ABSTRACT
Since 2020, the COVID-19 pandemic, triggered by SARS-CoV-2, represents the major global issue affecting the lifestyle of people around the world. Wuhan, China was the first city to detect the SARS-CoV-2 virus, but the virus soon spread around the world, forcing the World Health Organization to declare a global epidemic on March 11, 2020 (1). Previous pathological conditions or comorbidities such as old age are one of the main causes of premature death and increased morbidity and mortality due to COVID-19 (4). Inactivity due to hospitalization and bed rest and reduced physical activity due to constant quarantine and social distancing can reduce the ability of organ systems to resist viral infection and the risk of damage to the immune, respiratory, and Increase cardiovascular systems, musculoskeletal and nervous system (4). On the other hand, the health benefits of physical activity, from cardiovascular health to mental health, have been well established (5). Decreased physical activity and increased sedentary behaviors were reported during quarantine in several populations, including children and patients with a variety of medical conditions (6). In general, COVID-19 lifestyle changes have led to a decrease in physical activity and consequently more inactivity in different parts of the community, which can pose a risk to general or mental health, especially for certain populations. In this study, we have tried to review the neurological and psychological effects of COVID-19 and the resulting lifestyle changes, and specifically the role of exercise in relation to these effects. Central nervous system (CNS) and peripheral nervous system (PNS) manifestations can occur during and after COVID-19, but the underlying mechanisms, symptomatology, and frequency of these complications are not well understood (7). Limited postmortem studies have shown signs of hypoxic brain damage and inflammatory neurological changes in the brainstem, while neuropathological data from the PNS are almost non-existent. Due to the cause, direct invasion of acute respiratory syndrome of COVID-19 virus to nerve tissue has been suggested in several cases, but autoimmune damage and neurological complications related to intensive care management can also be effective. The contribution of these mechanisms to the overall burden of CNS and PNS complications of COVID-19 is unknown (7). Follow-ups in Germany and the United Kingdom have shown that neuropsychological symptoms after COVID-19 in 20 to 70% of patients, even in young adults, last for months after the onset of respiratory symptoms, suggesting brain involvement persists (9). COVID-19, which enters through angiotensin-converting enzyme receptors, can damage endothelial cells, leading to inflammation, thrombosis, and brain damage. In addition, systemic inflammation leads to a decrease in monoamines and neurotrophic factors and activation of microglia, which leads to an increase in glutamate and N-methyl-d-aspartate-3 and excitatory toxicity, and these factors cause the onset or exacerbation of existing neuropsychiatric symptoms. They are already (9). However, the extent of damage caused by the COVID-19 pandemic strain is still speculated;it has recently been suggested that irregular neuro-endocrine-immune interactions may be behind psychiatric manifestations observed in quarantined individuals (12, 13). Persistent and increased stressful events can direct immune, endocrine, and nervous system responses primarily through hypothalamic-pituitary-adrenal (HPA) mediated dysfunction (12), and changes in the levels of systemic inflammatory mediators or the brain predispose individuals to pathological psychological conditions. It acts like anxiety and depression. In addition, stress can be a potential trigger for neuroinflammation, a term used to indicate an imbalance or intensification of immune signals in the brain that can lead to several disorders such as aggression, psychosis, depression, and anxiety disorders (12). Covid 19 has also been shown to alter nerve growth factors that may affect the neurop
ABSTRACT
As the COVID-19 pandemic reshapes our social landscape, its lessons have far-reaching implications on how online service providers manage their infrastructure to mitigate risks. This paper presents Facebook's risk-driven backbone management strategy to ensure high service performance throughout the COVID-19 pandemic. We describe Risk Simulation System (RSS), a production system that identifies possible failures and quantifies their potential severity with a set of metrics for network risk. With a year-long risk measurement from RSS we show that our backbone resiliently withstood the COVID-19 stress test, achieving high service availability and low route dilation while efficiently handling traffic surges. We also share our operational practices to mitigate risk throughout the pandemic. Our findings give insights to further improve risk-driven network management. We argue for incorporating short-term failure statistics in modeling failures. Common failure prediction models based on long-term modeling achieve stable output at the cost of assigning low significance to unique short-term events of extreme importance such as COVID-19. Furthermore, we advocate augmenting network management techniques with non-networking signals. We support this by identifying and analyzing the correlation between network traffic and human mobility.