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<ArticleSet>
<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>32</Volume>
				<Issue>301</Issue>
				<PubDate PubStatus="epublish">
					<Year>2014</Year>
					<Month>10</Month>
					<Day>23</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Index</ArticleTitle>
<VernacularTitle>Index</VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">14429</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2015</Year>
					<Month>08</Month>
					<Day>26</Day>
				</PubDate>
			</History>
		<Abstract>Click to download the index of this issue.</Abstract>
			<OtherAbstract Language="FA">Click to download the index of this issue.</OtherAbstract>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_14429_3574cbb1010b32b07dd7f645153ee35c.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>32</Volume>
				<Issue>301</Issue>
				<PubDate PubStatus="epublish">
					<Year>2014</Year>
					<Month>10</Month>
					<Day>23</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Identification and Frequency of Colistin-Resistant Acintobacter Baumanii in Clinical Isolates Using Polymerase Chain Reaction</ArticleTitle>
<VernacularTitle>Identification and Frequency of Colistin-Resistant Acintobacter Baumanii in Clinical Isolates Using Polymerase Chain Reaction</VernacularTitle>
			<FirstPage>1466</FirstPage>
			<LastPage>1474</LastPage>
			<ELocationID EIdType="pii">14430</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Rozita</FirstName>
					<LastName>Yousefian</LastName>
<Affiliation>MSc Student, Department of Microbiology, School of Biology, Islamic Azad University, Falavarjan Branch, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0002-3765-8151</Identifier>

</Author>
<Author>
					<FirstName>Vajihe</FirstName>
					<LastName>Karbasizade</LastName>
<Affiliation>Assistant Professor, Department of Microbiology, School of Biology, Falavarjan Branch, Islamic Azad University, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0002-3765-8151</Identifier>

</Author>
<Author>
					<FirstName>Sharareh</FirstName>
					<LastName>Moghim</LastName>
<Affiliation>Associate Professor, Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0002-7134-3145</Identifier>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2014</Year>
					<Month>05</Month>
					<Day>10</Day>
				</PubDate>
			</History>
		<Abstract>Background: Antibiotic resistance among bacterial agents causing nosocomial infections is increasing. Acinetobacter baumannii is one of these agents that its increasing resistance to commonly used antibiotics makes it difficult to treat such infections. The aim of this study was to identify Acinetobacter baumannii isolates from clinical specimens using polymerase chain reaction (PCR) method and to determine relative frequency of colistin-resistant isolates.Methods: In a period of 7 months, 96 clinical specimens were isolated. All isolates were identified as Acinetobacter baumannii via standard biochemical tests and amplification of blaoxa-51 gene. To determine phenotypic resistance of isolates toward colistin, colony screening method was used and also minimum inhibitory concentration (MIC) of colistin was determined via broth microdilution.Findings: 51 isolates (53.1%) were resistant to colistin phenotypically and the minimum inhibitory concentration level for colistin resistant strains was more than 128 µg/ml.Conclusion: Based on our findings, the relative frequency of colistin-resistant Acinetobacter baumannii isolates was high. Therefore, more supervision and controlled use of this antibiotic is necessary; more infection control measurements are necessary to be done.</Abstract>
			<OtherAbstract Language="FA">Background: Antibiotic resistance among bacterial agents causing nosocomial infections is increasing. Acinetobacter baumannii is one of these agents that its increasing resistance to commonly used antibiotics makes it difficult to treat such infections. The aim of this study was to identify Acinetobacter baumannii isolates from clinical specimens using polymerase chain reaction (PCR) method and to determine relative frequency of colistin-resistant isolates.Methods: In a period of 7 months, 96 clinical specimens were isolated. All isolates were identified as Acinetobacter baumannii via standard biochemical tests and amplification of blaoxa-51 gene. To determine phenotypic resistance of isolates toward colistin, colony screening method was used and also minimum inhibitory concentration (MIC) of colistin was determined via broth microdilution.Findings: 51 isolates (53.1%) were resistant to colistin phenotypically and the minimum inhibitory concentration level for colistin resistant strains was more than 128 µg/ml.Conclusion: Based on our findings, the relative frequency of colistin-resistant Acinetobacter baumannii isolates was high. Therefore, more supervision and controlled use of this antibiotic is necessary; more infection control measurements are necessary to be done.</OtherAbstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">Acinetobacter baumannii</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Colistin, Nosocomial infections</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Polymerase chain reaction (PCR)</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_14430_48090e338b20a9d004c2ef18a335f3cf.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>32</Volume>
				<Issue>301</Issue>
				<PubDate PubStatus="epublish">
					<Year>2014</Year>
					<Month>10</Month>
					<Day>23</Day>
				</PubDate>
			</Journal>
<ArticleTitle>The Effects of Macronutrient Intake on the Risk of Pre-Diabetes in First-Degree Relatives of Patients with Type 2 Diabetes</ArticleTitle>
<VernacularTitle>The Effects of Macronutrient Intake on the Risk of Pre-Diabetes in First-Degree Relatives of Patients with Type 2 Diabetes</VernacularTitle>
			<FirstPage>1475</FirstPage>
			<LastPage>1486</LastPage>
			<ELocationID EIdType="pii">14431</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Akram</FirstName>
					<LastName>Yazdani</LastName>
<Affiliation>MSc Student, Department of Epidemiology and Biostatistics, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0002-7217-0282</Identifier>

</Author>
<Author>
					<FirstName>Marjan</FirstName>
					<LastName>Mansourian</LastName>
<Affiliation>Assistant Professor, Department of Epidemiology and Biostatistics, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Elham</FirstName>
					<LastName>Faghihimani</LastName>
<Affiliation>Isfahan Endocrinology and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Maryam</FirstName>
					<LastName>Zareh</LastName>
<Affiliation>Isfahan Endocrinology and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Masoud</FirstName>
					<LastName>Amini</LastName>
<Affiliation>Professor, Isfahan Endocrinology and Metabolism Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2014</Year>
					<Month>06</Month>
					<Day>06</Day>
				</PubDate>
			</History>
		<Abstract>Background: Previous studies showed that pre-diabetes often occurs prior to the incidence of type 2 diabetes. Accordingly, lifestyle modification has been suggested to prevent or delay the development of diabetes. The purpose of this study was to identify the impact of macronutrients consumption on recurrent events of pre-diabetes.Methods: This historical cohort study was performed for 9 years on first-degree relatives of patients with type 2 diabetes  attending to Isfahan endocrine and metabolism research center, Iran. The attendees completed laboratory tests including standard 75 g 2-hour current oral glucose tolerance test (OGTT). The outcome variables were the recurrence of a pre-diabetes event during follow-up and the assessed explanatory variables included protein, fat and carbohydrates intake, and a broad set of potential confounding variables were age categories, sex, overweight (body mas index or BMI), large waist-to-hip ratio (WHR), high-density lipoprotein (HDL), triglycerides, total cholesterol, high blood pressure, and low fiber intake. We considered the shared gamma frailty model to evaluate the association between recurrent pre-diabetes and explanatory variables. The R-software (version 2.15.2) was used to fit the models.Findings: Individuals with greater carbohydrate had a significantly higher hazard of recurrent pre-diabetes (hazard ratio = 1.04), adjusted by other variables. The hazards of recurrent pre-diabetes for individuals with fat intake of 25-35 unit were 1.52 higher than individuals with fat intake of lower than 25 unit; and for individuals with fat intake of more than 35 unit, hazards were 2.22 higher than individuals with fat intake of lower than 25 unit. Individuals with greater protein had a significantly higher hazard of recurrent pre-diabetes (hazard ratio = 1.05), adjusted by other variables.Conclusion: Macronutrient consumption can affect the metabolism of fat and glucose and cause changes in insulin resistance. The results of this study showed that macronutrients are effective in controlling diabetes. Further studies are recommended to achieve more accurate results. </Abstract>
