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July 28, 2009, 11:37 PM CT

Maternal, paternal genes' tug-of-war

Maternal, paternal genes' tug-of-war
An analysis of rare inherited disorders in which children lack some genes from one parent suggests that maternal and paternal genes engage in a subtle tug-of-war well into childhood, and possibly as late as the onset of puberty.

This striking new variety of intra-family conflict, described this week in the Proceedings of the National Academy of Sciences, is the latest wrinkle in the two-decades-old theory known as genomic imprinting, which holds that each parent contributes genes that seek to nudge his or her children's development in a direction most favorable, and least costly, to that parent.

"In comparison to other primates, human babies are weaned quite early, yet take a very long time to reach full nutritional independence and sexual maturity," says author David Haig, George Putnam Professor of Organismic and Evolutionary Biology in Harvard University's Faculty of Arts and Sciences. "Human mothers are also unusual among primates in that they often care for more than one child at a time. Evidence from disorders of genomic imprinting suggests that maternal and paternal genes may skirmish over the pace of human development".

Prior research has offered evidence of a genetic struggle for supremacy only during fetal development: In the womb, some genes of paternal origin have been shown to promote increased demands on mothers, leading to fetal overgrowth, while genes of maternal origin tend to have the opposite effect. This new work suggests maternal and paternal genes continue to engage in internal genetic conflict past childbirth.........

Posted by: Scott      Read more         Source


July 27, 2009, 11:02 PM CT

How the pathology of Parkinson's disease spreads?

How the pathology of Parkinson's disease spreads?
Accumulation of the synaptic protein alpha-synuclein, resulting in the formation of aggregates called Lewy bodies in the brain, is a hallmark of Parkinson's and other related neurodegenerative diseases. This pathology appears to spread throughout the brain as the disease progresses. Now, scientists at the University of California, San Diego School of Medicine and Konkuk University in Seoul, South Korea, have described how this mechanism works. Their findings the first to show neuron-to-neuron transmission of alpha-synuclein will appear in the Proceedings of the National Academy of Sciences (PNAS) on July 29.

"The discovery of cell-to-cell transmission of this protein may explain how alpha-synuclein aggregates can pass to new, healthy cells," said first author Paula Desplats, project scientist in UC San Diego's Department of Neurosciences. "We demonstrated how alpha-synuclein is taken up by neighboring cells, including grafted neuronal precursor cells, a mechanism that may cause Lewy bodies to spread to different brain structures." .

This insight will impact research into stem cell treatment for Parkinson's disease. "Our findings indicate that the stem cells used to replace lost or damaged cells in the brains of Parkinson's disease patients are also susceptible to degeneration," said Eliezer Masliah, MD, professor of neurosciences and pathology at UC San Diego School of Medicine. "Knowledge of the molecular basis of the intercellular transmission of alpha-synuclein may result in improved stem-cell based therapies with long-lasting benefits, by preventing the grafted cells to uptake α-synuclein or by making them more efficient in clearing the accumulated alpha-synuclein."........

Posted by: Daniel      Read more         Source


July 20, 2009, 11:40 PM CT

Gene that leads to breast cancer's aggressive behavior

Gene that leads to breast cancer's aggressive behavior
Aggressive forms of cancer are often driven by the abnormal over-expression of cancer-promoting genes, also known as oncogenes.

Studies at the Genome Institute of Singapore (GIS), a research institute under the Agency for Science, Technology and Research (A*STAR) of Singapore, have identified a gene, known as RCP (or RAB11FIP1), that is frequently amplified and over-expressed in breast cancer and functionally contributes to aggressive breast cancer behaviour.

The research findings appear in the July 20th online issue of Journal of Clinical Investigation (JCI).

The GIS team, led by Lance Miller, Ph.D., and Bing Lim, Ph.D., initially discovered that RCP expression was positively correlated with cancer recurrence in a population of patients with breast cancer. This suggested that RCP appears to be mandatory by some tumours for growth and metastatic spread to other organs.

When the scientists over-expressed RCP in non-malignant breast cells, they observed that RCP promotes migration, or cellular movement, which is a precursor to the ability of tumours to invade neighbouring tissues.

However, breast cancer cells in which RCP is over-expressed take on a more aggressive behaviour, including faster proliferation, enhanced migration/invasion and anchorage-independent growth.........

Posted by: Janet      Read more         Source


July 20, 2009, 11:39 PM CT

Insights into failed HIV-1 vaccine trial

Insights into failed HIV-1 vaccine trial
Following the disbandment of the STEP trial to test the efficacy of the Merck HIV-1 vaccine candidate in 2007, the leading explanation for why the vaccine was ineffective and may have even increased susceptibility to acquiring the virus centered on the hypothesis that high levels of baseline Ad5-specific neutralizing antibodies may have increased HIV-1 acquisition among the study subjects who received the vaccine by increasing Ad5-specific CD4+ T-cells that were susceptible to HIV-1 infection.

