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81.
反相离子对-高效液相色谱法测定河豚毒素 总被引:9,自引:0,他引:9
目的建立了反相离子对-高效液相色谱法测定河豚毒素含量的方法。方法选用SHIMADZUODS色谱柱(150×6mm5μm),以0.2%(v/v)醋酸液为流动相,流速为1.2mL/min,检测波长为230nm。结果河豚毒素线性范围20~100μg/mL,r=0.9960(n=5);回收率为93.32%,RSD=5.41%(n=5);日内精密度为6.10%,日间精密度为7.42%(n=5)最低检测限50ng。结论方法准确、快速、简便,可作为迅速确定河豚毒素含量的测定方法。 相似文献
82.
Bacterial joint infections in England and Wales: analysis of bacterial isolates over a four year period 总被引:7,自引:2,他引:7
Data from 1158 cases of septic arthritis reported to the Public Health
Laboratory Service (PHLS) Communicable Disease Control Centre (CDSC) from
England and Wales over a 4 yr period (January 1990 December 1993) are
presented. Reports where a bacterial organism was isolated from synovial
fluid, or where an organism was isolated from blood cultures where a
diagnosis of septic arthritis was reported, were examined. Reports of
infection were more common in children (12.7% of infections were in the
under 10 age group) and the elderly (54.7% aged 60 or over), and were
higher in males in all age groups except in the elderly. The most common
causative organisms remain staphylococcal and streptococcal species,
comprising 40.6% (470) and 28% (324) of cases, respectively. The most
common streptococci seen were Streptococcus pneumoniae and Lancefield group
A beta-haemolytic Streptococcus organisms, 60.8% (197/324), although group
B, C and G organisms accounted for 33.6% of streptococcal isolates
(109/324). Haemophilus influenzae septic arthritis is not exclusive to
children as 23.2% (16- 69) of cases occurred over the age of 15. A total of
48% (635) of isolates were identified from both synovial fluid and blood
cultures, 32.6% (378) from joint fluid alone and 12.5% (146) from blood
cultures. Although this study excludes cases of septic arthritis where no
organism was isolated, it presents important bacteriological information
from a large number of isolates from England and Wales over a 4 yr period.
Risk factors identified include a joint prosthesis, joint
disease/connective tissue disorder. immunosuppression and diabetes.
相似文献
83.
84.
To precisely determine the genotype of Epstein-Barr virus (EBV) in Hodgkin's disease (HD), we simultaneously analyzed three divergent gene loci (EBNA-2, EBNA-3C, and EBER) that distinguish type A and B viruses. The primers designed to amplify these three gene loci encompass either type-specific deletion sequences (EBNA-2 and EBNA-3C) or type-specific point mutations (EBER) that identify the virus strain based on the sizes of the polymerase chain reaction (PCR)-amplified products or the mobility shifts in single-strand conformation polymorphism analysis. The locations of point mutations were identified by direct sequencing of the PCR-amplified DNA. We analyzed 15 EBV-infected cell lines and found a good correlation between EBNA-2 and EBNA-3C typing results. In contrast, approximately 33% of the cell lines analyzed maintained type A sequences in EBNA-2 and EBNA-3C genes while carrying type B sequences in the EBER region. Data obtained from analysis of cell lines served as a reference for studying HD samples. EBV DNA was detected in about 70% of HD. Among the EBV-positive samples, 56% were associated with type A virus, 13% with type B, and 31% with dual viral sequences. Thus, type A virus is predominant in HD. Based on the histology, the frequencies of EBV positivity were 83%, 71%, and 33% for mixed cellularity, nodular sclerosis, and lymphocyte predominance, respectively. The detection of high frequency of both type A and B sequences in HD may provide a lead in investigating the role of dual viral infection in EBV pathogenesis. 相似文献
85.
Suppression of B-cell development as a result of selective expansion of donor T cells during the minor H antigen graft-versus-host reaction 总被引:1,自引:2,他引:1
A murine model of bone marrow (BM) transplantation in which donor (B10.D2) and recipient (BALB/c) mice were major histocompatibility complex (MHC) (H-2d) and Mls-1 identical, but incompatible at multiple non-MHC minor histocompatibility (H) antigens, and at Mls-2,3 was used to examine regeneration of B-cell development during the minor H antigen graft-versus-host reaction (GVHR). Mice that received T-cell- depleted allogeneic BM regained significant pre-B cells (sIg- 14.8+) in their BM. Mice undergoing GVHR after transplantation with allogeneic BM + T cells had less than 2% pre-B cells in their BM at day 7 and only 12% to 14% pre-B cells at days 21 and 28 compared with greater than 20% pre-B cells in the allogeneic controls. After partial recovery, the pre- B cells in the BM of GVH mice again decreased to less than 3% by day 42. This abnormal pattern of pre-B cell development in mice undergoing GVHR was associated with a reduced response to interleukin-7 (IL-7) in vitro. The delay in B-lineage cell reconstitution in mice with GVHR correlated with the expansion of donor V beta 3+ T cells in both the spleen and BM. BM T cells from mice with GVHR as well as isolated V beta 3+ T cells inhibited IL-7 colony-forming units from normal BM in co-culture assays. This inhibition could be reversed with anti- interferon gamma (IFN gamma) antibody. These data suggest that the delay in appearance and the reduction in proportion and number of pre-B cells observed early during the GVH reaction in this model is caused, in part, by the inhibitory actions of IFN gamma derived from donor V beta 3+ T cells on B-lineage cell development. 相似文献
86.
