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1.
Peacekeeping missions involve experiences that may impact the mental health of participating soldiers. However, research on the long-term mental health consequences of peacekeeping is sparse. The present study aimed to find the prevalence of mental health problems (MHPs), possible MHP predictors, and associations between predictors and MHPs in Norwegian peacekeepers 18–38 years after deployment to a United Nations peacekeeping mission. We used data from a cross-sectional, postdeployment survey of Norwegian peacekeepers who served in Lebanon between 1978 and 1998 (N = 10,605). Participants were assessed for posttraumatic stress disorder (PTSD); anxiety; depression; insomnia; alcohol misuse; drug misuse; and exposure to pre-, peri-, and postdeployment stressors. Logistic regressions were executed to explore key variables associated with MHPs. Total MHP prevalence was 15.1%, 95% CI [14.4, 15.8]. The estimates for specific disorders were 0.1% for drug misuse, 3.4% for alcohol misuse, 4.0% for depression, 6.2% for PTSD, 6.4% for anxiety, and 9.3% for insomnia. Postdeployment stressors, OR = 1.91, 95% CI [1.79, 2.04]; employment status, OR = 1.41, 95% CI [1.33, 1.48]; and traumatic exposure during deployment, OR = 1.11, 95% CI [1.09, 1.12], were positively related to PTSD, χ2(17, N = 8,568) = 1,791.299, p < .001. Similar patterns were found for the other MHPs. Considering that most participants (84.9%) reported low symptom levels, our findings challenge the widespread public perception that most peacekeepers have MHPs. Moreover, our results indicate that future peacekeepers should be prepared for challenges they may face not only during deployment but also in the years following their homecoming.  相似文献   
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BACKGROUND: The HOXA1 gene plays a major role in brainstem and cranial morphogenesis. The G allele of the HOXA1 A218G polymorphism has been previously found associated with autism. METHODS: We performed case-control and family-based association analyses, contrasting 127 autistic patients with 174 ethnically matched controls, and assessing for allelic transmission disequilibrium in 189 complete trios. RESULTS: A, and not G, alleles were associated with autism using both case-control (chi(2) = 8.96 and 5.71, 1 df, p <.005 and <.025 for genotypes and alleles, respectively), and family-based (transmission/disequilibrium test chi(2) = 8.80, 1 df, p <.005) association analyses. The head circumference of 31 patients carrying one or two copies of the G allele displayed significantly larger median values (95.0th vs. 82.5th percentile, p <.05) and dramatically reduced interindividual variability (p <.0001), compared with 166 patients carrying the A/A genotype. CONCLUSIONS: The HOXA1 A218G polymorphism explains approximately 5% of the variance in the head circumference of autistic patients and represents to our knowledge the first known gene variant providing sizable contributions to cranial morphology. The disease specificity of this finding is currently being investigated. Nonreplications in genetic linkage/association studies could partly stem from the dyshomogeneous distribution of an endophenotype morphologically defined by cranial circumference.  相似文献   
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Müller (glial) cells from the rabbit retina were isolated by means of papain and mechanical dissociation. Their Na+,K+-adenosine triphosphatase (ATPase) activity was measured using a radiochemical method, and its K+ dependence was determined. In contrast to that of photoreceptors (data from the literature), the Na+,K+-ATPase of Müller cells could be shown to increase its activity greatly when the [K+] was enhanced up to 10 mM. The functional implications of this behaviour for the K+ clearance in the retina are discussed.  相似文献   
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More than 10 years ago, it was shown by microdialysis that the excitatory transmitter glutamate accumulates in the interstitial space of brain subjected to ischemic insult. This was one of the key observations leading to the formulation of the `glutamate hypothesis' of ischemic cell death. It is now assumed that even a transient glutamate overflow may set in motion a number of events that ultimately cause cell loss in vulnerable neuronal populations. The aim of the present review is to discuss the intracellular changes that underlie the dysregulation of extracellular glutamate during and after ischemia, with emphasis on data obtained by postembedding, electron microscopic immunogold cytochemistry. While the time resolution of this approach is necessarily limited, it can reveal, quantitatively and at a high level of spatial resolution, how the intracellular pools of glutamate and metabolically related amino acids are perturbed during and after an ischemic insult. Moreover, this can be done in animals whose extracellular amino acid levels are monitored by microdialysis, allowing a direct correlation of extra- and intracellular changes. Immunogold analyses of brains subjected to ischemia have identified dendrites and neuronal somata as likely sources of glutamate efflux, probably mediated by reversal of glutamate uptake. The vesicular glutamate pool has been found to be largely unchanged after 20 min of ischemia. Ischemia causes an increased glutamate content and an increased glutamate/glutamine ratio in glial cells, as revealed by double immunogold labelling. This argues against the idea that glial cells contribute to the extracellular overflow of glutamate in the ischemic brain.  相似文献   
