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Objectives: The purpose of the present study was two-fold: (1) To analyse physical fitness changes of youth football players after a full-season; and (2) to examine whether physical fitness changes are explainable by estimated maturity status, 2digit:4digit ratio (2D:4D) from each hand and training load (TL) measures., Methods: Twenty-seven youth elite Under-15 football players were daily monitored for training load measures during 38 weeks. At the beginning and at the end of the season, all players were assessed for physical fitness. Also, the maturity status estimation and the length of the second and fourth digits of both hands were collected at the beginning of the season., Results: Significant differences were found for all physical fitness measures after the season. The second and fourth digits of left and right hands had negative moderate correlations with change of direction (COD) changes (r=-.39 to - 0.45 | p = .05 to 0.02). Also, the maturity offset measure had negative moderate correlations with COD changes (r=-.40 | p = .04). From the reported significant correlations, the maturity offset, Left 4D, Right 2D and Right 4D significantly predicted the Mod.505 COD test changes (β = 0.41, p = .04; β = -0.41, p = .04; β = -0.45, p = .02; and β = -0.44, p = .03, respectively)., Conclusion: The maturity offset and the 2D:4D measures have the potential to predict COD performance changes over-time in youth football players. Given the lack of associations between the maturity estimation, 2D:4D and training load measures, with the overall physical fitness measures, coaches should rely only at COD changes., (© 2022. The Author(s).) more...

Background: For a long time, in sports, researchers have tried to understand an expert by comparing them with novices, raising the doubts if the visual search characteristics distinguish experts from novices. Therefore, the aim of the present study was to review and conduct a meta-analysis to evaluate the differences in visual search behavior between experts and novices in team sports athletes., Methods: This systematic review with meta-analysis followed the PRISMA 2020 and Cochrane's guidelines. Healthy team athletes were included, which engaged in regular practice, from any sex or competitive level, specifically classified a priori as expert or novice in the original research (i.e., if they were classified after the experiment, based on one of the tests, the study would be excluded). We considered only research published in peer-reviewed journals, with no limitations regarding date or language. It was considered healthy team sport athletes engaged in regular practice. The scenarios could be in situ or film-based. The databases of EBSCO (Academic Search Complete, Academic Search Ultimate, APA PsycArticles, and APA PsycINFO), PubMed, Scopus, SPORTDiscus, and Web of Science were used to perform the searches. The risk of bias was calculated through the RoBANS tool., Results: From a total of 6,257 records, of which 985 were duplicates, titles and abstracts of 5,272 were screened, and 45 required full-text analysis. Of those, 23 were excluded due to not fulfilling the eligibility criteria regarding participants. In the end, 22 studies were selected, however, as two studies were part of the same trial and were analyzed conjointly., Discussion: Experts showed to be older and with more years of practice. The ability to distinguish experts from novices was not so clear regarding the variables analyzed. This could be due to the strategies chosen in each study, which were specific to each scenario, and when grouping all together, it was lost information within non-representative averages. The distinction between experts and novices was not clear, showing a lot of heterogeneity in the included studies. The expert classification itself may have been the conditioning aspect for these results, retaining the doubt and the need for more studies in the field., Systematic Review Registration: The protocol was pre-registered in OSF (project https://osf.io/3j4qv/, register https://osf.io/dvk2n)., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Silva, Afonso, Sampaio, Pimenta, Lima, Castro, Ramirez-Campillo, Teoldo, Sarmento, González Fernández, Kaczmarek, Oniszczuk and Murawska-Ciałowicz.) more...

