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Biomedical subjects

R Koide

Publications and source records attributed to R Koide.

At least 19 recordsLinked to original sources
PubMed2001

Local fundus response to blue (LED and laser) and infrared (LED and laser) sources.

Light damage research began during the early years of laser light exploration. There is a clear and significant literature that identifies an easily demonstrated retina-pigment epithelium pathology which is associated with short wavelength exposures below 520 nm. Recent interest has expanded because of the growing evidence for a blue light contribution to the retina aging process by way of a poorly understood chemical process(es) that involve circulation, oxidative reactions and the spectral absorption properties of the pigment epithelium. New powerful sources of relatively inexpensive blue energy have become available as a family of light emitting diodes. In this experiment, we examined funduscopic, angiographic and scanning laser tomographic measures of the retinal-pigment epithelium response to LED and laser spectral blue and infrared emissions closely matched in wavelengths and delivered under carefully matched circumstances. Ten retinas in normal young rhesus monkeys were locally exposed to various energy density values at 458 nm (Argon laser) ranging from 5 to 54 J cm(-2). Eight rhesus eyes were exposed to LED irradiation with a peak wavelength of 460 nm ranging from 9 to 62 J cm(-2). Similarly, a matched infrared (IR) laser and IR LED pair were used to expose an additional ten eyes for comparison of the long wavelengths. IR irradiance ranged from 21 to 306 J cm(-2). There was no response to IR exposure in any of the eyes. Blue light exposure results were measured from the color fundus photographs, scanning laser tomographs and early- and late-phase fluorescein angiogram responses at 2 and 30 days after the exposure. Results scores were accumulated for the four measures at the two time periods. The resulting lesion scores when plotted against the exposure in J cm(-2)showed no demonstrable effect at irradiance lower than 10 J cm(-2)and near 100% effectiveness for irradiance greater than 30 J cm(-2). The most sensitive and enduring indicator of change was the late fluorescein angiograms. Nonparametric statistical analysis of the scores from the two samples support the conclusion that there is no difference in the consequences of LED and laser light exposures under these matched conditions.

Analysis of Variance↗
PubMed2001

Effect of Antioxidants on Radical-initiated Peroxidation of Retinal Homogenate.

Purpose: To compare the effect of antioxidants on radical-initiated peroxidation of retinal homogenate.Methods: Lipid peroxides in bovine retinal homogenate were induced by 5 mM FeNO(3) (Fe), 25 mM 2, 2'-azobis(2, 4'-dimethylvaleronitrile) (lipid-soluble, AMVN) or 50 mM 2, 2'-azobis (2-amidinoprpane) dihydrochloride (water-soluble, AAPH) and the preventive effects of antioxidants were measured. Phosphatidylcholine hydroperoxide (PC-OOH) was analyzed with high performance liquid chromatography (HPLC) as the endpoint biomarker.Results and Conclusion: Troglitazone, an oral hypoglycemic agent, inhibited PC-OOH production by Fe and AMVN. Therefore, it may be effective for protecting against oxidative stress on the inner surface plasma membranes and subcellular organelle. Quercetin has radical scavenging effects on both sides of the membrane, because it prevents PC-OOH production by AMVN or AAPH. These results demonstrate the usefulness of an in vitro screening test that can accurately and rapidly determine the capacity of an antioxidant against lipid peroxidation or oxidative stress. (Jpn Ophthalmol Soc 104:466-70, 2000)

Journal Article↗
PubMed2001

[A case of visual agnosia for picture with right occipital lobe infarction].

We report a 74-year-old right-handed man with visual agnosia for picture due to right occipital lobe infarction. The patient had a remarkable impairment in visual recognition for standardized pictures made by Snodgrass and Vanderwart, in addition to left hemianopsia, left visuospatial neglect, and mild prosopagnosia. The visual agnosia for picture was generally recognized as a mild-type of the visual object agnosia, which was extremely rare in the patients with right occipital lesion. We discussed the mechanism of the visual agnosia in the right occipital lesion. Therefore, it raises the possibility that the broad impairment of the right occipital artery territory including parahippocampal gyrus as well as corpus callosum can cause the visual agnosia for picture.

Aged↗
PubMed2001

[Retinal hazard from blue light emitting diode].

