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71.
Julie M. Beaudet Leandra Mansur Eun Ji Joo Eyal Kamhi Bo Yang Thomas M. Clausen Ali Salanti Fuming Zhang Robert J. Linhardt 《Glycoconjugate journal》2014,31(2):109-116
Placental malaria is a serious problem in sub-Saharan Africa. Young women are particular susceptible to contracting this form of malaria during their first or second pregnancy despite previously acquired immunity from past infections. Placental malaria is caused by Plasmodium falciparum parasites expressing VAR2CSA on the erythrocyte surface. This protein adheres to a low-sulfated chondroitin sulfate-A found in placental tissue causing great harm to both mother and developing fetus. In rare cases, the localization of infected erythrocytes to the placenta can even result in the vertical transmission of malaria. In an effort to better understand this infection, chondroitin sulfate was isolated from the cotyledon part of the placenta, which should be accessible for parasite adhesion, as well as two non-accessible parts of the placenta to serve as controls. The placental chondroitin sulfate structures and their VAR2CSA binding were characterized. All portions of human placenta contained sufficient amounts of the appropriate low-sulfated chondroitin sulfate-A to display high-affinity binding to a recombinant truncated VAR2CSA construct, as determined using surface plasmon resonance. The cotyledon is the only placental tissue accessible to parasites in the bloodstream, suggesting it is the primary receptor for parasite infected red blood cells. 相似文献
72.
Chari Nithya Mansur Farzana Begum Shunmugiah Karutha Pandian 《Applied microbiology and biotechnology》2010,88(1):341-358
According to the Centers for Disease Control and Prevention, biofilms cause 65% of infections in developed countries. Pseudomonas aeruginosa biofilm cause life threatening infections in cystic fibrosis infection and they are 1,000 times more tolerant to antibiotic
than the planktonic cells. As quorum sensing, hydrophobicity index and extracellular polysaccharide play a crucial role in
biofilm formation, extracts from 46 marine bacterial isolates were screened against these factors in P. aeruginosa. Eleven extracts showed antibiofilm activity. Extracts of S6-01 (Bacillus indicus = MTCC 5559) and S6-15 (Bacillus pumilus = MTCC 5560) inhibited the formation of PAO1 biofilm up to 95% in their Biofilm Inhibitory Concentration(BIC) of 50 and 60 μg/ml
and 85% and 64% in the subinhibitory concentrations (1/4 and 1/8 of the BIC, respectively). Furthermore, the mature biofilm
was disrupted to 70–74% in their BIC. The antibiofilm compound from S6-15 was partially purified using solvent extraction
followed by TLC and silica column and further characterized by IR analysis. Current study for the first time reveals the antibiofilm
and antiquorum-sensing activity of B. pumilus, B. indicus, Bacillus arsenicus, Halobacillus trueperi, Ferrimonas balearica, and Marinobacter hydrocarbonoclasticus from marine habitat. 相似文献
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75.
Claudia Simões Tatiana Carvalho de Castro Lívia da Silva Cordeiro Norma Albarello Elisabeth Mansur Maria Teresa Villela Romanos 《World journal of microbiology & biotechnology》2010,26(1):93-99
Extracts from Cleome rosea were investigated for their activity against acyclovir-resistant strains of Herpes simplex type 1 (ACVr-HSV-1) and type 2 (ACVr-HSV-2). Methanolic and acidified (1% (v/v) HCl) methanolic extracts were prepared from
field-grown plants and in vitro propagated plants, as well as from calli and cell suspension cultures. The extracts presented
low cytotoxicity and caused virus titer reduction above 70%, with different mechanisms of action. Extracts from leaves of
field-grown plants inhibited viral infection mainly by affecting the virus particle itself (virucidal effect), while extracts
from calli acted mainly on cell receptors. On the other hand, all extracts evaluated affected the virus entry across the cell
membrane and the intracellular viral replication at similar percentages, causing reduction on titers in the range of 68–90%.
This study validated the potential use of in vitro materials as sources of antiherpetic agents from C. rosea. 相似文献
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77.
