News Letter

vol.4
2.2012● Chiba University Global COE ProgramC O N T E N T S・Research Highlights
Tomoaki Tanaka,
Shinichiro Motohashi,
Masayuki Miyagi,
Yusuke Endo and
Kenta Shinoda
・Reports of Study Abroad
・Events
・Seminars

Research
Highlights

Dr. Tomoaki Tanaka (Department of Clinical Cell Biology and Medicine) and Dr. Shinichiro
Motohashi (Department of Medical Immunology) both involved in this program, received
the Chiba Medical Society Award (2011). Dr. Motohashi’s research also received the 16th
Inohana Alumni Award.

Tomoaki Tanaka
Lecturer, Dept. of Clinical Cell Biology and Medicine“The p53 world”, a wide variety of physiological functions and common
pathogenesis of cancer, diabetes, and age-related disease〜Forefront of Molecular Biology of “Life-Aging-Disease-Death”〜
and characterize p53 chromatin complexes in vivo by manipulating
biochemical techniques and mass-spectrometry, and to performgenome-wide screening of RNA-seq and ChIP-seq using tumor andnon-tumor cells, including senescent cells and ES/iPS cells. We
found several chromatin regulators and transcriptional coactivatorssuch as CAS/CSE1 (chromosome segregation factor), Sp110(component of PML nuclear body protein forming a multiprotein
complex), and zinc finger proteins in association with p53
chromatin complexes (Figure 3). Given that they are components of
intranuclear structures and have functional domains such as thebromodomain and PHD zinc finger motif that potentially function
as “reader” for histone codes in epigenetic and chromatin-mediatedtranscriptional regulation, p53 is a bona-fide epigenetic regulators
acting as “the guardian of the genome” and “the cellular gatekeeper”.
Further, genome-wide analyses revealed that p53 can actively and/or
repressively control cell-cycle regulators, metabolic regulators,
senescence-associated secretary proteins (SASPs), and linc RNAsin cancer, senescent and ES/iPS cells. Thus, our study suggests thatp53 exerts multiple functions with a complexity of crosstalk to
intranuclear structure and transcriptional regulation for a wide
variety of transcripts, including linc RNAs in senescent and ES/iPS
cells, linking to a common mechanism of cancer, life-style-relateddisease, and age-related disease such as diabetes and cardiovasculardisorders (Figure 4).

While many processes in biology, for instance, temporal and spatial
control of gene profile during the development of organisms, increase
complexity, the aging process increases entropy and culminates inthe death of animals. Recent genetic studies have indicated that the
aging process is subjected to a regulatory network. It is now wellappreciated that the network includes the nutrient-sensing pathways(such as insulin and AKT/mTOR signals), and transcriptional andchromatin regulation (sirtuins, etc) with profound consequences.
Importantly as well, it is also evident that key molecules that
regulate cellular senescence and apoptosis, such as tumor suppressor
p53, are critically involved in the aging process and pathogenesis of
its associated diseases such as cancer, cardiovascular disease, andmetabolic disorders, a testament to the importance and crosstalk oftranscriptional and epigenetic regulators in the four inevitable eventsin our lives (Figure 1).
Tumor suppressor p53 receives multiple forms and a diverse rangeof stress signals such as DNA damage and oxidative or metabolic
stress, and then initiates different cellular outcomes, including
cell-cycle arrest, apoptosis, and/or cellular senescence. Recently
several lines of evidence have suggested that p53 pathway is linked
to the reprogramming process by pluripotent factors and oncogenic
signals, and p53 systematically regulates intracellular metabolic
pathways to preserve anti-oxidant and bioenergetic function (Figure2). To elucidate the p53 mechanisms, we have attempted to isolate
Figure 1. Epigenetic Regulators and Disease

Figure 3. Our Research Work about Tumor Suppressor p53
Analysis of p53 protein code

Search and functional analysis for p53 targets using

Histone methyltransferase

RNA-seq ChIP-sequence
Cell. 2000
Mol Cell 2001
PNAS 2010

Signal Cascade
Replication

Transcription

Recombination“Writer”
or“Eraser”

CommonMechanismHistone demethyltransferase“Reader”

Cell. 2000, Mol Cell 2001
JBC 2006, JBC 2007, Biochemistry

Epigenetic
regulators
in cancer

Chromatin complex analysis using

Fusion Identification of senescence regulator in

Cross-linking Technique

Nuclear Structure

Epigenetics andsenescencein life-style relateddiseaseCell 2007

Figure 4. Forefront of Molecular Biology of“Life-Aging-Disease-Death”

Figure 2. Wide Variety Function of p53 and its Metabolic Role

Life
Reprogramming

Guardian of
The Genome

Aging
Senescencep53
Chromatin
Complex

Epigenome
Analysis

Death

DiseaseApoptosis

CancerDiabetescommon mechanisms of and novel therapeutictargets for cancer and life-style related disease2

Research
Highlights
Shinichiro Motohashi
Associate Professor, Dept. of Medical Immunology

NKT cell-based Immunotherapy for non-small cell lung cancer(poor responder group). The median survival time (MST) of thegood responder group was significantly better than that of the poor
responder group (Figure 3). This result suggested IFN-γ might be avaluable biological marker for predicting the clinical course in
response to α-GalCer-pulsed APC administration. Two candidate
biomarkers that might be associated with immune responses werealso detected (Figure 4). From these results, “intravenous injectionof α-GalCer-pulsed APCs for the treatment of non-small cell lungcancer” was approved by the Japanese Ministry of Health, Labourand Welfare as “Highly Advanced Medicine” (Sep. 28th, 2011). In
addition, the phase I study of trans-bronchial intratumoral or
intranodal α-GalCer-pulsed APC injection was initiated in patientswith advanced NSCLC to activate iNKT cells in the tumor
microenvironment more efficiently. Further investigation to clarify
the mechanisms of iNKT cell-mediated anti-tumor immunity is inprogress. It would be advantageous to identify biomarkers that may
predict the clinical outcome before the treatment, and selectsubgroup(s) of patients who will most likely have a significant
clinical benefit in any or a specific type of iNKT cell-based
immunotherapy.

