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Biomedical subjects

M Rubio

Publications and source records attributed to M Rubio.

At least 109 records · Page 6Linked to original sources
PubMed1996

NADPH-diaphorase activity and vasopressin in the paraventricular nucleus of the hypothalamus following adrenalectomy.

In order to investigate novel neuroendocrine functions of the nitric oxide synthesizing enzyme a combined histochemical and immunocytochemical study focused on the paraventricular nucleus of the hypothalamus was conducted to check a possible influence of bilateral adrenalectomy on three different neuronal populations, NADPH diaphorase (ND)-positive, vasopressin (VP)-immunoreactive and neurons expressing both markers. In the adrenalectomized animals, a slight increase (P > 0.05) of the number of ND magnocellular neurons was detected, whereas no changes were observed in the ND-parvicellular population and in the neurons showing coexistence (magno- and parvicellular) (P > 0.05). By contrast, following bilateral adrenalectomy, a significant increase (P < 0.05) in the VP-parvicellular population (anterior, medial and periventricular subdivisions) was detected, which was reversed when the animals received daily doses of corticosterone. These results suggest that nitric oxide is not closely related to the hypothalamic regulation of the adenocorticotropin secretion exerted by the paraventricular nucleus.

Adrenal Glands↗
PubMed1996

Dopamine inhibits in vitro release of VIP and proliferation of VIP-immunoreactive pituitary cells.

A double immunohistochemical study for VIP and proliferating cell nuclear antigen (PCNA) was carried out on monolayer cultures from adult male rats pituitary glands treated with dopamine (ranging from 10(-9) to 10(-5) M), in order to establish whether or not dopamine is involved in the regulation of the proliferation rate of pituitary VIP-immunoreactive cells. For all doses of dopamine assayed, the release of VIP to the culture medium, the numerical density of VIP-immunoreactive cells and the percentages of VIP- and PCNA-immunoreactive cells decreased significantly after dopamine treatment. These results suggest that dopamine could be a physiological inhibitor involved in the modulation of pituitary VIP proliferation rate.

Animals↗
PubMed1996

Effects of S-adenosylmethionine on lipid peroxidation and liver fibrogenesis in carbon tetrachloride-induced cirrhosis.

BACKGROUND/AIM: The aim of this study was to investigate the effects of S-adenosylmethionine on liver peroxidation and liver fibrogenesis in carbon tetrachloride-induced cirrhosis. METHODS: Cirrhosis was induced in three groups of six rats by repeated injections of carbon tetrachloride over 9 weeks. One group of animals was treated only with carbon tetrachloride, and the other two received carbon tetrachloride plus S-adenosylmethionine (10 mg/kg intramuscularly daily) from week 3 to week 9, and from week 6 to week 9 of the study, respectively. Two additional groups of six rats, a control group and a group treated only with S-adenosylmethionine, were also studied. Glutathione concentration, thiobarbituric acid-reactive substances, collagen content, prolyl hydroxylase activity, and procollagen type I mRNA expression were determined in liver samples. RESULTS: All carbon tetrachloride-treated rats had cirrhosis at the end of the study. Cirrhosis was also present in five of the six carbon tetrachloride-treated rats receiving S-adenosylmethionine for 3 weeks, but in only one of the six rats that received S-adenosylmethionine for 6 weeks. Hepatic glutathione was significantly diminished in carbon tetrachloride-treated rats (2.7 +/- 0.3 mumol/g tissue) and returned to normal in rats receiving S-adenosylmethionine for 3 or 6 weeks (3.7 +/- 0.13 and 3.9 +/- 0.11 mumol/g tissue, respectively). The hepatic thiobarbituric acid-reactive substances were significantly lower in rats treated with carbon tetrachloride and S-adenosylmethionine for 6 weeks (98 +/- 5 nmol/g) than in rats treated with carbon tetrachloride (134 +/- 12 nmol/g) and in those treated with carbon tetrachloride and S-adenosylmethionine for 3 weeks (127 +/- 13 nmol/g). There were no differences in either hepatic collagen and prolyl hydroxylase activity between rats that received only carbon tetrachloride and those treated with S-adenosylmethionine for 3 weeks. In contrast, carbon tetrachloride-treated rats receiving S-adenosylmethionine for 6 weeks had significantly lower collagen and prolyl hydroxylase activity than the other two groups. A much greater increase in procollagen type I mRNA was found in carbon tetrachloride-treated rats than in rats treated with carbon tetrachloride and S-adenosylmethionine for 6 weeks. Furthermore, there was a significant correlation between the hepatic thiobarbituric acid-reactive substances and prolyl hydroxylase activity and hepatic collagen. CONCLUSIONS: We conclude that the early administration of S-adenosylmethionine in a model of carbon tetrachloride-induced liver injury restores glutathione levels and reduces lipid peroxidation, resulting in less advanced liver fibrosis.

