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In-depth characterization of heart-brain communication in critically ill patients with severe acute respiratory failure is attracting significant interest in the COronaVIrus Disease 19 (COVID-19) pandemic era during intensive care unit (ICU) stay and after ICU or hospital discharge. Emerging research has provided new insights into pathogenic role of the deregulation of the heart-brain axis (HBA), a bidirectional flow of information, in leading to severe multiorgan disease syndrome (MODS) in patients with confirmed infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Noteworthy, HBA dysfunction may worsen the outcome of the COVID-19 patients. In this review, we discuss the critical role HBA plays in both promoting and limiting MODS in COVID-19. We also highlight the role of HBA as new target for novel therapeutic strategies in COVID-19 in order to open new translational frontiers of care. This is a translational perspective from the Italian Society of Cardiovascular Researches.
To calculate and compare the National Institutes of Health (NIH) research investment for cardiac arrest (CA) to other leading causes of disability-adjusted life years (DALY) in the United States (U.S.).

A search within NIH RePORTER for 2017 was performed using single common resuscitation terms. Grants were individually reviewed and categorized as CA research (yes/no) using predefined criteria. DALY were calculated as the sum of years of life lost (YLL) and years lived with disability (YLD) using all adult non-traumatic out-of-hospital CA (OHCA) from the CARES database for 2017. Total DALY for the study population were extrapolated to a national level. Leading causes of DALY were obtained from the Global Burden of Disease study and funding data were extracted from the NIH Categorical Spending Report for comparison. The outcome measure was U.S. dollars invested per annual DALY.

The search yielded 290 grants, of which 87 (30%) were classified as CA research. Total funding for CA research in 2017 was $37.1M. A total of 73,915 (97%) cases from CARES met study inclusion criteria for the DALY analysis. The total DALY following adult OHCA in the U.S. population were 4,335,949 (YLL 4,332,166, YLD 3784). Per annual DALY, the NIH invested $287 for diabetes, $92 for stroke, $55 for ischemic heart disease, and $9 for CA research.

The NIH investment into CA research is far less than other comparable causes of death and disability in the U.S. These results should help inform utilization of limited resources to improve public health.
The NIH investment into CA research is far less than other comparable causes of death and disability in the U.S. These results should help inform utilization of limited resources to improve public health.Porcine epidemic diarrhea virus (PEDV), especially variants, causes a highly contagious enteric disease which could give rise to huge economic losses in the swine industry worldwide. Portulaca oleracea L. has been reported to regulate intestine disease and involved in viral infections. However, the underlying mechanisms of Portulaca oleracea L. extracts against PEDV have not been fully elucidated. In this study, the antiviral effects and potential mechanisms of Portulaca oleracea L. extracts against PEDV were investigated in vitro. We first examined the inhibitory effects of different Portulaca oleracea L. extracts on the PEDV(JX-16 strain) in vitro and found that the water extract of Portulaca oleracea L.(PO)could significantly inhibit PEDV replication by 92.73% on VH cells and 63.07% on Vero cells. Furthermore, time-course analysis showed PO inhibited PEDV replication during the adsorption period of infectious cycle. Western blot and indirect immunofluorescence assay indicated that PO down-regulated the S protein expression in a dose-dependent manner. In addition, our results demonstrated the ability of PO to inhibit PEDV replication in VH cells by down-regulating the cytokine levels (TNF-α,IL-22 and IFN-α) and inhibiting the NF-κB signaling pathway activated by PEDV. Thus, Portulaca oleracea L extracts have potential utility in the preventive and therapeutic strategies for PEDV infection.Recently efforts have been taken for unravelling mysteries between host-microbe interactions in gut microbiome studies of model organisms through metagenomics. SU5402 Co-existence and the co-evolution of the microorganisms is the significant cause of the growing antimicrobial menace. There needs a novel approach to develop potential antimicrobials with capabilities to act directly on the resistant microbes with reduced side effects. One such is to tap them from the natural resources, preferably the gut of the most closely related animal model. In this study, we employed metagenomics approaches to identify the large taxonomic genomes of the zebra fish gut. About 256 antimicrobial peptides were identified using gene ontology predictions from Macrel and Pubseed servers. Upon the property predictions, the top 10 antimicrobial peptides were screened based on their action against many resistant bacterial species, including Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus aureus, E. coli, and Bacillus cereus. Metabolic modelling and flux balance analysis (FBA) were computed to conclude the antibiotic such as tetracycline, cephalosporins, puromycin, neomycin biosynthesis pathways were adopted by the microbiome as protection strategies. Molecular modelling strategies, including molecular docking and dynamics, were performed to estimate the antimicrobial peptides' binding against the target-putative nucleic acid binding lipoprotein and confirm stable binding. One specific antimicrobial peptide with the sequence "MPPYLHEIQPHTASNCQTELVIKL" showed promising results with 53% hydrophobic residues and a net charge +2.5, significant for the development of antimicrobial peptides. The said peptide also showed promising interactions with the target protein and expressed stable binding with docking energy of -429.34 kcal/mol and the average root mean square deviation of 1 A0. The study is a novel approach focusing on tapping out potential antimicrobial peptides to be developed against most resistant bacterial species.
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