Civilization V - Genetic Engineering Mod
Have you ever wanted to bring down biological war fair on your fellow civs. If you do, then this is the Mod for you! Not only are their biological weapons but you also get to make Jurassic Park!

By: crazyPotatoz

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Civilization V - Genetic Engineering Mod - Video

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PALO ALTO, Calif. & CAMBRIDGE, England--(BUSINESS WIRE)--

Today, Open Monoclonal Technology, Inc. (OMT) and Recombinant Antibody Technology, Ltd (RAT) announced a publication about OmniRat in the Journal of Immunology (www.jimmunol.org/content/early/2013/01/09/jimmunol.1203041). The publication by scientists from OMT, RAT and Pfizer is entitled High-Affinity IgG Antibodies Develop Naturally in Ig- Knockout Rats Carrying Germline Human IgH/Igk/Igl Loci Bearing the Rat CH Region and covers eighteen months of close collaboration between the teams.

The manuscript describes a comprehensive comparison of wild type animals with OmniRat, the first genetically engineered rat to generate fully human antibody specificities. While there have been numerous transgenic mice expressing human antibodies, this is the first genetic engineering project that resulted in an animal that makes antibodies with fully human idiotypes as well as wild type animals make their own antibodies.

Antibodies from transgenic animals have proven to be the most productive platform for human antibody drug discovery and development. Six of eight currently approved human monoclonal antibodies are from transgenic animals and many more are in the pharmaceutical industry pipeline.

Dr. Marianne Brggemann, senior author of the manuscript, Research Director of RAT and scientific advisor to OMT, said: "We generated the first mouse expressing human antibodies 25 years ago. Many others followed but none of these worked as well as normal animals. I am pleased that we finally managed to generate an animal that makes antibodies with human idiotypes as well as wildtype animals. The data convinced Pfizer that OmniRat is a valuable tool for routine generation of high affinity human antibodies."

Open Monoclonal Technology, Inc.

Open Monoclonal Technology, Inc. (OMT) is a leader in genetic engineering of animals for the development of human therapeutic antibodies naturally optimized human antibodies.

OMT has created OmniRat, the first fully human monoclonal antibody platform based on transgenic rats. OMTs genetic engineering is based on an improved understanding of B cell development and a new approach to inactivation of endogenous antibody expression, which enables OmniRat to make antibodies with human idiotypes as efficiently as wild type rats make normal antibodies. OmniRat represents a novel and proprietary technology with unrestricted development options for fully human monoclonal antibodies, available worldwide for all targets and indications.

OMT also develops a transgenic mouse, OmniMouse, to complement OmniRat and further increase epitope coverage in human antibody development.

OmniAb integrates OMTs transgenic animal platforms, proven protein and DNA immunization and Gel-Encapsulated Microenvironment (GEM) deep antibody screening to enable fast and costefficient generation and identification of preferred human therapeutic antibody candidates.

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Open Monoclonal Technology and Recombinant Antibody Technology Announce OmniRat™ Scientific Publication

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Thousands of people braved the cold and demonstrated in the streets of Berlin as politicians and policymakers met to discuss changes to global agricultural policies.

Under the slogan, We are fed up, the protesters called for an end to food scandals, genetic engineering and animal cruelty in industrial livestock farming.

We are from the Friends of the Earth and we demonstrate for the peace of animals, small farmers, ecological farming, non-genetic produce animals and non-genetic food, Viola Wagner said, as she marched and chanted.

We got up at 4 oclock to come six hours by bus. Im here for my children and my grandchildren, to make sure they have a future and good food.

More than 120 groups representing farmers, industry, and animal rights and environmental activists organized the demonstration. It was timed to coincide with International Green Week, the Agriculture Ministers' Summit and the Global Forum for Agriculture, which are all taking place in Berlin this week.

The event also comes as another scandal in Germany has shaken consumer confidence in the safety and quality of the countrys food. Animal feed fats contaminated with the carcinogenic compound dioxin has again been discovered in the food chain, causing some countries to block German pork and egg imports.

Organizers said 22,000 people came from all over Germany, although police estimated turnout closer to 15,000.

