可吸收钉治疗髌骨横行骨折

目的探讨可吸收钉治疗髌骨横行骨折的优势与不足。方法回顾分析40例髌骨横行骨折患者采用可吸收钉固定髌骨,并对骨折愈合及膝关节功能进行评价,同时与40例采用克氏针张力带内固定进行对比分析。结果40例均获随访,时间为6~15个月(平均8.2月)。1例术后2个月因外伤导致髌骨再次骨折,其余均骨性愈合,无再移位,无伤口感染。根据胥少汀等疗效评级:优28例,良10例,差2例。两组病例膝关节功能无统计学意义。结论髌骨横行骨折采用可吸收钉内固定效果良好,但术后康复时间较长。     

关节局部注射罗哌卡因结合静脉PCA泵对全膝关节置换术后的镇痛研究

目的研究全膝关节置换术后关节周围注射罗哌卡因结合PCA泵的镇痛效果。方法选取择期行全膝关节置换手术患者90例,随机分为3组,每组30例（n=30）,第一组（A组）术后包括膝关节后关节囊和前侧切口周围组织浸润注射罗哌卡因,结合静脉PCA泵镇痛;第二组（B组）术后仅在前侧切口周围组织浸润注射罗哌卡因,而不注射后关节囊,结合静脉PCA泵镇痛。第三组（C组）术后仅采用静脉PCA泵镇痛。分别在术后2、12、24、48、72小时,以视觉模拟量表（visual analogue scale,VAS）评估患者术后的疼痛水平。结果术后2、12、24、48、72小时A、B、C组评分分别为2．0,2．1,4．9;2．7,2．6,5．5;3．5,3．4,4．6;2．4,2．5,3．8;1．4,1．4,2．8。A组和B组评分差异无统计学意义（P〉0．05）,A组和B组评分较C组差异有统计学意义（P〈0．05）。结论全膝关节置换术后应用罗哌卡因和静脉PCA泵能够有效缓解疼痛,后关节囊可不注射,镇痛效果优于单用PCA泵。     

儿童重症手足口病不同病情阶段视频脑电图特征与临床（附48例报告）

目的：探讨分析重症儿童手足口病（HFMD）不同病情阶段视频脑电图（VEEG）的特征。方法：对48例重症HFMD患儿的VEEG进行了回顾性分析。结果：发展期,48例患儿VEEG均有异常,异常度与脑炎改变基本符合,与临床表现不完全一致,一般以背景慢波及额颞区的放电为主要特征,重度VEEG异常者变化各异;好转期大多数患儿背景逐渐恢复,浅睡期额颞区出现散在的尖（棘）,尖慢（棘慢）波;康复期重度VEEG异常恢复慢,残留局灶或多灶性放电及背景慢波。结论：掌握HFMD不同病情阶段的VEEG特征,对病情的治疗、康复起到了重要的指导作用。     

WNT信号通路及其与唇腭裂发生

WNT信号通路作为调控胚胎发生的四大信号转导途径之一,主要参与细胞的增殖、分化和极化以及程序性细胞死亡和抗程序性细胞死亡等,近年来其研究逐渐成为热点。唇腭裂作为最常见的先天性畸形,其发病机制至今尚无定论。研究显示,WNT信号通路与唇腭裂发生关系密切,本文就WNT信号通路及其与唇腭裂发生的研究进展作一综述。     

Eritoran attenuates tissue damage and inflammation in hemorrhagic shock/trauma

Background

Severe injury and associated hemorrhagic shock lead to an inflammatory response and subsequent increased tissue damage. Numerous reports have shown that injury-induced inflammation and the associated end-organ damage is driven by Toll-like receptor 4 (TLR4) activation via damage-associated molecular patterns. We examined the effectiveness of Eritoran tetrasodium (E5564), an inhibitor of TLR4 function, in reducing inflammation induced during hemorrhagic shock with resuscitation (HS/R) or after peripheral tissue injury (bilateral femur fracture, BFF).

Material and methods

Mice underwent HS/R or BFF with or without injection of Eritoran (5 mg/kg body weight) or vehicle control given before, both before and after, or only after HS/R or BFF. Mice were sacrificed after 6 h and plasma and tissue cytokines, liver damage (histology; aspartate aminotransferase/alanine aminotransferase), and inflammation (NF-κB) and gut permeability were assessed.

Results

In HS/R Eritoran significantly reduced liver damage (values ± SEM: alanine aminotransferase 9910 ± 3680 U/L versus 1239 ± 327 U/L and aspartate aminotransferase 5863 ± 2000 U/L versus 1246 ± 243 U/L, P < 0.01) at 6 h compared with control when given just before HS and again just prior to resuscitation. Eritoran administration also led to lower IL-6 levels in plasma and liver and less NF-κB activation in liver. Increases in gut barrier permeability induced by HS/R were also prevented with Eritoran. Eritoran similarly diminished BFF-mediated systemic inflammatory responses.

Conclusion

These data suggest Eritoran can inhibit tissue damage and inflammation induced via TLR4/myeloid differentiation factor 2 signaling from damage-associated molecular patterns released during HS/R or BFF. Eritoran may represent a promising therapeutic for trauma patients to prevent multiple organ failure.     

