BackgroundSevere mental disorders are characterized by high recurrence rate， high disability rate， high rates of harmful incidents， and low treatment-seeking rate， with affected patients demonstrating increased frequencies of dangerous behaviors. Ningxia Hui Autonomous Region has implemented community management for patients with severe mental disorders across the region since 2004， while the current status and regional characteristics of the managed patients remain unclear. ObjectiveTo analyze the current status of management and treatment of patients with severe mental disorders in Ningxia Hui Autonomous Region， and to explore their regional distribution characteristics， so as to provide references for optimizing regional prevention and control strategies. MethodsPatients with severe mental disorders diagnosed and registered in the Severe Mental Disorder Management Information Platform of Ningxia Hui Autonomous Region from August 1， 2011 to December 31， 2021 were selected. Patients' basic information， management indicators， and treatment metrics were extracted from the platform， followed by descriptive statistical analysis of the corresponding data. ResultsAs of December 31， 2021， the permanent resident population of Ningxia Hui Autonomous Region was 6 946 540， with 29 787 registered patients with severe mental disorders. The majority of the patients were female （50.25%）， aged 18-59 years （79.01%）， with educational level of junior high school or below （84.63%）， married （52.87%）， farmers （56.01%）， and diagnosed with schizophrenia （55.91%）， while ethnic minority patients accounted for a relatively high proportion （31.35%）. In 2021， the reported prevalence rate of severe mental disorders in Ningxia Hui Autonomous Region was 0.43%， with standardized management and regular medication adherence rates at 90.39% and 66.34%， respectively. The standardized management rate in 8 counties/districts （36.36%） was lower than the average level of Ningxia Hui Autonomous Region， while 10 counties/districts （45.45%） showed below-average medication adherence rates， of which 6 counties/districts（60.00%） were located in the south-central region. ConclusionPatients with severe mental disorders in Ningxia Hui Autonomous Region are predominantly young and middle-aged adults with low level of education， and those in the central-southern region demonstrate lower medication adherence. ［Funded by Key Research and Development Program Project of Ningxia Hui Autonomous Region （number， 2023BEG02029）］

Objective To explore whether miR-146b can participate in the brain injury process of diabetic rats with cerebral infarction(DM-CI)by regulating the extracellular regulatory protein kinase(ERK1/2)-activated protein-1(AP-1)signaling pathway.Methods 80 SD rats were randomly divided into sham operation group,DM-CI group,low miR-146b expression group and ERK1/2 inhibition group,with 20 rats in each group.The National Institutes of Health Stroke Scale(NIHSS)score measures brain function in rats.The mRNA levels of miR-146b,ERK1/2 and AP-1 in rat brain tissue were detected by RT-qPCR.Western blotting detected ERK1/2,AP-1 protein levels in rat brain tissue.TTC staining was used to detect cerebral infarction volume in rats.H&E staining was used to detect brain histopathological changes.Random blood glucose levels were detected by glucose meter in rats.Results Compared with sham operation group,mRNA expression levels of miR-146b,ERK1/2 and AP-1 in brain tissue of rats in DM-CI group were significantly increased,with statistically differences(t=10.86,15.62,9.87,all P<0.05).ERK1/2 and AP-1 protein levels increased,with statistically differences(t=11.18,23.81,P<0.05).NIHSS score increased and random blood glucose level increased(t=44.49,30.02,all P<0.05),and increased cerebral infarction volume(t=51.05,P<0.05),the structure of brain tissue was disorganized and loose,and edema can be seen in the pericellular space.Compared with the DM-CI group,the mRNA expression levels of miR-146b,ERK1/2 and AP-1 in the brain tissue of rats with low expression of miR-146b were decreased,with statistically differences(t=38.00,20.03,24.25,all P<0.05).the protein expression of EPK1/2 and AP-1 decreased,and the differences were statistically significant(t=12.30,26.70,all P＜0.05).NIHSS score and random blood glucose level were decreased,with statistically differences(t=38.11,33.77,all P<0.05),cerebral infarction volume decreased(t=16.70,P<0.05),the degree of brain tissue in jury and edema was improved,and the expression levels of ERK1/2 and AP-1 protein and mRNA in brain tissue of rats inhibited by ERK1/2 were decreased,with statistically differences(t=13.61～38.00,all P<0.05),the NIHSS score of rats was decreased,and the random blood glucose level was decreased,with statistically differences(t=16.48,26.61,all P<0.05).Conclusion MiR-146b may be involved in brain functional and structural damage in DM-CI rats by regulating ERK1/2-AP-1 signaling pathway.

