Human ANA IgG Screen ELISA

Objective. Telomere shortening is a well-established marker of biological aging. Whether telomere erosion coincides with age-related increases in antinuclear antibody (ANA) seropositivity remains unknown. Our study aimed to determine the association between ANA seropositivity and shortened telomeres among 1999-2002 National Health and Nutrition Examination Survey (NHANES) subjects. Methods. We performed a cross-sectional analysis of 2,188 NHANES study participants with available ANA and telomere length data. ANA testing was performed using indirect immunofluorescence. Telomere lengths were measured via quantitative polymerase chain reaction methods. Applying appropriate sample weighting techniques, we used univariate and multivariate logistic regression methods to assess the association between shortened telomeres (i.e. lowest decile of the cohort) and ANA seropositivity. Results. ANAs were positive in 322 out of 2,188 (14.7%, 95% CI 13.3-16.3%) individuals. Subjects with shortened telomeres were more likely to be older (p<0.001), male (p=0.005), and have a cancer history (p<0.001). A higher proportion of non-Hispanic white participants (61.6% vs. 49.3%) and a lower proportion of non-Hispanic black participants (7.8% vs. 17.9%) had shortened telomeres (p<0.001). Shortened telomeres were not independently associated with ANA seropositivity (OR 1.48, 95% CI 0.87-2.52, p=0.14). However, female sex (OR 1.91, 95% CI 1.23-2.96, p=0.006), age >= 80 years (OR 2.06, 95% CI 1.08-3.92, p=0.03), and African American race (OR 1.58, 95% CI 1.00-2.51, p=0.05) were independent risk factors for ANA seropositivity. Neither sex nor race modified the relationship between ANA seropositivity and telomere length. Conclusion. Telomere erosion does not appear to be responsible for age-related increases in the prevalence of ANA seropositivity.

Biofilm mediated bacterial infections are the key factors in the progression of infectious diseases due to the evolution of antimicrobial resistance. Traditional therapy involving antibiotics is not adequate enough for treatment of such infections due to the increased resistance triggered by biofilm. To overcome this challenge, we developed anacardic acid (Ana) loaded solid lipid nanoparticles (SLNs), further coated with chitosan and DNase (Ana-SLNs-CH-DNase). The DNase coating was hypothesized to degrade the e-DNA, while chitosan was coated to yield positively charged SLNs with additional adhesion to biofilms. The SLNs were developed using homogenization method and further evaluated for particle size, polydispersity index, zeta potential, and entrapment efficiency. Drug excipient compatibility was confirmed by using FT-IR study, while encapsulation of Ana in SLNs was confirmed by X-ray diffraction study. The SLNs demonstrated sustained release for up to 24 h and excellent stability at room temperature for up to 3 months. The developed SLNs were found non-toxic against human immortalized keratinocyte (HaCaT) cells while demonstrated remarkably higher antimicrobial efficacy againstStaphylococcus aureus. Excellent effect of the developed SLNs on minimum biofilm inhibition concentration and minimum biofilm eradication concentration further confirmed the superiority of the developed formulation strategy. A significant (p< 0.05) reduction in biofilm thickness and biomass, as confirmed by confocal laser scanning microscopy, was observed in the case of developed SLNs in comparison with control. Cumulatively, the results suggest the enhanced efficacy of the developed formulation strategy to overcome the biofilm-mediated antimicrobial resistance.