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Biomedical subjects

R Honda

Publications and source records attributed to R Honda.

At least 109 records · Page 6Linked to original sources
PubMed1988

Selenium, zinc, copper and cadmium concentration in livers and kidneys of people exposed to environmental cadmium.

Selenium (Se), Cadmium (Cd), Zinc (Zn) and Copper (Cu) concentrations have been determined in the kidney cortex, medulla and liver of 21 Cd-exposed and 15 nonexposed autopsied subjects. In the kidney cortex, all four metals were significantly lower in the Cd-exposed subjects than in the nonexposed ones. In the liver Se levels were almost the same in both groups. Significant correlation coefficients between Se and the three metals were found in the kidney cortex of all the subjects. In the liver significant correlation coefficients were only seen between Se and Cu in the Cd-exposed subjects. These results indicated that the distribution of Se in humans chronically exposed to environmental Cd is different from that in humans exposed to environmental organic mercury.

Aged↗
PubMed1987

Cadmium, zinc and copper relationships in kidney and liver of humans exposed to environmental cadmium.

Cadmium, copper and zinc have been determined in kidney cortex, kidney medulla and liver from 51 cadmium-polluted and 122 nonpolluted autopsied subjects. Liver cadmium and zinc were significantly higher in the cadmium-polluted subjects than in the nonpolluted subjects. Kidney cadmium, copper and zinc were lower in the cadmium-polluted subjects because of renal damage. Significant correlations of the three metals were found in the kidney. In the liver the correlation coefficients were significant only between cadmium and zinc.

Adolescent↗
PubMed1987

Mechanism for bone disease found in inhabitants environmentally exposed to cadmium: decreased serum 1 alpha, 25-dihydroxyvitamin D level.

To investigate the mechanism for bone disease caused by exposure to cadmium serum samples were collected from 5 itai-itai disease patients, 36 Cd-exposed residents with renal tubular damage and 17 non-exposed individuals and analyzed for 1 alpha,25-dihydroxyvitamin D[1 alpha,25(OH)2D], parathyroid hormone, beta 2-microglobulin, calcium and inorganic phosphorus. Measurement of percentage tubular reabsorption of phosphate (%TRP) were performed only on the Cd-exposed subjects. Serum 1 alpha,25(OH)2D levels were lower in itai-itai disease patients and cadmium-exposed subjects with renal damage than in non-exposed subjects. Parathyroid hormone and beta 2-microglobulin concentrations in serum were higher in the Cd-exposed subjects. Decrease in serum 1 alpha,25(OH)2D levels were closely related to serum concentrations of parathyroid hormone, beta 2-microglobulin and %TRP. This study suggests that cadmium-induced bone effects were mainly due to a disturbance in vitamin D and parathyroid hormone metabolism, which was caused by the cadmium-induced kidney damage.

Aged↗
PubMed1987

[Influences of percutaneous nephrolithotomy on renal function, an observation using the NAG-index and beta 2-microglobulin as indices].

To examine the influence of percutaneous nephrolithotomy (PNL) on renal function, we measured the activity of urinary N-acetyl-beta-D-glucosaminidase (NAG) and beta 2-microglobulin (beta 2MG) in patients with nephrolithiasis, before and 3, 5, 7, 14 days and 1 month after PNL. With PNL, renal function was recovered within one month, and PNL was thought to be a more protective method than pyelolithotomy. Recovery of renal function was delayed in the cases in which PNL had been attempted over three times. In the patients with preoperative high-grade hydronephrosis, the excretion of NAG and beta 2MG in the urine was delayed. NAG-index was considered to be a more sensitive parameter than beta 2MG to evaluate renal function. The NAG-index and beta 2MG values of bladder urine were in good correlation with those of nephrostomy urine 5 days or more postoperatively. Measurement of the urinary NAG-index 3, 7, 14, 30 days after PNL operation was considered valuable for determining changes in renal function.

Acetylglucosaminidase↗
PubMed1986

Significance of elevated urinary N-acetyl-beta-D-glucosaminidase activity in chronic cadmium poisoning.

