乳腺癌患者保乳术联合腔镜腋窝淋巴结清扫术的临床研究

目的 探讨保乳手术联合腔镜腋窝淋巴结清扫术(MALND)对乳腺癌患者上肢功能、应激反应及血管细胞黏附分子-1 (VCAM-1)、细胞间黏附分子-1(ICAM-1)水平的影响。方法 回顾性分析98例乳腺癌患者的临床资料,依据手术方式的不同分为研究组53例和对照组45例。对照组行保乳手术联合传统腋窝淋巴结清扫术(CALND),研究组行保乳手术联合MALND。比较2组术前、术后6个月上肢功能;收集2组患者术前、术后12 h焦虑自评量表(SAS)、抑郁自评量表(SDS)评分以及心率(HR)、平均动脉压(MAP)水平,并对比2组应激反应程度;比较2组患者术前、术后5 d VCAM-1、ICAM-1水平。结果 术后6个月,研究组前屈、后伸、内收、外展、内旋、外旋活动角度大于对照组,差异有统计学意义(P<0.05);术后12 h,研究组SAS、SDS评分及HR、MAP水平低于对照组,差异有统计学意义(P<0.05);术后5 d,研究组VCAM-1、ICAM-1水平低于对照组,差异有统计学意义(P<0.05)。结论 保乳手术联合MALND对乳腺癌患者上肢功能影响小,术后应激反应程度轻...     

化瘀通络方对局灶性脑缺血大鼠再灌注(MCAO)后脑组织氧自由基和NOS表达的影响

目的:观察化瘀通络方治疗大鼠局灶性脑缺血-再灌注损伤对脑组织自由基及一氧化氮合成酶(NOS)和iNOS变化的影响。方法:制备大鼠局灶性脑缺血再灌注损伤模型,给予化瘀通络方治疗后观察丙二醛(MDA)、超氧化物歧化酶(SOD)及一氧化氮合成酶(NOS)和诱导型一氧化氮合成酶(iNOS)的变化。结果:化瘀通络方可显著降低MDA含量以及iNOS和NOS活性,SOD含量升高。结论:在脑缺血再灌注损伤后,化瘀通络方能抑制脑缺血再灌注后脂质过氧化反应,促进自由基清除,对抗自由基损伤,提高脑组织自身抗氧化能力,降低NOS和iNOS介导脑缺血-再灌注时的神经损伤,保护脑细胞。     

Validating self-reported strokes in a longitudinal UK cohort study (Whitehall II): Extracting information from hospital medical records versus the Hospital Episode Statistics database

Background

Quantiles are a staple of epidemiologic research: in contemporary epidemiologic practice, continuous variables are typically categorized into tertiles, quartiles and quintiles as a means to illustrate the relationship between a continuous exposure and a binary outcome.

Discussion

In this paper we argue that this approach is highly problematic and present several potential alternatives. We also discuss the perceived drawbacks of these newer statistical methods and the possible reasons for their slow adoption by epidemiologists.

Summary

The use of quantiles is often inadequate for epidemiologic research with continuous variables.     

左腋动脉和臂丛神经走行变异1例

笔者在标本解剖操作观察腋窝结构时发现1例左侧腋动脉与臂丛神经位置及走行出现变异,既往文献报道的变异多为腋动脉发出的分支与臂丛神经之间的位置与走行之间变异^[1-3],本次解剖观察发现腋动脉与臂丛神经的内侧束、外侧束和后束之间的位置关系出现变异,与既往报道有所不同,现报告如下。     

Hair cells in the inner ear of the pirouette and shaker 2 mutant mice

The shaker 2 (sh2) and pirouette (pi) mouse mutants display severe inner ear dysfunction that involves both auditory and vestibular manifestation. Pathology of the stereocilia of hair cells has been found in both mutants. This study was designed to further our knowledge of the pathological characteristics of the inner ear sensory epithelia in both the sh2 and pi strains. Measurements of auditory brainstem responses indicated that both mutants were profoundly deaf. The morphological assays were specifically designed to characterize a pathological actin bundle that is found in both the inner hair cells and the vestibular hair cells in all five vestibular organs in these two mutants. Using light microscope analysis of phalloidin-stained specimens, these actin bundles could first be detected on postnatal day 3. As the cochleae matured, each inner hair cell and type I vestibular hair cell contained a bundle that spans from the region of the cuticular plate to the basal end of the cell, then extends along with cytoplasm and membrane, towards the basement membrane. Abnormal contact with the basement membrane was found in vestibular hair cells. Based on the shape of the cellular extension and the actin bundle that supports it, we propose to name these extensions cytocauds. The data suggest that the cytocauds in type I vestibular hair cells and inner hair cells are associated with a failure to differentiate and detach from the basement membrane.     

