It is well known that functionally different two major subpopulations of lymphocytes are present-T lymphocytes (Thymus derived) and B lymphocytes (Bone marrow derived)-. Although they can be distinguished by specific surface receptors, surface antigen markers and electrophorectically different morbility, they are not morphologically distinguishable by light and electron microscopy. Recently it has been shown that the human T cells are smooth in surface, whereas B cells are villous by scanning electron microscopy (SEM). But Scott has reported by SEM used immunospecific latex markers that there was no distinct morphological difference between mouse T and B lymphocytes.
In the present study, we have observed lymphocytes of athymic nude mice (nu/nu) and nu/+ mice using freeze fracturing in an attempt to demonstrate the morphological difference between them.
Nude mice and nu/+ mice, ages 6-8 weeks were killed with ether and their inguinal lymphnodes were removed. One portion of each removed tissue was placed in 10% formalin and stained with hematoxylin and eosin for light microscopy. A second portion was immersed in 40% glycerol containing the cacodylate buffer and processed for freeze fracture.
The inguinal lymphnode of the nude mouse is relatively larger in size than that of nu/+ mouse. Although the small lymphocytes are present in the cortex, the expanded paracortical area completely lacks small lymphocytes. The lymphoid follicles are poorly developed and rather small in size.
Most of the lymphocytes of the nude mice are 4-8 μ in diameter, have a few short projections and only a few are villous.
In fracturing the membrane is often split along the middle of the lipid bilayer. Globular particles measuring 60 to 160 Å in diameter are present within the interior of the membrane exposed by freeze cleaving. The number of these particles per unit area (μ²) is 235-512(average density of 307) on the inner fracture face.
Most of the particles are present singly and only 2% of the nude mouse lymphocytes shows small aggregates of granule, while the lymphocytes of the thymus and the lymphnodes of the nu/+ mice show a higher percentage of particle aggregation by incubating in glycerol before freezing. Recently it has been suggested that the intramembranous particles may consist of protein and interact with a hydrophobic portion of glycoprotein or represent a receptor site. We agree with Mandel who suggested that the aggregates of the IP is one of the features of T-derived lymphocytes.
A relatively thick rim of the cytoplasm contain fairly well developed organelles in the nude mice. The nucleus is prominent and smooth in outline with scattered nuclear pores. The average pore density of the nude mouse is 19.2/10 μ² and is fairly lower than that of thymus and lymphnodes of nu/+ mice.
The density of the intramembranous particles and the nuclear pores of the nuclear envelope may show the degree of the nuclear metabolic activity and/or the degree of the cell maturity. Therefore we suggest that the lymphocytes of the nude mouse may have less metabolic activity, but further studies are needed.

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The preliminary clinical trial was carried out with a novel benzomorphan derivative of a non-narcotic analgesic, ID-1229, 2'-hydroxy-2-[γ (p-fluorobenzoyl)-n-propyl]-5, 9-dimethyl-6, 7-benzomorphan (Sumitomo Chemical Co., Ltd.). Employed in the test were five cancer and fourteen leprosy volunteers. All of these patients have had too severe pain to give sufficient relief with an ordinary analgesic. In most cases, one ampule of 15mg/ml of ID-1229 was intramuscularly injected. The clinical analgesic effect and other changes observed were as follows:
(1) The intramuscular injection of 15 mg of ID-1229 was equivalent to that of 30mg of pentazocine in analgesic potency.
(2) Administration of ID-1229 caused potent analgesic and hypnotic effects.
(3) ID-1229 was considered to act synergistically with pentazocine in analgesic effect, because the combination of both drugs increased the respective analgesic potencies.
(4) In the present trial, no influence was observed on respiration, heart rate and liver function.
(5) The administration produced reduction in blood pressure which was, in general, within the safety range.

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The leprosy epidemiological study in Okinawa was carried out with the historical change of leprosy control policy which was in operation by administrative measure of the Government, In Japan segregation policy for leprosy patients came into force in 1909 and five leprosaria were established to isolate the patients, according to the Leprosy Prevention Law which was carried into effect in 1907.
In Okinawa the Government had a plan to have two leprosaria but the Government did not succeed in establishment of leprosaria, because of opposition by the public. Finally Okinawa Airakuen Leprosarium was established in 1935 but during the time the number of leprosy patients in the communities has increased to about 1, 000, Hansen's Disease Prevention Law was put in force in 1961 by the Ryukyu Government and leprosy control policy was changed. In 1962 leprosy out-patient treatment started by Okinawa Anti-leprosy Association, Since then early treatment, early diagnosis and active contact tracing program have been performed under new policy and many patients in the community have been controlled by out-patient departments. In 1962 the incidence rate of leprosy was 0.078‰, in 1967 the rate increased to 0.180‰, and then in 1974 the rate decreased to 0.069‰. Recently the improvement of leprosy epidemiological status in Okinawa has been observed.

