Biomedical subjects

K Jinnai

Publications and source records attributed to K Jinnai.

At least 55 records · Page 3Linked to original sources

PubMed1994

Microinjection of LHRH and its antagonistic analog into the medial preoptic area does not affect pulsatile secretion of LH in ovariectomized rats.

To gain a better understanding of the existence of an ultra-short feedback mechanism controlling LHRH secretion in the medial preoptic area (MPO), we examined the effects of microinjections of LHRH or the LHRH antagonist [D-pGlu1, D-Phe2, D-Try3,6] into the MPO on pulsatile secretion of LH in ovariectomized rats and on the surge of LH secretion in proestrous rats. Neither the injection of 10 ng LHRH nor 100 ng its antagonist into the MPO had any effect on pulse frequency or the mean LH concentration in ovariectomized rats. The injection of 100 ng LHRH antagonist or 10 ng LHRH delayed or advanced, respectively, the LH surge in proestrous rats. Taking these results together with our previous report, the present study indicates that 1) endogenous LHRH in the MPO is involved in the ultra-short feedback regulation of LHRH release and 2) the ultra-short positive feedback mechanism in the MPO acts at the time of the proestrous LH surge but not under a hormonal milieu as in ovariectomized rats.

Animals↗

PubMed1993

A GABAB-receptor mechanism is involved in the prolactin release in both male and female rats.

In order to evaluate the possible involvement of a GABAB-receptor mechanism in the control of prolactin release, the effect of baclofen, a GABAB-receptor agonist, on prolactin release was studied in male and female rats. Baclofen at a dose of 2-12 mg/kg was injected i.v. and blood samples were collected through an intraatrial cannula in freely moving rats. Baclofen caused an immediate increase in the prolactin concentration in serum, peaking at 6 min, in female rats. The injection also caused an increase in prolactin in male rats, the increase being smaller than in female rats. Together with the previous finding that the pituitary gland does not have GABAB receptors, the results support the concept that GABA plays a role in the central stimulation of prolactin release, mediated by GABAB receptors.

Animals↗

PubMed1993

The distribution of the globus pallidus neurons with input from various cortical areas in the monkeys.

Single neuron activities of the globus pallidus were recorded in awake monkeys. Electrical stimulation of various cortical areas (the prefrontal, premotor, supplementary motor and arcuate premotor areas, and the motor cortex) inhibited spontaneous discharge of pallidal neurons. This inhibitory response was considered to be mediated through the striatum. Considerable number of pallidal neurons responded to the stimulation of more than one cortical areas. However, the neurons receiving inputs from the motor cortex and/or arcuate premotor area and those receiving inputs from the prefrontal, premotor and/or supplementary motor areas were segregated. The former neurons were located ventrolaterally in the caudal part of the globus pallidus, while the latter ones were located dorsomedially in the rostral part of the globus pallidus.

Animals↗

PubMed1993

Cerebello- and pallido-thalamic pathways to areas 6 and 4 in the monkey.

Projections from the cerebellar nuclei (CN) and the internal segment of the globus pallidus (GPi) to areas 6 and 4 via the thalamus were examined electrophysiologically in monkeys. In addition to the well-known pallido-thalamo-cortical projection to area 6, some thalamic neurons with CN input were found to project to area 6. Seventeen neurons in VLc, area X and the dorsal margin of VPLo were activated antidromically by stimulation of supplementary motor or premotor areas, and orthodromically by CN stimulation. Twelve neurons in area X and the medial part of VPLo were found to receive CN input and to project to the arcuate premotor area (APA). Four neurons in the VLo-X border region which were identified to project to APA were inhibited by GPi stimulation.

Animals↗

PubMed1993

Glycogenosis type V (McArdle's disease) with hyperuricemia. A case report and clinical investigation.

A 28-year-old male with glycogenosis type V associated with continuous hyperuricemia during mild daily activities is reported. An aerobic exercise test using a bicycle ergometer revealed that purine metabolites, i.e., ammonia, inosine, hypoxanthine and xanthine, were transiently increased by the exercise and that a subsequent increment in uric acid continued until the following day. The accelerated purine degradation by the muscle exercise was thus shown to be able to cause the overt hyperuricemia in a patient with glycogenosis type V. Therapeutic use of fructose for glycogenosis was disappointing due to fructose-induced hyperuricemia. A search for myogenic hyperuricemia is essential for therapeutic trials.

Adult↗

PubMed1993

[Surgical treatment of myasthenia gravis in patients with thymoma].

