Objective assessment of progressive increase in bite force post surgical correction of mandibular fractures using Nupai bite scan analyser

Background: Fracture of mandible is a common condition which is increasing in incidence in the trauma centers due to increasing motor vehicles and failure to abide by traffic regulations. Patients undergo surgical open reduction and internal fixation where post-operative occlusion and normal masticatory functions are targeted. Bite force can be taken as a guide of normal masticatory function of an individual which is dependent upon craniomandibular biomechanics. The aim of the study was to analyse bite force measurements post-operatively in patients who underwent open reduction and internal fixation for mandible fractures at different sites.Methods: Molar bite force was recorded in 31 post-operative patients who underwent open surgical procedure for fracture mandible in the department of plastic surgery from January 2018 to June 2019 by a pre-scale bite force recorder-Nupai bite force prescale system (FujiTM). Various parameters were recorded pre and post-operatively including age, gender, history, comorbidities, requirement of MMF, site and number of fractures and age of injury. Bite force were compared and improvement of bite force every 2 weeks was noted and analyzed upto 6 weeks postoperatively.Results: Bite force improvement was seen in all types of mandible fractures irrespective of the site and type of fractures over a period of 6 weeks post-operatively. This improvement was however not statistically significant. Decreased time interval form injury to surgery resulted in improved bite force measurements though not statistically significant.Conclusions: Although objective improvement in bite force could be demonstrated but extensive study involving more subjects and more patient variables would have statistical significance

Obesity and diabetes are major risk factors for epicardial adipose tissue inflammation

BACKGROUND. Epicardial adipose tissue (EAT) directly overlies the myocardium, with changes in its morphology and volume associated with myriad cardiovascular and metabolic diseases. However, EAT's immune structure and cellular characterization remain incompletely described. We aimed to define the immune phenotype of EAT in humans and compare such profiles across lean, obese, and diabetic patients. METHODS. We recruited 152 patients undergoing open-chest coronary artery bypass grafting (CABG), valve repair/replacement (VR) surgery, or combined CABG/VR. Patients' clinical and biochemical data and EAT, subcutaneous adipose tissue (SAT), and preoperative blood samples were collected. Immune cell profiling was evaluated by flow cytometry and complemented by gene expression studies of immune mediators. Bulk RNA-Seq was performed in EAT across metabolic profiles to assess whole-transcriptome changes observed in lean, obese, and diabetic groups. RESULTS. Flow cytometry analysis demonstrated EAT was highly enriched in adaptive immune (T and B) cells. Although overweight/obese and diabetic patients had similar EAT cellular profiles to lean control patients, the EAT exhibited significantly (P ≤ 0.01) raised expression of immune mediators, including IL-1, IL-6, TNF-α, and IFN-γ. These changes were not observed in SAT or blood. Neither underlying coronary artery disease nor the presence of hypertension significantly altered the immune profiles observed. Bulk RNA-Seq demonstrated significant alterations in metabolic and inflammatory pathways in the EAT of overweight/obese patients compared with lean controls. CONCLUSION. Adaptive immune cells are the predominant immune cell constituent in human EAT and SAT. The presence of underlying cardiometabolic conditions, specifically obesity and diabetes, rather than cardiac disease phenotype appears to alter the inflammatory profile of EAT. Obese states markedly alter EAT metabolic and inflammatory signaling genes, underlining the impact of obesity on the EAT transcriptome profile

Transcriptional characterization of human megakaryocyte polyploidization and lineage commitment

