHTS

Editor's note: Arthur Caplan is the Drs. William F and Virginia Connolly Mitty professor and director of the Division of Bioethics at New York University Langone Medical Center.

(CNN) -- So now we know -- there won't be a Neanderthal moving into your neighborhood.

Despite a lot of frenzied attention to the intentionally provocative suggestion by a renowned Harvard scientist that new genetic technology makes it possible to splice together a complete set of Neanderthal genes, find an adventurous surrogate mother and use cloning to gin up a Neanderthal baby -- it ain't gonna happen anytime soon.

Nor should it. But there are plenty of other things in the works involving genetic engineering that do merit serious ethical discussion at the national and international levels.

Arthur Caplan

Some thought that the Harvard scientist, George Church, was getting ready to put out an ad seeking volunteer surrogate moms to bear a 35,000-year-old, long-extinct Neanderthal baby. Church had to walk his comments back and note that he was just speculating, not incubating.

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Don't clone a Neanderthal baby

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Sixty years after scientists described the chemical code of life an interweaving double helix called DNA researchers have found four-stranded DNA is also lurking in human cells.

The odd structures are called G-quadruplexes because they form in regions of deoxyribonucleic acid (DNA) that are full of guanine, one of the DNA molecule's four building blocks, with the others being adenine, cytosine, thymine. The structure comprises four guanines held together by a type of hydrogen bonding to form a sort of squarelike shape. (The DNA molecule is itself a double strand held together by these building blocks and wrapped together like a helix.)

The new visualization of the G-quadruplex is detailed this week in the journal Nature Chemistry.

"I think this paper is important in showing directly the existence of this structure in vivo in the human genome, but it is not completely unexpected," said Hans-Joachim Lipps, of the University of Witten in Germany, who was not involved in the study. [See Images of the 4-Stranded DNA]

Scientists had shown in the past that such quadruplex DNA could form in test tubes and had even been found in the cells of ciliated protozoa, or single-celled organisms with hairlike appendages. Also there were hints of its existence in human cells, though no direct proof, Lipps said.

But scientists still didn't have concrete evidence for its existence in the human genome. In the new study, researchers, including chemist Shankar Balasubramanian, of the University of Cambridge and Cambridge Research Institute, crafted antibody proteins specifically for this type of DNA. The proteins were marked with a fluorescent chemical, so when they hooked up to areas in the human genome packed with G-quadruplexes, they lit up.

Next, they incubated the antibodies with human cells in the lab, finding these structures tended to occur in genes of cells that were rapidly dividing, a telltale feature of cancer cells. They also found a spike in quadruplexes during the s-phase of the cell cycle, or the phase when DNA replicates just before the cell divides.

As such, the researchers think the four-stranded DNA could be a target for personalized medicine in the future. If they could block these odd ducks perhaps they could stop the rapid cell division of cancer cells.

"We are seeing links between trapping the quadruplexes with molecules and the ability to stop cells dividing, which is hugely exciting," Balasubramanian said in a statement.

The finding "is certainly a technical (not scientific) breakthrough in designing antibodies sensitive enough to demonstrate this structure in vivo in the human genome," Lipps wrote.

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New Genetic Twist: 4-Stranded DNA Lurks in Human Cells

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Public release date: 24-Jan-2013 [ | E-mail | Share ]

Contact: Bill Hathaway 203-432-1322 Yale University

Nearly the entire genetic landscape of the most common form of brain tumor can be explained by abnormalities in just five genes, an international team of researchers led by Yale School of Medicine scientists report online in the Jan. 24 edition of the journal Science. Knowledge of the genomic profile of the tumors and their location in the brain make it possible for the first time to develop personalized medical therapies for meningiomas, which currently are only managed surgically.

Meningioma tumors affect about 170,000 patients in the United States. They are usually benign but can turn malignant in about 10 percent of cases. Even non-cancerous tumors can require surgery if they affect the surrounding brain tissue and disrupt neurological functions.

Approximately half of the tumors have already been linked to a mutation or deletion of a gene called neurofibromin 2, or NF2. The origins of the rest of the meningiomas had remained a mystery.

The Yale team conducted genomic analyses of 300 meningiomas and found four new genetic suspects, each of which yields clues to the origins and treatment of the condition. Tumors mutated with each of these genes tend to be located in different areas of the brain, which can indicate how likely they are to become malignant.

