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Biomedical subjects

M Jimenez

Publications and source records attributed to M Jimenez.

At least 55 records · Page 3Linked to original sources

Food of the gods: cure for humanity? A cultural history of the medicinal and ritual use of chocolate.

The medicinal use of cacao, or chocolate, both as a primary remedy and as a vehicle to deliver other medicines, originated in the New World and diffused to Europe in the mid 1500s. These practices originated among the Olmec, Maya and Mexica (Aztec). The word cacao is derived from Olmec and the subsequent Mayan languages (kakaw); the chocolate-related term cacahuatl is Nahuatl (Aztec language), derived from Olmec/Mayan etymology. Early colonial era documents included instructions for the medicinal use of cacao. The Badianus Codex (1552) noted the use of cacao flowers to treat fatigue, whereas the Florentine Codex (1590) offered a prescription of cacao beans, maize and the herb tlacoxochitl (Calliandra anomala) to alleviate fever and panting of breath and to treat the faint of heart. Subsequent 16th to early 20th century manuscripts produced in Europe and New Spain revealed >100 medicinal uses for cacao/chocolate. Three consistent roles can be identified: 1) to treat emaciated patients to gain weight; 2) to stimulate nervous systems of apathetic, exhausted or feeble patients; and 3) to improve digestion and elimination where cacao/chocolate countered the effects of stagnant or weak stomachs, stimulated kidneys and improved bowel function. Additional medical complaints treated with chocolate/cacao have included anemia, poor appetite, mental fatigue, poor breast milk production, consumption/tuberculosis, fever, gout, kidney stones, reduced longevity and poor sexual appetite/low virility. Chocolate paste was a medium used to administer drugs and to counter the taste of bitter pharmacological additives. In addition to cacao beans, preparations of cacao bark, oil (cacao butter), leaves and flowers have been used to treat burns, bowel dysfunction, cuts and skin irritations.

Cacao↗

Potential role of the alpha4 and alpha6 nicotinic receptor subunits in regulating nicotine-induced seizures.

Several studies have shown that genetic factors influence sensitivity to nicotine-induced seizures in the mouse. We used recombinant inbred (RI) strains derived from the Long-Sleep (LS) and Short-Sleep (SS) mouse lines to assess the possibility that polymorphisms associated with one or more of the nicotinic receptors cosegregate with differential sensitivity to nicotine-induced seizures. Restriction fragment length polymorphisms (RFLPs) associated with the alpha2, alpha3, alpha4, alpha5, and alpha6 nicotinic receptors were identified in the LS and SS mouse lines, but the RI strains were polymorphic for only the alpha4 and alpha6 RFLPs. The RI strains were tested for sensitivity to nicotine-induced seizures. Strain and gender effects on seizure sensitivity were obtained as assessed by ED(50) values and latency to seizure. Those RI strains with the LS-like alpha4 RFLP were, on average, more sensitive to nicotine-induced seizures than were those RI strains with SS-like alpha4 RFLP. The alpha6 nicotine receptor may also play a role in modulating nicotine-induced seizures, but this effect is markedly influenced by gender. Females of the RI strains with the LS-like alpha6 RFLP were more sensitive to nicotine than were females of the strains with the SS-like alpha6 RFLP. Similar trends were seen in the males, but these trends were not significant. Thus, these strain differences may be due to polymorphisms associated with both the alpha4 and alpha6 nicotinic receptors, but gender also plays an important role in regulating sensitivity to nicotine-induced seizure.

Animals↗

[Availabilty of juveniles from natural sources of the oyster Pteria colymbus (Bivalvia: Mytilidae), in the Gulf of Cariaco, Venezuela].

We examined the spat availability the oyster Pteria colymbus at 6-8 and 19-21 m depths for 15 months (March 1993-June 1994) in Turpialito, Golfo de Cariaco, Venezuela. Spats were trapped using artificial collectors (plastic filaments in bags, 30 x 60 mm), suspended from a long line. Each collector was replaced by a replica monthly to analyse abundance, shell dimension and mass of P. colymbus. Intraweekly, the temperature, salinity, oxygen and food availability (Chlorophyll a, total seston, organic and inorganic seston) were determinated. There is juvenile recruitment all year, suggesting continuous reproduction. Spat counts were higher at 6-8 m (generally 50-230 juveniles per collector) with peaks in August and December 1993 (April and June 93 at 19-21 m). The length-weigh mass relation was higher at 19-21 m, suggesting greater food availability because of lower organism density (including P. colymbus) and a greater water flux. Phytoplanktonic abundance and temperature were correlated (r2=0.38) with juvenile abundanc; this relationship and the association of juvenile abundance with higher temperature and Chlorophyll a levels, suggest that spat abundance was higher at the beginning of the water stratification period, when phytoplankton biomass is high.