Hepatocellular carcinoma (HCC) expresses abundant glycolytic enzymes and displays comprehensive glucose metabolism reprogramming. Aldolase A (ALDOA) plays a prominent role in glycolysis; however, little is known about its role in HCC development. In the present study, we aim to explore how ALDOA is involved in HCC proliferation. HCC proliferation was markedly suppressed both in vitro and in vivo following ALDOA knockout, which is consistent with ALDOA overexpression encouraging HCC proliferation. Mechanistically, ALDOA knockout partially limits the glycolytic flux in HCC cells. Meanwhile, ALDOA translocated to nuclei and directly interacted with c-Jun to facilitate its Thr93 phosphorylation by P21-activated protein kinase; ALDOA knockout markedly diminished c-Jun Thr93 phosphorylation and then dampened c-Jun transcription function. A crucial site Y364 mutation in ALDOA disrupted its interaction with c-Jun, and Y364S ALDOA expression failed to rescue cell proliferation in ALDOA deletion cells. In HCC patients, the expression level of ALDOA was correlated with the phosphorylation level of c-Jun (Thr93) and poor prognosis. Remarkably, hepatic ALDOA was significantly upregulated in the promotion and progression stages of diethylnitrosamine-induced HCC models, and the knockdown of A ldoa strikingly decreased HCC development in vivo. Our study demonstrated that ALDOA is a vital driver for HCC development by activating c-Jun-mediated oncogene transcription, opening additional avenues for anti-cancer therapies.

Objective : To explore whether chrysophanol(CHR) affects macrophage polarization by promoting mitochondrial biosynthesis through AMPK/PGC-1α pathway. Methods : The molecular docking and binding ability of CHR with AMPK and PGC-1α were predicted by Autodock vina software. Human monocytes(THP-1) were induced to M0 macrophages by phorbol myristate acetate(PMA), and to M1 macrophages by lipopolysaccharide(LPS) combined with interferon-γ(IFN-γ), which were set as Control group. M1 macrophages treated with CHR were set as CHR group. M1 macrophages treated with CHR combined with AMPK inhibitor(Compound C) were set as CHR+Compound C group. The mRNA expression levels of M1 macrophage markers(iNOS, CD86) and mitochondrial biosynthesis related genes(PGC-1α, NFR-1, TFAM) were detected by Quantitative real time polymerase chain reaction(qRT-PCR). The expression level of M1 macrophage marker iNOS was detected by immunofluorescence. The protein expression levels of AMPK, p-AMPK and PGC-1α were detected by Western blot. Results : The docking results showed that the binding energies of CHR with AMPK and PGC-1α were-8.4 kcal/mol and-7.4 kcal/mol, respectively. qRT-PCR results showed that the in vitro model of M1 macrophages was successfully established. Compared with the Control group, CHR treatment significantly increased the mRNA expression of mitochondrial biosynthesis-related genes PGC-1α, NFR-1, and TFAM(P<0.001). Compared with CHR treatment group, CHR combined with Compound C treatment significantly decreased the mRNA expression levels of mitochondrial biosynthesis-related genes PGC-1α, NFR-1, and TFAM(P<0.05). Immunofluorescence results showed that CHR treatment inhibited the protein expression of iNOS compared with the Control group(P<0.001). Compared with CHR treatment group,CHR combined with Compound C treatment reversed the inhibitory effect of CHR on i NOS protein expression(P<0.05). Western blot results showed that compared with the Control group,the CHR treatment group had significant increase in the protein expression levels of p-AMPK and PGC-1α(P<0.001).Compared with CHR treatment group,CHR combined with Compound C treatment significantly decreased the protein expression levels of p-AMPK and PGC-1α(P<0.05). Conclusion Chrysophanol may inhibit macrophage polarization to M1 by activating AMPK/PGC-1α signaling pathway to promote mitochondrial biosynthesis.

