The incidence of intracerebral hemorrhage over 13 years is compared between two Hisayama cohorts. Among men aged 40 years or older, the annual incidence declined significantly from 3.1/1,000 in the early cohort (1961-1970) to 1.2/1,000 in the recent cohort (1974-1983). Massive ganglionic hemorrhage decreased, while small or medium-sized intracerebral hemorrhage increased in the recent cohort on pathologic or computed tomographic examination. These trends could be due to the reduced prevalence of hypertension in the Hisayama population. The association of serum total cholesterol with intracerebral hemorrhage is discussed based on the results during a 22-year follow-up period.
SUMMARY l b elucidate the relation of hematocrit (Hct) to the incidence of cerebral infarction, a prospective follow-up study of 16 years (1965-81) was performed in a general population sample of 1220 Hisayama residents aged 44 and over, of both sexes. Most of the subjects who died during the follow-up period were autopskd, the rate being 89.0%.Hct decreased with advancing age in men, but not in women. The average value for Hct was significantly lower in women than in men. According to the mean value ± 1 SD of Hct, the subjects were grouped into 3, in each sex as follows: low (<35%), normal (35-45%) and high (2=45%) for men, and, low (<30%), normal (30-40%) and high (2:40%) for women.During the follow-up period, cerebral infarction occurred in 117 patients. The cumulative incidence of cerebral infarction In the low Hct group for men was the lowest, even after adjustments for age and blood pressure. Conversely, the incidence in the low Hct group of women was significantly higher than that in the normal Hct group and was consistently increased with tune during 2-5 years of the follow-up. After the 6th year or later, however, the incidence was gradually but significantly increased hi the Ugh Hct group, compared with the normal Hct group. Since Hct levels were related with other variables such as serum total cholesterol, serum total protein, Quetelet index and prevalence of hypertension in both sexes, heavy alcohol consumption in men, and glucose Intolerance in women, such variables were taken into account using Cox's proportional hazards regression model. The low Hct in women remained important as an independent risk factor of cerebral Infarction.The sex difference hi the role of Hct as a cause of cerebral infarction was discussed, taking into consideration the interrelationship between Hct and other risk factors.
Between October 1981 and September 1989, 564 patients admitted to the Department of Psychiatry of the Hospital of Oita Medical University received antipsychotic treatment. Ten (1.8%) of these patients developed neuroleptic malignant syndrome. This incidence is significantly greater than that reported in a group of other studies (27/17,811, 0.2%). We compared the characteristics of this sample with known risk factors for neuroleptic malignant syndrome. It is possible that Japanese people are at an increased risk for developing neuroleptic malignant syndrome. Psychomotor excitement, refusal of food, a weight loss of greater than 1 kg per week and oral administration of haloperidol at 15 mg/day or above were found to be risk factors for developing the neuroleptic malignant syndrome.
Monocytes from peripheral blood and synovial fluid of patients with definite and classic rheumatoid arthritis spontaneously produced significantly greater amounts of prostaglandin E2 (PGE2), leucotriene B4 (LTB4), and interleukin-l, (IL-10) than samples of peripheral blood from normal controls. Peripheral blood monocytes from patients with rheumatoid arthritis produced significantly greater amounts of PGE2 than control samples when stimulated with lipopolysaccharide. There were no significant differences in the spontaneous release of superoxide or N-acetyl-i-D-glucosaminidase by peripheral blood monocytes between patients and healthy controls. Both stimulated and unstimulated peripheral blood monocytes from patients with definite or classic rheumatoid arthritis produced significantly greater amounts of PGE2 than samples from normal controls. This was true, regardless of the stage of disease and the presence or absence of roentgenological joint abnormalities. Amounts of N-acetyl-P-Dglucosaminidase released by peripheral blood monocytes from patients correlated positively with the erythrocyte sedimentation rate (ESR) and negatively with duration of disease. Amounts of IL-1lB and N-acetyl-13-D-glucosaminidase released from the peripheral blood monocytes of patients who had had their disease for less than one year were significantly higher than those of normal controls. There were no significant correlations between the types of treatment and the amounts of PGE2, LTB4, IL-1l6 or N-acetyl-,3-D-glucosaminidase released by peripheral blood monocytes in patients with rheumatoid arthritis.The findings suggest that monocytes are activated in patients with rheumatoid arthritis both at the onset of disease and during its chronic phase, and that they produce large amounts of mediators which may have a role in the induction and extension of the inflammatory process which leads to tissue damage.
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