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Volume 34 (1979 - 198･･･
- Issue 6 Pages 719-
- Issue 5 Pages 643-
- Issue 4 Pages 565-
- Issue 3 Pages 465-
- Issue 2 Pages 371-
Volume 34, Issue 4
Displaying 1-10 of 10 articles from this issue
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Kiyomi Aoyama, Takero Kaido, Yoshihiko Miura, Keiko Nakazaki, Megumu K ...1979 Volume 34 Issue 4 Pages 565-573
Published: October 30, 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESS(1) Cohort analyses were made of the total and partial death rate for malignant neoplasms in both sexes.
(2) The cohort phenomenon was shown in the transition of the total death rate induced by malignant neoplasms in both sexes. The age-specific death rate curve forms a line similar to the rectilinear pattern seen in the middle age groups and above.
(3) Decreasing cohort phenomena were seen in the uterine and stomach cancer analyses. Both forms of cancer are now on the decrease.
(4) Increasing cohort phenomena were demonstrated in the lung and pancreas cancer analyses for both sexes. The rate of increase has nearly reached zero, and the age-specific death rate curves are approximately straight lines.
(5) A two-phase cohort phenomenon was observed in the liver cancer analysis for females.
(6) The transition of the death rate for leukemia showed cohort phenomena for both sexes. However, a final age-specific death rate curve is being reached, and the nature of this disease has changed.
(7) The transition of the death rates for malignant neoplasms according to site can be classified as with and without cohort phenomena. Those that showed cohort phenomena can be classified into four types.
a) The simple decreasing cohort phenomenon
b) The two-phase cohort phenomenon
c) The increasing cohort phenomenon that produces an age-specific death rate curve with a rectilinear pattern.
d) The increasing cohort phenomenon in all age groups.
(8) Suggestions for health control and related etiology were made in relation to the cohort phenomenon shown in malignant neoplasms.View full abstractDownload PDF (773K) -
Koji Nogawa, Etsuko Kobayashi, Arinobu Ishizaki, Takashi Kato, Chieko ...1979 Volume 34 Issue 4 Pages 574-579
Published: October 30, 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSThe study covered 40 Itai-itai disease patients and 61 suspected patients who were considered to be heavily damaged by cadmium. The reference group was comprised of 27 inhabitants in a nonpolluted area.
Blood specimens were collected, and the erythrocyte counts, hemoglobin and hematocrit values were measured. Blood and urine were also examined biochemically. Erythrocyte counts, hematocrit and hemoglobin values decreased significantly in the Cd-exposed groups. The mean M.C.H., M.C.V. and M.C.H.C. were higher in the Cd-exposed groups than in the reference group.
Significant correlation coefficients in the Cd-exposed groups were observed between the erythrocyte counts and abnormal blood or urine, e.g. Cd, RBP, β2-microglobulin and lysozyme in the urine and creatinine, BUN, total protein, uric acid, alkaline phosphatase, TRP%, LDH and iron in the plasma.
The correlation coefficients between the erythrocyte counts and the levels of creatinine and BUN in plasma were -0.61 and -0.50, respectively.
We concluded that anemia in patients with or suspected of having Itai-itai disease is not hypochromic nor microcytic. Renal damage caused by cadmium exposure may be one of the factors that cause the anemia.View full abstractDownload PDF (800K) -
Nobuhiro Konno1979 Volume 34 Issue 4 Pages 580-588
Published: October 30, 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSPhosvel is an organophosphorus pesticide that produces a delayed neurotoxic effect in hens. Residues of Phosvel have been reported to be present in adipose tissue of birds up to 21∼28 days following a single oral dose of 250mg/kg. We here describe accumulation of the pesticide in the fatty tissue of hens given a single, daily administrations of small doses.
Hens (22 months old) were given a single oral dose of 5, 10 or 20mg/kg b.w. of Phosvel daily, and were killed 24 hours after test periods of 7, 14, 21 or 28 days. Three birds that developed signs of paralysis died 3 days before the final dose (28 days).
