ABSTRACT - The performance and reliability of the Internet depend in large part on the operation of the underlying routing protocols. Today's IP routing protocols compute paths based on the network topology and configuration parameters, without regard to the current traffic load on the routers and links. This paper discusses routing optimization using Genetic Algorithm Then we study and analyze the problems of routing optimization in large networks. We will propose a detailed genetic algorithm in order to optimize routing tables and to enhance the performance of the routers.

الخلاصة ان الأداء والإتقان للانترنت يعتمد بدرجة كبيرة على سياقات اختيار المسارات . اليوم Internet protocol يقوم بعملية حساب المسارات بالاعتماد على ال Network topology بدون الاهتمام للزخم في المسارات . هذا البحث يبحث بتحقيق أفضل المسارات بالاعتماد على الخوارزمية الجينية . سنقوم بدراسة وتحليل مشكلة اختيار أفضل المسارات في الشبكات الكبيرة وسنقدم شرح للخوارزمية الجينية من اجل الحصول على جدول المسارات واختيار افضل المسارات الممكنة.

GA --- Crossover --- Mutation.

In this study, the geographical and demographical distribution of eighty clinically thalassaemic patients and fifty six apparently healthy individuals as a control group were studied. The geographical distribution of the samples revealed that the collected samples were from fifteen governorates which represent various regions in Iraq. The distribution of the samples according to some demographical parameters including: gender, age, and parent relationship was studied to reveal the effects of these parameters on the diversity of β-thalassaemia in both patient and control groups. Also, after molecular diagnosis of causative β-thalassaemia mutations using Amplification Refractory Mutation System (ARMS), the geographical distribution of positive diagnosed patients was studied in order to learn about the distribution of β-thalassaemia mutations, the results revealed the heterogeneity of diagnosed mutations within the Iraqi regions.

تم دراسة التوزيع الجغرافي والديموغرافي لثمانين مريض مصاب سريريا بالثلاسيميا– بيتا وستة وخمسون شخصاً من الأصحاء مظهرياً كمجموعة سيطرة. أظهر التوزيع الجغرافي للعينات أنها شملت خمس عشرة محافظة ممثلة لمختلف مناطق العراق. درس توزيع العينات طبقاً لبعض المعايير الديموغرافية التي شملت الجنس والعمر وعلاقة القربى بين الأباء لمعرفة تأثير هذه المعايير على تباين الإصابة بالثلاسيميا– بيتا في كلتا مجموعتي الدراسة. وبعد اجراء التشخيص الجزيئي للطفرات الوراثية المسببة للثلاسيميا-بيتا بإستخدام تقنية ARMS، درس التوزيع الجغرافي للعينات التي شخصت فيها الإصابة لمعرفة توزيع الطفرات الوراثية المسببة للثلاسيميا-بيتا، إذ أظهرت النتائج اختلاف أنواع الطفرات الوراثية لامدروسة ضمن المناطق العراقية.

Beta-Thalassaemia --- Mutation --- Iraq.

Background:Mutation within the FLT 3 and NPM 1 genes ranked within the most frequent recurrent known genetic markers in acute myeloid leukemia (AML) and show apparently opposite prognostic significance.Objective:To detect the frequency of FLT3-ITD and NPM-1 mutations in Iraqi pediatric AML patients using conventional polymerized chain reaction (PCR), and to relate their prevalence with the clinical presentation and the response to induction therapy.Methods:A prospective study of 30 children presented with AML and 16 children who were age and gender matched served as negative control for the mutation. AML cases were classified according to FAB classification. WBC count, platelet count and hematocrit were measured at diagnosis and after 30 days. Molecular analysis was done on peripheral blood or bone marrow aspirate samples by conventional PCR technology.Results:FLT 3-ITD mutation was detected in 3/30 (10%) patients, whereas NPM1 mutation was detected in 4/30 (13.33%) patients. Both mutations were detected in older age patients and predominantly in male. No significant correlation between each mutation and various hematological parameters, however WBC count was significantly higher in FLT-ITD unmutated patients. FLT3-ITD mutation was detected in M3 and M3 variant whereas NPM-1 mutation was detected in M2 and M3v. The three patients having FLT-3-ITD mutation (100%) did not achieved complete hematological remission, whereas 3/24 (12.5%) patients without the mutation did not achieve remission. On the other hand 2 out of 4 (50%) patients with NPM-1 mutation had not achieved complete hematological remission and 4/22 (18.18%) patients without mutation did not achieve remission. Finally regarding the interrelation between the two mutations, the two children who had NPM1 mutation and no FLT3-ITD mutation had achieved complete remission on induction therapy whereas the three children who had FLT3-ITD mutation with or without NPM1 mutation did not achieved complete remission.Conclusion:Prevalence of FLT3-ITD and NPM-1 mutations in Iraqi pediatric AML patients is comparable to that recorded worldwide and both mutations were observed in older age children and mainly in male. FLT3-ITD mutation unlike NPM-1 mutation associate with poor response to induction therapy and the adverse effect of FLT3-ITD mutation overcome the favorable effect of NPM-1 mutation when they exist together.Keywords:Pediatric AML, Flt3-ITD mutation, NPM1 mutation, PCR

