A promising strategy to improve the stability and immunogenicity of killed but metabolically active vaccines: low-temperature preparation and coating of nanoparticles.

Bacteria are becoming an increasingly serious threat to human health. The emergence of super bacteria makes clinical treatment more difficult. Vaccines are one of the most effective means of preventing and treating bacterial infections. As a new class of vaccines, killed but metabolically active (KBMA) vaccines provide the immunogenicity of live vaccines and the safety of inactivated vaccines. Herein, a promising strategy is proposed to improve the stability and immunogenicity of KBMA vaccines. KBMA vaccines were produced at low temperature (4 °C), and the bacterial surface was engineered using mesoporous silica nanoparticle (MSN) coating. Compared to vaccines prepared at room temperature, the metabolic activity of KBMA vaccines prepared at 4 °C remarkably improved. Benefiting from the induction of MSNs, the stability of KBMA vaccines was increased and the preservation time was prolonged at 4 °C. Meanwhile, metabolomics analysis showed that the metabolite spectrum of live bacteria changed after photochemical treatment and MSN coating, which interfered with organic acid metabolism pathways, lipid metabolism and biosynthesis of secondary metabolites. Furthermore, the immune response in the mice treated with KBMA/MSN vaccines was similar to that in those treated with live vaccines and stronger than that in those treated with inactivated vaccines. In comparison with the control group, bacteria tissue burdens of KBMA/MSN group were significantly reduced. CD4+ T cells dominated immune responses for the protection of mice. Thus, the current work promotes the application of KBMA vaccines, providing an alternative choice for treating bacterial infections.

[Clinical diagnosis of group A streptococcal pharyngitis and progress in the application of scoring systems]. / A族链球菌咽炎的临床诊断及评分制的应用进展.

Pharyngitis can be caused by various pathogens, including viruses and bacteria. Group A streptococcus (GAS) is the most common bacterial cause of pharyngitis. However, distinguishing GAS pharyngitis from other types of upper respiratory tract infections is challenging in clinical settings. This often leads to empirical treatments and, consequently, the overuse of antimicrobial drugs. With the advancement of antimicrobial drug management and healthcare payment reform initiatives in China, reducing unnecessary testing and prescriptions of antimicrobial drugs is imperative. To promote standardized diagnosis and treatment of GAS pharyngitis, this article reviews various international guidelines on the clinical diagnosis and differential diagnosis of GAS pharyngitis, particularly focusing on clinical scoring systems guiding laboratory testing and antimicrobial treatment decisions for GAS pharyngitis and their application recommendations, providing a reference for domestic researchers and clinical practitioners.

Identification of immunity- and ferroptosis-related signature genes as potential design targets for mRNA vaccines in AML patients.

Immune-associated ferroptosis plays an important role in the progression of acute myeloid leukemia (AML); however, the targets that play key roles in this process are currently unknown. This limits the development of mRNA vaccines based on immune-associated ferroptosis for clinical therapeutic applications. In this study, based on the rich data resources of the TCGA-LAML cohort, we analyzed the tumor mutational burden (TMB), gene mutation status, and associations between immune and ferroptosis genes to reveal the disease characteristics of AML patients. To gain a deeper understanding of differentially expressed genes, we applied the Limma package for differential expression analysis and integrated data sources such as ImmPort Shared Data and FerrDb V2. Moreover, we established gene modules related to TMB according to weighted gene coexpression network analysis (WGCNA) and explored the functions of these modules in AML and their relationships with TMB. We focused on the top 30 most frequent genes through a detailed survey of missense mutations and single nucleotide polymorphisms (SNPs) and selected potentially critical gene targets for subsequent analysis. Based on the expression of these genes, we successfully subgrouped AML patients and found that the subgroups associated with TMB (C1 and C2) exhibited significant differences in survival. The differences in the tumor microenvironment and immune cells between C1 and C2 patients were investigated with the ESTIMATE and MCP-counter algorithms. A predictive model of TMB-related genes (TMBRGs) was constructed, and the validity of the model was demonstrated by categorizing patients into high-risk and low-risk groups. The differences in survival between the high-risk patients and high-TMB patients were further investigated, and potential vaccine targets were identified via immune cell-level analysis. The identification of immunity- and ferroptosis-associated signature genes is an independent predictor of survival in AML patients and provides new information on immunotherapy for AML.

