364 results match your criteria: "First Clinic of Internal Medicine[Affiliation]"
Expert Opin Pharmacother
April 2020
Halal Research Center of IRI, FDA, Tehran, Iran.
: Mortality due to sepsis is still prevalent, peaking at extreme ages of life including infancy. Despite many efforts, the peculiarity of the infant immune system has limited further advances in its treatment. Indeed, neonates experience a dramatic physiological transition from immune tolerance to the maternal antigens to functional maturity.
View Article and Find Full Text PDFEur Heart J
August 2020
Center for Molecular Cardiology, University of Zürich, Wagistrasse 12, Schlieren CH-8952, Switzerland.
The ongoing worldwide increase in life expectancy portends a rising prevalence of age-related cardiovascular (CV) diseases in the coming decades that demands a deeper understanding of their molecular mechanisms. Inflammation has recently emerged as an important contributor for CV disease development. Indeed, a state of chronic sterile low-grade inflammation characterizes older organisms (also known as inflamm-ageing) and participates pivotally in the development of frailty, disability, and most chronic degenerative diseases including age-related CV and cerebrovascular afflictions.
View Article and Find Full Text PDFCells
January 2020
First Clinic of Internal Medicine, Department of Internal Medicine and Centre of Excellence for Biomedical Research (CEBR), University of Genoa, viale Benedetto XV 6, 16132 Genoa, Italy.
Neutrophil extracellular traps (NETs) are formed by decondensed chromatin, histones, and neutrophil granular proteins and have a role in entrapping microbial pathogens. NETs, however, have pro-thrombotic properties by stimulating fibrin deposition, and increased NET levels correlate with larger infarct size and predict major adverse cardiovascular (CV) events. NETs have been involved also in the pathogenesis of diabetes, as high glucose levels were found to induce NETosis.
View Article and Find Full Text PDFEur Heart J
September 2020
School of Life and Medical Sciences, Postgraduate Medical School, University of Hertfordshire, Hertfordshire, UK.
Cancer Immunol Immunother
March 2020
First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, viale Benedetto XV 6, 16132, Genoa, Italy.
J Am Coll Cardiol
January 2020
VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia. Electronic address:
Pericarditis refers to the inflammation of the pericardial layers, resulting from a variety of stimuli triggering a stereotyped immune response, and characterized by chest pain associated often with peculiar electrocardiographic changes and, at times, accompanied by pericardial effusion. Acute pericarditis is generally self-limited and not life-threatening; yet, it may cause significant short-term disability, be complicated by either a large pericardial effusion or tamponade, and carry a significant risk of recurrence. The mainstay of treatment of pericarditis is represented by anti-inflammatory drugs.
View Article and Find Full Text PDFInt J Cardiol
March 2020
Center for Molecular Cardiology, Schlieren Campus, University of Zurich, 8952 Schlieren, Switzerland; Department of Cardiology, University Hospital Zurich, 8091 Zurich, Switzerland; Department of Research and Education, University Hospital Zurich, 8001 Zurich, Switzerland. Electronic address:
Thromb Haemost
January 2020
Center for Molecular Cardiology, Schlieren Campus, University of Zurich, Zurich, Switzerland.
Ischemia/reperfusion (I/R) injury in acute myocardial infarction activates several deleterious molecular mechanisms. The transcription factor JunD regulates pathways involved in oxidative stress as well as in cellular proliferation, differentiation, and death. The present study investigated the potential role of JunD as a modulator of myocardial injury pathways in a mouse model of cardiac I/R injury.
View Article and Find Full Text PDFJ Cardiovasc Pharmacol
February 2020
Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Pauley Heart Center, Richmond, VA.
Eur J Clin Invest
February 2020
Center for Molecular Cardiology, University of Zurich, Schlieren, Switzerland.
Background: Endothelial cells regulate the formation of blood clots; thus, genes selectively expressed in these cells could primarily determine thrombus formation. Apold1 (apolipoprotein L domain containing 1) is a gene expressed by endothelial cells; whether Apold1 directly contributes to arterial thrombosis has not yet been investigated. Here, we assessed the effect of Apold1 deletion on arterial thrombus formation using an in vivo model of carotid thrombosis induced by photochemical injury.
View Article and Find Full Text PDFInt J Mol Sci
November 2019
Clinica Medica "A. Murri", Department of Biomedical Sciences & Human Oncology, University of Bari Medical School, Piazza Giulio Cesare 11, 70124 Bari, Italy.
Sexual dimorphism accounts for significant differences in adipose tissue mass and distribution. However, how the crosstalk between visceral and ectopic fat depots occurs and which are the determinants of ectopic fat expansion and dysfunction remains unknown. Here, we focused on the impact of gender in the crosstalk between visceral and epicardial fat depots and the role of adipocytokines and high-sensitivity C-reactive protein (hs-CRP).
