Objective:To investigate the clinical characteristics,contributing factors,and impacts of low-ratio cases under the Diagnosis-Intervention Packet(DIP)in tertiary hospitals,and propose actionable management strategies to promote the compliance and efficiency of medical insurance payment in tertiary hospitals.Methods:Based on retrospective analysis of 98 298 DIP-settled cases(January-October 2024)from a tertiary hospital in Henan,18 126 low-ratio and 80 172 normal-ratio cases were selected.Comparative metrics(demographics,hospitalization duration,primary care-sensitive conditions,medical insurance reimbursement ratios)were analyzed using non-parametric tests.Pareto analysis was applied to identify key diagnostic clusters.Results:Low-ratio cases exhibited distinct features:38.6％patients aged ≥61 years,32.5％hospital stays＜48 hours,l.0％primary care-sensitive conditions,Median reimbursement ratio was 0.69,with significant differences compared with general group.Seven diagnostic clusters(myeloproliferative disorders,poorly differentiated tumors,impact factors for health,medical treatment situation,etc.)accounted for 75.36％of low-ratio cases.Conclusion:It is suggested to optimize the medical service management under DIP payment through standardizing clinical pathways,enhanced coding quality,establishing policy feedback mechanisms,and promoting data governance.

Objective To investigate the effects of miR-483-3p on hypoxia/reoxygenation(H/R)-induced apoptosis and pyroptosis of H9c2 cardiomyocytes and its possible mechanism.Methods Rat H9c2 cardiomyocytes were cultured in vitro,adeno-associated virus-infected H9c2 and the H/R model were constructed by triple-air incuba-tor,and the cells were randomly divided into blank control(Sham)group,model(H/R)group,AAV-miR-483-3p mimic+H/R(AAV-miR-483-3p)group,AAV-miR-483-3p negative control+H/R(AAV-NC)group.The growth status of cells in each group was observed using an inverted microscope;cell proliferation activity was detected by cell counting kit-8(CCK-8);LDH release by lactate dehydrogenase(LDH)kit;apoptosis rate by flow cytometry;apoptosis by notched end labeling(TUNEL).Western blot(WB)was used to detect the expression levels of IL-1β and GSDMD proteins in each group.Results Compared with the Sham group,the H/R group showed abnormal cell status and increased cell death,decreased cell activity,increased LDH release,increased apoptosis rate and apopto-sis level,and increased expression levels of IL-1β and GSDMD proteins(P<0.05);compared with the H/R group,the AAV-miR-483-3p group showed improved cell status and less cell death,increased cell proliferation activity,increased LDH release,and increased IL-1β and GSDMD protein expression levels(P<0.05).Compared with the H/R group,the AAV-miR-483-3p group showed improved cell status and less cell death,increased cell proliferation activity,decreased LDH release,decreased apoptosis rate and apoptosis level,and decreased expression of IL-1β and GSDMD proteins(P<0.05).Conclusion Over-expression of miR-483-3p can improve H/R-inducedH9c2 cardiomyocyte injury by enhancing cell activity and cell metabolism,and inhibiting apoptosis and cell charring.

Objective:To investigate the clinical characteristics,contributing factors,and impacts of low-ratio cases under the Diagnosis-Intervention Packet(DIP)in tertiary hospitals,and propose actionable management strategies to promote the compliance and efficiency of medical insurance payment in tertiary hospitals.Methods:Based on retrospective analysis of 98 298 DIP-settled cases(January-October 2024)from a tertiary hospital in Henan,18 126 low-ratio and 80 172 normal-ratio cases were selected.Comparative metrics(demographics,hospitalization duration,primary care-sensitive conditions,medical insurance reimbursement ratios)were analyzed using non-parametric tests.Pareto analysis was applied to identify key diagnostic clusters.Results:Low-ratio cases exhibited distinct features:38.6％patients aged ≥61 years,32.5％hospital stays＜48 hours,l.0％primary care-sensitive conditions,Median reimbursement ratio was 0.69,with significant differences compared with general group.Seven diagnostic clusters(myeloproliferative disorders,poorly differentiated tumors,impact factors for health,medical treatment situation,etc.)accounted for 75.36％of low-ratio cases.Conclusion:It is suggested to optimize the medical service management under DIP payment through standardizing clinical pathways,enhanced coding quality,establishing policy feedback mechanisms,and promoting data governance.

