Shearmeter floats in the area of the WHOI Brazil Basin Tracer Release Experiment : technical and oceanographic data

Six drifting floats designed to measure shear were deployed in the vicinity of the Brazil Basin Tracer Release Experiment. The one-year long time series of oceanographic conditions obtained by the floats are for direct comparison with long-term tracer dispersion. The purpose of the tracer dispersion experiment was to study mixing of Antarctic Bottom Water at approximately 4000 m depth with less dense water above. Two of the floats returned shear records, one from about 1660 m depth and one from about 2800 m depth. Mean shear at 1660 m was 2.2 x 10 -3 s-1 with N = 1.1 cph, about 1.9 times the Garrett-Munk model amount. Mean shear at 2800 m was 1.1 x 10-3 with N = 0.5 cph, about 2.2 times Garrett-Munk. There was no apparent depth structure to the shear recorded by the near-bottom float moving over the mountainous seafloor. The two shear time series and the local tidal velocities were not strongly correlated, but the tide and shear series did have some similarities. Some variability in the 1660-m shear may be due to atmospheric forcing. Three floats deeper than 2800 m returned one-year long trajectories. Two trajectories were persistently eastward.Funding was provided by the National Science Foundation under Grant Nos. OCE-9416014 and OCE-9906685

The diagnosis of BCR/ABL-negative chronic myeloproliferative diseases (CMPD): a comprehensive approach based on morphology, cytogenetics, and molecular markers

Recent years showed significant progress in the molecular characterization of the chronic myeloproliferative disorders (CMPD) which are classified according to the WHO classification of 2001 as polycythemia vera (PV), chronic idiopathic myelofibrosis (CIMF), essential thrombocythemia (ET), CMPD/unclassifiable (CMPD-U), chronic neutrophilic leukemia, and chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome, all to be delineated from BCR/ABL-positive chronic myeloid leukemia (CML). After 2001, the detection of the high frequency of the JAK2V617F mutation in PV, CIMF, and ET, and of the FIP1L1–PDGFRA fusion gene in CEL further added important information in the diagnosis of CMPD. These findings also enhanced the importance of tyrosine kinase mutations in CMPD and paved the way to a more detailed classification and to an improved definition of prognosis using also novel minimal residual disease (MRD) markers. Simultaneously, the broadening of therapeutic strategies in the CMPD, e.g., due to reduced intensity conditioning in allogeneic hematopoietic stem cell transplantation and the introduction of tyrosine kinase inhibitors in CML, in CEL, and in other ABL and PDGRFB rearrangements, increased the demands to diagnostics. Therefore, today, a multimodal diagnostic approach combining cytomorphology, cytogenetics, and individual molecular methods is needed in BCR/ABL-negative CMPD. A stringent diagnostic algorithm for characterization, choice of treatment, and monitoring of MRD will be proposed in this review