Animals↗
PubMed1996

Pharmacokinetics of Dextran-70 in patients with cirrhosis and ascites undergoing therapeutic paracentesis.

BACKGROUND/AIM: Dextran-70 is frequently used as a plasma expander in patients with cirrhosis treated with large-volume paracentesis to prevent post-paracentesis hypovolemia, which is thought to develop after 24 h following the procedure. However, there are no studies on Dextran-70 pharmacokinetics in cirrhosis. METHODS: Nine patients with alcoholic cirrhosis and tense ascites treated with a 5-1 paracentesis were given 500 ml of Dextran-70. Blood samples to measure the plasma concentration of dextran were obtained 15 and 30 min, 1, 2, 3, 6, 12 and 24 h and 2 and 6 days after the end of the infusion. Nine healthy volunteers were studied in identical fashion after infusion of 100 ml of Dextran-70. The plasma concentration of dextran was determined by the anthrone method. A bicompartmental model was used to analyze the pharmacokinetic parameters. RESULTS: There were no significant differences between patients with cirrhosis and controls in the volume of distribution (7.7 +/- 0.6 vs. 7.3 +/- 1.21), half-life of the first and second component of plasma disappearance (2.96 +/- 0.69 and 80.3 5.9 h in patients with cirrhosis vs 2.82 +/- 0.69 and 67.1 +/- 10.7 h in controls). CONCLUSIONS: The pharmacokinetics of Dextran-70 in patients with cirrhosis and ascites after large-volume paracentesis is similar to that in controls. This may explain why Dextran-70 is less effective than albumin in preventing paracentesis-induced hypovolemia, which starts after most Dextran fraction has disappeared from plasma.

Ascites↗
PubMed1996

Nosocomial outbreak of Burkholderia pickettii infection due to a manufactured intravenous product used in three hospitals.

Forty-six cases of nosocomial infection caused by Burkholderia pickettii were reported between June and November 1993 in three metropolitan hospitals in Madrid. A case-control study of the outbreak was conducted to identify its cause. Seventy-four percent of the patients were males; the mean age +/- SD of the patients was 54 +/- 20 years. Sixty-five percent of the patients presented with some gastrointestinal disorder, and 80% had a peripheral catheter; 98% were treated with intravenous fluids, and 96% were treated with intravenous ranitidine. On the basis of results of a descriptive study and knowledge of the epidemiologic features of B. pickettii, a provisional causal hypothesis was formulated: intravenous ranitidine was the source of the outbreak. As a control measure, it was advised to stop treatment with this drug. On the basis of results of logistic regression and the microbiological isolation of B. pickettii in an ampule of the drug, we concluded that intravenous ranitidine was the cause of the outbreak.

Adult↗
PubMed1996

A study of Light's criteria and possible modifications for distinguishing exudative from transudative pleural effusions.

