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Biomedical subjects

M Hotta

Publications and source records attributed to M Hotta.

At least 91 records · Page 5Linked to original sources
PubMed1991

Steroid-responsive painful ophthalmoplegia in childhood: sphenoid sinusitis presenting as Tolosa-Hunt syndrome.

A childhood case of painful ophthalmoplegia which responded well to steroids was described. Although the clinical features suggested Tolosa-Hunt syndrome (THS), serial magnetic resonance imagings (MRI) revealed ethmoid and sphenoid sinusitis in this 7-year-old boy. It was considered that multiple factors such as allergy, viral infection and swimming predisposed him to develop severe sinusitis and gave rise to his painful ophthalmoplegia.

Child↗
PubMed1991

Solid phase synthesis of human growth hormone-releasing factor analogs containing a bicyclic beta-turn dipeptide.

Three analogs derived from the N-terminal 29-residue fragment of human growth hormone-releasing factor (hGRF) which contained a bicyclic beta-turn dipeptide (BTD) at 7-8, 8-9, and 9-10 positions were synthesized by solid phase methodology to ascertain if the beta-turns are important for the biological activity of hGRF and also to show the applicability of the BTD unit to solid phase synthesis. All three analogs were obtained in good yield and purity indicating that the BTD unit can be used in the usual condition of solid phase synthesis. The capacity of these analogs to release growth hormone (GH) was tested in an in vitro bioassay using rat anterior pituitary cells. All three BTD-containing analogs showed the same maximal GH secretion with parallel dose-response curves to that of hGRF(1-29)NH2, except their relative potencies were very low.

Amino Acid Sequence↗
PubMed1990

Insulin-induced hypoglycemia, L-dopa and arginine stimulate GH secretion through different mechanisms in man.

We sought to clarify the mechanisms of growth hormone (GH) secretion induced by insulin hypoglycemia, L-dopa, and arginine in man. The secretion of GH as measured by increased plasma level, in response to oral administration of 500 mg L-dopa or 30 min-infusion of arginine, was not modified by prior intravenous administration of 200 micrograms GH-releasing hormone (GHRH). It was, however, completely blocked by preadministered 50 micrograms SMS201-995, a long-acting somatostatin (SRIH) analog. GH release with 200 micrograms GHRH was completely blocked by 100 micrograms SMS201-995. GH secretion caused by insulin-induced hypoglycemia was significantly reduced but still present after administration of 100 micrograms of the analog. These results suggest that a suppression of SRIH release may be partially involved in the stimulatory mechanism of GH secretion by L-dopa. Coadministration of GHRH accentuated the stimulatory effect of arginine on GH secretion. Arginine significantly raised plasma TSH levels. These findings suggest that arginine suppresses SRIH release from the hypothalamus to cause GH secretion because SRIH suppresses TSH secretion. It is also suggested that some factor (or factors) other than GHRH and SRIH are involved in the mechanism by which insulin-induced hypoglycemia stimulates GH secretion, because the effect of insulin was not fully blocked in the presence of SRIH analog. Thus all the tests for GH release appear to act via different mechanisms.

Adult↗
PubMed1990

Synthetic analogs of growth hormone-releasing factor with antagonistic activity in vitro.

Analogs of human and rat growth hormone-releasing factor (hGRF and rGRF), related to [D-Arg2]hGRF(1-29)NH2, were synthesized by solid phase methodology. Their capacity to inhibit growth hormone secretion stimulated by hGRF(1-44)NH2 was tested on rat anterior pituitary cells in monolayer culture. Among the analogs of hGRF, [D-Arg2,29,Arg30]hGRF(1-30)NH2 showed the highest antagonistic potency of 3.64 relative to [D-Arg2]hGRF(1-29)NH2 = 1. However, the most potent analog synthesized thus far was [N-Ac-His1,D-Arg2,Ala15]rGRF(1-29)NH2, which showed a relative potency of 27.7.

Amino Acid Sequence↗
PubMed1990

Brain corticotropin-releasing factor acts as inhibitor of stress-induced gastric erosion in rats.

