he present prospective study was designed to conduct a local survey on patients under anti-tuberculosis therapy hospitalized in Abo-Seta hospital, Tripoli, Libya from the safety point of view. The study was carried out on 75 inpatients. The effects of the used drugs on some hematological parameters and liver function biomarkers were monitored for six-month period of treatment. Our survey showed that tuberculosis affects people with low and medium levels of education and with no job. The frequency of adverse effects related to treatment with Abo-Seta hospital regimen were decreases in WBCs count (-38.7%), RBCs count (-32.1%), platelets count (-33%) and hemoglobin concentration (-35.5%). However, in most of the cases, it was not necessary to modify the treatment regimen because of such side effects. Some parameters showed spontaneous recovery as RBCs count (+22.1%) and hemoglobin level (+20.1%). Combined therapy of ethambutol, isoniazid, pyrazinamide, and rifampicin has been used in Abo-Seta hospital, as a regimen for tuberculosis infection, may be associated with a high risk of hepatic toxicity during first month of treatment. However, during the remaining five months there was a good recovery of liver enzymes profile. Upon the data obtained from the present study, it could be concluded that TB patient after 6 month of treatment didn't develop multi-drug resistant tuberculosis (MDR-TB arabic 13 English 83
Marwan Draid(7-2013)

The human 11p15 region is divided into two independent imprinted domains, the H19/IGF2 and CDKN1C/KCNQ1 domains. Each domain is regulated by its own imprinting control regions, ICR1 and ICR2, which carry opposite germline imprints. The expression of 11p15 imprinted genes is regulated by two major mechanisms. ICR1 binds a zinc finger protein (CTCF) on the unmethylated maternal allele and acts as a chromatin insulator, whereas ICR2 is unmethylated on the paternal allele and serves as a promoter for a regulatory non-coding RNA (KCNQ1OT1). Dysregulation of 11p15 genomic imprinting results in two human foetal growth disorders: the Beckwith-Wiedemann (BWS) and the Silver-Russell (SRS) syndromes, which display opposite growth phenotypes. Various 11p15 epigenetic and genetic defects result in BWS and SRS. Gain or loss of DNA methylation account for 60% of BWS and SRS and, in most cases, the mechanism of the DNA methylation defect is unknown. The overall aim of this thesis was to decipher the mechanisms resulting in loss or gain of DNA methylation at ICR1 or ICR2 by investigating large cohorts of BWS and SRS patients displaying a “primary” DNA methylation defect. We aimed at establishing what was the incidence of copy number variations (CNVs) (duplications, deletions and segmental uniparental isodisomies) confined to one or one part of the H19/IGF2 or CDKN1C/KCNQ1 domains. We also screened extensively the ICR1 imprinting control region in BWS and SRS patients to identify new genetic defects. We show in this work that genetic defects in cis account for a significant proportion (approximately 30%) of BWS patients with ICR1 gain of DNA methylation but are rare in SRS and BWS patients with loss of DNA methylation at ICR1 and ICR2, respectively. We describe novel small gain and loss CNVs involving only part of the two domains in BWS and SRS. We also describe, for the first time, mutations and small deletions involving binding sites for the OCT4 and SOX2 pluripotency factors. Those defects account for approximately 14% of BWS cases and result in a BWS phenotype upon maternal transmission. We further characterize the role of OCT4/SOX2 pluripotency factors in the maintenance of genomic imprinting at the H19/IGF2 domain in mouse embryonic stem cells. By screening the whole 11p15 region for susceptibility alleles for loss or gain of DNA methylation, our group identified a novel 4.5 kb cis-regulatory region within the CDKN1C/KCNQ1 domain. A specific 4.5 kb haplotype confers, upon maternal transmission, a risk of ICR2 loss of DNA methylation in BWS patients. This study investigated the mechanism involved in the risk of ICR2 loss of DNA methylation in BWS and showed that within this 4.5 kb region, two SNPs (rs11823023 and rs179436) affect CTCF occupancy at DNA motifs flanking the CTCF 20 bp core motifs. This study identifies a new cis-regulatory region and highlights the crucial role of CTCF for the regulation of genomic imprinting at the CDKN1C/KCNQ1 domain. These recent findings bring new insights in the regulation of genomic imprinting at both the IGF2/H19 and CDKN1C/KCNQ1 domains. arabic 8 English 50
Mansur Ennuri Moftah Shmela(9-2014)

Investigation on the presence of antibodies against Chicken Infectious Anemia in Libya using the Enzyme-Linked Immunosorbent Assay
Abdulatif Asheg(4-2005)