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August 24, 2006, 5:16 AM CT

Microcapsules Open in Tumour Cells

Microcapsules Open in Tumour Cells Microcapsules in a cell, (a) before, and (b) after being illuminated with a laser
Treating cancerous tumours is difficult. Doctors have to destroy the tumour, but healthy tissue needs to be preserved. Chemotherapy tends to kill diseased cells, at the same time causing great damage to the body in general. So researchers are looking for ways to destroy only the rampant tumour cells. One way to achieve this is to transport substances inside of microcapsules into the tumour cells and release them there. Scientists led by Andre Skirtach and Gleb Sukhorukov at the Max Planck Institute of Colloids and Interfaces in Potsdam, Gera number of, along with Wolfgang Parak at Ludwig-Maximilian-University in Munich, have now used a laser as a means of opening microcapsules inserted into a tumour cell. The capsules subsequently release their contents, a fluorescent test substance, into the cell. The researchers used a light microscope to monitor how the luminous materials distribute themselves within the cell.

The vehicle that the scientists used was a polymer capsule only a few micrometres in diameter. The walls of the capsules were built from many layers of charged polymers, alternating positive and negative. In the laboratory, at least, this is an established way of producing transport containers for medicines, cosmetics, or nutrients, which can also pass through cell membranes. Andre Skirtach and colleagues equipped the capsules with a kind of "open sesame". But it didn't require any magic - just nanoparticles made of gold or silver atoms. The researchers mixed together charged metal nanoparticles along with the polymers composing the walls of the vesicle. The tumour cells absorbed the microcapsules and then the researchers aimed an infrared laser at them. Metal nanoparticles are especially good at absorbing the laser light and transmitting the heat further into their surroundings, heating up the walls. They became so hot that the bonds broke between the polymers and the shell and the capsules eventually opened.........

Posted by: Janet      Permalink         Source


August 23, 2006, 5:11 AM CT

Targeting Protein S14 In Breast Cancer Treatment

Targeting Protein S14 In Breast Cancer Treatment Dartmouth researchers Wendy Wells and William Kinlaw are looking into a protein called S14. (Photo by Joseph Mehling '69)
William Kinlaw, an associate professor of medicine at Dartmouth Medical School, has been working on a protein called S14 since 1990. Over the past few months, however, the news about S14 has picked up. Through a series of recently published academic studies, Kinlaw and colleagues are ready to pronounce S14 a potential drug target in treating breast cancer.

"Over the past three years, we've learned about S14 and its role in communicating information about the nutrient and energy supply to genes mandatory for fat metabolism in breast cancer cells," says Kinlaw, who is also affiliated with the Norris Cotton Cancer Center at Dartmouth-Hitchcock Medical Center. "With this knowledge has also come the understanding that most breast cancers have found a mechanism to turn on the S14 gene".

He explains that these tumors are 'addicted' to S14, because it is mandatory for the activation of a group of genes that allow the cancer cells to make fat. Kinlaw and his team have observed that breast cancer cells die if S14 is removed, and their analysis of human breast tumors indicates that S14 is critical for metastasis.

"This makes sense, as fat is a crucial fuel for breast cancers," he says. "We believe this is particularly so during a tumor cell's attempt to journey from the breast to other parts of the body, because the normal breast tissue supplies machinery that allows tumor cells to acquire fat from the bloodstream. Our data support the hypothesis that once the cells leave this metabolically friendly breast environment, the ability to manufacture their own fat becomes a make-or-break issue".........

Posted by: Janet      Permalink         Source


August 22, 2006, 7:03 PM CT

Cigarette smoke blocks cell repair mechanism

Cigarette smoke blocks cell repair mechanism
Cigarette smoke can turn normal breast cells malignant by blocking their ability to repair themselves, eventually triggering tumor development, University of Florida researchers report.

While some cells nonetheless rally and are able to fix their damaged DNA, a number of others become unable to access their own cellular first aid kit, as per findings from a UF study published recently (Aug. 21) in the journal Oncogene. If they survive long enough to divide and multiply, they pass along their mutations, acquiring cancerous properties.

Past research has been controversial. Tobacco smoke contains dozens of cancer-causing chemicals, but until more recently a number of studies found only weak correlations between smoking and breast cancer risk, or none at all. Those findings are increasingly being challenged by newer studies that are focusing on more than just single chemical components of tobacco, as past research often has done. In the UF study, scientists instead used a tar that contains all of the 4,000 chemicals found in cigarette smoke.

"Our study suggests the mechanism by which this may be happening," said Satya Narayan, Ph.D., an associate professor of anatomy and cell biology at UF's College of Medicine. "This is basically the important finding in our case: We are now describing how cigarette smoke condensate, which is a surrogate for cigarette smoke, can cause DNA damage and can block the DNA repair of a cell or compromise the DNA repair capacity of a cell. That can be detrimental for the cell and can lead to transformation or carcinogenesis".........

