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911.
Rats subcutaneously implanted with AH109A hepatoma cells show hyperlipidemia with high concentrations of serum triglyceride
and nonesterified fatty acid, suppression of lipoprotein lipase (LPL), and elevation of hormone-sensitive lipase (HSL) activities
during the growth of the hepatoma. Supplementation of the diet with sulfur amino acids such as l-methionine (Met) and l-cystine (Cys) improved hyperlipidemia by restoring LPL and HSL activities. In the present study, we have attempted to examine
the effects of sulfur amino acids on the activity and mRNA level of LPL and the activity of HSL using 3T3-L1 cells, which
are known to differentiate to adipocytes. The adipocytes were incubated with various concentrations of Met, Cys or l-cysteine (CysH) in the absence or presence of tumor necrosis factor-α (TNF-α). LPL activity was suppressed by TNF-α. In the
absence of TNF-α, Met, Cys and CysH did not change the LPL activity. In the presence of TNF-α, Met and Cys significantly increased
the LPL activity, and Met also enhanced the LPL mRNA level. HSL activity was also suppressed by TNF-α. In the absence of TNF-α,
Met enhanced the HSL activity. In the presence of TNF-α, Met, Cys and CysH suppressed the HSL activity. Sulfur amino acids
such as Met, Cys and CysH affected the LPL activity, mRNA level, and HSL activity in 3T3-L1 adipocytes. Some of these effects
of sulfur amino acids were different between LPL and HSL, between the absence and the presence of TNF-α, and between 3T3-L1
adipocytes and the adipose tissue from rats. 相似文献
912.
Nahoko Shikata Yukihiro Maki Masahiko Nakatsui Masato Mori Yasushi Noguchi Shintaro Yoshida Michio Takahashi Nobuo Kondo Masahiro Okamoto 《Amino acids》2010,38(1):179-187
The changes in the concentrations of plasma amino acids do not always follow the flow-based metabolic pathway network. We
have previously shown that there is a control-based network structure among plasma amino acids besides the metabolic pathway
map. Based on this network structure, in this study, we performed dynamic analysis using time-course data of the plasma samples
of rats fed single essential amino acid deficient diet. Using S-system model (conceptual mathematical model represented by
power-law formalism), we inferred the dynamic network structure which reproduces the actual time-courses within the error
allowance of 13.17%. By performing sensitivity analysis, three of the most dominant relations in this network were selected;
the control paths from leucine to valine, from methionine to threonine, and from leucine to isoleucine. This result is in
good agreement with the biological knowledge regarding branched-chain amino acids, and suggests the biological importance
of the effect from methionine to threonine. 相似文献
913.
Although anthracycline antibiotics daunorubicin (DR), doxorubicin (DX), and epirubicin (ER) possess minor differences in their
chemical structures, large differences are noted in their clinical use, as well as in cellular and plasma pharmacokinetic
parameters in vivo. Immunocytochemistry for DR, DX, or ER was developed using an anti-DR monoclonal antibody (ADM-1-11), which
has been demonstrated to react equally well with each of the three drugs, and therefore it was used for comparing their accumulation
in several rat tissue cells after a single i.v. injection of each drug. In the kidney, immunoreactivity for each drug was
distributed in essentially the same pattern and in the same strength 2 h after injection, but quite differently distributed
in kidney cells thereafter, so that at 120-h post-injection significant amounts of DX and ER remained, but DR had almost completely
vanished. Similar patterns of accumulation were observed in cells of other tissues including the pancreas, hair follicle,
and stomach, with the exception of the intestine in which none of the three drugs remained after 120 h. These results appear
to be supported by previous pharmacokinetic studies on the anthracyclines. The mechanism for such differences among the three
drugs remains obscure, but the hydroxyl group at C-14 of DX and ER molecule might be related to the strong propensity of DX
and ER to accumulate in tissue cells. The present results should contribute to the understanding of the mechanisms of the
differences in the pharmacokinetics, as well as the possibly in anti-tumor activities of the anthracyclines. 相似文献
914.