"Combining knowledge of these mutations with the location of tumor growth has direct clinical relevance and opens the door for personalized therapies," said Murat Gunel, the Nixdorff-German Professor of Neurosurgery, professor of genetics and of neurobiology, and senior author of the study. Gunel is also a member of Yale Cancer Center's Genetics and Genomics Research Program.

For instance, two of the mutations identified SMO and AKT1 have been linked to various cancers. SMO mutations had previously been found in basal cell carcinoma and are the target of an already approved drug for that form of skin cancer. Another, KLF4, activates a suite of genes and is known for its role in inducing stem cell formation, even in cells that have fully differentiated into a specific tissue type. Mutations in a TRAF7, a gene not previously associated with cancer, were found in approximately one-fourth of tumors. Meningiomas with these mutations are found in the skull base and are unlikely to become cancerous. In contrast, NF2 mutant tumors that flank the brain's hemispheres are more likely to progress to malignancy, especially in males.

Doctors may be able to use targeted chemotherapy on patients with non-NF2 mutations, especially those with recurrent or invasive meningiomas and those who are surgically at high risk. Individualized chemotherapies could also spare patients irradiation treatment, a risk factor for progression of these generally benign tumors. Gunel said it may also be possible to extend these approaches to more malignant tumors.

###

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Genetic landscape of common brain tumors holds key to personalized treatment

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Marfan Syndrome
Genetic Disorder Project assigned by Mr. Leal. Citations: medicalnewstoday.com, marfan.com, nhlbi.nih.gov, mayoclinic.com/marfan-syndrome/, genetics.emedtv.com/marfan-syndrome

By: Anna Green

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Nancy Drew: Shadow at the Water #39;s Edge- Part 5, I fail at finding my room and Origami
Yeaaah, so I keep on forgetting that there are certain times that I can and can NOT upload my videos. So I think that #39;s one of the many ways that gets me discouraged...don #39;t be like me and start something and just fail to finish it. This is not only a habit but literally a family trait...LITERALLY!!! (GENETICS!) XD Honestly, I have NO idea as to why the music is dominating everything. I can #39;t tell you how many times I have adjusted this...it just won #39;t listen! Since my fail to complete the first game, I #39;m going to go ahead and see if I can possibly- seriously- REALLY- complete this one. (Seeing as how I have done it already) One my biggest challenges of complete the last one (Phantom of Venice) were those dog #39;on lock picking puzzles and the very last ones. (Even though I have "cheat notes") A big thing that will be getting me by today will be Arglefumph #39;s videos and research from the internet. Anyone who is watching, if you are anything like me in this, do not be ashamed, for it is a weird/sad thing, but yet probably a normal thing. 🙂 Thank you for watching This game has been created by HER INTERACTIVE, clearly not me. This has been purchased through STEAM. (I believe.) As the others have been purchased through Amazon and BigFish games. THANK YOU!!! Phantom of Venice-(Most likely to be continued...) Shadow at the Water #39;s Edge... (MYSTERIOUS GAME CHOSEN BY THE UPLOADER. Should be coming soon as well...) TAGS: nancy drew her interactive dare to play ryokan hiei japan lol ...

By: IceInMySnowCone

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New Vision: Kontstantin Severinov at TEDxSkolkovo
Konstantin Severinov Professor of Biology at the Waksman Institute, Department of Molecular Biology and Biochemistry at Rutgers University, USA. He is also the Head of Laboratory of genetic regulation of prokaryotic mobile genetic elements at the Institute of Molecular Genetics of the Russian Academy of Sciences. He has also produced over 169 peer-reviewed publications and holds 6 patents in the US In thespirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience. At a TEDx event, TEDTalks video and live speakers combine to spark deep discussion and connection in a small group. These local, self-organized events are branded TEDx, where x = independently organized TED event. The TED Conference provides general guidance for the TEDx program, but individual TEDx events are self-organized.* (*Subject to certain rules and regulations)

By: TEDxTalks

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Kinnordy Domina
Sire: Danzante (imp) (De Niro / Weltmeyer) Dam: Gymnastic Star (imp) / Graf Landau (imp) A mature looking 3 year old filly with an absolutely faultless temperament. Domina has recently been started under saddle and has wisdom beyond her years. She is aso a breeding gold mine, a combination of highly sought-after dressage genetics, making her an excellent future breeding prospect. Currently in training with Brent Eastwell. More information at http://www.willowdowns.com.au

