1.Platelet aggregation induced by ADP and collagen in dyslipidemia patients
Nga Thi Hong Dao ; Ha Thi Thu Nguyen ; Khai Gia Pham
Journal of Medical Research 2007;51(4):44-48
Background: Dyslipidemia is an important risk factor of atherosclerosis. The endothelia can be injured by plaque that advantages for platelet adheadsion, aggregation and produces thrombosis. Objectives: (1) To evaluate the changes of platelet aggregation induced by ADP and collagen in hyperlipidemic patients; (2) To identify the relationship between platelet aggregation and various types of dyslipidemia. Subjects and methods: A descriptive cross sectional non-randomised control trial method was employed in this study. A total of 128 hyperlipidemic patients (in which 40 patients were type IIa, 36 were type lib, and 52 were type IV), and a control group of 88 people were measured the aggregation in platelet - rich plasma (PRP) induced by ADP and collagen. Results: There was no significant difference about the platelet counts in both intervention and control groups (p>0.05). ADP and collagen induced platelet aggregation increased significantly (p<0.01) in intervention group when compared to control group. A significant correlation was found between the plasma triglyceride concentration and platelet aggregation induced by ADP and collagen with r = 0,335 and 0,332 respectively, while that of cholesterol and ADP was 0,304. Conclusion: Platelet aggregation increased in hyperlipidemic patients and had a significant correlation with plasma triglyceride concentration. \r\n', u'\r\n', u'
Dyslipidemias/ pathology
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therapy
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Platelet Aggregation
2.Clinical and angiographic characteristics of premenopausal women with coronary artery disease.
Ke-fei DOU ; Bo XU ; Yue-jin YANG ; Rong LÜ ; Hong QIU ; Wei-xian YANG ; Zhao-wei MU ; Run-lin GAO ; Zhan GAO ; Ji-lin CHEN ; Shu-bin QIAO ; Jian-jun LI ; Xue-wen QIN ; Hai-bo LIU ; Yong-jian WU ; Jue CHEN ; Min YAO ; Shi-jie YOU ; Jin-qing YUAN ; Ju DAI
Chinese Medical Journal 2008;121(23):2392-2396
BACKGROUNDCoronary artery disease (CAD) is generally considered as a disease of middle-aged men. It is widely accepted that the risk for CAD of premenopausal women is low because of hormone protection. Based on our clinical experience, more and more premenopausal women suffer from angina and myocardial infarction without adequate concern. Even now, there are still limited detailed data to describe the characteristics, mechanism and prognosis of premenopausal CAD patients. This article aimed to analyze the clinical and angiographic characteristics of premenopausal women with CAD.
METHODSA total of 565 premenopausal women and 721 postmenopausal women (56 - 60 years old) who underwent coronary angiography for the first time from April 2004 to December 2007 were enrolled. The clinical data and coronary angiographic characteristics (presence, localization, length and severity) were compared between the premenopausal and postmenopausal CAD groups.
RESULTSPremenopausal CAD patients presented less frequently with hypertension, diabetes mellitus and dyslipidemia compared with postmenopausal CAD patients (55.0% vs 66.0%, 15.0% vs 31.5%, 23.9% vs 37.4%, respectively; all P < 0.05). Although we found more frequent involvement of single vessel in premenopausal CAD (43.2% vs 26.9%, P = 0), and triple vessels in postmenopausal (56 - 60 years old) CAD patients (33.8% vs 20.4%, P = 0), much more severe lesions (> or = 90%) at left main (2.9% vs 1.1%, P = 0.048) and proximal left anterior descending artery (LAD) (28.2% vs 16.6%, P = 0) in the premenopausal CAD group were found.
CONCLUSIONPremenopausal women with chest discomfort are always found to have obvious atherosclerosis, more inclined to be located at the left main and proximal LAD, which is a strong predictor of an adverse clinical outcome.
Coronary Angiography ; Coronary Artery Disease ; diagnostic imaging ; pathology ; Diabetes Mellitus ; pathology ; Dyslipidemias ; pathology ; Female ; Humans ; Hypertension ; pathology ; Middle Aged ; Postmenopause ; Premenopause
3.Elevated alanine aminotransferase activity is not associated with dyslipidemias, but related to insulin resistance and higher disease grades in non-diabetic non-alcoholic fatty liver disease.
