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Purpose: We investigated the hepatoprotective effect of Silibinin (SLB) to ischemia-reperfusion (I/R) rat model, by evaluating the histological expression of the tissue markers Fas/FasL, HMGB-1 and CD45, and SLB pharmacokinetics. Methods: Seventy-three Wistar-type male rats were randomized in 11 groups: Sham control group (open-close laparotomy); four I/R control groups (laparotomy, 45 min vascular occlusion, reperfusion, euthanasia after 60, 120, 180, and 240 min); four SLB (Si) groups (laparotomy, 45 min vascular occlusion, IV administration of SLB, reperfusion, euthanasia after 60, 120, 180, and 240 min); two SLB pharmacokinetics (PK) groups (IV administration of SLB, euthanasia after 45 and 240 min). Results: Fas/FasL increased with reperfusion time in I/R control groups and decreased in the Si groups, reaching, respectively, the highest and lowest values at 240 min of reperfusion (p <.0001). HMGB1 and CD45 increased with time in the I/R control groups up to 240 min and decreased in the Si groups, approaching zero expression after 180 and 60 min, respectively. Pharmacokinetic data showed higher liver accumulation and slower plasma elimination of SLB in ischemic animals. Conclusions: The hepatoprotective effect of SLB was demonstrated through the reduction of the expression of Fas/FasL, HMGB-1 and CD45 in liver tissue under I/R conditions, and in the pharmacokinetic study. The results document the efficacy of silibinin in the protection of the liver, and are particularly encouraging for its use in hepatic surgery. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. Despite the important progress observed in liver surgery, the survival rates are discouraging. The aim of this study was to investigate the expression of autotaxin in hepatocellular carcinoma. Materials and Methods: Liver tissues from 28 human hepatocellular carcinomas were evaluated for the expression of autotaxin by immunohistochemistry. The gender, age, histological grade, lymphovascular invasion, number of tumors, levels of serum alpha-fetoprotein (aFP), presence of liver cirrhosis, hepatitis, surgery and survival rates were recorded. Results: Immunohistochemistry confirmed the expression of autotaxin in hepatocellular carcinoma. The histological grade seems to be the only independent predictor of stronger autotaxin expression, as significantly higher levels of autotaxin were detected in histological grades II and III. In addition, levels of autotaxin seem to be the most important independent prognostic factor related to poor survival. There was an eight-fold higher risk of death in patients with high levels of autotaxin compared to patients with low levels. Conclusions: Autotaxin expression in hepatocellular carcinoma could be of great importance. High autotaxin expression in HCC is detected in patients with histological grade II and III. Further, patients with elevated expression levels were found to possess an eight-fold higher risk of death. Autotaxin role in HCC should be further elucidated. [ABSTRACT FROM AUTHOR]

Background: Remote kidney damage is a sequel of hepatic ischemia-reperfusion (I/R) injury. Silibinin is the main ingredient of the milk thistle plant seed extract with known antioxidant and hepatoprotective activity. Our study investigates the nephroprotective potential of intravenously administered silibinin, as a lyophilized SLB-hydoxypropyl-beta-cyclodextrin product, in hepatic I/R injury. Material and methods: 63 Wistar rats were divided into three groups: Sham (virtual intervention); Control (45 min ischemia and reperfusion); and Silibinin (200 μL intravenous silibinin administration after 45 min of ischemia). Kidney tissues were collected to determine TNF-α, M30 and histopathological changes at predetermined time intervals. Results: Comparing Sham vs. Control groups, proved that hepatic I/R injury increased renal TNF-α and M30 expression. Deterioration was observed in hyperemia/filtration of renal parenchyma and tubules, cortical filtration, tubular necrosis and edema (tissue swelling index). Intravenous silibinin administration and comparison of the Control vs. Silibinin groups showed a statistically significant decrease in TNF-α levels at 240 min following I/R (p < 0.0001), and in M30 at 180 min (p = 0.03) and 240 min (p < 0.0001). Renal parameters have significantly decreased in: hyperemia/filtration of renal parenchyma at 120 min (p = 0.003), 180 min (p = 0.0001) and 240 min (p = 0.0002); hyperemia/filtration of renal tubules at 120 min (p = 0.02), 180 min (p = 0.0001) and 240 min (p = 0.0005); cortical filtration (240 min - p = 0.005); tubular necrosis (240 min - p = 0.021); and edema (240 min - p = 0.001). Conclusion: Our study confirms that hepatic I/R injury causes remote renal damage while the intravenous administration of silibinin leads to statistically significant nephroprotective action. [ABSTRACT FROM AUTHOR]

