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501.
Shechinah Felice Choragudi Ganesh Kumar Veeramachaneni BV Raman Bondili JS 《Bioinformation》2014,10(8):507-511
Endo- β-N-acetylgucosaminidases (ENGases) are the enzymes that catalyze both hydrolysis and
transglycosylation reactions. It is of interest to study ENGases because of their ability to synthesize glycopeptides.
Homology models of Human, Arabidopsis thaliana and Sorghum ENGases were developed and their active sites
marked based on information available from Arthrobacter protophormiae (PDB ID: 3FHQ) ENGase. Further, these
models were docked with the natural substrate GlcNAc-Asn and the inhibitor Man3GlcNAc-thiazoline. The catalytic
triad of Asn, Glu and Tyr (N171, E173 and Y205 of bacteria) were found to be conserved across the phyla. The crucial
Y299F mutation showing 3 times higher transglycosylation activity than in wild type Endo-A is known. The hydrolytic
activity remained unchanged in bacteria, while the transglycosylation activity increased. This Y to F change is found
to be naturally evolved and should be attributing higher transglycosylation rates in human and Arabidopsis thaliana
ENGases. Ligand interactions Ligplots revealed the interaction of amino acids with hydrophobic side chains and polar
uncharged side chain amino acids. Thus, structure based molecular model-ligand interactions provide insights into
the catalytic mechanism of ENGases and assist in the rational engineering of ENGases. 相似文献
502.
Environmental variables that ameliorate extinction learning deficits in the 129S1/SvlmJ mouse strain
Victor A. Cazares Genesis Rodriguez Rachel Parent Lara Ouillette Katarzyna M. Glanowska Shannon J. Moore Geoffrey G. Murphy 《Genes, Brain & Behavior》2019,18(7)
Fear conditioning is an associative learning process by which organisms learn to avoid environmental stimuli that are predictive of aversive outcomes. Fear extinction learning is a process by which avoidance of fear‐conditioned stimuli is attenuated when the environmental stimuli is no longer predictive of the aversive outcome. Aberrant fear conditioning and extinction learning are key elements in the development of several anxiety disorders. The 129S1 inbred strain of mice is used as an animal model for maladaptive fear learning because this strain has been shown to generalize fear to other nonaversive stimuli and is less capable of extinguishing fear responses relative to other mouse strains, such as the C57BL/6. Here we report new environmental manipulations that enhance fear and extinction learning, including the ability to discriminate between an aversively paired tone and a neutral tone, in both the 129S1 and C57BL/6 strains of mice. Specifically, we show that discontinuous (“pipped”) tone stimuli significantly enhance within‐session extinction learning and the discrimination between neutral and aversively paired stimuli in both strains. Furthermore, we find that extinction training in novel contexts significantly enhances the consolidation and recall of extinction learning for both strains. Cumulatively, these results underscore how environmental changes can be leveraged to ameliorate maladaptive learning in animal models and may advance cognitive and behavioral therapeutic strategies. 相似文献
503.
Amélie Massemin Delphine Goehrig Jean-Michel Flaman Sara Jaber Audrey Griveau Sophia Djebali Elisabeth Marcos Léa Payen Jacqueline Marvel Romain Parent Serge Adnot Philippe Bertolino Jennifer Rieusset Antonin Tortereau David Vindrieux David Bernard 《Aging cell》2023,22(11):e13971
Cellular senescence is induced by many stresses including telomere shortening, DNA damage, oxidative, or metabolic stresses. Senescent cells are stably cell cycle arrested and they secrete many factors including cytokines and chemokines. Accumulation of senescent cells promotes many age-related alterations and diseases. In this study, we investigated the role of the pro-senescent phospholipase A2 receptor 1 (PLA2R1) in regulating some age-related alterations in old mice and in mice subjected to a Western diet, whereas aged wild-type mice displayed a decreased ability to regulate their glycemia during glucose and insulin tolerance tests, aged Pla2r1 knockout (KO) mice efficiently regulated their glycemia and displayed fewer signs of aging. Loss of Pla2r1 was also found protective against the deleterious effects of a Western diet. Moreover, these Pla2r1 KO mice were partially protected from diet-induced senescent cell accumulation, steatosis, and fibrosis. Together these results support that Pla2r1 drives several age-related alterations, especially in the liver, arising during aging or through a Western diet. 相似文献
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506.
Discordance between morphological and taxonomic diversity: land snails of oceanic archipelagos
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Kostas A. Triantis Christine E. Parent Robert A. D. Cameron Bernd Lenzner Aristeidis Parmakelis Norine W. Yeung María R. Alonso Miguel Ibáñez António M. de Frias Martins Dinarte N. F. Teixeira Owen L. Griffiths Yurena Yanes Kenneth A. Hayes Richard C. Preece Robert H. Cowie 《Journal of Biogeography》2016,43(10):2050-2061
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Prenatal diagnosis: The authors present a personal case of triose-phosphate-isomerase deficiency. Clinically the deficiency associates a constitutional non spherocytic anemia, paroxystic and precocius, and neuromuscular symptoms (axial hypotonia and limb palsies). A diaphragmatic paralysis may complicate the syndrome. Infections are frequent. Survival rarely goes beyond 5 years of age. Biochemical exams show the ubiquity of the deficiency. The physiopathology remains obscure. The TPI deficiency is heritable (autosomal recessive transmission). The gene has been mapped on the short arm of the chromosome 12. Prenatal diagnosis is possible. 相似文献
509.
The 5-methylcytosine (5mC) modification regulates multiple cellular processes and is faithfully maintained following DNA replication. In addition to DNA methyltransferase (DNMT) family proteins, ubiquitin-like PHD and ring finger domain-containing protein 1 (UHRF1) plays an important role in the maintenance of 5mC levels. Loss of UHRF1 abolishes 5mC in cells and leads to embryonic lethality in mice. Interestingly, UHRF1 has a paralog, UHRF2, that has similar sequence and domain architecture, but its biologic function is not clear. Here, we have generated Uhrf2 knockout mice and characterized the role of UHRF2 in vivo. Uhrf2 knockout mice are viable, but the adult mice develop frequent spontaneous seizures and display abnormal electrical activities in brain. Despite no global DNA methylation changes, 5mC levels are decreased at certain genomic loci in the brains of Uhrf2 knockout mice. Therefore, our study has revealed a unique role of UHRF2 in the maintenance of local 5mC levels in brain that is distinct from that of its paralog UHRF1. 相似文献
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