Search PubMed⌕ Search

Biomedical subjects

C Yamanaka

Publications and source records attributed to C Yamanaka.

At least 37 records · Page 2Linked to original sources
PubMed1997

Duality of glutamatergic and GABAergic control of pulsatile GnRH secretion by rat hypothalamic explants: II. Reduced NR2C- and GABAA-receptor-mediated inhibition at initiation of sexual maturation.

N-methyl-D-aspartate (NMDA) receptors and gamma-aminobutyric acid (GABA) receptors are involved in the mechanism of pulsatile gonadotrophin-releasing hormone (GnRH) secretion. The aim of this study was to elucidate the role of those receptors in the acceleration of pulsatile GnRH secretion seen at onset of puberty. Using hypothalamic explants from prepubertal (15 days), early pubertal (25 days) and adult (50 days) male rats, we studied the effects of pharmacological antagonists and antisense oligodeoxynucleotides on GnRH release evoked by NMDA and GABA receptor agonists as well as the interval between spontaneous GnRH secretory pulses. At the three studied ages, the muscimol-evoked release of GnRh is similarly inhibited by the GABAA receptor antagonist bicuculline. In contrast, the frequency of pulsatility is stimulated by bicuculline as indicated by a reduction of the mean GnRh interpulse interval from 60 to 40 min and such an effect is seen at 15 days only. The GnRH interpulse interval is also reduced by GABAA receptor antisense oligodeoxynucleotides at 15 days while no effects are seen at 25 days. At the three studied ages, the NMDA-evoked release of GnRH and the GnRh interpulse interval are similarly inhibited by 100 or 500 microM of the NMDA receptor antagonist 7-chlorokynurenic acid (7CK). These effects are consistent with the increase of GnRH interpulse interval caused by NR2A antisense oligodeoxynucleotides at 15 days (86 vs 64 min in controls) as well as 25 days (44 vs 36 min). A low (5 microM) concentration of 7CK does not result in any effect except a reduction of GnRH interpulse interval which is seen at 15 days only. A similar reduction of GnRh interpulse interval is obtained using NR2C antisense oligodeoxynucleotides at 15 days (50 vs 64 min in controls) while no effects are seen at 25 days (35 vs 36 min). At 25 days, muscimol can prevent the developmental increase in frequency of pulsatile GnRH secretion. In summary, pulsatile GnRH secretion by the prepubertal hypothalamus characteristically involves an inhibition mediated through GABAA receptors and the NR2C subunit of NMDA receptors. Based on these data, we propose a model for the mechanism of the onset of puberty which involves the disappearance or inactivation of GABAergic neurons located in the retrochiasmatic hypothalamus and expressing the NR2C subtype of NMDA receptors.

Animals↗
PubMed1997

A case of Robinow syndrome accompanied by partial growth hormone insufficiency treated with growth hormone.

We report on a 10-year-old Japanese girl with Robinow syndrome accompanied by partial growth hormone (GH) insufficiency. We started GH replacement therapy at the chronological age of 6.5 years. In this case, improvement in the growth velocity was remarkable, but bone maturation accelerated even more. In order to avoid further acceleration of bone maturation, we started to treat our patient at the chronological age of 9.8 years with GH combined with gonadal suppression therapy using a luteinizing hormone releasing hormone analogue. However, no improvement in height SDS for bone age was attained. Our observations suggest that the indication of GH therapy for patients with Robinow syndrome needs careful consideration.

Body Height↗
PubMed1996

Normal mutation frequencies of somatic cells in patients receiving growth hormone therapy.

