|山田 朋弘（やまだ ともひろ）||データ更新日：2019.07.11|
准教授 ／ 歯学研究院 歯学部門 口腔顎顔面病態学
|1.||Imajo I, Yamada T, Ishii K, Akahoshi T, Momii K, Kamizono K, Nakano H, Sumida T, Mori Y, Maxillofacial fractures caused by falls., Clinics in Surgery, 4, 2346, 2019.02.|
|2.||Tomohiro Yamada, Goro Sugiyama, Ken Higashimoto, Azusa Nakashima, Hiroyuki Nakano, Tomoki Sumida, Hidenobu Soejima, Yoshihide Mori, Beckwith-Wiedemann syndrome with asymmetric mosaic of paternal disomy causing hemihyperplasia, Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology, 10.1016/j.oooo.2018.07.053, 127, 3, e84-e88, 2019.03, [URL], Beckwith-Wiedemann syndrome (BWS) is a congenital disorder with 3 main features—overgrowth in infancy, macroglossia, and abdominal wall defects. Here, we report on a 5-month old girl with hemihyperplasia and macroglossia caused by paternal uniparental disomy (pUPD) asymmetric mosaic on chromosome 11p15.5. She could not retract her tongue into her mouth and the midline of the tongue was shifted to the left. Glossectomy was performed at age 1 year. A specimen of the tongue showed normal skeletal muscle, but the muscle fibers were closely spaced, and there were fewer stroma components in the tissue from the right side of the tongue than that from the left side. With respect to pUPD of chromosome 11p15.5, microsatellite marker analysis of the tongue tissue specimen revealed a higher mosaic rate in the tissue from the right side of the tongue (average 48.3%) than that from the left side (average 16.9%). Methylation analysis of Kv differentially methylated region (DMR) 1 (KvDMR1) and H19DMR revealed hypomethylation of KvDMR1 and hypermethylation of H19DMR in the tissue on the right side of the tongue (hyperplastic side). In this case, the difference in mosaic rate of pUPD in the 11p15.5 region was hypothesized to influence the expression level of insulin-like growth factor 2. This result may be helpful to clinicians, especially surgeons, when planning plastic surgery for hemihyperplasia..|
|3.||Kana Ishibashi, kotaro ishii, Goro Sugiyama, Yu Kamata, Azusa Suzuki, Kumamaru Wataru, Yukiko Ohyama, hiroyuki nakano, Tamotsu Kiyoshima, Tomoki Sumida, Tomohiro Yamada, Yoshihide Mori, Regulation of β-catenin phosphorylation by PR55β in adenoid cystic carcinoma, Cancer Genomics and Proteomics, 10.21873/cgp.20064, 15, 1, 53-60, 2018.01, [URL], Background/Aim: Adenoid cystic carcinoma (AdCC) is a rare cancer of the salivary gland with high risk of recurrence and metastasis. Wnt signalling is critical for determining tumor grade in AdCC, as it regulates invasion and migration. β-catenin dephosphorylation plays an important role in the Wnt pathway, but its underlying molecular mechanism remains unclear. Materials and Methods: Because the regulatory subunits of protein phosphatase 2A (PP2A) drive Wnt signalling via target molecules, including β-catenin, we used qRT-PCR and immunoblot analysis to investigate the expression of these subunits in an AdCC cell line (ACCS) and a more aggressive subline (ACCS-M). Results: PR55β was highly expressed in ACCS-M, suggesting its functional importance. In addition, PR55β expression was associated with tumor grade, with ACCS-M exhibiting higher PR55β levels. More importantly, knockdown of PR55β in ACCS-M cells significantly reduced invasiveness and metastatic ability. Furthermore, dephosphorylation and total levels of β-catenin were dependent on PR55β in ACCS-M. Finally, we confirmed a correlation between PR55β staining intensity and histopathological type in human AdCC tissues. Conclusion: Our study provides new insight into the interaction between PR55β and β-catenin and suggests that PR55β may be a target for the clinical treatment of AdCC..|
|4.||Hiroyuki Nakano, Kazuya Inoue, Tomoki Sumida, Tomohiro Yamada, Yoshihide Mori, Osteosynthesis using the uncalcined and unsintered hydroxyapatite/Poly-L-Lactic acid system, Annals of Maxillofacial Surgery, 10.4103/ams.ams_192_17, 8, 1, 116-117, 2018.01, [URL], The poly-L-lactic acid mini-plate system accomplished rapid development. However, the system still has a variety of problems. One such problem is the breakage of screws. In this technical report, we develop the temporary fixing screws made from stainless with hexagon steel that exhibit a hexagonal head and thread part that also features a tapping function..|
|5.||Kana Ishibashi, kotaro ishii, Goro Sugiyama, Tomoki Sumida, Tsuyoshi Sugiura, Yu Kamata, Katsuhiro Seki, Takahiro Fujinaga, Kumamaru Wataru, Yosuke Kobayashi, Naomi Hiyake, Hiroyuki Nakano, Tomohiro Yamada, Yoshihide Mori, Deregulation of nicotinamide N-methyltransferase and gap junction protein alpha-1 causes metastasis in adenoid cystic carcinoma, Anticancer Research, 10.21873/anticanres.12207, 38, 1, 187-197, 2018.01, [URL], Background/Aim: Adenoid cystic carcinoma (AdCC) is a malignant tumor that occurs in the salivary glands and frequently metastasizes. The aim of this study was to identify factors mediating AdCC metastasis. Materials and Methods: We established three AdCC cell lines by orthotropic transplantation and in vivo selection: parental, highly metastatic (ACCS-M-GFP), and lymph node metastatic (ACCS-LN-GFP) cells. Results: We examined the three cell lines. DNA microarray indicated significantly altered processes in ACCS-LN-GFP cells: particularly, the expression of nicotinamide N-methyltransferase (NNMT) was enhanced the most. NNMT is associated with tumorigenesis and is a potential tumor biomarker. Concomitantly, we found-significant down-regulation of gap junction protein alpha-1. We suggest that ACCS-LN-GFP cells acquire cancer stem cell features involving the up-regulation of NNMT and the loss of gap junction protein alpha-1, leading to epithelial-mesenchymal transition and consequent AdCC metastasis. Conclusion: NNMT is a potential biomarker of AdCC..|