STUDY OBJECTIVE: To determine the usefulness of modifying Light's criteria for the separation of pleural transudates from exudates. DESIGN: Retrospective review of patients who underwent a diagnostic thoracentesis during a 2-year period. SETTING: Community teaching hospital in Lleida, Spain. PATIENTS AND METHODS: Clinical records and pleural fluid characteristics of 230 consecutive patients with pleural effusion underwent a detailed review. Thirty-five of these patients were excluded from the analysis. As suggested recently by Romero et al, different cutoff levels for the criteria of Light et al were applied and their accuracies were calculated. RESULTS: Thirty-nine (20%) pleural effusions were transudates and 156 (80%) were exudates. The accuracy of the criteria of Light et al for identifying exudates was 94.7% (confidence interval, 91.6 to 97.9) in comparison to our own modified criteria (93.1%; confidence interval, 89.5 to 96.7) and the criteria suggested by Romero et al (92.6%; confidence interval, 88.9 to 96.3). These differences were not statistically significant. CONCLUSION: Changing the classic Light's criteria with different cutoff points offers no advantages for discriminating between transudative and exudative pleural effusions.

Adolescent↗
PubMed1996

Morphometric evidence of the regulation of the activity of LH-immunoreactive cells by corticosterone. An in vivo and in vitro study.

The present study was performed to investigate the morphometric effects of the administration of corticosterone on LH-immunoreactive cells of pituitary monolayer cultures. In addition, the effect of bilateral adrenalectomy on the LH-adenohypophyseal cells was explored. In vitro administration of corticosterone induced a marked decrease in the morphometric parameters considered (cellular, cytoplasmic and nuclear areas). In vivo, bilateral adrenalectomy produced a significant increase in these parameters when compared to those obtained in normal and sham-operated animals. However, when the bilaterally adrenalectomized rats received a daily dose of corticosterone no significant changes in the morphometric parameters were found. Morphometrically, these combined in vivo-in vitro findings confirm a corticosterone-induced hypoactivity of LH-cells together with a direct effect of this glucocorticoid on LH-adenohypophyseal cells.

Adrenalectomy↗
PubMed1995

Soluble CD23 directly activates monocytes to contribute to the antigen-independent stimulation of resting T cells.

The majority of T cells at the site of an inflammatory lesion do not appear to be Ag-specific, but they still contribute to the inflammatory response. Herein, we report that sCD23 activates monocytes to participate in the stimulation of resting T cells in the absence of TCR engagement. First, sCD23 selectively triggers monokine release by purified monocytes in the absence of costimulus. It induces TNF-alpha, IL-1 beta, IL-8, granulocyte-macrophage-CSF, and prostaglandin E2 but no IL-10, IL-12, TGF-beta, or leukotriene B4. The sCD23-induced TNF-alpha production is significantly inhibited by IL-4 and IL-10 but not by TGF-beta. Also, monocytes activated by sCD23 express decreased levels of HLA-DR and increased levels of CD14, CD54, CD40, and B7 Ag. Next, we show that, in the presence of monocytes, sCD23 is a potent costimulator of IL-2 or IL-12-induced IFN-gamma production by resting T cells in the absence of exogenous Ag and that this effect is partially reduced by anti-TNF-alpha mAb. B cells cannot substitute for monocytes, and CD4+ and CD8+ T cells are equal responders. The data further indicate that monocyte-T cell contact, more particularly CD40-CD40L interactions, is required for IFN-gamma production in response to IL-2 plus sCD23, and the response to IL-12 plus sCD23 is CD40- and B7-independent but is still partially contact-dependent. It is proposed that sCD23, when produced locally at a site of immune response, may trigger an inflammatory process via monokine release and may further amplify it via the stimulation of bystander non-Ag-specific T cells.

Cells, Cultured↗
PubMed1995

Calbindin D-28k and parvalbumin expression in mitotic cells of rat primary cortical cultures.

