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Biomedical subjects

L F Garcia

Publications and source records attributed to L F Garcia.

10 recordsLinked to original sources
PubMed1998

A randomized, blinded, comparative trial of one pepsin-digested and two whole IgG antivenoms for Bothrops snake bites in Uraba, Colombia. The Regional Group on Antivenom Therapy Research (REGATHER).

The therapeutic efficacy and the incidence of early antivenom reactions (EARs) were compared in a clinical trial performed in 79 patients bitten by Bothrops sp. in Urabá, Colombia. Patients were randomized into three groups according to the antivenom administered: A (n = 30, Butantan polyspecific, pepsin-digested Bothrops antivenom); B (n = 27, Butantan polyspecific, whole IgG Bothrops antivenom); and C (n = 22, Colombian commercial, monovalent, whole IgG Bothrops antivenom). The groups were comparable in all clinical and epidemiologic aspects; 33 patients had mild, 22 moderate, and 24 severe envenoming. At the doses used (two, four, and six vials [10 ml/vial] for mild, moderate, and severe envenomings, respectively) there were no differences between the antivenoms in restoring normal hemostatic parameters within 24 hr. The evolution of local envenoming was comparable in the three groups. Serum venom/antivenom kinetics determined by ELISA showed a complete clearance of venom levels 1 hr after treatment in mild/moderate envenomings. In severe cases, venom levels remained detectable up to 24 hr and recurrence of antigenemia was observed in some cases. Antivenom concentrations remained at high levels up to 24 hr of treatment. The incidence of EARs was significantly different in the groups: A (36.7%), B (11.1.%), and C (81.8%). There were no life-threatening anaphylactic reactions. We conclude that the efficacy of the three antivenoms was similar in neutralizing human Bothrops envenomings and that the production of whole IgG antivenoms by caprylic acid fractionation is a good alternative for reducing the incidence of EARs.

Adolescent↗
PubMed1997

Differential induction of apoptosis by virulent Mycobacterium tuberculosis in resistant and susceptible murine macrophages: role of nitric oxide and mycobacterial products.

Resistance and susceptibility of macrophages to mycobacteria are under the control of the Bcg/Nramp1 gene, which also controls the NO- production in response to macrophage activators. There is recent evidence indicating that mycobacteria induces apoptosis in infected macrophages. Using murine macrophage lines, congenic at the Bcg/Nramp1 gene, this report shows that B10R are more prone than B10S macrophages to undergo apoptosis after exposure to live virulent Mycobacterium tuberculosis H37Rv (Mtb) or PPD, as determined by cell viability, DNA fragmentation, hypoploidy, and the terminal deoxynucleotide transferase dUTP-biotin nick-end labeling assay. Induction of apoptosis correlated with NO- production. Aminoguanidine and anti-TNF-alpha inhibited NO- production and apoptosis. B10R and B10S macrophages were equally affected by sodium nitroprusside, a donor of NO-, but its effect, mainly in B10R cells, was enhanced by the presence of Mtb. Nonvirulent mycobacteria induced lower levels of NO- and did not cause cell death. Killed Mtb, mannose-capped lipoarabinomannan (ManLAM), and LPS rescued macrophages from apoptosis albeit induce NO-. These findings suggest the existence of opposite pathways: metabolically active mycobacteria promotes apoptosis whereas their structural components inhibit it. Apoptosis may be a critical mechanism by which Nramp1 gene controls the macrophage infection with virulent mycobacteria.

Animals↗
PubMed1997

Involvement of programmed cell death in morphogenesis of the vertebrate inner ear.

An outstanding challenge in developmental biology is to reveal the mechanisms underlying the morphogenesis of complex organs. A striking example is the developing inner ear of the vertebrate, which acquires a precise three-dimensional arrangement of its constituent epithelial cells to form three semicircular canals, a central vestibule and a coiled cochlea (in mammals). In generating a semicircular canal, epithelial cells seem to 'disappear' from the center of each canal. This phenomenon has been variously explained as (i) transdifferentiation of epithelium into mesenchyme, (ii) absorption of cells into the expanding canal or (iii) programmed cell death. In this study, an in situ DNA-end labeling technique (the TUNEL protocol) was used to map regions of cell death during inner ear morphogenesis in the chicken embryo from embryonic days 3.5-10. Regions of cell death previously identified in vertebrate ears have been confirmed, including the ventromedial otic vesicle, the base of the endolymphatic duct and the fusion plates of the semicircular canals. New regions of cell death are also described in and around the sensory organs. Reducing normal death using retrovirus-mediated overexpression of human bcl-2 causes abnormalities in ear morphogenesis: hollowing of the center of each canal is either delayed or fails entirely. These data provide new evidence to explain the role of cell death in morphogenesis of the semicircular canals.

Animals↗
PubMed1990

Natural killer cell activity in patients with pulmonary tuberculosis and in healthy controls.

Natural killer (NK) cell activity of freshly isolated peripheral blood mononuclear cells (MNC) or cells stimulated for 72 h with 10 micrograms/ml of a sonicate antigen of Mycobacterium tuberculosis H37Rv were studied in healthy responder and non-responder controls, as detected by lymphocyte proliferation with specific antigen, and in patients with pulmonary tuberculosis. K-652 cells were used as targets in a 4 h 51Cr release assay. MNC from patients exhibited a significant decrease in NK function as compared with responder controls (p less than 0.02). NK activity in responder individuals was highest 72 h after incubation with antigen. Non-stimulated cells were not cytotoxic. MNC from healthy responder and non-responder subjects incubated for 72 h with antigen yielded a significant increase in the percentage NK cytotoxicity at all effector/target ratios studied (p less than 0.01) as well as in the number of lytic units per culture (p less than 0.004). However, this increase was higher in responder individuals as compared to non-responder subjects (p = 0.02). The response to antigen was not significant in the group of patients although a net increase was also observed in the whole group. Only 4 of 9 patients exhibited significant increased responses after antigenic stimulation, 3 showed moderate responses, 1 did not respond and in a further patient a decrease was observed. The decreased NK activity could be secondary to abnormalities in the production of lymphokines by tuberculous patients. Although the role of non-specific cytotoxic cells in tuberculosis is unknown, their alterations could contribute to the pathogenesis of the disease.

Adolescent↗
PubMed1988

Blood transfusions and HLA compatibility in first cadaveric kidney transplants treated with cyclosporine A.

One-year graft survival of 54 first cadaveric kidney transplants that received immunosuppressive treatment with CsA was analyzed with respect to the number of random pretransplant blood transfusions and the HLA class 1 and class 2 matching. Overall graft survival at 1 year was 80.7%. Patients with 3 to 20 pretransplant transfusions had a survival of 93.7% compared with 66.7% in those with less than three or more than 20 transfusions. All kidneys transplanted with two or less HLA-A + B mismatches survived at 1 year. With three mismatched antigens survival was of 88.9%. This value was reduced to 66.7% for four incompatibilities. A similar situation was found for HLA-DR matching since all kidneys with full compatibility survived at 1 year compared with 90.9% and 66.7% for one and two mismatches, respectively. HLA-B and HLA-DR exhibited an additive effect since again all grafts with two or less mismatches survived, whereas in the group with three different antigens this figure was 90% and only 1 of the three kidneys with completely different antigens survived.

Blood Transfusion↗