Macro-creatine kinase type 1 possibly induced by intravenous hyperalimentation.
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Biomedical subjects
Publications and source records attributed to T Aoki.
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In vitro and in vivo antithrombogenicity of poly(propylene oxide) segmented nylon 610 was investigated. For the in vitro simulation of thrombosis on copolymer surfaces, a modified microsphere column method evaluated the thrombosis time of the copolymer column. For the in vivo evaluation of the antithrombogenicity of copolymer surfaces, small diameter tubing, precoated with copolymer, was implanted in rabbits as an arteriovenous shunt to determine the time of patency for the copolymer tubing. In both the in vitro and in vivo tests, the copolymer having a particular size and distribution of crystalline and amorphous microphases on its surface exhibited excellent antithrombogenicity; the copolymer with a long period of approximately 12 nm and a crystallite thickness of 6.5 nm suppressed the activation process of adhering platelets to show thromboresistant property. This paper emphasizes the importance of controlling the crystalline-amorphous microstructure for the antithrombogenicity of polymer surfaces with a semicrystalline microstructure.
The metabolism of chloral hydrate (CH) under anoxic conditions was investigated in the non-recirculating, hemoglobin-free liver perfusion system. CH uptake in the anoxic liver decreased to about 80% of that in the oxygen-supplied liver. The reduction of CH to trichloroethanol (TCE) increased and the oxidation of CH to trichloroacetic acid (TCA) decreased. The TCE/TCA ratio increased; however, the total trichloro compounds, that is TCE and TCA, were not significantly altered by anoxia. Though approximate 14% of the CH infused into the oxygen-supplied liver was changed to substances other than TCE or TCA, the unknown part was a very small portion in the anoxic liver. The decrease in CH uptake, by the anoxic liver, is thought to be equivalent to the decrease of the unknown metabolites. The TCE/TCA ratio under anoxia was also altered by pyruvate or lactate infusion.
We studied the effect of cortisol on the plastic synapses in the hippocampal region of the developing mouse brain. Ethanolic phosphotungustic acid-stained synaptic junctions were reduced in the cortisol-treated mouse brain dose-dependently and irreversibly. The steroid therapy in infancy requires circumspection.
The effects of 2-acetylaminofluorene (2-AAF), phenobarbital (PB) and butylated hydroxyanisole (BHA) on the competitive proliferation of glutathione S-transferase (GST-P) positive liver cell foci induced by diethylnitrosamine (DEN) and surrounding hepatocytes were studied. Rats were given a single i.p. injection of 200 mg/kg body wt of DEN and from 2 weeks later were given a diet containing 0.02% 2-AAF (group 1), 0.05% PB (group 2), 2.0% BHA (group 3), or no supplement (group 4) for 6 weeks. All rats were subjected to partial hepatectomy (PH) at the end of week 3. Animals from each group were killed 1, 2, 3 or 4 days or 1, 2, 3 or 5 weeks after PH. Sequential changes in cellular proliferations after PH were investigated by immunohistochemical staining for GST-P and autoradiography of [3H]thymidine. The development of GST-P positive foci was enhanced strongly by 2-AAF and slightly by PB and was inhibited by BHA. In the group treated with 2-AAF, proliferation of hepatocytes adjacent to foci was almost completely inhibited [labelling index (LI) = 0.4-1.5], but GST-P positive foci cells had a high LI (16.2-26.1) 1 week after PH. In the group treated with PB, proliferation of surrounding hepatocytes was slightly inhibited (LI one day after PH = 16.0) compared with that of control (LI = 24.2), but proliferation of cells in GST-P positive foci was not inhibited (LI one day after PH = 11.3; control value = 11.0). BHA retarded recovery of the LI (LI 4 days after PH = 8.1; control value, 4.0) and did not inhibit proliferation of surrounding hepatocytes. These results indicated an inverse relationship between the development of GST-P positive foci and proliferation of surrounding hepatocytes.
A large series of assays of the hepatocarcinogenic potential of 112 different compounds were carried out using a rapid bioassay system developed in this laboratory based on the two-step concept of hepatocarcinogenesis. Rats were initially given a single dose (200 mg/kg) of diethylnitrosamine (DEN) i.p. and starting 2 weeks later were treated with test compounds for 6 weeks and then killed, all rats being subjected to two-thirds partial hepatectomy (PH) at week 3. Carcinogenic potential was scored by comparing the number and area per cm2 of induced glutathione S-transferase placental form-positive (GST-P+) foci in the liver with those of the corresponding control group given DEN alone. Positive was scored for a significant increase in the value of GST-P+ foci, negative for no change or a decrease. Results were compared to reported Salmonella/microsome and long-term carcinogenicity test findings. Of the liver carcinogens, 10 out of 11 (90.9%) mutagenic, and 11 out of 13 (84.6%) non-mutagenic compounds gave positive results (mean, 87.5%). Carcinogens other than the hepatocarcinogens gave less positive results (two out of 17, 11.8%). None of the compounds reported as non-carcinogenic demonstrated positivity suggesting that the assay system does not suffer from the disadvantage of false-positive results. The protocol system also provided information concerning the inhibitory potential of compounds such as anti-oxidants. It is concluded that the present experimental protocol which requires far fewer animals and shorter duration than a long-term carcinogenicity test has practical applications for the rapid and economical screening of environmental hepatocarcinogens and their inhibitory agents.
