Predicting chlorophyll vertical distribution in response to epilimnetic nutrient enrichment in small stratified lakes

Light-limited metalimnetic phytoplankton communities are thoughtto be negatively impacted by epilimnetic nutrient enrichmentbecause of shading by increased epilimnetic phytoplankton biomass.We tested this expectation with a dynamic simulation model thatwas calibrated to three lakes undergoing whole-lake nutrientand food web manipulations. Total areal chlorophyll increaseddue to nutrient enrichment in each lake, but the magnitude ofthe response varied between lakes. Modeling experiments, whichallowed analysis of separate components of each lake's responseto nutrient enrichment, indicated that the response to enrichmentdepended on lake water color and food web structure. In weaklystained lakes ({small tilde}10 mg Pt 1^–1, k₄ = 0.4 m^–1),metalimnetic chlorophyll was stimulated by nutrient enrichmentup to moderate levels (1 µg Pt1^–1 day^–1).In more strongly colored lakes (25 mg Pt 1^–1, k₄ = 1.0),metalimnetic chlorophyll responded negatively to nutrient enrichmentat all P loading rates. Food web structure, as expressed byrates of zooplanktivory, interacted with water color in twoways. One impact was through direct grazing losses on metalimneticchlorophyll. The other process involved was indirect impactfrom grazing on epilimnetic phytoplankton, which reduced shadingon metalimnetic chlorophyll. Vertical redistribution of chlorophyllbetween the epilimnion and the metalimnion led to little accumulationof areal chlorophyll with increased P loading over limited rangesof water color and nutrient input rates. Model predictions maybe most effectively tested with whole-lake experiments contrastingfood web structure, water color and nutrient loading.     

Experimental Oesophagostomum dentatum infection in the pig: Worm populations resulting from single infections with three doses of larvae

This report describes the effect of different dose levels of infection upon worm burdens and development and fecundity of the parasites. Three groups each of 40, 9-week-old, helminth naïve pigs were inoculated once with either 2000 (group A), 20,000 (group B), or 200,000 (group C) infective third stage larvae of Oesophagostomum dentatum. Subgroups of 5 pigs from each major group were killed 3, 6, 11, 14, 18, 25, 34 and 47 days post inoculation (p.i.) and the large intestinal worm burdens were determined. Faecal egg counts were determined at frequent intervals after day 13 p.i. There were no overt clinical signs of gastrointestinal helminthosis during the experiment. Faecal egg counts became positive in groups A and B at around day 19 p.i., whereas most pigs in the high dose group C did not have positive egg counts until day 27–33 p.i. and some pigs remained with zero egg counts until the end of the study. Throughout the experiment the worm populations in group C consisted mainly of immature larval stages, while those in groups A and B were predominantly adult stages after days 14–18. Adult worms from the low dose group A were significantly longer than those from group C. At high population densities, stunted development of worms and reduced fecundity among female worms were found. Furthermore, there was a tendency for the distribution of the worms within the intestine to be altered with increasing population size.     

Restriction Fragment Length Polymorphism Mapping of Quantitative Trait Loci for Malaria Parasite Susceptibility in the Mosquito Aedes Aegypti

Susceptibility of the mosquito Aedes aegypti to the malarial parasite Plasmodium gallinaceum was investigated as a quantitative trait using restriction fragment length polymorphisms (RFLP). Two F(2) populations of mosquitoes were independently prepared from pairwise matings between a highly susceptible and a refractory strain of A. aegypti. RFLP were tested for association with oocyst development on the mosquito midgut. Two putative quantitative trait loci (QTL) were identified that significantly affect susceptibility. One QTL, pgs[2,LF98], is located on chromosome 2 and accounted for 65 and 49% of the observed phenotypic variance in the two populations, respectively. A second QTL, pgs[3,MalI], is located on chromosome 3 and accounted for 14 and 10% of the observed phenotypic variance in the two populations, respectively. Both QTL exhibit a partial dominance effect on susceptibility, wherein the dominance effect is derived from the refractory parent. No indication of epistasis between these QTL was detected. Evidence suggests that either a tightly linked cluster of independent genes or a single locus affecting susceptibility to various mosquito-borne parasites and pathogens has evolved near the LF98 locus; in addition to P. gallinaceum susceptibility, this general genome region has previously been implicated in susceptibility to the filarial nematode Brugia malayi and the yellow fever virus.     

The Triplo-Lethal Locus of Drosophila: Reexamination of Mutants and Discovery of a Second-Site Suppressor

In the genome of Drosophila melanogaster there is a single locus, Triplo-lethal (Tpl), that causes lethality when present in either one or three copies in an otherwise diploid animal. Previous attempts to mutagenize Tpl produced alleles that were viable over a chromosome bearing a duplication of Tpl, but were not lethal in combination with a wild-type chromosome, as deficiencies for Tpl are. These mutations were interpreted as hypomorphic alleles of Tpl. In this work, we show that these alleles are not mutations at Tpl; rather, they are dominant mutations in a tightly linked, but cytologically distant, locus that we have named Suppressor-of-Tpl (Su(Tpl)). Su(Tpl) mutations suppress the lethality associated with three copies of the Triplo-lethal locus and are recessive lethal. We have mapped Su(Tpl) to the approximate map position 3-46.5, within the cytological region 76B-76D.     