Following about 50 tractors, they marched from Berlins main train station, along one of the main shopping streets, through the government district, and ended with a rally in front of German Chancellor Angela Merkels offices.

The current dioxin scandal has suddenly highlighted the backlog of reforms in agricultural policy, Hubert Weiger, chairman of BUND (Friends of the Earth Germany), said in a speech.

In her weekly video message on Saturday, Merkel said the government would tighten controls in the animal feed industry.

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Berlin protests focus on farming and food safety

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--Johns Hopkins scientists identify epigenetic changes that referee genetic risk

Newswise In one of the first genome-wide studies to hunt for both genes and their regulatory tags in patients suffering from a common disease, researchers have found a clear role for the tags in mediating genetic risk for rheumatoid arthritis (RA), an immune disorder that afflicts an estimated 1.5 million American adults. By teasing apart the tagging events that result from RA from those that help cause it, the scientists say they were able to spot tagged DNA sequences that may be important for the development of RA. And they suspect their experimental method can be applied to predict similar risk factors for other common, noninfectious diseases, like type II diabetes and heart ailments.

In a report published in Nature Biotechnology Jan. 20, the researchers at Johns Hopkins and the Karolinska Institutet say their study bridges the gap between whole-genome genetic sequencing and diseases that have no single or direct genetic cause. Most genetic changes associated with disease do not occur in protein-coding regions of DNA, but in their regulatory regions, explains Andrew Feinberg, M.D., M.P.H., a Gilman scholar, professor of molecular medicine and director of the Center for Epigenetics at the Johns Hopkins University School of Medicines Institute for Basic Biomedical Sciences. Our study analyzed both and shows how genetics and epigenetics can work together to cause disease, he says.

Rheumatoid arthritis is a debilitating disease that causes inflammation, stiffness, pain and disfigurement in joints, especially the small joints of the hands and feet. It is thought to be an autoimmune disease, meaning that the bodys immune system attacks its own tissues, an assault led primarily by white blood cells. According to Feinberg, several DNA mutations are known to confer risk for RA, but there seem to be additional factors that suppress or enhance that risk. One probable factor involves chemical tags that attach to DNA sequences, part of a so-called epigenetic system that helps regulate when and how DNA sequences are read, how theyre used to create proteins and how they affect the onset or progress of disease.

To complicate matters, Feinberg notes, the attachment of the tags to particular DNA sequences can itself be regulated by genes. The details of what causes a particular sequence to be tagged are unclear, but it seems that some tagging events depend on certain DNA sequences. In other words, those tagging events are under genetic control, he says. Other tagging events, however, seem to depend on cellular processes and environmental changes, some of which could be the result, rather than the cause, of disease.

To tease apart these two types of tagging events, the researchers catalogued DNA sequences and their tagging patterns in the white blood cells of more than 300 people with and without one form of RA.

The team then began filtering out the tags that did not appear to affect RA risk. For example, if tags were seen on the same DNA sequence in those with and without RA, it was assumed that the tags at those sites were irrelevant to the cause or development of the disease. Then, from among the RA-relevant tags, they narrowed in on tags whose placement seemed to be dependent on DNA sequence. Finally, they made sure that the DNA sequences identified were themselves more prevalent in patients with RA. In this way, they created a list of DNA sequences associated with altered DNA tagging patterns, both of which were associated with RA.

Ultimately, the team identified 10 DNA sites that were tagged differently in RA patients and whose tagging seemed to affect risk for RA. Nine of the 10 sites were within a region of the genome known to play an important role in autoimmune diseases, while the 10th was on a gene that had never before been associated with the disease. Since RA is a disease in which the bodys immune system turns on itself, current treatments often involve suppressing the entire immune system, which can have serious side effects, Feinberg says. The results of this study may allow clinicians to instead directly target the culpable genes and/or their tags.

Our method allows us to predict which tagging sites are most important in the development of a disease. In this study, we looked for tagging sites under genetic control, but similar tags can be triggered by environmental exposures, like smoking, so there are many applications for this type of work, says Yun Liu, Ph.D., a lead researcher on the project.

The study also may shed light on how evolution works, explains Feinberg. It seems that natural selection might not simply be selecting for an individuals current fitness level but also for the adaptability of future generations given an unknown future. We think that certain genetic sequences may be biologically beneficial and conserved over time because they increase the amount of variation found in tagging patterns, giving individuals a greater chance of adapting to environmental changes.

