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C H Luo

Publications and source records attributed to C H Luo.

10 recordsLinked to original sources
PubMed1997

A Morse-code recognition system with LMS and matching algorithms for persons with disabilities.

Single-switch communication is an effective auxiliary method for persons with disabilities. However, it is not easy to recognize the Morse codes typed by them. In our earlier proposed Morse code auto-recognition method, using the Least-Mean-Square (LMS) adaptive algorithm, it was demonstrated that the system could successfully recognize the Morse-coded messages at unstable typing speeds. However, the speed variation had to be limited to a range between 0.67 and two times the present speed. In the case of beginners or those with heavy disabilities, this rule can not always be complied with, producing a low recognition rate of 20%. To address this limitation, this paper offers an advanced recognition method which combines the Least-Mean-Square algorithm with a character-by-character matching technique. The recognition rate for this method from simulated and real data from various sources is as high as 75% or more on average. This practical application of the single-switch method means a step forward toward alternative communication for disabled persons.

Algorithms↗
PubMed1996

Adaptive Morse-coded single-switch communication system for the disabled.

Automatic recognition of Morse-code is generally developed at a fixed typing rate. However, this is not suitable for the disabled due to their difficulty in maintaining a stable typing rate. In this paper, a system recognizing varying typing speeds is developed using an adaptive technique, the Least-Mean Square (LMS) algorithm. This system helps the disabled have a wide latitude and varying typing speeds in single-switch communication with the Morse-code.

Abbreviations as Topic↗
PubMed1994

A dynamic model of the cardiac ventricular action potential. I. Simulations of ionic currents and concentration changes.

A mathematical model of the cardiac ventricular action potential is presented. In our previous work, the membrane Na+ current and K+ currents were formulated. The present article focuses on processes that regulate intracellular Ca2+ and depend on its concentration. The model presented here for the mammalian ventricular action potential is based mostly on the guinea pig ventricular cell. However, it provides the framework for modeling other types of ventricular cells with appropriate modifications made to account for species differences. The following processes are formulated: Ca2+ current through the L-type channel (ICa), the Na(+)-Ca2+ exchanger, Ca2+ release and uptake by the sarcoplasmic reticulum (SR), buffering of Ca2+ in the SR and in the myoplasm, a Ca2+ pump in the sarcolemma, the Na(+)-K+ pump, and a nonspecific Ca(2+)-activated membrane current. Activation of ICa is an order of magnitude faster than in previous models. Inactivation of ICa depends on both the membrane voltage and [Ca2+]i. SR is divided into two subcompartments, a network SR (NSR) and a junctional SR (JSR). Functionally, Ca2+ enters the NSR and translocates to the JSR following a monoexponential function. Release of Ca2+ occurs at JSR and can be triggered by two different mechanisms, Ca(2+)-induced Ca2+ release and spontaneous release. The model provides the basis for the study of arrhythmogenic activity of the single myocyte including afterdepolarizations and triggered activity. It can simulate cellular responses under different degrees of Ca2+ overload. Such simulations are presented in our accompanying article in this issue of Circulation Research.

Action Potentials↗
PubMed1994

A dynamic model of the cardiac ventricular action potential. II. Afterdepolarizations, triggered activity, and potentiation.

The action potential model presented in our accompanying article in this journal is used to investigate phenomena that involve dynamic changes of [Ca2+]i, as described below. Delayed afterdepolarizations (DADs) are induced by spontaneous Ca2+ release from the sarcoplasmic reticulum (SR), which, in turn, activates both the Na(+)-Ca2+ exchanger (INaCa) and a nonspecific Ca(2+)-activated current (Ins(Ca)). The relative contributions of INaCa and of Ins(Ca) to the generation of DADs are different under different degrees of Ca2+ overload. Early afterdepolarizations (EADs) can be categorized into two types: (1) plateau EADs, resulting from a secondary activation of the L-type Ca2+ current during the plateau of an action potential, and (2) phase-3 EADs, resulting from activation of INaCa and Ins(Ca) by increased [Ca2+]i due to spontaneous Ca2+ release from the SR during the late repolarization phase. Spontaneous rhythmic activity and triggered activity are caused by spontaneous Ca2+ release from the SR under conditions of Ca2+ overload. Postextrasystolic potentiation reflects the time delay associated with translocation of Ca2+ from network SR to junctional SR. The cell is paced at high frequencies to investigate the long-term effects on the intracellular ionic concentrations.

