Relative Resistance (relative + resistance)

Distribution by Scientific Domains


Selected Abstracts


Relative resistance of Pacific salmon to infectious salmon anaemia virus

JOURNAL OF FISH DISEASES, Issue 9 2003
J B Rolland
Abstract Infectious salmon anaemia (ISA) is a major disease of Atlantic salmon, Salmo salar, caused by an orthomyxovirus (ISAV). Increases in global aquaculture and the international movement of fish made it important to determine if Pacific salmon are at risk. Steelhead trout, Oncorhynchus mykiss, and chum, O. keta, Chinook, O. tshawytscha, coho, O. kisutch, and Atlantic salmon were injected intraperitoneally with a high, medium, or low dose of a Norwegian strain of ISAV. In a second challenge, the same species, except chum salmon, were injected with a high dose of either a Canadian or the Norwegian strain. Average cumulative mortality of Atlantic salmon in trial 1 was 12% in the high dose group, 20% in the medium dose group and 16% in the low dose group. The average cumulative mortality of Atlantic salmon in trial 2 was 98%. No signs typical of ISA and no ISAV-related mortality occurred among any of the groups of Oncorhynchus spp. in either experiment, although ISAV was reisolated from some fish sampled at intervals post-challenge. The results indicate that while Oncorhynchus spp. are quite resistant to ISAV relative to Atlantic salmon, the potential for ISAV to adapt to Oncorhynchus spp. should not be ignored. [source]


Correlation between the high expression of C/EBP, protein in F442A cells and their relative resistance to antiadipogenic action of TCDD in comparison to 3T3-L1 cells

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 2 2002
Phillip C. C. Liu
Abstract We compared the ability of two clonally derived murine preadipocyte cell lines, 3T3-L1(L1) and 3T3-F442A (F442A), to differentiate after treatment by 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), and found that the former cell line was clearly suppressed by TCDD but the latter was not. It was initially postulated that the easiest way to explain the lack of response to TCDD in F442A cells could be an alteration in aryl hydrocarbon receptor (AhR) functionality. This hypothesis was tested first, but no differences were found in the levels or functions of AhR. To find an alternate explanation for such a differential effect of TCDD, we tested the action of several diagnostic agents on the process of adipocyte differentiation of these two cells. No differences were found between these two lines of cells in the susceptibility to the antiadipogenic action of 12-0-tetradecanoylphorbol-13-acetate (TPA), or to TNF,, indicating that the basic biochemical components engaged in the antiadipogenic actions of these agents in these two cell lines are similar. In contrast, F442A cells were found to be more resistant to the antiadipogenic action of EGF or TGF, than L1 cells which were tested side by side. Based on the knowledge that TNF, preferentially affects C/EBP, and that TGF, specifically controls C/EBP, and , in their antiadipogenic action, we hypothesized that the major cause for the differential response of these two similar cell lines could be the insensitivity of C/EBP, and/or , of F442A cells to the action of TCDD. We could obtain supporting data for this hypothesis, showing that in F442A cells, the level of C/EBP, is already high even before the addition of adipocyte differentiation factors and that TCDD did not cause any significant changes in the titer of C/EBP,. © 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol 16:70,83, 2002; Published online in Wiley Interscience (www.interscience.wiley.com). DOI 10.1002/jbt.10020 [source]


Use of a Mini-Dome Bioassay and Grafting to Study Resistance of Chickpea to Ascochyta Blight

JOURNAL OF PHYTOPATHOLOGY, Issue 10 2005
W. Chen
Abstract A mini-dome bioassay was developed to study pathogenicity of Ascochyta rabiei and relative resistance of chickpea (Cicer arietanium). It was determined that the best condition for assaying pathogenicity of A. rabiei was to use 2 × 105 spores/ml as inoculum and to maintain a leaf wetness period of 24 h under mini-domes at a temperature between 16 and 22°C. This mini-dome pathogenicity assay was used to determine relative resistance of six chickpea cultivars (cvs) to isolates of two pathotypes of A. rabiei. Grafting was employed to detect any translocated factors produced in the chickpea plant that mediate disease response, which could help elucidate possible resistance mechanisms to Ascochyta blight. The six chickpea cv. were grafted in all possible scion,rootstock combinations, and then inoculated with isolates of two pathotypes of A. rabiei using the mini-dome technique. Results showed that self-grafted-resistant plants remained resistant and self-grafted-susceptible plants stayed susceptible, indicating the grafting procedure did not alter host response to infection by A. rabiei. Susceptible scions always exhibited high and similar levels of disease severity regardless of rootstock genotypes, and resistant scions always showed low and similar levels of disease severity when they were grafted onto any of the six rootstock genotypes. Orthogonal contrasts showed that scion genotypes determined disease phenotype, and that rootstock genotypes had no contribution to disease phenotype of the scions. The pathogenicity assay did not detect any translocated disease-mediating agents responsible for susceptibility or resistance in chickpea. Disease phenotypes of Ascochyta blight of chickpea were conditioned locally by scion genotypes. [source]


