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    Displaying items by tag: mice

    mice with glioblastomaSwedish researchers have discovered a new method to combat cancer. In scientific journals it a completely new mechanism to fight cancer through the explosion of cancer cells.

    Experts on the science of cancer of the Karolinska Institute in Stockholm said that they were able to cause tumor growth in mice. Through the introduction of the drug they induce growth of a specific type of brain tumor called glioblastoma. Subsequently, after taking another drug they say they were able to prevent tumor development and growth of cancer cells.

    The substance, which is carried out the experiments is called 1 - Vakvinol, which may be administered in tablet form. It has been found that molecules of the particular drug may be incorporated in the cancer cells. In this way they cause the development of a process called vacuolation. In this order the cells swell by extracting fluid from the interstitial space and their incorporation in a vacuole inside the cell, which gradually increases in size. Subsequently, the cancer cell starts to break down, the walls thin and gradually this led to its literal explosion and death.

    Research and their research have been conducted on mice with glioblastoma, which scientists say is true and applicable to other types of cancer cells. This medicament is believed to have the same mechanism of action in humans, but in a different half-life, i.e. the dose in mice and will be different in different time intervals, while in humans will seek saturation and higher plasma concentration for maximum effect.

    The study is the result of many years of research into new methods of drug treatment of cancer, during which scientists have crashed millions of cancer cells particles to determine which of the tested drugs effect will be the strongest. Vakvinol-1 is defined as the definitive drug and scientists say the drug substance to be registered as soon as possible and move in phase 1 clinical trials compared to patients who are suffering from malignant forms of cancer.

    Claims of scientists are complemented by the fact that the experimental conditions in mice implanted tumor cells of human glioblastoma, which subsequently started his own development. Mice were fed with crushed tablets Vakvinol -1 in five consecutive days of drug experimentation. The results show that all six of the eight mice survived after drug administration, while in the control group of the infected mice with human glioblastoma, mortality is recorded as 100% , that is, 30 of each 30 mice were infected reached fatal. Surviving mice with specific therapy lived 80 more days, according to the researchers is equivalent to decades of human life, even allowing for full treatment.

    Professor Patrick Ernfors tissue from the Department of Biology at the Karolinska Institute, Stockholm, said he was proud of the scientific discovery of the research team, because this is an entirely new mechanism to fight cancer, which will be introduced in clinical trials. According to him, possible drug will combat cancer cells in an entirely new pathophysiological mechanism that would protect people from the harmful effects and side effects of other forms of drug therapy of cancers that currently exist.

    Published in News

    toxoplasmainChronic infection with the parasite Toxoplasma gondii can make mice lose their innate, hard-wired fear of cats. This loss of their innate fear may persist after the parasite is no longer detectable in their brains, suggesting that initial infection may cause permanent changes in the mechanisms underlying their fear of predators. The results are published September 18 in the open access journal PLOS ONE by Wendy Ingram and colleagues from the University of California, Berkeley.
    The Toxoplasma parasite can be deadly, causing spontaneous abortion in pregnant women or killing immune-compromised patients, but it has even stranger effects in mice.
    Infected mice lose their fear of cats, which is good for both cats and the parasite, because the cat gets an easy meal and the parasite gets into the cat's intestinal track, the only place it can sexually reproduce and continue its cycle of infection.
    New research by graduate student Wendy Ingram at the University of California, Berkeley, reveals a scary twist to this scenario: the parasite's effect seem to be permanent. The fearless behavior in mice persists long after the mouse recovers from the flu-like symptoms of toxoplasmosis, and for months after the parasitic infection is cleared from the body, according to research published today (Sept. 18) in the journal PLOS ONE.
    "Even when the parasite is cleared and it's no longer in the brains of the animals, some kind of permanent long-term behavior change has occurred, even though we don't know what the actual mechanism is," Ingram said. She speculated that the parasite could damage the smell center of the brain so that the odor of cat urine can't be detected. The parasite could also directly alter neurons involved in memory and learning, or it could trigger a damaging host response, as in many human autoimmune diseases.
    Ingram became interested in the protozoan parasite, Toxoplasma gondii, after reading about its behavior-altering effects in mice and rats and possible implications for its common host, the domesticated cat, and even humans. One-third of people around the world have been infected with Toxoplasma and probably have dormant cysts in their brains. Kept in check by the body's immune system, these cysts sometimes revive in immune-compromised people, leading to death, and some preliminary studies suggest that chronic infection may be linked to schizophrenia or suicidal behavior.