N-Acetyl-beta-D-glucosaminidase (NAG) activity and beta 2-microglobulin (beta 2-m) concentration were measured in the urine of inhabitants of a cadmium-polluted area (Cd), including patients with, or suspected, "itai-itai" disease and control subjects. Urinary NAG activity increased with increasing beta 2-m concentration up to about 100 U/g creatinine; above this value the NAG activity did not increase with increasing beta 2-m concentration. Urinary NAG activity thus represents another useful indicator of renal tubular damage caused by Cd poisoning since the mechanisms for the excretion of NAG and beta 2-m into urine are thought to be different.

Acetylglucosaminidase↗
PubMed1986

Sister-chromatid exchanges in the lymphocytes of people exposed to environmental cadmium.

Sister-chromatid exchanges (SCEs) were analyzed from peripheral lymphocyte cultures of 8 men and 16 women who had been exposed to environmental cadmium (Cd), and 6 controls. Average Cd concentrations in blood of the Cd-polluted group were 8.9 micrograms/l for men and 10.0 micrograms/l for women. These were no significant differences in SCE rates between the Cd-polluted and nonpolluted groups. There were no significant correlations between SCE rates and blood or urinary Cd concentrations. Cadmium alone may be an insignificant agent in producing chromosomal damage to peripheral blood lymphocytes.

Aged↗
PubMed1986

Critical concentration of cadmium in kidney cortex of humans exposed to environmental cadmium.

Cadmium (Cd) was determined in kidney cortex and liver of 173 autopsied Japanese. Subjects consisted of 51 persons from Cd-polluted areas ages between 61-94 years and 122 controls ages between 3-90 years. The mean Cd concentrations for the Cd-polluted group were 35.2 micrograms/g wet wt for kidney cortex and 66.7 micrograms/g wet wt for liver. Corresponding values for the control group aged over 60 were 90.1 and 10.7, respectively. Both liver and kidney cortex Cd were analyzed for 127 subjects (41 Cd-polluted and 86 control subjects). The kidney cortex concentration tended to increase linearly with increasing liver concentrations up to approximately 20 micrograms/g of liver Cd; above this value there was no further increase in kidney cortex level. Only three persons showed kidney cortex Cd levels above 200 micrograms/g. The lowest liver Cd levels of the Cd-polluted subjects with renal damage were around 30 micrograms/g. The critical level of kidney cortex Cd may exist below 200 micrograms/g in humans exposed to environmental Cd. The corresponding value for the liver may be below 30 micrograms/g wet wt.

Adolescent↗
PubMed1986

[A combination chemotherapy of cisplatin and etoposide in small cell lung cancer].

Fourteen patients with small cell lung cancer were treated with cisplatin (80 mg/m2 i.v.) and etoposide (300, 400, 500 mg/m2 i.v.). This combination chemotherapy was administered over a three- or four-week period. Eleven of 13 evaluable patients showed a greater than 50% tumor reduction, but there were 3 complete responses and 5 partial responses, giving a response rate of 61%. Four patients who were initially treated achieved major responses. In 9 patients who had received prior chemotherapy, 4 achieved a major response. Of 3 complete responders, 2 patients had previously received etoposide treatment alone. The renal toxicity of this regimen was minimal and no patients developed any clinical symptoms. Nausea and vomiting were well controlled by high-dose metoclopramide and methylprednisolone. All patients, however, experienced appetite loss after treatment. The dose-limiting toxic effect of this regimen was hematologic toxicity. We therefore concluded that the combination of etoposide (300 mg/m2 i.v.) and cisplatin (80 mg/m2 i.v.) is repeatable at 3 or 4 week intervals and effective in patients with small cell lung cancer.

Adult↗
PubMed1985

[Experience with induced hypertension chemotherapy for lung cancer].

Induced hypertension chemotherapy (IHC) using angiotensin II was applied for patients with lung cancer who had not been treated previously, and the results compared with those of preceding conventional chemotherapy as a sequential control. Twenty-nine patients with non-small cell lung cancer (non-SCLC) were treated with MTX and MMC. Response rate among evaluable cases was 23.1% (3/13) for conventional chemotherapy and 18.2% (2/11) for IHC. Twenty-eight patients with small cell lung cancer (SCLC) were treated with VCR, CPA and ACNU. Among evaluable cases, both chemotherapy groups with and without IHC showed the same response rate, 66.7% (8/12). With respect to response rate, there were no differences between conventional chemotherapy and IHC for non-SCLC or SCLC.