Gastric lesions are known to be caused by stress. Corticotropin-releasing factor (CRF) is a key peptide initiating various stress response. This study was designed to investigate how brain CRF is involved in the occurrence of stress-induced gastric erosion in rats. Intracerebroventricular (icv) administration of CRF suppressed the occurrence of gastric erosion induced by water-immersion restraint stress, and its suppressive effect was blocked by coadministration of a CRF receptor antagonist in rats. The peripheral administration of CRF had no influence on the occurrence of erosion. The icv administration of a CRF receptor antagonist or anti-rat CRF gamma-globulin increased gastric erosion induced by the stress. Ganglionic blockade with chlorisondamine, muscarinic blockade with atropine, or bilateral adrenalectomy by itself significantly inhibited the occurrence of stress-induced gastric erosion, and no additional effect of CRF on these treatments-induced inhibition of erosion was found. These results, therefore, suggest that the occurrence of stress-induced gastric erosion is mediated by the autonomic nervous system- and adrenal-dependent pathway, and that brain CRF reduces the occurrence of stress-induced gastric lesions by acting on its specific receptor within the central nervous system, probably through the autonomic nervous system- and adrenal-dependent mechanism.

Animals↗
PubMed1990

SEM evaluation of surface cracking in glass-ionomer cement.

In an effort to assess the influence of acid etching and air drying on the production of cracks in the surface of glass-ionomer cement, the two procedures were employed over progressively increased durations, and any resulting surface cracks in the cement, were examined by replica techniques under an SEM (Scanning Electron Microscope). The results showed that acid etching alone did not produce cracks, but air-drying by compressed air produced cracks at durations between 5 and 30 sec.

Acid Etching, Dental↗
PubMed1989

Effects of ingestion of glucose on GH and TSH secretion: evidence for stimulation of somatostatin release from the hypothalamus by acute hyperglycemia in normal man and its impairment in acromegalic patients.

Ingestion of glucose is known to induce suppression of GH secretion in normal subjects and this phenomenon is often absent in acromegalic patients. To clarify the mechanism of GH suppression in acute hyperglycemia in normal subjects and disturbed GH response in acromegalic patients, the effects of acute hyperglycemia on plasma GH and TSH levels were examined in normal subjects and acromegalic patients. Plasma GH levels were significantly lowered 45-60 min after ingestion of 75 g glucose and elevated at 210 and 240 min in nine normal subjects. Plasma TSH levels were also significantly lowered between 45 and 120 min after ingestion; levels then gradually rose. Subcutaneous administration of 50 micrograms SMS 201-995, a long acting somatostatin analog, lowered plasma TSH levels in both normal subjects and acromegalic patients, and there was no significant difference in the degree of decrease in plasma TSH levels between the normal subjects and patients. These results, taken together with several reports that somatostatin suppresses TSH secretion as well as GH secretion, suggest that acute hyperglycemia stimulates somatostatin release from the hypothalamus, thus causing inhibition of GH and TSH secretion. However, in ten acromegalic patients, only two showed suppression of plasma GH levels to below 50% of basal level and the degree of suppression of TSH secretion was significantly less than in normal subjects in the glucose tolerance test. It is, therefore, suggested that somatostatin release in response to acute hyperglycemia is impaired in most acromegalic patients and that this abnormality may be one of causes for the absence of the normal GH response to acute hyperglycemia in this disorder.

Acromegaly↗
PubMed1989

The somatostatin analog octreotide inhibits the secretion of growth hormone (GH)-releasing hormone, thyrotropin, and GH in man.

The effects of the somatostatin analog octreotide on plasma GH, TSH, and immunoreactive GH-releasing hormone (IR-GHRH) were studied in 10 normal men. After morning sc administration of 50 or 100 micrograms octreotide or placebo, plasma GH, TSH and GHRH were measured frequently for 6 h. Plasma GH or IR-GHRH concentrations did not change after placebo injection, but plasma TSH levels gradually decreased, in conformity with a circadian rhythm during the morning. The mean plasma GH levels after sc injection of 50 or 100 micrograms octreotide declined, and no spontaneous GH pulses occurred for 5 h. Plasma TSH decreased rapidly after both doses of octreotide and was significantly lower than the level after placebo treatment from 90-315 min (P less than 0.05) and 60-360 min (P less than 0.05 or P less than 0.01), respectively. Plasma IR-GHRH levels also were significantly lower from 30-360 min (P less than 0.05) in the group given 100 micrograms octreotide compared with the value in the placebo group. We conclude that octreotide inhibits not only GH and TSH secretion from the pituitary, but also GHRH release from the hypothalamus and/or peripheral tissues. These findings suggest that somatostatin controls GH secretion not only by suppressing pituitary secretion of GH but also by suppressing GHRH release from the hypothalamus.

