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㹃-mail㸸fusanori@dent.kyushu-u.ac.jp

Information for Speakers‫ڦ‬ᴾ Presentation Instruments
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PROGRAM㢌⬻ᚠ⎔࢟ࢵࢡ࢜ࣇࢩ࣏ࣥࢪ࣒࢘
Kick Off Symposium:
Program for Advancing Strategic International Networks to Accelerate theCirculation of Talented Researchers
2015 ᖺ 2 ᭶ 27 ᪥
ʄ 10:00ࠥ10: 30

Opening remarks Fusanori Nishimura

Program for Advancing Strategic International Networks to
Accelerate the Circulation of Talented Researchersʄ 10:30ࠥ11:50

Plenary Lecture 1                 Chair: Fusanori Nishimura

Denis F. Kinane㸸
Innate and Inflammatory host defenses against the oral biofilm               Morton Amsterdam Dean of the University of Pennsylvania Schoolof Dental Medicine.Professor of Pathology and of Periodontics

ʄ 13:00ࠥ14:00

Plenary Lecture 2                Chair: Hiroshi Nakanishi
Sim K. 6LQJKUDR 㸸Periodontitis and Alzheimer’s disease

University of Central Lancashire, School of Medicine and Dentistryʄ 14:00ࠥ14:10

Coffee Breakʄ 14:10ࠥ15:00 Special Lecture 1

Chair: Kazuaki Nonaka

Han-Sung Jung㸸
Teeth of the development, by the morphogenesis, for the future<RQVHL8QLYHUVLW\&ROOHJHRI'HQWLVWU\ʄ 15:00ࠥ15:50

Special Lecture 2&KDLU =KRX:X

Jianchun Yu 㸸Nutrition, inflammation and Mental HealthPeking Union Medical College and Postgraduate Schoolʄ 15:50ࠥ16:00

Coffee Breakʄ 16:00ࠥ17:20  Session by talented researchers for next circulation
Chair:  ʄ 17:40ࠥ17:50

16:00ࠥ16:20

Akihiro Furuhashi

16:20ࠥ16:40

Hiroki Kato

16:40ࠥ17:00

Shingo Takai

17:00ࠥ17:20

Urara Tanaka

17:20ࠥ17:40

Haruyoshi Yamaza

Closing remarks

Takayoshi Yamaza

ABSTRACTS

Opening remarks
Establishment of research base for the projects promoting healthy longevity from oral health

Fusanori Nishimura
Section of Periodontology, Division of Oral Rehabilitation,
Kyushu University Faculty of Dental Science

Oral health greatly contributes not only to the maintenance of quality of life in the elderly byrecovering mastication function, but also to the maintenance of cognitive function, prevention oflife-style related diseases such as obesity and diabetes, and maintenance of immune homeostasis,
all of which contributes to the establishment of societies full of health longevity. Additionally, inthe oral tissue or organs, stem cells are relatively abundant, and thus, are easy to extract.
Therefore, much attention has been being paid to the utilization of these cells for therapeutic
purpose against life-threatening diseases such as some autoimmune diseases and fatal liverdisease.
We, Kyushu University Faculty of Dental Science, consider “oral health sciences” which promotes
general health from oral health and “research on tissue regeneration and reconstruction” as two
major subjects and aim to build the world-wide research base with full of originality in these fields.
For that purpose, we re-confirm our mission as research-oriented university and are trying to
make any efforts to educate undergraduate and graduate students full of research-minds, and togrow the next leaders in these fields. To achieve our important mission, we create IN-CROSS-OUT
network with top-ranking laboratories in the world and aims to be the international research hub
in a next decade.
This year, we were able to get support from JSPS to promote our mission named “program foradvancing strategic international networks to accelerate the circulation of talented researchers”.
Our great partners are University of Pennsylvania, Harvard University, Monell Chemical Senses
center, University of Michigan, and University of Southern California. Here I will introduce thesummary of our project named “Establishment of research base for the projects promoting healthy
longevity from oral health” as an introduction of this three- year program. I hope the program
would produce great outcomes.
In 2017, we, Kyushu University Faculty of Dental Science, will celebrate 50th years of anniversary.
We all wish our dreams to build top-ranking research base come true when we celebrate 50th years
anniversary.

