Notes

Ethical Concerns within Trauma-Informed Care.
Forty-nine putative microRNAs were identified as being linked to the PDCD1/CD274 network, which were taken forward and further assessed for clinical relevance using OncomiR and previously published literature. One hundred and thirty significant survival associations for 46 microRNAs across fourteen groups of cancers were identified. Finally, a total of 23 putative repurposed drugs targeting multiple components of the PDCD1/CD274 network were identified, which may represent immunotherapeutic adjuvants. Taken together, these results shed light on the varying PDCD1/CD274 networks between individual cancers and signpost a need for more cancer-specific investigations and treatments.This study aimed to investigate the association between oral disease burden and oral health related quality of life (OHRQoL) among overweight/obese (OW/OB) and normal weight (NW) Malaysian adolescents. A total of 397 adolescents were involved in the two-year prospective observational cohort study. OHRQOL was measured through a self-administered questionnaire containing the short version of the Malaysian Oral Health Impact Profile (OHIP[M]). Body mass index (BMI) was used for anthropometric measurement. Whilst, decayed, missing, and filled teeth (DMFT) index, Significant Caries Index (SiC), simplified basic periodontal examination (S-BPE), and gingival bleeding index (GBI) were used for clinical assessment tools. Higher dental caries prevalence was observed in the NW group while higher SiC was reported in the OW/OB group. Regardless of the obesity status, the prevalence of gingivitis (BPE code 1 and 2) was high in this study. A reduction of GBI prevalence was observed in the two-year follow-up results with an increased prevalence of OHRQoL impact in the OW/OB group compared to the NW group (p > 0.05). The findings from this study suggested that obesity status did not have influence over the burden of oral diseases and OHRQoL. It offers insights referring to the changes in adolescents' oral diseases burden and OHRQoL.Plasma electrolytic oxidation (PEO) is a novel surface treatment process to produce thick, dense metal oxide coatings, especially on light metals, primarily to improve their wear and corrosion resistance. The coating manufactured from the PEO process is relatively superior to normal anodic oxidation. It is widely employed in the fields of mechanical, petrochemical, and biomedical industries, to name a few. JR-AB2-011 Several investigations have been carried out to study the coating performance developed through the PEO process in the past. This review attempts to summarize and explain some of the fundamental aspects of the PEO process, mechanism of coating formation, the processing conditions that impact the process, the main characteristics of the process, the microstructures evolved in the coating, the mechanical and tribological properties of the coating, and the influence of environmental conditions on the coating process. Recently, the PEO process has also been employed to produce nanocomposite coatings by incorporating nanoparticles in the electrolyte. This review also narrates some of the recent developments in the field of nanocomposite coatings with examples and their applications. Additionally, some of the applications of the PEO coatings have been demonstrated. Moreover, the significance of the PEO process, its current trends, and its scope of future work are highlighted.
Arrhythmogenic Cardiomyopathy (ACM) is a disease of the cardiac muscle, characterized by frequent ventricular arrhythmias and functional/ structural abnormalities, mainly of the right ventricle. To date, 20 different genes have been associated with ACM and the majority of them encode for desmosomal proteins. In this study, we describe the characterization of two novel variants in
gene, segregating in two ACM families. MYH7 encodes for myosin heavy chain β (MHC-β) isoform, involved in cardiac muscle contractility.

In family A, the autopsy revealed ACM with biventricular involvement in both the proband and his father. In family B, the proband had been diagnosed as affected by ACM and implanted with implantable cardioverter defibrillator (ICD), due to ECG evidence of monomorphic ventricular tachycardia after syncope. After clinical evaluation, a molecular diagnosis was performed using a NGS custom panel. The two novel variants identified predicted damaging, located in a highly conserved domain c. 2630T>C is not described while c.2609G>A has a frequency of 0.00000398. In silico analyses evaluated the docking characteristics between proteins using the Haddock2.2 webserver.

Our results reveal two variants in sarcomeric genes to be the molecular cause of ACM, further increasing the genetic heterogeneity of the disease; in fact, sarcomeric variants are usually associated with HCM phenotype. Studies on the role of sarcomere genes in the pathogenesis of ACM are surely recommended in those ACM patients negative for desmosomal mutation screening.
Our results reveal two variants in sarcomeric genes to be the molecular cause of ACM, further increasing the genetic heterogeneity of the disease; in fact, sarcomeric variants are usually associated with HCM phenotype. Studies on the role of sarcomere genes in the pathogenesis of ACM are surely recommended in those ACM patients negative for desmosomal mutation screening.A chronic inflammatory process characteristic of obstructive sleep apnea promotes vascular endothelial dysfunction and atherogenesis. This process can lead to destabilization and rupture of cardiovascular plaques, which clinically manifests as an acute coronary syndrome or stroke. The aim of this study was to investigate the inflammatory pathway leading to plaque destabilization in non-to-mild and moderate-to-severe groups of OSA patients. This prospective study involved enrollment of patients scheduled for endarterectomy. A sleep study was performed prior to surgery. Immunohistochemistry was performed on atherosclerotic plaques from carotid arteries obtained during standard open endarterectomy to determine levels of CD40, CD40L receptors, MCP-1, and MMP-9. The 46 patients included 14 controls, 13 with mild, 11 with moderate, and 8 with severe OSA. Increased expression of CD40, CD40L receptors, MCP-1, and MMP-9 were found to be proportionate with OSA severity. However, significant differences among groups were observed only for MCP-1 (p = 0.
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