Biomedical subjects

T Iwaki

Publications and source records attributed to T Iwaki.

At least 55 records · Page 3Linked to original sources

PubMed2001

Increased QT dispersion does not reflect the increased regional variation of cardiac sympathetic nervous activity in hypertrophic cardiomyopathy.

BACKGROUND: QT dispersion (QTD) reflects regional variation of ventricular repolarization. However, the relationship between QTD and the regional variation of cardiac sympathetic nerve activity in hypertrophic cardiomyopathy (HCM) is not yet elucidated. METHODS: Cardiac sympathetic nerve activity was evaluated in 25 patients with HCM by iodine 123 metaiodobenzylguanidine (MIBG) myocardial scintigraphy. With planar MIBG imaging, heart and mediastinum ratios (H/M) at early (20 minutes) and delayed (3 hours) acquisition and the washout rate (WR) were calculated. Polar maps of left ventricular myocardium were divided into 20 segments. The SD of early uptake (EU-SD), delayed uptake (DU-SD), and WR (WR-SD) in 20 segments as indices of regional variation were calculated. QT intervals were corrected by use of the Bazett formula. RESULTS: Maximum QTc correlated positively with H/M early, WR, and left ventricular wall thickness (LVWT). Minimum QTc correlated positively with WR and LVWT. Corrected QTD (QTDc) correlated negatively with EU-SD, DU-SD, and WR-SD and positively with the interventricular septal thickness/posterior wall thickness ratio. Stepwise regression analysis revealed that the most powerful determinants for maximum QTc, minimum QTc, and QTDc were WR, LVWT, and EU-SD, respectively. CONCLUSIONS: QTD correlated negatively rather than positively with the regional variability index of cardiac sympathetic nerve activity. These results suggest that increased QTD in patients with HCM may not reflect increased heterogeneity of cardiac sympathetic nerve activity.

Arrhythmias, Cardiac↗

PubMed2001

Significance of auditory evoked responses (EABR and P300) in cochlear implant subjects.

An electrically derived auditory brainstem response (EABR) was recorded intra-operatively, and the event-related potential (P300) postoperatively in post-lingually deaf adult cochlear implantees. EABR and P300 were recorded from two groups of 25 subjects each. All subjects had a cochlear mini-22 system implanted at our center between 1994 and 1998. Two parameters of EABR, threshold (T) and the gradient of the amplitude-growth (AG) curve, were used for correlation with postoperative speech reception scores. The consonant recognition score (CRS) measured 1 month postoperatively showed a significant correlation with the AG curve of EABR (Spearman rank order test, p = 0.004), but not at later points in time. No correlation was found between the T and CRS at any time postoperatively. As the AG curve reflects the number of remaining spiral ganglion cells in the inner ear, a large number of surviving neurons is thought to be advantageous only for initial speech learning. The latency of P300 was measured for correlation with the speech reception score. The division of the cochlear implant subjects into a fair and a good hearing group according to their CRS showed that the average latency of P300 was significantly longer for the fair hearing group than for the good hearing group. A follow-up study showed that P300 latency significantly correlated with CRS measured at 6 months, 1 year and at a later time. As the latency of P300 is thought to reflect the time for sound processing in the central auditory system, our results indicate that plasticity of the central auditory system is more important than that of the peripheral auditory system for speech learning in cochlear implant subjects.

Adult↗

PubMed2001

Accumulation of 8-oxo-2'-deoxyguanosine and increased expression of hMTH1 protein in brain tumors.

Oxidative DNA damage generated by an attack of reactive oxygen species causes mutation or cell death that may lead to various diseases and may be related to initiation or progression of carcinogenesis. 8-Oxo-2'-deoxyguanosine (8-oxo-dG) is a major oxidative DNA damage product that can result in mutation, and hMTH1, human MutT homolog protein 1, has been identified as an enzyme that hydrolyzes 8-oxo-dGTP to the monophosphate, thus preventing accumulation of 8-oxo-dG in DNA. With immunohistochemical approaches, we investigated accumulation of 8-oxo-dG and expression of hMTH1 in brain tumor tissues obtained from surgical and autopsy cases, including 42 neuroepithelial tumors, 5 meningiomas, 2 metastatic brain tumors, and 1 schwannoma. 8-Oxo-dG accumulation and hMTH1 expression were increased in various brain tumors. Nuclei of brain tumor cells were immunoreactive for 8-oxo-dG in all cases. In most cases, both nuclei and cytoplasm of the tumor cells were immunoreactive for hMTH1. Both 8-oxo-dG accumulation and hMTH1 expression were most evident in high-grade gliomas, indicating that oxidative stress was high in these gliomas. Thus, the defense mechanism against such oxidative stress may be enhanced as well. These results suggest that oxidative stress may play a role in tumor progression.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2001

The effect of breath termination criterion on breathing patterns and the work of breathing during pressure support ventilation.

