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Biomedical subjects

J Iwasaki

Publications and source records attributed to J Iwasaki.

At least 19 recordsLinked to original sources
PubMed2001

Growth and endocrine function during school age in very low-birth weight infants.

BACKGROUND: Short stature and low bodyweight are commonly encountered problems in the clinical follow up of premature infants. However, details about the underlying pathophysiology are unknown in these cases. METHODS: Evaluations of growth and endocrine function were performed in 23 very low-birth weight (VLBW) infants between 11.3 and 14.3 years of age. RESULTS: The mean (+/-SD) scores for height and weight were -0.50+/-0.97 and -0.50+/-1.10 SD, respectively. Mean serum insulin-like growth factor (IGF)-I and urine growth hormone (GH) levels were 402+/-138 ng/mL and 18.0+/-17.5 pg/mg creatinine, respectively. Serum IGF-I and urine GH levels were within the normal range for all patients. The bone age values were consistent with the patient's true age. Physical signs of puberty were detected in 15 of 23 patients (65%). Using bone ages to predict final adult height yielded a score of -0.52+/-1.08 SD. CONCLUSIONS: Despite the almost normal results of serum IGF-I, urine GH levels and bone age, the physical growth of these VLBW infants was less than that of normal birth weight children, as was their predicted adult growth.

Adolescent↗
PubMed1989

An investigation of capnography and pulse oximetry as monitors of pediatric patients sedated for dental treatment.

Traditional methods of monitoring sedated pediatric dental patients have major shortcomings. This study evaluated the use of capnography in conjunction with pulse oximetry for monitoring children during conscious sedation for dental treatment. The specific purposes of the study were to determine if capnography would: (1) detect ventilatory changes that subsequently cause an oxyhemoglobin desaturation as detected by pulse oximetry; and (2) detect an airway obstruction. Ten pediatric dental patients (mean age 2 years, 10 months) were sedated with 75 mg/kg of chloral hydrate in strict accordance with the Guidelines for the Elective Use of Conscious Sedation, Deep Sedation, and General Anesthesia in Pediatric Patients of the American Academy of Pediatric Dentistry and the American Academy of Pediatrics (1985). All patients were monitored continuously using both capnography and pulse oximetry. Analysis of data obtained using these monitors revealed that specific end-tidal CO2 values were not predictive for subsequent oxyhemoglobin desaturations and that capnography was very accurate in detecting complete obstruction of the airway. Pulse oximetry revealed that all patients had mild oxyhemoglobin desaturations and that 50% had moderate desaturations.

Anesthesia, Dental↗
PubMed1985

Pituitary 1,25-dihydroxyvitamin D3 receptors in hyperthyroid- and hypothyroid-rats.

The binding of 1 alpha,25-dihydroxy (26,27-methyl-[3H]) cholecalciferol ([3H]1,25-(OH)2D3) to its receptor in cytosol of the anterior pituitary cells was examined in hyperthyroid- and hypothyroid rats, as well as in normal rats. The binding capacity increased by 41% in L-Thyroxine-treated hyperthyroid rats and decreased by 49% in propylthiouracil-ingested hypothyroid rats as compared with normal control rats, whereas the affinity of the receptor for [3H]-1,25(OH)2D3 showed no difference among these 3 animal groups. These findings indicate that the number of 1,25(OH)2D3 receptors in the pituitary may be regulated by thyroid hormone, and further suggest that 1,25-(OH)2D3 may play some role in regulating functions of the anterior pituitary.

Animals↗
PubMed1985

Presence of growth hormone-releasing factor-like immunoreactivity in human cerebrospinal fluid.

Immunoreactive human growth hormone-releasing factor (I-hGRF) in human cerebrospinal fluid (CSF) was measured by radioimmunoassay using antiserum specific to the C-terminal portion of hGRF(1-44)NH2. Dilution curves of I-hGRF in the CSF were completely parallel to that of synthetic hGRF(1-44)NH2 standard. On Sephadex G-50 column chromatography a single peak of I-hGRF in the CSF was eluted at the position of synthetic hGRF(1-44)NH2. I-hGRF was present in the CSF of all control patients without any endocrine disease (mean +/- SE, 29.3 +/- 2.0 pg/ml) whereas I-hGRF in the CSF was not detectable (less than 5.8 pg/ml) in any of the patients with hypothalamic germinoma. In all patients with idiopathic GH deficiency, I-hGRF in the CSF was measurable but its concentration (15.1 +/- 1.0 pg/ml) was significantly (p less than 0.05) lower than that in the control subjects. No difference in I-hGRF levels of the CSF was observed between patients with acromegaly and control subjects. These findings demonstrate for the first time that I-hGRF is present in human CSF. Measurement of I-hGRF in the CSF may be useful for understanding the pathophysiology of hypothalamo-pituitary diseases.