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The effects of a variety of inhibitors suggested that the promastigote surface protease (PSP) of Leishmania might be a zinc metalloprotease. To investigate this possibility, we conducted atomic emission and absorption spectroscopic analyses, which show that PSP contains 1 atom of zinc per 63-kDa monomer. Further studies showed that the enzyme can be biosynthetically labeled with 65ZnCl2. The comparison of the amino acid sequence of Leishmania major PSP with nine other zinc metalloproteinases revealed significant similarity in the area of their zinc-binding sites. These data show clearly that the promastigote surface protease of Leishmania is a zinc metalloproteinase. Secondary structure analysis by circular dichroism spectroscopy indicates that PSP contains over 40% beta-strand and less than 20% alpha-helical structure. The molecular masses of amphiphilic PSP (152 kDa) and of hydrophilic PSP (142 kDa), determined by quantitative electron scattering, suggest that the purified enzyme occurs in solution, and presumably at the cell surface, as a non-covalent homodimer.  相似文献   
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Summary Haemangiosarcoma of bone is a very rare primary tumour with a variable history and differing radiographic and histological appearances. In some cases the lesion has similar features to the so-called adamantinoma of long bones in which the histogenesis is also unknown.Such a lesion is described which ocurred in the shaft of the right humerus of a 31-year-old man. Radiographically a centrally located area of osteolysis was seen without marginal sclerosis, but with erosion of the bony cortex. A biopsy was performed 16 months after the first radiographic examination and showed malignant tumour tissue which was difficult to classify histomorphologically. Several different neoplasms such as Ewing's sarcoma, myeloma, liposarcoma, malignant fibrous histiocytoma or a bone metastasis were suggested. Finally, a haemangiosarcoma or so-called adamantinoma of long bones was considered. The tumour was completely removed by en-bloc resection.Careful histomorphological investigation of the tumour tissue by means of light microscopy, cytology and electronmicroscopy showed a vascular pattern characteristic of a haemangiosarcoma. Using cytophotometric DNA measurements of the tumour cells, the lesion could be classified as being of lowgrade malignancy. This is confirmed since there has now been a 4-year follow up with no local recurrence or metastasis.There are many similarities between a well-differentiated haemangiosarcoma and an adamantinoma of long bones. The differential diagnosis and the histogenesis of the latter lesion is discussed. It is emphasized that the so-called adamantinoma of a long bone probably has a vascular origin.
Résumé L'hémangiosarcome est une tumeur osseuse primaire très rare, dont l'evolution est variable et dont les aspects radiologiques et histologiques sont divers. Dans quelques cas, la lésion ressemble à ce que l'on appelle «adamantinome des os longs», dont l'histogénèse est également inconnue.On présente ici un cas d'une telle tumeur, siégeant au niveau de la diaphyse humérale droite, chez un homme de 31 ans. Radiologiquement, il existait une zone centrale d'ostéolyse sans sclérose marginale mais avec érosion de la corticale. Une biopsie effectuée 16 mois après le premier examen radiologique a montré un tissu tumoral malin, difficile à classer histomorphologiquement.Plusieurs diagnostic ont été envisagée: sarcome d'Ewing, myélome, liposarcome, histiocystome fibreux malin, ou métastase osseuse. Finalement on a retenu le diagnostic soit d'hémangiosarcome, soit d'adamantinome. La tumeur a été complètement enlevée par résection en bloc.Des investigations histomorphologiques poussées du tissu tumoral par microscopie optique, cytologie et microscopie électronique ont mis en évidence les aspects vasculaires caractéristiques d'un hémangiosarcome. En utilisant les mesures cyto-photométriques d'ADN des cellules tumorales, la lésion a pu être classée comme ayant un degré de malignité peu élevé. Ceci a été confirmé par l'évolution, puisqu'avec 4 ans de recul il n'y a ni récidive locale ni métastase.Il y a beaucoup de similitudes entre un hémangiosarcome bien différencié et un adamantinome des os longs. Le diagnostic différentiel et l'histogénèse de cette dernière lésion sont discutes. L'origine vasculaire probable de l'adamentinome est soulignée.
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Notfall + Rettungsmedizin - Der plötzliche Brust- und der plötzliche Unterleibsschmerz gehören zu den häufigsten Gründen, die Patienten in die Notaufnahme führen. Das...  相似文献   
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