Naoaki Ishii

Isolation and genetic analysis of amber uvrA and uvrB mutants.

A mutation in succinate dehydrogenase cytochrome b causes oxidative stress and ageing in nematodes.

Oxidative stress and aging in Caenorhabditis elegans.

[Mitochondrial function and aging].

Protein oxidation during aging of the nematode Caenorhabditis elegans.

Adaptive responses to oxidative damage in three mutants of Caenorhabditis elegans (age-1, mev-1 and daf-16) that affect life span.

VBP-1 is necessary for morphogenesis in Caenorhabditis elegans.

A complex II defect affects mitochondrial structure, leading to ced-3- and ced-4-dependent apoptosis and aging.

Coenzyme Q10 can prolong C. elegans lifespan by lowering oxidative stress.

A mutation in the SDHC gene of complex II increases oxidative stress, resulting in apoptosis and tumorigenesis.

Direct measurement of oxygen consumption rate on the nematode Caenorhabditis elegans by using an optical technique.

Effect of oxidative stress on translocation of DAF-16 in oxygen-sensitive mutants, mev-1 and gas-1 of Caenorhabditis elegans.

The p38 signal transduction pathway participates in the oxidative stress-mediated translocation of DAF-16 to Caenorhabditis elegans nuclei.

Complex II inactivation is lethal in the nematode Caenorhabditis elegans.

The role of stress in ageing: research on the nematode, Caenorhabditis elegans.

[Why do peoples age? the mechanisms of organismal aging and longevity].

[Aging and age-related diseases caused by superoxide anion production from mitochondria].

Age-related changes of mitochondrial structure and function in Caenorhabditis elegans.

The role of the electron transport gene SDHC on lifespan and cancer.

The role of the electron transport SDHC gene on lifespan and cancer.

Basic principle of the lifespan in the nematode C. elegans.

Role of oxidative stress from mitochondria on aging and cancer.

The role of mitochondrial superoxide anion (O2(-)) on physiological aging in C57BL/6J mice.

Post-dauer life span of Caenorhabditis elegans dauer larvae can be modified by X-irradiation.

Cell growth of the mouse SDHC mutant cells was suppressed by apoptosis throughout mitochondrial pathway.

Mitochondrial reactive oxygen species generation by the SDHC V69E mutation causes low birth weight and neonatal growth retardation.

Interrelationships between mitochondrial fusion, energy metabolism and oxidative stress during development in Caenorhabditis elegans.

Beneficial effects of medical advice provided to elderly persons under the anti-aging health check-up system at Tokai University Tokyo Hospital.

Mitochondrial superoxide anion (O(2)(-)) inducible "mev-1" animal models for aging research.

Mitochondrial superoxide anion overproduction in Tet-mev-1 transgenic mice accelerates age-dependent corneal cell dysfunctions.

Oxidative stress induced inflammation initiates functional decline of tear production.

Model animals for the study of oxidative stress from complex II.

Haploinsufficiency of akt1 prolongs the lifespan of mice.

Genetically induced oxidative stress in mice causes thrombocytosis, splenomegaly and placental angiodysplasia that leads to recurrent abortion.

Ethyl methanesulfonate induces mutations in Caenorhabditis elegans embryos at a high frequency.

Association between insulin resistance and plasma amino acid profile in non-diabetic Japanese subjects.

A Combination of Mitochondrial Oxidative Stress and Excess Fat/Calorie Intake Accelerates Steatohepatitis by Enhancing Hepatic CC Chemokine Production in Mice.

Infertility and recurrent miscarriage with complex II deficiency-dependent mitochondrial oxidative stress in animal models.

Preparation of Clinically Useful Sennoside-reduced Rhubarb.

Endogenous reactive oxygen species cause astrocyte defects and neuronal dysfunctions in the hippocampus: a new model for aging brain.

Impaired p53/CEP-1 is associated with lifespan extension through an age-related imbalance in the energy metabolism of C. elegans.

Long-term administration of pDC stimulative lactic acid bacteria, Lactococcus lactis strain Plasma, prevents immune-senescence and decelerates individual senescence.