Search Results (6,647)

Crisis management has become a critical strategic concern in hospitality, particularly following the COVID-19 pandemic, which exposed limitations in conventional approaches to preparedness, response, and recovery. Although existing hospitality crisis management research has generated valuable insights into individual crisis phases, a limited understanding exists regarding how preparedness, crisis response, and organizational learning interact as an integrated strategic process across the crisis lifecycle. Addressing this gap, this study examines strategic crisis management within Jakarta’s five-star hotel sector and develops an integrated understanding of crisis management across pre-crisis, during-crisis, and post-crisis phases. A constructivist grounded theory approach was employed based on in-depth semi-structured interviews with 25 senior hospitality leaders, including hotel executives, owners, and industry association representatives. The findings suggest that crisis management is best understood as an integrated strategic capability rather than a series of discrete emergency responses. Three interrelated theoretical dimensions emerged: Continuous Strategic Preparedness, characterized by adaptive readiness, environmental sensemaking, decision readiness, and financial preparedness; Coordinated Strategic Crisis Response, encompassing liquidity discipline, operational adaptation, workforce adaptability, leadership coordination, and cross-functional alignment; and Strategic Renewal Through Organizational Learning, involving the retention of effective crisis practices, capability strengthening, and strategic reorientation toward ongoing uncertainty. The study proposes an Integrated Strategic Crisis Management Framework for Hospitality Organizations that explains the mechanisms linking preparedness, response, and organizational learning as a cyclical capability-building process. By reconceptualizing crisis management as an integrated strategic capability rather than a phase-based operational response, the study contributes to hospitality crisis management scholarship and provides practical insights for hospitality organizations operating in increasingly uncertain environments. Full article

Background/Objectives: Post-COVID-19 syndrome (PCS) is frequently accompanied by pain, which may coexist with alterations in multiple health domains. However, pain in PCS has rarely been explored from a multidimensional approach combining subjective and objective measures. Objective: To describe pain in subjects with PCS using pain intensity and the pressure pain threshold (PPT), and to examine the associations between these measures and descriptive characteristics as well as health status. Methods: A cross-sectional observational study was conducted in 45 previously hospitalised adults with PCS. Pain intensity was assessed using the visual analogue scale and PPT was assessed by algometry. Health status included fatigue, dyspnoea, anxiety, depression, quality of life, functionality, frailty, physical activity, muscle quality, muscle strength, physical performance, and functional capacity. Analyses were conducted using SPSS v30.0. Results: Participants showed moderate pain intensity and variability in PPT, with a significant inverse association between both measures. Bivariate analyses showed that higher pain intensity and lower PPT were associated with worse physical, psychological, and functional outcomes. In regression analyses, pain intensity was associated with sex, length of hospital stay, PPT, and quality of life; PPT was associated with sex, pain intensity, and grip strength. Model explanatory capacity varied, and some models were not statistically significant. Conclusions: Subjects with PCS exhibited moderate pain intensity and variability in pain sensitivity, with an association between subjective and objective pain measures. Pain measures were associated with multiple health domains at the bivariate level, while regression analyses identified a limited number of associations with variable explanatory capacity. These findings support comprehensive pain assessment in PCS. Full article

This paper examines the structural changes that the Indian equity market has experienced between 2015 and 2025 under the influence of major macroeconomic and geopolitical shocks—including the November 2016 demonetisation, the IL&FS liquidity crisis of 2018, the COVID-19 pandemic of 2020–2021, the Russo–Ukrainian conflict of 2022, and the synchronised global monetary tightening of 2022–2024. The primary objective is to test whether the volatility-modelling architecture proposed by a 2017 benchmark study for the 1992–2016 period continues to hold under the structurally different post-2015 regime, and to identify how persistence, asymmetry, and ARCH-order properties have evolved across the BSE Sensex, NSE CNX Nifty, and twenty-seven sectoral indices. A unified GARCH-family framework comprising GARCH(1,1), GJR-GARCH(1,1), and GARCH(2,1) is estimated on daily log-returns over an eleven-year sample of approximately 2750 observations per index. The empirical evidence confirms that volatility clustering and persistence are pervasive in the post-2015 decade, with the persistence measure (α1 + β1) rising relative to the initial 2017 study for most indices. Asymmetric volatility has intensified—negative shocks generate disproportionately larger volatility responses than positive shocks, particularly in the banking, FMCG, and energy sectors. A higher-order GARCH(2,1) specification is the preferred model for four indices in which lag-2 ARCH effects remain significant or in which integrated-GARCH behaviour rules out the standard GARCH(1,1). The findings have direct implications for portfolio risk management, option pricing, and the design of prudential policy in an increasingly retail-driven and derivative-intensive market ecosystem. Full article

