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Deep-ultraviolet (UV) light-emitting diodes (LEDs) based on AlGaN crystals have low light-emission efficiency; therefore, there is a need to improve this light-emission efficiency for a wide range of applications such as water and air sterilizations. UV-light-transparent device structures are considered one of the many solutions toward increasing light output power. To this end, the present study focused on developing a transparent AlGaN-based tunnel junction (TJ) as the anode of a deep-UV LED. Deep-UV LEDs composed of n+/p+-type AlGaN TJs were fabricated under the growth condition that reduced the carrier compensation in the n+-type AlGaN layers. The operating voltage was 10.8 V under the direct current (DC) operation of 63 A/cm2. In addition, magnesium zinc oxide (MgZnO)/Al reflective electrodes were fabricated to enhance the output power of the AlGaN homoepitaxial TJ LED. The output power was 57.3 mW under a DC operation of 63 A/cm2, and it was 1.7 times higher than that realized using the conventional Ti/Al electrodes. The combination of the AlGaN-based TJ and MgZnO/Al reflective contact allows further improvement of the light output power. This study confirms that the AlGaN TJ is a promising UV-transmittance structure that can obtain a high light-extraction efficiency.

Oral malignant melanoma, which frequently invades the hard palate or maxillary bone, is extremely rare and has a poor prognosis. Bone morphogenetic protein (BMP) is abundantly expressed in bone matrix and is highly expressed in malignant melanoma, inducing an aggressive phenotype. We examined the role of BMP signaling in the acquisition of an aggressive phenotype in melanoma cells in vitro and in vivo. In five cases, immunohistochemistry indicated the phosphorylation of Smad1/5 (p-Smad1/5) in the nuclei of melanoma cells. In the B16 mouse and A2058 human melanoma cell lines, BMP2, BMP4, or BMP7 induces morphological changes accompanied by the downregulation of E-cadherin, and the upregulation of N-cadherin and Snail, markers of epithelial-mesenchymal transition (EMT). BMP2 also stimulates cell invasion by increasing matrix metalloproteinase activity in B16 cells. These effects were canceled by the addition of LDN193189, a specific inhibitor of Smad1/5 signaling. In vivo, the injection of B16 cells expressing constitutively activated ALK3 enhanced zygoma destruction in comparison to empty B16 cells by increasing osteoclast numbers. These results suggest that the activation of BMP signaling induces EMT, thus driving the acquisition of an aggressive phenotype in malignant melanoma.

Bone invasion is a critical factor in determining the prognosis of oral squamous cell carcinoma (OSCC) patients. Transforming growth factor β (TGF-β) is abundantly expressed in the bone matrix and is involved in the acquisition of aggressiveness by tumors. TGF-β is also important to cytoskeletal changes during tumor progression. In this study, we examined the relationship between TGF-β signaling and cytoskeletal changes during bone invasion by OSCC. Immunohistochemical staining of OSCC samples from five patients showed the expression of p130Cas (Crk-associated substrate) in the cytoplasm and phosphorylated Smad3 expression in the nucleus in OSCC cells. TGF-β1 induced the phosphorylation of Smad3 and p130Cas, as well as epithelial–mesenchymal transition (EMT) accompanied by the downregulation of the expression of E-cadherin, a marker of epithelial cells, and the upregulation of the expression of N-cadherin, or Snail, a marker of mesenchymal cells, in human HSC-2 cells and mouse squamous cell carcinome VII (SCCVII) cells. SB431542, a specific inhibitor of Smad2/3 signaling, abrogated the TGF-β1-induced phosphorylation of p130Cas and morphological changes. Silencing p130Cas using an short hairpin RNA (shRNA) or small interfering RNA in SCCVII cells suppressed TGF-β1-induced cell migration, invasion, EMT and matrix metalloproteinase-9 (MMP-9) production. Compared with control SCCVII cells, SCCVII cells with silenced p130Cas strongly suppressed zygomatic and mandibular destruction in vivo by reducing the number of osteoclasts, cell proliferation and MMP-9 production. Taken together, these results showed that the expression of TGF-β/p130Cas might be a new target for the treatment of OSCC bone invasion.

We demonstrated the structural optimization of AlGaN tunnel junction (TJ) deep-ultraviolet light-emitting diodes by changing the thickness and impurity concentrations of p+-type and n+-type AlGaN constituting the TJ. By decreasing the total thickness of the TJ to 23 nm, the operating voltage reached a minimum of 8.8 V at 63 A cm−2. Further decrease in TJ thickness markedly increases the operating voltage. This finding implies that the depletion layer width becomes greater than the TJ thickness if it is smaller than 12 nm. Therefore, we conclude that the TJ thickness must be greater than the depletion layer width.

