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Biomedical subjects

J Barceló

Publications and source records attributed to J Barceló.

18 recordsLinked to original sources
PubMed1998

Surgical treatment of aortic dissections: initial experience with the adventitial inversion technique.

BACKGROUND: The adventitial inversion technique obliterates the false lumen and converts a dissected aorta into a conduit with tough adventitia on the inside and outside. Dacron grafts can be anastomosed to the aorta with fine sutures, which hold without tears. METHODS: From August 1995 to March 1997, we treated 6 patients with acute dissecting aneurysms. Three aneurysms were type I (A) involving the entire aorta, two type II (A) involving the ascending aorta, and one type III (B) involving the thoracoabdominal aorta. Circulatory arrest was used in 3 patients, 1 with type I aneurysm (A), 1 type II (A), and 1 type III (B). RESULTS: All Dacron-aorta anastomoses held sutures well and did not bleed intraoperatively or postoperatively. One patient (type II [A]) died of intraoperative low cardiac output. In patients with type I (A) aneurysms, the false lumen was obliterated, but 1 patient required resection of a 6-cm abdominal aortic aneurysm. CONCLUSIONS: The adventitial inversion technique is a safe technique for the treatment of acute dissecting aneurysms, which facilitates operation and solves the problem of intraoperative or postoperative bleeding due to tissue friability.

Acute Disease↗
PubMed1997

Anti-Sia-lb (anti-Gd) cold agglutinins bind the domain NeuNAc alpha2-3Gal in sialyl Lewis(x), sialyl Lewis(a), and related carbohydrates on nucleated cells and in soluble cancer-associated mucins.

Anti-Sia-lb (formerly anti-Gd) cold agglutinins (CAs) recognize sialylated carbohydrates on both adult and neonate red blood cells (RBCs). RBC CA activity inhibition experiments reported here indicate that the domain NeuNAc alpha2-3Gal, as found in sialyllactose, synthetic sialyl(s) Lewis(Le)(x) and sLe(a), sialyllactosamine, sialyl-fucosyllactose, and nonfucosylated sLe(a), constitutes the minimal epitope for these CAs, implicating that these autoantibodies could be able to bind this domain in sLe(x) and sLe(a) and related carbohydrates expressed on nucleated cells and in soluble cancer-related mucins. The following data obtained with the previously characterized monoclonal IgMk anti-Sia-lb CA, GAS, show that this is the case. GAS epitope expression among leukocytes that lack sLe(a) parallels that of sLe(x) determinant as detected by mouse monoclonal antibodies (MoAbs), especially MoAb KM-93. It is also found on epithelial malignant cells bearing both sLe(x) and sLe(a). GAS epitope on these nucleated cells, (1) like that present on RBC, is abolished by sialidase, unaffected by proteases, and inhibited by sialyllactose; and (2) is overlapping and/or proximal to that recognized by anti-sLe(x) MoAb, CSLEX-1, and KM-93. Moreover, CAGAS binds soluble cancer-associated mucins bearing sLe(x) and sLe(a) determinants. This binding is inhibited by sialyllactose and these mucins inhibit the RBC CA activity of CAGAS. The possible significance of anti-Sia-lb (anti-Gd) CAs as autoantibodies directed to carbohydrate ligands of host adhesion molecules that might be receptors of microbial adhesins of some CA-inducing pathogens is discussed.

Agglutinins↗
PubMed1997

Respiratory chain activity and mitochondrial DNA content of nonpurified and purified pancreatic islet cells.

