Biomedical subjects

T Mima

Publications and source records attributed to T Mima.

At least 55 records · Page 3Linked to original sources

PubMed1999

Intraventricular hemorrhage after carotid stenting.

PURPOSE: To report an important complication related to carotid stenting. METHODS AND RESULTS: A 71-year-old man with symptomatic subtotal occlusion of the left internal carotid artery had a 30-mm lesion treated percutaneously with implantation of 2 stents. Although the procedure was completed satisfactorily, left intraventricular hemorrhage occurred 4 hours later, possibly related to hyperperfusion injury. The patient expired 30 days after the stent procedure. Preoperative single-photon emission computed tomography revealed severely reduced vasoreactivity in the affected territory after acetazolamide challenge. CONCLUSIONS: The risk of hyperperfusion injury must be considered and minimized in patients with significant restriction of regional vasoreactivity. We recommend that cerebral hemodynamic status be determined prior to carotid stenting.

Aged↗

PubMed1999

[Brain oxygen extraction fraction as an indicator for shunting operation in normal pressure hydrocephalus].

It is still difficult for neurosurgeons to determine which patients with suspected idiopathic normal pressure hydrocephalus (NPH) should undergo shunting. We need to find a more accurate indicator to predict the effect of shunting. We introduced a new preoperative examination of brain oxygen extraction fraction (OEF) and examined whether preoperative OEF value is effective for prediction of the surgical results. Global brain OEF was calculated from oxygen contents of arterial blood (AO2) and jugular venous blood (VjO2) selectively sampled from the right jugular bulb using the Seldinger method: OEF = (AO2-VjO2)/AO2. Since June 1996 we have treated 9 patients suspected of idiopathic and 10 patients suspected of secondary NPH. OEF in non-NPH patients with dilated ventricle (n = 10) and in infarct patients (n = 85) were 0.33 +/- 0.02 and 0.38 +/- 0.06, respectively. In contrast, OEF increased both in idiopathic NPH (0.42 +/- 0.04) and secondary NPH (0.45 +/- 0.02), and the NPH patients with the higher preoperative OEF values showed the better symptomatic recovery. The present study suggests that brain function may be reversible when OEF can be increased and that OEF can be a useful indicator for predicting the effect of a shunting operation in NPH.

Aged↗

PubMed1999

Balloon angioplasty for embolic total occlusion of the middle cerebral artery and ipsilateral carotid stenting in an acute stroke stage.

A 66-year-old man suffering from neurologic symptoms caused by acute embolic total occlusion of the left middle cerebral artery was treated successfully with balloon angioplasty, and an ipsilateral carotid stenosis subsequently was dilated with stenting. The patient's clinical outcome 30 days later was favorable. This therapeutic option may prove to be a useful means of treating a patient with acute stroke, embolic total occlusion of the middle cerebral artery, and an ipsilateral carotid stenosis.

Acute Disease↗

PubMed1998

To what extent has the pathophysiology of normal-pressure hydrocephalus been clarified?

The causes and pathophysiology of idiopathic normal-pressure hydrocephalus (NPH) still remain poorly understood. We reviewed the recent pertinent literature on NPH from the past 3 years (1994- 1996) in this journal [Crit Rev Neurosurg (1997) 7:263-275] and here review further manuscripts that appeared mainly in 1997. Recent investigations suggest that idiopathic NPH may be a primary cerebral parenchymal disease rather than a disorder of cerebrospinal fluid (CSF) absorption. The pathophysiology of idiopathic NPH has a wide spectrum ranging from purely hydrodynamic problems owing to a CSF absorption defect to parenchymal changes caused by hemodynamic problems owing to ischemic vascular risk factors. Magnetic resonance imaging (MRI) of NPH frequently shows ischemic vas-cular encephalopathy. NPH may coexist with subcortical white matter vascular encephalopathy, because Binswanger's encephalopathy and idiopathic NPH share common clinical symptoms. Most patients with suspected NPH may suffer from both problems. Because of MRI findings of suspected NPH, ischemic parenchymal changes caused by vasculopathy have been receiving attention. Brain biopsy findings of suspected NPH suggest the presence of parenchymal changes caused by vasculopathy such as arteriosclerosis. Patients with brain biopsy findings of Alzheimer's disease may benefit from shunting. Pathological changes seen by brain biopsy are not specific for NPH. The information accumulated so far about NPH shows a wide clinical spectrum and multifactorial etiology. Therefore, patients with NPH are inhomogeneous, and this makes it difficult to diagnose and select patients for shunting.