In this study, we enhanced the emission power of AlGaN-based tunnel junction deep-ultraviolet LEDs (TJ LEDs) by using a MgZnO and aluminum stacked structure as UV reflective electrodes on the anode side. The emission wavelength of the fabricated TJ LED was 284 nm, and the emission power was 57.3 mW at 63 A cm−2. The polycrystalline MgZnO enabled both conductivity and UV transmittance to be achieved, approximately doubling with a reflectance of the fabricated TJ LED at 284 nm compared to conventional TJ LED with Ti/Al. These factors contributed to the increased emission power of TJ LEDs.

We analyzed the p–n junction of an aluminum gallium nitride (AlGaN) homojunction tunnel junction (TJ) deep-ultraviolet light-emitting diode by phase-shifting electron holography. We clearly obtained a phase image reflecting the band alinement of the p–n homojunction and derived a depletion layer width of approximately 10 nm. In addition, the observed depletion layer width for the AlGaN TJ was in good agreement with the simulated one reflecting the diffusion profile of Mg and Si, thus enabling a discussion on the electrical conduction mechanism for an AlGaN p–n junction.

AlGaN-based ultraviolet light-emitting diodes (UV-LEDs) are key components for the inactivation of viruses. Highly efficient and high-power UV-LEDs, capable of inactivating viruses in a short time, are in demand. For this purpose, the growth technologies of n-type AlGaN contact layers were developed from two points of view: first, to decrease the resistivity of n-type Al0.62Ga0.38N by minimizing the electron compensation, resulting in electronic degeneracy with metallic conduction;second, to improve the light emission uniformity in AlGaN multiquantum wells (MQWs) by controlling the morphology of the underlying n-type AlGaN layer to inhibit macrostep formation. A UV-LED module emitting at 275 nm was demonstrated with the developed growth technology, and illuminated with an irradiation power of 2.6 mW cm(-2) on SARS-CoV-2 samples. Over 99.999 % of viruses were inactivated within 5 s owing to the high power of this module.

Invited for this month's cover picture is the group of Dr. Satoko Hayashi at Faculty of Systems Engineering and Chemistry at Wakayama University. The cover picture shows the linear Se(16) σ(16c–30e) interactions, illustrated by the molecular graph type on the optimized structure of the dicationic octamer of 1,5‐(diselena)cane. HOMO‐1 of ψ(462) is drawn on the structure, which is located predominantly on the Se atoms. The optimized structure is stable, due to the nice engagement between the (CH(2))(3) moieties. The contour maps of ρ(r) are also drawn on the molecular C (s) planes of the dicationic dimer and trimer to demonstrate clearly the existence of the interactions between Se atoms. Read the full text of their Full Paper at 10.1002/open.202100017.

We previously demonstrated that the immunostimulatory activity of CpG DNA is increased by the formation of polypod-like structures. The present study was designed to elucidate the mechanism underlying this increase. Tripodna (three pods) and hexapodna (six pods) were prepared. The cellular uptake of Alexa Fluor 488-labeled DNA samples was examined in several cell lines by measuring the MFI of cells. TNF-α release from RAW264.7 cells was measured after addition of polypodna containing CpG motifs. Dissociation of double stranded DNA was evaluated using FRET. Tripodna and hexapodna were efficiently taken up by macrophage-like RAW264.7 cells and dendritic DC2.4 cells, but not by fibroblast or endothelial cell lines. The uptake by RAW264.7 cells was highest for hexapodna, followed by tripodna, dsDNA, and ssDNA. The release of TNF-α from RAW264.7 cells was also highest for hexapodna. The ratio of TNF-α release to cellular uptake was highest for ssDNA, and lowest for dsDNA. Tripodna and hexapodna were more easily dissociated into single strands after cellular uptake than was dsDNA. The efficient cellular uptake and prompt dissociation into single strands can be directly related to the high immunostimulatory activity of polypod-like structured DNAs containing CpG motifs.