Mohammad Ebrahim GHAMAR-CHEHREH ; Mohsen AMINI ; Hossein KHEDMAT ; Seyed Moayed ALAVIAN ; Fatemeh DARAEI ; Reza MOHTASHAMI ; Reza HADI ; Bent-Al-Hoda BEYRAM ; Saeed TAHERI
Asian Pacific Journal of Tropical Biomedicine 2012;2(9):702-706
OBJECTIVETo explore demographic and metabolic factors associated with increased alanine aminotransferase (ALT) activity in non-diabetic non-alcoholic fatty liver disease (NAFLD) patients.
METHODSOverall 372 patients who consecutively attended to Gastroenterology Clinic of Baqiyatallah University of Medical Sciences, Tehran, Iran awere diagnosed as NAFLD entered into analysis. Exclusion criteria were having diabetes mellitus and fasting blood glucose over 126 mg/dL, active hepatitis B virus infection, having hepatitis C virus positive serology, and to be under corticosteroid therapy. ALT levels were considered pathologically high when it was over 30 IU/L for men and over 19 IU/L for women.
RESULTSBivariate analyses using t test and chi-square test showed that patients with pathologically augmented ALT levels had significantly higher NAFLD grades in their ultrasonographic evaluations (P=0.003). Moreover, these patients represented significantly higher homeostatic model assessment levels (P=0.003), levels of serum insulin (P=0.002), fasting blood glucose (P<0.001), and uric acid (P=0.02). The prevalence of insulin resistance was also higher in patients with increased serum ALT concentrations. Multifactorial logistic regression models showed that ultrasonographic grading of NAFLD (P=0.027) and insulin resistance (P=0.013) were the only variables significantly associated with abnormal ALT levels.
CONCLUSIONSThis study shows that the associations of increased ALT serum levels in NAFLD patients are different from what are supposed before. By excluding diabetic patients from our population, we find that increased ALT levels are not associated with dyslipidemias but are independently associated with insulin resistance and NAFLD grading on ultrasonographic evaluations. Further studies are needed to confirm our results.
Adult ; Alanine Transaminase ; metabolism ; Blood Glucose ; Dyslipidemias ; metabolism ; Female ; Humans ; Insulin Resistance ; Male ; Middle Aged ; Non-alcoholic Fatty Liver Disease ; diagnostic imaging ; metabolism ; pathology ; Risk Factors ; Ultrasonography
4.Efficacy of fenofibrate for hepatic steatosis in rats after severe burn.
Zongwei HUANG ; Chengyue MENG ; Jing CHEN ; Yajie CHEN ; Yu CHEN ; Tao ZHOU ; Chao YANG
Chinese Journal of Burns 2016;32(5):277-282
OBJECTIVETo observe the efficacy of fenofibrate for hepatic steatosis in rats after severe burn.
METHODSTwenty-seven male SD rats were divided into sham injury group, burn group, and burn+ fenofibrate group according to the random number table, with 9 rats in each group. Rats in sham injury group were sham injured on the back by immersing in 37 ℃ warm water for 15 s and then remained without other treatment. Rats in burn group and burn+ fenofibrate group were inflicted with 30% total body surface area full-thickness scald (hereinafter referred to as burn) on the back by immersing in 98 ℃ hot water for 15 s, and then they were intraperitoneally injected with lactated Ringer's solution at post injury hour (PIH) 1. From PIH 24 to post injury day (PID) 8, rats in burn+ fenofibrate group were treated with fenofibrate in the dose of 80 mg·kg(-1)·d(-1), while those in burn group were treated with equivalent volume of saline. (1) Three rats of each group were respectively selected on PID 4, 6, and 8 for the collection of inferior vena caval blood samples. Serum content of total cholesterol (TC), triglyceride (TG), free fatty acid (FFA), high density lipoprotein (HDL), and low density lipoprotein (LDL) was determined with fully automatic biochemical analyzer. Body mass of each rat was measured immediately after blood sampling, and then rats were sacrificed to collect liver tissue for weighing wet mass. The ratio of wet mass of liver tissue to body mass (liver index) was calculated. Meanwhile, gross observation of liver was performed. (2) One liver tissue sample was harvested from each rat at each time point to observe histopathologic changes with HE staining. One liver tissue slice of each rat at each time point was collected to evaluate degree of hepatic steatosis, and the number of rats in each group in each grade of hepatic steatosis was recorded. Measurement data were processed with analysis of variance of factorial design and SNK test, and enumeration data were processed with Kruskal-Wallis test and Nemenyi test.
