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Background
Total hip arthroplasty is a successful surgery, that fails at a rate of approximately 10% at ten years from surgery. Causes for failure are mainly aseptic loosening of one or both components partially due to wear of articular surfaces and partially to design. The present analysis aimed to identify risk factors and quantify their effects on aseptic failure. 相似文献Empty sella is an anatomical condition caused by herniation of the subarachnoid space into the pituitary fossa through an incompetent seller diaphragm. Headache seems to be one of the most frequently reported symptoms. We studied 13 headache patients (12 females, 1 male) presenting with primary empty sella (PES) on CT scan. The characteristics of the headache were analyzed and plasma levels of pituitary hormones or cortisol assessed. We confirmed the nonspecific nature of the headache in PES even though the majority of our patients complained of daily headache, mostly localized anteriorly. Hormone plasma levels were within normal range in all the patients assessed. However, four patients reported earlier endocrine disorders and more than half of the patients presented with obesity.
In our opinion, PES should be suspected in middle-aged overweight women with daily headache even in the absence of endocrine symptomatology. 相似文献
Methods: Human and bovine endothelial cells and rat vascular smooth muscle cells were pretreated with isoflurane (1.5% for 30 min) and then exposed to cytokines (tumor necrosis factor-[alpha], interferon-[gamma], and interleukin-[beta]) for 72 h. Cytokine exposure was initiated immediately after isoflurane pretreatment or after a delay of 1-48 h. Cell survival and viability were evaluated by trypan blue exclusion and lactate dehydrogenase release. The role of mitochondrial and cell membrane adenosine triphosphate-sensitive potassium channels, or both, were evaluated with the antagonists 5-hydroxydecanoate, HMR-1098, or glybenclamide.
Results: Immediate isoflurane pretreatment was approximately 70% effective in increasing cell survival and prevented lactate dehydrogenase release in all cell lines. However, cellular protection was completely lost if the time between isoflurane and cytokine exposure was extended to 2-12 h, depending on the cell type. Delayed protection was equal to immediate protection when the interval was extended to 12-24 h, with protection being sustained at 48 h in human endothelial and rat vascular smooth muscle cells. The immediate and delayed protection was inhibited by glybenclamide and 5-hydroxydecanoate but not by HMR-1098, whereas diazoxide, a mitochondrial adenosine triphosphate-sensitive potassium channels agonist, mimicked the time course of isoflurane-induced immediate and delayed protection in all cell lines. 相似文献