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T Yanagihara

Publications and source records attributed to T Yanagihara.

At least 145 records · Page 8Linked to original sources
PubMed1997

[Evaluation of effective treatment drugs against Acanthamoeba cyst].

Cysts of 2 isolates of Acanthamoeba from the cornea of 2 patients with confirmed Acanthamoeba keratitis were tested in vitro for sensitivity to antimycotic agents such as fluconazole, miconazole, amphotericin-B, pimaricin, antiprotozoal agents such as pentamidine isetionate and antiseptics which could be use in the ophthamological region. Pimaricin was the most successful cysticidal agent against the two strains. Sensitivity to pentamidine isetionate showed variation. Fluconazole, miconazole and amphotericin-B were resistant against cysts with concentration of eye drops that have been used in the treatment of Acanthamoeba keratitis. It was supposed that 5% pimaricin eye drops could be use in the treatment of Acanthamoeba keratitis in addition to keratomycosis. Pentamidine isetionate which belong to the diamidine family, is not yet clear as to the side effects to corneal epithelium cell, but we believe that this drug could be expected as a new therapeutic agent for Acanthamoeba keratitis.

Acanthamoeba↗
PubMed1997

Distribution of endogenous tumour necrosis factor alpha in gliomas.

AIMS: To determine the distribution and cellular origin of endogenous tumour necrosis factor alpha (TNF alpha) in the cellular components of human gliomas. METHODS: Frozen sections of 26 gliomas (four astrocytomas (As); two oligoastrocytomas (OA); one ansplastic astrocytoma (AA); one anaplastic oligoastrocytoma (AOA); 18 glioblastomas (GB)) were examined immunohistochemically using antihuman TNF alpha and anti-Leu-M5 (CD11c) antibodies. Additional studies with double immunohistocchemical procedures were performed with anti-glial fibrillary acidic protein and anti-neurofilament antibodies. RESULTS: Eighty per cent of the AA, AOA, and GB (16 of 20) had a positive reaction for TNF alpha, but only 17% of As and OA (one of six) were positive. Positive cells were seen in both the tumour tissue and adjacent brain tissues. TNF alpha protein was detected not only in the tumour cells but also in the endothelium of tumour vessels as well as reactive astrocytes and neurons. CONCLUSIONS: Endogenous TNF alpha is present in cells of various origins in glial tumours including tumour vessels; however, the role of TNF alpha may be different in different types of cells or altered microenvironment.

Brain Chemistry↗
PubMed1997

A near-infrared spectroscopic study of cerebral ischemia and ischemic tolerance in gerbils.

BACKGROUND AND PURPOSE: To explore the physiological mechanism of ischemic tolerance, we studied intracerebral oxygenation states noninvasively using near-infrared spectroscopy after bilateral common carotid artery occlusion (BCO) in gerbils with and without ischemic pretreatment. METHODS: Under ether anesthesia, gerbils with sham operation (S group, n = 8) and those with pretreatment consisting of BCO for 2 minutes, twice at 3 days and 2 days earlier (T group, n = 8), were again subjected to BCO for 5 minutes. Changes in oxyhemoglobin (HbO2), deoxyhemoglobin (Hb), and total hemoglobin (HbT) as well as reduction in cytochrome oxidase (cyt.aa3) were calculated from the absorbance changes of the light transmitted through the brain. Seven days after the ischemic study, immunohistochemical examination was performed with an antiserum against microtubule-associated proteins. RESULTS: In both groups, the increase of Hb and decrease of HbO2 and HbT proceeded rapidly after BCO, and the maximal deoxygenation of hemoglobin occurred within 2.5 minutes. Reduction of cyt.aa3 also ensued rapidly and reached the maximal reduction within 3 minutes in both groups. In the T group, however, both deoxygenation of hemoglobin and reduction of cyt.aa3 progressed more slowly than in the S group. The time (seconds) necessary for a maximal change for cyt.aa3 was significantly longer in the T group (203.8 +/- 34.0 [mean +/- SD]; P < .01) than in the S group (68.0 +/- 14.7). The time necessary for a half-maximal change was also significantly longer in the T group than in the S group for both Hb (22.0 +/- 7.5 and 13.5 +/- 4.0, respectively; P < .05) and cyt.aa3 (23.9 +/- 5.7 and 11.6 +/- 4.3; P < .01). After recirculation for 7 days, all gerbils in the S group were found to have neuronal death in the hippocampus, while those in the T group did not. CONCLUSIONS: The present study indicated that mild ischemic stress can induce improvement in oxygen metabolism during subsequent ischemia, which might be causally related to the phenomenon known as "ischemic tolerance," in which a protective effect toward ischemic/postischemic injury is induced by earlier mild ischemic pretreatment.

