Lymphangioma of the pancreas: A case report.

INTRODUCTION: Lymphangiomas constitute a distinct subtype of benign lymphatic malformation. The occurrence of pancreatic involvement is exceedingly infrequent. Patients with this disease typically remain asymptomatic. Surgical resection serves as the primary therapeutic modality. CASE PRESENTATION: A female patient, aged 42, was revealed to have a mass located at the back of the pancreas and occupying the body of the pancreas during imaging examinations. As a result, she underwent laparoscopic surgery for resection. CLINICAL DISCUSSION: Lymphangioma is a congenital aberration of the lymphatic vessels without malignant properties. Patients typically present without symptoms, and laparoscopic surgery is the primary treatment approach. We have focused our discussion on the etiology, diagnosis, and management of this condition. CONCLUSION: Pancreatic lymphangioma, a clinical entity of rarity, often manifests with nonspecific symptoms. We believe that laparoscopic surgery is the preferred option for treating such diseases.

PRDX1 Influences The Occurrence and Progression of Liver Cancer by Inhibiting Mitochondrial Apoptosis Pathway.

OBJECTIVE: The aim of this study is to elucidate the role of PRDX1 in hepatocellular carcinoma using hepatoma cells. MATERIALS AND METHODS: In this experimental study, we elucidated role of PRDX1, using hepatoma cell lines. RESULTS: PRDX1 was upregulated in different types of cancers, including lung adenocarcinoma, breast cancer and liver cancer reported by several studies. nevertheless, mechanism of inducing liver cell death by PRDX1 remains largely unknown. Here, we showed that PRDX1 expression is enhanced in different cell lines. Here, we used western blot, quantitative real time polymerase chain reaction (qRT-PCR) and different biochemical assays to explore the role of PRDX1. We observed that overexpression of PRDX1 significantly enhanced proliferation of hepatoma cell lines, while knock-down of this gene showed significant inhibitory effects. We found that knock-down of PRDX1 activated cleaved caspase-3, caspase-9 proteins and Poly [ADP-ribose] polymerase 1 (PARP-1), which further executed apoptotic process, leading to cell death. We found that PRDX1 knock-down significantly produced mitochondrial fragmentation. We showed that silencing PRDX1 led to the loss of B-cell lymphoma 2 (Bcl-2) and activated Bcl-2-like protein 11 (Bim) which further induced Bax activation. Bax further released cytochrome c from mitochondria and induced apoptotic proteins, suggesting a significant role of PRDX1 knock-down in apoptosis. Finally, we showed that knock-down of PRDX1 significantly activated expression of Dynein-related protein 1 (Drp1), fission 1 (Fis1) and dynamin-2 (Dyn2) suggesting a crucial role of PRDX1 in mitochondrial fragmentation and apoptosis conditions. This study highlighted an important role of PRDX1 in regulating proliferation of hepatoma cells and thus future studies are required to validate its effect on hepatcoytes. CONCLUSION: We propose that future works on PRDX1 inhibitors may act as a therapeutic candidate for treatment of liver cancer.

Two new quinones and six additional metabolites with potential anti-inflammatory activities from the roots of Juglans mandshurica.

Two new quinones, 4-(5-hydroxy-1,4-dioxo-1,4-dihydronaphtha-len-3-ylamino)-butyric acid methyl ester (compound 1) and 1,3-dimethoxycarbonyl-8-hydroxy-9,10-anthraquinone (2), and six known compounds (3-8) were isolated from the roots of Juglans mandshurica Maxim., a member of the Juglandaceae family. The chemical structures of the compounds were elucidated by nuclear magnetic resonance spectroscopy and compared with data from the literature. The isolated compounds were evaluated for their ability to inhibit the production of nitric oxide, tumour necrosis factor-α, and interleukin-6 by the mouse macrophage RAW 264.7 cell line after lipopolysaccharide stimulation in vitro. We found that compounds 1-4 exhibited potent anti-inflammatory effects, as indicated by suppression of lipopolysaccharide-stimulated nitric oxide and cytokine production with 50% inhibitory concentrations between 20.09 µM and 27.63 µM. These results identify two novel quinones from J. mandshurica with potential utility as anti-inflammatory compounds.

