Microhardness of Calcium-enriched Mixture Cement and Covering Glass Ionomers after Different Time Periods of Application

Introduction: Various studies have recommended using calcium-enriched mixture (CEM) cement in different endodontic treatments, including vital pulp therapy. However, possible reciprocal effects of the covering glass ionomer cement (GIC) on their mechanical properties have not been yet investigated in detail. The current research aimed to experimentally evaluate the surface microhardness of CEM cement and the covering GICs after different application/testing times. Materials and Methods: Using stainless steel moulds (8×4×4 mm), CEM cement samples were prepared (n=120) and randomly divided into 12 experimental groups (n=10). CEM cement with thickness of 4 mm was inserted into the moulds, and the remaining spaces were filled with self-cured or light-cured resin-modified GICs at three-time intervals; immediate, in 15 min and after 24 h. Then, the samples were incubated for one and seven days. Using a Vickers microhardness tester, the microhardness of CEM and GICs was measured. The data were analyzed using two-way ANOVA and Tukey’s test, and the significance level was set at 5% (P<0.05). Results: The reciprocal effects of the type/time of application of GICs on the surface microhardness of CEM cement or GICs were statistically significant (P<0.001). The surface microhardness of CEM cement and both covering GICs significantly increased over time and in seven-day samples was significantly higher than in one-day samples (P<0.05). Conclusions: Low surface microhardness of CEM/GICs in short-term (24 h) seems transient; and appears to be compensated over a longer period (i.e. 7-day). Therefore, using GICs adjacent to CEM cement in single-visit restorative treatments may be advocate

Nerve Stimulator Guided Axillary Block in Painless Reduction of Distal Radius Fractures; a Randomized Clinical Trial

Introduction: Given the high prevalence of upper extremity fractures and increasing need to perform painless reduction in the emergency departments, the use of analgesic methods with fewer complications and more satisfaction appears to be essential. The aim of this study is comparison the nerve stimulator guided axillary block (NSAB) with intravenous sedation in induction of analgesia for painless reduction of distal radius fractures. Methods: In the present randomized clinical trial, 60 patients (18-70 years of age) suffered from distal radius fractures, were divided into two equal groups. One group received axillary nerve block by nerve stimulator guidance and the other procedural sedation and analgesia (PSA) using midazolam/fentanyl. Onset of analgesia, duration of analgesic effect, total procedure time and pain scores were recorded using visual analogue scale (VAS) and the outcomes were compared. Chi-squared and student t test were performed to evaluate differences between two groups. Results: Sixty patients were randomly divided into two groups (83.3% male). The mean age of patients was 31 ±0.7 years. While the onset of analgesia was significantly longer in the NSAB group, the mean total time of procedure was shorter than PSA (p<0.001). The NSAB group needed a shorter post-operative observation time (P<0.001). Both groups experienced equal pain relief before, during and after procedure (p>0.05). Conclusion: It seems that shorter post-operative monitoring time and consequently lesser total time of procedure, make nerve stimulator guided axillary block as an appropriate alternative for procedural sedation and analgesia in painless reduction of distal radius fractures in emergency department.

A Dietary Regimen of Caloric Restriction or Pharmacological Activation of SIRT1 to Delay the Onset of Neurodegeneration

Caloric restriction (CR) is a dietary regimen known to promote lifespan by slowing down the occurrence of age-dependent diseases. The greatest risk factor for neurodegeneration in the brain is age, from which follows that CR might also attenuate the progressive loss of neurons that is often associated with impaired cognitive capacities. In this study, we used a transgenic mouse model that allows for a temporally and spatially controlled onset of neurodegeneration to test the potentially beneficial effects of CR. We found that in this model, CR significantly delayed the onset of neurodegeneration and synaptic loss and dysfunction, and thereby preserved cognitive capacities. Mechanistically, CR induced the expression of the known lifespan-regulating protein SIRT1, prompting us to test whether a pharmacological activation of SIRT1 might recapitulate CR. We found that oral administration of a SIRT1-activating compound essentially replicated the beneficial effects of CR. Thus, SIRT1-activating compounds might provide a pharmacological alternative to the regimen of CR against neurodegeneration and its associated ailments.National Institutes of Health (U.S.) (Grant PO1 AG027916

Quantum dots: synthesis, bioapplications, and toxicity

This review introduces quantum dots (QDs) and explores their properties, synthesis, applications, delivery systems in biology, and their toxicity. QDs are one of the first nanotechnologies to be integrated with the biological sciences and are widely anticipated to eventually find application in a number of commercial consumer and clinical products. They exhibit unique luminescence characteristics and electronic properties such as wide and continuous absorption spectra, narrow emission spectra, and high light stability. The application of QDs, as a new technology for biosystems, has been typically studied on mammalian cells. Due to the small structures of QDs, some physical properties such as optical and electron transport characteristics are quite different from those of the bulk materials

Differences in right ventricular dysfunction in patients with idiopathic pulmonary hypertension versus secondary pulmonary hypertension

