Validation and Operational Implementation of the Navy Coastal Ocean Model Four Dimensional Variational Data Assimilation System (NCOM 4DVAR) In the Okinawa Trough

The Navy Coastal Ocean Model Four-Dimensional Variational Assimilation (NCOM 4DVAR) system is an analysis software package that is designed to supplement the current capability of the operational analysis/prediction system known as the Relocatable Navy Coupled Ocean Model (Relo NCOM) system. The present assimilation component of Relo NCOM employs the Navy Coupled Ocean Data Assimilation Three-Dimensional Variational Assimilation (NCODA 3DVAR) system to process and assimilate observations. The NCOM 4DVAR, on the other hand, uses a representer based 4DVAR method and has been found to improve the forecast-skill for several regional applications. This chapter presents the results of validation experiments performed in the Okinawa Trough. The analysis and resulting forecast skill of the two assimilation methods within Relo NCOM (NCOM 4DVAR and NCODA 3DVAR) are compared, and the operational implementation of NCOM 4DVAR is examined to verify that it satisfies operational constraints. The metrics used to validate the NCOM 4DVAR system include: computational efficiency, scalability, robustness, and the prediction accuracy of temperature, sea surface height, and sonic layer depth through NCOM 4DVAR and NCODA 3DVAR analyses. Forecast skill metrics are computed using surface observations of temperature, salinity and sea surface height, and profile observations from gliders and AXBTs (aerial expendable bathythermograph). Overall, the validation reveals that NCOM 4DVAR has lower root mean square errors for both analyses and forecasts than the operational NCODA 3DVAR system

Islet-brain1/C-Jun N-terminal kinase interacting protein-1 (IB1/JIP-1) promoter variant is associated with Alzheimer's disease.

Islet-brain1 (IB1) or c-Jun NH2 terminal kinase interacting protein-1 (JIP-1), the product of the MAPK8IP1 gene, functions as a neuronal scaffold protein to allow signalling specificity. IB1/JIP-1 interacts with many cellular components including the reelin receptor ApoER2, the low-density lipoprotein receptor-related protein (LRP), kinesin and the Alzheimer's amyloid precursor protein. Coexpression of IB1/JIP-1 with other components of the c-Jun NH2 terminal-kinase (JNK) pathway activates the JNK activity; conversely, selective disruption of IB1/JIP-1 in mice reduces the stress-induced apoptosis of neuronal cells. We therefore hypothesized that IB1/JIP-1 is a risk factor for Alzheimer's disease (AD). By immunocytochemistry, we first colocalized the presence of IB1/JIP-1 with JNK and phosphorylated tau in neurofibrillary tangles. We next identified a -499A>G polymorphism in the 5' regulatory region of the MAPK8IP1 gene. In two separate French populations the -499A>G polymorphism of MAPK8IP1 was not associated with an increased risk to AD. However, when stratified on the +766C>T polymorphism of exon 3 of the LRP gene, the IB1/JIP-1 polymorphism was strongly associated with AD in subjects bearing the CC genotype in the LRP gene. The functional consequences of the -499A>G polymorphism of MAPK8IP1 was investigated in vitro. In neuronal cells, the G allele increased transcriptional activity and was associated with an enhanced binding activity. Taken together, these data indicate that the increased transcriptional activity in the presence of the G allele of MAPK8IP1 is a risk factor to the onset of in patients bearing the CC genotype of the LRP gene