Background: Worldwide, the prevalence of sickle cell disease (SCD) as of 2016 was estimated at 2%; that is 300,000 births annually. This study was focused on homozygous sickle cell disease which leads to several complications notably hemolytic crises, aplastic crises and vaso-occlusive crises like stroke. Sickle cell disease is the most common cause of childhood stroke. Stroke occurs in 17% -24% of sickle cell children worldwide. Objectives: To determine the risk factors for overt stroke and outcome at discharge in sickle cell disease patients admitted in two reference hospitals in Cameroon. Method: This was a case-control study in two reference hospitals in Yaounde and Douala, carried out over the duration of 4 months, covering a 5-year period (December 2013 to December 2018). Included in the study, were all homozygous sickle cell children aged 6 months to 16 years during that period with or without stroke. A total of 1734 patients fulfilled the inclusion criteria. Out of these, 49 stroke patients participated and 687 were selected as controls. Data was collected from the patients' files and books on a pretested data collection form, then entered in the software C.S Pro 7.1 before analysis. Stroke outcome at discharge was assessed using the modified Rankin scale (mRs) with structured interview. A patient was classified as good outcome if mRs < 3 and poor outcome if mRs ≥ 3. Statistical analysis was done with SPSS software version 22.
lower than that for both of these agents added sequentially. Interestingly, when the sequence of addition of drugs was reversed using 5azaD/SAHA, the reduction in growth (66% vs. 85%, P , 0.05) and percentage of apoptotic cells were lower than in cultures treated with SAHA/5azaD. The greatest amount of glioma cell death induced by SAHA/5azaD corresponded with higher protein levels of the cyclin dependent kinase inhibitor, P 21 , and the minimum fraction of cells in active phases of cell cycle (19% in control vs. 11% in SAHA/5azaD). Furthermore, glioma cells treated with SAHA/ 5azaD or 5azaD/SAHA displayed the highest levels of acetylated histone H4 protein levels, indicating possible epigenetic changes. Our data indicating that the effects of SAHA/5azaD are likely mediated by epigenetic mechanisms is made evident by increases in P 21 and acetylated histone H4 protein levels. Whether such strategies are also effective in primary human glioma tumor cells will be tested, which may ultimately open untapped territories to search for curative therapies.
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