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1.
PLoS One ; 16(3): e0248995, 2021.
Article in English | MEDLINE | ID: covidwho-1575502

ABSTRACT

The COVID-19 pandemic forced healthcare services organization to adjust to mutating healthcare needs. Not exhaustive data are available on the consequences of this on non-COVID-19 patients. The aim of this study was to assess the impact of the pandemic on non-COVID-19 patients living in a one-million inhabitants' area in Northern Italy (Bologna Metropolitan Area-BMA), analyzing time trends of Emergency Department (ED) visits, hospitalizations and mortality. We conducted a retrospective observational study using data extracted from BMA healthcare informative systems. Weekly trends of ED visits, hospitalizations, in- and out-of-hospital, all-cause and cause-specific mortality between December 1st, 2019 to May 31st, 2020, were compared with those of the same period of the previous year. Non-COVID-19 ED visits and hospitalizations showed a stable trend until the first Italian case of COVID-19 has been recorded, on February 19th, 2020, when they dropped simultaneously. The reduction of ED visits was observed in all age groups and across all severity and diagnosis groups. In the lockdown period a significant increase was found in overall out-of-hospital mortality (43.2%) and cause-specific out-of-hospital mortality related to neoplasms (76.7%), endocrine, nutritional and metabolic (79.5%) as well as cardiovascular (32.7%) diseases. The pandemic caused a sudden drop of ED visits and hospitalizations of non-COVID-19 patients during the lockdown period, and a concurrent increase in out-of-hospital mortality mainly driven by deaths for neoplasms, cardiovascular and endocrine diseases. As recurrencies of the COVID-19 pandemic are underway, the scenario described in this study might be useful to understand both the population reaction and the healthcare system response at the early phases of the pandemic in terms of reduced demand of care and systems capability in intercepting it.


Subject(s)
Cause of Death , Emergency Service, Hospital/statistics & numerical data , Hospitalization/statistics & numerical data , COVID-19/epidemiology , COVID-19/pathology , COVID-19/virology , Cardiovascular Diseases/mortality , Cardiovascular Diseases/pathology , Humans , Italy/epidemiology , Metabolic Diseases/mortality , Metabolic Diseases/pathology , Neoplasms/mortality , Neoplasms/pathology , Pandemics , Quarantine , Retrospective Studies , SARS-CoV-2/isolation & purification
2.
Biomolecules ; 11(5)2021 05 11.
Article in English | MEDLINE | ID: covidwho-1299401

ABSTRACT

Lipoxygenases (LOXs) are lipid metabolizing enzymes that catalyze the di-oxygenation of polyunsaturated fatty acids to generate active eicosanoid products. 12-lipoxygenases (12-LOXs) primarily oxygenate the 12th carbon of its substrates. Many studies have demonstrated that 12-LOXs and their eicosanoid metabolite 12-hydroxyeicosatetraenoate (12-HETE), have significant pathological implications in inflammatory diseases. Increased level of 12-LOX activity promotes stress (both oxidative and endoplasmic reticulum)-mediated inflammation, leading to damage in these tissues. 12-LOXs are also associated with enhanced cellular migration of immune cells-a characteristic of several metabolic and autoimmune disorders. Genetic depletion or pharmacological inhibition of the enzyme in animal models of various diseases has shown to be protective against disease development and/or progression in animal models in the setting of diabetes, pulmonary, cardiovascular, and metabolic disease, suggesting a translational potential of targeting the enzyme for the treatment of several disorders. In this article, we review the role of 12-LOXs in the pathogenesis of several diseases in which chronic inflammation plays an underlying role.


Subject(s)
Arachidonate 12-Lipoxygenase/metabolism , Inflammation/immunology , Metabolic Diseases/immunology , Animals , Arachidonate 12-Lipoxygenase/genetics , Humans , Inflammation/metabolism , Inflammation/pathology , Lipid Metabolism , Metabolic Diseases/metabolism , Metabolic Diseases/pathology , Oxidation-Reduction
3.
Mol Genet Metab ; 132(2): S2-S6, 2021 02.
Article in English | MEDLINE | ID: covidwho-1091577
5.
Cell Metab ; 33(3): 479-498, 2021 03 02.
Article in English | MEDLINE | ID: covidwho-1039321

ABSTRACT

The increased prevalence of obesity, diabetes, and cardiovascular risk factors in people hospitalized with severe COVID-19 illness has engendered considerable interest in the metabolic aspects of SARS-CoV-2-induced pathophysiology. Here, I update concepts informing how metabolic disorders and their co-morbidities modify the susceptibility to, natural history, and potential treatment of SARS-CoV-2 infection, with a focus on human biology. New data informing genetic predisposition, epidemiology, immune responses, disease severity, and therapy of COVID-19 in people with obesity and diabetes are highlighted. The emerging relationships of metabolic disorders to viral-induced immune responses and viral persistence, and the putative importance of adipose and islet ACE2 expression, glycemic control, cholesterol metabolism, and glucose- and lipid-lowering drugs is reviewed, with attention to controversies and unresolved questions. Rapid progress in these areas informs our growing understanding of SARS-CoV-2 infection in people with diabetes and obesity, while refining the therapeutic strategies and research priorities in this vulnerable population.


Subject(s)
COVID-19/pathology , Diabetes Mellitus/pathology , Heart Disease Risk Factors , Metabolic Diseases/pathology , Obesity/pathology , Angiotensin-Converting Enzyme 2/metabolism , Blood Glucose/analysis , COVID-19/epidemiology , Cholesterol/metabolism , Comorbidity , Genetic Predisposition to Disease/genetics , Glucose/metabolism , Humans , Hyperglycemia/pathology , SARS-CoV-2 , COVID-19 Drug Treatment
6.
Nat Commun ; 11(1): 5165, 2020 10 14.
Article in English | MEDLINE | ID: covidwho-872694

ABSTRACT

Angiotensin-converting enzyme 2 (ACE2) has been identified as the host entry receptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) responsible for the COVID-19 pandemic. ACE2 is a regulatory enzyme of the renin-angiotensin system and has protective functions in many cardiovascular, pulmonary and metabolic diseases. This review summarizes available murine models with systemic or organ-specific deletion of ACE2, or with overexpression of murine or human ACE2. The purpose of this review is to provide researchers with the genetic tools available for further understanding of ACE2 biology and for the investigation of ACE2 in the pathogenesis and treatment of COVID-19.


Subject(s)
Cardiovascular Diseases/pathology , Disease Models, Animal , Lung Diseases/pathology , Peptidyl-Dipeptidase A/metabolism , Angiotensin-Converting Enzyme 2 , Animals , Betacoronavirus/physiology , COVID-19 , Cardiovascular Diseases/metabolism , Coronavirus Infections/metabolism , Coronavirus Infections/pathology , Coronavirus Infections/virology , Humans , Lung Diseases/metabolism , Metabolic Diseases/metabolism , Metabolic Diseases/pathology , Mice , Mice, Mutant Strains , Pandemics , Peptidyl-Dipeptidase A/genetics , Pneumonia, Viral/metabolism , Pneumonia, Viral/pathology , Pneumonia, Viral/virology , SARS-CoV-2
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