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<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>35</Volume>
				<Issue>432</Issue>
				<PubDate PubStatus="epublish">
					<Year>2017</Year>
					<Month>06</Month>
					<Day>22</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Index</ArticleTitle>
<VernacularTitle>Index</VernacularTitle>
			<FirstPage></FirstPage>
			<LastPage></LastPage>
			<ELocationID EIdType="pii">15258</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Journal</FirstName>
					<LastName>Index</LastName>
<Affiliation>--</Affiliation>
<Identifier Source="ORCID">0000-0003-0874-1906</Identifier>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2017</Year>
					<Month>11</Month>
					<Day>23</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_15258_10d4b366f410a1275f7b684f07a28456.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>35</Volume>
				<Issue>432</Issue>
				<PubDate PubStatus="epublish">
					<Year>2017</Year>
					<Month>06</Month>
					<Day>22</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Comparison of DNA Instability in Adenoma and Adenocarcinoma in Patients with Colorectal Cancer, Using Random Amplified Polymorphic DNA Polymerase Chain Reaction (RAPD-PCR)</ArticleTitle>
<VernacularTitle>Comparison of DNA Instability in Adenoma and Adenocarcinoma in Patients with Colorectal Cancer, Using Random Amplified Polymorphic DNA Polymerase Chain Reaction (RAPD-PCR)</VernacularTitle>
			<FirstPage>609</FirstPage>
			<LastPage>614</LastPage>
			<ELocationID EIdType="pii">15259</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Ardeshir</FirstName>
					<LastName>Talebi</LastName>
<Affiliation>Associate Professor, Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0001-7313-5086</Identifier>

</Author>
<Author>
					<FirstName>Samsam</FirstName>
					<LastName>Daneshbakhtiyar</LastName>
<Affiliation>Resident, Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Mahboobeh</FirstName>
					<LastName>Meshkat</LastName>
<Affiliation>Department of Cellular and Molecular Biology, School of Sciences, Nourdanesh Institute of Higher Education, Meymeh, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Marziyeh</FirstName>
					<LastName>Meshkat</LastName>
<Affiliation>Department of Cellular and Molecular Biology, School of Sciences, Nourdanesh Institute of Higher Education, Meymeh, Isfahan, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2016</Year>
					<Month>09</Month>
					<Day>18</Day>
				</PubDate>
			</History>
		<Abstract>Background: Colorectal cancer is the consequence of gathering numerous genetic alterations and it has been suggested that genomic instability is indispensable for the generation of multiple mutations underlying the development of cancer.Methods: Random amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) method was utilized to find genomic alterations in adenomas and adenocarcinomas compared with normal epithelial tissue obtained from 17 patients with colorectal cancer.Findings: Separated PCR products by 2% agarose determined approximate 370 base pairs band as a polymorphic fingerprint for normal (11.8%), adenoma (76.5%), and adenocarcinoma (88.2%) tissues. Polymorphic band could significantly discriminate adenomas [Odds ratio (OR) = 24.38, P = 0.0004] and adenocarcinomas (OR = 56.25, P &lt; 0.0001) from normal tissues. Furthermore, the 370 base pairs band could not distinguish adenomas from adenocarcinomas (P = 0.6600).</Abstract>
			<OtherAbstract Language="FA">Background: Colorectal cancer is the consequence of gathering numerous genetic alterations and it has been suggested that genomic instability is indispensable for the generation of multiple mutations underlying the development of cancer.Methods: Random amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) method was utilized to find genomic alterations in adenomas and adenocarcinomas compared with normal epithelial tissue obtained from 17 patients with colorectal cancer.Findings: Separated PCR products by 2% agarose determined approximate 370 base pairs band as a polymorphic fingerprint for normal (11.8%), adenoma (76.5%), and adenocarcinoma (88.2%) tissues. Polymorphic band could significantly discriminate adenomas [Odds ratio (OR) = 24.38, P = 0.0004] and adenocarcinomas (OR = 56.25, P &lt; 0.0001) from normal tissues. Furthermore, the 370 base pairs band could not distinguish adenomas from adenocarcinomas (P = 0.6600).</OtherAbstract>