By: Brent Eastwell

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Treating Cancer - Cancer Treatment
Treating Cancer. http://www.CancerUncensored.com. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I would like to present you with an overview of cancer. I #39;m going to briefly talk about what cancer is, what triggers it, what symptoms there are, how you can avoid it. We #39;ll also go over current treatment methods and alternative treatment. I #39;ll also show you where you can go to get the most up-to-date news and breakthroughs. Before we get stuck in, I would like to address two points Firstly, most people are terrified of cancer. I can understand that, as my wife has cancer, but as a society, we mustn #39;t let the dread of the disease prevent us from taking steps to understand it, because that way we can actively prevent it. One in three of us will be diagnosed with cancer within our lifetimes, yet 85% of cancer is avoidable! This video, and my book, cancer uncensored, can tell you how. So absorb as much of this data as you can, because it could save your life. Secondly, you must understand that cancer isn #39;t fully understood. We have a number of very solid theories, and plenty of study data, but if cancer was fully understood, we #39;d be closer to a cure. To quote Thomas Edison, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and prevent disease with nutrition." But as things stand at the ...

By: CancerUncensored

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What Prevents Cancer?
Keywordxxxx. Linkxxxx. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I want to give you an overview of cancer. I am going to briefly talk about what cancer is, what triggers it, what symptoms there are, how you can actively prevent it. I will also go over current treatment methods and alternative medicine. I #39;ll also tell you where you should go to get the most up-to-date news and advancements. Before we get stuck in, I would like to address two points: Firstly, most people are afraid of cancer. I can fully understand that, as my wife has cancer, but as a society, we must not allow the fear of the condition stop us from taking steps to understand it, because that way we can actively prevent it. One in three of us will be diagnosed with cancer during our lifetimes, yet 85% of cancer is avoidable! This video, and my book, cancer uncensored, can tell you how. So absorb as much of this information as you can, because it could save your life. Secondly, you need to realise that cancer is not totally understood. We have quite a few very solid theories, and a lot of study data, but if cancer was fully understood, we would be even closer to a cure. To quote Thomas Edison, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and prevent disease with nutrition." But as things stand at the ...

By: CancerUncensored

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Population and Genetics - Genesis Week, Episode 20, season 2 with Wazooloo/Ian Juby
christianima.com http In this episode, Ian responds to critics of his "population problem" rant, another dramatic example of the human genome in meltdown and why it matters, and a new rant on how you can know who the Intelligent Designer is. Random references: CrEvo Rant #71: The Population Problem http://www.youtube.com Population chart: en.wikipedia.org The formula for growth rates is compounding interest formula: Calculating growth rate: P = C (1 + r) ^t (P= Population, C = starting population? r=rate of change, % per year, t = time, in years.) Three sisters of agriculture: en.wikipedia.org Human genome in meltdown: crev.info Analysis of 6515 exomes reveals the recent origin of most human protein-coding variants Fu, et. al, Nature, January 10, 2013 http://www.nature.com DOI: 10.1038/nature11690 Sanford image: hort.cals.cornell.edu genetic entropy: creationresearch.org CrEvo Rant #78: Genetic Entropy: http://www.youtube.com My response to TLD on starvation: http://www.youtube.com CMI #39;s Evolution/Natural Selection tract: castore.creation.com wazooloo.com http

By: wazooloo

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Advancements In Cancer - Cancer Advancements
Advancements In Cancer. http://www.CancerUncensored.com. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I would like to present you with an overview of cancer. I #39;m going to briefly talk about exactly what cancer is, what triggers it, what symptoms there are, what you can do to actively prevent it. I will also go over current treatment methods and alternative medicine. I will also tell you where you can go to obtain the most up-to-date news and advancements. Before we get stuck in, I #39;d like to address two points Firstly, most people are terrified of cancer. I can understand that, as my wife has recently been diagnosed with cancer, but as a society, we must not allow the dread of the disease prevent us from taking steps to understand it, because that way we can actively prevent it. One in three of us will be diagnosed with cancer during our lifetimes, yet 85% of cancer is avoidable! This video, and my book, cancer uncensored, can tell you how. So absorb as much of this information as you can, as it could save your life. Secondly, you must understand that cancer is not entirely understood. We have quite a few very solid theories, and plenty of study data, but if cancer was fully understood, we might be even closer to a cure. To quote Thomas Edison, "The doctor of the future will no longer treat the human frame with drugs, but ...

