The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform
Naoki Mochizuki - One of the best experts on this subject based on the ideXlab platform.
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S1P-S1p2 Signaling in Cardiac Precursor Cells Migration
Etiology and Morphogenesis of Congenital Heart Disease, 2016Co-Authors: Hajime Fukui, Shigetomo Fukuhara, Naoki MochizukiAbstract:During embryogenesis, zebra fish Cardiac precursor cells (CPCs) originating from anterior lateral plate mesoderm migrate toward the midline between the endoderm and the yolk syncytial layer (YSL) to form Cardiac tube. The endoderm functions as a foothold for CPCs as evidenced by the endodermal mutants (cas/sox32, sox17, oep, fau/gata5, and bon) showing two hearts (Cardia bifida) [1]. Furthermore, mutant zebra fish (toh) lacking sphingosine-1-phosphate (S1P) transporter which is expressed in the YSL show two hearts [2], indicating the essential role for S1P-mediated signal in Cardiac development. This is also supported by a S1p2 receptor mutant (mil) which exhibits two hearts [3]. However, it is still unclear how S1P released from YSL regulates CPC migration.
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S1P-Yap1 Signaling Regulates Endoderm Formation Required for Cardiac Precursor Cell Migration in Zebrafish
Developmental Cell, 2014Co-Authors: Hajime Fukui, Kenta Terai, Hiroyuki Nakajima, Ayano Chiba, Shigetomo Fukuhara, Naoki MochizukiAbstract:Summary To form the primary heart tube in zebrafish, bilateral Cardiac precursor cells (CPCs) migrate toward the midline beneath the endoderm. Mutants lacking endoderm and fish with defective sphingosine 1-phosphate (S1P) signaling exhibit Cardia bifida. Endoderm defects lead to the lack of foothold for the CPCs, whereas the cause of Cardia bifida in S1P signaling mutants remains unclear. Here we show that S1P signaling regulates CPC migration through Yes-associated protein 1 (Yap1)-dependent endoderm survival. Cardia bifida seen in spns2 (S1P transporter) morphants and s1pr2 (S1P receptor-2) morphants could be rescued by endodermal expression of nuclear localized form of yap1 . yap1 morphants had decreased expression of the Yap1/Tead target connective tissue growth factor a (Ctgfa) and consequently increased endodermal cell apoptosis. Consistently, ctgfa morphants showed defects of the endodermal sheet and Cardia bifida. Collectively, we show that S1pr2/Yap1-regulated ctgfa expression is essential for the proper endoderm formation required for CPC migration.
Kazuaki Chayama - One of the best experts on this subject based on the ideXlab platform.
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Helicobacter pylori Infection Is the Major Risk Factor for Gastric Inflammation in the Cardia
Digestive Diseases and Sciences, 2006Co-Authors: Yasuo Egi, Sunjin Kim, Masanori Ito, Shinji Tanaka, Masaharu Yoshihara, Ken Haruma, Kazuaki ChayamaAbstract:We attempted to clarify the pathogenesis of gastric inflammation in the Cardia. Eighty Japanese participated in this study. Biopsy specimens of the gastric antrum, corpus, and Cardia (1 cm from the squamocolumnar junction) were obtained, and histological gastritis was evaluated. Cardiac inflammation was also evaluated using magnifying gastroscopy. We examined Helicobacter pylori infection, gastric juice pH/bile acid (BA), serum pepsinogen and gastrin levels, gastroesophageal reflux disease (GERD), and habitual smoking and assessed the relations between these factors and Cardiac inflammation. The prevalence of H. pylori infection was statistically higher in patients with Cardiac inflammation than in those without inflammation ( P < 0.05). The relationship was also demonstrated by magnifying gastroscopy. Cardiac inflammation was linked to low acid output but not linked to the BA concentration or habitual smoking. Cardiac inflammation was more pronounced in patients without GERD. These results suggest that H. pylori is a major risk factor for Cardiac inflammation in the Japanese.