Adenocarcinoma↗
PubMed1984

Parathyroid hormone concentration in the serum of people with cadmium-induced renal damage.

Serum parathyroid hormone (PTH) and renal functions were measured in thirty subjects with cadmium-induced renal damage and in the same number of control subjects. The negative correlations between PTH and creatinine clearance (Ccr) and between PTH and percentage renal phosphorus reabsorption (% TRP) were significant in the cadmium (Cd)-exposed group. Serum PTH concentrations were clearly high in two cases of the cadmium-exposed group. Their renal functions decreased severely compared with those of the other Cd-exposed people. The present study indicates that chronic cadmium intoxication could cause increased secretions of PTH, which may be related to cadmium-induced bone damage.

Aged↗
PubMed1984

Copper and zinc levels in serum and urine of cadmium-exposed people with special reference to renal tubular damage.

Urinary copper and zinc concentrations and their serum levels were determined in women environmentally exposed to cadmium, including "itai-itai" disease patients and suspected patients, for evaluating the effect of cadmium exposure on metabolism of such essential metals as copper and zinc in human beings. Copper concentrations in the urine of cadmium-exposed women, especially "itai-itai" patients and suspected patients, were much higher than those of nonexposed women. Zinc concentrations in the urine of cadmium-exposed women, however, were not different from those of nonexposed women. Zinc levels in the serum of the "itai-itai" patients were somewhat lower than those of the nonexposed women. On the other hand, serum copper was almost equal in the cadmium-exposed and the nonexposed women. The correlation coefficient between beta 2-microglobulin amounts and copper concentrations in the urine of all women examined was as high as 0.95. It is concluded that exposure to cadmium will cause an increase in the excretion of copper in urine, which is attributable to renal tubular damage due to the cadmium exposure, and that urinary zinc excretion is not increased by cadmium exposure, even in the patients who suffer from severe renal tubular damage.

Adult↗
PubMed1984

Alpha 1-microglobulin in urine as an indicator of renal tubular damage caused by environmental cadmium exposure.

Alpha1-Microglobulin (alpha 1-m) was determined in the urine of both the cadmium-exposed and nonexposed subjects and was compared with those of other urinary parameters such as beta 2-microglobulin (beta 2-m), glucose, total protein or amino acids. Large amounts of alpha 1-m were detected in the urine of cadmium-exposed subjects. There were significant correlations between alpha 1-m and other urinary parameters. The sensitivity and specificity of both alpha 1-m and beta 2-m as indices of tubular dysfunction caused by cadmium was similar. It was concluded that alpha 1-m in urine seemed to be a useful indicator of renal tubular dysfunction caused by cadmium.

Aged↗
PubMed1984

Iron concentrations in liver and kidney of cadmium-exposed human subjects.

Iron (Fe) concentrations in liver and kidney of cadmium (Cd)-exposed people (11 Itai-Itai patients, 13 persons requiring observation and 4 Cd-exposed persons) were compared with those of nonexposed people. No significant difference in Fe levels in liver was observed between the groups. This fact indicates that anaemia in environmentally Cd-exposed people was not due to iron deficiency in contrast to findings in animal experiments.

Cadmium Poisoning↗
PubMed1983

Urinary N-acetyl-beta-D-glucosaminidase and beta 2-microglobulin in 'itai-itai' disease.

N-acetyl-beta-D-glucosaminidase (NAG) activity in urine was measured in patients with 'itai-itai' disease, from chronically advanced cadmium poisoning. Elevation of NAG activity, however, was not so marked as that of beta 2-microglobulin (beta 2-MG) in the urine of patients and suspected patients. We conclude that the beta 2-MG test is more valuable than the NAG test for evaluating the severity of the renal tubular damage in chronically advanced cadmium (Cd) poisoning.

Acetylglucosaminidase↗