Validity of Chinese Version of the Composite International Diagnostic Interview-3.0 in Psychiatric Settings

Background:

The Composite International Diagnostic Interview-3.0 (CIDI-3.0) is a fully structured lay-administered diagnostic interview for the assessment of mental disorders according to ICD-10 and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria. The aim of the study was to investigate the concurrent validity of the Chinese CIDI in diagnosing mental disorders in psychiatric settings.

Methods:

We recruited 208 participants, of whom 148 were patients from two psychiatric hospitals and 60 healthy people from communities. These participants were administered with CIDI by six trained lay interviewers and the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I, gold standard) by two psychiatrists. Agreement between CIDI and SCID-I was assessed with sensitivity, specificity, positive predictive value and negative predictive value. Individual-level CIDI-SCID diagnostic concordance was evaluated using the area under the receiver operator characteristic curve and Cohen''s K.

Results:

Substantial to excellent CIDI to SCID concordance was found for any substance use disorder (area under the receiver operator characteristic curve [AUC] = 0.926), any anxiety disorder (AUC = 0.807) and any mood disorder (AUC = 0.806). The concordance between the CIDI and the SCID for psychotic and eating disorders is moderate. However, for individual mental disorders, the CIDI-SCID concordance for bipolar disorders (AUC = 0.55) and anorexia nervosa (AUC = 0.50) was insufficient.

Conclusions:

Overall, the Chinese version of CIDI-3.0 has acceptable validity in diagnosing the substance use disorder, anxiety disorder and mood disorder among Chinese adult population. However, we should be cautious when using it for bipolar disorders and anorexia nervosa.     

Short-term Rosuvastatin Treatment for the Prevention of Contrast-induced Acute Kidney Injury in Patients Receiving Moderate or High Volumes of Contrast Media: A Sub-analysis of the TRACK-D Study

Background:

Current randomized trials have demonstrated the effects of short-term rosuvastatin therapy in preventing contrast-induced acute kidney injury (CIAKI). However, the consistency of these effects on patients administered different volumes of contrast media is unknown.

Methods:

In the TRACK-D trial, 2998 patients with type 2 diabetes and concomitant chronic kidney disease (CKD) who underwent coronary/peripheral arterial angiography with or without percutaneous intervention were randomized to short-term (2 days before and 3 days after procedure) rosuvastatin therapy or standard-of-care. This prespecified analysis compared the effects of rosuvastatin versus standard therapy in patients exposed to (moderate contrast volume [MCV], 200–300 ml, n = 712) or (high contrast volume [HCV], ≥300 ml, n = 220). The primary outcome was the incidence of CIAKI. The secondary outcome was a composite of death, dialysis/hemofiltration or worsened heart failure at 30 days.

Results:

Rosuvastatin treatment was associated with a significant reduction in CIAKI compared with the controls (2.1% vs. 4.4%, P = 0.050) in the overall cohort and in patients with MCV (1.7% vs. 4.5%, P = 0.029), whereas no benefit was observed in patients with HCV (3.4% vs. 3.9%, P = 0.834). The incidence of secondary outcomes was significantly lower in the rosuvastatin group compared with control group (2.7% vs. 5.3%, P = 0.049) in the overall cohort, but it was similar between the patients with MCV (2.0% vs. 4.2%, P = 0.081) or HCV (5.1% vs. 8.8%, P = 0.273).

Conclusions:

Periprocedural short-term rosuvastatin treatment is effective in reducing CIAKI and adverse clinical events for patients with diabetes and CKD after their exposure to a moderate volume of contrast medium.     

腹腔镜下子宫/阴道骶骨固定术与改良全盆底功能重建术治疗中盆腔缺陷的疗效比较

目的 分析腹腔镜下子宫/阴道骶骨固定术与改良全盆底功能重建术治疗中盆腔缺陷所致的盆腔器官脱垂(pelvic organ prolapse,POP)的疗效比较.方法 回顾性收集2008年1月至2012年12月在我院接受腹腔镜下子宫/阴道骶骨固定术(观察组,57例)和改良全盆底功能重建术(对照组,55例)的患者临床资料.随访利用盆腔器官脱垂定量(pelvic organ prolapse quantification POP-Q)评分法比较患者客观满意度;主观症状改善评分(patient global impression of change,PGI-C)比较主观满意度;比较手术时间和出血量等围手术期参数;术后比较并发症、再次手术率;利用盆底生活质量问卷(pelvic floor distress inventory-short form 20,PFDI-20;pelvic floor impact questionnaire 7,PFIQ-7)比较2组术前、术后生活质量评分.结果 所有患者手术都有较好的结局.观察组与对照组相比,减少了出血量、留置尿管时间、术后住院时间.在平均42个月的随访中,主观满意度在观察组为57/57(100％),在对照组为51/55(92.73％) (P＞0.05);客观满意度在观察组为45/57 (78.95％),在对照组为38/55(69.09％)(P＞0.05).PGI-C评分在观察组显著优于对照组;PFDI-20、PFIQ-7问卷2组评分均较术前显著改善,但2组间并无显著差异;性生活质量问卷(pelvic organ prolapse/urinary incontinence sexualquestionnaire-12,PISQ-12)评分在观察组术前及术后均优于对照组(P＜0.01).结论 与改良全盆底功能重建术比较,腹腔镜子宫/阴道骶骨固定术可显著减少手术出血量、留置尿管时间和术后住院时间,有较好的主观症状改善.     