Calbindin D-28k and parvalbumin expression was studied immunocytochemically in monolayer mixed cortical cultures from rats aged 16 (E16), 17 (E17), and 19 (E19) days of gestation using monoclonal antibodies and the avidin-biotin immunoperoxidase method. Whereas in vivo both calcium-binding proteins are exclusively expressed in postmitotic neuronal populations, they were demonstrated in mitotic cultured cells at the three fetal ages and the three maturation times considered (6, 12, and 15 days). A subpopulation of immunostained mitotic cells was identified as astroglial cells after a double labelling study using an antibody against glial fibrillary acidic protein. These results suggest that conditions in vitro may induce the expression of calbindin D-28 and parvalbumin in mitotic cells.

Animals↗
PubMed1995

Type II cytokeratin expression in adult vertebrate spinal cord.

The phylogenetic evolution of the expression of type II cytokeratins (CKs) in the spinal cord of different adult vertebrates has been studied using an anti-CK immunohistochemical technique. Type II CK expression was stronger in lower vertebrates, specially anuran amphibians, than in higher vertebrates. No CK expression was found either in reptiles or birds, but a weak expression was demonstrated in mammals. The main neuroectodermal cell implicated in CK expression was the ependymocyte; some CK-positive radial astrocytes were also found in amphibians and fish, but neither CK-positive astrocytes nor neurons were observed in any vertebrate group. The functional significance of CK expression in the vertebrate spinal cord is not known. CKs do not have a consistent pattern of expression amongst vertebrates; however, the most common site is the ependyma.

Animals↗
PubMed1995

Adrenalectomy increases the glial fibrillary acidic immunoreactive-elements in the ventricular ependyma and adjacent neuropil of the rat third ventricle.

The reactions of bilateral adrenalectomy (14 days) on the rat glial fibrillary acidic-immunoreactive elements of the third ventricular ependyma and adjacent neuropil were analyzed using histological, immunohistochemical and morphometric methods. Bilateral adrenalectomy led to a drastic increase in the number of immunoreactive elements located in the neuropil adjacent to the third ventricle and the optic chiasm when compared to normal and sham-operated animals (p < 0.05). By contrast, the adrenalectomized animals receiving corticosterone showed the same characteristics and morphometric values as those found in normal and sham-operated animals. The results show that the participation of the adrenal gland in astroglial responses should be taken into account.

Adrenalectomy↗
PubMed1995

Regulation of expression of the LFA-1 and p150,95 leukocyte integrins: involvement of the CD11a and CD11c gene promoters.

Human Lymphocyte Associated Antigen-1 (LFA-1, CD11a/CD18, alpha L/beta 2) and p150,95 (CD11c/CD18, alpha X/beta 2) are cell surface alpha/beta heterodimers that, together with Mac-1 (CD11b/CD18, alpha M/beta 2) comprise the leukocyte-restricted beta 2 subfamily of integrins. LFA-1 is the only integrin expressed on all leukocyte lineages while p150,95 is exclusively expressed on cells of the myeloid lineage and on activated B lymphocytes and natural killer cells. The expression of the leukocyte integrins is regulated during cell activation and differentiation by transcriptional mechanisms. To dissect the molecular basis for the tissue-restricted and developmentally regulated expression of LFA-1 and p150,95, the promoter regions of their corresponding alpha subunits (CD11a and CD11c) were isolated and functionally characterized. Both promoters lack TATA and CAAT boxes, but exhibit initiator-like sequences at their major transcriptional start sites. Transient expression of CD11a- and CD11c-based reporter gene constructs have demonstrated the involvement of both promoters in the tissue-specific expression of LFA-1 and p150,95. Furthermore, a combination of DNAse I protection experiments and mobility band shift assays have revealed the existence of numerous DNA-protein interactions at the proximal region of both promoters, some of which overlap with consensus binding sequences for known transcription factors and correlate with the pattern of expression of both integrins.

Base Sequence↗
PubMed1995

Mortality associated with nosocomial bacteremia due to methicillin-resistant Staphylococcus aureus.

