急性冠状动脉综合征患者基质金属蛋白酶9基因多态性

目的 探讨基质金属蛋白酶9基因C1562T多态性与中国南方汉族人群冠心病的关系.方法 对经冠状动脉造影证实的急性冠状动脉综合征患者150例(急性冠状动脉综合征组)、稳定型心绞痛患者110例(稳定型心绞痛组)和同期冠状动脉造影阴性、排除冠心病诊断的患者70例(对照组)进行研究,采用酶联免疫吸附试验测定血浆基质金属蛋白酶9水平,采用聚合酶链反应-限制片长多态性技术分析基质金属蛋白酶9基因中C1562T基因多态性,比较各组的基因型和等位基因频率.结果 急性冠状动脉综合征组血浆基质金属蛋白酶9水平明显高于稳定型心绞痛组(P＜0.05)和对照组(P＜0.01),而稳定型心绞痛组与对照组比较,差异无统计学意义(P＞0.05).急性冠状动脉综合征组基质金属蛋白酶9基因CT、CT TT基因型频率以及T等位基因频率均高于对照组和稳定型心绞痛组(P＜0.05或0.01),稳定型心绞痛组与对照组各基因型和等位基因频率分布差异无统计学意义(P＞0.05).C1562T位点CT/TT基因型患者血浆基质金属蛋白酶9水平显著高于CC基因型患者(P＜0.01).结论 基质金属蛋白酶9基因C1562T多态性可能与中国南方汉族人群急性冠状动脉综合征有关,1562T等位基因是动脉粥样硬化斑块不稳定性的易感基因.     

胆道联合静脉超声造影在恶性梗阻性黄疸中的价值

目的:评价胆道联合静脉超声造影检查在恶性梗阻性黄疸治疗中的临床价值。方法:43例患者经增强CT或MRI诊断为恶性梗阻性黄疸,在手术前行经皮经肝胆管穿刺置管,并予以常规超声、静脉超声造影和胆道超声造影检查。以手术结果为金标准,分析常规超声、静脉超声造影、胆道超声造影、胆道联合静脉超声造影对恶性梗阻性黄疸的诊断符合率。结果:43例患者中,常规超声、静脉超声造影、胆道超声造影、胆道联合静脉超声造影的诊断符合率分别为72.1%(31/43)、83.7%(36/43)、81.4%(35/43)及93.0%(40/43)。其中胆道联合静脉超声造影的诊断符合率明显优于常规超声(P=0.021),而单独的静脉或胆道超声造影与常规超声之间的差异无统计学意义(P=0.194和0.307)。结论:胆道联合静脉超声造影可全面评估梗阻部位胆管的腔内和腔外的情况,提高超声对恶性梗阻性黄疸诊断符合率,有效判断手术的可切除性,具有较好的临床价值。     

A meta-analysis of the associations between the Q141K and Q126X ABCG2 gene variants and gout risk

Background: Gout is an inflammatory disease in which genetic factors play a role. ABCG2 is a urate transporter, and the Q141K and Q126X variants of ABCG2 have been associated with a risk of developing gout, though previous studies of these associations have been inconsistent. Therefore, we conducted a meta-analysis to explore the relationship between these genetic variants and gout. Methods: We examined 8 electronic literature databases. In total, 9 eligible articles on the associations between the Q141K (rs2231142) and Q126X (rs72552713) variants and gout risk, including 11 case-control studies were selected. We used odds ratios (OR) and 95% confidence intervals (CI) to assess the strength of these relationships in dominant, recessive, and co-dominant models. Results: This study included 6652 participants (2499 gout patients and 4153 controls). The Q141K variant was found to significantly increase the risk of gout in Asians (dominant model: OR=2.64, 95% CI=2.04-3.43, P=0.02 for heterogeneity; recessive model: OR=3.19, 95% CI=2.56-3.97, P=0.28 for heterogeneity; co-dominant model: OR=1.37, 95% CI=1.18-1.59, P=0.09 for heterogeneity) and other populations (dominant model: OR=1.85, 95% CI=1.20-2.85, P<0.0001 for heterogeneity; recessive model: OR=3.78, 95% CI=2.28-6.27, P=0.19 for heterogeneity; co-dominant model: OR=1.48, 95% CI=1.26-1.74, P=0.19 for heterogeneity). The Q126X variant also significantly increased the risk of gout in Asians (dominant model: OR=3.87, 95% CI=2.07-7.24, P=0.06 for heterogeneity). Conclusions: These results suggest associations between the rs2231142 and rs72552713 ABCG2 gene polymorphisms and gout risk, which led to unfavorable outcomes. However, studies with larger sample sizes and homogeneous populations should be performed to confirm these results.     

