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991.
使用一项定量测定大鼠前肢运动能力的新方法,训练大鼠抓握与张力传感器相接的圆柱形按钮并向上拉,以牛奶为奖励,利用强化阈值递增的方法测定前肢最大拉力。拉力波形可用微机记录和存储。本方法较为简便和经济,还具有能定量反映大鼠前肢抓握能力的优点。 相似文献
992.
采用定量的方法动态观察局部脑缺血-再灌注大鼠的行为和运动能力,旨在为缺血性脑损伤行为评价提供敏感的指标。用直径0.2mm的尼龙线经颈内动脉可逆性插入到大脑前动脉,建立局部脑缺血-再灌注大鼠模型。术后1、2、4、8、24、48h观察神经症状。运动能力的评价采用握-引测验、网屏测验和转棒测验,在术后1、2、3、7、14d进行。主要结果如下:该模型的偏瘫很快消失,术后4h就难以用肉眼观察出运动的异常。而提尾悬空试验的阳性体征持续到术后3d,转棒的成绩在术后1周恢复正常。握-引和网屏测验未能显示出肌力的异常,应考虑设计更完善的方法以排除干扰因素。上述结果提示提尾悬空和转棒测验是评价脑缺血大鼠运动缺陷的简便、客观且较敏感方法。 相似文献
993.
S. J. S. Flora S. N. Dube Usha Arora G. M. Kannan M. K. Shukla P. R. Malhotra 《Biometals》1995,8(2):111-116
The therapeutic efficacy of two thiol chelators, meso 2,3-dimercaptosuccinic acid (DMSA) or 2,3-dimercaptopropane sulfonate (DMPS) in treating chronic arsenic intoxication was investigated in male rats. Both the chelators were effective in promoting urinary arsenic excretion and restoring arsenic induced inhibition of blood -aminolevulinic acid dehydratase activity and hepatic glutathione level. Elevation of urinary -aminolevulinic acid excretion and arsenic concentration in blood, liver and kidneys were reduced significantly by both the chelators. Histopathological lesions induced by arsenic were also effectively reduced by the above chelators. DMSA being more effective than DMPS. The results suggest DMSA and DMPS to be effective antidotes for treating chronic arsenic toxicity in experimental animals. 相似文献
994.
本实验采用免疫细胞化学方法,研究了大白鼠中缝背核及中央上核内5-HT能神经元的生后转折变化,并结合图像分析对中缝中央上核内5-HT能神经元的生后发育进行了定量研究。结果显示,在生后第1天,中缝背核和中央上核内5-HT阳性胞体密集排列,突起较短。从P1到P30,中缝背核内,5-HT阳性胞体密度明显降低,外侧部5-HT阳性细胞突起的长度显著增加。中缝中央上核内,至P10,5-HT阳性胞体仍密集排列,且胞体增大,至P30,细胞排列变得疏松。从P90到P90,中缝背核和中央上核内阳性细胞的分布及形态无明显变化。统计学处理结果表明,中缝中央上核内5-HT能胞体数量从P1到P30有显著性增加,从P30到P90有显著性减少。胞体面积及周长从P1至P30逐渐增加,在P10至P30阶段增长最快。P1与P30以及P1与P90比较,胞体形状因子显著增加。从P1至P30,中缝中央上核外侧散布的5-HT阳性细胞逐渐减少,至成年只能偶尔见到,且胞体变得不规则。 相似文献
995.
A. Jawerbaum A.M. Franchi E.T. Gonzalez V. Novaro M.A.F. de Gimeno 《Prostaglandins & other lipid mediators》1995,50(1)
The relationship between high glucose concentrations and arachidonic acid metabolism in uterine tissue from control and diabetic ovariectomized rats was evaluated. Uterine tissue from diabetic rats produced amounts of PGE2 and PGF2α similar to controls, while a lower production of 6-keto-PGF1α (indicating the production of prostacyclin) and a higher production of TXB2 (indicating the generation of TXA2) was found in the diabetic group. A group of diabetic rats was treated with phlorizin to diminish plasma glucose levels. Phlorizin treatment did not alter production of PGE2, PGF2α, and 6-keto-PGF1α in the diabetic group. A diminished production of TXB2 was found in the treated diabetic uteri when compared to the non-treated diabetic group. Moreover, a positive correlation between plasma glucose levels and uterine TXB2 generation was observed. When control uterine tissue was exposed in vitro to high concentrations of glucose (22 mM) and compared to control tissue incubated in the presence of glucose 11 mM alterations in the generation of PGE2, PGF2α, and 6-keto-PGF1α were not found, but a higher production of TXB2 was observed and values were similar to those obtained in the diabetic tissue. Alteration in the production of the prostanoids evaluated were not observed when diabetic tissue was incubated in the presence of high concentrations of glucose. These results provide evidence of a direct relationship between plasma glucose levels and uterine production of TXA2. 相似文献
996.
