13 cases of miliary tuberculosis were experienced in 829 autopsy cases aged over 60 during January 1966 to December 1977 at Nagoya-shi Koseiin Geriatric Hospital. The series comprised 6 males and 7 females whose age distribution was 5 cases of 60-69, 3 cases of 70-79, 4 cases of 80-89 and 1 case over 90 years old.
12 cases of them were cryptic type only diagnosed at autopsy. 8 out of 13 cases died of miliary tuberculosis. Two cases had no underlying disorder. The other, however, had underlying disorders such as cerebrovascular disorder, neoplasma, liver disease, blood disease, and collagen disease.
As symptomes, general malaise, emaciation, loss of appetite were often observed. Body temperature were from 38 to 39°C in 61% of patients. Hepatomegaly in 2 cases and splenomegaly in 3 cases were also detected. 2 cases showed abnormal liver function. Miliary mottlings on chest X-ray films were present in only 3 out of 13 cases.
As predisposing factors to miliary tuberculosis, aging, underlying disorders, administration of corticosteroids or immunosuppressive agents were suggested.
The duration of clinical course were 3 weeks to 3 months. However, one case showed acute dissemination occured during the chronic course. The onset was sometimes obscure.
Lung, spleen and liver were the most frequently involved organ. They were followed by bone marrow. Liver biopsy revealed noncaseous granuloma in one case.
Dissemination originated from lung tuberculosis in many cases. However, there were 2 cases that dissemination originated from vertebral caries or lymph node tuberculosis of pancreatic head.
Tuberculosis in the aged should be followed carefully because lung tuberculosis was found in 15% of autopsy cases and be kept in mind hematcgeneous spread of tubercle bacilli might occured in the aged.

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Cardiac rupture occurred in 15 out of 82 cases of fresh myocardial infarction found among 1, 000 consecutive autopsies over 60 years of age. The average age of 15 cases was 75.8 years and they were 8 males and 7 females.
The cases with rupture were compared with the cases without rupture in reference to the clinical and pathological findings. No significant differences were found in age, sex, cardiovascular complications and pathological features except for fresh thrombotic occlusion.
The high incidence of lateral wall rupture (50%) contrasted to the relatively low incidence of isolated infarction in this area. The tear was present near the center of infarction.
Electrocardiograms were recorded in 10 at the time of rupture. Seven cases with pericardial tamponade showed sudden sinus bradycardia or junctional rhythm, 2 with subepicardial hematoma showed increasing pacing threshold and a case of septal rupture developed junctional rhythm.
Clinical course was less than 5 days in all. Recurrent chest pain was frequent. Persistent hypotension and recurrence of hypotension or congestive heart failure were observed in 5 of 6 cases, who survived more than 24 hours after the onset of symptom.
Patients having these symptoms and sudden electrocardiographic changes should be suspected of undergoing myocardial rupture.

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The purpose of this investigation was to characterize the non-cellular factors in immunologic deficiencies which occur in aged humans.
Phytohemagglutinin or pokeweed mitogen responsiveness of lymphocytes has been measured in young and older persons over 70 years of age without hematological and immunological disorders. The lymphocytes from older persons have been cultured in TC-199 medium with the autologous serum or young human AB serum, and the lymphocytes from young persons in TC-199 medium with the autologous serum or aged human AB-serum.
1) Lymphocytes from the older persons in the presence of autologous serum incorporated significantly less tritiated thymidine as compared with in the presence of young human AB serum when cultured with plant mitogens. Moreover lymphocyte reactivity from older persons was higher, as autologous serum decreased and young human AB serum increased in the medium.
2) Lymphocyte reactivity from young persons in the presence of the aged human AB serum was lower than that in the presence of autologous serum.
The difference in observed lymphocyte reactivity could be attributed to difference in the serum contained in the culture. These deficiencies of the aged human serum would include detrimental humoral factors present in the older persons which adversely affect lymphocyte responses to plant mitogens, or absence of humoral factors necessary for maintenance of growth and differentiation.
3) Lymphocyte reactivity from older persons in the culture medium with both 15% young human AB serum and 15% autologous serum was found to be lower than in the culture medium with only 15% young human AB serum.
These observation suggest that the aged human serum include detrimental humoral factors which adversely affect lymphocyte response to plant mitogens, and it would partly contribute to the immunological defficiencies of the aged persons.

