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Biomedical subjects

M Iwata

Publications and source records attributed to M Iwata.

At least 235 records · Page 13Linked to original sources
PubMed1997

[Efficacy of nasal bi-level positive airway pressure ventilation in a patient with olivo-ponto-cerebellar atrophy suffering from sleep apnea syndrome].

Sleep apnea with neuromuscular disorders has been successfully treated with bi-level positive airway pressure ventilation (BiPAP), which, unlike continuous positive airway pressure ventilation (CPAP), creates pressure difference between expiratory and inspiratory phases. Hence if the respiration of patients stops longer than a pre-set duration, BiPAP can automatically force them to breath through a nasal mask. We report a 60-year-old woman with olivo-ponto-cerebellar atrophy (OPCA), whose mixed-type sleep apnea was difficult to treat with conventional CPAP. We therefore tried BiPAP on this patient at night. Nocturnal CO2 retention was nearly resolved, and unexpectedly daytime PaCO2 was also corrected with marked improvement of daytime somnolence. BiPAP is totally non-invasive, and may be one of the most effective treatments in patients with OPCA suffering from sleep apnea.

Female↗
PubMed1997

[A case of dyskeratosis congenita with acute interstitial pneumonia].

This is a rare case of Dyskeratosis Congenita (DC) with acute interstitial pneumonia. A 51-year-old man with DC was admitted to our hospital because of cough, sputum and fever. Chest X-ray film showed ground glass opacities in all lung fields for a while steroid's therapy proved effective, but about seven months later the patient's condition became serious. Methylprednisolone, cyclophosphamide and mechanical ventilation therapy were not effective. He died and an autopsy was performed. The lung specimen showed Organizing Diffuse Alveolar Damage, and some parts pointed to bacterial infection. But Pneumocystic carinii pneumonia and Fungal infections were not found. It is therefore necessary to conduct intensive examinations of lung involvement of patients with Dyskeratosis Congenita.

Acute Disease↗
PubMed1997

[A case of paradoxical cerebral embolism with 'spectacular shrinking deficit'].

A 66-year-old woman was admitted to our hospital because of abrupt onset of left hemiparesis and confusional state. Ten hours prior to admission, she developed difficulty in left hand movement, and her family noticed cloudiness of consciousness and gait disturbance. Neurological examination revealed only a hollow hand sign of the left hand without other neurological deficits. Cranial CT showed a low density area in the right superior parietal region, and the follow up CT on 6th hospital day exhibited contrast enhancement and hemorrhagic transformation in this area. Cerebral angiography demonstrated capillary blush and early venous filling in the right posterior parietal region. Transesophageal color-coded Doppler echocardiography (TEE-CD) showed a shunt flow via patent foramen ovale (PFO). Thus, we diagnosed this case as paradoxical cerebral embolism through PFO, which is characterized by rapid recovery of clinical manifestation, so-called spectacular shrinking deficit. Even in elderly patients with embolic stroke of unknown origin, TEE-CD should be performed to investigate PFO.

Aged↗
PubMed1997

[A neuropsychological study on a patient with the resection of the right lateral frontal lobe].

We report a patient who underwent a resection of the right lateral frontal lobe after a venous thrombosis of the superior sagittal sinus. The patient showed inertia, obsessive-compulsive behavior and disinhibition two weeks after the operation and hyperlogia and hypergraphia four weeks later, all of which disappeared within six weeks. General intelligence, language and memory were consistently preserved, though the scores of the performance IQ and the visual memory were relatively decreased. A few months after the operation emotional and personality change such as impatience and apathy became evident. We suggest that the right lateral prefrontal area is concerned with personality and behavior and that the widespread resection holds general intelligence, language and memory within normal range but relatively decreases non-verbal cognitive function that requires manual responses.

Cerebral Infarction↗
PubMed1997

[Binocular functions in amblyopia and strabismus].

