心理干预对腹腔镜诊疗方法治疗不孕症患者的影响与护理对策

目的：探讨心理干预对腹腔镜诊疗方法治疗不孕症患者的影响与护理对策。方法：将60例不孕患者按随机数字表法分为观察组和对照组各30例，对照组采用常规护理，观察组在常规护理基础上进行心理干预。结果：观察组患者焦虑指数评分、治疗效果明显优于对照组。结论：不孕症患者经腹腔镜诊疗后，医疗护理人员需要及时采用有针对性的心理干预手段，帮助患者走出心理误区。     

Vitrectomy with Silicone Oil Tamponade in Rhegmatogenous Retinal Detachment following Acute Retinal Necrosis: Clinical Outcomes and Prognostic Factors

Purpose: The purpose of the study is to report the prognostic factors and outcomes of vitrectomy (PPV) with silicone oil tamponade in rhegmatogenous retinal detachment (RRD) secondary to acute retinal necrosis (ARN).

Methods: This retrospective, non-randomized, interventional comparative study included 38 eyes of 38 patients. All cases underwent PPV with silicone oil tamponade. The main outcome measure was improvement of final visual acuity relative to the presenting visual acuity and factors affecting the same Group A included eyes with favorable vision of 20/400 or better and Group B included the others.

Results: Group A included 16 eyes (42.10%), group B included 22 eyes (57.89%). In Group A 2 eyes out of 16 (12.5%) and in Group B 12 eyes out of 22 (54.54%) had RRD at presentation (p = 0.02, 95% CI for the difference 7.88–65.78%). The time interval between first presentation and development of RRD in Group A was 30.94 ± 38.8 days (median 30 days) whereas that in Group B was 10.81 ± 11.73 days (median 8 days) (p = 0.02). The odds of visual improvement post-vitrectomy when RRD occurred later was 8.4 (p = 0.01, 95% CI 1.53–46.1). The usage of systemic steroids (odds 5.2, p = 0.03, 95% CI 1.14–23.54) and oral valacyclovir (odds 4.33, p = 0.04, 95% CI 1.05–17.84) were associated with odds favoring a good visual outcome. Recurrent RRD was noted in 3/16 eyes (18.75%) in Group A and 13/22 eyes (59.09%) in Group B (p = 0.03).

Conclusion: Delayed occurrence of RRD after ARN is a good prognostic factor. Usage of systemic steroids and oral valacylocvir are associated with a favorable visual outcome when started before the onset of RRD.     

2型糖尿病合并冠心病患者心血管危险因素控制的临床分析

目的探讨心血管危险因素控制在2型糖尿病合并冠心病患者中的意义。方法筛选2型糖尿病合并冠心病患者140例,行问卷调查,对比心血管危险因素控制良好、差者血糖控制水平、近2年心血管事件发生情况。结果心血管危险因素控制水平良好93人、差者47人,心血管危险因素控制良好者血糖控制59.14%、一般34.41%、不佳6.45%,优于心血管危险因素控制者10.64%、53.19%、36.1%,急诊8.60%、门诊16.13%、医疗资源获取例次率24.73%,低于差者19.15%、104.26%、123.40%,心肌梗死4.30%、心衰3.23%、心绞痛37.63%、心血管事件合计发生例次率45.16%,低于差者14.89%、23.40%、93.62%、131.91%,差异具有统计学意义(P0.05)。结论对于2型糖尿病合并冠心病患者而言,积极控制心血管病危险因素,有助于提高血糖控制水平,降低心血管事件发生风险,进而改善预后。     

血尿酸与急性冠状动脉综合征367例的相关性研究

目的探讨血清尿酸（SUA）水平与急性冠状动脉综合征（ACS）的相关性。方法经临床确诊的冠心病（CHD）患者182例[其中慢性稳定型（A组）94例，ACS（B组）88例]与对照组185例。分别测定SUA及血脂。结果ACS组SUA水平显著高于对照组（P〈O．01），Logistic回归分析显示，SUA增高与ACS明显相关。结论高尿酸血症是ACS的主要危险因素之一。     

