ABSTRACT
Background:Despite progress in the health indexes in recent years, health inequalities remain as a global challenge within and between regions and countries. This study is the first to quantify the socioeconomic inequity in gastroesophageal reflux disease [GERD] using the concentration index
Methods: In this cross-sectional study, we used baseline data [7012 subjects] from the Fasa Cohort Study [the Southern Iran]. The principal component analysis was used to construct socioeconomic status of the participants. The concentration index and concentration curve were used to measure socioeconomic- related inequality in GERD. Decomposition of concentration index was also done to identify the contribution of each explanatory variable to the wealth-related inequality in GERD prevalence
Results: The prevalence of GERD was 16.9% [95% CI: 15.9-17.7%]. The overall concentration index for GERD was 0.093 [95% CI: 0.062-0.166]. Correspondingly, this figure for men and women were 0.116 [95% CI: 0.062-0.171%] and 0.091 [95% CI: 0.044-0.137%], respectively. The main contributors of socioeconomic-related inequality in GERD prevalence were socioeconomic status [64.4%], alcohol drinking [29%], and age [8.4%]
Conclusion: GERD is significantly more concentrated among richest people. There was significant socioeconomic inequality in GERD according to some individual factors. These inequalities need to be addressed by policy makers to identify the vulnerable subgroups and to reduce the disease burden in the community
ABSTRACT
Neurodegeneration is the pathophysiological basis for permanent neurological disabilities in multiple sclerosis [MS]; thus neuroprotection is emerging as a therapeutic approach in MS research. Modulation of excitotoxicity by inhibition of NMDARs has been suggested for neuroprotection. but selective antagonisation of the NR2B subtype of these receptors, a subtype believed to play a more pivotal role in neurodegeneration, has not been tested in MS. In this study inhibition of NR2B-containing NMDAR was evaluated on the animal model of MS, experimental autoimmune encephalomyelitis [EAE]. EAE induction was done using MOG in C57BL/6 mice. Therapeutic administration of different doses of highly selective NR2B-containing NMDAR inhibitor [RO25-6981] was compared with memantine [non-selective NMDAR antagonist] and vehicle. Neurological deficits in EAE animals were more efficiently decreased by selective inhibition of NR2B-containing NMDARs. Histological studies of the spinal cords also showed decreased inflammation, myelin degradation and neuro-axonal degeneration when RO25-6981was administered with higher doses. The effects were dose dependent. Regarding the role of NR2B-containing NMDARs in excitotoxicity, selective inhibition of these receptor subtypes seems to modulate the neurological disabilities and pathological changes in EAE. Further elucidation of the exact mechanism of action as well as more experimental studies can suggest NR2B-containing NMDAR inhibition as a potentially effective treatment strategy for slowing down the clinical deterioration of disability in MS