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Although the respiratory failure sets in as a consequence of impaired respiratory function, there would be causes of its onset. The most frequent causes of the respiratory failure are the deterioration of the pre-existing respiratory diseases and asthmatic attack, and these are followed by infectious complications of the respiratory system. Complications of non-respiratory systems are also seen as causes of respiratory failure by breaking down the balance of back ground factors within whole body.
The mortality of the patients with respiratory failure in this study is approximately 10%, the rate of which is one-third of the acute exacerbation state. About 60% of these patients recovered from respiratory failure, but 30% cases continue to be its chronic stable state.
To avoid the inducing factors-triggers, and to detect the pre-monitoring symptoms of acute exacerbation of respiratory failure for starting therapies as soon as possible, these are the important points for the management of respiratory failure in its chronic stable state. On acute exacerbation, careful treatment of each case is emphasized by analysis of autopsy.

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We compared the grade of breathness by the results of respiratory function. The results are shown in the table.
We investigated the actual conditions of respiratory failure.
The most frequent respiratory disease which caused respiratory failure was inactive pulmonary tuberculosis, the second was pulmonary tuberculosis, and the third was chronic obstructive lung disease and pulmonary cancer.
The restrictive type showed heavy mortality, on the contrary obstructive type showed slight mortality.
We discussed the indication of tracheotomy, and the arterial blood gas analysis was pH 7.22. Pao₂ 43.3mmHg and Paco₂ 100.0mmHg in the case of tracheotomy.

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The main causes of respiratory failure admitted to the Tokyo National Chest Hospital between January and August in 1975 are sequelae of tuberculosis (80% have had surgical treatments) and other chronic lung diseases (mainly chronic bronchitis and pulmonary fibrosis).
On the care of chronic stable stage, cardiac care was emphasized, because majority of cases show abnormal EKG patterns indicated right heart strain or hypertrophy. Oxygen administration for activities of daily living and home care has discussed especially refer to comparative merits of the equipments.
On the care of acute aggravation stage, establishment of well equipped and personelled intensive respiratory care unit at national sanatorium and hospital is strongly suggested.
It comes to a conclusion that a hospital with intensive respiratory care unit, a medicovocational rehabilitation center, and an accomodation and vocational aid center, should be in system for comprehensive care of respiratory failure.

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There are many diseases caused respiratory failure in childhood. Recently, mortality of bronchial asthma of children has increased abruptly. But, its cause is still unclear. Episodes of status asthmaticus has increased also in our hospital, the numbers of which were 254 cases from October 1974 to September 1975. Acute respiratory failure of bronchial asthma were 16 episodes of 8 subjects from 1971 to 1975. Clinical signs were well matched of criteria of Collins-Williams, O'Brien's triad, and Bierman's pulmonary index. Results of arterial blood gases and pH suggested severe respiratory acidosis and metabolic acidosis.
The administration of adrenocorticosteroids and humidified oxygen by recirculated O₂ tent should be applied. Especially, much doses of hydrocortisone intravenously are the effective pharmacological management of respiratory failure due to asthmatic attack.

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The pulmonary function of 61 patients with Duchenne type of progressive muscular dystrophy was examined, and from the obtained results the criteria of their respiratory failure were investigated.
The respiratory failure of the patients with DMP is caused by restrictive ventilatory disturbance (RVD). As the young patients with RVD grew older, their trouble degrees and the curve of their chest walls progressed the more. Therefore the aggravation of their RVD was obviously confirmed. In other words the development of DMP brought about the degeneration or the atrophy of skeletal muscles of their bodies, legs and arms. The degeneration and atrophy caused the curve of their chest walls and the decrease in their respiratory muscle force. The respiratory failure of the patients with DMP is summed up as a low ventilation of their pulmonary alveoli, which results from their chest-wall curve and the decrease in their respiratory muscle force.
%VC<60%·Po₂<81mmHg can be supposed to be the criteria of respiratory failure. From the view-point of the %VC<60%·Po₂<81mmHg, being looked upon as a border of DMP respiratory failure, the ventilatory responses of the patients after exercise were examined thoroughly.
In case of the patients with non-DMP respiratory failure their breathing was slow and deep. On the contrary, the patients with DMP respiratory failure breathed fast and shallow. In the latter the fall of pH·Pot·So₂ and the rise of Pco₂ were found out.
From the view-point of the most suitable breathing, it is the most desirable in the worst respiratory state after exercise that the patients adopt the breathing way of increasing in ventilation volume per one time and of decreasing in respiratory number of times. With regard to respiratory efficiency and the consumption of respiratory muscle force it is also the most economical. On the contrary, the patients with respiratory failure, as mentioned above, adopted the breathing way of making their respiratory muscle force exhausted.
It can readily be supposed that when a long term burden such as respiratory infection is imposed on the respiratory failure patients, they are apt to have ventilatory failure.
The remedial effect for the disease of DMP itself can't be expected. Such being the case, it is the most important, first of all, to take prophylactic measures for respiratory infections which are acutely aggravating factors. It is of great significance to train the patients with DMP respiratory failure to take abdominal breathing with high ventilatory efficiency.

