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71.
Francesca Prignano Veronica Rogai Elisabetta Cavallucci Alessandro Bitossi Volker Hammen Fabrizio Cantini 《Current rheumatology reports》2018,20(7):43
Purpose of Review
Understanding prevalence of diseases within specific regions of a country is important for optimal allocation of healthcare resources/funds. We performed a systematic review to obtain a clearer picture of the epidemiology of psoriasis and psoriatic arthritis across and within specific regions of Italy.Recent Findings
Prevalence of psoriasis in specific regions showed more variability (0.8–4.5%) than that in the total population (1.8–3.1%). Prevalence of psoriatic arthritis in the general population was reported for only two regions, Chiavari (0.09%) and Marche (0.42%). All other studies reported prevalence of psoriatic arthritis in patients with psoriasis in single centres and Italy-wide (4.7–47.1%). Prevalence of psoriatic arthritis was highest in patients with nail and/or scalp psoriasis and/or intergluteal/perianal region involvement.Summary
Based on current available data, these conditions appear to affect a substantial number of people and will likely have an important impact on the Italian healthcare system.72.
The role of the resting zone in growth plate chondrogenesis 总被引:8,自引:0,他引:8
Abad V Meyers JL Weise M Gafni RI Barnes KM Nilsson O Bacher JD Baron J 《Endocrinology》2002,143(5):1851-1857
In mammals, growth of long bones occurs at the growth plate, a cartilage structure that contains three principal layers: the resting, proliferative, and hypertrophic zones. The function of the resting zone is not well understood. We removed the proliferative and hypertrophic zones from the rabbit distal ulnar growth plate in vivo, leaving only the resting zone. Within 1 wk, a complete proliferative and hypertrophic zone often regenerated. Next, we manipulated growth plates in vivo to place resting zone cartilage ectopically alongside the proliferative columns. Ectopic resting zone cartilage induced a 90-degree shift in the orientation of nearby proliferative zone chondrocytes and seemed to inhibit their hypertrophic differentiation. Our findings suggest that resting zone cartilage makes important contributions to endochondral bone formation at the growth plate: 1) it contains stem-like cells that give rise to clones of proliferative chondrocytes; 2) it produces a growth plate-orienting factor, a morphogen, that directs the alignment of the proliferative clones into columns parallel to the long axis of the bone; and 3) it may also produce a morphogen that inhibits terminal differentiation of nearby proliferative zone chondrocytes and thus may be partially responsible for the organization of the growth plate into distinct zones of proliferation and hypertrophy. 相似文献
73.
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75.
Gabriella Marcon Antonio Indaco Giuseppe Di Fede Silvia Suardi Nicoletta Finato Valentino Moretti Sandro Micoli Paolo Fociani Pietro Zerbi Alessandro Pincherle Veronica Redaelli Fabrizio Tagliavini Giorgio Giaccone 《Brain pathology (Zurich, Switzerland)》2014,24(2):148-151
Prion diseases include sporadic, acquired and genetic forms linked to mutations of the prion protein (PrP) gene (PRNP). In subjects carrying the D178N PRNP mutation, distinct phenotypes can be observed, depending on the methionine/valine codon 129 polymorphism. We present here a 53‐year‐old woman with D178N mutation in the PRNP gene and homozygosity for valine at codon 129. The disease started at age 47 with memory deficits, progressive cognitive impairment and ataxia. The clinical picture slowly worsened to a state of akinetic mutism in about 2 years and the disease course was 6 years. The neuropathologic examination demonstrated severe diffuse cerebral atrophy with neuronal loss, spongiosis and marked myelin loss and tissue rarefaction in the hemispheric white matter, configuring panencephalopathic Creutzfeldt‐Jakob disease. PrP deposition was present in the cerebral cortex, basal ganglia and cerebellum with diffuse synaptic‐type pattern of immunoreactivity and clusters of countless, small PrP deposits, particularly evident in the lower cortical layers, in the striatum and in the molecular layer of the cerebellum. Western blot analysis showed the presence of type 1 PrPSc (Parchi classification). These findings underline the clear‐cut distinction between the neuropathological features of Creutzfeldt‐Jakob disease associated with D178N PRNP mutation and those of fatal familial insomnia. 相似文献
76.
Caryn Tatenda Mhangara Vaneshveri Naidoo Mokgobadibe Veronica Ntsiea 《Malawi medical journal : the journal of Medical Association of Malawi》2020,32(3):132
BackgroundCentral post-stroke pain (CPSP) is a poorly diagnosed chronic pain. It is under-treated and usually mismanaged.ObjectiveTo establish the prevalence of CPSP and its management in stroke clinics at a tertiary hospital.MethodsThis was a cross-sectional design with stroke patients and health professionals from the stroke clinic at the tertiary hospital in Zimbabwe.ResultsOut of 166 stroke survivors, 8% had CPSP. Younger age (<60 years) was significantly associated with CPSP (P<0.003). Pain characteristics of CPSP were hyperaesthesia (10, 71%), electric shocks (9, 64%), temperature allodynia (9, 64%) and allodynia (12, 86%). Ten health professionals participated in the study: one (10%) reported using Douleur Neuropathique 4 (to diagnose neuropathic pain) and two (20%) reported using sensory tests. Four patients (44%) were on paracetamol (acetaminophen) and on weak opiates such as codeine. None of the patients were on anticonvulsants or antidepressants. Two medical doctors (50%) used weak opiates as second-line management. Five patients (36%) reported receiving a combination of massage, stretching, general exercise and moist heat or cryotherapy.ConclusionThe prevalence of CPSP in the study group is within international range. There is a need for appropriate management and use of tests and outcome measures for diagnosis of CPSP. 相似文献
77.
