2004
Grenon, S Marlene; Hurwitz, Shelley; Sheynberg, Natalie; Xiao, Xinshu; Judson, Brad; Ramsdell, Craig D; Kim, Christine; Cohen, Richard J; Williams, Gordon H
Sleep restriction does not affect orthostatic tolerance in the simulated microgravity environment Journal Article
In: J Appl Physiol (1985), vol. 97, no. 5, pp. 1660–1666, 2004, ISSN: 8750-7587.
@article{pmid15234956,
title = {Sleep restriction does not affect orthostatic tolerance in the simulated microgravity environment},
author = {S Marlene Grenon and Shelley Hurwitz and Natalie Sheynberg and Xinshu Xiao and Brad Judson and Craig D Ramsdell and Christine Kim and Richard J Cohen and Gordon H Williams},
doi = {10.1152/japplphysiol.00328.2004},
issn = {8750-7587},
year = {2004},
date = {2004-11-01},
journal = {J Appl Physiol (1985)},
volume = {97},
number = {5},
pages = {1660--1666},
abstract = {Orthostatic intolerance (OI) is a major problem following spaceflight, and, during flight, astronauts also experience sleep restriction. We hypothesized that sleep restriction will compound the risk and severity of OI following simulated microgravity and exaggerate the renal, cardioendocrine, and cardiovascular adaptive responses to it. Nineteen healthy men were equilibrated on a constant diet, after which they underwent a tilt-stand test. They then completed 14-16 days of simulated microgravity [head-down tilt bed rest (HDTB)], followed by repeat tilt-stand test. During HDTB, 11 subjects were assigned to an 8-h sleep protocol (non-sleep restricted), and 8 were assigned to a sleep-restricted protocol with 6 h of sleep per night. During various phases, the following were performed: 24-h urine collections, hormonal measurements, and cardiovascular system identification. Development of presyncope or syncope defined OI. There was a significant decrease in time free of OI (P = 0.02) and an increase in OI occurrence (P = 0.06) after HDTB among all subjects. However, the increase in OI occurrence did not differ significantly between the two groups (P = 0.60). The two groups also experienced similar physiological changes with HDTB (initial increase in sodium excretion; increased excretion of potassium at the end of HDTB; increase in plasma renin activity secretion without a change in serum or urine aldosterone). No significant change in autonomic function or catecholamines was noted. Simulated microgravity leads to increased OI, and sleep restriction does not additively worsen OI in simulated microgravity. Furthermore, conditions of sleep restriction and nonsleep restriction are similar with respect to renal, cardioendocrine, and cardiovascular responses to simulated microgravity.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Orthostatic intolerance (OI) is a major problem following spaceflight, and, during flight, astronauts also experience sleep restriction. We hypothesized that sleep restriction will compound the risk and severity of OI following simulated microgravity and exaggerate the renal, cardioendocrine, and cardiovascular adaptive responses to it. Nineteen healthy men were equilibrated on a constant diet, after which they underwent a tilt-stand test. They then completed 14-16 days of simulated microgravity [head-down tilt bed rest (HDTB)], followed by repeat tilt-stand test. During HDTB, 11 subjects were assigned to an 8-h sleep protocol (non-sleep restricted), and 8 were assigned to a sleep-restricted protocol with 6 h of sleep per night. During various phases, the following were performed: 24-h urine collections, hormonal measurements, and cardiovascular system identification. Development of presyncope or syncope defined OI. There was a significant decrease in time free of OI (P = 0.02) and an increase in OI occurrence (P = 0.06) after HDTB among all subjects. However, the increase in OI occurrence did not differ significantly between the two groups (P = 0.60). The two groups also experienced similar physiological changes with HDTB (initial increase in sodium excretion; increased excretion of potassium at the end of HDTB; increase in plasma renin activity secretion without a change in serum or urine aldosterone). No significant change in autonomic function or catecholamines was noted. Simulated microgravity leads to increased OI, and sleep restriction does not additively worsen OI in simulated microgravity. Furthermore, conditions of sleep restriction and nonsleep restriction are similar with respect to renal, cardioendocrine, and cardiovascular responses to simulated microgravity.