RESULTS(1) The content of TC, TG, FFA, and HDL of rats in burn group on PID 4 was obviously different from that in sham injury group (with P values below 0.05). Compared with that in burn group, the content of TC, TG, and FFA of rats was significantly decreased (with P values below 0.05), while the content of HDL of rats was not obviously changed in burn+ fenofibrate group on PID 4 (P>0.05). There were no obvious differences in the content of LDL of rats among 3 groups on PID 4 (with P values above 0.05). The content of TC, TG, and HDL of rats in burn group on PID 6 was obviously different from that in sham injury group (with P values below 0.05). Compared with that in burn group, the content of TC and TG of rats was significantly decreased (with P values below 0.05), while the content of HDL of rats was significantly increased in burn+ fenofibrate group on PID 6 (P<0.05). There were no obvious differences in the content of FFA and LDL of rats among 3 groups on PID 6 (with P values above 0.05). The content of TC and HDL of rats in burn group on PID 8 was obviously different from that in sham injury group (with P values below 0.05). Compared with that in burn group, the content of TC of rats was significantly decreased (P<0.05), while the content of HDL of rats was not obviously changed in burn+ fenofibrate group on PID 8 (P>0.05). There were no obvious differences in content of TG, FFA, and LDL of rats among 3 groups on PID 8 (with P values above 0.05). (2) The texture of liver tissue of rats in burn+ fenofibrate group at each time point was tender and soft, without oil or fat on the section, which was close to the gross condition of liver of rats in sham injury group. Dark yellow plaque scattered on the surface of liver tissue of rats in burn group at each time point with oil and fat on the section, which was especially obvious on PID 6. There was no obvious difference in liver index of rats among 3 groups on PID 4 (F=1.63, P>0.05). On PID 6 and 8, the liver indexes of rats in sham injury group, burn group, and burn+ fenofibrate group were 0.0416±0.0016, 0.0533±0.0054, and 0.0370±0.0069; 0.0423±0.0034, 0.0624±0.0005, and 0.0444±0.0042 respectively. The liver indexes of rats in burn group on PID 6 and 8 were significantly higher than those in the other two groups (with P values below 0.05). There were no obvious differences in the liver indexes of rats between burn+ fenofibrate group and sham injury group on PID 6 and 8 (with P values above 0.05). (3) The liver tissue structure of rats in sham injury group was normal at each time point. Hepatic steatosis of rats in burn group at each time point appeared microvesicular and disperse, which was especially obvious on PID 6. Mild hepatic steatosis was observed in rats of burn+ fenofibrate group on PID 4, and then the structure of liver tissue gradually recovered to normal level from PID 6 on. The degree of hepatic steatosis of rats in sham injury group was 0 grade. One rat in I grade, 1 rat in II grade, and 7 rats in III grade were observed in hepatic steatosis of rats in burn group. Three rats in 0 grade, 4 rats in I grade, and 2 rats in II grade were observed in hepatic steatosis of rats in burn+ fenofibrate group. The degree of hepatic steatosis of rats in burn group was more severe than that in the other two groups (with χ(2) values respectively 56.25 and 162.44, P values below 0.05). The degree of hepatic steatosis of rats in burn+ fenofibrate group was more severe than that in sham injury group (χ(2)=27.51, P<0.05).
CONCLUSIONSFenofibrate can ameliorate the dyslipidemia of severely burned rat, and it can alleviate the degree of hepatic steatosis in certain degree.
Animals ; Burns ; pathology ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Dyslipidemias ; drug therapy ; Fatty Acids ; blood ; Fenofibrate ; pharmacology ; Liver ; pathology ; Liver Cirrhosis ; drug therapy ; Male ; Rats ; Rats, Sprague-Dawley ; Triglycerides ; blood
5.Electrocardiography series. Non-ischaemic causes of ST segment elevation.