The number of reported cases of malignancy developing in growth hormone (GH) users worldwide has increased to more than 40. However, the causal relationship between GH administration and the occurrence of malignancies is still uncertain. We investigated somatic cell mutation frequencies (Mfs) or variant frequency (Vf) at three gene loci in patients with pituitary dwarfism receiving GH therapy to clarify the genetic effect of GH. Eighty-eight patients receiving GH therapy for at least 3 months and 42 age-matched healthy controls were studied. Mfs at hypoxanthineguanine phosphoribosyltransferase (HPRT) and T-cell receptor (TCR) loci in GH users were not significantly higher than in the controls. Although a few patients seemed to have a slightly increased Vf at the glycophorin A (GPA) locus, the difference was not statistically significant. In addition, there was no tendency for the Mfs (Vf) at these loci to increase with the duration of the GH therapy. These data seem to exclude the possibility that GH induces genetic instability in patients with pituitary dwarfism who are receiving GH therapy.

Adolescent↗
PubMed1996

Effects of a high-protein diet on mineral metabolism and struvite activity product in clinically normal cats.

OBJECTIVE: To examine effects of high-protein diets (> 50% crude protein of dry matter) on urinary mineral excretion and struvite activity product ([Mg2+] x [NH4+] x [PO(4)3-]). ANIMALS: 14 clinically normal cats, 4 adult female and male cats for experiments 1 and 2, respectively, and 6 female kittens aged 4 months for experiment 3. PROCEDURE: Relations between dietary protein amount (25.9, 38.3, 51.4, and 65.4% crude protein [dry matter]) and urinary excretion of Mg, P, and Ca were examined in a 4 x 4-Latin square design (experiment 1). Struvite activity product, the index of solubility of struvite crystals, was determined when a high-protein diet (54.9%) was fed (experiment 2). Utilization of minerals in cats fed a high-protein diet long term was examined (experiment 3). RESULTS: Water intake and urine volume increased with increasing dietary protein concentration. Urinary Mg2+ excretion was not affected (experiment 1) or was decreased (experiment 3) by higher protein intake, leading to lower urine Mg2+ concentration in groups fed higher protein amounts. Urine pH was decreased by high-protein intake. As a result, PO(4)3- concentration was decreased by high-protein intake (experiment 2), although total daily urinary excretion of P was increased. Consequently, struvite activity product tended to decrease in cats fed high-protein diets, indicating increase in struvite solubility. High-protein intake decreased Ca and P retention by increasing their fecal and urinary excretions, respectively. CONCLUSION: As a consequence of the increase in urine volume and urine acidification, high-protein diets have potential ability to increase solubility of struvite crystals.

Animals↗
PubMed1995

Pyrrolidine dithiocarbamate inhibits intercellular adhesion molecule-1 biosynthesis induced by cytokines in human fibroblasts.

Intercellular adhesion molecule-1 (ICAM-1), the ligand of lymphocyte function-associated antigen-1, plays an important role in the interactions of a variety of hemopoietic and nonhemopoietic cells, including leukocytes, fibroblasts, and endothelial cells. ICAM-1 is known to be involved in the onset of several diseases such as inflammation, allograft rejection, and so on. In this report, we investigated the effects of dexamethasone, cyclosporin A, FK506, and pyrrolidine dithiocarbamate (PDTC) on the induction of the ICAM-1 gene by cytokines in fibroblasts. PDTC, a potent inhibitor of NF-kappa B, was shown by ELISA and FACS analysis to prevent dramatically the expression of the ICAM-1 gene stimulated by IL-1 alpha, IFN-gamma, and PMA, although the other reagents inhibited it only slightly. Ribonuclease protection assay revealed that PDTC blocked the expression of the ICAM-1 gene at the mRNA level. To elucidate the mechanism of this inhibition, we constructed a series of ICAM-1 promoter deletion mutants linked to the chloramphenicol acetyl transferase gene and analyzed the effect of PDTC on their activities. Transient transfection analysis indicated that the critical region for inhibition by PDTC is an NF-kappa B binding site-like motif (GGGAGGATTCC, ICAM-1 kappa B) that is located at position-540. Electrophoresis mobility shift assay revealed that PDTC actually inhibits the binding of NF-kappa B (or NF-kappa B-like) protein to the ICAM-1 kappa B site. These findings suggest that PDTC inhibits ICAM-1 gene expression by inhibiting the association of NF-kappa B (or NF-kappa B-like) protein with the ICAM-1 kappa B site.

