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1. Gastrin

Author

He, Hong, Shulkes, Arthur, Baldwin, Graham S., and Schwab, Manfred, editor

Published
2017
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3. Experimental rat models for contrast-induced nephropathy; a comprehensive review

Author

Marlon Perera, Joseph Ischia, Damien Bolton, Arthur Shulkes, Graham S. Baldwin, and Oneel Patel

Subjects
contrast-induced nephropathy, contrast, nephropathy, kidney injury, rat models, animal models, Pathology, RB1-214, Internal medicine, RC31-1245, Other systems of medicine, RZ201-999
Abstract

Contrast-induced nephropathy (CIN) is an iatrogenic disease caused by the parenteral administration of iodinated contrast media (CM). A number of agents are currently being assessed to minimise or prevent CIN. Such agents are typically assessed using rat models. The aim of this study was to provide a comprehensive review of the rat models of CIN used in pre-clinical research. The MEDLINE, EMBASE, Web of Science and Cochrane databases were systematically searched. Articles reporting rat models of CIN were included for assessment. Study designs, contrast agents and outcome measures were assessed. Of the assessed studies, a majority report a requirement for pre-existing renal impairment prior to the administration of CM. Outcome measures are heterogenous between studies, but typically include assessment and quantification of serum biochemical markers, cellular oxidative stress and histopathological changes. The significant variation in methodology reported in the current literature highlights the lack of consensus. The use of a reliable pre-contrast insult appears critical to result in the development of contrast nephropathy. The use of acceptable outcome measures appears to include serum laboratory markers, quantification of reactive oxygen species (ROS) and objective histopathological outcomes.

Published
2020
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19. Protective effect of zinc preconditioning against renal ischemia reperfusion injury is dose dependent.

Author

Kenny Rao, Kapil Sethi, Joseph Ischia, Luke Gibson, Laurence Galea, Lin Xiao, Mildred Yim, Mike Chang, Nathan Papa, Damien Bolton, Arthur Shulkes, Graham S Baldwin, and Oneel Patel

Subjects
Medicine, Science
Abstract

Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury and chronic kidney disease. Two promising preconditioning methods for the kidney, intermittent arterial clamping (IC) and treatment with the hypoxia mimetic cobalt chloride, have never been directly compared. Furthermore, the protective efficacy of the chemically related transition metal Zn2+ against renal IRI is unclear. Although Co2+ ions have been shown to protect the kidney via hypoxia inducible factor (HIF), the effect of Zn2+ ions on the induction of HIF1α, HIF2α and HIF3α has not been investigated previously.The efficacy of different preconditioning techniques was assessed using a Sprague-Dawley rat model of renal IRI. Induction of HIF proteins following Zn2+ treatment of the human kidney cell lines HK-2 (immortalized normal tubular cells) and ACHN (renal cancer) was measured using Western Blot.Following 40 minutes of renal ischemia in rats, cobalt preconditioning offered greater protection against renal IRI than IC as evidenced by lower peak serum creatinine and urea concentrations. ZnCl2 (10 mg/kg) significantly lowered the creatinine and urea concentrations compared to saline-treated control rats following a clinically relevant 60 minutes of ischemia. Zn2+ induced expression of HIF1α and HIF2α but not HIF3α in HK-2 and ACHN cells.ZnCl2 preconditioning protects against renal IRI in a dose-dependent manner. Further studies are warranted to determine the possible mechanisms involved, and to assess the benefit of ZnCl2 preconditioning for clinical applications.

Published
2017
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21. Gastrin

Author

He, Hong, primary, Shulkes, Arthur, additional, and Baldwin, Graham S., additional

Published
2016
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26. Metformin may offer no protective effect in men undergoing external beam radiation therapy for prostate cancer

Author

Arthur Shulkes, Weranja Ranasinghe, David Wetherell, Graham S. Baldwin, Shomik Sengupta, Oneel Patel, Damien M Bolton, Joseph Ischia, and Scott Williams

Subjects
Male, 0301 basic medicine, Oncology, medicine.medical_specialty, endocrine system diseases, Cell Survival, Urology, medicine.medical_treatment, Adenocarcinoma, Metastasis, Androgen deprivation therapy, 03 medical and health sciences, Prostate cancer, 0302 clinical medicine, Risk Factors, Internal medicine, Diabetes mellitus, medicine, Humans, Hypoglycemic Agents, Treatment Failure, Neoplasm Metastasis, Survival analysis, Neoplasm Staging, business.industry, Prostatic Neoplasms, nutritional and metabolic diseases, Androgen Antagonists, Radiotherapy Dosage, Middle Aged, Prostate-Specific Antigen, Hypoxia-Inducible Factor 1, alpha Subunit, medicine.disease, Survival Analysis, Metformin, Radiation therapy, Oxidative Stress, Prostate-specific antigen, 030104 developmental biology, Diabetes Mellitus, Type 2, 030220 oncology & carcinogenesis, PC-3 Cells, Neoplasm Grading, business, medicine.drug
Abstract