Identification of a gene (lpt-3) required for the addition of phosphoethanolamine to the lipopolysaccharide inner core of Neisseria meningitidis and its role in mediating susceptibility to bactericidal killing and opsonophagocytosis

MOLECULAR MICROBIOLOGY, Issue 4 2002
Fiona G. Mackinnon
Summary We have identified a gene, lpt-3, that is required for the addition of phosphoethanolamine to the 3-position (PEtn-3) on the , -chain heptose (HepII) of the inner core lipopolysaccharide (LPS) of Neisseria meningitidis (Nm). The presence of this PEtn-3 substituent is characteristic of the LPS of a majority (, 70%) of hypervirulent Nm strains, irrespective of capsular serogroup, and is required for the binding of a previously described monoclonal antibody (mAb B5) to a surface-accessible epitope. All strains of Nm that have PEtn-3 possess the lpt-3 gene. In some lpt-3 -containing strains, the 3-position on HepII is preferentially substituted by glucose instead of PEtn, the result of lgtG phase variation mediated by slippage of a homopolymeric tract of cytidines. Inactivation of lpt-3 resulted in loss of PEtn-3, lack of reactivity with mAb B5 and conferred relative resistance to bactericidal killing and opsonophagocytosis by mAb B5 in vitro. Thus, the identification of lpt-3 has facilitated rigorous genetic, structural and immunobiological definition of an immunodominant epitope that is a candidate immunogen for inclusion in an LPS-based vaccine to protect against invasive meningococcal disease. [source]


Association Between the Photodynamic Loss of Bcl-2 and the Sensitivity to Apoptosis Caused by Phthalocyanine Photodynamic Therapy,

PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 1 2003
Jitsuo Usuda
ABSTRACT We have reported that photodynamic therapy (PDT) using the photosensitizer phthalocyanine (Pc) 4 and red light damages the antiapoptotic protein Bcl-2. Recently, using transient transfection of Bcl-2 deletion mutants, we identified the membrane anchorage domains of Bcl-2 as necessary to form the photosensitive target. However, it is not clear how Bcl-2 photodamage sensitizes cells to Pc 4-PDT,induced apoptosis, whether overall cell killing is also sensitized or how upregulation of Bcl-2 in tumors might make them more or less responsive to Pc 4-PDT. In this study we report on MCF-7c3 cells (human breast cancer cells expressing stably transfected procaspase-3) overexpressing wild-type Bcl-2 or certain deletion mutants in either a transient or a stable mode. By flow cytometric analysis of transiently transfected cells, we found that wild-type Bcl-2, Bcl-2,33-54 and Bcl-2,37-63 (each of which can be photodamaged) protected cells from apoptosis caused by Pc 4-PDT. In contrast, Bcl-2,210-239, which lacks the C-terminal transmembrane domain and cannot be photodamaged, afforded no protection. We then evaluated the PDT sensitivity of transfected cell lines stably overexpressing high levels of wild-type Bcl-2 or one of the Bcl-2 mutants. Overexpression of wild-type Bcl-2, Bcl-2,33-54 or Bcl-2,37-63 resulted in relative resistance of cells to Pc 4-PDT, as assessed by morphological apoptosis or loss of clonogenicity. Furthermore, overexpression of Bcl-2 also inhibited the activation-associated conformational change of the proapoptotic protein Bax, and higher doses of Pc 4 and light were required to activate Bax in cells expressing high levels of Bcl-2. Many advanced cancer cells have elevated amounts of Bcl-2. Our results show that increasing the dose of Pc 4-PDT can overcome the resistance afforded by either Bcl-2 or the two mutants. PDT regimens that photodamage Bcl-2 lead to activation of Bax, induction of apoptosis and elimination of the otherwise resistant tumor cells. [source]


Investigation of unsaturated flow in woven, braided and stitched fiber mats during mold-filling in resin transfer molding