脑性瘫痪伴听力损失儿童的听力学特点及高危因素分析

目的探讨脑性瘫痪伴听力损失儿童的听力学特点及高危因素。方法对2009年1月～2010年12月诊断为脑性瘫痪的120例患儿进行听力学诊断,包括ABR、诊断型DPOAE测试,明确是否伴有听力损伤及听损伤的程度和部位,并对听力损伤的高危因素进行分析。结果 120例脑性瘫痪儿童中,双耳ABR反应阈正常82例(68.33%,82/120),其DPOAE均正常;38例(31.67%,38/120)ABR异常,其中,双耳35例,3例轻度、5例中度、3例重度、24例极重度;单耳3例,2例极重度、1例中度听力损失;23例双耳、3例单耳DPOAE未引出,与ABR检查结果一致,符合感音神经性聋诊断;12例双耳DPOAE正常,而ABR波形异常,符合蜗后聋诊断。38例听损伤脑瘫患儿的高危因素主要有高胆红素血症13例(34.21%)、窒息8例(21.05%)、早产低体重8例(21.05%),母孕期感染7例(18.42%)、伴其它新生儿疾病(先天性甲状腺机能低下症、败血症、化脓性脑膜炎、面神经麻痹等)6例(15.79%),脑瘫或耳聋家族史2例(5.26%),有两种或两种以上高危因素者11例。结论本组脑性瘫痪伴听力损失儿童以双耳极重度感音神经性聋为主,其次为双耳极重度蜗后聋,多数脑瘫伴听力损失儿童具有听力损伤高危因素。     

Inflammatory, haemostatic, and rheological markers for incident peripheral arterial disease: Edinburgh Artery Study.

AIMS: Recently, markers of inflammation, haemostasis, and blood rheology have received much attention as risk factors for coronary heart disease and stroke. However, their role in peripheral arterial disease (PAD) is not well established and some of them, including the pro-inflammatory cytokine interleukin-6 (IL-6), have not been examined before in prospective epidemiological studies. METHODS AND RESULTS: In the Edinburgh Artery Study, we studied the development of PAD in the general population and evaluated 17 potential blood markers as predictors of incident PAD. At baseline (1987), 1519 men and women free of PAD aged 55-74 were recruited. After 17 years, 208 subjects had developed symptomatic PAD. In analysis adjusted for cardiovascular risk factors and baseline cardiovascular disease (CVD), only C-reactive protein, fibrinogen, lipoprotein (a), and haematocrit [hazard ratio (95% CI) corresponding to an increase equal to the inter-tertile range 1.30 (1.08, 1.56), 1.16 (1.05, 1.17), 1.22 (1.04, 1.44), 1.22 (1.08, 1.38)] were significantly (P < 0.01) associated with PAD. However, these markers provided very little prognostic information for incident PAD to that obtained by cardiovascular risk factors and the ankle brachial index. Other markers including IL-6, intracellular adhesion molecule 1, d-dimer, tissue plasminogen activator antigen, and plasma and blood viscosities showed weak associations, which were considerably attenuated when CVD risk factors were accounted for. CONCLUSIONS: Our prospective data showed that several inflammatory, haemostatic, and rheological markers are associated with incident PAD; however, their clinical utility is likely to be limited. Future research is necessary to validate the importance of these biomarkers explicitly on PAD and to address the causality of the reported associations.     

Diabetes enhances lipopolysaccharide-induced cardiac toxicity in the mouse model

Diabetic patients have a higher rate of mortality from sepsis than do their nondiabetic septic counterparts. The hypothesis in this study is that chronic diabetes may make cardiovascular systems more sensitive to septicemia. To test this hypothesis, the authors investigated the effect of diabetes on endotoxin-induced cardiac toxicity. Diabetes was induced in FVB mice by injecting a single dose (150 mg/kg) of streptozotocin. Two months after streptozotocin treatment, the diabetic mice were treated with lipopolysaccharide by intraperitoneal injection at 2 mg/kg. Cardiac toxicity was evaluated by measuring levels of serum cardiac enzymes and cardiac morphology at 1 h, 4.5 h, and 24 h after lipopolysaccharide treatment. Serum and cardiac tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay methods at 1 h and 4.5 h after lipopolysaccharide treatment. Lipopolysaccharide treatment did not significantly affect the diabetic manifestations, including decreased body weight gain and increased glycated hemoglobin and serum triglyceride levels. However, diabetes significantly enhanced lipopolysaccharide-induced cardiac toxicity, which was demonstrated by significant increases in the levels of cardiac enzymes such as creatine phosphokinase and troponin T, abnormal morphological changes examined under light microscope with hematoxylin and eosin staining, and oxidative damage to proteins detected by 3-nitrotyrosine staining. Lipopolysaccharide treatment significantly increased serum and cardiac TNF-α and IL-6 concentrations. Diabetes did not alter the effect of lipopolysaccharide on serum and cardiac TNF-α elevation, but it significantly enhanced lipopolysaccharide-induced cardiac IL-6 production. These results suggest that diabetes significantly enhances endotoxin-induced cardiac toxicity, possibly through mechanisms that involve inflammatory/acute-phase cytokines.