Background/Objectives: Cardiovascular involvement is among the most consequential sequelae of SARS-CoV-2 infection. Myocardial injury, arrhythmia, and thromboembolic disease have been characterized in depth, yet the relationship between COVID-19 and valvular heart disease (VHD), and its interplay with heart failure (HF), has received comparatively limited synthesis. This narrative review consolidates current evidence on the mechanisms, diagnosis, differential assessment, and clinical outcomes linking acute and post-acute COVID-19 to valvular dysfunction and to incident or worsening heart failure, with emphasis on practical implications for cardiologists and internists. Methods: We searched PubMed, Scopus, and Web of Science (January 2020–January 2026) for studies on valvular dysfunction, heart failure, myocardial injury, and endothelial pathology in SARS-CoV-2 infection, and synthesized findings narratively. Results: Convergent pathways—endothelial injury, systemic hyperinflammation, micro- and macrovascular thrombosis, and pressure–volume overload—contribute to functional and, less frequently, structural valvular changes. Available evidence suggests that clinically relevant post-COVID valvular abnormalities are more often secondary/functional (mitral and tricuspid regurgitation) than primary structural lesions, although dedicated prospective valvular studies remain scarce. Pre-existing severe VHD markedly worsens acute COVID-19 prognosis. Elevated NT-proBNP, troponin, and interleukin-6 consistently predict decompensation and mortality, and a substantial minority of survivors show persistent fibrotic pulmonary changes and restrictive ventilatory defects on follow-up (pulmonary rather than cardiac findings). Conclusions: Post-COVID valvular dysfunction appears, on currently available but largely indirect evidence, predominantly functional and inflammation-related, and may overlap with HFpEF phenotypes in selected patients when objective diagnostic criteria are fulfilled. Biomarker-guided, multimodality follow-up is reasonable in high-risk survivors, and prospective longitudinal studies with standardized valvular endpoints remain a priority. Dedicated longitudinal evidence on valvular outcomes specifically remains very limited. Full article

Background and Objectives: Recovering from COVID-19 does not always imply a full return to health and may lead to the development of post-COVID-19 syndrome. Post-COVID-19 manifestations include, among others, symptoms of depression and/or anxiety. The aim of the study was to assess the prevalence of anxiety and depressive disorders and to identify their exogenous and endogenous predictors in individuals with post-COVID-19 syndrome. Materials and Methods: The study included 200 participants (116 women and 84 men, aged 18–80) diagnosed with post-COVID-19 syndrome. Participants completed psychological assessments, including the Hospital Anxiety and Depression Scale (HADS), the Generalized Anxiety Disorder 7 (GAD-7), and the Beck Depression Inventory (BDI). Comorbidities were also evaluated. Results: Based on the HADS, anxiety was identified in 41.5% of respondents and depression in 39.5%. Generalized anxiety disorder was screened positive for 36.5% of respondents (GAD-7), while mild depression was observed in 37.0% (BDI). Among participants with post-COVID-19 syndrome and diabetes, the risk of developing depression was three times higher than in individuals without comorbidities. In smoking women with post-COVID-19 syndrome and diabetes, the risk of developing depressive disorders was estimated to exceed 90%. Conclusions: The risk of developing anxiety and depressive disorders in individuals with post-COVID-19 syndrome and multimorbidity is very high, highlighting the need for preventive psychological care, including targeted screening programs, for those at greatest risk. Full article

