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Biomedical subjects

J L Alonso

Publications and source records attributed to J L Alonso.

At least 55 records · Page 3Linked to original sources
PubMed1995

Ecopathology in aquaculture: risk factors in infectious disease outbreak.

This paper describes a study of the risk factors associated with disease outbreaks in fish species of fish farms and rivers of north-east Spain. We focused our work on the isolation of fish pathogens (bacteria, virus), the water quality (physicochemical and microbiological quality) and management characteristics. We have observed 2 important viral diseases, infectious pancreatic necrosis and spring viraemia of carp, and 2 important bacterial ones, furunculosis (Aeromonas salmonicida) and bacterial kidney disease (BKD) (Renibacterium salmoninarum). Our preliminary results show that there are some potential risk factors associated with the main diseases of fish, such as fish age, fish species, production system, season and water temperature, but their role depends on the disease.

Age Factors↗
PubMed1995

Diagnostic survey of viral haemorrhagic disease in wild rabbits (Oryctolagus cuniculus) in four regions of Spain.

Samples of organs and serum were obtained from wild rabbits (Oryctolagus cuniculus) found dead in the field, shot or captured by hunters, or introduced for repopulation in various provinces of Spain over a two-year period, for the purposes of an epidemiological study of viral haemorrhagic disease (VHD) of rabbits. The efficacy of the haemagglutination test and the direct immunofluorescence test for the diagnosis of VHD was also examined.

Animals↗
PubMed1994

[Evaluation of the efficacy of chelation therapy with deferoxamine in patients with thalassemia major].

BACKGROUND: The current treatment of thalassaemia maior (TM) is based on a hypertransfusion regimen, with deferoxamine (DFO) chelation therapy to minimize the consequences of iron overload. To evaluate the long-term efficacy of chelation therapy, a group of 9 patients treated for a period of 9 years was studied. METHODS: The mean age of patients at the beginning of chelation therapy was 7 years. The age range at the moment of the study was 11 to 21 years. Pre-transfusion haemoglobin values were maintained above 10 gr/dl. DFO was administered by 10-hour sub-cutaneous infusion, 5 or 6 days a week at a dose of 40 mg/kg. Different iron overload parameters were considered, with special attention to cardiac function, growth and endocrinologic development. Signs of DFO toxicity were also studied. RESULTS: The final mean iron elimination rate was 72.6%. One patient died from cardiac haemosiderosis. Eight of the 9 patients showed significant growth impairment and 7, who have attained puberal or post-puberal age, suffer from one or more endocrinologic disorders (6 hypogonadism, 2 diabetes mellitus, 2 hypothyroidism and 1 hypoparathyroidism). The only toxic effect observed was transient crystalline opacity in 2 patients. CONCLUSIONS: Despite the early initiation of chelation therapy, TM patients receiving hypertransfusion regimen showed iron overload, with myocardiopathy, growth retardation and several endocrinologic disorders, mainly secondary hypogonadism, glucose metabolism disfunction and primary hypothyroidism.

Child↗
PubMed1994

Induction of tumor necrosis factor alpha production by human hepatocytes in chronic viral hepatitis.

Tumor necrosis factor alpha (TNF-alpha) is a multifunctional cytokine that has an important role in the pathogenesis of inflammation, cachexia, and septic shock. Although TNF-alpha is mainly produced by macrophages, there is evidence regarding TNF-alpha production by cells that are not derived from bone marrow. TNF-alpha production by normal and inflamed human liver was assessed at both mRNA and protein levels. Using a wide panel of novel anti-TNF-alpha monoclonal antibodies and a specific polyclonal antiserum, TNF-alpha immunoreactivity was found in hepatocytes from patients chronically infected with either hepatitis B virus (HBV) or hepatitis C virus. Minimal TNF-alpha immunoreactivity was detected in the mononuclear cell infiltrate and Kupffer cells. In situ hybridization experiments using a TNF-alpha RNA probe showed a significant expression of TNF-alpha mRNA in hepatocytes, Kupffer cells, and some infiltrating mononuclear cells. By contrast, TNF-alpha was detected at low levels in liver biopsies from normal individuals or patients with alcoholic liver disease and low expression of TNF-alpha mRNA was observed in these specimens. Transfection of HepG2 hepatoblastoma cells with either HBV genome or HBV X gene resulted in induction of TNF-alpha expression. Our results demonstrate that viral infection induces, both in vivo and in vitro, TNF-alpha production in hepatocytes, and indicate that the HBV X protein may regulate the expression of this cytokine. These findings suggest that TNF-alpha may have an important role in human liver diseases induced by viruses.

