膈肌功能对慢性阻塞肺疾病加重期插管患者撤机的指导价值分析

目的探讨膈肌功能对慢性阻塞性肺病加重期(AECOPD)插管患者撤机的指导价值。方法选取行机械通气并考虑撤机的AECOPD插管患者为研究对象,根据患者撤机成功与否分为撤机成功组与撤机失败组。具备撤机条件后行自主呼吸试验(SBT)30 min,监测SBT 0、5、30 min时膈肌电活动(Edi)、呼吸浅快指数(f/Vt)及口腔闭合压(P0.1)。结果 37例患者纳入本研究,其中撤机成功组25例,撤机失败组12例。撤机失败组患者血Pa CO2高于另一组患者(P0.05)。撤机成功与失败组患者的年龄、Pa O2、MAP等各方面均无显著差异(P0.05)。SBT 30 min时两组患者Edi均显著高于SBT 0 min;在SBT 30 min撤机成功组Edi低于撤机失败组,以Edi12V为临界值,撤机失败预测的灵敏度为100.0%和特异度为66.7%。在SBT 5、30min时撤机成功组患者f/Vt较撤机失败组低,两组患者P0.1无明显差别(P0.05)。结论 Edi对AECOPD患者撤机具有良好的预测价值。     

磷酸化Y盒结合蛋白1的抗体制备及其辅助诊断原发性肝癌合并肺转移的临床价值

目的 制备Y盒结合蛋白1磷酸化抗体(pAb/YB-1S102);探讨腹水中磷酸化YB-1 (pYB-1)作为标志物辅助诊断原发性肝癌合并肺转移的临床价值. 方法 通过生物信息学预测并化学合成102位丝氨酸磷酸化YB-1多肽,耦联载体蛋白后免疫家兔;protein A亲和层析法纯化抗血清pAb/YB-1S102,并验证其特异性.收集109例患者腹水并富集腹水中pYB-1,其中原发性肝细胞癌(HCC) 36例,HCC合并肺转移44例,肝硬化29例;采用Western blot定性检测腹水中pYB-1,并对定性结果进行回归判别与受试者工作特征(ROC)曲线分析.计数资料采用x2检验.结果 酶联免疫吸附法与十二烷基硫酸钠-聚丙烯酰胺凝胶电泳结果显示制备的pAb/YB-1S102效价≥1∶1×106,且纯度较高.Western blot结果证实pAb/YB-1S102能特异性识别内源性pYB-1S102.肝硬化患者腹水中未检出pYB-1S102,HCC合并肺转移患者腹水pYB-1S102阳性率(77.3％)显著高于HCC(30.6％,x2=11.69,P＜0.01);回归分析与ROC曲线结果表明pYB-1S102辅助诊断HCC合并肺转移的灵敏度为77.3％,符合率为73.8％(x2=17.56,P＜0.01). 结论 成功制备可识别内源性pYB-1的抗体pAb/YB-1102;通过定性检测腹水pYB-1,可鉴别诊断HCC合并肺转移.     

Estimating the predictive validity of diabetic animal models in rosiglitazone studies

For therapeutic studies, predictive validity of animal models – arguably the most important feature of animal models in terms of human relevance – can be calculated retrospectively by obtaining data on treatment efficacy from human and animal trials. Using rosiglitazone as a case study, we aim to determine the predictive validity of animal models of diabetes, by analysing which models perform most similarly to humans during rosiglitazone treatment in terms of changes in standard diabetes diagnosis parameters (glycosylated haemoglobin [HbA1c] and fasting glucose levels). A further objective of this paper was to explore the impact of four covariates on the predictive capacity: (i) diabetes induction method; (ii) drug administration route; (iii) sex of animals and (iv) diet during the experiments. Despite the variable consistency of animal species‐based models with the human reference for glucose and HbA1c treatment effects, our results show that glucose and HbA1c treatment effects in rats agreed better with the expected values based on human data than in other species. Induction method was also found to be a substantial factor affecting animal model performance. The study concluded that regular reassessment of animal models can help to identify human relevance of each model and adapt research design for actual research goals.     

