岡山大学シーズ・ニーズ創出強化イノベーション対話促進プログラム2013　→ Bound for the Future

平成25年度文部科学省「大学等シーズ・ニーズ創出強化支援事業（イノベーション対話促進プログラム）」採択課題において、SDGs推進研究大学である岡山大学が取り組んでいるイノベーション促進のための3つの対話コアである「①光技術と生命科学融合、②産官学連携強化、③未来志向型異分野ネットワーク構築」について紹介。さらに事業後も「地域中核・特色ある研究大学：岡山大学」からの未来を拓く教育研究・社会貢献活動などについて随時ご紹介。　since2013~2024, "All rights reserved" , OKAYAMA University, JAPAN.

2020年11月28日土曜日

【情報発信】資源植物科学研究所の馬建鋒教授、山地直樹准教授が2020年版の「世界で最も影響力のある科学者」に選出！

Clarivate Analytics社（旧トムソン・ロイターIP＆Science）が発表した高被引用論文著者リスト（Highly Cited Researchers）2020年版において、岡山大学資源植物科学研究所（IPSR）植物ストレス学グループの馬建鋒教授と山地直樹准教授が選出されました。馬建鋒教授は2015年版から6年連続、山地直樹准教授は5回目の受賞という快挙となります。

馬建鋒教授、山地直樹准教授は、植物の生育に不可欠な各種ミネラルの輸送メカニズムを数多く解明し、「植物・動物学/ Plant & Animal Science」分野において世界で最も影響力のある科学者として、国際的に高く評価されました。

毎年世界で注目されている本リストでは、科学と社会科学の21分野、および分野横断的なカテゴリにおいて、2009年1月から2019年12月の11年間に世界中で発表された全論文のうち、引用された回数が非常に高い（上位1％に入る）論文を複数発表した約6,200人の研究者が選出されています。引用数が顕著に高い論文は、科学コミュニティが意義深く有益であると判断した一つの目安となるため、これらの研究者は後続の研究に大きな影響を与えているといえます。

岡山大学は、2013年8月に文部科学省が日本のさらなる大学研究力向上や国際的な研究競争力強化などのために全国の大学・研究機関から選定した「研究大学強化促進事業」の選定大学（国内19大学）の一つであり、「リサーチ・ユニバーシティ（研究大学）：岡山大学」としての高い研究力を有しています。その一つとして資源植物科学研究所（IPSR）は、Top10%補正論文割合（Q値）の最も高い組織として評価されており、馬建鋒教授、山地直樹准教授は本学研究力強化促進の大きな原動力となる研究者です。

◯2020年版Highly Cited Researchers受賞者一覧はこちら

【本件問い合わせ先】
岡山大学資源植物科学研究所　教授　馬建鋒
TEL: 086-434-1209

https://www.okayama-u.ac.jp/tp/news/news_id9824.html

【offer information】Okayama University Medical Research Updates （OU-MRU）Vol.84「Friend to Foe—When Harmless Bacteria Turn Toxic」

Source: Okayama University (JAPAN), Public Relations Division
For immediate release: 27 November 2020
Okayama University research: Friend to Foe—When Harmless Bacteria Turn Toxic

(Okayama, 27 November) In a study recently published in PLoS Pathogens, researchers at Okayama University reveal novel mutations which transform bacteria into infectious bugs that are resistant to antibiotics.

Not all bacteria are naturally infectious. Several strains of innocuous bacteria turn infectious over their lifespan. However, the mechanisms by which such bacteria acquire pathogenic properties (known as virulence in microbiology terms) are still a mystery. Now, a research team led by Professor KAITO Chikara from Okayama University has identified specific gene mutations which drive this deadly switch in the microorganisms.

The researchers employed a non-pathogenic strain of Escherichia coli, bacteria commonly used in the laboratory, and exposed them to mutation-inducing processes. The bacteria were subsequently injected into silkworms. After multiple rounds of mutagen exposure, the E.coli started swiftly killing the worms, turning 500 times more lethal at a certain point. A closer look at the DNA of this dangerous strain revealed mutations in a protein known as the lipopolysaccharide (LPS) transporter. The LPS transporter resides on the bacterial membrane and funnels LPS, a bacterial toxin, from within the cell onto its surface. To understand how these mutations were linked to bacterial toxicity, the mutant E.coli were treated with host antimicrobial peptides or antibiotics. These antimicrobial molecules, however, did not hamper the growth of the mutant bacteria suggesting that the mutants had developed resistance against host immune response and antibiotics.

