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Biomedical subjects

I Akiguchi

Publications and source records attributed to I Akiguchi.

At least 19 recordsLinked to original sources
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↗
PubMed1992

Sphenoid sinus mucocele with recurrent visual disturbance.

We present a case of sphenoid sinus mucocele with recurrent visual disturbance on the same side. A 22-year-old female showed two episodes of visual disturbance in the left eye for 3 months, and acute retrobulbar optic neuritis was diagnosed. With corticosteroid, visual disturbance improved in 1 week. MRI and CT scans showed mucocele in the left sphenoid sinus, and left optic nerve swelling with high intensity was observed in T2-weighted MRI. No destruction of the optic canal was found. The contiguous inflammation in the optic nerve rather than compression was considered as pathogenesis.

Adult↗
PubMed1992

Thyroid hormone receptors and 3,5,3'-triiodothyronine biological effects in FRTL5 thyroid follicular cells.

Specific thyroid hormone (T3) receptors are present in thyroid follicular cells, including the rat FRTL5 clonal line, but little is known about the effects of T3 on the growth and differentiated function of the thyroid. Unlike primary cultures of animal or human thyroid cells, FRTL5 do not secrete appreciable amounts of thyroid hormones. We now have studied the effects of T3 by itself and in combination with TSH and insulin-like growth factor-I (IGF-I) on [3H]thymidine incorporation into DNA, iodide uptake, and cAMP production in FRTL5. We also have investigated the expression of different c-erbA mRNAs in these cells. Specific binding of T3 to FRTL5 cell nuclei in intact cells occurred with a binding capacity of 0.1-0.15 ng T3/mg DNA and an apparent Kd of 0.4 nM. Using an RNase protection assay on total cellular FRTL5 RNA and specific cRNA probes, we demonstrated the presence of c-erbA alpha and -beta mRNAs, both encoding T3 receptors. Biological effects were assessed in serum-free medium or buffer containing 0.1% BSA after maintaining quiescent culture of cells for at least 5 days in hormone-free medium containing 5% calf serum. T3 alone stimulated a dose-dependent increase in [3H]thymidine incorporation that reached a plateau at 188% of the control value at 10 nM T3. At 10(-11) M TSH, T3 potentiated TSH-stimulated [3H]thymidine incorporation (2.2-fold), but at TSH concentrations greater than 5 x 10(-11) M, T3 had no effect or reduced the response to TSH. T3 potentiated the [3H]thymidine response to 2 and 10 ng/ml IGF-I by 1.5- to 1.7-fold. T3 alone had no effect on iodide uptake, but attenuated iodide uptake stimulated by TSH. T3 was more potent in inhibiting TSH-stimulated iodide uptake than in enhancing TSH-stimulated DNA synthesis. T3 did not affect either basal or TSH-stimulated cAMP accumulation. Thus, in FRTL5 thyroid follicular cells 1) T3 receptors are expressed, as measured by direct binding assays and by the expression of c-erbA mRNAs; and 2) T3 acts as a growth factor and weak antidifferentiation factor. We suggest that T3 may modulate the actions of TSH and growth factors in thyroid epithelium.

Animals↗
PubMed1992

[Migrant sensory neuritis--electrophysiological and pathological study].

Migrant sensory neuritis, which was first proposed by Wartenberg, is very uncommon and only a few case reports have ever been published. We described one case of migrant sensory neuritis and discussed the pathogenesis of this disease. A 44-year-old man noticed numbness in the lateral aspect of the dorsum of the left foot in February 1985. Physically, there was hypoesthesia in the region of left sural nerve with positive Tinel's sign. During the next 4 years, pain, tingling sensation or hypoesthesia appeared in the regions of the right superficial radial nerve, right axillary nerve, left intercostal nerve, left lateral plantar nerve, digital nerve of the right second digit, left saphenous nerve, right superficial peroneal nerve, left superficial radial nerve, bilateral ulnar nerves and bilateral median antebrachial cutaneous nerves one after another in a migrating fashion. Tinel's sign was also positive at the right superficial radial nerve. In some occasions, decreased deep tendon reflexes were observed, but there had been no muscle weakness. Some nerves showed complete recovery, but others showed persistent involvement. Some nerves were affected repeatedly. Laboratory examination failed to clarify underlying disease except for mild liver dysfunction. Electrophysiological study showed reduced amplitude of the sensory nerve action potential (SNAP) of right sural nerve, left ulnar nerve, right superficial radial nerve and digital branch of right median nerve with preserved sensory nerve conduction velocity. SNAP of left sural nerve was absent. These findings mean the cause of the sensory disturbance is axonal degeneration rather than segmental demyelination. There were no abnormalities in motor nerve conduction study.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1992

