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Biomedical subjects

T Kido

Publications and source records attributed to T Kido.

At least 181 records · Page 10Linked to original sources
PubMed1988

Diaphragm function after pulmonary resection. Relationship to postoperative respiratory failure.

We studied the lung mechanics and respiratory muscle function in 20 patients undergoing pulmonary resection. Transdiaphragmatic pressure (delta Pdi) during quiet breathing did not show any remarkable change after the operation (9.5 +/- 1.1 to 10.9 +/- 1.0 cm H2O), while the ratio of abdominal to transdiaphragmatic pressure changes (delta Pab/delta Pdi) revealed a significant difference between the preoperative and the early postoperative periods (0.32 +/- 0.06 to 0.00 +/- 0.11, p less than 0.05). The postoperative delta Pab/delta Pdi correlated significantly with the work of breathing (r = -0.60, p less than 0.01). The maximal transdiaphragmatic pressure (Pdimax) decreased significantly after operation (75.0 +/- 15.8 to 32.8 +/- 12.4 cm H2O, p less than 0.05), with no significant change in the maximal inspiratory mouth pressure (MIP) (74.2 +/- 16.8 to 39.5 +/- 11.6 cm H2O). Four of 20 patients developed respiratory failure postoperatively and required mechanical ventilation. delta Pab/delta Pdi in these patients was significantly lower than in the other patients (-0.62 +/- 0.24 versus 0.16 +/- 0.09, p less than 0.005). Our results suggested that during quiet breathing diaphragmatic function was preserved and intercostal/accessory muscles recruitment increased, but maximal strength of the diaphragm might be reduced in patients undergoing pulmonary resection.

Adult↗
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

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

[Fundamental and clinical studies of flomoxef in the pediatric field].

Fundamental and clinical studies of flomoxef (FMOX, 6315-S) were conducted and the obtained results are summarized as follows. For the pharmacokinetic investigation, FMOX at 10 or 20 mg/kg was administered by intravenous drip infusion over 30 minutes. In the 10 mg/kg group, the maximum blood concentration was reached just after completion of the drip infusion with the mean concentration of 30.3 +/- 4.5 micrograms/ml, and the mean half-life was 0.734 +/- 0.196 hour. The 6-hour urinary excretion rate was 72.3%. In the 20 mg/kg group, which also showed the peak concentration immediately after completion of the drip infusion, the mean peak blood concentration was 54.3 +/- 9.7 micrograms/ml and the mean half-life was 0.628 +/- 0.185 hour. The 6-hour urinary excretion rate was 69.3%. The urinary recovery tended to be lower in children than in adults. Between 10 mg/kg and 20 mg/kg, a definite correlation was observed between dose levels and blood concentrations. In the clinical investigation conducted with a total of 30 patients (22 with respiratory tract infection, 3 with lymphadenitis, 2 each with urinary tract infection and cellulitis, and 1 with acute osteomyelitis), FMOX was found to be excellent in 14 cases, good in 9, fair in 1, poor in 1, and not evaluable in 5. The efficacy rate was, therefore, 92.0%. In the bacteriological evaluation, 8 out of 12 clinically isolated strains were eradicated, 2 unchanged and 2 unknown. The elimination rate was 80.0%. Regarding side effects, no abnormal clinical symptoms were observed. As abnormal laboratory values, eosinophilia, prolongation of APTT, increased platelet count, and a slight elevation of GOT were observed.

Adolescent↗
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↗