Abnormal platelet parameters in inflammatory bowel disease: a systematic review and meta-analysis.

BACKGROUND: Platelet dysfunction plays a critical role in the pathogenesis of inflammatory bowel disease (IBD). Despite clinical observations indicating abnormalities in platelet parameters among IBD patients, inconsistencies persist, and these parameters lack standardization for diagnosis or clinical assessment. METHODS: A comprehensive search was conducted in the PubMed, Embase, Web of Science, and Cochrane Library databases for relevant articles published up to December 16th, 2023. A random-effects model was employed to pool the weighted mean difference (WMD) and 95% confidence interval (95% CI) of platelet count (PLT), mean platelet volume (MPV), platelet distribution width (PDW), and plateletcrit (PCT) between IBD patients and healthy controls, and subgroup analyses were performed. RESULTS: The meta-analysis included 79 articles with 8,350 IBD patients and 13,181 healthy individuals. The results revealed significantly increased PLT and PCT levels (WMD: 69.910, 95% CI: 62.177, 77.643 109/L; WMD: 0.046%, 95% CI: 0.031%, 0.061%), and decreased MPV levels (WMD: -0.912, 95% CI: -1.086, -0.739 fL) in IBD patients compared to healthy individuals. No significant difference was found in PDW between the IBD and control groups (WMD: -0.207%, 95% CI: -0.655%, 0.241%). Subgroup analysis by disease type and disease activity showed no change in the differences for PLT, PCT, and MPV in the ulcerative colitis and Crohn's disease groups, as well as the active and inactive groups. Notably, the active group exhibited significantly lower PDW levels than the control group (WMD: -1.138%, 95% CI: -1.535%, -0.741%). CONCLUSIONS: Compared with healthy individuals, IBD patients display significantly higher PLT and PCT and significantly lower MPV. Monitoring the clinical manifestations of platelet abnormalities serves as a valuable means to obtain diagnostic and prognostic information. Conversely, proactive measures should be taken to prevent the consequences of platelet abnormalities in individuals with IBD. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42023493848.

Global research trend and hotspot in the low FODMAP diet: a bibliometric analysis.

BACKGROUND: According to national guidelines, a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) is a second-line therapy option for irritable bowel syndrome (IBS) and improves functional intestinal symptoms. Numerous noteworthy results have been published in this field over the past fifteen years. This study aims to analyze the global research trend and hotspot of the low FODMAP diet research, and provide a comprehensive perspective and direction for researchers. METHODS: The Science Citation Index-Expanded of the Web of Science Core Collection (WoSCC) was used to identify low FODMAP diet-related articles and reviews. Three bibliometric programs (CiteSpace, VOSviewer, Scimago Graphic) were utilized to analyze and visualize the annual publications, authors, countries, institutions, journals, citations, and keywords. RESULTS: In total, 843 documents related to the low FODMAP diet research were published in 227 journals by 3,343 authors in 1,233 institutions from 59 countries. The United States, which was the most engaged nation in international collaboration, had the largest annual production and the fastest growth. The most productive organization was Monash University, and the most fruitful researcher was Gibson PR. Nutrients ranked first in terms of the number of published documents. The article "A diet low in FODMAPs reduces symptoms of irritable bowel syndrome" (Halmos EP, 2014) received the most co-citations. Keywords that appear frequently in the literature mainly involve two main aspects: the clinical efficacy evaluation and mechanism exploration of the low FODMAP diet. The term "gut microbiota" stands out as the most prominent keyword among the burst keywords that have remained prevalent till date. CONCLUSION: The restriction stage of the low FODMAP diet is superior to other dietary therapies for IBS in terms of symptom response, but it has a negative impact on the abundance of gut Bifidobacteria and diet quality. Identification of biomarkers to predict response to the low FODMAP diet is of great interest and has become the current research hotspot.

Degradation of indole via a two-component indole oxygenase system from Enterococcus hirae GDIAS-5.