Ivandito KUNTJORO ; Swee Guan TEO ; Kian Keong POH
Singapore medical journal 2012;53(6):367-quiz 371
ST segment elevation is one of the most important electrocardiographic features that need to be recognised. Although ST segment elevation myocardial infarction is one of the main causes of this abnormality, there are other non-ischaemic causes that are also important. We discuss reversible apical ballooning syndrome or Takotsubo cardiomyopathy, pericarditis and a case of ST segment elevation due to 'early repolarisation pattern'.
Cardiology
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methods
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Coronary Angiography
;
methods
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Dyslipidemias
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complications
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Electrocardiography
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methods
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Female
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Humans
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Leukemia, Myeloid, Acute
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complications
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Male
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Middle Aged
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Myelodysplastic Syndromes
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complications
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Myocardial Infarction
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complications
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diagnosis
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Myocardial Ischemia
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pathology
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Prostatic Neoplasms
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complications
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Respiratory Tract Infections
;
complications
6.Apo E4 Genotype as the Alzheimer Indictor in Korean Senior Subjects Aged 50 to 64 Years Old.
Hyunhee OH ; Eunjung SHIN ; Hyunsook KIM ; Yunsook LIM ; Miyoung PARK ; Kkochbyul KIM ; Eunmee KIM ; Myoungsook LEE
The Korean Journal of Nutrition 2007;40(7):593-600
Recent studies described the epsilon 4 allele of apoE confers a two-to fourfold increased risk for late-onset Alzheimer's disease (LOAD), but LOAD pathology does not all fit neatly around apo E. Therefore, the goal of this study was to find the association between Alzheimer and apo E4 genotype in the 107 elderly between 50 to 64 years old who visited to FHWC of Sungshin Women's University. We conducted the questionnaire survey (general & 24 hr dietary recall), anthropometerics (BP, waist & BMI) and blood biochemistry (FBS & lipid profiles). LDL-c and HOMA-IR were calculated by Friedwald's and Matthew's formulas. The apo E genotyping was performed by PCR-RFLP method and subjects were divided into three allele groups (epsilon 3; wild, epsilon 2 & epsilon 4; mutants). The apo E allele frequencies were 7.0% for the epsilon 2, 83.6% for the epsilon 3 and 9.3% for the epsilon 4. In comparison with biochemistry characteristics by apo E genotype, FBS was significantly higher in epsilon 4 (129.2 +/- 6.8) than that in the others (epsilon 2: 117 +/- 7.4, epsilon 3: 107.3 +/- 2.2)(p < 0.01). More than forty percents of epsilon 4 group shown the dyslipidemia [high TG (> 150 mg/dl) & low HDL (< 40 mg/dl: male symbol or < 50 mg/dl: female symbol )]. The cytokines levels such as IL-1beta, IL-6 and TNF-alpha were not different among three apoE alleles. After the adjusting sex, age & dietary fiber, LDL-c level was significantly higher in epsilon 4 (108.3 +/- 7.7) than that in epsilon 2 (100.4 +/- 8.4)(p < 0.05). According to food intake and the recipe on the basis of 24 hr dietary recall, the elderly with epsilon 4 allele took higher intake frequency of the light -colored vegetable (radish, onion & cabbage) and pan-fried foods (sauteed beef and vegetables, stir-fried vienna with vegetables) than the others. We knew that the elderly with epsilon 4 allele had been restricted the calories intakes with high dietary fiber (33.6 + 2.5 g/d) to maintain the normal level of FBS and LDL-c. On next study, the prevalence of Alzheimer's disease in this population who has epsilon 4 allele on the condition of calories restriction will be continually follow-up.
Aged
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Alleles
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Alzheimer Disease
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Apolipoprotein E4*
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Apolipoproteins E
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Biochemistry
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Cytokines
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Dietary Fiber
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Dyslipidemias
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Eating
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Female
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Gene Frequency
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Genotype*
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Humans
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Interleukin-6
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Male
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Middle Aged*
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Onions
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Pathology
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Prevalence
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Surveys and Questionnaires
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Tumor Necrosis Factor-alpha
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Vegetables
7.Helicobacter pylori infection and gastric mucosa change and blood-lipid in people undergoing the physical examination in Changsha.
