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Biomedical subjects

K Jinnai

Publications and source records attributed to K Jinnai.

At least 37 records · Page 2Linked to original sources
PubMed1998

Nicotine given intracerebroventricularly does not inhibit the preovulatory surge of LH and PRL secretion in female rats.

To determine the effect of nicotine on LH and PRL secretion, nicotine bitartrate (nicotine) dissolved in saline was administered at 1400 h, just before the critical period for the preovulatory surge of LH and PRL secretion, either intracerebroventricularly (icv) or intravenously (iv) in female rats in proestrus. Nicotine neither at a dose of 5 microg nor at a dose of 10 microg injected icv at 1400 h caused significant changes in the surge of LH and PRL secretion. When nicotine was given iv at a dose of 100 microg, a significant decrease in LH and PRL concentrations occurred immediately, lasting for 2 h. After 1700 h, LH and PRL concentrations as high as that observed after 1700 h in saline-injected control rats were recovered, just as if nicotine caused a transient deficit of the surge secretion of these hormones. The results indicate that nicotine does not inhibit the preovulatory surge of LH and PRL secretion by acting at the hypothalamic level accessible via the third ventricle, but inhibits it by acting at certain other site(s).

Animals↗
PubMed1998

Fatal liver cirrhosis and esophageal variceal hemorrhage in a patient with type IIIa glycogen storage disease.

A 45-year-old woman with type IIIa glycogen storage disease (GSD IIIa) died of variceal hemorrhage secondary to liver cirrhosis. The postmortem examination disclosed increased intracellular glycogen in the liver as well as in the heart and skeletal muscle. Although most liver injuries in GSD IIIa have been considered to be non-progressive in adulthood, liver cirrhosis can be a cause of death in some patients.

Diagnosis, Differential↗
PubMed1997

Intracytoplasmic inclusion bodies of the substantia nigra in myotonic dystrophy. Immunohistochemical observations.

We recently reported a significantly higher incidence of intracytoplasmic inclusion bodies (IIBs) of the substantia nigra in patients with myotonic dystrophy (MyD) than in age-matched controls. The changes are, per se, not specific, since a small percentage of disease and normal controls also showed similar inclusions. To elucidate the pathological significance of the inclusion in MyD, we studied immunohistochemical characteristics of IIBs of the substantia nigra in eight patients with MyD. Many IIBs showed moderately intense immunoreactivity for ubiquitin, microtubule-associated protein (MAP) 1 and MAP 2. However, the IIBs did not react with any of the following: anti-neurofilament protein antibodies (Abs) (68, 160 and 200 kDa), anti-neuron-specific enolase antibody (Ab), anti-tau Ab, anti-tubulin Abs (alpha and beta), anti-paired helical filament Ab, anti-actin Ab, anti-phosphorylated epitope of neurofilaments Ab, anti-synaptophysin Ab, anti-myelin basic protein Ab, anti-actin Ab and anti-glial fibrillary acidic protein Ab. Our results suggest that IIBs of the substantia nigra in MyD are related to an alteration of neuronal cytoskeleton metabolism affecting microtubular proteins in conjunction with activation of ubiquitin proteolytic systems.

Aged↗
PubMed1997

Bicuculline infusion advances the timing of Fos expression in LHRH neurons in the preoptic area of proestrous rats.

The effect of bicuculline (BIC) on Fos expression in lutenizing hormone-releasing hormone (LHRH) neurons was examined by immunocytochemistry. Proestrous rats were infused with saline (SAL 1400, n = 4) or BIC (BIC 1400, n = 5) for 3 h (10.00-13.00 h) and were killed at 1400 h. Three control rats (SAL 1700), which received saline infusion, were killed at 1700 h. In both the BIC 1400 group and the SAL 1700 group, many LHRH neurons in the preoptic area expressed Fos, but those in the SAL 1400 group did not. The distribution and proportion of LHRH neurons expressing Fos in the BIC 1400 group were identical to those in the SAL 1700 group. We conclude that GABAergic neurons play a critical role in inducing LH surge by controlling LHRH neuronal activity.

Analysis of Variance↗
PubMed1997

Fos expression by naloxone in LHRH neurons of the mediobasal hypothalamus and effects of pentobarbital sodium in the proestrous rat.

