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921.
African savannah elephants (Loxodonta africana) occur in fragmented and isolated populations across southern Africa. Transfrontier conservation efforts aim at preventing the negative effects of population fragmentation by maintaining and restoring linkages between protected areas. We sought to identify genetic linkages by comparing the elephants in Kruger National Park (South Africa) to populations in nearby countries (Botswana, Mozambique, Zambia and Zimbabwe). We used a 446 base pair mitochondrial DNA (mtDNA) control region fragment (141 individuals) and 9 nuclear DNA (nDNA) microsatellite markers (69 individuals) to investigate phylogenetic relationships and gene flow among elephant populations. The mtDNA and nDNA phylogeographic patterns were incongruent, with mtDNA patterns likely reflecting the effects of ancient female migrations, with patterns persisting due to female philopatry, and nDNA patterns likely reflecting male-mediated dispersal. Kruger elephant heterozygosity and differentiation were examined, and were not consistent with genetic isolation, a depleted gene pool or a strong founder effect. Mitochondrial DNA geographic patterns suggested that the Kruger population was founded by elephants from areas both north and south of Kruger, or has been augmented through migration from more than one geographic source. We discuss our findings in light of the need for conservation initiatives that aim at maintaining or restoring connectivity among populations. Such initiatives may provide a sustainable, self-regulating management approach for elephants in southern Africa while maintaining genetic diversity within and gene flow between Kruger and nearby regions.  相似文献   
922.
Zusammenfassung Gestreifter Mausvogel(Colius striatus), Rotrückenmausvogel(Colius castanotus), Brillenmausvogel(Urocolius indicus) und Blaunackenmausvogel(Urocolius macrourus) zeigen einen ausgeprägten Tagesgang des Energiestoffwechsels, der mit dem Licht-Dunkel-Wechsel korreliert ist. Bei Fütterung ad lib. beträgt der Energiestoffwechsel während der Lichtphase 60–100 J/g · h (Umgebungstemperatur 23 °C). Während der Ruhephase sinkt er um 40–45 % auf 30–60 J/g · h ab. Läßt man Mausvögel hungern, sinkt das Niveau des Stoffwechsels kontinuierlich mit der fallenden Körpermasse ab. Wird eine bestimmte Gewichtsgrenze unterschritten, zeigen alle Mausvögel in der Nacht Torpor. Der Stoffwechsel sinkt dabei um 80–88 % gegenüber dem Lichtstoffwechsel. Im Extrem betrug der Energiestoffwechsel 1,26 J/g · h 98 % Reduktion beim Gestreiften Mausvogel. Der Ruhestoffwechsel von nicht hungernden Mausvögeln liegt im Mittel um + 4,5 % über dem errechenbaren Erwartungswert für kleine Nonpasseres. Mausvögel nutzen ihre Bananennahrung mit stark schwankender Effizienz von 30–70 %. Die Ausnutzungsrate der Nahrung steigt unter Hungerbedingungen an. Die höchste ermittelte Assimilationseffizienz betrug über 72 % beim Rotrückenmausvogel. Hungernde Mausvögel bauen Körpersubstanz ab, um daraus Energie zu gewinnen. Der Energiegewinn betrug bei allen untersuchten Arten zwischen 19 und 23 kJ pro g verlorener Körpermasse.
Torpor and utilization of food (metabolizable energy) in 4 species of mousebirds (Coliiformes)
Summary The Speckled Mousebird(Colius striatus), the Red-necked Mousebird(Colius castanotus), the Blue-naped Mousebird(Urocolius macrourus), and the Red-faced Mousebird(Urocolius indicus) show a diurnal cycle of energy metabolism correlated with the L:D-cycle. Fed ad libitum the level of activity metabolism (day time) is 60–100 J/g · h (ambient temperature 23°C). The level of resting metabolism decreases by 40–45 % to 30–60 J/g · h. Fasting leads to a gradual decrease of energy metabolism following continuously the loss of body mass. After reaching a distinct level of body mass all species show torpor during night. Metabolism decreases by 80–88 % in comparison to the activity levels. The lowest reduction observed was 98 % 1,26 J/g · h in the Speckled Mousebird. Mean resting metabolism of non-fasting mousebirds is about 4,5 % above the theoretically expected value for nonpasserine birds ( in the same range). The mousebirds utilize the metabolizable energy of bananas with greatly changing efficiencies of 30–70 %. Utilization efficiency increases during fasting conditions. The maximum rate observed was 72 % in the Red-nekked Mousebird. Fasting mousebirds show a catabolism of body mass for energy profit. This profit laid in all species investigated between 19–23 kJ per g body-mass loss.
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923.
Acetobacterium woodii is a Gram-positive anaerobic nonsporeforming bacterium able to grow on H2 and CO2 as sole sources of energy. The product of fermentation is acetic acid. Fine structural analysis showed rod-shaped flagellated cells, and coccoid cells without flagella arranged predominantly in pairs and chains. The cell wall was found to be composed of three layers. The cell surface exhibited a periodic array of particles consisting of subunits. The cytoplasmic membrane showed particles either either in random distribution or in a hexagonal pattern. Intracytoplasmic membranes were rarely observed, whereas inclusion bodies of varying shapes, predominantly in an uncommon disc-shape, could frequently be observed. Their content was dissolved in ultrathin sections indicating hydrophobic nature.  相似文献   
924.
Recognition of lipopolysaccharide (LPS) by Toll-like receptor (TLR)4 initiates an intracellular signaling pathway leading to the activation of nuclear factor-kappaB (NF-kappaB). Although LPS-induced activation of NF-kappaB is critical to the induction of an efficient immune response, excessive or prolonged signaling from TLR4 can be harmful to the host. Therefore, the NF-kappaB signal transduction pathway demands tight regulation. In the present study, we describe the human protein Listeria INDuced (LIND) as a novel A20-binding inhibitor of NF-kappaB activation (ABIN) that is related to ABIN-1 and -2 and, therefore, is further referred to as ABIN-3. Similar to the other ABINs, ABIN-3 binds to A20 and inhibits NF-kappaB activation induced by tumor necrosis factor, interleukin-1, and 12-O-tetradecanoylphorbol-13-acetate. However, unlike the other ABINs, constitutive expression of ABIN-3 could not be detected in different human cells. Treatment of human monocytic cells with LPS strongly induced ABIN-3 mRNA and protein expression, suggesting a role for ABIN-3 in the LPS/TLR4 pathway. Indeed, ABIN-3 overexpression was found to inhibit NF-kappaB-dependent gene expression in response to LPS/TLR4 at a level downstream of TRAF6 and upstream of IKKbeta. NF-kappaB inhibition was mediated by the ABIN-homology domain 2 and was independent of A20 binding. Moreover, in vivo adenoviral gene transfer of ABIN-3 in mice reduced LPS-induced NF-kappaB activity in the liver, thereby partially protecting mice against LPS/D-(+)-galactosamine-induced mortality. Taken together, these results implicate ABIN-3 as a novel negative feedback regulator of LPS-induced NF-kappaB activation.  相似文献   
925.
The encounter of individuals-prey, predators and mates-living in the surrounding environment is a fundamental process in the life of an organism. Along with the sensory abilities, this process will be regulated by the movement rules adopted by the individual. In this work we discuss the encounter-enhancement effect due to different natatorial modes by calculating the number of encounters realised by differently convoluted trajectories in two homogeneous distributions of particles. Using numerically generated trajectories representative of specific swimming behaviour, we demonstrate that high values of three-dimensional fractal dimension D(3D)(>1.9) are beneficial only at high concentration, whereas at low concentration less tortuous tracks (D(3D) approximately 1.5) are almost equally efficient. In the light of our results it is possible to better understand the behavioural adaptations evolved by individuals to thrive in their environment.  相似文献   
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Background

