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1.
It is widely believed that family planning has important benefits for both maternal and child health. Despite this, little work has been done to quantify the potential effect of family planning in reducing maternal mortality. This paper assesses the impact of family planning in averting maternal deaths, and discusses the overall ability of risk strategies to address the bulk of maternal mortality. The practical difficulties of providing effective contraception to populations with high maternal mortality are addressed, and the need for maternal health care services as an adjunct to useful family planning programs is emphasized. Although family planning cannot by itself cause a substantial reduction in risk of pregnancy, the combined strategies of general fertility reduction, abortion services, and family planning for high-risk groups might effectively address about half of all maternal mortality in the developing world. Pregnancy and delivery care have the potential for saving large numbers of lives with appropriate interventions. It is concluded that reproductive risks can be reduced only by preventing unwanted pregnancies and protecting maternal health during wanted ones. 相似文献
2.
The climbing fibre projection from the motor cortex to the cerebellar cortical C1 zone in the posterior lobe of the rat cerebellum was investigated using a combination of physiological, anatomical and neuropharmacological techniques. Electrical stimulation of the ipsilateral fore- or hindimbs or somatotopically corresponding parts of the contralateral motor cortex evoked climbing fibre field potentials at the same cerebellar recording sites. Forelimb-related responses were located in the C1 zone in the paramedian lobule or lobulus simplex and hindlimb-related responses were located in the C1 zone in the copula pyramidis. Microinjections of anterograde axonal tracer (Fluoro-Ruby or Fluoro-Emerald) were made into the fore- or hindlimb parts of the motor cortex where stimulation evoked the largest cerebellar responses. After a survival period of 7–10 days, the neuraxis was examined for anterograde labelling. No terminal labelling was ever found in the inferior olive, but labelled terminals were consistently found in a well-localized site in the dorso-medial medulla, ventral to the gracile nucleus, termed the matrix region. Pharmacological inactivation of the matrix region (2 mm caudal to the obex) selectively reduced transmission in descending (cerebro-olivocerebellar) but not ascending (spino-olivocerebellar) paths targeting fore- or hindlimb-receiving parts of the C1 zone. Transmission in spino-olivocerebellar paths was either unaffected, or in some cases increased. The identification of a novel pre-olivary relay in cerebro-olivocerebellar paths originating from fore- and hindlimb motor cortex has implications for the regulation of transmission in climbing fibre pathways during voluntary movements and motor learning. 相似文献
3.
The effects of arachidonic acid and its metabolites on gamma-aminobutyric acid (GABAA) receptor function were determined in rat cerebral cortical synaptoneurosomes. Incubation of synaptoneurosomes with phospholipase A2 decreased muscimol-induced 36Cl- uptake. Arachidonic acid, the major unsaturated fatty acid released by phospholipase A2, also inhibited muscimol-induced 36Cl uptake. Similar inhibition was obtained with other unsaturated fatty acids (docosahexaenoic, oleic) but not with saturated fatty acids (stearic, palmitic). The effect of arachidonic acid on muscimol responses was inhibited by bovine serum albumin (BSA), and BSA enhanced muscimol responses directly, indicating the generation of endogenous arachidonic acid in the synaptoneurosome preparation. The generation of endogenous arachidonic acid was also indicated by the ability of 2 inhibitors of arachidonic acid metabolism, indomethacin and nordihydroguaiaretic acid (NDGA), to inhibit muscimol-induced 36Cl uptake. We conclude that arachidonic acid probably has both direct and indirect actions on muscimol responses since both enzyme inhibitors inhibited muscimol responses but did not prevent the effect of exogenously added arachidonic acid. In additional experiments, arachidonic acid metabolites generated by cyclooxygenase, prostaglandins D2, E2 and F2 alpha, each decreased muscimol responses; prostaglandins F2 alpha was the most potent inhibitor. Since the unsaturated fatty acids and their metabolites are most susceptible to peroxidation, a generating system of superoxide radicals was tested on muscimol responses. A combination of xanthine and xanthine oxidase inhibited muscimol-induced 36Cl uptake in a concentration-dependent manner. We propose that the inhibition of GABAA neurotransmission by arachidonic acid and its metabolites can lead to increased neuronal excitability. This mechanism may play an important role in the development of neuronal damage following seizures or cerebral ischemia. 相似文献
4.