Because Fos is thought to be induced in neurons that are activated, we examined whether luteinizing hormone-releasing hormone (LHRH) neurons expressed Fos protein when they were stimulated by an opioid receptor antagonist naloxone (NAL), expecting to identify LHRH neurons which are regulated by opioid neurons directly or indirectly. Further, we examined whether an ovulation-blocking dosage of pentobarbital sodium (PB) would affect the NAL-induced Fos expression. Female rats were infused with naloxone (5 mg/kg/h) for 90 min (10.00-11.30) in the morning of proestrus, during which infusion blood sampling was done, and were killed by i.v. injection with an overdose of PB at 11.30-12.00. Dual immunoperoxidase/immunofluorescence staining for both Fos and LHRH revealed that some LHRH immunoreactive (ir) neurons in the forebrain expressed Fos-ir, associated with an increase in serum LH concentrations, but little co-localization was found in rats in proestrus which were infused with saline as the control. The proportion of LHRH-ir neurons which expressed Fos-ir was about 35-62% in the caudal part of the forebrain including the mediobasal hypothalamus, and this was larger than that (10%) in the rostral part of the forebrain including the preoptic area. PB injection (32 mg/kg bw, i.p.) 15 min prior to the beginning of NAL infusion significantly enhanced the increase in LH secretion due to NAL, and also enhanced Fos-ir expression in LHRH-ir neurons. Together with the well-established fact that PB blocks the LHRH surge generator and our previous findings that NAL stimulates the LHRH pulse generator even in the PB-blocked proestrous rat, these results strongly suggest that the LHRH pulse generator exists in the mediobasal hypothalamus which contains LHRH neurons that are responsive to NAL and express Fos protein.

Animals↗
PubMed1997

Possible role of the gamma-aminobutyric acid-A receptor system in the timing of the proestrous luteinizing hormone surge in rats.

To examine the role of the gamma-aminobutyric acid-A receptor-mediated system in the timing of the proestrous LH surge, we observed the free running activity rhythm and the timing of the LH surge simultaneously in blinded cycling female rats. Blood samples were obtained from unanesthetized freely moving rats through an intraatrial cannula. Five hours after the activity offset on the day of proestrus, bicuculline methiodide (BIC; 50 mg/kg x h) or saline was infused i.v. for 3 h into the freely moving rats. In the BIC group, the peak time of the surge occurred at 7.9 +/- 0.2 h after the activity offset, with a significant advance compared to the peak time in the saline group (i.e. 9.9 +/- 0.4 h), but neither BIC nor saline induced a significant phase shift in the circadian activity rhythm. We found that the infusion of BIC on the subjective morning of the proestrous day dissociates the timing of the LH surge from the circadian activity rhythm in rats.

Animals↗
PubMed1997

Decreased expression of full-length mRNA for cBCD541 does not correlate with spinal muscular atrophy phenotype severity.

Spinal muscular atrophy (SMA) is characterized by degeneration of spinal cord anterior horn cells and muscular atrophy and has three phenotypes based on clinical severity and age of onset. One of the responsible genes for SMA is the survival motor neuron (SMN) gene, which is homozygously absent or interrupted in more than 90% of SMA patients. The cBCD541 (BCD) gene is a highly homologous copy of the SMN gene, which has a single synonymous transition in the coding region and may compensate for the loss of the SMN gene. To evaluate the effects of the BCD gene expression on the phenotypes of SMA, we examined lymphocyte mRNA from 9 SMA patients lacking the SMN gene, 10 asymptomatic parents, and 15 control subjects. We amplified mRNA fragments containing exon 7 of the SMN or BCD genes using reverse transcription-polymerase chain reaction since the transcript lacking exon 7 encodes a putative protein with a different C-terminal end. We used glyceraldehyde-3-phosphate dehydrogenase (GAPDH) transcript as an internal control, and the relative expression level of the SMN or BCD gene was shown as the ratio of SMN or BCD transcript to GAPDH transcript (S/G ratio). The mean S/G ratios of the patients were significantly lower than that of the parents and controls. However, among the patients examined in this study, there was no relationship between the S/G ratios and phenotypes of SMA. The results showed that the BCD gene expression was not related to the phenotypes of SMA. Furthermore, there was an overlap between the S/G ratios in patients and controls. As our discrimination study showed that the S/G ratio reflected the expression of the BCD transcripts in patients and the SMN transcripts in controls, this finding suggested that the BCD gene expression per se does not compensate for the loss of the SMN gene.

Adolescent↗
PubMed1996

Immunohistochemical study of intracytoplasmic inclusion bodies of the thalamus in myotonic dystrophy.