UNLABELLED: With pressure support ventilation (PSV), each PSV breath is flow-cycled, and the breath termination criterion (TC) is usually nonadjustable. When TC does not match the interaction between the patient's inspiratory-expiratory efforts to the opening and closing of the inspiratory and expiratory valves, patient-ventilator asynchrony may occur, and the work of breathing (WOB) may increase. Therefore, we studied the effect of TC on breathing patterns and WOB during PSV in eight patients with acute respiratory distress syndrome or acute lung injury. We studied five levels of TC during PSV-1%, 5%, 20%, 35%, and 45% of the peak inspiratory flow. With increasing levels of TC, the tidal volume decreased and respiratory frequency increased, along with a decrease in duty cycle. WOB markedly increased with increasing levels of TC from 0.31 +/- 0.12 J/L with TC 1% to 0.51 +/- 0.11 J/L with TC 45%. Premature termination with double breathing occurred in one patient with TC 35% and four patients with TC 45%. Delayed termination with a duty cycle of >0.5 occurred in two patients with TC 1%. In conclusion, the proper adjustment of TC improves patient-ventilator synchrony and decreases WOB during PSV. IMPLICATIONS: Although termination criterion (TC) is usually nonadjustable, it influences the effectiveness of pressure support ventilation for mechanical ventilation. The proper adjustment of TC is crucial to improve patient-ventilator synchrony and decrease work of breathing. TC 5% of the peak inspiratory flow may be the optimal value for patients with acute respiratory distress syndrome or acute lung injury.

Aged↗

PubMed2001

Systolic dysfunction and blood pressure responses to supine exercise in patients with hypertrophic cardiomyopathy.

Left ventricular function and blood pressure responses were evaluated in 56 patients with non-obstructive hypertrophic cardiomyopathy (HCM) and 12 control subjects by using a radionuclide ventricular function monitor during supine ergometer exercise. Patients with HCM were divided into 2 groups: (i) group A had no decrease in ejection fraction (EF) during exercise; and (ii) group B had a decrease in EF during exercise. During exercise, the change in end-diastolic volume did not differ between the 3 groups. In contrast, the change in end-systolic volume differed between the 3 groups (p<0.0001). The change in systolic blood pressure (SBP) also differed significantly between the 3 groups. The change in SBP in group B was smaller than that in the control group and group A, and changes in the EF and changes in the SBP between rest and peak exercise showed a significant correlation (p<0.005). These results suggest that exercise-induced systolic dysfunction in patients with non-obstructive HCM may contribute to abnormal blood pressure response in those patients.

Adult↗

PubMed2001

Right ventricular metastasis from a primary cervical carcinoma.

A 49-year-old female presented with a 1-month history of cough and low-grade fever. Echocardiography showed a large mass in the right ventricle and percutaneous right ventricular endomyocardial biopsy provided the histologic diagnosis. Despite radiotherapy and chemotherapy, the patient died. At autopsy, the metastatic deposit in the heart was larger than the primary cervical carcinoma.

Carcinoma, Squamous Cell↗

PubMed2001

[Increased intracranial pressure caused by obstruction of torcular herophili with hemangiopericytoma: a case report].

A 49-year-old male had experienced diplopia for half a year. The intracranial pressure was markedly elevated (450 mmH2O). Neuroimaging revealed a tumor incompletely occluding the torcular herophili and the bilateral transverse sinuses without cerebral or cerebellar compression by the tumor. Both cortical veins and cervical veins were enlarged, and the Sylvian vein and Rabbe's vein and the tentorial sinus were collateral vessels. Biopsy was performed and histologic examination proved hemangiopericytoma. The patient underwent Gamma-knife treatment and the tumor decreased in size 3 months after the treatment.

Brain Neoplasms↗

PubMed2001

[Extracranial metastasis of glioblastoma to the lung and heart with a histological resemblance to small cell carcinoma of the lung: an autopsy case].

