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Biomedical subjects

K Asakawa

Publications and source records attributed to K Asakawa.

At least 37 records · Page 2Linked to original sources
PubMed1993

Responses of insulin-like growth factor binding protein-1 (IGFBP-1) and the IGFBP-3 complex to administration of insulin-like growth factor-I.

The importance of insulin-like growth factor binding proteins (IGFBPs) in modulating the bioactivity of administered IGFs is poorly understood. This study examines responses of IGFBP-1 and the IGFBP-3 complex to recombinant human IGF-I. Eight fasted subjects received a single dose of 0.1-0.125 mg/kg IGF-I sc. This caused a 10-fold rise in IGFBP-1 over 6 h, falling rapidly after food intake. Peak (6-h) IGFBP-1 values were highly correlated with peak post-prandial (8-h) glucose values (r = 0.941). IGFBP-3 showed little response, decreasing slightly over the 48-h period following IGF-I. Adaptive changes in IGFBPs were studied in fed adults injected daily for 7 days with IGF-I, 0.1 mg/kg sc. Following the first injection, IGFBP-1 had a markedly blunted response compared to that in fasted subjects. However, after the seventh IGF-I injection, a 3.5-fold greater IGFBP-1 response to the same IGF-I dose was seen. Concomitantly with the increased IGFBP-1 responsiveness, mean immunoreactive IGFBP-3 and acid-labile subunit levels decreased significantly (p < 0.005), whereas IGFBP-2 detected by immunoblotting increased. Thus IGF-I administration causes changes in IGFBPs which may be important in regulating IGF-I bioavailability.

Adult↗
PubMed1993

[A case report of BWG syndrome in an elderly patient performed with mitral valve replacement 11 years after single CABG].

A 46-year-old female who had undergone single CABG for BWG syndrome 11 years ago was referred to our hospital for paroxysmal atrial fibrillation. The roentgenogram showed slightly cardiomegaly and the enlargement of LA. Ischemic changes of ECG appeared at I, aVL, V5, V6, as inverted T wave, and low voltage R wave at V1-V4, but non Q wave. The thallium-201 emission computed tomogram at exercise revealed poor perfusion at apical region without redistribution pattern. Catheterization showed mitral regurgitation (grade III), big right coronary artery (RCA) arising from aorta, rich collateral to poor left coronary artery (LCA), and bypass graft was obstructed. The proximal end of LCA was closed, and didn't arise from both pulmonary artery and ascending aorta. In this cases, MVR only without re-CABG to LCA was selected and performed. Postoperative course was uneventful. The result of this case suggested that MVR was an effective surgical procedure for MR of BWG syndrome in the adult case and it was better to add CABG to LCA as much as possible if the ischemic region was large.

Coronary Artery Bypass↗
PubMed1993

[Late malfunction of the Björk-Shiley valve prosthesis due to Delrin disc defacement].

A 55-year-old woman eighteen years after mitral valvular replacement with Delrin disc Björk-Shiley valve prosthesis underwent a reoperation of prosthetic valve replacement for the prosthetic malfunction due to disc defacement. The patient suffered from faintness and vertigo at rest. An echocardiographic examination showed a moderate mitral insufficiency with a normal disc movement. Precise examination on the removed prosthesis revealed accelerated defacement of disc margin which made the ring-disc clearance up to 0.35 mm and strut-shaped groove formation on the inlet surface of the disc occluder. These findings suggested a pronouncedly earlier disc wear than predicted by Björk and co-workers. We concluded, therefore, that a patient undergone a valve replacement with Delrin disc Björk-Shiley valve should be examined periodically by echocardiography even though being without any symptoms.

Female↗
PubMed1993

[Scintigraphic comparison of graft patency between the left internal thoracic artery and saphenous vein graft after coronary bypass surgery].

