Phosphor-converted light-emitting diodes (LEDs) have recently become a promising candidate for next-generation agricultural and horticultural-use devices. In principle, they can overcome the limitations of regular daily sunshine. Here, the principle...

Patients with long-standing diabetes frequently demonstrate gastric hypersensitivity with an unknown mechanism. The present study was designed to investigate roles for nuclear factor-B (NF-B) and the endogenous H 2 S-producing enzyme cystathionine-␤-synthetase (CBS) signaling pathways by examining cbs gene methylation status in adult rats with diabetes. Intraperitoneal injection of streptozotocin (STZ) produced gastric hypersensitivity in female rats in response to gastric balloon distention. Treatment with the CBS inhibitor aminooxyacetic acid significantly attenuated STZ-induced gastric hypersensitivity in a dose-dependent fashion. Aminooxyacetic acid treatment also reversed hyperexcitability of gastric-specific dorsal root ganglion (DRG) neurons labeled by the dye DiI in diabetic rats. Conversely, the H 2 S donor NaHS enhanced neuronal excitability of gastric DRG neurons. Expression of CBS and p65 were markedly enhanced in gastric DRGs in diabetic rats. Blockade of NF-B signaling using pyrrolidine dithiocarbamate reversed the upregulation of CBS expression. Interestingly, STZ treatment led to a significant demethylation of CpG islands in the cbs gene promoter region, as determined by methylation-specific PCR and bisulfite sequencing. STZ treatment also remarkably downregulated the expression of DNA methyltransferase 3a and 3b. More importantly, STZ treatment significantly enhanced the ability of cbs to bind DNA at the p65 consensus site, as shown by chromatin immunoprecipitation assays. Our findings suggest that upregulation of cbs expression is attributed to cbs promoter DNA demethylation and p65 activation and that the enhanced interaction of the cbs gene and p65 contributes to gastric hypersensitivity in diabetes. This finding may guide the development and evaluation of new treatment modalities for patients with diabetic gastric hypersensitivity.

Increasing demand for clean energy has motivated considerable effort to exploit the properties of various materials in photovoltaics and related solar-harvesting devices. [1] Splitting of water by sunlight to generate hydrogen is one of the forms of energy production with the most potential. Metal oxides such as TiO 2 , ZnO, and WO 3 with various morphologies have been investigated for use in splitting water. [2][3][4][5][6] However, most of these metal oxides have large band gaps, which limit light absorption in the visible region and overall efficiency. To reduce the band gaps of nanostructured metal oxides, doping and utilization of transition metals, carbon, or nitrogen have been investigated. [7][8][9] One possibility is the use of semiconductor nanocrystals, known as quantum dots (QDs), as an alternative to photosensitive dyes. Quantum dots generally offer various significant advantages over dyes. [10] It was recently established that QDs generate multiple electronhole pairs per photon, improving device efficiency. [11] Quantum dot sensitized nanostructures are widely studied for use in solar cells. [12,13] However, little work has been done on metal oxide and semiconductor QD-based composite structures for use in water-splitting nanodevices.To elucidate this fundamental issue, we examined a combination of CdTe QDs and ZnO nanowires for splitting water photoelectrochemically (Scheme 1). One-dimensional nanostructures offer the additional potential advantage of improved charge transport over zero-dimensional nanostruc-tures such as nanocrystals. [6] Additionally, the typical electron mobility in ZnO is 10-100 times higher than that in TiO 2 , so the electrical resistance is lower and the electron-transfer efficiency higher. [14] However, since the overall water-splitting reaction is tough, sacrificial reagents are commonly adopted to evaluate the photocatalytic activity for water splitting. When the photocatalytic reaction is carried out in an aqueous solution that contains a reductant, electron donors, or hole scavengers such as sulfide ions or selenium ions, photogenerated holes irreversibly oxidize the reductant rather than the water. Employment of CdTe QDs in water splitting system has major advantages. CdTe with a more favorable conduction band energy (E CB = À1.0 V vs. NHE) can inject electrons into ZnO faster than CdSe (E CB = À0.6 V vs. NHE). In addition, monolayer deposition of CdTe QDs on the surface of ZnO nanowires would further improve the stability in electrochemical reaction, by avoiding anodic decomposition/corrosion of CdTe and thus enhancing the overall watersplitting performance. During the photoirradiation of CdTe, two reactions can be expected to dominate after initial charge separation [Eqs. (1) and (2)]. [15] Anodic decomposition : CdTe ðe þ hÞ ! Cd 0 þ Te 0Anodic corrosion : CdTe ðhÞ ! Cd 2þ þ TeC ÀMonolayer deposition of QDs can facilitate transfer from CdTe to ZnO and improve QD stability, so that the efficiency in the overall water-splitting reaction can be exactly measured in aqu...

Painful diabetic neuropathy is a common complication of diabetes produced by mechanisms that as yet are incompletely defined. The aim of this study was to investigate the roles of nuclear factor-kB (NF-kB) in the regulation of purinergic receptor P2X ligand-gated ion channel 3 (P2X3R) plasticity in dorsal root ganglion (DRG) neurons of rats with painful diabetes. Here, we showed that hindpaw pain hypersensitivity in streptozocininduced diabetic rats was attenuated by treatment with purinergic receptor antagonist suramin or A-317491. The expression and function of P2X3Rs was markedly enhanced in hindpaw-innervated DRG neurons in diabetic rats. The CpG (cytosine guanine dinucleotide) island in the p2x3r gene promoter region was significantly demethylated, and the expression of DNA methyltransferase 3b was remarkably downregulated in DRGs in diabetic rats. The binding ability of p65 (an active form of NF-kB) with the p2x3r gene promoter region and p65 expression were enhanced significantly in diabetes. The inhibition of p65 signaling using the NF-kB inhibitor pyrrolidine dithiocarbamate or recombinant lentiviral vectors designated as lentiviral vector-p65 small interfering RNA remarkably suppressed P2X3R activities and attenuated diabetic pain hypersensitivity. Insulin treatment significantly attenuated pain hypersensitivity and suppressed the expression of p65 and P2X3Rs. Our findings suggest that the p2x3r gene promoter DNA demethylation and enhanced interaction with p65 contributes to P2X3R sensitization and diabetic pain hypersensitivity.

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