• Journal of Trauma and Injury
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• v.32 no.1
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• pp.66-70
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• 2019

Traumatic diaphragmatic injuries (TDIs) are a rare complication in thoraco-abdominal trauma. The diagnosis is difficult and if left untreated, TDI can cause traumatic diaphragmatic hernia (TDH). Through an injured diaphragm, the liver, spleen, stomach, small intestine, and large intestine can be herniated to the thoracic cavity, but pancreatic herniation and pancreatitis are quite rare in TDH. This paper reports a case of pancreatitis developed by additional trauma in a patient with asymptomatic chronic TDH. A 58-year-old male visited the emergency department with a left abdominal injury after a fall 6 hours earlier. The vital signs were stable, but the amylase and lipase levels were elevated to 558 U/L and 1,664 U/L, respectively. Abdominal computed tomography (CT) revealed a left diaphragmatic hernia and an incarceration of the stomach, pancreatic ductal dilatation, and peripancreatic fatty infiltration. Additional history taking showed that he had suffered a fall approximately 20 years ago and had an accidentally diaphragmatic hernia through a chest CT 6 months earlier. A comparison with the previous CT revealed the pancreatitis to be caused by secondary pancreatic ductal obstruction due to the incarcerated stomach. For pancreatitis, gastrointestinal decompression was performed, and after 3 days, the pancreatic enzyme was normalized; hence, a thoracotomy was performed. A small ruptured diaphragm was found and reposition of the organs was performed. This paper reports the experience of successfully treating pancreatitis and pancreatic hernia developed after trauma without complications through a thoracotomy following gastrointestinal decompression.

• Journal of Ginseng Research
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• v.47 no.4
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• pp.572-582
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• 2023

Background: Free fatty acid-induced lipotoxicity is considered to play an important role in pancreatic β-cell dysfunction. The effect of ginsenosides on palmitic acid-induced pancreatic beta-cells cell death and failure of glucose-stimulated secretion of insulin (GSIS) was evaluated in this study. Methods: Enzyme-linked immunosorbent assay kit for a rat insulin was used to quantify glucose-stimulated insulin secretion. Protein expression was examined by western blotting analysis. Nuclear condensation was measured by staining with Hoechst 33342 stain. Apoptotic cell death was assessed by staining with Annexin V. Oil Red O staining was used to measure lipid accumulation. Results: We screened ginsenosides to prevent palmitic acid-induced cell death and impairment of GSIS in INS-1 pancreatic β-cells and identified protopanaxadiol (PPD) as a potential therapeutic agent. The protection effect of PPD was likely due to a reduction in apoptosis and lipid accumulation. PPD attenuated the palmitic acid-induced increase in the levels of B-cell lymphoma-2-associated X/B-cell lymphoma 2, poly (ADP-ribose) polymerase and cleaved caspase-3. Moreover, PPD prevented palmitic acid-induced impairment of insulin secretion, which was accompanied by an increase in the activation of phosphatidylinositol 3-kinase, peroxisome proliferator-activated receptor γ, insulin receptor substrate-2, serine-threonine kinase, and pancreatic and duodenal homeobox-1. Conclusion: Our results suggest that the protective effect of PPD on lipotoxicity and lipid accumulation induced by palmitic acid in pancreatic β-cells.

• Journal of Digestive Cancer Research
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• v.11 no.1
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• pp.21-29
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• 2023

Despite recent advancements in the diagnosis and treatment of pancreatic cancer, clinical results remain dismal. Furthermore, there are no reliable biomarkers or alternatives beyond carbohydrate antigen 19-9. Circulating tumor cells (CTCs) may be a potential biomarker, but their therapeutic application is constrained by their rarity in peripheral venous blood. Theoretically, the portal vein can be a more appropriate location for the detection of CTCs, because the first venous drainage of pancreatic cancer is portal circulation. According to several studies, the number and detection rate of CTCs may be higher in the portal blood than in the peripheral blood. CTC counts in the portal blood are strongly correlated with several prognostic parameters such as hepatic metastasis, recurrence after surgery, and survival. The phenotypic and genotypic properties analyzed in the captured portal CTCs can assist us to comprehend tumor heterogeneity and predicting the prognosis of pancreatic cancer. The investigations to date are limited by small sample sizes and varied CTC detection techniques. Therefore, a large number of prospective studies are required to confirm portal CTCs as a valid biomarker in pancreatic cancer.

