Publications by authors named "David Bode"

Article Synopsis
  • - Atrial fibrillation (AF) is becoming a major health issue, often linked with metabolic disorders like diabetes and obesity, and current treatments aren't very effective in preventing its negative impacts.
  • - Evidence shows that metabolic issues can lead to AF by causing structural and electrical changes in the heart, stressing the importance of personalized treatment strategies based on an individual's metabolic health.
  • - The article explores how AF itself can disrupt metabolism, affecting glucose and lipid processing, and discusses potential treatment approaches aimed at correcting these metabolic changes to enhance patient outcomes.
View Article and Find Full Text PDF

Aim: Exercise intolerance is the central symptom in patients with heart failure with preserved ejection fraction. In the present study, we investigated the adrenergic reserve both in vivo and in cardiomyocytes of a murine cardiometabolic HFpEF model.

Methods: 12-week-old male C57BL/6J mice were fed regular chow (control) or a high-fat diet and L-NAME (HFpEF) for 15 weeks.

View Article and Find Full Text PDF

Heart failure (HF) is marked by distinctive changes in myocardial uptake and utilization of energy substrates. Among the different types of HF, HF with preserved ejection fraction (HFpEF) is a highly prevalent, complex, and heterogeneous condition for which metabolic derangements seem to dictate disease progression. Changes in intermediate metabolism in cardiometabolic HFpEF-among the most prevalent forms of HFpEF-have a large impact both on energy provision and on a number of signalling pathways in the heart.

View Article and Find Full Text PDF

Atrial fibrillation (AF) is the most common sustained (atrial) arrhythmia, a considerable global health burden and often associated with heart failure. Perturbations of redox signalling in cardiomyocytes provide a cellular substrate for the manifestation and maintenance of atrial arrhythmias. Several clinical trials have shown that treatment with sodium-glucose linked transporter inhibitors (SGLTi) improves mortality and hospitalisation in heart failure patients independent of the presence of diabetes.

View Article and Find Full Text PDF

Aims: Heart failure with preserved ejection fraction (HFpEF) is frequently (30%) associated with right ventricular (RV) dysfunction, which increases morbidity and mortality in these patients. Yet cellular mechanisms of RV remodelling and RV dysfunction in HFpEF are not well understood. Here, we evaluated RV cardiomyocyte function in a rat model of metabolically induced HFpEF.

View Article and Find Full Text PDF

Aims: Heart failure with preserved ejection fraction (HFpEF) is an increasingly prevalent disease. Physical exercise has been shown to alter disease progression in HFpEF. We examined cardiomyocyte Ca homeostasis and left ventricular function in a metabolic HFpEF model in sedentary and trained rats following 8 weeks of moderate-intensity continuous training (MICT) or high-intensity interval training (HIIT).

View Article and Find Full Text PDF
Article Synopsis
  • SGLT-2 inhibitors like sotagliflozin have been shown to improve heart failure outcomes by reducing cardiovascular risks, particularly in heart failure with preserved ejection fraction (HFpEF), though the exact mechanisms remain unclear.
  • In a rat model of HFpEF, chronic treatment with sotagliflozin resulted in reduced left atrial enlargement and helped manage cellular arrhythmias linked to metabolic syndrome.
  • The study found that sotagliflozin decreased the occurrence of spontaneous calcium release events in heart cells without affecting their frequency, suggesting it may help stabilize heart function in this condition.
View Article and Find Full Text PDF

Metabolic syndrome-mediated heart failure with preserved ejection fraction (HFpEF) is commonly accompanied by left atrial (LA) cardiomyopathy, significantly affecting morbidity and mortality. We evaluate the role of reactive oxygen species (ROS) and intrinsic inflammation (TNF-α, IL-10) related to dysfunctional Ca homeostasis of LA cardiomyocytes in a rat model of metabolic HFpEF. ZFS-1 obese rats showed features of HFpEF and atrial cardiomyopathy in vivo: increased left ventricular (LV) mass, E/e' and LA size and preserved LV ejection fraction.

View Article and Find Full Text PDF

Introduction: Radiofrequency (RF) ablation is a commonly used tool in the invasive electrophysiology laboratory to treat a variety of rhythm disorders. Reliable creation of transmural ablation lesions is crucial for long-term success. Lesion size index (LSI) is a multiparametric index that incorporates time, power, contact force (CF), and impedance data recorded during RF ablation in a weighted formula and has been shown to predict the extent of myocardial tissue lesions.

