全文获取类型
收费全文 | 6386篇 |
免费 | 488篇 |
国内免费 | 2篇 |
出版年
2023年 | 29篇 |
2022年 | 85篇 |
2021年 | 157篇 |
2020年 | 106篇 |
2019年 | 126篇 |
2018年 | 159篇 |
2017年 | 140篇 |
2016年 | 227篇 |
2015年 | 330篇 |
2014年 | 330篇 |
2013年 | 559篇 |
2012年 | 563篇 |
2011年 | 499篇 |
2010年 | 332篇 |
2009年 | 254篇 |
2008年 | 405篇 |
2007年 | 396篇 |
2006年 | 365篇 |
2005年 | 267篇 |
2004年 | 283篇 |
2003年 | 264篇 |
2002年 | 239篇 |
2001年 | 51篇 |
2000年 | 36篇 |
1999年 | 57篇 |
1998年 | 57篇 |
1997年 | 51篇 |
1996年 | 45篇 |
1995年 | 29篇 |
1994年 | 40篇 |
1993年 | 42篇 |
1992年 | 27篇 |
1991年 | 22篇 |
1990年 | 31篇 |
1989年 | 19篇 |
1988年 | 17篇 |
1987年 | 18篇 |
1986年 | 14篇 |
1985年 | 16篇 |
1984年 | 21篇 |
1983年 | 15篇 |
1982年 | 20篇 |
1981年 | 21篇 |
1980年 | 8篇 |
1978年 | 15篇 |
1977年 | 10篇 |
1975年 | 8篇 |
1974年 | 10篇 |
1973年 | 9篇 |
1972年 | 7篇 |
排序方式: 共有6876条查询结果,搜索用时 31 毫秒
1.
Patrizia Vaccino Heinz-Albert Becker Andrea Brandolini Francesco Salamini Benjamin Kilian 《Molecular genetics and genomics : MGG》2009,281(3):289-300
The celiac disease (CD) is an inflammatory condition characterized by injury to the lining of the small-intestine on exposure
to the gluten of wheat, barley and rye. The involvement of gluten in the CD syndrome has been studied in detail in bread wheat,
where a set of “toxic” and “immunogenic” peptides has been defined. For wheat diploid species, information on CD epitopes
is poor. In the present paper, we have adopted a genomic approach in order to understand the potential CD danger represented
by storage proteins in diploid wheat and sequenced a sufficiently large number of cDNA clones related to storage protein genes
of Triticum monococcum. Four bona fide toxic peptides and 13 immunogenic peptides were found. All the classes of storage proteins were shown to contain harmful
sequences. The major conclusion is that einkorn has the full potential to induce the CD syndrome, as already evident for polyploid
wheats. In addition, a complete overview of the storage protein gene arsenal in T. monococcum is provided, including a full-length HMW x-type sequence and two partial HMW y-type sequences.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
2.
3.
4.
5.
Paolo d’Errico Marina Boido Antonio Piras Valeria Valsecchi Elena De Amicis Denise Locatelli Silvia Capra Francesco Vagni Alessandro Vercelli Giorgio Battaglia 《PloS one》2013,8(12)
Loss of the survival motor neuron gene (SMN1) is responsible for spinal muscular atrophy (SMA), the most common inherited cause of infant mortality. Even though the SMA phenotype is traditionally considered as related to spinal motor neuron loss, it remains debated whether the specific targeting of motor neurons could represent the best therapeutic option for the disease. We here investigated, using stereological quantification methods, the spinal cord and cerebral motor cortex of ∆7 SMA mice during development, to verify extent and selectivity of motor neuron loss. We found progressive post-natal loss of spinal motor neurons, already at pre-symptomatic stages, and a higher vulnerability of motor neurons innervating proximal and axial muscles. Larger motor neurons decreased in the course of disease, either for selective loss or specific developmental impairment. We also found a selective reduction of layer V pyramidal neurons associated with layer V gliosis in the cerebral motor cortex. Our data indicate that in the ∆7 SMA model SMN loss is critical for the spinal cord, particularly for specific motor neuron pools. Neuronal loss, however, is not selective for lower motor neurons. These data further suggest that SMA pathogenesis is likely more complex than previously anticipated. The better knowledge of SMA models might be instrumental in shaping better therapeutic options for affected patients. 相似文献
6.
