Childhood cancer survivors (CCS) are at increased risk for various health issues, including obesity, insulin resistance, hypertension, and dyslipidemia, resulting in the development of metabolic syndrome (MetS) later in life. It has been suggested that anticancer treatment may lead to alterations in lipid metabolism, which play a role in the pathogenesis of metabolic syndrome among CCS. The prospective study included 110 CCS, with a follow-up time of 6.39 years since the end of treatment. Fasting serum of fourteen fatty acids concentrations were measured in all children using gas-liquid chromatography. Among the study group, 41 CCS (37%) met 1 or more criteria for metabolic syndrome and exhibited higher concentrations of myristic (P = 0.002), palmitic (P = 0.003), stearic (P = 0.017), oleic (P = 0. 019), arachidonic (P = 0.002), lignoceric (P = 0.005), docosahexaenoic (P = 0.005), and total fatty acids compared to CCS without metabolic syndrome factors. Additionally, overweight or obese CCS presented higher levels of myristic (P = 0.048), palmitic (P = 0.016), oleopalmitic (P = 0.019), stearic (P = 0.024), oleic (P = 0.020), α-linoleic (P = 0.023) and behenic (P = 0.036) acids compared to survivors with a normal BMI. Childhood cancer survivors develop abnormalities in lipid metabolism, which may contribute to an earlier onset of metabolic syndrome. Additionally, overweight or obesity significantly exacerbates changes in lipid metabolism.

Although obesity and metabolic syndrome (comprising at least three of the following traits-abdominal obesity, elevated blood pressure, triglycerides and glucose/insulin resistance, and reduced high-density lipoprotein cholesterol in serum) are known to impact immune system activity, these conditions are often not considered when immune response characteristics are investigated in various rodent strains. In this work, metabolic syndrome indices are compared in 3 month-old (young) and 6 month-old (adult) rats of Dark Agouti (DA) and Albino Oxford (AO) strains, while parameters of coagulation, inflammation and oxidative stress were determined in young animals. Study reveals that both young and adult AO rats are obese, intolerant to glucose with higher levels of triglycerides and lower levels of high-density lipoprotein cholesterol when compared to age-matched DA rats. Parameters of coagulation, inflammation and oxidative stress that may contribute to the worsening of metabolic syndrome during aging are also higher in young AO rats. Metabolic syndrome observed in young and intensified in adult AO rats should be taken into consideration when analyzing alterations in immune reactivity during aging in this rat strain.

Radiomics is increasingly utilized in medical image analysis. This study evaluates the use of infrared thermography, a technique well-suited for radiomic analysis, in diagnosing metabolic syndrome (MS). Facial and palmar thermographs from 200 males (100 healthy controls and 100 MS patients) were analyzed. The dataset was split into a training cohort (n = 140) and a validation cohort (n = 60). All participants underwent laboratory testing on the same day as infrared thermography imaging. A total of 1656 radiomic features were extracted from each participant's thermographs and refined using Pearson correlation coefficients, two-sample t-tests, and LASSO regression. A binary random forest (RF) classification model was then constructed and evaluated based on its calibration, discrimination, and clinical utility. The RF model demonstrated strong diagnostic performance, achieving an AUC of 0.91 in the validation cohort. Calibration and decision curve analyses confirmed the model's clinical applicability. Infrared thermography-based radiomics offers a promising, non-invasive method for early screening of MS, highlighting its potential clinical utility.

Insulin resistance (IR), as quantified by the triglyceride glucose (TyG) index, and visceral obesity, as assessed by the body roundness index (BRI), have been identified as pivotal risk factors for stroke. However, the combined impact of these two indicators on stroke risk has not been thoroughly investigated. This study aims to investigate both the separate and combined associations, as well as potential interactions, between the TyG index and/or BRI with respect to stroke incidence.

This cohort study encompassed 6621 respondents who were free of stroke at baseline from the China Health and Retirement Longitudinal Study (CHARLS). Participants were categorized based on the median values of the TyG index or/and BRI. Cox proportional hazards regression models were employed to examine the associations between the TyG index alone, BRI alone, and their combined effects on stroke incidence. Both additive and multiplicative interaction effects were further estimated.

Among 6621 participants aged 45 years or older, the mean (SD) age was 58.06 (8.57) years, with 2951 (44.6%) being male. During a follow-up period of up to 9 years, 743 individuals experienced stroke events. Compared to participants with low TyG index and low BRI, the adjusted hazard ratios (HRs) were as follows: 1.36 (95% confidence interval [CI] 1.05-1.75) for high TyG index alone, 1.61 (95% CI 1.27-2.05) for high BRI alone, and 1.78 (95% CI 1.40-2.26) for high TyG index and high BRI. Neither additive nor multiplicative interactions between BRI and TyG for incident stroke were statistically significant. The combination of TyG and BRI enhanced the predictive capability for stroke compared to either biomarker alone.

We discovered that both the TyG index and BRI are strongly associated with stroke incidence. The joint assessment of TyG and BRI enhances the predictive capability for stroke, underscoring the critical role of IR and visceral adiposity in the identification and screening of stroke risk.

In the pursuit of an effortless "miracle cure", there has been a significant increase in the proliferation of fad diets. These diets generally exclude a food group or macronutrients and may also restrict energy intake; they become popular quickly but often lack substantial scientific evidence to support their efficacy and safety. They only show short-term results rather than promoting a lifestyle change. Fad diets are nutritionally unbalanced and can be dangerous for some individuals. Most fad diets are generally restrictive in carbohydrates, high in protein, or unbalanced and have low energy intake, which can harm patients with early stages of chronic kidney damage (CKD) who need a low-protein diet with adequate energy intake. This narrative review discusses the risk of fad diet prescriptions for non-dialysis CKD patients.

Platelet dysfunction plays a critical role in the pathogenesis of various disorders affecting the hemostatic-coagulant system. This review aims to explore the mechanisms by which platelet dysfunctions contribute to the disruption of hemostasis, leading to an increased risk of both thrombosis and bleeding. Platelets, traditionally known for their role in clot formation, can exhibit altered functionality under pathological conditions such as cardiovascular diseases, metabolic disorders, and autoimmune diseases, impacting their interaction with coagulation factors and vascular endothelium. The review discusses the molecular and cellular mechanisms underlying platelet dysfunction, including aberrations in platelet activation, aggregation, and secretion. It also highlights the interplay between platelets and other components of the coagulation cascade, such as fibrinogen and clotting factors, in maintaining vascular integrity. Moreover, the review examines clinical implications, including how platelet dysfunction can be a contributing factor in conditions like deep vein thrombosis, stroke, and disseminated intravascular coagulation (DIC). Finally, current therapeutic approaches targeting platelet dysfunctions, including antiplatelet agents and emerging therapies, are reviewed to provide insights into potential strategies for managing fluid-coagulation system imbalances. This review underscores the importance of a comprehensive understanding of platelet dysfunction to improve diagnosis and treatment of hemostatic disorders.