Hiroshi Yamamoto Toshiaki Endo Tamotsu Kiya Taeko Goto Satoru Sagae Eiki Ito Hiroshi Watanabe Ryuichi Kudo 《Prostaglandins & other lipid mediators》1995,50(4)
In rat luteal cells labeled with (3H]oleic acid, PGF2α-stimulated phospholipase D (PLD) activation was investigated. The PLD activity was detected by measuring the accumulation of [3H]phosphatidylethanol (PtdEt) in the presence of ethanol. PGF2α stimulated PtdEt accumulation at concentrations of more than 100 nM in the presence of ethanol. However, PtdEt accumulation did not change in the absence of ethanol. PGF2α (1 μM) increased PtdEt accumulation after 1 min, and the accumulation reached a plateau by 2–3 min. These results indicate that PGF2α activates PLD in rat luteal cells. U-73122, a phospholipase C (PLC) inhibitor, and staurosporine, a protein kinase C (PKC) inhibitor, did not inhibit PGF2α-stimulated [3H]PtdEt accumulation. These results suggest that PGF2α-induced PLD activation is different from PLC-PKC systems. We reported previously that PGF2α stimulated the release of arachidonic acid. The effects of indomethacin, nordihydroguaiaretic acid (NDGA), and 5,8,11,14-eicosatetraynoic acid (ETYA), inhibitors of arachidonic acid metabolism, on PGF2α-stimulated PtdEt accumulation were examined. Pretreatment with indomethacin enhanced PGF2α-induced PtdEt accumulation. In contrast, pretreatment with NDGA and ETYA inhibited PGF2α-induced PtdEt accumulation. It is suggested that PGF2α-stimulated PLD activation is mediated via lipoxygenase products. 相似文献
997.
Margherita Strolin Benedetti Enrico Frigerio Paola Tocchetti Giannantonio Brianceschi Maria Grazia Castelli Cinzia Pellizzoni Philippe Dostert 《Chirality》1995,7(4):285-289
Reboxetine, (RS)-2-[(RS)-α-(2-ethoxyphenoxy)benzyl]morpholine methanesulphonate, is a racemic compound and consists of a mixture of the (R,R)- and (S,S)-enantiomers. In this study, brain and plasma levels of both enantiomers were determined in mice and rats after oral administration of reboxetine at doses (1.1 mg/kg, mouse; 20 mg/kg, rat) twice the respective ED50 values in the antireserpine test. Plasma and brain concentrations of each enantiomer were measured up to 6 h postdosing using an HPLC method with fluorimetric detection after derivatization with a chiral agent (FLEC). In mice and rats, brain and plasma levels of the (R,R)-enantiomer were always higher than those of the (S,S)-enantiomer. After normalization for dose, the mean AUC0-tz values of both the (R,R)- and (S,S)-enantiomers in mouse brain were about 23 and 32 times higher than in rat brain, respectively. In plasma, the corrected mean AUC0-tz values were about 5 (R,R) and 10 (S,S) times higher in mice than in rats. These results provide evidence for the higher bioavailability and/or lower clearance of both enantiomers in mice than in rats, and for a higher penetration of both enantiomers into mouse brain compared to rat brain. © 1995 Wiley-Liss, Inc. 相似文献
998.
Keiichi Ozaki Reiko T. Lee Yuan C. Lee Toshisuke Kawasaki 《Glycoconjugate journal》1995,12(3):268-274
The Gal/GalNAc-specific lectin on the surface of rat peritoneal macrophages (macrophage asialoglycoprotein binding protein, M-ASGP-BP), which consists of a single polypeptide chain of 42 kDa, can form a homooligomeric receptor exhibiting high affinity for asialoorosomucoid (ASOR) [Ozaki K., Ii M., Itoh N., Kawasaki T. (1992)J Biol Chem
267: 9229–35]. In this study, the binding affinity of M-ASGP-BP was studied by using a series of synthetic or natural glycosides as inhibitors of125I-ASOR binding to recombinant M-ASGP-BP expressed on COS-1 cells (rM-ASGP-BP), and the results were compared with those of human hepatic lectin (HHL) on Hep G2 cells. Clustering of multiple Gal (or GalNAc) residues increased the binding affinity to M-ASGP-BP as well as to HHL. In contrast to HHL and other mammalian hepatic lectins, rM-ASGP-BP bound Gal residues tighter than GalNAc residues. A galactose-terminated triantennary N-glycoside, having oneN-acetyl-lactosamine unit on the 6 branch and twoN-acetyl-lactosamine units on the 3 branch of the trimannosyl core structure, showed affinity enhancement of 105 over a monovalent ligand for HHL, while the same glycopeptide showed enhancement of about 2000-fold for rM-ASGP-BP. These results suggest that spatial arrangements of sugar combining sites and subunit organization of macrophage and hepatic lectins are different. 相似文献
999.