Intracytoplasmic inclusion bodies of the thalamus in eight patients with myotonic dystrophy (MyD) were studied immunohistochemically. The intracytoplasmic inclusion bodies of the thalamus (thalamic inclusions, TIs) were strongly immunostained with anti-ubiquitin antibody (Ab) and some of them were mildly stained with anti-microtubule associated protein 1 (MAP 1) and anti-MAP 2 antibodies. However, TIs did not react with any of the following: anti-neurofilament protein Ab, anti-tau Ab, anti-paired helical filament Ab, anti-tubulin Abs (alpha and beta), anti-neuron-specific enolase Ab, anti-glial fibrillary acidic protein Ab, anti-synaptophysin Ab, anti-myelin basic protein Ab, anti-actin Ab and anti-phosphorylated epitope of neurofilaments Ab. Thus, our study demonstrates the unique immunohistochemistry of TIs in MyD which differentiates them from other intracytoplasmic inclusions in various neurodegenerative disorders.

Aged↗
PubMed1996

Novel ipriflavone receptors coupled to calcium influx regulate osteoclast differentiation and function.

Ipriflavone (7-isopropoxyisoflavone) is an effective antiresorptive agent used to treat osteoporosis. However, the mechanism of its action on osteoclasts and their precursor cells is not well understood. To determine whether the mechanism involves direct effects on osteoclasts or their precursors, we examined the effects of ipriflavone on cytosolic free calcium ([Ca2+]i) in osteoclasts and their precursors and measured specific binding of 3H-labeled ipriflavone. Highly purified chicken osteoclast precursors, which spontaneously differentiate into multinucleated osteoclasts in 3-6 days, were loaded with fura-2, and the subcellular [Ca2+]i distribution was monitored by videoimaging. Ipriflavone induced a rapid increase in [Ca2+]i followed by a sustained elevation [EC50 = 5 x 10(-7) M, 263 +/- 74 nM (SE) (n = 8) above basal levels, by 10(-6) M ipriflavone, sustained phase]. The responses were the same in differentiated chicken osteoclasts and isolated rabbit osteoclasts. An influx of extracellular Ca2+ is likely to be responsible for the ipriflavone-induced change in [Ca2+]i because the response was abolished by 0.5 mM LaCl3, or by Ca-free medium containing EGTA. Moreover, high [Ca2+]i levels were detected adjacent to the cell membrane after ipriflavone addition. Ipriflavone induced Ca influx mainly through dihydropyridine-insensitive Ca2+ channels, because nicardipine (10(-7)M) and verapamil (10(-7)M) had no effects on ipriflavone-induced [Ca2+]i responses. [3H]Ipriflavone binding studies indicated the presence of specific ipriflavone binding sites (two classes), both in precursor cells [dissociation constant (Kd), 7.60 x 10(-8)M, 2.67 x 10(-6)M] and in mature osteoclasts (Kd, 4.98 x 10(-8)M, 3.70 x 10(-6)M). Specific ipriflavone binding was not displaced by various modulators of avian osteoclast function, such as estradiol (10(-8)M) or retinoic acid (10(-6)M), indicating that ipriflavone receptors differ from the receptors for these Ca-regulating hormones. The fusion of osteoclast precursor cells was significantly inhibited by ipriflavone, which led to dose-dependent inhibition of bone resorption and tartrate-resistant acid phosphatase activity. Novel specific ipriflavone receptors that are coupled to Ca2+ influx were demonstrated in osteoclasts and their precursor cells. These ipriflavone receptors may provide a mechanism to regulate osteoclast differentiation and function.

Acid Phosphatase↗
PubMed1996

Neuronal loss in the medullary reticular formation in myotonic dystrophy: a clinicopathological study.

Respiratory insufficiency occurs frequently in patients with myotonic dystrophy (MyD). We have performed a quantitative study of neurons linked to respiratory function in the dorsal central medullary nucleus (DCMN), the ventral central medullary nucleus (VCMN), and the subtrigeminal medullary nucleus (SMN) in seven patients with MyD and eight age-matched controls. Alveolar hypoventilation of the central type occurred in three of the MyD patients but not in the remaining MyD patients or controls. The densities of neurons of the DCMN, the VCMN, and the SMN in MyD patients with hypoventilation were significantly lower than in MyD without hypoventilation and controls. These data suggest the neuronal loss of the DCMN, VCMN, and SMN is associated with the presence of hypoventilation in MyD and may be an important feature of MyD.

