Ligand-Based Reactivity of Oxygenation and Alkylation in Cobalt Complexes Binding with (Thiolato)phosphine Derivatives.

In our efforts to understand the nature of metal thiolates, we have explored the chemistry of cobalt ion supported by (thiolato)phosphine ligand derivatives. Herein, we synthesized and characterized a square-planar CoII complex binding with a bidentate (thiolato)phosphine ligand, Co(PS1″)2 (1) ([PS1″]- = [P(Ph)2(C6H3-3-SiMe3-2-S)]-). The complex activates O2 to form a ligand-based oxygenation product, Co(OPS1″)2 (2) ([OPS1″]- = [PO(Ph)2(C6H3-3-SiMe3-2-S)]-). In addition, an octahedral CoIII complex with a tridentate bis(thiolato)phosphine ligand, [NEt4][Co(PS2*)2] (3) ([PS2*]2- = [P(Ph)(C6H3-3-Ph-2-S)2]2-), was obtained. Compound 3 cleaves the C-Cl bond in dichloromethane via an S-based nucleophilic attack to generate a chloromethyl thioether group. Two isomeric products, [Co(PS2*)(PSSCH2Cl*)] (4 and 4') ([PSSCH2Cl*]- = [P(Ph)(C6H3-3-Ph-2-S)(C6H3-3-Ph-2-SCH2Cl)]-), were isolated and fully characterized. Both transformations, oxygenation of a CoII-bound phosphine donor in 1 and alkylation of a CoIII-bound thiolate in 3, were monitored by spectroscopic methods. These reaction products were isolated and fully characterized. Density functional theory (DFT, the B3LYP functional) calculations were performed to understand the electronic structure of 1 as well as the pathway of its transformation to 2.

An examination of the Northern Hemisphere mid-latitude storm track interannual variability simulated by climate models-sensitivity to model resolution and coupling.

The model fidelity in simulating the Northern Hemisphere storm track interannual variability and the connections of this variability to the low frequency atmospheric variations and oceanic variations are examined based on the atmospheric European Centre for Medium-Range Weather Forecasts (ECMWF) model and coupled NCAR Community Climate System Model (CCSM) systems at different horizontal resolutions. The atmospheric general circulation model (AGCM) runs are forced by observed sea surface temperatures (SST) with varying atmospheric resolutions, while the coupled general circulation model (CGCM) runs have a fixed atmospheric resolution but varying oceanic resolutions. The phases, between the North Pacific (NP) and North Atlantic (NA) sectors, of the simulated hemisphere-scale Empirical Orthogonal Function (EOF) modes of the storm track fluctuations change with the model resolution, suggesting the storm track variability in NP and NA basins are largely independent. The models can qualitatively reproduce the basin-scale EOFs of both NP and NA storm track variability. These EOFs are not sensitive to either atmospheric or oceanic model horizontal resolutions, but their magnitudes from the CGCM runs are substantially underestimated. The storm track variations over NP basin are hybrid of internal atmospheric variations and external forcing from the underlying conditions, but the fluctuations over the NA basin are merely atmospheric internal variability. The NP storm track variability from SST forcing accounts for 4.4% of the total variance in observations, while it only has less than 2% of the total in all AGCM simulations. The external forcing to the storm track variations is more realistically reproduced in the higher atmospheric resolution runs. The air-sea coupling makes the SST feedbacks to the atmospheric internal variability, absent in the atmospheric ECMWF model hindcasts, emerge in the coupled CCSM simulations.

Dynamical and Thermodynamical Influences of the Maritime Continent on ENSO Evolution.

