全文获取类型
收费全文 | 315篇 |
免费 | 19篇 |
出版年
2021年 | 2篇 |
2020年 | 3篇 |
2019年 | 2篇 |
2018年 | 8篇 |
2016年 | 6篇 |
2015年 | 12篇 |
2014年 | 10篇 |
2013年 | 17篇 |
2012年 | 14篇 |
2011年 | 18篇 |
2010年 | 5篇 |
2009年 | 6篇 |
2008年 | 17篇 |
2007年 | 18篇 |
2006年 | 6篇 |
2005年 | 9篇 |
2004年 | 12篇 |
2003年 | 11篇 |
2002年 | 13篇 |
2001年 | 5篇 |
2000年 | 10篇 |
1999年 | 11篇 |
1998年 | 2篇 |
1995年 | 4篇 |
1994年 | 5篇 |
1993年 | 4篇 |
1991年 | 6篇 |
1990年 | 10篇 |
1989年 | 2篇 |
1988年 | 6篇 |
1987年 | 14篇 |
1986年 | 9篇 |
1985年 | 6篇 |
1984年 | 11篇 |
1983年 | 7篇 |
1982年 | 1篇 |
1981年 | 1篇 |
1980年 | 1篇 |
1979年 | 1篇 |
1978年 | 1篇 |
1977年 | 2篇 |
1975年 | 1篇 |
1974年 | 2篇 |
1973年 | 2篇 |
1971年 | 5篇 |
1970年 | 1篇 |
1969年 | 1篇 |
1968年 | 2篇 |
1967年 | 4篇 |
1966年 | 5篇 |
排序方式: 共有334条查询结果,搜索用时 125 毫秒
121.
Tal Dagan Jan Riedel Pradipta Mandal Eva R. Pesce Gregory L. Blatch Brendan S. Crabb Paul R. Gilson Jude M. Przyborski 《Cellular microbiology》2012,14(11):1784-1795
Malaria parasites modify their host cell, the mature human erythrocyte. We are interested in the molecules mediating these processes, and have recently described a family of parasite‐encoded heat shock proteins (PfHsp40s) that are targeted to the host cell, and implicated in host cell modification. Hsp40s generally function as co‐chaperones of members of the Hsp70 family, and until now it was thought that human Hsp70 acts as the PfHsp40 interaction partner within the host cell. Here we revise this hypothesis, and identify and characterize an exported parasite‐encoded Hsp70, referred to as PfHsp70‐x. PfHsp70‐x is exported to the host erythrocyte where it forms a complex with PfHsp40s in structures known as J‐dots, and is closely associated with PfEMP1. Interestingly, Hsp70‐x is encoded only by parasite species that export the major virulence factor EMP1, implying a possible role for Hsp70‐x in EMP1 presentation at the surface of the infected erythrocyte. Our data strongly support the presence of parasite‐encoded chaperone/co‐chaperone complexes within the host erythrocyte, which are involved in protein traffic through the host cell. The host–pathogen interaction within the infected erythrocyte is more complex than previously thought, and is driven notonly by parasite co‐chaperones, but also by the parasite‐encoded chaperone Hsp70‐x itself. 相似文献
122.
123.
Salter MD Nienhaus K Nienhaus GU Dewilde S Moens L Pesce A Nardini M Bolognesi M Olson JS 《The Journal of biological chemistry》2008,283(51):35689-35702
The major pathway for O2 binding to mammalian myoglobins (Mb) and hemoglobins (Hb) involves transient upward movement of the distal histidine (His-64(E7)), allowing ligand capture in the distal pocket. The mini-globin from Cerebratulus lacteus (CerHb) appears to have an alternative pathway between the E and H helices that is made accessible by loss of the N-terminal A helix. To test this pathway, we examined the effects of changing the size of the E7 gate and closing the end of the apolar channel in CerHb by site-directed mutagenesis. Increasing the size of Gln-44(E7) from Ala to Trp causes variation of association (k'O2) and dissociation (kO2) rate coefficients, but the changes are not systematic. More significantly, the fractions (Fgem approximately 0.05-0.19) and rates (kgem approximately 50-100 micros(-1)) of geminate CO recombination in the Gln-44(E7) mutants are all similar. In contrast, blocking the entrance to the apolar channel by increasing the size of Ala-55(E18) to Phe and Trp causes the following: 1) both k'O2 and kO2 to decrease roughly 4-fold; 2) Fgem for CO to increase from approximately 0.05 to 0.45; and 3) kgem to decrease from approximately 80 to approximately 9 micros(-1), as ligands become trapped in the channel. Crystal structures and low temperature Fourier-transform infrared spectra of Phe-55 and Trp-55 CerHb confirm that the aromatic side chains block the channel entrance, with little effect on the distal pocket. These results provide unambiguous experimental proof that diatomic ligands can enter and exit a globin through an interior channel in preference to the more direct E7 pathway. 相似文献
124.
