以红皮病和口腔念珠菌感染为主要表现AIDS1例

报道以红皮病为突出表现AIDS 1例.患者男性,64岁,因“全身发疹2个月,伴发热1周”收入院.查体发现体重明显下降,双睑结膜充血,口腔上颚,颊黏膜密集点滴状白色伪膜,全身弥漫暗红色斑片,伴有褐色痂皮脱屑.口腔黏膜真菌涂片(+),HIV-1(+).确诊AIDS,红皮病,口腔念珠菌感染.后死于肺部感染.     

鼻咽癌放化疗患者口腔黏膜真菌感染调查

目的研究鼻咽癌放化疗患者口腔黏膜真菌感染情况.方法口腔咽拭子真菌镜检和真菌培养.结果鼻咽癌放化疗患者口腔黏膜真菌感染率较高,而以白色念珠菌为主.结论真菌为鼻咽癌放化疗患者口腔黏膜炎致病菌.     

中国痣斑金小蜂属分类研究(膜翅目：金小蜂科)

研究了中国金小蜂科、金小蜂亚科的痣斑金小蜂属Acrocormus Foerster,1856,描述2新种,美痣斑金小蜂Acrocrmus eucallus sp.nov.和棕唇痣斑金小蜂Acriocormus fuscussp.nov.,编制了中国痣斑金小蜂属分种检索表。美痣斑金小蜂Acrocrmus eucallus sp.nov.与榆痣斑金小蜂A.ulmi Yang较相似,新种与后者的主要区别为：盾纵沟伸至中胸盾片的1／2处;翅痣长为高的1.55倍;柄后腹长为宽的3.7倍,正模♀：河北献县,采集时间及采集人不详;模式标本保存于中国科学院动物研究所动物标本馆。棕痣斑金小蜂Acriocormus fuscussp.nov.与五营痣斑金小蜂A.wuyingensis Yang相近,比较杨忠岐（1996）的描述,新种与后者主要区别为：唇基区具明显的册形刻点;前胸背板前缘具脊;并胸腹节具完整的侧褶;缘脉为痣脉的1.5倍。正模♀：黑龙江伊春,1978－08－12,廖定熹采。模式标本保存于中国科学院动物研究所动物标本馆。     

斑痣悬茧蜂在黏虫寄主体内与中红侧沟茧蜂竞争下的存活和发育表现

【目的】不同种寄生蜂在同一小生境中可能寄生同一共享寄主。本研究旨在为认识寄生蜂种间互作关系,并为科学评价寄生性天敌控害效应提供依据。【方法】在室内以单寄生性斑痣悬茧蜂Meteorus pulchricornis(Wesmael)和中红侧沟茧蜂Microplitis mediator(Halidy)及其寄主黏虫Mythimna separata(Walker)低龄幼虫为材料,以寄生顺序和间隔时间为因素进行种间寄生竞争效应实验,观察比较两种蜂的存活和斑痣悬茧蜂子代的发育历期、体型大小和寿命等发育参数。【结果】不同寄生顺序和间隔时间组合处理下斑痣悬茧蜂子代蜂存活率始终高于中红侧沟茧蜂,且先寄生的斑痣悬茧蜂子代存活率高于后寄生的蜂,提前24 h寄生的斑痣悬茧蜂子代存活率可高达96.7%。当斑痣悬茧蜂先于中红侧沟茧蜂寄生时,其子代幼虫发育历期比单独寄生(对照)时显著延长;当后于中红侧沟茧蜂寄生时,其子代幼虫发育历期与单独寄生时无显著差异。各竞争处理下,斑痣悬茧蜂子代成虫寿命均长于单独寄生的子代成虫;子代成虫后足胫节长度与单独寄生相比明显缩短。【结论】结果说明,斑痣悬茧蜂在黏虫低龄幼虫体内与中红侧沟茧蜂的竞争中占有优势,但竞争对斑痣悬茧蜂子代生长发育具有负面影响。     