Delayed cardioprotection by sevoflurane preconditioning: a novel mechanism via inhibiting Beclin 1-mediated autophagic cell death in cardiac myocytes exposed to hypoxia/reoxygenation injury

Sevoflurane preconditioning has shown to exert delayed caridioprotection against subsequent ischemia and reperfusion injury, but the mechanisms underlying is unclear. Inhibition of autophagy by 3-methyladenine (3-MA) or knockdown of Beclin 1 leads to enhanced cardiac myocyte survival. Our study aimed to test whether sevoflurane preconditioning provides a second window of anesthetic preconditioning (SWOP) via inhibit Beclin 1-mediated autophagic cell death. H9c2 rat cardiomyocytes were randomly divided into five groups: Control (CON) group; hypoxia/reoxygenation (H/R) group, rat cardiomyocytes was exposed in the airtight container for 2 h followed by 1 h of reoxgenation; SWOP group, rat cardiomyocytes was exposed to 1 h of 2.5% sevoflurane 24 h before H/R; Autophagic inhibitors, 3-methyladenine (3-MA, 10 mM) was added to culture medium 15 min before sevoflurane exposure (3-MA+SWOP group) or cells were treated by 3-MA alone (3-MA group). The cell proliferation was significantly increased in SWOP group (79.49 ± 1.37%, P < 0.05) when compared to H/R group (62.2 ± 6.49%, P < 0.05). 3-MA administered before SWOP significantly attenuated the H/R induced autophagy and cell death. H/R injury up-regulated the expression of LC3-II and Beclin 1 proteins (342 ± 66% and 163 ± 18%, respectively, P < 0.05) compared to the CON group (100%), which were increased in SWOP group (202 ± 77% and 128 ± 8%, respectively, P < 0.05). The expression of LC3-II and Beclin 1 proteins was decreased in 3-MA group (110 ± 28% and 97 ± 6%, respectively) and 3-MA+SWOP group (93 ± 7% and 98 ± 6%, respectively) compared with H/R group, but Bcl-2 was upregulated in 3-MA group (158 ± 4%) and 3-MA+SWOP group (156 ± 5%) compared to H/R group (103 ± 7%). In conclusion, sevoflurane preconditioning confers delayed cardioprotection via inhibition Beclin 1-mediated autophagic cell death in cardiac myocytes 24 h before exposed to H/R injury.     

Immunolocalization of membrane-type 1 MMP in human rheumatoid synovium tissues

Membrane-type 1 matrix metalloproteinase (MT1-MMP, also known as MMP14), the best characterized membrane-anchored MMP, is an important matrix-degrading proteinase that could digest a broad spectrum of extracellular matrix proteins and accelerate angiogenesis. We have previously reported that some MMPs involved in the angiogenesis and the pannus formation within the joint, leading to the erosion of articular cartilage and bone in the pathological process of rheumatoid arthritis (RA). In the present study, we used immunohistochemistry assay and con-focal scanning technique to study the detailed immunolocalization of MT1-MMP in human RA synovium tissues as well as the infiltrating immune cell subsets. Our results showed that the positive MT1-MMP immunostaining could be found in synoviocytes, vascular endothelial cells, infiltrating macrophages and monocytes in RA synovium tissues, while weak or negative immunostaining could be found in infiltrating T cells, B cells and NK cells, respectively. Moreover, the Ki-67⁺ highly proliferating synoviocytes also showed higher MT1-MMP expression in RA synoviocytes. Thus, the aberrant expression of MT1-MMP in RA synoviocytes as well as infiltrating immune cells may contribute to the proliferation of the synoviocytes, and the angiogenesis and the pannus formation in RA pathological progression.     

