Primary hyperaldosteronism(PHA),the most common cause of secondary hypertension,can lead to cardiovascular and renal damage events.Early diagnosis and accurate typing of PHA is crucial to the choice of treatment options,and its diagnostic modalities usually include prone test screening,captopril test characterization and adrenal vein blood sampling for localization and typing diagnosis.However,with the development of imaging,molecular biology and morphology technologies,the use of nuclear medicine PET-CT,genetic testing and pathological diagnostic methods can also be used to accurately typify PHA.New technologies such as adrenal artery embolization and adrenal radiofrequency ablation are also increasingly being used in the treatment of PHA,which have the advantages of shorter and less costly surgery,fewer postoperative complications,and quicker recovery.This article provides a review of the developments in the screening,diagnosis and treatment of PHA with a view to informing clinical practice.

Primary hyperaldosteronism(PHA),the most common cause of secondary hypertension,can lead to cardiovascular and renal damage events.Early diagnosis and accurate typing of PHA is crucial to the choice of treatment options,and its diagnostic modalities usually include prone test screening,captopril test characterization and adrenal vein blood sampling for localization and typing diagnosis.However,with the development of imaging,molecular biology and morphology technologies,the use of nuclear medicine PET-CT,genetic testing and pathological diagnostic methods can also be used to accurately typify PHA.New technologies such as adrenal artery embolization and adrenal radiofrequency ablation are also increasingly being used in the treatment of PHA,which have the advantages of shorter and less costly surgery,fewer postoperative complications,and quicker recovery.This article provides a review of the developments in the screening,diagnosis and treatment of PHA with a view to informing clinical practice.

Objective:To investigate the clinical and pathological features of congenital hepatic fibrosis (CHF).Methods:The clinical and pathological findings of 20 patients diagnosed with CHF from 2017 to 2023 were retrospectively analyzed.Results:Among the 20 patients, 8 were males and 12 were females with a median age of 21.5 years. Mostly patients were admitted to the hospital with cirrhosis, portal hypertension and upper gastrointestinal bleeding. Pathological features were diffuse fibrosis in the portal area, formation of fibrous septa of varying width, segmentation of the liver parenchyma, with hyperplasia of small bile ducts. Among them, 1 case (5%) was complicated with Caroli's disease, and 1 case (5%) was HNF1α hepatocellular adenoma. IHC GS showed that was positively expressed in acinar region 3 in 75% cases.Conclusion:CHF is mainly manifested by portal hypertension and its complications. Histopathology is the gold standard for diagnosis. The possibility of CHF should be considered first in children and adolescents with portal hypertension but no history of hepatitis, and complicated kidney disease. The positive pattern of acinus-3 region of GS in IHC is helpful for the diagnosis of CHF.

Signal transducer and activator of transcription 3 (STAT3) and Chemokine CX3C ligand 1 (Fractalkine/CX3CL1) play important roles in vascular inflammation and injury. To study if STAT3 promotes vascular endothelial cell proliferation and migration through fractalkine, we overexpressed or knocked down STAT3 in vascular endothelial cells, and used quantitative real-time PCR and Western blotting to determine the effect of STAT3 on fractalkine expression. The wild type and STAT3 binding site mutant fractalkine promoter luciferase reporter plasmids were constructed, and luciferase activity assays were used to explore the effect of STAT3 on the transcriptional activity of the fractalkine promoter. MTT assays were used to detect the effect of overexpression or knockdown of STAT3 or fractalkine on the proliferation rate of vascular endothelial cells. Scratch assays were used to detect the effect of overexpression or knockdown of STAT3 or fractalkine on vascular endothelial cell migration. There results showed that overexpression of STAT3 could promote fractalkine expression, and knockdown of STAT3 could down-regulate fractalkine expression. STAT3 could directly bind to the promoter of fractalkine to promote its transcriptional activity via binding the GAS site of the fractalkine promoter. Knockdown of STAT3 could inhibit the migration of vascular endothelial cell, and overexpression of fractalkine antagonized this inhibition. Our data concluded that STAT3 promotes the proliferation and migration of vascular endothelial cell by binding the GAS site of the fractalkine promoter to promote fractalkine transcriptional activity and expression.
Cell Proliferation ; Chemokine CX3CL1 ; Endothelial Cells ; Promoter Regions, Genetic ; STAT3 Transcription Factor