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Biomedical subjects

A Ehsani

Publications and source records attributed to A Ehsani.

14 recordsLinked to original sources
PubMed1993

Characterization of a new allele of the human ERBB2 gene by allele-specific competition hybridization.

Nucleotide sequence analysis of the ERBB2 proton-oncogene in human breast tumors revealed a sequence variation at codons 654 and 655, corresponding to the transmembrane region of the protein. To investigate this polymorphism, genotyping of 340 unrelated individuals was conducted by allele-specific oligonucleotide (ASO) hybridization of DNA amplified from the ERBB2 transmembrane region. ASO hybridization under competition conditions allowed rapid and unambiguous assignment of alleles and revealed the occurrence of a new allele, B3, encoding Val-Val. The sensitivity and the specificity of the ASO competition hybridization technique indicate that the method is generally applicable to the analysis of polymorphisms in the human genome.

Alleles↗
PubMed1992

Detection of specific alleles by using allele-specific primer extension followed by capture on solid support.

This article describes a method for determining whether a particular nucleic acid sequence is present in a sample and for discriminating between any two nucleic acid sequences if such sequences differ only by a single nucleotide. The method entails extension of a novel two-component primer on templates that may or may not include a target nucleic acid sequence. The 3' portion of the primer is complementary to a portion of the template adjacent to the target sequence (for example, the polymorphic nucleotide). The 5' portion of the primer is complementary to a different preselected nucleic acid sequence. Extension of the 3' portion of the primer with a labeled deoxynucleoside triphosphate yields a labeled extension product, but only if the template includes the target sequence. The presence of such a labeled primer-extension product is detected by hybridization of the 5' portion to the preselected sequence. The preselected sequence is immobilized on a solid support. The method has been applied to genotyping individuals for the two-allele polymorphism of the human tyrosinase gene.

Alleles↗
PubMed1976

Effects of electrical countershock on serum creatine phosphokinase (CPK) isoenzyme activity.

Total and MB serum creatine phosphokinase (CPK) activity levels were measured serially in 30 patients treated with direct current electrical countershock, 17 patients with acute myocardial infarction and 25 normal subjects. In addition, serial determinations of total and MB CPK in serum were performed in 11 closed chest anesthetized dogs subjected to 10 repetitive countershocks at 15 second intervals with a delivered energy of 240 joules per countershock. Less than 4 milli-international units (mlU)/ml of MB CPK was found in the serum of normal subjects. Patients with myocardial infarction whose elevated total CPK levels were comparable with those of patients treated with cardioversion had a usbstantial rise in MB CPK activity, with peak values averaging 39 +/- 6 mlU/ml (mean +/- standard error). Fifteen of the 30 patients treated with countershock had elevated total CPK activity that peaked within 4 hours. In this group, MM CPK elevations accounted for the overall rise in CPK activity. In two patients, modest elevations of MB CPK (11 and 13 mlU/ml, respectively) were observed after cardioversion. In all 11 dogs total CPK increased after countershock, peaking to 1,888 +/- 410 MLU/ml within 6 hours. Six dogs had increased MB CPK activity (52+/- 6 mlU/ml) and myocardial necrosis demonstrable histologically 4 days later. The results indicate that (1) myocardial damage in dogs produced by intense, repetitive countershock is associated with increased serum MB CPK; and (2) countershock as conventionally used in patients does not generally produce myocardial damage and serum MB CPK elevation. Although release of MB CPK into serum occasionally occurs after countershock, perhaps reflecting myocardial damage, the elevations appear to be modest. Thus, electrical countershock does not obscure the diagnosis of myocardial infarction or impair quantitative assessment of the extent of myocardial damage based on analysis of serum MB CPK activity.

Adult↗
PubMed1975

Left ventricular performance after acute myocardial infarction. Sectrum of functional abnormalities and importance of wall motion disturbances during convalescent phase.

Seventeen patients underwent catheterization of the right and left sides of the heart and left ventricular (LV) angiography three to six weeks after acute myocardial infarction. Fourteen of 17 patients had abnormal LV function. Three patients had altered LV diastolic properties; five patients had abnormalities of diastolic properties and of systolic function; and six patients had abnormal systolic function, but diastolic function could not be assessed. Thirteen of the 14 patients with abnormal LV function had LV wall motion abnormalities, which were quantitatively related to impaired LV systolic function.

Adult↗
PubMed1975

Left atrial transport function in myocardial infarction. Importance of its booster pump function.

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.

Adolescent↗
PubMed1975

Ventricular fibrillation threshold in acute myocardial infarction and its relation to myocardial infarct size.

The effect of myocardial infarct size on ventricular fibrillation threshold (VFT) was evaluated by determining changes in VFT during acute myocardial infarction and relating those changes to infarct size. Infarct size was estimated from gross measurement and from serial changes in serum CPK activity in 25 dogs. VFT reduction correlated well with gross infarct size (r=0.92). This suggests that the severity of electrical instability during AMI is related to the size of the developing infarct, and that appropriate therapeutic interventions to reduce infarct size during this time may also render the heart more electrically stable.

Animals↗