https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38040 Wed 28 Jul 2021 10:17:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50276 Wed 28 Feb 2024 15:44:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50452 Wed 26 Jul 2023 13:14:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49619 2 GI tract areas are involved, the name should reflect all of the involved areas. Conclusions: This international process resulted in consensus for updated EGID nomenclature for both clinical and research use. EGID will be the umbrella term, rather than “eosinophilic gastroenteritis,” and specific naming conventions by location of GI tract involvement are recommended. As more data are developed, this framework can be updated to reflect best practices and the underlying science.]]> Wed 24 May 2023 11:40:45 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47509 Wed 24 Jan 2024 15:29:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30268 Wed 23 Feb 2022 16:06:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38722 Wed 19 Jan 2022 09:36:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37859 P = 0.04). The surrounding or invasion of nerves by cancer cells (perineural invasion) was detected in 12% of esophageal cancers and was associated with reduced survival (P = 0.04). Nerves were found to express the following receptors for nerve growth factor (NGF): neurotrophic receptor tyrosine kinase 1 and nerve growth factor receptor. An association was suggested between high production of NGF by cancer cells and the presence of nerves (P = 0.02). In vitro, NGF production in esophageal cancer cells was shown by Western blot, and esophageal cancer cells were able to induce neurite outgrowth in the PC12 neuronal cells. The neurotrophic activity of esophageal cancer cells was inhibited by anti-NGF blocking antibodies. Together, these data suggest that innervation is a feature in esophageal cancers that may be driven by cancer cell-released NGF.]]> Wed 17 Nov 2021 16:31:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36096 Helicobacter pylori pathologies, cancer, coeliac disease, and autoimmune gastritis. Recent research is unraveling pathophysiology beyond symptom-only definitions, focusing on the duodenum with innate immune disturbance (duodenal eosinophilia) and microbial disruption as possible cause. Management of functional dyspepsia includes making a secure diagnosis, treatment with first-line proton pump inhibitors (PPI), then tricyclic antidepressants, and careful choice of prokinetics. Herbal treatments (peppermint oil) and STW-5 have in this age group limited efficacy. Summary: Further studies are needed to define the prevalence of functional dyspepsia in the elderly and of prime importance, to exclude organic disease as a cause for symptoms of dyspepsia.]]> Wed 15 Dec 2021 16:10:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47086 0.05). Similar results were found for IBS subtypes. Higher serum L-arginine concentration had the strongest association with IBS diagnosis, with an odds ratio of 9.03 for those with serum L-arginine at the 75th (84 μmol/L) versus 25th (46 μmol/L) percentile (95% CI: 5.99–13.62). L-arginine had the best discriminative ability with a bias-adjusted area under the receiver operator characteristic curve of 0.859. Conclusions: Higher serum concentrations of L-arginine and endogenous methylarginines are strongly associated with IBS in adults.]]> Wed 14 Dec 2022 09:23:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50849 Wed 13 Mar 2024 15:39:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41179 Wed 12 Jul 2023 11:51:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27772 Wed 11 Apr 2018 15:54:06 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30281 Fbln1c protected against CS-induced airway fibrosis and emphysema-like alveolar enlargement. In experimental COPD, this occurred through disrupted collagen organization and interactions with fibronectin, periostin, and tenascin-c. Genetic inhibition of Fbln1c also reduced levels of pulmonary inflammatory cells and proinflammatory cytokines/chemokines (TNF-a, IL-33, and CXCL1) in experimental COPD. Fbln1c⌿ mice also had reduced airway remodeling in experimental chronic asthma and pulmonary fibrosis. Our data show that Fbln1c may be a therapeutic target in chronic respiratory diseases.]]> Wed 11 Apr 2018 13:33:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27771 In vitro, breast cancer cells were able to induce neurite outgrowth in PC12 cells, and this neurotrophic activity was partially inhibited by anti-NGF blocking antibodies. In conclusion, infiltration by nerve fibers is a feature of the tumor microenvironment that is associated with aggressiveness and involves NGF production by cancer cells. The potential participation of nerve fibers in breast cancer progression needs to be further considered.]]