OBJECTIVES: To assess whether metformin reduces radio-resistance and increases survival in men undergoing external beam radiation therapy (EBRT) for prostate cancer (PCa), and to determine its effect on hypoxia inducible factor 1-α (HIF1α). PATIENTS AND METHODS: All patients treated with curative intent with EBRT for PCa at a major cancer centre between 2000 and 2007 were included in this study. The outcome measures of time to biochemical failure (BF), metastasis, PCa-specific mortality and overall survival (OS) were analysed in those taking metformin vs those not, using competing risk and Cox regression models. To determine metformin's effect on HIF1α expression and survival in vitro, PC3 cells with high basal HIF1α levels were subjected to increasing doses of metformin after H2 O2 -induced oxidative stress. RESULTS: A total of 2055 eligible cases, including 113 who were on metformin, were identified, with a median follow-up of 95.7 months. There were no differences in age, initial prostate-specific antigen level, Gleason score, T-stage, D'Amico risk class or duration of androgen deprivation therapy (ADT) between patients who were or were not on metformin. Treatment with metformin did not result in any apparent improvement in time to BF, time to metastasis detection or OS, but there was a 1.5-fold increase in PCa-specific deaths (P = 0.045) in patients on metformin and ADT when adjusted for cancer risk and comorbidities. When comparing patients on high-dose metformin (>1 g/d) with those on low-dose metformin (≤1 g), there was no difference in either time to metastases or time to BF. In vitro metformin at a high concentration of 100 μM did not reduce HIF1α expression, nor did metformin affect the PC3 cell survival when exposed to oxidative stress (H2 O2 ). CONCLUSIONS: No association was found between the use of metformin and time to metastasis detection, time to BF or OS in patients undergoing radiation therapy with or without ADT for PCa. In vitro, low therapeutic concentrations of metformin had no effect on HIF1α, and this observation could explain the conflicting evidence for the effectiveness of metformin in men undergoing EBRT for PCa. Higher, more toxic doses of metformin may be required to inhibit the mammalian target of rapamycin-HIF1α pathway in this patient group.

Published
2019

28. CCK2R identifies and regulates gastric antral stem cell states and carcinogenesis

Author

Hayakawa, Yoku, Jin, Guangchun, Wang, Hongshan, Chen, Xiaowei, Westphalen, Christoph B, Asfaha, Samuel, Renz, Bernhard W, Ariyama, Hiroshi, Dubeykovskaya, Zinaida A, Takemoto, Yoshihiro, Lee, Yoomi, Muley, Ashlesha, Tailor, Yagnesh, Chen, Duan, Muthupalani, Sureshkumar, Fox, James G, Shulkes, Arthur, Worthley, Daniel L, Takaishi, Shigeo, and Wang, Timothy C

Published
2015
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29. Ketosis and appetite-mediating nutrients and hormones after weight loss

Author

Sumithran, P., Prendergast, L.A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., and Proietto, J.

Subjects
Obesity -- Comparative analysis -- Prevention, Ketones -- Health aspects, Reducing diets -- Methods, Weight loss -- Comparative analysis -- Methods, Food/cooking/nutrition, Health
Abstract

BACKGROUND/OBJECTIVES: Diet-induced weight loss is accompanied by compensatory changes, which increase appetite and encourage weight regain. There is some evidence that ketogenic diets suppress appetite. The objective is to examine the effect of ketosis on a number of circulating factors involved in appetite regulation, following diet-induced weight loss. SUBJECTS/METHODS: Of 50 non-diabetic overweight or obese subjects who began the study, 39 completed an 8-week ketogenic very-low-energy diet (VLED), followed by 2 weeks of reintroduction of foods. Following weight loss, circulating concentrations of glucose, insulin, non-esterified fatty acids (NEFA), β-hydroxybutyrate (BHB), leptin, gastrointestinal hormones and subjective ratings of appetite were compared when subjects were ketotic, and after refeeding. RESULTS: During the ketogenic VLED, subjects lost 13% of initial weight and fasting BHB increased from (mean ± s.e.m.) 0.07 ± 0.00 to 0.48 ±0.07 mmol/l (P < 0.001). BHB fell to 0.19 ± 0.03 mmol/l after 2 weeks of refeeding (P < 0.001 compared with week 8). When participants were ketotic, the weight loss induced increase in ghrelin was suppressed. Glucose and NEFA were higher, and amylin, leptin and subjective ratings of appetite were lower at week 8 than after refeeding. CONCLUSIONS: The circulating concentrations of several hormones and nutrients which influence appetite were altered after weight loss induced by a ketogenic diet, compared with after refeeding. The increase in circulating ghrelin and subjective appetite which accompany dietary weight reduction were mitigated when weight-reduced participants were ketotic. European Journal of Clinical Nutrition (2013) 67, 759-764; doi: 10.1038/ejcn.2013.90; published online 1 May 2013 Keywords: appetite; ketosis; very-low-energy diet; weight loss, INTRODUCTION The increasing prevalence of overweight and obesity has been widely reported. Ketogenic low-carbohydrate diets are a popular means of weight loss, and in the short-term, often result in greater [...]

