Background and Aims: Despite the well‑known association between human papillomavirus (HPV) and cervical cancer, yet there are no available data concerning the prevalence of HPV and its type distribution among Libyan women. The aim of this study was to investigate the prevalence of the most common high‑risk HPV types 16 and 18 among Libyan women in Tripoli and to compare it with the cytological findings of the cervix. Methods: A total of 132 cervical samples were collected from women who sought medical attention at the gynecology outpatient clinic of the Tripoli University Hospital and other gynecology private clinics in Tripoli region. Cervical cytological status was classified according to the Bethesda System 2014. Quantitative polymerase chain reaction was used to facilitate the specific detection of HPV types 16 and/or 18. Results: The cytopathological examination showed that 92.4% of women had normal cervical cytology (n = 122/132) and 7.5% (n = 10/132) of them had cervical lesions. The overall prevalence of the most common oncogenic HPV types was 4.5%, as only six samples (n = 6/132) were confirmed of harboring HPV‑DNA. Concerning the cytological status of the cervix, HPV‑DNA was not found (0%) in women with a normal cervix, and it was present in 60% of women with cervical lesions. The high‑risk HPV type 16 was the exclusive type among our all positive samples, with no detection of HPV type 18 among all our recruited subjects. Conclusion: Even though our findings showed a low overall prevalence of high‑risk HPV types among Libyan women, the burden of HPV 16 among women with cervical lesions highlights the need to raise attention toward expanding research about HPV and adopt measures to prevent cervical cancer by vaccination and national screening program. The introduction of HPV‑DNA testing in cervical cancer management will greatly benefit early‑stage HPV detection and help prevent cervical lesions from progression to cancer. arabic 15 English 81
H Alzaquzi, A Bashein(1-2019)

Reactive gliosis and inflammation are risk factors for white matter injury (WMI) development, which are correlated with the development of many neurodevelopmental deficits with no treatment. This study aimed to understand the mechanisms correlated with WMI, with a particular focus on the role of nuclear factor‑kappa B (NF‑kB) and p38 mitogen‑activated protein kinases (MAPKs) pathways. Seven‑day‑old Wistar rats were used to generate cerebellar tissue slices. Slices were cultured and randomly allocated to one of 3 groups and treated as follows: group‑I (control); group‑II (WMI), slices were subjected to 20 min of oxygen‑glucose deprivation (OGD); group‑III (WMI+ blockers), slices were subjected to OGD and treated with the blockers. Results showed that OGD insult triggered a marked increase in the apoptosis among WM elements, as confirmed by TUNEL assay. Immunocytochemical experiments revealed that there was a significant decrease in the percent of MBP+ OLs and NG2+ OPCs, and myelin integrity. There was also a significant increase in the percent of reactive microglia and astrocytes. BrdU immunostaining revealed there was an increase in the percent of proliferating microglia and astrocytes. Q‑RT‑PCR results showed OGD upregulated the expression levels of cytokines (TNF‑α, IL‑1, IL‑6, and IL‑1β) and inducible nitric oxide synthase (iNOS). On the other hand, treatment with BAY11 or SB203580 significantly enhanced the OL survival, restored myelin loss, and reduced microglia and astrocyte reactivity, and downregulated the iNOS and cytokine expression. Our findings demonstrate that blocking of NF‑KB/p38 MAPK pathways alleviated reactive gliosis, inflammation, and OL loss upon WMI. The findings may help to develop therapeutic interventions for WMI.
Mohamed A. Al-Griw, Michael G. Salter, Ian C. Wood(1-2022)

Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic kidney disorders with the incidence of 1 in 1,000 births. ADPKD is genetically heterogeneous with two genes identified: PKD1 (16p13.3, 46 exons) and PKD2 (4q21, 15 exons). Eighty five percent of the patients with ADPKD have at least one mutation in the PKD1 gene and fifteen percent of the patients have one mutation in PKD2 gene. Direct sequencing of one patient and his sequence of PKD1 gene demonstrated a missense mutation GCC----CCC substitution in exon 13 with cause change amino acid of Alanine to Proline at codon 1029. Three brothers have deletion mutation in exon 15, one patient missense mutation GGC---GCC in exon 19 which cause change amino acid of Glycine to Alanine at codon 2530. Molecular diagnostics of ADPKD relies on mutation screening of PKD1 and PKD2, which is complicated by extensive allelic heterogeneity and the presence of six highly homologous sequences of PKD1. PCR strategy was used to screen sequence variants with heteroduplex analysis and several affected individuals were discovered to have clusters of base pair substitutions in exons 13 and 19 with del 20 pb (3601-3620) in exon15. arabic 14 English 81
Refaat Tabagh, Ahmed Zaid(1-2018)