Plenary lecture 1

Innate and Inflammatory host defenses against
the oral biofilm
Denis F. Kinane
Morton Amsterdam Dean of the University of Pennsylvania
School of Dental Medicine.
Professor of Pathology and of Periodontics

This talk will address the innate and inflammatory host responses to the microbial biofilm
that constitutes the subgingival dental plaque. The host response to infection draws upon the
innate, inflammatory and adaptive immune systems, whose role is to provide the appropriate
response to the offending microorganisms. In some cases, this will be little or no response when
encountering ‘commensals’, and in other cases a gradated response depending very much on thehost’s own determination of the pathogenic nature of the microbial insult: and herein lies the rootof variation in host responses that govern individual susceptibility. In some individuals and withsome bacteria this will be an innate- only response, others will need to invoke the inflammatory
response, and yet others will require the adaptive immune response – be it cellular, humoral orboth – to reduce or remove the challenge from the microbes. Of course these responses would besomewhat easier to predict with a single pathogen challenge, and become infinitely more complex
as the biofilm
increases in complexity. In addition the host aspect of this interaction is immensely complex due
to environmental exposures which overlay on marked genetic variation in the host response foundin individual subjects. A further complexity that of epigenetic variation will also be addressed inthis presentation. An understanding of the interaction of structural and defensive host cells withthe biofilm is pivotal to understanding periodontal disease etiology and to developing tailoredtherapeutics. Thus, this talk addresses predominantly the innate responses of epithelial cells,
exposed to the biofilm

CURRICULUM VITAE

Denis F. Kinane, BDS, PhD, is the Morton Amsterdam Dean of the University of Pennsylvania
School of Dental Medicine. He also holds appointments as Professor of Pathology and of Periodontics.
Prior to joining Penn Dental Medicine in July 2009, Dr. Kinane served, as the Associate Dean
for Research and Enterprise, Director of the Oral Health and Systemic Disease Research Group,and Delta Dental Endowed Professor in the Department of Periodontics and Endodontics at the
University of Louisville School of Dentistry. He was also Professor of Microbiology and
Immunology there.
A native of Scotland, Dr. Kinane spent much of his distinguished career there, earning
his bachelor of dental surgery and his PhD in microbiology and immunology from the University of
Edinburgh in 1980 and 1983 respectively, and serving on the University of Glasgow Dental School
faculty for 14 years, where he held the posts of Professor and Chair of Periodontology and Oral
Immunology and Associate Dean for Research and Enterprise. Dr. Kinane is a member of theFaculties of Dental Surgery of the Royal College of Surgeons of Edinburgh in restorative dentistry
and the Royal College of Physicians and Surgeons of Glasgow in periodontics and oral medicine.
An active clinician and researcher, his research interests focus on periodontal immune andinflammatory processes, mainly addressing the causes, development, and susceptibility markers
of periodontal disease. His work also examines the relationships between periodontal disease
and systemic health and diseases such as diabetes and heart disease, involving research into
inflammation, immunity, microbial pathogenesis, genetics, and systemic disease markers. Among
his recent studies, has been an NIH-funded investigation into what genes make people more
susceptible to inflammation, gingivitis, and periodontitis (Epigenetics and cell receptors in Disease
Susceptibility).
An internationally respected lecturer, Dr. Kinane is widely published in U.S. and international
peer-reviewed journals and serves of the editorial boards of the Journal of Clinical Periodontology,
Clinical Oral Implants Research, Oral Diseases, British Dental Journal, Journal of Periodontal
Research, Genes and Immunity, and Journal of Dental Research. He was a member of the
Executive Committee of the European Academy of Periodontology and served as Chair of the Gordon
Conference on Periodontal Research, 2006-2009. Dr. Kinane is a highly sought-after international
speaker, frequently presents at symposia, conferences nationally and internationally. He regularlyorganizes international clinical and research symposia, including the 2013 and 2015 Penn Perio
Conference and the 2009 Gordon Conference. In Periodontology

