Freeze-fracture images of matrix vesicles of epiphyseal cartilage and non-calcified tracheal cartilage.
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Biomedical subjects
Publications and source records attributed to Y Toda.
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Pancreatic excretion of 5,5-dimethyl-2,4-oxazolidinedione (DMO) was studied in 25 normal subjects using the technique of the traditional pancreatic secretory test. The pancreozymin-secretin test was performed 4 days after the oral administration of trimethadione (3,5,5-trimethyl-2,4-oxazolidinedione, the precursor of DMO) for 3 consecutive days. When a dose of 1 unit/kg of pancreozymin was administered intravenously, both DMO concentration and output of a 10-min fractional specimen were rapidly increased and then decreased gradually. When a dose of 1 unit/kg of secretin was injected 30 min after pancreozymin, DMO concentration in duodenal aspirate showed no significant alteration, while DMO output of the aspirate was remarkably increased and then diminished in parallel to flow rate. DMO concentration in plasma varied widely from subject to subject, but was fairly constant during the course of the test in the same subject. Total DMO output in the postpancreozymin 30-min and postsecretin 60-min periods was linearly related to plasma DMO concentration. The output of DMO, when expressed as the output at a level of 10 mg/100 ml of plasma DMO, was linearly related to secretory volume and bicarbonate and amylase outputs in the postsecretin period. These results led to the conclusion that the human pancreas was capable of excreting a week organic acid of DMO with a molecular weight of 129.1 and that the excretion of DMO in normal subjects was a funciton of two factors: plasma DMO concentration and pancreatic secretory volume.
Abnormal pancreatic excretion of 5,5-dimethyl-2,4-oxazolidinedione (DMO) was demonstrated in 44 patients with chronic pancreatitis (14 with calcification and 30 without calcification). Pancreatic excretion of DMO in patients with chronic pancreatitis, as well as in normal subjects, depended on plasma DMO concentration and secretory volume. In the postsecretin 60-min period, almost all patients showed a decrease in total DMO output of duodenal aspirate over the observed range of plasma DMO concentration. More than half the patients without calcification gave a discordant pattern between the DMO output and volume, ie, decreased DMO output with normal volume secretion, while most of patients with calcification had low DMO output with decreased volume flow. The data of the pancreozymin-secretin test suggested that chornic pancreatic inflammation was moderate or minimal in patients without calcification and far advanced in those with calcification. From these results the hypothesis was advanced that DMO diffusion into the pancreatic ducts might be primarily impaired in the relatively early stage of chronic pancreatitis, and as the inflammation progressed to the final stage, DMO outflow from the ducts to the duodenum would be disturbed with evolving diffusion impairment of the compound. Total DMO output, when expressed as the output at a level of 10 mg/100 ml of plasma DMO (standard DMO output), was significantly reduced in chronic pancreatitis during a 60-min period after secretin stimulation. DMO in duodenal content, when expressed in terms of maximal concentration ratio of duodenal juice/plasma for the compound (maximal J/P ratio), was significantly low in chronic pancreatitis during the last 40-min period after secretin stimulation. These two parameters can therefore be used as indices of pancreatic excretion of DMO. The present technique may well become an effective diagnostic tool for early detection of chronic pancreatitis.
Detectability of abnormally high serum and urine amylases was investigated on patients with pancreatic diseases using amylase assays with substrates of different digestive rates to pancreatic amylase. Ratios of amylase activities determined by a chromogenic assay using a Remazolbrilliant Blue R starch (RBB assay) to those by Caraway's assay using a Lintner soluble starch (R/C ratio) were calculated on duodenal and salivary amylases obtained from 16 subjects undergoing a pancreozymin-secretin test. The R/C ratio of the duodenal amylase (M +/- SD = 0.56 +/- 0.12) was significantly higher (p less than 0.01 by F test) than that of the salivary amylase (M +/- SD = 0.36 +/- 0.10). Detectability of above-normal values of serum and urine amylases were compared with two assays in 77 pancreatic patients. The value for serum and urine amylases determined by the RBB and Caraway's assays exceeded the upper limit of normal in 37 and 58% by the RBB assay and 24 and 26% by Caraway's assay, respectively. Degrees of abnormality (ratio of the observed to the upper normal value) in serum and urine amylases were also significantly higher (p less than 0.05 for serum and p less than 0.01 upper for urine) by the RBB assay than by Caraway's assay. The RBB assay was more sensitive than Caraway's assay in detecting elevation of pancreatic amylase in serum and urine.
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