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  • American Physiological Society  (36)
  • 1
    Online-Ressource
    Online-Ressource
    WISE-2005: Countermeasures to prevent muscle deconditioning during bed rest in women
    American Physiological Society ; 2014
    In:  Journal of Applied Physiology Vol. 116, No. 6 ( 2014-03-15), p. 654-667
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 116, No. 6 ( 2014-03-15), p. 654-667
    Kurzfassung: The objectives of this study were to evaluate the efficacy of two separate countermeasures, exercise and protein supplementation, to prevent muscle strength and lean tissue mass losses during 60 days of bed rest (BR) in women and whether countermeasure efficacy was influenced by pre-BR muscular fitness (strength, endurance, tissue mass). Twenty-four women were assigned to an exercise (EX, n = 8), a no-exercise control (CON, n = 8), or a no-exercise protein supplementation group (PROT, n = 8). EX performed supine treadmill exercise within lower body negative pressure 3–4 days/wk and maximal concentric and eccentric supine leg- and calf-press exercises 2–4 days/wk. PROT consumed a diet with elevated protein content compared with CON and EX (1.6 vs. 1.0 g·kg −1 ·day −1 ). Knee and calf isokinetic strength and endurance, isotonic leg-press strength, and leg lean mass were measured before and after BR. Post-BR knee extensor strength and endurance, ankle strength, and leg lean mass were significantly greater and leg-press strength tended to be higher in EX than in CON and PROT. Post-BR measures in PROT were not different than those in CON. Exercise countermeasure efficacy was less, and strength, endurance, and leg lean mass losses in CON and PROT were greater, in subjects who were more fit pre-BR. An exercise protocol combining resistive and aerobic exercise training protects against losses in strength, endurance, and leg lean mass in women during BR, while a nutritional countermeasure without exercise was not effective. Exercise countermeasures may require individualization to protect higher levels of strength and endurance.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00590.2013
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2014
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    The effect of increased lung volume in chronic obstructive pulmonary disease on upper airway obstruction during sleep
    American Physiological Society ; 2015
    In:  Journal of Applied Physiology Vol. 119, No. 3 ( 2015-08-01), p. 266-271
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 119, No. 3 ( 2015-08-01), p. 266-271
    Kurzfassung: Patients with chronic obstructive pulmonary disease (COPD) exhibit increases in lung volume due to expiratory airflow limitation. Increases in lung volumes may affect upper airway patency and compensatory responses to inspiratory flow limitation (IFL) during sleep. We hypothesized that COPD patients have less collapsible airways inversely proportional to their lung volumes, and that the presence of expiratory airflow limitation limits duty cycle responses to defend ventilation in the presence of IFL. We enrolled 18 COPD patients and 18 controls, matched by age, body mass index, sex, and obstructive sleep apnea disease severity. Sleep studies, including quantitative assessment of airflow at various nasal pressure levels, were conducted to determine upper airway mechanical properties [passive critical closing pressure (Pcrit)] and for quantifying respiratory timing responses to experimentally induced IFL. COPD patients had lower passive Pcrit than their matched controls (COPD: −2.8 ± 0.9 cmH 2 O; controls: −0.5 ± 0.5 cmH 2 O, P = 0.03), and there was an inverse relationship of subject's functional residual capacity and passive Pcrit (−1.7 cmH 2 O/l increase in functional residual capacity, r 2 = 0.27, P = 0.002). In response to IFL, inspiratory duty cycle increased more ( P = 0.03) in COPD patients (0.40 to 0.54) than in controls (0.41 to 0.51) and led to a marked reduction in expiratory time from 2.5 to 1.5 s ( P 〈 0.01). COPD patients have a less collapsible airway and a greater, not reduced, compensatory timing response during upper airway obstruction. While these timing responses may reduce hypoventilation, it may also increase the risk for developing dynamic hyperinflation due to a marked reduction in expiratory time.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00455.2014
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2015
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Online-Ressource
    Online-Ressource
    Effect of alae nasi activation on maximal nasal inspiratory airflow in humans
    American Physiological Society ; 1998
    In:  Journal of Applied Physiology Vol. 84, No. 6 ( 1998-06-01), p. 2115-2122
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 84, No. 6 ( 1998-06-01), p. 2115-2122
