巻号一覧
前身誌
54 巻, 2 号
選択された号の論文の8件中1～8を表示しています
- |<
- <
- 1
- >
- >|
-
第I報 : Dexamethasoneのエステル型による抗エンドトキシン効果の相異今井 孝祐, 桜谷 憲彦1978 年 54 巻 2 号 p. 87-92
発行日: 1978/02/20
公開日: 2012/09/24
ジャーナル フリーThere have been controversial discussions as to the effectiveness of glucocorticoid treatment for various shock states, although more than a decade has passed since pharmacological doses of glucocorticoid was begun to be used for the treatment of various shock states. We have tried to investigate the anti-shock mechanism of glucocorticoids, and firstly we compared the anti-endotoxic potency of dexamethasone based on different ester types in mice.
Dexamethasone disodium phosphate (MD-P) and dexamethasone sodium sulfate (DM-S) were compared. Each steroid was diluted to 0.2 mg/ml with saline calculated as dexamethasone and administered intraperitoneally to mice. After intervals of 0, 1, 2, 3, 6, 12 and 24 hours, 0.5 mg of endotoxin (E-coli; 0127-B8, Difco, USA) was injected intraperitoneally, and the survival rates were calculated 72 hours later.
In the control group the survival rate was 20.4%. In the group administered DM-P, the survival rates were 65.0% initially, 57.1% after 1 hour, 45.7% after 2 hours, 25.0% after 3 hours, 25.0% after 6 hours, 15.0% after 12 hours and 16.6% after 24 hours. On the other hand, in the group administered DM-S the survival rates were 25.0%, 4.7%, 0%, 3.7%, 15.0%, 15.0% and 16.0% respectively. The groups pre-treated with DM-P at intervals of 0, 1 and 2 hours and pre-treated with DM-S at interval of 2 hours, exhibited a statistically significant difference in survival rates.
We speculate that these differences in anti-endotoxic potency are due to its rate and speed on the liberation of free steroids from their ester types in blood. This means that glucocorticoid will manifest its anti-endotoxic potency depending on its concentration of free form in blood.抄録全体を表示PDF形式でダウンロード (565K) -
井坂 勝利1978 年 54 巻 2 号 p. 93-106
発行日: 1978/02/20
公開日: 2012/09/24
ジャーナル フリーThe aspects of the secretion of the anterior pituitary hormones were studied using male rats with electrolytic lesions of the bilateral ventromedial hypothalamic area (HTL) in various experimental conditions.
The results obtained were as follows :
1. There was no significant difference in base-line level and in response of plasma growth hormone (GH) to the intravenous administration of prostaglandin E2 between the HTL and control groups, although plasma GH response to the intravenous administration of pentobarbital (PB) was significantly decreased in HTL rats. The decrease in GH secretion was observed even in the early stage after HTL. These results suggested that the impaired GH response to PB in HTL rats was induced by HTL itself rather than obesity due to HTL.
2. There was no significant difference in base-line level and in response of plasma prolactin (PRL) to the intravenous administration of sulpiride between the two groups at 1 week after the operation. Plasma PRL response to the intravenous administration of sulpiride in HTL rats at 10 weeks after the operation was significantly decreased, but showed a normal response after the consecutive loads of sulpiride given subcutaneously for 6 days. On the other hand, plasma PRL response to the intravenous administration of chlorpromazine in HTL rats was significantly decreased both at 1 and at 10 weeks after the operation. These results suggested that the decreased PRL response in HTL rats might have resulted from the reduced secretion of the PRL releasing factor, although the possibility of the increased secretion of the PRL-inhibiting factor cannot be excluded.
3. The plasma base-line level of luteinizing hormone (LH) was significantly decreased, but there was no change in the plasma follicle-stimulating hormone (FSH) level in HTL rats. There was no significant difference in plasma LH and FSH responses to the intravenous administration of LH-RH between the two groups. There was no significant change in plasma LH response to the subcutaneous administration of clomiphene in low and high doses for 5 days in HTL rats, but plasma FSH response was increased in both groups to the same degree. These results suggested that the LH-RH secretion was impaired in HTL rats and that the control mechanism of the secretion of LH and FSH by clomiphene might be different.
