Lethal and non-lethal effects of multiple indigenous predators on the invasive golden apple snail (Pomacea canaliculata)

1. We investigated the individual and combined effects of two predators (the climbing perch, Anabas testudineus, and the wetland crab, Esanthelphusa nimoafi) indigenous to wetlands in Laos, on the behaviour and survival of the invasive South American golden apple snail (Pomacea canaliculata). The snail is considered a pest, consuming large amounts of rice and other aquatic vegetation in the region. 2. Snail avoidance reactions to released predator chemical cues were investigated in aquaria while the effects of predators on a mixed snail population were studied in field enclosures that contained native aquatic plants (Salvinia cucullata, Ludwigia adscendens and Ipomoea aquatica). 3. In the aquaria experiment, neonate (2-3 mm) and medium-sized snails (8-10 mm) responded to fish chemical cues by going to the surface, whereas adult snails (35-40 mm) went to the bottom. In contrast, no size class of snails reacted to chemical cues released by crabs. 4. In the field experiment, fish reduced the abundance of neonate snails, and crabs reduced the abundance of all size classes. The effect of the combined predators could not be predicted from the mortality rate observed in single predator treatments. The survival of neonate and medium-sized snails was greater and of adults less than expected. The presence of predators did not affect egg production. Snails consumed significant amounts of plants despite the presence of predators. 5. Our findings suggest that some indigenous Asian predators have lethal and sublethal effects on P. canaliculata that depend on snail size and predator type. When in the presence of several predators the response of snails to one predator may either increase or decrease the vulnerability of snails to the others

Role of the \u3ci\u3eEscherichia coli\u3c/i\u3e FadR Regulator in Stasis Survival and Growth Phase-Dependent Expression of the \u3ci\u3euspA, fad\u3c/i\u3e, and \u3ci\u3efab\u3c/i\u3e Genes

The increased expression of the uspA gene of Escherichia coli is an essential part of the cell’s response to growth arrest. We demonstrate that stationary-phase activation of the uspA promoter is in part dependent on growth phase-dependent inactivation or repression of the FadR regulator. Transcription of uspA is derepressed during exponential growth in fadR null mutants or by including the fatty acid oleate in the growth medium of FadR1 cells. The results of DNA footprinting analysis show that FadR binds downstream of the uspA promoter in the noncoding region. Thus, uspA is a member of the fadR regulon. All the fad-lacZ fusions examined (fadBA, fadL, and fadD) are increasingly expressed in stationary phase with kinetics similar to that of the increased expression of uspA. In contrast, b-galactosidase levels decrease during stationary phase in a fabA-lacZ lysogen, consistent with the role of FadR as an activator of fabA. The growth phase-dependent increased and decreased transcription of fad genes and fabA, respectively, is dependent on the status of the fadR gene. Cells carrying a mutation in the FadR gene (fadRS219N) that makes it nonderepressible exhibit a weak stationary-phase induction of uspA and fad genes. In addition, cells carrying fadRS219N survive long-term stasis poorly, indicating that FadR-dependent alterations in fatty acid metabolism are an integral and important part of the adaptation to stationary phase

Role of the \u3ci\u3eEscherichia coli\u3c/i\u3e FadR Regulator in Stasis Survival and Growth Phase-Dependent Expression of the \u3ci\u3euspA, fad\u3c/i\u3e, and \u3ci\u3efab\u3c/i\u3e Genes

