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Aims This study aims to evaluate the short- and long-term associations between COVID-19 and development of cardiovascular disease (CVD) outcomes and mortality in the general population. Methods and Results A prospective cohort of patients with COVID-19 infection between 16 March 2020 and 30 November 2020 was identified from UK Biobank, and followed for up to 18 months, until 31 August 2021. Based on age (within 5 years) and sex, each case was randomly matched with up to 10 participants without COVID-19 infection from two cohorts—a contemporary cohort between 16 March 2020 and 30 November 2020 and a historical cohort between 16 March 2018 and 30 November 2018. The characteristics between groups were further adjusted with propensity score-based marginal mean weighting through stratification. To determine the association of COVID-19 with CVD and mortality within 21 days of diagnosis (acute phase) and after this period (post-acute phase), Cox regression was employed. In the acute phase, patients with COVID-19 (n = 7584) were associated with a significantly higher short-term risk of CVD {hazard ratio (HR): 4.3 [95% confidence interval (CI): 2.6– 6.9]; HR: 5.0 (95% CI: 3.0–8.1)} and all-cause mortality [HR: 81.1 (95% CI: 58.5–112.4); HR: 67.5 (95% CI: 49.9–91.1)] than the contemporary (n = 75 790) and historical controls (n = 75 774), respectively. Regarding the post-acute phase, patients with COVID-19 (n = 7139) persisted with a significantly higher risk of CVD in the long-term [HR: 1.4 (95% CI: 1.2–1.8); HR: 1.3 (95% CI: 1.1– 1.6)] and all-cause mortality [HR: 5.0 (95% CI: 4.3–5.8); HR: 4.5 (95% CI: 3.9–5.2) compared to the contemporary (n = 71 296) and historical controls (n = 71 314), respectively. Conclusions COVID-19 infection, including long-COVID, is associated with increased short- and long-term risks of CVD and mortality. Ongoing monitoring of signs and symptoms of developing these cardiovascular complications post diagnosis and up till at least a year post recovery may benefit infected patients, especially those with severe disease. [ABSTRACT FROM AUTHOR]

Objective(s): We evaluated the impact of the COVID-19 pandemic on the number of referrals for SPECT myocardial perfusion imaging (SPECT-MPI) as well as changes in the clinical and imaging characteristics. Methods: We respectively reviewed 1042 SPECT-MPI cases performed in a 4- month period during the COVID-19 pandemic (PAN; n=423) and compared their findings with those acquired in the same months before the pandemic (PRE; n=619). Results: The number of stress SPECT-MPI studies performed during the PAN period significantly dropped compared to the number of studies carried out in the PRE period (p = 0.014). In the PRE period, the rates of patients presenting with non-anginal, atypical and typical chest pain were 31%, 25% and 19%, respectively. The figures significantly changed in the PAN period to 19%, 42%, and 11%, respectively (all p-values <0.001). Regarding the pretest probability of coronary artery disease (CAD), a significant decrease and increase were noticed in patients with high and intermediate pretest probability, respectively (PRE: 18% and 55%, PAN: 6% and 65%, p <0.001 and 0.008, respectively). Neither the rates of myocardial ischemia nor infarction differed significantly in the PRE vs. PAN study periods . Conclusion: The number of referrals dropped significantly in the PAN era. While the proportion of patients with intermediate risk for CAD being referred for SPECTMPI increased, those with high pretest probability were less frequently referred. Image parameters were mostly comparable between the study groups in the PRE and PAN periods. [ABSTRACT FROM AUTHOR]

The COVID-19 infection caused by SARS-CoV-2 is a healthcare crisis that has led to unparalleled disruption and has impacted healthcare services, leading to significant morbidity and mortality in the worldwide population. Insufficient data on the management of COVID-19 complications such as hypercoagulability and the controversy about the benefits of anticoagulant therapy are major challenges encountered by clinicians, especially for patients with pre-existing cardiovascular diseases (CVD), and are still debatable. Therefore, we endeavored to conduct a systematic review to assess the clinical outcomes of prior anticoagulant therapy in patients with COVID-19 having pre-existing CVD. Electronic searches of the PubMed database and EBSCO Information Services were carried out, and all relevant articles were employed. Seven articles with data from 21,989 subjects were included. Despite the promised clinical outcomes of anticoagulant therapy, the results of the current systematic review indicated insignificant improvements in the reduction of mortality rate or ICU admission among patients with COVID-19 having pre-existing CVD. Furthermore, direct oral anticoagulant (DOAC) were favored over vitamin K antagonists (VKAs) due to better action and less side effects. In conclusion, the findings are controversial as we did not statistically analyze the results. The data showed inconsistent information with no clear effect of anticoagulant use before patient hospitalization or decreasing COVID-19 severity, particularly in those with CVD. Further studies including randomized controlled trials are required to describe the best course as well as optimal dose of anticoagulant use in the treatment of patients with COVID-19, particularly those with comorbidities such as CVD. [ABSTRACT FROM AUTHOR]

Introduction: We aimed to describe the extrapulmonary manifestations of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, including their frequency, onset with respect to respiratory symptoms, pathogenesis and association with disease severity. Methods: We searched the MEDLINE and Embase databases for SARS-CoV-2-related studies. Meta-analysis, observational studies, case series and case reports published in English or Chinese between 1 January 2020 and 1 May 2020 were included. Reports with only paediatric or obstetric cases were excluded. Results: 169 articles were included. Early manifestations (preceding respiratory symptoms until Day 6 of onset) included olfactory and gustatory disturbance (self-reported in up to 68% and 85% of cases, respectively), gastrointestinal symptoms (up to 65.9%) and rash (up to 20.4%). From Day 7 onwards, hypercytokinaemia, paralleled multi-organ complications including acute cardiac injury (pooled incidence of 17.7% in 1,412 patients, mostly with severe disease and 17.4% mortality), kidney and liver injury (up to 17% and 33%, respectively) and thrombocytopenia (up to 30%). Hypercoagulability resulted in venous thromboembolic events in up to 31% of all patients. Uncommon disease presentation and complications comprised Guillain-Barré syndrome, rhabdomyolysis, otitis media, meningoencephalitis and spontaneous pneumomediastinum. Conclusion: Although the systemic manifestations of SARS-CoV-2 infection are variegated, they are deeply interwoven by shared mechanisms. Two phases of extrapulmonary disease were identified: (a) an early phase with possible gastrointestinal, ocular and cutaneous involvement; and (b) a late phase characterised by multiorgan dysfunction and clinical deterioration. A clear, multidisciplinary consensus to define and approach thromboinflammation and cytokine release syndrome in SARS-CoV-2 is needed. [ABSTRACT FROM AUTHOR]

Background: Research has examined the relationships between coronary artery calcium (CAC) scores and mortality, mechanical ventilation, and intensive care unit admissions. This paper summarizes the predictive value of coronary artery calcification scoring for hospitalized COVID-19 patients in terms of mortality, mechanical ventilation, and intensive care unit admission. Methods: The patients in this single-center retrospective analysis have COVID-19 and were hospitalized at the Firouzabadi hospital in Tehran between 2019 and 2020. coronary artery calcificationscore was estimated based on chest non-contrast CT scans on the day of admission. Based on the coronary artery calcification score, the patients were categorized into Very Low, Mild to Moderate, and Moderate to Severe. After a univariate analysis of the critical factors, odds ratio (OR) analysis and multivariate analysis of variables that could be linked to COVID-19 advancement were carried out. Results: a total of 719 patients were examined. Among them, 414 patients were men. Mortality with a 17.1 % prevalence was statistically significant between CAS score levels (P < 0.001). This factor has high OR with mild to moderate and moderate to severe CAS (OR: 2.14; 95% CI: 1.71 to 3.06, and OR: 2.31; 95% CI: 1.84 to 3.57). Oxygen saturation was a significant statistic between CAS score levels (P = 0.02). This factor has a high OR with mild to moderate and moderate to severe CAS (OR: 1.09; 95% CI: 0.71 to 3.60, and OR: 2.38; 95% CI: 0.89 to 2.9). There was no statistical difference between the groups' outcomes of mechanical ventilation and admission types. Conclusion: In this study, the coronary artery calcification scores of patients with COVID-19 were compared, while the outcomes of interest mortality, mechanical ventilation, and intensive care unitU admission were closely investigated. In light of these findings, coronary artery calcificationscoring can help in patient stratification, enabling earlier therapies for disorders to progress quickly. [ABSTRACT FROM AUTHOR]

