CP-safe Gravity Mediation and Muon g-2

We propose a CP-safe gravity mediation model, where the phases of the Higgs B parameter, scalar trilinear couplings and gaugino mass parameters are all aligned. Since all dangerous CP violating phases are suppressed, we are now safe to consider low-energy SUSY scenarios. As an application, we consider a gravity mediation model explaining the observed muon $g-2$ anomaly. The CP-safe property originates in two simple assumptions: SUSY breaking in the K\"ahler potential and a shift symmetry of a SUSY breaking field $Z$. As a result of the shift symmetry, the imaginary part of $Z$ behaves as a QCD axion, leading to an intriguing possibility: the strong CP problem in QCD and the SUSY CP problem are solved simultaneously.Comment: 23 pages, 2 figures; v2 with additional explanation

ゾウゲガ サイボウ ノ ブンカ ト サイボウガイ キシツ

Tooth development is a complex process that includes interactions between oral epithelium-derived dental epithelial cells and neural crest-derived dental mesenchymal cells. In this process, the basement membrane at the epithelial-mesenchymal interface plays important roles in matrix-mediated cell interactions and for trapping growth factors, then dental epithelial and mesenchymal cells differentiate into enamel-forming ameloblasts and dentin-forming odontoblasts, respectively. For enamel and dentin formation, these cells produce large amounts of extracellular matrixes, thus cell-matrix and cell-cell interactions are crucial for both ameloblast and odontoblast differentiation. In this review, we focus on the role of the extracellular matrix in odontoblast differentiation. Dentin and bone are similar in several aspects, such as extracellular matrix composition and genetic diseases, which affect both bone and dentin mineralization, common between them. However, the process of odontoblast differentiation is completely different from that of osteoblast differentiation. For better understanding of tooth development, it is important to elucidate the differences between these cell types

Dental pulp stem cell factors for treating RISR

Radiation-induced skin ulceration is a frequent complication of radiotherapy for cancer treatment. Stem cells from human exfoliated deciduous teeth (SHEDs) can regenerate various tissues. In this study, we investigated the impact of SHED-conditioned media (SHED-CM) on radiation-induced ulceration. Mouse necks were locally irradiated with a single dose of 15 Gy of radiation. A week after the irradiation, most of the wild-type mice generated ulcer surrounded by severe erythema. Intra-venous administration of SHED-CM effectively inhibited the ulcer formation. Histological examination revealed that SHED-CM treatment inhibited radiation-induced dermal thickness and epithelial hyperplasia. SHED-CM could be a useful treatment option for radiation-induced skin ulceration

Allergic Oral Mucositis due to Musical Instrument Metal : A Case Report

金属アレルギーとは金属が皮膚や粘膜に接触し，その部位から溶出した金属イオンが体内に取り込まれることで起きるアレルギー反応である。今回われわれは，楽器のチューバのマウスピースによる金属アレルギーが原因と疑われる口腔粘膜炎を発症した1例を経験したのでその概要を報告する。 患児は10歳8か月女児。小学校の金管バンドクラブに所属して以降，歯肉の腫脹や口腔内の炎症所見を認めたため，近医にてパッチテストや血液検査を施行されるも金属アレルギーおよび自己免疫疾患は否定された。当科初診時には，唇頰側歯肉と頰粘膜に軽度自発痛ならびに発赤を伴う瀰漫性腫脹を認めた。歯肉は易出血性で，増殖し仮性ポケットが形成されていた。歯周病原細菌検査にて歯周病原細菌は基準値以下であった。歯肉増殖部位の病理組織検査は，歯肉炎の診断であり口腔衛生指導を徹底したが，症状の改善はみられなかった。ところが，楽器（チューバ）とマウスピースの変更を契機に口腔内の炎症が劇的に改善し，その1か月後には，健全な口腔粘膜の状態を呈していた。新旧のマウスピースを比較したところ，旧マウスピースではめっきが剥がれている箇所が多数みられた。金属組成分析ならびに金属パッチテスト検査を行ったところ，Crにアレルギーがある可能性が高いことが明らかとなり，金属アレルギーが原因で引き起こされた口腔粘膜炎と診断した。口腔内はマウスピースの変更以降，良好な状態が継続している。Metal allergy is an allergic reaction that occurs when metal touches the skin or mucous membranes, and eluted metal ions are taken into the body. Here we report a case of metal allergy caused by the mouthpiece of a musical instrument. The patient was a girl of 10 years and 8 months. Since joining the brass band club of her elementary school, gingival swelling and inflammation in the oral cavity had appeared. Therefore, a patch test and a blood test were performed by a local clinic, but both metal allergies and autoimmune diseases were denied. At the first visit to our hospital, the labial and buccal gingiva and buccal mucosa presented mild spontaneous pain and diffuse swelling with redness. The gingiva bled easily, and had grown over, forming false pockets. The periodontopathic bacteria were below reference values in the periodontopathic bacteria test. Histopathological examination revealed that the gingival overgrowth was periodontitis. Although we started to provide professional oral care, her condition did not improve. Eleven months later, the inflammation in the oral cavity drastically improved. We found that the musical instrument (tuba) had been changed to a new one. After that, the condition of the oral mucosa was healthy. The old mouthpieces had some spots where the plating had peeled off. Energy dispersive X-ray fluorescence spectrometry was carried out for an element analysis of the mouthpieces, and a metal patch test was also performed. The results showed that she may have had an allergic response to Cr. Finally, we diagnosed oral mucositis caused by metal allergies. The patient made steady progress after the mouthpiece was changed

