Drug-resistant staph infections are a major concern to health care providers. Hospitals in particular have become home to some strains of Staphylococcus aureus that resist every known antibiotic, including the last-resort vancomycin. But two researchers say they’ve discovered just how so-called “Hospital staph” develops resistance, potentially opening the door for development of new drugs that beat it to the punch.
It’s one of those stories that simultaneously gives great hope but also a little dread. Researchers in Pennsylvania say they’ve successfully stimulated the production of a pain-blocking protein in mice by using a modified herpes virus to attach the appropriate genes onto the animals’ DNA. That’s potentially terrific news. If the same technique held true in humans, it could offer a new way to treat the devastating pain associated with some forms of cancer, such as bone cancer. Of course, a hell of a lot of mice were bred specifically develop the extremely painful bone tumors, just so the technique could be tested. It’s no doubt a necessary sacrifice, but one that shouldn’t be overlooked entirely. You don’t have to be a wacko member of PETA to spare a thought for the millions of mice and other lab animals that are sacrificed each year so humans can live healthier lives.
Researchers say they’ve developed a new test for prions that improves the accuracy and speed with which the malformed and infectious proteins can be detected. Prions cause neurodegenerative diseases in sheep, deer and elk, plus Mad Cow disease in cattle and Creutzfeldt-Jakob in humans.
Researchers have discovered a gene mutation that causes a condition apparently identical to Huntington’s Disease, helping explain why some people with the disorder do not have a separate mutation found in most cases. The finding may help reveal why some diseases, like Huntington’s, Alzheimer’s and Parkinson’s, destroy some brain cells while sparing others. “For all practical purposes this is Huntington’s Disease, yet it’s caused by a different mutation on a completely different chromosome,” said Russell L. Margolis, M.D., associate professor of Psychiatry at Hopkins and director of the Johns Hopkins Laboratory of Genetic Neurobiology. “This is a rare version of an already rare disorder, but the mutation that causes it may not only help us better understand Huntington’s Disease, but could boost our understanding of many other neurodegenerative disorders.”
This is a little complex, but bear with us. Nearly all cells house their DNA inside a nucleus. But a little one-celled critter called Tetrahymena houses different versions of its DNA in each of its two nuclei. Researchers have found that the smaller nucleus (called the micronucleus) just keeps the cell’s full genome safe, acting as a sort of “lock box.” The larger nucleus (called the macronucleus) uses the DNA to regulate the cell’s life functions. When the cell mates to create a new generation, the two work together to compare the cell’s current DNA against what’s been stored in the lock box. If any foreign genes have snuck in (like from a virus) they nuclei eliminate it, to make sure baby gets a fresh start. Pretty neat, with possible implications for larger organisms, too.
Using neural stem cells to hunt down and kill cancer cells, researchers have successfully tested a new treatment for brain cancer. They now hope the technique will lead to an effective treatment for glioma, the most aggressive form of primary brain tumor in humans. As the Cedars-Sianai researchers note, the prognosis has historically been extremely poor for patients diagnosed with malignant gliomas. The tumors have poorly defined margins, and glioma cells often spread deep into healthy brain tissue making their surgical removal difficult. Often, pockets of tumor cells break off from the main tumor and migrate deep into non-tumorous areas of the brain. Therefore, even if the original tumor is completely removed or destroyed, the risk of recurrence is high as cells in these distant “satellites” multiply and eventually re-form a new brain tumor. Due to these characteristics, treating brain cancer has been extremely difficult.
Treating precancerous breast cells with chemopreventive agents like tamoxifen limits the development of breast cancer in genetically predisposed women, according to a new study. Precancerous breast cells may also provide an effective mechanism for screening new and current chemopreventive agents, the study found.
Researchers may have discovered the mechanism behind how prions ? pieces of protein molecules? can kill nerve cells in the brain and lead to some serious degenerative diseases. The key seems to lie in how one particular protein misfolds within an organelle inside the cell, transforming itself into a new agent and then poisoning the neuron in which it was made.
Men who test positive for elevated prostate specific antigen (PSA) levels sometimes freak out because they think it means they have cancer. To find out, a surgeon will often perform a biopsy. But researchers from the National Cancer Institute and the Food and Drug Administration report that a new test using a single drop of blood could help distinguish between prostate cancer and benign conditions. The trick is identifying patterns of proteins found in patients’ blood serum.
Stanford researchers have developed a technique that could cut the risks associated with gene therapy. Traditionally, gene therapy involves sneaking a snippet of genes into a person’s DNA via a virus messenger. But the result is the new sequence gets randomly placed within the patient’s existing genes, sometimes triggering other illnesses, such as leukemia. The new technique eliminates the need for a virus delivery system and places the genes in precise locations.