El Niño-Southern Oscillation (ENSO) exerts tremendous influences on the global climate. Through dynamic lifting and thermal forcing, the Maritime Continent (MC) plays an important role in affecting global atmospheric circulation. In spite of the extensive studies on ENSO mechanisms, the influence of MC on the characteristics of ENSO life cycle remains unclear. Our coupled model experiments reveal that the absence of the MC land contributes to a strong ENSO asymmetry and a weakened nonlinear atmospheric response to the combined seasonal and interannual SST variations (i.e. the combination mode) that prolongs the warm events, resulting in a reduction of ENSO frequency. On the other hand, our experiments suggest that the global climate model applied (NCAR CESM) overestimates the MC topographic uplifting effect on ENSO simulation. Overall, this study provides a new physical insight into the nature of the MC influence on ENSO evolution.

Verification of land-atmosphere coupling in forecast models, reanalyses and land surface models using flux site observations.

We confront four model systems in three configurations (LSM, LSM+GCM, and reanalysis) with global flux tower observations to validate states, surface fluxes, and coupling indices between land and atmosphere. Models clearly under-represent the feedback of surface fluxes on boundary layer properties (the atmospheric leg of land-atmosphere coupling), and may over-represent the connection between soil moisture and surface fluxes (the terrestrial leg). Models generally under-represent spatial and temporal variability relative to observations, which is at least partially an artifact of the differences in spatial scale between model grid boxes and flux tower footprints. All models bias high in near-surface humidity and downward shortwave radiation, struggle to represent precipitation accurately, and show serious problems in reproducing surface albedos. These errors create challenges for models to partition surface energy properly and errors are traceable through the surface energy and water cycles. The spatial distribution of the amplitude and phase of annual cycles (first harmonic) are generally well reproduced, but the biases in means tend to reflect in these amplitudes. Interannual variability is also a challenge for models to reproduce. Our analysis illuminates targets for coupled land-atmosphere model development, as well as the value of long-term globally-distributed observational monitoring.

On the Shortening of the Lead Time of Ocean Warm Water Volume to ENSO SST Since 2000.

The possible factors associated with the shortening of lead time between ocean warm water volume (WWV) variability along the equatorial Pacific and El Niño-Southern Oscillation (ENSO) variability after 2000 are documented. It is shown that the shortening of lead time is due to frequency increases of both WWV and ENSO. During 1979-99 the dominant frequencies were 1.5-3.5 years for both the Niño3.4 and WWV indices. In contrast, during 2000-16, both indices had a relatively flatter spectrum and were closer to a white noise process with a relative maximum at 1.5-2.0 years for the Niño3.4 index and 0.8-1.3 years for the WWV index. The frequency change of ENSO and WWV were linked to a westward shift of the Bjerknes feedback region. The results here are consistent with previous argument that the westward shift of the air-sea coupling region will cause an increase of ENSO frequency, as the corresponding zonal advection feedback reduces the period and growth of coupled instability, thus favoring more frequent and weak El Niño events.

The role of off-equatorial surface temperature anomalies in the 2014 El Niño prediction.

The 2014 El Niño, anticipated to be a strong event in early 2014, turned out to be fairly weak. In early 2014, the tropical Pacific exhibited persistent negative SST anomalies in the southeastern Pacific and positive SST anomalies in north, following the pattern of the Southern Pacific Meridional Mode. In this study, we explored the role of the off-equatorial SST anomalies in the 2014 prediction. Our experiments show that 40% of the amplitude error at the peak phase could be attributed to the lack of prediction of negative SST anomalies in the southeastern Pacific. However, the impact of this model error is partially compensated by the absence of the positive SST anomalies in the tropical western North Pacific in the model. The model response to the amplitude of negative southeastern Pacific SST anomalies is nonlinear in terms of equatorial warming, because the enhanced meridional pressure gradient forces very strong meridional winds without accelerating the zonal wind component near the equator. Our study suggests that reliable forecasts of ENSO strongly rely on correctly modeling the meridional SST gradient, as well as its delicate feedback with the zonal (ENSO) mode.

Salinity anomaly as a trigger for ENSO events.

