Biography
Currently working in academics with interest in research & hematology.
Abstract
Sickle-cell disease (SCD) is an autosomal recessive genetic blood disorder. Coenzyme Q10 is an oil-soluble, vitamin-like substance. The aim was to explore the possible role of coenzyme Q10 in improving the treatment and prognosis in sickle cell patient community. The first step towards this goal was to determine the levels of Coenzyme Q10 in sickle cell subjects. In this case controlled study of sickle cell disease patients and healthy matched controls, male and females were in 1:1 ratio. Both groups were submitted to data collection regarding age, sex, height, weight and average number of hospitalisations. Various haematological and physiological parameters were measured. Quantitative estimations of Coenzyme Q10 levels were done for both groups. Levels of Coenzyme Q10 were remarkably lower in sickle cell subjects as compared to normal ones. The levels of CoQ10 reported in this study are in the range of 1160 ngm/ml to 2309 ngm/ml for normal subjects while that among sickle cell subjects lies within a range of 650-1264 ngm/ml. On comparing the levels of CoQ10 with age, it was clearly evident in both males and females within each age subgroup that after initial increase, the levels of CoQ10 decreases with age. It can be concluded that Coenzyme Q10 levels showed significant variation between normal and sickle cell subjects and owing to its role in cellular bioenergetics and free radical metabolism, further research is needed to explore the effect of CoQ10 in sickle cell patients.
Biography
Hulya Cabadak is an Associate Professor at Marmara University, Turkey. Her research areas are Cancer Research, Cell Biology, Biology
Abstract
Acetylcholine is a neurotransmitter in the nervous system but it serves also as a paracrine or autocrine factor in different cell types, where it is linked to functions like proliferation and cell differentiation. Muscarinic receptors are relatively abundant in the central nervous system and peripheral parasympathetic nervous system. Many cells express a mixture of muscarinic receptor transcripts. Changes in muscarinic M2 and M3 receptor mRNA levels in response to agonist treatment have been reported in cerebellar granule cells, Chinese hamster ovary cells, lymphocytes and in the human neuroblasto macellline SH-SY5Y. Several researchers have suggested that non-neuronalacetylcholine and cholinergic agonists alter cell growth and proliferation of lymphocytes. Costa et al. demonstrated that acetylcholine released from T-lymphocytes acts via the M3 acetylcholine muscarinic receptor (mAChR) to trigger nuclear signaling and up-regulation of gene expression in T and B-lymphocytes. We have previously demonstrated the presence of M2, M3 and M4 mAChRs and M3 subtype mediated NO signaling in K562 chronic myelogenous leukemic cells. We also showed that carbacho (CCh), cholinergic agonist, treatment leads to changes in muscarinic M2, M3 and M4 receptor transcripts as well as M2 and M3 protein levels and enhances cyclic adenosine monophosphate (cAMP) accumulation in K562 cells. In this study, we investigated the levels of muscarinic receptor protein expression in megacaryocytic differentiated K562 leukemia cells. And we also investigated the effects of agonist stimulation on megacaryocytic differentiated K562 leukemia cells proliferation. Muscarinic cholinergic receptors activate stimulatory growth mechanisms in megacaryocytic differentiated K562 leukemia cells. stimulation on cell proliferation and expression in megacaryocytic differentiated K562 leukemia cells. We also found that CCh changed proliferation of megacaryocytic differentiated K562 cells proliferation in 24 hour, These results suggest that CCh modulates megacaryocytic differentiated K562 leukemic cells proliferation through muscarinic acetylcholine receptorsrnWe showed that CCh-treatment leads to changes in muscarinic M2, M3, and M4 receptor transcripts as well as M2 and M3 protein levels.rn