Medical hypotheses
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Postoperative cognitive dysfunction (POCD) is a decline in cognitive function for weeks or months after surgery. It may affect the patients' length of hospital stay, quality of life, the rehabilitation process, and work performance. Prolonged POCD occurs frequently after cardiac surgery, and the risk of POCD increases with age. ⋯ However, emerging evidences indicate that various inflammatory mediators are involved in the pathophysiology of POCD and inflammatory response may a potential pathogenic factor. The vagus nerve stimulation has been shown to decrease production and release of pro-inflammatory cytokines through the cholinergic anti-inflammatory pathway (CAP) in both animal model and human. Considering that the inflammation plays a definite role in the pathogenesis of POCD and the vagus nerve can mediate inflammation via CAP, we hypothesize that the transcutaneous vagus nerve stimulation may attenuate POCD by decreasing inflammatory response in elderly patients.
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In previous editorials I have written about the absent-minded and socially-inept 'nutty professor' stereotype in science, and the phenomenon of 'psychological neoteny' whereby intelligent modern people (including scientists) decline to grow-up and instead remain in a state of perpetual novelty-seeking adolescence. These can be seen as specific examples of the general phenomenon of 'clever sillies' whereby intelligent people with high levels of technical ability are seen (by the majority of the rest of the population) as having foolish ideas and behaviours outside the realm of their professional expertise. In short, it has often been observed that high IQ types are lacking in 'common sense'--and especially when it comes to dealing with other human beings. ⋯ I further suggest that this random silliness of the most intelligent people may be amplified to generate systematic wrongness when intellectuals are in addition 'advertising' their own high intelligence in the evolutionarily novel context of a modern IQ meritocracy. The cognitively-stratified context of communicating almost-exclusively with others of similar intelligence, generates opinions and behaviours among the highest IQ people which are not just lacking in common sense but perversely wrong. Hence the phenomenon of 'political correctness' (PC); whereby false and foolish ideas have come to dominate, and moralistically be enforced upon, the ruling elites of whole nations.
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Modic changes are bone marrow and endplate lesions visible in magnetic resonance imaging (MRI). They are regarded as a part of degenerative disc disease and associated with low back pain. And severe disc degeneration was occurred more in the patients with Modic changes. But there is still no study to analyze the relationship between Modic changes and intervertebral disc degeneration. We hypothesize that Modic changes are the possible causes and promotion of lumbar intervertebral disc degeneration. And there are three possible mechanisms for this hypothesis: a structural cause: Modic changes make cartilaginous material easier in extruded disc herniations, to destroy the structure of intervertebral disc and inhibit the absorption of the disc. A biomechanical cause: Modic changes alter the mechanical loading distribution on disc, to initiate a series of disc disruption and inhibit the self-recovery of the disc. A nutritional cause: Modic changes destroy the vascular architecture in vertebral endplate and block the most important metabolism pathway between vertebrae and disc. ⋯ (1) Find out procedures to cure Modic changes may be an important breakthrough for disc degenerative disease. (2) Treatment of Modic changes may be a critical step of biotherapy for disc degeneration disease.
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Synaptosomal-associated protein of 25 KD (SNAP-25) is a protein that participates in synaptic vesicle exocytosis through the formation of a SNARE complex; SNAP-25 also plays a pivotal role in modulating calcium homeostasis through negative regulation of voltage-gated calcium channels. SNAP-25 has been involved in different neuropsychiatric disorders, including attention deficit hyperactivity disorder. There are well known physiological gender differences in many neuropsychological skills, and there are even more striking gender differences in patients with attention deficit hyperactivity disorder and autism spectrum disorders. We hypothesize that these differences are the result of a mechanism involving SNAP-25 polymorphisms and its differential expression in specific brain areas.