中国栅蛛属2新种记述(蜘蛛目:栅蛛科)

本文记了分别采自云南高黎贡山的栅蛛科栅蛛属Hahnia 2新种:垭口栅蛛,新种S.yakouensis sp.nov.和肾形栅蛛,新种S.reniformis sp.nov..垭口栅蛛后眼列前曲,交媾腔大,扁圆形,交媾孔1个,位于交媾腔下缘,交媾管粗,呈"人"字形下行分成2支再向两侧扭曲.纳精囊有一肓管斜向上伸出,鉴于上述特征而与Hahnia mridulae Tikader,1970不同.肾形栅蛛交媾孔2个,位于生殖厣腹面中央,纳精囊1对,大,肾形,插入器始于生殖球左下方,鉴于上述特征而与Hahnia xinjiangensis Wang et Liang,1989不同. Abstract： The present paper deals with two new species of the genus Hahnia collected from the Gaoligong Mountains Region of Yunnan Province, China: Hahnia yakouensis sp. nov., Hahnia reniformis sp. nov..     

注重发挥博士后科研生力军作用

中国医科大学博士后科研流动站始建1995年。目前学校设有基础医学、临床医学和生物学3个博士后科研流动站。但由于每年国家财力有限,资助名额很少,在有限条件下建立、健全博士后制度,加强对博士后人员的培养,调动博士后人员的积极性是一项重要的研究课题。     

遗传物质的发现者之一——麦卡锡

1944年,3位科学家艾弗里、麦卡锡和麦克劳德在DNA遗传本质方面的发现是20世纪最重要的发现之一,这个发现打开了生物学革命的大门,从而改变了人类对自然界的看法,这项研究还为1953年沃森和克里克DNA双螺旋结构的发现奠定了坚实的基础,但不幸的是3位科学家都未曾荣获诺贝尔奖.通过介绍麦克林·麦卡锡的科学研究,从而对这项发现的基本状况有一个基本的了解.     

生命之树与进化模式:导言

One and half centuries ago, Charles Darwin (1859) presented overwhelming evidence and argued that all life on the earth shared common descent, and "from so simple a beginning endless forms most beautiful and most wonderful have been, and are being evolved". Ernst Haeckel (1886) and several of his contemporaries attempted to trace the pattern of descent among all extant and extinct forms in what Darwin referred to as "the great Tree of Life". Ever since then, systematists and evolutionary biologists have been exploring morphological, cytogenetic, chemical, developmental and molecular characters, and actively developing theories and methods to infer phylogenetic relationships among organisms from these characters. This endeavor has been especially stimulated by the rise of molecular biology and the emergence of computer science over the past 50 years. At the beginning of the 21st century, we are presented with an unprecedented opportunity to reconstruct the entire Tree of Life, and further, to study evolutionary processes and mechanisms in the context of a robust phylogenetic framework.     

我国微生态学的奠基人——魏曦

魏曦,字东升,1903年12月25日出生于湖南岳阳一个小职员家庭,父亲任职于邮政局.1914～1921年他在家乡湖滨中学读书,毕业后考入长沙湘雅医学院,学习两年后曾参加北伐军,任第四集团军警卫团三等军医.后退出军队,在长沙广雅中学任教.1928年入设立在上海的中央大学医学院(1932年独立为上海医学院)学习,1933年毕业,获博士学位.     

