Search Results (42,795)

Background/Objectives: The multifaceted concept of body image (BI) refers to an individual’s attitudes and impressions of their body. Negative BI is associated with a number of harmful health consequences, including obesity, eating disorders, and symptoms of sadness. The contemporary digital era, marked by the dominance of platforms, has brought about a considerable transformation in the landscape of BI issues. This study’s goal is to compile and assess the connections between social media (SM) use, body weight, and BI in adult populations. Methods: This is a narrative review that comprehensively searches across multiple academic databases, such as PubMed, Medline, Scopus, Web of Science, and Google Scholar. Studies that used SM (online blogs, microblogs, content communities, or social networking sites) for engagement (e.g., sharing, commenting, liking) or image-related activities (e.g., viewing, posting, or engaging with images) with healthy adults (aged 18–70 years) of any body mass index (BMI kg/m²) met the inclusion criteria. Included were observational and experimental studies that examined habitual SM use. Only peer-reviewed works published in English between 2015 and 2025 met the search criteria. Results: The currently available findings suggest that obese people are more dissatisfied with their bodies than people of normal weight, and obese women are more dissatisfied with their bodies than their peers of normal weight. Furthermore, experimental studies have demonstrated that immediate BI is adversely affected by acute exposure to idealized social media photographs. Conclusions: Policies should support specialized training that emphasizes a holistic approach to health and puts functionality and health above attractiveness. This training is crucial for dispelling weight-related stigmas and enabling healthcare providers to offer compassionate treatment that supports mental and physical health. Future research must concentrate on internalization and social pressure or reinforcement because these subjects have not gotten as much emphasis in prior studies. Such mechanism research could help better contextualize the role of recently introduced SM items. Full article

Background: Valproic acid (VPA) poisoning has a dynamic clinical course and may require extracorporeal toxin removal (ECTR) in severe cases. Intermittent hemodialysis is the preferred ECTR technique; however, clinical experience with expanded hemodialysis (HDx) using medium cut-off (MCO) membranes in acute VPA intoxication is scarce. We describe a case of severe VPA poisoning managed with intermittent HDx and outline the clinical rationale and kinetic response. Case Report: A 54-year-old woman presented to the emergency department after accidental presumably ingesting approximately 4 g of VPA, with depressed consciousness (Glasgow Coma Scale 7) and metabolic acidosis (pH 7.10, HCO₃⁻ 13 mmol/L, PCO₂ 50 mmHg, lactate 2.8 mmol/L, ionized calcium 0.8 mmol/L, elevated anion gap). Initial plasma VPA was 262.99 µg/mL, ammonia was 14 µmol/L, and cranial computed tomography showed no acute abnormalities. ECTR was initiated in the intensive care unit as intermittent HDx using an MCO dialyzer for 4 h. Serial VPA concentrations were obtained before treatment, at 2 h, and at the end of the session to guide real-time prescription adjustment, with an increase in blood flow from 200 to 230 mL/min. Results: VPA decreased from 262.99 µg/mL pre-HD to 141.48 µg/mL at 2 h (46.2% reduction) and 97.81 µg/mL at 4 h (62.8% reduction), with clear improvement in the level of consciousness. A mild post-dialysis rebound was observed (100.07 µg/mL at 14 h). The patient recovered without additional ECTR and was discharged with normalized VPA levels on follow-up. Conclusions: In this patient, intermittent HDx with an MCO membrane was feasible, well tolerated, and associated with rapid VPA clearance and neurological recovery. Serial drug monitoring enabled bedside optimization of the dialysis prescription and post-treatment evaluation. A single HDx session was sufficient, and VPA therapy was safely reintroduced under close monitoring. Full article

