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At least 433 records · Page 24Linked to original sources
PubMed2006

Role of the right dorsal premotor cortex in "physiological" mirror EMG activity.

A distributed cortical network enables the lateralization of intended unimanual movements, i.e., the transformation from a default mirror movement to a unimanual movement. Little is known about the exact functional organization of this "non-mirror transformation" network. Involvement of the right dorsal premotor cortex (dPMC) was suggested because its virtual lesion by high-frequency repetitive transcranial magnetic stimulation (rTMS) increased the excitability of the left primary motor cortex (M1) during unilateral isometric contraction of a left hand muscle (Cincotta et al., Neurosci Lett 367: 189-93, 2004). However, no behavioural effects were observed in that experimental protocol. Here we tested behaviourally twelve healthy volunteers to find out whether focal disruption of the right dPMC by "off-line" One Hz rTMS (900 pulses, 115% of resting motor threshold) enhances "physiological" mirroring. This was measured by an established protocol (Mayston et al., Ann Neurol 45: 583-94, 1999) that quantifies the mirror increase in the electromyographic (EMG) level in the isometrically contracting abductor pollicis brevis (APB) muscle of one hand during brief phasic contractions performed with the APB of the other hand. Mirroring in the right APB significantly increased after real rTMS of the right dPMC. In contrast, no change in mirroring was seen with sham rTMS of the right dPMC, real rTMS of the right M1, or real rTMS of the left dPMC. These findings strongly support the hypothesis that the right dPMC is part of the non-mirror transformation cortical network.

Action Potentials↗
PubMed2005

Bradykinin signaling counteracts cAMP-elicited aquaporin 2 translocation in renal cells.

Bradykinin (BK) is one of the most important peptides regulating vascular tone, water, and ionic balance in the body, playing a key role in controlling BP. It is interesting that patients with essential hypertension excrete less BK than normotensive individuals. For elucidating the mechanism by which BK regulates renal water transport that contributes to its antihypertensive effect, aquaporin 2 (AQP2)-transfected collecting duct CD8 cells, expressing the BK type II receptor (BK2R), were used as an experimental model. In CD8 cells, BK pretreatment impaired forskolin-induced AQP2 translocation to the apical plasma membrane. For clarifying the signal transduction cascade associated with this effect, whether BK induced an increase in cytosolic calcium, via the G protein Gq, known to be coupled to BK2R, first was investigated. Spectrofluorometry using fura-2-AM revealed that 100 nM BK elicited a significant increase in Ca(i), which was abolished by the receptor antagonist HOE-140. BK acts through BK2R coupled to both Gq and Galpha13, a known upstream effector of Rho protein. In CD8 cells, BK causes an increase in Rho activity, likely as a result of Galpha13 activation. This results in stabilization of the cortical F-actin network, thus impairing AQP2 trafficking. These effects counteract physiologic vasopressin stimulation, which instead has an opposite effect on actin network organization through Rho inactivation.

Animals↗
PubMed1991

The thalamic clock: emergent network properties.

Rhythmical oscillation of thalamic neuronal populations occurs under physiological conditions and in several disease states. In the present experiments we examined the network properties of population rhythmicity and the possible involvement of N-methyl-D-aspartate receptors in the frequency regulation and maintenance of rhythmic thalamic bursts. Multisite recording of neuronal activity and local microinjections of drugs were performed on the freely moving rat. Rhythmic thalamic population bursts at 6 to 9 Hz and concurrent neocortical high voltage spike-and-wave spindles were observed during awake immobility, with the thalamic rhythm leading the neocortical high voltage spindle. Even though all individual thalamocortical neurons fired in a phase-locked manner to the high-voltage spindle, the majority discharged at a significantly lower frequency than that of the population (multiunit) activity. In contrast, neurons in the nucleus reticularis thalami discharged at the frequency of the population bursts. Neurons in the extrapyramidal system and neocortex but not the hippocampal formation also fired in a phase-locked manner to the high-voltage spindle. Systemic administration or local microinjection of either non-competitive or competitive N-methyl-D-aspartate blockers (ketamine or ap-5) slowed the frequency of thalamic multiunit bursts and associated high-voltage spindles from 8 to 2 Hz, or completely blocked rhythmicity. Unilateral thalamic injection of ketamine or ap-5 resulted in a suppression of the amplitude of high-voltage spindles in the injected hemisphere. It is concluded that thalamic rhythmicity is not due to the "pacemaker" properties of thalamic cells but is rather an emergent property of the relay thalamus-nucleus reticularis network. Furthermore, we hypothesize that the frequency of network oscillation is regulated by the interplay between two major classes of voltage-dependent conductances in the thalamocortical cells: low-threshold calcium channels and high-threshold N-methyl-D-aspartate channels.