Graft patency after coronary bypass surgery (CABG) was evaluated with stress 201-thallium scintigraphy (stress 201Tl) in 26 cases, including 13 cases using the left internal thoracic artery (LITA group) in situ and 13 cases with saphenous vein graft (SVG group). All of them had effort or unstable angina caused by LAD lesion without apparent infarction. Stress 201Tl using a symptom-limited, graded bicycle exercise test was performed before CABG and 1 month, 6 months to 1 year, 1 year to 1.5 years after surgery. Five tomographic images including the apical side of the area fed by the bypass anastomosed to LAD in short axial sections were picked out and piled up. Fan-shaped ROI was made on this area and % Tl uptake was calculated using the following formula. 201Tl counts in ROI--Background counts/Maximum counts--Background counts x 100 (%) The normal % Tl uptake calculated in the control group (n = 11) in this ROI was 68.2 +/- 4.8%. Preoperative % Tl uptake showed 49.3 +/- 0.2% in the LITA group and 54.3 +/- 13.2% in the SVG group. % Tl uptake of the SVG group 1 month after CABG was slightly higher than that of the LITA group, (62.0 +/- 7.0% vs. 56.3 +/- 7.6%). However 6 months to 1 year after, % Tl uptake of the LITA group increased to 60.8 +/- 6.4%, inspite of a tendency on the decrease of that in the SVG group, (59.0 +/- 8.5%), and further more, 1 year to 1.5 years after CABG, increased to 62.3 +/- 5.1% near the normal % Tl uptake of the control group and the SVG group decreased to 58.8 +/- 6.8%. This result suggested that arterial in situ bypass graft might have an auto-regulation and "growing property" corresponding to flow demand, and this helps the excellent long-term patency of arterial bypass grafts.

Adult↗
PubMed1992

Effects of insulin-like growth factor I or human growth hormone in fasted rats.

To study the effect of insulin-like growth factor I (IGF-I) treatment on growth and metabolism in fasted rats and compare it with the effect of human growth hormone (hGH), we infused 120 micrograms/ml IGF-I continuously or injected 200 micrograms hGH twice a day in fasted rats. After a 3 1/2-day administration of IGF-I in fasted rats, the body weights, kidney, spleen and adrenal gland weights were greater than those for untreated fasted rats (control). The body weights and the organ weights in hGH treated rats did not differ from those in control rats. Serum IGF-I levels in control, hGH treated and IGF-I treated rats were 64.0 +/- 6.1, 107.5 +/- 6.9 and 129.8 +/- 6.3 ng/ml, respectively, which were significantly different from each other. Blood urea nitrogen (BUN) levels were 13.9 +/- 1.1 ng/ml in IGF-I treated rats, which were significantly lower than those of control rats. Human GH treatment did not change BUN but affected nonesterified fatty acid (NEFA) and triglyceride. In IGF-I treated rats three-day urinary excretion of nitrogen and creatine were 163.5 +/- 14.6 mg and 9.53 +/- 1.53 mg, which were significantly less than those in control rats. These data indicate that IGF-I infusion inhibits body weight loss and catabolism in fasted rats and might be a useful therapy in catabolic conditions.

Adrenal Glands↗
PubMed1991

Single sc administration of insulin-like growth factor I (IGF-I) in normal men.

Total and free form of IGF-I in plasma increased in a dose dependent manner after sc IGF-I administration. Peak values of total IGF-I were obtained at 3-4 h after the administration, and then the values decreased gradually. However, peak values of free form of IGF-I were obtained at 2 h, and then rapidly decreased thereafter. The blood glucose, serum insulin and C-peptide levels decreased until 4 h after IGF-I administration in a dose dependent manner. Plasma IGF-II values significantly decreased at 4-12 h after IGF-I administration. Urinary urea nitrogen and sodium excretion decreased after IGF-I administration. Urinary GH excretion also decreased after 0.06 mg/kg IGF-I administration. These data demonstrate that IGF-I may play a role in glucose, protein and electrolyte metabolism, and plasma IGF-II levels and GH secretion might be regulated by IGF-I in man.

