Modernizing Health Care: Private Sector, DoD and VA Innovations in Action
Healthcare in the military and civilian world is a dynamic field that is in a constant state of change. Given the unique environments of military medicine an...
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Modernizing Health Care: Private Sector, DoD and VA Innovations in Action - Video
Inside Health Care March 2014
A whole new world opened up for a women who started losing her hearing. Hear about Cochlear Implants. Dr. Wahlstrom will give some important tips on treatmen...
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This summer, Adventist Health Central Valley Network is launching an innovative program Discover Health Care: Volunteer Summer Program focusing on volunteer service and career development for high school- and college-aged students.
Discover Health Care: Volunteer Summer Program is an opportunity for high school and college students to utilize their summer break to volunteer at Adventist Health hospitals and learn more about a career in health care, said Clay Ipsen, Assistant Director of Volunteer Resources for Adventist Health. This unique combination will allow youth to really have a more complete understanding of health care and opportunities for future careers.
All student volunteers will take part in four career core sessions that allow them to explore various health care careers, assist them to be stronger applicants in the workforce and help them discover if health care is the right career choice for them, Ipsen said. During that time they will also volunteer in different areas of the hospital for 100 hours during the summer.
According to Ipsen, the four career core sessions that student volunteers will take part in are:
q Physician learning more about being a physician, the requirements, the skills it takes to be successful and what specialties they can study.
q Nursing presenting the wide variety of nursing opportunities, what qualifications they need to have and what skills they need to possess to be successful.
q Additional health care careers educating participants about health care careers they may not know of such as technicians, physical therapists and clinical engineers.
q Presenting yourself an opportunity to have a resume reviewed by HR professionals, be interviewed by hiring managers and learn more about presenting themselves for success.
Discover Health Care: Volunteer Summer Program will allow student volunteers to build their resume, gain experience, network with health care leaders and develop a greater understanding of the diverse health care industry in the Central Valley, Ipsen said.
The deadline to register for the program is March 24.
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PUBLIC RELEASE DATE:
5-Mar-2014
Contact: Shawna Williams shawna@jhmi.edu 410-955-8632 Johns Hopkins Medicine
Johns Hopkins researchers say they have found one way that a recently discovered genetic mutation might cause two nasty nervous system diseases. While the affected gene may build up toxic RNA and not make enough protein, the researchers report, the root of the problem seems to be snarls of defective genetic material created at the mutation site.
The research team, led by Jiou Wang, Ph.D., an assistant professor of biochemistry and molecular biology and neuroscience at the Johns Hopkins University School of Medicine, reports its finding March 5 on the journal Nature's website.
Two years ago, researchers linked the gene C9orf72, named for its location on the ninth human chromosome, to amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrig's disease, and to frontotemporal dementia (FTD).
In ALS, motor neurons nerve cells that carry messages from the brain to muscles degenerate and eventually die, which gradually paralyzes the patient. In FTD, neurons in the frontal and temporal lobes of the brain die. Some scientists think the same genetic and biological processes cause both disorders, but with very different symptoms, depending on where in the brain they occur.
The mutation in C9orf72 is called a hexanucleotide repeat expansion, a six-letter "word" of DNA repeated over and over, in a part of the gene that doesn't contain instructions for making any proteins. Although it's normal to have up to 20 such repeats, some people with ALS or FTD have dozens or even hundreds of them. Studies show the mutation is likely responsible for 4 to 8 percent of cases of sporadic ALS the kind that isn't necessarily hereditary and, in some groups, up to 40 percent of the kind that is.
To learn how the repeated sequence causes disease, the Johns Hopkins scientists looked at the structure of the DNA that makes up the gene and the RNA that carries its instructions. Although DNA and RNA are generally seen as long strands, they can bunch and curl to make 3-D structures.
Working with DNA and RNA they made that bore the six-letter "word" repeat, the researchers figured out that both were forming structures called G-quadruplexes. In these formations, guanines called "G" for short, one of the letters in the repeating DNA "word" link up, making stacks that stick together like tiny shelves. The RNA also forms other shapes in the repeating section hairpins and bulges. The researchers speculate that the G-quadruplexes and other structures might be getting in the way of the nucleic acids' normal functions.