Background: Long-term care facility (LTCF) residents are highly susceptible to healthcare-associated infections, and prevention is challenging given frailty, dementia, communal living, and resource constraints. Environmental surface and air contamination contribute to transmission. Novel no-touch automated disinfection technologies have been studied in hospitals, but evidence specific to LTCFs is scarce. This scoping review summarizes recent LTCF-focused interventions, their effectiveness, and implementation considerations. Methods: This scoping review was conducted following the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) Checklist. We searched PubMed, Medline, Embase, CINAHL, and Scopus for observational or experimental studies evaluating environmental disinfection in LTCFs/nursing homes, excluding body decolonization, non-LTCF settings, and reviews/protocols. Two reviewers independently screened and extracted data via Covidence. This review has been registered on OSF (Open Science Framework). Results: Of 1491 records, 7 studies met the inclusion criteria (6 from the USA, 1 from Australia): one cluster randomized trial, one interrupted time series studies, three prospective observational studies, and two pre–post designs. Interventions included physical methods (HVAC-integrated UV/UVGI, continuous UVGI) and chemical approaches (dry hydrogen peroxide, room fogging plus chlorine dioxide wipes, hydrogen peroxide wipes). Outcomes were heterogeneous (surface SARS-CoV-2 RNA, COVID-19 attack/case rates, airborne/surface microbial loads, and one clinical endpoint—acute respiratory illness). Several studies reported reductions in environmental or airborne bioburden; however, UV-based studies did not demonstrate statistically significant reductions in clinical infections. Certainty was limited by small numbers, non-randomized designs, and diverse outcome measures. Conclusions: No-touch automated disinfection methods appear promising as supplements to standard infection prevention control bundles for reducing environmental contamination in LTCFs. Nevertheless, consistent clinical benefits are unproven. Rigorous, LTCF-tailored, adequately powered trials with standardized clinical and environmental outcomes, plus implementation and cost-effectiveness evaluations, are needed. Full article

Background/Objectives: Our prior epigenome-wide association study (EWAS) on multiple sclerosis (MS) identified myeloid-associated methylation signatures and an association with enhancer regions. Here we compared differential DNA methylation across three central nervous system inflammatory disorders: MS, neuromyelitis optica (NMO), and neurologic post-acute sequelae of COVID-19 (neuro-PASC). Methods: Whole-blood DNA was profiled on Infinium MethylationEPIC arrays. Analyses included EWAS at the CpG level, differentially methylation region (DMR) analysis, and gene regulatory-element enrichment using Locus Overlap Analysis (LOLA). Limma linear models were adjusted for race, EPIC array version, age, sex, disease-modifying treatment class, and blood cell composition. Results: All three diseases were associated with broad CpG-level differential methylation. The most robust findings were disease-specific DMR signatures in gene regulatory regions. All three diseases shared Lamin B1-anchored chromatin states as an architectural genomic feature but differed in immune regulatory transcription factor binding sites (TFBS), RNA polymerase (Pol II) occupancy, and DNase accessibility. MS was enriched for TFBS in myeloid CEBPB and SPI1/PU.1 and lymphocyte-associated RUNX3, EBF1, and BATF. MS hypomethylated DMRs were concentrated at active enhancers and myeloid TFBS, suggestive of chronic myeloid activation. NMO showed the clearest promoter and B lymphocyte associated profile. Neuro-PASC was associated with hematopoietic DNase accessibility and TFBS for BATF and EBF1. Conclusions: These results suggest that DNA methylation in MS, NMO, and neuro-PASC differ meaningfully in regulatory architecture rather than conforming to a single shared disease-associated methylation model. A long-term goal is to develop immune therapies for newly recognized diseases such as neuro-PASC. Full article

