Comparative Analysis of Rhizosphere and Endophytic Microbial Communities Between Root Rot and Healthy Root of Psammosilene tunicoides.

The wild resources of Psammosilene tunicoides have decreased sharply because of the long-term mining and excavation, which has led to the increased demand for its artificial cultivation. However, root rot represents a significant obstacle leading to a poor quality and product of P. tunicoides. Previous reports have not focused on root rot in P. tunicoides. Therefore, this study explores the rhizospheric and root endophytic microbial community structure and composition of healthy and root rot P. tunicoides to understand the mechanism underlying root rot. The properties of the rhizosphere soil were assessed using physiochemical methods, and the bacterial and fungal populations were studied through amplicon sequencing of the 16S rRNA genes and ITS regions in the root and soil. Compared to healthy samples, the pH, hydrolysis N, available P, and available K were significantly decreased in the diseased samples while the organic matter and total organic carbon were significantly increased in the diseased samples. Redundancy analysis (RDA) showed that soil environmental factors are related to changes in the root and rhizosphere soil microbial community of P. tunicoides indicating that the physiochemical properties of soil affect plant health. Alpha diversity analysis showed that the microbial communities of healthy and diseased samples were similar. Some bacterial and fungal genera were significantly increased or decreased (P < 0.05) in diseased P. tunicoides, and certain microbial factors that antagonized root rot were further explored. This study provides an abundant microbial resource for future studies and contributes to improving soil quality and P. tunicoides agricultural production.

PATCHING RETINAL BREAKS WITH HEALAFLOW IN 27-GAUGE VITRECTOMY FOR THE TREATMENT OF RHEGMATOGENOUS RETINAL DETACHMENT.

PURPOSE: To report the surgical outcomes of primary rhegmatogenous retinal detachment (RRD) repaired by 27-gauge pars plana vitrectomy combined with Healaflow patch and air tamponade. METHODS: In an initial vitro experiment, we observed and compared the dissolution and displacement of the dispersion spots of 0.05-mL Healaflow and sodium hyaluronate. We then performed a prospective, interventional cohort study on 38 eyes in 37 consecutive patients with primary rhegmatogenous retinal detachment. All eyes underwent pars plana vitrectomy combined with Healaflow patch and air tamponade; the postoperative period did not involve prone positioning. The primary and final anatomical attachment rate, best-corrected visual acuity, and intraoperative and postoperative complications were evaluated. RESULTS: In the in vitro experiment, the viscoelastic Healaflow remained adherent with no change in the size of the area; however, the control dissolved completely in the balance solution. The patient study included 16 women (43.2%) and 21 men (56.8%) (mean age, 59.5 ± 9.5 years; mean follow-up period, 8.9 ± 3.8 months). A single break was present in 21 (55.3%) and 2 to 5 breaks in 17 cases (44.8%). The macula was involved in 25 (65.8%) and attached in 13 cases (34.2%) intraoperatively. Initial reattachment was achieved in 37 (97.4%) and final reattachment in 38 cases (100%). In one case (2.6%), the macula redetached because of failure of the chorioretinal scar to develop around the treated break. Mean preoperative and postoperative best-corrected visual acuities were 1.02 ± 0.82 logarithm of the minimum angle of resolution (median Snellen acuity: 20/125, range: 20/20,000-20/20) and 0.23 ± 0.17 logarithm of the minimum angle of resolution (median Snellen acuity: 20/32, range: 20/100-20/20), respectively (P < 0.001). Intraocular pressure was elevated transiently in 28 eyes (73.7%). There were no other intraoperative complications or postoperative scleral incision leakage. CONCLUSION: A 27-gauge pars plana vitrectomy combined with Healaflow patch, and air tamponade results in a high reattachment rate in the treatment of rhegmatogenous retinal detachment. Thus, patients can benefit from early visual recovery and less complications.

A decrease in phosphorylation of cAMP-response element-binding protein (CREBP) promotes retinal degeneration.

Excitotoxicity, induced either by N-Methyl-d-aspartate (NMDA) or kainic acid (KA), promotes irreversible loss of retinal ganglion cells (RGCs). Although the intracellular signaling mechanisms underlying excitotoxic cell death are still unclear, recent studies on the retina indicate that NMDA promotes RGC death by increasing phosphorylation of cyclic AMP (cAMP) response element (CRE)-binding protein (CREBP), while studies on the central nervous system indicate that KA promotes neuronal cell death by decreasing phosphorylation of CREBP, suggesting that CREBP can elicit dual responses depending on the excitotoxic-agent. Interestingly, the role of CREBP in KA-mediated death of RGCs has not been investigated. Therefore, by using an animal model of excitotoxicity, the aim of this study was to investigate whether excitotoxicity induces RGC death by decreasing Ser(133)-CREBP in the retina. Death of RGCs was induced in CD-1 mice by an intravitreal injection of 20 nmoles of kainic acid (KA). Decrease in CREBP levels was determined by immunohistochemistry, western blot analysis, and electrophoretic mobility gel shift assays (EMSAs). Immunohistochemical analysis indicated that CREBP was constitutively expressed in the nuclei of cells both in the ganglion cell layer (GCL) and in the inner nuclear layer (INL) of CD-1 mice. At 6 h after KA injection, nuclear localization of Ser(133)-CREBP was decreased in the GCL. At 24 h after KA injection, Ser(133)-CREBP was decreased further in GCL and the INL, and a decrease in Ser(133)-CREBP correlated with apoptotic death of RGCs and amacrine cells. Western blot analysis indicated that KA decreased Ser(133)-CREBP levels in retinal protein extracts. EMSA assays indicated that KA also reduced the binding of Ser(133)-CREBP to CRE consensus oligonucleotides. In contrast, intravitreal injection of CNQX, a non-NMDA glutamate receptor antagonist, restored the KA-induced decrease in Ser(133)-CREBP both in the GCL and INL, and inhibited loss of RGCs and amacrine cells. These results, for the first time, suggest that KA promotes retinal degeneration by reducing phosphorylation of Ser(133)-CREBP in the retina.