Antibodies, Monoclonal↗
PubMed1994

Increase of tumour necrosis factor alpha synthesis and gene expression in peripheral blood mononuclear cells of children with idiopathic nephrotic syndrome.

The pathogenesis of idiopathic nephrotic syndrome (minimal change nephropathy and its variants) is not completely understood. In recent years it has been speculated that a cytokine released by circulating blood mononuclear cells could alter the permeability of the glomerular capillary wall. In this study we have explored the potential participation of tumour necrosis factor alpha (TNF alpha), a cytokine mainly produced by monocytes, in 25 children with idiopathic nephrotic syndrome. TNF alpha was determined by cytotoxicity bioassay in the L-929 cell line and by double antibody/RIA. Patients in activity had higher serum TNF alpha levels and TNF alpha production by monocytes than patients in remission and controls. TNF alpha mRNA expression in blood mononuclear cells was analysed by Northern blot. The TNF alpha mRNA levels in patients in activity were increased compared to controls and to patients in remission. No significant differences in IL-1 beta and IL-6 synthesis were found between patients and controls. Our results suggest that TNF alpha, but not other cytokines such as IL-1 beta and IL-6, could play a role in the pathogenesis of the proteinuria in idiopathic nephrotic syndrome.

Child↗
PubMed1994

Subcellular localization of the segment polarity protein patched suggests an interaction with the wingless reception complex in Drosophila embryos.

The product of the segment polarity gene patched is a transmembrane protein involved in the cell communication processes that establish polarity within the embryonic segments of Drosophila. Monoclonal antibodies have been raised against the patched protein, and by immunoelectron microscopy part of the patched staining is found associated with discrete regions of the lateral plasma membrane of the embryonic epidermal cells. Using a mutation affecting endocytosis (shibire) we find that patched is a membrane-bound protein, which is internalized by endocytosis, and that the preferential sites of accumulation resemble the described localization of the cell-cell adhesive junctions of the epidermal cells. patched partially co-localizes with the wingless protein in the wingless-expressing and nearby cells, in structures that seem to be endocytic vesicles. These data suggest the interaction of patched protein with elements of the reception complex of wingless, as a way to control the wingless expression.

Animals↗
PubMed1994

[Esophageal carcinosarcoma: morphologic and cytometric study].

Carcinosarcoma of the esophagus is a rare malignant neoplasm composed by both carcinomatous (epithelial) and sarcomatous (mesodermal) elements. We report a case, diagnosed by biopsy an endoscopic brushing. Cytometric analysis was also performed.

Carcinosarcoma↗
PubMed1994

[Usefulness of endoscopic hemostasis in Dieulafoy's vascular disease].

We report three cases of "Dieulafoy's gastric erosion" or "Exulceratio simplex", which is rarely recognized but is not an uncommon cause of upper gastrointestinal hemorrhage, usually very dangerous, as it's an arterial bleeding. In all cases an emergency endoscopy was performed, and treatment with combination of local sclerosis and vessel's electrocoagulation was successful. We insist in the potential benefits of endoscopic treatment in all these occasions, if it's possible, since even exact diagnosis of the bleeding site is very difficult in some patients.

Adult↗
PubMed1994

[Intestinal pseudo-obstruction secondary to systemic neuropathies and myopathies].

The term intestinal pseudo-obstruction, is applied to a group of clinical disorders in which there are obstructive symptoms, in the absence of a mechanical agent, secondary to a disorder of intestinal motility. In this report, we show manometric studies done in four patients, with acute intestinal pseudo-obstructions, secondary to von Recklinghausen's neurofibromatosis (VRNF), in two patients, and in one patient with Duchenne's muscular dystrophy (DMD) and in another with Werdnig-Hoffmann's disease (WHD). We studied 24 hours antroduodenal motility, specially during phase 3 of the migratory motor complex (CMM), which showed a neuropathic disorder in one case of von Recklinghausen's disease and a myopathic disorder in patients with Duchenne's muscular dystrophy and Werdnig-Hoffmann's disease. We analysed results and conclusions and specially the kinetic action of erythromycin.

Adolescent↗
PubMed1993

Stimulation of IL-2-activated natural killer cells through the Kp43 surface antigen up-regulates TNF-alpha production involving the LFA-1 integrin.

