[Use of artificial neural networks in survival evaluation in heart failure].
Explore the source record for details and available documents.
Cardiac Output, Low↗
Biomedical subjects
J Ortiz
Publications and source records attributed to J Ortiz.
[Postural changes during echocardiography. Is this manoeuver necessary in the differential diagnosis of fixed and free floating thrombus?].
A case of a 62 year-old woman with mitral stenosis and thrombosis of the left atrium diagnosed by two-dimensional echocardiography (2D-Echo) is reported. During the procedure, postural changes were performed and characterized the thrombus as floating one. The postural changes during 2D-echo examination allows differential diagnosis among fixed and free floating atrial thrombus. Such postural manoeuvres are also important in evaluating prognosis and therapeutic management of mitral stenosis.
Coronary Thrombosis↗
[Consensus SOCESP-SBC on echocardiography].
Explore the source record for details and available documents.
Aortic Diseases↗
Second messenger and protein phosphorylation mechanisms underlying possible genetic vulnerability to alcoholism.
Explore the source record for details and available documents.
Alcoholism↗
Motor abnormalities in the terminal ileum of patients with chronic idiopathic constipation.
Abnormalities in oesophageal, gastric and jejunal motility have been described in patients with chronic idiopathic constipation, suggesting that this may be a panenteric disorder. To test the hypothesis that ileal motility is also abnormal in constipation, terminal ileal motility was studied in ten patients and six healthy controls by prolonged and ambulant manometry. Mean(s.e.m.) phase II activity was significantly prolonged in patients compared with controls, during wakefulness (61.6(7.3) versus 19.3(3.5) per cent, P < 0.001) and sleep (44.4(9.0) versus 1.1(0.8) per cent, P < 0.001). The mean(s.e.m.) duration of phase III fronts was shorter in patients (7.9(1.8) min) than in controls (13.2(1.3) min; P < 0.001). Retrograde propagation was seen in approximately 15 per cent of all phase IIIs in patients but not in control subjects. The mean(s.e.m.) duration of postprandial activity was significantly shorter in patients than in controls (30.1(6.2) versus 130.0(68.0) min, P < 0.001). Ileal motility is abnormal in patients with chronic idiopathic constipation. This may result from an abnormality of the enteric nervous system or abnormal modulation of this system by the central nervous system.
Adult↗
Chronic morphine administration increases beta-adrenergic receptor kinase (beta ARK) levels in the rat locus coeruleus.
Based on the established role of beta-adrenergic receptor kinase (beta ARK) and beta-arrestin in the desensitization of several G protein-coupled receptors, we investigated the effect of chronic morphine administration on beta ARK and beta-arrestin levels in selected brain areas. Levels of beta ARK were measured by blot immunolabeling analysis using antibodies specific for two known forms of beta ARK, i.e., beta ARK1 and beta ARK2. It was found that chronic morphine treatment produced an approximately 35% increase in levels of beta ARK1 immunoreactivity in the locus coeruleus, but not in several other brain regions studied. In contrast, chronic morphine treatment failed to alter levels of beta ARK2 immunoreactivity in any of the brain regions studied. Levels of beta-arrestin immunoreactivity, measured using an antiserum that recognizes two major forms of this protein in brain, were also found to increase (by approximately 20%) in the locus coeruleus. It is proposed that chronic morphine regulation of beta ARK1 and beta-arrestin levels may contribute to opioid-receptor tolerance that is known to occur in this brain region.
Animals↗
Mechanism of interruption of atrial flutter by moricizine. Electrophysiological and multiplexing studies in the canine sterile pericarditis model of atrial flutter.