Animals↗
PubMed1997

Measurement of tissue oxygen consumption in patients with mitochondrial myopathy by noninvasive tissue oximetry.

We measured oxygen consumption in the exercising lower limb by using noninvasive tissue oximetry with the near-infrared spectra of hemoglobin in the quadriceps muscle during bicycle ergometer exercise in four normal controls and three patients with chronic progressive external ophthalmoplegia (CPEO) as well as one patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS). Normal controls showed constant oxygenation during exercise and a rapid recovery after exercise. However, all four patients with mitochondrial myopathy showed abnormal oxygenation during exercise and a slow recovery afterward. The results reflected the defect in oxidative phosphorylation and the impairment in oxygen utilization in those patients. The distinctive patterns of imbalance between oxygen delivery and utilization correlated well with the severity of mitochondrial myopathy as judged by the sum of the serum lactate and pyruvate content during exercise. Noninvasive tissue oximetry may be useful to measure the severity of myopathy and exercise intolerance in patients with mitochondrial myopathy.

Adult↗
PubMed1997

Chronic inflammatory demyelinating polyneuropathy accompanied by hepatocellular carcinoma.

We report a patient with chronic inflammatory demyelinating polyneuropathy (CIDP) accompanied by hepatocellular carcinoma (HCC). Due to the remarkable weakness in the lower limbs and loss of the position sense, he could not walk. On neurophysiological examination, he had impaired nerve conduction velocities. Biopsied nerve and muscle specimens demonstrated demyelination of nerve fibers and neurogenic degeneration of muscles. After steroid therapy he showed marked improvement in muscle strength and sensory function.

Anti-Inflammatory Agents↗
PubMed1997

Ischemic damage and subsequent proliferation of oligodendrocytes in focal cerebral ischemia.

In order to achieve a better understanding of the pathophysiology of ischemic white matter lesions, oligodendrocytic degeneration and subsequent proliferation were examined in the mouse model of middle cerebral artery occlusion. In situ hybridization histochemistry for proteolipid protein messenger RNA was employed as a sensitive and specific marker of oligodendrocytes, and immunohistochemistry for myelin basic protein was used as a compact myelin marker. Immunohistochemistry for microtubule-associated protein 2 and albumin was employed to monitor neuronal degeneration and the breakdown of the blood brain barrier, respectively. In the ischemic core of the caudoputamen, the immunoreactivity for microtubule-associated protein 2 disappeared and massive albumin extravasation occurred several hours after vessel occlusion, while proteolipid protein messenger RNA signals remained relatively strong at this time. The messenger RNA signals began to attenuate 12 h after ischemia and were hardly detectable 24 h after ischemia in the whole ischemic lesion. In situ end-labeling of fragmented DNA showed some cells with proteolipid protein messenger RNAs to have DNA fragmentation at this period. In contrast to proteolipid protein messenger RNA signals, the immunoreactivity for myelin basic protein was detected as long as five days after ischemia. An apparent increase in the cells possessing strong proteolipid protein messenger RNA signals was found five days after ischemia, mainly in the corpus callosum and the cortex bordering the infarcted areas. A double simultaneous procedure with in situ hybridization for proteolipid protein messenger RNA and immunohistochemistry for glial fibrillary acid protein or lectin histochemistry for macrophages/microglia showed proliferating oligodendrocytes to be co-localized with reactive astrocytes and macrophages/microglia. These findings show that oligodendrocytic damage occurred following ischemic neuronal damage and the breakdown of the blood brain barrier, but preceded the breakdown of myelin proteins in the ischemic lesion, that an apoptosis-like process was involved in ischemic oligodendrocytic death, and that surviving oligodendrocytes responded and proliferated in the outer border of the infarcted area.

Animals↗
PubMed1997

[A case of red blood cell(RBC) agglutination on peripheral blood smear and effect of cefpirom sulfate].