Funder: National Institute for Health Research; Id: http://dx.doi.org/10.13039/501100014338Funder: NHS Blood and Transplant; Id: http://dx.doi.org/10.13039/100009033Funder: Bristol‐Myers Squibb; Id: http://dx.doi.org/10.13039/100002491Funder: European Commission; Id: http://dx.doi.org/10.13039/100013273Abstract: Background: Megakaryocytes (MKs) originate from cells immuno‐phenotypically indistinguishable from hematopoietic stem cells (HSCs), bypassing intermediate progenitors. They mature within the adult bone marrow and release platelets into the circulation. Until now, there have been no transcriptional studies of primary human bone marrow MKs. Objectives: To characterize MKs and HSCs from human bone marrow using single‐cell RNA sequencing, to investigate MK lineage commitment, maturation steps, and thrombopoiesis. Results: We show that MKs at different levels of polyploidization exhibit distinct transcriptional states. Although high levels of platelet‐specific gene expression occur in the lower ploidy classes, as polyploidization increases, gene expression is redirected toward translation and posttranslational processing transcriptional programs, in preparation for thrombopoiesis. Our findings are in keeping with studies of MK ultrastructure and supersede evidence generated using in vitro cultured MKs. Additionally, by analyzing transcriptional signatures of a single HSC, we identify two MK‐biased HSC subpopulations exhibiting unique differentiation kinetics. We show that human bone marrow MKs originate from these HSC subpopulations, supporting the notion that they display priming for MK differentiation. Finally, to investigate transcriptional changes in MKs associated with stress thrombopoiesis, we analyzed bone marrow MKs from individuals with recent myocardial infarction and found a specific gene expression signature. Our data support the modulation of MK differentiation in this thrombotic state. Conclusions: Here, we use single‐cell sequencing for the first time to characterize the human bone marrow MK transcriptome at different levels of polyploidization and investigate their differentiation from the HSC

A large ventricular septal defect complicating resuscitation after blunt trauma

A young adult pedestrian was admitted to hospital after being hit by a car. On arrival to the Accident and Emergency Department, the patient was tachycardic, hypotensive, hypoxic, and acidotic with a Glasgow Coma Scale of 3. Despite initial interventions, the patient remained persistently hypotensive. An echocardiogram demonstrated a traumatic ventricular septal defect (VSD) with right ventricular strain and increased pulmonary artery pressure. Following a period of stabilization, open cardiothoracic surgery was performed and revealed an aneurysmal septum with a single large defect. This was repaired with a bovine patch, resulting in normalization of right ventricular function. This case provides a vivid depiction of a large VSD in a patient following blunt chest trauma with hemodynamic compromise. In all thoracic trauma patients, and particularly those poorly responsive to resuscitation, VSDs should be considered. Relevant investigations and management strategies are discussed

Glucagon-like peptide-1 receptor agonists in the treatment of type 2 diabetes: Past, present, and future

Glucagon-like peptide-1 (GLP-1)–based therapy improves glycaemic control through multiple mechanisms, with a low risk of hypoglycaemia and the additional benefit of clinically relevant weight loss. Since Starling and Bayliss first proposed the existence of intestinal secretions that stimulate the pancreas, tremendous progress has been made in the area of incretins. As a number of GLP-1 receptor agonists (GLP-1 RAs) continue to become available, physicians will soon face the challenge of selecting the right option customized to their patient's needs. The following discussion, derived from an extensive literature search using the PubMed database, applying the terms incretin, GLP-1, exenatide, liraglutide, albiglutide, dulaglutide, lixisenatide, semaglutide, and taspoglutide, provides a comprehensive review of existing and upcoming molecules in the GLP-1 RA class in terms of their structure, pharmacological profiles, efficacy, safety, and convenience. Search Methodology: A literature search was conducted using the PubMed database, applying the terms incretin, GLP-1, exenatide, liraglutide, albiglutide, dulaglutide, lixisenatide, semaglutide, and taspoglutide. Relevant articles were those that discussed structural, pharmacokinetic and pharmacodynamic differences, classification, long-acting and short-acting GLP-1 RAs, phase 3 trials, and expert opinions. Additional targeted searches were conducted on diabetes treatment guidelines and reviews on safety, as well as the American Diabetes Association/European Society for Study of Diabetes (ADA/EASD) statement on pancreatic safety