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For the purpose of establishing clinical reference values, this paper reports results of ultrasonographic examination and measurement of accessory sex glands, ampullae, and the pelvic urethra of 102 mature, healthy breeding stallions (2-29 years of age) of various size types (7 Miniature Horses, 27 small ponies, 53 light horses and 15 heavy horses). Examinations were done per rectum in mostly unsedated stallions using an Aloka 210 scanner with a 7.5 MHz linear veterinary transrectal transducer (Corometrics Medical Systems, Inc., North Wallingford, CT, USA). Most measures of accessory sex glands, ampullae and the urethra were larger in horses of larger sizes. Except for vesicular glands, the majority of the measures for all glands were smaller for Miniature Horses and ponies than for light horses and heavy horses (P < 0.05). For vesicular glands, measures for heavy horses were greater than for those of other groups (P < 0.05). Measures were similar for Miniature Horses and ponies, and for light horses and heavy horses. For all measures, differences between left and right paired glands were not different (P > 0.10). The lumen diameter of vesicular glands and ampullae as well as prostate lobe thickness showed the greatest asymmetry. Although there were too few representatives of various breeds for statistical comparison, among the light horse breeds Arabian stallions had the smallest mean values for the majority of the measures. Among stallions, echogenic characteristics of accessory sex glands, particularly vesicular glands, varied widely, possibly related to variation in recent sexual activity. For some stallions, echogenic character, particularly that of vesicular glands, varied remarkably from left to right gland within stallions. For ampullae, there was also wide variation in lumen contents between stallions. These data are generally consistent with previous reports with smaller numbers of stallions, as well as consistent with in vitro measures in previous studies. The results provide useful clinical guidelines for size measures of accessory sex glands in horses. 相似文献
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C E Farin K Imakawa T R Hansen J J McDonnell C N Murphy P W Farin R M Roberts 《Biology of reproduction》1990,43(2):210-218
The trophoblastic interferons ovine and bovine trophoblast protein-1 (oTP-1 and bTP-1, respectively) have been implicated as mediators of maternal recognition of pregnancy in sheep and cattle. The objective of this study was to describe the onset and duration of gene expression for oTP-1 and bTP-1 in preimplantation ovine and bovine conceptuses by in situ hybridization and Northern analysis. Sections from paraffin-embedded ovine conceptuses, collected on Days 10, 11, 12, 13, and 15 of gestation (n = 1, 3, 3, 2, 2), and bovine conceptuses, collected on Days 12/13, 15/16, and 19 (n = 2, 4, 5), were hybridized to specific [35S]-labeled cDNA probes. Two different probes, one encompassing bases 442-918 and representing both coding and 3'-untranslated regions, and a second 3'-specific probe (bases 650-912) were used to detect oTP-1 mRNA. At all stages examined, oTP-1 mRNA was confined to trophectoderm of ovine conceptuses. Consistent with earlier studies, expression increased markedly at Day 13. oTP-1 mRNA was detected at low levels in seven of seven ovine conceptuses prior to Day 13 when the longer probe was employed. With the 3'-specific probe, however, oTP-1 mRNA was detected in only one of the seven ovine conceptuses prior to Day 13. Thus, although low amounts of oTP-1 mRNA may be present in ovine conceptuses prior to Day 13, massive induction of this mRNA occurs on Day 13 coincident with the initiation of maternal recognition of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
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Craig C. Teerlink Stephen N. Thibodeau Shannon K. McDonnell Daniel J. Schaid Antje Rinckleb Christiane Maier Walther Vogel Geraldine Cancel-Tassin Christophe Egrot Olivier Cussenot William D. Foulkes Graham G. Giles John L. Hopper Gianluca Severi Ros Eeles Douglas Easton Zsofia Kote-Jarai Michelle Guy Kathleen A. Cooney Anna M. Ray Kimberly A. Zuhlke Ethan M. Lange Liesel M. FitzGerald Janet L. Stanford Elaine A. Ostrander Kathleen E. Wiley Sarah D. Isaacs Patrick C. Walsh William B. Isaacs Tiina Wahlfors Teuvo Tammela Johanna Schleutker Fredrik Wiklund Henrik Grönberg Monica Emanuelsson John Carpten Joan Bailey-Wilson Alice S. Whittemore Ingrid Oakley-Girvan Chih-Lin Hsieh William J. Catalona S. Lilly Zheng Guangfu Jin Lingyi Lu Jianfeng Xu Nicola J. Camp Lisa A. Cannon-Albright 《Human genetics》2014,133(3):347-356
Previous GWAS studies have reported significant associations between various common SNPs and prostate cancer risk using cases unselected for family history. How these variants influence risk in familial prostate cancer is not well studied. Here, we analyzed 25 previously reported SNPs across 14 loci from prior prostate cancer GWAS. The International Consortium for Prostate Cancer Genetics (ICPCG) previously validated some of these using a family-based association method (FBAT). However, this approach suffered reduced power due to the conditional statistics implemented in FBAT. Here, we use a case–control design with an empirical analysis strategy to analyze the ICPCG resource for association between these 25 SNPs and familial prostate cancer risk. Fourteen sites contributed 12,506 samples (9,560 prostate cancer cases, 3,368 with aggressive disease, and 2,946 controls from 2,283 pedigrees). We performed association analysis with Genie software which accounts for relationships. We analyzed all familial prostate cancer cases and the subset of aggressive cases. For the familial prostate cancer phenotype, 20 of the 25 SNPs were at least nominally associated with prostate cancer and 16 remained significant after multiple testing correction (p ≤ 1E ?3) occurring on chromosomal bands 6q25, 7p15, 8q24, 10q11, 11q13, 17q12, 17q24, and Xp11. For aggressive disease, 16 of the SNPs had at least nominal evidence and 8 were statistically significant including 2p15. The results indicate that the majority of common, low-risk alleles identified in GWAS studies for all prostate cancer also contribute risk for familial prostate cancer, and that some may contribute risk to aggressive disease. 相似文献
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