Jennie Ponsford Rochelle Whelan-Goodinson Alex Bahar-Fuchs 《Brain injury : [BI]》2007,21(13):1385-1392
Primary objectives: To establish pre-morbid alcohol and drug use in persons with TBI, relative to controls, investigate how patterns of substance use change over time following TBI and identify factors associated with heavy post-injury substance use.
Methods and procedures: The Alcohol Use Disorders Identification test (AUDIT) and Drug Abuse Screening Test (DAST) was completed by 121 hospital inpatients with TBI, documenting pre-injury alcohol and drug use, and 133 demographically similar controls. Participants with TBI completed these measures and the Hospital Anxiety and Depression Scale (HADS) again 1 and 2 years post-injury and 76 also completed them at 3 years.
Results: Participants with TBI showed similar levels of drug and alcohol use to controls pre-injury, with 31.4% of the TBI group and 29.3% of controls drinking at hazardous levels. Alcohol and drug use declined in the first year post-injury, but increased by 2 years post-injury, with only 21.4% of participants with TBI reporting abstinence from alcohol and 25.4% drinking at hazardous levels. Only 9% showed a drug problem, but 24% had returned to some drug use. Those showing heavy alcohol use post-injury were young, male and heavy drinkers pre-injury. Drug and alcohol use was similar at 3 years post-injury.
Conclusions: More active intervention is needed to reduce alcohol and drug use following TBI. 相似文献
Methods and procedures: The Alcohol Use Disorders Identification test (AUDIT) and Drug Abuse Screening Test (DAST) was completed by 121 hospital inpatients with TBI, documenting pre-injury alcohol and drug use, and 133 demographically similar controls. Participants with TBI completed these measures and the Hospital Anxiety and Depression Scale (HADS) again 1 and 2 years post-injury and 76 also completed them at 3 years.
Results: Participants with TBI showed similar levels of drug and alcohol use to controls pre-injury, with 31.4% of the TBI group and 29.3% of controls drinking at hazardous levels. Alcohol and drug use declined in the first year post-injury, but increased by 2 years post-injury, with only 21.4% of participants with TBI reporting abstinence from alcohol and 25.4% drinking at hazardous levels. Only 9% showed a drug problem, but 24% had returned to some drug use. Those showing heavy alcohol use post-injury were young, male and heavy drinkers pre-injury. Drug and alcohol use was similar at 3 years post-injury.
Conclusions: More active intervention is needed to reduce alcohol and drug use following TBI. 相似文献
5.
Henry Krum MD PhD Rochelle Goldsmith PhD Michelle Wilshire-Clement BSc Myron Miller MD Milton Packer MD 《The American journal of cardiology》1995,75(17):1284-1286
In conclusion, plasma levels of the endothelialderived vasoconstrictor endothelin-1 (but not those of other neurohormonal vasoconstrictor factors), measured during exercise correlated closely with objective variables of exercise capacity in patients with heart failure. These findings suggest that endothelin-1 may contribute to exercise intolerance in patients with heart failure, perhaps by limiting the ability of the peripheral vasculature to dilate during exercise. 相似文献
6.
Pharmaceutical Research - 相似文献
7.
Thomas C. Rainbow Rochelle D. Schwartz Bruce Parsons Kenneth J. Kellar 《Neuroscience letters》1984,50(1-3):193-196
Quantitative autoradiography was used to localize nicotinic [3H]acetylcholine (ACh) binding sites in rat brain. High concentrations of nicotinic [3H]ACh binding sites were observed in the anterior and medial nuclei of the thalamus, the medial habenula and the superficial layer of the superior colliculus. Moderate levels of binding sites were observed in a variety of brain regions such as the frontoparietal cortex and the hippocampus. Low levels of nicotinic ACh sites occurred throughout the hypothalamus and the primary olfactory cortex. 相似文献
8.
