Quantification of flow during suction feeding in bluegill sunfish

Nearly all aquatic-feeding vertebrates use some amount of suction to capture prey items. Suction prey capture occurs by accelerating a volume of water into the mouth and taking a prey item along with it. Yet, until recently, we lacked the necessary techniques and analytical tools to quantify the flow regime generated by feeding fish. We used a new approach; Digital Particle Image Velocimetery (DPIV) to measure several attributes of the flow generated by feeding bluegill sunfish. We found that the temporal pattern of flow was notably compressed during prey capture. Flow velocity increased rapidly to its peak within 20 ms of the onset of the strike, and this peak corresponded to the time that the prey entered the mouth during capture. The rapid acceleration and deceleration of water suggests that timing is critical for the predator in positioning itself relative to the prey so that it can be drawn into the mouth along with the water. We also found that the volume of water affected by suction was spatially limited. Only rarely did we measure significant flow beyond 1.75 cm of the mouth aperture (in 20 cm fish), further emphasizing the importance of mechanisms, like locomotion, that place the fish mouth in close proximity to the prey. We found that the highest flows towards the mouth along the fish midline were generated not immediately in front of the open mouth, but approximately 0.5 cm anterior to the mouth opening. Away from the midline the peak in flow was closer to the mouth. We propose that this pattern indicates the presence of a bow wave created by the locomotor efforts of the fish. In this scheme, the bow wave acts antagonistically to the flow of water generated by suction, the net effect being to push the region of peak flow away from the open mouth. The peak was located farther from the mouth opening in strikes accompanied by faster locomotion, suggesting faster fish created larger bow waves.     

The role of oxidised regenerated cellulose/collagen in chronic wound repair and its potential mechanism of action

Normal wound healing is a carefully controlled balance of destructive processes necessary to remove damaged tissue and repair processes which lead to new tissue formation. Proteases and growth factors play a pivotal role in regulating this balance, and if disrupted in favour of degradation then delayed healing ensues; a trait of chronic wounds. Whilst there are many types of chronic wounds, biochemically they are thought to be similar in that they are characterised by a prolonged inflammatory phase, which results in elevated levels of proteases and diminished growth factor activity. This increase in proteolytic activity and subsequent degradation of growth factors is thought to contribute to the net tissue loss associated with these chronic wounds.

In this study, we describe a new wound treatment, comprising oxidised regenerated cellulose and collagen (ORC/collagen), which can redress this imbalance and modify the chronic wound environment. We demonstrate that ORC/collagen can inactivate potentially harmful factors such as proteases, oxygen free radicals and excess metal ions present in chronic wound fluid, whilst simultaneously protecting positive factors such as growth factors and delivering them back to the wound.

These characteristics suggest a beneficial role for this material in helping to re-balance the chronic wound environment and therefore promote healing.     

A scenario-based approach to modeling development: a prototype model of C. elegans vulval fate specification

Studies of developmental biology are often facilitated by diagram “models” that summarize the current understanding of underlying mechanisms. The increasing complexity of our understanding of development necessitates computational models that can extend these representations to include their dynamic behavior. Here we present a prototype model of Caenorhabditis elegans vulval precursor cell fate specification that represents many processes crucial for this developmental event but that are hard to integrate using other modeling methodologies. We demonstrate the integrative capabilities of our methodology by comprehensively incorporating the contents of three seminal papers, showing that this methodology can lead to comprehensive models of developmental biology. The prototype computational model was built and is run using a language (Live Sequence Charts) and tool (the Play-Engine) that facilitate the same conceptual processes biologists use to construct and probe diagram-type models. We demonstrate that this modeling approach permits rigorous tests of mutual consistency between experimental data and mechanistic hypotheses and can identify specific conflicting results, providing a useful approach to probe developmental systems.     

Suppression of acute anti-friend virus CD8+ T-cell responses by coinfection with lactate dehydrogenase-elevating virus

Friend virus (FV) and lactate dehydrogenase-elevating virus (LDV) are endemic mouse viruses that can cause long-term chronic infections in mice. We found that numerous mouse-passaged FV isolates also contained LDV and that coinfection with LDV delayed FV-specific CD8⁺ T-cell responses during acute infection. While LDV did not alter the type of acute pathology induced by FV, which was severe splenomegaly caused by erythroproliferation, the immunosuppression mediated by LDV increased both the severity and the duration of FV infection. Compared to mice infected with FV alone, those coinfected with both FV and LDV had delayed CD8⁺ T-cell responses, as measured by FV-specific tetramers. This delayed response accounted for the prolonged and exacerbated acute phase of FV infection. Suppression of FV-specific CD8⁺ T-cell responses occurred not only in mice infected concomitantly with LDV but also in mice chronically infected with LDV 8 weeks prior to infection with FV. The LDV-induced suppression was not mediated by T regulatory cells, and no inhibition of the CD4⁺ T-cell or antibody responses was observed. Considering that most human adults are carriers of chronically infectious viruses at the time of new virus insults and that coinfections with viruses such as human immunodeficiency virus and hepatitis C virus are currently epidemic, it is of great interest to determine how infection with one virus may impact host responses to a second infection. Coinfection of mice with LDV and FV provides a well-defined, natural host model for such studies.     

xRic-8 is a GEF for Gsalpha and participates in maintaining meiotic arrest in Xenopus laevis oocytes

Immature stage VI Xenopus oocytes are arrested at the G(2)/M border of meiosis I until exposed to progesterone, which induces meiotic resumption through a non-genomic mechanism. One of the earliest events produced by this hormone is inhibition of the plasma membrane enzyme adenylyl cyclase (AC), with the concomitant drop in intracellular cAMP levels and reinitiation of the cell cycle. Recently Gsalpha and Gbetagamma have been shown to play an important role as positive regulators of Xenopus oocyte AC, maintaining the oocyte in the arrested state. However, a question that still remains unanswered, is how the activated state of Gsalpha and Gbetagamma is achieved in the immature oocyte, since no receptor or ligand have been found to be required. Here we provide evidence that xRic-8 can act in vitro and in vivo as a GEF for Gsalpha. Overexpression of xRic-8, through mRNA injection, greatly inhibits progesterone induced oocyte maturation and endogenous xRic-8 mRNA depletion, through siRNA microinjection, induces spontaneous oocyte maturation. These results suggest that xRic-8 is participating in the immature oocyte by keeping Gsalpha-Gbetagamma-AC signaling complex in an activated state and therefore maintaining G2 arrest.