4. The plasma base-line level of thyrotropin (TSH) and plasma TSH response to methyl-mercapto-imidazole given subcutaneously for 5 days or to TRH given intravenously was decreased in HTL rats, although not significantly.
5. The Plasma base-line level of corticosterone showed no significant difference between the two groups.
These results indicate that the plasma base-line levels and/or pituitary reserves of anterior pituitary hormones are significantly decreased or tend to be reduced in HTL rats. The impaired secretion of these hormones, particularly of GH, probably contributes to the development of hypothalamic obesity.抄録全体を表示PDF形式でダウンロード (1218K) -
小川 さつき, 福地 総逸, 三浦 正1978 年 54 巻 2 号 p. 107-116
発行日: 1978/02/20
公開日: 2012/09/24
ジャーナル フリーA simple radioimmunoassay was applied to the measurement of oxytocin in human plasma.
Ten mg of synthetic oxytocin and 10 mg of porcine gamma globulin were dissolved in 4 ml of distilled water, and then added 150 mg of carbodiimide, after adjusted pH to 6-7. The solution was incubated 25°C for 4 hours and dialyzed overnight at 4°C against distilled water. An antibody to oxytocin was produced by intramuscular administration of the conjugate of oxytocin and globulin, emulsified with an equal volume of Freund's complete adjuvant, to rabbits at 2 weeks intervals. Oxytocin was radioiodinated by chloramine-T method, and then purified by gel filtration using Sephadex G-25. Plasma oxytocin was adsorbed by Florisil and extracted with acetone containing 1% acetic acid. Radioimmunoassay of oxytocin was performed by adding 0.1 ml of 125I-oxytocin and 0.1 ml of antisera to plasma extracts diluted with 0.05 M phosphate buffer containing 0.1% lysozyme (pH 7.4). After incubation at 4°C for 72 hours, antibody-bound antigen was separated using dextran-coated charcoal.
A high specificity of immunoassay was demonstrated by the fact that large excess of angiotensin I and II, and ACTH did not displace labelled oxytocin from the antibody. Lysine-8-vasopressin and arginine-8-vasopressin showed very little cross-reaction in the assay, possessing only 0.002% of the immunological potency of oxytocin. The specific activity of 125 I-oxytocin was 166 μCi/μg. Adsorption and extraction capacities of Florisil were 96.6±2.1% and 85.7±2.5%, respectively. Intra-and inter-assay variability were 7.2±4.9% and 4.3±2.2%, respectively. The sensitivity of the assay was below 1pg/tube.
Normal levels of plasma oxytocin were 0-2.2 pg/ml (n=13) in males and 0-10.4 pg/ml (n=10) in females. Plasma oxytocin levels in the 39th and 40th weeks of pregnancy were 27.9±4.14 pg/ml (n=4) and 29.8±17.1 pg/ml (n=13), respectively. The levels in creased to 33.1±12.1 pg/ml (n=7) and 37.1±17.5 pg/ml (n=7) in the first and third stages of labor, and decreased to 13.6±5.25 pg/ml (n=6) on the 2nd to 8th day after labor.
The radioimmunoassay for oxytocin in plasma is considered to be sufficiently applicable for clinical use.抄録全体を表示PDF形式でダウンロード (759K) -
国分 知子, 久富 優子, 大内 力男, 森 弘, 神戸川 明, 古屋 清英, 田 根培, 吉田 孝雄, 高木 繁夫1978 年 54 巻 2 号 p. 117-130
発行日: 1978/02/20
公開日: 2012/09/24
ジャーナル フリーIt is well-known that dehydroepiandrosterone (DHEA) and its sulfate (DHEA-S) are the major C 19 -secretory products of the human adrenal cortex. The measurement of these steroids in plasma may serve as a possibly superior index in assessing biologic function of adrenal.
