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93 results on '"Yatabe, Junichi"'

53. PS 02-47 RELATIONSHIPS BETWEEN SERUM SOLUBLE (PRO)RENIN RECEPTOR LEVELS AND OBESITY- OR METABOLISM-RELATED FACTORS IN ESSENTIAL HYPERTENSIVE PATIENTS

Author

Kimura, Shihori, primary, Morimoto, Satoshi, additional, Yamashita, Kaoru, additional, Takano, Noriyoshi, additional, Mizuguchi, Yuki, additional, Niiyama, Michita, additional, Bokuda, Kanako, additional, Yatabe, Midori, additional, Yatabe, Junichi, additional, Watanabe, Daisuke, additional, Ando, Takashi, additional, and Ichihara, Atsuhiro, additional

Published
2016
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56. PS 11-41 ASSOCIATION BETWEEN BODY MASS INDEX AND MORNING SURGE IN PATIENTS WITH ESSENTIAL HYPERTENSION

Author

Morimoto, Satoshi, primary, Niiyama, Michita, additional, Kimura, Shihori, additional, Mizuguchi, Yuki, additional, Seki, Yasufumi, additional, Yoshida, Naohiro, additional, Bokuda, Kanako, additional, Yatabe, Midori, additional, Yatabe, Junichi, additional, Watanabe, Daisuke, additional, Ando, Takashi, additional, and Ichihara, Atsuhiro, additional

Published
2016
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57. PS 02-46 URINARY SOLUBLE (PRO)RENIN RECEPTOR EXCRETION ASSOCIATED WITH URINE pH

Author

Morimoto, Satoshi, primary, Niiyama, Michita, additional, Kimura, Shihori, additional, Yamashita, Kaoru, additional, Takano, Noriyoshi, additional, Mizuguchi, Yuki, additional, Seki, Yasufumi, additional, Yatabe, Midori, additional, Yatabe, Junichi, additional, Watanabe, Daisuke, additional, Ando, Takashi, additional, and Ichihara, Atsuhiro, additional

Published
2016
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60. The rationale and design of reduction of uncontrolled hypertension by Remote Monitoring and Telemedicine (REMOTE) study.

Author

Yatabe, Midori Sasaki, Yatabe, Junichi, Asayama, Kei, Staessen, Jan A., Mujaj, Blerim, Thijs, Lutgarde, Ito, Kyotaro, Sonoo, Tomohiro, Morimoto, Satoshi, and Ichihara, Atsuhiro

Subjects
*HYPERTENSION, *THERAPEUTICS, *INTERNET in medicine, *TELEMEDICINE, *REGULATION of blood pressure, *BLOOD pressure, *PATIENTS, *PATIENT satisfaction, *COST effectiveness, *COMPUTER network resources
Abstract

Purpose: Although self-measurement of home blood pressure (HBP) is common in Japan and HBP telemonitoring via the Internet is possible, whether telemonitoring improves HBP control better than conventional practice remains unclear. Furthermore, hypertension care with online communication using telemonitored HBP is feasible, whereas the efficacy and safety of such telemedicine have not been established. We aim to compare traditional care, care with office visits using HBP telemonitoring, and antihypertensive telemedicine based on HBP telemonitoring. Methods and design: In total, 444 patients with uncontrolled hypertension will be recruited and randomly assigned to three groups: (1) control: usual care with office visits and HBP self-report, (2) telemonitoring: weekly assessment of transmitted HBP by physicians and treatment adjustment upon office visits, or (3) telemedicine: online communication instead of office visits to adjust medication using telemonitored HBP. Primary outcome is the time to control of HBP, and secondary outcomes include achieved HBP levels, adherence, treatment intensity, adverse events, patient satisfaction and cost-effectiveness. Discussion: Hypertension care with telemonitoring and telemedicine are expected to require shorter time to achieve HBP control compared to usual care. Combining HBP telemonitoring with telemedicine may lower the hurdles for starting and persisting to hypertension treatment and eventually reduce cardiovascular events. [ABSTRACT FROM AUTHOR]

Published
2018
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61. ACTH-Dependent Cyclic Cushing Syndrome Triggered by Glucocorticoid Excess Through a Positive-Feedback Mechanism.