Objectives: An analysis is made of the clinical profile, evolution and differences in morbidity and mortality of low cardiac output syndrome (LCOS) in the postoperative period of cardiac surgery, according to the 3 diagnostic subgroups defined by the SEMICYUC Consensus 2012., Design: A multicenter, prospective cohort study was carried out., Setting: ICUs of Spanish hospitals with cardiac surgery., Patients: A consecutive sample of 2,070 cardiac surgery patients was included, with the analysis of 137 patients with LCOS., Interventions: No intervention was carried out., Results: The mean patient age was 68.3±9.3 years (65.2% males), with a EuroSCORE II of 9.99±13. NYHA functional class III-IV (52.9%), left ventricular ejection fraction<35% (33.6%), AMI (31.9%), severe PHT (21.7%), critical preoperative condition (18.8%), prior cardiac surgery (18.1%), PTCA/stent placement (16.7%). According to subgroups, 46 patients fulfilled hemodynamic criteria of LCOS (group A), 50 clinical criteria (group B), and the rest (n=41) presented cardiogenic shock (group C). Significant differences were observed over the evolutive course between the subgroups in terms of time subjected to mechanical ventilation (114.4, 135.4 and 180.3min in groups A, B and C, respectively; P<.001), renal replacement requirements (11.4, 14.6 and 36.6%; P=.007), multiorgan failure (16.7, 13 and 47.5%), and mortality (13.6, 12.5 and 35.9%; P=.01). The mean maximum lactate concentration was higher in cardiogenic shock patients (P=.002)., Conclusions: The clinical evolution of these patients leads to high morbidity and mortality. We found differences between the subgroups in terms of the postoperative clinical course and mortality., (Copyright © 2017 Elsevier España, S.L.U. y SEMNIM. All rights reserved.) more...

Aim: To disclose whether mutations in the HFE gene inducing liver iron overload are related to the risk of hepatocellular carcinoma (HCC) in otherwise predisposed patients., Patients and Methods: One hundred and ninety-six patients (161 males) diagnosed with HCC and 181 healthy controls were included in the study. All subjects were white Spaniards.C282Y and H63D mutations in the HFE gene were identified in leucocyte genomic DNA using a polymerase chain reaction (PCR) and specific restriction enzymes. RESULTS (CASES/CONTROLS): 1. Genotype distribution: a) C282Y mutation: homozygotes 1/0, heterozygotes 12/23, wild type 183/158 (p = 0.07, non significant); b) H63D mutation: homozygotes 9/5, heterozygotes 85/52, wild type 102/124 (0dds ratio 2.00, 95% C.I. 1.29-3.12, p = 0.002. Four cases and 6 controls were carriers of heterozygous mixed genotypes. 2. Allele frequencies: a) C282Y mutation: wild type allele 378/339, mutated allele 14/23 (p = 0.11, non significant); b) H63D mutation: wild type allele 289/300, mutated allele 103/62 (0dds ratio 1.72, 95% C.I. 1.19-2.50, p = 0.004). Age at diagnosis, gender and etiology of the underlying liver disease do not influence these findings., Conclusion: The C282Y mutation in the HFE gene is not related to the risk of HCC in non-hemochromatosis patients. The H63D mutation is associated with a higher risk of HCC in cirrhotic patients irrespective of their underlying liver disease. more...

Dominant inherited beta-thalassemias describe those beta-thalassemia variants that result in a thalassemia intermediate phenotype in individuals who have inherited only a single copy of the abnormal beta gene. This form of thalassemia is characterized by moderately severe anemia with jaundice and splenomegaly; it is also characterized by the presence of inclusion bodies in the red blood cell precursors and has, therefore, previously been referred to as inclusion body beta-thalassemia. We describe a case of inclusion body beta-thalassemia in a 51-year-old Spanish male caused by a deletion of 11 bp (CD 131-134) in exon 3 of the beta-globin gene. The deletion of 11 bp in exon 3 of the beta-globin chain is predicted to produce an anomalous chain of 134 amino acids instead of the normal 146 with an extremely altered amino acid sequence from residues 131-134. Although this shortened variant would lead to a missing H helix, which is involved in alpha1beta1 contact and alpha1beta2 subunit interactions, the variant chain can still be bound to the heme group and acquire a secondary structure that is not suitable for the formation of stable dimers or tetramers and also less susceptible to proteolytic degradation. This is the first report of such a beta-thalassemia mutation. more...

