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71.
‘Fundamental causes’ of inequalities in mortality: an empirical test of the theory in 20 European populations 下载免费PDF全文
Johan P. Mackenbach Caspar W.N. Looman Barbara Artnik Matthias Bopp Patrick Deboosere Chris Dibben Ramune Kalediene Katalin Kovács Mall Leinsalu Pekka Martikainen Enrique Regidor Jitka Rychtaříková Rianne de Gelder 《Sociology of health & illness》2017,39(7):1117-1133
The ‘fundamental causes’ theory stipulates that when new opportunities for lowering mortality arise, higher socioeconomic groups will benefit more because of their greater material and non‐material resources. We tested this theory using harmonised mortality data by educational level for 22 causes of death and 20 European populations from the period 1980–2010. Across all causes and populations, mortality on average declined by 2.49 per cent (95%CI: 2.04–2.92), 1.83% (1.37–2.30) and 1.34% (0.89–1.78) per annum among the high, mid and low educated, respectively. In 69 per cent of cases of declining mortality, mortality declined faster among the high than among the low educated. However, when mortality increased, less increase among the high educated was found in only 46 per cent of cases. Faster mortality decline among the high educated was more manifest for causes of death amenable to intervention than for non‐amenable causes. The difference in mortality decline between education groups was not larger when income inequalities were greater. While our results provide support for the fundamental causes theory, our results suggest that other mechanisms than the theory implies also play a role. 相似文献
72.
Tomáš Mlčoch Jiří Klimeš Libor Fila Věra Vávrová Veronika Skalická Marek Turnovec Veronika Krulišová Jitka Jirčíková Dana Zemková Klára Vilimovská Dědečková Alena Bílková Vladimíra Frühaufová Lukáš Homola Zuzana Friedmannová Radovan Drnek Pavel Dřevínek Tomáš Doležal Milan MacekJr. 《The European journal of health economics》2017,18(1):73-82
Background
Economic data pertaining to cystic fibrosis (CF), is limited in Europe generally, and completely lacking in Central and Eastern Europe. We performed an analysis of all direct costs associated with CF relative to key disease features and laboratory examinations.Methods
A retrospective prevalence-based cost-of-illness (COI) study was performed in a representative cohort of 242 CF patients in the Czech Republic, which represents about 65 % of all Czech CF patients. Medical records and invoices to health insurance companies for reference year 2010 were analyzed.Results
The mean total health care costs were €14,486 per patient, with the majority of the costs going towards medicinal products and devices (€10,321). Medical procedures (€2676) and inpatient care (€1829) represented a much smaller percentage of costs. A generalized linear model showed that the strongest cost drivers, for all cost categories, were associated with patient age and lung disease severity (assessed using the FEV1 spirometric parameter), when compounded by chronic Pseudomonas aeruginosa airway infections. Specifically, maximum total costs are around the age 16 years; a FEV1 increase of 1 % point represented a cost decrease of: 0.9 % (medicinal products), 1.7 % (total costs), 2.8 % (procedures) and 7.0 % (inpatient care).Conclusions
COI analysis and regression modeling using the most recent data available can provide a better understanding of the overall economic CF burden. A comparison of our results with other methodologically similar studies demonstrates that although overall costs may differ, FEV1 can nonetheless be utilized as a generally transferrable indicator of the relative economic impact of CF.73.
Jitka Svobodová Karel Douda David Fischer Natalia Lapšanská Pavel Vlach 《Ecotoxicology (London, England)》2017,26(2):261-270
Mining activities are responsible for high concentrations of metals in river networks in many parts of the world. Mining activities and the resulting high loads of heavy metals interact with intensive acid rain, and often have great consequences for biodiversity. However, considering the frequently episodic nature of these heavy acid rains, there is little detailed evidence of direct impacts. In 2011 we observed a massive mortality of noble crayfish and stone crayfish in Padr?sko Special Area of Conservation (SAC) in the Brdy Mountain region of the Czech Republic. Based on concentrations of metals (Al, Fe, As, Cd, Pb, Cu, Zn and Hg) in various tissues (gills, hepatopancreas, muscle) of both dead and live crayfish in this locality compared to reference populations, these crayfish had experienced long-term exposure to increased levels of these metals. Here we give detailed documentation of crayfish mortality associated with high metal concentrations in the gills and other tissues of these endangered invertebrates. 相似文献
74.