【MEMO】

Plenary lecture 2

Periodontal pathogens and Alzheimer’s disease:Is there an association?
Sim K. Singhrao*, Lakshmyya Kesavalu1, StJohn Crean*The presenting authorOral & Dental Sciences Research Group,
University of Central Lancashire,
Preston, U.K. and 1Department of Periodontology and Oral Biology,
College of Dentistry, University of Florida, Gainesville, Florida, USA
The concept of chronic periodontal disease (PD) playing a role in Alzheimer’s disease (AD)comes from the seminal studies conducted by Kondo et al.,(1994) and Stein et al., (2007) who
have suggested a strong association between tooth loss due to PD and the development of AD.
Chronic, inflammatory, periodontal disease has a complex subgingival polymicrobial aetiology
involving key pathogens (Porphyromonas gingivalis Treponema denticola and Tannerella forsythia).
These pathogens are also linked with the development of other remote body organ inflammatory
pathologies including AD. AD is associated with memory loss and a number of aggregated hallmark
proteins such as Aβ4 deposits, hyperphosphorylated neurofibrillary tangles, neuronal loss and lossof synapses. Riviere et al., (2002) initiated experimental investigations and reported the detection ofseven oral species of the genus Treponema in brains of AD patients. Miklossy previously reported thatvarious types of spirochetes, belonging to the order Spirochaetales play a direct role in AD development(Miklossy 2011). Our investigation examined brain samples obtained from the “Brains for Dementia
Research” tissue bank, UK donated by ten patients with confirmed AD which were age-matched withindividuals without dementia. This study exclusively demonstrated the presence of lipopolysaccharide
from P. gingivalis in brains from subjects having suffered from AD. A subsequent collaborative study
was performed for proof of concept using ApoEnull mice animal models of experimental periodontitis
whereby mice were orally infected (N=12) with 109 P. gingivalis, T. denticola, T. forsythia andFusobacterium nucleatum as mono- and polymicrobial infections. Following chronic oral infection,
mice were sacrificed after 12 and 24 weeks. Genomic DNA was isolated from brain tissue of mice
infected with P. gingivalis, T. denticola, T. forsythia and to assess if these three infecting pathogens
accessed the brain. Their molecular identity was determined using universal 16s rDNA gene primers
and specific primer sets for each organism. Nucleotide sequencing demonstrated 6 out of 12 ApoEnullmice brains contained the P. gingivalis genomic DNA at 12 weeks (P = 0.006), and increased to 9 out of
12 at 24 weeks (P = 0.0001). Furthermore in-situ hybridisation has recently demonstrated the presenceof clusters of P. gingivalis in these mice brains supporting our published data. Next, the innate immune
responses were detected by using antibodies against complement activation products of C3 convertasestage and the membrane attack complex. Microglia in both infected and control groups demonstrated
strong intracellular labelling with C3 and C9, presumed on-going biosynthesis, but the pyramidal
neurons of the hippocampus in 4 out of 12 infected mice brains were clearly labelled with C3
activation fragments (P = 0.032). Statistically significant complement activation with bystander injury
of CA pyramidal neurons in the hippocampus up to 24 weeks of infection was only observed in the P.
gingivalis infected group. The data from the human brains and that from the animal model suggests
an emerging indirect link between PD and AD. Further research is needed to assess the direct role ofseveral oral infections in AD mouse models over longer infection episodes.

CURRICULUM VITAE

Sim’s interest in research in neurodegenerative diseases was nurtured by the influence of her
mentor Dr Gillian Cole (Consultant Neuropathologist) and later by Dr James W. Neal (Consultant
Neuropathologist). Sim obtained her M. Phil. degree at Cardiff University. Sim moved from thepathology Department to pursue her PhD in the Complement Biology Group at Cardiff University
headed by Professor B. Paul Morgan (Biochemistry and Immunology). This was a very interestingtime for establishing the inflammatory hypothesis of Alzheimer’s disease. Following three postdoctoral
research posts on aspects of non-CNS inflammatory diseases at Cardiff, Sim took up her current
Senior Research fellow position in the School of Medicine and Dentistry at the University of Central
Lancashire, where she is pursuing research in periodontal disease and its association with
Alzheimer’s disease in support of the aetiological hypothesis.
Publications
1. Singhrao SK, Nicholson K, Crean S (2012) Informed choices for challenging specimens
when choosing methacrylate resin systems for histology. Microsc Res Tech. 75(5):576-85.
2. Singhrao SK (2013) C1q, the classical complement pathway protein binds Hirano bodies in
Pick’s disease. Microsc Res Tech 76(6):606-11.
3. Poole S, Singhrao SK, Kesavalu L, Curtis MA, Crean S (2013) Determining the presenceof periodontopathic virulence factors in short-term post-mortem Alzheimer’s disease
braintissue. J Alzheimers Dis 36(4):665-77.
4. Dillon A, Achilles-Day U, Singhrao SK, Pearce M, Morton LHG, Crean S (2014) Biocide
sensitivity of Vermamoeba vermiformis isolated from dental-unit-waterline systems.
5. International Biodeterioration & Biodegradation 88:97-105.
6. Dillon A, Singhrao SK, Achilles-Day U, Pearce M, Morton LHG, Crean S (2014) Vermamoeba
vermiformis does not propagate Legionella pneumophila subsp. Pascullei in a simulated
laboratory dental-unit-waterline system. International Biodeterioration & Biodegradation
90:1-7.
7. Lal S, Singhrao SK, Bricknell M, Pearce M, Morton LHG, Ahmed W, Crean S (2014)
Monitoring dental unit water line output water by current in-office test kits. Curr Microbiol
69(2):135-142.
8. Singhrao SK, Harding A, Simmons T, Robinson S, Kesavalu L, Crean StJ (2014) Oral
inflammation, tooth loss, risk factors and association with progression of Alzheimer’s
disease. J Alzheimers Dis. 1;42(3):723-37.
9. Poole S, Singhrao SK, Chukkapalli S, Rivera M, Velsko I, Kesavalu L, Crean StJ Active
invasion of an oral bacterium and infection-induced complement activation in ApoEnull micebrains. Accepted 2014 JAD