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ALS-linked gene causes disease by changing genetic material's shape
(PRWEB) March 05, 2014
In Latin America, Mexico is the pioneer in genetic test applications. Personalized medicine has only been around for the last 15 years. The ALAMPs intention with personalized medicines was to decrease and identify the predisposition of diseases, and to increase the success rate of therapy.
A list of international and national guests gathered at this ALAMP sponsored event. Attendees included Stefan Long, director of the science department at General Genetics Corporation, the number one laboratory in the study of ADN in the world; Dr Felipe Vzquez Estupin, specialist in family therapy; and Dr. Bernard Esquivel, president of ALAMP, who discussed the transition that personalized medicine proposes for healthy and sick individuals, as well as for health systems, through the integration of personalized medicine into clinical practice of genetic examinations that strengthen such care.
The first international symposium of personalized medicine was directed at any health professional that wanted to incorporate their field in the diverse areas of personalized medicine. This included establishment of the protocols of prevention, follow up and monitoring to the development of specific adequate treatments, and the genetic characteristics of each individual.
As defined by the Presidents Council of Advisors of Science and Technology, personalized medicine discerns if the processes that apply to a patient, or a to a group of patients, are appropriate from view point of the proposed strategies as the response to a specific medicine will be different from the present responses of a patient affected by the same condition. This has allowed, and will continue to allow, the introduction of predictors of any disease, whether it be the presence of mutations of oncogenes, or of regular tumor genes.
This algorithm explains the vision of Mexico for personalized medicine: based on the molecular profile of the patient (his genome), regardless of his age, it identifies the susceptibility of various conditions to develop in the patient. Subsequently they establish educational mechanisms/institutions like nutrition (Nutrigenomics; the individualization of micro-macro nutrients according to the metabolic level expressed by the genes), habits, etc., with the intention of preventing the onset of the disease. Since we are not aware of all the environmental factors that trigger diseases, there is always the possibility of more developing factors. Therefore, it is very important to establish a customized program aimed at the early detection of such pathogens. If one detects many diseases in their initial stage (among these are many types of cancer), one can implement appropriate therapeutic measures that eradicate these diseases or control them quickly, preventing further damage and degeneration of the patient (which is the case in non-communicable chronic diseases, or diabetes).
The first international symposium of personalized medicine addressed issues in various areas of genetic medicine, and addressed the steps that Mexico is taking as the pioneer in its application of personalized medicine in Latin America. As a country, Mexico hopes to reduce the unfavorable economic impact of the 25 chronic-degenerative prevalent diseases in the next 20 years by applying immediate preventive measures through a simple genetic test. The proposed test would cost $420 dollars, which will allow saving on treatment costs. Currently, there are 12.8 million future diabetics that could spend up to $448,000 if they dont detect their disease earlier.
For example, as we know, type 2 diabetes mellitus is one of the major causes of death in Mexico and has a pre-pathogenic period (before it appears, which highlights the genetic susceptibility), and a pathogenic period (with the onset of the disease) stage that doesnt present symptoms. Approximately two years later after the onset of the disease, a large number of the patients are not yet diagnosed, until they have an acute complication, i.e., with the hospital emergency room.
Applying the proposed model of personalized medicine to these patients may:
A)Delay the onset of the diseases by many years, which allows for a better quality of life for the patient and a very important economic savings cost for his or her social security.
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Personalized Medicine: The New Paradigm in the Prevention and Treatment of Diseases
New tests could spare soldiers from debilitating sickness at high altitudes--and mitigate cattle deaths in the Rockies
Chris 73, Wikimedia Commons
On his 27th birthday, David Hillebrandt and his wife Sally began to climb Mount Kenya, the second-highest mountain in Africa after Kilimanjaro. Instead of gearing up and heading straight for the mountain's tallest peakwhich reaches 5,199 metersthe couple started their journey more leisurely, trekking through scenic ridges and valleys around the mountain at an altitude of about 3,000 meters.
