6 research outputs found
Microscopy analysis of soils at the Phoenix landing site, Mars: Classification of soil particles and description of their optical and magnetic properties
No full textThe optical microscope onboard the Phoenix spacecraft has returned color images (4 ?m pixel?1) of soils that were delivered to and held on various substrates. A preliminary taxonomy of Phoenix soil particles, based on color, size, and shape, identifies the following particle types [generic names in brackets]: (1) reddish fines, mostly unresolved, that are spectrally similar to (though slightly darker than) global airborne dust [red fines], (2) silt? to sand?sized brownish grains [brown sand], (3) silt? to sand?sized black grains [black sand], and (4) small amounts of whitish fines, possibly salts [white fines]. Most particles have a saturation magnetization in the range 0.5?2 Am2 kg?1 as inferred from their interaction with magnetic substrates. The particle size distribution has two distinct peaks below 10 ?m (fines) and in the range 20–100 ?m (grains), respectively, and is different from that of ripple soils in Gusev crater. In particular medium to large sand grains appear to be absent in Phoenix soils. Most sand grains have subrounded shape with variable texture. A fractured grain (observed on sol 112) reveals evidence of micrometer?sized crystal facets. The brown sand category displays a large diversity in color including shiny, almost colorless particles. Potential source regions for these grains may be the Tharsis volcanoes or Heimdal crater (20 km east of the landing site). The black grains are suggested to belong to a more widespread population of particles with mafic mineralogy. The absence of black/brown composite grains is consistent with different formation pathways and source regions for each grain type.Precision and Microsystems EngineeringMechanical, Maritime and Materials Engineerin
Actin Cross-Linking Effector Domain of the Vibrio vulnificus F-Type MARTX Toxin Dominates Disease Progression During Intestinal Infection
No full textVibrio vulnificus is an opportunistic pathogen that causes gastroenteritis and septicemia in humans. The V. vulnificus multifunctional-autoprocessing repeats-in-toxin (MARTX) toxin is a pore-forming toxin that translocates multiple functionally independent effector domains into target cells and an essential virulence factor for fatal disease. The effector repertoire delivered and thus the mechanism of action of the toxin can differ dramatically across V. vulnificus isolates. Here, we utilize a strain of V. vulnificus that carries an F-type MARTX toxin that delivers an actin cross-linking domain (ACD) and four other effector domains. We demonstrate that ACD is the primary driver of virulence following intragastric infection and of bacterial dissemination to distal organs. We additionally show that ACD activates the transcription of intermediate early response genes in cultured intestinal epithelial cells (IECs). However, the genes activated by ACD are suppressed, at least in part, by the codelivered Ras/Rap1-specific endopeptidase (RRSP). The transcriptional response induced by strains translocating only RRSP results in a unique transcriptional profile, demonstrating that the transcriptional response to V. vulnificus is remodeled rather than simply suppressed by the MARTX toxin effector repertoire. Regardless, the transcriptional response in the intestinal tissue of infected mice is dominated by ACD-mediated induction of genes associated with response to tissue damage and is not impacted by RRSP or the three other effectors codelivered with ACD and RRSP. These data demonstrate that while other effectors do remodel early intestinal innate immune responses, ACD is the dominant driver of disease progression by ACD(+) V. vulnificus during intestinal infection
Direct Cloning Method for Expression of Recombinant Proteins with an Inositol Hexakisphosphate Inducible Self-Cleaving Tag
No full text
TRPV1 and the MCP-1/CCR2 Axis Modulate Post-UTI Chronic Pain
No full textAbstractThe etiology of chronic pelvic pain syndromes remains unknown. In a murine urinary tract infection (UTI) model, lipopolysaccharide of uropathogenic E. coli and its receptor TLR4 are required for post-UTI chronic pain development. However, downstream mechanisms of post-UTI chronic pelvic pain remain unclear. Because the TRPV1 and MCP-1/CCR2 pathways are implicated in chronic neuropathic pain, we explored their role in post-UTI chronic pain. Mice were infected with the E. coli strain SΦ874, known to produce chronic allodynia, and treated with the TRPV1 antagonist capsazepine. Mice treated with capsazepine at the time of SΦ874 infection failed to develop chronic allodynia, whereas capsazepine treatment of mice at two weeks following SΦ874 infection did not reduce chronic allodynia. TRPV1-deficient mice did not develop chronic allodynia either. Similar results were found using novelty-suppressed feeding (NSF) to assess depressive behavior associated with neuropathic pain. Imaging of reporter mice also revealed induction of MCP-1 and CCR2 expression in sacral dorsal root ganglia following SΦ874 infection. Treatment with a CCR2 receptor antagonist at two weeks post-infection reduced chronic allodynia. Taken together, these results suggest that TRPV1 has a role in the establishment of post-UTI chronic pain, and CCR2 has a role in maintenance of post-UTI chronic pain.</jats:p
