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Decreased expression of phospholipase C-beta 2 isozyme in human platelets with impaired function 总被引:4,自引:4,他引:4
Platelets from a patient with a mild inherited bleeding disorder and abnormal platelet aggregation and secretion show reduced generation of inositol 1,4,5-trisphosphate, mobilization of intracellular Ca2+, and phosphorylation of pleckstrin in response to several G protein mediated agonists, suggesting a possible defect at the level of phospholipase C (PLC) activation (see accompanying report). A procedure was developed that allows quantitation of platelet PLC isozymes. After fractionation of platelet extracts by high-performance liquid chromatography, 7 out of 10 known PLC isoforms were detected by immunoblot analysis. The amount of these isoforms in normal platelets decreased in the order PLC- gamma 2 > PLC-beta 2 > PLC-beta 3 > PLC-beta 1 > PLC-gamma 1 > PLC- delta 1 > PLC-beta 4. Compared with normal platelets, platelets from the patient contained approximately one-third the amount of PLC-beta 2, whereas PLC-beta 4 was increased threefold. These results suggest that the impaired platelet function in the patient in response to multiple G protein mediated agonists is attributable to a deficiency of PLC-beta 2. They document for the first time a specific PLC isozyme deficiency in human platelets and provide an unique opportunity to understand the role of different PLC isozymes in normal platelet function. 相似文献
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SG Lindquist M Duno M Batbayli A Puschmann H Braendgaard S Mardosiene K Svenstrup LH Pinborg K Vestergaard LE Hjermind J Stokholm BB Andersen P Johannsen JE Nielsen 《Clinical genetics》2013,83(3):279-283
Recently, a hexanucleotide (GGGGCC) repeat expansion in the first intron of C9ORF72 was reported as the cause of chromosome 9p21‐linked frontotemporal dementia‐amyotrophic lateral sclerosis (FTD‐ALS). We here report the prevalence of the expansion in a hospital‐based cohort and associated clinical features indicating a wider clinical spectrum of C9ORF72 disease than previously described. We studied 280 patients previously screened for mutations in genes involved in early onset autosomal dominant inherited dementia disorders. A repeat‐primed polymerase chain reaction amplification assay was used to identify pathogenic GGGGCC expansions. As a potential modifier, confirmed cases were further investigated for abnormal CAG expansions in ATXN2. A pathogenic GGGGCC expansion was identified in a total of 14 probands. Three of these presented with atypical clinical features and were previously diagnosed with clinical olivopontocerebellar degeneration (OPCD), atypical Parkinsonian syndrome (APS) and a corticobasal syndrome (CBS). Further, the pathogenic expansion was identified in six FTD patients, four patients with FTD‐ALS and one ALS patient. All confirmed cases had normal ATXN2 repeat sizes. Our study widens the clinical spectrum of C9ORF72related disease and confirms the hexanucleotide expansion as a prevalent cause of FTD‐ALS disorders. There was no indication of a modifying effect of the ATXN2 gene. 相似文献
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Ahmed Z Elmaadawi Peter S Jensen L Eugene Arnold Brooke SG Molina Lily Hechtman Howard B Abikoff Stephen P Hinshaw Jeffrey H Newcorn Laurence Lee Greenhill James M Swanson Cathryn A Galanter 《World Journal of Psychiatry》2015,5(4):412-424
AIM: To determine the prevalence of bipolar disorder (BD) and sub-threshold symptoms in
children with attention deficit hyperactivity disorder (ADHD) through 14 years’
follow-up, when participants were between 21-24 years old.METHODS: First, we examined rates of BD type I and II diagnoses in youth
participating in the NIMH-funded Multimodal Treatment Study of ADHD (MTA). We used the
diagnostic interview schedule for children (DISC), administered to both parents (DISC-P) and
youth (DISCY). We compared the MTA study subjects with ADHD (n = 579) to a
local normative comparison group (LNCG, n = 289) at 4 different assessment
points: 6, 8, 12, and 14 years of follow-ups. To evaluate the bipolar variants, we compared
total symptom counts (TSC) of DSM manic and hypomanic symptoms that were generated by DISC in
ADHD and LNCG subjects. Then we sub-divided the TSC into pathognomonic manic (PM) and
non-specific manic (NSM) symptoms. We compared the PM and NSM in ADHD and LNCG at each
assessment point and over time. We also evaluated the irritability as category A2 manic symptom
in both groups and over time. Finally, we studied the irritability symptom in correlation with
PM and NSM in ADHD and LNCG subjects.RESULTS: DISC-generated BD diagnosis did not differ significantly in rates between ADHD
(1.89%) and LNCG 1.38%). Interestingly, no participant met BD diagnosis more than once in the 4
assessment points in 14 years. However, on the symptom level, ADHD subjects reported
significantly higher mean TSC scores: ADHD 3.0; LNCG 1.7; P < 0.001. ADHD
status was associated with higher mean NSM: ADHD 2.0 vs LNCG 1.1;
P < 0.0001. Also, ADHD subjects had higher PM symptoms than LNCG, with PM
means over all time points of 1.3 ADHD; 0.9 LNCG; P = 0.0001. Examining both
NSM and PM, ADHD status associated with greater NSM than PM. However, Over 14 years, the NSM
symptoms declined and changed to PM over time (df 3, 2523; F = 20.1; P <
0.0001). Finally, Irritability (BD DSM criterion-A2) rates were significantly higher in ADHD
than LNCG (χ2 = 122.2, P < 0.0001), but irritability was
associated more strongly with NSM than PM (df 3, 2538; F = 43.2; P <
0.0001).CONCLUSION: Individuals with ADHD do not appear to be at significantly greater risk for
developing BD, but do show higher rates of BD symptoms, especially NSM. The greater linkage of
irritability to NSM than to PM suggests caution when making BD diagnoses based on irritability
alone as one of 2 (A-level) symptoms for BD diagnosis, particularly in view of its frequent
presentation with other psychopathologies. 相似文献
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Mesenchymal stem cells exert differential effects on alloantigen and virus-specific T-cell responses 总被引:2,自引:0,他引:2
Karlsson H Samarasinghe S Ball LM Sundberg B Lankester AC Dazzi F Uzunel M Rao K Veys P Le Blanc K Ringdén O Amrolia PJ 《Blood》2008,112(3):532-541
Mesenchymal stem cells (MSCs) suppress alloantigen-induced T-cell functions in vitro and infusion of third-party MSCs seems to be a promising therapy for graft-versus-host disease (GVHD). Little is known about the specificity of immunosuppression by MSCs, in particular the effect on immunity to pathogens. We have studied how MSCs affect T-cell responses specific to Epstein-Barr virus (EBV) and cytomegalovirus (CMV). We found that EBV- and CMV-induced proliferation and interferon- (IFN-) production from peripheral blood mononuclear cells (PBMCs) was less affected by third-party MSCs than the response to alloantigen and that MSCs had no effect on expansion of EBV and CMV pentamer-specific T cells. Established EBV-specific cytotoxic T cells (CTL) or CMV-CTL cultured with MSCs retained the ability to proliferate and produce IFN- in response to their cognate antigen and to kill virally infected targets. Finally, PBMCs from 2 patients who received MSCs for acute GVHD showed persistence of CMV-specific T cells and retained IFN- response to CMV after MSC infusion. In summary, MSCs have little effect on T-cell responses to EBV and CMV, which contrasts to their strong immunosuppressive effects on alloreactive T cells. These data have major implications for immunotherapy of GVHD with MSCs and suggest that the effector functions of virus-specific T cells may be retained after MSC infusion. 相似文献
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