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<!DOCTYPE ArticleSet PUBLIC "-//NLM//DTD PubMed 2.7//EN" "https://dtd.nlm.nih.gov/ncbi/pubmed/in/PubMed.dtd">
<ArticleSet>
<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2008</Year>
					<Month>12</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>EFFECTS OF COOKED LENTILS ON GLYCEMIC CONTROL AND BLOOD LIPIDS OF PATIENTS WITH TYPE 2 DIABETES</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10077</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Hamidreza</FirstName>
					<LastName>Shams</LastName>
<Affiliation>BSc, Department of Nutrition and Food Science, Shahid Beheshti University of Medical Sciences and Health Services, Tehran.</Affiliation>

</Author>
<Author>
					<FirstName>Farideh</FirstName>
					<LastName>Tahbaz</LastName>
<Affiliation>PhD, Department of Nutrition and Food Science, Shahid Beheshti University of Medical Sciences and Health Services, Tehran.</Affiliation>

</Author>
<Author>
					<FirstName>Mohammad Hassan</FirstName>
					<LastName>Entezari</LastName>
<Affiliation>PhD, Department of Nutrition and Food Science, School of Health, Isfahan University of Medical Sciences &amp; Health Services, Isfahan.</Affiliation>

</Author>
<Author>
					<FirstName>Alireza</FirstName>
					<LastName>Abadi</LastName>
<Affiliation>4) PhD, Department of Social Medicine, Shahid Beheshti University of Medical Sciences and Health Services, Tehran.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Abstract    INTRODUCTION: Diabetes mellitus is the most important endocrine disease worldwide. Scientists recommend consumption of low glycemic index (LGI) foods for prevention and control of diabetess. This study was designed to test the effects of cooked lentil as a LGI food on blood glucose and lipid profile among type 2 diabetic patients.    METHODS: In a randomized cross-over clinical trial, 30 individuals with type 2 diabetes were randomly divided into 2 groups (A and B). At the 1st step, group A followed the normal diet and group B followed normal diet plus 50 g cooked lentil and 6 g canula oil substitute of 30g bread and 20 g cheese. After 6 weeks these two groups stopped their diets and put on wash out period for 3 weeks and later the diets were switched between them and continued for another 6-week-period. Anthropometric measurements, dietary intakes, serum lipids and glucose levels were determined at the beginning and the end of each period. Data was analyzed by Food Processor II and SPSS-13 softwares.    RESULTS: Body mass index, LDL-C, HDL-C ,triglycerides and serum Fructozamine were not significantly influenced by treatment whereas total cholesterol and fasting blood glucose decreased significantly (P &lt; 0.05).    CONCLUSION: Cooked lentil consumption as a LGI food in breakfast can control FBS and serum total cholesterol. It might be a good regimen for improving glycemic control in type 2 diabetic patients.        Keywords: Diabetes mellitus, Lentil, Lipid profiles, Blood glucose, Glycemic index.</Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10077_70803c1acb1ee113c07ec6bddc4929bd.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</Journal>
<ArticleTitle>EARLY AND LATE EFFECT OF HIGH DOSE ATORVASTATIN AND LOW DOSE ATORVASTATIN ON SERUM C - REACTIVE PROTEIN REDUCTION IN NON ST ELEVATION MYOCARDIAL INFARCTION</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10079</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Masoumeh</FirstName>
					<LastName>Sadeghi</LastName>
<Affiliation>Associate Professor of Cardiology, Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.</Affiliation>
<Identifier Source="ORCID">0000-0001-7179-5558</Identifier>