Bacteria store an arsenal of chemicals on their surface within small vesicles. The mutant E.coli had an abundance of such vesicles which were also rich in LPS. It thus seemed that the bugs had developed a clever mechanism to expel toxins and chemicals out of the cell. The team then analysed the LPS transporter to investigate whether its mutations played a role in this regard. Indeed, the structure of the LPS transporter was found altered in the mutant strains. A plug which keeps the channel of the transporter closed, appeared defective. Lastly, to see whether similar mutations in the LPS transporter occur naturally, the team examined bacterial samples taken from patients. As expected, these samples contained similar mutants of E.coli which were also resistant to antimicrobials. Mutations in the LPS transporter were thus conferring bacteria with crafty mechanisms to stay alive and infect host cells.

“These findings suggest that non-pathogenic bacteria can gain virulence traits by changing the functions of essential genes, and provide new insight to bacterial evolution in a host environment,” conclude the researchers. Information on such toxic mutations in bacteria are vital for diagnosing infections and developing appropriate antibacterial drugs.

Background

Virulence – A microorganism's ability to infect a host cell is known as virulence. Organisms have varying mechanisms of virulence known as virulence factors. Common virulence factors driving bacterial toxicity are chemicals that help bacteria invade and adhere to host cells or poisons that damage host cells. A thorough understanding of these factors is key to developing strategies for combatting bacterial toxicity.

Lipopolysaccharide (LPS) – LPS is a chemical that forms a major component of the outer membrane of bacteria. Once synthesized within the bacterial cell, it is pushed out through a channel known as the LPS transporter to subsequently reside within the outer membrane. LPS protects the bacterial membrane from foreign attacks and induces responses such as inflammation, fever, and septic shock when bacteria infect hosts. Thus, LPS is a crucial component of the bacterial defense system.

Reference

Chikara Kaito, Hirono Yoshikai, Ai Wakamatsu, Atsushi Miyashita, Yasuhiko Matsumoto, Tomoko Fujiyuki, Masaru Kato, Yoshitoshi Ogura, Tetsuya Hayashi, Takao Isogai, Kazuhisa Sekimizu. Non-pathogenic Escherichia coli acquires virulence by mutating a growth-essential LPS transporter. PLoS Pathogens, 2020 Apr; 16(4): e1008469.

DOI : 10.1371/journal.ppat.1008469

Correspondence to
Professor KAITO Chikara, Ph.D.
Division of Immunobiology,
Graduate School of Medicine, Dentistry and Pharmaceutical
Sciences, Okayama University, 1-1-1, Tsushima-naka, Kita-ku,
Okayama 700-8530, Japan
e-mail : ckaito(a)okayama-u.ac.jp
For inquiries, please contact us by replacing (a) with the @ mark.
http://www.pharm.okayama-u.ac.jp/lab/bunsei/

Further information
Okayama University
1-1-1 Tsushima-naka , Kita-ku , Okayama 700-8530, Japan
Public Relations Division
E-mail: www-adm(a)adm.okayama-u.ac.jp
For inquiries, please contact us by replacing (a) with the @ mark.

Website: //www.okayama-u.ac.jp/index_e.html
Okayama Univ. e-Bulletin: //www.okayama-u.ac.jp/user/kouhou/ebulletin/
We love OKAYAMA UNIVERSITY: https://www.youtube.com/watch?v=7cXlttQIk3E
Okayama University Image Movie（2020）
https://www.youtube.com/watch?v=vQxeL0ztSLA

