Haploinsufficiency of the glutamate decarboxylase 67 gene in a subset of GABAergic neurons induces schizophrenia-related behavioral phenotypes

学位記番号：医博甲147

Numerical simulation of hydrogen entering a second phase particle in aluminum

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Role of T phase in the hydrogen embrittlement suppression for Al-Zn-Mg- Cu alloys

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Assessment of hydrogen embrittlement behavior in Al-Zn-Mg alloys by multi- modal 3D image-based simulation

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Prevention of hydrogen embrittlement in Al-Zn-Mg alloys by dispersion of novel phases

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Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma

Approximately half of surgically-treated patients with low-grade-glioma (LGG) suffer recurrence or metastasis. Currently there is no effective drug treatment. While the selective COX-2 inhibitor celecoxib showed anti-neoplastic activity against several malignant tumors, its effects against LGG remain to be elucidated. Ours is the first report that the expression level of COX-2 in brain tissue samples from patients with LGG and in LGG cell lines is higher than in the non-neoplastic region and in normal brain cells. We found that celecoxib attenuated LGG cell proliferation in a dose-dependent manner. It inhibited the generation of prostaglandin E2 and induced apoptosis and cell-cycle arrest. We also show that celecoxib hampered the activation of the Akt/survivin- and the Akt/ID3 pathway in LGGs. These findings suggest that celecoxib may have a promising therapeutic potential and that the early treatment of LGG patients with the drug may be beneficial

膠芽腫においてAd-DKK3の抗腫瘍効果はWnt蛋白と受容体の相互作用の阻害によりもたらされる

Field log book of Mike Gagner, labeled WM-7, 4/14/04, WM-7, 06/26/04, and WM-7, 8/20/04 of project 1418.01 PHABSIM site

Genetic deletion of the 67‐kDa isoform of glutamate decarboxylase alters conditioned fear behavior in rats

The GABAergic system is thought to play an important role in the control of cognition and emotion, such as fear, and is related to the pathophysiology of psychiatric disorders. For example, the expression of the 67‐kDa isoform of glutamate decarboxylase (GAD67), a GABA‐producing enzyme, is downregulated in the postmortem brains of patients with major depressive disorder and schizophrenia. However, knocking out the Gad1 gene, which encodes GAD67, is lethal in mice, and thus, the association between Gad1 and cognitive/emotional functions is unclear. We recently developed Gad1 knockout rats and found that some of them can grow into adulthood. Here, we performed fear‐conditioning tests in adult Gad1 knockout rats to assess the impact of the loss of Gad1 on fear‐related behaviors and the formation of fear memory. In a protocol assessing both cued and contextual memory, Gad1 knockout rats showed a partial antiphase pattern of freezing during training and significantly excessive freezing during the contextual test compared with wild‐type rats. However, Gad1 knockout rats did not show any synchronous increase in freezing with auditory tones in the cued test. On the other hand, in a contextual memory specialized protocol, Gad1 knockout rats exhibited comparable freezing behavior to wild‐type rats, while their fear extinction was markedly impaired. These results suggest that GABA synthesis by GAD67 has differential roles in cued and contextual fear memory