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Luise Aamann Else Marie Vestergaard Henning Grφnbk 《World journal of gastroenterology : WJG》2014,20(12):3223-3230
Inflammatory bowel disease(IBD),which comprises ulcerative colitis and Crohn’s disease,is characterized by inflammation of the gastrointestinal tract.The trefoil factors 1,2,and 3(TFF1-3)are a family of peptides that play important roles in the protection and repair of epithelial surfaces,including the gastrointestinal tract.TFFs may be involved in IBD pathogenesis and are a potential treatment option.In the present review,we describe the TFF family and their potential role in IBD by summarizing the current knowledge of their expression,possible function and pharmacological role in IBD. 相似文献
23.
Keith B. Burt Robert Whelan Patricia J. Conrod Tobias Banaschewski Gareth J. Barker Arun L.W. Bokde Uli Bromberg Christian Büchel Mira Fauth‐Bühler Herta Flor André Galinowski Juergen Gallinat Penny Gowland Andreas Heinz Bernd Ittermann Karl Mann Frauke Nees Dimitri Papadopoulos‐Orfanos Tomas Paus Zdenka Pausova Luise Poustka Marcella Rietschel Trevor W. Robbins Michael N. Smolka Andreas Ströhle Gunter Schumann Hugh Garavan the IMAGEN Consortium 《Journal of child psychology and psychiatry, and allied disciplines》2016,57(11):1287-1296
24.
Luise Erpenbeck Melanie Demers Zsuzsanna K. Zsengellér Maureen Gallant Stephen M. Cifuni Isaac E. Stillman S. Ananth Karumanchi Denisa D. Wagner 《Journal of the American Society of Nephrology : JASN》2016,27(1):120-131
Thrombotic microangiopathy (TMA) is a life-threatening condition that affects some, but not all, recipients of vascular endothelial growth factor (VEGF) inhibitors given as part of chemotherapy. TMA is also a complication of preeclampsia, a disease characterized by excess production of the VEGF-scavenging soluble VEGF receptor 1 (soluble fms-like tyrosine kinase 1; sFlt-1). Risk factors for VEGF inhibitor–related TMA remain unknown. We hypothesized that deficiency of the VWF-cleaving ADAMTS13 endopeptidase contributes to the development of VEGF inhibitor–related TMA. ADAMTS13−/− mice overexpressing sFlt-1 presented all hallmarks of TMA, including thrombocytopenia, schistocytosis, anemia, and VWF-positive microthrombi in multiple organs. Similar to VEGF inhibitor–related TMA in humans, these mice exhibited severely impaired kidney function and hypertension. In contrast, wild-type mice overexpressing sFlt-1 developed modest hypertension but no other features of TMA. Recombinant ADAMTS13 therapy ameliorated all symptoms of TMA in ADAMTS13−/− mice overexpressing sFlt-1 and normalized BP in wild-type mice. ADAMTS13 activity may thus be a critical determinant for the development of TMA secondary to VEGF inhibition. Administration of recombinant ADAMTS13 may serve as a therapeutic approach to treat or prevent thrombotic complications of VEGF inhibition. 相似文献
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26.
Arlette F. Buchmann Katrin Zohsel Dorothea Blomeyer Erika Hohm Sarah Hohmann Christine Jennen-Steinmetz Jens Treutlein Katja Becker Tobias Banaschewski Martin H. Schmidt Günter Esser Daniel Brandeis Luise Poustka Ulrich S. Zimmermann Manfred Laucht 《Psychopharmacology》2014,231(16):3089-3097
Rationale
Considerable evidence suggests that genetic factors combine with environmental influences to impact on the development of aggressive behavior. A genetic variant that has repeatedly been reported to render individuals more sensitive to the presence of adverse experiences, including stress exposure during fetal life, is the seven-repeat allele of the dopamine D4 receptor (DRD4) gene.Objectives
The present investigation concentrated on the interplay of prenatal maternal stress and DRD4 genotype in predicting self-reported aggression in young adults. As disruption of the hypothalamic-pituitary-adrenal system has been discussed as a pathophysiological pathway to aggression, cortisol stress reactivity was additionally examined.Methods
As part of an epidemiological cohort study, prenatal maternal stress was assessed by maternal interview 3 months after childbirth. Between the ages of 19 and 23 years, 298 offspring (140 males, 158 females) completed the Young Adult Self-Report to measure aggressive behavior and were genotyped for the DRD4 gene. At 19 years, 219 participants additionally underwent the Trier Social Stress Test to determine cortisol reactivity.Results
Extending earlier findings with respect to childhood antisocial behavior, the results revealed that, under conditions of higher prenatal maternal stress, carriers of the DRD4 seven-repeat allele displayed more aggression in adulthood (p?=?0.032). Moreover, the same conditions which seemed to promote aggression were found to predict attenuated cortisol secretion (p?=?0.028).Conclusions
This is the first study to indicate a long-term impact of prenatal stress exposure on the cortisol stress response depending on DRD4 genotype. 相似文献27.
