Objective: To investigate c-myc proto-oncogene expression and the relationship of PCNA protein expression of extrahepatic vascular smooth muscle cell in patients with portal hypertension and normal vessels.
Methods: RT-PCR was used to demonstrate the expression of c-myc mRNA and immuno-chemistry strain was performed to detect the expression of PCNA protein in splenic veins of 28 patients with portal hypertension and 12 normal vessels.
Results: The straining of PCNA protein was (29.8 +/- 4.7)% in splenic veins with portal hypertension, Normal vessels did not detect PCNA protein expression (P < 0.01); RT-PCR showed that the expression of c-myc mRNA in PCNA-positive control and in negative control of splenic veins with portal hypertension were (7.61 +/- 1.04)% and (3.82 +/- 0.92)%, respectively. There ws different between two groups (P < 0.01) and significant different (P < 0.01) when compared with (1.01 +/- 0.21)% in normal vessels.
Conclusions: The c-myc was immediate-early gene when it modulated proliferation of vascular smooth muscle cell. Hemodynamic disturbance of portal vein system activate the proto-oncogene of smooth muscle cells in splenic vein of patients with portal hypertension, promoting the proliferation, migrating and phenotypic change and resulting in vascular remodelling of splenic veins.
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Pflugers Arch
January 2025
Leibniz Institute for Prevention Research and Epidemiology - BIPS, Bremen, Germany.
The global increase of overweight and obesity in children and adults is one of the most prominent public health threats, often accompanied by insulin resistance, hypertension, and dyslipidemia. The simultaneous occurrence of these health problems is referred to as metabolic syndrome. Various criteria have been proposed to define this syndrome, but no general consensus on the specific markers and the respective cut-offs has been achieved yet.
View Article and Find Full Text PDFHPB (Oxford)
January 2025
Hepato-Biliary Center, AP-HP Paul Brousse Hospital, Paris-Saclay University, INSERM Unit 1193, 94800 Villejuif, France. Electronic address:
Background: Liver cirrhosis accounts for more than 90 % of portal hypertension cases, and the other cases are due to noncirrhotic portal hypertension (NCPH). Variceal bleeding is the most life-threatening complication of portal hypertension and its primary treatment is medical according to the Baveno VII guidelines. This review discusses the evidence on surgical portal decompression for adult patients with NCPH secondary to chronic extrahepatic portal vein obstruction (EHPVO).
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January 2025
Department of Radiology, University Medical Center Regensburg, 93053 Regensburg, Germany.
Background: Portal vein thrombosis (PVT) leads to portal hypertension (PH) with its sequelae. Computed tomography spleno-mesenterico-portography (CT-SMPG) combines sequential CT spleno-portography and CT mesenterico-portography. CT-SMPG comprehensively illustrates the venous hemodynamic changes due to PH.
View Article and Find Full Text PDFMedicina (Kaunas)
December 2024
Clinic for Gastroenterology and Hepatology, University Clinical Centre of Serbia, 11 000 Belgrade, Serbia.
Cirrhotic cardiomyopathy (CCM) is a diagnostic entity defined as cardiac dysfunction (diastolic and/or systolic) in patients with liver cirrhosis, in the absence of overt cardiac disorder. Pathogenically, CCM stems from a combination of systemic and local hepatic factors that, through hemodynamic and neurohormonal changes, affect the balance of cardiac function and lead to its remodeling. Vascular changes in cirrhosis, mostly driven by portal hypertension, splanchnic vasodilatation, and increased cardiac output alongside maladaptively upregulated feedback systems, lead to fluid accumulation, venostasis, and cardiac dysfunction.
View Article and Find Full Text PDFAnn Med
December 2025
Department of Internal Medicine, Hallym Medical Center, Hallym University College of Medicine, Chuncheon, Republic of Korea.
Background/aims: Acute decompensation (AD) is defined as the development of complications related to portal hypertension and liver dysfunction that affect the progression of chronic liver disease (CLD) or liver cirrhosis (LC). Variations exist in patient demographics and prognostic outcomes of AD based on the aetiology of CLD, encompassing LC. However, limited research has been conducted to analyse these discrepancies across aetiologies.
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