A dynamic zero-COVID policy is not identical to a zero-COVID policy, which seeks to completely eliminate the virus. It throws light on a problem of statistics on pandemics in general with special insights into the COVID-19 pandemic. What have we learned in the 3 years of the COVID-19 pandemic? After 3 long years of the Corona virus disease 2019 (COVID-19) pandemic, several thoughts come to our minds: We have survived and even successfully managed the pandemic in our country. [Extracted from the article]

Background: The clinical manifestation of COVID-19 is associated with infection and inflammation of the lungs, but there is evidence to suggest that COVID-19 may also affect the structure and function of the cardiovascular system. At present, it is not fully understood to what extent COVID-19 impacts cardiovascular function in the short- and long-term following infection. The aim of the present study is twofold: (i) to define the effect of COVID-19 on cardiovascular function (i.e. arterial stiffness, cardiac systolic and diastolic function) in otherwise healthy individuals and (ii) to evaluate the effect of a home-based physical activity intervention on cardiovascular function in people with a history of COVID-19. Methods: This prospective, single-centre, observational study will recruit 120 COVID-19-vaccinated adult participants aged between 50 and 85 years, i.e. 80 with a history of COVID-19 and 40 healthy controls without a history of COVID-19. All participants will undergo baseline assessments including 12-lead electrocardiography, heart rate variability, arterial stiffness, rest and stress echocardiography with speckle tracking imaging, spirometry, maximal cardiopulmonary exercise testing, 7-day physical activity and sleep measures and quality of life questionnaires. Blood samples will be collected to assess the microRNA expression profiles, cardiac and inflammatory biomarkers, i.e. cardiac troponin T; N-terminal pro B-type natriuretic peptide; tumour necrosis factor alpha; interleukins 1, 6 and 10; C-reactive protein; d-dimer; and vascular endothelial growth factors. Following baseline assessments, COVID-19 participants will be randomised 1:1 into a 12-week home-based physical activity intervention aiming to increase their daily number of steps by 2000 from baseline. The primary outcome is change in left ventricular global longitudinal strain. Secondary outcomes are arterial stiffness, systolic and diastolic function of the heart, functional capacity, lung function, sleep measures, quality of life and well-being (depression, anxiety, stress and sleep efficiency). Discussion: The study will provide insights into the cardiovascular implications of COVID-19 and their malleability with a home-based physical activity intervention. Trial registration: ClinicalTrials.gov NCT05492552. Registered on 7 April 2022. [ABSTRACT FROM AUTHOR]

Introduction: Various diagnostic tools are used to assess the severity of COVID-19 symptoms and the risk of mortality, including laboratory tests and scoring indices such as the Modified Early Warning Score (MEWS). The diagnostic value of inflammatory markers for assessing patients with different severity of COVID-19 symptoms according to the MEWS was evaluated in this study. Materials and Methods: The concentrations of CRP (C-reactive protein) (immunoassay) and IL6 (interleukin 6) (electrochemiluminescence assay) were determined, and CRP/IL6, CRP/L, and LCR ratios were calculated in blood serum samples collected from 374 COVID-19 patients. Results: We demonstrated that CRP, IL6, CRP/IL6, CRP/L, LCR inflammatory markers increase significantly with disease progression assessed based on the MEWS in COVID-19 patients and may be used to differentiating patients with severe and non-severe COVID-19 and to assess the mortality. Conclusion: The diagnostic value of inflammatory markers for assessing the risk of mortality and differentiating between patients with mild and severe COVID-19 was confirmed. [ABSTRACT FROM AUTHOR]

COVID-19 is a major worldwide health concern that is linked to severe morbidity and mortality. In contrast to the majority of COVID-19 patients who experience moderate symptoms, about 5% of the patients experience serious manifestations such as acute respiratory distress syndrome, septic shock, and fatal organ failure. Although pneumonia is the main symptom of COVID-19, other organs, such as the kidneys, might also be affected by the condition. Acute kidney injury is one of the most frequent extrapulmonary symptoms of severe COVID-19. Indeed, it has been suggested that COVID-19 affects the kidney as the second most common organ after the lungs. This is due to the fact that the virus attaches to angiotensin-converting enzyme 2 (ACE2) receptors, which have significant expression in the kidney, before entering the host cells. It is important to follow up and monitor patients with COVID-19 for the occurrence of kidney damage, as timely treatment measures will lead to better clinical results and lower patient mortality. Even minor renal function impairment is a distinct risk factor for COVID-19 infection, hospitalization, and death. Furthermore, SARSCoV-2 infections can raise mortality for those with underlying renal disorders as well as make it more difficult to treat and care for them. It can also produce new kidney damage. Kidney tubular damage is the predominant symptom of SARS-CoV-2 infection's impact on the kidney, with proteinuria as the primary clinical symptom. The pathogenesis of kidney and damage in COVID-19 patients is varied and complicated. In COVID-19 patients, the virus has the ability to infect renal tubular epithelium and podocytes directly, which is linked to Bowman's capsule protein leakage, acute tubular necrosis, mitochondrial dysfunction, and collapsing glomerulopathy. Other causes of acute kidney injury (AKI) in COVID-19 patients, including cytokine storm, lymphopenia, and macrophage activation syndrome, have been caused by SARS-CoV2-induced immune response dysregulation. Interactions between organs, endothelial dysfunction, hypercoagulability, sepsis, and rhabdomyolysis are considered other major AKI mechanisms. In the present review, we focus on the role of each of these factors involved in AKI in COVID-19 patients. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 (COVID-19) infection was first discovered in December 2019 and was soon declared a worldwide pandemic. With the decrease in the severity of the deadly disease, there is a false sense of relief globally. However, there has been an increasing trend in the cases of cardiovascular and other complications of COVID-19 which has raised concern about the sequelae of this infection. The number of cases of sudden cardiac death and myocardial infection, post-COVID-19 has seen a major leap, especially in healthy people of both genders. Systemic comorbidities and immunocompromised states have a direct effect on the prognosis of patients. The SARS-CoV-2 infection not just affects the respiratory system but multi-organ involvement is seen due to this deadly virus. The heart is a vital organ that has acute-acute and long-term consequences, what is known as long-COVID, which lead to increased morbidity and mortality. There are increased cases of multiple cardiovascular problems such as blood clots, cardiovascular accidents, myocarditis, myocardial infarction, and heart failure in people after recovering from SARS-CoV-2 infection. The histopathological findings in the heart due to COVID-19 infection can be interstitial edema with the presence or absence of myocarditis, lymphocytic endotheliitis, microvascular microthrombi, thrombosis, interstitial fibrosis with no endothelins, or rarely myocarditis. While the tissue diagnosis during acute illness is less likely feasible, autopsy findings can be helpful to understand better pathophysiology of the disease and thus help in the better management of the patient. This review was performed to analyze the postmortem findings of the heart in patients infected with the SARS-COV-2 virus, to understand the effect of COVID-19 and its complications on the heart. The pathological changes in the cardiovascular system need to be explained and correlated with the clinical findings and prognosis of the patients. We also want to hypothesize that these findings, especially myocarditis lead to sudden death in the young, which gets undetected on routine investigations. [ABSTRACT FROM AUTHOR]

Background: COVID-19 affects the cardiovascular system and ECG abnormalities may be associated with worse prognosis. We evaluated the prognostic value of ECG abnormalities in individuals with COVID-19.Methods: Multicentre cohort study with adults hospitalised with COVID-19 from 40 hospitals across 23 countries. Patients were followed-up from admission until 30 days. ECG were obtained at each participating site and coded according to the Minnesota coding criteria. The primary outcome was defined as death from any cause. Secondary outcomes were admission to the intensive care unit (ICU) and major adverse cardiovascular events (MACE). Multiple logistic regression was used to evaluate the association of ECG abnormalities with the outcomes.Results: Among 5313 participants, 2451 had at least one ECG and were included in this analysis. The mean age (SD) was 58.0 (16.1) years, 60.7% were male and 61.1% from lower-income to middle-income countries. The prevalence of major ECG abnormalities was 21.3% (n=521), 447 (18.2%) patients died, 196 (8.0%) had MACE and 1115 (45.5%) were admitted to an ICU. After adjustment, the presence of any major ECG abnormality was associated with a higher risk of death (OR 1.39; 95% CI 1.09 to 1.78) and cardiovascular events (OR 1.81; 95% CI 1.30 to 2.51). Sinus tachycardia (>120 bpm) with an increased risk of death (OR 3.86; 95% CI 1.97 to 7.48), MACE (OR 2.68; 95% CI 1.10 to 5.85) and ICU admission OR 1.99; 95% CI 1.03 to 4.00). Atrial fibrillation, bundle branch block, ischaemic abnormalities and prolonged QT interval did not relate to the outcomes.Conclusion: Major ECG abnormalities and a heart rate >120 bpm were prognostic markers in adults hospitalised with COVID-19. [ABSTRACT FROM AUTHOR]