By: CancerUncensored

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It's not clear. While psychological stress can lead to DNA damage associated with aging, it's not clear whether this damage manifests itself visibly. But that hasn't stopped some news outlets from heralding a link between stress and graying hair. When a 2011 study showed a mechanism through which stress could cause DNA damage, articles in the Daily Mail, Yahoo, and elsewhere touted the study as proof that stress can cause visible aging. "Stress Really Does Make Your Hair Go Gray, Scientists Find," proclaimed the headline in the Telegraph.

However, the study had little or nothing to do with gray hair, with the words gray and hair never even appearing. Furthermore, the study used adrenaline, not stress, and it was conducted on mice, not people.

As William Saletan pointed out in Slate in 2009, many other studies have found no relationship between early graying and aging. A Danish study of 20,000 men and women could find no relationship between deaths from heart disease and outward signs of aging, such as balding, wrinkly skin, and gray hair. Instead, most graying seems to be determined by genetics. If presidents tend to go gray in office, it may simply be because most normal graying happens during the same years in which presidents serve.

"Overnight" graying from stress is extremely rare, if it exists at all. Though traumatized fictional characters have had their hair suddenly turn white since at least the days of Shakespeare, the phenomenon remains unproven.

Photo selection can also exaggerate the appearance of aging. While Obama's sprinkles of gray started making headlines just 44 days into his presidency, a Huffington Post article this week actually complimented the president's "amazing glow." A CNN commentator agreed, remarking that he "looks five years younger."

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Stress or genetics?

Recommendation and review posted by Bethany Smith

AUSTRALIAN Wool Innovation has outlined the direction of a new sheep genetics program to be considered by its board later this year that will investigate the accuracy of early-life assessment of the genetic merit of sheep.

The proposed new Lifetime Productivity Project is based on feedback from the industry of moves toward collecting more information on individual animals at younger ages.

And while the project may draw criticism as being a replacement for AWIs Information Nucleus Flock investment, AWI says the need for improved lifetime productivity data has been around for decades, well before the nucleus flock, and requires data from larger numbers of sheep.

A planning team including up to nine organisations and research bodies with a history of sheep breeding research is drafting the project proposal to go to the AWI board for consideration in July or August. There will be a three to four-month industry consultation period before then to receive feedback on the proposal from growers groups, researchers and other stakeholders.

AWI head of on-farm R&D Jane Littlejohn said while breeding values were increasingly accepted by sheep breeders as an effective genetic evaluation tool, there were still issues to resolve to improve their acceptance.

We must focus on the reasons why more wool producers and stud breeders have not taken up these new technologies faster and whether it can be improved, she said.

Dr Littlejohn said the proposed project would examine issues around adoption by breeders of Australian Sheep Breeding Values including:

This project will significantly improve our understanding of the genetics of lifetime reproductive performance and its interaction with other traits such as growth and wool production, she said.

The progeny bred in the project would be evaluated over their lifetime for a range of wool, meat, disease and reproduction traits. DNA samples will be collected for genomic evaluation of predictors of lifetime performance.

Additionally, the availability of lifetime performance information, effects such as birth-rearing type and age-of-dam, pedigree and genomic information will contribute to the development of genomic-enhanced breeding values for lifetime traits.

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AWI's new genetics

Recommendation and review posted by Bethany Smith

BOTHELL, Wash. & CAMBRIDGE, Mass.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) and Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited (TSE:4502), today announced the initiation of a global phase III clinical trial evaluating ADCETRIS (brentuximab vedotin) in combination with chemotherapy for the treatment of newly diagnosed CD30-positive mature T-cell lymphoma (MTCL) patients, including patients with systemic anaplastic large cell lymphoma (sALCL) and other types of peripheral T-cell lymphomas. The trial, also known as ECHELON-2, is being conducted under a Special Protocol Assessment (SPA) agreement from the U.S. Food and Drug Administration (FDA) and also received scientific advice from the European Medicines Agency (EMA). ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30. ADCETRIS is currently not approved for use in the front-line treatment of MTCL.

The standard of care for newly diagnosed MTCL, a chemotherapy regimen called CHOP, has not changed in more than three decades, and there is a significant need to identify enhanced treatment options for these patients, said Clay B. Siegall, Ph.D., President and Chief Executive Officer at Seattle Genetics. Recent phase I data from 26 patients presented at the ASH annual meeting showed that adding ADCETRIS to CHP resulted in compelling antitumor activity, with 100 percent of the patients experiencing a response, and a manageable safety profile. Our goal with this phase III trial is to redefine the standard of care for front-line treatment of MTCL.