Adult↗
PubMed1991

Measurement of free form of insulin-like growth factor I in human plasma.

A method to measure free form of insulin-like growth factor I (IGF-I) in human plasma using octadecylsilyl silica (Sep-Pak C18) cartridge has been developed. IGF-I was adsorbed by Sep-Pak C18 cartridge and eluted with 75% ethanol--0.01 M HCl. Labeled and non-labeled IGF-I were recovered in yields 92.5 +/- 2.1% (Mean +/- SEM) and 94.4 +/- 6.3% after adsorption to and elution from the Sep-Pak, respectively. When EDTA plasma was applied to the Sep-Pak, less than 5% of total IGF-I was recovered in the eluate. However, when acid-ethanol extracted plasma was applied to the Sep-Pak, IGF-I was recovered in yields greater than 75% of total IGF-I. When the Sep-Pak eluate was gel filtered, 88.4 +/- 4.0% of immunoreactive IGF-I eluted in the same fraction as synthetic IGF-I did, but the fraction passed through the Sep-Pak was observed as a high molecular weight form (bound form) of IGF-I. These data indicate that this Sep-Pak method does not extract all of the IGF-I in plasma, but extracts mainly the free form IGF-I. Using this method, IGF-I values of free form (fIGF-I) in EDTA plasma were measured. The fIGF-I values in normal adults, patients with acromegaly, and patients with growth hormone (GH)-deficiency were 2.4 +/- 0.1, 13.8 +/- 1.6, and 1.1 +/- 0.1 ng/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1991

Repeated sc administration of recombinant human insulin-like growth factor I (IGF-I) to human subjects for 7 days.

Recombinant human insulin-like growth factor I (rhIGF-I) was administered subcutaneously to 6 normal subjects and 2 patients with GH deficiency at a dose of 0.1 mg/kg for 7 consecutive days after breakfast. In normal subjects, plasma IGF-I levels increased from 217 +/- 22 ng/ml (Mean +/- SEM) to maximal levels of 581 +/- 6 ng/ml 4 h after the first administration of IGF-I. The blood glucose levels were statistically depressed 4 h after injection at 69 +/- 2 mg/dl. Similar plasma IGF-I and blood glucose profiles were observed after the seventh administration of IGF-I. The free form of IGF-I in plasma was 2.3 +/- 0.3 ng/ml in normal subjects and increased to maximal levels of 43.5 +/- 5.1 ng/ml 2 h after the first IGF-I administration. A similar pattern for the free form of IGF-I was observed after the seventh administration; however, the values obtained at 0, 1 and 2 h were greater after the seventh administration. In patients with G-deficiency, the plasma IGF-I and blood glucose profiles were similar to those observed in normal subjects, although the total IGF-I levels were low in these patients at all sampling points during the study. Slight decreases in serum insulin, uric acid, and creatinine were observed after the seventh administration of IGF-I. There were no changes in the excretion of urea nitrogen, creatine, creatinine, sodium, potassium, chlorine, calcium or C-peptide in the urine during the 7 days of IGF-I administration.

Adult↗
PubMed1990

Effects of short-term growth hormone therapy in short children without growth hormone deficiency.