Yasukazu Yoshida Nanako Itoh Mieko Hayakawa Yoko Habuchi Yoshiro Saito Yoshitane Tsukamoto Osamu Cynshi Kou-ichi Jishage Hiroyuki Arai Etsuo Niki 《The Journal of nutritional biochemistry》2010,21(1):66-76
It has been hypothesized that oxidative stress plays a key role in aging. In order to elucidate the role of the antioxidant network — including α-tocopherol (αT) and αT transfer protein — in aging in vivo, α-tocopherol transfer protein knockout (αTTP?/?) mice were fed a vitamin-E-depleted diet, and wild-type (WT) mice were fed a diet containing 0.002 wt.% αT from the age of 3 months to 1 1/2 years. The lipid oxidation markers total hydroxyoctadecadienoic acid (tHODE) and 8-iso-prostaglandin F2α, and antioxidant levels in the blood, liver and brain were measured at 3, 6, 12 and 18 months. tHODE levels in the plasma of αTTP?/? mice were elevated at 6 months compared to 3 months, and were significantly higher those in WT mice, although they decreased thereafter. On the other hand, tHODE levels in the liver and brain were constantly higher in αTTP?/? mice than in WT mice. Motor activities decreased with aging in both mouse types; however, those in the αTTP?/? mice were lower than those in the WT mice. It is intriguing to note that motor activities were significantly correlated with the stereoisomer ratio (Z,E/E,E) of HODE, which is a measure of antioxidant capacity in vivo, in the plasma, in the liver and even in the brain, but not with other factors such as antioxidant levels.In summary, using the biomarker tHODE and its stereoisomer ratio, we demonstrated that αT depletion was associated with a decrease in motor function, and that this may be primarily attributable to a decrease in the total antioxidant capacity in vivo. 相似文献
915.
916.
917.
Comprehensive analysis of rice DREB2-type genes that encode transcription factors involved in the expression of abiotic stress-responsive genes 总被引:4,自引:0,他引:4
918.
Circulating muscle-specific microRNA, miR-206, as a potential diagnostic marker for rhabdomyosarcoma 总被引:1,自引:0,他引:1
Mitsuru Miyachi Hideki Yoshida Ken Kikuchi Tomoko Iehara 《Biochemical and biophysical research communications》2010,400(1):89-93
Presently there is no serum biomarker of rhabdomyosarcoma (RMS). Several studies have shown that profiles of microRNA (miRNA) expression differ among tumor types. Here we evaluated the feasibility of using muscle-specific miRNAs (miR-1, -133a, -133b and -206) as biomarkers of RMS. Expression of muscle-specific miRNAs, especially miR-206, was significantly higher in RMS cell lines than in other tumor cell lines, as well as in RMS tumor specimens. Further, serum levels of muscle-specific miRNAs were significantly higher in patients with RMS tumors than in patients with non-RMS tumors. Normalized serum miR-206 expression level could be used to differentiate between RMS and non-RMS tumors, with sensitivity of 1.0 and specificity of 0.913. These results raise the possibility of using circulating muscle-specific miRNAs, especially miR-206, as landmark biomarkers for RMS. 相似文献
919.
Mihoko Kondo-Nakamura Koichi Uemura Ken-ichi Yoshida 《Biochemical and biophysical research communications》2010,393(3):449-163
We examined whether and how pretreatment with carbon monoxide (CO) prevents apoptosis of cardioblastic H9c2 cells in ischemia-reperfusion. Reperfusion (6 h) following brief ischemia (10 min) induced cytochrome c release, activation of caspase-9 and caspase-3, and apoptotic nuclear condensation. Brief CO pretreatment (10 min) or a caspase-9 inhibitor (Z-LEHD-FMK) attenuated these apoptotic changes. Ischemia-reperfusion increased phosphorylation of Akt at Ser472/473/474, and this was enhanced by CO pretreatment. A specific Akt inhibitor (API-2) blunted the anti-apoptotic effects of CO in reperfusion. In normoxic cells, CO enhanced generation, which was inhibited by a mitochondrial complex III inhibitor (antimycin A) but not by a NADH oxidase inhibitor (apocynin). The CO-enhanced Akt phosphorylation was suppressed by an scavenger (Tiron), catalase or a superoxide dismutase (SOD) inhibitor (DETC). These results suggest that CO pretreatment induces mitochondrial generation of , which is then converted by SOD to H2O2, and subsequent Akt activation by H2O2 attenuates apoptosis in ischemia-reperfusion. 相似文献
920.
Yoshida T Mizuta T Shimizu S 《Biochemical and biophysical research communications》2010,402(4):676-679
Parkinson’s disease (PD) is a common neurodegenerative disorder. The motor neuron degeneration 2 mutant (mnd2) mouse is considered to be an animal model of PD, and exhibits striatal neuron loss, severe muscle wasting, weight loss and death before 40 days of age. We found for the first time that parkin expression was decreased in the mnd2 mouse brain. Since parkin is a crucial protein for PD, the neurodegenerative disorder in mnd2 mice may be caused by parkin protein loss. We therefore examined whether compensation of parkin protein prevents neurodegenerative disorders in mnd2 mice by generating parkin-transgenic (parkin-Tg) mnd2 mice. However, both parkin-Tg mnd2 mice and mnd2 mice were smaller than wild type mice. In muscle strength and survival rate, parkin-Tg mnd2 mice showed similar values to mnd2 mice. Our data suggest that repression of parkin protein does not play a major role in neurodegeneration of mnd2 mice and administration of parkin protein does not rescue mnd2 mice. 相似文献