Animal farming copiously generates indoles, which contribute to odor and pose a challenge for deodorization. While biodegradation is widely accepted, there is a lack of suitable indole-degrading bacteria for animal husbandry. In this study, we aimed to construct genetically engineered strains with indole-degrading abilities. Enterococcus hirae GDIAS-5 is a highly efficient indole-degrading bacterium, which functions via a monooxygenase YcnE presumably contributes to indole oxidation. However, the efficiency of engineered Escherichia coli expressing YcnE for indole degradation is lower than that of GDIAS-5. To improve its efficacy, the underlying indole-degradation mechanisms in GDIAS-5 were analyzed. An ido operon that responds to a two-component indole oxygenase system was identified. In vitro experiments showed that the reductase component of YcnE, YdgI, can improve the catalytic efficiency. The reconstruction of the two-component system in E. coli exhibited higher indole removal efficiency than GDIAS-5. Furthermore, isatin, the key intermediate metabolite in indole degradation, might be degraded via a novel isatin-acetaminophen-aminophenol pathway involving an amidase whose coding gene is located near the ido operon. The two-component anaerobic oxidation system, upstream degradation pathway, and engineering strains investigated in this study provide important insights into indole degradation metabolism and offer efficient resources for achieving bacterial odor elimination.

Distinct molecular subtypes of systemic sclerosis and gene signature with diagnostic capability.

Background: As Systemic Sclerosis (SSc) is a connective tissue ailment that impacts various bodily systems. The study aims to clarify the molecular subtypes of SSc, with the ultimate objective of establishing a diagnostic model that can inform clinical treatment decisions. Methods: Five microarray datasets of SSc were retrieved from the GEO database. To eliminate batch effects, the combat algorithm was applied. Immune cell infiltration was evaluated using the xCell algorithm. The ConsensusClusterPlus algorithm was utilized to identify SSc subtypes. Limma was used to determine differential expression genes (DEGs). GSEA was used to determine pathway enrichment. A support vector machine (SVM), Random Forest(RF), Boruta and LASSO algorithm have been used to select the feature gene. Diagnostic models were developed using SVM, RF, and Logistic Regression (LR). A ROC curve was used to evaluate the performance of the model. The compound-gene relationship was obtained from the Comparative Toxicogenomics Database (CTD). Results: The identification of three immune subtypes in SSc samples was based on the expression profiles of immune cells. The utilization of 19 key intersectional DEGs among subtypes facilitated the classification of SSc patients into three robust subtypes (gene_ClusterA-C). Gene_ClusterA exhibited significant enrichment of B cells, while gene_ClusterC showed significant enrichment of monocytes. Moderate activation of various immune cells was observed in gene_ClusterB. We identified 8 feature genes. The SVM model demonstrating superior diagnostic performance. Furthermore, correlation analysis revealed a robust association between the feature genes and immune cells. Eight pertinent compounds, namely methotrexate, resveratrol, paclitaxel, trichloroethylene, formaldehyde, silicon dioxide, benzene, and tetrachloroethylene, were identified from the CTD. Conclusion: The present study has effectively devised an innovative molecular subtyping methodology for patients with SSc and a diagnostic model based on machine learning to aid in clinical treatment. The study has identified potential molecular targets for therapy, thereby offering novel perspectives for the treatment and investigation of SSc.

[Joint action of phoxim and fenvalerate on spermatogenesis of male rats].

