Sperm conceive cues in surprising ways.
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Biomedical subjects
Publications and source records attributed to D Gurwitz.
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Transdermal nicotine patches have been successfully introduced as a safe and powerful aid to smoking cessation; this has contributed to the rising interest in additional therapeutic applications for nicotine and synthetic nicotinic agonists. Nicotine and nicotinic agonists may have a therapeutic potential for a variety of disorders, including Alzheimer's and Parkinson's diseases, depression, attention deficit disorder, Tourette's syndrome and ulcerative colitis. These interests are partially fuelled by the urgent need of the tobacco industry to find new niches for nicotine in a world bound eventually to retire from cigarette smoking. At the same time, there is an increased interest in developing drugs for fighting obesity, a growing affliction of industrialised nations. This review presents data on the potential of nicotine, and in particular synthetic nicotinic agonists, for controlling body weight. Nicotinic agonists may become relatively safe, effective and inexpensive alternatives for several optional drugs currently being developed for treating human obesity, including beta-3-adrenergic agonists, leptin and its agonists, and neuropeptide Y antagonists.
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Activation of receptor tyrosine kinases stimulates a diverse array of cellular responses such as proliferation and differentiation. The first events in the signal transduction pathways mediated by different receptor tyrosine kinases are similar and include activation of the mitogen-activated protein kinase (MAPK) pathway and the induction of immediate early genes. The precise signaling pathways leading to each of the cellular responses mediated by receptor tyrosine kinases are still unknown, although it has been proposed that sustained activation of the MAPK pathway by receptor tyrosine kinases such as the nerve growth factor (NGF) receptor TrkA is sufficient to induce differentiation in PC12 cells. In the present study we examined the effect of NGF on mutant PC12 cells that were derived spontaneously in our cultures. NGF induced normal activation of immediate early genes in these cells, whereas the activation of some delayed response genes, as well as neurite outgrowth, was impaired. Furthermore, activation of the NGF-induced extracellular signal-regulated kinase (ERK) in these cells was transient, not sustained. These results support the hypothesis that sustained activation of ERK plays an important role in activating the induction of delayed response genes. However, sustained ERK activation is not a mandatory condition for the promotion of all the features of differentiated PC12 cells, as NGF could induce transcription of the delayed response gene, transin, in PC12 mutant cells. Taken together, our results suggest that NGF induces differentiation of PC12 cells via several signaling pathways, an important one of which is the MAPK pathway.
The failure of the immune system to mount a successful attack on the human immunodeficiency virus (HIV) is an old enigma for AIDS research. The high mutational capacity of HIV, which unremittingly confuses the immune system, is a major factor in immune failure. But this alone cannot fully explain the certain and inescapable failure of the immune system, leading to full-blown AIDS. Here, we propose the hypothesis that endogenous cannabinoids, derived mostly from macrophages, might participate in the general failure of the immune system in HIV-infected individuals.
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There are no simple answers when it comes to the genetic study of complex traits, and schizophrenia is no exception. Debate will continue over the interaction between genes and environment. But now there are new clues.