昆虫学名中属名和种名的属性

<正> 采用双名法命名生物,一般包括一个名词的属名和一个形容词的神名.例如意大利蜜蜂Apt。。。Ilif。,a L.、葡萄十星甲虫 Oidc。dccc-。pu。c。。。。Billb.;但是,少数属名是名词而种名也是名词。例如牛羽虱Bo。icola ho。i。(L.)、狗林头蚤 c。,,co。p4。l。pos ca。。。(nit1S卜··。 拉丁文及拉丁化的其他文字,名词和形容词都有文法性的,阳性、阴性、中性三者,各从词尾表现出,阳性词尾为:-u。、-or、-7r、-o’、-”、。O。等;阴性词尾为:-。、-。、-S、-x、-cs、-。s、-eo。-。G、-。。等;中性词尾为:-。m、-G。、-O。、。。r、-ar、-ma、J。、-r。、J、-。、-C等,其中阳性词尾较多用一us,阴性词尾用一a,中性词尾用一。。,总的用一a为最多。     

美生物工学公司的财政数据,1982(百万美元)

公司名NOVO Industri介eh America GrouPGenenteehCetUSCollagen合作研究公司Hybritech50以he饥Biotech分子遗传学公司CytoxEnz。生化公司遗传工程公司Ribi免疫化学公司单克隆抗体公司Bio ResPonse52/81赚 56。7 %82/81 22 0。941084081上八bC︸厅‘OOn舀Q︺︸8 :。..…n,﹄O八On︸ot了,曰qU 一﹄一一出售额%324。2637.4 2328。89016。0 627。4 2756。5 904。8 1681。5 541。1 1461。1一20。9 420。5 1910。3 780。1 88一1.4一一1。3一一1。1一一0。3,一1。1一一1。6一美生物工学公司的财政数据,1982(百万美元)@聂世芳…     

我国部分城市市花一览

一市两种市花的: 北京月季、菊花。青岛耐冬、月季。南昌月季、金边瑞香。芜湖月季、菊花。新乡月季、石榴。信阳紫薇、月季。恩施月季、桂花。济宁荷花、月季。无锡杜鹃花、梅花。合肥石榴、桂花。肇庆荷花、鸡蛋花。一市一种市花的:     

光系统Ⅱ颗粒放氧的钙激活和钙定位

1IntroductionTheoxyg6n－evolvingco…。（OEC）ofphotosystem11（ppfi）isahighlycideredstructllleofvanouspolpotideswhichp～dethebindingsltesfortheInompccofactorsandmedi-atetheactionofthem．（GhanotaldsandYoc1990,DebuS1992,Yoc1991）．Thep。essof…。lutiontakesplaceinmD。arthel。佃。－faceofthethylakoidmembrane．Itis“v。byl…恤mpresfo。。－ganese,2。3calciumandsevendCIions．OfthetllleekindsOfionsinvolvedinthephotOSyntheticsPlittingofwater,陶峙见。［［ene——。Ivelyc佃n－tenzed（Ghanota…     

八类特种养殖品在海外走俏

据外贸部门有关资料介绍,近两年有如下特种养殖产品在国外走俏,可以适时发展: 1.甲鱼。国内外均为席上佳品。2.泥鳅。日本可年耗4000余吨,大部分从我国进口。3.金钱龟。一些国家招待贵客不可少。4.蛇。香港每年耗活蛇50万条,冻蛇肉数十吨。5.黄鳝。国际市场走俏。6.鸭。鸭舌、鸭掌、鸭内脏被视为席上珍品,价格昂贵。7.蚕品。蚕丝织品在世界市场上常年不衰。8.长毛兔。需求量与日俱增。     

Exact Controllability of Age-Structured Predator-Prey Populations

1IntroductionT5e劝dysisd8贝ami。dpTdatO。preynit。ti。is4iquitousinthebiologicalworldandlsd。id既曲ienit。estan6ipeceto。IOgy．Thetheoretidstudydpredation晌hadahghistoryho。lugwiththe。nalworkofInne．aandVolt。,andcontin。tobeofwid聊readinterest咖y．仇iiithelateof1980’s,most…ator－pteystUdieshavebudonInteractingspedeswithoutsg。sin．－Cture（forexmple,sce［1」,［2」,［3」and［4］）．HOwever,asthelin阿mceof明卜s刎cmreInpoPulaMnhasbecomemorewidelyrecognized,thereisanIn－er。lugnum…     