Objective To observe the effect of pirfenidone on myocardial fibrosis in rats and inves-tigate its underlying mechanism.Methods Twenty-four SD rats were randomly divided into sham-operation group,model group,low-and high-dose pirfenidone groups,with 6 rats in each group.Rat model of myocardial fibrosis was established by injecting isoprenaline into the tail vein,while normal saline was given to the sham operation group.Pirfenidone of 150 and 300 mg/(kg·d)were infused gastrically to the rats of low-and high-dose pirfenidone groups after modeling.Mas-son staining was used to observe the severity of myocardial fibrosis,immunohistochemical assay was employed to detect the expression of Collagen-1,NOD-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome,cysteinyl aspartate-specific protease-1(Caspase-1),and Western blotting was performed to detect the protein levels of Collogen-1 and atrial desmo-plakin D(gasdermin D,GSDMD).Results The model group showed obvious myocardial fibrosis,and elevated expression of Collogen-1,NLRP3,Caspase-1 and GSDMD when compared with the sham operation group(P＜0.05).Low-and high-dose pirfenidone treatment resulted in signifi-cantly reduced myocardial fibrosis and reduced expression of Collogen-1,NLRP3,Caspase-1 and GSDMD[(8.14±1.40)％,(6.56±0.75)％vs(22.15±2.57)％,P＜0.05;0.14±0.03 vs 0.33±0.05,0.42±0.13,P＜0.05;(10.34±1.40)％,(10.33±3.40)％vs(23.22±1.99)％,P＜0.05;(15.67±0.56)％,(17.33±0.78)％vs(22.87±1.92)％,P＜0.05;0.43±0.06,0.46±0.11 vs 0.65±0.03,P＜0.05].Conclusion Pirfenidone inhibits cardiomyocyte pyroptosis and attenuates myocar-dial fibrosis through the NLRP3/Caspase-1/GSDMD signaling axis.

Objective To observe the effect of pirfenidone on myocardial fibrosis in rats and inves-tigate its underlying mechanism.Methods Twenty-four SD rats were randomly divided into sham-operation group,model group,low-and high-dose pirfenidone groups,with 6 rats in each group.Rat model of myocardial fibrosis was established by injecting isoprenaline into the tail vein,while normal saline was given to the sham operation group.Pirfenidone of 150 and 300 mg/(kg·d)were infused gastrically to the rats of low-and high-dose pirfenidone groups after modeling.Mas-son staining was used to observe the severity of myocardial fibrosis,immunohistochemical assay was employed to detect the expression of Collagen-1,NOD-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome,cysteinyl aspartate-specific protease-1(Caspase-1),and Western blotting was performed to detect the protein levels of Collogen-1 and atrial desmo-plakin D(gasdermin D,GSDMD).Results The model group showed obvious myocardial fibrosis,and elevated expression of Collogen-1,NLRP3,Caspase-1 and GSDMD when compared with the sham operation group(P＜0.05).Low-and high-dose pirfenidone treatment resulted in signifi-cantly reduced myocardial fibrosis and reduced expression of Collogen-1,NLRP3,Caspase-1 and GSDMD[(8.14±1.40)％,(6.56±0.75)％vs(22.15±2.57)％,P＜0.05;0.14±0.03 vs 0.33±0.05,0.42±0.13,P＜0.05;(10.34±1.40)％,(10.33±3.40)％vs(23.22±1.99)％,P＜0.05;(15.67±0.56)％,(17.33±0.78)％vs(22.87±1.92)％,P＜0.05;0.43±0.06,0.46±0.11 vs 0.65±0.03,P＜0.05].Conclusion Pirfenidone inhibits cardiomyocyte pyroptosis and attenuates myocar-dial fibrosis through the NLRP3/Caspase-1/GSDMD signaling axis.

Objective To investigate the effects of miR-483-3p on hypoxia/reoxygenation(H/R)-induced apoptosis and pyroptosis of H9c2 cardiomyocytes and its possible mechanism.Methods Rat H9c2 cardiomyocytes were cultured in vitro,adeno-associated virus-infected H9c2 and the H/R model were constructed by triple-air incuba-tor,and the cells were randomly divided into blank control(Sham)group,model(H/R)group,AAV-miR-483-3p mimic+H/R(AAV-miR-483-3p)group,AAV-miR-483-3p negative control+H/R(AAV-NC)group.The growth status of cells in each group was observed using an inverted microscope;cell proliferation activity was detected by cell counting kit-8(CCK-8);LDH release by lactate dehydrogenase(LDH)kit;apoptosis rate by flow cytometry;apoptosis by notched end labeling(TUNEL).Western blot(WB)was used to detect the expression levels of IL-1β and GSDMD proteins in each group.Results Compared with the Sham group,the H/R group showed abnormal cell status and increased cell death,decreased cell activity,increased LDH release,increased apoptosis rate and apopto-sis level,and increased expression levels of IL-1β and GSDMD proteins(P<0.05);compared with the H/R group,the AAV-miR-483-3p group showed improved cell status and less cell death,increased cell proliferation activity,increased LDH release,and increased IL-1β and GSDMD protein expression levels(P<0.05).Compared with the H/R group,the AAV-miR-483-3p group showed improved cell status and less cell death,increased cell proliferation activity,decreased LDH release,decreased apoptosis rate and apoptosis level,and decreased expression of IL-1β and GSDMD proteins(P<0.05).Conclusion Over-expression of miR-483-3p can improve H/R-inducedH9c2 cardiomyocyte injury by enhancing cell activity and cell metabolism,and inhibiting apoptosis and cell charring.

