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721.
722.
Kelvin S.-H. Peh 《Biodiversity and Conservation》2010,19(4):1083-1099
This review deals with alien species invasion in Southeast Asia, an important conservation and management concern in the region.
I report on the current and potential future impacts of biological invasions on biodiversity in Southeast Asia. Current knowledge
of the invasive species in Southeast Asia is mostly based on anecdotal observations. Nevertheless, I attempt to compile existing
empirical evidence on the negative effects of the biological invaders found in the region. These impacts include displacement
of native biota, modification of ecosystems, hybridization, environmental disturbance, and economic loss. Any effective counter-measure
will need to involve a multi-national strategy, yet such measure is challenging due to a broad spectrum of political and economic
development models among the Southeast Asian countries. An overview of the taxonomic structure of the invasive species in
Southeast Asia shows that the invasive plant and fish are the most represented taxonomic groups in all countries. The current
research effort in invasion ecology from Southeast Asia is not being up to international standard in comparison to other regions,
and the absence of recent international journal articles on invasive plant species reveals the biases in biological invasion-related
research. The lack of research capacity and financial support from governments, and the inability to disseminate scholarly
data in international journals are the possible reasons for the dearth of research literature on biological invasions from
the region. Finally, a forward-looking agenda for the region should include improving the quality and quantity of biological
invasion research; adopting a tough approach to the illegal release of wildlife; and applying multi-national strategies that
integrate data sharing, prioritization, public awareness, policy work, capacity building, conservation actions and surveillance. 相似文献
723.
Alzheimer's disease is a progressive neurodegenerative disorder and the most common form of dementia. The disease is confirmed by the presence of neuritic plaques and neurofibrillary tangles in the cerebral cortex at autopsy, but the accuracy of antemortem diagnosis, especially at the early stages of the disease, is not ideal. Thus, there is a substantial need for the discovery and validation of diagnostic biomarkers. Many Alzheimer's disease biomarker discovery studies emphasize the analysis of cerebrospinal fluid (CSF) because of its close association with the brain. Here, we review recent mass spectrometry-based studies of Alzheimer's disease CSF, and additionally discuss issues associated with CSF in proteomics studies. 相似文献
724.
725.
726.
Pirbhai M Dong F Zhong Y Pan KZ Zhong G 《The Journal of biological chemistry》2006,281(42):31495-31501
Chlamydia trachomatis has evolved a profound anti-apoptotic activity that may aid in chlamydial evasion of host defense. The C. trachomatis anti-apoptotic activity has been correlated with blockade of mitochondrial cytochrome c release, inhibition of Bax and Bak activation, and degradation of BH3-only proteins. This study presents evidence that a chlamydia-secreted protease factor designated CPAF is both necessary and sufficient for degrading the BH3-only proteins. When the C. trachomatis-infected cell cytosolic extracts were fractionated by column chromatography, both the CPAF protein and activity elution peaks overlapped with the BH3-only protein degradation activity peak. Depletion of CPAF with a CPAF-specific antibody removed the BH3-only protein degradation activity from the infected cell cytosolic extracts, whereas depletion with control antibodies failed to do so. Notably, recombinant CPAF expressed in bacteria was able to degrade the BH3-only proteins, whereas CPAF mutants similarly prepared from bacteria failed to do so. Finally, bacterium-expressed CPAF also degraded the human BH3-only protein Pumaalpha purified from bacteria. These results demonstrate that CPAF contributes to the chlamydial anti-apoptotic activity by degrading the pro-apoptotic BH3-only Bcl-2 subfamily members. 相似文献
727.
With a view to establishing whether first-trimester human placentas possess the ability to synthesize DHEA from cholesterol, homogenates of this tissue obtained from two groups of women undergoing elective termination of normally progressing pregnancy between 10 - 12 weeks gestation (n = 5, age 23 - 29 years and n = 5, age 21 - 27 years) were incubated separately with [26-(14)C]cholesterol for the generation of [14C]isocaproic acid + pregnenolone and [7n-3H]pregnenolone for the biosynthesis of [3H]DHEA. Controls consisted of homogenates heated in a boiling water bath for 10 min. Using the reverse-isotope dilution analysis, desmolase efficiency expressed as mean specific activity of [14C]isocaproic acid varied from 282 to 725 dpm/mmol, while that of 17 alpha-hydroxylase and steroid C-17,20-lyase, catalyzed conversion of [7n-3H]pregnenolone to [3H]DHEA varied from 3498 to 26 258 dpm/mmol. The corresponding efficiencies of enzymicconversion varied between 5.8 x 10( -2) and 1.5 x 10( -1) % for [14C]isocaproic acid, but between 5.5 x 10( -2) and 4.1 x 10( -1) % for [3H]DHEA. No such metabolite was evident in the controls of heat-denatured homogenates. These are the first study results to demonstrate that early placentas are capable of converting cholesterol to pregnenolone to DHEA, contrary to the widely held concept of DHEA production by fetal and maternal adrenal glands. This finding has important physiological implications and could provide a new dimension to the concept of fetoplacental steroidogenesis. 相似文献
728.
