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941.
942.
Ernesto Shimizu Analía Macías Fernando Paolicchi Gabriel Magnano Laura Zapata Analía Fernández Ana Canal Sergio Garbaccio Angel Cataldi Karina Caimi Martín Zumárraga 《Memórias do Instituto Oswaldo Cruz》2014,109(2):236-245
Mycobacterium bovis is the causative agent of bovine tuberculosis
(TB), a disease that affects approximately 5% of Argentinean cattle. Among the
molecular methods for genotyping, the most convenient are spoligotyping and variable
number of tandem repeats (VNTR). A total of 378 samples from bovines with visible
lesions consistent with TB were collected at slaughterhouses in three provinces,
yielding 265 M. bovis spoligotyped isolates, which were distributed
into 35 spoligotypes. In addition, 197 isolates were also typed by the VNTR method
and 54 combined VNTR types were detected. There were 24 clusters and 27 orphan types.
When both typing methods were combined, 98 spoligotypes and VNTR types were observed
with 27 clusters and 71 orphan types. By performing a meta-analysis with previous
spoligotyping results, we identified regional and temporal trends in the population
structure of M. bovis. For SB0140, the most predominant spoligotype
in Argentina, the prevalence percentage remained high during different periods,
varying from 25.5-57.8% (1994-2011). By contrast, the second and third most prevalent
spoligotypes exhibited important fluctuations. This study shows that there has been
an expansion in ancestral lineages as demonstrated by spoligotyping. However, exact
tandem repeat typing suggests dynamic changes in the clonal population of this
microorganism. 相似文献
943.
944.
Ono E Inoue J Hashidume T Shimizu M Sato R 《Biochemical and biophysical research communications》2011,(3):677-681
TGR5 is a member of the G protein-coupled receptor family and is activated by bile acids (BAs). TGR5 is thought to be a promising drug target for metabolic diseases because the activation of TGR5 prevents obesity and hyperglycemia in mice fed a high-fat diet (HFD). In the present study, we identified a naturally occurring limonoid, nomilin, as an activator of TGR5. Unlike BAs, nomilin did not exhibit the farnesoid X receptor ligand activity. Although the nomilin derivative obacunone was capable of activating TGR5, limonin (the most abundant limonoid in citrus seeds) was not a TGR5 activator. When male C57BL/6J mice fed a HFD for 9 weeks were further fed a HFD either alone or supplemented with 0.2% w/w nomilin for 77 days, nomilin-treated mice had lower body weight, serum glucose, serum insulin, and enhanced glucose tolerance. Our results suggest a novel biological function of nomilin as an agent having anti-obesity and anti-hyperglycemic effects that are likely to be mediated through the activation of TGR5. 相似文献
945.
946.
Saito F Saito-Arai Y Nakamura-Okuma A Ikeda M Hagiwara H Masaki T Shimizu T Matsumura K 《Biochemical and biophysical research communications》2011,(2):494-369
α-Dystroglycan (α-DG) plays crucial roles in maintaining the stability of cells. We demonstrated previously that the N-terminal domain of α-DG (α-DG-N) is secreted by cultured cells into the culture medium. In the present study, to clarify its function in vivo, we generated a monoclonal antibody against α-DG-N and investigated the secretion of α-DG-N in human cerebrospinal fluid (CSF). Interestingly, we found that a considerable amount of α-DG-N was present in CSF. α-DG-N in CSF was a sialylated glycoprotein with both N- and O-linked glycan. These observations suggest that secreted α-DG-N may be transported via CSF and have yet unidentified effects on the nervous system. 相似文献
947.
948.
