学习风格特征对腹腔镜扶镜技能训练的影响

目的 分析医学生的学习风格特征,探讨不同的学习风格特征对腹腔镜扶镜助手技能训练的影响。方法 在腹腔镜扶镜助手扶镜技能训练前采用Kolb学习风格量表于2020年9月至12月对哈尔滨医科大学附属第四医院60名实习医生和40名专硕研究生学习风格特征进行评估;然后分析比较实习医生和专硕研究生学习风格特征的差异,以及不同学习风格特征对腹腔镜扶镜技能训练效果的影响。结果 实习医生和专硕研究生学习风格特征差异有统计学意义(P<0.001)。实习生群体中以发散型学习风格为主,研究生群体中以聚合型学习风格为主。学习风格特征对腹腔镜扶镜技能效果有显著影响。实习医生和专硕研究生聚合型学习风格受试者在扶镜技能训练中,视野居中、水平位、最佳视野每个周期平均失误数均明显少于发散、同化和调节型学习风格的受试者。结论 医学生中不同学习群体有着不同的学习风格特征。在腹腔镜扶镜技能训练中学习风格特征对训练效果有显著影响。医学教育中应该充分兼顾不同学习风格特征的特点,充分发挥学生学习风格优势。     

未成熟树突状细胞表面CD1d分子在体外移植免疫中的作用

背景:树突状细胞具有双向免疫调节作用,成熟树突状细胞激活免疫应答,而未成熟树突状细胞则倾向诱导免疫耐受。目的:探讨鼠CD1d分子在未成熟树突状细胞诱导移植免疫耐受中的作用,以及在此过程中细胞因子的参与机制。方法:利用vIL-10转染的BALB/c小鼠未成熟树突状细胞在体外用粒细胞-巨噬细胞集落刺激因子基因、脂多糖刺激成熟,经抗CD1d(anti-CD1d)干预。观察培养后的细胞表型、细胞因子表达。为探明CD1d分子在异体T细胞存在下的免疫作用,进行不同实验条件的初次、再次混合淋巴细胞培养(1stMLC、2ndMLC),观察T细胞增殖、细胞因子表达。结果与结论:Anti-CD1d的干预降低了未成熟树突状细胞增殖异体T细胞的能力,anti-CD1d干预的未成熟树突状细胞致敏异体T细胞后其免疫功能低下;anti-CD1d干预在异体T细胞存在时影响未成熟树突状细胞在功能上的成熟,主要表现在抑制白细胞介素12的分泌,加强白细胞介素10的分泌。     

老年冠心病患者下肢动脉硬化危险因素分析

目的 探讨影响老年冠心病患者下肢动脉硬化闭塞症(LEASD)发生发展的相关危险因素。方法 选择2014年1~3月哈尔滨医科大学附属第四医院冠心病患者114例为研究对象,采用彩色多普勒超声观察下肢血管狭窄程度,根据狭窄程度将其分为狭窄率≥70%组(n=21)和狭窄率<70%组(n=53)。观察并分析两组患者年龄及伴发高血压、糖尿病、腔隙性脑梗死、高密度脂蛋白-胆固醇(HDL-C)降低、载脂蛋白A(apoA)降低、高同型半胱氨酸血症(HHCY)、超敏C反应蛋白(hs-CRP)增高等因素,并进行狭窄率≥70%者危险因素分析。结果 1114例入选者检出下肢动脉硬化者74例,检出率为64.9%,平均年龄高于未检出下肢动脉硬化者,差异有统计学意义(P<0.05),下肢动脉硬化患者均伴发腔隙性脑梗死。2狭窄率≥70%组≥90岁的患者所占比例明显高于狭窄率<70%组,差异有高度统计学意义(P<0.01)。3狭窄率≥70%组伴发高血压、糖尿病、HDL-C降低、HHCY、hs-CRP增高者多于狭窄率<70%组,差异有统计学意义(P<0.05);而两组伴发apoA降低者比较,差异无统计学意义(P>0.05)。4Logistic分析表明老年LEASD患者下肢血管狭窄率≥70%与高龄(>90岁)、高血压、糖尿病、HDL-C降低、HHCY、hs-CRP增高密切相关(P=0.033、0.036、0.021、0.028、0.034、0.046)。结论 170岁以上老年冠心病患者下肢动脉硬化发生率高达64.9%;2 LEASD血管狭窄程度与年龄具有一定的相关性;3高龄(>90岁)、高血压、糖尿病、HDL-C降低、HHCY、hs-CRP增高是预测老年冠心病患者下肢动脉硬化狭窄率≥70%的独立危险因素。     