Acromegaly↗
PubMed1984

Specific binding of 1,25 dihydroxyvitamin D3 in lymphocytes.

We examined ten cellular or tissue sources of lymphocytes for specific binding of 1,25(OH)2D3, the hormonally active form of vitamin D3. A specific-binding protein was found in three of these sources. Scatchard analysis of cytosol from a follicular lymphoma cell line revealed binding sites with a Kd of 7.0 X 10(-11) and a receptor concentration of 6.6 fmol/mg protein. Sucrose density centrifugation of 3H-1,25(OH)2D3 labeled cytosol showed a 3.75 peak which was absent in cytosols incubated with excess nonradioactive 1,25(OH)2D3. The relative amounts of vitamin D3 metabolites required to displace 50% of the specifically bound 3H-1,25(OH)2D3 were 1,25(OH)2D3: 1,24,25(OH)3D3: 25(OH)D3: 24,25(OH)2D3 = 1: 180: 1000: 2700. Excess vitamin D3, cortisol, and estradiol failed to displace 3H-1,25(OH)2D3. Scatchard analysis of spleen cytosol from a patient with prolymphocytic transformation of chronic lymphocytic leukemia demonstrated a binding protein with a Kd of 1.2 X 10(-10) and a receptor concentration of 0.2 fmol/mg protein. DNA cellulose binding confirmed the presence of the specific-binding protein in this cytosol. Specific binding of 3H-1,25(OH)2D3 was also quantitated in a cell line from a patient with Burkitt's lymphoma with a Kd of 0.3 X 10(-10) and a receptor concentration of 29.6 fmol/mg protein. No specific binding of 3H-1,25(OH)2D3 was observed in lymphocytes from seven other malignant and nonmalignant sources. These results are the first to demonstrate a specific-binding protein for 1,25(OH)2D3 in lymphocytes from tissue and from these specific cell lines. The presence of this protein in some lymphocytes but not others may reflect the state of activation of the lymphocytes.

Binding, Competitive↗
PubMed1984

Prolactin secretion from human prolactinomas perifused in vitro: effect of TRH, prostaglandin E1, theophylline, dopamine and dopamine receptor blockers.

To clarify the functional characteristics of prolactin (Prl)-producing adenoma cells, the effect of TRH, prostaglandin E1 (PGE1), theophylline, dopamine and dopaminergic antagonists on Prl secretion was examined in vitro in perifused pituitary adenoma tissues obtained at surgery from 8 patients with prolactinoma. Perifusion with TRH at a concentration of 10(-6) to 10(-5) M resulted in a significant increase in effluent Prl levels in 3 of the 8 adenoma tissues. In the remaining 5 adenomas, TRH produced no effect on Prl release in vitro. On the other hand, PGE1 (10(-5) M) stimulated Prl secretion in 2 of the 4 adenomas examined. Addition of theophylline (5.5 mM) caused a marked increase of effluent Prl levels in all 8 prolactinomas regardless of the reactivity to TRH or PGE1. Dopamine (5 X 10(-7) M) suppressed Prl secretion from adenoma tissue in 5 of 7 patients tested but had no effect in the remaining two adenomas. When perifused simultaneously with dopamine, sulpiride (D2-selective dopamine receptor blocker, 5 X 10(-7) M) blocked the inhibitory effect of dopamine on Prl release in 3 of the 4 dopamine-sensitive prolactinomas. In one adenoma responsive to dopamine but resistant to sulpiride, YM-09151-2 (relatively specific D1-dopamine receptor blocker, 5 X 10(-7) M) antagonized the dopaminergic inhibition of Prl release. When perifused alone, neither sulpiride nor YM-09151-2 affected Prl release from any of the adenoma tissues tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Measurement of 1,25-dihydroxyvitamin D3 receptors in breast cancer and their relationship to biochemical and clinical indices.

