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Biomedical subjects

J C Flores

Publications and source records attributed to J C Flores.

15 recordsLinked to original sources
PubMed1998

A mathematical model for Neanderthal extinction.

A simple mathematical homogeneous model of competition is used to describe Neanderthal extinction in Europe. It considers two interacting species, Neanderthals and Early Modern Men, in the same ecological niche. Using paleontological data we claim that the parameter of similarity, between both species, fluctuates between 0.992 and 0.997. An extension of the model including migration (diffusion) is also discussed; nevertheless, extinction of Neanderthal seems unavoidable. Numerical analysis of travelling wave solutions (fronts) confirms the extinction. The wave-front-velocity is estimated from linear analysis and numerical simulations confirm this estimation. We conjecture a mathematical formulation for the principle of exclusion between competitive interacting species (Gause).

Animals↗
PubMed1995

Adenoid cystic carcinoma initially diagnosed and treated as hemangioma.

Adenoid cystic carcinoma initially diagnosed and treated as hemangioma. A case diagnosed as having a hemangioma of the soft palate according to clinical and arteriographic findings is discussed. Recurrence appeared one year after embolization. Arteriography showed no vascular lesion and histopathologic study revealed an adenoid cystic carcinoma. It is stated that imaging studies may be insufficient.

Carcinoma, Adenoid Cystic↗
PubMed1990

[IgA nephropathy (Berger's disease). Our experience in 78 cases].

We studied 78 patients with a diagnosis of IgA nephropathy. Renal biopsy was indicated in 69 patients by the presence of macroscopic hematuria (52%), microhematuria or proteinuria (22%), nephrotic syndrome (10%), severe hypertension with microhematuria or renal failure (14%) or nephritic syndrome (1%). Nine were healthy subjects being studied as live kidney donors. An association with IgG and/or IgM was present in 92% of patients. Serum IgA was elevated in 36% of patients. Hypertension was present in 30% and decreased renal function in 29%. Patients with serum creatinine above 1.5 mg/dl tended to be older (33.8 vs 28.7 years) and to have hypertension (52% vs 19%). Among 25 patients followed for more than 12 months renal function remained stable in 44%, deteriorated in 20% and 36% developed renal failure. The latter was associated to older age, hypertension, absence of macroscopic hematuria and nephrotic syndrome. The 9 live donors had no clinical manifestations of renal disease. Thus, IgA nephropathy is a highly variable clinical entity, both in its manifestations and its prognosis. An asymptomatic course is demonstrated in some subjects.

Adolescent↗
PubMed1989

[Lupus nephropathy: difficulties in its treatment].

The management of the patient with lupus nephropathy is still difficult. A new classification considering activity and chronicity indexes has revalued the histologic assessment as a prognostic and therapeutic guide. The benefits of immunosuppressive drugs in preventing progression of renal disease have been clarified and adverse effects reduced by new methods of administration. A key aspect of therapy is still individual selection of type and intensity of immunosuppression, that must be adjusted to the changing nature of the disease. Therapy must be balanced between optimal levels of efficacy and minimal toxicity.

Adrenal Cortex Hormones↗
PubMed1988

DNA binding factors for the CpG-rich island containing the promoter of the human X-linked PGK gene.

The gene coding for the glycolytic enzyme phosphoglycerate kinase (PGK-1) is X-linked in mammals and has a G+C-rich 5' region characteristic of several constitutive genes. Despite the fact that PGK-1 is constitutively expressed, it is transcriptionally regulated in female cells by X chromosome inactivation. To study the expression and regulation of the PGK-1 gene, we have analyzed the binding of trans-acting factors to the 5' region of the PGK-1 gene. We detect at least three distinct binding activities that interact in a sequence-specific manner in vitro with at least six different sites in the 5' region. Two of these binding activities generate DNase I-protected footprints centered approximately 360 bp and 130 bp upstream of the transcription start point. We have examined the promoter specificity of the three binding activities in gel mobility-shift assays by competition with cloned promoter fragments of other genes. None of the binding activities interacts exclusively with X-linked promoters. However, one activity binds preferentially to G+C-rich promoters, and another activity appears to bind preferentially to only two of the promoters tested. Previous studies have demonstrated that one HpaII/MspI site, which is included within a footprinted region observed in this study, is fully methylated in the inactive X chromosome and totally unmethylated on the active X chromosome. Competition studies using synthetic oligonucleotides containing 5-methylcytosine at all CpG sites in this region demonstrate that DNA methylation does not significantly alter the affinity between the corresponding binding activity and this binding site.

Base Sequence↗
PubMed1986

Response of Drosophila embryonic cells to tumor promoters.

Several recent observations on tumor promoters point to the many developmental and embryonic characteristics associated with their mode of action. These observations have led us to investigate the effects of a series of tumor promoters on Drosophila embryonic cultures at both the morphological and molecular levels. The cultures have been used with some success by us to assess the teratogenic potential of a large number of molecules, including drugs, chemicals, and environmental pollutants. In this culture system, 12-O-tetradecanoylphorbol 13-acetate (TPA), the most potent of the tumor promoters tested, disrupted normal muscle and neuron differentiation at concentrations ranging from 0.1 to 10 microM; 4-O-methylphorbol 12-myristate a weak stage I promoter, used at concentrations the same as or higher than those of TPA had no inhibitory effect on cell differentiation. A selected group of tumor promoters was also investigated at the molecular level for their effects on differentiating Drosophila cells. All tumor promoters tested induced synthesis of three heat shock proteins. On the basis of these two levels of effects (morphological and molecular) it is apparent that the tumor promoters tested act similarly as teratogens do in the Drosophila embryonic cultures. This finding confirms some recent published reports suggesting that a large number of tumor promoters act as teratogens if the exposure interval is during the embryonic rather than the adult stage. We suggest that this system can be usefully employed to investigate some of the common mechanisms involved in tumor promotion and teratogenesis.

Abnormalities, Drug-Induced↗
PubMed1986

Clinical and immunological evolution of oligoanuric anti-GBM nephritis treated by haemodialysis.

Eight patients with oligoanuric anti-glomerular-basement-membrane (GBM), antibody-mediated glomerulonephritis without lung haemorrhage who were not treated with plasma exchange therapy were reviewed. All had severe crescentic nephritis and required dialysis. Circulating anti-GBM antibodies disappeared gradually and spontaneously in all patients. The autoantibodies became undetectable in five patients after an average of 11 months. No patient recovered renal function. Two patients have been successfully transplanted and anti-GBM nephritis has not recurred. One of these needed a pre-transplant course of plasma exchange and immunosuppression to reduce a slightly raised anti-GBM antibody titre. Of five patients who remain on dialysis, only two cannot be transplanted due to the persistence of circulating autoantibodies. One patient died from causes unrelated to renal disease. Oligoanuric patients with anti-GBM nephritis who need dialysis rarely benefit from aggressive therapy unless lung haemorrhage is present.

Acute Disease↗
PubMedDate not supplied

[Non-syndromic familial deafness. Review and genetic study].

Many cases of hearing impairment are of genetic origin. Non-syndromic recessive transmission is the most frequent form. A genetic study was made of cases of non-syndromic familial hearing impairment seen in our service. The pattern of Mendelian inheritance was studied in the disorders associated with deafness. Four families had non-syndromic deafness and autosomal inheritance (3 dominant and one recessive) and one had a probable sex-linked inheritance. Genetic counseling was given and guidelines were created after reviewing the literature.

Adolescent↗