Evaluation of 24-hour endogenous growth hormone (GH) secretion was carried out in 62 children, aged 7-16 years, who did not have classic GH deficiency (GHD). The mean 24-hour GH concentration, determined at 20-minute intervals over 24 hours, was variable, ranging from 1.28 to 11.39 micrograms/l with a mean of 4.95 +/- 2.55 micrograms/l (+/- SD). There was a positive correlation between mean 24-hour GH concentration and plasma insulin-like growth factor I (IGF-I) values (r = 0.54; p less than 0.01). Recombinant human GH, 0.1 IU/kg/day was administered to 30 of the 62 children for 6 months followed by 6 months' observation without treatment. Thereafter, GH was administered at the same dose for a further 6 months to 16 children. The mean height velocities before, during, and after the first treatment period were 4.3 +/- 0.9, 7.3 +/- 1.9 and 4.9 +/- 2.0 cm/year (mean +/- SD), respectively. The height velocity during treatment was greater than pre- and post-treatment values (p less than 0.001). The height velocity increased again during the second treatment period to a mean of 8.5 +/- 2.0 cm/year (p less than 0.001). Nine other children were treated continuously in a similar manner for 1 year and their height velocity increased significantly from 4.1 +/- 1.4 to 6.0 +/- 1.9 cm/year (p less than 0.001). According to our criteria, 29 of the 39 children (74.4%) who were treated for 6-12 months showed a GH-dependent height increase during therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Effects of sc administration of recombinant human insulin-like growth factor I (IGF-I) on normal human subjects.

Recombinant human insulin-like growth factor I (IGF-I) was administered subcutaneously to each of 5 normal human subjects at doses of 0 mg/kg (control), 0.06 mg/kg, or 0.12 mg/kg successively at one week intervals. After 0.06 mg/kg or 0.12 mg/kg IGF-I injections, plasma IGF-I levels increased from 185 +/- 17 ng/ml (mean +/- SEM) to maximal levels of 396 +/- 21 ng/ml at 3 hours and from 169 +/- 14 ng/ml to 480 +/- 27 ng/ml at 4 hours, respectively. These two peak values were statistically different (p less than 0.05). After 0.06 mg/kg and 0.12 mg/kg IGF-I administration, blood glucose levels decreased from 85 +/- 2 mg/dl to minimal levels of 73 +/- 3 mg/dl at 3 hours and from 83 +/- 1 mg/dl to 50 +/- 4 mg/dl at 2 hours, respectively. These two minimal values were statistically different (p less than 0.001). Serum insulin and C-peptide levels were decreased in a dose dependent manner after IGF-I administration. There were no changes between blood urea nitrogen levels before and 4 hours after IGF-I administration. The urinary GH concentration decreased after 0.06 mg/kg IGF-I administration, but increased and maintained normal values after 0.12 mg/kg IGF-I administration.

Adult↗
PubMed1990

Radioimmunoassay for insulin-like growth factor II (IGF-II).

Insulin-like growth factor II (IGF-II) levels in human plasma were measured in physiological and pathological conditions by radioimmunoassay (RIA) with biosynthetic IGF-II. This RIA was specific for IGF-II and cross-reactivity with IGF-I was 1%. The sensitivity was 15 pg/tube with 50% displacement at 50 pg/tube. The intra- and inter-assay coefficients of variation for IGF-II were 6.3 and 9.3%, respectively. The plasma IGF-II levels in normal adults, patients with hypopituitarism and patients with active acromegaly were 589.6 +/- 15.8, 800.9 +/- 45.6 and 330.3 +/- 24.3 ng/ml, respectively. After human growth hormone (hGH) treatment in hypopituitarism, IGF-II slightly increased, but not significantly. After adenomectomy in patients with acromegaly, IGF-II significantly decreased. These data indicate that IGF-II concentrations in plasma were partially GH dependent. This GH dependency was less than that of IGF-I. IGF-II was low in patients with anorexia nervosa and with liver cirrhosis and high in patients with renal failure. In two cases with extrapancreatic tumor-associated hypoglycemia, plasma IGF-II was increased to 1123.8 and 843.5 ng/ml, and returned to normal after tumor resection. These data showed that IGF-II was partly dependent on GH and nutritional conditions and that IGF-II was the most likely cause of some cases of hypoglycemia with extrapancreatic tumor. This specific and sensitive RIA of IGF-II would be useful in evaluating its physiological and pathological role in plasma and tissue.

