Observation of own exploration movements impairs haptic spatial perception

The present study was designed to assess whether the visibility of ones’ own exploratory movements impairs or enhances perceptual speed and precision of haptic stimuli with varying complexity. Previous studies have shown that noninformative vision of steady surroundings improves haptic spatial perception. However, due to the serial nature of haptic processing and limited capacity of working memory resources, we hypothesized that noninformative vision of limb movements may impair haptic perception. The study sample consisted of ninety-eight healthy adults who were randomized into two groups, matched for sex and age. Participants were required to explore two-dimensional haptic stimuli with varying complexity and to recognize them visually. The difference between the two experimental groups was a screen that would prevent the participants from viewing their hands during exploration in the nonobservation condition (NonOb). The other half of participants were able to see their hands in the manual movement observation condition (MovOb) thanks to the special design of the stimuli. As hypothesized, the persons in the MovOb condition made significantly more errors. The difference in error frequency between participants of the MovOb and NonOb condition was greater for complex stimuli than for simple ones. These results suggest that incoming visual information about own manual exploration movements increases competitive pressure for limited working memory resources, and therefore, more recognition errors are made. Covering the hands during exploration may constitute a helpful simplification of the task’s demands by supporting the maintenance of information in working memory. Additionally, the relation of haptic complexity and stimulus characteristics was analyzed.     

Surface expression and function of Cav3.2 T-type calcium channels are controlled by asparagine-linked glycosylation

Low-voltage-activated T-type calcium channels play important roles in neuronal physiology where they control cellular excitability and synaptic transmission. Alteration in T-type channel expression has been linked to various pathophysiological conditions such as pain arising from diabetic neuropathy. In the present study, we looked at the role of asparagine (N)-linked glycosylation on human Ca_v3.2 T-type channel expression and function. Manipulation of N-glycans on cells expressing a recombinant Ca_v3.2 channel revealed that N-linked glycosylation is critical for proper functional expression of the channel. Using site-directed mutagenesis to disrupt the canonical N-linked glycosylation sites of Ca_v3.2 channel, we show that glycosylation at asparagine N192 is critical for channel expression at the surface, whereas glycosylation at asparagine N1466 controls channel activity. Moreover, we demonstrate that N-linked glycosylation of Ca_v3.2 not only controls surface expression and activity of the channel but also underlies glucose-dependent potentiation of T-type Ca²⁺ current. Our data suggest that N-linked glycosylation of T-type channels may play an important role in aberrant upregulation of T-type channel activity in response to glucose elevations.     

Inhibition of BMP activity protects epithelial barrier function in lung injury

Epithelial injury is a central finding in pulmonary disease and is accompanied by disruption of epithelial barrier function, leading to pulmonary oedema and inflammation. Injured epithelial cells lose their properties and gain mesenchymal characteristics, a phenotypic switch that contributes to lung remodelling after injury. Here we studied bone morphogenetic protein (BMP) signalling and, in particular, the role of BMP2 and the BMP modulator BMPER in injured lung epithelium. Increased BMP activity, reflected by up‐regulation of the Smad1/5–Id1 axis, is detected after injury of lung epithelium in vitro and in vivo. Two members of the BMP family, BMP2 and BMPER, have opposing effects. BMP2 is up‐regulated after epithelial injury and causes epithelial dysfunction and hyperpermeability, mediated by the Smad1/5–Id1‐dependent down‐regulation of E‐cadherin. In contrast, BMPER expression is decreased following injury, which in turn impairs epithelial integrity, characterized by reduction of E‐cadherin and epithelial leakage in vitro and in vivo. High levels of BMPER antagonized BMP2‐Smad5–Id1 signalling and prevented BMP2‐mediated decrease of E‐cadherin and hyperpermeability, suggesting that BMPER restores epithelial homeostasis. Supporting this notion, pharmacological inhibition of BMP signalling by LDN193189 prevented reduction of E‐cadherin and disruption of epithelial barrier function. Inhibition of excessive BMP activation could be a new approach to restore epithelial integrity and prevent disruption of epithelial barrier function after lung injury. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Postmortem age estimation via DNA methylation analysis in buccal swabs from corpses in different stages of decomposition—a “proof of principle” study

International Journal of Legal Medicine - Age estimation based on the analysis of DNA methylation patterns has become a focus of forensic research within the past few years. However, there is...     

Metabolomics in postmortem cerebrospinal fluid diagnostics: a state-of-the-art method to interpret central nervous system–related pathological processes

International Journal of Legal Medicine - In the last few years, quantitative analysis of metabolites in body fluids using LC/MS has become an established method in laboratory medicine and...     

Effect of bone quality and quantity on the primary stability of dental implants in a simulated bicortical placement

Clinical Oral Investigations - Conventional dental implants inserted in the molar region of the maxilla will reach into the sinus maxillaris when alveolar ridge height is limited. When surgery is...     

Anxiety as Predictor of the Cortisol Awakening Response in Patients with Coronary Heart Disease

Background

Anxiety is associated with worse outcomes in patients with coronary heart disease (CHD). A dysregulation of the HPA axis is a potential mechanism linking psychological factors and coronary disease. No study has yet investigated the relationship between anxiety and cortisol among patients with established CHD.

Purpose

The aim of this study was to assess the association between anxiety and the cortisol awakening response in patients with CHD.

Method

Four salivary cortisol samples were used to assess two measures of the cortisol awakening response (CAR) in 47 patients with established CHD. Anxiety was measured using the Hospital Anxiety and Depression Scale (HADS).

Results

Higher anxiety values were associated with a higher total output of cortisol in the first hour after awakening (AUCg, area under the curve with respect to ground) (p?=?0.04) and a nonsignificant trend towards a more pronounced increase (AUCi, area under the curve with respect to increase) (p?=?0.08). In patients who had a history of myocardial infarction (MI), the cortisol output was lower compared to patients who had no previous MI (p?=?0.02). In linear regression analyses, anxiety emerged as significant predictor of AUCg and AUCi after controlling for MI, ejection fraction (LVEF, left ventricular ejection fraction), and depression.

Conclusions

Our results provide further indications for an association between anxiety and a dysregulation of the HPA axis. History of MI emerged as second predictor of cortisol output in the morning.     

Correction: Tantalum(v) 1,3-propanediolate β-diketonate solution as a precursor to sol–gel derived,metal oxide thin films

Correction for ‘Tantalum(v) 1,3-propanediolate β-diketonate solution as a precursor to sol–gel derived, metal oxide thin films’ by Christopher Beale et al., RSC Adv., 2020, 10, 13737–13748, DOI: 10.1039/D0RA02558E.

The authors regret that the plasma treatment and printing parameters were reported incorrectly in the subsection “Deposition on a-SiO₂ for UV/Vis spectrophotometry” in the Experimental section of the original article.Before printing, the substrate for both samples was subjected to an argon plasma treatment for 5 minutes (150 W, 0.6 mbar). The plasma power is now corrected to be the same as stated in the “Deposition on a-SiO₂ for Raman/XRD” subsection, where originally it was incorrectly stated that “the power was set slightly higher” for the Raman/XRD samples. For both the acetylacetone and benzoylacetone inks, the inks were printed on their respective substrates with a 75 μm drop pitch having dimensions of 400 × 220 drops to create a uniform layer.The correct section is as follows: