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Biomedical subjects

A Gil

Publications and source records attributed to A Gil.

At least 127 records · Page 7Linked to original sources
PubMed1999

Experimental colitis induced by trinitrobenzenesulfonic acid: an ultrastructural and histochemical study.

Inflammatory bowel disease (IBD) of humans is a chronic and devastating disease of unknown etiology. Models of acute colitis in animals have been achieved by intrarectal administration of agents such as 2,4,6-trinitrobenzenesulfonic acid (TNBS) into rat colon. This agent induces focal inflammation and alterations in the colon with features similar to those found in chronic inflammatory diseases in humans. The aim of this study was to assess the effect of TNBS administration on histological and ultrastructural features of the rat colon, especially in areas not affected by transmural inflammation. Also in areas without transmural inflammation, we observed a significant increase in crypt diameter and in the number and area of the goblet cells, as well as alterations in the contents of mucin in goblet cells. We conclude that TNBS treatment in rats led to severe changes in normal architecture of the colon and also in damaged areas where no direct inflammation was produced.

Animals↗
PubMed1999

Extra-virgin olive oil increases the resistance of LDL to oxidation more than refined olive oil in free-living men with peripheral vascular disease.

Patients with peripheral vascular disease (Fontaine stage II) are characterized by ischemia of the lower extremities, atherosclerosis and alteration of blood coagulation and fibrinolysis. A randomized, two-period, crossover design was used to compare the effects of extra-virgin (VO) and refined olive (RO) oils on plasma lipids and lipoprotein composition and LDL oxidation susceptibility in free-living men with peripheral vascular disease. The oils differed in their antioxidant profile (alpha-tocopherol: 300 vs. 200 mg/kg; phenolic compounds 800 vs. 60) and concentration but not in their fatty acid composition. Subjects were randomly assigned to two groups. The first group (n = 12) received VO with which to freely cook all meals for 3 mo, followed by a 3-mo wash-out period; they then received RO for the final 3 mo. The second group (n = 12) consumed the oils in the opposite order. Energy, fat, polyunsaturated fatty acids (PUFA) and alpha-tocopherol intakes were not different when patients consumed the two oils. Profiles of the major fatty acids in plasma and LDL were not different after consumption of VO and RO. The slope of the line for LDL oxidation vs. the line for copper concentration was significantly higher after the intake of RO than after the intake of VO. Total LDL taken up by macrophages was significantly greater when the men consumed RO rather than VO. We suggest that antioxidants present in VO may protect LDL against oxidation more than does RO in men with peripheral vascular disease.

Aged↗
PubMed1999

Dietary phospholipids rich in long-chain polyunsaturated fatty acids improve the repair of small intestine in previously malnourished piglets.

Malnourished piglets were studied to establish how a diet containing long-chain polyunsaturated fatty acids (LC-PUFA) of the (n-6) and (n-3) series, esterified in the form of phospholipids, affects intestinal recovery after severe malnutrition. Piglets (7-d-old) were randomly assigned to two groups. One group was fed a piglet milk formula and the other was malnourished by protein-energy restriction for 30 d. Healthy and malnourished piglets were then divided into two subgroups fed for 10 d either an adapted milk formula (C and M) or the same diet supplemented with LC-PUFA phospholipids (C-P and M-P). The M-P group had greater protein, DNA, cholesterol and phospholipid levels and a lower triglyceride level in the jejunal segment than did the M group. The fatty acid composition of the jejunal mucosa and microsomes of the M-P piglets did not differ from that of healthy piglets (C). However, in jejunal mucosa, microsomes and phospholipids from malnourished piglets that did not receive LC-PUFA (group M) had significantly lower percentages of (n-6) LC-PUFA than those in healthy piglets (C). The (n-3) LC-PUFA percentages of jejunal mucosa were also lower in the M group than in the C group. The small intestine of piglets fed the LC-PUFA-supplemented formula recovered more completely from histologic lesions and biochemical alterations caused by the malnutrition process than the small intestine of piglets fed the control formula without LC-PUFA.

Animals↗
PubMed1999

Mutation in GDP-fucose synthesis genes of Sinorhizobium fredii alters Nod factors and significantly decreases competitiveness to nodulate soybeans.