Considerable interest has recently focused on the possible role of alterations in mitochondrial activity and mutations in the mitochondrial genome for the development of non-insulin-dependent diabetes. Our study aimed at investigating the normal mitochondrial respiratory chain activity of nonpurified and purified islet cells to further explore whether some diabetic states are associated with alterations of mitochondrial oxidative processes. For this purpose, pancreatic islets were isolated from Wistar rats. Unpurified islet cells were obtained in the presence of trypsin and DNAse, and purified beta and non-beta cells were prepared by autofluorescence-activated sorting using a flowcytometer. Intact cell respiration and substrate oxidation in digitonin-permeabilized cells were measured polarographically with a Clark oxygen electrode in a micro-water-jacketed cell. Specific activity of the individual complexes of the respiratory chain was determined spectrophotometrically in unpurified islet cells. The relative amount of mitochondrial (mtDNA) and nuclear (nDNA) DNA in all three cell populations and in rat brain and skeletal muscle was estimated by dot blotting. The intact cell respiration of unpurified islet cells corresponds to the mean of values obtained for beta and non-beta islet cells. Oxidation rates of different substrates by permeabilized beta cells were lower than those for unpurified and non-beta cells. The amount of mtDNA relative to nDNA was similar in all three groups of cells, and was also similar to that obtained from brain and skeletal muscle. In summary, we have described mitochondrial respiratory chain activity in unpurified, beta, and non-beta islet cells. Our results represent an initial step in investigating the potential pathogenic role that alterations in oxidative phosphorylation could play in some diabetic states.

Animals↗
PubMed1996

Stimulation through CD50 (ICAM-3) induces both activation and programmed cell death of human thymocytes.

CD50 (ICAM-3) has been identified as the third CD11a/CD18 (LFA-1) counter receptor. We investigated the expression and possible role of this molecule in the induction of early and late activation events in human thymocytes. We observed that CD50 expression is acquired by early T cell progenitors (CD34+) and maintained during thymic development, reaching the highest levels in the most mature population of thymocytes (CD3high). Neither basal nor cytokine-induced expression of CD50 was observed on untransformed human thymic epithelial cell lines. Cross-linking of CD50 expressed on the surface of human thymocytes, by using mAbs recognizing epitopes not related to the CD11a binding site, transduced transmembrane signals leading to an increase of intracellular calcium concentration. This calcium mobilization was inhibited when CD50 was co-cross-linked with CD45, suggesting that tyrosine phosphorylation is also involved in CD50 signaling. The same anti-CD50 mAbs that were able to affect intracellular calcium levels were shown to induce CD69 but not CD25 expression on human thymocytes. This effect was preferentially observed on CD3low/CD3high thymocyte subpopulations. Cross-linking of CD50 also significantly increased activation-induced cell death of human thymocytes. These results support the idea that CD50 molecule can play a role in developing functionally mature T lymphocytes.

Antibodies, Monoclonal↗
PubMed1995

Anti-islet cell and anti-insulin antibody production by CD5+ and CD5- B lymphocytes in IDDM.

Although CD5 + B lymphocytes are mostly committed to the production of polyreactive natural autoantibodies, CD5 + B lymphocytes committed to the production of somatically mutated and monoreactive high-affinity IgM autoantibodies have been also shown. Increased proportions of CD5 + B lymphocytes in some autoimmune diseases, including insulin-dependent diabetes mellitus (IDDM), have been noticed. The present study was undertaken to analyse the differences between CD5 + and CD5- B lymphocyte subsets for production of IDDM-related autoantibodies, i.e. anti-human insulin antibodies (IA) and anti-human islet cell antibodies (ICA). For this purpose, Epstein-Barr Virus (EBV)-transformation of FACS cell-sorted CD5 + and CD5- B lymphocytes and unfractionated enriched B lymphocytes from nine IDDM patients treated exclusively with recombinant human insulin, and from four healthy control subjects was performed; a mean of 102-216 microcultures with a mean of 1,000-2,333 cells/microculture for each B-lymphocyte fraction and individual was established. Data show that both CD5 + and CD5- B-lymphocyte subsets from either normal subjects or from IDDM patients receiving recombinant human insulin, contain B lymphocytes committed to the production of IA-IgM as a common element of their repertoire. In contrast, cells committed to the production of IA-IgG were only detected among the CD5- B lymphocyte subset from some IDDM patients. Only one microculture, out of a total of 6,211 screened (from control subjects and patients), in the CD5- B-cell subset from a recently-diagnosed IDDM patient, was found to produce ICA-IgM lambda. This might suggest that the frequency of circulating B lymphocytes committed to the production of ICA is very low even in IDDM patients bearing serum ICA. EBV-transformed B cells producing the ICA-IgM lambda were stabilized and cloned by somatic hybridization technique. This ICA-IgM lambda human monoclonal antibody, designated HY1-MB91, is not polyreactive, but shows a restricted reactivity with human pancreatic islets, failing to react with other human tissues including cerebellar cortex, and lacking rheumatoid factor and anti-DNA antibody activities. It also lacks reactivity with pancreatic islets from other mammalian species (rat, mouse and monkey) as well as with other rat tissues, including cerebellar cortex. The antigen recognized by HY1-MB91 antibody in human islet cells is a cytoplasmic component mostly found in beta cells.