恶性梗阻性黄疸伴急性化脓性胆管炎一期行胰十二指肠切除术的可行性分析

目的对恶性梗阻性黄疸伴急性化脓性胆管炎一期行胰十二指肠切除术进行可行性分析。方法回顾分析我院1999年至2004年施行PD手术治疗恶性梗阻性黄疸病人128例，其中，PD手术治疗恶性梗阻性黄疸伴Asc24例（A组），PD手术治疗不伴有Asc病例104例（B组）。术前按Knaus法计算每例APACHEⅢ评分，对比分析两组术后并发症的发生率和死亡率，以及APACHEⅢ不同计分段下死亡率的差异。结果A组术后并发症发生率为45．8％，死亡率8．3％；B组术后并发症发生率为34．6％，死亡率7．7％。两组术后并发症发生率有显著性差异（P〈O．05），死亡率无显著性差异（P〉O．05）。APACHEⅢ计分段分别为40分以下、41～70分、71分以上统计死亡率，两组死亡率差异无显著性（P〉O．05），组内比较，不同计分段死亡率有显著性差异（P％0．05）。结论恶性梗阻性黄疸伴ASC病例术前全面和客观的评估、及时的手术探查和决断、术中的精细操作和围手术期的综合处理是保证一期PD术良好预后的决定因素。     

腹腔镜与开腹肝门部胆管癌根治术的对比研究

目的:对比腹腔镜肝门部胆管癌根治术与开腹肝门部胆管癌根治术的临床疗效,探讨腹腔镜肝门部胆管癌根治术的安全性及可行性。方法:回顾分析2011年3月至2013年10月收治的19例肝门部胆管癌患者的临床资料,术前根据患者及家属的要求,14例行四孔法腹腔镜肝门部胆管癌根治术(A组),5例行开腹肝门部胆管癌根治术(B组),对比分析两组患者术中及术后情况。结果:患者均完成相应术式。A组中12例于腹腔镜下使用吻合器完成肠间吻合;2例先扩大右上腹小切口于腹外完成肠间吻合后还纳腹腔,重新建立气腹完成胆肠吻合;1例Ⅳ型患者未达到完全根治。A组手术时间长于B组,差异有统计学意义(P<0.05),术后镇痛时间、住院时间短于B组,差异有统计学意义(P<0.05);术中出血量、术中淋巴结清扫数量、术后进食时间、术后并发症及住院总费用两组相比差异无统计学意义(P>0.05)。术后随访5~30个月,平均(17.6±0.8)个月,无一例死亡。结论:腹腔镜肝门部胆管癌根治术由腹腔镜技术熟练及手术经验丰富的手术团队开展是安全、可行的,具有患者创伤小、痛苦少、康复快、并发症少、美容效果好等优点。     

Gene transfer of antisense B7.1 attenuates acute rejection against splenic allografts in rats