We have previously described that a mAb directed against a surface dimer (Kp43) expressed by NK cells was able to regulate cell proliferation, enhance the cytotoxicity of IL-2-activated NK cells, and activate phospholipase D. In this work we have analyzed the ability of the anti-Kp43 mAb to regulate the production of TNF-alpha. Our results show that the stimulation of IL-2-activated NK cells with soluble anti-Kp43 mAb or its F(ab')2 activated the secretion of the cytokine, inasmuch as this effect is associated with the induction of cellular aggregation. The intensity of the Kp43-mediated stimulation varied among different IL-2-activated NK cell samples. Even in those instances where the anti-Kp43 mAb alone could not detectably enhance TNF-alpha production, it displayed a synergistic effect combined to a soluble anti-CD16 mAb, which on its own did not efficiently activate cytokine production. The anti-Kp43 mAb also cooperated with a phorbol ester, although it did not modify the TNF-alpha production triggered by a Ca2+ ionophore. The anti-Kp43-mediated effect, which required the preactivation of cells with IL-2, was inhibited by cycloheximide and actinomycin D and was associated with an increase in the levels of TNF-alpha-specific mRNA. It is noteworthy that the Kp43-mediated production of TNF-alpha was partially inhibited by anti-CD18, anti-CD11a and anti-ICAM-1 mAb that blocked LFA-1-dependent cellular interactions, which impaired NK cell aggregation and, moreover, was dependent on the presence of extracellular Mg2+, thus suggesting that the leukocyte integrin is involved in the activation process triggered through Kp43.

Antibodies, Monoclonal↗
PubMed1993

Signaling through the LFA-1 leucocyte integrin actively regulates intercellular adhesion and tumor necrosis factor-alpha production in natural killer cells.

The LFA-1 leucocyte integrin is known to participate in natural killer (NK) cytolytic activity, mediating effector target interactions. The possibility that LFA-1 may also play an active regulatory role in NK cells has been explored. To this end, we have employed a monoclonal antibody (HP1N) raised against recombinant interleukin-2 (rIL-2)-activated NK cells, which recognizes the alpha chain of the LFA-1 heterodimer (CD11a). In contrast to other anti-CD11a mAb the HP1N and its F(ab')2 fragment did not affect NK cell-mediated cytotoxicity and triggered a strong homotypic adhesion of NK cells and other LFA-1+ cells. Cellular aggregation was inhibited by anti-CD18 mAb, anti-ICAM-1 mAb, and other anti-CD11a mAb. Remarkably, the HP1N mAb was also shown to induce tumor necrosis factor-alpha (TNF-alpha) production from NK cells upon costimulation with anti-CD16 mAb. Such an effect appeared to be independent from homotypic adhesion since it took place in Mg(2+)-free medium, where NK cell aggregation was inhibited. Moreover, incubation with the HP1N mAb triggered a Ca2+ influx into the cytosol; this effect was clearly observed upon cross-linking of cell bound HP1N and was also substantiated with other anti LFA-1 (CD11a and CD18) mAb. Taken together these results indicate that the LFA-1 molecule is capable of transducing signals in NK cells, which regulate the intercellular interaction with its ligand, and enhance the activation via Fc gamma receptor type III.

Antibodies, Monoclonal↗
PubMed1993

Survey of rotavirus infection in a dairy herd: comparison between polyacrylamide gel electrophoresis and two commercial tests.

A survey of rotavirus infection in a dairy herd with a history of neonatal diarrhoea was carried out. Faecal samples taken from 15 cows before and after calving as well as faeces taken from their calves daily from birth to two weeks of life were tested for rotavirus by polyacrylamide gel electrophoresis (PAGE) and compared with an ELISA and a latex agglutination commercial test. Rotavirus excretion was not detected in faeces from cows around parturition by any of the three tests. However, all of their calves shed rotaviruses during the observation period. The onset of rotavirus excretion determined by PAGE ranged from day 2 to day 8 of life (day 4.8 +/- 1.8 on average) and lasted for 4 to 7 days (5.3 +/- 1.1 days on average). Chi-square test showed a significant association (P = 0.0001) between the presence of rotavirus and the altered consistency of calves faeces. All the three tests showed similar results (overall agreement 92.5%) but discrepancies were detected mainly at the beginning or at the end of the rotavirus excretion period. Results obtained with both commercial kits closely paralleled each other and parameters other than sensitivity, specificity, diagnostic accuracy or predictive values have to be considered as selection criteria.