An autopsy case of small cell glioblastoma, showing multiple extracranial metastases, is reported with special reference to histopathological differentiation from metastatic small cell carcinoma. Widely spread lesions in the bilateral lungs were developed after an operation and chemo-radiotherapy for glioblastoma, and the lung lesions led to fatal respiratory failure. Postmortem examination revealed multiple tumors in the lung, lymph nodes, and the heart, as well as local invasion of the primary tumor to the dura, skull, and the scalp. The mechanism of extracranial metastasis of brain tumor is discussed.

Adult↗

PubMed2001

[A case of Gerstmann-Sträussler-Scheinker syndrome (GSS) with late onset--a haplotype analysis of Glu219Lys polymorphism in PrP gene].

We report a 74-year-old man with late onset Gerstmann-Sträussler-Scheinker syndrome (GSS). In this family, 3 out of 6 siblings and his father developed cerebellar ataxia and mental deterioration in their fifth decades. He complained of unsteady walking and tingling pain in the legs at the age of 70. Neurological examination revealed moderate truncal ataxia, mild limb ataxia, ataxic speech, sensory impairment, paresthesia and areflexia in the lower extremities. CSF examination showed elevated CSF and 14-3-3 proteins with a normal cell count. EEG and brain MRI demonstrated no abnormality. Somatosensory evoked potential (SEP) study showed delayed N13-N20 interpeak latencies in the upper extremities and delayed N20 at 12th thoracic spinous process, indicating dysfunction of the posterior roots or columns of the spinal cord including the dorsal horns and proximal peripheral nerve. Analysis of the prion protein gene demonstrated a Pro102Leu amino acid substitution, which is compatible with classical GSS. Haplotype analysis of the PrP gene identified a Glu219Lys polymorphism on another allele. Recently, it was confirmed that protein X, which accelerates the conversion of the normal type of PrP (PrPC) into a pathological type of PrP (PrPSc), binds to the 219th amino acid residue of PrP. Therefore, the 219Lys polymorphism theoretically inhibited formation of PrPSc and may thus have delayed the onset of the disease in this patient.

Aged↗

PubMed2001

[A patient with vitamin E deficient, myopathy presenting with amyotrophy].

We report a 61-year-old man with vitamin E deficiency, presenting with, myopathy as an only clinical symptom. In 1997, at 59 years of age, he noted mild proxymal-muscle weakness and atrophy in the four extremities, nine years after he received a Billroth II partial gastrectomy for a gastric ulcer. His muscle weakness slowly exacerbated, and he was admitted to our hospital in 1999. On admission, neurological examination confirmed mild proximal-muscle weakness and atrophy in the four extremities. Intelligence, cranial nerves, coordination, sensation and tendon reflexes were all normal. Laboratory examination showed normochromic anemia (Hb 9.9 g/dl, Ht 30.9%, MCV 97.5 fl, MCHC 31.2 pg), hypoproteinemia (5.0 g/dl), and hypocholesterolemia (107 mg/dl). The levels of serum CK, lactate and pyruvate were normal. The serum vitamin E level was markedly reduced (0.17 mg/dl; normal 0.75-1.41). Cerebrospinal fluid was normal. Nerve conduction, sensory evoked potentials (SEP), electromyography (EMG), head CT and electroencephalography (EEG) were all normal. Muscle biopsy from the right deltoid muscle showed both mild myogenic and neurogenic changes. Remarkably, type 1 muscle fiber predominance and granular accumulation of autofluorescent lipofuscin granules in the muscle fibers were found. These pathological findings were compatible with those of vitamin E-deficient myopathy. Thus, he was diagnosed as having vitamin E-deficient myopathy, which was confirmed by apparent effective supplementation of vitamin E. Interestingly, our present case did not show any other neurological manifestations such as deep sensory disturbance, sensory ataxia or polyneuropathy. A long-term workload due to hard physical labor and smoking in our patient may have accelerated oxidative muscle damage, resulting in amyotrophy mainly due to vitamin E deficient myopathy.

Gastrectomy↗

PubMed2001

[An autopsy case of dementia with motor neuron disease accompanying Alzheimer's disease lesion].

