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Little is known regarding the extent by which patients undergoing outpatient cataract surgery are at risk for postoperative hospitalization. We sought to determine the percentage of patients undergoing cataract surgery who were subsequently hospitalized, the patient characteristics associated with postoperative hospitalization, and the reasons for hospitalization.We identified all beneficiaries of a large U.S. managed care network age ≥40 years old who underwent ≥1 cataract surgery from 2001-2011. All enrollees who required inpatient hospitalization within 7, 14, 30, and 90 days following initial cataract surgery and the reasons for hospitalization were determined. Logistic regression was performed to assess factors that significantly impacted the odds of requiring postoperative hospitalization.Among the 64,981 patients who underwent cataract surgery, rates of hospitalization within 7, 14, 30, and 90 days were 0.3%, 0.5%, 1.3% and 4.2%, respectively. Among the 10,674 patients who had no major preexisting medical comorbidities, 0.1% were hospitalized within 7 days. The odds of hospitalization increased by 35% (OR = 1.35 [CI, 1.23-1.48]) with the presence of each additional comorbidity and by 14% with each additional hospitalization in the 3 years prior to cataract surgery (OR = 1.14 [CI, 1.10-1,18]). Those who were hospitalized in the 30 days prior to cataract surgery had 524% increased odds of being hospitalized within 7 days after cataract surgery (OR = 6.24, [CI, 3.37-11.57]) compared to those with no record of preoperative hospitalization. Postoperative hospitalizations were most commonly due to cardiovascular conditions, comprising over 25% of primary diagnoses associated with hospitalization.The risk of hospitalization after cataract surgery is low, and is very low among those with no major preexisting medical comorbidities. Opportunities may exist to limit comprehensive preoperative evaluation and testing to those who have serious pre-existing medical comorbidities.

Background: Following reduction of public health and social measures concurrent with SARS-CoV-2 Omicron emergence in late 2021 in Australia, COVID-19 case notification rates rose rapidly. As rates of direct viral testing and reporting dropped, true infection rates were most likely to be underestimated., Objective: To better understand infection rates and immunity in this population, we aimed to estimate SARS-CoV-2 seroprevalence in Australians aged 0-19 years., Methods: We conducted a national cross sectional serosurvey from June 1, 2022, to August 31, 2022, in children aged 0-19 years undergoing an anesthetic procedure at eight tertiary pediatric hospitals. Participant questionnaires were administered, and blood samples tested using the Roche Elecsys Anti-SARS-CoV-2 total spike and nucleocapsid antibody assays. Spike and nucleocapsid seroprevalence adjusted for geographic and socioeconomic imbalances in the participant sample compared to the Australian population was estimated using multilevel regression and poststratification within a Bayesian framework., Results: Blood was collected from 2,046 participants (median age: 6.6 years). The overall adjusted seroprevalence of spike-antibody was 92.1% (95% credible interval (CrI) 91.0-93.3%) and nucleocapsid-antibody was 67.0% (95% CrI 64.6-69.3). In unvaccinated children spike and nucleocapsid antibody seroprevalences were 84.2% (95% CrI 81.9-86.5) and 67.1% (95%CrI 64.0-69.8), respectively. Seroprevalence was similar across geographic remoteness index and socioeconomic quintiles. Nucleocapsid antibody seroprevalence increased with age while the point seroprevalence of the spike antibody seroprevalence decreased in the first year of life and then increased to 97.8 (95% Crl 96.1-99.2) by 12-15 years of age., Conclusion: Most Australian children and adolescents aged 0-19 years, across all jurisdictions were infected with SARS-CoV-2 by August 2022, suggesting rapid and uniform spread across the population in a very short time period. High seropositivity in unvaccinated children informed COVID-19 vaccine recommendations in Australia., Competing Interests: All authors have no financial interests/personal relationships that may be considered as potential competing interests with this study. Some authors have received institutional research grants and travel funding from the Australian Government, non-government or private organisations for other bodies of work. Dr Archana Koirala, Professor Kristine Macartney and Professor Nicholas Wood declare funding support from the Australian Government Department of Health and Aged Care (DoHAC) to the institution National Centre for Immunisation Research and Surveillance (NCIRS). Dr Archana Koirala has received a travel and accommodation grant to present and attend the World Society of Paediatric Infectious Diseases scientific meeting in 2023. Professor Kristine Macartney received payment as an expert witness for Australian Health Departments against proceedings against COVID-19 health regulations in 2021-2022. Professor Kristine Macartney declares institutional directed funding support from the WHO and GAVI the Vaccine Alliance, Welcome Trust and the Australian NHMR, to NCIRS and the University of Sydney; payment as an expert witness for Australian health departments against proceedings against COVID-19 health regulations in 2021-2022, payment less than USD $5,000 for international travel for expert speaking engagements, non-pharmaceutical company sources. Professor Nicholas Wood, Professor Britta S von Ungern-Sternberg and Dr Brendan McMullan declare funding from the National Health and Medical Research Council (NHMRC) grants. Professor Britta S von Ungern-Sternberg declared funding support from Stan Perron Charitable Foundation. Professor Helen S Marshall declares a research grant from Pfizer to Women’s and Children’s Health Network (WCHN), no personal remuneration, for meningococcal research. Professor Peter Richmond declares research grants from Merck Sharpe & Dohme, GlaxoSmithKline (GSK) directed at the Telethon Kids Institute (TKI), no personal remuneration, on RSV, pneumococcal disease, varicella, meningococcal research and a COVID-19 vaccine study to assess immunogenicity and safety of homologous or heterologous vaccine schedules. Professor Peter Richmond, Professor Helen S Marshall and Professor Nicholas Wood declare a research grant from the Australian Government Department of Health and Aged Care to WCHN, TKI and University of Sydney for a COVID-19 DNA vaccine clinical trial Ms Alissa McMinn declares funding support from Pfizer provided support for flights/accommodation to attend the Public Health Association Australia Communicable Diseases & Immunisation Conference in 2023. Dr Ushma Wadia declares funding from Pfizer for flights and accommodation to attend Meningococcal Disease Vaccine Education in 2023. This does not alter our adherence to PLOS ONE policies on sharing data and materials., (Copyright: © 2024 Koirala et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

