Urothelial carcinoma of the urinary bladder with a component of acinar/tubular type differentiation simulating prostatic adenocarcinoma

We report a case of an 83-year-old man with a high-grade carcinoma of the urinary bladder who underwent cystoprostatectomy. The invasive carcinoma showed mixed, morphologically distinct patterns consisting of conventional high-grade urothelial carcinoma, glandular differentiation resembling enteric type adenocarcinoma, and acinar/tubular type differentiation, morphologically similar to Gleason grade 3 prostatic adenocarcinoma. Immunohistochemical studies revealed the acinar/tubular component of the tumor to be negative for prostate-specific antigen and prostatic acid phosphatase, but positive for cytokeratin 7, cytokeratin 20, high molecular weight cytokeratin (34 beta E12), and thrombomodulin, consistent with origin from the bladder rather than the prostate. Although bladder carcinomas composed of mixed morphologic patterns are not uncommon, to our knowledge, the presence of acinar/tubular type features simulating prostatic adenocarcinoma in such tumors has not been described elsewhere.     

对Bem性别角色量表的考察与修订

目的：对在性别角色研究中使用得最为广泛的工具-Bem量表进行介绍，考察它在中国文化下的信、效度并进行修订。方法：选取两个城市三所大学中的340名本科生为被试。经过项目分析、因素分析等统计方法，对构成量表的条目进行删除和保留。结果：最后由14项男性化条目和12项女性化条目构成新的Bem量表简本。结论：修订后的Bem量表在信、效度上有了明显的提高，可以成为进一步研究的工具。     

NO及NO合成酶与感染性休克

感染性休克病理生理学过程十分复杂。NO在其中的作用既具有有害的一面，同时也存在有利的一面。受内毒素、细胞因子等诱导，iNOS表达上调并产生大量NO，引起循环衰竭、组织细胞损伤以及通过调节炎症介质基因表达扩大全身炎症反应。另一方面，eNOS所产生的NO对机体具有保护作用。然而，感染性休克时，eNOS蛋白质合成及其功能受到损害，反而成为血管内皮功能失常、诱发多器官功能障碍的重要原因。     

Evidence for a major gene underlying bone size variation in the Chinese

Osteoporosis is a major public health problem defined as a loss of bone strength, of which bone size is an important determinant. In the present study, familial correlation and segregation analyses for the spine and hip bone sizes were performed for the first time in a Chinese sample composed of 393 nuclear families with a total of 1,193 individuals. The results indicate a major gene of codominant inheritance for spine bone size; however, there is no evidence of a major gene influencing hip bone size. Significant familial residual effects are found for both traits, suggesting their polygenic inheritance. Heritability estimates (±SE) for spine and hip bone size were 0.62 (0.13) and 0.59 (0.12), respectively. Sex and age differences in genotype‐specific average bone size were observed. Compared with our previous study on bone mineral density (BMD) in the same population, this study suggests that genetic determination of bone size may be different from that of BMD, and thus studying bone size as one surrogate phenotype for osteoporotic fractures may be necessary. Am. J. Hum. Biol. 16:68–77, 2004. © 2003 Wiley‐Liss, Inc.     

Lysine methylation within the globular domain of histone H3 by Dot1 is important for telomeric silencing and Sir protein association

The amino-terminal histone tails are subject to covalent post-translational modifications such as acetylation, methylation, and phosphorylation. In the histone code hypothesis, these exposed and unstructured histone tails are accessible to a repertoire of regulatory factors that specifically recognize the various modified histones, thereby generating altered chromatin structures that mediate specific biological responses. Here, we report that lysine (Lys) 79 of histone H3, which resides in the globular domain, is methylated in eukaryotic organisms. In the yeast Saccharomyces cerevisiae, Lys 79 of histone H3 is methylated by Dot1, a protein shown previously to play a role in telomeric silencing. Mutations of Lys 79 of histone H3 and mutations that abolish the catalytic activity of Dot1 impair telomeric silencing, suggesting that Dot1 mediates telomeric silencing largely through methylation of Lys 79. This defect in telomeric silencing might reflect an interaction between Sir proteins and Lys 79, because dot1 and Lys 79 mutations weaken the interaction of Sir2 and Sir3 with the telomeric region in vivo. Our results indicate that histone modifications in the core globular domain have important biological functions.     

Encoding of location and intensity of noxious indentation into rat skin by spatial populations of cutaneous mechano-nociceptors

The ability of a spatial population of cutaneous, Adelta, and C mechano-nociceptors to encode the location and intensity of a noxious, cutaneous indentation was examined using an isolated preparation in a rat model. Skin and its intact innervation were harvested from the medial thigh of the rat hindlimb and placed in a dish, with the corium side down, containing synthetic interstitial fluid. The margins of the skin were coupled to an apparatus that could stretch and apply compression to the skin. The skin was suspended on top of a deformable platform whose bulk, nonlinear, compressive compliance emulated that found in vivo. The isolated preparation facilitated examination of the spatial population response by eliminating the nonlinear geometry and inhomogeneous compressive compliance present in-vivo. Spatial population responses (SPR) were formed from recordings of single neurons that were stimulated by compressing the skin with an indenter (flat cylinder, 3-mm diam) at discrete intervals from the center of their receptive fields. SPR were composed of the neural responses (z axis) at each indentation location (x, y plane), and were analyzed quantitatively using nonlinear regression to fit an equation of a Gaussian surface. Both Adelta and C SPR accurately encoded the location and intensity of noxious indentation. The intensity of the stimulus was encoded in the peak neural response of the SPR, which had a nonlinear relationship to the compressive force. The location of the stimulus was encoded in the x, y position of the peak of the SPR. The position of the peak remained constant with increasing magnitudes of compressive force. The overall form of the SPR also remained constant with changes of compressive load, suggesting a possible role for encoding in the SPR some aspects of shape of a noxious stimulus.     

