Search

Abstract Purpose Benign skin lesions in zygomatic-infraorbital regions severely influence pediatric patients’ appearance as well as mental health. Treatments are difficult for the high requirements of patients’ guardians in both function and aesthetics. The present study aims to introduce a surgical method, Expanded Multi-Lobe Cervicofacial Flap, which combines the advantages of the classical cervicofacial advancement rotation flap and the tissue expansion technique. Methods A total of 21 pediatric patients were enrolled. The treatment process included 2 stages: implantation of the skin tissue expander and flap transfer. The excessive skin created by tissue expansion extended the coverage area of the multi-lobe flap. Results In this retrospective study, follow-up periods were all more than 12 months (20.8 ± 6.7). In the last follow-ups, the flaps were all in good condition, and No facial organ displacement was observed. The patients’ guardians were satisfied with the outcomes. Conclusions Using the expanded multi-lobe cervicofacial flap for the zygomatic-infraorbital benign skin lesion repair is effective, and this method is especially applicable to the pediatric population.

Abstract Extracellular adenosine triphosphate (ATP) and its receptor, P2X7 receptor (P2X7R), are playing an important role in the pathological process of renal ischemia-reperfusion injury, but their underlying mechanism remains unclear. Also, the effects of tubular epithelium-expressed P2X7 receptor on ischemia acute kidney injury is still unknown. The aim of this study is to clarify if this mechanism involves the activation of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome in the renal tubular epithelial cells. In our research, we used male C57BL/6 wild type and P2X7R (−/−) mice, cultured human proximal tubular epithelial cells, and kidneys from acute kidney injury patients. Mice underwent for unilateral nephrectomy combined with the lateral renal pedicle clamping. Cultured cells were subjected to hypoxia/reoxygenation or ATP. Apyrase and A438079 were used to block the extracellular ATP/P2X7 receptor pathway. We also constructed radiation-induced bone marrow (BM) chimeras by using P2X7R (−/−) mice and P2X7R (+/+) wild-type mice. P2X7 receptor deficiency protected from renal ischemia-reperfusion injury and attenuated the formation of NLRP3 inflammasome. By using BM chimeras, we found a partial reduction of serum creatinine and less histological impairment in group wild-type BM to P2X7R (−/−) recipient, compared with group wild-type BM to wild-type recipient. In renal tubular epithelial cells, hypoxia/reoxygenation induced ATP release and extracellular ATP depletion reduced the expression of active IL-1β. ATP activated the NLRP3 inflammasome in renal tubular epithelial cells, which were blunted by transient silence of P2X7 receptor, as well as by P2X7 receptor blocking with A438079. In human samples, we found that patients with Stage 3 AKI had higher levels of P2X7 receptor expression than patients with Stage 1 or Stage 2. Extracellular ATP/P2X7 receptor axis blocking may protect renal tubular epithelial cells from ischemia-reperfusion injury through the regulation of NLRP3 inflammasome.

Aim The accumulation of uremic toxins, such as asymmetric dimethylarginine (ADMA), has emerged as one of the major cardiovascular disease-related risk factors in patients with end-stage renal disease (ESRD). Based on the low molecular weight of ADMA, hemodialysis (HD) should theoretically effectively remove ADMA. In this study, we investigated the clearance behavior of ADMA during high-flux HD. Methods Eight HD patients without residual renal function were included. Blood samples were collected at 0, 30, 60, 120 and 240 min after dialysis started, as well as 1 h and 48 h after dialysis. ADMA level was detected by HPLC-MS/MS. Herein, the ADMA level in blood cells and the ADMA protein binding rate were measured. Accordingly, the dialyzer extraction ratio was also determined. Results The reduction ratio (RR) of ADMA (corrected for hemoconcentration) was significantly lower, at only 37.21 ± 6.44%, than that of urea and creatinine (p .05). Urea and creatinine had a slight rebound ratio of less than 10% at 1 h after the completion of HD. In contrast, considerable rebound of approximately 30% was detected in ADMA. Conclusion This study suggests that ADMA may present a multicompartmental distribution that cannot be representatively reflected by the urea kinetics model.