BACKGROUND: Moricizine is said to have potent effects on cardiac conduction but little or no effect on cardiac refractoriness. METHODS AND RESULTS: The effects of moricizine (2 mg/kg IV) on induced atrial flutter were studied 2 to 4 days after the creation of sterile pericarditis in 11 dogs. Ten episodes of stable atrial flutter before and after the administration of moricizine were studied in 9 dogs in the conscious, nonsedated state, and 7 episodes were studied in 6 dogs in the anesthetized, open chest state. In the conscious state, the effects of moricizine on atrial excitability, atrial effective refractory period, and intra-atrial conduction times were studied by recording during overdrive pacing of sinus rhythm from epicardial electrodes placed at selected atrial sites. Moricizine prolonged the atrial flutter cycle length in all the episodes, from a mean of 133 +/- 9 to 172 +/- 27 milliseconds (P < .001), and then terminated 7 of the 10 episodes. Moricizine increased the atrial threshold of excitability from a mean of 2.3 +/- 1.4 to 3.3 +/- 2.2 mA (P < .01) and prolonged intra-atrial conduction times (measured from the sulcus terminalis to the posteroinferior left atrium) from a mean of 58 +/- 6 to 64 +/- 5 milliseconds (P < .005). Prolongation of the atrial effective refractory period from 166 +/- 20 to 174 +/- 24 milliseconds (P < .05) was observed only at the sulcus terminalis site. In the open chest studies, administration of moricizine prolonged the atrial flutter cycle length from a mean of 150 +/- 15 to 216 +/- 30 milliseconds (P < .001) and then terminated the atrial flutter in all 7 episodes. As demonstrated by simultaneous multisite mapping from 95 bipolar sites on the right atrial free wall, the atrial flutter cycle length prolongation was either due to further slowing of conduction in an area of slow conduction in the reentrant circuit of the atrial flutter (5 episodes) or further slowing of conduction in an area of slow conduction plus the development of a second area of slow conduction (2 episodes). The change in conduction times in the rest of the reentrant circuit was negligible (10.9 +/- 8.7% of the total change). In all 7 episodes, the last circulating reentrant wave front blocked in an area of slow conduction. CONCLUSIONS: Moricizine (1) prolongs the atrial flutter cycle length, primarily by slowing conduction in an area of slow conduction in the reentrant circuit, (2) terminates atrial flutter by causing block of the circulating reentrant wave front in an area of slow conduction of the reentrant circuit, and (3) effectively interrupts otherwise stable atrial flutter in this canine model. The reason for these effects of moricizine are not readily explained by its effects on global atrial conduction times and refractoriness studied during sinus rhythm. Local changes in conduction in an area(s) of slow conduction are responsible for both cycle length prolongation and atrial flutter termination rather than the traditional wavelength concept of head-tail interaction.
Animals↗
Characterization of the excitable gap in a functionally determined reentrant circuit. Studies in the sterile pericarditis model of atrial flutter.
BACKGROUND: Single premature beats were introduced in the reentrant circuit during stable atrial flutter in the canine sterile pericarditis model to test the hypotheses that (1) despite the fact that the reentrant circuit is functionally determined, there is a fully excitable gap; (2) the excitable gap in the reentrant circuit is not uniform; and (3) inhomogeneities of conduction in the reentrant circuit explain the effects of premature beats. METHODS AND RESULTS: A multiplexing system was used to record 190 unipolar electrograms from the right atrial free wall during 18 atrial flutter episodes in 9 dogs. In all 18 episodes, premature stimuli captured the atrial flutter reentrant circuit. At the longest coupling intervals, the return cycle at the site closest to the pacing site did not prolong. As the coupling interval of the premature stimulus decreased, the return cycle then progressively increased, associated with changes in conduction in the reentrant circuit that were not uniform. The result was that coupling intervals associated with introduction of the premature beat also were not constant. The mean duration of the total (ie, fully plus partially) excitable gap was 12 +/- 4 ms in areas of slow conduction, and it was always shorter than the total excitable gap in other areas (22 +/- 6 ms, P < .001). The mean duration of the fully excitable gap based on analysis of the return cycle was 4 +/- 1 ms in the reentrant circuit. In 13 of 18 atrial flutter episodes, a premature stimulus terminated atrial flutter by causing block of the orthodromic wave front of the premature beat in an area of slow conduction. The mean coupling interval that caused orthodromic block was 113 +/- 5 ms (recorded at the site just proximal to the area of block), and it was always longer than the delivered stimulus coupling interval at the pacing site (96 +/- 8 ms, P < .001). CONCLUSIONS: We conclude that in this functionally determined atrial flutter reentrant circuit in the canine sterile pericarditis model, (1) a fully excitable gap is present in at least part of the reentrant circuit; (2) the duration of the excitable gap in the reentrant circuit is shortest in areas of slow conduction; and (3) when a premature beat encounters the partially excitable gap of the reentrant circuit, it results in changes in conduction such that the coupling intervals are not uniform throughout in the reentrant circuit.
Animals↗
Mapping the conversion of atrial flutter to atrial fibrillation and atrial fibrillation to atrial flutter. Insights into mechanisms.
