Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 8 de 8
Filter
1.
Front Biosci (Landmark Ed) ; 26(6): 135-148, 2021 05 30.
Article in English | MEDLINE | ID: covidwho-1281062

ABSTRACT

The human body is colonized from the birth by a large number of microorganisms. This will constitute a real "functional microbial organ" that is fundamental for homeostasis and therefore for health in humans. Those microorganisms. The microbial populations that colonize humans creating a specific ecosystem they have been collectively referred to as "human microbiota" or "human normal microflora". The microbiota play an important pathophysiological role in the various locations of the human body. This article focuses on one of the most important, that is the enteric microbiota. The composition (quantitative and qualitative) of microbes is analyzed in relation to age and environment during the course of human life. It also highlights eubiosis and dysbiosis as key terms for its role in health and disease. Finally, it analyzes its bi-directional relationship with the microbiota of the lungs, skin and that of the brain, and consequently for the whole central and peripheral nervous system for the maintenance of health in the human body.


Subject(s)
Bacteria/metabolism , Gastrointestinal Microbiome/physiology , Health Status , Homeostasis/physiology , Bacteria/classification , Brain/physiology , Cytokines/metabolism , Gastrointestinal Tract/physiology , Humans , Lung/physiology , Population Dynamics
2.
Rev Recent Clin Trials ; 16(3): 262-271, 2021.
Article in English | MEDLINE | ID: covidwho-1171287

ABSTRACT

BACKGROUND: Infectious agents may be involved in the pathogenesis of vascular disease and related complications. The aim of this review is to analyze the most relevant information on the common infections related to vascular disease, discussing the main pathophysiological mechanisms. METHODS: In the current review, the most important evidence on the issue of infections and vascular disease is searched on Medline, Scopus, and ScienceDirect database. RESULTS: Among infectious agents, herpesviruses, parvovirus B19, hepatitis viruses, human immunodeficiency virus, severe acute respiratory syndrome coronavirus 2, treponema pallidum, mycobacterium tuberculosis, pseudomonas aeruginosa, staphylococcus aureus, and candida albicans seem to particularly related to vascular disease. CONCLUSION: Infectious agents may affect vessel's homeostasis and functionality, both on the arterial and venous side, by means of several pathophysiological mechanisms such as dysregulation in vasomotor function, thromboembolic complications, initiation and progression of atherosclerosis, alteration of perivascular adipose tissue, recruiting inflammatory cells and molecules.


Subject(s)
Infections/physiopathology , Vascular Diseases/physiopathology , Disease Progression , Homeostasis/physiology , Humans
3.
Curr Pain Headache Rep ; 25(3): 19, 2021 Feb 25.
Article in English | MEDLINE | ID: covidwho-1100995

ABSTRACT

PURPOSE OF REVIEW: This review provides an updated discussion on the clinical presentation, diagnosis and radiographic features, mechanisms, associations and epidemiology, treatment, and prognosis of posterior reversible encephalopathy syndrome (PRES). Headache is common in PRES, though headache associated with PRES was not identified as a separate entity in the 2018 International Classification of Headache Disorders. Here, we review the relevant literature and suggest criteria for consideration of its inclusion. RECENT FINDINGS: COVID-19 has been identified as a potential risk factor for PRES, with a prevalence of 1-4% in patients with SARS-CoV-2 infection undergoing neuroimaging, thus making a discussion of its identification and treatment particularly timely given the ongoing global pandemic at the time of this writing. PRES is a neuro-clinical syndrome with specific imaging findings. The clinical manifestations of PRES include headache, seizures, encephalopathy, visual disturbances, and focal neurologic deficits. Associations with PRES include renal failure, preeclampsia and eclampsia, autoimmune conditions, and immunosuppression. PRES is theorized to be a syndrome of disordered autoregulation and endothelial dysfunction resulting in preferential hyperperfusion of the posterior circulation. Treatment typically focuses on treating the underlying cause and removal of the offending agents.


