Isolation of a Campylobacter lanienae-like Bacterium from Laboratory Chinchillas (Chinchilla laniger)

Routine necropsies of 27 asymptomatic juvenile chinchillas revealed a high prevalence of gastric ulcers with microscopic lymphoplasmacytic gastroenteritis and typhlocolitis. Polymerase chain reaction (PCR) analysis using Campylobacter genus-specific partial 16S rRNA primers revealed the presence of Campylobacter spp. DNA in the faeces of 12 of 27 animals (44.4%). Species-specific partial 16S rRNA PCR and sequencing confirmed that these animals were colonized with Campylobacter lanienae, a gram-negative, microaerophilic bacterium that was first identified on routine faecal screening of slaughterhouse employees and subsequently isolated from faeces of livestock. Campylobacter lanienae was isolated from the faeces of six PCR-positive animals and identified with species-specific PCR and full 16S rRNA sequencing. Phylogenetic analysis showed that these isolates clustered with C. lanienae strain NCTC 13004. PCR analysis of DNA extracted from gastrointestinal tissues revealed the presence of C. lanienae DNA in the caecum and colon of these chinchillas. Gastrointestinal lesions were scored and compared between C. lanienae-positive and C. lanienae-negative animals. There was no correlation between colonization status and lesion severity in the stomach, liver, duodenum, or colon. Possible routes of C. lanienae infection in chinchillas could include waterborne transmission and faecal–oral transmission from wild mice and rats or livestock. Based on these findings, the authors conclude that C. lanienae colonizes the lower bowel of chinchillas in the absence of clinical disease. This is the first report of C. lanienae in any rodent species. Campylobacter lanienae isolates from different mammalian species demonstrate heterogeneity by 16S rRNA sequence comparison. Analysis using rpoB suggests that isolates and clones currently identified as C. lanienae may represent multiple species or subspecies.Ruth L. Kirschstein National Research Service AwardNational Institutes of Health (U.S.) (Grant R01-OD011141)National Institutes of Health (U.S.) (Grant T32-OD007036)National Institutes of Health (U.S.) (Grant P30-ES02109

Testing fluvial erosion models using the transient response of bedrock rivers to tectonic forcing in the Apennines, Italy

The transient response of bedrock rivers to a drop in base level can be used to discriminate between competing fluvial erosion models. However, some recent studies of bedrock erosion conclude that transient river long profiles can be approximately characterized by a transport‐limited erosion model, while other authors suggest that a detachment‐limited model best explains their field data. The difference is thought to be due to the relative volume of sediment being fluxed through the fluvial system. Using a pragmatic approach, we address this debate by testing the ability of end‐member fluvial erosion models to reproduce the well‐documented evolution of three catchments in the central Apennines (Italy) which have been perturbed to various extents by an independently constrained increase in relative uplift rate. The transport‐limited model is unable to account for the catchments’response to the increase in uplift rate, consistent with the observed low rates of sediment supply to the channels. Instead, a detachment‐limited model with a threshold corresponding to the field‐derived median grain size of the sediment plus a slope‐dependent channel width satisfactorily reproduces the overall convex long profiles along the studied rivers. Importantly, we find that the prefactor in the hydraulic scaling relationship is uplift dependent, leading to landscapes responding faster the higher the uplift rate, consistent with field observations. We conclude that a slope‐ dependent channel width and an entrainment/erosion threshold are necessary ingredients when modeling landscape evolution or mapping the distribution of fluvial erosion rates in areas where the rate of sediment supply to channels is low