Published
2013
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31. Gastrin

Author

He, Hong, primary, Shulkes, Arthur, additional, and Baldwin, Graham S., additional

Published
2014
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34. Zinc Preconditioning Provides Cytoprotection following Iodinated Contrast Media Exposure in In Vitro Models

Author

Arthur Shulkes, Damien M Bolton, Graham S. Baldwin, Marlon Perera, Oneel Patel, and Joseph Ischia

Subjects
0301 basic medicine, Radiographic contrast media, Article Subject, Iohexol, Contrast-induced nephropathy, Contrast Media, Apoptosis, 030204 cardiovascular system & hematology, Pharmacology, medicine.disease_cause, Kidney, Cell Line, Kidney Tubules, Proximal, 03 medical and health sciences, 0302 clinical medicine, medicine, Medical technology, Animals, Humans, Radiology, Nuclear Medicine and imaging, R855-855.5, Cytotoxicity, chemistry.chemical_classification, Reactive oxygen species, medicine.disease, Cytoprotection, Oxidative Stress, Zinc, 030104 developmental biology, medicine.anatomical_structure, chemistry, Oxidative stress, Research Article, medicine.drug
Abstract

Introduction & Objectives. Contrast media (CM) causes renal injury through both direct cellular injury (cytotoxicity) and regional vascular changes (renal hypoxia) mediated by reactive oxygen species (ROS). Zinc may be able to provide protection against CM-induced cytotoxicity due to its indirect antioxidant properties and subsequent effect on ROS. We aimed to determine the protective role of zinc preconditioning against contrast-induced renal injury in vitro. Methods. Normal human proximal renal kidney cells (HK-2) were preconditioned with either increasing doses of ZnCl2 or control. Following this preconditioning, cells were exposed to increasing concentrations of Iohexol 300 mg I2/ml for four hours. Key outcome measures included cell survival (MTT colorimetric assay) and ROS generation (H2DCFDA fluorescence assay). Results. Contrast media induced a dose-dependent reduction in survival of HK-2 cells. Compared to control, contrast media at 150, 225, and 300 mg I2/ml resulted in 69.5% (SD 8.8%), 37.3% (SD 4.8%), and 4.8% (SD 6.6%) cell survival, respectively ( p < 0.001 ). Preconditioning with 37.5 μM and 50 μM ZnCl2 increased cell survival by 173% (SD 27.8%) ( p < 0.001 ) and 219% (SD 32.2%) ( p < 0.001 ), respectively, compared to control preconditioning. Zinc preconditioning resulted in a reduction of ROS generation. Zinc pre-conditioning with 37.5 μM μM ZnCl2 reduced ROS generation by 46% ( p < 0.001 ) compared to control pre-conditioning. Conclusions. Zinc preconditioning reduces oxidative stress following exposure to radiographic contrast media which in turn results in increased survival of renal cells. Translation of this in vitro finding in animal models will lay the foundation for future use of zinc preconditioning against contrast induced nephropathy.

Published
2021

36. Stimulation of proliferation in the colorectal mucosa by gastrin precursors is blocked by desferrioxamine

Author

Ferrand, Audrey, Lachal, Shamilah, Bramante, Gianni, Kovac, Suzana, Shulkes, Arthur, and Baldwin, Graham S.

Subjects
Gastrin -- Properties, Iron in the body -- Properties, Deferoxamine -- Dosage and administration, Colon (Anatomy) -- Properties, Biological sciences
Abstract

Precursors of the peptide hormone gastrin stimulate proliferation in the colorectal mucosa and promote the development of colorectal carcinoma. Gastrins bind two ferric ions selectively and with high affinity, and the biological activity of glycine-extended gastrin (Ggly) in vitro is dependent on the presence of ferric ions. The aim of the present study was to determine whether or not iron is required for biological activity of progastrin and Ggly in vivo. Rats that had undergone a colostomy were infused with Ggly, and proliferation was measured in the defunctioned rectal mucosa. Proliferation was also measured in the colonic mucosa of hGAS and MTI-Ggly mice, which, by definition, overexpress progastrin and Ggly, respectively. The requirement for iron was assessed by thrice-weekly injection of the chelating agent desferrioxamine (DFO). The proliferation index in the defunctioned rectal mucosa was significantly increased in the Ggly-infused rats, and the increase was significantly reduced after treatment with DFO. Treatment with DFO significantly reduced the crypt height and proliferation index in the colonic mucosa of hGAS and MTI-Ggly mice but had no effect on the same variables in wild-type mice. These observations are consistent with the hypothesis that the biological activity of progastrin and Ggly in vivo is dependent on the presence of ferric ions and further suggest that chelating agents may block the stimulatory effects of gastrin precursors in the development of colorectal carcinoma. colon; iron doi: 10.1152/ajpgi.00046.2010.

Published
2010

40. The role of hypoxia-inducible factor 1α in determining the properties of castrate-resistant prostate cancers.

Author

Weranja K B Ranasinghe, Lin Xiao, Suzana Kovac, Mike Chang, Carine Michiels, Damien Bolton, Arthur Shulkes, Graham S Baldwin, and Oneel Patel