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Genes and Their Regulatory 'Tags' Conspire to Promote Rheumatoid Arthritis

Recommendation and review posted by Bethany Smith

Jan. 21, 2013 Cancer cells are resourceful survivors with plenty of tricks for staying alive. Researchers have uncovered one of these stratagems, showing how cells lacking the tumor suppressor BRCA1 can resume one form of DNA repair, sparing themselves from stagnation or death. The study appears in the January 21st issue of The Journal of Cell Biology.

The BRCA1 protein helps to mend double-strand DNA breaks by promoting homologous recombination. Without it, cells can amass broken, jumbled, and fused chromosomes, which may cause them to stop growing or die. Although cells lacking BRCA1 seem like they should be vulnerable, loss of the protein instead seems to boost abnormal growth.

Recent studies have shown that cells lacking BRCA1 compensate by cutting back on 53BP1. This protein helps orchestrate a different DNA repair mechanism, nonhomologous end joining (NHEJ), and it thwarts a key step in homologous recombination. Researchers think that, in cells without BRCA1, 53BP1 spurs excessive NHEJ that can cause fatal chromosomal chaos. But with 53BP1 out of the way, the cells are able to resume homologous recombination. That might explain why cells that lack BRCA1 and eliminate 53BP1 can withstand traditional chemotherapy compounds and PARP inhibitors, a new generation of anti-cancer drugs that are in clinical trials. But how do cancer cells turn down 53BP1?

Researchers previously found that certain mutant fibroblasts increase production of cathepsin L, a protease that destroys 53BP1. BRCA1-deficient cancer cells take advantage of the same mechanism, according to a team of researchers led by Susana Gonzalo from the Washington University School of Medicine. When they cultured breast cancer cells that were missing BRCA1, the cells stopped growing. After two weeks of lethargy, however, some cells, which the researchers dubbed BOGA cells (BRCA1-deficient cells that overcome growth arrest), began to divide again. These cells showed increased levels of cathepsin L and reduced amounts of 53BP1. Eliminating cathepsin L from BOGA cells or dosing them with vitamin D, a cathepsin L inhibitor, prevented the decline in 53BP1 abundance.

To find out whether boosting cathepsin L levels enabled the cancer cells to restart homologous recombination, the researchers monitored sites of DNA damage tagged by RAD51, a protein that helps promote homologous recombination. The cells that had stopped growing did not display RAD51 foci, but these foci were prevalent in BOGA cells with reduced 53BP1. Removing cathepsin L from BOGA cells increased 53BP1 levels and diminished the number of RAD51 foci.

If cells can't perform homologous recombination, they turn to repair mechanisms such as NHEJ that can lead to jumbled chromosomes. However, after DNA-breaking doses of radiation, BOGA cells exhibited few chromosome defects. The number of these flaws climbed after the researchers stabilized 53BP1 levels by inhibiting cathepsin L or trimming its abundance.

The team then analyzed tumor samples from breast cancer patients. Researchers suspect that cathepsin L attacks 53BP1 by entering the nucleus. Samples from patients with BRCA1 mutations or with triple-negative breast cancer -- an aggressive form of the disease -- showed high levels of nuclear cathepsin L and reduced quantities of 53BP1. That suggests tumors in these patients hike the amounts of cathepsin L in the nucleus to break down 53BP1 and restore homologous recombination.

"It's a new pathway that explains how breast cancer cells lose 53BP1," says Gonzalo. How cancer cells boost nuclear cathepsin L levels is unclear, she notes.

Triple-negative breast cancers are currently identified by their lack of Her2 and the estrogen and progesterone receptors. The work suggests that another trio of measurements -- the amounts of 53BP1, cathepsin L, and vitamin D receptor in the nucleus -- might help identify patients that are resistant to current breast cancer treatments. These people might respond to cathepsin inhibitors, some of which are undergoing animal testing. These compounds might steer the cells away from homologous recombination and leave them vulnerable to other therapies.

