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Biomedical subjects

I Akiguchi

Publications and source records attributed to I Akiguchi.

At least 181 records · Page 10Linked to original sources
PubMed1993

A case of foreign accent syndrome without aphasia caused by a lesion of the left precentral gyrus.

We report a case of foreign accent syndrome (FAS) without aphasia. The patient was a right-handed, 44-year-old woman, a native Japanese. Disposition and inversion of pitch accents and appearance of unnecessary stress accents made her speech sound foreign, like that of a Korean. MRI demonstrated an infarction in the middle fifth of the posterior lateral aspect of the left precentral gyrus. Limited motor cortex damage causes FAS without dysarthria, apraxia of speech, or aphasia.

Adult↗
PubMed1993

Effects of phorbol ester on protein kinase C activity and effects of depletion of its activity on thyrotrophin, forskolin and 8'-bromoadenosine 3',5'-cyclic monophosphate-induced [3H]thymidine incorporation in rat FRTL-5 cells.

Protein kinase C (PKC) activity was measured in rat FRTL-5 cells cultured in medium containing insulin and transferrin (2H medium), in cells treated with phorbol 12,13-dibutyrate (PDBu), an activator of PKC, and in cells treated with 4 alpha-12,13-phorbol didecanoate (4 alpha-PDD), an inactive phorbol ester, in order to study the translocation and down-regulation of its activity. Provided the PDBu induced translocation and down-regulation of PKC activity, we used the down-regulated cells to study the roles played by PKC in DNA synthesis induced by stimuli which increase cyclic AMP (cAMP) and a cAMP analogue. Cytosolic preparations obtained from cells cultured in 2H media were fractionated on a DEAE-cellulose column, and fractions were assayed for PKC activity. PKC activity was eluted at concentrations between 0.06 and 0.15 mol NaCl/l with a peak at 0.1 mol/l. Exposure of cells to PDBu (100 ng/ml) resulted in 53% loss of initial PKC activity in the cytosolic fraction in concert with reciprocal augmentation of PKC activity in the particulate fraction that peaked at 321% of the initial level at 15 min of exposure. When cells were stimulated with 100 ng PDBu/ml for 15 min, three- and 1.9-fold greater PKC activity appeared in the particular and total cellular (cytosol plus particulate) fractions respectively than was the case for stimulation with 10 ng PDBu/ml. The total cellular PKC activity transiently increased at 15 min to 137% and subsequently decreased to 74, 40 and 25% of the initial level at 1, 12 and 24 h respectively. However, translocation of PKC activity to the particulate fraction was not observed in cells treated for 15 min with either 10 or 100 ng 4 alpha-PDD/ml and total cellular PKC activity was modestly reduced, to 97% of the initial level in cells exposed to 4 alpha-PDD (100 ng/ml) for 24 h. [3H]Thymidine incorporation was measured in cells whose PKC activity was stimulated by TSH, forskolin or 8-bromoadenosine cAMP simultaneously with PDBu (100 ng/ml), and also in cells whose PKC activity had been down-regulated by pretreatment with PDBu prior to the addition of each stimulant. The [3H]thymidine incorporation induced by each of the stimulants was inhibited in cells whose PKC activity was subjected to simultaneous stimulation, but was enhanced in cells whose PKC activity had previously been depleted. This potentiating effect of PDBu pretreatment on subsequent TSH-induced [3H]thymidine incorporation was not observed in cells exposed to PDBu for less than 12 h, but was observed in cells exposed for 24 h or longer.(ABSTRACT TRUNCATED AT 400 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1993

T-cell infiltration and expression of MHC class II antigen by macrophages and microglia in a heterogeneous group in leukoencephalopathy.

We report here on T-cell infiltration and diffuse expression of the major histocompatibility complex (MHC) class II antigen in a heterogeneous group of macrophages and microglia in leukoencephalopathy (LE). Microglia reacting positively for HLA-DR were five times more numerous in LE than those in non-LE cases and were distributed densely in the degenerated white matter but sparsely in the subcortical arcuate fibers. CD4- and CD8-positive lymphocytes were 9 and 15 times more plentiful, respectively, in LE cases; they aggregated in the expanded Virchow-Robin spaces and frequently infiltrated the neural parenchyma. An intimate association of T cells with macrophages, and the expression of leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1), accessory molecules in antigen presentation, were observed in each cell in the region of macrophage clusters. These results indicate that expression of MHC antigen is accompanied by cell adhesion molecules and by infiltration of T cells in a heterogeneous group in leukoencephalopathy and suggests their immunocompetence, although it may be secondary to destruction of myelin.

