Evaluating frailty assessment tools and biological frailty markers in C57BL/6 female mice.

Frailty is a complex condition characterized by a decline in multiple physiological systems, compromising an individual's ability to maintain homeostasis. The onset and progression of frailty are linked to negative health outcomes such as disability, hospitalization, and mortality. To better understand frailty mechanisms, animal models have become valuable due to their accessibility to critical tissues and the ability to control variables.

Protectin DX as a therapeutic strategy against frailty in mice.

Frailty in aging is driven by the dysregulation of multiple biological pathways. Protectin DX (PDX) is a docosahexaenoic acid (DHA)-derived molecule that alleviates many chronic inflammatory disorders, but its potential effects on frailty remain unknown. Our goal is to identify age-related impairments in metabolic systems and to evaluate the therapeutic potential of PDX on frailty, physical performance, and health parameters.

Fast and slow skeletal myosin binding protein-C and aging.

Aging is associated with skeletal muscle strength decline and cardiac diastolic dysfunction. The structural arrangements of the sarcomeric proteins, such as myosin binding protein-C (MyBP-C) are shown to be pivotal in the pathogenesis of diastolic dysfunction. Yet, the role of fast (fMyBP-C) and slow (sMyBP-C) skeletal muscle MyBP-C remains to be elucidated.

Physiological Systems in Promoting Frailty.

Frailty is a complex syndrome affecting a growing sector of the global population as medical developments have advanced human mortality rates across the world. Our current understanding of frailty is derived from studies conducted in the laboratory as well as the clinic, which have generated largely phenotypic information. Far fewer studies have uncovered biological underpinnings driving the onset and progression of frailty, but the stage is set to advance the field with preclinical and clinical assessment tools, multiomics approaches together with physiological and biochemical methodologies.

Adipocyte-specific Nos2 deletion improves insulin resistance and dyslipidemia through brown fat activation in diet-induced obese mice.

Objective: Inducible nitric oxide (NO) synthase (NOS2) is a well-documented inflammatory mediator of insulin resistance in obesity. NOS2 expression is induced in both adipocytes and macrophages within adipose tissue during high-fat (HF)-induced obesity.

Methods: Eight-week-old male mice with adipocyte selective deletion of the Nos2 gene (Nos2) and their wildtype littermates (Nos2) were subjected to chow or high-fat high-sucrose (HFHS) diet for 10 weeks followed by metabolic phenotyping and determination of brown adipose tissue (BAT) thermogenesis.

Vena cava presents endothelial dysfunction prior to thoracic aorta in heart failure: the pivotal role of nNOS uncoupling/oxidative stress.

Arterial endothelial dysfunction has been extensively studied in heart failure (HF). However, little is known about the adjustments shown by the venous system in this condition. Considering that inferior vena cava (VC) tone could influence cardiac performance and HF prognosis, the aim of the present study was to assess the VC and thoracic aorta (TA) endothelial function of HF-post-myocardial infarction (MI) rats, comparing both endothelial responses and signaling pathways developed.

Electroanatomic voltage mapping for tissue characterization beyond arrhythmia definition: A systematic review.

Three-dimensional (3D) reconstruction by means of electroanatomic mapping (EAM) systems, allows for the understanding of the mechanism of focal or re-entrant arrhythmic circuits, which can be identified by means of dynamic (activation and propagation) and static (voltage) color-coded maps. However, besides this conventional use, EAM may offer helpful anatomical and functional information for tissue characterisation in several clinical settings. Today, data regarding electromechanical myocardial viability, scar detection in ischaemic and nonischaemic cardiomyopathy and arrhythmogenic right ventricle dysplasia (ARVC/D) definition are mostly consolidated, while emerging results are becoming available in contexts such as Brugada syndrome and cardiac resynchronisation therapy (CRT) implant procedures.

Bacterial Postbiotics as Promising Tools to Mitigate Cardiometabolic Diseases.

Gut microbes dictate critical features of host immunometabolism. Certain bacterial components and metabolites (termed postbiotics) mitigate cardiometabolic diseases whereas others potentiate pathological processes. In this review, we discuss key aspects related to the usefulness of bacterial-related molecules strategically positioned as promising treatment strategies for cardiometabolic diseases.

