The MAP-IO (Marion Dusfresne Atmospheric Program - Indian Ocean) program aims to make up for the lack of observation in this region of the earth by equipping the Marion Dufresne vessel (https://taaf.fr/en/marion-dufresne-and-astrolabe/) with a set of in-situ instruments and remote sensing for the atmosphere and marine biology studies. This program has been labeled by the French Commission Nationale de la Flotte Hauturière (CNFH, https://www.flotteoceanographique.fr/) for the period 2021 to 2024. During this period, MAP-IO will operate as a scientific program for the acquisition and scientific enhancement of four years of data. This period will also serve as an operational prototype to study the feasibility of switching the program to a permanent observatory aimed at integration into international infrastructures networks such as ACTRIS (https://www.actris.eu/) or ICOS (https://www.icos-cp.eu/). More informations on the project : http://www.mapio.re/. MAP-IO is a scientific program led by the University of La Reunion (LACy and OSU-R) and was funded by the European Union through the ERDF programme, the University of Reunion, the SGAR-Réunion, the Région Réunion, the CNRS, IFREMER and the Flotte Océanographique Française. The Cytosense automated flow cytometer from the cytobuoy compagny was installed onboard the Marion Dufresnes Sea Water supply, to run semi continuously samples for phytoplankton functional groups resolution. Sample acquisition was schedulled once avery two hours. The data corresponds to abundances in cells/ml, mean forward scatter and red fluorescence in arbitrary units, per group. The groups are identified as standard groups following the BODC F02 vocabulary and the corresponding selections sets named following expert names.

IntroductionBryostatin-1, a potent agonist of the protein kinase C, has been studied for HIV and cancer therapies. In HIV research, it has shown anti-HIV effects during acute infection and reactivation of latent HIV in chronic infection. As effective CD8+ T cell responses are essential for eliminating reactivated virus and achieving a cure, it is important to investigate how bryostatin-1 affects HIV-specific CD8+ T cells. HIV-specific CD8+ T cells often become exhausted, showing reduced proliferative potential and impaired cytokine production, a dysfunction also observed in cancer. Therefore, we further investigated how bryostatin-1 directly impacts exhausted CD8+ T cells.MethodsPBMCs from people with HIV (PWH) were treated with bryostatin-1 and tracked with proliferation dye for cell expansion. One day 6, HIV-specific CD8+ T cells were detected by tetramers staining and examined by flow cytometry. By utilizing an established in vitro murine T cell exhaustion system, changes in inhibitory receptors, transcription factors, cytokine production and killing capacity of bryostatin-1 treated exhausted CD8+ T cells were determined by flow cytometry. RNA-seq analysis was performed to study transcriptional changes in these cells.ResultsWe found that bryostatin-1 improved the expansion and decreased PD-1 expression of HIV-specific CD8+ T cells. Bryostatin-1 enhanced the functionality and proliferation while decreasing inhibitory receptor expression of in vitro generated exhausted CD8+ T cells. Bryostatin-1 upregulated TCF-1 and decreased TOX expression. These changes were confirmed through RNA-seq analysis. RNA-seq revealed that mitogen-activated protein kinases (MAPK) 11 was significantly downregulated in exhausted CD8+ T cells, however, it greatly upregulated after bryostatin-1 treatment. Inhibition of MAPK11 in bryostatin-1-treated cells blocked the increased proliferation and IFN-γ production induced by bryostatin-1, but did not affect other bryostatin-1 induced effects, such as the reduction of inhibitory receptors.DiscussionOur data demonstrate that bryostatin-1 induces a MAPK 11-dependent improvement in the proliferative and functional capacity of exhausted T cells. This study provides a rationale for bryostatin-1's potential to help eradicate the HIV reservoir during treatment, and it may also contribute to cancer immunotherapy by functionally improving exhausted CD8+ T cells.

