Studies on the phospholipid composition of pathogenic cell membranes of Mycoplasma hyopneumoniae

The membrane phospholipid and fatty acid compositions of Mycoplasma hyopneumoniae, a pathogen of porcine enzootic pneumoniae isolated in China, was studied by thin-layer chromatography and gas chromatography. The results showed that membrane phospholipids consisted predominantly of diphosphatidylglycerol. The percentage of C16 - C18 fatty acids comprised 79% of the total fatty acids, of which oleic acid as well as palmitic acid are the major fatty acids. Some differences were shown in fatty acid composition as compared with membranes of other species of Mycoplasma.     

Biosynthesis of monensins a and b: the role of isoleucine

Isoleucine added to the cultivation medium of Streptomyces cinnamonensis C-100-5 induced a relative increase of the production of monensin B at the expense of monensin A. U-14C-Isoleucine was found not to be a specific monensin B precursor. The incorporation of 1-13C-2-methylbutyrate into monensins A and B showed the label to be evenly incorporated in both products at carbon atoms originating from C(1) of propionate. In regulatory mutants insensitive to 2-amino-3-chlorobutyrate isoleucine influenced the production of monensins only slightly but strains resistant to 2-aminobutyrate and norleucine decreased their total production by 2-12% in the presence of isoleucine which was associated with a decrease of monensin A content by 14-52%. The inhibitory effect of isoleucine on the biosynthesis of valine, a specific precursor of the butyrate unit of monensin A, is discussed.     

Characteristics of the saprophytic reference strain FA ofClaviceps paspali

Growth properties and morphological features of the saprophytic collection cultureClaviceps paspali strain FA were investigated. The strain was characterized by a range of utilization of 13 carbon sources in a basic synthetic and a peptone medium. A temperature of 23 °C was more favourable for growth than 28 °C. Stages of changes of the culture cultivated for a long time on Sabouraud’s medium were detected by electron microscopy. The white culture was characterized by true septated mycelium with different types of terminal parts of hyphae. Arthrospores occurred after a 14-d cultivation, small spherical conidia released individually from hyphae were quite rare. As compared with other strains of the same species, strain FA did not form spherical clusters of conidia. On the other hand, a spontaneous rupture of the surface cell wall in different parts of hyphae and release of the cytoplasm were observed. In corn-steep containing media the formation of individual, pair and chain-like forms of arthritic conidia was stimulated. Destructive autolytic changes of hyphae were detected in the medium with potato extract.     

Saprophytic production of Clavine alkaloids and activity of Hydroxymethylglutaryl-CoA reductase

In submerged Claviceps cultures the activity of hydroxymethylglutaryl-CoA reductase preceded the increase of alkaloid production and of sterol content. During the first alkaloid phase, cell mevalonate was involved in the biosynthesis of both alkaloids and steroids. In the second production phase, it was predominantly used for alkaloid synthesis. Hydroxymethylglutaryl-CoA reductase appears to be a suitable target for physiological manipulation to increase clavine alkaloid yields.     

Amiodarone inhibits T4 to T3 conversion and alpha-glycerophosphate dehydrogenase and malic enzyme levels in rat liver

Amiodarone has been found to decrease serum T3 by blocking peripheral T4 5'-deiodinase. This reduction in T3 levels may contribute to the effectiveness of this drug in moderating cardiac arrhythmias. To further characterize the effect of amiodarone on thyroid hormone metabolism and biological action, male Sprague-Dawley rats were thyroidectomized and then fed 500 ug T4 or 50 ug T3 and 500 mg amiodarone/kg of powdered diet for 6 to 8 weeks. Hepatic and cardiac levels of T4, T3, alpha-glycerophosphate dehydrogenase (GPD) and malic enzyme (ME) were used as indicators of thyroid hormone availability and action at the cellular level. Conversion of T4 to T3 was measured in liver homogenates. Serum TSH, T4 and T3 were also measured. Amiodarone reduced hepatic GPD and ME in thyroidectomized rats receiving dietary T4. Liver T4 levels were significantly increased by amiodarone and the T3/T4 ratio was reduced (P less than .05). Amiodarone inhibited hepatic T4 to T3 conversion and decreased serum T3. The decreased T3 action at the cellular level, indicated by the reduction in hepatic GPD and ME, is not due to pharmacologic effects of amiodarone since these enzyme levels were not affected by amiodarone in thyroidectomized rats replaced with T3.     

Morphine induced thyroxine release from rat thyroid gland in vitro

Male rat thyroid glands were incubated for two hours in Krebs-Ringer bicarbonate buffer with different amounts of morphine and/or naloxone. Five micrograms/ml morphine produced a significant increase in the T4 concentration of incubation medium, and resulted in an accumulation of cAMP in the tissue. Naloxone did not change the T4 release but its incubation with morphine prevented the morphine-induced changes. Similarly, naloxone inhibited the morphine-induced accumulation of cAMP in the thyroid tissue.     

Subregional assignment of the linked marker G8 (D4S10) for Huntington disease to chromosome 4p16.1-16.3.

The linked DNA marker for Huntington disease has recently been mapped to the short arm of chromosome 4 by somatic cell hybridization studies. Southern blot analysis of DNA from patients with Wolf-Hirschhorn syndrome (WHS) has suggested that the linked marker maps within the terminal 4p16 band. We have now accomplished subregional assignment of G8 (D4S10) to 4p16.1-16.3 using in situ hybridization techniques on two patients with nonoverlapping interstitial deletions of 4p. The mapping of G8 (D4S10) to a region deleted in patients with WHS will allow the application of new strategies for detecting DNA sequences closer to the locus for Huntington disease.     

Paternal age and the occurrence of birth defects

The association between paternal age and the occurrence of birth defects was studied using data collected in Metropolitan Atlanta. Paternal-age information for babies born with defects was obtained from birth certificates, hospital records, and interviews with mothers; for babies born without defects, the information was obtained from birth certificates. Several statistical techniques were used to evaluate the paternal-age-birth-defects associations for 86 groups of defects. Logistic regression analysis that controlled for maternal age and race indicated that older fathers had a somewhat higher risk for having babies with defects, when all types of defects were combined; an equivalent association for older mothers was not found. Logistic regression analyses also indicated modestly higher risks for older fathers for having babies with ventricular septal defects and atrial septal defects and substantially higher risks for having babies with defects classified in the category chondrodystrophy (largely sporadic achondroplasia) and babies with situs inversus. An association between elevated paternal age and situs inversus has not been reported before; the magnitude of the estimated increased risk for situs inversus was about the same as that found in this study for chondrodystrophy.     

The relationship between maternal age and chromosome size in autosomal trisomy.

The pattern of maternal age-specific incidence of autosomal trisomy in spontaneous abortions was examined for each chromosome for which a sufficient number of trisomies was observed. This included chromosomes 2, 4, 7-10, 13-16, 18, and 20-22. The rate of increase after age 30 for each of the small chromosomes (groups D-G) was similar, with the exception of chromosome 16, which showed a significantly shallower rate. The C group chromosomes tended to have an intermediate rate of increase after age 30, with the exception of chromosome 7, which had a pattern similar to the smaller chromosomes. The larger chromosomes (2 and 4) had the smallest rate of increase. There was a significant relationship between chromosome size and rate of increase after age 30 (after excluding chromosome 16), but not with rate of increase before age 30. The results suggest that autosomal trisomies may be of heterogeneous origin, with a maternal age-related factor associated with chromosome size and other sources unrelated to chromosome size. Additional evidence for and against this hypothesis is discussed.