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Disease Parameters (disease + parameter)
Selected AbstractsInterleukin-10 gene promoter polymorphism in Polish rheumatoid arthritis patientsINTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 4 2010A. Paradowska-Gorycka Summary Interleukin (IL)-10 is an important multifunctional cytokine with both anti-inflammatory and immunoregulatory effects in rheumatoid arthritis (RA). In the present study, we evaluated the frequency and potential impact of IL-10 promoter polymorphisms on susceptibility to and severity of RA in Polish in , patients with a high disease activity (mean DAS 28 C-reactive protein 5.25). DNA was obtained from 244 RA patients and 106 healthy controls. The ,592C/A and ,1082G/A IL-10 gene polymorphisms were amplified by polymerase chain reaction with restriction endonuclease mapping. The frequency of the IL-10-592CA, -592AA genotypes (respectively: 30% vs 5% and 7% vs 0%) and allele ,592A (37% vs 5%) were significantly higher in RA patients as compared with a control group. We did not find any association of the IL-10-592C/A genotype distribution with disease parameters, except for an increased ESR (erythrocyte sedimentation rate) in patients with the ,592CC genotype as compared with those with ,592CA or ,592AA genotypes (P = 0.01). The frequency of the IL-10-1082GG genotype was lower (P = 0.0001), and that of the IL-10-1082GA genotype was higher (P = 0.009) in RA patients comparing with the control group. In RA patients with ,1082GA or ,1082AA genotypes the time duration of the disease (P = 0.03), Health Assessment Questionnaire (HAQ) Score (P = 0.04) and PLT count (P = 0.001) were significantly increased as compared with subjects with ,1082GG genotype. Presented findings indicate that IL-10-592C/A and IL-10-1082G/A polymorphisms may be considered genetic risk factors for RA susceptibility and severity. [source] Effect of oral hygiene instruction and scaling on oral malodour in a population of Turkish children with gingival inflammationINTERNATIONAL JOURNAL OF PAEDIATRIC DENTISTRY, Issue 6 2006C. KARA Summary. Aim., Oral malodour affects a large proportion of the population, and may cause a significant social or psychological handicap to those suffering from it. The condition has a positive correlation with the accumulation of bacterial plaque in the oral cavity. The aim of the present study was twofold: first, to determine whether oral malodour and periodontal disease parameters are associated with one another in 150 Turkish subjects (mean age ± SD = 9·1 ± 2·7 years; age range = 7,12 years); and secondly, to investigate the impact of oral hygiene instruction and scaling on oral malodour. Design., The parameters measured included whole-mouth odour judge scoring, halimeter measurements, saliva pH scores, gingival index, plaque index, and probing depth before and after the treatment procedures. Results., Odour judge scores were significantly associated with halimeter findings. However, gingival index, plaque index and probing depth were significantly associated with odour judge scores and halimeter scores. The statistical analysis revealed that periodontal treatments caused a significant reduction (P < 0·001) in volatile sulphur compound formation. Conclusion., These results suggest that, in the population studied, periodontal health and oral malodour are associated with one another. Oral malodour levels were significantly reduced after treating gingival inflammation. Thus, in order to avoid oral malodour in children, oral care should not be neglected. [source] JOINTLY-DETERMINED ECOLOGICAL THRESHOLDS AND ECONOMIC TRADE-OFFS IN WILDLIFE DISEASE MANAGEMENTNATURAL RESOURCE MODELING, Issue 4 2007ELI P. FENICHEL ABSTRACT. We investigate wildlife disease management, in a bioeconomic framework, when the wildlife host is valuable and disease transmission is density-dependent. Disease prevalence is reduced in density-dependent models whenever the population is harvested below a host-density threshold a threshold population density below which disease prevalence declines and above which a disease becomes epidemic. In conventional models, the threshold is an exogenous function of disease parameters. We consider this case and find a steady state with positive disease prevalence to be optimal. Next, we consider a case in which disease dynamics are affected by both population controls and changes in human-environmental interactions. The host-density threshold is endogenous in this case. That is, the manager does not simply manage the population relative to the threshold, but rather manages both the population and the threshold. The optimal threshold depends on the economic and ecological trade-offs arising from the jointly-determined system. Accounting for this endogene-ity can lead to reduced disease prevalence rates and higher population