Anti-oxidant/Pro-oxidant oxidant imbalance leads to chronic inflammation and insulin resistance can lead to the development of metabolic syndrome (MetS). The oxidative balance score (OBS) is a tool for assessing oxidative stress associated with MetS risk. However, the association between OBS and mortality in patients with MetS remains unclear. This study analyzed 10,647 MetS patients from the 1999-2018 National Health and Nutrition Examination Survey (NHANES). OBS were calculated using a combination of 16 dietary and 4 lifestyle factors. Multivariate Cox proportional hazards regression models, Kaplan-Meier survival analysis, restricted cubic splines (RCS), and subgroup analyses were used to evaluate the potential association between OBS and the risk of all-cause and cardiovascular mortality. Sensitivity analyses confirmed the robustness of the results. This study found that OBS was inversely associated with all-cause and cardiovascular mortality in patients with MetS, a result consistent across most subgroups. Both the Kaplan-Meier curve and RCS analysis supported these findings. Sensitivity analysis was used to verify the robustness of the results. Maintaining an antioxidant-based diet and lifestyle may help reduce the risk of all-cause and cardiovascular mortality in patients with MetS. These findings underscore the significance of incorporating antioxidant-rich dietary patterns and behavioral practices in strategies aimed at preventing and managing MetS.

Globally, traumatic injuries and severe hemorrhagic wounds resulting from natural disasters, wars, traffic accidents, and operation rooms, especially during birth, are among the most difficult humanitarian and economic problems. Thus, the priority in emergency medical treatment is reducing unexpected blood loss, which can significantly influence a patient's rescue and recovery speed. For the immediate cessation of bleeding in severe hemorrhagic wounds and to speed up their healing, environmentally friendly γ-ionizing irradiation technology was used to develop innovative natural-based hydrogels impregnated with traditional medicinal plant extracts (MPE) with proven hemostatic and bactericidal potential as potential dressings for hemostasis, infection control, and wound healing. A series of superabsorbent hemostatic dressings composed of (hydroxypropyl methylcellulose/agar-agar/carbopol) (HPMC/AA/Cp) assisted with Salvadora persica (Miswak) (Mis), Achillea millefolium L. (Yarrow) (Yaro), (shepherd's purse) (Sheph), and Equisetum arvense L. (horsetail) (HoTa) extracts were prepared. The freeze-drying technique was used to obtain spongious (HPMC/AA/Cp)-Mis, (HPMC/AA/Cp)-Yaro, (HPMC/AA/Cp)-Sheph, and (HPMC/AA/Cp)-Hota, respectively. The developed dressings' swelling characteristics and the In-vitro cytocompatibility, hemostatic efficacy, and bactericidal potential were evaluated. The In-vivo hemostatic potential was assessed using a hemorrhaging liver rat model. Transferrin and calcium levels were measured to document their impact on the hemostasis process.

Changing poor dietary habits is effective for treating metabolic syndrome (MetS). Despite the global reputation of the Mediterranean diet (MD) for health, research on its link to MetS is limited, especially in non-Mediterranean regions. This study aimed to investigate the relationship between the MD and MetS. Data from the 2007 to 2020 NHANES were analysed using multiple logistic regression, restricted cubic spline (RCS) regression, and subgroup analysis. Among 20,991 participants, a negative association between Mediterranean diet score (MDS) and MetS prevalence was observed. RCS regression indicated a linear relationship. Subgroup analysis revealed a significant negative association in most groups, except those with high school education, other Hispanics, and non-Hispanic blacks. In the American population, greater adherence to the Mediterranean diet is associated with a reduced risk of metabolic syndrome, emphasising its protective effects and relevance in public health strategies. Future research should focus on promoting its adoption and investigating causal mechanisms and the impact of specific dietary components through longitudinal studies.

The Systemic Immune-Inflammation Index (SII) is a novel biomarker of systemic inflammation. We explored the association between the SII and metabolic syndrome (MetS) and its components in middle-aged and older adults.

We included 2755 participants (1305 men) aged 45-84 years from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort from examination 5 (2010-2012). Logistic regression was employed to assess the relationship between the SII and MetS, as well as its components.

A total of 1082 participants (463 men) were diagnosed with MetS. On a continuous scale, the SII was positively associated with MetS (odds ratio (OR): 1.23, 95% confidence interval (CI): 1.05-1.46) and its components including hyperglycemia (1.23: 1.05-1.44) and elevated blood pressure (BP) (1.47: 1.14-1.89). When analyzed on a quartile scale, participants in the quartile 4 of SII had 32% and 63% higher prevalence of hyperglycemia and elevated BP, respectively, compared to those in the quartile 1 (P for trend: 0.021 and < 0.001, respectively). Additionally, we identified 40% higher prevalence of low HDL-C in quartile 2 of the SII compared to quartile 1 (1.40; 1.07-1.83) (P trend = 0.454). In subgroup analysis, general obesity status modified the relationship between SII and abdominal obesity, showing a positive association in obese individuals (1.72: 1.00-2.95) and a negative association (0.80: 0.66-0.97) in non-obese individuals (P for interaction = 0.009).

Higher SII scores were associated with an increased likelihood of MetS, hyperglycemia, and high BP among middle-aged and older adults. Longitudinal studies are needed to determine the causal relationships between SII and the development of MetS, as well as to assess the potential role of SII as a screening tool in clinical practice.

Metabolic syndrome (MetS) and sarcopenia (SP) are increasingly significant public health issues in aging societies, sharing common pathophysiological mechanisms and being associated with severe health consequences. This study investigates the impact of MetS and SP on all-cause and cause-specific mortality using a longitudinal, nationally representative population-based cohort.

The study analyzed data from the National Health and Nutrition Examination Survey (NHANES) conducted between 1999 and 2018. Mortality data were obtained from the National Death Index up to December 2019.

Among the 21,962 participants, 13,517 (61.5%) had neither MetS nor SP(MetS-/SP-), 5,407 (24.6%) had MetS only(MetS+/SP-), 2,698 (12.2%) had SP only(MetS-/SP+), and 340 (1.5%) had both MetS and SP(MetS+/SP+). Compared to the group without MetS and SP, the groups with MetS only, SP only, and both MetS and SP showed increased all-cause mortality, with adjusted hazard ratios (HR) of 1.23 (95% CI: 1.11-1.37), 1.63 (95% CI: 1.41-1.89), and 1.61 (95% CI: 1.33-1.95), respectively. The MetS+/SP+ group had the highest overall mortality risk (trend test p<0.0001). For cause-specific mortality, the MetS+/SP+ group exhibited increased cardiovascular mortality (HR: 1.89, 95% CI: 1.27-2.81), cardiac mortality (HR: 1.89, 95% CI: 1.25-2.86), respiratory mortality (HR: 2.63, 95% CI: 1.29-5.35), and diabetes mortality (HR: 8.79, 95% CI: 2.62-29.45) compared to the group without MetS and SP.

The coexistence of MetS and SP significantly increases the risk of all-cause and cause-specific mortality. Individuals with either condition may require more vigilant management to prevent the onset of the other condition, thereby reducing mortality rates. These findings highlight the importance of integrated healthcare strategies targeting both MetS and SP to improve patient outcomes and longevity.