Regarding the changing trends in the concept, definition, etiological classification, and criteria for diagnosis of amblyopia, we reviewed a total of 4,693 cases of amblyopia seen during the past 37 years. The amblyopia was divided into four types: strabismic, anisometropic, ametropic, and form vision deprivative. There was a definite trend for the incidence to decrease and for the diagnosis to be made during earlier age in recent years. Although favorable recovery of visual acuity is obtained after treatment of amblyopia and strabismus, there are difficulties in obtaining good binocular functions in early-onset amblyopia and strabismus. This feature was evaluated in regard to motion perception asymmetry (MPA) and binocular depth from motion (DFM). Many cases of early-onset amblyopia and strabismus showed no disparity stereopsis, or position stereopsis, in spite of the presence of DFM. The MPA appeared to be closely related to early-onset esotropia regardless of age, while it disappeared and motion perception became symmetric 4 to 5 months after birth in normal infants. The DFM seemed to play an important role in maintaining good motor alignment for several years after surgery. I developed a checkerboard pattern stimulator in 1978. This method proved to be useful in developing binocular functions and motor alignment by applying simultaneous bifoveolar stimulation and anti-suppression. Extensive exposure to the stimulation was essential for therapeutic success.

Adolescent↗
PubMed1997

[A case of acute inflammatory demyelinating neuropathy associated with autoimmune-type chronic active hepatitis].

We presented a case of acute inflammatory demyelinating polyneuropathy associated with autoimmune chronic active hepatitis (AI-CAH). This is the third case report of neuropathy in AI-CAH. A 64-year-old male with chronic liver dysfunction was admitted to the hospital because of high fever, distal weakness and sensory disturbance of all extremities, bilateral facial weakness and dysphagia. On neurologic examination, there was bilateral weakness of the upper and lower facial muscles, bulbar palsy and severe distal weakness of all extremities. The deep tendon reflexes were absent and the sensation of touch, pinprick, temperature, and vibration was impaired bilaterally symmetrically in all extremities. Serum biochemistry revealed hyperproteinemia, hypergammaglobulinemia and elevated liver enzymes. Rheumatoid factor, antinuclear antibody anti-smooth muscle antibody were positive. Serological tests for hepatitis B surface antigen and its antibody hepatitis B core antibody, and hepatitis C antibody were all negative. Serum anti-GM1, anti-GD1b, anti-GQ1b and anti-MAG antibodies were negative. Liver biopsy findings were consistent with AI-CAH with marked lymphocytic infiltration in the portal tracts. Albuminocytologic dissociation was noted in CSF. Motorconduction velocity of the median, ulnar and facial nerves were markedly reduced with temporal dispersion. No motor response was evoked in the lower extremities. Needle electromyography revealed denervation and reinnervation potentials in the arm and leg. The sural nerve biopsy showed segmental de- and re-myelination and deposition of IgG components in endoneurium. Neurological symptoms and liver dysfunction improved with corticosteroid treatment. In this case, hypergammaglobulinemia associated with an exacerbation of AI-CAH may be responsible for the acute inflammatory demyelinating neuropathy through an unknown autoimmune mechanism.

Acute Disease↗
PubMed1997

[Neurosarcoidosis with an alternating and recurrent external ophthalmoplegia].

We report a 62-year-old woman who was admitted to our hospital because of abrupt onset of ptosis, and alternating and recurrent bilateral external ophthalmoplegia in a short period without pupillary sphincter muscle abnormality. She had been suffering from uveitis of unknown origin for four years before admission, which was improved with the local administration of steroid. Her brain CT and MRI showed a parasellar mass lesion, and cerebral angiography revealed total occlusion of the right internal carotid artery with little arteriosclerotic change in other blood vessels. She was diagnosed as having sarcoidosis because of elevated serum creatinine kinase and lysozyme levels, and the pathological finding of granuloma in muscle biopsy. The oral administration of prednisolone resulted in disappearance of her external ophthalmoplegia completely in ten months. We postulate that in this patient, the alternating and recurrent external ophthalmoplegia in a short period was related to ischemic neuropathy caused by vascular lesion of neurosarcoidosis.

Cranial Nerve Diseases↗
PubMed1996

Ultrastructural study of synapses in the anterior horn neurons of patients with amyotrophic lateral sclerosis.

This report concerns an ultrastructural examination of the synapses present on the surface of somata of anterior horn neurons of the lumbar spinal cord of seven patients with amyotrophic lateral sclerosis (ALS). Specimens from six age-matched, neurologically normal control individuals were included for comparison. Examination of presynaptic terminals revealed a wide range of changes not only in degenerated neurons (central chromatolytic neurons), but, to a lesser extent, in normal-appearing neurons. The alterations included dense conglomerates of aggregated dark mitochondria and presynaptic vesicles, bundles of neurofilaments, as well as marked increase of presynaptic vesicles. Our observations suggest that in patients with ALS a substantial synaptic alteration does take place in the early stages of anterior horn neuron degeneration and degeneration of axosomatic synapses of anterior horn neurons in ALS may be of consequence on lower motor neuron degeneration.