View Article and Find Full Text PDFBiomed Res Int
April 2020
Clinic of Cardiovascular Diseases, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, Italy.
J Clin Med
November 2019
Center for Molecular Cardiology, Schlieren Campus, University of Zurich, 8952 Schlieren, Switzerland.
CANTOS reported reduced secondary atherothrombotic events in patients with residual inflammatory risk treated with the inhibitory anti-IL-1β antibody, Canakinumab. Yet, mechanisms that underlie this benefit remain elusive. Recent work has implicated formation of neutrophil extracellular traps (NETosis) in arterial thrombosis.
View Article and Find Full Text PDFJACC Basic Transl Sci
September 2019
IRCCS Ospedale Policlinico San Martino Genoa, Italian Cardiovascular Network, Genoa, Italy.
Eur J Clin Invest
January 2020
Department of Internal Medicine, First Clinic of Internal Medicine, University of Genoa, Genoa, Italy.
Curr Pharm Des
June 2020
IRCCS Ospedale Policlinico San Martino Genoa - Italian Cardiovascular Network, 10 Largo Benzi 16132 Genoa, Italy.
J Clin Med
October 2019
IRCCS Ospedale Policlinico San Martino Genoa-Italian Cardiovascular Network, 16132 Genoa, Italy.
Statins are effective lipid-lowering drugs with a good safety profile that have become, over the years, the first-line therapy for patients with dyslipidemia and a real cornerstone of cardiovascular (CV) preventive therapy. Thanks to both cholesterol-related and "pleiotropic" effects, statins have a beneficial impact against CV diseases. In particular, by reducing lipids and inflammation statins, they can influence the pathogenesis of both myocardial infarction and diabetic cardiomyopathy.
View Article and Find Full Text PDFIUBMB Life
April 2020
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Familial hypercholesterolemia (FH) is an autosomal dominant disorder of lipoprotein metabolism that mainly occurs due to mutations in the low-density lipoprotein receptor gene and is characterized by increased levels of low-density lipoprotein cholesterol, leading to accelerated atherogenesis and premature coronary heart disease. Both innate and adaptive immune responses, which mainly include monocytes, macrophages, neutrophils, T lymphocytes, and B lymphocytes, have been shown to play a key role for the initiation and progression of atherogenesis in the general population. In FH patients, these immune cells have been suggested to play specific pro-atherosclerotic activities, from the initial leukocyte recruitment to plaque rupture.
View Article and Find Full Text PDFEur Heart J
April 2020
Center for Molecular Cardiology, Schlieren Campus, University of Zurich, Wagistrasse 12, Schlieren 8952, Switzerland.
Aims: Aging is an established risk factor for stroke; genes regulating longevity are implicated in the pathogenesis of ischaemic stroke where to date, therapeutic options remain limited. The blood-brain barrier (BBB) is crucially involved in ischaemia/reperfusion (I/R) brain injury thus representing an attractive target for developing novel therapeutic agents. Given the role of endothelial cells in the BBB, we hypothesized that the endothelial-specific expression of the recently described longevity gene SIRT6 may exhibit protective properties in stroke.
View Article and Find Full Text PDFBiomark Med
November 2019
Ospedale Policlinico San Martino Genoa - Italian Cardiovascular Network, 10 Largo Benzi, Genoa 16132, Italy.
J Cardiovasc Med (Hagerstown)
January 2020
IRCCS Ospedale Policlinico San Martino Genoa - Italian Cardiovascular Network, Genoa, Italy.
Eur J Clin Invest
October 2019
School of Allied Health, Faculty of Health, Education, Medicine and Social Care, Anglia Ruskin University, Chelmsford, UK.
Circ Arrhythm Electrophysiol
September 2019
Pauley Heart Center, Department of Internal Medicine, Virginia Commonwealth University, Richmond (J.K., A.G.M., A.B., S.T., F.N.S., K.A.E., A.A.).
Curr Pharm Des
June 2020
First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, 6 viale Benedetto XV, 16132 Genoa, Italy.
Background: Diabetes is increasing over time, mainly driven by obesity, aging, and urbanization. Classical macro- and microvascular complications represent the final result of a complex interplay involving atherosclerosis at all stages.
Methods: In this review, we aim at focusing on current updates in the pathophysiology of vascular disease in diabetes and discussing how new therapies might influence the management of these patients at high cardiovascular risk.
Biomolecules
August 2019
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran.
Chronic inflammation is one of the main determinants of atherogenesis. The traditional medications for treatment of atherosclerosis are not very efficient in targeting atherosclerotic inflammation. Most of these drugs are non-selective, anti-inflammatory and immunosuppressive agents that have adverse effects and very limited anti-atherosclerotic effects, which limits their systemic administration.
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