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1.
Transportation Research Part E-Logistics and Transportation Review ; 165, 2022.
Artigo em Inglês | Web of Science | ID: covidwho-2069756

RESUMO

One of the profound impacts of digitalization on supply chains is manifested through e -commerce. The latter has significantly grown during the last two decades, with further amplifications during the COVID-19 pandemic. This has created operational and policy making challenges for firms when deciding about how best to manage the resulting growth in e -commerce. While the impact of e-commerce on supply chains has been widely recognized in the literature, there was no effort to systematically review the literature, conceptualize some of the challenges and propose future research directions. This paper fills this gap by reviewing 153 publications from 1999 to 2019. We classify the reviewed literature based on which supply chain drivers were investigated, as well as, the employed research methodology. In addition, we conduct network and content analysis to uncover the main research themes and potential research directions namely, developing analytical centred;modelling based ecosystem for environment;leveraging data mining to enhance sustainability;balance between growth and sustainability;consumer demand and uncertainty;coordination in e-commerce logistics;last mile alternatives and cost management of innovative technique implementations. Furthermore, based on our literature review, we propose a conceptual framework where we interlink supply chain stages with a firm's business strategy, digital transformation strategy and performance.

2.
Chest ; 162(4):A601, 2022.
Artigo em Inglês | EMBASE | ID: covidwho-2060643

RESUMO

SESSION TITLE: What Lessons Will We Take From the Pandemic? SESSION TYPE: Rapid Fire Original Inv PRESENTED ON: 10/19/2022 11:15 am - 12:15 pm PURPOSE: Physical distancing is a fundamental community mitigation strategy that averts adverse health outcomes from COVID-19 and other transmissible illnesses. Despite national policies in place, racial/ethnic minority groups and individuals with lower socioeconomic status had disproportionately worse COVID-19 outcomes. Barriers to adherence to these public health recommendations may underlie some of these disparities. We, therefore, examined physical distancing practices according to racial/ethnic group, educational attainment, and income level in the US. METHODS: The National Health Interview Survey (NHIS), an annual cross-sectional survey that collects health indicators for noninstitutionalized civilians, was queried for adult respondents interviewed in 2020. We included adults who were working at any point in the past 12 months prior to the interview. Respondents working the week prior to the interview were identified in subgroup analyses. The outcomes of interest were rates of self-reported physical distancing measures in the workplace and non-adherence to these measures. Sample-weighted proportions and 95% confidence intervals were estimated and Pearson χ2 tests (α=0.05) were conducted to compare outcomes across racial/ethnic, educational, and income categories. Data were publicly available and deidentified, therefore institutional review was not sought. RESULTS: 9,501 respondents aged ≥18 years reported working at any point in the past 12 months prior to the interview. After weighting, 88.3% (n=8,427) reported having physical distancing measures in the workplace. In subgroup analyses of 8,394 individuals who worked in the last week, 91.2% (n=7,713) reported currently having physical distancing measures in the workplace. Rates of having social distancing measures in the workplace were higher with increasing educational attainment and income level (Table). Black and Hispanic individuals worked at places with higher rates of non-adherence to physical distancing measures compared with White and Asian respondents. Rates of non-adherence to physical distancing in the workplace were lower with increasing educational attainment and income level (Table). CONCLUSIONS: In 2020, higher rates of having physical distancing measures in the workplace were seen among more educated and higher-income individuals. Higher rates of non-adherence to these measures at the place of work were seen among Black and Hispanic individuals and those with lower educational attainment and income level. Limitations of this study include the self-reported nature of data, small sample sizes of some minority populations, and lack of granularity in work settings. CLINICAL IMPLICATIONS: Varying working conditions are possible barriers to adherence to public policies. Future efforts are needed to elucidate and mitigate the factors behind inequities in the ability to adhere to public health recommendations and disparities in health outcomes. DISCLOSURES: No relevant relationships by Deepak Bhatt No relevant relationships by Edward Christopher Dee No relevant relationships by Enrico Ferro No relevant relationships by Bhav Jain No relevant relationships by Bisola Ojikutu No relevant relationships by Joseph Alexander Paguio No relevant relationships by Jasper Seth Yao

