[A fundamental study on periodontal examination--comparison of probing depth between whole- and partial-mouth recording methods].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to I Kato.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Family history of cancer was examined for 9,131 cancer patients who were reported to the Aichi Cancer Registry in 1979-1981, and were over 20 years old at diagnosis. The rate of patients whose parents and/or siblings had cancer of any site was 24.5%. The rate was 9.2% for father, 8.4% for mother, 6.0% for brother(s), and 5.2% for sister(s). A significant site concordance between study patient and family member with cancer was observed for cancer of the breast, colon and rectum, and stomach. The rate of family history of breast cancer patients was 3.3 times higher than the corresponding rate for other cancer patients (3.1% vs 0.9%). Similarly, the ratio was 2.2 in colon and rectum cancer (4.2% vs 1.9%), and 1.6 in stomach cancer (16.5% vs 10.1%). An increased risk of cancer was observed when both brother and sister had cancer. This may suggest an important role of environmental exposure at an early age, as well as genetic factors, in the development of cancer. The age distribution curve of the colon and rectum cancer patients who had a family history of the same cancer was found to be bimodal with the larger peak in the 40s and the smaller peak in the 70s. This may suggest a differential contribution of genetic and environmental factors to the development of colon and rectum cancer.
In order to contribute to the etiological study of thyroid lymphomas, the development of lymphomas in pre-existing chronic thyroiditis was statistically investigated. A total of 5592 female patients (older than 25 years) with chronic thyroiditis diagnosed between 1965 and 1982 at Kuma Hospital in Hyogo Prefecture were followed up until December 31, 1984. From a total of 45623 person-years, 8 new cases of primary thyroid lymphoma were observed (O), all of which were judged to be B-cell type from their immunological or histopathological characteristics. Since the expected number of cases with malignant lymphomas (E1) and the expected number of cases with thyroid lymphomas (E2) were 2.45 and 0.10, respectively, the O/E1 and O/E2 ratios were 3.3 (P less than 0.01) and 80.0 (P less than 0.001), respectively. The average follow-up interval for the patients with thyroid lymphoma was 9.2 years. In the reference group, consisting of cases with Basedow's disease, an increased risk of thyroid lymphoma was not observed. The present results suggest that autoimmune reactions with a notable lymphocytic infiltrate may play an important role in the etiology of lymphomas in the thyroid gland.
To elucidate the risk factors of multiple primary cancer a case-control analysis was performed on 265 cases of multiple primary cancer (a total of 490 cancers) and 1,412 cases of single cancer which were matched for sex, age, year of diagnosis and site of cancer using the data of the Aichi Cancer Registry from 1962 to 1983. As to the family history of cancer three characteristics of multiple primary cancer were revealed, a larger percentage of cancer history in two or more members of their family (8.3% vs 3.6%), a larger percentage of a cancer history in sisters (11.2% vs 5.2%), and a larger percentage of family history of colorectal cancer (4.4% vs 1.6%). These differences were statistically significant and more pronounced in females. In male heavy smokers (30 or more cigarettes per day) the relative risk was elevated to 2.17, in particular for multiple primary cancers including lung cancer. In females the relative risk for drinkers and daily drinkers was 2.02 and 4.22 respectively. As to the kind of alcoholic beverage, the relative risk was highest for beer drinkers. Some kinds of occupations were related to increased or decreased risk of multiple primary cancers, especially in males. The data on family history suggest both genetic predisposition and environmental similarity among family members. Smoking, especially heavy smoking, could be a risk factor of multiple primary cancers which involve smoking-related cancers, but drinking seems to influence the multiplicity of cancer either directly or indirectly.