Okayama University Medical Research Updates （OU-MRU）
The whole volume : OU-MRU (1- )
Vol.1：Innovative non-invasive ‘liquid biopsy’ method to capture circulating tumor cells from blood samples for genetic testing
Vol.2：Ensuring a cool recovery from cardiac arrest
Vol.3：Organ regeneration research leaps forward
Vol.4：Cardiac mechanosensitive integrator
Vol.5：Cell injections get to the heart of congenital defects
Vol.6：Fourth key molecule identified in bone development
Vol.7：Anticancer virus solution provides an alternative to surgery
Vol.8：Light-responsive dye stimulates sight in genetically blind patients
Vol.9：Diabetes drug helps towards immunity against cancer
Vol.10：Enzyme-inhibitors treat drug-resistant epilepsy
Vol.11：Compound-protein combination shows promise for arthritis treatment
Vol.12：Molecular features of the circadian clock system in fruit flies
Vol.13：Peptide directs artificial tissue growth
Vol.14：Simplified boron compound may treat brain tumours
Vol.15：Metamaterial absorbers for infrared inspection technologies
Vol.16：Epigenetics research traces how crickets restore lost limbs
Vol.17：Cell research shows pathway for suppressing hepatitis B virus
Vol.18：Therapeutic protein targets liver disease
Vol.19：Study links signalling protein to osteoarthritis
Vol.20：Lack of enzyme promotes fatty liver disease in thin patients
Vol.21：Combined gene transduction and light therapy targets gastric cancer
Vol.22：Medical supportive device for hemodialysis catheter puncture
Vol.23：Development of low cost oral inactivated vaccines for dysentery
Vol.24：Sticky molecules to tackle obesity and diabetes
Vol.25：Self-administered aroma foot massage may reduce symptoms of anxiety
Vol.26：Protein for preventing heart failure
Vol.27：Keeping cells in shape to fight sepsis
Vol.28：Viral-based therapy for bone cancer
Vol.29：Photoreactive compound allows protein synthesis control with light
Vol.30：Cancer stem cells’ role in tumor growth revealed
Vol.31：Prevention of RNA virus replication
Vol.32：Enzyme target for slowing bladder cancer invasion
Vol.33：Attacking tumors from the inside
Vol.34：Novel mouse model for studying pancreatic cancer
Vol.35：Potential cause of Lafora disease revealed
Vol.36：Overloading of protein localization triggers cellular defects
Vol.37：Protein dosage compensation mechanism unravelled
Vol.38：Bioengineered tooth restoration in a large mammal
Vol.39：Successful test of retinal prosthesis implanted in rats
Vol.40：Antibodies prolong seizure latency in epileptic mice
Vol.41：Inorganic biomaterials for soft-tissue adhesion
Vol.42：Potential drug for treating chronic pain with few side effects
Vol.43：Potential origin of cancer-associated cells revealed
Vol.44：Protection from plant extracts
Vol.45：Link between biological-clock disturbance and brain dysfunction uncovered
Vol.46：New method for suppressing lung cancer oncogene
Vol.47：Candidate genes for eye misalignment identified
Vol.48：Nanotechnology-based approach to cancer virotherapy
Vol.49：Cell membrane as material for bone formation
Vol.50：Iron removal as a potential cancer therapy
Vol.51：Potential of 3D nanoenvironments for experimental cancer
Vol.52：A protein found on the surface of cells plays an integral role in tumor growth and sustenance
Vol.53：Successful implantation and testing of retinal prosthesis in monkey eyes with retinal degeneration
Vol.54：Measuring ion concentration in solutions for clinical and environmental research
Vol.55：Diabetic kidney disease: new biomarkers improve the prediction of the renal prognosis
Vol.56：New device for assisting accurate hemodialysis catheter placement
Vol.57：Possible link between excess chewing muscle activity and dental disease
Vol.58：Insights into mechanisms governing the resistance to the anti-cancer medication cetuximab
Vol.59：Role of commensal flora in periodontal immune response investigated
Vol.60：Role of commensal microbiota in bone remodeling
Vol.61：Mechanical stress affects normal bone development
Vol.62：3D tissue model offers insights into treating pancreatic cancer
Vol.63：Promising biomarker for vascular disease relapse revealed
Vol.64：Inflammation in the brain enhances the side-effects of hypnotic medication
Vol.65：Game changer: How do bacteria play Tag ?
Vol.66：Is too much protein a bad thing?
Vol.67：Technology to rapidly detect cancer markers for cancer diagnosis
Vol.68：Improving the diagnosis of pancreatic cancer
Vol.69：Early gastric cancer endoscopic diagnosis system using artificial intelligence
Vol.70：Prosthetics for Retinal Stimulation
Vol.71：The nervous system can contribute to breast cancer progression
Vol.72：Synthetic compound provides fast screening for potential drugs
Vol.73：Primary intraocular lymphoma does not always spread to the central nervous system

Vol.74：Rising from the ashes—dead brain cells can be regenerated after traumatic injury
Vol.75：More than just daily supplements — herbal medicines can treat stomach disorders
Vol.76：The molecular pathogenesis of muscular dystrophy-associated cardiomyopathy
Vol.77：Green leafy vegetables contain a compound which can fight cancer cells
Vol.78：Disrupting blood supply to tumors as a new strategy to treat oral cancer
Vol.79：Novel blood-based markers to detect Alzheimer’s disease

