Medical hypotheses
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In a recent Medical Hypotheses editorial, I suggested the name psychological neoteny (PN) to refer to the widely-observed phenomenon that adults in modernizing liberal democracies increasingly retain many of the attitudes and behaviors traditionally associated with youth. I further suggested that PN is a useful trait for both individuals and the culture in modernizing societies; because people need to be somewhat child-like in their psychology order to keep learning, developing and adapting to the rapid and accelerating pace of change. Thirdly, I put forward the hypothesis that the major cause of PN in modernizing societies is the prolonged duration of formal education. ⋯ However, the economic effect is different in men and women: after parenthood men are more likely to have a job and work more hours while women change in the opposite direction. The conclusion is that psychological neoteny is indeed increasing, and mainly as a consequence of the increasing percentage of school leavers going into higher education. But at present it is unclear whether this trend is overall beneficial or harmful; and the answer may be different for men and women.
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The mechanisms responsible for symptom expression in fibromyalgia (FM) are complex. The most consistently detected objective abnormalities in FM involve pain-processing systems. Up to recently, central nervous system was a primary focus of investigations in FM. ⋯ This paper suggests that patients with FM represent a state of the dysfunction of descending, antinociceptive pathways and low hypothalamic-pituitary-adrenal function. This state is further proposed to result in many skin biopsy findings associated with the disorder, including increased N-methyl-d-aspartate receptors subtype 2D expression, neurogenic inflammation and characteristic electron microscopic findings. Future direction of research would be identification of specific laboratory markers such as skin biopsy for diagnostic and clinical evaluation purposes in FM.
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Postoperative delirium represents a serious complication after major surgery. Patients suffer from anxiety, hallucinations and delusions, and have higher postoperative morbidity and mortality. Generally, the role of acetylcholine deficiency in delirium pathophysiology is widely accepted. ⋯ These morphological changes lead to a decrease of nutritive perfusion and to longer diffusion distance for oxygen. Because acetylcholine synthesis is especially sensitive to low oxygen tension, symptoms of its deficiency readily develop. Therapeutic tools to modulate excessive inflammation are available, therefore new strategies of delirium treatment should be implemented in clinical praxis, as well as in preventive measures.
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Since the launch in 1998 of the anti-impotence drug sildenafil (viagra), the American food and drug administration has identified 50 cases of drug-related blindness, the so-called nonarteritic anterior ischemic optic neuropathy. This, very serious, side effect frequently leads to sudden, mostly irreversible loss of vision, and there is no proven effective treatment to cure patients or to prevent recurrence. ⋯ These data are consistent with the hypothesis that sildenafil, surgery and anesthesia, taken together, could be a potentially dangerous cocktail of risk factors for sudden irreversible loss of vision. To reduce the risk, sildenafil use should be avoided at least one week before surgical operations, since the reported cases of blindness developed 36h after drug ingestion.
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Vascular calcification is a common feature in advanced atherosclerosis and also a predictor of future cardiovascular events such as unstable angina and myocardial infarction, especially in diabetes. There is a growing body of evidence that advanced glycation end products (AGEs), senescent macroprotein derivatives formed at an accelerated rate in diabetes, exist within atherosclerotic lesions, thereby being implicated in the pathogenesis of accelerated atherosclerosis in diabetes. Indeed, we have previously shown that AGE - their receptor (RAGE) interaction could induce angiogenesis through autocrine production of vascular endothelial growth factor, suggesting its role for plaque formation and enlargement in diabetes. ⋯ Since we, along with others, have shown that nifedipine inhibits glycation of low-density lipoprotein in vitro and blocks the AGE-induced RAGE expression in endothelial cells through its anti-oxidative properties, nifedipine could inhibit vascular calcification by blocking the AGE formation or the downstream signaling in diabetes. In this paper, we would like to propose the possible ways of testing our hypothesis. Does nifedipine treatment slow down the progression of coronary calcification in diabetic patients? If the answer is yes, is this beneficial effect of nifedipine superior to that of other DHPs with equihypotensive properties? Does nifedipine treatment decrease expression levels of AGEs and RAGE in diabetic atherosclerosis? Is the unique effect of nifedipine on vascular calcification correlated with its AGE or RAGE-suppressing properties? These prospective studies will provide further valuable information whether nifedipine could prevent vascular calcification in diabetic atherosclerosis by blockade the AGE-RAGE signaling in vascular wall cells.