    Kurzfassung: The upper airway is a complicated structure that is usually widely patent during inspiration. However, on inspiration during certain physiological and pathophysiological states, the nares, pharynx, and larynx may collapse. Collapse at these locations occurs when the transmural pressure (Ptm) at a flow-limiting site (FLS) falls below a critical level (Ptm′). On airway collapse, inspiratory airflow is limited to a maximal level (V˙i max ) determined by (−Ptm′)/Rus, where Rus is the resistance upstream to the FLS. The airflow dynamics of the upper airway are affected by the activity of its associated muscles. In this study, we examine the modulation ofV˙i max by muscle activity in the nasal airway under conditions of inspiratory airflow limitation. Each of six subjects performed sniffs through one patent nostril (pretreated with an alpha agonist) while flaring the nostril at varying levels of dilator muscle (alae nasi) EMG activity (EMGan). For each sniff, we located the nasal FLS with an airway catheter and determinedV˙i max , Ptm′, and Rus. Activation of the alae nasi from the lowest to the highest values of EMGan increasedV˙i max from 422 ± 156 to 753 ± 291 ml/s ( P 〈 0.01) and decreased Ptm′ from −3.6 ± 3.0 to −6.0 ± 4.7 cmH 2 O ( P 〈 0.05). Activation of the alae nasi had no consistent effect on Rus.V˙i max was positively correlated with EMGan, and Ptm′ was negatively correlated with EMGan in all subjects. Our findings demonstrate that alae nasi activation increasesV˙i max through the nasal airway by decreasing airway collapsibility.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1998.84.6.2115
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1998
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    Online-Ressource
    Chronic intermittent hypoxia upregulates genes of lipid biosynthesis in obese mice
    American Physiological Society ; 2005
    In:  Journal of Applied Physiology Vol. 99, No. 5 ( 2005-11), p. 1643-1648
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 99, No. 5 ( 2005-11), p. 1643-1648
    Kurzfassung: Obstructive sleep apnea (OSA), a condition tightly linked to obesity, leads to chronic intermittent hypoxia (CIH) during sleep. There is emerging evidence that OSA is independently associated with insulin resistance and fatty liver disease, suggesting that OSA may affect hepatic lipid metabolism. To test this hypothesis, leptin-deficient obese ( ob/ob) mice were exposed to CIH during the light phase (9 AM–9 PM) for 12 wk. Liver lipid content and gene expression profile in the liver (Affymetrix 430 GeneChip with real-time PCR validation) were determined on completion of the exposure. CIH caused a 30% increase in triglyceride and phospholipid liver content ( P 〈 0.05), whereas liver cholesterol content was unchanged. Gene expression analysis showed that CIH upregulated multiple genes controlling 1) cholesterol and fatty acid biosynthesis [malic enzyme and acetyl coenzyme A (CoA) synthetase], 2) predominantly fatty acid biosynthesis (acetyl-CoA carboxylase and stearoyl-CoA desaturases 1 and 2), and 3) triglyceride and phospholipid biosynthesis (mitochondrial glycerol-3-phosphate acyltransferase). A majority of overexpressed genes were transcriptionally regulated by sterol regulatory element-binding protein (SREBP) 1, a master regulator of lipogenesis. A 2.8-fold increase in SREBP-1 gene expression in CIH was confirmed by real-time PCR ( P = 0.001). Expression of major genes of cholesterol biosynthesis, SREBP-2 and 3-hydroxy-3-methylglutaryl-CoA reductase, was unchanged. In conclusion, we have shown that CIH may exacerbate preexisting fatty liver of obesity via upregulation of the pathways of lipid biosynthesis in the liver.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00522.2005
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2005
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Dynamic modulation of upper airway function during sleep: a novel single-breath method
    American Physiological Society ; 2006
    In:  Journal of Applied Physiology Vol. 101, No. 5 ( 2006-11), p. 1489-1494
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 101, No. 5 ( 2006-11), p. 1489-1494
    Kurzfassung: To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18–50 yr; 20–35 kg/m 2 ; apnea-hypopnea index 〉 20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 ± 2.0 cmH 2 O) was significantly lower than the opening pressure (10.8 ± 2.4 cmH 2 O). Rus was higher for deflation (18.1 ± 2.4 cmH 2 O·l −1 ·s) than during inflation (7.5 ± 1.9 cmH 2 O·l −1 ·s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by ∼4 cmH 2 O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00173.2006
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2006
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Neuromechanical control of the isolated upper airway of mice
    American Physiological Society ; 2008
    In:  Journal of Applied Physiology Vol. 105, No. 4 ( 2008-10), p. 1237-1245
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 105, No. 4 ( 2008-10), p. 1237-1245
