Citations

ABSTRACT The ninth American Society for Microbiology Conference on Biofilms was convened in-person on 13–17 November 2022 in Charlotte, NC. As the first of these conferences since prior to the start of the COVID-19 pandemic, the energy among the participants of the conference was clear, and the meeting was a tremendous success. The mixture of >330 oral and poster presentations resoundingly embodied the vitality of biofilm research across a wide range of topics and multiple scientific disciplines. Special activities, including a pre-conference symposium for early career researchers, further enhanced the attendee experience. As a general theme, the conference was deliberately structured to provide high levels of participation and engagement among early career scientists.

Background: Graft-versus-host disease (GVHD) is a common complication of hematopoietic cell transplantation, and its incidence is low in liver transplantation (LT). Estimating the incidence of GVHD after LT is challenging due to the paucity of available data from the United Network for Organ Sharing. This is the first national analysis of the incidence and risk factors of GVHD after LT. Methods: This retrospective cohort study used the National Readmission Database to calculate the incidence rate of GVHD within 1 year of LT using survival analysis. The predictors of GVHD were identified using univariate and multivariate Cox regression analyses. Results: From 2010 to 2020, of 88,433 LTs, 383 cases of GVHD occurred within 1 year after LT, resulting in an incidence rate of 1.0% (95% CI: 0.8%–1.3%). We observed no statistically significant change in the incidence of GVHD after LT from 2010 to 2020 (beta-coefficient, −0.07%; 95% CI: −0.17% to 0.04%, p = 0.188). Interestingly, alcohol-associated liver disease was associated with a lower risk of GVHD (adjusted HR, 0.57; 95% CI: 0.36–0.91, p = 0.018), whereas a higher risk was found to be related to a secondary diagnosis of COVID-19 on index admission. Conclusion: Our study found that the incidence rate of GVHD within 1 year of LT in the United States was 1.0% and remained stable from 2010 to 2020. The predictors associated with GVHD include alcohol-associated liver disease and COVID-19. Our study provides valuable insights into the incidence, risk factors, and outcomes of GVHD after LT.

Background: Tobacco smoking during pregnancy is associated with metabolic dysfunction in children, but mechanistic insights remain limited. Hypomethylation of cg05575921 in the aryl hydrocarbon receptor repressor (AHRR) gene is associated with in utero tobacco smoke exposure. In this study, we evaluated whether AHRR hypomethylation mediates the association between maternal smoking and metabolic dysfunction in children. Methods: We assessed metabolic dysfunction using liver fat content (LFC), serum, and clinical data in children aged 7–12 years (n=78) followed since birth. Maternal smoking was self-reported at 12 weeks gestation. Methylation was measured by means of pyrosequencing at 3 sequential CpG sites, including cg05575921, at birth and at ages 7–12. Regression models were used to evaluate whether AHRR methylation mediated the association between maternal smoking and child metabolic dysfunction. Results: Average AHRR methylation at birth was significantly higher among children of nonsmoking mothers compared with children of mothers who smoked (69.8% ± 4.4% vs. 63.5% ± 5.5, p=0.0006). AHRR hypomethylation at birth was associated with higher liver fat content (p=0.01), triglycerides (p=0.01), and alanine aminotransferase levels (p=0.03), and lower HDL cholesterol (p=0.01) in childhood. AHRR hypomethylation significantly mediated associations between maternal smoking and liver fat content (indirect effect=0.213, p=0.018), triglycerides (indirect effect=0.297, p=0.044), and HDL cholesterol (indirect effect = -0.413, p=0.007). AHRR methylation in childhood (n=78) was no longer significantly associated with prenatal smoke exposure or child metabolic parameters (p>0.05). Conclusions: AHRR hypomethylation significantly mediates the association between prenatal tobacco smoke exposure and features of childhood metabolic dysfunction, despite the lack of persistent hypomethylation of AHRR into childhood. Further studies are needed to replicate these findings and to explore their causal and long-term significance.

