The Experts below are selected from a list of 309 Experts worldwide ranked by ideXlab platform
Therese Sørlie - One of the best experts on this subject based on the ideXlab platform.
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abstract a18 the tankyrase inhibitor g007 lk inhibits Small Intestine lgr5 stem cell proliferation without altering Tissue morphology
Cancer Research, 2016Co-Authors: Jens Henrik Norum, Raoul Kuiper, Jo Waaler, Stefan Krauss, Ellen Skarpen, Andreas Brech, Therese SørlieAbstract:Tankyrase enzymes play crucial roles in the Wnt signaling pathway, involved in the regulation of intestinal stem cells and Tissue homeostasis. Aberrant Wnt signaling is known to cause intestinal cancers and the tankyrase inhibitor G007-LK has previously been shown to inhibit tumor growth in an APC-mutant colorectal cancer xenograft model. We have used in vivo models to address the effect of G007-LK on Small Intestine Tissue homeostasis. The mice were treated for up to 3 weeks with the tankyrase inhibitor, without affecting the body mass or observed clinical condition of the mice. HE 2015 Oct 23-26; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2016;76(3 Suppl):Abstract nr A18.
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abstract 3032 the effect of a tankyrase inhibitor on the Small Intestine Tissue homeostasis
Cancer Research, 2014Co-Authors: Jens Henrik Norum, Raoul Kuiper, Jo Waaler, Stefan Krauss, Ellen Skarpen, Andreas Brech, Therese SørlieAbstract:Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA In the Small Intestine the Wnt/β-catenin pathway is involved in regulation of stem cells and Tissue homeostasis. Aberrant Wnt signaling is known to cause intestinal cancers. Tankyrase enzymes play crucial roles in the regulation of the Wnt signaling pathway. Inhibition of tankyrase activity is an effective way of inhibiting Wnt/β-catenin signaling. A Small molecule tankyrase inhibitor, G007-LK, was developed that inhibits tumor growth in a APC-mutant colorectal cancer xenograft model. In in vivo experiments at high doses (60 mg/kg), G007-LK treatment resulted in severe necrosis and inflammation in the Small Intestine, possibly affecting the stem cells. Different cell populations in the Small Intestine have been shown to have stem cell properties, including the Lgr5+ cell population located at the bottom of the crypts and the cells residing in +4 position counting from the crypt base. Both of these cell populations can give rise to all the various cell types of the Small Intestine. In the current project, we have used in vivo models to address the effect of the tankyrase inhibitor, G007-LK, on Small Intestine Tissue homeostasis. H&E staining of fixed Tissue sections showed no significant differences between mice treated with 10 mg/kg G007-LK or vehicle. We performed lineage tracing from the Lgr5+ stem cells of the Small Intestine and observed that treatment with G007-LK reduced the number of cells traced from Lgr5+ stem cells. Immunohistochemistry (IHC) staining for the proliferation marker Ki67 showed reduced number of positive cells in the Small intestinal crypts of the G007-LK- compared to vehicle-treated mice. As expected, IHC staining for β-catenin showed reduced number of positive nuclei in the G007-LK- compared to vehicle-treated mice, suggesting reduced signaling via the Wnt/β-catenin pathway. Taken together, our data show that a daily dose of the tankyrase inhibitor G007-LK (10 mg/kg), is well tolerated by mice. Administration of the tankyrase inhibitor to the mice reduces the number of lineage traced cells from the Lgr5+ stem cell population in the Small Intestine, without altering the general histology of the Tissue. Citation Format: Jens Henrik Norum, Ellen Skarpen, Andreas Brech, Raoul Kuiper, Jo Waaler, Stefan Krauss, Therese Sorlie. The effect of a tankyrase inhibitor on the Small Intestine Tissue homeostasis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3032. doi:10.1158/1538-7445.AM2014-3032
J F Huntley - One of the best experts on this subject based on the ideXlab platform.