Odontomas, developmental anomalies of tooth germ, frequently occur in familial adenomatous polyposis patients with activated Wnt/β-catenin signaling. However, roles of Wnt/β-catenin signaling in odontomas or odontogenic cells are unclear. Herein, we investigated β-catenin expression in odontomas and functions of Wnt/β-catenin signaling in tooth germ development. β-catenin frequently accumulated in nucleus and/or cellular cytoplasm of odontogenic epithelial cells in human odontoma specimens, immunohistochemically. Wnt/β-catenin signaling inhibited odontogenic epithelial cell proliferation in both cell line and tooth germ development, while inducing immature epithelial bud formation. We identified Semaphorin 3A (Sema3A) as a downstream molecule of Wnt/β-catenin signaling and showed that Wnt/β-catenin signaling-dependent reduction of Sema3A expression resulted in suppressed odontogenic epithelial cell proliferation. Sema3A expression is required in appropriate epithelial budding morphogenesis. These results suggest that Wnt/β-catenin signaling negatively regulates odontogenic epithelial cell proliferation and tooth germ development through decreased-Sema3A expression, and aberrant activation of Wnt/β-catenin signaling may associate with odontoma formation.

Electronic degeneracy to express metallic conduction in Al-rich AlGaN for the electron injection layer enhances the efficiencies of deep ultraviolet light emitters. This study systematically demonstrates the Si doping range and conditions to realize degenerate n-type Al0.6Ga0.4N layers based on the electron compensation effect. The temperature-independent electron concentrations resulting from the degenerate band appear in high Si doping conditions to overcome the electron compensation due to carbon on nitrogen sites (CN). However, excessive Si doping of over 4.0 × 1019 cm−3 leads to the collapse of the electronic degeneracy and a switch to the temperature-dependent electron transport via the impurity bands, where the luminescence bands originating from III vacancy-Si complexes (VIII-nSi) are dominant. The key parameter is the effective donor concentration, Nd − Na, based on the reduction in electron concentrations via acceptor-like deep levels such as CN and VIII-nSi. The Hall-effect analyses for n-type Al0.6Ga0.4N layers with various Si concentrations yielded an Nd − Na value of (9.5 ± 2.9) × 1018 cm−3 to vanish the ionization energy of Si donors, which is approximately six times higher than that in GaN. The results suggest not only the optimal doping range to obtain an Al-rich AlGaN layer with metallic conduction but also the necessity of the growth condition to minimize electron compensation.

Abnormal expression of Facioscapulohumeral muscular dystrophy (FSHD) region gene 1 (FRG1) is involved in the pathogenesis of FSHD. FRG1 is also important for the normal muscular and vascular development. Our previous study showed that FRG1 is one of the highly expressed genes in the mandible on embryonic day 10.5 (E10.5) than on E12.0. In this study, we investigated the temporospatial expression pattern of FRG1 mRNA and protein during the development of the mouse lower first molar, and also evaluated the subcellular localization of the FRG1 protein in mouse dental epithelial (mDE6) cells. The FRG1 expression was identified in the dental epithelial and mesenchymal cells at the initiation and bud stages. It was detected in the inner enamel epithelium at the cap and early bell stages. At the late bell and root formation stages, these signals were detected in ameloblasts and odontoblasts during the formation of enamel and dentin matrices, respectively. The FRG1 protein was localized in the cytoplasm in the mouse tooth germ in vivo, while FRG1 was detected predominantly in the nucleus and faintly in the cytoplasm in mDE6 cells in vitro. In mDE6 cells treated with bone morphogenetic protein 4 (BMP4), the protein expression of FRG1 increased in cytoplasm, suggesting that FRG1 may translocate to the cytoplasm. These findings suggest that FRG1 is involved in the morphogenesis of the tooth germ, as well as in the formation of enamel and dentin matrices and that FRG1 may play a role in the odontogenesis in the mouse following BMP4 stimulation.

The formation mechanism of Ga-rich streaks in the AlGaN layers formed at macro-step edges was investigated by analyzing AlGaN layers grown by metalorganic vapor phase epitaxy on AlN/sapphire-templates. Energy dispersive X-ray spectroscopy in the cross-sectional scanning transmission electron microscopy revealed that the macro-steps formed during AlN growth were maintained through the upper AlGaN layer. This can be explained by the less interaction between adjacent macro-steps due to the sufficiently smaller surface diffusion lengths of Ga and Al species than the inter-macro-step distance of submicron to a few microns. Moreover, atomic force microscopy indicated that the apparent smooth region between macro-steps involved many atomic steps and terrace width of a few ten nanometers which may be the actual scale of the diffusion lengths. At the macro-step edge, facets that are different from a c-plane are formed. The higher incorporation efficiency of Ga atoms on these facets compared with that of the c-plane likely led to the formation of Ga-rich streaks due to the less inter-surface diffusion between the facets and c-plane regions. We demonstrated AlGaN growth without Ga-rich streaks using the flattened AlN/sapphire-template by polishing; this resulted in the achievement of homogeneous emission energies in AlGaN-based quantum wells.