Tauopathy is one of the pathological features of Alzheimer's disease and related dementias (ADRD). At present, there have been many studies on the formation, deposition, and intercellular transmission of tau in neurons and immune cells. The vasculature is an important component of the central nervous system. This review discusses the interaction between vasculature and tau in detail from three aspects. (1) The vascular risk factors (VRFs) discussed in this review include diabetes mellitus (DM), abnormal blood pressure (BP), and hypercholesterolemia. (2) In ADRD pathology, the hyperphosphorylation and deposition of tau interact with disrupted vasculature, such as different cells (endothelial cells, smooth muscular cells, and pericytes), the blood-brain barrier (BBB), and the cerebral lymphatic system. (3) The functions of vasculature are regulated by various signaling transductions. Endothelial nitric oxide synthase/nitric oxide, calcium signaling, Rho/Rho-associated coiled-coil containing Kinase, and receptors for advanced glycation end products are discussed in this review. Our findings indicate that the prevention and treatment of vascular health may be a potential target for ADRD combination therapy. HIGHLIGHTS: Persistent VRFs increase early disruption of vascular mechanisms and are strongly associated with tau pathology in ADRD. Cell dysfunction in the vasculature causes BBB leakage and drainage incapacity of the cerebral lymphatic system, which interacts with tau pathology. Signaling molecules in the vasculature regulate vasodilation and contraction, angiogenesis, and CBF. Abnormal signaling transduction is related to tau hyperphosphorylation and deposition.

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder, and critically ill patients with T2DM in intensive care unit (ICU) have an increased risk of mortality. In this study, we investigated the relationship between nine inflammatory indicators and prognosis in critically ill patients with T2DM to provide a clinical reference for assessing the prognosis of patients admitted to the ICU. Critically ill patients with T2DM were extracted from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database and divided into training and testing sets (7:3 ratio). An external validation cohort was collected from a single center in China using identical criteria. Logistic and Cox regression analyses were used to evaluate the relationship between nine inflammatory indicators and ICU, 30-day, and 90-day mortality rates. Significant predictive variables were chosen using least absolute shrinkage selection operator (LASSO) regression from logistic regression results, and a prognostic prediction model was built with multivariate logistic regression. The model was validated in both test and external validation sets. A total of 4,783 patients were included for model development and testing; an additional 204 served as the external validation set. The levels of eight inflammatory indicators were significantly correlated with short-term prognosis in critically ill patients with T2DM (P < 0.05 for all). The prediction model showed excellent discrimination performance, with AUC values of 0.825 (95% CI, 0.785-0.864) in the test set and 0.741 (95% CI, 0.630-0.851) in the external validation set. Calibration curves demonstrated strong consistency in both sets. In addition, decision curve analysis showed a net clinical benefit within 1-60% threshold probability in the test set and 10-41% threshold probability in the external validation set. Eight inflammatory indicators were identified as independent risk factors for prognosis in critically ill patients with T2DM. The prediction model showed promising performance in both internal and external validation cohorts, highlighting its potential as a valuable tool for early risk stratification and prediction of the outcomes of personalized treatment strategies in ICU settings.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting women of reproductive age characterized by a spectrum of clinical, metabolic, reproductive, and psychological abnormalities. This syndrome is associated with significant long-term health risks, necessitating elucidation of its pathophysiology, early diagnosis, and comprehensive management strategies. Several contributory factors in PCOS, including androgen excess and insulin resistance, collectively enhance oxidative stress, which subsequently leads to mitochondrial dysfunction. However, the precise mechanisms through which oxidative stress induces mitochondrial dysfunction remain incompletely understood. Comprehensive searches of electronic databases were conducted to identify relevant studies published up to 30 September 2024. Mitochondria, the primary sites of reactive oxygen species (ROS) generation, play critical roles in energy metabolism and cellular homeostasis. Oxidative stress can inflict damage on components, including lipids, proteins, and DNA. Damage to mitochondrial DNA (mtDNA), which lacks efficient repair mechanisms, may result in mutations that impair mitochondrial function. Dysfunctional mitochondrial activity further amplifies ROS production, thereby perpetuating oxidative stress. These disruptions are implicated in the complications associated with the syndrome. Advances in genetic analysis technologies, including next-generation sequencing, have identified point mutations and deletions in mtDNA, drawing significant attention to their association with oxidative stress. Emerging data from mtDNA mutation analyses challenge conventional paradigms and provide new insights into the role of oxidative stress in mitochondrial dysfunction. We are rethinking the pathogenesis of PCOS based on these database analyses. In conclusion, this review explores the intricate relationship between oxidative stress, mtDNA mutations, and mitochondrial dysfunction, offers an updated perspective on the pathophysiology of PCOS, and outlines directions for future research.

Insulin resistance (IR) is linked to an increased risk of frailty, yet it remains unclear whether the non-insulin-based IR indicators are associated with frailty trajectories and physical function decline. It aimed to examine the associations of triglyceride-glucose (TyG) index, metabolic score for insulin resistance (METS-IR), estimated glucose disposal rate (eGDR) and with long-term deficit-accumulation frailty trajectories and physical function decline.

Data from 6722 participants in the China Health and Retirement Longitudinal Study (CHARLS) were analyzed. Baseline TyG index, METS-IR, eGDR, along with the frailty index (FI) over nine years, were calculated. FI trajectories were assessed using group-based trajectory model (GBTM). Logistic regression models were used to analyze the associations between IR indicators with FI trajectory and frailty risk. Restricted cubic splines (RCS) models were utilized to detect potential dose-response associations. Linear mixed-effects model was used to evaluate associations with FI development speed. Age, gender, educational level, marital status, smoking status, drinking status, life satisfaction, social activity and sleep duration were adjusted. Additionally, a two-sample Mendelian randomization (MR) was performed to assess the causality of observed associations.

Three FI trajectories including low-stable frailty, moderate-increasing frailty, and accelerated rising frailty were identified. Regarding the frail risk, each SD increment in TyG index was associated with a 16.1% increase in the risk of frailty (OR = 1.161; 95%CI: 1.092, 1.235). An inverse association was observed for eGDR with the OR (95%CI) being 0.741 (0.696, 0.788). A linear relationship was observed between baseline TyG index and frailty risk (P nonlinear = 0.696), but nonlinear association patterns for eGDR (P nonlinearity < 0.010) and METS-IR (P nonlinearity < 0.010). Each SD increment of TyG index was associated with greater FI increase (β = 0.005 SD/y; 95%CI = 0.002, 0.008 SD/y; P < 0.001). A similar association pattern was observed for METS-IR, and participants in the highest quartile of METS-IR showed significantly greater FI progression, with β value of 0.013 (95% CI = 0.004, 0.022). Each SD increment of eGDR was associated with a slower increase in FI (β=-0.006 SD/y, 95% CI=-0.009, -0.003 SD/y; P < 0.001). Participants in the highest quartile of eGDR presented a lower annual change in FI compared with participants in quartile 1 group during follow-up (β=-0.013 SD/y, 95% CI=-0.022, -0.005 SD/y; P for trend = 0.001). Similar findings were observed for physical function decline. Findings from MR analysis showed a causal relationship between higher TyG index and increased risk of frailty (β = 0.214, 95% CI = 0.079, 0.349; P = 0.002).

The non-insulin-based IR indicators, including TyG index, METS-IR and eGDR, were independently associated with the frailty progression and physical function decline. Monitoring and managing abnormal glucose metabolism should be recommended as a part of comprehensive strategies to prevent or delay the progression of frailty.