Aged↗
PubMed1993

[Chronic herpes simplex encephalitis initially presenting with persistent myoclonus].

A 59-year-old female patient with atypical chronic herpes simplex encephalitis was reported. Initial symptom was persistent myoclonus involving the trunk and limb muscles, and later lateral gaze palsy to the left side, cerebellar ataxia, consciousness disturbance and other brainstem symptoms including absence of corneal and gag reflex and vocal cord palsy developed. The patient was successfully treated with high dose of acyclovir. Electroencephalogram was normal in the initial stage but later showed diffuse slow waves. Although CT scan and MRI showed no abnormal finding in the cerebral cortex, brainstem lesion was observed on PD weighted image of MRI. Lumbar puncture yielded a clear cerebrospinal fluid, with slightly elevated protein, increased lymphocytes, and elevated titer of herpes simplex virus type I. The serological data, albumin ratio (10.3), antibody index (12.3) and antibody ratio (7.1) were consistent with herpes simplex encephalitis. Ten days' administration of acyclovir, 1,200 mg a day and repeated three times, was prominently effective for the myoclonus and consciousness disturbance. A diagnosis of chronic herpes simplex encephalitis initially presenting with brainstem encephalitis was made. Judging from the clinical and EEG findings, the brainstem lesion was initially thought to be a cause of myoclonus in this case. However, somatosensory evoked potential (SPE) of both upper and lower extremities revealed enlarged amplitude (giant SEP), and long loop reflex was enhanced (C-reflex) on the left. Giant SEP and C-reflex imply cerebral cortex as the origin of the myoclonus. Brainstem inflammatory lesion might have involved the ascending inhibitory system, thus disinhibiting the cortical sensorimotor area and causing cortical myoclonus.

Chronic Disease↗
PubMed1993

[Oral dyskinesis, facial dystonia].

Oral dyskinesia or orofacial dyskinesia is considered to be one of the most severe side-effects of a chronic treatment with neuroleptics or 1-dopa, although it has also been described in nontreated people. In oral or orofacial dyskinesia, involuntary spasms cause arrhythmic movements of the tongue, sometimes with protrusion and drooling, opening of the mouth, clenching of the teeth, or pursuing and retraction of the lips. Each spasm lasts seconds to a minute or two. In orofacial dyskinesia, lip smacking, chewing and tongue movements occur in a repetitive pattern interrupting speech. The pathophysiology of the orofacial dyskinesia has been still unknown. However, previous clinical observations and basic pharmacological studies have suggested that the dopaminergic receptors, especially of D1 type, play a crucial role in causing this condition. Based on this assumption, dopaminergic receptor antagonists have been introduced as medical treatments.

Dyskinesia, Drug-Induced↗
PubMed1993

Beta/A4 proteinlike immunoreactive granular structures in the brain of senescence-accelerated mouse.

The immunohistochemical localization of amyloid beta/A4 protein in the senescence-accelerated mouse brain was studied using six different antisera against human amyloid precursor protein peptides. beta/A4 proteinlike immunoreactivity was observed in the form of granular structures (beta-LIGS) in various regions, including the medial septum, cerebral cortex, hippocampus, cerebellum, and some cranial nerve roots. beta-LIGS were 1.5 to 2.5 mu in diameter and irregularly shaped. They increased significantly in number with aging, predominantly in animals with a phenotype of age-related deterioration of memory and learning abilities. Congo red and thioflavine S did not stain the granules. On immunoblots, the main immunoreactive bands were observed at 14 to 18 kd. The staining intensities of these bands also increased with advancing age. We consider that beta-LIGS are not only a new morphological manifestation of senescence in mice, but also a pertinent clue in understanding the mechanisms of amyloid deposition.

Aging↗
PubMed1992

Regional accumulation of amyloid beta/A4 protein precursor in the gerbil brain following transient cerebral ischemia.

