https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42656 Wed 31 Aug 2022 13:02:16 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46760 Wed 30 Nov 2022 09:30:58 AEDT ]]> 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:54300 Wed 28 Feb 2024 15:46:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45030 TAS2R4 (rs2233998 and rs2234001) and TAS2R5 (rs2227264) were associated with body mass index (BMI). Genotyping (Taqman qPCR assays) was performed on DNA extracted from blood samples (n = 563) from an elderly cohort. Homozygosity for the minor allele of all polymorphisms was significantly associated with a lower BMI in males. The TAS2R4-rs2233998 CC genotype, the TAS2R4-rs2234001 CC genotype and the TAS2R5-rs2227264 TT genotype were associated with lower BMI (2.1, 2.1 and 2.2 units; p = 0.002, 0.003 and 0.001, respectively). Epicatechin intake was not associated with BMI and genotype was not associated with epicatechin intake. This suggests that the association between TAS2R genotype and elevated BMI risk occurs through altered extra-oral responses and not directly via altered epicatechin intake.]]> Wed 26 Oct 2022 10:43:50 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:47717 Wed 25 Jan 2023 13:01:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42463 p < 0.002) and smallest with metronidazole (22.7%, p = 0.18). Overall, 8.9% (95% confidence interval: 3.9-13.9) of patients had AEs severe enough to discontinue antibiotic therapy. In PSC patients, antibiotic treatment results in a significant improvement in markers of cholestasis and MRS. Antibiotics, particularly vancomycin, may have a positive effect on PSC either via direct effects on the microbiome or via host-mediated mechanisms.]]> Wed 24 Aug 2022 11:23:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52909 Wed 22 May 2024 15:08:38 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34904 Wed 22 May 2019 12:08:39 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37585 Wed 19 Jan 2022 15:19:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33649 Wed 19 Jan 2022 15:16:53 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:50280 Wed 15 May 2024 10:35:38 AEST ]]> 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:14215 Wed 11 Apr 2018 13:17:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13807 2 wk after inflammation). Blinded outcomes were used in 42% studies, randomization in 10%, and evidence of visceral inflammation in 54%. Only 3 studies fulfilled our criteria for high methodological quality, and no study reported sample size calculations. Conclusions: The included studies provide strong evidence for CNS plasticity following GIT inflammation, specifically in the spinal cord dorsal horn. This evidence includes altered visceromotor responses and indices of referred pain, elevated neural activation and peptide content, and increased neuronal excitability. This evidence supports continued use of this approach for preclinical studies; however, there is substantial scope to improve study design.]]> Wed 11 Apr 2018 12:29:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14158 Wed 11 Apr 2018 10:28:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49859 Wed 07 Jun 2023 10:25:30 AEST ]]> 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:36106 Wed 06 Apr 2022 13:57:21 AEST ]]> 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:55535 Wed 05 Jun 2024 09:38:22 AEST ]]> 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:36082 Wed 05 Feb 2020 13:13:07 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48779 Wed 05 Apr 2023 14:30:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50715 Wed 02 Aug 2023 16:17:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48579 Tue 21 Mar 2023 17:43:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40879 Tue 19 Jul 2022 14:31:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55703 Tue 18 Jun 2024 12:51:29 AEST ]]> 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:55301 Tue 14 May 2024 17:51:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55623 Tue 11 Jun 2024 16:02:37 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:54158 Tue 06 Feb 2024 12:17:30 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:35651 84 cell monolayers grown on transparent, permeable supports was assessed over 48 h with or without bile acids. Cell migration was measured in Boyden chambers. mRNA and protein expression were measured by RT-PCR and Western blotting. DCA (50-150 μM) significantly inhibited wound closure in cultured epithelial monolayers and attenuated cell migration in Boyden chamber assays. DCA also induced nuclear accumulation of the farnesoid X receptor (FXR), whereas an FXR agonist, GW4064 (10 µM), inhibited wound closure. Both DCA and GW4064 attenuated the expression of CFTR Cl⁻ channels, whereas inhibition of CFTR activity with either CFTR-_inh-172 (10 μM) or GlyH-101 (25 µM) also prevented wound healing. Promoter/reporter assays revealed that FXR-induced downregulation of CFTR is mediated at the transcriptional level. In contrast, UDCA (50-150 µM) enhanced wound healing in vitro and prevented the effects of DCA. Finally, DCA inhibited and UDCA promoted mucosal healing in an in vivo mouse model. In conclusion, these studies suggest bile acids are important regulators of epithelial wound healing and are therefore good targets for development of new drugs to modulate intestinal barrier function in disease treatment. New & Noteworthy: The secondary bile acid, deoxycholic acid, inhibits colonic epithelial wound healing, an effect which appears to be mediated by activation of the nuclear bile acid receptor, FXR, with subsequent downregulation of CFTR expression and activity. In contrast, ursodeoxycholic acid promotes wound healing, suggesting it may provide an alternative approach to prevent the losses of barrier function that are associated with mucosal inflammation in IBD patients.]]