Background Robotic liver resection has emerged as a new modality in the field of minimally invasive surgery. However, the effectiveness of this approach for liver resection is not yet known. Methods A literature survey was performed using specific search phrases in PubMed. Case series that focused on biliary reconstruction were excluded. Characteristics, such as patient demographics, perioperative outcomes, and oncological results for colorectal liver metastasis and hepatocellular carcinoma were analyzed. Results Nineteen series that described the cases of 217 eligible patients were reviewed. The most commonly performed procedures were wedge resection and segmentectomy. Right hepatectomy was performed in a few specialized centers. The conversion and complication rates were 4.6 and 20.3 %, respectively. The most common reason for conversion was unclear tumor margin. Intra-abdominal fluid collection was the most frequently occurring morbidity. Mean operation time was 200–507 min. Mean intraoperative blood loss was 50–660 mL, with a tendency toward increased blood loss observed in series that included major hepatectomies. Mean postoperative hospital stay was 5.5–11.7 days. The longest mean follow-up time was 36 months for colorectal liver metastasis and 25.1 months in hepatocellular carcinoma. Disease-free survival for mixed malignancies was comparable to that after laparoscopic procedures. Overall survival was not reported. Conclusions Robotic liver resection is safe and feasible for experienced surgeons with advanced laparoscopic skills. Long-term oncologic outcomes are unclear, but short-term perioperative results seem comparable to those of conventional laparoscopic liver resection.

Macrophages engulf oxidized-LDL (oxLDL) leading to accumulation of cellular cholesterol and formation of foam cells, which is a hallmark of atherosclerosis. Moreover, recent studies showed that accumulation of free cholesterol in macrophages leading to activation of NLRP3 inflammasome and production of interleukin-1β (IL-1β) has been linked to atherosclerosis-associated inflammation. However, it is not clear if cholesterol accumulation is associated with hepatic inflammation and fibrosis in the liver. In this study, we investigated the association of free cholesterol and oxLDL accumulation in portal vein with the inflammation, atherosclerosis, and fibrosis in human nonalcoholic fatty liver disease (NAFLD). Serial sections derived from surgical specimens of NAFLD were stained with filipin and antibodies against IL-1β, CD68, α-smooth muscle actin (α-SMA), oxLDL and lectin-like oxLDL receptor-1 (LOX-1). We show that free cholesterol was colocalized with oxLDL in the wall of portal vein, and which was associated with lumen narrowing, plaque formation, endothelium deformation, and portal venous inflammation. The inflammation was evidenced by the colocalization of Kupffer cells and IL-1β and the expression of LOX-1. Notably, ruptured plaque was closely associated with portal venous inflammation. Moreover, free cholesterol and oxLDL accumulation in periportal and sinusoidal fibrosis, which was associated with regional stellate cell activation and chicken-wire fibrosis. These findings reveal a direct association between cholesterol accumulation, portal venous inflammation and fibrosis in NAFLD.

Insulin-like growth factor, (IGF)-1, is produced mainly by the liver and plays important roles in promoting growth and regulating metabolism. Previous study reported that development of hepatocellular carcinoma (HCC) was accompanied by a significant reduction in serum IGF-1 levels. Here, we hypothesized that dysregulation of microRNAs (miRNA) in HCC can modulate IGF-1 expression post-transcriptionally. The miRNAs expression profiles in a dataset of 29 HCC patients were examined using illumina BeadArray. Specific miRNA (miR)-190b, which was significantly up-regulated in HCC tumor tissues when compared with paired non-tumor tissues, was among those predicted to interact with 3′-untranslated region (UTR) of IGF-1. In order to explore the regulatory effects of miR-190b on IGF-1 expression, luciferase reporter assay, quantitative real-time PCR, western blotting and immunofluorecence analysis were performed in HCC cells. Overexpression of miR-190b in Huh7 cells attenuated the expression of IGF-1, whereas inhibition of miR-190b resulted in up-regulation of IGF-1. Restoration of IGF-1 expression reversed miR-190b-mediated impaired insulin signaling in Huh7 cells, supporting that IGF-1 was a direct and functional target of miR-190b. Additionally, low serum IGF-1 level was associated with insulin resistance and poor overall survival in HCC patients. Increased expression of miR-190 may cause decreased IGF-1 in HCC development. Insulin resistance appears to be a part of the physiopathologic significance of decreased IGF-1 levels in HCC progression. This study provides a novel miRNA-mediated regulatory mechanism for controlling IGF-1 expression in HCC and elucidates the biological relevance of this interaction in HCC.