Acromegaly↗
PubMed1989

Growth hormone and insulin-like growth factor I stimulate Leydig cell steroidogenesis.

Leydig cells from 40 days old rats were incubated with or without human growth hormone (hGH) or insulin-like growth factor I (IGF-I) in the presence or absence of human chorionic gonadotropin (hCG), and testosterone and cyclic AMP (cAMP) levels in the medium were measured. Neither hGH nor IGF-I increased testosterone production in the absence of hCG in concentrations up to 1000 and 100 ng/ml, respectively. However, both peptides increased hCG-induced testosterone production in a dose-dependent manner. The maximal stimulatory concentrations of hGH and IGF-I were 100 and 50 ng/ml, respectively. Human GH did not further enhance the IGF-I-stimulated steroidogenesis. The hGH-augmented steroidogenesis was inhibited by anti-hGH IgG and anti-IGF-I IgG. hGH also enhanced hCG-stimulated cAMP production time dependently, suggesting that the stimulatory effect of hGH on steroidogenesis was due to an increased cAMP production. These data suggest that the effect of hGH might be mediated by locally produced IGF-I, which may act as a modulator on gonadal development in the presence of gonadotropin.

Animals↗
PubMed1989

Human growth hormone stimulates liver regeneration in rats.

To study the effect of human growth hormone (hGH) on liver regeneration in rats, 200 micrograms hGH was administered to partial hepatectomized rats twice a day for three days. The bw of hGH-treated rats was higher than that in untreated rats. After three day administration, the liver weight was 3.18 +/- 0.13 g, significant higher than that of untreated rats (2.68 +/- 0.17 g). Human GH also stimulated the mitosis in the liver. Serum insulin-like growth factor I (IGF-I) and albumin levels were significantly increased and urea nitrogen levels were significantly decreased in hGH-treated rats compared with those in untreated rats. When 120 micrograms/day IGF-I was continuously administered to partial hepatectomized rats for three days, the bw and the liver weight were not higher than those of controls. These data indicate that hGH directly stimulates liver regeneration and recover liver dysfunction in rats.

Animals↗
PubMed1989

Measurement of nocturnal urinary growth hormone values.

Nocturnal urinary growth hormone values were measured by a sensitive enzyme immunoassay in normal adults, patients with GH deficiency, patients with Turner's syndrome, normal but short children who had normal plasma GH responses to provocative tests, and patients with acromegaly. The mean nocturnal urinary GH values in patients with acromegaly were significantly greater than those in normal adults (1582.3 +/- 579.8 vs 53.5 +/- 8.6 pmol/mmol creatinine (+/- SEM); p less than 0.05). In the normal but short children and patients with Turner's syndrome, the mean nocturnal urinary GH values were 83.1 +/- 5.2 and 79.8 +/- 29.5 pmol/mmol creatinine, respectively. In patients with GH deficiency, the nocturnal urinary GH values were undetectable (less than 5.3 pmol/mmol creatinine) except in one patient where the value was 6.3 pmol/mmol creatinine. The nocturnal urinary GH values of the patients with GH deficiency were significantly lower than those of the other groups (p less than 0.05). In normal but short children, the nocturnal urinary GH values correlated significantly with mean plasma nocturnal GH concentrations (r = 0.76, p less than 0.001), and 24-hour urinary GH values (r = 0.84, p less than 0.001), respectively. In 4 patients with GH deficiency who had circulating anti-hGH antibody, the urinary GH values were also undetectable. These data indicate that nocturnal urinary GH value reflects endogenous GH secretion during collection time, and that measurement of the nocturnal urinary GH values is a useful method for screening of patients with GH deficiency and acromegaly.

Acromegaly↗
PubMed1988

Urinary growth hormone (GH) measurements are useful for evaluating endogenous GH secretion.