The main drivers of COVID-19 disease severity and the impact of COVID-19 on long-term health after recovery are yet to be fully understood. Medical imaging studies investigating COVID-19 to date have mostly been limited to small datasets and post-hoc analyses of severe cases. The UK Biobank recruited recovered SARS-CoV-2 positive individuals (n = 967) and matched controls (n = 913) who were extensively imaged prior to the pandemic and underwent follow-up scanning. In this study, we investigated longitudinal changes in body composition, as well as the associations of pre-pandemic image-derived phenotypes with COVID-19 severity. Our longitudinal analysis, in a population of mostly mild cases, associated a decrease in lung volume with SARS-CoV-2 positivity. We also observed that increased visceral adipose tissue and liver fat, and reduced muscle volume, prior to COVID-19, were associated with COVID-19 disease severity. Finally, we trained a machine classifier with demographic, anthropometric and imaging traits, and showed that visceral fat, liver fat and muscle volume have prognostic value for COVID-19 disease severity beyond the standard demographic and anthropometric measurements. This combination of image-derived phenotypes from abdominal MRI scans and ensemble learning to predict risk may have future clinical utility in identifying populations at-risk for a severe COVID-19 outcome. [ABSTRACT FROM AUTHOR]

Purpose: New lethal coronavirus disease 2019 (COVID-19), currently, has been converted to a disastrous pandemic worldwide. As there has been found no definitive treatment for the infection in this review we focused on molecular aspects of coenzyme Q10 (CoQ10) and possible therapeutic potencies of CoQ10 against COVID-19 and similar infections. Methods: This is a narrative review in which we used some authentic resources including PubMed, ISI, Scopus, Science Direct, Cochrane, and some preprint databases, the molecular aspects of CoQ10 effects, regarding to the COVID-19 pathogenesis, have been analyzed and discussed. Results: CoQ10 is an essential cofactor in the electron transport chain of the phosphorylative oxidation system. It is a powerful lipophilic antioxidant, anti-apoptotic, immunomodulatory and anti-inflammatory supplement which has been tested for the management and prevention of a variety of diseases particularly diseases with inflammatory pathogenesis. CoQ10 is a strong anti-inflammatory agent which can reduce tumor necrosis factor-α (TNF-α), interleukin (IL)- 6, C-reactive protein (CRP), and other inflammatory cytokines. The cardio-protective role of CoQ10 in improving viral myocarditis and drug induced cardiotoxicity has been determined in different studies. CoQ10 could also improve the interference in the RAS system caused by COVID-19 through exerting anti-Angiotensin II effects and decreasing oxidative stress. CoQ10 passes easily through blood–brain barrier (BBB). As a neuroprotective agent CoQ10 can reduce oxidative stress and modulate the immunologic reactions. These properties may help to reduce CNS inflammation and prevent BBB damage and neuronal apoptosis in COVID-19 patients. Conclusion: CoQ10 supplementation may prevent the COVID-19-induced morbidities with a potential protective role against the deleterious consequences of the disease, further clinical evaluations are encouraged. [ABSTRACT FROM AUTHOR]

Background: The coronavirus disease 2019 (COVID‐19) poses special challenges for societies, as the disease causes millions of deaths. Although the direct prevention measures affect the prevalence and mortality the most, the other indirect factors, including natural environments and economics, could not be neglected. Evaluating the effect of natural land cover on COVID-19 health outcomes is an urgent and crucial public health topic. Methods: Here, we examine the relationships between natural land cover and the prevalence and mortality of COVID-19 in the United States. To probe the effects of long-term living with natural land cover, we extract county-level land cover data from 2001 to 2019. Based on statistically spatial tests, we employ the Spatial Simultaneous Autoregressive (SAC) Model to estimate natural land cover’s impact and monetary values on COVID-19 health outcomes. To examine the short-term effects of natural environments, we build a seasonal panel data set about the greenery index and COVID-19 health outcomes. The panel SAC model is used to detect the relationship between the greenery index and seasonal COVID-19 health outcomes. Results: A 1% increase in open water or deciduous forest is associated with a 0.004-death and 0.163-conformed-case, or 0.006-death and 0.099-confirmed-case decrease in every 1,000 people. Converting them into monetary value, for the mortality, a 1% increase in open water, deciduous forest, or evergreen forest in a county is equivalent to a 212-, 313-, or 219-USD increase in household income in the long term. Moreover, for the prevalence, a 1% change in open water, deciduous forest, or mixed forest is worth a 382-, 230-, or 650-USD increase in household income. Furthermore, a rational development intensity is also critical to reduce the risk of the COVID-19 pandemic. More greenery in the short term is also linked to lower prevalence and mortality. Conclusions: Our study underscores the importance of incorporating natural land cover as a means of mitigating the risks and negative consequences of future pandemics like COVID-19 and promoting overall public health. [ABSTRACT FROM AUTHOR]

Cytokine release syndrome (CRS) due to severe acute respiratory coronavirus-2 (SARS-CoV-2) infection leads to life-threatening pneumonia which has been associated with coronavirus disease (COVID-19) pathologies. Centuries-old Asian traditional medicines such as Withania somnifera (L.) Dunal (WS) and Tinospora cordifolia (Willd.) Miers (TC) possess potent immunomodulatory effects and were used by the AYUSH ministry, in India during the COVID-19 pandemic. In the present study, we investigated WS and TC's anti-viral and immunomodulatory efficacy at the human equivalent doses using suitable in vitro and in vivo models. While both WS and TC showed immuno-modulatory potential, WS showed robust protection against loss in body weight, viral load, and pulmonary pathology in the hamster model of SARS-CoV2. In vitro pretreatment of mice and human neutrophils with WS and TC had no adverse effect on PMA, calcium ionophore, and TRLM-induced ROS generation, phagocytosis, bactericidal activity, and NETs formation. Interestingly, WS significantly suppressed the pro-inflammatory cytokines-induced Th1, Th2, and Th17 differentiation. We also used hACE2 transgenic mice to further investigate the efficacy of WS against acute SARS-CoV2 infection. Prophylactic treatment of WS in the hACE2 mice model showed significant protection against body weight loss, inflammation, and the lung viral load. The results obtained indicate that WS promoted the immunosuppressive environment in the hamster and hACE2 transgenic mice models and limited the worsening of the disease by reducing inflammation, suggesting that WS might be useful against other acute viral infections. The present study thus provides pre-clinical efficacy data to demonstrate a robust protective effect of WS against COVID-19 through its broader immunomodulatory activity [ABSTRACT FROM AUTHOR]

The rapid spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in recent years not only caused a global pandemic but resulted in enormous social, economic, and health burdens worldwide. Despite considerable efforts to combat coronavirus disease 2019 (COVID-19), various SARS-CoV-2 variants have emerged, and their underlying mechanisms of pathogenicity remain largely unknown. Furthermore, effective therapeutic drugs are still under development. Thus, an ideal animal model is crucial for studying the pathogenesis of COVID-19 and for the preclinical evaluation of vaccines and antivirals against SARS-CoV-2 and variant infections. Currently, several animal models, including mice, hamsters, ferrets, and non-human primates (NHPs), have been established to study COVID-19. Among them, ferrets are naturally susceptible to SARS-CoV-2 infection and are considered suitable for COVID-19 study. Here, we summarize recent developments and application of SARS-CoV-2 ferret models in studies on pathogenesis, therapeutic agents, and vaccines, and provide a perspective on the role of these models in preventing COVID-19 spread. [ABSTRACT FROM AUTHOR]

