PIKE is essential for oligodendroglia development and CNS myelination

Oligodendrocyte (OL) differentiation and myelin development are complex events regulated by numerous signal transduction factors. Here, we report that phosphoinositide-3 kinase enhancer L (PIKE-L) is required for OL development and myelination. PIKE-L expression is up-regulated when oligodendrocyte progenitor cells commit to differentiation. Conversely, depleting phosphoinositide-3 kinase enhancer (PIKE) expression by shRNA prevents oligodendrocyte progenitor cell differentiation. In both conventional PIKE knockout (PIKE^−/−) and OL-specific PIKE knockout mice, the number of OLs is reduced in the corpus callosum. PIKE^−/− OLs also display defects when forming myelin sheath on neuronal axons during neonatal development, which is partially rescued when PTEN is ablated. In addition, Akt/mTOR signaling is impaired in OL-enriched tissues of the PIKE^−/− mutant, leading to reduced expression of critical proteins for myelin development and hypomyelination. Moreover, myelin repair of lysolecithin-induced lesions is delayed in PIKE^−/− brain. Thus, PIKE plays pivotal roles to advance OL development and myelinogenesis through Akt/mTOR activation.Efficient propagation of action potentials depends on the presence of myelin sheath that spirals around the axon. As a membrane extension from oligodendrocytes (OLs), the myelin sheath has a unique lipid-rich composition that allows electrical insulation for high-speed conduction and fidelity of signal transfer (1). Generation of OLs is a developmentally regulated process, which involves the proliferation of oligodendrocyte progenitor cells (OPCs) at the germinal subventricular zones (SVZ), migration throughout the CNS, differentiation into mature OLs, and adhesion to the axon to form myelin (2). Although most OPCs first appear in early neonatal brain, maturation and myelination of OLs in rodents occur largely in postnatal life between P10 and P60 (1). The timing of s differentiation and myelin formation requires highly localized signaling mechanisms, which involves the coordinated activation/inactivation of Wnt/β-catenin, Hedgehog/Gli1, Jagged1/Notch, and PI3K/Akt/mTOR cascades (3). Disruption of these pathways via gene manipulation or modulation of their regulators results in defective OL development. For example, PI3K depletion causes reduced myelin expression in the cerebral cortex and striatum (4). On the other hand, mutation of PTEN, the negative regulator of PI3K/Akt cascade, causes thickening and unraveling of the myelin sheath surrounding hypertrophic axons in the corpus callosum (CC) (5).Phosphoinositide 3-kinase enhancer L (PIKE-L) is a CNS-specific GTPase that belongs to the centaurin family (6, 7). It participates in numerous cellular events to regulate neuronal activity and survival. Our previous studies show that PIKE-L interacts with both netrin receptor (UNC5H) and metabotropic glutamate receptor I (mGlu₁) to prevent apoptotic cell death (8, 9). In addition, PIKE-L controls cell-surface trafficking of 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl) propanoic acid receptor and the formation of long-term potentiation in the postsynaptic neurons (10). Moreover, PIKE controls the neuronal dendritogenesis and survival through maintaining the integrity of the PI3K/Akt pathway (11). Indeed, PIKE is an important molecular switch to control the cellular PI3K/Akt activation as it links extracellular stimuli including netrin, glutamate, and neurotrophins to the intrinsic PI3K/Akt activities (12–14). Nevertheless, the functions of PIKE-L in nonneuronal cells such as OLs and astrocytes still remain unexplored. In this paper, we report that PIKE-L signals through the PI3K/Akt pathway to advance CNS myelinogenesis.     

C1q nephropathy in an old woman with acute renal failure: a case report and literature review

Reports on the clinical entity of C1q nephropathy have focused on older children and young adult, data on old people are rare. In this report, we would introduce a 77-year-old woman who was diagnosed as C1q nephropathy by means of electron microscopic and immunofluorescence examination. Facial and lower extremity edema was the main reason for her to go for medical treatment, and she developed into acute renal failure within 5?d. Complete remission was observed after hemodialysis and steroid drugs treatments.     