Author

Seki, Yasufumi, Morimoto, Satoshi, Saito, Fumiko, Takano, Noriyoshi, Kimura, Shihori, Yamashita, Kaoru, Yoshida, Naohiro, Bokuda, Kanako, Sasaki, Nobukazu, Yatabe, Midori, Watanabe, Daisuke, Yatabe, Junichi, Ando, Takashi, Amano, Kosaku, Kawamata, Takakazu, and Ichihara, Atsuhiro

Abstract

Cyclic Cushing syndrome is a rare variant of Cushing syndrome that demonstrates periodic cortisol excess. It has been thought that inhibition of a glucocorticoid positive-feedback loop is associated with remission of hypercortisolism in ACTH-dependent cyclic Cushing syndrome. However, the underlying mechanism that triggers the development of the hypercortisolism is still unknown. We observed a case of ACTH-dependent cyclic Cushing syndrome that was developed by exogenous glucocorticoids, possibly through a glucocorticoid positive-feedback loop.

Published
2019
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63. Abstract MP03: Relationships between Serum Soluble (Pro)Renin Receptor Levels and Endocrine or Metabolic Factors in Patients with Essential Hypertension

Author

Kimura, Shihori, primary, Morimoto, Satoshi, additional, Yamashita, Kaoru, additional, Takano, Noriyoshi, additional, Mizuguchi, Yuki, additional, Seki, Yasufumi, additional, Niiyama, Michita, additional, Yoshida, Naohiro, additional, Bokuda, Kanako, additional, Yatabe, Midori, additional, Yatabe, Junichi, additional, Watanabe, Daisuke, additional, Ando, Takashi, additional, and Ichihara, Atsuhiro, additional

Published
2015
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67. Abstract 072: Newly Developed Personal Device can Detect Changes and Variations of Urinary Na/K Ratio with Standardized Low- and High-salt Meals in Healthy Volunteers

Author

Yatabe, Junichi, primary, Yatabe, Midori S, additional, Takano, Kozue, additional, Watanabe, Ami, additional, Kurosawa, Satsuki, additional, Yonemoto, Mizuho, additional, Nochi, Momoko, additional, Ikeda, Yuri, additional, Iwahori, Toshiyuki, additional, Shiga, Toshikazu, additional, Watanabe, Tsuyoshi, additional, and Kimura, Junko, additional

Published
2014
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68. Mini Nutritional Assessment as a useful method to predict the development of pressure ulcer among elderly inpatients

Author

Yatabe, Midori Sasaki, Taguchi, Fumie, Ishida, Izumi, Sato, Atsuko, Kameda, Toshio, Ueno, Shuichi, Takano, Kozue, Watanabe, Tsuyoshi, Sanada, Hironobu, Yatabe, Junichi, Yatabe, Midori Sasaki, Taguchi, Fumie, Ishida, Izumi, Sato, Atsuko, Kameda, Toshio, Ueno, Shuichi, Takano, Kozue, Watanabe, Tsuyoshi, Sanada, Hironobu, and Yatabe, Junichi

Abstract

type:Text, Author Manuscript (Submitted version), OBJECTIVES: Malnutrition is a major risk factor of pressure ulcers (PU). However, the best method of nutritional assessment to prevent PU is still unclear. This study was designed to determine the usefulness of Mini Nutritional Assessment (MNA) and plasma amino acid analysis to predict the formation of PU among inpatients. DESIGN: This was a prospective, observational cohort study with a mean observation period of 62.2±86.4 days. SETTING: Intermediate and acute care wards of a hospital in rural Japan. PARTICIPANTS: The 422 patients analyzed had an average age of 85.0±7.6 years. MEASUREMENTS: MNA, Subjective Global Assessment (SGA), Braden Scale (PU prognostic score), pressure ulcer formation, and biochemical analysis including plasma amino acid concentrations. RESULTS: PU developed in 7.1% of the patients. A MNA score of less than 8 was more sensitive than a rating of moderate or severe malnourishment on the SGA combined with a Braden Scale score of <15 in predicting future PU. Area under the receiver operating characteristic curve (AUC) of MNA was superior to that of the Braden Scale. Braden Scale nutrition subscore had the lowest AUC among the six Braden Scale subscores. The PU group showed significantly lower plasma arginine concentrations than the No PU group. CONCLUSION: MNA was able to predict the development of PU. A MNA of <8 performed better than the SGA, Braden Scale, and plasma arginine levels in predicting PU development. Although lower plasma arginine concentration at time of admission was associated with PU development, the area under the ROC curve was not significant. The findings from this prospective study support the use of nutritional assessment among inpatients in order to predict PU risk and target appropriate interventions.