			<OtherAbstract Language="FA">Background: Previous studies showed that pre-diabetes often occurs prior to the incidence of type 2 diabetes. Accordingly, lifestyle modification has been suggested to prevent or delay the development of diabetes. The purpose of this study was to identify the impact of macronutrients consumption on recurrent events of pre-diabetes.Methods: This historical cohort study was performed for 9 years on first-degree relatives of patients with type 2 diabetes  attending to Isfahan endocrine and metabolism research center, Iran. The attendees completed laboratory tests including standard 75 g 2-hour current oral glucose tolerance test (OGTT). The outcome variables were the recurrence of a pre-diabetes event during follow-up and the assessed explanatory variables included protein, fat and carbohydrates intake, and a broad set of potential confounding variables were age categories, sex, overweight (body mas index or BMI), large waist-to-hip ratio (WHR), high-density lipoprotein (HDL), triglycerides, total cholesterol, high blood pressure, and low fiber intake. We considered the shared gamma frailty model to evaluate the association between recurrent pre-diabetes and explanatory variables. The R-software (version 2.15.2) was used to fit the models.Findings: Individuals with greater carbohydrate had a significantly higher hazard of recurrent pre-diabetes (hazard ratio = 1.04), adjusted by other variables. The hazards of recurrent pre-diabetes for individuals with fat intake of 25-35 unit were 1.52 higher than individuals with fat intake of lower than 25 unit; and for individuals with fat intake of more than 35 unit, hazards were 2.22 higher than individuals with fat intake of lower than 25 unit. Individuals with greater protein had a significantly higher hazard of recurrent pre-diabetes (hazard ratio = 1.05), adjusted by other variables.Conclusion: Macronutrient consumption can affect the metabolism of fat and glucose and cause changes in insulin resistance. The results of this study showed that macronutrients are effective in controlling diabetes. Further studies are recommended to achieve more accurate results. </OtherAbstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">Carbohydrate</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Fat</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Macronutrient</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Pre-diabetes</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Protein</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_14431_6e2c22ab08479b1da4206a0c5d7da31e.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>32</Volume>
				<Issue>301</Issue>
				<PubDate PubStatus="epublish">
					<Year>2014</Year>
					<Month>10</Month>
					<Day>23</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Frequency of c-MPL and JAK2V617F Mutations in Iranian Patients with Philadelphia-Negative Myeloproliferative Disorders and its Association with Clinical and Laboratory Findings</ArticleTitle>
<VernacularTitle>Frequency of c-MPL and JAK2V617F Mutations in Iranian Patients with Philadelphia-Negative Myeloproliferative Disorders and its Association with Clinical and Laboratory Findings</VernacularTitle>
			<FirstPage>1487</FirstPage>
			<LastPage>1495</LastPage>
			<ELocationID EIdType="pii">14432</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Abbas</FirstName>
					<LastName>Ghotaslou</LastName>
<Affiliation>MSc Student, Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Fatemeh</FirstName>
					<LastName>Nadali</LastName>
<Affiliation>Associate Professor, Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Bahram</FirstName>
					<LastName>Chahardouli</LastName>
<Affiliation>Hematology-Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Ali</FirstName>
					<LastName>Ghasemi</LastName>
<Affiliation>MSc Student, Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Sadegh</FirstName>
					<LastName>Abbasian</LastName>
<Affiliation>MSc Student, Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Kazem</FirstName>
					<LastName>Ghaffari</LastName>
<Affiliation>MSc Student, Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Shahrbanoo</FirstName>
					<LastName>Rostami</LastName>
<Affiliation>Hematology-Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2014</Year>
					<Month>08</Month>
					<Day>04</Day>
				</PubDate>
			</History>
