Since its emergence as a major cause of coronavirus pneumonia, SARS-CoV-2 has spread quickly all over the world. The pandemic has affected all aspects of life and continues to spread despite the stringent control measures. Meanwhile, scientists all around the world have been scrambling to ascertain how the virus spreads and find out the effective ways to put this outbreak quickly under control, focusing on both persistent strict domestic interventions and vigilance against exogenous imported cases (1,2). Several cases of family clusters have been reported and evidence of person-to-person transmission has been confirmed. Indicating the importance of early detection and isolation of infected patients (3,4). Hence then special caution is needed for asymptomatic patients particularly for family members.
Daw MA, Ahmed MO, ET AL.(1-2021)

Several reports have discussed possible bony morphological causes of fetlock pathology but without relating them to its morphometry. Radiographic measurement is widely used in constructing numerical databases of bone morphometry. Such measurements would not be reliable unless all factors affecting the radiographs were considered. Therefore, this study aimed to establish a specific dorsopalmar view (DP) for fetlock radiographic measurements, and then to develop reliable and repeatable fetlock parameters that represent fetlock conformation on those DP radiographs. Ten cadaveric forelimbs from ten adult horses were cut at the distal third of the radius and mounted in a normal posture for DP radiography. Specific features on fetlock bones were used as landmarks to identify the DP at zero degrees. Other bony features were selected as landmarks for developing fetlock parameters on these radiographs. Twenty-seven parameters were designed in the form of angles (12) and ratios (15). The repeatability and consistency of each parameter was tested. A specific fetlock DP view was determined at zero degrees based on certain landmarks. All angular and ratio parameters showed high reliability and consistency in their measurements. The established parameters provide an opportunity to test the relationship between fetlock morphometrics and performance, or the likelihood of certain pathologies.
Abdulrhman Mohamed Salah Alrtib, Aiman Hussein Saleh Oheida, Mohamed Hamrouni S. Abushhiwa, Helen M S Davies(3-2019)

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)