The parameter tuning of a multi-stable energy harvester is crucial to enhancing harvesting efficiency. In this paper, the bifurcation theory is applied to quantitatively reveal the effects of structural parameters on the statics and dynamics of a quad-stable energy harvester (QEH). Firstly, a novel QEH system utilizing the geometric nonlinearity of springs is proposed. Static bifurcation analysis is carried out to design quad-stable working conditions. To investigate the cross-well and high-energy vibration, the complex dynamic frequency (CDF) method, suitable for both weakly and strongly nonlinear dynamic problems, is then applied to deduce the primary response solution. By using the unfolding analysis in singularity theory, four steady-state properties and dozens of primary resonance modes are demonstrated. Based on the transition set, the effective bandwidth for energy harvesting can be customized to adapt well to various vibration environments by parametric adjustment. Finally, the experimental tests verify that the output power can reach up to 1 mW. The proposed QEH and its mechanics optimization can guide energy supply for next-generation wireless systems and low-power sensors under magnetic forbidding environments.

Abstract Background Current paradigms of detecting acute kidney injury (AKI) are insensitive and non-specific. Klotho is a pleiotropic protein that is predominantly expressed in renal tubules. In this study, we evaluated the diagnostic and prognostic roles of urine Klotho for AKI following cardiac surgery. Methods We conducted a prospective study involving 91 patients undergoing cardiac surgery. AKI was defined according to the AKIN definition. The renal outcomes within 7 days after operation were evaluated. Perioperative levels of urine Klotho and urine neutrophil gelatinase-associated lipocalin (NGAL) were measured by using ELISA. Results Of 91 participants, 33 patients (36.26%) developed AKI. Of these AKI patients, 21 (63.64%), 8 (24.24%), and 4 (12.12%) were staged 1, 2, and 3, respectively. Serum creatinine in AKI patients began to slightly increase at first postoperative time and reached the AKI diagnostic value 1 day after operation. Postoperative urine Klotho peaked at the first postoperative time (0 h after admission to the intensive care unit (ICU)) in patients with AKI, and was higher than that in non-AKI patients up to day 3. The AUC of detecting AKI for urine Klotho was higher than urine NGAL at the first postoperative time and 4 h after admission to the ICU. In a multivariate model, increased first postoperative urine Klotho may be an independent predictor for AKI occurrence following cardiac surgery. The concentrations of first postoperative urine Klotho were higher in AKI stage 2 and 3 than those in stage 1 (p

Background/Aims: Cardiac surgery-associated acute kidney injury (CSA-AKI) was traditionally defined as an increase in serum creatinine (sCr) after cardiac surgery. Recently, serum cystatin C (sCyC) has been proposed to be a better biomarker in the prediction of AKI. The clinical utility and performance of combining sCyC and sCr in patients with AKI, particularly for the prediction of long-term outcomes, remain unknown. Methods: We measured sCyC together with sCr in 628 patients undergoing cardiac surgery. sCyC and sCr were assessed at baseline and 24 and 48 h after surgery. CSA-AKI determined by sCr (CSA-AKIsCr) was defined as an sCr increase greater than 0.3 mg/dL or 50% from baseline. Major adverse events (MAEs; including death of any cause and dialysis) at 3 years were assessed. Results: CSA-AKIsCr developed in 178 patients (28.3%). Three-year follow-up was available for 621 patients; MAEs occurred in 42 patients (6.8%). An increase in sCyC concentration ≥30% within 48 h after surgery was detected in 228 patients (36.3%). This was the best sCyC cutoff for CSA-AKIsCr detection (negative predictive value = 88.8%, positive predictive value = 58.3%). To evaluate the use of both sCyC and sCr as CSA-AKI diagnostic criteria, we stratified patients into 3 groups: non-CSA-AKI, CSA-AKI detected by a single marker, and CSA-AKI detected by both markers. By multivariable logistic regression analysis, the independent predictors of MAEs at 3 years were group 2 (non-CSA-AKI group as the reference, CSA-AKI detected by a single marker: odds ratio [OR] = 3.48, 95% confidence interval [CI]: 1.27–9.58, p = 0.016), group 3 (CSA-AKI detected by both markers: OR = 5.12, 95% CI: 2.01–13.09; p = 0.001), and baseline glomerular filtration rate (OR = 2.24; 95% CI: 1.27–3.95; p = 0.005). Conclusion: Combining sCyC and sCr to diagnose CSA-AKI would be beneficial for risk stratification and prognosis in patients after cardiac surgery.