Diabetes is closely related to hypertension, and insulin resistance-related indices are novel metrics used to evaluate the risk of diabetes and cardiovascular diseases. This study aims to explore the relationships between the TyG index, METS-IR, TG/HDL-C, and HOMA-IR with hypertension.

Data from the NHANES spanning ten consecutive survey cycles from 1998 to 2018 were utilized, focusing on adults with complete blood pressure data and comprehensive information for calculating the TyG index, METS-IR, TG/HDL-C, and HOMA-IR. A multivariable logistic regression model was employed to examine the relationship between insulin resistance indices and hypertension as well as blood pressure levels, while subgroup analyses were conducted to explore potential influencing factors. RCS curves were used to describe both linear and non-linear relationships.

This NHANES-based study included 16,062 adults. Regardless of the adjustment for covariates, significant associations were found between the TyG index, METS-IR, TG/HDL-C, HOMA-IR and hypertension risk. The ROC curve demonstrated the stability of the TyG index, METS-IR, TG/HDL-C, and HOMA-IR in predicting hypertension risk. The RCS curves uncovered a linear relationship between the TyG index, METS-IR, and hypertension, whereas TG/HDL-C and HOMA-IR exhibited a non-linear association with hypertension. Subgroup analyses indicated that smoking and diabetes may influence the relationship between insulin resistance-related indices and hypertension.

Elevated levels of the insulin resistance indices TyG index, METS-IR, TG/HDL-C, and HOMA-IR are closely associated with hypertension risk. These indices can serve as effective markers for monitoring hypertension risk in clinical practice. However, larger-scale prospective cohort studies are needed to validate these findings and further explore the clinical application potential of the TyG index, METS-IR, TG/HDL-C, and HOMA-IR as tools for cardiovascular risk assessment. Such studies will help elucidate the specific causal relationships between these insulin resistance-related indices and hypertension and advance their practical application in clinical settings.

This study aimed to explore the risk factors of hypokalemia after radical resection of esophageal cancer (EC) and establish a nomogram risk prediction model to evaluate hypokalemia risk after esophagectomy. Thus, this study provides a reference for the clinical development of intervention measures.

Clinical data of EC patients who underwent radical surgery from January 2020 to November 2022 in the First Affiliated Hospital of Guangxi Medical University were retrospectively collected. The relevant variables were screened using multivariate logistic regression analysis with IBM SPSS 25.0 and R 4.2.0 software, and a nomogram for predicting hypokalemia risk was established. The established nomogram was evaluated by receiver operating characteristic (ROC), calibration, and decision curves. The model was also internally validated by 1000 bootstrap resampling methods.

After radical EC resection, the incidence rate of hypokalemia in 213 patients was 19.2% (41/213). The hemoglobin levels, total serum protein, serum albumin, calcium ion concentration, direct bilirubin, prothrombin time (PT), and activated partial thromboplastin time (APTT) were related (p < 0.05). The multivariate logistic analysis showed that the white blood cell count, serum albumin level, direct bilirubin, and operation time were risk factors for hypokalemia after radical EC resection (p < 0.05). The area under the ROC curve (AUC) was 0.764, demonstrating the good discriminative ability of the established nomogram for hypokalemia prediction. The calibration curve showed a good fit between the predicted and actual observed probabilities. The model maintained a high C-index in the internal validation (C-index = 0.758), supporting that the nomogram can be widely used for hypokalemia prediction.

The prediction model for hypokalemia risk with individualized scores based on the patient's white blood cell count, serum albumin level, direct bilirubin, and operation time can screen out high-risk patients who might develop hypokalemia. It is of certain reference value for clinicians to screen and follow up with patients with emphasis and to formulate preoperative and postoperative intervention strategies.

Phthalate exposures have been shown to be inversely associated with reproductive success among women undergoing assisted reproductive technology (ART). However, the underlying mechanisms are unknown.

To explore blood coagulation function as the mediating role of associations between exposure to phthalates and ART outcomes.

A total of 735 women from the Tongji Reproductive and Environmental (TREE) study were included. Urine samples collected at recruitment were quantified for 8 phthalate metabolites, and blood clotting time and platelet indices were also determined. Generalized linear regression, logistic regression, weighted quantile sum (WQS) regression, or Bayesian kernel machine regression (BKMR) models were applied to investigate the associations among individual and mixture of phthalate metabolites, blood coagulation parameters, and ART outcomes. The mediation role of blood coagulation parameters was estimated by mediation analysis.

Mono-n-butyl phthalate (MBP), mono-isobutyl phthalate (MiBP), monobenzyl phthalate (MBzP), mono(2-ethyl-5-carboxypentyl) phthalate (MECPP), and molar sum of di(2-ethylhexyl) phthalate metabolites (∑DEHP) were positively associated with platelet indices. Phthalate metabolite mixture was also positively associated with platelet count (PLT), mean platelet volume (MPV), and plateletcrit (PCT), whereas inversely associated with international normalized ratio (INR). Meanwhile, PLT and PCT were inversely associated with the odds of implantation success and live birth, while prothrombin time and INR were positively associated with the odds of implantation success. Mediation analyses showed indirect effects of above-mentioned phthalate metabolites and phthalate mixture on the odds of implantation success and live birth through PLT or PCT, with the proportion mediated ranging from 3.44% to 8.96%.

Phthalates may increase the risks of ART failure through enhancing blood coagulation function. More studies are warranted to verify the findings.

Studies have reported an association among systemic immune inflammation index (SII), all-cause and cause-specific mortality, but the results are inconsistent.

To comprehensively explore the association between Systemic Immune Inflammation (SII) and the risk of all-cause mortality, cardiovascular disease (CVD), and cancer mortality.

A meta-analysis was conducted by reviewing existing literature. The search encompassed prominent databases including PubMed, Embase, Cochrane, and the Web of Science, with the cutoff date set at March 1, 2024. Furthermore, subgroup analyses and dose-response assessments were undertaken to provide a nuanced exploration of mortality risk factors.

A total of 33 articles were included (427,819 participants). In the study, SII was associated with an increased risk of all-cause mortality (HR = 1.45, 95%CI [1.36,1.54], P < 0.05). SII increased the risk of CVD mortality (HR = 1.44, 95%CI [1.29,1.60], P < 0.05). The Linear independence shows that for every 100 units increase in SII, the risk of all-cause and CVD death increases by 5% and 6%. SII was not associated with a statistically significant risk of cancer death (HR = 1.09, 95%CI [0.96,1.23], P < 0.05).

Meta-analysis showed that SII was associated with all-cause mortality and CVD mortality. More data and basic research are needed to confirm the association.

This study utilized large-scale population data from the National Health and Nutrition Examination Survey (NHANES) to elucidate the relationship between the Klotho protein and metabolic syndrome along with its components. We further investigated the possible mediating effect of inflammation on these relationships. Our objective was to identify biomarkers for risk stratification and potential therapeutic targets for metabolic syndrome.

