Зависимость свойств толстопленочных терморезисторов от состава базовой шпинели

Изменением соотношения компонентов шпинели Cu1-x-yCo2yMn2-yO4 получены толстопленочные терморезисторы с удельным объемным электросопротивлением 1,5-33 Омм и тепловой константой В25/85 2980-3690 К

Associations between APOE genotypes and disease susceptibility, joint damage and lipid levels in patients with rheumatoid arthritis.

OBJECTIVE: Apolipoprotein E (APOE) genotypes are associated with cardiovascular disease (CVD) and lipid levels. In rheumatoid arthritis (RA), an association has been found with disease activity. We examined the associations between APOE genotypes and disease susceptibility and markers of disease severity in RA, including radiographic joint damage, inflammatory markers, lipid levels and cardiovascular markers. METHOD: A Norwegian cohort of 945 RA patients and 988 controls were genotyped for two APOE polymorphisms. We examined longitudinal associations between APOE genotypes and C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) as well as hand radiographs (van der Heijde Sharp Score(SHS)) in 207 patients with 10 year longitudinal data. Lipid levels, cardiovascular markers and history of CVD were compared across genotypes in a cross sectional study of 136 patients. Longitudinal radiological data of cohorts from Lund and Leiden were available for replication. (N = 935, with 4799 radiographs). RESULTS: In the Norwegian cohort, associations between APOE genotypes and total cholesterol (TC) and low-density lipoproteins (LDL) were observed (ε2 < ε3/ε3 < ε4, p = 0.03 and p = 0.02, respectively). No association was present for acute phase reactant or CVD markers, but a longitudinal linear association between APOE genotypes and radiographic joint damage was observed (p = 0.007). No association between APOE genotypes and the severity of joint destruction was observed in the Lund and Leiden cohorts, and a meta- analysis combining all data was negative. CONCLUSION: APOE genotypes are associated with lipid levels in patients with RA, and may contribute to dyslipidemia in some patients. APOE genotypes are not consistently associated with markers of inflammation or joint destruction in RA

Longitudinal analyses and meta-analyses for <i>APOE</i> and radiographic joint damage for 3 cohorts.

<p>For <i>APOE</i>, the three genotype groups, ε2 carrier, ε3/ε3, and ε4 carrier are coded 0, 1 and 2 respectively. The coefficient estimates and 95% confidence interval (95% CI) from the longitudinal analyses give a measure of the difference in radiographic joint damage score of adjacent <i>APOE</i> genotype groups within each cohort. E.g. in the Norwegian cohort individuals with ε3/ε3 genotype had 0.36 lower radiographic joint damage score than individuals carrying ε2. The coefficient estimates are given on the natural log (ln) scale for radiographic joint damage score. Longitudinal analyses were adjusted for time, age, gender and treatment. Additional adjustments including presence of anti citrullinated protein antibodies and disease duration at baseline were included in the analyses of the Norwegian cohort. A fixed effect meta-analysis was carried out and the p-value is shown.</p

Mean radiographic joint damage in patients with RA in the three different cohorts grouped by <i>APOE</i> genotype.

<p>A = Norway, B = Lund (Sweden) and C = Leiden (Netherland). The Y-axes shows radiographic damage, either as log-transformed van der Heijde Sharp score or log transformed Larsen score (Lund). The x-axes show years of follow-up. Number of patients included: Norway (EURIDISS); n = 176, Leiden n = 621, Lund n = 138.</p

Demographics and clinical measures of the 136 patients included in the lipid and CVD analyses.

<p>sd; standard deviation, Disease duration; disease duration in years at follow-up in 2007, ACPA; anti-citrullinated protein antibodies, RF; rheumatoid factor, CDAI; Clinical Disease Activity Index, DAS28; Diseases Activity Score 28, HAQ; Health Assessment Questionnaire, Statins; lipid lowering medications, sDMARD and bDMARD; synthetic and biologic disease-modifying antirheumatic drug,</p>*<p>The three genotype groups (ε2carriers, ε3/ε3, and ε4 carriers) were compared by ANOVA or chi square test.</p>¤<p>Not all patients had data available for all analyses, but the maximum number of patients in each group was ε2 n = 15, ε3/ε3 n = 81, ε4 n = 40. Patients with ε2/ε4 gentoype were excluded (n = 4).</p

Lipid levels and CVD outcome in RA patients across different <i>APOE</i> genotype groups.

<p>LDL: low density lipoproteins, HDL; High density lipoproteins, IMT; intima-media thickness (mm), CVD event; cardiovascular disease event (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0060970#s2" target="_blank">Methods</a> sections). All lipids are measured in mmol/L. Lipid levels and IMT were compared using ANCOVA, and unadjusted mean values with standard deviation (sd) are given in column 2, 3 and 4. CVD outcomes, which included previous CVD events or carotid plaques present on ultrasound (or both) were compared using Chi-square test; and the number of individuals affected with percentages [%] are given in column 2, 3 and 4. Multivariate analyses were adjusted for age, sex and current statin use. Not all patients had data on all variables and patients with genotype ε2/ε4 (n = 4) were omitted from the analyses.</p>*<p>p-values were corrected for multiple testing using Dunnets-Hsu adjustment.</p>$<p>Exact test.</p

Longitudinal analyses of <i>APOE</i> genotype and radiographic score, CRP and ESR as dependent variables in the EURIDISS cohort.

<p>SHS, CRP and ESR have all been log-transformed.</p>¥<p>Models were adjusted for: a = time, b = time, age, sex, disease duration, ACPA and DMARD treatment (ever/never).</p>¤<p>Model B with SHS outcome was also adjusted for CRP. For the models investigating CRP or ESR n = 207, while for joint damage (SHS) n = 176. Patients with genotype ε2/ε4 were omitted from the analyses.</p>£<p>In the analyses where <i>APOE</i> genotype is a categorical factor, ε3/ε3 is the reference group.</p>$<p>In the linear analyses (<i>APOE</i> linear), ε2, ε3/ε3, and ε4 are coded 0, 1 and 2 respectively.</p>§<p>Overall p-value.</p>*<p>P-values corrected for multiple testing using Sidaks’ adjustment.</p

Demographic and baseline clinical data on patients included in the Norwegian longitudinal analyses (EURIDISS cohort), grouped by APOE genotype.

<p>sd; standard deviation, Disease duration; disease duration at baseline in years, ACPA; anti-citrullinated protein antibodies, RF; rheumatoid factor, CRP; C-reactive protein (mg/L), ESR; erythrocyte sedimentation rate (mm/hour), HAQ; Health Assessment Questionnaire, LnSHS; log transformed Sharp van der Heijde score, sDMARD; synthetic disease-modifying anti rheumatic drugs.</p>*<p>The three genotype groups (ε2 carriers, ε3/ε3, and ε4 carriers) were compared by ANOVA or Chi-square test.</p>£<p>For RF and ACPA, patients were viewed as positive if they had at least one positive test during the 10 year follow-up.</p

<i>APOE</i> genotypes in RA patients and controls.

<p>ACPA; anti-citrullinated protein antibodies, RF; rheumatoid factor. Frequencies of genotypes were compared between all patients or subsets of patients (i.e. ACPA positive patients) and controls using chi square test.</p>*<p>Odds ratios were calculated using ε3/ε3 as the reference group.</p