Case Report: Infant-onset Degos disease with nervous system involvement and a literature review.

Degos disease also known as malignant atrophic papulosis (MAP), is an autoinflammatory disease that mainly affects small- to medium-sized arteries. Gastrointestinal and nervous system are most commonly affected systems. Herein, we reported a case of Degos disease with disease onset during infantile and had severe neurological involvement.

Gas-Phase Regeneration of Metal-Poisoned V2O5-WO3/TiO2 NH3-SCR Catalysts via a Masking and Reconstruction Strategy.

Renewing metal-poisoned NH3-SCR catalysts holds great potential for mitigating environmental pollution and utilizing hazardous wastes simultaneously. Ionic compounds containing heavy metals often exhibit limited solubility due to their high polarizability, making traditional washing techniques ineffective in removing heavy metal poisons. This study presents a gas-based method for regenerating heavy-metal-poisoned V2O5-WO3/TiO2 catalysts employed in NH3-SCR techniques. The regeneration is achieved by employing a masking and reconstruction strategy, which involves the in situ formation of NO2 to mediate the production of SO3. This enables the effective bonding of Pb and triggers the reconstruction of active VOx sites. In situ spectroscopy confirms that the sulfation of PbO restores acidity, while the occupied effect resulting from the sulfation of TiO2 promotes the formation of more polymeric VOx species. Consequently, the regenerated catalyst exhibits enhanced activity and superior resistance to metal poisons compared with the fresh catalyst. The innovative method offers a promising solution for extending the lifespan of poisoned catalysts, reducing waste generation, and enhancing the efficiency of NH3-SCR systems.

Identification of immune- and oxidative stress-related signature genes as potential targets for mRNA vaccines for pancreatic cancer patients.

Adenocarcinoma of the pancreas (PAAD) is one of the deadliest malignant tumors, and messenger ribonucleic acid vaccines, which constitute the latest generation of vaccine technology, are expected to lead to new ideas for the treatment of pancreatic cancer. The Cancer Genome Atlas-PAAD and Genotype-Tissue Expression data were merged and analyzed. Weighted gene coexpression network analysis was used to identify gene modules associated with tumor mutational burden among the genes related to both immunity and oxidative stress. Differentially expressed immune-related oxidative stress genes were screened via univariate Cox regression analysis, and these genes were analyzed via nonnegative matrix factorization. After immune infiltration analysis, least absolute shrinkage and selection operator regression combined with Cox regression was used to construct the model, and the usefulness of the model was predicted based on the receiver operating characteristic curve and decision curve analysis curves after model construction. Finally, metabolic pathway enrichment was analyzed using gene set enrichment analysis combined with Kyoto Encyclopedia of Genes and Genomes and gene ontology biological process analyses. This model consisting of the ERAP2, mesenchymal-epithelial transition factor (MET), CXCL9, and angiotensinogen (AGT) genes can be used to help predict the prognosis of pancreatic cancer patients more accurately than existing models. ERAP2 is involved in immune activation and is important in cancer immune evasion. MET binds to hepatocyte growth factor, leading to the dimerization and phosphorylation of c-MET. This activates various signaling pathways, including MAPK and PI3K, to regulate the proliferation, invasion, and migration of cancer cells. CXCL9 overexpression is associated with a poor patient prognosis and reduces the number of CD8 + cytotoxic T lymphocytes in the PAAD tumor microenvironment. AGT is cleaved by the renin enzyme to produce angiotensin 1, and AGT-converting enzyme cleaves angiotensin 1 to produce angiotensin 2. Exposure to AGT-converting enzyme inhibitors after pancreatic cancer diagnosis is associated with improved survival. The 4 genes identified in the present study - ERAP2, MET, CXCL9, and AGT - are expected to serve as targets for messenger ribonucleic acid vaccine development and need to be further investigated in depth.

Modular access to diarylmethyl sulfonamides via visible light-promoted cross-coupling reactions.