It is not generally believed that there is a relation between atrial flutter, thought to be due to a single reentrant circuit, and atrial fibrillation, thought to be due to simultaneously circulating multiple-reentrant wave fronts. However, there are many reasons to suggest that these rhythms are more closely related than previously thought. To test the hypothesis that the length of an area of functional block in the right atrial free wall is critical to the conversion of atrial flutter to atrial fibrillation and of atrial fibrillation to atrial flutter, we studied spontaneous and ATP-induced conversion of stable atrial flutter to sustained atrial fibrillation and spontaneous conversion of sustained atrial fibrillation to stable atrial flutter. We studied 13 episodes of the conversion of stable atrial flutter to sustained atrial fibrillation and sustained atrial fibrillation to stable atrial flutter in seven dogs with sterile pericarditis. Six episodes were spontaneous and seven were ATP related. All episodes were studied by using a multisite mapping system to record 190 unipolar electrograms (converted in the software to 95 bipolar electrograms) from the right atrial free wall along with ECG lead II. Atrial flutter induction was attempted by atrial stimulation (S1S2 or S1S2S3) or by rapid atrial pacing for > or = 20 beats from selected sites at selected rates. For both the spontaneous and the ATP-related episodes, stable atrial flutter was defined as any episode of > or = 5 minutes, and sustained atrial fibrillation was any episode of > or = 1 minute. During all the episodes of stable atrial flutter, a line of functional block with a mean length of 24 +/- 4 mm was localized on the right atrial free wall. When the previously stable line of functional block decreased to a mean of 16 +/- 3 mm (P < .05), either spontaneously or after ATP administration (40 mg i.v.), the new line of functional block was not long enough to maintain stable atrial flutter, and conversion to atrial fibrillation resulted. This shortened line of functional block continued to change and migrate over the right atrial free wall throughout sustained atrial fibrillation. These observations were similar for both spontaneous and ATP-induced conversions. When sustained atrial fibrillation evolved to stable atrial flutter, there was reformation of a long line of functional block, long enough (> or = prior length) to create a stable reentrant circuit, which then captured the right atrial free wall and subsequently both atria.(ABSTRACT TRUNCATED AT 400 WORDS)
Adenosine Triphosphate↗
Alcohol dehydrogenase from human stomach: variability in normal mucosa and effect of age, gender, ADH3 phenotype and gastric region.
Alcohol dehydrogenase (ADH) has been analysed in 36 endoscopic biopsies of normal gastric body and/or antrum mucosa, from 31 individuals with an age between 17 and 79 years. Oesophageal, duodenal and oral mucosa specimens have been also examined. Stomach mucosa contains three isozyme types: the gamma gamma-ADH forms (class I), sigma sigma-ADH (class IV) and chi chi-ADH (class III). gamma gamma-ADH was present in all gastric samples, while sigma sigma-ADH was detected in all body specimens (n = 15) but only in eight of 20 antrum biopsies. The presence of high sigma sigma-ADH activity in oral and oesophageal mucosa confirms the distribution of class IV in the upper gastrointestinal tract where it may serve as a first metabolic barrier against ingested alcohols and aldehydes. Considering all gastric specimens, ADH activity was 5.78 +/- 2.61 mU/mg of protein with 100 mM ethanol, pH 10.0. ADH activity was higher in men than women and in gastric body than in antrum, although differences did not reach statistical significance. However, activity was significantly higher in subjects below 50 years than those older than 50 years. Furthermore, an inverse correlation was found between gastric ADH activity and age (r = -0.40, P < 0.02). In old subjects ADH activity was significantly higher in gastric body (5.87 +/- 1.22 mU/mg) than in antrum (4.14 +/- 1.78 mU/mg) (P = 0.03). Differences in activity between samples from each ADH3 phenotype were statistically not significant but corresponded to those expected from the kinetic constants of the respective gamma gamma-ADH isozymes, which suggests that ADH3 polymorphism affects activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Randomized trial comparing three forms of pelvic floor repair for neuropathic faecal incontinence.
A randomized controlled trial in women with neuropathic faecal incontinence compared total pelvic floor repair (n = 12) with anterior levatorplasty and sphincter plication alone (n = 12) and postanal repair alone (n = 12). Review at 6 and 24 months indicated that results were significantly better for total pelvic floor repair than either of the other procedures. Complete continence was achieved in eight of the 12 patients 2 years after total pelvic floor repair. Only total repair significantly elongated the anal canal. Both total pelvic floor repair and anterior levatorplasty improved sensation in the upper anal canal.
