SARS-2 virus has reached its most harmful mutated form and has damaged the world's economy, integrity, health system and peace to a limit. An open problem is to address the release of antibodies after the infection and after getting the individuals vaccinated against the virus. The viral fusion process is linked with the furin enzyme and the adaptation is linked with the mutation, called D614G mutation. The cell-protein studies are extremely challenging. We have developed a mathematical model to address the process at the cell-protein level and the delay is linked with this biological process. Genetic algorithm is used to approximate the parametric values. The mathematical model proposed during this research consists of virus concentration, the infected cells count at different stages and the effect of interferon. To improve the understanding of this model of SARS-CoV2 infection process, the action of interferon (IFN) is quantified using a variable for the non-linear mathematical model, that is based on a degradation parameter . This parameter is responsible for the delay in the dynamics of this viral action. We emphasize that this delay responds to the evasion by SARS-CoV2 via antagonizing IFN production, inhibiting IFN signaling and improving viral IFN resistance. We have provided videos to explain the modeling scheme.
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http://dx.doi.org/10.1007/s40808-021-01260-y | DOI Listing |
Front Biosci (Landmark Ed)
January 2025
Institute of Translational Medicine, Shanghai University, 200444 Shanghai, China.
Background: Dexamethasone has proven life-saving in severe acute respiratory syndrome (SARS) and COVID-19 cases. However, its systemic administration is accompanied by serious side effects. Inhalation delivery of dexamethasone (Dex) faces challenges such as low lung deposition, brief residence in the respiratory tract, and the pulmonary mucus barrier, limiting its clinical use.
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January 2025
HUN-REN-SZTE Neuroscience Research Group, Hungarian Research Network, University of Szeged (HUN-REN-SZTE), Danube Neuroscience Research Laboratory, H-6725 Szeged, Hungary.
Backgrounds: Memory and emotion are especially vulnerable to psychiatric disorders such as post-traumatic stress disorder (PTSD), which is linked to disruptions in serotonin (5-HT) metabolism. Over 90% of the 5-HT precursor tryptophan (Trp) is metabolized via the Trp-kynurenine (KYN) metabolic pathway, which generates a variety of bioactive molecules. Dysregulation of KYN metabolism, particularly low levels of kynurenic acid (KYNA), appears to be linked to neuropsychiatric disorders.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, 530021 Nanning, Guangxi, China.
Background: Rheumatic heart disease (RHD), which is caused mainly by Group A Streptococcus, leads to fibrotic damage to heart valves. Recently, endothelial‒mesenchymal transition (EndMT), in which activin plays an important role, has been shown to be an important factor in RHD valvular injury. However, the mechanism of activin activity and EndMT in RHD valvular injury is not clear.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, 401336 Chongqing, China.
Background: Myocardial ischemia-reperfusion (I/R) injury and coronary microcirculation dysfunction (CMD) are observed in patients with myocardial infarction after vascular recanalization. The antianginal drug trimetazidine has been demonstrated to exert a protective effect in myocardial ischemia-reperfusion injury.
Objectives: This study aimed to investigate the role of trimetazidine in endothelial cell dysfunction caused by myocardial I/R injury and thus improve coronary microcirculation.
Pharm Biol
December 2025
The Affiliated Hospital, Changchun University of Chinese Medicine, Changchun, China.
Context: The decline in ovarian reserve is a major concern in female reproductive health, often associated with oxidative stress and mitochondrial dysfunction. Although ginsenoside Rg1 is known to modulate mitophagy, its effectiveness in mitigating ovarian reserve decline remains unclear.
Objective: To investigate the role of ginsenoside Rg1 in promoting mitophagy to preserve ovarian reserve.
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