</Author>
<Author>
					<FirstName>Narges</FirstName>
					<LastName>Sadat Razavi</LastName>
<Affiliation>Resident of cardiology, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
<Author>
					<FirstName>Nizal</FirstName>
					<LastName>Sarrafzadegan</LastName>
<Affiliation>Professor of Cardiology, Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
<Author>
					<FirstName>Mahzad</FirstName>
					<LastName>Saeedifar</LastName>
<Affiliation>Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
<Author>
					<FirstName>Mohammad</FirstName>
					<LastName>Talaee</LastName>
<Affiliation>Researcher Methodology and statistic consultant, Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Abstract    INTRODUCTION: Inflammation is now recognized to play an important role at all stages of the atherogenic process that are precursors of myocardial infarction (MI). hs-CRP is one of this markers of inflammation and Statins have both lipid lowering and anti inflammatory effects and it is proposed that aggressive statins treatment can cause lower serum CRP levels. In this study, we compared intensive and moderate atorvastatin treatment effects on mean serum CRP reduction.    METHODS: This study is a double-blind clinical trial. Some patients who were up 21 years old and recently suffered non-ST elevation MI during 24 hours and went to the emergency department of Feiz hospital and/or Chamran hospital and were confined to bed in the CCU were entered in study. A total number of 50 patients were divided to two groups of equal number: A-25 patients under treatment with 80 mg Atorvastatin B-25 patients under treatment with 20 mg Atorvastatin. The examinations hs-CRP and lipid profile were done at admission to CCU, discharge from hospital and two months after treatments and results compared in two groups.    RESULTS: It was specified that in group treated with 80 mg atorvastatin 12 patients (48%) were males and 9 patients (52%) were females and mean age was 60.1 ± 13.4 years. In group treated with 20mg atorvastatin, 16 patients (64%) were males and 9 patients (36%) were males and mean age was 59.6 ± 11.2 years. In group treated with 80mg atorvastatin mean CRP at CCU admission (baseline), discharge and two months latter was 7 ± 5.5, 5.3 ± 4.1 and 2.3 ± 4.3 respectively and in group treated with 20mg atorvastatin was 7.1 ± 8.3, 5.7 ± 7.4 and 3.5 ± 5.1 respectively. Mean  serum LDL (Low density lipoprotein) in patients before and after treatment in group treated with 80 mg atorvastatin was 134.2 ± 33.2 and 117.5 ± 31.9 and  in   group  treated  with  20 mg  atorvastatin  was  141.07 ± 33.4 and 126.4 ± 32.5. Mean serum CRP decreased in both groups after treatment but mean CRP decreased to lower levels in patients treated with 80mg atorvastatin either at discharge from hospital (P = 0.32) or two months after treatment(P = 0.02) compared patients treated with 20mg atorvastatin and this difference between two groups was more significant two months after treatment than at discharge. Also serum LDL was decrease in both groups after treatment but no significant difference was detected (P = 0.77). With Pearson correlation there was correlation between the percent reductions in LDL cholesterol and in CRP levels only for the total patients (P &lt; 0.001), not for the high dose atorvastatin group alone or the low dose atorvastatin group alone (P &gt; 0.05).    CONCLUSION: high dose statins cause lower serum CRP levels and their effect on lowering CRP is separated from their lipid lowering effects and is due to their anti inflammatory effects.        Keywords: atorvastatin, CRP, MI, st elevation MI</Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10079_96e76211d21b66fbdaf1a05498b4417a.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2008</Year>
					<Month>12</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>RELATION OF MICROALBUMINURIA AND CORONARY ARTERY DISEASE IN NON DIABETIC PATIENTS</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10080</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Vida</FirstName>
					<LastName>Nesar Hoseini</LastName>
<Affiliation></Affiliation>

</Author>
<Author>
					<FirstName>Omolbanin</FirstName>
					<LastName>Taziki</LastName>
<Affiliation>FatemeZahra Hospital, Artesh Boulevard, Sari, Mazandaran.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Abstract    INTRODUCTION: Prospective studies confirmed that microalbuminuria is a predictor of cardiovascular diseases, independent of classical risk factors and is associated with all-cause mortality in patients with diabetes or hypertension and in the general population. However, there is few data linking angiographic severity of coronary artery disease (CAD) to microalbuninuria (MA). We examined coronary angiograms for extent of severe CAD (luminal narrowing 50%) in patients without Diabetes Mellitus (DM) and general population.    METHODS: Our study comprised of 153 patients undergoing coronary angiography in Hazrat Fatemeh hospital in Iran (M/F 80/73, mean age 57 ± 11 y). Urine albumin excretion was measured in 24h urine samples by immune precipitation technique. Age-sex, distribution of coronary risk factors and MA were compared between patients with and without CAD.    RESULTS: Overall, 70.5% (108) of patients had CAD and 29.4% (45) had no coronary lesion. MA was detected in 62.9% of patients with CAD and 8.8% of those without coronary artery lesion (P &lt; 0.05). The presence of 1 or 2 vessels CAD showed a linear increase from group to group without microalbuminuria (P &lt; 0.05).    CONCLUSION: Patients with MA have more severe angiographic CAD compared to those without MA. This relation is independent of other risk factors.       Keywords: Coronary artery disease, diabetes, microalbuminuria</Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10080_ebd774c929a7f6c7e5df19e355f61e23.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2008</Year>
					<Month>12</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>C-REACTIVE PROTEIN AND CORONARY CALCIUM SCORE ASSOCIATION IN CORONARY ARTERY DISEASE</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10081</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Ali</FirstName>
					<LastName>Hosseinsabet</LastName>
<Affiliation>Cardiologist, Department of Cardiology, Shaheed Rajaei Cardivascular Center, Vali-e-asr Avenue, Tehran.</Affiliation>