Invariant natural killer T (iNKT) cells are activated by a specificligand, α-Galactosylceramide (α-GalCer), in a CD1d-dependent
manner, and upon activation iNKT cells modulate the function of awide variety of other immune cells, including anti-tumor effector
cells in both a direct and an indirect manner (Figure 1). Early
clinical trials of iNKT cell-based immunotherapy demonstrated thatthe infusion of ligand-pulsed antigen presenting cells (APCs) or invitro activated iNKT cells was safe and well tolerated in patientswith non-small cell lung cancer (NSCLC). Intravenous injection of
α-GalCer-pulsed APCs, which induces the activation ofendogenous NKT cells and NKT cell-dependent responses, waswell tolerated. In this clinical trial, whole PBMCs cultured with
GM-CSF and IL-2 are used as antigen presenting cells (Figure 2).
These APCs include DCs that can activate iNKT cells efficiently.
The number of IFN-γ-producing cells in PBMCs after restimulation
with α-GalCer in vitro was detected to evaluate the functional
iNKT cells and NK cells that were subsequently activated by
activated iNKT cells. The number of IFN-γ-producing cells wasclearly elevated (good responder group) in 10 patients, while theremaining 7 patients did not show any increased IFN-γ production
Figure 1

Figure 3
NK cellα-GalCer
CD1d
DC

Vα
α 24/Vββ11
Antigenreceptor

CD8+ Tcell
Indirect killing

IFN- γResponse group

Direct killingtumor

NKT cellNonresponse
group

Figure 2

Figure 4
LTB4DH102

p=0.0117DPYSL3
101

101

100

p=0.0117

100

101

10-1

100
10-1
100

10-2
10-2

10-1

apheresis
IL-2 and GM-CSF

PBMC

α-GalCer

IIntravenous
injection

10-1

10-2

α-GalCer pulsed DCs

10-3

10-3

pre

post

good responder
group

3

10-2

pre

post

poor responder
group

10-4

pre

post

good responder
group

10-4

pre

post

poor responder
groupResearch Highlights

Annual Best Research Award 2011

This award is given to Ph.D. students in the G-COE relevant
fields whose research is recognized as most outstanding
through the year. The Annual Best Research Award 2011 went to
Dr. Masayuki Miyagi (G-COE-RA) and Dr. Yusuke Endo who is
now a G-COE Fellow.

Masayuki Miyagi
G-COE Research Assistant
Dept. of Orthopaedic Surgery

The pathomechanism of chronic diskogenic low back pain
higher in the injured group than in the non-injured group for theentire eight weeks studied (Figure 2). Thus, in this lumbar IVD
injury model, local inflammation calmed down to normal levels
within two weeks, but activation of the sensory nervous system
continued for at least eight weeks. (Miyagi M, et al., Spine 2011 inpress)
There are two limitations to this study. First, there are somedifferences in the findings between animal models such as the IVD
injury model and human specimens. When considering diskogenic
low back pain, not only injury but also mechanical stress such as
dynamic compression may be an important factor in humandegenerated IVDs. Now, we are proceeding with a new project toinvestigate in a newly developed IVD dynamic compression model(Figure 3). Second, the evaluation of low back pain behavior is alimitation of most basic research animal models. We previously
reported the gait changes using the CatWalk system (Figure 4) in a
rat model of lumbar myofascial inflammation and suggested that
we may be able to apply this system to the evaluation of low backpain behavior in rats. (Miyagi M, et al., Spine, 36(21):1760-4,
2011.) Now we are proceeding with a new project to investigate thelow back pain behavior using the CatWalk system in a rat model ofthe IVD injury model.

Low back pain is one of the most common and important
medical problems. Intervertebral disk (IVD) pathology is thought tobe a significant contributor to low back pain. However, its
pathophysiology remains incompletely understood. Shinohara firstreported the presence of nerve fibers in the deep layers of IVDs in
diskogenic low back pain patients. Further investigations havefound high levels of inflammatory mediators in degenerated human
IVDs. The results of these studies suggest that the presence ofsensory nerve fibers in IVDs and the persistent production of
inflammatory mediators in degenerated IVDs may lead todiskogenic low back pain.
However, the pathomechanism of “chronic” diskogenic low backpain was not absolutely clear. We compared in rats the behavior of
the sensory nervous system (neuropeptides in dorsal root ganglion(DRGs) and glia in the spinal dorsal horn) and inflammatory
mediators (nerve growth factor: NGF, TNF-alpha, IL-6) inexperimentally injured IVDs over the first eight weeks following
experimental IVD injury. In this study, inflammatory mediator
levels in injured IVDs were significantly higher than control levels
for four days but by the end of second week no longer significantly
differed from control levels (Figure 1). On the other hand, theup-regulation of neuropeptides in DRG neurons and the microglia
and astrocytes in the spinal dorsal horn remained significantly
Figure 1. The production of inflammatory mediators in IVDs
(pg/mg)20

NGF(pg/mg)0.1

TNFα

vertebra 5
IVDvertebra 6
IVD
vertebra 7

0.8

0.08

15

(pg/mg)1

Figure 3. IVD injury or/and dynamic compression model

IL-6

0.06

0.6

0.04

0.4

0.02

0.2

0

0

non-inj
1d
4d
1w
2w
4w
8w

0

non-inj
1d
4d
1w
2w
4w
8w

5

non-inj
1d
4d
1w
2w
4w
8w

10

Figure 2. ImmunohistochemistryNon-Injury
Iba-1(microglia)

6
7

7

Figure 4. CatWalk gait analysis system

Spinal dorsal horn

InjuryCGRP(neuropeptide)

5
6

conventional IVD
IVD injury &IVD dynamic
injury model compression model compression model

p<0.05 difference compared with control group SNK test

DRG

5

GFAP(astrocyte)

4Research Highlights

Annual Best Research Award 2011

Dr. Endo also received the Dean’s Excellent Record Award,
Graduate School of Medical and Pharmaceutical Sciences,
Chiba University.

Yusuke Endo
G-COE Fellow
Dept. of Immunology

Identification of pathogenic memory Th2 cells, which are required for allergic
inflammation and clarification of molecular mechanisms controlling IL-5
production in memory Th2 cells.
Th cells remains to be analyzed in detail. Therefore, this study is an
important subject that needs to be further analyzed to understandthe development of disease including allergic disorders.
Recently, we found that memory Th2 cells expressed CXCR3, awell-known marker for Th1 cells, and were subdivided into four
distinct subpopulations according to the expression of CD62L and
CXCR3. IL-5-producing cells were predominantly detected in the
CD62LloCXCR3lo population in memory Th2 cells (Figure 3) andthis population played a critical role in the memory Th2-dependent
allergic airway inflammation. Furthermore, T-box transcription
factor, Eomesodermin (Eomes) was up-regulated in memory Th2cells and suppressed GATA3-dependent IL-5 production, which
resulted in reduced airway inflammation (Figure 4). This study was
published in the November issue of Immunity (Endo et al.,Immunity 35, 733).
In this study, we have identified pathogenic memory Th2 cells
and clarified molecular mechanisms, which are required for the
induction of memory Th2-dependent eosinophilic airway
inflammation. We will apply this study to human memory CD4 T
cells for the treatment of allergic disorders.

