Biomedical subjects
Publications and source records attributed to H Mikami.
Renal dipeptidase purified from swine kidney hydrolyzed N-formimidoyl thienamycin, carpetimycins A and B, and Sch29482, but not azthreonam, penicillin G, or cephaloridine.
The activities of T-1982 (sodium 7 beta-[(2R, 3S)-2-(4-ethyl-2, 3-dioxo-1-piperazine-carboxamido)-3-hydroxybutanamido]-7 alpha-methoxy-3-[(1-methyl-1H-tetrazol-5-yl)thiomethyl]-3-cephem-4-carboxylate) against various gram-positive and gram-negative bacteria were compare with those of cefmetazole, cefoxitin, cefazolin, and cefoperazone. T-1982 was active against both gram-positive and gram-negative bacteria, including genera resistant to the other cephalosporins. T-1982 exhibited greater activity than did cefmetazole, cefoxitin, cefazolin, or cefoperazone against Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, and Serratia marcescens and was also highly active against Bacteroides fragilis. T-1982 was as stable to various beta-lactamases as were cefmetazole and cefoxitin. The therapeutic activities of T-1982 in mice experimentally infected with various gram-negative bacteria were superior to those of cefmetazole, cefoxitin, cefazolin, and cefoperazone.
In spontaneoulsy hypertensive rats (SHR), the hypotensive effect of captopril (30 mg/kg/day per os for 4 days), which inhibits the converting enzyme when given orally was significantly potentiated rather than suppressed by aprotonin (100,000 KIU/day s.c. for 7 days), but was not affected by indomethacin. These findings suggest that neither the kallikrein-kinin system nor the prostaglandin system is involved in any of the hypotensive actions of captopril in SHR other than the inhibition of the converting enzyme.
We examined the role of dietary electrolytes and humoral factors in causing seasonal changes in blood pressure. Normal subjects had no seasonal difference in blood pressure, although urinary sodium and norepinephrine were significantly higher in winter than in summer. In patients with essential hypertension blood pressure, urinary sodium and norepinephrine excretion and plasma norepinephrine concentration were significantly higher in winter. Plasma renin activity, plasma and urinary aldosterone and urinary kallikrein excretion were not significantly different between the two seasons in both normal subjects and hypertensive patients. In conclusions, the blood pressure of patients with essential hypertension has a seasonal variation with higher pressures in the winter than in the summer. Increased sympathetic nervous activity and an increased load of sodium presented to the kidney for excretion may be contributing factors in the rise in blood pressure in winter in patients with essential hypertension.
Two sisters were found to have Bartter's syndrome. Both had hypokalemia, hyperreninemia, normal BPs, and decreased pressor responses to angiotensin II. During a water diuresis, patient 1 had an abnormally low distal tubular fractional reabsorption of chloride initially, but this normalized after hypokalemia was corrected for one year. Patient 2 had no demonstrable defect in chloride transport. Hypokalemia in Bartter's syndrome may be caused by some hereditary mechanisms other than defective reabsorption of chloride in the distal tubules.
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There have been many reports on lung cancer among chromate workers. Chromate compounds are thought to be a carcinogen and lung cancer among chromate workers is considered one of the occupational lung cancers. Recently, it is debated that metaplastic and hyperplastic changes of bronchial epithelium are revealed or not to the development of bronchogenic carcinoma. Histopathological study on changes of bronchial epithelium among chromate workers was performed in order to clarify the effect of chromate compounds to bronchial epithelium. The subjects were 14 cases of lung cancer among chromate workers. As a control, 18 cases of non cancer among chromate workers. Lung tissue which was obtained at necropsy or surgery was fixed by formalin and was produced cross-sections and was stained on Haematoxylin-Eosin. The results were as follows. 1. Of examined 235 cross-sections, basal cell hyperplasia of bronchial epithelium was found in 13 per cent. Squamous metaplasia was found in 29 per cent, on the contrary, atypical metaplastic changes were observed in 34 per cent. 2. Of four cases of carcinoma in situ and two cases of small invasive carcinoma, four cases revealed development from atypical squamous metaplasia to precancerous changes. 3. These cases developed invasive carcinoma from atypical squamous metaplasia for a long period, of which were found by successive exfoliative cytology of sputum. From these findings, it was concluded that inhalation of chromate dust affected bronchial epithelium and caused highly atypical squamous metaplasia which developed to carcinoma in situ and finally to invasive carcinoma.
