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The increased interest in cost-effective outpatient therapy and the expected difficulty in surgical treatment of recurrent endometriomas made aspiration and sclerotherapy of endometrioma an attractive option before ovulation induction.

Purpose: Uniportal video-assisted thoracoscopic surgery (VATS) complex segmentectomy has been challenging for thoracic surgeons. This study was designed to compare the perioperative outcomes between uniportal and multiportal VATS complex segmentectomy. Methods: Data on a total of 122 uniportal and 57 multiportal VATS complex segmentectomies were assessed. Propensity score (PS) matching yielded 56 patients in each group. A crude comparison and PS matching analyses, incorporating preoperative variables, were conducted to elucidate the short-term outcomes between uniportal and multiportal VATS complex segmentectomies. Results: The uniportal group had a significantly shorter operation time (173 min vs. 195 min, p = 0.004), pleural drainage duration (2.5 d vs. 3.5 d, p <0.001), and postoperative hospital stay (4.2 d vs. 5.3 d, p <0.001) before matching, and a significant difference was also observed after matching for pleural drainage duration (2.5 d vs. 3.6 d, p <0.001) and postoperative hospital stay (4.5 d vs. 5.2 d, p = 0.001). The numbers of dissected lymph nodes in N1 and N2 stations, the intraoperative and postoperative complication rates were not significantly different between these two groups. Conclusions: The uniportal VATS complex segmentectomy was not inferior to multiportal VATS in terms of perioperative outcomes and therefore should be considered as a viable surgical approach for treatment.

This study investigated the pro-fibrogenic role of high mobility group box 1 (HMGB1) peptides in liver fibrogenesis. An animal model of carbon tetrachloride (CCl4)-induced liver fibrosis was used to examine the serum HMGB1 levels and its intrahepatic distribution. The increased serum HMGB1 levels were positively correlated with elevation of transforming growth factor-β1 (TGF-β1) and collagen deposition during fibrogenesis. The cytoplasmic distribution of HMGB1 was noted in the parenchymal hepatocytes of fibrotic livers. In vitro studies confirmed that exposure to hydrogen peroxide and CCl4 induced an intracellular mobilization and extracellular release of nuclear HMGB1 peptides in clone-9 and primary hepatocytes, respectively. An uptake of exogenous HMGB1 by hepatic stellate cells (HSCs) T6 cells indicated a possible paracrine action of hepatocytes on HSCs. Moreover, HMGB1 dose-dependently stimulated HSC proliferation, up-regulated de novo synthesis of collagen type I and α-smooth muscle actin (α-SMA), and triggered Smad2 phosphorylation and its nuclear translocation through a TGF-β1-independent mechanism. Blockade with neutralizing antibodies and gene silencing demonstrated the involvement of the receptor for advanced glycation end-products (RAGE), but not toll-like receptor 4, in cellular uptake of HMGB1 and the HMGB1-mediated Smad2 and ERK1/2 phosphorylation as well as α-SMA up-regulation in HSC-T6 cells. Furthermore, anti-RAGE treatment significantly ameliorated CCl4-induced liver fibrosis. In conclusion, the nuclear HMGB1 peptides released from parenchymal hepatocytes during liver injuries may directly activate HSCs through stimulating HSC proliferation and transformation, eventually leading to the fibrotic changes of livers. Blockade of HMGB1/RAGE signaling cascade may constitute a therapeutic strategy for treatment of liver fibrosis.