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81.
Kemmer D Huang Y Shah SP Lim J Brumm J Yuen MM Ling J Xu T Wasserman WW Ouellette BF 《Genome biology》2005,6(12):R106
We developed Ulysses as a user-oriented system that uses a process called Interolog Analysis for the parallel analysis and
display of protein interactions detected in various species. Ulysses was designed to perform such Interolog Analysis by the
projection of model organism interaction data onto homologous human proteins, and thus serves as an accelerator for the analysis
of uncharacterized human proteins. The relevance of projections was assessed and validated against published reference collections.
All source code is freely available, and the Ulysses system can be accessed via a web interface . 相似文献
82.
83.
Proliferation Rates of Bovine Primary Muscle Cells Relate to Liveweight and Carcase Weight in Cattle
Chantal A. Coles Jenny Wadeson Carolina P. Leyton Jason P. Siddell Paul L. Greenwood Jason D. White Matthew B. McDonagh 《PloS one》2015,10(4)
Muscling in cattle is largely influenced by genetic background, ultimately affecting beef yield and is of major interest to the beef industry. This investigation aimed to determine whether primary skeletal muscle cells isolated from different breeds of cattle with a varying genetic potential for muscling differ in their myogenic proliferative capacity. Primary skeletal muscle cells were isolated and cultured from the Longissimus muscle (LM) of 6 month old Angus, Hereford and Wagyu X Angus cattle. Cells were assessed for rate of proliferation and gene expression of PAX7, MYOD, MYF5, and MYOG. Proliferation rates were found to differ between breeds of cattle whereby myoblasts from Angus cattle were found to proliferate at a greater rate than those of Hereford and Wagyu X Angus during early stages of growth (5–20 hours in culture) in vitro (P < 0.05). The proliferation rates of myoblasts during early stages of culture in vitro were also found to be positively related to the liveweight and carcase weight of cattle (P < 0.05). Gene expression of MYF5 was also found to be significantly down-regulated in WagyuX compared with Angus cattle (P < 0.05). These findings suggest that early events during myogenesis are important for determining liveweight and caracase weights in cattle. 相似文献
84.
Greiciane MS Florim Heloisa C Caldas Julio CR de Melo Maria Alice SF Baptista Ida MM Fernandes Marcela Savoldi-Barbosa Gustavo H Goldman Mario Abbud-Filho 《Arthritis research & therapy》2015,17(1)
IntroductionMicrochimeric male fetal cells (MFCs) have been associated with systemic lupus erythematosus, and published studies have further correlated MFC with lupus nephritis (LN). In the present study, we evaluated the frequency of MFC in the renal tissue of patients with LN.MethodsTwenty-seven renal biopsies were evaluated: Fourteen were from women with clinical and laboratory findings of LN, and thirteen were from controls. Genomic DNA was extracted from kidney biopsies, and the male fetal DNA was quantified using real-time quantitative polymerase chain reactions for the detection of specific Y chromosome sequences.ResultsMFCs were detected in 9 (64%) of 14 of patients with LN, whereas no MFCs were found in the control group (P = 0.0006). No differences in pregnancy history were found between patients with LN and the control group. Significantly higher amounts of MFCs were found in patients with LN with serum creatinine ≤1.5 mg/dl. Furthermore, women with MFCs had significantly better renal function at the time of biopsy (P = 0.03). In contrast, patients with LN without MFCs presented with more severe forms of glomerulonephritis (World Health Organization class IV = 60% and class V = 40%).ConclusionsOur data indicate a high prevalence of MFCs in renal biopsy specimens from women with LN, suggesting a role for MFCs in the etiology of LN. The present report also provides some evidence that MFCs could have a beneficial effect in this disease.
Electronic supplementary material
The online version of this article (doi:10.1186/s13075-015-0615-4) contains supplementary material, which is available to authorized users. 相似文献85.
