Dendritic cell-mediated T cell polarization

Effective defense against diverse types of micro-organisms that invade our body requires specialized classes of antigen-specific immune responses initiated and maintained by distinct subsets of effector CD4⁺ T helper (Th) cells. Excessive or detrimental (e.g., autoimmune) responses by effector T cells are controlled by regulatory T cells. The optimal balance in the development of the different types of effector and regulatory Th cells is orchestrated by dendritic cells (DC). This review discusses the way DC adapt the T cell response to the type of pathogen, focusing on the tools that DC use in this management of the T cell response.     

Nucleotide sequence and coding capacity of the large (L) genomic RNA segment of Seoul 80-39 virus, a member of the hantavirus genus.

The nucleotide sequence of the large (L) genomic RNA segment of Seoul 80-39 virus was determined from overlapping cDNA clones. The virion L RNA segment is 6530 nucleotides long. The 3' and 5' terminal sequences are inversely complementary for 15 bases. The viral complementary-sense RNA contains a single open reading frame from an AUG codon at nucleotide position 37-39 to a UAA stop codon at nucleotide position 6490-6492. This ORF could encode a polypeptide of 2151 amino acids (246,662 kDa) which likely corresponds to the L protein detected in purified viral particles (Elliott et al., 1984) and is assumed to be an RNA-dependent RNA polymerase molecule (Schmaljohn and Dalrymple, 1983). Comparison of the L protein of the Seoul 80-39 virus with the polymerase proteins encoded by other negative-stranded RNA viruses revealed 44% similarity only with the part of the Bunyamwera virus L protein (Elliott, 1989) and a very weak homology with the PB1 protein of influenza virus.     

人文医学视域下构建《惠世医学人文素养》课程的教学实践

目的研究医学教育如何将人文精神内化于心,为医疗实践提供思路和方向。方法以《惠世医学人文素养》课程为载体,将心理营养教育融入人文教育,整体化教学整合人文和医学;应用Kirkpatrick模型从反应、学习、行为和结果等4个层次分析课程的教学效果。结果学生对课程满意度高;课程学习后学生增强了信息管理能力、团队合作能力、语言表达能力、自我发展能力等,提高了专业认知度,加强了职业认同感,在技能考核中展现了良好的人文关怀精神和优良的职业素质。结论《惠世医学人文素养》课程作为医学人文教育模式创新的有益尝试,有助于提高医学人文教育的有效性和针对性。     

Problem case: two-dimensional enlargement of the upper lip after excision of a vascular malformation

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Problem case: two-dimensional enlargement of the upper lip after excision of a vascular malformation     

2.5g/L罗哌卡因高位硬膜外阻滞对呼吸功能的影响

目的 观察2.5g/L罗哌卡因用于上胸段硬膜外阻滞时对呼吸功能的影响。方法 20例行择期乳癌改良根治术患者,于T3－4硬膜外腔注入2.5g/L罗哌卡因10－15ml,观察用药前及用药后10、15、30min4个时点的呼吸功能变化,同时监测麻醉平面和循环功能。结果 硬膜外腔注入2.5g/L罗哌卡因后10、15、30min与麻醉前相比,潮气量、补呼气量和肺活量明显降低（P＜0．05－0．01）,呼吸频率增快（P＜0．05）,分钟通气量与SpO2保持不变（P＞0．05）。胸部皮肤痛觉消失平面T1－2－T6－7,循环功能（HR、ECG、MAP、SBP、DBP）稳定。麻醉期间无其它不良反应。结论 2.5g/L罗哌卡因用于高位硬膜外阻滞,在获得满意镇痛范围及循环功能稳定的同时,肺通气功能基本保持不变。     

苏拉明对肺癌血管生成的抑制作用

目的　研究苏拉明对肺癌血管生成的抑制作用及其机制。方法　采用细胞培养和免疫组织化学的方法离体研究肺癌A5 49细胞、人血管内皮ECV 30 4细胞VEGF及其受体 (Flt、KDR)的表达及苏拉明的影响。结果　苏拉明对肺癌细胞产生和分泌VEGF无影响 ;ECV 30 4细胞KDR、Flt的蛋白表达在苏拉明浓度为 0 .2 5ng/ml和 2 .5ng/ml时 ,受到显著抑制 ;而苏拉明浓度为 0 .2 5ng/ml和 2 5ng/ml时Flt的表达 ,以及苏拉明浓度为 2 .5ng/ml和 2 5ng/ml时KDR的表达则无明显变化 (与对照组比较 ,P >0 .0 5 ) ;苏拉明对A5 49、ECV 30 4细胞增生无影响。结论　苏拉明抑制肺癌血管生成的作用机制可能是通过抑制血管内皮细胞上的VEGF受体表达 ,减少VEGF与其受体结合所致。     

