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Biomedical subjects

M A Arias

Publications and source records attributed to M A Arias.

8 recordsLinked to original sources
PubMed2006

[Determining cardiac output by carbon dioxide rebreathing in patients with sleep apnea-hypopnea syndrome].

The objective of the present study was to determine the relation between resting cardiac output in patients with sleep apnea-hypopnea syndrome but without arterial hypertension or heart failure as measured indirectly by the carbon dioxide rebreathing method and left ventricular function evaluated by transthoracic echocardiography. We also compared the variability and reproducibility of the measurements obtained by the equilibrium and exponential methods. In patients with sleep apnea-hypopnea syndrome there was a modest but significant association between resting cardiac output and left ventricular shortening fraction (r=0.690; P<.001) and left ventricular ejection fraction (r=0.690; P<.001). In addition, mean (SD) cardiac output obtained by the equilibrium method showed a lower coefficient of variability (0.21 [0.08]) than that of the exponential method (0.16 [0.09]) (P<.01) as well as a narrower reproducibility interval.

Carbon Dioxide↗
PubMed2000

Cutting edge: human B cell function is regulated by interaction with soluble CD14: opposite effects on IgG1 and IgE production.

The mechanism(s) controlling activation of naive B cells, their proliferation, Ag receptor affinity maturation, isotype switching, and their fate as memory or plasma cells is not fully elucidated. Here we show that between 24 and 60% of CD19+ cells in PBMC bind soluble CD14 (sCD14). Tonsillar B cells also bind sCD14, but preferentially the CD38-ve/low cells. Interaction of sCD14 with B cells resulted in higher levels of IgG1 and marked inhibition of IgE production by activated tonsillar B cells and Ag-stimulated PBMC. We found that sCD14 interfered with CD40 signaling in B cells, inhibited IL-6 production by activated B cells, and increased the kinetics and magnitude of CD40 ligand expression on T cells. Together with the previously reported effects on T cells, these findings define sCD14 as a novel soluble regulatory factor capable of modulating cellular and humoral immune responses by interacting directly with T and B cells.

B-Lymphocyte Subsets↗
PubMed2000

The effect of melatonin in patients with fibromyalgia: a pilot study.

The aim of the study was to determine the possible effect of melatonin treatment on disturbed sleep, fatigue and pain symptoms observed in fibromyalgia (FM) patients. Twenty-one consecutive patients with FM were included in an open 4-week-duration pilot study. Before and after treatment with melatonin 3 mg at bedtime, patients were evaluated using tender point count by palpation of 18 classic anatomical regions, pain score in four predesignated areas, pain severity on a 10 cm visual analogue scale (VAS), sleep disturbances, fatigue, depression, anxiety, and patient and physician global assessments, also by a VAS. Urine 6-sulphatoxymelatonin levels (aMT-6S) were measured in the patients and 20 age- and sex-matched controls. Nineteen patients completed the study. One patient withdrew because of migraine and another was lost to follow-up. At day 30, median values for the tender point count and severity of pain at selected points, patient and physician global assessments and VAS for sleep significantly improved with melatonin treatment. Other variables improved but did not reach statistical significance. Adverse events were mild and transient. Lower levels of aMT-6S were found in FM patients compared with normal median controls (+/-SD, 9.16 +/- 7.9 microg/24 h vs 16.8 +/- 12.8 microg/24 h) (p = 0.06). Although this is an open study, our preliminary results suggest that melatonin can be an alternative and safe treatment for patients with FM. Double-blind placebo controlled studies are needed.

Administration, Oral↗
PubMed1999

Soluble CD14 acts as a negative regulator of human T cell activation and function.

T cell activation is controlled by the coordination of stimulatory and negative regulatory signals which are not completely defined. In this study we tested for a possible direct effect of CD14 on the regulation of T cell activation and function. We show that soluble CD14 (sCD14) induces inhibition of antigen-mediated peripheral blood mononuclear cells (PBMC) proliferation and anti-CD3-mediated proliferation of CD4+CD8+, CD4+CD8+ and CD4+CD8+ Tcell clones. This effect is not due to cell death, but results from a marked inhibition of IL-2 production. Proliferation of T cell clones due to exogenous IL-2 is not affected by sCD14. We also found that sCD14 inhibits production of another Th1-like cytokine, IFN-gamma and a Th2-like cytokine, IL-4. Importantly, sCD14 induces a progressive accumulation of the inhibitory protein IkappaB-alpha. We show that sCD14 binds to activated T cells. Following cell activation, biotinylated sCD14 stains CD3+ PBMC, as well as human T cell clones with varying intensity. The binding is saturable, can be inhibited by excess of unlabeled sCD14 and, following binding, sCD14 is internalized. Collectively, these findings reveal a previously unrecognized function of sCD14, namely its capacity to negatively regulate T lymphocyte activation and function by interacting directly with activated T cells.

Biological Transport, Active↗
PubMed1998

Aeromonas hydrophila associated with a severe outbreak of infection in farmed rabbits.

An outbreak of infection with a high rate of mortality has been detected in an industrial rabbitry in Spain. Aeromonas hydrophila was isolated in pure culture from liver, lung, heart and spleen of ill and moribund animals. All the isolates belonged to O:11 serogroup, autogglutinated after boiling, were resistant to the bactericidal action of the fresh rabbit serum and did not agglutinate in acriflavine. They were producers of hemolysins and proteases but were not enterotoxigenic.

Aeromonas hydrophila↗
PubMed1982

Mice with the xid defect have helper cells for T15 idiotype-dominant anti-phosphorylcholine primary and secondary plaque-forming cells responses.

We have examined the abilities of helper T cells from commercially available (CBA/N X BALB/c)F1 (NBF1) xid male and phenotypically normal female mice to help T15+ and T15- B cells to produce thymus-dependent phosphorylcholine (PC)-specific direct plaque-forming cell responses. Carrier-primed T cells from both male and female mice were found (a) to restore T15+ TD responses in congenitally athymic BALB/c mice, (b) to help PC-primed BALB/c splenic B cells produce predominantly T15+ responses, and (c) to provide help for T15+ and T15- PFC responses generated by PC-primed normal F1 splenic B cells. Furthermore, carrier-primed irradiated xid and normal recipients contributed adequate helper activity for T15 dominant responses. We therefore conclude that male and female NBF1 mice are equally capable of helping T15+ responses.

Animals↗