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M Villanueva

Publications and source records attributed to M Villanueva.

17 recordsLinked to original sources
PubMed2001

Use of comparative physical and sequence mapping to annotate mouse chromosome 16 and human chromosome 21.

Distal mouse chromosome 16 (MMU16) shares conserved linkage with human chromosome 21 (HSA21), trisomy for which causes Down syndrome (DS). A 4.5-Mb physical map extending from Cbr1 to Tmprss2 on MMU16 provides a minimal tiling path of P1 artificial chromosomes (PACs) for comparative mapping and genomic sequencing. Thirty-four expressed sequences were positioned on the mouse map, including 19 that were not physically mapped previously. This region of the mouse:human comparative map shows a high degree of evolutionary conservation of gene order and content, which differs only by insertion of one gene (in mouse) and a small inversion involving two adjacent genes. "Low-pass" (2.2x) mouse sequence from a portion of the contig was ordered and oriented along 510 kb of finished HSA21 sequence. In combination with 68 kb of unique PAC end sequence, the comparison provided confirmation of genes predicted by comparative mapping, indicated gene predictions that are likely to be incorrect, and identified three candidate genes in mouse and human that were not observed in the initial HSA21 sequence annotation. This comparative map and sequence derived from it are powerful tools for identifying genes and regulatory regions, information that will in turn provide insights into the genetic mechanisms by which trisomy 21 results in DS.

Animals↗
PubMed1999

Perfect conserved linkage across the entire mouse chromosome 10 region homologous to human chromosome 21.

The distal end of human Chromosome (HSA) 21 from PDXK to the telomere shows perfect conserved linkage with mouse Chromosome (MMU) 10. This region is bounded on the proximal side by a segment of homology to HSA22q11.2, and on the distal side by a region of homology with HSA19p13.1. A high-resolution PAC-based physical map is described that spans 2.8 Mb, including the entire 2.1 Mb from Pdxk to Prmt2 corresponding to HSA21. Thirty-four expressed sequences are mapped, three of which were not mapped previously in any species and nine more that are mapped in mouse for the first time. These genes confirm and extend the conserved linkage between MMU10 and HSA21. The ordered PACs and dense STS map provide a clone resource for biological experiments, for rapid and accurate mapping, and for genomic sequencing. The new genes identified here may be involved in Down syndrome (DS) or in several genetic diseases that map to this conserved region of HSA21.

Animals↗
PubMed1996

[Truth disclosure to patients diagnosed with cancer].

OBJECTIVE: To find the sort of information given to cancer patients in PC and the factors which affect the disclosure of the diagnosis. DESIGN: A descriptive crossover study, carried out through a personal interview. SETTING: A county hospital with no oncology service. PATIENTS: All those patients with cancer (histologically confirmed) admitted to the hospital during April and May 1993. MEASUREMENTS AND MAIN RESULTS: Each patient was asked what illness he/she had, who told him/her and where, along with his/her sociodemographic details. Later the date of diagnosis and the site and spread of the tumour were taken from the medical records. Out of 108 patients under study, 8 knew they had cancer, 1 said he/she had a tumour and 11 believed they had "something bad". 7 patients had no information about their illness and 81 gave alternative diagnoses (inflammation, cyst...). Disclosure was more common in the cases of breast cancer, haematological cancer and those diagnosed over 6 months previously. No significant differences regarding the spread of the tumour or the sociodemographic variables were found. CONCLUSIONS: The disclosure of a diagnosis of cancer is the exception, not the rule. Concealment is only abandoned in the case of potentially curable tumours and those which offer a longer life expectancy.

Aged↗
PubMed1993

Muscle carnitine deficiency and lipid storage myopathy in patients with mitochondrial myopathy.

Abnormal carnitine distribution in muscle was found in 22 of 77 patients (29%), with mitochondrial myopathy. Furthermore, total (TC) and free (FC) carnitine levels in muscle were lower in patients than in controls (P < 0.01). Muscle long-chain acylcarnitines (LCAC) were significantly increased in these patients (P < 0.01). Muscle carnitine deficiency was found in 31.5% of patients with lipid storage myopathy (LSM) and in 25.6% of patients with ragged-red fibers (RRF). Therefore, carnitine deficiency can be found in patients with mitochondrial myopathy even in the absence of LSM. Muscle levels of TC and FC were lower in patients with respiratory chain defects than in those with normal respiratory chain (P < 0.01). In contrast, LCAC levels were significantly increased (P < 0.05). Carnitine levels did not differ significantly, among patients with different respiratory-chain defects. Consequently, these patients, owing to their biochemical block, reduce progressively the muscle carnitine pool and subsequent LCAC rise, due to long-chain fatty acid (LCFA) accumulation.