David, who today serves as a medical advisor to the British Mountaineering Council, already had considerable climbing experience at the time: he had scaled a 5,790-meter peak in Pakistan and 3,960-meter peaks in the European Alps. Sally, in contrast, had never done any serious climbing and did not consider herself a mountaineer.
But Sally wasn't the one who needed to stop and turn around.
"I am meant to be this tough, rugged mountaineer," David says, "and I celebrated my birthday by throwing up all over the place." Plagued by a throbbing headache and relentless nausea, David retreated to lower ground. He knew from previous climbs that he was prone to altitude sickness, but he thought circling the mountain at 3,000 meters would be a good way to acclimatize. This time it didn't do the trick. Even though she was a far less experienced climber, Sally adjusted to the altitude much faster.
It wasn't experience that made the differenceit was genetics. Scientists have known for a while that some people are inherently more susceptible to altitude sickness than othersand that this susceptibility is heritablebut only now are they on the trail of the culprit genes. Preliminary studies suggest that a group of six genes predicts who will get altitude sickness with greater than 90 percent accuracy. Such a precise genetic test would greatly benefit the military, which currently has no way of predicting which soldiers will fall ill when flown to high altitudes and would rather not waste money on expensive acclimatization drugs. In a parallel research effort, scientists have been searching for the genes that determine which cows develop altitude sickness, also known as brisket disease, when they graze in the Rocky Mountains. Because tens of thousands of cows die in the western U.S. from brisket disease annually, ranchers would like nothing more than to strip the responsible genes from the breeding population.
Written in blood The pursuit of a genetic test for altitude sickness began in earnest a few years ago in Robert Roach's laboratory at the University of Colorado. In 2010, 28 people in Roach's lab ascended to an altitude of 4,875 meters without ever leaving the ground. Roach placed his volunteers in a large metal box called a hypobaric chamber and gradually sucked out air with a vacuum pump, reducing atmospheric pressure to mimic a high altitude, low-oxygen environment. Roach purposefully recruited a mixture of people who were susceptible to altitude sickness and people who had never had problems in high climes. As expected, about half of the 28 volunteers felt sick in the chamber, whereas the others felt fine.
Roach took samples of his volunteers' blood, isolated their DNA and programmed a computer to search for genetic differences between the people who got sick and those who didn't mind hanging out in thin air. The program identified six genes that are expressed at unusually high or low levels in people who felt sick; some of the genes are linked to oxygen transport. Looking at the expression levels of those six genes alone was enough to distinguish people who became ill from those who did not with about 95 percent accuracy.
The following year, Roach collaborated with Benjamin Levine of the University of Texas Southwestern Medical Center to try the rudimentary genetic test on a larger group of volunteers. This time, instead of bringing the mountain to his lab, Roach decided to move his lab to the mountain.
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Mountain Maladies: Genetic Screening Susses Out Susceptibility to Altitude Sickness
Cloned Human Embryos As Well As Animal Human Hybrids?
abominationFebruary 2014 Breaking News Labs Mixing Human DNA with Animal DNA 1 of 5 Last days final hour news prophecy update 2 of 4 ... 3 of 4 ... 4 of 4 .....
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Cloned Human Embryos As Well As Animal Human Hybrids? - Video
Genetic engineering talk show
By: Victor Rodriguez
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PUBLIC RELEASE DATE:
4-Mar-2014
Contact: Vicki Cohn vcohn@liebertpub.com 914-710-2100 Mary Ann Liebert, Inc./Genetic Engineering News
New Rochelle, NY, March 4, 2014Only about 37% of babies around the world are exclusively breastfed for the first 6 months of life, as recommended by the World Health Organization (WHO). The benefits of breastfeeding for both infants and mothers are well-established. The effectiveness of different types of interventions for promoting exclusive breastfeeding in high-income countries is the focus of a Review article published in Breastfeeding Medicine, the official journal of the Academy of Breastfeeding Medicine published by Mary Ann Liebert, Inc., publishers. The article is available free on the Breastfeeding Medicine website at http://www.liebertpub.com/bfm.
Most interventions designed to encourage women to breastfeed use supportive or educational approaches, with varying levels of success, according to study authors Helen Skouteris and colleagues from Deakin University and University of Melbourne (Melbourne, Australia), and Leeds Metropolitan University (Leeds, UK).
