Publications by authors named "Ke-Yan Wu"

Article Synopsis
  • The study investigates the role of serum glycosylated hemoglobin A1c (HbA1c) levels in assessing the severity and outcomes of acute pancreatitis (AP), focusing on two groups: normal HbA1c levels (<6.5%) and high levels.
  • It was found that higher HbA1c levels correlate with increased disease severity, complications, and the risk of organ failure in AP patients, with the optimal cutoff for predicting organ failure at 7.05%.
  • The results suggest that better glycemic control may lead to improved outcomes in AP, emphasizing the importance of monitoring HbA1c levels prior to the onset of the condition.
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Apigenin is an edible flavonoid with anticancer properties; however, the underlying mechanisms in hepatocellular carcinoma (HCC) remain to be clarified. In the present study, we demonstrated that apigenin decreased the viability of both SMMC-7721 and SK-Hep1 cells in a dose-dependent manner, and inhibited the migration and invasion of HCC cells with different metastatic potential by regulating actin cytoskeletal rearrangements. Moreover, we showed that apigenin decreased the expression of YAP, and subsequently reduced migration and invasion by modulating the expression of the epithelial-mesenchymal transition (EMT) markers, and promoted the autophagy of HCC cells by regulating the expression of autophagy-related genes.

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Introduction: Acute pancreatitis (AP) is a common clinical pancreatic disease. Patients with different severity levels have different clinical outcomes. With the advantages of algorithms, machine learning (ML) has gradually emerged in the field of disease prediction, assisting doctors in decision-making.

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Emerin (EMD) plays diverse roles in cellular polarity organization, nuclear stability, and cell motility, however, the biological role of EMD relevant to the migration and invasion of hepatocellular carcinoma (HCC) cells has not yet been illustrated. In the present study, we initially found that the upregulation of EMD in HCC tissues, and EMD expression was negatively correlated with the spontaneous metastatic potential of HCC cell lines. Loss of EMD in HCC cells facilitated cell migration and invasion in vitro and metastasis in vivo.

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Long non-coding RNAs (lncRNAs) have been identified in cerebral ischemia-reperfusion (I/R) injury nowadays. Herein, we uncovered the function and underlying mechanism of the lncRNA Rian in cerebral I/R injury. The oxygen-glucose deprivation model in N2a cells was offered to mimic cerebral I/R injury in vitro.

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Article Synopsis
  • The study aimed to examine how common fatty pancreas is in Yangzhou, China, and what factors contribute to its development.
  • Out of 2,093 participants, 56 (2.7%) were found to have fatty pancreas after excluding incomplete data, leading to a total of 1,228 subjects analyzed.
  • Results indicated that older age, central obesity, and fatty liver disease are significant independent risk factors for developing fatty pancreas.
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Objective: To study the regulation of luteolin on spleen cells and sarcoma S180 cells in normal ICR mice.

Methods: Spleen cells and S180 cells were incubated with different concentrations of luteolin (50, 100, 200, and 400 μmol/L). The effect of luteolin on spleen cells and sarcoma S180 cells was determined by MTT assay.

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Background: The integrin α6 subunit is part of the integrin α6β1 and α6β4 complexes, which are known to mediate the invasion of carcinoma cells. However, the precise role of integrin α6 in intrahepatic cholangiocarcinoma (ICC) has not yet been addressed.

Methods: Twenty cases of ICCs and matched nontumor samples were used to analyze integrin α6 expression by immunohistochemistry.

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Aim: To prepare a monoclonal antibody against human vascular endothelial growth factor (VEGF165), for further study the VEGF165 in the tumorigenesis, tumor cell migration and the tumor cells escape from the immune response.

Methods: VEGF165 gene was cloned from the human umbilical vein endothelial cells (HUVEC) by RT-PCR, and then cloned into the pGEX-6P1, constructed the prokaryotic expression of pGEX-6P1-VEGF165. The fusion -protein of VEGF165 was expressed in E.

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