OBJECTIVE To compare the antihypertensive efficacy of sacubitril/valsartan versus benazepril in patients with perimenopausal hypertension， as well as their impacts on ventricular remodeling and inflammatory fibrosis. METHODS A total of 206 perimenopausal hypertensive patients in our hospital from January 1， 2023 to December 30， 2024 were retrospectively included.These patients were enrolled and divided into benazepril group （105 cases） and sacubitril/valsartan group （101 cases）. Benazepril group received Benazepril hydrochloride tablet， and sacubitril/valsartan group received Sacubitril valsartan sodium tablet. All patients were treated for 6 months. The blood pressure（systolic blood pressure and diastolic blood pressure） and blood pressure control status before and after treatment， echocardiographic indicators （left ventricular ejection fraction， left ventricular mass index， relative wall thickness， and early-diastolic peak transmitral flow velocity/early-diastolic peak velocity of the mitral annulus）， inflammatory fibrosis related indicators（high-sensitivity C-reactive protein，ratio of monocytes to lymphocytes，and ratio of neutrophils to lymphocytes）， as well as the occurrence of adverse reactions（hypotension，hyperkalemia，and angioedema） were observed in both groups before and after treatment. RESULTS The blood pressure control rate was significantly higher in the sacubitril/valsartan group than in benazepril group （ P ＜0.05）. After treatment， the blood pressure， echocardiographic indicators（except for left ventricular ejection fraction） ，and inflammatory fibrosis related indicators were significantly lower than those before treatment within the same group， and the sacubitril/valsartan group were significantly lower than the benazepril group （ P ＜0.05）. There were no statistically significant differences in the incidence of hypotension， hyperkalemia， angioedema， and overall adverse drug reactions between the two groups （ P ＞0.05）. CONCLUSIONS Compared with benazepril， sacubitril/valsartan provides superior blood-pressure control， reverses ventricular remodeling， attenuates inflammatory fibrosis in perimenopausal hypertensive patients， while maintaining a similar safety profile.

[Objective] To explore the optimal pressure parameters for chyle plasma filtration under low-temperature conditions, and to improve the quality of chyle plasma treatment and filtration efficiency by improving experimental methods. [Methods] The filtration efficiency and filtration time of 30 severe chyle plasma samples under conventional preparation environment pressure and under preparation environment with a controlled filtration membrane pressure difference of 0.5 bar were compared. [Results] The absorbance of severe chyle plasma samples before and after filtration under two different preparation pressures was statistically significant (P<0.05), and both achieved the expected filtration effect. Under the preparation environment of controlling the pressure difference of the filtration membrane to 0.5 bar, the filtration was faster and with better effect, which was statistically significant compared to the conventional preparation environment pressure (P<0.05). [Conclusion] By selecting the optimal pressure parameters for filtering chyle plasma under low-temperature conditions, the efficiency of chyle plasma filtration under low-temperature conditions has been improved, and the practicality and reliability of low-temperature filtration technology have been enhanced.