Background/Objectives: Acute myeloid leukemia (AML) remains a hematologic malignancy with poor prognosis. The neddylation inhibitor MLN4924 has demonstrated potent anti-leukemic activity in preclinical models, yet its clinical translation faces significant challenges. The aim of this study was to explore combination therapy strategies that could further enhance MLN4924’s anti-leukemia potential. Methods: AML cell lines used in this study were Kasumi-1 and MOLM-13. Cell viability was assessed using CCK-8 assays. mRNA and protein expression levels were determined through RT-qPCR and Western blot, respectively. Flow cytometry was employed to analyze surface markers (SLC1A5, CD11b, CD14, CD16), mitochondrial membrane potential (JC-1), and apoptosis (Annexin V-FITC/PI). In vivo efficacy was validated using an NCG mouse xenograft model. Transcriptomic profiling was performed to explore the potential mechanism by which MLN4924 in combination with V9302 inhibits leukemia. Results: Treatment with MLN4924 significantly upregulated key glutamine metabolic proteins, GLUL and the glutamine transporter SLC1A5, in AML cells. Knockdown of SLC1A5 significantly enhanced AML cell sensitivity to MLN4924. The combination of MLN4924 and the SLC1A5 inhibitor V9302 synergistically inhibited AML cell proliferation, induced monocytic differentiation, and promoted apoptosis. Transcriptomic analysis revealed that this combination therapy prominently suppressed the tricarboxylic acid (TCA) cycle. Conclusions: Neddylation inhibition induces compensatory upregulation of glutamine metabolism in AML. Co-targeting neddylation and glutamine transporter SLC1A5 synergistically exerts anti-leukemic effects, at least in part through disruption of the TCA cycle. This combination represents a novel and effective therapeutic strategy against AML. Full article

Background: Previous research has found that mindfulness-based techniques are beneficial for reducing stress in heavy-drinking individuals. However, the underlying neurobiology of these stress-reducing effects are unclear. Moreover, much of the research examining neurobiological correlates of mindfulness has used static functional connectivity, suggesting that brain activity goes unchanged for the entire length of an MRI scan. Methods: In the current study, we used a state-based dynamic functional connectivity model to examine brain states during either a 10 min mindfulness session or resting control that followed an individually tailored stress imagery task. Using a hidden semi-Markov model (HSMM), six brain states and the associated dynamics of state traversal were estimated for a population of moderate-to-heavy drinkers (N = 32). We modeled the 36 Schaefer atlas regions spanning the salience and default mode networks, and the HSMM characterized each state by its distinct multivariate pattern of activity and covariance structure. Group differences in dwell times, transition behavior, and overall state dynamics were evaluated using permutation tests and mixed-effects models. Results: Participants that experienced the mindfulness session had more transitions and longer time spent in states in which the salience network was more active. Participants assigned to the control group had more transitions and increased time spent in states in which nodes of the default mode network were more active. Moreover, for control participants, increased occupancy time to SN-dominant states was associated with lower perceived stress. Conclusions: Using HSMM provided a unique insight into network connectivity during mindful states; we believe it offers a novel approach to testing and optimizing mindful-based therapies. Full article

Background/Objectives: Sex and age influence inflammatory responses, but researchers have not fully characterized their combined association with complicated acute appendicitis (CAA). This study assessed the independent and interactive associations of sex, age, and inflammatory cell counts with CAA. Methods: We conducted a retrospective observational study of 708 patients with histopathologically confirmed uncomplicated appendicitis (UAA) or CAA. We analyzed demographic and clinical data, including preoperative complete blood counts, stratified by sex. We used multivariable logistic regression models with interaction terms to evaluate associations and possible effect modification by sex and age. We explored the direction and magnitude of these interactions by estimating marginal predicted probabilities. Results: The incidence of CAA was significantly higher in men than in women. In men with CAA, complete blood count analysis showed elevated neutrophil and monocyte counts and reduced lymphocyte counts. Male sex (odds ratio (OR) 2.197, 95% confidence interval (CI) 1.610–2.999), continuous age (1.017, 1.002–1.033), lymphocyte count (0.656, 0.526–0.820), monocyte count (1.551, 1.036–2.321), and platelet count (1.004, 1.001–1.006) were independently associated with CAA. Interaction analysis revealed significant interactions between neutrophils and both sex and age (p < 0.05), while lymphocyte counts showed significant interaction with age but not with sex. Conclusions: This study provides new insight into complex sex- and age-related immune cell patterns in CAA and may inform future diagnostic and management strategies by highlighting immune profile variability. Full article