Microvascular dysfunction is a major complication in hypertensive patients. We previously reported that CD4+CD25+ T regulatory cells (Treg) play an important preventive role in hypertension-induced vascular dysfunction. However, whether Treg cells therapy and autophagy inhibition could rescue Treg cells survival and microvascular function in established hypertension is an important question that remained unanswered.

Methods & results

Here we showed that Treg cells from mice model of established hypertension displayed an enhanced apoptotic rate, which was rescued with Treg cells transfer and autophagy inhibition. We also showed increased autophagy in mesenteric resistance artery (MRA) in mice with established hypertension. Importantly, the inhibition of autophagy or one single transfer of Treg cells into mice with established hypertension improved the microvascular function independently of high blood pressure. The protection involves the modulation of interleukin-10 (IL-10), inflammation, endoplasmic reticulum (ER) stress, oxidative stress, Akt, and eNOS.

Conclusions

The present study suggests that Treg cells survival is regulated by autophagy. Also, Treg cells as a cellular therapy aimed at rescuing the microvascular function through an autophagy-dependent mechanism and independently of arterial blood pressure lowering effects. Because our mouse model of established hypertension mimics the clinical situation, our results have the potential for new therapeutic approaches that involve the manipulation of Treg cells and autophagy to overcome established hypertension-induced cardiovascular complications.  相似文献   
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