Sequential changes of numbers of pepsinogen 1 (Pg 1)-decreased pyloric glands (PDPG) detected by immunohistochemistry and of the incidence of gastric carcinomas were examined in five different strains of rats treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG;CAS:70-25-7). Male SD (Crj:CD), WKY (WKY/NCrj), Lewis (LEW/Crj), Wistar (Crj:Wistar) and F344 (F344/DuCrj) rats (40 per strain), were given drinking water containing 100 micrograms/ml MNNG for 30 weeks and then normal tap water, and were killed at week 10, 30 and 50 of the experiment. Adenocarcinomas of the glandular stomach were found in nine of 15 SD rats (60%), in eight of 12 WKY rats (67%), in eight of 15 Lewis rats (53%), in three of 13 Wistar rats (23%) and in one of 18 F344 rats (6%) at week 50. These incidences of carcinomas in SD, WKY and Lewis were significantly higher (P less than 0.01) than that in F344 rats. From week 10, the numbers of PDPG in SD, WKY and Lewis rats were significantly greater (P less than 0.01) than that in F344 rats. From week 30, the numbers of PDPG in Wistar rats were also significantly greater (P less than 0.05-0.01) than that of F344. The susceptibility of rats to induction of gastric carcinoma by MNNG correlated with the susceptibility to induction of PDPG by MNNG in each strain, suggesting that induction of PDPG is a preneoplastic change in chemical gastric carcinogenesis.
Two wide-spectrum initiation models were investigated in F344 male rats. Model I: After sequential treatment with diethylnitrosamine (DEN), N-methylnitrosourea (MNU) and dihydroxy-di-N-propylnitrosamine (DHPN), animals were given phenobarbital (PB) or N,N-dibutylnitrosamine (DBN) as a test compound for 14 weeks and sacrificed at week 18. Model II: Animals were treated with DHPN, followed by N-ethyl-N-hydroxyethylnitrosamine (EHEN), and then 3,2'-dimethyl-4-aminobiphenyl (DMAB) as initiators and were subsequently given 3-methylcholanthrene (MCA) or PB as a test compound for 11 weeks. Animals were sacrificed 16 weeks after the commencement. In both models, assessment of lesion yield revealed significant enhancement of carcinogenesis by the test compounds in their respective target organs. Since, in many cases, treatment with PB, DBN and MCA subsequent to the combined initiation procedures brought about a marked increase in lesion development, far greater than a simple sum of the yields given by initiators and test compounds alone, the presently described approach appears promising for development of medium-term bioassay systems for detection of environmental carcinogens.
The purpose of this study was to analyse the magnitude and direction of lateral forces exerted on the abutment tooth of a complete mandibular overdenture. A newly developed transducer was used for measuring forces. It was small enough to be embedded in the lower denture base, and could detect the magnitude and direction of forces. Five subjects, 38 to 77 years of age, with an edentulous maxilla and one or two canines remaining in the mandible were selected for this experiment. An upper complete denture and a lower complete overdenture with only one abutment tooth were fabricated for each subject. Forces exerted on the abutment tooth were measured during tapping and chewing of kamaboko (a Japanese cooked fish paste with soft consistency) and also peanuts, a few days and about 20 days after the denture insertion. The following results were obtained: (i) the average magnitude of lateral forces ranged from 0.5 to 2.0 kgf, and there were significant differences of the mean value between subjects; (ii) lateral forces were mainly observed on an imaginary line drawn through the experimental tooth (lower canine) and the opposite retromolar pad. There were no significant differences between the first and the second measurement.
The respiratory burst activity (generation of hydrogen peroxide) of peripheral polymorphonuclear leukocytes (PMN) in both phorbol myristate acetate (PMA)-stimulated and unstimulated states and phagocytosis were assessed using flow cytometry on 46 patients with chronic renal failure: 33 patients undergoing chronic hemodialysis (CHD), 8 patients who have never been on dialysis (nonhemodialysis; NHD), 5 patients undergoing continuous ambulatory peritoneal dialysis (CAPD); these patients were compared with 27 normal control subjects. In patients just before the initiation of dialysis, impaired hydrogen peroxide production by PMA-stimulated PMN and depressed phagocytosis were noted, which was restored to the control levels by hemodialysis. A mild but significant reduction of hydrogen peroxide production in a PMA-stimulated state was found in NHD patients, and an inverse correlation was noted between the impairment of this function and the degree of diminished renal function. There was no significant difference between CAPD patients and controls in hydrogen peroxide production by PMA-stimulated PMN. Decreased hydrogen peroxide production by unstimulated PMN was observed in both CHD and CAPD patients. These findings may explain, at least partly, the enhanced susceptibility to bacterial and fungal infections of these patients.
Although muscle is considered to be the most important site for postprandial glucose disposal, the metabolic fate of oral glucose taken up by muscle remains unclear. We, therefore, employed the dual isotope technique (intravenous, [6-3H]-glucose; oral, [1-14C]glucose), indirect calorimetry, and forearm balance measurements of glucose, lactate, alanine, pyruvate, O2, and CO2 in nine normal volunteers to determine the relative importance of muscle glycogenic, glycolytic, and oxidative pathways in disposal of an oral glucose load. During the 5 h after glucose ingestion (1 g/kg), 37 +/- 3% (24.9 +/- 2.3 g) of the load was oxidized and 63 +/- 3% (42.8 +/- 2.7 g) was stored. At least 29% (19.4 +/- 1.3 g) was taken up by splanchnic tissues. Muscle took up 26% (17.9 +/- 2.9 g) of the oral glucose coincident with a 50% reduction in its oxidation of fat. 15% of the oral glucose taken up by muscle (2.5 +/- 0.9 g) was released as lactate, alanine, or pyruvate; 50% (8.9 +/- 1.4 g) was oxidized, and 35% (6.4 +/- 2.3 g) was available for storage. We conclude that muscle and splanchnic tissues take up a comparable percentage of an oral glucose load and that oxidation is the predominant fate of glucose taken up by muscle, with storage in muscle accounting for less than 10% of the oral load. Thus, contrary to the prevailing view, muscle is neither the major site of storage nor the predominant site of disposal of an oral glucose load.
The motor activity of the canine lower esophageal sphincter (LES) was studied under conscious states by means of the strain gage transducer, and gastroesophageal reflux was investigated after injection of the contrast medium through the silastic tube inserted in gastric fundus by x-ray. The motor activity and function of LES were observed in the dogs with selective proximal vagotomy (SPV), truncal vagotomy (TV) and TV + gastrectomy. Results were summarized as follows; 1. In the postprandial period, so called receptive relaxation was observed in gastric body, and tonic contraction was observed in LES. On the other hand, the occurrence of the LES contraction was consistent with gastric periodic motor activity in the interdigestive state. It was found that such a contractile pattern of LES and gastric body prevented the reflux of gastric juice from stomach to esophagus in the digestive and interdigestive state. 2. In the postprandial period, the tonic contraction of LES was inhibited by the venous injection of atropine sulfate. Mechanisms of digestive contractile activity of LES were mainly regulated by cholinergic nerve. 3. After SPV and TV, the motility of LES and gastric body was disturbed. Namely, receptive relaxation disappeared, and tonic contraction was observed in gastric body, but the relaxation of the LES was found after ingestion. These findings suggested that discordant LES contractiles with the contraction of the gastric body after vagotomy produced a gastroesophageal reflux. 4. After TV + gastrectomy, the synchronous motor activity of the LES, remnant stomach and duodenum disappeared. Namely, it was thought that the reflux esophagitis occurred after gastric surgery with vagotomy and lymphnodes dissection was caused by the duodenal juice reflux to remnant stomach and esophagus.
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Demonstration of the exact site of dural fistulas in cases of cerebrospinal fluid rhinorrhea is difficult. Previous reports have described the use of metrizamide cisternography combined with either hypocycloidal tomography or computerized tomography; however, direct, dynamic, real-time visualization of the fistula is difficult with instillation of a minimal dose of metrizamide using those methods. A digital video subtraction fluoroscopy system can visualize the actual site of the fistula directly and dynamically using only a small amount of metrizamide.
The synthesis and in vitro activity of 7 beta-(substituted vinylthioacetamido)-1-oxacephem antibiotics are described. The compounds having a cis-chlorovinylthioacetamido group at C-7 showed high activity against Gram-positive as well as Gram-negative bacteria. The most interesting compound of the series was 51 I because of its high activity and high plasma level in mice.
The synthesis and in vitro activity of 1-oxacephem derivatives having a substituted or a non-substituted cis-fluorovinylthioacetamido side chain at C-7 are described. Of these new 1-oxacephem antibiotics, 2355-S (42a) shows good antibacterial activity against Gram-positive and Gram-negative bacteria, and very favorable pharmacokinetic properties.
Prostatic acid phosphatase (PAP) and prostate specific antigen (PA), which are useful markers of diagnosis for prostatic cancer, have been purified from human seminal plasma. Total of 54.4 mg PAP and 3.0 mg PA were purified from 426.5 ml human seminal plasma. The purified antigens were demonstrated a single band by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), having a molecular weight of about 50,000 and 34,000, respectively. The PAP and PA purified from human seminal plasma were considered similar to that of prostatic tissue immunologically and biochemically.