Grenon, S M; Hurwitz, S; Sheynberg, N; Xiao, X; Ramsdell, C D; Mai, C L; Kim, C; Cohen, R J; Williams, G H
Role of individual predisposition in orthostatic intolerance before and after simulated microgravity Journal Article
In: J Appl Physiol (1985), vol. 96, no. 5, pp. 1714–1722, 2004, ISSN: 8750-7587.
@article{pmid15075309,
title = {Role of individual predisposition in orthostatic intolerance before and after simulated microgravity},
author = {S M Grenon and S Hurwitz and N Sheynberg and X Xiao and C D Ramsdell and C L Mai and C Kim and R J Cohen and G H Williams},
doi = {10.1152/japplphysiol.01274.2003},
issn = {8750-7587},
year = {2004},
date = {2004-05-01},
journal = {J Appl Physiol (1985)},
volume = {96},
number = {5},
pages = {1714--1722},
abstract = {Orthostatic intolerance (OI) is a major problem after spaceflight. Its etiology remains uncertain, but reports have pointed toward an individual susceptibility to OI. We hypothesized that individual predisposition plays an important role in post-bed rest OI. Twenty-four healthy male subjects were equilibrated on a constant diet, after which they underwent tilt-stand test (pre-TST). They then completed 14-16 days of head-down-tilt bed rest, and 14 of the subjects underwent repeat tilt-stand test (post-TST). During various phases, the following were performed: 24-h urine collections and hormonal measurements, plethysmography, and cardiovascular system identification (a noninvasive method to assess autonomic function and separately quantify parasympathetic and sympathetic responsiveness). Development of presyncope or syncope defined OI. During pre-TST, 11 subjects were intolerant and 13 were tolerant. At baseline, intolerant subjects had lower serum aldosterone (P < 0.01), higher excretion of potassium (P = 0.01), lower leg venous compliance (P = 0.03), higher supine parasympathetic responsiveness (P = 0.02), and lower standing sympathetic responsiveness (P = 0.048). Of the 14 subjects who completed post-TST, 9 were intolerant and 5 were tolerant. Intolerant subjects had lower baseline serum cortisol (P = 0.03) and a higher sodium level (P = 0.02) compared with tolerant subjects. Thus several physiological characteristics were associated with increased susceptibility to OI. We propose a new model for OI, whereby individuals with greater leg venous compliance recruit compensatory mechanisms (activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, and withdrawal of the parasympathetic nervous system) in the face of daily postural challenges, which places them at an advantage to face orthostatic stress. With head-down-tilt bed rest, the stimulus to recruit compensatory mechanisms disappears, and differences between the two subgroups attenuate.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Orthostatic intolerance (OI) is a major problem after spaceflight. Its etiology remains uncertain, but reports have pointed toward an individual susceptibility to OI. We hypothesized that individual predisposition plays an important role in post-bed rest OI. Twenty-four healthy male subjects were equilibrated on a constant diet, after which they underwent tilt-stand test (pre-TST). They then completed 14-16 days of head-down-tilt bed rest, and 14 of the subjects underwent repeat tilt-stand test (post-TST). During various phases, the following were performed: 24-h urine collections and hormonal measurements, plethysmography, and cardiovascular system identification (a noninvasive method to assess autonomic function and separately quantify parasympathetic and sympathetic responsiveness). Development of presyncope or syncope defined OI. During pre-TST, 11 subjects were intolerant and 13 were tolerant. At baseline, intolerant subjects had lower serum aldosterone (P < 0.01), higher excretion of potassium (P = 0.01), lower leg venous compliance (P = 0.03), higher supine parasympathetic responsiveness (P = 0.02), and lower standing sympathetic responsiveness (P = 0.048). Of the 14 subjects who completed post-TST, 9 were intolerant and 5 were tolerant. Intolerant subjects had lower baseline serum cortisol (P = 0.03) and a higher sodium level (P = 0.02) compared with tolerant subjects. Thus several physiological characteristics were associated with increased susceptibility to OI. We propose a new model for OI, whereby individuals with greater leg venous compliance recruit compensatory mechanisms (activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, and withdrawal of the parasympathetic nervous system) in the face of daily postural challenges, which places them at an advantage to face orthostatic stress. With head-down-tilt bed rest, the stimulus to recruit compensatory mechanisms disappears, and differences between the two subgroups attenuate.