This study enrolled 13,119 participants aged 40-79 years, spanning five NHANES cycles from 2007 to 2016, with complete information on metabolic syndrome and the Klotho protein. The definition of metabolic syndrome followed the criteria of the National Cholesterol Education Program-Adult Treatment Panel III. Survey-weighted logistic regression and subgroup analysis were used to explore the associations between serum Klotho protein levels and metabolic syndrome, along with its components. Mediation analysis was performed to investigate the mediating effects of inflammation-related markers, including white blood cells, neutrophils, lymphocytes, monocytes, the neutrophil-to-lymphocyte ratio (NLR), the platelet-to-lymphocyte ratio (PLR), the systemic immune-inflammation index (SII) and the monocyte-to-HDL ratio (MHR), with the aim of elucidating how the Klotho protein influences the onset and progression of metabolic syndrome.

The study participants had an average age of 56.06 years (95% CI: 55.76-56.37), with a Klotho protein concentration of 798.10 pg/ml (95% CI: 656.50-980.50) and a 43.77% prevalence of metabolic syndrome (n = 5742). In the crude model, Klotho was negatively correlated with metabolic syndrome and its components, including central obesity, hypertension, and hypertriglyceridemia. After adjusting for all confounding factors, Klotho was demonstrated to be negatively associated only with metabolic syndrome (OR: 0.82, 95% CI: 0.70-0.97), hypertension (OR: 0.83, 95% CI: 0.70-0.98), and hypertriglyceridemia (OR: 0.78, 95% CI: 0.67-0.91). Subgroup and interaction analyses revealed significant interactions between age, sex, race/ethnicity, body mass index, and Klotho. Additionally, mediation analysis demonstrated that leukocytes, neutrophils and monocytes accounted for 34.78%, 31.91% and 7.13%, respectively, of the associations between Klotho and metabolic syndrome.

The serum concentration of Klotho protein was negatively associated with metabolic syndrome, with the relationship being partly mediated by systemic immune inflammation. The findings of this research revealed that the Klotho protein may be a valuable biomarker for risk stratification and a potential therapeutic target for metabolic syndrome.

Observational studies support that altered immunoglobulin G (IgG) N-glycosylation and inflammatory factors are associated with cardiometabolic diseases (CMDs); nevertheless, the causality between them remains unclear.

Two-sample Mendelian randomization (MR) analyses were conducted to systematically investigate the bidirectional causality between IgG N-glycans and nine CMDs in both East Asians and Europeans.

In the forward MR analysis, the univariable MR analysis presented suggestive causality of 14 and eight genetically instrumented IgG N-glycans with CMDs in East Asians and Europeans, respectively; the multivariable MR analysis showed that ten and 11 pairs of glycan-CMD associations were identified in East Asian and European populations, respectively. In the reverse MR analysis, based on East Asians and Europeans, the univariable MR analysis presented suggestive causality of seven and 12 genetically instrumented CMDs with IgG N-glycans, respectively; the multivariable MR analysis presented that six and five CMD-glycan causality were found in East Asian and Europeans, respectively.

The comprehensive MR analyses provide suggestive evidence of bidirectional causality between IgG N-glycans and CMDs. This work helps to understand the molecular mechanism of the occurrence/progression of CMDs, optimize existing and develop new strategies to prevent CMDs, and contribute to the early identification of high-risk groups of CMDs.

The neutrophil-to-lymphocyte ratio (NLR) has emerged as a novel inflammatory marker related to disease prognosis, this study aimed to evaluate the association between NLR and mortality in metabolic syndrome (MetS) patients.

This study used data from 13,156 participants with MetS, derived from the National Health and Nutrition Examination Survey from 1999 to 2020. The NLR was calculated, and its associations with cardiovascular disease (CVD) mortality and all-cause mortality were assessed by multivariate Cox regression, restricted cubic spline and Kaplan-Meier curves. The study performed subgroup analyses to validate the robustness of the findings in different populations. The predictive ability of NLR was evaluated using time-dependent receiver operating characteristic curve. The indirect impact of eGFR was explored by mediation analysis.

As NLR values increased, there was an obvious rise in the risk of mortality in MetS. The fully adjusted continuous model revealed a 16.0%, 14.4% elevated risk of CVD mortality (HR = 1.160; 95% CI: 1. 090-1.234, p < 0.0001) and all-cause mortality (HR = 1.144; 95% CI: 1. 086-1.206, p < 0.0001), respectively, with each one-unit increment in NLR. Comparing the highest to the lowest quartile of NLR, the top quartile exhibited a significantly increased risk of CVD mortality (HR = 2. 447; 95% CI: 1. 561-3. 836, p < 0.0001), and all-cause mortality (HR = 1. 53; 95% CI: 1. 188-1. 972, p = 0.001) among individuals with MetS. Subgroup analyses substantiated the stability of these associations in most populations. The curve under area for the 3, 5, and 10 years were 0.650, 0.716, and 0.645 for CVD mortality, and 0.746, 0.688, and 0.635 for all-cause mortality. Significantly, the eGFR acted as an intermediary in the relationship of NLR with CVD mortality and all-cause mortality, accounting for 9.85% and 9.86% of the effect, respectively.

The NLR served as a significant indicator for assessing the risk of mortality in the MetS population. Consequently, we recommended the regular assessment of NLR in MetS populations as a potentially advantageous method for evaluating their risk of mortality.

Hepatic ischemia and reperfusion (I/R) injury is a common problem faced by patients undergoing clinical liver transplantation and hepatectomy, but the specific mechanism of liver I/R injury has not been fully elucidated. The protein degradation complex 11S proteasome is involved in apoptosis, proliferation and cell cycle regulation by regulating the 11S proteasome regulatory complex (REG)γ. The main objective of this study is to explore the role and specific mechanism of REGγ in liver I/R.

By constructing a model of in vivo hepatic I/R injury in mice and a model of hypoxia and reoxygenation (H/R) in isolated hepatocytes. First, the REGγ expression were detected during hepatic I/R in mice. Second, to investigate the effects of REGγ knockout (KO) on liver necrosis, inflammatory response, apoptosis and mitochondrial function. Finally, mouse liver Src homology collagen (p66shc) mitochondrial translocation was detected.

The expression of REGγ was up-regulated during hepatic I/R. REGγ KO had significantly reduced liver tissue infarct size, liver transaminases, inflammatory cells infiltration, inflammatory cytokine and activation of nuclear factor kappa-B (NF-κB) signaling pathway and cell apoptosis. REGγ KO had significantly alleviated the mitochondrial damage, decreased the up-regulated level of cytochrome C, reactive oxygen species (ROS). REGγ KO had significantly reduced p66shc mitochondrial translocation in mice.

The experimental results of this study indicated that REGγ has an important role in preventing liver I/R injury and may play a role through the mitochondrial p66shc signaling pathway.