Journal Article↗

PubMed1998

Interleukin 6 plays a key role in the development of antigen-induced arthritis.

To investigate the direct role of interleukin (IL) 6 in the development of rheumatoid arthritis, IL-6-deficient (IL-6 -/-) mice were backcrossed for eight generations into C57BL/6 mice, a strain of mice with a genetic background of susceptibility for antigen-induced arthritis (AIA). Both histological and immunological comparisons were made between IL-6-deficient (IL-6 -/-) mice and wild-type (IL-6 +/+) littermates after the induction of AIA. Although all IL-6 +/+ mice developed severe arthritis, only mild arthritis was observed in IL-6 -/- mice. Safranin O staining demonstrated that articular cartilage was well preserved in IL-6 -/- mice, whereas it was destroyed completely in IL-6 +/+ mice. In addition, comparable mRNA expression for both IL-1beta and tumor necrosis factor alpha, but not for IL-6, was detected in the inflamed joints of IL-6 -/- mice, suggesting that IL-6 may play a more crucial role in cartilage destruction than either IL-1beta or tumor necrosis factor alpha. In immunological comparisons, both antigen-specific in vitro proliferative response in lymph node cells and in vivo antibody production were elicited in IL-6 -/- mice, but they were reduced to less than half of that found in IL-6 +/+ mice. Lymph node cells of IL-6 -/- mice produced many more Th2 cytokines than did IL-6 +/+ mice with either antigen-specific or nonspecific stimulation in in vitro culture. Taken together, these results indicate that IL-6 may play a key role in the development of AIA at the inductive as well as the effector phase, and the blockade of IL-6 is possibly beneficial in the treatment of rheumatoid arthritis.

Animals↗

PubMed1998

Serial processing of the somesthetic information revealed by different effects of stimulus rate on the somatosensory-evoked potentials and magnetic fields.

In order to evaluate information processing in the somatosensory cortex, the effect of two different stimulus rates was investigated by simultaneously recording somatosensory-evoked potentials (SEPs) and magnetic fields (SEFs) in nine healthy adults. During electric stimulation of the median nerve at the wrist, SEFs were recorded with the helmet-shaped whole-head coverage magnetometer array with 122 first-order planar gradiometers while SEPs were simultaneously recorded from seven scalp positions. Interstimulus intervals (ISIs) of 0.9 s and 4 s were compared. In all subjects, N20 as well as its magnetic counterpart, N20m, was clearly demonstrated over the contralateral somatosensory area. Subsequent deflections around 80-200 ms did not make any clear peak and were smaller than those at 20-60 ms (P30m, P40m, N50m and P60m). After 200 ms, SEFs were negligible, whereas SEPs had larger amplitude than those of shorter latencies, constituting a peak around 250 ms (P250). Both SEF and SEP deflections later than 40 ms were decreased in responses at the shorter ISI; this diminution was most prominent for P250. Therefore, it is concluded that the tangential currents in the somatosensory cortex (area 3b) mainly contribute to responses during the first 200 ms after the stimulus, whereas the radially oriented currents (most likely in the crown of the postcentral gyrus) take over for subsequent information processing.

Adult↗

PubMed1998

Human supplementary motor area is active in preparation for both voluntary muscle relaxation and contraction: subdural recording of Bereitschaftspotential.

