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Biomedical subjects

S A Cook

Publications and source records attributed to S A Cook.

At least 55 records · Page 3Linked to original sources
PubMed1992

Genetic mapping of the murine gene and 14 related sequences encoding chromosomal protein HMG-14.

The high-mobility-group chromosomal protein HMG-14 preferentially binds to nucleosomal core particles of mammalian chromatin and may modulate the chromatin configuration of transcriptionally active genes. The human gene for HMG-14 has been localized to the Down syndrome region of Chromosome (Chr) 21 and may be involved in the etiology of this syndrome. Here we show, by means of genetic linkage analysis of interspecific and intersubspecific backcross mice, that the murine functional gene, Hmg14, is located on the distal end of mouse Chr 16, a region known to have conserved synteny with human Chr 21. In addition to the functional gene for HMG-14, both human and mouse genomes contain many related sequences that are probably processed pseudogenes. Here we map the locations of 14 Hmg14-related sequences in two mouse genomes. The 14 mapped loci are widely dispersed on ten chromosomes (Chrs 3, 5, 7, 9, 11, 12, 16, 17, 19, and X) and can be detected efficiently with a single cDNA probe. Thus, the Hmg14 multigene family is well suited to serve as genetic markers for other linkage studies in mice.

Animals↗
PubMed1992

Chromosomal localization of the murine gene and two related sequences encoding high-mobility-group I and Y proteins.

HMG-I and its isoform HMG-Y are members of the abundant high-mobility-group of nonhistone chromatin proteins; they bind to A + T-rich regions of chromosomal DNA and are expressed at high levels in rapidly dividing, undifferentiated mammalian cells. HMG-I and HMG-Y are alternatively spliced products of a single functional gene, designated Hmgi in the mouse. Here, we report the occurrence of at least three distinct Hmgi-related loci in the mouse. Only one of these loci was present in all of the 10 mouse strains examined; therefore, this locus most likely represents the transcriptionally active, functional gene, Hmgi. Genetic linkage analysis of interspecific and intersubspecific backcrosses showed that Hmgi is located in the t-complex region of mouse Chromosome 17. Two additional Hmgi-related sequences, Hmgi-rs1 and Hmgi-rs2, were found only in certain mouse strains and probably represent pseudogenes. Hmgi-rs1 is located on Chromosome 11; it was present in all of the standard laboratory inbred mouse strains examined but was absent in wild-derived inbred strains of Mus spretus, M. musculus castaneus, and M. m. molossinus. Hmgi-rs2 was found only in M. m. castaneus and is located on Chromosome 6. Hmgi genes have not been previously mapped in any species, but the location of the probable functional gene on murine Chromosome 17 suggests that the homologous gene in humans is located on Chromosome 6.

Animals↗
PubMed1992

Myocardial perfusion imaging in the diagnosis of coronary artery disease.

The role of myocardial perfusion imaging has been extended from diagnosis to management and prognosis in patients with coronary artery disease. Great emphasis has been placed on improving the accuracy of the test to better define perfusion, viability, and the extent of damage of the myocardium. To achieve this goal, investigators have focused on several areas including imaging technique, in which the accuracy of single-photon emission CT has been compared with that of positron emission tomography; radiopharmaceuticals, in which 201Tl has been compared with 99mTc-sestamibi and 99mTc-teboroxime; stress modalities, in which dipyridamole and adenosine stress have been compared with exercise; myocardial viability, as determined by delayed and reinjection 201Tl imaging or by measurement of cellular integrity using 82Rb compared with 18fluorodeoxyglucose metabolic PET imaging; and assessment of myocardial salvage and prognosis by exercise or dipyridamole 201Tl imaging in acute myocardial infarction.

Adenosine↗
PubMed1991

Influence of left ventricular mass on the diagnostic accuracy of myocardial perfusion imaging using positron emission tomography with dipyridamole stress.

This study assesses the influence of left ventricular hypertrophy (LVH) on the accuracy of myocardial perfusion imaging using pharmacologic coronary vasodilation. Seventy-five patients without previous infarction, and with known coronary anatomy, were studied by echocardiography and PET. LVH (defined by mass greater than 131 g/m2 in males or greater than 100 g/m2 in females) was identified in 25 patients; this group did not differ significantly from the remainder in terms of clinical or angiographic parameters. Twenty patients with hypertrophy had significant coronary artery stenoses, which were identified correctly by PET in 11 (55%), in contrast to 29 of 34 patients (85%, p = 0.03) with coronary disease but normal LV mass. Normal perfusion images were obtained in three of five patients (60%) with hypertrophy but no coronary disease; in contrast, 14 of 16 patients without either coronary disease or hypertrophy (88%, p = ns) had normal scans. The accuracy of PET was 14/25 (56%) in those with hypertrophy, and 43/50 (86%, p = 0.01) in patients with normal LV mass. In this group, the presence of hypertrophy was associated with reduction in the diagnostic accuracy of PET using dipyridamole stress. These findings may account for the phenomenon of "dipyridamole nonresponsiveness" in some patients.