Background: COVID-19-related mobility restrictions may have affected physical activity and post-fracture care in older adults. This study compared outcomes before and after age-based mobility restrictions, focusing on reported activity, documented combined postoperative physiotherapy and anti-osteoporotic pharmacologic treatment, and secondary fragility fractures. Methods: This retrospective single-center pre–post study included patients aged 65 years or older who underwent bipolar hemiarthroplasty for low-energy osteoporotic femoral neck fracture. Patients treated during the year before restrictions were compared with those treated during the post-restriction year. Outcomes included reported pre-fracture activity category, all-cause mortality, mobility among survivors, documented combined postoperative physiotherapy and anti-osteoporotic pharmacologic treatment, and secondary fragility fractures. Results: The pre-pandemic and post-restriction groups included 65 and 122 patients, respectively. Regular outdoor walking/activity before fracture was less frequent in the post-restriction group than in the pre-pandemic group (45.1% vs. 72.3%; p < 0.001), whereas home-limited activity was more frequent (54.9% vs. 27.7%). All-cause mortality during follow-up was 24.6% and 29.5%, respectively (p = 0.499). Mobility among survivors did not differ significantly (p = 0.832). Among survivors, documented combined postoperative physiotherapy and anti-osteoporotic pharmacologic treatment was uncommon: 14.3% and 17.4%, respectively (p = 0.809). Secondary fragility fractures were recorded only in the post-restriction group (8/86 survivors, 9.3%; p = 0.051). Conclusions: In this retrospective pre–post comparison, the post-restriction group showed a lower proportion of reported outdoor activity, while documented combined postoperative physiotherapy and anti-osteoporotic pharmacologic treatment remained uncommon among survivors. Secondary fragility fractures were observed only in the post-restriction group and should be interpreted with caution, given the exploratory design and limited number of events. Structured rehabilitation referral, osteoporosis treatment, fall-prevention strategies, and follow-up pathways remain important components of post-fracture care following femoral neck fracture. Full article

Background: During the COVID-19 pandemic, uncertainty regarding the safety of kidneys from COVID-19-positive donors led to a reduction in kidney transplants and increased organ non-use in the United States. This study aims to evaluate whether donor COVID-19 positivity is associated with one-year post-transplant estimated glomerular filtration rate (eGFR) among kidney transplant recipients. Methods: This retrospective cohort study used data from the United States Organ Procurement and Transplantation Network (OPTN) 2020–2024. Donor COVID-19 status was determined by the SARS-CoV-2 nucleic acid amplification technique (NAT) and antibody test results. The main outcome was recipients’ one-year eGFR, estimated by the CKD-EPI 2021 formula. Linear regression models were used to compare the mean one-year eGFR among donor COVID-19 groups, adjusted by inverse probability of treatment weights. Interaction terms of donor acute kidney injury status and race were assessed to evaluate effect modification. Results: Among 38,199 included kidney transplant recipients, 1090 (2.9%) received kidneys from donors with active COVID-19 infection, 423 (1.1%) from donors with resolved infection, and 36,686 (96.0%) from COVID-19-negative donors. After weighting and adjustment, there was no significant difference in one-year eGFR for recipients of kidneys from donors with active COVID-19 (mean difference, 0.05 [95% CI, −1.08 to 1.18]) or resolved infection (mean difference, −0.27 [95% CI, −2.19 to 1.64]) compared with COVID-19-negative donors. Neither donor AKI nor donor race modified the association between donor COVID-19 status and one-year eGFR. Conclusions: This study suggests that kidneys from COVID-19-positive donors may be a viable option without compromising short-term allograft function as measured by 1-year eGFR. Full article

Background: The coronavirus disease 2019 (COVID-19) pandemic coincided with substantial changes in healthcare delivery and antimicrobial resistance (AMR) patterns worldwide, particularly in intensive care units (ICUs), where invasive procedures and broad-spectrum antibiotics are commonly used. Data from Türkiye remains limited. Methods: This retrospective observational study evaluated bacterial and fungal isolates from adult ICU patients at a tertiary hospital from 2016 to 2025. Microorganisms were identified, and antimicrobial susceptibility testing was performed using standardized methods. Resistance patterns were compared between the pre-pandemic (January 2016–February 2020) and post-pandemic (March 2020–May 2025) periods. Results: A total of 2666 patients and 5433 isolates were analyzed. Gram-negative pathogens showed marked increases in resistance: carbapenem and colistin resistance in Klebsiella pneumoniae were significantly higher in the post-pandemic period (69.6% vs. 44.4% and 60.5% vs. 22.5%, respectively; p < 0.001). Resistance rates to multiple antimicrobial agents also increased in Acinetobacter baumannii and Pseudomonas aeruginosa (p < 0.05). Among Gram-positive bacteria, vancomycin-resistant Enterococcus faecium increased from 10% to 47.1%. Candida auris emerged only in the post-pandemic period, showing high resistance to fluconazole (75%) and amphotericin B (36.7%). Conclusions: Significant differences in AMR patterns were observed between the pre- and post-pandemic periods in this ICU population. Higher resistance rates were observed among several clinically important bacterial pathogens, and Candida auris emerged exclusively during the post-pandemic period. Given the study’s observational design, these findings should be interpreted as temporal associations rather than evidence of a causal effect of the COVID-19 pandemic. Continued antimicrobial stewardship and infection-control measures remain essential to address the growing burden of AMR. Full article

