Kim, Hye Ran;Kang, Mun Ju;Kim, Yong Hwan;Lee, Jun Ho;Cho, Kwang Won;Hwang, Seong Youn;Lee, Dong Woo
Journal of The Korean Society of Clinical Toxicology
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v.14
no.1
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pp.16-25
/
2016
Purpose: Patients suffering from acute poisoning by different substances often visit the emergency department (ED) and receive various prognoses according to the toxic material and patients' condition. Hyperlactatemia, which is an increased blood lactate level that generally indicates tissue hypoperfusion, is commonly utilized as a prognostic marker in critically ill patients such as those with sepsis. This study was conducted to investigate the relationships between blood lactate and clinical prognosis in acute poisoned patients. Methods: This retrospective study was conducted from January 2013 to June 2014 at a single and regional-tertiary ED. We enrolled study patients who were examined for blood test with lactate among acute intoxicated patients. The toxic materials, patient demographics, laboratory data, and mortalities were also reviewed. Additionally, we analyzed variables including blood lactate to verify the correlation with patient mortality. Results: A total of 531 patients were enrolled, including 24 (4.5%) non-survivors. Patient age, Glasgow coma scale (GCS), serum creatinine (Cr), aspartate transaminase (AST), and serum lactate differed significantly between survivors and non-survivors in the binary logistic regression analysis. Among these variables, GCS, AST, and lactate differed significantly. The median serum lactate levels were 2.0 mmol/L among survivors and 6.9 mmol/L among non-survivors. The AUC with the ROC curve and odds ratio of the initial serum lactate were 0.881 and 3.06 (0.89-8.64), respectively. Conclusion: Serum lactate was correlated with fatalities of acute poisoning patients in the ED; therefore, it may be used as a clinical predictor to anticipate their prognoses.
Endothelial cells are a vital constituent of most mammalian organs and are required to maintain the integrity of these tissues. These cells also play a major role in angiogenesis, inflammatory reactions, and in the regulation of thrombosis. Angiogenesis facilitates pulp formation and produces the vessels which are essential for the maintenance of tooth homeostasis. These vessels can also be used in bone and tissue regeneration, and in surgical procedures to place implants or to remove cancerous tissue. Furthermore, endothelial cell regeneration is the most critical component of the tooth generation process. The aim of the present study was to stimulate endothelial regeneration at a site of acute cyclophosphamide (CP)-induced endothelial injury by treatment with human umbilical cord-derived endothelial/mesenchymal stem cells (hEPCs). We randomly assigned 16 to 20-week-old female NOD/SCID mice into three separate groups, a hEPC ($1{\times}10^5$ cells) transplanted, 300mg/kg CP treated and saline (control) group. The mice were sacrificed on days 5 and 10 and blood was collected via the abdominal aorta for analysis. The alanine transaminase (ALT), aspartate aminotransferase (AST), serum alkaline phosphatase (s-ALP), and albumin (ALB) levels were then evaluated. Tissue sections from the livers and kidneys were stained with hematoxylin and eosin (HE) for microscopic analysis and were subjected to immunohistochemistry to evaluate any changes in the endothelial layer. CP treatment caused a weight reduction after one day. The kidney/body weight ratio increased in the hEPC treated animals compared with the CP only group at 10 days. Moreover, hEPC treatment resulted in reduced s-ALP, AST, ALT levels compared with the CP only group at 10 days. The CP only animals further showed endothelial injuries at five days which were recovered by hEPC treatment at 10 days. The number of CD31-positive cells was increased by hEPC treatment at both 5 and 10 days. In conclusion, the CP-induced disruption of endothelial cells is recovered by hEPC treatment, indicating that hEPC transplantation has potential benefits in the treatment of endothelial damage.
