White blood cells (WBCs) are considered a reliable biomarker of inflammation. Elevations in both WBCs and pro-inflammatory cytokines are associated with several chronic conditions. Diet is a strong moderator of inflammation and WBCs. The purpose of this study was to examine the association between the Dietary Inflammatory Index (DII®) and WBCs using data from the United States National Health and Nutrition Examination Survey (NHANES). NHANES is a cross-sectional study that occurs in two-year cycles. Respondents from five cycles (n = 26,046) with available data on diet (collected through a single 24-h dietary recall [24HR]) and WBCs (derived using the Coulter method) were included. The DII (theoretical range is about -8 to +8) was derived from the micro and macronutrients calculated from the 24HR. Linear regression models, using survey design procedures, were used to estimate adjusted mean WBC (i.e., total, lymphocytes, monocytes, and neutrophils) counts and percentages by DII quartiles. Among all participants no statistically significant difference in WBCs were observed when comparing DII quartile 4 (most pro-inflammatory) to quartile 1 (most anti-inflammatory). However, a one-unit increase in the DII was associated with a 0.028 (1000 per µL) increase in total WBCs (p = .01). Additionally, a 0.024 increase in neutrophils (p < .01) was observed for a one-unit increase in the DII. In the group of participants with normal body mass index (BMI, 18.5-24.9 kg/m), those in DII quartile 4 had higher levels of total WBCs compared to subjects with normal BMI in DII quartile 1 (7.12 vs. 6.88, p = .01). Similar comparisons were observed for monocytes and neutrophils. However, these relationships were not observed for participants who were overweight or obese, which are pro-inflammatory conditions. Normal-weight individuals consuming more pro-inflammatory diets were more likely to have elevated WBCs. Because of its cross-sectional design, NHANES cannot inform directly on temporal relations, thus limiting causal inference. Future research is needed to examine the impact of anti-inflammatory diet adoption on lowering levels of WBCs, in addition to other inflammatory mediators.

Objective: To determine whether or not the use of colchicine decreases the risk of amyloidosis among Armenian patients with familial Mediterranean fever (FMF). Subjects and Methods: The study included 99 Armenian patients from the Center of Medical Genetics database with genetically ascertained FMF; 33 had renal amyloidosis and 66 were randomly selected control patients without renal amyloidosis. Self- reported colchicine use was assessed by interviewer-based questionnaire. Results: The patients with incident amyloidosis were more likely to be older men, but younger at the time of disease onset, and more likely to have had a family history of amyloidosis and M694F mutation in the MEFV gene compared to patients without amyloidosis. The risk of amyloidosis decreased with adequate colchicine use rather than nonadequate use (adjusted odds ratio, OR, 0.48, 95% confidence interval, CI, 0.16–1.43), continuous colchicine use rather than interrupted use (adjusted OR 0.15, 95% CI 0.04–0.53), earlier rather than later initiation age of colchicine treatment (adjusted OR 0.95, 95% CI 0.90–1.01), current colchicine rather than ever/never colchicine use (adjusted OR 0.20, 95% CI 0.05–0.89). Conclusion: The study demonstrated that colchicine treatment is effective in preventing amyloidosis among Armenian patients with FMF and that earlier initiation and continuous therapy at an adequate dose of 1.2–1.8 mg/day may be associated with a decreased amyloidosis risk among Armenian patients with FMF.

No abstract

The study aims to explore variation in scholarly productivity outcomes by underrepresented status among a diverse sample of researchers in a community-engaged training program. We identified 141 trainees from a web-based survey of researchers in the National Cancer Institute-funded, Community Networks Program Centers (CNPCs) (2011-2016). We conducted a series of multiple logistic regression models to estimate the effect of National Institutes of Health (NIH)-defined underrepresented status on four, self-reported, scholarly productivity outcomes in the previous 5 years: number of publications (first-authored and total) and funded grants (NIH and any agency). Sixty-five percent (n = 92) indicated NIH underrepresented status. In final adjusted models, non-NIH underrepresented (vs. underrepresented) trainees reported an increased odds of having more than the median number of total publications (> 9) (OR = 3.14, 95% CI 1.21-8.65) and any grant funding (OR = 5.10, 95% CI 1.77-14.65). Reporting ≥ 1 mentors (vs. none) was also positively associated (p < 0.05) with these outcomes. The CNPC underrepresented trainees had similar success in first-authored publications and NIH funding as non-underrepresented trainees, but not total publications and grants. Examining trainees' mentoring experiences over time in relation to scholarly productivity outcomes is needed.

No abstract