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41.
As the nation moves to reform Medicare and the health care industry becomes more competitive which will dramatically change the means by which health care is organized and financed, state governments ought to be establishing administrative capacity to administer new systems. This article describes past experiences of states in similar efforts and uses the legislation written in 13 states to analyze in greater detail current state health reform activities. Policies that create new central authorities have the greatest likelihood of building the appropriate administrative infrastructures. Provisions related to establishing data bases, creating regional authorities or advisory committees, establishing uniform claims, and facilitating integrated systems of care are common to several proposals. Previous state experiences with health planning and citizen involvement are evident in the schemes being proposed and enacted. 相似文献
42.
The acute morphological response to amosite asbestos in the guinea pig was studied by light microscopy and by transmission, scanning, and scanning transmission electron microscopy. Fiber identification was carried out by energy dispersive X-ray analysis. Animals were studied at postinjection intervals of 2, 4, and 12 hr and 1-7 days. Three groups of test animals were studied for each time interval. These consisted of a vascularly perfused parenchymal group and a free cell lavaged group. The information obtained was compared with saline-injected and normal control animals. The acute tissue response was characterized by intraalveolar, not interstitial, events. The early phagocytic response was shared between polymorphs and macrophages, while in the longer intervals, the macrophages were the phagocytic cell type. Packaging differences within the two types of phagocytes were seen. Endothelial stability was noted, while some edematous type I pneumocytes were observed. Fibrotic involvement was limited to some intraalveolar fibrin deposits. It is suggested that the term "free asbestos fibers" refers to an extracellular event, while intracellular fibers are coated with either a membranous sheath, a siderosome, or a classical ferruginous coating. 相似文献
43.
44.
Alterations in tyrosine protein kinase activities upon activation of human neutrophils 总被引:2,自引:0,他引:2
Human neutrophils are phagocytic cells that can be activated by a variety of agonists to undergo a group of physiologic responses. This "stimulus-response" coupling is thought to be dependent on the phosphorylation of specific proteins. We have previously shown that, in addition to the widely distributed serine and threonine protein kinases, neutrophils contain tryosine protein kinase activity in the cell cytosol and particulate fractions. When neutrophils are treated with a variety of agents, phosphorylation of both cytosolic and particulate proteins on tyrosine residues occurs. Increases in tyrosine phosphorylation may be a result of increases in the activity of tyrosine kinases or a decrease in the activity of phosphotyrosine phosphatases. In this study, we have used a novel nondenaturing polyacrylamide gel electrophoretic method to demonstrate that treatment of human neutrophils with the chemotactic peptide FMLP or the phorbol ester phorbol myristate acetate induces a time- and concentration-dependent increase in the tyrosine protein kinase activity found in the cell cytosol and cell particulate fraction. The time course and concentration range over which these changes occur are similar to those seen for activation of the neutrophil oxidative burst and phosphorylation of proteins on tyrosine residues, suggesting that these events may be related. 相似文献
45.
Frequency of the ATM IVS10-6T→G variant in Australian multiple-case breast cancer families
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46.
Hypospadias trends in two US surveillance systems 总被引:6,自引:0,他引:6
OBJECTIVE: Hypospadias is a common congenital anomaly, the cause of which is unknown. Unexplained increases in the rates of hypospadias occurred in five European countries in the 1970s and 1980s. We examined data from two birth defects surveillance systems in the United States for evidence of similar trends. METHODOLOGY: The Metropolitan Atlanta Congenital Defects Program (MACDP) provided birth prevalence rates from 1968 to 1993. The nationwide Birth Defects Monitoring Program (BDMP) provided rates from 1970 to 1993. MACDP data are population-based and could be categorized by the severity of the hypospadias. BDMP data allowed analysis of rate trends for the four census regions of the United States. RESULTS: Data from both surveillance systems showed an approximate doubling of hypospadias rates in the 1970s and 1980s. MACDP data showed that the rate of severe cases increased while the ratio of mild to severe cases decreased. BDMP data showed that hypospadias rates increased markedly in all four regions of the United States. CONCLUSIONS: The observed increases are unlikely to be attributable to increased sensitivity of the surveillance systems or the identification of more mild cases by physicians over time, because either trend would have increased rather than decreased the ratio of mild to severe cases. If real, these trends represent the largest number of cases and the first report of an increase in hypospadias rates outside of Europe. Additional investigation of a possible increase in hypospadias rates is warranted. 相似文献
47.
