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Journal: European journal of clinical investigation


The most restrictive non-pharmaceutical interventions (NPIs) for controlling the spread of COVID-19 are mandatory stay-at-home and business closures. Given the consequences of these policies, it is important to assess their effects. We evaluate the effects on epidemic case growth of more restrictive NPIs (mrNPIs), above and beyond those of less restrictive NPIs (lrNPIs).


As of October 2020, there are >1 million documented deaths with COVID-19. Excess deaths can be caused by both COVID-19 and the measures taken. COVID-19 shows extremely strong risk stratification across age, socioeconomic factors, and clinical factors. Calculation of years-of-life-lost from COVID-19 is methodologically challenging that can yield misleading over-estimates. Many early deaths may have been due to suboptimal management, malfunctional health systems, hydroxychloroquine, sending COVID-19 patients to nursing homes, and nosocomial infections; such deaths are partially avoidable moving forward. About 10% of the global population may be infected by October 2020. Global infection fatality rate is 0.15-0.20% (0.03-0.04% in those <70 years), with large variability across locations with different age-structure, institutionalization rates, socioeconomic inequalities, population-level clinical risk profile, public health measures, and health care. There is debate on whether at least 60% of the global population must be infected for herd immunity, or, conversely, mixing heterogeneity and pre-existing cross-immunity may allow substantially lower thresholds. Simulations are presented with a total of 1.58-8.76 million COVID-19 deaths over 5-years (1/2000-12/2024) globally (0.5-2.9% of total global deaths). The most favorable figures in that range would be feasible if high risk groups can be preferentially protected with lower infection rates than the remaining population. Death toll may also be further affected by potential availability of effective vaccines and treatments, optimal management and measures taken, COVID-19 interplay with influenza and other health problems, reinfection potential, and any chronic COVID-19 consequences. Targeted, precise management of the pandemic and avoiding past mistakes would help minimize mortality.


Estimates of community spread and infection fatality rate (IFR) of COVID-19 have varied across studies. Efforts to synthesize the evidence reach seemingly discrepant conclusions.


The evolving coronavirus disease 2019 (COVID-19) epidemic1 is certainly cause for concern. Proper communication and optimal decision-making is an ongoing challenge, as data evolve. The challenge is compounded, however, by exaggerated information. This can lead to inappropriate actions. It is important to differentiate promptly the true epidemic from an epidemic of false claims and potentially harmful actions.


A key question concerning coronavirus disease 2019 (COVID-19) is how effective and long lasting immunity against this disease is in individuals who were previously infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We aimed to evaluate the risk of SARS-CoV-2 re-infections in the general population in Austria.


Systematic reviews are generally placed above narrative reviews in an assumed hierarchy of secondary research evidence. We argue that systematic reviews and narrative reviews serve different purposes and should be viewed as complementary. Conventional systematic reviews address narrowly focused questions; their key contribution is summarising data. Narrative reviews provide interpretation and critique; their key contribution is deepening understanding. This article is protected by copyright. All rights reserved.

Concepts: Evidence-based medicine, All rights reserved, All rights reversed, Copyright, Critic


The employment of dietary strategies such as ketogenic diets, which force cells to alter their energy source, has shown efficacy in the treatment of several diseases. Ketogenic diets are composed of high fat, moderate protein and low carbohydrates, which favor mitochondrial respiration rather than glycolysis for energy metabolism.

Concepts: Protein, Metabolism, Nutrition, Adenosine triphosphate, Glucose, Mitochondrion, Cellular respiration, Citric acid cycle


BRD7 is a member of bromodomain-containing protein and was found to be a cofactor of P53. Down-regulation of BRD7 has been shown in nasopharyngeal carcinoma cell lines and tissues. However, the clinical role of BRD7 in colorectal cancer remains unknown.

Concepts: Gene, Cell, Cancer, Lung cancer, Cell biology, Colorectal cancer, Adenocarcinoma, Nasopharyngeal carcinoma


Eur J Clin Invest 2012 Backgroud  Apelin, a potential agent for treating heart failure, has various ionic effects on ventricular myocytes. However, the effects of apelin on the atrium are not clear. The purpose of this study was to investigate the acute effects of apelin on the electrophysiological characteristics of atrial myocytes. Method  Whole-cell patch-clamp techniques were used to investigate the action potential (AP) and ionic currents in isolated rabbit left atrial (LA) myocytes before and after the administration of apelin. Result  Apelin reduced LA AP duration measured at 90%, 50% and 20% repolarization of the amplitude by 11 ± 3%, 24 ± 5%, 30 ± 7% at 1 nM (n = 11), and by 14 ± 4%, 36 ± 6% and 45 ± 5% at 10 nM (n = 11), but not at 0·1 nM. Apeline (0·1, 1, 10 nM) did not change the amplitude, or resting membrane potential in LA myocytes. Apelin (1 nM) increased sodium currents, ultra-rapid potassium currents and the reverse mode of sodium-calcium exchanger currents, but decreased late sodium currents and L-type calcium currents and did not change transient outward currents or inward rectifier potassium currents in LA myocytes. Conclusions  Apelin significantly changed the atrial electrophysiology with a shortening of AP duration, which may be caused by its effects on multiple ionic currents.

Concepts: Neuron, Action potential, Ion channel, Electrophysiology, Membrane potential, Resting potential, Inward-rectifier potassium ion channel, Cardiac action potential


Hypoxia precedes cardiomyocyte necrosis in acute myocardial infarction (AMI). We therefore hypothesized that uric acid - as a marker of oxidative stress and hypoxia - might be useful in the early diagnosis and risk stratification of patients with suspected AMI.

Concepts: Myocardial infarction, Atherosclerosis, Oxidative stress, Stroke, Infarction, Troponin, Necrosis, Uric acid