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91.
92.
Alterations in neural Theory of Mind processing in euthymic patients with bipolar disorder and unaffected relatives 下载免费PDF全文
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Dionisio KL Howie SR Dominici F Fornace KM Spengler JD Donkor S Chimah O Oluwalana C Ideh RC Ebruke B Adegbola RA Ezzati M 《Journal of exposure science & environmental epidemiology》2012,22(2):173-181
Smoke from biomass fuels is a risk factor for pneumonia, the leading cause of child death worldwide. Although particulate matter (PM) is the metric of choice for studying the health effects of biomass smoke, measuring children's PM exposure is difficult. Carbon monoxide (CO), which is easier to measure, can be used as a proxy for PM exposure. We measured the exposure of children ≤ 5 years of age in The Gambia to CO using small, passive, color stain diffusion tubes. We conducted multiple CO measurements on a subset of children to measure day-to-day exposure variability. Usual CO exposure was modeled using a mixed effects model, which also included individual and household level exposure predictors. Mean measured CO exposure for 1181 children (n=2263 measurements) was 1.04 ± 1.46?p.p.m., indicating that the Gambian children in this study on average have a relatively low CO exposure. However, 25% of children had exposures of 1.3?p.p.m. or higher. CO exposure was higher during the rainy months (1.33 ± 1.62?p.p.m.). Burning insect coils, using charcoal, and measurement done in the rainy season were associated with higher exposure. A parsimonious model with fuel, season, and other PM sources as covariates explained 39% of between-child variation in exposure and helped remove within-child variability. 相似文献
95.
Jedrychowski W Perera FP Tang D Stigter L Mroz E Flak E Spengler J Budzyn-Mrozek D Kaim I Jacek R 《Nutrition (Burbank, Los Angeles County, Calif.)》2012,28(4):372-377
ObjectiveWe previously reported an association between prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAH) and lower birth weight, birth length, and head circumference. The main goal of the present analysis was to assess the possible impact of coexposure to PAH-containing barbecued meat consumed during pregnancy on birth outcomes.Materials and methodsThe birth cohort consisted of 432 pregnant women who gave birth at term (>36 wk of gestation). Only non-smoking women with singleton pregnancies, 18–35 y of age, and who were free from chronic diseases such as diabetes and hypertension, were included in the study. Detailed information on diet over pregnancy was collected through interviews and the measurement of exposure to airborne PAHs was carried out by personal air monitoring during the second trimester of pregnancy. The effect of barbecued meat consumption on birth outcomes (birth weight, length, and head circumference at birth) was adjusted in multiple linear regression models for potential confounding factors such as prenatal exposure to airborne PAHs, child's sex, gestational age, parity, size of mother (maternal prepregnancy weight, weight gain in pregnancy), and prenatal environmental tobacco smoke.ResultsThe multivariable regression model showed a significant deficit in birth weight associated with barbecued meat consumption in pregnancy (coeff = ?106.0 g; 95%CI: ?293.3, ?35.8). The effect of exposure to airborne PAHs was about the same magnitude order (coeff. = ?164.6 g; 95%CI: ?172.3, ?34.7). Combined effect of both sources of exposure amounted to birth weight deficit of 214.3 g (95%CI: ?419.0, ?9.6). Regression models performed for birth length and head circumference showed similar trends but the estimated effects were of borderline significance level. As the intake of barbecued meat did not affect the duration of pregnancy, the reduced birth weight could not have been mediated by a shortened gestation period.ConclusionIn conclusion, the study results provided epidemiologic evidence that prenatal PAH exposure from diet including grilled meat might be hazardous for fetal development. 相似文献
96.
Rainer P Woitas Golo Ahlenstiel Tilman Sauerbruch Ulrich Spengler 《Gastroenterology》2003,124(5):1560-1555
Readers are encouraged to write letters to the editor concerning articles that have been published in Gastroenterology. Short, general comments are also considered, but use of the Correspondence section for publication of original data in preliminary form is not encouraged. Letters should be typewritten double-spaced and submitted in triplicate. 相似文献
97.
Zum Thema
Leberzirrhosen unterschiedlichster Genese pr?disponieren zur Bildung maligner Tumoren der Leber und der Galleng?nge. Die Entstehung
und Einwirkung von reaktiven Sauerstoffmediaten scheint ein gemeinsamer Pathomechanismus zu sein, der zu Sch?den an DNA, Lipiden
und Proteinen der Leber- und Gallezellen führt. Darüber hinaus spielen spezifische molekulare Mechanismen für die maligne
Entartung bei alkoholinduzierter, posthepatitischer oder stoffwechselbedingter Leberzirrhose sowie prim?r sklerosierender
Cholangitis eine Rolle. 相似文献
98.
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100.
Interleukin 6/gp130-dependent pathways are protective during chronic liver diseases 总被引:15,自引:0,他引:15
Streetz KL Tacke F Leifeld L Wüstefeld T Graw A Klein C Kamino K Spengler U Kreipe H Kubicka S Müller W Manns MP Trautwein C 《Hepatology (Baltimore, Md.)》2003,38(1):218-229
The contribution of the acute phase inducer interleukin 6 (IL-6) in the pathogenesis of liver diseases is yet unclear. Our analysis showed enhanced expression of IL-6 in livers derived from patients with acute and chronic liver diseases. Additionally, IL-6 plasma levels were significantly increased in patients with chronic liver diseases and showed an inverse correlation with biochemical markers of liver function and a positive correlation with inflammatory markers, signs of portal hypertension, and the degree of liver fibrosis. To prove the relevance of these clinical findings, we applied the tetrachlorcarbonide (CCl(4)) model to conditional knockout animals (Cre/loxP system) for gp130, the common signal transducer of IL-6 family cytokines. Cre recombinases were expressed through a hepatocyte (AlfpCre) and a ubiquitous (MxCre) control element. Gp130 deleted mice had a totally abolished STAT3 activation and acute phase response induction, but gp130 deletion had no effect on the degree of acute liver injury and subsequent hepatocyte proliferation. In contrast, during chronic liver injury induced by biweekly application of CCl(4), deletion of the gp130 receptor in nonparenchymal liver cells and not hepatocytes resulted in fibrosis progression. In conclusion, our experiments indicate an involvement of IL-6 in the pathogenesis of liver diseases and suggest a protective role of IL-6/gp130-dependent pathways in nonparenchymal liver cells during fibrosis progression in chronic liver diseases. (Hepatology 2003;38:218-229). 相似文献