Architectural/Environmental Handbook for Extraterrestrial Design

Handbook on environmental and space utilization criteria for design of extraterrestrial manned spacecraft and shelter

Bone marrow transplantation alters the tremor phenotype in the murine model of globoid-cell leukodystrophy

Tremor is a prominent phenotype of the twitcher mouse, an authentic genetic model of Globoid-Cell Leukodystrophy (GLD, Krabbe’s disease). In the current study, the tremor was quantified using a force-plate actometer designed to accommodate low-weight mice. The actometer records the force oscillations caused by a mouse’s movements, and the rhythmic structure of the force variations can be revealed. Results showed that twitcher mice had significantly increased power across a broad band of higher frequencies compared to wildtype mice. Bone marrow transplantation (BMT), the only available therapy for GLD, worsened the tremor in the twitcher mice and induced a measureable alteration of movement phenotype in the wildtype mice. These data highlight the damaging effects of conditioning radiation and BMT in the neonatal period. The behavioral methodology used herein provides a quantitative approach for assessing the efficacy of potential therapeutic interventions for Krabbe’s disease

Cosmic ray tables - Asymptotic directions, variational coefficients and cut-off rigidities IQSY instruction manual no. 10

Cosmic ray deflections in geomagnetic field, variational coefficients, and diurnal intensity variations - table

Invariants of the Haldane-Shastry SU(N)SU(N) Chain

Using a formalism developed by Polychronakos, we explicitly construct a set of invariants of the motion for the Haldane-Shastry $SU(N)$ chain.Comment: 11 pages, UVA-92-0

Proper Sanitization of Broiler and Pullet Houses.

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The effect of anaesthetics on blood perfusion in transplanted mouse tumours.

Rubidium-86, 125I-human serum albumin and 51Cr-labelled red cells have been used to investigate the effects of the anaesthetics Nembutal (pentobarbitone sodium) and urethane on blood perfusion, blood volume and albumin leakage in 5 types of transplanted mouse tumour and in normal organs. Nembutal was found to increase the relative blood perfusion by a factor of 1-3 to 2-0 in tumours and by a factor of 1-7 to 3-0 in kidneys but muscle perfusion fell to 0-3-0-5 that of controls. The effects of urethane were found to be dose dependent, generally in the same direction as for Nembutal, and smaller. Both anaesthetics reduced the blood volume of tumours (except for the C3H mammary carcinoma) and of kidneys by factors of 0-2 to 0-8. The duration of anaesthesia had no effect on the plateau values of relative blood perfusion and blood volume in either tumours or normal organs, but Nembutal delayed slightly the 86Rb uptake and decreased the rate of albumin leakage

Gene identification for the cblD defect of vitamin B12 metabolism

Background Vitamin B12 (cobalamin) is an essential cofactor in several metabolic pathways. Intracellular conversion of cobalamin to its two coenzymes, adenosylcobalamin in mitochondria and methylcobalamin in the cytoplasm, is necessary for the homeostasis of methylmalonic acid and homocysteine. Nine defects of intracellular cobalamin metabolism have been defined by means of somatic complementation analysis. One of these defects, the cblD defect, can cause isolated methylmalonic aciduria, isolated homocystinuria, or both. Affected persons present with multisystem clinical abnormalities, including developmental, hematologic, neurologic, and metabolic findings. The gene responsible for the cblD defect has not been identified. Methods We studied seven patients with the cblD defect, and skin fibroblasts from each were investigated in cell culture. Microcell-mediated chromosome transfer and refined genetic mapping were used to localize the responsible gene. This gene was transfected into cblD fibroblasts to test for the rescue of adenosylcobalamin and methylcobalamin synthesis. Results The cblD gene was localized to human chromosome 2q23.2, and a candidate gene, designated MMADHC (methylmalonic aciduria, cblD type, and homocystinuria), was identified in this region. Transfection of wild-type MMADHC rescued the cellular phenotype, and the functional importance of mutant alleles was shown by means of transfection with mutant constructs. The predicted MMADHC protein has sequence homology with a bacterial ATP-binding cassette transporter and contains a putative cobalamin binding motif and a putative mitochondrial targeting sequence. Conclusions Mutations in a gene we designated MMADHC are responsible for the cblD defect in vitamin B12 metabolism. Various mutations are associated with each of the three biochemical phenotypes of the disorder