Too hot for comfort: The heatwaves in Greece in 1987 and 1988

The heatwaves that affected Greece in July 1987 and July 1988 are considered in terms of (i) the relative strain index. For different types of activity, and (ii) the discomfort index. Hourly values of air temperature and humidity for Thessaloniki and Athens were used as the data base. Both indices show that in terms of physiological strain and general discomfort, Thessaloniki suffered a little more and a little longer than Athens. We conclude that the relative strain index is probably a useful tool in studies of the adverse effects of humid heatwaves on different sections of a population.     

Physiology and pathophysiology of selectins, integrins, and IgSF cell adhesion molecules focusing on inflammation. A paradigm model on infectious endocarditis

The development of adhesion bonds, either among cells or among cells and components of the extracellular matrix, is a crucial process. These interactions are mediated by some molecules collectively known as adhesion molecules (CAMs). CAMs are ubiquitously expressed proteins playing a central role in controlling cell migration, proliferation, survival, and apoptosis. Besides their key function in physiological maintenance of tissue integrity, CAMs play an eminent role in various pathological processes such as cardiovascular disorders, atherogenesis, atherosclerotic plaque progression and regulation of the inflammatory response. CAMs such as selectins, integrins, and immunoglobulin superfamily take part in interactions between leukocyte and vascular endothelium (leukocyte rolling, arrest, firm adhesion, migration). Experimental data and pathologic observations support the assumption that pathogenic microorganisms attach to vascular endothelial cells or sites of vascular injury initiating intravascular infections. In this review a paradigm focusing on cell adhesion molecules pathophysiology and infective endocarditis development is given.     

Multiphysics and multiscale modeling of microthrombosis in COVID-19

Emerging clinical evidence suggests that thrombosis in the microvasculature of patients with Coronavirus disease 2019 (COVID-19) plays an essential role in dictating the disease progression. Because of the infectious nature of SARS-CoV-2, patients’ fresh blood samples are limited to access for in vitro experimental investigations. Herein, we employ a novel multiscale and multiphysics computational framework to perform predictive modeling of the pathological thrombus formation in the microvasculature using data from patients with COVID-19. This framework seamlessly integrates the key components in the process of blood clotting, including hemodynamics, transport of coagulation factors and coagulation kinetics, blood cell mechanics and adhesive dynamics, and thus allows us to quantify the contributions of many prothrombotic factors reported in the literature, such as stasis, the derangement in blood coagulation factor levels and activities, inflammatory responses of endothelial cells and leukocytes to the microthrombus formation in COVID-19. Our simulation results show that among the coagulation factors considered, antithrombin and factor V play more prominent roles in promoting thrombosis. Our simulations also suggest that recruitment of WBCs to the endothelial cells exacerbates thrombogenesis and contributes to the blockage of the blood flow. Additionally, we show that the recent identification of flowing blood cell clusters could be a result of detachment of WBCs from thrombogenic sites, which may serve as a nidus for new clot formation. These findings point to potential targets that should be further evaluated, and prioritized in the anti-thrombotic treatment of patients with COVID-19. Altogether, our computational framework provides a powerful tool for quantitative understanding of the mechanism of pathological thrombus formation and offers insights into new therapeutic approaches for treating COVID-19 associated thrombosis.     

In vitro evolution predicts emerging SARS-CoV-2 mutations with high affinity for ACE2 and cross-species binding

Emerging SARS-CoV-2 variants are creating major challenges in the ongoing COVID-19 pandemic. Being able to predict mutations that could arise in SARS-CoV-2 leading to increased transmissibility or immune evasion would be extremely valuable in development of broad-acting therapeutics and vaccines, and prioritising viral monitoring and containment. Here we use in vitro evolution to seek mutations in SARS-CoV-2 receptor binding domain (RBD) that would substantially increase binding to ACE2. We find a double mutation, S477N and Q498H, that increases affinity of RBD for ACE2 by 6.5-fold. This affinity gain is largely driven by the Q498H mutation. We determine the structure of the mutant-RBD:ACE2 complex by cryo-electron microscopy to reveal the mechanism for increased affinity. Addition of Q498H to SARS-CoV-2 RBD variants is found to boost binding affinity of the variants for human ACE2 and confer a new ability to bind rat ACE2 with high affinity. Surprisingly however, in the presence of the common N501Y mutation, Q498H inhibits binding, due to a clash between H498 and Y501 side chains. To achieve an intermolecular bonding network, affinity gain and cross-species binding similar to Q498H alone, RBD variants with the N501Y mutation must acquire instead the related Q498R mutation. Thus, SARS-CoV-2 RBD can access large affinity gains and cross-species binding via two alternative mutational routes involving Q498, with route selection determined by whether a variant already has the N501Y mutation. These mutations are now appearing in emerging SARS-CoV-2 variants where they have the potential to influence human-to-human and cross-species transmission.     

Using EEG Frontal Asymmetry to Predict IT User’s Perceptions Regarding Usefulness,Ease of Use and Playfulness

Information systems (IS) community is increasingly interested in employing neuroscience tools and methods in order to develop new theories concerning Human–computer interaction (HCI) and further understand IS acceptance models. The new field of NeuroIS has been introduced to address these issues. NeuroIS researchers have proposed encephalography (EEG), among other neuroscience instruments, as a valuable usability metric, when used effectively in appropriately designed experiments. Moreover, numerous researchers have suggested that EEG frontal asymmetry may serve as an important metric of user experience. Based on the aforementioned evidence, this study aims to integrate frontal asymmetry with Technology acceptance model (TAM). Particularly, we assumed that frontal asymmetry might predict users’ perceptions regarding Usefulness and Ease of Use. Furthermore, we hypothesized that frontal asymmetry might also affect (influence) users’ Perceived Playfulness. Specifically, 82 (43 females and 39 males) undergraduate students were chosen to use a Computer-Based Assessment (while being connected to the EEG) in the context of an introductory informatics course. Results confirmed our hypothesis as well as points of theory about Information technology (IT) acceptance variables. This is one of the first studies to suggest that frontal asymmetry could serve as a valuable tool for examining IT acceptance constructs and better understanding HCI.     

A rare case of a 39 year old male with a parasite called Dioctophyma renale mimicking renal cancer at the computed tomography of the right kidney. A case report

We present a very rare case of a 39 year old patient with Dioctophyma renale depicted as a Bosniak cyst IV of the right kidney who was finally subjected to a robotic assisted radical nephrectomy.