Drug resistance of Streptococcus pyogenes and Haemophilus influenzae isolated from respiratory tract were surveyed. Drug resistance and resistance patterns of S. pyogenes strains isolated in various districts in Japan were compared with those of the strains isolated in Europe. Of 1021 strains isolated in Japan, tetracycline (TC) -, macrolide antibiotic (Mac) -, lincomycin (Lcm) -and chloramphenicol (CM) -resistant strains were demonstrated respectively, at the frequencies of 80.3, 62.3, 60.8, and 57.9%. It was characteristic that quadruple and triple resistance to TC, Mac, Lcm and CM were manifested among the strains and their serotype was confined to the T type 12. The emergence of multiply resistant streptococcal strains was due mostly to the rapid increase in the isolation fre quency of Mac- and Lcm-resistant strains. Of 258 strains isolated in Europe, TC-resistant strains were merely demonstrated at the frequency of 23.6%.
To know the presence of drug resistance plasmid curing of resistance to Mac, TC, and CM was tested. These resistances were lost after cultivation at 41°C or in the presence of acriflavine (0.2, μ g/ ml). These results suggest that the determinants governing resistance to these antibiotics are located on extrachromosomal genetic elements (plasmid) that are widely distributed in streptococci.
From 60 strains of H. influenzae, TC-and APC-resistant strains were demonstrated at frequencies of 8.3% and 5.0%, respectively. No other antibiotic-resistant strains were isolated. Drug resistances were not conjugally transferred. Curing of resistance to TC and APC was tested. APC resistance was lost after cultivation in the presence of ethidium bromide (1μ g/ml). APC-resistant H. influenzae MI-74 produced a type I β-lactamase (PCase). This strain carried nonconjugative plasmid and its size was estimated to be 18 μm.

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It has been reported that large dose of sodium L-thyroxine (T₄) administration to the neonatal rats produces persistent alterations in hypothalamo-pituitary-thyroid axis on adult rats. The neonatal animals treated with T₄ exhibited retarded growth and produced a variety of endocrine abnormalities through the course of adult life. Thus this group of abnormalities has been called as neo T₄ syndrom. These neo T₄ rats, however, were injected with 15-30μ g of T₄ daily during the first 7days of life. It is clear that such large dose of T₄ administration produces severe hypermetabolic situations on neonatal animals as indicated by the increase of oxgen consumption, elevation of body temperature, increased basal metabolic rate and so much caloric consumption. Although it is generally accepted that metabolic disorders in neonatal period modify various endocrine and central nervous system, disagree exsists whether these kinds of abnormalities are specific for neo T₄ syndrome or not. 2, 4-Dinitrophenol (DNP) has been recognized as an agent of inducing hypermetabolism in various animals by virture of its uncoupling effect on oxidative phospholyration with the Krebs tricarboxylic acid cycle.
It is also well known that administration of DNP decreases plasma PBI levels and produces T₄ displacement from serum protein. We employed DNP in our study to produce hypermetabolism on neonatal rats. Our present study was undertaken to compare DNP treated neonatal rats (neo DNP) with neo T₄ rats and to compare both of groups to neo saline rats as control to see the effect of neonatal hypermetabolism on the hypothalamo-pituitary-thyroid axis in adult stage. Neonatal rats which had received 7daily injection of 50μ g of DNP or 30μ g of L-T₄beginning with the day of birth were used in the present study.
The following results were obtained ;
1) Neo DNP and neo T₄ rats revealed persistent retardation of growth compared with neo saline rats.
2) Neo T₄ rats at 22days of age showed low plasma T₄ and T₃ levels compared with neo saline control rats but neo DNP rats did not show it.
3) Neo DNP and neo T₄ rats at 22days of age showed lower response to synthetic TRH administration (I.P) than that of neo saline rats. Moreover neo T₄ rats showed almost no response to TRH.
4) Neo DNP and neo T₄ rats at 22days of age showed low pituitary TSH contents compared to neo saline rats and also neo T₄ rats showed apparently high pituitary prolactin contents compared with neo saline rats but neo DNP rats did not show it.
5) Neo DNP and neo T₄rats in adult stage showed also blunted response to TRH administration (I, V) compared with neo saline rats.
6) Neo DNP and neo T₄rats in adult stage showed abnormal response to PTU or T₄ administration.
7) Neo T₄ rats at 161days of age showed lower pituitary TSH contents and endocrine organ weights than neo saline and neo DNP rats.
Thus, the present study has shown that neonatal hypermetabolism causes hypofunction of pituitary-thyroid axis through adult life and that alternation of hypothalamus may be more prominent in neo T₄ rats than neo DNP rats.

