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To investigate whether seafarers in Norway who were declared unfit for service at sea or received a time-limited health certificate had a higher risk of acute somatic hospital admissions compared with those who received a full health certificate.
Registry-based cohort study.
Seafarers in Norway who presented to a seafarer’s doctor to obtain a health certificate between 2018 and 2019, as required for work aboard Norwegian vessels. The study was conducted within Norway’s publicly funded healthcare system.
Norwegian seafarers aged 18–70 years who underwent medical examinations (n=43 758), including n=5452 females (12.5%).
Acute somatic hospital admission within 2 years of medical examination. HRs were estimated using Cox regression models in two separate time periods (0–3 months and 3–24 months), with adjustment for possible confounding from age, gender, level of education and centrality of residence (proximity to healthcare services).
The crude risk of acute somatic hospital admissions was higher for individuals who received a declaration of unfitness, as compared with those who received a full health certificate, in both follow-up periods: 0–3 months (HR=5.13, 95% CI: 3.27 to 8.04) and 3–24 months (HR=2.63, 95% CI: 2.07 to 3.34). Similarly, those with time-limited health certificates had a higher risk in both periods: 0–3 months (HR=2.02, 95% CI: 1.39 to 2.93) and 3–24 months (HR=2.45, 95% CI: 2.15 to 2.79). Adjustment of the analyses for socio-demographic factors did not change the effect estimates substantially.
These findings highlight the importance of comprehensive and continuous health assessments to help prevent adverse health outcomes and ensure safety at sea, particularly among vulnerable subgroups of seafarers.
Existing patient-reported outcome measures (PROMs) do not meet accepted international criteria for measuring health outcomes of hypospadias treatment. This protocol describes the qualitative development (phase I) of a novel PROM to evaluate outcomes of hypospadias treatments.
Participants aged 7 years and older with hypospadias and caregivers of children under 8 years seeking treatment at Boston Children’s Hospital, Children’s Hospital of Eastern Ontario (CHEO), Children’s Hospital of Philadelphia (CHOP) and McMaster Children’s Hospital), will be invited to participate in concept elicitation and cognitive interviews. Concept elicitation interviews will be in-depth and semi-structured to understand concepts important to patients seeking treatment for hypospadias. Cognitive interviews will be performed concurrently to ensure that the scale items, instructions and response options are relevant, understandable and comprehensive. Cognitive interviews will be complemented by expert input. Concept elicitation and cognitive interview transcripts will be coded line-by-line. Participant quotes will be categorised into top-level domains, themes and subthemes. The primary outcome of this research will be to develop a conceptual model representing the patient experience of hypospadias and a novel PROM.
Ethics approval was obtained from Boston Children’s Hospital’s Institutional Review Board (HHS Registration: IRB00000352; Protocol number IRB-P00042425). CHOP, McMaster and CHEO have reliance agreements with Boston Children’s Hospital. Findings from this research will be disseminated at national and international conferences and published in relevant peer-reviewed journals for the target audience.
by Kenneth K.Y. Ting, Hisham M. Ibrahim, Nitya Gulati, Yufeng Wang, Jonathan V. Rocheleau, Myron I. Cybulsky
The formation of macrophage (Mφ) foam cells is a hallmark of atherosclerosis, yet how the process of lipid loading can modulate Mφ inflammatory responses by rewiring their intracellular metabolic circuits is not well understood. Our previous studies have shown that the accumulation of oxidized LDL (oxLDL) or free cholesterol in Mφs impaired their inflammatory response by suppressing HIF-1α-mediated glycolysis and upregulating NRF2 antioxidative response. However, it remains unclear if other metabolic processes are also contributory. In this study, we found that the accumulation of free cholesterol, but not oxLDL, in primary murine thioglycolate-elicited peritoneal Mφs (PMφs) enhanced a PARP1-dependent response associated with repair of DNA damage, which was characterized by poly ADP-ribosylation of proteins, phosphorylation of histone 2A.X and consumption of NAD + . Both oxLDL and cholesterol enhanced the PARP1 response after LPS stimulation. Treatment of PMφs with mitoTEMPO, a specific mitochondrial reactive oxygen species (mtROS) scavenger, alleviated mtROS during cholesterol loading, blocked the PARP1 response and partially restored LPS- induced inflammatory gene expression. In contrast to inhibition of PARP1 enzymatic activity, knockdown of PARP1 expression in RAW264.7 Mφs with siRNA elevated LPS-induced inflammatory gene expression. Overall, our study suggests that cholesterol accumulation triggers a PARP1 response to DNA damage in Mφs and that PARP1 inhibits LPS-mediated inflammation through a non-enzymatic function.
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