Intestinal permeability plays a pivotal role in the gut-liver axis and has emerged as a critical target for the prevention and treatment of liver diseases. Based on recent studies in China and globally， this article reviews the definitions and interrelationship of intestinal barrier function and intestinal permeability， the methods for assessing intestinal permeability， and the mechanism of action and clinical significance of intestinal permeability in the development and progression of various liver diseases. Studies have shown that increased intestinal permeability is a significant hallmark and an important driving factor for multiple liver diseases， and this state leads to the translocation of bacteria and harmful substances， trigger a systemic inflammatory response， and thus exacerbates liver injury， fibrosis， and metabolic dysregulation. Therefore， it is closely associated with the development and progression of metabolic associated fatty liver disease， alcoholic liver disease， autoimmune liver diseases， and their end-stage events， including liver cirrhosis， liver failure， and hepatocellular carcinoma. Future research should focus on the standardization of assessment methods， the exploration of underlying mechanisms， and the clinical translation of these findings.

BACKGROUND: Arsenic trioxide (ATO) is indicated as a broad-spectrum medicine for a variety of diseases, including cancer and cardiac disease. While the role of ATO in hepatic ischemia/reperfusion injury (HIRI) has not been reported. Thus, the purpose of this study was to identify the effects of ATO on HIRI. METHODS: In the present study, we established a 70% hepatic warm I/R injury and partial hepatectomy (30% resection) animal models in vivo and hepatocytes anoxia/reoxygenation (A/R) models in vitro with ATO pretreatment and further assessed liver function by histopathologic changes, enzyme-linked immunosorbent assay, cell counting kit-8, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. Small interfering RNA (siRNA) for extracellular signal-regulated kinase (ERK) 1/2 was transfected to evaluate the role of ERK1/2 pathway during HIRI, followed by ATO pretreatment. The dynamic process of autophagic flux and numbers of autophagosomes were detected by green fluorescent protein-monomeric red fluorescent protein-LC3 (GFP-mRFP-LC3) staining and transmission electron microscopy. RESULTS: A low dose of ATO (0.75 μmol/L in vitro and 1 mg/kg in vivo ) significantly reduced tissue necrosis, inflammatory infiltration, and hepatocyte apoptosis during the process of hepatic I/R. Meanwhile, ATO obviously promoted the ability of cell proliferation and liver regeneration. Mechanistically, in vitro  studies have shown that nontoxic concentrations of ATO can activate both ERK and phosphoinositide 3-kinase-serine/threonine kinase (PI3K-AKT) pathways and further induce autophagy. The hepatoprotective mechanism of ATO, at least in part, relies on the effects of ATO on the activation of autophagy, which is ERK-dependent. CONCLUSION Low, non-toxic doses of ATO can activate ERK/PI3K-AKT pathways and induce ERK-dependent autophagy in hepatocytes, protecting liver against I/R injury and accelerating hepatocyte regeneration after partial hepatectomy.
Animals ; Arsenic Trioxide ; Autophagy/physiology* ; Reperfusion Injury/prevention & control* ; Mice ; Male ; Proto-Oncogene Proteins c-akt/physiology* ; Arsenicals/therapeutic use* ; Oxides/therapeutic use* ; Liver/metabolism* ; Extracellular Signal-Regulated MAP Kinases/metabolism* ; Mice, Inbred C57BL

Purpose: Prostate cancer (PCa) is an epithelial malignancy that originates in the prostate gland and is generally categorized into low, intermediate, and high-risk groups. The primary diagnostic indicator for PCa is the measurement of serum prostate-specific antigen (PSA) values. However, reliance on PSA levels can result in false positives, leading to unnecessary biopsies and an increased risk of invasive injuries. Therefore, it is imperative to develop an efficient and accurate method for PCa risk stratification. Many recent studies on PCa risk stratification based on clinical data have employed a binary classification, distinguishing between low to intermediate and high risk. In this paper, we propose a novel machine learning (ML) approach utilizing a stacking learning strategy for predicting the tripartite risk stratification of PCa. Methods: Clinical records, featuring attributes selected using the lasso method, were utilized with 5 ML classifiers. The outputs of these classifiers underwent transformation by various nonlinear transformers and were then concatenated with the lasso-selected features, resulting in a set of new features. A stacking learning strategy, integrating different ML classifiers, was developed based on these new features. Results: Our proposed approach demonstrated superior performance, achieving an accuracy of 0.83 and an area under the receiver operating characteristic curve value of 0.88 in a dataset comprising 197 PCa patients with 42 clinical characteristics. Conclusions This study aimed to improve clinicians’ ability to rapidly assess PCa risk stratification while reducing the burden on patients. This was achieved by using artificial intelligence-related technologies as an auxiliary method for diagnosing PCa.