levels. Additionally, we show that ecological parameters that may be unimportant in conventional models that do not account for the endogeneity of the host-density threshold are potentially important when host density threshold is recognized as endogenous. [source] Resistance in water yam (Dioscorea alata) cultivars in the French West Indies to anthracnose disease based on tissue culture-derived whole-plant assayPLANT PATHOLOGY, Issue 5 2006T. J. Onyeka Reactions of 60 water yam (Dioscorea alata) cultivars to three isolates of the yam anthracnose fungal pathogen (Colletotrichum gloeosporioides) were evaluated using tissue culture-derived whole-plant assay. Three disease parameters: single score on a scale of 0,6 at the seventh day after inoculation (SD7); area under the disease progress curve (AUDPC); and disease progress rate (Rd) were compared, and cultivars were classified into disease-response groups using a rank-sum method based on AUDPC scores for the two most virulent isolates. A wide range of variation in resistance of the D. alata cultivars, and significant effects of pathogen isolate and isolate,cultivar interactions, were observed for all disease parameters. The three disease parameters were positively correlated; however, four cultivars showed great dispersions from the regression lines for comparisons of SD7 with the multiple assessments based AUDPC and Rd. The 60 cultivars were separated into resistant (n = 12), moderately resistant (n = 19), moderately susceptible (n = 18) and susceptible (n = 11) groups. The potential of the tissue culture-derived whole-plant assay to resistance breeding programmes and further understanding of the yam anthracnose pathosystem is discussed. [source] Aberrant IgG galactosylation precedes disease onset, correlates with disease activity, and is prevalent in autoantibodies in rheumatoid arthritis,ARTHRITIS & RHEUMATISM, Issue 8 2010Altan Ercan Objective To examine the association between aberrant IgG galactosylation and disease parameters in rheumatoid arthritis (RA). Methods Analysis of N -glycan in serum samples from multiple cohorts was performed. The IgG N -glycan content and the timing of N -glycan aberrancy relative to disease onset were compared in healthy subjects and in patients with RA. Correlations between aberrant galactosylation and disease activity were assessed in the RA cohorts. The impact of disease activity, sex, age, anti,cyclic citrullinated peptide (anti-CCP) antibody titer, disease duration, and C-reactive protein level on aberrant galactosylation was determined using multivariate analysis. The N -glycan content was also compared between epitope affinity,purified autoantibodies and the remaining IgG repertoire in RA patients. Results Our results confirm the aberrant galactosylation of IgG in RA patients as compared with healthy controls (mean ± SD 1.36 ± 0.43 versus 1.01 ± 0.23; P < 0.0001). We observed a significant correlation between levels of aberrant IgG galactosylation and disease activity (Spearman's , = 0.37, P < 0.0001). This correlation was higher in women (Spearman's , = 0.60, P < 0.0001) than in men (Spearman's , = 0.16, P = 0.10). Further, aberrant IgG galactosylation substantially predated the onset of arthritis and the diagnosis of RA (3.5 years) and resided selectively in the anticitrullinated antigen fraction. Conclusion Our findings identify aberrant IgG galactosylation as a dysregulated component of the humoral immune response in RA that begins prior to disease onset, associates with disease activity in a sex-specific manner, and resides preferentially in autoantibodies. [source] Increased expression of interleukin-7 in labial salivary glands of patients with primary Sjögren's syndrome correlates with increased inflammationARTHRITIS & RHEUMATISM, Issue 4 2010A. Bikker Objective To study the expression levels and immunostimulatory capacities of interleukin-7 (IL-7) in primary Sjögren's syndrome. Methods Labial salivary gland (LSG) IL-7 expression was determined by immunohistochemistry, using a quantitative scoring system, in 30 patients with sicca syndrome: 15 patients with primary Sjögren's syndrome (SS) and 15 patients with non-SS sicca syndrome. The correlation of IL-7 expression in LSGs with parameters of local and peripheral disease was studied, and serum and salivary IL-7 levels were determined. Additionally, the effects of IL-7 on cytokine production by peripheral blood mononuclear cells (PBMCs) from patients with primary SS were determined in vitro by Luminex multicytokine assay and compared with the effects in control subjects. Results The expression of IL-7 in LSGs was higher in patients with primary SS compared with that in patients with non-SS sicca syndrome. IL-7 was observed primarily in the vicinity of lymphocytic infiltrates. Salivary IL-7 levels in patients with primary SS were higher than