The concentraion of Phosvel in the fat of hens given 5mg/kg and 10mg/kg increased during the first 21 days, but fell slightly by the termination of the experiment at day 28. Phosvel storage in the fat of birds given 20mg/kg was relatively stable up to 14 days of administration, but increased sharply thereafter. At day 25, the Phosvel concentration in the fat reached a maximum. The level of Phosvel in the fat was proportional to the amount of the daily dose. Three birds given 10mg/kg showed signs of ataxia after the 19th∼26th dose and paralysis after the 20th∼28th dose. Six hens given 20mg/kg showed signs of ataxia after the 17th∼20th dose and paralysis after the 21st∼26th dose.
The results clearly show that Phosvel accumulated in the adipose tissue of hens after continuous exposure and that delayed neurotoxicity in hens was produced following the daily oral administration of 10∼20mg/kg.View full abstractDownload PDF (1221K) -
Hisao Matsumoto1979 Volume 34 Issue 4 Pages 589-597
Published: October 30, 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSAdsorption of HgCl2 and CH3HgCl in aqueous solutions by the hair was measured at 20°C and 30 °C. The concentration of adsorbed Hg was higher at 30°C than 20°C; both isotherms adapted well to Freundrich equation.
An increased mercury concentration on the hair was clear even in extremely dilute mercury solutions.
Desorption of HgCl2 adsorbed by the hair was poor when hair was washed with HCl solutions. But the CH3HgCl on the hair was eluted very well with 1N HCl solution. A washing with 1mM of L-cysteine did not elute the mercury on the hair much.
Thus, desorption of only the outer-adsorbed mercury on head hair is considered impossible. Measurement of methylmercury is recomended as a sign of internal organic mercury absorption.View full abstractDownload PDF (1253K) -
Kotaro Yamamura, Keiko Aoshima1979 Volume 34 Issue 4 Pages 598-604
Published: October 30, 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSAudiometrically normal, male students (ages 18 to 22, 6-12 persons) were exposed to intermittent and steady-state noise (480 minutes, pink noise), after which the Temporary Threshold Shift (TTS) and urinary 17 OHCS levels were measured.
The rise-decay time of an exposed noise (trapezoidal noise, cf, Fig. 1) was ca 500ms and the duration was 6.5 seconds. Peak levels of the intermittent noises were 80dB (A) and 90dB (A).
Experimental Conditions
Exposure 1: Control
Exposure 2: Peak level 90dB (A); duty cycle 2 minutes.
Exposure 3: Peak level 90dB (A); duty cycle 1 minute.
Exposure 4: Peak level 90dB (A); duty cycle 24 seconds.
Exposure 5: Peak level 90dB (A); duty cycle 12 seconds.
Exposure 6: Peak level 80dB (A); duty cycle 2 minutes.
Exposure 7: Peak level 80dB (A); duty cycle 1 minute.
Exposure 8: Peak level 80dB (A); duty cycle 24 seconds.
Exposure 9: Peak level 80dB (A); duty cycle 12 seconds.
Exposure 10: Steady state noise; sound level 90dB (A).
Exposure 11: Steady state noise; sound level 80dB (A).
Results
(1) TTS growth
The coefficients of regression of TTS growth by exposures 1, 2, 3, 6, 7 and 8 were not significant. The coefficient of regression of TTS growth induced by exposures 4, 5, 9, 10 and 11 were significant.
The TTS2 of noise exposure for 480 minutes, calculated according to regression equations, were determined by the on fraction rule. This gave a TTS for exposures 4 and 5 (on fraction 25%, 50%) that equaled 29% and 40% respectively of the TTS of exposure 10.
(2) Urinary 17 OHCS levels
There was a significant difference between the 8 hours-urinary 17 OHCS levels induced by exposures 6 and 7 and that induced by the control. No significant difference appeared between the urinary 17 OHCS levels induced by other noise exposures (exposures 8, 9 and 11) and that induced by the control.
