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Biomedical subjects

M Jay

Publications and source records attributed to M Jay.

At least 127 records · Page 7Linked to original sources
PubMed1989

Demonstration of bias in series of retinoblastoma.

A register of retinoblastoma is being compiled with the aim of complete ascertainment of all cases with a recorded diagnosis of retinoblastoma in the United Kingdom. Sources of ascertainment include patients seen at St Bartholomew's and Moorfields Eye Hospitals, cases recorded in regional cancer registries, and pathology reports. Ascertainment of the Hospital series is complete, but that of the rest of the country is still incomplete. Comparison between the proportions of bilateral and unilateral cases in an age cohort in the Hospital series and the country as a whole shows that the Hospital series is biased towards an excess of bilateral cases.

Eye Neoplasms↗
PubMed1989

Genetic and cytogenetic analysis of patients showing reduced esterase-D levels and mental retardation from a survey of 500 individuals with retinoblastoma.

The authors have analysed the esterase-D levels in 500 retinoblastoma patients of whom 15 showed red cell enzyme activities of approximately 50% that of normal controls. Chromosome analysis of these 15 patients confirmed the presence of a deletion involving region 13q14 in all cases. Seven of the 15 cases had not previously been diagnosed and all of these showed sub-band deletions within 13q14. None of these seven patients were mentally retarded although the remaining eight who showed larger chromosome deletions demonstrated the full spectrum of psychomotor abnormalities associated with 13q deletions. Two other mentally retarded retinoblastoma patients with normal esterase-D activity showed no karyotypic abnormality, demonstrating that mental retardation cannot be taken to indicate a chromosome deletion in all cases. Eight of the 15 deletion cases were only unilaterally affected. The data presented in this article suggest that esterase-D quantitation could provide the primary means of detection of chromosome deletions in retinoblastoma patients.

Adult↗
PubMed1988

Detection of the carrier state of X-linked retinoschisis.

We determined the extent of suppressive rod-cone interaction in 11 obligate carriers and eight potential carriers of X-linked retinoschisis from eight families. Despite otherwise normal ophthalmoscopic and functional testing, all of the obligate heterozygous carriers demonstrated a complete absence of normal rod-cone interaction. Of the potential heterozygous carriers, three had normal rod-cone interactions, two had no detectable interaction, and two yielded technically unsatisfactory results. This lack of rod-cone interactions allows heterozygous individuals to be identified clinically and has implications concerning the origin of this inherited disorder.

Flicker Fusion↗
PubMed1988

Deletion of chromosome region 13q14 is transmissible and does not always predispose to retinoblastoma.

During routine screening of retinoblastoma patients for esterase D activity in red blood cell lysates a patient was identified with only 50% of normal enzyme activity. Chromosome analysis showed that this patient had a small deletion within chromosome region 13q14. Parental studies showed that, whereas the father had normal enzyme levels, the mother had esterase D levels which were also 50% of normal and a similar small 13q14 deletion. Ophthalmological examination failed to demonstrate any retinal abnormality in either parent. Thus we present the first case not only of the direct transmission of a 13q14 deletion within a family but also of an individual in whom the deletion has not predisposed to tumour formation.

Cell Line↗
PubMed1988

Impact of nicotine on myocardial neutrophil uptake.

Excessive cigarette smoking is recognized as a major risk factor for ischemic heart disease. Although the mechanism by which smoking enhances this risk is not known, multiple lines of indirect evidence suggest that an adverse effect of nicotine on the interaction between neutrophils and the myocardium may play a central pathogenic role. Accordingly, this study employed an isolated rabbit heart preparation perfused at a constant flow rate with physiologic salt solution containing autologous neutrophils to test the hypotheses that nicotine promotes myocardial neutrophil uptake and that an augmented myocardial neutrophil burden intensifies the actions of stimulated neutrophils on the coronary circulation. Addition of 10(-7) M nicotine to the perfusion medium caused an abrupt and sustained sequestration of 111In-labeled neutrophils by isolated rabbit hearts. In contrast, preincubation of neutrophils in 10(-7) M nicotine without inclusion of the alkaloid in the perfusion medium failed to promote neutrophil uptake. Nicotine neither enhanced myocardial neutrophil sequestration induced by perfusion with hypoxic medium nor potentiated neutrophil chemotactic responses evoked by leukotriene B4, the putative mediator of hypoxia-induced myocardial neutrophil uptake. In addition, nicotine failed to influence either baseline levels or the hypoxia-induced accumulation of immunoreactive leukotriene B4 detected in myocardial biopsies. The inflammatory cell stimulant, formylmethionyl-leucyl-phenylalanine (fMLP), increased coronary vascular resistance in neutrophil-perfused hearts but not in hearts perfused with neutrophil-free medium. The magnitude of the fMLP-induced coronary response was augmented when the myocardial neutrophil burden was increased by the addition of nicotine to the perfusion medium or by perfusion with hypoxic medium. These observations suggest that nicotine promotes myocardial neutrophil uptake by mechanisms that do not relate to enhanced release and/or effects of endogenous leukotriene B4 and that sequestration of neutrophils intensifies their actions on the coronary circulation.

