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Biomedical subjects

D Chin

Publications and source records attributed to D Chin.

88 records · Page 5Linked to original sources
PubMed1983

Bone imaging in infections: artefacts from spectral overlap between a Tc-99m tracer and In-111 leukocytes.

In three patients with skeletal infectious disease, scintigrams with a Tc-99m bone-seeker and In-111-tagged leukocytes, made within 24 hr of each other, showed striking similarities. In two cases, the findings from the In-111 WBC images were ultimately determined to be artefacts due to Tc-99m crosstalk within the 173-keV photopeak of In-111. In the second case, the error was traced to failure to use a pure In-111 source for energy calibration: the camera had been peaked on the radiation from the patient himself, who had had an earlier Tc-99m bone scan.

Aged↗
PubMed1982

A study of the implicit criteria used in diagnosing chest pain.

Although previous studies have reported the prevalence of coronary artery disease among patients with typical and atypical angina, criteria for the definition of these chest pain syndromes have not been well described. We studied the implicit criteria used by physicians to classify patients with chest pain. Five internists reviewed the histories of 190 subjects admitted to the hospital for elective coronary arteriography and rated each history as indicating either high or low risk of coronary disease. We applied logistic discriminant analysis to these ratings to create a decision rule for the classification of patients with anginal syndromes. The prevalence of confirmed coronary artery disease in subjects classified by the rule as at high risk was 0.83; the prevalence was 0.57 in subjects classified as at low risk. These prevalences are similar to those found for typical and atypical angina in previous large studies. We conclude that this linear model represents the physicians' decisions and provides criteria for defining anginal pain syndromes in certain settings.

Angina Pectoris↗
PubMed1981

Hypotensive central spinal cord infarction: a clinicopathological study of 3 cases of aortic disease.

Neuropathological studies of 3 cases of aortic disease, complicated by severe prolonged hypotension, revealed a spectrum of central spinal cord infarction not corresponding to a specific arterial territory. The findings support the concept that the central grey matter of the caudal spinal cord is most vulnerable to oligaemic hypoxia. Variation in the longitudinal distribution of ischaemic damage in the individual case depends primarily on the anatomical pattern of the spinal arterial net and on the nature and distribution of the vascular pathology.

Aged↗
PubMed1981

Intraoperative anticoagulation in cardiovascular surgery.

The optimal heparin dose to prevent intraoperative thrombosis or excessive bleeding during the occlusive phase of cardiovascular operations has not been determined. Therefore, we studied the kinetics of heparin effect in 28 patient undergoing peripheral vascular and cardiac operations. The activated clotting time (ACT) was measured in seconds by an electronic clot timer. The maximum ACT after initial heparin administration, the time to reach maximum ACT, and the half-time of heparin effect (t1/2) were determined. The anticoagulant effect of a given dose of heparin varies greatly among patients. No correlation was found between the t1/2 and the dosage of heparin administered. Despite higher doses of heparin administered to cardiac patients, the t1/2 in cardiac and vascular patients was not significantly different. Four patients received the same dose of heparin preoperatively and intraoperatively in an effort to predict the intraoperative effect. The times to maximum effect were the same but t1/2 intraoperatively was longer. These results indicate: (1) maximum heparin effect occurs later than previously believed and is different for cardiac and peripheral vascular patients; (2) the recommendation to give more heparin based on the 5-minute ACT is not valid; (3) individual response to a standard dose of heparin is unpredictable, both in duration and maximum effect; and (4) intraoperative monitoring of the heparin effect is practical and is the only way that any consistent, specific and point of heparin can be achieved.

Aged↗
PubMed1979

Biochemical and genetic characterization of three hamster cell mutants resistant to diphtheria toxin.