Daily (24-h) urinary GH excretion was measured using a highly sensitive sandwich enzyme immunoassay in 10 normal adults, 6 patients with hypopituitarism, 25 normal but short children who had normal plasma GH responses (peak plasma GH level, greater than 10 micrograms/L) to provocative tests, and 8 patients with acromegaly. The mean urinary GH values in the normal adults, patients with acromegaly, and patients with hypopituitarism were 13.8 +/- 4.0 (+/- SE) and 431.1 +/- 149.1 ng/g creatinine (Cr) (1.56 +/- 0.45 and 48.77 +/- 16.87 ng/mmol Cr) and undetectable, respectively; these mean values were significantly different from each other. In the normal but short children the urinary values ranged from undetectable to 55.8 ng/g Cr (6.31 ng/mmol Cr). All of the normal but short children and 4 patients with hypopituitarism participated in a 24-h endogenous GH secretion study. The urinary GH values correlated significantly with the mean 24-h plasma GH concentrations as an index of endogenous GH secretion (r = 0.81; P less than 0.001) and plasma somatomedin-C levels (r = 0.67; P less than 0.001), respectively. In 6 patients with acromegaly whose plasma GH levels were constant throughout a 4-h period, the urinary GH values also significantly correlated with the mean plasma GH levels (r = 0.95; P less than 0.01). These data indicate that urinary GH measurements reflect endogenous GH secretion and that measurement of urinary GH excretion is a useful, simple, and practical method for evaluating endogenous GH secretion.

Acromegaly↗
PubMed1988

Twenty-four hour plasma GH, FSH and LH profiles in patients with Turner's syndrome.

We studied the plasma GH profiles in 6 patients with Turner's syndrome and 6 normal girls of short stature by sampling every 20 min for 24 hours. We observed episodic secretion of GH in these subjects. The mean plasma 24 h GH level in patients with Turner's syndrome was 3.6 +/- 1.4 (SD) ng/ml which was significantly lower than that of normal short girls (7.1 +/- 2.2 ng/ml, p less than 0.01). The GH secretion during both nighttime and daytime was decreased in the patients with Turner's syndrome, however the number of pulses did not differ significantly. There were no correlations between the mean plasma 24 h GH level on one hand and peak GH level obtained after GH provocative test and plasma somatomedin C on the other. Plasma FSH and LH levels were also measured in 4 patients with Turner's syndrome. Both levels were elevated and there observed no clear pulsatile secretion of FSH, but, some pulsatile secretion of LH was observed in two patients. These data indicate that patients with Turner's syndrome have decreased endogenous GH secretion, even though they show normal GH responses to GH provocative tests.

Adolescent↗
PubMed1988

Treatment of acromegaly with long acting somatostatin analogue SMS 201-995.

Ten acromegalic patients were treated with the somatostatin analogue SMS 201-995 (SMS) for 3-38 weeks in various doses and by different administration routines (thrice daily or multiple sc injection). Plasma GH daily profiles, plasma IGF-I, urinary GH, serum TSH, IRI and fasting blood glucose (FBG) concentrations were measured before and during SMS treatment. Plasma GH rapidly decreased within one hour in all patients and was suppressed for at least 4 h after a 50 micrograms sc injection of SMS in 8 patients. Multiple injections of 300-600 micrograms/day SMS (25-50 micrograms X 12) suppressed GH throughout the day. Plasma IGF-I was completely normalized in 4 patients, and, in all but one of the others, decreased markedly. Urinary GH decreased within the first week of treatment in all patients and normalization was obtained in 3 patients. Shrinkage of the pituitary tumor, as determined by CT or MRI, was observed in 7 of 9 patients. Other clinical improvements, such as diminution or complete disappearance of swelling of soft tissues, excessive perspiration, and headache, were observed in 7 of 8 patients. Changes in serum TSH, IRI and FBG were seen in 3-4 patients, but without any apparent clinical problems. In conclusion, SMS is a useful clinical tool for treatment of acromegaly, and a multiple sc injection method seems to be preferable.

Acromegaly↗