【MEMO】

Special lecture 1

Teeth of the development, by themorphogenesis, for the future
Han-Sung Jung
Yonsei University College of Dentistry, Seoul, Korea

Tooth development is regulated by progressive and mutual interactions between epithelium andmesenchyme. The molecular mechanisms underlying this instruction are well-preserved and mostof the contributing molecules belong to several signalling families. Research focusing on mouseteeth has uncovered many aspects of tooth development, including molecular and evolutionary
detailed and in addition offered a valuable system to analyse the regulation of epithelial stem
cells. In mice, the spatial and temporal regulation of cell differentiation and the mechanisms ofpatterning during development can be analysed both in vivo and in vitro.
The mouse teeth that modulating the balance between inductive and inhibitory signals
constitutes a key mechanism regulating the epithelial stem cells and cellular differentiation.
I would share current ideas with additional maintenance for the location of the putative dental
stem cells and for the stemness. Fine-tuning of the signalling in the regulation of the toothmorphogenesis, and that altering the levels of an inhibitor can cause variation in the toothpatterning. Furthermore, clinical implications including in the diagnosis, prevention andtreatment of congenital defects as well as in the design of regenerative therapies would be offundamental importance in Oral Biosciences.

CURRICULUM VITAE

Education:
1997

PhD,

Dept. of Anatomy & Developmental Biology, University College London, UK.

1993

BSc,

Dept. of Anatomy & Developmental Biology, University College London, UK.

Position:
2000 〜 present

Assistant, Associate and Professor, Yonsei University, Korea.

2013 〜 present

Adjunct Professor, Guangzhou Medical University, China

2012 〜 present

Adjunct Professor, The University of Hong kong2010 〜 present

Adjunct Professor, Kanagawa Dental College, Japan

2003 〜 present

Adjunct Professor, Tokyo Dental College, Japan

1999 − 2000

Instructor, Harvard Medical School, USA.

1997 − 1999

Post-doctoral fellow, University of Helsinki, Finland.

Publications:
Lai WF, Lee JM, Jung HS. (2014) Molecular and engineering approaches to regenerate and repair teeth inmammals. Cell Mol Life Sci.71(9):1691-701
Kim EJ, Cho SW, Shin JO, Lee MJ, Kim KS, Jung HS (2013). Ihh and Runx2/Runx3 signaling
interact to coordinate early chondrogenesis: a mouse model. PLoS One 8:e55296 Nakagawa E,
Zhang L, Shin JO, Kim EJ, Cho SW, Ohshima H, Chen Z, Jung HS (2012) The novel expression of
Oct3/4 and Bmi1 in the root development of mouse molars. Cell Tissue Res.
347,479-484
Shin JO, Kim EJ, Cho KW, Nakagawa E, Kwon HJ, Cho SW, Jung HS (2012) BMP4 signaling
mediates Zeb family in developing mouse tooth. Histochem Cell Biol 13,791-800 Cho SW, Kwak S,
Woolley TE, Lee MJ, Kim EJ, Baker RE, Kim HJ, Shin JS, Tickle C, Maini PK, Jung HS (2011)
Interactions between Shh, Sostdc1 and Wnt signaling and a new feedback loop for spatial patterningof the teeth. Development 138,1807-1816 Lee JM, Kim JY, Cho KW, Lee MJ, Cho SW, Kwak S, Cai J,
Jung HS (2008) Wnt11/Fgfr1b cross-talk modulates the fate of cells in palate development.
Developmental Biology 314,341-350 Cho SW, Kim JY, Cai J, Lee JM, Kim EJ, Lee HA, Yamamoto
H, Jung HS (2007) Temperospatial tissue interactions regulating the regeneration of the enamelknot in the developing mouse tooth. Differentiation 75,158-165 Cho SW, Lee HA, Cai J, Lee MJ,
Kim JY, Ohshima H, Jung HS (2007) The primary enamel knot determines the position of the firstbuccal cusp in developing mice molars. Diffrentiation 75,441-451 Cai J, Cho SWKim JY, Lee MJ,
Cha YG, Jung HS (2007) Patterning the size and number of tooth and its cusps. Developmental
Biology 304, 499-507
Lee JM, Kim JY, Cho KW, Zhang Y, Byun SK, Yi CK, Jung HS (2006) Modulation of cell proliferation
during palatogenesis by the interplay between Tbx3 and BMP4. Proceedings of the national
Academy of Sciences USA 103,16788-16793