Introduction: In China, a quarter of patients are undergoing 2-times weekly hemodialysis. Using data from the China Dialysis Outcomes and Practice Patterns Study (DOPPS), we tested the hypothesis that whereas survival and hospitalizations would be similar in the presence of residual kidney function (RKF), patients without RKF would fare worse on 2-times weekly hemodialysis. Methods: In our cohort derived from 15 units randomly selected from each of 3 major cities (total N = 45), we generated a propensity score for the probability of dialysis frequency assignment, estimated a survival function by propensity score quintiles, and averaged stratum-specific survival functions to generate mean survival time. We used the proportional rates model to assess hospitalizations. We stratified all analyses by RKF, as reported by patients (urine output

Background/Aims: Klotho is a multifunctional protein expressed predominantly in kidney tubular epithelium. Here, we investigated the protective effects of Klotho on necroptosis in renal ischemic-reperfusion injury (IRI) and the role of oxidative stress in this process. Methods: Mice were subjected to bilateral renal pedicle clamping. Mouse renal tubular epithelial (TCMK-1) cells were exposed to hypoxia/reoxygenation (H/R) or H2O2. Kidney samples from acute kidney injury (AKI) patients and controls were examined by immunofluorescence. Klotho protein and N-acetyl-L-cysteine (NAC) were used to define their roles in mediating necroptosis. Necroptosis was assessed by TUNEL staining, immunoblotting, and real-time PCR. Oxidative stress was studied via ELISA, immunoblotting, colorimetric, and thiobarbituric acid reactive substances assays. Results: Renal IRI induced Klotho deficiency in the serum and kidney, but an increase in the urine. The levels of the necroptotic markers receptor-interacting protein kinase (RIP) 1, RIP3, IL-1β, and TUNEL-positive cells increased after IRI; all increases were ameliorated by Klotho. In TCMK-1 cells, Klotho and NAC attenuated the elevation in RIP1, RIP3, and LDH release induced by H/R or H2O2. Moreover, Klotho decreased the levels of oxidative stress biomarkers and elevated superoxide dismutase 2 expression in both in vivo and in vitro experiments. Studies in human samples further confirmed the Klotho deficiency and increased formation of RIP3 puncta in AKI kidneys. Conclusion: Klotho protects tubular epithelial cells from IRI and its anti-necroptotic role may be associated with oxidative stress inhibition.

Background/Aims: Autophagy is a dynamic catabolic process that maintains cellular homeostasis. Whether it plays a role in promoting cell survival or cell death in the process of renal ischemia/reperfusion (I/R) remains controversial, partly because renal autophagy is usually examined at a certain time point. Therefore, monitoring of the whole time course of autophagy and apoptosis may help better understand the role of autophagy in renal I/R. Methods: Autophagy and apoptosis were detected after mice were subjected to bilateral renal ischemia followed by 0-h to 7-day reperfusion, exposure of TCMK-1 cells to 24-h hypoxia, and 2 to 24-h reoxygenation. The effect of autophagy on apoptosis was assessed in the presence of autophagy inhibitor 3-methyladenine (3-MA) and autophagy activator rapamycin. Results: Earlier than apoptosis, autophagy increased from 2-h reperfusion, reached the maximum at day 2, and then began declining from day 3 when renal damage had nearly recovered to normal. Exposure to 24-h hypoxia induced autophagy markedly, but it decreased drastically after 4 and 8-h reoxygenation, which was accompanied with increased cell apoptosis. Inhibition of autophagy with 3-MA increased the apoptosis of renal tubular cells during I/R in vivo and hypoxia/reoxygenation (H/R) in vitro. In contrast, activation of autophagy by rapamycin significantly alleviated renal tissue damage and tubular cell apoptosis in the two models. Conclusion: Autophagy was induced in a time-dependent manner and occurred earlier than the onset of cell apoptosis as an early response that played a renoprotective role during renal I/R and cell H/R. Up-regulation of autophagy may prove to be a potential strategy for the treatment of acute kidney injury.