Posted by: Janet      Permalink         Source


August 22, 2006, 6:04 PM CT

Ever-happy Mice And Treatment Of Depression

Ever-happy Mice And Treatment Of Depression
Can you think of being permanently happy and cheerful? That's what a team of scientists did. A new breed of permanently 'cheerful' mouse is providing hope of a new therapy for clinical depression. TREK-1 is a gene that can affect transmission of serotonin in the brain. Serotonin is known to play an important role in mood, sleep and sexuality. By breeding mice with an absence of TREK-1, scientists were able create a depression-resistant strain. The details of this research, which involved an international collaboration with researchers from the University of Nice, France, are published in Nature Neuroscience this week.

"Depression is a devastating illness, which affects around 10% of people at some point in their life," says Dr. Guy Debonnel an MUHC psychiatry expert, professor in the Department of Psychiatry at McGill University, and principal author of the new research. "Current medications for clinical depression are ineffective for a third of patients, which is why the development of alternate therapys is so important".

Mice without the TREK-1 gene ('knock-out' mice) were created and bred in collaboration with Dr. Michel Lazdunski, co-author of the research, in his laboratory at the University of Nice, France. "These 'knock-out' mice were then tested using separate behavioral, electrophysiological and biochemical measures known to gauge 'depression' in animals," says Dr. Debonnel. "The results really surprised us; our 'knock-out' mice acted as if they had been treated with antidepressants for at least three weeks."........

Posted by: JoAnn      Permalink         Source


August 21, 2006, 10:06 PM CT

Protein That Protect Breast Cancer Tumors

Protein That Protect Breast Cancer Tumors
About half of women whose breast cancer is treated with standard chemotherapy have their cancer return within five years. Most chemotherapeutic drugs have undesirable side effects, but there has been no way to predict who would benefit and who wouldn't. Fortunately, new research findings at the University of Southern California could change that.

Scientists at the USC/Norris Comprehensive Cancer Center have discovered a new biological marker in tumors that can help indicate whether a woman's breast cancer will respond to the most usually prescribed chemotherapy drugs.

Amy S. Lee, Ph.D., professor of biochemistry and molecular biology in the Keck School of Medicine of the University of Southern California, isolated the gene for the GRP78 protein (78-kDA glucose-regulated protein) in 1980. It normally helps protect cells from dying, especially when they are under stress from a lack of glucose. In her current research, Lee finds that breast cancer tumors with high levels of GRP78 are protected from a common chemotherapy regimen based on Adriamycin, a topoisomerase inhibitor. Her findings are published as a "Priority Report" in the August 15 issue of Cancer Research.

"The importance of this study is in its potential to help clinicians who treat cancer," Lee says. "It will help sort out the patients who won't respond to particular therapy regimens and will have a higher chance of cancer recurrence."........

Posted by: Janet      Permalink         Source


August 21, 2006, 9:07 PM CT

Bulls-eye For Antibiotic Target

Bulls-eye For Antibiotic Target
A Purdue University researcher has opened the door for possible antibiotic therapys for a variety of diseases by determining the structure of a protein that controls the starvation response of E. coli.

This research is applicable to the therapy of a number of diseases because that same protein is found in numerous harmful bacteria, including those that cause ulcers, leprosy, food poisoning, whooping cough, meningitis, sexually transmitted diseases, respiratory infections and stomach cancer, said David Sanders, an associate professor of biology. Sanders, who is part of the Markey Center for Structural Biology at Purdue, detailed his research in a paper reported in the Aug. 16 issue of the journal Structure.

"This is an important discovery for the field of antibiotics, which was greatly in need of something new," Sanders said. "The antibiotics available today face a challenge of increasing resistance and failure. This research suggests a whole new approach to combat bacterial infections. In addition, this protein is an excellent antibiotic target because it only exists in bacteria and some plants, which means the therapy will only affect the targeted bacterial cells and will be harmless to human cells".

Sanders and his collaborator, Miriam Hasson, studied the structure of exopolyphosphatase, a protein in E. coli bacteria that functions as an enzyme and catalyzes chemical reactions within the bacteria. This enzyme provides the signal for bacteria to enter starvation mode and limit.........

Posted by: Mark      Permalink         Source


August 20, 2006, 9:26 PM CT

How HIV 'exhausts' killer T cells

How HIV 'exhausts' killer T cells
American and South African researchers working at the epicenter of the AIDS epidemic in South Africa have discovered how the human immunodeficiency virus (HIV) "exhausts" killer T cells that would otherwise attack the virus. The scientists observed that HIV can simply "turn off" fully functional T cells by flipping a molecular switch on the cells. In test tube studies, however, the researchers showed that they could reinvigorate the killer T cells by blocking that inhibitory switch, which is called programmed death-1 (PD-1).