【MEMO】

Special lecture 2

Nutrition, inflammation and Mental Health

Yu Jianchun
Professor in Dept. of General Surgery,
Peking Union Medical College Hospital, Peking Union Medical College

Chronic low-grade inflammation has been known to associate with many systemic diseases,
including obesity, inflammatory bowel diseases. The low-grade chronic inflammation results inoxidative stress and DNA damage in several of cells, including adipocytes, macrophages, and thedamaged cells produce cytokines to secondarily amplify inflammation. It is well accepted thatchronic systemic inflammation for continuous cytokine production involves in the pathogenesis
of neurodegenerative diseases, including Alzheimer’s diseases.
On the other hand, stress may induces oxidative stress refers to the effect of greater thannormal production of free radical molecules in the mitochondria during energy metabolism and thepotential damage to lipid to cell membranes are particularly vulnerable to damage by free
radicals. In clinically, acute stress may be related to gut problems such as acid stomach, diarrhea,
constipation, and irritable bowel syndrome, and chronic stress may result in mental healthproblems, including depression.
The concept of “Surgeon General’s report on mental health” is first given by the U.S Surgeon
General David Satcher in the early of 1999, because the nutrients necessary for keeping a healthy
heart as well as a healthy brain. The mental health problems is rising in the West countries during
the 21th century in place of the explosion of heart disease during the 20th century. Depression is
now the second-leading cause of global disability and mental health problems make high cost eachyear in the developing countries.
Nutrition is known as one of the major factors influencing the translation of genotype to thephenotype. This reflects the principles and application of systems biology, which sees health as thereflection of the genetic molecular, and biochemical interactions between bodily systems, a networkof relationships that has the capacity for self-regulation. In this talk, I will introduce the concept
about “Mental health is influenced by nutrition” and discuss how nutrition, including functional
medicine for reduction of inflammation as well as oxidation stress. We need more basic and clinicalevidence to expand the concept in near future.

CURRICULUM VITAE

Education:
1980-1985

Bethune Medical College, JiLin University, China.（Bechler Degree in Medicine）

1985-1988

Peking Union Medical College Hospital Chinese Academy of Medical Sciences, Beijing, China.
(MD Degree in General Surgery）

1995-1998

Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
（PhD Degree in General Surgery）

Position:
1985-1989

Resident in Dept. of surgery, Peking Union Medical College Hospital, Chinese Academy ofMedical Sciences, Beijing, China.

1990-1994

Attending Surgeon in Dept. of surgery, Peking Union Medical College Hospital, Chinese
Academy of Medical Sciences, Beijing, China.

1995-1996

Visiting scholar for Department of Surgery, Okayama University, Japan.

1997

Visiting scholar for Nutrition Science Institute of Stuttgart University, Germany.

1998

MDS Harris training in global Standard Operating Procedures for the position of Study
Coordinator, USA.

2002

Laparoscopic surgery training, training center in Union Christian Hospital，Hong Kong，China

2011

Bariatric (Laparoscopic) surgery training, in training center in YiDa University Hospital，Taiwan.

1995-1999

Associate professor: Dept. of general surgery, Peking Union Medical College Hospital.
Chinese Academy of Medical Sciences, Beijing, China.

2000-

Professor: Dept. of surgery, Peking Union Medical College Hospital, Chinese Academy ofMedical Sciences, Beijing, China.

Award:
Ministry of Health for medical and health technology second prize, 1996.
United Nations Information System Technology Prize for Invention and Innovation in China: parenteraland enteral nutrition improvement, 1996.
Medical and health science and technology, Beijing, second prize, 2000.
The National Science and Technology Progress Award, 2002.
Beijing Medical Society best work and Contribution Award, 2010.
Chinese Medical Society of Parenteral and Enteral Nutrition Committee: Excellence Award Perioperative
enteral nutrition and parenteral nutrition controlled prospective multicenter clinical study, 2010.
Peking Union Medical College Outstanding Teacher Award, 2002, 2005, 2005, 2009, 2009, 2010, 2011,
2012
Beijing Parenteral Enteral Nutrition Board of Medicine Award, 2010.
Chinese Nutrition Society Award for Outstanding Paper, 2010.
Beijing science and technology award, 2012.
Chinese science and technology award (second prize), 2013.