BACKGROUND:Multiple studies have confirmed that mitogen-activated protein kinase(MAPK)signaling pathway is involved in cell proliferation,and microRNA(miR)is involved in the occurrence and development of hypertrophic scars.Therefore,the role of miR-27a-3p and MAPK signaling pathways in pathological scar formation has been further explored. OBJECTIVE:To explore the effect of miR-27a-3p on the proliferation of human hypertrophic scar fibroblasts through the MAPK signaling pathway. METHODS:The primary fibroblasts were isolated and collected from the skin samples.The primary fibroblasts were observed by inverted microscope and verified by immunofluorescence.The relative expression level of miR-27a-3p in tissues was detected by qRT-PCR.The target genes of hsa-miR-27a-3p were predicted using the database,and then the predicted target genes were enriched by gene ontology function analysis and biological pathway enrichment analysis of the Kyoto Encyclopedia of Genes and Genomes.There were seven groups:blank control,negative control,miR-27a-3p mimic,miR-27a-3p inhibitor,miR-27a-3p mimic+p38 MAPK inhibitor,miR-27a-3p mimic+extracellular regulated protein kinase inhibitor,miR-27a-3p mimic+c-Jun N-terminal kinase inhibitor.Western blot was used to detect the levels of extracellular regulated protein kinase,c-Jun N-terminal kinase inhibitor.and p38 kinase and their phosphorylation levels.Cell counting kit-8 and EdU were used to detect cell proliferation. RESULTS AND CONCLUSION:Compared with normal skin fibroblasts,hypertrophic scar fibroblasts had stronger proliferative activity(P<0.05)and faster proliferation level(P<0.001).Compared with normal skin,miR-27a-3p was highly expressed in hypertrophic scars(P<0.001).Compared with the negative control group,overexpression of miR-27a-3p could promote cell proliferation activity(P<0.001)and proliferation levels(P<0.001).Compared with the negative control group,knockdown of miR-27a-3p could inhibit the proliferation activity(P<0.05)and proliferation levels(P<0.001).Compared with the negative control group,overexpression of miR-27a-3p promoted the phosphorylated levels of extracellular regulated protein kinase,c-Jun N-terminal kinase,and p38 mitogen-activated protein kinase(P<0.05).Compared with the negative control group,knockdown of miR-27a-3p inhibited the phosphorylated levels of extracellular regulated protein kinase,c-Jun N-terminal kinase,and p38 MAPK(P<0.05).Compared with the miR-27a-3p mimic group,specific inhibitors of extracellular regulated protein kinase,c-Jun N-terminal kinase,and p38 MAPK reversed the effects of miR-27a-3p on the proliferative activity(P<0.01)and proliferation level(P<0.001)of fibroblasts.To conclude,these results suggest that miR-27a-3p promotes the proliferation of human hypertrophic scar fibroblasts by activating the MAPK signaling pathway.

To investigate the in vitro inhibitory mechanism of Nymphaea candida total flavonoids(NCTF)against Staphylococcus aureus(S.aureus)and its safety in mice,this study first deter-mined the antibacterial effect of NCTF on the clinically isolated strain S.aureus-C1.Subsequently,the inhibitory mechanism of NCTF on S.aureus-C1 was explored by measuring its effects on bac-terial growth curves,microstructure,intracellular AKP and LDH levels,and biofilm formation.Safety evaluation included determination of LD50 and MDT in mice,as well as analysis of serum biochemical parameters,organ indices,and histopathological observations.Results showed that NCTF effectively inhibited S.aureus-C1 proliferation,with an inhibition zone diameter of(18.98±0.67)mm and a MIC of 6.25 g/L.A concentration of 2×MIC nearly completely suppressed bacte-rial growth.Scanning electron microscopy revealed structural damage to bacterial cells,including collapse and shrinkage.AKP and LDH assays indicated significantly increased AKP activity(P＜0.05)and decreased intracellular LDH activity(P＜0.05)in the supernatant of drug-treated groups,demonstrating NCTF-induced disruption of cell walls and membranes leading to leakage of AKP and LDH.Crystal violet staining of biofilms showed significant inhibition rates of(43.77±9.16)％and(61.71±9.82)％at 2 × MIC and 4 × MIC concentrations,respectively(P＜0.05).Safe-ty assessments indicated low toxicity of NCTF in mice,with transient effects that returned to nor-mal levels within a short period.These findings demonstrate that NCTF exhibits potent antibacte-rial activity against S.aureus-C1 by damaging bacterial cell structures,increasing cell wall/mem-brane permeability,reducing biofilm formation,and displaying low toxicity.This study provides scientific evidence for clinical drug screening against bovine mastitis and the development of Nym-phaea candida resources.