We report a novel and efficient method for the preparation of diarylmethyl sulfonamide derivatives through visible-light-induced sulfamoylation of para-quinone methides with sulfamoyl chlorides under mild, metal-free conditions. This protocol demonstrates excellent tolerance toward a wide range of functional groups, affording the corresponding products in moderate to high yields. Preliminary mechanism studies revealed that the excited photocatalyst rhodamine 6G* was mainly quenched by para-quinone methides and the generated diarylmethyl radical intermediates then underwent radical-radical cross-coupling with sulfamoyl radicals to yield the diarylmethyl sulfonamides.

Case report: A case of renal vessel rupture caused by severe vomiting in early pregnancy.

OBJECTIVE: Spontaneous renal vessel rupture is a rare clinical emergency. However, pregnancy symptoms and signs are not obvious, and the limited examination methods obscure the observation. Thus, early renal rupture is challenging to detect, leading to misdiagnosis and poor prognosis. This paper aims to improve clinicians' understanding of this disease and reduce the rate of clinical misdiagnosis. PATIENT CONCERNS: The patient, aged 23 and 11 weeks pregnant, developed severe right lumbar and abdominal pain for 14 hours after severe nausea, vomiting, and paroxysmal intensification. Color ultrasound of the urinary system at another hospital revealed right kidney stones and right ureter dilation. Thus, the patient came to our hospital for treatment. DIAGNOSES: Spontaneous renal vessel rupture. INTERVENTIONS: In this case, the diagnosis of spontaneous renal vascular rupture and hemorrhage was confirmed. Following conservative treatment such as fluid replenishment, blood transfusion, and hemostasis, the patient was given an emergency renal artery embolization due to unstable hemodynamics during treatment and poor conservative treatment effect. OUTCOMES: Nephrectomy was performed after 1-week follow-up for renal necrosis. LESSONS: To avoid missed diagnosis and misdiagnosis, patients with abdominal pain caused by severe vomiting during pregnancy must be closely monitored. Additionally, treatment should be considered individually to ensure the safety of both mother and child. Therefore, spontaneous renal vessel rupture should be considered as the differential diagnosis.

NGF-BMSC-SF/CS composites for repairing knee joint osteochondral defects in rabbits: evaluation of the repair effect and potential underlying mechanisms.

BACKGROUND: With the rapid growth of the ageing population, chronic diseases such as osteoarthritis have become one of the major diseases affecting the quality of life of elderly people. The main pathological manifestation of osteoarthritis is articular cartilage damage. Alleviating and repairing damaged cartilage has always been a challenge. The application of cartilage tissue engineering methods has shown promise for articular cartilage repair. Many studies have used cartilage tissue engineering methods to repair damaged cartilage and obtained good results, but these methods still cannot be used clinically. Therefore, this study aimed to investigate the effect of incorporating nerve growth factor (NGF) into a silk fibroin (SF)/chitosan (CS) scaffold containing bone marrow-derived mesenchymal stem cells (BMSCs) on the repair of articular cartilage defects in the knees of rabbits and to explore the possible underlying mechanism involved. MATERIALS AND METHODS: Nerve growth factor-loaded sustained-release microspheres were prepared by a double emulsion solvent evaporation method. SF/CS scaffolds were prepared by vacuum drying and chemical crosslinking. BMSCs were isolated and cultured by density gradient centrifugation and adherent culture. NGF-SF/CS-BMSC composites were prepared and implanted into articular cartilage defects in the knees of rabbits. The repair of articular cartilage was assessed by gross observation, imaging and histological staining at different time points after surgery. The repair effect was evaluated by the International Cartilage Repair Society (ICRS) score and a modified Wakitani score. In vitro experiments were also performed to observe the effect of different concentrations of NGF on the proliferation and directional differentiation of BMSCs on the SF/CS scaffold. RESULTS: In the repair of cartilage defects in rabbit knees, NGF-SF/CS-BMSCs resulted in higher ICRS scores and lower modified Wakitani scores. The in vitro results showed that there was no significant correlation between the proliferation of BMSCs and the addition of different concentrations of NGF. Additionally, there was no significant difference in the protein and mRNA expression of COL2a1 and ACAN between the groups after the addition of different concentrations of NGF. CONCLUSION: NGF-SF/CS-BMSCs improved the repair of articular cartilage defects in the knees of rabbits. This repair effect may be related to the early promotion of subchondral bone repair.

