Polyethylene glycol matrix reduces the rates of photochemical and thermal release of nitric oxide from S-nitroso-N-acetylcysteine

S -nitrosothiols have many biological activities and may act as nitric oxide (NO) carriers and donors, prolonging NO half-life in vivo. In spite of their great potential as therapeutic agents, most S -nitrosothiols are too unstable to isolate. We have shown that the S -nitroso adduct of N -acetylcysteine (SNAC) can be synthesized directly in aqueous and polyethylene glycol (PEG) 400 matrix by using a reactive gaseous (NO/O₂) mixture. Spectral monitoring of the S–N bond cleavage showed that SNAC, synthesized by this method, is relatively stable in nonbuf-fered aqueous solution at 25°C in the dark and that its stability is greatly increased in PEG matrix, resulting in a 28-fold decrease in its initial rate of thermal decomposition. Irradiation with UV light (λ= 333 nm) accelerated the rate of decomposition of SNAC to NO in both matrices, indicating that SNAC may find use for the photogeneration of NO. The quantum yield for SNAC decomposition decreased from 0.65 ± 0.15 in aqueous solution to 0.047 ± 0.005 in PEG 400 matrix. This increased stability in PEG matrix was assigned to a cage effect promoted by the PEG microenvironment that increases the rate of geminated radical pair recombination in the homolytic S–N bond cleavage process. This effect allowed for the storage of SNAC in PEG at −20°C in the dark for more than 10 weeks with negligible decomposition. Such stabilization may represent a viable option for the synthesis, storage and handling of S -nitrosothiol solutions for biomedical applications.     

Nickel carbonyl adsorption on the Ni(111) surface

Overlayers formed by the adsorption of Ni(CO)₄ in CO on the Ni(111) surface at 100 K were characterized using high resolution electron energy loss spectroscopy and thermal desorption spectroscopy. At temperatures below 135 K, molecular nickel carbonyl adsorbs on the CO saturated Ni(111) surface as suggested by several observations. Vibrational transitions characteristic of molecular Ni(CO)₄ are dominant. The energy dependence of both the elastic and inelastic electron scattering cross sections are dramatically altered by Ni(CO)₄ adsorption. All of the mass spectrometer ionization fragments typical of molecular Ni(CO)₄ are observed in the narrow thermal desorption peak at 150 K. The inelastic scattering cross sections for both adsorbed nickel carbonyl and adsorbed CO on the Ni(111) surface suggest that a nonresonant dipole scattering mechanism is dominant.     

New high permittivity tetragonal tungsten bronze dielectrics Ba2LaMNb4O15: M=Mn, Fe

The new phases Ba₂LaMNb₄O₁₅: M=Mn, Fe were prepared by solid state reaction at 1100 °C. They have the tetragonal tungsten bronze structure, space group P4/mbm, at room temperature. The two octahedral sites show partial order of M and Nb with preferential occupancy of the smaller B(1) sites by M. Both phases have high permittivities 90±15 over the range 10-320 K. Ba₂LaFeNb₄O₁₅ is highly insulating with bulk conductivity ?10⁻⁸ ohm⁻¹ cm⁻¹ at 25 °C and tan δ?0.001 over the range 100-320 K and at 10⁵ Hz. Solid solutions between these new phases and the compositionally and structurally related relaxor ferroelectric Ba₂LaTi₂Nb₃O₁₅ show gradual loss of ferroelectric behaviour attributed to replacement of polarisable Ti⁴⁺ by a mixture of (Mn, Fe)³⁺ and Nb⁵⁺.     

Conservation of position and exclusive expression of mouse Xist from the inactive X chromosome

X-chromosome inactivation in mammals is a regulatory phenomenon whereby one of the two X chromosomes in female cells is genetically inactivated, resulting in dosage compensation for X-linked genes between males and females. In both man and mouse, X-chromosome inactivation is thought to proceed from a single cis-acting switch region or inactivation centre (XIC/Xic). In the human, XIC has been mapped to band Xq13 (ref. 6) and in the mouse to band XD (ref. 7), and comparative mapping has shown that the XIC regions in the two species are syntenic. The recently described human XIST gene maps to the XIC region and seems to be expressed only from the inactive X chromosome. We report here that the mouse Xist gene maps to the Xic region of the mouse X chromosome and, using an interspecific Mus spretus/Mus musculus domesticus F1 hybrid mouse carrying the T(X;16)16H translocation, show that Xist is exclusively expressed from the inactive X chromosome. Conservation between man and mouse of chromosomal position and unique expression exclusively from the inactive X chromosome lends support to the hypothesis that XIST and its mouse homologue are involved in X-chromosome inactivation.