> Wed 11 Apr 2018 11:44:48 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53695 Wed 10 Jan 2024 10:42:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33706 Wed 09 Mar 2022 16:04:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36867 NTR, and the proneurotrophin receptor sortilin were analyzed with immunohistochemistry in a cohort of thyroid cancers (n = 128) and compared with adenomas and normal thyroid tissues (n = 62). TrkA was detected in 20% of thyroid cancers, compared with none of the benign samples (P = 0.0007). TrkA expression was independent of histologic subtypes but associated with lymph node metastasis (P = 0.0148), suggesting the involvement of TrkA in tumor invasiveness. Nerves in the tumor microenvironment were positive for TrkA. p75^NTR was overexpressed in anaplastic thyroid cancers compared with papillary and follicular subtypes (P < 0.0001). Sortilin was overexpressed in thyroid cancers compared with benign thyroid tissues (P < 0.0001). Neurotrophin receptor expression was confirmed in a panel of thyroid cancer cell lines at the mRNA and protein levels. Functional investigations using the anaplastic thyroid cancer cell line CAL-62 found that siRNA against TrkA, p75^NTR, and sortilin decreased cell survival and cell migration through decreased SRC and ERK activation. Together, these data reveal TrkA, p75^NTR, and sortilin as potential therapeutic targets in thyroid cancer.]]> Wed 09 Feb 2022 15:52:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36862 Wed 07 Apr 2021 20:17:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34069 in vivo preparation and patch-clamp electrophysiology to test whether the synaptic and intrinsic properties of superficial dorsal horn (SDH) neurons are altered 5 days after the induction of mild colitis in adult male mice (i.e. during acute inflammation of the colon). Whole-cell recordings were made from lumbosacral (L6-S1) superficial dorsal horn neurons (SDH), in animals under isoflurane anesthesia. Noxious colorectal distension (CRD) was used to identify SDH neurons with colonic inputs, while stimulation of the hind paw and tail was employed to assess convergent cutaneous input. Following inflammation, a significantly increased proportion of SDH neurons received both colonic and cutaneous inputs, compared to neurons in naïve animals. In addition, the nature and magnitude of responses to CRD and cutaneous stimulation differed in inflamed animals, as was spontaneous excitatory synaptic drive. Conversely, several measures of intrinsic excitability were altered in a manner that would decrease SDH network excitability following colitis. We propose that during inflammation, sensitization of colonic afferents results in increased signaling to the SDH. This is accompanied by plasticity in SDH neurons whereby their intrinsic properties are changed to compensate for altered afferent activity.]]> Wed 06 Feb 2019 09:51:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44040 Wed 05 Oct 2022 15:32:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36083 Wed 05 Feb 2020 13:13:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49006 Wed 03 May 2023 12:17:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41421 Wed 03 Aug 2022 11:59:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47794 Tue 31 Jan 2023 15:19:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49759 Tue 30 May 2023 18:25:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46669 Brachyspira aalborgi type strain, 513A. Also, 16S analysis of the mucosa-associated microbiota was performed in the cases and nonspirochetosis controls. We found one isolate to be of the species Brachyspira pilosicoli; all remaining isolates were of the species Brachyspira aalborgi. Besides displaying extensive genetic heterogeneity, the isolates harbored several mucin-degrading enzymes and other virulence-associated genes that could confer a pathogenic potential in the human colon. We also showed that 16S amplicon sequencing using standard primers for human microbiota studies failed to detect Brachyspira due to primer incompatibility. IMPORTANCE This is the first report of whole-genome analysis of clinical isolates from individuals with colonic spirochetosis. This characterization provides new opportunities in understanding the physiology and potentials of these bacteria that densely colonize the gut in the individuals infected. The observation that standard 16S amplicon primers fail to detect colonic spirochetosis may have major implications for studies searching for associations between members of the microbiota and clinical conditions such as irritable bowel syndrome (IBS) and should be taken into consideration in project design and interpretation of gastrointestinal tract microbiota in population-based and clinical settings.]]