骨髓源间充质干细胞在异基因小鼠免疫器官内的分布及其免疫功能调节作用

目的：探讨骨髓源间充质干细胞(Bone marrow mesenchymal stem cells，BMSC)在异基因小鼠免疫器官内的分布及其免疫调节作用。方法：以CM-Dil荧光染料示踪BMSC的体内分布情况，并辅以PCR检测Y染色体的方法进一步鉴定；体外实验采用MTT法、ELISA和FACS等方法检测BMSC的免疫调节作用。结果：BMSC可进入并较长期(30天)存在于异基因小鼠免疫器官内；在体外，BALB／C小鼠的BMSC对由ConA诱导的BALB／C和C57BL／6(B6)和BXSB小鼠的T细胞增殖均有抑制作用；而对前两种小鼠由12S诱导的B细胞增殖和分泌k方面表现为促进作用，对BXSB小鼠由IPS诱导的B细胞增殖和k分泌有抑制作用。BALB／C小鼠的BMSC对BALB／C和B6小鼠由ConA诱导的IL-4生成细胞的数量无明显影响，却可降低由ConA诱导的两种品系小鼠的IFN-γ生成细胞的数量；但对于BXSB小鼠却不同，BALB／C的BMSC可降低由ConA诱导的BXSB小鼠的IL-4生成细胞的数量，而提高由ConA诱导的IFN-γ生成细胞的数量。结论：异基因BMSC不但可进入受体的免疫器官，且可较长期(30天)存在；另外，BMSC对同基因正常、异基因正常和异基因自身免疫病的个体均有一定程度的免疫调节作用。     

Endogenous Immune Response to Glutamic Acid Decarboxylase (GAD67) in NOD Mice is Modulated by Adjuvant Immunotherapy

We have shown that immunization of non-obese diabetic (NOD) mice with adjuvants (CFA or BCG) prevents the onset of diabetes by induction of regulatory cells. Since autoimmune responses to glutamic acid decarboxylase (GAD) are up-regulated in insulin-dependent diabetes mellitus (IDDM), in this study GAD67-specific antibody, T cell proliferation and lymphokine production patterns were analysed in the adjuvant-treated mice to characterize the regulatory mechanisms underlying the protection. We used both spontaneous diabetes and syngeneic islet transplantation models in NOD mice. Protection against spontaneous diabetes and prevention of syngeneic islet graft rejection by CFA or BCG treatment was found to be accompanied by the production of long lasting and high titre anti-GAD67 antibody of IgG1 isotype in the sera. Uponin vitrostimulation with GAD67, draining lymph node and spleen cells from CFA-immunized NOD mice or syngeneic islet-grafted and BCG-protected NOD mice produced much more IL-4, whereas there was no significant change in IFN-γ production. The strong early T cell proliferative response to GAD67 in CFA or BCG-immunized NOD mice was followed by a low or unresponsiveness state. Taken together, these results suggest a shift in Th1/Th2 balance in the GAD67-specific endogenous immune response to a change in Th2 levels after adjuvant treatment. We postulate that the protective effect of CFA or BCG is due to the diversion of GAD-specific endogenous cellular immune response to a non-pathogenic humoral response.     

人际交往训练降低医学生心理应激反应的实验研究

目的　探讨人际交往训练降低医学生心理应激反应的有效模式 ,以培养交往手段 ,促进身心健康 ,提高学习效率。方法　从云南中医学院中医专业 2 0 0 0级 8个班 ,41 2名学生中随机抽取 2个班 ,共 1 0 6人为被试对象 ,结合专业学习 ,在生理学课堂教学中贯穿人际交往训练 ,训练前后分别测查 90项症状自评量表 ( SCL-90 )和防御方式问卷 ( DSQ) ,并用 Q分类法检验被试课前和课后自我评价。最后 ,对被试和其余 6个班的学生进行生理测验 ,并对测验成绩进行比较。结果　被试在交友信心、乐观豁达、口头表达、积极接纳、说服技巧方面均比训练前有显著和极显著提高 ;且考前心理应激反应明显降低 ,防御方式趋向成熟 ,测验及格率高于其余 6个班。结论　结合专业进行人际交往训练可在近期内改善医学生的心理健康水平 ,有利于提高学习效率 ,深受大学生欢迎     

Follicular dendritic cell accessory activity crosses MHC and species barriers

Productive follicular dendritic cell (FDC)-B cell interactions appear to involve critical ligand-receptor interactions. Immune complexes (IC) on FDC activate complement and provide FDC with a complement-derived CD21 ligand (CD21L), which bind CD21, while antigen in the IC binds on the B cell-BCR. Further, FDC-FcgammaRIIB binds Fc regions of antibodies in IC and reduces coligation of BCR and FcgammaRIIB minimizing an inhibitor of B cell activation. Given that Fc receptors and complement receptors bind immunoglobulins and complement fragments of other species, we reasoned that FDC accessory activity should cross MHC and species barriers. This prediction was tested using memory lymphocytes from OVA-immune mice and TT-immune humans in combination with FDC from murine lymph nodes and human tonsils. Human and murine FDC converted IC into potent immunogens (specific antibody increased from background to thousands of ng / ml). MHC barriers did not restrict this activity and human FDC worked with murine lymphocytes and murine FDC worked with human lymphocytes. Furthermore, stimulation via MHC-dependent allogeneic or zenogeneic mechanisms did not promote antibody production by FDC. Polyclonal responses stimulated by lipopolysaccharide and pokeweed mitogen were also promoted (10 - 100-fold) and anti-CD21 blocked FDC activity. These results substantiate the hypothesis that FDC are necessary for strong recall responses and that FDC-CD21L is critical.