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Background: Hospitals play a crucial role in responding to disasters and public health emergencies. However, they are also vulnerable to threats such as fire or flooding and can fail to respond or evacuate adequately due to unpreparedness and lack of evacuation measures. The United Nations Office for Disaster Risk Reduction has emphasised the importance of partnerships and capacity building in disaster response. One effective way to improve and develop disaster response is through exercises that focus on collaboration and leadership. This study aimed to examine the effectiveness of using the 3-level collaboration (3LC) exercise in developing collaboration and leadership in districts in Thailand, using the concept of flexible surge capacity (FSC) and its collaborative tool during a hospital evacuation simulation., Methods: A mixed-method cross-sectional study was conducted with 40 participants recruited from disaster-response organisations and communities. The data from several scenario-based simulations were collected according to the collaborative elements (Command and control, Safety, Communication, Assessment, Triage, Treatment, Transport), in the disaster response education, "Major Incident Medical Management and Support" using self-evaluation survey pre- and post-exercises, and direct observation., Results: The 3LC exercise effectively facilitated participants to gain a mutual understanding of collaboration, leadership, and individual and organisational flexibility. The exercise also identified gaps in communication and the utilisation of available resources. Additionally, the importance of early community engagement was highlighted to build up a flexible surge capacity during hospital evacuation preparedness., Conclusions: the 3LC exercise is valuable for improving leadership skills and multiagency collaboration by incorporating the collaborative factors of Flexible Surge Capacity concept in hospital evacuation preparedness., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Background: Since its initial appearance in December 2019, coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread globally. Wastewater surveillance has been demonstrated as capable of identifying infection clusters early. The purpose of this study was to investigate a quick and simple method to detect SARS-CoV-2 in wastewater in Thailand during the early stages of the second outbreak wave when the prevalence of the disease and the virus concentration in wastewater were low., Methods: Wastewater samples were collected from a hospital caring for patients with COVID-19 and from 35 markets, two of which were associated with recently reported COVID-19 cases. Then, samples were concentrated by membrane filtering prior to SARS-CoV-2 detection by RT-qPCR., Results: SARS-CoV-2 RNA was detected in the wastewater samples from the hospital; the Ct values for the N, ORF1ab, and S genes progressively increased as the number of patients admitted to the treatment floor decreased. Notably, the ORF1ab and S genes were still detectable in wastewater even when only one patient with COVID-19 remained at the hospital. SARS-CoV-2 RNA was detected in the wastewater samples from fresh market where COVID-19 cases were reported., Conclusions: Our findings suggest that wastewater surveillance for SARS-CoV-2 is sensitive and can detect the virus even in places with a high ambient temperature and relatively low prevalence of COVID-19., Competing Interests: The authors declare conflicts of interest., (Copyright © 2022 Supranee Thongpradit et al.)

Objectives: The coronavirus disease 2019 (COVID-19) has become a worst pandemic. The clinical characteristics vary from asymptomatic to fatal. This study aims to examine the association between body mass index (BMI) levels and the severity of COVID-19., Methods and Study Design: A cohort study included 147 adult patients with confirmed COVID-19 were categorized into 4 groups by BMI levels on admission: <18.5 (underweight), 18.5-22.9 (normal weight), 23.0-24.9 (overweight), and ≥25.0 kg/m2 (obese). Rates of pneumonia, severe pneumonia, acute kidney injury (AKI), and ICU stay during hospitalization across BMI group was determined. Logistic regression analysis was used to determine the association between BMI and severe pneumonia., Results: Of the totals, patients having a BMI <18.5, 18.5-22.9, 23.0-24.9, and ≥25.0 kg/m2 were 12.9%, 38.1%, 17.7%, and 31.3%, respectively. The rates of pneumonia and severe pneumonia tended to be higher in patients with higher BMI, whereas the rates of AKI and ICU stay were higher in patients with BMI <18.5 kg/m2 and ≥ 25 kg/m2, when compared to patients with normal BMI. After controlling for age, sex, diabetes, hypertension and dyslipidemia in the logistic regression analysis, having a BMI ≥25.0 kg/m2 was associated with higher risk of severe pneumonia (OR 4.73; 95% CI, 1.50-14.94; p = 0.003) compared to having a BMI 18.5-22.9 kg/m2. During admission, elevated hemoglobin and alanine aminotransferase levels on day 7 and 14 of illness were associated with higher BMI levels. In contrast, rising of serum creatinine levels was observed in underweight patients on days 12 and 14 of illness., Conclusions: Obesity in patients with COVID-19 was associated with severe pneumonia and adverse outcomes such as AKI, transaminitis and ICU stay. Underweight patients should be closely monitored for AKI. Further studies in body composition are warranted to explore the links between adiposity and COVID-19 pathogenesis., Competing Interests: The authors have declared that no competing interests exist.

