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Biomedical subjects

N Terao

Publications and source records attributed to N Terao.

At least 37 records · Page 2Linked to original sources
PubMed1992

Suppressive effect of soluble factor(s) derived from Prevotella loescheii ATCC 15930 on proliferation of human lymphocytes.

Soluble sonic extracts of Prevotella loescheii caused a dose-dependent inhibition of human peripheral blood lymphocyte proliferation by mitogen and of the proliferation of a leukemic cell line, BALL-1, when assessed by DNA synthesis (3H-thymidine incorporation). RNA (3H-uridine incorporation) and protein (3H-leucine incorporation) synthesis were similarly altered after exposure to the extract. There was no effect on cell viability as measured by either trypan blue exclusion or extracellular release of the cytoplasmic enzyme lactate dehydrogenase. Preliminary characterization indicates the suppressive factor(s) derived from P. loescheii to be a protein since it is heat-labile and trypsin-sensitive. The factor eluted in a peak on a high-pressure liquid chromatography gel filtration corresponding to a molecular weight of approximately 32,000. Since black-pigmented anaerobic rods have been implicated in the pathogenesis of periodontal disease, the data suggest that P. loescheii contributes to the disease process by suppressing lymphocyte function.

Bacterial Proteins↗
PubMed1989

Calcium phosphate cements: study of the beta-tricalcium phosphate--monocalcium phosphate system.

The possibility of making cements based on beta-tricalcium phosphate (beta-TCP), a promising bone graft material, was investigated. Upon admixture with water, beta-TCP/monocalcium phosphate monohydrate (MCPM) mixtures were found to set and harden like conventional hydraulic cements. Beta-TCP powders with larger particle size, obtained by sintering at higher temperatures, increased the ultimate strength of the cement. Results show that setting occurs after dissolution of MCPM, as a result of the precipitation of dicalcium phosphate dihydrate (DCPD) in the paste. The ultimate tensile strength of the hardened cement is proportional to the amount of DCPD formed. Upon ageing above 40 degrees C, DCPD transforms progressively into anhydrous dicalcium phosphate (DCP), thereby decreasing the strength. Ageing of the pastes in 100% r.h. results in a decay of the mechanical properties. This can be ascribed to an intergranular dissolution of the beta-TCP aggregates as a result of the pH lowering brought about by the MCPM to DCPD conversion.

Biocompatible Materials↗
PubMed1989

A simplified aluminum stain in paraffin sections of bone from hemodialysis patients.

A new simplified method has been devised for staining aluminum and has been tested in paraffin sections of bone from 60 patients who have undergone hemodialysis. Iliac crest bone fragments were fixed in 20% phosphate-buffered formalin for less than a day and demineralized at room temperature in 10% phosphate-buffered formalin containing 5% formic acid for only 2 to 3 hr. Four-micron paraffin sections, accompanied by positive controls, were stained with Maloney's aluminum stain, the Berlin blue reaction for iron, dylon or Congo red for amyloid and von Kossa's reaction for calcium. Aluminum and iron were demonstrated particularly at the mineralizing front of bony tissues; aluminum in 52 cases, iron in 45. Dylon staining also gave positive results in 52 cases. It is important in determining whether aluminum deposition is present that the von Kossa reaction remains positive even after demineralization. This method may be more useful for demonstrating aluminum in bony tissues than the complicated and time-consuming resin-embedding method currently used.

Aluminum↗
PubMed1988

[Renal cell carcinoma in the solitary kidney].

We have treated surgically 5 patients with renal cell carcinoma in the solitary kidney. The cause of renal absence was nephrectomy for renal stones, in 2 patients and renal tuberculosis, renal cyst and renal hypoplasia in 1 patient each. Four of the 5 patients died. One of the 4 patients died 5 days after surgery due to gastrointestinal bleeding, 1 due to metastasis, 1 due to gastric cancer and one due to hemodialysis complications. Surgical management of renal cell carcinoma of solitary kidney is discussed.

Aged↗
PubMed1987

Adaptive changes of H+ and/or bicarbonate transport in chronic metabolic acidosis: its quantitative evaluation by using isolated perfused kidney.