POLYMER COMPOSITES, Issue 4 2001
J. Slade
In Resin Transfer Molding (RPM), which is a process to manufacture polymer composites, the impregnation of fibrous reinforcement In the form of mats by a thermosetting resin is modeled as the flow of a Newtonian liquid through a single length-scale porous medium. While this approach is sufficiently accurate for random fiber-mats, it can lead to appreciable errors when applied to woven, braided, or stitched fiber-mats that contain two length scales. This work investigates the primary factors governing the isothermal unsaturated flow through such dual-scale porous media. Two studies were conducted to better understand this phenomenon: the first experimenatally investigated the flow, while the second theoretically modeled the flow and identified important parameters affecting such a flow with the help of dimensionless analysis. In the first study, one-dimensional constant injection rate experiments were performed using various fiber mats. The unsaturated flow behavior of various mats was characterized using a constant "sink" term in the continuity equation. Results indicated that for a given fiber-mat, the magnitude of the sink effect was a function of the capillary number. In the second study, a numerical model was developed to describe flow through dual-scale preforms in which the two flow domains, the inter- and intra-tow regions, were coupled. We identified a dimensionless number called the sink effect index , that characterizes the magnitude of liquid absorption by the tows and is a function of the relative resistance to flow in the tow and inter-tow regions, and the packing density of the tows. The parametric study of this index with the help of numerical simulations reveals its influence on the flow and identifies the distinct transient and steady-state flow regimes. [source]


Enzymatic and structural analysis of the I47A mutation contributing to the reduced susceptibility to HIV protease inhibitor lopinavir

PROTEIN SCIENCE, Issue 9 2008
Klára Grantz, ková
Abstract Lopinavir (LPV) is a second-generation HIV protease inhibitor (PI) designed to overcome resistance development in patients undergoing long-term antiviral therapy. The mutation of isoleucine at position 47 of the HIV protease (PR) to alanine is associated with a high level of resistance to LPV. In this study, we show that recombinant PR containing a single I47A substitution has the inhibition constant (Ki) value for lopinavir by two orders of magnitude higher than for the wild-type PR. The addition of the I47A substitution to the background of a multiply mutated PR species from an AIDS patient showed a three-order-of-magnitude increase in Ki in vitro relative to the patient PR without the I47A mutation. The crystal structure of I47A PR in complex with LPV showed the loss of van der Waals interactions in the S2/S2, subsites. This is caused by the loss of three side-chain methyl groups due to the I47A substitution and by structural changes in the A47 main chain that lead to structural changes in the flap antiparallel ,-strand. Furthermore, we analyzed possible interaction of the I47A mutation with secondary mutations V32I and I54V. We show that both mutations in combination with I47A synergistically increase the relative resistance to LPV in vitro. The crystal structure of the I47A/I54V PR double mutant in complex with LPV shows that the I54V mutation leads to a compaction of the flap, and molecular modeling suggests that the introduction of the I54V mutation indirectly affects the strain of the bound inhibitor in the PR binding cleft. [source]


Selective Neuronal Vulnerability Following Mild Focal Brain Ischemia in the Mouse

BRAIN PATHOLOGY, Issue 4 2003
Juri Katchanov
The evolution of cellular damage over time and the selective vulnerability of different neuronal subtypes was characterized in the striatum following 30-minute middle cerebral artery occlusion and reperfusion in the mouse. Using autoradiography we found an increase in the density of [3H]PK11195 binding sites,likely reflecting microglial activation,in the lesion border at 3 days and in the whole striatum from 10 days to 6 weeks. This was accompanied by a distinct loss of [3H]flumazenil and [3H]CGP39653 binding sites from 10 days up to 6 weeks reflecting neuronal loss. Brain ischemia resulted in a substantial loss of medium spiny projection neurons as seen at three days by Nissl staining, TUNEL and immunocytochemistry using antibodies against microtubule-associated protein (MAP2), NeuN, (,-opioid receptors, substance P, Lenkephalin, neurokinin B, choline acetyltransferase, parvalbumin, calretinin and somatostatin. Both patch and matrix compartments were involved in ischemic damage. In contrast, the numbers of cholinergic, GABAergic, and somatostatin-containing interneurons in the ischemic striatum were not different from those in the contralateral hemisphere at 3 and 14 days. A low density of glutamate receptors, the ability to sequester calcium by calcium-binding proteins and other hitherto unidentified factors may explain this relative resistance of interneurons to acute ischemia. [source]


Genetic variation and susceptibility to infection: the red cell and malaria

BRITISH JOURNAL OF HAEMATOLOGY, Issue 3 2008
D. J. Weatherall
Summary There is now convincing evidence that the extremely high frequencies of certain genetic disorders of the red cell involving haemoglobin, the red-cell membrane, or its metabolic pathways reflect relative resistance to malaria over thousands of years. At least some progress has been made towards an understanding of the cellular mechanisms involved, although much remains to be learnt. As well as the extremely valuable information that this field is providing about how exposure to infection has moulded the current structure of the human genome, recent research in this field is starting to provide some valuable new approaches to the better control of parasitic and other infections that remain a major global health problem. [source]


