To evaluate the effect of obesity on atherosclerosis, health, and longevity in the elderly, we studied the relationship between body mass index, atherosclerosis, and the duration of disability by multivariate analyses.
We analyzed data from 521 residents of the Yokufu-kai home for the aged. They underwent a 50 g oral glucose tolerance test, and autopsies were done after they died. All functional evaluations were done retrospectively from the hospital records. The mean age of the time of death was significantly higher in the overweight group than in the lean group. The incidence of marked cerebral atherosclerosis was significantly higher in the overweight and the obese groups than in the lean and the medium-weight groups. The incidence of cerebral infarction with neurological deficits was significantly higher in the overweight group than in the lean group, but there were no differences in other types of infarction. The incidence of severe coronary artery stenosis was significantly higher in the obese group than in the lean and medium-weight groups, but there was no difference in the incidence of myocardial infarction between groups. There were no differences in the incidence of severe atherosclerosis of the aorta, femoral artery, or renal artery between groups. Patients in the overweight group were bedridden for a significantly longer time than those in the lean group.
We conclude that body weight in the elderly is positively associated with survival. However, overweight subjects suffered from non-fatal cerebral infarction, and prolonged survival was associated with greater disability.

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mas, 8 squamous cell carcinomas, 1 large cell carcinoma, and 1 adeno-squamous cell carcinoma. PCR-SSCP analysis showed that 3 small cell carcinomas (50%), 3 adenocarcinomas (23%), 2 squamous cell carcinomas (25%), and 1 large cell carcinoma (100%) had p53 gene mutations. The abnormalities were found between exons five and eight. The metastatic tumor and the primary tumor had similar mutations. These results suggest that p53 gene mutation may occur before distant metastasis and may be stable during the process of metastasis.

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Bone mineral density (BMD) in the lumbar vertebra was measured by dual energy X-ray absorptiometry (DXA) for diagnosis of spinal osteoporosis. Generally, osteoporosis begins with cortical and trabecular bone loss, and some authors have described the importance of trabecular bone loss in the diagnosis of spinal osteoporosis. Estimated bone mineral content (EBMC) expresses the lowest bone mineral content per square centimeter in the trabecular bone.
We studied EBMC in the os calcis by single energy X-ray absorptiometry (SXA) and BMD in the third lumbar vertebra by DXA. The results were as follows.
1) A phantom, and both EBMC and BMD in the left and right os calcis of a male volunteer were measured by SXA. EBMC was significantly correlated with BMD, and was usually lower than BMD. EBMC and BMD on the X-ray side tended to be higher than those on the opposite side.
2) EBMC and BMD of the os calcis of nine men and eight women with chronic renal failure and diabetes mellitus were measured. EMBC of the os calcis was significantly correlated with BMD, EBMC and BMD in women were lower than those in the men.
3) EBMC of the os calcis in SXA and BMD of the third lumbar vertebra in DXA were measured in 30 female volunteers. Age, weight, height and EBMC of the os calcis were significantly correlated with BMD of the third lumbar vertebra.
EBMC of the os calcis and BMD of the third lumbar vertebra tended to be lower in older subjects. Both of them tended to be higher in heavier subjects and in taller subjects. EBMC of the os calcis and BMD of the third lumbar vertebra in subjects who exercised regularly were significantly higher than those in subjects who did not.
In conclusion, EBMC of the os calcis may indicate trabecular bone mineral content, the loss of which may reflect osteoporosis.

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Macrophage colony-stimulating factor (M-CSF) is a cytokine involed in the development and proliferation of the monocyte/macrophage lineage cells. M-CSF has also been reported to participate in the induction of osteoclasts, and may be important in the destruction of bone and cartilage and the periarticular osteoporotic changes seen in patients with rheumatoid arthritis (RA). We developed a new ELISA technique to measure M-CSF levels in synovial fluid with high sensitivity and reproducibility. The mean M-CSF level in the synovial fluid of patients with RA was 1.38±0.56ng/ml, and that of patients with osteoarthritis (OA) was 0.67±0.13ng/ml. In contrast, serum levels of M-CSF in patients with RA and in normal controls were 1.32±0.50ng/ml and 0.90±0.09 ng/ml, respectively. These differences were both statistically significant.
Since serum M-CSF levels correlate with inflammatory signs obtained from examination of blood, they indicate the general condition of patients with RA. Synovial fuid M-CSF levels increase even in the early phase of RA and remain high despite drug therapy, which suggests that they reflect the condition of affected joints including joint spaces and inflamed synovia more directly than do the levels of serum M-CSF.
Measurement of the M-CSF level in the synovial fluid may be useful in the diagnosis, clinical evaluation, and assessment of the effects of treatment in patients with RA.

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The effect of coenzyme Q₁₀ (CoQ₁₀) on hepatocyte injury during endotoxin (ET) shock in rats was studied with special reference to the role of polymorphonuclear neutrophils (PMN). ET shock was induced by intravenous administration of 5 mg/kg ET, and CoQ₁₀ was given at 20 mg/kg once or 3 times orally or intravenously. We examined plasma glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and glutamate dehydrogenase (GLDH) levels, superoxide production by PMN, the phagocytic activity of PMN, the cytotoxity of PMN to liver cells, and histological changes in the liver.
The CoQ₁₀-treated rats showed lower levels of GOT, GPT, and GLDH than rats treated with ET only. When compared to the group given ET only superoxide production by PMN induced by 2-methyl-6-phenyl-3, 7-dihydroimidazol [1, 2-α] pyrazin-3-one (MCLA) was signifi-cantly inhibited in the group given CoQ₁₀ intravenously and 3 times orally, but there was no significant difference in the group given CoQ₁₀ once orally. However, the level of superoxide production by PMN stimulated by phorbol myristate acetate (PMA) was lower in all CoQ₁₀-treated rats than in those given ET only. There was no difference in either peripheral PMN counts or PMN phagocytes between the CoQ₁₀-treated group and the group given ET only. Histologically, the hepatocyte injury in all groups that received CoQ₁₀ was milder than that in the ET-only group. No hepatocyte cytotoxity by PMN was observed in any group that received CoQ₁₀. These results suggest that both intravenous and oral administration of CoQ₁₀ can modulate the endotoxin-activated PMN, and is useful for preventing hepatocyte injury during ET shock.

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