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Four cases of the congenital craniovertebral anomalies with onset of the symptoms after the age of 50 were reported. Then, the incidence of the anomalies was examined among the older outpatients of the university hospitals and the causes of late onset were discussed.
Case 1, a 61-year-old female with odontoid agenesis, occipitalization of the atlas, fusion of C2 and C3, developmental cervical spinal canal stenosis and spondylosis deformans, developed hypesthesia of the hands at the age of 51, with subsequent spastic and ataxic tetraparesis and atrophy of the hand muscles. Case 2, a 55-year-old female with atlanto-axial dislocation, occipitalization of the atlas and fusion of C2 and C3, showed gait disturbance at 53, followed by spastic tetraparesis and occipital neuralgia. Case 3, a 67-year-old male with basilar impression, occipitalization of the atlas, fusion of C2 and C3, developmental cervical canal stenosis and spondylosis deformans, developed paresthesia of the hands and feet at 67, associated with bilateral pyramidal signs. Case 4, a 51-year-old male with fusion of C2 and C3, anomalous vertebral bodies of C4-C6, developmental cervical canal stenosis and spondylosis deformans, had neck pain and muscle weakness of the right arm at 51, later developing muscle atrophy of the bilateral shoulder girdles.
Of 535 consecutive outpatients aged 50 and over whose skulls and/or cervical spines were examined roentgenologically in the geriatric clinic of University of Tokyo Hospital and in the neurologic clinic of University of Gunma Hospital, there were 13 patients (2.4%) with major congenital craniovertebral anomalies except Arnold-Chiari malformation. In four patients of these 13 the onset of the symptoms was after 50 (aforementioned), in 3 it was before 50, and the rest had no symptoms and signs. The incidence of each anomaly was 1.7% in block vertebrae, 0.7% in occipitalization of the atlas, atlanto-axial dislocation, and odontoid dysgenesis, respectively, and 0.4% in basilar impression. Developmental cervical canal stenosis was defined as the narrowest antero-posterior diameter of the cervical spinal canal not exceeding 13mm, excluding such stenotic portions as secondary to spondylosis deformans. The canal stenosis was observed in 23% of the patients with the craniovertebral anomalies and in 7% of those without, the former being significantly higher than the latter.
The causes of late onset of the symptoms in four patients were analysed by referring to the asymptomatic patients and the literature. In Case 2 with atlanto-axial dislocation, a moderately narrow diameter (13mm) between the odontoid and the posterior arch of the atlas seemed to play a role in late onset. In the remaining three patients, the concomitant developmental cervical canal stenosis and spondylosis deformans were probably the cause of late progressive impairment of the functions of the middle or lower cervical nerves added to the upper cervical cord dysfunction.

