Model of ammonia volatilization from calcareous soils

A quantitative model of ammonia volatilization from the calcareous soil uppermost 1-cm layer was developed and tested. The model accounts for the following processes: ammonium-ammonia equilibration in the soil solution, cation exchange between calcium and ammonium which results in ammonium distribution between soil liquid and solid phases, nitrification of dissolved ammonium, distribution of ammonia between liquid and gaseous phases and diffusion of gaseous ammonia in the soil air. The combined effect of various characteristics such as soil pH, cation exchange capacity, water capacity and nitrification rate on ammonia losses from various soil types have been studied. The model was validated against experimental results of ammonia losses from different soils for its use as a predicting tool. The model shows that most of ammonia losses can be explained by the interactive effect of high soil pH and low cation exchange capacity. Computations show increased ammonia volatilization with decreasing soil water capacity. Increasing fertilizer application rate has a small effect on percentage of ammonia losses. Increased nitrification rate and shorter “lag” period of nitrification reduce ammonia losses considerably. Good agreement was obtained between model calculations and experimental results of ammonia volatilization from 13 soils.     

Two-color flow cytometric analysis of monocyte depleted human blood lymphocyte subsets

Peripheral blood mononuclear cells (PBMC) from normal individuals were examined using 16 pairs of FITC and phycoerythrin (PE) directly conjugated monoclonal antibodies. Each pair of reagents was used to evaluate a conventional lymphocyte gate as well as open (non) gate of monocyte depleted PBMC. Parallel studies using the same panel of monoclonal antibodies were carried out on selected, nonmonocyte depleted samples. The major findings of this analysis were that 1,000-1,200 lymphocytes in a 10,000 cell analysis are found outside the lymphocyte gate and of these approximately 2/5 are CD16 positive LGL/NK cells, 2/5 are CD3 positive T cells, and 1/5 are CD19/CD20 positive B cells. Thus, it appears that 10-15% of the lymphoid cells fall outside of the conventional lymphocyte gate, and in certain settings monocyte depletion may be useful to perform more complete evaluation of the total lymphoid cell population obtained after ficoll-hypaque separation.     

Dexamethasone blocks increased leukotriene B4 production during endotoxin-induced lung injury

We hypothesized that leukotriene B4 (LTB4) might be produced during endotoxemia in pigs and, if so, might play a role in the pathophysiology of acute respiratory failure. Escherichia coli endotoxin (055-B5) was infused intravenously into anesthetized pigs at 5 micrograms/kg the 1st h, followed by 2 micrograms.kg-1.h-1 for 3 h. Endotoxemic pigs were treated with dexamethasone (DEX, iv) 18 h (5 mg/kg) and 1 h (5 mg/kg) before onset of endotoxemia. During phases I (i.e., 0-2 h) and II (i.e., 2-4 h), endotoxin decreased cardiac index, caused granulocytopenia, and increased mean pulmonary arterial pressure, pulmonary vascular resistance, alveolar-arterial O2 gradient, and hematocrit. During phase II, plasma LTB4 levels were increased (as determined by radioimmunoassay, reverse-phase high-performance liquid chromatography, and ultraviolet spectroscopy). Endotoxin increased the levels of LTB4 and albumin in bronchoalveolar lavage fluid (BALF). DEX blocked or greatly attenuated the endotoxin-induced hemodynamic abnormalities and blocked the increases in plasma and BALF LTB4 levels. We conclude that LTB4 is produced during porcine endotoxemia and could possibly play a role in the pathophysiology of endotoxin-induced lung injury in anesthetized pigs.     

Phylogeny of Greya (Lepidoptera: Prodoxidae), based on nucleotide sequence variation in mitochondrial cytochrome oxidase I and II: congruence with morphological data

The phylogeny of Greya Busck (Lepidoptera: Prodoxidae) was inferred from nucleotide sequence variation across a 765-bp region in the cytochrome oxidase I and II genes of the mitochondrial genome. Most parsimonious relationships of 25 haplotypes from 16 Greya species and two outgroup genera (Tetragma and Prodoxus) showed substantial congruence with the species relationships indicated by morphological variation. Differences between mitochondrial and morphological trees were found primarily in the positions of two species, G. variabilis and G. pectinifera, and in the branching order of the three major species groups in the genus. Conflicts between the data sets were examined by comparing levels of homoplasy in characters supporting alternative hypotheses. The phylogeny of Greya species suggests that host-plant association at the family level and larval feeding mode are conservative characters. Transition/transversion ratios estimated by reconstruction of nucleotide substitutions on the phylogeny had a range of 2.0-9.3, when different subsets of the phylogeny were used. The decline of this ratio with the increase in maximum sequence divergence among taxa indicates that transitions are masked by transversions along deeper internodes or long branches of the phylogeny. Among transitions, substitutions of A-->G and T-->C outnumbered their reciprocal substitutions by 2-6 times, presumably because of the approximately 4:1 (77%) A+T-bias in nucleotide base composition. Of all transversions, 73%-80% were A<-->T substitutions, 85% of which occurred at third positions of codons; these estimates did not decrease with an increase in maximum sequence divergence of taxa included in the analysis. The high frequency of A<-->T substitutions is either a reflection or an explanation of the 92% A+T bias at third codon positions.      

Argininosuccinic aciduria: prenatal studies in a family at risk.

We have monitored two successive pregnancies in a family which we found to be at risk for argininosuccinic aciduria. We measured argininosuccinic acid (ASA) concentrations in amniotic fluid and utilized an indirect assay of ASA lyase activity in cultured amniotic fluid cells. The assay procedure is based on the uptake of 14C from [14C]citrulline and of [3H]leucine into protein. ASA was easily measured in amniotic fluid from the first fetus at risk, whereas none was detectable in control fluids. Amniotic fluid cells cultured from this fetus had only 5.5% of control ASA lyase activity. The pregnancy was terminated, and hepatic ASA lyase activity in the fetus was shown to be about 1.3% of control values. In addition, eight fetal tissues were analyzed for ASA, and all had significant accumulation. ASA was not detected in amniotic fluid from the second fetus at risk, and ASA lyase activity in cultured cells was 80% of control activity. Enzymatic analysis of erythrocyte lysate confirmed the diagnosis of an unaffected child (ASA lyase = 46% of control) and indicated heterozygosity. Thus, we provide further evidence that argininosuccinic aciduria can be diagnosed successfully in utero by indirect assay of ASA lyase activity in cultured amniotic fluid cells. In addition, high amniotic fluid ASA concentrations provide strong adjunctive evidence for such a prenatal determination, and may prove to be sufficient for diagnosis.