Sepsis is characterized by dysregulated immune responses induced by damage-associated molecular patterns, such as extracellular cold-inducible RNA-binding protein (eCIRP), that frequently lead to acute lung injury (ALI) and high mortality. Recently, a subset of CD4⁺ T cells possessing both T helper 1 (Th1) and regulatory T cell (Treg) phenotypes, termed Th1-Treg cells, has been identified; however, their function in sepsis remains unknown. In this study, we investigated the dynamics, induction mechanisms, and functional roles of Th1-Treg cells in the development of sepsis-induced ALI. Polymicrobial sepsis was induced in mice using cecal ligation and puncture. In vivo, Th1-Treg cell accumulation in the lungs was analyzed in WT and CIRP^−/− mice following sepsis. In vitro, isolated CD4⁺ T cells from WT and TLR4^−/− mice were treated with eCIRP to evaluate Th1-Treg cell differentiation and downstream signaling pathways. STAT1 and STAT5 activation were evaluated, and pharmacological inhibitors were used to assess their involvement. Adoptive transfer of Th1-Treg cells was conducted to determine their functional impact on ALI and mortality in septic mice. We observed a significant accumulation of Th1-Treg cells in the lungs of WT septic mice compared to sham mice. eCIRP drove the induction of Th1-Treg cells in vitro, and CIRP^−/− mice exhibited decreased Th1-Treg cell accumulation in the lungs compared to WT mice after sepsis. In parallel to Th1-Treg cell induction, eCIRP activated signal transducer and activator of transcription, STAT1 and STAT5. Both the induction of Th1-Treg cells and the activation of STAT1/5 proteins were significantly attenuated in TLR4^−/− mice. Furthermore, pharmacological inhibition of STAT1/5 signaling significantly reduced eCIRP-induced Th1-Treg cell differentiation. Intriguingly, adoptive transfer of Th1-Treg cells significantly exacerbated ALI, resulting in increased mortality in sepsis. Our findings indicate Th1-Treg cells induced by the eCIRP–TLR4–STAT1/5 axis aggravate ALI, worsening mortality in sepsis. Targeting these pathogenic cells potentially alleviates sepsis-induced ALI. Full article

Death from acute radiation syndrome (ARS) has been a long-standing threat. Given the current heightened risk of a nuclear event, e.g., a conflict bomb, terror bomb, reactor core dispersion, or recurrent exposure to medical radiation, a systemic treatment to reduce or eliminate ARS death would be beneficial. This study utilizes step-wise progression to (i) identify why lethally irradiated mice die from ARS and (ii) identify a multidrug regimen, administered before or after irradiation, that prevents or treats ARS pathologies to significantly suppress or eliminate ARS death. Lethal blood-borne E. coli septic infection was found in 97% of near-death, irradiated mice; this observation was consistent with the numerous breaches observed in GI histology showing a broken and breached GI epithelium and GI muscularis externa. Our study found (i) a new and clear explanation of why irradiated mice die from ARS; (ii) identified two drugs (PrC-210, ciprofloxacin), which, when administered minutes pre-radiation, conferred 100% survival benefit or 56% when administered a day after irradiation; and (iii) a three-drug regimen (PrC-210, ciprofloxacin, GCSF) that conferred 92% survival benefit when administered 1–2 days after radiation. These drug regimens can be “field-deployed” to field staging areas and home medicine chests to enable the simple, widespread use of the regimens in the face of radiation threat. Full article

