Biomedical subjects
Publications and source records attributed to E Garcia.
We present a case of Uhl's anomaly associated with atresia of the pulmonary valve. The rarity of this association is noteworthy, only three cases having previously been published. Our case presents the peculiarity of a patient with a normal tricuspid valve.
Explore the source record for details and available documents.
Four experiments were conducted to determine whether in conditioning to a serial compound, CS1-CS2-UCS, there are (a) associative mechanisms operating to extend conditioning beyond the bounds of a CS-UCS contiguity gradient and (b) stimulus selection processes acting to attenuate the potency of CS-UCS contiguity. In Experiments 1 and 2, the CS2-UCS interval was held at .35 sec while the CS1-UCS interval was varied across groups from .75 to 2.75 sec. CS1 test trials revealed substantial CR acquisition at all CS1-UCS intervals. Moreover, Experiment 2 indicated that when the contribution of cross-modal generalization from CS2 to CS1 was factored out, there still remained a substantial level of conditioning, which Experiment 3 indicated was attributable to an associative mechanism like higher-order or sensory conditioning. The observation of CR acquisition at CS1-UCS intervals of 4.75, 8.75, and 18.75 sec in Experiment 4 suggested that serial compound training yields conditioning to CSs located well beyond the single CS contiguity gradient for the rabbit's nictitating membrane response. Experiments 1 and 2 also indicated the presence of stimulus selection processes because, at the shorter CS1-UCS intervals (.75 and 1.25 sec), the levels of test-trial responding to CS2 fell below those observed to the less contiguous CS1.
The product of the glnR gene is required for nitrogen regulation of the synthesis of glutamine synthesis (Gln synthetase) [L-glutamate:ammonia ligase (ADP-forming), EC 6.3.1.2] and two periplasmic transport proteins that are subject to nitrogen control in Salmonella. Strains with mutations to loss of function of the glnR product [e.g., a strain with a Tn10 insertion or one with an ICR-induced (frameshift) mutation in glnR] have about 3% as much Gln synthetase as a fully derepressed wild-type strain and are unable to increase synthesis of this enzyme or periplasmic transport proteins in response to nitrogen limitation. The structural gene for Gln synthetase, glnA, and those for the periplasmic transport proteins are unlinked on the chromosome; thus, glnR appears to encode a diffusible positive regulatory element. Consistent with this, the mutant glnR allele is recessive to the wild-type allele with regard to expression of glnA (synthesis of Gln synthetase). Although glnR is closely linked to glnA, strains with mutations to complete loss of function of the glnR product can be distinguished from glnA strains by their ability to produce detectable Gln synthetase and to grow in the absence of glutamine. To demonstrate unequivocally that glnR is distinct from glnA, we have purified and characterized Gln synthetase from a strain with a Tn10 insertion in glnR. Because the properties of Gln synthetase from the insertion mutant, most importantly the carboxyl-terminal sequence of amino acids, are the same as those of synthetase from wild type, the Tn10 insertion cannot be in glnA (if it were, the carboxyl terminus of Gln synthetase would have to be altered); therefore we conclude that the Tn10 insertion is in a regulatory gene, glnR, which is distinct from glnA. A model for the function of the glnR product together with the previously defined glnF product in mediating nitrogen control is discussed.
6 clinically normal subjects underwent a 3-month physical conditioning program with the ejection fractions determined before and after physical conditioning using a scintillation probe. All subjects achieved a conditioning effect as evidenced by increased treadmill test duration after conditioning (mean duration before conditioning: 658 vs. 715 sec after conditioning; p less than 0.02). All 6 subjects increased resting ejection fractions after conditioning (mean ejection fraction before conditioning: 54.5 +/- 5.4%; mean ejection fraction after conditioning: 67.0 +/- 9.0%; p less than 0.01). Thus, an aerobic physical conditioning program appears to increase resting ejection fractions in normal subjects.
Explore the source record for details and available documents.
The design and function of a device that holds an ultrasound transducer against the chest wall in a stationary position is described. This holder is useful for obtaining echocardiograms during cinefluoroscopic procedures, various positional maneuvers, and exercise testing.
Explore the source record for details and available documents.
To aid in the study of coronary artery disease, 57 patients with complete left bundle branch block underwent clinical evaluation, treadmill exercise testing and cardiac catheterization. The patients were classified into two groups according to coronary angiographic findings: 30 patients with significant stenosis (70 percent or greater luminal narrowing) of at least one major vessel and 27 with no significant coronary artery disease. There was no difference in age, presenting symptoms or previous medical treatment between the two groups. There were more men in the group with coronary artery disease. Exercise-induced S-T changes were similar in the two groups; the sensitivity and specificity of these changes for the diagnosis of coronary artery disease were unacceptable irrespective of the criterion chosen. With additional S-T depression of either 1 or 2 mm below the baseline value, the predictive accuracy was only 53 percent. Combined exertional chest pain and 1 mm S-T depression increased the predictive accuracy of exercise testing to 71 percent. These data indicate that exercise-induced electrocardiographic changes do not facilitate detection of coronary artery disease in patients with complete left bundle branch block.
