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Biomedical subjects

D C Lin

Publications and source records attributed to D C Lin.

At least 19 recordsLinked to original sources
PubMed2006

Scaling and organization of electroencephalographic background activity and alpha rhythm in healthy young adults.

The coexistence of the broad-band fluctuation and alpha rhythm of the brain dynamics is studied based on the zero-crossing property of the local electroencephalographic (EEG) recording in eyes closed and eyes open. A two-component zero-crossing scenario, consisting of a broad-band fractal and narrow-band rhythm components, is assumed. Scaling is found in the power law distribution p(tau) approximately tau(-nu) of the crossing time interval tau of the broad-band fluctuation. In alpha dominant brain state, the alpha rhythm interval L also exhibits scaling in the form of power law distribution: p(L) approximately L(phi). Our main result is the relationship nu + phi approximately 3 that characterizes the organization of these two prominent features of the brain dynamics. The possible role of self-organized criticality of punctuated equilibrium in this organization is discussed.

Adult↗
PubMed2004

Hierarchical structure in healthy and diseased human heart rate variability.

It is shown that the healthy and diseased human heart rate variability (HRV) possesses a hierarchical structure of the She-Leveque (SL) form. This structure, first found in measurements in turbulent fluid flows, implies further details in the HRV multifractal scaling. The potential of diagnosis is also discussed based on the characteristics derived from the SL hierarchy.

Biophysical Phenomena↗
PubMed2003

Robustness and perturbation in the modeled cascade heart rate variability.

In this study, numerical experiments are conducted to examine the robustness of using cascade to describe the multifractal heart rate variability (HRV) by perturbing the hierarchical time scale structure and the multiplicative rule of the cascade. It is shown that a rigid structure of the multiple time scales is not essential for the multifractal scaling in healthy HRV. So long as there exists a tree structure for the multiplication to take place, a multifractal HRV and related properties can be captured by using the cascade. But the perturbation of the multiplicative rule can lead to a qualitative change. In particular, a multifractal to monofractal HRV transition can result after the product law is perturbed to an additive one at the fast time scale. We suggest that this explains the similar HRV scaling transition in the parasympathetic nervous system blockade.

Animals↗
PubMed2002

Acute thoracolumbar burst fractures: a new view of loading mechanisms.

STUDY DESIGN: An in vitro investigation of loading mechanisms in acute thoracolumbar burst fractures. OBJECTIVES: To assess the validity of the authors' hypothesis that anterior shear forces transmitted by the facet joints are responsible for causing the severe canal compromise associated with acute thoracolumbar burst fractures. SUMMARY OF BACKGROUND DATA: Thoracolumbar burst fractures created in the laboratory rarely match the severity of clinical cases. To date, no studies have examined in great detail the role of facet joint loading in the burst-fracture mechanism. An incomplete understanding of loading mechanisms may contribute to the controversies regarding management. METHODS: Nine human cadaveric motion segments were instrumented with strain gages and subjected to axial compression or axial impact coupled with an extension moment. Failure loads, strain information, and radiographs were collected. RESULTS: Fracture patterns characteristic of acute thoracolumbar burst fractures were observed in the three specimens tested with an extension moment. In this group, high strains were also recorded at the bases of the pedicles, indicating a probable site of fracture initiation. Specimens tested in a neutral orientation experienced crush fractures without an increase in interpedicular distance. Strain patterns were more uniform in this group. CONCLUSIONS: The severity and clinical relevance of the injuries sustained by the specimens tested in extension suggest that facet joint loading plays a critical role in the acute thoracolumbar burst-fracture loading mechanism. Fracture patterns and strain concentrations are in agreement with clinical observations as well as past experimental studies.

Acute Disease↗
PubMed2002

Simulate heart rate variability in different physiological conditions.

Heart rate variability is assumed to result from a multiplicative or cascade mechanism based on its multifractal property. Numerical results on the perturbation of the cascade are given to compare HRV under parasympathetic (PNS) and sympathetic (SNS) autonomic blockades. It was found that qualitative change of the HRV multifractal, which was observed in PNS blockade, is due to the change from a multiplicative to an additive mechanism.

Biophysical Phenomena↗
PubMed2001

Cytomegalovirus ventriculoencephalitis in a bone marrow transplant recipient receiving antiviral maintenance: clinical and molecular evidence of drug resistance.

We describe a case of CMV ventriculoencephalitis in a severely immunocompromised bone marrow transplant recipient who was receiving combination therapy with ganciclovir and foscarnet for treatment of viremia and retinitis. Analysis of sequential viral isolates recovered from the patient's cerebrospinal fluid suggested that disease developed because of the presence of viral resistance and, possibly, low tissue penetration of antiviral agents.

Antiviral Agents↗
PubMed2001

Modeling heart rate variability in healthy humans: a turbulence analogy.

