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101.
以D-氨基半乳糖(D-Galactosamine,D-GalN)造成急性肝损伤(急性肝炎、急性肝坏死)大鼠模型后、对照观察了急性肝损伤大鼠血浆氨基酸的变化,建立了大鼠急性肝损伤时血浆氨基酸的变化模式并对其发生机理进行了探讨。大鼠血浆氨基酸的测定采用聚酰薄层荧光分析技术,其测定结果是:急性肝炎组,酪氨酸(Tyr)、天冬氨酸(Asp)、谷氨酰胺(Gln)和鸟氨酸(Orn)升高,精氨酸(Arg)下降,其余氨基酸无显著变化。急性肝坏死组,除Arg显著下降外,其余所有氨基酸都显著升高,而两组支链氨基酸(BCAA)/芳香族氨基酸(AAA)克分子比值均显著下降。 相似文献
102.
Effect of 20 days exposure of juvenile gilthead seabream ( Sparus aurata ) to elevated levels of ammonia on growth and survival was examined in a continuous flow system. Suppressed growth and reduced survival were observed at concentrations of 8.2 and 13 mg l−1 total ammonia-N (0.5 and 0.7 mg l−1 un-ionized ammonia-N, respectively) and higher. The maximum acceptable toxic concentration (MATC) for growth was between 4.8 to 8.2 mg l−1 total ammonia-N (0.3 and 0.5 mg l−1 un-ionized ammonia-N, respectively). Fish exposed to high ammonia levels (13 mg l−1 total ammonia-N, 0.7 mg l−1 un-ionized ammonia-N) displayed clear signs of liver pathology. Existing evidence suggests that S. aurata is less sensitive to ammonia than other reported marine and freshwater fish.
Under certain conditions ammonia concentration in the intensive fish ponds in Eilat may exceed the no observed effect concentration for S. aurata . 相似文献
Under certain conditions ammonia concentration in the intensive fish ponds in Eilat may exceed the no observed effect concentration for S. aurata . 相似文献
103.
Livers of juvenile cabrilla sea basses ( Serranus cabrilla ) were subjected to light and electron transmission microscopy following different periods of maintenance in an aquarium. Since this fish is easy to feed in captivity and the hepatic structure was found to be comparable at the four periods tested (0, 5, 10 and 20 days), both at the histological and ultrastructural level, the liver of S. cabrilla could be an available model for marine contamination experimental studies. As in other fish species, it is not possible to distinguish the portal lobules and the triads. The Melano-Macrophage Centres contain tipofuscins, ceroids and haemosiderin, but they do not contain any melanin. The hepatocytes are arranged in cords (two cells thick), and, at the ultrastructural level, they show numerous microvilli in the perisinusoidal and canalicular areas. The hyaloplasm includes a considerable amount of glycogen and some lipid droplets are occasionally observed. Mitochondria, rough endoplasmic reticulum and the Golgi apparatus are relatively scarce. 相似文献
104.
Ashok K. Srivastava Rafick-Pierre Sékaly Jean-Louis Chiasson 《Molecular and cellular biochemistry》1993,121(2):127-133
The effect of nicotinamide-adenine dinucleotides (NAD+ and NADP+) on Ca2+ transport in rat liver nuclei was investigated. Ca2+ uptake and release were determined with a Ca2+ electrode. Ca2+ uptake was dependent on adenosine triphosphate (ATP; 2mM). The presence of NAD+ (2mM) or NADP+ (1 and 2mM) caused a significant inhibition of Ca2+ uptake following addition of 2mM ATP. Ca2+, which accumulated in the nuclei during 6 min after ATP addition, was significantly released by the addition of NAD+ (0.5–2mM) or NADP+ (0.1–2mM). However, the effect of NADH (2mM) or NADPH (2mM) on Ca2+ uptake and release clearly weakened in comparison with the effects of NAD+ and NADP+. Meanwhile, ryanodine (10M), thapsigargin (10M) or oxalate (0.5mM) had no effect on Ca2+ uptake and release in rat liver nuclei. These reagents did not significantly alter the effects of 2mM NAD+ on Ca2+ uptake and release. Thus, NAD+ and NADP+ had a potent effect on Ca2+ transport in rat liver nuclei. The present findings suggest that the liver cytosolic NAD+ (NADP+) is a factor in the regulation of the nuclear Ca2+ concentration. (Mol Cell Biochem121: 127–133, 1993) 相似文献
105.