• Journal of Trauma and Injury
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• v.36 no.3
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• pp.242-248
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• 2023

Purpose: Blunt pancreatic trauma in pediatric patients is relatively rare, yet it is associated with high risks of morbidity and mortality This study aimed to review pediatric patients with blunt pancreatic trauma treated at a single center and provide treatment guidelines. Methods: This study included patients under the age of 18 years who visited our center's pediatric emergency department and were diagnosed with pancreatic injury due to abdominal trauma via radiological examination between January 2007 and December 2022. Patients' medical records were retrospectively reviewed and analyzed. Results: Among 107 patients with abdominal trauma, 14 had pancreatic injury, with a median age of 8.2 years (interquartile range, 3.1-12.3 years). Eight patients were male and six were female. The most common mechanism of injury was falls from a height and bicycle handlebars (four cases each). Six patients had associated injuries. Two patients had American Association for the Surgery of Trauma grade I or II, eight had grade III, and four had grade IV or V injuries. Eight patients underwent surgical resection, and four were discharged with only an intervention for duct injuries. Conclusions: Patients with blunt pancreatic trauma at our center have been successfully treated with surgical modalities, and more recently through nonsurgical approaches involving active endoscopic and radiologic interventions.

• Annals of Hepato-Biliary-Pancreatic Surgery
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• v.26 no.4
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• pp.401-406
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• 2022

Abdominal hydatid cyst disease mostly involves the liver. Involvement of the pancreas as an isolated primary organ is rare accounting for < 2% of all systemic echinococcosis cases. It mostly involves the head of the pancreas. Symptoms depend on the location, size, and associated complications; therefore, it can have varied presentations including acute pancreatitis. On imaging, it can mimic other common pancreatic cystic lesions like pseudocyst or cystic neoplasm. Accurate preoperative diagnosis is usually difficult and requires a very high index of suspicion even in endemic areas. Herein, a case of primary isolated hydatid cyst of the pancreas that was initially diagnosed and managed as acute pancreatic pseudocyst is reported.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.1
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• pp.391-395
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• 2014

Background: We aimed to evaluate the role of genetic polymorphisms in tobacco carcinogen-metabolizing genes and their interactions with smoking in a hospital-based case-control study of Japanese subjects. Materials and Methods: We examine the associations of pancreatic cancer risk with genetic polymorphisms in GSTM1, GSTT1 and GSTP1, phase II enzymes that catalyze the conjugation of toxic and carcinogenic electrophilic molecules. The study population consisted of 360 patients and 400 control subjects, who were recruited from several medical facilities in Japan. Unconditional logistic regression methods were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between genotypes and pancreatic cancer risk. Results: Among the control subjects, the prevalence of the GSTM1-null genotype and the GSTT1-null genotype was approximately 56% and 48%, respectively. Cases and controls were comparable in terms of GSTM1 and GSTT1 genotype distributions. Neither of the deleted polymorphisms in GSTM1 and GSTT1 was associated with the risk of pancreatic cancer, with an age- and sex-adjusted OR of 0.99 (95%CI: 0.74-1.32) for the GSTM1-null genotype, and 0.98 (95%CI: 0.73-1.31) for the GSTT1-null genotype. The OR was 0.97 (95%CI: 0.64-1.47) for individuals with the GSTM1 and GSTT1-null genotypes compared with those with the GSTM1 and GSTT1- present genotypes. No synergistic effects of smoking or GST genotypes were observed. Conclusions: Our results indicate no overall association between the GSTM1 and GSTT1 deletion polymorphisms and pancreatic cancer risk in the Japanese subjects in our study.

• Asian-Australasian Journal of Animal Sciences
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• v.33 no.11
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• pp.1837-1847
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• 2020

Objective: To evaluate the pancreatic differentiation potential of α-1,3-galactosyltransferase knockout (GalTKO) pig-derived bone marrow-derived mesenchymal stem cells (BM-MSCs) using epigenetic modifiers with different pancreatic induction media. Methods: The BM-MSCs have been differentiated into pancreatic β-like cells by inducing the overexpression of key transcription regulatory factors or by exposure to specific soluble inducers/small molecules. In this study, we evaluated the pancreatic differentiation of GalTKO pig-derived BM-MSCs using epigenetic modifiers, 5-azacytidine (5-Aza) and valproic acid (VPA), and two types of pancreatic induction media - advanced Dulbecco's modified Eagle's medium (ADMEM)-based and N2B27-based media. GalTKO BM-MSCs were treated with pancreatic induction media and the expression of pancreas-islets-specific markers was evaluated by real-time quantitative polymerase chain reaction, Western blotting, and immunofluorescence. Morphological changes and changes in the 5'-C-phosphate-G-3' (CpG) island methylation patterns were also evaluated. Results: The expression of the pluripotent marker (POU class 5 homeobox 1 [OCT4]) was upregulated upon exposure to 5-Aza and/or VPA. GalTKO BM-MSCs showed increased expression of neurogenic differentiation 1 in the ADMEM-based (5-Aza) media, while the expression of NK6 homeobox 1 was elevated in cells induced with the N2B27-based (5-Aza) media. Moreover, the morphological transition and formation of islets-like cellular clusters were also prominent in the cells induced with the N2B27-based media with 5-Aza. The higher insulin expression revealed the augmented trans-differentiation ability of GalTKO BM-MSCs into pancreatic β-like cells in the N2B27-based media than in the ADMEM-based media. Conclusion: 5-Aza treated GalTKO BM-MSCs showed an enhanced demethylation pattern in the second CpG island of the OCT4 promoter region compared to that in the GalTKO BM-MSCs. The exposure of GalTKO pig-derived BM-MSCs to the N2B27-based microenvironment can significantly enhance their trans-differentiation ability into pancreatic β-like cells.