Refuse storage and collection systems are potential sources of food and harbourage areas for rodents which transmit pathogens. We examined the factors associated with rodent activity in public housing municipal waste collection premises in a highly urbanized city-state. We analysed data from April 2019 to March 2020 in mixed-effects logistic regression models to examine the independent factors associated with rodent activity in central refuse chute rooms (CRCs), individual refuse chute (IRC) bin chambers and bin centres. We accounted for within-year patterns, repeated measures and nested effects. We observed a heterogeneous spatial distribution of rodent activity. Rodent droppings were strongly associated with rodent activity in CRCs (aOR: 6.20, 95% CI: 4.20–9.15), bin centres (aOR: 3.61, 95% CI: 1.70–7.64) and IRC bin chambers (aOR: 90.84, 95% CI: 70.13–117.67). Gnaw marks were positively associated with rodent activity in CRCs (aOR: 5.61, 95% CI: 3.55–8.97) and IRC bin chambers (aOR: 2.05, 95% CI: 1.43–2.95), as were rub marks in CRCs (aOR: 5.04, 95% CI: 3.44–7.37) and IRC bin chambers (aOR: 3.07, 95% CI: 1.74–5.42). Each burrow increased the odds of rodent sightings in bin centres (aOR: 1.03, 95% CI: 1.00–1.06). The odds of rodent sightings in an IRC bin chamber increased with every additional bin chute chamber within the same block (aOR: 1.04, 95% CI: 1.01–1.07). We identified several factors that well predicted rodent activity in waste collection premises. Municipal estate managers with limited resources can adopt a risk-based approach in tailoring the focus of their rodent control interventions. [ABSTRACT FROM AUTHOR]

The high magnitude zoonotic event has caused by Severe Acute Respitarory Syndrome CoronaVirus-2 (SARS-CoV-2) is Coronavirus Disease-2019 (COVID-19) epidemics. This disease has high rate of spreading than mortality in humans. The human receptor, Angiotensin-Converting Enzyme 2 (ACE2), is the leading target site for viral Spike-protein (S-protein) that function as binding ligands and are responsible for their entry in humans. The patients infected with COVID-19 with comorbidities, particularly cancer patients, have a severe effect or high mortality rate because of the suppressed immune system. Nevertheless, there might be a chance wherein cancer patients cannot be infected with SARS-CoV-2 because of mutations in the ACE2, which may be resistant to the spillover between species. This study aimed to determine the mutations in the sequence of the human ACE2 protein and its dissociation with SARS-CoV-2 that might be rejecting viral transmission. The in silico approaches were performed to identify the impact of SARS-CoV-2 S-protein with ACE2 mutations, validated experimentally, occurred in the patient, and reported in cell lines. The identified changes significantly affect SARS-CoV-2 S-protein interaction with ACE2, demonstrating the reduction in the binding affinity compared to SARS-CoV. The data presented in this study suggest ACE2 mutants have a higher and lower affinity with SARS-Cov-2 S-protein to the wild-type human ACE2 receptor. This study would likely be used to report SARS-CoV-2 resistant ACE2 mutations and can be used to design active peptide development to inactivate the viral spread of SARS-CoV-2 in humans. [ABSTRACT FROM AUTHOR]

The cardiovascular system is frequently affected by coronavirus disease-19 (COVID-19), particularly in hospitalized cases, and these manifestations are associated with a worse prognosis. Most commonly, heart involvement is represented by myocarditis, myocardial infarction, and pulmonary embolism, while arrhythmias, heart valve damage, and pericarditis are less frequent. While the clinical suspicion is necessary for a prompt disease recognition, imaging allows the early detection of cardiovascular complications in patients with COVID-19. The combination of cardiothoracic approaches has been proposed for advanced imaging techniques, i.e., CT scan and MRI, for a simultaneous evaluation of cardiovascular structures, pulmonary arteries, and lung parenchyma. Several mechanisms have been proposed to explain the cardiovascular injury, and among these, it is established that the host immune system is responsible for the aberrant response characterizing severe COVID-19 and inducing organ-specific injury. We illustrate novel evidence to support the hypothesis that molecular mimicry may be the immunological mechanism for myocarditis in COVID-19. The present article provides a comprehensive review of the available evidence of the immune mechanisms of the COVID-19 cardiovascular injury and the imaging tools to be used in the diagnostic workup. As some of these techniques cannot be implemented for general screening of all cases, we critically discuss the need to maximize the sustainability and the specificity of the proposed tests while illustrating the findings of some paradigmatic cases. [ABSTRACT FROM AUTHOR]

Heparanase (HPSE) is an endoglycosidase cleaves heparan sulfate (HS) and this contributes to the degradation and remodeling of the extracellular matrix. HS cleaved by HPSE induces activation of autophagy and formation of autophagosommes which facilitate binding of HPSE to the HS and subsequent release of growth factors. The interaction between HPSE and HS triggers releases of chemokines and cytokines which affect inflammatory response and cell signaling pathways with development of hyperinflammation, cytokine storm (CS) and coagulopathy. HPSE expression is induced by both SARS-CoV-2 and monkeypox virus (MPXV) leading to induction release of pro-inflammatory cytokines, endothelial dysfunction and thrombotic events. Co-infection of MPX with SARS-CoV-2 may occur as we facing many outbreaks of MPX cases during Covid-19 pandemic. Therefore, targeting of HPSE by specific inhibitors may reduce the risk of complications in both SARS-CoV-2 and MPXV infections. Taken together, HPSE could be a potential link between MPX with SARS-CoV-2 in Covid-19 era. [ABSTRACT FROM AUTHOR]

Background: The success of early dexamethasone therapy for hospitalised COVID-19 cases in treatment of Sars-CoV-2 infection may predominantly reflect its anti-inflammatory action against a hyperinflammation (HI) response. It is likely that there is substantial heterogeneity in HI responses in COVID-19. Methods: Blood CRP, ferritin, neutrophil, lymphocyte and platelet counts were scored to assess HI (HI5) and combined with a validated measure of generalised medical deterioration (NEWS2) before day 2. Our primary outcome was 28 day mortality from early treatment with dexamethasone stratified by HI5-NEWS2 status. Findings: Of 1265 patients, high risk of HI (high HI5-NEWS2) (n = 367, 29.0%) conferred a strikingly increased mortality (36.0% vs 7.8%; Age adjusted hazard ratio (aHR) 5.9; 95% CI 3.6–9.8, p<0.001) compared to the low risk group (n = 455, 36.0%). An intermediate risk group (n = 443, 35.0%) also showed significantly higher mortality than the low risk group (17.6% vs 7.8%), aHR 2.2, p = 0.005). Early dexamethasone treatment conferred a 50.0% reduction in mortality in the high risk group (36.0% to 18.0%, aHR 0.56, p = 0.007). The intermediate risk group showed a trend to reduction in mortality (17.8% to 10.3%, aHR 0.82, p = 0.46) which was not observed in the low risk group (7.8% to 9.2%, aHR 1.4, p = 0.31). Interpretation: Higher HI5-NEWS2 scores measured at COVID-19 diagnosis, strongly associate with increased mortality at 28 days. Significant reduction in mortality with early dexamethasone treatment was only observed in the high risk group. Therefore, the HI5-NEWS2 score could be utilised to stratify randomised clinical trials to test whether intensified anti-inflammatory therapy would further benefit high risk patients and whether alternative approaches would benefit low risk groups. Considering its recognised morbidity, we suggest that early dexamethasone should not be routinely prescribed for HI5-NEWS2 low risk individuals with COVID-19 and clinicians should cautiously assess the risk benefit of this intervention in all cases. [ABSTRACT FROM AUTHOR]

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Background: At the end of December 2019, a new infectious disease was reported in Wuhan, China. It was a new type of coronavirus named COVID-19. The spread of COVID-19 created an emergency in the global health system and the elderly was identified as a vulnerable group to the disease. Materials and Methods: This is a systematic review conducted to manage the vulnerability of the elderly during the COVID-19 pandemic. Accordingly, all articles published in this field from the beginning of March 2019 to the end of June 2021 have been extracted from the following databases: Web of Science, PubMed, Scopus, Cochrane Library, Google Scholar, Irandoc, Magiran, MedLib, and SID. Results: High incidences of COVID-19 are exacerbated in the elderly with cognitive disorders, immunodeficiency, malnutrition, use of various medicines and social problems, anxiety, distance from the family, lack of healthcare, history of falls, multidrug use due to old age during the COVID-19 pandemic, in addition to the elderly with underlying diseases, such as kidney failure, diabetes, high blood pressure, arthritis, heart, and respiratory diseases. Conclusion: The prevalence of vulnerability in the elderly was high during the COVID-19 pandemic, which can be a significant risk factor for health. Suffering from several simultaneous diseases, the number of medicines used, the history of falls, underlying diseases, and living alone were some of the vital determinants of vulnerability and considering the adverse consequences of vulnerability, difficulty in designing and implementing appropriate interventions and self-care education for the elderly and their families to manage drug use, treating chronic diseases, and preventing falls, it seems necessary to observe health protocols and stay at home. [ABSTRACT FROM AUTHOR]