To investigate the in vitro inhibitory mechanism of Nymphaea candida total flavonoids(NCTF)against Staphylococcus aureus(S.aureus)and its safety in mice,this study first deter-mined the antibacterial effect of NCTF on the clinically isolated strain S.aureus-C1.Subsequently,the inhibitory mechanism of NCTF on S.aureus-C1 was explored by measuring its effects on bac-terial growth curves,microstructure,intracellular AKP and LDH levels,and biofilm formation.Safety evaluation included determination of LD50 and MDT in mice,as well as analysis of serum biochemical parameters,organ indices,and histopathological observations.Results showed that NCTF effectively inhibited S.aureus-C1 proliferation,with an inhibition zone diameter of(18.98±0.67)mm and a MIC of 6.25 g/L.A concentration of 2×MIC nearly completely suppressed bacte-rial growth.Scanning electron microscopy revealed structural damage to bacterial cells,including collapse and shrinkage.AKP and LDH assays indicated significantly increased AKP activity(P＜0.05)and decreased intracellular LDH activity(P＜0.05)in the supernatant of drug-treated groups,demonstrating NCTF-induced disruption of cell walls and membranes leading to leakage of AKP and LDH.Crystal violet staining of biofilms showed significant inhibition rates of(43.77±9.16)％and(61.71±9.82)％at 2 × MIC and 4 × MIC concentrations,respectively(P＜0.05).Safe-ty assessments indicated low toxicity of NCTF in mice,with transient effects that returned to nor-mal levels within a short period.These findings demonstrate that NCTF exhibits potent antibacte-rial activity against S.aureus-C1 by damaging bacterial cell structures,increasing cell wall/mem-brane permeability,reducing biofilm formation,and displaying low toxicity.This study provides scientific evidence for clinical drug screening against bovine mastitis and the development of Nym-phaea candida resources.

OBJECTIVE To explore the therapeutic effect and safety of tolvaptan in the treatment of heart failure with preserved ejection fraction （HFpEF） complicated with hyponatremia. METHODS Overall 106 patients with HFpEF complicated with hyponatremia were collected from the Department of Cardiology in the First Affiliated Hospital of Nanyang Medical College from January 1， 2020 to June 1， 2023. According to the random number table， the patients were divided into conventional treatment group （n＝53） and tolvaptan group （n＝53）. The conventional treatment group was given conventional treatment. Tolvaptan group additionally received Tolvaptan tablets 15 mg on the basis of conventional treatment group， increasing to 30 mg after 24 h， and then adjusting the dosage according to the levels of serum sodium； the maximum dose should not exceed 60 mg/d， and the medication should be stopped when the serum sodium level was≥150 mmol/L. Both groups of patients were treated for 6 months. The levels and changes of cardiac function indexes [left ventricular ejection fraction （LVEF）， left ventricular end systolic diameter （LVESD）， left ventricular end diastolic diameter （LVEDD）， N-terminal pro-brain natriuretic peptide （NT-proBNP）]， 24 h urine output， serum sodium， blood creatinine and urea nitrogen were compared between 2 groups before and after treatment. The occurrence of adverse drug reaction （ADR） was recorded. RESULTS Before treatment， there was no statistically significant difference in those indexes between 2 groups （P＞0.05）. After treatment， the levels of LVEF， 24 h urine output and serum sodium in 2 groups were significantly higher than before treatment， and the tolvaptan group was significantly higher than the conventional treatment group； the levels of LVESD， LVEDD and NT-proBNP were significantly lower than before treatment， and the tolvaptan group was significantly lower than the conventional treatment group （P＜0.05 or P＜0.01）. The changes in cardiac function indexes， 24 h urine output and serum sodium levels in the atorvastatin group were more significant than the conventional treatment group （P＜0.05）. There was no statistically significant difference in the levels and changes of blood creatinine and urea nitrogen before and after treatment， as well as the incidence of nausea and vomiting， dizziness， hypernatremia and frequent urination between 2 groups （P＞0.05）. CONCLUSIONS Tolvaptan can improve cardiac function and increase the blood sodium levels in patients with HFpEF complicated with hyponatremia， without affecting their renal function or increasing the risk of ADR.