Feasibility and safety of cryoballoon ablation for atrial fibrillation and closing patent foramen ovale without implantation：A pilot study.

BACKGROUND: Patent foramen ovale (PFO) affects 20%-34% of adults and is associated with strokes and other disorders. The conventional treatment of PFO-related strokes is a closure procedure. The metal device is associated with some adverse events. OBJECTIVE: Our aim was to investigate the efficacy and safety of PFO closure using cryoablation without implantation in patients with atrial fibrillation (AF) who underwent pulmonary vein isolation (PVI). METHODS: We divided the 22 patients with both PFO and AF who underwent PVI via cryoablation into 2 groups: standard PVI + atrial septal (AS) cryoablation group (group 1, n = 11) and standard PVI group (group 2, n = 11). The guidewire accesses the left atrium through the PFO without AS puncture during the procedure. Standard PVI via cryoablation was performed. The cryoballoon was retracted to the right atrium and inflated against the AS post-PVI. Patients in group 1 had cryoablation for 120-150 seconds, whereas patients in group 2 received sham ablation. The co-primary end points were the PFO closure rate and a composite of AF recurrence and stroke/transient ischemic attack (TIA) events. RESULTS: There were no differences in procedure-related adverse events between the 2 groups. Neither group had an ischemic stroke report at 1-year follow-up. The PFO closure rate at 6 months in group 1 was significantly higher than that in group 2 (7 [63.6%] vs 1 [9.1%]; P = .002). AF recurrence post ablation was comparable in both groups at 3 months (3 [27.3%] vs 1 [9.1%]; P = .269), 6 months (0 vs 0), and 12 months (2 [18.2%%] vs 1 [9.1%]; P = .534) of follow-up. CONCLUSION: Cryoablation is a safe and effective approach to close PFO in patients with AF undergoing PVI in a single procedure.

AP-1 and SP1 trans-activate the expression of hepatic CYP1A1 and CYP2A6 in the bioactivation of AFB1 in chicken.

Dietary exposure to aflatoxin B1 (AFB1) is harmful to the health and performance of domestic animals. The hepatic cytochrome P450s (CYPs), CYP1A1 and CYP2A6, are the primary enzymes responsible for the bioactivation of AFB1 to the highly toxic exo-AFB1-8,9-epoxide (AFBO) in chicks. However, the transcriptional regulation mechanism of these CYP genes in the liver of chicks in AFB1 metabolism remains unknown. Dual-luciferase reporter assay, bioinformatics and site-directed mutation results indicated that specificity protein 1 (SP1) and activator protein-1 (AP-1) motifs were located in the core region -1,063/-948, -606/-541 of the CYP1A1 promoter as well as -636/-595, -503/-462, -147/-1 of the CYP2A6 promoter. Furthermore, overexpression and decoy oligodeoxynucleotide technologies demonstrated that SP1 and AP-1 were pivotal transcriptional activators regulating the promoter activity of CYP1A1 and CYP2A6. Moreover, bioactivation of AFB1 to AFBO could be increased by upregulation of CYP1A1 and CYP2A6 expression, which was trans-activated owing to the upregulalion of AP-1, rather than SP1, stimulated by AFB1-induced reactive oxygen species. Additionally, nano-selenium could reduce ROS, downregulate AP-1 expression and then decrease the expression of CYP1A1 and CYP2A6, thus alleviating the toxicity of AFB1. In conclusion, AP-1 and SP1 played important roles in the transactivation of CYP1A1 and CYP2A6 expression and further bioactivated AFB1 to AFBO in chicken liver, which could provide novel targets for the remediation of aflatoxicosis in chicks.

Prohibitin 1 inhibits cell proliferation and induces apoptosis via the p53-mediated mitochondrial pathway in vitro.