Antifibrotic effect of adrenomedullin on coronary adventitia in angiotensin II-induced hypertensive rats

OBJECTIVE: The extracellular matrix (ECM) determines the structural integrity of the heart and vasculature, participating in cardiovascular remodeling. We previously reported that adrenomedullin (AM) inhibited cellular proliferation and protein synthesis of cardiac fibroblasts; however, the precise mechanisms of AM actions as an antifibrotic factor remain unknown. The purpose of this study was to examine the biological actions of AM against the profibrotic factor angiotensin II (Ang II) in coronary adventitia. METHODS AND RESULTS: Rats with hypertension induced by Ang II infusion were administered 0.06 mug/kg/min recombinant human AM subcutaneously for 14 days. The AM infusion significantly (p<0.05) reduced the Ang II-induced increase of coronary adventitial fibroblasts expressing Ki-67 and alpha-smooth muscle actin (alpha-SMA) in the left ventricle, by 65%, and 62%, respectively, without affecting systolic blood pressure, left ventricle/body weight, or cross-sectional area of myocardial fibers. Collagen deposition of coronary arteries was reduced by the AM infusion (-24%, p<0.01), and these effects of AM were accompanied by significant reductions in gene expression of type 1 collagen (-49%, p<0.05) and transforming growth factor-beta1 (TGF-beta1) (-55%, p<0.01). In cultured cardiac fibroblasts, 10(-7) mol/L AM exerted an inhibitory effect on TGF-beta1-induced alpha-SMA expression (p<0.01) that was mimicked by 8-bromo-cAMP and attenuated by the protein kinase A inhibitor H-89. CONCLUSION: AM decreased Ang II-induced collagen deposition surrounding the coronary arteries, inhibiting myofibroblast differentiation and expressions of ECM-related genes in rats. The present findings further support the biological action of AM as an antifibrotic factor in vascular remodeling.     

胰岛素短期强化治疗对初诊2型糖尿病患者胰岛β细胞功能的影响

目的　观察胰岛素短期强化治疗对初诊 2型糖尿病患者胰岛β细胞功能的改善作用及降糖效果。方法对 2 4例初诊 2型糖尿病患者应用胰岛素泵进行 2周的胰岛素强化治疗 ,治疗第 15天时对比治疗前后静脉葡萄糖耐量试验所诱发的胰岛素第 1时相的分泌、胰岛素曲线下面积及由 Homa模型计算胰岛素分泌指数 (Homa B)、胰岛素抵抗指数 (Homa A) ,同时观察空腹血糖、餐后 2小时血糖变化 ;3个月时对比糖化血红蛋白变化。结果　患者空腹血糖及餐后 2小时血糖分别在治疗 (3.7± 1.8)天、 (5 .5± 1.7)天达到控制标准 ,胰岛 β细胞功能显著改善 ,静脉葡萄糖耐量试验各时点的胰岛素分泌及 Homa B值较治疗前明显升高 (P<0 .0 5 ) ,Hom a A指数下降(P<0 .0 5 )。随访 3个月 ,13例患者单纯控制饮食即可维持血糖控制标准 ,糖化血红蛋白由治疗前的 (9.8± 1.2 ) %降至 (6 .3± 0 .7) %。结论　胰岛素短期强化治疗可明显改善及恢复初诊 2型糖尿病患者胰岛素第 1时相分泌 ,不同程度的缓解病情     

通冠胶囊对冠心病介入术后病人GMP-140和vWF的影响

目的探讨通冠胶囊对冠心病经皮冠状动脉介入治疗(PCI)后病人血浆血小板α颗粒膜蛋白-140(GMP-140)、血管性假性血友病因子(vWF)的影响.方法将52例PCI术后的冠心病病人随机分为治疗组(西药加通冠胶囊组)与对照组(西药组).于手术当日、术后1月及术后3月检测GMP-140、vWF含量.结果治疗3月后治疗组GMP-140、vWF含量均明显低于对照组(P＜0.01,P＜0.05).结论通冠胶囊配合西药治疗能显著降低GMP-140、vWF水平,抑制血小板活化从而减少血栓形成是其重要机制之一.     

