Objectives
Rheumatoid arthritis (RA) has been rarely reported in association with sickle cell disease (SCD). Our study aimed to estimate the prevalence of RA in SCD population and to describe the clinical characteristics of RA associated with SCD.
Methods
Retrospective chart review of SCD and RA patients followed at 2 large urban hospitals. Seven RA/SCD patients were identified and compared to age and sex matched cohort of SCD only and of RA only group. All patients were Black.
Results
There were 739 SCD cases, seven (0.94%) met ACR criteria for RA (SCD-RA), 411 cases were RA only group. Mean age was significantly higher in SCD-RA compared to the entire population of SCD and RA (41.7 ± 3.9 (± SEM) vs. 33.26 ± 0.47, vs. 61.39 ± 0.79, p<0.01).
SCD-RA patients had lower hemoglobin (g/dl) when compared to the age and sex matched SCD or RA only patients (7.4 ± 0.49 vs. 8.3 ± 0.60 vs. 11 ± 0.59, p <0.01) respectively.
There were no significant differences in laboratory and treatment approach between SCD-RA and RA only groups, except for the radiographic evidence of periarticular osteopenia and greater difficulty in the activities of daily living (ADL) among SCD-RA cohort, compared to the age and sex matched RA cohort (p=0.01)
Conclusion
In contrast to older reports, the prevalence of RA among SCD patients in our study (0.94%) was similar to that reported in the general population (0.5–1%) and was to be associated with difficulty in ADL and periarticular osteopenia. Since RA manifests at an older age, our reported prevalence is likely explainable by improved survival of SCD patients due to enhanced medical care and the advent of hydroxyurea as a major therapeutic breakthrough for SCD.
Gill lateral cells of the bivalve Crassostrea virginica are innervated by serotonin and dopamine (DA) nerves from their ganglia and regulate cilia beating rates. DA slows down cilia beating and serotonin speeds them up. GABA a neurotransmitter in vertebrates and many invertebrates rarely has been reported in bivalves. We showed GABA is present in C. virginica and GABA acts as a ganglionic neurotransmitter modulating gill lateral cell cilia activity. We used immunohistofluorescence to localize GABA receptors in ganglia and gill and identify DA receptors in gill lateral cells as D2‐like (D2DR). We hypothesize Western Blot (WB) would verify D2DR and GABA receptors in gill. For WB gill cell lysate was prepared by in NP‐40 detergent buffer containing protease inhibitor, followed by centrifuging to obtain supernatant with solubilized membrane proteins. Up to 30 µg of solubilized protein was subjected to SDS‐PAGE with 10% acrylamide gels and electroblotted onto nitrocellulose. D2DR and GABA receptor immunoreactivity was revealed by 1̊ antibodies followed by HRP‐conjugated 2̊ antibodies. WB showed 70 ‐ 75 kD bands corresponding to DA D2DR and GABA RA1‐6 receptors in gill. The present project allows us to confirm our previous studies showing the presence of DA and GABA and furthers the understanding of their physiological roles in C. virginica.
Accumulations of manganese (Mn) or copper (Cu) is characteristic of the neurodegenerative disorders Manganism and Wilsonˈs Disease, respectively. Mitochondria are a source and target of oxidative stress. Previously we found gill mitochondria from the oyster Crassostrea virginica, treated with Mn or Cu had impaired oxygen utilization. Oxidative damage causes a loss of mitochondrial membrane potential (MMP) with associated mitochondrial dysfunction. Here we used two fluorescent dyes, TMRM and JC‐1, to determine effects of Mn and Cu treatments on MMP. Mitochondria from gill of C. virginica were isolated and treated. For JC‐1 we compared fluorescence intensities at 525/590 nm of Mn treated mitochondria to that of control. Mn treated showed dose dependant decreases in fluorescence. For TMRM we compared slopes of the fluorescence intensity ratios. Treating isolated mitochondria with Cu resulted in a dose dependant reversal in the slopes. Cu was more toxic than Mn. Both fluorescent dyes were effective in demonstrating short term treatments with Mn or Cu could de energize gill MMP. This information correlates well with our previous findings on the toxic effects of Mn and Cu on mitochondrial respiration. Identifying the molecular and cellular mechanisms of metal induced oxidative stress will provide a better understanding of the pathophysiological of neurodegenerative disorders associated with metal toxicity.
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