The leucocyte migration inhibition test (LMT) using the agarose plate method introduced by Clausen is simple and highly reproducible.
Using thyroglobulin, mitochondria and thyroid microsomal fractions as antigens, LMT was performed on ten patients with insulin dependent diabetics, twenty patients with insulin independent diabetics, eleven patients with Graves' diseases, ten patients with chronic thyroiditis and ten healthy controls.
The migration index was expressed as a percentage of migration and calculated from the following formula.
Migration index (M I) =average areas of migration in test suspension/average areas of migration in control suspension×100
Using a thyroid microsomal fraction, the mean migration index for the insulin dependent diabetics (93.2±11.6) was significantly lower than in the normal subjects (104.3±10.9) (0.025<p<0.05).
Using thyroglobulin as an antigen for the insulin dependent diabetics and insulin independent diabetics, the mean migration indices (±SD) were 93.7±10.8 and 102.8±10.6 respectively.
The corresponding values for the control group were 100.6±7.3.
Using a mitochondria, MI values for insulin dependent and independent diabetics were 97.7±5.5 and 99.6±12.6 respectively, while MI value for the control group was 103.9±13.6.
The mean migration indices obtained with the mitochondria and thyroglobulin were not significantly depressed when the diabetic groups were compared with the normal subjects.

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The galactose tolerance tests were performed using the recently developed galactose-dehydrogenase technique in normal, hepatic and diabetic cases. The results obtained were compared with glucose tolerance tests, and in particular the changes of carbohydrate metabolites were investigated.
In all cases, no significant changes of plasma IRI during galactose loading tests were found with both oral and intravenous administration. Furthermore, a correlation between ΔIRI and Δgalactose was not statistically recognized.
The correlation between ΔIRI and Δglucose was significant in normal subjects in oral glucose tolerance tests, but not significant in galactose tolerance tests. However, no correlation was observed in the groups of diseases in both oral glucose and galactose tolerance tests.
In the relationship between ΔIRI and ΔNEFA, slightly positive correlation was found in normal subjects during oral glucose loading, whereas a tendency of negative correlation was found in them during oral galactose loading. This tendency was particularly remarkable in patients with liver diseases whose blood galactose levels were retarded.
The decrease in blood NEFA levels during oral galactose loading were compared with the glucose tolerance tests. The decrease of NEFA following oral galactose loading reached a maximum level after 1 hour. On the other hand, the decrease following glucose loading was still maintained after 2 hours, and was more remarkably compared to galactose loading. It was thought that the initial decrease in blood NEFA levels between 30 and 60 minutes after loading was induced by the direct action of galactose or glucose, and the continuous decrease up to 2 hours after glucose loading was caused by insulin release.

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It is well-known that thyroidal ¹³¹I-uptake is not suppressed by the T₃-suppression test in Graves' disease. However, it has not been elucidated whether serum TSH is suppressed or not. As the basal level of TSH in Graves' disease is generally very low, a comparision of TSH levels before and after the T₃-suppression test is difficult. An investigation was made of changes in serum T₃, T₄, TSH before and after the T₃-suppression test in patients treated for Graves' disease (Group I.....non suppressed patients whose TSH decreased after the suppression test, Group II.....suppressed patients, Group III.....non suppressed patients in whom a TSH decrease after the suppression test was not confirmed). After daily administration of 75γ of T₃ for 8 days, serum TSH was significantly reduced from 16.5±2.7μU/ml (mean±SE) to 0.6±0.3/μU/ml in Group I, whereas thyroidal ¹³¹I-uptake was not suppressed (26.4±3.7% before; 26.6±3.4% after). Immediately after the suppression test serum T₄ did not show a significant decrease in non-suppressed patients (Group I, III), but in suppressed patients (Group II) serum T₄ was significantly reduced from 8.6±0.3μg/dl to 6.7±0.5μg/dl.
The conclusions were as follows :
1. The non-suppressibility of ¹³¹I-uptake may be due to thyroidal autonomy or the existence of thyroid stimulators other than TSH.
2. In general, during recovery from Graves' disease the secretion of pituitary TSH occurs earlier than the suppression of the thyroidal gland.
3. It is suggested, that to evaluate the T₃ suppression test, reduction of serum T₄ is a more useful indicator than changes in 24-hr thyroidal ¹³¹I-uptake.