Background: The serum transferrin receptor (TfR) presents certain advantages over other parameters of cellular iron status because it does not vary in acute or chronic diseases., Objective: To establish reference ranges of TfR in healthy children for our laboratory, to define the distribution of this variable in children with acute illness and in those with iron deficiency, and to evaluate the diagnostic yield of TfR, the transferrin-receptor/ferritin ratio (TfR/F) and the transferrin-receptor-ferritin index (TfR-F) in distinguishing ferropenic from infectious anemia., Patients and Methods: A descriptive, cross-sectional analysis was conducted in 132 children aged from 6 months to 16 years for a period of 18 months. The subjects were classified in three groups: healthy children, children with acute illness, and children with iron deficiency. The distribution of TfR and its diagnostic yield were evaluated., Results: Of the 132 subjects, 30 were excluded because they lacked one or more of the parameters under analysis and 19 were excluded because they showed a thalassemic trait. In the 30 healthy children, the mean TfR concentration was 1.2 mg/l (SD 0.36) and the median was 1.02 (IQR 0.7-1.7). In the 32 children with acute illness, with or without anemia, TfR values were similar to those found in healthy children (p > 0.05). TfR values were higher in children with iron deficiency (21 patients; mean TfR value: 1.67 mg/l SD 0:98) than in healthy children but this difference was not statistically significant (p 0.08). The highest TfR values were found in the group with ferropenic anemia (mean TfR value: 2.13 mg/l SD 1.14) with a statistically significant difference between healthy children (p 0.04) and those with iron deficiency without anemia (p 0.01). The TfR/F ratio showed an optimal diagnostic yield in distinguishing ferropenic from acute disease anemia. If this ratio is higher than 80.7 ferropenia can be suspected as the cause of the anemia with a global value of the test of 100 % (95 % CI: 75.91-99.42)., Conclusions: TfR could be useful in evaluating intracellular iron status in children. Acute disease does not alter TfR values and, in combination with ferritin, TfR offers an optimal diagnostical yield in distinguishing ferropenic from acute illness anemia. more...

Objective: To test the hypothesis that the heterozygous state for HFE gene mutations involved in the pathogenesis of hemochromatosis, that may induce an increase of hepatic iron content, may aggravate the liver damage induced by prolonged and excessive use of ethanol., Patients and Methods: C282Y and H63D mutations of HFE gene were identified through polymerase chain reaction (PCR) on leukocyte DNA, in 125 consecutive patients diagnosed of advanced alcoholic liver disease (109 men, mean age 54 years, SD 11) and 181 healthy controls. All subjects were white Spaniards. RESULTS (CASES/CONTROLS): 1. Genotype distribution: a) mutation C282Y: no homozygotes, 10/23 heterozygotes, 115/158 normal (p = 0.60); b) mutation H63D: 9/5 homozygotes, 46/52 heterozygotes, 70/124 normal (Chi square 6.51, p = 0.039). 2. Allele frequencies: a) mutation C282Y: 240/339 normal, 10/23 mutated (p = 0.21); b) mutation H63D: 186/300 normal, 64/62 mutated (odds ratio 1.66, 95% CI 1.10-2.52, p = 0.01)., Conclusions: Our results suggest that H63D mutation of the HFE gene, but not the C282Y mutation, is associated to the risk of developing advanced liver alcoholic disease. more...