Tobias Goldmann Nicolas Zeller Jenni Raasch Katrin Kierdorf Kathrin Frenzel Lars Ketscher Anja Basters Ori Staszewski Stefanie M Brendecke Alena Spiess Tuan Leng Tay Clemens Kreutz Jens Timmer Grazia MS Mancini Thomas Blank Günter Fritz Knut Biber Roland Lang Danielle Malo Doron Merkler Mathias Heikenwälder Marco Prinz 《The EMBO journal》2015,34(12):1612-1629
Microglia are tissue macrophages of the central nervous system (CNS) that control tissue homeostasis. Microglia dysregulation is thought to be causal for a group of neuropsychiatric, neurodegenerative and neuroinflammatory diseases, called “microgliopathies”. However, how the intracellular stimulation machinery in microglia is controlled is poorly understood. Here, we identified the ubiquitin‐specific protease (Usp) 18 in white matter microglia that essentially contributes to microglial quiescence. We further found that microglial Usp18 negatively regulates the activation of Stat1 and concomitant induction of interferon‐induced genes, thereby terminating IFN signaling. The Usp18‐mediated control was independent from its catalytic activity but instead required the interaction with Ifnar2. Additionally, the absence of Ifnar1 restored microglial activation, indicating a tonic IFN signal which needs to be negatively controlled by Usp18 under non‐diseased conditions. These results identify Usp18 as a critical negative regulator of microglia activation and demonstrate a protective role of Usp18 for microglia function by regulating the Ifnar pathway. The findings establish Usp18 as a new molecule preventing destructive microgliopathy. 相似文献
86.
Marina GM Viturino Jamil M Neto Flvia F Bajano Sueli MS Costa Alicia B Roque Gessica FS Borges Galina Ananina Priscila HH Rim Flvio M Medina Fernando F Costa Jos PC de Vasconcellos Mnica B de Melo 《Experimental biology and medicine (Maywood, N.J.)》2021,246(10):1148
This study aimed to evaluate the role of APOE polymorphisms (rs429358 and rs7412) in the risk of age-related macular degeneration in a sample of the Southeastern Brazilian population. Seven hundred and five unrelated individuals were analyzed, 334 with age-related macular degeneration (case group), and 371 without the disease (control group). In the case group, patients were further stratified according to disease phenotypes, divided into dry and wet age-related macular degeneration, and non-advanced and advanced age-related macular degeneration. APOE polymorphisms (rs429358 and rs7412) were evaluated through polymerase chain reaction and direct sequencing. In the comparison of cases vs. controls, none of the associations reached statistical significance, considering the Bonferroni-adjusted P-value, although there was a suggestive protection for the E3/E4 genotype (OR = 0.626; P-value = 0.037) and E4 carriers (OR = 0.6515; P-value = 0.047). Statistically significant protection for both the E3/E4 genotype and E4 carriers was observed in the comparisons: advanced age-related macular degeneration vs. controls (OR = 0.3665, P-value = 0.491 × 10−3 and OR = 0.4031, P-value = 0.814 × 10−3, respectively), advanced age-related macular degeneration vs. non-advanced age-related macular degeneration (OR = 0.2529, P-value = 0.659 × 10−4 and OR = 0.2692, P-value = 0.631 × 10−4, respectively). In the comparison of wet age-related macular degeneration vs. control, protection was statistically significant only for E3/E4 (OR = 0.4052, P-value = 0.001). None of the comparisons demonstrated any significant association for E2 genotypes or E2 carriers in age-related macular degeneration risk in this study. Findings suggest a protective role of the E4 haplotype in the APOE gene in the risk for advanced and wet forms of age-related macular degeneration, in a sample of the Brazilian population. To our knowledge, this is the first Brazilian study to show the association between APOE polymorphisms and age-related macular degeneration. 相似文献
87.
88.
