白念珠菌侵袭宿主毒力因子研究进展

白念珠菌是一种寄生于人类黏膜表面的条件致病菌,是导致免疫功能低下人群侵袭性真菌感染的主要病原菌。白念珠菌形成侵袭性感染的过程主要分为黏附、侵袭、播散、形成感染灶等步骤,其中黏附和侵袭过程最为关键。黏附是白念珠菌入侵宿主的前提,该过程主要依赖于细胞壁表面的黏附素。侵袭阶段主要与菌丝形成、细胞壁表面毒力蛋白表达和蛋白水解酶分泌增加有关。形成菌丝是白念珠菌侵袭宿主的关键因素,主要由细胞内cAMP/PKA和MAPK等信号通路调控;侵袭素主要位于白念珠菌细胞壁表面,可以协助其穿刺宿主上皮细胞、诱导内吞作用;白念珠菌还可分泌多种蛋白水解酶,它能够破坏宿主组织细胞,协助白念珠菌形成感染灶。该文主要对白念珠菌黏附和侵袭宿主过程中关键的毒力因子进行综述,为理解白念珠菌致病机制以及选择潜在的药物靶点提供参考。     

白念珠菌与血管内皮细胞黏附后的作用机制

白念珠菌与血管内皮细胞的相互作用是其是否造成血源性播散感染的中心环节,两者的黏附仅仅是作用的初级阶段、黏附的程度对两者作用的性质一感染控制和感染播散之间的关系并不明确。而在黏附后的相互作用研究中提示白念珠菌进入血管内皮细胞并造成其损伤继而进入其他组织,同时血管内皮细胞对白念珠菌感染也具有重要的保护作用,这种作用与血管内皮细胞对白念珠菌的内吞也密切相关。本文对两者黏附后血管内皮细胞对白念珠菌的吞噬,白念珠菌对血管内皮细胞的损伤以及血管内皮细胞对白念珠菌感染的保护作用方面作一综述。     

白念珠菌对宿主的黏附机制

白念珠菌对宿主的黏附是白念珠菌感染过程的关键的第一步,因此阐明白念珠菌对宿主的黏附机制对探索新的方法预防和治疗白念珠菌感染至关重要。近年来,研究者们从白念珠菌的表面结构、黏附素以及黏附相关基因等方面对白念珠菌与宿主的黏附机制进行了大量研究。该文就白念珠菌对宿主的黏附机制进行综述。     

黄芩素与氟康唑协同抗白念珠菌生物被膜作用研究

目的：研究黄芩素与氟康唑合用对白念珠菌生物被膜形成的影响。方法采用激光共聚焦显微镜观察黄芩素与氟康唑合用对白念珠菌生物被膜生长形态的影响;采用 XTT 法考察黄芩素与氟康唑合用对白念珠菌生物被膜形成能力的影响;应用水-烃两相测定实验考察黄芩素与氟康唑合用对白念珠菌生物被膜细胞表面疏水性（ Cell surface hydrophobicity, CSH）的影响;应用实时定量 RT-PCR（Real Time RT-PCR）实验考察黄芩素与氟康唑合用对白念珠菌 CSH1、EFG1、HWP1、ALS1基因表达的影响。结果黄芩素与氟康唑合用能够协同抑制白念珠菌生物被膜的形成,经黄芩素与氟康唑处理的白念珠菌不能形成正常的生物被膜,其生长动力学及细胞表面疏水性下降,细胞疏水性相关基 CSH1、菌丝形成调控基因EFG1、黏附相关基因 HWP1基因的表达水平降低。结论黄芩素与氟康唑合用可协同抑制白念珠菌生物被膜的形成。     

白念珠菌Ras/cAMP/PKA通路的研究进展

白念珠菌是一种重要的条件致病真菌,Ras/cAMP/PKA信号通路在白念珠菌的多种生理过程中发挥作用,如形态转换、黏附、生物被膜形成等,对于维持白念珠菌的毒力以及侵袭能力是十分重要的。对这一信号通路的深入研究有助于更好地了解白念珠菌对人体致病的机制,给抗真菌新药的研发提供新的思路。该文重点阐述通路相关蛋白功能、上下游调控关系及机制。     

