• Asian Pacific Journal of Cancer Prevention
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• v.13 no.3
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• pp.847-850
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• 2012

Tumor necrosis factor (TNF)-alpha-induced protein 8 (TNFAIP8 or TIPE) is a recently identified protein considered to be associated with carcinogenesis. To investigate its expression pattern in pancreatic cancer patients and to analyse its correlation with clinicopathological significance and the expression levels of epithelial growth factor receptor (EGFR), immunohistochemistry was performed to detect the TNFAIP8 and EGFR proteins in pancreatic cancers, pancreatitis tissues, and healthy controls. The results showed stronger staining of TNFAIP8 protein in pancreatic cancer tissues compared with normal pancreas tissue. Furthermore, in 56 patients with pancreatic cancer, the expression levels of TNFAIP8 in patients with low tumor stage was higher than that with high tumor stage, and correlated with tumor staging and lymph node metastasis (P<0.05). Furthermore, TNFAIP8 expression positively correlated with EGFR levels (r=0.671135, P<0.05). These results indicate that TNFAIP8 may play important roles in the progression of pancreatic cancer.

• Archives of Obesity and Metabolism
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• v.3 no.1
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• pp.35-42
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• 2024

Serotonin, a biogenic amine widely found in many organisms, functions as both a neurotransmitter and hormone. Although serotonin is involved in various physiological processes, this study aimed to review its role in energy metabolism. Given that serotonin cannot cross the blood-brain barrier and is synthesized by two different isoforms of tryptophan hydroxylase in the central nervous system (CNS) and peripheral tissues, it is reasonable to assume that serotonin in the CNS and peripheral tissues functions independently. Recent studies have demonstrated how serotonin influences energy metabolism in metabolic target organs such as the intestines, liver, pancreas, and adipose tissue. In summary, serotonin in the CNS induces satiety and appetite suppression, stimulates thermogenesis, and reduces body weight. Conversely, serotonin in the periphery increases intestinal motility, stimulates gluconeogenesis in the liver, suppresses glucose uptake by hepatocytes, promotes fat uptake by liver cells, stimulates insulin secretion while suppressing glucagon secretion in the pancreatic islets, promotes lipogenesis in white adipose tissue, inhibits lipolysis and browning of white adipose tissue, and suppresses thermogenesis in brown adipose tissue, thereby storing energy and increasing body weight. However, considering that most experimental results were obtained using mice and conducted under specific nutritional conditions, such as high-fat diets, whether serotonin acts in the same way in humans, whether it will act similarly in individuals with normal versus obese weights, and whether its effects vary depending on the type of food consumed, remain unknown.

• Journal of Veterinary Clinics
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• v.27 no.6
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• pp.686-692
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• 2010

Computed tomography (CT) is considered as gold standard in evaluating pancreatitis in human, but there have been only a few studies in veterinary field. Balthazar CT severity index (CTSI) used to assess the severity of acute necrotizing pancreatitis in human could be applicable to dogs, because the severity of acute pancreatitis depends on the area of pancreatic necrosis in dogs more than in human. In this study, 25 adult, clinically healthy beagle dogs were used. CT examinations was performed in normal pancreas, positive control group and acute necrotizing pancreatitis induced by autologous bile injection. Balthazar CTSI was applied to canine acute necrotizing pancreatitis in contrastenhanced CT image and compared with the result of histopathologic examination. The Hounsfield unit (HU) of normal canine pancreas was $52.44{\pm}4.58$ and the density was significantly decreased in acute necrotizing pancreatitis (P < .05). In contrast-enhanced CT examination, pancreatic density was decreased significantly and this area was compatible to pancreatic necrosis. Balthazar CTSI showed positive correlation with histopathologic evaluation with a sensitivity of 100% and a specificity of 88.89%. Balthazar CTSI can be applied to evaluate the severity of acute necrotizing pancreatitis in dogs.

• Journal of Pharmacopuncture
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• v.22 no.2
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• pp.83-89
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• 2019