Kelvin F. Conrad Karen H. Willson Katherine Whitfield Ian F. Harvey Chris J. Thomas Thomas N. Sherratt 《Ecography》2002,25(4):439-445
In this study we assessed whether individuals of the damselfly species Ischnura elegans and Coenagrion puella that moved between ponds differed in their mean characteristics from individuals that did not move. Overall, the sex (female) and species ( C. puella ) that spent the most time away from the breeding site was more likely to move between ponds. Ischnura elegans males that dispersed had significantly longer forewings than males that did not, while male C. puella parasitised by water mites were more likely to disperse than unparasitised males. There was no evidence for differences in dispersal rates among the female colour forms of either I. elegans or C. puella . In general, the differences in dispersal characteristics between sexes and species could be explained by underlying variation in activity and mobility. The majority of dispersal between breeding sites by C. puella and I. elegans did not appear to be directed, but probably arose from chance movements occasionally taking individuals to a different pond from which they emerged. 相似文献
729.
The peroxisomal Lon protease LonP2 in aging and disease: functions and comparisons with mitochondrial Lon protease LonP1
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Laura C. D. Pomatto Rachel Raynes Kelvin J. A. Davies 《Biological reviews of the Cambridge Philosophical Society》2017,92(2):739-753
Peroxisomes are ubiquitous eukaryotic organelles with the primary role of breaking down very long‐ and branched‐chain fatty acids for subsequent β‐oxidation in the mitochondrion. Like mitochondria, peroxisomes are major sites for oxygen utilization and potential contributors to cellular oxidative stress. The accumulation of oxidatively damaged proteins, which often develop into inclusion bodies (of oxidized, aggregated, and cross‐linked proteins) within both mitochondria and peroxisomes, results in loss of organelle function that may contribute to the aging process. Both organelles possess an isoform of the Lon protease that is responsible for degrading proteins damaged by oxidation. While the importance of mitochondrial Lon (LonP1) in relation to oxidative stress and aging has been established, little is known regarding the role of LonP2 and aging‐related changes in the peroxisome. Recently, peroxisome dysfunction has been associated with aging‐related diseases indicating that peroxisome maintenance is a critical component of ‘healthy aging’. Although mitochondria and peroxisomes are both needed for fatty acid metabolism, little work has focused on understanding the relationship between these two organelles including how age‐dependent changes in one organelle may be detrimental for the other. Herein, we summarize findings that establish proteolytic degradation of damaged proteins by the Lon protease as a vital mechanism to maintain protein homeostasis within the peroxisome. Due to the metabolic coordination between peroxisomes and mitochondria, understanding the role of Lon in the aging peroxisome may help to elucidate cellular causes for both peroxisome and mitochondrial dysfunction. 相似文献
730.
End stage renal disease‐induced hypercalcemia may promote aortic valve calcification via Annexin VI enrichment of valve interstitial cell derived‐matrix vesicles
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Lin Cui Nabil A. Rashdan Dongxing Zhu Elspeth M. Milne Paul Ajuh Gillian Milne Miep H. Helfrich Kelvin Lim Sai Prasad Daniel A. Lerman Alex T. Vesey Marc R. Dweck William S. Jenkins David E. Newby Colin Farquharson Vicky E. Macrae 《Journal of cellular physiology》2017,232(11):2985-2995
Patients with end‐stage renal disease (ESRD) have elevated circulating calcium (Ca) and phosphate (Pi), and exhibit accelerated progression of calcific aortic valve disease (CAVD). We hypothesized that matrix vesicles (MVs) initiate the calcification process in CAVD. Ca induced rat valve interstitial cells (VICs) calcification at 4.5 mM (16.4‐fold; p < 0.05) whereas Pi treatment alone had no effect. Ca (2.7 mM) and Pi (2.5 mM) synergistically induced calcium deposition (10.8‐fold; p < 0.001) in VICs. Ca treatment increased the mRNA of the osteogenic markers Msx2, Runx2, and Alpl (p < 0.01). MVs were harvested by ultracentrifugation from VICs cultured with control or calcification media (containing 2.7 mM Ca and 2.5 mM Pi) for 16 hr. Proteomics analysis revealed the marked enrichment of exosomal proteins, including CD9, CD63, LAMP‐1, and LAMP‐2 and a concomitant up‐regulation of the Annexin family of calcium‐binding proteins. Of particular note Annexin VI was shown to be enriched in calcifying VIC‐derived MVs (51.9‐fold; p < 0.05). Through bioinformatic analysis using Ingenuity Pathway Analysis (IPA), the up‐regulation of canonical signaling pathways relevant to cardiovascular function were identified in calcifying VIC‐derived MVs, including aldosterone, Rho kinase, and metal binding. Further studies using human calcified valve tissue revealed the co‐localization of Annexin VI with areas of MVs in the extracellular matrix by transmission electron microscopy (TEM). Together these findings highlight a critical role for VIC‐derived MVs in CAVD. Furthermore, we identify calcium as a key driver of aortic valve calcification, which may directly underpin the increased susceptibility of ESRD patients to accelerated development of CAVD. 相似文献