BACKGROUND/OBJECTIVES: Previous studies have reported that protein supplementation contributes to the attenuation of inflammation. Serious trauma such as burn injury usually results in the excessive release of inflammatory factors and organs dysfunction. However, a few reports continued to focus on the function of protein ingestion in regulating burn-induced inflammation and organ dysfunction. MATERIALS/METHODS: This study established the rat model of 30% total body surface area burn injury, and evaluated the function of blended protein (mixture of whey and soybean proteins). Blood routine examination, inflammatory factors, blood biochemistry, and immunohistochemical assays were employed to analyze the samples from different treatment groups. RESULTS: Our results indicated a decrease in the numbers of white blood cells, monocytes, and neutrophils in the burn injury group administered with the blended protein nutritional support (Burn+BP), as compared to the burn injury group administered normal saline supplementation (Burn+S). Expressions of the pro-inflammatory factors (tumor necrosis factor-α and interleukin-6 [IL-6]) and chemokines (macrophage chemoattractant protein-1, regulated upon activation normal T cell expressed and secreted factor, and C-C motif chemokine 11) were dramatically decreased, whereas anti-inflammatory factors (IL-4, IL-10, and IL-13) were significantly increased in the Burn+BP group. Kidney function related markers blood urea nitrogen and serum creatinine, and the liver function related markers alanine transaminase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase were remarkably reduced, whereas albumin levels were elevated in the Burn+BP group as compared to levels obtained in the Burn+S group. Furthermore, inflammatory cells infiltration of the kidney and liver was also attenuated after burn injury administered with blended protein supplementation. CONCLUSIONS: In summary, nutritional support with blended proteins dramatically attenuates the burn-induced inflammatory reaction and protects organ functions. We believe this is a new insight into a potential therapeutic strategy for nutritional support of burn patients.
Yura Ahn;Sung-Cheol Yun;Seung Soo Lee;Jung Hee Son;Sora Jo;Jieun Byun;Yu Sub Sung;Ho Sung Kim;Eun Sil Yu
Korean Journal of Radiology
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v.21
no.4
/
pp.413-421
/
2020
Objective: A widely applicable, non-invasive screening method for non-alcoholic fatty liver disease (NAFLD) is needed. We aimed to develop and validate an index combining computed tomography (CT) and routine clinical data for screening for NAFLD in a large cohort of adults with pathologically proven NAFLD. Materials and Methods: This retrospective study included 2218 living liver donors who had undergone liver biopsy and CT within a span of 3 days. Donors were randomized 2:1 into development and test cohorts. CTL-S was measured by subtracting splenic attenuation from hepatic attenuation on non-enhanced CT. Multivariable logistic regression analysis of the development cohort was utilized to develop a clinical-CT index predicting pathologically proven NAFLD. The diagnostic performance was evaluated by analyzing the areas under the receiver operating characteristic curve (AUC). The cutoffs for the clinical-CT index were determined for 90% sensitivity and 90% specificity in the development cohort, and their diagnostic performance was evaluated in the test cohort. Results: The clinical-CT index included CTL-S, body mass index, and aspartate transaminase and triglyceride concentrations. In the test cohort, the clinical-CT index (AUC, 0.81) outperformed CTL-S (0.74; p < 0.001) and clinical indices (0.73-0.75; p < 0.001) in diagnosing NAFLD. A cutoff of ≥ 46 had a sensitivity of 89% and a specificity of 41%, whereas a cutoff of ≥ 56.5 had a sensitivity of 57% and a specificity of 89%. Conclusion: The clinical-CT index is more accurate than CTL-S and clinical indices alone for the diagnosis of NAFLD and may be clinically useful in screening for NAFLD.
People with higher genetic predisposition to obesity are more susceptible to cardiovascular diseases (CVDs) and healthy plant-based foods may be associated with reduced risks of obesity and other metabolic markers. We investigated whether healthy plant-foods-rich dietary patterns might have inverse associations with cardiometabolic risk factors in participants at genetically elevated risk of obesity. For this cross-sectional study, 377 obese and overweight women were chosen from health centers in Tehran, Iran. We calculated a healthy plant-based diet index (h-PDI) in which healthy plant foods received positive scores, and unhealthy plant and animal foods received reversed scores. A genetic risk score (GRS) was developed based on 3 polymorphisms. The interaction between GRS and h-PDI on cardiometabolic traits was analyzed using a generalized linear model (GLM). We found significant interactions between GRS and h-PDI on body mass index (BMI) (p = 0.02), body fat mass (p = 0.04), and waist circumference (p = 0.056). There were significant gene-diet interactions for healthful plant-derived diets and BMI-GRS on high-sensitivity C-reactive protein (p = 0.03), aspartate aminotransferase (p = 0.04), alanine transaminase (p = 0.05), insulin (p = 0.04), and plasminogen activator inhibitor 1 (p = 0.002). Adherence to h-PDI was more strongly related to decreased levels of the aforementioned markers among participants in the second or top tertile of GRS than those with low GRS. These results highlight that following a plant-based dietary pattern considering genetics appears to be a protective factor against the risks of cardiometabolic abnormalities.