Objective:To investigate the risk factors of refracture of the injured vertebrae after percutaneous vertebral augmentation for acute symptomatic thoracolumbar osteoporotic compression fractures (ASTOCFs).Methods:A case-control study was conducted to analyze the clinical data of 2 237 ASTOCFs patients admitted to three hospitals from January 2010 to January 2019. There were 569 males and 1 668 females, with age range of 50-85 years [(66.7±4.8)years]. The patients underwent percutaneous vertebroplasty (PVP) or percutaneous kyphoplasty (PKP). According to the radiographic outcomes, the patients were divided into refracture group ( n=315) and non-refracture group ( n=1 922). Data were recorded for the two groups, including basic demographics (gender, age, height and weight), personal habits (smoking and alcohol consumption), basic diseases (diabetes, hypertension, coronary heart disease and chronic obstructive pulmonary disease), preoperative bone mineral density, fracture segment, number of injured vertebrae, surgical method (PVP or PKP), surgical approach, bone cement viscosity, distance from cement to the upper and lower endplate, cement volume in injured vertebrae, cement leakage, postoperative exercise, and postoperative anti-osteoporosis treatment. The above data were analyzed to identify their correlation with postoperative refracture of the injured vertebrae by univariate analysis. The independent risk factors for postoperative refracture of the injured vertebrae were determined by multivariate Logistic regression analysis. Results:Univariate analysis showed that refracture of injured vertebrae was correlated with gender, age, diabetes, fracture segment, surgical method, distance from cement to the upper and lower endplate, postoperative exercise, and postoperative anti-osteoporosis treatment ( P<0.05 or 0.01), but there was no correlation with height, weight, smoking, alcohol consumption, hypertension, coronary heart disease, chronic obstructive pulmonary disease, preoperative bone mineral density, number of fractured vertebrae, surgical approach, bone cement viscosity, cement volume in injured vertebrae or cement leakage (all P>0.05). Multivariate Logistic regression analysis showed that female ( OR=1.92, 95% CI 1.34-2.64, P<0.01), age ≥80 years ( OR=1.21, 95%CI 1.17-1.25, P<0.01), diabetes ( OR=1.92, 95% CI 0.44-2.55, P<0.01), thoracolumbar fracture ( OR=1.46, 95% CI 1.82-7.51, P<0.05), PKP ( OR=4.56, 95% CI 0.86-1.44, P<0.05), no postoperative exercise ( OR=2.14,95% CI 0.27-0.38, P<0.01), and no postoperative anti-osteoporosis treatment ( OR=2.36,95% CI 0.13-0.47, P<0.05) were positively correlated with refracture of injured vertebrae. Conclusion:Female, age ≥80 years, diabetes, thoracolumbar fracture, PKP, no postoperative exercise, and no postoperative anti-osteoporosis treatment are independent risk factors for refracture of injured vertebrae after percutaneous vertebral augmentation for ASTOCFs.

OBJECTIVETo investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro.

METHODSCultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80 µmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1% DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment.

RESULTSEmodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time- and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05).

CONCLUSIONEmodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.

Carcinoma, Squamous Cell ; pathology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; drug effects ; Cyclin E ; metabolism ; Cyclin-Dependent Kinase 2 ; metabolism ; Cyclin-Dependent Kinase Inhibitor p21 ; metabolism ; Emodin ; pharmacology ; Humans ; Mouth Neoplasms ; pathology ; Oncogene Proteins ; metabolism ; Signal Transduction

Objective To investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro. Methods Cultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80μmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1%DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment. Results Emodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time-and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05). Conclusion Emodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.

Objective To investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro. Methods Cultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80μmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1%DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment. Results Emodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time-and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05). Conclusion Emodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.