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1.
Adv Exp Med Biol ; 1327: 63-78, 2021.
Article in English | MEDLINE | ID: covidwho-1316238

ABSTRACT

In severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, children experience mild symptoms compared to adults. However, the precise explanations for this disparity are not clear. Thus, we attempted to identify rational explanations about age-related differences as reported in different studies. Given the incomplete data on SARS-CoV-2, some information has been gathered from other studies of earlier coronavirus or influenza outbreaks. Age-related differences in disease severity are important with regard to diagnosis, prognosis, and treatment of SARS-CoV-2 infections. In addition, these differences impact social distancing needs, since pediatric patients with mild or asymptomatic are likely to play a significant role in disease transmission.


Subject(s)
COVID-19 , Influenza, Human , Adult , Age Factors , Child , Disease Outbreaks , Humans , SARS-CoV-2
2.
Adv Exp Med Biol ; 1321: 277-286, 2021.
Article in English | MEDLINE | ID: covidwho-1114256

ABSTRACT

There is data from individual clinical trials suggesting that procalcitonin (PCT) may be a prognostic factor in the severity of COVID-19 disease. Therefore, this systematic review and meta-analysis was performed to investigate PCT levels in severe COVID-19 patients. We searched Embase, ProQuest, MEDLINE/PubMed, Scopus, and ISI/Web of Science for studies that reported the level of PCT of patient with severe COVID-19. We included all studies regardless of design that reported the level of PCT in patients with severe COVID-19. We excluded articles not regarding COVID-19 or not reporting PCT level, studies not in severe patients, review articles, editorials or letters, expert opinions, comments, and animal studies. Nine studies were included in the analysis. The odds of having more severe COVID-19 disease was higher in subjects with elevated PCT (≥0.05 ng/mL) compared with those having low procalcitonin (<0.05 ng/mL) [n = 6, OR(95% CI) = 2.91(1.14, 7.42), p = 0.025). After estimating the mean and standard deviation values from the sample size, median, and interquartile range, a pooled effect analysis indicated higher serum PCT concentrations in patients with severe versus less severe disease [n = 6, SMD(95% CI) = 0.64(0.02, 1.26), p = 0.042]. The results of this study showed that PCT is increased in patients with severe COVID-19 infection.


Subject(s)
COVID-19 , Procalcitonin , Humans , SARS-CoV-2
3.
Expert Rev Anti Infect Ther ; 19(3): 345-357, 2021 03.
Article in English | MEDLINE | ID: covidwho-759815

ABSTRACT

INTRODUCTION: Coronavirus disease 2019 (COVID-19) has the characteristics of high transmission, diverse clinical manifestations, and a long incubation period. In addition to infecting the respiratory system, COVID-19 also has adverse effects on the cardiovascular system. COVID-19 causes acute myocardial injuries, as well as chronic damage to the cardiovascular system. AREAS COVERED: The present review is aimed at providing current information on COVID-19 and the cardiovascular system. PubMed, Scopus, Science direct, and Google Scholar were searched. EXPERT OPINION: It is suggested that heart injury caused by COVID-19 infection might be an important cause of severe clinical phenotypes or adverse events in affected patients. Myocardial damage is closely related to the severity of the disease and even the prognosis in patients with COVID-19. In addition to disorders that are caused by COVID-19 on the cardiovascular system, more protection should be employed for patients with preexisting cardiovascular disease (CVD). Hence, it is very important that once relevant symptoms appear, patients with COVID-19 be rapidly treated to reduce mortality. Thus, early measurements of cardiac damage via biomarkers following hospitalization for COVID-19 infections in a patient with preexisting CVD are recommended, together with careful monitoring of any myocardial injury that might be caused by the infection.Abbreviations: ICU: An intensive care unit; 2019-nCoV: 2019 novel coronavirus; ACEI: ACE inhibitor; ACS: Acute coronary syndrome; ARDS: Acute respiratory distress syndrome; AT1R: Ang II type 1 receptor; ATP: Adenosine triphosphate; ACC: American College of Cardiology; ACE: Angiotensin converting enzyme; Ang II: Angiotensin II; ARB: Angiotensin II receptor blocker; AV block: Atrioventricular block; CAD: Coronary artery disease; CVD: Cardiovascular disease; CT: Computerized tomography; CHF: Congestive heart failure; CHD: Coronary heart disease; CK-MB: Creatine kinase isoenzyme-MB; CRP: C-reactive protein; cTnI: Cardiac troponin I; EAT: Epicardial adipose tissue; ECMO: Extracorporeal membrane oxygenation; FDA: Food and Drug Administration; G-CSF: Granulocyte colony-stimulating factor; HFrEF: HF with a reduced ejection fraction; synhACE2: Human isoform of ACE2; IL: Interleukin; IABP: Intra-aortic balloon counterpulsation; IP10: Interferon γ-induced protein 10 kDa; LPC: Lysophosphatidylcholine; Mas: Mitochondrial assembly receptor; MCP1: Monocyte chemoattractant protein-1; MERS: Middle East respiratory syndrome; MIP1a: macrophage inflammatory protein 1a: MOF: Multiple organ failure; MI: Myocardial infarction; MRI: Magnetic resonance imaging; MYO: Myohe-moglobin; NT-proBNP: N-terminal pro-brain natriuretic peptide; PCPS: Percutaneous cardiopulmonary assistance; rhACE2: Recombinant human ACE2; SARS: Severe acute respiratory syndrome; Th: T helper; RAS: Renin-angiotensin system; TNF-α: Tumor necrosis factor-α; WHO: World Health Organization.


Subject(s)
COVID-19 , Cardiovascular System , Heart Diseases , SARS-CoV-2 , COVID-19/epidemiology , COVID-19/immunology , COVID-19/physiopathology , COVID-19/therapy , Cardiovascular System/metabolism , Cardiovascular System/physiopathology , Comorbidity , Disease Management , Heart Diseases/metabolism , Heart Diseases/physiopathology , Heart Diseases/therapy , Heart Diseases/virology , Humans , Prognosis , SARS-CoV-2/pathogenicity , SARS-CoV-2/physiology
4.
Health Aff (Millwood) ; 39(9): 1633-1642, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-671627

ABSTRACT

A widely accessible vaccine is essential to mitigate the health and economic ravages of coronavirus disease 2019 (COVID-19). Without appropriate incentives and coordination, however, firms might not respond at sufficient speed or scale, and competition among countries for limited supply could drive up prices and undercut efficient allocation. Programs relying on "push" incentives (direct cost reimbursement) can be complicated by the funder's inability to observe firms' private cost information. To address these challenges, we propose a "pull" program that incentivizes late-stage development (Phase III trials and manufacturing) for COVID-19 vaccines by awarding advance purchase agreements to bidding firms. Using novel cost and demand data, we calculated the optimal size and number of awards. In baseline simulations, the optimal program induced the participation of virtually all ten viable vaccine candidates, spending an average of $110 billion to generate net benefits of $2.8 trillion-nearly double the net benefits generated by the free market.


Subject(s)
Coronavirus Infections/prevention & control , Financial Management/economics , Marketing of Health Services , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , Viral Vaccines/economics , Viral Vaccines/pharmacology , COVID-19 , Coronavirus Infections/epidemiology , Drug Industry , Female , Global Health , Humans , Male , Pneumonia, Viral/epidemiology
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