Alterations of beta/A4 amyloid protein precursor (APP) were investigated immunohistochemically in the gerbil brain after transient global ischemia and subsequent reperfusion. Marked accumulation of this protein peaking at 24 h occurred in the neurons of the CA3 and paramedian region of the hippocampus as well as layers III, V and VI of the cerebral cortex. On the contrary, the accumulation was not observed in the neurons of the CA1 region. These results indicate that distribution of APP is altered depending on tissue viabilities after cerebral ischemia.

Amyloid beta-Protein Precursor↗
PubMed1992

Soybean agglutinin binds commonly to a subpopulation of small-diameter neurons in dorsal root ganglion, vascular endothelium and microglia in human spinal cord.

Soybean agglutinin (SBA) was used to identify the location of N-acetylgalactosaminyl glycoconjugates in human dorsal root ganglia (DRG) and spinal cord. SBA bound to a subpopulation of small-diameter neurons in DRG and their central projections. It also bound to microglia and vascular endothelium. Vascular endothelium, DRG neurons and microglia do not originate from the neural tube, but penetrate into the neural tube in the embryonic stage and thereafter are located in the spinal cord. SBA binding glycoconjugates may be responsible for cell-cell interaction between these three cell types and tissues in human spinal cord.

Acetylglucosamine↗
PubMed1992

Topographic projections from the subiculum to the limbic regions of the medial frontal cortex in the cat.

When WGA-HRP was injected into the subicular cortex of the ventral hippocampal formation (Hv) in the cat, terminal labeling was seen ipsilaterally in the caudoventral parts of the medial frontal cortex: in the infralimbic cortex (area 25), ventral part of the prelimbic cortex (area 32), and caudoventral part of the orbitofrontal cortex (area 12). The terminal labeling was observed in all cortical layers except layer 1. The cells of origin of these projections were then confirmed to be pyramidal neurons in the subiculum of the Hv. The projections were topographically organized: the temporal-septal shift along the long axis of the subiculum of the Hv corresponded to a rostroventral-caudodorsal shift in the anterogradely labeled limbic regions of the medial frontal cortex.

Animals↗
PubMed1992

Localization of protein kinase C in human skeletal muscle.

The immunolocalization of protein kinase C (PKC) isozymes alpha, beta I and beta II, was investigated in human skeletal muscle. All three isozymes were present on the muscle fiber surface membrane and within the muscle fibers. The alpha-isozyme was most clearly delineated on the surface membrane of the muscle fiber and on small blood vessels in the connective tissue. The axons of myelinated intramuscular nerves stained intensely for the beta I isozyme, whereas the endoneurial connective tissue reacted more strongly for the alpha- and beta II-isozymes. PKC isozymes may regulate intracellular signal transduction in human skeletal muscle, as in the other tissues, but their exact role in muscle remains unknown.

Adult↗
PubMed1992

Occurrence of acetylcholinesterase activity closely associated with amyloid beta/A4 protein is not correlated with acetylcholinesterase-positive fiber density in amygdala of Alzheimer's disease.

To investigate the possible relationship between acetylcholinesterase (AChE)-containing fiber density and senile plaque density and between AChE-positive plaques and beta/A4 protein deposition, AChE histochemistry, the modified Bielschowsky's method and beta/A4 protein immunohistochemistry were performed on the amygdala of Alzheimer's disease (AD) and aged control cases. Abundant AChE-positive senile plaques were found in the amygdala and related structures in AD. These AChE-positive plaques were mainly of the primitive or diffuse type. In addition to senile plaques of typical morphologies a variety of AChE-positive structures were observed in the amygdala and related regions in AD. A comparison of serial sections stained alternatively with AChE histochemistry and beta/A4 protein immunohistochemistry has revealed that these AChE-positive structures with variable morphological appearances displayed beta/A4 protein immunoreactivity, indicating that AChE is localized in a variety of beta/A4 protein deposition including the diffuse plaque. Thus, it is suggested that AChE is present in some senile plaques at the earliest stage. However, there was no apparent correlation between the numerical density of AChE-positive fibers and senile plaque density. These findings suggest that the degeneration of cholinergic neurons is not attributed to the occurrence of AChE activity in beta/A4 protein.

Acetylcholinesterase↗
PubMed1992

Immunohistochemical localization of the proteinase inhibitor region of amyloid precursor proteins in the neocortex of Alzheimer's disease and aged controls.