Animals↗
PubMed1993

[A ventriculoperitoneal shunt as a rare cause of ascites].

We report the case of a 22-year-old man with a craniopharyngioma, who developed ascites following a ventriculoperitoneal shunt procedure for hydrocephalus. The ascites was resolved with diversion of the distal catheter into the right atrium. A ventriculoperitoneal shunt can cause ascites, even without neurological symptoms suggestive of shunt malfunction.

Adult↗
PubMed1992

Molinate decontamination processes in effluent water from rice fields.

The performance of aeration, photodecomposition and biological degradation processes as methods to reduce molinate contamination levels in effluent water from rice fields was studied. Aeration produced a molinate dissipation of 84%, as against 22% without aeration. Application of UV-light to clean water solutions achieved a molinate photodecomposition of 96% in 24 h. Maximal degradation obtained in algal cultures was 55% in 20 days and 78% in 40 days. In micro-organism cultures, kept in darkness and with a continuous flow of aqueous solution of molinate and inorganic salts, a degradation of 97% was achieved.

Azepines↗
PubMed1992

Tumor necrosis factor-alpha production induced in T lymphocytes through the AIM/CD69 activation pathway.

Human activation inducer molecule (AIM/CD69), a dimeric glycoprotein of 33 and 27 kDa, is the earliest inducible cell surface antigen expressed during lymphocyte activation, which has been also involved in lymphocyte proliferation. Although AIM is absent from peripheral blood resting lymphocytes, it is expressed by in vivo activated lymphocytes infiltrating sites of chronic inflammation in several pathologies, as well as by lymphocytes after in vitro activation with different stimuli. We have investigated the possibility that tumor necrosis factor-alpha (TNF-alpha) gene expression and protein secretion could be induced in peripheral blood T cells through the AIM/CD69 molecule. Anti-AIM monoclonal antibodies (mAb) were able to induce TNF-alpha secretion in T cells when protein kinase C (PKC) was simultaneously activated by treatment with phorbol esters. TNF-alpha secretion was detected at 24 h and peaked at day 3 upon T lymphocyte activation with anti-AIM mAb. Immunoprecipitation studies with an anti-TNF-alpha mAb from surface iodinated T cells activated through AIM, demonstrated that TNF-alpha first appeared as a cell surface molecular form of 26 kDa, which is subsequently released to the extracellular medium as the 17-kDa molecular form of TNF-alpha. AIM stimulation dramatically increased TNF-alpha mRNA levels, and this mRNA induction and subsequent TNF-alpha secretion were virtually abrogated by the immunosuppressive drug cyclosporin A. Taken together these results indicate that AIM constitutes a novel molecular pathway in T lymphocytes for induction of TNF-alpha, and suggest a relevant pathologic role for AIM+ lymphocytes located at sites of tissue injury in the pathogenesis of different chronic inflammatory diseases.

Animals↗
PubMed1992

Regulation of tumor necrosis factor (TNF)-alpha synthesis and TNF receptors expression in T lymphocytes through the CD2 activation pathway.

The involvement of the CD2 (T11) molecule, an alternative activation pathway for T lymphocytes, in the regulation of tumor necrosis factor (TNF)-alpha/TNF receptor system in human T lymphocytes has been investigated. It has been found that both TNF-alpha synthesis and secretion were induced after incubation of purified T lymphocytes with the appropriate mitogenic combination of antibodies specific for two different epitopes on the CD2 molecule. Moreover, TNF-alpha secretion was also observed by activation of T lymphocytes either through CD3 or CD69 molecular pathways, or with other stimulating agents such as Ca2+ ionophore in combination with phorbol esters. The expression of TNF receptors has been studied in both nonactivated and CD2-activated T lymphocytes. Unstimulated T cells weakly expressed a functional 75-kDa receptor form, whereas they lacked detectable levels of the 55-kDa receptor form. Triggering of T cell activation through the CD2 molecule also markedly increased the expression of the p75-kDa TNF receptor form, but did not exert any inductive effect on the expression of the p55-kDa TNF receptor. In addition, we have found that TNF-alpha enhanced the proliferative response triggered by the mixture of anti-CD2 monoclonal antibodies. Taken together, these results support a role for the CD2 activation pathway in the functional regulation of TNF-alpha/TNF receptor system in T lymphocytes, and reinforce the view of CD2 as an alternative pathway for regulation of the cytokine network that modulates the function of T lymphocytes.

Antibodies, Monoclonal↗