Grenon, S Marlene; Sheynberg, Natalie; Hurwitz, Shelley; Xiao, Grace; Ramsdell, Craig D; Ehrman, Michael D; Mai, C Lan; Kristjansson, Siri Rostoft; Sundby, Grete H; Cohen, Richard J; Williams, Gordon H
Renal, endocrine, and cardiovascular responses to bed rest in male subjects on a constant diet Journal Article
In: J Investig Med, vol. 52, no. 2, pp. 117–128, 2004, ISSN: 1081-5589.
@article{pmid15068228,
title = {Renal, endocrine, and cardiovascular responses to bed rest in male subjects on a constant diet},
author = {S Marlene Grenon and Natalie Sheynberg and Shelley Hurwitz and Grace Xiao and Craig D Ramsdell and Michael D Ehrman and C Lan Mai and Siri Rostoft Kristjansson and Grete H Sundby and Richard J Cohen and Gordon H Williams},
doi = {10.1136/jim-52-02-21},
issn = {1081-5589},
year = {2004},
date = {2004-03-01},
journal = {J Investig Med},
volume = {52},
number = {2},
pages = {117--128},
abstract = {BACKGROUND: Exposure to actual and simulated microgravity induces cardiovascular deconditioning through a variety of factors. Although the mechanisms involved remain uncertain, one involves alterations in volume-regulating systems--the hypothesis being tested in this study. To maximize our ability to detect subtle changes in the volume-regulating systems, subjects were studied on a high-average salt intake to maximally suppress these systems basally.
METHODS: Fourteen healthy male subjects underwent 14-day head-down tilt bed rest (HDTB) during which a constant 200 mEq sodium, 100 mEq potassium diet was maintained. Daily 24-hour urine collection was performed; plasma renin activity, serum aldosterone, plethysmography, and cardiovascular system identification were performed during a control period (pre-HDTB) and at the end of HDTB (end HDTB).
RESULTS: Sodium excretion increased initially (pre-HDTB = 182.8 +/- 10.4 mEq/total volume; early HDTB = 236.4 +/- 13.0; p = .002) and then returned to baseline values. Potassium excretion increased 4 days after the initiation of HDTB and remained elevated thereafter (pre-HDTB = 82.2 +/- 2.4/total volume; mid- to late HDTB = 89.4 +/- 2.1; p = .02). Plasma renin activity increased significantly with HDTB (pre-HDTB = 1.28 +/- 0.21 ng/mL/h; end HDTB = 1.69 +/- 0.18; p = .01), but serum aldosterone did not change. A significant decrease in autonomic responsiveness and an increase in leg compliance were observed.
CONCLUSIONS: We conclude that even in the presence of a high-average salt intake diet, simulated microgravity leads to renal, cardioendocrine, and cardiovascular system alterations that likely contribute to cardiovascular deconditioning.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
BACKGROUND: Exposure to actual and simulated microgravity induces cardiovascular deconditioning through a variety of factors. Although the mechanisms involved remain uncertain, one involves alterations in volume-regulating systems--the hypothesis being tested in this study. To maximize our ability to detect subtle changes in the volume-regulating systems, subjects were studied on a high-average salt intake to maximally suppress these systems basally.
METHODS: Fourteen healthy male subjects underwent 14-day head-down tilt bed rest (HDTB) during which a constant 200 mEq sodium, 100 mEq potassium diet was maintained. Daily 24-hour urine collection was performed; plasma renin activity, serum aldosterone, plethysmography, and cardiovascular system identification were performed during a control period (pre-HDTB) and at the end of HDTB (end HDTB).
RESULTS: Sodium excretion increased initially (pre-HDTB = 182.8 +/- 10.4 mEq/total volume; early HDTB = 236.4 +/- 13.0; p = .002) and then returned to baseline values. Potassium excretion increased 4 days after the initiation of HDTB and remained elevated thereafter (pre-HDTB = 82.2 +/- 2.4/total volume; mid- to late HDTB = 89.4 +/- 2.1; p = .02). Plasma renin activity increased significantly with HDTB (pre-HDTB = 1.28 +/- 0.21 ng/mL/h; end HDTB = 1.69 +/- 0.18; p = .01), but serum aldosterone did not change. A significant decrease in autonomic responsiveness and an increase in leg compliance were observed.
CONCLUSIONS: We conclude that even in the presence of a high-average salt intake diet, simulated microgravity leads to renal, cardioendocrine, and cardiovascular system alterations that likely contribute to cardiovascular deconditioning.