六州歌头——乘东风 攀高峰

扫除妖魅,寰宇凯歌宏。篡权者,黄粱梦。彩霞飞,壮鲲鹏,蓬雀徒目送。忆导师,千秋颂。松柏青,鲜花盛,岁峥嵘。抓纲治国,决策雄威重,领袖英明。齐中华步伍,开始新长征,万里东风。战旗红。科学实验,人欢动。学大庆,志无穷。求红专,合工农,苦钻研,永不松。打好这一仗,现代化,出奇功。真战士,骨头硬,竞争锋。锦绣前程,展     

1991年第1期“高中毕业班生物检测题”参考答案

一、选择题 1 .D 2.C 3.B 4.C 5。A 6.C 7.CS。C 9。B 10.A 11。A 12.B 13。D 14。D 15。D 16。D 17。B 18。A 19.B20。B 21。B 22。C 23。B 24。D 25。B 26。C 27。A 28。D 29.C 30。C 31.B 32.D 33。A 34。D 35。D 二、简答题 36.水的光解葡萄糖和丙酮酸的分解37.70%95%ATP 38。(l)8283(2)第一营养级(绿色植物)(3)鹰增多,植物减少(4)田鼠数量变动而引起的39.(1)转氛基作用、缩合反应、脱氛基作用(2)尿素肝脏肾(3)CO:、H:O(4)脂肪糖类(5)食物通过转氛基作用体内蛋白质的水解40(l)①珍尸巢(2)②偷卵管(3)⑧子宫(4)胎膜子…     

Large-Scale Comparison Analysis of Genome Sequences

IIntMuctiona习nenC6allpoent13asenondynamiCpmpCgIsthemostWidely11。dllethed11。－quencecompgnsonatpresent．Wbenmpingon18I’ge一切degenomempence肛dyslswiththiskindofmethed,wefacetwomperdifficulties,the18ig6stompandtheIOllgmptationaltdrie．My。。dMill。［“spplyHi。比那’stecheniqJ‘、mpen。alipentpwhl。,wb。dgofl山mconsumeSpaceMypZ’Oportlonaltothesumd山eapuencelmphs．AnewpIOgTgnSIM”,utilizingthealgorithm,hasbeenueding。eequ。ceallpoent．How。,themptationaltimebySIMisstilltoolO…     

中国的驼鹿

驼鹿是鹿科中最大的动物。分布于我国大、小兴安岭及阿尔泰山。中国有３个亚种。它们的栖息地,可以划分为７种植被类型。草食性动物。食物种类在２５０种以上。食物中以树的枝条为主。一般在２．５岁左右开始繁殖。怀孕期２２５￣２３７天。产１￣２仔。此外,还介绍了驼鹿的行为、分类、分布和资源等。     

内源性一氧化碳在大鼠败血症休克时低血压发生机制中的作用

A sepsis model induced by cecal ligation and puncture was used to study the role of endogenous carbon monoxide in hypotension pathogenesis of rats during septic shock. After administration of zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG),an inhibitor of heme oxygenase (HO),blood pressure (BP),HO activity and carbon monoxide (CO) release from vascular muscle tissue were measured. The results showed that BP of sepsis rats, including systolic and diastolic arterial BP, decreased significantly while HO activity and CO content were significantly increased. In contrast, after administration of ZnDPBG, BP of sepsis rats was significantly increased while the HO activity and CO production were significantly decreased. These findings suggest that HO activity and CO release within vascular musculature are increased during septic shock; inhibition of HO may elevate BP of rats during septic shock through a decrease of endogenous CO production. It is concluded that endogenous CO derived from vascular muscle cells plays an important role in regulating vascular tone, and the up-regulation of HO activity followed by subsequent CO production contributes to hypotension pathogenesis during septic shock.     

内源性一氧化碳在大鼠败血症性休克时低血压发生机制中的作用

应用盲肠结扎法制备大鼠败血症休克模型,研究内源性一氧化碳（ＣＯ）在败血症休克时低血压发病中的作用。用血红素加氧酶（ｈｅｍｅｏｘｙｇｅｎａｓｅ,ＨＯ）抑制剂２,４二甘油次卟啉锌（ｚｉｎｃｄｅｕｔｅｒｏｐｏｒｐｈｙｒｉｎ２,４ｂｉｓｇｌｙｃｏｌ,ＺｎＤＰＢＧ）处理大鼠后,观察动物动脉血压,同时测定主动脉平滑肌组织中ＨＯ活性和ＣＯ生成量。结果发现：败血症大鼠动脉收缩压、舒张压降低,同时血管平滑肌ＨＯ活性和ＣＯ生成明显增加。败血症大鼠用ＺｎＤＰＢＧ处理后,动脉血压明显回升,同时ＨＯ活性和ＣＯ生成明显被抑制。实验表明败血症休克时低血压的发生与血管平滑肌细胞ＨＯ活性增加和内源性ＣＯ生成增多明显相关;应用ＨＯ抑制剂阻断ＨＯ活性能导致内源性ＣＯ生成减少,继而使败血症休克时大鼠血压明显回升。实验提示,内源性ＣＯ对血管张力具有重要的调节作用;ＨＯ活性和内源性ＣＯ生成增加是败血症休克时低血压发生的重要机制之一。     