Adolescent↗
PubMed1994

Severe homozygous protein C deficiency: identification of a splice site missense mutation (184, Q-->H) in exon 7 of the protein C gene.

Single strand conformation polymorphism (SSCP) analysis of exon 7 of the protein C gene has identified a novel splice site missense mutation (184, Q-->H), in a newborn child with purpura fulminans and undetectable protein C levels. The mutations, seen in the homozygous state in the child and in the heterozygous state in her mother, was characterized and found to be a G to C nucleotide substitution at the -1 position of the donor splice site of intron 7 of the protein C gene, which changes histidine 184 for glutamine (184, Q-->H). According to analysis of the normal and mutated sequences, this mutation should also abolish the function of the donor splice site of intron 7 of the protein C gene. Since such a mutation is compatible with the absence of gene product in plasma and since DNA sequencing of all protein C gene exons in this patient did not reveal any other mutation, we postulate that mutation 184, Q-->H results in the absence of protein C gene product in plasma, which could be the cause of the severe phenotype observed in this patient.

Base Sequence↗
PubMed1993

Reduction in size of the myotonic dystrophy trinucleotide repeat mutation during transmission.

Myotonic dystrophy (DM) is an autosomal-dominant disorder that affects 1 in 8000 individuals. Amplification of an unstable trinucleotide CTG repeat, located within the 3' untranslated region of a gene, correlates with a more severe DM phenotype. In three cases, the number of CTG repeats was reduced during the transmission of the DM allele; in one of these cases, the number was reduced to within the normal range and correlated at least with a delay in the onset of clinical signs of DM. Haplotype data of six polymorphic markers in the DM gene region indicate that, in this latter case, two stretches of the affected chromosome had been exchanged with that region of the wild-type chromosome.

Adult↗
PubMed1993

Isolation and characterisation of a CDw50 negative Jurkat T-cell line variant (PPL.1).

PPL.1, a Jurkat cell line variant deficient in CDw50 surface expression, has been selected by fluorescence-activated cell sorting and expanded in cell culture. We have studied the expression of several leukocyte surface markers (CD2, CD3, CD4, CD8, CD7, CD26, CD25, CD14, CD18, kCD20, CD43, CD45, CD45R, CD71 and HLA class I and II) and we find no differences in their expression between PPL.1 and its parental Jurkat cell line. Immunoprecipitation analysis of metabolically labelled PPL.1 cells ([35S]-cysteine plus [35S]-methionine) fails to detect the presence of a preformed cytoplasmic pool of CDw50 molecules. The deficient CDw50 expression on PPL.1 cells is stable after several weeks of continuous culture and even after exposure of cells to several lymphocyte activating agents (PGE2, PHA, Con A, calcium ionophore A23187 and human recombinant IFN-gamma). No karyotype changes responsible for such phenotype deficiency are found. PPL.1 cells are as efficient as wild-type Jurkat or K562 cells, when used as targets in cytotoxicity assays with fresh or PHA-stimulated peripheral blood lymphocytes. No blocking effects of CDw50-specific mAb are observed in such assay. These results are consistent with the fact that CDw50 is not involved in alloreactive T-cell-specific cytotoxicity. They also suggest that this antigen is implicated only on a very specialized type of cell-cell interactions.

