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101.
102.
Putman CT Dixon WT Pearcey JA Maclean IM Jendral MJ Kiricsi M Murdoch GK Pette D 《American journal of physiology. Regulatory, integrative and comparative physiology》2004,287(6):R1419-R1426
The purpose of this investigation was to examine the temporal changes in uncoupling protein (UCP)-3 expression, as well as related adaptive changes in mitochondrial density and fast-to-slow fiber type transitions during chronically enhanced contractile activity. We examined the effects of 1-42 days of chronic low-frequency electrical stimulation (CLFS), applied to rat tibialis anterior (TA) for 10 h/day, on the expression of UCP-3 and concomitant changes in myosin heavy chain (MHC) protein expression and increases in oxidative capacity. UCP-3 protein content increased from 1 to 12 days, reaching 1.5-fold over control (P < 0.0005); it remained elevated for up to 42 days. In contrast, UCP-3 mRNA decreased in response to CLFS, reaching a level that was threefold lower than control (P < 0.0007). The activities of the mitochondrial reference enzymes citrate synthase (EC 4.1.3.7) and 3-hydroxyacyl-CoA-dehydrogenase (EC 1.1.1.35), which are known to increase in proportion to mitochondrial density, progressively increased up to an average of 2.3-fold (P < 0.00001). These changes were accompanied by fast-to-slow fiber type transitions, characterized by a shift in the pattern of MHC expression (P <0.0002): MHCI and MHCIIa expression increased by 1.7- and 4-fold, whereas MHCIIb displayed a 2.4-fold reduction. We conclude that absolute increases in UCP-3 protein content in the early adaptive phase were associated with the genesis of mitochondria containing a normal complement of UCP-3. However, during exposure to long-term CLFS, mitochondria were generated with a lower complement of UCP-3 and coincided with the emergence of a growing population of oxidative type IIA fibers. 相似文献
103.
Goh KL Hiller J Haston JL Holmes DF Kadler KE Murdoch A Meakin JR Wess TJ 《Biochimica et biophysica acta》2005,1722(2):183-188
Analysis of the diameters of collagen fibrils provides insight into the structure and physical processes occurring in the tissue. This paper describes a method for analyzing the frequency distribution of the diameters of collagen fibrils from small-angle X-ray scattering (SAXS) patterns. Frequency values of fibril diameters were input into a mathematical model of the form factor to calculate the equatorial intensity which best fits the experimentally derived data from SAXS patterns. A minimization algorithm utilizing simulated annealing (SA) was used in the fitting procedure. The SA algorithm allowed for random sampling of the frequency values, and was run iteratively to build up an optimized frequency distribution of fibril diameters. Results were obtained for collagen samples from sheep spine ligaments. The mean fibril diameter value obtained from this data-fitting method was 73 nm+/-20 nm (S.D.). From scanning transmission electron microscopy, the mean diameter was found to be 69 nm+/-14 nm (S.D.). The good agreement between the two methods demonstrates the reliability of the SAXS method for the tissue examined. The non-destructive nature of this technique, as well as its statistical robusticity and capacity for large sampling, means that this method is both quick and effective. 相似文献
104.
Murdoch WJ 《Biology of reproduction》2005,73(4):586-590
Ovulation is a rate-limiting event for the perpetuation of a species; unfortunately, it imparts a cancer risk. Reactive oxidants generated during the mechanics of ovulatory follicular rupture damage the DNA of ovarian surface epithelial cells that are located within a limited diffusion radius. Those cells that survive the trauma of ovulation, along the margins of a ruptured follicle, proliferate and migrate to reconcile the discontinuity within the ovarian epithelium created at the site of oocyte release. It is conceivable that clonal expansion of an ovarian surface epithelial cell with unrepaired DNA, but not committed to death, could be an initiating factor in the etiology of common ovarian cancer. In fact, the majority of cancers of the ovary are derived from the surface epithelium; and circumstances that avert ovulation (oral contraceptive use, pregnancy/lactation) protect against ovarian adenocarcinoma. Not surprisingly, the genotoxic potential of ovulation is exacerbated by malfunctions in tumor suppressor/cell-cycle arrest and base-excision repair mechanisms. Recent experimental evidence indicates that vitamin E and progesterone protect against ovarian metaplasia by negating the oxidative stress of ovulation and by enhancing the repair capacity (genomic integrity) of the surface epithelium, respectively. Ovarian cancer of surface epithelial origin is a deadly insidious disease because it characteristically remains asymptomatic until it has metastasized throughout the abdominal cavity; therefore, prevention is a high priority. 相似文献
105.
