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排序方式: 共有355条查询结果,搜索用时 31 毫秒
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Lankin VZ Sherenesheva NI Konovalova GG Tikhaze AK 《Bulletin of experimental biology and medicine》2000,130(7):694-696
The effects of pretreatment with β-carotene-containing preparation carinat on the development of renal tumors in rats receiving
single intravenous injection of chemical carcinogen 3-(1-α-L-arabinopyranosyl)-1-methyl-1-nitrosourea were studied. Fourteen
months after carcinogen administration, the degree of lipid oxidation in rat kidneys 2.5-fold surpassed that in animals receiving
carinat in a dose producingin vivo antioxidant effect. Carinat decreased the total number of induced tumors and the incidence of mesenchymal renal tumors and
suppressed the development of multiple tumors. The accumulation of lipoperoxides in the kidneys during carcinogenesis is associated
with activation of free radical processes and carcinogen-induced inhibition of lipoperoxide enzymatic degradation and probably
promotes renal malignancies due to co-carcinogenic action of these compounds. The data suggest that carinat-induced suppression
of tumor development attests to antioxidant effects of β-carotene.
Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 130, No. 7, pp. 95–97, July, 2000 相似文献
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Gene conversion is a likely cause of mutation in PKD1 总被引:3,自引:0,他引:3
Watnick TJ; Gandolph MA; Weber H; Neumann HP; Germino GG 《Human molecular genetics》1998,7(8):1239-1243
Approximately 70% of the gene responsible for the most common form of
autosomal dominant polycystic kidney disease ( PKD1 ) is replicated in
several highly homologous copies located more proximally on chromosome 16.
We recently have described a novel technique for mutation detection in the
duplicated region of PKD1 that circumvents the difficulties posed by these
homologs. We have used this method to identify two patients with a nearly
identical cluster of base pair substitutions in exon 23. Since pseudogenes
are known to be reservoirs for mutation via gene conversion events for a
number of other diseases, we decided to test whether these sequence
differences in PKD1 could have arisen as a result of this mechanism. Using
changes in restriction digest patterns, we were able to show that these
sequence substitutions are also present in N23HA, a rodent-human somatic
cell hybrid that contains only the PKD1 homologs. Moreover, these changes
were also detected in total DNA from several affected and unaffected
individuals that did not harbor this mutation in their PKD1 gene copy. This
is the first example of gene conversion in PKD1 , and our findings
highlight the importance of using gene-specific reagents in defining PKD1
mutations.
相似文献
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V. P. Tverdokhlib G. G. Konovalova V. Z. Lankin F. Z. Meerson 《Bulletin of experimental biology and medicine》1988,106(5):1526-1528
All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR. Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Grenburg Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR I. K. Shkhvatsabaya.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 106, No. 11, pp. 528–529, November, 1988. 相似文献
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BACKGROUND & AIMS: Shwachman syndrome is an inherited condition with multisystemic abnormalities, including exocrine pancreatic dysfunction. The aim of this study was to evaluate the occurrence and progression of features in a large cohort of patients. METHODS: Clinical records of 25 patients with Shwachman syndrome were reviewed. RESULTS: Mean birth weight (2.92 +/- 0.51 kg) was at the 25th percentile. However, by 6 months of age, mean heights and weights were less than the 5th percentile. After 6 months of age, growth velocity was normal. Severe fat maldigestion due to pancreatic insufficiency was present in early life (fecal fat, 26% +/- 17% of fat intake; age, < 2 years). Serial assessment of exocrine pancreatic function showed persistent deficits of enzyme secretion, but 45% of patients showed moderate age-related improvements leading to pancreatic sufficiency. Neutropenia was the most common hematologic abnormality (88%), but leukopenia, thrombocytopenia, and anemia were also frequently encountered. Patients with hypoplasia of all three bone marrow cellular lines (n = 11) had the worst prognosis; 5 patients died, 2 of sepsis and 3 of acute myelogenous leukemia. Other findings included hepatomegaly and/or abnormal liver function test results and skeletal abnormalities. CONCLUSIONS: A wide and varied spectrum of phenotypic abnormalities among patients with Shwachman syndrome is described. Pancreatic acinar dysfunction is an invariable abnormality. Patients with severe bone marrow involvement may have a guarded prognosis. (Gastroenterology 1996 Dec;111(6):1593-602) 相似文献
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Sedankin M. K. Gudkov A. G. Vesnin S. G. Konovalova A. A. Leushin V. Yu. Solov’ev Yu. V. Sidorov I. A. Agasieva S. V. Chizhikov S. V. Gorlacheva E. N. 《Biomedical engineering》2021,55(3):224-228
Biomedical Engineering - We present here an analytical review of technical means used for intracavity thermometry of biological objects. Radiometers can be effective both in medicine and veterinary... 相似文献
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Prostaglandin E2 (PGE2) is produced by activated platelets and by several other cells, including capillary endothelial cells. PGE2 exerts a dual effect on platelet aggregation: inhibitory, at high, supraphysiologic concentrations, and potentiating, at low concentrations. No information exists on the biochemical mechanisms through which PGE2 exerts its proaggregatory effect on human platelets. We have evaluated the activity of PGE2 on human platelets and have analyzed the second messenger pathways involved. PGE2 (5 to 500 nmol/L) significantly enhanced aggregation induced by subthreshold concentrations of U46619, thrombin, adenosine diphosphate (ADP), and phorbol 12-myristate 13-acetate (PMA) without simultaneously increasing calcium transients. At a high concentration (50 mumol/L), PGE2 inhibited both aggregation and calcium movements. PGE2 (5 to 500 nmol/L) significantly enhanced secretion of beta-thromboglobulin (beta TG) and adenosine triphosphate from U46619- and ADP-stimulated platelets, but it did not affect platelet shape change. PGE2 also increased the binding of radiolabeled fibrinogen to the platelet surface and increased the phosphorylation of the 47-kD protein in 32P- labeled platelets stimulated with subthreshold doses of U46619. Finally, the amplification of U46619-induced aggregation by PGE2 (500 nmol/L) was abolished by four different protein kinase C (PKC) inhibitors (calphostin C, staurosporine, H7, and TMB8). Our results suggest that PGE2 exerts its facilitating activity on agonist-induced platelet activation by priming PKC to activation by other agonists. PGE2 potentiates platelet activation at concentrations produced by activated platelets and may thus be of pathophysiologic relevance. 相似文献