We have recently improved the technique of the isolated perfused rat kidney by addition of amino acids to the perfusion solution. Utilizing this improved preparation, we examined to what extent chronic acid-base status can alter H+ and/or bicarbonate transport in the whole kidney and the effect of acetazolamide (10(-4) M) on this process. Kidneys from rats that had been drinking tap water (control), 1.5% NH4Cl (acidotic), or 1.5% NaHCO3 (alkalotic) were perfused with a solution of identical pH and PCO2. During the control period, the fractional bicarbonate reabsorption was higher in acidotic rats than in control rats by 1.0% and urine pH was lower than those in control. On the other hand, the two parameters were not different between control and alkalotic rats. Acetazolamide increased urine pH and decreased the fractional bicarbonate reabsorption in all, but these parameters in acidotic and alkalotic rats were not different compared with those in control. We conclude that adaptive changes of H+ and/or bicarbonate transport in chronic metabolic acidosis corresponds to about 1.0% as fractional bicarbonate reabsorption by the isolated perfused kidney and is largely carbonic anhydrase dependent.

Absorption↗
PubMed1986

Earlobe crease and coronary heart disease in Japanese.

To evaluate whether a significant statistical correlation exists between earlobe crease (EC) and coronary heart disease (CHD), 1000 Japanese adult patients (573 males, 427 females) were examined for the presence or absence of EC, clinical or angiographic evidence of CHD, and the following coronary risk factors: male sex, age over 50 years, obesity, hypertension, diabetes mellitus, cigarette smoking, and hyperlipidemia. Patients were divided into two groups according to clinical evidence of CHD: 237 patients with angina pectoris and/or myocardial infarction (CHD+ group); 720 patients without evidence of CHD (CHD- group). Coronary angiography was performed on 200 patients from this sample population; these patients were also divided into two groups: 119 patients with greater than 50% luminal narrowing of at least one major coronary artery (stenosis+ group); 81 patients with no significant atherosclerotic changes in the coronary arteries (stenosis- group). EC was present in 58 of 237 CHD+ patients (24.5%) but in only 35 of 720 CHD- patients (4.8%; P less than 0.001); it was present in 31 of 199 stenosis+ patients (26.1%) but in only 3 of 81 stenosis- patients (3.7%; P less than 0.01). EC was also found to correlate significantly with some coronary risk factors; the correlations between the presence of EC and the presence of CHD and coronary risk factors were investigated by multivariate analysis. In a multivariate setting, the existence of CHD and an age of over 50 years was significantly related to the presence of EC. To investigate the relationship between EC and advancing age, all patients were separated into age-groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Reduced extraction of I-propranolol by perfused rat liver in the presence of uremic blood.

Previous in vivo studies have shown that the presystemic clearance of p.o.-administered levo-isomer of propranolol is inhibited in rats with uranyl nitrate-induced acute renal failure. A series of steady-state single-pass rat liver perfusion studies were performed to explore the probable mechanism of the observed metabolic inhibition. When livers from normal rats were perfused with blood perfusate prepared from normal donor animals, a high extraction ratio (Eh) of 0.974 +/- 0.005 (mean +/- S.D.) was observed at an influent I-propranolol concentration of 400 ng/ml, i.e., only 2.6% of drug entering the liver escaped single-pass extraction. The extraction of I-propranolol was significantly lower (i.e., Eh = 0.906 +/- 0.017) when livers isolated from uranyl nitrate-induced renal failure rats were perfused with uremic blood; such that there was an approximate 3-fold increase in the amount of drug escaping single-pass extraction (i.e., from 2.6 to 9.4%). This difference in hepatic extraction is quantitatively consistent with the increase in p.o. systemic availability of I-propranolol observed in our previous in vivo study with the uranyl nitrate-induced renal failure rat model. When livers from normal rats were cross-perfused with uremic blood, extraction of I-propranolol was depressed to almost the same level (i.e., Eh = 0.927 +/- 0.009) as when livers from renal failure animals were perfused with uremic blood. In contrast, livers from renal failure rats cross-perfused with normal blood exhibited comparable extraction for I-propranolol (Eh = 0.970 +/- 0.010) as normal livers perfused with normal blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1984

Pharmacokinetics of l-propranolol during repetitive dosing in normal and uranyl nitrate-induced renal failure rats.