Adult↗
PubMed1989

Cerebral artery blood flow velocity waveforms in normal and small for dates fetuses.

Middle cerebral artery (MCA) blood flow velocity waveforms were recorded by a pulsed Doppler system in normal and small for dates (SFD) fetuses. Eighty four normal growth fetuses and 15 SFD fetuses were studied between the 28th and 40th gestational week. The flow velocity waveforms were analysed to determine the resistance index (RI = peak systolic velocity minus end diastolic velocity/peak systolic velocity). The results obtained were as follows: 1. The mean values of RI in the MCA had a peak of 0.802 +/- 0.049 at 32-33 gestational weeks and decreased gradually to a level of 0.686 +/- 0.087 at 40 gestational weeks. 2. In 8 asymmetrical SFD fetuses, the RI values for the MCA were below the normal range (mean -1.5 SD) in 6 cases and normal in 2 cases. 3. The RI values for MCA in all 7 symmetrical SFD fetuses were in the normal range.

Blood Flow Velocity↗
PubMed1989

[Color change by thickness and background color on visible light-cured composite resins].

The effects of thickness and background color on the color of five commercial light-cured composite resins were studied by a dental color meter using the CIE 1976 L*a*b* color system. As thickness increased from 1.0 to 4.0 mm, values of L*a*b* decreased for white and dentin color background but showed no obvious difference in color for a black background. the color of composite resins were not in fluenced by background color in a thickness of 4.0 mm. The values of color difference for 1.0 and 2.0 mm thick samples have a larger value than the same 4.0 mm samples. The color difference was recognized even for the same shade name in five representative kinds of composite resins.

Color↗
PubMed1989

[Color shades of visible light-cured composite resins].

The color of visible light-cured composite resins was examined by a dental color meter. The color shade guide was used as reference material in this study. The color difference value ranged from 5.5 to 11.0, suggesting that the color of composite resins is out of range of the shade guide.

Color↗
PubMed1989

[Adhesive efficiency of new bonding agents to dentin on bonding agent using urethane acrylate oligomer].

The tensile bond strength of new bonding agents on human dentin treated with 37% phosphoric acid solution for 60 sec to a photocurable composite resin was measured and the fractured surface was then observed by SEM. The new bonding agents consisted of various 20 wt% high molecular monomers (MW. 1500, 5000, urethane acrylate oligomer) as a base monomer. The best bonding agent was a mixture of 20 wt% 1500 molecular monomer as a base monomer and the value of the tensile bond strength was 91 +/- 17 kgf/cm2. The tensile bond test and SEM image of the fracture surface suggested that a high molecular monomer as a base monomer promoted the adhesive efficiency to human dentin.

Acrylic Resins↗
PubMed1988

Study on the mechanism of abnormal growth hormone (GH) secretion in anorexia nervosa: no evidence of involvement of a low somatomedin-C level in the abnormal GH secretion.

The response of plasma growth hormone (GH) to an iv injection of synthetic human growth hormone-releasing factor (hGHRF-44) (2 micrograms/kg bw) was studied in 23 patients with anorexia nervosa. The basal plasma concentrations of somatomedin-C (Sm-C) in these patients were also measured. Basal plasma GH levels were above normal in 8 out of 23 patients and an exaggerated GH response to hGHRF-44 compared to that in age-matched normal females was found in 9 patients. Mean basal plasma Sm-C concentration in the patients was 0.41 +/- 0.04 U/ml (mean +/- SE), which was in the low normal limit. When 6 patients were reexamined after their weight gain of 4-18 kg as well as their normalization of basal plasma Sm-C levels, their elevation of basal plasma GH level was lowered and the responsiveness to hGHRF-44 improved. However, there was no significant correlation between the Sm-C concentration and basal plasma GH level as well as the integrated GH response to hGHRF-44 expressed as the area under the curve (OhGH). These findings, therefore, suggest that some factor(s) other than the lowered plasma Sm-C level are involved in the mechanism of abnormal GH secretion in patients with anorexia nervosa.