Subjects
Medicine, Science
Abstract

BackgroundCastrate-resistant prostate cancer (CRPC) is a lethal condition in patients receiving androgen deprivation therapy for prostate cancer (PC). Despite numerous studies showing the expression of HIF1α protein under normoxia in PC cell lines, the role of this normoxic HIF1α expression in chemo-resistance and migration has not been investigated previously. As no method is currently available to determine which tumors will progress to CRPC, the role of HIF1α in PC and its potential for predicting the development of CRPC was also investigated.MethodsThe effect of HIF1α protein knockdown on chemo-resistance and migration of PC3 cells was assessed by cell counting and Transwell assays, respectively. Translation efficiency of HIF1α mRNA was determined in PC cells using a HIF1α 5'UTR-luciferase construct. Clinical outcomes were correlated following the staining of 100 prostate tumors for HIF1α expression.ResultsThe CRPC-like cell lines (PC3 and DU145) expressed more HIF1α protein than an androgen sensitive cell line (LNCaP). Migration rate and chemo-resistance were higher in the PC3 cells and both were decreased when HIF1α expression was reduced. Increased translation of HIF1α mRNA may be responsible for HIF1α overexpression in PC3 cells. Patients whose tumors expressed HIF1α had significantly decreased metastasis-free survival and the patients who were on androgen-deprivation therapy had decreased CRPC-free survival on Kaplan-Meier analysis. On multivariate analysis HIF1α was an independent risk factor for progression to metastatic PC (Hazard ratio (HR) 9.8, p = 0.017) and development of CRPC (HR 10.0, p = 0.021) in patients on androgen-deprivation therapy. Notably the tumors which did not express HIF1α did not metastasize or develop CRPC.ConclusionsHIF1α is likely to contribute to metastasis and chemo-resistance of CRPC and targeted reduction of HIF1α may increase the responsiveness of CRPCs to chemotherapy. Expression of HIF1α may be a useful screening tool for development of CRPC.

Published
2013
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41. Inactivating cholecystokinin-2 receptor inhibits progastrin-dependent colonic crypt fission, proliferation, and colorectal cancer in mice

Author

Jin, Guangchun, Ramanathan, Vigneshwaran, Quante, Michael, Baik, Gwang Ho, Yang, Xiangdong, Wang, Sophie S.W., Tu, Shuiping, Gordon, Shanisha A.K., Pritchard, David Mark, Varro, Andrea, Shulkes, Arthur, and Wang, Timothy C.

Subjects
Cholecystokinin -- Health aspects, Tumors -- Health aspects, Gastrin -- Health aspects, Stem cells -- Health aspects, Colorectal cancer -- Health aspects, Cancer -- Genetic aspects -- Care and treatment, Membrane proteins -- Health aspects, Calmodulin -- Health aspects, Health care industry
Abstract

Hyperproliferation of the colonic epithelium, leading to expansion of colonic crypt progenitors, is a recognized risk factor for colorectal cancer. Overexpression of progastrin, a nonamidated and incompletely processed product of the gastrin gene, has been shown to induce colonic hyperproliferation and promote colorectal cancer in mice, but the mechanism of pathogenesis has not been defined. Cholecystokinin-2 receptor (CCK2R) is the primary receptor for cholecystokinin (CCK) and amidated gastrin. Here, we show that Cck2r was expressed in murine colonic crypts and upregulated in the transgenic mice that overexpress human progastrin. Murine deletion of Cck2r abrogated progastrin-dependent increases in colonic proliferation, mucosal thickness, and β-catenin and CD44 expression in the colon tumor. In addition, either deletion or antagonism of Cck2r resulted in the inhibition of progastrin-dependent increases in progenitors expressing doublecortin and CaM kinase-like-1 (DCAMKL1), stem cells expressing leucine rich repeat-containing G protein-coupled receptor 5 (LgR5), and colonic crypt fission. Furthermore, in the azoxymethane mouse model of colorectal carcinogenesis, Cck2r deletion in human progastrin-overexpressing mice resulted in markedly decreased aberrant crypt foci formation and substantially reduced tumor size and multiplicity. Taken together, these observations indicate that progastrin induces proliferative effects, primarily in colonic progenitor cells, through a CCK2R-dependent pathway. Moreover, our data suggest that CCK2R may be a potential target in the treatment or prevention of colorectal cancer., Introduction Colorectal cancer is one of the most common cancers and the second leading cause of cancer-related death in the United States (1). The majority of colorectal cancers originate in [...]

Published
2009
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42. Interrelationships between circulating gastrin and iron status in mice and humans

Author

Kovac, Suzana, Smith, Kelly, Anderson, Gregory J., Burgess, John R., Shulkes, Arthur, and Baldwin, Graham S.

Subjects
Rats as laboratory animals -- Testing, Gastrin -- Physiological aspects, Biological sciences
Abstract

The observations that the peptide hormone gastrin interacts with transferrin in vitro and that circulating gastrin concentrations are increased in the iron-loading disorder hemochromatosis suggest a possible link between gastrin and iron homeostasis. This study tested the hypothesis that gastrin and iron status are interrelated by measurement of iron homeostasis in mice and humans with abnormal circulating gastrin concentrations. Intestinal iron absorption was determined by [sup.59]Fe uptake following oral gavage, and concentrations of duodenal divalent metal transporter-1 (DMT-1) and hepatic hepcidin mRNAs were determined by quantitative real-time PCR in agastrinemic (GasKO), hypergastrinemic cholecystokinin 2 receptor-deficient (CCK2RKO), or wild-type mice. Iron status was measured by standard methods in the same mice and in hypergastrinemic humans with multiple endocrine neoplasia type 1 (MEN-1). Iron absorption was increased sixfold and DMT-1 mRNA concentration fourfold, and transferrin saturation was reduced 0.8-fold and hepcidin mRNA expression 0.5-fold in juvenile GasKO mice compared with age-matched wild-type mice. In mature mice, few differences were observed between the strains. Juvenile CCK2RKO mice were hypergastrinemic and had a 5.4-fold higher DMT-1 mRNA concentration than wild-type mice without any increase in iron absorption. In contrast to juvenile GasKO mice, juvenile CCK2RKO mice had a 1.5-fold greater transferrin saturation, which was reflected in a twofold increase in liver iron deposition at maturity compared with wild-type mice. The correlation between transferrin saturation and circulating gastrin concentration observed in mutant mice was also observed in human patients with MEN, in whom hypergastrinemia correlated positively (P = 0.004) with an increased transferrin saturation. Our data indicate that, in juvenile animals when iron demand is high, circulating gastrin concentrations may alter iron status by a CCK2R-independent mechanism. anemia; ferric; hemochromatosis