Cardiovascular disease is accompanied by an impaired endothelium-dependent vasodilatory response. Loss of endothelial nitric oxide synthase (eNOS) expression may contribute to endothelial dysfunction. The aim of the present study was to analyze the effect of cerivastatin, a novel HMG CoA reductase inhibitor, on tumor necrosis factor-alpha (TNF-alpha)-induced downregulation of eNOS protein expression in bovine aortic endothelial cells (BAEC). TNF-alpha (10 ng/ml)- incubated BAEC showed a reduced expression of eNOS protein and decreased eNOS mRNA stabilization. This effect was associated with an increased binding activity of BAEC cytosolic proteins to the 3'-untranslated region (3'UTR) of eNOS mRNA. Cerivastatin prevented TNF-alpha-induced downregulation of eNOS protein expression in a concentration-dependent manner (10(-8) to 10(-5) M). Cerivastatin also prevented the binding of the cytosolic proteins to 3'-UTR of eNOS mRNA and was associated with eNOS mRNA stabilization. The reduced expression of eNOS protein by TNF-alpha was also prevented by coincubation with cycloheximide. In addition cycloheximide inhibited the binding activity of the cytosolic proteins to 3'-UTR of eNOS mRNA, suggesting the inducible character of the mentioned-cytosolic proteins. TNF-alpha stimulated the translocation of nuclear factor-kappaB (NF-kappaB), an effect that was not modified by cerivastatin. Furthermore, an inhibitor of NF-kappaB translocation, pyrrolidine dithiocarbamate failed to modify both the downregulation of eNOS expression and the increased binding activity of the cytosolic proteins to 3'-UTR of eNOS mRNA by TNF-alpha. The effect of cerivastatin on eNOS expression and the binding activity of the cytosolic proteins were reversed by coincubation with L-mevalonate. In conclusion, cerivastatin stabilized eNOS mRNA and upregulated eNOS expression in the endothelium, and this was associated with a decreased binding activity of cytosolic proteins to 3'-UTR of eNOS mRNA. The effect of cerivastatin on the regulation of eNOS expression was independent of NF-kappaB mobilization by TNF-alpha. These findings suggest that cerivastatin may have beneficial effects on the endothelial dysfunction associated with cardiovascular diseases beyond its effect on lowering cholesterol. more...

Changes in the expression of endothelial nitric oxide synthase (eNOS) in the peritoneum could be involved in the peritoneal dysfunction associated with peritoneal inflammation. Demonstrated recently in bovine endothelial cells was the existence of cytosolic proteins that bind to the 3'-untranslated region (3'-UTR) of eNOS mRNA and could be implicated in eNOS mRNA stabilization. The present work demonstrates that eNOS protein is expressed in human endothelial and mesothelial peritoneal cells. Escherichia coli lipopolysaccharide shortened the half-life of eNOS message, reducing eNOS protein expression in peritoneal mesothelial and endothelial cells. Moreover, under basal conditions, human peritoneal samples expressed cytosolic proteins that bind to the 3'-UTR of eNOS mRNA. The cytosolic proteins that directly bind to 3'-UTR were identified as a 60-kD protein. After incubation of human peritoneal samples with lipopolysaccharide, the binding activity of the cytosolic 60-kD protein increased in a time-dependent manner. Studies are now necessary to determine the involvement of this 60-kD protein in the regulation of eNOS expression in peritoneal cells and particularly its involvement in the peritoneal dysfunction associated with inflammatory reactions. more...

Introduction and Aims: The thrombotic process is a multicellular phenomenon in which not only platelets are involved but also neutrophils are involved. Recent in vitro studies performed in our laboratory have demonstrated that triflusal reduced platelet aggregation by stimulating nitric oxide (NO) production by neutrophils. The aim of the present study was to evaluate whether the in vivo treatment with triflusal could also modify the ability of neutrophils to produce NO. Furthermore, the role of NO released by neutrophils on platelet aggregation and secretion was also tested., Methods: The study was performed in 12 healthy volunteers of 32 +/- 6 years of age. The volunteers were treated with triflusal (600 mg/day) for 5 days and platelets and neutrophils were isolated before and after treatment. The ability of neutrophils to produce NO and the capacity of inhibiting platelet aggregation and secretion of transforming growth factor-beta (TGF-beta) were assessed., Results: After the treatment with triflusal we obtained the following results: a) an increase in NO production by neutrophils; b) potentiation of the inhibition of platelet aggregation by neutrophils, an effect that was reverted by incubating neutrophils with an L-arginine antagonist, L-NAME, and c) the presence of neutrophils reduced the release of TGF-beta by platelets measured as index of platelet secretion by a NO-independent mechanism., Conclusions: Triflusal (600 mg/day/5 days) stimulated NO production by neutrophils. After the treatment with triflusal, neutrophils inhibited both platelet aggregation and secretion. The antiaggregating effect of neutrophils was an NO-dependent mechanism while the inhibition of platelet secretion mediated by neutrophils after the treatment with triflusal was an NO-independent mechanism. more...