In the article "Interventions Designed to Promote Exclusive Breastfeeding in High-Income Countries: A Systematic Review" the authors evaluate the effectiveness of different interventions, comparing prenatal and postnatal approaches, the duration of the interventions, and identify whether they focus on educating mothers or providing emotional support.
"The search for successful interventions that promote the international goal of exclusive breastfeeding for the first six months of an infant's life has been continual but inconclusive," says Ruth Lawrence, MD, Editor-in-Chief of Breastfeeding Medicine and Professor of Pediatrics, University of Rochester School of Medicine. "Authors Helen Skouteris and colleagues in their extensive review point out that a trial of more support and interventions in the postpartum period may be critical to solving this issue."
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About the Journal
Breastfeeding Medicine, the Official Journal of the Academy of Breastfeeding Medicine, is an authoritative, peer-reviewed, multidisciplinary journal published 10 times per year in print and online. The Journal publishes original scientific papers, reviews, and case studies on a broad spectrum of topics in lactation medicine. It presents evidence-based research advances and explores the immediate and long-term outcomes of breastfeeding, including the epidemiologic, physiologic, and psychological benefits of breastfeeding. Tables of content and a sample issue may be viewed on the Breastfeeding Medicine website at http://www.liebertpub.com/bfm.
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Which interventions are most effective to promote exclusive breastfeeding?
PUBLIC RELEASE DATE:
5-Mar-2014
Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News
New Rochelle, NY, March 5, 2014Chronic hepatitis C virus (HCV) infection can lead to serious diseases such as cirrhosis and cancer of the liver, so viral clearance and prevention of relapse are important treatment goals. Low-dose oral interferon may reduce the risk of HCV relapse in patients with mild liver fibrosis according to a study published in Journal of Interferon & Cytokine Research, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Interferon & Cytokine Research website.
In "A Double-Blind Randomized Controlled Study to Evaluate the Efficacy of Low-Dose Oral Interferon-Alpha in Preventing Hepatitis C Relapse," Chuan-Mo Lee and coauthors from several universities and hospitals in Taiwan present the results of a clinical trial comparing the effects of 24 weeks of treatment with two doses of oral interferon-alpha or placebo in patients who achieved viral clearance after successful HCV therapy.
"This is a highly significant study relevant to the optimal use of IFN for HCV treatment," says Co-Editor-in-Chief Ganes C. Sen, PhD, Chairman, Department of Molecular Genetics, Cleveland Clinic Foundation, Ohio.
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About the Journal
Journal of Interferon & Cytokine Research (JICR), led by Co-Editors-in-Chief Ganes C. Sen, PhD, and Thomas A. Hamilton, PhD, Chairman, Department of Immunology, Cleveland Clinic Foundation, is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that covers all aspects of interferons and cytokines from basic science to clinical applications. JICR is an official journal of the International Cytokine and Interferon Society. Complete tables of content and a sample issue may be viewed online on the Journal of Interferon & Cytokine Research website.
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Can low-dose interferon prevent relapse of hepatitis C virus infection?
Engineering a patients own immune cells to resist HIV could eliminate the need for lifelong antiretroviral therapies.
The immune cells of HIV patients can be genetically engineered to resist infection, say researchers. In a small study in humans, scientists report that by creating a beneficial mutation in T cells, they may be able to nearly cure patients of HIV.
In a study published in the New England Journal of Medicine on Wednesday, researchers report that they can use genome editing to re-create the rare mutations responsible for protecting about 1 percent of the population from the virus in infected patients. They report that some of the patients receiving the genome-modifying treatment showed decreased viral loads during a temporary halt of their antiretroviral drugs. In one patient, the virus could no longer be detected in his blood.
Zinc-finger nucleases are one of a few genome-editing tools that researchers use to create specific changes to the genomes of living organisms and cells (see Genome Surgery). Scientists have previously used genome-editing techniques to modify DNA in human cells and nonhuman animals, including monkeys (see Monkeys Modified with Genome Editing). Now, the NEJM study suggests the method can also be safely used in humans.