Introduction: Right ventricular (RV) function in the setting of pulmonary hypertension based on different etiologies has not been well studied. In this study, we evaluated the RV function in patients with idiopathic pulmonary hypertension (IPH) versus secon-dary pulmonary hypertension (SPH) due to congestive heart failure. Material and method: Forty-five patients with pulmonary hypertension and New York Heart Association (NYHA) functional class II or III were enrolled. Of these, 22 were diagnosed with IPH and 23 with SPH. Echocardiographic data, including Doppler and Doppler based strain, were assessed according to the American Society of Echocardiography (ASE) guidelines for detailed evaluation of RV function in these two groups. Results: Mean PAP was 60 ± 14.5 mm Hg in patients with IPH versus 43 ± 11.5 mm Hg in patients with SPH (p = 0.001). Considering conventional indexes of RV function, only Sm and dp/dt were significantly better in the first group compared with the second group (p-value for Sm = 0.042 and for dp/dt = 0.039). RV end diastolic dimension was significantly higher in the IPH group (p = 0.013). Using deformation indexes of RV function, the basal and mid portion of RV free wall strain and basal RV strain rates were significantly worse in the chronic systolic heart failure (PH-HF) group in comparison to the IPH group (p < 0.001 in basal RV strain, p = 0.034 in mid RV strain and p = 0.046 in basal RV strain rate respectively).Conclusion: IPH has less impact on RV function in comparison to PH-HF. Considering both entities are in the category of RV pressure overload, we conclude that the etiology of pulmonary hypertension also plays an important role in RV function in addition to pressure overload

Aortic Valve Area and Strain Measurements by Cardiac MRI and Transthoracic Echocardiography in Severe Aortic Stenosis with Normal Left Ventricular Function

Background: Transthoracic echocardiography (TTE) is the recommended imaging technique for the evaluation of patients with aortic stenosis (AS). However, in cases with inconclusive findings, cardiac magnetic resonance (CMR) planimetry is used to grade AS severity. This study aimed to compare the results derived from TTE and CMR in patients with severe AS with normal left ventricular (LV) function.Methods: In a prospective study, 20 patients with severe AS were recruited and data derived from TTE and CMR modalities were compared with the archived records of 28 age- and sex-matched healthy controls. The data included aortic valve area (AVA), MRI-derived biventricular global strains, and TTE-derived global longitudinal strain (GLS). SPSS software was used to analyze the data with independent samples t test, intraclass correlation coefficient (ICC), and Pearson correlation. P<0.05 was considered statistically significant.Results: An excellent agreement was found in AVA values derived from CMR and TTE with an average ICC of 0.932 (95% CI=0.829-0.973). There was a significant difference in LV-GLS, LV global radial strain (GRS), right ventricular (RV) GRS, and RV global circumferential strain between the groups. A good correlation was found between CMR- and TTE-derived GLS with an average ICC of 0.721 (95% C=0.255-0.896). The mean aortic valve pressure gradient in TTE had a significant inverse linear correlation with LV-GRS in CMR (r=-0.537). All P values were <0.05.Conclusion: There was a good agreement between AVA and strain values derived from cardiac MRI and TTE. The myocardial strain was impaired in patients with severe AS and normal LV function and correlated with disease severity

An epigenetic blockade of cognitive functions in the neurodegenerating brain

Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer’s disease [superscript 1]. The causes leading to such impairment are only poorly understood and effective treatments are slow to emerge [superscript 2]. Here we show that cognitive capacities in the neurodegenerating brain are constrained by an epigenetic blockade of gene transcription that is potentially reversible. This blockade is mediated by histone deacetylase 2, which is increased by Alzheimer’s-disease-related neurotoxic insults in vitro, in two mouse models of neurodegeneration and in patients with Alzheimer’s disease. Histone deacetylase 2 associates with and reduces the histone acetylation of genes important for learning and memory, which show a concomitant decrease in expression. Importantly, reversing the build-up of histone deacetylase 2 by short-hairpin-RNA-mediated knockdown unlocks the repression of these genes, reinstates structural and synaptic plasticity, and abolishes neurodegeneration-associated memory impairments. These findings advocate for the development of selective inhibitors of histone deacetylase 2 and suggest that cognitive capacities following neurodegeneration are not entirely lost, but merely impaired by this epigenetic blockade.Stanley Medical Research InstituteNational Institute of Neurological Disorders and Stroke (U.S.) (RO1NS078839)Swiss National Science FoundationBard Richmond (Fellowship)Simons FoundationTheodor und Ida Herzog-Egli Foundatio

An Epigenetic Blockade of Cognitive Functions in the Neurodegenerating Brain

Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer’s disease. The causes leading to such impairment are only poorly understood and effective treatments are slow to emerge. Here we show that cognitive capacities in the neurodegenerating brain are constrained by an epigenetic blockade of gene transcription that is potentially reversible. This blockade is mediated by histone deacetylase 2, which is increased by Alzheimer’s-disease-related neurotoxic insults in vitro, in two mouse models of neurodegeneration and in patients with Alzheimer’s disease. Histone deacetylase 2 associates with and reduces the histone acetylation of genes important for learning and memory, which show a concomitant decrease in expression. Importantly, reversing the build-up of histone deacetylase 2 by short-hairpin-RNA-mediated knockdown unlocks the repression of these genes, reinstates structural and synaptic plasticity, and abolishes neurodegeneration-associated memory impairments. These findings advocate for the development of selective inhibitors of histone deacetylase 2 and suggest that cognitive capacities following neurodegeneration are not entirely lost, but merely impaired by this epigenetic blockade