Recent studies have postulated the contribution of nitric oxide (NO) released by the endothelium to the beneficial effects of estrogen. Despite a neuronal-type NO synthase (nNOS) described in neutrophils, less is known about the effect of estrogen in these cells. The aim of the present study was to analyze the expression of nNOS protein in human neutrophils under different estrogenic conditions. We first analyzed nNOS expression in neutrophils obtained from premenopausal women. During the first 2 days of the follicular phase (low circulating estrogen concentrations), nNOS expression in neutrophils was reduced with respect to that found in neutrophils obtained from the same donors during the ovulatory phase (high circulating estrogen concentrations). Moreover, the expression of nNOS protein in neutrophils obtained from postmenopausal women after transdermal estrogen therapy was markedly enhanced with respect to that observed before the treatment. In vitro incubation of neutrophils derived from men for 6 hours with 17beta-estradiol (10(-10) to 10(-8) mol/L) upregulated the expression of nNOS protein. The 17beta-estradiol receptor antagonists, tamoxifen (10(-8) mol/L) and ICI 182780 (10(-8) mol/L), inhibited the upregulation of nNOS protein induced by 17beta-estradiol. The putative functional implication was denoted by a reduced expression of the CD18 antigen on the surface of 17beta-estradiol-incubated neutrophils, which was accompanied by a decreased adhesive capacity. Both effects were prevented by an NO antagonist. In conclusion, the in vivo levels of circulating estrogen concentrations seem to be associated with the level of nNOS protein expression in neutrophils from women. Moreover, low doses of 17beta-estradiol upregulate nNOS protein expression in neutrophils from men. The increased ability of 17beta-estradiol-incubated neutrophils derived from men to produce NO reduced their adhesive properties. more...

Despite the evidence that cytokines stimulate nitric oxide (NO) production by inducible nitric oxide synthase (iNOS), several reports recently demonstrated that the hypotensive response related to endothelial nitric oxide synthase (eNOS) activity could be inhibited by the same cytokines. The aim of the present work was to analyze whether NO generated by vascular smooth muscle cells (VSMC) could modify eNOS protein expression in endothelial cells. Bovine aortic endothelial cells (BAEC) and bovine VSMC (BVSMC) in coculture were used for the study. Interleukin-1beta (IL-1beta, 10 ng/ml)-treated BVSMC, which expressed iNOS protein, decreased eNOS protein expression in BAEC. The presence of NO antagonists N(omega)-nitro-L-arginine methyl ester (10(-3) mol/l) or N(G)-monomethyl-L-arginine (10(-3) mol/l) prevented the decrease in eNOS protein expression induced by IL-1beta-treated BVSMC. Surprisingly, two different NO donors, 3-morpholinosydnonimine (10(-4) mol/l) and S-nitroso-N-acetyl-D,L-penicillamine (10(-4) mol/l), failed to modify eNOS expression in BAEC, suggesting the existence of a diffusible mediator released from IL-1beta-treated BVSMC that acts on endothelial cells by reducing eNOS expression. The presence of NO antagonists reduced tumor necrosis factor-alpha (TNF-alpha) production by IL-1beta-stimulated BVSMC. This effect was also produced in the presence of a protein kinase G inhibitor, guanosine-5'-O-(2-thiodiphosphate) trilithium salt. A polyclonal antibody against TNF-alpha prevented eNOS expression in the BAEC-BVSMC coculture. In conclusion, NO by itself failed to modify eNOS protein expression in endothelial cells but increased TNF-alpha generation by IL-1beta-stimulated BVSMC and, in this way, reduced eNOS expression in the endothelium. more...