those in control subjects. In all 30 patients with sicca syndrome, IL-7 expression in LSGs correlated with parameters of both local and peripheral disease. Furthermore, IL-7 stimulated T cell,attracting and T cell,differentiating cytokines (monokine induced by interferon-, [IFN,], IFN,-inducible 10-kd protein, IL-12, and IL-15), as well as Th1 (IFN,), Th2 (IL-4), Th17 (IL-17A), proinflammatory (tumor necrosis factor , and IL-1,), and regulatory (IL-10 and IL-13) cytokine production by PBMCs. All of these cytokines were previously shown to be associated with primary SS. The IL-7,induced increase in IL-10 production in patients with primary SS was reduced compared with that in control subjects. Conclusion The correlation between LSG IL-7 expression and (local) disease parameters in primary SS as well as the IL-7,mediated induction of inflammatory cytokines indicate that IL-7 might contribute to the immunopathology of primary SS. [source] Biomarkers of periodontal inflammation in the Australian adult populationAUSTRALIAN DENTAL JOURNAL, Issue 2 2009TR Fitzsimmons Abstract Background:, Several inflammatory biomarkers are implicated in the pathogenesis of periodontitis including interleukin-1, (IL-1,) and C-reactive protein (CRP). This study investigated the presence of these factors in gingival crevicular fluid (GCF) and their relationship to clinical and social determinants of periodontitis in the Australian population. Methods:, Equal numbers of periodontitis cases and non-cases were sampled during oral epidemiologic examination in the National Survey of Adult Oral Health. GCF was sampled from four sites where probing pocket depth (PPD) and recession were recorded. From these, IL-1, and CRP were quantified by ELISA and the log amount of GCF IL-1, (pg) per person and the proportion of adults with detectable CRP was computed. Results:, Periodontitis cases (n = 511) had significantly higher levels of IL-1, and CRP than non-cases (n = 562). PPD, clinical attachment loss, plaque and gingivitis indices were positively associated with elevated levels of both biomarkers. Levels of both were positively associated with age, low socio-economic position and non-Australian birth. Conclusions:, The presence of IL-1, and CRP in GCF are associated with periodontal disease parameters within the Australian population. The levels of both biomarkers are influenced by age, education and eligibility for public dental care. [source] Aiming towards effective preventive medicine against Japanese cedar pollinosis: epidemiology, patient investigation and integrated research including genotype analysesCLINICAL & EXPERIMENTAL ALLERGY REVIEWS, Issue 2 2005N. Terada Summary Environmental rather than genetic factors appear to play the major role in the recent increased prevalence of Japanese cedar pollinosis in Japan. However, investigating the genes that determine IgE levels and analysing gene polymorphisms may assist in finding new methods of treatment and establishing preventive medicine against this disease. Among a total of 219 asymptomatic individuals who were anti-Japanese cedar pollen IgE antibody positive as determined by radioallergosorbent test (RAST), only a handful subsequently developed symptoms of Japanese cedar pollinosis or secondary onset of Japanese cedar pollinosis over 5,14 years of follow-up. Among those who subsequently developed secondary onset of disease, >50% were found to have high initial RAST scores, suggesting that the incidence of Japanese cedar pollinosis is correlated with RAST score. Hence, it may be prudent to advise asymptomatic individuals with high RAST scores to avoid exposure to Japanese cedar pollen so as to delay onset of the disease. Analysis of sequence variants of the Fc,RI, gene revealed that patients with nasal allergy exhibit a single-nucleotide polymorphism in which the amino acid at 237 of the intracellular domain changes from glutamine to glycine more frequently than individuals without nasal allergy. Furthermore, Il homo polymorphism of the IL-4R, gene is associated with higher serum nonspecific IgE and Japanese cedar pollen-specific IgE levels than are seen in individuals showing Il,Val hetero and Val homo expression types. When the age of pollinosis onset was compared among these three genotypes, it was found to be significantly lower among Il homo type than the other two expression types, suggesting that Il homo type individuals seem characteristically pre-disposed to early onset of pollinosis. Studies comparing eosinophil-associated gene polymorphism in healthy and pollinosis phenotypes have revealed several relationships among the various genotypes and specific disease parameters and suggest that Eotaxin G (123G/A) and IL5 (,703C/T) genotypes can affect the timing of symptom onset after sensitization as well as nasal mucosal hyper-responsiveness. [source] | |||||||||||||