Ishida, Junichi

[["dc.bibliographiccitation.firstpage","497"],["dc.bibliographiccitation.journal","Wiener klinische Wochenschrift"],["dc.bibliographiccitation.lastpage","504"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","dos Santos, Marcelo Rodrigues"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Emami, Amir"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","von Haehling, Stephan"],["dc.date.accessioned","2018-11-07T10:05:07Z"],["dc.date.available","2018-11-07T10:05:07Z"],["dc.date.issued","2016"],["dc.description.abstract","Inadequate nutritional status has been linked to poor outcomes in patients with heart failure (HF). Skeletal muscle wasting affects about 20% of ambulatory patients with HF. The impact of nutritional intake and appetite on skeletal muscle wasting has not been investigated so far. We sought to investigate the impact of nutritional status on muscle wasting and mortality in ambulatory patients with HF. We studied 130 ambulatory patients with HF who were recruited as a part of the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) program. Muscle wasting was defined according to criteria of sarcopenia, i.e., appendicular skeletal muscle mass two standard deviations below the mean of a healthy reference group aged 18-40 years. Nutritional status was evaluated using the Mini-Nutritional Assessment-Short Form (MNA-SF). Functional capacity was assessed as peak oxygen consumption (peak VO2) by cardiopulmonary exercise testing, 6aEurominute walk testing, and the Short Physical Performance Battery (SPPB). At baseline, 19 patients (15%) presented with muscle wasting. Patients with muscle wasting had significantly lower values of peak VO2, 6aEurominute walk distance, SPPB, and MNA-SF score than patients without (all p < 0.05). In multivariate analysis, MNA-SF remained an independent predictor of muscle wasting after adjustment for age and New York Heart Association class (odds ratio [OR] 0.66; confidence interval [CI] 0.50-0.88; p < 0.01). A total of 16 (12%) patients died during a mean follow-up of 21 months. In Cox regression analysis, MNA-SF (OR 0.80, CI 0.64-0.99, p = 0.04), left ventricular ejection fraction (OR 0.93, CI 0.86-0.99, p = 0.05), and peak VO2 (OR 0.78, CI 0.65-0.94, p = 0.008) were predictors of death. MNA-SF is an independent predictor of muscle wasting and mortality in ambulatory patients with HF. Nutritional screening should be included as a fundamental part of the overall assessment of these patients."],["dc.identifier.doi","10.1007/s00508-016-1112-8"],["dc.identifier.isi","000390034100011"],["dc.identifier.pmid","27853883"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38838"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","1613-7671"],["dc.relation.issn","0043-5325"],["dc.title","Nutritional status and its effects on muscle wasting in patients with chronic heart failure: insights from Studies Investigating Co-morbidities Aggravating Heart Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","37"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","42"],["dc.bibliographiccitation.volume","238"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Anker, Markus S."],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T10:22:26Z"],["dc.date.available","2018-11-07T10:22:26Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Myostatin, a negative regulator of skeletal muscle mass, is up-regulated in the myocardiumof heart failure (HF) and increasedmyostatin is associatedwithweight loss in animal models with HF. Although there are disparities in pathophysiology and epidemiology between male and female patients with HF, it remains unclear whether there is gender difference in myostatin expression and whether it is associated with weight loss in HF patients. Methods: Heart tissue sampleswere collected frompatientswith advanced heart failure (n= 31, female n= 5) as well as healthy control donors (n= 14, female n= 6). Expression levels of myostatin and its related proteins in the heart were evaluated by western blotting analysis. Results: Body mass index was significantly lower in female HF patients than inmale counterparts (20.0 +/- 4.2 in female vs 25.2 +/- 3.8 in male, p= 0.04). In female HF patients, both mature myostatin and pSmad2 were significantly up-regulated by 1.9 fold (p= 0.05) and 2.5 fold (p < 0.01) respectively compared to female donors, while expression of pSmad2was increased by 2.8 times inmale HF patients compared to male healthy subjects, but that of myostatinwas not. Therewas no significant difference in protein expression related tomyostatin signaling between male and female patients. Conclusion: In this study, myostatin and pSmad2 were significantly up-regulated in the failing heart of female patients, but notmale patients, and female patients displayed lower body mass index. Enhancedmyostatin signaling in female failing heart may causally contribute to pathogenesis of HF and cardiac cachexia. (C) 2017 Elsevier B. V. All rights reserved."],["dc.identifier.doi","10.1016/j.ijcard.2017.03.153"],["dc.identifier.isi","000402478900007"],["dc.identifier.pmid","28465115"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42273"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.title","Myostatin signaling is up-regulated in female patients with advanced heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","12"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","18"],["dc.bibliographiccitation.volume","238"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Markus S."],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T10:22:25Z"],["dc.date.available","2018-11-07T10:22:25Z"],["dc.date.issued","2017"],["dc.description.abstract","Cachexia is defined as a complex metabolic syndrome associated with underlying illness that is characterized by the loss of body weight consisting of muscle and fat mass wasting. Sarcopenia is defined as the ageing related loss of muscle mass in health and disease that may not have an effect on body weight. As millions of patients are in cachectic or sarcopenic states, both