Aged↗
PubMed1996

Differential induction of helper and killer T cells from isolated CD4+CD8+ thymocytes in suspension culture.

Thymocytes of T cell receptor transgenic mice with nonselecting and RAG-2 -/- backgrounds were developmentally arrested at the CD4+CD8+ stage before positive selection. These thymocytes underwent lineage commitment upon transient stimulation with a combination of ionomycin, a calcium ionophore, and phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator, in suspension culture. The effective drug doses were limited within narrow ranges and much lower than those which induce proliferation of mature T cells. The doses corresponded to those which inhibit glucocorticoid-induced apoptosis in these thymocytes. CD4 lineage commitment required longer duration, higher intensity of the stimulation, or both, than CD8 lineage commitment. Functional helper T cells (Th1 and Th2) were induced from the CD4 lineage-committed cells upon secondary stimulation with a combination of ionomycin and PMA followed by lymphokine treatment. Cytotoxic T cells were induced from the CD8 lineage-committed cells upon incubation with concanavalin A and irradiated splenic dendritic cells, but not with the combination of ionomycin and PMA. These results indicate that positive selection is mimicked by the pharmacological stimulation in the absence of other cell types, but that final maturation of CD8 T cells may require a different signal.

Animals↗
PubMed1996

Regulation of T cell apoptosis via T cell receptors and steroid receptors.

Less than 5% of immature CD4/CD8 double-positive (DP) thymocytes are positively selected to survive and differentiate into single-positive CD4 and CD8 T cells, while self-reactive DP thymocytes undergo apoptosis (negative selection). Both positive and negative selection events are active processes that involve signaling through the T cell receptors (TCRs) and through some accessory molecules. The two events differ quantitatively in the strength of the interaction between TCR and peptide/major histocompatibility complex molecules. We established an in vitro model of positive selection that can be analyzed quantitatively. Positive selection is likely to inhibit glucocorticoid-induced apoptosis in DP thymocytes. Proper crosslinking of TCR together with CD4, CD8, or LFA-1 inhibits the death, and its inhibitory activity is mimicked by proper combinations of ionomycin, a calcium ionophore, and phorbol myristate acetate (PMA), a protein kinase C (PKC) activator. The drug concentrations are within narrow ranges, and are lower than those which are required for the proliferation of mature T cells. Transient stimulation with the combinations of ionomycin and PMA induces differentiation and commitment of isolated DP thymocytes to the CD4 or CD8 T cell lineage in suspension cultures. The level of PKC activity appears to determine the lineage to commit. Functional mature T cells are induced from the committed cells upon secondary stimulation. Activation of calcineurin, a Ca2+/calmodulin-dependent protein phosphatase, also appears to be essential for positive selection as well as for the inhibition of glucocorticoid-induced apoptosis. Negative selection and the regulation of mature T cell apoptosis through TCR and steroid receptors are also discussed.

Animals↗
PubMed1996

Dendritic synapses of anterior horn neurons in amyotrophic lateral sclerosis: an ultrastructural study.

This ultrastructural study deals with the synapses of primary dendrites of the anterior horn neurons in the lower lumbar spinal cords of seven patients with amyotrophic lateral sclerosis (ALS) who had mild neuronal depletion. Specimens from seven age-matched, neurologically normal individuals served as controls. In each instance, the autopsy was performed within 6 h after death. Our results indicate a statistically significant increase in degenerative changes in the dendrite presynapses of normal-appearing neurons of the ALS patients. The alterations included aggregation of electron-dense synaptic vesicles and dark mitochondria with dense cristae, and bundles of neurofilaments. However, we found no significant difference between controls and patients with respect to cross-sectional area and length of the dendrites, number of synapses per dendrite, and lengths of individual synapses and their active zones in the normal-appearing neurons, even though the patients' neurons had a smaller cross-sectional area. In chromatolytic neurons, the number of synapses and the length of the active zone of the primary dendrites were significantly diminished. These findings suggest that despite degenerative changes of the presynapses, the synapses in the primary dendrites of the anterior horn neurons are preserved at the early stage of ALS. The preservation of these synapses may be due to their relative resistance to degenerative processes, or may represent a compensatory mechanism of the synapses for diminished synaptic function in distal dendrites.