> Tue 29 Nov 2022 08:39:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47656 Tue 24 Jan 2023 15:26:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44768 Tue 21 Mar 2023 16:48:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37101 Tue 18 Aug 2020 10:23:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33176 6× upper limit of normal (ULN) and 4 had >10× ULN. TTG Ab-positive patients were classified as having either potential CD with (n = 3, 16%) and without lymphocytic duodenosis (LD; n = 12, 63%), and no CD (n = 4, 21%) on human leukocyte antigen typing. There was an increase in duodenal eosinophils in patients with elevated TTG Ab (P = 0.01), which remained when patients with LD were excluded (P = 0.018). Of 19 patients with EoE and elevated TTG Ab, 5 responded to elimination diet involving exclusion of wheat, including 2 with a sole wheat trigger and TTG Ab >10× ULN that were CD-associated human leukocyte antigen-negative. Conclusions: Serum TTG Ab was elevated in almost one-quarter of our total EoE cohort, and at least 20% of these patients did not have potential CD, suggesting EoE is a heterogeneous disease with differing immune mechanisms activated in some patients. These findings also support routine esophageal biopsy during upper endoscopy in children with elevated TTG Ab.]]> Tue 11 Sep 2018 12:15:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50115 Tue 11 Jul 2023 15:54:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25796 Tue 11 Feb 2020 09:19:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46015  0.5). Conclusions: In FD patients, the response to antimicrobial therapy with rifaximin is not influenced by concomitant IBS symptoms.]]> Tue 08 Nov 2022 18:38:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43821 +ß7⁺ gut-homing T cells appear to be linked to the pathophysiology of both FD and IBS. Studies in the area are complicated by poor phenotyping of patients into subgroups and the subtle nature of the immune activity involved in FD and IBS. CONCLUSIONS: Alterations in proportions of gut-homing T lymphocytes in both FD and IBS indicate that a loss of mucosal homeostasis may drive the symptoms of FD and IBS. There is indirect evidence that Th17 responses may play a role in FGIDs, however the evidence for a Th2 immune phenotype in FD and IBS is limited. Although immune involvement is evident, large, well-characterised patient cohorts are required to elucidate the immune mechanisms driving the development of FGIDs.]]> Tue 04 Oct 2022 10:29:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33993 Firmicutes, specifically Streptococcus and Veillonella spp. The relative abundance of the genus Rothia was also observed to be greater in current smokers; while in contrast, levels of Prevotella and Neisseria were lower. The MAM profiles and diversity of previous smokers were observed to be intermediate between current and never smokers. Smoking did not impact the total density of bacteria present on the mucosa. Conclusions: These data indicate the duodenal MAM of current smokers is characterised by reduced bacterial diversity, which is partially but not completely restored in previous smokers. While the precise mechanisms remain to be elucidated, these microbiota changes may in some part explain the adverse effects of smoking on mucosa-associated diseases of the GI tract. Smoking status requires consideration when interpreting MAM data.]]> Tue 03 Sep 2019 17:58:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23037 Thu 28 Oct 2021 12:35:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45013 Thu 27 Oct 2022 17:46:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45363 Thu 27 Oct 2022 11:46:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41003 Thu 21 Jul 2022 10:51:13 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41177 Thu 18 Apr 2024 12:11:34 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33627 Thu 17 Feb 2022 09:31:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36101 Thu 17 Feb 2022 09:25:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40083 Helicobacter pylori induces strong inflammatory responses that are directed at clearing the infection, but if not controlled, these responses can be harmful to the host. We investigated the immune-regulatory effects of the innate immune molecule, nucleotide-binding oligomerization domain-like receptors (NLR) family CARD domain-containing 5 (NLRC5), in patients and mice with Helicobacter infection. Methods: We obtained gastric biopsies