A general approach to the location of radiopaque objects, with applications in radiotherapy.
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Biomedical subjects
Publications and source records attributed to D Jones.
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The time course of changes in plasma cyclic AMP, heart rate and bronchial tone after inhalation of fenoterol or isoprenaline from a dose-metered aerosol are reported in a group of normal subjects. After isoprenaline, plasma cyclic AMP increased rapidly reaching a peak by 10 min and returned to basal levels within 60 min. A rapid, transient rise in heart rate occurred that was maximal by 5 min and returned to a basal level by 45 min. After fenoterol, the changes in cyclic AMP and heart rate were of much longer duration. The rise in plasma cyclic AMP was slower in onset and of greater magnitude than for isoprenaline, reaching a peak by 20 min and remaining above basal level for more than 6 h. The maximum increase in heart rate after fenoterol was less than that observed with isoprenaline but an elevated rate persisted for 4 h after inhalation of fenoterol. Fenoterol is known to have a longer duration of action as a bronchodilator in comparison with isoprenaline. The prolonged rise in plasma cyclic AMP in normal subjects given inhaled fenoterol may reflect this long duration of action. The concomitant rise in heart rate, however, suggests that the duration of plasma cyclic AMP response may in part be due to the systemic effect of the fraction of inhaled fenoterol known to be absorbed via the buccal and intestinal routes.
A monoclonal antibody, designated M148, produced by the hybridoma technique from spleen cells of mice immunized with human medulloblastoma, was found by indirect immunofluorescence to bind to normal human platelets (both PlA1 positive and PlA1 negative) and megakaryocytes, as well as to some medulloblastoma and neuroblastoma cells and cell lines and certain other solid tumours. No binding was observed to other marrow constituents, nor to any other normal tissue examined. The antibody bound to platelets from a patient with the Bernard-Soulier syndrome but not to thrombasthenic platelets. It immunoprecipitated glycoproteins IIb and IIIa from 125I-labelled normal platelet membranes, and completely inhibited ADP-induced fibrinogen binding and aggregation of platelets. Aggregation was also inhibited in response to adrenaline, collagen, thrombin, sodium arachidonate and the ionophore A23187; clot retraction was partially inhibited. The antibody was without effect on thromboxane formation or 5-hydroxytryptamine (5HT) secretion in response to thrombin, but inhibited 5HT secretion in response to arachidonate. It did not inhibit factor VIII binding or agglutination in response to ristocetin, but completely inhibited factor VIII binding in response to thrombin. These findings suggest that the epitopes are close to the fibrinogen and factor VIII binding sites on glycoproteins IIb/IIIa, and that the lack of these glycoproteins is sufficient explanation for the pattern of dysfunction observed in thrombasthenic platelets, without invoking any other membrane abnormality.
A survey of methicillin-resistant strains of Staphylococcus aureus received for phage typing indicated a marked increase of resistant strains received in 1982 and 1983. Of 62 hospitals in New York City which sent strains for phage typing, 35 had methicillin-resistant isolates. A significant development was the presence of strains of the same phage type at several hospitals, indicating a possible inter-hospital spread of these strains. Among strains present at several hospitals, the largest group was of experimental phage type 88. Strains of type 88 were received from 23 hospitals, representing 56% of all methicillin-resistant strains received from New York City hospitals. Strains of type 88 were resistant to all antistaphylococcal antibiotics, with the exception of vancomycin, and represented a major source of nosocomial infections at 13 hospitals. As experimental phage 88 is not routinely used for typing in U.S. laboratories, the nationwide distribution of strains of type 88 is difficult to assess.
RTG-2 cells, a line of fibroblasts from rainbow trout (Salmo gairdnerii), are induced to synthesize a distinct set of heat-shock polypeptides after exposure to elevated temperature or to low concentrations of sodium arsenite. We isolated and characterized two cDNA sequences, THS70.7 and THS70.14, encoding partial information for two distinct species of 70-kilodalton heat shock polypeptide (hsp70) from these cells. These sequences are identical at 73.3% of the nucleotide positions in their regions of overlap, and their degree of sequence conservation at the polypeptide level is 88.1%. The two derived trout hsp70 polypeptide sequences show extensive homology with derived amino acid sequences for hsp70 polypeptides from Drosophila melanogaster and Saccharomyces cerevisiae. Northern blot analysis of RNA from arsenite-induced RTG-2 cells, with the trout hsp70 cDNAs as probes, revealed the presence of three hsp70 mRNA species. Southern blot analysis of trout testis DNA cleaved with various restriction endonucleases revealed a small number of bands hybridizing to the hsp70 cDNAs, suggesting the existence of a small family of hsp70 genes in this species. Finally, trout hsp70 cDNA sequences cross-hybridized with restriction fragments in genomic DNA from HeLa cells, bovine liver, Caenorhabditis elegans, and D. melanogaster.
In patients with chronic obstructive pulmonary disease, respiratory drive as estimated from occlusion pressures (PO.1 and PO.1/PCO2, cm H2O/mm Hg) and respiratory timing (T1, T1/TTOT) were predicted accurately by multiple regression analysis from the respiratory parameters PO2, PCO2, and blood HCO3 in conjunction with estimates of cerebral blood flow. We used four linear models to obtain essentially the same multiple correlation coefficient, indicating that these independent variables are all important factors in controlling both the drive and timing of respiration.
