Pigment ratios and phytoplankton assessment in northern Wisconsin lakes

Nine lakes in northern Wisconsin were sampled from February through September 1996, and HPLC analysis of water column pigments was carried out on epilimnetic seston. Pigment distributions were evaluated throughout the water column during summer in Crystal Lake and Little Rock Lake. The purpose of our study was to investigate the use of phytopigments as markers of the main taxonomic groups of algae. As a first approach, multiple regression of marker pigments against chlorophyll a (chl a) was used to derive the best linear combination of the main xanthophylls (peridinin, fucoxanthin, alloxanthin, lutein, and zeaxanthin). A significant regression equation (r²= 0.98) was obtained for epilimnion data. The good fit indicates that the chl a:xanthophyll ratios were fairly constant in the epilimnion of the nine lakes over time. Chlorophyll a recalculated from the main xanthophylls in each sample showed good agreement with measured chl a in epilimnetic waters. A second approach used the CHEMTAX program to analyze the same data set. CHEMTAX provided estimates of chl a biomass for all algal classes and allowed distinction between diatoms and chrysophytes, and between chlorophytes and euglenophytes. These results showed a reasonably good agreement with biomass estimates from microscope counts, despite uncertainties associated with differences in sampling procedure. Changes of pigment ratios over time in the epilimnetic waters were also investigated, as well as differences between surface and deep samples of Little Rock Lake and Crystal Lake. We found evidence that changes in the ratio of photoprotective pigments to chl a occurred as a response to changes in light climate. Changes were also observed for certain light‐harvesting pigments. The comparison between multiple regression and CHEMTAX analyses for inferring chl a biomass from concentrations of marker pigments highlighted the need to take account of variations in pigment ratio, as well as the need to acquire additional data on the pigment composition of planktonic algae.     

Effect of mild-to-moderate airflow limitation on exercise capacity

To determine the effect of mild-to-moderate airflow limitation on exercise tolerance and end-expiratory lung volume (EELV), we studied 9 control subjects with normal pulmonary function [forced expired volume in 1 s (FEV1) 105% pred; % of forced vital capacity expired in 1 s (FEV1/FVC%) 81] and 12 patients with mild-to-moderate airflow limitation (FEV1 72% pred; FEV1/FVC % 58) during progressive cycle ergometry. Maximal exercise capacity was reduced in patients [69% of pred maximal O2 uptake (VO2max)] compared with controls (104% pred VO2max, P less than 0.01); however, maximal expired minute ventilation-to-maximum voluntary ventilation ratio and maximal heart rate were not significantly different between controls and patients. Overall, there was a close relationship between VO2max and FEV1 (r2 = 0.62). Resting EELV was similar between controls and patients [53% of total lung capacity (TLC)], but at maximal exercise the controls decreased EELV to 45% of TLC (P less than 0.01), whereas the patients increased EELV to 58% of TLC (P less than 0.05). Overall, EELV was significantly correlated to both VO2max (r = -0.71, P less than 0.001) and FEV1 (r = -0.68, P less than 0.001). This relationship suggests a ventilatory influence on exercise capacity; however, the increased EELV and associated pleural pressures could influence cardiovascular function during exercise. We suggest that the increase in EELV should be considered a response reflective of the effect of airflow limitation on the ventilatory response to exercise.     

Effect of the (+)-CC-1065-(N3-adenine)DNA adduct on in vitro DNA synthesis mediated by Escherichia coli DNA polymerase.