Gonzales AJ; Christensen JG; Preston RJ; Goldsworthy TL; Tlsty TD; Fox TR 《Carcinogenesis》1998,19(7):1173-1183
48.
Guo RJ; Wang Y; Kaneko E; Wang DY; Arai H; Hanai H; Takenoshita S; Hagiwara K; Harris CC; Sugimura H 《Carcinogenesis》1998,19(9):1539-1544
Mutations in the transforming growth factor beta type II receptor
(TGFbetaRII) gene have been detected in several human cancer types
exhibiting microsatellite instability. Using intron primers previously
reported for examination of the entire coding region of the TGFbetaRII
gene, 29 sporadic gastric cancers were screened with non-radioactive single
strand conformation polymorphism and subsequent DNA sequencing analysis.
Mutations of the TGFbetaRII gene were detected in three out of 29 tumors
(10%). Two cases showed deletions in a polyadenine tract in both alleles
and was positively associated with replication error. One case had an
insertion of GA dinucleotide sequence in one allele. Mutations of the
TGFbetaRII gene were restricted to exon 3 and other coding regions were not
affected. Loss of heterozygosity was detected by analyzing a polymorphic
site in intron 2. Three out of nine (33%) informative cases, which were all
of intestinal type and advanced cases, showed loss of heterozygosity but
neither TGFbetaRII mutation nor replication error was found in these cases.
Immunoreactivity of TGFbetaRII in tumor tissues was reduced to a different
extent in the gastric cancer with genetically abnormal transforming growth
factor. Although the numbers studied are small, homozygous (A)10 deletion
or loss of heterozygosity of TGFbetaRII is involved in tumorigenesis and
progression of at least some part of sporadic gastric cancer.
相似文献
49.
50.
Tumour cell growth may be accelerated by protein kinase C (PKC) agonists
such as phorbol esters and receptor tyrosine kinases, but receptor tyrosine
kinases are in turn desensitized to growth factors by PKC agonists. To
clarify this apparent PKC bifunctionality, we have used phosphoantibodies
to determine the relationship between PKC- dependent phosphorylation events
affecting the ErbB2 oncoprotein in G8/DHFR 3T3 cells. Neither the kinetics
nor the extent of phorbol- induced juxtamembrane domain (Thr686)
phosphorylation vary directly with C-terminal (Tyr1222) dephosphorylation,
with Tyr1222 continuing to be dephosphorylated long after Thr686
phosphorylation has also declined. Platelet-derived growth factor (PDGF)
mimics the short-term effects of phorbol on Thr686 and Tyr1222
phosphorylation, and confocal microscopy reveals that both of these PKC
agonists induce rapid internalization of PKC-modified ErbB2. Phorbol causes
sustained cytoplasmic accumulation of PKC-phosphorylated receptors,
however, whereas PDGF triggers the appearance of this ErbB2 subset only
briefly. Metabolic labelling and co-precipitation studies fail to implicate
heterologous molecules in either the tyrosine dephosphorylation or
internalization of PKC-modified ErbB2. Taken in the context of earlier
juxtamembrane domain mutagenesis studies, these findings indicate that
phorbol-activated PKC may desensitize growth factor receptors to
extracellular ligands solely by triggering sustained receptor
internalization. We submit that PKC-dependent juxtamembrane domain
phosphorylation represents a physiological mechanism for shortening the
duration and enhancing the specificity of growth factor signalling by
promoting internalization of liganded and unliganded receptors,
respectively.
相似文献