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.     

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).     

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…     

Activation of Protein Kinase C Augments Peptide Release from Rat Sensory Neurons

Abstract: To determine whether protein kinase C (PKC) mediates release of peptides from sensory neurons, we examined the effects of altering PKC activity on resting and evoked release of substance P (SP) and calcitonin gene-related peptide (CGRP). Exposing rat sensory neurons in culture to 10 or 50 n M phorbol 12,13-dibutyrate (PDBu) significantly increased SP and CGRP release at least 10-fold above resting levels, whereas the inactive 4α-PDBu analogue at 100 n M had no effect on release. Furthermore, 100 n M bradykinin increased peptide release approximately fivefold. Down-regulation of PKC significantly attenuated the release of peptides evoked by either PDBu or bradykinin. PDBu at 1 n M or 1-oleoyl-2-acetyl- sn -glycerol at 50 µ M did not alter resting release of peptides, but augmented potassium- and capsaicin-stimulated release of both SP and CGRP approximately twofold. This sensitizing action of PKC activators on peptide release was significantly reduced by PKC down-regulation or by pretreating cultures with 10 n M staurosporine. These results establish that activation of PKC is important in the regulation of peptide release from sensory neurons. The PKC-induced enhancement of peptide release may be a mechanism underlying the neuronal sensitization that produces hyperalgesia.     

Transient receptor potential vanilloid 1, calcitonin gene-related peptide, and substance P mediate nociception in acute pancreatitis

The mechanism of pancreatitis-induced pain is unknown. In other tissues, inflammation activates transient receptor potential vanilloid 1 (TRPV1) on sensory nerves to liberate CGRP and substance P (SP) in peripheral tissues and the dorsal horn to cause neurogenic inflammation and pain, respectively. We evaluated the contribution of TRPV1, CGRP, and SP to pancreatic pain in rats. TRPV1, CGRP, and SP were coexpressed in nerve fibers of the pancreas. Injection of the TRPV1 agonist capsaicin into the pancreatic duct induced endocytosis of the neurokinin 1 receptor in spinal neurons in the dorsal horn (T10), indicative of SP release upon stimulation of pancreatic sensory nerves. Induction of necrotizing pancreatitis by treatment with L-arginine caused a 12-fold increase in the number of spinal neurons expressing the proto-oncogene c-fos in laminae I and II of L1, suggesting activation of nociceptive pathways. L-arginine also caused a threefold increase in spontaneous abdominal contractions detected by electromyography, suggestive of referred pain. Systemic administration of the TRPV1 antagonist capsazepine inhibited c-fos expression by 2.5-fold and abdominal contractions by 4-fold. Intrathecal, but not systemic, administration of antagonists of CGRP (CGRP(8-37)) and SP (SR140333) receptors attenuated c-fos expression in spinal neurons by twofold. Thus necrotizing pancreatitis activates TRPV1 on pancreatic sensory nerves to release SP and CGRP in the dorsal horn, resulting in nociception. Antagonism of TRPV1, SP, and CGRP receptors may suppress pancreatitis pain.     

Activation of transient receptor potential ankyrin 1 evokes nociception through substance P release from primary sensory neurons

To examine mechanisms underlying substance P (SP) release from primary sensory neurons in response to activation of the non-selective cation channel transient receptor potential ankyrin 1 (TRPA1), SP release from cultured rat dorsal root ganglion neurons was measured, using radioimmunoassay, by stimulating TRPA1 with allyl isothiocyanate (AITC), a TRPA1 agonist. AITC-evoked SP release occurred in a concentration- and time-dependent manner. Interestingly, p38 mitogen-activated protein kinase (p38) inhibitor SB203580 significantly attenuated AITC-evoked SP release. The in vivo effect of AITC-evoked SP release from primary sensory neurons in mice was evaluated. Hind paw intraplantar injection of AITC induced nociceptive behaviors and inflammation (edema, thermal hyperalgesia). AITC-induced thermal hyperalgesia and edema were inhibited by intraplantar pre-treatment with either SB203580 or neurokinin-1 receptor antagonist CP96345. Moreover, intrathecal pre-treatment with either CP96345 or SB203580 inhibited AITC-induced nociceptive behaviors and thermal hyperalgesia. Immunohistochemical studies demonstrated that intraplantar AITC injection induced the phosphorylation of p38 in mouse dorsal root ganglion neurons containing SP. These findings suggest that activation of TRPA1 evokes SP release from the primary sensory neurons through phosphorylation of p38, subsequent nociceptive behaviors and inflammatory responses. Furthermore, the data also indicate that blocking the effects of TRPA1 activation at the periphery leads to significant antinociception.     