Published
2013

69. Effects of a high-sodium diet on renal tubule Ca2+ transporter and claudin expression in Wistar-Kyoto rats

Author

Yatabe, Midori Sasaki, Yatabe, Junichi, Takano, Kozue, Murakami, Yuta, Sakuta, Rina, Abe, Sadahiko, Sanada, Hironobu, Kimura, Junko, Watanabe, Tsuyoshi, Yatabe, Midori Sasaki, Yatabe, Junichi, Takano, Kozue, Murakami, Yuta, Sakuta, Rina, Abe, Sadahiko, Sanada, Hironobu, Kimura, Junko, and Watanabe, Tsuyoshi

Abstract

type:Text, Background: Urinary Ca^{2+} excretion increases with dietary NaCl. NaCl-induced calciuria may be associated with hypertension, urinary stone formation and osteoporosis, but its mechanism and long-term effects are not fully understood. This study examined alterations in the expressions of renal Ca^{2+} transporters, channels and claudins upon salt loading to better understand the mechanism of salt-induced urinary Ca^{2+} loss. Methods: Eight-week old Wistar-Kyoto rats were fed either 0.3% or 8% NaCl diet for 8 weeks. Renal cortical expressions of Na+/Ca2+ exchanger 1 (NCX1), Ca^{2+} pump (PCMA1b), Ca^{2+} channel (TRPV5), calbindin-D28k, and claudins (CLDN-2, -7, -8, -16 and −19) were analyzed by quantitative PCR, western blot and/or immunohistochemistry. Results: Fractional excretion of Ca^{2+} increased 6.0 fold with high-salt diet. Renal cortical claudin-2 protein decreased by approximately 20% with decreased immunological staining on tissue sections. Claudin-16 and −19 expressions were not altered. Renal cortical TRPV5, calbindin-D28k and NCX1 expressions increased 1.6, 1.5 and 1.2 fold, respectively. Conclusions: Chronic high-salt diet decreased claudin-2 protein and increased renal TRPV5, calbindin-D28k, and NCX1. Salt loading is known to reduce the proximal tubular reabsorption of both Na+ and Ca^{2+}. The reduction in claudin-2 protein expression may be partly responsible for the reduced Ca^{2+} reabsorption in this segment. The concerted upregulation of more distal Ca^{2+}-transporting molecules may be a physiological response to curtail the loss of Ca^{2+}, although the magnitude of compensation does not seem adequate to bring the urinary Ca^{2+} excretion down to that of the normal-diet group.

Published
2012

79. Amelioration of Genetic Hypertension by Suppression of Renal G Protein–Coupled Receptor Kinase Type 4 Expression

Author

Sanada, Hironobu, primary, Yatabe, Junichi, additional, Midorikawa, Sanae, additional, Katoh, Tetsuo, additional, Hashimoto, Shigeatsu, additional, Watanabe, Tsuyoshi, additional, Xu, Jing, additional, Luo, Yingjin, additional, Wang, Xiaoyan, additional, Zeng, Chunyu, additional, Armando, Ines, additional, Felder, Robin A., additional, and Jose, Pedro A., additional

Published
2006
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80. Single-Nucleotide Polymorphisms for Diagnosis of Salt-Sensitive Hypertension

Author

Sanada, Hironobu, primary, Yatabe, Junichi, primary, Midorikawa, Sanae, primary, Hashimoto, Shigeatsu, primary, Watanabe, Tsuyoshi, primary, Moore, Jason H, primary, Ritchie, Marylyn D, primary, Williams, Scott M, primary, Pezzullo, John C, primary, Sasaki, Midori, primary, Eisner, Gilbert M, primary, Jose, Pedro A, primary, and Felder, Robin A, primary

