锁定接骨板弹性内固定治疗股骨远端骨折

目的探讨锁定接骨板弹性内固定治疗股骨远端骨折的疗效。方法2015 年 1 月—2016 年 6 月，采用锁定接骨板弹性内固定治疗股骨远端骨折 21 例。男 5 例，女 16 例；年龄 32～88 岁，平均 62 岁。摔伤 14 例，交通事故伤 5 例，高处坠落伤 2 例。左侧 13 例，右侧 8 例。闭合性骨折 20 例，开放性骨折 1 例。骨折根据 AO/OTA 分型：33-A1 型 5 例，33-A2 型 3 例，33-A3 型 8 例，33-C2 型 2 例，33-C3 型 3 例。受伤至手术时间 3～13 d，平均 6.5 d。结果术后患者切口均Ⅰ期愈合。18 例患者获随访，随访时间 12～24 个月，平均 16 个月。X 线片复查示骨折均愈合，愈合时间 8～24 周，平均 16.6 周；关节面恢复平整，下肢长度恢复。随访期间无螺钉松动、钢板断裂，无膝关节内外翻畸形，未出现明显膝关节僵硬。术后 6、12 个月间疼痛视觉模拟评分（VAS）比较，差异无统计学意义（P>0.05）；其余各时间点间比较，差异均有统计学意义（P<0.05）。术后 3、6、12 个月膝关节活动度较 1 个月时明显增大，比较差异均有统计学意义（P<0.05）；3、6、12 个月间比较，差异均无统计学意义（P>0.05）。各时间点间 Neer 评分比较，差异均有统计学意义（P<0.05）；术后 12 个月，按 Neer 评分标准评定膝关节功能，获优 12 例、良 6 例。 结论锁定接骨板弹性内固定治疗股骨远端骨折临床效果良好，是治疗该类型骨折的有效方法之一。     

提上睑肌缩短术联合 Mustarde 双 Z 形切除术矫正儿童小睑裂综合征

目的探讨提上睑肌缩短术联合 Mustarde 双 Z 形切除术矫正儿童小睑裂综合征（blepharophimosis-ptosis-epicanthus inversus syndrome，BPES）的疗效。方法2015 年 3 月—2017 年 6 月，采用提上睑肌缩短术联合 Mustarde 双 Z 形切除术一期矫正 26 例儿童双眼 BPES。其中，男 16 例，女 10 例；年龄 4～14 岁，平均 7 岁。均有典型的小睑裂四联征。7 例伴有鼻梁低平，20 例伴有弱视和斜视。睑裂长度（19.5±4.5）mm，睑裂宽度（2.5±1.6）mm，内眦间距（42.1±6.5）mm，提上睑肌肌力（5.5±1.3）mm。结果术后切口均Ⅰ期愈合。23 例获随访，随访时间 2～12 个月，平均 10 个月。其中 2 例矫正不足、3 例过度矫正，6 例眼睑线弧度欠佳，均无眼睑内外翻和角膜炎发生。其余患儿均成功矫正上睑下垂和内眦赘皮，眼睑线弧度自然。术后 7 d 测量睑裂长度（27.2±1.9）mm，睑裂宽度（12.5±1.3）mm，内眦间距（29.4±2.6）mm；以上指标均较术前显著改善，差异有统计学意义（t=0.127，P=0.042；t=0.341，P=0.029；t=0.258，P=0.038）。术后无因睑裂宽度、长度回退导致的成角畸形发生。 结论提上睑肌缩短术联合 Mustarde 双 Z 形切除术能达到一期矫正儿童 BPES 目的，可获得较好临床疗效。     

CCR2 and CCR5 chemokine receptors differentially influence the development of autoimmune diabetes in the NOD mouse

The infiltration of monocytes represents an important early event in the development of autoimmune diabetes in NOD mice. Given that chemokines are key regulators of leukocyte trafficking, we examined the requirement for the chemokine receptors β(CC)-chemokine receptor-5 (CCR5) and β(CC)-chemokine receptor-2 (CCR2), which recruit monocytes, in disease development in the NOD mouse. Whereas the onset of diabetes was significantly delayed in CCR2-/-NOD mice (25% at 30 weeks) compared to NOD mice (50% at 28 weeks), the pathogenesis of diabetes was accelerated in CCR5-/-NOD mice (75% at 23 weeks). The rapid development of diabetes in CCR5-/-NOD mice was associated with aggressive destructive insulitis and was accompanied by altered leukocyte migration into islets. In contrast, CCR2-/- NOD mice exhibited delayed inflammatory cell recruitment. Nevertheless, total diabetogenic splenocytes from CCR2-/-NOD and CCR5-/-NOD showed similar capability to adoptively transfer diabetes into NOD.scid recipients. Importantly, our data suggest that targeting of CCR2 may lead to therapies against Type 1 diabetes.     

Genotoxicity studies of glycidol fatty acid ester (glycidol linoleate) and glycidol

Glycidol fatty acid esters (GEs) are found in refined edible oils. Safety concerns have been alleged due to the possible release of glycidol (G), an animal carcinogen.     