Action Potentials↗
PubMed1993

Cellular responses to electrical stimulation: a study using a model of the ventricular cardiac action potential.

A mathematical model of the membrane action potential of a ventricular cardiac cell is used to examine the cellular responses to premature stimulation. Results demonstrate the importance of the slow recovery of INa in determining the response of the cell. Simulated responses to periodic stimulation include monotonic Wenckebach patterns and alternans in APD at normal [K]O. At low [K]O, nonmonotonic Wenckebach periodicities, aperiodic patterns, and enhanced supernormal excitability that results in unstable responses ("chaotic activity") are observed. These observations are consistent with recent experimental results, and the simulations provide insights into the underlying mechanisms at the level of membrane ionic channel kinetics.

Action Potentials↗
PubMed1991

Null-balance transducer for isometric force measurements and length control of single heart cells.

Recently, an ultrasensitive, optical-fiber-based force transducer was developed to measure the microscopic force of contraction of single heart cells. Since force in cardiac muscle is length and velocity dependent, it is desirable to maintain a constant (isometric) cell length. The original design permits approximately 1% shortening of cell length to occur during twitch contractions. The shortening can be reduced significantly by adding a piezoelectric bimorph actuator and closed-loop control, as described in this paper. As a result, the effective stiffness of the transducer can be increased by a factor of about 100, and cell shortening reduced to approximately 0.01%. For the force probes typically used, this is equivalent to a movement of less than 20 nm for a typical value of 100 nN peak cell force in single frog ventricular cells. The gain in stiffness is obtained without sacrificing sensitivity, although at the expense of frequency response. The new design also permits control of cell length and is applicable to studies of the mechanical stiffness of cardiac cells.

Animals↗
PubMed1991

A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction.

A mathematical model of the membrane action potential of the mammalian ventricular cell is introduced. The model is based, whenever possible, on recent single-cell and single-channel data and incorporates the possibility of changing extracellular potassium concentration [K]o. The fast sodium current, INa, is characterized by fast upstroke velocity (Vmax = 400 V/sec) and slow recovery from inactivation. The time-independent potassium current, IK1, includes a negative-slope phase and displays significant crossover phenomenon as [K]o is varied. The time-dependent potassium current, IK, shows only a minimal degree of crossover. A novel potassium current that activates at plateau potentials is included in the model. The simulated action potential duplicates the experimentally observed effects of changes in [K]o on action potential duration and rest potential. Physiological simulations focus on the interaction between depolarization and repolarization (i.e., premature stimulation). Results demonstrate the importance of the slow recovery of INa in determining the response of the cell. Simulated responses to periodic stimulation include monotonic Wenckebach patterns and alternans at normal [K]o, whereas at low [K]o nonmonotonic Wenckebach periodicities, aperiodic patterns, and enhanced supernormal excitability that results in unstable responses ("chaotic activity") are observed. The results are consistent with recent experimental observations, and the model simulations relate these phenomena to the underlying ionic channel kinetics.

Action Potentials↗
PubMed1989

[Influence of zinc deprivation on thymus, spleen development and adenosine deaminase activity in young rats].

This study on the thymus and spleen development and ADA activity was done in young rats with zinc deprivation and supplementation. The serum zinc level, body weight, absolute and relative weight, and ADA activity of the thymus and spleen were compared between the experimental rats and the control group. Above indications were all decreased; especially both the thymus weight and the thymus ADA activity were markedly decreased in the zinc deficient group. The averages of thymic absolute weight, relative weight and ADA activity were dropped by 61.32%, 54.54% and 47.59%, respectively. After zinc supplementation for one month, all the body weight, weight of the thymus and spleen, and ADA activity of the spleen were recovered to the control group's level, while ADA activity of the thymus was 33.03% higher than that of the control group. Our data suggested that zinc was not only an important trace element in maintaining the growth of the body, the development of the thymus and spleen, but it may be an important agent to activate the ADA or to prompt synthesis of ADA.

Adenosine Deaminase↗