ABSTRACT
Due to the prevalence of COVID-19, providing safe environments and reducing the risks of virus exposure play pivotal roles in our daily lives. Contact tracing is a well-established and widely-used approach to track and suppress the spread of viruses. Most digital contact tracing systems can detect direct face-to-face contact based on estimated proximity, without quantifying the exposed virus concentration. In particular, they rarely allow for quantitative analysis of indirect environmental exposure due to virus survival time in the air and constant airborne transmission. In this work, we propose an indoor spatiotemporal contact awareness framework (iSTCA), which explicitly considers the self-containing quantitative contact analytics approach with spatiotemporal information to provide accurate awareness of the virus quanta concentration in different origins at various times. Smartphone-based pedestrian dead reckoning (PDR) is employed to precisely detect the locations and trajectories for distance estimation and time assessment without the need to deploy extra infrastructure. The PDR technique we employ calibrates the accumulative error by identifying spatial landmarks automatically. We utilized a custom deep learning model composed of bidirectional long short-term memory (Bi-LSTM) and multi-head convolutional neural networks (CNNs) for extracting the local correlation and long-term dependency to recognize landmarks. By considering the spatial distance and time difference in an integrated manner, we can quantify the virus quanta concentration of the entire indoor environment at any time with all contributed virus particles. We conducted an extensive experiment based on practical scenarios to evaluate the performance of the proposed system, showing that the average positioning error is reduced to less than 0.7 m with high confidence and demonstrating the validity of our system for the virus quanta concentration quantification involving virus movement in a complex indoor environment. © 2022 by the authors.
ABSTRACT
Since the end of 2019, the world has faced a major crisis because of the outbreak of COVID-19 disease which has created a severe threat to humanity. To control this pandemic, the World Health Organization gave some guidelines like wearing PPE (personal protective equipment) (e.g., face masks, overshoes, gloves), social distancing, hand hygiene and shutting down all modes of public transport services. During this pandemic, plastic products (e.g., household plastics, PPE and sanitizer bottles) have substantially prevented the spread of this virus. Since the outbreak, approximately 1.6 million tons of plastic waste have been generated daily. However, single-use PPE like face masks (N95), surgical masks and hand gloves contain many non-biodegradable plastics materials. These abandoned products have created a huge number of plastic debris which ended up as microplastics (MPs) followed by nanoplastics (NPs) in nature that are hazardous to the eco-system. These MPs and NPs also act as vectors for the various pathogenic contaminants. The goal of this review is to offer an extensive discussion on the formation of NPs and MPs from all of these abandoned plastics and their long-term impact on the environment as well as human health. This review paper also attempts to assess the present global scenario and the main challenge of waste management to reduce the potential NP/MPs pollution to improve the eco-systems. © 2022 Elsevier Ltd
ABSTRACT
The coronavirus disease 2019 (COVID-19) pandemic has resulted in millions of patients infected worldwide and indirectly affecting even more individuals through disruption of daily living. Long-term adverse outcomes have been reported with similar diseases from other coronaviruses, namely Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS). Emerging evidence suggests that COVID-19 adversely affects different systems in the human body. This review summarizes the current evidence on the short-term adverse health outcomes and assesses the risk of potential long-term adverse outcomes of COVID-19. Major adverse outcomes were found to affect different body systems: immune system (including but not limited to Guillain-Barré syndrome and paediatric inflammatory multisystem syndrome), respiratory system (lung fibrosis and pulmonary thromboembolism), cardiovascular system (cardiomyopathy and coagulopathy), neurological system (sensory dysfunction and stroke), as well as cutaneous and gastrointestinal manifestations, impaired hepatic and renal function. Mental health in patients with COVID-19 was also found to be adversely affected. The burden of caring for COVID-19 survivors is likely to be huge. Therefore, it is important for policy makers to develop comprehensive strategies in providing resources and capacity in the healthcare system. Future epidemiological studies are needed to further investigate the long-term impact on COVID-19 survivors.
Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Patient Outcome Assessment , Pneumonia, Viral/complications , Pneumonia, Viral/epidemiology , Betacoronavirus/immunology , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/virology , Host-Pathogen Interactions/immunology , Humans , Organ Specificity , Pandemics , Pneumonia, Viral/immunology , Pneumonia, Viral/virology , SARS-CoV-2 , Time FactorsABSTRACT
Objective: To explore and analyze the possible mechanism of liver injury in patients with coronavirus disease 2019 (novel coronavirus pneumonia, NCP). Methods: The correlation between ALT, AST and other liver enzyme changes condition and NCP patients' disease status reported in the literature was comprehensively analyzed. ACE2 expression in liver tissue for novel coronavirus was analyzed based on single cell sequencing (GSE115469) data. RNA-Seq method was used to analyze Ace2 expression and transcription factors related to its expression in liver tissues at various time-points after hepatectomy in mouse model of acute liver injury with partial hepatectomy. t-test or Spearman rank correlation analysis was used for statistical analysis. Results: ALT and AST were abnormally elevated in some patients with novel coronavirus infection, and the rate and extent of ALT and AST elevation in severe NCP patients were higher than those in non-severe patients. Liver tissue results of single cell sequencing and immunohistochemistry showed that ACE2 was only expressed in bile duct epithelial cells of normal liver tissues, and very low in hepatocytes. In a mouse model of acute liver injury with partial hepatectomy, Ace2 expression was down-regulated on the first day, but it was elevated up to twice of the normal level on the third day, and returned to normal level on seventh day when the liver recovered and hepatocyte proliferation stopped. Whether this phenomenon suggests that the bile duct epithelial cells with positive expression of Ace2 participate in the process of liver regeneration after partial hepatectomy deserves further study. In RNA-Seq data, 77 transcription factors were positively correlated with the expression of Ace2 (r > 0.2, FDR < 0.05), which were mainly enriched in the development, differentiation, morphogenesis and cell proliferation of glandular epithelial cells. Conclusion: We assumed that in addition to the over activated inflammatory response in patients with NCP, the up-regulation of ACE2 expression in liver tissue caused by compensatory proliferation of hepatocytes derived from bile duct epithelial cells may also be the possible mechanism of liver tissue injury caused by 2019 novel coronavirus infection.