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BACKGROUND: There have been no previous studies on the role of inflammation in the brain for the second most common dementing disorder, dementia with Lewy bodies. OBJECTIVE: To investigate the degree of cortical inflammation in dementia with Lewy bodies (DLB) compared with Alzheimer disease (AD) and control brains. DESIGN AND MAIN OUTCOME MEASURES: Post-mortem tissue collection from a brain donor program using standardized diagnostic criteria. Brains collected from January 1, 1993, through December 31, 1996, were screened and selected only for the presence or absence of tau neuritic plaques. Results of immunohistochemistry for HLA-DR were quantified using area fraction counts. Counts were performed by investigators who were unaware of the diagnosis. Results were compared across groups using analysis of variance and posthoc testing. SETTING: A medical research institute in Sydney, Australia. PATIENTS: Eight brains with DLB and without the tau neuritic plaques typical of AD, 10 brains with AD and no Lewy bodies, and 11 nondemented controls without significant neuropathological features were selected from a consecutive sample. RESULTS: Compared with AD, DLB demonstrated significantly less inflammation in the form of HLA-DR-reactive microglia in all cortical regions (P<.001, posthoc). The level of inflammation in DLB was comparable to that seen in controls (P=.54, post hoc). CONCLUSIONS: Inflammation appears related to the tau neuritic plaques of AD. Despite similar clinical presentations, therapeutic anti-inflammatory strategies are not likely to be effective for pure DLB. Arch Neurol. 2000. 相似文献
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School sport is a major cause of injury in the post-primary age group. The importance of primary prevention in sport has been identified; however secondary prevention of school related sport injury has not been described in Ireland. A random sample of 450 schools in Northern Ireland and the Republic of Ireland was studied using a postal questionnaire. Current management of sport injury, with particular interest in the expertise and training of teachers and coaches, was explored. Replies were received from 333 (74%) schools. There was no physical education teacher with up to date first aid training in 37% schools. Immediate care in terms of mechanisms and equipment to deal with injury was available in 35%-81% of schools responding. Correct response ranged from 65%-90% to four scenarios: commonly presenting yet potentially serious management problems. This study demonstrated deficiencies in sport injury care. In addition to concern about current training, a need for basic life support training is highlighted. These findings have implications for the prevention of school sports injuries. 相似文献
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Oberyszyn TM; Conti CJ; Ross MS; Oberyszyn AS; Tober KL; Rackoff AI; Robertson FM 《Carcinogenesis》1998,19(3):445-455
The beta2 integrin (CD 18/CD 11 a, b, c) family of proteins mediate
adherence of leukocytes to vascular endothelium and the associated ligand,
intercellular adhesion molecule-1 (ICAM-1; CD 54), interacts with beta2
integrin proteins to allow transendothelial migration of leukocytes into
sites of inflammation. The present study examines the function of these
proteins in a murine model of acute cutaneous inflammation induced
following topical application of 12-O- tetradecanoylphorbol-13-acetate
(TPA) to the dorsal epidermis of SENCAR mice and in a model of skin
multistage carcinogenesis. At 24 h following topical application of TPA to
the dorsal epidermis of mice, dermal leukocytes expressed higher levels of
beta2 integrin protein compared with the lower levels of beta2 integrin
protein expression by peripheral blood leukocytes. ICAM-1 protein was
localized to epidermal keratinocytes and vascular endothelium in
TPA-treated skin and to proliferating papilloma cells. Intravenous (i.v.)
injection of either 50 microg anti-beta2 integrin antibody alone or in
combination with anti-ICAM-1 antibody significantly inhibited both
TPA-stimulated neutrophil infiltration into the dermis (P < 0.001) and
myeloperoxidase (MPO) activity (P < 0.03 anti-beta2 integrin antibody; P
< 0.01 anti- beta2 integrin + ICAM-1 adhesion molecule antibodies), but
had no effect on TPA-induced epidermal hyperplasia. In addition, injection
of either anti-ICAM-1 adhesion molecule antibody alone (P < 0.004) or in
combination with anti-beta2 integrin antibody (P < 0.001) significantly
inhibited TPA-induced production of 7,8-dihydroxy-2'-deoxyguanosine (8-
OHdG) immunoreactive proteins by epidermal keratinocytes. Beta2
integrin/ICAM-1 adhesion molecules work in concert to regulate migration,
retention and functional activation of leukocytes within the dermis during
TPA-induced skin inflammation and within stromal tissue of papillomas that
form during multi-stage carcinogenesis. Agents that inhibit these
receptor/ligand interactions may be useful in defining the roles of
specific cell populations in cutaneous inflammation and multistage
carcinogenesis and may also have potential as anti-promoting and
anti-progression agents.
相似文献
57.
Bolontrade MF; Stern MC; Binder RL; Zenklusen JC; Gimenez-Conti IB; Conti CJ 《Carcinogenesis》1998,19(12):2107-2113
In this study we have analyzed the vascular response induced in the two-
stage carcinogenesis model in SENCAR mice. The role of angiogenesis has not
been explored in this model, which is the paradigm of multistage
carcinogenesis and a model for neoplastic lesions derived from exophytic
premalignant lesions (e.g. colon carcinoma, bladder papilloma). We
investigated if angiogenesis is involved in the formation of papillomas and
in the progression from papilloma to carcinoma. To this end we analyzed the
vasculature of normal and hyperplastic skin, focal epidermal hyperplasias
that are precursors of papillomas, papillomas at different stages and
squamous cell carcinomas. We also analyzed the vascularization of
papillomas induced in two strains of mice that differ in their
susceptibility to malignant progression. We show here that angiogenesis is
turned on in the earliest stages of papilloma formation. In late stages,
regardless of state of progression, the predominant response is an increase
in the size of blood vessels. Thus, in the SENCAR mouse model,
representative of exophytic tumors, the angiogenesis switch is a very early
event, probably mechanistically related to the development of the primarily
exophytic lesions. Therefore, the density of blood vessels cannot be used
as a predictor of malignant progression in this model.
相似文献
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