穿山甲主要食物营养成分研究

穿山甲（Ｍａｎｉｓｐｅｎｔａｄａｃｔｙｌａ）为国家Ⅱ级保护动物,主要分布于长江以南各省区的丘陵山地。由于穿山甲被视为滋补和药用珍品,又无有效的保护措施,遭到乱捕滥猎;加上山地林木被砍伐,使穿山甲的衍生地不断减少,目前各地区穿山甲资源都面临绝境。因此,研究穿山甲的繁衍已十分必要和迫切。近年来,许多学者进行过人工养殖的研究（顾文仪,１９８３;梁庭敏,１９９６）,但迄今均没有完全成功的先例,其中关键的因素是穿山甲的人工食物难以解决。配制的人工混合饲料,往往造成穿山甲拒食或不适应,患胃肠疾病死亡。因此,…     

Mechanism of action of GTP in the induction of Ca2+ release from hepatic microsomes

The mechanism by which GTP induces Ca2+ release from Ca2(+)-preloaded rat hepatic microsomes was studied. In the same concentration range as that for Ca2+ release, GTP inhibited the initial rate of ATP-driven Ca2+ uptake. It also inhibited the formation by ATP of the phosphorylated intermediate of Ca2(+)-ATPase, which had previously been identified by us as a 97-116 kDa protein (Fleschner, C.R., et al. (1985) Biochem. J. 226, 839). Vanadate, an inhibitor of Ca2(+)-ATPase, also caused Ca2+ release in a similar fashion, but its effect was not additive to that of GTP. Although the non-metabolizable GTP analogues, GMPPNP and GTP gamma S, did not cause Ca2+ release by themselves, GTP gamma S completely and GMPPNP partially blocked the effect of GTP. Pretreatment of vesicles with either cholera or pertussis toxin did not alter the responsiveness to GTP. These results indicate that GTP inhibits microsomal Ca2(+)-ATPase, independently of the Gs and Gi proteins. Because a decrease in Ca2+ uptake results in a net increase in Ca+ release, this effect of GTP seems to account, at least partially, for the GTP-induced Ca2+ release from microsomes.     

多重聚合酶链反应与荚膜肿胀试验对肺炎链球菌血清分型的比较研究

为评估多重聚合酶链反应（PCR ）对肺炎链球菌血清分型的可行性,分别采用多重PCR和荚膜肿胀试验对568株肺炎链球菌进行血清分型,并对分型结果进行比较分析。结果显示,568株肺炎链球菌中,213株通过荚膜肿胀试验分出16个血清群,主要有血清群19（23．1％,131／568）、6（5．3％,30／568）、23（1．6％,9／568）、14（1．4％,8／568）、9（1．1％,6／568）、15（1．1％,6／568）等,分型率为37．5％（213／568）;356株通过多重PCR分出21个血清群,主要有血清群19（27．8％,158／568）、23（8．5％,48／568）、6（7．4％,42／568）、14（4．4％,25／568）、3（4．2％,24／568）、15（3．5％,20／568）等,分型率为62．7％（356／568）。荚膜肿胀试验鉴定出血清群4和18,但多重PCR未能鉴定;多重PCR鉴定出血清群5、12、35、16、17和22,但荚膜肿胀试验未能鉴定。多重PCR与荚膜肿胀试验对19F、19A血清型的鉴定无显著差异。结果提示,这2种方法对肺炎链球菌血清分型结果有差别,多重PCR的分型率高于荚膜肿胀试验。对来源复杂的标本进行肺炎链球菌血清分型,2种方法可相互补充,以提高分型率。     

红芽芋球茎片两步法离体快繁及其再生苗生理和光合特性研究

以江西铅山红芽芋(Colocasia esculenta L.Schott var.cormosus‘Hongyayu’)试管苗为材料,建立了芋球茎片两步法离体快繁体系,并对其再生苗的形态指标、染色体数目、生理和光合特性以及叶绿素荧光特性进行了检测。结果表明:(1)红芽芋球茎片单芽诱导的最佳培养基为MS+KT 2 mg/L+6-BA 1 mg/L+NAA0.1mg/L,诱导培养30d后将单芽从球茎片上分离,再接种到生根培养基(MS+KT 2mg/L+NAA 0.1mg/L)上培养30d即可形成完整植株,移栽成活率高达98%;(2)由球茎片单芽、丛生芽、不定芽离体快繁获得的红芽芋再生苗在形态指标、叶下表皮气孔参数、染色体数目、生理生化指标以及叶片光合特性参数和叶绿素荧光特性方面均无显著差异。说明红芽芋球茎片两步法离体培养的再生苗繁殖系数高、染色体数目稳定,该离体快繁体系可应用于江西铅山红芽芋的工厂化生产。     

不明原因男性不育人群中睾丸特异性乳酸脱氢酶基因突变的发现及其意义

为了研究睾丸特异性乳酸脱氢酶,即乳酸脱氢酶C4(LDH-C4)基因突变在男性不育发病中的作用,利用LDH-C4特异性底物对100名不明原因男性不育症患者的精子LDH-C4进行活性显色,用变性高效液相色谱(DHPLC)技术对LDH-C4活性低下的患者进行LDHC基因PCR产物的突变筛查,对DHPLC峰形异常的PCR产物进行序列测定.筛选到一组精子LDH-C4活性明显下降的患者,其中1名患者的LDHC基因PCR产物在DHPLC中呈异常洗脱峰.对这一PCR产物进行序列测定,发现患者LDHC基因第5外显子的115位碱基发生了T→A的杂合改变(GenBank登录号GU479375),该突变使LDHC基因的178位密码子由原来的TTG(编码亮氨酸)变为TAG(终止密码子),形成截短的C亚基.T克隆-测序进一步证实了该无义突变的杂合状态.这是在人类LDHC基因上发现的第一个突变,提示LDHC基因突变可能是男性不育发病的原因之一.     

