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1.
World J Clin Cases ; 11(24): 5692-5699, 2023 Aug 26.
Article in English | MEDLINE | ID: mdl-37727708

ABSTRACT

BACKGROUND: Biliary adenomas that occur in the extrahepatic biliary tree are rare. It is difficult to distinguish it from cholangiocarcinoma or cholangiolithiasis by various imaging examinations, and it is very easy to be misdiagnosed. AIM: To evaluate the cumulative experiences including clinical characteristics and treatments of nine patients diagnosed with extrahepatic biliary adenoma admitted to the First Affiliated Hospital of Xi'an Jiaotong University from 2016 to 2022. METHODS: A total of nine patients were included in our study. The laboratory examinations, disease diagnosis, therapy and pathological characteristics, and follow-up of every patient were evaluated. RESULTS: Our cohort consisted of six females and three males with an average diagnosis age of 65.1 years (range 46-87). Six extrahepatic biliary adenomas were located in the common bile ducts and three in the hepatic duct. On initial presentation, all of the patients have symptom of biliary origin, including obstructive jaundice (4/9, 44.4%), abdominal pain (6/9, 66.7%), and fever (3/9, 33.3%). Preoperative imaging examination considered bile duct carcinoma in 6 cases and bile duct calculi in 3 cases. All the patients received surgical treatment and were confirmed by pathology as biliary adenoma. The symptoms improved significantly in all 9 patients after surgery. Seven of nine patients recovered well at follow-up without tumor recurrence. One patient died 2 mo after the surgery due to heart failure. One patient developed jaundice again 8 mo after surgery, underwent endoscopic retrograde cholangiopancreatography and biliary stent placement. CONCLUSION: Benign extrahepatic biliary tumors are rare and difficult to diagnosis preoperatively. Intraoperative choledochoscopy and timely biopsy may offer great advantages.

2.
World J Clin Cases ; 7(22): 3728-3733, 2019 Nov 26.
Article in English | MEDLINE | ID: mdl-31799297

ABSTRACT

BACKGROUND: Acute gastrointestinal bleeding is an emergency condition that can lead to significant morbidity and mortality. Embolization is considered the preferred therapy in the treatment of lower gastrointestinal bleeding when it is unrealistic to perform the surgery or vasopressin infusion in this population. Treatment of acute lower gastrointestinal (GI) bleeding (any site below the ligament of Treitz) using this technique has not reached a consensus, because of the belief that the risk of intestinal infarction in this condition is extremely high. The purpose of the study is to evaluate the effectiveness and safety of this technique in a retrospective group of patients who underwent embolization for acute lower GI bleeding. AIM: To evaluate the efficacy and safety of super-selective arterial embolization in the management of acute lower GI bleeding. METHODS: A series of 31 consecutive patients with angiographically demonstrated small intestinal or colonic bleeding was retrospectively reviewed. The success rate and complication rate of super-selective embolization were recorded. RESULTS: Five out of thirty-one patients (16.1%) could not achieve sufficiently selective catheterization to permit embolization. Initial control of bleeding was achieved in 26 patients (100%), and relapsed GI bleeding occurred in 1 of them at 1 wk after the operation. No clinically apparent bowel infarctions were observed in patients undergoing embolization. CONCLUSION: Super-selective embolization is a safe therapeutic method for acute lower GI bleeding, and it is suitable and effective for many patients suffering this disease. Importantly, careful technique and suitable embolic agent are essential to the successful operation.

3.
Eur J Pharmacol ; 863: 172696, 2019 Nov 15.
Article in English | MEDLINE | ID: mdl-31562866

ABSTRACT

Placental growth factor (PlGF) related signaling pathway has been shown to have close relationship with the progression of cancers. Metformin has been reported to have an inhibitory effect on PlGF expression in a breast cancer model. However, little is known about whether the anti-neoplastic activity of metformin is contributed by its inhibitory effect on PlGF expression. Protein, mRNA and secretion levels of PlGF were tested and the proliferation of cancer cells was determined. After treatment of metformin, BALB/c mice bearing 4T1 tumors were sacrificed and immunohistochemistry staining of the tumor sections was obtained. Baseline expression of autocrine PlGF varied between different breast cancer cell lines, while the expression of vascular endothelial growth factor receptor-1 (VEGFR-1) was comparable between cell lines. Other clinical data showed that the expression of PlGF other than VEGFR-1 had a prognostic value for patients with breast cancers. Metformin significantly decreased the secretion and mRNA levels of PlGF, which greatly contributed to its inhibitory effect on the proliferation of breast cancer cells with high P1GF expression. The unresponsiveness of tumor cells with low PlGF expression to genetic silencing was reversed by the supplementation of exogenous PlGF. Systemic metformin administration apparently inhibited the in vivo growth of 4T1 carcinoma, which was accompanied by the repolarization of macrophages from M2 to M1. These findings indicated that both autocrine and paracrine PlGF signaling and macrophage repolarization are involved in the progression of breast cancer, which could be targeted by metformin.


Subject(s)
Antineoplastic Agents/pharmacology , Macrophages/cytology , Macrophages/drug effects , Membrane Proteins/metabolism , Metformin/pharmacology , Signal Transduction/drug effects , Autocrine Communication/drug effects , Breast Neoplasms/diagnosis , Breast Neoplasms/pathology , Cell Line, Tumor , Cell Proliferation/drug effects , Gene Expression Regulation, Neoplastic/drug effects , Humans , Membrane Proteins/genetics , Prognosis , RNA, Messenger/genetics , Vascular Endothelial Growth Factor Receptor-1/metabolism , Vascular Endothelial Growth Factor Receptor-2/metabolism , Xenograft Model Antitumor Assays
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