Nickel-cobalt hydroxide nanosheets: Synthesis, morphology and electrochemical properties.

This paper reports the synthesis, characterization, and electrochemical performance of nickel-cobalt hydroxide nanosheets. The hydroxide nanosheets of approximately 0.7nm thickness were prepared by delamination of layered nickel-cobalt hydroxide lactate in water and formed transparent colloids that were stable for months.

Electrochemical performance of cobalt hydroxide nanosheets formed by the delamination of layered cobalt hydroxide in water.

We report the preparation of monometallic Co(2+)/Co(3+) layered double hydroxide, intercalated with lactate anions (LCoH-Lactate), and its spontaneous delamination in water to form cobalt hydroxide nanosheets. These hydroxide nanosheets formed stable aqueous dispersions. The thickness of a nanosheet was estimated to be approximately 1 nm by atomic force microscopy and small angle X-ray scattering experiments, and corresponds to a single hydroxide layer.

Lethal cutaneous disease in transgenic mice conditionally expressing type I human T cell leukemia virus Tax.

Type I human T cell leukemia virus (HTLV-I) is etiologically linked with adult T cell leukemia, an aggressive and usually fatal expansion of activated CD4+ T lymphocytes that frequently traffic to skin. T cell transformation induced by HTLV-I involves the action of the 40-kDa viral Tax transactivator protein. Tax both stimulates the HTLV-I long terminal repeat and deregulates the expression of select cellular genes by altering the activity of specific host transcription factors, including cyclic AMP-responsive element-binding protein (CREB)/activating transcription factor, NF-kappaB/Rel, and serum response factor.

p53 induces NF-kappaB activation by an IkappaB kinase-independent mechanism involving phosphorylation of p65 by ribosomal S6 kinase 1.

Apoptosis induced by p53 has been proposed to involve activation of the transcription factor NF-kappaB. Here we describe the novel molecular mechanism through which p53 and DNA-damaging agents activate NF-kappaB. NF-kappaB induction by p53 does not occur through classical activation of the IkappaB kinases and degradation of IkappaBalpha.

The NF-kappa B-inducing kinase induces PC12 cell differentiation and prevents apoptosis.

NF-kappa B has been implicated in the survival and differentiation of PC12 cells. In this study, we examined the effect of the NF-kappa B-inducing kinase (NIK) on these processes. When inducibly expressed in PC12 cells, a kinase-proficient but not -deficient form of NIK promoted neurite process formation and mediated anti-apoptotic signaling.