Sensory nerve induced inflammation contributes to heterotopic ossification

Heterotopic ossification (HO), or bone formation in soft tissues, is often the result of traumatic injury. Much evidence has linked the release of BMPs (bone morphogenetic proteins) upon injury to this process. HO was once thought to be a rare occurrence, but recent statistics from the military suggest that as many as 60% of traumatic injuries, resulting from bomb blasts, have associated HO. In this study, we attempt to define the role of peripheral nerves in this process. Since BMP2 has been shown previously to induce release of the neuroinflammatory molecules, substance P (SP) and calcitonin gene related peptide (CGRP), from peripheral, sensory neurons, we examined this process in vivo. SP and CGRP are rapidly expressed upon delivery of BMP2 and remain elevated throughout bone formation. In animals lacking functional sensory neurons (TRPV1(-/-) ), BMP2-mediated increases in SP and CGRP were suppressed as compared to the normal animals, and HO was dramatically inhibited in these deficient mice, suggesting that neuroinflammation plays a functional role. Mast cells, known to be recruited by SP and CGRP, were elevated after BMP2 induction. These mast cells were localized to the nerve structures and underwent degranulation. When degranulation was inhibited using cromolyn, HO was again reduced significantly. Immunohistochemical analysis revealed nerves expressing the stem cell markers nanog and Klf4, as well as the osteoblast marker osterix, after BMP2 induction, in mice treated with cromolyn. The data collectively suggest that BMP2 can act directly on sensory neurons to induce neurogenic inflammation, resulting in nerve remodeling and the migration/release of osteogenic and other stem cells from the nerve. Further, blocking this process significantly reduces HO, suggesting that the stem cell population contributes to bone formation.     

Formation of Neuromuscular Junctions and Synthesis of Sensory Neuropeptides in the Co-cultures of Dorsal Root Ganglion and Cardiac Myocytes

Aim The interactions between primary sensory neurons and cardiac myocytes are still unclear. In the present study, the co-culture model of dorsal root ganglion (DRG) explant and cardiac myocytes was used to characterize the morphological relationship between primary sensory nerve endings and cardiac myocytes and to investigate whether cardiac myocytes could induce substance P (SP) and calcitonin gene-related peptide (CGRP) synthesis in DRG neurons and release from DRG neurons in the neuromuscular co-cultures. Methods The formation of neuromuscular junctions was observed with scanning electron microscopy (SEM). SP and CGRP expression were detected by immunocytochemistry. Basal SP and CGRP release and capsaicin-evoked SP and CGRP release were analyzed by radioimmunoassay (RIA). Results In this study, neuromuscular junctions were observed in the co-cultures of DRG explant and cardiac myocytes. SP-immunoreactive (IR) and CGRP-IR neurons were detected in both neuromuscular co-cultures and DRG explant cultures, but the number of SP-IR and CGRP-IR neurons migrating from DRG explant was significantly increased in neuromuscular co-cultures. Capsaicin-evoked SP and CGRP release but not basal SP and CGRP release in neuromuscular co-cultures increased significantly as compared with that in the cultures of DRG explant alone. Conclusions The results implicated that the morphological relationship between sensory nerve terminal and cardiac myocyte is much more close in vitro than it is in vivo. Cardiac myocytes may induce sensory neuropeptide synthesis and capsaicin-evoked neuropeptide release in neuromuscular co-cultures. Further experiment needs to be performed about the significance of neuropeptide synthesis and capsaicin-evoked neuropeptide release induced by target cardiac myocytes. Zhen Liu and Huaxiang Liu contributed equally to this article.     

Nuclear Localization of SP, CGRP, and NK 1 R in a Subpopulation of Dorsal Root Ganglia Subpopulation Cells in Rats

Signals generated by renal pelvic afferent nerves in response to stimulation are transmitted from peripheral processes of dorsal root ganglia neurons to their central terminals in the dorsal horn of the spinal cord to cause the release of neuropeptides, including SP and CGRP. All of the cellular activities of SP are considered to be mediated through interaction with NK₁R located on the cell surface. We have investigated the colocalization and subcellular distribution of NK₁R, SP, and CGRP in different subpopulations of neurons that innervate renal tissue. Our findings therefore provide the first evidence for the presence of NK₁R, SP, and CGRP in the nuclei of DGR neural cells. The physiological significance of this localization remains unknown. One possibility is that pelvic sensory neurons may regulate their responses to different stimuli by modulating the ratio of CGRP and SP release and/or nuclear NK₁R expression.     