We describe here three different hamster cell mutants which are resistant to diphtheria toxin and which provide models for investigating some of the functions required by the toxin inactivates elongation factor 2 (EF-2). Cell-free extracts from mutants Dtx(r)-3 was codominant. The evidence suggests that the codominant phenotype is the result of a mutation in a gene coding for EF-2. The recessive phenotype might arise by alteration of an enzyme which modifies the structure of EF-2 so that it becomes a substrate for reaction with the toxin. Another mutant, Dtx(r)-2, contained EF-2 that was sensitive to the toxin and this phenotype was recessive. Pseudomonas aeruginosa exotoxin is known to inactivate EF-2 as does diphtheria toxin and we tested the mutants for cross-resistance to pseudomonas exotoxin. Dtx(r)-1 and Dtx(r)-3 were cross-resistant while Dtx(r)-2 was not. It is known that diphtheria toxin does not penetrate to the cytoplasm of mouse cells and that these cell have a naturally occurring phenotype of diphtheria toxin resistance. We fused each of the mutants with mouse 3T3 cells and measured the resistance. We fused each of the mutants with mouse 3T3 cells and measured the resistance of the hybrid cells to diphtheria toxin. Intraspecies hybrids containing the genome of mutants Dtx(r)-1 and Dtx(r)-3 had some resistance while those formed with Dtx(r)-2 were as sensitive as hybrids derived from fusions between wild-type hamster cells and mouse 3T3 cells.

Animals↗
PubMed1978

Studies of the diphtheria toxin receptor on Chinese hamster cells.

Concanavalin A, wheat germ agglutinin and the ovalbumin glycopeptide are all inhibitors of the cytotoxic effect of diphtheria toxin on Chinese hamster cells. Ovalbumin glycopeptide loses its inhibitory property after treatment with beta-N-acetylglucosaminidase. This demonstrates the importance of the glycopeptide structure for the mechanism of inhibition. The glycopeptide may be a toxin cell-surface receptor analogue. Diphtheria toxin-resistant mutants were isolated in order to search for cells that might have an altered toxin receptor. One mutant was 10- to 15-fold more resistant to diphtheria toxin than wild-type cells when protein synthesis was measured as a function of toxin concentration. However, when protein synthesis was measured as a function of time at a high toxin concentration, the time before onset of inhibition was identical in the mutant and wild-type cells. We present evidence indicating that the resistance of this mutant can be accounted for by a decreased affinity of toxin for a cell-surface receptor.

Cell Line↗
PubMed1978

Diphtheria toxin has the properties of a lectin.

The inhibition of protein synthesis in Chinese hamster V79 cells by diphtheria toxin is antagonized by the lectins concanavalin A, succinylated concanavalin A, and wheat germ agglutinin but not by Proteus vulgaris phytohemagglutinin or abrus agglutinin. The effects of concanavalin A and wheat germ agglutinin are reversed by methyl alpha-mannoside and N-acetylglucosamine, respectively. The inhibition of diphtheria toxin as a function of concanavalin A concentration fits a model of competitive inhibition with an apparent dissociation constant for concanavalin A of 3 X 10(-8) M. These results suggest that the diphtheria toxin receptor may be an oligosaccharide. To test this hypothesis, we screened several oligosaccharides for the ability to inhibit diphtheria toxin. The cell wall polysaccharide of Salmonella cholera suis and the ovalbumin glycopeptide were effective inhibitors. These studies suggest that diphtheria toxin may have the oligosaccharide binding properties of a lectin with specificity for N-acetylglucosamine and mannose.

Cell Line↗
PubMed1978

Use of an internal standard in monitoring the bacterial degradation of crude oil.

Hexachloroethane is nonvolatile, insoluble in water, and apparently not toxic to or metabolized by bacteria. Its addition to cultures growing at the expense of crude oil thus provides an internal standard against which the rate of degradation of individual crude oil components can be conveniently and reproducibly measured.

Bacteria↗
PubMed1975

The mechanism of action of vinblastine. Binding of [acetyl-3H]vinblastine to embryonic chick brain tubulin and tubulin from sea urchin sperm tail outer doublet microtubules.