3.
International Journal of Health Sciences ; 6:3686-3700, 2022.
Artigo em Inglês | Scopus | ID: covidwho-1995072

RESUMO

COVID-19 has significantly affected the teaching-learning continuum in India. Most of the educational institutes had adopted online mode for the delivery of content and pedagogies enabled by digital technology, devices, and platforms. The pandemic has adversely affected English language learning in India, for learners used to learning ESL in a real-life situation through regular face-to-face mode experienced challenges in earning ESL through virtual mode. Learning English to develop the required language skills in virtual classrooms was anything but easy. Nonetheless, Indian students, as this study finds, took up the challenge by their stride and survived the altered learning conditions forced by the pandemic. This student-centric study aims to explore the impact of COVID-19 on language learning, the problems and challenges faced by student-learners, and the strategies to overcome them. An online survey was conducted to collect data from a group of students (n=400) using a survey questionnaire and mixed methods were used for data analysis and interpretation. The results indicate that the students experienced moderate to high-level difficulty in language learning and their coping strategies worked out. © 2022 International Journal of Health Sciences.

4.
Critical Care Medicine ; 50(1 SUPPL):539, 2022.
Artigo em Inglês | EMBASE | ID: covidwho-1691827

RESUMO

INTRODUCTION: Infectious agents, including SARSCoV- 2, cause pulmonary endothelial cell (EC) dysfunction that leads to acute respiratory distress syndrome (ARDS). EC dysfunction involves increased leukocyte recruitment and cell permeability mediated by various junctional proteins, integrins, and adhesion molecules. The omega-3 fatty acid eicosapentaenoic acid (EPA) and its metabolites modulate inflammation and vascular function. These actions of EPA may contribute to reduced cardiovascular events as reported in outcome trials such as REDUCE-IT. Currently, EPA is being tested in patients at risk for or with COVID-19. This study tested the effects of EPA on protein expression in human pulmonary ECs following challenge by the cytokine IL-6 to simulate conditions encountered in advanced viral infections. METHODS: Human lung microvascular endothelial cells (HMVEC-L) were post-treated with vehicle or EPA (40 μM) in 2% FBS after a 2 hr challenge with IL-6 at 12 ng/ml for 24 h. Proteomic analysis used LC/MS to assess relative expression levels of EC proteins. Only significant (p< 0.05) changes in protein expression between treatment groups >1-fold were analyzed. Specific pathway analysis was carried out using gene set enrichment analysis (GSEA). RESULTS: HMVEC-L treated with EPA following challenge with IL-6 showed significant changes in over 400 proteins compared with IL-6 treatment alone. EPA specifically diminished eleven proteins in the “integrin cell surface interactions” pathway. These pathways proteins included integrins alpha-V, alpha-6, and beta-1, along with PECAM-1, junction adhesion molecule C (JAM3), fibronectin, and ICAM- 2. CONCLUSIONS: EPA reduced expression of pulmonary endothelial adhesion and permeability proteins following IL-6 treatment. The ability of EPA to inhibit EC dysfunction and inflammation may have benefits for patients with or at risk for ARDS due to viruses such as SARS-CoV-2 or sepsis.