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			<Param Name="value">Colorectal Cancer</Param>
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			<Object Type="keyword">
			<Param Name="value">Adenoma</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Adenocarcinoma</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Random amplified polymorphic DNA polymerase chain reaction</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Genomic instability</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_15259_e3d389ef8c92b280760c6ebd647c2cee.pdf</ArchiveCopySource>
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<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>35</Volume>
				<Issue>432</Issue>
				<PubDate PubStatus="epublish">
					<Year>2017</Year>
					<Month>06</Month>
					<Day>22</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Comparison of Serum Level of Magnesium in Patients Received Pantoprazole or Ranitidine in Intensive Care Unit</ArticleTitle>
<VernacularTitle>Comparison of Serum Level of Magnesium in Patients Received Pantoprazole or Ranitidine in Intensive Care Unit</VernacularTitle>
			<FirstPage>615</FirstPage>
			<LastPage>621</LastPage>
			<ELocationID EIdType="pii">15260</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Babak</FirstName>
					<LastName>Alikiaii</LastName>
<Affiliation>Assistant Professor, Anesthesiology and Critical Care Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0003-3236-1970</Identifier>

</Author>
<Author>
					<FirstName>Parviz</FirstName>
					<LastName>Kashefi</LastName>
<Affiliation>Professor, Anesthesiology and Critical Care Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0002-7254-204X</Identifier>

</Author>
<Author>
					<FirstName>Saeed</FirstName>
					<LastName>Abbasi</LastName>
<Affiliation>Assistant Professor, Anesthesiology and Critical Care Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0003-0930-5698</Identifier>

</Author>
<Author>
					<FirstName>Elahe</FirstName>
					<LastName>Askari-Barzani</LastName>
<Affiliation>Student of Medicine, Student Research Committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2017</Year>
					<Month>01</Month>
					<Day>29</Day>
				</PubDate>
			</History>
		<Abstract>Background: Some of studies showed that using proton-pump inhibitors (PPIs) in hospitalized patients is one of the causes of decreased serum magnesium level that leads to electrolytic imbalance. This study aimed to compare serum level of magnesium in patients who received pantoprazole or ranitidine in intensive care unit.Methods: In a clinical trial study, 50 patients hospitalized in intensive care units of Alzahra hospital, Isfahan, Iran, were randomly divided in to two groups of 25. Patients were treated with pantoprazole and ranitidine in first and second groups, respectively. Serum level of magnesium was measured during two weeks after entrance to intensive care units and compared between the groups.Findings: Mean serum level of magnesium in the two groups of pantoprazole and ranitidine in second day of hospitalization was 1.90 ± 0.11 and 1.98 ± 0.13 mg/dl, respectively and there was statistically difference between the two groups (P = 0.017). Serum level of magnesium until the 10th day of hospitalization was significantly different between the two groups. In addition, the trend of serum level of magnesium was different between the two groups (P &lt; 0.001).Conclusion: Our study showed that consumption of ranitidine led to less decrease of serum level of magnesium among patients hospitalized in internal care units. But, considering our limitations as the amount of cases, more studies on using ranitidine are recommended.</Abstract>
			<OtherAbstract Language="FA">Background: Some of studies showed that using proton-pump inhibitors (PPIs) in hospitalized patients is one of the causes of decreased serum magnesium level that leads to electrolytic imbalance. This study aimed to compare serum level of magnesium in patients who received pantoprazole or ranitidine in intensive care unit.Methods: In a clinical trial study, 50 patients hospitalized in intensive care units of Alzahra hospital, Isfahan, Iran, were randomly divided in to two groups of 25. Patients were treated with pantoprazole and ranitidine in first and second groups, respectively. Serum level of magnesium was measured during two weeks