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631.
A total of 18 fallow does, including pubertal, non-pregnant and pregnant adult does (6 per class), each received a single subcutaneous implant containing 18 mg melatonin on 4 occasions at 29-30-day intervals from 10 November 1986 (approximately 120-day treatment period). A further 18 contemporary does served as herd-mate controls. Two adult fallow bucks were treated the same and were run with the does until 16 March. Thereafter, 1 of 4 control bucks was run with the does until 1 June. Of the 6 pregnant does receiving implants within the last 40 days of their gestation, 4 failed to lactate after parturition in December 1986. The remaining 2 does successfully reared their fawns, as did the 6 contemporary controls. Mean (+/- s.e.m.) dates of first oestrus in 1987 were 27.6 February (+/- 3.0 days) and 22.9 April (+/- 0.8 days) for all treated and all control does respectively (P less than 0.001). Pubertal does were generally later to exhibit first oestrus than were older does within their respective treatment groups. Return oestrus occurred only in 2 pubertal does (1 treated and 1 control) with remaining does conceiving to their first oestrus, as verified by plasma progesterone profiles. However, 5 (28%) of the treated does and 3 (17%) of the control does failed to maintain pregnancy and fawn in 1987. The mean (+/- s.e.m.) 1987 fawning date of the remaining does was 22.4 October (+/- 2.7 days) for the treated group (N = 13) and 13.1 December (+/- 0.8 days) for the control group (N = 15; P less than 0.001). Mean (+/- s.e.m.) gestation length of treated does (238.9 +/- 0.6 days) was significantly longer than that of control does (234.5 +/- 0.4 days; P less than 0.001). Of 13 fawns born to treated does, 4 (31%) died within 24 h of birth (mainly due to hypothermia) whereas all 15 fawns born to control does survived to weaning. Melatonin-treated bucks exhibited a marked advancement of neck muscle hypertrophy during the treatment period and displayed normal rutting activity (e.g. vocalization) in response to early oestrus in the treated does.  相似文献   
632.
A 16-year-old rhesus macaque presented with progressive, ascending quadriparesis following measles vaccination. He was diagnosed with transverse myelitis following MRI, gross necropsy, and histopathology. This is the first report of transverse myelitis in a rhesus macaque following measles vaccination.  相似文献   
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634.
As a champion of small RNA research for two decades, Caenorhabditis elegans has revealed the essential Argonaute CSR-1 to play key nuclear roles in modulating chromatin, chromosome segregation and germline gene expression via 22G-small RNAs. Despite CSR-1 being preserved among diverse nematodes, the conservation and divergence in function of the targets of small RNA pathways remains poorly resolved. Here we apply comparative functional genomic analysis between C. elegans and Caenorhabditis briggsae to characterize the CSR-1 pathway, its targets and their evolution. C. briggsae CSR-1-associated small RNAs that we identified by immunoprecipitation-small RNA sequencing overlap with 22G-RNAs depleted in cbr-csr-1 RNAi-treated worms. By comparing 22G-RNAs and target genes between species, we defined a set of CSR-1 target genes with conserved germline expression, enrichment in operons and more slowly evolving coding sequences than other genes, along with a small group of evolutionarily labile targets. We demonstrate that the association of CSR-1 with chromatin is preserved, and show that depletion of cbr-csr-1 leads to chromosome segregation defects and embryonic lethality. This first comparative characterization of a small RNA pathway in Caenorhabditis establishes a conserved nuclear role for CSR-1 and highlights its key role in germline gene regulation across multiple animal species.  相似文献   
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636.
The construct General Sleep-related Experiences (GSEs, such as elevated dream recall, vivid or bizarre dreams, flying dreams, hypnagogic hallucinations, nightmares, and recurrent dreams) has been previously linked to various forms of psychopathology in nonclinical populations. The aim of this pilot study was to explore this relationship in the context of severe psychopathology. Nineteen outpatients of a mental health clinic were compared to 26 controls on sleep experiences, psychopathology, sleep quality, life stress, and transliminality. Outpatients also reported illness intrusiveness levels. As expected, the outpatient group had elevated GSEs. Within the outpatient group, illness intrusiveness, stress, and transliminality were correlated with GSEs. These findings elucidate the association between GSEs and distress in the context of severe psychopathology. (PsycINFO Database Record (c) 2011 APA, all rights reserved)  相似文献   
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638.
The role of the antioxidant defense mechanism in diabetesinduced anomalies was studied in the Cohen diabetes-sensitive (CDs) and -resistant (CDr) rats, a genetic model of nutritionally induced type 2 diabetes mellitus. Embryos, 12.5-day-old, of CDs and CDr rats fed regular diet (RD) or a diabetogenic high-sucrose diet (HSD) were monitored for growth retardation and congenital anomalies. Activity of superoxide dismutase (SOD) and catalaselike enzymes and levels of ascorbic acid (AA), uric acid (UA), and dehydroascorbic acid (DHAA) were measured in embryonic homogenates. When fed RD, CDs rats had a decreased rate of pregnancy, and an increased embryonic resorption. CDs embryos were smaller than CDr embryos; 46% were maldeveloped and 7% exhibited neural tube defects (NTDs). When fed HSD, rate of pregnancy was reduced, resorption rate was greatly increased (56%; P < .001), 47.6% of the embryos were retrieved without heart beats, and 27% exhibited NTD. In contrast, all the CDr embryos were normal when fed RD or HSD. Activity of SOD and catalase was not different in embryos of CDs and CDr rats fedRD. When fed HSD, levels of AA were significantly reduced, the ratio DHAA/AA was significantly increased, and SOD activity was not sufficiently increased when compared to embryos of CDr. The reduced fertility of the CDs rats, the growth retardation, and NTD seem to be genetically determined. Maternal hyperglycemia seems to result in environmentally induced embryonic oxidative stress, resulting in further embryonic damage.  相似文献   
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