Vol.80：A novel 3D cell culture model sheds light on the mechanisms driving fibrosis in pancreatic cancer

Vol.81：Innovative method for determining carcinogenicity of chemicals using iPS cells

Vol.82：Making memories — the workings of a neuron revealed

Vol.83：Skipping a beat — a novel method to study heart attacks

https://www.okayama-u.ac.jp/eng/research_highlights/index_id119.html

2020年11月26日木曜日

【offer information】Okayama University Medical Research Updates (OU-MRU) Vol.83「Skipping a beat—a novel method to study heart attacks」

Source: Okayama University (JAPAN), Public Relations Division
For immediate release: 12 November 2020
Okayama University research: Skipping a beat—a novel method to study heart attacks

(Okayama, 12 November) In a video-based study recently published in the Journal of Visualized Experiments (JoVE), researchers at Okayama University use stem cells to create a model of ischemic heart disease that closely replicates cardiac cells under stress.

Ischemic heart disease often leads to heart attacks and is the leading cause of death worldwide. The condition manifests when the heart muscle does not receive adequate oxygen and eventually starts giving way. Scientists rely on animal models such as rats and mice to study ischemic heart disease. However, there are pronounced differences between the rodent and human heart, creating the need for a more “humanized” model. Now, a research team led by Research Associate Professor TAKAHASHI Ken and Professor NARUSE Keiji at Okayama University has created such a model using human stem cells.

Stem cells have the unique ability to grow into any kind of specialized cell if given the right cocktail of growth factors. The team leveraged this property of stem cells and transformed them into heart muscle cells, or cardiomyocytes. To do so, human induced pluripotent stem cells (hiPSCs), a subset of stem cells, were first grown in incubators. Steadily growing hiPSCs were then differentiated into cardiomyocytes using a mix of factors promoting cardiac cell growth and subsequently incubated for 30 days. After this period, the cells were observed under a microscope to find that almost half of them had started contracting spontaneously, a property native to cardiomyocytes. Additionally, chemical assays showed that the cells were positive for cellular markers typically found within cardiac cells.

To then induce ischemic heart disease, the newly formed cardiomyocytes were grown in a medium deprived of glucose, their primary energy source. Next, nitrogen gas was gradually released into the incubators holding the cells for 24 hours, creating a hypoxic environment. When observed again, only a small number of viable cells remained which were accompanied by a conspicuous reduction in contractility. Ischemia was thus successfully simulated, closely replicating the cell death that develops in ischemic cardiac disease.

This study reports a novel and clinically relevant technique for studying ischemic cardiac disease in the laboratory. The condition was induced in cardiomyocytes derived from human stem cells mimicking patterns of damage seen in the human heart. This platform can eliminate the need for conducting complex procedures in animals and circumvent animal sacrifice. Moreover, the applications of the model in heart disease research are endless. “[This] model of ischemic heart disease, based on iPS CMs of human origin, can provide a useful platform for drug screening and further research on ischemic heart disease”, conclude the researchers.

【offer information】Okayama University Medical Research Updates （OU-MRU） Vol.82「Making memories—the workings of a neuron revealed」

Source: Okayama University (JAPAN), Public Relations Division
For immediate release: 27 October 2020

Okayama University research: Making memories—the workings of a neuron revealed

(Okayama, 27 October) In a study published in Scientific Reports researchers at Okayama University use simulations to depict changes that occur within neurons during the processes of learning and memory formation.

Two antagonist phenomena in the brain are known to drive learning and memory. Long-term potentiation (LTP) strengthens communication between adjacent neurons to facilitate the integration of new memories. Long-term depression (LTD) weakens such interactions to relieve the brain of redundant information. However, the molecular changes driving these processes are still unclear to neuroscientists. Now, in a collaboration between Associate Professor SUMI Tomonari from Okayama University and Assistant Professor HARADA Kouji from Toyohashi University of Technology, a pair of scientists has revealed how the competitive shuttling of one molecule between in and out of synapses play an important role in this regard.

LTP and LTD are initiated by flux of calcium ions into neighbouring (post-synaptic) neurons when those receive signals from the pre-synaptic ones. The post-synaptic neurons then do so by presenting a signal reader known as the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) on their surface during LTP, which fades away during LTD. To understand the dynamics of AMPAR increase and decrease on post-synaptic membranes better, the duo created a mathematical model of post-synaptic neuron that closely mimicked physiological LTP and LTD. Neurons of the hippocampus—the seat of learning and memory within the brain—were used as a model system.