after entrance to intensive care units and compared between the groups.Findings: Mean serum level of magnesium in the two groups of pantoprazole and ranitidine in second day of hospitalization was 1.90 ± 0.11 and 1.98 ± 0.13 mg/dl, respectively and there was statistically difference between the two groups (P = 0.017). Serum level of magnesium until the 10th day of hospitalization was significantly different between the two groups. In addition, the trend of serum level of magnesium was different between the two groups (P &lt; 0.001).Conclusion: Our study showed that consumption of ranitidine led to less decrease of serum level of magnesium among patients hospitalized in internal care units. But, considering our limitations as the amount of cases, more studies on using ranitidine are recommended.</OtherAbstract>
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			<Param Name="value">Magnesium</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Pantoprazole</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Ranitidine</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Intensive Care Unit</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_15260_4e4f8804bf781c81ea45e97aecb24427.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>35</Volume>
				<Issue>432</Issue>
				<PubDate PubStatus="epublish">
					<Year>2017</Year>
					<Month>06</Month>
					<Day>22</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Comparative Study on Mutations in CDH1 Gene in Iranian Patients with Hereditary Diffuse Gastric Cancer (HDGC) and Sporadic Diffuse Gastric Cancer (SDGC)</ArticleTitle>
<VernacularTitle>Comparative Study on Mutations in CDH1 Gene in Iranian Patients with Hereditary Diffuse Gastric Cancer (HDGC) and Sporadic Diffuse Gastric Cancer (SDGC)</VernacularTitle>
			<FirstPage>622</FirstPage>
			<LastPage>628</LastPage>
			<ELocationID EIdType="pii">15261</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Abbas</FirstName>
					<LastName>Moridnia</LastName>
<Affiliation>Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Majid</FirstName>
					<LastName>Kheirollahi</LastName>
<Affiliation>Associate Professor, Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-Communicable Disease AND Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0002-8393-839X</Identifier>

</Author>
<Author>
					<FirstName>Mohammad Amin</FirstName>
					<LastName>Tabatabaeefar</LastName>
<Affiliation>Associate Professor, Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0003-0730-750X</Identifier>

</Author>
<Author>
					<FirstName>Mehrdad</FirstName>
					<LastName>Zeinalian</LastName>
<Affiliation>Assistant Professor, Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0003-1381-0582</Identifier>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2017</Year>
					<Month>02</Month>
					<Day>22</Day>
				</PubDate>
			</History>
		<Abstract>Background: Gastric cancer (GC) is the fourth common cancer worldwide and the second cause of mortality among all cancers. Mutations in the CDH1 gene are the most common cause of hereditary diffuse gastric cancer (HDGC) and sporadic diffuse gastric cancer (SDGC). CDH1 gene encode for E-cadherin protein. We compared the nucleotide alterations and copy number variations in CDH1 gene between Iranian patients with HDGC and SDGC.Methods: We evaluated 45 patients including 17 cases with HDGC and 28 cases with SDGC identified according to the histopathological criteria and familial history. DNA extraction was obtained from peripheral blood and formalin-fixed paraffin-embedded (FFPE) tissues. The DNA sequencing was completed using polymerase chain reaction (PCR) amplification of 16 exons of the CDH1 gene. Multiplex ligation-dependent probe amplification (MLPA) method was accomplished on samples with no pathogenic variants in sequencing.Findings: Synonymous substitution of L116L and A692A was detected in patients with HDGC and SDGC; but non-synonymous substitution of D777E, c.889delA, and c.1177delA deletions only detected in patients with HDGC. MLPA results revealed one deletion in exon 1 of CDH1 gene in patients with HDGC and one deletion in exon 2, and one duplication in exon 9 of CDH1 gene in patients with SDGC.Conclusion: According to the results, different variants in CDH1 gene was presented in patients with HDGC and SDGC that emphasis the survey of CDH1 variants and especially detected variants in this study in the diagnosis of diffuse gastric cancer disease.</Abstract>