Activity Cycles↗
PubMed2004

The adipose tissue as a source of vasoactive factors.

Obesity is associated with increased incidence of cardiovascular mortality. However, the mechanisms that link increased fat mass with hypercholesterolemia, hypertension, endothelial dysfunction and coronary heart disease have not been fully elucidated. Unravelling the diverse neuroendocrine systems, which regulate energy balance and body fat has been a long-standing challenge in biology, with obesity as an increasingly important public health focus. Until recently, the adipocyte has been considered only a passive tissue for the storage of excess energy in the form of fat. However, there is now compelling evidence that adipocytes act as endocrine, secretory cells. It has been shown that several hormones, growth factors and cytokines are actually expressed in white adipose tissue. In a dynamic view of the adipocyte a wide range of signals emanates from white adipose tissue such as tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and their respective soluble receptors. White adipose tissue also secretes important regulators of lipoprotein metabolism like lipoprotein lipase (LPL), apolipoprotein E (apoE) and cholesteryl ester transfer protein (CETP). The increasing number of products secreted by adipocytes also includes leptin, estrogen, angiotensinogen, plasminogen activator inhibitor-1 (PAI-1), tissue factor and transforming growth factor-beta (TGF-beta). Nitric oxide synthase (NOS) has been also reported to be expressed in white adipose tissue. Acylation stimulating protein (ASP), adipophilin, adipoQ, adipsin, monobutyrin, agouti protein and factors related to pro-inflammatory and immune processes have also been shown to be released by white adipocytes. Since blood vessels express receptors for most of the adipocyte-derived factors, adipose tissue seems to play a key role in cardiovascular physiology through the existence of a network of local and systemic signals. The current knowledge in this field will be reviewed in the broader perspective of cardiovascular physiology and pathophysiology.

Adipose Tissue↗
PubMed1996

New modalities for understanding dynamic regulation of the somatotropic (GH) axis: explication of gender differences in GH neuroregulation in the human.

BACKGROUND: Neuroendocrine regulation of the somatotropic (GH) axis is under the direction of hypothalamic signals, intrapituitary mechanisms, and multi-level feedback control. Consequently, understanding the regulation of the physiologically pulsatile mode of GH release in vivo is a substantial challenge. OBJECTIVES: To present and review several new modalities designed to unmask novel features of physiological regulation of the GH axis. To this end, I emphasize gender differences in the control of pulsatile GH release, while highlighting the new approaches to uncovering such differences. SUBJECTS: Human volunteers. METHODS: Novel investigative modalities include: (1) a high-sensitivity chemiluminescence GH assay capable of measuring 0.002 microgram/l of GH when utilized with a new discrete variance model for assay data reduction; (2) the technique of standardized linear regression to compare GH measures in men versus women; (3) the application of so-called deconvolution analysis, which is designed to estimate underlying rates of pulsatile hormone (GH) secretion as well as hormone half-life from a given plasma GH concentration profile; (4) an approximate entropy (ApEn) statistic to quantify the regularity or orderliness of hormone release, by assigning a single non-negative number that is a measure of the pattern reproducibility in the data; and (5) the evolution of network models to represent the physiological connections and feedback activities of the GH axis. RESULTS: The foregoing new methodologies have collectively uncovered prominent gender differences in the regulation of the GH axis, which encompass: (i) higher mean serum GH concentrations due to greater GH secretory burst mass in women than men; (ii) relatively reduced suppressibility of GH by oral glucose administration due to greater GH secretory burst mass in women compared to men, with no apparent gender differences in the frequency of GH secretory bursts or the GH half-life in plasma; (iv) a remarkably higher degree of irregularity or disorder in the GH release process in women or female rats compared to male counterparts, indicating significantly reduced pattern reproducibility in the female; (v) an approximately two-fold greater sensitivity of men compared to women to the negative effects of age and increased percentage body fat and the positive impact of physical fitness on mean serum GH concentrations; and (vi) the ability of a multinodal network to capture the feedback relationships observed in vivo among GHRH, somatostatin, GH secretion, and GH and IGF-I negative feedback. CONCLUSIONS: New analytical modalities for understanding dynamic regulation of the GH axis disclose a wide array of specific, prominent, and quantifiable gender differences in the physiological control mechanisms that direct this important neuroendocrine axis.

