Thermoregulatory control during pregnancy and lactation in rats

Eliason, Heather L., and James E. Fewell.Thermoregulatory control during pregnancy and lactation in rats.J. Appl. Physiol. 83(3): 837-844, 1997.Although the mechanisms remain unknown, maternal coretemperature (T_c) decreases nearterm of pregnancy and is increased throughout lactation in rats. Thepurpose of our present experiments was to determine whether pregnancy and lactation shift the thermoneutral zone of rats and to investigate whether the changes in maternal T_cduring pregnancy and lactation result from "forced" or"regulated" thermoregulatory responses. Conscious, chronicallyinstrumented nonpregnant and pregnant and lactating rats were studiedboth in a thermocline (a chamber with a linear temperature gradientfrom 12 to 36°C) and in a metabolic chamber to determine theinfluence of pregnancy and lactation on selected ambient temperature aswell as the thermoregulatory response to changes in ambienttemperature. We found that selected ambient temperature, oxygenconsumption, and thermal conductance did not change in rats studied ina thermocline as T_c decreased nearterm of pregnancy. There was, however, a downward shift in thethermoneutral zone of rats studied in a metabolic chamber near term ofpregnancy. During lactation, selected ambient temperature decreased inrats studied in a thermocline as oxygen consumption andT_c increased. The thermoneutralzone of lactating rats was not different from that of nonpregnantanimals. Thus our data provide evidence that the decrease inT_c near term of pregnancy in ratsresults from a regulated thermoregulatory response,whereas the increase in T_c duringlactation results from a forced thermoregulatory response.

     

Oxidation of Indole-3-acetic Acid and Oxindole-3-acetic Acid to 2,3-Dihydro-7-hydroxy-2-oxo-1H Indole-3-acetic Acid-7′-O-β-d-Glucopyranoside in Zea mays Seedlings

Radiolabeled oxindole-3-acetic acid was metabolized by roots, shoots, and caryopses of dark grown Zea mays seedlings to 2,3-dihydro-7-hydroxy-2-oxo-1H indole-3-acetic acid-7′-O-β-d-glycopyranoside with the simpler name of 7-hydroxyoxindole-3-acetic acid-glucoside. This compound was also formed from labeled indole-3-acetic acid supplied to intact seedlings and root segments. The glucoside of 7-hydroxyoxindole-3-acetic acid was also isolated as an endogenous compound in the caryopses and shoots of 4-day-old seedlings. It accumulates to a level of 4.8 nanomoles per plant in the kernel, more than 10 times the amount of oxindole-3-acetic acid. In the shoot it is present at levels comparable to that of oxindole-3-acetic acid and indole-3-acetic acid (62 picomoles per shoot). We conclude that 7-hydroxyoxindole-3-acetic acid-glucoside is a natural metabolite of indole-3-acetic acid in Z. mays seedlings. From the data presented in this paper and in previous work, we propose the following route as the principal catabolic pathway for indole-3-acetic acid in Zea seedlings: Indole-3-acetic acid → Oxindole-3-acetic acid → 7-Hydroxyoxindole-3-acetic acid → 7-Hydroxyoxindole-3-acetic acid-glucoside.     

Twins and Q-banded chromosome polymorphisms

Summary Q-banded chromosomal analyses were performed on 24 pairs of twins to determine the stability and heritability of chromosome polymorphisms, and to establish the use of these markers in the determination of twin zygosity. Sixteen twin pairs were determined monozygotic by chromosome polymorphism analysis and confirmed monozygotic by blood group genotyping. No two genetically distinct individuals had the same polymorphic pattern, suggesting the individuality of each morphological karyotype. The frequencies for the various types of chromosome polymorphisms, including stalk length variations, were determined. Analysis of frequency distribution for variant combinations showed random association.     

Structure and Barr body formation of an Xp + chromosome with two inactivation centers.

A patients with seizures, Von Willebrand disease, and symptoms of Turner syndrome was a chromosomal mosaic. In blood culture (1974), 56% of the cells were 45, X 33% 46, XXp+ and 11% 47,XXp + Xp +; in the skin, no cells with 47 chromosomes were found. Presumably the Xp + chromosome arose through a break in the Q-banded dark region next to the centromere on Xp to which an Xq had been attached. The abnormal X was late-labeling and formed a larger than normal Barr body. Of the chromatin-positive fibroblasts, 18.2% showed bipartite Barr bodies, which agrees with the hypothesis that the X inactivation center lies on the proximal part of the Xq. On the basis of the structure and behavior of the bipartite bodies in the present patient, as compared to those formed by other chromosomes with two presumed inactivation centers, we propose that the dark region next to the centromere of Xp remains active in the inactive X. In cells with 45,X and 46,XY, this region has the same relative size, whereas it is significantly shorter in the active X of three females, including the present patient, with one abnormal X. We propose that this region on the active X reveals different states of activity, as reflected in its length, depending on how many other X chromosomes are in the cell.     

