Depressive Symptoms and Perception of COVID-19 Risk in Ohio Adults

Background: We assessed the relationship between depressive symptoms and perceived COVID-19 risk in the next month. Methods: This analysis used survey data collected during a July 2020 cross-sectional study using a household-based probability sampling design. A total of 615 noninstitutionalized, English- and/or Spanish-speaking adults in Ohio were included. Depressive symptoms screening occurred using the Patient Health Questionnaire-2 (PHQ-2). We applied survey weights so that presented analyses represent the adult population in Ohio. We performed log-risk regression modeling (generalized linear model with binomial distribution and log link) to estimate unadjusted and covariate-adjusted prevalence ratios examining the association between screening positive for depressive symptoms and perceived risk of COVID-19 in the next month. Results: The study population was majority female (59.1%) and White (90.3%). The mean age was 55.9 years (standard deviation (SD)=17.3). About 1 in 20 (4.6%) screened positive for depressive symptoms. A positive depressive symptoms screen was not significantly associated with perceived risk of COVID-19 in the next month (prevalence ratio [PR]=0.75; 95% confidence interval [CI]=0.25–2.24). After confounder adjustment, the adjusted prevalence ratio (aPR) was nearly unchanged (aPR=0.78; 95% CI=0.24–2.55). Conclusion: As depression is often associated with anxiety and pessimism toward the future, the lack of association between depressive symptoms screening and perception of COVID-19 risk in the next month is surprising. Social withdrawal, which is also associated with depression, may have concealed any increased perceived COVID-19 risk, as depressed individuals who remained socially isolated may have had lower perceived COVID-19 risk

Experimental Evolution of Escherichia coli K-12 at High pH and with RpoS Induction

Experimental evolution of Escherichia coli K-12 W3110 by serial dilutions for 2,200 generations at high pH extended the range of sustained growth from pH 9.0 to pH 9.3. pH 9.3-adapted isolates showed mutations in DNA-binding regulators and envelope proteins. One population showed an IS1 knockout of phoB (encoding the positive regulator of the phosphate regulon). A phoB::kanR knockout increased growth at high pH. phoB mutants are known to increase production of fermentation acids, which could enhance fitness at high pH. Mutations in pcnB [poly(A) polymerase] also increased growth at high pH. Three out of four populations showed deletions of torI, an inhibitor of TorR, which activates expression of torCAD (trimethylamine N-oxide respiration) at high pH. All populations showed point mutations affecting the stationary-phase sigma factor RpoS, either in the coding gene or in genes for regulators of RpoS expression. RpoS is required for survival at extremely high pH. In our microplate assay, rpoS deletion slightly decreased growth at pH 9.1. RpoS protein accumulated faster at pH 9 than at pH 7. The RpoS accumulation at high pH required the presence of one or more antiadaptors that block degradation (IraM, IraD, and IraP). Other genes with mutations after high-pH evolution encode regulators, such as those encoded by yobG (mgrB) (PhoPQ regulator), rpoN (nitrogen starvation sigma factor), malI, and purR, as well as envelope proteins, such as those encoded by ompT and yahO Overall, E. coli evolution at high pH selects for mutations in key transcriptional regulators, including phoB and the stationary-phase sigma factor RpoS.IMPORTANCEEscherichia coli in its native habitat encounters high-pH stress such as that of pancreatic secretions. Experimental evolution over 2,000 generations showed selection for mutations in regulatory factors, such as deletion of the phosphate regulator PhoB and mutations that alter the function of the global stress regulator RpoS. RpoS is induced at high pH via multiple mechanisms

Gamma-glutamyltransferase, arterial remodeling and prehypertension in a healthy population at low cardiometabolic risk

International audiencePlasma gamma-glutamyltransferase (GGT) was suggested to reflect the level of systemic oxidative stress. Oxidative stress induces changes in arterial structure and function and contributes to the development of hypertension. Therefore, GGT may be associated with arterial remodeling and blood pressure (BP) increment, even in absence of disease. To test this hypothesis, we evaluated, in 825 healthy subjects at low cardiometabolic risk, the associations of plasma GGT with carotid artery intima-media thickness (IMT), luminal diameter and prehypertension; in 154 subjects was evaluated also the association with aortic stiffness (cfPWV). Associations were controlled for insulin sensitivity, C-reactive protein, and life-style habits. In the main population, BP was remeasured after 3 years. Carotid diameter and cfPWV, but not IMT, were directly and independently related to plasma GGT. Subjects with prehypertension (N = 330) had higher GGT as compared with subjects with normal BP (22 [14] vs 17 [11] IU/L; adjusted P = 0.001), and within prehypertensive subjects, those who developed hypertension during 3 years had higher GGT than those without incident hypertension (27 [16] vs 21 [14] IU/L; adjusted P < 0.05). Within subjects with arterial stiffness measurement, those with prehypertension (N = 79) had higher both GGT and arterial stiffness (25 [14] vs 16 [20] IU/L and 9.11 ± 1.24 vs 7.90 ± 0.94 m/s; adjusted P < 0.01 and <0.05). In the view of previous evidence linking plasma GGT concentration to the level of systemic oxidative stress, our findings suggest a role of oxidative stress in subclinical arterial damage and in prehypertension, even in healthy subjects free of cardiometabolic risk. Arterial organ damage may represent the link between GGT and hypertension