In 1982, the number of deaths from hematopoietic neoplasms was 5,885 for males and 4,237 for females, which corresponded to about 6% of all malignant neoplasms. The increase in the age-adjusted death rate in the last 10 years was highest for lymphatic leukemia (1.8 times), followed by multiple myeloma (1.7 times), malignant lymphomas (1.3 times) and myelogenous leukemia (1.1 times). In the old-age group, i.e., over 70, the death rate for all types of hematopoietic neoplasms markedly during this period, particularly for multiple myeloma. In children, however, an increase in lymphatic leukemia and a decrease in decrease in myelogenous leukemia were observed. Geographical marked excess in the death rates for malignant lymphomas and lymphatic leukemia in the Kyushu district, especially in the middle- and old-age groups. This may be attributed to the high incidence of adult T-cell leukemia/lymphoma in the southwestern part of Japan. The age-adjusted death rate for malignant lymphomas was slightly higher in rural areas than in urban areas in males in Kyushu.
With regard to the geographical distribution of pancreatic cancer mortality, the relationship of the latitude and of the average temperature to pancreatic cancer mortality was examined. Both internationally and within Japan, a strong positive association between latitude and pancreatic cancer mortality and a strong negative association with the average temperature were observed. The simple correlation coefficient between pancreatic cancer mortality and the latitude was 0.724 for males and 0.725 for females, and that between pancreatic cancer mortality and the average temperature was -0.773 for males and -0.729 for females in 26 countries. In the 47 prefectures in Japan, the coefficient was 0.612, 0.615, -0.589, and -0.630 respectively. Most of these relationships remained statistically significant after controlling for per capita consumption of food which was also related to the pancreatic cancer mortality internationally, such as sugar, eggs, milk and dairy products, oils and fats, pulse, coffee, and fat. Within Japan, an urban-rural effect on the pancreatic cancer mortality was not observed in spite of a higher intake of fat in large cities. There remains the possibility that factors related to latitude or average temperature other than diet may be involved in the occurrence of pancreatic cancer.
Explore the source record for details and available documents.
Lactobacillus casei YIT 9018 (LC 9018) augmented the natural killer (NK) cell activity of spleen cells from inbred BALB/c mice injected intravenously with LC 9018 or intraperitoneally with polyinosinate -polycytidylate. Augmentation of this activity by LC 9018 was also observed in male C3H/He, CBA/N, and C57BL/6 mice. The spleen cells exhibited no cytolytic activity against P815, a cell line insensitive to NK cells. The cytolytic activity of the spleen cells increased 2 days after the injection of 250 micrograms of LC 9018/mouse, peaked on day 3, and gradually declined thereafter. The increase caused by LC 9018 was also observed in normal and Meth A-bearing mice. In vitro treatment with anti-asialo GM1 antibody plus complement completely abrogated the LC 9018-augmented murine NK cell activity. The NK activity on the 3rd day after LC 9018 injection was reduced by in vitro treatment with anti-Thy 1.2 monoclonal antibody plus complement to half of that observed when treatment was with complement alone. This suggests that there were two populations of NK cells in the spleen cell suspension derived from LC 9018-treated mice. One population was asialo GM1-positive and Thy 1-negative, the other was asialo GM1-positive and Thy 1-positive.
The cytotoxic action of leukocidin from Pseudomonas aeruginosa was supported by the following observations. (i) The destruction of rabbit leukocytes by the toxin was reduced in the absence of Ca2+ and stimulated by the addition of calcium ionophore A23187 but inhibited by EDTA, EGTA, and TMB-8, an antagonist of intracellular Ca2+ transport. (ii) Uptake of 45Ca into leukocytes exposed to the toxin was enhanced about threefold the rate of uptake into untreated cells. The increased 45Ca uptake into the cells was slightly inhibited by trifluoperazine, an inhibitor of Ca2+-calmodulin activity, but not by ruthenium red. (iii) Pseudomonal leukocidin enhanced rapidly the labeling of phosphatidylinositol, polyphosphoinositides, phosphatidic acid, and lysophosphatidic acid from [32P]phosphate. The time course experiments of the labeling and breakdown of these phospholipids suggested that the initial action of this toxin was to stimulate phosphatidic acid production, presumably causing a rapid metabolic change of phosphatidylinositol correlating with the activities of phosphatidylinositol-specific phospholipase C and 1,2-diacylglycerol kinase. It was considered that a rapid formation of phosphatidic acid and degradation of polyphosphoinositides might be related to a Ca2+ movement from extra- and intracellular space. (iv) In leukocytes exposed to the toxin, acid phosphatase activity as a marker enzyme of lysosome was activated up to 75% of the lysosomal enzyme before cell destruction. The leakage of lysosomal enzyme from the cells occurred at the almost same time as leukocyte destruction. The mode of cytotoxic action of pseudomonal leukocidin is discussed.
