Surface adsorption, intracellular accumulation and compartmentalization of Pb(II) in batch-operated lagoons with Salvinia minima as affected by environmental conditions, EDTA and nutrients

The effects of environmental factors and nutrients on the various possible removal mechanisms (surface adsorption, intracellular accumulation and precipitation to sediments) and partitioning of lead among various compartments (plant biomass, water column and sediments) in Salvinia minima batch-operated lagoons, were evaluated. Surface adsorption was found to be the predominant mechanism for Pb(II) removal under all environmental conditions tested in the absence of nutrients (an average of 54.3%) and in a nutrient medium (modified Hutner 1/10 medium) free of EDTA and phosphates (54.41%) at "high" initial Pb(II) concentrations (in the range of 10.3+/-0.13 to 15.2+/-0.05 mg/L). Under these conditions, the bioconcentration factors (BCFs) were 2,431+/-276 and 2,065+/-35, respectively. Lead removal was very rapid during the first 4 h and reached 70% in the absence of nutrients at the "medium" light intensity and temperature (LIT) tested, 88% in nutrient medium free of EDTA and supplemented with synthetic wastewater (at the "lowest" LIT tested), and 85% in medium free of EDTA and phosphates. It was concluded that the mechanisms of lead removal by S. minima, and the compartmentalization of this metal in the microcosm of batch-operated lagoons, are primarily a function of the presence of certain nutrients and chelants, with secondary dependence on environmental conditions. In addition, the results indicate that the percentage of lead removed is only a gross parameter and that the complementary use of BCF and compartmentalization analysis is required to gain a full insight into the metal removal process.     

Climate variability and campylobacter infection: an international study

Campylobacter is among the most important agents of enteritis in developed countries. We have described the potential environmental determinants of the seasonal pattern of infection with campylobacter in Europe, Canada, Australia and New Zealand. Specifically, we investigated the role of climate variability on laboratory-confirmed cases of campylobacter infection from 15 populations. Regression analysis was used to quantify the associations between timing of seasonal peaks in infection in space and time. The short-term association between weekly weather and cases was also investigated using Poisson regression adapted for time series data. All countries in our study showed a distinct seasonality in campylobacter transmission, with many, but not all, populations showing a peak in spring. Countries with milder winters have peaks of infection earlier in the year. The timing of the peak of infection is weakly associated with high temperatures 3 months previously. Weekly variation in campylobacter infection in one region of the UK appeared to be little affected by short-term changes in weather patterns. The geographical variation in the timing of the seasonal peak suggests that climate may be a contributing factor to campylobacter transmission. The main driver of seasonality of campylobacter remains elusive and underscores the need to identify the major serotypes and routes of transmission for this disease.     

The FK506 binding protein Fpr3 counteracts protein phosphatase 1 to maintain meiotic recombination checkpoint activity

The meiotic recombination checkpoint delays gamete precursors in G2 until DNA breaks created during recombination are repaired and chromosome structure has been restored. Here, we show that the FK506 binding protein Fpr3 prevents premature adaptation to damage and thus serves to maintain recombination checkpoint activity. Impaired checkpoint function is observed both in cells lacking FPR3 and in cells treated with rapamycin, a small molecule inhibitor that binds to the proline isomerase (PPIase) domain of Fpr3. FPR3 functions in the checkpoint through controlling protein phosphatase 1 (PP1). Fpr3 interacts with PP1 through its PPIase domain, regulates PP1 localization, and counteracts the activity of PP1 in vivo. Our findings define a branch of the recombination checkpoint involved in the adaptation to persistent chromosomal damage and a critical function for FK506 binding proteins during meiosis.     

High-pressure inactivation of hepatitis A virus within oysters

Previous results demonstrated that hepatitis A virus (HAV) could be inactivated by high hydrostatic pressure (HHP) (D. H. Kingsley, D. Hoover, E. Papafragkou, and G. P. Richards, J. Food Prot. 65:1605-1609, 2002); however, direct evaluation of HAV inactivation within contaminated oysters was not performed. In this study, we report confirmation that HAV within contaminated shellfish is inactivated by HHP. Shellfish were initially contaminated with HAV by using a flowthrough system. PFU reductions of >1, >2, and >3 log(10) were observed for 1-min treatments at 350, 375, and 400 megapascals, respectively, within a temperature range of 8.7 to 10.3 degrees C. Bioconcentration of nearly 6 log(10) PFU of HAV per oyster was achieved under simulated natural conditions. These results suggest that HHP treatment of raw shellfish will be a viable strategy for the reduction of infectious HAV.     