高黎贡山北段东西坡种子植物区系的比较研究

高黎贡山北段的东西坡由于在降雨量和热量分配等方面存在着显著的差异,致使东西坡在植物的种类、组成及区系特征等方面表现出明显的差异.东坡记载野生种子植物152科,580属,1475种及192变种(亚种),西坡记载野生种子植物162科,659属,1804种及186变种(亚种).东西坡种子植物科、属、种的对比分析表明:1)东西坡现代种子植物区系具有相同的历史渊源,但其区系联系减弱了,东西坡区系相似性程度,依科、属、种的顺序依次递减;2)西坡现代种子植物区系比东坡具有更为深刻的热带起源烙印.就科、属、种三个水平来说,东坡的热带成分低于西坡,温带成分高于西坡.许多典型的泛热带大科在西坡比东坡有着更为丰富的种类,其中有些泛热带科分子在东坡缺乏分布,而在西坡找到了合适的驻留之地;3)西坡现代种子植物区系与东喜马拉雅植物区系的联系比东坡紧密,而东坡与高黎贡山以东的区系联系比西坡密切,由于高黎贡山山脉的阻隔,近代植物物种的东西坡交流发生了障碍;4)西坡生态地理环境比东坡更有利于物种的生存、繁衍和分化,它既是古老成分的避难所,又是孕育新生成分的摇篮.     

用叶绿体ndhF和核核糖体ITS序列推断李属(蔷薇科)的系统发育

Sequences of the chloroplast ndhF gene and the nuclear ribosomal ITS regions are employed to reconstruct the phylogeny of Prunus (Rosaceae), and evaluate the classification schemes of this genus. The two data sets are congruent in that the genera Prunus s.l. and Maddenia form a monophyletic group, with Maddenia nested within Prunus. However, the ndhF data set is incongruent with the ITS data supporting two major groups within Prunus one consisting of subgenera Laurocerasus (including Pygeum) and Padus as well as the genus Maddenia and another of subgenera Amygdalus, Cerasus, and Prunus. The ITS data, on the other hand, support a clade composed of subgenera Amygdalus and Prunus and Prunus sect. Microcerasus in addition to a paraphyletic grade of subgenera Laurocerasus and Padus (and the genus Maddenia) taxa. In general, the subgeneric classifications of Prunus s.l. are not supported. The ITS and ndhF phylogenies differ mainly in interspecific relationships and the relative position of the Padus/Laurocerasus group. Both ITS and ndhF data sets suggest that the formerly recognized genus Pygeum is polyphyletic and that the distinction of the subgenera Padus and Laurocerasus is not supported. The biogeographic interactions of the temperate and tropical members in the Padus/Laurocera- sus/Maddenia alliance including Pygeum are shown to be highly dynamic and complex.     

途经甘肃的3种水鸟新纪录

2007年10月13日至11月5日进行敦煌市湿地鸟类调查时,分别在南湖湿地与候鸟自然保护区及党河水库使用Leica apo77高倍望远镜观察到3种水鸟,在以往的文献资料中未见其分布于甘肃的报道,应为甘肃鸟类新纪录。笔者用500mm镜头分别拍下3种水鸟的照片。1.赤颈(Podiceps grisegena)2007年10月13日13:30时,在南湖湿地与候鸟自然保护区的阳关水库(渥洼池)记录到2只赤颈。当时水面上同时有凤头(P.cristatus)、黑颈(P.nigricollis)以及大量鸭类、潜鸭类游禽活动,赤颈体形较凤头小,而又明显比黑颈大。其中一只赤颈的…     

鸡的瞬膜

瞬膜(nictitating membrane),又称第三眼睑,是一种保护眼球、防止灰尘的结构.鸟类的瞬膜位于眼眶的前眼角,为半透明的膜,其内缘具有一种羽毛上皮,借以刷洗角膜上的灰尘.在飞行时能遮覆眼球,以避免干燥气流和灰尘对眼球的伤害.由于瞬膜在鸟类睁眼的一瞬间迅速缩回前眼角,很难拍摄到.最近费了好大的周折,终于拍到了理想的鸡瞬膜照片,现予以发表供生物学界的同行共享(友情提示:如引用请注明原作者).     

