[Intraplatelet serotonin levels in renal and collagen diseases].
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Blood Platelets↗
Biomedical subjects
A Tsuchida
Publications and source records attributed to A Tsuchida.
[A study on reducing radiation dose in dental radiography for children. Part 1. The sheltering effects of lead content rubber sheet and ready-made apron].
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Child↗
Selective glomerular thrombosis in rats induced by combined injections of nephrotoxic antiserum and lipopolysaccharide.
Experimental glomerular thrombosis was induced in rats by combined injections of nephrotoxic antiserum and lipopolysaccharide. For the development of glomerular thrombosis, administration of nephrotoxic antiserum (greater than or equal to 0.1 ml pooled material) was required as a preparatory agent and greater than or equal to 100 ng lipopolysaccharide as a provoking agent. The severity of renal lesions was not parallel with the amounts of nephrotoxic antiserum and lipopolysaccharide injected. Transient clamping of a unilateral renal artery for 10 to 20 minutes at the time of the nephrotoxic antiserum injection partially prevented the development of glomerular thrombosis in the clamped side. Intervals between the preparatory and provoking injections were found to be -4 to 72 hours for the development of renal lesions. With the preparatory injection of 0.1 to 0.3 ml nephrotoxic antiserum a thrombotic lesion developed exclusively in glomerular capillary walls greater than or equal to 2 hours after the lipopolysaccharide injection. No thrombotic lesion was observed in other tissues such as lung, liver, or intestine, but a generalized Shwartz-manlike phenomenon was observed with the preparatory injection of 0.5 ml nephrotoxic antiserum. When rats were pretreated with nephrotoxic antiserum and 3 hours thereafter transfused with 1 to 3 X 10(8) polymorphonuclear leukocytes, which had been incubated with lipopolysaccharide for 30 minutes in vitro and washed three times with buffered physiologic saline solution, a marked glomerular thrombosis was also induced. The result indicates that lipopolysaccharide plays a role in the development of thrombosis by a direct effect on leukocytes. The development of glomerular thrombosis was prevented in a leukocytopenic state when leukocyte count was less than 600/microliter, but not in thrombocytopenic rats with a platelet count 8.7 to 30 X 10(3)/microliter. Leukocyte count and plasma fibrinogen level decreased, and prothrombin time and activated partial thromboplastin time were prolonged significantly during the pathologic course. Platelet count and FDP did not change significantly. This experimental model has a basic similarity to the generalized Shwartzman reaction, but the lesions develop exclusively in glomeruli.
Animals↗
[Effectiveness of cefotaxime in pediatric infectious diseases].
Cefotaxime (CTX) was administered to 117 pediatric patients. Although 26 of these patients were excluded from the clinical evaluation of the study because other antimicrobial agents were given concomitantly with CTX or because no infectious diseases were proved, these cases were evaluated for adverse effects of the drug. The remaining 91 cases were evaluated for clinical effect; pneumonia in 56 cases, septicemia in 5, suspected septicemia in 5, meningitis (aseptic cases included) in 3, urinary tract infection in 5 and other diseases in 17. No pathogenic organisms were identified in any of the pneumonia cases, even either by bacterial culture or other laboratory test methods. Pathogens of septicemia were E. coli in 3 cases, K. pneumoniae in 1 and E. agglomerans in 1. Those of urinary tract infections were E. coli in 3 cases, a mixed infection of S. aureus and an unidentified species of Gram-negative rods in 1, and unknown in 1. Clinical effectiveness rates of CTX were 78.6% in pneumonia and 100% in septicemia, suspected septicemia and urinary tract infections. One patient with purulent meningitis caused by H. influenzae was also treated with CTX successfully. Adverse reactions and abnormal laboratory findings were observed in 12 cases (12/117 = 10.3%); rash in 2 cases, vomiting in 1, abdominal pain in 1, diarrhea in 5, granulocytopenia and thrombocytopenia in 1, eosinophilia in 3 and elevation of liver enzymes (GOT and LDH) in 1.
Bacterial Infections↗
Multiple primary malignancies in childhood cancer.
A total of 2,609 cases of childhood cancer (9,012 person-years), among which there were nine cases of second primary malignant neoplasms, were collected from six institutions. The expected number of second primary cancers was 0.88, and the observed/expected (O/E) ratio was 10.22. The estimated incidence of multiple primary cancers in children with primary cancers was 99.9 per 100,000. The tumor registry of Kanagawa Prefecture had 1,317 cases of childhood cancer with 3,326.4 person-years, among which six multiple primary cancer cases were reported. The O/E ratio was 18.4 with 180.3/100,000 person-years at risk in this series. A total of 51 cases of multiple primary cancer, including 20 synchronous cases, were reported by four major registries of childhood cancers. Frequent association with nervous tissue tumors was noted. In 17 cases the second tumor followed retinoblastoma, and most second tumors were related to radiation therapy. In the remaining 14 cases the second tumors varied; hematopoietic neoplasms in seven, thyroid carcinoma in three, and bone and connective tissue tumors in four.
Adolescent↗
[Pharmacokinetic and clinical studies of latamoxef (moxalactam) in neonates and premature infants].
Studies were carried out on the in vivo kinetics and clinical efficacy of latamoxef (LMOX) in neonates and premature infants. The results are summarized below. Serum concentration and T1/2 following intravenous injection of LMOX to neonates LMOX was intravenously administered to neonates as one shot doses of 10 mg/kg and 20 mg/kg. The serum concentration of LMOX showed a dose-response to the 10 and 20 mg/kg doses in each of the 0--3 day-old group, 4--7 day-old group and 8--28 day-old group. The T 1/2 values were as follows; for the 10 mg/kg dose, 5.17 hours in the 0--3 day-old group, 3.28 hours in the 4--7 day-old group and 2.79 hours in the 8--28 day-old group; for the 20 mg/kg dose, 5.58 hours in the 0--3 day-old group, 3.46 hours in the 4--7 day-old group and 3.14 hours in the 8--28 day-old group. Thus, it is seen that the half-life of both dosages decreased as the infants became older. Serum concentration and T 1/2 following intravenous injection of LMOX to premature infants Similar to the case of neonates described above, the concentration of LMOX in the serum of the premature infants showed a dose-response to the 10 mg/kg and 20 mg/kg dosages. The T 1/2 values for the 0--3, 4--7 day-old and 8--28 day-old groups were 7.54, 3.93 hours and 6.25 hours, respectively, for the 10 mg/kg dose, and 10.8, 4.05 hours and 3.23 hours, respectively, for the 20 mg/kg dose. Again, it is seen that the half-life of both dosages decreased as the age of the prematurely-born infants increased. Serum concentration and T1/2 following 1-hour intravenous drip infusion of LMOX to neonates LMOX was administered to neonates in doses of 10 mg/kg and 20 mg/kg, by i.v. drip infusion over a 1-hour period. With both dosages, the peak serum concentration of LMOX occurred at the time of completion of the infusion. The T1/2 values for the 0--3, 4--7 day-old and 8--28 day-old groups were 5.41, 3.68 hours and 1.92 hours, respectively, for the 10 mg/kg dose, and 5.31, 2.67 hours and 4.86 hours, respectively, for the 20 mg/kg dose. Urinary excretion of LMOX in neonates and premature infants. The percentage of the administered LMOX dose contained in the urine excreted during the 6-hour period following intravenous administration of LMOX to neonates and premature infants was determined.(ABSTRACT TRUNCATED AT 400 WORDS)
Humans↗
[Benign mixed tumor in the trachea].
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Adenoma↗
[Clinical efficacy and pharmacokinetics of cefpiramide in children].
Thirty-six febrile patients were administered cefpiramide (CPM) of 20 approximately 75 mg/kg/day for 3 approximately 11 days, and the clinical and side effects were evaluated. Among children with bacterial infections, including pneumonia, urinary tract infection, sepsis, pharyngitis and bronchitis, the results were excellent in 9, good in 13, and fair in 3 patients. Out of 36 patients, adverse reactions were observed in 9 cases, i.e. vascular pain at one shot intravenous injection in 4, diarrhea in 2, eosinophilia in 2, and diarrhea and eosinophilia in 1 case. One shot intravenous administration of CPM of 10 mg/kg to 4 patients yielded mean serum level of 100 micrograms/ml at 15 minutes and mean serum half-life of 2.5 hours, and administration of 20 mg/kg to 3 patients yielded mean serum level of 200 micrograms/ml at 15 minutes and mean serum half-life of 3.5 hours. The half-life in 1 patient with slight liver lesion was 5.36 hours. The rates of urinary recovery within 8 approximately 12 hours were 7.2 to 28.0% in 5 patients, 45.1% in a patient with nephrotic syndrome, and 50.9% in a patient with slight liver lesion.
