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1.
Central and peripheral effects of iminodipropionitrile on catecholamine metabolism in rats 总被引:1,自引:0,他引:1
Chronic treatment with iminodipropionitrile (IDPN) causes a behavioral syndrome characterized by lateral and vertical neck dyskinesias, hyperactivity, random circling, and increased startle response (the "ECC syndrome"). The effects of the neurotoxin on norepinephrine (NE), dopamine (DA), and their metabolites were evaluated in the hypothalamus and the striatum of IDPN-treated animals. Urinary excretion of the amines was also measured. There was no significant persistent change in central metabolism of dopamine. There was a transient increase in NE metabolism in the hypothalamus after the third injection of IDPN that lasted until the development of the syndrome at 7 days of drug treatment. Urinary excretion of NE and its metabolites was increased on the day that the syndrome developed. Urinary excretion of homovanillic acid was persistently decreased throughout and after cessation of drug treatment. There was no change in the excretion of either dopamine or dihydroxyphenyl acetic acid. The ratio of total NE/total DA excreted by IDPN-treated rats was the inverse of that of control animals. These results suggest that persistent dyskinesias may be associated with a relative increase in facilitatory NE-dependent mechanisms at the cortical, subcortical, or spinal cord level. 相似文献
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The 16189 variant of mitochondrial DNA occurs more frequently in C282Y homozygotes with haemochromatosis than those without iron loading 总被引:3,自引:1,他引:3
Livesey KJ Wimhurst VL Carter K Worwood M Cadet E Rochette J Roberts AG Pointon JJ Merryweather-Clarke AT Bassett ML Jouanolle AM Mosser A David V Poulton J Robson KJ 《Journal of medical genetics》2004,41(1):6-10
Background:Patients with hereditary haemochromatosis (HH) are usually homozygous for the C282Y mutation in the HFE gene. They have variable expression of iron overload and present with a variety of complications, including liver disease, diabetes, arthropathy, fatigue, and cardiomyopathy. The mitochondrial 16189 variant is associated with diabetes, dilated cardiomyopathy, and low body fat at birth, and might contribute to genetic predisposition in further multifactorial disorders. The objective of this study was to determine the frequency of the 16189 variant in a range of patients with haemochromatosis, who had mutations in the HFE gene.
Methods:Blood DNA was analysed for the presence of the 16189 variant in British, French, and Australian C282Y homozygotes and controls, with known iron status, and in birth cohorts.
Results:The frequency of the mitochondrial 16189 variant was found to be elevated in individuals with haemochromatosis who were homozygous for the C282Y allele, compared with population controls and with C282Y homozygotes who were asymptomatic (42/292 (14.4%); 102/1186 (8.6%) (p = 0.003); and 2/64 (3.1%) (p = 0.023), respectively).
Conclusions:Iron loading in C282Y homozygotes with HH was exacerbated by the presence of the mitochondrial 16189 variant.
相似文献4.
J. J. Hoarau M. Cesari A. Dieye N. Kotea S. K. Surrun A. Moine H. Caillens F. Cadet M. Pabion 《International journal of immunogenetics》2003,30(3):207-211
In order to determine the ethnic origin of the transporter associated with antigen processing 2 (TAP2) G allele, initially discovered by us in a group of type 1 diabetes (insulin‐dependent diabetes mellitus) patients living on Reunion Island, HLA TAP2 typing was performed using the polymerase chain reaction–amplification refractory mutation system (PCR‐ARMS) method in type 1 diabetes patients and unrelated healthy controls of three different ethnic groups (Caucasians, Indians and black Africans from Senegal and Mauritius). The comparison of TAP2 allele frequencies in controls showed significant racial (ethnic) differences. The TAP2*0101 and TAP2 C alleles were increased, respectively, in the Caucasian (50% in Caucasians vs. 40% in other groups) and Senegalese (27% in Senegalese vs. 10% in other groups) populations. In comparison with Caucasians, the TAP2*0201 variant was significantly increased in the Indian population and decreased in the Senegalese black population. In addition, the TAP2 G allele was observed in the two African populations studied but not in the Caucasian or Indian population. This observation is consistent with the view that this allele is restricted to populations of African origin. In addition, we have determined the large extended haplotype DQA1‐DQB1‐DRB1 associated with TAP2 G. We found that this allele is preferentially associated with the large conserved haplotype HLA DQA1*0501‐DQB1*0201‐DRB1*0301. 相似文献
5.