5.
Critical Care Medicine ; 50(1 SUPPL):539, 2022.
Artigo em Inglês | EMBASE | ID: covidwho-1691826

RESUMO

INTRODUCTION: Endothelial cell (EC) dysfunction results in reduced nitric oxide (NO) bioavailability leading to inflammation and increased susceptibility to infectious agents. Heme oxygenase-1 (HO-1) produces potent antioxidant and anti-inflammatory products including carbon monoxide. SARS-CoV-2 and influenza affect ECs in multiple vascular beds, including pulmonary tissue. The omega-3 fatty acid eicosapentaenoic acid (EPA) and its metabolites preserve EC function in a manner that may contribute to reduced incident cardiovascular events (REDUCE-IT). Currently, EPA is being tested in patients with or at risk for COVID-19. This study tested the effects of EPA on NO and peroxynitrite (ONOO-) release under conditions of inflammation using lipopolysaccharide (LPS) and the cytokine IL-6. We also measured expression of HO-1 after cell challenge with IL-6. METHODS: Human lung microvascular endothelial cells (HMVEC-L) were pretreated with vehicle or EPA (40 μM) in 2% FBS for 2 h, then challenged with either IL-6 (12 ng/ml) or LPS (200 ng/ml) for 24 h. Cells (including untreated controls) were stimulated with calcium ionophore to measure maximum production of NO and peroxynitrite (ONOO-) using tandem porphyrinic nanosensors. Proteomic analysis was performed using LC/MS to assess relative expression levels. Only significant (p< 0.05) changes in protein expression between treatment groups >1-fold were analyzed. RESULTS: HMVEC-L challenged with LPS and IL-6 showed a pronounced loss of NO release by 22% (p< 0.01) and 18% (p< 0.01), respectively, concomitant with an increase in ONOO- by 28% (p< 0.01) and 26% (p< 0.01), respectively. As a result, the [NO]/[ONOO-] ratio, a marker of eNOS coupling efficiency, decreased by 39% (p< 0.001) and 35% (p< 0.001) with LPS and IL-6, respectively. However, EPA increased this ratio by 39% (p< 0.01) in both LPS and IL-6 treated cells. EPA also caused a 5.7-fold (p = 4.4 × 10-38) increase in expression of HO-1 with IL-6. CONCLUSIONS: These findings indicate that EPA improves NO bioavailability and reduces nitroxidative stress in pulmonary ECs during inflammation with LPS or IL-6. These studies indicate a protective effect of EPA on pulmonary ECs that may reduce inflammatory activation during sepsis, influenza, or advanced COVID-19 that may mediate many aspects of multiorgan system failure.

6.
Critical Care Medicine ; 50(1 SUPPL):540, 2022.
Artigo em Inglês | EMBASE | ID: covidwho-1691825

RESUMO

INTRODUCTION: SARS-CoV-2 and other viruses can cause endothelial cell (EC) dysfunction in multiple vascular beds, including pulmonary tissue. Infected patients may then develop acute respiratory distress syndrome (ARDS) and cardiovascular (CV) complications. The omega-3 fatty acid eicosapentaenoic acid (EPA) and its bioactive metabolites favorably modulate inflammation and EC function. These benefits of EPA may contribute to reduced CV events as reported in outcome trials (REDUCE-IT). Currently, EPA is being tested in patients with or at risk for COVID-19. This study tested the effects of either EPA pre- or post-treatment on global protein expression in human pulmonary ECs under conditions of inflammation using the cytokine IL-6 to simulate conditions of advanced viral infections. METHODS: Human lung microvascular endothelial cells (HMVEC-L) were pre-treated with either EPA (40 μM) or IL-6 (12 ng/mL) for 2 hr and then treated with IL-6 or EPA, respectively, for 24 hr in media with 2% FBS. Proteomic analysis was performed using LC/MS to assess relative protein expression levels. Only significant (p< 0.05) changes in protein expression between treatment groups >1-fold were analyzed. Expression of soluble intercellular adhesion molecule-1 (sICAM-1) was separately measured with immunochemistry. RESULTS: HMVEC-L pre- and post-treated with EPA during challenge with IL-6 showed significant changes in 100 (49/51 up/down) and 441 (229/212 up/down) proteins, respectively, compared with IL-6 treatment alone. Among the 31 proteins that were significantly modulated by both EPA pre- and post-treatment, thioredoxin reductase 1 increased relative to IL-6 alone, while matrix metalloproteinase 1 and fibronectin both decreased. Other proteins, such as hypoxia up-regulated protein 1, were differentially modulated by EPA relative to IL-6 (increased in pre-treatment, decreased in post-treatment). Finally, EPA significantly reduced sICAM- 1expression by 41% and 12% compared with IL-6 alone in the pre- and post-treatment models, respectively. CONCLUSIONS: These findings indicate that EPA favorably modulates the expression of multiple inflammatory and cytoprotective proteins during inflammation. These studies support a broad anti-inflammatory effect of EPA on pulmonary ECs that may have therapeutic implications for patients at risk for ARDS due to infectious agents including SARS-CoV-2 or other viruses.

