Advances in isolated phages that affect Ralstonia solanacearum and their application in the biocontrol of bacterial wilt in plants.

Bacterial wilt is a widespread and devastating disease that impacts the production of numerous crucial crops worldwide. The main causative agent of the disease is Ralstonia solanacearum. Due to the pathogen's broad host range and prolonged survival in the soil, it is challenging to control the disease with conventional strategies. Therefore, it is of great importance to develop effective alternative disease control strategies. In recent years, phage therapy has emerged as an environmentally friendly and sustainable biocontrol alternative, demonstrating significant potential in controlling this severe disease. This paper summarized basic information about isolated phages that infect R. solanacearum, and presented some examples of their application in the biocontrol of bacterial wilt. The risks of phage application and future prospect in this area were also discussed. Overall, R. solanacearum phages have been isolated from various regions and environments worldwide. These phages belong mainly to the Inoviridae, Autographiviridae, Peduoviridae, and Cystoviridae families, with some being unclassified. Studies on the application of these phages have demonstrated their ability to reduce pathogenicity of R. solanacearum through direct lysis or indirect alteration of the pathogen's physiological properties. These findings suggested bacteriophage is a promising tool for biocontrol of bacterial wilt in plants.

Effect of high intensity ultrasound on transglutaminase-catalyzed soy protein isolate cold set gel.

The effects of high intensity ultrasound (HIU, 105-110 W/cm(2) for 5 or 40 min) pre-treatment of soy protein isolate (SPI) on the physicochemical properties of ensuing transglutaminase-catalyzed soy protein isolate cold set gel (TSCG) were investigated in this study. The gel strength of TSCG increased remarkably from 34.5 to 207.1 g for TSCG produced from SPI with 40 min HIU pre-treatment. Moreover, gel yield and water holding capacity also increased after HIU pre-treatments. Scanning electron microscopy showed that HIU of SPI resulted in a more uniform and denser microstructure of TSCG. The content of free sulfhydryl (SH) groups was higher in HIU TSCG than non-HIU TSG, even though greater decrease of the SH groups present in HIU treated SPI was observed when the TSCG was formed, suggesting the involvement of disulfide bonds in gel formation. Protein solubility of TSCG in both denaturing and non-denaturing solvents was higher after HIU pretreatment, and changes in hydrophobic amino acid residues as well as in polypeptide backbone conformation and secondary structure of TSCG were demonstrated by Raman spectroscopy. These results suggest that increased inter-molecular ε-(γ-glutamyl) lysine isopeptide bonds, disulfide bonds and hydrophobic interactions might have contributed to the HIU TSCG gel network. In conclusion, HIU changed physicochemical and structural properties of SPI, producing better substrates for TGase. The resulting TSCG network structure was formed with greater involvement of covalent and non-covalent interactions between SPI molecules and aggregates than in the TSCG from non-HIU SPI.

Activation of opioid µ-receptors, but not δ- or κ-receptors, switches pulmonary C-fiber-mediated rapid shallow breathing into an apnea in anesthetized rats.

Rapid shallow breathing (RSB) is mainly mediated by bronchopulmonary C-fibers (PCFs). We asked whether this RSB could be modulated by opioids. In anesthetized rats right atrial bolus injection of phenylbiguanide (PBG) to evoke RSB was repeated after: (1) intravenously giving fentanyl (µ-receptor agonist), DPDPE (δ-receptor agonist), or U-50488H (κ-receptor agonist); (2) fentanyl (iv) following naloxone methiodide, a peripheral opioid receptor antagonist; (3) bilateral microinjection of fentanyl into the nodose ganglia; (4) fentanyl (iv) with pre-blocking histamine H(1) and H(2) receptors by diphenhydramine and ranitidine. Systemic fentanyl challenge, but not DPDPE or U-50488H, switched the PBG-induced RSB to a long lasting apnea. This switch was blocked by naloxone methiodide rather than diphenhydramine and ranitidine. After microinjecting fentanyl into the nodose ganglia, PBG also produced an apnea. Our results suggest that activating µ-receptors is capable of turning the PCF-mediated RSB into an apnea, at least partly, via facilitating PCFs' activity and this switching effect appears independent of the released histamine.