1.The coordinated effect of the excessive protein and cholesterin intake on inducing rat myocardial fibrosis and its mechanism.
Xiao-Hua XIE ; Zhao-Hui LI ; Wen CHEN ; Wen-Ning LU ; Ning LIU ; Xiu-Hua LIU ; Chao-Shu TANG
Chinese Journal of Applied Physiology 2004;20(1):43-45
AIMTo investigate the coordinated role and its mechanism of the high protein and hypercholesterol intake on inducing rat myocardial fibrosis.
METHODSThe tissue level of the collagen in left ventricule, the concentrations of the plasma and the cardiac tissue angiotensin II (Ang II) and Aldosterone (Ald), the serum concentration of nitrite (NO2-), in the Wistar rats on diet which adding 20% protein or/and 100 mg/d cholesterin in the rat standard foods for 8 weeks, were measured by the colorimetric analysis of the hydroxyproline, by the radioimmunoassay, and by the assay of Griess, respectively.
RESULTS1.69 times left ventricular collagen contents, 0.7 times plasma concentrations of total cholesterin, 1.5 times levels of the plasma Ang II and 1 time myocardial ald contents were higher, and the serum NO2- concentration was significant lower, in the rats of the high protein and hypercholesterol intake than in the rats of the high protein intake. That 0.48 times left ventricular collagen contents, 0.23 times plasma Ang II in the high protein and hypercholesterol intake rats were higher than in the high cholesterin intake rats.
CONCLUSIONThe excessive protein and cholesterin intake can induce the coordinated effect on developing the myocardial fibrosis of rats. And the mechanism of the fibrosis in rat left ventricule maybe result with the activation of RAAS and the endothelial injury.
Animals ; Cardiomyopathies ; etiology ; pathology ; Cholesterol, Dietary ; adverse effects ; Dietary Proteins ; adverse effects ; Fibrosis ; Male ; Myocardium ; pathology ; Rats ; Rats, Wistar
2.Advanced Criteria for Clinicopathological Diagnosis of Food Protein-induced Proctocolitis.
Jin Bok HWANG ; Moon Ho PARK ; Yu Na KANG ; Sang Pyo KIM ; Seong Il SUH ; Sin KAM
Journal of Korean Medical Science 2007;22(2):213-217
The clinicopathological findings in previous studies concerning food protein-induced proctocolitis (FPIPC) are quite diverse in terms of results and conclusions. The aim of this study was to suggest advanced clinicopathological diagnostic criteria that facilitate the early confirmation of FPIPC. Data of 38 FPIPC patients, who had received sigmoidoscopy and biopsy, was analyzed. Microscopic findings were compared with observations of previous studies. Feeding at onset of bleeding was exclusively breast-fed (94.7%) and formula-fed or mixed-fed (5.3%). Endoscopic abnormalities were observed in all patients; nodular hyperplasias with circumscribed and/or central pit-like erosions in 94.7% and erythema in 5.3%. Histopathological findings were; lymphoid aggregates in 94.7%, eosinophils in lamina propria of > or =60 cells/10 HPF in 97.4% and of >20 cells/HPF in 63.2%, epithelial or muscularis mucosa eosinophil infiltration in 97.4%, and crypt abscess in 2.6%. The majority of FPIPC patients are exclusively breast-fed and nodular hyperplasias with erosions may be a disease specific endoscopic finding. Histologic diagnosis of FPIPC is compatible with eosinophils in the lamina propria of > or =60 cells/10 high power fields; however, >20 cells/HPF is not an appropriate diagnostic criterion.
Sensitivity and Specificity
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Reproducibility of Results
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Rectal Diseases/*diagnosis/etiology
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Proctocolitis/*diagnosis/*etiology
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Male
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Infant, Newborn
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Infant
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Humans
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Gastrointestinal Hemorrhage/*diagnosis/etiology
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Female
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Dietary Proteins/*adverse effects
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Diagnosis, Differential
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Breast Feeding/*adverse effects
3.Prevalence of self-reported allergy, food hypersensitivity and food intolerance and their influencing factors in 0-36 months old infants in 8 cities in China.
Fang-li LIU ; Yi-bing NING ; De-fu MA ; Ying-dong ZHENG ; Xiao-guang YANG ; Wen-jun LI ; Yu-mei ZHANG ; Pei-yu WANG
Chinese Journal of Pediatrics 2013;51(11):801-806
OBJECTIVETo measure the prevalence, the possible causes and the influencing factors of allergy, food hypersensitivity and food intolerance in 0-36 month old infants in 8 cities in China.