Both normal and malignant breast tissue contain the specific receptor for 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3). A recent study has shown its presence in 80% of surgically removed breast tumors, although only at low levels. We have measured the 1,25-(OH)2D3 receptor in breast tumors from 68 patients and have found it at similar frequency (75%) but at much higher concentrations (range, less than 1 to 30 fmol/mg protein). This receptor has the same characteristics as that measured in classic 1,25-(OH)2D3 target tissues and was distinguished by sucrose gradient centrifugation from plasma contaminants. Complete case histories and follow-up were available on 56 of these patients, and 1,25-(OH)2D3 receptor status (less than 8 or greater than or equal to 8 fmol/mg protein) was not related to the level of estrogen receptors, menopausal status, T-stage or histology of tumors, or presence of 99mTc phosphate hot spots on bone scans. The lack of relationship between the level of 1,25-(OH)2D3 receptors and other prognostic indicators suggests its potential as a new independent variable for assessing breast cancer patients. However, at this stage, 1,25-(OH)2D3 receptor status did not result in any significant difference in probability of survival or metastasis-free survival. Assessment of the importance of this variable for treatment or outcome must await an increased number of patients and a longer time since surgery.

Breast Neoplasms↗
PubMed1984

Specific uptake of 1,25-dihydroxycholecalciferol by human chronic myeloid leukemia cells.

We have examined mononuclear cell preparations from patients with chronic myeloid leukemia [CML] for binding of and response to 1,25-dihydroxycholecalciferol [1,25-(OH)2D3]. Whole cells specifically took up [3H]-1,25-(OH)2D3 with high affinity (Kd 3.6 X 10(-11) M) and low capacity. Subcellular fractionation of labeled cells showed that binding was restricted to cytosols and nuclei. Sucrose gradient centrifugation of cells preincubated with [3H]-1,25-(OH)2D3 revealed a single 3.6S peak which was totally displaced with 100-fold excess nonradioactive hormone. However, we were unable to demonstrate specific binding of 1,25-(OH)2D3 by postlabeling standard cytosol preparations. In addition, cytosols prepared from a mixture of CML cells and 1,25-(OH)2D3 receptor-positive T47D (human breast cancer) cells had less than 10% of the binding measured in T47D cytosol alone. However, the levels of binding in T47D cytosols were not reduced if the receptors were occupied with [3H]-1,25-(OH)2D3 prior to the addition of the CML cytosols. Thus, CML cells appear to contain both the receptor for 1,25-(OH)2D3 and an unknown substance which prevents its detection following the preparation of cytosol. Cells from patients with CML in the chronic phase specifically bound more 1,25-(OH)2D3 [18.0 +/- 3.2 (S.E.) fmol/10(7) cells] than did those in acute myeloid transformation [7.2 +/- 1.5] or than did cells from patients with acute myeloid leukemia [2.6 +/- 0.8]. Only cells from the first group of patients responded to the addition of 1,25-(OH)2D3 by differentiating along the monocyte-macrophage pathway. We conclude that the differentiation-induction effect of 1,25-(OH)2D3 is likely to depend on adequate levels of receptor and that intact cells rather than cytosol preparations should be studied before cells of a particular tissue are designated as receptor negative.

Calcitriol↗
PubMed1983

Growth inhibition of human breast cancer cells induced by calcitonin.

The human breast cancer cell line (T47D) has specific, high affinity calcitonin receptors and calcitonin-responsive adenylate cyclase. Human, salmon and [Asu1,7]eel calcitonin inhibited cell growth in a dose-related manner with almost equipotency. Analogues of human calcitonin demonstrated slight cell growth inhibition. We found extreme growth inhibition with daily treatment with dibutyryl cyclic AMP (10(-4) M). In contrast to calcitonin 1,25-(OH)2D3 had a biphasic effect on cell growth. Physiological doses (5 X 10(-10) M) of 1,25-(OH)2D3 stimulated growth of T47D, whereas treatment by supraphysiological amounts (2.5 X 10(-7) M) caused significant inhibition of growth. Calcitonin and 1,25-(OH)2D3 appeared to have additive effects.

Animals↗
PubMed1982

Central nervous system effect of calcitonin: stimulation of prolactin release in rats.