Now, a study by Dan Barouch, MD, PhD, and a scientific team at Beth Israel Deaconess Medical Center (BIDMC), published in the July 20 Advance Online issue of Nature Medicine, shows this was likely not the case.

"Our findings demonstrate that there is no connection between Ad5 neutralizing antibodies and T-cell immune responses," explains Barouch, who is Chief of the Division of Vaccine Research at BIDMC and Associate Professor of Medicine at Harvard Medical School. "Moreover, subjects with baseline Ad5-specific neutralizing antibodies did not develop higher levels of Ad5-specific T-cell responses as compared with subjects without baseline Ad5-specific neutralizing antibodies".

The Ad5 virus is a weakened form of adenovirus, which is responsible for the common cold and is extremely widespread in the general population. In the Merck vaccine candidate, Ad5 was used as a vector to transport three HIV-1 genes, a strategy that helps to overcome limitations posed by the HIV-1 virus.........

Posted by: Mark      Read more         Source


July 20, 2009, 11:37 PM CT

Stem cells in sutures to enhance healing

Stem cells in sutures to enhance healing
Surgical thread can be embedded with a patient's own adult stem cells to promote healing.

Credit: JHU

Johns Hopkins biomedical engineering students have demonstrated a practical way to embed a patient's own adult stem cells in the surgical thread that doctors use to repair serious orthopedic injuries such as ruptured tendons. The goal, the students said, is to enhance healing and reduce the likelihood of re-injury without changing the surgical procedure itself.

The project team -- 10 undergraduates sponsored by Bioactive Surgical Inc., a Maryland medical technology company -- won first place in the recent Design Day 2009 competition conducted by the university's Department of Biomedical Engineering. In collaboration with orthopedic physicians, the students have begun testing the stem cellbearing sutures in an animal model, paving the way for possible human trials within about five years.

The students believe this technology has great promise for the therapy of debilitating tendon, ligament and muscle injuries, often sports-related, that affect thousands of young and middle-aged adults annually. "Using sutures that carry stems cells to the injury site would not change the way surgeons repair the injury," said Matt Rubashkin, the student team leader, "but we believe the stem cells will significantly speed up and improve the healing process. And because the stem cells will come from the patient, there should be no rejection problems".........

Posted by: Scott      Read more         Source


July 20, 2009, 11:04 PM CT

Why placebos work?

Why placebos work?
Placebos are a sham commonly mere sugar pills designed to represent "no therapy" in a clinical therapy study. The effectiveness of the actual medicine is compared with the placebo to determine if the medicine works.

And yet, for some people, the placebo works nearly as well as the medication. How well placebos work varies widely among individuals. Why that is so, and why they work at all, remains a mystery, believed to be based on some combination of biological and psychological factors.

Now, scientists at UCLA have found a new explanation: genetics. Dr. Andrew Leuchter, a professor of psychiatry at the UCLA Semel Institute for Neuroscience and Human Behavior, and his colleagues report that in people suffering from major depressive disorder, or MDD, genes that influence the brain's reward pathways may modulate the response to placebos. The research appears in the August edition of the Journal of Clinical Psychopharmacology (currently available online by subscription).

Placebos are thought to act by stimulating the brain's central reward pathways by releasing a class of neurotransmitters called monoamines, specifically dopamine and norepinephrine. These are the brain chemicals that make us "feel good." Because the chemical signaling done by monoamines is under strong genetic control, the researchers reasoned that common genetic variations between individuals called genetic polymorphisms could influence the placebo response.........

Posted by: Janet      Read more         Source


July 16, 2009, 11:50 PM CT

Understanding of DNA repair mechanism could lead to better cancer drugs

Understanding of DNA repair mechanism could lead to better cancer drugs
Scientists at Washington University School of Medicine in St. Louis have shed new light on a process that fixes breaks in the genetic material of the body's cells. Their findings could lead to ways of enhancing chemotherapy drugs that destroy cancer cells by damaging their DNA.

Using yeast cells, the researchers studied protein molecules that have an important role in homologous recombination, which is one way that cells repair breaks in the DNA double helix. The process in yeast is similar to that in humans and other organisms.

Earlier research had established that a protein molecule named Srs2 regulates homologous recombination by counteracting the work of another protein, Rad51. Reporting in the July 10 issue of the journal Molecular Cell, the research team reveals the mechanism of how Srs2 removes Rad51 from DNA and thereby prevents it from making repairs to broken strands.

