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Pacing Clin Electrophysiol
January 2025
Second Division of Cardiology, Cardiac-Thoracic and Vascular Department, University Hospital of Pisa, Pisa, Italy.
This case details the successful implantation of a leadless pacemaker following the extraction of transvenous leads in a 72-year-old female patient with a complex cardiovascular history. The patient had undergone a series of cardiac interventions, including a recent percutaneous tricuspid valve repair with a metal clip implant due to severe regurgitation. After presenting with an infection at the pacemaker site, methicillin-resistant Staphylococcus hominis was identified, necessitating the removal of the entire pacing system.
View Article and Find Full Text PDFJ Cell Biol
April 2025
Department of Genetics and Cell Biology, College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
TBC1D20 deficiency causes Warburg Micro Syndrome in humans, characterized by multiple eye abnormalities, severe intellectual disability, and abnormal sexual development, but the molecular mechanisms remain unknown. Here, we identify TBC1D20 as a novel Rab11 GTPase-activating protein that coordinates vesicle transport and actin remodeling to regulate ciliogenesis. Depletion of TBC1D20 promotes Rab11 vesicle accumulation and actin deconstruction around the centrosome, facilitating the initiation of ciliogenesis even in cycling cells.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
January 2025
Johns Hopkins University, Division of Pulmonary and Critical Care Medicine, Baltimore, MD, USA.
Obesity is a risk factor for asthma morbidity, associated with less responsiveness to inhaled corticosteroids. CD4+ T-cells are central to the immunology of asthma and may contribute to the unique obese asthma phenotype. We sought to characterize the single cell CD4+ Transcriptional profile differences in obese children with asthma compared to normal weight children with asthma.
View Article and Find Full Text PDFUnlabelled: SYNGAP1 is a key Ras-GAP protein enriched at excitatory synapses, with mutations causing intellectual disability and epilepsy in humans. Recent studies have revealed that in addition to its role as a negative regulator of G-protein signaling through its GAP enzymatic activity, SYNGAP1 plays an important structural role through its interaction with post-synaptic density proteins. Here, we reveal that intrinsic excitability deficits and seizure phenotypes in heterozygous Syngap1 knockout (KO) mice are differentially dependent on Syngap1 GAP activity.
View Article and Find Full Text PDFRationale: Airflow obstruction refractory to β2 adrenergic receptor (β2AR) agonists is an important clinical feature of infant respiratory syncytial virus (RSV) bronchiolitis, with limited treatment options. This resistance is often linked to poor drug delivery and potential viral infection of airway smooth muscle cells (ASMCs). Whether RSV inflammation causes β2AR desensitization in infant ASMCs is unknown.
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