We report the case of a 60-year-old man with autopsy-proven dementia with motor neuron disease (D-MND) and Alzheimer's disease lesion. The patient presented with clumsiness of his right hand at the age of 55 years old and subsequently developed dysarthria, weakness and atrophy of his upper limbs. He was unaffectionate towards his family, repeated the same phrase, and showed severe disorientation of time and place. Neurological examination on admission showed not only diffuse lower motor neuron signs, such as weakness, atrophy, fasciculation and areflexia in both upper limbs, but also dementia (HDS-R 9/30). He died of respiratory insufficiency. Neuropathological examination showed mild atrophy of the frontal and temporal lobes and anterior spinal roots. Microscopic examination of cortical sections revealed degenerative changes with simple atrophy and gliosis, and these changes were predominant in layers 1 and 2 of the frontal and temporal cortices. Using immunohistochemical staining, ubiquitin-positive but tau-negative inclusions were frequently found in neurons of the hippocampal granular cell layers and temporal lobes. Many senile plaques and neurofibrillary tangles were present in all sections of the brain. Our final diagnosis was dementia with motor neuron disease accompanying Alzheimer's disease lesion, because of hypoperfusion in the parietal lobe as well as the frontal lobe demonstrated by SPECT, and the presence of many senile plaques and neurofibrillary tangles in the cerebral cortex. Overlapping of pathologically-proven D-MND and Alzheimer's disease lesion is extremely rare, and this case may improve our understanding of the process of neurodegeneration.

Alzheimer Disease↗

PubMed2000

Neural plasticity detected in short- and long-term cochlear implant users using PET.

The interaction of listening to words and watching sign language in short-term and long-term cochlear implant (CI) users who have learned sign language after becoming deaf was measured using PET. In short-term CI users the auditory cortex was inactive while in long-term CI users it was fully activated with the simultaneous presentation of auditory and visual input. The result suggests the possibility that the interference of rival modalities may be diminished with experience and the preference switchover from the visual input to the auditory input could be accomplished by means of the neural plasticity persisting in the mature human auditory cortex.

Adolescent↗

PubMed2000

Molecular cloning of a novel apoptosis-related gene, human Nap1 (NCKAP1), and its possible relation to Alzheimer disease.

Expression profiles of thousands of genes (cDNAs) were analyzed in sporadic Alzheimer disease (AD)-affected brains in comparison with normal subjects by using the high-density cDNA filter method and differential display analysis. Among 31 differentially expressed genes, one gene was found to be markedly depressed in AD-affected brains. A full-length (or nearly full-length) cDNA of the gene was isolated and sequenced. The cDNA turned out to be an orthologue of rat Nap1. The gene was thus designated human Nap1 (HGMW-approved symbol NCKAP1) and was mapped to human chromosome 2q32 by fluorescence in situ hybridization. Northern blotting and in situ hybridization studies showed that in brain, the gene is predominantly expressed in neuronal cells. Antisense oligo DNA of human Nap1 transcripts was found to induce apoptosis of neuronal cells. Based on these results, the possible role of human Nap1 in AD is discussed.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Two autopsy cases with Pelizaeus-Merzbacher disease phenotype of adult onset, without mutation of proteolipid protein gene.

We report the autopsy cases of two brothers which are pathologically compatible with Pelizaeus-Merzbacher disease (PMD). Both patients had a late onset (at the ages of 29 and 42 years) and chronic neurological symptoms including tremor, ataxia and dementia. The T2-weighted magnetic resonance imaging of the younger brother demonstrated increased signal areas with sparing of small areas in the cerebral white matter. The postmortem examinations, obtained at the ages of 45 and 61 years, showed similar neuropathological findings. Histologically, a cardinal finding was a lack of myelin in large parts of white matter with the preservation of islands of intact myelin, resulting in a "tigroid" appearance. Only small amounts of sudanophilic material were present. The axons were relatively well preserved, but oligodendrocytes were numerically reduced. Ultrastructurally, myelin sheaths in the white matter were markedly thin. Immunohistochemistry showed that proteolipid protein (PLP) was reduced in the affected white matter. However, genetic studies did not reveal exonic mutations or duplications of the PLP gene. We conclude that the two cases are a rare type of dysmyelinating disorder with PMD phenotype of adult onset and could be caused by previously unrecognized abnormalities of the PLP gene or other genes.