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Captopril was given alone and in combination with diuretics to 49 patients with hypertension for 1 to 12 mol Within 2 mo blood pressure reduction correlated with pretreatment plasma renin activity and response to the infusion of angiotensin II antagonist, but these effects were not present at 4 mo. Plasma and urinary aldosterone were suppressed but serum converting enzyme activity, plasma bradykinin, kallikren, and prostaglandins (E and F) were in the normal range effect of captopril. Despite sustained reduction of blood pressure, plasma catecholamines were not elevated and urinary catecholamines were suppressed in patients on captopril alone. It is concluded that another mechanism, such as enhancement of renal or local kinin-prostaglandin system, as well as suppression of the renin-angiotensin-aldosterone system may be involved in the long-term efficacy of captopril. Sympathetic activity may also be depressed and contribute to the hypotensive effect.
The effect of age on the levels of active and trypsin-activatable inactive plasma renin was examined in 41 normal subjects and 54 patients with essential hypertension, during recumbency and after stimulation with furosemide and ambulation. Active renin levels in supine subjects and patients decreased with age. Inactive renin levels did not change with age in normal subjects, whereas in hypertensive patients they decreased with age. Following stimulation with furosemide and ambulation, the levels of active renin increased but the responsiveness to stimulus decreased with age in both groups. In contrast, inactive renin levels slightly increased after furosemide administration and ambulation, resulting in increased proportion of active to total renin. These data show that an acute stimulation with furosemide and ambulation affects mainly the active form of plasma renin, and the effect of age on inactive plasma renin in normal subjects may be different from that in patients with essential hypertension.
Methylguanidine concentration in blood cell of nondialysed patients with chronic renal failure was quantitatively determined by the method of the present authors. We also determined tissue methylguanidine concentrations in the liver, blood cell, kidney, colon, muscle and brain of uremic rat experimentally produced by Platt's method. Methylguanidine concentrations in blood cell and tissues except the brain of the uremic rats and in blood cell of the uremic patients were 5--7 times higher than those in their serums. An increased methylguanidine concentration in the liver of the uremic rat receiving 40% protein diet was observed. These results imply that methylguanidine acts as one of the important uremic toxins in the intracellular space except for the brain, and suggest that the liver specifically affects the formation of methylguanidine.
The effect of aging on urinary kallikrein excretion (UkalV) was investigated in 54 normal subjects, 11-88 yr old, and 37 patients with essential hypertension, 17-82 yr old. Urinary sodium, potassium, and aldosterone excretion (U(Ald)V) were also measured in these subjects. Urinary sodium and potassium excretion in both normal subjects and hypertensive patients did not significantly change with aging. In normal subjects, U(kal)V (r = 0.45; P less than 0.001) and U(Ald)V (r = 0.58; P less than 0.01) significantly decreased with increasing age. U(kal)V was positively correlated with U(Ald)V (r = 0.44; P less than 0.001). In contrast, the hypertensive patients had a significant decrease with age in U(Ald)V (r = -0.36; P less than 0.05), but no significant age-related change in U(kal)V. No significant correlation between U(kal)V and U(Ald)V was observed in the hypertensive patients. In individuals less than 60 yr old, there was no significant difference in U(kal)V values between normal subjects and hypertensive patients. Hypertensive patients more than 60 yr old excreted more urinary kallikrein than normal subjects of the same age group (P less than 0.05). In conclusion, the age-related decrease of U(kal)V in normal subjects may be due to the reduced activity of the renin-angiotensin-aldosterone system. It remains to be elucidated whether the absence of the age-related decrease in U(kal)V in hypertensive patients is related to the pathogenesis or pathophysiology of essential hypertension.
The effect of age on active and cryoactivatable inactive plasma renin levels was examined in 58 normal subjects and 58 patients with essential hypertension during recumbency and after stimulation with furosemide and ambulation. Active renin levels declined with age in both supine subjects and patients. Inactive renin levels did not change with age in normal subjects, while in hypertensive patients they decreased with age. Following stimulation with furosemide and ambulation, the levels of active renin increased but its responsiveness to the stimulus decreased with age in both groups. In contrast, inactive renin was not significantly influenced by furosemide administration and ambulation. These data show that an acute stimulation with furosemide and ambulation affects mainly the active form of plasma renin, and that the effect of age on inactive plasma renin in normal subjects may be different from that in patients with essential hypertension.
The genesis of unusual radiographic shadows by bronchi filled with tumor cells is reported. These shadows, similar to those caused by mucus or pus, are rod-like and indicate the replacement of air by water dense materials. The unifying term, "bronchial cast shadow" is proposed as the radiographic diagnostic sign.
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