Protein arginine methyltransferase-1 stimulates dopaminergic neuronal cell death in a Parkinson's disease model.

Recent studies have revealed that protein arginine methyltransferases (PRMTs) are responsible for diverse neurodegenerative diseases. However, their pathophysiological role in dopaminergic neuronal death in Parkinson's disease (PD) has not been evaluated. In this study, we demonstrated that 1-Methyl-4-phenylpyridinium iodide (MPP+), rotenone and paraquat, which cause dopaminergic neuronal cell death, increased PRMT1 expression in dopaminergic cell line. Dopaminergic neuronal cell death was increased by PRMT1 overexpression. MPP+-induced cell death was attenuated by PRMT1 knockdown. Poly (ADP-ribose) polymerase-1 (PARP1) expression and activity, poly-ADP-ribosylation (PARylation), were elevated by MPP+. Moreover, we found that PRMT1 positively regulates nuclear translocation of apoptosis-inducing factor (AIF). Elevated PRMT1 expression was observed in the substantia nigra pars compacta of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-injected mice. Furthermore, MPTP-induced dopaminergic neuronal death was reduced in PRMT1 haploinsufficient (prmt1+/-) mice. These data suggest that PRMT1 is implicated in PARP1/AIF-mediated dopaminergic neuronal cell death, which might be involved in the pathology of PD. Therefore, our results propose PRMT1 as a new target to develop a potential treatment of PD.

17ß-Estradiol induces odontoblastic differentiation via activation of the c-Src/MAPK pathway in human dental pulp cells.

The present study is aimed at investigating the effects of the exogenous estrogen 17ß-estradiol (E2) on odontoblastic differentiation in human dental pulp cells (HDPCs) immotalized with hTERT gene and their molecular mechanism. Proliferation was detected by BrdU assay, and odontoblast differentiation induction was evaluated by the expression of dentin sialophosphoprotein (DSPP), dentin sialoprotein (DSP) and dentin matrix protein1 (DMP1), and alkaline phosphatase (ALP) activity and mineralization. Estrogen receptor-α (ER-α), c-Src, and mitogen-activated protein kinases (MAPKs) were examined and their inhibitors were used to determine the roles on odontogenic induction. E2 significantly promoted the HDPC proliferation, which was mediated by extracellular signal-related kinase 1/2. E2 upregulated DSPP, DSP, and DMP1 as the odontogenic differentiation markers and enhanced ALP activity and mineralization. E2 increased phosphorylation of ER-α and fulvestrant, an ER downregulator, significantly downregulated DSPP, DMP1, and DSP induced by E2. Moreover, E2 treatment activated c-Src and MAPKs upon odontogenic induction, whereas chemical inhibition of c-Src and MAPKs decreased expression of DSPP, DMP1, and DSP and mineralization augmented by E2. Moreover, fulvestrant reduced E2-induced phosphorylation of c-Src and MAPK and inhibition of c-Src by PP2 attenuated activation of MAPKs during E2-induced odontoblastic differentiation. Taken together, these results indicated that E2 stimulates odontoblastic differentiation of HDPCs via coordinated regulation of ER-α, c-Src, and MAPK signaling pathways, which may play a key role in the regeneration of dentin.

CoCl2 induces apoptosis through the mitochondria- and death receptor-mediated pathway in the mouse embryonic stem cells.

Embryonic hypoxia/ischemia is a major cause of a poor fetal outcome and future neonatal and adult handicaps. However, biochemical cellular events in mouse embryonic stem (mES) cells during hypoxia remains unclear. This study investigated the underlying mechanism of apoptosis in mES cells under CoCl2-induced hypoxic/ischemic conditions. CoCl2 enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the accumulation of reactive oxygen species in mES cells. The CoCl2-treated mES cells showed a decrease in cell viability as well as typical apoptotic changes, cell shrinkage, chromatin condensation, and nuclear fragmentation and an extended G2/M phase of the cell cycle. CoCl2 augmented the release of cytochrome c into the cytosol from the mitochondria with a concomitant loss of the mitochondrial transmembrane potential (ΔΨm) and upregulated the voltage-dependent anion channel. In addition, CoCl2-induced caspase-3, -8, and -9 activation and upregulation of p53 level, whereas downregulated Bcl-2 and Bcl-xL, a member of the anti-apoptotic Bcl-2 family in mES cells. Furthermore, CoCl2 led to the upregulation of Fas and Fas-ligand, which are the death receptor assemblies, as well as the cleavage of Bid in mES cells. These results suggest that CoCl2 induces apoptosis through both mitochondria- and death receptor-mediated pathways that are regulated by the Bcl-2 family in mES cells.

Effects of lanthanum ion modifications on the photoelectrochemical properties of ZnO nanorods-based dye-sensitized solar cells.

We investigated the photoelectrochemical effects on La ion-modified ZnO nanorods for dye-sensitized solar cells (DSSCs), preparing four kinds of samples grown in solutions with 0, 1, 2, and 3 at% of La precursors. It was found that La ion modifications lead to an increase in the lattice constant of ZnO nanorods, resulting in widening of their energy bandgap. I-V results tell that the photoelectrochemical properties increase in the order of 2, 1, 0, and 3 at% La ion-modified ZnO nanorod-based DSSCs. To further analyze and explain the experimental results, we measured absorbance, IPCE, and EIS and concluded that the DSSCs fabricated by using 3 at% La ion-modified ZnO nanorods exhibit better device performances such as Voc, Jsc, and efficiency, suggesting that the amount of La ions is a key parameter of La modified-DSSCs. The results can be explained by Burstein-Mott effects, vertical growth, and La oxide coating effects of the ZnO nanorods.

