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1.
World J Gastrointest Surg ; 16(1): 59-66, 2024 Jan 27.
Article in English | MEDLINE | ID: mdl-38328327

ABSTRACT

BACKGROUND: Severe acute pancreatitis (SAP), a condition with rapid onset, critical condition and unsatisfactory prognosis, poses a certain threat to human health, warranting optimization of relevant treatment plans to improve treatment efficacy. AIM: To evaluate the efficacy and safety of computerized tomography-guided therapeutic percutaneous puncture catheter drainage (CT-TPPCD) combined with somatostatin (SS) in the treatment of SAP. METHODS: Forty-two SAP patients admitted to The Second Affiliated Hospital of Fujian Medical University from June 2020 to June 2023 were selected. On the basis of routine treatment, 20 patients received SS therapy (control group) and 22 patients were given CT-TPPCD plus SS intervention (research group). The efficacy, safety (pancreatic fistula, intra-abdominal hemorrhage, sepsis, and organ dysfunction syndrome), abdominal bloating and pain relief time, bowel recovery time, hospital stay, inflammatory indicators (C-reactive protein, interleukin-6, and procalcitonin), and Acute Physiology and Chronic Health Evaluation (APACHE) II score of both groups were evaluated for comparison. RESULTS: Compared with the control group, the research group had a markedly higher total effective rate, faster abdominal bloating and pain relief and bowel recovery, shorter hospital length of stay, fewer complications, and lower posttreatment inflammatory indices and APACHE-II scores. CONCLUSION: CT-TPPCD in combination with SS is effective for SAP patients, which can reduce complications, accelerate symptom resolution, inhibit inflammation, and improve patient condition, with promising prospects for clinical promotion.

3.
Cell Physiol Biochem ; 47(4): 1533-1545, 2018.
Article in English | MEDLINE | ID: mdl-29940566

ABSTRACT

BACKGROUND/AIMS: Gastric cancer (GC) is the most common gastrointestinal malignancy, causing cancer-related deaths in East Asia. MicroRNAs (miRNAs) are small non-coding RNAs aberrantly expressed in human tumors. In this study, we aim to investigate the roles of miR-204 in the epithelial to mesenchymal transition (EMT)-associated chemosensitivity. METHODS: The expression of miR-204 was detected in clinical tumor samples and GC cell lines by real time PCR. Tumor cell's growth, invasion, and migration were measured by MTT assay, wound healing assay, and transwell invasion assay, respectively. Western blot method was used to detect the protein levels of indicated genes. Luciferase reporter assay was performed to validate the target gene of miR-204. The in vivo role of miR-204 was measured using a xenograft mouse model of GC. RESULTS: By comparing the expressions of miR-204 in human gastric tumors and their adjacent normal tissues, it was disclosed that miR-204 was significantly downregulated in gastric tumors. Moreover, miR-204 was downregulated in multiple GC cell lines compared with normal gastric epithelial cells. Overexpression of miR-204 suppressed GC cells' proliferation, invasion, and migration. It is noteworthy that 5-FU treatments induced miR-204 expression and suppressed TGF-ß pathway. By establishment of 5-FU resistant GC cell line, it was revealed that miR-204 was significantly downregulated in 5-FU resistant GC cells, representing mesenchymal features with downregulation of epithelial marker, while mesenchymal markers were upregulated. We identified TGFBR2 as a direct target of miR-204 by Western blot method and luciferase assay in GC cells and tumor samples as well. In addition, overexpression of miR-204 sensitized GC cells to 5-FU in vitro. Xenograft experiments demonstrated that the combination of miR-204 and 5-FU efficiently inhibited tumor growth and improved survival rate of mice as well. Eventually, we illustrated the restoration of TGFBR2 in miR-204 overexpression GC cells, which recovered resistance to 5-FU treatments compared with miR-204 overexpression GC cells. CONCLUSION: This study describes a miRNA-based therapeutic strategy against 5-FU resistance in GC, contributing to the development of anti-chemoresistance therapeutic agents.


Subject(s)
Drug Resistance, Neoplasm , Epithelial-Mesenchymal Transition , Fluorouracil/pharmacology , MicroRNAs , Neoplasm Proteins , Protein Serine-Threonine Kinases , RNA, Neoplasm , Receptors, Transforming Growth Factor beta , Stomach Neoplasms , Animals , Cell Line, Tumor , Drug Resistance, Neoplasm/drug effects , Drug Resistance, Neoplasm/genetics , Epithelial-Mesenchymal Transition/drug effects , Epithelial-Mesenchymal Transition/genetics , Humans , Mice , MicroRNAs/genetics , MicroRNAs/metabolism , Neoplasm Proteins/genetics , Neoplasm Proteins/metabolism , Protein Serine-Threonine Kinases/genetics , Protein Serine-Threonine Kinases/metabolism , RNA, Neoplasm/genetics , RNA, Neoplasm/metabolism , Receptor, Transforming Growth Factor-beta Type II , Receptors, Transforming Growth Factor beta/genetics , Receptors, Transforming Growth Factor beta/metabolism , Stomach Neoplasms/genetics , Stomach Neoplasms/metabolism , Stomach Neoplasms/pathology , Stomach Neoplasms/therapy , Xenograft Model Antitumor Assays
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