[Abulia: a case of cerebral infarction in the bilateral genua of internal capsules].

A patient was presented with an outstanding symptom of abulia due to cerebral infarcts in the bilateral genua of internal capsules. A 53-year-old woman, generally in good health and active, had no contributory medical history except for hypertension. She was well until August 20, 1988, when she was noted to have become taciturn and absent-minded. In the morning, she got up and went to work as usual. Although she worked without trouble, she hardly talked with her colleagues. After getting home from work, she would lie down without doing any housework, and this was continued on the following day. However, she had no physical problems. She was thus admitted to a hospital on August 22. Lethargy and urinary incontinence were apparent for a few days. Thereafter she became awakeful and could take care of herself. She sat on her bed all the time, and could talk normally with her daughter. She was referred subsequently to the Department of Neurology, Hyogo Prefectural Tsukaguchi Hospital on August 30. On examination, the patient was alert, polite and cooperative with no physical abnormalities except for high blood pressure. Neurological examination indicated the patient to be attentive and well-oriented. Cranial nerves and eye movements were normal except for slight anisocoria and sluggish pupils. There were no muscle weakness, extrapyramidal signs, or cerebellar signs. Deep tendon reflexes were normal. Babinski signs and forced grasping were not noted. A neuropsychological study showed the patient not to be demented, aphasic, or apraxic.(ABSTRACT TRUNCATED AT 250 WORDS)

Akinetic Mutism↗
PubMed1992

[An adult case of transverse myelitis with erythema infectiosum].

We reported an adult case of transverse myelitis with erythema infectiosum. A 33-year-old female was admitted to Kyoto University Hospital because of a weakness in the lower extremities and "cloth-wearing" sensation of the trunk and legs. One month before admission, she became febrile and developed a symmetrical erythema on the extremities. At the same time she noticed a slight weakness of the legs and numbness in her fingers and toes, which disappeared next few days. A week later, she again developed a fever, severe weakness of the legs and "cloth-wearing" sensation on the trunk, and erythema appeared on the cheek. Physical examination on admission revealed a weakness and hyperreflexia in the extremities, in particular, knee and ankle jerk, and hypesthesia of the trunk and legs below the level of Th6. Cerebrospinal fluid (CSF) examination revealed 181/mm3 cells (mononuclear cell dominant) and 30 mg/dl protein. Magnetic resonance imaging, CT and electrophysiological studies indicated no abnormalities. IgM antibody against human parvovirus (B19) was detected in the serum and CSF. She was diagnosed as transverse myelitis with parvovirus infection and was medicated with prednisolone 40-60 mg/day, and improved gradually with the residua of a mild weakness of the legs and hypesthesia on the trunk between the level of Th6 and Th10.

Adult↗
PubMed1992

[A case of herpes simplex encephalitis diagnosed by polymerase chain reaction].

A case of a 55-year-old male with herpes simplex encephalitis (HSE) was reported. He was admitted because of fever, headache and memory disturbance. T1 weighted MRI showed low signal intensity and T2 weighted imaging revealed high signal intensity in the medial portions of bilateral temporal lobes. Herpes simplex virus (HSV) antibody titer in cerebrospinal fluid (CSF) was not elevated. HSV DNA in CSF was amplified by polymerase chain reaction (PCR) and identified by the microplate hybridization method. The PCR technique would be useful for the diagnosis of HSE.

DNA, Viral↗