Lupus nephritis (LN) is among the most serious complications of systemic lupus erythematosus (SLE), which causes significant morbidity and mortality. Renalase is a novel, kidney-secreted cytokine-like protein that promotes cell survival. Here, we aimed to investigate the relationship of serum renalase levels with LN and its role in the disease progression of LN.For this cross-sectional study, 67 LN patients and 35 healthy controls were enrolled. Seventeen active LN patients who received standard therapies were followed up for six months. Disease activity was determined by the SLE Disease Activity-2000 (SLEDAI-2K) scoring system and serum renalase amounts were determined by ELISA. Predictive value of renalase for disease activity was assessed. Furthermore, the expression of renalase in the kidneys of patients and macrophage infiltration was assessed by immunohistochemistry.Serum renalase amounts were significantly higher in LN patients than in healthy controls. Moreover, patients with proliferative LN had more elevated serum renalase levels than Class V LN patients. In proliferative LN patients, serum renalase levels were significantly higher in patients with active LN than those with inactive LN. Serum renalase levels were positively correlated with SLEDAI-2K, 24-h urine protein excretion, ds-DNA and ESR but inversely correlated with serum albumin and C3. Renalase amounts decreased significantly after six-months of standard therapy. The performance of renalase as a marker for diagnosis of active LN was 0.906 with a cutoff value of 66.67 μg/ml. We also observed that the amount of renalase was significantly higher in glomerular of proliferative LN along with the co-expression of macrophages.Serum renalase levels were correlated with disease activity in LN. Serum renalase might serve as a potential indicator for disease activity in LN. The marked increase of glomerular renalase and its association with macrophages suggest that it might play an important role in disease progression of LN.

Abstract Alkaline metal sulfur (AMS) batteries offer a promising solution for grid-level energy storage due to their low cost and long cycle life. However, the formation of solid compounds such as M2S2 and M2S (M = Na, K) during cycling limits their performance. Here we unveil intermediate-temperature K-Na/S batteries utilizing advanced electrolytes that dissolve all polysulfides and sulfides (K2Sx, x = 1–8), significantly enhancing reaction kinetics, specific capacity, and energy density. These batteries achieve near-theoretical capacity (1655 mAh g−1 sulfur) at 75 °C with a 1 M sulfur concentration. At a 4 M sulfur concentration, they deliver 830 mAh g−1 at 2 mA cm−2, retaining 71% capacity after 1000 cycles. This new K-Na/S battery with specific energy of 150-250 Wh kg−1 only employs earth-abundant elements, making it attractive for long-duration energy storage.

The cryogenic treatment of near β Ti–5Al–5Mo–5V–3Cr–1Zr (Ti55531) alloy was conducted using the liquid nitrogen refrigeration method. The microstructure and properties were characterized by scanning electron microscopy (SEM), electron backscatter diffraction (EBSD), X-ray diffraction (XRD), and transmission electron microscopy (TEM). The results show that the alloy achieves optimal properties at a cryogenic time of 8h. Compared to samples that were not cryogenically treated, microhardness, ultimate tensile strength (UTS), and elongation increased by 12.9%, 6.8%, and 8.0% respectively. Detailed microstructural characterization indicated that the cryogenic processing can lead to grain refinement, enhanced dislocation density, and accelerate the transformation of the metastable β phase into the stable α phase, resulting in a higher volume fraction of the α phase. After cryogenic treatment, the lath-shaped α phase reorients from a vertical to a parallel orientation, and its average width is reduced. Simultaneously, cryogenic treatment diminished texture strength but enhanced the uniformity of the alloy. Improvements induced by cryogenic treatment are attributed to alloy volume and lattice contraction caused by cold compression forces at cryogenic temperatures, which generate internal stress and grain deflection.