Publications:(Some papers within 5 years)
Jianchun Yu. Bariatric Surgery in Adolescents: a multidisciplinary Approach. Essentials and Controversies
in Bariatric Surgery Edited by Chih-Kun Huang ( Copyright C©2014 INTECH (First published October,
2014)
Tian SB, Yu JC, Kang WM, Ma ZQ, Ye X, Cao ZJ. Association between dairy intake and gastric cancer:
a meta-analysis of observational studies. PLoS One, 9(7):e101728, 2014.
Tian SB, Yu JC, Kang WM, Ma ZQ, Ye X, Cao ZJ, Yan C. Combined detection of CEA, CA 19-9, CA
242 and CA 50 in the diagnosis and prognosis of resettable gastric cancer. Asian Pac J Cancer Prev.,
15(15):6295-300, 2014.
Wang J, Kang WM, Yu JC, Liu YQ, Meng QB, Cao ZJ. Cadherin-17 induces tumorigenesis and lymphatic
metastasis in gastric cancer through activation of NF-κB signaling pathway. Cancer Biol Ther.
14(3):262-270, 2013.
Meng QB, Yu JC, Ma ZQ, Kang WM, Zhou L, Ye X. Benefits of intra-operative systemic chemotherapy
during curative surgery in patients with locally advanced gastric cancer. Chin Med J (Engl).,
126(18):3493-3498, 2013.
Kang WM, Yu JC, Ma ZQ, Zhao ZR, Meng QB, Ye X. Laparoscopic-endoscopic cooperative surgery for
gastric submucosal tumors. World J Gastroenterol. 19(34):5720-5726, 2013.
Wang J, Yu JC, Kang WM, Ma ZQ. Prognostic significance of intraoperative chemotherapy andextensive lymphadenectomy in patients with node-negative gastric cancer. J Surg Oncol. 105(4):400-4,
2012.
Sun H, Jin Z, Li X, Qian J, Yu JC, Zhu F, Zhu H. Detection and localization of active gastrointestinal
bleeding with multidetector row computed tomography angiography: a 5-year prospective study in one
medical center. J Clin Gastroenterol., 46 (1):31-41, 2012.
Zhou L, He XD, Yu JC, Zhou RL, Shan Y, Rui JA. Overexpression of LAPTM4B-35 attenuates
epirubucin-induced apoptosis of gallbladder carcinoma GBC-SD cells. Surgery., 150(1):25-31, 2011.
Wang J, Yu JC, Kang WM, Ma ZQ. Treatment strategy for early gastric cancer. Surg Oncol., Jan 21,
2011.
Wang J, Yu JC, Kang WM, Wang WZ, Liu YQ, Gu P. The Predictive Effect of Cadherin-17 on Lymph
Node Micrometastasis in pN0 Gastric Cancer. Ann Surg Oncol. Oct 19, 2011.
Wu Q, Yu JC, Kang WM, Ma ZQ. Short-term effects of supplementary feeding with enteral nutrition
via jejunostomy catheter on post-gastrectomy gastric cancer patients. Chin Med J (Engl)., 124(20):3297-301., 2011.
Zhang Q, Yu JC, Kang WM, Zhu GJ. Effect of ω-3 fatty acid on gastrointestinal motility after abdominal
operation in rats. Mediators Inflamm., 2011:152137, 2011.
Liu XX, Yu JC. n-3 polyunsatured fatty acid enhance chemotherapy sensitivity by inhibiting NF-kB
pathway 2010

e-Clinical Nutrition 2011

Wang J, Yu JC, Kang WM, Ma ZQ. Treatment strategy for early gastric cancer. Surg Oncol. 2011,
doi:10.1016/j.suronc.2010.12.004.
Wang J, Yu JC, Kang WM, Ma ZQ. Superiority of a fish oil-enriched emulsion to medium-chain
triacylglycerols/long-chain triacylglycerols in gastrointestinal surgery patients: A randomized clinical
trial. Nutrition., Nov 22, 2011.
Zhou L, Zhang JS, Yu JC, Cui QC, Zhou WX, Kang WM, Ma ZQ. Negative association of c-fos expression
as a favorable prognostic indicator in gastric cancer. Arch Med Res., 41(3):201-6, 2010.