Animals↗

Immunohistological and ultrastructural analysis of the intimal thickening in coarctation of human aorta.

OBJECTIVES: The histological nature and characteristics of aortic coarctation are not clearly defined, the aim of this study is to analyse intimal thickening in aortic coarctation. METHODS: In order to characterize the components of intimal thickening in coarctation, narrowed segments of aorta obtained after surgery from ten children were examined immunocytochemically and by electron microscopy. RESULTS: Histological analysis of aortic coarctation demonstrated a widened subendothelial region with separation of endothelial cells from the internal elastic lamina. Masson's trichrome staining showed a marked increase in extracellular matrix and cell numbers in the intimal thickening compared with normal aorta. Cellular component analysis demonstrated invagination of the intima by smooth muscle actin-positive cells, with a fragmentation of the internal elastic lamina. No proliferating smooth muscle and inflammatory cells were identified in the intima. In order to characterize the smooth muscle cell phenotypes, various smooth muscle cell markers were sought using specific monoclonal antibodies: alpha-smooth muscle actin, smooth muscle-myosin heavy chain, heavy caldesmon, desmin. In moderate coarcted aorta, at least two distinct smooth muscle phenotypes were identified. In the juxtamedial part of the intima smooth muscle, cells were differentiated and expressed all smooth muscle markers; in the subendothelial part of the intimal thickening, the majority of smooth muscle cells expressed only alpha-smooth muscle actin and appeared dedifferentiated. In regions of marked stenosis, a strong expression of smooth muscle-myosin heavy chain, and heavy caldesmon in the intimal thickening pointed to the presence of redifferentiated smooth muscle cells, not still expressing desmin. Electron microscopic examination also revealed a variety of smooth muscle cell phenotypes in the intimal thickening. In the superficial layer, smooth muscle cells appeared to be in the synthetic state, while in the deeper part, both synthetic and contractile components were identified. CONCLUSIONS: These observations indicated that human coarctation was characterized by intimal recruitment of non-proliferating smooth muscle cells with dedifferentiated phenotype. However, the presence of smooth muscle cells with an intermediate phenotype in the narrowest part of the coarctation suggest that the redifferentiation process could participate in the pathogenesis of aortic coarctation.

Actins↗

Differentiating with fluorescence spectroscopy the sources of dissolved organic matter in soils subjected to drying

The relative fluorescence, normalised on dissolved organic carbon (DOC), and a humification index, based on the location of the fluorescence emission spectra, were used to investigate the possible sources of the increase in dissolved organic matter (DOM) when a soil is dried. From these 2 parameters it could be seen that air drying resulted in a minor increase of more humified material in DOM while the effect of oven drying was mainly due to cell lysis.

Journal Article↗

Potential of polymeric lamellar substrate particles (PLSP) as adjuvants for vaccines.

In recent years microspheres or microparticles produced from biodegradable polymers such as poly(D,L-lactide) (PLA) and poly(D, L-lactide-co-glycolide) (PLGA) containing encapsulated vaccine antigens have been investigated for administration via parenteral, oral, and intranasal routes. These microparticles allow the controlled release of vaccines with an aim to reduce the number of doses for primary immunisation or to develop single dose vaccines. The polymer materials have been widely regarded as being of minimal toxicity. Evaluation of candidate systems in animal studies have shown antibody levels and cell responses similar to or greater than those observed with adjuvants such as alum. However, there are concerns regarding the integrity and immunogenicity of the antigen during the encapsulation process when the antigen is exposed to organic solvents, high shear stresses and the exposure of antigen to low pH which is caused by polymer degradation. An alternative approach would be to adsorb antigens to the surface of biodegradable polymer particles. Polymeric lamellar substrate particles (PLSP), produced by a simple precipitation of PLA, are suitable for this purpose. The adsorption of antigens onto these particles is a simple procedure. It avoids pH changes due to bulk polymer degradation and the use of solvents and therefore will be less damaging to the vaccine. Moreover, such systems will be much easier to scale up for a clinical study and eventual manufacture. The aim of this article is to discuss the preparation and physical characteristics of PLSP, antigen adsorption, in vivo efficacy of PLSP antigen systems and to consider the potential of PLSP as controlled release adjuvants for protein, peptide or viral vaccines.

