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The quick-release technique to estimate musculotendinous (MT) stiffness has been extensively used over the last years, in both animals and humans, to gain insights in the adaptive process of the series elastic component (SEC). Recently, MT stiffness quantification, i.e., SEC behavior, has been revisited for subjects not able to fully activate their muscles (effects of long-term spaceflight or non-mature muscles). Such a phenomenon can also be encountered in stunted children. So, the aim of the present study was to analyze the effect of stunting on MT stiffness taking into account possible defect in muscle activation. For this study, 20 eutrophic children (EU) with an average age of 9 years ± 4 months were compared to 11age matched stunted children (S) evaluated by the height-to-age index. The MT stiffness index was obtained with regard to stiffness–torque and stiffness–soleus EMG relationships. The children of the S group presented a significantly lower Maximal Voluntary Contraction (MVC) in plantar flexion in comparison with children of the EU group (?37.8%). The significantly lower MT stiffness index for S children (?42.6%) was evidenced only when quantified with regard to the stiffness–soleus EMG relationship (66.5 ± 42.8 vs. 38.2 ± 19.9 Nm rad?1%?1). Possible delay in fiber type differentiation or tendinous structure maturation can account for the lower MT stiffness index in S children. In conclusion, stunting during early childhood delays the differentiation and maturation processes of musculotendinous structures as shown by the lower MT stiffness quantified with regards to muscle activity, also altered for stunted prepubertal children.  相似文献   
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Harlequin (Hq) mice develop ataxia due to an X-linked recessive mutation in the gene encoding apoptosis-inducing factor (Aif). Brain cells in Hq mice contain the modified base 8-hydroxydeoxyguanosine (8-OHdG), suggesting that the defect in Aif causes increased DNA oxidation in these cells. Because oxidative damage is mutagenic, Hq mice might suffer increased mutation in the brain. To examine this possibility, mutation in the brain was assessed using the Tg(βA-G11PLAP) mouse model, which allows mutant cells to be visualized in tissue sections in situ. Hq mice exhibited more and larger patches of PLAP positive tissue in the brain. PLAP+ cells were observed in all areas of the brain. No increase in the number of PLAP+ cells was seen in three other tissues, suggesting that the effect of Aif deficiency on mutation was specific to brain.  相似文献   
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AimThis research aims to analyze the acute effect of incremental inspiratory loads on respiratory pattern and on the predominant activity frequency of inspiratory muscle, taking into account differences in gender responses. Optoelectronic Plethysmography was performed during loads in 39 healthy subjects (20 women), placing 89 markers on the thoracic-abdominal wall to obtain total and regional volumes. Surface electromyography (SEMG) was taken simultaneously on the Sternocleidomastoid and Diaphragm muscles, to calculate the predominant muscle activity frequency through wavelet analysis. Inspiratory loads were performed using Threshold® with 2 min of breathing at different levels, ranging from a load of 10 cmH2O plus 5 cmH2O to 40 cmH2O or fatigue.ResultsInspiratory Time increased during loads. Total and compartmental volumes increased with different regions, changing at different loads. These changes in volume occur earlier in women (20 cmH2O) than in men (30 cmH2O). The predominant activity frequency of Sternocleidmastoid muscle decreased at 30 cmH2O, while Diaphragm activity decreased at 40 cmH2O.ConclusionThe acute effects of incremental inspiratory loads are increases of total and regional volumes and inspiratory time. As for muscle activity, the predominant activity frequency declined in Sternocleidomastoid and Diaphragm muscles, but at different loads. Such respiratory and SEMG patterns and gender differences should be considered when clinical interventions are performed.  相似文献   
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Synthetic lethality is a promising strategy for specific targeting of cancer cells that carry mutations that are absent in normal cells. This approach may help overcome the challenge associated with targeting dysfunctional tumour suppressors, such as p53 and Rb?(refs?, ). Here we show that Dicer1 targeting prevents retinoblastoma formation in mice by synthetic lethality with combined inactivation of p53 and Rb. Although Dicer1 functions as a haploinsufficient tumour suppressor, its complete loss of function is selected against during tumorigenesis. We show that Dicer1 deficiency is tolerated in Rb-deficient retinal progenitor cells harbouring an intact p53 pathway, but not in the absence of p53. This synthetic lethality is mediated by the oncogenic miR-17-92 cluster because its deletion phenocopies Dicer1 loss in this context. miR-17-92?inactivation suppresses retinoblastoma formation in mice and co-silencing of miR-17/20a and p53 cooperatively decreases the viability of human retinoblastoma cells. These data provide an explanation for the selective pressure against loss of Dicer1 during tumorigenesis and a proof-of-concept that targeting miRNAs may potentially represent a general approach for synthetic lethal targeting of cancer cells that harbour specific cancer-inducing genotypes.  相似文献   
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A sensitive and specific assay for detection of food-borne pathogenic Yersinia pseudotuberculosis was developed. The primer-probe set was designed to target a 157-bp sequence of the chromosomally located gene ail. The complete method, including an internal amplification control, was evaluated for several different food items.  相似文献   
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