    Kurzfassung: We characterized the passive structural and active neuromuscular control of pharyngeal collapsibility in mice and hypothesized that pharyngeal collapsibility, which is elevated by anatomic loads, is reduced by active neuromuscular responses to airflow obstruction. To address this hypothesis, we examined the dynamic control of upper airway function in the isolated upper airway of anesthetized C57BL/6J mice. Pressures were lowered downstream and upstream to the upper airway to induce inspiratory airflow limitation and critical closure of the upper airway, respectively. After hyperventilating the mice to central apnea, we demonstrated a critical closing pressure (Pcrit) of −6.2 ± 1.1 cmH 2 O under passive conditions that was unaltered by the state of lung inflation. After a period of central apnea, lower airway occlusion led to progressive increases in phasic genioglossal electromyographic activity (EMG GG ), and in maximal inspiratory airflow (V̇i max ) through the isolated upper airway, particularly as the nasal pressure was lowered toward the passive Pcrit level. Moreover, the active Pcrit fell during inspiration by 8.2 ± 1.4 cmH 2 O relative to the passive condition ( P 〈 0.0005). We conclude that upper airway collapsibility (passive Pcrit) in the C57BL/6J mouse is similar to that in the anesthetized canine, feline, and sleeping human upper airway, and that collapsibility falls markedly under active conditions. Active EMG GG and V̇i max responses dissociated at higher upstream pressure levels, suggesting a decrease in the mechanical efficiency of upper airway dilators. Our findings in mice imply that anatomic and neuromuscular factors interact dynamically to modulate upper airway function, and provide a novel approach to modeling the impact of genetic and environmental factors in inbred murine strains.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.90461.2008
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2008
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    Effect of age and weight on upper airway function in a mouse model
    American Physiological Society ; 2011
    In:  Journal of Applied Physiology Vol. 111, No. 3 ( 2011-09), p. 696-703
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 111, No. 3 ( 2011-09), p. 696-703
    Kurzfassung: Defects in pharyngeal mechanical and neuromuscular control are required for the development of obstructive sleep apnea. Obesity and age are known sleep apnea risk factors, leading us to hypothesize that specific defects in upper airway neuromechanical control are associated with weight and age in a mouse model. In anesthetized, spontaneously breathing young and old wild-type C57BL/6J mice, genioglossus electromyographic activity (EMG GG ) was monitored and upper airway pressure-flow dynamics were characterized during ramp decreases in nasal pressure (Pn, cmH 2 O). Specific body weights were targeted by controlling caloric intake. The passive critical pressure (Pcrit) was derived from pressure-flow relationships during expiration. The Pn threshold at which inspiratory flow limitation (IFL) developed and tonic and phasic EMG GG activity during IFL were quantified to assess the phasic modulation of pharyngeal patency. The passive Pcrit increased progressively with increasing body weight and increased more in the old than young mice. Tonic EMG GG decreased and phasic EMG GG increased significantly with obesity. During ramp decreases in Pn, IFL developed at a higher (less negative) Pn threshold in the obese than lean mice, although the frequency of IFL decreased with age and weight. The findings suggest that weight imposes mechanical loads on the upper airway that are greater in the old than young mice. The susceptibility to upper airway obstruction increases with age and weight as tonic neuromuscular activity falls. IFL can elicit phasic responses in normal mice that mitigate or eliminate the obstruction altogether.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00123.2011
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2011
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    Online-Ressource
    Endothelium-derived GM-CSF influences expression of oncostatin M
    American Physiological Society ; 2011
    In:  American Journal of Physiology-Cell Physiology Vol. 301, No. 4 ( 2011-10), p. C947-C953
    Details
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 301, No. 4 ( 2011-10), p. C947-C953
    Kurzfassung: During and after transendothelial migration, neutrophils undergo a number of phenotypic changes resulting from encounters with endothelium-derived factors. This report uses an in vitro model with human umbilical vein endothelial cells and isolated human neutrophils to examine the effects of two locally derived cytokines, granulocyte (G)-macrophage (M) colony-stimulating factor (GM-CSF) and G-CSF, on oncostatin M (OSM) expression. Neutrophils contacting activated HUVEC expressed and released increased amounts of oncostatin M (OSM), a proinflammatory cytokine known to induce polymorphonuclear neutrophil adhesion and chemotaxis. Neutrophil transendothelial migration resulted in threefold higher OSM expression and protein levels compared with nontransmigrated cells. Addition of anti-GM-CSF neutralizing antibody reduced OSM expression level but anti-G-CSF was without effect. GM-CSF but not G-CSF protein addition to cultures of isolated neutrophils resulted in a significant increase in OSM protein secretion. However, inhibition of β 2 integrins by neutralizing antibody significantly reduced GM-CSF-induced OSM production indicating this phenomenon is adhesion dependent. Thus cytokine-stimulated endothelial cells can produce sufficient quantities of GM-CSF to influence in an adhesion-dependent manner, the phenotypic characteristics of neutrophils resulting in the latter's transmigration. Both transmigration and adhesion phenomenon lead to increased production of OSM by neutrophils that then play a major role in inflammatory response.