We have been investigating the potential use of cell-penetrating peptide-linked polymers as a novel penetration enhancer. Since previous in vivo studies demonstrated that poly(N-vinylacetamide-co-acrylic acid) bearing D-octaarginine, a typical cell-penetrating peptide, enhanced membrane permeation of biomolecules, its potential as an in vitro transfection tool was evaluated in this study. A plasmid DNA encoding green fluorescent protein (pGFP-C1), β-galactosidase, and bovine serum albumin (BSA) were used as model biomolecules. Anionic pGFP-C1 interacted electrostatically with cationic d-octaarginine-linked polymers. When the ratio of mass concentration of polymers to that of pGFP-C1 reached 2.5, complexes whose size and zeta potential were approximately 200 nm and 15 mV, respectively, were obtained. GFP expression was observed in cells incubated with complexes prepared under conditions in which the polymer/pDNA concentration ratio exceeded 2.5. The expression level elevated with an increase in the concentration ratio, but physicochemical properties of the complexes remained unchanged. Results suggested that free polymers contributed to pGFP-C1 internalization. Another cell study demonstrated that β-galactosidase premixed with polymers was taken up into cells in its active tetrameric form. Similar electrostatic interaction-driven complex formation was observed for BSA charged negatively in neutral solution. However, it appeared that the internalization processes of BSA differed from those of pGFP-C1. A mass concentration-dependent increase in internalized BSA was observed, irrespective of the polymer/protein concentration ratio. Due to frail interactions, polymers that were released from the complexes and subsequently immobilized on cell membranes might also contribute to membrane permeation of BSA.

In previous studies by our group, we reported that thymosin beta 4 (Tb4) is closely associated with the initiation and development of the tooth germ, and can induce the expression of runt-related transcription factor 2 (RUNX2) during the development of the tooth germ. RUNX2 regulates the expression of odontogenesis-related genes, such as amelogenin, X-linked (Amelx), ameloblastin (Ambn) and enamelin (Enam), as well as the differentiation of osteoblasts during bone formation. However, the mechanisms through which Tb4 induces the expression of RUNX2 remain unknown. In the present study, we employed a mouse dental epithelial cell line, mDE6, with the aim to elucidate these mechanisms. The mDE6 cells expressed odontogenesis-related genes, such as Runx2, Amelx, Ambn and Enam, and formed calcified matrices upon the induction of calcification, thus showing characteristics of odontogenic epithelial cells. The expression of odontogenesis-related genes, and the calcification of the mDE6 cells were reduced by the inhibition of phosphorylated Smad1/5 (p-Smad1/5) and phosphorylated Akt (p-Akt) proteins. Furthermore, we used siRNA against Tb4 to determine whether RUNX2 expression and calcification are associated with Tb4 expression in the mDE6 cells. The protein expression of p-Smad1/5 and p-Akt in the mDE6 cells was reduced by treatment with Tb4-siRNA. These results suggest that Tb4 is associated with RUNX2 expression through the Smad and PI3K-Akt signaling pathways, and with calcification through RUNX2 expression in the mDE6 cells. This study provides putative information concerning the signaling pathway through which Tb4 induces RUNX2 expression, which may help to understand the regulation of tooth development and tooth regeneration.

The dynamic and static nature of extended hypervalent interactions of the BE···AE···AE···BE type are elucidated for four center–seven electron interactions (4c–7e) in the radical cationic dimers (1·+) and 4c–6e in the dicationic dimers (12+) of 1,5-(dichalcogena)canes (2: AE(CH2CH2CH2)2BE: AE, BE = S, Se, Te, and O). The quantum theory of atoms-in-molecules dual functional analysis (QTAIM-DFA) is applied for the analysis. Total electron energy densities Hb(rc) are plotted versus Hb(rc) – Vb(rc)/2 [= (ℏ2/8m)∇2ρb(rc)] at bond critical points (BCPs) of the interactions, where Vb(rc) values show potential energy densities at BCPs. Data from the fully optimized structures correspond to the static nature of the interactions. Those from the perturbed structures around the fully optimized ones are also plotted, in addition to those of the fully optimized ones, which represent the dynamic nature of interactions. The BE···AE–AE···BE interactions in 12+ are stronger than the corresponding ones in 1·+, respectively. ...