</Author>
<Author>
					<FirstName>Ahmad</FirstName>
					<LastName>Mohebbi</LastName>
<Affiliation>Professor of Cardiology ,Department of Cardiology, Shaheed Rajaei Cardivascular Center, Iran University of Medical Science, Tehran.</Affiliation>

</Author>
<Author>
					<FirstName>Alireza</FirstName>
					<LastName>Almasi</LastName>
<Affiliation>Assistant Professor of Radiology, Department of Rardiology, Shaheed Rajaei Cardivascular Center, Iran University of Medical Science, Tehran.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Abstract    BACKGROUND: Both high-sensitivity C-reactive protein (hs-CRP) and spiral computed tomography coronary artery calcium score (CCS) are valid markers of cardiovascular risk. It is unknown whether hs-CRP is a marker of atherosclerotic burden or whether it reflects a process (eg, inflammatory fibrous cap degradation) leading to acute coronary events.    METHOD AND MATERIALS: In a cross-sectional study, we studied association between hs-CRP and coronary calcium score in 143 patients that were candidate for coronary artery bypass grafting (CABG).    RESULTS: In our study, we found no significant association between hs-CRP and CCS in bivariants (P = 0.162) and multivariable (P = 0.062) analysis but in patients that didn’t take statins, this association was significant and positive in bivariant (P = 0.001) but in multivariant analysis this association was negative and significant (P = 0.008).     CONCLUSION: hs-CRP was not associated with CCS. The relation between CRP and clinical events might not be related to atherosclerotic burden. Markers of inflammation, like CRP, and indices of atherosclerosis, such as CAC, are likely to provide distinct information regarding cardiovascular risk.        Keywords: coronary calcification, inflammation, risk factors, Multislice spiral CT, h-CRP.  </Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10081_725215ed82ab6306919b485b81ff9615.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2008</Year>
					<Month>12</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>CENTRAL OBESITY AS A PREDICTOR OF CORONARY ARTERY OCCLUSION</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10082</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Javad</FirstName>
					<LastName>Ramazani</LastName>
<Affiliation>MD, Cardiology Department, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
<Author>
					<FirstName>Hamid</FirstName>
					<LastName>Sanei</LastName>
<Affiliation>Associate professor, Cardiology Department, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
<Author>
					<FirstName>Masoumeh</FirstName>
					<LastName>Sadeghi</LastName>
<Affiliation>Associate professor, Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.</Affiliation>
<Identifier Source="ORCID">0000-0001-7179-5558</Identifier>