Base Sequence↗
PubMed1995

Type 3 GM1 gangliosidosis: clinical and neuroradiological findings in an 11-year-old girl.

An 11-year-old Japanese girl was diagnosed as having type 3 GM1 gangliosidosis by clinical symptoms and enzyme assay. She was the youngest among the patients with type 3 GM1 gangliosidosis whose clinical and neuroradiological findings have been documented. Clumsiness since early infancy and dystonia since early childhood which progressed slowly without mental deterioration and dysmorphism led us to the diagnosis of type 3 GM1 gangliosidosis. Genotype determination showed point mutation in exon 2 of the beta-galactosidase gene, which is common among the patients reported in Japan. T2-weighted MRI demonstrated bilateral symmetrical hypointensity in the putamen and globus pallidus. Single photon emission computed tomography using 99mTc-HMPAO showed bilateral hyperperfusion in the basal ganglia which decreased gradually during 1 year of observation. Twenty-two patients with type 3 GM1 gangliosidosis reported in the literature whose onset was at under 15 years of age were reviewed.

Child↗
PubMed1995

Elevation of serum creatine phosphokinase during growth hormone treatment in patients with multiple pituitary hormone deficiency.

Serum creatinine phosphokinase (s-CPK) increased to more than 500 U/l in 5 out of 21 patients with growth hormone (GH) deficiency during the 2 years of treatment with biosynthetic GH. In three of these five patients, s-CPK had elevated gradually after the start of GH treatment and remained high in one patient except in the period when GH injection was interrupted, and gradually decreased in the other two patients during treatment. These three patients had complete GH deficiency associated with multiple pituitary hormone deficiency due to pituitary stalk transection. One of the remaining two patients had Noonan syndrome and his s-CPK levels before therapy were relatively high. The fifth patient was a baseball athlete and the elevation of s-CPK seemed to be attributable to the strenuous exercise. Conclusion. s-CPK increases significantly in a certain group of patients with GH deficiency during GH replacement therapy. Measurement of s-CPK is to be included in the follow up laboratory tests at least in the 1st treatment year to evaluate the potential hazardous effects of GH on muscle.

Adolescent↗
PubMed1993

Protein-losing gastroenteropathy with facial anomaly and growth retardation: a mild case of Hennekam syndrome.

A 7-year-old boy with a peculiar face, protein-losing gastroenteropathy and growth retardation is reported. Although he has a face similar to those 5 cases reported previously by Hennekam et al. (Am J Med Genet 34:593-600, 1989) and Gabrielli et al. (Am J Med Genet 40:244-247, 1991), he is not mentally retarded nor does he have severe lymphedema. This patient seems to have a mild case of the Hennekam syndrome.

Albumins↗
PubMed1993

Acquired growth hormone deficiency due to pituitary stalk transection after head trauma in childhood.

Two patients are reported with growth hormone deficiency due to head trauma in childhood. Although their injuries were outwardly only slight and there was no loss of consciousness and no subsequent neurological deficits, they exhibited gradual growth retardation from the time of the trauma. Provocative endocrinological tests showed growth hormone deficiency and MRI showed transection of the pituitary stalk. These findings suggest that ordinary head trauma, as well as perinatal insult and congenital abnormalities, could be a cause of growth hormone deficiency.

Child↗
PubMed1993

[Nutritional assessment for patients with neurosurgical diseases].