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Cardiac hypertrophy develops from pressure overloading due to hypertension.
This compensatory hypertrophic process may be not only affected by the quantitative or qualitative characteristics of the diposed pressure but the ongoing intrinsic cardiac metabolism, mainly protein metabolism and finally affect on total cardiac function. We classified 85 patients with hypertensive heart disease into 3 groups on the basis of the left ventricular echocardiographic findings as follows.
1) Left ventricular hypertrophic group (LVH group), 30 patients; symmetric hypertrophy of the left ventricle and the summation of the interventricular septum thickness (IVST) and posterior left ventricular wall thickness (PWT), IVST+PWT≥30mm.
2) Left ventricular dilatation group (LVD group), 29 patients; dilatated left ventricular cavity, LVDd≥60mm.
3) Asymmetric septal hypertrophic group (ASH group), 20 patients; asymmetric septal hypertrophy caracterized by IVST≥15mm and IVST/PWT≥1.3. And we checked serum albumin, A/G ratio, total cholesterol and total protein level of each individual. Average serum albumin level was significantly lower in LVD group of 3.7±0.35g/dl compart to that of LVH group and ASH group, 4.3±0.3g/dl and 4.5±0.42g/dl respectively (p<0.001). No statisfical difference was noted between LVH group and ASH group. Also the average value of A/G ratio, total protein and total cholesterol were significantly lower in LVD group that that of the other 2 groups (p<0.001).
It was suspected that the cause of disturbed liver function due to congestion may be responsible for hypoalbuminemia.
Then the correlation between serum albumin and venous pressure regarding as the index of liver congestion was evaluated in LVD group and in hemodynamically different RHD group.
Although no correlation was found between serum albumin and venous pressure in LVD group, significant negative correlation was found in RHD groups.
We considered that the cause of this hypoalbuminemia in LVD group was mainly due to liver congestion, but the roles of the other factor like lack of dietary protein intake and disturbance of intrinsic protein metabolism were suspected.

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Small Infarctions account for about 40% of the cases of cerebral infarction. With the development of the CT scan has come the opportunity to expand our knowledge of the clinical presentation, etiology, and pathophysiology of small infarctions. This papne will deal with the clinical manifestations of cases of small infarctions of the basal ganglia, as demonstrated by CT scan. For purposes of the study, small infarctions have been defined as those which exhibit a low density area less than 15mms in diameter on CT scan. During the presentation we will emphasize the correlation of small infarctions of the basal ganglia with transient ischemic attacks.
Two hundred twenty-three patients with symptoms suggestive of cerebral ischemic infarction were studied by CT scan. In 42.4% of the patients small infarctions of the basal ganglia found on CT scan; of these 65 patients were also studied by angiography.
The clinical presentation of 60 patients with small infarctions of the basal ganglia was compared with that of 41 patients with major cerebral artery occlusion. About half of the patients exhibited a similar degree of weakness in the affected upper and lower extremities. In most of the other patients the upper extremity was more involved than the lower extremity. However, only 3.3% of the patients with small basal ganglia infarctions demonstrated complete hemiplegia as compared with 36.6% of the patients with major artery occlusion. Half of the patients with basal ganglia infarction had no sensory impairment.
Sixty-five per cent of the patients with small infarctions of the basal ganglia showed good recovery compared with 17% of the patients with major artery occlusion cerebral infarctions.
Motor deficits were mild in patients with lesions in the anterior limb or genu of the internal capsule, whereas the patients who sustained small infarctions in the posterior two-thirds of the posterior limb generally had much more marked motor involvement.
There was a striking difference on the prognosis for improvement of the motor deficit when the patients were divided into those with lesions less than 10mm in diameter and those with lesions 10-15mm in diameter.
Of the 65 patients with small infarctions of the basal ganglia demonstrated on CT scan who also were studied angiographically 39 (or 60%) had normal arteriograms.
In 21.7% of the patients with small infarctions of the basal ganglia a past history of TIAs was found, compared with 15.6% of the group without lesions on the CT scan and only 9% of the patients with infarctions elsewhere on CT scan. In 61.5% of the cases of small infarction who had a history of TIAs their stroke was occurred within one day after the last TIA whereas this short interval between TIA and stroke was not prominent in the major artery occlusion group. In 10 of the cases with small infarction the pattern of neurological involvement was similar between the TIAs and stroke.
Five of 65 cases with low density area on basal ganglia were diagnosed transient ischemic attack clinically. Two of 5 cases with transient ischemic attack reveals the positive contrast enhancement on CT scan, two weeks or 17 days later from onset.