血管钙化对血脂的影响及维生素K干预研究

目的：探讨在正常饮食情况下血管钙化是否影响血脂浓度。方法：Wistar大鼠30只,随机抽取10只作为阴性对照组,其余20只用维生素D3和尼古丁制备血管钙化模型。将造模大鼠随机分为钙化组和钙化+维生素K组：钙化组喂饲普通基础饲料,钙化+维生素K组喂饲含有维生素K2的饲料,维生素K2按30mg/（kg·d）给予。12w后,全自动生化分析仪检测血清TC、TG、LDL-C、HDL-C,取胸主动脉Von kossa染色进行病理学观察。结果：钙化组von Kossa染色血管弹性纤维间可见大量棕黄色钙化斑,而阴性对照组大鼠血管中膜弹力纤维正常,无钙沉积现象,钙化+维生素K2组无钙化斑或只有少量的棕黄色钙化斑。各组大鼠血清TC、TG、LDL-C、HDL-C浓度接近（P＞0-05）。结论：在本实验条件下,血管钙化对大鼠血脂无影响;维生素K对正常血脂无影响。     

斑痣盘菌科一新种及一中国新记录种

报道斑痣盘菌科的2个分类单元,其中生于八角Illiciumverum上的八角生散斑壳Lophodermiumilliciicolasp.nov.是新种,寄生于柳属植物Salixspp.上的脐突斑痣盘菌Rhytismaumbonatum为中国新记录种。对此二种进行了汉文描述、图解和讨论,新种附有拉丁文特征简介。供研究标本保藏于安徽农业大学森林保护教研室(AAUFP)。     

斑痣悬茧蜂对不同寄主密度斑块的选择和最优搜寻行为

在圆柱形透明有机玻璃罩内,观察了斑痣悬茧蜂对不同寄主密度斑块的选择和滞留时间,并用Cox比例风险模型分析了寄主密度、产卵次数和搜寻特征对斑痣悬茧蜂在斑块上的驻留时间及其影响因素.结果表明:斑痣悬茧蜂对高密度寄主斑块的初次选择次数、访问次数均高于低密度寄主斑块,导致在高密度斑块上具有更高的寄生率;斑痣悬茧蜂在各斑块的驻留时间随寄主密度的增加而增加.Cox模型分析结果显示,斑块内寄主密度和产卵数均对其离开斑块的倾向起消极作用,即随寄主密度和产卵数的增加而倾向于留在斑块上;而寄主密度与产卵数的互作反而对寄生蜂离开斑块倾向具有促进作用,这两种作用可使寄生蜂利用寄主斑块获得最大适合度.     

斑痣悬茧蜂的寄主辨别能力及其影响因素

为评价斑痣悬茧蜂Meteorus pulchricornis (Wesmael)的寄主辨别能力及其影响因素, 采用双选试验（斜纹夜蛾2龄寄主幼虫, 健康∶被寄生=5∶5）, 观察了寄生经历（无寄生经历、 有1次寄生经历、 有1次过寄生经历）和寄主被首次寄生后的间隔时间（1 - 7 d）对斑痣悬茧蜂在健康寄主和被寄生寄主之间的选择; 为探究斑痣悬茧蜂是否能够辨别寄主斑块质量, 观察了斑痣悬茧蜂连续3次访问不同质量寄主斑块（被寄生寄主∶健康寄主分别为 2∶8, 5∶5和 8∶2）时的产卵刺扎次数。对选择频次进行的分析表明, 寄主被首次寄生后的间隔时间和寄生蜂的寄生经历均对过寄生发生有显著影响(P<0.05), 过寄生概率随寄主首次被寄生后的间隔时间延长而降低; 有寄生经历的寄生蜂发生过寄生的概率低于无寄生经历的寄生蜂。用Cox比例风险模型对寄主辨别时间进行的分析表明, 发生过寄生的风险随寄主被初次寄生后间隔时间的延长而减小, 也因寄生蜂具有过寄生经历而减小。斑痣悬茧蜂在连续3次访问不同质量寄主斑块中, 产卵刺扎次数随寄主斑块的质量提高而显著增多。据此推论, 斑痣悬茧蜂不仅能够辨别被寄生寄主, 而且能够辨别含有被寄生寄主的寄主斑块。     