The Us3 Protein of Herpes Simplex Virus 1 Inhibits T Cell Signaling by Confining Linker for Activation of T Cells (LAT) Activation via TRAF6 Protein

Herpes simplex virus 1 (HSV-1) is the most prevalent human virus and causes global morbidity because the virus is able to infect multiple cell types. Remarkably, HSV infection switches between lytic and latent cycles, where T cells play a critical role. However, the precise way of virus-host interactions is incompletely understood. Here we report that HSV-1 productively infected Jurkat T-cells and inhibited antigen-induced T cell receptor activation. We discovered that HSV-1-encoded Us3 protein interrupted TCR signaling and interleukin-2 production by inactivation of the linker for activation of T cells. This study unveils a mechanism by which HSV-1 intrudes into early events of TCR-mediated cell signaling and may provide novel insights into HSV infection, during which the virus escapes from host immune surveillance.     

Functional interaction between herpes simplex virus type 2 gD and HVEM transiently dampens local chemokine production after murine mucosal infection

Herpes virus entry mediator (HVEM) is one of two principal receptors mediating herpes simplex virus (HSV) entry into murine and human cells. It functions naturally as an immune signaling co-receptor, and may participate in enhancing or repressing immune responses depending on the natural ligand used. To investigate whether engagement of HVEM by HSV affects the in vivo response to HSV infection, we generated recombinants of HSV-2(333) that expressed wild-type gD (HSV-2/gD) or mutant gD able to bind to nectin-1 (the other principal entry receptor) but not HVEM. Replication kinetics and yields of the recombinant strains on Vero cells were indistinguishable from those of wild-type HSV-2(333). After intravaginal inoculation with mutant or wild-type virus, adult female C57BL/6 mice developed vaginal lesions and mortality in similar proportions, and mucosal viral titers were similar or lower for mutant strains at different times. Relative to HSV-2/gD, percentages of HSV-specific CD8(+) T-cells were similar or only slightly reduced after infection with the mutant strain HSV-2/gD-Δ7-15, in all tissues up to 9 days after infection. Levels of HSV-specific CD4(+) T-cells five days after infection also did not differ after infection with either strain. Levels of the cytokine IL-6 and of the chemokines CXCL9, CXCL10, and CCL4 were significantly lower in vaginal washes one day after infection with HSV-2/gD compared with HSV-2/gD-Δ7-15. We conclude that the interaction of HSV gD with HVEM may alter early innate events in the murine immune response to infection, without significantly affecting acute mortality, morbidity, or initial T-cell responses after lethal challenge.     

Mitochondria-derived reactive oxygen species negatively regulates immune innate signaling pathways triggered by a DNA virus, but not by an RNA virus

Reactive oxygen species (ROS) are crucial secondary messengers of signaling pathways. Redox-dependent signaling events have been previously described in the innate immune response. However, the mechanism by which ROS modulates anti-viral innate immune signaling is not fully clarified. Here, we report that mitochondria-derived ROS differentially regulate the innate response to DNA and RNA viruses (herpes simplex virus (HSV) and Sendai virus (SeV), respectively), with the cytokine response to HSV being negatively regulated by mitochondrial ROS. Importantly, specific activation of Toll-like receptors (TLRs) and DNA receptors (DNARs) but not retinoic acid inducible gene I (RIG-I)-like receptors (RLRs), led to signaling cascades that were inhibited by mitochondrial ROS production. Thus, localized mitochondrial ROS exerts negative modulation of innate immune responses to the DNA virus HSV-2 but not the RNA virus SeV.     

Enhancement of Chemokine Function as an Immunomodulatory Strategy Employed by Human Herpesviruses