青海湟水流域蝶类

1995～2003年调查并整理分析青海湟水流域的蝶类,有9科52属80种,其中凤蝶科1属2种,绢蝶科1属6种,粉蝶科8属22种,斑蝶科1属1种,眼蝶科12属13种,蛱蝶科15属18种,蚬蝶科1属3种,灰蝶科9属10种,弄蝶科4属5种.以古北界为主,青藏区最为丰富.     

Analysis of metal-induced DNA lesions and DNA-repair replication in mammalian cells

The potency of several metal compounds in causing lesions in DNA either directly or by exposure of intact cultured cells has been examined using the neutral conditions of nucleoid gradient sedimentation. HgCl2 was clearly the most potent inducer of single-strand breakage when added to isolated nucleoids or when nucleoids were prepared from cells treated with this compound. CaCrO4 , however, caused DNA-strand breaks in nucleoids isolated from cells treated with this agent but did not induce DNA strand breaks when added directly to nucleoids. Although less potent than HgCl2, NiCl2 also caused significant single strand breakage in isolated nucleoids or in nucleoids prepared from cells treated with this metal. Since strand breakage of DNA in intact cells may occur secondary to activation of DNA-dependent nucleases during repair replication, CsCl gradient density sedimentation was utilized to examine whether repair processes were induced by exposure of cells to NiCl2, HgCl2 and CaCrO4 . CaCrO4 and NiCl2 induced substantial DNA-repair activity at concentrations and exposure times where DNA lesions could not be detected whereas HgCl2 induced a 10-fold lower level of DNA-repair activity compared to CaCrO4 at optimal concentrations which again were below the concentrations of this metal that produced measurable DNA lesions. Both the induction of DNA-repair activity and DNA-strand breakage by these metals was concentration- and time-dependent. These results demonstrate some unique aspects of the interaction of HgCl2, NiCl2 and CaCrO4 with the DNA of intact cells and point to the possible important correlation of induction of DNA repair to carcinogenesis since nickel and chromate have clearly been implicated as carcinogens and induce considerable repair whereas HgCl2 is not considered a carcinogen and induces the least DNA repair despite its potency in producing DNA lesions.     

Generation and characterization of a recombinant vesicular stomatitis virus expressing the glycoprotein of Borna disease virus

Borna disease virus (BDV) is an enveloped virus with a nonsegmented negative-strand RNA genome whose organization is characteristic of mononegavirales. However, based on its unique genetics and biological features, BDV is considered to be the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales. BDV cell entry occurs via receptor-mediated endocytosis, a process initiated by the recognition of an as yet unidentified receptor at the cell surface by the BDV surface glycoprotein (G). The paucity of cell-free virus associated with BDV infection has hindered studies aimed at the elucidation of cellular receptors and detailed mechanisms involved in BDV cell entry. To overcome this problem, we generated and characterized a replication-competent recombinant vesicular stomatitis virus expressing BDV G (rVSVDeltaG*/BDVG). Cells infected with rVSVDeltaG*/BDVG produced high titers (10(7) PFU/ml) of cell-free virus progeny, but this virus exhibited a highly attenuated phenotype both in cell culture and in vivo. Attenuation of rVSVDeltaG*/BDVG was associated with a delayed kinetics of viral RNA replication and altered genome/N mRNA ratios compared to results for rVSVDeltaG*/VSVG. Likewise, incorporation of BDV G into virions appeared to be restricted despite its high levels of expression and efficient processing in rVSVDeltaG*/BDVG-infected cells. Notably, rVSVDeltaG*/BDVG recreated the cell tropism and entry pathway of bona fide BDV. Our results indicate that rVSVDeltaG*/BDVG represents a unique tool for the investigation of BDV G-mediated cell entry, as well as the roles of BDV G in host immune responses and pathogenesis associated with BDV infection.     

15年前后细菌L型临床耐药性的变迁

目的检测15年前后细菌L型临床耐药性的变迁,分析影响因素,指导临床用药。方法对新乡市中心医院15年来临床检出的常见细菌L型菌株逐个进行药敏监测,逐年进行耐药性变化分析研究。结果1990年至1999年细菌L型常见菌株耐药性逐年上升,特别是青霉素类大部耐药;2000年至2005年,耐药性趋势变缓,青霉素类耐药率有所下降。结论合理应用抗生素,不滥用抗生素是细菌L型耐药性变迁的重要原因,药物敏感试验是良好的监测方法。