From each participating patient, the team harvested bone marrow stem cells, which give rise to T cells in the body. They then used a zinc finger nuclease to break copies of the CCR5 gene that encodes for proteins on the surface of immune cells that are a critical entry point of HIV. The stem cells were then infused back into each patients bloodstream. The modification process isnt perfect, so only some of the cells end up carrying the modification. About 25 percent of the cells have at least one of the CCR5 genes interrupted, says Edward Lanphier, CEO of Sangamo Biosciences, the Richmond, California, biotech company that manufactures zinc finger nucleases.
Because the cells are a patients own, there is no risk of tissue rejection. The modified stem cells then give rise to modified T cells that are more resistant to infection by HIV, say the researchers.
One week after the infusion, researchers were able to find modified T cells in the patients blood. Four weeks after the infusion, six of the 12 patients in the study temporarily stopped taking their antiretroviral drugs so the researchers could assess the effect of the genome-editing treatment on the amount of the virus in the patients bodies. In four of these patients, the amount of HIV in the blood dropped. In one patient, the virus could no longer be detected at all. The team later discovered that this best responder had naturally already had one mutated copy of the CCR5 gene.
Patients who carry one broken copy of the CCR5 progress to AIDS more slowly than those who dont, says Bruce Levine, a cell and gene therapy researcher at the University of Pennsylvania School of Medicine and coauthor on the study. Because all of the cells in that best-responder patient already carried one disrupted copy of CCR5, the modification by the zinc finger nuclease led to T cells with no functional copies of the gene. That means the cells are fully resistant to HIV infection. The team is now working to increase the number of immune cells that end up carrying two broken copies of CCR5.
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PUBLIC RELEASE DATE:
5-Mar-2014
Contact: Steve Graff stephen.graff@uphs.upenn.edu 215-349-5653 University of Pennsylvania School of Medicine
PHILADELPHIAUniversity of Pennsylvania researchers have successfully genetically engineered the immune cells of 12 HIV positive patients to resist infection, and decreased the viral loads of some patients taken off antiretroviral drug therapy (ADT) entirelyincluding one patient whose levels became undetectable. The study, appearing today in the New England Journal of Medicine, is the first published report of any gene editing approach in humans.
The phase I study was co-authored by researchers at Penn Medicine, the Albert Einstein College of Medicine and scientists from Sangamo BioSciences, which developed the zinc finger nuclease (ZFN) technology, the T cell therapy approach used in the clinical trial.
"This study shows that we can safely and effectively engineer an HIV patient's own T cells to mimic a naturally occurring resistance to the virus, infuse those engineered cells, have them persist in the body, and potentially keep viral loads at bay without the use of drugs," said senior author Carl H. June, MD, the Richard W. Vague Professor in Immunotherapy in the department of Pathology and Laboratory Medicine at Penn's Perelman School of Medicine. "This reinforces our belief that modified T cells are the key that could eliminate the need for lifelong ADT and potentially lead to functionally curative approaches for HIV/AIDS."
June and his colleagues, including Bruce L. Levine, PhD, the Barbara and Edward Netter Associate Professor in Cancer Gene Therapy in the department of Pathology and Laboratory Medicine and the director of the Clinical Cell and Vaccine Production Facility at Penn, used the ZFN technology to modify the T cells in the patientsa "molecular scissors," of sorts, to mimic the CCR5-delta-32 mutation. That rare mutation is of interest because it provides a natural resistance to the virus, but in only 1 percent of the general population. By inducing the mutations, the scientists reduced the expression of CCR5 surface proteins. Without those, HIV cannot enter, rendering the patients' cells resistant to infection.
For the study, the team infused the modified cells known as SB-728-Tinto two cohorts of patients, all treated with single infusionsabout 10 billion cellsbetween May 2009 and July 2012. Six were taken off antiretroviral therapy altogether for up to 12 weeks, beginning four weeks after infusion, while six patients remained on treatment.