The coefficient of regression between the 8-hour-urinary 17 OHCS levels to the logarithm of the on fraction was significant.View full abstractDownload PDF (834K) -
Mutsuo Ishizaki1979 Volume 34 Issue 4 Pages 605-611
Published: October 30, 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSThe amounts of daily arsenic intake from food have been reported by the joint FAO/WHO Expert Commitee on Food Additives, by Schroeder and Balassa, and by Nakao. Published values vary widely from 0.073mg per capita per day to 2.0mg per capita per day, mainly because no accurate methods for the determination of arsenic in various foods have been established.
I previously reported an accurate and highly sensitive method for the determination of arsenic in biological material that uses combined solvent extraction and carbon furnace atomic absorption spectrometry. I here report the accurate amounts of arsenic contained in various fuods. The amount of arsenic in the average Japanese diet was calculated based on the analyzed data from this study, and the per capita intake of foods was compiled by food groups. The daily intake of arsenic was determined to be approximately 0.126mg per capita per day in a diet of 1, 399g per day. This value compared fairly with Nakao's reported value of 0.073mg to 0.173mg per capita per day. The principal source of arsenic in the Japanese diet is fish, 72%; followed by seaweed, 10%; and rice, 10%.View full abstractDownload PDF (913K) -
Hideki Ohno, Hideo Watanabe, Chiaki Kishihara, Hitoshi Ochi, Eimatsu T ...1979 Volume 34 Issue 4 Pages 612-619
Published: October 30, 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSUntrained healthy male volunteers were studied to observe the effects of muscular exercise (bicycle ergometer, 920kpm/min for 15min and 30min) on the levels of carbonic anhydrase B (CA-B) and C (CA-C) isozymes and 2, 3-diphosphoglycerate (2, 3-DPG) in the blood. Significant decreases in the levels of CA-B and total esterase activity were observed after 15min and 30min of exercise, but the level of CA-C did not vary much. The level of 2, 3-DPG increased after 30min of exercise. Positive correlations were observed between the levels of CA-B and total esterase activity after each exercise (r=0.675, 0.619). The decrease in total esterase activity is caused by the decrease in CA-B. The mean value of 2, 3-DPG after exercise increased to 19.3per cent after 30min of exercise. This indicates that the magnitude of increase in 2, 3-DPG was sufficient to shift the oxygen dissociation curve to the right. A negative correlation was found between the levels of CA-B and 2, 3-DPG after 30min of exercise (r=-0, 618), but no significant correlation was found after 15min of exercise. The blood lactate-pyruvate ratio increased above the pre-exercise values after 15min, but not after 30min of exercise. After 30min of exercise the increase in lactate concentration and the change in 2, 3-DPG showed good correlation (r=0.667). These observations suggest that the decrease in CA-B plays a part in the combination of 2, 3-DPG and deoxyhemoglobin under hypoxic conditions, and that enhancement of oxygen delivery through an increase in 2, 3-DPG is important for adequate homeostatic adjustment to prolonged exercise.View full abstractDownload PDF (1046K) -
Kanji Matsui, Kazuo Nomiyama1979 Volume 34 Issue 4 Pages 620-623
Published: October 30, 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSTesticular injury is known to be provoked by a single dose of cadmium administered to rats or mice. We have studied the effects of environmental temperatures on cadmium-induced testicular injury. Macroscopic experiments were performed twice. In the first experiment, 18, 4-week-old male rats of the Sprague-Dawley strain were acclimatized to environmental temperatures of 8°, 22°or 32°C for 10 weeks; then they were given a single subcutaneous dose of cadmium chloride at levels of 0, 3, 6 or 12mg/kg. In the second experiment, 37, 4-week-old male rats were acclimatized to 8°, 22°or 38°C for 4 weeks, after which they were given a single injection of 0, 3, 6, 12 or 24mg/kg cadmium chloride. The degree of cadmium-induced testicular and epididymal hemorrhage was related to the environmental temperature: the higher the environmental temperature, the more severe the cadmium-induced testicular injury.View full abstractDownload PDF (3987K) -
1979 Volume 34 Issue 4 Pages 639a
Published: 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSDownload PDF (88K) -
1979 Volume 34 Issue 4 Pages 639b
Published: 1979
Released on J-STAGE: February 17, 2009
JOURNAL FREE ACCESSDownload PDF (88K)
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