Background: Functional evidence suggests that endothelial denudation stimulates inducible nitric oxide synthase (iNOS) activity in the vascular wall. In vitro studies done in our laboratory have shown that iNOS expression in smooth muscle cells is reduced by endothelial cells. The object of this study was to analyze the iNOS protein expression in the arterial wall after in vivo deendothelialization, and the role of platelet activation abciximab in the expression of this protein., Materials and Methods: Endothelial denudation was performed in the left carotid artery of Wistar rats. The right carotid artery was used as control., Results: iNOS protein was only weakly expressed at 6, 24 and 48 hours after endothelial denudation. Since platelet adhesion and aggregation occur early after endothelial damage, we have analyzed the role of activated platelets in iNOS protein expression during the first two days after angioplasty. Early after in vivo endothelial injury, thrombocytopenic rats showed a marked iNOS protein expression. Similar results were obtained by blocking the platelet glycoprotein IIb/IIIa in rats treated with abciximab (Reopro)., Conclusions: iNOS protein is weakly expressed in the arterial wall after endothelial denudation. Platelets play a crucial role preventing iNOS protein expression early after endothelial damage through a mechanism that depends on GP IIb/IIIa, an effect that can be avoided with glycoprotein IIb/IIIa, blockers, such as abciximab. more...

Changes in the endothelial nitric oxide synthase (eNOS) expression could be involved in the endothelium-dependent vasorelaxing dysfunction associated with cardiovascular diseases. We have recently demonstrated the existence of endothelial cytosolic proteins that bind to the 3'-untranslated region (3'-UTR) of eNOS mRNA and could be involved in eNOS mRNA stabilization. In the present work, we have characterized the cytosolic proteins that bind to 3'-UTR eNOS mRNA. An endothelial cytosolic protein (MW 60-kD) specifically bound to 3'-UTR eNOS mRNA as determined by a cross-linking assay followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The endothelial cytosolic protein recognized a cytidine (C)-rich region within 3'-UTR eNOS mRNA. Furthermore, tumor necrosis factor-alpha (TNF-alpha) increased the level of the 60-kD endothelial cytosolic protein. In addition, TNF-alpha reduced eNOS mRNA levels and this was prevented by coincubation with cycloheximide. Cycloheximide also prevented the binding activity of the endothelial cytosolic protein to 3'-UTR eNOS mRNA. In summary, these data suggest that a 60-kD endothelial cytosolic protein binds to 3'-UTR eNOS mRNA. TNF-alpha increased the 60-kD protein levels. Cycloheximide prevented the binding activity of the cytosolic protein to 3'-UTR eNOS mRNA related to TNF-alpha; this effect was associated with greater eNOS mRNA levels. Further specific studies are needed to determine the involvement of this 60-kD endothelial cytosolic protein in the regulation of eNOS mRNA stabilization and in the endothelial dysfunction associated with cardiovascular diseases. more...