A Comparison of Purified Host Specific Toxin from Helminthosporium maydis, Race T, and Its Acetate Derivative on Oxidation by Mitochondria from Susceptible and Resistant Plants

NADH or succinate oxidation and malate oxidation were differentially affected in mitochondria from both susceptible and resistant corn by a purified and chemically characterized preparation of host-specific toxin from Bipolaris (Helminthosporium) maydis, race T. NADH and succinate oxidation by susceptible T corn mitochondria were stimulated 50 to 200% with apparent uncoupling from the cytochrome chain at approximately 10(-9)m toxin (5 to 20 ng/ml). Significant inhibition of malate oxidation was observed at slightly higher toxin concentrations, but oxidation was still coupled to ADP utilization. Inhibition of malate oxidation also was observed in N corn (resistant) and soybean mitochondria at approximately 1,000-fold greater concentrations, but stimulation of NADH and succinate oxidation was not found at any toxin concentration tested.A fully acetylated toxin derivative at approximately 1 microgram per milliliter also caused stimulation of NADH or succinate oxidation in T corn mitochondria, but not those of N corn or soybean mitochondria at 100 micrograms per milliliter. Malate oxidation was inhibited to the same extent by toxin acetate with mitochondria from T corn, N corn, and soybean. The blocking of hydroxyl groups in race T toxin by acetyl functions eliminated selectivity toward malate oxidation only. The data suggest that inhibition of malate oxidation is either a separate or secondary effect of selective action of toxin on T corn mitochondria, perhaps by interference with transport in or out of the matrix. Sensitivity of T, but not N, corn mitochondria to purified toxin decays within minutes after pellets are suspended in aqueous osmotica, with no obvious change in mitochondrial integrity. The action of race T toxin seems to involve a labile process, such as ion gradient(s), or an unstable structural conformation of T corn mitochondria.     

Alkylxanthines: inhibition of adenosine-elicited accumulation of cyclic AMP in brain slices and of brain phosphodiesterase activity.

A series of 1, 3-dialkylxanthines was examined as antagonists of adenosine-induced accumulation of cyclic AMP in guinea pig cerebral cortical slices and as inhibitors of brain phosphodiesterases. The order of potency as adenosine-antagonists was: 8-phenyltheophylline (IC₅₀ 6 μM) > 1, 3-dibutylxanthine (IC₅₀ 30 μM), 1, 3-dipropylxanthine > theophylline (IC₅₀ 60 μM), 3-isobutyl-1-methylxanthine (IBMX), 1, 3, 7-triethylxanthine > 7-benzyl IBMX (IC₅₀ 100 μM), 8-methyl IBMX > 7-benzyl-8-bromo IBMX, 9-methyl IBMX, 8-bromo IBMX, 1-isoamyl-3-isobutylxanthine. The order of potency as inhibitors of brain calcium-dependent phosphodiesterase was: 7-benzyl IBMX (IC₅₀ 1.5 μM), 7-benzyl-8-bromo IBMX > 8-methyl IBMX (IC₅₀ 4.5 μM) > IBMX (IC₅₀ 7.5 μM), 8-bromo IBMX > 9-methyl IBMX (IC₅₀ 40 μM), 1, 3, 7-triethylxanthine > 1, 3-dibutylxanthine (IC₅₀ 100 μM), 1-isoamyl-3-isobutylxanthine > theophylline. 8-Phenyltheophylline and 1, 3-dibutylxanthine represented potent adenosine-antagonists with relatively low activity as phosphodiesterase inhibitors whereas 7-benzyl IBMX and 7-benzyl-8-bromo-IBMX were potent inhibitors of the calcium-dependent phosphodiesterase with relatively low activity as adenosine-antagonists. None of the compounds were potent inhibitors of the brain calcium-independent phosphodiesterase, although 1-isoamyl-3-isobutylxanthine might prove useful as an inhibitor of this enzyme because of its very low activity as an adenosine-antagonist.     

Dominant and recessive informational suppressors of a missense mutation in Coprinus

Summary Twenty-one suppressor gene mutations which suppress the met-5.1 missense mutation of Coprinus were separated into six groups (A-F) on the basis of dominance or recessiveness, linkage to the met-5 locus, comlementation in heterozygous cells and growth behaviour. The actual number of suppressor loci could not be determined because crosses between suppressed mutants were inviable. The allele specificity of group A, C, D and F suppressors was confirmed by appropriate crosses. Group B and E suppressors were not tested because of close linkage to the met-5 locus. No evidence for functional suppression of met-5 mutations was obtained thus it is likely that all the suppressors cause translational corelation of met-5.1. Suppressors in four groups (C-F) have properties expected of tRNA structural gene mutations: the group C mutation is dominant, the other mutations are recessive but do not complement in heterozygous cells. The relative efficiencies of the tRNA species involved was assessed by comparing the degree to which the different sup ⁺ mutations depressed the growth rate on methionine supplemented medium. The dominant mutation depressed growth to the greatest extent and is, therefore, the most efficient suppressor. The least efficient suppressors did not depress growth at all. When growth was compared on minimal medium it was found that the more efficient the suppressor the less well it restored growth. The mutations in groups A and B depressed growth more than the tRNA mutations but affect some other component in translation because they are recessive and complement normally. It is suggested that they may act to alter tRNA modifying enzymes.     

Long term effect on mortality of stopping smoking after unstable angina and myocardial infarction.

Subjects who stop smoking cigarettes after myocardial infarction have an improved rate of survival compared with those who continue, but to date it was not known whether the benefit persisted for more than six years. A total of 498 men aged under 60 years who had survived a first episode of unstable angina or myocardial infarction by two years were followed up by life table methods for a further 13 years. Mortality in those who continued to smoke was significantly higher (82.1%) than in those who stopped smoking (36.9%). These differences increased with time. Mortality in those who were non-smokers initially and who continued not to smoke was intermediate (62.1%). The adverse effect of continued smoking was most pronounced in those with unstable angina. Continuing to smoke increased the rate of sudden death to a greater degree in those with less severe initial attacks, while the effect of smoking on fatal reinfarctions was most apparent in those with a more complicated presentation. These findings suggest that stopping cigarette smoking is the most effective single action in the management of patients with coronary heart disease.