Subject(s)
Endothelium/physiopathology , Headache/physiopathology , Posterior Leukoencephalopathy Syndrome/physiopathology , Seizures/physiopathology , Vision Disorders/physiopathology , Acute Chest Syndrome/epidemiology , Aminolevulinic Acid/analogs & derivatives , Anemia, Sickle Cell/epidemiology , Autoimmune Diseases/epidemiology , Blood-Brain Barrier/metabolism , Brain Edema/diagnostic imaging , Brain Edema/physiopathology , COVID-19/epidemiology , Cerebrovascular Circulation/physiology , Cytokines/metabolism , Eclampsia/epidemiology , Female , Homeostasis/physiology , Humans , Hypertension/physiopathology , Magnetic Resonance Imaging , Posterior Leukoencephalopathy Syndrome/diagnostic imaging , Posterior Leukoencephalopathy Syndrome/epidemiology , Posterior Leukoencephalopathy Syndrome/therapy , Pre-Eclampsia/epidemiology , Pregnancy , Prognosis , Renal Insufficiency/epidemiology , SARS-CoV-2 , Vasospasm, Intracranial/physiopathology
4.
Free Radic Res ; 55(4): 364-374, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1010202

ABSTRACT

The COVID-19 pandemic has so far affected more than 45 million people and has caused over 1 million deaths worldwide. Infection with SARS-CoV-2, the pathogenic agent, which is associated with an imbalanced redox status, causes hyperinflammation and a cytokine storm, leading to cell death. Glucose-6-phosphate dehydrogenase (G6PD) deficient individuals may experience a hemolytic crisis after being exposed to oxidants or infection. Individuals with G6PD deficiency are more susceptible to coronavirus infection than individuals with normally functioning G6PD. An altered immune response to viral infections is found in individuals with G6PD deficiency. Evidence indicates that G6PD deficiency is a predisposing factor of COVID-19.


Subject(s)
COVID-19 , Glucosephosphate Dehydrogenase Deficiency , SARS-CoV-2/physiology , Virus Diseases , COVID-19/complications , COVID-19/epidemiology , COVID-19/genetics , COVID-19/metabolism , Disease Susceptibility , Glucosephosphate Dehydrogenase/genetics , Glucosephosphate Dehydrogenase/metabolism , Glucosephosphate Dehydrogenase Deficiency/complications , Glucosephosphate Dehydrogenase Deficiency/epidemiology , Glucosephosphate Dehydrogenase Deficiency/genetics , Glucosephosphate Dehydrogenase Deficiency/metabolism , Homeostasis/physiology , Humans , Oxidation-Reduction , Pandemics , Virus Diseases/epidemiology , Virus Diseases/genetics , Virus Diseases/metabolism
5.
Semin Cell Dev Biol ; 115: 37-44, 2021 07.
Article in English | MEDLINE | ID: covidwho-933484

ABSTRACT

Magnesium is an essential element of life, involved in the regulation of metabolism and homeostasis of all the tissues. It also regulates immunological functions, acting on the cells of innate and adaptive immune systems. Magnesium deficiency primes phagocytes, enhances granulocyte oxidative burst, activates endothelial cells and increases the levels of cytokines, thus promoting inflammation. Consequently, a low magnesium status, which is often underdiagnosed, potentiates the reactivity to various immune challenges and is implicated in the pathophysiology of many common chronic diseases. Here we summarize recent advances supporting the link between magnesium deficiency, inflammatory responses and diseases, and offer new hints towards a better understanding of the underlying mechanisms.


Subject(s)
Endothelial Cells/metabolism , Inflammation/metabolism , Magnesium Deficiency/metabolism , Magnesium/metabolism , Animals , Cation Transport Proteins/metabolism , Homeostasis/physiology , Humans
6.
Biochem Pharmacol ; 183: 114278, 2021 01.
Article in English | MEDLINE | ID: covidwho-845710

ABSTRACT

Baking soda and vinegar have been used as home remedies for generations and today we are only a mouse-click away from claims that baking soda, lemon juice, and apple cider vinegar are miracles cures for everything from cancer to COVID-19. Despite these specious claims, the therapeutic value of controlling acid-base balance is indisputable and is the basis of Food and Drug Administration-approved treatments for constipation, epilepsy, metabolic acidosis, and peptic ulcers. In this narrative review, we present evidence in support of the current and potential therapeutic value of countering local and systemic acid-base imbalances, several of which do in fact involve the administration of baking soda (sodium bicarbonate). Furthermore, we discuss the side effects of pharmaceuticals on acid-base balance as well as the influence of acid-base status on the pharmacokinetic properties of drugs. Our review considers all major organ systems as well as information relevant to several clinical specialties such as anesthesiology, infectious disease, oncology, dentistry, and surgery.