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Enzyme helps cancer cells avoid genetic instability

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Jan. 20, 2013 In one of the first genome-wide studies to hunt for both genes and their regulatory "tags" in patients suffering from a common disease, researchers have found a clear role for the tags in mediating genetic risk for rheumatoid arthritis (RA), an immune disorder that afflicts an estimated 1.5 million American adults. By teasing apart the tagging events that result from RA from those that help cause it, the scientists say they were able to spot tagged DNA sequences that may be important for the development of RA. And they suspect their experimental method can be applied to predict similar risk factors for other common, noninfectious diseases, like type II diabetes and heart ailments.

In a report published in Nature Biotechnology Jan. 20, the researchers at Johns Hopkins and the Karolinska Institutet say their study bridges the gap between whole-genome genetic sequencing and diseases that have no single or direct genetic cause. Most genetic changes associated with disease do not occur in protein-coding regions of DNA, but in their regulatory regions, explains Andrew Feinberg, M.D., M.P.H., a Gilman scholar, professor of molecular medicine and director of the Center for Epigenetics at the Johns Hopkins University School of Medicine's Institute for Basic Biomedical Sciences. "Our study analyzed both and shows how genetics and epigenetics can work together to cause disease," he says.

Rheumatoid arthritis is a debilitating disease that causes inflammation, stiffness, pain and disfigurement in joints, especially the small joints of the hands and feet. It is thought to be an autoimmune disease, meaning that the body's immune system attacks its own tissues, an assault led primarily by white blood cells. According to Feinberg, several DNA mutations are known to confer risk for RA, but there seem to be additional factors that suppress or enhance that risk. One probable factor involves chemical "tags" that attach to DNA sequences, part of a so-called epigenetic system that helps regulate when and how DNA sequences are "read," how they're used to create proteins and how they affect the onset or progress of disease.

To complicate matters, Feinberg notes, the attachment of the tags to particular DNA sequences can itself be regulated by genes. "The details of what causes a particular sequence to be tagged are unclear, but it seems that some tagging events depend on certain DNA sequences. In other words, those tagging events are under genetic control," he says. Other tagging events, however, seem to depend on cellular processes and environmental changes, some of which could be the result, rather than the cause, of disease.

To tease apart these two types of tagging events, the researchers catalogued DNA sequences and their tagging patterns in the white blood cells of more than 300 people with and without one form of RA.

The team then began filtering out the tags that did not appear to affect RA risk. For example, if tags were seen on the same DNA sequence in those with and without RA, it was assumed that the tags at those sites were irrelevant to the cause or development of the disease. Then, from among the RA-relevant tags, they narrowed in on tags whose placement seemed to be dependent on DNA sequence. Finally, they made sure that the DNA sequences identified were themselves more prevalent in patients with RA. In this way, they created a list of DNA sequences associated with altered DNA tagging patterns, both of which were associated with RA.

Ultimately, the team identified 10 DNA sites that were tagged differently in RA patients and whose tagging seemed to affect risk for RA. Nine of the 10 sites were within a region of the genome known to play an important role in autoimmune diseases, while the 10th was on a gene that had never before been associated with the disease. "Since RA is a disease in which the body's immune system turns on itself, current treatments often involve suppressing the entire immune system, which can have serious side effects," Feinberg says. "The results of this study may allow clinicians to instead directly target the culpable genes and/or their tags."

"Our method allows us to predict which tagging sites are most important in the development of a disease. In this study, we looked for tagging sites under genetic control, but similar tags can be triggered by environmental exposures, like smoking, so there are many applications for this type of work," says Yun Liu, Ph.D., a lead researcher on the project.

The study also may shed light on how evolution works, explains Feinberg. "It seems that natural selection might not simply be selecting for an individual's current fitness level but also for the adaptability of future generations given an unknown future. We think that certain genetic sequences may be biologically beneficial and conserved over time because they increase the amount of variation found in tagging patterns, giving individuals a greater chance of adapting to environmental changes."

Other authors of the report include Martin J. Aryee, M. Daniele Fallin, Arni Runarsson and Margaret Taub of the Johns Hopkins University School of Medicine; and Leonid Padyukov, Espen Hesselberg, Lovisa Reinius, Nathalie Acevedo, Marcus Ronninger, Lementy Shchetynsky, Annika Scheynius, Juha Kere, Lars Alfredsson, Lars Klareskog and Tomas J. Ekstrm of the Karolinska Institutet, Sweden.