Murakami K Murata N Noda Y Tahara S Kaneko T Kinoshita N Hatsuta H Murayama S Barnham KJ Irie K Shirasawa T Shimizu T 《The Journal of biological chemistry》2011,286(52):44557-44568
Oxidative stress is closely linked to the pathogenesis of neurodegeneration. Soluble amyloid β (Aβ) oligomers cause cognitive impairment and synaptic dysfunction in Alzheimer disease (AD). However, the relationship between oligomers, oxidative stress, and their localization during disease progression is uncertain. Our previous study demonstrated that mice deficient in cytoplasmic copper/zinc superoxide dismutase (CuZn-SOD, SOD1) have features of drusen formation, a hallmark of age-related macular degeneration (Imamura, Y., Noda, S., Hashizume, K., Shinoda, K., Yamaguchi, M., Uchiyama, S., Shimizu, T., Mizushima, Y., Shirasawa, T., and Tsubota, K. (2006) Proc. Natl. Acad. Sci. U.S.A. 103, 11282-11287). Amyloid assembly has been implicated as a common mechanism of plaque and drusen formation. Here, we show that Sod1 deficiency in an amyloid precursor protein-overexpressing mouse model (AD mouse, Tg2576) accelerated Aβ oligomerization and memory impairment as compared with control AD mouse and that these phenomena were basically mediated by oxidative damage. The increased plaque and neuronal inflammation were accompanied by the generation of N(ε)-carboxymethyl lysine in advanced glycation end products, a rapid marker of oxidative damage, induced by Sod1 gene-dependent reduction. The Sod1 deletion also caused Tau phosphorylation and the lower levels of synaptophysin. Furthermore, the levels of SOD1 were significantly decreased in human AD patients rather than non-AD age-matched individuals, but mitochondrial SOD (Mn-SOD, SOD2) and extracellular SOD (CuZn-SOD, SOD3) were not. These findings suggest that cytoplasmic superoxide radical plays a critical role in the pathogenesis of AD. Activation of Sod1 may be a therapeutic strategy for the inhibition of AD progression. 相似文献
949.
Tamura Y Chiba Y Tanioka T Shimizu N Shinozaki S Yamada M Kaneki K Mori S Araki A Ito H Kaneki M 《FEBS letters》2011,585(19):3058-3064
Nitric oxide (NO) has been implicated in pancreatic β-cell death in the development of diabetes. The mechanisms underlying NO-induced β-cell death have not been clearly defined. Recently, receptor-interacting protein-1 (RIP1)-dependent necrosis, which is inhibited by necrostatin-1, an inhibitor of RIP1, has emerged as a form of regulated necrosis. Here, we show that NO donor-induced β-cell death was inhibited by necrostatin-1. Unexpectedly, however, RIP1 knockdown neither inhibited cell death nor altered the protective effects of necrostatin-1 in NO donor-treated β-cells. These results indicate that NO donor induces necrostatin-1-inhibitable necrotic β-cell death independent of RIP1. Our findings raise the possibility that NO-mediated β-cell necrosis may be a novel form of signal-regulated necrosis, which play a role in the progression of diabetes. 相似文献
950.
Contribution of central versus sweat gland mechanisms to the seasonal change of sweating function in young sedentary males and females 总被引:1,自引:0,他引:1
Yumiko Taniguchi Junichi Sugenoya Naoki Nishimura Satoshi Iwase Takaaki Matsumoto Yuuki Shimizu Yoko Inukai Maki Sato 《International journal of biometeorology》2011,55(2):203-212
In summer and winter, young, sedentary male (N = 5) and female (N = 7) subjects were exposed to heat in a climate chamber in which ambient temperature (Ta) was raised continuously from 30
to 42°C at a rate of 0.1°C min−1 at a relative humidity of 40%. Sweat rates (SR) were measured continuously on forearm, chest and forehead together with tympanic
temperature (Tty), mean skin temperature ( [`T] s ) \left( {\overline {\hbox{T}} {\hbox{s}}} \right) and mean body temperature ( [`T] b ) \left( {\overline {\hbox{T}} {\hbox{b}}} \right) . The rate of sweat expulsions (Fsw) was obtained as an indicator of central sudomotor activity. Tty and ( [`T] b ) \left( {\overline {\hbox{T}} {\hbox{b}}} \right) were significantly lower during summer compared with winter in males; SR was not significantly different between summer and
winter in males, but was significantly higher during summer in females; SR during winter was higher in males compared with
females. The regression line relating Fsw to ( [`T] b ) \left( {\overline {\hbox{T}} {\hbox{b}}} \right) shifted significantly from winter to summer in males and females, but the magnitude of the shift was not significantly different
between the two subject groups. The regression line relating SR to Fsw was steepened significantly from winter to summer in
males and females, and the change in the slope was significantly greater in females than in males. Females showed a lower
slope in winter and a similar slope in summer compared to males. It was concluded that sweating function was improved during
summer mediated by central sudomotor and sweat gland mechanisms in males and females, and, although the change of sweat gland
function from winter to summer was greater in females as compared with males, the level of increased sweat gland function
during summer was similar between the two subject groups. 相似文献