Infusions were deemed safe and tolerable, the authors report, and modified T cells continued to persist in the patients when tested during follow up visits. One week after the initial infusion, testing revealed a dramatic spike in modified T cells inside the patients' bodies. While those cells declined over a number of weeks in the blood, the decrease of modified cells was significantly less than that of unmodified T cells during ADT treatment interruption. Modified cells were also observed in the gut-associated lymphoid tissue, which is a major reservoir of immune cells and a critical reservoir of HIV infection, suggesting that the modified cells are functioning and trafficking normally in the body.
The study also shows promise in the approach's ability to suppress the virus. The viral loads (HIV-RNA) dropped in four patients whose treatment was interrupted for 12 weeks. One of those patients' viral loads dropped below the limit of detection; interestingly, it was later discovered that the patient was found to be heterozygous for the CCR5 delta-32 gene mutation.
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Gene therapy locks out HIV, paving the way to control virus without antiretroviral drug
WASHINGTON, March 5 -- U.S. researchers said Wednesday they have used gene therapy involving genetically engineered T- cells to successfully decrease the amount of the AIDS virus in several patients taken off antiretroviral drug therapy (ADT) entirely, including one patient whose levels became undetectable.
The study, published in the U.S. journal New England Journal of Medicine, is the first published report of any gene editing approach in humans, the researchers said.
"This study shows that we can safely and effectively engineer an HIV patient's own T cells to mimic a naturally occurring resistance to the virus, infuse those engineered cells, have them persist in the body, and potentially keep viral loads at bay without the use of drugs," senior author Carl June, professor of the University of Pennsylvania, said in a statement.
"This reinforces our belief that modified T cells are the key that could eliminate the need for lifelong ADT and potentially lead to functionally curative approaches for HIV/AIDS," June said.
In their study, the researchers used a technology called the zinc finger nuclease (ZFN) to modify the T cells in 12 patients with the AIDS virus in order to mimic the CCR5-delta-32 mutation that can provide a natural HIV resistance. Only one percent of the general population carries that rare mutation.
They then infused the modified cells known as SB-728-T into two groups of patients, all treated with single infusions of about 10 billion cells, between May 2009 and July 2012.
Six were taken off antiretroviral therapy altogether for up to 12 weeks, beginning four weeks after infusion, while six patients remained on treatment.
The researchers found that the amount of HIV dropped in four patients whose treatment was interrupted for 12 weeks.
One of those patients' viral loads dropped below the limit of detection before reinstitution of ADT and the patient was later found to be "heterozygous" for the CCR5-delta-32 gene mutation, they said.
"This case gives us a better understanding of the mutation and the body's response to the therapy, opening up another door for study," co-author Bruce Levine, associate professor of the University of Pennsylvania said.
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Gene therapy shows promise for HIV control without drugs: study-Eastday
Scientists have modified genes in the blood cells of HIV patients to help them resist the AIDS virus, and say the treatment seems safe and promising.
The results give hope that this approach might one day free at least some people from needing medicines to keep HIV under control, a form of cure.
The idea came from an AIDS patient who appears cured after getting a cell transplant seven years ago in Berlin from a donor with natural immunity to HIV. Only about one per cent of people have two copies of the gene that gives this protection.
Researchers are seeking a more practical way to get similar results by using gene therapy to modify patients' own blood cells.
A study of this in 12 patients was led by Dr Carl June at the University of Pennsylvania with results publishedon Thursday in the New England Journal of Medicine. These are the first published results from this method, which also has been tried in several smaller studies of patients in California.
HIV usually infects blood cells through a protein on their surface, a 'docking station' called CCR5. A California company, Sangamo BioSciences, makes a treatment that can knock out a gene that makes CCR5.
The 12 HIV patients had their blood filtered to remove some of their cells. The gene-snipping compound was added in the lab, and the cells were infused back into the patients.
Four weeks later, half of the patients were temporarily taken off AIDS medicines to see the gene therapy's effect. The virus returned in all but one of them, but the modified cells seemed to be protected from HIV infection and were more likely to survive than the cells that had not been treated.
'We knew that the virus was going to come back in most of the patients,' but the hope is that the modified cells eventually will outnumber the rest and give the patient a way to control viral levels without medicines, said Dr Pablo Tebas, one of the Penn researchers. That would be what doctors call a 'functional cure,' because the virus would still be present but held in check without treatment.
