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排序方式: 共有261条查询结果,搜索用时 35 毫秒
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Armando Pérez-Rangel José Manuel Hernández Araceli Castillo-Romero Lilián Yépez-Mulia Rafael Castillo Francisco Hernández-Luis Benjamín Nogueda-Torres Juan Pedro Luna-Arias Gerardo Radilla Gloria León-Avila 《Parasitology research》2013,112(9):3251-3257
In the present study, we evaluated the effect of an albendazole (ABZ) derivative JVG9 on cultured Giardia intestinalis. To assess the JVG9 effects, we evaluated the tubulin cytoskeleton by confocal microscopy, and we found that the characteristic staining was modified. The scanning electron microscopy images revealed extremely damaged trophozoites and cyst-like cells. The confocal images revealed that this drug triggered the expression of cyst wall protein 1 and encystation. We also found that at low doses, AL triggered the encystation process too. 相似文献
3.
Casademont J Rodriguez-Santiago B Miró O Beato A López S Nunes V Cardellach F 《Aging clinical and experimental research》2005,17(1):1-7
BACKGROUND AND AIMS: The potential influence of impaired oxidative metabolism in the modulation of manifestations in sporadic Alzheimer's disease (AD) has attracted much attention in the last 50 years. Unfortunately, many clinical and experimental results aiming at proving this hypothesis are still controversial. The aim was to study the enzymatic activities of respiratory chain (RC) complexes I through V in three brain areas of a group of patients with definite AD, and to compare the results with a group of normal brains. We simultaneously assessed the lipid peroxidation of the samples as a measure of free radical damage. METHODS: The specific activity of the individual complexes of the RC was measured spectrophotometrically, and the loss of cis-parinaric acid fluorescence was used to determine the chemical process of lipid peroxidation. RESULTS: We were not able to detect differences in any of the analyzed RC enzymatic activities, or in the level of lipid peroxidation between patients with AD and controls. Instead, differences were found in the number of mitochondria and in the intrinsic enzymatic activities of complexes III and IV in various brain areas. CONCLUSIONS: Spectrophotometric enzymatic analyses of respiratory complexes in brain homogenates do not support the primary contribution of mitochondrial RC dysfunction in the pathogenesis of AD. 相似文献
4.
Anti-Trypanosoma cruzi and anti-leishmanial activity by quinoxaline-7-carboxylate 1,4-di-N-oxide derivatives 总被引:1,自引:0,他引:1
Juan Carlos Villalobos-Rocha Luvia Sánchez-Torres Benjamín Nogueda-Torres Aldo Segura-Cabrera Carlos A. García-Pérez Virgilio Bocanegra-García Isidro Palos Antonio Monge Gildardo Rivera 《Parasitology research》2014,113(6):2027-2035
In this work, a novel series of ethyl and methyl quinoxaline-7-carboxylate 1,4-di-N-oxide derivatives were evaluated in vitro on Trypanosoma cruzi trypomastigotes and Leishmania mexicana promastigotes, and cytotoxicity activity in murine macrophages was tested. In silico molecular docking simulations of trypanothione reductase were also done. Three compounds of 33 quinoxaline-7-carboxylate 1,4-di-N-oxide derivatives showed better anti-T. cruzi activity than nifurtimox and beznidazole; two compounds had better anti-leishmanial activity that amphotericin-B, and two compounds showed better activity against both parasites than reference drugs. Compounds M2, M7, M8 and E5, showed low cytotoxic activity on the host cell. The in silico studies suggest that compound M2 is a potential trypanothione reductase inhibitor. 相似文献
5.
de Gonzalo-Calvo D Fernández-García B de Luxán-Delgado B Rodríguez-González S García-Macia M Suárez FM Solano JJ Rodríguez-Colunga MJ Coto-Montes A 《Age (Dordrecht, Netherlands)》2012,34(3):761-771
The objective of the present study was to investigate the changes in a large panel of emergent geriatric biomarkers in long-term
trained elderly men to analyze the effects of long-term exercise on an aged population. We collected blood samples from two
groups of male volunteers older than 65 years who maintain a measure of functional independence: one group of sedentary subjects
without a history of regular physical activity and the other of subjects who have sustained training, starting during adulthood
(mean training time = 49 ± 8 years). We studied morbidity, polypharmacy, cellular and serological inflammatory parameters,
and endocrine mediators. After adjusting for confounding factors, we observed reduced medication intake per subject and lower
number of diseases per subject with statistical differences nearly significant in the long-term exercise group. We showed
that long-term training was associated with lower levels of white blood cell counts, neutrophil counts, interleukin-6, interleukin-10,
interleukin-1 receptor antagonist, and soluble TNF receptor-I. Furthermore, we noted an increase in the concentrations of
insulin-like growth factor-1 and dehydroepiandrosterone in the long-term training group. We concluded that long-term exercise
training from adulthood to old age is clearly associated with a healthy profile of emergent geriatric biomarkers. Long-term
training could improve the inflammatory–endocrine imbalance associated with disease, frailty, functional decline, and mortality
in elderly men. Our results point to the benefits of prolonged exercise from adulthood to old age. 相似文献
6.