Adjuvants, Immunologic↗

Successful treatment of refractory supraventricular tachycardia by repeat intravascular injection of amiodarone in a fetus with hydrops.

We report the case of a fetus with supraventricular tachycardia complicated by congestive heart failure and ascites. After failure of initial transplacental treatment, the injection of amiodarone into the umbilical vein combined with evacuation of ascites achieved conversion to sinus rhythm and restored cardiac function thus allowing pregnancy to go to term. This report suggests that direct fetal therapy by umbilical vein puncture and evacuation of effusions constitutes an effective treatment for supraventricular tachycardias with massive fetal hydrops which do not respond to transplacental treatment.

Adult↗

Renal function in compensated hepatic cirrhosis: effects of an amino acid infusion and relationship with nitric acid.

AIMS: In order to assess the possible participation of nitric oxide (NO) in renal function during compensated hepatic cirrhosis, we studied renal function, the plasma and urinary levels of cGMP and the concentration of nitrates and nitrites, as markers of NO synthesis in blood and urine, in 10 patients with Child A hepatic cirrhosis as compared with 10 control subjects, both under basal conditions and during stimulation (amino acid-induced glomerular hyperfiltration). METHODS: To study renal function, the glomerular filtration rate (GFR), effective renal plasma flow (ERPF), renal functional reserve (RFR), renal venous resistance (RVR) and the filtration fraction (FF) were measured. Renin and aldosterone levels were determined to assess the possible involvement of these compounds in the renin-angiotensin-aldosterone axis. RESULTS: GFR and ERPF were significantly lower in the patients with cirrhosis than in the controls (mean GFR: 82+/-12.3 vs. 105+/-15 ml/min, p = 0. 01; ERPF 452+/-86 vs. 543+/-56 ml/min, p = 0.002). The RFR value was similar in both groups. In the basal situation cGMP levels were higher in plasma and urine in patients with cirrhosis than in the controls (plasma cGMP in cirrhosis 8.4+/-2.4 vs. 4.2+/-3.5 pmol/ml; urine cGMP in cirrhosis 1.2+/-2.1 vs. 0.68+/-0.1 pmol/ml). The NO levels were also higher in plasma and urine in patients with cirrhosis vs. controls (plasma NO in cirrhosis 45.5+/-9.2 vs. 30. 3+/-1.2 micromol/l; urinary NO in cirrhosis 6.2+/-1.3 vs. 3.1+/-2.3 micromol/ml). In both groups the amino acid perfusion increased GFR, ERPF, cGMP and NO levels in plasma and urine. In the patients with cirrhosis the RVR decreased significantly during perfusion and no noteworthy changes in FF were observed. The GFR values observed during amino acid perfusion were similar in patients with cirrhosis and portal hypertension to those observed in the controls (27.2+/-12 vs. 25.3+/-16%). However, the changes induced the ERPF were more marked in patients with cirrhosis (cirrhosis 35.3+/-15 vs. 22. 2+/-13%, p = 0.02). CONCLUSIONS: The present findings point to certain alterations in renal function in patients with hepatic cirrhosis and portal hypertension without ascitis, a clear difference being visible between the ERPF and GFR following amino acid-induced stimulation. The significant elevation in cGMP and NO levels in plasma and urine implies a maintained vasodilatory action that may at least partly compensate the vasoconstrictor effects of angiotensin II.

Adult↗

[Surgical evaluation of transthoracic tridimensional echocardiography in the anatomic study of atrial septal defect].

