Objective Under the operation background of Diagnosis-Intervention Packet(DIP),whether there is interaction between reducing medical cost and average length of stay combined with pre-hospitalization mode,and whether there is difference between different departments and diseases in interaction.Methods Based on real-world data from 71 453 patients admitted to Guizhou Provincial People's Hospital from July to December 2021,a two-way analysis of variance was employed.When the interaction effect was statistically significant,parameter estimation was used to determine the magnitude and direction of the interaction effect,followed by subgroup analyses by department and disease.Results Without adjustment,both total medical costs and average length of stay exhibited a negative interaction effect(P＜0.05).Subgroup analyses revealed that in terms of total medical costs,the effect size for the surgical system was 0.18％,lower than that for the internal medicine system(0.70％);for core diseases,it was 6.62％,lower than that for comprehensive diseases(7.71％).Regarding average length of stay,the effect size for the surgical system was 0.55％,better than that for the internal medicine system(0.22％);for core diseases,it was 8.70％,higher than that for comprehensive diseases(2.90％).Conclusion The combination of DIP payment reform and pre-admission management model demonstrates a synergistic effect,effectively reducing patients' medical costs and length of stay.This effect is influenced by disease complexity and the standardization of diagnostic and treatment processes.

Objective To investigate the expression of Nucleophosmin 3(NPM3)in lung adenocarcinoma and its impact on the biological functions of the lung adenocarcinoma cell line H 292,with the goal of providing innovative insights for the diagno-sis and therapeutic strategies of lung adenocarcinoma.Methods The differential expression of the NPM3 gene between lung ad-enocarcinoma and normal controls was analyzed,along with its correlation with the clinicopathological characteristics and prog-nosis of lung adenocarcinoma patients,using the TCGA bioinformatics database.A cell model with reduced NPM3 expression(si-NPM3-H292)was developed by gene interference technology,and the efficiency of this knockdown was assessed by real-time fluorescence quantitative PCR(qRT-PCR)and Western blotting.The impact of NPM3 knockdown on the proliferative capacity of lung adenocarcinoma cells was evaluated by using CCK-8 and plate clone formation assays.The scratch and Transwell assays were employed to assess the effect of NPM 3 knockdown on the migratory potential of H 292 cells.The mRNA and protein ex-pression levels of markers associated with epithelial-mesenchymal transition(EMT)were determined by qRT-PCR and Western blotting.Additionally,the expression levels of proteins involved in the PI3K/Akt signaling pathway were examined by Western blotting.Results Analysis of the TCGA database indicated that NPM 3 is highly expressed in lung adenocarcinoma and is sig-nificantly associated with the clinicopathological classification of lung adenocarcinoma patients.The survival outcomes for pa-tients with high NPM 3 expression were notably worse than those with low expression(P＜0.05).The knockdown cell model was successfully established,and the proliferation and migration capabilities of H292 cells were significantly diminished after NPM3 knockdown(P＜0.05).Compared to the control group,mRNA and protein levels of E-cadherin were increased in si-NPM 3-H292 cells,while the expression level of N-cadherin was reduced at both mRNA and protein levels(P＜0.05).Although no significant change was observed in the protein expressions of Akt and PI3K in si-NPM3-H292 cells compared to the control,there was a decrease in phosphorylation levels,accompanied by an increase in protein expression of PTEN(P＜0.05).Conclusion NPM3 is highly expressed in lung adenocarcinoma,which is associated with poor prognosis of patients.NPM3 may facilitate the proliferation and migration of lung adenocarcinoma cells through regulation of the PI 3K/Akt signaling pathway.

Objective Under the operation background of Diagnosis-Intervention Packet(DIP),whether there is interaction between reducing medical cost and average length of stay combined with pre-hospitalization mode,and whether there is difference between different departments and diseases in interaction.Methods Based on real-world data from 71 453 patients admitted to Guizhou Provincial People's Hospital from July to December 2021,a two-way analysis of variance was employed.When the interaction effect was statistically significant,parameter estimation was used to determine the magnitude and direction of the interaction effect,followed by subgroup analyses by department and disease.Results Without adjustment,both total medical costs and average length of stay exhibited a negative interaction effect(P＜0.05).Subgroup analyses revealed that in terms of total medical costs,the effect size for the surgical system was 0.18％,lower than that for the internal medicine system(0.70％);for core diseases,it was 6.62％,lower than that for comprehensive diseases(7.71％).Regarding average length of stay,the effect size for the surgical system was 0.55％,better than that for the internal medicine system(0.22％);for core diseases,it was 8.70％,higher than that for comprehensive diseases(2.90％).Conclusion The combination of DIP payment reform and pre-admission management model demonstrates a synergistic effect,effectively reducing patients' medical costs and length of stay.This effect is influenced by disease complexity and the standardization of diagnostic and treatment processes.

