排序方式: 共有37条查询结果,搜索用时 31 毫秒
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胡子鲶(Claris fuscus Lacepede)雄性泌尿系统组织学的观察研究 总被引:3,自引:1,他引:2
对胡子鲶(Claris fuscus Lacepede)泌尿系统,即肾脏、输尿管、膀胱以及尿道的组织学特征进行了初步观察和研究。结果表明,胡子鲶泌尿系统组织学特征与鲤科(Cyprinider)鱼类泌尿系统组织学特征大致相同,但也有一定区别。为今后鲶亚目(Siluroidei)鱼类的研究和养殖,提供一定的参考资料。 相似文献
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杨雪特 《重庆大学学报(自然科学版)》2002,25(6):35-38
文章为了精确地求出一个直线加速运动荷电黑洞时空中的粒子能级 ,并在此基础之上 ,对此黑洞视界附近的粒子能级的分布特征进行研究 ,从而搞清楚此黑洞的非热辐射特征。作者采用在直线加速运动荷电黑洞时空中求解Hamilton -Jacobi方程 ,并采用广义的乌龟坐标变换将Havnilton -Jacobi方程变成乌龟坐标下的形式 ,以便求出粒子广义动量的径向分量 ,进一步求出粒子能量 ,有了粒子的能量表达式便可以研究此黑洞视界附近的能级及此黑洞的非热辐射。结果表明 ,粒子能级分布与黑洞荷电产生的电磁四维势有关 ,还与黑洞的蒸发率等因素有关 ,黑洞非热辐射粒子的能量范围与四维电磁势的A0 和A1分量有关 ,还与黑洞的蒸发率 ( rH)有关。因此 ,此黑洞有非热辐射 ,辐射粒子的能量范围与A0 、A1和 rH 有关 相似文献
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'Inverse' melting of a vortex lattice 总被引:1,自引:0,他引:1
Avraham N Khaykovich B Myasoedov Y Rappaport M Shtrikman H Feldman DE Tamegai T Kes PH Li M Konczykowski M van der Beek K Zeldov E 《Nature》2001,411(6836):451-454
Inverse melting is the process in which a crystal reversibly transforms into a liquid or amorphous phase when its temperature is decreased. Such a process is considered to be very rare, and the search for it is often hampered by the formation of non-equilibrium states or intermediate phases. Here we report the discovery of first-order inverse melting of the lattice formed by magnetic flux lines in a high-temperature superconductor. At low temperatures, disorder in the material pins the vortices, preventing the observation of their equilibrium properties and therefore the determination of whether a phase transition occurs. But by using a technique to 'dither' the vortices, we were able to equilibrate the lattice, which enabled us to obtain direct thermodynamic evidence of inverse melting of the ordered lattice into a disordered vortex phase as the temperature is decreased. The ordered lattice has larger entropy than the low-temperature disordered phase. The mechanism of the first-order phase transition changes gradually from thermally induced melting at high temperatures to a disorder-induced transition at low temperatures. 相似文献
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N de Wind M Dekker N Claij L Jansen Y van Klink M Radman G Riggins M van der Valk K van't Wout H te Riele 《Nature genetics》1999,23(3):359-362
Cancer predisposition in hereditary non-polyposis colon cancer (HNPCC) is caused by defects in DNA mismatch repair (MMR). Mismatch recognition is attributed to two heterodimeric protein complexes: MutSalpha (refs 2, 3, 4, 5), a dimer of MutS homologues MSH2 and MSH6; and MutSbeta (refs 2,7), a dimer of MSH2 and MSH3. These complexes have specific and redundant mismatch recognition capacity. Whereas MSH2 deficiency ablates the activity of both dimers, causing strong cancer predisposition in mice and men, loss of MSH3 or MSH6 (also known as GTBP) function causes a partial MMR defect. This may explain the rarity of MSH6 and absence of MSH3 germline mutations in HNPCC families. To test this, we have inactivated the mouse genes Msh3 (formerly Rep3 ) and Msh6 (formerly Gtmbp). Msh6-deficient mice were prone to cancer; most animals developed lymphomas or epithelial tumours originating from the skin and uterus but only rarely from the intestine. Msh3 deficiency did not cause cancer predisposition, but in an Msh6 -deficient background, loss of Msh3 accelerated intestinal tumorigenesis. Lymphomagenesis was not affected. Furthermore, mismatch-directed anti-recombination and sensitivity to methylating agents required Msh2 and Msh6, but not Msh3. Thus, loss of MMR functions specific to Msh2/Msh6 is sufficient for lymphoma development in mice, whereas predisposition to intestinal cancer requires loss of function of both Msh2/Msh6 and Msh2/Msh3. 相似文献
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R. Seïte 《Cellular and molecular life sciences : CMLS》1963,19(3):162-163