    Materialart: Online-Ressource
    ISSN: 0363-6143 , 1522-1563
    URL: Article
    DOI: 10.1152/ajpcell.00205.2011
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2011
    ZDB Id: 1477334-X
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    Online-Ressource
    Electrical stimulation of the hypoglossal nerve: a potential therapy
    American Physiological Society ; 2014
    In:  Journal of Applied Physiology Vol. 116, No. 3 ( 2014-02-01), p. 337-344
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 116, No. 3 ( 2014-02-01), p. 337-344
    Kurzfassung: Obstructive sleep apnea is characterized by recurrent episodes of pharyngeal collapse, which result from a decrease in pharyngeal dilator muscle tone. The genioglossus is a major pharyngeal dilator that maintains airway patency during sleep. Early studies in animal and humans have demonstrated that electrical stimulation of this muscle reduces pharyngeal collapsibility, increases airflow, and mitigates obstructive sleep apnea. These findings impelled the development of fully implantable hypoglossal nerve stimulating systems (HGNS), for which feasibility trial results are now available. These pilot studies have confirmed that hypoglossal nerve stimulation can prevent pharyngeal collapse without arousing patients from sleep. Potentially, a substantial segment of the patient population with obstructive sleep apnea can be treated with this novel approach. Furthermore, the feasibility trial findings suggest that the therapeutic potential of HGNS can be optimized by selecting patients judiciously, titrating the stimulus intensity optimally, and characterizing the underlying function and anatomy of the pharynx. These strategies are currently being examined in ongoing pivotal trials of HGNS.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00423.2013
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2014
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 10
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    Online-Ressource
    Leptin and the control of pharyngeal patency during sleep in severe obesity
    American Physiological Society ; 2014
    In:  Journal of Applied Physiology Vol. 116, No. 10 ( 2014-05-15), p. 1334-1341
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 116, No. 10 ( 2014-05-15), p. 1334-1341
    Kurzfassung: Rationale: Obesity imposes mechanical loads on the upper airway, resulting in flow limitation and obstructive sleep apnea (OSA). In previous animal models, leptin has been considered to serve as a stimulant of ventilation and may prevent respiratory depression during sleep. We hypothesized that variations in leptin concentration among similarly obese individuals will predict differences in compensatory responses to upper airway obstruction during sleep. Methods: An observational study was conducted in 23 obese women [body mass index (BMI): 46 ± 3 kg/m 2 , age: 41 ± 12 yr] and 3 obese men (BMI: 46 ± 3 kg/m 2 , age: 43 ± 4 yr). Subjects who were candidates for bariatric surgery were recruited to determine upper airway collapsibility under hypotonic conditions [pharyngeal critical pressure (passive P CRIT )], active neuromuscular responses to upper airway obstruction during sleep, and overnight fasting serum leptin levels. Compensatory responses were defined as the differences in peak inspiratory airflow (ΔV I max), inspired minute ventilation (ΔV I ), and pharyngeal critical pressure (ΔP CRIT ) between the active and passive conditions. Results: Leptin concentration was not associated with sleep disordered breathing severity, passive P CRIT , or baseline ventilation. In the women, increases in serum leptin concentrations were significantly associated with increases in ΔV I max ( r 2 = 0.44, P 〈 0.001), ΔV I ( r 2 = 0.40, P 〈 0.001), and ΔP CRIT ( r 2 = 0.19, P 〈 0.04). These responses were independent of BMI, waist-to-hip ratio, neck circumference, or sagittal girth. Conclusion: Leptin may augment neural compensatory mechanisms in response to upper airway obstruction, minimizing upper airway collapse, and/or mitigating potential OSA severity. Variability in leptin concentration among similarly obese individuals may contribute to differences in OSA susceptibility.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00958.2013
    RVK:
    WA 15000
    RVK:
    XA 52094
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2014
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
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