Unveiling the interplay between rational, psychological and functional factors in continuous glucose monitoring early adoption: Novel evidence from the Dexcom ONE case in Italy.

Background: The escalating prevalence of diabetes, with its multifaceted complications, poses a pressing challenge for healthcare systems globally. In response, the advent of continuous glucose monitoring (CGM) systems, offering technological solutions for daily diabetes management, presents significant opportunities. However, the widespread adoption faces several barriers, linked both to the technological configuration of the devices and to the psychological dimension of patients.

What drives patients' acceptance of Digital Therapeutics? Establishing a new framework to measure the interplay between rational and institutional factors.

Background: The rising incidence of chronic diseases among the population, further exacerbated by the phenomenon of aging, is a primary concern and a serious challenge for the healthcare systems worldwide. Among the wide realm of health digital technologies, the rise of Digital Therapeutics (DTx), which are medical devices able to deliver evidence-based treatments to manage and treat diseases, opens new opportunities. However, their diffusion and usage are still fragmented among countries.

Comparison between real-world practice and application of the FRAX algorithm in the treatment of osteoporosis.

Background And Aims: The most recent guidelines suggest treating patients whose FRAX 10-year fracture risk scores are ≥ 20%. However, this method of evaluation does not take into account parameters that are nonetheless relevant to the therapeutic choice. Our aim was to compare the therapeutic choices for treatment based on a wider assessment (real-world practice) with those based on FRAX scores, taking 20% as the cut-off score.

Dietary inflammatory index is associated with lung function in healthy older adults.

Objectives: Aging is associated with low-grade chronic inflammation contributing to a decline in lung performance. The Dietary Inflammatory Index (DII) has been introduced to evaluate the inflammatory potential of different diets, which may further affect individuals' respiratory function. This study investigates the association between DII and lung performance in older adults.

Communicating Bad News to Older Patients from the Physician's Point of View: Focus on the Influence of Gender and Length of Work Experience.

Background: Communicating bad news is of great interest in the geriatric field, but few works have considered the physician's point of view in this regard.

Objectives: The aim of this study was to explore possible differences related to physicians' gender and work experience in how a terminal diagnosis is disclosed to older patients.

Methods: Study participants were 420 Italian physicians (277 M, 143 F) working in clinical medicine (58.

Association of body surface area with fat mass, free fat mass and total weight in healthy individuals, and implications for the dosage of cytotoxic drugs.

Background & Aims: In oncology, the dosage of anti-neoplastic drugs is generally adapted to the patient's body surface area (BSA). We investigated the potential differences between BSA and body weight (BW) in estimating the variability in body composition among individuals, especially older adults.

Materials And Methods: The study population included 322 community-dwelling individuals with different age and sex: 45 adult men (AM, age 18-65 years), 86 older men (OM, age >65 years), 54 adult women (AW, age 18-65 years), and 137 older women (OW, age >65 years).

The Impact of Smoking on Bone Metabolism, Bone Mineral Density and Vertebral Fractures in Postmenopausal Women.

Background: Smoking is recognized among the risk factors for osteoporosis, but only few studies have comprehensively explored its influence on bone metabolism and strength. We aimed to evaluate smoking effects on calcium-phosphate metabolism, bone mineral density (BMD) and fracture risk in postmenopausal women.

Methods: Our sample included 1067 postmenopausal women who arrived to our osteoporosis outpatient clinic.

Phase angle and metabolic equivalents as predictors of frailty transitions in advanced age.

Objectives: The aim of this prospective study was to investigate whether two cellular and metabolic health indices, phase angle (PhA) and metabolic equivalents (METs), can predict changes in frailty states in fit community-dwelling older people.

Methods: A sample of 118 individuals aged ≥65 years who attended a twice-weekly mild fitness program of aerobic and/or resistance exercises was enrolled in the study. At baseline and after three years, individuals underwent a clinical examination, biochemical determinations, bioelectrical impedance analysis, body composition assessment with dual energy X-ray absorptiometry, physical performance tests, and frailty and sarcopenia assessment.

Identification of asymptomatic frailty vertebral fractures in post-menopausal women.