METHODS: Fourteen healthy male subjects underwent 14-day head-down tilt bed rest (HDTB) during which a constant 200 mEq sodium, 100 mEq potassium diet was maintained. Daily 24-hour urine collection was performed; plasma renin activity, serum aldosterone, plethysmography, and cardiovascular system identification were performed during a control period (pre-HDTB) and at the end of HDTB (end HDTB).
RESULTS: Sodium excretion increased initially (pre-HDTB = 182.8 +/- 10.4 mEq/total volume; early HDTB = 236.4 +/- 13.0; p = .002) and then returned to baseline values. Potassium excretion increased 4 days after the initiation of HDTB and remained elevated thereafter (pre-HDTB = 82.2 +/- 2.4/total volume; mid- to late HDTB = 89.4 +/- 2.1; p = .02). Plasma renin activity increased significantly with HDTB (pre-HDTB = 1.28 +/- 0.21 ng/mL/h; end HDTB = 1.69 +/- 0.18; p = .01), but serum aldosterone did not change. A significant decrease in autonomic responsiveness and an increase in leg compliance were observed.
CONCLUSIONS: We conclude that even in the presence of a high-average salt intake diet, simulated microgravity leads to renal, cardioendocrine, and cardiovascular system alterations that likely contribute to cardiovascular deconditioning.
Xiao, Xinshu; Mukkamala, Ramakrishna; Sheynberg, Natalie; Grenon, S Marlene; Ehrman, Michael D; Mullen, Thomas J; Ramsdell, Craig D; Williams, Gordon H; Cohen, Richard J
In: J Appl Physiol (1985), vol. 96, no. 2, pp. 489–497, 2004, ISSN: 8750-7587.
@article{pmid14514703,
title = {Effects of simulated microgravity on closed-loop cardiovascular regulation and orthostatic intolerance: analysis by means of system identification},
author = {Xinshu Xiao and Ramakrishna Mukkamala and Natalie Sheynberg and S Marlene Grenon and Michael D Ehrman and Thomas J Mullen and Craig D Ramsdell and Gordon H Williams and Richard J Cohen},
doi = {10.1152/japplphysiol.00602.2003},
issn = {8750-7587},
year = {2004},
date = {2004-02-01},
journal = {J Appl Physiol (1985)},
volume = {96},
number = {2},
pages = {489--497},
abstract = {Microgravity-induced orthostatic intolerance (OI) continues to be a primary concern for the human space program. To test the hypothesis that exposure to simulated microgravity significantly alters autonomic nervous control and, thus, contributes to increased incidence of OI, we employed the cardiovascular system identification (CSI) technique to evaluate quantitatively parasympathetic and sympathetic regulation of heart rate (HR). The CSI method analyzes second-to-second fluctuations in noninvasively measured HR, arterial blood pressure, and instantaneous lung volume. The coupling mechanisms between these signals are characterized by using a closed-loop model. Parameters reflecting parasympathetic and sympathetic responsiveness with regard to HR regulation can be extracted from the identified coupling mechanisms. We analyzed data collected from 29 human subjects before and after 16 days of head-down-tilt bed rest (simulated microgravity). Statistical analyses showed that parasympathetic and sympathetic responsiveness was impaired by bed rest. A lower sympathetic responsiveness and a higher parasympathetic responsiveness measured before bed rest identified individuals at greater risk of OI before and after bed rest. We propose an algorithm to predict OI after bed rest from measures obtained before bed rest.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Microgravity-induced orthostatic intolerance (OI) continues to be a primary concern for the human space program. To test the hypothesis that exposure to simulated microgravity significantly alters autonomic nervous control and, thus, contributes to increased incidence of OI, we employed the cardiovascular system identification (CSI) technique to evaluate quantitatively parasympathetic and sympathetic regulation of heart rate (HR). The CSI method analyzes second-to-second fluctuations in noninvasively measured HR, arterial blood pressure, and instantaneous lung volume. The coupling mechanisms between these signals are characterized by using a closed-loop model. Parameters reflecting parasympathetic and sympathetic responsiveness with regard to HR regulation can be extracted from the identified coupling mechanisms. We analyzed data collected from 29 human subjects before and after 16 days of head-down-tilt bed rest (simulated microgravity). Statistical analyses showed that parasympathetic and sympathetic responsiveness was impaired by bed rest. A lower sympathetic responsiveness and a higher parasympathetic responsiveness measured before bed rest identified individuals at greater risk of OI before and after bed rest. We propose an algorithm to predict OI after bed rest from measures obtained before bed rest.