Absence of human T-cell lymphotropic virus type I coinfection in human immunodeficiency virus-infected hemophilic men 总被引:2,自引:0,他引:2
Concern for transmission of human T-cell lymphotropic virus, type 1 (HTLV-1) infection to recipients of infected cellular blood products has prompted development of tests to eliminate blood units with HTLV-I antibodies. Most hemophilic men from the United States became infected with human immunodeficiency virus (HIV) before HIV donor screening and before blood products were processed to inactivate the virus. To assess whether these men might also be infected with HTLV-I, we examined the HTLV-I antibody status of 127 factor VIII (hemophilia A) recipients and 71 factor IX (hemophilia B) recipients. One HIV-seronegative and four HIV-seropositive persons were HTLV-I reactive by enzyme-linked immunosorbent assay (ELISA). Four of five ELISA-reactive serum samples were negative by HTLV-I immunoblot assay (IB); 1 reactive and 1 borderline reactive serum were indeterminate on IB (p19 reactivity), but negative by radioimmunoprecipitation assay (RIPA). Peripheral blood mononuclear cells from one patient with indeterminate HTLV-I IB were negative for HTLV-I genomic sequences by polymerase chain reaction. The other indeterminate patient's serum antibody pattern was stable over a 2-year period, suggesting this was not an instance of early HTLV-I seroconversion. These results reaffirm the safety of factor components in the United States with regard to HTLV-I but emphasize the importance and need for further testing of reactive HTLV-I ELISA results with a second more specific technique. 相似文献
87.
88.
89.
Transformed T lymphocytes infected by a novel isolate of human T cell leukemia virus type II 总被引:1,自引:0,他引:1
Chorba TL; Brynes R; Kalyanaraman VS; Telfer M; Ramsey R; Mawle A; Palmer EL; Chen AT; Feorino P; Evatt BL 《Blood》1985,66(6):1336-1342
Human T cell leukemia virus type II (HTLV-II) has been isolated from a patient (Mo) with features of leukemic reticuloendotheliosis (LRE) and from a patient with acquired immunodeficiency syndrome (AIDS). We have obtained another isolate of HTLV-II from a patient (CM) with severe hemophilia A, pancytopenia, and a 14-year history of staphylococcal and candidal infections but no evidence of T cell leukemia/lymphoma, AIDS, or LRE. Fresh mononuclear cells and cultured lymphocytes from CM express retroviral antigens indistinguishable by molecular criteria from HTLV-IIMo. Leukocyte cultures from CM yield hyperdiploid (48,XY, +2, +19) continuous lymphoid lines; human fetal cord blood lymphocytes (CBL) are transformed by cocultivation with these CM cell cultures but retain normal cytogenetic constitution. Electron microscopic examination of the CM cultures and transformed CBL reveals budding of extracellular viral particles, intracellular tubuloreticular structures, and viral particles contained within intracellular vesicles. CM cell cultures and the transformed CBL do not require exogenous interleukin 2, have T cell cytochemical features and mature T helper phenotypes, and exhibit minimal T helper and profound T suppressor activity on pokeweed mitogen-stimulated differentiation of normal B cells. These characteristics, which are similar to those observed with the first HTLV-II isolate, may represent properties of all HTLV-II-infected T cells. 相似文献
90.
Hooper WC; Phillips DJ; Ribeiro MJ; Benson JM; George VG; Ades EW; Evatt BL 《Blood》1994,84(2):483-489
Protein S deficiency, which is associated with thrombosis, can either be inherited or acquired. Recently, we reported that a decrease in free protein S was observed in 19 of 25 persons with HIV/AIDS. The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), has been reported to be elevated in human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) patients and has been shown to induce a procoagulant state on the surface of endothelial cells. We report here that recombinant TNF-alpha (rTNF-alpha) downregulated protein S synthesis in the SV-40T transfected human microvascular endothelial cell line (HMEC-1) model system by approximately 70% and in primary human umbilical vein and dermal microvascular endothelial cell cultures by approximately 50%. Using the HMEC-1 model, Northern blot analysis showed a decrease in protein S RNA at 24 hours that was corroborated by Western blot analysis and enzyme- linked immunosorbent assay (ELISA) quantification. Evidence supporting the specificity of the TNF-alpha effect included the following: (1) TNF- alpha down-regulation of protein S was completely blocked by TNF neutralizing antibody; (2) the effect was transient, and protein S was restored to near normal levels after TNF was removed from cell cultures; (3) an antibody directed to the TNF RI (55-kD receptor) was shown to mimic the action of TNF-alpha on HMEC-1 cells; and (4) other proinflammatory cytokines, interleukin (IL)-1, IL-6, and TGF-beta, had no effect on protein S secretion. However, TNF-alpha showed no regulatory control over protein S synthesis in the human hepatocellular carcinoma cell line HepG-2. We suggest that TNF-alpha downregulation of protein S may be a mechanism for localized procoagulant activity and thrombosis recently reported in some AIDS patients with associated protein S deficiency. 相似文献