Purpose: Vertebral fractures are associated with persistent pain, disability and mortality. However, around two thirds of women with vertebral fractures are unaware of them. We aimed to analyze which factors could mostly be associated to the presence of vertebral fractures in post-menopausal women, and evaluate the effectiveness of current screening criteria for the detection of vertebral fractures in an outpatient setting.

The control of mitochondrial succinate-dependent H2O2 production.

In brain mitochondria succinate activates H(2)O(2) release, concentration dependently (starting at 15 μM), and in the presence of NAD dependent substrates (glutamate, pyruvate, β-hydroxybutyrate). We report that TCA cycle metabolites (citrate, isocitrate, α-ketoglutarate, fumarate, malate) individually and quickly inhibit H(2)O(2) release. When they are present together at physiological concentration (0.

Different effects of SNP and GSNO on mitochondrial O2 .- /H 2O2 production.

Sodium Nitroprusside (SNP) and S-Nitrosoglutathione (GSNO) differently affect mitochondrial H(2)O(2) release at Complex-I. mM SNP increases while GSNO decreases the release induced by succinate alone or added on top of NAD-linked substrates. Stimulation likely depends on Nitric Oxide ((.

Succinate is the controller of O2-/H2O2 release at mitochondrial complex I : negative modulation by malate, positive by cyanide.

Mitochondrial production of H(2)O(2) is low with NAD substrates (glutamate/pyruvate, 3 and 2 mM) (G/P) and increases over ten times upon further addition of succinate, with the formation of a sigmoidal curve (semimaximal value at 290 microM, maximal H(2)O(2) production at 600 microM succinate). Malate counteracts rapidly the succinate induced increased H(2)O(2) release and moves the succinate dependent H(2)O(2) production curve to the right. Nitric oxide (NO) and carbon monoxide (CO) are cytochrome c oxidase inhibitors which increase mitochondrial ROS production.

Clorgyline and other propargylamine derivatives as inhibitors of succinate-dependent H(2)O(2) release at NADH:UBIQUINONE oxidoreductase (Complex I) in brain mitochondria.

Complex I is the main O(2)(-) producer of the mitochondrial respiratory chain. O(2)(-) release is low with NAD-linked substrates and increases strongly during succinate oxidation, which increases the QH(2)/Q ratio and is rotenone sensitive. We show that the succinate dependent O(2)(-) production (measured as H(2)O(2) release) is inhibited by propargylamine containing compounds (clorgyline, CGP 3466B, rasagiline and TVP-1012).

Succinate modulation of H2O2 release at NADH:ubiquinone oxidoreductase (Complex I) in brain mitochondria.

Complex I (NADH:ubiquinone oxidoreductase) is responsible for most of the mitochondrial H2O2 release, both during the oxidation of NAD-linked substrates and during succinate oxidation. The much faster succinate-dependent H2O2 production is ascribed to Complex I, being rotenone-sensitive. In the present paper, we report high-affinity succinate-supported H2O2 generation in the absence as well as in the presence of GM (glutamate/malate) (1 or 2 mM of each).

Dopamine-derived dopaminochrome promotes H(2)O(2) release at mitochondrial complex I: stimulation by rotenone, control by Ca(2+), and relevance to Parkinson disease.

Inhibitors of Complex I of the mitochondrial respiratory chain, such as rotenone, promote Parkinson disease-like symptoms and signs of oxidative stress. Dopamine (DA) oxidation products may be implicated in such a process. We show here that the o-quinone dopaminochrome (DACHR), a relatively stable DA oxidation product, promotes concentration (0.

Respiration-dependent removal of exogenous H2O2 in brain mitochondria: inhibition by Ca2+.

In brain mitochondria, state 4 respiration supported by the NAD-linked substrates glutamate/malate in the presence of EGTA promotes a high rate of exogenous H2O2 removal. Omitting EGTA decreases the H2O2 removal rate by almost 80%. The decrease depends on the influx of contaminating Ca2+, being prevented by the Ca2+ uniporter inhibitor ruthenium red.