Establishment of mice model with human viral hepatitis B

AIM:To establish a mice model of hepatitis B by using HBV-transgenic mice, and to transfer HBV-specific cytotoxic T lymphoo/tes (CTL) induced from syngeneic BALB/c mice immunized by a eukaryotic expression vector containing HBV complete genome DNA.METHODS: HBV DNA was obtained from digested pBR3222HBV and ligated with the vector pcDNA3. Recombinant pcDNA3-HBV was identified by restriction endonuclease assay and transfected into human hepatoma cell line HepG2 with lipofectin. ELISA was used to detect the expression of HBsAg in culture supernatant, and RT-PCR to determine the existence of HBV PreS1 mRNA.BALB/c mice were immunized with pcDNA3-HBV or pcDNA3 by intramuscular injection.ELISA was used to detect the expression of HBsAb in serum. MTT assay was used to measure non-specific or specific proliferation ability and specific killing activity of spleen lymphocytes. Lymphocytes from immunized mice were transferred into HBV-transgenic mice (2.5&#215;10^7 per mouse).Forty-eight hours later,the level of serum protein and transaminase was detected with biochemical method,liver and kidney were sectioned and stained by HE to observe the pathological changes.RESULTS: By enzyme digestion with Eco RI, Xho I and Hind Ⅲ,the recombinant pcDNA3-HBV was verified to contain a single copy of HBV genome,which was inserted in the positive direction.HepG2 cells transfected with the recombinant could stably express PreS1 mRNA and HBsAg.After immunized by pcDNA3-HBV for 4 weeks,HBsAb was detected in the serum of BALB/c mice. The potential of spleen lymphoo/tes for both non-specific and specific proliferation and the specific killing activity against target cells were enhanced. The transgenic mice in model group had no significant changes in the level of serum protein but had an obvious increase of ALT and AST. The liver had obvious pathological changes, while the kidney had no evident damage.CONCLUSION:A eukaryotic expression vector pcDNA3-HBV containing HBV complete genome is constructed successfully. HepG2 cells transfected with the recombinant can express PreS1 mRNA and HBsAg stably.Specific cellular immune response can be induced in mice immunized by pcDNA3-HBV.A mice model of acute hepatitis with HBV has been established.     

Activation of p38 mitogen-activated protein kinase contributes to the early cardiodepressant action of tumor necrosis factor.

OBJECTIVES: The purpose of this study was to determine whether p38 mitogen-activated protein kinase (p38-MAPK) contributes to tumor necrosis factor-alpha (TNFalpha)-induced contractile depression. BACKGROUND: Tumor necrosis factor has both beneficial and detrimental consequences that may result from the activation of different downstream pathways. Tumor necrosis factor activates p38-MAPK, a stress-responsive kinase implicated in contractile depression and cardiac injury. METHODS: In isolated hearts from mice lacking the p38-MAPK activator, MAPK kinase 3 (MKK3), perfused at constant coronary pressure or flow, we measured the left ventricular developed pressure (LVDP) and the relationship between end-diastolic volume and LVDP in the presence and absence of 10 ng/ml TNFalpha. RESULTS: Within 15 min at constant pressure, TNFalpha significantly reduced LVDP and coronary flow in outbred and mkk3(+/+) mice. This early negative inotropic effect was associated with a marked phosphorylation of both p38-MAPK and its indirect substrate, HSP27. In hearts lacking MKK3, TNFalpha failed to activate p38-MAPK or to cause significant contractile dysfunction. The actions of TNFalpha were similarly attenuated in MAPK-activated protein kinase 2 (MK2)-deficient hearts, which have a marked reduction in myocardial p38-MAPK protein content, and by the p38-MAPK catalytic site inhibitor SB203580 (1 micromol/l). Under conditions of constant coronary flow, the p38-MAPK activation and contractile depression induced by TNFalpha, though attenuated, remained sensitive to the absence of MKK3 or the presence of SB203580. The role of p38-MAPK in TNFalpha-induced contractile depression was confirmed in isolated murine cardiac myocytes exposed to SB203580 or lacking MKK3. CONCLUSIONS: Tumor necrosis factor activates p38-MAPK in the intact heart and in isolated cardiac myocytes through MKK3. This activation likely contributes to the early cardiodepressant action of TNFalpha.     

An anti-CD45RO immunotoxin kills latently infected human immunodeficiency virus (HIV) CD4 T cells in the blood of HIV-positive persons.

Highly active antiretroviral therapy has decreased the morbidity and mortality of human immunodeficiency virus (HIV) infection, but latently infected cells remain for prolonged periods. CD4(+) CD45RO(+) T cells are a major latent virus reservoir in HIV-infected persons. Replication-competent, latently HIV-infected T cells can be generated in vitro by infecting peripheral blood mononuclear cells with HIV and then eliminating the HIV-producing cells with an anti-CD25 immunotoxin (IT). The CD25(-) latently infected cells then can be eliminated with an anti-CD45RO IT. This study determined whether this IT also could kill latently infected CD4 T cells from HIV-infected persons with or without detectable plasma viremia. The results show that ex vivo treatment of cells from HIV-positive persons by anti-CD45RO IT reduces the frequency of both productively and latently infected cells. In contrast, CD4(+) CD45RA(+) naive T cells and a proportion of CD4(+) CD45RO(lo) memory T cells are spared.