190例5岁以下儿童死亡原因监测分析

目的通过对5岁以下儿童死亡原因分析,探索有效的策略和干预措施,降低5岁以下儿童死亡率。方法对蚌埠市第一人民医院2008年1月-2012年12月报告的190例5岁以下儿童死亡监测资料进行整理、汇总和回顾分析。结果 190例5岁以下儿童死亡原因前3位依次是：早产和低出生体重（35例）、呼吸系统疾病（32例）、出生窒息（24例）。新生儿组死亡构成比明显高于其他3组（P〈0.01）,提示年龄越小儿童死亡率越高;在28 d~5岁儿童死因中,意外死亡排在首位;城镇儿童与农村儿童死前接受医疗服务情况基本一致（P〉0.05）。结论只有家庭、医疗保健机构和社会各部门共同努力,才能保证儿童健康成长。     

Sarpogrelate: cardiovascular and renal clinical potential

Sarpogrelate is a selective 5-hydroxytryptamine receptor subtype 2A (5-HT_2A) antagonist. It is metabolised to racemic M-1 and both enantiomers of M-1 are also antagonists of 5-HT_2A receptors. Sarpogrelate inhibits responses to 5-HT mediated by 5-HT_2A receptors such as platelet aggregation, vasoconstriction and vascular smooth muscle proliferation. There is no information available on the pharmacokinetics of sarpogrelate. Sarpogrelate is efficacious in animal models of thrombosis, coronary artery spasm, atherosclerosis, restenosis, peripheral vascular disease, pulmonary hypertension, ischaemic heart disease, myocardial infarction, diabetes and kidney disease. Small clinical trials indicate that sarpogrelate may be beneficial in the treatment of coronary artery disease, angina, restenosis, heart valve prostheses surgery, diabetes mellitus, Raynaud’s phenomenon, systemic sclerosis and Buerger’s disease. Larger, randomised, double-blind, placebo-controlled clinical trials of sarpogrelate in intermittent claudication, coronary artery disease, restenosis and diabetes should be considered.     

Activation of 5-hydroxytryptamine1B/1D/1F receptors as a mechanism of action of antimigraine drugs

Introduction: The introduction of the triptans (5-hydroxytryptamine (5-HT)_1B/1D receptor agonists) was a great improvement in the acute treatment of migraine. However, shortcomings of the triptans have prompted research on novel serotonergic targets for the treatment of migraine.

Areas covered: In this review the different types of antimigraine drugs acting at 5-HT receptors, their discovery and development are discussed. The first specific antimigraine drugs were the ergot alkaloids, consisting of ergotamine, dihydroergotamine and methysergide, which are agonists at 5-HT receptors, but can also bind α-adrenoceptors and dopamine receptors. In the 1990s, the triptans became available on the market. They are 5-HT_1B/1D receptor agonists, showing fewer side effects due to their receptor specificity. In the last years, compounds that bind specifically to 5-HT_1D, 5-HT_1F and 5-HT₇ receptors have been explored for their antimigraine potential. Furthermore, the serotonergic system seems to act in tight connection with the glutamatergic as well as the CGRP-ergic systems, which may open novel therapeutic avenues.

Expert opinion: Although the triptans are very effective in treating migraine attacks, their shortcomings have stimulated the search for novel drugs. Currently, the focus is on 5-HT_1F receptor agonists, which seem devoid of vascular side effects. Moreover, novel compounds that affect multiple transmitter and/or neuropeptide systems that are involved in migraine could be of therapeutic relevance.     

Engineering the niche for stem cells

Abstract

Much has been made about the potential for stem cells in regenerative medicine but the reality is that the development of actual therapies has been slow. Adult stem cells rely heavily on the assortment of biochemical and biophysical elements that constitute the local microenvironment in which they exist. One goal of biomedicine is to create an artificial yet biofunctional niche to support multipotency, differentiation and proliferation. Such tools would facilitate more conclusive experimentation by biologists, pharmaceutical scientists and tissue engineers. While many bioengineering techniques and platforms are already in use, technological innovations now allow this to be done at a higher resolution and specificity. Ultimately, the multidisciplinary integration of engineering and biology will allow the niche to be generated at a scale that can be clinically exploited. Using the systems that constitute the intestinal, hematopoietic and epidermal tissues, this article summarizes the various approaches and tools currently employed to recreate stem cell niches and also explores recent advances in the field.     

Cytokine network and dysregulated apoptosis in atopic dermatitis

Activation and skin-selective homing of peripheral blood memory/effector T cells and effector functions in the skin represent sequential immunological events in the pathogenesis of atopic dermatitis (AD). T cells infiltrating the skin utilize the cutaneous lymphocyte-associated antigen (CLA) and other receptors to recognize and cross the vascular endothelium. In the peripheral blood of AD patients, both CD4⁺ and CD8⁺ subsets of CLA+CD45RO⁺ T cells are in an activated state with high CD25, HLA-DR, and CD40- ligand expression. They express upregulated Fas and Fas-ligand and undergo activation-induced apoptosis. After homing to skin these T cells form dermal infiltrates which play a key role in the pathogenesis of the disease. Skin-infiltrating T cells in AD are protected from activation-induced cell death, although they express both Fas and Fas-ligand. They are protected from apoptosis by cytokines such as IL-2, IL-4, and IL-15 and extracellular matrix components such as fibronectin and transferrin. CLA⁺, skin-homing T cells may play a role in peripheral blood eosinophilia and hyper IgE production by high IL-5 and IL-13 expression, respectively. These T cells secrete IFN-γ in the skin, which upregulates Fas on keratinocytes and renders them susceptible to apoptosis. Keratinocyte apoptosis is induced by Fas-ligand, either soluble or expressed on the surface of T cells, leading to eczema formation. Here we discuss the mechanisms of skin-selective T cell homing and activation, and emphasize the concept of dysregulated apoptosis of T cells, eosinophils, and keratinocytes as essential pathogenetic episodes in AD and other eczematous disorders.