7.
García-Reyna Benjamín Castillo-García Gilberto Daniel Barbosa-Camacho Francisco José Cervantes-Cardona Guillermo Alonso Cervantes-Pérez Enrique Torres-Mendoza Blanca Miriam Fuentes-Orozco Clotilde Pintor-Belmontes Kevin Josue Guzmán-Ramírez Bertha Georgina Bernal-Hernández Aldo González-Ojeda Alejandro Cervantes-Guevara Gabino 《International journal of mental health and addiction》2022,20(2):895-906
International Journal of Mental Health and Addiction - The presence of COVID-19 has had psychological consequences among health personnel; these include fear, anxiety, and depression. In the... 相似文献
8.
Helena Codina-Martínez Benjamín Fernández-García Carlos Díez-Planelles Álvaro F. Fernández Sara G. Higarza Manuel Fernández-Sanjurjo Sergio Díez-Robles Eduardo Iglesias-Gutiérrez Cristina Tomás-Zapico 《Scandinavian journal of medicine & science in sports》2020,30(2):238-253
Endurance training promotes exercise-induced adaptations in brain, like hippocampal adult neurogenesis and autophagy induction. However, resistance training effect on the autophagy response in the brain has not been much explored. Questions such as whether partial systemic autophagy or the length of training intervention affect this response deserve further attention. Therefore, 8-week-old male wild-type (Wt; n = 36) and systemic autophagy-deficient (atg4b−/−, KO; n = 36) mice were randomly distributed in three training groups, resistance (R), endurance (E), and control (non-trained), and in two training periods, 2 or 14 weeks. R and E maximal tests were evaluated before and after the training period. Forty-eight hours after the end of training program, cerebral cortex, striatum, hippocampus, and cerebellum were extracted for the analysis of autophagy proteins (LC3B-I, LC3B-II, and p62). Additionally, hippocampal adult neurogenesis was determined by doublecortin-positive cells count (DCX+) in brain sections. Our results show that, in contrast to Wt, KO were unable to improve R after both trainings. Autophagy levels in brain areas may be modified by E training only in cerebral cortex of Wt trained for 14 weeks, and in KO trained for 2 weeks. DCX + in Wt increased in R and E after both periods of training, with R for 14 weeks more effective than E. Interestingly, no changes in DCX + were observed in KO after 2 weeks, being even undetectable after 14 weeks of intervention. Thus, autophagy is crucial for R performance and for exercise-induced adult neurogenesis. 相似文献
9.
10.
Maria G. Zavala-Cerna Erika A. Martínez-García Olivia Torres-Bugarín Benjamín Rubio-Jurado Carlos Riebeling Arnulfo Nava 《Clinical reviews in allergy & immunology》2014,47(1):73-90
Posttranslational modifications (PTMs) are defined as covalent modifications occurring in a specific protein amino acid in a time- and signal-dependent manner. Under physiological conditions, proteins are posttranslationally modified to carry out a large number of cellular events from cell signaling to DNA replication. However, an absence, deficiency, or excess in PTMs of a given protein can evolve into a target to trigger autoimmunity, since PTMs arise in the periphery and may not occur in the thymus; hence, proteins with PTMs never tolerize developing thymocytes. Consequently, when PTMs arise during cellular responses, such as inflammation, these modified self-antigens can be taken up and processed by the antigen-presenting cells (APCs). Autoreactive T cells, which recognize peptides presented by APCs, can then infiltrate into host tissue where the modified antigen serves to amplify the autoimmune response, eventually leading to autoimmune pathology. Furthermore, a PTM occurring in an amino acid residue can induce changes in the net charge of the protein, leading to conformational modifications in the tertiary and quaternary structure of the protein, especially interaction with human leukocyte antigen (HLA) molecules. Molecular mimicry (MM) was until now the prevailing hypothesis explaining generation of autoimmunity; nevertheless, experimental animal models need inflammation via infection or other immunogens to ensure autoimmunity; MM alone is not sufficient to develop autoimmunity. PTMs could arise as an additive factor to MM, which is required to start an autoimmune response. PTMs have been found to be present in different pathologic conditions such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), antiphospholipid syndrome, and primary biliary cirrhosis. The aim of the present review is to expose protein posttranslational modifications and the evidence suggesting their role in the generation of autoimmunity. 相似文献