Introduction: Oxidative stress (OS) during uncontrolled hyperglycemia has a pivotal role in pancreatic dysfunction. Our study aimed to demonstrate that crocin can potentiate anti-oxidant defense systems of pancreatic cells to improve oxidative stress. Methods: Male Wistar rats were divided randomly into four groups: a normal group, a normal-treated group, a diabetic group and a diabetic-treated group (n = 6 rats per group). Diabetes was induced by a single dose of streptozotocin (45 mg/kg/IV). The treated groups received crocin daily for 8 weeks (40 mg/kg/IP). At the end of the experiment, rats were sacrificed and pancreas tissue was obtained. Subsequently, the concentrations of malondialdehyde (MDA), nitrate and glutathione as well as the enzymatic activities of catalase and superoxide dismutase (SOD) were determined in all animals. Data were analyzed by two-way ANOVA with appropriate post hoc testing and a probability value of P < 0.05 was considered to represent a statistically significant difference in mean values. Results: Uncontrolled hyperglycemia weakened the anti-oxidant system by decreasing SOD and catalase enzyme activity in pancreatic tissues and induced OS by increasing the MDA content in diabetic non-treated animals. Crocin potentiated the anti-oxidant defense system by increasing the activity of both SOD and catalase, and improved OS by diminishing MDA production in pancreatic cells of rats contained in the diabetic-treated group. Conclusion: Based on our results, it is concluded that uncontrolled hyperglycemia can weaken the anti-oxidant defense system and cause the development of OS. Also, crocin can improve OS in pancreatic cells by potentiating the anti-oxidant defense system.

• The Journal of Internal Korean Medicine
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• v.19 no.2
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• pp.278-299
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• 1998

This study was aimed to evaluate the anti-stress effect of danchisoyosan on the rats stressed by immobilization. The experimental animals were immobilized in the stress box($5{\times}5{\times}20cm$) for 12 hours in a day during 3 days, and administered $500mg/5m{\ell}/g$ of Danchisoyosan extract for 14 days before stress. There were measured the change of body weight and organ weight under immobilized-stress. The norepinephrine, epinephrine, dopamine, serotonine contents were measured by HPLC method in rat brain. There were measured the GOT, GPT contents in serum and tissue lipid peroxidation in the brain, liver, spleen, adrenalgland, pancreas, testes, thymus, heart. The following results were obtained: 1. The change of organ weight was significantly lower in control than normal group. Sample group inhibited decreased weight from stress comparing to control group. 2. Lipid peroxidation in the liver was significantly higher in control than normal group. Sample group shows significant decrease comparing to control group. 3. Lipid peroxidation in the kidney was significantly higher in control than normal group. Sample group shows significant decrease comparing to control group. 4. GPT contents in serum was significantly higher in control than normal group. Sample up shows significant decrease comparing to control group. 5. Dopamine contents in the brain was significantly higher in control than normal group. Sample group shows significant decrease comparing to control group. 6. Serotonine contents in the brain was significantly higher in control than normal group. Sample group shows significant decrease comparing to control group.

• Journal of Life Science
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• v.19 no.12
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• pp.1777-1786
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• 2009

Thymosin ${\beta}4$, a small protein containing 43 amino acids, has multi-functional roles in cell physiology. It was first identified as a thymic maturation factor and recently has been shown to accelerate wound healing, hair growth, angiogenesis, tumor growth, and metastasis. It was also reported to play a key role in developing organs, including the nervous system and heart. Thymosin ${\beta}4$ induces the expression of vascular endothelial cell growth factor (VEGF), laminin-5, and other important biologically active genes. Using tissue microarray analysis, we investigated the expression patterns of thymosin ${\beta}4$ and VEGF in various normal human adult tissues. Thymosin ${\beta}4$ was highly expressed in the liver, pancreas, ductal epithelium of the salivary gland, and heart, and moderately expressed in the skin, lung, spleen, lymph node, thymus, ureter, and blood endothelial cells in both the lung and adrenal gland. The expression of VEGF generally co-localized with thymosin ${\beta}4$ and VEGF was highly expressed in the pancreas, ureter, mammary gland, liver, esophagus, and blood endothelial cells in both the lung and adrenal gland. These results suggest that thymosin ${\beta}4$ plays an important role in the function of various organs and since the expression pattern of thymosin ${\beta}4$ co-localized with VEGF, part of that function may be to induce or maintain angiogenesis.

• Journal of The Korean Society of Clinical Toxicology
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• v.10 no.1
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• pp.33-36
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• 2012