Bereitschaftspotentials (BPs) preceding muscle relaxation and contraction were compared by using subdural electrodes which were implanted onto the right medial frontal surface in two patients with supplementary motor area (SMA) seizure. The applied movement paradigm (muscle relaxation and contraction tasks) was completely the same as employed in our previous study [Terada, K., Ikeda, A., Nagamine, T. and Shibasaki, H., Electroenceph. clin. Neurophysiol., 95 (1995) 335-345]. In both patients, either negative or positive BPs were observed in the SMA-proper and supplementary negative motor area (SNMA) starting at 1.2-1.8 prior to both movements. In one patient, BP was more widespread in the relaxation task whereas more restricted to the hand area in the contraction task. In the other patient, the BPs were observed in the cortical area rostral to SNMA (pre-SMA), in addition to the SMA-proper, in both tasks. It is concluded that SMA-proper and SNMA, and probably pre-SMA as well, in humans are similarly active in preparation for both voluntary muscle contraction and relaxation.

Adult↗

PubMed1998

Trabecular myocytes of the embryonic heart require N-cadherin for migratory unit identity.

The myocardial wall of the vertebrate heart changes from a simple epithelium to a trabeculated structure during embryogenesis. This process occurs when epithelioid cardiomyocytes migrate toward the endocardium, which we show is coincident with up-regulation of the cell adhesion molecule, N-cadherin. To study the role of N-cadherin expressed at the trabeculation stage, a replication-defective retrovirus expressing a dominant negative mutant of N-cadherin (delta N-cadherin) was engineered. Control viruses were designed to express beta-galactosidase or a full-length N-cadherin. Viruses were introduced into epithelioid presumptive myocytes at the time they initiate the epithelial-mesenchymal transformation. Individual cells infected with control viruses generated daughter myocytes which migrated toward endocardium as a tight cluster, thereby generating a clone that forms a single or at most two trabeculae. In contrast, myocytes expressing delta N-cadherin were sparsely distributed within the myocardium and failed to form the ridge-shaped clone. Thus, in addition to its known roles in myocyte epithelialization and intercalated disc formation, N-cadherin appears to play a role in homotypic interactions between nonepithelial migratory myocytes during trabecular formation of the embryonic heart.

Animals↗

PubMed1998

Pathogenesis of cortical myoclonus studied by magnetoencephalography.

Myoclonus-associated cortical activities were studied by simultaneous recording of a magnetoencephalogram and an electroencephalogram in 6 patients with cortical myoclonus due to various causes. Cortical activities were averaged, with respect to the precise onset of the myoclonic jerk, to evaluate the myoclonus-associated cortical magnetic fields. The estimated generator of their earliest peak was localized at the contralateral precentral gyrus in all patients. As judged from the direction of the electrical current, surface positive activity preceding the electromyographic discharge was detected in 3 patients with cortical reflex myoclonus and in 1 patient with possible corticobasal degeneration. In contrast, in the remaining 2 patients (Lennox-Gastaut syndrome and Alzheimer's disease), magnetic fields time-locked to the myoclonic jerk were associated with surface negative activity at the precentral cortex. The present study, applying for the first time an off-line jerk-locked back-averaging analysis to magnetoencephalography, demonstrated the important role of the precentral cortex in generating spontaneous myoclonus. It is most likely that the differing polarity of the electromagnetic activity reflects the differing activation patterns within the cortical laminar structure in the precentral area, underlying the generation of various types of myoclonus.

Adult↗

PubMed1998

Electrophysiological studies of early stage corticobasal degeneration.

We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic-rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon-emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor-evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input from the sensory cortex.

Aged↗

PubMed1998

In vitro growth suppression of vascular smooth muscle cells using adenovirus-mediated gene transfer of a truncated form of fibroblast growth factor receptor.

Vascular smooth muscle cell (VSMC) proliferation associated with arterial injury causes restenosis, which remains to be resolved in cardiovascular and ischemic cerebrovascular disease, especially after balloon angioplasty. Fibroblast growth factor (FGF) is a potent mitogen and a trophic factor for a variety of cells, including VSMCs. We constructed a replication-deficient adenovirus vector, designated AxCA delta FR, coding a truncated form of fibroblast growth factor receptor-1 (FGFR-1) gene lacking the intracellular domain to interrupt receptor-mediated FGF signaling, and examined its effect on the proliferation of primary-cultured rat VSMCs. We transferred the truncated form of the FGFR-1 gene to the VSMCs and confirmed its expression and localization in infected cells by Western blotting and immunofluorescence study. The VSMCs infected with AxCA delta FR degenerated and the proliferation of these cells was suppressed markedly by the infection with this virus in vitro. Our results suggest that the receptor-mediated signal of FGFs has an important role in VSMC proliferation and gene transfer of a truncated form of FGFR using adenoviral vector may be useful for the treatment of the diseases caused by excessive proliferation of VSMCs like restenosis after percutaneous transluminal angioplasty or carotid endoarterectomy.