Soukaloun D Lee SJ Chamberlain K Taylor AM Mayxay M Sisouk K Soumphonphakdy B Latsavong K Akkhavong K Phommachanh D Sengmeuang V Luangxay K McDonagh T White NJ Newton PN 《PLoS neglected tropical diseases》2011,5(2):e971
Background
Infantile beriberi is a potentially lethal manifestation of thiamin deficiency, associated with traditional post-partum maternal food avoidance, which persists in the Lao PDR (Laos). There are few data on biochemical markers of infantile thiamin deficiency or indices of cardiac dysfunction as potential surrogate markers.Methodology/Principal Findings
A case control study of 47 infants with beriberi and age-matched afebrile and febrile controls was conducted in Vientiane, Laos. Basal and activated erythrocyte transketolase activities (ETK) and activation (α) coefficients were assayed along with plasma brain natriuretic peptide, N-terminal pro-brain natriuretic peptide and troponin T. Basal ETK (and to a lesser extent activated ETK) and plasma troponin T were the only infant biochemical markers that predicted infantile beriberi. A basal ETK≤0.59 micromoles/min/gHb gave a sensitivity (95%CI) of 75.0 (47.6 to 92.7)% and specificity (95%CI) of 85.2 (66.3 to 95.8)% for predicting infantile beriberi (OR (95%CI) 15.9 (2.03–124.2); p = 0.008) (area under ROC curve = 0.80). In contrast, the α coefficient did not discriminate between cases and controls. Maternal basal ETK was linearly correlated with infant basal ETK (Pearson''s r = 0.66, p<0.001). The odds of beriberi in infants with detectable plasma troponin T was 3.4 times higher in comparison to infants without detectable troponin T (OR 3.4, 95%CI 1.22–9.73, p = 0.019). Detectable troponin T had a sensitivity (95%CI) of 78.6 (59.0 to 91.7) % and specificity (95%CI) of 56.1 (39.7 to 71.5) % for predicting infantile beriberi.Conclusions/Significance
Basal ETK is a more accurate biochemical marker of infantile beriberi than the activation coefficient. Raised plasma troponin T may be a useful indicator of infantile beriberi in infants at risk and in the absence of other evident causes. 相似文献89.
Weifeng Xu MS Xinwei Chen MD Yexin Wang MS Baoting Fan MS Ke Guo MS Chi Yang MD Shiqi Yu MD Yichuan Pang MD Shanyong Zhang MD 《Journal of cellular physiology》2020,235(3):3022-3032
Considering the high rate of osteoclast-related diseases worldwide, research targeting osteoclast formation/function is crucial. In vitro, we demonstrated that chitooligosaccharide (CS) dramatically inhibited osteoclastogenesis as well as osteoclast function dose-dependently. CS suppressed osteoclast-specific genes expression during osteoclastogenesis. Furthermore, we found that CS attenuated receptor activator of nuclear factor kappa B ligand (RANKL)-mediated mitogen-activated protein kinase (MAPK) pathway involving p38, erk1/2, and jnk, leading to the reduced expression of c-fos and nuclear factor of activated T cells c1 (NFATc1) during osteoclast differentiation. In vivo, we found CS protected rats from periodontitis-induced alveolar bone loss by micro-computerized tomography and histological analysis. Overall, CS inhibited RANKL-induced osteoclastogenesis and ligature-induced rat periodontitis model, probably by suppressing the MAPK/c-fos/NFATc1 signaling pathway. Therefore, CS may be a safe and promising treatment for osteoclast-related diseases. 相似文献
90.
Katarzyna Goljanek‐Whysall Ana Soriano‐Arroquia Rachel McCormick Caroline Chinda Brian McDonagh 《Aging cell》2020,19(4)
One of the key mechanisms underlying skeletal muscle functional deterioration during aging is disrupted mitochondrial dynamics. Regulation of mitochondrial dynamics is essential to maintain a healthy mitochondrial population and prevent the accumulation of damaged mitochondria; however, the regulatory mechanisms are poorly understood. We demonstrated loss of mitochondrial content and disrupted mitochondrial dynamics in muscle during aging concomitant with dysregulation of miR‐181a target interactions. Using functional approaches and mito‐QC assay, we have established that miR‐181a is an endogenous regulator of mitochondrial dynamics through concerted regulation of Park2, p62/SQSTM1, and DJ‐1 in vitro. Downregulation of miR‐181a with age was associated with an accumulation of autophagy‐related proteins and abnormal mitochondria. Restoring miR‐181a levels in old mice prevented accumulation of p62, DJ‐1, and PARK2, and improved mitochondrial quality and muscle function. These results provide physiological evidence for the potential of microRNA‐based interventions for age‐related muscle atrophy and of wider significance for diseases with disrupted mitochondrial dynamics. 相似文献