Three relatively clear-cut diagnostic groups, namely primary major depressive disorder-endogenous subtype (PRI MDD-E), primary anxiety disorder with no depression (PRI ANX), and normal controls as well as two additional patient groups with mixed or coexisting anxious/depressive diagnoses were studied. Clinical assessment was made by routine psychiatric interview, Schedule of Affective Disorder and Schizophrenia (SADS) research interview, and obtaining family history of MDD. Subjects underwent both routine 'baseline' sleep EEG polygraphic arecoline, a muscarinic, cholinergic agonist infused during sleep. Cholinergic sensitivity was assessed by measuring the time to induction of REM sleep after arecoline infusion. In addition, a subgroup of MDD patients underwent pupillographic testing. Peripheral alpha-adrenergic responsivity was measured by the magnitude of pupillary mydriatic response after local ocular instillation of phenylephrine. Successful separation (83% correct classification) of the 'pure' groups (PRI MDD-E, PRI ANX, and normal) was achieved by discriminant function analysis of sleep EEG variables. Compared to PRI ANX and normal groups, patients with PRI MDD-E had supersensitive cholinergic REM-induction response, shorter REM latency, increased first REM density and REM percent. Separation of the PRI ANX and normal groups was by intermittent awake time, delta sleep percent, and total REM density. Classification of the mixed anxious/depressive groups was next attempted using the discriminant coefficients derived from the above analysis of 'pure' groups. We found that the presence of absence of family history of MDD in patients with mixed diagnosis offered the best prediction of classification into PRI MDD-E and PRI ANX groups, respectively. MDD patients with coexisting panic disorder were significantly subsensitive to phenylephrine-induced mydriasis compared to MDD patients without anxiety.
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The clinical evaluation of an ultralightweight polypropylene below-knee prosthesis conducted by the University of Strathclyde identified a number of potential problems which can arise from the use of polypropylene. This paper describes the problems associated with manufacture, loss of alignment and fitting, and indicates handling techniques to minimize these problems.
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A six-months out-patient study of chronic alcoholics with undecompensated liver disease has shown a statistically significant inverse correlation between the change in mean corpuscular volume and the change in body weight (r = -0.4, P less than 0.01). A fall in body weight over this period was the best clinical indicator of apparently continuing alcohol abuse. Previous anthropometric studies have indicated that reduced adipose tissue is one cause of lower body weights in such patients. To determine whether this is due to the effects of alcohol or of poor nutrition, the epididymal fat pad weights of rats following 28 days administration of alcohol (36% of total calories) as part of a nutritionally adequate liquid diet were compared with those of pair-fed controls initially matched for body weight. At the end of the experiment, body weight gain was the same in both groups but the mean weight of the fat pads of alcohol-fed animals (371.7 mg +/- 60.0 mg SD) all of which developed hepatic steatosis was 29% greater than that of pair-fed controls (288.7 mg +/- 42.4 mg). This difference was statistically significant (P less than 0.025). This study shows that alcohol intake per se does not prevent an increase in body weight or fat even if hepatic steatosis is induced and that loss of adipose tissue in chronic alcoholics who continue to drink is probably due to simultaneous inadequate nutritional intake.
The precise nature of the motion of the knee during a pivot shift is of interest when types of knee instability are correlated with specific injuries. Ten subjects with anterior cruciate ligament injuries and demonstrable pivot shift instabilities were examined with a triaxial electrogoniometer to detect angular motion at the joint during the performance of a pivot shift test. By varying the method of test performance and observing the patterns of motion by eye and in the electrogoniometric data, the pivot shift was shown to be a dominantly translational event during nonstressed knee testing and a dominantly rotational event during stressed knee testing.
The nucleotide sequences of two different cDNAs, CEHS48 and CEHS41, coding for the 16,000 dalton heat shock proteins (hsps) of Caenorhabditis elegans have been determined. CEHS48 codes for a polypeptide of 135 amino acids, approximately 15 fewer than the complete protein while CEHS41 is missing approximately 46 amino acids. From nucleotide 113 to the TAA termination signal the extent of homology between the sequences is 91%. Toward the 5' ends, the homology drops to 20% and results in completely divergent amino acid sequences. The 3' noncoding regions are only 30% homologous. Only CEHS48 contains a poly(A) signal and a poly(A) tail, suggesting that CEHS41 has an incomplete 3' end. The region from amino acid 43 to amino acid 115 shows extensive homology with corresponding regions in the four small hsps of Drosophila melanogaster and in mammalian alpha-crystallin. Two-dimensional gel analysis of in vitro synthesized hsp16 reveals the existence of five distinct components of identical molecular weights, but with different isoelectric points.
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Monoamine metabolite measurements are being increasingly used for making nosological, symptomatological and pharmacological profiles of the affective disorders. A number of unresolved methodological issues question the validity of using baseline metabolite levels for predicting treatment response. Some studies show correlations between baseline metabolite levels and response to treatment with specific antidepressant agents. Effects of antidepressant treatment on metabolite levels may be useful in predicting drug response.