Context.— Respiratory infections complicate lung transplantation and increase the risk of allograft dysfunction. Allograft lungs may have different susceptibilities to infection than native lungs, potentially leading to different disease severity in lungs of single lung transplant recipients (SLTRs). Objective.— To study whether infections affect allograft and native lungs differently in SLTRs but similarly in double LTRs (DLTRs). Design.— Using an institutional database of LTRs, medical records were searched, chest computed tomography studies were systematically reviewed, and histopathologic features were recorded per lung lobe and graded semiquantitatively. A multilobar-histopathology score (MLHS) including histopathologic data from each lung and a bilateral ratio (MLHSratio) comparing histopathologies between both lungs were calculated in SLTRs and compared to DLTRs. Results.— Six SLTRs died of infection involving the lungs. All allografts showed multifocal histopathologic evidence of infection, but at least 1 lobe of the native lung was uninvolved. In 4 of 5 DLTRs, histopathologic evidence of infection was seen in all lung lobes. On computed tomography, multifocal ground-glass and/or nodular opacities were found in a bilateral distribution in all DLTRs but in only 2 of 6 SLTRs. In SLTRs, the MLHSAllograft was higher than MLHSNative (P = .02). The MLHSratio values of SLTR and DLTR were significantly different (P < .001). Conclusions.— Allograft and native lungs appear to harbor different susceptibilities to infections. The results are important for the management of LTRs.

Context.— Misdiagnosis of antiphospholipid syndrome can occur owing to the wide diversity of antiphospholipid (aPL) assays and a lack of international calibrators and harmonized reference intervals. Objective.— To assess laboratory practices regarding reporting and establishing reference intervals for immunoglobulin (Ig) G/IgM anti-cardiolipin (aCL) and anti–beta-2 glycoprotein I (anti-β2GPI) assays. Design.— Supplemental questions related to reporting and establishing reference ranges for aPL assays were sent as part of the Antiphospholipid Antibody (ACL)-B 2019 College of American Pathologists (CAP) proficiency testing survey. The response rate and methods assessment details were determined, as well as qualitative and quantitative results for 3 test samples. Results.— The number of participants reporting results for IgG aCL (n = 489), IgM aCL (n = 476), IgG anti-β2GPI (n = 354), and IgM anti-β2GPI (n = 331) varied by antibody type. The enzyme-linked immunosorbent assay (ELISA) (up to 58.6%, 260 of 444) was the most used method; others included multiplex (from 18.9% to 23.9%), fluorescence enzyme immunoassay (14.4%–17.6%), and chemiluminescence immunoassay (6.5%–9.0%). More respondents reported quantitative than qualitative results, and manufacturer cutoff ranges were used by 92.9% and 94.2% of respondents for aCL and anti-β2GPI, respectively. Despite variation in the use of semiquantitative ranges, qualitative negative/positive reporting of the test samples achieved almost 100% consensus. Qualitative consensus was met in contrast to the wide range of quantitative results obtained for each analyte across different kits. Conclusions.— ELISA remains the most used method for detecting aPL antibodies, with most laboratories reporting quantitative results based on manufacturers' suggested reference ranges. The categorization of quantitative results as equivocal, weak positive, or positive for responders using kits from the same manufacturer was variable.

This article discusses the widespread implementation of surgical video replay to improve technical and nontechnical performance of surgeons.

Summary HLA evolutionary divergence reflects the ability to recognize diverse neoantigens as non-self, and as a biomarker is conceptually distinct from programmed cell death ligand 1 expression and tumor mutation burden. HLA-based assays to predict benefit from immunotherapy in lung cancer require prospective validation. See related article by Jiang et al., p. 4830

AbstractPurposeDental amalgam contains mercury and is commonly used in dental restorations. The impact of MRI on mercury excretion from dental amalgam is not well understood across clinical field strengths, especially 7T. We investigated the effects of MRI exposure on mercury excretion using fresh, lab‐created dental amalgam restorations and in extracted teeth with old, pre‐existing restorations.MethodsDonated, unfilled human teeth (n = 120) were restored with amalgam before being stored in saline, artificial saliva, or a dry box prior to MRI scanning. The teeth were placed in individual tubes of fresh artificial saliva and scanned at 1.5T, 3T, or 7T or left unscanned as controls. Mercury concentrations were measured 24–30 h later. Donated teeth with pre‐existing restorations (n = 40) were stored in artificial saliva, scanned at 7T or left unscanned as controls, and mercury concentration tested.ResultsFor teeth extracted and restored in a laboratory, no significant difference was found (F = 2.42, P = 0.072) between mean mercury concentrations of unscanned teeth (13.72 μg/L) and teeth scanned at 1.5T (10.88 μg/L), 3T (12.65 μg/L), or 7T (8.88 μg/L). For teeth extracted with previously placed restorations, no significant difference (P = 0.288) was found between unscanned controls (4.28 μg/L) and teeth scanned at 7T (6.63 μg/L).ConclusionMRI of dental amalgam does not significantly increase mercury excretion at 1.5T, 3T, or 7T compared to unscanned teeth. This holds true for controlled laboratory restorations as well as for those placed and lived with prior to extraction and scanning, demonstrating no added risk to the clinical patient or research subject.