Ōsaka, Japan
Ōsaka, Japan

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Meinhardt L.W.,U.S. Department of Agriculture | Costa G.G.L.,University of Campinas | Thomazella D.P.T.,University of Campinas | Teixeira P.J.P.L.,University of Campinas | And 11 more authors.
BMC Genomics | Year: 2014

Background: The basidiomycete Moniliophthora roreri is the causal agent of Frosty pod rot (FPR) disease of cacao (Theobroma cacao), the source of chocolate, and FPR is one of the most destructive diseases of this important perennial crop in the Americas. This hemibiotroph infects only cacao pods and has an extended biotrophic phase lasting up to sixty days, culminating in plant necrosis and sporulation of the fungus without the formation of a basidiocarp.Results: We sequenced and assembled 52.3 Mb into 3,298 contigs that represent the M. roreri genome. Of the 17,920 predicted open reading frames (OFRs), 13,760 were validated by RNA-Seq. Using read count data from RNA sequencing of cacao pods at 30 and 60 days post infection, differential gene expression was estimated for the biotrophic and necrotrophic phases of this plant-pathogen interaction. The sequencing data were used to develop a genome based secretome for the infected pods. Of the 1,535 genes encoding putative secreted proteins, 1,355 were expressed in the biotrophic and necrotrophic phases. Analysis of the data revealed secretome gene expression that correlated with infection and intercellular growth in the biotrophic phase and invasive growth and plant cellular death in the necrotrophic phase.Conclusions: Genome sequencing and RNA-Seq was used to determine and validate the Moniliophthora roreri genome and secretome. High sequence identity between Moniliophthora roreri genes and Moniliophthora perniciosa genes supports the taxonomic relationship with Moniliophthora perniciosa and the relatedness of this fungus to other basidiomycetes. Analysis of RNA-Seq data from infected plant tissues revealed differentially expressed genes in the biotrophic and necrotrophic phases. The secreted protein genes that were upregulated in the biotrophic phase are primarily associated with breakdown of the intercellular matrix and modification of the fungal mycelia, possibly to mask the fungus from plant defenses. Based on the transcriptome data, the upregulated secreted proteins in the necrotrophic phase are hypothesized to be actively attacking the plant cell walls and plant cellular components resulting in necrosis. These genes are being used to develop a new understanding of how this disease interaction progresses and to identify potential targets to reduce the impact of this devastating disease. © 2014 Meinhardt et al.; licensee BioMed Central Ltd.

O'Connor B.J.,King's College London | Kilfeather S.,Bioscience Center | Cheung D.,Vlietland Hospital | Kafe H.,Cabinet de Pneumologie | And 5 more authors.
Expert Opinion on Pharmacotherapy | Year: 2010

Objective: To investigate the efficacy and safety of ciclesonide in patients with severe asthma over a 1-year period. Research design and methods: Patients aged 18 75 years with persistent asthma were enrolled in a 12-week, double-blind, randomized study and treated with ciclesonide 320 or 640 μg twice daily (b.i.d.) with the option of continuing in a 40-week extension phase (EP). Main outcomes measures: Change in morning peak expiratory flow (PEF) from baseline to 12 weeks and safety over 1 year. Results: 365 patients were randomized and 275 continued into the EP. During 12 weeks' treatment, morning peak expiratory flow significantly increased by 16 l/min (p < 0.001) and 14 l/min (p 0.001) in the 320 and 640 μg b.i.d. groups, respectively. Both doses significantly reduced total asthma symptom scores by 0.29 (p < 0.0001). In both groups, the incidence of adverse effects (AEs) was low and mean cortisol levels in serum and urine were not suppressed during the EP. Conclusions: Ciclesonide 320 μg b.i.d. sustained lung function and asthma symptoms in patients with severe asthma over 12 weeks' treatment, and maintained lung function during a 40-week EP; ciclesonide 640 μg b.i.d. did not provide additional benefits. Long-term use of ciclesonide was not associated with increased local AEs or negative effects on cortisol levels. © 2010 Informa UK, Ltd.

Taura A.,Kyoto University | Ohgita H.,Kyoto University | Funabiki K.,Bioscience Center | Miura M.,Red Cross | And 2 more authors.
Acta Oto-Laryngologica | Year: 2010

Conclusion: The epidemiology of vertigo remains unclear. This study might contribute to an understanding of the mechanisms underlying vestibular disease. Objective: To investigate the epidemiological features of patients with vertigo. Methods: A retrospective study on 612 patients with vertigo who visited Kyoto University Hospital. Results: Elderly individuals comprised > 30% of patients presenting with vertigo, with more female patients than male patients. © 2010 Informa Healthcare.

