<?xml version="1.0" encoding="utf-8"?>
<XML>
<JOURNAL>
<YEAR>2012</YEAR>
<VOL>4</VOL>
<NO>2</NO>
<MOSALSAL>0</MOSALSAL>
<PAGE_NO>102</PAGE_NO>


<ARTICLES>

	<ARTICLE> 
		<TitleF>Table of contents</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>0</FPAGE>
			<TPAGE>0</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/2
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1393/12/11
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Members Information Pack</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>0</FPAGE>
			<TPAGE>0</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/2
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1393/12/11
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Editorial note</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>51</FPAGE>
			<TPAGE>51</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/2
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1393/12/11
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Faranoush</Name>
				<MidName></MidName>
				<Family>M</Family>
				<NameE>Faranoush</NameE>
				<MidNameE></MidNameE>
				<FamilyE>M</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Changing Pattern of Histone H3 Methylation following treatment of erythroid progenitors derived from cord blood CD133+ cells with sodium butyrate and thalidomide</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background: Human β-like globin genes regulaon during development from embyonic to adult stage results in
generaon of different types of hemoglobin with different funcons. As β-thalassemia and sickle cell disease are
disorders of β-globin chain, epigenec drugs such as thalidomide and sodium butyrate which can induce γ-globin
gene are considered as a novel therapeuc approach. Drugs effecve in decreasing DNA methylaon and alteraon
of histone methylaon pa$ern can result in γ-globin gene upregulaon.
Materials and Methods: This study was performed on erythroid progenitors derived from cord blood CD133+ cells.
Erythroid progenitors were treated with thalidomide and sodium butyrate as single and combinaon therapies in
10 μM concentraons. Chroman Immuno Percipitaon (ChIP) assay was used to evaluate the change in H3K27
methylaon pa$ern. Also, Real-me PCR assay was used to compare the number of DNA fragments resulng from
immunoprecipitaon in different drug treatment groups.
Results: Real-me PCR assay indicated considerable effect of thalidomide single therapy in decreasing H3K27
methylaon compared with sodium butyrate and combinaon therapy.
Conclusion: According to the results of this study, it seems that the synergisc effect of thalidomide and sodium
butyrate combinaon therapy on γ-globin gene inducon arises from other epigenec mechanisms.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>53</FPAGE>
			<TPAGE>59</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Epigenesis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Genec</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>thalidomide</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>sodium butyrate</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>methylaon</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>ABO blood groups and prognosis of breast cancer: a case-control study in Arak/Iran</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background: To explore a possible rela!onship among blood groups and the prognosis of breast cancer, this case-
control study was carried out in Arak city, Arak province, Iran.
Materials and Methods: One hundred and thirty four pa!ents with breast cancer were inves!gated. ABO blood
groups were obtained from medical records. Mul!variate analyses were performed, including size of tumor, axillary
lymph nodes involvement and prognosis of the pa!ents.
Results: We found that there is a significant rela!onship between the blood type and the size of tumor (P.V=0.035),
axillary lymph nodes involvement (P.V=0.001) and the prognosis of the breast cancer (P.V=0.014).
Conclusion: The blood type of among our pa!ents with breast cancer seems to be a prognos!c factor and the
presence of B-an!gen shows associa!on with poor prognosis of breast cancer.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>61</FPAGE>
			<TPAGE>65</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Breast cancer</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>blood group</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>prognosis</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Peykan check, a simple continuous quality control method for hematology analyzers</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>A simple inexpensive con!nuous quality control method, by means of eight basic blood coun!ng parameters,
obtained from automated hematology analyzers, using pa!ent samples, is described.
A few samples with low, normal and high values were selected and introduced to the instrument early in the morning
as the first count, the results of which are plo#ed on the appropriate chart as dots. The same samples were again
given to the instrument at noon and the results were plo#ed on the same chart as the arrow heads. An arrow is then
drawn from each pair of consecu!ve counts. The same procedure is repeated every 6 hours, using a newly selected