Approximately 30% of the Japanese population suffers fromallergic disease. However, only symptomatic therapies are presently
available, and no curative therapeutic strategies have beendeveloped. We are trying to clarify the underlying molecularmechanisms of allergic disease, focusing on the role of CD4-positive
helper T (Th) cells. Effector Th cells are subdivided into at least
three distinct subsets (Th1, Th2, and Th17 cells) according to theircytokine production profiles (Figure 1). Among them, Th2 cells
produce IL-4, IL-5, and IL-13 (so-called Th2 cytokines) and arethought to play a critical role in allergic disease.
After antigen clearance, some of the effector Th cells aremaintained as memory Th cells for long periods in vivo through thecontraction phase (Figure 2). Memory Th cells play an importantrole in ‘immunological memory’ that is central in immune responses,
and they are involved in a wide variety of diseases. Memory Th
cells displayed higher heterogeneity as compared to effector Th
cells and are subdivided into several subpopulations according to
the expression of cell surface molecules, cytokine production, andexpression of transcription factors even in the same Th subsets.
However, functional difference of each subpopulation in memory
Figure 1. Differentiation and function of helper T cell (Th) subsets

Figure 3. The CD62LloCXCR3lo population of memory Th2 cells
selectively produces IL-5

Host defense

Involved in autoimmune disease

Th1

TCR

y
Humoral immunity
IL-4

GATA3
IL-4,IL-5,IL-13

Naive CD4

Post cell sorting

Memory Th2 cell
CXCR3IL-12/IFNγ

Against intracellular pathogens

IFNg

CXCR3

APC

T-bet

Against helminth infections

H/H

L/L

H/L

CD62L

CD62L

Involved in allergic disease

IL-4

Th2

L/H

IL-5

CD62L/CXCR3
H/L
H/H Memory Th2
L/L
L/H

IL-13

IFNγ

IL-6/TGFβ
Against extracellular bacteria
RORγt
IL-17

0

10

0

5

0

5

0

10

20

Relative expression (/HPRT)

Involved in autoimmune disease

Th17

Figure 4. Identification of pathogenic memory Th2 cell andmechanisms controlling IL-5 production

Figure 2. Overview of memory Th cell generation

Cell number

Expansion
p
Ag
stim.

Contraction
Maintenance ofgPathogenic
Memory Th2

Memoryycell number
functionA

Memory Th2

Naive

TCR
Eomes

Time

Effector(Th1, Th2, and Th17)

Eomes
IL-5
IL-4
IL-13

Memory5

CD62LhiCXCR3hi
CD62LhiCXCR3lo
CD62Llo CXCR3hi
C
TCR

CD62LloCXCR3lo
B
TCR
Eomes

Eomes

GATA3

GATA3

GATA3

Il5

Il5

Il5

++
++
++

+
++
++

+
++
++

Research
Highlights

Dr. Kenta Shinoda, who is now a G-COE Fellow, was awarded the Dean’s Excellent
Record Award, Graduate School of Medical and Pharmaceutical Sciences, Chiba
University, at the graduation ceremony. His research is shown below.

Kenta Shinoda
G-COE Fellow
Dept. of Immunology

Role of CD69 for the generation of memory T helper lymphocytes
Immunity is said to have a memory for most invading agentsencountered before, because a second encounter with the same
agent prompts a rapid and vigorous response. Memory T helper(Th) lymphocytes play an essential role in immunological memory.
In their absence, the generation of long-lived plasma cells and themaintenance and secondary expansion of memory cytotoxic T cells
are impaired. Despite their eminent importance for the regulation of
immune reactions and immunological memory, little is known
about the molecular mechanisms of the generation and maintenanceof memory Th cells.
After antigen recognition, naive Th cells activate and expand
into a large pool of effector Th cells in secondary lymphoid organs,such as spleen and lymph nodes. Most of the effector Th cells die
during a phase of contraction; however, a small proportion survive
and differentiate into memory Th cells in body. To date, we haveshowed that effector Th cells relocated to the bone marrow (BM)after their activation in secondary lymphoid organs, and weremaintained as memory Th cells in the BM. In addition, memory Th
cells persist as resting in the BM, next to IL-7-secreting stromal cells,suggesting that IL-7 is the prime survival signal for these memory
cells. Upon challenge with the antigen, they could efficiently
induce the production of high-affinity antibodies by B lymphocytes.
Taken together, these results suggest that effector Th cells relocate

2

Figure 3. CD69-deficient Th cells fail to provide
efficient help for B cells
High-afffinity antibodies (μg/ml)

Figure 2. CD69 is required for the generation of
antigen-specific memory Th cells
Bone marrow antigen-spe
ecific
CD44hi CD4
T cells (x104)
C

Figure 1. Memory Th cells (red) reside on stromalcells (blue) and express CD69 (green)

to the BM and maintain on a survival niche for a long period.
However, mechanisms involved in this process remain unknown.
In the steady states, resting memory Th cells mostly express
CD69 (Figure 1), which is well-known as an early activation
marker of lymphocytes. We focused on CD69 and examined toclarify the role of CD69 in memory Th cells. We enumerated
memory Th cells in CD69-deficient mice. Although CD69 does notappear to be required for the development of effector Th cells, thenumber of antigen-specific memory Th cells in CD69-deficient
mice dramatically decreased compared to wild-type mice (Figure2). In addition, CD69-deficient Th cells failed to induce an efficient
production of high-affinity antibodies in vivo (Figure 3). In the wayof generation of memory Th cells, we show that CD69 regulates thehoming of effector Th cells to BM as an adhesion molecule. These
data suggest that CD69 plays a crucial role in the generation ofmemory Th cells and that the relocation of effector Th cells to thebone marrow is essential for generation of memory Th cells (Figure4). In the case of allergy or autoimmune diseases, we think there
are similar mechanisms underlying the generation and maintenanceof harmful memory Th cells. We will clarify the mechanisms
involved in the maintenance of harmful memory Th cells in chronic
diseases.

CD69 +/+
CD69 -/-

1

CD69 +/+
CD69 -/-

6

4

2

0

0

20

0

40

60

Days

Figure 4. CD69 regulates the generation of memory Th cells
Expansion ofeffector Th cells

Invasion of pathogens

Generation and maintenanceof memory Th cells

Secondary lymphoid organs

Production ofhigh-affinity antibodies
BM
CD69

Naive
Th

EffectorTh

Homing

CD69

MemoryTh

Provide help for the
production of highaffinity antibodies

niche㸦IL-7+ stroma㸧

Antigen-presenting cells
Th: helper T lymphocytes

6ReportsofStudy Abroad

Eight young researchers involved in this program contributed reportsof study abroad. Let’s hear their experience and advice.