F. Schroeder J. R. Jefferson D. Powell S. Incerpi J. K. Woodford S. M. Colles S. Myers-Payne T. Emge T. Hubbell D. Moncecchi D. R. Prows C. E. Heyliger 《Molecular and cellular biochemistry》1993,123(1-2):73-83
Fatty acid-binding proteins (FABP) are abundant cytosolic proteins whose level is responsive to nutritional, endocrine, and a variety of pathological states. Although FABPs have been investigatedin vitro for several decades, little is known of their physiological function. Liver L-FABP binds both fatty acids and cholesterol. Competitive binding analysis and molecular modeling studies of L-FABP indicate the presence of two ligand binding pockets that accomodate one fatty acid each. One fatty acid binding site is identical to the cholesterol binding site. To test whether these observations obtainedin vitro were physiologically relevant, the cDNA encoding L-FABP was transfected into L-cells, a cell line with very low endogenous FABP and sterol carrier proteins. Uptake of both ligands did not differ between control cells and low expression clones. In contrast, both fatty acid uptake and cholesterol uptake were stimulated in the high expression cells. In high expression cells, uptake of fluorescent cis-parinaric acid was enhanced more than that of trans-parinaric acid. This is consistent with the preferential binding of cis-fatty acids to L-FABP but in contrast to the preferential binding of trans-parinaric acid to the L-cell plasma membrane fatty acid transporter (PMFABP). These data show that the level of cytosolic fatty acids in intact cells can regulate both the extent and specificity of fatty acid uptake. Last, sphingomyelinase treatment of L-cells released cholesterol from the plasma membrane to the cytoplasm and stimulated microsomal acyl-CoA: cholesteryl acyl transferase (ACAT). This process was accelerated in high expression cells. These observations show for the first time in intact cells that L-FABP, a protein most prevalent in liver and intestine where much fat absorption takes place, may have a role in fatty acid and cholesterol absorption.Abbreviations FABP
fatty acid-binding protein
- L-FABP
liver fatty acid-binding protein
- I-FABP
intestinal fatty acid-binding protein
- H-FABP
heart fatty acid-binding protein
- A-FABP
adipocyte fatty acid-binding protein
- PMFABP
plasma membrane fatty acid-binding protein
- SCP-2
sterol carrier protein-2
- Dehydroergosterol (DHE)
d-5,7,9(11),22-ergostatetraene-3b-ol
- cis-parinaric
acid-9Z, 11E, 13E, 15Z-octatetraenoic acid
- trans
parinaric acid, 9E, 11E, 13E, 14E-octatetraenoic acid
- BSA
bovine serum albumin
- KRH
Krebs-Ringer-Henseleit buffer 相似文献
106.
Patrick van Dijck Kristina Schoonjans Paolo Sassone-Corsi Johan Auwerx Guido Verhoeven 《Molecular and cellular biochemistry》1993,125(2):127-136
The hepatic expression of the 2u gene family is controlled by a variety of hormones including steroids, growth hormone and insulin. The mechanisms by which these hormones affect -globulin expression are only partially understood. Recently we isolated and characterized clone RAP 01, an 2u-globulin gene expressed in the liver. In preliminary experiments we noted that partial hepatectomy, a procedure which results in a sharp rise in the level of the oncoproteins c-Fos and c-Jun, also causes a transient induction of the messenger RNA corresponding to clone RAP 01. Using the DNAseI footprinting technique we were able to show that this clone contains a TPA (phorbol 12-myristate 13-acetate)-responsive element (TRE) in its first intron. This element (denoted as element X) is identical to the consensus AP-1 binding site (TGACTCAG) and is protected by rat liver nuclear extracts as well as by purified c-Jun. Gel retardation experiments show that an oligonucleotide containing the TRE consensus sequence competes for binding of liver nuclear proteins to element X and that antibodies directed against the M2 peptide of the mouse Fos protein or the PEP-2 peptide of Jun prevent the formation of specific complexes with the same element. Moreover, element X functions as a TRE in transfected BWTG3 hepatoma cells treated with TPA. Co-transfection withfos andjun expression vectors mimics the effects of TPA suggesting that AP-1 is in fact the mediator of the observed response. It is concluded that the first intron of RAP 01 contains a functional Fos-Jun element. 相似文献
107.
Shikha Bakshi Maninder Kaur Arpana Verma Sadhna Sharma 《Journal of biochemical and molecular toxicology》2023,37(8):e23386
Drug-induced liver injury (DILI) is an adverse outcome of the currently used tuberculosis treatment regimen, which results in patient noncompliance, poor treatment outcomes, and the emergence of drug-resistant tuberculosis. DILI is primarily caused by the toxicity of the drugs and their metabolites, which affect liver cells, biliary epithelial cells, and liver vasculature. However, the precise mechanism behind the cellular damage attributable to first-line antitubercular drugs (ATDs), as well as the effect of toxicity on the cell survival strategies, is yet to be elucidated. In the current study, HepG2 cells upon treatment with a high concentration of ATDs showed increased perforation within the cell, cuboidal shape, and membrane blebbing as compared with control/untreated cells. It was observed that ATD-induced toxicity in HepG2 cells leads to altered mitochondrial membrane permeability, which was depicted by the decreased fluorescence intensity of the MitoRed tracker dye at higher drug concentrations. In addition, high doses of ATDs caused cell damage through an increase in reactive oxygen species production in HepG2 cells and a simultaneous reduction in glutathione levels. Further, high dose of isoniazid (50–200 mM), pyrazinamide (50–200 mM), and rifampicin (20–100 µM) causes cell apoptosis and affects cell survival during toxic conditions by decreasing the expression of potent autophagy markers Atg5, Atg7, and LC3B. Thus, ATD-mediated toxicity contributes to the reduced ability of hepatocytes to tolerate cellular damage caused by altered mitochondrial membrane permeability, increased apoptosis, and decreased autophagy. These findings further emphasize the need to develop adjuvant therapies that can mitigate ATD-induced toxicity for the effective treatment of tuberculosis. 相似文献
108.