75.
JNK inhibitor SP600125 is a partial agonist of human aryl hydrocarbon receptor and induces CYP1A1 and CYP1A2 genes in primary human hepatocytes 总被引:2,自引:0,他引:2
Dvorak Z Vrzal R Henklova P Jancova P Anzenbacherova E Maurel P Svecova L Pavek P Ehrmann J Havlik R Bednar P Lemr K Ulrichova J 《Biochemical pharmacology》2008,75(2):580-588
SP600125, a specific inhibitor of c-Jun-N-Terminal kinase (JNK), was reported as a ligand and antagonist of aryl hydrocarbon receptor (AhR) [Joiakim A, Mathieu PA, Palermo C, Gasiewicz TA, Reiners Jr JJ. The Jun N terminal kinase inhibitor SP600125 is a ligand and antagonist of the aryl hydrocarbon receptor. Drug Metab Dispos 2003;31(11):1279-82]. Here we show that SP600125 is not an antagonist but a partial agonist of human AhR. SP600125 significantly induced CYP1A1 and CYP1A2 mRNAs in primary human hepatocytes and CYP1A1 mRNA in human hepatoma cells HepG2. This effect was abolished by resveratrol, an antagonist of AhR. Consistent with the recent report, SP600125 dose-dependently inhibited CYP1A1 and CYP1A2 genes induction by a prototype AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in human hepatocytes. Moreover, SP600125 displayed typical behavior of a partial agonist in HepG2 cells transiently transfected with a reporter plasmid containing two inverted repeats of the dioxin responsive element or with a plasmid containing 5'-flanking region of human CYP1A1 gene. SP600125 transactivated the reporter plasmids with EC(50) of 0.005 and 1.89 microM, respectively. On the other hand, TCDD-dependent transactivation of the reporter plasmids was inhibited by SP600125 with IC(50) values of 1.54 and 2.63 microM, respectively. We also tested, whether the effects of SP600125 are due to metabolism. Using liquid chromatography/mass spectrometry approach, we observed formation of two minor monohydroxylated metabolites of SP600125 in human hepatocytes, human liver microsomes but not in HepG2 cells. These data imply that biotransformation is not responsible for the effects of SP600125 on AhR signaling. In conclusion, we demonstrate that SP600125 is a partial agonist of human AhR, which induces CYP1A genes. 相似文献
76.
77.
Jitka?VeldemaEmail authorView authors OrcID profile Kathrin?B?sl Dennis?Alexander?Nowak 《Journal of neurology》2018,265(5):1071-1078
Objective
To describe the relationship between changes of cortico-spinal excitability and motor recovery of the affected hand after stroke.Methods
Eighteen hemiparetic stroke patients with a severe-to-mild upper limb motor impairment were randomized. Cortico-spinal excitability measures (resting motor thresholds and motor evoked potentials) obtained from a distal (abductor pollicis brevis) and proximal (biceps brachii) upper limb muscle were assessed for both hemispheres. Motor function of the affected hand was tested by the Wolf Motor Function and Action Research Arm tests. The evaluations were performed at baseline and weekly over 7 weeks of in-patient neurological rehabilitation.Results
Severe hand dysfunction was associated with a strong suppression of ipsilesional cortico-spinal excitability and a shift of excitability towards the contralesional hemisphere. Mild hand impairment was associated with a shift of cortico-spinal excitability towards the ipsilesional hemisphere. Favorable motor recovery correlated with an increase of ipsilesional cortico-spinal excitability.78.
Jitka Annen MSc Gianluca Frasso Ph.D. Julia Sophia Crone Ph.D. Lizette Heine Ph.D. Carol Di Perri M.D. Ph.D. Charlotte Martial MSc Helena Cassol MSc Athena Demertzi Ph.D. Lionel Naccache M.D. Ph.D. Steven Laureys M.D. Ph.D. and Coma Science Group Collaborators 《Annals of neurology》2018,83(4):842-853
79.
80.
Jitka Fricova Martin Vejra?ka Pavel Stopka Jana Krizova Jaromír Bělá?ek Richard Rokyta 《Archives of Medical Science》2010,6(5):764-771