Objective To investigate the characteristics of a novel FANCL mutation identified in a patient with premature ovarian insufficiency(POI)and to explore its potential functional impacts in vitro.Methods A novel FANCL heterozygous mutation c.1033G>A(p.Glu345Lys)was screened in a patient with POI using whole exome sequencing(WES),which was found to be inherited from a mother who had undergone early menopause.The authenticity of the mutation was identified by Sanger sequencing and the conserved nature of the mutation site was predicted by software.Overexpressing FANCL mutant and wildtype plasmids were constructed and transiently transfected into HEK293T cell lines,and the effect of the mutation was detected by qPCR,immunofluorescence and Western blot.Results The mutation site of FANCL was located within the Ring domain of FANCL,which was highly conserved across multiple species.The mutant showed no significant change in mRNA expression level,while the protein expression level was significantly down-regulated.In vitro cellular experiments further revealed that the mutation leads to decreased expression levels by reducing protein stability.Conclusion A FANCL c.1033G>A mutation was found and it may cause disease in the POI patient due to decreased protein stability.

Objective To investigate the expression of Nucleophosmin 3(NPM3)in lung adenocarcinoma and its impact on the biological functions of the lung adenocarcinoma cell line H 292,with the goal of providing innovative insights for the diagno-sis and therapeutic strategies of lung adenocarcinoma.Methods The differential expression of the NPM3 gene between lung ad-enocarcinoma and normal controls was analyzed,along with its correlation with the clinicopathological characteristics and prog-nosis of lung adenocarcinoma patients,using the TCGA bioinformatics database.A cell model with reduced NPM3 expression(si-NPM3-H292)was developed by gene interference technology,and the efficiency of this knockdown was assessed by real-time fluorescence quantitative PCR(qRT-PCR)and Western blotting.The impact of NPM3 knockdown on the proliferative capacity of lung adenocarcinoma cells was evaluated by using CCK-8 and plate clone formation assays.The scratch and Transwell assays were employed to assess the effect of NPM 3 knockdown on the migratory potential of H 292 cells.The mRNA and protein ex-pression levels of markers associated with epithelial-mesenchymal transition(EMT)were determined by qRT-PCR and Western blotting.Additionally,the expression levels of proteins involved in the PI3K/Akt signaling pathway were examined by Western blotting.Results Analysis of the TCGA database indicated that NPM 3 is highly expressed in lung adenocarcinoma and is sig-nificantly associated with the clinicopathological classification of lung adenocarcinoma patients.The survival outcomes for pa-tients with high NPM 3 expression were notably worse than those with low expression(P＜0.05).The knockdown cell model was successfully established,and the proliferation and migration capabilities of H292 cells were significantly diminished after NPM3 knockdown(P＜0.05).Compared to the control group,mRNA and protein levels of E-cadherin were increased in si-NPM 3-H292 cells,while the expression level of N-cadherin was reduced at both mRNA and protein levels(P＜0.05).Although no significant change was observed in the protein expressions of Akt and PI3K in si-NPM3-H292 cells compared to the control,there was a decrease in phosphorylation levels,accompanied by an increase in protein expression of PTEN(P＜0.05).Conclusion NPM3 is highly expressed in lung adenocarcinoma,which is associated with poor prognosis of patients.NPM3 may facilitate the proliferation and migration of lung adenocarcinoma cells through regulation of the PI 3K/Akt signaling pathway.

Objective To investigate the characteristics of a novel FANCL mutation identified in a patient with premature ovarian insufficiency(POI)and to explore its potential functional impacts in vitro.Methods A novel FANCL heterozygous mutation c.1033G>A(p.Glu345Lys)was screened in a patient with POI using whole exome sequencing(WES),which was found to be inherited from a mother who had undergone early menopause.The authenticity of the mutation was identified by Sanger sequencing and the conserved nature of the mutation site was predicted by software.Overexpressing FANCL mutant and wildtype plasmids were constructed and transiently transfected into HEK293T cell lines,and the effect of the mutation was detected by qPCR,immunofluorescence and Western blot.Results The mutation site of FANCL was located within the Ring domain of FANCL,which was highly conserved across multiple species.The mutant showed no significant change in mRNA expression level,while the protein expression level was significantly down-regulated.In vitro cellular experiments further revealed that the mutation leads to decreased expression levels by reducing protein stability.Conclusion A FANCL c.1033G>A mutation was found and it may cause disease in the POI patient due to decreased protein stability.