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Recently, anoxia in tissues has been attracting attention as a causative factor in the onset of complications of diabetes mellitus. We determined erythrocyte deformability in diabetics as one of the factors involved in the onset of anoxia in tissues, and studied the changes of erythrocyte deformability, erythrocyte osmotic fragility, HbAI and erythrocyte 2, 3-DPG.
Erythrocyte deformability was determined by an improved filtration method described by Reid et al, and erythrocyte osmotic fragility by a CPC method, HbAI by the microcolumn-chromatography method, i.e. an improved method discovered by Trivelli et al., and 2, 3-DPG by our own modified Ericson's method.
Erythrocyte deformability was 0.53±0.03ml.RBC/min in diabetics, compared with 0.78±0.04ml/RBC/min in normal subjects, displaying a significant decline. A further decline was observed in a group of diabetic patients with severe complications. A significant negative correlation was noted between erythrocyte deformability and HbAI.
Erythrocyte osmotic fragility was 64.3±0.6mOsm, compared with 60.0±0.5mOsm in normal subjects, representing a significant shift to the hypertonic side in diabetics, and a negative correlation with erythrocyte deformability was demonstrated. A decline of erythrocyte 2, 3-DPG was also found in the group of diabetic patients with severe complications.
As described above, the fragility of the erythrocyte membrane and an increase in HbAI seem to be causative factors largely affecting erythrocyte deformability in diabetes mellitus, and it is suggested that a decline in erythrocyte deformability as well as in 2, 3-DPG is involved in the onset of complications of diabetes mellitus.

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The purpose of this study is to examine the effect of age on active and inactive plasma renin levels. Twenty-two young (15 to 35 years), 17 middle-aged (36 to 60 years) and 19 old (62 to 84 years) normal subjects and 9 young (16 to 35 years), 17 middle-aged (38 to 59 years) and 32 old (61 to 81 years) patients with essential hypertension were studied.
Blood samples were collected after 1 hour of recumbency and after hour of upright standing with 40mg of intravenous furosemide injection for the measurement of plasma renin activity (PRA) and total renin activity. Total renin activity was measured by the cryoactivation method of Sealey et al. Inactive renin activity was calculated as the difference between total renin activity and PRA.
PRA levels in supine position declined with age in both normal subjects and hypertensive patients. Inactive renin activity levels did not change with age in normal subjects, while in hypertensive patients those decreased with age.
Following stimulation of furosemide and standing, PRA levels increased but its responsiveness to the stimuli decreased with age in both groups. In contrast, inactive renin activity levels were not significantly influenced.
These data suggest that a disturbance in the conversion of inactive to active renin may contribute to the low PRA levels in normal elderly subjects and that acute stimulation by furosemide and standing affects mainly active renin.

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Japanese have been considered to have low mortality rate on cardiovascular disease due to less severity of atherosclerotic risk factors. Plasma lipid levels are also suspected to be lower among Japanese than those among foreigners, especially from western countries. The present study was conducted to compare the plasma lipids of other Oriental foreigners with those of Japanese based on the strict matched comparison.
Total cholesterol, triglyceride, phospholipids, free fatty acids and HDL-cholesterol were determined on the fasting plasma obtained from 23 subjects of each group, in which age, sex, and obesity index were strictly identical.
Mean total cholesterol was 230.5mg/dl among Japanese and 232.8mg/dl among foreigners, mean LDL-cholesterol calculated from the equation of Friedewald et al was 136.9mg/dl and 145.4mg/dl respectively, and HDL-cholesterol was 62.4mg/dl and 59.3mg/dl respectively. Mean plasma triglyceride level was 155.8mg/dl among Japanese and 140.2mg/dl among foreigners. Those plasma lipid levels were not statistically different in both groups.
Comparison was also made based on the matched alcohol and smoking habits. There were neither significant differences in plasma lipids in both groups.
This study indicated that there seemed to be absent the racial differences in plasma lipids among Orientals when compared strictly on the basis of the same age, sex and obesity index.