• Food Science and Preservation
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• v.18 no.3
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• pp.390-396
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• 2011

Ginger (Zingiber officinale) is a well-known herb that is widely consumed as spice for the flavoring of foods. As part of our continuing search for bioactive materials, the in vitro pancreatic lipase inhibition and antioxidant properties of an aqueous ethanolic extract of Z. officinale were investigated. The total phenolic content was determined using a spectrophotometric method. The antioxidant efficacies of the extract was studied with radical scavenging assays using DPPH and $ABTS^+$ radicals. Further more, the antiobesity effect of the extract was evaluated by porcine pancreatic lipase assay. In particularly, the pancreatic lipase inhibitory activity of the ethyl acetate (EtOAc)-soluble portion from Z. officinale was significantly higher than that of the other solvent-soluble portions. The results suggest that Z. officinale may have therapeutic potential that may be useful in development of an anti-obesity agent or its precursors.

• Biomolecules & Therapeutics
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• v.32 no.1
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• pp.123-135
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• 2024

Although gemcitabine-based regimens are widely used as an effective treatment for pancreatic cancer, acquired resistance to gemcitabine has become an increasingly common problem. Therefore, a novel therapeutic strategy to treat gemcitabine-resistant pancreatic cancer is urgently required. Piceamycin has been reported to exhibit antiproliferative activity against various cancer cells; however, its underlying molecular mechanism for anticancer activity in pancreatic cancer cells remains unexplored. Therefore, the present study evaluated the antiproliferation activity of piceamycin in a gemcitabine-resistant pancreatic cancer cell line and patient-derived pancreatic cancer organoids. Piceamycin effectively inhibited the proliferation and suppressed the expression of alpha-actinin-4, a gene that plays a pivotal role in tumorigenesis and metastasis of various cancers, in gemcitabine-resistant cells. Long-term exposure to piceamycin induced cell cycle arrest at the G₀/G₁ phase and caused apoptosis. Piceamycin also inhibited the invasion and migration of gemcitabine-resistant cells by modulating focal adhesion and epithelial-mesenchymal transition biomarkers. Moreover, the combination of piceamycin and gemcitabine exhibited a synergistic antiproliferative activity in gemcitabine-resistant cells. Piceamycin also effectively inhibited patient-derived pancreatic cancer organoid growth and induced apoptosis in the organoids. Taken together, these findings demonstrate that piceamycin may be an effective agent for overcoming gemcitabine resistance in pancreatic cancer.

• The Korean Journal of Physiology
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• v.30 no.2
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• pp.219-229
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• 1996

In order to investigate intra-pancreatic cholinergic roles on insulin action in exocrine secretion, the pancreas was isolated from rats and continuously perfused with modified Krebs-Henseleit solution. Intra-arterial infusion of insulin (100 nM) or cholecystokinin (CCK, 14 pM) alone resulted in stimulation of the volume flow and amylase output. Also insulin potentiated the action of CCK in the exocrine secretion. Tetrodotoxin and atropine completely abolished the potentiating action of insulin and CCK as well as the action of insulin alone, but did not change the action of CCK alone. In order to see an effect of intra-pancreatic neural activation on the insulin action, electrical field stimulation (EFS) with parameters of 20 V, 2 msec and 8 Hz was applied to the isolated pancreas for 10 min under 2.5 or 18 mM glucose background. The EFS voltage-dependently elevated the flow rate and amylase output, and potentiated exocrine secretion in 18 mM glucose infusion compared with 2.5 mM glucose. The potentiating effects of EFS and 18 mM glucose were not observed in the streptozotocin-treated pancreas although it was perfused with 18 mM glucose. However, it was restored when the diabetic pancreas was perfused with porcine insulin(100 nM). Tetrodotoxin and atropine inhibited the pancreatic secretion induced by EFS with the background of 18 mM glucose. The results of present investigation indicate that the intra-pancreatic cholinergic tone exerts a stimulatory influence on the action of insulin in pancreatic exocrine secretion of rats.