Background: Dysbiosis of the gut microbiota is common in children with autism spectrum disorder (ASD). Probiotics have the potential to improve outcomes in ASD by modulating the gut microbiota–brain axis. Methods: In a pilot randomised trial, children (2 to 5 years) with confirmed ASD (DSM-5 criteria) received either a multi-strain probiotic (450 billion CFU twice daily for one month, followed by once daily for three months) or placebo supplementation. Faecal microbiota profiles were assessed using pre- and post-supplementation samples. The primary outcome involved changes in gut microbiota diversity. Secondary outcomes included faecal short-chain fatty acid levels and behavioural changes. Results: Difficulties in recruitment and loss to follow-up for reasons including COVID-19 resulted in the enrolment of only 23 (probiotic: 9; placebo: 14) instead of the planned 40 children. There was no evidence of changes in the gut microbiota in probiotic-supplemented children. The common phyla were Bacillota_A (~50%), Bacteroidota (~18%) and Actinobacteriota (~10%). Alpha- and Beta-diversity showed no significant difference between pre- vs. post-supplementation samples. Bifodobacteriaceae increased significantly in the probiotic-supplemented group (p = 0.046). Conclusions: The increase in faecal Bifodobacteriaceae supports an evaluation of probiotics in ASD. Addressing the reasons for loss to follow-up is important when designing trials in this field. Full article

There is no proven therapy for Long COVID, a post-acute condition characterized by persistent symptoms following SARS-CoV-2 infection. Extracellular vesicles (EVs) are emerging as mediators of disease pathogenesis through their molecular cargo. We investigated whether EV glycosylation is altered in Long COVID plasma and whether these vesicles can be selectively targeted using a glycan-binding affinity resin. Large (100–500 nm) and small (40–200 nm) EVs were isolated from post-acute COVID-19 plasma and analyzed by nanoparticle flow cytometry to assess surface glycosylation. Small EV capture assays were performed using Galanthus nivalis agglutinin (GNA) affinity resin. Plasma miRNA profiles before and after GNA treatment were evaluated using NanoString nCounter analysis, and potential downstream pathway effects were computationally inferred using validated miRNA–mRNA interactions and PROGENy. Mannose-positive large EVs were significantly increased in Long COVID compared to recovered controls (p < 0.05). GNA-mediated small EV capture correlated with mannose-positive EV abundance (r = 0.341, p < 0.05), and seven miRNAs were significantly reduced following treatment. Computational pathway analysis suggested modulation of key signaling pathways, including JAK-STAT, Estrogen, VEGF, and PI3K. These findings suggest a glycan-associated EV signature in Long COVID and support further investigation of lectin-based capture as a potential strategy to target vesicle-associated molecular cargo. Full article

Background: SARS-CoV-2 infection has been associated with metabolic disturbances and endocrine alterations, including effects on pancreatic β-cell function and thyroid hormone regulation. However, the relationship between thyroid function and β-cell compensatory capacity in the post-COVID state remains unclear. Methods: In this cross-sectional study, we evaluated β-cell compensation (HOMA-B/HOMA-IR) and thyroid parameters in three groups: patients with active COVID-19, individuals with post-COVID metabolic disturbances, and a COVID-negative metabolic syndrome reference group. Thyroid status was assessed using both comprehensive clinical classification and biochemical criteria. Associations between thyroid hormones and β-cell function were analyzed using Spearman correlation. Results: β-cell compensatory capacity differed significantly across groups, with the lowest values observed during active COVID-19 and intermediate impairment in the post-COVID cohort compared with the metabolic syndrome group. FT3 concentrations and the FT3/FT4 ratio were significantly reduced during active infection and were positively associated with β-cell compensation in the post-COVID group (ρ = 0.421, p = 0.018 and ρ = 0.382, p = 0.031, respectively). Although thyroid dysfunction appeared more prevalent in the post-COVID cohort when defined by overall clinical classification, no significant differences were observed when thyroid status was evaluated based solely on biochemical criteria, excluding clinical history and euthyroid sick syndrome. Conclusions: Post-COVID metabolic disturbances are characterized by impaired β-cell compensatory capacity and alterations in peripheral thyroid hormone dynamics. The apparent increase in thyroid dysfunction is largely driven by pre-existing thyroid disease and non-thyroidal illness effects rather than intrinsic thyroid pathology. These findings are consistent with the hypothesis of a potential post-COVID immunometabolic phenotype involving both pancreatic and thyroid-related mechanisms. Full article