TSLP in Allergic Diseases
Masayuki Kitajima
Immunology Program
Benaroya Research Institute at Virginia Mason(from October 2008)
With collaborators and graduate students, we reported that enhanced
Th2 differentiation and allergen-induced airway inflammation in Zfp35deficient mice (Kitajima et al, J Immunol, 2009) and memory Th2 cells
induce antitumor immunity by activating NK cells (Kitajima et al,
Cancer Res, 2011). With strong hope in international collaboration
cultivated in the research activities I have begun research activities as afellow researcher in unison with the idea of Global COE program. Aftera year and half as G-COE fellow, now I am a postdoctoral fellow in thesame laboratory (that of Dr. Steven Ziegler).
The cytokine thymic stromal lymphopoietin (TSLP) has been
implicated in the development and progression of allergic inflammationin both humans and mice. We reported that TSLP enhances the functionof Th2 cells as a result of studying as a G-COE fellow (Kitajima et al,
Eur J Immunol, 2011). Thus, the novel function of TSLP suggests that
TSLP is involved in homeostasis of Th2 cells in allergic inflammation
directly. Next, I am investigating TSLP-activated DCs, which have notbeen extensively investigated. In this study, using CCL17-eGFP
transgenic mouse-derived FLT3L-induced bone marrow DC subsets(CD11bHigh DC, CD24High DC, and pDC), we found that CCL17-eGFPexpressing DCs induced by TSLP were part of CD11bHigh DCs. And the
GFP-positive DCs had a high level of costimulatory molecules and
MHCII expression compared to the GFP-negative DCs, and they had
increased Th2 differentiation in vitro. Taken together, these results may
indicate identification of TSLP-targeted DCs and establishment of theStudy at University of Wisconsin-Madison
Jiro Terada
Dept. of Respirology, Graduate School of Medicine, Chiba University
Dept. of Comparative, University of Wisconsin Madison（from April 2009 to March 2011）[]

I’d like to express my appreciation of the opportunity to have worked
as a G-COE-RA. I’ll briefly present my research life from 2005 to
2011.
My PhD study started after I had worked as a respiratory physician
for five years. The goal of my research was to study basic science in
respiratory medicine. The first half of my PhD research was respiratoryneuro-regulation using physiological methods under professors Fukuda
and Kuwaki in Dept. of Autonomic Physiology, while the second half
was cell-cell communication using pancreas cell-line with moleculartechnique. After the completion of my PhD study, I went to the
University of Wisconsin Madison with my sons and wife. I worked
there for two years under Gordon Mitchell who is well known in the
study of respiratory neuroplasticity. My research projects were 1)
Diaphragm long-term facilitation during sleep in unanesthetized ratsand 2) Respiratory neuroplasticity for respiratory failure in spinally
injured rats. Madison is a beautiful and safe capital city of the state of
Wisconsin in the midwestern U.S. It was more difficult at first tounderstand the culture and English than I expected. But thanks to myboss, colleagues and friends in Japan, I’ve finished my projects there.

7

DC assay system, and suggest that it has a potential for providing new
information on the role of TSLP-activated DCs in allergic inflammation.
In research activities that keep evolving with the globalization,
learning the research form of real overseas research laboratories is sure
to become a provision of the postgraduate who conducts research
activities of Japan in the future. Moreover, I am convinced that theprocess of piling discussion and study results with a worldwide
researcher has touched off the growth of the postgraduate who has theconnection with the fellow researcher's own growth.

With members of the laboratory
Masayuki Kitajima (first from left in top raw), Steven F. Ziegler (third from leftin middle raw)

Now I think I had great and irreplaceable experience with my family.
So I think it would be good challenge for young researchers to do someresearch in foreign countries. Again, I was deeply grateful to everyone
who encourages my research life in Chiba and Madison, especially themembers of the G-COE program.

With members of the laboratory
Jiro Terada (second from right in front raw), Gordon Mitchell (third from right in
middle raw)

A research project report: from Universityof Michigan

the NLRP3 inflammasome is involved in avariety of metabolic diseases including
obesity, atherosclerosis and type 2 diabetes. I
believe our current project in this field may
have the potential to lead to better treatment
for inflammasome-associated diseases.

Yuumi Nakamura
Department of Pathology, University of Michigan(from May 2009)
I had finished a graduate degree, and then worked as
G-COE research fellow at Chiba University in 2009.
During that period, my research project was focused on therole of the NLRP3-inflammasome in mast cells. After that,to investigate this more deeply, I started to work as a
research fellow in Dr. Gabriel Nunez’s lab at the Universityof Michigan. I’m now using a “human disease-associatedNlrp3 mutant knock-in mouse” that is a very powerful tool
for analyzing the role of Nlrp3-inflammasome in vivo.
Recently, many studies have suggested the activation of

At Dr. Nunez’s home(from left, Gabriel Nunez, Nakamura’s family)

Crucial role of CD8αα for T cell memory survival
Ryo Shinnakasu
Division of Developmental Immunology
La Jolla Institute for Allergy & Immunology(from May 2009)
A hallmark of immune T cell memory is that repeated infections
with a pathogen are met with more rapid and enhanced protective
immunity against that organism. Effector memory T cells (EM) arelocated in various tissues and have a heightened and immediate
effector function. By contrast, central memory T cells (CM) residewithin lymphoid tissues and require proliferation and differentiation
to become effector cells.
On the other hand, allergy responses are caused by an abnormal
immunoresponse to antigens that are non-pathogen originally.
Memory T cells are known to affect these allergy responses.
When I belonged to Chiba University I performed my basic
researches about generation of EM and CM for the development of
the allergic prevention and cure by the immune system.
Currently, I belong to the laboratory of Dr. Hilde Cheroutre at the
La Jolla Institute for Allergy & Immunology. It becomes clear fromour past study gradually that CD8αα serve as key components formaintain the intraepithelial lymphocytes which is a kind of effector
memory T cells and now I am performing the analysis from amolecule level about the function mechanism of CD8αα.
I have had a lot of precious experience since I started research in
U.S. 2 years ago. I want to make the most of these experiences for
my future research in Japan and I want to tell students what I felt
through research life in U.S for about the differences of how to leadand the way of thinking for research in comparison to Japan.

With members of the laboratory
Haruhiro Toko (fifth from left), Mark Sussman (center in back raw)

Heart Institute in San Diego State University
Haruhiro Toko
Department of Biology
San Diego State University(from February 2010)
I belonged in Cardiovascular Science and Medicine, Chiba
University Graduate School of Medicine. From Feb., 2010, I havestudied at Heart Institute in San Diego State University (P.I. Mark
Sussman). In this lab., almost all researchers study about the role ofkinases such as Akt and Pim1, or the role of cardiac progenitor cells
in the pathological heart.
Before coming here, I studied about the molecular mechanismsof how some gene mutations induce dilated cardiomyopathy. I
clarified that a kinase, CaMKII, is an important factor to induce
cardiac dysfunction in dilated cardiomyopathy. From the results, I
was interested in the role of kinases in the heart diseases. Kinases /phosphatases regulate crucial aspects of growth and survival
through phosphorylation / dephosphorylation of target substrates.
Many reports involved in my study demonstrated that processes ofcardiac hypertrophy, myocardial infarction, and heart failure are
dictated in part by which kinases / phosphatases are involved andalso by the intensity and duration of specific enzymatic activities.
While research has identified numerous critical regulatory kinases
and phosphatases in the myocardium, the intracellular mechanism
for temporal regulation of signaling duration and intensity remains
obscure. I would like to clarify the mechanism, so I decided tocome here. Now, I have focused on an enzyme, which regulates
phosphorylated kinases / phosphatases, and have examined the roleof the enzyme in the physiological and pathological heart.