Kang, Nan Hui;Park, Ji Sook;Lee, Hongchan;Yim, Jung-Eun
Journal of Nutrition and Health
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v.53
no.4
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pp.381-389
/
2020
Purpose: This study examined the relationships among serum ferritin, vitamin D, folate, iron, and vitamin B12 as indicators of obesity. The results provide the basic data for the prevention and treatment of obese and severely obese people. Methods: This study selected 44 people from 18 years of age or older to 59 years. This study used the indicators of the body mass index (BMI) to analyze obesity as the obesity group (BMI of 25.0-29.9 kg/㎡) and as the severe obesity group (BMI ≥ 30.0 kg/㎡). Of the 44 subjects, 23 and 21 subjects were in the obesity and severe obesity groups, respectively. Their height, weight, body fat, skeletal muscle mass measured using bioimpedance analysis, and measured serum nutrients and biochemical parameters. Results: The obesity group showed a significantly lower age, body weight, BMI and body composition, body fat mass, and body fat percentage, and the height was significantly lower in the severe obesity group. The results of the biochemical parameters of the subjects showed that the levels of aspartate transaminase, alanine transaminase, hemoglobin A1c, total cholesterol, and triglyceride were within the normal range, and there was no significant difference between the 2 groups. The levels of folate, vitamin B12, 25-hydroxyvitamin D3, iron, and ferritin were almost normal, and there was no significant difference between the 2 groups. Conclusion: This study revealed an association with the serum nutrients and obesity, but there was no difference between the obesity group and severe obesity group. Observations of the nutrient levels in not only the blood in obesity and severe obesity but also in red blood cells and tissues will be necessary.
Purpose: The objective of this study was to describe the frequency of hepatobiliary dysfunction (HD) at our hospital and determine the possible risk factors and complications associated with the development of HD in very low birth weight infants (VLBWI) treated with parenteral nutrition (PN). Methods: A retrospective study of VLBWI (n=92) that required PN between 2004 and 2008 in the NICU at the Bucheon St. Marys Hospital of Catholic University was performed. HD was defined by a direct bilirubin (DB) >2 mg and a transaminase of 60 IU/L defined cholestasis and liver injury. Groups I, II, and III were limited to cases of cholestasis, liver injury without cholestasis, and no abnormalities, respectively. The VLBWI were compared to each other. Results: Thirty-six subjects (39.1%) had cholestasis and 51 (55.4%) had liver injury. In addition, 36 (39.1%), 19 (20.7%), and 37 (40.2%) subjects were classified as groups I, II, and III, respectively. The three groups showed significant differences in gestational age, 1- and 5-minute Apgar scores, use of surfactant, duration of parenteral nutrition, frequency of RBC transfusions, bronchopulmonary dysplasia (BPD), and patent ductus arteriosus (PDA) (P<0.05). The multiple regression analysis with cholestasis as the dependent variable, showed a significant correlation with gestational age, use of surfactant, frequency of RBC transfusions, and PDA. Conclusion: Various factors, such as birth weight, gestational age, 1- and 5-minute Apgar scores, use of surfactant for respiratory distress syndrome (RDS), frequency of RBC transfusions, BPD, and PDA may be related to hepatobiliary dysfunction in VLBWI treated with PN.