Many complex systems share similar statistical characteristics. In this Letter, a turbulence analogy is proposed for the long-term heart rate variability of healthy humans. Based on such an analogy, the equivalence of an inertial range is found and a cascade model, which captures the statistical properties of the heart rate data, is given.

Electrocardiography, Ambulatory↗
PubMed2001

An integrated circuit implementation of the Huxley sarcomere model.

We have developed an integrated circuit to simulate the mechanical behavior demonstrated by sarcomeres found in skeletal muscle. The circuit is based upon the mathematical description of the attachment and detachment dynamics of crossbridge populations and the force generated by the crossbridges, originally formulated by A. F. Huxley. We describe the process of designing the circuit model from the mathematical model, present the sarcomere circuit implementation, and demonstrate the transient and steady-state behaviors that the fabricated circuit produces. Comparison of our results to published mechanical behavior of skeletal muscle shows qualitative similarities. We conclude that the circuit muscle model exhibits the potential for real-time simulation of muscle contractions and could be used to give engineered systems muscle-like properties.

Models, Biological↗
PubMed2001

Damping actions of the neuromuscular system with inertial loads: human flexor pollicis longus muscle.

Our previous work in an animal model showed that neuromuscular damping properties help maintain limb posture by effectively dissipating mechanical energy arising from disturbances. The purpose of this study was to determine whether similar damping properties were expressed in intact, normal human muscles. To review briefly, when the reflexively active soleus muscle in a decerebrate cat is coupled to an inertial load, application of a force impulse to the load results in lightly damped oscillations. By calculating the logarithmic decrement in muscle velocity following the impulse (the decrement being related to the amount of energy dissipated from the inertia), we found that damping increased with oscillation amplitude, a nonlinear property. This nonlinearity represents an automatic compensation for larger perturbations. Our findings in parallel experiments on the interphalangeal joint of the human thumb were that the long thumb flexor, the flexor pollicis longus (FPL), displayed mechanical and reflex behavior closely comparable to that reported earlier for the cat soleus, despite differences in architectural and metabolic properties between these muscles. Specifically, by selecting experimental trials that did not include voluntary interventions, we observed amplitude-dependent differences in damping in which larger amplitude movements elicited larger damping than did smaller movements. In addition, even after accounting for amplitude-dependent differences in damping, damping was found to be larger in later cycles than in the first cycle. This nonlinearity indicates that both mechanical properties of muscle and reflex mechanisms are dependent on prior movement history. We propose that this history-dependent behavior arises from the effects of prior movement on stretch reflex gain, and these effects are mediated primarily via changes in muscle spindle properties. Recordings of electromyographic activity from the FPL, during the first and second cycles of oscillation supported this postulate of a reduced reflex gain following prior motion. The functional significance of these nonlinear damping properties is that during the initial muscle stretch, the stiffness is high, which helps to preserve the initial position (although at the expense of promoting oscillation). Subsequently, the ensuing increase in damping helps suppress continuing oscillation. This sequence of varying mechanical properties is broadly analogous to the features of a predictive, or feed-forward controller, designed to produce a response that initially maintains position, and subsequently dampens oscillations. These results show that the intrinsic properties of muscle and spinal reflexes automatically provide a complex time-varying response, appropriate for maintenance of stable limb posture.

Adult↗
PubMed2000

Tensin can induce JNK and p38 activation.

Cells organize diverse types of specialized adhesion sites upon attachment to extracellular matrix (ECM) components. One of the physiological roles of such cell-ECM interactions is to initiate and regulate adhesion-mediated signal transduction responses. The association of cells with fibronectin fibrils has been shown to regulate the JNK and p38 signaling pathways. We tested whether tensin, a cytoskeletal component localized to both focal contacts and fibronectin-associated fibrillar adhesions, can induce these signaling pathways. We found that tensin overexpression resulted in activation of both the c-Jun amino-terminal kinase (JNK) and p38 pathways. Tensin-mediated JNK activation was independent of the activities of the small GTP binding proteins Rac and Cdc42, but did depend on SEK, a kinase involved in the JNK pathway. We suggest that tensin may directly activate the JNK and p38 pathways, acting downstream or independent of the activities of the small GTP binding proteins Rac and Cdc42.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed2000

Integrin dynamics and matrix assembly: tensin-dependent translocation of alpha(5)beta(1) integrins promotes early fibronectin fibrillogenesis.