Adolescent↗
PubMed1993

Biological monitoring of occupational exposure to n-hexane by exhaled air analysis and urinalysis.

To compare two methods of biological monitoring for the evaluation of risk of occupational exposure to n-hexane, we analyze the relationship between environmental exposure to this solvent and urinary excretion of 2,5-hexanedione and n-hexane in exhaled air in 69 workers employed in the shoe industry. Environmental exposure to the solvent was monitored with personal diffusive samplers, which were desorbed with carbon sulfide and analyzed by gas chromatography. To measure 2,5-hexanedione, urine was subjected to acid hydrolysis, separation in octadecyl silane columns, elution with 5% aqueous acetonitrile solution and extraction with dichloromethane, followed by gas chromatography. In exhaled air, n-hexane was measured with a sampling system that permitted concentration of aliquots of end-exhaled air (alveolar air) from one or more exhalations in a tube packed with activated charcoal, which was then desorbed with carbon sulfide and analyzed by gas chromatography. Concentrations of n-hexane in breathing zone air were significantly correlated with urinary concentrations of 2,5-hexanedione (r = 0.88) and with exhaled air n-hexane (r = 0.86); in addition, the two biological indicators correlated significantly (r = 0.70). Analyses in both exhaled air and urine were thus considered useful for biological monitoring of the risk of exposure to n-hexane.

Adhesives↗
PubMed1993

Equipotent inhibition by R(-)-, S(+)- and racemic ibuprofen of human polymorphonuclear cell function in vitro.

1. The effects of racemic (rac) ibuprofen and its S(+)- and R(-)-enantiomers on functions of human polymorphonuclear cells (PMN) and platelets were studied in vitro. 2. Rac-ibuprofen inhibited PMN functions (O2- generation, beta-glucuronidase release, LTB4 formation). Similar IC50 values (40-100 microM) were obtained for the S(+)- and R(-)-enantiomers. 3. All forms of ibuprofen inhibited cyclooxygenase-related platelet functions (aggregation, thromboxane formation). The S(+)-enantiomer was about twice as active as the racemate while the R(-)-enantiomer was at least 10-fold less active. This demonstrates that the S(+) is the only cyclooxygenase inhibitory component of the racemate. 4. The concentrations of rac-ibuprofen in PMN and platelets were similar to those in the incubation medium and represented equal concentrations of the enantiomers. This indicates that neither interconversion nor tissue accumulation of the compounds occurred. 5. These data indicate that antineutrophil effects of ibuprofen on human PMN are independent of cyclooxygenase inhibition. Therefore, R(-)-ibuprofen may be superior to the S(+)-isomer for the treatment of PMN-dependent inflammatory diseases. However, effective free drug concentrations may not be obtained in vivo.

Blood Platelets↗
PubMed1992

Stereospecific and non-stereospecific effects of ibuprofen on human platelet and polymorphonuclear leukocyte functions.

This study compares biological activities of racemic ibuprofen (rac-IBU) and its S(+) and R(-) enantiomeres in human platelet and polymorphonuclear cells (PMN). Rac-IBU inhibited cyclooxygenase-related platelet functions (aggregation, thromboxane (TX) B2 formation) in vitro, the S-(+) enantiomer being 40-100-times more active than the R-(-) form. rac-IBU also inhibited PMN functions (O2- generation, beta-glucuronidase release). These effects in PMN were not stereospecific. The data suggest cyclooxygenase-independent actions of ibuprofen in human PMN which may contribute to its antiinflammatory effects in vivo.

Blood Platelets↗
PubMed1989

Action of methylene blue and haemoglobin in rabbit aorta in relation to the surface of drug entry.