Objective:This study investigated the changes of cortical thickness in patients with Parkinson's cognitive dysfunction.Methods:In this cross-sectional study, general clinical data and head magnetic resonance imaging data were collected from Parkinson's disease(PD)patients and healthy controls who were hospitalized or outpatient in the Department of Geriatric Neurology of the First Affiliated Hospital of Kunming Medical University from January 2019 to December 2020.We observed the changes of cortical thickness in each group, and analyzed the correlation between cortical thickness and cognitive dysfunction in PD.Results:Compared with PD normal cognitive group, the cortical thickness of the left superiortemporal gyrus[(2.7±0.1)mm, (2.4±0.1)mm, t=-4.194], left supramarginal[(2.4±0.1)mm, (2.2±0.1)mm, t=-4.845], right insula[(3.0±0.1)mm, (2.7±0.1)mm, t=-4.170], left parahippocampal[(2.8±0.3)mm, (2.4±0.3)mm, t=-4.164]decreased in PD cognitive impairment group(all P<0.05), and cortical thickness of the right parsorbitalis[(2.5±0.2)mm, (2.4±0.2)mm, t=-4.226], left entorhinal[(3.5±0.3)mm, (3.1±0.4)mm, t=-4.583], left inferiortemporal[(2.7±0.2)mm, (2.5±0.1)mm, t=-6.229], left supramarginal[(2.4±0.1)mm, (2.1±0.1)mm, t=-3.236], right fusiform[(2.8±0.1)mm, (2.5±0.1)mm, t=-5.364], right lingual[(2.0±0.1)mm, (1.9±0.1)mm, t=-3.887], right insula[(3.0±0.1)mm, (2.7±0.2)mm, t=-5.326], right isthmuscingulate[(2.6±0.2)mm, (2.3±0.2)mm, t=-3.743]decreased in PD severe cognitive impairment group, the statistical difference was significant(all P<0.05). The cerebral cortex thickness was positively correlated with Mini-Mental State Examination and different cognitive areas, and negatively correlated with Hoehn-Yahrr grading. Conclusions:Local cortical thinning was observed in PD patients with cognitive impairment, whereas cortical involvement was more extensive in PD patients with severe cognitive impairment.

Objective:To investigate the relationship between rapid eye movement sleep behavior disorder(RBD)and neurofilament light chain(NfL)levels in patients with Parkinson's disease(PD).Methods:General clinical data of 121 PD patients and 38 healthy controls(HC)who visited the Department of Geriatric Neurology of the First Affiliated Hospital of Kunming Medical University from June 2019 to January 2021 were collected in a prospective study.According to the Rapid Eye Movement Sleep Behavior Disorder Questionnaire(RBDSQ), PD patients were divided into a PD with RBD group(PD-RBD, RBDSQ≥6)and a PD without RBD group(PD-NRBD, RBDSQ<6). General clinical data and plasma NfL levels of patients in the groups were compared.In addition, symptoms during exercise, during non-exercise, and sleep quality in the groups were also compared.Results:Plasma NfL levels were higher in the PD group than in the HC group(19.39 ng/L, 12.58-31.78; 14.85 ng/L, 9.78-22.15; Z=-2.492, P<0.05); plasma NfL levels were significantly higher in the PD-RBD group than in the PD-NRBD group and in the HC group(25.29 ng/L, 19.09-34.75; 17.14 ng/L, 11.70-26.67; 14.85 ng/L, 9.78-22.15; Z=-3.434, P<0.01); there was no significant difference in plasma NfL levels between the HC group and the PD-NRBD group( P>0.05). Receiver operating characteristic(ROC)curve analysis showed that, when the plasma NfL cutoff was set at 17.86 ng/L, PD-RBD and PD-NRBD could be distinguished( AUC=0.70, 95% CI=0.60-0.80, sensitivity 82%, specificity 54%). Binary logistic regression identified NfL level as an independent predictor of PD-RBD( β=0.068, OR=1.103, P=0.003). Conclusions:PD-RBD patients have increased plasma NfL levels, which can potentially serve as a biomarker for PD with RBD.

A total of 189 stool samples from swine with diarrhea, collected in various porcine farms in the central region of China were tested for porcine enteric caliciviruses (PEC) member porcine sapoviruses (SaV) by reverse transcription polymerase chain reaction (RT-PCR) amplification using primers designed to detect porcine SaV. Selected amplicons were sequenced to establish phylogenetic relationships with reference strains. Porcine SaV were detected in 12.70% (24/189) of the samples. Phylogenetic studies based on partial RNA polymerase gene sequences indicated that the field strains of viruses isolated in China were closely related (75.6 88.3% identity) to the porcine SaV Cowden reference strain. These results provide evidence that caliciviruses of the genus sapovirus circulate in piglets in China, but further studies are needed to clarify their importance as cause of diarrhea. This is the first report of PEC in China.