Lezza AM Fallacara FP Pesce V Leeuwenburgh C Cantatore P Gadaleta MN 《Neurochemical research》2008,33(12):2609-2614
According to the “mitochondrial theory of aging” the lifelong accumulation of various kinds of damage to mitochondrial DNA
(mtDNA) has been related to the age-dependent mitochondrial bioenergetic dysfunction. Caloric restriction (CR) diet is able
to prevent or delay the onset of several age-related damages to mtDNA. The effects of aging and CR on the presence of abasic
sites and single-strand breaks of the sugar–phosphate backbone in mtDNA have been analyzed by applying Ligation Mediated-PCR
to a H strand region of brain mtDNA from young and old ad libitum-fed and old CR-treated rats. The region, encompassing the
Direct Repeat 1 of the 4,834 bp-long deletion, is highly damaged in the old ad libitum-fed animals with respect to the young
ones, whereas in the CR rats it shows a much lower extent of damage. The data confirm, at single nucleotide resolution, the
protective effect of CR on the age-related mtDNA damage.
Special issue article in honor of Dr. Anna Maria Giuffrida-Stella. 相似文献
125.
Moriggi M Cassano P Vasso M Capitanio D Fania C Musicco C Pesce V Gadaleta MN Gelfi C 《Proteomics》2008,8(17):3588-3604
After hind limb suspension, a remodeling of postural muscle phenotype is observed. This remodeling results in a shift of muscle profile from slow-oxidative to fast-glycolytic. These metabolic changes and fiber type shift increase muscle fatigability. Acetyl-L-carnitine (ALCAR) influences the skeletal muscle phenotype of soleus muscle suggesting a positive role of dietary supplementation of ALCAR during unloading. In the present study, we applied a 2-D DIGE, mass spectrometry and biochemical assays, to assess qualitative and quantitative differences in the proteome of rat slow-twitch soleus muscle subjected to disuse. Meanwhile, the effects of ALCAR administration on muscle proteomic profile in both unloading and normal-loading conditions were evaluated. The results indicate a modulation of troponin I and tropomyosin complex to regulate fiber type transition. Associated, or induced, metabolic changes with an increment of glycolytic enzymes and a decreased capacity of fat oxidation are observed. These metabolic changes appear to be counteracted by ALCAR treatment, which restores the mitochondrial mass and decreases the glycolytic enzyme expression, suggesting a normalization of the metabolic shift observed in unloaded animals. This normalization is accompanied by a maintenance of body weight and seems to prevent a switch of fiber type. 相似文献
126.
De Flora S D'Agostini F Balansky R Camoirano A Cartiglia C Longobardi M Travaini G Steele VE Pesce C Izzotti A 《Mutation research》2008,659(1-2):137-146
Our recent studies have shown that both cigarette smoke and UV-containing light, which are the most widespread and ubiquitous mutagens and carcinogens in the world, cause systemic genotoxic damage in hairless mice. Further studies were designed with the aim of evaluating the induction of genotoxic and carcinogenic effects in Swiss albino mice exposed to smoke and/or light since birth. We observed that a 4-month whole-body exposure of mice to mainstream cigarette smoke, starting at birth, caused an early and potent carcinogenic response in the lung and other organs. Our further experiments showed that exposure of mice to environmental cigarette smoke, during the first 5 weeks of life, resulted in a variety of significant alterations of intermediate biomarkers, including cytogenetic damage in bone marrow and peripheral blood, formation of lipid peroxidation products, increase of bulky DNA adduct levels, induction of oxidative DNA damage, and overexpression of OGG1 gene in lung, stimulation of apoptosis, hyperproliferation and loss of Fhit protein in pulmonary alveolar macrophages and/or bronchial epithelial cells, and early histopathological alterations in the respiratory tract. Moreover, exposure of mice to UV-containing light, mimicking solar irradiation, significantly enhanced oxidative DNA damage and bulky DNA adduct levels in lung, and synergized with smoke in inducing molecular alterations in the respiratory tract. The baseline OGG1 expression in lung was particularly high at birth and decreased in post-weanling mice. Oxidative DNA damage and other investigated end-points exhibited differential patterns in post-weanling mice and adult mice. The findings of these studies provide a mechanistic clue to the general concept that the neonatal period and early stages of life are critical in affecting susceptibility to carcinogens. 相似文献
127.
Characterization of a Bacteriocin-Like Substance Produced by a Vaginal Lactobacillus salivarius Strain 总被引:7,自引:0,他引:7 下载免费PDF全文
Virginia S. Ocaa Aída A. Pesce de Ruiz Holgado María Elena Nader-Macías 《Applied microbiology》1999,65(12):5631-5635
A novel bacteriocin-like substance produced by vaginal Lactobacillus salivarius subsp. salivarius CRL 1328 with activity against Enterococcus faecalis, Enterococcus faecium, and Neisseria gonorrhoeae was characterized. The highest level of production of this heat-resistant peptide or protein occurred during the late exponential phase. Its mode of action was shown to be bactericidal. L. salivarius subsp. salivarius CRL 1328 could be used for the design of a probiotic to prevent urogenital infections. 相似文献
128.
129.
130.
Martha S. Núñez de Kairúz Guillermo Oliver Aída A. Pesce de Ruiz Holgado Ricardo N. Farías 《Current microbiology》1983,9(2):105-109
The effect of saturated fatty acids from 6∶0 to 16∶0 and oleic acid onLactobacillus leichmanii ATCC 4797 growing in non-skim-milk media was determined. The inhibition by lauric acid was higher than that obtained with any other fatty acid. A mutant (MC12) resistant to the fatty acid inhibition with high β-oxidation activity was also studied. A positive correlation between the ability ofL. leichmanii ATCC 4797 and its derivative MC12 to degrade fatty acids and their resistance to the fatty acid inhibition is shown in this report. 相似文献