With members of the laboratory
Ryo Shinnakasu (third from left), Hilde Cheroutre (third from right)

8

Reports ofStudy
AbroadMy professional and cultural experiences in the
United States

A report of studying abroad at Haverd Medical
SchoolJun Ikari

Kaoru Ito

Pulmonary, Critical Care, Sleep and Allergy Medicine, Department
of Internal Medicine, University of Nebraska Medical Center(from April 2011)

Department of Genetics, Harvard Medical School(from April 2011)
I did the research about heart failure and its pathophysiology in
Chiba University. Since the mechanisms of heart failure arediversified, I studied a molecular biological approach. At the sametime, I got interested in the genetic approach. Next generation
sequencer (NGS) and the new methods which can be performed in
NGS might increase my interest in genetics. And I thought it was agood idea to pursue the pathophysiology of heart failure by
investigating cardiomyopathy which is an extreme model ofgenetic heart failure. So I asked my boss and my superiors where
the best lab was to study cardiomyopathy by genetic approach andI got valuable advices. Fortunately, now I work for the lab which isfamous for cardiomyopathy.
Our research subjects are familial heart diseases, the large cohort
study regarding cardiac hypertrophy and mouse models of heart
failure. Now I am engaged in the first and second ones. Because
we deal with huge data of genome, RNAseq and ChIPseq and soon, our lab members are divided into two groups, a dry groupwhich is engaged in the computer work and a wet group which isengaged in small animal experiments. Because I am curious about
the new technique, I also do some work which is related with asmall animal experiment though I am in a dry group.
In our lab, when we conduct experiments which are concernedwith NGS, what I need to do is just to prepare the samples because
our research assistants and technicians do the other experiments.
I thought that division of labor improves the efficiency. But I
make an effort to watch the experiment because I am a beginner inthe field. Our lab uses human samples mainly and we can get
human samples easier than we do so in Japan, not only blood
samples for DNA extraction but also fresh organ samples for RNA
extraction. In addition, a lot of collaborations with other institutes
are being made and many labs provide their ideas to advance theresearch. I was surprised at the systematic and effective research
environment.
Finally, just before I went to the US to study abroad, the biggest
earthquake we have ever experienced hit Japan. So being in
anguish over whether I should leave Japan or not, I came to
Boston. Now I still think about it. But I believe that I must do what
I should do in the US and I will find a way to give something backto Japan after returing to my country.

I have researched at The University of Nebraska Medical Center
since April 2011 under the supervision of Professor Stephen I.
Rennard who is one of the leading authorities on chronic
obstructive pulmonary disease (COPD) around the world.
In Japan, I researched on ‘A role of PHF11 in activated B cells’.
Polymorphism of the PHF11 is highly associated with high serum
IgE levels and clinical severity of asthma. We found exogenous
murine Phf11 in activated B cells augments frequencies of classswitch recombination to IgE and generation of IgE-secretinglong-lived plasma cells.
In the United States, I am evaluating the altered repair function oflung fibroblast that contributes to the development of COPD. Also I
am exploring the therapeutic approach to restore the repair function
in COPD. As for my advice for studying abroad, I recommend
cultivating the ability to research independently, because theautonomy of the individual is valued in the United States. I also
think it is important to improve discussion skills in English, because
researchers are requested to actively join discussions at a meeting.
The experience of communicating in English at the G-COE
conferences and the laboratory meetings at the Department ofDevelopmental Genetics has been really great help for me
professionally.
I live in the city of Omaha, Nebraska. Omaha is a very quiet, safe
and serene place to live. I enjoy watching sports, sharing meals withfriends at my home and travelling. I can feel America’s dynamism
through the vast extent of land and diverse cultures. I want to growas a person and a researcher utilizing these experiences. I’m deeply
grateful that my position here will afford me that opportunity.

With members of the laboratory
Jun Ikari (second from right), Stephen I Rennard (second from left)

How solve the drug lag and how improve
Translational Research
Masaya Koshizaka
Duke Clinical Research Institute, Duke University(from July 2011)
Since 2007, I engaged in improving the management of the clinical
trials scientifically and ethically at the Chiba University Clinical ResearchCenter. It is necessary to have the objective data center for clinical trials.
I involved in setting up and operating the data center, in order to manage
large clinical data properly.
Japan lags behind the other countries in clinical trials.
It is told that it takes more time and money to do clinical trials inJapan than the other Asian countries. It is one reason of the drug lag, thedelay of domestic introduction of overseas innovative medicine.
It is necessary to clear up the drug lag, in order to use new drugs forJapanese patients as soon as possible. Thus we have to participate in the
global clinical trials. For this goal, I participate in the actual global
clinical trials of cardiovascular diseases and diabetes, as a researcher at
Duke Clinical Research Institute (DCRI), the top level research institute.
DCRI is in North Carolina, which has nature and enough resources ofstudy. In DCRI there are many research fellows, who came from

9With members of the laboratory
Kaoru Ito (first from left in top raw), Jonathan.G.Seidman(Professor, first from right in top raw), Cristine.E.Seidman(Professor, third from right in top raw)

Australia, Brazil, Canada, China, Denmark, Holland, Italy, and Taiwan.
I could learn not only clinical trials, but also western communicationand culture.
After going back to Japan, I would
like to improve Japanese clinicalresearches.
IN DCRI I also participate in the
Biomarker project in order to learn
about Translational Research (TR). I
would like to contribute to TR of
Chiba University in the future, too.
At the home of Dr. John H. Alexander (Koshizaka’s mentor)(From left, Koshizaka’s family, Alexander’s family, andHideki Hanaoka)

The 8th
Global COE
WorkshopPresentation and Discussionby G-COE-RA
1st Lecture Hall, Main Building 1F, Faculty of Medicine, Chiba University

February 19,
2011

The 8th Global COE Workshop that was the fifth workshop in “Presentation andDiscussion by G-COE-RA” took place on February 19. Thirty-three G-COE-RAs presented
the progress of each research. Some of them talked coolly about the results in an assuming
tone, and some kept on talking with much enthusiasm that might be brought from passion totheir own research studies, or other might have got nervous for their first experience ofpresentation in English. The audiences were drawn into their presentations that were full ofeach RA’s characteristics and charm, while also being impressed with the research quality
on which each RA is working. Most of the presentations were assertive and sophisticate.
Students took English Presentation Seminar, which was introduced at the Graduate Schoolof Medicine and Pharmaceutical Science last summer; we believe it has contributed a lot for
their improvement. The participants enjoyed discussions through a barrage of questions
made by the students in the Q and A periods. This workshop was very active and fruitful.
We have seen the RA grow by increasing experience in presentation and discussion in thismanner, and realized the significance and evident progress of the workshop as well as the
Global COE Program.

