大学生网络交往动机的差异研究

目的探讨大学生网络交往动机,为有效引导大学生认识和参与网络交往,同时为社会、学校、家长制定相应干预措施提供一定的心理依据。方法采用自编的大学生网络交往动机量表和Wrightsman编制的人性哲学量表—独立性分量表,对646名大学生的网络交往动机的差异进行研究。结果电大学生的网络交往动机更倾向于"交往/寻求帮助",而普通全日制高校学生更倾向于"消遣/娱乐";男生更倾向于"交往/寻求帮助"、"消遣/娱乐"、"好奇/追求时尚"、"网络优越感";理科学生更倾向于"交往/寻求帮助"、"网络优越感"、"消遣/娱乐"、"好奇/追求时尚";高年级大学生更倾向于"消遣/娱乐"、"好奇/追求时尚";独立性高的大学生网络交往的动机更倾向于"交往/寻求帮助"、"网络优越感"。结论大学生的网络交往动机因学校、专业、年级、性别、独立性人格特征不同而存在不同程度的差异。     

唑来膦酸联合泰索帝治疗晚期非小细胞肺癌骨转移疗效分析

目的 评价唑来磷酸联合泰索帝治疗晚期非小细胞肺癌骨转移的疗效及安全性.方法 41例晚期非小细胞肺癌骨转移患者随机分为唑来膦酸联合泰索帝(A组)及单用唑来磷酸(B组)治疗,对两组疗效进行分析比较.结果 A组骨痛缓率、生存质量改善率略好于B组(P>0.05).毒副作用差异无显著性.A组骨转移灶修复率52.4%(11/29),B组20.0%(4/20).差异有显著性(P<0.05).结论 唑来膦酸联合泰索帝治疗晚期非小细胞肺癌骨转移有较好的治疗用,毒性可耐受.     

软组织磷酸盐尿性间叶肿瘤的临床病理分析

目的研究磷酸盐尿性间叶肿瘤（混合结缔组织亚型）的临床与病理学特点。方法对1例骨软化症患者的肿块切除标本进行光镜、电镜和免疫组化SP法检测。结合临床资料，并复习相关文献。结果患者表现为顽固性骨软化症、低磷酸盐血症，高磷酸盐尿，高血清碱性磷酸酶，外周血单核细胞增多，血钙浓度正常。经99mTc—OCT（奥曲肽）检查指导临床发现左胭窝区小肿块并切除之。术后3天，血磷恢复正常。光镜下肿瘤主要由肥胖的梭形细胞和破骨细胞样多核巨细胞构成，具有丰富的血管，可见血管外皮瘤样血管、散在脂肪岛、明显的出血及含铁血黄素沉积，肿瘤边缘有不完整的膜状骨样或软骨样组织。电镜下见梭形细胞内含数量不等的细颗粒状电子致密物，其中部分为结晶样高电子致密度颗粒。免疫组化显示多核细胞和单核间质细胞CD68阳性。结论该例为肿瘤源性骨软化症，其病理类型为磷酸盐尿性间叶肿瘤，混合结缔组织亚型。外科切除后治愈，99mTc-OCT对于指导临床发现小的隐蔽病灶很有价值。     

骨髓增生异常综合征中的微环境异常

Myelodysplastic syndrome (MDS) is considered as a preleukemic course, characteristic of hypercellular marrow and pancytopenia. Many studies have demonstrated that defects occur in the heamtopoiet-ic cells from patients with MDS. Recently, many abnormal changes in apoptosis, proliferation, ability of hematopoietic support, cytokine secretion, clonal origin of stromal cells and angiogenesis have also been re-vealed in the bone marrow mieroenvironment of MDS patients.     

从人分离出两株甲型流感H9N2亚型毒株内部基因特性的研究

目的 了解2株从人分离出的H9N2亚型毒株内部基因特性，并弄清其来源。方法 用RT-PCR扩增目的基因，用P^CEM-T Vector(美国Promega公司)，4℃过夜连接，重组质粒转入dH5a细菌，筛选阳性菌落，酶切鉴定，送六合通公司自动测序。然后进行进化树分析。结果 2株测定毒株内部基因均为G9基因系，它们相互间除PA基因有差异外，其余5个基因均相同。结论 2株测定毒株的基因组均为G9基因系，它们是由携带不同基因特性H9N2毒株的禽群分别直接感染人，而不是来自同一禽的H9N2亚型流感病毒。     

Mutation spectrum and genotype-phenotype analyses in Cowden disease and Bannayan-Zonana syndrome, two hamartoma syndromes with germline PTEN mutation