Zhou L, He XD, Yu JC, Zhou RL, Xiong FX, Qu Q, Rui JA. Expression of LAPTM4B in gallbladdercarcinoma cells: the role in invasive potential. Hepatogastroenterology., 57(98):207-11, 2010.
Zhou L, He XD, Yu JC, Zhou RL, Yang H, Qu Q, Rui JA. Overexpression of LAPTM4B promotes growthof gallbladder carcinoma cells in vitro. Am J Surg., 199(4):515-21, 2010.
Kang WM, Zhang JS, Wang MS, Gu YC, Yu JC. Prevalence of metabolic syndrome and its associations
with other metabolic disorders and cardiovascular changes in health examination population in Beijing.
Chin Med Sci J., 24(4):227-30, 2009.
FanYP, Yu JC. Effects of Glutamine Supplementation on patients undergoing abdominal surgery Chin
Med Sci J., 24(1):55-59, 2009.
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【MEMO】

Presentation by
talented researchers
for next circulation

Soft Tissue Response to Dental Implant Materials
Akihiro Furuhashi, Yasunori Ayukawa, Ikiru Atsuta, Yunia Dwi Rakhmatia,
Noriyuki Yasunami, Kiyoshi Koyano
Section of Implant and Rehabilitative Dentistry, Division of Oral Rehabilitation,
Faculty of Dental Science, Kyushu University

Objectives:
As implants are inserted into jaw bone and penetrating oral mucosa into the oral environment, a
number of stimuli attack the gingival margin. Around dental implant, weak epithelial attachment
has been reported. For the long time stability of dental implants, understanding of the relationshipbetween soft tissue and dental implant materials are important. Thus, the purpose of our researchis to evaluate the soft tissue reaction to dental implant materials.
Materials and Methods:
In the first research, the difference of soft tissue reaction to the various titanium surface topographies
such as rough surface, machined surface, micro-grooved surface was evaluated in vitro and in vivo.
In the second research, the difference of soft tissue reaction to various kinds of materials such astitanium, zirconia, platinum-gold alloy was evaluated in vitro and in vivo. In the third research,
the effect of titanium surface modification with hydrothermal treatment with CaCl2 solution on
soft tissue was evaluated in vitro and in vivo.
Results:
From the first and the second researches, it is revealed that titanium surface topography and thedental implant materials have some influences on the soft tissue response.
From the third research, it is revealed that calcium-modified titanium surface has some positiveeffect on soft tissue attachment to dental implant.
Discussion and Conclusion:
For the long time stability of dental implant, consideration for the selection of implant surface
topography, materials in the trans-mucosal part might be important. In the present study, novelsurface treatment with calcium hydrothermal procedure showed the potential for the enhancementof soft tissue attachment.

Tom70 is essential for PINK1 import into mitochondria
Hiroki Kato
Department of Pediatric Dentistry, Graduate School of Dental Science, Kyushu University

PTEN induced kinase 1 (PINK1) is a serine/threonine kinase in the outer membrane of mitochondria(OMM), and known as a responsible gene of Parkinson’s disease (PD). The precursor of PINK1 issynthesized in the cytosol and then imported into the mitochondria via the translocase of the OMM(TOM) complex. However, a large part of PINK1 import mechanism remains unclear. In this study,
we examined using cell-free system the mechanism by which PINK1 is targeted to and assembled
into mitochondria. Surprisingly, the main component of the import channel, Tom40 was notnecessary for PINK1 import. Furthermore, we revealed that the import receptor Tom70 is essential
for PINK1 import. In addition, we observed that although PINK1 has predicted mitochondrial
targeting signal, it was not processed by the mitochondrial processing peptidase. Thus, our results
suggest that PINK1 is imported into mitochondria by a unique pathway that is independent of the
TOM core complex but crucially depends on the import receptor Tom70.

Glucagon like peptide-1 (GLP-1) underlies sweet taste transmission
Shingo Takai*, Keiko Yasumatsu*, Shusuke Iwata*, Mayuko Inoue*,
Ryusuke Yoshida*, Noriatsu Shigemura*,
Daniel J. Drucker**, Robert F. Margolskee***,Yuzo Ninomiya** Sect. Oral Neurosci., Grad. Sch. Dental Sci., Kyushu Univ., Fukuoka, Japan** Dept. Med., Mt. Sinai Hosp., Lunenfeld Tanenbaum Res. Inst., Univ. Toronto, Tronto, Canada*** Monell Chemical Senses Center, Philadelphia, USA

Recent studies demonstrated that taste bud cells express several gut peptides, such as GLP-1(glucagon like peptide-1), NPY (neuropeptide Y), and glucagon, and secrete these peptides in response
to various taste stimuli. Interestingly, the secretion patterns of peptides are correlated with taste
qualities, suggesting the possibility that these gut peptides would contribute to taste quality coding.
In this study, we report that around a half of GLP-1 expressing taste cells possess sweet taste
receptor subunit T1R3, and GLP-1 receptor is expressed in gustatory nerve neurons in wild typemice. Mice genetically lacking of GLP-1 receptor showed decreased behavioral responses to sweetcompounds in short-time lick test and reduced sweet taste responses in chorda tympani (CT) nerve
recordings. Additionally, we measured GLP-1 concentrations released from single taste buds, andcells in response to various kinds of taste stimuli by using ELISA method. As a result, we found that
GLP-1 is secreted from a subset of sweet responsive cells by sweet taste stimulation in a concentration
dependent manner. Furthermore, i.v. injection of GLP-1 produced transient increase of neuralactivities in a subset of sweet specific single nerve fibers without affecting those of other taste fibers.
All these findings suggest that GLP-1 may be involved in normal sweet taste signal transmission inmice.

