金属对金属全髋关节表面置换术治疗股骨头骨坏死

背景：近来，随着改进型金属对金属关节假体的出现，全髋关节表面置换术发展成为一种可行的关节成形术式。然而，这种术式是否适用于股骨头坏死患者尚存争议，因为这类患者股骨侧假体是用骨水泥固定于坏死的股骨头表面。本研究的目的是分析股骨头坏死患者应用金属对金属全髋关节表面置换术后的临床和影像学结果，并将本组结果与诊断为骨关节炎的患者进行比较。 方法：对42个股骨头骨坏死的髋关节行金属对金属全髋关节表面置换术。根据年龄、性别、术者和手术入路，选择42个同样进行金属对金属全髋关节表面置换术的骨关节炎性髋作为对照。在骨坏死组，男25例，女11例；在骨关节炎组，男28例，女13例。手术时平均年龄42岁。对患者进行临床和影像学随访，平均随访41个月。 结果：两组临床结果相似，骨坏死组，效果优或良39髋（93％）；骨关节炎组，效果优或良41髋（98％）。两组各有2例失败而行标准的全髋关节成形术。两组患者生存曲线相似。 结论：对于活动量大的骨坏死患者进行金属对金属全髋关节表面置换术，短期随访可获得与骨关节炎患者相似的优良效果。我们期待长期随访是否也能得到类似的结果。 可信水平：治疗性研究，Ⅱ级。进一步可信度参见作者介绍。     

七氟醚抑制突触后胆碱能突触传递而不影响短时程增强

背景：目前人们已了解全身麻醉对兴奋性和抑制性突触的作用。但全身麻醉影响突触可塑性，从而影响学习和记忆的机制在细胞水平上尚不清晰。本研究选取体细胞一体细胞之间一致的突触后神经元，验证临床浓度的七氟醚是否影响胆碱能突触传递的短时程增强。     

Anesthetics Inhibit Acetylcholine-promoted Guanine Nucleotide Exchange of Heterotrimeric G Proteins of Airway Smooth Muscle

Background: Anesthetics inhibit airway smooth muscle contraction in part by a direct effect on the smooth muscle cell. This study tested the hypothesis that the anesthetics halothane and hexanol, which both relax airway smooth muscle in vitro, inhibit acetylcholine-promoted nucleotide exchange at the [alpha] subunit of the Gq/11 heterotrimeric G protein (G[alpha]q/11; i.e., they inhibit muscarinic receptor-G[alpha]q/11 coupling).

Methods: The effect of halothane (0.38 +/- 0.02 mm) and hexanol (10 mm) on basal and acetylcholine-stimulated G[alpha]q/11 guanosine nucleotide exchange was determined in membranes prepared from porcine tracheal smooth muscle. The nonhydrolyzable, radioactive form of guanosine-5'-triphosphate, [35S]GTP[gamma]S, was used as the reporter for G[alpha]q/11 subunit dissociation from the membrane to soluble fraction, which was immunoprecipitated with rabbit polyclonal anti-G[alpha]q/11 antiserum.

Results: Acetylcholine caused a significant time- and concentration-dependent increase in the magnitude of G[alpha]q/11 nucleotide exchange compared with basal values (i.e., without acetylcholine), reaching a maximal difference at 100 [mu]m (35.9 +/- 2.9 vs. 9.8 +/- 1.2 fmol/mg protein, respectively). Whereas neither anesthetic had an effect on basal G[alpha]q/11 nucleotide exchange, both halothane and hexanol significantly inhibited the increase in G[alpha]q/11 nucleotide exchange produced by 30 [mu]m acetylcholine (by 59% and 68%, respectively).     

Morphine Preconditions Purkinje Cells against Cell Death under In Vitro Simulated Ischemia-Reperfusion Conditions

Background: Morphine pretreatment via activation of [delta]1-opioid receptors induces cardioprotection. In this study, the authors determined whether morphine preconditioning induces ischemic tolerance in neurons.

Methods: Cerebellar brain slices from adult Sprague-Dawley rats were incubated with morphine at 0.1-10 [mu]m in the presence or absence of various antagonists for 30 min. They were then kept in morphine- and antagonist-free buffer for 30 min before they were subjected to simulated ischemia (oxygen-glucose deprivation) for 20 min. After being recovered in oxygenated artificial cerebrospinal fluid for 5 h, they were fixed for morphologic examination to determine the percentage of undamaged Purkinje cells.

Results: The survival rate of Purkinje cells was significantly higher in slices preconditioned with morphine (>= 0.3 [mu]m) before the oxygen-glucose deprivation (57 +/- 4% at 0.3 [mu]m morphine) than that of the oxygen-glucose deprivation alone (39 +/- 3%, P < 0.05). This morphine preconditioning-induced neuroprotection was abolished by naloxone, a non-type-selective opioid receptor antagonist, by naltrindole, a selective [delta]-opioid receptor antagonist, or by 7-benzylidenenaltrexone, a selective [delta]1-opioid receptor antagonist. However, the effects were not blocked by the [mu]-, [kappa]-, or [delta]2-opioid receptor antagonists, [beta]-funaltrexamine, nor-binaltorphimine, or naltriben, respectively. Morphine preconditioning-induced neuroprotection was partially blocked by the selective mitochondrial adenosine triphosphate-sensitive potassium channel antagonist, 5-hydroxydecanoate, or the mitochondrial electron transport inhibitor, myxothiazol. None of the inhibitors used in this study alone affected the simulated ischemia-induced neuronal death.     

Isoflurane Pretreatment Has Immediate and Delayed Protective Effects against Cytokine-induced Injury in Endothelial and Vascular Smooth Muscle Cells

Background: Volatile anesthetics have protective effects against cytokine-induced injury in endothelial and vascular smooth muscle cells. The authors hypothesized that isoflurane pretreatment may trigger immediate and delayed protection that is modulated by adenosine triphosphate-sensitive potassium channels.

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.     

Mild Hypercapnia Induces Vasodilation via Adenosine Triphosphate-sensitive K+ Channels in Parenchymal Microvessels of the Rat Cerebral Cortex

Background: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex.

Methods: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 [mu]m) was monitored using computerized videomicroscopy.

Results: During contraction to prostaglandin F2[alpha] (5 x 10-7 m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10-6 m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10-7 m) as well as the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (10-4 m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10-8 to 3 x 10-7 m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide.     

接种疫苗后皮肤淋巴组织增生及边缘带B细胞淋巴瘤

2例成年女性患者在接种流感疫苗后,接种部位出现不典型淋巴组织浸润。1例患者发展为低度恶性皮肤边缘带B细胞淋巴瘤(M ZL),尽管已扩散至远端皮肤,但仍对局部切除及放疗敏感。另1例患者临床进程以局部侵袭为特征,多次尝试外科切除术失败后,组织学表现为仅对放疗有反应的炎症性反应。接种疫苗后皮肤淋巴组织增生及边缘带B细胞淋巴瘤@May S.A. @Netto G. @Domiati- Saad R. @Kasper C.$Dr. Southwest Dermatopathology Consultants, 13016 Bee St, Dallas, TX 75234, United States @张莹…