Previous studies have shown that the recombination of cells liberated from developing tooth germs develop into teeth. However, it is difficult to use human developing tooth germ as a source of cells because of ethical issues. Previous studies have reported that thymosin beta 4 (Tmsb4x) is closely related to the initiation and development of the tooth germ. We herein attempted to establish odontogenic epithelial cells from non-odontogenic HaCaT cells by transfection with TMSB4X. TMSB4X-transfected cells formed nodules that were positive for Alizarin-red S (ALZ) and von Kossa staining (calcium phosphate deposits) when cultured in calcification-inducing medium. Three selected clones showing larger amounts of calcium deposits than the other clones, expressed PITX2, Cytokeratin 14, and Sonic Hedgehog. The upregulation of odontogenesis-related genes, such as runt-related transcription factor 2 (RUNX2), Amelogenin (AMELX), Ameloblastin (AMBN) and Enamelin (ENAM) was also detected. These proteins were immunohistochemically observed in nodules positive for the ALZ and von Kossa staining. RUNX2-positive selected TMSB4X-transfected cells implanted into the dorsal subcutaneous tissue of nude mice formed matrix deposits. Immunohistochemically, AMELX, AMBN and ENAM were observed in the matrix deposits. This study demonstrated the possibility of induction of dental epithelial cell differentiation marker gene expression in non-odontogenic HaCaT cells by TMSB4X.

Keratin 17 (KRT17) has been suggested as a potential diagnostic marker of squamous cell carcinoma including oral squamous cell carcinoma (OSCC). The current study was conducted to clarify the function of KRT17 and its expression mechanism in OSCC. Immunohistochemical analyses were carried out to examine the expression of KRT17, GLI family zinc finger (GLI)-1, GLI-2, or cleaved caspase-3 in OSCCs. The expression of KRT17, GLI-1, or GLI-2 was investigated among OSCC cell lines, and the effects of loss-of-function of KRT17 or GLI, using siRNA or inhibitor, on the cell growth of the OSCC cell line HSC-2 particularly with respect to apoptosis were examined. Immunohistochemical analyses of tissue specimens obtained from 78 OSCC patients revealed that KRT17 was not observed in non-tumor regions but was strongly expressed at high frequencies in tumor regions. Knockdown of KRT17 increased the number of cleaved caspase-3-positive cells, leading to the reduction of cell number. Loss-of-function of GLI-1 or GLI-2 also increased the cell numbers of apoptotic cells positive for staining of Annexin-V and propidium iodide (PI) and the terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling (TUNEL) method, and induced DNA fragmentation. This inhibitory effect on cell growth was partially rescued by exogenous KRT17 expression. In the KRT17-positive regions in OSCCs, GLI-1 or GLI-2 was frequently detected, and the number of cells with cleaved caspase-3 positive was decreased. KRT17 promotes tumor cell growth, at least partially, through its anti-apoptotic effect as a result of the KRT17 overexpression by GLIs in OSCC.

Interest in implantable microchips for medical sensors is increasing. To reduce the invasiveness of implantation, wireless data transmission in a living body is an important issue shared by all such sensors. Here, the authors report on a light-based wireless data transmission method for implantable biomedical sensor chips. An implantable micro-sized image sensor (400 × 1200 μm2) that was designed to modulate a small light-emitting diode (λ = 855 nm) with pulse-width modulation for intra-vital optical communication (IOC) was developed. Both a transmitter device and a receiver device for IOC were prepared, and optical image data transmission through biological tissue (a mouse skull bone) was successfully demonstrated.

We deposited a 4-inch crack-free aluminum nitride (AlN) layer on a flat sapphire substrate and a patterned sapphire substrate grown using metal-organic vapor phase epitaxy method. To use the 4-inch sapphire substrate, we introduce air voids in the AlN layer in the initial growth region. Moreover, we discovered that optical absorption exists in the AlN layer with air voids. The secondary ion mass spectrometry (SIMS) results show that the impurity concentrations are high at the regions where the air voids exist, though the growth conditions are same throughout the AlN layer. We considered that it is most probable that the optical absorption is mainly attributed to the complexes of Al and O. The origin of the optical absorption was identified as a deep emission band due to impurities such as carbon and oxygen around the air voids. In this study, it was possible to obtain a transparent AlN template without air voids by changing the growth conditions and the layer structure. In addition, we could further suppress the underlying layer with the air voids.

