Does the balance strategy during walking in elderly persons show an association with fall risk assessment?

The primary objective of this study was to clarify whether balance evaluation during walking in elderly people was related to fall risk assessment; the second objective was to clarify the difference in balance strategy between young and elderly people based on the balance evaluation through a gait cycle. Thirty healthy young adults and 25 healthy elderly adults participated. All participants performed walking at their preferred speed and at a fast speed. Based on the margin of stability (MoS), balance during a gait cycle was divided into medial/lateral and anterior/posterior direction (ML/AP-MoS). Positive/negative integral values of ML-MoS were defined as ML-MoSPOS/ML-MoSNEG, and the average of AP-MoS over the gait cycle was defined as AP-MoSmean. The fast/preferred ratio of AP-MoSmean/ML-MoSPOS (AP-MoSmean (Fast/Preferred)/ML-MoSPOS (Fast/Preferred)) and the fast-preferred difference of ML-MoSNEG (ML-MoSNEG (Fast-Preferred)) were compared between groups. ML/AP-MoS at the preferred/fast gait was also compared between 12 gait events and groups. The Japanese version of the Mini-Balance Evaluation Systems Test (J-Mini-BESTest), the Japanese version of the Activities-specific Balance Confidence Scale (J-ABC scale), and the number of falls in the past year were obtained from all subjects. ML-MoSPOS (Fast/Preferred), ML-MoSNEG (Fast-Preferred), and AP-MoSmean (Fast/Preferred) were significantly correlated with J-Mini-BESTest. Gait balance evaluation based on MoS may reflect an individual's balance function. In fast gait, ML-MoS at foot flat and toe off and AP-MoS at just before heel strike were highly likely to be gait events to identify elderly adults with balance disorders.

Investigation of balance strategy over gait cycle based on margin of stability.

This study was conducted to investigate the balance strategy of healthy young adults through a gait cycle using the margin of stability (MoS). Thirty healthy young adults participated in this study. Each performed walking five times at a preferred speed and at a fast speed. The MoS was calculated over a gait cycle by defining the base of support (BoS) changes during a gait cycle. The MoS was divided into medial/lateral and anterior/posterior components (ML MoS and AP MoS). The central values and the values at 12 gait events of the MoS were compared. Positive/negative integration of ML MoS (ML MoSPOS and ML MoSNEG, respectively) and the average ML/AP MoS over a cycle (ML/AP MoSmean) were significantly lower at a fast gait than at a preferred gait. ML/AP MoS were lower at a fast speed than at the preferred speed, except for the ML MoS immediately before left heel strike (pre left HS) and right and left heel strike (HS). ML/AP MoS were significantly lower immediately before heel strike (pre-HS) than in other gait events, regardless of walking speed. It was suggested that pre-HS is the most unstable moment in both ML/AP directions and a crucial moment in control of gait stability. The results presented above might be applicable as basic data regarding dynamic stability of healthy young adults through a gait cycle for comparisons with elderly people and patients with orthopedic disorders or neurological disorders.

Differential inotropic effects of endothelin-1, angiotensin II, and phenylephrine induced by crosstalk with cAMP-mediated signaling process in dog ventricular myocardium.

Endothelin-1 (ET-1), angiotensin II (Ang II), and phenylephrine, an alpha1-adrenoceptor agonist, share the common signaling process, resulting in activation of Gq protein-coupled receptor (GqPCR) to activate the hydrolysis of phosphoinositide (PI). They do not elicit any inotropic effect in isolated dog ventricular muscle. In the presence of forskolin or IBMX (3-isobutyl-1-methylxanthine), ET-1 produced a dual effect, that is, a positive inotropic effect (PIE) and/or a negative inotropic effect (NIE) depending on concentrations of forskolin or IBMX present simultaneously with ET-1. Phenylephrine produced a definite PIE and Ang II induced a small and transient PIE in the presence of forskolin or IBMX, but they did not elicit a NIE. Facilitation of Ca2+ influx via L-type Ca2+ channel may play a crucial role in the crosstalk because GqPCR agonists produced, likewise a PIE in the presence of Bay k 8644. GqPCR agonists failed to induce a PIE in the presence of dihydroouabain or elevated [Ca2+]o. These findings indicate that the accumulation of cAMP or activation of L-type Ca2+ channels markedly modulates the inotropic response to GqPCR agonists in a manner that leads to a PIE in dog ventricular myocardium. In addition, ET-1, but not Ang II or phenylephrine, activates the signal transduction process that results in a NIE.

Differential inhibition by TAK-044 of the inotropic effects of endothelin-1 and endothelin-3.

The influence of a nonselective antagonist of endothelin receptors, TAK-044 (cyclo-[d-alpha-aspartyl-3-[(4-phenylpiperazin-1-yl)carbonyl]-l-alanyl-l-alpha-aspartyl-d-2-(2-thienyl)glycyl-l-leucyl-d-tryptophyl] disodium), on the positive inotropic effect of endothelin-1 and endothelin-3 was investigated in isolated rabbit myocardium. While TAK-044 produced a concentration-dependent rightward shift of the concentration-response curve for endothelin-1 and endothelin-3, the effect of endothelin-3 was hundred times more sensitive to TAK-044 than that of endothelin-1. The combination of FR139317 ([2-(R)-[2(R)-[2(S)-[[1-(hexahydro-1H-azepinyl)]carbonyl]amino-4-methylpentanoyl]amino-3-[3-(1-methyl-1H-indolyl)]propionyl] amino-3-(2-pyridyl)propionic acid]) and BQ-788 (N-cis-2,6-dimethylpiperidinocarbonyl-l-gamma-methylleucyl-d-1-methoxycarbonyltryptophanyl-d-norleucine) mimicked the inhibitory action of TAK-044 on the positive inotropic effect of endothelin-3 but enhanced the effect of endothelin-1. In a receptor-binding assay, TAK-044 was four times more potent in antagonizing the specific binding of endothelin-1 than that of endothelin-3. Endothelin-1 may activate receptor subtypes that trigger both positive and negative inotropic effects, the latter being more susceptible to the antagonistic action of TAK-044, which may explain in part the differential antagonistic action of TAK-044 on the inotropic effect of endothelin-1 and endothelin-3.