It is widely assumed that all exercise, regardless of the degree of difficulty or strenuousness, is good (no pain-no gain). In this speculative review of the literature and our research findings we highlight the fact that strenuous exercise taken to the extreme initiates an immune and vascular proinflammatory situation. However, mild cyclic exercise appears to produce health benefits for an individual. In part, this is due to vascular cyclic pulsations, occurring in mild exercise, stimulating constitutive nitric oxide synthase derived nitric oxide release. This in turn down-regulates vascular endothelial cells and immunocytes, as well as their interaction and inhibits the disassociation of NF-kappaB, preventing the production of proinflammatory cytokines. The nitric oxide so generated may even scavenge excess free radicals, preventing tissue damage. Prolonged strenuous exercise appears to limit these positive phenomena because of the maintained and prolonged high blood pressure that reduces the cyclic pulsations, limiting nitric oxide production. We further note that pathological conditions, i.e., Parkinson's disorder, may benefit from mild exercise, i.e., cyclic nitric oxide production, since the inactivity associated with this disease may lead to compromised nitric oxide production, initiating a progressive deterioration of tissues, including peripheral adrenergic neurons, due to a lack of adequate basal nitric oxide levels required to maintain the vascular microenvironment in a mild state of inhibition. We conclude that mild exercise represents an alternate and economical therapy to preserve health and/or diminish the rate of decline of the normal physiological processes that may even be associated with aging. 相似文献
6.
The accumulated evidence suggests that the overproduction of nitric oxide (NO) is involved in methamphetamine (METH)-induced neurotoxicity. Using NADPH-diaphorase histochemistry, neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) antibody immunohistochemistry, the possible overexpression of nNOS and iNOS was investigated in the brains of mice treated with METH. The number of positive cells or the density of positive fibers was assessed at 1 h, 24 h and 1 week after METH injections. There were no clear positive iNOS cells and fibers demonstrated in the brains of mice after METH treatment. In contrast, METH caused marked increases in nNOS in the striatum and hippocampus at 1 and 24 h post-treatment. The nNOS expression normalized by 1 week. There were no statistical changes in nNOS expression in the frontal cortex, the cerebellar cortex, nor in the substantia nigra. These results provide further support for the idea that NO is involved in the neurotoxic effects of METH. 相似文献
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Michael A. Weber MD Ernesto L. Schiffrin MD William B. White MD Samuel Mann MD Lars H. Lindholm MD John G. Kenerson MD John M. Flack MD Barry L. Carter Pharm D Barry J. Materson MD C. Venkata S. Ram MD Debbie L. Cohen MD Jean‐Claude Cadet MD Roger R. Jean‐Charles MD Sandra Taler MD David Kountz MD Raymond R. Townsend MD John Chalmers MD Agustin J. Ramirez MD George L. Bakris MD Jiguang Wang MD Aletta E. Schutte MD John D. Bisognano MD Rhian M. Touyz MD Dominic Sica MD Stephen B. Harrap MD 《Journal of clinical hypertension (Greenwich, Conn.)》2014,16(1):14-26
10.
Addictions to licit and illicit drugs are chronic relapsing brain disorders that affect circuits that regulate reward, motivation, memory, and decision-making. Drug-induced pathological changes in these brain regions are associated with characteristic enduring behaviors that continue despite adverse biopsychosocial consequences. Repeated exposure to these substances leads to egocentric behaviors that focus on obtaining the drug by any means and on taking the drug under adverse psychosocial and medical conditions. Addiction also includes craving for the substances and, in some cases, involvement in risky behaviors that can cause death. These patterns of behaviors are associated with specific cognitive disturbances and neuroimaging evidence for brain dysfunctions in a diverse population of drug addicts. Postmortem studies have also revealed significant biochemical and/or structural abnormalities in some addicted individuals. The present review provides a summary of the evidence that has accumulated over the past few years to implicate brain dysfunctions in the varied manifestations of drug addiction. We thus review data on cerebrovascular alterations, brain structural abnormalities, and postmortem studies of patients who abuse cannabis, cocaine, amphetamines, heroin, and “bath salts”. We also discuss potential molecular, biochemical, and cellular bases for the varied clinical presentations of these patients. Elucidation of the biological bases of addiction will help to develop better therapeutic approaches to these patient populations. 相似文献