set of samples, and the last sample which is selected in late evening on each day, is introduced to the instrument
on the next morning. Hence pa!ent samples are run at the beginning and the end of three daily work shi$s. An
explana!on is given to use the direc!on of the arrows as the main factor to assess the quality of the instrument
performance. This method can be easily applied to any hematological laboratory and can simply be performed even
by laboratory technicians.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>67</FPAGE>
			<TPAGE>73</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Quality control</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>blood</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>cell count</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Evaluating the frequency of HTLV-Ι/Π infection among blood donors, major thalassemic patients and individuals infected with hepatitis B and C viruses in Isfahan, Iran</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background: The human T-cell lymphotropic virus type I is the first retrovirus idenfied in humans. The virus has
been associated with adult T-cell leukemia/lymphoma, human T-lymphotropic virus type I, myelopathy/tropical
spasc paraparesis, uveis, arthris, pulmonary lymphocyc alveolis, keratoconjuncvis sicca, and infecous
dermas. Human T-lymphotropic virus type Iis endemic in Japan, parts of central Africa, the Caribbean basin and
South America, Melanesia and Iran (city of Mashhad). The aim of this study was to evaluate serological prevalence
of human T-lymphotropic virus type I/IIinfecon among blood donors, major thalassemic paents and individuals
infected with hepas B and C viruses in the city of Isfahan, Iran.
Materials and Methods: Sera were collected from 140 blood donors (440 samples), 150 major thalassemic paents
,150 and individuals with hepas B and C and were tested for the presence of human T-lymphotropic virus type I/
IIspecific anbody in a 6 months period in 2007using ELISA and Western Blot tests
Results: Blood donors tested were negave for human T-lymphotropic virus type I/IIinfecon, but in major thalassemic
paents including 88 males and 62 females, 5 were posive (3.3%). Stascal analyses did not show any significant
difference between genders. In individuals with hepas one was border line (HCV).
Conclusion: The results indicate a low level of coinfecon of human T-lymphotropic virus with HCV in this part
of the country. However, the observaon of a case with borderline findings, among this group and also posive
cases among thalassemic paents, suggests the presence of the virus in blood donor populaon so this virus could
be present in Isfahan but more invesgaon is needed to evaluate the need for screening tests to detec human
T-lymphotropic virus type I among blood donors in Isfahan.connuing screening and educaon of parents and also
mass media educaon against consuming “Fava bean” and “Naphtalen”.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>75</FPAGE>
			<TPAGE>80</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/292012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>HTLV-I/II</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Hepas C virus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Hepas B virus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Thalassemia</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Co-inheritance of α-and β-thalassemia: challenges in prenatal diagnosis of thalassemia</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Background: The double heterozygous state of α/β thalassemia may alter the hematological indices and modify the
phonotype. In addion, definite characterizaon of co-inheritance of α- and β-thalassemia heterozygous carriers
may change the process of genec counseling.
Materials and Methods: An Iranian couple with low hematological indices was analyzed for α-globin gene deleons
using mulplex gap PCR method and β-globin gene mutaons by ARMS-PCR method and DNA sequencing.
Results: The -20.5kb α-globin gene deleon was found in both individuals, and the IVSI-110(G&#62;A) mutaon in β-
globin gene in male partner. The β -globin gene sequence was normal in female partner. Therefore, the couple was
informed about the risk of having fetuses with hemoglobin Bart’s hydrops fetalis.
Conclusion:The co-inheritance of α/β thalassemia should be considered in genec counseling of families screened
for β-thalassemia major prevenon.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>81</FPAGE>
			<TPAGE>84</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/292012/04/292012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>α-thalassemia</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>β-thalassemia</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Polymerase Chain Reacon</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Mutaon</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Factor XIII deficiency: a review of literature</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Coagulaon factor XIII gene, protein structure and funcon Coagulaon factor XIII (FXIII) is a tetrameric (FXIII-
A2B2) pro-transglutaminase enzyme with an essenal role in the final stage of coagulaon cascade by cross linking
the fibrin monomers and stabilizing the fibrin clot. Congenital FXIII deficiency is a rare bleeding disorder, with an