Adenoviridae↗

PubMed1998

Simultaneous expression of brain-derived neurotrophic factor and neurotrophin-3 in Cajal-Retzius, subplate and ventricular progenitor cells during early development stages of the rat cerebral cortex.

To identify production sites and action targets of neurotrophins during neurogenesis, we investigated immunoreactivities of neurotrophins and their tyrosine kinase receptors in the cerebral cortex of rat embryos. Two sets of ligand-receptor systems, brain-derived neurotrophic factor/TrkB and neurotrophin-3/TrkC, were expressed simultaneously in Cajal-Retzius, subplate neurons and ventricular multipotent stem cells at embryonic days 13 and 15. Intraventricular administration of brain-derived neurotrophic factor or neurotrophin-3 at embryonic day 16 markedly modulated microtubule-associated protein II and/or Hu protein expression in different ways in the cortical plate cells by embryonic day 20. These observations indicate the involvement of autocrine and/or local paracrine action of brain-derived neurotrophic factor and/or neurotrophin-3 during formation of the cerebral cortex.

Aging↗

PubMed1998

Suboptimal clinical response to anti-tumor necrosis factor alpha (TNFalpha) antibody therapy in a patient with severe rheumatoid arthritis and lymphadenopathy.

This concerns a patient with severe rheumatoid arthritis (RA) and lymphadenopathy (LA) who showed suboptimal clinical response to antitumor necrosis factor alpha (TNFalpha) antibody (Ab), cA2 therapy. The assessment of TNFalpha and IL-6 mRNA expression in the swollen lymph-node (LN) of the patient by reverse transcription, polymerase chain reaction (RT-PCR) before cA2 treatment, showed only enhanced IL-6 production, but not TNFalpha. Moreover, cA2 failed to inhibit in-vitro spontaneous IL-6 production in the LN block culture from the patient. Taken together, these results indicate that IL-6 production in the swollen LNs of the patient might not depend on TNFalpha. This might partly cause suboptimal clinical response to anti-TNFalpha Ab therapy in the patient.

Antibodies, Monoclonal↗

PubMed1998

Attention modulates both primary and second somatosensory cortical activities in humans: a magnetoencephalographic study.

To clarify the role of primary and second somatosensory cortex (SI and SII) in somatosensory discrimination, we recorded somatosensory evoked magnetic fields during a stimulus strength discrimination task. The temporal pattern of cortical activation was analyzed by dipole source model coregistered with magnetic resonance image. Stimulus intensity was represented in SI as early as 20 ms after the stimulus presentation. The later components of SI response (latency 37.7 and 67.9 ms) were enhanced by rarely presented stimuli (stimulus deviancy) during passive and active attention. This supports an early haptic memory mechanism in human primary sensory cortex. Contra- and ipsilateral SII responses followed the SI responses (latency 124.6 and 138.3 ms, respectively) and were enhanced by attention more prominently than the SI responses. Active attention increased SII but not SI activity. These results are consistent with the concept of ventral somatosensory pathway that SI and SII are hierarchically organized for passive and active detection of discrete stimuli.

Adult↗

PubMed1998

Cortical myoclonus: sensorimotor hyperexcitability.