Ian G. Town Gary J. Phillips Edile Murdoch Stephen T. Holgate Frank J. Kelly 《Free radical research》1993,18(4):211-221
The time course and nature of the pulmonary inflammatory and antioxidant responses, both during and after hyperoxic-induced acute lung injury were studied in the preterm guinea pig. Three-day preterm (65 days gestation) guinea pigs were randomly exposed to either 21% O2 (control) or 95% O2 (hyperoxia) for 72 hours. All pups were then maintained in ambient conditions for up to a further 11 days, during which time lung damage was monitored. In animals exposed to hyperoxia, evidence of acute lung injury and inflammation was characterized by a marked increase in microvascular permeability and elevated numbers of neutrophils in bronchoalveolar lavage fluid. Protein concentration, elastase-like activity and elastase-inhibitory capacity in lavage fluid were at a maximum at the end of the 72 hours hyperoxic exposure. Four days later, all values had returned to control levels. In contrast, increased numbers of neutrophils, macrophages and lymphocytes were recovered in the lavage fluid during this early recovery period. Coinciding with the influx of inflammatory cells, there was a significant increase in glutathione peroxidase, manganese superoxide dismutase and catalase activities in immature lung. Lung copper/zinc superoxide dismutase activity remained unchanged during both experimental periods. The strong temporal relationship between the influx of inflammatory cells to the lung and the induction of pulmonary antioxidant enzyme defences suggests that a common mechanism underlies both responses. These findings have led us to regard inflammation in the hyperoxic-injured immature lung as a beneficial event and not, as previously suggested, as part of the injurious process. 相似文献
109.
Daniel E. Gomez Jacqueline L. Hartzler Robert H. Corbitt Alexander M. Nason Unnur P. Thorgeirsson 《In vitro cellular & developmental biology. Animal》1993,29(6):451-455
Summary We describe a fast and reproducible method that can be used as a final step in obtaining pure populations of liver endothelial
cells. This method employs endothelial cell specific lectin covalently bound to magnetic polystyrene beads (Dynabeads). Evonymus
europaeus agglutinin (EEA)-coated Dynabeads were used to purify monkey liver endothelium from Percoll gradient separated nonparenchymal
cells. EEA-coated beads were also successfully used to purify monkey aortic endothelial cells. The endothelial cells grew
to confluence as a cobblestonelike monolayer, expressed Factor VIII related antigen, and incorporated acetylated-low density
lipoprotein. The magnetic beads seemed not to modify the normal properties of the isolated endothelium, thus facilitating
their use in experimental studies. This immunomagnetic separation technique may be applicable for purification of endothelial
cells from a wide variety of tissue sources. 相似文献
110.
Pei Shi Wentao Zhu Jiwei Fu An Liang Ting Zheng Zhilong Wen Xincheng Wu Yuchen Peng Songsong Yuan Xiaoping Wu 《Journal of cellular and molecular medicine》2023,27(21):3326-3338
Acute liver failure (ALF) is an inflammation-mediated hepatocyte death process associated with ferroptosis. Avicularin (AL), a Chinese herbal medicine, exerts anti-inflammatory and antioxidative effects. However, the protective effect of AL and the mechanism on ALF have not been reported. Our in vivo results suggest that AL significantly alleviated lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced hepatic pathological injury, liver enzymes, inflammatory cytokines, reactive oxygen species and iron levels and increased the antioxidant enzyme activities (malondialdehyde and glutathione). Our further in vitro experiments demonstrated that AL suppressed inflammatory response in LPS-stimulated RAW 264.7 cells via blocking the toll-like receptor 4 (TLR4)/myeloid differentiation protein-88 (MyD88)/nuclear factor kappa B (NF-κB) pathway. Moreover, AL attenuated ferroptosis in D-GalN-induced HepG2 cells by activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1)/glutathione peroxidase 4 (GPX4) pathway. Therefore, AL can alleviate inflammatory response and ferroptosis in LPS/D-GalN-induced ALF, and its protective effects are associated with blocking TLR4/MyD88/NF-κB pathway and activating Nrf2/HO-1/GPX4 pathway. Moreover, AL is a promising therapeutic option for ALF and should be clinically explored. 相似文献