Zhiheng CHEN ; Canxia XU ; Ling LUO ; Jing XIAO ; Pingting YANG ; Chang LIU
Journal of Central South University(Medical Sciences) 2014;39(3):265-269
OBJECTIVE:
To explore the relationship between the Helicobacter pylori (H.pylori) infection and gastric mucosa change and blood-lipid in people undergoing the physical examination in Changsha.
METHODS:
A total of 2 264 people undergoing physical examination were divided into an H. pyloripositive group (n=1 068) and an H. pylori-negative group (n=1 196). Gastric mucosa change was diagnosed by gastroscopy, blood-lipid and blood sugar were detected, and the statistical analysis was performed.
RESULTS:
The incidence rate of H.pylori infection was 47.2%. The incidence rate of gastric mucosal erosion, gastric ulcer, duodenal ulcer, gastric mucosal atrophy, gastric polyp, dyslipidemia, increase of triglyceride were (TG) and decrease of the high density lipoprotein cholesterol (HDL-C) in the H.pylori-positive group were all higher than those in the H.pylori-negative group (P<0.01 or P<0.05). In the H. pylori-positive group, the level of TG in people with gastric mucosal erosion, gastric ulcer and duodenal ulcer was higher than that in people with normal gastric mucosa or mild gastritis, and HDL-C was lower than that in people with normal gastric mucosa or mild gastritis.
CONCLUSION
H. pylori infection can induce the gastric mucosa injury and dyslipidemia, which may result in the occurrence and development of coronary heart disease by increasing TG and decreasing HDL-C, thus increasing the risk of atherosclerosis.
Adenomatous Polyps
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Cholesterol, HDL
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blood
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Duodenal Ulcer
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microbiology
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physiopathology
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Dyslipidemias
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microbiology
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Gastric Mucosa
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microbiology
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pathology
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Gastritis
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microbiology
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physiopathology
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Helicobacter Infections
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physiopathology
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Helicobacter pylori
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Humans
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Lipids
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blood
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Physical Examination
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Stomach Neoplasms
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Stomach Ulcer
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microbiology
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physiopathology
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Triglycerides
;
blood
8.Study of the relationship between carotid intima-media thickness and traditional Chinese medicine syndrome of dyslipidemia.
Yan LEI ; Zhen-hua WANG ; Hao ZHAO ; Jian-gang LIU
Chinese journal of integrative medicine 2009;15(2):112-116
OBJECTIVEThe study aimed to explore the relationship between the carotid intima-media thickness (IMT), lipids, high-sensitivity C-reactive protein (hs-CRP), homocysteine (Hcy) and other indices of laboratory and the traditional Chinese medicine (TCM) syndrome of dyslipidemia.
METHODSA total of 152 dyslipidemia patients and 8 healthy people (taken as the control group) were recruited. According to the theory of the TCM syndrome, 152 dyslipidemia patients were assigned to 4 groups: the stagnation of phlegm (SP) group, the blood stasis blocking channels (BSBC) group, the stagnation of phlegm and blood (SPB) group and the non-stagnation of phlegm and blood (NSPB) group. The carotid ultrasonic test, hs-CRP, Hcy, blood rheology and blood lipids were examined for all the recruited patients. The relationships among carotid IMT, laboratory indices and TCM syndrome of dyslipidemia were analyzed by the methods of F test and multiple linear regressions.
RESULTS(1) Carotid IMT was significantly different among groups of healthy people and different TCM syndromes. The sequence from lowest to highest was: healthy group, NSPB group, SP group, SPB group and BSBC group. (2) Triglyceride (TG) and blood rheology were significantly different between the groups of healthy people and different TCM syndromes. Among different TCM syndrome groups, TG and blood rheology in the NSPB group were the lowest, but were the highest in SPB group. (3) Hcy, very low density lipoprotein and TG were correlated with atherosclerosis of the carotid.
CONCLUSIONCarotid IMT, TG and blood rheology were closely correlated with the TCM syndrome of dyslipidemia. Atherosclerosis of the carotids would be prone to occur if one of these factors was heightened.
Adult ; Aged ; Biomarkers ; analysis ; blood ; C-Reactive Protein ; analysis ; Carotid Arteries ; anatomy & histology ; diagnostic imaging ; pathology ; Case-Control Studies ; Dyslipidemias ; blood ; diagnosis ; pathology ; Female ; Homocysteine ; analysis ; blood ; Humans ; Male ; Medicine, Chinese Traditional ; methods ; Middle Aged ; Organ Size ; Research Design ; Syndrome ; Triglycerides ; analysis ; blood ; Tunica Intima ; anatomy & histology ; diagnostic imaging ; pathology ; Ultrasonography
9.Research progress on pharmacotherapy of calcific aortic valve disease.