			<OtherAbstract Language="FA">Background: Gastric cancer (GC) is the fourth common cancer worldwide and the second cause of mortality among all cancers. Mutations in the CDH1 gene are the most common cause of hereditary diffuse gastric cancer (HDGC) and sporadic diffuse gastric cancer (SDGC). CDH1 gene encode for E-cadherin protein. We compared the nucleotide alterations and copy number variations in CDH1 gene between Iranian patients with HDGC and SDGC.Methods: We evaluated 45 patients including 17 cases with HDGC and 28 cases with SDGC identified according to the histopathological criteria and familial history. DNA extraction was obtained from peripheral blood and formalin-fixed paraffin-embedded (FFPE) tissues. The DNA sequencing was completed using polymerase chain reaction (PCR) amplification of 16 exons of the CDH1 gene. Multiplex ligation-dependent probe amplification (MLPA) method was accomplished on samples with no pathogenic variants in sequencing.Findings: Synonymous substitution of L116L and A692A was detected in patients with HDGC and SDGC; but non-synonymous substitution of D777E, c.889delA, and c.1177delA deletions only detected in patients with HDGC. MLPA results revealed one deletion in exon 1 of CDH1 gene in patients with HDGC and one deletion in exon 2, and one duplication in exon 9 of CDH1 gene in patients with SDGC.Conclusion: According to the results, different variants in CDH1 gene was presented in patients with HDGC and SDGC that emphasis the survey of CDH1 variants and especially detected variants in this study in the diagnosis of diffuse gastric cancer disease.</OtherAbstract>
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			<Object Type="keyword">
			<Param Name="value">CDH1</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Diffuse gastric cancer</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Iran</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_15261_1d72d067ad71fc47c245e249dc16cb7f.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>35</Volume>
				<Issue>432</Issue>
				<PubDate PubStatus="epublish">
					<Year>2017</Year>
					<Month>06</Month>
					<Day>22</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Assessment of the Expression Level of B-Cell Lymphoma 6 (BCL6) in Peripheral Blood CD38+ B Lymphocytes in Patients with Common Variable Immunodeficiency (CVID)</ArticleTitle>
<VernacularTitle>Assessment of the Expression Level of B-Cell Lymphoma 6 (BCL6) in Peripheral Blood CD38+ B Lymphocytes in Patients with Common Variable Immunodeficiency (CVID)</VernacularTitle>
			<FirstPage>629</FirstPage>
			<LastPage>634</LastPage>
			<ELocationID EIdType="pii">15262</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Faezeh</FirstName>
					<LastName>Abbasirad</LastName>
<Affiliation>MSc Student, Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Mazdak</FirstName>
					<LastName>Ganjalikhani-Hakemi</LastName>
<Affiliation>Assistant Professor, Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Nafiseh</FirstName>
					<LastName>Esmaeil</LastName>
<Affiliation>Assistant Professor, Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0001-9854-3043</Identifier>

</Author>
<Author>
					<FirstName>Shokrollah</FirstName>
					<LastName>Farrokhi</LastName>
<Affiliation>Assistant Professor, Department of Immunology and Allergy, The Persian Gulf Tropical Medicine Research Center, The Persian Gulf Biomedical Research Institute, Bushehr University of Medical Sciences, Bushehr, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Roya</FirstName>
					<LastName>Sherkat</LastName>
<Affiliation>Associate Professor, Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0002-8574-2091</Identifier>

</Author>
<Author>
					<FirstName>Reza</FirstName>
					<LastName>Yazdani</LastName>
<Affiliation>Assistant Professor, Primary Immunodeficiency Research Center, Tehran University of Medical Sciences, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Sanaz</FirstName>
					<LastName>Afshar-Ghasemlou</LastName>
<Affiliation>MSc Student, Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2017</Year>
					<Month>02</Month>
					<Day>22</Day>
				</PubDate>
			</History>