However one of the disadvantages of competitive protein binding assays and radioimmunoassays (RIA), which have usually been used, exists in the need for preliminary extraction or troublesome purification of steroids. Now, RIA method which do not require any extraction or chromatographic purification have been developed. Antiserum I and II were derived from rabbits immunized by 11α-succinoyloxy-DHEA-BSA and DHEA 3-succinate-BSA, respectively. Antiserum I was highly specific to DHEA and was used for determination of DHEA, and its reactivity titer was 1 : 2,000. Antiserum II was used for DHEA-S assay at dilution of 1 : 60,000.
Comparison experiment on plasma samples were carried out as follows.
1) DHEA in plasma was determined by RIA using antiserum I for samples obtained by the method A and B.
A : DHEA was extracted from plasma with ether and purified by chromatography (Sephadex LH-20).
B : The sample was obtained by extraction as a similar described above (without chromatography). 2) DHEA-S in plasma was determined using antiserum I (C) and antiserum II (D and E) for samples obtained by the method C, D and E.
C) DHEA-S was hydrolyzed by acid and DHEA thus obtained was purified by the method A.
D) A saturated ammonium sulfate was added to plasma and DHEA-S was extracted with ethyl acetate.
E) Plasma was directly used for RIA.
All results were found to be fully reliable. Coefficient of correlation in A-B, C-D and C-E were 0.965, 0.858 and 0.880, respectively.
It was found that RIA methods for obtained by method B and E are very useful for clinical application.抄録全体を表示PDF形式でダウンロード (1154K) -
田中 敏章, 諏訪 城三, 高橋 剛, 寺島 和光1978 年 54 巻 2 号 p. 131-142
発行日: 1978/02/20
公開日: 2012/09/24
ジャーナル フリーThe response of serum testosterone to human chorionic gonadotropin (HCG) was investigated in male children with normal endocrine function (control subjects) and those with hypothalamo-pituitary dysfunctions and gonadal disorders. Serum testosterone concentrations were determined by radioimmunoassay. HCG (3,000 units/m2 of body surface) was injected once a day for three days, and blood samples for testosterone assay were drawn before the first injection (basal testosterone level) and at 24 hours after the last injection (post-HCG testosterone level). The mean basal and post-HCG testosterone levels in 7 control
The mean basal and post-HCG testosterone levels in 7 control boys, aged from 7 months to 9-10/12 years, were 18.1±8.8 ng/dl and 240.0±28.9 ng/dl respectively. Serum testosterone rose from a mean basal level of 14.0±5.7 ng/dl to a mean post-HCG level of 117.8±50.4 ng/dl in 30 patients with cryptorchidism (aged from 1-4/12 yr. to 12-11/12 yr.), from 12 ng/dl to 34 ng/dl in a patient with XO/XY male (1-2/12 yr.), from 31.4±29.6 ng/dl to 200.7±127.7 ng/dl in 7 patients with pituitary dwarfism (aged from 3-9/12 yr. to 15-9/12 yr.), from 12.5±9.2 ng/dl to 30.5±26.2 ng/dl in two patients with Prader-Willi syndrome (aged 3-2/12 yr. and 5-1/12 yr.), and from 11.4±5.0 ng/dl to 33.4±16.8 ng/dl in 5 patients with small penis with small cryptoid tests (aged from 2-2/12 yr. to 15-9/12 yr.).
Mean basal testosterone levels were not significantly different in these various groups. Response of testosterone to HCG was significantly lower (p<0.005) in patients with cryptorchidism, XO/XY male, Prader-Willi syndrome, and small penis with small cryptoid testes than that in the control pre-pubertal boys. Although the mean post-HCG testosterone level in patients with pituitary dwarfism did not differ from that in the control boys, each case showed variable response. Three out of 7 patients with pituitary dwarfism showed lower responses, and one patient with secondary sexual development showed a significantly higher response than did the control pre-pubertal boys. Two patients with Prader-Willi syndrome, whose testosterone responses to HCG were minimal, exhibited normal responses of serum LH and FSH to LH-RH. This fact suggests that the genesis of hypogonadism in Prader-Willi syndrome was not only hypothalamic dysfunction but also primary dysgenetic testicular function. Serum gonadotropin response to LH-RH was low in two out of 5 patients with small penis with small cryptoid testes, and basal FSH level was significantly high in the other three. These findings in these patients suggest that secondary hypogonadism and primary hypogonadism were included in this symptomen complex.