Advanced Medicine Progress Seminar by
Seeds Grant Competition Winners 2010
March 8,2011

The 3rd Auditorium, Chiba University Hospital 3F
We held a seed grant competition for advanced medicine for the purpose of seed
exploitation, acceleration of Translational Research (TR) and enhancing young researchers’
motivation to do clinical study, at Chiba University. We have been supporting eight selected
excellent study proposals in providing research grants and regular discussions, in order toaccelerate the realization of TR. An open seminar took place on March 8, 2011 to reportprogress in these studies.
Each of the studies is aimed at developing tumor markers, diagnostic drug for tumor
localization, or novel therapeutic agents and treatments targeting various diseases including
neurodegenerative diseases and malignant tumors. From the reports at the seminar, we
recognized that the stage of research varied greatly among the studies, however, energetic
efforts have been made to promote them toward realizing TR. Two studies we make acontinuing support were reported the steady progress compared to last year. We willcontinue to support by holding this seed grant competition until we will establish a clear
trend to promote the research for diagnostic or therapeutic development generated from
Chiba University starting from this in-house seed exploitation.
Shinichiro Motohashi
Program Leader,Seeds Grant Competition10

March 29,
2011

Inaugural Joint Scientific Meeting– Medical University of Vienna andChiba University –Conference Room, Main Building 2F, Faculty of Medicine, Chiba University

Inaugural Joint Scientific Meeting --Medical University of Vienna (MUV) and Chiba University-- was heldon March 29, 2011. This was the first event on the academic and research collaboration activities agreed on in2010 between Medical University of Vienna in Austria and Chiba University. The symposium program wasdesigned by the Chiba University Graduate School of Medicine and Chiba University Hospital in order toencourage the medical research activities between both universities, with supports by Chiba University
G-COE program and the Health and Labor Science Research programs for Translational Research.
The symposium began with the opening remarks by Dr. Yoichi Kohno, director of University Hospital. The
focus of this workshop was on “The LDL receptor to immature cell diseases”. At first, Dr. Hideaki Bujo,
Graduate School of Medicine (Chaired by Dr. Takashi Miki, Graduate School of Medicine) made apresentation on the LDL receptor family study overview. Dr. Chiaki Nakaseko, Graduate School of Medicine
and University Hospital (Chaired by Dr. Atsushi Iwama, Graduate School of Medicine), then spoke about the
prognostic impact of serum soluble LR11 on acute leukemia.
Message with Selected Slides
The last presentation was on the adipocyte-based gene therapy
for interactive serum protein deficiencies by Dr. Masayuki
Dear President Dr. Saito, dear Colleagues!
Kuroda, Chiba University Hospital (Chaired by Dr. Koutaro
I deeply regret that unfortunate events bringing sadness to many
Yokote, Graduate School of Medicine). The symposium
Japanese people preclude my participation in this Inauguralfinished with the closing remarks by Dr. Haruaki Nakaya, dean
Joint Scientific Meeting of our Universities.
of Graduate School of Medicine.
My thoughts and hopes are with all of you.
I wish you and your colleagues a successful meeting now, and a
The symposium was much productive with the enthusiastic
rapid recovery from the dire consequences of the powers of
discussion by many participants for the future collaborative
nature.
research projects. The joint meeting will be next held at MUV.
Hoping that we will be able to meet soon,
With best regards,

Hideaki Bujo
Joint Program Chiba University Office

Wolfgang J. Schneider

The 9thGlobal COE
WorkshopPresentation and Discussion by
G-COE-RA
1st Lecture Hall, Main Building 1F, Faculty of Medicine, Chiba University

June 4,2011

The 9th Global COE Workshop that was the sixth workshop in “Presentation and Discussion by G-COE-RA”
was held on Saturday, June 4. This year 33 graduate students selected as G-COE-RAs, including the 17 RAs
newly selected. The RA has been widely recruited from the related research field of this program, thus theincreasing number of departments has been involved in this program every year. In particular, in the Graduate
School of Pharmaceutical Sciences, the number of the RAs has doubled from last year to 10 and consequently
three departments have newly involved. New RAs made a presentation on their experimental plan, and theRAs selected again this year on research results and progresses additionally in English. In the Q and A periods,
each RA was pelted with questions. To respond them smoothly actually requires higher English communicative
ability. We are sure that the RAs will further improve theability making use of program designed for that purpose,including a video of the presentation and Presentation
Seminar for scientific seminar in English, in addition toexperience in the workshop. Besides the student’s mentors,
two advisory professors evaluated each presentation. The
increasing number of advisory professors newly involved
could be a sign for fulfillment and progress of thisprogram.
11

IMSUT/RCAST - Chiba University
Global COE Joint Retreat 2011

“Toward new era in the basic and clinical immunology”
Date: September 17-18, 2011
Place: Oiso Prince Hotel

IMSUT/RCAST - Chiba University Global COE Joint Retreat was held for the first time in cooperation withThe IMSUT (Institute of Medical Science, The University of Tokyo) & RCAST (Research Center for Advanced
Science and Technology, The University of Tokyo) Global COE Program “Center of Education and Research
for the Advanced Genome-Based Medicine: For personalized medicine and the control of worldwide infectious
diseases”. One-hundred and ten graduate students and researchers from the both G-COE programs gathered andstudied together for two days, developing new interaction and stimulating active discussion. Dr. Toshio Suda,
Professor of Keio University, gave a keynote lecture entitled “Stem Cells and Cancer Stem Cells”. The program
was organized by the program committee
in which members are Drs. Taishin
Akiyama and Jun Kunisawa from the
IMSUT and Dr. Hiroshi Nakajima from
Chiba University. The followings arereports from some participants.

Toshio Suda

Professor
Department of Cell Differentiation,
Keio University School of Medicine

At the poster session, Soichi Tofukuji, G-COE-RA,
Department of Immunology, Graduate School of Medicine,
Chiba University, received the Best Poster Award.

Kotaro Suzuki

Department of Molecular
Genetics, Graduate School of
Medicine, Chiba University
The Chiba University G-COE Retreat 2011was held on September 17 and 18 at Oiso
Prince Hotel. This was our 3rd Retreat and
IMSUT/RCAST-Chiba University G-COE Joint
Retreat. The maximum number of graduate
students and PI researchers participatedcompared with the past 2 times of conventions.
Also in the contents, almost all presentations
in each field were high quality. In Poster
Presentation as well as Oral Presentation, we
had in-depth discussion. We believe that thisprogram provided mutual understanding
between students and PI.

Ryuta Uraki

Division of Virology,
The Institute of Medical Science,
The University of Tokyo
I am a master course’s student researching
the pathogenicity of influenza virus. I was so
nervous because the theme of this seminar
was immunology, not virology which is mymajor. However, in spite of my anxiety, thisseminar was so attractive and exciting for me
to get fruitful advice about the interesting
phenomenon I have focused on fromwonderful professors and seniors. Further, thisseminar gave me fine chance to present myresearch orally in English and to communicate
with researchers in other fields. I would like tomake use of what I learned in this seminar to
perform more creative research.

Tomokazu Sumida
Hiroshi Ashida

Division of Bacterial infection,
The Institute of Medical Science,
The University of Tokyo
I attended the “IMSUT/RCAST - Chiba
University Global COE Joint Retreat 2011” at
Oiso. In this retreat, young scientists andgraduate students, who specialize in immunology, from Chiba University and IMSUT
presented recent data on oral presentations or
poster sessions. Although I am unfamiliar to
immunology (I am a bacteriologist), it wasgood opportunity to motivate myself throughdiscussion and communicate with samegeneration. In particular, advises and questions from another field specialists to myresearch subject will provide me turning
points to further execute research.
Finally, I thank retreat secretaries, executive
committees, and all participants for theirsupport and participation.