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Epigenetics explains rheumatism? Genes and their regulatory 'tags' conspire to promote rheumatoid arthritis

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In what is being billed as the largest private donation for cancer research in Canadian history, Princess Margaret Hospital announced a $50-million gift on Monday.

The money will support personalized medicine, a burgeoning field in which doctors use patients genetic information to diagnose disease and deliver customized treatments.

This gift literally is a game changer for cancer research, said Paul Alofs, president and CEO of Princess Margaret Cancer Foundation.

The $50-million donation, which has been pledged over 10 years, is from philanthropists Emmanuelle Gattuso and her husband, broadcast tycoon Allan Slaight. Ms. Gattuso is a breast cancer survivor who was treated at Princess Margaret in Toronto.

We believe that personalized cancer medicine will revolutionize the way that cancer patients are treated, Ms. Gattuso, 65, told a crowd of staff and journalists in the hospitals atrium.

The money will be used to hire more cancer specialists and support their research, said Benjamin Neel, the hospitals research director.

Their unprecedented $50-million donation will enable us to create a superfund to provide the necessary long-term sustainable funding to attract, support and retain the best and brightest scientists in the world, he said.

Princess Margaret Hospital is developing a model of personalized cancer medicine that focuses on earlier detection, more precise diagnosis, targeted treatment and better support for patients.

In 2009, Ms. Gattuso and Mr. Slaight donated $22-million to Princess Margaret to create a rapid diagnostic centre for breast cancer, which provides diagnoses and treatment plans in one day.

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Philanthropist gives Princess Margaret hospital $50-million to fight cancer

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Public release date: 20-Jan-2013 [ | E-mail | Share ]

Contact: Carrie Strehlau media@stjude.org 901-595-2295 St. Jude Children's Research Hospital

(MEMPHIS, Tenn. January 20, 2013) Research led by St. Jude Children's Research Hospital scientists has identified a possible lead in treatment of two childhood leukemia subtypes known for their dramatic loss of chromosomes and poor treatment outcomes.

The findings also provide the first evidence of the genetic basis for this high-risk leukemia, which is known as hypodiploid acute lymphoblastic leukemia (ALL). Normal human cells have 46 chromosomes, half from each parent, but hypodiploid ALL is characterized by fewer than 44 chromosomes. Chromosomes are highly condensed pieces of DNA, the molecule that carries the inherited instructions for assembling and sustaining a person. The research appears in the January 20 advance online edition of the scientific journal Nature Genetics.

The study, the largest ever focused on hypodiploid ALL, confirmed that this tumor has distinct subtypes distinguished by the number of chromosomes lost and the submicroscopic genetic alterations they harbor. Researchers found evidence suggesting more than one-third of patients with a subtype known as low hypodiploid ALL have Li-Fraumeni syndrome. Families with Li-Fraumeni syndrome harbor inherited mutations in the TP53 tumor suppressor gene and have a high risk of a range of cancers. Hypodiploid ALL had not previously been recognized as a common manifestation of Li-Fraumeni syndrome.

Researchers reported that the major hypodiploid subtypes are both sensitive to a family of compounds that block the proliferation of cancer cells. The compounds include drugs already used to treat other cancers. The subtypes are low hypodiploid ALL, characterized by 32 to 39 chromosomes, and near haploid ALL, which has 24 to 31 chromosomes.

"This study is a good example of the important insights that can be gained by studying the largest possible number of patients in as much detail as possible. This approach led us to key insights about these leukemia subtypes that we would otherwise have missed," said the study's senior and corresponding author, Charles Mullighan, MBBS(Hons), MSc, M.D., an associate member of the St. Jude Pathology Department. Mullighan is a Pew Scholar in Biomedical Sciences.

The near haploid and low hypodiploid ALL subtypes represent 1 to 2 percent of the estimated 3,000 pediatric ALL cases diagnosed annually in the U.S. But they account for a much larger number of ALL treatment failures. Today more than 90 percent of young ALL patients will become long-term survivors, compared to 40 percent for patients with these two high-risk subtypes. St. Jude researchers led the study in collaboration with investigators from the Children's Oncology Group, the world's largest organization devoted exclusively to childhood and adolescent cancer research.