There have been few guidelines in the field of nutritional management with regard to neurosurgical patients. In this review, caloric intake and nutritional parameters were measured in 24 patients in the acute stage and 32 patients in the chronic stage (prolonged unconscious state). We ascertained (1) whether the caloric intake was adequate or not, (2) the relationship between the grade of neurological damage and the nutritional assessment, and (3) we discussed the relationship between diseases and the nutritional assessments. The acute-stage patients, 14 male and 13 female, consisted of both a neurologically good prognostic group and a neurologically poor prognostic group. All of the prolonged-unconscious patients revealed poor prognosis. The nutritional assessment was referred to such parameters as, diet and nutrition, anthropometric measurements, laboratory tests, immunological parameters and prognostic nutritional index. The results were, 1) the acute stage patients received less caloric intake than their resting energy expenditure, 2) the neurologically poor prognostic patients showed muscle atrophy and decrease of creatinine-height index which represents muscle content, 3) there was no significant differences between the assessment parameters in each disease, and 4) serum electrolytes decreased in prolonged-unconscious patients with a small amount of caloric intake.

Acute Disease↗
PubMed1993

[A case of intra- and extracranially extensive metastatic brain tumor of tracheal cancer origin].

The authors report a case of metastatic brain tumor of tracheal cancer origin, itself a rare condition. A 55-year-old man was admitted with complaints of headache, atonic seizure of left lower limb and right temporal swelling. On admission, the patient had left recurrent nerve palsy. CT scan displayed right temporal bone destruction and ring-enhanced mass. MRI disclosed that the mass contained an inner necrotic region and a perifocal edema. Right common carotid angiogram revealed that the tumor was fed only by narrowed vessels of the middle meningeal artery. Subtotal removal of the tumor was performed, and histological examination revealed cranial metastasis of tracheal squamous cell carcinoma. Postoperative course was uneventful, and the patient underwent medical treatment for the primary lesion before post-operative brain-irradiation.

Brain Neoplasms↗
PubMed1992

Glycogen storage disease type III with muscle involvement: reappraisal of phenotypic variability and prognosis.

A review of the case histories of 19 Japanese patients with enzymatically proven glycogen storage disease (GSD) III who developed muscular symptoms at various ages illustrates the phenotypic variability of this disease. There seem to be 4 subgroups of GSD III with muscle involvement according to the clinical symptoms. The first group of patients is characterized by the childhood onset of muscle weakness and hepatic disorders. The second group of patients develops muscular symptoms in adult years while the liver symptoms start in childhood. The third group includes the patients whose muscle weakness started in adult years long after liver symptoms in childhood had disappeared. The fourth group shows only muscular symptoms as adults without any sign or history of liver dysfunction since childhood. The prognosis for each subgroup seems to be different; however, none of them appears to be better than that for GSD I, as has been suggested previously.

Female↗
PubMed1992

Short stature with normal growth hormone and elevated IGF-I.

We report on a Japanese girl with short stature, malar hypoplasia, up-slanting palpebral fissures, blue sclerae and thin, stiff and slightly brownish hair. Short stature started in utero and her psychomotor development was normal. Menarche appeared at 13 years 8 months. Height at 14 years 5 months was 132 cm (-4.6 SD). Her growth hormone (GH) sleep pattern and responses to insulin, L-dopa, arginine, propranolol-glucagon and growth hormone-releasing hormone were normal. Plasma insulin-like growth factor I (IGF-I) was high (2170-4860 units/l) and increased from 4860 to 7080 units/l 20 h after biosynthetic GH injection. Gel infiltration patterns of the free and protein-bound IGF-I in plasma from the patient were not different from the controls; IGF-I fraction of the high and low molecular weight binding protein and the non-protein bound fraction were 75.5%, 15.8% and 8.7%, respectively. IGF-I from the patient showed normal bioactivities when determined by [35S]sulphate and [3H]thymidine uptake into cultured rat chondrocytes, and by [3H]thymidine and [3H]alpha-aminoisobutyric acid uptake into the patient's skin fibroblasts. IGF-I binding to cultured skin fibroblasts from the patient was comparable to that of controls. These results suggest that tissue specific defects of IGF-I receptors may be the cause of increased IGF-I levels in the patient.

Animals↗