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There have been many reports, using pancreatic specific glucagon-antibody “K30”. Since some clearly stated that after pancreatectomy, plasma pancreatic glucagon levels increased, it has become a major problem whether, in the normal state, the gastrointestinal glucagon which react the pancreatic specific glucagon antibody is determined, or whether there is any physiological activity of the extrapancreatic glucagon on the blood sugar metabolism.
The present study was designed to detect any increase in the gastrointestinal glucagon which react the pancreatic specific glucagon antibody in the normal state, and also to examine the function of the extrapancreatic glucagon on the blood sugar metabolism.
Twenty healthy dogs, weighing from 10 to 12kg, were used. These dogs were operated on under Ketalar anesthesia. After insertion of polyethlene catheters into the femoral and axillar veins, tracheal catheters were intubated. Under additional Ravonal anesthesia, gastroenterectomy of these dogs was performed, resecting from the end of the esophagus to the end of the ampulla of the rectum with a midline abdominal incision. The pancreases of all the dogs were preserved almost intact. The bleeding volumes and packed cell volumes (PCV) were measured during this operation at ten minute intervals. At the end of this operation, which took one hour and a half, PCV decreased from 43% to 32% in each dog. The five control dogs were exsanguinated at 32% of PCV for one and a half hours and only laparotomy was performed as a sham-operation under Ketalar anesthesia.
1) Immediately after surgery, Arginine was administered at the rate of 130mg/kg/min for 15 minutes to the five gastroenterectomized dogs and to the five dogs who had under-gone the Sham operation. Plasma glucagon immunoreactivity (GI) (measured using pancreatic specific glucagon-antibody “K30” (Unger, Texas)) rose from a mean baseline value of 115 ± 9pg/ml up to a mean peak value of 200 ± 9pg/ml at 10 minutes in the gastroenterectomized dogs, and also, in the control dogs, GI rose from a mean baseline value of 158 ± 16 pg/ml to a mean peak value of 300 ±25pg/ml at 15 minutes. Total GLI (measured using non-specific glucagon-antibody “K4023” (Novo, Denmark)) increased from a mean baseline value of 130 ±14pg/ml to a mean peak value of 220 ±18pg/ml at 15 minutes in the gastroenterectomized. dogs, and also, in the control dogs, total GLI increased from a mean baseline value of 330 ±13pg/ml to a mean peak value of 705 ±62pg/ml at 10 minutes. IRI (measured by the two-antibody method) rose from a mean baseline value of 13 ±2μU/ml to a mean peak value of 46 ±812U/ml at 15 minutes in the gastroenterectomized dogs, and also, in the control dogs, IRI rose from a mean baseline value of 16 ±4/.2U/ml to a mean peak value of 32 ±3μU/ml. Blood sugar levels (BS) (measured by the glucose oxidase method) decreased from 152±2mg/dl to a mean trough value of 127 ±4mg/dl at 15 minutes in the gastroenterectomized dogs, but showed little change in the control dogs.
2) At 2 hours after surgery, Arginine was administered at the same rate and the same volume as that at just after surgery to the five gastroenterectomized dogs and the five control dogs. There was no remarkable difference between the responses of GI, total GLI, IRI and BS to that at 2 hours after surgery and those responses at just after surgery.
GI responses in arginine experiments showed significantly lower values at any point in the gastroenterectomized dogs than those in the control dogs (with the Student's t-test P<0.05). There was no significant difference between the response of GI and that of total GLI in the arginine experiments in the gastroenterectomized dogs at any point. Also IRI response showed no significant difference between the gastroenterectomized dogs and the control dogs.

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To determine the central neuronal mekchanisms essentially involved in the regulation of ovulatory LH release in cycling female rats, and to confirm the role of ovarian steroid feedback on the central regulatory mechanisms, the following experiments were carried out. A) The effects of electrical stimulation of the preoptic area (MPO) upon unit firing in the periventricular arcuate uncleus (ARC) were investigated in Wister female rats throughout the 4-day estrous cycle. Unit activity was recorded using a stereo-taxic oriented tungsten microelectrode under light urethane anesthesia. Repetitive stimulation of monophasic square waves varying only in current intensity was used. The following results were obtained. (a) An increase in activity of all ARC neurones recorded was induced by MPO stimulation on each day of the estrous cycle. (b) The minimum current (threshold) effective in increasing activity in the ARC neurones varied throughout the estrous cycle; the lowest threshold was observed in the proestrus and the highest on the first day of diestrus. Moreover, thereshold current of MPO stimulation required to increase ARC activity was found to be 'elevated after long-term ovariectomy and markedly lowered to the level of proestrus by estrogen treatment, but less affected by progesterone. (c) The spontaneous activity of the MPO and ARC neurones were increased at proestrus in cycling rats and after estrogen injection in spayed rats.
B) To clarify the conflicting data in the literature on which a dual regulatory mechanism for gonadotrophine release has been proposed, the ovulatory responses to electrochemical stimulation (ECS) of the medical septal-preoptic complex were compared in pentobarbital blocked normal proestrus and neonatally androgenized female rats. Increasing the stimulus strength enhanced the induction of ovulation in normal but not in androgenized rats. However, the ovaries in androgenized rats are relatively insensitive to LH, while pituitary responsiveness to LRH is identical. Therefore, the response to ECS was further evaluated in terms of plasma LH concentration. Radioimmunoassayable plasma LH was significantly elevated 30 min after ECS. Peak LH levels occured 90 min after ECS and were returning toward basseline after 120 min. There was no difference in mean plasma LH values in normal and androgenized rats at any time in each stimulus strength. Stimulation of the diagonal band of Broca, antero-medial septum as well as MPO equally elicited similar LH responses in both animals.
C) Changes of plasma LH were investigated in ovariectomized rats to study the effects of electrolytic lesions of medial or lateral septum by platinum electrode or preoptichypothalamic deafferentation (supracommissural roof cut) upon plasma LH rise after ovari-ectomy, on decrease of LH secretion after a single injection of 20 jig estradiol benzoate (EB) in long-term spayed rats, and on LH release induced by a second injection of EB or 5 mg progesterone given 72 hours after the first EB injection. Septal interruptions did not alter the time sequence and the level of plasma LH rise after ovariectomy, LH decrease created by the first injection of EB and LH release inducted by progesterone in the after-noon of the injection. However, LH release in the afternoon of the day after the second injection of EB was remarkably reduced in rats with supracommissural roof cut in which all the transseptal fiber connections were completely transected. This reduction of LH release was not observed in the cases where in postcommissural component of stria terminalis was left untransected or even partially so. In the rats with either medial or lateral septal lesions, estrogen-induced LH release appeared to differ from intact spayed rats in timing and quantity of peak LH secretion on each afternoon of the second EB injection.

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