There is functional evidence suggesting that endothelial denudation stimulates inducible nitric oxide synthase (iNOS) activity in the vascular wall. In vitro studies have shown that iNOS expression in smooth muscle cells is reduced by endothelial cells. In the present study we have analyzed the time course of iNOS protein expression in the arterial wall after in vivo deendothelialization. Endothelial denudation was performed in the left carotid artery of Wistar rats, and the right carotid artery was used as control. Whereas iNOS protein was weakly expressed 6, 24, and 48 hours after endothelial denudation, a marked iNOS expression was found 7, 14, and 30 days after vascular damage. Because platelet adhesion and aggregation occur early after endothelial damage, we studied the role of activated platelets in the negative modulation of iNOS protein expression during the first 2 days after endothelial denudation. Early after in vivo endothelial injury, platelet-depleted rats showed a marked iNOS protein expression in the vascular wall. Similar results were obtained by blocking the platelet glycoprotein (GP) IIb/IIIa. Although iNOS protein is present in the arterial wall several days after endothelial denudation, early after arterial wall injury iNOS protein is weakly expressed. Platelets play a crucial role in preventing iNOS protein expression early after endothelial damage, an effect that can be avoided with GP IIb/IIIa blockers. Although iNOS protein was weakly expressed in vivo in the rat carotid artery wall 6, 24, and 48 hours after balloon endothelial denudation, a marked iNOS expression was found 7, 14, and 30 days after arterial damage. iNOS expression could be increased early after endothelial injury by removing circulating platelets and by an antibody against the GP IIb/IIIa. In conclusion, platelets prevent iNOS protein expression early after endothelial balloon damage, an effect that can be avoided with GP IIb/IIIa blocking agents. more...

Two NO synthase (NOS) isoforms have been described in vessels, an endothelial constitutive NOS (eNOS) and an inducible NOS (iNOS). The purpose of the present study was to examine the endothelium-dependent and endothelium-independent hypotensive response in aging rats, analyzing the ability of their vessels to produce NO. The studies were performed in 2 groups of euvolemic, conscious, male Wistar rats: aging rats (n=20, 18 months old) and young rats (n=20, 5 months old). The hypotensive responses to acetylcholine, bradykinin, and sodium nitroprusside were determined. Furthermore, the expression of the NOS isoforms by Western blot and the eNOS and iNOS activities, defined as Ca2+-dependent and Ca2+-independent conversion of [14C]L-arginine into [14C]L-citrulline, respectively, were also determined. In the aging rats, we found an impaired hypotensive response to acetylcholine and bradykinin (2 NO- and endothelium-dependent hypotensive agents) that was accompanied by a preserved hypotensive response to sodium nitroprusside. Aging rats also demonstrated an enhanced sensitivity response to the pressor effect of the L-arginine antagonist L-Nomega-nitro-L-arginine and a reduced vasoconstrictor response to angiotensin II. The inhibition of NO synthesis normalized the pressor effect of angiotensin II in the aging animals. Nitrite plus nitrate plasma levels were increased in aging rats. Furthermore, cGMP content was also higher in the aging vessels. In the aging aortas, the expression of both eNOS and iNOS isoforms was enhanced. However, in aging rats, the activity of the eNOS isoform was markedly reduced, a finding that was accompanied by the presence of iNOS activity. The vessel wall of aging rats showed an enhanced expression of eNOS and iNOS isoforms. However, eNOS activity was reduced in the aging animals. These findings could explain the impaired endothelium-dependent hypotensive response associated with aging. more...

The endothelium is a dynamic organ involved in the genesis and development of the cardiovascular diseases. Nitric oxide (NO) is one of the factors released from endothelium. NO is generated by endothelial cells through the activity of a constitutive nitric oxide synthase (cNOS). Smooth muscle cells generate NO by an inducible NOS isoform (iNOS). NO regulates vascular tone, different mechanisms involved in the interaction of blood cells to the vascular wall, the growth of smooth muscle cells and the matrix protein synthesis. The lack of an endothelium-dependent vasodilatory response has been defined as endothelial dysfunction. It has been demonstrated a reduced endothelium-dependent vasodilation response in hypertension, aging, atherosclerosis ... and in patients without evident coronary disease. Although the cNOS has been initially described as constitutive, in recent years it has been demonstrated that several pathophysiological stimuli such as hypoxia, chronic exercise, cytokines regulate its level of expression. Our laboratory has demonstrated that an endothelial cytosolic protein regulates the half-lives of eNOS mRNA. This endothelial cytosolic protein could be a target for specific drugs to prevent endothelial dysfunction. more...