A Clinical and Angiographic Scoring System to Predict the Probability of Successful First-Attempt Percutaneous Coronary Intervention in Patients With Total Chronic Coronary Occlusion

ObjectivesThis study sought to develop a scoring model predicting percutaneous coronary intervention (PCI) success in chronic total occlusions.BackgroundCoronary chronic total occlusion is the lesion subtype in which angioplasty is most likely to fail. Chronic total occlusion for PCI (CTO-PCI) failure is associated with higher 1-year mortality and major adverse cardiac events compared with successful CTO-PCI. Although several independent predictors of final procedural success have been identified, no study has yet produced a model predicting final procedural outcome.MethodsData from 1,657 consecutive patients who underwent a first-attempt CTO-PCI were prospectively collected. The scoring model was developed in a derivation cohort of 1,143 patients (70%) using a multivariable stepwise analysis to identify independent predictors of CTO-PCI failure. The model was then validated in the remaining 514 (30%).ResultsThe overall procedural success rate was 72.5%. Independent predictors of CTO-PCI failure were identified and included in the clinical and lesion-related score (CL-score) as follows: previous coronary artery bypass graft surgery +1.5 (odds ratio [OR]: 2.49, 95% confidence interval [CI]: 1.56 to 3.96), previous myocardial infarction +1 (OR: 1.6, 95% CI: 1.17 to 2.2), severe lesion calcification +2 (OR: 2.72, 95% CI :1.78 to 4.16), longer CTOs +1.5 (≥20 mm OR: 2.04, 95% CI: 1.54 to 2.7), non–left anterior descending coronary artery location +1 (OR: 1.56, 95% CI: 1.14 to 2.15), and blunt stump morphology +1 (OR: 1.39, 95% CI: 1.05 to 1.81). Score values of 0 to 1, >1 and <3, ≥3 and <5, and ≥5 identified subgroups at high, intermediate, low, and very low probability, respectively, of CTO-PCI success (derivation cohort: 84.9%, 74.9%, 58%, and 31.9%; p < 0,0001; validation cohort: 88.3%, 73.1%, 59.4%, and 46.2%; p < 0.0001).ConclusionsThis clinical and angiographic score predicted the final CTO-PCI procedural outcome of our study population.     

Identification of immunohistochemical markers for distinguishing lung adenocarcinoma from squamous cell carcinoma

Background

Immunohistochemical staining has been widely used in distinguishing lung adenocarcinoma (LUAD) from lung squamous cell carcinoma (LUSC), which is of vital importance for the diagnosis and treatment of lung cancer. Due to the lack of a comprehensive analysis of different lung cancer subtypes, there may still be undiscovered markers with higher diagnostic accuracy.

Methods

Herein first, we systematically analyzed high-throughput data obtained from The Cancer Genome Atlas (TCGA) database. Combining differently expressed gene screening and receiver operating characteristic (ROC) curve analysis, we attempted to identify the genes which might be suitable as immunohistochemical markers in distinguishing LUAD from LUSC. Then we detected the expression of six of these genes (MLPH, TMC5, SFTA3, DSG3, DSC3 and CALML3) in lung cancer sections using immunohistochemical staining.

Results

A number of genes were identified as candidate immunohistochemical markers with high sensitivity and specificity in distinguishing LUAD from LUSC. Then the staining results confirmed the potentials of the six genes (MLPH, TMC5, SFTA3, DSG3, DSC3 and CALML3) in distinguishing LUAD from LUSC, and their sensitivity and specificity were not less than many commonly used markers.

Conclusions

The results revealed that the six genes (MLPH, TMC5, SFTA3, DSG3, DSC3 and CALML3) might be suitable markers in distinguishing LUAD from LUSC, and also validated the feasibility of our methods for identification of candidate markers from high-throughput data.