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A 47-years-old female, suffering from cirrhosis after having been treated tuberculosis for a long, visited our hospital with complaints of cyanosis, dyspnea and faintness for several years. After laboratory examination, cyanosis was confirmed by a low arterial oxygen saturation (82% and oxygen tension (30mmHg)). Pulmonary function studies revealed mild disturbance of ventilatory function (%VC 62%, %FEV₁ 72%) with raised minute volume (V 14.5 1/m). Alveolar-arterial oxygen difference was wide (80mmHg) and that of pure oxygen inhalation was more wide (164mmHg). Because of our thought that hypoxemia of this case was due to venous blood admixture, right cardiac catheterization, pulmonary angiography and whole body scanning using ^99mTc-Macroaggregated Albumin (MAA) was performed. From these results, r-l shunt ratio (68.8%) was calculated. Hypoxemia of this case was thought to be caused by multiple small pulmonary arteriovenous fistulas.

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I. The characteristics of patients with chronic respiratory failure resulting from arterial blood gas analysis:
From Jan. 1974 to June 1975, we treated 21 patients with chronic respiratory failure involving acute exacerbation at Akashi National Hospital.
The blood gas analysis of these Patients showed that 15 cases of them were alveolar hypoventilation type (71.4%) and 6 cases were anoxemia alone type (28.6%).
II. Pulmonary circulation in chronic respiratory failure patients with acute exacerbation:
Eighteen cases of chronic respiratory failure with exacerbation were observed. Their pulmonary circulation was recorded with the use of the Swan-Ganz flow direct recorded balloon catheter.
The results: 1) Significant high level negative correlation was shown between the arterial blood oxygen tension (Pao₂) and the mean pulmonary arterial blood pressure (PPA) during normal air respiration at rest, (r=-0.841, ρ<0.001)
2) This pulmonary hypertension was significantly reduced by oxygen inhalation. However, in the event that the patient shows increased pulmonary artery pressure and takes more dense oxygen, the blood pressure decreased to an even greater degree.
3) In three of the above cases, an “Iron Lung” was used for the purpose of artificial ventilation. The pulmonary circulation showed increased tidal pressure of the pulmonary artery and right ventricle as the result of the box pressure pulsation of the “Iron Lung” treatment.

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In the first part of this report, a conventional portable oxygen producing apparatus, Solid Oxygen System (Life Support Co. U.S.A.), was evaluated on two patients with chronic respiratory failure from the view-point of improving activities of daily life. The results were rather satisfactory except for the limitation of duration.
In the second part, a portable oxygen supplying apparatus invented by us was introduced. The point of our apparatus is a inflatable jacket. The jacket serves as an oxygen reservoir in normal atmospheric pressure. The oxygen is supplied to this jacket from a con-ventional portable high pressure oxygen cartridge. The patients may inspire at their own will the oxygen in normal pressure from within the jacket, for this simple device does not require ordinary complicated heavy pressure-ajusting valve.

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Recently, three cases of acute exacerbation of chronic pulmonary disease were treated in our intensive care unit (ICU). These were of chronic bronchitis, pulmonary tuberculosis and emphysema with cor pulmonale chronicum respectively. The former two cases were successfully treated with artificial respiration and tracheostomy. The latter one only needed oxygen inhalation therapy, physiotherapy, bronchodilator, diuretics and digitalization. During staying in ICU, the patient's condition was improved, but about one month after returning to the medical ward, he died from heart failure.
It is absolutely advisable to have ICU or such special care unit for treatment of severely ill patients such as acute exacerbation of chronic pulmonary disease.

