PubMed Health⌕ Search

Biomedical subjects

R Ramírez

Publications and source records attributed to R Ramírez.

At least 73 records · Page 4Linked to original sources
PubMed1995

Immunohistochemical quantitative study of the peritubular lamina propria after induction of testicular atrophy induced by epinephrine.

Changes in the testicular peritubular lamina propria in rats treated for 1-11 weeks with intra-scrotal injections of epinephrine were studied by quantitative immunohistochemical methods. In control testes, BrdU-labelled nuclei (proliferating cells) were observed only in spermatogonia and some primary spermatocytes, whereas testes from epinephrine-treated rats showed BrdU labelling in some of the spermatogonia and in peritubular cells. Immunostaining for transforming growth factor beta 1 (TGF-beta 1) was present in germ cells, Sertoli cells and Leydig cells; vimentin immunostaining was found mainly in Sertoli cells; desmin immunostaining was found in the peritubular cells, and immunostaining for type IV collagen, laminin and fibronectin was found in the extracellular matrix of the lamina propria. The volume densities of seminiferous tubules (including seminiferous epithelium, lamina propria and tubular lumen) that immunostained for TGF-beta 1, vimentin, laminin, desmin or fibronectin were calculated. All of these parameters increased significantly in testes from epinephrine-treated animals during the course of the experiment, except for desmin immunostaining which showed no significant change in volume density. Since total seminiferous tubule volume decreased markedly in the testes of treated rats during the experiment, the transformation of relative values for immunostaining into absolute volumes per testis revealed a significant increase in TGF-beta 1 immunostaining, no significant change in vimentin immunostaining, and a significant decrease in desmin immunostaining during the time of the study. The absolute volume occupied by laminin and fibronectin immunostaining decreased from the 3rd to the 8th weeks of treatment, and increased from the 8th to the 11th weeks. These changes, associated with germ cell depletion and tubular fibrosis, suggest that tubular ischaemic atrophy caused by epinephrine alters the peritubular myoid cells, which change immunophenotype and increase their secretion of the extracellular matrix components producing tubular fibrosis. The mechanism of this alteration may involve direct effects on the peritubular cells or the changes may be secondary to germ cell and/or Sertoli cell lesions.

Animals↗
PubMed1994

Leukotriene C4 upregulates collagenase expression and synthesis in human lung fibroblasts.

Leukotriene C4 (LTC4), a mediator generated by a variety of inflammatory cells, participates in several physiological and pathological processes. It has been shown that LTC4 stimulates collagen synthesis by fibroblasts, suggesting a role in collagen turnover. However, the possible effect of this mediator on collagen degradation has not been examined. In this study we explored the role of LTC4 in the modulation of fibroblast interstitial collagenase and TIMP-1. Confluent cultures of three human normal lung fibroblast cell lines, and one derived from idiopathic pulmonary fibrosis (IPF) were exposed to LTC4 0.1, 1 and 10 nM, and to IL-1 beta as positive control. Collagenase and TIMP mRNAs expression were analyzed by Northern blot followed by densitometric scanning. Immunoreactive procollagenase was detected by immunoblot, and collagenase activity was measured using [3H]collagen. Our results showed that LTC4 enhanced several-fold collagenase mRNA expression in collagenase-producing fibroblasts, and induced the expression of the enzyme mRNA in collagenase-nonproducing fibroblasts, both in normal and IPF derived cell lines. LTC4 1 nM induced the highest response. Collagenolytic activity and immunoreactive collagenase paralleled collagenase mRNA expression. Interestingly, simultaneous exposure of fibroblasts to LTC4 plus IL-1 failed to show additive effects. Moreover, in two cell lines the combination resulted in a decrease of collagenase mRNA expression compared with both mediators separately. TIMP mRNA levels were not significantly modified by LTC4, nor IL1 beta. Our findings suggest that LTC4 plays a role in the modulation of fibroblast collagenase, and it may participate in extracellular matrix remodeling during lung inflammation.

Collagenases↗
PubMed1994

Pertussis toxin inhibits activation-induced cell death of human thymocytes, pre-B leukemia cells and monocytes.