Abstract Background To systematically analyze differences in atherosclerotic cardiovascular disease (ASCVD) burden between young and older adults. Methods We estimated the prevalence, mortality, and disability-adjusted life years (DALYs) of ASCVD, including ischemic heart disease (IHD), ischemic stroke (IS), and peripheral artery disease (PAD), in individuals aged 20–54 and > 55 years from 1990–2019, utilizing data from the 2019 Global Burden of Disease Study. The annual percentage changes (EAPCs) for age-specific prevalence, mortality, or DALY rates were calculated to quantify the temporal trends of ASCVD burden. We also analyzed population attribution fractions (PAF) of premature ASCVD mortality and DALYs for different risk factors and compared the burden of extremely premature, premature, and non-premature ASCVD cases based on clinical classifications. Results From 1990–2019, the global prevalence rates of IHD, IS, and PAD in the 20–54 years age group increased by 20.55% (from 694.74 to 837.49 per 100,000 population), 11.50% (from 439.48 to 490.03 per 100,000 population), and 7.38% (from 384.24 to 412.59 per 100,000 population), respectively. Conversely, the ASCVD prevalence in > 55years age group decreased. Adverse outcome burdens, including mortality and DALYs, varied among ASCVD subtypes. The decrease in the mortality/DALY burden of IHD and IS was lower in the 20–54 years group than in the > 55 years group. For PAD, DALYs among those aged 20–54 increased but decreased among those aged > 55 years. When grouped according to socio-demographic index (SDI) values, lower SDI regions exhibited a higher proportion of young ASCVD burden. The prevalence of young IHD, IS, and PAD in low SDI regions reached 20.70%, 40.05%, and 19.31% in 2019, respectively, compared with 12.14%, 16.32%, and 9.54%, respectively, in high SDI regions. Metabolic risks were the primary contributors to the ASCVD burden in both age groups. Increased susceptibility to ambient particulate matter pollution and inadequate control of high body-mass index and high fasting plasma glucose in young individuals may partially explain the differing temporal trends between young and older individuals. Conclusions The ASCVD burden in young individuals may become a growing global health concern, especially in areas with lower socioeconomic development levels that require more effective primary prevention strategies.

Summary: Background: Dementia among younger people is rapidly emerging as a global health concern; however, comprehensive research on its shifting burden trends remains insufficient. Methods: Data on the prevalence, incidence, mortality, and disability-adjusted life years (DALYs) associated with dementia occurring in individuals

The escalating prevalence of non-alcoholic fatty liver disease (NAFLD), driven by inadequate dietary habits and metabolic imbalances, underscores the urgent need for effective dietary interventions. This study investigated the potential of 80 % peanut diacylglycerol (DAG) as a functional lipid component in preventing NAFLD and associated intestinal microenvironment based on a high-cholesterol diet (HCD)-induced zebrafish model. We first found that the zebrafish fatty liver model shared multiple similar pathways like lipid-induced atherosclerosis, insulin resistance with NAFLD patient in terms of lipid metabolism. Employing larvae and grown zebrafish, we aimed to elucidate the preventive and alleviating effect of a DAG diet on NAFLD respectively. Results showed that DAG post-intervention significantly decreased hepatic lipid accumulation and diminished intestinal inflammatory in fatty liver zebrafish model. Notably, transcriptomic sequencing illuminated upregulation in genes related to lipid metabolism (e.g., fasn, mogat2, cd36), suggesting that peanut DAG accelerated lipid transportation and fostered a metabolic environment less conducive to NAFLD symptoms. Besides, reduced liver lipid droplets and hepatic inflammatory suggested DAG feeding could also prevent the formation of NAFLD. The study provided compelling evidence supporting the incorporation of DAG into the diet as a strategy for the prevention and management of fatty liver disease, proposing a novel approach to functional food development aimed at combating metabolic diseases.