During the 18 years period from 1972 to 1990 fifty-two patients with thymoma, including 13 with thymoma and myasthenia gravis (MG), underwent surgical treatment in our hospital. During the same period 27 patients without thymoma underwent surgical intervention for MG. These patients were assessed from the clinical manifestations, clinical effects for MG, and prognosis. The improved effects of surgery for MG with or without thymoma could be yearly obtained after operation. Palliation and remission rates of the 10 patients of MG with thymoma, excluded postthymectomy MG, were very poor in comparison with that of the 27 patients of MG without thymoma. Further more, the prognosis of the 13 patients of thymoma with MG was worse than that of 39 patients of thymoma without MG. The association of thymoma and progressive severity of disease related closely the influence of delayed response to surgical intervention and prognosis. In conclusion, aggressive surgical resection followed by chemo-radiotherapy was the best treatment for the invasive thymoma. Postoperative intensive care for MG crisis and recurrence of thymoma improved the effect to surgical intervention and revealed the good prognosis.

Adolescent↗

PubMed1992

Epitope-specific suppression of antibody response in experimental autoimmune myasthenia gravis by a monomethoxypolyethylene glycol conjugate of a myasthenogenic synthetic peptide.

A synthetic peptide corresponding to a myasthenogenic region of Torpedo californica acetylcholine (AcCho) receptor (AcChoR) alpha subunit, AcChoR alpha-(125-148), was conjugated to monomethoxypolyethylene glycol (mPEG). Injection of mice with the mPEG-AcChoR alpha-(125-148) conjugate and subsequent immunization with whole Torpedo AcChoR suppressed the development of experimental autoimmune myasthenia gravis (EAMG) by electrophysiological criteria. In anti-AcChoR sera from these animals, the antibody response against unconjugated AcChoR alpha-(125-148) was decreased, while the antibody responses against whole AcChoR and other epitopes were not altered. There were no detectable changes in T-cell proliferation responses to AcChoR alpha-(125-148) or to whole AcChoR in these animals. Prior injections with a "nonsense" peptide-mPEG conjugate had no effect on responses to the subsequent immunization with whole Torpedo AcChoR. The results indicate that the mPEG-AcChoR alpha-(125-148) conjugate has epitope-specific tolerogenicity for antibody responses in EAMG and that the AcChoR alpha-subunit region comprising residues 125-148 plays an important pathophysiological role in EAMG. The epitope-directed tolerogenic conjugates may be useful for future immunotherapies of human myasthenia gravis. The strategy of specific suppression of the antibody response to a predetermined epitope by using a synthetic mPEG-peptide conjugate may prove useful in manipulation and suppression of unwanted immune responses such as autoimmunity and allergy.

Amino Acid Sequence↗

PubMed1992

Profile of the regions on the alpha-chain of human acetylcholine receptor recognized by autoantibodies in myasthenia gravis.

Eighteen synthetic overlapping peptides encompassing the entire extracellular part (residues alpha 1-210) of the alpha-chain of human acetylcholine receptor (AChR) and a 19th peptide (residues alpha 262-276) corresponding to an extracellular connection between two transmembrane regions were prepared and used for the measurement, by solid-phase radioimmunoassay, of the binding of autoantibodies in plasma from myasthenia gravis (MG) patients. Autoantibodies were found to recognize only a limited number of the synthetic peptides. The regions recognized resided predominantly within the areas alpha 10-30, alpha 111-145 and alpha 175-198 and, less frequently, region alpha 45-77. Differences in the recognition profile of the peptides from patient to patient indicated that the autoantibody responses were under genetic control. However, by using a mixture of the appropriate peptides, it was possible to determine autoantibodies in all 15 myasthenia sera and to distinguish between these, normal human sera and other neurological or autoimmune diseases. The mapping of the continuous antigenic regions recognized by autoantibodies on the alpha-chain of human AChR has permitted a comparison of the regions recognized by autoantibodies and autoimmune T-cells from the same donor. It also provided a peptide-based direct antibody binding method for diagnosis of MG.

Adolescent↗

PubMed1991

Movement-related activity of thalamic neurons with input from the globus pallidus and projection to the motor cortex in the monkey.

Thalamic neurons projecting to the arm area of the motor cortex were identified by their antidromic response to stimulation of that area in two awake monkeys. Neurons were further identified as receiving inputs from the cerebellar nuclei or the internal segment of the globus pallidus by excitatory or inhibitory response to stimulation of these nuclei. Most (33/34) of the thalamic neurons in the cerebello-thalamo-cortical projection and more than half (12/18) of those in the pallido-thalamo-cortical projection changed their firing rate on the lever-lifting hand movement in the reaction-time task. A considerable number of neurons of both groups (14/23 and 3/10) changed their firing rate prior to the onset of the earliest EMG. These findings agree with the model that activities of pallidal as well as cerebellar nuclear neurons related to motor control are transmitted to the motor cortex through the thalamus.

