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BackgroundPrevious studies have observed that haemoglobin concentrations can be affected by type of blood collection, analysis methods and device, and that near-in-time population-based surveys report substantially different anaemia prevalence. We investigated whether differences in mean haemoglobin or prevalence of anaemia between near-in-time surveys of the same population were associated with differences in type of blood collection or analytic approach to haemoglobin measurement.MethodsWe systematically identified pairs of population-based surveys that measured haemoglobin in the same population of women of reproductive age (WRA) or preschool-aged children (PSC). Surveys were matched on geographic coverage, urban/rural place of residence, inclusion of pregnant women, time of data collection (within 18 months), and, to the extent feasible, age range. Differences in anaemia prevalence were presented graphically. Random-effects meta-analysis and meta-regression of difference in mean haemoglobin were carried out, with subgroups defined by comparison of type of blood collection and analytic approach within each survey pair.ResultsWe included 23 survey pairs from 17 countries for PSC and 17 survey pairs from 11 countries for WRA. Meta-regression indicates that surveys measuring haemoglobin with HemoCue® Hb 301 found higher haemoglobin concentrations than near-in-time surveys using HemoCue® Hb 201+ in non-pregnant women ((NPW); 5.8 g/L (95% confidence interval (CI) = 3.2-8.3) mean difference, n = 5 pairs) and PSC (4.3 g/L (1.4-7.2), n = 6). Surveys collecting venous blood found higher haemoglobin concentrations than near-in-time surveys collecting capillary blood in PSC (3.8 g/L (0.8-6.7), n = 8), but not NPW (0.4 g/L (-1.9-2.8), n = 9).ConclusionsBecause this study is observational, differences in haemoglobin concentrations in near-in-time surveys may be caused by other factors associated with choice of analytic approach or type of blood collected. The source or sources of differences should be clarified to improve use of surveys to prioritize and evaluate public health programs.RegistrationPROSPERO CRD42022296553.

BackgroundTo ensure that National Institutes of Health-funded research is relevant to the population's needs, specific emphasis on proportional representation of minority/sex groups into National Cancer Institute (NCI) cancer centers' clinical research programs is reported to the NCI.MethodsEMPaCT investigators at 5 regionally diverse comprehensive cancer centers compared data reported to the NCI for their most recent Cancer Center Support Grant competitive renewal to assess and compare the centers' catchment area designations, data definitions, data elements, collection processes, reporting, and performance regarding proportional representation of race/ethnicity and sex subsets.ResultsCancer centers' catchment area definitions differed widely in terms of their cancer patient versus general population specificity, levels of specificity, and geographic coverage. Racial/ethnic categories were similar, yet were defined differently, across institutions. Patients' socioeconomic status and insurance status were inconsistently captured across the 5 centers.ConclusionsCatchment area definitions and the collection of patient-level demographic factors varied widely across the 5 comprehensive cancer centers. This challenged the assessment of success by cancer centers in accruing representative populations into the cancer research enterprise. Accrual of minorities was less than desired for at least 1 racial/ethnic subcategory at 4 of the 5 centers. Institutions should clearly and consistently declare their primary catchment area and the rationale and should report how race/ethnicity and sex are defined, determined, collected, and reported. More standardized, frequent, consistent collection, reporting, and review of these data are recommended, as is a commitment to collecting socioeconomic data, given that socioeconomic status is a primary driver of cancer disparities in the United States.

Tregs restrain both the innate and adaptive immune systems to maintain homeostasis. Allergic airway inflammation, characterized by a Th2 response that results from a breakdown of tolerance to innocuous environmental antigens, is negatively regulated by Tregs. We previously reported that prostaglandin I2 ([PGI.sub.2]) promoted immune tolerance in models of allergic inflammation; however, the effect of [PGI.sub.2] on Treg function was not investigated. Tregs from mice deficient in the [PGI.sub.2] receptor IP (IP KO) had impaired suppressive capabilities during allergic airway inflammatory responses compared with mice in which [PGI.sub.2] signaling was intact. IP KO Tregs had significantly enhanced expression of immunoglobulin-like transcript 3 (ILT3) compared with WT Tregs, which may contribute to the impairment of the IP KO Treg's ability to suppress Th2 responses. Using fate-mapping mice, we reported that [PGI.sub.2] signaling prevents Treg reprogramming toward a pathogenic phenotype. [PGI.sub.2] analogs promoted the differentiation of naive T cells to Tregs in both mice and humans via repression of [beta]-catenin signaling. Finally, a missense variant in IP in humans was strongly associated with chronic obstructive asthma. Together, these data support that [PGI.sub.2] signaling licenses Treg suppressive function and that [PGI.sub.2] is a therapeutic target for enhancing Treg function., Introduction Tregs are important components of the adaptive immune system that promote tolerance, prevent the development of autoimmune diseases, and suppress inflammation (1, 2). Tregs are characterized by their expression [...]

