The Feasibility of Hepatic Resections Using a Bipolar Radiofrequency Device (Habib?)

The bipolar radiofrequency device (Habib®) has been recently introduced in order to reduce intraoperative bleeding for a safe hepatic resection as an alternative to the conventional tools. However, indications, perioperative findings, and outcome of the device for hepatic resections remain and deserve to be analyzed. The current study aims to analyze the feasibility of the bipolar radiofrequency device (Habib®) for hepatic resections. Information of the patients that underwent hepatic resection using with the Habib® device between 2007 and 2011 was abstracted. Patient, disease, and operation-related findings and perioperative data were investigated. A total of 71 cases (38 [53.5 %] males, mean age was 56.8 ± 11.9) were analyzed. Metastatic disease (n = 55; 77.5 %) was the leading indication followed by primary liver and biliary malignancies (n = 7; 9.9 %), hemangioma (n = 5; 7 %), hydatid disease (n = 3; 2.8 %), and hepatic gunshot trauma (n = 1; 1.4 %). Metastasectomy was the most commonly performed procedure (n = 31; 56.3 %), but in 24 (77.4 %) cases, it was performed in addition to extended resections. Other procedures in the study patients include segmentectomy in 17, bisegmentectomy in 19, trisegmentectomy in 17, right or left hepatectomy in 8, and extended right/left hepatectomy in 3. The mean (±SD) operation time was 241.7 ± 78.2 min. The median amount of bleeding was 300 cc (range 25–2500), and 23 (32.4 %) cases required perioperative transfusion. The median hospitalization period was 5 days (range 1–47). Lengthened drainage (n = 9, 12.7 %) and intraabdominal abscess (n = 8, 11.23 %) were the most common problems. Hepatic resections using the Habib® device seem to be feasible in cases with primary and metastatic hepatic lesions and benign liver masses and even those with hepatic trauma. It may lessen the amount of intraoperative hemorrhage, although lengthened drainage and intraabdominal abscess were the major postoperative problems in these cases.     

Melatonin reduces dimethylnitrosamine-induced liver fibrosis in rats

Increased deposition of the extracellular matrix components, particularly collagen, is a central phenomenon in liver fibrosis. Stellate cells, the central mediators in the pathogenesis of fibrosis are activated by free radicals, and synthesize collagen. Melatonin is a potent physiological scavenger of hydroxyl radicals. Melatonin has also been shown to be involved in the inhibitory regulation of collagen content in tissues. At present, no effective treatment of liver fibrosis is available for clinical use. We aimed to test the effects of melatonin on dimethylnitrosamine (DMN)-induced liver damage in rats. Wistar albino rats were injected with DMN intraperitoneally. Following a single dose of 40 mg/kg DMN, either saline (DMN) or 100 mg/kg daily melatonin was administered for 14 days. In other rats, physiologic saline or melatonin were injected for 14 days, following a single injection of saline as control. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examination. Malondialdehyde (MDA), an end product of lipid peroxidation, and glutathione (GSH) and superoxide dismutase (SOD) levels were evaluated in blood and tissue homogenates. DMN caused hepatic fibrotic changes, whereas melatonin suppressed these changes in five of 14 rats (P < 0.05). DMN administration resulted in increased hydroxyproline and MDA levels, and decreased GSH and SOD levels, whereas melatonin reversed these effects. When melatonin was administered alone, no significant changes in biochemical parameters were noted. In conclusion, the present study suggests that melatonin functions as a potent fibrosuppressant and antioxidant, and may be a therapeutic choice.     

Evaluating the landscape of gene cooperativity with receptor tyrosine kinases in liver tumorigenesis using transposon-mediated mutagenesis

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Effects of 2-Hydroxypropyl-Beta-Cyclodextrin on Cardiovascular Signs of Amitriptyline Poisoning in a Rat Model

The aim of this study was to investigate the efficacy of 2-hydroxypropyl-beta-cyclodextrin (HPBCD) as an antidotal treatment for the in vivo cardiovascular effects of amitriptyline poisoning. Experiments were carried out on 33 Wistar rats. To evaluate cardiovascular effects of HPBCD, rats were infused with dextrose or HPBCD. In the poisoning model, amitriptyline (0.94 mg/kg/min) was infused until the mean arterial blood pressure (MAP) dropped to 50 % of the baseline. Following amitriptyline infusion, dextrose, low-dose HPBCD (4.19 mg/kg/min), or high-dose HPBCD (16.76 mg/kg/min) was infused, and MAP, heart rate (HR), and electrocardiogram were recorded for 60 min. Hearts were examined for tissue damage and apoptosis. HPBCD infusion alone did not yield significant difference for MAP, HR, QRS duration, QT interval, and cardiac tissue damage when compared to dextrose (p > 0.05). In the poisoning model, MAP and HR decreased, while QRS duration and QT interval prolonged significantly following amitriptyline infusion (p < 0.0167). Dextrose, low-dose HPBCD, and high-dose HPBCD infusion similarly corrected MAP, HR, QRS duration, and QT interval values at the end-experiment time point (p > 0.05). Histological scores for tissue damage and apoptosis showed no significant difference between the groups (p > 0.05). Based on our results, HPBCD did not show cardiovascular toxicity, while it was not more effective than dextrose for the treatment of amitriptyline poisoning. Further antidotal studies of cyclodextrins with higher doses and/or binding affinities are needed for poisonings.