		<Abstract>Background: Myeloproliferative disorders are a group of diseases characterized by increased proliferation of myeloid lineage. In addition to JAK2V617F mutation, several mutations in the c-MPL gene were described in patients with Philadelphia-negative Chronic Myeloproliferative disorders  (Ph-negative MPNs) that could be important in the pathogenesis of diseases. The aim of the present study was to investigate the frequency of c-MPL and JAK2V617F mutations in Iranian patients with Philadelphia-negative Myeloproliferative disorders.Methods: Peripheral blood samples from 60 patients with Philadelphia-negative Myeloproliferative disorders, subgroups of essential thrombocythemia (ET) and primary myelofibrosis (PMF) and 25 healthy subjects, as control, were taken. In order to investigate the mutation status of c-MPL and Jak2 V617F via using sequencing, the amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) and allele specific-polymerase chain reaction (AS-PCR) were used.Findings: Of the total of 60 patients, 34 (56.6%) and 1 (1.7%) had Jak2V617F and c-MPL mutations, respectively. Patients with Jak2V617F mutation had higher white blood cell (WBC) counts (P = 0.005) and hemoglobin concentrations than those without the mutation (P = 0.003). In addition, for all healthy subjects in control group, mutation was negative.Conclusion: The present study revealed that the c-MPL mutations, unlike the Jak2V617F mutations, are rare in Iranian patients with Philadelphia-negative Chronic Myeloproliferative disorders and the low mutation rate should be considered in the design of screening strategies of patients with myeloproliferative disorders.</Abstract>
			<OtherAbstract Language="FA">Background: Myeloproliferative disorders are a group of diseases characterized by increased proliferation of myeloid lineage. In addition to JAK2V617F mutation, several mutations in the c-MPL gene were described in patients with Philadelphia-negative Chronic Myeloproliferative disorders  (Ph-negative MPNs) that could be important in the pathogenesis of diseases. The aim of the present study was to investigate the frequency of c-MPL and JAK2V617F mutations in Iranian patients with Philadelphia-negative Myeloproliferative disorders.Methods: Peripheral blood samples from 60 patients with Philadelphia-negative Myeloproliferative disorders, subgroups of essential thrombocythemia (ET) and primary myelofibrosis (PMF) and 25 healthy subjects, as control, were taken. In order to investigate the mutation status of c-MPL and Jak2 V617F via using sequencing, the amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) and allele specific-polymerase chain reaction (AS-PCR) were used.Findings: Of the total of 60 patients, 34 (56.6%) and 1 (1.7%) had Jak2V617F and c-MPL mutations, respectively. Patients with Jak2V617F mutation had higher white blood cell (WBC) counts (P = 0.005) and hemoglobin concentrations than those without the mutation (P = 0.003). In addition, for all healthy subjects in control group, mutation was negative.Conclusion: The present study revealed that the c-MPL mutations, unlike the Jak2V617F mutations, are rare in Iranian patients with Philadelphia-negative Chronic Myeloproliferative disorders and the low mutation rate should be considered in the design of screening strategies of patients with myeloproliferative disorders.</OtherAbstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">Amplification refractory mutation system-polymerase chain reaction (ARMS-PCR)</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">c-MPL mutation</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">JAK2V617F</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Myeloproliferative disorders</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_14432_e9bbcc76e4c32d0a1276efc5e6c1d6c8.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>32</Volume>
				<Issue>301</Issue>
				<PubDate PubStatus="epublish">
					<Year>2014</Year>
					<Month>10</Month>
					<Day>23</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Identification New Angiotansin-1 Converting Enzyme Inhibitory Peptide from Ostrich Egg White Protein Hydrolysate</ArticleTitle>
<VernacularTitle>Identification New Angiotansin-1 Converting Enzyme Inhibitory Peptide from Ostrich Egg White Protein Hydrolysate</VernacularTitle>
			<FirstPage>1496</FirstPage>
			<LastPage>1508</LastPage>
			<ELocationID EIdType="pii">14433</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Masoud</FirstName>
					<LastName>Homayouni-Tabrizi</LastName>
<Affiliation>PhD Student, Department of Biology, Islamic Azad University, Science and Research Branch, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Ahmad</FirstName>