We observed red blood cell (RBC) agglutination on peripheral blood smear and an abnormal RBC distribution histogram that suggested the influence of cefpirom sulfate. The patient was receiving cefpirom sulfate when RBC agglutination and the abnormal pattern were recognized, but these abnormalities disappeared as soon as the drug was withdrawn. When the peripheral blood sample was re-examined after warming for an hour at 37 degrees C, the abnormal pattern almost disappeared and RBC agglutination became minimal. We also observed cold agglutination reaction by using O type washed RBCs from a healthy individual that were reacted with cefpirom sulfate, but found only minimal agglutination at RT. As the drug concentration and plasma concentration were increased, we observed more agglutination at 4 degrees C, but this agglutination disappeared after incubation for an hour at 37 degrees C. The cold agglutinin titer was normal. We thus believe that the cause of RBC agglutination in this case was caused by cefpirom sulfate.

Cells, Cultured↗
PubMed1997

Podocyte detachment and epithelial cell reaction in focal segmental glomerulosclerosis with cellular variants.

In primary focal segmental glomerulosclerosis with cellular variants the type of epithelial cells that segmentally or globally increased and their relation to sites where podocytes detached from the capillary wall, remain unclear. Two renal samples containing glomeruli with cellular variants were serially examined using transmission electron microscopy. A total of 10 lesions, including 2 collapsing glomerulopathy, 7 cellular lesions, and 1 sclerosis, were examined. Disappearance of the dense basal band of microfilaments from portions of podocytes was followed by detachment from the capillary basement membrane, resulting in segmental denudation of the capillary wall. The defects were not covered by other portions of epithelial cells, when the defects occurred in more central regions of the glomerulus. When detachment of podocytes occurred in the peripheral areas of the glomerulus, the defects were covered with new basement membrane and by other epithelial cells. These epithelial cells were characterized by the formation of intercellular junctional complexes of zonula adherens and desmosomes between each other and with the parietal epithelial cells (PECs), by showing occasional cilia, apoptotic nuclei, and mitosis. Thus, repair is achieved as the defect is covered by the participation of PECs; synechia and glomerular sclerosis result, depending upon the extent of the original podocyte injury.

Apoptosis↗
PubMed1997

Fully automated measurement of total iron-binding capacity in serum.

We established a method for fully automated measurement of total iron-binding capacity (TIBC) in serum without separation of the unbound excess iron after saturating serum transferrin. After saturation of serum transferrin with an excess amount of iron (first step), the unbound iron was eliminated by formation of a complex with ferrozine, which was used as a chromogenic reagent (second step). For the TIBC assay, iron dissociated from transferrin by shifting the pH to acidic was reacted with ferrozine, and the increase in the absorbance at 570 nm was measured (third step). Because the iron used as a calibrator, which was added to saturate transferrin, reacted completely with ferrozine in the second step (elimination of unbound iron), the change in the absorbance to generate a calibration factor could not be monitored in the third step. To solve this problem, we used N-(2-hydroxyethyl)ethylenediamine-N,N',N'-triacetic acid (HEDTA) to complex with the iron added to saturate transferrin in the second step. This made it possible to form an iron-ferrozine complex at acidic pH because iron was dissociated from HEDTA at acidic pH. The within-run CVs of this method were 0.66-2.43% at 17.7-77.0 mumol/L, and the day-to-day CVs were 1.06-1.57% at 29.9-60.4 mumol/L (n = 10). The correlation between the values obtained with this method (y) and those from the direct TIBC assay, which involved removal of unbound iron by ion-exchange resin (x), was: y = 0.963x + 0.29 mumol/L (r = 0.973, Sy/x = 2.83, n = 59), and with the TIBC values calculated from the serum iron concentrations and the unbound iron-binding capacities measured by a direct colorimetric method (x) was: y = 1.01x - 1.06 mumol/L (r = 0.994, Sy/x = 1.66, n = 51).

Blood Proteins↗
PubMed1996

Effect of systemic zinc administration on delayed neuronal death in the gerbil hippocampus.