Published
2006
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81. Differential Effects of Angiotensin II Type-1 Receptor Antisense Oligonucleotides on Renal Function in Spontaneously Hypertensive Rats

Author

Yoneda, Minoru, primary, Sanada, Hironobu, additional, Yatabe, Junichi, additional, Midorikawa, Sanae, additional, Hashimoto, Shigeatsu, additional, Sasaki, Midori, additional, Katoh, Tetsuo, additional, Watanabe, Tsuyoshi, additional, Andrews, Peter M., additional, Jose, Pedro A., additional, and Felder, Robin A., additional

Published
2005
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86. Direction‐independent block of bi‐directional Na+/Ca2+exchange current by KB‐R7943 in guinea‐pig cardiac myocytes

Author

Kimura, Junko, Watano, Tomokazu, Kawahara, Masanori, Sakai, Eiichi, and Yatabe, Junichi

Abstract

We investigated the inhibitory effect of KB‐R7943 on ‘bi‐directional’ Na+/Ca2+exchange current (iNCX) with the reversal potential of iNCX(ENCX) in the middle of the ramp voltage pulse employed.Bi‐directional iNCXwas recorded with ‘full’ ramp pulses given every 10 s from the holding potential of −60 mV over the voltage range between 30 and −150 mV under the ionic conditions of 140 mM[Na]o, 20 mM[Na]i, 1 mM[Ca]oand 433 nM[Ca]iwith calculated ENCXat −50 mV.KB‐R7943 (0.1–100 μM) concentration‐dependently inhibited the current, which reversed near the calculated ENCX, indicating that the blocked current was iNCX.The inhibition levels were not significantly different between outward and inward iNCXmeasured at 0 and −120 mV, respectively. IC50of KB‐R7943 was approximately 1 μMfor both directions of iNCX.Under the bi‐directional ionic conditions, only an outward or inward iNCXwas induced by positive or negative ‘half’ ramp pulses, respectively, from the holding potential of −60 mV. KB‐R7943 inhibited both direction of iNCXand the concentration‐inhibition relations were superimposable to the ones obtained by ‘full’ ramp pulses.These results indicate that KB‐R7943 inhibits iNCXdirection‐independently under bi‐directional conditions. This conclusion is different from that of our previous results obtained from iNCXunder uni‐directional ionic conditions, where KB‐R7943 inhibited iNCXdirection‐dependently. The difference could be attributed to slow dissociation of the drug from the exchanger.

Published
1999
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88. Abstract 072.

Author

Yatabe, Junichi, Yatabe, Midori S, Takano, Kozue, Watanabe, Ami, Kurosawa, Satsuki, Yonemoto, Mizuho, Nochi, Momoko, Ikeda, Yuri, Iwahori, Toshiyuki, Shiga, Toshikazu, Watanabe, Tsuyoshi, and Kimura, Junko

Abstract

Background: A low-sodium (Na), high-potassium (K) diet is recommended to suppress blood pressure elevation, but determining the absolute amounts of Na and K in a diet is difficult. A novel portable device was developed to allow easy measurement of urinary Na/K ratio on the spot. In this study, our aims were 1): to observe the changes of urinary Na/K ratio in subjects on low- and high-Na diet and 2): to determine if there are differences in urinary Na/K ratio between subjects with and without salt sensitivity.Methods: Healthy volunteers (14 subjects) ingested standardized low- (3 g NaCl /day) and high-Na (20 g NaCl/day) meals for 7 days each. Urinary Na/K ratio was measured at each voiding using a prototype device (Omron Healthcare). Collection of blood and 24-hour urine was conducted at the end of each diet period (unrestricted (NS), low-salt (LS), and high-salt (HS)). Those with mean blood pressure difference (LS vs. HS) ≥ 5% were determined as salt-sensitive (SS) and others salt-resistant (SR).Results: Urinary Na/K ratio reached a plateau approximately 3 days after each change in the Na level of the diet. Urinary Na/K ratio of spot urine correlated well with Na/K ratio of 24-hour urine. Average urinary Na/K ratio was 3.9 ± 1.9 on the last day of NS, 0.8 ± 0.3 on LS, and 6.9 ± 2.1 on HS. The variation of urinary Na/K ratio was small during the LS diet period. The change in urinary Na/K ratio of SS group tended to be slower than that of SR. This device may also be useful in diabetic and proteinuric patients as Na/K ratio was affected minimally by experimental glucose and protein addition.Conclusion: Using an easy-to-use device, measurements of urinary Na/K ratio keenly reflected the sodium level of the diet. [ABSTRACT FROM AUTHOR]