2002
Xiao, Xinshu; Ozawa, Edwin T; Huang, Yaqi; Kamm, Roger D
Model-based assessment of cardiovascular health from noninvasive measurements Journal Article
In: Ann Biomed Eng, vol. 30, no. 5, pp. 612–623, 2002, ISSN: 0090-6964.
@article{pmid12108836,
title = {Model-based assessment of cardiovascular health from noninvasive measurements},
author = {Xinshu Xiao and Edwin T Ozawa and Yaqi Huang and Roger D Kamm},
doi = {10.1114/1.1484217},
issn = {0090-6964},
year = {2002},
date = {2002-05-01},
journal = {Ann Biomed Eng},
volume = {30},
number = {5},
pages = {612--623},
abstract = {Cardiovascular health is currently assessed through a variety of hemodynamic parameters, many of which can only be determined by invasive measurement often requiring hospitalization. A noninvasive method of evaluating several of these parameters such as systemic vascular resistance (SVR), maximum left ventricular elasticity (E(LV)), end diastolic volume (VED), and cardiac output, is presented. The method has three elements: (1) a distributed model of the human cardiovascular system (Ozawa et aL, Ann. Biomed. Eng. 29:284-297, 2001) to generate a solution library that spans the anticipated range of parameter values, (2) a method for establishing the multidimensional relationship between features computed from the arterial blood pressure and/or flow traces (e.g., mean arterial pressure, pulse amplitude, mean flow velocity) and the critical hemodynamic parameters, and (3) a parameter estimation method that yields the best fit between measured and computed data. Sensitivity analyses were used to determine the critical parameters, and the influence of fixed model parameters. Using computer-generated brachial pressure and velocity profiles (which can be measured noninvasively), the error associated with this method was found to be less than 3% for SVR, and less than 10% for E(LV) and V(ED). Simulations were also performed to test the ability of the approach to predict changes in SVR and E(LV) from an initial base line state.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Cardiovascular health is currently assessed through a variety of hemodynamic parameters, many of which can only be determined by invasive measurement often requiring hospitalization. A noninvasive method of evaluating several of these parameters such as systemic vascular resistance (SVR), maximum left ventricular elasticity (E(LV)), end diastolic volume (VED), and cardiac output, is presented. The method has three elements: (1) a distributed model of the human cardiovascular system (Ozawa et aL, Ann. Biomed. Eng. 29:284-297, 2001) to generate a solution library that spans the anticipated range of parameter values, (2) a method for establishing the multidimensional relationship between features computed from the arterial blood pressure and/or flow traces (e.g., mean arterial pressure, pulse amplitude, mean flow velocity) and the critical hemodynamic parameters, and (3) a parameter estimation method that yields the best fit between measured and computed data. Sensitivity analyses were used to determine the critical parameters, and the influence of fixed model parameters. Using computer-generated brachial pressure and velocity profiles (which can be measured noninvasively), the error associated with this method was found to be less than 3% for SVR, and less than 10% for E(LV) and V(ED). Simulations were also performed to test the ability of the approach to predict changes in SVR and E(LV) from an initial base line state.
Xiao, X; Mukkamala, R; Sheynberg, N; Williams, G H; Cohen, R J
Effects of prolonged bed rest on the total peripheral resistance baroreflex Journal Article
In: Comput Cardiol, vol. 29, pp. 53–56, 2002, ISSN: 0276-6574.