Inhibition of Migration of Mouse Macrophages by Tuberculin-Sensitive Mouse Lymphocytes and by Mouse Migration Inhibitory Factor
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The guinea pig migration inhibition technique, an accepted in vitro correlate of delayed hypersensitivity, has been adapted to a murine system. Peritoneal exudate cells from CF-1 mice vaccinated with viable cells of the H37Ra strain of Mycobacterium tuberculosis were inhibited in vitro by purified protein derivative (PPD) or whole H37Ra microorganisms. Peritoneal exudate cells from the inbred C57Bl/6 mice immunized with H37Ra cells also were inhibited in vitro by PPD or whole H37Ra microorganisms. Migration inhibitory factor (MIF) was produced by splenic lymphocytes from the H37Ra-immunized C57Bl/6 mice when incubated with either antigen. Intravenous injection of PPD or viable H37Ra organisms into H37Ra mice resulted in MIF production in vitro by splenic lymphocytes without further antigenic stimulation. Peritoneal exudate cells from nonimmunized C57Bl/6 mice and supernatant fluids from cultures of lymphocytes from nonimmunized C57Bl/6 mice were not inhibited in the presence of antigen. The production of MIF by splenic lymphocytes from immunized C57Bl/6 mice depended upon the conditions under which the lymphocytes were cultured, the time of exposure to antigen (3 days), the use of a higher concentration of PPD for stimulation of lymphocytes than that required for guinea pig cells, and also the use of cells from a highly inbred mouse strain. 相似文献
9.
Moallem HJ Taningo G Jiang CK Hirschhorn R Fikrig S 《Clinical immunology (Orlando, Fla.)》2002,105(1):75-80
Purine nucleoside phosphorylase (PNP) deficiency results in an autosomal recessive immunodeficiency disease characterized by initial involvement of cellular immunity and neurological manifestations with subsequent abnormalities of humoral immunity. The initial presentation and clinical course has varied widely in the relatively few published cases. The molecular basis has been reported in only 10 patients, precluding evaluation of phenotype-genotype relationships. We now report clinical, immunologic, and molecular findings in a new case of relatively early onset that emphasizes hypotonia and developmental delay as early manifestations. The patient carried two novel missense mutations (Gly56A1a and Val217Ile) on the same allele in apparent homozygosity. Expression of each of the mutant enzymes in vitro demonstrated that the Gly156A1a mutation abolished enzyme activity while the Val217Ile mutation was without obvious effect and is therefore a normal variant. Such "normal" polymorphisms might be associated with a variable response to the immunosuppressive PNP inhibitors currently in clinical trials. 相似文献
10.
Steven M. Kubersky Rochelle Hirschhorn M. Johan Broekman Bruce N. Cronstein 《Inflammation》1989,13(5):591-599
Chemoattractants are generated at inflammatory loci that not only induce neutrophils (PMNs) to leave the vasculature but also stimulate PMNs to release potentially toxic agents (e.g., H2O2, O
2
–
or OH). We have recently demonstrated that endothelium releases adenosine which, when bound to a specific receptor on the PMN surface, inhibits release of toxic oxygen metabolites from stimulated PMN. To determine whether occupancy of adenosine receptors modulates generation and release of oxygen metabolites, we have studied the effect of 2-chloroadenosine on O
2
–
generation and O2 consumption in response to opsonized zymosan particles (STZ) and immune complexes (IC). 2-Chloroadenosine inhibits, in a dose-dependent fashion, Of generation by neutrophils that have been exposed to C3b-coated particles (STZ). Inhibition of Of generation is similar in the presence or absence of cytochalasin B (IC50=53 ±19 and 16 ±5nM, respectively,P=NS). Since occupancy of adenosine receptors might inhibit only externalization but not generation of oxygen metabolites, we studied the effect of 2-chloroadenosine on oxygen consumption by activated neutrophils. 2-Chloroadenosine inhibited O2 consumption stimulated by STZ and the surrogate bacterial chemoattractant FMLP; however, inhibition of O2 consumption varied with the presence or absence of cytochalasin B. In contrast, when neutrophils were stimulated by immune complexes, 2-chloroadenosine only minimally inhibited O
2
–
release and O2 consumption (10 ± 5 and 5 ± 4% inhibition, respectively). Thus, occupancy of adenosine receptors inhibits O2 consumption in parallel with inhibition of O
2
–
release. These results support the hypothesis that ingestion of complement-opsonized particles stimulates the respiratory burst by a mechanism different from that by which the respiratory burst is stimulated after occupancy of Fc receptors. Moreover, these observations suggest that endothelium, by releasing adenosine, prevent activated neutrophils from damaging the microvasculature at inflammatory loci. In contrast, deposition of immune complexes in vessel walls leads to vascular damage because endothelial cells are incapable of preventing attack by immune complex-stimulated neutrophils.This research was supported by grants from the U.S. Public Health Service (AI-10343 and HL29034) and the Veterans Administration.Dr. Cronstein is the recipient of a Clinical Investigator Award (K11-AR-01490) and was a fellow of the Arthritis Foundation. Dr. Broekman was an Established Investigator of the American Heart Association. 相似文献