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The increasing sodium salts (NaCl, NaHCO3, NaSO4 etc.) in agricultural soil is a serious global concern for sustainable agricultural production and food security. Soybean is an important food crop, and their cultivation is severely challenged by high salt concentration in soils. Classical transgenic and innovative breeding technologies are immediately needed to engineer salt tolerant soybean plants. Additionally, unfolding the molecular switches and the key components of the soybean salt tolerance network are crucial for soybean salt tolerance improvement. Here we review our understandings of the core salt stress response mechanism in soybean. Recent findings described that salt stress sensing, signalling, ionic homeostasis (Na+/K+) and osmotic stress adjustment might be important in regulating the soybean salinity stress response. We also evaluated the importance of antiporters and transporters such as Arabidopsis K+ Transporter 1 (AKT1) potassium channel and the impact of epigenetic modification on soybean salt tolerance. We also review key phytohormones, and osmo-protectants and their role in salt tolerance in soybean. In addition, we discuss the progress of omics technologies for identifying salt stress responsive molecular switches and their targeted engineering for salt tolerance in soybean. This review summarizes recent progress in soybean salt stress functional genomics and way forward for molecular breeding for developing salt-tolerant soybean plant.

Background: High flow nasal cannula (HFNC) therapy is widely employed in acute hypoxemic respiratory failure (AHRF) patients. However, the techniques for predicting HFNC outcome remain scarce.Methods: PubMed, EMBASE, and Cochrane Library were searched until April 20, 2021. We included the studies that evaluated the potential predictive value of ROX (respiratory rate-oxygenation) index for HFNC outcome. This meta-analysis determined sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic score, diagnostic odds ratio (DOR), and pooled area under the summary receiver operating characteristic (SROC) curve.Results: We assessed nine studies with 1933 patients, of which 745 patients experienced HFNC failure. This meta-analysis found that sensitivity, specificity, PLR, NLR, diagnostic score, and DOR of ROX index in predicting HFNC failure were 0.67 (95% CI 0.57-0.76), 0.72 (95% CI 0.65-0.78), 2.4 (95% CI 2.0-2.8), 0.46 (95% CI 0.37-0.58), 1.65(95% CI 1.37-1.93), and 5.0 (95% CI 4.0-7.0), respectively. In addition, SROC was 0.75 (95% CI 0.71-0.79). Besides, our subgroup analyses revealed that ROX index had higher sensitivity and specificity for predicting HFNC failure in COVID-19 patients from non-European countries, while the acquisition time of 6 h after receiving HFNC had a lower sensitivity and specificity when compared to other times.Conclusions: This study demonstrated that ROX index could function as a novel potential marker to identify patients with a higher risk of HFNC failure. However, the prediction efficiency was moderate, and additional research is required to determine the optimal cut-off value and propel acquisition time of ROX index in the future.PROSPERO registration number: CRD42021240607.

Following ligand stimulation, several Toll-like receptors (TLRs) are phosphorylated at tyrosine residues in their intracellular domains. However, the precise chain of events leading to tyrosine-phosphorylation-dependent TLR-mediated cytokine secretion has not been defined. We focused on elaborating the signaling pathway of tyrosine-phosphorylated TLR2. We demonstrated that two tyrosine residues in the intracellular domain of TLR2, Y616 and Y761, were important for cytokine secretion. We also showed that the src-kinase, Fyn, is constitutively associated with TLR2. TLR2-ligand stimulation increases the amount of phosphorylated Fyn and phosphorylated TLR2. The p85-PI3K complex together with PKC associated with TLR2 in a src-kinase dependent manner. We identified crosstalk between this complex and two components of the TLR2 tyrosine-phosphorylation-independent pathway, IRAK-1 and TRAF6. Our results demonstrate that the downstream events of ligand-stimulated TLR2, including activation of NF B and Erk1/2 as well as cytokine secretion, are src-kinase dependent.

Previous studies suggest an association of cardiac microvascular endothelial cells (CMECs) hyperpermeability with sepsis-related cardiac injury. Our results showed that CMECs permeability was dependent upon concentration and time of lipopolysaccharides (LPS) stimulation. Integrin ανβ3 expression decreased after LPS stimulation. Pretreatment with anti-integrin ανβ3 antibody enhanced LPS-induced hyperpermeability. Upregulation of integrin ανβ3 decreased LPS-induced hyperpermeability. F-actin remodeling was enhanced after LPS stimulation and was inhibited by up-regulation of integrin ανβ3. Inhibition of Src or Rac1 reduced CMECs permeability after LPS stimulation, but there were no differences in the phosphorylation of Src and Rac1 when over-expressing or blocking integrin β3. After pretreatment with Src or Rac1 inhibitor, no significant difference was found in the expression of integrin ανβ3 in LPS-induced CMECs. These finding suggested that integrin ανβ3 overexpression decreased LPS-stimulated CMECS permeability by inhibition of cytoskeletal remodeling, but the mechanism might not be mediated via Src/Rac1 signaling.