流式细胞仪检测尖锐湿疣患者的T细胞亚群及NK细胞

目的 研究尖锐湿疣患者的细胞免疫功能。方法 用流式细胞仪检测了３０例尖锐湿疣患者外周血Ｔ细胞亚群及ＮＫ细胞百分率。结果 尖锐湿疣患者ＣＤ４细胞百分率下降,ＣＤ８细胞百分率增高,ＮＫ细胞数降低,与对照组相比差异均有显著性。结论 尖锐湿疣患者存在细胞免疫功能缺陷。     

牛蒡苷元钙拮抗作用的研究（英文）

对牛蒡苷元（ＡＣＴ）的钙拮作用进行探讨,为确认ＡＣＴ是牛蒡子解表功能的有效成分提供实验依据,描记给ＡＣＴ前后,各标本对ＫＣ１或ＣａＣ１２诱发收缩的量效曲线,按Ｓｃｏｔｔ法计算ＰＤ’２;测定给ＡＣＴ后,标本对乙酰胆硷（Ａｃｈ）诱发的两相收缩的抑制百分率。ＡＣＴ对离体大鼠气管、结肠、肮动脉、胸主动脉平滑肌由ＫＣ１引起的收缩产生非竞争性拮抗作用,其ＰＤ’２分别为４．０１,５．９８,６．０５;ＡＣＴ和维拉     

高密度脂蛋白介导大鼠皮肤成纤维细胞内胆固醇流出的机制

目的研究高密度脂蛋白-3(HDL3)介导大鼠皮肤成纤维细胞胆固醇(ch)流出机制。方法用N-乙酰咪唑修饰HDL,阻断HDL与细胞受体相互作用,观察其对HDL3介导细胞ch流出的影响。用FITC标记HDL示踪HDL3在介导细胞ch流出中自身代谢过程。结果牛血清白蛋白(对照组)介导4.74%细胞ch流出,HDL3组和N-乙酰咪唑HDL组分别为31.85%和8.41%。FITC-HDL3与细胞37-℃培养3h后,细胞内吞荧光强度(FS)占细胞结合FS的65.78%,其中93.5%FS存在于TCA可沉淀部分。细胞进一步37-     

Temporal Bone Histopathology in Connexin 26–Related Hearing Loss

Objective: Mutations in GJB2, a gene that encodes a gap junction protein, Connexin 26 (Cx26), are responsible for approximately one third of sporadic severe‐to‐profound or profound congenital deafness and half of severe‐to‐profound or profound autosomal recessive nonsyndromic hearing loss (ARNSHL). Mouse mutants homozygous for knockouts of this gene are nonviable, precluding histopathologic studies of the associated inner ear pathology in this animal model. Therefore, we studied archival temporal bone sections to identify temporal bone donors with Cx26‐related deafness. Study Design: Temporal bone donors with a history of congenital severe‐to‐profound or profound deafness were identified in the registry of the Temporal Bone Library at the University of Iowa. Histological findings were interpreted in a blinded fashion. DNA extracted from two celloidin‐embedded mid‐modiolar sections from each temporal bone was screened for the 35delG Cx26 mutation. The entire coding region of Cx26 was screened for other deafness‐causing mutations if the 35delG mutation was detected. Results: Of five temporal bone donors with congenital severe‐to‐profound deafness, one donor was found to have Cx26‐related deafness. This individual was a Cx26 compound heterozygote, carrying the 35delG mutation and a noncomplementary Cx26 missense mutation on the opposing allele. Microscopic evaluation of this temporal bone showed no neural degeneration, a good population of spiral ganglion cells, near‐total degeneration of hair cells in the organ of Corti, a detached and rolled‐up tectorial membrane, agenesis of the stria vascularis, and a large cyst in the scala media in the region of the stria vascularis. Conclusion: This study is the first to report the temporal bone histopathology associated with Cx26‐related deafness. Preservation of neurons in the spiral ganglion suggests that long‐term successful habilitation with cochlear implants may be possible in persons with severe‐to‐profound or profound Cx26‐related deafness.