Published
2014

89. Abstract 102.

Author

Kitada, Kento, Nakano, Daisuke, Hitomi, Hirofumi, Yatabe, Junichi, Felder, Robin A, Kobori, Hiroyuki, and Nishiyama, Akira

Abstract

We previously reported that aldosterone/mineralocorticoid receptor activation caused cell senescence via p21, a cell cycle regulator, -dependent pathway in proximal tubules of rat kidney and human proximal tubular cells. However, functional influences of cell senescent on the kidney are still unclear. In the present study, we hypothesized that aldosterone-induced cell senescence caused cell apoptosis by increasing the secretion of apoptotic factors (n=6 in all groups). Aldosterone increased senescent cells at day 3 and day 5 in human proximal tubular cells, and the changes were accompanied by the increase in p21 protein expression (day 3: 2.9±0.7 fold, day 5: 6.5±0.9 fold, p<0.05) and TNF-α mRNA (day 3: 2.3±0.3 fold, day 5: 2.4±0.6 fold, p<0.05). In addition, aldosterone also increased secretion of TNF-α into the culture medium compared with vehicle-treated group (day 3: 15.7±1.2 vs 7.2±1.6 pg/ml; day 5: 33.3±5.7 vs 11.8±2.3 pg/ml; p<0.05, respectively): gene silencing of p21 abolished these changes. Meanwhile, 3-day treatment with aldosterone showed no sign of cell apoptosis, which was evaluated by terminal nick end labeling (TUNEL) and annexin V/propidium iodide (PI) staining, and 5-day treatment with aldosterone increased cell apoptosis (TUNEL: aldosterone, 6.4±1.5%; vehicle, 0.6±0.3%; annexin V/PI: aldosterone, 5.8±0.8%; vehicle, 0.8±0.3%; p<0.05). Importantly, p21 siRNA and TNF-α neutralizing antibody abolished these aldosterone-induced apoptotic changes (TUNEL: 1.4±0.1 and 0.9±0.5%; annexin V/PI: 0.9±0.3 and 1.5±0.9%; respectively). These results indicate that aldosterone increases TNF-α synthesis and secretion in proximal tubular cells via p21/senescence-dependent pathway, and that the secreted TNF-α plays an important role as an autocrine/paracrine factor to mediate cell apoptosis, which may be involved in aldosterone-induced renal damage. [ABSTRACT FROM AUTHOR]

Published
2012

92. [3,4-Dihydroxyphenyl alanine (DOPA)].

Author

Yatabe J and Sanada H

Subjects
Adrenal Gland Neoplasms diagnosis, Biomarkers analysis, Chromatography, High Pressure Liquid, Dihydroxyphenylalanine physiology, Humans, Melanoma diagnosis, Nervous System Neoplasms diagnosis, Neuroblastoma diagnosis, Parkinson Disease diagnosis, Pheochromocytoma diagnosis, Reference Values, Specimen Handling, Dihydroxyphenylalanine analysis
Published
2005

93. [Involvement of dopamine receptor in the pathogenesis of hypertension and hypertensive target-organ damage].

Author

Sanada H, Yatabe J, Sasaki M, and Watanabe T

Subjects
Animals, Dopamine physiology, Dopamine Agonists therapeutic use, Fenoldopam therapeutic use, G-Protein-Coupled Receptor Kinase 4, Humans, Hypertension drug therapy, Kidney Tubules, Proximal metabolism, Natriuresis, Protein Serine-Threonine Kinases physiology, Receptors, Dopamine classification, Signal Transduction, Sodium metabolism, Hypertension etiology, Receptors, Dopamine physiology
Published
2004

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