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Background: This study aimed to produce Odontoglossum ringspot virus (ORSV)-free Cymbidium orchid 'New True' plants from ORSV-infected mother plants by culturing their meristems and successively repeating subcultures of protocorm-like bodies (PLBs) derived from the meristems. Results: Initially, ORSV was confirmed as the causative agent of viral symptoms in orchid leaves via reverse transcription-polymerase chain reaction (RT-PCR) analysis. Meristems from infected plants were cultured to generate PLBs, which in sequence were repeatedly subcultured up to four times. RT-PCR and quantitative RT-PCR analyses revealed that while ORSV was undetectable in shoots derived from the first subculture, complete elimination of the virus required at least a second subculture. Genetic analysis using inter-simple sequence repeat markers indicated no somaclonal variation between regenerated plants and the mother plant, suggesting that genetic consistency was maintained. Conclusion: Overall, our findings demonstrate that subculturing PLBs for a second time is ideal for producing genetically stable, ORSV-free Cymbidium orchids, thus offering a practical means of generating genetically stable, virus-free plants and enhancing plant health and quality in the orchid industry. [ABSTRACT FROM AUTHOR]

The article offers information on the Gq alpha subunit and hyper-phosphorylated ERK expression in Sturge–Weber syndrome. Topics discussed include information on the association of syndrome with leptomeningeal blood vessel endothelial cells; discussions on the increased number of leptomeningeal blood vessels with thin or disorganized vessel walls; and the increased endothelial p-ERK expression in port-wine birthmarks.

Oxidative stress is known to be a primary risk factor for neuronal diseases. Glutaredoxin (GLRX)‑1, a redox‑regulator of the thioredoxin superfamily, is known to exhibit an important role in cell survival via various cellular functions. However, the precise roles of GLRX1 in brain ischemia are still not fully understood. The present study investigated whether transduced PEP‑1‑GLRX1 protein has protective effects against oxidative stress in cells and in an animal model. Transduced PEP‑1‑GLRX1 protein increased HT‑22 cell viability under oxidative stress and this fusion protein significantly reduced intracellular reactive oxygen species and levels of DNA damage. In addition, PEP‑1‑GLRX1 protein regulated RAC‑a serine/threonine‑protein kinase and mitogen‑activated protein kinase signaling, in addition to apoptotic signaling including B cell lymphoma (Bcl)‑2, Bcl‑2 associated X, apoptosis regulator, pro‑caspase‑9 and p53 expression levels. In an ischemic animal model, it was verified that PEP‑1‑GLRX1 transduced into the Cornu Ammonis 1 region of the animal brain, where it markedly protected against ischemic injury. These results indicate that PEP‑1‑GLRX1 attenuates neuronal cell death resulting from oxidative stress in vitro and in vivo. Therefore, PEP‑1‑GLRX1 may exhibit a beneficial role in the treatment of neuronal disorders, including ischemic injury. [ABSTRACT FROM AUTHOR]

Radiotherapy is an essential step during the treatment of glioblastoma multiforme (GBM), one of the most lethal malignancies. The survival in patients with GBM was improved by the current standard of care for GBM established in 2005 but has stagnated since then. Since GBM is a radioresistant malignancy and the most of GBM recurrences occur in the radiotherapy field, increasing the effectiveness of radiotherapy using high-Z metal nanoparticles (NPs) has recently attracted attention. This review summarizes the progress in radiotherapy approaches for the current treatment of GBM, the physical and biological mechanisms of radiosensitization through high-Z metal NPs, and the results of studies on radiosensitization in the in vitro and in vivo GBM models using high-Z metal NPs to date. [ABSTRACT FROM AUTHOR]

In a previous study, we utilized a proteomic approach and found a significant reduction in phosphatidylethanolamine-binding protein 1 (PEBP1) protein level in the spinal cord at 3 h after ischemia. In the present study, we investigated the role of PEBP1 against oxidative stress in NSC34 cells in vitro, and ischemic damage in the rabbit spinal cord in vivo. We generated a PEP-1-PEBP1 fusion protein to facilitate the penetration of blood-brain barrier and intracellular delivery of PEBP1 protein. Treatment with PEP-1-PEBP1 significantly decreased cell death and the induction of oxidative stress in NSC34 cells. Furthermore, administering PEP-1-PEBP1 did not show any significant side effects immediately before and after ischemia/reperfusion. Administration of PEP-PEBP1 improved the Tarlov's neurological score at 24 and 72 h after ischemia, and significantly improved neuronal survival at 72 h after ischemia based on neuronal nuclei (NeuN) immunohistochemistry, Flouro-Jade B staining, and western blot study for cleaved caspase 3. PEP-1-PEBP1 administration decreased oxidative stress based on malondialdehyde level, advanced oxidation protein products, and 8-iso-prostaglandin F2α in the spinal cord. In addition, inflammation based on myeloperoxidase level, tumor necrosis factor-α level, and high mobility group box 1 level was decreased by PEP-1-PEBP1 treatment at 72 h after ischemia. Thus, PEP-1-PEBP1 treatment, which decreases oxidative stress, inflammatory cytokines, and neuronal death, may be an effective therapeutic strategy for spinal cord ischemia. [ABSTRACT FROM AUTHOR]