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1.
Summary Amo 1618 inhibits germination and root growth of Lentil seedlings in the dark and in the light, with some symptoms of toxicity; CCC has no effect.Both CCC and Amo 1618 inhibit the catalase activity of a lentil root extract.Increasing concentrations of Amo 1618 progressively increase the activity of peroxidase and IAA-oxidase in vivo; the catalase activity remains unchanged.The effect of Amo 1618 on root growth can thus be explained by a diminished auxin level mediated by an increased auxin catabolism.The effect of Amo 1618 and that of kinetin on root growth and enzymes are parallet. Gibberellic acid has an opposite effect on auxin catabolism.
Une partie de ce travail a fait l'objet du mémoire de Licence de J. L. et a été réalisée au Laboratoire de Biochimie végétale de l'Institut de Botanique de Liège. 相似文献
Une partie de ce travail a fait l'objet du mémoire de Licence de J. L. et a été réalisée au Laboratoire de Biochimie végétale de l'Institut de Botanique de Liège. 相似文献
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Hybrids were generated between mouse hepatoma cells which exhibit a transformed phenotype, and rat normal diploid fibroblasts. Most isolated hybrid clones contain a single set of chromosomes from each parent. Such clones grow to low saturation densities and are unable to grow or to form colonies in soft agar. The transformed phenotype of the parental hepatoma cells is thus suppressed in these hybrids. Suppression is very stable; however, subclones which have regained a transformed phenotype could be selected; these subclones show a significant reduction of their chromosome number. Amongst the hybrid clones isolated after fusion, a few are characterized by an excess of mouse chromosomes and a reduced number of rat chromosomes. Such clones exhibit a transformed phenotype. Our results show that, provided the hybrids contain an almost complete single set of chromosomes of each parent, spontaneous transformation behaves as a recessive trait in hybrids formed with normal diploid cells. 相似文献
4.
Martin Gael Oyono Sebastien Kenmoe Ngu Njei Abanda Guy Roussel Takuissu Jean Thierry Ebogo-Belobo Raoul Kenfack-Momo Cyprien Kengne-Nde Donatien Serge Mbaga Serges Tchatchouang Josiane Kenfack-Zanguim Robertine Lontuo Fogang Elisabeth Zeukoo Menkem Juliette Laure Ndzie Ondigui Ginette Irma Kame-Ngasse Jeannette Nina Magoudjou-Pekam Arnol Bowo-Ngandji Seraphine Nkie Esemu Lucy Ndip 《PLoS neglected tropical diseases》2022,16(7)
Yellow fever (YF) has re-emerged in the last two decades causing several outbreaks in endemic countries and spreading to new receptive regions. This changing epidemiology of YF creates new challenges for global public health efforts. Yellow fever is caused by the yellow fever virus (YFV) that circulates between humans, the mosquito vector, and non-human primates (NHP). In this systematic review and meta-analysis, we review and analyse data on the case fatality rate (CFR) and prevalence of YFV in humans, and on the prevalence of YFV in arthropods, and NHP in sub-Saharan Africa (SSA). We performed a comprehensive literature search in PubMed, Web of Science, African Journal Online, and African Index Medicus databases. We included studies reporting data on the CFR and/or prevalence of YFV. Extracted data was verified and analysed using the random effect meta-analysis. We conducted subgroup, sensitivity analysis, and publication bias analyses using the random effect meta-analysis while I2 statistic was employed to determine heterogeneity. This review was registered with PROSPERO under the identification CRD42021242444. The final meta-analysis included 55 studies. The overall case fatality rate due to YFV was 31.1% (18.3–45.4) in humans and pooled prevalence of YFV infection was 9.4% (6.9–12.2) in humans. Only five studies in West and East Africa detected the YFV in mosquito species of the genus Aedes and in Anopheles funestus. In NHP, YFV antibodies were found only in members of the Cercopithecidae family. Our analysis provides evidence on the ongoing circulation of the YFV in humans, Aedes mosquitoes and NHP in SSA. These observations highlight the ongoing transmission of the YFV and its potential to cause large outbreaks in SSA. As such, strategies such as those proposed by the WHO’s Eliminate Yellow Fever Epidemics (EYE) initiative are urgently needed to control and prevent yellow fever outbreaks in SSA. 相似文献
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Fragile X related protein 1 isoforms differentially modulate the affinity of fragile X mental retardation protein for G-quartet RNA structure 总被引:2,自引:2,他引:2
Bechara E Davidovic L Melko M Bensaid M Tremblay S Grosgeorge J Khandjian EW Lalli E Bardoni B 《Nucleic acids research》2007,35(1):299-306
Fragile X syndrome, the most frequent form of inherited mental retardation, is due to the absence of expression of the Fragile X Mental Retardation Protein (FMRP), an RNA binding protein with high specificity for G-quartet RNA structure. FMRP is involved in several steps of mRNA metabolism: nucleocytoplasmic trafficking, translational control and transport along dendrites in neurons. Fragile X Related Protein 1 (FXR1P), a homologue and interactor of FMRP, has been postulated to have a function similar to FMRP, leading to the hypothesis that it can compensate for the absence of FMRP in Fragile X patients. Here we analyze the ability of three isoforms of FXR1P, expressed in different tissues, to bind G-quartet RNA structure specifically. Only the longest FXR1P isoform was found to be able to bind specifically the G-quartet RNA, albeit with a lower affinity as compared to FMRP, whereas the other two isoforms negatively regulate the affinity of FMRP for G-quartet RNA. This result is important to decipher the molecular basis of fragile X syndrome, through the understanding of FMRP action in the context of its multimolecular complex in different tissues. In addition, we show that the action of FXR1P is synergistic rather than compensatory for FMRP function. 相似文献
7.
