Catalytic hydroboration of aldehydes and ketones with an electron-rich acyclic metallasilylene.

The application of main group metal complexes in catalytic reactions is of increasing interest. Here we show that the electron-rich, acyclic metallasilylene L'(Cl)GaSiL C (L' = HC[C(Me)NDipp]2, Dipp = 2,6-iPr2C6H3; L = PhC(NtBu)2) acts as a precatalyst in the hydroboration of aldehydes with HBPin. Mechanistic studies with iso-valeraldehyde show that silylene C first reacts with the aldehyde with [2 + 1] cycloaddition in an oxidative addition to the oxasilirane 1, followed by formation of the alkoxysilylene LSiOCH[Ga(Cl)L']CH2CHMe2 (2), whose formation formally results from a reductive elimination reaction at the Si center. Alkoxysilylene 2 represents the active hydroboration catalyst and shows the highest catalytic activity with n-hexanal (reaction time: 40 min, yield: >99%, TOF = 150 h-1) at room temperature with a catalytic load of only 1 mol%. Furthermore, the hydroboration reaction catalysed by alkoxysilylene 2 is a living reaction with good chemoselectivity. Quantum chemical calculations not only provide mechanistic insights into the formation of alkoxysilylene 2 but also show that two completely different hydroboration mechanisms are possible.

Homoleptic and heteroleptic ketodiiminate zinc complexes for the ROP of cyclic l-lactide.

Homo- and heteroleptic ketodiiminate zinc complexes L12Zn2 (1, L1 = [Me2NC2H4NC(Me)CH]2CO), L2(ZnCp)2 (2, L2 = [Me2NC3H6NC(Me)CH]2CO, Cp = C5H5) and L2HZnCp* (3, Cp* = C5Me5) were synthesized and characterized by 1H and 13C NMR and IR spectroscopy as well as by elemental analysis and single crystal X-ray diffraction (sc-XRD, 2, 3). The catalytical activity of heteroleptic complexes 2 and 3 were tested in the ring-opening polymerization (ROP) of l-lactide. Homobimetallic complex 2 showed the highest activity and selectivity for the synthesis of cyclic polylactide (cPLLA; TOF = 17 460 h-1) at 100 °C in toluene solution, while linear polymers are formed with mononuclear complex 3.

Suppression of anchorage-independent growth by expression of the ataxia-telangiectasia group D complementing gene, ATDC.

The ataxia-telangiectasia group D complementing gene, ATDC, is located at 11q23, where loss of heterozygosity (LOH) is frequently observed in many kinds of cancers including breast cancer. Underexpression of ATDC in breast and prostate cancer has been reported using serial analysis of gene expression (SAGE) and DNA microarray analysis. We previously reported that SV-40-transformation down-regulates the expression of ATDC. In the present study, we investigated the roles of ATDC in carcinogenesis. First, we investigated the expression of ATDC in 11 cancer cell lines. No detectable transcript was observed in 4 tumor cell lines, and no ATDC protein was detected in 8 tumor cell lines. We transfected ATDC expression vector into Saos-2 and BT-549 that lacked detectable mRNA and protein expression of ATDC. Colony-forming efficiency in soft agar was significantly suppressed in all of the ATDC transfectants. These results suggest that suppressed ATDC expression is associated with malignant phenotype.

Injection of human primary effusion lymphoma cells or associated macrophages into severe combined immunodeficient mice causes murine lymphomas.

The pathogenesis of immunodeficiency-associated lymphoma is poorly understood. During the past several years, numerous lines of evidence implicating a multistep process of malignant transformation, also known as sequential pathogenesis, have emerged. Tumor-associated macrophage production of specific lymphostimulatory products has been demonstrated and hypothesized to be central to this process. While attempting to establish primary effusion lymphoma in severe combined immunodeficient (SCID) mice, we discovered a potential model of murine lymphomagenesis consistent with the sequential pathogenesis model. This pathogenesis-based model of lymphoma could significantly impact the current thinking about posttransplantation and other immunodeficiency-related lymphoproliferative disorders. Human primary effusion lymphoma-derived CD14+ cell-injected SCID mice developed aggressive murine large cell lymphomas. Tumor cell preparations containing CD14 cells or isolated CD14 cells induced lymphoma/lymphoproliferative diseases in 74% (20 of 27) of injected SCID mice. No tumors were induced by tumor-associated CD3 cells (0 of 4), normal human macrophages (0 of 13), or a murine macrophage cell line (0 of 10). Human macrophages were detected in tumor-bearing animals up to 6 months postinjection in association with the murine T-cell tumors but were not detected in controls or unaffected animals. These observations are consistent with the macrophage-initiated sequential pathogenesis model of disease (M. S. McGrath et al., Acquir. Immune Defic. Syndr., 8: 379-385, 1995; M. S. McGrath et al., Infectious Causes of Cancer: Targets for Intervention, pp. 231-242, Totowa, NJ: Humana Press, 2000).