Efecto de algunas prácticas de manejo del agua sobre las perdidas de nitrógeno en el cultivo del arroz

El experimento se realizó durante el primer semestre de 1986 en el Instituto Colombiano Agropecuario, Palmira, con el objetivo de cuantificar las pérdidas de nitrógeno asimilable según el manejo del agua, en las fases vegetativa, reproductiva y de maduración del arroz (Línea 25702). A mayor volumen de agua aplicado mayores fueron las pérdidas de nitrógeno asimilable en el suelo. Las menores pérdidas de nitrógeno se presentaron entre los 47 y 67 días en todos los tratamientos y las mayores en la fase reproductiva (68 a 105 días después de la siembra).Experiment was carried out at Colombian Agropecuary Institute (lCA) Palmira for 1986 a, with primary aim to estimate available N losts in soil under some water management practices on rice (L 25702) during vegetative, reproductive and ripening stages. The greater volumen of applied irrigation water the greater available N losts was showed. Less N losts was showed between 47 and 67 days in all treatments, it being greater in the reproductive stage (68 to 105 days)

Role of c-Abl Kinase in DNA Mismatch Repair-dependent G2 Cell Cycle Checkpoint Arrest Responses*S⃞

Current published data suggest that DNA mismatch repair (MMR) triggers prolonged G2 cell cycle checkpoint arrest after alkylation damage from N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) by activating ATR (ataxia telangiectasia-Rad3-related kinase). However, analyses of isogenic MMR-proficient and MMR-deficient human RKO colon cancer cells revealed that although ATR/Chk1 signaling controlled G2 arrest in MMR-deficient cells, ATR/Chk1 activation was not involved in MMR-dependent G2 arrest. Instead, we discovered that disrupting c-Abl activity using STI571 (Gleevec™, a c-Abl inhibitor) or stable c-Abl knockdown abolished MMR-dependent p73α stabilization, induction of GADD45α protein expression, and G2 arrest. In addition, inhibition of c-Abl also increased the survival of MNNG-exposed MMR-proficient cells to a level comparable with MMR-deficient cells. Furthermore, knocking down GADD45α (but not p73α) protein levels affected MMR-dependent G2 arrest responses. Thus, MMR-dependent G2 arrest responses triggered by MNNG are dependent on a human MLH1/c-Abl/GADD45α signaling pathway and activity. Furthermore, our data suggest that caution should be taken with therapies targeting c-Abl kinase because increased survival of mutator phenotypes may be an unwanted consequence