At the crossroads of epidemiology and biology: Bridging the gap between SARS-CoV-2 viral strain properties and epidemic wave characteristics.

The COVID-19 pandemic has given rise to numerous articles from different scientific fields (epidemiology, virology, immunology, airflow physics …) without any effort to link these different insights. In this review, we aim to establish relationships between epidemiological data and the characteristics of the virus strain responsible for the epidemic wave concerned. We have carried out this study on the Wuhan, Alpha, Delta and Omicron strains allowing us to illustrate the evolution of the relationships we have highlighted according to these different viral strains.

Risk assessment for long- and short-range airborne transmission of SARS-CoV-2, indoors and outdoors.

Preventive measures to reduce infection are needed to combat the COVID-19 pandemic and prepare for a possible endemic phase. Current prophylactic vaccines are highly effective to prevent disease but lose their ability to reduce viral transmission as viral evolution leads to increasing immune escape. Long-term proactive public health policies must therefore complement vaccination with available nonpharmaceutical interventions aiming to reduce the viral transmission risk in public spaces.

Facts and conjectures on calmodulin and its cousin proteins, parvalbumin and troponin C.

This review aims at giving a rational frame to understand the diversity of EF hand containing calcium binding proteins and their roles, with special focus on three members of this huge protein family, namely calmodulin, troponin C and parvalbumin. We propose that these proteins are members of structured macromolecular complexes, termed calcisomes, which constitute building devices allowing treatment of information within eukaryotic cells and namely calcium signals encoding and decoding, as well as control of cytosolic calcium levels in resting cells. Calmodulin is ubiquitous, present in all eukaryotic cells, and pleiotropic.

Using Data Mining to Explore Calmodulin Bibliography.

In this chapter, we present a strategy and the techniques to approach a scientific field from a set of articles gathered from the bibliographic database "Web of Science." The strategy is based on methods developed to analyze social networks. We illustrate its use in studying the calmodulin field.

Ca-Dependent Transcriptional Repressors KCNIP and Regulation of Prognosis Genes in Glioblastoma.

Glioblastomas (GBMs) are the most aggressive and lethal primary astrocytic tumors in adults, with very poor prognosis. Recurrence in GBM is attributed to glioblastoma stem-like cells (GSLCs). The behavior of the tumor, including proliferation, progression, invasion, and significant resistance to therapies, is a consequence of the self-renewing properties of the GSLCs, and their high resistance to chemotherapies have been attributed to their capacity to enter quiescence.

Discovery of a Locally and Orally Active CXCL12 Neutraligand (LIT-927) with Anti-inflammatory Effect in a Murine Model of Allergic Airway Hypereosinophilia.

We previously reported Chalcone-4 (1) that binds the chemokine CXCL12, not its cognate receptors CXCR4 or CXCR7, and neutralizes its biological activity. However, this neutraligand suffers from limitations such as poor chemical stability, solubility, and oral activity. Herein, we report on the discovery of pyrimidinone 57 (LIT-927), a novel neutraligand of CXCL12 which displays a higher solubility than 1 and is no longer a Michael acceptor.

Quiescence status of glioblastoma stem-like cells involves remodelling of Ca signalling and mitochondrial shape.

Quiescence is a reversible cell-cycle arrest which allows cancer stem-like cells to evade killing following therapies. Here, we show that proliferating glioblastoma stem-like cells (GSLCs) can be induced and maintained in a quiescent state by lowering the extracellular pH. Through RNAseq analysis we identified Ca signalling genes differentially expressed between proliferating and quiescent GSLCs.

Efficient Modeling and Simulation of Space-Dependent Biological Systems.

We recently demonstrated the possibility to model and to simulate biological functions using hardware description languages (HDLs) and associated simulators traditionally used for microelectronics. Nevertheless, those languages are not suitable to model and simulate space-dependent systems described by partial differential equations. However, in more and more applications space- and time-dependent models are unavoidable.

Changes in chromatin state reveal ARNT2 at a node of a tumorigenic transcription factor signature driving glioblastoma cell aggressiveness.

Although a growing body of evidence indicates that phenotypic plasticity exhibited by glioblastoma cells plays a central role in tumor development and post-therapy recurrence, the master drivers of their aggressiveness remain elusive. Here we mapped the changes in active (H3K4me3) and repressive (H3K27me3) histone modifications accompanying the repression of glioblastoma stem-like cells tumorigenicity. Genes with changing histone marks delineated a network of transcription factors related to cancerous behavior, stem state, and neural development, highlighting a previously unsuspected association between repression of ARNT2 and loss of cell tumorigenicity.

Modeling and simulation of biological systems using SPICE language.

The article deals with BB-SPICE (SPICE for Biochemical and Biological Systems), an extension of the famous Simulation Program with Integrated Circuit Emphasis (SPICE). BB-SPICE environment is composed of three modules: a new textual and compact description formalism for biological systems, a converter that handles this description and generates the SPICE netlist of the equivalent electronic circuit and NGSPICE which is an open-source SPICE simulator. In addition, the environment provides back and forth interfaces with SBML (System Biology Markup Language), a very common description language used in systems biology.

The adaptors Grb10 and Grb14 are calmodulin-binding proteins.

We identified the Grb7 family members, Grb10 and Grb14, as Ca -dependent CaM-binding proteins using Ca -dependent CaM-affinity chromatography as we previously did with Grb7. The potential CaM-binding sites were identified and experimentally tested using fluorescent-labeled peptides corresponding to these sites. The apparent affinity constant of these peptides for CaM, and the minimum number of calcium ions bound to CaM that are required for effective binding to these peptides were also determined.

[Application of microelectronics CAD tools to synthetic biology].

Synthetic biology is an emerging science that aims to create new biological functions that do not exist in nature, based on the knowledge acquired in life science over the last century. Since the beginning of this century, several projects in synthetic biology have emerged. The complexity of the developed artificial bio-functions is relatively low so that empirical design methods could be used for the design process.

Bisacodyl and its cytotoxic activity on human glioblastoma stem-like cells. Implication of inositol 1,4,5-triphosphate receptor dependent calcium signaling.

Glioblastoma is the most common malignant brain tumor. The heterogeneity at the cellular level, metabolic specificities and plasticity of the cancer cells are a challenge for glioblastoma treatment. Identification of cancer cells endowed with stem properties and able to propagate the tumor in animal xenografts has opened a new paradigm in cancer therapy.

GeNeDA: An Open-Source Workflow for Design Automation of Gene Regulatory Networks Inspired from Microelectronics.

The topic of this article is the development of an open-source automated design framework for synthetic biology, specifically for the design of artificial gene regulatory networks based on a digital approach. In opposition to other tools, GeNeDA is an open-source online software based on existing tools used in microelectronics that have proven their efficiency over the last 30 years. The complete framework is composed of a computation core directly adapted from an Electronic Design Automation tool, input and output interfaces, a library of elementary parts that can be achieved with gene regulatory networks, and an interface with an electrical circuit simulator.

The anti-hypertensive drug prazosin inhibits glioblastoma growth via the PKCδ-dependent inhibition of the AKT pathway.

A variety of drugs targeting monoamine receptors are routinely used in human pharmacology. We assessed the effect of these drugs on the viability of tumor-initiating cells isolated from patients with glioblastoma. Among the drugs targeting monoamine receptors, we identified prazosin, an α1- and α2B-adrenergic receptor antagonist, as the most potent inducer of patient-derived glioblastoma-initiating cell death.