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Biomedical subjects

J Benitez

Publications and source records attributed to J Benitez.

At least 73 records · Page 4Linked to original sources
PubMed1990

Establishment and characterization of a new human colon adenocarcinoma cell line: BCS-TC2.

A new cell line designated as BCS-TC2 was established in culture from a primary human colon adenocarcinoma. This cell line has been in continuous culture over a 36-month period. The cells grow as a monolayer sheet, displaying areas with a multilayered pattern as well as single cells and free-floating aggregates. The morphological, immunological, and ultrastructural features of these cells are in agreement with their epithelial origin. The characterization of this cell line indicated a 38 hr doubling time, and a colony forming efficiency of 2% in semisolid media and 22% in liquid culture, at low cell densities. These cells produce low amounts of carcinoembryonic antigen in culture (0.1 ng of CEA/10(6) cells). Sub-cutaneous injection into athymic mice shows that these cells have a non-tumorigenic capacity. Chromosomal analysis showed a karyotype 46 XX, -15, +der (15), inv (16) (p13::q13). BCS-TC2 cell line, which maintains in culture several characteristics of the original tumor, represents a useful model system for cell biology studies of primary and non-metastatic tumors.

Adenocarcinoma↗
PubMed1990

Mapping of human chromosome 22 by in situ hybridization.

The second smallest chromosome of the human karyotype, i.e., chromosome 22, is involved in many congenital or acquired structural aberrations. This variety can be taken advantage of to determine the exact linear order, from centromere to telomere, of cloned probes and chromosomal breakpoints. Eleven probes were localized with respect to breakpoints of 11 der(22) of independent cell lines using in situ hybridization on metaphasic spreads. The deduced order of the tested probes and that of the breakpoints are in complete agreement with the published genetic map and the karyotypic analysis, respectively. This approach enables a correlation of the genetic map with the chromosomal banding.

Cell Line↗
PubMed1990

Oxidative polymorphism of debrisoquine in Parkinson's disease.

Oxidative phenotype and metabolic ratio (MR) of debrisoquine (DBQ) have been determined in 87 patients with Parkinson's disease and in 556 healthy control subjects. Three patients (3.45%) and 34 control subjects (6.12%), having an MR greater than 12.6, were classified as poor metabolisers (PM) of DBQ (ns). The distribution of MR values in the 84 Parkinsonian patients classified as extensive metabolisers (EM) showed a less efficient oxidative rate when compared with controls of the same phenotype (p less than 0.001). This difference may be due to enzymatic inhibition caused by drug treatment in 40 of these patients. As in patients not taking any drug known to inhibit the oxidation of DBQ, distribution of MR values was not different from that in controls. A negative correlation (r = -0.36, p less than 0.02) was found between MR of DBQ and age at onset of disease in patients free of drugs known to interact with DBQ metabolism. A higher rate of DBQ oxidation could be a genetic factor that delays the clinical onset of Parkinson's disease in predisposed people.

Adult↗
PubMed1990

Study of the parental origin of sexual aneuploidy in ten families using RFLPs.

We have studied 10 families with sexual aneuploidy by means of recombinant DNA techniques. The X linked probes were F814 (DXS52), FIX (FVIII gene), pert 87.15 (DXS164), L754 (DXS84) and 47Z (DXYS5). The observed banding patterns allowed us to determine the parental origin of such aneuploidy in nine of our cases. It was paternal in seven cases and maternal in two.

Cells, Cultured↗
PubMed1990

[Myelodysplastic syndromes. Hematologic phenotypes, cytogenetic expression and clinical course in 133 cases (1979-1989)].

One hundred and thirty-three cases of myelodysplastic syndromes studied during the last ten years were revised. Of them, 79 were males and 54 females, and their ages ranged between 15 and 91 years (median, 69 years). Five patients (3.7%) had secondary myelodysplasias. The haematological phenotype (FAB) of the cases was: RA, 41.3%; SRA, 24%; RAEB, 18%; RAEBT, 3.7%; CMML, 8.3%. Leucopenia/thrombocytopenia without initial anaemia was present in 4.5% of the cases. Abnormal karyotype was found in 54 patients (40.6%), MIKA in 41 cases and MAKA in 13 cases. The cytogenetic anomalies most commonly found were +8, 5q-, -7, 11q- and 13q-. Cytogenetic abnormalities were commonest amongst the RAEB (50%), and least frequent in CMML (18.2%). Thirty-one patients evolved into acute leukaemia (29 ANLL and 2 ALL). Such blastic changes were more frequent in RAEB (62.5%) and rarest in SRA (9.4%), and they appeared mostly in patients with complex karyotype (MAKA) (53.8%) as compared with those who had normal karyotype (17.7%). Short-lasting complete remission was achieved by 40% of the patients treated with conventional chemotherapy. The survival of the group as a whole (median 30 months) varied in accordance with the haematological phenotype: SRA, 81 months; RA, 65 months; CMML, 13 months; RAEB +/- T, 8 months. The finding of a MAKA karyotype significantly shortened the survival (4 months) with regard to MIKA (44 months) or normal karyotype (39 months). The following median survivals were attained after patients' staging (Bournemouth's criteria): stage A, 84 months; stage B, 22 months, and stage C, 5 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1989

Acetylator polymorphism in Parkinson's disease.