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Two cases of Sjögren-Larsson Syndrome were reported. Interesting clinical findings of each patient were elevation of serum copper and high excretion of urinary copper.
Patient I. 9 Yo. male: The patient had characteristic ichthyosis, spastic paralysis, mental retardation, right strabismus and both retentio testis. Abnormal laboratory findings were as below: serum γ-gl 1.7g/dl, α-gl 0.4g/dl. Cu 196-170μg/dl, urinary Cu 17-14μg/mg of creatinine, fundus: atrophy of both optic nerves.
Patient II. 19 Yo. female: The patient had same triad as patient I, especially the ichthyosis was severe. Abnormal laboratory findings were as below: serum γ-gl 1.5g/dl, α-gl 0.3g/dl, Cu 166-160μg/dl, urinary Cu 72-33μg/mg of creatinine. fundus: degeneration of both macula. EEG: typical spike & wave complex in all area. Liver disease, thyroid disease, Wilson's disease and anemia were negrected in both patients. Since Sjögren & Larsson first described this syndrome in 1957, a number of cases have been reported, but the pathogenesis of this syndrome are not yet known. Sjögren-Larsson syndrome with abnormal Cu metabolism has not been reported. In this report, the relation between high serum copper and the pathogenesis of Sjögren-Larsson syndrome was dicussed.

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Two cases of hypothyroid myopathy were reported. Case 1. A 45-years-old man was admitted to our hospital with a history of diffuse muscular stiffness in the legs and arms for the preceeding 8 years. He was treated with ¹³¹I for hyperthyroidism 9 years prior to admission and since then had had symptoms of myxedema and had received substitution therapy occasionally.
On physical examination he had athletic appearance, a large tongue, slurred speech with a hoarse voice, dry skin and dry and sparse hair. Neurological examination revealed marked generalized muscular hypertrophy, particularly in the proximal parts of the upper limbs. All the muscles were exceedingly firm in consistency. There was no gross muscular weakness. There was a prolonged relaxation phase in achilles tendon reflex and no neurological deficit was detected except for the above.
Serum cholesterol was 266 mg/dl, and no abnormal findings were obtained on other routine laboratory investigations. Protein bound iodine, ¹³¹I uptake at 24h, T₃, T₄ and the basal metabolic rate were 2.0 mg/dl, 15.5%, 21.1%, 2.9μg/dl and -25% respectively. Serum creatine phosphokinase was 33 unit (normal 0-12). The thyroid scintigram was normal. The cerebrospinal fluid was normal. The electroencephalogram was normal. The electromyogram revealed myogenic pattern.
Biopsied specimen from left deltoid muscle showed the variety of changes. Thers was a variation in the diameter of the fibers (rarely up to 100μ) and in a few fibers there were loss of striation, fragmentation, central invasion of sarcolemmal nuclei, granular degeneration, hyaline degeneration and marked metachromasia. Endomysium was sometimes edematous, and the homogenous, PAS negative, eosinophilic material was found beneath the sarcolemmal sheath in rare instances.
Case 2. A 38-years-old woman visited our hospital with a symptoms of myxedema. She received substitution therapy, but discontinued the treatment by herself. In the following year she noticed the tiredness and occasional aching and stiffness of the extremities, and visited our neurological unit.
On physical examination she had a low pitched voice, coarse hair and dry skin. Neurological examination revealed generalized muscular stiffness and slight weakness of the proximal muscles of all four extremities. There was no muscular hypertrophy or atrophy. The muscles were not tender. There was marked mounding phenomenon on percussion of the bilateral gastrocnemius muscles and was a prolonged relaxation phase in achilles tendon reflex. Except for the above, no neurological abnormalities were obtained.
Routine laboratory investigations including the thyroid functions were normal except for the slight elevation of the value of serum cholesterol (265mg/dl). Serum creatine phosphokinase was 17 unit. The cerebrospinal fluid was normal.
The electroencephalogram was normal. The electromyogram revealed myogenic pattern.
Biopsied specimen from left deltoid muscle showed the resembling changes to the findings obtained in case 1.
Thyroid extracts was given, and about one month after the treatment muscular symptoms were almost disappeared in each case. And the diagnosis of hypothyroid myopathy was made.
Serum enzyme activities such as creatine phosphokinase, and histological findings were discussed in contrast with the previous literatures, and we reviewed the muscular manifestations in hypothyroidism and attempted to classify the clinical types of hypothyroid myopathy making reference to the previous reports.

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F.T.A. 175±2 was the mean value in standing position with both legs in normal adult Japanese.
The close relationship was noted in the following items; age, duration of pain, X ray-findings, gross O or X appearance of the knee, effusion, walking ability and contracture of the joint.

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