BACKGROUND: Prohibitin 1 (PHB1) has been identified as an antiproliferative protein that is highly conserved and ubiquitously expressed, and it participates in a variety of essential cellular functions, including apoptosis, cell cycle regulation, proliferation, and survival. Emerging evidence indicates that PHB1 may play an important role in the progression of hepatocellular carcinoma (HCC). However, the role of PHB1 in HCC is controversial. AIM: To investigate the effects of PHB1 on the proliferation and apoptosis of human HCC cells and the relevant mechanisms in vitro. METHODS: HCC patients and healthy individuals were enrolled in this study according to the inclusion and exclusion criteria; then, PHB1 levels in the sera and liver tissues of these participates were determined using ELISA, RT-PCR, and immunohistochemistry. Human HepG2 and SMMC-7721 cells were transfected with the pEGFP-PHB1 plasmid and PHB1-specific shRNA (shRNA-PHB1) for 24-72 h. Cell proliferation was analysed with an MTT assay. Cell cycle progression and apoptosis were analysed using flow cytometry (FACS). The mRNA and protein expression levels of the cell cycle-related molecules p21, Cyclin A2, Cyclin E1, and CDK2 and the cell apoptosis-related molecules cytochrome C (Cyt C), p53, Bcl-2, Bax, caspase 3, and caspase 9 were measured by real-time PCR and Western blot, respectively. RESULTS: Decreased levels of PHB1 were found in the sera and liver tissues of HCC patients compared to those of healthy individuals, and decreased PHB1 was positively correlated with low differentiation, TNM stage III-IV, and alpha-fetoprotein ≥ 400 µg/L. Overexpression of PHB1 significantly inhibited human HCC cell proliferation in a time-dependent manner. FACS revealed that the overexpression of PHB1 arrested HCC cells in the G0/G1 phase of the cell cycle and induced apoptosis. The proportion of cells in the G0/G1 phase was significantly increased and the proportion of cells in the S phase was decreased in HepG2 cells that were transfected with pEGFP-PHB1 compared with untreated control and empty vector-transfected cells. The percentage of apoptotic HepG2 cells that were transfected with pEGFP-PHB1 was 15.41% ± 1.06%, which was significantly greater than that of apoptotic control cells (3.65% ± 0.85%, P < 0.01) and empty vector-transfected cells (4.21% ± 0.52%, P < 0.01). Similar results were obtained with SMMC-7721 cells. Furthermore, the mRNA and protein expression levels of p53, p21, Bax, caspase 3, and caspase 9 were increased while the mRNA and protein expression levels of Cyclin A2, Cyclin E1, CDK2, and Bcl-2 were decreased when PHB1 was overexpressed in human HCC cells. However, when PHB1 was upregulated in human HCC cells, Cyt C expression levels were increased in the cytosol and decreased in the mitochondria, which indicated that Cyt C had been released into the cytosol. Conversely, these effects were reversed when PHB1 was knocked down. CONCLUSION: PHB1 inhibits human HCC cell viability by arresting the cell cycle and inducing cell apoptosis via activation of the p53-mediated mitochondrial pathway.

Macrod1 suppresses diabetic cardiomyopathy via regulating PARP1-NAD+-SIRT3 pathway.

Diabetic cardiomyopathy (DCM), one of the most serious long-term consequences of diabetes, is closely associated with oxidative stress, inflammation and apoptosis in the heart. MACRO domain containing 1 (Macrod1) is an ADP-ribosylhydrolase 1 that is highly enriched in mitochondria, participating in the pathogenesis of cardiovascular diseases. In this study, we investigated the role of Macrod1 in DCM. A mice model was established by feeding a high-fat diet (HFD) and intraperitoneal injection of streptozotocin (STZ). We showed that Macrod1 expression levels were significantly downregulated in cardiac tissue of DCM mice. Reduced expression of Macrod1 was also observed in neonatal rat cardiomyocytes (NRCMs) treated with palmitic acid (PA, 400 µM) in vitro. Knockout of Macrod1 in DCM mice not only worsened glycemic control, but also aggravated cardiac remodeling, mitochondrial dysfunction, NAD+ consumption and oxidative stress, whereas cardiac-specific overexpression of Macrod1 partially reversed these pathological processes. In PA-treated NRCMs, overexpression of Macrod1 significantly inhibited PARP1 expression and restored NAD+ levels, activating SIRT3 to resist oxidative stress. Supplementation with the NAD+ precursor Niacin (50 µM) alleviated oxidative stress in PA-stimulated cardiomyocytes. We revealed that Macrod1 reduced NAD+ consumption by inhibiting PARP1 expression, thereby activating SIRT3 and anti-oxidative stress signaling. This study identifies Macrod1 as a novel target for DCM treatment. Targeting the PARP1-NAD+-SIRT3 axis may open a novel avenue to development of new intervention strategies in DCM. Schematic illustration of macrod1 ameliorating diabetic cardiomyopathy oxidative stress via PARP1-NAD+-SIRT3 axis.