This study presents the expression pattern and functions of thymosin beta 10 (Tbeta10), a Tbeta4 homologue during the development of mouse lower first molars. An in situ signal of Tbeta10 was detected on embryonic day 10.5 (E10.5)-E15.5 mainly in dental mesenchymal cells as well as in dental epithelial cells, while Tbeta4 was expressed in dental epithelial cells. In the late bell stage, preodontoblasts with strong Tbeta10 expression and preameloblasts with strong Tbeta4 expression exhibited face-to-face localization, suggesting that an intimate cell-cell interaction might exist between preodontoblasts and preameloblasts to form dentin and enamel matrices. A strong Tbeta10 signal was found in odontoblasts in the lateral side of the dental pulp and in Hertwig’s epithelial root sheath, thus suggesting that Tbeta10 participates in the formation of the outline of the tooth root. An inhibition assay using Tbeta10-siRNA in E11.0 mandibles showed significant growth inhibition in the tooth germ. The Tbeta10-siRNA-treated E15.0 tooth germ also showed significant developmental arrest. The number of Ki67-positive cells significantly decreased in the Tbeta10-siRNA-treated mandibles. The cellular proliferative activity was also significantly suppressed in Tb10-siRNA-treated cultured mouse dental pulpal and epithelial cells. These results indicate that developmental arrest of the tooth germ might be caused by a reduction in cell proliferative activity. The stage-specific temporal and spatial expression pattern of Tbeta10 in the developing tooth germ is indicative of multiple functions of Tbeta10 in the developmental course from initiation to root formation of the tooth germ.

Thymosin beta-4 (Tβ4) is known to be ubiquitously involved in the actin monomer sequestering on the cytoskeleton. Our previous study showed specific temporal and special in situ expression pattern of Tβ4 mRNA in dental epithelial and mesenchymal cells in the developing tooth germ of the mouse lower first molar. In this study, we examined the functional implications of Tβ4 in the developmental course of the mouse lower first molar. An inhibition assay using Tβ4 antisense sulfur-substituted oligodeoxynucleotide (AS S-ODN) in cultured embryonic day 11.0 (E11.0) mandibles showed a significant growth inhibition of the tooth germ. However, no growth arrest of the cultured E15.0 tooth germ was observed by using Tβ4 AS S-ODN. The Tβ4 knockdown led to significantly decreased expression levels of type II/III runt-related transcription factor 2 (Runx2) and nucleolin (Ncl) in the cultured E11.0 mandibles. Since our previous studies proved that the inhibition of type II/III Runx2 and Ncl translations resulted in the developmental arrest of the tooth germ in the cultured E11.0 mandible, Tβ4 appears to play roles in tooth germ development via the regulation of the type II/III Runx2 and Ncl expressions. Tβ4 knockdown also resulted in decreased secretion of matrix metalloproteinase (Mmp)-2, a reduced cell motility activity and upregulation of E-cadherin in dental epithelial mDE6 cells. These results suggest that Tβ4 plays multiple functional roles in odontogenic epithelial cells in the early stages of tooth germ development by regulating the expression of odontogenesis-related genes.

Interleukin (IL)-22 is a member of the IL-10 family. Its main targets are epithelial cells, not immune cells. We examined IL-22 signal transduction in oral squamous cell carcinoma (OSCC) cells. Immunohistochemical staining revealed that IL-22R was expressed more highly in OSCC compared to normal regions. An IL-22R signal was also observed in metastatic OSCC cells in the lymph node. RT-PCR showed that the human OSCC cell lines MISK81-5, HSC-3, HSC-4, SAS and SQUU-B expressed IL-22 receptor chains. Immunoblotting showed that IL-22 induced a transient tyrosine phosphorylation of STAT3 (pY705-STAT3) in MISK81-5 cells. The change in the serine phosphorylation of STAT3 was subtle during the examination periods. Simultaneously, pY705-STAT3 activation in HSC-3 cells was undetectable after IL-22 stimulation. Immunocytochemistry demonstrated that IL-22 induced the translocation of phosphorylated STAT3 into the nucleus of MISK81-5 cells. IL-22 temporarily upregulated the expression of anti-apoptotic and mitogenic genes such as Bcl-x, survivin and c-Myc, as well as SOCS3. IL-22 transiently activated ERK1/2 and induced a delayed phosphorylation of p38 MAP kinase, but negligibly involved the activation of NF-κB in MISK81-5 cells. MISK81-5 and SQUU-B cells treated with IL-22 showed mild cellular proliferation. MISK81-5, HSC-4 and SAS cells treated with IL-22 downregulated the keratinocyte differentiation-related genes compared with unstimulated cells. Conversely, STAT3 suppression by STAT3 siRNA strongly disrupted the downregulation of these genes by IL-22, but it did not significantly affect the activation of ERK1/2 by IL-22. The OSCC cells used in this study upregulated the expression of SERPINB3/4 (SCCA1/2), well-known SCC markers, following treatment with IL-22. These results indicate that IL-22 differentially activates the STAT3 signaling system depending on the type of OSCC. IL-22 may therefore play a role in tumor growth, cell differentiation and progression through STAT3-dependent and -independent pathways.

