Toward a mechanistic understanding of the formation of 2D-GaNxin epitaxial graphene

WOS:000907017300001 PubMed ID:36580283Ultrathin 2D-GaNx can be formed by Ga intercalation into epitaxial graphene (EG) on SiC followed by nitridation in ammonia. Defects in the graphene provide routes for intercalation, but the nature and role of the defects have remained elusive. Here we examine the influence of graphene layer thickness and chemical functionalization on Ga intercalation and 2D-GaNx formation using a combination of experimental and theoretical studies. Thin buffer layer regions of graphene near steps on SiC readily undergo oxygen functionalization when exposed to air or a He/O2 plasma in contrast to thicker regions which are not chemically modified. Oxygen functionalization is found to inhibit Ga intercalation leading to accumulation of Ga droplets on the surface. In contrast, Ga readily intercalates between EG and SiC in the thicker graphene regions that do not contain oxygen. When NH3 annealing is carried out immediately after Ga exposure, 2D-GaNx formation is observed only in the oxygen-functionalized regions, and Ga intercalated under thicker nonfunctionalized graphene does not convert to GaNx. Density functional theory calculations demonstrate that oxygen functionalization of graphene alters the binding energy of Ga and NH3 species to the graphene surface. The presence of hydroxyl groups on graphene inhibits binding of Ga to the surface; however, it enhances the chemical reactivity of the graphene surface to NH3 which, in turn, enhances Ga binding and facilitates the formation of 2D-GaNx. By modifying the EG process to produce oxygen-functionalized buffer layer graphene, uniformly intercalated 2D-GaNx is obtained across the entire substrate surface

Multidisciplinary early intervention in a child with autism and childhood apraxia of speech

Background: Childhood apraxia of speech (CAS) is a neurological pediatric speech sound disorder, in which the precision and consistency of movements underlying speech are impaired in the absence of neuromuscular deficits. It is a common comorbidity in autism spectrum disorder (ASD) and requires detailed analysis to identify the typical errors in speech. Clinical Description: A 25-month-old boy presented with speech delay. The evaluation revealed an impaired absence of meaningful speech, impaired nonverbal communication and social skills, repetitive atypical behavior, and sensory issues with normal hearing. Although autism was suspected, the diagnosis could not be established, and intervention was started based on strengths and weaknesses. There was minimal improvement and discordance between receptive and expressive language was noted. Manifestations evolved over 15 months until a diagnosis of ASD was established by standard protocol. CAS was diagnosed at almost 4 years when a few meaningful words had developed and errors in oral movements, articulation, and phonological development were identified. Management and Outcome: Initially, the child received multidisciplinary management customized according to the strengths, weaknesses, and needs of the child. There was minimal improvement in communication, social interaction, and overall functioning. Identification of autism and slight changes in intervention did not bring about any remarkable changes. Once CAS was identified, and the focus of management changed there was a remarkable improvement in speech, and mild improvement in other aspects. Conclusion: Nonverbal or minimally verbal children with autism should be evaluated for CAS, especially if there is discordance between expressive and receptive language

Comparative Evaluation of Efficacy of Chlorhexidine and Herbal Mouthwash as a Preprocedural Rinse in Reducing Dental Aerosols: A Microbiological Study

Objective. The risk to dentists, assistants, and patients of infectious diseases through aerosols has long been recognized. The aim of this study was to evaluate and compare the efficacy of commercially available preprocedural mouth rinses containing 0.2% chlorhexidine (CHX) gluconate, Befresh™ herbal mouthwash, and water in reducing the levels of viable bacteria in aerosols. Materials & Methods. This was a single-center, double-masked, placebo-controlled, randomized, three-group parallel design study. 30 patients (10 patients in each group) were recruited in the study. Patient rinsed mouth with 10 ml of CHX, 10 ml Befresh™, or 10 ml water. All the patients underwent supragingival ultrasonic scaling for a minimum of 30 min. The aerosol collection was done using a blood agar plate. The blood agar plates were kept approximately 12 inches from the patient’s mouth. The microbial culture was analyzed. The colony-forming unit (CFU) counting in all three groups was assessed using one-way ANOVA test to compare among the groups (p value <0.001). The intergroup comparison was done using the post hoc Tukey test. Result. There was a marked reduction in the CFU in the CHX group in all three areas. This was followed by Befresh™ (Sagar Pharmaceuticals) mouthwash. There was no reduction in the CFU of the water group. Conclusion. This study proves that a regular preprocedural mouth rinse could significantly reduce the majority bacteria present in aerosols generated by the use of an ultrasonic unit, and Befresh™ mouth rinse was found to be equally effective in reducing the aerosol contamination to 0.2% CHX gluconate

The E3 ubiquitin ligase HectD3 attenuates cardiac hypertrophy and inflammation in mice

Myocardial inflammation has recently been recognized as a distinct feature of cardiac hypertrophy and heart failure. HectD3, a HECT domain containing E3 ubiquitin ligase has previously been investigated in the host defense against infections as well as neuroinflammation; its cardiac function however is still unknown. Here we show that HectD3 simultaneously attenuates Calcineurin-NFAT driven cardiomyocyte hypertrophy and the pro-inflammatory actions of LPS/interferon-gamma via its cardiac substrates SUMO2 and Stat1, respectively. AAV9-mediated overexpression of HectD3 in mice in vivo not only reduced cardiac SUMO2/Stat1 levels and pathological hypertrophy but also largely abolished macrophage infiltration and fibrosis induced by pressure overload. Taken together, we describe a novel cardioprotective mechanism involving the ubiquitin ligase HectD3, which links anti-hypertrophic and anti-inflammatory effects via dual regulation of SUMO2 and Stat1. In a broader perspective, these findings support the notion that cardiomyocyte growth and inflammation are more intertwined than previously anticipated. Rangrez et al. show that overexpression of the HECT domain E3 ubiquitin protein ligase 3 (HectD3) reduces cardiac hypertrophy while reducing macrophage infiltration in mice. This study provides a cardioprotective mechanism, where HectD3 targets SUMO2 and Stat1 to exert its anti-hypertrophic and anti-inflammatory effects