Effect of [Asu 1,7]eel calcitonin (CT) on prolactin (PRL) release was examined in male rats under urethane anesthesia. Intravenous injection of 4-20 micrograms [Asu1,7]eel CT did not modify plasma PRL levels. Injections of 0.5-2.5 micrograms [Asu1,7]eel CT into the lateral ventricle produce a significant and dose-related increase of plasma PRL within 10 min of injection. When intraventricularly injected in an equimolar dose (0.74 nmol/10 microliters), eel CT11-32, eel CT15-32, [Asu1,7]eel CT1-16 and [Asu1,7]eel CT1-9 showed 44.8, 25.7, 19.9 and 10.1% the potencies of [Asu1,7]eel CT, respectively, in stimulating activity of PRL release. The rise of plasma PRL after [Asu1,7]eel CT injection were significantly less or abolished not only in hypothalamic-lesioned rats but also in rats with complete deafferentation. Pretreatment with alpha-methyl-p-tyrosine (250 mg/kg, 12 h before) but not with p-chlorophenylalanine (300 mg/kg, 72 and 24 h before) resulted in a suppression of [Asu1,7]eel CT-induced PRL release. These results suggest the following: first, PRL release is stimulated by centrally injected [Asu1,7]eel CT, the action site of which may exist in the extrahypothalamic area; second, brain catecholamines may be involved in the mechanism of [Asu1,7]eel CT-evoked PRL release; third, the C-terminal portion of the peptide may play an important role in stimulating PRL release.

Animals↗
PubMed1982

Attenuation by hypocalcemia of pulsatile growth hormone secretion in conscious male rats.

The effect of hypocalcemia following parathyroidectomy (PTX) on growth hormone (GH) secretion was investigated in unrestrained, unanesthetized male rats bearing chronically implanted indwelling cannulae. During a 6-hour period, starting at about 10 a.m., control rats with a serum calcium (Ca) value of 8.11 +/- 0.38 mg/dl (mean +/- SEM) 2 weeks after sham-operation showed secretory bursts of GH similar to those observed in conscious intact rats. Under hypocalcemia of 4.88 +/- 0.32 mg/dl 2 weeks after PTX, GH secretory episodes were completely suppressed throughout the study. Plasma prolactin (PRL) levels were also decreased in PTX rats as compared with those of sham-operated rats. Daily food intake and body weight gain as well as serum T4 levels in PTX rats were not different from those of sham-operated and intact rats. Pituitary GH content of PTX rats was significantly lower than that of sham-operated and control rats. Pulsatile GH secretion was partially restored in PTX rats by raising serum Ca to 8.43 +/- 0.27 mg/dl through feeding with high Ca diet containing 7% Ca. Immediately after intravenous injection of antisomatostatin sheep serum, pulsatile GH surges recovered in PTX rats despite hypocalcemia of 4.48 +/- 0.74 mg/dl. The mean plasma 6-hour GH levels were significantly higher than those of normal sheep-serum-treated PTX rats (p less than 0.001). These findings suggest that the episodic release of GH is suppressed in hypocalcemic rats after PTX, at least partially via circulating endogenous somatostatin.

Animals↗
PubMed1982

Effect of vasoactive intestinal polypeptide on growth hormone secretion in perifused acromegalic pituitary adenoma tissues.

The effects of vasoactive intestinal polypeptide (VIP), dopamine, and somatostatin (SRIF) on GH secretion were examined in vitro in perifused pituitary adenoma tissues obtained at surgery from seven patients with acromegaly. The perifusion of VIP at 5 x 10(-8) M resulted in a significant increase in effluent GH levels in five of the seven adenomas. A dose-related GH response was observed from 5 x 10(-9) to 5 x 10(-7) M VIP in two adenomas examined. SRIF at 5 x 10(-8) to 10(-7) M suppressed not only baseline secretion of GH but also inhibited GH rises elicited by VIP in six of the seven adenomas. Dopamine at 5 x 10(-7) to 5 x 10(-6) M decreased the baseline secretion of GH in six of the seven adenomas. In four of the six adenomas responsive to dopamine, dopamine suppressed VIP-induced GH release when perifused simultaneously. In the remaining two dopamine-sensitive adenomas in which VIP alone failed to affect GH release, the inhibition by dopamine of GH release was blocked by VIP perifused concomitantly with dopamine. Synthetic TRH or theophylline perifused at the end of the experiment stimulated GH release in all of the adenomas, indicating the viability of tumor cells throughout the study. These results suggest that VIP stimulates GH release by its direct action on pituitary adenoma cells of acromegalic patients and that VIP, SRIF, and dopamine interact at the pituitary level in modulating GH secretion from these adenomas.

Acromegaly↗