It is concluded that a HCG test is a useful tool for the examination of testicular function and for the differential diagnosis of hypogonadism in childhood as well as a LH-RH test.抄録全体を表示PDF形式でダウンロード (1026K) -
小林 正巳, 下田 新一, 笠井 貴久男1978 年 54 巻 2 号 p. 143-157
発行日: 1978/02/20
公開日: 2012/09/24
ジャーナル フリーThe basal values and changes of gastrin in serum produced by tolbutamide (Tol.) induced hypoglycemia were studied in the present experiment where 30 normal controls, 23 patients with hyperthyroidism, 9 patients with primary hypothyroidism and 7 diabetics were employed. After overnight fasting, 1.0 or 0.5 g of Tol was administered iv to each subject immediately after the basal blood sample was taken. Venous blood samples were again withdrawn at 5, 15, 30, 45, 60, 90,120,150 and 180 min after the start of the injections. An acute and marked increase of immunoreactive insulin within 15 min was followed by a clear decrease of blood sugar (BS), the so-called Tol-induced hypoglycemia, after the Tol injection. In the normal control, the Tol injection resulted in hypoglycemia, (46.0±2.0 mg/100 ml) at 30 min. The mean basal gastrin level was 61±3 pg/ml. The gastrin level in serum began to increase at 30 min and reached a maximum (95±10 pg/ml) at 45 min after the treatment. This peak value of gastrin was significantly higher (P<0.001) than the basal one. The basal value of gastrin in all of the hyperthyroid patients was 90±6 pg/ml, and this value was significantly higher (P<0.05) than in the normal controls. In these subjects, 0.5 g of Tol was administered to obtain almost the same hypoglycemic effect as that in controls injected with 1.0 g of the agent. In 7 out of 23 patients, marked basal hypergastrinemia (140±10 pg/ml) was found. These patients didn't show the consistent response of serum gastrin to Tol injection despite the adequately induced hypoglycemia (47.1±6.4 mg/100 ml). In the other 16 patients, the initial values of serum gastrin were less than 100 pg/ml, and in 11 out of these subjects, Tol stimulated clearly to increase the gastrin level in serum at 60 min up to approximately twice as much as the basal one (from 73±5 to 145 ± 17 pg/ml). In contrast, no response of serum gastrin to Tol was observed in the rest of the 16 patients who showed relatively milder hypoglycemia (nadir of BS 56.0±4.6 mg/100 ml) than the former group (47.5± 4.6 mg/100 ml). In primary hypothyroidism, they had relatively low initial levels of serum gastrin (49±11 pg/ml). This value was not significant compared with normal controls, but significantly (P<0.02) lower than that of hyperthyroidism. Moreover, no response of serum gastrin to 1 g Tol injection was observed, although the induced hypoglycemia ensued adequately (43.0±2.6 mg/100 ml). This hyporesponsiveness of serum gastrin in hypothyroidism was significantly lower compared with normal controls and hyperthyroidism (P<0.05 and P<0.05, respectively). Also in the diabetics who had normal gastrin levels in basal state (59±7 pg/ml), no response of serum gastrin to Tol (1.0 g) was noticed. This would be due to slow decrease of BS.
From these results, we confirmed that the Tol-induced hypoglycemia clearly stimulates an increase in serum gastrin levels and that in response to Tol serum thyroid hormone promotes basal gastrin release.抄録全体を表示PDF形式でダウンロード (1354K) -
二岡 清昇1978 年 54 巻 2 号 p. 158-173
発行日: 1978/02/20
公開日: 2012/09/24
ジャーナル フリーThe estrogen receptor (ER) and progesterone receptor (PR) were investigated in normal uterine endometrium and uterine adenocarcinoma of human subjects. In the normal endometrial cytosols, either estradiol-17β (E2) or progesterone (P) bound to 8S proteins and the kinetic analysis by charcoal adsorption showed Kd (E2) = 2.5×10-9M and Kd (P) = 2.0×10-9M.