J. S. Lakind S. T. Holgate D. R. Ownby A. H. Mansur P. J. Helms D. Pyatt S. M. Hays 《Biomarkers》2007,12(5):445-467
Biomarkers associated with asthma aetiology and exacerbation have been sought to shed light on this multifactorial disease. One candidate is the serum concentration of the Clara cell secretory protein (CC16, sometimes referred to as CC10 or uteroglobin). In this review, we examine serum CC16's relation to asthma aetiology and exacerbation. There is evidence that acute exposures to certain pulmonary irritants can cause a transient increase in serum CC16 levels, and limited evidence also suggests that a transient increase in serum CC16 levels can be caused by a localized pulmonary inflammation. Research also indicates that a transient increase in serum CC16 is not associated with measurable pulmonary damage or impairment of pulmonary function. The biological interpretation of chronic changes in serum CC16 is less clear. Changes in serum CC16 concentrations (either transient or chronic) are not specific to any one agent, disease state, or aetiology. This lack of specificity limits the use of serum CC16 as a biomarker of specific exposures. To date, many of the critical issues that must be understood before serum CC16 levels can have an application as a biomarker of effect or exposure have not been adequately addressed. 相似文献
78.
Boeger Walter A.; Pie Marcio R.; Falleiros Renan M.; Ostrensky Antonio; Darrigran Gustavo; Mansur Maria Cristina Dreher; Belz Carlos E. 《Journal of plankton research》2007,29(11):1015-1019
The golden mussel (Limnoperna fortunei, Mollusca: Mytilidae)is an emerging invasive species in freshwater environments inSouth America, causing extensive environmental and economicimpacts. A molecular method to detect larvae of the golden musselin plankton samples has been recently developed and holds promisefor becoming an important way to monitor the expansion of goldenmussel populations. In the present study, we conduct, for thefirst time, field tests of this method by comparing its performancewith alternative sampling efforts (microscopy and manual searchfor adults). In addition, we test different modifications ofthe molecular method to deal with PCR inhibition in environmentalsamples. The results indicate that the molecular method is veryefficient, being faster and more sensitive that microscopy methods.Therefore, the molecular method tested in the present studycan represent an invaluable tool in large-scale monitoring effortsof the golden mussel throughout its introduced range. 相似文献
79.
Unterholzner L Sumner RP Baran M Ren H Mansur DS Bourke NM Randow F Smith GL Bowie AG 《PLoS pathogens》2011,7(9):e1002247
Recognition of viruses by pattern recognition receptors (PRRs) causes interferon-β (IFN-β) induction, a key event in the anti-viral innate immune response, and also a target of viral immune evasion. Here the vaccinia virus (VACV) protein C6 is identified as an inhibitor of PRR-induced IFN-β expression by a functional screen of select VACV open reading frames expressed individually in mammalian cells. C6 is a member of a family of Bcl-2-like poxvirus proteins, many of which have been shown to inhibit innate immune signalling pathways. PRRs activate both NF-κB and IFN regulatory factors (IRFs) to activate the IFN-β promoter induction. Data presented here show that C6 inhibits IRF3 activation and translocation into the nucleus, but does not inhibit NF-κB activation. C6 inhibits IRF3 and IRF7 activation downstream of the kinases TANK binding kinase 1 (TBK1) and IκB kinase-ε (IKKε), which phosphorylate and activate these IRFs. However, C6 does not inhibit TBK1- and IKKε-independent IRF7 activation or the induction of promoters by constitutively active forms of IRF3 or IRF7, indicating that C6 acts at the level of the TBK1/IKKε complex. Consistent with this notion, C6 immunoprecipitated with the TBK1 complex scaffold proteins TANK, SINTBAD and NAP1. C6 is expressed early during infection and is present in both nucleus and cytoplasm. Mutant viruses in which the C6L gene is deleted, or mutated so that the C6 protein is not expressed, replicated normally in cell culture but were attenuated in two in vivo models of infection compared to wild type and revertant controls. Thus C6 contributes to VACV virulence and might do so via the inhibition of PRR-induced activation of IRF3 and IRF7. 相似文献