Permeability to phi chi 174 bacteriophages in polyolephin membrane condoms

Membranes used for the manufacture of condoms eventually can develop tiny pores, thereby decreasing dramatically their effectiveness as a physical barrier against the transmission of infectious agents. A technique was designed that was based on the ability of bacteriophage viruses to trespass membranes and to infect certain bacteria species, and then developing lysis plaques in the colonies of the host bacteria. The effectiveness of 60 polyolefin condoms in preventing the diffusion of the bacteriophage phi chi 174(ATCC13706-B1), 27 nm diameter, was compared to 20 latex condoms. Physiological conditions such as pressure, pH, superficial tension, length, time of exposure and viral titre were simulated. A pressurization system was designed, in which compressed air was injected simultaneously to ten condoms. Four of the 60 polyolefin condoms and one of the 20 latex condoms were permeable to the virus. Therefore, at least 93% of the condoms evaluated were able to contain the virus. The difference in permeability between the two types of membranes was not statistically significant (P = 0.79).     

Cannabinoid receptor-induced neurite outgrowth is mediated by Rap1 activation through G(alpha)o/i-triggered proteasomal degradation of Rap1GAPII

The G(alpha)o/i-coupled CB1 cannabionoid receptor induces neurite outgrowth in Neuro-2A cells. The mechanisms of signaling through G(alpha)o/i to induce neurite outgrowth were studied. The expression of G(alpha)o/i reduces the stability of its direct interactor protein, Rap1GAPII, by targeting it for ubiquitination and proteasomal degradation. This results in the activation of Rap1. G(alpha)o/i-induced activation of endogenous Rap1 in Neuro-2A cells is blocked by the proteasomal inhibitor lactacystin. G(alpha)o/i stimulates neurite outgrowth that is blocked by the expression of dominant negative Rap1. Expression of Rap1GAPII also blocks the G(alpha)o/i-induced neurite outgrowth and treatment with proteasomal inhibitors potentiates this inhibition. The endogenous G(alpha)o/i-coupled cannabinoid (CB1) receptor in Neuro-2A cells stimulates the degradation of Rap1GAPII; activation of Rap1 and treatment with pertussis toxin or lactacystin blocks these effects. The CB1 receptor-stimulated neurite outgrowth is blocked by treatment with pertussis toxin, small interfering RNA for Rap, lactacystin, and expression of Rap1GAPII. Thus, the G(alpha)o/i-coupled cannabinoid receptor, by regulating the proteasomal degradation of Rap1GAPII, activates Rap1 to induce neurite outgrowth.     

Is root growth under phosphorus deficiency affected by source or sink limitations?

Reduced net photosynthesis (Pn) and decreasing shoot and root biomass are typical effects of phosphorus deficiency in plants. Lower biomass accumulation could be the result of reduced Pn (source limitation), but may also be due to direct negative effects of low P availability on growth (sink limitation). Because of the principal importance of root growth for P uptake, this study specifically examined the question whether source or sink limitations were responsible for reduced root growth rates under P deficiency. Rice plants were grown in nutrient solutions with four levels of P supply and at two light treatments and the effect of Pxlight treatments on growth and carbohydrate distribution was observed. Plants had up to 70% higher Pn when grown with natural (high) light compared with low light. Higher Pn, however, did not lead to additional growth under P deficiency, suggesting that assimilate supply from source leaves to roots was not a limiting factor under P deficiency. This was supported by observations that root starch concentrations increased in P-deficient roots. The comparison of two genotypes with different tolerance to P deficiency showed that the more tolerant one preferentially distributed P to roots where the additional P stimulated root growth and, ultimately, P uptake. The results therefore suggest that source limitation is of little importance under P deficiency. Even at highly sub-optimal tissue P concentrations of below 0.7 mg P g(-1) dry weight, plants were able to produce enough assimilates to sustain growth rates that were directly limited by low P availability.