PlasPi TDM: Augmentation of a low-cost camera platform for advanced underwater physical-ecological observations.

Marine ecosystem dynamics in the context of climate change is a growing scientific, political and social concern requiring regular monitoring through appropriate observational technologies and studies. Thus, a wide range of tools comprising chemical, biogeochemical, physical, and biological sensors, as well as other platforms exists for marine monitoring. However, their high acquisition and maintenance costs are often a major obstacle, especially in low-income developing countries. We designed an advanced low-cost synoptic marine ecosystem observation system that operates at relatively high temporal frequencies, named PlasPi TDM. This instrument is an improved version of the camera system (PlasPI marine cameras) developed in 2020 by Autun Purser from the Alfred Wegener Institute Helmholtz Center for Polar and Marine Research (Germany), and collaborators. It incorporates several innovative developments such as multispectral (records the spectrum of any object photographed), temperature and pressure sensors. The PlasPi TDM operates to a depth of 200 m. The various field deployments demonstrate the operational capability of the PlasPi TDM for different applications and illustrate its considerable potential for in-situ observations and marine surveillance in Africa. This device is intended as an open-source project and its continued development is encouraged for a more integrated, sustainable and low-cost ocean observing system.

Probing leukocyte traffic in lymph from oro-nasal mucosae by cervical catheterization in a sheep model.

Lymph nodes are instructed via the lymph about ongoing events in tissues both during the steady state and under provoked inflammation. In order to probe for tissue-to-node transduction mechanisms, we have developed a novel in vivo technique of pseudo-afferent lymph collection from the oro-nasal mucosae which represent the main portals of entry of micro-organisms and efficient routes for vaccination. After lateral lymph node resection of the head, a network of lymph ducts was reconstructed as checked by lymphography. Subsequent catheterization of the cervical lymph duct allowed the collection of cells that were shown to originate from the oro-nasal mucosae. These cells included dendritic cells, monocytes, granulocytes, memory CD45RAneg CD2pos integrin beta7lo CD4 T cells, CD25pos CD4, CD8, gamma/delta T cells, and B lymphocytes. This approach, which permits lymph collection over several weeks, opens a valuable and unique way to study leukocyte and particulate (micro-organisms, vaccines) trafficking from head tissue to nodes under homeostastic and immuno-stimulatory conditions in a highly physiological setting.

Inflammatory activation enhances NMDA-triggered Ca2+ signalling and IL-1ß secretion in primary cultures of rat astrocytes.

The aim of the present study was to measure the effects of NMDA receptor antagonists on rat astroglial-enriched primary cultures after incubation with lipopolysaccharide (LPS), with a view to explaining the role of NMDA receptors in the inflammatory activation of astrocytes. First, the presence of NMDA receptor subunits was confirmed at the protein level by immunocytochemical methods. The presence of functional NMDA receptors containing GluN2B subunits was then established by ratiometric fluorescent Ca(2+) imaging which revealed transient NMDA-triggered Ca(2+) responses. These responses could be blocked by the competitive antagonist 2-amino-5-phosphonopentoate (APV) and the non-competitive GluN2B subunit-selective antagonist ifenprodil. The NMDA-evoked Ca(2+) transients were dependent on Ca(2+) release from intracellular stores via interaction with InsP3-sensitive receptors as they were blocked by thapsigargin or xestospongin C. Following 24h incubation with LPS, astroglial inflammatory activation increased IL-1ß secretion and NMDA-triggered Ca(2+) transients. The addition of APV or ifenprodil inhibited these enhanced responses, suggesting that LPS exposure stimulates IL-1ß release from astrocytes through a mechanism that requires NMDA receptor stimulation.