The effect of experimental renal failure on the intravenous and oral pharmacokinetics of l-propranolol was studied in rats. Renal failure was induced by a single intravenous injection of uranyl nitrate (5 mg/kg). Pharmacokinetic studies were carried out on the fifth day after injection of the renal toxin (renal failure group) or saline (control group). Serum concentration time course of l-propranolol was characterized after a single intravenous or oral dose as well as after five consecutive doses of the drug given at 3-hr intervals. During repetitive intravenous drug administration, steady state was reached by the second dose, i.e., within 6 hr after initiation of repetitive dosing. No significant difference in the serum concentration time course of l-propranolol was observed between control and renal failure animals. In both groups the AUC over the steady-state dosing interval was on the average 21-27% higher than the AUC after a single dose, indicating a slight decrease in the systemic clearance of l-propranolol during repetitive intravenous drug administration. An approximately two- to three-fold higher serum l-propranolol concentration was observed in renal failure animals as compared to the normal controls after both single or repetitive oral dosing. The apparent reduction in oral clearance probably reflected an inhibition of the hepatic first-pass metabolism of l-propranolol in the renal failure rat. An unexpectedly high and protracted accumulation of serum l-propranolol concentration was observed during repetitive oral drug administration. Continuing accumulation was still evident after the fifth oral dose, i.e., a period of 15 hr or approximately 10 half-lives. The mean AUC over the last dosing interval was 32.0 and 17.8 times higher than the predicted steady-state estimate based on single oral dose data for control and renal failure rats, respectively. The substantial reduction in the oral clearance during repetitive drug administration may be due to an auto-inhibition of l-propranolol metabolism.

Acute Kidney Injury↗
PubMed1984

Acute and chronic hypotensive effects of nifedipine and niludipine in hypertensive patients with chronic renal failure.

The present study was aimed to evaluate the acute and chronic hypotensive effects of nifedipine (Bay a 1040, Adalat) and niludipine (Bay a 7168) in hypertensive patients with chronic renal failure. 1. The decrease of blood pressure lasted for at least 3 h and maximum decrement was achieved in 60 min (26% decrement, p less than 0.05) after oral administration of nifedipine (10 mg). On the other hand, niludipine (20 mg) caused decrease of blood pressure for at least 4 h and attained maximum decrement in 90 min (13% decrement, p less than 0.05) after oral administration. 2. In chronic studies of both drugs, the maximum decrease of blood pressure (p less than 0.05) was attained after one week and lasted at least 4 weeks. There were no significant changes of pulse rate, body weight and urine volume in both nifedipine and niludipine groups. 3. Nifedipine caused great diurnal or day-to-day fluctuations of blood pressures after chronic administrations. On the other hand niludipine did not cause any significant fluctuations. Any serious complications could not be seen during these studies. In conclusion, these results provide clinical evidence that niludipine could be usefused great diurnal or day-to-day fluctuations of blood pressures after chronic administrations. On the other hand niludipine did not cause any significant fluctuations. Any serious complications could not be seen during these studies. In conclusion, these results provide clinical evidence that niludipine could be useful for treatment of hypertension associated with chronic renal failure. Results also suggest that the optimal efficacy of nifedipine and niludipine in part depends on the specific clinical situation at hand. For example, nifedipine seems to be the drug of choice in hypertensive emergencies when there is a need for rapid lowering of blood pressure.

Adolescent↗
PubMed1983

Effect of pyridoxal 5'-phosphate on Ca2+-stimulated adenosine triphosphatase activity in microsomes of rat submandibular gland in vitro.

1. The Ca2+-ATPase activity in microsomes of rat submandibular gland was inhibited by pyridoxal 5'-phosphate in vitro. 2. The dissociation constant of the enzyme-pyridoxal 5'-phosphate complex was estimated to be 6.5 mM. 3. The inhibition of pyridoxal 5'-phosphate for both ATP and Ca2+ was competitive. 4. The order of inhibitory effectiveness of pyridoxal 5'-phosphate analogs was pyridoxal 5'-phosphate greater than pyridoxal HCl greater than pyridoxamine 5'-phosphate greater than pyridoxamine HCl. 5. The enzyme-pyridoxal 5'-phosphate complex was nonreducible with sodium borohydride.

Adenosine Triphosphate↗
PubMed1983

Effect of prostaglandin A2 on Na+-K+-ATPase in basolateral plasma membrane of rat intestine in vitro inhibition of activation of K+-dependent p-nitrophenylphosphatase by Na+ and ATP.

1. The activation of K+-dependent p-nitrophenylphosphatase (EC 3.6.1.7) by both Na+ and ATP in rat intestinal basolateral plasma membrane is inhibited by prostaglandin A2. 2. The drug's inhibition of the activation of the enzyme by both Na+ and ATP is due to a decrease in the affinity of the enzyme for Na+ and in the Vmax of the enzyme. 3. The Ki values for this drug for Na+ and ATP in the activation of the enzyme were 45 and 70 microM, respectively.

4-Nitrophenylphosphatase↗