Animals↗

PubMed1990

Discharge patterns of pallidal neurons with input from various cortical areas during movement in the monkey.

Activities of pallidal neurons were studied in awake monkeys which were implanted with stimulating electrodes in the various cortical areas in the frontal lobe. Cortical inputs to each pallidal neuron were examined by inhibitory responses to stimulation through these electrodes. Discharge patterns of pallidal neurons were observed during performance of the reaction-time, delayed go/no-go discrimination and self-paced movement tasks. Most of the pallidal neurons with input from the arm of the motor cortex changed their firing rate in close relation to the arm movement (movement-related activity). Many of the neurons with input from the supplementary motor and cingulate areas showed sustained changes in discharge rate during the delay period in addition to movement-related activity. Most of the neurons with input from prefrontal cortex responded to light stimulus.

Animals↗

PubMed1990

Acute autonomic and sensory neuropathy: a case report.

A female patient with acute autonomic and sensory neuropathy is described. Urinary disturbance developed rapidly and was followed by orthostatic syncope, absence of lacrimation, salivation and sweating, and sensory impairment. Muscle strength had been consistently normal despite diffuse muscular atrophy. Marked decrease in the number of small myelinated and unmyelinated fibres was revealed in biopsied sural nerve. Eighteen months after the onset, her autonomic symptoms have partially improved.

Acute Disease↗

PubMed1990

Somatosensory evoked potentials in acute renal failure: effect of parathyroidectomy.

Effects of acute renal failure (ARF) on somatosensory evoked potentials (SEP) were studied in rats. Cervical and cortical SEPs were measured both before and after bilateral ureteral ligation. A significant augmentation of amplitudes and an increase in latencies of the cortical SEP were observed in ARF. The peripheral nerve conduction velocities were unchanged. Serum parathyroid hormone (PTH) levels in uremic rats were significantly elevated after the bilateral ureteral ligation. In previously parathyroidectomized rats, the bilateral ureteral ligation had no effects on amplitudes of SEP or serum PTH levels.

Acute Kidney Injury↗

PubMed1990

A case of mitochondrial myopathy, encephalopathy and lactic acidosis due to cytochrome c oxidase deficiency with neurogenic muscular changes.

An 18-year-old male with mitochondrial myopathy, encephalopathy and lactic acidosis was studied by electromyography (EMG) along with histological and biochemical studies on his biopsied muscle. Mitochondrial cytochrome c oxidase deficiency with a decrease in the amounts of the subunits 2, 6, and 7 was discovered. Although no apparent symptoms of peripheral neuropathy were present, EMG revealed high-amplitude motor unit action potentials with a reduced interference pattern and the histochemical study revealed fiber type grouping without grouped atrophy. These findings indicated lower motor neuron damage, probably due to the mitochondrial disorder, followed by reinnervation. Coenzyme Q10 administration was effective in reducing both the lactate and pyruvate levels and for recovering the muscle atrophy.

Acidosis, Lactic↗

PubMed1990

Diurnal variation of cerebral blood flow in rat hippocampus.

We measured local cerebral blood flow over 24 hours in 10 unanesthetized, freely moving rats to determine whether blood flow in the hippocampus fluctuated as a function of time of day. We measured hydrogen clearance at 1-hour intervals using a polyurethane-coated platinum electrode with a 1-mm bare tip implanted in the dorsal hippocampus. Individual rats displayed a wide range of local cerebral blood flow values (from 30 to 100 ml/min/100 g tissue) in a day. In seven of the 10 rats, the overall mean hippocampal blood flow for the dark cycle (7 PM-5 AM) was significantly (p less than 0.001, 0.01, or 0.05) greater than that for the light cycle (6 AM-6 PM), showing an average increase of 20%. Further, the maximum mean hippocampal blood flow at 11 PM in all 10 rats was 42% greater than the minimum at noon. Our study demonstrates for the first time that local cerebral blood flow in the hippocampus shows diurnal variation.

Animals↗

PubMed1990

The roles of endogenous opioids in the inhibitory action of the hippocampus on preovulatory luteinizing hormone in rats.