The addition of ethylenediaminetetraacetate to competent cultures of Bacillus subtilis irreversibly inhibited the transformability as well as the cellular binding of DNA. Our results show that the inhibition of DNA binding by ethylenediaminetetraacetate in whole cells, protoplasts, and membrane vesicles is mainly due to a permanent alteration of the DNA receptors. Transformation absolutely requires free magnesium ions, whereas DNA binding is a magnesium-independent step. In contrast to ethylenediaminetetraacetate, the absence of Mg2+ does not irreversibly affect the capacity of the competent cells to be transformed DNA-binding receptors located at the cell surface remain associated with the plasma membrane after protoplasting and after isolation of membrane vesicles. A Mg2+-dependent endonucleolytic activity associated with the membrane appears to be responsible for the lower levels of binding by protoplasts in the presence of this ion.
Explore the source record for details and available documents.
A patient with tetralogy of Fallot who underwent a successful Blalock shunt procedure as a child was evaluated 28 years later because of clinical deterioration. Results of cardiac catheterization and angiography disclosed, in addition to a functioning shunt, evidence of an infundibular, subvalvular tumor and a large anastomosis between the left circumflex coronary artery and the bronchial arteries of the right lung with the possibility of "coronary steal". At operation, the Blalock and coronary-to-bronchial artery anastomoses were ligated; and total correction was performed including resection of the pulmonary valve and infundibulum, excision of the tumor, closure of the ventricular septal defect, and application of an outflow patch to enlarge the pulmonary annulus. The patient was discharged nine days after surgical correction.
Explore the source record for details and available documents.
The product of a newly identified gene, glnF, which is distinct from the glutamine synthetase structural gene (glnA), is required for synthesis of glutamine synthetase [L-glutamate:ammonia ligase (ADP-forming), EC 6.3.1.2[ in Salmonella typhimurium and probably in Escherichia coli. Salmonella strains with ICR (2-chloro-6-methoxy-9-[3-(2-chloroethyl)aminopropylamino]acridine dihyodrochloride)-induced (frameshift) mutations in glnF are glutamine auxotrophs; they have less than 10% oof wild-type glutamine synthetase activity or antigen and are unable to derepress the synthesis of the enzyme. The mutant allele is recessive to the wild-type allele, indicating that the glnF gene encodes a diffusible product. Mutant glnF strains have normal activities of all proteins involved in covalent modification of glutamine synthetase: adenylyltransferase (EC 2.7.7.42), PII, uridylyltransferase, and uridylyl removing enzyme. In addition, they have glutamate synthase (EC 1.4.1.13) and glutamate dehydrogenase (EC 1.4.1.4) activities. Thus, glnF does not encode the structure of any of these proteins. The above evidence suggests that the product of the glnF gene is (or produces) a positive regulatory factor that is required for synthesis of glutamine synthetase; it indicates that auto-regulation cannot account for control of the synthesis of glutamine synthetase in Salmonella.
Recognition of thrombosis of a Björk-Shiley aortic valve prosthesis 4 years after insertion in a patient was based upon sudden clinical deterioration, loss of prosthetic sounds, and development of new stenotic and regurgitant murmurs. Thrombotic fixation was confirmed by diagnostic alterations on the echocardiogram. All manifestations reverted to normal after successful surgical debridement of the prosthesis. Echocardiography is a valuable noninvasive adjunct in the differential diagnosis of prosthetic valve malfunction.
Explore the source record for details and available documents.
Coliphage BF23 develops in Salmonella typhimurium rough strains. The phage is neither restricted nor modified by S. typhimurium. The growth patterns of the phage were slightly different in S. typhimurium than in Escherichia coli, although phage propagated on S. typhimurium is identical to the phage propagated in E. coli by several criteria used. Mutants of S. typhimurium resistant to BF23 were isolated and found to map (by P22- and Pl-mediated transduction) in the same position as bfe mutants of E. coli. The order of genes was: metB - argC - bfe - rif - purD - metA. Phage BF23 does not form plaques on smooth S. typhimurium strains, since the phage fails to adsorb irreversibly to smooth cells. Nevertheless, on solid agar, the phage prevents growth of many (but not all) smooth strains. Moreover, UV- and alkali-inactivated phage BF23, although unable to form plaques on sensitive hosts, retains the ability to prevent growth of the host on solid medium. This ability is sensitive to protease and resistant to DNAse and RNase. Heat treatment of the phage causes rapid loss of the cell-growth-preventing-ability whereas the ability to form plaques is lost much more slowly. These results lead to a proposal that phage BF23 virions carry a colicin-like factor that kills sensitive cells.
The influence of adenosine-3',5'-cyclic monophosphate (cAMP) and other nucleotides on the competence development of Bacillus subtilis was studied. The stimulation of competence which can be achieved by exposing physiologically low-competent cells to supernatants from highly competent cultures can be inhibited with different cAMP doses. When the same cells were suspended in a minimal medium with cAMP, varying degrees of stimulatin- of competence were observed depending on the time of addition of the drug. This effect is not specific for cAMP. It appears to be correlated to an increase of the amount of DNA bound to the competent cells. cAMP activities were antagonized by equimolar doses of adenosine-triphosphate (ATP) and guanosine-triphosphate (GTP).