					<LastName>Asoodeh</LastName>
<Affiliation>Associate Professor, Department of Chemistry, School of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Mohammad-Reza</FirstName>
					<LastName>Abbaszadegan</LastName>
<Affiliation>Professor, Department of Human Genetics, Immunology Research Center, Avicenna Research Institute AND Medical Genetics Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Khadijeh</FirstName>
					<LastName>Shahrokhabadi</LastName>
<Affiliation>Assistant Professor, Department of Biology, School of Sciences, Islamic Azad University, Mashhad Branch, Mashhad, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Mahboobeh</FirstName>
					<LastName>Nakhaei Moghaddam</LastName>
<Affiliation>Assistant Professor, Department of Biology, School of Sciences, Islamic Azad University, Mashhad Branch, Mashhad, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2014</Year>
					<Month>08</Month>
					<Day>06</Day>
				</PubDate>
			</History>
		<Abstract>Background: Due to the side effects of anti-hypertension drugs, extracting bioactive peptides from natural sources is of great importance. The mail goal of this study was identifying a peptide for enzyme hydrolytic of ostrich egg white protein hydrolysate (OEWPH) and investigating its inhibitory effects on angiotansin-1 converting enzyme (ACE).Methods: The ostrich egg white protein hydrolysate was prepared using pepsin and pancreatin and then fractionated using evaluated reveres-phase high-performance liquid chromatography (RP-HPLC). Tandem mass analysis of the puriﬁed peptide was used to reveal peptide sequence. ACE inhibitory effect and kinetic parameters of the reaction in the presence of the peptide was evaluated. Molecular docking was used to determine the interaction parameters of ACE-peptide comp.Findings: Peptide sequencing of the selected peptide revealed a DAESLSRLLG (MW = 1060/18 Da) and named DG-10. The DG-10 peptide showed a potent inhibitory effect on ACE with the half maximal inhibitory concentration (IC50) value of 0.133 mg/ml. Lineweaver-Burk plot exhibited a non-competitive behavior in the presence of the DG-10 peptide. Molecular interactions and energy binding of the peptide with ACE were investigated via molecular docking.Conclusion: The DG-10 peptide isolated from ostrich egg white protein hydrolysate displayed a potent inhibitory effect on ACE.</Abstract>
			<OtherAbstract Language="FA">Background: Due to the side effects of anti-hypertension drugs, extracting bioactive peptides from natural sources is of great importance. The mail goal of this study was identifying a peptide for enzyme hydrolytic of ostrich egg white protein hydrolysate (OEWPH) and investigating its inhibitory effects on angiotansin-1 converting enzyme (ACE).Methods: The ostrich egg white protein hydrolysate was prepared using pepsin and pancreatin and then fractionated using evaluated reveres-phase high-performance liquid chromatography (RP-HPLC). Tandem mass analysis of the puriﬁed peptide was used to reveal peptide sequence. ACE inhibitory effect and kinetic parameters of the reaction in the presence of the peptide was evaluated. Molecular docking was used to determine the interaction parameters of ACE-peptide comp.Findings: Peptide sequencing of the selected peptide revealed a DAESLSRLLG (MW = 1060/18 Da) and named DG-10. The DG-10 peptide showed a potent inhibitory effect on ACE with the half maximal inhibitory concentration (IC50) value of 0.133 mg/ml. Lineweaver-Burk plot exhibited a non-competitive behavior in the presence of the DG-10 peptide. Molecular interactions and energy binding of the peptide with ACE were investigated via molecular docking.Conclusion: The DG-10 peptide isolated from ostrich egg white protein hydrolysate displayed a potent inhibitory effect on ACE.</OtherAbstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">Angiotansin-1 converting enzyme (ACE)</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Ostrich egg white protein hydrolysate (OEWPH)</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Peptide</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_14433_4915f20d2c36611cb101e95e5c34b4e7.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>32</Volume>
				<Issue>301</Issue>
				<PubDate PubStatus="epublish">
					<Year>2014</Year>
					<Month>10</Month>
					<Day>23</Day>
				</PubDate>
			</Journal>
<ArticleTitle>An Overview on the Evolution of Language and Genetics of Speech Disorders</ArticleTitle>
<VernacularTitle>An Overview on the Evolution of Language and Genetics of Speech Disorders</VernacularTitle>