Carotenoids play a central role in photosynthesis and cellular protection, and microalgae represent a sustainable platform for their commercial production. Here, we optimized the accumulation of the high-value carotenoids astaxanthin and lutein in continuous photoautotrophic cultures of Chromochloris zofingiensis by modulating nitrogen supply and light intensity. Reducing nitrate availability strongly promoted astaxanthin accumulation, whereas lutein levels remained largely unaffected. For 4% N in the dry biomass, accumulation of astaxanthin was highest and that of lutein lowest, while the opposite was recorded for 9% N. Average irradiance positively affected lutein accumulation independently of nitrate, whereas that of astaxanthin only increased under nitrogen-limiting conditions. Integrated transcriptomics and carotenoid profiling analysis revealed nitrogen availability as the dominant regulatory factor, with a synergistic interaction with light that enhances their individual effects. Nitrate limitation redirected metabolic flux from lycopene toward β-carotene and its subsequent conversion to astaxanthin via BKT1 overexpression, while high irradiance induced CYP97A1 and CYP97C expression, favoring lutein biosynthesis. Together, these findings demonstrate that targeted control of nitrogen and light enables the continuous and programmable production of C. zofingiensis biomass with a specific astaxanthin-to-lutein ratio, highlighting its potential for industrial carotenoid bioprocesses. Full article

Candida species are frequently detected in bile cultures during endoscopic retrograde cholangiopancreatography (ERCP), but their clinical significance and the value of antifungal treatment remain unclear. We performed a retrospective single-center cohort study of adults with growth of Candida species from bile cultures collected by ERCP performed between 2010 and 2023. We compared inpatients who received vs. those who did not receive antifungals within one week of ERCP and a subgroup with acute cholangitis. The primary outcome was a composite of death and invasive candidiasis within one year. Secondary outcomes included death, invasive candidiasis, and rehospitalization. Inverse probability of treatment weighting (IPTW) was performed using baseline characteristics. Adjusted hazard ratios and odds ratios were calculated. Among 197 inpatients, 51 (25.9%) received antifungals. At one year, the primary outcome occurred in 23 of 51 patients (45.1%) receiving antifungal therapy and in 67 of 146 patients (45.9%) who did not; the IPTW-adjusted hazard ratio was 0.93 (95% confidence interval 0.69–1.27; p = 0.66). No significant differences were seen in the acute cholangitis subgroup (n = 117). In this study, antifungal therapy was not associated with improved survival, lower rates of invasive candidiasis, or fewer readmissions. Findings support a conservative, stewardship-oriented approach to managing Candida-positive bile cultures in the absence of invasive disease. Full article

COVID-19 not only affects the respiratory system but also increases the risk of cerebrovascular complications, including ischemic stroke. Experimental and clinical data suggest that cytokine dysregulation and polymorphisms of thrombophilia-related genes (MTHFR, MTR, and MTRR) may jointly promote hypercoagulation, endothelial dysfunction, and thromboinflammation, thereby contributing to post-COVID ischemic stroke. This study included 160 patients treated at Zangiota Infectious Diseases Hospitals (2021–2023): 60 patients with ischemic stroke in the acute or post-COVID period (experiment group), 50 COVID-19 patients without ischemic stroke (comparison group), and 50 ischemic stroke patients without COVID-19 (control group). Clinical–neurological and immunological parameters were assessed, and polymorphisms in thrombophilia/folate cycle genes (MTHFR C677T, MTR, and MTRR) were genotyped by PCR/real-time PCR. Statistical analysis included χ² tests, t-tests, logistic regression with odds ratios (OR) and 95% confidence intervals (CI); Hardy–Weinberg equilibrium was verified. A strong association was identified between the MTHFR C677T polymorphism and ischemic stroke on the background of COVID-19 (OR = 5.4; 95% CI: 2.1–13.8; p < 0.001). The TNF-α rs1800629 polymorphism was also significantly associated with COVID-19-related cerebrovascular events (OR = 3.27; 95% CI: 1.4–7.6; p = 0.006). Carriage of two or more minor alleles produced a synergistic effect, markedly increasing the risk of post-COVID ischemic stroke (OR = 5.59; 95% CI: 2.3–13.6; p < 0.001). These polymorphisms were linked to hyperhomocysteinemia, endothelial dysfunction, and mechanisms contributing to multifactorial arterial ischemic events. The combined assessment of thrombophilia and folate cycle-related genotypes and clinical indicators may provide a potential framework for improved risk stratification. Polymorphisms in MTHFR may appear to represent important genetic determinants of ischemic stroke following COVID-19, particularly in the context of arterial ischemic mechanisms. Full article