华山松上的斑痣盘菌

根据作者野外调查、室内研究以及查阅有关文献获得的数据,发现我国华山松Pinus armandii上斑痣盘菌科Rhytismataceae菌物6属18种,其中玉龙舟皮盘菌Ploioderma yulongense为一新种。文中对新种进行了描述、图解和讨论,编制了18个种的检索表,讨论了华山松上斑痣盘菌的生态习性及致病性。     

建立维生素K_1微生物限度测定方法

目的:根据计数培养基适用性检查和计数方法适用性试验结果,建立维生素K1微生物限度测定方法。方法:以聚山梨酯80作为乳化剂,使维生素K1在p H 7.0无菌氯化钠-蛋白胨缓冲液中充分乳化。取1:20供试液1 m L,按平皿法分别用营养琼脂培养基和玫瑰红钠琼脂培养基培养,以计数细菌、霉菌和酵母菌。结果:验证所用培养基的菌落平均数均大于对照培养基上的70%,且菌落形态大小一致。稀释液对照组和试验组培养基上菌落平均数的回收率均大于70%,且菌落形态大小一致。三批维生素K1及其加速和长期稳定性样品中均未见菌落。结论:所选培养基适宜大肠埃希菌、金黄色葡萄球菌和白色念珠菌生长。且含聚山梨酯80的p H 7.0无菌氯化钠-蛋白胨缓冲液和维生素K1对所含大肠埃希菌、金黄色葡萄球菌和白色念珠菌无抑菌性。     

角蛋白与肿瘤

角蛋白属于I型和II型中间纤维,是上皮细胞中间纤维的主要组成蛋白。角蛋白对上皮细胞及组织的稳定性和完整性具有重要的功能,此外,许多角蛋白还参与细胞内的信号转导通路。角蛋白的基因突变会导致一系列的遗传性皮肤病,还能引起肝脏、口腔粘膜、食管、外阴、直肠粘膜的白海绵痣等疾病。最近大量研究发现,角蛋白在人类多种类型肿瘤中也存在特异性表达,角蛋白及其抗体在肿瘤的免疫化学诊断、核转移、精确的分型或分类等方面具有重要的作用,并且还有助于预测肿瘤治疗反应和预后情况。因此,研究角蛋白与肿瘤之间的相互联系,揭示它们的作用机制对肿瘤的诊断和治疗有着重要意义。该文回顾了近年来角蛋白的分子生物学研究概况及临床应用,对各种角蛋白与肿瘤发生、进展、诊断以及预后的关系进行综述,同时对存在的问题及困难作了探讨并对未来的研究进行了展望。     

角蛋白与肿瘤

角蛋白属于I型和II型中间纤维,是上皮细胞中间纤维的主要组成蛋白。角蛋白对上皮细胞及组织的稳定性和完整性具有重要的功能,此外,许多角蛋白还参与细胞内的信号转导通路。角蛋白的基因突变会导致一系列的遗传性皮肤病,还能引起肝脏、口腔粘膜、食管、外阴、直肠粘膜的白海绵痣等疾病。最近大量研究发现,角蛋白在人类多种类型肿瘤中也存在特异性表达,角蛋白及其抗体在肿瘤的免疫化学诊断、核转移、精确的分型或分类等方面具有重要的作用,并且还有助于预测肿瘤治疗反应和预后情况。因此,研究角蛋白与肿瘤之间的相互联系,揭示它们的作用机制对肿瘤的诊断和治疗有着重要意义。该文回顾了近年来角蛋白的分子生物学研究概况及临床应用,对各种角蛋白与肿瘤发生、进展、诊断以及预后的关系进行综述,同时对存在的问题及困难作了探讨并对未来的研究进行了展望。     

Roles of the trkB and trkC gene products of Escherichia coli in K+ transport

Mutations at the trkB and trkC loci of Escherichia coli produce an abnormal efflux of K+. The mutations are partially dominant in diploids and revert frequently by what appears to be intragenic suppression to the null state. The mutations can be reverted by insertion of Tn10 into the mutated gene, and spontaneous revertants are fully recessive to the mutant allele in diploids. K+ efflux produced by NEM* and by DNP* persists in strains with presumed null mutations at either locus, indicating neither gene product is the primary target for the effect of these inhibitors on K+ efflux. The results are consistent with the view that trkB and trkC encode independent systems for K+ efflux. Mutations at these loci alter regulation of the process so that K+ efflux occurs inappropriately. A second mutation to the null state abolishes this abnormal K+ efflux. These genes may encode K+/H+ antiporters, an activity postulated to mediate K+ efflux and demonstrated to exist in E. coli and other bacteria.     

