Medical hypotheses
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Clostridium difficile infection (CDI) remains a devastating cause of hospital-acquired diarrhea. Treatment modalities have centered traditionally on two antibiotics, metronidazole and oral vancomycin. Both drugs, however, have been associated with variable relapse rates up to 20%. ⋯ We believe that antibiotic selection for the treatment of patients with any infectious disease must account for the possibility of subsequent severe CDI. We posit 'upstream' antibiotic selection will prevent 'downstream' CDI and potentially ameliorate deficiencies in infection prevention practices. Formal studies evaluating such an endpoint would be useful in this era of dangerous CDI.
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Deep brain stimulation of the pedunculopontine tegmental nucleus (PPTg) had usually been reported to improve the symptoms of advanced Parkinson's disease. Previous studies showed that neurons in the PPTg involved in the control of the sympathetic outflow to the kidneys. ⋯ We propose a hypothesis that deep brain stimulation of the PPTg may influence renal function by serotonergic and catecholaminergic pathways. Because PRV-614/tryptophan hydroxylase and PRV-614/tyrosine hydroxylase double-labeled neurons in the compact parts of PPTg (cpPPTg) were not detected, deep brain stimulation of the cpPPTg might not influence renal function.
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Involuntary medication is one of the coercive measures used in psychiatry. We argue that direct extrapolation of placebo and nocebo effects of psychiatric medication in the voluntary setting to the situation of coercive treatment is probably not justified. ⋯ As a consequence, placebo effects are likely to be diminished in coercive treatment, while nocebo effects are probably increased. This may result in an overall decreased effectiveness of medication in coercive settings.
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Evidence indicates that smokers have hyperalgesia perioperatively as characterized by a higher postoperative pain score as well as increased requirements of opioids during surgery and postoperative patient-controlled analgesia compared with non-smokers. The possible mechanism of hyperalgesia for smokers is related to nicotinic acetylcholine receptor (nAChR) desensitization as well as competitive occupancy for binding sites. For smokers, high doses of opioids are needed perioperatively whereas small doses of nicotine do not reduce postoperative opioid requirements. ⋯ The serotonergic system plays an important part in modulating anti-nociception, and decreasing the concentration of serotonin in vesicles in neurons of the brain and spinal cord is an effective method. Intraoperative application of tramadol could result in an analgesic effect via enhancement of descending inhibitory pain pathways. Therefore, increasing the amount of tramadol given intraoperatively and postoperatively may reduce overall opioid requirements, and decrease the pain score as well as morphine consumption postoperatively.
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Despite a large body of epidemiologic and clinical evidence suggesting that sleep disordered breathing is an independent risk factor for development of type 2 diabetes (T2DM), the underlying pathogenesis of altered glucose metabolism in sleep apnea remains to be unraveled. While previous studies have proposed some causal pathways linking sleep apnea with T2DM through increased insulin resistance and deterioration in insulin sensitivity, there has been a particular lack of research into sleep apnea-related alterations in pancreatic beta-cell function. Drawing upon our previous observation that sleep apnea is independently associated with an increased basal pancreatic beta-cell function in adults with normal glucose metabolism, the idea presented here suggests that sleep apnea imposes an excessive demand for insulin secretion, which may lead to progressive pancreatic beta-cell failure in high-risk individuals. ⋯ The ideas and hypotheses presented here address the unexplored pathophysiological mechanisms underlying the potential causal link between sleep apnea and T2DM. Future hypotheses-testing will seek to delineate the role of sleep apnea in the development of T2DM, probe the underlying molecular mechanisms for pancreatic beta-cell dysfunction in sleep apnea, and obtain information on clinical, epidemiologic, and other factors responsible for protecting individuals from alterations in insulin-glucose homeostasis. These results could further be utilized in testing genetic susceptibilities and various therapy modalities to prevent pancreatic beta-cell dysfunction and maintain normal glucose status in persons with sleep apnea in the long term.