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direct anthelmintic and immunostimulatory effects of oral dosing semi purified phytohaemagglutinin lectin in sheep infected with teladorsagia circumcincta and trichostrongylus colubriformis
Veterinary Parasitology, 2012Co-Authors: Riosde L Alvarez, F Jackson, A W Greer, G Grant, E Jackson, Alison A Morrison, J F HuntleyAbstract:Lectins are plant secondary compounds that can have anthelmintic properties in vitro. In particular, the phytohaemagglutinin lectin extracted from Phaseolus vulgaris has been shown to inhibit the feeding of Trichostrongylus colubriformis and Teladorsagia circumcincta L1 larvae. However, little is known about the potential anthelmintic properties of this lectin in vivo and its suitability to control gastrointestinal parasite infections in lambs. In a 2 × 2 study, lambs were either orally dosed, or not, with 2.3 mg semi-purified PHA lectin per kg live weight (LW) per day, whilst concurrently infected, or not, with 1000 T. circumcincta and 1000 T. colubriformis L3 infective larvae per day for 42 days. There were no adverse clinical effects observed with this dose of PHA lectin. Although worm burdens were similar, animals dosed with PHA lectin had reduced concentration of nematode eggs in the faeces compared with their non-lectin dosed counterparts (P = 0.026), suggesting that there may be a direct effect of PHA lectin on parasite fecundity. Irrespective of infection, PHA lectin had immune-stimulatory properties with increased eosinophillia in both abomasal and Small Intestine Tissue sections taken at slaughter on day 42 (P < 0.02 for both) and a tendency for decreased ability of Teladorsagia larvae to penetrate abomasal Tissue explants (P = 0.06). Compared with infection alone, concurrent PHA lectin dosing and infection further increased the number of eosinophils (P < 0.01), PAS-positive (mucin-producing cells) (P = 0.03) and tended to increase the number of T helper cells (P = 0.06). No interactions were observed for cell populations in Small Intestine Tissue sections. These results suggest PHA lectin could have two possible modes of action against T. circumcincta and T. colubriformis, a direct anthelmintic effect on nematode fecundity and an indirect effect through enhancing local immune responses in the host.
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Direct anthelmintic and immunostimulatory effects of oral dosing semi-purified phytohaemagglutinin lectin in sheep infected with Teladorsagia circumcincta and Trichostrongylus colubriformis.
Veterinary parasitology, 2012Co-Authors: L Ríos-de Álvarez, F Jackson, A W Greer, G Grant, E Jackson, Alison A Morrison, J F HuntleyAbstract:Lectins are plant secondary compounds that can have anthelmintic properties in vitro. In particular, the phytohaemagglutinin lectin extracted from Phaseolus vulgaris has been shown to inhibit the feeding of Trichostrongylus colubriformis and Teladorsagia circumcincta L1 larvae. However, little is known about the potential anthelmintic properties of this lectin in vivo and its suitability to control gastrointestinal parasite infections in lambs. In a 2 × 2 study, lambs were either orally dosed, or not, with 2.3mg semi-purified PHA lectin per kg live weight (LW) per day, whilst concurrently infected, or not, with 1000 T. circumcincta and 1000 T. colubriformis L3 infective larvae per day for 42 days. There were no adverse clinical effects observed with this dose of PHA lectin. Although worm burdens were similar, animals dosed with PHA lectin had reduced concentration of nematode eggs in the faeces compared with their non-lectin dosed counterparts (P=0.026), suggesting that there may be a direct effect of PHA lectin on parasite fecundity. Irrespective of infection, PHA lectin had immune-stimulatory properties with increased eosinophillia in both abomasal and Small Intestine Tissue sections taken at slaughter on day 42 (P
Jens Henrik Norum - One of the best experts on this subject based on the ideXlab platform.
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abstract a18 the tankyrase inhibitor g007 lk inhibits Small Intestine lgr5 stem cell proliferation without altering Tissue morphology
Cancer Research, 2016Co-Authors: Jens Henrik Norum, Raoul Kuiper, Jo Waaler, Stefan Krauss, Ellen Skarpen, Andreas Brech, Therese SørlieAbstract:Tankyrase enzymes play crucial roles in the Wnt signaling pathway, involved in the regulation of intestinal stem cells and Tissue homeostasis. Aberrant Wnt signaling is known to cause intestinal cancers and the tankyrase inhibitor G007-LK has previously been shown to inhibit tumor growth in an APC-mutant colorectal cancer xenograft model. We have used in vivo models to address the effect of G007-LK on Small Intestine Tissue homeostasis. The mice were treated for up to 3 weeks with the tankyrase inhibitor, without affecting the body mass or observed clinical condition of the mice. HE 2015 Oct 23-26; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2016;76(3 Suppl):Abstract nr A18.