Adolescent↗
PubMed1988

Effect of human growth hormone-releasing hormone on GH secretion in Cushing's syndrome and non-endocrine disease patients treated with glucocorticoids.

The GH response to 100 micrograms human growth hormone-releasing hormone (hGRH) given intravenously was evaluated in eleven patients with Cushing's syndrome who had been ill for more than one year and in six patients with non-endocrine diseases who were treated with glucocorticoid for one to twelve weeks. Extremely low to no response of plasma GH to hGRH injection was noted in all seven patients with Cushing's disease and in four patients with Cushing's syndrome due to an adrenal adenoma or carcinoma. In contrast, all six patients with non-endocrine diseases who were treated with glucocorticoid showed normal GH responses to hGRH. These results suggest that the diminished hGRH-induced GH secretion in patients with Cushing's syndrome might be caused by the prolonged period of hypercortisolemia.

Adult↗
PubMed1988

Involvement of corticotropin-releasing factor in restraint stress-induced anorexia and reversion of the anorexia by somatostatin in the rat.

The mechanism by which restraint stress induces suppression of food intake and the influence of intracerebroventricular (icv) administration of somatostatin on the anorexia induced by restraint stress were examined in the rat. Ninety minutes of restraint stress reduced food intake of rats to approximately 60% that of control. Anorexia induced by 90 min restraint stress was partially reversed by icv administration of alpha-helical CRF (9-41), a corticotropin-releasing factor (CRF) antagonist, and completely reversed by anti-CRF gamma-globulin. These results provide further evidence in support of the theory that CRF is involved in the inhibitory mechanism of food intake in restraint stress. ICV administration of somatostatin 14 and SMS 201-995, an analog of somatostatin, also reversed restraint stress-induced anorexia. It is, therefore, suggested that somatostatin may counteract the suppressive action of CRF on food intake in stress.

Animals↗
PubMed1988

Antagonistic effect of somatostatin on corticotropin-releasing factor-induced anorexia in the rat.

The effect of somatostatin on corticotropin-releasing factor (CRF)-induced anorexia was examined in rats. Intracerebroventricular (icv) administration of 0.11 nmol and 0.21 nmol ovine CRF significantly suppressed food intake of 24 h-starved rats. Icv administration of 0.31 nmol somatostatin 14 and somatostatin 28 partially reversed suppression of food intake induced by icv injection of 0.21 nmol CRF in 24 h-starved rats. These results suggest that somatostatin may counteract the suppressive effect of CRF on food intake within the central nervous system.

Animals↗
PubMed1988

Ontogeny of pituitary responsiveness to corticotropin-releasing hormone in rat.

The ontogeny of the pituitary's responsiveness to synthetic rat corticotropin-releasing hormone (CRH) in the late prenatal and early postnatal periods of rats was studied by a superfusion system using whole pituitaries. A significant increase of immunoreactive beta-endorphin (IR-beta-Ep) secretion in response to 10(-10) M CRH but not to 10(-11) M CRH was observed in pituitaries from the 15th day of gestation, the earliest day that we tested, whereas 10(-11) M CRH stimulated IR-beta-Ep release from the pituitaries of 17.5-day-old fetuses. Dose-related IR-beta-Ep secretions induced by 10(-12) M to 10(-10) M CRH were observed in pituitaries of 19.5- and 21.5-day-old fetuses, and 1-, 3- and 9-day-old newborn pups. CRH stimulated not only IR-beta-Ep and IR-adrenocorticotropic hormone (ACTH) but also IR-alpha-melanocyte-stimulating hormone (IR-alpha-MSH) secretions from fetal pituitaries. The content of IR-CRH in the hypothalamic extract from 15-day-old fetus was 6.6 +/- 3.6 pg/hypothalamus (mean +/- S.E.M.) and it gradually increased to reach 212.7 +/- 20.3 pg/hypothalamus on the 21.5th day of gestation. However, the content of IR-CRH in the hypothalamus dramatically decreased just after birth and then rapidly increased again from the 5th day after birth. These data indicate that the responsiveness of corticotrophs to CRH is already present on the 15th day of gestation, when the content of IR-CRH in the hypothalamus is extremely low and that the amount of hypothalamic IR-CRH dramatically dropped for several days just after birth in rats.

Animals↗