PIAS3/SOCS1-STAT3 axis responses to oxidative stress in hepatocellular cancer cells.

The participation of STAT3 and its upstream inhibitors, PIAS3 and SOCS1, in the oxidative response of hepatocellular carcinoma (HCC) cells was uncertain. Here, the expression of PIAS3 and SOCS1 in HCC tissues and cell lines was explored, and we sought to determine whether oxidative stress epigenetically regulated PIAS3 and SOCS1 expression and STAT3 activation in HCC cells. The expression of PIAS3 and SOCS1 was markedly decreased in HCC cell lines and tissues compared to normal hepatic cells and tissues. In HCC patients, low PIAS3 and SOCS1 expression were associated with poor survival. Oxidative stress induced by H2O2 in HepG2 cells was indicated by low antioxidant levels and high protein carbonyl content. Moreover, oxidative stress in HepG2 cells contributed to reduced proliferation but increased apoptosis, migration, and invasion capacity, which might be counteracted by antioxidants, such as tocopheryl acetate (TA). PIAS3 and SOCS1 expression was markedly decreased, while STAT3 was activated in HepG2 cells in response to H2O2 exposure. Co-treatment with antioxidant TA effectively increased the expression of PIAS3 and SOCS1, but it dephosphorylated STAT3 in H2O2-treated cells. PIAS1 or SOCS1 overexpression in HepG2 cells after H2O2 treatment restored cell viability and anti-oxidative responses and decreased apoptosis, migration, and invasion ability, and dephosphorylated STAT3 levels. Co-administration of the STAT3 activator, colivelin, partially abolished the effect of PIAS3 and SOCS1 overexpression in these processes. Therefore, oxidative stress in HCC cells may improve their migration and reduce proliferation through STAT3 activation through the repression of PIAS3 and SOCS1 expression.

The effect of bilateral U-sutures in pancreaticojejunostomy in 75 consecutive cases.

BACKGROUND: Various technical interventions have been suggested to decrease the frequency of postoperative pancreatic fistulas but the effect is not particularly satisfactory. We have analyzed our application of bilateral U-sutures in pancreaticojejunostomy. METHODS: The pancreatic stump is freed over approximately 2 cm, an appropriate diameter silicone catheter with 2-4 lateral holes was inserted into the remnant pancreatic duct (>2 mm in diameter is required) over 2-3 cm as a stent in 69 patients. In six patients with soft pancreas and very small pancreatic duct (<2 mm in diameter), the silicone catheter was not used. An incision was made on the side of the distal section of the jejunum and end-to-side an invaginated pancreaticojejunostomy was performed using bilateral U-sutures. RESULTS: Only two (2.67%) cases developed pancreatic 'biochemical leaks'. None of the 75 patients developed grade B and grade C pancreatic leakage. The overall morbidity was 29.33%. The anastomosis time was 14 minutes on average. There were no symptoms such as abdominal discomfort, dyspepsia and diarrhea, and no dilatation of pancreatic duct was found by CT in 75 patients after discharge from hospital. CONCLUSIONS: Bilateral U-sutures are a safe, simple, and effective technique in pancreaticojejunostomy, preventing the primary complication of anastomotic leakage, and worthy of wide use.

The effect of no naked pancreatic surface in the cavity of jejunum on pancreaticojejunostomy in 132 consecutive cases.

BACKGROUND/AIMS: To prevent the pancreatic fistulas, we designed a technique termed "no naked pancreatic surface in the cavity of jejunum" on pancreaticojejunostomy. METHODOLOGY: We adopted pancreatic exocrine secretions following the pancreatic duct by drainage; there was no naked pancreatic surface in the cavity of jejunum, and entail 2-3 cm sheath of the jejunum to the pancreatic stump. RESULTS: Only 3 (2.27%) cases developed pancreatic fistulas, 1 patient had a grade A leak, and 2 patients had grade B leakage. The overall morbidity was 25.76%. There was no dilatation of pancreatic duct or pancreatic enzyme deficiency shown during followed-up. The duration for accomplishing the anastomosis was 20 minutes averagely. CONCLUSIONS: The technique of no naked pancreatic surface in the cavity of jejunum can be routinely used in any case with pancreaticojejunostomy. It is a safe, simple, and effective technique that avoids the primary complication of anastomotic leakage.

