How to Minimize the Impact of Pandemic Events: Lessons From the COVID-19 Crisis

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the current pandemic of coronavirus disease 2019 (COVID-19). This pandemic is characterized by a high variability in death rate (defined as the ratio between the number of deaths and the total number of infected people) across world countries. Several possible explanations have been proposed, but it is not clear whether this variability is due to a single predominant factor or instead to multiple causes. Here we addressed this issue using multivariable regression analysis to test the impact of the following factors: the hospital stress (defined as the ratio between the number of infected cases and the total number of hospital beds), the population median age, and the quality of the National Health System (NHS). For this analysis, we chose countries of the world with over 3000 infected cases as of April 1, 2020. Hospital stress was found to be the crucial factor in explaining the variability of death rate, while the others had negligible relevance. Different procedures for quantifying cases of infection and death for COVID-19 could affect the variability in death rate across countries. We therefore applied the same statistical approach to Italy, which is divided into 20 Regions that share the same protocol for counting the outcomes of this pandemic. Correlation between hospital stress and death rate was even stronger than that observed for countries of the world. Based on our findings and the historical trend for the availability of hospital beds, we propose guidelines for policy-makers to properly manage future pandemics

Nicotine and the taste allure for salty food

Smoking has been recognized as one agent that may decrease the effectiveness of the gustatory system to detect salt (Na+) in foodstuffs. As a consequence, smokers tend to ingest saltier foods than nonsmokers. An increase in sodium intake has been associated with hypertension: thus, smoking may concur to the development of hypertension by impairing salt perception. Understanding the mechanisms underlying the action of smoking on salty taste represents the premise to design proper intervention aiming at restoring normal sensitivity to sodium in smokers. I addressed this issue by studying the effect of nicotine, one of the main components of tobacco smoke, on the sodium detection mechanism in rat taste cells. Electrophysiological analysis of these cells revealed that long-term exposure to nicotine reduced the ion current mediated by the Epithelial Sodium Channel (ENaC), one of the sodium receptors occurring in taste cells. As to the molecular mechanism responsible for such a current decrease, data were consistent with a reduction in the number of functional ENaCs in the membrane of taste cells. Therefore, nicotine reduces the capability of taste cells to respond to sodium ions. This might explain, at least in part, why smokers tend to use salt more abundantly when flavoring their food: they are just boosting the sensory information to be relayed to the brain

Electrophysiology of Sodium Receptors in Taste Cells

Sodium intake is important to maintain proper osmolarity and volume of extracellular fluid in vertebrates. The ability to find sources of sodium ions for managing electrolyte homeostasis relies on the activity of the taste system to sense salt. Several studies have been performed to understand the mechanisms underlying Na+ reception in taste cells, the peripheral detectors for food chemicals. It is now generally accepted that Na+ interacts with specific ion channels in taste cell membrane, called sodium receptors. As ion channels, these proteins mediate transmembrane ion fluxes (that is, electrical currents) during their operation. Thus, a lot of information on the functional properties of sodium receptors has been obtained by using electrophysiological techniques. Here, I review our current knowledge on the biophysical and physiological features of these receptors obtained by applying the patch-clamp recording techniques to single taste cells

Salt Taste, Nutrition, and Health

The sodium ion (Na+) is essential for life [...

Does ENaC Work as Sodium Taste Receptor in Humans?

Taste reception is fundamental for the proper selection of food and beverages. Among the several chemicals recognized by the human taste system, sodium ions (Na+) are of particular relevance. Na+ represents the main extracellular cation and is a key factor in many physiological processes. Na+ elicits a specific sensation, called salty taste, and low-medium concentrations of table salt (NaCl, the common sodium-containing chemical we use to season foods) are perceived as pleasant and appetitive. How we detect this cation in foodstuffs is scarcely understood. In animal models, such as the mouse and the rat, the epithelial sodium channel (ENaC) has been proposed as a key protein for recognizing Na+ and for mediating preference responses to low-medium salt concentrations. Here, I will review our current understanding regarding the possible involvement of ENaC in the detection of food Na+ by the human taste system

Effect of kokumi taste-active γ-glutamyl peptides on amiloride-sensitive epithelial Na+ channels in rat fungiform taste cells