The divalent cation zinc has been reported to possess several physiological properties such as blocking apoptotic cell death through an inhibitory effect on Ca(2+)-Mg2+ endonuclease activity, or modulating the neurotoxicity via glutamate receptor subtypes. In the present study, we investigated the effect of peripherally injected zinc on delayed neuronal death seen in the hippocampus after transient global ischemia, in order to elucidate a possible beneficial role on zinc in ischemic neuronal cell death. Forty-five adult Mongolian gerbils of both sexes underwent transient bilateral clipping of the common carotid arteries for 3 min. In the pretreated animals, ZnCl2 (20 mg/kg) was injected subcutaneously once, 1 h before ischemia (superacute group; n = 6) or twice at 24 and 48 h before ischemia (subacute group; n = 14). Histological survey was carried out 3 days later by in situ DNA fragmentation method and 4 days later by hematoxylin-eosin staining by semiquantatively counting dead neurons in the CA1 sector. Subacute zinc pre-administration significantly reduced the nuclear damage and subsequent neuronal death; however, superacutely pre-administered zinc did not protect hippocampal neurons against ischemia but it did not aggravate the effect of ischemia, either. The present study suggested that transfer of exogenous zinc into the intracellular space is required for neuroprotection, presumably via the anti-endonuclease activity.

Animals↗
PubMed1996

Induction of cyclooxygenase-2 mRNA in gerbil hippocampal neurons after transient forebrain ischemia.

We examined the effect of brain ischemia on neuronal expression of cyclooxygenase-2 gene in the hippocampus. Transient forebrain ischemia was produced by occluding bilateral carotid arteries for 5 min in Mongolian gerbil. Northern blotting and in situ hybridization demonstrated that expression of cyclooxygenase-2 mRNA was transiently induced in the hippocampal neurons. Although future studies will be needed to clarify if induced cyclooxygenase-2 following ischemia is involved in neuronal damage or neuronal protection, selective cyclooxygenase-2 inhibitors may be a new therapeutical approach for the treatment of stroke.

Animals↗
PubMed1996

Ischemic tolerance in moderately symptomatic gerbils after unilateral carotid occlusion.

Ischemic tolerance following transient global cerebral ischemia has drawn considerable attention because of the putative cell defense mechanism which may be inducible by ischemic stress. The purpose of this study is to investigate the inducibility of ischemic tolerance in moderately symptomatic gerbils after unilateral carotid occlusion. Adult Mongolian gerbils were used. Under ether inhalation, the right common carotid artery was occluded for up to 30 min with an aneurysmal clip. Immediately after occlusion, neurological signs and motor function were evaluated and gerbils with moderate signs were selected for investigation of ischemic tolerance. Ischemia for 30 min to gerbils with moderate signs constantly caused neuronal death in the caudoputamen, but it was prevented by pretreatment with 10 min ischemia which was reversible but strong enough to produce heat shock protein 70. The results show that ischemic tolerance can be induced after hemispheric cerebral ischemia as in the case of global cerebral ischemia and suggest that ischemic tolerance may be relevant in human stroke.

Animals↗
PubMed1996

Hemiparkinsonism following haemorrhage in the contralateral substantia nigra.

We report a patient with right hemiparkinsonism following haemorrhage in the left substantia nigra. The hemiparkinsonism responded to treatment with trihexyphenidyl hydrochloride and deteriorated after temporary discontinuation of the drug. Single photon emission computed tomography using technetium 99m d, l-hexamethylpropyleneamine oxide showed reduced uptake in the left putamen, globus pallidus and thalamus.

Cerebral Hemorrhage↗
PubMed1996

Cation binding at the node of Ranvier in biopsied peripheral nerves of patients with Charcot-Marie-Tooth disease type 1A and hereditary neuropathy with liability to pressure palsies.

The node of Ranvier in myelinated fibers is known to have an affinity to bind cations. Demyelination and remyelination due to abnormal expression of a myelin protein may affect cation binding or vice versa under pathological conditions. To study the cation binding at the node of Ranvier in inherited demyelinating neuropathies associated with over- and under-expression of the peripheral myelin protein 22 (PMP-22), the reaction with ferric ion and ferrocyanide was used to visualize the cation binding sites in biopsied nerves of four patients with Charcot-Marie-Tooth disease type 1A (CMT1A) and two patients with hereditary neuropathy with liability to pressure palsies (HNPP), and the results were compared with those of four patients having acquired neuropathies with normal PMP-22 expression. In CMT1A, nodal widening or paranodal demyelination was associated with dense precipitates focally on both sides of the widened node. Although fainter precipitates were present at the node between remyelinated internodes, the percentage of nodes exhibiting the reaction product between normal and remyelinated internodes was not statistically different from that between normal internodes in CMT1A. In acquired neuropathies, on the other hand, the difference was significant between the two (P < 0.05), with reduction between normal and remyelinated internodes. At the nodes neighboring demylinated internodes, the percentage of nodes exhibiting the reaction product was reduced significantly in both CMT1A and acquired neuropathies, but to a lesser degree in CMT1A. Precipitates were clearly seen at the nodes neighboring a tomaculum in HNPP. The results suggest that preserved cation binding at the node may allow nerves to keep the electrical excitability in CMT1A and HNPP where myelin remodeling takes place at high frequency.