The closure of atrial septal defects by interventional catheterisation requires an accurate assessment of their morphology and anatomical relationships. This study evaluated transthoracic three-dimensional echocardiography for the selection of atrial septal defects accessible to an occlusive prosthesis. The transthoracic three-dimensional echocardiographic measurements of 17 patients (4 to 55 years) with ostium secundum atrial septal defects were compared with those of the surgeon in a prospective study. The maximal diameters of the defect, the height of the interatrial septum, the distances to the superior vena cava (postero-superior border) and inferior vena cava (postero-inferior border), to the coronary sinus and the tricuspid valve were measured as a reconstruction of the interatrial septum seen from the right atrium. The aortic border was measured from a three-dimensional view from the left atrium. Thirteen of the 17 investigations (76%) were exploitable. The diameters of the defect varied during the cardiac cycle (p = 0.0002). Ther correlations between the surgical and echocardiographic measurements varied from 0.82 for the maximal diameter to 0.6 for the postero-inferior limits. Three-dimensional echocardiography is capable of detecting all the contra-indications of an occlusive prosthesis: 2 inadequate postero-inferior and 1 inadequate aortic borders, 9 maximal diameters which were too large, 3 insufficiently high atrial septa, 1 double atrial septal defect. The coronary sinus was only visualised in 1 case. Transthoracic three-dimensional echocardiography is a non-invasive technique capable of improving the selection of atrial septal defects for interventional closure. The transoesophageal approach should be reserved for candidates selected by the transthoracic investigation for the detection of small structures (coronary sinus) and when the transthoracic window is poor.

Adolescent↗

Hemorrhagic shock primes for increased expression of cytokine-induced neutrophil chemoattractant in the lung: role in pulmonary inflammation following lipopolysaccharide.

Recent studies have suggested that hemorrhagic shock followed by resuscitation renders patients more susceptible to lung injury by priming for an exaggerated response to a second stimulus, the so-called "two-hit" hypothesis. We investigated the role of C-X-C chemokines in mediating the augmented lung inflammation in response to LPS following resuscitated shock. In a rodent model, animals exposed to antecedent shock exhibited enhanced lung neutrophil sequestration and transpulmonary albumin flux in response to intratracheal LPS. This effect correlated with an exaggerated expression of cytokine-induced neutrophil chemoattractant (CINC) protein and mRNA, but not macrophage-inflammatory protein 2. Strategies designed to inhibit CINC, both anti-CINC Ab and supplementation with the antioxidant N-acetyl-cysteine, prevented the enhanced neutrophil sequestration, suggesting that CINC played a central role in the enhanced leukocyte accumulation following shock plus LPS treatment. Shock alone increased lung nuclear factor-kappaB expression and augmented the response to LPS. Prevention of this effect by N-acetylcysteine supplementation of the resuscitation fluid implicates a role for oxidant stress in the priming for lung inflammation following shock. Finally, alveolar macrophages recovered from shock-resuscitated animals released more CINC protein in vitro in response to LPS than macrophages from sham animals. Considered together, these findings show that augmented release of CINC, in part from primed alveolar macrophages, contributes significantly to the enhanced lung leukosequestration and transpulmonary albumin flux in response to LPS following resuscitated shock.

Acetylcysteine↗

Catecholamine and cortisol responses of horses to incremental exertion.

The responses of the plasma concentrations of catecholamines and cortisol in horses to varied relative intensities of exertion were examined. The plasma concentrations of cortisol, epinephrine and norepinephrine increased significantly (p < 0.05) with exertion. The plasma cortisol concentrations at relative work intensities of 48.3% +/- 1.4%, 82.3% +/- 2.0% and 99.6% +/- 0.4% of VO2max were 114%, 124%, and 126%, respectively, of those at rest, whereas the plasma epinephrine concentrations were 239%, 772% and 3483%, and the norepinephrine concentrations were 138%, 255%, and 1121% of the values at rest. There was a significant (p < 0.0001) relationship between the plasma epinephrine and norepinephrine concentrations. The blood lactate concentration and the plasma epinephrine and norepinephrine concentrations were significantly (p < 0.0001) related, as were the relative work intensity (%VO2max) and the plasma epinephrine and norepinephrine concentrations. The relationships between the plasma cortisol concentration and work intensity or blood lactate concentration were not significant (p > 0.05). This study demonstrates a relationship between work intensity and indicators of adrenal medullary and sympathetic activity during brief exertion in horses.

Adrenal Medulla↗

[Study of the cardiorespiratory response and chronotropic function after correction of tetralogy of Fallot. Important role of residual pulmonary regurgitation].