</Author>
<Author>
					<FirstName>Ramin</FirstName>
					<LastName>Hidari</LastName>
<Affiliation>Associated professor, Cardiology Department, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
<Author>
					<FirstName>Poneh</FirstName>
					<LastName>Haghani</LastName>
<Affiliation>Research Assistant, Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Abstract    INTRODUCTION: Central obesity is one of the coronary artery diseases (CAD) risk factors that has been regarded, recently. There are several methods for measuring abdominal obesity. We used abdominal diameter index (ADI) as an index of abdominal obesity and studied its relation to CAD.    METHODS: 180 patients [90 male and 90 female] with CAD were studied in Shahid  Chamran  Hospital affiliated to Isfahan  University of Medical Sciences. Patients were stratified as normal group (without significant occlusion of CAD) and group with coronary artery diseases (over than 75% occlusion in at least one of the coronary arteries: LMA, LAD, RCA, LCX). People with diabetes, hypertension, hyperlipidemia, foot paralysis, edema, hypertriglyceridemia and ascitis were excluded. ADI was compared between groups. The relationship between ADI and coronary artery occlusion was tested in patients with CAD.    RESULTS: The mean of ADI in patients with CAD was significantly higher than normal group (0.52 ±0.85 versus 0.41 ± 0.082 in men and 0.51 ± 0.15 versus 0.42 ± 0.07 in women, respectively) (P &lt; 0.05). Significant correlation was seen between ADI and coronary artery occlusion only in women (P &lt; 0.05). ADI had not any significant correlation with hyperlipidemia, diabetes, high blood pressure, sex, and smoking.    CONCLUSION: It seems that ADI, as an index of central obesity might be included as an independent predictor of CAD. This hypothesis needs large follow up studies to be tested in future.        Keywords: Abdominal diameter, central obesity, waist to hip ratio, coronary artery disease.</Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10082_9b22a40256b079f338827b0ff1f4792b.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</Journal>
<ArticleTitle>RELATION BETWEEN PREECLAMPSIA AND CARDIAC ENZYMES</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10083</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Rubina</FirstName>
					<LastName>Aziz</LastName>
<Affiliation>Department of Biochemistry, Federal Govt Urdu University for Arts, Sciences and Technology, Karachi.</Affiliation>

</Author>
<Author>
					<FirstName>Tabassum</FirstName>
					<LastName>Mahboob</LastName>
<Affiliation>Dr. Tabassum Mahboob Department of Biochemistry, University of Karachi, Karachi.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Abstract    INTRODUCTION: Preeclampsia affects about 5-10% of all pregnancies and is a major cause of maternal, fetal and neonatal mortality and morbidity. The cardiovascular system undergoes a host of changes in association with development of preeclampsia. LDH is a useful biochemical marker that reflects the severity of the occurrence of preeclampsia.    METHOD AND MATERIALS: One hundred pregnant women were selected for this study, 50 normal pregnant women as controls and 50 preeclamptic women as the study group.  Cardiac enzymes (serum LDH, serum AST, serum CK and serum CKMB) of these women were analyzed.    RESULTS: Mean Serum LDH and mean serum AST concentrations were significantly higher in preeclamptic patients compared to normal pregnant women (348.34 ± 59.17 vs. 255.92 ± 43.26, P &lt; 0.01) and (34.32 ± 10.37 vs. 22.06 ± 5.10, P &lt; 0.01) respectively.     CONCLUSION: LDH and AST may be increased due to liver damage. This endothelial vascular damage is the main cause in the occurrence of preeclampsia. Higher levels of LDH and AST are very useful markers to identify the occurrence of preeclampsia.        Keywords: LDH, Preeclampsia, AST, Cardiac Enzymes.</Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10083_c5f79d384b8024d5adddb872f9651f38.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</Journal>
<ArticleTitle>CARDIAC PERFORMANCE IN END STAGE RENAL DISEASE DIABETIC PATIENTS WITH ARTERIOVENOUS FISTULA</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10084</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Ali-Akbar</FirstName>
					<LastName>Beigi</LastName>
<Affiliation>Assistant Professor, Vascular surgery department, Chamran Hospital, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
<Author>
					<FirstName>Alireza</FirstName>
					<LastName>Khosravi</LastName>
<Affiliation>Assistant Professor, Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.</Affiliation>
<Identifier Source="ORCID">0000-0003-0736-2090</Identifier>

</Author>
<Author>
					<FirstName>Amir</FirstName>
					<LastName>Mir-Mohammad Sadeghi</LastName>
<Affiliation>Assistant Professor, Department of General Surgery, Kashan University of Medical Scienses, Kashan.</Affiliation>
<Identifier Source="ORCID">0000-0001-9212-0138</Identifier>