Background/Objectives: Patients with pre-existing heart failure (HF) represent a clinically vulnerable population with increased susceptibility to adverse outcomes during acute systemic illnesses, including coronavirus disease 2019 (COVID-19). Systemic inflammation is increasingly recognized as a central pathophysiological mechanism linking cardiovascular vulnerability with infection-related organ dysfunction. However, the prognostic role of inflammatory biomarkers in hospitalized COVID-19 patients with pre-existing HF remains incompletely defined. This study aimed to evaluate the association between inflammatory biomarkers and clinical outcomes in this high-risk population. Methods: This retrospective single-center cohort study included 395 consecutive adult patients hospitalized with confirmed COVID-19 between March 2020 and December 2024 at a tertiary referral center. Pre-existing HF was documented in 143 patients (36.2%). Inflammatory biomarkers, including C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin, and D-dimer, were measured at admission. The primary outcomes were development of sepsis and in-hospital mortality. Multivariable logistic regression models were constructed to identify independent predictors of adverse outcomes after adjustment for demographic characteristics, comorbidities, disease severity, and cardiac biomarkers. Results: Patients with pre-existing HF had significantly higher in-hospital mortality compared with those without HF (11.9% vs. 4.8%, p = 0.016) and showed a trend toward increased intensive care unit admission. HF patients exhibited higher admission IL-6 levels, indicating enhanced inflammatory activation. In univariable analysis, HF was associated with mortality (OR 2.67, 95% CI 1.22–5.83, p = 0.014). After multivariable adjustment, the association between HF and mortality was attenuated, whereas IL-6 remained an independent predictor of mortality (adjusted OR 1.38, 95% CI 1.04–1.82, p = 0.021). Elevated IL-6 and procalcitonin levels were also independently associated with sepsis development. Conclusions: Pre-existing heart failure identifies a population at increased risk of adverse outcomes in hospitalized COVID-19 patients, and this excess risk appears to be partly mediated by systemic inflammatory activation. Interleukin-6 emerged as a key biomarker linking cardiovascular vulnerability, immune dysregulation, and clinical deterioration. These findings support the potential role of inflammation-based risk stratification to improve prognostic assessment and guide personalized management in high-risk patients with underlying cardiovascular disease. Full article

Sudden disruptions can destabilize everyday routines and open the door to pro-environmental behavioral change. This paper examines whether exogenous Moments of Change (MoC) with different temporal profiles—an acute nationwide power outage in Spain and the prolonged COVID-19 disruption—reshape employees’ workplace pro-environmental behavior (PEB) by weakening the relationship between habits and PEB. Study 1 surveyed 226 Spanish office workers 38 days after a brief blackout, while Study 2 followed 135 employees in Spain and the Netherlands longitudinally across the COVID-19 period. We found that, while reported PEB increased after both disruptions, the short-term blackout was insufficient to weaken the relationship between habits and behavior significantly, or to strengthen individual and organizational drivers of behavior. In contrast, the more prolonged COVID-19 disruption significantly weakened the influence of habits on PEB and strengthened the relationship between perceived corporate environmental responsibility and behavior. These findings suggest that the duration of a disruption is a critical factor. Specifically, brief shocks may elicit specific new behaviors; only prolonged disruptions appear sufficient to break established habits and enhance the influence of organizational factors on employees’ pro-environmental actions. Full article

Ubiquitin-specific peptidase 10 (USP10) deubiquitinates multiple signaling proteins in cancer cells. These USP10 substrates contain both tumor suppressors and oncogenic proteins, thus conferring both inhibitory and promoting effects of USP10 on tumorigenesis and progression. This review focuses on the dual roles of USP10 in various cancer types and addresses the association of aberrant USP10 expression with the development of various types of cancers, including hepatocellular carcinoma, lung cancer, breast cancer, prostate cancer, gastric cancer, and acute and chronic myelogenous leukemia. In addition, this review discusses the potential applications of USP10 inhibitors as targeted drugs for cancer therapy. Full article