> Tue 01 Oct 2019 13:39:00 AEST ]]> 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:45352 Thu 27 Oct 2022 11:46:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45328 30% response to the run-in diet, as measured by the Nepean Dyspepsia Index, were then re-challenged with 'muesli' bars containing either gluten, fructan, or placebo in randomised order. Those with symptoms which significantly reduced during the elimination diet, but reliably reappeared (a mean change in overall dyspeptic symptoms of >30%) with gluten or fructan re-challenge were deemed to have wheat induced FD. Results: Eleven participants were enrolled in the study (75% female, mean age 43 years). Of the initial cohort, nine participants completed the elimination diet phase of whom four qualified for the rechallenge phase. The gluten-free, low FODMAP diet led to an overall (albeit non-significant) improvement in symptoms of functional dyspepsia in the diet elimination phase (mean NDI symptom score 71.2 vs. 47.1, p = 0.087). A specific food trigger could not be reliably demonstrated. Conclusions: Although a gluten-free, low-FODMAP diet led to a modest overall reduction in symptoms in this cohort of FD patients, a specific trigger could not be identified. The modified Salerno criteria for NCG/WS identification trialled in this dietary rechallenge protocol was fit-for-purpose. However, larger trials are required to determine whether particular components of wheat induce symptoms in functional dyspepsia.]]> Thu 27 Oct 2022 08:44:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53983 Thu 25 Jan 2024 13:04:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48574 Thu 24 Aug 2023 15:19:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51213 Thu 24 Aug 2023 14:59:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45598 Thu 23 Mar 2023 13:55:28 AEDT ]]> 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:36101 Thu 17 Feb 2022 09:25:33 AEDT ]]> 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:48841 Thu 13 Apr 2023 09:46:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47378 Thu 06 Jul 2023 13:38:08 AEST ]]> 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:37534 Thu 04 Feb 2021 16:22:20 AEDT ]]> 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:13806 Sat 24 Mar 2018 08:22:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17715 Sat 24 Mar 2018 07:57:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27093 Sat 24 Mar 2018 07:40:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29359 Sat 24 Mar 2018 07:34:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22162 Immunity, Griseri et al. (2015) identify a new GM-CSF-dependent role for eosinophils in the pathogenesis of IL-23-Th17 cell-induced colitis.]]> Sat 24 Mar 2018 07:14:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24895 Sat 24 Mar 2018 07:14:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24935 Sat 24 Mar 2018 07:14:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22110 Sat 24 Mar 2018 07:13:17 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:22126 Sat 24 Mar 2018 07:09:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53532 Mon 24 Jun 2024 16:05:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43435 P_app), with differences in ML retention and complexation amongst the chelants and the gut microbes. The decrease in ML permeability varied amongst the MLs. Chelating agents reduce intestinal absorption of MLs by forming complexes thereby making them less permeable. In the case of gut bacteria, the decrease in the intestinal permeability of MLs may be associated to a direct protection of the intestinal barrier against the MLs or indirect intestinal ML sequestration by the gut bacteria through adsorption on bacterial surface. Thus, both gut microbes and chelating agents can be used to decrease the intestinal permeability of MLs, thereby mitigating their toxicity.]]> Mon 19 Sep 2022 11:35:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55689 Mon 17 Jun 2024 10:25:59 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:41872 Mon 15 Aug 2022 10:03:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46206 Mon 14 Nov 2022 11:29:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53620 Mon 13 May 2024 12:39:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37467 Mon 11 Jan 2021 16:16:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52306 Mon 09 Oct 2023 10:16:43 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:55080 Mon 08 Apr 2024 14:10:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45729 Mon 07 Nov 2022 13:12:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51416 Mon 04 Sep 2023 14:58:25 AEST ]]> 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:40013 Mon 04 Jul 2022 08:54:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34081 Fri 27 Sep 2019 10:22:06 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:33077 Chlamydia, Haemophilus influenzae, influenza, and respiratory syncytial virus respiratory tract infections and ovalbumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed and interrogated. Results: Infection induced increases in the levels of microRNA (miRNA)-21 (miR-21) expression in the lung during SSIAAD, whereas expression of the miR-21 target phosphatase and tensin homolog was reduced. This was associated with an increase in levels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased nuclear histone deacetylase (HDAC)2 levels. Treatment with an miR-21-specific antagomir (Ant-21) increased phosphatase and tensin homolog levels. Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels. This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to allergic airway disease. These observations were replicated with SSIAAD associated with 4 different pathogens. Conclusion: We identify a previously unrecognized role for an miR-21/PI3K/HDAC2 axis in SSIAAD. Our data highlight miR-21 as a novel therapeutic target for the treatment of this form of asthma.]]> Fri 24 Aug 2018 14:41:05 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:40012 Streptococcus pneumoniae, Haemophilus influenzae and Pseudomonas aeruginosa)to induce infection in both the respiratory and gastroin-testinal (GI) tracts. However, the importance and mechanism of HIF-1αin augmenting PAFR-dependent bacterial infections in COPD are poorly understood. Here, we review the evidence for the roles of local tissue hypoxia-induced inflammation, HIF-1α and PAFR in facilitating bacterial infections in COPD. Blocking PAFR may provide a novel antimicrobial approach to manage bacterial infections in COPD.]]> Fri 22 Jul 2022 13:06:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41982 Fri 19 Apr 2024 11:58:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53126 Fri 17 Nov 2023 12:21:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53162 Fri 17 Nov 2023 12:00:09 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:40046 Fri 15 Jul 2022 10:05:42 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: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 ]]>