"The cure rate for hypodiploid ALL is only about half that obtained overall for children with ALL. The findings of this study are very important and have the potential to impact how this high-risk subset of childhood ALL is treated," said Stephen Hunger, M.D., chair of the Children's Oncology Group ALL committee and one of the paper's co-authors. "This study grew out of the efforts of Hank Schueler, a teenager who died from hypodiploid ALL. He wanted to find ways to help treat other children with this type of leukemia. After he passed away, his parents established a foundation to support research in hypodiploid ALL. We thought that one way to do this was to conduct the genomic analyses reported in this paper. These findings would not have been possible without Hank's idea and without support from the Schueler family."

Researchers used a variety of laboratory techniques to look for genetic abnormalities in cancer cells from 124 pediatric patients missing at least one chromosome. The patients included 68 with near haploid ALL and 34 with low hypodiploid ALL. Investigators also checked white blood cells collected when 89 of the 124 patients were in remission. The study included whole-genome sequencing of the entire cancer and normal genomes of 20 patients with near haploid or low hypodiploid subtypes. For another 20 patients, investigators deciphered just DNA involved in protein production. Researchers also screened cancer cells from 117 adult ALL patients, including 11 with the low hypodiploid subtype.

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Genetic basis of high-risk childhood cancer points to possible new drug treatment strategy

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Kimberly Ho - Posing Practice 2013 with Advanced Genetics
Hey Everyone! Watch my latest video as I practice posing for the 2013 competition season. It is never ever too early to start practicing. Practice makes perfect!!!

By: Kim Ho

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Kimberly Ho - Posing Practice 2013 with Advanced Genetics - Video

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Welcome to cox genetics
This video was uploaded from an Android phone.

By: spenlottacash

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Welcome to cox genetics - Video

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99 Lost Aliens ~ Green Beanz Seeds Test Grow Ep. 1
Whats up everyone. This is Episode #1 of a long journey thru this test grow that I am doing for Green Beanz Seeds. Im sooo stoked too be running these genetics and how they are crossed! Should be LOTS of FIYAH comin outta these testers. You guys will see every step in how I sow these, too sexing, too weeding out weaklings in veg, too picking phenos and why. They were put in wet paper towels today and put away in a drawer in my dresser in my bedroom. Temps are about 65-70 degrees in that room. Now its just a waiting game. I have ran GBS gear before and ALWAYS have a GREAT germination rate... 90-100% all the time and in LESS than 36hrs.... most times in LESS than 24hrs. Come along for the journey... should be a GREAT ride!! Lost Alien = Aliendog V2 x BWOG ET (Berry White F4 x Fire Alien OG) (the BerryWhite in this cross is (DJ Short BB (sativa pheno) x Ceres Seeds White Indica)) 99 Aliens = Joey #39;s Weed C-99 x Alien Kush F2

By: PNWGardenOfFunk

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99 Lost Aliens ~ Green Beanz Seeds Test Grow Ep. 1 - Video

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Titan Genetics ~ Test Grow ~ BlueDawg StarHaze
Hey Guys! Another test grow that Im doing for another local breeder here in the PNW. I will run these side by side with my GBS gear. These were bred by Titan from Titan Genetics. He is doing his thing and using STABLE lines. Killin the game up here!! Cant wait too see what these produce! Stay tuned.... BlueDawg = Blue Dream (Snoops cut) x (Stardawg x Alien Kush) StarHaze = D Haze x (Stardawg x Alien Kush)

By: PNWGardenOfFunk

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Titan Genetics ~ Test Grow ~ BlueDawg

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rules of probability
This video was uploaded for General Biology 2. It describes how to do a trihybrid genetics problem using the rules of probability, specifically the multiplication rule and the addition rule. Thanks.

By: Anne Macek lachelt

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rules of probability - Video

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Open Your Mind Internet Radio (OYM) Simon Parkes - 20th Jan 2012
Guest - Simon Parkes - Elected Labour party Councillor in Whitby England, Mother Worked For MI5, Grandfather Worked For MI6, Involved With The White Illuminati, Abducted For Genetics, Pedophiles, Ted Heath, Annunaki, Hadron Collider, Hilary Clinton, Tesla, Advanced Technology With Crowd Control, Project Blue Beam, Microchip The Population, Solutions.