Objective To explore the differences and similarities in the changes of pulp repair response after direct pulp capping with iRoot BP Plus and MTA.Methods A total of 36 male SD rats were randomly divided into 3 groups,namely iRoot BP Plus group,MTA group and blank control group.Dental pulp exposure and direct pulp capping was performed on both sides of maxillary first molars of each rat.Four rats were randomly selected and sacrificed from each group at 7,14,and 28 days postoperatively,and the specimens were taken for hematoxylin-eosin(HE)staining,and then each index was observed.Results ①From the perspective of dentin tubular formation quality,at 14 d and 28 d,there were statistical differences between iRoot BP Plus group and MTA group(P＜0.05),and iRoot BP Plus was significantly better than MTA in terms of quality of restorative dentin formation.②At 14 days after operation,iRoot BP Plus had a greater area of neodontinin than that in MTA group(P＜0.05).Conclusion Both iRoot BP Plus and MTA can promote the formation of restorative dentin bridges after direct pulp capping,and the formation quality is high.The long-term effects need to be further studied.

This study was a single-center retrospective study, to investigate the correlation between the relative level of miR-200a in exfoliated cells of peritoneal dialysis (PD) effluent and clinical indicators of peritoneal function in PD patients. Clinical data of PD patients who underwent treatment in the Department of Nephrology, the First Affiliated Hospital of Nanchang University, from January 2024 to December 2024 were collected, and the relative level of miR-200a in exfoliated cells of PD effluent was assessed. Patients were divided into three groups according to dialysis duration (Group A:≤1 year; Group B:>1 to <5 years; Group C:≥5 years), and differences in clinical data among the groups were compared. The correlation between the relative level of miR-200a and serum albumin, serum calcium, serum phosphorus, serum creatinine, hemoglobin, the neutrophil/high-density lipoprotein cholesterol ratio, the monocyte/high-density lipoprotein cholesterol ratio, the lymphocyte/high-density lipoprotein cholesterol ratio, and 24-hour urine volume in PD patients was analyzed. The results showed that there were no statistically significant differences among the three groups in gender, age, creatinine clearance rate, or Kt/V (all P>0.05). However, statistically significant differences were found among the three groups in peritoneal transport type ( χ2=13.518, P=0.001) and ultrafiltration volume ( H=6.905, P=0.032). Based on the 4-hour PD effluent creatinine/blood creatinine in the peritoneal equilibration test, patients were divided into the low transporter/low average transporter group (L group) and the high transporter/high average transporter group (H group). A statistically significant difference in the relative level of miR-200a was observed between the two groups [11.70 (1.09, 20.49) vs. 0.73 (0.46, 1.98), t=4.545, P<0.001]. The relative level of miR-200a was positively correlated with ultrafiltration volume and 24-hour urine output ( r=0.328, P=0.030; r=0.516, P<0.001), and negatively correlated with dialysis vintage ( r=-0.496, P<0.001). These results indicate that miR-200a level in PD effluent may, to some extent, reflect patients' peritoneal membrane function.

Objective To develop a risk management system for complications associated with peripheral venous indwelling needles and to evaluate its application effect in order to reduce the risk of related complications.Methods We designed a comprehensive risk management system for peripheral intravenous indwelling needle complications,integrating specialized evidence-based guidelines with clinical practice insights,including 5 modules:intelligent assessment and decision support,intelligent inspection reminders,educational modules,collaborative case management procedures,and a knowledge base.Patients admitted to the neurology and internal classification metabolism departments of a tertiary hospital in Jilin Province were conveniently selected as the research subjects.Patients were assigned to a control group(from May to July 2022,before the implementation of the system)and an experimental group(from September to December 2022,after the implementation of the system).The incidence of complications,duration of indwelling needle,compliance rate of core indicators for nursing quality and number of nursing consultations were compared between the groups.Additionally,a self-administered questionnaire was used to assess clinical nurses'evaluations of the system.Results A total of 189 patients were included in the experimental group and 177 patients in the control group.The incidence of complications associated with peripheral intravenous indwelling needles was lower than that in the control group.The duration of indwelling peripheral intravenous needles was longer than that in the control group.The quality compliance rate of peripheral venous indwelling needle care in the experimental group was higher than that in the control group,and the number of consultation cases in the experimental group was higher than that in the control group.Comparisons between the 2 groups showed statistically significant differences for all indicators(P＜0.05).The nurses'recognition rates for the system's user-friendliness,professional guidance,and patient benefit were 77.78％,81.74％,and 82.13％,respectively.Conclusion The application of a peripheral vein indwelling needle complication risk management system can reduce the incidence of complications,prolong the duration of indwelling,and improve nursing quality.Nurses have a high recognition of this system.