OBJECTIVE: To assess the joint toxicity of phoxim (Pho) and fenvalerate (Fen) on the spermatogenesis of male rats and to clarify its mechanism. METHODS: Based on the three administrative levels of factorial analysis (3 x 3) of Pho and Fen, i. e. their half lethal dose (LD50) 1/250 LD50 (5.9, 2.4 mg/kg) and 1/50 LD50 (29.4, 12.0 mg/kg) and the control, 135 adult male SD rats were randomly assigned to9 groups, the control (0.0 mg/kg), Pho (5.9, 29.4 mg/kg), Fen (2.4, 12.0 mg/kg), Pho + Fen (5.9 + 2.4, 5.9 + 12.0, 29.4 + 2.4, 29.4 + 12.0 mg/kg), and treated intragastrically with different doses of Pho, Fen and Pho + Fen for 15 and 30 days. The levels of serum follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone (T) and testis homogenate T were determined by radioimmunoassay (RIA), the activity of testicular marker enzymes such as acid phosphatases (ACP) and gamma-glutamyl transpeptidase (gamma-GT) examined, and the sperm head count measured for the changes of daily sperm production (Spr). RESULTS: At 15 days, obvious interaction was observed between Pho and Fen in both serum LH and FSH (P < 0.05), as well as between their reproductive toxicities. With the increase in doses, the joint action was synergistic in LH (P < 0.05) and antagonistic in FSH (P < 0.01) at a high dose ( 29.4 + 12.0 mg/kg). At 30 days, marked interaction between Pho and Fen was noted in the content of homogenate T (P < 0.05) , with a joint synergistic effect. At 15 and 30 days, with the increase of doses, both Pho and Fen reduced Spr and the activity of ACP and gamma-GT, but Pho + Fen showed no obvious interaction in them (P > 0.05) , and their joint action was an additive effect. CONCLUSION: Pho and Fen jointly impaired spermatogenesis in a dose- and time-dependent manner. Their joint action exhibited mainly as a synergistic effect, an additive effect and increased toxicity.

Level of hepatitis B surface antigen might serve as a new marker to predict hepatocellular carcinoma recurrence following curative resection in patients with low viral load.

To investigate the association between preoperative HBsAg (hepatitis B surface antigen) level and risk of HCC (hepatocellular carcinoma) recurrence following curative resection, we enrolled 826 HBV-related HCC patients who underwent curative resection and received long-term follow-up at the Eastern Hepatobiliary Surgery Hospital (Shanghai, China). Multivariate analyses showed that serum HBsAg ≥ 2000 S/CO, seropositive hepatitis B e antigen (HBeAg), γ-glutamyl transpeptidase > 61 U/L, prothrombin time > 13 s, multinodularity, lager tumor size, and major portal vein invasion were independently associated with a increased risk of HCC recurrence. Compared with HCC patients with HBsAg level < 2000 S/CO, HCC patients with HBsAg level ≥ 2000 S/CO had a higher prevalence of seropositive HBeAg, antiviral therapy, and cirrhosis; were younger; and had a higher levels of alanine transaminase (ALT), aspartate aminotransferase (AST), and HBV viral load. Multivariable stratified analyses showed HCC patients with HBsAg level < 2000 S/CO tended to have a lower incidence of HCC recurrence in following subgroups of patients, including for noncirrhotic (HR, 0.561; 95% CI, 0.345-0.914), HBV DNA < 2000 IU/mL (HR, 0.604; 95% CI, 0.401-0.912), ALT ≤ 41 U/L (HR, 0.643; 95% CI, 0.440-0.942), AST ≤ 37 U/L (HR, 0.672; 95% CI, 0.459-0.983), and seronegative HBeAg (HR, 0.682; 95% CI, 0.486-0.958). When we evaluated HBeAg-negative patients with HBV DNA < 2000 IU/mL, HBsAg level still determined risk of HCC recurrence (p = 0.014), but not HBV DNA (p = 0.550) and ALT (p = 0.186). These results suggest high levels of HBsAg increase risk of HCC recurrence following curative resection. HBsAg level might serve as a new marker to complement HBV DNA level in predicting HCC recurrence, especially in HBeAg-negative patients with low viral load.

[Effects of fenvalerate on reproductive and endocrine systems of male rats].