By: OYMInternetRadio

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Open Your Mind Internet Radio (OYM) Simon Parkes - 20th Jan 2012 - Video

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How to Pronounce Enhancers
Learn how to say Enhancers correctly with EmmaSaying #39;s "how do you pronounce" free tutorials. Definition of enhancer (oxford dictionary): noun a person or thing that enhances something: a sweetener and flavour enhancer Genetics a DNA sequence that increases the level of transcription of a gene that is located nearby on the same chromosome. http://www.emmasaying.com Take a look at my comparison tutorials here http://www.youtube.com Subscribe to my channel here : http://www.youtube.com

By: Emma Saying

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How to Pronounce Enhancers - Video

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Genetics: Trailer
Music: (c)Kevin MacLeod #39;s STEEL AND SEETHING Software Used: Sony Vegas Pro 9.0 Camera Used: Nikon D3100 Location: La Salle College Antipolo 🙂 While waiting for the next shooting day, I just decided to make a trailer of our second Science Informational Video project (first with these helluva fellas .. so talented and very cooperative xD). Though the entire video that we are planning to come up with is not as creepy as this one, I am sure that it #39;ll be better than this one 🙂 Kaila Aniqa Canlas Christine Loise Deala Ann Sharmaine Mendiola Beverly Caluma Jonna Mae Escobar Nicole Kate Balangue Rachel Ann Piliin Kath Mendoza Jeremiah Torres Renato Icasiano Monster Basister Francis Esporlas (Guest Tripod ^^) Entire video will be uploaded on Kaila Aniqa #39;s YouTube channel. #Dominate

By: BGKrookie

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Genetics: Trailer - Video

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Yearling bucking bull calf FOR SALE
Athletic bull calf with some great genetics! 1st time bucked. Blood lines include Skate Kat, Reindeer Dippin and Gunslinger!

By: hideawayhillsfarm

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Yearling bucking bull calf FOR SALE - Video

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Controlling the Cell Cycle in Cancer Therapy - by Norman E. Sharpless, MD
Controlling the Cell Cycle in Cancer Therapy Lecture by Norman E. Sharpless, MD Professor of Medicine and Genetics, UNC School of Medicine

By: TheOncologistJournal

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Controlling the Cell Cycle in Cancer Therapy - by Norman E. Sharpless, MD - Video

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Young Goats Learn Accents From One Another
Calls from goat kids who live together become more similar over time. Scientists say these accents suggest goats are capable of basic vocal learning, since their environment, not just genetics, influences their calls.

By: LiveScienceVideos

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Young Goats Learn Accents From One Another - Video

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Genome and Clinic in the Care of Renal Cell Carcinoma - by W. Kimryn Rathmell, MD, PhD
Uniting the Genome and Clinic to Advance the Science and Care of Renal Cell Carcinoma Lecture by W. Kimryn Rathmell, MD, PhD Associate Professor of Medicine and Genetics, UNC School of Medicine

By: TheOncologistJournal

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Genome and Clinic in the Care of Renal Cell Carcinoma - by W. Kimryn Rathmell, MD, PhD - Video

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Blood Centers of America, Inc. continues to drive market diversification into the cell therapy and regenerative medicine sectors.

West Warwick, RI (PRWEB) January 21, 2013

BCA will be hosting one-on-one meetings with senior executives of leading cell therapy and cell-based immunotherapy companies, participating in sessions and high-profile networking events, and showcasing BCA member capabilities in the event's 3-day tradeshow.

"Participating in what is often described as one of the leading cell therapy industry conferences of the year is a great way to launch our 2013 initiative to raise the profile of BCA in the cell therapy industry and engage in one-on-one discussions about what BCA has to offer companies in the cell therapy sector," stated BCA's newly appointed CEO, Bill Block.