A live-attenuated DEN-2 virus, DEN-2 strain 16681-PDK53, has been found to be attenuated for both humans and mice with an unknown mechanism. To partially answer this question, responses of flavivirus-naïve primary human PBMC to infection with attenuated DEN-2 PDK53 (D2/IC-VV45R) virus and its parental, virulent DEN-2 16681 virus (D2/IC-30P-A) were investigated at the cellular and genetic levels using cDNA array analysis. Both DEN-2 viruses produced similar replication kinetics in flavivirus-naïve PBMC. In contrast, virulent DEN-2 virus caused a higher percentage of apoptotic death. A macro-array analysis showed that the virulent D2/IC-30P-A virus induced changes in the expression of a greater number of genes than did the attenuated D2/IC-VV45R virus, 31 genes versus 19 genes, respectively, by 24 h post-infection. Interestingly, both viruses stimulated cytokines known to be virulence factors for DEN virus infection, such as IL-1beta, IL-6, IL-8, IL-10, MIP-1beta, and MIP-1alpha. The virulent virus additionally up-regulates immune suppression factors and down-regulates immune activator and growth factors. In conclusion, our data demonstrated that D2-PDK53 effected less change in PBMC than D2-16681 in terms of observable cellular effect and expression of cytokine and chemokine related genes.

Systemic lupus erythematosus (SLE) is a complex autoimmune disorder that affects various organs and systems. Increased apoptosis, together with defects in the uptake of apoptotic bodies, are thought to have a pathogenic role in SLE. By detection of chromatin condensation, 30% of apoptosis was detected in peripheral blood mononuclear cells (PBMC) from Thai patients with active SLE. Therefore, understanding of the molecular processes in PBMC apoptosis may allow us to gain insight into pathophysiology of SLE. Thus, genes involved in the apoptosis of PBMC from these patients were investigated ex vivo by cDNA array analysis. Seventeen apoptosis-related genes were stimulated in active SLE, more than twofold higher than in inactive SLE. These genes are classified into six groups, namely death receptors, death ligands, caspases, bcl-family, and neutral proteases and genes involved in endoplasmic reticulum stress-mediated apoptosis, such as caspase-4 and GADD153. Among those stimulated genes, tumor necrosis factor (TNF) and the TNF-receptor family were drastically up-regulated 60- and 19-fold higher than in healthy controls, respectively. Moreover, the degree of apoptosis correlated with the level of TNF-alpha in plasma, suggesting that the TNF family plays a role in the induction of apoptosis in SLE. To verify this hypothesis, PBMC from healthy individuals were treated with plasma from active SLE patients in the presence or absence of etanercept, a TNF inhibitor. In the presence of etanercept, active SLE plasma reduced the level of apoptosis to 26.43%. In conclusion, massive apoptotic death of PBMC occurred during the active stage of SLE. The molecular pathway of SLE-PBMC apoptosis was mediated at least via TNF/TNFR signaling pathway, which was confirmed by functional test of TNF-alpha in SLE patients' plasma.

Rabies virus (RABV) is able to induce apoptotic death of target cells. The molecular pathway of RABV-induced cell death is partially known. In the present study, cDNA array analysis was used as a tool to screen for pro-apoptotic genes that may be involved in RABV induction. RNA was extracted from the infected CNS and from mock-infected controls. When the mean gene expression was compared between the infected group and controls, 21 potential apoptotic genes were identified that exhibited more than 2.5-fold difference in their expression levels. These 21 genes can be grouped into two groups, those genes that participate in the commitment phase and those that play a role as executioners. Examples of genes in commitment phase were death receptors (Fas-L receptor, TNF-receptor), lysosomal proteases, calpain, caspase-1, signaling molecules (ERK, p38MAPK) and bcl-2 family members. Cytochrome c and caspase-3 were representatives of executioners. Based on types of genes activated during the commitment phase, two independent apoptotic mechanisms may be activated in response to the RV infection. The first is immune-mediated death which may operate through the receptor-ligand pathway activated by caspase-1 and the pro-inflammatory cytokine, IL-1beta. The other mechanism is a protease-mediated process which involves lysosomal proteases and calcium-dependent neutral proteases. These two stimulating pathways were followed by Bad, Bak, Bid activation and subsequently the upregulation of cytochrome c and caspase-3. In addition, mobilization of K+ ion and other accessory apoptotic genes such as annexins and clusterin were also upregulated.