In the cytosols of adenocarcinomas, Kd (E2) values were ranged from 2.5-0.6×10-9M in the presence of E2-8S protein binding, Kd (P) value in the presence of P-8S protein binding was the same as that in the normal endometrial cytosol, but Kd (P) value was 1.3×10-8M in the absence of P-8S protein. Even when E2-8S existed, P-8S was not always detected, but whenever P-8S existed, E2-8S was detected. These results indicate that the ER of the adenocarcinoma is altered in quality, resulting in no synthesis of PR in some cases.
Steroid specificity of PR in the estrogen-primed endometrial cytosol was studied by kinetics. All steroids demonstrated competitive inhibition for PR binding. Especially did studies of the steroids related to progesterone demonstrate that the plane of ring A/B, _??_4 double bond and C-3, 20 ketones were important for PR binding. The binding of PR was tolerated when the side chain of the acetyl group was replaced by the 17α-ethynyl-17β-hydroxy group. And the binding affinities of most steroids were related to their biological activities.
In the menstrual cycle, the maximum binding site (Bm) of the steroid receptor was investigated by kinetics. The results were as follows; in the proliferative phase, Bm (E2) in creased from the early to the middle, and decreased in the late. Bm (E2) increased again in the ovulatory period, and in the secretory phase, Bm (E2) increased slightly in the middle and decreased in the late. Bm (P) also demonstrated almost the same alteration of Bm (E2).
The nuclear binding quantities of steroids were measured by exchange assay. Nuclear E2 bindings were at almost the same level in proliferative and secretory phases of the menstrual cycle, but nuclear P binding was detected slightly in the secretory phase and much less than nuclear E2 bindings. These results suggested that the nuclear P-receptor may be metabolized rapidly in vivo and the nuclear E2-receptor may stay longer.抄録全体を表示PDF形式でダウンロード (1424K) -
佐藤 勝男1978 年 54 巻 2 号 p. 174-186
発行日: 1978/02/20
公開日: 2012/09/24
ジャーナル フリーIt is known that the changes of the kidney and the eye-ground in workers exposed to carbon disulphide (CS2) are very similar to diabetic microangiopathy, however, the influences of CS2 exposure on glucose tolerance and pancreatic α, β cell function are still obscure.
In order to throw some light on this problem in this paper, the responses of blood glucose, serum insulin (IRI), serum C-peptide (CPR), plasma pancreatic glucagon (IRG), and serum growth hormone (HGH) to oral glucose loading (100gm.) and retinal changes were studied in workers exposed to CS2 (CS2 group).
The CS2 group averaged 45 years of age and had been exposed to CS2 for an average of 13 years. Age and body index of healthy control subjects (control group) were matched with these of the CS2 group. Both groups had not a hereditary predisposition to diabetes, The results were as follows :
a) Neither proteinuria nor glycosuria was found after fasting in the case of the CS2 group.
b) The types of glucose tolerance in the CS2 group were normoglycemic and borderline-hyperglycemic, and there were no significant differences between the CS2 group and the control group in the response of blood glucose.
c) In comparison with the control group, the responses of IRI and CPR were significantly lower, and the response of HGH had a tendency to be lower in the CS2 group. The response of IRG in the CS2 group was identical to the one in the control group.
d) The changes of the eye-ground in the CS2 group were very similar to these of diabetics, corresponding to AIAIII of Shikano's classification.
e) In comparison with the group exposed to CS2 for less than 10 years, the incidence of AI-AIII was higher, and the response of IRI was lower in the group exposed to CS2 for more than 10 years.
f) In the cases with AI-AIII of the CS2 group, the response of IRI had a tendency to be lower in comparison with the one without these changes (AI-AIII). No differences were found in the incidence of AI-AIII between normoglycemic and borderline-hyperglycemic types of the CS2 group.
The results suggest that CS2 exposure causes the hypofunction of the pancreatic β cell, despite glucose intolerance, and has an influence on the hyposecretion of HGH. And a correlation is thought to exist between the low response of IRI and the pathogenesis of diabetic-like retinopathy in workers exposed to CS2.抄録全体を表示PDF形式でダウンロード (1226K)
- |<
- <
- 1
- >
- >|