Evidence for (and Against) Progenitor Bias in the Size Growth of Compact Red Galaxies

Most massive passive galaxies are compact at high redshifts, but similarly compact massive galaxies are rare in the local universe. The most common interpretation of this phenomenon is that massive galaxies have grown in size by a factor of about five since redshift z=2. An alternative explanation is that recently quenched massive galaxies are larger (a "progenitor bias"). In this paper we explore the importance of progenitor bias by looking for systematic differences in the stellar populations of compact early-type galaxies in the DEEP2 survey as a function of size. Our analysis is based on applying the statistical technique of bootstrap resampling to constrain differences in the median ages of our samples and to begin to characterize the distribution of stellar populations in our co-added spectra. The light-weighted ages of compact early-type galaxies at redshifts 0.5 < z < 1.4 are compared to those of a control sample of larger galaxies at similar redshifts. We find that massive compact early-type galaxies selected on the basis of red color and high bulge-to-total ratio are younger than similarly selected larger galaxies, suggesting that size growth in these objects is not driven mainly by progenitor bias, and that individual galaxies grow as their stellar populations age. However, compact early-type galaxies selected on the basis of image smoothness and high bulge-to-total ratio are older than a control sample of larger galaxies. Progenitor bias will play a significant role in defining the apparent size changes of early-type galaxies if they are selected on the basis of the smoothness of their light distributions.Comment: 39 pages, 10 figures. Astrophysical Journal (in press

Clinical practice guideline for best practice management of pediatric patients by chiropractors: Results of a Delphi consensus process

Objective: To build upon existing recommendations on best practices for chiropractic management of children by conducting a formal consensus process and best evidence synthesis. Design: Best practice guide based on recommendations from current best available evidence and formal consensus of a panel of experienced practitioners, consumers, and experts for chiropractic management of pediatric patients. Methods: Synthesis of results of a literature search to inform the development of recommendations from a multidisciplinary steering committee, including experts in pediatrics, followed by a formal Delphi panel consensus process. Results: The consensus process was conducted June to August 2022. All 60 panelists completed the process and reached at least 80% consensus on all recommendations after three Delphi rounds. Recommendations for best practices for chiropractic care for children addressed these aspects of the clinical encounter: patient communication, including informed consent; appropriate clinical history, including health habits; appropriate physical examination procedures; red flags/contraindications to chiropractic care and/or spinal manipulation; aspects of chiropractic management of pediatric patients, including infants; modifications of spinal manipulation and other manual procedures for pediatric patients; appropriate referral and comanagement; and appropriate health promotion and disease prevention practices. Conclusion: This set of recommendations represents a general framework for an evidence-informed and reasonable approach to the management of pediatric patients by chiropractors

Impaired IL-23-dependent induction of IFN-gamma underlies mycobacterial disease in patients with inherited TYK2 deficiency

Human cells homozygous for rare loss-of-expression (LOE) TYK2 alleles have impaired, but not abolished, cellular responses to IFN-alpha/beta (underlying viral diseases in the patients) and to IL-12 and IL-23 (underlying mycobacterial diseases). Cells homozygous for the common P1104A TYK2 allele have selectively impaired responses to IL-23 (underlying isolated mycobacterial disease). We report three new forms of TYK2 deficiency in six patients from five families homozygous for rare TYK2 alleles (R864C, G996R, G634E, or G1010D) or compound heterozygous for P1104A and a rare allele (A928V). All these missense alleles encode detectable proteins. The R864C and G1010D alleles are hypomorphic and loss-of-function (LOF), respectively, across signaling pathways. By contrast, hypomorphic G996R, G634E, and A928V mutations selectively impair responses to IL-23, like P1104A. Impairment of the IL-23-dependent induction of IFN-gamma is the only mechanism of mycobacterial disease common to patients with complete TYK2 deficiency with or without TYK2 expression, partial TYK2 deficiency across signaling pathways, or rare or common partial TYK2 deficiency specific for IL-23 signaling.ANRS Nord-Sud ; CIBSS ; CODI ; Comité para el Desarrollo de la Investigación ; Fulbright Future Scholarshi