内源性一氧化碳在大鼠败血症性休克时 低血压发生机制中的作用

A sepsis model induced by cecal ligation and puncture was used to study the role of endogenous carbon monoxide in hypotension pathogenesis of rats during septic shock. After administration of zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG),an inhibitor of heme oxygenase (HO),blood pressure (BP),HO activity and carbon monoxide (CO) release from vascular muscle tissue were measured. The results showed that BP of sepsis rats,including systolic and diastolic arterial BP,decreased significantly while HO activity and CO content were significantly increased. In contrast,after administration of ZnDPBG,BP of sepsis rats was significantly increased while the HO activity and CO production were significantly decreased. These findings suggest that HO activity and CO release within vascular musculature are increased during septic shock;inhibition of HO may elevate BP of rats during septic shock through a decrease of endogenous CO production. It is concluded that endogenous CO derived from vascular muscle cells plays an important role in regulating vascular tone,and the up-regulation of HO activity followed by subsequent CO production contributes to hypotension pathogenesis during septic shock.     

内源性一氧化碳与一氧化氮在高血压发病中的相互作用 …

目的和方法：采用ＨＯ活性抑制剂诱导大鼠高血压模型,观察血压变化、主动脉ＨＯ和ＮＯＳ活性、ＣＯ和ＮＯ产生释放,并测定血浆和主动脉平滑肌组织中ｃＧＭＰ含量,以探讨内源性ＮＯ和ＣＯ在高血压发生机制中的作用及其相互关系。结果：大鼠应用ＨＯ抑制剂ＺｎＤＰＢＧ腹腔注射２周后,继续饲养到第４周出现持续而稳定的高血压,同时总ＮＯＳ（ｔＮＯＳ）和诱导型ＮＯＳ（ｉＮＯＳ）的活性分别增加４５．４％和７３．３％（均为Ｐ〉     

内源性一氧化碳减轻大鼠双侧后肢缺血再灌注所致的肺损伤

通过观察血红素氧化酶（HO）阻断剂－－锌原卟啉（ZnPP)对肺组织、肺泡间质多形核白细胞数目肺组织丙二醛含量和湿重干重之比的影响,并对肺组织HO活性和血内碳氧血红蛋白水平（COHb）进行检测,以探讨内源性HO／一氧化碳（CO）在肢体缺血再灌注（I／R）所致肺损伤中的作用。结果发现,大鼠双侧后肢I／R可导致急性肺损伤,同时使肺组织中HO活性和血内COHb水平显著升高;应用ZnPP预处理可使HO活性和COHb水平显著降低,但肺损伤却进一步加重。上述实验结果表明,肢体I／R致肺损伤时,肺组织中HO活性和内源性CO生成增多或减轻大鼠肢体I／R所致的肺损伤。     

The regulating effect of heme oxygenase/carbon monoxide on hypoxic pulmonary vascular structural remodeling

Hypoxic pulmonary vascular structural remodeling (HPVSR) is the important pathologic basis of hypoxic pulmonary hypertension (HPH). The discoveries of endogenous gaseous messenger molecules, nitric oxide (NO) and carbon monoxide (CO), have been moving the research of HPVSR to a very new phase. But the effect and significance of heme oxygenase (HO)/CO on the development of HPVSR have not been fully understood. In this study, we observed the alteration of endogenous HO/CO system in five time points during 14 days and found that the content of CO in lung homogenates in rats with HPVSR increased in a time-dependent double-peak manner. Exogenous supply of ZnPP-IX, an inhibitor of HO-1, decreased the content of CO in lung homogenate, decreased the expression of Fas and apoptotic cells in pulmonary artery smooth muscle cells (PASMCs), up-regulated the expression of PCNA in PASMCs, and worsened HPH and HPVSR of hypoxic rats. Meanwhile, exogenous supply of CO played an adverse action. The results showed that the up-regulation of HO/CO exerted a protective role in the development of HPVSR.     