|6.||Chisato Sakuma, Hideto Imura, Tomohiro Yamada, Toshio Sugahara, Azumi Hirata, Yayoi Ikeda, Nagato Natsume, Cleft palate formation after palatal fusion occurs due to the rupture of epithelial basement membranes, Journal of Cranio-Maxillofacial Surgery, 10.1016/j.jcms.2018.09.016, 46, 12, 2027-2031, 2018.12, [URL], 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces cleft palate and hydronephrosis in the mouse embryo. Cleft palate occurs due to failure in palatal grow, but the underlying mechanisms are unclear. We investigated the mechanisms of cleft palate development in TCDD-exposed mouse embryos. We administered olive oil (control group) or TCDD diluted in olive oil (40 μg/kg) via gastric tubes to pregnant mice on gestational day (GD) 12. Embryos of control and TCDD-exposed groups were removed from pregnant mice on GD 14 and GD 15, respectively. One mouse embryo from the control group had anteroposterior palatal fusion. Palatal fusion was observed in three TCDD-exposed mouse embryos. Palates of TCDD-exposed mice fused from the interior to the middle of the palates, while the palates were separated in the posterior region. The middle of the embryonic palatal shelves in TCDD-exposed animals was narrow and split at the fusional position. At this position, palatal and blood cells were dispersed from the palatal tissue and the epithelium was split, with a discontinuous basement membrane. The results suggest that decreased intercellular adhesion or insufficient tissue strength of the palatal shelves may be involved in the development of cleft palate following palatal fusion..|
|7.||Nakashima A, Yamada T,Nakano H, Sugiyama G, Sugi T, Kamata YU, Sumida T, Mori Y., Jaw asymmetry may cause bad posture of the head and the spine –a preliminary study-., Journal of Oral and Maxillofacial Surgery, Medicine and Pathology, 30, 3, 242-246, 2018.06.|
|8.||Kamata Y, Yamada T, Sumida T, Nakano H, Sugiyama G, Nakashima A, Mori Y., Pediatric treatment-resistant nonbacterial osteomyelitis of the mandible associated with SAPHO syndrome., Journal of Dental and Oral Health, 3, 7, 084, 2017.06.|
|9.||Nakashima A, Nakano H, Yamada T,Inoue K, Sugiyama G, Kumamaru W, Nakajima Y, Sumida T, Yokoyama T, Mishima K, Mori Y., The relationship between lateral displacement of the mandible and scoliosis., Oral Maxillofac Surg, 21, 1, 59-63, 2016.06.|
|10.||Tomoki Sumida, Tomohiro Yamada, A clinical investigation of oral sarcomas at multi-institutions over the past 30 years., 2016.08.|
|11.||山田 朋弘, 北村直也, 習慣性顎関節脱臼に対する外科的処置とその問題点 -Buckley Terry法と関節結節削除術の比較-, 日本口腔外科学会, 60, 1, 2-6, 2014.01.|
|12.||Tomohiro Yamada, SPARC is associated with carcinogenesis of oral squamous epithelium and consistent with cell competition., 日本臨床分子形態学会, 2014.10.|
|13.||Tomohiro Yamada, Azumi Hirata, Eri Sasabe, Tomohide Yoshimura, Seiji Ohno, Naoya Kitamura, Tatsuya Yamamoto, TCDD disrupts posterior palatogenesis and causes cleft palate., J Craniomaxillofacial Surgery, 42, 1, 1-6, 2014.01, Dioxins (e.g. 2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD) cause cleft palate at a high rate. A post-fusional split may contribute to the pathogenesis, and tissue fragility may be a concern. The objective of this study was to investigate the effects of TCDD on the palatal epithelium, bone and muscle, which contribute to tissue integrity.
ICR mice (10–12 weeks old) were used. TCDD was administered on E12.5 at 40 mg/kg. Immunohistochemical staining for AhR, ER-α, laminin, collagen IV, osteopontin, Runx2, MyoD, and desmin were performed. Furthermore, western blot analysis for osteopontin, Runx2, MyoD, and desmin were performed to evaluate protein expression in the palatal tissue.
Immunohistologically, there was little difference in the collagen IV and laminin localization in the palatal epithelium between control versus TCDD-treated mice. Runx2 and osteopontin immunoreactivity decreased in the TCDD-treated palatal bone, and MyoD and desmin decreased in the TCDD-treated palatal muscle. AhR and ER-α immunoreactivity were localized to the normal palatal bone, but ER-α was diminished in the TCDD-treated palate. On western blot analysis, Runx2, MyoD, and desmin were all downregulated in the TCDD-treated palate.
TCDD may suppress palatal osteogenesis and myogenesis via AhR, and cause cleft palates via a post-fusional split mechanism, in addition to a failure of palatal fusion..
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