@article{pmid14686446,
title = {Effects of prolonged bed rest on the total peripheral resistance baroreflex},
author = {X Xiao and R Mukkamala and N Sheynberg and G H Williams and R J Cohen},
issn = {0276-6574},
year = {2002},
date = {2002-01-01},
journal = {Comput Cardiol},
volume = {29},
pages = {53--56},
abstract = {Orthostatic intolerance following prolonged exposure to microgravity continues to be a primary concern of the human space program. Reduced autonomic tone has been demonstrated to contribute to this phenomenon, and the heart rate baroreflex, in particular, has been repeatedly shown to be impaired. However, only the works of Yelle et al. have attempted to address the role of the total peripheral resistance (TPR) baroreflex, a potentially more significant contributor to blood pressure regulation. We applied a previously developed method for estimating the static gains of both the arterial and cardiopulmonary TPR baroreflexes to data obtained before and after 16-day bed rest. Reductions in the estimated static gains of the arterial (statistically significant) and cardiopulmonary TPR baroreflexes were found after bed rest. This study supports the works of Yelle et al, which imply that the TPR baroreflex is reduced after spaceflight.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Orthostatic intolerance following prolonged exposure to microgravity continues to be a primary concern of the human space program. Reduced autonomic tone has been demonstrated to contribute to this phenomenon, and the heart rate baroreflex, in particular, has been repeatedly shown to be impaired. However, only the works of Yelle et al. have attempted to address the role of the total peripheral resistance (TPR) baroreflex, a potentially more significant contributor to blood pressure regulation. We applied a previously developed method for estimating the static gains of both the arterial and cardiopulmonary TPR baroreflexes to data obtained before and after 16-day bed rest. Reductions in the estimated static gains of the arterial (statistically significant) and cardiopulmonary TPR baroreflexes were found after bed rest. This study supports the works of Yelle et al, which imply that the TPR baroreflex is reduced after spaceflight.
2001
Ozawa, E T; Bottom, K E; Xiao, X; Kamm, R D
Numerical simulation of enhanced external counterpulsation Journal Article
In: Ann Biomed Eng, vol. 29, no. 4, pp. 284–297, 2001, ISSN: 0090-6964.
@article{pmid11339326,
title = {Numerical simulation of enhanced external counterpulsation},
author = {E T Ozawa and K E Bottom and X Xiao and R D Kamm},
doi = {10.1114/1.1359448},
issn = {0090-6964},
year = {2001},
date = {2001-04-01},
journal = {Ann Biomed Eng},
volume = {29},
number = {4},
pages = {284--297},
abstract = {Enhanced external counterpulsation (EECP) is a noninvasive, counterpulsative method to provide temporary aid to the failing heart by sequentially inflating cuffs on the lower extremity out-of-phase with the left ventricle. Optimization of the method necessitates consideration of the hemodynamics created by EECP and the mode of action providing patient benefit. A computational model based on the governing one-dimensional equations is developed that simulates cardiovascular hemodynamics during EECP. The model includes a 30-element arterial system including the left ventricle, bifurcations, and peripheral arterial vessels. Effects of vessel collapse as external pressure is applied, arterial refilling on pressure release, changes in aortic pressure, and shear stress generated in the arteries are each investigated. Device parameters are systematically varied to determine their effect on system performance. Results show the potential for significant collapse and shear augmentation throughout the arteries of the lower extremity. Performance is strongly influenced by the mean level of external pressurization and the timing of cuff inflation, but less so by the relative timing and pressure differences between cuff segments.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Enhanced external counterpulsation (EECP) is a noninvasive, counterpulsative method to provide temporary aid to the failing heart by sequentially inflating cuffs on the lower extremity out-of-phase with the left ventricle. Optimization of the method necessitates consideration of the hemodynamics created by EECP and the mode of action providing patient benefit. A computational model based on the governing one-dimensional equations is developed that simulates cardiovascular hemodynamics during EECP. The model includes a 30-element arterial system including the left ventricle, bifurcations, and peripheral arterial vessels. Effects of vessel collapse as external pressure is applied, arterial refilling on pressure release, changes in aortic pressure, and shear stress generated in the arteries are each investigated. Device parameters are systematically varied to determine their effect on system performance. Results show the potential for significant collapse and shear augmentation throughout the arteries of the lower extremity. Performance is strongly influenced by the mean level of external pressurization and the timing of cuff inflation, but less so by the relative timing and pressure differences between cuff segments.
0000
Yamamoto, Ryo
dsRID: Editing-free in silico identification of dsRNA region using long-read RNA-seq data Journal Article
In: 0000.
@article{nokey,
title = {dsRID: Editing-free in silico identification of dsRNA region using long-read RNA-seq data},
author = {Ryo Yamamoto},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity Journal Article
In: 0000.
@article{nokey,
title = {LINE-associated cryptic splicing induces dsRNA-mediated interferon response and tumor immunity},
keywords = {},
pubstate = {published},
tppubtype = {article}
}