The chemical composition and serological reactions of lipopolysaccharides from serogroups A,B,X, and Y Neisseria meningitidis.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The accuracy of the scintigraphic diagnosis of acute myocardial infarction with 99mTc-pyrophosphate, 99mTc-tetracycline and 99mTc-glucoheptonate was assessed in 63 patients, 43 of whom had clinical evidence of acute myocardial infarction. In 15, studies with both 99mTc-tetracycline and 99mTc-pyrophosphate were performed. Accuracy was greatest with 99mTc-pyrophosphate (17/17 true positives, 8/10 true negatives) contrasted with 99mTc-tetracycline (12/25 true positives, 6/11 true negatives) and 99mTc-glucoheptonate (3/13 true positives, 2/2 true negatives). 99mTc-pyrophosphate was the most sensitive tracer for the detection of acute myocardial infarction. The diagnostic accuracy with 99mTc-glucoheptonate was poor.
The brain imaging properties of 99mTc glucoheptonate, 99mTc pertechnetate, and 99mTc DPTA are compared. Results demonstrate that optimum images are obtained at 90, 180, and 180 min., for 99mTc GH, 99mTc DTPA, and 99mTc perterchnetate, respectively. The former two images are not affected by prior bone imaging with 99mTc pyrophosphate, while 99mTc pertechnetate images are adversely affected. 99mTc glucoheptonate appears to be the superior agent for brain imaging, followed by 99mTc DTPA and 99mTc pertechnetate.
In a comparison study of three commonly employed 99mTc brain imaging pharmaceuticals, 16 patients with proven brain lesions had imaging performed with DTPA, glucoheptonate, and pertechnetate over a short interval of time. Lesion detectability was assessed by a data processing system which evaluated average lesion-to-background activity ratios for each patient examination. Statistical analysis of the resultant data demonstrated a significant improvement (20%) in lesion-to-background ratio in favor of one hour delayed DTPA images versus two hour delayed pertechnetate images. Comparison of one hour delayed DTPA images with one hour delayed glucoheptonate images did not reveal a significant difference in lesion-to-background ratio. The authors conclude that both Tc-DTPA and Tc-glucoheptonate are superior alternatives to pertechnetate when employed in the manner described.
99mTc glucoheptonate was used as a brain imaging agent in a consecutive series of 859 patients. Sensitivity was 94% in patients with proved CNS tumors. Static imaging of patients with infarction showed a sensitivity of 62%. When the perfusion study was included, this valve increased to 90%. Overall sensitivity was 83%, specificity 99%, and accuracy 95% without inclusion of perfusion results. When these results were included, overall sensitivity was 93%, specificity 99%, and accuracy 98%.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Suppression of pancreatic glucagon secretion by hyperglycemia is a characteristic of normal alpha cell function. However, in diabetic subjects, plasma glucagon is normal or high despite hyperglycemia. It seemed possible that the presence of glucose or its metabolites within the alpha cell might be essential for suppression of glucagon secretion, and that in diabetes an intracellular deficiency of glucose secondary to insulin lack might be responsible for the nonsuppressibility. The present study was designed to determine the effect upon glucagon secretion of blockade of glucose metabolism and of experimental insulin deficiency. Blockade of glucose metabolism was induced in dogs by administration of 2-deoxyglucose or mannoheptulose. A striking rise in glucagon was observed despite accompanying hyperglycemia and hyperinsulinemia, which, in the case of mannoheptulose, was induced by infusing crystalline insulin. To determine if insulin lack also causes paradoxical hyperglucagonemia, dogs were made severely diabetic by alloxan. Fasting glucagon levels ranged from 3 to 22 times normal despite severe hyperglycemia, and were quickly restored to normal by infusing insulin. Diabetes induced in rats by anti-insulin serum was also associated with significant elevation in plasma glucagon. However, diazoxide-induced insulin lack did not increase glucagon in dogs. It is concluded that normal suppression of glucagon secretion by hyperglycemia does not occur when glucose metabolism is blocked or when severe insulin deficiency is produced. It is suggested that normal glucose metabolism within the alpha cell may be an insulin-requiring process without which hyperglycemic suppression of glucagon release cannot occur.