The study's senior author, Bruce Walker, a Howard Hughes Medical Institute researcher at Massachusetts General Hospital, said that clinical testing of drugs that block the PD-1 switch could begin very soon, since such drugs exist already. However, he cautioned that these kinds of drugs could cause serious side effects, including autoimmune reactions that trigger the immune system to attack the body. Walker added that the researchers' findings will also likely have application in understanding other chronic viral diseases.

The findings by Walker and colleagues were published in an advance online publication on August 20, 2006, by the journal Nature. Walker is also at the Partners AIDS Research Center and Harvard Medical School. Other co-authors were from the University of KwaZulu Natal in South Africa, Oxford University, Dana-Farber Cancer Institute of Harvard Medical School, Emory University School of Medicine, and The Wistar Institute.........

Posted by: Mark      Permalink         Source


August 20, 2006, 9:23 PM CT

A New Tool Against Brain Disease

A New Tool Against Brain Disease A shell from the venomous cone snail Conus omaria, which lives in the Pacific and Indian oceans and eats other snails
Credit: Kerry Matz, University of Utah
University of Utah researchers isolated an unusual nerve toxin in an ocean-dwelling snail, and say its ability to glom onto the brain's nicotine receptors may be useful for designing new drugs to treat a variety of psychiatric and brain diseases.

"We discovered a new toxin from a venomous cone snail that may enable scientists to more effectively develop medications for a wide range of nervous system disorders including Parkinson's disease, Alzheimer's disease, depression, nicotine addiction and perhaps even schizophrenia," says J. Michael McIntosh.

Discovery of the new cone snail toxin will be published Friday, Aug. 25 in The Journal of Biological Chemistry by a team led by McIntosh, a University of Utah research professor of biology, professor and research director of psychiatry, member of the Center for Peptide Neuropharmacology and member of The Brain Institute.

McIntosh is the same University of Utah researcher who as an incoming freshman student in 1979 discovered another "conotoxin" that was developed into Prialt, a drug injected into fluid surrounding the spinal cord to treat severe pain due to cancer, AIDS, injury, failed back surgery and certain nervous system disorders. Prialt was approved in late 2004 in the United States and was introduced in Europe last month.........

Posted by: Daniel      Permalink         Source


August 20, 2006, 2:27 PM CT

Trial Of New Asthma Treatment Calls For Volunteers

Trial Of New Asthma Treatment Calls For Volunteers
Scientists at Washington University School of Medicine in St. Louis are seeking participants for the AIR2 (Asthma Interventional Research) international, multi-center clinical trial, which explores whether a new asthma therapy improves asthma care.

The trial, the first test of the procedure in the United States, focuses on a procedure called bronchial thermoplasty to treat asthma. Early patient data from trials outside the United States suggest it may hold promise for moderate and severe asthmatic patients.

"This is an exciting trial because for the first time ever in the U.S., we are looking at a non-pharmacological therapy for asthma," says Mario Castro, M.D., principal investigator of the study at the School of Medicine and associate professor of medicine in the Division of Pulmonary and Critical Care Medicine. "Currently, if you suffer from asthma, medicine is the only therapy available to you for relief, so there is the potential this clinical trial may change the way we care for millions of asthma sufferers."

Asthma is one of the most common and costly diseases in the world. It affects more than 20 million people in the United States alone, with an estimated 2 million emergency room visits and 5,000 deaths per year. The prevalence of asthma is on the rise, and there is no cure.........

Posted by: Scott      Permalink         Source


August 20, 2006, 2:21 PM CT

Immune cells protect retina from damage

Immune cells protect retina from damage Abnormal blood vessels and hemorrhage underneath the retina in the wet form of age-related macular degeneration
Eventhough some recent studies have suggested that inflammation promotes retinal damage in age-related macular degeneration (AMD), new work from Washington University ophthalmology scientists has observed that a particular type of inflammation, regulated by cells called macrophages, actually protects the eye from damage due to AMD.

The scientists report in the Aug. 15 issue of Public Library of Science (PLoS) Medicine that in a mouse model of AMD, macrophages help prevent the formation of blood vessels that grow underneath the retina and cause the majority of severe vision loss linked to AMD.

Age-related macular degeneration is the leading cause of blindness in the United States in people over the age of 50. It accounts for more than 40 percent of blindness among the institutionalized elderly, and as baby boomers get older, the problem is expected to grow, with at least 8 million cases of AMD predicted by the year 2020.

There are two varieties of AMD: a "dry" form and a "wet" form. Most patients have the dry form of the disease, and eventhough this can progress and cause severe vision loss in some, between 80 and 90 percent of the blindness and severe vision loss occurs in the wet form of the disease, as per the paper's first author Rajendra S. Apte, M.D., Ph.D.........

Posted by: Mike      Permalink         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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