VEGF-C表达和微淋巴管密度与胃癌淋巴转移的关系及意义

目的探讨胃癌组织血管内皮生长因子C(VEGF-C)表达和微淋巴管密度(MLVD)及两者与胃癌淋巴转移的关系。方法应用免疫组织化学方法检测208例人胃癌组织、40例癌浸润前缘组织及139例人胃正常粘膜组织中VEGF-C、D2-40的表达,对D2-40阳性脉管进行MLVD计数,并结合病理资料进行统计学分析。结果胃癌组织VEGF-C的表达明显高于正常胃粘膜组织(χ2=109.199,P<0.01);胃癌组织中有淋巴结转移(χ2=14.496,P<0.01)或浸润透浆膜(χ2=11.586,P<0.01)组VEGF-C表达水平分别较无转移或浸润未及浆膜组增高。癌浸润前缘组织中MLVD(18.36±15.60个/mm2)明显高于胃癌组(9.41±9.32个/mm2,t=-3.681,P<0.01)和胃正常粘膜组织(7.70±7.69个/mm2,t=-4.180,P<0.01);胃癌淋巴结转移组MLVD(9.81±9.97个/mm2)高于无转移组(6.41±7.85个/mm2,t=2.516,P<0.01),而在浸润透浆膜组(11.20±10.55个/mm2)和未及浆膜组(8.54±9.36个/mm2)MLVD无差别(t=1.467,P=0.472)。另外,在胃癌组织中VEGF-C表达与MLVD呈正相关(F=2.910,P<0.05)。结论VEGF-C在胃癌中的高表达与胃癌浸润深度、淋巴转移密切相关。     

Victims of war—Psychoendocrine evidence for the impact of traumatic stress on psychological well-being of adolescents growing up during the Israeli–Palestinian conflict

Violent conflicts are severe traumatic stressors with detrimental effects on physical and mental health, with children and adolescents being particularly at risk. For the hypothalamic–pituitary–adrenal (HPA) axis, characteristic patterns of dysregulation in trauma-exposed individuals have been shown. This study set out to investigate self-reported mental well-being in Palestinian adolescents growing up during the Israeli–Palestinian conflict. Hair cortisol concentrations (HCC) as a psychoendocrine marker for long-term HPA axis aberrations along with the potential protective factor sense of coherence (SoC; i.e., the global mindset to interpret the world and emerging stressors as comprehensible, manageable, and meaningful) were examined. Between 2014 and 2016, posttraumatic stress disorder (PTSD), depression, anxiety, HCC, and SoC were examined in 233 adolescents aged 11 to 16 from the West Bank. More than half of the participants reported trauma exposure, with 40% fulfilling the criteria of a preliminary PTSD diagnosis and a high prevalence of anxiety and depression. HCC was significantly elevated in the PTSD subgroup compared to the subgroup not exposed to any traumatic events (p = 0.046), with trauma-exposed individuals in between. HCC was further associated with typical sequelae of traumatic stress. Notably, SoC was inversely related to self-reported psychopathology, as well as to HCC in the trauma group. The results illustrate the situation of adolescents exposed to chronic traumatic stress and extend the literature on aberrant HPA axis functioning under such conditions. They also point out a central role of SoC, which may imply new strategies to aid individuals exposed to ongoing conflicts.     

Reciprocal effect of Waardenburg syndrome mutations on DNA binding by the Pax-3 paired domain and homeodomain

The Pax-3 protein contains two DNA-binding domains, a paired domain and a homeodomain. Mutations in Pax-3 cause Waardenburg syndrome (WS) in humans and the mouse Splotch (Sp) phenotype. In the Sp-delayed mouse, a mutation in the Pax-3 paired domain (G9R) abrogates the DNA-binding activity of both the paired domain and the homeodomain, suggesting that they may functionally interact. To investigate this possibility further, we have analyzed the DNA-binding properties of additional point mutants in the Pax-3 paired domain and homeodomain that occur in WS patients (F12L, N14H, G15S, P17L, R23L, G48A, S51F and G66D in the paired domain, V47F and R53G in the homeodomain), the Pax-1 un mutation (G15A) and a substitution associated with Peters' anomaly in the PAX-6 gene (R23G). Within the paired domain, seven of 10 mutations were found to abrogate DNA-binding by the paired domain. Remarkably, these seven mutations also affected DNA binding by the homeodomain, causing either a complete loss (P17L and G66D), a reduction (R23G, R23L, G15S and G15A) or an increase in DNA-binding activity (N14H). In addition, the effect of paired domain mutations occurred at the level of monomer formation by the homeodomain, while the dimerization potential of this domain seemed unaffected in mutants where it could be analyzed. Furthermore, while both homeodomain mutations were found to abolish DNA binding by this domain, the R53G mutation also abrogated DNA binding by the paired domain. The important observation that independent mutations in either domain can affect DNA binding by the other in the intact Pax- 3 protein strongly suggests that the two domains are not functionally independent but bind DNA through cooperative interactions. Modeling the deleterlous mutations on the three-dimensional structure of the paired domain of Drosophila Prd shows that these mutations cluster at the DNA interface, thus suggesting that a series of DNA contacts are essential for DNA binding by both the paired domain and the homeodomain of Pax-3.