Severe abnormalities in the oral mucosa induced by suprabasal expression of epidermal keratin K10 in transgenic mice

Previous studies have demonstrated that keratin K10 plays an important role in mediating cell signaling processes, since the ectopic expression of this keratin induces cell cycle arrest in proliferating cells in vitro and in vivo. However, apart from its well known function of providing epithelial cells with resilience to mechanical trauma, little is known about its possible roles in nondividing cells. To investigate what these might be, transgenic mice were generated in which the expression of K10 was driven by bovine K6beta gene control elements (bK6(beta)hK10). The transgenic mice displayed severe abnormalities in the tongue and palate but not in other K6-expressing cells such as those of the esophagus, nails, and hair follicles. The lesions in the tongue and palate included the cytolysis of epithelial suprabasal cells associated with an acute inflammatory response and lymphocyte infiltration. The alterations in the oral mucosa caused the death of transgenic pups soon after birth, probably because suckling was impaired. These anomalies, together with others found in the teeth, are reminiscent of the lesions observed in some patients with pachyonychia congenita, an inherited epithelial fragility associated with mutations in keratins K6 and K16. Although no epithelial fragility was observed in the bK6(beta)hK10 oral epithelia of the experimental mice, necrotic processes were seen. Collectively, these data show that the carefully regulated tissue- and differentiation-specific patterns displayed by the keratin genes have dramatic consequences on the biological behavior of epithelial cells and that changes in the specific composition of the keratin intermediate filament cytoskeleton can affect their physiology, in particular those of the oral mucosa.     

Allelic somatic mutations may explain vascular twin nevi

Summary Vascular twin nevi, i.e., telangiectatic nevus and nevus anemicus occurring together and adjacent to each other, can be explained as twin spots resulting from a somatic recombination. It is so far unclear, however, whether the postulated underlying autosomal recessive mutations are allelic. This problem can be approached by studying another cutaneous phenotype, phacomatosis pigmentovascularis. Within this diagnosis, several authors have reported the simultaneous occurrence of three different birthmarks, viz., a pigmentary nevus, a telangiectatic nevus and a nevus anemicus. These cases can also be explained as a twin-spot phenomenon, provided two of these nevi are considered allelic traits. The two vascular nevi are most probably allelic, whereas the pigmentary nevus may be a nonallelic component of this syndrome. In conclusion, phacomatosis pigmentovascularis provides circumstantial evidence suggesting allelism of somatic mutations giving rise to two different vascular nevi.     

Molecular pathogenesis of malignant melanoma: a different perspective from the studies of melanocytic nevus and acral melanoma

The Clark model for melanoma progression emphasizes a series of histopathological changes beginning from benign melanocytic nevus to melanoma via dysplastic nevus. Several models of the genetic basis of melanoma development and progression are based on this Clark’s multi-step model, and predict that the acquisition of a BRAF mutation can be a founder event in melanocytic neoplasia. However, our recent investigations have challenged this view, showing the polyclonality of BRAF mutations in melanocytic nevi. Furthermore, it is suggested that many melanomas, including acral and mucosal melanomas, arise de novo, not from melanocytic nevus. While mutations of the BRAF gene are frequent in melanomas on non-chronic sun damaged skin which are prevalent in Caucasians, acral and mucosal melanomas harbor mutations of the KIT gene as well as the amplifications of cyclin D1 or cyclin-dependent kinase 4 gene. Amplifications of the cyclin D1 gene are detected in normal-looking ‘field melanocytes’, which represent a latent progression phase of acral melanoma that precedes the stage of atypical melanocyte proliferation in the epidermis. Based on these observations, we propose an alternative genetic progression model for melanoma.     