Summary It has been extensively demonstrated that perfusion is the best fixation procedure for providing good morphological evidence ofstructures, especially in the case of nervous tissue. But it might be questioned if it should also be preferred whencytochemical data have to be obtained or compared.As a preliminary attempt to answer this question, lipoproteic inclusions in nerve cells of vegetative ganglia of adult cat have been considered. These occur in about 25% of cells after immersion in fixative, whereas if perfusion is used, a relation appears between the amount of saline perfused before the fixative fluid and the percentage of cells containing inclusions: this falls to 10% after 300 ml saline, to 1% after 800 ml. In conclusion, though structural artefacts have been avoided and fixation appears excellent, perfusion is significantly responsible for a definite cytochemical alteration. 相似文献
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The superior cervical ganglia of the rat have been incubated in vitro for 1 h in basal medium Eagle (BME) with Hanks' salts, BME with Earle's salts, Kreb's solution and NCTC 109 medium. Comparison of the cell areas, established by a semi-automatic quantitative method, shows that the three former induce a 30--35% neuronal retraction, whereas NCTC 109 has no effect. Thus this latter medium seems the best one for studies using incubation of these cells. 相似文献
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Todd JA Walker NM Cooper JD Smyth DJ Downes K Plagnol V Bailey R Nejentsev S Field SF Payne F Lowe CE Szeszko JS Hafler JP Zeitels L Yang JH Vella A Nutland S Stevens HE Schuilenburg H Coleman G Maisuria M Meadows W Smink LJ Healy B Burren OS Lam AA Ovington NR Allen J Adlem E Leung HT Wallace C Howson JM Guja C Ionescu-Tîrgovişte C;Genetics of Type Diabetes in Finland Simmonds MJ Heward JM Gough SC;Wellcome Trust Case Control Consortium Dunger DB Wicker LS Clayton DG 《Nature genetics》2007,39(7):857-864
The Wellcome Trust Case Control Consortium (WTCCC) primary genome-wide association (GWA) scan on seven diseases, including the multifactorial autoimmune disease type 1 diabetes (T1D), shows associations at P < 5 x 10(-7) between T1D and six chromosome regions: 12q24, 12q13, 16p13, 18p11, 12p13 and 4q27. Here, we attempted to validate these and six other top findings in 4,000 individuals with T1D, 5,000 controls and 2,997 family trios independent of the WTCCC study. We confirmed unequivocally the associations of 12q24, 12q13, 16p13 and 18p11 (P(follow-up) 相似文献
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Rosendahl J Witt H Szmola R Bhatia E Ozsvári B Landt O Schulz HU Gress TM Pfützer R Löhr M Kovacs P Blüher M Stumvoll M Choudhuri G Hegyi P te Morsche RH Drenth JP Truninger K Macek M Puhl G Witt U Schmidt H Büning C Ockenga J Kage A Groneberg DA Nickel R Berg T Wiedenmann B Bödeker H Keim V Mössner J Teich N Sahin-Tóth M 《Nature genetics》2008,40(1):78-82
Chronic pancreatitis is a persistent inflammatory disease of the pancreas, in which the digestive protease trypsin has a fundamental pathogenetic role. Here we have analyzed the gene encoding the trypsin-degrading enzyme chymotrypsin C (CTRC) in German subjects with idiopathic or hereditary chronic pancreatitis. Two alterations in this gene, p.R254W and p.K247_R254del, were significantly overrepresented in the pancreatitis group, being present in 30 of 901 (3.3%) affected individuals but only 21 of 2,804 (0.7%) controls (odds ratio (OR) = 4.6; confidence interval (CI) = 2.6-8.0; P = 1.3 x 10(-7)). A replication study identified these two variants in 10 of 348 (2.9%) individuals with alcoholic chronic pancreatitis but only 3 of 432 (0.7%) subjects with alcoholic liver disease (OR = 4.2; CI = 1.2-15.5; P = 0.02). CTRC variants were also found in 10 of 71 (14.1%) Indian subjects with tropical pancreatitis but only 1 of 84 (1.2%) healthy controls (OR = 13.6; CI = 1.7-109.2; P = 0.0028). Functional analysis of the CTRC variants showed impaired activity and/or reduced secretion. The results indicate that loss-of-function alterations in CTRC predispose to pancreatitis by diminishing its protective trypsin-degrading activity. 相似文献