Published
2008

43. Experimental rat models for contrast-induced nephropathy; A comprehensive review

Author

Perera, M, Ischia, J, Bolton, D, Shulkes, A, Baldwin, GS, Patel, O, Perera, M, Ischia, J, Bolton, D, Shulkes, A, Baldwin, GS, and Patel, O

Abstract

Contrast-induced nephropathy (CIN) is an iatrogenic disease caused by the parenteral administration of iodinated contrast media (CM). A number of agents are currently being assessed to minimise or prevent CIN. Such agents are typically assessed using rat models. The aim of this study was to provide a comprehensive review of the rat models of CIN used in pre-clinical research. The MEDLINE, EMBASE, Web of Science and Cochrane databases were systematically searched. Articles reporting rat models of CIN were included for assessment. Study designs, contrast agents and outcome measures were assessed. Of the assessed studies, a majority report a requirement for pre-existing renal impairment prior to the administration of CM. Outcome measures are heterogenous between studies, but typically include assessment and quantification of serum biochemical markers, cellular oxidative stress and histopathological changes. The significant variation in methodology reported in the current literature highlights the lack of consensus. The use of a reliable pre-contrast insult appears critical to result in the development of contrast nephropathy. The use of acceptable outcome measures appears to include serum laboratory markers, quantification of reactive oxygen species (ROS) and objective histopathological outcomes.