Blockade of CD80-CD28 costimulatory pathway induces unresponsiveness of T cells to alloantigens and protects allografts against immune rejection in numerous animal models. The aim of this study was to investigate whether blocking expression of B7.1 (CD80) on donor splenocytes by an antisense technique protected splenic allografts against immune rejection. Splenic grafts from Wistar-Furth rats were intra-arterially transfused with an antisense B7.1 expression vector, before they were transplanted into Sprague-Dawley rats. The rats were sacrificed at scheduled times, and the splenic allografts histologically examined. Antisense gene transfer resulted in marked down-regulation of B7.1 in donor spleens, hyporesponsiveness of recipient T cells, and attenuated acute immune rejection against splenic allografts. No obvious damage to skin, liver, or gut due to graft-versus-host disease was detected in the recipients. In conclusion, blocking expression of B7.1 in donor spleens by antisense gene therapy represented a potential alloantigen-specific immunosuppressive strategy to inhibit acute rejection against splenic allografts.     

Association of interleukin-6 methylation in leukocyte DNA with serum level and the risk of ischemic heart disease

Background Interleukin-6 (IL-6), a multifunctional cytokine, plays an important role in the development of ischemic heart disease (IHD), and DNA hypomethylation of 2 CpGs, located downstream in the proximity of the IL-6 gene promoter, has been associated with risk factor for IHD. This study was to examine the association of blood leukocyte DNA methylation of the 2 CpGs in IL-6 with the risk of IHD and the serum IL-6 level. Methods IL-6 methylation levels of 582 cases and 673 controls were measured using the bisulfite pyrosequencing technology. Serum level of IL-6 was measured using enzyme-linked immunosorbent assay. Results The IL-6 methylation was significantly lower in IHD cases than in the controls, irrespective of CpG site. After multivariate adjustment, lower (< median) average IL-6 methylation was associated with an increased risk of IHD (OR 1.57, 95% CI 1.22–2.02, p?β?=??1.02?pg/mL per increase in IL-6 methylation, p?=?0.002) among IHD cases. This significant relationship was not observed among controls. Conclusions DNA hypomethylation of IL-6 gene measured in blood leukocytes was associated with increased risk of IHD. IL-6 demethylation may upregulate its expression, whereby exerting its risk effect on the development of IHD.     

Cell-specific roles of GRK2 in onset and severity of hypoxic-ischemic brain damage in neonatal mice

The ubiquitously expressed kinase GRK2 protects against cellular overstimulation by desensitizing G protein-coupled receptors and regulating intracellular signaling. Recently, we described that hypoxia-ischemia (HI)-induced brain damage was accelerated and increased in GRK2^+/? neonatal mice. Using Cre-Lox technology we now investigated the role of decreased GRK2 in only microglia/macrophages or forebrain neurons in development of HI brain injury.Low GRK2 in microglia/macrophages (LysM-GRK2^f/+ mice) was sufficient to accelerate onset of HI damage, without affecting the severity of brain injury at 24 h post-HI as compared to LysM-GRK2^+/+ littermates. Consistently, the ipsilateral hemisphere of GRK2^+/? mice contained microglia with a more rounded phenotype compared to WT mice at 3 h post-HI. Inhibition of microglial/macrophage activity by minocycline treatment prevented the early onset of HI injury in GRK2^+/? mice. In vitro, primary GRK2^+/? microglia stimulated with LPS produced more TNF-α than WT microglia via a p38-dependent pathway. In vivo, HI-induced cerebral p38 activation and TNF-α production were increased in GRK2^+/? mice or in LysM-GRK2^f/+ mice. Our findings indicate that low GRK2 in microglia/macrophages accelerates brain damage via a GRK2/p38/TNF-α-dependent pathway.Reduced GRK2 only in forebrain neurons (CamKIIα-GRK2^f/+ mice) significantly increased severity of HI brain damage without affecting the onset of brain damage.In conclusion, our data indicate that low GRK2 in microglia/macrophages facilitates activation of these cells which may contribute to the earlier onset of cerebral HI injury associated with increased p38 phosphorylation and TNF-α production. The level of GRK2 in neurons is crucial for determining the ultimate severity of HI damage in the newborn brain.