Metabolic syndrome (MetS) is an important risk factor for atherosclerotic cardiovascular disease (ASCVD). Elevated triglyceride (TG) levels and decreased high-density lipoprotein levels (HDL-C) are predisposing factors for the development of ASCVD. Evidence on the association between atherosclerotic index of plasma [AIP = log (TG/HDL-C)] and MetS is limited. Our study aimed to investigate the association between AIP and MetS. This is a cross-sectional study that determines the presence of MetS by assessing anthropometric and biochemical parameters. Multivariate log-binomial regression models were used to analyze the relationship between AIP and MetS risk. To further test the stability of the results, we performed sensitivity analyses in young, non-obese, and normal lipid population. Smoothing plots explored the potential nonlinear relationship between the AIP index for MetS and the estimated potential risk threshold. Predictive power of AIP for MetS using respondent operating characteristic (ROC) curves. The prevalence of MetS was 67.35%. Multivariate logistic regression analysis showed an independent and positive association between AIP and MetS (Per 1 SD increase, PR = 1.31, 95% CI: 1.15-1.47). Sensitivity analysis demonstrated the stability of the results. Smoothing plot showed a nonlinear relationship between AIP and MetS, with an inflection point of 0.66. ROC curve analysis, AIP was an accurate indicator for assessing MetS in type 2 diabetics (AUC = 0.840, 95% CI: 0.819-0.862). AIP is a stable and independently powerful predictor of MetS in T2DM patients. AIP can be used as a simple assessment tool for the early detection of MetS and disease management for the prevention of cardiovascular disease.

Obesity is linked to the increasing prevalence of metabolic syndrome (MetS), even among the pediatric population. Some inflammatory and cardioembolic indexes derived from routine laboratory tests have captivated the attention of the medical community.

The aim of our study was to evaluate whether these markers are effective in distinguishing varying degrees of obesity and MetS in children and adolescents.

We conducted a retrospective study. A total of 71 children and adolescents, aged between 6 and 16, were included in the study. Among them, 5 were overweight, 35 had obesity, and 31 had severe obesity. According to the NCEP ATP III criteria, 32 individuals had Metabolic Syndrome (MetS), while 39 did not have MetS.

The MetS positive group had higher values of TG/HDL-C (p < 0.001), TC/HDL-C (p < 0.001), MHR (p = 0.015), LHR (p = 0.001), NHR (p = 0.001), atherogenic index of plasma (p < 0.001), and PHR (p < 0.001). ESR, NLR, PLR, and SII did not progressively increase with the number of MetS criteria. The ROC curve analysis demonstrated that markers such as TG/HDL-C, the atherogenic index of plasma, TC/HDL-C, LHR, NHR, and PHR were effective in identifying MetS in children and adolescents with obesity.

In conclusion, we determined that some novel inflammatory and cardioembolic indexes are useful in assessing MetS and obesity in children and adolescents.

Background: Subclinical myocardial injury (SCMI) is associated with an increased risk of poor cardiovascular disease (CVD) outcomes. Understanding the underlying risk factors for SCMI is crucial for the prevention and management of CVD. We hypothesized that atherogenic dyslipidemia, a combination of high triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C), is associated with an increased risk of SCMI. Methods: This analysis from the third National Health and Nutrition Examination Survey (NHANES-III) included 7093 participants (age 59.3 ± 13.4 years, 52.8% women, and 49.4% White) free of CVD. Atherogenic dyslipidemia was defined as TG ≥ 150 mg/dL and HDL-C < 40 mg/dL in men or <50 mg/dL in women. A validated electrocardiographic-based cardiac infarction injury score (CIIS) ≥ 10 was considered positive for SCMI. Multivariable logistic regression analysis was used to examine the association of different combinations of TG and HDL-C groups, including atherogenic dyslipidemia with SCMI. Results: About 22.5% (n = 1594) of participants had atherogenic dyslipidemia, and 26.3% (n = 1862) had SCMI. Compared to participants with normal TG and normal HDL-C, those with atherogenic dyslipidemia had a higher prevalence of SCMI (31.2% vs. 23.9%, p-value < 0.001). In a multivariable logistic regression model, atherogenic dyslipidemia was associated with the highest odds of SCMI followed by high TG/normal HDL-C, then low HDL-C/normal TG [OR (95% CI): 131 (1.14, 1.52), 1.13 (0.97, 1.33), and 1.01 (0.86, 1.20), respectively). Conclusions: Atherogenic dyslipidemia is associated with a higher risk of SCMI, which highlights the role of nontraditional risk factors in the development of subclinical CVD.

The aim of this study was to investigate the relationship between triglyceride-glucose (TyG) index and cardiovascular disease (CVD) and all-cause mortality in adults with metabolic syndrome (MeS) and explore the mediating role of oxidative stress.

This study included 6131 adults with MeS from the National Health and Nutrition Examination Survey (NHANES). The relationships between TyG index and mortality were elucidated using multivariate Cox proportional hazards models, restricted cubic splines (RCS) Fine-Gray competing risk model. In addition, mediation analysis was used to test the indirect effect of oxidative stress indicators.

Over a median 106-month follow-up, a total of 357 CVD and 1292 all-cause deaths were recorded. After multivariate adjustment, there was a J-type relationship between TyG index and CVD and all-cause mortality, with optimal inflection point of 9.13 and 8.92. After the threshold point, TyG index was positively associated with CVD (HR: 4.21, 95%CI: 1.82, 9.78) and all-cause mortality(HR: 2.93, 95%CI: 2.05, 4.18). Even using non-cardiovascular mortality as a competitive risk, the Fine-Gray model also illustrated that the cumulative CVD mortality incidence was higher in MeS with TyG index >9.13 (Fine-Gray P< 0.01). Mediation analysis revealed that biomarkers of oxidative stress, including gamma-glutamyl transferase and uric acid, collectively mediated 10.53% of the association between the TyG index and CVD mortality, and 8.44% of the association with all-cause mortality (P < 0.05).

In the cohort study, TyG index was found to have a J-shaped association with CVD mortality and all-cause mortality in MeS population and oxidative stress may play a key mediating role in this relationship.

The binary diagnosis of Metabolic Syndrome(MetS) fails to accurately evaluate its severity, and the association between MetS severity and frailty progression remains inadequately elucidated. This study aims to clarify the relationship between the severity of MetS and the progression of frailty among the middle-aged and elderly population in China.

Participants from the 2011-2018 China Health and Retirement Longitudinal Study(CHARLS) were included for a longitudinal analysis. The study employs a frailty index(FI) based on 32 health deficits to diagnose frailty and to assess FI trajectories. An age-sex-ethnicity-specific MetS scoring model (MetS score) was used to assess metabolic syndrome severity in Chinese adults. The Cumulative MetS score from 2012 to 2015 was calculated using the formula: (MetS score in wave 1 + MetS score in wave 3) / 2 × time(2015 - 2012). The association between MetS score, Cumulative MetS score, and the risk and trajectory of frailty were evaluated using Cox regression/logistic regression, and linear mixed models. Restricted Cubic Splines(RCS) models were utilized to detect potential non-linear associations.

A higher MetS score was significantly associated with an increased risk of frailty(HR per 1 SD increase = 1.205; 95%CI: 1.14 to 1.273) and an accelerated FI trajectory(β per 1 SD increase = 0.113 per year; 95%CI: 0.075 to 0.15 per year). Evaluating changes in MetS score using a Cumulative MetS score indicated that each 1 SD increase in the Cumulative MetS score increased the risk of frailty by 22.2%(OR = 1.222; 95%CI: 1.133 to 1.319) and accelerated the rate of increase in FI(β = 0.098 per year; 95%CI: 0.058 to 0.138 per year). RCS model results demonstrated a dose-response curve relationship between MetS score and Cumulative MetS score with frailty risk. Stratified analysis showed consistency across subgroups. The interaction results indicate that in males and individuals under aged 60, MetS score may accelerate the increase in FI, a finding consistent across both models.