Aged↗
PubMed1996

Synaptic loss in anterior horn neurons in lower motor neuron disease.

This report concerns an ultrastructural investigation of the synapses of anterior horn neurons in the lumbar spinal cord of four patients with lower motor neuron disease (LMND) who had no upper motor neuron and corticospinal tract involvement. Anterior horn neurons of five normal individuals served as controls. The cell body area and the number of synapses of the normal-appearing neurons of the LMND patients were significantly reduced (P < 0.0001). These findings suggest that synaptic changes of anterior horn neurons could be ascribed to the degeneration of lower motor neurons rather than to the influence of upper motor neuron system degeneration. On the other hand, the lengths of individual synapses (P < 0.0001) and of their active zones (P < 0.05) were significantly increased in the patients. These increases would indicate that synapses on anterior horn neurons of individuals with LMND appear to have the capacity to react to progressive degeneration and loss of other synapses by means of a compensatory response or plasticity that enhances their efficiency.

Adult↗
PubMed1996

Novel polymorphisms and haplotypes in the human coagulation factor XIII A-subunit gene.

Novel polymorphic sites within the coding region of the human coagulation factor XIII A-subunit (F13A) gene and their haplotypic combinations with the other polymorphic sites thus far reported are presented. Polymorphic bands were detected in exons 2, 5, 8, 12 and 14 by using single strand conformational polymorphism analysis and antithetic forms of the polymorphic exons were linked with each other, cosegregating as distinct sequence haplotypes. In Finnish, German, and Russian populations a total of 18 haplotypes were observed of possible 72 haplotypic combinations of the 5 exons. Ten of the haplotypes detected were found to have no novel mutations but to be only combinations of preexisting mutations. No tightly associated combinations in pairwise comparisons between antithetic forms of the polymorphic exons were observed, indicating that there may be recombinational hotspots within the F13A gene region.

Amino Acid Sequence↗
PubMed1996

Increased Fas antigen on T cells in multiple sclerosis.

Programmed cell death of antigen specific T cells (apoptosis) may be an important process in the pathogenesis of autoimmune diseases such as multiple sclerosis (MS). Fas antigen was recognized as an apoptosis-related antigen. To investigate Fas antigen in multiple sclerosis (MS), we measured the expression rate of Fas antigen and activation markers on T cells in peripheral blood (PB) of 19 MS patients, 18 controls and in cerebrospinal fluid (CSF) of nine MS patients by flow cytometry. The positive rate of Fas antigen in MS patients was higher than that of healthy controls in PB. In patients with MS, the expression rates of Fas antigen and activation markers were higher in CSF than in PB. The above findings suggest that there is acceleration or impairment of apoptosis on activated T cells in MS.

Antigens, CD↗
PubMed1996

Intracerebral expression of gonadotropin-releasing hormone and growth hormone-releasing hormone is delayed until smoltification in the salmon.

A developmental strategy was employed to investigate the functional assembly of neuropeptidergic systems in the migratory species of chum salmon Oncorhynchus keta. Using immunocytochemistry we have demonstrated that different groups of gonadotropin-releasing hormone- (GnRH)- and growth hormone-releasing hormone- (GHRH)-synthesizing neurons emerged according to very different developmental timetables. From the eye pigmentation stage (23 +/- 2 days after fertilisation (DAF)) through to the pre-smoltification stage (136 DAF), salmon-GnRH neurons originating from the olfactory placodes remained restricted to the extracerebral course of the terminal nerve. At the climax of smoltification (downstream migration 167 DAF), basal forebrain and midbrain GnRH neurons with elaborate neurite outgrowths in the brain and the pituitary became detectable. The GnRH neuroanatomical organization in the post-smoltification stage (197 DAF) was similar to that in the smoltification stage (167 DAF). In contrast to the case for other teleosts, chicken-GnRHII neurons were not found in the midbrain but were localized along the medial regions of the olfactory nerve. Growth hormone-releasing hormone immunoreactivity in the olfactory apparatus (21 DAF), and fibers along the basal telencephalon and hypothalamus and in the pituitary were observed during early embryogenesis (51 DAF) and in cells in the preoptic area on 167 DAF. The intracerebral expression of GnRH and GHRH was not detected until the peak of smoltification, which coincided with a peak in thyroid hormones, and precisely with downstream migratory behavior.

