[Mechanism of biosynthesis of fatty acids].
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Biomedical subjects
Publications and source records attributed to E Schweizer.
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The trifunctional FAS2 gene encoding subunit alpha of the Saccharomyces cerevisiae fatty acid synthetase complex was mapped on the left arm of chromosome XVI 24 centimorgans proximal to GAL4 and 39 centimorgans distal to PEP4 relative to the centromere. Mapping was achieved by three independent methods: meiotic co-segregation of FAS2 and ARO7 in recombination-deficient spo11-mutants: tetrad analysis of crosses between FAS2, GAL4 and PEP4; and Southern hybridization of purified FAS2 DNA with individual yeast chromosomes separated by pulsed-field gel electrophoresis.
The Saccharomyces cerevisiae nuclear gene MRP-L6 was cloned by complementation of the respiratory-deficient mutant pet-ts 2523 with a library of wild-type yeast genomic DNA. The isolated gene was part of a 3.8-kb sequenced DNA fragment containing, in addition to MRP-L6, two unassigned reading frames, ORF1 and ORF2. MRP-L6 codes for a basic protein of 205 amino acids and a molecular mass of 22.8 kDa. The protein exhibits significant sequence similarity to the ribosomal protein L6 of bacteria and chloroplasts. Unlike the corresponding bacterial proteins, however, the MRP-L6 protein (MRP-L6p) contains at its N-terminus a 16 amino-acid leader sequence exhibiting the known characteristics of mitochondrial import signals. Disruption of MRP-L6 leads to the phenotype of a mitochondrial translation-defective, rho-negative yeast mutant. The results are consistent with MRP-L6p representing an essential component of yeast mitochondrial ribosomes. Expression of MRP-L6 was examined, under conditions of glucose repression and derepression, in wild-type cells and in a series of catabolite repression-defective yeast mutants. In most cases, a distinct though small influence of the carbon source on the expression of an MRP-L6/lacZ reported construct was observed.
The recently developed Tridimensional Personality Questionnaire (TPQ) was used to examine personality correlates in women diagnosed with premenstrual syndrome (PMS). The hypotheses were that the TPQ scores, specifically harm avoidance (HA), would be higher in PMS subjects than in the general population but lower than in depressed populations because major mood disorder is an exclusion from the PMS diagnosis; harm avoidance would have the strongest association with PMS, but other TPQ factors might characterize nondysphoric subgroups in the PMS population. The sample included 157 women who sought medical treatment and met clearly defined criteria for PMS. Two comparison groups of age-matched women with major depression (MDD, N = 20) and premenstrual exacerbation of major depression (MDD + PMS, N = 24) were also evaluated. TPQ scores were significantly higher for PMS subjects on all three dimensions compared with external normative TPQ data. The TPQ dimensions of HA and novelty seeking (NS) were modestly correlated with the premenstrual symptom scores. The HA dimension correlated with premenstrual depression and physical aches; high NS scores correlated with premenstrual food cravings, headache, and mood swings. As hypothesized, the HA scores were significantly higher in the comparison groups diagnosed with major depression; the NS and reward dependence (RD) dimensions did not differ between the PMS and MDD groups. PMS was associated with only modest nonnormative personality correlates, as assessed by the TPQ. Elevations of the HA and NS dimensions were associated with a tendency for the PMS to present with specific symptom patterns: depressive symptoms for the HA factor and food cravings and mood swings for the NS factor. Further research employing other assessment methods is needed to confirm these findings.
BACKGROUND: Total parenteral nutrition (TPN) is associated with intestinal atrophy and dysfunction possibly attributed to the absence of the nonessential amino acid glutamine from commercially available TPN solutions because of the instability of the monoamino acid during heat sterilization and storage. The use of stable dipeptides may overcome this problem. In this study we tested the hypothesis that glutamine dipeptide supplementation with alanyl-L-glutamine during TPN for 10 days would reverse small bowel atrophy and TPN-induced dysfunction in rats. METHODS: A conventional TPN solution (250 kcal/kg bw) was compared with an isocaloric and isonitrogenous TPN supplemented with alanyl-L-glutamine dipeptide. A food-fed control group was included (n = 6 each group). Jejunum mucosal architecture, absorption of water and glucose, and disaccharidase activity of maltase and alkaline phosphatase were evaluated. RESULTS: TPN-induced villous atrophy, significantly reduced absorption rate, and decreased activity of villous enzymes, compared with the TPN group, could be reversed by supplementation of glutamine dipeptide alanyl-L-glutamine to parenteral nutrition solutions with no difference to the control group. CONCLUSIONS: Glutamine dipeptide-enriched parenteral nutrition preserves mucosal structure and reversed atrophy-associated dysfunction.