Introduction: COVID-19 has spread globally in waves, and Danish treatment guidelines have been updated following the first wave. We sought to investigate whether the prognostic values of echocardiographic parameters changed with updates in treatment guidelines and the emergence of novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants, 20E (EU1) and alpha (B.1.1.7), and further to compare cardiac parameters between patients from the first and second wave. Methods: A total of 305 patients hospitalized with COVID-19 were prospectively included, 215 and 90 during the first and second wave, respectively. Treatment in the study was defined as treatment with remdesivir, dexamethasone, or both. Patients were assumed to be infected with the dominant SARS-CoV-2 variant at the time of their hospitalization. Results: Mean age for the first versus second wave was 68.7 ± 13.6 versus 69.7 ± 15.8 years, and 55% versus 62% were males. Left ventricular (LV) systolic and diastolic function was worse in patients hospitalized during the second wave (LV ejection fraction [LVEF] for first vs. second wave = 58.5 ± 8.1% vs. 52.4 ± 10.6%, p < 0.001; and global longitudinal strain [GLS] = 16.4 ± 4.3% vs. 14.2 ± 4.3%, p < 0.001). In univariable Cox regressions, reduced LVEF (hazard ratio [HR] = 1.07 per 1% decrease, p = 0.002), GLS (HR = 1.21 per 1% decrease, p < 0.001), and tricuspid annular plane systolic excursion (HR = 1.18 per 1 mm decrease, p < 0.001) were associated with COVID-related mortality, but only GLS remained significant in fully adjusted analysis (HR = 1.14, p = 0.02). Conclusion: Reduced GLS was associated with COVID-related mortality independently of wave, treatment, and the SARS-CoV-2 variant. LV function was significantly impaired in patients hospitalized during the second wave. [ABSTRACT FROM AUTHOR]

Keywords: acute coronary syndrome (ACS); coronary artery disease (CAD); COVID-19; myocardial ischemia; percutaneous coronary intervention (PCI); SARS-CoV-2 EN acute coronary syndrome (ACS) coronary artery disease (CAD) COVID-19 myocardial ischemia percutaneous coronary intervention (PCI) SARS-CoV-2 1 4 4 01/17/23 20230101 NES 230101 The coronavirus disease 2019 (COVID-19) pandemic was an event of exceptional, unforeseen, and unexpected nature that has caught unprepared the world's public decision-makers, healthcare professionals, the pharmaceutical industry, and patients. A meta-analysis of data on 1,527 patients with COVID-19 revealed that at least 8% of patients had an acute myocardial injury, the risk of which was 13-fold higher in patients with a more severe clinical presentation [[1]]. Patients presenting with ST-elevation myocardial infarction (STEMI) and concomitant COVID-19 infection showed a higher thrombus burden and worse prognosis [[2]]. [Extracted from the article]

Background Indigenous individuals have higher rates of mortality and poverty in Mexico and more than half are marginalised, and COVID-19 pandemic aggravated the existing burden of health disparities. We aimed to analyse the effects of being indigenous and marginalised on coronavirus (COVID-19) infection fatality in Mexico. Methods We identified 3424690 non-pregnant, COVID-19 positive adults ≥19 years in the Mexico national COVID-19 database with known date of symptom. We used demographic information, indigenous status, marginalisation status, and co-morbidities in binary logistic regression to predict mortality, adjusting for covariates, including hospitalisation, admission to the intensive care unit (ICU), and mechanical ventilation use. We also assessed the interaction between indigenous status and marginalisation. Results Marginalisation was much higher among indigenous (53.7%) compared to non-indigenous individuals (4.8%). COVID-19 fatalities were approximately 20 years older (64.4 and 63.0 years) than survivors (44.7 and 41.2 years) among indigenous vs non-indigenous individuals, respectively. The unadjusted risk of COVID-19 fatality among indigenous individuals was nearly two-fold (odds ratio (OR)=1.92)) compared to non-indigenous individuals (OR=1.05). COVID-19 fatality was higher among highly marginalised individuals (upper quartile) (OR=1.51; 95% confidence interval (CI)=1.49-1.54). Marginalised indigenous individuals had a significantly lower likelihood of ICU admission compared to non-indigenous non-marginalised individuals. The likelihood of mechanical ventilation for indigenous individuals was 4% higher compared to non-indigenous individuals. Indigenous marginalised individuals had a significantly lower probability of mechanical ventilation compared to non-indigenous non-marginalised individuals. COVID-19 comorbidity risks of fatality significantly differed between the two groups in the Cox survival analysis. In the fully adjusted model, indigenous individuals were 4% more likely to die from COVID-19 compared to non-indigenous. Conclusions Indigenous, marginalised individuals with COVID-19 had higher risk of hospitalisation and ICU admission than non-indigenous patients. Marginalised, indigenous individuals were less likely to receive mechanical ventilation compared to non-indigenous, but had a higher risk of COVID-19. Indigenous individuals had a 4% higher COVID-19 mortality risk COVID-19 compared to non-indigenous individuals. Improved community medical care and augmented health services in rural hospitals could mitigate barriers to health care access in indigenous, marginalised populations. [ABSTRACT FROM AUTHOR]

Copyright of Revista Enfermagem Contemporânea is the property of Revista Enfermagem Contemporanea and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: COVID-19 has rapidly become a global health emergency. This infection can cause damage to various organs. Injury to myocardial cells is one of the salient manifestations of COVID-19. The clinical course and outcome of acute coronary syndrome (ACS) are influenced by various factors, including comorbidities and concomitant diseases. One of these acute concomitant diseases is COVID-19, which can affect the clinical course and outcome of acute myocardial infarction (MI). Methods: The present cross-sectional study compared the clinical course and outcome of MI and some of its practical factors between patients with and without COVID-19. The study population consisted of 180 patients (129 males and 51 females) diagnosed with acute MI. Eighty patients had COVID-19 infection concurrently. Results: The mean age of the patients was 65.62 years. The frequencies of non--ST-elevation MI (vs ST-elevation MI), lower ejection fractions (<30), and arrhythmias were significantly higher in the COVID-19 group than in the non--COVID-19 group (P=0.006, 0.003, and P<0.001, respectively). The single-vessel disease was the most frequent angiographic result in the COVID-19 group, while the double-vessel disease was the most frequent angiographic result in the non--COVID-19 group (P<0.001). Conclusion: It appears that patients with ACS who are co-infected with COVID-19 infection need essential care. [ABSTRACT FROM AUTHOR]

Purpose: This study, on this basis of Turkey, determined physiological factors affecting individuals' being infected by the COVID-19 virus. Material and Methods: For this purpose, on 1104 individuals above the age of 18; necessary data are collected and assessed. Results: The women went through COVID-19 more severely when compared with men. It is also seen that smokers were less infected by COVID-19. It is seen that sunbathing, exercises, sleeping and using minerals did not have positive effects against the disease; usage of plant-based agents did not have positive effects on individuals' resistance against COVID-19 on severeness of the disease and results obtained after usage of medicines; surprisingly, individuals, who used probiotics/prebiotics were in a disadvantageous position against COVID-19. It is seen that individuals had significant changes in their feeding habits. Participants mostly preferred organic animalbased products. It is also seen that there were significant changes in individuals' habits on consumption. It is determined that there was a decrease in the amount of shopping from supermarkets, while at the same time, there was an increase in the amount of shopping from online platforms. Conclusion: The COVID 19 pandemic disrupted many known memories for other pandemics and led to unique new situations. [ABSTRACT FROM AUTHOR]