Effort tolerance is reduced after correction of Tetralogy of Fallot. This prospective study investigated the cardiorespiratory response and the chronotropic function (mean follow-up 11.1 years) of 70 patients (43 boys and 27 girls) with an average age of 14.9 +/- 7.2 years (group 1) compared with 65 normal, sedentary subjects paired red for age and gender (group 2). All underwent exercise testing (Bruce protocol) with measurement of respiratory gases. Quantification of pulmonary regurgitation was performed by Doppler echocardiography. The chronotropic response to exercise was assessed by calculating the mean of slopes established by chronotropic metabolic relationship of Wilkoff. The cardiorespiratory response to exercise was abnormal in group 1: the duration of exercise (11.3 vs 13.6 min; p = 0.005), peak VO2 (35.5 vs 46 ml/min/kg; p < 0.001) and anareobic threshold (8.3 vs 9.2 min; p = 0.001) were decreased. Maximal heart rate (172 vs 190bpm; p < 0.001) and the mean of the metabolic-chronotropic slopes (0.68 vs 0.83; p < 0.001) were decreased in the patient group, showing abnormal chronotropic response to exercise. The latter seemed to be related to the severity of pulmonary regurgitation. The duration of exercise (10.6 vs 11.5 min; p = 0.001), peak VO2 (33 vs 37 ml/min/kg; p < 0.001), maximal heart rate (161 vs 177 bpm; p = 0.002) and the mean of the slopes of the metabolic-chronotropic relationship (0.59 vs 0.72; p < 0.001) were decreased in patients with moderate to severe pulmonary regurgitation. This study shows that significant pulmonary regurgitation is responsible for a poor cardiorespiratory response to exercise and for an abnormal chronotropic response which seems to be multifactorial but probably related to an adaptation favouring left ventricular filling during exercise.

Adolescent↗

Augmented intracellular glutathione inhibits Fas-triggered apoptosis of activated human neutrophils.

Agonist signals delivered through cell surface Fas induce apoptosis. However, the apoptotic program can be modulated by signals from the environment, and in particular, by signals delivered through adhesion molecules. Because neutrophil functional activity in inflammation is contingent on cell survival, and because circulating neutrophils normally die rapidly through a constitutively expressed apoptotic program, we evaluated Fas-mediated apoptosis in resting and inflammatory human neutrophils. We show that normal neutrophils respond to Fas engagement with accelerated rates of apoptosis, but cross-linking of beta2 integrins or priming with bacterial lipopolysaccharide (LPS) prevents this increase. Adhesion molecule cross-linking results in increased intracellular glutathione (GSH). Augmentation of intracellular GSH with exogenous GSH or N-acetylcysteine is sufficient to reduce the Fas-triggered increase in apoptotic rates. Prevention of the activation induced GSH increase by buthionine sulfoximine, a cell permeable inhibitor of GSH biosynthesis, restored Fas responsiveness in activated neutrophils, an effect that could be blocked with exogenous GSH. Taken together, these data show that Fas-induced signaling for neutrophil apoptosis is blocked in a redox sensitive manner by costimulatory signals delivered through beta2 integrins or activation by LPS, and provide a biologic explanation for sustained neutrophil survival in the inflammatory environment.

Apoptosis↗

Impaired apoptotic death signaling in inflammatory lung neutrophils is associated with decreased expression of interleukin-1 beta converting enzyme family proteases (caspases).

BACKGROUND: Fas and tumor necrosis factor receptor 1 (TNFR1) are membrane proteins that signal for apoptotic cell death by downstream activation of proteins of the interleukin-1 beta converting enzyme (ICE) family. Spontaneous apoptosis is delayed in neutrophils activated by transmigration into an inflammatory focus. In this study we evaluated the effects of transmigration on Fas and TNFR1-induced apoptosis and apoptotic gene expression. METHODS: Sprague-Dawley rats were killed 4 hours after intratracheal challenge with 500 micrograms lipopolysaccharide (LPS). Neutrophils isolated from the systemic circulation (circulation) or bronchoalveolar lavage fluid (lung) were incubated with or without an agonistic antibody to Fas (clone CH-11, 100 ng/ml) or TNF (10 ng/ml) for 24 hours. Apoptosis and Fas expression were assessed by flow cytometry. Expression of the antiapoptotic protein Bcl-2 and proapoptotic proteins ICE and CPP32 were measured by Western blots. RESULTS: Neutrophils transmigrating into the lung in response to LPS showed delayed apoptosis compared with circulating neutrophils and failed to undergo apoptosis in response to anti-Fas antibody or TNF-alpha. Fas expression was unaltered; however, TNFR1 expression was reduced. Bcl-2 was not detected in either group; both the pro- and active forms of ICE and active CPP32 were significantly decreased in lung neutrophils. The specific ICE inhibitor, YVAD-CMK, partially blocked the increased rates of apoptosis resulting from engagement of Fas or TNFR1. CONCLUSIONS: Neutrophil transmigration retards apoptosis through engagement of the death receptors Fas and TNFR1. This refractory state is associated with reduced levels of proapoptotic proteins. Blunted responsiveness to physiologic apoptotic stimuli prolongs neutrophil functional survival during acute inflammation and may contribute to the tissue injury associated with acute respiratory distress syndrome.