This is the third global phase III trial with ADCETRIS to be initiated in the past nine months, said Karen Ferrante, M.D., Chief Medical Officer, Millennium. This trial represents another major achievement in our aspiration to bring important new therapies to patients with CD30-expressing malignancies by evaluating ADCETRIS in the front-line setting.

The ECHELON-2 study is a randomized, double-blind, placebo-controlled multi-center global phase III trial designed to investigate ADCETRIS in combination with cyclophosphamide, doxorubicin and prednisone (A+CHP) versus cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) as front-line therapy in patients with CD30-expressing MTCL. The primary endpoint is progression-free survival (PFS) per independent review facility assessment using the Revised Response Criteria for malignant lymphoma (Cheson, 2007). Secondary endpoints include overall survival (OS), complete remission (CR) rate and safety. The trial will be conducted in North America, Europe and Asia and is expected to enroll approximately 300 patients (approximately 150 patients per treatment arm). A molecular companion diagnostic test will be used in this trial to identify eligible patients based on CD30 expression. The companion diagnostic test is being developed under a previously announced collaboration agreement with Ventana Medical Systems, Inc. (Ventana), Millennium and Seattle Genetics.

At the recent 54th American Society of Hematology (ASH) Annual Meeting and Exposition held December 8-11, 2012 in Atlanta, GA, encouraging phase I data were presented from an abstract titled Brentuximab Vedotin Administered Concurrently with Multi-Agent Chemotherapy as Front-line Treatment of ALCL and Other CD30-Positive Mature T-Cell and NK-Cell Lymphomas (Abstract #60). The clinical trial was conducted to evaluate ADCETRIS in combination with chemotherapy for the treatment of newly diagnosed MTCL patients, including patients with sALCL. Data were reported from 26 previously untreated patients who received the combination regimen of ADCETRIS plus CHP.

After completing a combination regimen of ADCETRIS plus CHP, 26 of 26 patients (100 percent) treated with ADCETRIS plus CHP had an objective response, including 23 patients (88 percent) with a complete remission. The most common treatment-emergent adverse events of any grade regardless of relationship occurring in more than 30 percent of patients were nausea (62 percent), peripheral sensory neuropathy (62 percent), diarrhea (58 percent), fatigue (54 percent) and alopecia (46 percent). The most common Grade 3 or 4 treatment-emergent adverse events regardless of relationship included Grade 3 febrile neutropenia, peripheral sensory neuropathy, nausea and dyspnea and Grade 4 nausea and diarrhea. The abstract can be found at http://www.hematology.org.

More information about the ECHELON-2 phase III trial of ADCETRIS in front-line CD30-expressing MTCL, including enrolling centers, will be available by visiting http://www.clinicaltrials.gov.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

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Seattle Genetics and Millennium Initiate Global Phase III Clinical Trial of ADCETRIS® (Brentuximab Vedotin) in Front ...

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BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today presented interim results from a phase I clinical trial evaluating ASG-5ME for the treatment of metastatic pancreatic ductal adenocarcinoma (PDA) at the American Society of Clinical Oncology (ASCO) 2013 Gastrointestinal Cancers Symposium being held January 24-26, 2013 in San Francisco, CA. ASG-5ME is an antibody-drug conjugate (ADC) targeting the SLC44A4 antigen and is being co-developed by Seattle Genetics and Agensys, Inc., an affiliate of Tokyo-based Astellas Pharma Inc., for the treatment of solid tumors. The phase I data from the ASG-5ME clinical trial in advanced pancreatic cancer identified the maximum tolerated dose (MTD) for weekly administration, demonstrated tolerability and provided preliminary evidence for antitumor activity.

Pancreatic cancer is a terrible disease, with a median survival of only six months for metastatic disease and a five-year survival rate of less than six percent, said Jonathan Drachman, M.D., Senior Vice President, Research and Translational Medicine of Seattle Genetics. There is an urgent need to identify more effective therapeutic options for these patients, and we are encouraged by the tolerability and evidence of antitumor activity observed in this phase I trial. We look forward to further results from ongoing trials of ASG-5ME in prostate and gastric cancer.