Background and Objective: Despite advances in operative techniques and perioperative care, complications following coronary artery bypass grafting (CABG) remain an important cause of postoperative morbidity and organ dysfunction. This study aimed to evaluate the association between preoperative epicardial adipose tissue (EAT) thickness measured using computed tomography and postoperative morbidity and mortality in patients undergoing isolated CABG, and to explore whether EAT thickness may serve as a potential imaging-based risk marker for postoperative complications. Materials and Methods: The study was a retrospective single-center observational cohort study. Patients who underwent isolated coronary artery bypass grafting between 1 January 2019 and 2 January 2023, and had available preoperative computed tomography (CT) imaging were retrospectively reviewed. Epicardial adipose tissue thickness was measured on CT images at three predefined anatomical regions, yielding two parameters: total EAT thickness and right ventricular EAT thickness. Postoperative complications were evaluated using established definitions, with atrial fibrillation (AF) assessed according to European Society of Cardiology (ESC) criteria and acute kidney injury defined based on Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. Results: Patients who developed postoperative complications after coronary artery bypass grafting tended to have thicker epicardial adipose tissue. Increased total epicardial adipose tissue thickness was associated with postoperative paroxysmal atrial fibrillation, whereas greater right ventricular epicardial adipose tissue thickness was associated with postoperative acute kidney injury. Multivariable analysis confirmed that both total and right ventricular epicardial adipose tissue thickness were independently associated with postoperative complications (total EAT: OR 1.74, 95% CI 1.10–2.76; right ventricular EAT: OR 2.03, 95% CI 1.31–3.15). ROC analysis showed modest discrimination for postoperative atrial fibrillation (AUC 0.69) and acceptable discrimination for acute kidney injury (AUC 0.79). No association was observed between epicardial adipose tissue measurements and postoperative mortality. Conclusions: Increased preoperative epicardial adipose tissue thickness was associated with several early postoperative complications following coronary artery bypass grafting, including atrial fibrillation, acute kidney injury, and in-hospital infection. Preoperative epicardial adipose tissue thickness measured by computed tomography may represent a potentially useful imaging-based risk marker for early postoperative complications following isolated CABG, although confirmation in larger prospective studies is required. Full article

Background/Objectives: Q fever, caused by Coxiella burnetii, is typically treated with doxycycline, but its efficacy is limited in chronic cases and may be poorly tolerated. Systemic ciprofloxacin shows limited activity for acute Q fever. However, inhaled liposomal formulations may provide therapeutic benefit. Methods: Two inhaled ciprofloxacin formulations (Lipoquin^® and Apulmiq^®) were evaluated in an A/J mouse model of Q fever and compared with intraperitoneal ciprofloxacin and oral doxycycline. Initially, pharmacokinetic studies were performed to determine an appropriate dosing regimen for the inhaled ciprofloxacin formulations. A separate cohort of mice were then infected with C. burnetii and treated once daily via nebulisation with Lipoquin or Apulmiq, initiated at 24, 48, or 72 h post-challenge. Clinical signs, weight change, splenomegaly, bacterial burden, and lung histopathology were evaluated. Results: Pharmacokinetic analysis confirmed sustained lung concentrations of inhaled ciprofloxacin, supporting once-daily dosing. Inhaled Lipoquin and Apulmiq significantly reduced clinical signs, weight loss, splenomegaly, and pulmonary bacterial burden compared to untreated controls and doxycycline-treated mice. Histopathology revealed decreased lung inflammation and lesion severity following inhalational dosing. Systemic ciprofloxacin slightly reduced splenic bacterial burden but was less effective in controlling pulmonary infection. Conclusions: Inhaled liposomal ciprofloxacin demonstrated superior protection and reduced respiratory manifestations of Q fever compared to doxycycline and systemic ciprofloxacin. These findings suggest inhaled formulations may represent a viable alternative for the treatment of Q fever pneumonia. Further studies are needed to evaluate clinical applicability and long-term outcomes. Full article