Inflammatory bowel disease (IBD) is a general term describing chronic, idiopathic relapsing, inflammatory conditions of the gastrointestinal tract of unknown etiology. Previous studies have indicated that Malva parviflora leaf extract possesses anti-inflammatory, antioxidant, and antiulcerogenic activity. activity. This work aimed to investigatee the anti-inflammatory effect of the methanolic (MEMP) and aqueous (AEMP) extracts of M. parviflora leaves on acetic acid-induced colitis in rats. arabic 19 English 104
Aisha Mohamed Dugani, Soad Treesh(5-2016)

Cellular elements of maturing brain are vulnerable to insults, which lead to neurodevelopmental defects. There are no established treatments at present. Here we examined the efficacy of selective adenosine A2A receptor inhibitor SCH58261 to combat brain injury, particularly oligodendrocyte (OL) lineage cells, in young rats. Wistar rats (n = 24, 6.5 days old) were randomly divided into equal groups of four. The sham (SHAM) group received no treatment, the vehicle (VEHICLE) group received 0.1% dimethylsufoxide, the injury (INJ) group was exposed to oxygen-glucose deprivation insult, and the injury+SCH58261 (INJ+SCH58261) group was exposed to the insult and received 1 μM SCH58261. Immunocytochemical experiments revealed that there was a significant reduction in the populations of mature OL (MBP+ OLs) and immature OL precursors (NG2+ OPCs) in the INJ group compared to SHAM group. Furthermore, there was also a significant increase in the percent of apoptotic MBP+ OL and NG2+ OPC populations as evidenced by TUNEL assay. In addition, there was a significant reduction in the proliferation rate among NG2+ OPCs, which was confirmed by BrdU immunostaining. On the other hand, treatment with SCH58261 significantly enhanced survival, evidenced by the reduction in apoptotic indices for both cell types, and it is preserved the NG2+ OPC proliferation. Activation of adenosine A2A receptors may contribute to OL lineage cell loss in association with decreased mitotic behavior of OPCs in neonatal brains upon injury. Future investigations assessing ability of SCH58261 to regenerate myelin will provide insights into its wider clinical relevance.
Mohamed A. Al-Griw, Rabia O. Alghazeer, Nuri Awayn, Ghalia Shamlan, Areej A. Eskandrani, Afnan M. Alnajeebi, Nouf A. Babteen, Wafa S. Alansari(1-2020)

Mutations in the TAL1 (T-cell acute leukemia 1) gene were recently described in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and in those with lymphoblastic T-cell non-Hodgkin’s lymphoma (T-NHL). The purpose of this pilot study was to assess the prevalence of mutations in TAL1 gene in T-ALL and TNHL. DNA samples from 15 unrelated healthy controls, 20 T-ALL patients, and 10 T-NHL patients were analyzed using DNA-PCR and direct DNA sequencing to identify sequence genetic variations in TAL1 gene (exons 2 and 3). TAL1 exon 2 mutations were identified in 7.7% adult and 12.5% adolescent T-ALL patients analyzed. TAL1 exon 2 mutations were detected in 16.7% of the adult TNHL patients analyzed. Sequencing of TAL1 exon 3 showed no sequence variation for the T-ALL and T-NHL cancer patients analyzed. No sex difference where observed in the incidences of TAL1 exons 2 mutations between T-ALL and T-NHL patients with and without TAL1 mutations. TAL1 exon 2 missense and frame-shift mutations were present in 44.4% (4/9) and 55.6% (5/9) of T-ALL patients, respectively. However, the frame-shift and missense mutations in the T-NHL patients accounted for, where respectively, 60% (3/5) and 40% (4/5) of all TAL1 exon 2 mutations. Comparing the clinical features showed that there are no differences in PLT and WBC counts as well as the average age between T-ALL and T-NHL patients with and without TAL1 mutations. Overall, these findings indicate that TAL1 mutations are too rare to be of clinical relevance, and do not seem to be significantly associated with the increased T-ALL and T-NHL susceptibility, implying different pathways with respect to TAL1 genetic polymorphisms as a risk factor for T-ALL and T-NHL at least in this population of Libyans.
Amal E. Elarifi, Othman A. El-Ansari, Mohamed A. Al-Griw(12-2016)