Some patients found to have clonal panmyelopathies develop an acquired defect of haemoglobin synthesis clinically similar to haemoglobin H disease. A 58 year-old male diagnosed of simple refractory anaemia developed microcytosis and hypochromia. At the same time, his myelodysplastic syndrome became a refractory anaemia with excess of blasts. 33% of the red blood cells had "golf ball" inclusions after incubation with brilliant cresyl blue. Cellulose acetate electrophoresis revealed an haemoglobin H band. The globin chain synthesis alpha/beta ratio was 0.69. The molecular analysis demonstrated the integrity of both alpha genes in each chromosome. There were no familiar antecedent of haemoglobinopathy. more...

In this study, 63 infants, 38 males and 25 females, with pathology that suggested gastro-esophageal reflux, were studied. These patients were between one month and 7-1/2 years of age, with a mean age of 29 months and a standard deviation of 28.1 months. All patients underwent a barium study of the esophagus and the stomach, evaluated according to the criteria of Cleveland, an esophageal scintigram to detect GER, performed according to the criteria of Fernández and Argüelles, and an abdominal echography according to the technique of Naik and Moore. The test was considered a true positive if the echography was positive along with one other positive examination. A false positive was considered if only the echography were positive. A true negative was when the echography was negative along with another negative test. A false negative was when the echography was negative and some other test was positive. The following results were obtained for the echography: a sensitivity of 68%, a specificity of 84.61% and a safety factor of 71.2%. We conclude that echography can be considered as a complimentary examination for the study of GER, given it harmless nature, the availability of the equipment and the possibility of prolonging the exploration which can be recorded on videotape. more...

Hemolytic-uremic syndrome is a disease of different etiology, characterized by thrombocytopenia, hemolytic anemia and renal failure. A case of lethal evolution that afflicted a 18 year old male is presented. The exceptional presentation with massive pulmonary hemorrhage highlighted. more...

In order to evaluate the use of sucralfate in the treatment of children with reflux esophagitis, we studied 66 children aged from 4 months to 12 years (mean 5.9 years, SD 3.5) diagnosed to have gastroesophageal reflux by means of esophageal isotopic examination and radiology. An endoscopic examination was carried out in all cases. None of the patients suffered from kidney disease or had taken antacids, cimetidine, sucralfate or antirheumatic drugs in the two weeks prior to the study. Patients were divided into three groups matched according to age, grade of esophagitis, sex, nutritional state and semiology and treated with sucralfate in tablets, cimetidine, or sucralfate in suspension; no dietetic or postural measures were used. On days 14, 28, 42 and 56, clinical control was carried out and endoscopy was done on day 28, this being repeated on day 56 if the course was not satisfactory. From the statistical analysis of the results we deduce that there are no differences between the three groups. Therefore sucralfate appears to be a useful drug for the treatment of children with esophagitis due to GER. more...

We present a research work on the diagnosis of the malabsorption syndrome in childhood. The study is based on two diagnostic tests which are: the xylose test and the histological examination of intestinal mucosa. We have tried to assess the usefulness of the determination of the blood xylose after an extra oral load of xylose, comparing the results with the morphological findings in the intestinal mucosa, making a correlation between both, in order to discern the contribution of this examination to the diagnosis of the malabsorption syndrome in childhood. We come to the following conclusions: The determination of the blood xylose after an extra oral load with a single dose is a useful test in the diagnosis of malabsorption syndromes in childhood, and gives us facts about the status of the intestinal mucosa. The abnormality of the results of this test is an important indication for an intestinal biopsy. The xylose test cannot replace the intestinal biopsy. more...

Ninety children with signs and symptoms of gastroesophageal (GE) reflux were studied. All of them had GE scintigraphy, barium, and endoscopy, and 50, in addition, ultrasound examination. The sensitivity of the GE scintigraphy, in comparison with the other methods, was 92.5%. It is a useful screening test for GE reflux. more...