Objective To study the role of microRNA(miR)-483-3p in reducing myocardial fibrosis in rats,and explore the relationship between its mechanism and autophagy.Methods A total of 24 male SD rats were randomly divided into sham operation group,model group,blank transfec-tion group and high expression group,with 6 rats in each group.The blank transfection group and the high-expression group were pretreated with a single injection of adeno-associated virus(AAV)-blank transfection and AAV-miR-483-3p(5×1011 vg)in the tail vein,respectively.In 14 d later,the sham group was injected with 2.5 ml/(kg·d)normal saline for 14 d,and rat model of myocardial fibrosis was established by 2 mg/ml isoproterenol[2.5 ml/(kg·d)]injection through tail vein for 14 consecutive days.Myocardial pathological damage,severity of myocardial fibrosis,and expression levels of collagen-Ⅰ,microtubule-associated protein light chain 3(LC3),autoph-agy-related protein 5(Atg5)and autophagy degradation substrate(P62)in cardiomyocytes were evaluated and measured.Results Compared with the sham operation group,the model group had obviously larger myocardial fibrosis area,higher positive expression of Collagen-Ⅰ,and increased protein levels of Atg5 and LC3-Ⅱ/LC3-Ⅰ,and decreased expression level of P62 protein(P＜0.05).The myocardial fibrosis area,positive expression of Collagen-Ⅰ,the expression levels of Atg5 and LC3-Ⅱ/LC3-Ⅰ protein[(13.64±1.51)％vs(27.47±1.55)％,(13.48±3.07)％vs(30.91±2.45)％,0.98±0.17 vs 1.24±0.28,0.66±0.05 vs 1.26±0.09,P＜0.05]were significant-ly decreased,and the expression level of P62 was notably increased(0.91±0.11 vs 0.74±0.06,P＜0.05)in the high expression group than the model group.Conclusion MiR-483-3p attenuates myocardial fibrosis in rats,and the mechanism may be related to the inhibition of cardiomyocyte autophagy.

Objective To explore the therapeutic effect of bicyclol(BIC)on rat model of myocardial fibrosis and its possible mechanism.Methods Twenty-four SPF male SD rats were randomly di-vided into sham group,model group,low-and high-dose groups,with 6 rats in each group.Except for the sham group,all other groups were injected with 5 mg/(kg·d)isoproterenol by tail vein to establish myocardial fibrosis model,and the low-and high-dose groups were administered by ga-vage with 100 and 200 mg/(kg·d)BIC,respectively for 14 consecutive days.HE staining and Masson staining were used respectively to observe the severity of myocardial injury and fibrosis.Western blot assay was employed to detect the protein expression of Collagen Ⅰ,Collagen Ⅲ,al-pha smooth muscle actin(α-SMA),methyltransferase-like protein 3(METTL3),α-ketoglutarate-dependent dioxygenase AlkB homolog 5(ALKBH5)and YTH domain family protein 1(YTHDF1)in rat myocardium.Results Compared with the sham group,myocardial cell necrosis and myocardial fibrosis were significantly more serious in the model group.Low-and high-dose BIC treatment reduced myocardial cell rupture and necrosis and myocardial fibrosis when com-pared with the model group.The expression levels of Collagen Ⅰ,Collagen Ⅲ,α-SMA,METTL3 and YTHDF1(P＜0.05)were significantly higher,and that of ALKBH5(0.58±0.02 vs 0.88±0.07,P＜0.05)was notably lower in the myocardial tissues of the model group than the sham group.While,both doses of BIC treatment significantly reversed above changes in protein levels(P＜0.05).Conclusion BIC can effectively alleviate myocardial structural damage and interstitial collagen deposition in rats with isoproterenol-induced myocardial fibrosis,and its mechanism may be related to m6A methylation modification.

Objective:To construct the postgraduate teaching case database of rotation in department of cardiology, and to explore its application effect.Methods:The postgraduate teaching case base of rotation in department of cardiology was constructed during April 2020 to December 2020. A total of 32 graduate students rotating in Department of Cardiology of Affiliated Hospital of Guilin Medical University from January 2021 to April 2021 were selected and randomly divided into two groups. The routine group adopted the traditional teaching method, and the research group applied the teaching case base on this basis, both for one month. The examination results, the changes of clinical practice ability before and after the teaching, and the satisfaction with the teaching mode were compared between the two groups. SPSS 22.0 was used for t test and chi-square test. Results:The final results of the theoretical examination and practical operation examination of the two groups were higher than those of the entrance examination ( P<0.05), and the results of the theoretical examination and practical operation examination of the research group were higher than those of the routine group ( P<0.05). The scores of clinical practice ability of inquiry, case analysis, diagnosis, treatment and follow-up in the two groups after teaching were higher than those before teaching ( P<0.05), and the scores of clinical practice ability in the research group after teaching were higher than those in the routine group ( P<0.05). The satisfaction scores on improving examination results, enhancing clinical practice ability, deepening professional understanding and enhancing professional confidence of the teaching mode of the research group were higher than those of the routine group ( P<0.05). Conclusion:The construction and application of postgraduate teaching case base of cardiology rotation can improve the examination results, enhance the clinical practice ability, and achieve the satisfaction of postgraduates.