Change in social status and risk of low birth weight in Denmark: population based cohort study.

OBJECTIVE: To estimate the risk of having a low birthweight infant associated with changes in social, environmental, and genetic factors. DESIGN: Population based, historical cohort study using the Danish medical birth registry and Statistic Denmark''s fertility database. SUBJECTS: All women who had a low birthweight infant (< 2500 g) (index birth) and a subsequent liveborn infant (outcome birth) in Denmark between 1980 and 1992 (exposed cohort, n = 11,069) and a random sample of the population who gave birth to an infant weighing > or = 2500 g and to a subsequent liveborn infant (unexposed cohort, n = 10,211). MAIN OUTCOME MEASURES: Risk of having a low birthweight infant in the outcome birth as a function of changes in male partner, area of residence, type of job, and social status between the two births. RESULTS: Women in the exposed cohort showed a high risk (18.5%) of having a subsequent low birthweight infant while women in the unexposed cohort had a risk of 2.8%. After adjustment for initial social status, a decline in social status increased the absolute risk of having a low birthweight infant by about 5% in both cohorts, though this was significant only in the unexposed cohort. Change of male partner did not modify the risk of low birth weight in either cohort. CONCLUSION: Having had a low birthweight infant and a decline in social status are strong risk factors for having a low birthweight infant subsequently.     

Myocardial uptake kinetics of tocainide enantiomers in the isolated perfused rabbit heart

The extent of myocardial accumulation of tocainide, administered as single enantiomers and as well as racemate, was determined in the isolated, spontaneous beating rabbit heart. The heart was retrogradely perfused at a constant rate and fractions of the perfusate were collected during and after infusion. Kinetic parameters for myocardial accumulation and disposition of tocainide were indirectly determined from drug concentration/time course in the outflow perfusate. No stereoselectivity in myocardial accumulation was observed. A two compartment model with mean half-lives for distribution and elimination of 0.60 and 3.78 min, respectively, was fitted to the accumulation and disposition data. At steady-state, tocainide enantiomers were accumulated about three times in the myocardium relative to the perfusion liquid. © 1995 Wiley-Liss, Inc.     

Blood and gastrointestinal parasites of eastern wild turkeys from Kentucky and Tennessee

Fifty-nine gastrointestinal tracts and 52 blood samples were collected from eastern wild turkeys (Meleagris gallopavo silvestris Vieillot) during the spring turkey hunts of 1979-1980 from two areas in western Kentucky and Tennessee. Eight species of parasites were recovered, and included (combined prevalence): Haemoproteus meleagridis Levine, 1961 (25%), Hymenolepis carioca (Magalhaes, 1898) (44%), Metroliasthes lucida Ransom, 1900 (25%), Raillietina georgiensis (Reid and Nugara, 1961) (15%), R. williamsi Fuhrmann, 1932 (64%), Ascaridia dissimilis Perez Vigueras, 1931 (83%), Capillaria caudinflata (Molin, 1858) (2%), and Heterakis gallinarum (Schrank, 1788) (27%). A significant difference existed between the intensities of A. dissimilis from the two states. Twenty-two subinoculations of collected blood were made in 1979, but no Plasmodium infections were recovered. Helminths of wild turkeys from 11 southeastern states were compared using similarity and diversity indices. High similarities were observed in helminth populations of two groups of states: 1) Alabama, Mississippi, Arkansas, Virginia, and Tennessee; and 2) Tennessee, Kentucky, and Illinois. Simpson's diversity index indicated helminth populations of wild turkeys in Florida were the most diverse (0.10), while those in Louisiana turkeys were the least diverse (0.33).     

RNA secondary structure and translation inhibition: analysis of mutants in the rplJ leader

We have carried out measurements of the stable binding of the ribosomal protein (r-protein) complex L10-L7/L12 to mutant forms of the mRNA leader of the rplJ operon of Escherichia coli. One of the point mutations, base 1548, which lies within the L10-L7/L12-protected region, almost completely abolishes in vitro formation of a stable complex of L10-L7/L12 with rplJ mRNA leader, and a second point mutation, base 1634, strongly reduces it. These observations constitute strong support for the proposition that L10-L7/L12 binds to the rplJ leader in bringing about translational feedback. To account for the action of these and other mutations, and to explain the mechanism of translation feedback inhibition, we suggest a secondary structure model involving alternate forms of the rplJ mRNA leader.