</Author>
<Author>
					<FirstName>Mansour</FirstName>
					<LastName>Safaei</LastName>
<Affiliation>Associate Professor, Department of Surgery, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Abstract    BACKGROUND: Access to vascular system needed for hemodialysis among patients in end stage renal disease (ESRD). Cardiac performance has been affected by chronic renal failure based on several known causes during diseases process. We have compared in this study some of cardiac performance indicators before and after fistulization in diabetic and non-diabetic ESRD patients.    METHODS: Fifty ESRD patients were included in the study. Systolic pulmonary arterial pressure (PAP), cardiac output (CO) and ejection fraction (EF) were measured by echocardiography before fistulization and was repeated at least 8 months after fistulization. Data analyzed in diabetic and non-diabetic patients. RESULTS: Thirty four patients were included in analysis (28 men and 6 women). Mean time of follow up was 10.5 ± 1.3 months. The mean of PAP before and after fistulization was 25.16 mmHg and 21.3 mmHg, respectively in all individuals (P &gt; 0.05). The mean of cardiac output before and after making fistula was 5580 ml/min and 5680 ml/min, respectively (P &lt; 0.05). Diabetic patients showed a significant reduction in their mean of cardiac ejection fraction before and after intervention (EF1 = 66.9%, EF2 = 51.4%) comparing with non-diabetic patients  (EF1 = 58.5, EF2 = 57.5) (P &lt; 0.05). PAP changes and CO changes had not any significant difference between diabetic and non-diabetic patients. DISCUSSION: Fistulization in ESRD patients can improve cardiac performance among these patients. This change may be differing among patients based on the cause of renal failure. Diabetes mellitus may be one of the parameters that can modulate this affect. This should be test in more detailed studies.        Keywords: Fistulization, End Stage Renal Diseases, Cardiac Performance, Diabetes mellitus</Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10084_c1aff6753244c6ee93d489992b51f012.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</Journal>
<ArticleTitle>OBESITY PATTERN IN SOUTH OF IRAN: 2002-2006</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10085</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Hossein</FirstName>
					<LastName>Farshidi</LastName>
<Affiliation>MD. Associate Professor, Cardiology Department, Hormozgan University of Medical Sciences, Bandar Abbas.</Affiliation>

</Author>
<Author>
					<FirstName>Marzieh</FirstName>
					<LastName>Nikparvar</LastName>
<Affiliation>MD. Assistant Professor, Cardiology Department, Hormozgan University of Medical Sciences, Bandar Abbas.</Affiliation>

</Author>
<Author>
					<FirstName>Shahram</FirstName>
					<LastName>Zare</LastName>
<Affiliation>PhD. Associate Professor, Preventive Medicine, Hormozgan University of Medical Sciences, Bandar Abbas.</Affiliation>

</Author>
<Author>
					<FirstName>Elham</FirstName>
					<LastName>Bushehri</LastName>
<Affiliation>M.Sc. Health &amp; Welfare Sciences School, Hormozgan University of Medical Sciences, Bandar Abbas.</Affiliation>

</Author>
<Author>
					<FirstName>Tasnim</FirstName>
					<LastName>Eghbal Eftekhaari</LastName>
<Affiliation>MD. Research Assistant, Hormozgan University of Medical Sciences, Bandar Abbas.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Abstract    INTRODUCTION: The most important factor in mortality and morbidity and disability in most world countries is cardiovascular disease. Preventable risk factors include smoking, hyperlipidemia, hypertension, sedentary life and obesity. Unfortunately, in these eras, obesity is an important health challenge. We assessed the trend of obesity in the southern Iran community.    METHODS: Two cross-sectional community-based studies in 2002 and 2006 in 1% of community aged over 18 years residing in southern Iran were performed. City population was selected using cluster-based sampling. The questionnaires were filled by trained interviewers who went on house visits and obtained variables including age, sex, weight and height using standard measurements. Findings were divided according to WHO criteria as low-weight, normal-weight, overweight and extreme obesity, and morbid obesity; data were analyzed using descriptive statistics and SPSS software.    RESULTS: The population studied in 2002 and 2006 numbered 1500 (956 women and 544 men) and 1329 (943 women and 386 men), respectively. Body mass index in 2002 and 2006 was 24.29 ± 10.9 and 28.24 ± 4.3 kg/m2, respectively which is statistically significant (P &lt; 0.5). Despite the decrease in absolute obesity of the community, the population is faced with statistically significant obesity.    CONCLUSION: Multiple studies have shown the relation between sedentary life and weight gain and loss of health. In comparison with studies in different countries, obesity in south of Iran is alarming, especially as number of overweight women was twice that of men.        Keywords: Obesity, cardiovascular disease, body mass index.  </Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10085_5e62c1998206e0110459a6143546fe2e.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Cardiovascular research institute, Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>ARYA Atherosclerosis Journal</JournalTitle>
				<Issn>1735-3955</Issn>
				<Volume>4</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</Journal>
<ArticleTitle>FACTS ABOUT TRANS FATTY ACIDS</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">10078</ELocationID>
			
