Little information is available regarding the mode of neuroendocrine control of pituitary tropic hormone secretion in low environmental temperature or hypoxic condition. To assess the control of pituitary TSH secretion in cold and hypoxic environment, the changes of rat plasma TSH were determined by means McKenzies direct measurement with a slight modification. In some experiments changes of plasma 11-hydroxycortico-steroid (11-OHCS) were also estimated using fluorophotometric method following DeMoor's method.
Male rats (weighing 190-220g, Swiss-Webster strain) fed on a low iodine diet were used as experimental animals. The rats were divided into two groups : one group was kept at the room temperature of 29±1°C at least for 14 days before experiment, the other was kept at diurnal fluctuating temperature of 27°C to 23°C for 10 days. These two groups were exposed to cold at 0-1°C for 60 minutes. The hypoxic condition was set at 10% and 5% O₂ in N₂, and the animals were exposed to the continuous low oxygen gas flow for 60 minutes. Blood samples were obtained with heparinized syringes at the end of exposure by puncture of jugular vein under Pentobarbital anesthesia, and immediately centrifuged.
To determine the arterial blood p02, pCO2, pH and buffer excess, arterial blood samples were obtained anaerobically from the carotid artery 15 minutes after hypoxic exposure. Rectal temperature was measured using electropotentiometer after cold exposure to 0°C for 60 minutes. Administration of Dexamethasone (Dexa.) in 3 doses (50,100 & 200μg in 0.25 ml saline per 100g B.W.) was given at 9 : 00 A.M. subcutaneously, 4 hours prior to experiment. Synthetic Thyrotropin-Releasing Hormone (syn TRH : synthesized after Gillessen's method) was administered into jugular vein, and blood sample was taken 8 minutes after injection.
Results obtained are summarised as follows :
When the rats acclimated to 29°C were exposed to cold 0°C for 60 minutes, mean rectal temperature fell from 36.11 : ±0.10°C to 34.85±0.41°C. Under this condition of acute cold exposure, both plasma TSH and 11-0HCS levels were increased significantly. The influence of hypoxic exposure to rats' arterial blood pO₂ was observed. The rats exposed to room air, 10% and 5% O₂ showed 112.8±5.54, 70.8±1.65 and 40.5±2.49 mmHg in pO₂, respectively. When the animals were exposed to acute cold (0°C for 60 min.) under hypoxic condition of 10% O₂no increase of plasma TSH was observed, while plasma 11-0HCS increased significantly. The rats exposed to cold under hypoxic condition of 5% O₂ also showed the inhibition of plasma TSH increase. The effect of Dexamethasone pretreatment on rat plasma TSH was studied under both cold and hypoxic cold exposure.
In the condition of cold exposure under 10% or 5% O₂ gas, the rats pretreated with Dexa. 50-200μg/100g B.W. showed high plasma TSH levels, whereas pretreatment with Dexa. blocked the increase of plasma 11-OHCS. Dexamethasone has no effect on resting plasma TSH levels or plasma TSH increase following cold exposure (29→0°C).
The rats acclimated to the fluctuating temperature from 27 to 23°C showed no plama TSH increase after cold exposure, while pretreatment with Dexamethasone facilitated the pituitary TSH release under the same condition.
In an attempt to study the mechanism of pituitary TSH secretion following cold exposure under hypoxic condition, it was found that synthetic TRH in several doses induced a prominent TSH release in the rats exposed to hypoxia with or without pretreatment of Dexamethasone.
From the findings mentioned aboved it was speculated that the mechanism of the reduction of plasma TSH levels after cold exposure under hypoxic condition, was mainly due to lack of TRH secretion,

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Radioimmunoassay (RIA) and competetive protein binding assay (CBPA) provide dose-response curves which show severe non-linearity. These non-linear dose-response curves make graphical or numerical dose interpolation difficult. Accordingly, several classic “least squares” statistical procedures commonly used for bioassay data are not directly applicable.
Several methods have been proposed for the linearization of dose-response curves in order to facilitate the rapid and accurate calculation of radioimmunoassay or competetive protein binding assay results. Among methods, linearization obtained by the use of the logit transformation is the best one and by this transformation statistical methods commonly used for bioassay results become directly applicable to the calculation of radioimmunoassay results.

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An electron microscopic study was performed on the multinucleated giant cell which is characteristic of the histological feature of subacute thyroiditis (de Quervain). Materials were thyroids obtained from six patients showing typical features of this disease both clinically and histologically. The following findings were obtained.
1) Most remarkable findings of electron microscopic features of the giant cell are the presence of numerous and various kinds of granules, mitochondria, and well-developed rough-surfaced endoplasmic reticulum and Golgi apparatus. The granules were classified into three types ; lysosome (Gr I), colloid droplets (Gr II) and secretory granules (Gr III). Well-developed rough-surfaced endoplasmic reticulum and Golgi apparatus were noted and this seems to suggest that the giant cell has the secretive function.
2) Numerous microvilli were observed at the apical portion of the giant cell facing the remaining colloid. These microvilli were generally elongated and branched out. And, in this portion, pinocytotic figures were observed. The author presumed this feature to be reabsorption colloid. From this electron microscopic study, the feature which had been called “colloidphagia” on light microscopic observation of the giant cells was recognized as the reabsorption of colloid i.e. a great number of closely packed colloid droplets (Gr II).
3) Nuclei of the giant cell generally showed round or oval shapes. They were generally larger than those of the thyroid epithelium. Nucleoli were moderately larger, too. Centrioles were frequently observed near the nucleus. These findings and the fact that the giant cell has numerous nuclei suggested an active nucleic fission.
4) The basement membrane of the thyroid follicle ad joining giant cells showed thickening and/or thinning, and some slits were observed. But the giant cell is itself in close and wide contact with the basement membrane.
Therefore, it is difficult to consider that the cells forming the giant cell had infiltrated into the follicle from the outside.
5) Whereas junction of the giant cell to other cells was definitely simple, that of the giant cell to another was complicated with remarkable interdigitation. And these findings seem to suggest that the giant cell originates from the thyroid follicular epithelium.
6) From the above-mentioned electron microscopic findings, it is considered that the multinucleated giant cell which appears in the thyroid of the cases with subacute thyroiditis (de Quervain) is derived from the epithelium of the thyroid follicle.

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The biological activities of deshistidine-glucagon (DH-glucagon) which was prepared by removal of a N-terminal aminoacid, histidine, from glucagon were compared both in vitro and in vivo experiments with those of native glucagon. DH-glucagon was supplied from Novo laboratories. The results of the experiments obtained were as follows :
1) DH-glucagon (in an amount of 30 μg) lacked the blood-sugar increasing action due to the glycogenolysis after intraperitoneal administration in rats.
2) Increase of the glucose uptake by the epididymal adipose tissue of a rat could not be found in a in vitro experiment in the presence of DH-glucagon in an amount of 0.μg to 10.0 μg/ml
3) Lypolysis increasing action of DH-glucagon (in an amount of 0.1 μg to 10.0 μg/ml) as indicated by the release of glycerol in vitro was also apparently absent as compared to that of glucagon.
From the above results the biological activities of DH-glucagon were discussed.

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