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Free thyroxine (T₄) has been suggested as the active component available to the cells in vivo for the initiation of the hormonal action and thyrotropin (TSH) regulation. It is known that hypolipemic agent clofibrate displaces T₄ from plasma protein in vitro. If the free T₄ would be elevated after administration of the drug, the pituitary TSH secretion might be decreased through the negative feedback mechanism, as suggested previously. The present study was undertaken to determine the effect of clofibrate and related compound on serum TSH concentrations in man and experimental animals.
The results obtained herein were as follows :
A single and chronic administration of clofibrate (750mg/day) significantly suppressed serum TSH levels in patients with primary hypothyroidism. There was no change in serum levels of T₄-iodine, triiodothyronine (T₃) and % free T₄ after clofibrate treatment. On the other hand, clofibrate failed to produce discernible changes in serum T₄-I, T₃, and basal and thyrotropin-releasing hormone (TRH) -induced TSH levels in euthyroid subjects.
Similar results were also obtained with brain-stimulating compound meclofenoxate hydrochloride (750mg drip infusion or 600mg/day x 7days. oral), similar in structure to clofibrate.
In thyroidectomized rats with undetectable levels of serum T₄ and T₃, both clofibrate and meclofenoxate hydrochloride suppressed elevated serum TSH levels. The pituitary TSH content was lower in these drugs-treated groups than in controls, while no change in the hypothalamic TRH content was observed in these animals.
These observations suggest that clofibrate and structurally related compound suppressed TSH secretion in patients with primary hypothyroidism and in thyroidectomized rats, presumably at the hypothalamic-pituitary levels.

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Bronchial angiograms performed on 74 patients with pulmonary mass lesion from 1973 through 1977 were reviewed. Angiographic findings of 43 patients with pathologically proven lung cancer were evaluated for histopathology and hilar lymph node metastasis. Angiographic patterns of lung cancer were classified into 6 types. I : Bronchial arterial branches pour into the center of mass density, and then tumor vessels radiate peripherally. II : Neovascularity and tumor stain throughout mass density. III : Neovascularity and/or tumor stain at central portion of mass density. N : Neovascularity and/or tumor stain at peripheral portion of mass density. V : Neovascularity and/or tumor stain at proximal portion of mass density. VI : Non-visualized mass density.
Among 25 cases of adenocarcinoma, 16 cases were grouped as type I, 4 as type II, 1 as type N, 2 as type V and 2 as type VI, All the cases showing type I were adenocarcinoma. Fourteen cases of squamous cell carcinoma were classified 8 cases in type II, 1 in type III, 1 in type IV, 3 in type V and 1 in type VI. Small cell carcinoma (non-oat cell type) were 2 cases in type III and 1 in type V.
Hilar lymph node metastases were investigated in 35surgically proven cases. Seventeen cases showed angiographic findings of lymph node metastases, and 13 out of these 17 cases were proved to be correct pathologically. Eighteen cases were free of angiographic findings of metastases ;13 cases to be correctly diagnosed and 5 cases showed metastasis pathologically.

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Case 1 was a 4-year-old boy with macular cherry red spots, myoclonus and pyramidal tract signs. The clinical diagnosis was Tay-Sachs disease. Tay-Sachs ganglioside was increased in his brain obtained at autopsy.
Case 2 was a 7-year-old girl with onset at age of 3 years with epileptic seizures. Macular degeneration, pyramidal and cerebellar signs followed. The clinical diagnosis was late infantile form of amaurotic family idiocy. GM1-ganglioside was increased in the brain at autopsy.
Case 3 was a 27-year-old man with macular degeneration, myoclonus, convulsive seizures, cerebellar and pyramidal signs. The clinical diagnosis was adult type of amaurotic family idiocy (Kufs disease). In the brain at autopsy, ganglioside showed a normal pattern.
Case 4 was a 33-year-old man with spastic paraplegia and progressive dementia. Neuropathologically, atypical leucodystrophy was diagnosed by a mild increase of cerebroside-sulfuric ester. Aryl sulphatase A activity was 50% of control in the brain at autopsy.
Electron microscopy showed in Case 1 that the neurons were swollen by membranous cytoplasmic bodies (MCB) in cytoplasm. There were MCB, zebra bodies and some other organelles in a limiting membrane. It seemed that these formed autophagolysosome, some of which were similar to the so-called curvilinear bodies (CLB).
In Case 2, there were several MCB and CLB enclosed with a limiting membrane in neurons from the frontal lobe. filamentous or reticular substance filled the cavities of dilated cisternae of the rough endoplasmic reticulum (ER). Besides dilated ER, CLB, small MCB and zebra bodies were observed in neurons from the occipital lobe. In Purkinje cells, there were many vesicles, cored vesicles and small MCB near cisternae of rough ER grown in the cytoplasm. Some of them were enclosed with a limiting membrane, being suggestive of their transformation into CLB.
In Case 3, neurons at ammon's horn were swollen with finger print-like patterns. Glial cells from this region and neurons from the occipital lobe contained multilamellar cytosomes (MLC) with a limiting membrane.
In Case 4, there were large osmiophilic myelin figures surrounded by a limiting membrane among myelin sheaths in the white matter. Some glial cells contained myelin figures in cisternae of ER, some of which were changed into large inclusions with osmiophilic myelin figures.
These inclusions were generally regarded as residual bodies, but in our cases the origin of inclusion bodies were considered to be swollen cisternae of ER, many vesicles, cored vesicles, small MCB near the ER and myelin figures in the cisternae of ER.

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