The adenosine inhibition of glutamate exocytosis in synaptosomes is removed by the collapse of the vesicle-cytosol deltapH plus the opening of farnesol-sensitive Ca(2+) channels.

Adenosine inhibits synaptosomal exocytosis of glutamate, triggered by KCl or by the K(+) channel inhibitor, 4-aminopyridine (4-AP), without affecting Ca(2+) influx. Its effect is removed by the activation of protein kinase C (PKC). We show that in the presence of the protein kinase inhibitor, staurosporine, the adenosine inhibition is removed also by collapsing deltapH between secretory vesicle and the cytosol with methylamine (MA), provided that exocytosis is triggered by KCl (which activates an initial transient spike of Ca(2+) influx) but not by 4-AP.

Adenosine inhibits glutamate exocytosis largely without interfering with Ca2+ influx in rat cerebrocortical synaptosomes.

Adenosine is an inhibitor of glutamate release in synaptosomes. The inhibition is removed by the A(1) adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). We monitored the variations of cytoplasmic free Ca(2+) concentrations ([Ca(2+)](i)) in KCl or 4-aminopyridine-stimulated synaptosomes, in the presence of adenosine or adenosine plus DPCPX.

Involvement of nuclear factor-kappa B (NF-kappaB) activation in mitogen-induced lymphocyte proliferation: inhibitory effects of lymphoproliferation by salicylates acting as NF-kappaB inhibitors.

The transcription factor nuclear factor-kappa B (NF-kappaB) is involved in the production of inflammatory cytokines and in the control of the inflammatory response. Some nonsteroidal anti-inflammatory drugs such as acetylsalicylic acid (ASA) or salicylate are known to exert some of their anti-inflammatory pharmacological properties independently of cyclooxygenase inhibition. For ASA and salicylate, an NF-kappaB inhibitory effect at mM concentrations (pharmacological plasma concentrations reached in vivo) has been shown.

Modulation of glutamate exocytosis by redox changes of superficial thiol groups in rat cerebrocortical synaptosomes.

The treatment of cerebral cortex synaptosomes with the membrane impermeable thiol reagent 5,5'-dithio-bis-(2-nitrobenzoic acid) (DTNB) induces a long-lasting partial inhibition (about 40%) of the KCl-stimulated Ca2+-dependent exocytosis of glutamate. Synaptosomes are not damaged by the treatment. The increase of cytoplasmic free Ca2+ concentration ([Ca2+]i) upon depolarization is not affected by DTNB.

The pH-sensitive dye acridine orange as a tool to monitor exocytosis/endocytosis in synaptosomes.

We introduce the use of the pH-sensitive dye acridine orange (AO) to monitor exo/endocytosis of acidic neurotransmitter-containing vesicles in synaptosomes. AO is accumulated exclusively in acidic v-ATPase-dependent bafilomycin (Baf)-sensitive compartments. A fraction of the accumulated AO is rapidly released (fluorescence increase) upon depolarization with KCl in the presence of Ca2+.

Pretreatment with H2O2 decreases the Ca2+ sensitivity of the exocytosis of glutamate in cerebrocortical synaptosomes.

The treatment of cerebrocortical synaptosomes with low concentrations of H2O2 induces a long-lasting inhibition of the Ca2+ -dependent release of glutamate induced by KCl or ionomycin, without interfering with the cytosolic calcium and without damaging the synaptosomes (Zoccarato, F., Valente, M., and Alexandre, A.

Hydrogen peroxide induces a long-lasting inhibition of the Ca(2+)-dependent glutamate release in cerebrocortical synaptosomes without interfering with cytosolic Ca2+.

We studied the action of H2O2 on the exocytosis of glutamate by cerebrocortical synaptosomes. The treatment of synaptosomes with H2O2 (50-150 microM) for a few minutes results in a long-lasting depression of the Ca(2+)-dependent exocytosis of glutamate, induced by KCl or by the K(+)-channel inhibitor 4-aminopyridine. The energy state of synaptosomes, as judged by the level of phosphocreatine and the ATP/ADP ratio, was not affected by H2O2, although a transient decrease was observed after the treatment.