Dose- and Sex-related Carcinogenesis by N-Bis(2-hydroxypropyl)nitrosamine in Wistar Rats

CANCER SCIENCE, Issue 4 2000
Eduardo L. T. Moreira
An initiation-promotion medium-term bioassay for detection of chemical carcinogens, developed in the male F344 rat, uses 0.1% N-bis(2-hydroxypropyl)nitrosamine (DHPN) among five genotoxic chemicals for the initiation of carcinogenesis in multiple organs. To establish this bioassay in the Wistar strain, the effects of two dose levels of DHPN were evaluated on the main DHPN rat target organs: lung, thyroid gland, kidneys and liver. Four groups of male and female animals were studied: Control,untreated group; Multi-organ initiated group (also referred to as DMBDD, based on the initials of the five initiators),treated sequentially with N-diethylnitrosamine (DEN, i.p.), N-methyl-N-nitrosourea (MNU, i.p.), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN, drinking water), N, ,N,-dimethylhydrazine (DMH, s.c.) and DHPN (drinking water) for 4 weeks; a third group treated with 0.1% DHPN in drinking water for 2 weeks and the last group treated with 0.2% DHPN in drinking water for 4 weeks. The animals were sacrificed after 30 weeks. DHPN at 0.2% induced preneoplasia in the liver and kidneys of rats of both sexes, the number and area of the putative preneoplastic liver glutathione S-transferase-positive hepatocyte foci being significantly increased in these animals. It also induced benign and malignant tumors in female and in male rats. However, there was no relationship between the increased incidence of preneoplastic lesions and tumor development in the 0.2% DHPN-exposed groups of both sexes. DHPN at 0.1% induced only a few preneoplastic lesions in the liver and kidney and no tumors in both male and female rats. A clear dose and sex-related carcinogenic activity of DHPN was registered, although Wistar rats of both sexes showed a relative resistance to the carcinogenic activity of this compound. [source]


Drosophila melanogaster as a model for elucidating the pathogenicity of Francisella tularensis

CELLULAR MICROBIOLOGY, Issue 6 2008
Malin Vonkavaara
Summary Drosophila melanogaster is a widely used model organism for research on innate immunity and serves as an experimental model for infectious diseases. The aetiological agent of the zoonotic disease tularaemia, Francisella tularensis, can be transmitted by ticks and mosquitoes and Drosophila might be a useful, genetically amenable model host to elucidate the interactions between the bacterium and its arthropod vectors. We found that the live vaccine strain of F. tularensis was phagocytosed by Drosophila and multiplied in fly haemocytes in vitro and in vivo. Bacteria injected into flies resided both inside haemocytes and extracellularly in the open circulatory system. A continuous activation of the humoral immune response, i.e. production of antimicrobial peptides under control of the imd/Relish signalling pathway, was observed and it may have contributed to the relative resistance to F. tularensis as flies defective in the imd/Relish pathway died rapidly. Importantly, bacterial strains deficient for genes of the F. tularensis intracellular growth locus or the macrophage growth locus were attenuated in D. melanogaster. Our results demonstrate that D. melanogaster is a suitable model for the analysis of interactions between F. tularensis and its arthropod hosts and that it can also be used to identify F. tularensis virulence factors relevant for mammalian hosts. [source]


Growth of Brucella abortus in macrophages from resistant and susceptible mouse strains

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2000
J. Sathiyaseelan
C57Bl/10 mice have a superior ability to control chronic infections with virulent strains of the intracellular bacteria Brucella abortus compared with BALB/c mice. While a number of differences in the cytokines produced by lymphocytes following infection of these two strains of mice have been shown, macrophages have not been evaluated for their role in conveying relative resistance. The importance of macrophages in control of brucella infections is demonstrated by the observations that intracellular survival of various strains of B. abortus directly correlates with their virulence in vivo, and the ability of macrophages to control brucellae in vitro has been shown to correlate with a brucella-resistant phenotype in ruminants. While both BALB/c and C57Bl are Nramp -susceptible mouse strains, additional differences in macrophage function outside of the Nramp1 gene effects could influence susceptibility to brucellosis. The studies conducted here comparing the ability of macrophages from C57Bl/10 and BALB/c mice indicate that the macrophages from resistant mice did not control intracellular growth of B. abortus strain 2308 more efficiently than those from the susceptible mice, either in the absence of, or following, interferon-gamma activation or iron supplementation. A number of different conditions for culturing macrophages were evaluated to rule out the influence of antibiotics on the conclusions drawn from the results. [source]