Periodontitis and diabetes mellitus are two prevalent chronic diseases that have been recognized to exhibit a bidirectional relationship. Individuals with diabetes are more susceptible to periodontitis, and conversely, periodontitis can exacerbate glycemic control in diabetic patients. The underlying mechanisms of this interrelationship involve complex pathways, including inflammatory responses, altered immune functions, and microbial dysbiosis. The mechanistic insights into the interrelationship between periodontitis and diabetes mellitus revolve around the role of inflammation as a common link between the two diseases. Inflammatory mediators such as cytokines, chemokines, and prostaglandins play a crucial role in the pathogenesis and progression of the diseases. The dysregulation of the immune response in diabetes can exacerbate the inflammatory response in periodontitis, leading to increased tissue destruction and bone resorption. The chronic inflammation in periodontitis can contribute to insulin resistance and impaired glycemic control in diabetic patients. Future directions in research aim to further elucidate the molecular mechanisms underlying the interrelationship between periodontitis and diabetes mellitus. Modulating the inflammatory response, restoring microbial balance, and improving glycemic control hold promise in managing both conditions simultaneously. Herein, we will provide an overview of the interrelationship of periodontitis and diabetes mellitus, and retrospect the underlying mechanisms, which may inspire investigators with further research directions.

BackgroundThe recent hemoglobin, albumin, lymphocyte, and platelet (HALP) scores, combined with various clinically available indicators, can comprehensively evaluate the nutritional and immune status of patients. Some observational studies have found a positive correlation between HALP score and cancer prognosis, but the clinical application of HALP score has raised concerns due to the presence of confounding factors. The aim of this study is to explore the relationship between HALP score and long-term mortality in cancer patients.MethodsWe extracted 3832 cancer patients with complete baseline information from the National Health and Nutrition Examination Survey (NHANES). The COX regressions and restricted cubic spline (RCS) curves were used to explore the nonlinear relationship between HALP score and long-term mortality risk in cancer patients. Kaplan-Meier (K-M) curve was conducted to evaluate the impact of HALP score on long-term mortality risk. Additionally, subgroup analysis was conducted to verify the stability of the above results.ResultsWe divided participants into 4 groups based on HALP score, and the COX regression results showed that risk of long-term mortality tended to be lower in cancer patients with high HALP scores. Meanwhile, the RCS curves showed that there was a nonlinear association. The results remained stable in subgroup analyses and in breast cancer, colorectal cancer, cervix and uterus cancer, melanoma, prostate cancer and skin cancer.ConclusionsHALP score were independently associated with the risk of long-term mortality in cancer patients, and there is also a non-linear association. This will provide new perspectives on clinical and nutritional interventions for cancer patients.

Abstract Background Sarcopenic obesity, a clinical and functional condition characterized by the coexistence of obesity and sarcopenia, has not been investigated in relation to dementia risk and its onset. Methods We included 208,867 participants from UK biobank, who aged 60 to 69 years at baseline. Dementia diagnoses were identified using hospital records and death register data. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models to evaluate the associations of obesity, sarcopenia, and sarcopenic obesity with dementia risk, stratified by sex. Stratified analyses were performed across dementia-related polygenic risk score (PRS). Restricted mean survival time models were established to estimate the difference and 95%CIs of dementia onset across different status. Additionally, linear regression models were employed to estimate associations of different status with brain imaging parameters. The mediation effects of chronic diseases were also examined. Results Obese women with high PRS had a decreased risk (HR = 0.855 [0.761–0.961]), but obese men with low PRS had an increased risk (HR = 1.223 [1.045–1.431]). Additionally, sarcopenia was associated with elevated dementia risk (HRwomen = 1.323 [1.064–1.644]; HRmen = 2.144 [1.753–2.621]) in those with low PRS. Among those with high PRS, however, the association was only significant in early-life (HRwomen = 1.679 [1.355–2.081]; HRmen = 2.069 [1.656–2.585]). Of note, sarcopenic obesity was associated with higher dementia risk (HRwomen = 1.424 [1.227–1.653]; HRmen = 1.989 [1.702–2.323]), and results remained similar stratified by PRS. Considering dementia onset, obesity was associated with dementia by 1.114 years delayed in women, however, 0.170 years advanced in men. Sarcopenia (women: 0.080 years; men: 0.192 years) and sarcopenic obesity (women: 0.109 years; men: 0.511 years) respectively advanced dementia onset. Obesity, sarcopenia, and sarcopenic obesity were respectively related to alterations in different brain regions. Association between sarcopenic obesity and dementia was mediated by chronic diseases. Conclusions Sarcopenic obesity and sarcopenia were respectively associated with increased dementia risk and advanced dementia onset to vary degree. The role of obesity in dementia may differ by sex and genetic background.