We mutagenized Sinorhizobium fredii HH103-1 with Tn5-B20 and screened about 2,000 colonies for increased beta-galactosidase activity in the presence of the flavonoid naringenin. One mutant, designated SVQ287, produces lipochitooligosaccharide Nod factors (LCOs) that differ from those of the parental strain. The nonreducing N-acetylglucosamine residues of all of the LCOs of mutant SVQ287 lack fucose and 2-O-methylfucose substituents. In addition, SVQ287 synthesizes an LCO with an unusually long, C20:1 fatty acyl side chain. The transposon insertion of mutant SVQ287 lies within a 1.1-kb HindIII fragment. This and an adjacent 2.4-kb HindIII fragment were sequenced. The sequence contains the 3' end of noeK, nodZ, and noeL (the gene interrupted by Tn5-B20), and the 5' end of nolK, all in the same orientation. Although each of these genes has a similarly oriented counterpart on the symbiosis plasmid of the broad-host-range Rhizobium sp. strain NGR234, there are significant differences in the noeK/nodZ intergenic region. Based on amino acid sequence homology, noeL encodes GDP-D-mannose dehydratase, an enzyme involved in the synthesis of GDP-L-fucose, and nolK encodes a NAD-dependent nucleotide sugar epimerase/dehydrogenase. We show that expression of the noeL gene is under the control of NodD1 in S. fredii and is most probably mediated by the nod box that precedes nodZ. Transposon insertion into neoL has two impacts on symbiosis with Williams soybean: nodulation rate is reduced slightly and competitiveness for nodulation is decreased significantly. Mutant SVQ287 retains its ability to form nitrogen-fixing nodules on other legumes, but final nodule number is attenuated on Cajanus cajan.

Amino Acid Sequence↗
PubMed1999

Morbidity and mortality in systemic lupus erythematosus during a 5-year period. A multicenter prospective study of 1,000 patients. European Working Party on Systemic Lupus Erythematosus.

In the present study we assessed the frequency and characteristics of the main causes of morbidity and mortality in SLE during a 5-year period and analyzed the prognostic significance for morbidity and mortality of the main immunologic parameters used in clinical practice. We started in 1990 a multicenter study of 1,000 patients from 7 European countries. All had medical histories documented and underwent medical interview and routine general physical examination when entered in the study, and all were followed prospectively by the same physicians during the ensuing 5 years (1990-1995). Four hundred thirteen patients (41.3%) presented 1 or more episodes of arthritis, 264 (26.4%) had malar rash, 222 (22.2%) active nephropathy, 139 (13.9%) fever, 136 (13.6%) neurologic involvement, 132 (13.2%) Raynaud phenomenon, 129 (12.9%) serositis (pleuritis and/or pericarditis), 95 (9.5%) thrombocytopenia, and 72 (7.2%) thrombosis. Two hundred seventy patients (27%) presented infections, 113 (11.3%) hypertension, 75 (7.5%) osteoporosis, and 59 (5.9%) cytopenia due to immunosuppressive agents. Sixteen patients (1.6%) developed malignancies, with the most frequent primary localizations the uterus and the breast. Several immunologic parameters (anti-dsDNA or antiphospholipid antibodies) were found to have a predictive value for the development of SLE manifestations during the period of the study. Forty-five patients (4.5%) died; the most frequent causes of death were divided similarly among active SLE (28.9%), infections (28.9%), and thromboses (26.7%). A survival probability of 95% at 5 years was found. A lower survival probability (92%) was detected in those patients who presented at the beginning of the study with nephropathy.

Adolescent↗
PubMed1999

Effect of spontaneous breathing trial duration on outcome of attempts to discontinue mechanical ventilation. Spanish Lung Failure Collaborative Group.

The duration of spontaneous breathing trials before extubation has been set at 2 h in research studies, but the optimal duration is not known. We conducted a prospective, multicenter study involving 526 ventilator-supported patients considered ready for weaning, to compare clinical outcomes for trials of spontaneous breathing with target durations of 30 and 120 min. Of the 270 and 256 patients in the 30- and 120-min trial groups, respectively, 237 (87.8%) and 216 (84.8%), respectively, completed the trial without distress and were extubated (p = 0.32); 32 (13.5%) and 29 (13.4%), respectively, of these patients required reintubation within 48 h. The percentage of patients who remained extubated for 48 h after a spontaneous breathing trial did not differ in the 30- and 120-min trial groups (75.9% versus 73.0%, respectively, p = 0.43). The 30- and 120-min trial groups had similar within-unit mortality rates (13 and 9%, respectively) and in-hospital mortality rates (19 and 18%, respectively). Reintubation was required in 61 (13.5%) patients, and these patients had a higher mortality (20 of 61, 32.8%) than did patients who tolerated extubation (18 of 392, 4.6%) (p < 0.001). Neither measurements of respiratory frequency, heart rate, systolic blood pressure, and oxygen saturation during the trial, nor other functional measurements before the trial discriminated between patients who required reintubation from those who tolerated extubation. In conclusion, after a first trial of spontaneous breathing, successful extubation was achieved equally effectively with trials targeted to last 30 and 120 min.

Aged↗
PubMed1999

[Prevalence of antibodies against tetanus, diphtheria and Bordetella pertussis in health care professionals].