Distribution and ontogeny of SP, CGRP, SOM, and VIP in chick sensory and sympathetic ganglia

The distribution and ontogeny of four neuropeptides in developing chick lumbosacral sensory and sympathetic ganglia were studied using immunohistochemical techniques. Antibodies to two of these peptides, substance P (SP) and calcitonin gene-related peptide (CGRP), stained small neurons in the medial part of the dorsal root ganglia from embryonic Day 5 and Day 10, respectively, whereas neurons in the lateral part of the ganglia were negative; this distribution persisted throughout development. Both sets of neurons apparently send fibers to the dorsal horn of the spinal cord: SP to laminae I and II, and CGRP to lamina I, suggesting that the SP- and CGRP-positive sensory neurons are nociceptive or thermoreceptive. This correlation between the presence of SP or CGRP in a neuron and a particular functional modality thus provides evidence for a functional distinction between the mediodorsal and ventrolateral zones that are apparent during the development of chick dorsal root ganglia. Moreover, this study suggests that the type of neuron that develops within the dorsal root ganglion correlates with its position within the ganglion. In contrast to SP and CGRP, somatostatin (SOM) and vasoactive intestinal polypeptide (VIP) immunoreactivities were not seen in the lumbosacral sensory ganglia at any stage during development. However, both were present in sympathetic ganglia: SOM from embryonic Day 4.5 and VIP from embryonic Day 10. VIP immunoreactivity persisted throughout development in a large number of sympathetic neurons, but the number of cells with SOM immunoreactivity decreased from embryonic Day 10 onward. SOM therefore appears to be present only transiently in most chick lumbosacral sympathetic cells.     

Functional interaction between transforming growth factor alpha and capsaicin-sensitive sensory neurons in the rat stomach

BACKGROUND AND AIMS: Transforming growth alpha (TGFalpha) and sensory neurons have been shown to promote gastric mucosal protection and healing. Aims were to examine in vitro interactions between gastric sensory neurons, the sensory neuropeptide calcitonin gene-related peptide (CGRP), and TGFalpha. METHODS: Gastric mucosal/submucosal tissue fragments from Sprague-Dawley (SD) rats were incubated in short-term (30 min) culture. Peptide release into media and TGFalpha tissue content were measured by radioimmunoassay. RESULTS: TGFalpha (1 x 10(-8) to 1 x 10(-6) M) caused dose-dependent stimulation of CGRP release. Maximal CGRP release (+87%) was observed with 1 x 10(-6) M TGFalpha: 28.6+/-3.8 vs. control of 15.5+/-2.7 pg/g tissue; P<0.05. Both CGRP (1 x 10(-7) to 1 x 10(-5) M) and capsaicin (1 x 10-(8) to 1 x 10(-6)M) significantly inhibited basal TGFalpha release in a dose-dependent fashion that ranged from -20% to -39%. In contrast, capsaicin-induced sensory denervation caused significant increases in both basal TGFalpha release and TGFalpha tissue content. CONCLUSION: Function interactions between TGFalpha and gastric sensory neurons are suggested by the observations that (1) TGFalpha stimulated CGRP release from gastric sensory neurons; (2) CGRP and acute capsaicin treatment inhibited TGFalpha release and; (3) capsaicin-induced sensory denervation caused significant increases in both gastric TGFalpha basal release and tissue content.     

Nociceptive neurons detect cytokines in arthritis

Proinflammatory cytokines are major mediators in the pathogenesis of diseases of joints such as rheumatoid arthritis and osteoarthritis. This review emphasizes that proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1beta, interleukin-6 and interleukin-17 are also mediators of pain by directly acting on the nociceptive system. Proportions of nociceptive sensory neurons express receptors for these cytokines, and the application of cytokines rapidly changes the excitability, ion currents and second messenger systems of these neurons. By inducing persistent sensitization of nociceptive sensory neurons (C- and a proportion of Aδ-fibers) for mechanical stimuli in the joint (a process called peripheral sensitization), these cytokines significantly contribute to the persistent hyperalgesia typical for many disease states of the joint. In addition, the disease-associated release of cytokines in the spinal cord supports the generation of central sensitization. The therapeutic neutralization of proinflammatory cytokines thus not only reduces the process of inflammation but may directly reduce hyperalgesia and pain by reversing the neuronal effects of cytokines. It is emerging that different cytokines have different actions on neurons. The neutralization of tumor necrosis factor-alpha reduces both mechanical and thermal hyperalgesia of the joint. The neutralization of interleukin-1beta attenuates thermal hyperalgesia whereas the neutralization of interleukin-6 and interleukin-17 mainly reduces mechanical hyperalgesia. These different effects are partly explained by influencing different target molecules in sensory neurons. For example, in cultured sensory neurons tumor necrosis factor-alpha and interleukin-1beta upregulate the TRPV1 ion channel, which is involved in the transduction of heat stimuli, consistent with an effect of these cytokines in thermal hyperalgesia. By contrast, interleukin-17 upregulates the TRPV4 ion channel, which has a role in the transduction of mechanical stimuli. Thus, the analgesic potential of neutralizing cytokines seems to depend on which cytokine is mainly involved in the particular pain state.