Kokumi taste-active compounds enhance salty taste perception. In animal models, sodium (salt) detection is mediated by the amiloride-sensitive epithelial sodium channel, ENaC. This ion channel works as a sodium receptor in the so-called sodium-taste cells. It is not known whether kokumi taste substances are able to affect the activity of functional ENaCs in these cells. Here, we use the patch-clamp technique to study the effect of kokumi-active tripeptides, glutathione (GSH) and γ-glutamyl-valyl-glycine (EVG), on the ENaC-mediated membrane current in rat fungiform sodium-taste cells. GSH and EVG reduced slightly this current and the effect disappeared in the presence of amiloride, a specific ENaC blocker. No effect on membrane current was detected in other taste cells (Type II and Type III cells) that do not express functional ENaC. Our findings suggest that the enhancing effect of kokumi taste-active γ-glutamyl peptides on salt reception is not explained by an increase in the activity of ENaC

How to Minimize the Impact of Pandemic Events: Lessons From the COVID-19 Crisis

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the current pandemic of coronavirus disease 2019 (COVID-19). This pandemic is characterized by a high variability in death rate (defined as the ratio between the number of deaths and the total number of infected people) across world countries. Several possible explanations have been proposed, but it is not clear whether this variability is due to a single predominant factor or instead to multiple causes. Here we addressed this issue using multivariable regression analysis to test the impact of the following factors: the hospital stress (defined as the ratio between the number of infected cases and the total number of hospital beds), the population median age, and the quality of the National Health System (NHS). For this analysis, we chose countries of the world with over 3000 infected cases as of April 1, 2020. Hospital stress was found to be the crucial factor in explaining the variability of death rate, while the others had negligible relevance. Different procedures for quantifying cases of infection and death for COVID-19 could affect the variability in death rate across countries. We therefore applied the same statistical approach to Italy, which is divided into 20 Regions that share the same protocol for counting the outcomes of this pandemic. Correlation between hospital stress and death rate was even stronger than that observed for countries of the world. Based on our findings and the historical trend for the availability of hospital beds, we propose guidelines for policy-makers to properly manage future pandemics

Molecular and Cellular Mechanisms Underlying Somatostatin-Based Signaling in Two Model Neural Networks, the Retina and the Hippocampus

Neural inhibition plays a key role in determining the specific computational tasks of different brain circuitries. This functional \u201cbraking\u201d activity is provided by inhibitory interneurons that use different neurochemicals for signaling. One of these substances, somatostatin, is found in several neural networks, raising questions about the significance of its widespread occurrence and usage. Here, we address this issue by analyzing the somatostatinergic system in two regions of the central nervous system, the retina and the hippocampus. By comparing the available information on these structures, we have identified common motifs in the action of somatostatin that may explain its involvement in such diverse circuitries. The emerging concept is that somatostatin-based signaling, through conserved molecular and cellular mechanisms, allows neural networks to operate correctly

Inhibitory Plasticity: From Molecules to Computation and Beyond

Synaptic plasticity is the cellular and molecular counterpart of learning and memory and, since its first discovery, the analysis of the mechanisms underlying long-term changes of synaptic strength has been almost exclusively focused on excitatory connections. Conversely, inhibition was considered as a fixed controller of circuit excitability. Only recently, inhibitory networks were shown to be finely regulated by a wide number of mechanisms residing in their synaptic connections. Here, we review recent findings on the forms of inhibitory plasticity (IP) that have been discovered and characterized in different brain areas. In particular, we focus our attention on the molecular pathways involved in the induction and expression mechanisms leading to changes in synaptic efficacy, and we discuss, from the computational perspective, how IP can contribute to the emergence of functional properties of brain circuits

Scattering Compensation for Deep Brain Microscopy: The Long Road to Get Proper Images

Multiphoton microscopy is the most widespread method for preclinical brain imaging when sub-micrometer resolution is required. Nonetheless, even in the case of optimal experimental conditions, only a few hundred micrometers under the brain surface can be imaged by multiphoton microscopy. The main limitation preventing the acquisition of images from deep brain structures is the random light scattering which, until recently, was considered an unsurmountable obstacle. When in 2007 a breakthrough work by Vellekoop and Mosk [1] proved it is indeed possible to compensate for random scattering by using high resolution phase modulators, the neuro-photonics community started chasing the dream of a multiphoton microscopy capable of reaching arbitrary depths within the brain. Unfortunately, more than 10 years later, despite a massive improvement of technologies for scattering compensation in terms of speed, performances and reliability, clear images from deep layers of biological tissues are still lacking. In this work, we review recent technological and methodological advances in the field of multiphoton microscopy analyzing the big issue of scattering compensation. We will highlight the limits hampering image acquisition, and we will try to analyze the road scientists must tackle to target one of the most challenging issue in the field of biomedical imaging