Relax promotes ectopic neuronal differentiation in Xenopus embryos

We previously isolated a novel rat cDNA encoding a basic helix–loop–helix transcription factor named Relax, whose expression in the developing central nervous system is strictly limited to discrete domains containing precursor cells. The timing of Relax expression coincides with neuronal differentiation. To investigate the involvement of Relax in neurogenesis we tested whether Relax activated neural genes in the ectoderm by injecting Relax RNA into Xenopus embryos. We demonstrate that ectopic Relax expression induces a persistent enlargement of the neural plate and converts presumptive epidermal cells into neurons. This indicates that Relax, when overexpressed in Xenopus embryos, has a neuronal fate-determination function. Analyses both of Relax overexpression in the frog and of the distribution of Relax in the rat neural tube strongly suggest that Relax is a neuronal fate-determination gene.

Characterization of the stable L-arginine-derived relaxing factor released from cytokine-stimulated vascular smooth muscle cells as an NG-hydroxyl-L-arginine-nitric oxide adduct.

The nature of an L-arginine-derived relaxing factor released from vascular smooth muscle cells cultured on microcarrier beads and stimulated for 20 h with interleukin 1 beta was investigated. Unlike the unstable relaxation elicited by authentic nitric oxide (NO) in a cascade superfusion bioassay system, the effluate from vascular smooth muscle cells induced a stable relaxation that was susceptible to inhibition by oxyhemoglobin. Three putative endogenous NO carriers mimicked this stable relaxing effect: S-nitroso-L-cysteine, low molecular weight dinitrosyl-iron complexes (DNICs), and the adduct of NG-hydroxy-L-arginine (HOArg) with NO. Inactivation of S-nitroso-L-cysteine by Hg2+ ions or trapping of DNICs with agarose-bound bovine serum albumin abolished their relaxing effects, whereas that of the vascular smooth muscle cell effluate remained unaffected. In addition, neither S-nitrosothiols nor DNICs were detectable in the effluate from these cells, as judged by UV and electron spin resonance (ESR) spectroscopy. The HOArg-NO adduct was instantaneously generated upon reaction of HOArg with authentic NO under bioassay conditions. Its pharmacological profile was indistinguishable from that of the vascular smooth muscle cell effluate, as judged by comparative bioassay with different vascular and nonvascular smooth muscle preparations. Moreover, up to 100 nM HOArg was detected in the effluate from interleukin 1 beta-stimulated vascular smooth muscle cells, suggesting that sufficient amounts of HOArg are released from these cells to spontaneously generate the HOArg-NO adduct. This intercellular NO carrier probably accounts for the stable L-arginine-derived relaxing factor released from cytokine-stimulated vascular smooth muscle cells and also from other NO-producing cells, such as macrophages and neutrophils.

Otuz iki esnafnıng birbiri ile köp talaşkanı

In Eastern Turkic (Arabic script).

Sudo chŏnsŏ : chʻojŏng /

Mode of access: Internet.

Samut sathiti rāi pī khō̜ng prathet Thai = Statistical yearbook, Thailand

Mode of access: Internet.

Thống kê niên giám Việt-nam /

Mode of access: Internet.

Taò te Kīng : aus dem chinesischen ins deutsche /

Translation of Tao-te ching.

Phlēng yāo konlabot læ konlaʻaksō̜n : tǣng čhārưk thī Wat Phrachētuphon nai ratchakān thī 3.

Introduction by Prince Damrong: p. (1)-(32).

Talēng phāi /

At head of title: Bǣp sō̜n ʻān čhintakrawī niphon.

Jahāngīrʹnāmah /

Poems.

Nu-gu-mo-nun O-je-boa an-oad Ge-ë-se-uü-ne-gu-noo-du-be-üng ...

Preface signed J. Stinson.

Die politiker : Komödie in füng Aufzügen. Umschlag von Ernest Inch /

Mode of access: Internet.

Reanalysis of the effect of proposals to relax vehicle emission standards on Chicago air quality : three reports and a summary.

"April, 1982."

Kajŏng samsipillyŏn Imja Sama pangmok.

Photocopy of the movable type (Ŭrhaeja) ed. in the Mansong Kim Wan-sŏp munʾgo in the Korea University Library, Seoul, Korea.