(+)-CC-1065 is a potent antitumor antibiotic produced by Streptomyces zelensis. Previous studies have shown that the potent cytotoxic and antitumor activities of (+)-CC-1065 are due to the ability of this compound to covalently modify DNA. (+)-CC-1065 reacts with duplex DNA to form an N3-adenine DNA adduct which lies in the minor groove of the DNA helix overlapping with a 5-base-pair region. As a consequence of covalent modification with (+)-CC-1065, the DNA helix bends into the minor groove and also undergoes winding and stiffening [Lee, C.-S., Sun, D., Kizu, R., & Hurley, L. H. (1991) Chem. Res. Toxicol. 4, 203-213]. In the studies described here, in which we have constructed site-directed DNA adducts on single-stranded DNA templates, we have shown that (+)-CC-1065 and select synthetic analogues, which have different levels of cytotoxicity, all show strong blocks against progression of Klenow fragment, E. coli DNA polymerase, and T4 DNA polymerase. The inhibition of bypass of drug lesions by polymerase could be partially alleviated by increasing the concentration of dNTPs and, to a small extent, by increasing polymerase levels. Klenow fragment binds equally well to a DNA template adjacent to a drug modification site and to unmodified DNA. These results taken together lead us to suspect that it is primarily inhibition of base pairing around the drug modification site and not prevention of polymerase binding that leads to blockage of DNA synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Factors influencing parasitism of Sirex noctilio (Hymenoptera: Siricidae) by the nematode Deladenus siricidicola (Nematoda: Neotylenchidae) in summer rainfall areas of South Africa

Control of the invasive wasp, Sirex noctilio Fabricius using the parasitic nematode Deladenus siricidicola Bedding is a well known example of a successful classical biological control program. Despite its wide-scale success, this control method has recently had poor success in the summer rainfall areas of South Africa. Data from previous studies showed variation in nematode parasitism from inoculated trees (inoculation success) between different tree sections and among inoculation times. They also pointed to moisture content of the wood or virulence of the nematode as the most likely underlying factors influencing variations in inoculation success. The results from our study showed that the highest levels of parasitism was obtained from early inoculations and from the bottom sections of trees, where moisture content of the wood was highest, supporting the hypothesis that moisture content influences parasitism. However, even when moisture content was adequate, average inoculation success remained below 25% and was often 0%, suggesting that there are other barriers to inoculation success. Different sources from which the nematodes were produced did not influence inoculation success, indicating that nematode virulence is most likely not the cause of the low success. Another interesting finding was that parasitized wasps were larger than unparasitized wasps. Background parasitism was present despite the poor success with past inoculations, but the data also suggest that the natural build-up of this population could be constrained by the same factors that influence inoculations.     

Prostaglandin F2alpha involves heparan sulphate sugar chains and FGFRs to modulate osteoblast growth and differentiation

The present investigation extends our previous studies on PGF2alpha-mediated signalling in osteoblast metabolism. In particular, the role of PGF2alpha as modulator of heparan sulphate proteoglycans (HSPGs), fibroblast growth factor 2 (FGF-2) and fibroblast growth factor receptors (FGFRs) was evaluated. We hereby reported the novel observation that PGF2alpha was able to promote the formation of HSPGs/FGF-2/FGFRs complexes. Moreover, our data suggested that PGF2alpha could induce new synthesis of heparan sulphate (HS) chains on osteoblasts by a mechanism involving a modulation of MAPK signalling and that HS is required for the regulation of FGF-2 induced by PGF2alpha. Indeed, a proteolytic cleavage of HSPGs with heparinase III (Hep III) prior to PGF2alpha administration down-regulated the basal expression of phospho-p44/42, likely inhibiting FGFRs tyrosine kinase activity. Interestingly, MAPK signalling influenced syntheses and subcellular localization of FGF-2, its specific receptor and HS. In addition, the proteolytic cleavage by Hep III and the MAPK kinase inhibition by PD-98059 also revealed that PGF2alpha induced cell proliferation is dependent on HSPGs and FGF-2 specific receptor, respectively. Of further relevance of this study, we demonstrated, by using a specific siRNA for FGFR1, that PGF2alpha modulates Runx2 expression by FGFR1 and HS.     