PURPOSE: To compare the effect of exposure time from a blue(460 nm) light emitting diode(LED) on the morphology of the outer retina and determine conditions where damage occurs. MATERIALS AND METHODS: Young adult rhesus monkeys were anesthetized, and received blue LED exposure from a modified slit-lamp. A 3 mm beam of 0.85 mW was imaged onto the retina through a lens positioned before the cornea and exposure damage was determined at time intervals for 12 to 90 min. Fundus photography, fluorescein angiography(FAG), retinal tomography(HRT), and s-cone electororetinogram(S-ERG) were recorded at baseline, 2, and 30 days. RESULTS: Two days after 40 min exposure, there was a grey, discolored region, which was over-fluorescent in FAG, and an incresse in HRT and S-ERG corresponding to the site which was exposed to LED light. In histological examination at 30 days, the LED had caused produced a marked disruption of the disks of photoreceptor cells, damaged retinal pigment epithelium(RPE) apical villi, and a loss of RPE melanin after 90 min exposure. CONCLUSION: A threshold level was found around 40 min. This morphological damage may impair function and continuous exposure to blue light is potentially dangerous to vision.

Animals↗
PubMed2000

Juvenile-onset generalized neuroaxonal dystrophy (Hallervorden-Spatz disease) with diffuse neurofibrillary and lewy body pathology.

We describe an unusual case of Hallervorden-Spatz disease (HSD). After presenting with limb rigidospasticity at the age of 9 years, our patient developed progressive dementia, spastic tetraparesis and myoclonic movements, leading to akinetic mutism. He died of pneumonia at the age of 39 years. Autopsy revealed a severely atrophic brain, weighing 510 g. Histologically, there were iron deposits in the globus pallidus and substantia nigra pars reticulata, and numerous axonal spheroids throughout the brain and spinal cord. Neurofibrillary tangles were abundant in the hippocampus, cerebral neocortex, basal ganglia and brain stem. Neuritic plaques and amyloid deposits were absent. Lewy bodies and Lewy neurites, which were immunolabeled by anti-alpha-synuclein, were found in the brain stem, cerebral cortex and spinal gray matter. Sarkosyl-insoluble tau extracted from the temporal cortex resolved on immunoblots into three major bands of 60, 64 and 68 kDa and a minor band of 72 kDa, as reported for Alzheimer's disease. The present case, together with a few similar cases reported previously, may represent a particular subset of neuroaxonal dystrophy, i.e., HSD associated with extensive accumulation of both tau and alpha-synuclein.

Adolescent↗
PubMed2000

Electron microscopic observation of pituitary adenylate cyclase-activating polypeptide (PACAP)-containing neurons in the rat retina.

The distribution and localization of pituitary adenylate cyclase-activating polypeptide (PACAP) in the rat retina were studied by immunocytochemistry with both light and electron microscopy. PACAP-like immunoreactivity (PACAP-LI) was detected in the amacrine and horizontal cells as well as in the inner plexiform layer, the ganglion cell layer and the nerve fiber layer. PACAP-LI seemed to be concentrated predominantly in the neuronal perikarya and their processes, but not in other cells in the retina. At the ultrastructural level, PACAP-LI was visible in the plasma membranes, rough endoplasmic reticulum, and cytoplasmic matrix in the PACAP-positive neurons in the inner nuclear layer. In the inner plexiform layer, PACAP-positive amacrine cell processes made synaptic contact with immunonegative amacrine cell processes, bipolar cell processes, and ganglion cell terminals. These findings suggest that PACAP may function as a neurotransmitter and/or neuromodulator.

Animals↗
PubMed2000

Diplopia after cataract surgery.

PURPOSE: To evaluate the cause of diplopia after cataract surgery. SETTING: Cataract surgery at 7 hospitals and examination of diplopia at a central eye hospital. METHODS: This study comprised 18 eyes of 17 patients with diplopia that developed after cataract surgery in which retrobulbar anesthesia was used. The Hess screen test was done to diagnose oculomotor dysfunction. RESULTS: Several cases showed superior or inferior deviation of the globe, but most patients had nonuniform disturbances of eye movement. Examination of 3 patients by the Hess chart within 1 week after surgery showed paralysis of eye muscles but an overaction at a later stage, evident by reversal of eye position 1 month later. Surgery for strabismus was performed in 6 cases. One case with diplopia improved spontaneously 3 months after cataract surgery and achieved good alignment. CONCLUSIONS: The Hess screen test was useful for comparing changes in oculomotor function before and after surgery. Oculomotor dysfunction after cataract surgery may be caused directly by traumatic injury during administration of anesthesia or surgery using bridle sutures or indirectly from sensitivity to anesthetic agents.

Aged↗
PubMed2000

Expanded polyglutamine stretches interact with TAFII130, interfering with CREB-dependent transcription.

At least eight inherited neurodegenerative diseases are caused by expanded CAG repeats encoding polyglutamine (polyQ) stretches. Although cytotoxicities of expanded polyQ stretches are implicated, the molecular mechanisms of neurodegeneration remain unclear. We found that expanded polyQ stretches preferentially bind to TAFII130, a coactivator involved in cAMP-responsive element binding protein (CREB)-dependent transcriptional activation, and strongly suppress CREB-dependent transcriptional activation. The suppression of CREB-dependent transcription and the cell death induced by polyQ stretches were restored by the co-expression of TAFII130. Our results indicate that interference of transcription by the binding of TAFII130 with expanded polyQ stretches is involved in the pathogenetic mechanisms underlying neurodegeneration.

