Objective This study was to investigate the ameliorative effects of mangiferin on prostatic fibrosis in benign prostatic hyperplasia(BPH)and the mechanism of action of regulating microRNA(miRNA)-483-3p.Methods The male mice were randomly divided into five groups:normal control group,BPH model control group,finasteride group,mangiferin group,and mangiferin+miRNA-483-3p antagonist group.The mice model of BPH was induced by castration and subcutaneous injection of tes-tosterone propionate.After 30 days,the prostatic collagen deposition was observed by masson and sirius red stain,and the level of hydroxyproline was detected.Prostatic mRNA levels of transforming grouth factor-β1(TGF-β1),mitogen-activated protein kinase 2(MK2),and mitogen-activated protein kinase kinase 6(MKK6),as well as the level of miRNA-483-3p,were detected by quantita-tive real-time PCR.Prostatic protein levels of TGF-β1,MK2,phosphorylated MK2(p-MK2),MKK6,and p-MKK6 were detected by western blotting.Finally,the binding effect of miRNA-483-3p on MK2 was evaluated by luciferase assay.Results Compared to normal control group,the prostatic collagen deposition,mRNA levels of TGF-β1,MK2,and MKK6,as well as protein levels of TGF-β1,p-MK2,and p-MKK6 were significantly increased(P＜0.01),while the miRNA-483-3p level was significantly decreased in BPH model control group(P＜0.01).Compared with BPH model control group,the mangiferin group was able to up-regulate the level of miRNA-483-3p,reduce the mRNA levels of TGF-β1,MK2,and MKK6,as well as the protein levels of TGF-β1,p-MK2,and p-MKK6,and alleviate prostatic collagen deposition.When compared to the mangiferin group,mangiferin+miRNA-483-3p antagomir significantly decreased the miRNA-483-3p level,increased the prostatic collagen deposition,mRNA levels of TGF-β1,MK2,and MKK6,as well as protein levels of TGF-β1,p-MK2,and p-MKK6(P＜0.01).Luciferase assay showed that miRNA-483-3p could tar-get binding with MK2.Conclusion Mangiferin can attenuate prostatic fibrosis by regulating miRNA-483-3p and inhibiting MK2.

Objective:To investigate the prognosis and risk factors for children diagnosed with all types of subaortic stenosis(SAS) who developed recurrent left ventricular outflow tract obstruction after surgical treatment.Methods:The study retrospectively included patients aged 0-18 years old who underwent open heart SAS surgery at Fuwai Hospital from 2016-2019. Children with hypertrophic obstructive cardiomyopathy were excluded. Detailed operative notes, medical records and ultrasound information, and follow-ups were extracted. Recurrent SAS was defined as left ventricular outflow tract gradient 30 mmHg(1 mmHg=0.133 kPa) 1 month after SAS surgical treatment.Results:A total of 137 children were included in this study. The medium age of children at the time of SAS surgery was 4.6 years old(3 months-17.8 years old). After a median follow-up of 4.36 years(3.2-5.7 years), a total of 30 patients developed recurrent LVOTO, with a recurrence rate of 21.9%, and 7(5.1%) underwent a second surgery. Compared to the non-recurrent group, children in the recurrent group were younger at the time of surgery( P=0.0443), had a smaller body surface area( P=0.0485), and a longer length of stay( P=0.0380). In Cox analysis, when only considering preoperative variables, the independent risk factor for LVOTO recurrence were a peak left ventricular outflow tract gradient higher than 50 mmHg( HR=5.25, P=0.001), a BSA less than 0.9( HR=2.5, P=0.023), and a length of SAS 5 mm( HR=2.29, P=0.050). When both preoperative and intraoperative variables were considered, preoperative peak left ventricular outflow tract gradient 50 mmHg( HR=4.91, P=0.002) and peeling from the aortic valve( HR=3.23, P=0.010) were independent risk factors for postoperative recurrence. Conclusion:Recurrent LVOTO after SAS surgical repair is common, and regular postoperative follow-up is crucial to evaluate whether a secondary intervention is required. Regular postoperative follow-up is needed for children at high risk.

ObjectiveTo investigate the objective characteristics of tongue manifestations in patients with coronary heart disease （CHD）. MethodsA total of 315 participants with CHD were recruited in the CHD group， and 211 healthy participants who underwent physical examination were recruited as the healthy control group. In addition， according to the common comorbidities （primary hypertension， carotid atherosclerosis， type 2 diabetes mellitus， fatty liver， hyperlipidaemia， heart failure， and cerebral infarction） in 315 participants with CHD， each comorbidity was classified into a group of comorbidities with that disease and a group of non-comorbidities. Tongue images were captured using a TFDA-1 tongue diagnostic instrument to characterise the tongue body （TB） and tongue coating （TC）， comparing the RGB， HIS， and Lab colour spaces in the chromaticity index （R， red； G， green； B， blue； H， hue； I， intensity； S， saturation； L， lightness； a， red-green axis； b， yellow-blue axis）， the tongue coating thickness index （per-All）， contrast （CON）， angular second moment （ASM）， entropy （ENT）， and mean （MEAN） in texture metrics. ResultsCompared with the healthy control group， the characteristic indexes of tongue body in CHD group showed lower TB-R， TB-G， TB-B， TB-I， TB-L and higher TB-H， TB-b； and the characteristic indexes of tongue coating in CHD group showed lower TC-R， TC-B and higher TC-CON， TC-MEAN， TC-H， TC-b （P＜0.05 or P＜0.01）. Compared with non-combined primary hypertension group， CHD combined primary hypertension group showed higher per-All， TB-G， TB-L， and lower TB-a， TC-a （P＜0.05）； compared with the non-combined carotid atherosclerosis group， CHD combined carotid atherosclerosis group showed higher TB-CON， TB-ENT， TB-MEAN， and lower TB-ASM （P＜0.05 or P＜0.01）； compared with the non-combined type 2 diabetes mellitus group， CHD combined type 2 diabetes mellitus group showed lower per-All and higher TB-H （P＜0.05 or P＜0.01）； compared with the non-combined fatty liver group， CHD combined fatty liver group showed higher TB-CON， TB-MEAN， TB-ENT， and lower TB-ASM and TC-S （P＜0.05 or P＜0.01）； compared with the non-combined hyperlipidaemia group， CHD combined hyperlipidaemia group showed lower TB-S and TB-a （P＜0.05）； compared with non-combined heart failure group， CHD combined heart failure group showed lower TB-R， TB-G， TB-I， TB-L， and higher TB-a （P＜0.05 or P＜0.01）； compared with non-combined cerebral infarction group， CHD combined cerebral infarction group showed higher TC-CON， TC-ENT， TC-MEAN， and lower TC-ASM （P＜0.05 or P＜0.01）. ConclusionCompared to healthy individuals， patients with CHD tend to have darker tongue colours and rougher TC textures. Compared with non-comorbidity participants， those with primary hypertension tended to be lighter tongue colour and thicker tongue coating， those with carotid atherosclerosis had paler tongue body， those with type 2 diabetes mellitus had thinner tongue coating， those with fatty liver disease had paler tongue body and whiter tongue colour， those with hyperlipidaemia and heart failure had paler tongue colour， and those with cerebral infarction had rougher tongue texture.