Controlled cavity collapse: scaling laws of drop formation

The formation of transient cavities at liquid interfaces occurs in an immense variety of natural processes, among which the bursting of surface bubbles and the impact of a drop on a liquid pool are salient. The collapse of a surface liquid cavity is a well documented natural process that leads to the ejection of a thin and fast jet. Droplets generated through this process can be one order of magnitude smaller than the cavity's aperture, and they are consequently of interest in drop on demand inkjet applications. In this work, the controlled formation and collapse of a liquid cavity is analyzed, and the conditions for minimizing the resulting size and number of ejected drops are determined. The experimental and numerical models are simple and consist of a liquid reservoir, a nozzle plate with the discharge orifice, and a moving piston actuated by single half-sine-shaped pull-mode pulses. The size of the jetted droplet is described by a physical model resulting in a scaling law that is numerically and experimentally validated

Controlled cavity collapse: scaling laws of drop formation

The formation of transient cavities at liquid interfaces occurs in an immense variety of natural processes, among which the bursting of surface bubbles and the impact of a drop on a liquid pool are salient. The collapse of a surface liquid cavity is a well documented natural process that leads to the ejection of a thin and fast jet. Droplets generated through this process can be one order of magnitude smaller than the cavity's aperture, and they are consequently of interest in drop on demand inkjet applications. In this work, the controlled formation and collapse of a liquid cavity is analyzed, and the conditions for minimizing the resulting size and number of ejected drops are determined. The experimental and numerical models are simple and consist of a liquid reservoir, a nozzle plate with the discharge orifice, and a moving piston actuated by single half-sine-shaped pull-mode pulses. The size of the jetted droplet is described by a physical model resulting in a scaling law that is numerically and experimentally validated

The role of B cells in COVID-19 infection and vaccination

B cells secrete antibodies and mediate the humoral immune response, making them extremely important in protective immunity against SARS-CoV-2, which caused the coronavirus disease 2019 (COVID-19) pandemic. In this review, we summarize the positive function and pathological response of B cells in SARS-CoV-2 infection and re-infection. Then, we structure the immunity responses that B cells mediated in peripheral tissues. Furthermore, we discuss the role of B cells during vaccination including the effectiveness of antibodies and memory B cells, viral evolution mechanisms, and future vaccine development. This review might help medical workers and researchers to have a better understanding of the interaction between B cells and SARS-CoV-2 and broaden their vision for future investigations

Gene cluster lock after pheromone receptor gene choice

In mammals, perception of pheromones is based on the expression in each vomeronasal sensory neuron of a limited set of receptor genes, chosen among a large repertoire. Here, we report an extremely tight control of the monogenic and monoallelic transcription of the V1rb2 receptor gene. Combining genetic and electrophysiological approaches, we show that the transcription of a non-functional V1r allele leads to the coexpression of another, functional V1r gene. The choice of this coexpressed gene surprisingly includes genes located on the cluster homologous to the one from which the mutant allele is transcribed. However, V1r genes located in cis relative to the transcribed mutant allele are excluded from the coexpression choice. Our observations strongly suggest a monogenic regulatory mechanism acting (a) at a general level, via the expression of the V1r receptor itself, and (b) at a more local level, defined by the V1r gene cluster

p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours.

p73 (ref. 1) has high homology with the tumour suppressor p53 (refs 2-4), as well as with p63, a gene implicated in the maintenance of epithelial stem cells. Despite the localization of the p73 gene to chromosome 1p36.3 a region of frequent aberration in a wide range of human cancers, and the ability of p73 to transactivate p53 target genes, it is unclear whether p73 functions as a tumour suppressor. Here we show that mice functionally deficient for all p73 isoforms exhibit profound defects, including hippocampal dysgenesis, hydrocephalus, chronic infections and inflammation, as well as abnormalities in pheromone sensory pathways. In contrast to p53-deficient mice, however, those lacking p73 show no increased susceptibility to spontaneous tumorigenesis. We report the mechanistic basis of the hippocampal dysgenesis and the loss of pheromone responses, and show that new, potentially dominant-negative, p73 variants are the predominant expression products of this gene in developing and adult tissues. Our data suggest that there is a marked divergence in the physiological functions of the p53 family members, and reveal unique roles for p73 in neurogenesis, sensory pathways and homeostatic control