Influxes of calcium ions were applied as the input of the simulations, and successfully trigger LTP and LTD. As expected, calcium-induced LTP stimulus resulted in AMPAR being shuttled out of the post-synaptic neurons, whereas LTD resulted in AMPAR being shunted back in. A deeper dive revealed that two opposing calcium sensors, namely synaptotagmin 1/7 (Syt1/7) and protein interacting with C-kinase 1 (PICK1), were driving these movements. Both sensors were active during LTP and LTD albeit in varying amounts. The Syt1/7 activity overtook the PICK1 during LTP resulting in a release of AMPAR from vesicles, whereas the former was overtook by the latter during LTD resulting in a recapture of the released AMPAR. A competition between Syt1/7 and PICK1 was thus behind the increase and decrease of AMPAR on the post-synaptic membranes.

The research duo then closely examined the fate of AMPAR once it was shunted back into post synaptic neurons. Instead of degrading, AMPAR was stored in little vesicles near the neuron surface and kept ready for the next LTP signal. This resulted in an almost instantaneous incorporation of AMPAR into the postsynaptic membranes upon LTP stimulus. Myosin Vb, a molecular motor protein, was responsible for this dynamic recycling of AMPAR within the neuron.

This study showed two competing mechanisms underlying LTP and LTD instead of two mutually exclusive processes. Additionally, the role of key molecules driving this dynamic competition was revealed. Deciphering the complexities of LTP and LTD is instrumental in understanding memory related disorders such as Alzheimer’s disease and amnesia.

Background

LTP, LTD, and AMPAR: Long-term potentiation (LTP) is the strengthening, and long-term depression (LTD) is the weakening of inter-neuron connections in response to chemicals known as neurotransmitters. The chemically induced inflow of calcium ions into adjacent (post-synaptic) neurons warns to prepare for either LTP or LTD. Subsequently, the initiating (pre-synaptic) neuron fires neurotransmitters such as glutamate to communicate with the post-synaptic neurons.

α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) is a molecule that closely resembles glutamate. Thus, the post-synaptic neuron presents the AMPA receptor (AMPAR) on its surface to read glutamate signals. LTP leads to more AMPAR incorporation into postsynaptic membranes and better glutamate binding, whereas LTD leads to the opposite. The increase and decrease of AMPAR on post-synaptic membranes is a key factor in facilitating neuronal connections. Understanding the dynamics of AMPAR shuttling is vital for research on the normal development of learning and memory and disorders that implicate them.

Reference

Tomonari Sumi, Kouji Harada. Mechanism underlying hippocampal long-term potentiation and depression based on competition between endocytosis and exocytosis of AMPA receptors. Scientific Reports, volume.10, Article number: 14711 (2020)

DOI : 10.1038/s41598-020-71528-3
https://www.nature.com/articles/s41598-020-71528-3#citeas

Correspondence to
Associate Professor SUMI Tomonari, Ph.D.
Research Institute for Interdisciplinary Science, Okayama University,
3-1-1 Tsushimanaka, Kita-ku, Okayama 700-8530, Japan
e-mail : sumi(a) cc.okayama-u.ac.jp
For inquiries, please contact us by replacing (a) with the @ mark.
http://www.cc.okayama-u.ac.jp/~sumi/index_e.html

Further information
Okayama University
1-1-1 Tsushima-naka , Kita-ku , Okayama 700-8530, Japan
Public Relations Division
E-mail: www-adm(a)adm.okayama-u.ac.jp
For inquiries, please contact us by replacing (a) with the @ mark.

Website: //www.okayama-u.ac.jp/index_e.html
Okayama Univ. e-Bulletin: //www.okayama-u.ac.jp/user/kouhou/ebulletin/
We love OKAYAMA UNIVERSITY: https://www.youtube.com/watch?v=7cXlttQIk3E
Okayama University Image Movie（2020）
https://www.youtube.com/watch?v=vQxeL0ztSLA

Vol.80：A novel 3D cell culture model sheds light on the mechanisms driving fibrosis in pancreatic cancer

Vol.81：Innovative method for determining carcinogenicity of chemicals using iPS cells

https://www.okayama-u.ac.jp/eng/research_highlights/index_id116.html

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