		<Abstract>immunodeficiency, is a heterogeneous set of immunological abnormalities including decreased serum levels of antibodies, and impaired antibody response to infections or vaccination. The syndrome includes impaired B-cell maturation, impaired somatic hypermutation, reduced numbers of circulating memory B cells, and absent or reduced plasma cells. B cell lymphoma 6 (BCL6) is a transcription factor which is important for the evolution and proliferation of B cells. This study aimed to investigate the expression of BCL6 in peripheral blood CD38+ B lymphocytes in patients with CVID.Methods: Blood samples were collected from 14 patients with CVID under substitutive immunoglobulin (Ig) therapy before immunoglobulin infusion and 14 normal controls. Then, peripheral blood mononuclear cells (PBMCs) were isolated using Ficoll-Hypaque density centrifugation. CD19+ B lymphocytes were purified from PBMCs by positive selection using B-cell isolation kit. Flow cytometery method was employed to determine the expression of the BCL6 in CD38+ B cells.Findings: The expression of BCL6 in CD38 +B lymphocytes was 1.51% and 0.58% in patients and healthy subjects, respectively; the difference was not statistically significant (P &gt; 0.05).Conclusion: The results showed that there is no significant difference in the mean expression of BCL6 of the CD38+ B cells in patients with CVID, compared with control group. However, the average BCL6 expression of CD38+ B lymphocytes in patients was more than control group.</Abstract>
			<OtherAbstract Language="FA">immunodeficiency, is a heterogeneous set of immunological abnormalities including decreased serum levels of antibodies, and impaired antibody response to infections or vaccination. The syndrome includes impaired B-cell maturation, impaired somatic hypermutation, reduced numbers of circulating memory B cells, and absent or reduced plasma cells. B cell lymphoma 6 (BCL6) is a transcription factor which is important for the evolution and proliferation of B cells. This study aimed to investigate the expression of BCL6 in peripheral blood CD38+ B lymphocytes in patients with CVID.Methods: Blood samples were collected from 14 patients with CVID under substitutive immunoglobulin (Ig) therapy before immunoglobulin infusion and 14 normal controls. Then, peripheral blood mononuclear cells (PBMCs) were isolated using Ficoll-Hypaque density centrifugation. CD19+ B lymphocytes were purified from PBMCs by positive selection using B-cell isolation kit. Flow cytometery method was employed to determine the expression of the BCL6 in CD38+ B cells.Findings: The expression of BCL6 in CD38 +B lymphocytes was 1.51% and 0.58% in patients and healthy subjects, respectively; the difference was not statistically significant (P &gt; 0.05).Conclusion: The results showed that there is no significant difference in the mean expression of BCL6 of the CD38+ B cells in patients with CVID, compared with control group. However, the average BCL6 expression of CD38+ B lymphocytes in patients was more than control group.</OtherAbstract>
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			<Object Type="keyword">
			<Param Name="value">B-lymphocytes</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Plasma cells</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">B-Cell Lymphoma 6</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">CD38</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_15262_19c81ddc9575bacf2a6f73b428065821.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Isfahan University of Medical Sciences</PublisherName>
				<JournalTitle>Journal of Isfahan Medical School</JournalTitle>
				<Issn>1027-7595</Issn>
				<Volume>35</Volume>
				<Issue>432</Issue>
				<PubDate PubStatus="epublish">
					<Year>2017</Year>
					<Month>06</Month>
					<Day>22</Day>
				</PubDate>
			</Journal>
<ArticleTitle>The Epidemiologic Assessment of Children with Acute Pyelonephritis in a 5-Years Period, Based on American Academy of Pediatrics (AAP) 2011 Guidelinee</ArticleTitle>
<VernacularTitle>The Epidemiologic Assessment of Children with Acute Pyelonephritis in a 5-Years Period, Based on American Academy of Pediatrics (AAP) 2011 Guidelinee</VernacularTitle>
			<FirstPage>635</FirstPage>
			<LastPage>642</LastPage>
			<ELocationID EIdType="pii">15263</ELocationID>
			
			
			<Language>FA</Language>
<AuthorList>
<Author>
					<FirstName>Hamid</FirstName>
					<LastName>Mohammadjafari</LastName>
<Affiliation>Professor, Infectious Diseases Research Center with Focus on Nosocomial Infections, Mazandaran University of Medical Sciences, Sari, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Abbas</FirstName>