ObjectiveThe meta-analysis aimed to explore the cardiac adaptation in hypothyroidism patients by cardiac magnetic resonance.Research methods and proceduresDatabases including PubMed, Cochrane Library, Embase, CNKI, and Sinomed for clinical studies of hypothyroidism on cardiac function changes. Databases were searched from the earliest data to 15 June 2023. Two authors retrieved studies and evaluated their quality. Review Manager 5.4.1 and Stata18 were used to analyze the data. This study is registered with the International Platform of Registered Systematic Review and Meta-analysis Protocols (INPLASY), 202440114.ResultsSix studies were selected for further analysis. Five of them reported differences in cardiac function measures between patients with hypothyroidism and healthy controls, and three studies reported cardiac function parameters after treatment in patients with hypothyroidism. The fixed-effect model combined WMD values for left ventricular ejection fraction (LVEF) had a pooled effect size of -1.98 (95% CI -3.50 to -0.44], P=0.01), implying that LVEF was lower in patients with hypothyroidism than in healthy people. Analysis of heterogeneity found moderate heterogeneity (P = 0.08, I² = 50%). WMD values for stroke volume (SV), cardiac index (CI), left ventricular end-diastolic volume index(LVEDVI), left ventricular end-systolic volume (LESVI), and left ventricular mass index(LVMI) were also analyzed, and pooled effect sizes showed the CI and LVEDVI of patients with hypothyroidism ware significantly decrease (WMD=-0.47, 95% CI [-0.93 to -0.00], P=0.05, WMD=-7.99, 95%CI [-14.01 to -1.96], P=0.009, respectively). Patients with hypothyroidism tended to recover cardiac function after treatment [LVEF (WMD = 6.37, 95%CI [2.05, 10.69], P=0.004), SV (WMD = 7.67, 95%CI [1.61, 13.74], P=0.01), CI (WMD = 0.40, 95%CI [0.01, 0.79], P=0.05)], and there was no difference from the healthy controls.ConclusionHypothyroidism could affect cardiac function, although this does not cause significant heart failure. It may be an adaptation of the heart to the hypothyroid state. There was a risk that this adaptation may turn into myocardial damage. Cardiac function could be restored after treatment in patients with hypothyroidism. Aggressive levothyroxine replacement therapy should be used to reverse cardiac function.Systematic review registrationhttps://inplasy.com, identifier (INPLASY202440114).

The efficient fault detection (FD) of traction control systems (TCSs) is crucial for ensuring the safe operation of high-speed trains. Transient faults (TFs) can arise due to prolonged operation and harsh environmental conditions, often being masked by background noise, particularly during dynamic operating conditions. Moreover, acquiring a sufficient number of samples across the entire scenario presents a challenging task, resulting in imbalanced data for FD. To address these limitations, an unsupervised transfer learning (TL) method via federated Cycle-Flow adversarial networks (CFANs) is proposed to effectively detect TFs under various operating conditions. Firstly, a CFAN is specifically designed for extracting latent features and reconstructing data in the source domain. Subsequently, a transfer learning framework employing federated CFANs collectively adjusts the modified knowledge resulting from domain alterations. Finally, the designed federated CFANs execute transient FD by constructing residuals in the target domain. The efficacy of the proposed methodology is demonstrated through comparative experiments.