Department of Cardiovascular
Science and Medicine,
Graduate School of Medicine,
Chiba University
The G-COE retreat was held at Oiso
overlooking the blue ocean and the whitebeach. As this year’s retreat was co-hosted by
IMSUT/RCAST and Chiba University, moreprograms became available and it seemed
there was educational consideration for
training young researchers.
Many of the presentation based on thelatest immunological research provided mewith great learning experience, since I usually
study about cardiology and do not have muchopportunity to encounter basic immunologicalstudy. Learning that the immunological system
was associated with so many pathophysiological conditions and also finding the possibility of its relevance with cardiovasculardiseases, I developed deeper interest in
medical science.
During this 2-day meeting, the communication with researchers from other universities
through poster sessions and reception,encouraged and motivated me to researchharder and deeper. I really appreciate having
the opportunity to join this occasion.

12

Satomi Tanaka

Department of Cellular Molecular
Medicine, Graduate School of
Medicine, Chiba University
This year’s Global COE Joint Retreat washeld in a hotel that faced on Oiso long beach.
I felt quite nervous because I had to present
our recent work in English in front of a large
audience. However, we had a social gathering
the night before and dressed in plain clothes,
unlike an ordinary academic conference, so
we were able to have a more lively discussion
in a pleasant atmosphere. It was also a goodchance to talk to a lot of researchers fromother departments. Furthermore, I was very
impressed with the lecture on normal andcancer stem cells presented by Dr. Suda.
Thank you for giving me the valuable
opportunity.

Yosuke Kurashima

Division of Mucosal Immunology,
The Institute of Medical Science,
The University of Tokyo
I was participated in the Global COE Joint
Retreat on September 17 to 18th. It was agreat opportunity for me to learn recent research direction in the medical fields such as
Immunology, Infection, and Cancer at once. In
the keynote lecture, Prof. Suda from Keio
Univ. presented the data indicating the importance of hypoxic microenvironment for the
maintenance of hematopoietic stem cells inthe stem cell niche. Because “Immune Cell
Metabolism” is becoming one of the recent
notable fields in the immunology, theexperimental results indicating the importanceof H1F1a for the regulation of TCA cycle instem cell niche was very impressive for me.
Last but not least, I would like to express mysincere appreciation for setting up this wonderful meeting to the organizers and administrators. I'd definitely want to participate nexttime, if there is a chance like this time.

The 6th Chiba University Global COE Symposium

Immune System Regulation toward Disease Control
November 30, 2011
Hotel New Otani Makuhari, Chiba

The G-COE Program
held the 6th Chiba
University Global COE
Symposium at Makuhari
in Chiba prefecture and I
could learn the latest
immunological knowledge. At this symposium, the seminar of Dr.
Chen Dong who is oneof the authorities on Th17 cell research was very
impressive. Not only could I learn the most recent
findings in Th17 cells from his study, but this seminaralso increased my motivation for my study. Additionally,
I could gain a further understanding of signaling pathway
and cytokines for the immune system. Overall, thisseminar was beneficial for advancing my research. Moreover, when I saw the researchers vigorously discussing on
the newest topics, I persuaded myself that research in the
immunological field made further progress in the near
future. By using the knowledge acquired at this symposium, I would like to work hard and contribute to thedevelopment of medicine and bioscience.
I worked as a stuff member in this symposium and had
the opportunities to speak with some researchers directly.
However, I keenly felt the importance of English
speaking ability for communication. I
will make a conscious effort to study
English in order to be able to communicate more smoothly when participatingin the next symposium.

The G-COE Program held the 6th Chiba University
Global COE Symposium at Makuhari, on Wednesday,
November 30th, co-organized by IMSUT & RCAST
G-COE Program, The University of Tokyo. This sixth
symposium, entitled “Immune System Regulation
toward Disease Control”, focused on immune-relateddiseases. Since the regular annual meeting of theJapanese Society for Immunology was held for 3 days until thepreceding day at the Makuhari Messe, the symposium was filled withenthusiasm. Participants listened intently to presentations and discussed
topics of mutual interest heatedly. The fact that the hall was fully packed
with audience suggests that we successfully lined up attractive
researchers from home and abroad. A total of 15 talks were presented insymposium, starting with a session on lymphocyte development andhomeostasis, followed by those on immunological memory and T
lymphocyte function, and ending with one on allergy and inflammation.
Personally, I was most interested in Dr. Meinrad Busslinger’s
presentation about a genome-wide analysis of the transcriptional
regulation in B cells by ChIP-Seq and RNA-Seq. His lecture provided mewith useful information to precede my study based on the same
technology he used. At lunchtime, I happened to sit next to him andfortunately talked with him directly. I asked him some questions anddiscussed new insights into the genome-wide study. Additionally, I led
the symposium as MC and made several announcements in English. I
also took over the management of the symposium cooperating with
G-COE office members. This was my first time to do MC work andmanagement, so I found somepoints to improve at next chance.
However, it was a great
experience for me. I believe this
symposium will transmit new
information toward the rest of theworld from Chiba University,and lead to progress in the
research of immunological fieldin the future.

Atsushi Onodera
G-COE Independent Research
Associate, Dept. of Immunology

Yukiko Watanabe
G-COE-RA
Dept. of Immunology

13G-COE Seminar
Learn from the forefront
For our graduate students,
top-ranked world
researchers gave lectures
including recent findingsof their studies.

Allergy Clinical Conference
Go beyond the borders
In the conference
researchers from Dept. ofAllergy and Clinical
Immunology, Dept. ofPediatrics, Dept. of
Otorhinolaryngology andDept. of Dermatology
cross-disciplinarily
discuss allergic diseases.

Basic Science Joint Meeting (BSJM)
Coordinated by PhD student working group

This seminar has been held every week coordinated by graduate students working group.
59. January 7, 2011
Yuichi Michikawa, Senior Researcher,
RadGenomics Project, Research Center for
Charged Particle Therapy, National Instituteof Radiological Sciences
60. January 14, 2011
Harukiyo Kawamura, Assistant Professor,
Dept. of Medical Physiology
61. January 21, 2011
Kentaro Takahashi, Graduate Student, Dept.
of Molecular Genetics
62. January 28, 2011
Chiaki Iwamura, Assistant Professor, Dept. of
Immunology
63. February 4, 2011
Akira Matsuura, Professor, Div. of
Nanoscience, Graduate School of Advanced
Integration Science/Department of Biology,
Faculty of Science
64. February 18, 2011
Shinichiro Motohashi, Associate Professor,
Dept. of Medical Immunology
65. February 25, 2011
Ayako Inamine, G-COE Fellow, Dept. of
Otolaryngology, Head and Neck Surgery
66. April 1, 2011
Haruko Takano, Post Doctoral Fellow,
Biomedical Research Center
67. April 8, 2011
Mitsujirou Osawa, Lecturer, Dept. of
Cellular and Molecular Medicine
68. April 15, 2011
Kouya Suzuki, Graduate Student, Dept. of
Immunology
69. April 22, 2011
Junji Yamashita, Research Fellow, Dept. of
Immunology
70. May 6, 2011
Ayako Matsumoto, JSPS Fellow, Dept. of
Pharmacology/Dept. of Neurobiology

