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Serum thymus and activation‐regulated chemokine/CCL17 (sTARC) is known as a good indicator for atopic dermatitis severity. Herein, we investigate whether sTARC correlates with severity and therapeutic response for alopecia areata (AA) in our 121 patients. The sTARC mean of AA totalis and universalis was significantly higher than mild AA. Next, we compared sTARC of diffuse AA (n = 14) and severity‐controlled patchy AA (n = 32) and found that sTARC in diffuse AA (564.2 ± 400.0 pg/mL) was significantly higher than that of the patchy type (344.0 ± 239.8 pg/mL), suggesting a potential role of TARC in active progression of diffuse AA. Ten patients with diffuse AA were treated with i.v. corticosteroid pulse therapy. Then, we tested whether sTARC can predict prognosis after the pulse therapy and found that baseline sTARC in the poor responders (1025.5 ± 484.8 pg/mL) was significantly higher than that in the good responders (complete remission at 24 months after the pulse therapy, 347.8 ± 135.7 pg/mL), indicating sTARC as a response biomarker in the corticosteroid pulse therapy for diffuse AA. Finally, to investigate TARC production in the affected hair follicles, we performed immunohistochemical double staining of TARC and CD68 using scalp skin specimens of diffuse AA with high titers of sTARC. The results showed their co‐localization in the infiltrating cells around the AA hair follicles, suggesting that TARC is mainly produced from CD68+ histiocytes. In conclusion, sTARC is a disease activity and response biomarker in AA, providing new insight beyond the T‐helper 1/2 paradigm to solve the immunological pathogenesis of AA.  相似文献   
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Vitiligo is an acquired disorder in which depigmented macules result from mostly autoimmune loss of melanocytes. The initiating process in vitiligo has still been uncertain. Here, we report the case of a 19‐year‐old man with undetermined/unclassified vitiligo with a new periphery‐spreading vitiligo lesion on the right dorsal hand after rigorous sun exposure. Histopathological evaluation showed noticeable infiltration of CD68+ macrophages, moderate infiltration of CD3+ T cells, little infiltration of CD8+ T cells and CD11c+ myeloid dendritic cells, HMB45/CD11c double‐positive cells, and Melan‐A/MART1+ deposits in the dermis. We surmised that melanocyte‐derived deposits were mostly phagocytosed by CD68+ macrophages and were faintly phagocytosed by CD11c+ myeloid dendritic cells, referring distribution of CD68+ mononuclear cells and melanocyte biomarkers. Complete repigmentation was achieved following topical application of hydrocortisone butyrate propionate 0.1% ointment. We summarize that prompt clearance of debris by macrophages would be essential to an excellent prognosis of complete repigmentation.  相似文献   
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We describe a 34‐year‐old Japanese man with syringotropic CD8+ mycosis fungoides (MF) accompanied by hypohidrosis who was treated with vorinostat and retinoids. Interestingly, immunohistochemical staining for dermcidin revealed a decrease of sweat in the eccrine glands, and a sweat test by the iodine starch method proved hypohidrosis in the MF‐affected areas. Six months after treatment with this combination therapy, the patient's advanced MF was under control.  相似文献   
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Objective: The role of inflammation in cognitive alterations in a post-operative setting is still not fully understood. Surgical interventions can cause systemic inflammations which eventually can induce neuroinflammation. However, the main causes of functional changes after surgery are still elusive. In this study, we investigated the role of CD38, a TNFα-inducible NADH+ cyclase and hydrolase. We assume that CD38 overexpression impairs mitochondrial ATP synthesis. Within the hippocampus, the resulting cellular death could lead to cognitive impairment.

Methods: Seventy-nine Wistar-HAN rats were subjected for three hours either to partial hepatectomy under sevoflurane anaesthesia (‘surgery’), sevoflurane anaesthesia alone (‘anaesthesia’) or control. Rats were randomly selected to determine levels of CD38, TNFα, IL-6, and ATP, for GFAP immunohistochemistry and for Morris Water Maze testing.

