Motor actions of myosin were directly visualized by electron tomography of insect flight muscle quick-frozen during contraction. In 3D images, active cross-bridges are usually single myosin heads, bound preferentially to actin target zones sited midway between troponins. Active attached bridges (approximately 30% of all heads) depart markedly in axial and azimuthal angles from Rayment's rigor acto-S1 model, one-third requiring motor domain (MD) tilting on actin, and two-thirds keeping rigor contact with actin while the light chain domain (LCD) tilts axially from approximately 105 degrees to approximately 70 degrees. The results suggest the MD tilts and slews on actin from weak to strong binding, followed by swinging of the LCD through an approximately 35 degrees axial angle, giving an approximately 13 nm interaction distance and an approximately 4-6 nm working stroke.
We aimed at investigating the effect of honokiol on heatstroke in an experimental rat model. Sprogue-Dawley rats were divided into 3 groups: normothermic diabetic rats treated with vehicle solution (NTDR+V), heatstroke-diabetic rats treated with vehicle (HSDR+V), and heatstroke rats treated with konokiol (0.5–5 mg/ml/kg) (HSDR+H). Sixty minutes before the start of heat stress, honokiol or vehicle solution was administered. (HSDR+H) significantly (a) attenuated hyperthermia, hypotension and hypothalamic ischemia, hypoxia, and neuronal apoptosis; (b) reduced the plasma index of the toxic oxidizing radicals; (c) diminished the indices of hepatic and renal dysfunction; (d) attenuated the plasma systemic inflammatory response molecules; (e) promoted plasma levels of an anti-inflammatory cytokine; (f) reduced the index of infiltration of polymorphonuclear neutrophils in the serum; and (g) promoted the survival time fourfold compared with the (HSDR+V) group. In conclusion, honokiol protected against the outcome of heatstroke by reducing inflammation and oxidative stress-mediated multiple organ dysfunction in diabetic rats.
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