Glass fiber posts relining: can composite opacity influence retention to root canal dentin?

Odontology - This study aimed at evaluating the influence of glass-fiber post (GFP) relining with composites of different opacities on resin cement layer thickness (CLT), bond strength (BS) to root...     

Facial expression recognition in Alzheimer’s disease: A systematic review

Introduction: It is well established that behavioral variant frontotemporal dementia can impair social and emotional function. However, there is no consensus regarding how Alzheimer’s disease can affect facial expression recognition. We aim to systematically review all the literature addressing this issue over the last 10 years.

Method: We conducted a search based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The search for literature was undertaken on 19 September 2017, using Pubmed, SciELO, BIREME, and Thomson Reuters Web of Science electronic databases. The key terms for the search were: Alzheimer’s disease, dementia, and facial expression recognition.

Results: We screened 173 articles, and 22 of them were selected. The most common methodology involved showing participants photographs of people expressing the six basic emotions—fear, anger, sadness, disgust, surprise, and happiness. Results were ambiguous. Among people with mild Alzheimer’s disease, happiness was easier to recognize than the other five basic emotions, with sadness and anger the most difficult to recognize. In addition, the intensity level of the emotions presented seems to be important, and facial expression recognition is related to specific cognitive capacities, including executive function and visuoperceptual abilities. Impairment in facial expression recognition does not appear to be a consistent neuropsychological finding in Alzheimer’s disease.

Conclusions: The lack of standardized assessment instruments and the heterogeneity of the methods and samples used across studies hamper comparisons. Future researches should investigate facial expression recognition through more ecological and standardized methods.     

Ethanol upregulates the P2X7 purinergic receptor in human macrophages

Alcohol consumption is considered to be the third leading cause of death in the United States. In addition to its direct toxicity, ethanol has two contrasting effects on the immune system: the nucleotide oligomerization domain‐like receptor pyrin domain‐containing‐3 (NLRP3) inflammasome is inhibited by acute ethanol exposure but activated by chronic ethanol exposure. Purinergic receptors (especially the P2X7 receptor) are able to activate the NLRP3 inflammasome and are involved in many ethanol‐related diseases (such as gout, pulmonary fibrosis, alcoholic steatohepatitis, and certain cancers). We hypothesized that ethanol regulates purinergic receptors and thus modulates the NLRP3 inflammasome's activity. In experiments with monocyte‐derived macrophages, we found that interleukin (IL)‐1β secretion was inhibited after 7 h of exposure (but not 48 h of exposure) to ethanol. The disappearance of ethanol's inhibitory effect on IL‐1β secretion after 48 h was not mediated by the upregulated production of IL‐1β, IL‐1α, IL‐6 or the inflammasome components NLRP3, apoptosis‐associated speck‐like protein containing a caspase recruitment domain, and caspase 1. P2X7R expression was upregulated by ethanol, whereas expression of the P2X4 and P2X1 receptors was not. Taken as a whole, our results suggest that ethanol induces NLRP3 inflammasome activation by upregulating the P2X7 receptor. This observation might have revealed a new mechanism for inflammation in ethanol‐related diseases.     

Psychopathological Comorbid Symptoms in Animal Hoarding Disorder

Psychiatric Quarterly - The main goal of this research is to describe the psychopathological symptoms comorbid to animal hoarding disorder. This is a cross-sectional study with a sample of a 33...     

A novel SNCA E83Q mutation in a case of dementia with Lewy bodies and atypical frontotemporal lobar degeneration

In this case report, we discuss a patient presenting with parkinsonism followed by a non-amnestic dementia with aphasic clinical features, as well as frontal dysexecutive syndrome. There was a family history of dementia with an autopsy diagnosis of “Pick's disease” in the proband's father. Neuroimaging of the patient revealed focal and severe temporal lobe and lesser frontoparietal lobe atrophy. At autopsy, there was severe frontotemporal lobar degeneration. Histologic evaluation revealed an absence of tau or transactivation response DNA-binding protein of 43 kDa (TDP) pathology but rather severe Lewy body deposition in the affected cortices. Genetic phenotyping revealed a novel missense mutation (p.E83Q) in exon 4 of the gene encoding α-synuclein (SNCA). This case study presents a patient with a novel SNCA E83Q mutation associated with widespread Lewy body pathology with prominent severe atrophy of the frontotemporal lobes and corresponding cognitive impairment.