Abnormal Exercise Electrocardiography With Normal Stress Echocardiography Is Associated With Subclinical Coronary Atherosclerosis.

Background: Patients with abnormal (positive) exercise electrocardiography, but normal stress echocardiography (+ECG/-Echo), have an increased risk of adverse cardiovascular events compared with patients with a normal (negative) ECG and a normal stress Echo (-ECG/-Echo). However, it is unclear if +ECG/-Echo discordance is associated with a greater burden of subclinical coronary atherosclerosis.

Methods: Project Baseline Health Study participants who underwent a stress Echo and coronary artery calcium (CAC) scan were stratified by stress Echo result: -ECG/-Echo or +ECG/-Echo.

A Case of Leukemia Cutis (Acute Myeloid Leukemia) With Epidermotropism.

Acute myeloid leukemia is a cancer involving uncontrolled proliferation of hematopoietic cells. Cutaneous involvement is referred to as leukemia cutis (LC). The histopathologic presentation of LC is variable, and may present with perivascular, periadnexal, dermal, or subcutaneous infiltrate.

Glycogenin is dispensable for normal liver glycogen metabolism and body glucose homeostasis.

Glycogen is a glucose-storage polysaccharide molecule present in animals, fungi and bacteria. The enzyme glycogenin can self-glycosylate, forming an oligosaccharide chain that primes glycogen synthesis. This priming role of glycogenin was first believed to be essential for glycogen synthesis, but glycogen was then found in the skeletal muscle, heart, liver and brain of glycogenin-knockout mice (Gyg KO), thereby showing that glycogen can be synthesized without glycogenin.

Altered Purinergic Signaling and CD8+ T Cell Dysregulation in STAT3 GOF Syndrome.

Signal transduction downstream of activating stimuli controls CD8+ T cell biology, however these external inputs can become uncoupled from transcriptional regulation in Primary Immune Regulatory Disorders (PIRDs). Gain-of-function (GOF) variants in STAT3 amplify cytokine signaling and cause a severe PIRD characterized by early onset autoimmunity, lymphoproliferation, recurrent infections, and immune dysregulation. In both primary human and mouse models of STAT3 GOF, CD8+ T cells have been implicated as pathogenic drivers of autoimmunity.