    Pregnant women are already warned to steer clear of kitty litter, since the parasite is passed through cat feces and can cause blindness or death in the fetus. One main source of spread is undercooked pork, Ingram said.
    With the help of Michael Eisen and Ellen Robey, UC Berkeley professors of molecular and cell biology, Ingram set out three years ago to discover how Toxoplasma affects mice's hard-wired fear of cats. She tested mice by seeing whether they avoided bobcat urine, which is normal behavior, versus rabbit urine, to which mice don't react. While earlier studies showed that mice lose their fear of bobcat urine for a few weeks after infection, Ingram showed that the three most common strains of Toxoplasma gondii make mice less fearful of cats for at least four months.
    Using a genetically altered strain of Toxoplasma that is not able to form cysts and thus is unable to cause chronic infections in the brain, she demonstrated that the effect persisted for four months even after the mice completely cleared the microbe from their bodies. She is now looking at how the mouse immune system attacks the parasite to see whether the host's response to the infection is the culprit.
    "This would seem to refute – or at least make less likely – models in which the behavior effects are the result of direct physical action of parasites on specific parts of the brain," Eisen wrote in a blog post about the research.
    "The idea that this parasite knows more about our brains than we do, and has the ability to exert desired change in complicated rodent behavior, is absolutely fascinating," Ingram said. "Toxoplasma has done a phenomenal job of figuring out mammalian brains in order to enhance its transmission through a complicated life cycle."

    Published in News

    M Id 416855 J-assay-kits-cell-monoclonal-polyclonal-peptide-biological-research-products

    If the gene has a similar role in humans will be able to develop new screening tests

    British scientists have identified a gene in mice, which increases the risk of ovarian cancer, as defective.

    Rodents lacking gene are twice as likely to develop cancer, ovarian cancer, and to show signs of infertility. If the gene has a similar role in humans will be able to develop new screening tests, said scientists from the charity Cancer Research UK.

    They focus on gene Helq, who was involved in the restoration of damaged DNA. It turned out that mice deprived of it, are two-fold higher risk of ovarian cancer.

    "The results show that if there are problems with Helq in mice increases the likelihood of developing ovarian cancer and other tumors, said study leader Dr. Simon Boultan. This is exciting because it is possible the same effect was observed in women with a defective gene Helq. The next step is to check whether this is so."

    Published in News

    Scientists at Indiana University and international collaborators have found a way to link two hormones into a single molecule, producing a more effective therapy with fewer side effects for potential use as treatment for obesity and related medical conditions.

    The studies were carried out in the laboratories of Richard DiMarchi, the Standiford H. Cox Distinguished Professor of Chemistry and the Linda & Jack Gill Chair in Biomolecular Sciences in the IU Bloomington College of Arts and Sciences, and of Matthias Tschöp, professor of medicine and director of the Institute of Diabetes and Obesity, Helmholtz Center Munich, Germany.

    Results were published online this week by the journal Nature Medicine.

    Researchers combined a peptide hormone from the digestive system, GLP-1, with the hormone estrogen and administered it to obese laboratory mice. While both GLP-1 and estrogen have demonstrated efficacy as therapy for obesity and adult-onset diabetes, the combination was more effective in producing weight loss and other beneficial results than using either compound on its own. And it produced fewer adverse effects, such as excessive tissue growth linked to tumor formation.

    "We find that combining the hormones as a single molecule dramatically enhanced their efficacy and their safety," DiMarchi said. "The combination improves the ability to lower body weight and the ability to manage glucose, and it does so without showing the hallmark toxicities associated with estrogen."

    The researchers believe GLP-1 acts as a "medicinal chaperone," targeting estrogen to the hypothalamus and pancreas, which are involved with metabolic processes. The precise targeting reduces the likelihood that the estrogen will produce negative effects, such as cancer and stroke.

    Brian Finan, a former doctoral student in DiMarchi's lab, is the lead author of the paper, "Targeted estrogen delivery reverses the metabolic syndrome." Co-authors include Bin Yang and Vasily Gelfanov, research scientists in the IU Bloomington Department of Chemistry, and DiMarchi. Finan is now a post-doctoral researcher at the Helmholtz Zentrum München in Germany, directed by Tschöp, who is DiMarchi's longtime collaborator and a corresponding co-author. Affiliations of the other 20 co-authors include the University of Cincinnati where, also led by Tschöp, many of the in vivo pharmacology and molecular mechanism studies were conducted; Northwestern University; and research laboratories in Germany and China.

    Associated with what health authorities are calling a global epidemic of obesity, the metabolic syndrome consists of obesity associated with other factors such as high blood pressure, high triglycerides, hyperglycemia and low HDL cholesterol. The International Diabetes Federation estimates that as much as 20 percent of the world's adult population has some form of the metabolic syndrome and that they are three times as likely to have a heart attack or stroke and five times as likely to develop adult-onset diabetes as people without the syndrome.

    DiMarchi said investigation continues in the optimization of the peptide-based hormone conjugates with an emphasis on determining the specific mechanism of biological action and identification of an optimal drug candidate suitable for human study. The combination of other peptides and nuclear hormones for targeting other medical conditions holds considerable promise and opportunity for future research.