AIM: The aim of the present study was to determine the prevalence of antibodies versus tetanus, diphtheria and Bordetella pertussis in a population of health care personnel. PATIENTS AND METHODS: A transversal study was carried out in a population of healthy health care professionals from two hospitalary centers in the Community of Madrid (Spain). The ELISA method was used for antibody determinations. The determination of antibodies versus tetanus and diphtheria was performed in a total of 344 individuals (mean age 32 years) and that of whooping cough in 104 subjects (mean age 23 years). RESULTS: The global prevalence of tetanus, diphtheria and whooping cough was of 76.5, 48 and 57%, respectively. The prevalence of antibodies versus tetanus was significantly greater in males than in females. CONCLUSIONS: Revaccination versus tetanus and diphtheria is recommended every 10 years to guarantee protector antibody concentrations in adults. With regard to whooping cough, revaccination could be a strategy to consider in the future, particularly in risk groups in contact with cases of this disease.

Adult↗
PubMed1999

Stability of the FMR1 CGG repeat in a Basque sample.

The fragile X syndrome is an X-chromosome-linked dominant disorder with reduced penetrance. It is the most common inherited form of mental retardation. The molecular basis is usually the unstable expansion of a CGG trinucleotide repeat in the 5' untranslated region of the first exon of the FMR1 gene, which resides at chromosome position Xq27.3 and is coincident with the cytogenetic fragile site FRAXA, which characterizes the syndrome. In the Biscay province of the Basque Country the prevalence of FRAXA in a mentally retarded sample of non-Basque origin is in the range of other analyzed Spanish populations. In the sample of Basque origin we have not found FRAXA site expression and the repeat size is in the normal range. Based on this, we have examined FMR1 gene stability in normal individuals of Basque origin from the Biscay province. This study is based on a sample of 242 X chromosomes. The results from the CGG repeat region of FMR1 indicate that a prevalence of predisposing normal alleles toward repeat instability in the Basque population is 0.00% or near to it. This could be 1 of the explanations of the apparently low fragile X syndrome incidence found in the Basque mentally retarded sample analyzed by us. This low incidence does not seem to be associated with the flanking microsatellite markers.

Analysis of Variance↗
PubMed1998

The 26-mer peptide released from SNAP-25 cleavage by botulinum neurotoxin E inhibits vesicle docking.

Botulinum neurotoxin E (BoNT E) cleaves SNAP-25 at the C-terminal domain releasing a 26-mer peptide. This peptide product may act as an excitation-secretion uncoupling peptide (ESUP) to inhibit vesicle fusion and thus contribute to the efficacy of BoNT E in disabling neurosecretion. We have addressed this question using a synthetic 26-mer peptide which mimics the amino acid sequence of the naturally released peptide, and is hereafter denoted as ESUP E. This synthetic peptide is a potent inhibitor of Ca2+-evoked exocytosis in permeabilized chromaffin cells and reduces neurotransmitter release from identified cholinergic synapses in in vitro buccal ganglia of Aplysia californica. In chromaffin cells, both ESUP E and BoNT E abrogate the slow component of secretion without affecting the fast, Ca2+-mediated fusion event. Analysis of immunoprecipitates of the synaptic ternary complex involving SNAP-25, VAMP and syntaxin demonstrates that ESUP E interferes with the assembly of the docking complex. Thus, the efficacy of BoNTs as inhibitors of neurosecretion may arise from the synergistic action of cleaving the substrate and releasing peptide products that disable the fusion process by blocking specific steps of the exocytotic cascade.

Amino Acid Sequence↗
PubMed1998

An ethanolic-aqueous extract of Curcuma longa decreases the susceptibility of liver microsomes and mitochondria to lipid peroxidation in atherosclerotic rabbits.

Atherosclerosis is characterized by oxidative damage which affects lipoproteins, the walls of blood vessels and subcellular membranes. This study evaluates the antioxidant capacity of a Curcuma longa extract on the lipid peroxidation of liver mitochondria and microsome membranes in atherosclerotic rabbits. Male rabbits fed a 3% (w/w) lard and 1.3% (w/w) cholesterol diet were randomly assigned to three groups. Two groups were treated with different dosages of a turmeric extract (A and B) and the third group (control) with a curcumin-free solution. Basal and in vitro 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH)-induced hydroperoxide and TBARS productions in liver mitochondria and microsomes were analyzed. Group A had the lowest concentration of mitochondrial hydroperoxides. In microsomes, the basal hydroperoxide levels were similar in all groups but, after the induction of oxidation, group C registered the highest value; TBARS production followed the same trend in mitochondria. These findings suggest that active compounds in curcuma extract may be protective in preventing lipoperoxidation of subcellular membranes in a dosage-dependent manner.

Animals↗
PubMed1998

Influence of dietary lipids on lipoprotein composition and LDL Cu(2+)-induced oxidation in rabbits with experimental atherosclerosis.

