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2024/08/06
Validation of a new protocol for a zebrafish MEFL (malformation or embryo-fetal lethality) test method that conforms to the ICH S5 (R3) guideline.
2024/05/21
In vivo assessment of individual and total proteinuria in zebrafish larvae using the solvatochromic compound ZMB741
2021/10/31
Generation of a Transgenic Zebrafish Line for In Vivo Assessment of Hepatic Apoptosis
2021/08/19
Patient-Derived Cancer Xenograft Zebrafish Model (PDXZ) for Drug Discovery Screening and Personalized Medicine
2021/07/09
Establishment of a Quality Control Protocol for Zebrafish Developmental Toxicity Studies
2020/10/13
Gap junction protein beta 4 plays an important role in cardiac function in humans, rodents, and zebrafish
2020/05/28
A novel orexin antagonist from a natural plant was discovered using zebrafish behavioural analysis
2019/10/15
C3orf70 Is Involved in Neural and Neurobehavioral Development
2019/09/22
Generation of a Triple-Transgenic Zebrafish Line for Assessment of Developmental Neurotoxicity during Neuronal Differentiation
2019/07/17
Aging-associated microstructural deterioration of vertebra in zebrafish

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2000/01/01
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Pharmacogenomics and therapeutic target validation in cerebral vasospasm.

T.Tanaka,Y.Nishimura,H.Tsunoda,M.Naka
J Cardiovasc. Pharm. 36(Suppl.2) S1-S4 2000

Abstract

One of the most important pharmacogenomic technologies is transcriptome analysis. We used this method to study the change of gene expression profiles in animal models of cerebral vasospasm. We found novel drug target candidates in cerebral vasospasm through pharmacogenomics. By using differential display and quantitative reverse transcriptase-polymerase chain reaction, we found that heme oxygenase-1 (HO-1) mRNA was prominently induced in the basilar artery and modestly in brain tissue in a murine vasospasm model. There was a significant correlation between the degree of vasospasm and HO-1 mRNA levels in the basilar arteries exhibiting vasospasm. Antisense HO-1 oligodeoxynucleotides (ODN) inhibited HO-1 induction in the basilar arteries, but not in the whole brain tissue. This phenomenon was not observed in the nontreatment, sense HO-1 ODN and scrambled ODN treatment arteries. We report, for the first time, the protective effects of HO-1 gene induction by endogenous or clinical compounds in cerebral vasospasm after subarachnoid hemorrhage, a finding that should provide a novel therapeutic target for cerebral vasospasm.

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