Metabolic syndrome increases endogenous carbon monoxide production to promote hypertension and endothelial dysfunction in obese Zucker rats

Vascular heme oxygenase (HO) metabolizes heme to form carbon monoxide (CO). Increased heme-derived CO inhibits nitric oxide synthase and can contribute to hypertension via endothelial dysfunction in Dahl salt-sensitive rats. Obese Zucker rats (ZR) are models of metabolic syndrome. This study tests the hypothesis that endogenous CO formation is increased and contributes to hypertension and endothelial dysfunction in obese ZR. Awake obese ZR showed increased respiratory CO excretion, which was lowered by HO inhibitor administration [zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG) 25 micromol.kg(-1).24 h(-1) ip]. In awake obese ZR, chronically instrumented with femoral arterial catheters, blood pressure was elevated but was decreased by the HO inhibitor ZnDPBG. Body weight, blood glucose, glycated hemoglobin, plasma insulin, total and LDL cholesterol, oxidized LDL, and triglyceride levels were elevated in obese ZR, and, except for LDL cholesterol, were unchanged by HO inhibition. Total HO-1 protein levels were not different between lean and obese ZR aortas. In vitro experiments used isolated skeletal muscle arterioles with constant pressure and no flow, or constant midpoint, but altered endpoint pressures to establish graded levels of luminal flow. In obese ZR arterioles, responses to ACh and flow were attenuated. Acute in vitro pretreatment with an HO inhibitor, chromium mesoporphyrin, enhanced ACh and flow-induced dilation and abolished the differences between groups. Furthermore, exogenous CO prevented the restoration of flow-induced dilation by the HO inhibitor in obese ZR arterioles. These results suggest that HO-derived CO production is increased and promotes hypertension and arteriolar endothelial dysfunction in obese ZR with metabolic syndrome independent of affecting metabolic parameters.     

Alterations in heme oxygenase/carbon monoxide system in pulmonary arteries in hypertension

Enhancement of the heme oxygenase/carbon monoxide (HO/CO) system has been shown to lower blood pressure (BP) in young (8 weeks), but not in adult (20 weeks) spontaneously hypertensive (SHR) rats. The reasons for this selective effect still remain puzzling. We investigated the effects of hemin on the HO/CO system of the pulmonary artery (PA) in SHR and Wistar-Kyoto (WKY) rats at different ages and evaluated the hemin-dependent changes in sGC and cGMP pathways. Hemin administration resulted in an evident reduction of BP (from 148.6 +/- 3.2 to 125.8 +/- 2.6 mmHg, P < 0.01) in young, but not in prehypertensive (4 weeks) or adult SHR or WKY rats at all ages. Coadministration of the HO inhibitor, chromium mesoporphyrin, with hemin, cancelled the BP-lowering effect of hemin. Remarkably, lower expression levels of HO-1, HO-2, and sGC paralleled with reduced HO activity and cGMP content were observed in PA from 8-week SHR rats, but not from adult SHR or WKY rats of all ages. Interestingly, hemin treatment restored these deficiencies, although the expression level of non-inducible HO-2 protein remained unchanged. We conclude that in young and prehypertensive SHR rats, an impaired HO/CO-sGC/cGMP system in the PA might be indicative of the pathogenesis and development of hypertension. In contrast, the HO/CO system in the PA of adult SHR rats was upregulated as a compensatory reaction to elevated BP and desensitization of the downstream targets of the sGC/cGMP pathway occurred.     

Inhibition of heme oxygenase augments tubular sodium reabsorption

Heme oxygenase (HO) catalyzes the degradation of heme to form iron, biliverdin, and carbon monoxide (CO). The vascular actions of CO include direct vasodilation of vascular smooth muscle and indirect vasoconstriction through inhibition of nitric oxide synthase (NOS). This study was performed to examine the effects in the kidney of inhibition of heme oxygenase alone or combined with NOS inhibition. Chromium mesoporphyrin (CrMP; 45 μmol/kg ip), a photostable HO inhibitor, was given to control rats and N(G)-nitro-l-arginine methyl ester (l-NAME)-treated hypertensive rats (50 mg·kg?1·day?1), 12 h, 4 days). In control animals, CrMP decreased CO levels, renal HO-1 levels, urine volume, and sodium excretion, but had no effect on arterial pressure, renal blood flow (RBF), plasma renin activity (PRA), or glomerular filtration rate (GFR). In l-NAME-treated hypertensive rats, CrMP decreased endogenous CO and renal HO-1 levels and had no effect on arterial pressure, RBF, or GFR but decreased sodium and water excretion in a similar manner to control animals. An increase in PRA was observed in untreated rats but not in l-NAME-infused rats, indicating that this effect is associated with an absent NO system. The results suggest that inhibition of HO promotes water and sodium excretion by a direct tubular action that is independent of renal hemodynamics or the NO system.