Opioids are the one of the most commonly used drugs to control cancer pain all over the world. But, we should not overlook the potential risk of opioid intoxication because they have well-known detrimental side effects. The opioid intoxication can be diagnosed thorough various clinical manifestations. The altered mental status, respiratory depression, and miosis is very representative clinical features although these symptoms don't always appear together. Unfortunately the opioid-toxidrome can be varied. A 42 years old man came to our emergency room after taking about 900 mg morphine sulfate per oral. He was nearly alert and his respiration was normal. Even though his symptoms didn't deteriorated clinically, serial arterial blood gas analysis showed increase in PaCO2. So we decided to use intravenous naloxone. Soon, he was fully awaked and his pupils size was increased. After a continuous infusion of intravenous naloxone for 2 hours, PaCO2 decreased to normal range and his pupil size also returned to normal after 12 hours. Though the levels of serum amylase and lipase increased slightly, his pancreas was normal according to the abdominal computed tomography. He had nausea, vomit, and whole body itching after naloxone continuous infusion, but conservatively treated. We stopped the continuos infusion after 1 day because his laboratory results and physical examinations showed normal. As this case shows, it is very important to prescribe naloxone initially. If you suspect opioid intoxication, we recommend the initial use of naloxone even though a patient has atypical clinical features. In addition, we suggest intranasal administration of naloxone as safe and effective alternative and it's necessary to consider nalmefene that has a longer duration for opioid intoxication.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.1
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• pp.373-376
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• 2015

Background: EVA1A (eva-1 homolog A) is a novel gene that regulates programmed cell death through autophagy and apoptosis. Our objective was to investigate the expression profiles and potential role of EVA1A in normal and neoplastic human pancreatic tissues. Materials and Methods: The expression pattern of EVA1A in normal pancreatic tissue was examined by indirect immunofluorescence and confocal microscopy. Protein levels in paraffin-embedded specimens from normal and diseased pancreatic and matched non-tumor tissues were evaluated by immunohistochemistry. Results: EVA1A colocalized with glucagon but not with insulin, demonstrating production in islet alpha cells. Itwas strongly expressed in chronic pancreatitis, moderately or weakly expressed in the plasma membrane and cytoplasm in pancreatic acinar cell carcinoma, and absent in normal pancreatic acinar cells. Although the tissue architecture was deformed, EVA1A was absent in the alpha cells of pancreatic ductal adenocarcinomas, intraductal papillary mucinous neoplasms, mucinous cystadenomas, solid papillary tumors and pancreatic neuroendocrine tumors. Conclusions: EVA1A protein is specifically expressed in islet alpha cells, suggesting it may play an important role in regulating alpha-cell function. The ectopic expression of EVA1A in pancreatic neoplasms may contribute to their pathogenesis and warrants further investigation.

• Journal of Nutrition and Health
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• v.37 no.10
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• pp.865-871
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• 2004

This study was designed to examine the effects of diets containing different levels of seeds of Benincasa hispida(wax gourd) on glycogen, protein levels and lipid profiles as well as malondialdehyde (MDA) in streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley rats were induced diabetes mellitus by STZ injection (45 mg/kg) into the tail vein and were divided into four groups: normal, STZ-control, and two experimental groups. Normal and STZ-control groups were fed the AIN-93 diet and the two experimental groups were fed a modified diet containing 2.5% and 5.0% of wax gourd seed powder for four weeks. The liver, muscle, lung, kidney, and pancreas were excised after sacrifice, then the glycogen, protein, and lipid peroxidation products were measured. The rats fed 2.5% wax gourd seed group showed higher levels of liver glycogen compared with that of the STZ-control group. The levels of kidney protein were significantly increased in the 2.5% and 5.0% wax gourd seed groups. There were no significant difference cholesterol and liver triglyceride levels of the liver and MDA concentration in the liver, lung, and kidney among all four groups. These results show that wax gourd seed treatment of 2.5% and 5.0% doses did not exhibit profound anti-lipid peroxidation properities.

• BMB Reports
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• v.48 no.11
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• pp.609-617
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• 2015

NAD(P)H:quinone oxidoreductase (NQO1), an obligatory two-electron reductase, is a ubiquitous cytosolic enzyme that catalyzes the reduction of quinone substrates. The NQO1- mediated two-electron reduction of quinones can be either chemoprotection/detoxification or a chemotherapeutic response, depending on the target quinones. When toxic quinones are reduced by NQO1, they are conjugated with glutathione or glucuronic acid and excreted from the cells. Based on this protective effect of NQO1, the use of dietary compounds to induce the expression of NQO1 has emerged as a promising strategy for cancer prevention. On the other hand, NQO1-mediated two-electron reduction converts certain quinone compounds (such as mitomycin C, E09, RH1 and β-lapachone) to cytotoxic agents, leading to cell death. It has been known that NQO1 is expressed at high levels in numerous human cancers, including breast, colon, cervix, lung, and pancreas, as compared with normal tissues. This implies that tumors can be preferentially damaged relative to normal tissue by cytotoxic quinone drugs. Importantly, NQO1 has been shown to stabilize many proteins, including p53 and p33ING1b, by inhibiting their proteasomal degradation. This review will summarize the biological roles of NQO1 in cancer, with emphasis on recent findings and the potential of NQO1 as a therapeutic target for the cancer therapy.