Strong metal oxide-zeolite interactions during selective catalytic reduction of nitrogen oxides.

In response to the stricter EU VII emission standards and the "150 â„ƒ challenge", selective catalytic reduction by ammonia (NH3-SCR) catalysts for motor vehicles are required to achieve high NO conversion below 200 °C. Compounding metal oxides with zeolites is an important strategy to design the low-temperature SCR catalysts. Here, we original prepared Cu-SSZ-13 @ MnGdOx (Cu-Z @ MGO), which achieved over 90% NO conversion and 95% N2 selectivity at 150 â„ƒ. It has been demonstrated that a uniform mesoporous loaded layer of MGO grows on Cu-Z, and a recrystallization zone appears at the MGO-Cu-Z interface. We discover that the excellent low-temperature SCR activity derives from the strong metal oxide-zeolite interaction (SMZI) effects. The SMZI effects cause the anchor and high dispersion of MGO on the surface of Cu-Z. Driven by the SMZI effects, the Mn3+/Mn4+ redox cycle ensures the low and medium temperature-SCR activity and the Cu2+/Cu+ redox cycle guarantees the medium and high temperature-SCR activity. The introduction of MGO improves the reaction activity of -NH2 species adsorbed at Mn sites at 150 â„ƒ, achieving a cycle of reduction and oxidation reactions at low temperatures. This strategy of inducing SMZI effects of metal oxides and zeolites paves a way for development of high-performance catalysts.

ADP-ribosylation: An emerging direction for disease treatment.

ADP-ribosylation (ADPr) is a dynamically reversible post-translational modification (PTM) driven primarily by ADP-ribosyltransferases (ADPRTs or ARTs), which have ADP-ribosyl transfer activity. ADPr modification is involved in signaling pathways, DNA damage repair, metabolism, immunity, and inflammation. In recent years, several studies have revealed that new targets or treatments for tumors, cardiovascular diseases, neuromuscular diseases and infectious diseases can be explored by regulating ADPr. Here, we review the recent research progress on ART-mediated ADP-ribosylation and the latest findings in the diagnosis and treatment of related diseases.

An integrated mycotoxin-mitigating agent can effectively mitigate the combined toxicity of AFB1, DON and OTA on the production performance, liver and oviduct health in broiler breeder hens.

This study was to evaluate the efficacy of an integrated mycotoxin-mitigating agent in reducing the adverse effects of co-occurring dietary aflatoxin B1 deoxynivalenol and ochratoxin A on broiler breeder hens. 360 30-week-old Hubbard Efficiency Plus broiler breeder hens were allocated into four groups and received a basal diet (BD; Control), BD added 0.15 mg/kg aflatoxin B1+1.5 mg/kg deoxynivalenol+0.12 mg/kg ochratoxin A (Toxins), BD plus Toxins with 0.1% TOXO-XL (Toxins + XL1), and BD plus Toxins with 0.2% TOXO-XL (Toxins + XL2), respectively, for 8 weeks, and then received the same BD for another 4 weeks. Compared with control, mycotoxins decreased total egg weigh, egg laying rate, settable eggs rate, hatch of total eggs rate, egg quality, but increased feed/egg ratio and mortality rate, and impaired the liver and oviduct health during weeks 1-8 and(or) 9-12. It also increased PC and MDA concentrations, TUNEL-positive cells and IL-1ß and IL-6 expression, and decreased T-AOC, GPX and CAT activities in liver and/or oviduct. Notably, most of these negative changes were mitigated by both dosages of TOXO-XL. Generally, 0.2% TOXO-XL displayed better mitigation effects than 0.1% TOXO-XL. Conclusively, these findings revealed that TOXO-XL could mitigate the combined mycotoxins-induced toxicity on the performance, liver and oviduct health, through the regulation of redox, immunity, and apoptosis in broiler breeder hens.