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abstract 3032 the effect of a tankyrase inhibitor on the Small Intestine Tissue homeostasis
Cancer Research, 2014Co-Authors: Jens Henrik Norum, Raoul Kuiper, Jo Waaler, Stefan Krauss, Ellen Skarpen, Andreas Brech, Therese SørlieAbstract:Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA In the Small Intestine the Wnt/β-catenin pathway is involved in regulation of stem cells and Tissue homeostasis. Aberrant Wnt signaling is known to cause intestinal cancers. Tankyrase enzymes play crucial roles in the regulation of the Wnt signaling pathway. Inhibition of tankyrase activity is an effective way of inhibiting Wnt/β-catenin signaling. A Small molecule tankyrase inhibitor, G007-LK, was developed that inhibits tumor growth in a APC-mutant colorectal cancer xenograft model. In in vivo experiments at high doses (60 mg/kg), G007-LK treatment resulted in severe necrosis and inflammation in the Small Intestine, possibly affecting the stem cells. Different cell populations in the Small Intestine have been shown to have stem cell properties, including the Lgr5+ cell population located at the bottom of the crypts and the cells residing in +4 position counting from the crypt base. Both of these cell populations can give rise to all the various cell types of the Small Intestine. In the current project, we have used in vivo models to address the effect of the tankyrase inhibitor, G007-LK, on Small Intestine Tissue homeostasis. H&E staining of fixed Tissue sections showed no significant differences between mice treated with 10 mg/kg G007-LK or vehicle. We performed lineage tracing from the Lgr5+ stem cells of the Small Intestine and observed that treatment with G007-LK reduced the number of cells traced from Lgr5+ stem cells. Immunohistochemistry (IHC) staining for the proliferation marker Ki67 showed reduced number of positive cells in the Small intestinal crypts of the G007-LK- compared to vehicle-treated mice. As expected, IHC staining for β-catenin showed reduced number of positive nuclei in the G007-LK- compared to vehicle-treated mice, suggesting reduced signaling via the Wnt/β-catenin pathway. Taken together, our data show that a daily dose of the tankyrase inhibitor G007-LK (10 mg/kg), is well tolerated by mice. Administration of the tankyrase inhibitor to the mice reduces the number of lineage traced cells from the Lgr5+ stem cell population in the Small Intestine, without altering the general histology of the Tissue. Citation Format: Jens Henrik Norum, Ellen Skarpen, Andreas Brech, Raoul Kuiper, Jo Waaler, Stefan Krauss, Therese Sorlie. The effect of a tankyrase inhibitor on the Small Intestine Tissue homeostasis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3032. doi:10.1158/1538-7445.AM2014-3032
Zhongrong Zhou - One of the best experts on this subject based on the ideXlab platform.
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Influence of clamping parameters on the trauma of rabbit Small Intestine Tissue.
Clinical Biomechanics, 2019Co-Authors: Jin Wang, Bing-rui Wang, Wei Li, Zhongrong ZhouAbstract:Abstract Background During clamping operation for minimally invasive intestinal surgery, patients often suffer from Small Intestine trauma. This phenomenon will lead to various complications, increase recovery time and cause pain for patients. Methods In this paper, preliminary simulations of Small Intestine clamping operations in the minimally invasive surgery were made by conducting compression tests under different clamping stresses, durations and loading rates. A pathological grading system was designed after microscope observation to quantitatively evaluate the trauma of Small Intestine Tissue. Findings Results showed that different traumas: inflammatory cell infiltration, hyperemia, hemorrhage and rupture between serosa and muscularis, as well as villi destruction could be observed on the clamping sites of the Small Intestine Tissue. When the clamping parameters (clamping stress, duration and loading rate) increased, the degree of the Tissue trauma increased. There existed safe thresholds for clamping operations, at which severe trauma of Small Intestine Tissues could be avoided in the clamping process. Interpretation As the clamping parameters increased, the strain, that is the deformation of the Small Intestine Tissue increased. The increase in the deformation would induce the aggravation of trauma degree.