Adult↗

PubMed2000

alpha-Synuclein is expressed in a variety of brain tumors showing neuronal differentiation.

alpha-Synuclein is presynaptic nerve terminal protein and its immunoreactivity has been observed in such neurodegenerative structures as senile plaques of Alzheimer's disease or Lewy bodies of Parkinson's disease. The physiological role of alpha-synuclein is still unknown. It is speculated that alpha-synuclein may be expressed in brain tumors, especially in those showing neuronal differentiation. We examined the immunohistochemical localization of alpha-synuclein in 77 human brain tumors. alpha-Synuclein was widely distributed in the brain tumors showing neuronal differentiation. As a result, positive immunostaining for alpha-synuclein was observed in ganglioglioma, medulloblastoma, neuroblastoma, primitive neuroectodermal tumor, pineocytoma/pineoblastoma, and central neurocytoma. Compared with other neuronal markers, the positive ratio of alpha-synuclein was not as high as synaptophysin, microtubule-associated protein 2, neuron-specific enolase and tau, but it was higher than neurofilament and chromogranin A. The expression of synaptophysin was diffusely observed in the cytoplasm, cellular processes and nucleus in tumors showing neuronal differentiation; however, the expression of alpha-synuclein was predominantly observed in the cytoplasm of the tumors as well as in the cellular processes. On the other hand, non-neuronal brain tumors such as astrocytic tumors or meningiomas were totally negative for alpha-synuclein. In conclusion, the appearance of an alpha-synuclein-positive structure was not limited to neurodegenerative diseases, but could also be detected in neoplastic cells showing neuronal differentiation.

Adolescent↗

PubMed2000

Ubiquitin-immunoreactive skein-like inclusions in the neostriatum are not restricted to amyotrophic lateral sclerosis, but are rather aging-related structures.

We examined the presence of ubiquitin-immunoreactive skein-like inclusions (SLI) in the neostriatum and spinal cord in normal individuals and patients with different neurodegenerative diseases. Ubiquitin-immunoreactive SLI in the neostriatum were observed both in the normal individuals and in the patients with a variety of neurodegenerative diseases. In particular, SLI were frequently seen in normal aged subjects and certain neurodegenerative diseases, such as progressive supranuclear palsy and myotonic dystrophy. In contrast, the occurrence rate of SLI in cases with Pick's disease and multiple system atrophy tended to decrease. On the other hand, SLI in the spinal anterior horn were detected in cases of amyotrophic lateral sclerosis, but not in any cases with other neurodegenerative diseases. SLI in the neostriatum were also identifiable using phosphotungstic acid-hematoxylin and Gomori trichrome staining. Ubiquitin immunoelectron microscopy demonstrated that the SLI in the neostriatum corresponded to bundles of filaments. These features of SLI in the neostriatum were quite similar to those of intracytoplasmic rod-like inclusions (RLI) in the large neurons of caudate nucleus, which were first described by Kojima and Ogawa in 1974. Our findings indicate that SLI in the neostriatum are ubiquitin-related structures whose occurrence increases by aging, and less frequently accompany several neurodegenerative diseases, and are identical to at least some RLI.

Aging↗

PubMed2000

Immunohistochemistry of chondromodulin-I in the human intervertebral discs with special reference to the degenerative changes.

The expression of the matrix protein chondromodulin-I has been studied in human intervertebral discs of 101 people using immunohistochemical analyses. The purpose of this report is to present data on the metabolic changes that were found to occur in the chondrocytes of intervertebral discs during development and aging. Chondromodulin-I was highly expressed during the gestational period and gradually decreased after maturation. It was detected in both the extracellular matrix and chondrocytes in the zone of hypertrophic cartilage, the zone of proliferative cartilage and the zone of resting cartilage in fetal discs. It was also present in the annulus fibrosus, nucleus pulposus and end-plate cartilage in mature discs. In degenerative discs, chondromodulin-1 immunoreactivity tended to be elevated in the remaining chondrocytes. Our findings suggest that the expression of the protein is developmentally regulated and upregulated through a defense mechanism against the degenerative processes of the aged intervertebral disc.

Adolescent↗

PubMed2000

Amplification and overexpression of mdm2 gene in ependymomas.

Ependymomas rarely show p53 gene alteration, and the tumorigenic mechanism of ependymomas still remains to be elucidated. We investigated the amplification and overexpression of mdm2 gene, whose product (MDM2) is considered to be one of the major cellular regulators of p53-mediated growth control, in 26 specimens of ependymomas obtained from 20 patients. The majority of the ependymomatous samples (96%) showed at least focal immunopositivity for MDM2; however, only 8% of the samples were immunopositive for p53. mdm2 gene amplification was detected in 35% of the samples by differential polymerase chain reaction, all of which overexpressed MDM2. These results suggest that the amplification and/or overexpression of mdm2 may be one of the major molecular events occurring in the tumorigenesis of ependymomas.

Adolescent↗