Adolescent↗
PubMed1996

Alzheimer-type pathology in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS).

A 53-year-old Japanese woman with a point mutation in mitochondrial DNA (tRNALeu(UUR), nt3243) consistent with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and Alzheimer-type brain pathology is reported. This woman had suffered myopathy and psychosis without any clinical evidence of, stroke-like episodes during the last 10 years of her life, and had died after an accident. At autopsy 30 h post mortem, a part of the brain was snap frozen for biochemical and histochemical studies, and the remaining part was processed for a routine examination and electron microscopy. In the brain there were no ischemic lesions. Instead, primitive/diffuse senile plaques were found throughout the brain, predominantly in the frontal and temporal lobes, while Alzheimer neurofibrillary tangles were found only in the parahippocampal gyrus. These plaques were positive for beta-protein and mostly negative for tau protein, ubiquitin, neurofilaments, alpha-choline acetyltransferase, and acetylcholinesterase. Mutations in codon 331 of the ND2 gene as well as codons 693, 713 and 717 of the beta-amyloid precursor protein gene, known to be responsible for some cases of familial Alzheimer disease, were not found. Furthermore, coincidental Down syndrome was ruled out by chromosome analysis. The results suggest a possible correlation between this mitochondrial DNA abnormality and Alzheimer-type pathology.

Alzheimer Disease↗
PubMed1996

Accumulation of peripheral myelin protein 22 in onion bulbs and Schwann cells of biopsied nerves from patients with Charcot-Marie-Tooth disease type 1A.

Peripheral myelin protein 22 (PMP-22) is a glycoprotein expressed in the myelin sheath of myelinated Schwann cells. Duplication of the PMP-22 gene and its gene dosage effect have been postulated to be involved in the pathogenesis in the majority of individuals with Charcot-Marie-Tooth disease type 1A (CMT1A). Northern blot analysis has demonstrated that the mean relative ratio of PMP-22 mRNA/beta-actin mRNA in biopsied nerves of patients with CMT1A is significantly higher than that in disease controls. To investigate whether the elevated expression of PMP-22 mRNA is reflected in the amount and the localization of PMP-22, we analyzed PMP-22, myelin basic protein (MBP), protein zero (P0), and S-100 immunoreactivities in biopsied nerves from six patients with CMT1A, five patients with other types of CMT, five patients with acquired demyelinating neuropathies, and two normal subjects. In all patients with CMT other than CMT1A and acquired demyelinating neuropathy, as well as in normal subjects, the myelin sheath was immunoreactive for PMP-22, MBP, and P0, while the Schwann cell cytoplasm was immunoreactive only for S-100. In five out of six patients with CMT1A, however, the PMP-22 immunoreactivity was present not only on the myelin sheath but also in the Schwann cell cytoplasm and onion bulbs (OBs). Although OBs are nonspecific and also seen in other inherited or acquired demyelinating neuropathies, the PMP-22-positive OBs were seen exclusively in CMT1A. The finding suggested that the expression of PMP-22 was abnormal for its localization and probably for the amount in patients with CMT1A carrying duplication of the PMP-22 gene.

Adolescent↗
PubMed1996

Bifemelane hydrochloride enhances 'ischemic tolerance' phenomenon in gerbil hippocampal CA1 neurons.

Neurons are so vulnerable to ischemic insults that transient forebrain ischemia for 5 min killed most CA1 neurons in the gerbil hippocampus (surviving neurons: 4%). In contrast, 2 days after a nonlethal challenge of 2-min ischemia, 51% of CA1 neurons became resistant to subsequent, otherwise lethal ischemia for 5 min. Bifemelane hydrochloride (20 mg/kg, i.p.), which helps ischemic brain recover from oxidative stress and inhibition of protein synthesis, significantly enhanced the 'ischemic tolerance' phenomenon if injected 1 day after 2-min ischemia: 94% of neurons survived after 5-min ischemia. This finding carries implications for possible preventive treatment following warning signs of transient ischemic attack.

Adaptation, Physiological↗