Deep sequencing identifies deregulation of microRNAs involved with vincristine drug-resistance of colon cancer cells

Background: Vincristine (VCR) is a chemical that is widely used in tumor therapy. While long-term use can make tumor cells resistant to VCR, the underlying mechanisms of this resistance are still unclear. Objective: This study aimed at investigating the role of microRNA (miRNA) in colon cancer drug resistance. Methods: HCT-8 colon carcinoma cells were cultured and treated with different VCR concentrations to establish an HCT-8/VCR resistant cell line. Whole-genome screens, HiSeq 2500 sequencing, and bioinformatics methods were used to detect and analyze differences in miRNA expression between the drug-resistant HCT-8/VCR cells and non-resistant HCT-8 cells. Differential expression profiles of miRNAs were constructed based on sequencing result. Results: The HCT-8/VCR resistant colon carcinoma cell line was established. With regard to the difference in drug resistance between HCT-8/VCR and HCT-8 cells, 24 miRNAs showed statistically significant differences in their expression (fold change > 4), of which 17 were up-regulated. Seven miRNAs were down-regulated. Conclusion: As abnormal expression of miRNAs was associated with VCR resistance of colon carcinoma cells, differences in miRNA expression may play a key role in VCR resistance of colon cancer cells.     

Role of transcriptional factor Nrf2 in the acute lung injury of mice

Objective: This study aimed to investigate the expression and role of Nrf2 in the acute lung injury (ALI) of mice. Methods: A total of 60 BABL/c mice were randomly divided into 2 groups: ALI group and control group. In ALI group, ALI was introduced by injection of LPS. Immunohistochemistry was performed to detect Nrf2 expression in the lung; Western blot assay was employed to detect the expression of Nrf2 in the lung homogenate; ELISA was conducted to detect the expression of Nrf2 in the lung homogenate and BALF. Results: As compared to control group, ALI mice had a high Nrf2 expression in the lung as shown in immunohistochemistry, and the Nrf2 expression in the lung homogenate and BALF also increased markedly (P<0.05). Conclusion: The Nrf2 expression increases in the lung and BALF of ALI mice, suggesting that Nrf2 is involved in the inflammation during ALI and may serve as a new target in the therapy of ALI.     

行为疗法在功能性舌根音障碍矫治中的应用

目的:探讨功能性语音障碍患者应用行为疗法矫治异常舌根音,提高舌根音清晰度的方法。方法:对12例功能性异常舌根音患者运用行为疗法进行语音治疗,收集治疗前后的语音资料进行对比评估。结果:患者舌根音的语音清晰度由治疗前的52.67±11.49提高到治疗后的77.67±6.11,差异具有统计学意义(P<0.05)。结论:应用行为疗法在矫治功能性异常舌根音,可达到提高语音清晰度,改善语音功能的目的。     

肺诺卡菌病胸部CT特征

目的 探讨肺诺卡菌病的胸部CT特点。方法 回顾性分析经病原学培养确诊的8例肺诺卡菌病患者的胸部CT表现、临床资料。结果 8例患者中,5例为单纯肺诺卡菌病,3例为播散型肺诺卡菌病。肺部病变以斑片、实变影最为多见(n=8),其次为结节影(n=5)、空洞影(n=4)、团块影(n=2)。4例合并胸腔积液或积脓,5例肺内病灶区域胸膜增厚,3例合并纵隔、肺门淋巴结肿大,1例合并气胸、1例合并心包积液。结论 肺诺卡菌病的胸部CT表现多样,常合并四肢或躯干皮肤或皮下软组织感染;当肺部病灶发展迅速,出现实变、结节、空洞、肿块等多样病灶时,应考虑肺部诺卡菌感染的可能。