APACHEⅡ评分在外科ICU感染防治中的应用

外科 ICU(SICU)是三级甲等医院内重要的抢救单元 ,也是医院内感染的高发病区。急性生理学及慢性健康状况评分 系统 (APACHE )已广泛用于ICU疾病严重程度的评估及预后评价、疾病变化趋势的动态观察、动态评价救治水平、制订和修正医疗护理计划等各领域〔1 ,2〕 ,我们也探讨过其在 SICU中的应用价值〔3〕。现将 APACHE 用于SICU医院内下呼吸道感染发生和防治中的结果总结如下。1　临床资料1.1　病例 :我院 1999年 1月— 2 0 0 2年6月 SICU中 APACHE 评分准确者32 6例 ,其中男 2 5 0例 ,女 76例 ;年龄2～ 82岁 ,平均 (5 3.4 …     

疼痛对切口愈合影响的研究

在临床护理工作中，疼痛已成为继体温、脉搏、呼吸、血压四大生命体征之后的第五生命体征。被日益受到重视，解除疼痛已成为护理工作的重要内容之一。疼痛常常导致病人的睡眠不足，造成情绪低落，妨碍组织康复。严重的疼痛还会影响手术切．日的愈合，手术切口愈合不良，会给病人带来额外的痛苦和经济负担，严重者甚至会给病人造成病残或死亡。所以控制疼痛要与维持足够血容量及保证体温正常同等对待。现将我院对此做的研究作一介绍。     

肾上腺外嗜铬细胞瘤的超声诊断与鉴别

本文报告经手术与病理证实的肾上腺外嗜铬细胞瘤29例32个瘤体。超声检出率为90．6％，定位准确率93．8％。肿瘤声像表现无特异性，与其他肿瘤较难鉴别。同时讨论了良性、恶性肿瘤鉴别点。     

纽扣钢板悬吊固定自体胴绳肌肌腱前交叉韧带重建术后远端骨隧道填充磷酸三钙人工骨的临床分析

目的：判断微孔磷酸三钙（ mp-TCP）临床上是否可以有效促进腱骨愈合,提高膝关节稳定性,减少胫骨隧道的扩大,恢复关节功能。方法本研究对2007年6月至2008年10月,120例进行前交叉韧带（ ACL）自体腘绳肌肌腱重建手术的患者进行研究,随机填充mp-TCP,符合实验标准共105例患者。术后随访1年,进行临床、影像学指标统计分析。结果 TCP填充组及TCP非填充组两组在术后12个月的临床指标中,膝关节活动度（ ROM）、单腿跳跃检查、大腿周径差别、Lachman试验和轴移试验结果均无统计学差异;Tegner评分,Lysholm评分和IKDC主观功能量化评分统计学上也均无统计学差异（P＜0.05）;但是双侧膝关节前向松弛度差异（SSD）上则有统计学差异。重建术后影像学指标统计分析示骨隧道填充TCP可以有效减少术后骨隧道扩大的程度。结论前交叉韧带自体腘绳肌肌腱重建手术骨隧道填充TCP可以有效减少术后骨隧道扩大的程度。     

护理资料归档与管理

为了使护理资料能进一步清晰化和规范化，我们采取及时准确归档、合理分卷管理的方法。现总结如下。     

低分子肝素治疗糖尿病肾病的疗效观察

目的 :探讨低分子肝素 (LMWH)治疗糖尿病肾病的疗效。方法 :随机将 2 3例糖尿病肾病患者分为二组 ,对照组 12例 ,给予降糖以及洛丁新和肠溶阿斯匹林口服治疗。观察组 11例则在此基础上加用低分子肝素。结果 :治疗 6周后观测二组尿蛋白、血浆蛋白、肌酐清除率、血脂、纤维蛋白原及浮肿程度均较治疗前改善 ,而治疗组明显优于对照组 (P <0 .0 1及P <0 .0 5 ) ,凝血指标无明显差异。结论 :LMWH可明显改善糖尿病肾病的蛋白尿和浮肿 ,而无明显出血等副作用。