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Cardiac glands hyperplastic polyp of the stomach
Journal of Gastroenterology and Hepatology, 2005Co-Authors: Shinji Nagata, Shinji Tanaka, Masaharu Yoshihara, Ken Haruma, Kazuaki ChayamaAbstract:Abstract Reported herein is a very rare polyp in the gastric Cardia of a 49-year-old man. He was referred because of a polyp detected by upper gastrointestinal examination in an affiliated hospital. Endoscopic examination revealed a polyp-like submucosal tumor. Endoscopic ultrasonography revealed minute cystic dilatations and thickening of the submucosal layer. Accordingly, a preliminary diagnosis of Cardiac gland hyperplasia was made. The lesion was removed successfully by snare polypectomy. Observed macroscopically, the polyp was 30 mm in diameter and covered with normal gastric mucosa. Examined histologically, the polyp comprised a hyperplastic submucosal Cardiac gland.
Hajime Fukui - One of the best experts on this subject based on the ideXlab platform.
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S1P-S1p2 Signaling in Cardiac Precursor Cells Migration
Etiology and Morphogenesis of Congenital Heart Disease, 2016Co-Authors: Hajime Fukui, Shigetomo Fukuhara, Naoki MochizukiAbstract:During embryogenesis, zebra fish Cardiac precursor cells (CPCs) originating from anterior lateral plate mesoderm migrate toward the midline between the endoderm and the yolk syncytial layer (YSL) to form Cardiac tube. The endoderm functions as a foothold for CPCs as evidenced by the endodermal mutants (cas/sox32, sox17, oep, fau/gata5, and bon) showing two hearts (Cardia bifida) [1]. Furthermore, mutant zebra fish (toh) lacking sphingosine-1-phosphate (S1P) transporter which is expressed in the YSL show two hearts [2], indicating the essential role for S1P-mediated signal in Cardiac development. This is also supported by a S1p2 receptor mutant (mil) which exhibits two hearts [3]. However, it is still unclear how S1P released from YSL regulates CPC migration.
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S1P-Yap1 Signaling Regulates Endoderm Formation Required for Cardiac Precursor Cell Migration in Zebrafish
Developmental Cell, 2014Co-Authors: Hajime Fukui, Kenta Terai, Hiroyuki Nakajima, Ayano Chiba, Shigetomo Fukuhara, Naoki MochizukiAbstract:Summary To form the primary heart tube in zebrafish, bilateral Cardiac precursor cells (CPCs) migrate toward the midline beneath the endoderm. Mutants lacking endoderm and fish with defective sphingosine 1-phosphate (S1P) signaling exhibit Cardia bifida. Endoderm defects lead to the lack of foothold for the CPCs, whereas the cause of Cardia bifida in S1P signaling mutants remains unclear. Here we show that S1P signaling regulates CPC migration through Yes-associated protein 1 (Yap1)-dependent endoderm survival. Cardia bifida seen in spns2 (S1P transporter) morphants and s1pr2 (S1P receptor-2) morphants could be rescued by endodermal expression of nuclear localized form of yap1 . yap1 morphants had decreased expression of the Yap1/Tead target connective tissue growth factor a (Ctgfa) and consequently increased endodermal cell apoptosis. Consistently, ctgfa morphants showed defects of the endodermal sheet and Cardia bifida. Collectively, we show that S1pr2/Yap1-regulated ctgfa expression is essential for the proper endoderm formation required for CPC migration.