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Sedighe</FirstName>
					<LastName>Asgary</LastName>
<Affiliation>Isfahan Cardiovascular Research Center, Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan.</Affiliation>
<Identifier Source="ORCID">0000-0001-7724-4802</Identifier>

</Author>
<Author>
					<FirstName>Bahar</FirstName>
					<LastName>Nazari</LastName>
<Affiliation>Research Assistant, Basic Research Department, Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan.</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2010</Year>
					<Month>12</Month>
					<Day>02</Day>
				</PubDate>
			</History>
		<Abstract>Introduction Fatty acids constitute the main class of lipids in the human diet, being found in nature mainly as glycerol esters that originate triacylglycerols. In the vegetal and animal kingdoms, fatty acids generally have cis unsaturations. In this form, the hydrogens bound to the double bond carbons are on the same side. In another possible configuration, called trans, the hydrogens are bound to un saturations, carbons on opposing sides. Fatty acids with one or more un saturations in the trans configuration are called trans fatty acids (TFAs).1-4      There are two major sources of TFA, those that come from ruminant animals and those that are industrially produced.      The majority of TFAs are found in partially hydrogenated vegetable oils, which contain 10–40% as TFA.5 Hydrogenation is based on the reaction of unsaturated fatty acids of either vegetable or marine oil in the presence of a catalyst, in general nickel. The objective is to increase the oxidative stability of oils by reduction of the concentration of more unsaturated fatty acids and changing their physical properties, thus extending their application. Hydrogenation depends mainly on oil temperature, hydrogen pressure, stirring speed, reaction time, and the catalyst type and concentration. According to the process conditions, hydrogenation is classified as either partial or total and either selective or nonselective.6 It has been estimated that dietary TFAs from partially hydrogenated oils may be responsible for between 30,000 and 100,000 premature coronary deaths per year in the United States.7      The concentration of TFA in meat and milk from ruminants (i.e., cattle, sheep, goats, etc.) contain 3 to 8% of total fat.5 It is hypothesized that ruminant TFAs, or certain TFA isomers from ruminant sources, may confer some health benefits; however, since TFA from animal sources accompany saturated fatty acids (SFA), an increase in a single ruminant TFA in the diet is not appropriate because it will increase SFAs.8 In addition, processes such as edible oil refining, meat irradiation, food frying, also contribute to increase the daily intake of TFA.9,10      Intake of TFAs has been consistently shown in multiple and rigorous randomized trials to have adverse effects on blood lipids, most notably on the LDL: HDL cholesterol ratio, which is a strong cardiovascular risk factor.11-13 When a mixture of TFA isomers, obtained by partial hydrogenation of vegetable oils, is used to replace oleic acid, there is a dose-dependent increase in the LDL: HDL ratio. The relationship between amount of TFA as the percent of energy and the increase in the LDL: HDL ratio appears to be approximately linear (figure 1),12 with no evidence of a threshold at low levels of intake, and with slope twice as steep as that observed by replacing oleic with saturated fats. The average impact of TFA induces changes in the LDL: HDL ratio corresponds to tens of thousands premature deaths in the US alone. Although dramatic, this effect is substantially smaller than the increase in cardiovascular mortality associated with TFA intake in epidemiological studies, suggesting that other mechanisms are likely to be contributing in the toxicity of TFA.11    Figure 1: Results of randomized studies of the influence of industrially produced trans fatty acids (circles) and saturated fat (squares) on the LDL: HDL cholesterol ratio (y-axis). A diet with isocaloric levels of unsaturated fatty acids was used as a comparative basis.12 The x-axis indicates in per cent energy a replacement of unsaturated fat with either saturated fatty acids or industrially produced trans fatty acids.    