Published
2020

44. Contributors

Author

Aalen, Reidunn B., primary, Abdel-Wahab, Yasser H.A., additional, Adams, Michael E., additional, Adan, Roger A.H., additional, Ahima, Rexford S., additional, Ahmed, Naima, additional, Al-Massadi, Omar, additional, Altstein, Miriam, additional, Anouar, Youssef, additional, Anselmi, Laura, additional, Ansorge, Siegfried, additional, Antcheva, Nikolinka, additional, Antonova-Koch, Yevgeniya, additional, Appel, Jon R., additional, Arik, Anam J., additional, Arter, Alison L., additional, Arvan, Peter, additional, Ashkenazi, Avraham, additional, Baas, P.W., additional, Bado, André, additional, Baird, Andrew, additional, Baiula, Monica, additional, Bakaletz, Lauren O., additional, Bakken, Earl E., additional, Balaskó, Márta, additional, Baldwin, Graham S., additional, Banks, William A., additional, Barra, Donatella, additional, Barson, Jessica R., additional, Basille, Magali, additional, Bauer, Natalie N., additional, Bedini, Andrea, additional, Beeton, Christine, additional, Begley, David J., additional, Beinfeld, Margery C., additional, Bendena, William G., additional, Benoit, Stephen C., additional, Bentov, Itay, additional, Bern, Howard, additional, Bierbaum, Gabriele, additional, Billington, Charles J., additional, Blasiak, Anna, additional, Block, Norman L., additional, Bloom, Stephen. R., additional, Bonney, Iwona, additional, Bowie, John H., additional, Boyd, Sunny K., additional, Brain, Susan D., additional, Brede, Dag A., additional, Broeck, Jozef Vanden, additional, Brown, Kelly L., additional, Brown, Mark R., additional, Bugni, James M., additional, Bundgaard, Jens R., additional, Burel, Delphine, additional, Butenko, Melinka A., additional, Call, Melissa J., additional, Calò, Girolamo, additional, Campbell, Duncan John, additional, Carlsson, Anna, additional, Carr, Daniel B., additional, Carraway, Robert E., additional, Carreira, Marcos C., additional, Casanueva, Felipe F., additional, Cassella, Sarah N., additional, Casson, Stuart A., additional, Castaño, Justo P., additional, Cebrat, Marek, additional, Chappe, Valerie, additional, Chatenet, David, additional, Chen, Keqiang, additional, Chen, Chen, additional, Chen, Longchuan, additional, Chen, Duan, additional, Cheng, Carrie Y.Y., additional, Cho, Sung Ki, additional, Chow, Billy K.C., additional, Christopoulos, Arthur, additional, Chu, Shijian, additional, Clarke, Iain J., additional, Coast, Geoffrey M., additional, Compere, Vincent, additional, Concepcion, Gisela P., additional, Cone, Roger D., additional, Conlon, J. Michael, additional, Cornélissen, Germaine, additional, Courel, Maité, additional, Couture, Réjean, additional, Cramer, W.A., additional, Croft, Nathan P., additional, Crujeiras, Ana B., additional, Cuttitta, Frank, additional, Cynis, Holger, additional, D’Acquisto, F., additional, Davis, Jon F., additional, Davis, Thomas P., additional, de La Serre, Claire Barbier, additional, de Lartigue, Guillaume, additional, de Lecea, Luis, additional, de Oliveira Santos, Marcelo, additional, De Waard, Michel, additional, Bolette Hartmann, Carolyn F. Deacon, additional, Delestre, Charlène, additional, Delgado, Mario, additional, Demuth, Hans-Ulrich, additional, Deng, Xiaoming, additional, Dharmawardhana, Palitha, additional, Di Cosmo, Anna, additional, Dias, Simoni Campos, additional, Dickerson, Jonathan W., additional, Diep, Dzung B., additional, Dircksen, H., additional, Dischinger, Jasmin, additional, do Rego, Jean-Claude, additional, Dobner, Paul R., additional, Dockray, Graham J., additional, Dores, Robert M., additional, Ducroc, Robert, additional, Dudek, Nadine L., additional, Dumont, Yvan, additional, Duraffourd, Celine, additional, Duterte-Boucher, Dominique, additional, Eberlé, Alex N., additional, Egleton, Richard D., additional, Eipper, Betty A., additional, Engel, Jorg B., additional, Englander, Ella W., additional, Epelbaum, Jacques, additional, Erlanson-Albertsson, Charlotte, additional, Evangelista, S., additional, Fagan, Karen A., additional, Farber, Joshua M., additional, Farkasfalvi, Klára, additional, Fekete, Csaba, additional, Flatt, Peter R., additional, Flower, R.J., additional, Forssmann, Wolf-Georg, additional, Fournier, Alain, additional, Foy, Kevin Chu, additional, Franco, Octávio Luiz, additional, Frenkel, Dan, additional, Fricker, Lloyd D., additional, de la Fuente-Núñez, César, additional, Fukuda, Hiroo, additional, Gäde, Gerd, additional, Galas, Ludovic, additional, Gallagher, Patricia E., additional, Gandolfo, Pierrick, additional, Garcia-Espinosa, Maria A., additional, García-Sanmartín, Josune, additional, Geary, Nori, additional, Geng, Hua, additional, Germano, Patrizia M., additional, Goetze, Jens P., additional, Gonzalez, Alexis A., additional, Gonzalez, Ana, additional, Gosnell, Blake A., additional, Goto, Katsutoshi, additional, Gourcerol, Guillaume, additional, Gozes, I., additional, Gracia-Navarro, Francisco, additional, Grayson, Bernadette E., additional, Greeley, George H., additional, Greenwald-Yarnell, Megan, additional, Gressens, Pierre, additional, Grider, John R., additional, Grünewald, Jan, additional, Guerreiro, Juliano R., additional, Guerrini, Remo, additional, Guida, Filomena, additional, Guilhaudis, Laure, additional, Guilmeau, Sandra, additional, Gundlach, Andrew L., additional, Gutkowska, Jolanta, additional, Hackbarth, Clifton, additional, Haim Ohana, Y., additional, Halberg, Franz, additional, Hallberg, Mathias, additional, Hamidi, Sayyed A., additional, Han, Song, additional, Han, Ji-Sheng, additional, Hancock, Robert E.W., additional, Haque, Samer-ul, additional, Hara-Nishimura, Ikuko, additional, Hariton, Aliza, additional, Hartsock, Wendy J., additional, Harvey, Alan L., additional, Hasunuma, Itaru, additional, Henning, Robert J., additional, Heppner, Kristy M., additional, Hertweck, Kate L., additional, Herzog, Herbert, additional, Higashiyama, Tetsuya, additional, Hinuma, Shuji, additional, Hippenstiel, Stefan, additional, Hirakawa, Yuki, additional, Hirose, Shuichi, additional, Hirsch, Jochen R., additional, Hocke, Andreas C., additional, Hodges, Robert S., additional, Hoffmann, Werner, additional, Hökfelt, Tomas, additional, Holst, Jens