Miaomiao DU ; Gaigai MA ; Yuping SHI
Journal of Zhejiang University. Medical sciences 2016;45(4):432-438
With the population aging and declining incidence of rheumatic heart disease, calcific aortic valve disease (CAVD) has become the most frequent valve disease and the common cause of aortic valve replacement. Patients with CAVD need to cope with a deteriorating quality of life and valve replacement is the only effective clinical option for the patients. Therefore, early pharmacotherapy is of great significance in prevention or slow-down of the progression of CAVD. For years CAVD was considered to be a passive wear and tear process of valves, but now it is recognized as an active and multi-factorial process. Histopathologic studies have revealed that inflammation, disorder of calcium and phosphorus metabolism and dyslipidemia are involved in the process of CAVD. Clinical trials of CAVD pharmacotherapy have been carried out based on those histopathologic studies. Statin, renin-angiotensin inhibitors and anti-osteoporosis drug are well studied in recent years. This article reviews the recent research progress of the pharmacotherapy for CAVD.
Angiotensin Receptor Antagonists
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therapeutic use
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Angiotensin-Converting Enzyme Inhibitors
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therapeutic use
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Aortic Valve
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pathology
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Aortic Valve Stenosis
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complications
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drug therapy
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etiology
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Calcinosis
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complications
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drug therapy
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etiology
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Calcium Metabolism Disorders
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complications
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Disease Progression
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Dyslipidemias
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complications
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Humans
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Hydroxymethylglutaryl-CoA Reductase Inhibitors
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therapeutic use
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Inflammation
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complications
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Phosphorus Metabolism Disorders
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complications
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Quality of Life
10.Therapeutic effect of fibroblast growth factor 21 on NAFLD in MSG-iR mice and its mechanism.
Sheng-Long ZHU ; Zhen-Yu ZHANG ; Gui-Ping REN ; Xian-Long YE ; Lei MA ; Dan YU ; Miao-Miao HAN ; Jing-Zhuang ZHAO ; Tian-Yuan ZHANG ; De-Shan LI
Acta Pharmaceutica Sinica 2013;48(12):1778-1784
This study is to evaluate the therapeutic effect of fibroblast growth factor 21 (FGF21) on NAFLD in MSG-IR mice and to provide mechanism insights into its therapeutic effect. The MSG-IR mice with insulin resistance were treated with high dose (0.1 micromol.kg-1d-1) and low dose (0.025 micromol.kg-1d-1) of FGF21 once a day for 5 weeks. Body weight was measured weekly. At the end of the experiment, serum lipids, insulin and aminotransferases were measured. Hepatic steatosis was observed. The expression of key genes regulating energy metabolism were detected by real-time PCR. The results showed that after 5 weeks treatment, both doses of FGF21 reduced body weight (P<0.01), corrected dyslipidemia (P<0.01), reversed steatosis and restored the liver morphology in the MSG model mice and significantly ameliorated insulin resistance. Additionally, real-time PCR showed that FGF21 significantly reduced transcription levels of fat synthetic genes, decreased fat synthesis and promoted lipolysis and energy metabolism by up-regulating key genes of lipolysis, thereby liver fat accumulation was reduced and liver function was restored to normal levels. In conclusion, FGF21 significantly reduces body weight of the MSG-IR mice, ameliorates insulin resistance, reverses hepatic steatosis. These findings provide a theoretical support for clinical application of FGF21 as a novel therapeutics for treatment of NAFLD.
Animals
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Body Weight
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drug effects
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Dose-Response Relationship, Drug
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Dyslipidemias
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metabolism
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Energy Metabolism
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drug effects
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Fatty Liver
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chemically induced
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complications
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Female
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Fibroblast Growth Factors
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administration & dosage
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pharmacology
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therapeutic use
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Insulin Resistance
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Lipolysis
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drug effects
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Liver
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metabolism
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pathology
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Male
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Mice
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Non-alcoholic Fatty Liver Disease
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drug therapy
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Sodium Glutamate