Pediatric AML --- Flt3-ITD mutation --- NPM1 mutation --- PCR

Abstract: The study was conducted on 90 blood samples divided into 35 samples Hypothyroidism 35 samples hyperthyroidism (group of patients ) and 20samples from healthy people ( control group). DNA of two groups was extracted and exon 10 was amplified by using PCR. Mutations were diagnosed and analyzed by using Sequencing. The present study found seven novel mutations in exon 10, divided into five mutations among hypothyroidism patients compared to control (who did not appear to have any type of mutations diagnosed). All mutations diagnosed were substitution included transition or transversion depending on the nature of the mutant base, three missense mutation in three hypothyroidism patients with a proportion of 20% each. They are as follows c.1330 T>C, Y444H; c.1424 T>C, L475P and c.1435 T>C, S479P and two silent mutation in two hypothyroidism patients (c.1338G>A, L446L and c.2300 G>A Untranscrib).While the result showed two mutation in hyperthyroidism, one was missense mutation (c.1832 C>A, P610Q) and the other silent mutation (c.2103 C>A, R701R).The current study pointed out the occurrence of the disease linked with mutations in specific areas of linking stimulating hormone and the interaction between the protein receptor and α-subunit for G-protein.

الخلاصة: استخدمت الدراسة الحالية90 عينة دم مقسمة إلى 35عينة من مصابين بحالة القصور في نشاط الغدة و35 عينة من مرضى فرط نشاط الغدة ومثلت بمجموعة المرضى (Patients Group )) و20 عينة من أشخاص أصحاء تمثلت بمجموعة السيطرة (Control Group ). استخلص DNA للمجموعتين وضخمت المنطقة المشفرة العاشرة (Exons 10) لجين TSHR باستخدام تقنية Polymerase Chain Reaction ( PCR) بعدها تم تشخيص الطفرات وتحليلها بطريقة التتابعSequencing . وجدت الدراسة الحاليةسبعة طفرات جديدة Novel Mutations في المنطقة المشفرة موزعة الى خمسة طفرات لدى مصابين بحالة القصور مقارنة بمجموعة السيطرة (الذين لم تظهر لديهم أي نوع من الطفرات المشخصة ) وان جميع الطفرات المشخصة هي طفرات نقطية تعويضية استبدالية Substitution أما من نوع Transition أو Transversion اعتمادا على طبيعة القاعدة الطافره ثلاث منهاMissense Mutations في ثلاث مصابين بحالة القصورنسبة كل منها 20% وهي كالتالي c.1330 T>C , Y444H ; c.1424 T>C ,L475P and c.1435 T>C , S479Pو طفرتين صامتتين Silent Mutations في اثنين من مرضى بحالة القصور (c.1338 G>A, L446L and c.2300 G>A , Untranscribt ). بينما سجلت النتائج وجود طفرتين فقط في حالة الفرط في نشاط الغدة بنسبة 5.71% احدهما Missense (c.1832 C>A, P610Q ) والأخرى صامته (c.2103 C>A ,R701R ). أشارت الدراسة الحالية إلى احتمالية ارتباط الطفرات بحدوث المرض وذلك من خلال موقع الطفرات في المناطق الخاصة للارتباط بالهرمون المحفز ومنطقة التفاعل بين البروتين المستقبل و الوحدة الثانوية ألفا لكوانين- بروتين (G-protein ).

Thyroid disorders --- TSHR gene --- Mutation.

the study was carried out in period between “1 August 2005 to 30 of December 2006”.Blood samples of 80 clinically thalassaemic patients were collected from three thalassaemiacenters in Iraq, namely: Ibn Albalady central thalassaemia center in Baghdad, and also fromKerbalaa and Al-Qadissya governorates. Blood samples were also collected from 56 apparentlyhealthy individuals to serve as a control group.DNA was isolated from blood and used for molecular detection of seven types of β-thalassaemiamutations (IVS1 nt.1 G--A , IVS1nt.5 G--C, IVS1 nt.6 T--C, IVS1 nt.110 G --A, codon 39 C--T,IVS2 nt.1G--A, and IVS2 nt.745 C--G) using the PCR based technique called ARMS(Amplification Refractory Mutation System).Five out of seven of these diagnosed mutations were reported for the first time in Iraq, and themost frequent β-thalassaemia mutations were codon 39 and IVS1 nt.110 with the proportions(26.76%) and (20.34%), respectively. No IVS2nt.745 was detected within the studied samples.Genotypic distribution of the samples indicated that there is no significant difference (p > 0.05)between the frequency of homozygotes and heterozygotes within patient group, while there is asignificant difference at (P < 0.01) in comparison with the control group.The study of association between the number and the types of mutations revealed that 28(58%) ofpositive cases have single mutation in a homozygous state or heterozygous state whichsignificantly associated at (P < 0.05) with β-thalassaemia mutations, whereas 20(42%) of thesecases have compound mutations. The most frequent association appeared between IVS1 nt.110 andCodon 39 mutations.Finally, mutations within families, pointed to a positive correlation between the types of mutationsin sons or daughters and their fathers and/or mothers; this indicates the accuracy of the ARMStechnique in detection of β-thalassaemia mutations. This conclusion should be taken with cautiondue to the limited number of families.

Beta-thalassaemia --- mutation --- ARMS-PCR --- Iraq