Juul, additional, Holzer, Peter, additional, Horodyski, Frank M., additional, Hosoda, Hiroshi, additional, Hou, Xiaowen, additional, Huffaker, Alisa, additional, Iijima, Norio, additional, Ikeuchi, Momoko, additional, Imperial, Julita S., additional, Improta, Giovanna, additional, Inui, Akio, additional, Irwin, Nigel, additional, Ishii, Munehiro, additional, Iturrioz, Xavier, additional, Ivanisevic, Ljubica, additional, Iwao, Hiroshi, additional, Iwata, Takeo, additional, Izumi, Yasukatsu, additional, Izumiyama, Hajime, additional, Jankowski, Marek, additional, Janssen, Tom, additional, Jégou, Sylvie, additional, Jensen, Robert T., additional, Jethwa, Preeti H., additional, Johannessen, Helene, additional, Johanson, Conrad, additional, Judkowski, Valeria, additional, Kaczmarek, Przemyslaw, additional, Kageyama, Haruaki, additional, Kakimoto, Tatsuo, additional, Kang, Ki Sung, additional, Kangawa, Kenji, additional, Kastin, Abba J., additional, Kato, Johji, additional, Kaumaya, Pravin T.P., additional, Keep, Richard F., additional, Kem, William R., additional, Khomenko, Tetyana, additional, Kikuyama, Sakae, additional, Kim, Young-Joon, additional, Kimura, Sadao, additional, King, Ross, additional, Kiptoo, Paul, additional, Kishimoto, Ichiro, additional, Kitamura, Kazuo, additional, Kluczyk, Alicja, additional, Kobori, Hiroyuki, additional, Kodama, Yosuke, additional, Kojima, Masayasu, additional, Kondo, Yuki, additional, Körner, Meike, additional, Kosson, Piotr, additional, Kotz, Catherine M., additional, Krishnan, Bhavani, additional, Kulseng, Bård, additional, Kumpf, Robert, additional, Laburthe, Marc, additional, Lacaille, Hélène, additional, Ladenheim, Ellen E., additional, Ladram, Ali, additional, Laksitorini, Marlyn D., additional, Lambert, David G., additional, Lange, Angela B., additional, Langhans, Wolfgang, additional, Larauche, Muriel, additional, Larhammar, Dan, additional, Larráyoz, Ignacio M., additional, Lattanzi, Roberta, additional, Lechan, Ronald M., additional, Lefranc, Benjamin, additional, Leibowitz, Sarah F., additional, Lelièvre, Vincent, additional, Leprince, Jérôme, additional, Levine, Allen S., additional, Li, Qun, additional, Lifshitz, Veronica, additional, Lihrmann, Isabelle, additional, Chi-Jen Lin, James, additional, Lindberg, Iris, additional, Lindsey, Keith, additional, Lipkowski, Andrzej W., additional, Liron, T., additional, Liu, Junli, additional, Liu, Ying, additional, Liu, Min, additional, Llorens-Cortes, Catherine, additional, Loizidou, Marilena, additional, Lopez, C., additional, Lovejoy, David A., additional, Luca, Vincenzo, additional, Lutz, Thomas A., additional, Ma, Sherie, additional, Mains, Richard E., additional, Malagon, Maria M., additional, Malendowicz, Ludwik K., additional, Wan, Jennifer Man-Fan, additional, Mangoni, Maria Luisa, additional, Manigrasso, Michaele B, additional, Marahiel, Mohamed A., additional, Marco, Heather G., additional, Maric-Bilkan, Christine, additional, Marks, Nikki J., additional, Martin, Roland, additional, Martinez, Vicente, additional, Martínez, Alfredo, additional, Martinez-Fuentes, Antonio J., additional, Masler, Edward P., additional, Matsubayashi, Yoshikatsu, additional, Mattu, Harman S., additional, Maule, Aaron G., additional, McLaughlin, Patricia J., additional, McMurtry, Ivan F., additional, Meelkop, Ellen, additional, Mehdi, Saher, additional, Melchiorri, Pietro, additional, Millar, R.P., additional, Miller, Laurence J., additional, Miller, Miles, additional, Million, Mulugeta, additional, Minamino, Naoto, additional, Mittelman, M., additional, Miyauchi, Takashi, additional, Miyazato, Mikiya, additional, Mizoguchi, Hirokazu, additional, Mohme, Malte, additional, Montero-Hadjadje, Maité, additional, Moody, Terry W., additional, Mookherjee, Neeloffer, additional, Moran, Timothy H., additional, Morganstern, Irene, 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Ann, additional, Tan, Tricia M., additional, Temmerman, Liesbet, additional, Temmesfeld-Wollbrück, Bettina, additional, Tena-Sempere, Manuel, additional, Thorsell, Annika, additional, Tilakaratne, Nanda, additional, Tobe, Stephen S., additional, Tokudome, Takeshi, additional, Tolstanova, Ganna, additional, Tonon, Marie-Christine, additional, Topping, Jennifer F., additional, Tossi, Alessandro, additional, Tostivint, Hervé, additional, Toth, Istvan, additional, Totsune, Kazuhito, additional, Toyoda, Fumiyo, additional, Troke, Rachel, additional, Tschöp, Matthias H., additional, Tso, Patrick, additional, Tsukaya, Hirokazu, additional, Tsutsui, Kazuyoshi, additional, Tu, Hong, additional, Turner, Anthony J., additional, Ubuka, Takayoshi, additional, Valdivia, Elene R., additional, Vandersmissen, Hans Peter, additional, Vaudry, David, additional, Vaudry, Hubert, additional, Vazquez-Martinez, Rafael, additional, Verbalis, Joseph G., additional, Vicari, Daniele, additional, Vidal, Nicolas, additional, Vignoni, Marzia, additional, Viollet, Cécile, additional, Vishwanatha, K.S., additional, Vivoli, Mirella, additional, Voisin, Thierry, additional, Vu, John P., additional, Walker, John C., additional, Wallace, B.A., additional, Wang, Ji Ming, additional, Wang, Lixin, additional, Wardman, Jonathan H., additional, Watanabe, Takuya, additional, Welch, Hazel, additional, Werner, Haim, additional, Whitmore, L., additional, Wiedemann, Imke, additional, Winsky-Sommerer, Raphaelle, additional, Witt, Ken A., additional, Wojciechowicz, Tatiana, additional, Wong, Jack Ho, additional, Woods, Stephen C., additional, Wootten, Denise, additional, Wu, Vincent, additional, Wurtz, Olivier, additional, Xiong, Ximing, additional, David Xu, Zhi-Qing, additional, Yamaguchi, Yube, additional, Yamaguchi, Takahiro, additional, Yamamoto, Kazutoshi, additional, Yamashita, E., additional, Yamazaki, Hiroyuki, additional, Yang, De, additional, Yoshikawa, Masaaki, additional, Yuan, Pu-Qing, additional, Yung, Sunny C., additional, Zagon, Ian S., additional, Zakharov, S.D., additional, Zaman, Mehfuz, additional, Zhalnina, M.V., additional, Zhang, Ning, additional, Zhang-Auberson, Lixin, additional, Zhao, Chun-Mei, additional, Ziolkowska, Agnieszka, additional, and Zitnan, Dusan, additional