Age Factors↗
[Clinical effect of latamoxef on newborn and premature infants].
Eleven infants ranging 2 days to 3 months of age were studied for clinical evaluation. Ten of them were diagnosed as sepsis or suspected to be septic. Another one contracted umbilical infection. In 7 of 10 cases, causative bacteria were detected by blood culture, that is S. epidermidis in 3 cases, E. cloacae in 2 cases, K. pneumoniae in 1 case and A. calcoaceticus in another. Those infants were treated by parenteral LMOX. Dosage was 30 to 75 mg/kg per day. Clinical results were excellent in 6 cases (3 cases of S. epidermidis, 2 of E. cloacae and 1 of K. pneumoniae) and good in another case (A. calcoaceticus). The other 3 infants clinically diagnosed as sepsis but not proven by blood culture were also treated successfully. The result of the umbilical infection in 1 case was good. Another group of 5 infants ranging 4 to 22 days of age were also treated by LMOX because of suspected bacterial infections. With these infants pharmacokinetic study was done. Peak serum levels after 1 hour drip infusion of 20 mg/kg ranged from 43 to 53 micrograms/ml. Average of half-lives was 2.7 hours. Estimation of distribution volume resulted in 350 to 523 ml/kg body weight.
Bacterial Infections↗
Effects of anesthesia and K+ ATP channel blockade on interstitial adenosine accumulation in ischemic rabbit myocardium.
Glibenclamide, a K+ ATP channel antagonist, blocks the anti-infarct effect of ischemic preconditioning in rabbits, but only when the latter are anesthetized with ketamine-xylazine. Furthermore, the protection triggered by pinacidil, a K+ ATP channel opener, can be aborted by treatment with the adenosine antagonist 8-(P-sulfophenyl)theophylline. This study tests whether either the anesthetic regimen or glibenclamide affects infarct size by modulating interstitial adenosine levels. Interstitial adenosine and total purine concentrations were assessed in open-chest rabbits by the microdialysis technique. Dialysis fibers were inserted into myocardium served by a coronary artery branch surrounded by a snare. All animals sustained a 30-min coronary occlusion and then 120-min reperfusion. Rabbits were anesthetized with either sodium pentobarbital or a ketamine-xylazine mixture. Half of the latter animals also received glibenclamide. The control levels of adenosine in the dialysate were comparable in the three groups, as were those of total purines, and the infusion of glibenclamide caused no change. Ischemia led to 10- to 20-fold increases in interstitial adenosine and 10- to 40-fold rises in total purine concentrations. These increases were equivalent in all groups. Further-more, infarct size as a percentage of the myocardium at risk was also comparable in the three groups. Neither the anesthetic agent nor glibenclamide appears to modulate interstitial adenosine release from ischemic tissue.
Adenosine↗
Suppression of reperfusion arrhythmia by ischemic preconditioning in the rat: is it mediated by the adenosine receptor, prostaglandin, or bradykinin receptor?
The mechanism for the suppression of reperfusion arrhythmia by preconditioning (PC) remains unknown. This study aimed to examine the roles of the adenosine receptor, prostaglandin (PG), and bradykinin (BK) receptor in PC. Under pentobarbital anesthesia, the coronary artery of the rat was occluded for 5 min and then reperfused. In untreated controls, this protocol induced ventricular tachycardia (VT) in 100% of the rats and ventricular fibrillation (VF) in 60%. PC with 2 min ischemia/5 min reperfusion prior to the 5 min coronary occlusion significantly reduced the incidence of reperfusion VT and VF to 30% and 0%, respectively. This antiarrhythmic effect of the PC was not blocked when rats were pretreated with 8-phenyltheophylline (8-PT, 10 mg/kg), aspirin-DL-lysin (18 mg/kg), or a specific BK receptor antagonist, Hoe140 (20 nmol/kg). None of these agents alone significantly modified the incidence of reperfusion VT or VF. These results suggest that neither the adenosine receptor, endogenous PG, nor BK receptor play a major role in the mechanism of suppression of perfusion arrhythmias by PC in the rat heart.