Adult↗
Effects of the antidepressant drug tianeptine on plasma and platelet serotonin of depressive patients and healthy controls.
We have examined the effects of a single 12.5 mg dose and of 12 weeks treatment up to 37.5 mg daily with tianeptine, a new antidepressant drug that potentiates in vivo the uptake of serotonin (5-HT). On day 0, tianeptine reduced plasma 5-HT concentration. This acute effect occurred also on subsequent examination days. However, long-term treatment tended (P < 0.06) to increase basal plasma 5-HT concentrations, in covariation with decreases of MADRS (Montgomery-Asberg Depression Rating Scale) and HARS (Hamilton Anxiety Rating Scale). Platelet 5-HT increased only in elderly patients, probably due to the higher plasma concentration of the drug in this group than in younger patients. These results show that the acute effects of therapeutic doses of tianeptine are consistent with an enhancement of the 5-HT uptake. However, long-term treatment does not result in a decreased plasma 5-HT, as might be expected from the acute effects of the drug.
Adult↗
Propylthiouracil (PTU)-induced agranulocytosis treated with recombinant human granulocyte colony-stimulating factor (G-CSF).
Two premenopausal female patients with Graves' hyperthyroidism and propylthiouracil (PTU)-induced agranulocytosis are presented. The first patient, age 47, received 300 mg of PTU per day and developed agranulocytosis within 6 weeks of the commencement of therapy. There were no granulocytes in the peripheral smear and a bone marrow biopsy demonstrated an absence of the entire myeloid cell line as well as the presence of many granulomas. The second patient, age 39, received PTU 1600 mg per day for two and half weeks and then 2 days of methimazole, 200 mg per day. She developed complete agranulocytosis on peripheral smear within 3 weeks of the initiation of therapy. Her bone marrow biopsy demonstrated maturation arrest of the granulocytic cell line at the myelocyte stage. In addition to discontinuing their antithyroid drugs, both patients were treated with G-CSF subcutaneously. The first patient received 300 micrograms of G-CSF on days 2 and 4 after discontinuing PTU with the appearance of 4.7 x 10(9)/L granulocytes and granulocyte precursors on day 4. The second patient received 575 micrograms of G-CSF for 2 days and 300 micrograms for 1 additional day beginning on the third day after discontinuing antithyroid drugs. On the second treatment day there were 5.8 x 10(9)/L granulocytes and granulocyte precursors on the peripheral smear. A comparison to previously published cases on antithyroid drug induced agranulocytosis suggests that the use of G-CSF decreased the amount of time required for marrow recovery after the cessation of the offending drug.
Adult↗
Mechanism of spontaneous termination of stable atrial flutter in the canine sterile pericarditis model.
BACKGROUND: We tested the hypotheses that spontaneous termination of stable atrial flutter is directly related to spontaneous beat-to-beat cycle length oscillations and that block of the circulating reentrant wave front occurs in an area of slow conduction. METHODS AND RESULTS: We studied 30 episodes of spontaneous termination of stable atrial flutter induced by atrial stimulation in 11 conscious, nonsedated dogs with sterile pericarditis. Additionally, in 5 dogs, 14 episodes of spontaneous termination of stable atrial flutter were studied with a multisite mapping system to record simultaneously from 190 right atrial electrodes. In the conscious-state studies, atrial flutter cycle length oscillations began 6 +/- 1 (mean +/- SEM) beats before termination in 26 episodes, stable atrial flutter evolved into atrial fibrillation in 3 episodes, and no cycle length change occurred before termination in 1 episode. In the open-chest studies, in all instances, spontaneous oscillations began 7 +/- 1 beats before termination. The only consistent oscillation pattern occurred for the last two beats: a long cycle length (149 +/- 9 milliseconds) followed by a much shorter cycle length (110 +/- 6 milliseconds) (P < .01). Activation maps demonstrated that all cycle length oscillations were explained by changes of conduction in an area(s) of slow conduction in the reentrant circuit. In two instances, the last (short) cycle length was associated with disappearance of an area of slow conduction. In all episodes, the last circulating reentrant wave front blocked in an area of slow conduction in the reentrant circuit. Although not tested, during the last beat, the very early arrival of the circulating reentrant wave front at an area of slow conduction suggests an important role for refractoriness, with head and tail interactions, resulting in block. CONCLUSIONS: Spontaneous termination of stable atrial flutter in the sterile pericarditis model (1) is preceded by beat-to-beat cycle length oscillations that result from changes in conduction in areas of slow conduction in the reentrant circuit and (2) results from block of the circulating reentrant wave front in an area of slow conduction.
