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3-Ketothiolase deficiency (3KTD) is the result of a deficiency in mitochondrial acetoacetyl-CoA thiolase (T2). The molecular basis of 3KTD was analyzed in a patient (GK10) and his family at the protein, cDNA and gene levels. Protein analyses showed that GK10's T2 protein was undetectable in fibroblasts even with the pulse-protein labeling method and that his parents were carriers of 3KTD. Complementary DNA analyses with PCR showed that T2 cDNA in the patient lacked the normal exon 11 sequence and that his parents were obligatory carriers of the DNA sequence which canceled exon 11. When the PCR-amplified genomic fragments around exon 11 were sequenced, an AG to AC mutation at the 3' splice site of intron 10 was detected. This mutation is presumed to be responsible for exon 11 skipping. 相似文献
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Brenda Rocamonde Nicolas Futsch Noemia Orii Omran Allatif Augusto Cesar Penalva de Oliveira Renaud Mahieux Jorge Casseb Hlne Dutartre 《PLoS neglected tropical diseases》2021,15(11)
The Human T-cell Leukemia Virus-1 (HTLV-1)-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) is a devastating neurodegenerative disease with no effective treatment, which affects an increasing number of people in Brazil. Immune cells from the adaptive compartment are involved in disease manifestation but whether innate cell functions participate in disease occurrence has not been evaluated. In this study, we analyzed innate cell responses at steady state and after blood cell stimulation using an agonist of the toll-like receptor (TLR)7/8-signaling pathway in blood samples from HTLV-1-infected volunteers, including asymptomatic carriers and HAM/TSP patients. We observed a lower response of IFNα+ DCs and monocytes in HAM/TSP compared to asymptomatic carriers, as a potential consequence of corticosteroid treatments. In contrast, a higher frequency of monocytes producing MIP-1α and pDC producing IL-12 was detected in HAM/TSP blood samples, together with higher IFNγ responsiveness of NK cells, suggesting an increased sensitivity to inflammatory response in HAM/TSP patients compared to asymptomatic carriers. This sustained inflammatory responsiveness could be linked or be at the origin of the neuroinflammatory status in HAM/TSP patients. Therefore, the mechanism underlying this dysregulations could shed light onto the origins of HAM/TSP disease. 相似文献
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Kogo N Tazaki A Kashino Y Morichika K Orii H Mochii M Watanabe K 《Developmental biology》2011,(2):462-469
Mitochondria are accurately transmitted to the next generation through a female germ cell in most animals. Mitochondria produce most ATP, accompanied by the generation of reactive oxygen species (ROS). A specialized mechanism should be necessary for inherited mitochondria to escape from impairments of mtDNA by ROS. Inherited mitochondria are named germ-line mitochondria, in contrast with somatic ones. We hypothesized that germ-line mitochondria are distinct from somatic ones. The protein profiles of germ-line and somatic mitochondria were compared, using oocytes at two different stages in Xenopus laevis. Some subunits of ATP synthase were at a low level in germ-line mitochondria, which was confirmed immunologically. Ultrastructural histochemistry using 3,3′-diaminobenzidine (DAB) showed that cytochrome c oxidase (COX) activity of germ-line mitochondria was also at a low level. Mitochondria in one oocyte were segregated into germ-line mitochondria and somatic mitochondria, during growth from stage I to VI oocytes. Respiratory activity represented by ATP synthase expression and COX activity was shown to be low during most of the long gametogenetic period. We propose that germ-line mitochondria that exhibit suppressed respiration alleviate production of ROS and enable transmission of accurate mtDNA from generation to generation. 相似文献
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Mary C. Hunt Per J. G. Lindquist Sari Nousiainen Merja Huttunen Kenji Orii Thomas L. T. Svensson T. Aoyama Takashi Hashimoto Uulf Diczfalusy Stefan E. H. Alexson 《Cell biochemistry and biophysics》2000,32(1-3):317-324
Acyl-CoA thioesterases hydrolyze acyl-CoAs to the corresponding free fatty acid plus coenzyme A. The activity is strongly
induced in rat and mouse liver after feeding the animals peroxisome proliferators (PPs). To elucidate the role of these enzymes
in lipid metabolism, the authors have cloned the cDNAs corresponding to the inducible cytosolic and mitochondrial type I enzymes
(CTE-I and MTE-I), and studied tissue expression and nutritional regulation of expression of the mRNAs in mice. The constitutive
expression of both mRNAs was low in liver, with CTE-I expressed mainly in kidney and brown adipose tissue, and MTE-I expressed
in brown adipose tissue and heart. As expected, the expression in liver of both the CTE-I and MTE-I mRNAs were strongly induced
(>50-fold) by treatment with clofibrate. A similar level of induction was observed by fasting and a time-course study showed
that the CTE-I and MTE-I mRNAs were increased already at 6 h after removal of the diet. Refeeding normal chow diet to mice
fasted for 24h normalized the mRNA levels with a T
1/2 of about 3–4 h. Feeding mice a fat-free diet further decreased the expression, possibly indicating repression of expression.
The strong expression of MTE-I and CTE-I in the heart was increased about 10-fold by fasting. To further characterize these
highly regulated enzymes, the authors have cloned the corresponding genes and promoter regions. The structures of the two
genes were found to be very similar, consisting of three exons and two introns. Exon-intron borders conform to general consensus
sequences, and, especially, the first exon appears to be highly conserved. The promoter regions of both the CTE-I and MTE-I
genes contain putative PP response elements, suggesting an involvement of PP-activated receptors in the regulation of these
genes. 相似文献