Objective To evaluate the efficacy and safety of brexpiprazole in treating acute schizophrenia.Methods Patients with schizophrenia were randomly divided into treatment group and control group.The treatment group was given brexpiprozole 2-4 mg·d-1 orally and the control group was given aripiprazole 10-20 mg·d-1orally,both were treated for 6 weeks.Clinical efficacy of the two groups,the response rate at endpoint,the changes from baseline to endpoint of Positive and Negative Syndrome Scale(PANSS),Clinical Global Impression-Improvement(CGI-S),Personal and Social Performance scale(PSP),PANSS Positive syndrome subscale,PANSS negative syndrome subscale were compared.The incidence of treatment-related adverse events in two groups were compared.Results There were 184 patients in treatment group and 186 patients in control group.After treatment,the response rates of treatment group and control group were 79.50％(140 cases/184 cases)and 82.40％(150 cases/186 cases),the scores of CGI-I of treatment group and control group were(2.00±1.20)and(1.90±1.01),with no significant difference(all P＞0.05).From baseline to Week 6,the mean change of PANSS total score wese(-30.70±16.96)points in treatment group and(-32.20±17.00)points in control group,with no significant difference(P＞0.05).The changes of CGI-S scores in treatment group and control group were(-2.00±1.27)and(-1.90±1.22)points,PSP scores were(18.80±14.77)and(19.20±14.55)points,PANSS positive syndrome scores were(-10.30±5.93)and(-10.80±5.81)points,PANSS negative syndrome scores were(-6.80±5.98)and(-7.30±5.15)points,with no significant difference(P＞0.05).There was no significant difference in the incidence of treatment-related adverse events between the two group(69.00％vs.64.50％,P＞0.05).Conclusion The non-inferiority of Brexpiprazole to aripiprazole was established,with comparable efficacy and acceptability.

Metastasis-associated lung adenocarcinoma transcript 1 ( MALAT1) is a well-established oncogenic long non-coding RNA, the higher expression of which is strongly correlated with cancer events such as tumorigenesis, progression, metastasis, drug resistance, and treatment outcome in solid cancers. Recently, a series of studies has highlighted its potential role in hematological malignancies in terms of these events. Similar to solid cancers, MALAT1 can regulate various target genes via sponging and epigenetic mechanisms, but the miRNAs sponged by MALAT1 differ from those identified in solid cancers. In this review, we systematically describe the role and underlying mechanisms of MALAT1 in multiple types of hematological malignancies, including regulation of cell proliferation, metastasis, stress response, and glycolysis. Clinically, MALAT1 expression is related to poor treatment outcome and drug resistance, therefore exhibiting potential prognostic value in multiple myeloma, lymphoma, and leukemia. Finally, we discuss the evaluation of MALAT1 as a novel therapeutic target against cancer in preclinical studies.

Objective To explore the causal relationship between ischemic stroke and different types of epilepsy so as to provide genetic evidence for the risk of epilepsy after ischemic stroke.Methods Based on the summary data of genome-wide association study,Mendelian randomization (MR ) analysis was performed with MR-Egger regression,weighted median and inverse-variance weighting.Sensitivity analysis was conducted by using MR-Egger regression test,MR-PRESSO test and leave-one-out method.Results Two-sample MR analysis showed that there was a causal relationship between ischemic stroke and the risk of epilepsy (OR=1.10,P=0.036)and generalized epilepsy (OR=1.25,P=0.001 ),but no such relationship was observed with the risk of focal epilepsy (OR=1.06,P=0.360).In addition,diastolic blood pressure (OR=1.12,P=0.002)and BMI (OR=1.08,P=0.015)also had a causal relationship with the risk of epilepsy. After adjusting confounding factors,multivariate MR analysis revealed that only ischemic stroke (OR=1.18,P=3.770×10-6)and epilepsy risk had a causal relationship.Conclusion There is a causal relationship between ischemic stroke and the risk of generalized epilepsy,which can be used to stratify the risk of post-stroke epilepsy.

Objective To detect the expression changes of interleukin-10(IL-10)and transforming growth factor-β1(TGF-β1)during the development of deep vein thrombosis in mice,and to explore the application value of them in thrombus age estimation.Methods The mice in the experimental group were subjected to ligation of inferior vena cava.The mice were sacrificed by excessive anesthesia at 1 d,3 d,5 d,7 d,10 d,14 d and 21 d after ligation,respectively.The inferior vena cava segment with thrombosis was extracted below the ligation point.The mice in the control group were not ligated,and the inferior vena cava segment at the same position as the experimental group was extracted.The ex-pression changes of IL-10 and TGF-β1 were detected by immunohistochemistry(IHC),Western blot-ting and real-time qPCR.Results IHC results revealed that IL-10 was mainly expressed in monocytes in thrombosis and TGF-β1 was mainly expressed in monocytes and fibroblast-like cells in thrombosis.Western blotting and real-time qPCR showed that the relative expression levels of IL-10 and TGF-β1 in each experimental group were higher than those in the control group.The mRNA and protein levels of IL-10 reached the peak at 7 d and 10 d after ligation,respectively.The mRNA expression level at 7 d after ligation was 4.72±0.15 times that of the control group,and the protein expression level at 10 d after ligation was 7.15±0.28 times that of the control group.The mRNA and protein levels of TGF-β1 reached the peak at 10 d and 14 d after ligation,respectively.The mRNA expression level at 10 d after ligation was 2.58±0.14 times that of the control group,and the protein expression level at 14 d after ligation was 4.34±0.19 times that of the control group.Conclusion The expressions of IL-10 and TGF-β1 during the evolution of deep vein thrombosis present time-dependent sequential changes,and the expression levels of IL-10 and TGF-β1 can provide a reference basis for thrombus age estimation.