TNF-α is essential in the induction of fatal autoimmune hepatitis in mice through upregulation of hepatic CCL20 expression.

It is unclear what roles TNF-α has in the development of autoimmune hepatitis (AIH) and whether AIH is responsive to anti-TNF-α. We recently developed a mouse model of fatal AIH that develops in PD-1-deficient mice thymectomized three days after birth, finding that CCR6-CCL20 axis-dependent migration of dysregulated splenic T cells is crucial to induce AIH. In this study, we show the indispensable role of TNF-α in the development of AIH. Administering anti-TNF-α prevented the induction, but treatment by anti-TNF-α after the induction did not suppress progression. Administering anti-TNF-α did not prevent splenic T-cell activation, but did suppress hepatic CCL20 expression. In contrast, administering anti-CCL20 suppressed AIH but not elevated serum TNF-α levels. TNF-α stimulation enhanced CCL20 expression in hepatocytes. These findings suggest that TNF-α is essential in the induction of AIH through upregulation of hepatic CCL20 expression, which allows migration of dysregulated splenic T cells

Fibronectin-β1 Integrin Interaction in Teeth

The dental epithelium and extracellular matrix interact to ensure that cell growth and differentiation lead to the formation of teeth of appropriate size and quality. To determine the role of fibronectin in differentiation of the dental epithelium and tooth formation, we analyzed its expression in developing incisors. Fibronectin mRNA was expressed during the presecretory stage in developing dental epithelium, decreased in the secretory and early maturation stages, and then reappeared during the late maturation stage. The binding of dental epithelial cells derived from postnatal day-1 molars to a fibronectin-coated dish was inhibited by the RGD but not RAD peptide, and by a β1 integrin-neutralizing antibody, suggesting that fibronectin-β1 integrin interactions contribute to dental epithelial-cell binding. Because fibronectin and β1 integrin are highly expressed in the dental mesenchyme, it is difficult to determine precisely how their interactions influence dental epithelial differentiation in vivo. Therefore, we analyzed β1 integrin conditional knockout mice (Intβ1lox-/lox-/K14-Cre) and found that they exhibited partial enamel hypoplasia, and delayed eruption of molars and differentiation of ameloblasts, but not of odontoblasts. Furthermore, a cyst-like structure was observed during late ameloblast maturation. Dental epithelial cells from knockout mice did not bind to fibronectin, and induction of ameloblastin expression in these cells by neurotrophic factor-4 was inhibited by treatment with RGD peptide or a fibronectin siRNA, suggesting that the epithelial interaction between fibronectin and β1 integrin is important for ameloblast differentiation and enamel formation

miR-1 and Tooth Development

Many genes encoding growth factors, receptors, and transcription factors are induced by the epithelial-mesenchymal interaction during tooth development. Recently, numerous functions of microRNAs (miRNAs) are reportedly involved in organogenesis and disease. miRNAs regulate gene expression by inhibiting translation and destabilizing mRNAs. However, the expression and function of miRNAs in tooth development remain poorly understood. This study aimed to analyze the expression of miRNAs produced during tooth development using a microarray system to clarify the role of miRNAs in dental development. miR-1 showed a unique expression pattern in the developing tooth. miR-1 expression in the tooth germ peaked on embryonic day 16.5, decreasing gradually on postnatal days 1 and 3. An in situ hybridization assay revealed that miR-1 is expressed at the cervical loop of the dental epithelium. The expression of miR-1 and connexin (Cx) 43, a target of miR-1, were inversely correlated both in vitro and in vivo. Knockdown of miR-1 induced the expression of Cx43 in dental epithelial cells. Interestingly, cells with miR-1 downregulation proliferated slower than the control cells. Immunocytochemistry revealed that Cx43 in cells with miR-1 knockdown formed both cell-cell gap junctions and hemichannels at the plasma membrane. Furthermore, the rate of ATP release was higher in cells with miR-1 knockdown than in control cells. Furthermore, Cx43 downregulation in developing molars was observed in Epiprofin-knockout mice, along with the induction of miR-1 expression. These results suggest that the expression pattern of Cx43 is modulated by miR-1 to control cell proliferation activity during dental epithelial cell differentiation