白念珠菌致病性研究进展

白念珠菌是一种重要的条件致病菌,多在体表及黏膜宿主共栖生存,可引起皮肤黏膜及内脏的广泛感染。白念珠菌是单细胞假菌丝酵母菌,形态上具有双相性,即菌丝相和孢子相。其中菌丝相更易黏附和入侵宿主组织,是该菌在体内的主要致病形式。白念珠菌的致病机制与多种因素如黏附、芽管、水解酶、生物膜、群体感应等有关。该文综述了白念珠菌致病机制的研究新进展。     

白念珠菌黏附基因的研究进展

白念珠菌能引起免疫力低下患者的皮肤黏膜和全身系统性持续感染,对宿主组织的黏附是其侵入和感染的先决条件。对白念珠菌黏附相关基因的研究有助于揭示白念珠菌的致病机制。近年来,越来越多的研究者从黏附基因的结构、影响其表达的因素以及黏附机制等方面进行了研究。本文就黏附基因的相关研究进展进行综述,旨在为新型抗真菌药物和白念珠菌疫苗的研究提供参考。     

白念珠菌黏附、侵袭黏膜屏障机制的研究进展

随着深部真菌感染率的上升,白念珠菌病已成为国内、外学者的研究热点.白念珠菌之所以能引起全身播散性的感染,黏附并侵袭黏膜屏障在其致病过程中发挥着非常关键的作用.本文总结目前国内外研究成果,对白念珠菌黏附、侵袭黏膜屏障相关的机制做一综述,为更好的了解和治疗念珠菌病提供理论依据.     

CRK1基因缺失对白念珠菌形态、黏附、生物被膜的影响

目的 研究CRK1基因缺失对白念珠菌形态、黏附、生物被膜的影响.方法 显微镜下观察,计算菌丝形成率,比较CRK1基因缺失菌（Δcrk1菌）及标准菌SC5314形成菌丝的能力;建立肠黏膜模型,计算黏附率,评价CRK1基因缺失对白念珠菌黏附的影响;MTT法及结晶紫法（CV）评价CRK1基因缺失对白念珠菌生物被膜形成的影响.结果 与SC5314相比,Δcrk1菌分别在10％胎牛血清和RPMI-1640培养条件下形成菌丝能力均较弱,两者之间有统计学差异;Δcrk1菌在60、90、120 min时对肠黏膜的黏附数明显少于标准菌SC5314,两者之间有统计学差异;通过MTT法、结晶紫法两种方法证实了,在经48 h培养后,Δcrk1菌与其标准菌SC5314相比,形成生物膜的能力弱,两者之间差异有统计学差异.结论 CRK 1基因缺失影响白念珠菌菌丝二态性的转化,进而影响黏附力和生物被膜的形成.     

抑癌蛋白PTEN及PDZ蛋白对其的调节

pten基因是迄今为止发现的第1个具有双特异性磷酸酶活性的抑癌基因,该基因的编码产物PTEN蛋白,是具有蛋白与脂质磷酸酯酶活性的双特异性磷酸酯酶,作为1种重要的信号分子参与细胞增殖、分化、黏附、迁移、凋亡以及基因转录的调控. 最近,关于PTEN在信号转导中的作用以及细胞内PTEN的调节机制研究较多,尤其是PDZ蛋白对PTEN的调节作用. PTEN蛋白包括1个氨基端（N端）磷酸酯酶区域,1个与脂质结合的C2区域和1个含有PDZ结合序列的羧基端（C端）区域. PDZ结构域通过识别目标蛋白羧基端PDZ结合序列与目标蛋白相互作用,调控多种重要的细胞生理过程和信号传导途径.本文就抑癌基因pten编码产物PTEN蛋白的结构、PTEN的生物学功能和PDZ蛋白对PTEN调节的研究进展进行综述.     

