ABSTRACT
Background Past research has suggested a cross-sectional association between COVID-19-related discrimination and PTSD symptom severity. However, no cohort study has examined the longitudinal association that allows causal interpretation. Also, even if such an association genuinely exists, the mechanism remains unclear.Methods We conducted a two-year follow-up study, obtaining data from healthcare workers in a hospital setting. We first evaluated how COVID-19-related discrimination in 2021 was associated with subsequent PTSD symptom severity in 2023. Thereafter, we conducted causal mediation analysis to examine how this association was mediated by psychological distress in 2022, accounting for exposure-mediator interaction. Missing data were handled using random forest imputation.Results A total of 660 hospital staff were included. The fully adjusted model showed greater PTSD symptom severity in individuals who experienced any COVID-19-related discrimination compared with those without such experiences (β, 0.44; 95% CI, 0.04–0.90). Regarding each type of discrimination, perceived discrimination was associated with greater PTSD symptom severity (β, 0.52; 95% CI, 0.08–0.96), whereas verbal discrimination did not reach statistical significance. Psychological distress consistently mediated 28.1–38.8% of the observed associations.Conclusions COVID-19-related discrimination is associated with subsequent PTSD symptom severity in healthcare workers. Psychological distress may serve as an important mediator, underscoring the potential need for interventions targeting this factor.
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COVID-19 , Stress Disorders, Post-TraumaticABSTRACT
In order to determine recent behaviors in atmospheric polycyclic aromatic hydrocarbon (PAH) concentrations at the west end of Japan and to reveal the causes of these behaviors, atmospheric PAH concentrations were measured in suburban and forest sites of Nagasaki, Japan from 2017 to 2021. The results showed that the total concentration of PAHs decreased considerably by 60% and 57% in suburban and forest sites, respectively, over this period. When analyzed by season, the rate of decrease in winter was markedly high. Therefore, the decreasing behavior in PAH concentrations in Nagasaki in recent years was considered to be mainly due to less PAHs originating from cold continental regions such as northern China. In particular, the reduction in coal and biomass combustion for winter heating in households, the efforts to improve air quality, and the limitation of economic activities in response to COVID-19 were likely responsible for the decrease in atmospheric PAH concentrations. In addition, although the PAH concentrations decreased, there was no significant change in the breakdown of the number of benzene rings in the PAH or in the attributes of their sources.
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Background: Coronavirus disease 2019 (COVID-19)-associated pulmonary aspergillosis (CAPA) is a fatal complication in the general population. However, there are few reports on CAPA in patients undergoing hemodialysis (HD). Methods: This retrospective observational cohort study was conducted at a single center between December 2020 and June 2021. We enrolled 21 HD patients with COVID-19 undergoing treatment and divided them into two groups, CAPA and non-CAPA (COVID-19 with and without pulmonary aspergillosis), and evaluated their characteristics, clinical outcomes and comorbidities. Results: The log-rank test revealed that the 90-day survival rate after the initiation of treatment for COVID-19 was significantly lower in the CAPA (n = 6) than in the non-CAPA group (n = 15) (P = 0.0002), and the 90-day mortality rates were 66.6% and 0% in the CAPA and non-CAPA groups, respectively. In the CAPA group, four patients died due to respiratory failure (on Days 6 and 20), gastrointestinal bleeding (Day 8) and sepsis (Day 33); the reverse transcription-polymerase chain reaction (RT-PCR) for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remained positive when they died. The remaining two patients survived and the negative conversion of RT-PCR for SARS-CoV-2 was confirmed on Days 10 and 15. The negative conversion of serum (1, 3)-ß-d-glucan (BDG) was confirmed on Day 15 in one patient; the BDG remained positive on Day 64 in the other. Conclusions: CAPA is a fatal complication in HD patients and the general population. Therefore, clinicians should consider the possibility of testing for CAPA in patients undergoing HD. Mycological workups may be helpful for the early detection of CAPA.
ABSTRACT
Hypoxia is a common pathway to the progression of end-stage kidney disease. Retinoic acid-inducible gene I (RIG-I) encodes an RNA helicase that recognizes viruses including SARS-CoV2, which is responsible for the production of interferon (IFN)-α/ß to prevent the spread of viral infection. Recently, RIG-I activation was found under hypoxic conditions, and klotho deficiency was shown to intensify the activation of RIG-I in mouse brains. However, the roles of these functions in renal inflammation remain elusive. Here, for in vitro study, the expression of RIG-I and IFN-α/ß was examined in normal rat kidney (NRK)-52E cells incubated under hypoxic conditions (1% O2). Next, siRNA targeting RIG-I or scramble siRNA was transfected into NRK52E cells to examine the expression of RIG-I and IFN-α/ß under hypoxic conditions. We also investigated the expression levels of RIG-I and IFN-α/ß in 33 human kidney biopsy samples diagnosed with IgA nephropathy. For in vivo study, we induced renal hypoxia by clamping the renal artery for 10 min in wild-type mice (WT mice) and Klotho-knockout mice (Kl-/- mice). Incubation under hypoxic conditions increased the expression of RIG-I and IFN-α/ß in NRK52E cells. Their upregulation was inhibited in NRK52E cells transfected with siRNA targeting RIG-I. In patients with IgA nephropathy, immunohistochemical staining of renal biopsy samples revealed that the expression of RIG-I was correlated with that of IFN-α/ß (r = 0.57, P<0.001, and r = 0.81, P<0.001, respectively). The expression levels of RIG-I and IFN-α/ß were upregulated in kidneys of hypoxic WT mice and further upregulation was observed in hypoxic Kl-/- mice. These findings suggest that hypoxia induces the expression of IFN-α/ß through the upregulation of RIG-I, and that klotho deficiency intensifies this hypoxia-induced expression in kidneys.