			<FirstPage>1509</FirstPage>
			<LastPage>1529</LastPage>
			<ELocationID EIdType="pii">14434</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Seyyed Mohammad</FirstName>
					<LastName>Mousavi</LastName>
<Affiliation>Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord AND General Office of Legal Medicine, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Elaheh</FirstName>
					<LastName>Kamali</LastName>
<Affiliation>PhD Student, Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Padideh</FirstName>
					<LastName>Karimi</LastName>
<Affiliation>PhD Student, Department of Genetics, School of Biological Sciences, Tarbiat Modares University, Tehran, Iran</Affiliation>
<Identifier Source="ORCID">0000-0003-0675-7373</Identifier>

</Author>
<Author>
					<FirstName>Mansour</FirstName>
					<LastName>Salehi</LastName>
<Affiliation>Associate Professor, Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences AND Medical Genetics Center of Genome, Isfahan, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2013</Year>
					<Month>12</Month>
					<Day>29</Day>
				</PubDate>
			</History>
		<Abstract>Language, as an exclusive salient of human kind, is the requisite of development and formation of the human society; thus, it is at the topmost of human evolutionary features. Language and speech can be studied in various fields such as biology. Biolinguistics is an interdisciplinary field in which biological development of language is studied. It aims to find the functioning cycle in mind that enables humans to perceive the principles and bases of language. Language genetics, a subfield of biolinguistics, traces genetic factors in the formation and perception of language. Although a variety of theories have been introduced to explain the origins of language, considering recent studies, acquiring essential genetic abilities for speaking are undoubtedly of the most crucial necessities of this skill. Researchers have recently found defective genes in a wide spectrum of language disorders, through which they strongly confirm that speech systems rely on these genes to function properly. However, there is no report on a study which answers this question clearly: considering the origins of language and human evolution, is the proper function of genes, genetic structures, and general requirements necessary for speaking? The evolution of language and genetics of speech disorders along with the outstanding improvements and recent studies are discussed in this review article.</Abstract>
			<OtherAbstract Language="FA">Language, as an exclusive salient of human kind, is the requisite of development and formation of the human society; thus, it is at the topmost of human evolutionary features. Language and speech can be studied in various fields such as biology. Biolinguistics is an interdisciplinary field in which biological development of language is studied. It aims to find the functioning cycle in mind that enables humans to perceive the principles and bases of language. Language genetics, a subfield of biolinguistics, traces genetic factors in the formation and perception of language. Although a variety of theories have been introduced to explain the origins of language, considering recent studies, acquiring essential genetic abilities for speaking are undoubtedly of the most crucial necessities of this skill. Researchers have recently found defective genes in a wide spectrum of language disorders, through which they strongly confirm that speech systems rely on these genes to function properly. However, there is no report on a study which answers this question clearly: considering the origins of language and human evolution, is the proper function of genes, genetic structures, and general requirements necessary for speaking? The evolution of language and genetics of speech disorders along with the outstanding improvements and recent studies are discussed in this review article.</OtherAbstract>
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			<Param Name="value">Language</Param>
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			<Param Name="value">Genetics</Param>
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			<Object Type="keyword">
			<Param Name="value">Evolution</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Speech disorders</Param>
			</Object>
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<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_14434_e1f9b39289e1893622852cf8de6e14db.pdf</ArchiveCopySource>
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