Periodontal tissue deteriorates under persistent oxidative stress induced by inflammatory reactions in the microflora of the oral cavity. This study aimed to evaluate the cellular properties of mouse gingival fibroblasts (MGFs) in the presence of oxidative stress. MGFs from 10-, 30- and 52-week-old mice were used to evaluate the changes in the cellular properties with aging. The study investigated the effects of oxidative stress on the cellular properties of MGFs from 10-week-old mice. The expression of p53, p21 and murine double minute 2 (Mdm2) in the MGFs in response to oxidative stress was also examined. By day 8, the number of MGFs increased in culture. However, the increase was markedly lower in MGFs derived from aged mice. Oxidative stress due to hydrogen peroxide (H2O2)-induced morphological changes characterized by a round shape with enlarged nuclei and expanded cytoplasm. The cell number of MGFs was decreased subsequent to treatment with 50 µM or a higher concentration of H₂O₂. MGFs treated with H₂O₂ at 20 µM showed a similar cell growth curve as the one seen in 52-week-old mice. Phosphorylated p53 protein was increased in MGFs subsequent to treatment with 20 µM H2O2, along with an upregulated transcription of p21 and Mdm2 mRNAs. These results suggest that treatment with a lower concentration of H₂O₂ in MGFs induces cell cycle arrest, resulting in stress-induced premature senescence, possibly correlated with the development of periodontal diseases.

A transmission queuing scheme is described that increases downlink throughput on wireless local area networks (WLANs) while also increasing the total throughput. When the amount of uplink traffic increases on a WLAN, the carrier sense multiple access with collision avoidance (CSMA/CA) protocol, which is the prescribed scheme for IEEE 802.11 WLAN channel access, may substantially reduce the rate of downlink data frame transmission. This results in severe throughput degradation for mobile stations with downlink traffic. The proposed scheme comprises a transmission control function based on consecutive transmission, as described in the IEEE 802.11e standard, and a dynamic queue prioritization algorithm. Simulation results demonstrate that the proposed scheme increases the maximum total throughput for uplink and downlink traffic by 17% compared with the conventional distributed coordination function (DCF) scheme and that it reduces the difference between uplink and downlink throughput. In an environment where transmission errors occur, the difference in throughput is reduced by about 50% compared with the conventional schemes.

The crystalline quality of GaN and Al0.08Ga0.92N epitaxial layers on (100) β-Ga2O3 substrates was significantly improved by the facet-controlled growth method. The facets were controlled by changing the nitrogen ambient thermal annealing temperature. We demonstrated the high-crystalline-quality GaN and Al0.08Ga0.92N on β-Ga2O3 substrates, which were comparable to GaN and AlGaN on sapphire substrates using low-temperature buffer layers. This method is useful for the fabrication of vertical-type ultraviolet (UV) light-emitting diodes (LEDs) on β-Ga2O3 substrates. (© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

We previously performed cDNA subtraction between the mouse mandibles on embryonic day 10.5 (E10.5) in the pre-initiation stage of the odontogenesis and E12.0 in the late initiation stage to identify genes expressed at its beginning. Adenosine triphosphate synthase subunit a (Atpase6) is one of the highly expressed genes in the E12.0 mandible including tooth germs. In situ hybridization was conducted using the mouse mandibular first molar from E10.5 to E18.0 to determine the precise expression patterns of Atpase6 mRNA in the developing tooth germ. Atpase6 mRNA was strongly expressed in the presumptive dental epithelium and the underlying mesenchyme at E10.5, and in the thickened dental epithelium at E12.0 and E13.0. Strong in situ signals were observed in the epithelium at E14.0, and in the enamel organ excluded the area of the primary enamel knot at E15.0. Atpase6 was strongly expressed in the inner enamel epithelium, the adjacent stratum intermedium, and the outer enamel epithelium in the cervical loops from E16.0 to E18.0. In addition, strong Atpase6 signals were coincidently demonstrated in various developing cranio-facial organs. These results suggest that Atpase6 participates in the high energy-utilizing functions of the cells related to the initiation and the development of the tooth germ as well as those of the other cranio-facial organs.