METHODTotally 2632 infants from the outpatient departments of prevention and health care of two representative hospitals in 8 Chinese cities were randomly selected by applying multistage cluster sampling method from October 2011 to March 2012, and a one-on-one survey to infants' parents was conducted to investigate infants' sensitization status.
RESULTSelf-reported infant allergy rate was 17.97% (473/2632) ; self-reported food hypersensitivity and food intolerance rates were 6.53% (172/2632) and 4.26% (112/2632) , respectively. The proportion of self-reported food hypersensitivity of 0-12 months old infants was 4.47% (74/1656) and their top five allergens in a descending order were eggs (28.38%) , shrimp (25.68%) , fish (21.62%) , milk (18.92%) and wheat (4.05%) . The proportion of self-reported 13-36 months old infant's food hypersensitivity was 10.05% (98/976) . The top five allergens were shrimp (33.93%) , fish (26.79%) , eggs (23.21%) , milk (12.50%) and soy (3.57%) in 13-24 months group, while fish (38.24%) , shrimp (35.29%) , eggs (20.59%) , milk (20.59%) and peanuts (2.94%) in 25-36 months group. Both 7-12 and 13-24 month old were the highest incidence (both of them were 11.98%, 58/484) of age for developing food hypersensitivity and 7-12-month old was also the highest incidence (8.47%, 41/484) of age for food intolerance. The self-reported food intolerance rate was 3.68% (61/1656) and 5.23% (51/976) in the two age groups, respectively. Age, parental history of allergy and father's educational level (OR was 2.452, 1.482 and 2.598, respectively, P < 0.01) were the risk factors of food hypersensitivity; within two weeks of sickness (OR = 1.267, P < 0.05) was the risk factor of food intolerance.
CONCLUSIONInfancy was the most vulnerable period of life of getting allergy, therefore, it is necessary for all infants to prevent allergy through a variety of effective strategies.
Age Distribution ; Child, Preschool ; China ; epidemiology ; Dietary Proteins ; adverse effects ; Egg Hypersensitivity ; epidemiology ; etiology ; Eggs ; adverse effects ; Female ; Food Hypersensitivity ; epidemiology ; etiology ; prevention & control ; Humans ; Incidence ; Infant ; Infant Food ; adverse effects ; Infant Formula ; Infant, Newborn ; Male ; Milk Hypersensitivity ; epidemiology ; etiology ; prevention & control ; Risk Factors ; Sampling Studies ; Sex Distribution ; Surveys and Questionnaires
4.Influence of long-used staphylokinase derivative on hemoagglutinative and fibrinolytic systems.
Yuan-Yuan WANG ; Min-Hui LONG ; Jin-Feng WANG ; He ZHU ; Min WANG ; Min-Ji ZOU ; Shen LIU ; Tao XU ; Jia-Xi WANG ; Dong-Gang XU
Journal of Experimental Hematology 2009;17(3):670-673
This study was aimed to explore the influence of staphylokinase derivative (SAKD) on the hemoagglutinative and fibrinolytic systems, and to determine the safety of the staphylokinase derivative in application. The normal and model rats each 30 were divided into normal saline, SAKD and rSAK groups. The hemorrhage, bleeding time (BT), blood platelet count (BPC), activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), fibrinogen (Fg), D-dimer (D-D), plasminogen (PLG) and plasmin inhibitor activity (PI) were detected before and after the administration with staphylokinase derivative 0.5 mg/kg body weight, once three days for consecutive 15 days. The results indicated that one case of normal rats with SAKD and two cases of high fat diet model group had mild hemorrhage, all of which showed automatic hemostasis; and 3 cases in rSAK group had mild hemorrhage. And the platelet counting, D-D, PLG and PI in all groups did not significantly change. The rats of high fat diet group treated with SAKD showed the significant extension of APTT, PT and TT times, and the decrease of Fg time (p < 0.05). All the experimental results demonstrated that the influence of SAKD on the hemagglutination of the normal animals was lower, however, which can improve the high-hemagglutination status of the rats with high fat diet. It is concluded that the SAKD at the dosage of this study has the higher safety, which can alleviate the high hemagglutination symptoms of the rats with high fat diet.