Besides the increase of the LDL: HDL ratio, TFA increase lipo-protein (a) and triglycerides when substitute saturated fat.13-16 Other reported effects of TFA on blood lipids include alterations in the LDL particle size profile and in the composition of postprandial lipoproteins. The mechanisms mediating the effects of trans fatty acid on blood lipids are still incompletely understood, but may involve opposite effects on ApoA-I and LDL ApoB-100 catabolism.14 N.R. Matthan et al, Dietary hydrogenated fat increases high-density lipoprotein apoA-I catabolism and decreases low-density lipoprotein apoB-100 catabolism in hypercholesterolemic women.17,18      Consumption of TFA predicts higher risk of coronary heart disease, sudden death, cancer and possibly diabetes mellitus.19-22 Additionally, the high consumption of TFA during pregnancy has been associated with effects on intrauterine development.23 TFA may have adverse effects on growth and development by interfering with essential fatty acid metabolism, direct effects on membrane structures or metabolism, or secondary to reducing the intakes of the cis essential fatty acids in either mother or child. TFA are transported across the placenta and secreted in human milk in amounts that depend on the maternal dietary intake.24-26 Inverse associations have been shown between TFA and the essential n − 6 and n − 3 fatty acids in newborn infants, human milk and preschool children. It supports the need to reduce industrially produced TFA and improve dietary fat quality, particularly by increasing intake of n − 3 fatty acids. The use of partially hydrogenated fats and oils by industry, particularly in baked and processed foods that are widely consumed by women and children result in exposure to TFA in amounts shown to have adverse health effects on blood lipids and inflammatory markers in adults. In addition, high exposure to TFA is consistently related to lower levels of Docosahexaenoic acid, a fatty acid that is crucial for normal neural development and function.24,27-29      It has also been observed a rise in allergic diseases upon the high ingestion of this fatty acid.30 These associations are greater than would be predicted by effects of TFA on serum lipoproteins alone. Systemic inflammation and endothelial dysfunction may be involved in the pathogenesis of atherosclerosis, acute coronary syndromes, sudden death, insulin resistance, dyslipidemia, and heart failure. Fatty acids may also directly or indirectly modulate metabolic and inflammatory responses of the endoplasmic reticulum 31 (Figure 2). Evidence from both observational and experimental studies indicates that TFA are pro-inflammatory.  Inflammation is an independent risk factor for cardiovascular diseases (CVD). Epidemiologic studies have suggested that TFA may have an adverse effect on inflammatory markers. In the Nurses’ Health Study, TFA intake, assessed by semi-quantitative food - frequency questionnaires, was  positively associated with tumor necrosis factor receptor (TNFR) levels in healthy women (P for trend &lt; 0.001), and was also associated with levels of C-reactive protein (CRP) and IL-6 in women with higher BMI (P &lt; 0.05) [32-35]. Limited evidence suggests that pro-inflammatory effects may be stronger for trans isomers of linoleic acid (trans-C18:2) and oleic acid (trans-C18:1), rather than of palmitoleic acid (trans-C16:1), but further study of potential isomer-specific effects is needed. TFA also appear to induce endothelial dysfunction. The mechanisms underlying this effect is not well-established, but may involve TFA incorporation into endothelial cell, monocyte/macrophage, or adipocyte cell membranes (affecting membrane signaling pathway relating to inflammation) or ligand-dependent effects on peroxisome proliferator-activated receptor (PPAR) or retinoid X receptor (RXR) pathways.36,37 Activation of inflammatory responses and endothelial dysfunction may represent important mediating pathways between TFA consumption and risk of coronary heart disease, sudden death, and diabetes.16      The possibility that TFAs decrease the threshold for cardiac arrhythmias has been supported by the results from a more recent case control study of the risk of sudden cardiac death. When levels of TFAs in red blood cells as a marker for trans fatty acid intake were compared in 179 cases of sudden cardiac death with 285 controls, it was found that dietary levels of TFAs were associated with a moderately increased risk and that levels of trans linoleic acids were associated with a markedly increased risk of sudden cardiac death.38 The mechanism behind this finding can theoretically be related to changes in the fatty acid composition of muscle cell membranes39-42 (Figure 2). This affects the function of the ion channels, which are important for the formation and propagation of the electrical impulses in the cells.      