The effect of methylene blue and haemoglobin has been evaluated by using a procedure of restricting drug entry to one surface of rabbit aortic rings. In preparations precontracted with noradrenaline, methylene blue and haemoglobin produced, via the intima, an additional rapid and endothelium-dependent contraction. While haemoglobin was without effect via the adventitia, methylene blue produced a slow endothelium-independent contraction that was diminished but not abolished in reserpine-pretreated animals. This augmentation of the noradrenaline-induced contraction produced by methylene blue via the adventitia in reserpine-pretreated rabbits was observed also with phenylephrine but not with methoxamine. Methylene blue, when added to aortic rings incubated with 3H-(-)-noradrenaline, interfered with the neuronal uptake of this amine and enhanced the outflow of 3H. In conclusion, methylene blue and haemoglobin enhanced noradrenaline-induced contraction by an endothelium-dependent mechanism when applied via the intima. Haemoglobin is devoid of effects via the adventitia but methylene blue has indirect sympathomimetic effects. In experiments using intact rings with no restriction to drug entry it was found that the enhancement by haemoglobin of the tyramine-induced response was markedly less than that observed for noradrenaline for the same level of plateau contraction. This finding indicates that the endothelium-derived relaxing factor is more effective on smooth muscle cell layers in the vicinity of intima than on those close to adventitia.

Animals↗
PubMed1987

Corynebacterium pyogenes mastitis outbreak in inbred heifers in a California dairy.

An outbreak of Corynebacterium pyogenes mastitis ("Summer Mastitis") was observed in a group of 96 heifers. The outbreak affected 8 animals, of which 7 were too young for breeding. The disease incidence was highest in calves 2 to 4 months old. Cases were observed over an initial estimated 14 day period with a further case being detected 14 days subsequently. Corynebacterium pyogenes mastitis has not been reported in calves this age. Factors postulated to influence the outbreak include the presence of large numbers of flies, intersucking of calves, and possible viral disease.

Animals↗
PubMedDate not supplied

Correlation between concentrations of n-hexane and toluene in exhaled and environmental air in an occupationally exposed population.

We determined the correlations between the concentrations of n-hexane and toluene in exhaled and environmental air in the shoe manufacturing industry. Data were collected in 1988 and in 1992 from a total of 265 subjects. Environmental air samples were collected with personal diffusive samplers by adsorption on activated charcoal during exposure and from end-expired air (alveolar air) on cartridges of activated charcoal after exposure. Both compounds were desorbed with carbon disulphide and analysed by gas chromatography. Linear regression analyses showed a good correlation between environmental and end-expired air concentrations (r = 0.82 for n-hexane and r = 0.81 for toluene). These correlations allowed us to calculate the concentrations in expired air corresponding to current environmental limit values. The calculated concentrations in end-expired air that correspond to current environmental threshold limit values of 176 mg m-3 for n-hexane and 377 mg m-3 for toluene are 28 mg m-3 (95% confidence limit, 27-29 mg m-3) and 40 mg m-3 (95% confidence limit, 39-41 mg m-3), respectively. Similar correlations were found when the data from the two study periods were analysed separately.

Adolescent↗
PubMedDate not supplied

[Effect of isoflurane on gas exchange and systemic and pulmonary hemodynamics in man during single lung ventilation].

OBJECTIVE: We studied the effect of 1.5% isoflurane end expiratory fraction on arterial oxygenation and on systemic and pulmonary hemodynamics during nonsurgical single lung ventilation. MATERIAL AND METHODS: The study includes 6 patients undergoing surgical thoracotomy. In all cases a double lumen endotracheal tube was inserted and pulmonary ventilation was performed with a FiO2 = 1. Patients were placed on lateral decubitus position. The following variables were measured: mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), central venous pressure (CVP), capillary pulmonary pressure (CPP), cardiac output (CO), and Qs/Qt. Measurements were taken at three different situations. The first was done under bilateral pulmonary ventilation and intravenous anesthesia with thiopental, fentanyl, and diazepam. The nondependent lung was collapsed by means of a selective ventilation of the dependent lung, and the second series of measurements was done 20 min after intravenous anesthesia. The third block of data was obtained after 15 min of respiratory ventilation with 1.5% isoflurane. RESULTS: Single lung ventilation induced a significant decrease of Pa O2 (379 +/- 96 mmHg vs 208 +/- 93 mmHg) and a significant increase in Qs/Qt (20 +/- 8% vs 30 +/- 10%). However, during isoflurane ventilation there were no significant changes in PaO2 (208 +/- 93 mmHg vs 204 +/- 94 mmHg) nor in Qs/Qt (30 +/- 10 vs 28 +/- 8). Isoflurane elicited a significant decrease of the CO, whereas MPAP, RVS, and PvO2 did not show significant variations. CONCLUSIONS: We conclude that 1.5% isoflurane end expiratory concentrations did not significantly affect pulmonary oxygenation during single lung ventilation.

Aged↗