"BCA is a network of centers geographically dispersed throughout North America with considerable experience in collecting, processing and distributing regulatory-compliant, clinical-grade biologial materials", continued Block. "We are keen to engage cell therapy leadership in a discussion about how we can leverage BCA member infastructure and capabilities in the development and processing of cell therapy products and their safe and cost-effective delivery to patients."

About BCA

BCA is a member-owned organization comprised of 37 independent blood centers geographically dispersed throughout the North America, providing more than 46% of the U.S. blood supply. Along with their core business of providing a substantial portion of U.S. blood supply, BCA members provide a myriad of other services in cell therapies, blood management, therapeutic apheresis, tissue and cord blood banking, etc.

BCA provides thousands of units of biological materials annually to life science researchers, clinicians, therapeutic companies, or companies doing medical device, diagnostic or therapeutic development work.

BCA assists cell therapy companies with securing reliable and compliant sources for the cells used in their therapeutic products and/or pre-clinical research. Where a client need exceeds the capacity of a single center, BCA can assist with putting in place a multi-center supply agreement around cell collections, processing, storage or other handling.

In 2012, BCA generated over $6 million in custom products and services to cell therapy companies including patient-donor collections for autologous cell therapies in clinical trial and commercial distribution.

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BCA Represents Independent Blood Centers at Phacilitate Cell & Gene Therapy Forum

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New Discoveries Provide a Path to a More Complete Cure with Gene Therapy Treatment

Newswise PHILADELPHIA - Independent clinical trials, including one conducted at the Scheie Eye Institute at the Perelman School of Medicine, have reported safety and efficacy for Leber congenital amaurosis (LCA), a congenital form of blindness caused by mutations in a gene (RPE65) required for recycling vitamin A in the retina. Inherited retinal degenerative diseases were previously considered untreatable and incurable. There were early improvements in vision observed in the trials, but a key question about the long-term efficacy of gene therapy for curing the retinal degeneration in LCA has remained unanswered. Now, new research from the Scheie Eye Institute, published this week in the Proceedings of the National Academy of Sciences, finds that gene therapy for LCA shows enduring improvement in vision but also advancing degeneration of affected retinal cells, both in LCA patients and animal models of the same condition.

LCA disease from RPE65 mutations has two-components: a biochemical blockade leading to impaired vision, and a progressive loss of the light-sensing photoreceptor cells throughout life of the affected patient. The authors of the new study explain that until now gene therapy has been optimistically assumed, but not proven, to solve both disease components at the same time.

We all hoped that the gene injections cured both components re-establishing the cycle of vision and also preventing further loss of cells to the second disease component said Artur V. Cideciyan, PhD, lead author and co-investigator of an LCA clinical trial at Penn.

Yet, when the otherwise invisible cell layers of the retina were measured by optical imaging in clinical trial participants serially over many years, the rate of cell loss was the same in treated and untreated regions. In other words, gene therapy improved vision but did not slow or halt the progression of cell loss, commented Cideciyan.

These unexpected observations should help to advance the current treatment by making it better and longer lasting, commented co-author Samuel G. Jacobson, MD, PhD, principal investigator of the clinical trial. Slowing cell loss in different retinal degenerations has been a major research direction long before the current gene therapy trials. Now, the two directions must converge to ensure the longevity of the beneficial visual effects in this form of LCA.

In a continuation of the longstanding collaboration between the Scheie investigators and the Section of Ophthalmology at Penn School of Veterinary Medicine headed by co-authors Gustavo D. Aguirre, VMD, PhD, and William A. Beltran, DVM, PhD, studies were performed to test whether the clinical results were also present in the canine model of this LCA at disease stages equivalent to those in human patients.

Our gene treatment in this canine model provided the groundwork for the clinical trials of patients, and now we added data to confirm the fact that retinal degeneration does continue despite improved vision said Aguirre. The next step is to perform the relevant experiments to ask what intervention will stop the degeneration if added to the gene therapy.

These new findings contribute to greater clarity in understanding the natural history and complexity of the RPE65 form of LCA and provide a firm foundation for future investigations, said Joan M. OBrien MD, professor and chair of the Department of Ophthalmology and director of the Scheie Eye Institute.

Co-authors, in addition to the Penn researchers include, William W. Hauswirth, PhD, professor of Ophthalmology, at the University of Florida, Gainesville.

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