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Influence of different lubricating fluids on friction trauma of Small Intestine during enteroscopy
Tribology International, 2018Co-Authors: Jin Wang, L. Ma, W. Li, Zhongrong ZhouAbstract:Abstract Given the increasing attention to abdominal pain problem caused by Small Intestine damage during enteroscopy, the development of lubricating fluids for injury prevention has become an urgent task. In this study, in vivo friction experiments were conducted by using rabbit Small Intestine Tissue under natural condition and lubricated conditions of Normal Saline, Calf Serum and Hyaluronic Acid, respectively. A quantitative grading system was designed to assess the friction trauma of the Small Intestine Tissue. Results showed that the Calf Serum or Hyaluronic Acid lubricant could relieve the traumas and reduce the friction at the probe-Small Intestine mucosa interface. These results can be useful to identify the suitable lubricating fluids for the safe operation of enteroscopy.
Raoul Kuiper - One of the best experts on this subject based on the ideXlab platform.
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abstract a18 the tankyrase inhibitor g007 lk inhibits Small Intestine lgr5 stem cell proliferation without altering Tissue morphology
Cancer Research, 2016Co-Authors: Jens Henrik Norum, Raoul Kuiper, Jo Waaler, Stefan Krauss, Ellen Skarpen, Andreas Brech, Therese SørlieAbstract:Tankyrase enzymes play crucial roles in the Wnt signaling pathway, involved in the regulation of intestinal stem cells and Tissue homeostasis. Aberrant Wnt signaling is known to cause intestinal cancers and the tankyrase inhibitor G007-LK has previously been shown to inhibit tumor growth in an APC-mutant colorectal cancer xenograft model. We have used in vivo models to address the effect of G007-LK on Small Intestine Tissue homeostasis. The mice were treated for up to 3 weeks with the tankyrase inhibitor, without affecting the body mass or observed clinical condition of the mice. HE 2015 Oct 23-26; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2016;76(3 Suppl):Abstract nr A18.
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abstract 3032 the effect of a tankyrase inhibitor on the Small Intestine Tissue homeostasis
Cancer Research, 2014Co-Authors: Jens Henrik Norum, Raoul Kuiper, Jo Waaler, Stefan Krauss, Ellen Skarpen, Andreas Brech, Therese SørlieAbstract:Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA In the Small Intestine the Wnt/β-catenin pathway is involved in regulation of stem cells and Tissue homeostasis. Aberrant Wnt signaling is known to cause intestinal cancers. Tankyrase enzymes play crucial roles in the regulation of the Wnt signaling pathway. Inhibition of tankyrase activity is an effective way of inhibiting Wnt/β-catenin signaling. A Small molecule tankyrase inhibitor, G007-LK, was developed that inhibits tumor growth in a APC-mutant colorectal cancer xenograft model. In in vivo experiments at high doses (60 mg/kg), G007-LK treatment resulted in severe necrosis and inflammation in the Small Intestine, possibly affecting the stem cells. Different cell populations in the Small Intestine have been shown to have stem cell properties, including the Lgr5+ cell population located at the bottom of the crypts and the cells residing in +4 position counting from the crypt base. Both of these cell populations can give rise to all the various cell types of the Small Intestine. In the current project, we have used in vivo models to address the effect of the tankyrase inhibitor, G007-LK, on Small Intestine Tissue homeostasis. H&E staining of fixed Tissue sections showed no significant differences between mice treated with 10 mg/kg G007-LK or vehicle. We performed lineage tracing from the Lgr5+ stem cells of the Small Intestine and observed that treatment with G007-LK reduced the number of cells traced from Lgr5+ stem cells. Immunohistochemistry (IHC) staining for the proliferation marker Ki67 showed reduced number of positive cells in the Small intestinal crypts of the G007-LK- compared to vehicle-treated mice. As expected, IHC staining for β-catenin showed reduced number of positive nuclei in the G007-LK- compared to vehicle-treated mice, suggesting reduced signaling via the Wnt/β-catenin pathway. Taken together, our data show that a daily dose of the tankyrase inhibitor G007-LK (10 mg/kg), is well tolerated by mice. Administration of the tankyrase inhibitor to the mice reduces the number of lineage traced cells from the Lgr5+ stem cell population in the Small Intestine, without altering the general histology of the Tissue. Citation Format: Jens Henrik Norum, Ellen Skarpen, Andreas Brech, Raoul Kuiper, Jo Waaler, Stefan Krauss, Therese Sorlie. The effect of a tankyrase inhibitor on the Small Intestine Tissue homeostasis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3032. doi:10.1158/1538-7445.AM2014-3032