View Article and Find Full Text PDF

Aims: Atrial contractile dysfunction is associated with increased mortality in heart failure (HF). We have shown previously that a metabolic syndrome-based model of HFpEF and a model of hypertensive heart disease (HHD) have impaired left atrial (LA) function in vivo (rat). In this study we postulate, that left atrial cardiomyocyte (CM) and cardiac fibroblast (CF) paracrine interaction related to the inositol 1,4,5-trisphosphate signalling cascade is pivotal for the manifestation of atrial mechanical dysfunction in HF and that quantitative atrial remodeling is highly disease-dependent.

View Article and Find Full Text PDF

The ability of amyloid-β peptide (Aβ) to disrupt membrane integrity and cellular homeostasis is believed to be central to Alzheimer's disease pathology. Aβ is reported to have various impacts on the lipid bilayer, but a clearer picture of Aβ influence on membranes is required. Here, we use atomic force and transmission electron microscopies to image the impact of different isolated Aβ assembly types on lipid bilayers.

View Article and Find Full Text PDF

Oxidative stress and the formation of plaques which contain amyloid-β (Aβ) peptides are two key hallmarks of Alzheimer's disease (AD). Dityrosine is found in the plaques of AD patients and Aβ dimers have been linked to neurotoxicity. Here we investigate the formation of Aβ dityrosine dimers promoted by Cu Fenton reactions.

View Article and Find Full Text PDF
Article Synopsis
  • Alzheimer’s disease (AD) is characterized by the aggregation of amyloid-β (Aβ) peptides into toxic structures, but human serum albumin can inhibit this process by binding to Aβ and preventing its fibrous formation.
  • A phase II clinical trial demonstrated that albumin-plasma exchange can reduce cognitive decline in AD patients, suggesting albumin's potential protective role.
  • The presence of other hydrophobic molecules like cholesterol and fatty acids can interfere with albumin’s ability to inhibit Aβ fibrillization, linking dietary factors to AD risk.
View Article and Find Full Text PDF

Unlabelled: Heart failure (HF) with preserved ejection fraction (HFpEF) is present in about 50% of HF patients. Atrial remodeling is common in HFpEF and associated with increased mortality. We postulate that atrial remodeling is associated with atrial dysfunction in vivo related to alterations in cardiomyocyte Calcium (Ca) signaling and remodeling.

View Article and Find Full Text PDF

A central hallmark of Alzheimer's disease is the presence of extracellular amyloid plaques chiefly consisting of amyloid-β (Aβ) peptides in the brain interstitium. Aβ largely exists in two isoforms, 40 and 42 amino acids long, but a large body of evidence points to Aβ(1-42) rather than Aβ(1-40) as the cytotoxic form. One proposed mechanism by which Aβ exerts toxicity is the formation of ion channel pores that disrupt intracellular Ca homeostasis.

View Article and Find Full Text PDF

Enuresis is defined as intermittent urinary incontinence during sleep in a child at least five years of age. Approximately 5% to 10% of all seven-year-olds have enuresis, and an estimated 5 to 7 million children in the United States have enuresis. The pathophysiology of primary nocturnal enuresis involves the inability to awaken from sleep in response to a full bladder, coupled with excessive nighttime urine production or a decreased functional capacity of the bladder.

View Article and Find Full Text PDF

Dyspareunia is recurrent or persistent pain with sexual activity that causes marked distress or interpersonal conflict. It affects approximately 10% to 20% of U.S.

View Article and Find Full Text PDF

Aprataxin (APTX) deficiency causes progressive cerebellar degeneration, ataxia and oculomotor apraxia in man. Cell free assays and crystal structure studies demonstrate a role for APTX in resolving 5'-adenylated nucleic acid breaks, however, APTX function in vertebrates remains unclear due to the lack of an appropriate model system. Here, we generated a murine model in which a pathogenic mutant of superoxide dismutase 1 (SOD1(G93A)) is expressed in an Aptx-/- mouse strain.

View Article and Find Full Text PDF

Objective: The purpose of this project was to improve provider documentation of adolescent overweight and obesity through body mass index percentile (BMI%) documentation in the military's electronic medical record (EMR).

Methods: Using the FOCUS-PDCA (Find-Organize-Clarify-Understand-Select-Plan-Do-Check-Act) model, we developed an intervention to improve rates of diagnosis of overweight/obesity in our adolescent medicine clinic. Medical technicians documented the patient's BMI% and growth chart in the EMR.

View Article and Find Full Text PDF