conditions contribute to high numbers to death worldwide. A number of treatments have been proposed for cachexia and sarcopenia, but these are either in the preclinical stage or in clinical trials and hence not available to the general population. Particularly in cachexia there is a massive problem of recruiting patients for trials and also with the follow-up, due to the seriousness of the disease. This underlines the importance of well-characterized animal models. Obviously, most of the widely used cachexia and sarcopenia animal models have limitations in reproducibility of the condition and novel models are warranted in this context. The key findings of developing models in the field of cachexia and sarcopenia are that more types of the conditions have been taken into the researchers' interest. In cardiac cachexia, technical issues, which limit the preciseness and reproducibility in surgical heart failure models, have been overcome by a combination of surgery and the use of transgenic mouse models or salt sensitive rat models. Fatigue is the most pronounced symptom of cachexia and may be caused by reduced cardiac function independent of the underlying disease. Sarcopenia models often suffer from the use of young animals, due to the limited availability and very high costs of using aged animals. This review will focus on rodent models designed to mimic cachexia and sarcopenia including co-morbidities such as cancer, heart failure, as well as other diseases and conditions. (C) 2017 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.ijcard.2017.03.154"],["dc.identifier.isi","000402478900003"],["dc.identifier.pmid","28476513"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42270"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.title","Animal models of cachexia and sarcopenia in chronic illness: Cardiac function, body composition changes and therapeutic results"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","48"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.volume","247"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2020-12-10T14:24:31Z"],["dc.date.available","2020-12-10T14:24:31Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.ijcard.2017.06.094"],["dc.identifier.issn","0167-5273"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72275"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Reply to letter to the editor “suramin against myostatin signaling may be considered to intervene in female patients with advanced heart failure”"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","391"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cachexia Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","392"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Saito, Masakazu"],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T09:48:30Z"],["dc.date.available","2018-11-07T09:48:30Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1002/jcsm.12080"],["dc.identifier.isi","000365536800017"],["dc.identifier.pmid","26674220"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35320"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.title","Hypermetabolism: should cancer types, pathological stages and races be considered in assessing metabolism and could elevated resting energy expenditure be the therapeutic target in patients with advanced cancer?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Springer, Jochen"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Haehling, Stephan von"],["dc.date.accessioned","2019-07-15T10:49:08Z"],["dc.date.available","2019-07-15T10:49:08Z"],["dc.date.issued","2019"],["dc.description.abstract","Growth hormone secretagogues (GHSs) are a generic term to describe compounds which increase growth hormone (GH) release. GHSs include agonists of the growth hormone secretagogue receptor (GHS‐R), whose natural ligand is ghrelin, and agonists of the growth hormone‐releasing hormone receptor (GHRH‐R), to which the growth hormonereleasing hormone (GHRH) binds as a native ligand. Several GHSs have been developed with a view to treating or diagnosisg of GH deficiency, which causes growth retardation, gastrointestinal dysfunction and altered body composition, in parallel with extensive research to identify GHRH, GHS‐R and ghrelin. This review will focus on the research history and the pharmacology of each GHS, which reached randomized clinical trials. Furthermore, we will highlight the publicly disclosed clinical trials regarding GHSs."],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16281"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61499"],["dc.language.iso","en"],["dc.title","Growth hormone secretagogues: history, mechanism of action and clinical development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","240"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of the American Medical Directors Association"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Dos Santos, Marcelo Rodrigues"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Emami, Amir"],["dc.contributor.author","Springer, Jochen"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","von Haehling, Stephan"],["dc.date.accessioned","2018-11-07T10:26:22Z"],["dc.date.available","2018-11-07T10:26:22Z"],["dc.date.issued","2017"],["dc.description.abstract","Objectives: Skeletal muscle wasting, also known as sarcopenia, has recently been identified as a serious comorbidity in patients with heart failure (HF). We aimed to assess the impact of sarcopenia on endothelial dysfunction in patients with HF with reduced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF). Design: Cross-sectional study. Setting: Ambulatory patients with HF were recruited at Charite Medical School, Campus Virchow-Klinikum, Berlin, Germany. Participants: We assessed peripheral blood flow (arm and leg) in 228 patients with HF and 32 controls who participated in the Studies Investigating Comorbidities Aggravating HF (SICA-HF). Measurements: The appendicular skeletal muscle mass of the arms and the legs combined was assessed by dual energy x-ray absorptiometry (DEXA). Sarcopenia was defined as the appendicular muscle mass two standard deviations below the mean of a healthy reference group of adults aged 18 to 40 years, as suggested for the diagnosis of muscle wasting in healthy aging. All patients underwent a 6-minute walk test and spiroergometry testing. Forearm and leg blood flow were measured by venous occlusion plethysmography. Peak blood flow was assessed after a period of ischemia in the limbs to test endothelial function. Results: Sarcopenia was identified in 37 patients (19.5%). Patients with sarcopenia presented with lower baseline forearm blood flow (2.30 +/- 1.21 vs. 3.06 +/- 1.49 vs. 4.00 +/- 1.66 mL min(-1) 100 mL(-1); P = .02) than those without sarcopenia or controls. The group of patients with sarcopenia showed similar baseline leg blood flow (2.06 +/- 1.62 vs. 2.39 +/- 1.39 mL min(-1) 100 mL(-1); P = .11) to those without but lower values when compared to controls (2.06 +/- 1.62 vs. 2.99 +/- 1.28 mL min(-1) 100 mL(-1); P = .03). In addition, patients with and without sarcopenia presented with lower peak flow in the forearm when compared to controls (18.37 +/- 7.07 vs. 22.19 +/- 8.64 vs. 33.63 +/- 8.57 mL min(-1) 100 mL(-1); P < .001). A similar result was observed in the leg (10.89 +/- 5.61 vs. 14.66 +/- 7.19 vs. 21.37 +/- 13.16 mL min(-1) 100 mL(-1); P < .001). Peak flow in the forearm showed a significant correlation with exercise capacity (relative peak VO2: R = 0.47; P < .001; absolute peak VO2: R = 0.35; P < .001; and 6-min walk distance: R = 0.20; P < .01). Similar correlations were observed between peak flow in the leg and exercise capacity (absolute peak VO2: R = 0.42, P < .001; relative peak VO2: R = 0.41, P < .001; and 6-min walk test: R = 0.33; P < .001). Logistic regression showed peak flow in the leg to be independently associated with the 6-min walk distance adjusted for age, hemoglobin level, albumin, creatinine, presence of sarcopenia, and coronary artery disease (hazard ratio, 0.903; 95% confidence interval, 0.835-0.976; P = .01). Conclusion: Patients with HF associated with sarcopenia have impaired endothelial function. Lower vasodilatation had a negative impact on exercise capacity, particularly prevalent in patients with sarcopenia. (C) 2016 AMDA - The Society for Post-Acute and Long-Term Care Medicine."],["dc.identifier.doi","10.1016/j.jamda.2016.09.006"],["dc.identifier.isi","000398943400010"],["dc.identifier.pmid","27816483"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43027"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1538-9375"],["dc.relation.issn","1525-8610"],["dc.title","Sarcopenia and Endothelial Function in Patients With Chronic Heart Failure: Results From the Studies Investigating Comorbidities Aggravating Heart Failure (SICA-HF)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","852"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","853"],["dc.bibliographiccitation.volume","223"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T10:05:47Z"],["dc.date.available","2018-11-07T10:05:47Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1016/j.ijcard.2016.08.289"],["dc.identifier.isi","000387036200224"],["dc.identifier.pmid","27580220"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38966"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.title","Significance of animal models of cardiac cachexia and impact of gender on cardiac cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","11"],["dc.bibliographiccitation.volume","238"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Markus S."],["dc.contributor.author","Coats, Andrew J. Stewart"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T10:22:24Z"],["dc.date.available","2018-11-07T10:22:24Z"],["dc.date.issued","2017"],["dc.description.abstract","Cachexia in the context of heart failure (HF) has been termed cardiac cachexia, and represents a progressive in-voluntary weight loss. Cachexia is mainly the result of an imbalance in the homeostasis of muscle protein synthesis and degradation due to a lower activity of protein synthesis pathways and an over-activation of protein degradation. In addition, muscle wasting leads to of impaired functional capacity, even after adjusting for clinical relevant variables in patients with HF. However, there is no sufficient therapeutic strategy in muscle wasting in HF patients and very few studies in animal models. Exercise training represents a promising intervention that can prevent or even reverse the process of muscle wasting, and worsening the muscle function and performance in HF with muscle wasting and cachexia. The pathological mechanisms and effective therapeutic approach of cardiac cachexia remain uncertain, because of the difficulty to establish animal cardiac cachexia models, thus novel animal models are warranted. Furthermore, the use of improved animal models will lead to a better understanding of the pathways that modulate muscle wasting and therapeutics of muscle wasting of cardiac cachexia. (C) 2017 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.ijcard.2017.03.155"],["dc.identifier.isi","000402478900002"],["dc.identifier.pmid","28427849"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42267"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.title","Sarcopenia, cachexia, and muscle performance in heart failure: Review update 2016"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","62"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","64"],["dc.bibliographiccitation.volume","225"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Baumgarten, Anna"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T10:04:29Z"],["dc.date.available","2018-11-07T10:04:29Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1016/j.ijcard.2016.09.128"],["dc.identifier.isi","000390472000015"],["dc.identifier.pmid","27710805"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38703"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.title","Protein levels in Keap1-Nrf2 system in human failing heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]