Fish oil replacement prevents, while docosahexaenoic acid-derived protectin DX mitigates end-stage-renal-disease in atherosclerotic diabetic mice.

Diabetic nephropathy (DN) remains the major cause of end-stage renal disease (ESRD). We used high-fat/high-sucrose (HFHS)-fed LDLr /ApoB mice with transgenic overexpression of IGFII in pancreatic β-cells (LRKOB100/IGFII) as a model of ESRD to test whether dietary long chain omega-3 polyunsaturated fatty acids LCω3FA-rich fish oil (FO) could prevent ESRD development. We further evaluated the potential of docosahexaenoic acid (DHA)-derived pro-resolving lipid mediators, 17-hydroxy-DHA (17-HDHA) and Protectin DX (PDX), to reverse established ESRD damage.

Electroanatomic voltage mapping and characterisation imaging for "right ventricle arrhythmic syndromes" beyond the arrhythmia definition: a comprehensive review.

Three-dimensional (3D) reconstruction by means of electroanatomic mapping (EAM) systems, allows for the understanding of the mechanism of focal or re-entrant arrhythmic circuits along with pacing techniques. However, besides this conventional use, EAM may offer helpful anatomical and functional information. Data regarding electromechanical scar detection in ischaemic (and nonischaemic) cardiomyopathy are mostly consolidated, while emerging results are becoming available in contexts such as arrhythmogenic right ventricular dysplasia (ARVC/D) definition and Brugada syndrome.

Distinct Effects of Milk-Derived and Fermented Dairy Protein on Gut Microbiota and Cardiometabolic Markers in Diet-Induced Obese Mice.

Background: Recent meta-analyses suggest that the consumption of fermented dairy products reduces type 2 diabetes and cardiovascular disease (CVD) risk, although the underlying mechanisms remain unclear.

Objective: We evaluated whether dairy protein products modulated gut microbiota and cardiometabolic features in mouse models of diet-induced obesity and CVD.

Methods: Eight-week-old C57BL/6J wild-type (WT) and LDLr-/-ApoB100/100 (LRKO) male mice were fed for 12 and 24 wk, respectively, with a high-fat/high-sucrose diet [66% kcal lipids, 22% kcal carbohydrates (100% sucrose), 12% kcal proteins].

Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLrApoB mice.

Background And Aims: Poor dietary habits contribute to the obesity pandemic and related cardiovascular diseases but the respective impact of high saturated fat versus added sugar consumption remains debated. Herein, we aimed to disentangle the individual role of dietary fat versus sugar in cardiometabolic disease progression.

Methods: We fed pro-atherogenic LDLrApoB mice either a low-fat/high-sucrose (LFHS) or a high-fat/low-sucrose (HFLS) diet for 24 weeks.

Ventricular tachycardia oversensing in S-ICD patients: Case-based brief review.

A 76-year-old woman with permanent atrial fibrillation and a mechanical aortic valve came to our attention. Echocardiography showed a 50-55% ejection fraction (EF) with good prosthesis performance. For symptomatic bradyarrhythmia, she received a VVI pacemaker (Proponent MRI L2010 model; Boston Scientific.

[Remarks on angina pectoris].

In the first volume of the New England Journal of Medicine of 1812, J. Warren published a paper on the subject of angina pectoris, in which clearly emerge the difficulties facing the physicians of that time in trying to formulate a correct diagnosis and prescribe the right therapy. We thought it would be certainly of interest to offer our readers an Italian translation of this article, obviously with some stylistic modifications and supplemented with information coming from other historical scientific works.

[Amiodarone and thyroid dysfunction: a pending problem].

Amiodarone is an antiarhytmic drug used in many clinical situations for its probed effect; it is also preferred in particular groups of patients (heart failure, post-ischemical) for its safe and its prognostic benefits. However, a substantial proportion of amiodarone treated patients develop either hypothyroidism or thyrotoxicosis. Both abnormalities may occur in apparently normal glands or in glandes with pre-existed abnormalities.