Skeletal Muscle Triacylglycerol Hydrolysis Does Not Influence Metabolic Complications of Obesity

Intramyocellular triacylglycerol (IMTG) accumulation is highly associated with insulin resistance and metabolic complications of obesity (lipotoxicity), whereas comparable IMTG accumulation in endurance-trained athletes is associated with insulin sensitivity (the athlete’s paradox). Despite these findings, it remains unclear whether changes in IMTG accumulation and metabolism per se influence muscle-specific and systemic metabolic homeostasis and insulin responsiveness. By mediating the rate-limiting step in triacylglycerol hydrolysis, adipose triglyceride lipase (ATGL) has been proposed to influence the storage/production of deleterious as well as essential lipid metabolites. However, the physiological relevance of ATGL-mediated triacylglycerol hydrolysis in skeletal muscle remains unknown. To determine the contribution of IMTG hydrolysis to tissue-specific and systemic metabolic phenotypes in the context of obesity, we generated mice with targeted deletion or transgenic overexpression of ATGL exclusively in skeletal muscle. Despite dramatic changes in IMTG content on both chow and high-fat diets, modulation of ATGL-mediated IMTG hydrolysis did not significantly influence systemic energy, lipid, or glucose homeostasis, nor did it influence insulin responsiveness or mitochondrial function. These data argue against a role for altered IMTG accumulation and lipolysis in muscle insulin resistance and metabolic complications of obesity.Obesity is a global public health problem and a major risk factor for insulin resistance and type 2 diabetes. These disorders are characterized by excess lipid accumulation in multiple tissues, primarily as triacylglycerols (TAGs). The lipotoxicity hypothesis suggests that this lipid excess promotes cellular dysfunction and cell death, which ultimately contribute to insulin resistance and metabolic disease (1). However, intracellular TAG accumulation is not always associated with adverse metabolic outcomes, suggesting that TAGs themselves are not pathogenic (2). In contrast, other non-TAG lipid metabolites such as fatty acids (FAs), diacylglycerols (DAGs), and ceramides have been shown to influence glucose homeostasis and insulin action by interfering with insulin signaling and glucose transport, promoting endoplasmic reticulum stress and mitochondrial dysfunction, and activating inflammatory and apoptotic pathways (reviewed in ref. 3). Nevertheless, the precise identities and sources of these bioactive lipid intermediates remain elusive (4,5). Furthermore, whether intracellular TAGs serve as a protective sink or a toxic source of deleterious lipid metabolites that contribute to insulin resistance remains unclear (6).Since skeletal muscle is the major contributor to insulin-mediated glucose disposal, lipid excess in this tissue could have serious implications for systemic glucose homeostasis and insulin responsiveness (7). Indeed, numerous studies have demonstrated a strong association between intramyocellular triacylglycerol (IMTG) accumulation and insulin resistance (reviewed in ref. 8). In contrast, endurance exercise training is characterized by IMTG accumulation and insulin sensitivity (the athlete’s paradox) (2). This variable association between IMTG accumulation and insulin responsiveness has largely been attributed to differences in the balance between lipid delivery and muscle oxidative capacity (8–10). Not surprisingly then, most studies have focused on the impact of muscle FA uptake and/or oxidation on glucose homeostasis and insulin action (11). However, experimental manipulations of these parameters cannot distinguish among the effects of IMTGs, IMTG metabolism, and other lipid intermediates. Furthermore, accumulating evidence suggests that muscle oxidative capacity cannot entirely explain differences in IMTGs or insulin responsiveness (12). These findings have led to speculation that dynamic IMTG metabolism (i.e., TAG synthesis or hydrolysis) may be critically involved in lipid-induced insulin resistance (6). However, few studies have specifically addressed the contribution of IMTG metabolism per se to this process.The regulated storage and release of IMTGs remain poorly understood, but require the coordinated action of synthetic enzymes (i.e., diacylglycerol acyltransferases [DGATs]), hydrolytic enzymes (i.e., adipose triglyceride lipase [ATGL] and hormone sensitive lipase [HSL]), and other lipid droplet proteins (6). Specifically, modulating IMTG synthesis in murine skeletal muscle alters IMTG content and systemic glucose homeostasis, supporting a role for IMTG metabolism in metabolic disease (13–15). However, the metabolic impact of modulating IMTG hydrolysis in vivo remains unclear. Global deletion of either ATGL (16–19) or HSL (20) has produced variable results. The former, but not the latter, results in massive IMTG accumulation with improvement in systemic glucose homeostasis, suggesting that inhibition of ATGL-mediated TAG hydrolysis protects against insulin resistance. In contrast, recent studies in cardiac muscle (21) and other tissues (22,23) indicate that ATGL-mediated TAG hydrolysis is required for mitochondrial function such that enhancing, rather than inhibiting, ATGL action may improve metabolic outcomes. Nevertheless, the autonomous role of skeletal muscle TAG catabolism in influencing muscle-specific and systemic metabolic phenotypes remains unknown.The goal of the current study was to understand the contribution of IMTG hydrolysis to tissue-specific and systemic metabolic phenotypes, particularly glucose homeostasis and insulin action, in the context of obesity. We therefore generated animal models with decreased (skeletal muscle-specific ATGL knockout [SMAKO] mice) and increased (muscle creatine kinase [Ckm]-ATGL transgenic [Tg] mice) ATGL action exclusively in skeletal muscle, and assessed the metabolic consequences at baseline and in response to chronic high-fat feeding. Interestingly, modulation of IMTG hydrolysis via ATGL action did not significantly influence glucose homeostasis, insulin action, or other metabolic phenotypes in the context of obesity despite dramatic changes in IMTG content.     

Nash equilibrium solutions of tracking game for bilinear systems with exponential reference signals

In this paper, we consider the problem of Nash equilibrium solutions of two players tracking game for bilinear systems. A successive approximation approach is modified to design optimal controllers for bilinear systems. More specifically, a sequence of extended Sylvester differential equations are solved by this modified approach. A simulation example is given to demonstrate the validity of this approach. Copyright © 2012 John Wiley & Sons, Ltd.