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Objective:To evaluate the diagnosis and treatment of abdominal cocoon.Methods:The clinical data of 8 patients with abdominal cocoon in our hospital from Jan 2015 to Dec 2021 were retrospectively reviewed including clinical and imaging manifestations, treatment and follow-up.Results:One case was asymptomatic, and the other 7 cases suffered from recurrent abdominal pain with complete or incomplete intestinal obstruction. The median course of disease was 6 months (15 days to 40 years). Six cases underwent laparcoscopic cocoon membrane resection and intestinal adhesion lysis, of which 2 cases underwent laparotomy, one case was converted to open surgery, 4 cases underwent concomitant appendectomy. Follow-up ranged from 3 to 69 months, there were 2 cases complicating early inflammatory intestinal obstruction, 1 case suffred wound fat liquefaction and infection, 1 case with a colic 5 months after operation, and the others were doing well.Conclusions:The clinical characteristics of abdominal cocoon disease are not typical. Surgery is the main treatment. The prognosis of the disease is generally fair.
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<p><b>OBJECTIVE</b>To investigate whether SIS3, a specific inhibitor of Smad3 phosphorylation, can reverse the stemness of multidrug-resistant(MDR) hepatocellular carcinoma cells.</p><p><b>METHODS</b>MDR HCC Huh7.5.1/ADM cell lines were developed by exposing parental cells to stepwise increasing concentrations of ADM. CCK-8 assay was used to determine the cellular sensitivity of various anticancer drugs. Flow cytometry (FCM) was used to analyze the expression level of cancer stem cell marker CD133. Clone formation assay and mouse subcutaneous xenograft tumors were used to investigate the tumorigenicity in vitro and in vivo. Western blotting (WB) was used to analyze the changes of expressions of CD133, Smad3, Bcl-2, Bax and p-Smad3 in different conditions.</p><p><b>RESULTS</b>ADM treatment of HCC cells in vitro resulted in a development of subline, Huh7.5.1/ADM cells, with CSC phenotypes: stable MDR phenotype (besides ADMc Huh7.5.1/ADM cells were also more resistant to some other anticancer drugs including VCR, MMC and CTX ) (IC50: 0.215 ± 0.018 vs. 0.123 ± 0.004, 0.145 ± 0.009 vs. 0.014 ± 0.002, 1.021 ± 0.119 vs. 0.071 ± 0.006, 27.007 ± 1.606 vs. 1.919 ± 0.032) (unit: µg/ml) (P<0.05). Huh7.5.1/ADM cells enriched the cancer stem-like cell fraction (CD133-positive subpopulation) (76.06 ± 2.948% vs. 25.38 ± 4.349%) (P<0.05), had stronger tumorigenicity in vivo and colony formation ability, and activated the Smad3 activity. Inhibition of Smad3 activity by SIS3 decreased stemness of the Huh7.5.1/ADM cells: CD133-positive subpopulation (48.49 ± 2.304% vs. 76.06 ± 2.948%) (P<0.05); ADM IC50: (0.112 ± 0.019 vs. 0.215 ± 0.018), VCR IC50 (0.065 ± 0.013 vs. 0.145±0.009), MMC IC₅₀ (0.749 ± 0.121 vs. 1.021 ± 0.119), CTX IC50 (10.576 ± 1.248 vs. 27.007 ± 1.606) (unit: µg/ml) (P<0.05), and decreased tumorigenicity and colony formation ability.</p><p><b>CONCLUSION</b>SIS3 as a specific inhibitor of Smad3 signal is involved in the stemness of multidrug resistant hepatocellular carcinoma cells.</p>