Our findings underscore the positive correlation between the severity of MetS and frailty progression in the middle-aged and elderly, highlighting the urgent need for early identification of MetS and targeted interventions to reduce the risk of frailty.

The escalating global burden of diabetes and its associated cognitive impairment underscores the urgency for effective interventions. Bergenin shows promise in regulating glucose metabolism, mitigating inflammation, and improving cognitive function. Zebrafish models offer a unique platform for assessing drug efficacy and exploring pharmacological mechanisms, complemented by subsequent investigations in cell and rat models.

The experimental subjects included zebrafish larvae (CZ98:Tg (mpeg1:EGFP) ihb20Tg/+ ), adult zebrafish (immersed in 2% glucose), BV2 cell line (50 mM glucose + 10 μm Aβ1-42), and a streptozotocin (STZ) bilateral intracerebroventricular injection rat model. Bergenin's effects on the toxicity, behavior, and cognitive function of zebrafish larvae and adults were evaluated. The Morris water maze assessed cognitive function in rats. Neuronal histopathological changes were evaluated using HE and Nissl staining. qPCR and Western blot detected the expression of glycolysis enzymes, inflammatory factors, and Bergenin's regulation of PPAR/NF-κB pathway in these three models.

1) In zebrafish larvae, Bergenin interventions significantly reduced glucose levels and increased survival rates while decreasing teratogenicity rates. Microglial cell fluorescence in the brain notably decreased, and altered swimming behavior tended to normalize. 2) In adult zebrafish, Bergenin administration reduced BMI and blood glucose levels, altered swimming behavior to slower speeds and more regular trajectories, enhanced recognition ability, decreased brain glucose and lactate levels, weakened glycolytic enzyme activities, improved pathological changes in the telencephalon and gills, reduced expression of pro-inflammatory cytokines, decreased ins expression and increased expression of irs1, irs2a, and irs2b, suggesting a reduction in insulin resistance. It also altered the expression of pparg and rela. 3) In BV2 cell line, Bergenin significantly reduced the protein expression of glycolytic enzymes (GLUT1, HK2, PKFKB3, and PKM2), lowered IL-1β, IL-6, and TNF-α mRNA expression, elevated PPAR-γ protein expression, and decreased P-NF-κB-p65 protein expression. 4) In the rat model, Bergenin improves learning and memory abilities in STZ-induced rats, mitigates neuronal damage in the hippocampal region, and reduces the expression of inflammatory factors IL-1β, IL-6, and TNF-α. Bergenin decreases brain glucose and lactate levels, as well as glycolytic enzyme activity. Furthermore, Bergenin increases PPARγ expression and decreases p-NF-κB p65/NF-κB p65 expression in the hippocampus.

Bergenin intervenes through the PPAR-γ/NF-κB pathway, redirecting glucose metabolism, alleviating inflammation, and preventing high glucose-induced neuronal damage.

Chronic low‑grade inflammation defines obesity as a metabolic disorder. Alterations in the structure of gut flora are strongly associated with obesity. Lactoferrin (LF) has a biological function in regulating intestinal flora. The present study aimed to investigate the therapeutic and anti‑-inflammatory effects of LF in obese mice based on intestinal flora. A total of 30 C57BL/6 mice were divided into three groups consisting of 10 mice each. Subsequently, one group was fed a normal diet (Group K), another group was fed a high‑fat diet (Group M) and the remaining group switched from regular drinking to drinking 2% LF water (Group Z2) after 2 weeks of high‑fat diet; all mice were fed for 12 weeks. After the experiment, the mouse blood lipid and lipopolysaccharide levels, levels of inflammatory factors and intestinal tight junction proteins were assessed. Mouse stool samples were analyzed using 16S ribosomal RNA sequencing. The results showed that LF reduced serum total cholesterol, triglycerides and low‑density lipoprotein levels, elevated high‑density lipoprotein levels, suppressed metabolic endotoxemia and attenuated chronic low‑grade inflammatory responses in obese mice. In addition, LF upregulated zonula occludens‑1 and occludin protein expression levels in the intestine, thereby improving intestinal barrier integrity. LF altered the intestinal microbial structure of obese mice, reduced the ratio of Firmicutes and an elevated ratio of Bacteroidota, modifying the bacterial population to the increased relative abundance of Alistipes, Acidobacteriota, Psychrobacter and Bryobacter.

Evidence has shown that the individual metrics in Life's Essential 8 (LE8), an updated cardiovascular health (CVH) concept proposed by the American Heart Association, play a role in the development of inflammatory bowel disease (IBD). However, epidemiological evidence on the overall LE8 on IBD risk remains limited. We aimed to assess the longitudinal associations of LE8-defined CVH and the risks of IBD and its subtypes, ulcerative colitis (UC) and Crohn's disease (CD). We also tested whether genetic susceptibility could modify these associations.

A total of 260,836 participants from the UK Biobank were included. LE8 scores were determined by 8 metrics (physical activity, diet, nicotine exposure, sleep, body mass index, blood pressure, blood glucose, and blood lipids), and were divided into three levels: low CVH (0-49), moderate CVH (50-79), and high CVH (80-100). Cox proportional hazards models were used to calculate the hazard ratios (HRs) and confidence intervals (CIs) of the risk of IBD in relation to CVH status.

Over a median follow-up 12.3 years, we documented 1,500 IBD cases (including 1,070 UC and 502 CD). Compared to participants with low CVH, the HRs (95% CIs) of those with high CVH for IBD, UC, and CD were 0.67 (0.52, 0.83), 0.70 (0.52, 0.93), and 0.55 (0.38, 0.80), respectively. These associations were not modified by genetic susceptibility (all P for interactions > 0.05). The lowest HR (UC: 0.30, 95% CI: 0.20-0.45; CD: 0.33, 95% CI: 0.20-0.57) was observed in participants with both high CVH and low genetic risk.

Better CVH, defined by LE8, was associated with significantly lower risks of IBD, UC, and CD, irrespective of genetic predisposition. Our results underscore the importance of adherence to LE8 guidelines for maintaining CVH as a potential strategy in the prevention of IBD.

The influence of metabolic syndrome (MetS) on long-term prognosis of patients with myocardial infarction (MI), the most severe type of coronary artery disease, remains not fully determined. This systematic review and meta-analysis were conducted to investigate the association between MetS and long-term clinical outcomes of patients with MI. A systematic search of Medline, Web of Science, and Embase databases from inception to June 25, 2023, was conducted to obtain eligible studies. Only studies with follow-up duration for at least one year were considered. A random-effects model was utilized to pool the results, accounting for heterogeneity. Ten observational studies were included, which included 33 197 patients with MI. Among them, 17 244 (51.9%) were with MetS at baseline. During a follow-up duration of 12 to 48 months (mean: 22.5 months), patients with MetS were associated with higher incidence of major adverse cardiovascular events [risk ratio (RR): 1.35. 95% confidence interval (CI): 1.19 to 1.54, p<0.001; I2=64%] and all-cause deaths (RR: 1.34, 95% CI: 1.18 to 1.52, p<0.001; I2=23%), as compared to those without MetS at baseline. Subgroup analyses showed that the results were not significantly affected by study characteristics such as study country, design, type of MI, mean age of the patients, treatment with percutaneous coronary intervention, follow-up durations, or study quality scores (p for subgroup difference all>0.05). In patients with MI, MetS may be a risk factor of poor long-term prognosis.