from 30 patients in Australia. We performed studies with mice that lack NLRC5 in the myeloid linage (Nlrc5^møKO) and mice without Nlrc5 gene disruption (controls). Some mice were gavaged with H pylori SS1 or Helicobacter felis; 3 months later, stomachs, spleens, and sera were collected, along with macrophages derived from bone marrow. Human and mouse gastric tissues and mouse macrophages were analyzed by histology, immunohistochemistry, immunoblots, and quantitative polymerase chain reaction. THP-1 cells (human macrophages, controls) and NLRC5^-/- THP-1 cells (generated by CRISPR-Cas9 gene editing) were incubated with Helicobacter and gene expression and production of cytokines were analyzed. Results: Levels of NLRC5 messenger RNA were significantly increased in gastric tissues from patients with H pylori infection, compared with patients without infection (P <.01), and correlated with gastritis severity (P <.05). H pylori bacteria induced significantly higher levels of chemokine and cytokine production by NLRC5^-/- THP-1 macrophages than by control THP-1 cells (P <.05). After 3 months of infection with H felis, Nlrc5^mø-KO mice developed gastric hyperplasia (P <.0001), splenomegaly (P <.0001), and increased serum antibody titers (P <.01), whereas control mice did not. Nlrc5^mø-KO mice with chronic H felis infection had increased numbers of gastric B-cell follicles expressing CD19 (P <.0001); these follicles had features of mucosa-associated lymphoid tissue lymphoma. We identified B-cell-activating factor as a protein that promoted B-cell hyperproliferation in Nlrc5^mø-KO mice. Conclusions: NLRC5 is a negative regulator of gastric inflammation and mucosal lymphoid formation in response to Helicobacter infection. Aberrant NLRC5 signaling in macrophages can promote B-cell lymphomagenesis during chronic Helicobacter infection.]]> Thu 14 Jul 2022 12:19:41 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34597 Thu 13 Jan 2022 10:31:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48867 Thu 13 Apr 2023 10:07:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48841 Thu 13 Apr 2023 09:46:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46068 Thu 10 Nov 2022 14:23:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48154 Thu 09 Mar 2023 09:37:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36110 Thu 06 Feb 2020 14:11:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36102 Thu 06 Feb 2020 12:12:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36099 Thu 06 Feb 2020 11:37:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50509  3 bowel motions a day (OR 1.50, 95% CI 1.08, 2.07, p = 0.02; OR = 1.67, 95% CI 1.11, 2.51, p = 0.01), and loose stools (OR 1.40, 95% CI 1.04, 1.90, p = 0.03; OR = 1.68, 95% CI 1.13, 2.51, p = 0.01) at the 1- and 3-year follow-ups, respectively. Conclusions & Inferences: Diabetes is an independent risk factor for a greater frequency of early satiation and diarrhea, adjusting for lifestyle and psychological factors.]]> Thu 03 Aug 2023 11:12:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49117 Thu 02 May 2024 12:18:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48476 Sun 19 Mar 2023 15:13:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31133 Sat 24 Mar 2018 08:44:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14790 Sat 24 Mar 2018 08:26:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19968 Sat 24 Mar 2018 07:58:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19564 Sat 24 Mar 2018 07:58:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17888 Sat 24 Mar 2018 07:56:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21293 Sat 24 Mar 2018 07:54:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18376 Sat 24 Mar 2018 07:52:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20655 Sat 24 Mar 2018 07:49:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29439 Sat 24 Mar 2018 07:39:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27400 Helicobacter pylori testing and eradication is recommended. Based on currently available data, acotiamide appears promising, particularly in postprandial distress syndrome. Further large-scale multicentered trials are required to define the duration of treatment and the side-effect profile.]]