Cortical or cortical reflex myoclonus is characterized by abnormally enlarged cortical somatosensory evoked potentials (giant SEPs), which most likely reflect pathologically hyperexcitable sensorimotor cortex. To clarify the pathogenesis of myoclonus of cortical origin, we simultaneously recorded SEPs and whole head somatosensory evoked magnetic fields (SEFs) following electric stimulation of the median nerve at the wrist in six patients with cortical myoclonus. N20m and enlarged P30m were observed in all patients and were localized at the posterior bank of the central sulcus (Brodmann area 3b of the primary somatosensory cortex). In addition, P25m and N35m components of SEFs were recognized in five and four patients, respectively. P25m component, that is, the magnetic counterpart of P25 in EEG, was the earliest cortical component showing enhancement in patients. Multidipole analysis combined with magnetic resonance imaging (MRI) coregistration revealed that the generators of P25m were in the precentral gyrus in four patients and in the postcentral gyrus in one patient. The second SEFs around 200 msec after the single stimulus were recorded in three patients at area 3b (repetitive SEFs); two of whom showed negative as well as positive myoclonus. The importance of motor cortex for the generation of cortical reflex myoclonus was thus demonstrated. The pathologic features of SEFs suggest abnormal excitability of primary sensorimotor cortex.

Adult↗

PubMed1998

FGF1 patterns the optic vesicle by directing the placement of the neural retina domain.

Patterning of the bipotential retinal primordia (the optic vesicles) into neural retina and retinal pigmented epithelium depends on its interaction with overlaying surface ectoderm. The surface ectoderm expresses FGFs and the optic vesicles express FGF receptors. Previous FGF-expression data and in vitro analyses support the hypothesis that FGF signaling plays a significant role in patterning the optic vesicle. To test this hypothesis in vivo we removed surface ectoderm, a rich source of FGFs. This ablation generated retinas in which neural and pigmented cell phenotypes were co-mingled. Two in vivo protocols were used to replace FGF secretion by surface ectoderm: (1) implantation of FGF-secreting fibroblasts, and (2) injection of replication-incompetent FGF retroviral expression vectors. The retinas in such embryos exhibited segregated neural and pigmented epithelial domains. The neural retina domains were always close to a source of FGF secretion. These results indicate that, in the absense of surface ectoderm, cells of the optic vesicles display both neural and pigmented retinal phenotypes, and that positional cues provided by FGF organize the bipotential optic vesicle into specific neural retina and pigmented epithelium domains. We conclude that FGF can mimic one of the earliest functions of surface ectoderm during eye development, namely the demarcation of neural retina from pigmented epithelium.

Animals↗

PubMed1997

Functional localization of pain perception in the human brain studied by PET.

To elucidate the functional localization and somatotopic organization of pain perception in the human cerebral cortex, we studied the regional cerebral blood flow using positron emission tomography during selective painful stimulation in six normal subjects. Response to a painful stimulus was elicited using a special CO2 laser, which selectively activates nociceptive receptors, to the hand and foot. Multiple brain areas, including bilateral secondary somatosensory cortices (SII) and insula, and the frontal lobe and thalamus contralateral to the stimulus side, were found to be involved in the response to painful stimulation. While our data indicate that the bilateral SII play an important role in pain perception, they also indicate that there is no pain-related somatotopic organization in the human SII or insula.

Adult↗

PubMed1997

Familial cortical myoclonic tremor as a unique form of cortical reflex myoclonus.

Previously it was reported that some patients with tremor had the same electrophysiological findings as those seen in patients with cortical reflex myoclonus, and consequently the tremor was named "cortical tremor." In the present study, we examined six patients from three families with cortical tremor of relatively late onset. The inheritance pattern of cortical tremor was compatible with autosomal dominant trait. Those patients had relatively rhythmic involuntary movements (tremor) in the distal upper and lower limbs, especially during posture and/or fine movements. There was no cerebellar ataxia or dementia, and fits of loss of consciousness occurred only infrequently. Electrophysiologically, they had generalized spikes on electroencephalogram (EEG), giant cortical components of somatosensory evoked potential, an enhanced long-loop reflex (C-reflex), and cortical spikes preceding the rhythmic jerk demonstrable by the jerk-locked back averaging method, thus fulfilling the criteria of cortical reflex myoclonus. Furthermore, they had slow negative EEG shift starting 1-2 s prior to voluntary movements, suggesting that, as opposed to the conventional form of progressive myoclonus epilepsy (PME), the cerebellar efferent input to the motor cortices was normal. These clinical and electrophysiological pictures are distinct from those of familial essential tremor, familial essential myoclonus, or the conventional form of PME, and the term "familial cortical myoclonic tremor" will represent the clinical and electrophysiological features of this unique entity most appropriately.

Adult↗