Animals↗
PubMed1988

fMLP provokes coronary vasoconstriction and myocardial ischemia in rabbits.

Recent pathological studies of coronary arteries from humans with suspected coronary spasm have revealed an augmented intramural burden of inflammatory cells. To test the hypothesis that inappropriate activation of inflammatory cells participates in the evolution of coronary vasospasm, the present experiments employed a newly developed coronary arteriographic technique for use in pentobarbital-anesthetized rabbits to evaluate the coronary vasomotor actions of the nonselective inflammatory cell stimulant, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP). In 10 of 10 animals, selective left intracoronary injection of 200 ng fMLP evoked profound left coronary narrowing accompanied in all cases by ST segment deviation and dysrhythmias. Thallium-201 scintigraphy demonstrated hypoperfusion of the left ventricular free wall and septum supplied by the spastic coronary artery. The fMLP-induced epicardial vaso-constriction, ischemic electrocardiogram (ECG) changes, and thallium perfusion defects were reversed by intravenous nitroglycerin. Neither the right coronary artery nor its distribution were influenced by left coronary injection of fMLP. Additional experiments in isolated, salt solution-perfused rabbit hearts demonstrated that fMLP failed to exert direct coronary vasoconstrictor effects. These observations indicate that the non-selective inflammatory cell stimulant, fMLP, provokes arteriographically demonstrable coronary spasm with attendant myocardial hypoperfusion and ischemic ECG changes in anesthetized rabbits. Such a model may be useful in exploring the dynamic role of inflammatory cells in development of coronary spasm.

Angiography↗
PubMed1988

Reversible depression in Binswanger's disease.

The authors describe four elderly patients with Binswanger's disease in whom depression was prominent. Therapy with antidepressant drugs in three patients produced major improvement in psychological and physical functions. The one patient who could not be given an adequate course of antidepressant therapy because of intercurrent illness improved spontaneously after many months. The authors conclude that depression associated with Binswanger's disease is reversible despite persistence of neurological abnormalities. They speculate that this depressive syndrome is an example of organic affective disorder due to diffuse subcortical white matter ischemic lesions of the cerebral hemispheres and discuss the possible neuroanatomical basis of the depression.

Aged↗
PubMed1987

Alternations in lipid membrane fluidity and the physical state of cell-surface sialic acid in zinc-deficient rat erythrocyte ghosts.

Erythrocyte ghosts, prepared from the blood of rats fed zinc-deficient diets, were evaluated for membrane fluidity and surface sialic acid properties using spin-labeled probes and electron spin resonance (ESR) spectroscopy. These physical parameters of the erythrocyte ghosts from the zinc-deficient group were compared to those for erythrocyte ghosts obtained from ad libitum and pair fed controls consuming zinc-adequate diets. As the animals became progressively zinc deficient, the erythrocyte ghost membranes became more fluid than those from the control groups. In addition, the apparent rotational correlation time of Tempamine spin probes on surface sialic acid residues was smaller for the zinc deficient group, indicative of an increased rotational mobility of the spin label. These results suggest that zinc deficiency can have pronounced effects on the physical state of membrane bilayer lipids and cell surface carbohydrates and supports the view that many of the pathological signs of zinc deficiency are due to a general membrane defect.

Animals↗
PubMed1987

Comparisons of labeling efficiency, biological activity and biodistribution among 125I-, 67Ga-DTPA-and 67Ga-DFO-lectins.

The labeling efficiency, biological activity and biodistribution of 125I labeled and 67Ga chelating agent conjugated lectins were investigated. Pisum sativum agglutinin (PSA) and Lens culinaris agglutinin (LCH) were efficiently labeled with 67Ga using bifunctional chelating agents such as diethylenetriaminepentaacetic acid (DTPA) and deferoxamine (DFO), whereas labeling with 125I was significantly less efficient. The agglutinating activity of these lectins towards Ehrlich ascites tumor (EAT) cells was retained on conjugation with DFO, but not with DTPA. The in vitro binding ratio of 67Ga-DFO-lectins for EAT cells was almost the same as that of 125I-lectins. However, the value was significantly decreased in the case of 67Ga-DTPA-lectins. In the biodistribution study of radiolabeled lectins in Ehrlich solid tumor (EST) bearing mice, the accumulation of radioactivity in tumor tissue was very much less with 67Ga-DTPA-lectins than with 125I-lectins. However, the concentration was significantly elevated in the case of 67Ga-DFO-lectins. While, these lectins accumulated in liver, spleen, lung, and kidney to a greater extent than 67Ga citrate, the tumor to organ ratios became very low. These low tumor to organ ratios, in contrast to 67Ga citrate, will certainly inhibit the tumor delineation, and therefore it seems that in spite of a high accumulation ratio of 67Ga-DFO-lectins in tumor tissue, these agents are not useful in tumor detection.