Fibronectin matrix assembly is a multistep, integrin-dependent process. To investigate the role of integrin dynamics in fibronectin fibrillogenesis, we developed an antibody-chasing technique for simultaneous tracking of two integrin populations by different antibodies. We established that whereas the vitronectin receptor alpha(v)beta(3) remains within focal contacts, the fibronectin receptor alpha(5)beta(1) translocates from focal contacts into and along extracellular matrix (ECM) contacts. This escalator-like translocation occurs relative to the focal contacts at 6.5 +/- 0.7 microm/h and is independent of cell migration. It is induced by ligation of alpha(5)beta(1) integrins and depends on interactions with a functional actin cytoskeleton and vitronectin receptor ligation. During cell spreading, translocation of ligand-occupied alpha(5)beta(1) integrins away from focal contacts and along bundles of actin filaments generates ECM contacts. Tensin is a primary cytoskeletal component of these ECM contacts, and a novel dominant-negative inhibitor of tensin blocked ECM contact formation, integrin translocation, and fibronectin fibrillogenesis without affecting focal contacts. We propose that translocating alpha(5)beta(1) integrins induce initial fibronectin fibrillogenesis by transmitting cytoskeleton-generated tension to extracellular fibronectin molecules. Blocking this integrin translocation by a variety of treatments prevents the formation of ECM contacts and fibronectin fibrillogenesis. These studies identify a localized, directional, integrin translocation mechanism for matrix assembly.

Biological Transport↗
PubMed2000

Dynamics and segregation of cell-matrix adhesions in cultured fibroblasts.

Here we use time-lapse microscopy to analyse cell-matrix adhesions in cells expressing one of two different cytoskeletal proteins, paxillin or tensin, tagged with green fluorescent protein (GFP). Use of GFP-paxillin to analyse focal contacts and GFP-tensin to study fibrillar adhesions reveals that both types of major adhesion are highly dynamic. Small focal contacts often translocate, by extending centripetally and contracting peripherally, at a mean rate of 19 micrometers per hour. Fibrillar adhesions arise from the medial ends of stationary focal contacts, contain alpha5beta1 integrin and tensin but not other focal-contact components, and associate with fibronectin fibrils. Fibrillar adhesions translocate centripetally at a mean rate of 18 micrometers per hour in an actomyosin-dependent manner. We propose a dynamic model for the regulation of cell-matrix adhesions and for transitions between focal contacts and fibrillar adhesions, with the ability of the matrix to deform functioning as a mechanical switch.

Actins↗
PubMed2000

Damping actions of the neuromuscular system with inertial loads: soleus muscle of the decerebrate cat.

A transient perturbation applied to a limb held in a given posture can induce oscillations. To restore the initial posture, the neuromuscular system must provide damping, which is the dissipation of the mechanical energy imparted by such a perturbation. Despite their importance, damping properties of the neuromuscular system have been poorly characterized. Accordingly, this paper describes the damping characteristics of the neuromuscular system interacting with inertial loads. To quantitatively examine damping, we coupled simulated inertial loads to surgically isolated, reflexively active soleus muscles in decerebrate cats. A simulated force impulse was applied to the load, causing a muscle stretch, which elicited a reflex response. The resulting deviation from the initial position gave rise to oscillations, which decayed progressively. Damping provided by the neuromuscular system was then calculated from the load kinetics. To help interpret our experimental results, we compared our kinetic measurements with those of an analogous linear viscoelastic system and found that the experimental damping properties differed in two respects. First, the amount of damping was greater for large oscillation amplitudes than for small (damping is independent of amplitude in a linear system). Second, plots of force against length during the induced movements showed that damping was greater for shortening than lengthening movements, reflecting greater effective viscosity during shortening. This again is different from the behavior of a linear system, in which damping effects would be symmetrical. This asymmetric and nonlinear damping behavior appears to be related to both the intrinsic nonlinear mechanical properties of the soleus muscle and to stretch reflex properties. The muscle nonlinearities include a change in muscle force-generating capacity induced by forced lengthening, akin to muscle yield, and the nonlinear force-velocity property of muscle, which is different for lengthening versus shortening. Stretch reflex responses are also known to be asymmetric and amplitude dependent. The finding that damping is greater for larger amplitude motion represents a form of automatic gain adjustment to a larger perturbation. In contrast, because of reduced damping at small amplitudes, smaller oscillations would tend to persist, perhaps contributing to normal or "physiological" tremor. This lack of damping for small amplitudes may represent an acceptable compromise for postural regulation in that there is substantial damping for larger movements, where energy dissipation is more critical. Finally, the directional asymmetry in energy dissipation provided by muscle and reflex properties must be reflected in the neural mechanisms for a stable posture.

Animals↗
PubMed1999

Control of development by altered localization of a transcription factor in B. subtilis.

In B. subtilis, the chromosome partitioning proteins Soj (ParA) and Spo0J (ParB) regulate the initiation of sporulation. Soj is a negative regulator of sporulation gene expression, and Spo0J antagonizes Soj function. Using fusions of Soj to green fluorescent protein, we found that Soj localized near the cell poles and upon entry into stationary phase oscillated from pole to pole. In the absence of Spo0J, Soj was associated predominantly with DNA. By in vivo cross-linking and immunoprecipitation, we found that Soj physically associates with developmentally regulated promoters, and this association increased in the absence of Spo0J. These results show that Soj switches localization and function depending on the chromosome partitioning protein Spo0J. We further show that mutations in the Soj ATPase domain disrupt localization and function and render Soj insensitive to regulation by Spo0J.

Adenosine Triphosphatases↗