> Sat 24 Mar 2018 07:34:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27132 Brachyspira in colonic biopsies, is uncommon and considered of doubtful significance. We aimed to determine the prevalence of CS in the general population, identify subtle colon pathologies, and evaluate a link with symptoms of IBS. Colonoscopy was performed in 745 subjects (aged 19-70 years, mean age 51 years, 43% male) with biopsies (ileum and 4 colonic sites) from a random population sample, Stockholm, Sweden, who completed a validated questionnaire of gastrointestinal symptoms; IBS was identified by Rome III criteria. CS was identified by histology and immunohistochemistry. In a general population, 17 individuals (2.28%; 95% confidence interval, 1.2%-3.5%) were diagnosed as having CS by histology; 6 (35%) had IBS. CS was always present in the sigmoid colon, but only 14 rectal biopsies. Eosinophils were increased in colon biopsies in CS cases versus controls, in the transverse (P =.02), sigmoid colon (P =.001), and rectum (P =.0005) with subepithelial eosinophil clusters (P =.053). Lymphoid follicles (at any site) were present in 13 CS (P =.0003). There was a 3-fold increased risk of IBS in CS (odds ratio, 3.59; 95% confidence interval, 1.27-10.11; P =.015). Polyps and diverticular disease were similar in CS cases and controls. The prevalence of CS in a general population is 2% and associated with nonconstipating IBS. Colonic eosinophilia with lymphoid follicles may signify the presence of CS.]]> Sat 24 Mar 2018 07:33:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30502 Sat 24 Mar 2018 07:26:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28919 Sat 24 Mar 2018 07:25:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24892 Sat 24 Mar 2018 07:14:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24504 Sat 24 Mar 2018 07:13:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22734 Sat 24 Mar 2018 07:12:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23828 Sat 24 Mar 2018 07:12:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54589 Sat 02 Mar 2024 10:51:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32805 Mon 23 Sep 2019 10:39:48 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49546 Mon 22 May 2023 08:45:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42367 Mon 22 Aug 2022 14:08:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50098 Mon 17 Jul 2023 11:05:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46215 Mon 14 Nov 2022 12:04:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48208 Mon 08 May 2023 15:57:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37123 Mon 06 Mar 2023 16:12:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36442 Mon 04 May 2020 14:01:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34348 Mon 04 Mar 2019 14:57:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40013 Mon 04 Jul 2022 08:54:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39241 P = 0.022 adjusted for age, sex, and smoking). Cecal IELs were increased in IBS—diarrhea (relative risk ratio = 2.03, 95% confidence interval 1.13–3.63, P = 0.017). No difference was observed in alpha diversity of MaM or fecal microbiota based on IEL count. There was no difference in beta diversity of the MaM according to IEL count in the terminal ileal (TI) (P = 0.079). High TI IEL counts associated with a significant expansion of the genus Blautia (P = 0.024) and unclassified Clostridiales (P = 0.036) in colon MaM. Discussion: A modest but significant increase in IELs was observed in IBS vs. controls in a population-based setting. Subtle TI and cecal inflammation may play a pathogenic role in IBS but needs confirmation. Modest but discernible differences in the colonic MaM were seen according to TI IEL count but not IBS status.]]> Fri 27 May 2022 14:39:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27125 Fri 25 Sep 2020 11:41:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35708 Indian Journal of Medical Research, 149, April 2019, pp 437-440.]]> Fri 25 Oct 2019 15:19:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49999 Fri 23 Jun 2023 11:40:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51590 Fri 22 Sep 2023 13:41:03 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24284 Fri 18 Nov 2016 10:49:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51709 Fri 15 Sep 2023 14:09:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44360 Fri 14 Oct 2022 08:44:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47355 Fri 13 Jan 2023 13:26:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49401 Fri 12 May 2023 14:41:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49370 Fri 12 May 2023 13:38:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55276 Fri 10 May 2024 11:13:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36857 Fri 10 Jul 2020 19:14:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49107 Fri 05 May 2023 11:32:08 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49104 Fri 05 May 2023 11:32:06 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36750 Fri 03 Jul 2020 09:05:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39978 Fri 01 Jul 2022 09:58:32 AEST ]]>