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Biomedical subjects

Miguel Muñoz

Publications and source records attributed to Miguel Muñoz.

8 recordsLinked to original sources
PubMed2006

Thin-layer boilover in diesel-oil fires: Determining the increase of thermal hazards and safety distances.

A study of the effects of thin-layer boilover on large hydrocarbon fires was carried out. In the experiments, diesel-oil was burned in pools with diameters ranging from 1.5 to 6m. Previous models used to predict emissive power during the stationary state were analysed and successively modified in order to accurately predict thermal hazard during the water ebullition phase. It was discovered that the increase in emissive power during thin-layer boilover is greater when the pool diameter is smaller. Furthermore, the required increases in safety distances in the case of accidents involving this dangerous phenomenon are provided.

Fires↗
PubMed2006

Experimental study of thin-layer boilover in large-scale pool fires.

By performing a series of pool fire experiments, the authors attempt to apply knowledge of thin-layer boilover to the large scale (pool diameter from 1.5 to 6 m). Two commercial hydrocarbons were used: gasoline and diesel. As expected, only in the case of diesel did the phenomenon of thin-layer boilover occur. Data were used to analyze various features of thin-layer boilover in fires, particularly its intensity and onset time. A comparison with results published in the literature shows the importance of this study.

Fires↗
PubMed2005

Consequences of major accidents: assessing the number of injured people.

Quantitative risk assessment studies of accident scenarios usually involve estimating the number of fatalities that can be expected. The number of people injured, however, is seldom evaluated because it implies significant additional effort and often the information required to perform this evaluation is not available. However, the number of injured people can be very important for emergency planning, especially in relatively large accidents. In this paper, a set of 975 accidents were selected for analysis, with the aim of searching for a relationship between the number of people killed and the number of people injured. As the data were scattered, principal component analysis and clustering analysis were applied to identify the data subsets that could undergo a selective, specific statistical treatment. Further treatment of these subsets led to mathematical expressions that are used to estimate the probable number of injured people as a function of the number of fatalities for all accidents, as well as for gas cloud, fire and explosion events, respectively.

Accidents↗
PubMed2005

Antitumoral action of the neurokinin-1-receptor antagonist L-733,060 and mitogenic action of substance P on human retinoblastoma cell lines.

PURPOSE: Activation of the neurokinin-1 receptor is known to induce proliferation in tumor cells, but it is as yet unknown whether this applies to retinoblastoma. This was an in vitro study of the growth inhibitory capacity of the potent and long-acting neurokinin-1 receptor antagonist L-733,060, at concentrations ranging from 7.5 to 20 microM, against the human retinoblastoma line WERI-Rb-1 and from 10 to 25 microM against the human retinoblastoma line Y-79. The ability of substance P (an neurokinin-1 stimulator) to activate the cell growth of these retinoblastoma cell lines was also determined. METHODS: A cell counter was used to determine the number of viable cells, followed by application of the tetrazolium compound WST-8 [2-(2-methoxy-4-nitrophenyl)-3-(4 nitrophenyl))-5-(2,4-disulfophenyl)-2H-tetrazolium, monosodium salt, colorimetric method to evaluate cell viability in this cytotoxicity assay. RESULTS: Nanomolar concentrations of substance P increased the growth of both cell lines and micromolar concentrations of L-733,060 inhibited the growth of the two cell lines studied, with and without previous administration of substance P. L-733,060 inhibited the growth of the WERI-Rb-1 and Y-79 cell lines in a dose-dependent manner. IC50 was 12.15 microM for 49 hours for WERI-Rb1 and 17.38 microM for 40 hours for Y-79. CONCLUSIONS: The findings demonstrate that substance P is a mitogen and also indicate that the neurokinin-1 receptor antagonist L-733,060 acts on both human retinoblastoma cell lines as an antitumoral agent.

Antineoplastic Agents↗
PubMed2004

Antitumoral action of the neurokinin-1 receptor antagonist L-733 060 on human melanoma cell lines.

Melanoma represents 1% of all cancers and accounts for approximately 65% of skin cancer deaths. At present, effective treatment does not exist. Substance P (SP) is a neuropeptide expressed in invasive malignant melanomas. We studied the in vitro growth inhibitory capacity of the potent and long-acting neurokinin-1 (NK1) receptor antagonist L-733 060 at concentration ranges of 2.5-20 microM, 10-30 microM and 20-50 microM in the melanoma cell lines COLO 858, MEL H0 and COLO 679, respectively. A Coulter counter was used to determine the number of viable cells, and the tetrazolium compound 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)2-(4-sulphophenyl)-2H-tetrazolium, inner salt (MTS) colorimetric method was used to evaluate cell proliferation. L-733 060 inhibited the growth of all three cell lines in a dose-dependent manner. The 50% inhibition concentration (IC(50)) was 8.7 microM at 48 h and 7.1 microM at 96 h for COLO 858, 27.5 microM at 24 h and 18.9 microM at 48 h for MEL H0, and 33.8 microM at 30 h and 31.5 microM at 72 h for COLO 679. These findings indicate that the NK1 receptor antagonist L-733 060 acts as an antitumoral agent. This action, shown here for the first time, suggests that the NK1 receptor antagonist L-733 060 could be a promising therapeutic drug in the treatment of the human melanoma.

Antineoplastic Agents↗
PubMed2004

Entry and transcription as key determinants of differences in CD4 T-cell permissiveness to human immunodeficiency virus type 1 infection.

Isolated primary human cells from different donors vary in their permissiveness-the ability of cells to be infected and sustain the replication of human immunodeficiency virus type 1 (HIV-1). We used replicating HIV-1 and single-cycle lentivirus vectors in a population approach to identify polymorphic steps during viral replication. We found that phytohemagglutinin-stimulated CD4(+) CD45RO(+) CD57(-) T cells from healthy blood donors (n = 128) exhibited a 5.2-log-unit range in virus production. For 20 selected donors representing the spectrum of CD4 T-cell permissiveness, we could attribute up to 42% of the total variance in virus production to entry factors and 48% to postentry steps. Efficacy at key intracellular steps of the replicative cycle (reverse transcription, integration, transcription and splicing, translation, and budding and release) varied from 0.71 to 1.45 log units among donors. However, interindividual differences in transcription efficiency alone accounted for 64 to 83% of the total variance in virus production that was attributable to postentry factors. While vesicular stomatitis virus G protein-mediated fusion was more efficacious than CCR5/CD4 entry, the latter resulted in greater transcriptional activity per proviral copy. The phenotype of provirus transcription was stable over time, indicating that it represents a genetic trait.

Biological Transport↗
PubMed2003

Protection from HIV-1 infection of primary CD4 T cells by CCR5 silencing is effective for the full spectrum of CCR5 expression.

Stable gene silencing by RNA interference (RNAi) can be achieved by expression of small hairpin RNAs (shRNAs) from RNA polymerase III promoters. We have tested lentiviral vectors expressing shRNAs targetting CCR5 in primary CD4 T cells from donors representing various CCR5 and CCR2 genetic backgrounds covering the full spectrum of CCR5 expression levels and permissiveness for HIV-1 infection. A linear decrease in CCR5 expression resulted in a logarithmic decrease in cellular infection, giving up to three logs protection from HIV-1 infection in vitro. Protection was maintained at very high multiplicity of infection. This and other recent reports on RNAi should open a debate about the use of RNAi gene therapy for HIV infection.

CD4-Positive T-Lymphocytes↗