Formation and distribution of modified FAD between isozymes of alcohol oxidase in the methylotrophic yeast pichia methanolica

The content of modified FAD (mFAD) in isoforms of alcohol oxidase (AO) in the methylotrophic yeast Pichia methanolica MH4 is increased in the stationary growth phase of the culture or under lower dilution rates. The isoform with slower electrophoretic mobility has the higher mFAD content. The results of in vitro experiments and the occurrence of mFAD in AO-lacking mutants of Hansenula polymorpha DL-1 imply a biosynthetic origin of this cofactor. HPLC analysis of tryptic hydrolysates of the first and the ninth isoforms of AO from P. methanolica MH4 revealed two different types of subunits. Possible mechanism of mFAD formation and distribution between the AO isozymes is discussed.     

Phenotypic and genetic analysis of a variant of human immunodeficiency virus (HIV-1) subtype B, isolated in Russia]

Oral malignant neoplasms are very common in old dogs. The prognosis of oral malignant melanoma (MM) for long-term survival is poor, because of early metastasis and delayed diagnosis. Oral MM in immature dogs is rare. A case of oral MM in an immature dog is described. The diagnostic workup includes radiographs of the tumor and thorax, a cytologic examination of the regional lymph nodes and a biopsy of the tumor. The therapy with the best chance of success is the radical surgical excision of the tumor.     

The effect of short peptides isolated from the brain of a hibernating suslik on the rat EEG and behavior

In the Drosophila embryo, at specific choice points along the major motor nerves, subsets of motor axons defasciculate and then steer into their muscle target regions. Here we describe the analysis of beaten path (beat), a gene required for the selective defasciculation of motor axons at these choice points. In beat mutant embryos, motor axons fail to defasciculate and bypass their targets. This phenotype is suppressed by mutations in FasII and conn, two genes encoding cell adhesion molecules expressed on motor axons, suggesting that beat provides an antiadhesive function. beat encodes a novel secreted protein that is expressed by motoneurons during outgrowth. Rescue and ectopic expression experiments support the model that Beat protein is secreted by motor axons where it functions to regulate their selective defasciculation at specific choice points.     

Modelling DNA damage induced by different energy photons and tritium beta-particles

PURPOSE: To model the production of single- and double-strand breaks (ssb and dsb) in DNA by ionizing radiations. To compare the predicted effectiveness of different energy photon radiations and tritium beta-particles. MATERIALS AND METHODS: Modelling is carried out by Monte Carlo and includes consideration of direct energy depositions in DNA molecules, the production of species, their diffusion and interactions with each other and DNA. Computer-generated electron tracks in liquid water are used to model energy deposition and to derive the initial positions of chemical species. Atomistic representation of the DNA in B form with a first hydration shell is used. Photon radiations in the energy range 70keV-1MeV and tritium beta-particles are considered. RESULTS: A tentative increase for dsb yield has been predicted for 70 keV photons and tritium compared with 137Cs. This increase is more pronounced for complex dsb. Double-strand breaks are much more prone compared with ssb to combine with additional strand breaks and base damage, which contributes to break complexity. At least half of DNA breaks are hydroxyl radical mediated. CONCLUSIONS: The developed model makes predictions compatible with features of available experimental data. Break complexity has to be addressed in biophysical modelling when the relative effectiveness of radiations in DNA damage is studied. Obtained data strongly argue against the dominance of direct radiation action in DNA damage in the cellular environment predicted by some theoretical studies.     

Cluster organization of ion channels formed by the antibiotic syringomycin E in bilayer lipid membranes

The cyclic lipodepsipeptide, syringomycin E, when incorporated into planar lipid bilayer membranes, forms two types of channels (small and large) that are different in conductance by a factor of sixfold. To discriminate between a cluster organization-type channel structure and other possible different structures for the two channel types, their ionic selectivity and pore size were determined. Pore size was assessed using water-soluble polymers. Ion selectivity was found to be essentially the same for both the small and large channels. Their reversal (zero current) potentials with the sign corresponding to anionic selectivity did not differ by more than 3 mV at a twofold electrolyte gradient across the bilayer. Reduction in the single-channel conductance induced by poly(ethylene glycol)s of different molecular weights demonstrated that the aqueous pore sizes of the small and large channels did not differ by more than 2% and were close to 1 nm. Based on their virtually identical selectivity and size, we conclude that large syringomycin E channels are clusters of small ones exhibiting synchronous opening and closing.     

Lethal neonatal autosomal recessive axonal sensorimotor polyneuropathy

Peripheral neuropathy is an uncommon cause of generalized hypotonia and weakness in infancy. It occurs as a part of the clinical syndrome in some neurodegenerative disorders of infancy, but seldom causes respiratory failure or swallowing difficulties. We report a lethal autosomal recessive axonal polyneuropathy with neonatal onset in a large kindred from Northern Mississippi. One patient was studied in detail at our medical center and the information on 12 other affected infants in this large family were gathered from medical records and by interviewing the family members. Patients were symptomatic for the polyneuropathy before birth and died in the first year of life from respiratory complications. Thirteen babies were affected by this clinical phenotype in four generations of this family with a high frequency of consanguinity. Affected babies were of both sexes and were born to healthy consanguineous parents. The clinical phenotype of polyneuropathy in our index patient and other affected babies in this family was similar, and represents a unique form of hereditary neonatal polyneuropathy.