Numerous expert committees have made evidence-based statements that recommend limiting dietary TFA intake; Institute of Medicine, TFA consumption should be as low as possible.43Dietary Guidelines Advisory Committee (DGAC), TFA consumption by all population groups should be kept as low as possible, which is about 1% of energy intake or less.44 Dietary Guidelines for Americans, keep TFA consumption as low as possible.45WHO/FAO report, Diet, Nutrition, and Chronic Disease, the population nutrient intake goal for TFA is less than 1% of energy from TFA.46International Society for the Study of Fatty Acids and Lipids (ISSFAL), the maximum level of TFA should be 1% of energy.47Nutrition and Diet for Healthy Lifestyles in Europe, EURODIET, a population goal of less than 2% energy from TFA.48UK Ministry of Agriculture, less than 2% of energy.49Netherlands Health Council, less than 1% of energy intake should be from TFA.50National Cholesterol Education Program, intakes of TFA should be kept low.51American Heart Association (AHA), less than 1% of energy as TFA.52American Diabetes Association, intake of TFA should be minimized.53      Thus, according to the American Heart Association, the best message for consumers presently is limitation of dietary TFA, SFA, and cholesterol by following a healthy overall dietary pattern that emphasizes fruits, vegetables, whole-grain foods, fat free and low fat dairy products, lean meats, poultry and fish twice a week. Following this dietary pattern will limit TFA and SFA intake and is consistent with current dietary recommendations made by many organizations worldwide.8      Elimination of hydrogenation of vegetable oils represents a cost-effective means of improving heath. It also avoids destruction of essential polyunsaturated fatty acids.7      Review articles have special structure that is not considered in this article. A review article begin with introduction that explain the aim of this review clearly, then it continues with the description of the subject using other articles, it is necessary to explain how did you extract other articles, which data banks you used for search and what     Figure 2. Potential Physiological Effects of Trans Fatty Acids.    was the inclusion and exclusion criteria of articles you used for your review. Finally you should have a clear conclusion that persuades the readers of your review. Usually review article is written by an expert person that is about that subject. Changes in hepatocyte production, secretion, and catabolism of lipoproteins, together with effects on plasma cholesteryl ester transfer protein (CETP), probably account for adverse effects of trans fatty acids on serum lipid levels (Panel A). The effect on CETP is probably not direct but mediated through effects on membrane or nuclear receptors (dashed line). Trans fatty acids also alter fatty acid metabolism and, possibly, inflammatory responses of adipocytes. In addition, nitric oxide–dependent endothelial dysfunction and increased levels of circulating adhesion molecules (soluble intercellular adhesion molecule 1 [sICAM-1] and soluble vascular-cell adhesion molecule 1 [sVCAM-1]) are seen with trans fat intake. Trans fatty acids also modulate monocyte and macrophage activity (Panel D), as manifested by increased production of inflammatory mediators. Each of these effects has been seen in controlled studies in humans and may, individually or in concert, increase the risk of atherosclerosis, plaque rupture, sudden death from cardiac causes, and diabetes. The subcellular mechanisms for these effects are not well established, but they may be mediated by effects on membrane receptors that localize with and are influenced by specific membrane phospholipids (Panel B), such as endothelial nitric oxide (NO) synthase or toll-like receptors; by direct binding of trans fatty acids to nuclear receptors regulating gene transcription, such as liver X receptor (Panel C); and by direct or indirect effects on endoplasmic reticulum (ER) responses, such as activation of Jun N-terminal kinase (JNK). Such hypothesized subcellular pathways — which have been shown to exist for other fatty acids — require further investigation. TNF- denotes tumor necrosis factor , ROS reactive oxygen species, NF-B nuclear factor B, and mRNA messenger RNA.</Abstract>
<ArchiveCopySource DocType="pdf">https://arya.mui.ac.ir/article_10078_2754518221cfbc8d25c13a06a4cb8421.pdf</ArchiveCopySource>
</Article>
</ArticleSet>