Herpes simplex virus (HSV) types 1 and 2 are highly prevalent human neurotropic pathogens that cause a variety of diseases, including lethal encephalitis. The relationship between HSV and the host immune system is one of the main determinants of the infection outcome. Chemokines play relevant roles in antiviral response and immunopathology, but the modulation of chemokine function by HSV is not well understood. We have addressed the modulation of chemokine function mediated by HSV. By using surface plasmon resonance and crosslinking assays we show that secreted glycoprotein G (SgG) from both HSV-1 and HSV-2 binds chemokines with high affinity. Chemokine binding activity was also observed in the supernatant of HSV-2 infected cells and in the plasma membrane of cells infected with HSV-1 wild type but not with a gG deficient HSV-1 mutant. Cell-binding and competition experiments indicate that the interaction takes place through the glycosaminoglycan-binding domain of the chemokine. The functional relevance of the interaction was determined both in vitro, by performing transwell assays, time-lapse microscopy, and signal transduction experiments; and in vivo, using the air pouch model of inflammation. Interestingly, and in contrast to what has been observed for previously described viral chemokine binding proteins, HSV SgGs do not inhibit chemokine function. On the contrary, HSV SgGs enhance chemotaxis both in vitro and in vivo through increasing directionality, potency and receptor signaling. This is the first report, to our knowledge, of a viral chemokine binding protein from a human pathogen that increases chemokine function and points towards a previously undescribed strategy of immune modulation mediated by viruses.     

T cell immunity to herpes simplex viruses in seronegative subjects: silent infection or acquired immunity?

During the course of investigating T cell responses to HSV among volunteers entering trials of investigational genital herpes vaccines, 6 of the 24 immunocompetent subjects with no prior history of oral/labial or genital herpes possessed HSV-specific T cell immunity but, by multiple determinants of even the most sensitive serological assays, remained seronegative to HSV-1 and -2. Of these six immune seronegative (IS; HSV-seronegative with HSV-specific T cell responses) subjects, two had transient HSV-specific T cell responses, while four had CD4(+) and CD8(+) T cell responses directed at HSV that persisted for up to 4 years. CD4(+) T cell clones were isolated that recognized and had high binding affinities to epitopes in HSV-2 tegument proteins. All six IS subjects had potential sexual exposure to an HSV-2-infected sexual partner. Oral and genital mucosal secretions were sampled and tested for the presence of infectious HSV and HSV DNA. No evidence of HSV was detected in >1500 samples obtained from these IS subjects. The identification of persistent T cell responses to HSV in seronegative subjects is a novel finding in the herpesvirus field and suggests either undetected infection or acquired immunity in the absence of infection. Understanding the basis of these acquired immune responses may be critical in developing effective vaccines for genital herpes.     

Cervical antibodies in patients with oral herpes simplex virus type 1 (HSV-1) infection: local anamnestic responses after genital HSV-2 infection.

Herpes simplex virus (HSV)-specific immunoglobulin A, immunoglobulin G, and secretory-component-containing immunoglobulins were identified in cervical and salivary secretions from six subjects with oral HSV type 1 (HSV-1) infections. Anamnestic cervical and salivary antibody responses were detected in two HSV-1-seropositive women with newly acquired genital HSV-2 infections. These data implicate the common mucosal immune system in antibody responses to HSV.     

Neuronal Interferon Signaling Is Required for Protection against Herpes Simplex Virus Replication and Pathogenesis

Interferon (IFN) responses are critical for controlling herpes simplex virus 1 (HSV-1). The importance of neuronal IFN signaling in controlling acute and latent HSV-1 infection remains unclear. Compartmentalized neuron cultures revealed that mature sensory neurons respond to IFNβ at both the axon and cell body through distinct mechanisms, resulting in control of HSV-1. Mice specifically lacking neural IFN signaling succumbed rapidly to HSV-1 corneal infection, demonstrating that IFN responses of the immune system and non-neuronal tissues are insufficient to confer survival following virus challenge. Furthermore, neurovirulence was restored to an HSV strain lacking the IFN-modulating gene, γ34.5, despite its expected attenuation in peripheral tissues. These studies define a crucial role for neuronal IFN signaling for protection against HSV-1 pathogenesis and replication, and they provide a novel framework to enhance our understanding of the interface between host innate immunity and neurotropic pathogens.     