Purpose/aim: To examine with immunohistochemical assay MTA1 protein expression levels in pancreatic cancer tissues defining its prognostic value. Material and Methods: The specimens derived from 51 patients who underwent surgery. The levels of MTA1 protein were compared with the age of the patients, their survival, and prognosis. Also, we studied clinical and histopathological factors such as the degree of tumor differentiation and its stage in correlation with MTA1 protein levels. In parallel, there was correlation between the expression of the ΜΤΑ1 protein and the aforementioned factors regarding survival rate. Furthermore, we independently correlated the patient's survival in relation to whether they had undergone adjuvant chemotherapy or not. Results: It has been found to be low, moderate, or high expression of MTA1 levels in 48 out of 51 cancer tissues. Specifically, 49.0% of patients had low expression, 33.3% moderate, and 11.8% high expression of MTA1. Regarding the expression of MTA1 protein in correlation with various clinical and histopathological factors, a statistically significant correlation was observed with the degree of differentiation (p = 0.0068) and with the stage of the disease (p = 0.0173), but not with survival (p = 0.0740) or the age of them (p = 0.1547). Finally, it was found that overexpression of the MTA1protein is a prognostic factor for shorter survival in patients with pancreatic cancer (average 4.67 ± 0.95 months). Conclusions: MTA 1 protein may constitute an important prognostic marker in pancreatic cancer and could improve prognosis and treatment. [ABSTRACT FROM AUTHOR]

Background:Acute pancreatitis is associated with acute lung injury. The aim of the present study is to evaluate alterations of lungs in an experimental model of acute pancreatitis (AP) following both bilio-pancreatic duct obstruction close to the duodenum. Acute pancreatitis is a common disease with significant mortality. This situation makes the need of finding protective factors for the lung parenchyma, imperative. In the present study there is an effort to clarify the role of apigenin, a substance which is well known for its antioxidant and anti-inflammatory effects, on lung injury, following acute pancreatitis in rats.Materials and methods:In the present study, 126 male Wistar-type rats 3–4 months old and 220–350 g weight were used. At time 0 we randomly assigned the following groups: Group Sham: Rats were subjected to virtual surgery. Group Control: Rats were subjected to surgery for induction of acute pancreatitis. Group Apigenin: Rats were subjected to surgery for induction of acute pancreatitis and enteral feeding with apigenin. Immunochemistry for TNF-α and IL-6 as well as MPO activity were measured at predetermined time intervals 6, 12, 24, 48, and 72 h, in order to evaluate architectural disturbances of the lung tissue.Results:From the pathological reports we realized that comparing the control group with the apigenin group, there is an improvement of lung tissue damage following apigenin administration, with statistical significance. Apigenin reduces most histopathological alterations of the pulmonary tissue, reduces MPO and TNF-α activity at 48 hours and, furthermore, reduces IL-6 activity at 72 hours post-administration.Conclusions:Oral Apigenin administration in rats, following experimental induced acute pancreatitis, seems to be protective on the lung tissue. Apigenin administration to humans could potentially ameliorate acute lung injuries. However, special caution is required for humans' use, as more detailed studies are needed. [ABSTRACT FROM AUTHOR]

