Papers by ibraheem bamaga
Open Access Macedonian Journal of Medical Sciences, 2021
AIM: The aim of the study is to investigate the role of myoepithelial cells in the pathogenesis o... more AIM: The aim of the study is to investigate the role of myoepithelial cells in the pathogenesis of mucoepidermoid carcinoma (MEC) using the double immunohistochemical staining; α _smooth muscle actin (_α-SMA)as specific marker for the myoepithelial cell differentiation and proliferative cell nuclear antigen (PCNA) as a marker for proliferative activity of myoepithelial cells. MATERIAL AND METHODS: Retrospective study of twenty salivary gland specimens (ten MEC and ten normal salivary glands) were studied using double immunohistochemical labeling for α _smooth muscle actin α-SMA) and proliferative cell nuclear antigen (PCNA). The SPSS statistical package was used for data analysis (IBM SPSS Statistics for Windows, Version 20.0, Released 2011, IBM Corp, and Armonk, NY, USA). RESULTS: In mucoepidermoid carcinomas, no positivity of α-SMA was seen in neoplastic cells (Frequent test), and it was just observed in the stroma of tumor, in the walls of blood vessels whereas, PCNA was positive...
Neurofibromatosis Type I (NF1) syndrome is characterized by neurofibromas and neural tumors but i... more Neurofibromatosis Type I (NF1) syndrome is characterized by neurofibromas and neural tumors but is also associated with skeletal abnormalities. The cellular pathophysiology of skeletal abnormalities in NF1 is not understood. These abnormalities result from constitutive active RAS and its downstream effectors, RASERK pathway, due to mutation of NF1 gene which converts active RAS-GTP into inactive RAS-GDP. In osteoblast cells, RAS-ERK pathway is involved in cell proliferation and differentiation and is also involved in mechanical signals transduction. In this study, we propose that Nf1 mutation in osteoblast cells will affect the response to mechanical stimulation through the RAS pathway. The Flexcell tension system was used to mechanically stimulate calvarial osteoblast precursor from conditional knockout mice, Nf1(ob-/-), and wild type calvarial osteoblast precursor cells, (WT. The protocol of cyclic mechanical strain was 2% to 4% elongation at 0.16 Hz (10 cycles per minute) for 24 ...
Journal of Dental Health, Oral Disorders & Therapy, 2017
Sphenoid wing dysplasia (SWD), which results in a craniofacial deformity, is the third most commo... more Sphenoid wing dysplasia (SWD), which results in a craniofacial deformity, is the third most common skeletal deformity in Neurofibromatosis Type I (NF1) patients. A neurofibromin osteoblast conditional deletion mouse model (Nf1ob-/-) has been developed to study the skeletal abnormalities in NF1. No overt morphological phenotype is seen in the appendicular or axial skeleton of these mice. Nf1ob-/-mice have been shown to have increased bone porosity and lower bone density. We noted a progressive craniofacial deformity, which results in cranial asymmetry, malocclusion and unilateral proptosis of an eye. To assess this deformity, we employed micro-computed tomography (mCT) and geometric morphometric analysis to compare Nf1ob-/-mouse skulls to control animals. Landmarks were placed on the images at 13 biologically relevant cranial anatomical sites. Analysis of distances and angles between these landmarks revealed that there is significant variation between the Nf1ob-/-mice and controls. We found that the nasal and frontal bones of Nf1ob-/-mice skulls are deviated from the central line, whereas it was straight in controls. The nasal region is tipped downward in Nf1ob-/-mice. We also noted that the cranium shows a trend toward macrocephaly in Nf1ob-/-mice whereas other measurements were within the range of normal control mice. These differences correspond to those seen in craniofacial dysplasia and SWD in NF1 patients. No tumors were found associated with the craniofacial dysplasia in Nf1ob-/-mice. Our results identify a primarily osteoblast origin for the pathogenesis of craniofacial dysplasia in Nf1ob-/-mice and strongly support an osteoblast origin for SWD in NF1. In addition, we identify and validate a novel mouse model with which to explore molecular mechanisms and test preventative treatments for SWD in NF1.
Journal of Dental and Craniofacial Research
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Papers by ibraheem bamaga