Aged↗
PubMed2000

[Effect of antioxidants on radical-initiated peroxidation of retinal homogenate].

PURPOSE: To compare the effect of antioxidants on radical-initiated peroxidation of retinal homogenate. METHODS: Lipid peroxides in bovine retinal homogenate were induced by 5 mM FeNO3 (Fe), 25 mM 2, 2'-azobis(2,4'-dimethylvaleronitrile) (lipid-soluble, AMVN) or 50 mM 2,2'-azobis (2-amidinoprpane) dihydrochloride (water-soluble, AAPH) and the preventive effects of antioxidants were measured. Phosphatidylcholine hydroperoxide (PC-OOH) was analyzed with high performance liquid chromatography (HPLC) as the endpoint biomarker. RESULTS AND CONCLUSION: Troglitazone, an oral hypoglycemic agent, inhibited PC-OOH production by Fe and AMVN. Therefore, it may be effective for protecting against oxidative stress on the inner surface plasma membranes and subcellular organelle. Quercetin has radical scavenging effects on both sides of the membrane, because it prevents PC-OOH production by AMVN or AAPH. These results demonstrate the usefulness of an in vitro screening test that can accurately and rapidly determine the capacity of an antioxidant against lipid peroxidation or oxidative stress.

Animals↗
PubMed2000

[A case of NARP (neurogenic muscle weakness, ataxia, and retinitis pigmentosa) with a T-to-C point mutation at nt 8993 of mitochondrial DNA].

We report a case of NARP with a T-to-C point mutation at nt 8993 of mitochondrial DNA. A 37-year old man with mild mental retardation, retinitis pigmentosa, and clonic-tonic seizure was admitted to our hospital. The neurological examination revealed scanning speech, dystonic neck turning to the left side, and pyramidal tract signs. Serum-, CSF-lactate and pyruvate level were slightly elevated. Brain MRI findings showed cerebral atrophy, cerebellar cortical atrophy accompanied with dilation of forth ventricle, and high intensity lesions in the bilateral lenticular nuclei on T2 weighted images. Nucleotide sequence analysis of the mitochondrial DNA in the leukocytes demonstrated a T-to-C point mutation at nt 8993. To our knowledge, this is the first report of a Japanese patient with NARP associated with the T-to-C mutation at nt 8993 of mt DNA. Mitochondrial DNA analysis should be considered in the differential diagnosis of patients with retinitis pigmentosa and various neurological signs.

Adult↗
PubMed1999

No mutation in the entire coding region of the alpha-synuclein gene in pathologically confirmed cases of multiple system atrophy.

To determine whether mutations in the coding region of the alpha-synuclein gene are relevant in cases of multiple system atrophy (MSA), detailed nucleotide sequence analysis of the alpha-synuclein gene was performed using total RNA obtained from autopsied brain specimens of 11 pathologically confirmed cases of MSA. The brain specimens used in this study contained both gray and white matter, which were dissected from the frontal, temporal or occipital lobe. No nucleotide alterations were found in the entire coding region of the alpha-synuclein gene in any of the cases. While mutations in the regulatory or intronic regions of the gene were not ruled out, our results suggest that mutations in the coding region of the alpha-synuclein gene are unlikely to contribute to the pathogenesis of MSA.

Aged↗
PubMed1999

Widespread occurrence of alpha-synuclein/NACP-immunoreactive neuronal inclusions in juvenile and adult-onset Hallervorden-Spatz disease with Lewy bodies.

Alpha-Synuclein (originally called precursor of the non-Abeta component of Alzheimer's disease amyloid-NACP) is a presynaptic nerve terminal protein and is now known to be a major component of Lewy bodies (LBs) in Parkinson's disease. Previous studies have shown that LBs are occasionally found in patients with Hallervorden-Spatz disease (HSD), a hereditary or sporadic neuroaxonal dystrophy. Therefore, an immunocytochemical examination of the brain tissues from two patients with HSD for alpha-synuclein/NACP was performed. In both cases, LBs were observed in the substantia nigra, locus ceruleus and other subcortical nuclei. These LBs were strongly immunolabelled with anti-alpha-synuclein/NACP. Moreover, abnormal alpha-synuclein/NACP-immunoreactive structures in the neuronal somata and processes were found in the cerebral neocortex, hippocampus, basal ganglia, thalamus, pontine and inferior olivary nuclei, spinal grey matter, and peripheral sympathetic ganglia. Although numerous dystrophic axons (spheroids) were found throughout the brain, either none or only a few were positive for alpha-synuclein/NACP. These findings suggest that widespread accumulation of alpha-synuclein/NACP is a pathological feature in patients suffering from HSD with LBs, and that this phenomenon is unrelated to axonal spheroid formation.