Antigens, CD↗
PubMed1992

Myotonic dystrophy mutation: an unstable CTG repeat in the 3' untranslated region of the gene.

Myotonic dystrophy (DM) is the most common inherited neuromuscular disease in adults, with a global incidence of 1 in 8000 individuals. DM is an autosomal dominant, multisystemic disorder characterized primarily by myotonia and progressive muscle weakness. Genomic and complementary DNA probes that map to a 10-kilobase Eco RI genomic fragment from human chromosome 19q13.3 have been used to detect a variable length polymorphism in individuals with DM. Increases in the size of the allele in patients with DM are now shown to be due to an increased number of trinucleotide CTG repeats in the 3' untranslated region of a DM candidate gene. An increase in the severity of the disease in successive generations (genetic anticipation) is accompanied by an increase in the number of trinucleotide repeats. Nearly all cases of DM (98 percent or 253 of 258 individuals) displayed expansion of the CTG repeat region. These results suggest that DM is primarily caused by mutations that generate an amplification of a specific CTG repeat.

Base Sequence↗
PubMed1992

Correlation between CTG trinucleotide repeat length and frequency of severe congenital myotonic dystrophy.

The myotonic dystrophy (DM) mutation has recently been identified as an unstable trinucleotide CTG repeat which is present 5-30 times in the normal population but which is amplified up to 2,000 times in DM. We have determined the status of the CTG repeat in 272 DM individuals. Infants with severe congenital DM, as well as their mothers, are shown to have on average a greater amplification of the CTG repeat than is seen in the noncongenital DM population. This fact, when viewed in conjunction with the tendency to increased CTG repeat length in our DM kindreds, provides evidence for the existence of genetic anticipation in the transmission of DM.

Base Sequence↗
PubMed1991

[Hemoptysis: a prospective study of 108 cases in an emergency service].

A prospective study is performed in 108 patients presenting hemoptysis who were attended in the emergency department. Final diagnosis was achieved in 89 cases (82.4%), being lung infections of tuberculous origin or not, neoplasias, and chronic obstructive lung emphysema the main observed etiologies. A low percentage of severe hemoptysis is found (5.6%). Diagnosis was obtained in 79.6% of patients by clinical history, physical exam, chest x-ray and ORL exam. Only 13.6% of patients who were not diagnosed in the Emergency department were later diagnosed by follow up and performance of complementary tests. Similarly, the lack of an initial etiological diagnosis had no repercussion, by itself, in a worse prognosis. Therefore, it is recommended to perform a single strict evolution control in patients with hemoptysis of unknown origin who present risk factors of lung neoplasia (male sex, age greater than 40 years, smoking greater than 45 packs/year).

Age Factors↗
PubMedDate not supplied

Cardiac surgery on Jehova's Witnesses at Instituto Cardiovascular-Hospital Pavia.

Jehovah's Witnesses (J.W.) can undergo successful cardiac operations. We have operated five J.W. patients. Of these patients, two had coronary artery bypass surgery and three had correction of congenital anomalies. These included an atrial septal defect with infundibular pulmonic stenosis, a tetralogy of Fallot and a patient with a ventricular septal defect. Our treatment protocol includes a meticulous surgery, the use of early heparinization to collect all shed blood into the pump oxygenator, observation in the operating room for early exploration if the patient bleeds and administration of iron preparations. Recombinant human erythropoietin, although available and in our treatment protocol, has not been used yet. All patients survived the operation and left the hospital with an excellent hemoglobin and hematocrit. The length of stay varied from 7 to 15 days.

Adolescent↗