The aim of this study was to investigate the composition of plasma lipoproteins and their susceptibility to oxidation in rabbits with experimental atherosclerosis provoked by the intake of a diet rich in cholesterol and saturated fat as well as the influence of the intake of four diets differing in their lipid profiles (fish (F), refined olive (R), virgin olive (V) and sunflower (S) oils) on plasma lipoprotein composition and susceptibility to oxidation of these atherosclerotic rabbits. Plasma and lipoproteins concentrations of cholesterol, phospholipids and triglycerides were markedly higher in atherosclerotic rabbits but decreased with the experimental diets. LDL oxidation damage increased in atherosclerotic rabbits; the F diet led to a higher LDL oxidation susceptibility whereas groups fed either S, R, or V showed LDL oxidation values close to those of the control group. Diets rich in monounsaturated and n-3 polyunsaturated oils showed efficacy in restoring the normal lipid profiles in atherosclerotic rabbits provided in fish oil is adequately stabilized with antioxidants.

Animals↗
PubMed1998

Influence of mechanical ventilation on blood lactate in patients with acute respiratory failure.

OBJECTIVES: To determine whether mechanical ventilation (MV) may affect blood lactate concentration in patients with acute respiratory failure. DESIGN: Prospective observational study with follow-up to hospital discharge. SETTING: A 17-bed medical and coronary intensive care unit in a 650-bed general hospital. PATIENTS: 55 adult patients mechanically ventilated for acute respiratory failure between May 1996 and April 1997 were recruited. MEASUREMENTS AND RESULTS: Arterial blood samples for determination of plasma lactate and blood gas analysis were taken just before tracheal intubation on spontaneous breathing, and 20 and 60 min after the initiation of controlled MV. Cuff systemic arterial pressure was measured before tracheal intubation and every 10 min during the first h of MV. Hyperlactatemia (arterial blood lactate > or = 2 mmol/l) was present in 21 of the 55 patients studied. After 20 min of MV, there was a decrease in blood lactate from 4.74 +/- 1.78 to 3.07 +/- 1.69 mmol/l (p < 0.01); 40 min later there was a further decrease to 2.63 +/- 1.35 mmol/l (p < 0.05). The decrease in blood lactate was also observed in those patients who after starting MV developed systemic arterial hypotension (p < 0.01). In patients with a normal lactate concentration at the entry to the study, lactate remained the same after 60 min on MV (NS). CONCLUSIONS: Controlled MV decreases substantially the severity of hyperlactatemia in patients with acute respiratory failure, and any adverse circulatory effects of MV do not alter this beneficial outcome.

Adult↗
PubMed1998

Addition of gangliosides to an adapted milk formula modifies levels of fecal Escherichia coli in preterm newborn infants.

Because some gangliosides bind bacteria, we tested the influence of supplementating an adapted milk formula with gangliosides, at a total concentration of 1.43 mg/100 kcal, on the fecal microflora of preterm infants. At all sampling times, feces from infants fed with ganglioside-supplemented formula had significantly lower relative content of Escherichia coli than feces from infants fed with control milk formula: the difference was especially significant at age 7 days postnatal < .001). At age 30 days postnatal, fecal bifidobacterial counts were higher in infants fed with ganglioside-supplemented formula (P < .05). We conclude that gangliosides at concentrations present in human milk significantly modify the fecal flora.

Escherichia coli↗
PubMed1998

Dietary nucleotides have cytoprotective properties in rat liver damaged by thioacetamide.

Liver cirrhosis has been induced with thioacetamide administered via different routes in rats and other species. The oral intake of thioacetamide causes nodular liver cirrhosis in rats characterized by extensive fibrosis occupying most of the hepatic parenchyma. To characterize the cytological features of cirrhosis induced by thioacetamide, and the degree of recovery obtained with dietary nucleotides, we made a morphometric study of the hepatocytes in rats administered 300 mg/l of thioacetamide for 4 months, and in rats receiving the same hepatotoxic treatment but allowed a 2-weeks recovery period on a nucleotide-free diet or a 250 mg/100 g nucleotide-supplemented diet. Thioacetamide caused to cell damage and affected the ultrastructure of hepatocytes leading to a decrease in cytoplasmic area together with increased nuclear and nucleolar size. Dietary supplementation with nucleotides favoured recovery, restoring the cytoplasmic (TN=491.7+/-9.6 vs TAA=305.1+/-3.7), nuclear (73.6+/-2.8 vs 97.4+/-2.9), and nucleolar area of damaged hepatocytes (5.6+/-0.3 vs 14.0+/-0.9). The injury from thioacetamide intake increased liver collagen, but dietary nucleotides prevented hepatic deposition of this protein. This study supports the hypothesis that dietary supplementation with nucleotides is decisive in ensuring hepatocyte recovery after thioacetamide-induced liver damage, and that dietary nucleotides have antifibrotic properties.

Animals↗