Adrenergic beta-Antagonists↗
The detection and prognosis of small pancreatic carcinoma.
During a period of 16 years, 203 proven pancreatic ductal adenocarcinomas were studied. Tumor size was measured on either the resected or the autopsy specimen. Four tumors were smaller than 1 cm, and 17 tumors were between 1.1 and 2 cm. ERCP has been found to be the most accurate in the diagnosis of small pancreatic carcinoma. Followup of 44 patients in whom the tumor was resected showed that survival depended on tumor size. In four patients with tumors smaller than 1 cm without parenchymal invasion, the postoperative 5-yr cumulative survival rate was 100%. Pancreatic carcinoma smaller than 1 cm limited to duct epithelium is considered as early cancer. Various diagnostic imaging modalities are now available to evaluate patients in whom pancreatic carcinoma is clinically suspected. These include ultrasonography (US), computed tomography (CT), endoscopic retrograde cholangiopancreatography (ERCP), and angiography. More recently magnetic resonance imaging (MRI), endoscopic ultrasound (EUS), and peroral pancreatic ductal biopsy also have been used. This report compares diagnostic modalities for pancreatic carcinoma in order to provide a data base for their rational use in the diagnosis of small resectable pancreatic carcinomas.
Adult↗
Expression of vascular endothelial growth factor in human gallbladder lesions.
The purpose of this study was to examine whether vascular endothelial growth factor (VEGF) regulates angiogenesis in human gallbladder carcinomas. We examined the expression of VEGF in 131 gallbladder lesions by immunohistochemistry and in situ mRNA hybridization technique. VEGF immunoreactivity was detected in 100% (9/9) of hyperplasias, 75% (3/4) of adenomas and 91% (107/118) of carcinomas. In gallbladder carcinoma tissues, VEGF mRNA level directly correlated with its protein level. VEGF expression in the neoplasms significantly correlated with vascularization, but not prognostic parameters. These findings suggest that VEGF is commonly expressed in human gallbladder carcinomas and may contribute to neovascularization during carcinogenesis.
Adenoma↗
Cyclin E overexpression in human gallbladder carcinomas.
The expression of cyclin E, one of the important positive cell cycle regulators, was examined immunohistochemically in gallbladder carcinomas. Cyclin E gene product was detected in 58 (49%) out of 118 cases. The degree of cyclin E expression was not associated with any clinicopathological factor including histology, the depth of tumor invasion, tumor stage and patient prognosis. Cyclin E expression was not correlated with that of p53 protein statistically, whereas it was correlated with the proliferative activity of the tumor cells by PCNA (p<0.05). These results suggested that cyclin E expression may confer progression of gallbladder carcinomas.
Biomarkers↗
Plasma levels of myeloperoxidase and elastase are differentially regulated by hemodialysis membranes and anticoagulants.
To examine effects of dialyzer membranes and anticoagulants on hemodialysis (HD)-triggered neutrophil degranulation. We measured plasma myeloperoxidase (MPO) and elastase (ELT) by an enzyme-linked immunoabsorbent assay. During routine HD with a cuprophane membrane and high molecular weight (HMW) heparin, plasma MPO was rapidly upregulated to maximal levels within 15 min after starting extracorporeal circulation. In contrast, the level of plasma ELT gradually increased such that the highest level was achieved at the end of the procedure. When polysulfone and polymethylmethacrylate membranes were substituted for cuprophane, the rise in ELT was markedly suppressed. Polysulfone was also capable of reducing the MPO response, although the effect was less prominent than that for ELT. As for anticoagulants, nafamostat mesylate (NM) completely suppressed the rise in plasma MPO during HD with cuprophane. Low molecular weight (LMW) heparin also partially inhibited this response. In sharp contrast, there was no significant difference in the ELT response between nafamostat, HMW, and LMW heparins. Thus, NM maximally suppressed the rise of plasma MPO but had no effect on the ELT response. Our results suggest that neutrophil degranulation of MPO and ELT is differentially regulated during HD. Polysulfone and NM appear to maximally reduce excessive neutrophil activation.
Adult↗