Fausto Biancari Tomas Gudbjartsson Jouni Heikkinen Vesa Anttila Timo Mäkikallio Anders Jeppsson Linda Thimour-Bergström Carmelo Mignosa Antonino S. Rubino Kari Kuttila Jarmo Gunn Jan-Ola Wistbacka Kari Teittinen Kari Korpilahti Francesco Onorati Giuseppe Faggian Giulia Vinco Corrado Vassanelli Flavio Ribichini Tatu Juvonen Tomas A. Axelsson Axel F. Sigurdsson Pasi P. Karjalainen Ari Mennander Olli Kajander Markku Eskola Erkki Ilveskoski Veronica D'Oria Marisa De Feo Tuomas Kiviniemi K.E. Juhani Airaksinen 《The American journal of cardiology》2014
78.
Addictions to licit and illicit drugs are chronic relapsing brain disorders that affect circuits that regulate reward, motivation, memory, and decision-making. Drug-induced pathological changes in these brain regions are associated with characteristic enduring behaviors that continue despite adverse biopsychosocial consequences. Repeated exposure to these substances leads to egocentric behaviors that focus on obtaining the drug by any means and on taking the drug under adverse psychosocial and medical conditions. Addiction also includes craving for the substances and, in some cases, involvement in risky behaviors that can cause death. These patterns of behaviors are associated with specific cognitive disturbances and neuroimaging evidence for brain dysfunctions in a diverse population of drug addicts. Postmortem studies have also revealed significant biochemical and/or structural abnormalities in some addicted individuals. The present review provides a summary of the evidence that has accumulated over the past few years to implicate brain dysfunctions in the varied manifestations of drug addiction. We thus review data on cerebrovascular alterations, brain structural abnormalities, and postmortem studies of patients who abuse cannabis, cocaine, amphetamines, heroin, and “bath salts”. We also discuss potential molecular, biochemical, and cellular bases for the varied clinical presentations of these patients. Elucidation of the biological bases of addiction will help to develop better therapeutic approaches to these patient populations. 相似文献
79.
Gianetti E Hall JE Au MG Kaiser UB Quinton R Stewart JA Metzger DL Pitteloud N Mericq V Merino PM Levitsky LL Izatt L Lang-Muritano M Fujimoto VY Dluhy RG Chase ML Crowley WF Plummer L Seminara SB 《The Journal of clinical endocrinology and metabolism》2012,97(9):E1798-E1807
Context: A broad spectrum of GnRH-deficient phenotypes has been identified in individuals with both mono- and biallelic GNRHR mutations. Objective: The objective of the study was to determine the correlation between the severity of the reproductive phenotype(s) and the number and functional severity of rare sequence variants in GNRHR. Subjects: Eight hundred sixty-three probands with different forms of GnRH deficiency, 46 family members and 422 controls were screened for GNRHR mutations. The 70 subjects (32 patients and 38 family members) harboring mutations were divided into four groups (G1-G4) based on the functional severity of the mutations (complete or partial loss of function) and the number of affected alleles (monoallelic or biallelic) with mutations, and these classes were mapped on their clinical phenotypes. Results: The prevalence of heterozygous rare sequence variants in GNRHR was significantly higher in probands vs. controls (P < 0.01). Among the G1-G3 groups (homozygous subjects with successively decreasing severity and number of mutations), the hypogonadotropic phenotype related to their genetic load. In contrast, subjects in G4, with only monoallelic mutations, demonstrated a greater diversity of clinical phenotypes. Conclusions: In patients with GnRH deficiency and biallelic mutations in GNRHR, genetic burden defined by severity and dose is associated with clinical phenotype. In contrast, for patients with monoallelic GNRHR mutations this correlation does not hold. Taken together, these data indicate that as-yet-unidentified genetic and/or environmental factors may combine with singly mutated GNRHR alleles to produce reproductive phenotypes. 相似文献
80.
Palamarchuk A Yan PS Zanesi N Wang L Rodrigues B Murphy M Balatti V Bottoni A Nazaryan N Alder H Rassenti L Kipps TJ Freitas M Croce CM Pekarsky Y 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(7):2555-2560
B-cell chronic lymphocytic leukemia (CLL) is the most common human leukemia. Deregulation of the T-cell leukemia/lymphoma 1 oncogene (TCL1) in mouse B cells causes a CD5(+) leukemia similar to aggressive human CLL. To examine the mechanisms by which Tcl1 protein exerts its oncogenic activity in B cells, we performed proteomics experiments to identify its interacting partners. We found that Tcl1 physically interacts with de novo DNA methylthansferases Dnmt3A and Dnmt3B. We further investigated the effects of Tcl1 up-regulation on the enzymatic activity of Dnmt3A and found that Tcl1 overexpression drastically inhibits Dnmt3A function. In addition, B cells from TCL1 transgenic mice showed a significant decrease in DNA methylation compared with WT controls. Similarly, CLL samples with high Tcl1 expression showed a decrease in DNA methylation compared with CLL samples with low Tcl1 expression. Given the previous reports of inactivating mutations of DNMT3A in acute myelogenous leukemia and myelodysplastic syndrome, our results suggest that inhibition of de novo DNA methylation may be a common oncogenic mechanism in leukemogenesis. 相似文献