ADCs are monoclonal antibodies that are designed to deliver cytotoxic agents selectively to tumor cells. This approach is designed to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing antitumor activity. With over a decade of experience and knowledge in ADC innovation, Seattle Genetics has developed proprietary technology employing synthetic cytotoxic agents, such as monomethyl auristatin E (MMAE), and stable linker systems that attach these cytotoxic agents to the antibody. Seattle Genetics linker systems are designed to be stable in the bloodstream and release the cell-killing agent once inside targeted cancer cells. ADCETRIS (brentuximab vedotin) is the first drug approved utilizing Seattle Genetics ADC technology.

A Phase I Study of ASG-5ME, a Novel Antibody-Drug Conjugate, in Pancreatic Ductal Adenocarcinoma (Abstract #176)

A phase I clinical trial was conducted to evaluate the safety and activity and to identify the MTD of ASG-5ME in patients with metastatic PDA. At the time of data analysis, 35 patients with metastatic PDA were enrolled in the trial. These patients had a median age of 63 and were heavily pretreated with a median of three prior therapies. The median time since initial PDA diagnosis and time since identification of metastatic disease was 1.4 years and 0.59 years, respectively. Patients received doses ranging from 0.3 milligrams per kilogram (mg/kg) to 1.5 mg/kg administered weekly for three out of every four weeks.

Key findings included:

Enrollment of PDA patients to this ASG-5ME phase I trial is complete. Enrollment of patients with relapsed or refractory gastric adenocarcinoma is ongoing. In addition, Seattle Genetics and Agensys are evaluating ASG-5ME in a phase I study for castration-resistant prostate cancer (CRPC). For more information about the trials, visit http://www.clinicaltrials.gov.

About Pancreatic Cancer

Pancreatic cancer occurs when malignant (cancerous) cells grow, divide and spread in the tissues of the pancreas. The most common type of pancreatic cancer, accounting for 95 percent of tumors, is adenocarcinoma arising within the exocrine component of the pancreas. Pancreatic cancer is the fourth leading cause of cancer-related death in the United States and for all stages of the disease combined, the one- and five-year relative survival rates are 25 percent and six percent, respectively.

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Seattle Genetics Announces Data from ASG-5ME Phase I Clinical Trial for Pancreatic Cancer

Recommendation and review posted by Bethany Smith

Gene Therapy OA Video v1

By: deanthompsonbeehive

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Gene Therapy OA Video v1 - Video

Recommendation and review posted by Bethany Smith

Public release date: 24-Jan-2013 [ | E-mail | Share ]

Contact: Gregory Harris gregory.harris@albertahealthservices.ca 403-619-3108 Alberta Health Services

CALGARY Researchers in Calgary have launched the first gene therapy clinical trial in the world for Fabry disease, a rare inherited enzyme deficiency that can shorten the lifespan of people who have it by as much as 40 years.

Researchers will first remove a quantity of stem cells from a Fabry patient's blood. Then a working copy of a new gene will be inserted into the stem cells using a specially engineered virus. During the final phase of the trial, researchers hope to transplant these stem cells back into the donor patient and the new, working copy of the gene will make the missing enzyme.

The clinical trial has been prompted by promising gene therapy results in mice performed in the laboratory of Dr. Jeffrey Medin at the University Health Network in Toronto. Dr. Medin is the principal investigator of the pan-Canada team grant that is supporting this trial.

"We hope this will one day become a form of treatment that effectively cures Fabry disease," says Dr. Aneal Khan, a medical geneticist based at Alberta Children's Hospital, who is leading the Calgary segment of the national project.

"It could also help establish a platform on which we can create gene therapies for other illnesses and establish Calgary as a national leader in this experimental field of interventional genetics."

Although several gene therapies have been used in Canada for cancer, this study will be the first in the country to test a gene therapy for an inherited metabolic disorder.

People with Fabry disease have a change in a gene called GLA and can't make enough enzyme to break down a fatty substance called Gb3. The build-up of Gb3 can lead to problems in the kidneys, heart and brain. About 400 Canadians, including 25 Calgarians, have Fabry disease.

Although the project is headquartered in Toronto, physicians and scientists in Calgary will play a major role in the clinical trial. In particular, the lab at Foothills Medical Centre in Calgary has specialized expertise in the stem cell filtering process that will be used for the clinical trial.

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Canada launches first gene therapy trial for Fabry disease

Recommendation and review posted by Bethany Smith