Effects of different membrane integrity inhibitors on total membrane transfer from PKH26-labeled T cells to PMNs and PMN functions after 1 h pre-incubation detected by flow cytometry

Effects of different inhibitors on PMN-MNC trogocytosis detected by flow cytometry.

Cox proportional-hazards regression analysis for independent associations between the survival time and the IPI, CD4 count and a N:L >6:1.

The primary objective of this work was to delve into the potential therapeutic advantages and dissect the molecular mechanisms of salidroside in enhancing erectile function in rats afflicted with diabetic microvascular erectile dysfunction (DMED), addressing both the whole-animal and cellular dimensions.We established a DMED model in Sprague‒Dawley (SD) rats and conducted in vivo experiments. The DMED rats were administered varying doses of salidroside, the effects of which on DMED were compared. Erectile function was evaluated by applying electrical stimulation to the cavernous nerves and measuring intracavernous pressure in real time. The penile tissue underwent histological examination and Western blotting. Hydrogen peroxide (H2O2) was employed in the in vitro trial to induce an oxidative stress for the purpose of identifying alterations in cell viability. The CCK-8 assay was used to measure the viability of corpus cavernous smooth muscle cells (CCSMCs) treated with vs. without salidroside. Flow cytometry was utilized to detect alterations in intracellular reactive oxygen species (ROS). Apoptosis was assessed through Western blotting and TdT-mediated dUTP nick-end labelling (TUNEL). Animal and cellular experiments indicate that the Nrf2/HO-1 signalling pathway may be upregulated by salidroside, leading to the improvement of erectile function in diabetic male rats by alleviating oxidative stress and reducing apoptosis in corpus cavernosum tissue.

(A) Schematic of the BAC reporter construct. Destabilization of the Mx1deGFP or IFIT1deGFP fusion protein was achieved by C-terminal fusion with the degradation domain of mouse ornithine decarboxylase (mODC). (B) A549-IFIT1deGFP cells were stimulated with 10 IU/ml IFN-α for 24 h and subjected to FACS to separate cells according to expression of IFIT1deGFP. Right after sorting, GFP-positive and -negative cells were lysed and total RNA was extracted. Amounts of mRNAs specified in the bottom of the graph were quantified by RT-qPCR and normalized to GAPDH mRNA levels. Note that the IFIT1 specific RT-qPCR detected both the endogenous ISG and the reporter mRNA. Data represent the mean from two independent experiments and their respective SDs. (C) A549-IFIT1deGFP cells were stimulated with 100 IU/ml IFN-α (to achieve high level expression of the endogenous ISG), harvested at time points specified in the top (hours) and analyzed by Western blot to detect proteins specified in the right. A representative blot from 3 independent experiments is shown. Mock-treated cells are shown in the right lane of each panel. (D) Induction kinetics of IFIT1deGFP and Mx1deGFP after stimulation of A549 reporter cell lines with IFN-α. Cells were treated with 100 IU/ml of IFN-α, harvested at time points specified in the bottom of the graph and number of GFP-positive cells was determined by flow cytometry. Data are mean from 3 independent experiments and their respective SDs. (E) IFN-α dose response assay with A549 reporter cell lines. Cells were stimulated for 24 h with 100 IU/ml IFN-α and analyzed for mean GFP intensity (left panel) or number of GFP-expressing cells (right panel) by using flow cytometry. Data are mean from 3 independent experiments and their respective SDs. (F) Half-life of IFIT1deGFP (left panel) and Mx1deGFP (right panel) as determined by CHX treatment of cells after pre-stimulation with 100 IU/ml IFN-α for 15 h. Cells were harvested at time points given in the bottom of the graph and cell lysates were analyzed by Western blot using GFP-, IFIT1-, Mx1- and β-actin-specific antisera. Representative blots are shown in the bottom of each panel; quantifications from 4 independent experiments and their respective SDs are depicted in the upper graphs of each panel. In panels C and F, numbers in the left of Western blots refer to molecular weights of size standards in kiloDalton (kDa), respectively.