Aged↗
PubMed1995

Thymoma: tumour type related to expression of epidermal growth factor (EGF), EGF-receptor, p53, v-erb B and ras p21.

As clinicopathological features may not be sufficient to predict the progression of thymoma, we have carried out what we believe to be the first immunohistochemical study describing the relationship between the different types of thymoma and the tumour stage, on the one hand, and the expression of epidermal growth factor (EGF), EGF-receptor (EGFR), p53, v-erb B and ras p21, on the other. The positive rates versus histological types and Masaoka's clinical stages in the 47 cases were as follows: p53 (non-invasive thymoma: 41.7%; malignant thymoma category I: 82.4%; malignant thymoma category II: 83.3%), EGF (non-invasive thymoma: 4.2%; malignant thymoma category I: 11.8%; malignant thymoma category II: 33.3%) and EGFR (non-invasive thymoma: 8.3%; malignant thymoma category I: 35.3%; malignant thymoma category II: 66.7%); p53 (stages I and II: 51.7%; stages III and IV: 77.8%), EGF (stages I and II: 3.4%; stages III and IV: 22.2%) and EGFR (stages I and II: 13.8%; stages III and IV: 44.4%). These data suggest that p53 may be implicated in the initial stages of tumorigenesis and that increased expression of EGF and EGFR may play a role in thymoma progression.

Adult↗
PubMed1995

Neuronal cell loss in the dorsal raphe nucleus and the superior central nucleus in myotonic dystrophy: a clinicopathological correlation.

A quantitative study of neurons in the dorsal raphe nucleus (DRN) and the superior central nucleus (SCN) was performed in seven patients with myotonic dystrophy (MyD), five of whom showed hypersomnia, and in eight age-matched controls. The densities of neurons in the DRN and the SCN were significantly lower in MyD patients with hypersomnia than in MyD patients without hypersomnia and control subjects. There was an appreciable positive correlation in the density of neurons between the DRN and the SCN in all MyD patients. These data suggest that the neuronal loss of the DRN and the SCN is associated with the presence of hypersomnia in MyD.

Aged↗
PubMed1995

LHRH pulse generator is stimulated by naloxone in the pentobarbital-blocked proestrous rat.

Previous studies by us and others led us to hypothesize that there are separate LHRH pulse and surge generators in the rat brain. The present study was designed to detect the activity of LHRH pulse generator by checking changes in LH secretion and the multiunit activity (MUA) of the arcuate-median eminence region of the hypothalamus during infusions of naloxone (NAL, 2 mg/h) in the proestrous rat in which the LHRH surge generator activity was blocked by pentobarbital sodium (PB, 32 mg/kg bw, ip). The animals were subjected to blood sampling in the morning (1000-1300 h) or afternoon (1400-1700), and injected with PB at 09.45 or 13.45, respectively. During saline infusions in the rat given PB injection at either 09.45 or 13.45, serum LH levels were low but fluctuated significantly, suggesting a pulsatile secretion in either the morning or the afternoon period. The pulse intervals were an average 28.2 min in the morning and 42.2 min in the afternoon. NAL infusions decreased the pulse interval significantly, to 22.0 min in the morning and to 27.0 min in the afternoon. In the electrophysiological experiment, characteristic increases in the MUA (volleys), which occur in association with the initiation of an LH pulse and therefore are considered to represent an increased activity of the LHRH pulse generator, appeared during NAL (5 mg/h) infusions in either the morning or the afternoon. These results strongly suggest that separate LHRH pulse and surge generators exist in the brain, and that, even during the critical period of proestrus, the activity of LHRH pulse generator is disclosed by PB, which, on the other hand, arrests the surge generator.

Animals↗
PubMed1995

[A case of hereditary pressure-sensitive neuropathy, confirmed by a gene analysis].

A 21-year-old male patient with hereditary pressure-sensitive neuropathy (HPSN) is reported. He had been well and was working as a carpenter until February 6, 1993, when he developed difficulty in raising his left arm and numbness in the radial aspect of his left forearm in the morning. Left musculocutaneous nerve palsy, a left winged-scapula, absence of the left biceps and right Achilles reflexes, and distal dominant nerve conduction delay were positive findings. His father and younger brother showed similar conduction delays. Sural nerve biopsy revealed the presence of tomacula, segmental demyelination and thinly myelinated fibers. Gene analyses of the patient's cultured lymphoblastoid cells disclosed deletion of the marker 6G1 and peripheral myelin protein-22 (PMP-22) gene of a single allele of chromosome 17 in 90% of his intermitotic cells by in situ hybridization, and also a 57% gene dosage of PMP-22 of normal control using Southern blotting. These findings indicate the deletion in 17p11.2 of the genomic DNA of this patient, which is diagnostic for HPSN.

