Rice SRO1a contributes to Xanthomonas TAL effector-mediated expression of host susceptible gene.

Xanthomonas species infect many important crops and cause huge yield loss. These pathogens deliver transcription activator-like (TAL) effectors into the cytoplasm of plant cells. TAL effectors move to host nuclei, directly bind to the promoters of host susceptible genes, and activate their transcription. However, the molecular mechanisms by which TAL effectors induce host transcription remain unclear. We herein demonstrated that TAL effectors interacted with the SIMILAR TO RCD ONE (SRO) family proteins OsSRO1a and OsSRO1b in nuclei. A transactivation assay using rice protoplasts indicated that OsSRO1a and OsSRO1b enhanced the activation of the OsSWEET14 promoter by the TAL effector AvrXa7. The AvrXa7-mediated expression of OsSWEET14 was significantly reduced in ossro1a mutants. However, the overexpression of OsSRO1a increased disease resistance by up-regulating the expression of defense-related genes, such as WRKY62 and PBZ1. This was attributed to OsSRO1a and OsSRO1b also enhancing the transcriptional activity of WRKY45, a direct regulator of WRKY62 expression. Therefore, OsSRO1a and OsSRO1b appear to positively contribute to transcription mediated by bacterial TAL effectors and rice transcription factors.

A tissue-silicone integrated simulator for right ventricular pulsatile circulation with severe functional tricuspid regurgitation.

There is a great demand for development of a functional tricuspid regurgitation (FTR) model for accelerating development and preclinical study of tricuspid interventional repair devices. This study aimed to develop a severe FTR model by creating a tissue-silicone integrated right ventricular pulsatile circulatory simulator. The simulator incorporates the porcine tricuspid annulus, valve leaflets, chordae tendineae, papillary muscles, and right ventricular wall as one continuous piece of tissue, thereby preserving essential anatomical relationships of the tricuspid valve (TV) complex. We dilated the TV annulus with collagenolytic enzymes under applying stepwise dilation, and successfully achieved a severe FTR model with a regurgitant volume of 45 ± 9 mL/beat and a flow jet area of 15.8 ± 2.3 cm2 (n = 6). Compared to a normal model, the severe FTR model exhibited a larger annular circumference (133.1 ± 8.2 mm vs. 115.7 ± 5.5 mm; p = 0.009) and lower coaptation height (6.6 ± 1.0 mm vs. 17.7 ± 1.3 mm; p = 0.003). Following the De-Vega annular augmentation procedure to the severe FTR model, a significant reduction in regurgitant volume and flow jet area were observed. This severe FTR model may open new avenues for the development and evaluation of transcatheter TV devices.

Repairable ex vivo model of functional and degenerative mitral regurgitation.

OBJECTIVES: Transcatheter mitral valve repair is an emerging alternative to the surgical repair. This technology requires preclinical studies to assess efficacy in mitigating mitral regurgitation (MR). However, ex vivo MR models are not established. We developed 2 novel repairable models, functional and degenerative, which can quantitatively assess regurgitation and effect of intervention. METHODS: We used porcine mitral valves and a pulsatile flow circulation system. In the functional MR model, the annulus was immersed in 0.1% collagenase solution and dilated using 3D-printed dilators. To control the regurgitation grade, the sizes of the dilator and silicone sheet in which the valve was sutured to were adjusted. Chordae of P2 were severed in the degenerative model, and the number of severed chordae was adjusted to control the regurgitation grade. Models were repaired using the edge-to-edge or artificial chordae technique. RESULTS: The mean regurgitant fraction of the moderate-severe functional and degenerative models were 47.9% [standard deviation (SD): 2.2%] and 58.5% (SD: 8.0%), which were significantly reduced to 28.7% (SD: 4.4%) (P < 0.001) and 26.0% (SD: 4.4%) (P < 0.001) after the valve repair procedures. Severe functional model had a mean regurgitant fraction of 59.4% (SD: 6.0%). CONCLUSIONS: Both functional and degenerative models could produce sufficient MR levels that meet the interventional indication criteria. The repairable models are valuable in evaluating the efficacy of valve repair procedures and devices. The ability to control the amount of regurgitation enhances the versatility and reliability of these models. These reproducible models could expedite the development of novel devices.

Central and Enteric Neuroprotective Effects by Eucommia ulmoides Extracts on Neurodegeneration in Rotenone-induced Parkinsonian Mouse.

Parkinson's disease (PD) is a progressive neurodegenerative disease of both the central and peripheral / enteric nervous systems. Oxidative stress and neuroinflammation are associated with the pathogenesis of PD, suggesting that anti-oxidative and anti-inflammatory compounds could be neuroprotective agents for PD. Eucommia ulmoides (EU) is a traditional herbal medicine which exerts neuroprotective effects by anti-inflammatory and anti-oxidative properties. Our previous study showed that treatment with chlorogenic acid, a component of EU, protected against neurodegeneration in the central and enteric nervous systems in a PD model. In this study, we examined the effects of EU extract (EUE) administration on dopaminergic neurodegeneration, glial response and α-synuclein expression in the substantia nigra pars compacta (SNpc), and intestinal enteric neurodegeneration in low-dose rotenone-induced PD model mice. Daily oral administration of EUE ameliorated dopaminergic neurodegeneration and α-synuclein accumulation in the SNpc. EUE treatment inhibited rotenone-induced decreases in the number of total astrocytes and in those expressing the antioxidant molecule metallothionein. EUE also prevented rotenone-induced microglial activation. Furthermore, EUE treatment exerted protective effects against intestinal neuronal loss in the PD model. These results suggest that EU exerts neuroprotective effects in the central and enteric nervous systems of rotenone-induced parkinsonism mice, in part by glial modification.