28.
Juliane H. Fröhner Stephan Ripke Sarah Jurk Shu-Chen Li Tobias Banaschewski Arun L.W. Bokde Erin Burke Quinlan Sylvane Desrivières Herta Flor Antoine Grigis Hugh Garavan Andreas Heinz Rüdiger Brühl Jean-Luc Martinot Marie-Laure Paillère Martinot Eric Artiges Frauke Nees Dimitri Papadopoulos Orfanos Luise Poustka Sarah Hohmann Henrik Walter Robert Whelan Gunter Schumann Michael N. Smolka the IMAGEN Consortium 《Alcoholism, clinical and experimental research》2022,46(4):667-681
Background
While drinking alcohol, one must choose between the immediate rewarding effects and the delayed reward of a healthier lifestyle. Individuals differ in their devaluation of a delayed reward based on the time required to receive it, i.e., delay discounting (DD). Previous studies have shown that adolescents discount more steeply than adults and that steeper DD is associated with heavier alcohol use in both groups.Methods
In a large-scale longitudinal study, we investigated whether higher rates of DD are an antecedent or a consequence of alcohol use during adolescent development. As part of the IMAGEN project, 2220 adolescents completed the Monetary Choice Questionnaire as a DD measure, the Alcohol Use Disorders Identification Test, and the Timeline Follow Back interview at ages 14, 16, 18, and 22. Bivariate latent growth curve models were applied to investigate the relationship between DD and drinking. To explore the consequences of drinking, we computed the cumulative alcohol consumption and correlated it with the development of discounting. A subsample of 221 participants completed an intertemporal choice task (iTeCh) during functional magnetic resonance imaging at ages 14, 16, and 18. Repeated-measures ANOVA was used to differentiate between high-risk and low-risk drinkers on the development of neural processing during intertemporal choices.Results
Overall, high rates of DD at age 14 predicted a greater increase in drinking over 8 years. In contrast, on average, moderate alcohol use did not affect DD from ages 14 to 22. Of note, we found indicators for less brain activity in top-down control areas during intertemporal choices in the participants who drank more.Conclusions
Steep DD was shown to be a predictor rather than a consequence of alcohol use in low-level drinking adolescents. Important considerations for future longitudinal studies are the sampling strategies to be used and the reliability of the assessments.29.
Ryan J. Wood-Bradley Sarah L. Henry Sanna Barrand Anais Giot Luke Eipper John F. Bertram Luise A. Cullen-McEwen James A. Armitage 《Anatomical record (Hoboken, N.J. : 2007)》2020,303(10):2657-2667
A maternal low protein (LP) diet in rodents often results in low nephron endowment and renal pathophysiology in adult life, with outcomes often differing between male and female offspring. Precisely how a maternal LP diet results in low nephron endowment is unknown. We conducted morphological and molecular studies of branching morphogenesis and nephrogenesis to identify mechanisms and timepoints that might give rise to low nephron endowment. Sprague–Dawley rats were fed a normal protein (19.4% protein, NP) or LP (9% protein) diet for 3 weeks prior to mating and throughout gestation. Embryonic day 14.25 (E14.25) kidneys from males and females were either cultured for 2 days after which branching morphogenesis was quantified, or frozen for gene expression analysis. Real-time PCR was used to quantify expression of key nephrogenesis and branching morphogenesis genes at E14.25 and 17.25. At E17.25, nephron number was determined in fixed tissue. There was no effect of either maternal diet or sex on branching morphogenesis. Nephron number at E17.25 was 14% lower in male and female LP offspring than in NP controls. At E14.25 expression levels of genes involved in branching morphogenesis (Gfrα1, Bmp4, Gdnf) and nephrogenesis (Hnf4a, Pax2, Wnt4) were similar in the dietary groups, but significant differences between sexes were identified. At E17.25, expression of Gfrα1, Gdnf, Bmp4, Pax2 and Six2 was lower in LP offspring than NP offspring, in both male and female offspring. These findings provide new insights into how a LP diet leads to low nephron endowment and renal sexual dimorphism. 相似文献