Three novel forms of autosomal recessive TYK2 deficiency

Human cells homozygous for rare loss-of-expression (LOE) TYK2 alleles have impaired, but not abolished, cellular responses to IFN-α/β (underlying viral diseases in the patients) and to IL-12 and IL-23 (underlying mycobacterial diseases). Cells homozygous for the commonP1104A TYK2 allele have selectively impaired responses to IL-23 (underlying isolated mycobacterial disease). We report three new forms of TYK2 deficiency in six patients from five families homozygous for rare TYK2 alleles (R864C, G996R, G634E, or G1010D) or compound heterozygous for P1104A and a rare allele (A928V). All these missense alleles encode detectable proteins. The R864C and G1010D alleles are hypomorphic and loss-of-function (LOF), respectively, across signaling pathways. By contrast, hypomorphic G996R, G634E, and A928V mutations selectively impair responses to IL-23, like P1104A. Impairment of the IL-23–dependent induction of IFN-γ is the only mechanism of mycobacterial disease common to patients with complete TYK2 deficiency with or without TYK2 expression, partial TYK2 deficiency across signaling pathways, or rare or common partial TYK2 deficiency specific for IL-23 signaling

Risk of COVID-19 after natural infection or vaccinationResearch in context

Summary: Background: While vaccines have established utility against COVID-19, phase 3 efficacy studies have generally not comprehensively evaluated protection provided by previous infection or hybrid immunity (previous infection plus vaccination). Individual patient data from US government-supported harmonized vaccine trials provide an unprecedented sample population to address this issue. We characterized the protective efficacy of previous SARS-CoV-2 infection and hybrid immunity against COVID-19 early in the pandemic over three-to six-month follow-up and compared with vaccine-associated protection. Methods: In this post-hoc cross-protocol analysis of the Moderna, AstraZeneca, Janssen, and Novavax COVID-19 vaccine clinical trials, we allocated participants into four groups based on previous-infection status at enrolment and treatment: no previous infection/placebo; previous infection/placebo; no previous infection/vaccine; and previous infection/vaccine. The main outcome was RT-PCR-confirmed COVID-19 >7–15 days (per original protocols) after final study injection. We calculated crude and adjusted efficacy measures. Findings: Previous infection/placebo participants had a 92% decreased risk of future COVID-19 compared to no previous infection/placebo participants (overall hazard ratio [HR] ratio: 0.08; 95% CI: 0.05–0.13). Among single-dose Janssen participants, hybrid immunity conferred greater protection than vaccine alone (HR: 0.03; 95% CI: 0.01–0.10). Too few infections were observed to draw statistical inferences comparing hybrid immunity to vaccine alone for other trials. Vaccination, previous infection, and hybrid immunity all provided near-complete protection against severe disease. Interpretation: Previous infection, any hybrid immunity, and two-dose vaccination all provided substantial protection against symptomatic and severe COVID-19 through the early Delta period. Thus, as a surrogate for natural infection, vaccination remains the safest approach to protection. Funding: National Institutes of Health

Risk of COVID-19 after natural infection or vaccinationResearch in context

Background: While vaccines have established utility against COVID-19, phase 3 efficacy studies have generally not comprehensively evaluated protection provided by previous infection or hybrid immunity (previous infection plus vaccination). Individual patient data from US government-supported harmonized vaccine trials provide an unprecedented sample population to address this issue. We characterized the protective efficacy of previous SARS-CoV-2 infection and hybrid immunity against COVID-19 early in the pandemic over three-to six-month follow-up and compared with vaccine-associated protection. Methods: In this post-hoc cross-protocol analysis of the Moderna, AstraZeneca, Janssen, and Novavax COVID-19 vaccine clinical trials, we allocated participants into four groups based on previous-infection status at enrolment and treatment: no previous infection/placebo; previous infection/placebo; no previous infection/vaccine; and previous infection/vaccine. The main outcome was RT-PCR-confirmed COVID-19 >7–15 days (per original protocols) after final study injection. We calculated crude and adjusted efficacy measures. Findings: Previous infection/placebo participants had a 92% decreased risk of future COVID-19 compared to no previous infection/placebo participants (overall hazard ratio [HR] ratio: 0.08; 95% CI: 0.05–0.13). Among single-dose Janssen participants, hybrid immunity conferred greater protection than vaccine alone (HR: 0.03; 95% CI: 0.01–0.10). Too few infections were observed to draw statistical inferences comparing hybrid immunity to vaccine alone for other trials. Vaccination, previous infection, and hybrid immunity all provided near-complete protection against severe disease. Interpretation: Previous infection, any hybrid immunity, and two-dose vaccination all provided substantial protection against symptomatic and severe COVID-19 through the early Delta period. Thus, as a surrogate for natural infection, vaccination remains the safest approach to protection. Funding: National Institutes of Health