BACKGROUND: In this retrospective study, we investigated the outcomes and demographic characteristics of COVID-19 patients with and without a history of CVD. METHODS: This large retrospective, multicenter study was performed on inpatients with suspected COVID-19 pneumonia who were admitted across four hospitals in Babol, Northern Iran. Demographic data, clinical data, and cycle threshold value (Ct) results of Real Time PCR were obtained. Then, participants were divided into two groups: (1) cases with CVDs, (2) cases without CVDs. RESULTS: A total of 11097 suspected COVID-19 cases with a mean ± SD age of 53 ±25.3 (range: 0 to 99) years were involved in the present study. Out of whom 4599 (41.4%) had a positive RT-PCR result. Of those, 1558 (33.9%) had underlying CVD. Patients with CVD had significantly more co-morbidities such as hypertension, kidney disease, and diabetes. Moreover, 187 (12%) and 281 (9.2%) of patients with and without CVD died, respectively. Also, mortality rate was significantly high among the three groups of Ct value in patients with CVD, with the highest mortality in those with Ct between 10 and 20 (Group A = 19.9%). CONCLUSION: In summary, our results highlight that CVD is a major risk factor for hospitalization and the severe consequences of COVID-19. Death in CVD group is significantly higher compared to non-CVD. In addition, the results show that age-related diseases can be a serious risk factor for the severe consequences of COVID-19. [ABSTRACT FROM AUTHOR]

Muntner I et al. i in a large cohort study evaluated indirectly, the RAS Inhibitor medication controversy, whether it led to a significant number of patients discontinuing RAS inhibitor treatment.[22] The findings are important to inform responses to future public health emergencies. Despite the controversy at the beginning of the COVID-19 pandemic, overwhelming scientific evidence has shown RAS inhibitors to be safe and beneficial in COVID-19. [Extracted from the article]

Introduction: Diabetes mellitus (DM) and hyperglycemia are important risk factors for poor outcomes in hospitalized patients with coronavirus disease 2019 (COVID-19). The aim of the present study was to analyze the factors associated with the composite outcome of the necessity of invasive mechanical ventilation (IMV) or admission to the intensive care unit (ICU) in subjects with severe COVID-19 infection treated with dexamethasone comparing patients with DM vs. patients without DM. Research design and methods: An observational retrospective cohort study was performed, including hospitalized subjects with a diagnosis of SARS-CoV-2 pneumonia. Inclusion criteria were: age ≥18 years old with severe COVID-19 disease requiring daily intravenous 6mg dexamethasone treatment for 10 days. Exclusion criteria were: <18 years old, non-severe illness and/or patients in charge of ICU. Variables related to clinical and analytical parameters, glycemic control, acquired-hospital superinfections, mortality, IMV requirement, ICU admission and length of stay were included. Results: Two hundred and nine individuals with COVID-19 disease treated with dexamethasone were included. One hundred twenty-five out of these subjects (59.8%) were patients with DM. Overall, from the 209 subjects, 66 (31.6%) required IMV or were admitted to the ICU, with significant differences between patients with DM (n=50) vs. patients without DM (n=16) (76% vs. 24%, p=0.002). Among the group of subjects with DM (n=125), those who required IMV or were admitted to the ICU showed higher serum concentrations of C-reactive protein, interleukin-6, D-dimer, ferritin and pro-calcitonin and significantly lower serum concentrations of albumin compared to those who did not require IMV or were not admitted to the ICU. Besides, between these two groups of patients with DM, we observed no differences in glycemic parameters, including median capillary blood glucose values, glycosylated hemoglobin, coefficient of variability and hypoglycemic episodes. In the multinomial analysis, factors independently associated with the composite outcome of IMV or admission to the ICU in the insulin-treated group were the National Early Warning Score (NEWS) 2 score (OR 1.55 [1.17-2.17], p=0.005) and the presence of hospital-acquired superinfections (OR 35.21 [5.11-386.99], p=0.001). Conclusions: In our study, parameters related to glycemic control were not associated with IMV requirement nor admission to the ICU in patients with DM and severe COVID-19 disease receiving daily 6 mg of dexamethasone for 10 days. However, hospital-acquired superinfections and disease severity at admission were independent factors associated with this composite outcome. [ABSTRACT FROM AUTHOR]

SARS-CoV-2 is the causative agent of COVID-19 that has infected over 642 million and killed over 6.6 million people around the globe. Underlying a wide range of clinical manifestations of this disease, from moderate to extremely severe systemic conditions, could be genes or pathways differentially expressing in the hosts. It is therefore important to gain insights into pathways involved in COVID-19 pathogenesis and host defense and thus understand the host response to this pathogen at the physiological and molecular level. To uncover genes and pathways involved in the differential clinical manifestations of this disease, we developed a novel gene co-expression network based pipeline that uses gene expression obtained from different SARS-CoV-2 infected human tissues. We leveraged the network to identify novel genes or pathways that likely differentially express and could be physiologically significant in the COVID-19 pathogenesis and progression but were deemed statistically non-significant and therefore not further investigated in the original studies. Our network-based approach aided in the identification of co-expression modules enriched in differentially expressing genes (DEGs) during different stages of COVID-19 and enabled discovery of novel genes involved in the COVID-19 pathogenesis, by virtue of their transcript abundance and association with genes expressing differentially in modules enriched in DEGs. We further prioritized by considering only those enriched gene modules that have most of their genes differentially expressed, inferred by the original studies or this study, and document here 7 novel genes potentially involved in moderate, 2 in severe, 48 in extremely severe COVID-19, and 96 novel genes involved in the progression of COVID-19 from severe to extremely severe conditions. Our study shines a new light on genes and their networks (modules) that drive the progression of COVID-19 from moderate to extremely severe condition. These findings could aid development of new therapeutics to combat COVID-19. [ABSTRACT FROM AUTHOR]

Introduction: To analyze the current state, hotspots, and cutting-edge trends of genomics research on the outbreak of Corona Virus Disease 2019 (COVID-19) from 2019 to the present (March 2022). Methods: Statistical and visual analysis of COVID-19 genomics results published in the 2019-2022 Web of Science Core Collection Database (WOSCC) was performed using CiteSpace software, including data on countries, institutions, authors, journals, co-citations, keywords, etc. Results: A total of 9133 English literature were included. The number of publications has significantly increased in 2021, and it is expected that this upward trend will last into the future. The research hotspots of COVID-19 revolve around quarantine, biological management, angiotensin-converting enzyme-2, RNA-dependent RNA polymerase, etc. Research frontiers and trends focus on molecular docking, messenger RNA, functional receptor, etc. Conclusion: The last two years have seen a significant increase in research interest in the field of novel coronavirus pneumonia genomics. [ABSTRACT FROM AUTHOR]

The frequency of pericarditis as a complication in COVID‐19 patients without underlying disease is not well known. We report a case of COVID‐19 presenting with pericarditis without myocarditis or severe respiratory symptoms in a middle‐aged woman, who had neither underlying disease nor previous diagnosis of COVID‐19. [ABSTRACT FROM AUTHOR]

Lactate dehydrogenase (LDH) is a terminating enzyme in the metabolic pathway of anaerobic glycolysis with end product of lactate from glucose. The lactate formation is crucial in the metabolism of glucose when oxygen is in inadequate supply. Lactate can also be formed and utilised by different cell types under fully aerobic conditions. Blood LDH is the marker enzyme, which predicts mortality in many conditions such as ARDS, serious COVID-19 and cancer patients. Lactate plays a critical role in normal physiology of humans including an energy source, a signaling molecule and a pH regulator. Depending on the pH, lactate exists as the protonated acidic form (lactic acid) at low pH or as sodium salt (sodium lactate) at basic pH. Lactate can affect the immune system and act as a signaling molecule, which can provide a "danger" signal for life. Several reports provide evidence that the serum lactate represents a chemical marker of severity of disease similar to LDH under inflammatory conditions. Since the mortality rate is much higher among COVID-19 patients, associated with high serum LDH, this article is aimed to review the LDH as a therapeutic target and lactate as potential marker for monitoring treatment response of inflammatory diseases. Finally, the review summarises various LDH inhibitors, which offer potential applications as therapeutic agents for inflammatory diseases, associated with high blood LDH. Both blood LDH and blood lactate are suggested as risk factors for the mortality of patients in serious inflammatory diseases. [ABSTRACT FROM AUTHOR]

