Browsing by Subject "Gastrointestinal Tract"
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Item A revised model for radiation dosimetry in the human gastrointestinal tract(Texas A&M University, 2004-09-30) Bhuiyan, Md. Nasir UddinA new model for an adult human gastrointestinal tract (GIT) has been developed for use in internal dose estimations to the wall of the GIT and to the other organs and tissues of the body from radionuclides deposited in the lumenal contents of the five sections of the GIT. These sections were the esophagus, stomach, small intestine, upper large intestine, and the lower large intestine. The wall of each section was separated from its lumenal contents. Each wall was divided into many small regions so that the histologic and radiosensitive variations of the tissues across the wall could be distinguished. The characteristic parameters were determined based on the newest information available in the literature. Each of these sections except the stomach was subdivided into multiple subsections to include the spatiotemporal variations in the shape and characteristic parameters. This new GIT was integrated into an anthropomorphic phantom representing both an adult male and a larger-than-average adult female. The current phantom contains 14 different types of tissue. This phantom was coupled with the MCNP 4C Monte Carlo simulation package. The initial design and coding of the phantom and the Monte Carlo treatment employed in this study were validated using the results obtained by Cristy and Eckerman (1987). The code was used for calculating specific absorbed fractions (SAFs) in various organs and radiosensitive tissues from uniformly distributed sources of fifteen monoenergetic photons and electrons, 10 keV - 4 MeV, in the lumenal contents of the five sections of the GIT. The present studies showed that the average photon SAFs to the walls were significantly different from that to the radiosensitive cells (stem cells) for the energies below 50 keV. Above 50 keV, the photon SAFs were found to be almost constant across the walls. The electron SAF at the depth of the stem cells was a small fraction of the SAF routinely estimated at the contents-mucus interface. Electron studies showed that the ?self-dose? for the energies below 300 keV and the ?cross-dose? below 2 MeV were only from bremsstrahlung and fluorescent radiations at the depth of the stem cells and were not important.Item Analysis of Bacterial-Host Interactions Between Campylobacter jejuni and the Avian Host During Commensalism(2009-06-15) Bingham-Ramos, Lacey Kathleen; Hendrixson, David R.Campylobacter jejuni is a leading cause of bacterial enteritis in humans throughout the world. In contrast to the disease seen in humans upon infection, C. jejuni promotes an asymptomatic, intestinal colonization of many animals, especially avian species, to result in commensalism. The primary route of transmission to humans is through the consumption or handling of undercooked poultry meats, making C. jejuni of particular importance to the agricultural industry. The direct interplay between C. jejuni and the natural avian host was examined to better understand the interactions that contribute to commensalism. We analyzed the colonization dynamics of C. jejuni over 28 days and identified a previously uncharacterized prolonged, robust colonization of the bursa of Fabricius, a major lymphoid organ. C. jejuni localized to the mucus layer lining the epithelium of the bursal lumen, with no invasion of or damage to host tissue apparent. However, C. jejuni was detected invading the cecal epithelium of chicks but only at day 1 post-infection, which may contribute to the observed transient, infection of the spleen and liver. Additionally, certain colonization factors of C. jejuni were shown to promote persistence in specific organs. Mutants lacking catalase and the cytolethal distending toxin demonstrated a reduction in levels in the bursa but not the ceca during prolonged colonization, whereas an unencapsulated mutant showed a global colonization defect of all organs. These findings suggest that persistent colonization of the bursa and the ceca, and the ability of the avian host to largely confine C. jejuni to mucosal surfaces may be specific for the development of commensalism. Separate analyses of additional colonization factors of C. jejuni revealed the importance of two putative cytochrome c peroxidases (CCP), DocA and Cjj0382, in promoting efficient cecal colonization. Further analysis of DocA and Cjj0382 revealed that both proteins have typical characteristics of CCPs, as they are periplasmic proteins with heme-dependent peroxidase activity. Our data suggest that although DocA and Cjj0382 have characteristics of CCPs, they likely perform different physiological functions for the bacterium during colonization. Overall, this study enhances our understanding of the interactions between C. jejuni and a natural host that contribute to the development of commensalism.Item The Characterization of the Fucose Sensing Kinase (FUSK) and the Fucose Sensing Response Regulator (FUSR) and Their Role in Virulence Regulation in Enterohemorrhagic Escherichia Coli O157:H7(2013-01-17) Pacheco, Alline Roberta; Sperandio, Vanessa, Ph.D.EHEC causes outbreaks of bloody diarrhea worldwide, by colonizing the human large intestine, where it forms attaching and effacing (AE) lesions on the intestinal epithelium. AE lesion development requires the presence of the locus of enterocyte effacement (LEE) that encodes for a molecular syringe, a type three secretion system (T3SS), which translocates effectors to the host cell. Expression of the LEE is controlled by the AI-3/Epi/NE interkingdom signaling cascade. The two-component systems QseBC and QseEF are at the core of the AI-3/Epi/NE signaling, controlling expression of flagellar motility genes, the LEE and type 3 secreted effectors in response to AI-3 and the catecholamine hormones Epi and NE. The network of regulatory proteins that form the AI-3/Epi/NE continues to expand, as shown by recent studies from our laboratory. Microarray analyses indicate that a putative two-component system (TCS), herein named FusKR, is repressed by QseBC and QseEF. FusK is the histidine kinase and FusR is the response regulator. In this work, we started to unravel the role of FusKR in EHEC pathogenicity. We constructed isogenic knockouts of fusK and fusR, and investigated their participation in virulence gene regulation in EHEC. Microarray analysis shows that deletion of fusK and fusR alters transcription of virulence and metabolic genes. Phenotypic analyses show that fusK- and fusR- strains are hypervirulent in vitro, overexpress the LEE genes and produces higher amounts of the T3 secreted protein EspB. Nonetheless, the fusK mutant is attenuated for colonization of the mammalian intestine. Biochemical studies revealed that FusK senses fucose. Fucose is an important carbon source for commensal and pathogenic bacteria during intestinal colonization. Transcriptional analyses shows that FusKR signal transduction system regulates fucose utilization indirectly, through regulation of the predicted membrane transporter Z0461, involved in optimal fucose uptake. Gut commensal Bacteroides thetaiomicron (B.theta) degrades mucin, releasing free monosaccharides, including fucose, into the gut lumen. Co-culture of B.theta and EHEC on mucin indicates that this commensal supplies mucin-derived fucose to EHEC, reducing expression of the LEE. Our studies demonstrate that a novel TCS, FusKR, modulates intestinal colonization by EHEC, and it is involved in complex interactions with the microbiota during infection.