Tritium-labeled viblastine, specific activity 107 Ci/mol, was prepared by acetylation of desacetylvinblastine with [3H]acetic anhydride, and has been employed in a study of vinblastine binding to tubulin. There are two high affinity vinblastine-binding sites per mole of embryonic chick brain tubulin (KA = 3-5 X 10(5) l./mol). Binding to these sites was rapid, and relatively independent of temperature between 37 and 0degreeC. Vincristin sulfate and desacetylvinblastine sulfate, two other active vinca alkaloid derivatives, competitively inhibited the binding of vinblastine. The inhibition constant for vincristine was 1.7 X 10(-5) M; and for desacetylvinblastine, 2 X 10(-5) M. The vinblastine binding activity of tubulin decayed upon aging, but this property was not studied in detail. Vinblastine did not depolymerize stable sea urchin sperm tail outer doublet microtubules, nor did it bind to these microtubules. However, tubulin solubilized from the B subfiber of the outer doublet microtubules possessed the two high affinity binding sites (KA = 1-3 X 105 l./mol). These data suggest that vinblastine destroys microtubules in cells primarily by inhibition of microtubule polymerization, and does not directly destroy preformed microtubules.

Animals↗
PubMedDate not supplied

Detection of distinct isoform patterns of the beta-amyloid precursor protein in human platelets and lymphocytes.

Cerebral deposition of the amyloid beta-protein (A beta P), approximately 40 residue fragment of the integral membrane protein, beta-amyloid precursor protein (beta APP), has been implicated as the probable cause of some cases of familial Alzheimer's disease (AD). The parallels between A beta P deposition in AD and the deposition of certain plasma proteins in systemic amyloid diseases has heightened interest in the analysis of beta APP in circulating cells and plasma. Here, we describe distinct isoform patterns of beta APP in peripheral platelets and lymphocytes. PCR-mediated amplification of mRNA from purified platelets demonstrated the expression of all three major beta APP transcripts (beta APP770,751,695). The full-length, approximately 140 kDa form of beta APP751,770 was detected in membranes of resting and activated platelets but very little immature, approximately 122 kDa beta APP751,770 was found, suggesting a different processing of beta APP in platelets than that described in a variety of cultured cells and tissues. Platelets stimulated with thrombin, calcium ionophore, or collagen released the soluble, carboxyl-truncated form of beta APP (protease nexin-II), but no evidence for the shedding of full-length beta APP associated with platelet microparticles was found, in contrast to previous reports. As a positive control marker for microparticles, the fibrinogen receptor subunit, GPIIIa, was readily detected in platelet releasates. Resting and activated platelets contained similar amounts of the approximately 10 kDa carboxyl terminal beta APP fragment that is retained in platelet membranes following the constitutive cleavage of protease nexin-II. Nonstimulated peripheral B and T lymphocytes contained small amounts of membrane-associated mature and immature beta APP751,770. The potentially amyloidogenic full-length beta APP molecules present in circulating platelets and lymphocytes but not in microparticles could serve as a source of the microvascular A beta P deposited during aging and particularly in AD.

Adult↗
PubMedDate not supplied

Assessment of cardiopulmonary resuscitation in the membership examination of the Royal College of Physicians.

The poor performance of doctors in cardiopulmonary resuscitation has been described in several studies. The problem has been addressed in the last few years by simplifying treatment algorithms, establishing standards of competence, and creating a training framework. Resuscitation skills are also assessed during formal examinations such as those for the membership of the Royal College of Physicians (MRCP(UK)). In 1994 and 1996, we assessed the resuscitation skills of the candidates at our centre during the short-case section of the MRCP examination. With the correct preparation, there was no difficulty in carrying out detailed assessment of basic life support, defibrillation and advanced life support. This assessment was carried out separately from that of the examiners and did not interfere with the running of the short cases. The resuscitation skills of this small sample of an important group of doctors in training grades were unsatisfactory, and we suggest that more should be done to raise standards.

Cardiopulmonary Resuscitation↗