Ryu, Ji Hyeon;Kim, Eun-Jin;Xie, Chengliang;Nyiramana, Marie Merci;Siregar, Adrian S.;Park, Si-Hyang;Cho, Soo Buem;Song, Dae Hyun;Kim, Nam-Gil;Choi, Yeung Joon;Kang, Sang Soo;Kang, Dawon
Journal of the Korean Society of Food Science and Nutrition
/
v.46
no.6
/
pp.659-670
/
2017
Oxidative stress and inflammation are key factors responsible for progression of liver injury. A variety of functions of oyster hydrolysate (OH) are affected by their antioxidant and anti-inflammatory activities. However, little is known regarding the effects of OH on a liver injury model. This study was performed to evaluate the effects of OH on acute liver injury induced by lipopolysaccharide/D-galactosamine (LPS/D-GalN) in mice. Experimental groups were divided into six groups as follows (each group, n=10): control (saline), LPS/D-GalN, LPS/D-GalN+OH (100 mg/kg), LPS/D-GalN+OH (200 mg/kg), LPS/D-GalN+OH (400 mg/kg), and LPS/D-GalN+silymarin (25 mg/kg, positive control). The experimental acute liver injury model was induced with LPS ($1{\mu}g/kg$) and D-GalN (400 mg/kg). We first analyzed antioxidant and anti-inflammatory activities in OH. OH showed high DPPH and ABTS radical scavenging activities and reduced ROS generation in Chang cells in a dose-dependent manner. In addition, OH showed anti-inflammatory activities, such as inhibition of cyclooxygenase-2 and 5-lipooxygenase. Treatment with OH down-regulated tumor necrosis factor $(TNF)-{\alpha}$, interleukin (IL)-6, and $IL-1{\alpha}$ expression levels in LPS-stimulated RAW264.7 cells. OH significantly reduced LPS/D-GalN-induced increases in the concentrations of alanine transaminase and aspartate aminotransferase in serum. In the LPS/D-GalN group, liver tissues exhibited apoptosis of hepatocytes with hemorrhages. These pathological alterations were ameliorated by OH treatment. Consistently, hepatic catalase activity was low in the LPS/D-GalN group compared to the control group, and catalase activity was significantly restored by OH treatment (P<0.05). Furthermore, OH markedly reduced the LPS/D-GalN-induced increase in $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 levels in liver tissue. Taken together, these results show that OH has hepatoprotective effects on LPS/D-GalN-induced acute liver injury via inhibition of oxidative stress and inflammation, suggesting that OH could be used as a health functional food and potential therapeutic agent for acute liver injury.
Kim, Ae-Jung;Kim, Sun-Yeou;Choi, Mi-Kyeong;Kim, Myung-Hwan;Han, Myung-Ryun;Chung, Kun-Sub
Korean Journal of Food Science and Technology
/
v.37
no.4
/
pp.636-641
/
2005
Mulberry leaves, high in dietary fiber and some nutritional materials, are thought to have hypocholesterolemic effect. Therefore, effect of mulberry leaf powder on serum lipid profiles were studied using rats with diet-induced hypercholesterolemia. Male Sprague-Dawley rats were fed AIN-93 diet (control group), and diets containing high-cholesterol and 0% mulberry leaves powder, high-cholesterol and 5% mulberry leaves powder, and high-cholesterol and 10% mulberry leaves powder for 4 weeks. Hypercholesterolemia was induced by adding 1% cholesterol and 0.5% cholic acid to all diets except in control group. Although no differences were observed in food intake and initial body weight among groups, mulberry leaf treatment resulted in significant decreases in food efficiency ratio and body weight gain. Mulberry leaf treatment decreased serum lipid profiles, atherogenic index, cardiac risk factor, low density lipoprotein cholesterol ratio, serum aspartate transaminase, and liver lipid levels. High density lipoprotein cholesterol, total cholesterol, serum HDL-cholesterol, and fecal lipid levels increased, suggesting mulberry leaves could improve hyperlipidemia and liver action, thereby proventing cardiovascular disease.
This study investigated the antioxidant and hepatoprotective effects of Ainsliaea acerifolia water extract (AAWE) on HepG2 cells. Five types of caffeoylquinic acid (CQA) were detected in AAWE, namely, 4,5-di-O-caffeoylquinic acid (4,5-DCQA; 11.16 mg/g), 3,4-di-O-caffeoylquinic acid (3,4-DCQA; 5.23 mg/g), 5-O-caffeoylquinic acid (5-CQA; 4.88 mg/g), 3,5-di-O-caffeoylquinic acid (3,5-DCQA; 3.51 mg/g), and 4-O-caffeoylquinic acid (4-CQA; 3.31 mg/g). AAWE exerted ABTS+ antioxidant effects, evidenced by polyphenol content and 2,2'2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) and 2,2-diphenyl-1-picryl-hydrazyl-hydrate (DPPH radical scavenging) activities. AAWE (300 ㎍/mL) treatment significantly decreased the activities of gamma glutamyl transferase (GGT), aspartate transaminase (AST), and lactate dehydrogenase (LDH) as compared to control and exerted protective effects against the increase in liver function index induced by lipopolysaccharide (LPS)/galactosamine (D-GalN) in HepG2 cells. In addition, the secretion of tumor necrosis factor (TNF)-α by HepG2 cells induced by LPS/D-GalN significantly increased in all treatment groups compared to that in the control. However, AAWE (100-300 ㎍/mL) treatment significantly decreased the secretion of TNF-α compared to that in the control. These results suggest that AAWE treatment reduces hepatotoxicity by increasing antioxidant activities, reducing GGT, AST, and LDH activities, and inhibiting TNF-α secretion.
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