The lone patient whose HIV did not return turned out to have one copy of the protective gene, so 'nature had done half of the job already,' Tebas said.
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PHILADELPHIA University of Pennsylvania researchers have successfully genetically engineered the immune cells of 12 HIV positive patients to resist infection, and decreased the viral loads of some patients taken off antiretroviral drug therapy (ADT) entirelyincluding one patient whose levels became undetectable. The study, appearingtoday in the New England Journal of Medicine, is the first published report of any gene editing approach in humans.
The phase I study was co-authored by researchers at Penn Medicine, the Albert Einstein College of Medicine and scientists from Sangamo BioSciences, which developed the zinc finger nuclease (ZFN) technology, the T cell therapy approach used in the clinical trial.
This study shows that we can safely and effectively engineer an HIV patients own T cells to mimic a naturally occurring resistance to the virus, infuse those engineered cells, have them persist in the body, and potentially keep viral loads at bay without the use of drugs, said senior author Carl H. June, MD, the Richard W. Vague Professor in Immunotherapy in the department of Pathology and Laboratory Medicine at Penns Perelman School of Medicine. This reinforces our belief that modified T cells are the key that could eliminate the need for lifelong ADT and potentially lead to functionally curative approaches for HIV/AIDS.
June and his colleagues, including Bruce L. Levine, PhD, the Barbara and Edward Netter Associate Professor in Cancer Gene Therapy in the department of Pathology and Laboratory Medicine and the director of the Clinical Cell and Vaccine Production Facility at Penn, used the ZFN technology to modify the T cells in the patientsa molecular scissors, of sorts, to mimic the CCR5-delta-32 mutation. That rare mutation is of interest because it provides a natural resistance to the virus, but in only 1 percent of the general population. By inducing the mutations, the scientists reduced the expression of CCR5 surface proteins. Without those, HIV cannot enter, rendering the patients cells resistant to infection.
For the study, the team infused the modified cells known as SB-728-Tinto two cohorts of patients, all treated with single infusionsabout 10 billion cellsbetween May 2009 and July 2012. Six were taken off antiretroviral therapy altogether for up to 12 weeks, beginning four weeks after infusion, while six patients remained on treatment.
Infusions were deemed safe and tolerable, the authors report, and modified T cells continued to persist in the patients during follow up visits. One week after the initial infusion, testing revealed a dramatic spike in modified T cells inside the patients bodies. While those cells declined over a number of weeks in the blood, the decrease of modified cells was significantly less than that of unmodified T cells during ADT treatment interruption. Modified cells were also observed in the gut-associated lymphoid tissue, which is a major reservoir of immune cells and a critical reservoir of HIV infection, suggesting that the modified cells are functioning and trafficking normally in the body.
The study also shows promise in the approachs ability to suppress the virus. The viral loads (HIV-RNA) dropped in four patients whose treatment was interrupted for 12 weeks. One of those patients viral loads dropped below the limit of detection; interestingly, it was later discovered that the patient was found to be heterozygous for the CCR5 delta-32 gene mutation.
Since half the subject's CCR5 genes were naturally disrupted, the gene editing approach was building on the head start provided by inheriting the mutation from one parent, said Levine. This case gives us a better understanding of the mutation and the bodys response to the therapy, opening up another door for study.
Therapies based on the CCR5 mutation have gained steam over the last six years, particularly after a man known as the Berlin Patient was functionally cured. Diagnosed with acute myeloid leukemia (AML), he received a stem cell transplant from a donor who had the CCR5 mutation in both alleles (from both parents) and has remained off ADT since 2008. Researchers are attempting to replicate this phenomenon because allogeneic transplantswhich carry a high mortality risk and require lengthy hospitalizationsare not a practical solution for HIV patients who do not have blood cancers. Nor are they effective in ridding the body of HIV unless the donor has the mutated gene in both alleles, as shown recently in two Boston patients who were thought to have been functionally cured from transplants, only to see their viral loads spike.
Though disappointing to the research community, the Boston patients results highlight key factors when combating the virus.
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NIBSC/Science Photo Library
HIV attacks a type of immune cell known as a T cell (shown here) using a protein encoded by the CCR5 gene.