Variation in the temperature preference and growth rate of individual fish reconciles differences between two growth models

1. A growth model, originally developed for brown trout (Salmo trutta), has now been fitted to data for Atlantic salmon (S. salar) and stone‐loach (Barbatula barbatula) from English populations, and Arctic charr (Salvelinus alpinus) from Sweden. The model relates growth rate to temperature for a fish of standard size and the functional relationship has a triangular shape with a sharp peak at the optimal temperature for growth and zero growth at the base of the triangle. It was unsuitable for growth data for Norwegian salmon, and a curvilinear Ratkowsky model provided a better fit, though the experimental protocol was different in the Norwegian and English experiments. 2. The Norwegian salmon were kept in groups in each tank, had to compete for food, and had to be divided into slow, moderate and fast growers before the Ratkowsky model could be fitted. Each English salmon was kept in its own tank and fed individually. For replicate experiments, fish of similar size were selected. Variation among fish kept under similar conditions was therefore small, and the triangular model was essentially for individual fish, not groups of fish. 3. The present simulation study tests the hypothesis that individual differences in the growth response could account for the curvilinear growth‐temperature relationship for the Norwegian salmon. The triangular model was used to generate the growth response to temperature for a group of salmon, each fish having a slightly different temperature preference and growth rate. The result was a curvilinear response, well approximated by the Ratkowsky model (adjusted R² = 0.96). When the variability in individual temperature preference was increased, the Ratkowsky model was an even better fit (adjusted R² = 0.98). Therefore, the apparent discrepancy between the two models was reconciled by allowing for individual differences in temperature preference and growth rate within groups of fish.     

Does age, sex, or ACE genotype affect glucose and insulin responses to strength training?

The purpose of the present study was to determine whether age, sex, or angiotensin I-converting enzyme (ACE) genotype influences the effects of strength training (ST) on glucose homeostasis. Nineteen sedentary young (age = 20-30 yr) men (n = 10) and women (n = 9) were studied and compared with 21 sedentary older (age = 65-75 yr) men (n = 12) and women (n = 9) before and after a 6-mo total body ST program. Fasting insulin concentrations were reduced in young men and in older men with ST (P < 0.05 in both). In addition, total insulin area under the curve decreased by 21% in young men (P < 0.05), and there was a trend for a decrease (11%) in older men (P = 0.06). No improvements in insulin responses were observed in young or older women. The ACE deletion/deletion genotype group had the lowest fasting insulin and insulin areas under the oral glucose tolerance test (OGTT) curve before training (all P < 0.05), but those with at least one insertion allele had a trend for a greater reduction in total insulin area than deletion homozygotes (P = 0.07). These results indicate that ST has a more favorable effect on insulin response to an OGTT in men than in women and offer some support for the hypothesis that ACE genotype may influence insulin responses to ST.     

FGF and FGFR signaling in chondrodysplasias and craniosynostosis

The first experimental mouse model for FGF2 in bone dysplasia was made serendipitously by overexpression of FGF from a constitutive promoter. The results were not widely accepted, rightfully drew skepticism, and were difficult to publish; because of over 2,000 studies published on FGF‐2 at the time (1993), only a few reported a role of FGF‐2 in bone growth and differentiation. However, mapping of human dwarfisms to mutations of the FGFRs shortly, thereafter, made the case that bone growth and remodeling was a major physiological function for FGF. Subsequent production of numerous transgenic and targeted null mice for several genes in the bone growth and remodeling pathways have marvelously elucidated the role of FGFs and their interactions with other genes. Indeed, studies of the FGF pathway present one of the best success stories for use of experimental genetics in functionally parsing morphogenetic regulatory pathways. What remains largely unresolved is the pleiotropic nature of FGF‐2. How does it accelerate growth in one cell then stimulate apoptosis or retard growth for another cell in the same type of tissue? Some of the answers may come through distinguishing the FGF‐2 protein isoforms, made from alternative translation start sites, these appear to have substantially different functions. Although we have made substantial progress, there is still much to be learned regarding FGF‐2 as a most complex, enigmatic protein. Studies of genetic models in mice and human FGFR mutations have provided strong evidence that FGFRs are important modulators of osteoblast function during membranous bone formation. However, there is some controversy regarding the effects of FGFR signaling in human and murine genetic models. Although significant progress has been made in our understanding of FGFR signaling, several questions remain concerning the signaling pathways involved in osteoblast regulation by activated FGFR. Additionally, little is known about the specific role of FGFR target genes involved in cranial bone formation. These issues need to be addressed in future in in vitro and in vivo approaches to better understand the molecular mechanisms of action of FGFR signaling in osteoblasts that result in anabolic effects in bone formation. J. Cell. Biochem. © 2005 Wiley‐Liss, Inc.