Congenital Hearing Loss

thrombophilia genetic testing :: Article Creator New Prenatal Genetic Testing Could Predict Your Baby I have two children. At the moment, all I know about their genes is that they both have 46 chromosomes, and one is XY and one is XX. I try to treat them equally, to assume equal potential. But what if I knew my daughter carried a "smart" gene and my son did not? When he came home from school with a B, would I assume it was just his genes, and not push him to try harder? And what if I could have known this before he were born, at a time when he was just a little blip on an ultrasound? Frankly, I'm not sure I would trust myself with this information. Such knowledge isn't, of course, possible yet. For one thing, we haven't yet found many genes that can reliably predict intelligence. And at the moment, even if we did know what genes we were looking for, we wouldn't be able to find them very early in pregnancy. But thanks to a

marfan syndrome x linked :: Article Creator X Chromosome: X Inactivation Bacher, C. P., et al. Transient colocalization of X-inactivation centres accompanies the initiation of X inactivation. Nature Cell Biology 8, 293-299 (2006) doi:10.1038/ncb1365 (link to article) Borsani, G., et al. Characterization of a murine gene expressed from the inactive X chromosome. Nature 351, 325–329 (1991) doi:10.1038/351325a0 (link to article) Boumil, R. M., & Lee, J. T. Forty years of decoding the silence in X-chromosome inactivation. Human Molecular Genetics 10, 2225–2232 (2001) Brockdorff, N., et al. Conservation of position and exclusive expression of mouse Xist from the inactive X chromosome. Nature 351, 329–331 (1991) doi:10.1038/351329a0 (link to article) ———. The product of the mouse Xist gene is a 15 kb inactive X-specific transcript containing no conserved ORF and located in the nucleus. Cell 71, 515–526 (1992) Brown, C. J., et al. A gene from

thrombocytopenia clots :: Article Creator What Is Drug-induced Thrombocytopenia? Some medications can destroy blood-clotting cells called platelets or prevent bone marrow from producing enough. This can lead to a low platelet count called thrombocytopenia. Drugs that may cause thrombocytopenia include heparin, acetaminophen (Tylenol), and some chemotherapy drugs. Certain medications may cause thrombocytopenia. The condition may lead to severe complications and can be life threatening. Drug-induced thrombocytopenia occurs when medications cause a low platelet level. Platelets are blood cells that help blood clot to slow or stop bleeding. If a person's blood does not clot, they may bleed excessively. A normal platelet count is 150,000 to 450,000 per microliter (µl) of blood. A platelet count below 150,000/µl is considered low. Without treatment, thrombocytopenia may cause severe internal or external blee

low platelets :: Article Creator Can Beta Blockers Cause Low Platelet Count? Exploring The Connection Beta blockers are a class of medications commonly prescribed for a variety of cardiovascular conditions, including hypertension, heart rhythm disorders, and heart failure. While they are effective in managing these conditions, there are concerns regarding their potential side effects. One such concern is whether beta blockers can cause low platelet counts, a condition known as thrombocytopenia. This article aims to explore the relationship between beta blockers and platelet count, examining the mechanisms involved, potential risks, and the importance of monitoring. Understanding Beta Blockers Beta blockers work by blocking the effects of epinephrine (adrenaline) on beta-adrenergic receptors in the heart and blood vessels. By doing so, they help to lower heart rate, reduce blood pressure, and decrease the workload on the heart. Some commonly p

chromosome disease list :: Article Creator The 'Molecular Devils' That Cause The Most Fatal Diseases Ever Known A tiny protein is responsible for one of the most horrific ways to die: the prion, a germ unlike any other. Despite not having any genetic signature of life—like bacteria, fungi, and even viruses do—these proteins can fold into a malignant, zombie-like form that converts normal prions into a copy of themselves, which eventually destroys the brain from the inside out. In a new book The Power of Prions, author and scientist Michel Brahic provides a close-up view of these mysterious proteins. Brahic is a French microbiologist who's been connected to the world of prions for decades. Though he personally focused on unraveling the viral triggers of brain diseases, he was an early colleague of Stanley Prusiner, one of the eventual Nobel Prize-winning discoverers of prions. Later in his career, Brahic's research veered to