Adult↗
PubMed1986

Verification of Fourier phase and amplitude values from simulated heart motion using a hydrodynamic cardiac model.

Using pusher-plate-type artificial hearts, changes in the degree of synchrony and stroke volume were compared to phase and amplitude calculations from the first Fourier component of individual-pixel time-activity curves generated from gated radionuclide images (RNA) of these hearts. In addition, the ability of Fourier analysis to quantify paradoxical volume shifts was tested using a ventricular aneurysm model by which the Fourier amplitude was correlated to known increments of paradoxical volume. Predetermined phase-angle differences (incremental increases in asynchrony) and the mean phase-angle difference calculated from RNAs showed an agreement of -7 degrees +/- 4.4 degrees (mean +/- SD). A strong correlation was noted between stroke volume and Fourier amplitude (r = 0.98; P less than 0.0001) as well as between the paradoxical volume accepted by the 'aneurysm' and the Fourier amplitude (r = 0.97; P less than 0.0001). The degree of asynchrony and changes in stroke volume were accurately reflected by the Fourier phase and amplitude values, respectively. In the specific case of ventricular aneurysms, the data demonstrate that using this method, the paradoxically moving areas may be localized, and the expansile volume within these regions can be quantified.

Fourier Analysis↗
PubMed1985

Prediction of improvement in left ventricular function after ventricular aneurysmectomy using Fourier phase and amplitude analysis of radionuclide cardiac blood pool scans.

Postoperative improvement in left ventricular (LV) function is a common objective of LV aneurysmectomy, but is difficult to predict. The first Fourier component of time-activity curves of pre- and postoperative gated radionuclide angiographic studies was evaluated for this purpose in 20 patients who had undergone aneurysmectomy. LV aneurysms had portions that characteristically exhibited marked phase delay with varying degrees of amplitude. Total aneurysmal amplitude was obtained preoperatively by summing the amplitude component of all pixels that exhibited phase delay, suggesting paradoxical motion. LV ejection fraction (EF) before and after aneurysmectomy and the absolute postoperative increase in LVEF were calculated. Nine of 20 patients had an absolute increase of EF less than 10% despite resection of large aneurysms. A strong correlation was found between the absolute increase in EF after aneurysmectomy and the total amplitude within paradoxically moving areas (r = 0.93, p less than 0.0001). Thus, preoperative measurement of the total paradoxical amplitude predicts absolute change in EF and may be important in selecting patients for aneurysmectomy. The data also suggest that the total aneurysmal amplitude reflects the stroke volume ejected into an aneurysm in systole and that paradoxical expansion of an aneurysm contributes to LV dysfunction in some of these patients.

Adult↗
PubMed1981

Recirculation subtraction for analysis of left-to-right-cardiac shunts: concise communication.

The object of this study is to improve the techniques for describing the lung dilution curve for shunt quantification by separating the effects of systemic recirculation on the curve form those of direct shunt return. The time of the systemic recirculation peak was estimated by determination of transit times from the right and left ventricles and lung. A gamma variate fit based on the distribution of points at that segment was applied to the recirculation curve and subtracted from the original lung dilution curve. Similar gamma variate fitting was performed for both primary and shunt curves. Rather than fitting the gamma variate of the shunt curve by the leading edge only, a larger portion could now be used since the trailing edge of the curve is clearer following recirculation subtraction. The algorithm is completely automatic, requiring no operator intervention or selection of curve-fitting regions. The correlation coefficient for comparison of the dilution-curve analysis with oximetry determinations was 0.92 in a series of 29 patients.

Adolescent↗
PubMed1981

Failure of LeVeen shunting in refractory ascites--a view from the other side.

We have reviewed our experience with 11 patients treated with LeVeen peritoneovenous shunts during a 22-month period from March, 1976, through December, 1977, to assess long-term results and shunt patency. Nine patients had follow-up studies to assess shunt patency at a mean of 26 months. After insertion of the shunt, the mean weight loss was 7.9 kg at hospital discharge. At 26-month follow-up evaluation, six patients had minimal ascites (responders), whereas five had massive ascites (nonresponders). Of the six responders, three patients with nonfunctioning shunts lost an average of 15.8 kg of ascites, three whereas with patent shunts lost an average of 15.0 kg. Eight of 11 patients (73%) required revision or replacement of the shunt because of malfunction; clotting was the most common cause of failure. We conclude that the role and effectiveness of LeVeen peritoneovenous shunts remain questionable. They may cause diuresis, maintain it, or not be responsible for it all. Clinical reports that cite their effectiveness should document patency of these shunts.

Adult↗