Alice in Wonderland

Illustration of Alice sitting in chair and mad hatter fussing at rabbithttps://scholarsjunction.msstate.edu/cht-sheet-music/6620/thumbnail.jp

Alice in Wonderland

Illustration of Alice, the Mad Hatter, and rabbit; inset photo of Eddie Cantorhttps://scholarsjunction.msstate.edu/cht-sheet-music/8669/thumbnail.jp

Estimation of Dietary Iron Bioavailability from Food Iron Intake and Iron Status

Currently there are no satisfactory methods for estimating dietary iron absorption (bioavailability) at a population level, but this is essential for deriving dietary reference values using the factorial approach. The aim of this work was to develop a novel approach for estimating dietary iron absorption using a population sample from a sub-section of the UK National Diet and Nutrition Survey (NDNS). Data were analyzed in 873 subjects from the 2000–2001 adult cohort of the NDNS, for whom both dietary intake data and hematological measures (hemoglobin and serum ferritin (SF) concentrations) were available. There were 495 men aged 19–64 y (mean age 42.7±12.1 y) and 378 pre-menopausal women (mean age 35.7±8.2 y). Individual dietary iron requirements were estimated using the Institute of Medicine calculations. A full probability approach was then applied to estimate the prevalence of dietary intakes that were insufficient to meet the needs of the men and women separately, based on their estimated daily iron intake and a series of absorption values ranging from 1–40%. The prevalence of SF concentrations below selected cut-off values (indicating that absorption was not high enough to maintain iron stores) was derived from individual SF concentrations. An estimate of dietary iron absorption required to maintain specified SF values was then calculated by matching the observed prevalence of insufficiency with the prevalence predicted for the series of absorption estimates. Mean daily dietary iron intakes were 13.5 mg for men and 9.8 mg for women. Mean calculated dietary absorption was 8% in men (50th percentile for SF 85 µg/L) and 17% in women (50th percentile for SF 38 µg/L). At a ferritin level of 45 µg/L estimated absorption was similar in men (14%) and women (13%). This new method can be used to calculate dietary iron absorption at a population level using data describing total iron intake and SF concentration

Non-renormalization theorems in softly broken SQED and the soft β\beta-functions

The renormalization of softly broken SQED is related to the one of supersymmetric QED by using the construction with a local gauge supercoupling and by taking into account softly broken anomalous axial U(1) symmetry. From this extended model one obtains the non-renormalization theorems of SQED and the counterterms of the soft breaking parameters as functions of the supersymmetric counterterms. Due to the Adler-Bardeen anomaly of the axial current an invariant regularization scheme does not exist, and therefore the $\beta$-functions of soft breaking parameters are derived from an algebraic construction of the Callan-Symanzik equation and of the renormalization group equation. We obtain the soft $\beta$-functions in terms of the gauge $\beta$-function and of the anomalous dimension of the supersymmetric matter mass. In particular, we find that the X-term of the scalar mass $\beta$-function as well as the gauge $\beta$-function in $l\geq 2$ are due to the Adler-Bardeen anomaly of the axial symmetry.Comment: 28 page

Some Remarks On Gauge-Mediated Supersymmetry Breaking

We investigate the communication of supersymmetry breaking to the Standard Model in theories of gauge mediated supersymmetry breaking with general weakly coupled messenger sectors. We calculate the one loop gaugino and two loop soft scalar masses for nonvanishing Str M^2 of the messenger sector. The soft scalar masses are sensitive to physics at scales higher than the messenger scale, in contrast to models with vanishing messenger supertrace. We discuss the implications of this ultraviolet sensitivity in theories with renormalizable and nonrenormalizable supersymmetry breaking sectors. We note that the standard relation, in minimal gauge mediation, between soft scalar and gaugino masses is altered in models with nonvanishing messenger supertrace.Comment: 14 pages, LaTeX, uses epsf, 4 .eps figures included; minor corrections,version to appear in Phys.Lett.

Exact beta-functions in softly-broken N=2 Chern-Simons matter theories

We present exact results for the beta-functions for the soft-breaking parameters in softly-broken N=2 Chern-Simons matter theories in terms of the anomalous dimension in the unbroken theory. We check our results explicitly up to the two loop level.Comment: 11 pages; 3 figures; references adde

Loss of CD4+ T cell-intrinsic arginase 1 accelerates Th1 response kinetics and reduces lung pathology during influenza infection

Arginase 1 (Arg1), the enzyme catalyzing the conversion of arginine to ornithine, is a hallmark of IL-10-producing immunoregulatory M2 macrophages. However, its expression in T cells is disputed. Here, we demonstrate that induction of Arg1 expression is a key feature of lung CD4+ T cells during mouse in vivo influenza infection. Conditional ablation of Arg1 in CD4+ T cells accelerated both virus-specific T helper 1 (Th1) effector responses and its resolution, resulting in efficient viral clearance and reduced lung pathology. Using unbiased transcriptomics and metabolomics, we found that Arg1-deficiency was distinct from Arg2-deficiency and caused altered glutamine metabolism. Rebalancing this perturbed glutamine flux normalized the cellular Th1 response. CD4+ T cells from rare ARG1-deficient patients or CRISPR-Cas9-mediated ARG1-deletion in healthy donor cells phenocopied the murine cellular phenotype. Collectively, CD4+ T cell-intrinsic Arg1 functions as an unexpected rheostat regulating the kinetics of the mammalian Th1 lifecycle with implications for Th1-associated tissue pathologies

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

Pretty Polly Perkins: Fox-Trot Song

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