To determine mechanisms underlying the transgenerational presence of metabolic perturbations in the intrauterine growth-restricted second-generation adult females (F2 IUGR) despite normalizing the in utero metabolic environment, we examined in vivo glucose kinetics and in vitro skeletal muscle postinsulin receptor signaling after embryo transfer of first generation (F1 IUGR) to control maternal environment. Female F2 rats, procreated by F1 pre- and postnatally nutrient- and growth-restricted (IUGR) mothers but embryo transferred to gestate in control mothers, were compared with similarly gestating age- and sex-matched control (CON) F2 progeny. Although there were no differences in birth weight or postnatal growth patterns, the F2 IUGR had increased hepatic weight, fasting hyperglycemia, hyperinsulinemia, and unsuppressed hepatic glucose production, with no change in glucose futile cycling or clearance, compared with F2 CON. These hormonal and metabolic aberrations were associated with increased skeletal muscle total GLUT4 and pAkt concentrations but decreased plasma membrane-associated GLUT4, total pPKC[zeta], and PKC[zeta] enzyme activity, with no change in total SHP2 and PTP1B concentrations in IUGR F2 compared with F2 CON. We conclude that transgenerational presence of aberrant glucose/insulin metabolism and skeletal muscle insulin signaling of the adult F2 IUGR female offspring is independent of the immediate intrauterine environment, supporting nutritionally induced heritable mechanisms contributing to the epidemic of type 2 diabetes mellitus. glucose transporter; metabolic imprinting; epigenetic inheritance doi:10.1152/ajpendo.00462.2006.

The effect of K(super +)-induced dimerization of tetrakis(benzo-15-crown-5)porphyrin and its metal derivatives on the redox, optical, and ESR behavior is reported. Electrochemical HOMO-LUMO energy levels revealed destabilization of HOMO and stabilization of LUMO upon dimerization.

Stable isotopic protocols for the study of folate absorption were conducted to determine the following: (1) the equivalence of the [13[C.sub.5]] and [2[H.sub.2]] forms of folic acid, and (2) the merits of short-term plasma kinetics from injected and oral doses vs. urinary excretion of [13[C.sub.5]] and [2[H.sub.2]] folates. Another objective was to evaluate the merits of protocols not involving 'saturation' of subjects with nonlabeled folate. Oral administration of [13[C.sub.5]] and [2[H.sub.2]] folic acid ([approximately]500 nmol each) to adult subjects (n = 4) yielded an equivalent 24-h urinary excretion of [approximately]2% of each dose (molar ratio of urinary [13[C.sub.5]]/[2[H.sub.2]]folates = 0.96 [+ or -] 0.055; mean [+ or -] SEM). Expression of urinary excretion as a ratio of [13[C.sub.5]]/[2[H.sub.2]]folates yielded less within-group variability than seen for absolute excretion of each form of labeled folate. In the second study, subjects received 226 nmol of [2[H.sub.2]]folic acid intravenously and 1010 nmol of [13[C.sub.5]]folic acid orally. Isotopic enrichment of plasma [2[H.sub.2]]folates rose rapidly and returned to near basal values by [approximately]2 h postdose. In contrast, enrichment of plasma [13[C.sub.5]]folates was detected until 4 h after dose, whereas enrichment values were far lower than seen with [2[H.sub.2]]folate. Adjusting for the difference in dose, the molar response of plasma area under the curve for isotopic enrichment was 15- to 20-fold greater for injected folates. In view of this very limited short-term plasma response even with a relatively large oral dose, presumably due to hepatic first-pass uptake, these findings suggest that plasma kinetics would be of limited usefulness in assessing the relative bioavailability of nutritionally relevant oral doses of labeled folate. KEY WORDS: folic acid folate human bioavailability stable isotopes