Suppression of Sprouty2 enhances cell proliferation and migration inperiodontal ligament cells
Urara Tanaka, Terukazu Sanui, Takao Fukuda, Kyosuke Toyoda, Ryo Atomura,Kensuke Yamamichi and Fusanori Nishimura

Department of Periodontology, Division of Oral Rehabilitation, Faculty of Dental Science,
Kyushu University, Fukuoka, Japan

Objectives: The periodontal ligament (PDL) plays an important role as a reservoir of mesenchymal
stem cell. The cells in PDL tissue are critical participants during periodontal tissue regeneration.
Sprouty (Spry) is an intracellular protein includes four mammalian homologs, which are expressedin most tissues. Mammalian Spry proteins were originally identified as an inhibitor of fibroblast
growth factor (FGF) receptor, and it functions as a negative regulator of receptor tyrosine kinases(RTKs) signaling. However, Spry2 does not affect epidermal growth factor (EGF)-induced ERK
activation. Since both FGF and EGF have been suggested as possible growth factor for periodontal
cytokine therapy, we aimed to investigate whether Spry2 could be new therapeutic targets forenhancing periodontal tissue regeneration.
Methods: We used multipotent clonal human PDL cell line 1-17. The cells were transfected withsmall interfering RNA (siRNA) specific for Spry2. Using WST-8 assay and Ki-67 staining, growth
factor-induced cell proliferation was investigated. In order to evaluate osteoblastic differentiation,
ALP staining and Real-time PCR detecting genes associated with calcification were performed.
Cell migration was assessed by a scratch wound healing assay and boyden chamber assay, andlamellipodia formation was confirmed by fluorescence microscope.
Results: Transfection of Spry2 siRNA enhanced bFGF+EGF-induced ERK activation in 1-17 cells.
Spry2 siRNA 1-17 cells stimulated by bFGF+EGF proliferated faster than control cells.
Migration activity and lamellipodia formation of bFGF+EGF-stimulated Spry2 siRNA 1-17 cells
were promoted compared with control cells accompanied by increase in PI3K, Akt and Rac1 activity.
On the other hand, osteoblastic differentiation of Spry2 siRNA 1-17 cells was inhibited.
Conclusions: bFGF+EGF induced proliferation and migration was up-regulated in Spry2 siRNA
1-17 cells, whereas osteogenic differentiation was inhibited. Since selective proliferation and migrationof PDL cells are important for periodontal tissue regeneration, Spry2 could be new therapeutictargets for periodontal regeneration.

Dihydroorotate dehydrogenase depletion hampersmitochondrial
function and osteogenic differentiation in osteoblasts
Haruyoshi Yamaza
Section of Pediatric Dentistry, Division of Oral Health Growth and Development,
Faculty of Dental Science, Kyushu University, Fukuoka, Japan

Mutation of the dihydroorotate dehydrogenase (DHODH) gene is responsible for Miller syndrome
which is characterized by craniofacial malformations in association with limb abnormalities.
We previously demonstrated that the DHODH enzyme is involved in forming a mitochondrialsupercomplex in HeLa cells. Moreover, mutated DHODH led to protein instability, loss of enzyme
activity, and increased reactive oxygen species. In order to explore the etiology of Miller syndrome
in more detail, we here investigated the effects of DHODH inhibition in cells involved in skeletal
structure. MC3T3-E1 cells are derived from mouse calvaria osteoblast precursor cells. DHODH
in MC3T3-E1 cells was knocked down by specific siRNAs after which cell proliferation, ATPproduction and expression of bone-related genes were investigated. After depletion of DHODH
using specific siRNAs, inhibition of cell proliferation and cell cycle arrest occurred in MC3T3-E1
cells. In addition, ATP production was reduced in whole cells, especially in mitochondria.
Furthermore, mRNA levels of the osteogenic genes Runt-related transcription factor 2 (Runx2)
and Osteocalcin (Ocn) decreased in DHODH siRNA-treated cells compared to controls. These datasuggest that depletion of DHODH affects the differentiation and maturation of osteoblasts.