Although SARS-CoV-2, the causative virus of the global COVID-19 pandemic, primarily affects the respiratory tract, it is now recognized to have broad multi-organ tropism and systemic effects. Early reports indicated that SARS-CoV-2 infection could lead to cardiac damage, suggesting the virus may directly impact the heart. Cardiac cell types derived from human pluripotent stem cells (hPSCs) enable mechanistic interrogation of SARS-CoV-2 infection in human cardiac tissue. Purpose of Review: To review the studies published since the emergence of the COVID-19 pandemic which utilize hPSCs and their cardiovascular derivative cell types to interrogate the tropism and effects of SARS-CoV-2 infection in the heart, as well as explore potential therapies. Recent Findings: Recent studies reveal that SARS-CoV-2 is capable of infecting and replicating within hPSC-derived cardiomyocytes and sinoatrial nodal cells, but not as extensively in their non-parenchymal counterparts. Additionally, they show striking viral effects on cardiomyocyte structure, transcriptional activity, and survival, along with potential mechanisms and therapeutic targets. Summary: Cardiac models derived from hPSCs are a viable platform to study the impact of SARS-CoV-2 on cardiac tissue and may lead to novel mechanistic insight as well as therapeutic interventions. [ABSTRACT FROM AUTHOR]

Background: The coronavirus disease 2019 (COVID-19) severely hindered the timely receipt of health care for patients with cancer, especially female patients. Depression and anxiety were more pronounced in female patients than their male counterparts with cancer during treatment wait-time intervals. Herein, investigating the impact of treatment delays on the survival outcomes of female patients with early-stage cancers can enhance the rational and precise clinical decisions of physicians.Methods: We analyzed five types of cancers in women from the Surveillance, Epidemiology, and End Results (SEER) program between Jan 2010 and Dec 2015. Univariate and multivariate Cox regression analyses were used to determine the impacts of treatment delays on the overall survival (OS) and cancer-specific survival (CSS) of the patients.Results: A total of 241,661 females with early-stage cancer were analyzed (12,617 cases of non-small cell lung cancer (NSCLC), 166,051 cases of infiltrating breast cancer, 31,096 cases of differentiated thyroid cancer, 23,550 cases of colorectal cancer, and 8347 cases of cervical cancer). Worse OS rates were observed in patients with treatment delays ≥ 3 months in stage I NSCLC (adjustedHazard ratio (HR) = 1.11, 95% Confidence Interval (CI): 1.01-1.23, p = 0.044) and stage I infiltrating breast cancer (adjustedHR = 1.23, 95% CI 1.11-1.37, p < 0.001). When the treatment delay intervals were analyzed as continuous variables, similar results were observed in patients with stage I NSCLC (adjustedHR = 1.04, 95% CI 1.01-1.06, p = 0.010) and in those with stage I breast cancer (adjustedHR = 1.03, 95% CI 1.00-1.06, p = 0.029). However, treatment delays did not reduce the OS of patients with differentiated thyroid cancer, cervical cancer, or colorectal cancer in the early-stage. Only intermediate treatment delays impaired the CSS of patients with cervical cancer in stage I (adjustedHR = 1.31, 95% CI 1.02-1.68, p = 0.032).Conclusion: After adjusting for confounders, the prolonged time from diagnosis to the initiation of treatment (< 6 months) showed limited negative effects on the survival of most of the patients with early-stage female cancers. Whether our findings serve as evidence supporting the treatment deferral decisions of clinicians for patients with different cancers in resource-limited situations needs further validation. [ABSTRACT FROM AUTHOR]

Background There is evidence for a bi-directional relationship between COVID-19 and the cardiovascular (CV) system. Source of data Published literature. Areas of agreement Pre-existing heart failure (HF) increases the risk of mortality with COVID-19. CV complications are recognized, including increased rates of acute coronary syndromes, HF, arrhythmia and myocarditis. Drugs targeting the angiotensin system are safe and may provide prognostic benefit. Areas of controversy Vaccination as a cause of myocarditis remains a key area of contention. Growing points As the pandemic progresses, we are gaining more data about the long-term effects of COVID-19 on the CV system: long COVID, and medium-to-long-term increases in CV risk. Areas timely for developing research Large-scale longitudinal studies will shed light on long-term CV outcomes with COVID-19. Furthermore, the differential effects of COVID-19 variants on the CV system must be investigated. [ABSTRACT FROM AUTHOR]

Aim: Recent reports of potential harmful effects of nonsteroidal anti‐inflammatory drugs (NSAIDs) in treating patients with coronavirus disease 2019 (COVID‐19) have raised great concern. Methods: We searched the PubMed, EMBASE, Cochrane Library and MedRxiv databases to examine the prevalence of NSAID use and associated COVID‐19 risk, outcomes and safety. Results: Twenty‐five studies with a total of 101 215 COVID‐19 patients were included. Prevalence of NSAID use among COVID‐19 patients was 19% (95% confidence interval [CI] 14‐23%, no. of studies [n] = 22) and NSAID use prior to admission or diagnosis of COVID‐19 was not associated with an increased risk of COVID‐19 (adjusted odds ratio [aOR] = 0.93, 95% CI 0.82‐1.06, I2 = 34%, n = 3), hospitalization (aOR = 1.06, 95% CI 0.76‐1.48, I2 = 81%, n = 5), mechanical ventilation (aOR = 0.71, 95% CI 0.47‐1.06, I2 = 38%, n = 4) or length of hospital stay. Moreover, prior use of NSAIDs was associated with a decreased risk of severe COVID‐19 (aOR = 0.79, 95% CI 0.71‐0.89, I2 = 0%, n = 7) and death (aOR = 0.68, 95% CI 0.52‐0.89, I2 = 85%, n = 10). Prior NSAID administration might also be associated with an increased risk of stroke (aOR = 2.32, 95% CI 1.04‐5.2, I2 = 0%, n = 2), but not myocardial infarction (aOR = 1.49, 95% CI 0.25‐8.92, I2 = 0, n = 2) and composite thrombotic events (aOR = 1.56, 95% CI 0.66‐3.69, I2 = 52%, n = 2). Conclusion: Based on current evidence, NSAID use prior to admission or diagnosis of COVID‐19 was not linked with increased odds or exacerbation of COVID‐19. NSAIDs might provide a survival benefit, although they might potentially increase the risk of stroke. Controlled trials are still required to further assess the clinical benefit and safety (e.g., stroke and acute renal failure) of NSAIDs in treating patients with COVID‐19. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Health Sciences / Sağlık Bilimleri Dergisi is the property of Erciyes Universitesi Saglik Bilimleri Dergisi and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aims: Delivery of clinical dental education, as opposed to clinical medicine, is particularly challenging due to the obligatory aerosol-generating procedures (AGPs) used in dentistry, which are known to facilitate the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Hence, using AGPs and working in close proximity to patients for extended periods in dental hospital/university settings with multiple teaching clinics have been a formidable prospect for all stake holders. Therefore, several professional and governmental organizations have promulgated variations of infection control guidelines for general practice dentistry in the pandemic era to mitigate SARS-CoV-2 transmission. Materials and methods: In the absence of unified guidelines for modified infection control/clinical procedures for dental education. We implemented a clinical protocol template and modified operating procedures (MOP) for teaching clinical dentistry to fit the infection control requirements during the pandemic/post-pandemic period at the Sharjah University, College of Dentistry, UAE. MOPs ranged from various engineering control measures (e.g., negative-pressure ventilation systems in operatories) to administrative control measures featuring post-procedure fallow periods of treatment-abeyance between patient sessions. Results: The new MOPs for clinical dentistry in the COVID-19 pandemic era, trialled in a UAE dental teaching hospital, have successfully eliminated infection transmission amongst the students, clinicians, ancillary staff, or attending patients, thus far. Conclusions: The proposed MOPs that complement the standard operating protocols in clinical dentistry were an attempt to mitigate nosocomial infection transmission and protect four different groups of stakeholders, i) the patients, ii) the dental students, iii) the clinical academics, and iv) the para-dental personnel/assistants. Due to the endemicity of the COVID-19 in many regions of the World, the suggested MOPs need periodic review and revision, to fit the emerging data on the disease. Finally, as there are no studies to date comparing the relative efficacy of the MOPs in various dental academic institutions, there is an urgent need for future workers to address this issue. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged as a contemporary hazard to people. It has been known that COVID-19 can both induce heart failure (HF) and raise the risk of patient mortality. However, the mechanism underlying the association between COVID-19 and HF remains unclear. The common molecular pathways between COVID-19 and HF were identified using bioinformatic and systems biology techniques. Transcriptome analysis was performed to identify differentially expressed genes (DEGs). To identify gene ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways, common DEGs were used for enrichment analysis. The results showed that COVID-19 and HF have several common immune mechanisms, including differentiation of T helper (Th) 1, Th 2, Th 17 cells; activation of lymphocytes; and binding of major histocompatibility complex class I and II protein complexes. Furthermore, a protein-protein interaction network was constructed to identify hub genes, and immune cell infiltration analysis was performed. Six hub genes (FCGR3A, CD69, IFNG, CCR7, CCL5, and CCL4) were closely associated with COVID-19 and HF. These targets were associated with immune cells (central memory CD8 T cells, T follicular helper cells, regulatory T cells, myeloid-derived suppressor cells, plasmacytoid dendritic cells, macrophages, eosinophils, and neutrophils). Additionally, transcription factors, microRNAs, drugs, and chemicals that are closely associated with COVID-19 and HF were identified through the interaction network. [ABSTRACT FROM AUTHOR]