Activation of human thymocytes and pre-B cells via the CD3/T cell receptor (TCR) complex or the IgM/B cell receptor complex, respectively, results in apoptotic cell death. Similarly, cross-linking of the activation marker CD69, which belongs to the natural killer complex, causes apoptosis of lipopolysaccharide-preactivated monocytes. Here we show that pertussis toxin (PTX) inhibits the activation-induced apoptosis of these three cell types, though it fails to prevent the programmed cell death that follows exposure of cells to the synthetic glucocorticoid dexamethasone (thymocytes, pre-B cells) or to interleukin 4 (monocytes). The capacity of pertussis toxin to suppress activation-induced death is not due to quenching of the activation signal, because thymocytes exposed to PTX are still capable of mobilizing Ca2+ after TCR-alpha/beta cross-linking and proliferate in response to costimulation with PTX and CD3/TCR ligation. The apoptosis-inhibitory effect of PTX depends on the presence of an intact adenosine diphosphate (ADP)-ribosylating moiety, since a mutant pertussis toxin molecule that lacks enzymatic activity, but still possesses the membrane translocating activity, fails to interfere with activation-induced cell death. A toxin that induces a different spectrum of ADP ribosylation than PTX, cholera toxin, fails to inhibit apoptosis. To suppress apoptosis, the intact PTX holotoxin must be added to cells before the lethal activation step; its addition 30 min after initial activation remains without effect on apoptosis. These data unravel a PTX sensitive signal transduction event that intervenes during an early step of activation-induced cell death of immune cells.

Apoptosis↗
PubMed1993

[The use of antibiotics in surgical prophylaxis. The characteristics and consequences].

BACKGROUND: The efficacy of antibiotic prophylaxis in certain surgical procedures has been demonstrated in clinical trials. The present study aimed at getting knowledge on the way how it is used in a certain hospital. METHODS: In a certain day, all patients receiving antibiotics to prevent a postoperative infection were identified in a medical school hospital. Information on the operative procedure, prescribed antibiotics and clinical course of the patients was recorded. RESULTS: Out of 714 patients admitted, 255 (36%) were treated with antibiotics and, of these, 85 were given them to prevent a postoperative infection. In 52% of patients, two or more antibiotics were given. The mean (SD) duration of prophylaxis was 8.4 (8.6) days. It was judged as really indicated in 34 cases (40%). Only in 17 (20%) the first choice antibiotic was selected; in 11 (13%) a preoperative dose of the right antibiotic was administered and only in 3 (3.5%) a preoperative dose of the first choice antibiotic was administered and prophylaxis lasted up to 48 hours. CONCLUSIONS: The use of antibiotics in surgical prophylaxis in a medical school hospital is inappropriate in more than 95% of cases. The situation in other centres should be quantified and the universally accepted norms of prophylaxis should be implemented.

Anti-Bacterial Agents↗
PubMed1992

Production of collagenase and tissue inhibitor of metalloproteinases by fibroblasts derived from normal and fibrotic human lungs.

Several experiments have demonstrated low collagenolytic activity during the development of pulmonary fibrosis. In order to determine if fibroblasts play a role in this alteration, procollagenase and tissue inhibitor of metalloproteinases (TIMP) were quantified in fibroblasts derived from 12 human lung specimens (normal = 6, idiopathic pulmonary fibrosis [IPF] = 6). Under basal conditions, three cell strains from normal and three from fibrotic lung specimens did not synthesize collagenase and a similar number of normal and IPF-derived fibroblast strains produced the enzyme. However, the rate of enzyme synthesis among normal and fibrotic collagenase producing fibroblasts exhibited significant differences. Thus, whereas normal fibroblasts produced more than 300 ng/ml, fibrotic lung fibroblasts secreted approximately half of this amount (115 +/- 67 ng/ml). Phorbol myristate acetate (PMA) enhanced collagenase production in all of the 12 lung fibroblast lines tested. In four IPF fibroblasts, PMA increased collagenase secretion close to those of normal stimulated lung fibroblasts; however, a lower induction was observed in cell strains from two fibrotic lung specimens. There was a wide variation in TIMP production both in normal and fibrotic lung fibroblasts, and no statistically significant difference was observed. Under basal conditions, TIMP levels ranged from 329 to 16,911 ng/ml in normal lung cells, and from 377 to 17,557 in fibrotic lung fibroblasts. PMA induced a severalfold increase in all cell lines. These results suggest that there are subpopulations of lung fibroblasts with different potential to produce collagenase and TIMP in vitro, and that the predominance of low collagenase-producing subsets may contribute to the development of fibrosis.

Adult↗