Subject(s)
Acid-Base Equilibrium/physiology , Acid-Base Imbalance/metabolism , Acid-Base Imbalance/therapy , Acid-Base Equilibrium/drug effects , Animals , COVID-19/metabolism , COVID-19/therapy , Homeostasis/drug effects , Homeostasis/physiology , Humans , Medicine, Traditional/methods , Medicine, Traditional/trends , Sodium Bicarbonate/administration & dosage , Sodium Bicarbonate/metabolism
7.
Am J Physiol Cell Physiol ; 319(6): C991-C996, 2020 12 01.
Article in English | MEDLINE | ID: covidwho-751459

ABSTRACT

Alveoli are the gas-exchanging units of the lung, and the alveolar barrier is often a key battleground where pathogens, allergens, and other insults from the environment are encountered. This is seen in the current coronavirus disease 2019 (COVID-19) pandemic, as alveolar epithelium is one of the major targets of SARS-COV-2, the virus that causes COVID-19. Thus, it is essential to understand the mechanisms in order to maintain the integrity of alveoli epithelium. Alveolar type II (AT2) cells behave as tissue stem cells that repair alveoli epithelium during steady-state replacement and after injury. However, not all AT2 cells are equal in their ability for self-renewal or differentiation. Through marker gene identification, lineage tracing, and single-cell RNA-sequencing (scRNA-seq), distinct subpopulations of AT2 cells have been identified that play the progenitor role in a different context. The revelation of AT2 heterogeneity has brought new insights into the role of AT2 cells in various lung disease settings and potentiates the finding of more therapeutics targets. In this mini review, we discuss the recently identified subpopulations of AT2 cells and their functions under steady-state, postinjury, and pathological conditions.


Subject(s)
COVID-19/pathology , Homeostasis/physiology , Pulmonary Alveoli/cytology , Pulmonary Alveoli/physiology , SARS-CoV-2 , Animals , Humans , Pulmonary Alveoli/pathology
8.
Clin Auton Res ; 30(4): 299-315, 2020 08.
Article in English | MEDLINE | ID: covidwho-705370

ABSTRACT

The pandemic viral illness COVID-19 is especially life-threatening in the elderly and in those with any of a variety of chronic medical conditions. This essay explores the possibility that the heightened risk may involve activation of the "extended autonomic system" (EAS). Traditionally, the autonomic nervous system has been viewed as consisting of the sympathetic nervous system, the parasympathetic nervous system, and the enteric nervous system. Over the past century, however, neuroendocrine and neuroimmune systems have come to the fore, justifying expansion of the meaning of "autonomic." Additional facets include the sympathetic adrenergic system, for which adrenaline is the key effector; the hypothalamic-pituitary-adrenocortical axis; arginine vasopressin (synonymous with anti-diuretic hormone); the renin-angiotensin-aldosterone system, with angiotensin II and aldosterone the main effectors; and cholinergic anti-inflammatory and sympathetic inflammasomal pathways. A hierarchical brain network-the "central autonomic network"-regulates these systems; embedded within it are components of the Chrousos/Gold "stress system." Acute, coordinated alterations in homeostatic settings (allostasis) can be crucial for surviving stressors such as traumatic hemorrhage, asphyxiation, and sepsis, which throughout human evolution have threatened homeostasis; however, intense or long-term EAS activation may cause harm. While required for appropriate responses in emergencies, EAS activation in the setting of chronically decreased homeostatic efficiencies (dyshomeostasis) may reduce thresholds for induction of destabilizing, lethal vicious cycles. Testable hypotheses derived from these concepts are that biomarkers of EAS activation correlate with clinical and pathophysiologic data and predict outcome in COVID-19 and that treatments targeting specific abnormalities identified in individual patients may be beneficial.


Subject(s)
Autonomic Nervous System/physiology , Betacoronavirus , Coronavirus Infections/physiopathology , Homeostasis/physiology , Pneumonia, Viral/physiopathology , Stress, Physiological/physiology , COVID-19 , Coronavirus Infections/diagnosis , Humans , Pandemics , Pneumonia, Viral/diagnosis , SARS-CoV-2
SELECTION OF CITATIONS
SEARCH DETAIL