In a new mouse mutant, circletail (Crc), failure of neural tube closure (embryonic day [E] 8-9) is associated with errors in retinal axon projection at the optic chiasm (E12-18), such that many axons normally projecting contralaterally instead grow to ipsilateral targets. Although the architecture of the chiasmatic region is altered, neurons and glia containing putative cues for axon guidance are present. The aberrant ipsilateral-projecting cells originate from a nonrandom expansion of the wild-type uncrossed retinal region. These axon pathway defects are found in two other mutants with cephalic neural tube defects (NTD), loop-tail (Lp) and Pax3 (splotch; Sp(2H)). Crc is phenotypically similar to Lp, exhibiting an open neural tube from midbrain to tail (craniorachischisis), while splotch has spina bifida with or without a cranial NTD. The retinal axon abnormalities occur only in the presence of NTD and not in homozygous mutants lacking cranial NTD. Thus, failure of neural tube closure is associated with failure of many retinal axons to cross the ventral midline. This study therefore reveals an unexpected connection between closure of the neural tube at the dorsal midline and development of ventral axon tracts. genesis 27:32-47, 2000. 相似文献
106.
Murdoch WJ Van Kirk EA Alexander BM 《Experimental biology and medicine (Maywood, N.J.)》2005,230(6):429-433
A cause-effect relationship between ovulation and common (surface) epithelial ovarian cancer has been suspected for many years. The ovarian surface epithelium apparently becomes exposed to genotoxins that are generated during the ovulatory process. Intensive egg-laying hens readily develop ovarian carcinomatosis. Indeed, elevated levels of potentially mutagenic 8-oxo-guanine adducts were detected in avian ovarian epithelial cells isolated from the apical surfaces and perimeters of pre-and postovulatory follicles, respectively. Internucleosomal DNA fragmentation indicative of apoptosis was evident in ovarian surface epithelial cells associated with the formative site of ovulation (stigma line) and regressive ruptured follicles. It is conceivable that a genetically altered progenitor cell with unrepaired DNA but not committed to death (i.e., a unifocal "escape") could give rise to a transformed phenotype. Hence, the high rate of ovarian cancer in egg-laying hens could be the consequence of genomic damages to the ovarian surface epithelium associated with incessant ovulations, thereby increasing the likelihood of mutation and clonal expansion. 相似文献
107.
108.
Todd N. Pearsons Andrew R. Murdoch Greg Mackey Keely G. Murdoch Tracy W. Hillman Matthew R. Cooper Joseph L. MIller 《Environmental Biology of Fishes》2012,94(1):87-100
Ecological risks of Pacific salmon (spring, summer, and fall run Chinook, coho, and sockeye salmon) and steelhead trout hatchery
programs operated between 2013 and 2023 in the Upper Columbia Watershed will be assessed using Delphi and modeling approaches.
Committees composed of resource managers and public utility districts identified non-target taxa of concern (i.e., taxa that
are not the target of supplementation), and acceptable hatchery impacts (i.e., change in population status) to those taxa.
Biologists assembled information about hatchery programs, non-target taxa, and ecological interactions and this information
will be provided to expert panelists in the Delphi process to facilitate assessment of risks and also used to populate the
Predation, Competition, and Disease (PCD) Risk 1 model. Delphi panelists will independently estimate the proportion of a non-target
taxa population that will be affected by each individual hatchery program. Estimates from each of the two approaches will
be independently averaged, a measure of dispersion calculated (e.g., standard deviation), and subsequently compared to the
acceptable hatchery impact levels that were determined previously by committees of resource managers and public utility districts.
Measures of dispersion will be used to estimate the scientific uncertainty associated with risk estimates. Delphi and model
results will be compared to evaluate the qualities of the two approaches. Furthermore, estimates of impacts from each hatchery
program will be combined together to generate an estimate of cumulative impact to each non-target taxon. 相似文献
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