Amino Acid Chloromethyl Ketones↗

Mycotoxin production by fusarium species isolated from bananas.

The ability of Fusarium species isolated from bananas to produce mycotoxins was studied with 66 isolates of the following species: F. semitectum var. majus (8 isolates), F. camptoceras (3 isolates), a Fusarium sp. (3 isolates), F. moniliforme (16 isolates), F. proliferatum (9 isolates), F. subglutinans (3 isolates), F. solani (3 isolates), F. oxysporum (5 isolates), F. graminearum (7 isolates), F. dimerum (3 isolates), F. acuminatum (3 isolates), and F. equiseti (3 isolates). All isolates were cultured on autoclaved corn grains. Their toxicity to Artemia salina L. larvae was examined. Some of the toxic effects observed arose from the production of known mycotoxins that were determined by thin-layer chromatography, gas chromatography, or high-performance liquid chromatography. All F. camptoceras and Fusarium sp. isolates proved toxic to A. salina larvae; however, no specific toxic metabolites could be identified. This was also the case with eight isolates of F. moniliforme and three of F. proliferatum. The following mycotoxins were encountered in the corn culture extracts: fumonisin B(inf1) (40 to 2,900 (mu)g/g), fumonisin B(inf2) (150 to 320 (mu)g/g), moniliformin (10 to 1,670 (mu)g/g), zearalenone (5 to 470 (mu)g/g), (alpha)-zearalenol (5 to 10 (mu)g/g), deoxynivalenol (8 to 35 (mu)g/g), 3-acetyldeoxynivalenol (5 to 10 (mu)g/g), neosolaniol (50 to 180 (mu)g/g), and T-2 tetraol (5 to 15 (mu)g/g). Based on the results, additional compounds produced by the fungal isolates may play prominent roles in the toxic effects on larvae observed. This is the first reported study on the mycotoxin-producing abilities of Fusarium species that contaminate bananas.

Journal Article↗

[Alteration of myocardial viability and systemic ventricular dysfunction after Senning procedure].

After a Senning procedure for transposition of the great arteries (TGA), systolic dysfunction of the right ventricle (RV) is common. Pre and peroperative chronicale hypoxia may be the cause of this ventricular myocardial alteration. In order to detect abnormalities of myocardial viability and to study their relationship to RV function, the authors studied 41 patients (pts), 11.3 +/- 3 years after a Senning procedure. All patients underwent myocardial scintigraphy of the RV under basal conditions. 1 hour after injection of 1.5 mCi of Thallium 201. The RV ejection fraction (n = 41) and at peak effort (n = 25). Exercise ability and aerobic capacity were assessed by exercise testing (Bruce) with gas exchange measurement and compared with 41 normal matched subjects. The cardiorespiratory response to exercise was altered in the Senning group : duration of effort (10.5 +/- 2 vs 13.2 +/- 2 min; p < 0.0001), peak VO2 (33 +/- 5 vs 44.4 +/- 6 ml/min/kg; p < 0.0001), anaerobic threshold (6 +/- 1 vs 8.4 +/- 1.9 min; p < 0.05) were lower compared to controls. Abnormalities of RV viability were observed in 18/41 pts (44%), moderate in 12 cases and severe in 6 cases. Resting and exercise RVEF were significantly lower in patients with myocardial defects (45 +/- 5 vs 51 +/- 7%; p < 0.0005, and 49 +/- 9 vs 58 +/- 9%; p < 0.05 respectively). In conclusion, after the Senning procedure for TGA, scintigraphic abnormalities of the systemic ventricule are common and associated with an alteration of systolic function at rest and on exercise.

Adolescent↗