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J Val

Publications and source records attributed to J Val.

8 recordsLinked to original sources
PubMed2000

Kinetic analysis of a molecular model of the budding yeast cell cycle.

The molecular machinery of cell cycle control is known in more detail for budding yeast, Saccharomyces cerevisiae, than for any other eukaryotic organism. In recent years, many elegant experiments on budding yeast have dissected the roles of cyclin molecules (Cln1-3 and Clb1-6) in coordinating the events of DNA synthesis, bud emergence, spindle formation, nuclear division, and cell separation. These experimental clues suggest a mechanism for the principal molecular interactions controlling cyclin synthesis and degradation. Using standard techniques of biochemical kinetics, we convert the mechanism into a set of differential equations, which describe the time courses of three major classes of cyclin-dependent kinase activities. Model in hand, we examine the molecular events controlling "Start" (the commitment step to a new round of chromosome replication, bud formation, and mitosis) and "Finish" (the transition from metaphase to anaphase, when sister chromatids are pulled apart and the bud separates from the mother cell) in wild-type cells and 50 mutants. The model accounts for many details of the physiology, biochemistry, and genetics of cell cycle control in budding yeast.

Cell Cycle↗
PubMed1998

[Effectiveness of the eradication of Helicobacter pylori by treatment with omeprazol, amoxicillin, and clarithromycin according to dosage and administration schedule].

BACKGROUND: There are many reports that evaluate the efficacy of the combination of omeprazole, amoxicillin and clarithromycin in the eradication of Helicobacter pylori, but data about effectivity in clinical practice are sparse. The goal of our study is to evaluate the effectivity in the clinical setting of this combination with diverse durations and doses. METHODS: This is a retrospective analysis of 187 patients (128 male and 59 female), with an endoscopic diagnosis of duodenal ulcer (156), gastric ulcer (25) and both (6) with Helicobacter pylori infection as defined by both: a positive ureasa test and histology. After diagnosis the patient were treated with one of three combinations: a) omeprazole: 20 mg/12 h + amoxicillin: 1 g/12 h + clarithromycin: 500 mg/12 h, during 6 days (n = 60); b) omeprazole: 20 mg/12 h + amoxicillin: 1 g/12 h + clarithromycin: 500 mg/12 h, during 7 days (n = 74), and c) omeprazole: 20 mg/12 h + amoxicillin: 1 g/8 h + clarithromycin: 500 mg/8 h, during 7 days (n = 53). After the 6 or 7 day treatment period the patients did not receive any further treatment until a follow-up control unit. Eradication was evaluated with one of two tests: endoscopy (with ureasa test and at least 4 histologic samples) (n = 90) or urea breath test according to european protocol (n = 97). RESULTS: No patient dropped out because of side effects and compliance was above 80% in all cases. The global eradication rate was 87.2% (CI 95%: 82.4-92%). According to treatment the rate were respectively 80% (CI 95%: 67.7-89.2%) with scheme A; 89.2% (CI 95%: 79.8-95.2%) with scheme B, and 92.5% (CI 95%: 81.8-97.9%) with scheme C, with no statistically significant differences among groups. Difference between schemes and C, however, was almost reached (p = 0.053). CONCLUSIONS: The combination of omeprazole, amoxicillin and clarithromycin at standard doses (scheme B) is effective in clinical practice. Higher dose of amoxicillin and clarithromycin does not improve the results, and shorter duration of therapy associated with lower, although not significant rate of eradication.

Adult↗
PubMed1995

Checkpoints in the cell cycle from a modeler's perspective.

The cell division cycle is a complex process by which cells grow and divide into two viable daughter cells. So that mistakes are not made in this crucial replication process, cells stop at one or more "checkpoints" in the cycle to query their internal state and external conditions, before proceeding to the next stage of the cycle. In this paper we study some simple mathematical models of cell cycle arrest in G1 ("Start") and G2. Our models help to relate the molecular mechanisms of these checkpoints with physiological properties of the cell cycle.

Animals↗
PubMed1991

Anticardiolipin antibodies and lupus anticoagulant in end-stage renal disease.

Anticardiolipin antibodies are autoantibodies clinically associated with hypercoagulability. Systemic thrombosis and thrombosis of the vascular access for haemodialysis coexist with immunoregulation abnormalities in end-stage renal disease (ESRD). The aim of the present study was to analyse the incidence of thrombotic episodes and the presence of anticardiolipin antibodies and lupus anticoagulant in 73 patients with ESRD--51 on haemodialysis and 22 on conservative treatment. Four (18%) patients on conservative treatment had IgG-anticardiolipin, three of them also having lupus anticoagulant. Sixteen (31%) patients on haemodialysis showed IgG-anticardiolipin and 11 (22%) lupus anticoagulant; overall, 19 (37%) patients on haemodialysis had IgG-anticardiolipin and/or lupus anticoagulant. This greater incidence in haemodialysis was associated with a more frequent use of cuprophane membranes (68% versus 34%, P less than 0.05). Six patients with ESRD--one on conservative treatment--met criteria for the diagnosis of primary antiphospholipid syndrome, clinically characterised by thrombosis of the vascular access. IgG-anticardiolipin and/or lupus anticoagulant are frequently found in ESRD and their incidence increases with haemodialysis, probably due to some kind of membrane bioincompatibility. IgG-anticardiolipin and lupus anticoagulant can be associated with thrombotic episodes, being constituents of an ESRD-related antiphospholipid syndrome.

Adult↗