The hypothetical roles of arsenic in multiple sclerosis by induction of inflammation and aggregation of tau protein: A commentary

Multiple sclerosis (MS) is a disease which manifests demyelination of neuronal cells in the brain. Despite extensive research on the mechanisms of disease development and progression, the exact mechanism is not elucidated yet, which has hampered drug development and subsequent treatment of the disease. We have recently shown that the serum levels of arsenic and malondialdehyde, a lipid peroxidation marker, are high in MS patients. In this article, we would like to formulate the hypothesis that arsenic may cause MS by induction of inflammation, degeneration, and apoptosis in neuronal cells. The induction of ROS generation in cells upon exposure to arsenic as a heavy metal may be involved in the pathogenesis of MS. Tau protein, a member of the family of microtubule-associated proteins, is mainly expressed in neurons and contribute to the assembly of neuronal microtubules network. Arsenic may affect the hyperphosphorylation and aggregation of tau proteins and may be involved in the cascade leading to deregulation of tau function associated with neurodegeneration. For validation of this hypothesis, studies might be conducted to evaluate the association of arsenic levels and tau protein levels in MS patients. Further studies might also focus on the trafficking along microtubules in neurons of MS patient with regard to hyperphosphorylation of tau protein. This hypothesis may add a new dimension to the understanding of MS etiology and help to design novel therapeutic agents against potential targets that might be discovered. If this hypothesis proves to be true, tau phosphorylation inhibitors can be potential candidates for MS drug development.     

The Jefferson Scale of Empathy: a nationwide study of measurement properties,underlying components,latent variable structure,and national norms in medical students

The Jefferson Scale of Empathy (JSE) is a broadly used instrument developed to measure empathy in the context of health professions education and patient care. Evidence in support of psychometrics of the JSE has been reported in health professions students and practitioners with the exception of osteopathic medical students. This study was designed to examine measurement properties, underlying components, and latent variable structure of the JSE in a nationwide sample of first-year matriculants at U.S. colleges of osteopathic medicine, and to develop a national norm table for the assessment of JSE scores. A web-based survey was administered at the beginning of the 2017–2018 academic year which included the JSE, a scale to detect “good impression” responses, and demographic/background information. Usable surveys were received from 6009 students enrolled in 41 college campuses (median response rate?=?92%). The JSE mean score and standard deviation for the sample were 116.54 and 10.85, respectively. Item-total score correlations were positive and statistically significant (p?<?0.01), and Cronbach α?=?0.82. Significant gender differences were observed on the JSE scores in favor of women. Also, significant differences were found on item scores between top and bottom third scorers on the JSE. Three factors of Perspective Taking, Compassionate Care, and Walking in Patient’s Shoes emerged in an exploratory factor analysis by using half of the sample. Results of confirmatory factor analysis with another half of the sample confirmed the 3-factor model. We also developed a national norm table which is the first to assess students’ JSE scores against national data.     

Predictive ability of C-reactive protein for early mortality after ischemic stroke: comparison with NIHSS score

We aimed to compare the association of high-sensitivity C-reactive protein (CRP) and National Institutes of Health Stroke Scale (NIHSS) score with mortality risk and to determine the optimal threshold of CRP for prediction of mortality in ischemic-stroke patients. A series of 162 patients with first-ever ischemic-stroke admitted within 24 h after onset of symptoms was enrolled. CRP and NIHSS score were estimated on admission and their predictive abilities for mortality at 7 days were determined by logistic-regression analyses. Receiver-Operating Characteristic (ROC) curves were depicted to identify the optimal cut-off of CRP, using the maximum Youden-index and the shortest-distance methods. Deceased patients had higher levels of CRP and NIHSS on admission (8.87 ± 7.11 vs. 2.20 ± 4.71 mg/l for CRP, and 17.31 ± 6.36 vs. 8.70 ± 4.85 U for NIHSS, respectively, P < 0.01). CRP and NIHSS were correlated with each other (r ² = 0.39, P < 0.001) and were also independently associated with increased risk of mortality [odds ratios (95 % confidence interval) of 1.16 (1.05–1.28) and 1.20 (1.07–1.35) for CRP and NIHSS, respectively, P < 0.01]. The areas under the ROC curves of CRP and NIHSS for mortality were 0.82 and 0.84, respectively. The CRP value of 2.2 mg/l was identified as the optimal cut-off value for prediction of mortality within 7 days (sensitivity: 0.81, specificity: 0.80). Thus, CRP as an independent predictor of mortality following ischemic-stroke is comparable with NIHSS and the value of 2.2 mg/l yields the optimum sensitivity and specificity for mortality prediction.     

Acid and Microhardness of Mineral Trioxide Aggregate and Mineral Trioxide Aggregate–like Materials

Introduction

The aim of this study was to compare the surface microhardness of BioAggregate, ProRoot MTA, and CEM Cement when exposed to an acidic environment or phosphate-buffered saline (PBS) as a synthetic tissue fluid.

Methods

Ninety cylindrical molds made of polymethyl methacrylate with an internal diameter of 6 mm and height of 4 mm (according to ASTM E384 standard for microhardness tests) were fabricated and filled with BioAggregate (n = 30), tooth-colored ProRoot MTA (n = 30), or CEM Cement (n = 30). Each group was then divided into 3 subgroups of 10 specimens consisting of those exposed to distilled water, exposed to PBS (pH = 7.4), or exposed to butyric acid (pH = 5.4). After 1 week the Vickers surface microhardness test was performed. Statistical analysis included 2-way analysis of variance, followed by post hoc Dunnett T3 in cases with lack of homoscedasticity and Tukey honestly significant difference in cases with homoscedasticity.

Results

The indentations obtained from the CEM Cement specimens exposed to an acidic pH were not readable because of incomplete setting. There was a significant difference between the microhardness of the materials regardless of the environmental conditions (P < .001). In all the environmental conditions, MTA had significantly higher and CEM Cement had significantly lower microhardness values (P < .001). All experimental cements had significantly higher microhardness values when exposed to PBS (P < .001) and had significantly lower microhardness values when exposed to butyric acid (P < .001).

Conclusions

The surface microhardness of BioAggregate, ProRoot MTA, and CEM Cement was reduced significantly by exposure to butyric acid and increased significantly by exposure to PBS. In all environmental conditions, MTA had significantly higher microhardness values.