OBJECTIVES: To evaluate the impairment of fenvalerate on reproductive and endocrine systems and clarify the mechanism of action. METHODS: Different doses of fenvalerate (0, 2, 4, 12, 60 mg/kg) were orally treated to the adult male SD rats for 15 days and 30 days, respectively. The levels of serum follicle stimulating hormone(FSH), luteinizing hormone (LH), testosterone(T) and testis homogenate T were determined by radioimmunoassay(RIA). Besides, the activity of testicular marked enzymes such as acid phosphatases(ACP) and gamma-glutamyl transpeptidase(gamma-GT) were examined, and sperm head counts were measured to explain the changes of daily sperm production(Spr). RESULTS: In fifteen days, serum FSH levels markedly increased in rats exposed to fenvalerate of < or = 12 mg/kg groups(P < 0.01) and serum levels of LH increased in 12 mg/kg group(P < 0.01). In addition, T levels in testis homogenates decreased after treated with the doses of > or = 12 mg/kg groups compared with the control group(P < 0.01). In thirty days, serum contents of FSH were significantly elevated in the doses of > or = 12 mg/kg groups(P < 0.01) and homogenate levels of T were diminished in the low dose group(2.4 mg/kg) (P < 0.05). Activity of ACP increased in 12 mg/kg group after fifteen days(P < 0.05) and was restrained in the high dose group(60 mg/kg) in thirty days(P < 0.05), but the contents of gamma-GT were arrested with different doses dependently in the testis(P < 0.05). Fenvalerate caused dose-dependent reduction in sperm head counts and daily sperm production, which markedly reduced at the doses of > or = 12 mg/kg groups(P < 0.01). CONCLUSIONS: Fenvalerate has obvious reproductive toxicity on male rats and can change their serum and testis homogenate levels of sex hormone or activity of testicular marked enzymes, which may be correlated with the impairment of Sertoli cell and spermatogenic epithelium.

Hepatitis B virus infection and intrahepatic cholangiocarcinoma.

Intrahepatic cholangiocarcinoma (ICC) is a devastating malignant tumor arising from the peripheral intrahepatic bile duct epithelium. The incidence and mortality of ICC is markedly increasing over the past two decades worldwide, though the cause for this rise in incidence is unclear, thus intensifying the search for alternative etiological agents and pathogenetic mechanisms. Hepatolithiasis, primary sclerosing cholangitis, parasitic infection (Opisthorchis viverrini or Clonorchis sinensis), fibropolycystic liver disease, and chemical carcinogen exposure are thought to be the risk factors for ICC. Nevertheless, the majority of ICC patients do not have any of these risk factors, and none of the established risk factors can explain the recent increasing trend of ICC. Therefore, identifying other risk factors may lead to the prevention and early detection of ICC. Chronic hepatitis B virus (HBV) infection is the predominant cause of hepatocellular carcinoma in HBV-endemic areas. This review discusses the evidence implicating chronic HBV infection as a likely etiology of ICC and the pathogenetic mechanisms that might be involved.

Fate of hydrolyzed Al species in humic acid coagulation.

The hydrolysis of Al-based coagulants in acidic conditions is necessary for the removal of organic matter by the coagulation/sedimentation process. However, interactions between hydrolyzed Al species and organic matter are complicated and this makes it difficult to optimize coagulant dosing for organics removal. The goal of this study was to investigate the reactions of hydrolyzed Al species in the coagulation of organic matter. Two polyaluminum chloride (PACl) coagulants, a commercial product with sulfate (PACl-C) and lab-prepared material (PACl-Al13) containing 7% and 96% of total Al as Al13, respectively, have been applied to investigate the coagulation of humic acid (HA). At pH 6, a lower dosage of PACl-Al13 than of PACl-C was required for optimized HA removal through coagulation/sedimentation due to the strong complexation and charge neutralization by Al13. Observation of the coagulation process using wet scanning electron microscopy showed that PACl-C produced both clustered flocs and linear precipitates in the presence of sulfate while PACl-Al13 produced curled precipitates due to the formation of intermolecular complex, when both coagulants were added at the optimum doses. Investigation of Al-HA floc by (27)Al-NMR and Al 2p XPS suggested that monomeric Al (Alm) was hydrolyzed into Al(OH)3 with tetrahedron for PACl-C coagulation while a half of Al13 slowly decomposed into octahedral Al-HA precipitates for PACl-Al13 coagulation. Meanwhile, C ls XPS indicated that aromatic CC of HA was preferentially removed from solution to Al-HA flocs for both PACl-C and PACl-Al13 coagulation. It was concluded that Al-HA complexation strongly affects the reaction pathways for Al hydrolysis and the final nature of the precipitates during PACl coagulation of HA and that the hydrolysis products are also strongly affected by the characteristics of the PACl coagulant.