11 research outputs found

    The Physics of the B Factories

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    Elevated lactate dehydrogenase isoenzyme 1 as a tumour marker in patients with germ cell testicular tumours

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    In a series of 50 patients with testicular tumours evaluated prior to orchidectomy, 12 out of 19 with pure seminoma and seven out of 31 with non-seminomatous or mixed seminomatous and non-seminomatous germ cell tumours had elevated plasma lactate dehydrogenase isoenzyme 1 concentrations. In contrast, seven of the 19 seminoma patients had elevated serum human chorionic gonadotrophin (hCG) concentrations and 25 of the 31 non-seminomatous and mixed seminomatous and non-seminomatous germ cell tumour patients had elevations of hCG and/or alpha-fetoprotein. Using these three markers, 12 out of 19 seminoma patients and 27 out of 31 non-seminomatous or mixed seminomatous and non-seminomatous tumour patients were positive for one or more of these tumour markers

    Post-infarct sympathetic hyperactivity differentially stimulates expression of tyrosine hydroxylase and norepinephrine transporter

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    The balance between norepinephrine (NE) synthesis, release, and reuptake is disrupted after acute myocardial infarction resulting in elevated extracellular NE. Stimulation of sympathetic neurons in vitro increases NE synthesis and the synthetic enzyme tyrosine hydroxylase (TH) to a greater extent than it increases NE reuptake and the NE transporter (NET) which removes NE from the extracellular space. We used TGR(ASrAOGEN) transgenic rats, which lack post-infarct sympathetic hyperactivity, to test the hypothesis that increased cardiac sympathetic nerve activity accounts for the imbalance in TH and NET expression in these neurons after myocardial infarction. TH and NET mRNA levels were identical in the stellate ganglia of unoperated TGR(ASrAOGEN) rats compared to Sprague Dawley (SD) controls, but the 3-fold increase in TH and 2-fold increase in NET mRNA seen in the stellate ganglia of SD rats one week after ischemia-reperfusion was absent in TGR(ASrAOGEN) rats. Similarly, the increase in TH and NET protein observed in the base of the SD ventricle was absent in the base of the TGR(ASrAOGEN) ventricle. Neuronal TH content was depleted in the left ventricle of both genotypes while NET was unchanged. Basal heart rate and cardiac function were similar in both genotypes, but TGR(ASrAOGEN) hearts were more sensitive to the beta agonist dobutamine. Tyramine-induced release of endogenous NE generated similar changes in ventricular pressure and contractility in both genotypes, but post-infarct relaxation was enhanced in TGR(ASrAOGEN) hearts. These data support the hypothesis that post-infarct sympathetic hyperactivity is the major stimulus increasing TH and NET expression in cardiac neurons

    Fatal ventricular tachycardia in association with propafenone, a new class IC antiarrhythmic agent.

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    A man with a past history of malignant ventricular arrhythmias occurring late after myocardial infarction was admitted for assessment. Monitoring revealed frequent ventricular premature beats and occasional non-sustained runs of ventricular tachycardia. Other drugs having failed, he was started on oral propafenone which is a new Vaughan Williams class IC antiarrhythmic agent. Several hours after starting this drug he had incessant ventricular tachycardia and subsequently died. Other class IC agents have been shown to have a high incidence of proarrhythmic effects, and particular care should be taken with these potent new drugs

    The BaBar detector: Upgrades, operation and performance

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    Contains fulltext : 121729.pdf (preprint version ) (Open Access
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