    Partial funding of the research was provided by Marcadia Biotech and more recently Roche Pharma. Marcadia is a company that DiMarchi co-founded and was acquired in 2010 by Roche Pharma, to which he remains a research consultant.

     

    Published in News
    Monday, 27 May 2013 08:51

    What Makes Us Feel an Itch?

    It's a burning question in science—what makes us feel an itch?

    bear-itch-gentaur-antibodiesScientists experimenting in mice may have found the culprit: A molecule used by the heart is pulling double duty, sending a message to the spinal cord that ultimately produces that familiar tickle on our skin.

    The finding elevates itch—previously thought to be a mild form of pain—to a separate phenomenon, with "its own dedicated landline to the brain," study co-author Mark Hoon, a molecular geneticist at the National Institute of Dental and Craniofacial Research in Bethesda, Maryland, said in a statement.

    And because mice and people share similar biology, the scientists suspect that people also have this circuit.

    The discovery could also someday identify a way to block the molecule from producing itching—a potentially life-changing intervention for millions of people who suffer from chronic itch, particularly those with eczema and psoriasis.

    "Itch is coming into its own as a serious medical condition that deserves treatment above and beyond pain," said Earl Carstens, a neurobiologist and itch expert at the University of California, Davis, who wasn't involved in the study.

    There's even a case of a woman whose itch was so severe that she scratched through her skull into her brain, Carstens said.

    "We know much less about itch than we know about pain, and this paper advances our knowledge about the basic mechanism of itching."

    Getting to the Root of the Itch

    Called natriuretic polypeptide b (Nppb), the itch-causing molecule is already known to be released by the heart, where it controls blood pressure by regulating the amount of sodium released by the kidneys.

    The team decided to focus their research on Nppb because it showed up as a promising candidate in their search to find molecules in itch-sensing cells.

    But first the team had to show that Nppb acts as a neurotransmitter by signaling the brain to itch. 

    So they injected the molecule into mouse skin, with no results. But when the team injected the molecule into a place on the spinal cord that communicates with other nerves, the mice started scratching—a main indicator of itch.

    Next, the team genetically engineered mice that did not have the Nppb molecule.

    In an "aha moment," Hoon said, the team exposed the mice to compounds known to produce itch—and the animals didn't scratch at all. Without Nppb, the animals didn't feel an itch, according to the study.

    Itching itself likely evolved to protect us from disease, Hoon added. 

    "If you think about all of the nasty critters that come through our skin ... it's a way to protect ourselves and remove irritants on the skin before they can do damage," he said.

    Double-Duty Molecules

    UC-Davis's Carstens said "he never would have predicted" that Nppb is the itchmaker, since it has such a different role in the body.

    Co-author Hoon agreed that it's "really weird that this [molecule] is from the heart."

    But both experts noted that our bodies are extremely efficient, often finding ways to make certain parts work multiple jobs, as in the case of Nppb.

    Hoon likens it to "biological cassettes" that produce different responses when "played" in various organs of the body.

    He also suspects there are more such double-duty molecules in our body—just itching to be found.

     

    Published in News
    Monday, 11 March 2013 16:35

    Pills may help you live to 150 years ...

    knockinout-mice-rat

    Scientists develop pill that can help people to live to 150 years, slowing the aging process, reported the British newspaper "Daily Telegraph".

    Drugs are synthetic versions of the organic chemical resveratrol, found in red wine, which is believed to slow aging, enhances the activity of the protein SIRT1. The pharmaceutical company GlaxoSmithKline (GSK) drug testing on people suffering from diabetes of the second type and psoriasis.

    Professor of Genetics at Harvard University David Sinclair said that aging can not "irreversible catastrophe." "We now investigate whether a benefit for people who are already healthy. Results are promising. We find that aging is irreversible disaster, as previously thought. Certain people may live up to 150 years, but it will not get there without further research" he said.

    Professor Sinclair said that the efforts of the activity of SIRT1 protein enhances cell activity, reducing their laziness. Previous experiments on mice, bees and flies that received the substances that enhance the activity of the protein showed that they live longer.

    Professor Sinclair allegedly performed experiments which showed that the substances based on resveratrol have a direct impact on health. Some scholars argue that the impact is real and experimental stealth. The results were published in the scientific journal "Science", wrote Thursday.

    Despite the controversy, some experiments that promise for diseases such as cancer, cardiovascular disease and heart failure, diabetes of the second type, Alzheimer's, Parkinson's, fatty liver disease, cataracts, osteoporosis, muscle atrophy, sleep disorders and inflammatory diseases such as psoriasis, arthritis and colitis.

    In the present study aimed to determine how these substances can help cure diseases associated with aging. But Professor Sinclair believes that in time will also examine the preventive effect. As statins are used today to prevent heart disease and stroke, as these substances can be used to delay many diseases, says the researcher.

    Published in News