MicroRNA­122 regulation of the morphology and cytoarchitecture of hepatoma carcinoma cells.

MicroRNAs (miRNAs) are a large family of post­transcriptional regulators of gene expression that control a number of developmental and cellular processes in eukaryotic organisms and are ~23 nucleotides in length. miRNA­122 is an abundant liver­specific miRNA, implicated in fatty acid and cholesterol metabolism, as well as in hepatitis C viral replication and is frequently suppressed in primary hepatocellular carcinomas. In the current study, the Hep3B cell line with stable overexpression of miR­122 was successfully established through gene transfection methods and drug screening. miR­122 was observed to alter cell morphology in vitro by stable overexpression in Hep3B cells. This alteration was viewed by light microscopy and transmission electron microscopy. These alterations included increases in the cell volume, the appearance of lipid granules and vacuoles, thickening of nuclear membrane, swelling of the mitochondria, cytoplasm vacuolization and a more prominent nucleolus. Furthermore, the study provided novel evidence that miR­122 function was dependent upon its expression level. In addition, it was observed to negatively regulate mitochondria.

Effect of OSW-1 on microRNA expression profiles of hepatoma cells and functions of novel microRNAs.

3ß,16ß,17α-trihydroxycholest-5-en-22-one 16-O-(2-O-4-methoxybenzoyl-ß-D-xylopyranosyl)-(1→3)- (2-O-acet​yl-α-L-arabinopyranoside) (OSW-1) is a member of the cholestane saponin family, which was first isolated from the bulbs of Ornithogalum saundersiae and previously reported to be cytotoxic against several types of malignant cells. However, its antitumor mechanism remains unclear. Therefore, we investigated microRNA (miRNA) expression profiles in order to explore the antitumor activities of OSW-1. Furthermore, following study of differentially expressed miRNAs, the function of novel miRNAs and OSW-1 was determined using known miRNAs and anticarcinogens. The present study demonstrated that treatment with OSW-1 leads to the upregulation and downregulation of a large set of tumor-related miRNAs, including miR-299, miR-1908, miR-125b, miR-187a, miR-1275, hav1-miR-H6-3p, miR-181, miR-210, miR-483, miR-126, miR-208 and others. Notably, miR-141, miR-142, miR-200C and miR-1275 were found to be upregulated by OSW-1 and doxorubicine, as compared with doxorubicine alone. Additionally, the expression fold-change of miR-142-3P was ~58 times higher than its expression with a different treatment. These miRNAs are linked to cancer, including proliferation, differentiation, apoptosis, cell adhesion, migration, polarity and epithelial to mesenchymal transition (EMT).

Signaling network of OSW­1­induced apoptosis and necroptosis in hepatocellular carcinoma.

The compound 3ß, 16ß, 17α­trihydroxycholest­5­en­22­one 16­O­(2­O­4­methoxybenzoyl­ß­D­xylopyranosyl)­ (1→3)­(2­O­acetyl­α­L­arabinopyranoside (OSW­1) is a member of the cholestane saponin family that was created in the bulbs of Ornithogalum saudersiae. OSW­1 has previously been shown as cytotoxic against numerous types of malignant cells, however, its antitumoral mechanisms remain unclear. The present study aimed to examine the potential changes in the gene expression of a hepatocellular carcinoma (HCC) cell line (Hep3B) incubated with OSW­1 in vitro. The results showed that OSW­1 inhibited tumors through invasiveness, angiogenesis, cell polarity and cell adhesion (as shown by Roche NimbleGen gene expression analysis), in addition to inducing apoptosis through the mitochondrial pathway. This affected the expression of a number of core genes in a number of signaling pathways, including WNT, MAPK, VEGF and P53. To the best of our knowledge, the present study is the first to report that OSW­1, as a molecular compound, induces necroptotic death in hepatocellular carcinoma (HCC).