Acetylator phenotype has been determined using sulphamethazine in 100 patients with Parkinson's disease and in 93 age-matched normal control subjects. Sixty-nine patients and 54 control subjects were classified as slow acetylators (NS). No relation was found among acetylator polymorphism and age at onset or clinical stage of disease. Amongst slow acetylators, the percentage of acetylated sulphamethazine in plasma was significantly lower in patients than in controls. Despite this finding, the results do not support any relationship between acetylator polymorphism and the risk of developing Parkinson's disease.

Acetylation↗
PubMed1989

Assessment of the debrisoquin and dextromethorphan phenotyping tests by gaussian mixture distributions analysis.

From a sample of 149 unrelated Spaniards, individuals were phenotyped for their ability to hydroxylate debrisoquin and O-demethylate dextromethorphan. The distribution of urinary metabolic ratios for each test was analyzed by univariate gaussian mixture distributions analysis to determine the number of populations, the mean and standard deviation of the metabolic ratios for each population, and the proportion belonging to each population. For the 124 subjects phenotyped with both the debrisoquin and dextromethorphan tests a bivariate analysis was performed. The results demonstrate that both tests similarly separated this sample into two populations, with 10% belonging to poor metabolizer phenotypes. In addition, the correlation between the metabolic ratios from each test is significant, indicating that they are measuring the same biologic trait and the certainty of correctly identifying the debrisoquin oxidation phenotype of an individual is improved by using the results of both tests.

Debrisoquin↗
PubMed1987

Effect of pentobarbital on the contraction and calcium movements in cat cerebral and peripheral arteries.

Pentobarbital (PB) induced concentration-dependent vasodilation in cylindrical segments of cat cerebral and femoral arteries precontracted with 75 mM K+ or 10(-5) M serotonin (5-HT). PB (10(-4) or 10(-3) M, 10 min preincubations) caused concentration-dependent inhibition of the contraction produced by both agents. The exposure of the vessels to a Ca2+-free medium annulled the response elicited by K+ in both kinds of arteries. In this medium, the contraction induced by 5-HT in cerebral arteries was abolished, whereas in femoral ones it was significantly reduced. This residual response was abolished by PB. The intracellular 45Ca2+ uptake (La3+ method) elicited by K+ in both kinds of arteries and by 5-HT in cerebral ones was reduced in a concentration-dependent manner by PB (10(-4)-10(-3) M). The spontaneous 45Ca2+ efflux from these arteries and that induced by La3+ (10 mM) were unaffected by PB (10(-3) M). These results indicate that the vasodepressor effects induced by PB are essentially due to an interference of the barbiturate with the Ca2+ entry into the vascular smooth muscle cell in both kinds of arteries and with the intracellular Ca2+ movements in femoral ones. It does not seem to exist a clear selectivity of PB for brain or peripheral arteries for antagonizing the responses caused by K+ or 5-HT.

Animals↗
PubMed1987

Leukemic transformation in patients with the 5q- alteration: analysis of the behavior of the 5q- clones in preleukemic to leukemic phases.

Serial cytogenetic studies have been performed in four patients with myelodysplastic syndromes. In all four a 5q- alteration was present, but with a different pattern of presentation. One patient presented 5q- as the only alteration since diagnosis; two patients acquired this alteration during the course of the disease; and the fourth showed a 5q- plus other alterations since the first cytogenetic study. Likewise, three of the four patients showed a clone with trisomy 8 and without 5q-. According to these observations and others from the literature with similar cytogenetic behavior, we have analyzed the following points: 5q- as a primary event and as the only alteration, 5q- as a secondary event, 5q- plus other alterations, and presence of cytogenetically different clones. Analysis of these points suggests that the 5q- alteration can represent an early mutation conferring a slow capacity of expansion to the affected clones, with the possibility of cytogenetic evolution during the progression of the disease (about 30% of the patients). Likewise, the association of trisomy 8 clones with 5q- clones can be a nonrandom event.

Aged↗
PubMed1987

Frequency of constitutional chromosome alterations in patients with hematologic neoplasias.

From 1978 to 1985 cytogenetic studies were performed on 718 patients with different hematologic diseases. Nine (1.25%) had a constitutional chromosome alteration. One patient had trisomy 21, four had balanced translocations and four had sex chromosome anomalies. Although the frequency of constitutional alterations was twice that seen in the newborn population, an analysis of these data and also from the literature shows a random association between constitutional chromosome alterations and hematologic neoplasias, except for patients with Down's syndrome.

Adolescent↗
PubMed1987

Chromosomal patterns in human malignant astrocytomas.

Cytogenetic analysis by direct and/or in vitro preparations was performed on 34 malignant astrocytomas. Thirty tumors showed near-diploid chromosome numbers, whereas, tritetraploid chromosome complements were present in four tumors. The most frequent chromosomal changes implied numerical deviations by a gain of chromosomes #7, #19, and #20, and by losses of #10, #22, and Y. Structural rearrangements were present in stem- or side lines of 24 tumors. Although no common chromosomal rearrangement seems to exist among those tumors, chromosomes #1, #6, #7, and #9 were predominantly involved. Polysomy and structural rearrangements of chromosome #7 could be related to the overexpression of epidermal growth factor gene, previously observed in some malignant gliomas.

Adult↗