The short-term effects of various oral care methods in dependent elderly: comparison between toothbrushing, tongue cleaning with sponge brush and wiping on oral mucous membrane by chlorhexidine

doi: 10.1111/j.1741‐2358.2011.00577.x The short‐term effects of various oral care methods in dependent elderly: comparison between toothbrushing, tongue cleaning with sponge brush and wiping on oral mucous membrane by chlorhexidine Objectives: To explore the short‐term effects from toothbrushing, tongue cleaning with sponge brush and wiping on oral mucous membrane by chlorhexidine. Background: Numerous reports have been seen in recent years proving the effectiveness of mouth cleaning with a toothbrush for the prevention of respiratory infections among the dependent elderly. However, the short‐term effects from each oral care method have not yet been clarified. Hence, an investigation was conducted by having each subject independently perform various oral care methods for five consecutive days. Materials and Methods: The subjects consisted of 12 assistance‐dependent elderly who have difficulties with tooth brushing by themselves, have 10 or more residual teeth and are not yet using plate dentures. After the pre‐intervention examination, each of the following oral care methods were performed on the same subject on an approximately three week basis: 1) Tooth brushing 2)Tongue cleaning with sponge brush 3)Wiping on oral mucous with sponge brush by chlorhexidine. Each method was performed independently, once a day for 5 consecutive days and the subjects were reexamined on the sixth day for comparative verification. Results: Consequently, toothbrushing decreased the plaque index and gingival index significantly and an improvement of oral malodour was also acknowledged (p < 0.01). Tongue cleaning with a sponge brush decreased the tongue coat score significantly (p < 0.05) and oral malodour was also improved (p < 0.01). Wiping on oral mucous with a sponge brush soaked in chlorhexidine significantly decreased opportunistic infections in the pharynx region (p < 0.05). Conclusions: It was suggested that the use of not only a toothbrush but also chlorhexidine gluconate may be indicated for dependent elderly people in whom pathogens of opportunistic infection are detected.     

口腔鳞状细胞癌线粒体DNA的HVRⅢ区突变的研究（英文）

目的：检测口腔鳞状细胞癌患者线粒体DNA复制控制区（mtDNA D-loop）高变Ⅲ区（hypervariable regionⅢ,HVRⅢ）的突变情况,并探讨其意义。方法：以口腔鳞状细胞癌患者癌旁组织及正常组织作为对照,对7例口腔鳞状细胞癌组织样本的mtDNA D-loop HVRⅢ区进行PCR扩增和测序分析。结果：在7例患者的癌组织、癌旁组织、正常组织样本中共发现72个（56种）核苷酸改变,其中51个（26种）为核苷酸多态性改变;3个肿瘤组织样本中共发现21个突变,其中16个位于HVRⅢ区范围内;癌旁组织及正常组织未发现突变;口腔鳞状细胞癌的mtDNA D-loop HVRⅢ区突变率为42.9%（3/7）。结论：mtDNA D-loop HVRⅢ区的变异可能与口腔鳞状细胞癌的易感性有一定的联系;本研究为寻找新的肿瘤基因诊断和肿瘤遗传易感性的标志物提供了依据。     

Histological and histochemical evaluation of human oral mucosa constructs developed by tissue engineering

Reconstruction of large oral mucosa defects is often challenging, since the shortage of healthy oral mucosa to replace the excised tissues is very common. In this context, tissue engineering techniques may provide a source of autologous tissues available for transplant in these patients. In this work, we developed a new model of artificial oral mucosa generated by tissue engineering using a fibrin-agarose scaffold. For that purpose, we generated primary cultures of human oral mucosa fibroblasts and keratinocytes from small biopsies of normal oral mucosa using enzymatic treatments. Then we determined the viability of the cultured cells by electron probe quantitative X-ray microanalysis, and we demonstrated that most of the cells in the primary cultures were alive and had high K/Na ratios. Once cell viability was determined, we used the cultured fibroblasts and keratinocytes to develop an artificial oral mucosa construct by using a fibrin-agarose extracellular matrix and a sequential culture technique using porous culture inserts. Histological analysis of the artificial tissues showed high similarities with normal oral mucosa controls. The epithelium of the oral substitutes had several layers, with desmosomes and apical microvilli and microplicae. Both the controls and the oral mucosa substitutes showed high suprabasal expression of cytokeratin 13 and low expression of cytokeratin 10. All these results suggest that our model of oral mucosa using fibrin-agarose scaffolds show several similarities with native human oral mucosa.