Adult↗
PubMed1994

The inhibitory input from the substantia nigra to the mediodorsal nucleus neurons projecting to the prefrontal cortex in the cat.

The effects of stimulation of the substantia nigra pars reticulata (SNr) on the neurons of the mediodorsal nucleus (MD) projecting to the prefrontal cortex (PF) were studied in cats. The MD neurons projecting to the ventral part of the PF tended to be located in the ventral part of the MD, while those projecting to the dorsal part of the PF in the dorsal part. Spontaneous discharges of 30/57 tested MD neurons were suppressed by SNr stimulation at a latency ranging from 2 to 15 ms. The latency of the suppression corresponded well to that of antidromic responses of SNr neurons elicited by MD stimulation (from 1.4 to 14.0 ms). Intracellular recordings in a few MD neurons showed IPSP by SNr stimulation. The SNr is considered to exert an inhibitory effect on the MD neurons projecting to the PF.

Animals↗
PubMed1994

Bicuculline infusions advance the timing of luteinizing hormone surge in proestrous rats: comparisons with naloxone effects.

The role of GABA neurons in the control of the surge of LH secretion was investigated by examining whether GABAA receptor antagonist bicuculline (BIC) infusion prior to the LH surge could advance the timing of the proestrous surge in the rat. The effect of the opioid receptor antagonist naloxone (NAL) was also examined for comparison. Female rats in proestrus were iv infused with NAL (2 or 5 mg/hr) or BIC (50 mg/kg/hr) for a 3-hr (1000-1300 hr) period during which blood samples were collected at 6-min intervals through an intraatrial cannula in freely moving rats. The animals that received infusion were bled again over a 7-hr period (1400-2000 hr) at 1-hr intervals. NAL infusions at 2 mg/hr induced an increase in pulsatile LH secretion, but did not affect the timing, magnitude, and duration of the LH surge. NAL infusions at 5 mg/hr not only induced a greater increase in pulsatile LH secretion but also resulted in a pronounced LH surge prematurely. In contrast, during BIC infusion, no significant changes in LH secretion were seen until 1200 hr, but afterward a rapid and sharp rise in LH secretion occurred, suggesting the premature LH surge. These results are consistent with the hypothesis that the tonic LH secretion is sensitive to NAL, but not to BIC, whereas the surge of LH secretion is sensitive to barbiturates that have been known as the activator of GABAA receptor complex. Therefore, we suggest that there is a LHRH surge generator, distinct from the pulse generator, in the brain, and it has GABA neurons in its circuitry.

Animals↗
PubMed1994

Analysis of exposed regions on the main extracellular domain of mouse acetylcholine receptor alpha subunit in live muscle cells by binding profiles of antipeptide antibodies.

To study the structural organization of the main extracellular domain of the nicotinic acetylcholine receptor (AChR) alpha subunit in live muscle cells, we examined the native membrane-bound receptors in cultured mouse skeletal muscle cells for their ability to bind a panel of antibodies against uniform-sized overlapping synthetic peptides which collectively represent this entire domain. The binding profile indicated that the regions alpha 23-49, alpha 78-126, alpha 146-174, and alpha 182-210 are accessible to binding with antibody. Residues alpha 23-49, alpha 78-126, and alpha 194-210 contain binding regions for alpha-neurotoxin and some myasthenia gravis autoantibodies. A comparison of this binding profile with the profile obtained for membrane-bound Torpedo californica AChR in isolated membrane fractions showed some similarities as well as significant differences between the subunit organization in the isolated membrane fraction and that in the membrane of live muscle cells. Regions alpha 89-104 and alpha 158-174, which are exposed in the isolated membrane fraction, are also exposed in the live cell. On the other hand, regions alpha 23-49, and alpha 182-210, which are exposed in the live cell, are not accessible in the isolated membrane and, furthermore, the region alpha 1-16, which has marginal accessibility in the cell, becomes highly accessible in the membrane isolates. The exposed regions defined by this study may be the primary targets for the initial autoimmune attack on the receptors in experimental autoimmune myasthenia gravis.

Amino Acid Sequence↗