We prospectively studied all cases of Staphylococcus aureus bacteremia that occurred during an extensive outbreak of methicillin-resistant S. aureus (MRSA) in our hospital over a 4-year period (January 1990 through September 1993). We report the results of a comparative analysis of the clinical characteristics and mortality rates among patients with nosocomial bacteremia caused by MRSA (84 cases) or methicillin-susceptible S. aureus (MSSA; 100 cases). The patients with MRSA bacteremia were older than those with MSSA bacteremia (69 years vs. 54 years, respectively; P < .01) and were more likely than those with MSSA bacteremia to have the following predisposing factors: a prolonged hospitalization (32 days vs. 14 days, respectively; P < .01); prior antimicrobial therapy (61% vs. 34%, respectively; P < .01); urinary catheterization (58% vs. 27%, respectively; P < .01); nasogastric tube placement (31% vs. 13%, respectively; P < .01); and prior surgery (45% vs. 31%, respectively; P = .05). Multivariate analysis with use of the stepwise logistic regression method showed a relationship between mortality and the following variables: methicillin resistance (odds ratio [OR], 3), meningitis (OR, 13), and inadequate treatment (OR, 11).

Aged↗
PubMed1995

The two CD23 isoforms display differential regulation in chronic lymphocytic leukaemia.

B lymphocytes from chronic lymphocytic leukaemia (B-CLL) patients express the two CD23 isoforms (type A and B), which differ only in their intracytoplasmic domain. The abnormal regulation of the CD23 antigen in response to IL-4, IFNs alpha and gamma results in CD23 over-expression on B-CLL cells. Our present study shows that the two CD23 isoforms are differentially and abnormally regulated on B-CLL cells. IL-4 selectively up-regulates CD23 type A mRNA in five different B-CLL patients, whereas in normal B cells it enhances CD23 type A and is the most potent inducer of type B. In contrast, phorbol esters (PMA) up-regulate both CD23 isoforms in the malignant B cells and specifically increases type B in normal B cells. We next postulated that cytokines other than IL-4 regulate CD23 B isoform in B-CLL cells and therefore examined the effect of IL-2, IFN-gamma and IFN-alpha. We found that the ability of a given cytokine to induce B-CLL growth (i.e. IL-2 and IFN alpha) is concurrent with a selective up-regulation of CD23 type B mRNA, whereas lymphokines that have no B cell growth activity (i.e. IL-4 and IFN-gamma) specifically increase CD23 type A mRNA. We next showed that IL-4 and IFN gamma prevent hydrocortisone-induced programmed cell death and that the rescued malignant B cells mainly express CD23 type A. Given that CD23 molecule has been reported to play a role in normal B cell proliferation and survival, it is therefore proposed that in B-CLL cells the expression of CD23 type A may be related to cell viability and that of type B to cell proliferation. These data suggest that the CD23 molecule may contribute to the physiopathology of the disease which is characterized by the accumulation of long-lived and slow-dividing monoclonal B cells.

Adult↗
PubMed1995

In vitro morphometric and proliferative variations in VIP-immunoreactive pituitary cells induced by estradiol.

Using double labelling for proliferating cell nuclear antigen (PCNA) and vasoactive intestinal peptide (VIP), a study was conducted to elucidate the repercussions of the addition of estradiol to monolayer pituitary cultures on the morphology, size, number, mitotic index and PCNA labelling index of VIP-immunoreactive cells, comparing the results with those obtained in control cultures. The addition of estradiol (100 nM) over 3 h of incubation led to a significant increase (p < 0.01) in the cellular, cytoplasmic and nuclear areas of VIP-immunoreactive cells and in the number of these cells. The same treatment elicited an even greater increase in the mitotic index (p < 0.01) and PCNA labelling index (p < 0.01) of VIP-immunoreactive cells. The results obtained suggest that estrogens induce proliferation and hyperplasia of in vitro VIP-immunoreactive pituitary cells.

Animals↗