Most patients infected with SARS-CoV-2 display mild symptoms with good prognosis, while 20% of patients suffer from severe viral pneumonia and up to 5% may require intensive care unit (ICU) admission due to severe acute respiratory syndrome, which could be accompanied by multiorgan failure. Plasma proteomics provide valuable and unbiased information about disease progression and therapeutic candidates. Recent proteomic studies have identified molecular changes in plasma of COVID-19 patients that implied significant dysregulation of several aspects of the inflammatory response accompanied by a general metabolic suppression. However, which of these plasma alterations are associated with disease severity remains only partly characterized. A known limitation of proteomic studies of plasma samples is the large difference in the macromolecule abundance, with concentration spanning at least 10 orders of magnitude. To improve the coverage of plasma contents, we performed a deep proteomic analysis of plasma from 10 COVID-19 patients with severe/fatal pneumonia compared to 10 COVID-19 patients with pneumonia who did not require ICU admission (non-ICU). To this aim, plasma samples were first depleted of the most abundant proteins, trypsin digested and peptides subjected to a high pH reversed-phase peptide fractionation before LC–MS analysis. These results highlighted an increase of proteins involved in neutrophil and platelet activity and acute phase response, which is significantly higher in severe/fatal COVID-19 patients when compared to non-ICU ones. Importantly, these changes are associated with a selective induction of complement cascade factors in severe/fatal COVID-19 patients. Data are available via ProteomeXchange with identifier PXD036491. Among these alterations, we confirmed by ELISA that higher levels of the neutrophil granule proteins DEFA3 and LCN2 are present in COVID-19 patients requiring ICU admission when compared to non-ICU and healthy donors. Altogether, our study provided an in-depth view of plasma proteome changes that occur in COVID-19 patients in relation to disease severity, which can be helpful to identify therapeutic strategies to improve the disease outcome. [ABSTRACT FROM AUTHOR]

The ongoing Coronavirus Disease 2019 (COVID-19) pandemic is caused by the highly infectious Severe Acute Respiratory Syndrome Coronavirus-2 (SARSCoV-2). There is an urgent need for biomarkers that will help in better stratification of patients and contribute to personalized treatments. We performed targeted proteomics using the Olink platform and systematically investigated protein concentrations in 350 hospitalized COVID-19 patients, 186 post-COVID-19 individuals, and 61 healthy individuals from 3 independent cohorts. Results revealed a signature of acute SARS-CoV-2 infection, which is represented by inflammatory biomarkers, chemokines and complementrelated factors. Furthermore, the circulating proteome is still significantly affected in post-COVID-19 samples several weeks after infection. Post-COVID-19 individuals are characterized by upregulation of mediators of the tumor necrosis (TNF)-a signaling pathways and proteins related to transforming growth factor (TGF)-ß. In addition, the circulating proteome is able to differentiate between patients with different COVID-19 disease severities, and is associated with the time after infection. These results provide important insights into changes induced by SARS-CoV-2 infection at the proteomic level by integrating several cohorts to obtain a large disease spectrum, including variation in disease severity and time after infection. These findings could guide the development of host-directed therapy in COVID-19. [ABSTRACT FROM AUTHOR]

Objective: Cardiac involvement in recovered COVID‐19 patients assessed by cardiac magnetic resonance imaging (MRI). Methods: Subjects recently recovered from COVID‐19 and with an abnormal left ventricular global longitudinal strain were enrolled. Cardiac MRI in all the enrolled subjects was done at baseline (within 30–90 days following recovery from COVID‐19) with a follow‐up scan at 6 months in individuals with an abnormal baseline scan. Additionally, 20 age‐and sex‐matched individuals were enrolled as healthy controls (HCs). Results: All the 30 enrolled subjects were symptomatic during active COVID‐19 disease and were categorized as mild: 11 (36.7%), moderate: 6 (20%), and severe: 13 (43.3%). Of the 30 patients, 16 (53.3%) had abnormal CMR findings. Myocardial edema was reported in 12 (40%) patients while 10 (33.3%) had late gadolinium enhancement (LGE). No difference was observed in terms of conventional left ventricular (LV) parameters; however, COVID‐19‐recovered patients had significantly lower right ventricular (RV) ejection fraction, RV stroke volume, and RV cardiac index compared to HCs. Follow‐up scan was abnormal in 4/16 (25%) with LGE persisting in three patients (who had severe COVID‐19 [3/4;75%]). Subjects with severe COVID‐19 had a greater frequency of LGE (53.8%) and myocardial edema (61.5%) as compared to mild and moderate cases. Myocardial T1 (1284 ± 43.8 ms vs. 1147.6 ± 68.4 ms; p <.0001) and T2 values (50.8 ± 16.7 ms vs. 42.6 ± 3.6 ms; p =.04) were significantly higher in post COVID‐19 subjects compared to HCs. Similarly, T1 and T2 values of severe COVID‐19 patients were significantly higher compared to mild and moderate cases. Conclusions: An abnormal CMR was seen in half of the recovered patients with persistent abnormality in one‐fourth at 6 months. Our study suggests a need for closer follow‐up among recovered subjects in order to evaluate for long‐term cardiovascular sequelae. COVID‐19 causes structural changes in the myocardium in a small segment of patients with partial spontaneous resolution. [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is a member of the coronavirus family that causes the novel coronavirus disease first diagnosed in 2019 (COVID‐19). Although many studies have been carried out in recent months to determine why the disease clinical presentations and outcomes can vary significantly from asymptomatic to severe or lethal, the underlying mechanisms are not fully understood. It is likely that unique individual characteristics can strongly influence the broad disease variability; thus, tailored diagnostic and therapeutic approaches are needed to improve clinical outcomes. The circadian clock is a critical regulatory mechanism orchestrating major physiological and pathological processes. It is generally accepted that more than half of the cell‐specific genes in any given organ are under circadian control. Although it is known that a specific role of the circadian clock is to coordinate the immune system's steady‐state function and response to infectious threats, the links between the circadian clock and SARS‐CoV‐2 infection are only now emerging. How inter‐individual variability of the circadian profile and its dysregulation may play a role in the differences noted in the COVID‐19‐related disease presentations, and outcome remains largely underinvestigated. This review summarizes the current evidence on the potential links between circadian clock dysregulation and SARS‐CoV‐2 infection susceptibility, disease presentation and progression, and clinical outcomes. Further research in this area may contribute towards novel circadian‐centred prognostic, diagnostic and therapeutic approaches for COVID‐19 in the era of precision health. [ABSTRACT FROM AUTHOR]

The pathogenesis of long-Covid symptoms remains incompletely understood. Therefore, we aimed to determine cardiopulmonary limitations 6 months after surviving COVID-19 using pulmonary function tests, echocardiographic studies to the point of analysis of global-longitudinal-strain (GLS), which describes the cycling myocardium deformation and provides better data on left ventricular (LV) dysfunction than LV ejection fraction (LVEF), and validated questionnaires. Overall, 60 consecutive hospitalized patients were included (61 ± 2 years, 40% treated in the ICU). At follow-up (194 ± 3 days after discharge), fatigue was the most prevalent symptom (28%). Patients with fatigue were more symptomatic overall and characterized by worse quality of life (QoL) scores compared to patients without fatigue (all p < 0.05), mainly due to limited mobility and high symptom burden. While PFT variables and LVEF were normal in the vast majority of patients (LVEF = 52% (45–52%)), GLS was significantly reduced (− 15% (− 18 to − 14%)). However, GLS values were not different between patients with and without fatigue. In conclusion, fatigue was the most prevalent long-Covid symptom in our cohort, which was associated with worse QoL mainly due to limited mobility and the high burden of concomitant symptoms. Patients showed a subtle myocardial dysfunction 6 months after surviving COVID-19, but this did not relate to the presence of fatigue. [ABSTRACT FROM AUTHOR]