Animals↗
PubMed1987

An experimental study on differential diagnosis of tumor from inflammation by using 125I labeled Pisum sativum agglutinin.

We have reported that Pisum sativum agglutinin (PSA), a plant lectin which recognizes mannosyl residues, accumulates markedly in Ehrlich solid tumor (EST) and suggested the possibility of applying PSA to tumor imaging radiopharmaceuticals. In the present work, an inflammation was induced by implantation of cotton thread in the left rear leg skeletal muscle of ddY mice and Ehrlich ascites tumor cells were inoculated into the right rear leg. 67Ga-citrate accumulated in the tumor tissue and the inflammatory lesion to almost equal extents. On the other hand, 125I-PSA preferentially accumulated in tumor tissues in mice bearing both tumor and inflammation. The results suggest that differential diagnosis of tumor from inflammation using radiolabeled PSA may be possible.

Animals↗
PubMed1987

A chromosomal breakpoint that separates the esterase D and retinoblastoma predisposition loci in a patient with del(13)(q14q31).

A patient with severe mental retardation and other congenital abnormalities who developed retinoblastoma was shown to have a deletion on the long arm of chromosome #13 with breakpoints in regions q14 and q31. Quantitation of enzyme activity of the esterase-D gene which, together with the retinoblastoma locus, is located in region 13q14 showed levels that were equal to those of normal controls. The 13q14 breakpoint, therefore, appears to have occurred between the two loci, which places the esterase D gene in a more proximal position in this band than the retinoblastoma locus.

Carboxylesterase↗
PubMed1987

Enhanced chemotaxis and superoxide anion production by polymorphonuclear leukocytes from nicotine-treated and smoke-exposed rats.

Although previous studies have shown that polymorphonuclear leukocytes (PMNs) exposed to nicotine in vitro exhibit enhanced superoxide anion generation and chemotactic responses, it is not known whether in vivo exposure to the alkaloid causes the same alterations in PMN function. Accordingly, this study evaluated superoxide anion generation evoked by phorbol myristate acetate (PMA) and chemotactic responses to formylmethionylleucylphenylalanine (fMLP) in PMNs isolated from rats treated acutely or subchronically with nicotine and from rats chronically exposed to cigarette smoke. Acute or subchronic (twice daily for 7 days) i.p. injection of 0.2 or 0.02 mg/kg nicotine potentiated PMA-induced superoxide anion generation by PMNs. Similarly, acute i.p. injection of 0.2 mg/kg nicotine or subchronic treatment with 0.02 mg/kg nicotine potentiated fMLP-induced chemotaxis. Subchronic treatment with 0.2 mg/kg of the alkaloid blunted fMLP-induced chemotaxis, in contrast to the potentiating actions of the lower dose. Treatment with nicotine mimicked the effects of tobacco smoke exposure. A 15-week exposure regimen to either sidestream and mainstream smoke from University of Kentucky 2R1 reference cigarettes potentiated PMA-induced superoxide anion generation. Mainstream but not sidestream smoke also enhanced chemotactic responses to fMLP. Viewed collectively, these observations indicate that in vivo exposure to nicotine or to tobacco smoke augment PMN superoxide anion generation and chemotactic responses to selected stimuli and thus implicate such adverse actions of smoking on PMN function in certain pathologies associated with excessive tobacco smoke exposure.

Animals↗
PubMed1987

Correlation of ibuprofen bioavailability with gastrointestinal transit by scintigraphic monitoring of 171Er-labeled sustained-release tablets.

External gamma scintigraphy was used to monitor the gastrointestinal (GI) transit of radiolabeled sustained-release tablets containing 800 mg ibuprofen in eight fasted healthy volunteers. Ibuprofen serum concentrations were determined from blood samples drawn sequentially over a 24-hr period. Serum concentrations and related parameters were correlated to the position of the dosage form in the GI tract from the scintiphotos. The sustained-release tablets were radiolabeled intact utilizing a neutron activation procedure, by incorporating 0.18% of 170Er2O3 (enriched to greater than 96% 170Er) into the bulk formulation. After manufacture of the final dosage forms, the tablets were irradiated in a neutron flux (4.4 x 10(13) n/cm2.sec) for 2 min, converting the stable 170Er to radioactive 171Er (t1/2 = 7.5 hr). Each tablet contained 50 microCi of 171Er at the time of administration. The scintigraphy studies suggested that the greatest proportion of ibuprofen was absorbed from this dosage form while the tablet was in the large bowel. The dosage forms eroded slowly in the small bowel and appeared to lose their integrity in the large bowel. In vitro studies showed only minimal effects of the neutron irradiation procedure on the dosage form performance.

Biological Availability↗