Geotechnical controls on erodibility in fluvial impact erosion

Bedrock incision by rivers is commonly driven by the impacts of moving bedload particles. The speed of incision is modulated by rock properties, which is quantified within a parameter known as erodibility that scales the erosion rate to the erosive action of the flow. Although basic models for the geotechnical controls on rock erodibility have been suggested, large scatter and trends in the remaining relationships indicate that they are incompletely understood. Here, we conducted dedicated laboratory experiments measuring erodibility using erosion mills. In parallel, we measured uniaxial compressive strength, tensile strength, Young's modulus, bulk density, and the Poisson's ratio for the tested lithologies. We find that under the same flow conditions, erosion rates of samples from the same lithology can vary by a factor of up to 60. This indicates that rock properties that may vary over short distances within the same rock can exert a strong control on its erosional properties. The geotechnical properties of the tested lithologies are strongly cross-correlated, preventing a purely empirical determination of their controls on erodibility. The currently prevailing model predicts that erosion rates should scale linearly with Young's modulus and inversely with the square of the tensile strength. We extend this model using first-principle physical arguments, taking into account the geotechnical properties of the impactor. The extended model provides a better description of the data than the existing model. Yet, the fit is far from satisfactory. We suggest that the ratio of mineral grain size to the impactor diameter presents a strong control on erodibility that has not been quantified so far. We also discuss how our laboratory results upscale to real landscapes and long timescales. For both a revised stream power incision model and a sediment-flux-dependent incision model, we suggest that long-term erosion rates scale linearly with erodibility and that, within this theoretical framework, relative laboratory measurements of erodibility can be applied at the landscape scale.</p

A discrete random model describing bedrock profile abrasion

We use a simple, collision-based, discrete, random abrasion model to compute the profiles for the stoss faces in a bedrock abrasion process. The model is the discrete equivalent of the generalized version of a classical, collision based model of abrasion. Three control parameters (which describe the average size of the colliding objects, the expected direction of the impacts and the average volume removed from the body due to one collision) are sufficient for realistic predictions. Our computations show the robust emergence of steady state shapes, both the geometry and the time evolution of which shows good quantitative agreement with laboratory experiments.Comment: 9 pages, 6 figure

Contributions Made by CDC25 Phosphatases to Proliferation of Intestinal Epithelial Stem and Progenitor Cells

The CDC25 protein phosphatases drive cell cycle advancement by activating cyclin-dependent protein kinases (CDKs). Humans and mice encode three family members denoted CDC25A, -B and -C and genes encoding these family members can be disrupted individually with minimal phenotypic consequences in adult mice. However, adult mice globally deleted for all three phosphatases die within one week after Cdc25 disruption. A severe loss of absorptive villi due to a failure of crypt epithelial cells to proliferate was observed in the small intestines of these mice. Because the Cdc25s were globally deleted, the small intestinal phenotype and loss of animal viability could not be solely attributed to an intrinsic defect in the inability of small intestinal stem and progenitor cells to divide. Here, we report the consequences of deleting different combinations of Cdc25s specifically in intestinal epithelial cells. The phenotypes arising in these mice were then compared with those arising in mice globally deleted for the Cdc25s and in mice treated with irinotecan, a chemotherapeutic agent commonly used to treat colorectal cancer. We report that the phenotypes arising in mice globally deleted for the Cdc25s are due to the failure of small intestinal stem and progenitor cells to proliferate and that blocking cell division by inhibiting the cell cycle engine (through Cdc25 loss) versus by inducing DNA damage (via irinotecan) provokes a markedly different response of small intestinal epithelial cells. Finally, we demonstrate that CDC25A and CDC25B but not CDC25C compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells

Protein Phosphatase 2A Interacts with the Na+,K+-ATPase and Modulates Its Trafficking by Inhibition of Its Association with Arrestin

Background: The P-type ATPase family constitutes a collection of ion pumps that form phosphorylated intermediates during ion transport. One of the best known members of this family is the Na +,K +-ATPase. The catalytic subunit of the Na +,K +-ATPase includes several functional domains that determine its enzymatic and trafficking properties. Methodology/Principal Findings: Using the yeast two-hybrid system we found that protein phosphatase 2A (PP2A) catalytic C-subunit is a specific Na +,K +-ATPase interacting protein. PP-2A C-subunit interacted with the Na +,K +-ATPase, but not with the homologous sequences of the H +,K +-ATPase. We confirmed that the Na +,K +-ATPase interacts with a complex of A- and C-subunits in native rat kidney. Arrestins and G-protein coupled receptor kinases (GRKs) are important regulators of G-protein coupled receptor (GPCR) signaling, and they also regulate Na +,K +-ATPase trafficking through direct association. PP2A inhibits association between the Na +,K +-ATPase and arrestin, and diminishes the effect of arrestin on Na +,K +-ATPase trafficking. GRK phosphorylates the Na +,K +-ATPase and PP2A can at least partially reverse this phosphorylation. Conclusions/Significance: Taken together, these data demonstrate that the sodium pump belongs to a growing list of io