Results: Plasma TNFα and IL-6 levels were significantly higher in the surgery group in the immediate post-operative phase. GFAP expression and hippocampal CD38 concentration were significantly elevated 24 h after the intervention in the surgery group as compared to anaesthesia alone and controls. ATP levels did not differ significantly between the three groups. No treatment differences in spatial cognition parameters were found.

Conclusions: Surgery in the form of partial hepatectomy activated the peripheral immune system and induced hippocampal glial activation and a CD38 increase. These changes, however, were not associated with rats’ cognitive impairment ≥24 h after surgery.  相似文献   
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Purpose: MRL-lpr/lpr mice, a model for various autoimmune diseases, were repeatedly irradiated with 0.5 Gy of γ-rays, and changes in their autoimmune manifestations were investigated.

Materials and methods: MRL-lpr/lpr mice at 13 weeks of age were maintained in plastic cages and exposed whole-body to 0.5 Gy γ-ray irradiation from a 137Cs source 5 times per week for 4 weeks, from the time they were 13 weeks old until they reached 17 weeks old. Changes of autoimmune manifestations were examined 3 weeks later at the 20th week.

Results: Splenomegaly, lymphadenopathy, and proteinuria in MRL-lpr/lpr mice were clearly ameliorated by a total dose of 10 Gy (0.5 Gy/day×5 days/week for 4 weeks). Histologically severe disease-specific damage to the kidney and the salivary gland, i.e., glomerulonephritis and sialoadenitis, was also improved after irradiation. CD3+ CD4? CD8? CD45R/B220+ T cell numbers, which proliferate abnormally in MRL-lpr/lpr mice, were significantly decreased by the irradiation, possibly through induction of apoptosis. The elevated NO2? and NO3? (NOx?) production by macrophages of MRL-lpr/lpr mice was lowered by the irradiation. The irradiation also prolonged the life span of MRL-lpr/lpr mice. These phenomena may contribute to the amelioration of autoimmune manifestations in MRL-lpr/lpr mice exposed to repeated small-doses of γ-rays.

Conclusions: Repeated small-dose γ-ray exposure ameliorates the autoimmune manifestations in MRL-lpr/lpr model mice.  相似文献   
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Clinical observations report a greater propensity to develop Parkinson's disease (PD) in amphetamine users. 3,4‐Methylenedioxymethamphetamine (MDMA; “ecstasy”) is an amphetamine‐related drug that is largely consumed by adolescents and young adults, which may have neuroinflammatory and neurotoxic effects. Here, the objective was to evaluate in mice whether consumption of MDMA during adolescence might influence the neuroinflammatory and neurotoxic effects of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP), a toxin known to induce PD in humans. The activation of astroglia and microglia by glial fibrillary acidic protein (GFAP) and complement receptor type 3 (CD11b) immunohistochemistry and the degeneration of dopaminergic neurons by tyrosine hydroxylase (TH) immunohistochemistry were evaluated. MPTP (20 mg/kg × 4) was administered to mice treated from ages 8 weeks to 17 weeks with MDMA (10 mg/kg twice daily, two times a week). In mice that were chronically treated with MDMA, administration of MPTP induced a higher microglial and astroglial response in both the striatum and the substantia nigra pars compacta (SNc) compared with vehicle‐treated or vehicle + MPTP‐treated mice. Inflammatory changes were associated with a decrease in TH immunoreactivity in the SNc of MDMA‐treated mice and with a further decrease in the striatum and the SNc of MDMA + MPTP‐treated mice compared with vehicle‐treated, MDMA‐treated, and MPTP‐treated mice. The results demonstrate that chronic administration of MDMA during late adolescence in mice exacerbates the neurodegeneration and neuroinflammation caused by MPTP, suggesting that MDMA may constitute a risk factor for dopaminergic neuron degeneration. © 2013 International Parkinson and Movement Disorder Society  相似文献   
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