Whether endogenous opioid peptides were involved in the inhibitory action of the hippocampus (HPC) on luteinizing hormone (LH) release was studied examining the effect of naloxone, an opioid antagonist, on the inhibitory action of electrical stimulation of the HPC and also by examining the effect of metenkephalin administration in the HPC, on preovulatory release of LH in proestrous rats. In rats treated with saline at 13:00 h, either sham stimulation or electrical stimulation of the dorsal HPC, which was performed acutely under ether anesthesia, significantly inhibited the afternoon rise in serum LH. In animals treated with naloxone at a dose of 2.0 mg/kg body weight, the afternoon rise in LH appeared smaller than that in the control group. However, statistical analysis showed no significant difference in LH values compared to the control group. Direct administration of met-enkephalin at a dose of 10 micrograms at 13:00 h through a chronically implanted cannula in the HPC did not induce any significant change in the afternoon rise in LH, regardless of whether it induced behavioral seizures or not. The results suggest that opioid peptides in the HPC do not play a significant role in the inhibitory action of HPC on LH release. Opioids existing in areas other than the HPC may play a certain, but small role.

Animals↗

PubMed1989

Calcitonin gene-related peptide enhances spontaneous acetylcholine release from the rat motor nerve terminal.

The effect of synthetic rat calcitonin gene-related peptide (rCGRP) on neuromuscular transmission was examined in a superfused rat phrenic nerve-diaphragm preparation using an intracellular microelectrode technique. The superfusion with rCGRP (10(-8) to 2 x 10(-7) M) caused significant increases in the frequency of miniature endplate potentials (MEPPs). It, however, had no effect on the resting membrane potential, amplitude of MEPPs, or acetylcholine quantum size and content. Enhancement of spontaneous acetylcholine release from the motor nerve terminal by rCGRP was demonstrated.

Acetylcholine↗

PubMed1989

Intracytoplasmic inclusion bodies of the thalamus and the substantia nigra, and Marinesco bodies in myotonic dystrophy: a quantitative morphological study.

Intracytoplasmic inclusion bodies of the thalamus and the substantia nigra, and Marinesco bodies have been studied in four patients with myotonic dystrophy (MyD), eight patients with other neurological diseases (control A), and eight patients without neurological diseases (control B). The percentages of the affected cells were calculated by dividing the number of neurons including intracytoplasmic inclusion bodies of the thalamus and the substantia nigra, and Marinesco bodies, by the total cell count in these respective regions. Statistical analyses were performed with regard to the frequency of these bodies by using Student's t test. There was a significantly higher incidence of intracytoplasmic inclusion bodies of the thalamus (13.2% versus 0.7%, P less than 0.001) and the substantia nigra (20.4% versus 2.7%, P less than 0.001), and Marinesco bodies (37.4% versus 4.1%, P less than 0.001) in patients with MyD than in controls A and B. From our observations, it is suggested that the presence with a high frequency, in combination, of these bodies is not an incidental finding but may have an intimate and important relationship with the pathogenesis of MyD, and may be a conspicuous and diagnostically important feature of MyD.

Adult↗

PubMed1989

[A case of adrenomyeloneuropathy with localized cerebral white matter degeneration].

A male with an atypical adrenomyeloneuropathy is described, who developed spastic paraparesis at the age of 37. Because his gait deteriorated further and he had a bladder dysfunction, he was admitted to National Sanatorium Hyogo Central Hospital at the age of 51. A diagnosis of adrenomyeloneuropathy was supported by increased level of very long chain fatty acids in plasma. He became demented and suffered from grand mal seizures during the last one year of his life. CT scan showed symmetrical hypodense lesions in the centrum semiovale. He died of pneumonia and renal failure at the age of 53. Autopsy revealed symmetrical degeneration throughout the corticospinal tracts from cerebral white matter to lumbar spinal cord. Degeneration of the optic radiation, posterior half of the corpus callosum, thalamus, cerebellar white matter, and gracile tract in high cervical segments were also observed. In these area, there was a loss of myelin and axon with marked gliosis and foamy macrophages, as well as mild perivascular cuffing. In our case, symmetrical and well-defined lesion in cerebral white matter is atypical for adrenomyeloneuropathy, while destruction of the gracile tracts is not a feature of adrenoleukodystrophy. In addition, well-demarcated "pseudosystemic" type of fiber tract degeneration appears to be different from a feature of primary demyelination which has been considered to be an essential alteration of adrenoleukomyeloneuropathy-complex. We propose another hypothesis, therefore, that neurons are primarily altered, thereby leading to the degeneration of myelins in this disease.

Adrenoleukodystrophy↗