Neoagarooligosaccharides (NAOS), possessing a variety of bioactivities, are mainly produced by β-agarases cleaving the β-1,4-glycosidic bond of agar or agarose. Previous study indicated that NAOS has antioxidant effect, however, the NAOS monomers on the activity of scavenging ROS has not been deeply clarified till now. In this study, the protective effects of NAOS especially neoagarotetraose (NA4) against H2O2-stimulated oxidative damage in HepG2 cells and their underlying molecular mechanism were investigated. The results indicated that NA4 could inhibit the production of reactive oxygen species (ROS) and enhance the activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in H2O2-induced HepG2 cells. Moreover, NA4 activated the mRNA and protein expression levels of the nuclear factor erythroid-2-related factor 2 (Nrf2), which further up-regulated the mRNA and protein expression of the downstream antioxidant enzymes including heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1), indicating that NA4 could attenuate H2O2-induced oxidative damage through Nrf2 pathway in HepG2 cells. The study suggested that NA4 could be an effective antioxidant candidate and it may be developed as a promising component in healthy food exerting antioxidation effect.

Summary: Eosinophilic chronic rhinosinusitis (ECRS) is a distinct subset of chronic rhinosinusitis characterized by heightened eosinophilic infiltration and increased symptom severity, often resisting standard treatments. Traditional diagnosis requires invasive histological evaluation. This study aims to develop predictive models for ECRS based on patient clinical parameters, eliminating the need for invasive biopsy. Utilizing logistic regression with lasso regularization, random forest (RF), gradient-boosted decision tree (GBDT), and deep neural network (DNN), we trained models on common clinical data. The predictive performance was evaluated using metrics such as area under the curve (AUC) for receiver operator characteristics, decision curves, and feature ranking analysis. In a cohort of 437 eligible patients, the models identified peripheral blood eosinophil ratio, absolute peripheral blood eosinophil, and the ethmoidal/maxillary sinus density ratio (E/M) on computed tomography as crucial predictors for ECRS. This predictive model offers a valuable tool for identifying ECRS without resorting to histological biopsy, enhancing clinical decision-making.

Objective: Our study aimed to elucidate the effect of PAI-1 (Plasminogen Activator Inhibitor-1) and t-PA (Tissue-type Plasminogen Activator) in tissue remodeling in nasal polyps patients. Methods: Samples were streamed as early Nasal Polyps (eNP, n = 10) and inferior tissue from the same patient, mature Nasal Polyps (mNP, n = 14), and Control group (n = 15), respectively. Immunohistochemistry and immunofluorescence were applied to detect localization. Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and Western blot were used to measure different levels among three groups. The mNP tissue was cultured in vitro and treated with TGF-β1 (Transforming Growth Factor-beta 1) activator, TGF-β1 inhibitor (SB431542), and PAI-1 inhibitor (TM5275); then Western blot, qRT-PCR, and ELISA were used to assess changes. Results: The immunohistochemistry and immunofluorescence showed that PAI-1 expression decreased in eNP and mNP, mainly in epithelium and glands. The transcriptional expression and protein level of TGF-β1/t-PA/PAI-1/Collagen1 were lower in eNP than IT while mNP group demonstrated lower mRNA expression and protein level of TGF-β1/t-PA/PAI-1/Collagen1 than Control group. In mNP tissue culture in vitro, TGF-β1 activator elevated t-PA, PAI-1, and Collagen1 with higher release of PAI-1 and Collagen1 in supernatant, whereas SB431542 suppressed above reactions; TM5275 lowered transcriptional and protein level of Collagen1 in supernatant. Conclusion: Early Nasal polyps’ formation in middle meatus mucous is related with fibrillation system PAI-1/t-PA and tissue remodeling; moreover, nasal polyps’ development is regulated by TGF-β1-mediated PAI-1 reduction. Level of evidence: 3b.