Purpose:Complete surgical resection with negative margins without lymphadenectomy is the treatment of choice for nonmetastatic Gastrointestinal Stromal Tumors (GISTs). Laparoscopic resection of gastric GISTs <5 cm is an acceptable and oncologically feasible, safe, and effective treatment. We present our experience of an endoscopically assisted minimally invasive transumbilical single-incision laparoscopic (SILS) technique for gastric GISTs resection.Methods:Four patients with small gastric GISTs ≤5 cm located on the greater curvature or the anterior wall were resected with SILS by using a lesion-lifting technique under the guidance of flexible gastroscopy.Results:The technique was feasible and safe and offered significant advantages in locating the tumor and controlling the resection margins. There were no major intraoperative or postoperative complications, conversions, or tumor ruptures. Pathology showed low-risk GISTs resected with disease-free margins without tumor rupture. No recurrences have been observed.Conclusion:The endoscopically assisted SILS wedge gastrectomy is a feasible, safe, and advantageous technique for the treatment of the greater curvature or anterior wall gastric GISTs. [ABSTRACT FROM PUBLISHER]

Introduction: Acinar cell death is a crucial event in acute pancreatitis (AP) and may occur either by apoptosis or necrosis. The aim of this study was to investigate the expression of the apoptosis associated proteins Fas and FasL in experimentally induced severe AP. Methods: AP was induced in 30 rats by injecting 0.2 ml of 4.5% sodium taurocholate solution into the biliopancreatic duct. Sham operated animals ( n = 30) and 10 normal controls were used for comparisons. Animals were killed at 6, 12, 24, 48, 72 hr and 1 week after operation (five animals at each time point) and both serum and pancreatic tissue were obtained. The severity of AP was graded by morphological evaluation and by measuring serum amylase levels. Acinar cell apoptosis was detected by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. Tissue expressions of Fas and FasL were evaluated by immunohistochemistry. Results: Sodium taurocholate injection resulted in severe acute necrotizing pancreatitis as early as six hr after taurocholate infusion with gradually increasing severity and a peak at 72 hr, and a significant increase of serum amylase at 6 and 12 hr. Apoptotic acinar cells were observed between 48 and 72 hr. The expression of both Fas and FasL in pancreatic tissue was induced in comparison with normal controls. Fas expression in AP was higher and statistically significant at 24 hr whereas FasL expression was consistently lower with a statistical significance observed at 12 hr when compared to sham-operated animals suggesting Fas upregulation and FasL downregulation in this model of AP. Conclusions: Induction and sequential changes in the expressions of Fas and FasL occur during taurocholate induced severe AP in rats and their temporal modulation might associate with acinar cell death by apoptosis. [ABSTRACT FROM AUTHOR]

Background: Emerging evidence supports the role of matrix metalloproteinases (MMPs) in hernia formation. However, the imbalance between the proteolytic activity of MMPs and their endogenous inhibitors (TIMPs) has not been investigated. The aim of the present study was to determine changes of MMP and TIMP levels in patients with inguinal hernia. Methods: Two matrix metalloproteinases (MMP-9 and MMP-2) and their main inhibitors TIMP-1 and TIMP-2 were evaluated in consecutive patients undergoing inguinal hernia repair and control subjects. MMP/TIMP quantification was performed using ELISA in abdominal fascia tissue specimens and preoperative plasma samples. Results: Tissue explants from hernia patients produced significantly higher levels of MMP-9 and MMP-2, and reduced TIMP-1 and TIMP-2 concentrations compared to those of controls. In plasma, a reverse correlation was found regarding the concentrations of MMPs; the circulating levels of MMP-9 and MMP-2 were significantly lower in patients with inguinal hernia than controls. Furthermore, hernia patients were found to have elevated plasma levels of TIMP-2 and reduced plasma levels of TIMP-1. Conclusions: The imbalance in MMP/TIMP activity indicates a dysregulation of the extracellular matrix degradation process in patients with inguinal hernia. The results of the present study suggest that impaired collagen metabolism may be an underlying pathophysiological mechanism of inguinal hernia formation. [ABSTRACT FROM AUTHOR]