Biocompatibility of Accelerated Mineral Trioxide Aggregate on Stem Cells Derived from Human Dental Pulp

The aim of this study was to evaluate the effects of several additives on the setting time and cytotoxicity of accelerated-set mineral trioxide aggregate (MTA) on stem cells of human dental pulp. ProRoot white MTA (WMTA) (Dentsply Tulsa Dental, Johnson City, TN) was mixed with various additives including distilled water, 2.5% disodium hydrogen phosphate (Na2HPO4) (Merck, Darmstadt, Germany), K-Y Jelly (Johnson & Johnson, Markham, ON, Canada), and 5% and 10% calcium chloride (CaCl2) (Merck). The setting times were evaluated using a Vicat apparatus (Alsa Lab, Istanbul, Turkey). Human dental pulp stem cells were isolated and seeded into 48-well plates at 2 x 10(3) cells per well and incubated with MTA samples for 24 hours, 3 days, and 7 days. Cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. MTA mixed with 10% CaCl2 showed the lowest setting time (P < .05). According to the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sullophenyl)-2H-tetrazolium results on the 1st, 3rd, and 7th days, a statistically significant difference was found (P < .05) between MTA groups and the control group. MTA mixed with K-Y Jelly in all groups showed the lowest cell viability at all time points (P < .05). The cell viability of MTA mixed with distilled water, 5% CaCl2, 10% CaCl2, and Na2HPO4 increased significantly through time (P < .05). This in vitro study found MTA mixed with 5% and 10% CaCl2 and Na2HPO4 is biocompatible with dental pulp stem cells in terms of cell viability. Further in vitro and in vivo investigations are required to prove the clinical applications of MTA mixed with various additives

Seasonality of 7

This study aims at analysing the latitudinal variability of both the yearly and seasonal pattern of 7Be surface activity concentrations, at addressing the impact of tropopause height (TPH) on 7Be distribution and at evaluating the time lag between TPH and 7Be at European level. With this aim, weekly 7Be and daily TPH data at 17 sampling stations during 10 yr (2001–2010) are analysed. 7Be shows a clear increasing tendency in the period and generally tends to increase with decreasing latitude. The seasonal pattern generally shows maxima during the warm period and minima during the cold one. The seasonal variogram analysis points out a good spatial correlation for TPH data while a weaker one is observed for 7Be, having TPH a larger influence on 7Be during summer. The influence of TPH on 7Be exhibits a large spatial variability, with a clear gap between south and north in the area of the polar front jet. The results identify the presence of two main groups, in particular separating between stations located in northern Europe (50 °N and higher) and stations in southern Europe (south of 50 °N). A similar behaviour for stations located in the same geographical area is also observed when looking at the day of maximum impact of TPH on 7Be concentrations. The results suggest that 7Be concentrations respond in different time ranges to changes in the TPH, observing seasonal differences in each group. These results represent the first European approach to the understanding of the TPH impact on 7Be concentrations at surface levels

Is hypertensive left ventricular hypertrophy a cause of sustained ventricular arrhythmias in humans?

Sudden cardiac death (SCD) is most commonly secondary to sustained ventricular arrhythmias (VAs). This review aimed to evaluate if left ventricular hypertrophy (LVH) secondary to systemic hypertension in humans is an isolated risk factor for ventricular arrhythmogenesis. Animal models of hypertensive LVH have shown changes in ion channel function and distribution, gap junction re-distribution and fibrotic deposition. Clinical data has consistently exhibited an increase in prevalence and complexity of non-sustained VAs on electrocardiographic monitoring. However, there is a dearth of trials suggesting progression to sustained VAs and SCD, with extrapolations being confounded by presence of co-existent asymptomatic coronary artery disease (CAD). Putatively, this lack of data may be due to the presence of more homogenous distribution of pathophysiological changes seen in those with hypertensive LVH versus known pro-arrhythmic conditions such as HCM and myocardial infarction. The overall impression is that sustained VAs in the context of hypertensive LVH are most likely to be precipitated by other causes such as CAD or electrolyte disturbance