The tumour suppressor gene PTEN , which maps to 10q23.3 and encodes a 403 amino acid dual specificity phosphatase (protein tyrosine phosphatase; PTPase), was shown recently to play a broad role in human malignancy. Somatic PTEN deletions and mutations were observed in sporadic breast, brain, prostate and kidney cancer cell lines and in several primary tumours such as endometrial carcinomas, malignant melanoma and thyroid tumours. In addition, PTEN was identified as the susceptibility gene for two hamartoma syndromes: Cowden disease (CD; MIM 158350) and Bannayan-Zonana (BZS) or Ruvalcaba-Riley-Smith syndrome (MIM 153480). Constitutive DNA from 37 CD families and seven BZS families was screened for germline PTEN mutations. PTEN mutations were identified in 30 of 37 (81%) CD families, including missense and nonsense point mutations, deletions, insertions, a deletion/insertion and splice site mutations. These mutations were scattered over the entire length of PTEN , with the exception of the first, fourth and last exons. A 'hot spot' for PTEN mutation in CD was identified in exon 5 that contains the PTPase core motif, with 13 of 30 (43%) CD mutations identified in this exon. Seven of 30 (23%) were within the core motif, the majority (five of seven) of which were missense mutations, possibly pointing to the functional significance of this region. Germline PTEN mutations were identified in four of seven (57%) BZS families studied. Interestingly, none of these mutations was observed in the PTPase core motif. It is also worthy of note that a single nonsense point mutation, R233X, was observed in the germline DNA from two unrelated CD families and one BZS family. Genotype-phenotype studies were not performed on this small group of BZS families. However, genotype-phenotype analysis inthe group of CD families revealed two possible associations worthy of follow-up in independent analyses. The first was an association noted in the group of CD families with breast disease. A correlation was observed between the presence/absence of a PTEN mutation and the type of breast involvement (unaffected versus benign versus malignant). Specifically and more directly, an association was also observed between the presence of a PTEN mutation and malignant breast disease. Secondly, there appeared to be an interdependent association between mutations upstream and within the PTPase core motif, the core motif containing the majority of missense mutations, and the involvement of all major organ systems (central nervous system, thyroid, breast, skin and gastrointestinal tract). However, these observations would need to be confirmed by studying a larger number of CD families.      

Mouse homologues of the human AZF candidate gene RBM are expressed in spermatogonia and spermatids, and map to a Y chromosome deletion interval associated with a high incidence of sperm abnormalities

An RNA-binding motif (RBM) gene family has been identified on the human Y chromosome that maps to the same deletion interval as the 'azoospermia factor' (AZF). We have identified the homologous gene family (Rbm) on the mouse Y with a view to investigating the proposal that this gene family plays a role in spermatogenesis. At least 25 and probably >50 copies of Rbm are present on the mouse Y chromosome short arm located between Sry and the centromere. As in the human, a role in spermatogenesis is indicated by a germ cell-specific pattern of expression in the testis, but there are distinct differences in the pattern of expression between the two species. Mice carrying the deletion Yd1, that maps to the proximal Y short arm, are female due to a position effect resulting in non-expression of Sry ; sex-reversing such mice with an Sry transgene produces males with a high incidence of abnormal sperm, making this the third deletion interval on the mouse Y that affects some aspect of spermatogenesis. Most of the copies of Rbm map to this deletion interval, and the Yd1males have markedly reduced Rbm expression, suggesting that RBM deficiency may be responsible for, or contribute to, the abnormal sperm development. In man, deletion of the functional copies of RBM is associated with meiotic arrest rather than sperm anomalies; however, the different effects of deletion are consistent with the differences in expression between the two species.      

ATRX encodes a novel member of the SNF2 family of proteins: mutations point to a common mechanism underlying the ATR-X syndrome

It was shown recently that mutations of the ATRX gene give rise to a severe, X-linked form of syndromal mental retardation associated with alpha thalassaemia (ATR-X syndrome). In this study, we have characterised the full-length cDNA and predicted structure of the ATRX protein. Comparative analysis shows that it is an entirely new member of the SNF2 subgroup of a superfamily of proteins with similar ATPase and helicase domains. ATRX probably acts as a regulator of gene expression. Definition of its genomic structure enabled us to identify four novel splicing defects by screening 52 affected individuals. Correlation between these and previously identified mutations with variations in the ATR-X phenotype provides insights into the pathophysiology of this disease and the normal role of the ATRX protein in vivo.      

CO对局灶性缺血脑组织血脑屏障通透性的影响

目的:研究一氧化碳及其限速酶(血红素氧合酶-1)对局灶性缺血脑组织血脑屏障通透性的影响。方法:将SD大鼠随机分为3组(n=6),使用血红素氧合酶诱导剂及抑制剂腹腔注射,用等量生理盐水腹腔注射作为对照组,12h后复制MCAO模型。梗塞后24h后检测血液中一氧化碳浓度、血脑屏障通透性。结果:诱导剂组一氧化碳浓度明显高于对照组(P＜0.01),血脑屏障通透性明显低于对照组(P＜0.05),而抑制剂组一氧化碳浓度明显低于对照组(P＜0.01),血脑屏障通透性明显高于对照组(P＜0.05)。血红素氧合酶诱导剂、抑制剂对非梗塞侧的血脑屏障通透性没有影响(P＞0.05)。结论:一氧化碳作为一种信使分子,脑缺血时浓度升高具有保护血脑屏障的作用。