Annals of the New York Academy of Sciences
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Ann. N. Y. Acad. Sci. · May 2004
ReviewCardiac fiber orientation and the left-right asymmetry determining mechanism.
The invariant nature of body situs within and across vertebrate species implies that a highly conserved pathway controls the specification of the left-right (L/R) axis. Situs-specific morphogenesis begins at the end of this pathway and leads to normal organ arrangement, also known as situs solitus. Occasionally, individuals have a complete, mirror image reversal of this asymmetry, called situs inversus totalis (SIT). ⋯ However, the helical myofiber pattern within the left ventricle (LV) wall is only partially mirror imaged: apical and superficial basal fiber orientation are as in normal persons, whereas the deeper basal layers have an inverted fiber orientation. Because of this bivalent fiber orientation pattern, LV deformation in humans with SIT is mirror imaged only near the base, but near the apex it is as in normal subjects. Apparently, the embryonic L/R controlling genetic pathway does determine situs-specific gross anatomy morphogenesis, but it is not the only factor regulating fiber architecture within the LV wall.
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Recent years have witnessed a dramatic increase in publications implicating free radicals and oxidative stress in virtually every aspect of biology and medicine. Redox Neurology may be defined as the study of the roles of free radicals, transition metals, oxidative stress, and antioxidant defenses in diseases of the nervous system. ⋯ Opportunities for research and teaching careers in the redox neurosciences are outlined. The paper concludes with a forecast of several research themes likely to preoccupy this nascent discipline in the days ahead.
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Ann. N. Y. Acad. Sci. · Dec 2003
ReviewMoxonidine, a mixed alpha(2)-adrenergic and imidazoline receptor agonist, identifies a novel adrenergic target for spinal analgesia.
Moxonidine is a mixed alpha(2)-adrenergic and imidazoline receptor agonist with an improved side effect profile compared to clonidine. Intrathecal (i.t.) moxonidine has been found to possess analgesic activity that, in contrast to the majority of alpha(2)-adrenoceptor (alpha(2)AR) agonists, does not require activation of the alpha(2A)AR subtype, which mediates many of the side effects associated with alpha(2)AR use. In addition, moxonidine (i.t.) interacts in a synergistic manner with opioid agonists and this synergy is retained in neuropathic pain states. Moxonidine may therefore be clinically useful in the treatment of chronic neuropathic pain, either alone or as a coadjuvant with opioids.
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The art of medicine provides a rare opportunity to understand human values and to contribute toward the well-being of one's fellow humans--women in the case of ob-gyn--a contribution that fits in with the mission of the International Federation of Gynaecology Obstetrics (FIGO). Obstetricians and gynecologists should indeed take it upon themselves to improve conditions for women, since the bond and respect between the two is a significant one. It is obstetricians-gynecologists who can provide the much needed technical information to throw light on justifying services that deal with devastating, debilitating, degenerating, and devaluating situations, such as neglected pregnancy, disregard toward cancer detection, and humiliating genital mutilation. ⋯ Ob-gyn must look a little beyond just the lucrative practice of the plain science of obstetrics and gynecology and undertake the responsibility to help and protect the health and life of women around the world. A conscientious doctor cannot practice medicine on women's bodies alone, but must also "practice" against several social evils, the prevention of which is crucial to women's health. Obstetricians and gynecologists can utilize their access to policymakers and health "builders" to carry this brief for women's health, and can urge governments to take a second look at women's rights to ensure that they are on par with the accepted norms of human rights, to be protected and propagated.
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Ann. N. Y. Acad. Sci. · Sep 2003
ReviewCongenital myasthenic syndromes: multiple molecular targets at the neuromuscular junction.
Congenital myasthenic syndromes (CMS) stem from defects in presynaptic, synaptic, and postsynaptic proteins. The presynaptic CMS are associated with defects that curtail the evoked release of acetylcholine (ACh) quanta or ACh resynthesis. Defects in ACh resynthesis have now been traced to mutations in choline acetyltransferase. ⋯ The kinetic mutations increase or decrease the synaptic response to ACh and result in slow- and fast-channel syndromes, respectively. Most low-expressor mutations reside in the AChR epsilon subunit and are partially compensated by residual expression of the fetal-type gamma subunit. In a subset of CMS patients, endplate AChR deficiency is caused by mutations in rapsyn, a molecule that plays a critical role in concentrating AChR in the postsynaptic membrane.