GNE myopathy (GNEM), also known as hereditary inclusion body myopathy (HIBM), is a late- onset, progressive myopathy caused by mutations in the GNE gene encoding the enzyme responsible for the first regulated step in the biosynthesis of sialic acid (SA). The disease is characterized by distal muscle weakness in both the lower and upper extremities, with the quadriceps muscle relatively spared until the late stages of disease. To explore the role of SA synthesis in the disease, we conducted a comprehensive and systematic analysis of both free and total SA levels in a large cohort of GNEM patients and a mouse model. A sensitive LC/MS/MS assay was developed to quantify SA in serum and muscle homogenates. Mean serum free SA level was 0.166 μg/mL in patients and 18% lower (p<0.001) than that of age-matched control samples (0.203 μg/mL). In biopsies obtained from patients, mean free SA levels of different muscles ranged from 0.046-0.075 μg/μmol Cr and were markedly lower by 72-85% (p<0.001) than free SA from normal controls. Free SA was shown to constitute a small fraction (3-7%) of the total SA pool in muscle tissue. Differences in mean total SA levels in muscle from patients compared with normal controls were less distinct and more variable between different muscles, suggesting a small subset of sialylation targets could be responsible for the pathogenesis of GNEM. Normal quadriceps had significantly lower levels of free SA (reduced by 39%) and total SA (reduced by 53%) compared to normal gastrocnemius. A lower SA requirement for quadriceps may be linked to the reported quadriceps sparing in GNEM. Analysis of SA levels in GneM743T/M743T mutant mice corroborated the human study results. These results show that serum and muscle free SA is severely reduced in GNEM, which is consistent with the biochemical defect in SA synthesis associated with GNE mutations. These results therefore support the approach of reversing SA depletion as a potential treatment for GNEM patients.

For successful bone tissue engineering, a scaffold needs to be osteoconductive, porous, and biodegradable, thus able to support attachment and proliferation of bone cells and guide bone formation. Recently, hydroxyapatites (HA), a major inorganic component of natural bone, and biodegrade polymers have drawn much attention as bone scaffolds. The present study was designed to investigate whether the bone regenerative properties of nano-HA/polycaprolactone (PCL) spiral scaffolds are augmented in an HA dose dependent manner, thereby establishing a suitable composition as a bone formation material. Nano-HA/PCL spiral scaffolds were prepared with different weight ratios of HA and PCL, while porosity was introduced by a modified salt leaching technique. Human fetal osteoblasts (hFOBs) were cultured on the nano-HA/PCL spiral scaffolds up to 14 days. Cellular responses in terms of cell adhesion, viability, proliferation, differentiation, and the expression of bone-related genes were investigated. These scaffolds supported hFOBs adhesion, viability and proliferation. Cell proliferation trend was quite similar on polymer-ceramic and neat polymer spiral scaffolds on days 1, 7, and 14. However, the significantly increased amount of alkaline phosphatase (ALP) activity and mineralized matrix synthesis was evident on the nano-HA/PCL spiral scaffolds. The HA composition in the scaffolds showed a significant effect on ALP and mineralization. Bone phenotypic markers such as bone sialoprotein (BSP), osteonectin (ON), osteocalcin (OC), and type I collagen (Col-1) were semi-quantitatively estimated by reverse transcriptase polymerase chain reaction analysis. All of these results suggested the osteoconductive characteristics of HA/PCL nanocomposite and cell maturation were HA dose dependent. For instance, HA∶PCL = 1∶4 group showed significantly higher ALP mineralization and elevated levels of BSP, ON, OC and Col-I expression as compared other lower or higher ceramic ratios. Amongst the different nano-HA/PCL spiral scaffolds, the 1∶4 weight ratio of HA and PCL is shown to be the most optimal composition for bone tissue regeneration.