A Tabucchi R Rainis M Lorenzi R Pagani E Marinello 《Biochimica et biophysica acta》1987,926(2):177-185
We examined the effects of a two-thirds hepatectomy in the adult rat on the activities of the three L-threonine-degrading enzymes, L-threonine dehydratase, L-threonine aldolase and L-threonine dehydrogenase. Noticeable variations were observed which did not occur in either sham-operated or turpentine-treated rats and were not linked to food intake. They were considered specific to the regenerating liver. When the reactions were followed in vitro, L-threonine deaminase and L-threonine aldolase were significantly lower for the first 12-24 h: L-threonine dehydrogenase decreased only after 48 h. These results are linked to a decrease in the enzyme concentration in the tissue. L-Serine and L-threonine liver concentrations increased 2-3-fold during the same periods. When the activities were evaluated in vivo, the levels of the first two enzymes remained constant for 24 h, but increased after 48 h; L-threonine dehydrogenase increased between 12 and 48 h. The in vivo activity of the enzymes was reflected by total L-threonine degradation, which had a single sharp peak at 48 h. The asynchronous variations in enzyme activity are related to the differences in protein metabolism which occur in the regenerating liver, and are the consequence of a new transient differential control. The changes observed are significant in liver regeneration; they regulate the consumption and the serum and liver levels of L-serine and L-threonine, setting them aside for protein synthesis. They minutely control the flux of amino acids toward gluconeogenesis, since, during the first 48 h after partial hepatectomy, the production of glucose is ensured principally by lactate; the contribution of L-threonine seems to be more significant only at 48 h. These findings are useful in the study of the regulation of the enzymes involved in amino acid metabolism during liver regeneration. 相似文献
7.
8.
Mapping of a restriction fragment length polymorphism within the human aldolase B gene 总被引:1,自引:0,他引:1
Giovanni Paolella Rita Santamaria Pasqualina Buono Francesco Salvatore 《Human genetics》1987,77(2):115-117
Summary Peripheral blood DNA was hybridized to the full-length cDNA and the cloned structural gene of human aldolase B. With PvuII endonuclease a restriction fragment length polymorphism was detected that was present in the heterozygous state in about 21% of the individuals tested. A map of the human aldolase gene was constructed for the two groups of individuals found to produce different fragments after PvuII digestion. This allowed the localization of the polymorphic site within the gene, which was found to be due to the loss of a PvuII site in the last intron upstream from the 3 end. This polymorphism may be used as a genetic marker to study individuals affected by hereditary fructose intolerance. 相似文献
9.
B Porcelli M Pizzichini A Di Stefano R Leoncini A Taddeo E Marinello 《Bollettino della Società italiana di biologia sperimentale》1989,65(12):1201-1205
The behavior of plasma and urine oxypurines (hypoxanthine and xanthine) and of uric acid has been studied in normal subjects and in gout patients. Oxypurines and uric acid were increased in the plasma of gout patients but only the urinary excretion of hypoxanthine was higher in this group. The interpretation of the observed variations is discussed. 相似文献
10.
A Tabucchi L Terzuoli A Di Stefano M Pizzichini R Leoncini E Dispensa E Marinello 《Bollettino della Società italiana di biologia sperimentale》1989,65(11):1097-1103
Phosphoribosyl-1-pyrophosphate (PRPP) amidotransferase is the "key anabolic enzyme" of purine nucleotide synthesis; PRPP synthetase connects the pentose cycle with the same pathway. We have studied their behavior in 5 control subjects and in 8 affected by CLL. Determination of PRPP amidotransferase was carried out through the evaluation of 14C-glutamic acid (released by 14C-glutamine) in the incubation mixture. PRPP synthetase was followed by adding ATP and ribose 5-phosphate to the incubation mixtures, and by evaluating the PRPP formed through the release of CO2 in a coupled reaction. In the case of PRPP-amidotransferase, our values are in the range reported in the literature: in patients affected by CLL, the enzyme activity is much higher and the increase is more evident when values referred to the patients, than when to the cells. Our values of PRPP synthetase are consistent with those of Peters and Veerkamp, but no definite conclusion is possible in the case of leukemic patients. 相似文献