71. May 13, 2011
Koji Onomoto, Assistant Professor, Div. of
Molecular Immunology, Medical Mycology
Research Center
72. May 20, 2011
Hideki Hanaoka, Director/Professor, Chiba
University Hospital Clinical Research Center
73. May 27, 2011
Jing Pan, G-COE RA, Dept. ofDevelopmental Genetics
74. June 4, 2011
Hiroyuki Ishikawa, Associate Professor,
Dept. of Biology, Graduate School of Science
75. June 10, 2011
Akio Matsumoto, Associate Professor, Dept.
of Pharmacology
76. June 17, 2011
Masayuki Kuroda, Associate Professor,
Center for Advanced Medicine
77. June 24, 2011
Atsushi Onodera, Assistant Professor, Dept.
of Immunology
78. July 1, 2011
Tatsuya Sato, Assistant Professor, Dept. ofDevelopmental Biology
79. July 8, 2011
Takaaki Konuma, Graduate Student, Dept.
of Cellular and Molecular Medicine
80. July 15, 2011
Masaya Yokota, Graduate Student, Dept. of
Molecular Genetics
81. July 22, 2011
Nobuhide Tsuruoka, Clinical Fellow, Dept. of
Reproductive Medicine/Dept. ofDevelopmental Genetics
82. September 2, 2011
Takeshi Murata, Associate Professor,
Graduate School of Science14

83. September 9, 2011
Tomoaki Tanaka, Lecturer, Dept. of Clinical
Cell Biology and Medicine
84. September 16, 2011
Tohru Minamino, Lecturer, Dept. of
Cardiovascular Science and Medicine
85. October 7, 2011
Shunsuke Nakamura, Graduate Student,
Dept. of Cellular and Molecular Medicine
86. October 14, 2011
Arifumi Iwata, Clinical Fellow, Dept. of
Molecular Genetics
87. October 28, 2011
Asami Hanazawa, Graduate Student, Dept.
of Immunology
88. November 4, 2011
Motoo Kitagawa, Associate Professor, Dept.
of Molecular and Tumor Pathology
89. November 11, 2011
Tetsuhiro Chiba, Assistant Professor, Dept.
of Medicine and Clinical Oncology
90. November 18, 2011
Daiju Sakurai, Lecturer, Dept. of
Otolaryngology, Head and Neck Surgery
91. November 25, 2011
Naohiko Seki, Associate Professor, Dept. of
Functional Genomics
92. December 2, 2011
Susumu Kawamoto, Professor, Molecular
Biology, Medical Mycology Research Center
93. December 9, 2011
Soichi Tofukuji, Graduate Student, Dept. of
Immunology/Kazusa DNA Research Institute
94. December 16, 2011
Fumihiro Ishibashi, Graduate Student, Dept.
of Immunology/Dept. of Thoracic Surgery

New Members
RAs Newly Selected in 2011
Kenta Watanabe
Department of ClinicalPharmacology

Taiji Nakano
Department of Pediatrics

Satomi Tanaka
Depertment of Cellular andMolecular Medicine

Aika Nojima
Department of Cardiovascular
Science and Medicine

Mani Kohno
Department of Developmental
Genetics

Go Sasahara
Depertment of Otorhinolaryngology,
Head & Neck Surgery

Tomohiko Makiyama
Lab. of Chemical Pharmacology

Jing Pan
Department of Developmental
Genetics

Muradil Mutallip
Depertment of Otorhinolaryngology,
Head & Neck Surgery

Jun Matsumoto
Department of ClinicalPharmacology

Xin Wang
Department of Biochemistry

Yoshiki Kaneko
Department of Molecular Biology
and Oncology

Eriko Suwa
Department of GeriatricPharmacology and Therapeutics

Kenichi Ishibashi
Department of Molecular Cell
Biology

Hiroyuki Suzuki
Department of Molecular Imaging
and Radiotherapy

Moeko Hino
Department of Pediatrics

Tadashi Shiohama
Department of Pediatrics

Upcoming Events

G-COE Collaborators
Itsuko Ishii
Associate Professor, Department of Clinical Pharmacology
Noritaka Ariyoshi
Associate Professor, Division of Pharmacy, Chiba University Hospital
Koichi Ueno
Professor, Department of Geriatric Pharmacology and Therapeutics
Toshihiko Murayama
Professor, Laboratory of Chemical Pharmacology
Mitsutoshi Yoneyama
Professor, Division of Molecular Immunology, MMRC
Shinobu Saijo
Associate Professor, Division of Molecular Immunology, MMRC

G-COE Independent Research Associate
Tumes Damon
Department of Immunology

The 10th Chiba University G-COE Workshop (Presentation
and Discussion by G-COE-RA)
Date: February 11, 2012
Venue: The 1st Lecture Hall, Main Building 1F, Faculty of
Medicine, Chiba University
CCRC 10th Anniversary and CFMRC Inauguration
Symposium
Date: March 19, 2012
Venue: The Auditorium, Medical and Pharmaceutical Science
Building II 1F, Chiba University

The 11th Chiba University G-COE Workshop (Presentation
and Discussion by G-COE-RA)
Date: June 2012
G-COE Retreat 2012
Date: September 8-9, 2012
Venue: Seimei-no-Mori Resort

G-COE Fellows

The University of Auckland – RCAI- Chiba University
Symposium (tentative)
Date: Autumn 2012 / Venue: New Zealand

Yusuke Endo
Department of Immunology
Kenta Shinoda
Department of Immunology
Masaya Koshizaka
Chiba University Hospital Clinical Research Center
Shunsuke Furuta
Department of Molecular Genetics

The 7th Chiba University G-COE Symposium
Date: January 2013
The 12th Chiba University G-COE Workshop (Presentation
and Discussion by G-COE-RA)
Date: February 2013

Editor’s
Note

Here is vol.4 of our newsletter. There were earthquakes, tsunami and a nuclear power plant accident last year, but medical andclinical researches have steadily progressed. Seeing from vol. 1, you may recognize how the promotion of this G-COE program
has contributed to provide a better environment for young researchers who aim to do medical research or develop treatments.
Also events have expanded in many different directions from an international perspective. We are sure that this G-COE program
will produce many young researchers capable of working on the international stage. (Kazuo Suzuki, G-COE Coordinator)

15

Chiba University Global COE Program
Graduate School of Medicine, Chiba University
1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Tel: +81-43-226-2515 Fax: +81-43-226-2503
e-mail: igaku-gcoejimu@office.chiba-u.jp
URL: http://www.isrt-gcoe-chiba.jp