According to the classical theories of ENSO, subsurface anomalies in ocean thermal structure are precursors for ENSO events and their initial specification is essential for skillful ENSO forecast. Although ocean salinity in the tropical Pacific (particularly in the western Pacific warm pool) can vary in response to El Niño events, its effect on ENSO evolution and forecasts of ENSO has been less explored. Here we present evidence that, in addition to the passive response, salinity variability may also play an active role in ENSO evolution, and thus important in forecasting El Niño events. By comparing two forecast experiments in which the interannually variability of salinity in the ocean initial states is either included or excluded, the salinity variability is shown to be essential to correctly forecast the 2007/08 La Niña starting from April 2007. With realistic salinity initial states, the tendency to decay of the subsurface cold condition during the spring and early summer 2007 was interrupted by positive salinity anomalies in the upper central Pacific, which working together with the Bjerknes positive feedback, contributed to the development of the La Niña event. Our study suggests that ENSO forecasts will benefit from more accurate salinity observations with large-scale spatial coverage.

[Specific immune against pancreatic cancer induced by dendritic cells pulsed with mutant K-ras peptide].

OBJECTIVE: To investigate whether dendritic cells (DCs) pulsed with mutant K-ras peptide (12-Val) can induce efficiently specific anti-tumor immune response against pancreatic cancer. METHODS: Immature DCs were isolated from the peripheral blood of a volunteer and were pulsed with synthesized mutant K-ras peptide (YKLVVVGAV). When the DCs were matured the expression rate of Kras antigen epitope on the DC's surface was detected by mono antibody (K-ras-12-Val). Autogeneic and homologous T cells were mixed with the mutant K-ras peptide-pulsed DCs. Human pancreatic cancer cells of the line Patu8988 were mixed with cytotoxic T lymphocytes (CTLs) cultured for 5 days, and the killing effects of the CTLs on the cells was assessed by MTT method. Patu8988 cells were injected subcutaneously into nude mice, cancer cells were obtained from the tumor masses and injected subcutaneously into other nude mice to establish mice models of pancreatic cancer. Then 32 mice with pancreatic cancer were randomly divided into 4 equal groups: control group, K-ras specific CTL intra-tumor injection group, CTL caudal vein injection group, and IL-2 activated non-specific CTL intra-tumor injection group. The tumor size was measure regularly. Immunohistochemistry was used to detect the pathological analysis of the transplanted tumors. RESULTS: The mutational epitope (K-ras-12-Val) induced by mutant peptide could be found on the DCs'surface efficiently. After co-incubation with the mature DCs pulsed with tumor antigen the autogeneic T cells were activated, the CD8 T cells accounted for (44.8 +/- 2.1)%. Without damage the normal tissue cells, the killing rate of activated K-ras specific CTLs to the tumor cell when the ratios of CTL: Patu8988 cells were 10:1, 20:1, and 50:1 were (21.2 +/- 1.9)%, (32.4 +/- 2.1)%, and (45.7 +/- 5.3)% respectively, all while the killing efficiency significantly superior to those of the non-specific activated T lymphocyte (all P < 0.05). Eight days after CTL injection into the nude mice the tumor size of the intratumor injection group was (68 +/- 13) mm3, significantly smaller than those of the control group and IL-2 activated non-specific CTL intra-tumor injection group [(87 +/- 14) mm3 and (79 +/- 19) mm3, both P < 0.05]. The survival rates of the nude mice of the K-ras specific CTL intra-tumor injection group, CTL caudal vein injection group, and IL-2 activated non-specific CTL intra-tumor injection group were all significantly higher than that of the control group (all P < 0.05), and the survival rate of the K-ras specific CTL intra-tumor injection group was significantly higher than that of the IL-2 activated non-specific CTL intra-tumor injection group (P < 0.05). Immunohistochemical staining confirmed that K-ras specific CTL had the ability to move toward tumor. CONCLUSION: DCs pulsed with mutant K-ras peptide (12-Val) induces specific anti-tumor immune response in pancreatic cancer efficiently.