Annular pancreas associated with nutcracker syndrome: A case report

The pancreas usually develops from the fusion of thedorsal and ventral pancreatic buds between the first 4-8weeks of embryonic life. Annular pancreas consists of aring of pancreatic tissue, which partially or completely surroundsthe descending portion of the duodenum. Annularpancreas is an uncommon congenital anomaly. The etiologyof this anomaly is still unknown. It has been associatedwith other congenital anomalies and various clinicalsymptoms. The nutcracker phenomenon is definedas compression of the left renal vein between the aortaand superior mesenteric artery. We report the case of a54-year-old patient who presented with a 15-day historyof nausea and vomiting associated with weight loss. Onmagnetic resonance cholangiopancreatography (MRCP)and computer tomography (CT) examination, an annularpancreas and nutcracker syndrome were diagnosed, respectively.In this study, we founded that the radiologicand clinical findings of associated annular pancreas withnutcracker syndrome may be of clinical importance forsurgical procedures.Key words: Annular pancreas, congenital anomaly, nutcrackerphenomenon, MRCP, C

Macrolipasemia secondary to colon cancer chemotherapy: a case report

We reported macrolipasemia in a colon cancer patient during the chemotherapy period without any evidence of pancreatitis. A 52-year-old man formerly treated for papillary thyroid carcinoma had elevated a carcinoembryonic antigen (CEA) concentration in the latest control and was diagnosed with colon cancer. Xelox chemotherapy (oxaliplatin and capecitabine) protocol was planned for six months. Interestingly, the lipase activities gradually increased from 30 U/L to 434 U/L, and exceeded three times the upper limit of the reference range (13-60 U/L). There were no symptoms of pancreatitis, and the abdominal computed tomography (CT) scan was also normal. Polyethylene glycol (PEG) recovery % values of serum samples gradually decreased and were 27% in the recent sample before the end of chemotherapy. Interestingly, the serum lipase activity fell a month after chemotherapy, and PEG recovery % increased (39%). We considered the following possibilities: (1) macrolipasemia due to chemotherapy drugs, (2) macrolipasemia due to antibodies against chemotherapy drugs

Suberoylanilide Hydroxamic Acid (SAHA) Reduces Fibrosis Markers and Deactivates Human Stellate Cells via the Epithelial-Mesenchymal Transition (EMT)

Hepatic fibrosis is known as the accumulation of connective tissue secondary to chronic damage to the liver. Epithelial-mesenchymal transition (EMT) corresponding increase in liver fibrogenesis was shown with immunohistochemistry and PCR-based studies. Suberoylanilide hydroxamic acid (SAHA), a synthetic compound approved as a histone deacetylase inhibitor (HDAC) by the FDA to treat cutaneous T-cell lymphoma is under investigation for the treatment of lung and renal fibrosis. Experimental modeling for hepatic fibrosis can be constructed with an LX2 cell line isolated from human hepatic stellate cells (HSCs). In this study, we aimed to investigate the modulation of SAHA in the pathogenesis of liver fibrosis by detecting the levels of proteins; (E-cadherin (E-cad), N-cadherin (N-cad), Vimentin (Vim), and genes; E-cad, N-cad, Vim, transforming growth factor-beta (TGF-beta), alpha-smooth muscle actin (alpha-SMA), type 1 collagen (COL1A1), type 3 collagen (COL3A1)) that play a significant role in EMT with the LX2 cell line. We also evaluated the action of SAHA with cell proliferation, clonogenic, and migration assay. Cell proliferation was performed by flow cytometry. All the protein levels were determined by Western blot analysis, and gene expression levels were measured by Real-Time PCR. Our study observed that SAHA treatment decreased cell viability, colony formation and migration in LX2 cells. We found that SAHA increased E-cad expression level, while it decreased N-cad, Vim, COL1A1, COL3A1, alpha-SMA TGF-beta genes expression levels. SAHA decreased the level of E-cad, N-cad, and Vim protein levels. We thought that SAHA possesses potent antifibrotic and anti-EMT properties in LX2

The Effect of EZH2 Inhibition through DZNep on Epithelial-Mesenchymal Transition Mechanism

Although the molecular pathogenesis of hepatocellular carcinoma (HCC) is uncertain, it is known that the epithelial-mesenchymal transition (EMT) mechanism and epigenetic changes have an important role. This study was focused on evaluating the relationship of 3-Deazaneplanocin A (DZNep) with the EMT mechanism, which is a histone methyltransferase inhibitor on HCC and is also known as an enhancer of zeste homolog 2 (EZH2) inhibitor. Cell viability of HepG2 cells (HCC cell line) assessed for DZNep over 72 hours with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Additionally, colony-forming assay, apoptosis assay, RNA isolation, cDNA synthesis, and real-time PCR (RT-PCR) were performed to see the effect of DZNep on HepG2 cells. DZNep reduced cell proliferation for 72 hours, also significantly reduced colony formation in addition it increased the total apoptosis. DZNep on EZH2, E-cadherin, N-cadherin, and Vimentin (Vim) gene expressions was given different results by either decreasing or increasing the expressions. In this study, we observed a positive effect of DZNep on apoptosis and TIMP3 expression level and decreased colony formation. However, it gave complicated results with the level of gene expression E-cadherin and TIMP2, increase the level of Vim and MMP2 expression. Therefore, we think that further studies are necessary to clarify the role of DZNep

A new marker for lipid peroxidation: Serum paraoxonase activity in non-alcoholic steatohepatitis

Background/aims: Relationship between hepatic antioxidant paraoxonase 1 (PON1) activity, lipid peroxidation and liver injury was investigated in patients with non-alcoholic steatohepatitis. Methods: A total of 23 patients with non-alcoholic steatohepatitis (15 males, 8 females; mean age: 40.30±7.67 yrs) and 23 healthy controls (14 males, 9 females; mean age: 39.70±8.78 yrs) were enrolled in the study. Serum paraoxonase 1 activity and levels of a well-known lipid peroxidation marker, serum malondialdehyde, were determined. Results: Serum paraoxonase 1 activity decreased significantly in non-alcoholic steatohepatitis compared to the control group (p0.05). Conclusions: Increased lipid peroxidation may be either a cause or a result of liver injury in patients with non-alcoholic steatohepatitis. Although serum paraoxonase 1 activity does not reflect the degree of liver damage in non-alcoholic steatohepatitis, reduced paraoxonase 1 activity, especially in the presence of mild disease, could be interpreted as a biochemical marker of the lipid peroxidation

Suberoylanilide hydroxamic acid inhibits LX2 cells proliferation via decreasing yes-associated protein/transcriptional coactivator with PDZ-binding motif proteins

Background: Hepatic fibrosis is a complex and dynamic process similar to "wound healing" that results in the progressive accumulation of connective tissue. We aimed to investigate the epigenetic control of liver fibrosis and Hippo pathway in human hepatic stellate cell (HSC) line. We examined the effect of Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor on the LX2 cell line