					<LastName>Alipour</LastName>
<Affiliation>Assistant Professor, Department of Epidemiology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Fereshteh</FirstName>
					<LastName>Saeedi</LastName>
<Affiliation>Student of Medicine, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2017</Year>
					<Month>02</Month>
					<Day>16</Day>
				</PubDate>
			</History>
		<Abstract>Background: Acute pyelonephritis (APN) is the second common significant infection in infants and children. Long-term complications of APN, scar nephropathy and hypertension, make it a serious disease at this period of life. American Academy of Pediatrics (AAP) suggested newer approach to patients with APN from 2011. We studied the epidemiologic aspect of the patients since 2011.Methods: This retrospective study was performed by assessing the documented history of patients with APN. Patients&#039; demographic and clinical data were recorded. Age, sex, urine culture, sensitivity status, and imaging findings were analyzed. Long-term findings such as recurrent urinary tract infection (UTI), kidney scar, and outcome of vesicoureteral reflux were assessed.Findings: A total of 360 children with mean age of 35.2 months, (81% female) were enrolled in study. The most common organism was Escherichia coli (78%) with at least 82% sensitivity to third generation cephalosporins, aminoglycosides, and carbapneme. The resistance of Escherichia coli to co-trimoxazole and nalidixic acid was 44% and 38%, respectively. 26 patients (7.6%) suffered from recurrent UTI; and recurrence was related patient&#039;s age. Hydronephrosis, vesicoureteral reflux, and scar were respectively reported in 20%, 46%, and 47% of children imaging were performed for them.Conclusion: APN is a serious and significant infection in children yet. The most common organism is Escherichia coli. Long-term complications confirm that strict follow up and assessment of the patients is very advisable.</Abstract>
			<OtherAbstract Language="FA">Background: Acute pyelonephritis (APN) is the second common significant infection in infants and children. Long-term complications of APN, scar nephropathy and hypertension, make it a serious disease at this period of life. American Academy of Pediatrics (AAP) suggested newer approach to patients with APN from 2011. We studied the epidemiologic aspect of the patients since 2011.Methods: This retrospective study was performed by assessing the documented history of patients with APN. Patients&#039; demographic and clinical data were recorded. Age, sex, urine culture, sensitivity status, and imaging findings were analyzed. Long-term findings such as recurrent urinary tract infection (UTI), kidney scar, and outcome of vesicoureteral reflux were assessed.Findings: A total of 360 children with mean age of 35.2 months, (81% female) were enrolled in study. The most common organism was Escherichia coli (78%) with at least 82% sensitivity to third generation cephalosporins, aminoglycosides, and carbapneme. The resistance of Escherichia coli to co-trimoxazole and nalidixic acid was 44% and 38%, respectively. 26 patients (7.6%) suffered from recurrent UTI; and recurrence was related patient&#039;s age. Hydronephrosis, vesicoureteral reflux, and scar were respectively reported in 20%, 46%, and 47% of children imaging were performed for them.Conclusion: APN is a serious and significant infection in children yet. The most common organism is Escherichia coli. Long-term complications confirm that strict follow up and assessment of the patients is very advisable.</OtherAbstract>
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			<Param Name="value">Pyelonephritis</Param>
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			<Param Name="value">Urinary tract infections</Param>
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			<Param Name="value">Vesicoureteral reflux</Param>
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			<Param Name="value">Scar</Param>
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			<Object Type="keyword">
			<Param Name="value">Hydronephrosis</Param>
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<ArchiveCopySource DocType="pdf">https://jims.mui.ac.ir/article_15263_c018ae0e48e90aa4093c5a37af897fb1.pdf</ArchiveCopySource>
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