Mohammad Mohsen Arié Pinson Renliang Zhang Amram Samuni 《Molecular and cellular biochemistry》1995,145(2):103-110
The aim of the research was to study the role played by extracellular O
2
.-
radicals, which are implicated in cardiac cell damage and the protective effect by cell-permeable, nitroxide, superoxide dismutase-mimics. Cardiomyocytes cultures from 1-day-old rats served as the test-system. Experiments were performed since 5th day in culture when >80% of the cells were beating myocardial cells. Oxidative damage was induced by 0.5 mM hypoxanthine and 0.06 U/ml xanthine oxidase or by 10 mM glucose and 0.15 U/ml glucose oxidase. The parameters used to evaluate damages were spontaneous beating, lactate dehydrogenase release and ATP level. The rhythmic pulsation was followed microscopically. To determine the kinetics of cytosolic enzyme release from the cells, media samples were collected at various points of time and assayed for enzyme activity. To determine the cellular ATP, cells were washed with sodium phosphate buffer, scraped off and boiled for 3 min with sodium phosphate buffer. Following centrifugation the supernatant was collected and ATP was determined by the chemiluminogenic assay using firefly tails. The present results indicate that nitroxide stable free radicals, in the millimolar concentration range, provide full protection without toxic side-effect. Unlike exogenously added SOD that failed to protect, exogenous catalase provided almost full protection. In addition, the metal-chelating agent dipyridyl, but not diethylene-triamine-pentaacetate or desferrioxamine, protected the cultured cells. The present results suggest that H2O2 is the predominant toxic species mediating the oxidative damage whereas extracellular superoxide radical does not contribute to cultured cardiomyocyte damage. Since nitroxides do not remove H2O2 they can protect the cells possibly by oxidizing the metal ions and inhibiting the Fenton reaction. The superoxide dismutase-mimic activity of nitroxides does not seem to underlie their protective effect, however, the involvement of intracellular O
2
.-
cannot be excluded.Abbreviations CHDO
2-spirocyclohexane doxyl (2-cyclohexane-5,5-demethyl-3-oxazolidinoxyl)
- DF
desferrioxamine
- DTPA
diethylene-triamine-pentaacetate
- EPR
electron paramagnetic resonance
- HX
hypoxanthine
- LDH
lactate dehydrogenase
- SOD
superoxide dismutase
- SEM
standard error of mean: TEMPOL, 4-hydroxy-2,2,6,6-tetramethyl-piperidinoxyl
- TEMPAMINE
4-amino-2,2,6,6-tetramethyl-piperidinoxyl
- XO
xanthine oxidase
- CAT
catalase 相似文献
1000.
Federico Bennardini Antonella Mattana Elisabetta Pinna Nossai Marco Mignano Flavia Franconi Claudia Juliano Luigi Sciola Proto Pippia Michele Chiesi 《Molecular and cellular biochemistry》1995,152(1):23-30
B crystallin, a structural protein of the mammalian lens essential for the maintenance of lens transparency, is also expressed, at variable levels, in many extraocular tissues where it plays a protective role in stress conditions. In fact, heat or toxic shocks, as well as pathological states, increase B crystallin levels in many cell types. Here we show that B crystallin expression is also modulated in subcultures of rat fibroblasts and Galliera sarcoma cells. Western blots analysis with anti B crystallin antibodies reveals the presence of the protein in both cell populations, although the kinetic pattern of expression is different. Galliera fibroblasts constitutively express the protein up to the 70th subculture and afterwards the synthesis ceases. On the other hand, Galliera sarcoma cells do not contain B crystallin in the early stages of the culture, but there is a progressive increases between the 20th and 40th cell subculture. Differences also exist concerning the intracellular distribution: B crystallin is diffusely localized in the cytoplasm of fibroblasts while in sarcoma cells it localizes mainly to the perinuclear region. B crystallin is totally recovered as soluble protein in the supernatants obtained after low speed centrifugation of fibroblast homogenates, while in sarcoma cells a portion of the protein is also recovered in the insoluble pellet. Intracellular pH measurements show an alkaline cytosol in sarcoma cells compared to fibroblasts. Heat shock treatment of fibroblast subcultures constitutively expressing B crystallin induces an over-expression of the protein, while in fibroblasts whose biosynthetic capacity is lost, heat shock is unable to activate the crystallin gene. Correlation between B crystallin expression and proliferative rate shows that highly proliferating fibroblasts do not express B crystallin, while neoplastic cells do. 相似文献