Recent advances in the study of Kaposi's sarcoma-associated herpesvirus replication and pathogenesis

It has now been over twenty years since a novel herpesviral genome was identified in Kaposi's sarcoma biopsies. Since then, the cumulative research effort by molecular biologists, virologists, clinicians, and epidemiologists alike has led to the extensive characterization of this tumor virus, Kaposi's sarcoma-associated herpesvirus(KSHV; also known as human herpesvirus 8(HHV-8)), and its associated diseases. Here we review the current knowledge of KSHV biology and pathogenesis, with a particular emphasis on new and exciting advances in the field of epigenetics. We also discuss the development and practicality of various cell culture and animal model systems to study KSHV replication and pathogenesis.     

The structure, reproduction and taxonomy of Vidalia and Osmundaria (Rhodophyta, Rhodomelaceae)

Comprises species occurring mostly in subtidal habitats in tropical, subtropical and warm-temperate areas of the world. An analysis of the type species, V. spiralis (Sonder) Lamouroux ex J. Agardh, a species from Australia, establishes basic characters for distinguishing species in the genus. These characters are (1) branching patterns of thalli, (2) flat blades that may be spiralled on their axis, (3) width of the blade, (4) primary or secondary derivation of sterile and fertile branchlets and (5) position of sterile and fertile branchlets on the thalli. Application of the latter two characters provides an important basic method for separation of species into three major groups. Osmundaria , a genus known only in southern Australia, was studied in relation to Vidalia , and its separation from the Vidalia assemblage is not accepted. Species of Vidalia therefore are transferred to the older genus name, Osmundaria. Two new species, Osmundaria papenfussii and Osmundaria oliveae are described from Natal. Confusion in the usage of the epithet, Vidalia fimbriala Brown ex Turner has been clarified, and Vidalia gregaria Falkenberg, described as an epiphyte on Osmundaria pro/ifera Lamouroux, is revealed to be young branches of the host, Osmundaria prolifera.     

New or rare chromosome counts in Artemisia L. (Asteraceae, Anthemideae) and related genera from Kazakhstan

Fifteen chromosome counts of six Artemisia taxa and one species of each of the genera Brachanthemum, Hippolytia, Kaschgaria, Lepidolopsis and Turaniphytum are reported from Kazakhstan. Three of them are new reports, two are not consistent with previous counts and the remainder are confirmations of very scarce (one to four) earlier records. All the populations studied have the same basic chromosome number, x = 9, with ploidy levels ranging from 2x to 6x. Some correlations between ploidy level, morphological characters and distribution are noted.     

肝癌中HBV和HCV基因和抗原的分布及意义

采用原位分子杂交方法检测HCV RNA及HBV X基因;采用免疫组织化学方法研究HCV核心抗原,非结构区C33c抗原及HBxAg在肝细胞肝癌中的定位及分布.结果表明(1)HCV RNA、HBV X基因在肝细胞肝癌组织检出率分别为40%(55/136)和82%(112/136).HCV RNA定位于癌细胞的胞浆内,阳性细胞呈散在、灶状及弥漫分布三种形式;HBV X基因在肝癌细胞中的分布呈胞浆型、核型及核浆型,阳性细胞也呈上述三种分布形式;(2)HCV C33c抗原、核心抗原在肝细胞肝癌中的阳性率为81%(133/164)及86%(141/164).C33c抗原定位于癌细胞及肝细胞的胞浆内;核心抗原既定位于癌细胞核中,又可定位于胞浆中.C33c抗原阳性细胞以灶状分布为主;而核心抗原阳性细     

Selection with two alleles and complete dominance

For a plant selection model with frequency-independent viabilities, fertilities and selfing rates, it is shown that apart from global fixation, for certain parameter combinations a protected polymorphism and facultative fixation (either allele may become fixed according to initial frequencies) may both occur. Facultative fixation requires different selling rates for the dominant and recessive type. Protection of the polymorphism requires resource allocation for male and female function. In this connection the problem of purely genetically caused population extinction is discussed.
For general frequency dependence and regular segregation, the chances for establishment of a completely recessive gene are compared to those of a completely dominant gene. It is proven that the process of establishment of the recessive gene, despite a fitness advantage, may be considerably endangered by drift effects if random mating prevails. The recessive gene may reach the same effectivity in establishment as a dominant gene, only if the recessive homozygote mates exclusively with its own type during the period of establishment.