A clinical trial has shown that a gene-editing technique can be safe and effective in humans. For the first time, researchers used enzymes called zinc-finger nucleases (ZFNs) to target and destroy a gene in the immune cells of 12 people with HIV, increasing their resistance to the virus to the virus. The findings are published today in The New England Journal of Medicine1.
This is the first major advance in HIV gene therapy since it was demonstrated that the Berlin patient Timothy Brown was free of HIV, says John Rossi, a molecular biologist at the Beckman Research Institute of the City of Hope National Medical Center in Duarte, California. In 2008, researchers reported that Brown gained the ability to control his HIV infection after they treated him with donor bone-marrow stem cells that carried a mutation in a gene called CCR5. Most HIV strains use a protein encoded by CCR5 as a gateway into the T cells of a hosts immune system. People who carry a mutated version of the gene, including Brown's donor, are resistant to HIV.
But similar treatment is not feasible for most people with HIV: it is invasive, and the body is likely to attack the donor cells. So a team led by Carl June and Pablo Tebas, immunologists at the University of Pennsylvania in Philadelphia, sought to create the beneficial CCR5 mutation in a persons own cells, using targeted gene editing.
The researchers drew blood from 12 people with HIV who had been taking antiretroviral drugs to keep the virus in check. After culturing blood cells from each participant, the team used a commercially available ZFN to target the CCR5 gene in those cells. The treatment succeeded in disrupting the gene in about 25% of each participants cultured cells; the researchers then transfused all of the cultured cells into the participants. After treatment, all had elevated levels of T cells in their blood, suggesting that the virus was less capable of destroying them.
Six of the 12 participants then stopped their antiretroviral drug therapy, while the team monitored their levels of virus and T cells. Their HIV levels rebounded more slowly than normal, and their T-cell levels remained high for weeks. In short, the presence of HIV seemed to drive the modified immune cells, which lacked a functional CCR5 gene, to proliferate in the body. Researchers suspect that the virus was unable to infect and destroy the altered cells.
They used HIV to help in its own demise, says Paula Cannon, who studies gene therapy at the University of Southern California in Los Angeles. They throw the cells back at it and say, Ha, now what?
In this first small trial, the gene-editing approach seemed to be safe: Tebas says that the worst side effect was that the chemical used in the process made the patients bodies smell bad for several days.
The trial isnt the end game, but its an important advance in the direction of this kind of research, says Anthony Fauci, director of the US National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. Its more practical and applicable than doing a stem-cell transplant, he says, although it remains to be seen whether it is as effective.
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Futurist Flight Radio #3
Welcome back to Futurist Flight. We #39;re now bringing you powerfull anthems like "Check This Out" and "Rock Like This", to make your week even better. Hope you...
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3UA3 Kurt Vonnegut Futurist Slidecast
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REGINA Its April 2024 and farmer Hank Fairfields mind has turned to seeding.
He summons his computerized butler and requests a report on moisture and temperature. A flock of mini-drones to cruise over the fields, looking into them to a depth of three feet.
That lets Hank create a map of where fertilizer and pesticides must be applied.
He can even release natural predators like ladybugs to consume the pests before they hatch.
And from all this, he can prepare a schedule of seeding using robot tractors.
Thats the future farm, as sketched by Toronto-based futurist Richard Worzel who conceded to a standing-room-only audience of farmers and allies that things wont work out this way as there are too many events we havent anticipated.
Still, scenarios like this give an ideas of whats to come in whats already one of the most high-tech of all North American industries: farming.
Clearly, its going to involve more computers, robots, biotechnology and computer intelligence, he told chemical giant BASFs Knowledge Harvest event for elite farmers in Regina Tuesday.
Painting a picture of a world in which a farmer can monitor every bit of land and every animal around the clock, Worzel said one of its key economic drivers will be continued growth in developing economies like China, where the average daily calorie intake has gone from 1,400 in 1960 to 2,600 at present, with consumption of meat and dairy products growing particularly fast.
The same demand will come from India, and some countries in Asia, Africa and Latin America, causing him to say that for the first time in a century, the future of farming is better than ever.
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