Animals↗
cAMP receptor protein from Trypanosoma cruzi: purification and cloning of a short sequence of the corresponding cDNA.
cAMP is involved in the differentiation of Trypanosoma cruzi, the causative agent of Chagas' disease. cAMP levels are elevated in the infective, non-dividing metacyclic trypomastigote stage, with respect to the non-infective, proliferative, epimastigote stage. In both stages three is a cAMP receptor protein (CARPT), with unique properties that differentiate it from the regulatory subunits of the cAMP-dependent protein kinase (RI and RII). The CARPT from T. cruzi epimastigotes was purified using ion-exchange chromatography, affinity chromatography and gel filtration. After the final step of purification, two protein bands were obtained, p89 and p70, corresponding to the intact CARPT and its proteolytic product. These two CARPT polypeptides were utilized to prepare polyclonal antibodies in rabbits. Previous results from our laboratory showed that CARPT cross-reacts with polyclonal antibodies prepared against the regulatory subunit (RII) of the cAMP-dependent protein kinase (PKA). As expected from these results, the anti-CARPT antibody recognized purified RII protein in an ELISA assay. The anti-CARPT antibodies were used for immunoblot analyses of epimastigote lysates. The two bands corresponding to the CARPT (p89 and p70), as well as a p40 band, were recognized. Immunoscreening of a T. cruzi lambda ZAP cDNA library with these anti-CARPT polyclonal antibodies yielded one positive clone (pBSCARPT) which contained a 540 bp insert. Northern analyses using the pBSCARPT clone as a probe, showed a 5.2 kb mRNA band in epimastigotes, which were grown in culture from 2 to 10 days in LIT medium. Sequence analyses of the 540 bp insert have failed to show homology to other gene sequences in the database.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Mucinous adenocarcinoma of the urachus. Apropos of a case].
This report present one case of mucinous adenocarcinoma of the urachus, a very uncommon tumour with eccentric clinical behaviour. It includes a brief description of both its macro and microscopic appearance, establishing the differential diagnosis both with adenocarcinoma of the vesical dome and the metastatic tumours which can affect the bladder. Also, there is a brief comment on the main anatomo-clinical characteristics of these tumours.
Adenocarcinoma, Mucinous↗
Total pelvic floor repair for the treatment of neuropathic fecal incontinence.
Long-term results of postanal repair are poor. Many patients with neuropathic incontinence have evidence of anterior pelvic floor weakness. A more comprehensive surgical repair has therefore been developed that involves postanal repair, anterior levatorplasty, and external sphincter plication. Primary total pelvic floor repair was performed in 22 women with neuropathic fecal incontinence. Fourteen patients who remained incontinent after conventional postanal repair underwent secondary anterior levatorplasty and external sphincter plication (two stages). Neither resting nor squeeze anal pressures were influenced by any of these procedures. However, pelvic floor descent at rest and straining was significantly decreased following primary total pelvic floor repair and secondary pelvic floor repair (p less than 0.05) but not by postanal repair. Complete continence for liquids, solids, and flatus was achieved in 41% of patients after primary total pelvic floor repair and in 14% after secondary anterior levatorplasty and external sphincter plication, but in only 4% after postanal repair. Only one patient after primary total pelvic floor repair and one after secondary anterior levatorplasty and external sphincter plication had persistent incontinence compared with 18 (38%) after postanal repair.
Anal Canal↗
Cation-induced aggregation and fusion of N-acyl-N-methyl-phosphatidylethanolamine vesicles.
Aggregation and fusion of unilamellar vesicles consisting of N-acyl-N-methylphosphatidylethanolamine were studied as a function of mono- and divalent cation concentrations. The aggregation reactions were irreversible processes, as demonstrated by changes in monovalent ion concentrations and by the addition of ethylenediaminetetraacetic acid (EDTA) to chelate divalent cations, suggesting the possibility of some cation-induced vesicle fusion. An increase in the NaCl ionic strength of the vesicle suspension solutions diminishes the threshold concentration for Li+ and K+ and increases that corresponding to Mn2+, Mg2+ and Ca2+. However NaCl concentrations above 300 mM yield smaller threshold values for the divalent cation-induced processes, probably due to the increased size of phospholipid vesicles as the ionic strength of the medium increases.
Cations↗