Published
2013
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45. Gastrin

Author

Shulkes, Arthur, primary and Baldwin, Graham S., additional

Published
2013
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47. An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Author

Sartor, Daniela M., Shulkes, Arthur, and Verberne, Anthony J.M.

Subjects
Cholecystokinin -- Research, Rats as laboratory animals -- Research, Peptides -- Research, Gastrointestinal system -- Motility, Gastrointestinal system -- Research, Biological sciences
Abstract

Ingestion of a meal results in gastrointestinal (GI) hyperemia and is associated with systemic and paracrine release of a number of peptide hormones, including chole-cystokinin (CCK) and 5-hydroxytryptamine (5-HT). Systemic administration of CCK octapeptide inhibits a subset of presympathetic neurons of the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor tone to the GI viscera. The aim of this study was to determine whether endogenous release of CCK and/or 5-HT also inhibits CCK-sensitive RVLM neurons. The effects of intraduodenal administration of the secretagogues sodium oleate (SO) and soybean trypsin inhibitor (SBTI) on circulating levels of CCK and 5-HT were examined. In separate experiments, the discharge rates of barosensitive, medullospinal, CCK-sensitive RVLM presympathetic vasomotor neurons were recorded after rapid intraduodenal infusion of SO-SBTI or water. Alternatively, animals were pretreated with the [CCK.sub.1] receptor antagonists devazepide and lorglumide or the 5-[HT.sub.3] antagonist MDL-72222 before SO-SBTI administration. Secretagogue infusion significantly increased the level of circulating CCK, but not 5-HT. SOSBTI significantly decreased (58%) the neuronal firing rate of CCK-sensitive RVLM neurons compared with water (5%). [CCK.sub.1] receptor antagonists did not reverse SO-SBTI-induced neuronal inhibition (58%), whereas the 5-[HT.sub.3] antagonist significantly attenuated the effect (22%). This study demonstrates a functional relation between a subset of RVLM presympathetic vasomotor neurons and meal-related signals arising from the GI tract. It is likely that endogenously released 5-HT acts in a paracrine fashion on GI 5-[HT.sub.3] receptors to initiate reflex inhibition of these neurons, resulting in GI vasodilatation by withdrawal of sympathetic tone. rostroventrolateral medulla; cholecystokinin; devazepide; MDL-72222; 5-hydroxytryptamine

Published
2006

49. Glycine-extended gastrin stimulates cell proliferation and migration through a Rho- and ROCK-dependent pathway, not a Rac/Cdc42-dependent pathways

Author

He, Hong, Pannequin, Julie, Tantiongeo, John-Paul, Shulkes, Arthur, and Baldwin, Graham S.

Subjects
Protein kinases -- Research, Cytoskeleton -- Research, G proteins -- Research, Biological sciences
Abstract

Both amidated gastrin (Gamide) and glycine-extended gastrin (Ggly) stimulate gastrointestinal cell proliferation and migration. Binding of Gamide to the cholecystokinin-2 receptor activates small GTP-binding proteins of the Rho family (Rho, Rac, and Cdc42), and dominant-negative mutants of Rho or Cdc42 block Gamide-stimulated cell proliferation and survival. In comparison, little is known about the Ggly signaling transduction pathway leading to cell proliferation and migration. The present study examined the roles of the small G proteins Rho, Rac, and Cdc42 in Ggly-induced proliferation and migration of the mouse gastric epithelial cell line IMGE-5. Ggly stimulated the activation of Rho and its downstream effector protein ROCK. The activation of Rho and ROCK mediated Ggly-induced cell proliferation and migration as inhibition of Rho by C3, or ROCK by Y-27632, completely blocked these effects of Ggly. Ggly also stimulated tyrosine phosphorylation of focal adhesion kinase, and stimulation was reversed by addition of C3 and Y-27632. In contrast to the effects of Rho and ROCK, inhibition of the Rac or Cdc42 pathways by expression of dominant-negative mutants of Rac or Cdc42 did not affect Ggly-induced cell proliferation and migration. These results demonstrate that Ggly stimulates IMGE-5 cell proliferation and migration through a Rho/ROCK-dependent pathway but not via Rac- or Cdc42-dependent pathways. G proteins; cytoskeleton; focal adhesion kinase

Published
2005

50. Biological activity and ferric ion binding of fragments of glycine-extended gastrin

Author

He, Hong, Baldwin, Graham S., Shehan, Philip B., Barnham, Kevin J., Norton, Raymond S., and Shulkes, Arthur

Subjects
Gastrin -- Research, Glycine -- Research, Binding sites (Biochemistry) -- Research, Biological sciences, Chemistry
Abstract

Nonamidated gastrins such as progastrin and glycine-extended gastrin 17 (Ggly) induce cell proliferation, migration in vitro, and colonicmucosal proliferation in vivo. The aim of the study was to define the minimum biologically active fragment of Ggly and to determine whether ferric ions are required for the activity.

Published
2004

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