Goodfellow, a graduate student in the University of Georgia's Regenerative Bioscience Center, has developed a unique approach of marrying stem cell biology and 3-D imaging to track and label neural stem cells. His findings were published in the journal Advanced Functional Materials. Using microscopic iron beads and a chicken egg, he and his colleagues were able to label neural stem cells and watch them for multiple days using magnetic resonance imaging—without harming the cell. Very little is known about the unusual behavior of neural stem cells after experimental treatment. Understanding their whereabouts, keeping them safe from the body's own immune system and tracking the intended destination for repair in a noninvasive manner is the next important step in regenerative medicine therapy. "The unknown is that big 'black box' when people inject neural stem cells and have no idea where they go, or what they do-it's pretty invasive and inaccurate," said Steven Stice, a Georgia Research Alliance Eminent Scholar and director of the Regenerative Bioscience Center who is housed in the College of Agricultural and Environmental Sciences. The question remains, he said, of whether injecting neural stem cells to restore damaged neurons and allowing the body to heal as it is meant to naturally really delay the onset of symptoms, such as Alzheimer's and Parkinson's diseases. To answer that question, Goodfellow painstakingly labeled neural stem cells with extremely small iron beads and then transplanted the cell into a chicken embryo. "We went to great pains to prove and demonstrate that our labeling method does not harm the stem cells," said Goodfellow, who started as an undergraduate in Stice's lab while majoring in animal and dairy science in the UGA College of Agricultural and Environmental Sciences. "If we are altering transplanted stem cells that we hope will be an effective treatment, then it's a moot point if we do it blindly." Before proving that neural stem cells could be tracked with MRI, the RBC research collaboration, which included Qun Zhao, Luke Mortensen and Gregory Simchick, first had to determine if the iron beads were harmful to the neural stem cells. For 14 days, they tracked and compared live cells and evaluated the fate of derived cells based on their gene expression profile. "We had to take it to the next level and be able to follow the process through for a period of time," Stice said. "No one has really been able to follow neural cells at any great depth to the level of specificity that we were able to do." The findings focus mainly on neural stem cells, but Goodfellow sees potential for their use with mesenchymal stem cells. "One novel aspect of this iron nanoparticle is the iron center covered in synthetic polymers," Goodfellow said. "The covering can be manipulated to show up in green, red or a spectrum of colors with fluorescent microscopy and MRI for a multitude of regenerative therapies-but the surface is what helps it to not harm the cells." The dextran coating used around the nanoparticle increases the nanoparticles biocompatibility, allowing for a larger loading capacity and the protection of a stable environment, he said. In addition to developing a chick model and applications for toxicology testing in the near future, Goodfellow and his team hope that this project may finally shed some light on the uncertainty surrounding neural stem cells and the great therapeutic promise for healing patients after stroke, traumatic brain and spinal cord injuries. "The hope is that this research will get stem cells to clinical applications faster, even if we are just doing rodent studies," he said. "If we are able to see that the cells are surviving and integrating and not adversely affecting the animal, then the likelihood of us getting through clinical trials and onto a real therapy is a lot greater and a lot faster." More information: Forrest T. Goodfellow et al. Tracking and Quantification of Magnetically Labeled Stem Cells Using Magnetic Resonance Imaging, Advanced Functional Materials (2016). DOI: 10.1002/adfm.201504444

Perry C.N.,University of California at San Diego | Huang C.,Bioscience Center | Liu W.,Bioscience Center | Magee N.,Bioscience Center | And 2 more authors.
PLoS ONE | Year: 2011

A significant consequence of ischemia/reperfusion (I/R) is mitochondrial respiratory dysfunction, leading to energetic deficits and cellular toxicity from reactive oxygen species (ROS). Mammalian complex I, a NADH-quinone oxidoreductase enzyme, is a multiple subunit enzyme that oxidizes NADH and pumps protons across the inner membrane. Damage to complex I leads to superoxide production which further damages complex I as well as other proteins, lipids and mtDNA. The yeast, S. cerevisiae, expresses internal rotenone insensitive NADH-quinone oxidoreductase (Ndi1); a single 56kDa polypeptide which, like the multi-subunit mammalian complex I, serves as the entry site of electrons to the respiratory chain, but without proton pumping. Heterologous expression of Ndi1 in mammalian cells results in protein localization to the inner mitochondrial membrane which can function in parallel with endogenous complex I to oxidize NADH and pass electrons to ubiquinone. Expression of Ndi1 in HL-1 cardiomyocytes and in neonatal rat ventricular myocytes protected the cells from simulated ischemia/reperfusion (sI/R), accompanied by lower ROS production, and preservation of ATP levels and NAD+/NADH ratios. We next generated a fusion protein of Ndi1 and the 11aa protein transduction domain from HIV TAT. TAT-Ndi1 entered cardiomyocytes and localized to mitochondrial membranes. Furthermore, TAT-Ndi1 introduced into Langendorff-perfused rat hearts also localized to mitochondria. Perfusion of TAT-Ndi1 before 30 min no-flow ischemia and up to 2 hr reperfusion suppressed ROS production and preserved ATP stores. Importantly, TAT-Ndi1 infused before ischemia reduced infarct size by 62%; TAT-Ndi1 infused at the onset of reperfusion was equally cardioprotective. These results indicate that restoring NADH oxidation and electron flow at reperfusion can profoundly ameliorate reperfusion injury. © 2011 Perry et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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