Bleeding and thrombosis are common complications during immune thrombocytopenic purpura (ITP) treatment. There is a strong need to predict bleeding and thrombosis risks before ITP treatment to optimize therapy and appropriately manage these complications. We performed a retrospective cohort study of 120 patients with primary ITP to identify a biomarker to predict bleeding and thrombosis. We compared blood test results at diagnosis between patients with and without bleeding or thrombosis episodes. The standard deviation of red blood cell distribution width (RDW-SD) differed significantly between those with and without bleeding and between those with and without thrombosis, leading us to identify it as a variable representative of risk. RDW-SD was significantly associated with patient age and with histories of several vascular diseases. Multivariate regression analyses showed that RDW integrated several variables associated with vascular risks. RDW-SD was significantly associated with difficulty with corticosteroid discontinuation (hazard ratio [HR], 2.22, p = 0.01), incidence of bleeding (HR, 2.75, p< 0.01), incidence of thrombosis (HR, 2.67, p< 0.01) and incidence of infection (HR, 1.78, p = 0.04). The RDW-SD value at the time of ITP diagnosis is a useful biomarker to predict the risks of bleeding, thrombosis, and other complications.

The occurrence and development of diabetic vascular diseases are closely linked to inflammation-induced endothelial dysfunction. Puerarin (Pue), the primary component of Pueraria lobata, possesses potent anti-inflammatory properties. However, its vasoprotective role remains elusive. Therefore, we investigated whether Pue can effectively protect against vascular damage induced by diabetes. In the study, Pue ameliorated lipopolysaccharide-adenosine triphosphate (LPS-ATP) or HG-primed cytotoxicity and apoptosis, while inhibited reactive oxygen species (ROS)-mediated NLR family pyrin domain containing 3 (NLRP3) inflammasome in HUVECs, as evidenced by significantly decreased ROS level, NOX4, Caspase-1 activity and expression of NLRP3, GSDMD, cleaved caspase-1, IL-1β and IL-18. Meanwhile, ROS inducer CoCI2 efficiently weakened the effects of Pue against LPS-ATP-primed pyroptosis. In addition, NLRP3 knockdown notably enhanced Pue's ability to suppress pyroptosis in LPS-ATP-primed HUVECs, whereas overexpression of NLRP3 reversed the inhibitory effects of Pue. Furthermore, Pue inhibited the expression of ROS and NLRP3 inflammasome-associated proteins on the aorta in type 2 diabetes mellitus rats. Our findings indicated that Pue might ameliorate LPS-ATP or HG-primed damage in HUVECs by inactivating the ROS-NLRP3 signalling pathway.

Populational aging is marked by chronic noncommunicable diseases, such as metabolic syndrome (MetS). IL-10 and IL-1β are pleiotropic cytokines with multiple biological effects linked to metabolic disorders. This cross-sectional study assessed 193 participants' IL-10 and IL-1β serum levels regarding their role in developing MetS, clinical characteristics, and their IL1B rs1143627 and IL10 rs1800890 variants' genotype frequencies in a population over 60. IL-10 levels correlated weakly with HDL levels and fat mass and inversely with triglycerides, glucose, glycated hemoglobin, and estimated average blood glucose levels. IL-10 levels were also indirectly influenced by the patient's T2DM duration, lean mass amount, and bone mineral content. Participants with altered HDL, elevated serum glucose, raised HbA1c levels, or those over 80 had reduced serum IL-10 levels compared to those with normal levels or other age groups, respectively. Women also had higher serum IL-10 levels than men. Dissimilarly, IL-1β levels correlated directly only with the number of total leukocytes and segmented neutrophils, showing only significant variations with self-reported alcohol consumption. Our study also found that those with the IL10 AA genotype (lower IL-10 levels) had a significantly higher risk of developing MetS. These findings may help direct future research and more targeted therapeutic approaches in older adults.

Postoperative delirium (POD) is more prevalent among elderly patients with type 2 diabetes mellitus (T2DM). Insulin resistance (IR) can be assessed using the triglyceride-glucose (TyG) index, a novel biomarker. This study aims to investigate the predictive potential of the TyG index for POD in elderly patients with T2DM.

Elderly patients (≥ 65) with T2DM who underwent non-neurosurgery and non-cardiac surgery were enrolled. Univariate and multivariate logistic regression analyses were conducted to assess the association between the TyG index and POD. Additionally, subgroup analyses were performed to compare the sex-specific differences in the predictive ability of the TyG index for POD.

A total of 4566 patients were included in this retrospective cohort. The receiver operating characteristic (ROC) curve analysis determined the optimal cut-off value for the TyG index to be 8.678. In the univariate model, a TyG index > 8.678 exhibited an odds ratio (OR) of 1.668 (95% CI: 1.210-2.324, P = 0.002) for predicting POD. In the multivariate regression models, the ORs were 1.590 (95% CI: 1.133-2.252, P < 0.008), 1.661 (95% CI: 1.199-2.325, P < 0.003), and 1.603 (95% CI: 1.137-2.283, P = 0.008) for different models. Subgroup analyses demonstrated that the predictive ability of the TyG index was more pronounced in females compared to males.

The TyG index shows promise as a novel biomarker for predicting the occurrence of POD in elderly surgical patients with T2DM.

Elevated platelet count (PLTc) is associated with first-episode schizophrenia and adverse outcomes in individuals with precursory psychosis. However, the impact of antipsychotic medications on PLTc and its association with symptom improvement remain unclear.

We aimed to investigate changes in PLTc levels following antipsychotic treatment and assess whether PLTc can predict antipsychotic responses and metabolic changes after accounting for other related variables.

A total of 2985 patients with schizophrenia were randomised into seven groups. Each group received one of seven antipsychotic treatments and was assessed at 2, 4 and 6 weeks. Clinical symptoms were evaluated using the positive and negative syndrome scale (PANSS). Additionally, we measured blood cell counts and metabolic parameters, such as blood lipids. Repeated measures analysis of variance was used to examine the effect of antipsychotics on PLTc changes, while structural equation modelling was used to assess the predictive value of PLTc on PANSS changes.

PLTc significantly increased in patients treated with aripiprazole (F=6.00, p=0.003), ziprasidone (F=7.10, p<0.001) and haloperidol (F=3.59, p=0.029). It exhibited a positive association with white blood cell count and metabolic indicators. Higher baseline PLTc was observed in non-responders, particularly in those defined by the PANSS-negative subscale. In the structural equation model, PLTc, white blood cell count and a latent metabolic variable predicted the rate of change in the PANSS-negative subscale scores. Moreover, higher baseline PLTc was observed in individuals with less metabolic change, although this association was no longer significant after accounting for baseline metabolic values.

Platelet parameters, specifically PLTc, are influenced by antipsychotic treatment and could potentially elevate the risk of venous thromboembolism in patients with schizophrenia. Elevated PLTc levels and associated factors may impede symptom improvement by promoting inflammation. Given PLTc's easy measurement and clinical relevance, it warrants increased attention from psychiatrists.

ChiCTR-TRC-10000934.