Background: The coronavirus disease 2019 (COVID-19) pandemic significantly disrupted cancer screening, diagnosis, and care. This phase of the Hungarian Cancer Epidemiology (HUN-CANCER-EPI) study evaluated trends in cancer incidence and mortality in Hungary during the pre-COVID (2011–2019), COVID (2020–2021), and post-COVID (2022–2023) periods. Methods: Nationwide data from the Hungarian National Health Insurance Fund database were analysed. Age- and sex-adjusted incidence and mortality trends from 2011 to 2019 were modeled using Poisson regression. Changes from trends in 2020–2023 were compared to pre-COVID projections with 95% confidence intervals. Results: From 2011 to 2019, age-standardised cancer incidence declined by 1.9% (95% CI: 1.3% to 2.4%) annually in males and by 1.0% (95% CI: 0.6% to 1.4%) in females. During 2020–2021, incidence dropped sharply below the expected: in 2020 (−12.8% in males and −11.8% in females) and in 2021 (−11.7% and −7.9%, respectively). The largest declines affected prostate, melanoma, and kidney cancer. Rapidly progressing tumors like pancreatic and esophageal showed smaller decreases. By 2023, partial incidence rebounds were observed for prostate cancer, kidney cancer, and melanoma, likely reflecting the recovery of pandemic-delayed diagnoses. Lung and liver cancers showed no rebound. The steepest drops were in males aged 70+, with incomplete recovery. Mortality stayed near expected levels overall, with some exceptions, like melanoma, where the rebound in incidence coincided with increased mortality rates in 2023, which may reflect delayed diagnosis, although this cannot be directly confirmed. Conclusions: The pandemic had lasting, cancer-type-specific impacts on incidence patterns, particularly affecting screening-dependent, slow-growing tumors. Mortality remained largely stable overall during the available follow-up, highlighting the need for targeted recovery strategies and strengthened healthcare system resilience. Full article

Background: Following the coronavirus disease 2019 (COVID-19) pandemic, increased reports of severe acute hepatitis of unknown etiology in children have raised concerns about virus-associated liver injury. Acute respiratory tract infections (ARTIs) are a common cause of pediatric hospitalization and may be accompanied by reactive hepatitis; however, virus-specific patterns of hepatic involvement remain incompletely defined. This study aimed to evaluate liver involvement associated with ARTIs in hospitalized children. Methods: This retrospective study included pediatric patients (<18 years) hospitalized with ARTIs between October 2021 and May 2023. Respiratory viruses were identified via multiplex real-time polymerase chain reaction assays. Liver function tests were systematically evaluated during hospitalization. Transaminase elevations were categorized according to the upper limit of normal (ULN = 40 U/L). Acute hepatic failure was defined according to the Pediatric Acute Liver Failure criteria. Results: A total of 179 patients were analyzed (median age: 38 months; 59.2% male). Elevated AST and ALT levels were observed in 24.0% and 8.4% of patients, respectively. Adenovirus was the most frequently detected virus (11.2%), followed by influenza A (7.3%) and parainfluenza virus (6.7%). Severe transaminase elevations (>5 × ULN and >500 U/L) were observed in patients with influenza infection. All cases of acute hepatic failure (n = 3) were associated with influenza infection. Other respiratory viruses were associated with mild or transient liver enzyme abnormalities. Conclusions: Severe hepatic involvement—including severe transaminase elevation and acute hepatic failure—occurred exclusively in children with influenza infection, particularly influenza B, while mild and transient liver enzyme abnormalities were common across other respiratory viral infections. These findings highlight the importance of targeted liver function monitoring in pediatric influenza patients and provide clinically relevant data on virus-specific hepatic involvement in the post-COVID-19 era. Full article