We previously performed cDNA subtraction between the mouse mandibles at embryonic day 10.5 (E10.5) and E12.0 to make a profile of the regulator genes for odontogenesis. Fifteen kDa interferon alpha responsive gene (Ifrg15) is one of several highly-expressed genes in the E12.0 mandible. The current study examined the precise expression patterns of Ifrg15 mRNA in the mouse mandibular first molar by in situ hybridization to evaluate the possible functional roles of this gene in odontogenesis. Ifrg15 mRNA was expressed in the epithelial and mesenchymal tissues of the mandible at E10.5 and E12.0. The Ifrg15 in situ signal was detected in the epithelial bud and the surrounding mesenchyme at E14.0, and was present in the enamel organ including the primary enamel knot, and in the underlying mesenchyme at E15.0. The in situ signal was restricted in the inner and outer enamel epithelia and the stratum intermedium at E16.0. The signal of Ifrg15 mRNA was further restricted to the inner enamel epithelium and the adjacent stratum intermedium at E17.0 and E18.0. Consequently, the expression of Ifrg15 mRNA was localized in the ameloblasts and odontoblasts at postnatal days 1.0 to 3.0. However, the in situ signal was markedly weaker than at the embryonic period. The expression of Ifrg15 mRNA was coincidently observed in various craniofacial organs as well as in the tooth germ. These results suggest that Ifrg15 is closely related to odontogenesis, especially the differentiation of the ameloblasts and odontoblasts, and to the morphogenesis of the craniofacial organs.

We demonstrated activation annealing of Mg-doped p-type Al 0.17 Ga 0.83 N in different gases. The hole concentration of Al 0.17 Ga 0.83 N annealed in oxygen is higher than that annealed in nitrogen or air. A hole concentration of 1.3 × 10 16 cm -3 at room temperature was achieved by annealing in oxygen flow at 900 °C. Secondary ion mass spectroscopy shows that hydrogen dissociation from Mg-doped Al 0.17 Ga 0.83 N is found to be enhanced by annealing in a flow of oxygen, compared with annealing in a flow of nitrogen. We confirmed the effect of activation annealing in oxygen flow on the performance of UV light-emitting diode (LED). At a DC current of 100 mA, the output power of the LED annealed in oxygen flow at 900 °C is four times higher than that of the LED annealed in nitrogen flow at 800 °C.

Galectin-3 is a beta-galactoside-binding animal lectin having pleiotropic effects on cell growth, differentiation, and apoptosis. This lectin has been shown to be involved in phagocytosis by macrophages and in inflammation. Here we investigated an involvement of galectin-3 in the regulatory process of inflammatory bone resorption in rats with adjuvant-induced arthritis (AA rats) accompanying severe bone destruction in the ankle joints. The protein level of galectin-3 in the ankle-joint extracts was markedly augmented at week 3 after adjuvant injection, at the time when severe bone destruction was observed. Immunohistochemical analysis revealed an extremely high expression of galectin-3 in macrophages and granulocytes infiltrated in the area of severe bone destruction. To estimate the role of galectin-3 in osteoclastogenesis and osteoclastic bone resorption, recombinant galectin-3 was added to in vitro culture systems. Galectin-3 markedly inhibited the formation of osteoclasts in cultures of murine osteoclast precursor cell line as well as in rat bone marrow culture systems. This inhibition was not observed by heat-inactivated galectin-3 or by galectin-7. Although recombinant galectin-3 did not affect signaling through mitogen-activated protein kinase (MAPK) or nuclear factor-kappaB (NF-kappaB), it specifically suppressed the induction of nuclear factor of activated T-cells c1 (NFATc1). Galectin-3 significantly inhibited dentine resorption by mature osteoclasts in vitro. Furthermore, in vivo studies clearly showed a significant suppression of bone destruction and osteoclast recruitment accompanying arthritis, when galectin-3 was injected into the cavity of ankle joint of AA rats. Thus, abundant galectin-3 observed in the area of severe bone destruction may act as a negative regulator for the upregulated osteoclastogenesis accompanying inflammation to prevent excess bone destruction.

Periapical granulomas contain a large number of T lymphocytes and monocytes/macrophages and a small number of B lymphocytes and polymorphonuclear leukocytes. Sections from eight periapical granulomas were stained by a variety of immunohistochemical methods. The vascular endothelial cells stained positively for intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. Helper T cells were identified by immunostaining for CD4 and stained positively for interferon-gamma (IFN-gamma). However, CD4-positive T cells did not stain for interleukin-4 (IL-4). Monocytes/macrophages were identified by immunostaining for CD68 and stained positively for IL-1alpha or inducible nitric oxide synthase (iNOS). IL-1beta could not be detected in the same samples. No cytokine expression was observed in B cells identified by immunostaining for CD20. IFN-gamma- and iNOS-positive cells could not be detected in clinically healthy periodontal ligament being used as a negative control. These results suggest that the IFN-gamma-producing T cells and iNOS-positive cells may modulate the progress of disease in local inflammation sites such as in periapical granulomas.