E. Grundmann - One of the best experts on this subject based on the ideXlab platform.
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Adenocarcinomas of esophagus and Cardia in comparison with gastric carcinoma
Journal of Cancer Research and Clinical Oncology, 1993Co-Authors: G. Heidl, P. Langhans, W. Mellin, H. Bünte, E. GrundmannAbstract:Since the carcinomas of the Cardia and the adenocarcinomas of the esophagus show many similarities in their histological and morphological descriptions, a detailed comparative study was attempted on the basis of 66 esophageal carcinomas in adenoid differentiation, 359 carcinomas of the Cardia, 1288 gastric carcinomas in infraCardial localisation, and 492 squamous carcinomas of the esophagus. The evaluation yielded no significant differences between the adenocarcinomas of the esophagus and the Cardia neither in age and sex distribution nor with regard to the classifications of Borrmann, WHO, Ming, and Laurén, but a significant discrimination was possible between esophageal and Cardial adenocarcinoma together, on the one hand, and infraCardial gastric carcinoma on the other. Furthermore, esophageal adenocarcinomas were localized preferentially in the lower third, unlike squamous carcinomas of the same organ. These results suggest that esophageal adenocarcinoma and carcinoma of the Cardia must be considered as one separate entity, probably originating from a common stem cell. They further suggest that the Cardia belongs to the esophagus rather than to the stomach.
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Adenocarcinomas of esophagus and Cardia in comparison with gastric carcinoma
Journal of Cancer Research and Clinical Oncology, 1993Co-Authors: G. Heidl, P. Langhans, W. Mellin, H. Bünte, E. GrundmannAbstract:Since the carcinomas of the Cardia and the adenocarcinomas of the esophagus show many similarities in their histological and morphological descriptions, a detailed comparative study was attempted on the basis of 66 esophageal carcinomas in adenoid differentiation, 359 carcinomas of the Cardia, 1288 gastric carcinomas in infraCardial localisation, and 492 squamous carcinomas of the esophagus. The evaluation yielded no significant differences between the adenocarcinomas of the esophagus and the Cardia neither in age and sex distribution nor with regard to the classifications of Borrmann, WHO, Ming, and Lauren, but a significant discrimination was possible between esophageal and Cardial adenocarcinoma together, on the one hand, and infraCardial gastric carcinoma on the other. Furthermore, esophageal adenocarcinomas were localized preferentially in the lower third, unlike squamous carcinomas of the same organ. These results suggest that esophageal adenocarcinoma and carcinoma of the Cardia must be considered as one separate entity, probably originating from a common stem cell. They further suggest that the Cardia belongs to the esophagus rather than to the stomach.
Pamela J. Schreiner - One of the best experts on this subject based on the ideXlab platform.
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Temporal Changes in Resting Heart Rate, Left Ventricular Dysfunction, Heart Failure and Cardiovascular Disease: Cardia Study
The American Journal of Medicine, 2020Co-Authors: Chike C. Nwabuo, Appiah, Henrique T. Moreira, Henrique D. Vasconcellos, N. Aghaji, Bharath Ambale-venkatesh, Jamal S. Rana, Norrina B. Allen, Donald M. Lloyd-jones, Pamela J. SchreinerAbstract:ABSTRACT Background The prognostic significance of temporal changes in resting heart rate in young adults for premature heart failure and cardiovascular disease is unclear. We investigated the association between temporal changes in resting heart rate in young adults and early adult risk factors, subsequent Cardiac function, and the risk of heart failure and cardiovascular by middle age. Methods We examined 4343 Coronary Artery Risk Development in Young Adults (Cardia) study participants (mean [SD] age was 29.9 [3.6] years at the Cardia Year-5 examination [1990-1991], 49% of participants were men, and 45% were African-American). Adjusted linear regression models were used to assess the association between temporal changes in resting heart rate, early life cardiovascular disease risk factors, and midlife Cardiac function. Cox proportional hazard regression models were used to relate temporal changes in resting heart rate to heart failure and cardiovascular disease. Outcomes were followed up until August 31, 2017. Results Higher alcohol consumption (β = 0.03, P Conclusions Baseline and temporal changes in resting heart rate in young adults were associated with incident heart failure and cardiovascular disease by midlife. Contributory factors were associations between temporal increases in resting heart rate and early adult risk factors and subsequent Cardiac dysfunction.