Animals
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Dietary Fats
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Fibrin Fibrinogen Degradation Products
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Fibrinolysis
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drug effects
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Fibrinolytic Agents
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adverse effects
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pharmacology
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Hemagglutination
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drug effects
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Hemostasis
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Male
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Metalloendopeptidases
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pharmacology
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Partial Thromboplastin Time
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Platelet Count
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Prothrombin Time
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Rats
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Rats, Wistar
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Recombinant Fusion Proteins
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adverse effects
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pharmacology
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Thrombin Time
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Thrombolytic Therapy
5.Level and effect of anti-HSP70 antibody changed in the procession of rat atherosclerosis.
Xue LENG ; Rui ZHAN ; Xin-Xing WANG ; Xiao-Hua LU ; Li-Qun WANG ; Xiu-Jie GAO ; Ling-Jia QIAN
Chinese Journal of Applied Physiology 2009;25(4):450-454
AIMTo explore the level of anti-HSP70 antibody in plasma during atherosclerosis procedure induced by high-fat diet in rat and the relationship of them.
METHODSTwenty eight rat were divided into high-fat diet group (H) and control group (C). The total cholesterol (TC), Glyceride (TG), low density lipoprotein cholesterol (LDL-C) in serum, pathology change of rat Arch of the aorta were determined, the level of anti-HSP70 antibody and their Phenotype were evaluated by ELISA.
RESULTSAfter two weeks, the serum concentrations of TC and LDL-C in rat supplemented by high-fat diet were significantly higher than those in control group (P < 0.01), the serum TG were much lower than those in control group (P < 0.01). Four weeks later the level of anti-HSP70 antibody, IgM, IgG phenotype were significantly higher than those in control group (P < 0.01). There were lipin deposition and mottling formation in rat Arch of the aorta in rat supplemented by high-fat diet in 12th week.
CONCLUSIONAtherosclerosis could be induced by high-fat diet in rat. Accompany with the atherosclerosis procession, the level of anti-HSP70 antibody was continuously elevated, the level of anti-HSP70 antibody was related to atherosclerosis. The level of anti-HSP70 antibody was closely associated with atherosclerosis.
Animals ; Antibodies ; blood ; Atherosclerosis ; immunology ; physiopathology ; Diet, High-Fat ; adverse effects ; Dietary Fats ; administration & dosage ; HSP70 Heat-Shock Proteins ; immunology ; Immunoglobulin G ; blood ; Immunoglobulin M ; blood ; Male ; Rats ; Rats, Wistar
6.Helicobacter pylori infection enhances atherosclerosis in high-cholesterol diet fed C57BL/6 mice.
Xing-hai CHEN ; Jiang-bin WANG ; Yu-shan WANG ; Zhong-min LIU ; Yan LI
Chinese Journal of Cardiology 2010;38(3):259-263
OBJECTIVETo evaluate the impacts of Helicobacter pylori (H. pylori) infection on atherosclerosis and plasma lipid levels in high-cholesterol diet fed C57BL/6 mice.
METHODFemale C57BL/6 mice were randomly divided into 4 groups (n = 12 each): fed with normal chow diet (A), infected with H. pylori (B), fed with high-cholesterol diet (C) and infected with H. pylori and fed with high-cholesterol diet (D). After 52 weeks, plasma levels of lipids were measured and aortic atherosclerosis was observed. The ureA, ureC, cagA and vacA DNA were also detected by PCR in the aortic arteries.
RESULT(1) Prevalence of atherosclerosis was similar between group C and D (91.6% vs. 100%, P > 0.05) while there was no atherosclerosis in group A and B. H. pylori infected mice showed more obvious inflammation in gastric mucosa than mice without H. pylori infection. (2) The plasma levels of triglyceride, total cholesterol and LDL were higher and HDL was lower in group B, C and D than those in group A and in group D than in group C (all P < 0.05). (3) Roberts & Thompson scores and number of foam cells in plaques were significantly higher in group D compared with those in group C (all P < 0.05). (4) ureC DNA was detected in 5 out of 12 aortic arteries of mice in group D but not in group A, B and C.
CONCLUSIONOur results suggested that H. pylori infection might enhance the atherosclerotic lesion formation in this mouse model.
Animals ; Atherosclerosis ; microbiology ; pathology ; Bacterial Proteins ; genetics ; Bacterial Toxins ; genetics ; Cholesterol ; blood ; Cholesterol, Dietary ; adverse effects ; DNA, Bacterial ; analysis ; Female ; Helicobacter Infections ; pathology ; Helicobacter pylori ; genetics ; Mice ; Mice, Inbred C57BL ; Triglycerides ; blood ; Urease ; genetics