Expression of human immunodeficiency virus type 1 gp120 from herpes simplex virus type 1-derived amplicons results in potent, specific, and durable cellular and humoral immune responses

Herpes simplex virus type 1 (HSV-1) infects a wide range of cells, including dendritic cells. Consequently, HSV-1 vectors may be capable of eliciting strong immune responses to vectored antigens. To test this hypothesis, an HSV-1 amplicon plasmid encoding human immunodeficiency virus type 1 gp120 was constructed, and murine immune responses to helper virus-free amplicon preparations derived from this construct were evaluated. Initial studies revealed that a single intramuscular (i.m.) injection of 10(6) infectious units (i.u.) of HSV:gp120 amplicon particles (HSV:gp120) elicited Env-specific cellular and humoral immune responses. A potent, CD8(+)-T-cell-mediated response to an H-2D(d)-restricted peptide from gp120 (RGPGRAFVTI) was measured by a gamma interferon ELISPOT and was confirmed by standard cytotoxic-T-lymphocyte assays. Immunoglobulin G enzyme-linked immunosorbent assay analysis showed the induction of a strong, Env-specific antibody response. An i.m. or an intradermal administration of HSV:gp120 at the tail base elicited a more potent cellular immune response than did an intraperitoneal (i.p.) inoculation, although an i.p. introduction generated a stronger humoral response. The immune response to HSV:gp120 was durable, with robust cellular and humoral responses persisting at 171 days after a single 10(6)-i.u. inoculation. The immune response to HSV:gp120 was also found to be dose dependent: as few as 10(4) i.u. elicited a strong T-cell response. Finally, HSV:gp120 elicited significant Env-specific cellular immune responses even in animals that had been previously infected with wild-type HSV-1. Taken together, these data strongly support the use of helper-free HSV-1 amplicon particles as vaccine delivery vectors.     

HSV hepatitis in the mouse: a light and electron microscopic study with immunohistology and in situ hybridization

In order to characterize better the morphology and immune response in acute necrotizing HSV infection, murine HSV hepatitis was examined. BALB/c mice were inoculated intraperitoneally with 10(6) plaque-forming units (PFU) of HSV-1 (Lenette) and HSV-2 (D316). In both groups half the animals were pretreated with silica particles to block macrophage function. Up to 6 days after infection four mice from each group were sacrificed at daily intervals and the livers were examined by light and electron microscopy, immunohistology, in situ hybridization, combined immunohistology/in situ hybridization and titration of viral PFU. HSV-2 infected mice developed severe necrotizing hepatitis with persistence of HSV in the liver tissue until the end of the study. HSV-1 infected mice rapidly eliminated the virus and revealed only small necrotic foci. Early phase alterations and necrotic phase lesions were distinguished and characterized and morphologic evidence of a direct cytopathic effect of HSV was detected. A specific immune reaction in late stages appeared to be mediated by T4-positive T-lymphocytes. In situ hybridization and immunohistochemistry showed a close correlation with virus titration and were valuable in characterizing early phases and in the assessment of prognosis and differential diagnosis.     

Neurokinin 1 receptor signaling affects the local innate immune defense against genital herpes virus infection

We show that genital infection with neurotropic HSV type 2 (HSV-2) induced a significant increase of the neuropeptide substance P (SP) within the genital tract of mice. SP was shown to weakly interfere with the HSV-2 replication. Furthermore, lack of SP signaling through the use of mice deficient in the SP receptor, neurokinin 1 receptor (NK1R), revealed an important role for SP in the innate defense against HSV-2. NK1R-deficient mice had significantly enhanced levels of HSV-2 in the genital tract and in the CNS following infection and a significantly accelerated disease progression, which was associated with an impaired NK cell activity locally in the vagina. Lack of NK1R signaling did, however, not impair the animals' ability to mount a protective immune response to HSV-2 following vaccination with an attenuated virus. Both NK1R+/+ and NK1R-/- mice developed strong HSV-2-specific Th1 T cell responses following vaccination. No genital viral replication was observed in either vaccinated NK1R-deficient or NK1R+/+ control animals following a genital HSV-2 challenge, and all of these animals survived without any symptoms of disease. In conclusion, the present results indicate that SP and NK1R signaling contributes to the innate resistance against HSV-2 infection in mice.