7.
Lecture Notes on Data Engineering and Communications Technologies ; 91:113-123, 2022.
Artigo em Inglês | Scopus | ID: covidwho-1540199

RESUMO

The COVID-19 infection has firmly affected all nations globally. COVID-19 disease is a lung infection by the novel CORONA virus. The present study aims to develop a binary classification deep neural network that identifies the COVID-19 disease on chest X-ray scans. The proposed model divides the chest X-rays is two classes;one is a normal chest X-ray or the other is covid infected. The model has utilized the benefit of the transfer learning method and implemented the ResNet-50 pre-trained model as the backbone model. 1200 chest X-rays have been used to conduct this study while the achieved accuracy is 97.92%. The proposed model also manifests the effect of deep learning techniques in the medical imaging domain. © 2022, The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd.

8.
Topics in Antiviral Medicine ; 29(1):61, 2021.
Artigo em Inglês | EMBASE | ID: covidwho-1250615

RESUMO

Background: Established in vitro models for SARS-CoV-2 infection are limited and include cell lines of non-human origin and those engineered to overexpress ACE2, the cognate host cell receptor. Although Calu-3, a human lung cell line which endogenously expresses ACE2, supports SARS-CoV-2 replication, they are significantly less permissive to infection than other models. Furthermore, ACE2 expression in the respiratory tract is low and emerging evidence suggests the utilization of alternative host cell receptors and attachment factors may compensate for low ACE2 expression levels in the lung. We identified human H522 lung adenocarcinoma cells as naturally permissive to SARS-CoV-2 infection despite complete absence of ACE2. Methods: A panel of 10 cell lines, with variable expression levels of ACE2 and TMPRSS2 were infected with SARS-CoV-2 strain 2019-nCoV/USA-WA1/2020. Viral replication was monitored through assessment of cell-associated and cell-free viral RNA (vRNA) by QRT-PCR as well as N staining by FACS and in situ hybridization. Effect of blocking S protein by neutralizing antibodies and an ACE2-Fc decoy peptide, ACE2 blocking by a specific antibody, and ACE2 knockout by CRISPR on SARS-CoV-2 replication was determined by Q-RT-PCR for vRNAs. Various viral entry inhibitors were used to pathway of SARS-CoV-2 entry in H522 cells. RNA sequencing and proteomics was used to study the cell and innate immune responses in infected H522 cells. siRNA-mediated knockdown was utilized to further characterize the pathway of immune sensing. Results: Infection of H522 cells required the SARS-CoV-2 spike protein, though in contrast to ACE2-dependent models, spike alone was not sufficient for H522 infection. Temporally resolved transcriptomic and proteomic profiling revealed alterations in cell cycle and the antiviral host cell response, including MDA5- dependent activation of type-I interferon signaling. Focused chemical screens point to important roles for clathrin-mediated endocytosis and endosomal cathepsins in SARS-CoV-2 infection of H522 cells. Conclusion: These findings imply the utilization of an alternative SARS-CoV-2 host cell receptor which may impact tropism of SARS-CoV-2 and consequently human disease pathogenesis.

