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1.
G. Röhrborn V. Sezer I. -D. Adler A. Schmaltz I. H. Pawlowitzki Ch. Nautsch 《Human genetics》1978,42(1):55-58
Summary Mutagenic damages in female germ, cells of mice have been tested with the dominant, lethal assay and the cytogenetic analysis of unfertilized M II-oocytes. Concluding one can say that from the experimental data presented here do not show any mutagenic effect of INH on oogenesis of different strains of mice can be stated. 相似文献
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Köse Çınar Rugül Görgülü Yasemin Çalıyurt Okan Sönmez Bülent 《Sleep and biological rhythms》2016,14(4):387-396
Sleep and Biological Rhythms - Sleep deprivation (SD) is known to modulate inflammatory and oxidative stress markers. How these markers change over the SD period have seldom been studied in healthy... 相似文献
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The primary structure of the calmodulin-sensitive adenylate cyclase toxin from Bacillus anthracis has been determined from the corresponding nucleotide sequence and compared to that of the homologous toxin secreted by Bordetella pertussis. The cya gene of Bacillus anthracis encodes an 800 amino acid (aa) protein beginning with an N-terminal signal peptide. The central part of the B. anthracis adenylate cyclase includes a region of striking homology with the N-terminal part of the B. pertussis enzyme. In this region a particularly well conserved 24-aa peptide and two other less homologous peptides have been identified. These data corroborate the immunological relatedness of the two enzymes and suggest that the two prokaryotic calmodulin-sensitive adenylate cyclases originate from a common ancestor. 相似文献
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Luft FC Toka O Toka HR Jordan J Bahring S 《American journal of physiology. Regulatory, integrative and comparative physiology》2003,285(4):R709-R714
Mendelian forms of hypertension have delivered a treasure trove of novel genes. To date, the molecular mechanisms of five such syndromes have been largely clarified, including glucocorticoid-remediable aldosteronism, Liddle's syndrome, apparent mineralocorticoid excess, an activating mutation of the mineralocorticoid receptor, and pseudohypoaldosteronism type 2. Each of these conditions features salt sensitivity with increased sodium and volume reabsorption by the kidney and low plasma renin activity. None of the gene loci for these syndromes has been convincingly linked to hypertension in the general population. We are investigating kindreds who have autosomal-dominant hypertension and brachydactyly. Affected persons invariably have both anomalies. The hypertension is severe and results in death at about age 50 years from stroke. The condition resembles essential hypertension, because renin, aldosterone, and norepinephrine responses are normal and no salt sensitivity is present. The response to antihypertensive drugs is general. Another feature is diminished baroreflex sensitivity with markedly impaired blood pressure buffering. Furthermore, the ventrolateral medulla may be compromised in these patients, because neurovascular anomalies are a regular finding. We mapped the gene(s) for this disease to chromosome 12p and narrowed the chromosomal region by studying more affected families. Interestingly, the same locus was recently mapped in Chinese families with essential hypertension. Our 3-centimorgan region contains genes encoding a phosphodiesterase, an ATP-dependent potassium channel, and its regulator the sulfonylurea receptor 2. Screening of the coding regions revealed that none of these candidate genes harbor obvious mutations; however, other genetic mechanisms may nevertheless compromise their function. Our study underscores the importance of regulatory physiology to the understanding of a complex genetic syndrome. 相似文献
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