Age Factors↗
PubMed1996

A chondroitin sulfate/keratan sulfate proteoglycan, PG-1000, forms complexes which are concentrated in the reticular laminae of electric organ basement membranes.

Previously, we identified PG-1000 as part of a disulfide-linked complex of two large proteoglycans (PG-1000 and the beta component) and three smaller proteins purified from the extracellular matrix of elasmobranch electric organ (Iwata and Carlson, 1991, J. Biol. Chem. 266: 323-333). PG-1000 is a chondroitin sulfate/keratan sulfate proteoglycan with a molecular mass of about 1.2 x 16(6) daltons. When visualized in the electron microscope, PG-1000 has the typical "bottle-brush" appearance expected for a proteoglycan with an average total length of about 345 nm and about 20 chains of approximately 110 nm (Carlson and Wight, 1987, J. Cell Biol. 105: 3075-3086). Using immunocytochemical methods, we now demonstrate that PG-1000 is a component of the interstitial extracellular matrix of the electric organ. PG-1000 immunoreactivity is found throughout the interstitial matrix, but it is highly concentrated in that region of the matrix immediately adjacent to the basal lamina, the reticular lamina. The reticular and basal laminae together form the basement membrane. PG-1000 immunoreactivity is especially apparent on basal laminae that surround nerve fibers and nerve terminals. When the disulfide-linked PG-1000 complexes are purified and examined in the electron microscope following rotary shadowing, they appear as bottle-brush structures which are often attached at a central region and radiate like spokes of a wheel. These aggregates contain two to six proteoglycan monomers. We hypothesize that the PG-1000 complexes are disulfide-stabilized parts of an extended network of linked proteoglycans in the reticular lamina.

Animals↗
PubMed1996

Myoglobin inhibits proliferation of cultured human proximal tubular (HK-2) cells.

Following nephrotoxic injury, renal repair is dependent on tubular regeneration. In the case of myoglobinuric acute renal failure (ARF), persistence of myoglobin within tubular cells, or sublethal injury sustained at the height of exposure to it, might retard this process. To test this hypothesis, a human proximal tubular cell line (HK-2) was cultured for 24 hours in the absence or presence of clinically relevant myoglobin concentrations (0.5, 1, 2, 4 mg/ml). Immediately following myoglobin removal, lethal cell injury (vital dye uptake), lipid peroxidation, and DNA damage (alkaline unwinding assay) were assessed. The extent of cell proliferation was estimated over the next four days by a tetrazolium based (MTT) assay and by determining total intracellular LDH. Myoglobin's effects on protein and DNA synthesis were also assessed (35S-methionine and bromodeoxyuridine incorporation, respectively). Myoglobin induced dose-dependent lipid peroxidation (malondialdehyde generation) and cell death (up to 80% vital dye uptake with the 4 mg/ml challenge). Although 1 mg/ml myoglobin caused no cell death, it induced nearly complete growth arrest. This lasted for approximately three days following myoglobin removal from the media. Neither of two control proteins (albumin; lysozyme) nor a second nephrotoxin (gentamicin; 1 mg/ml) reproduced this effect. The 1 mg/ml myoglobin challenge caused an 80 to 90% depression in protein and DNA synthesis. It also induced significant DNA damage, as assessed by the alkaline unwinding assay (P < 0.01). Iron chelation therapy (deferoxamine) mitigated myoglobin-induced cell killing. However, its addition following myoglobin loading worsened HK-2 outgrowth by exerting a direct anti-proliferative effect. These results indicate that: (1) sublethal myoglobin toxicity can induce transient proximal tubular cell growth arrest, potentially slowing recovery from ARF; (2) this effect correlates with, and could result from, heme-induced DNA damage and a blockade in DNA/protein synthesis; and (3) deferoxamine can inhibit proximal tubular cell proliferation. This possibility needs to be considered in designing clinical trials with DFO for myohemoglobinuric ARF.

Acute Kidney Injury↗