Laparoscopic excision of a urachal cyst containing large stones in an adult.

Stone-containing urachal cysts are extremely rare in adults. Here, we report the case of a 58-year-old man with a urachal cyst who had lower abdominal pain and urinary frequency. Abdominal ultrasonography and computed tomography showed hyperdense stones in the urachus. He was treated with a laparoscopic excision using a transperitoneal approach. The pathological diagnosis was an inflammed urachal cyst. This rare case illustrates an inflammed urachal cyst containing stones treated with laparoscopy.

Ambient atmosphere-processable, printable Cu electrodes for flexible device applications: structural welding on a millisecond timescale of surface oxide-free Cu nanoparticles.

Recently, various functional devices based on printing technologies have been of paramount interest, owing to their characteristic processing advantages along with excellent device performance. In particular, printable metallic electrodes have drawn attention in a variety of optoelectronic applications; however, research into printable metallic nanoparticles has been limited mainly to the case of an environmentally stable Ag phase. Despite its earth-abundance and highly conductive nature, the Cu phase, to date, has not been exploited as an ambient atmosphere-processable, printable material due to its critical oxidation problem in air. In this study, we demonstrate a facile route for generating highly conductive, flexible Cu electrodes in air by introducing the well-optimized photonic sintering at a time frame of 10(-3) s, at which the photon energy, rather than conventional thermal energy, is instantly provided. It is elucidated here how the surface oxide-free, printed Cu particulate films undergo chemical structural/microstructural evolution depending on the instantly irradiated photon energy, and a successful demonstration is provided of large-area, flexible, printed Cu conductors on various substrates, including polyimide (PI), polyethersulfone (PES), polyethylene terephthalate (PET), and paper. The applicability of the resulting printed Cu electrodes is evaluated via implementation into both flexible capacitor devices and indium-gallium-zinc oxide (IGZO) flexible thin-film transistors.

Formamide mediated, air-brush printable, indium-free soluble Zn-Sn-O semiconductors for thin-film transistor applications.

In this study, for high-performance indium-free metal oxide channel layer, we synthesize Zn-Sn-O (ZTO) precursor solutions in which formamide is incorporated as an additive for catalyzing the subsequent sol-gel reactions and the evolution of chemical structure. It is revealed that the formamide plays a critical chemical role in evolving a chemical structure with more oxygen-deficient oxide lattice and with less hydroxide, allowing for high field-effect mobility over 7 cm(2)/V·s. Furthermore, it is for the first time demonstrated that electrically active metal-oxide films can be patterned, using an air-brush printing technique, by directly depositing formamide-mediated ZTO-precursor solutions in patterned geometries.

EGCG induces apoptosis in human laryngeal epidermoid carcinoma Hep2 cells via mitochondria with the release of apoptosis-inducing factor and endonuclease G.

(-)-Epigallocatechin-3-gallate (EGCG), a major green tea polyphenol, was tested for in vitro cytotoxicity against human laryngeal epidermoid carcinoma of the larynx Hep2 cells. EGCG-induced apoptotic cell death accompanied by a change in the cell cycle. However, EGCG did not result in caspase activation, nor did a caspase inhibitor block cell death. Furthermore, EGCG caused no change in the intracellular levels of reactive oxygen species (ROS). The levels of p53 were increased in the EGCG-treated cells, with a corresponding decrease in Bcl-2 and Bid protein levels as well as an increase in the Bax level. In addition, EGCG induced the cytoplasmic release of cytochrome c from the mitochondria accompanied by a decreased mitochondrial membrane potential, and subsequently upregulated translocation of apoptosis-inducing factor (AIF) and endonuclease G (EndoG) into the nucleus during the apoptotic process. Taken together, these findings indicate that the p53-mediated mitochondrial pathway and the nuclear translocation of AIF and EndoG play a crucial role in EGCG-induced apoptosis of human laryngeal epidermoid carcinoma Hep2 cells, which proceeds through a caspase-independent pathway.

Antioxidant and antiinflammatory activities of xanthorrhizol in hippocampal neurons and primary cultured microglia.

Xanthorrhizol, a natural sesquiterpenoid isolated from the rhizome of Curcuma xanthorrhiza Roxb (Zingiberaceae), has antibacterial activities and protective effects against cisplatin-induced hepatotoxicity. In this study, we investigated the activities of xanthorrhizol as an antioxidant or antiinflammatory agent using neuronal and microglial cells. Xanthorrhizol had potent neuroprotective effects on glutamate-induced neurotoxicity and reactive oxygen species (ROS) generation in the murine hippocampal HT22 cell line. Also, xanthorrhizol inhibited H(2)O(2)-induced lipid peroxidation in rat brain homogenates. The properties of xanthorrhizol as an antiinflammatory agent were investigated in microglial activation by lipopolysaccharide. It reduced the expression of cyclooxygenase-2 and the inducible nitric oxide synthase, which consequently resulted in the reduction of nitric oxide. The production of proinflammatory cytokines, such as interleukin-6 and tumor necrosis factor-alpha in activated microglial cells, was reduced by xanthorrhizol. These results suggest that xanthorrhizol could be an effective candidate for the treatment of Alzheimer's disease- and other neurological disease-related ROS and inflammation.