The immunohistochemical localization of the proteinase inhibitor region of amyloid protein precursors (APPI) in the postmortem human neocortex was studied using a polyclonal antibody raised against a purified recombinant human APPI derivative produced by COS-1 cells. APPI-like immunoreactivity (APPI-LI) was found diffusely in the human neocortex. APPI-LI appeared as irregularly shaped granular structures. The size of the APPI-LI structures was 1-4 microns in diameter. APPI-LI usually formed a cluster of 10- to 20-microns diameter in the cortical gray matter and 20- to 40-microns diameter in the subcortical white matter. Double staining for APPI and glial fibrillary acidic protein indicated that APPI-LI in the white matter and molecular layer was localized exclusively in the fibrillary astrocytes. In contrast, APPI-LI was found in neurons as well as in the fibrillary astrocytes in layers II through to VI. Under fluorescence microscopy, APPI-LI in both neurons and fibrillary astrocytes were found in close association with lipofuscin. The present observations indicate that APPI is localized in neurons and astrocytes in the human neocortex and that APPI may be associated with lipofuscin or lysosome in the human neocortex.

Aged↗
PubMed1992

Detailed distribution of nerve growth factor in rat brain determined by a highly sensitive enzyme immunoassay.

We modified a previously reported enzyme immunoassay method to make it more sensitive for quantification of nerve growth factor (NGF), and succeeded in measuring the NGF content in as small as 2 mg (wet weight) of rat brain tissue. Rat brain was cut into about 600 pieces of the same size, and the NGF content in each piece was determined by this method. The findings were as follows: (i) In the cerebral cortex, NGF contents were unevenly distributed, ranging from less than 0.1 to 1.8 ng/g wet wt. The level was highest in the caudal parietal and rostral occipital cortices and lowest in the lateral parietal cortex. (ii) Areas comprising the limbic system such as the cingulate gyrus, pyriform cortex, amygdala, anterior and medial thalamus, hippocampus, septum, and diagonal band of Broca contained high levels of NGF. (iii) In the brain stem and cerebellum, the levels were low; however, a relatively high level was registered in the cerebellar nuclei, lateral vestibular nucleus, ventral cochlear nucleus, superior olive, and pontine reticular nuclei. These findings, taken together with previously published information, suggest that the neurons in the anterior and medial thalamus, pontine reticular nuclei, superior olive, ventral cochlear nucleus, and cerebellar Purkinje cells may be additional populations of NGF-responsive neurons in the rat brain.

Animals↗
PubMed1992

Inbred SAM-P/10 as a mouse model of spontaneous, inherited brain atrophy.

We developed a novel inbred strain of mouse with age-related brain atrophy and it was named "Senescence Accelerated Mouse (SAM)-P/10." Macroscopic morphometry indicated that the brains of SAM-P/10 showed age-dependent involutional changes mainly in the frontal portion of the cerebrum. The brain weight decreased by 8.6% throughout the life-span. There were no obvious defects in postnatal development. Semi-macroscopic morphometry revealed a prominent atrophy in the neocortex, olfactory cortex and amygdala. Microscopic morphometry showed that the neocortical neurons were lost with aging, with mostly the large neurons being affected which were lost by 35.6% throughout the life-span. Somata of the neocortical neurons shrank with advancing age. In a control SAM-R/1 strain with only a slight macroscopic involutional change in the brain without weight loss, neither loss of the neocortical large neurons nor shrinkage of the neocortical neurons was evident with aging. Learning and memory skills were evaluated using the one-trial passive avoidance task and conditional avoidance task. Young SAM-P/10 mice performed well in both tasks but older SAM-P/10 showed a poorer performance in both tasks, and this was even poorer than the performance of very old SAM-R/1 mice. Thus, SAM-P/10 can serve as a spontaneous animal model of brain atrophy for a variety of studies of aging of the brain. A better understanding of neurodegenerative diseases with dementia should be forthcoming.

Aging↗
PubMed1992

Cheiro-oral-pedal syndrome.

The cheiro-oral syndrome is a well-known peculiar sensory disturbance seen around the corner of the mouth and in the palm of the hand on the same side. However, sensory disturbance around the corner of the mouth, in the palm of the hand and in the foot on the same side (cheiro-oral-pedal syndrome) has not been reported until now. We examined 2 cases of cheiro-oral-pedal syndrome; the lesion responsible was confirmed by magnetic resonance imaging to be in the medial lemniscus and in the ventral ascending tract of the trigeminal nerve.

Aged↗