Ana Paula Kallaur Josiane Lopes Sayonara Rangel Oliveira Andrea Name Colado Simão Edna Maria Vissoci Reiche Elaine Regina Delicato de Almeida Helena Kaminami Morimoto Wildea Lice Carvalho Jennings de Pereira Daniele Frizon Alfieri Sueli Donizete Borelli Domacio Ramon Kaimen-Maciel Michael Maes 《Molecular neurobiology》2016,53(8):5191-5202
8.
Marie J. Richard Veronique Ducros Michel Rorêt Josiane Arnaud Charles Coudray Michèle Fusselier Alain Favier 《Biological trace element research》1993,39(2-3):149-159
In six chronic dialyzed uremic patients, an intravenous sodium selenite (Se 50 μg during 5 wk and then 100 μg) and zinc gluconate
(Zn 5 mg) supplementation was performed during 20 wk at each dialysis session three times weekly. Before supplementation,
plasma Se and Zn, plasma and erythrocytes (RBC) antioxidant metalloenzymes glutathione peroxidase (GPX), and superoxide dismutase
(SOD) were significantly decreased, whereas lipid peroxidation (as thiobarbituric acid reactants TBARs) was increased. To
obtain a significative change in plasma selenium, we had to use an Se dose of 100 μg/dialysis session. Then, treatment-increased
plasma Se (from 0.58 ±0.09 to 0.89±0.16 μmol/L) led to a repletion of RBC-GPX (from 29.6±6 to 43±5.8 U/g Hb) and increased
plasma GPX levels (from 62±13 to 151±43 U/L). Plasma Zn and RBC-SOD did not vary significantly. The change of TBARs was not
observed between wk 1 and 4. They decreased significantly between wk 4 (4.80±0.21μmol/L) and wk 20 (4.16±0.26 μmol/L). We
noted a low correlation between TBARs and plasma GPX. A strong correlation was observed between Se and plasma GPX. The reversal
of Se deficiencies should reduce oxidative damage observed in these patients. 相似文献
9.
Sophie Creuzet Laurent Lescaudron Zhenlin Li Josiane Fontaine-Pérus 《Experimental cell research》1998,243(2):241
Although satellite cell differentiation is involved in postnatal myogenesis from growth to posttrauma regeneration, the early stages of this process remain unclear. This study investigatedpHuDes-nls-lacZtransgene activity, as revealed by X-gal staining and the accumulation of MyoD, myogenin, endogenous desmin, and myosin, in order to determine whether satellite cells share the same activation program during growth and regeneration. After birth, skeletal myonuclei in which myogenin expression was limited were briefly characterized by transgene activity. Satellite cells were only evidenced by MyoD and slow myosin accumulation, but failed to initiate transgene expression. After freeze trauma, satellite cell activation led to MyoD, myogenin, and desmin expression. Subsequently, when myosin expression occurred, transgene activation was apparent in regenerating structures, with more intense X-gal staining in mononucleated cells than regenerating myotubes. After the second week posttrauma, only desmin and myogenin expression were maintained in regenerating structures. In culture, the behavior of satellite cells showed that desmin expression was committed before transgene activation occurred, i.e., concurrently with MyoD, myogenin, myosin expression, and the first fusion events. Quantitative analysis confirmed the discrepancy between endogenous desmin and transgene expression and demonstrated the close correlation between transgene activation and the fusion index. Our results strongly suggest that satellite cells promote distinct pathways of myogenic response during growth and regeneration. 相似文献
10.
Hafida Merzouk Sihem Madani Aziz Hichami Josiane Prost Jacques Belleville Naim A. Khan 《Obesity (Silver Spring, Md.)》2002,10(7):703-714
Objective: The long‐term effects of fetal hyperinsulinemia, time course of changes in liver and very‐low‐density lipoprotein (VLDL) lipid levels and fatty acid compositions were investigated in obese offspring of streptozotocin‐induced mildly diabetic rats. Research Methods and Procedures: Mild hyperglycemia in pregnant rats was induced by intraperitoneal injection of streptozotocin on day 5 of gestation. Control pregnant rats were injected with citrate buffer. Liver and VLDL lipids and fatty acids were analyzed in offspring at different ages. Results: At birth, obese pups had higher VLDL triglyceride levels, saturated fatty acids, and C20:4n‐6. They also had lower C18:2n‐6 proportions in VLDL triglycerides, phospholipids, and cholesteryl esters than controls pups. In 1‐month‐old male and female obese rats, VLDL and liver lipid amounts were similar to those in their respective controls; however, high levels of C18:2n‐6 and C20:4n‐6 were noted in liver and VLDL lipids. At the age of 2 months, liver and VLDL triglyceride levels were higher in obese females than in control females. Fatty acid abnormalities seen in obese rats included low C18:3n‐3 and high C22:6n‐3 proportions in liver triglycerides and phospholipids. At the age of 3 months, obese rats, both males and females, compared with control animals, had higher VLDL and hepatic lipids with reduced C20:4n‐6 levels and polyunsaturated/saturated fatty acids ratios in hepatic and VLDL triglycerides and phospholipids. Discussion: Fetal obesity, associated with alterations in VLDL lipid fatty acid composition, represents an important risk factor for adult obesity and diabetes. 相似文献