The increased expression of the uspA gene of Escherichia coli is an essential part of the cell’s response to growth arrest. We demonstrate that stationary-phase activation of the uspA promoter is in part dependent on growth phase-dependent inactivation or repression of the FadR regulator. Transcription of uspA is derepressed during exponential growth in fadR null mutants or by including the fatty acid oleate in the growth medium of FadR1 cells. The results of DNA footprinting analysis show that FadR binds downstream of the uspA promoter in the noncoding region. Thus, uspA is a member of the fadR regulon. All the fad-lacZ fusions examined (fadBA, fadL, and fadD) are increasingly expressed in stationary phase with kinetics similar to that of the increased expression of uspA. In contrast, b-galactosidase levels decrease during stationary phase in a fabA-lacZ lysogen, consistent with the role of FadR as an activator of fabA. The growth phase-dependent increased and decreased transcription of fad genes and fabA, respectively, is dependent on the status of the fadR gene. Cells carrying a mutation in the FadR gene (fadRS219N) that makes it nonderepressible exhibit a weak stationary-phase induction of uspA and fad genes. In addition, cells carrying fadRS219N survive long-term stasis poorly, indicating that FadR-dependent alterations in fatty acid metabolism are an integral and important part of the adaptation to stationary phase

Numerical Analysis of Etoposide Induced DNA Breaks

Background: Etoposide is a cancer drug that induces strand breaks in cellular DNA by inhibiting topoisomerase II (topoII) religation of cleaved DNA molecules. Although DNA cleavage by topoisomerase II always produces topoisomerase II-linked DNA double-strand breaks (DSBs), the action of etoposide also results in single-strand breaks (SSBs), since religation of the two strands are independently inhibited by etoposide. In addition, recent studies indicate that topoisomerase II-linked DSBs remain undetected unless topoisomerase II is removed to produce free DSBs. Methodology/Principal Findings: To examine etoposide-induced DNA damage in more detail we compared the relative amount of SSBs and DSBs, survival and H2AX phosphorylation in cells treated with etoposide or calicheamicin, a drug that produces free DSBs and SSBs. With this combination of methods we found that only 3 % of the DNA strand breaks induced by etoposide were DSBs. By comparing the level of DSBs, H2AX phosphorylation and toxicity induced by etoposide and calicheamicin, we found that only 10 % of etoposide-induced DSBs resulted in histone H2AX phosphorylation and toxicity. There was a close match between toxicity and histone H2AX phosphorylation for calicheamicin and etoposide suggesting that the few etoposide-induced DSBs that activated H2AX phosphorylation were responsible for toxicity. Conclusions/Significance: These results show that only 0.3 % of all strand breaks produced by etoposide activate H2A

A bridge between a lonely soul and the surrounding world: A study on existential consequences of being closely related to a person with aphasia

This study illuminates existential consequences of being closely related to a person suffering from aphasia. Seventeen close relatives were interviewed and their narratives were interpreted with inspiration from Ricoeur, Levinas, Husserl, Winnicot, and Maurice Merleau-Ponty. The emerging interpretations resulted in four themes that illuminate a life characterized by lost freedom, staying, a new form of relationship, and growing strong together with others. An overarching theme suggests that a life together with an aphasic person means being used as a bridge between the aphasic person and the surrounding world. Moreover, it illuminates that a close relative to a person with aphasia is a person who does not leave, despite a heavy burden of lonely responsibility. It is concluded that community services need to fulfill their responsibility of providing support to informal caregivers as suggested by the Swedish lawmakers

Using force covariance to derive effective stochastic interactions in dissipative particle dynamics

There exist methods for determining effective conservative interactions in coarse grained particle based mesoscopic simulations. The resulting models can be used to capture thermal equilibrium behavior, but in the model system we study do not correctly represent transport properties. In this article we suggest the use of force covariance to determine the full functional form of dissipative and stochastic interactions. We show that a combination of the radial distribution function and a force covariance function can be used to determine all interactions in dissipative particle dynamics. Furthermore we use the method to test if the effective interactions in dissipative particle dynamics (DPD) can be adjusted to produce a force covariance consistent with a projection of a microscopic Lennard-Jones simulation. The results indicate that the DPD ansatz may not be consistent with the underlying microscopic dynamics. We discuss how this result relates to theoretical studies reported in the literature.Comment: 10 pages, 10 figure