9.
Critical Care Medicine ; 49(1 SUPPL 1):488, 2021.
Artigo em Inglês | EMBASE | ID: covidwho-1194040

RESUMO

INTRODUCTION: Loss of pulmonary endothelial cell (EC) nitric oxide (NO) bioavailability following infection by SARS-CoV-2 or influenza leads to increased viral uptake, thrombosis and enhanced inflammation. EC production of NO by its synthase (eNOS) is downregulated by proteins in membrane caveolae, including caveolae-associated protein 2. The omega-3 fatty acid eicosapentaenoic acid (EPA) and its bioactive lipid metabolites reduce inflammation and improve EC function in various tissues. These benefits of EPA may contribute to the pronounced cardiovascular event reduction reported in REDUCE-IT. As a result, EPA is now being tested in patients at risk for COVID-19. This study tested the effects of EPA on expression of caveolae-associated protein 2 and NO bioavailability in pulmonary ECs under conditions of inflammation caused by the cytokine interleukin-6 (IL-6). METHODS: Human lung microvascular endothelial cells (HMVEC-L) were pretreated with vehicle or EPA (40 μM) in 2% FBS for 2 h, then challenged with IL-6 at 12 ng/ml for 24 h. Cells (including untreated controls) were stimulated with calcium ionophore to measure maximum production of NO and peroxynitrite (ONOO-) using tandem porphyrinic nanosensors. Proteomic analysis was performed using LC/ MS to capture relative expression levels >1,000 proteins. Only significant (p<0.05) changes in protein expression between treatment groups >2-fold were further analyzed. RESULTS: HMVEC-L challenged with IL-6 showed a pronounced loss of NO bioavailability. EPA treatment increased NO release (17%, p<0.05) and decreased ONOO- release (16%, p<0.05) compared with IL-6 treatment. The [NO]/[ONOO-] ratio, a marker of eNOS coupling efficiency, decreased by 35% (p<0.001) following exposure to IL-6 but EPA treatment increased the ratio by 39% (p<0.001). Improved NO bioavailability correlated with >3-fold reduction in caveolae-associated protein 2 (p<0.05). CONCLUSIONS: EPA restored NO bioavailability and reduced expression of caveolae-associated protein 2 in pulmonary ECs following IL-6 treatment. The ability of EPA to inhibit endothelial inflammatory changes and restore NO bioavailability has therapeutic implications for patients at risk for SARS-CoV-2 infection and other inflammatory states.

10.
Critical Care Medicine ; 49(1 SUPPL 1):488, 2021.
Artigo em Inglês | EMBASE | ID: covidwho-1194039

RESUMO

INTRODUCTION: Infectious agents like SARS-CoV-2 can cause endothelial cell (EC) dysfunction in multiple vascular beds from different organs in infected patients, including pulmonary tissue that leads to acute respiratory distress syndrome (ARDS). The omega-3 fatty acid eicosapentaenoic acid (EPA) has multifactorial effects that lead to reduced inflammation and improved EC function. These benefits of EPA may contribute to reduced cardiovascular events as reported in REDUCE-IT. EPA is currently being tested in patients at risk for COVID-19 in multiple trials. This study tested the effects of EPA on protein expression in human pulmonary ECs under conditions of inflammation using the cytokine IL-6 to simulate viral infection conditions. METHODS: Human lung microvascular endothelial cells (HMVEC-L) were pretreated with vehicle or EPA (40 μM) in 2% FBS for 2 h, then challenged with IL-6 at 12 ng/ml for 24 h. Proteomic analysis of cell lysates was performed using LC/MS to capture relative expression levels of over 1,000 proteins. Only significant changes in protein expression between treatment groups >2-fold were analyzed. Specific pathway analysis was carried out using gene set enrichment analysis (GSEA). Expression levels of intercellular adhesion molecule-1 (ICAM-1) were measured by Western blot analysis. RESULTS: HMVEC-L pretreated with EPA and then challenged with IL-6 showed reduced release of >60 proteins compared with untreated controls. Among the proteins significantly suppressed were those involved in inflammation, including protein LYRIC, integrin alpha-5, peroxiredoxin-1, macrophage migration inhibitory factor, and lysine-tRNA ligase. GSEA analysis revealed changes in several pathways related to transcription regulation. Exposure to IL-6 also caused a >5-fold increase in ICAM-1 expression compared with vehicle (p<0.001). EPA reduced ICAM-1 expression compared with control by 41% (p<0.05). CONCLUSIONS: These findings indicate that EPA reduces the expression of multiple inflammatory proteins triggered by cytokine treatment. These studies support a broad antiinflammatory effect of EPA on pulmonary ECs that may have therapeutic implications for patients at risk for influenza or SARS-CoV-2 or other pro-inflammatory stimuli.