Adult↗
PubMed1999

Transgenic mice harboring a full-length human mutant DRPLA gene exhibit age-dependent intergenerational and somatic instabilities of CAG repeats comparable with those in DRPLA patients.

Dentatorubral-pallidoluysian atrophy (DRPLA) is one among an increasing number of hereditary neurodegenerative diseases determined as being caused by unstable expansion of CAG repeats coding for polyglutamine stretches. To investigate the molecular mechanisms underlying CAG repeat instability, we established three transgenic lines each harboring a single copy of a full-length human mutant DRPLA gene carrying a CAG repeat expansion. These transgenic mice exhibited an age-dependent increase (+0.31 per year) in male transmission and an age-dependent contraction (-1.21 per year) in female transmission. Similar tendencies in intergenerational instabilities were also observed in human DRPLA parent-offspring pairs. The intergenerational instabilities of the CAG repeats may be interpreted as being derived from the instability occurring during continuous cell division of spermatogonia in the male, and that occurring during the period of meiotic arrest in the female. The transgenic mice also exhibited an age-dependent increase in the degree of somatic mosaicism which occurred in a cell lineage-dependent manner, with the size range of CAG repeats being smaller in the cerebellum than in other tissues including the cerebrum, consistent with observations in autopsied tissues of DRPLA patients. Thus, the transgenic mice described in this study exhibited age-dependent intergenerational as well as somatic instabilities of expanded CAG repeats comparable with those observed in human DRPLA patients, and are therefore expected to serve as good models for investigating the molecular mechanisms of instabilities of CAG repeats.

Adult↗
PubMed1999

A neurological disease caused by an expanded CAG trinucleotide repeat in the TATA-binding protein gene: a new polyglutamine disease?

To investigate whether the expansion of CAG repeats of the TATA-binding protein (TBP) gene is involved in the pathogenesis of neurodegenerative diseases, we have screened 118 patients with various forms of neurological disease and identified a sporadic-onset patient with unique neurologic symptoms consisting of ataxia and intellectual deterioration associated with de novo expansion of the CAG repeat of the TBP gene. The mutant TBP with an expanded polyglutamine stretch (63 glutamines) was demonstrated to be expressed in lymphoblastoid cell lines at a level comparable with that of wild-type TBP. The CAG repeat of the TBP gene consists of impure CAG repeat and the de novo expansion involves partial duplication of the CAG repeat. The present study provides new insights into sporadic-onset trinucleotide repeat diseases that involve de novo CAG repeat expansion.

Adolescent↗
PubMed1999

Adenovirus-mediated expression of mutant DRPLA proteins with expanded polyglutamine stretches in neuronally differentiated PC12 cells. Preferential intranuclear aggregate formation and apoptosis.

To investigate the molecular mechanisms of neurodegeneration caused by expanded CAG repeats in dentatorubral-pallidoluysian atrophy (DRPLA), an autosomal dominant neuro degrees enerative disorder caused by unstable expansion of a CAG trinucleotide repeat in the DRPLA gene on 12p13.31, we established an efficient expression system for truncated and full-length DRPLA proteins with normal or expanded polyglutamine stretches in neuronally differentiated PC12 cells and fibroblasts using an adenovirus expression system. Although aggregate body formation was observed both in neuronally differentiated PC12 cells and in fibroblasts expressing truncated DRPLA proteins with Q82, >97% ( n = 3) of neuronally differentiated PC12 cells showed intra-nuclear inclusions, while only 31 21% ( n = 3) of fibro-blasts had intranuclear inclusions at 3 days after infection. The percentage of apoptotic cells was significantly higher in neuronally differentiated PC12 cells expressing the truncated DRPLA protein with Q82 than in fibroblasts, suggesting the possibility that intranuclear aggregate bodies are formed preferentially in neuronally differentiated PC12 cells and that these cells are more vulnerable than fibroblasts to the toxic effects of expanded polyglutamine stretches in the DRPLA protein. When the full-length DRPLA protein with Q82 was expressed, aggregate bodies were found exclusively in the nuclei of the neuronally differentiated PC12 cells, while they were found in the cytoplasm of fibroblasts. Despite the presence of aggregate bodies, apoptosis was not induced by expression of the full-length DRPLA protein with Q82 in either neuronally differentiated PC12 cells or fibroblasts, suggesting that the presence of intranuclear aggregate bodies is in itself not necessarily toxic to cells.

Adenoviridae↗