Myo/Nog cells expressing muscle proteins are present in preretinal membranes from patients with proliferative vitreoretinopathy.

Proliferative vitreoretinopathy (PVR) is a complication of rhegmatogenous retinal detachment and ocular trauma. The disease is characterized by development of membranes that may apply traction to the retina and cause redetachment. Membrane contractions are attributed to myofibroblasts arising from retinal pigment epithelial cells, glia and fibroblasts. The progenitors of myofibrobasts in the lens are Myo/Nog cells that express the skeletal muscle transcription factor MyoD and bone morphogenetic protein inhibitor Noggin. The retina and choroid also contain Myo/Nog cells that respond to stress. We examined preretinal PVR membranes from three ocular trauma patients with retinal detachment for Myo/Nog cells and their expression of muscle proteins. Myo/Nog cells were identified by co-localization of antibodies to the G8 antigen and Noggin. Greater than 80% of all cells in sections from two of three patients expressed both G8 and Noggin. Myo/Nog cells lacked pigment. Alpha smooth muscle actin (α-SMA) and striated myosin II heavy chain were present in the majority of Myo/Nog cells in these two patients. Differentiation of Myo/Nog cells was paralleled by low levels of MyoD. Membrane sections from the third patient consisted mostly of connective tissue with very few cells. A small subpopulation in these sections expressed both G8 and Noggin, and muscle proteins were detected in only a minority of G8-positive (+) cells. In all three patients, greater than 99% of cells with MyoD, α-SMA and striated muscle myosin co-expressed G8. These findings suggest that contractile myofibroblasts in PVR membranes may be derived from differentiating Myo/Nog cells.

A Case of 25 Inappropriate Automatic Implantable Cardioverter Defibrillator Shocks and 22 Episodes of Antitachycardia Pacing.

An implantable cardioverter defibrillator (ICD) can save lives from fatal tachyarrhythmias. In rare cases, these devices can fail or malfunction. We present a case of a patient that suffered from 25 inappropriate shocks and 22 episodes of antitachycardia pacing (ATP), secondary to a probable non-traumatic dual lead fracture. One episode of ATP induced an R-on-T phenomenon, causing monomorphic ventricular tachycardia in the patient. The inappropriately functioning ICD also required two magnets to be placed on the patient's chest in the emergency department to convert the device to an asynchronous mode. An unexpected case of this magnitude and in such a brief timeframe has not been reported in prior ICD studies.

Acute Response and Neuroprotective Role of Myo/Nog Cells Assessed in a Rat Model of Focal Brain Injury.

Focal brain injury in the form of a needlestick (NS) results in cell death and induces a self-protective response flanking the lesion. Myo/Nog cells are identified by their expression of bone morphogenetic protein inhibitor Noggin, brain-specific angiogenesis inhibitor 1 (BAI1) and the skeletal muscle specific transcription factor MyoD. Myo/Nog cells limit cell death in two forms of retinopathy. In this study, we examined the acute response of Myo/Nog cells to a NS lesion that extended from the rat posterior parietal cortex to the hippocampus. Myo/Nog cells were identified with antibodies to Noggin and BAI1. These cells were the primary source of both molecules in the uninjured and injured brain. One day after the NS, the normally small population of Myo/Nog cells expanded approximately eightfold within a 1 mm area surrounding the lesion. Myo/Nog cells were reduced by approximately 50% along the lesion with an injection of the BAI1 monoclonal antibody and complement. The number of dying cells, identified by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), was unchanged at this early time point in response to the decrease in Myo/Nog cells. However, increasing the number of Myo/Nog cells within the lesion by injecting BAI1-positive (+) cells isolated from the brains of other animals, significantly reduced cell death and increased the number of NeuN+ neurons compared to brains injected with phosphate buffered saline or exogenous BAI1-negative cells. These findings demonstrate that Myo/Nog cells rapidly react to injury within the brain and increasing their number within the lesion is neuroprotective.

Stuttering and Word-Finding Difficulties in a Patient With COVID-19 Presenting to the Emergency Department.

Coronavirus disease 2019 (COVID-19) was designated as a global pandemic by the World Health Organization (WHO) on March 11, 2020. The Cochrane Database of Systematic Reviews documents that COVID-19 has a wide range of common symptoms, which have made it difficult to characterize the disease. To date, the neurological symptoms of stuttering and word-finding difficulties have not been reported in confirmed COVID-19 cases. This case report describes the clinical course of a 53-year-old female that presented to the emergency department (ED) twice with varying symptoms consistent with COVID-19. At the second ED visit, she complained of new-onset stuttering and word-finding difficulties and tested positive for COVID-19 using the polymerase chain reaction (PCR) nasopharynx test. When contacted, the patient stated that her speech issues persisted at least seven days after discharge from her second ED visit. As a result, the virus may cause symptoms of an acute neurological event and should be taken into diagnostic consideration. These neurological findings may be explained by the recent discovery of the COVID-19 spike protein's ability to destabilize the blood-brain barrier (BBB) and enter the central nervous system (CNS). Increased classification of unrecognized COVID-19 symptoms and complications may aid in the characterization, surveillance, and prevention of the disease.

A Case of Euglycemic Diabetic Ketoacidosis in a Patient With Type 2 Diabetes Mellitus and COVID-19.

Diabetic ketoacidosis (DKA) can cause significant morbidity and mortality in patients with type 1 or type 2 diabetes mellitus. DKA causes an approximate annual hospitalization rate of 6.3% and in-hospital case-fatality rate of 0.4%. A subset of DKA cases termed euglycemic diabetic ketoacidosis (eu-DKA) is characterized by euglycemia (<200 mg/dL), high anion gap metabolic acidosis, and an increased plasma ketone concentration. This clinical syndrome comprises approximately 2.6% to 3.2% of total DKA admissions, making it a rare condition. In this case report, a male patient was diagnosed with coronavirus disease 2019 (COVID-19) three days prior to arriving at the emergency department. Upon evaluation, he displayed severe acidemia and was diagnosed with eu-DKA. He was started on intravenous regular insulin and D5 one-half normal saline, which markedly improved his metabolic status. Notably, his admission was uncomplicated by respiratory symptoms of COVID-19. It is proposed that his eu-DKA was catalyzed by his recent COVID-19 infection. Recent studies that have shown COVID-19 may increase lipolysis and induce ketogenesis in susceptible patients.