11.
Critical Care Medicine ; 49(1 SUPPL 1):477, 2021.
Artigo em Inglês | EMBASE | ID: covidwho-1194037

RESUMO

INTRODUCTION: Infectious agents like SARS-CoV-2 trigger inflammation in endothelial cells (EC) in multiple vascular beds in infected patients, including pulmonary tissue that leads to acute respiratory distress syndrome (ARDS). Due to its anti-inflammatory effects, the omega-3 fatty acid eicosapentaenoic acid (EPA) is being tested in patients at risk for COVID-19. Additionally, EPA has been shown to significantly reduce cardiovascular events in high risk patients with elevated triglycerides as reported in the REDUCE-IT trial. The objective, then, of this study was to test the ability of EPA to reduce inflammatory changes in pulmonary ECs. METHODS: Human lung microvascular endothelial cells (HMVEC-L) were pretreated with vehicle or EPA (40 μM) in 2% FBS for 2 h, then challenged with lipopolysaccharide (LPS) at 200 ng/mL for 24 h. The expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in pulmonary ECs was measured with immunochemistry using SDS-PAGE and compared with β- Actin as a control. RESULTS: HMVEC-L challenged with LPS dramatically increased ICAM-1 expression by 1135% (p<0.001) compared with vehicle treatment. Pulmonary ECs pretreated with EPA had reduced expression of ICAM-1 by 47% (p<0.001). LPS modestly increased VCAM-1 expression (45%, p<0.05) in a manner that was reduced by EPA (12%), but it was not significant. CONCLUSIONS: EPA significantly reduced the expression of ICAM-1 in human pulmonary ECs following LPS exposure. These studies indicate a protective effect of EPA on the pulmonary endothelium that may reduce inflammation associated with infectious agents such as SARS-CoV-2.

12.
Critical Care Medicine ; 49(1 SUPPL 1):179, 2021.
Artigo em Inglês | EMBASE | ID: covidwho-1194016

RESUMO

INTRODUCTION: Endothelial cell (EC) dysfunction results in reduced nitric oxide (NO) bioavailability leading to inflammation and thrombus formation. Infectious agents like SARS-CoV-2 and influenza can infect ECs in multiple vascular beds from different organs in infected patients, especially in the lung. The omega-3 fatty acid eicosapentaenoic acid (EPA) and its metabolites can preserve EC function and reduce inflammation. These effects of EPA likely contribute to reduced cardiovascular events as reported in REDUCE-IT. Currently, EPA is being tested in patients at risk for COVID-19. This study tested the effects of EPA on NO bioavailability in pulmonary ECs under conditions of inflammation induced by lipopolysaccharide (LPS). METHODS: Human lung microvascular endothelial cells (HMVEC-L) were pretreated with vehicle or EPA (40 μM) in 2% FBS for 2 h, then challenged with LPS at 200 ng/ml for 24 h. Cells (including untreated controls) were stimulated with calcium ionophore to measure maximum production of NO and peroxynitrite (ONOO-) using tandem porphyrinic nanosensors. RESULTS: HMVEC-L challenged with LPS showed a pronounced loss of NO bioavailability. Cells treated with EPA increased NO release (20%, p<0.05) and decreased ONOO- release (14%, p<0.01) compared with LPS treatment. The [NO]/[ONOO-] ratio, a marker of eNOS coupling efficiency, decreased by 39% (p<0.001) following exposure to LPS. However, EPA increased the ratio by 39% (p<0.01) compared with LPS alone. CONCLUSIONS: These findings indicate that EPA preserves NO bioavailability and reduces nitroxidative stress in pulmonary ECs following LPS treatment. These studies indicate a protective effect of EPA on pulmonary ECs that may reduce the inflammatory changes caused by infectious agents such as influenza or SARS-CoV-2 among other stimuli.

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