The leukocytotoxic toxin pseudomonal leukocidin, produced by Pseudomonas aeruginosa, was radioiodinated with chloramine-T reagent. Binding of [125I]leukocidin to rabbit polymorphonuclear leukocytes was found to be concentration dependent at 37 degrees C. A Scatchard plot of binding data was linear, indicating that leukocidin binds to a single population of sites. The dissociation constant, KD, was calculated from the Scatchard plot to be 2.5 X 10(-7) M, and the number of binding sites per leukocyte was approximately 4.4 X 10(5). Unlabeled leukocidin or antileukocidin antibody reduced the binding of [125I]leukocidin to the leukocytes. A leukocidin-binding protein was extracted from rabbit polymorphonuclear leukocytes with Triton X-100 and purified by leukocidin-Sepharose 4B affinity column chromatography. Approximately 60 micrograms of binding protein was obtained from 8.1 mg of material extracted from the leukocytes. The binding protein had a molecular weight of about 50,000 as shown by sodium dodecyl sulfate-polyacrylamide slab gel electrophoresis and staining with silver nitrate. Under nondenaturing conditions, its molecular weight was also about 50,000, as shown by gel filtration-Sephadex G-200 chromatography. The 50,000-dalton protein purified in this way from rabbit polymorphonuclear leukocytes competitively inhibited the binding of leukocidin to leukocytes and inactivated leukocidin activity. With equimolar amounts of the 50,000-dalton protein and leukocidin, up to 90% inactivation of leukocidin was observed.
The ratio of leukocidin-producing strains to clinical isolates of Pseudomonas aeruginosa was investigated together with the production of protease, elastase, and exotoxin A. We also examined whether these strains contain the common antigen which resides in the cell wall. By using the agar gel diffusion test with specific antisera, we found that 87 of 90 (96.7%) of clinical isolates produced leukocidin. Protease, elastase, and exotoxin A were also produced at high percentages. The common antigen was found to exist in all strains. Next, to estimate antileukocidin antibody in the sera of patients, we used an enzyme-linked immunosorbent assay with horseradish peroxidase-protein A. The sera of 39 patients with diffuse panbronchiolitis (DPB) were investigated for antileukocidin antibody. The mean antileukocidin titer in the sera of 17 DPB patients who were not infected with P. aeruginosa and 5 DPB patients who were transiently infected with the bacteria was about the same as the mean antileukocidin titer in the sera of 11 healthy controls, whereas the mean antileukocidin titer in the sera of 17 DPB patients who were persistently colonized was significantly higher than that in healthy controls. These results indicate that leukocidin was produced at the local site of infection in DPB patients.
The effects of visual fixation upon caloric nystagmus were computed in each parameter as a measure. The percentage reduction established with slow-phase velocity best distinguished normal from abnormal visual fixation at the line of 60%. However, if a +/- 5% safety margin is taken into account, 11 of 176 ears showed false-negatives. The number of nystagmus beats in normals decreased markedly during the period of fixation. In abnormals, the number of nystagmus beats increased definitely during the fixation period. Based on this fact, the product of slow-phase velocity multiplied by the number of nystagmus beats was assessed as the fixation-suppression index. As a result, 11 ears showing false-negative slow-phase velocity decreased to 2 ears. Thus, this modified fixation-suppression index seems to be an appropriate parameter to separate normal from abnormal fixation-suppression of caloric nystagmus.
Explore the source record for details and available documents.
Explore the source record for details and available documents.