Objective To explore the relationship between serum miRNA-126a,miRNA-130b levels and cognitive impairment(CI)in patients with diabetes mellitus(DM)complicated with acute stroke(AS).Methods A retrospective analysis was conducted on 70 DM patients with AS admitted to Wuhan First Hospital from January 2019 to December 2021.Patients were divided into CI group(41 cases)and non-CI group(29 cases)based on the occurrence of CI.Real-time fluorescence quantitative PCR was used to detect the relative expression levels of miRNA-126a and miRNA-130b in peripheral blood.Results Compared with non-CI group,the CI group showed increased albumin(P<0.05)and decreased levels of miRNA-126a and miRNA-130b(P<0.05).Logistic regression analysis showed that albumin(OR=19.045,95%CI=2.001～181.230),miRNA-126a(OR=200.603,95%CI=15.663～2569.162),miRNA-130b(OR=11.770,95%CI=1.966～70.474)were related factors affecting CI occurrence in DM patients with AS.ROC curve analysis showed that peripheral blood miRNA-126a had the highest AUC(0.958)for diagnosing CI in DM patients with AS,with a sensitivity of 97.6%and specificity of 89.7%.The AUC for miRNA-130b(0.669)was lower,with a sensitivity of 73.2%and specificity of 62.1%.Conclusion Decreased expression of peripheral blood miRNA-126a has good diagnostic value for CI in DM patients with AS.

Based on the viewpoints of turbidity and toxin and years of clinical experience,professor Wei Aisheng proposed that spleen qi deficiency leading to internal retention of turbidity and toxin contributes to the key pathogenesis of patients with type 2 diabetes mellitus(T2DM)characterized by obesity or metabolic disorders.For T2DM patients with obesity or metabolic disorders in the middle and end stages,long-term retention of turbidity and toxin leads to unsmooth qi movement of triple energizer and damage of viscera.Therefore,Professor Wei put forward the viewpoint of cutting off the toxin in the early stage,and established the therapy of replenishing qi,respectively expelling pathogens and eliminating turbidity from triple energizer.Professor Wei formulated Sanhuang Yinchen Wuling San as the primary prescription for T2DM.The prescription is derived from the classical formula Yinchen Wuling San with the herbs of Astragali Radix,Coptidis Rhizoma and Ephedrae Herba added,having the actions of replenishing qi and supporting healthy qi,respectively expelling pathogens from triple-energizer to resolve phlegm-damp and stagnated heat.The application of Sanhuang Yinchen Wuling San for T2DM can invigorate spleen qi,smooth qi movement of triple energizer,and eliminate turbidity and toxin,and enhance the efficacy for T2DM.

Hepatocellular carcinoma(HCC)expresses abundant glycolytic enzymes and displays comprehensive glucose metabolism reprogramming.Aldolase A(ALDOA)plays a prominent role in glycolysis;however,little is known about its role in HCC development.In the present study,we aim to explore how ALDOA is involved in HCC proliferation.HCC proliferation was markedly suppressed both in vitro and in vivo following ALDOA knockout,which is consistent with ALDOA overexpression encouraging HCC prolifera-tion.Mechanistically,ALDOA knockout partially limits the glycolytic flux in HCC cells.Meanwhile,ALDOA translocated to nuclei and directly interacted with c-Jun to facilitate its Thr93 phosphorylation by P21-activated protein kinase;ALDOA knockout markedly diminished c-Jun Thr93 phosphorylation and then dampened c-Jun transcription function.A crucial site Y364 mutation in ALDOA disrupted its interaction with c-Jun,and Y364S ALDOA expression failed to rescue cell proliferation in ALDOA deletion cells.In HCC patients,the expression level of ALDOA was correlated with the phosphorylation level of c-Jun(Thr93)and poor prognosis.Remarkably,hepatic ALDOA was significantly upregulated in the promotion and progression stages of diethylnitrosamine-induced HCC models,and the knockdown of Aldoa strikingly decreased HCC development in vivo.Our study demonstrated that ALDOA is a vital driver for HCC development by activating c-Jun-mediated oncogene transcription,opening additional avenues for anti-cancer therapies.