autosomal recessive trait inheritance, and a frequency of about 1 in 2 million people. Most cases of FXIII deficiency
are associated with FXIII-A subunit deficiency and only few FXIII-B subunit deficiencies have been reported. Severe
FXIII-A deficiencies are associated with some moderate to severe clinical complicaons including umbilical bleeding
during infancy, impaired wound healing, pregnancy loss in affected women, life-threatening intracranial bleeding and
also subcutaneous and so# ssue bleeding. Diagnosis of FXIII deficiency can be achieved by clot solubility tests in 5
M urea or 1% monochloracec acid as a screening assay, and also quantave evaluaon of the acvity or angenic
levels of FXIII A and B subunits. There have been recommendaons for primary prophylaxis or replacement therapy
in FXIII deficient paents, in order to prevent spontaneous bleeding, bleeding during minor and major surgeries, or
prevenon of pregnancy loss in women. Acquired FXIII deficiency has also been reported as a result of decreased
producon or high consumpon of FXIII as well as the secreon of autoanbodies against FXIII subunits.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>85</FPAGE>
			<TPAGE>91</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/292012/04/292012/04/292012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>FXIII deficiency</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>bleeding disorders</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>wound healing</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>pregnancy</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>prophylaxis</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>replacement therapy</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Acute Hemorrhagic Edema of Infancy: Report of Two Cases Report</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introducon: Acute hemorrhagic edema of infancy (AHEI) is a cutaneous leukocytoclas!c vasculi!s of infants, clinically
characterized by acute development of peripheral edema and targetoid purpuric lesions on face and extremi!es. It is
considered to be an uncommon form of cutaneous vasculi!s occurring in children younger than 2 years old.
The clinical picture has a violent onset, a short benign course followed by spontaneous complete recovery.
Case presenta!on: We describe two males with acute hemorrhagic edema. In one case the disease appeared a"er
upper respiratory tract infec!on.
Conclusion: AHEI is a benign disorder despite its drama!c appearance. The most striking classic features of the
disease are the contrast between the acuteness of the cutaneous lesions and the good general condi!on of the
pa!ent. Considering its clinical features, AHEI can be jus!fiably characterized as a unique disorder, dis!nct from
Henoch–Schenlein Purpura (HSP).</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>93</FPAGE>
			<TPAGE>96</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Acute hemorrhagic edema (this is not a MESH keyword)</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Infancy</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Vasculi!s</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>Leukocytoclas!c</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Large Ovarian Hemorrhagic Cyst and Immune Thrombocytopenia as Early Manifestations of Systemic Lupus Erythematosus (SLE)</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Hematologic abnormali"es are generally present among systemic lupus erythematosus pa"ents. Idiopathic
thrombocytopenic purpura can be the first manifesta"on of SLE, followed by other symptoms and signs of disease
appearing several years later. Although bleeding due to immune thrombocytopenic purpura is usually mild and
occurs in mucocutaneous surfaces, but it may be severe and represent in unusual sites such as an ovarian cyst .We
report a case of SLE presented with immune thrombocytopenia and a large hemorrhagic ovarian cyst.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>97</FPAGE>
			<TPAGE>98</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Hemorrhagic</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>ovarian cysts</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>lupus erythematosus</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>systemic</KeyText>
			</KEYWORD>

			<KEYWORD>
				<KeyText>thrombocytopenia</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Very late recurrence of gastric cancer with bone mar-row anemia as a stem cell disease: a lesson for future</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>99</FPAGE>
			<TPAGE>100</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Homogeneously Staining Regions or Double Minute Chromosomes in Leukemia (Brief Communication)</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>101</FPAGE>
			<TPAGE>102</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2015/03/22015/03/22015/03/22012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/292012/04/29
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1391/2/10
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/22015/03/2
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/12/11
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>

</ARTICLES>

</JOURNAL>
</XML>