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The purpose of this series of studies is to evaluate clinical findings in elderly patients under prolonged bed-rest, who show poor prognosis. One of the major reasons for the poor prognosis in these patients seems to be impairment of cardiac function. To evaluate the impaired cardiac function in elderly bed-fast patients, cardiac function was measured in 106 patients with cerebrovascular disorders (CVD) and 25 elderly patients bed-fast due to reasons other than CVD, such as bone fracture; comparison was made with 36 age-matched healthy subjects. Heart rate (HR), blood pressure (BP), and cardiac function (cardiac index (CI), stroke index (SI), and total peripheral vascular resistance index (TPRI)) were measured by ECG, sphygmomanometer, and a dyedilution method using indocyanine green dye and ear-piece photocell, respectively. When compaired with healthy subjects, all the patients bed-fast for any reason showed similar HR and BP. CI and SI in the bed-fast patients were 2.17±5.7 (male), 2.02±0.40L/min. M² (female), and 32.0±5.7 (m), 27.7±5.3ml min. M² (f), respectively, which were lower than those of healthy subjects; 2.97±0.44 (m), 2.56±0.51 (f), and 44.1±7.9 (m), 35.6±5.7 (f). TPRIs in the bedfast patients were 3630±950 (m) and 4100±1140 dyns.sec.cm^-15/M²(f), which were higher than those in healthy subjects: 2690±520 (m) and 2990±670 (f). The patients with CVD showed similar HR and BP lower CI and SI, and higher TPRI than those in healthy subjects. According to their activity of daily living (ADL, 0-15), these patients with CVD were classified into three groups; good ADL group (>10) moderate ADL group (>5, ≤10), and poor ADL group (≤5, bed-fast patients). As their ADL became lower, CI and SI became lower and TPRI became higher, although heart rate and blood pressure remained almost constant. The bed-fast patients due to CVD showed more significant impairment of cardiac function than those in patients bedfast due to causes other than CVD, such as bone fracture. However, incidences of complicated diseases such as hypertension, coronary heart disease (ischemic ST-T change in ECG), and myocardial infarction, showed no difference between these two groups.
These findings indicate that elderly patients under prolonged bed-rest have impaired cardiac function and that the impairment is more significant in the patients bed-fast due to cerebrovascular disoders than in the patients with other diseases, such as bone fracture. This impairment of cardiac function seemed to be caused by impossibility of physical movement (bed-rest), the underlying and complicated diseases, and possibly by cerebrovascular disorders themselves.

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Sephadex G-15 column chromatography on Acid Mucopolysaccharide (AMPS) and Total Binding Hexose (TBH) in 24-hour urine specimens were performed to clarify the relationship between these substances and age as well as glucose tolerance.
The examinees were 5 cases of young non-diabetics from 20 to 30 years of age, 5 cases of aged non-diabetics over 60 years old and 6 cases of aged diabetics over 60 years old. In this study, the diabetics were treated with sulfonylureas, but poorly controlled. AMPS and TBH in 24-hour urine specimens were fractionated into three fractions of Fr-I, Fr-II and Fr-III by sephadex G-15 column chromatography. Molecular weight is in order of Fr-I>Fr-II>Fr-III.
1) In non-diabetics, the amount of 24-hour urine AMPS is lower in the aged than that in the young. Also, each amount of AMPS in three fractions is lower in the aged than that in the young.
2) The amount of 24-hour urine AMPS tends to be higher in the aged diabetics than that in the aged non-diabetics. In each AMPS of Fr-I and Fr-II, there is no difference between aged non-diabetics and aged diabetics. Only the AMPS of Fr-III is higher in the aged diabetics than that in the aged non-diabetics. Accordingly, the higher level of 24-hour urine AMPS in the aged diabetics is caused by the higher level of Fr-III AMPS.
3) In non-diabetics, the amount of 24-hour urine TBH is lower in the aged than that in the young. Also, each amount of TBH in three fractions is lower or tends to be lower in the aged than that in the young.
4) The amount of 24-hour urine TBH is higher in the aged diabetics than that in the aged non-diabetics. Also, each amount of TBH in three fractions is lower or tends to be lower in the aged non-diabetics than that in the aged diabetics.
Age and glucose intolerance are accelerating factors for arteriosclerosis. But the present results may suggest that these factors have different roles on the progressive course of arteriosclerosis.

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