"Our findings may make it possible to uncover ways to augment the effect of DNA-damaging agents that are used for cancer chemotherapy," says senior author Tom Ellenberger, D.V.M, Ph.D., the Raymond H. Wittcoff Professor and head of the Department of Biochemistry and Molecular Biophysics. "A number of chemotherapeutic agents work by causing DNA damage in cancer cells, leading to their death, and tumors can become resistant to chemotherapy by using DNA repair mechanisms to keep the cells alive. Drugs that inhibit the DNA repair process could help increase the efficiency of chemotherapeutic agents".........

Posted by: Janet      Read more         Source


June 16, 2009, 5:03 AM CT

RNA snippet suppresses spread of aggressive breast cancer

RNA snippet suppresses spread of aggressive breast cancer
Image courtesy of University of Illinois
A low cellular level of a tiny fragment of RNA appears to increase the spread of breast cancer in mouse models of the disease, as per scientists at Whitehead Institute for Biomedical Research.

Measuring levels of this so-called microRNA, which is also linked to metastatic breast cancer in humans, may more accurately predict the likelihood of metastasis (which accounts for 90% of cancer-related deaths) and ultimately help determine patient prognoses.

In the study, whose results are published in the June 12 issue of Cell, Scott Valastyan, a graduate student in Whitehead Member Robert Weinberg's laboratory, screened patient breast cancer samples for microRNAs with potential roles in metastasis. MicroRNAs are single strands of RNA about 21-23 nucleotides long. Within a cell, a single microRNA can fine-tune the expression of dozens of genes simultaneously. This capability could be especially important in metastasis, a multi-step process that could be influenced by a single microRNA at several points.

The screened samples were classified as either metastatic cancer or non-metastatic cancer. After analysis, the microRNA miR-31 stood out because of its inverse correlation with metastasis. In samples where a patient's original tumor had not metastasized, the cancer cells retained high levels of the microRNA. But where the tumor had metastasized, the cancer cells came to possess lower levels of miR-31.........

Posted by: Janet      Read more         Source


June 12, 2009, 5:22 AM CT

Gene therapy technique for cancer by cutting off blood supply

Gene therapy technique for cancer by cutting off blood supply
University of Florida scientists have come up with a new gene treatment method to disrupt cancer growth by using a synthetic protein to induce blood clotting that cuts off a tumor's blood and nutrient supply.

In mice implanted with human colorectal cancer cells, tumor volume decreased 53 percent and cancer cell growth slowed by 49 percent in those treated with a gene that encodes for the artificial protein, compared with those that were untreated.

The research team, led by Dr. Bradley S. Fletcher, an assistant professor of pharmacology and therapeutics in the College of Medicine, created the so-called fusion protein to target another protein called tumor endothelial marker 8, or TEM8, which was recently found to be preferentially expressed in the inner lining of tumor vessels. Such differences in protein expression enable delivery of drug molecules to the cells that harbor these proteins.

"The protein we created did a very good job of homing to the tumor and binding," said Stephen Fernando, who recently completed his doctoral studies. "By targeting TEM8, we can potentially create a treatment against cancer".

The Fletcher group is the first to target cancer cells through protein binding to TEM8. The findings, now available online, are featured on the cover of the June 15 edition of Cancer Research........

Posted by: Janet      Read more         Source


June 12, 2009, 5:20 AM CT

Simple chemical system that mimics DNA

Simple chemical system that mimics DNA
A team of Scripps Research researchers has created a new analog to DNA that assembles and disassembles itself without the need for enzymes. Because the new system comprises components that might reasonably be expected in a primordial world, the new chemical system could answer questions about how life could emerge.

The work, published in the June 11, 2009 issue of Science Express, an advance, online publication of the journal Science, might also be a starting point on the way to exotic new materials that repair themselves or transform in response to their environment.

Researchers are both bemused and fascinated by the question of how life could have arisen on Earth. One of the most prominent theories is that, before the emergence of DNA, the earliest forms of life used RNA to transmit their genetic codes. The late Leslie Orgel, a co-author of the new paper, first suggested this idea, known as the "RNA World".

One of the theory's challenges is that RNA is still so complex that a number of scientists believer something still simpler must have preceded it. "I have been working for years to learn what replicators and genetic systems might have come before the advent of the RNA World," says team leader of the new research Professor Reza Ghadiri, a Scripps Research chemist.........

Posted by: Scott      Read more         Source



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Did you know?
Scientists at Yale have brought to light a mechanism that regulates the way an internal organelle, the Golgi apparatus, duplicates as cells prepare to divide, according to a report in Science Express.Graham Warren, professor of cell biology, and colleagues at Yale study Trypanosoma brucei, the parasite that causes Sleeping Sickness. Like a number of parasites, it is exceptionally streamlined and has only one of each internal organelle, making it ideal for studying processes of more complex organisms that have a number of copies in each cell.

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