Population attributable fractions of fatty liver disease for type 2 diabetes Mellitus.

PURPOSE: To determine the population attributable fraction (PAF) of fatty liver disease (FLD) for type 2 diabetes mellitus (T2DM) and compare it to the PAFs of other metabolic abnormalities. METHODS: We conducted a 10-year retrospective cohort study of 33,346 individuals in Karamay Central Hospital of Xinjiang. Individuals were followed up for T2DM occurrence based on FBS. The PAFs of FLD were calculated generally and respectively in different sex and age groups. A comparison of the PAF of FLD and that of other metabolic abnormalities, as well as the PAFs of FLD in different groups classified based on age and sex, was performed using Cox regression. RESULTS: During an average follow-up period of 3.71 years, 1486 T2DM were diagnosed. The incidence density of T2DM was 1.2/100 person-years, and cumulative incidence rate was 4456.31/100,000 person-years. Partial PAF (PAFp) of FLD in the entire population was 23.11%. In the male population, PAFp was higher at 30-40 years old. In the female population, it was higher when age ≥ 60 years old. In multivariable Cox regression model, FLD, male sex, age ≥ 45 years old, overweight, hypertriglyceridaemia, and systolic hypertension were independent risk factors for T2DM, with corresponding PAFp of 25.00%, 24.99%, 36.47%, 24.96%, 5.71%, and 6.76%, respectively. Age ≥ 45 years old showed the highest PAFp and adjusted hazard ratio, followed by FLD. CONCLUSIONS: FLD contributes more to T2DM incidence than other metabolic disorders. Particular attention should be given to male populations of 30-40 and female populations above 60 for FLD prevention and treatment.

Remediation Strategies for Mycotoxins in Animal Feed.

Mycotoxins occur widely in various animal feedstuffs, with more than 500 mycotoxins identified so far [...].

Lipid profiles in patients with juvenile idiopathic arthritis: a systematic literature review and meta-analysis.

OBJECTIVE: The purpose of this study was to comprehensively evaluate the lipid profiles in patients with juvenile idiopathic arthritis (JIA). METHODS: The literature and relevant reviews were searched for published clinical studies on the relationship between JIA and blood lipid levels. The Newcastle-Ottawa scale (NOS) was applied to evaluate the risk and methodological value of the included case‒control and cohort studies. Standardized mean differences (SMDs) and 95% confidence intervals were derived for all variables with adequate unprocessed data. This meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) guidelines. RESULTS: In total, 16 studies were incorporated through screening. The analysis findings revealed that the levels of very low-density lipoprotein cholesterol [SMD=-0.411, 95% CI (-0.774~-0.048), P = 0.026], high-density lipoprotein cholesterol [SMD=-0.528, 95% CI (-0.976~-0.079), P = 0.021], and apolipoprotein A1 [SMD=-1.050, 95% CI (-1.452~-0.647), P = 0.000] in JIA patients were statistically lower than those observed in healthy controls. The level of low-density lipoprotein cholesterol [SMD = 0.202, 95% CI (0.003 ~ 0.400), P = 0.046] was significantly higher in JIA patients than in healthy controls. In JIA patients, body mass index [SMD=-0.189, 95% CI (-0.690 ~ 0.311), P = 0.459], high-density lipoprotein [SMD =-1.235, 95% CI (-2.845 ~ 0.374), P = 0.133), low-density lipoprotein [SMD = 0.616, 95% CI (-0.813 ~ 2.046), P = 0.398), triglycerides (SMD = 0.278, 95% CI (-0.182 ~ 0.738), P = 0.236], total cholesterol [SMD=-0.073, 95% CI (-0.438 ~ 0.293), P = 0.696] and apolipoprotein B levels [SMD = 0.226, 95% CI (-0.133 ~ 0.585), P = 0.217] were not significantly different from those in healthy controls. CONCLUSIONS: The outcomes of this meta-analysis suggest that dyslipidemia is common in JIA patients compared to healthy controls. Patients with JIA have a significantly increased risk of atherosclerosis and cardiovascular disease later in life.