Female↗
PubMed2006

Noise-induced coherence and network oscillations in a reduced bursting model.

The dynamics of the Hindmarsh-Rose (HR) model of bursting thalamic neurons is reduced to a system of two linear differential equations that retains the subthreshold resonance properties of the HR model. Introducing a reset mechanism after a threshold crossing, we turn this system into a resonant integrate-and-fire (RIF) model. Using Monte-Carlo simulations and mathematical analysis, we examine the effects of noise and the subthreshold dynamic properties of the RIF model on the occurrence of coherence resonance (CR). Synchronized burst firing occurs in a network of such model neurons with excitatory pulse-coupling. The coherence level of the network oscillations shows a stochastic resonance-like dependence on the noise level. Stochastic analysis of the equations shows that the slow recovery from the spike-induced inhibition is crucial in determining the frequencies of the CR and the subthreshold resonance in the original HR model. In this particular type of CR, the oscillation frequency strongly depends on the intrinsic time scales but changes little with the noise intensity. We give analytical quantities to describe this CR mechanism and illustrate its influence on the emerging network oscillations. We discuss the profound physiological roles this kind of CR may have in information processing in neurons possessing a subthreshold resonant frequency and in generating synchronized network oscillations with a frequency that is determined by intrinsic properties of the neurons.

Biological Clocks↗
PubMed2005

Activation of early silent synapses by spontaneous synchronous network activity limits the range of neocortical connections.

During the early development of neocortical networks, many glutamatergic synapses lack AMPA receptors and are physiologically silent. We show in neocortical cultures that spontaneous synchronous network activity is able to convert silent synapses to active synapses by the incorporation of AMPA receptors into synaptic complexes throughout the network within a few minutes. To test the effect of synaptic activation on the connectivity of neuronal populations, we created separated neuronal networks that could innervate each other. We allowed outgrowing axons to invade the neighboring network either before or after the onset of synchronous network activity. In the first case, both subnetworks connected to each other and synchronized their activity, whereas in the second case, axonal connections failed to form and network activity did not synchronize between compartments. We conclude that early spontaneous synchronous network activity triggers a global AMPAfication of immature synapses, which in turn prevents later-arriving axons from forming afferent connections. This activity-dependent process may set the range of corticocortical connections during early network development before experience-dependent mechanisms begin elaborating the mature layout of the neocortical connections and modules.

2-Amino-5-phosphonovalerate↗
PubMed2005

Systematic intervention of transcription for identifying network response to disease and cellular phenotypes.

MOTIVATION: A major challenge in post-genomic research has been to understand how physiological and pathological phenotypes arise from the networks of expressed genes. Here, we addressed this issue by developing an algorithm to mimic the behavior of regulatory networks in silico and to identify the dynamic response to disease and changing cellular conditions. RESULTS: With regulatory pathway and gene expression data as input, the algorithm provides quantitative assessments of a wide range of responses, including susceptibility to disease, potential usefulness of a given drug, or consequences to such external stimuli as pharmacological interventions or caloric restriction. The algorithm is particularly amenable to the analysis of systems that are difficult to recapitulate in vitro, yet they may have important clinical value. The hypotheses derived from the algorithm were biologically relevant and were successfully validated via independent experiments, as illustrated here in the analysis of the leukemia-associated BCR-ABL pathway and the insulin/IGF pathway related to longevity. The algorithm correctly identified the leukemia drug target and genes important for longevity, and also provided new insights into our understanding of these two processes. AVAILABILITY: The software package is available upon request to the authors.

Aging↗
PubMed1991

Two dynamic modes of striatal function under dopaminergic-cholinergic control: simulation and analysis of a model.

A neural network model based on the anatomy and physiology of the matrix compartment of the striatum is described. The model consists of a network of neurons which are mutually inhibitory within a defined domain. A membrane potassium conductance (GK) under dopaminergic-cholinergic control is included in the model. Computer simulation results show that changes in GmaxK can modulate the behaviour of the network to produce either competition or coactivation among striatal output neurons. An analysis of a two-neuron system based on the model shows that the maximum steepness of the threshold function plays a decisive role in the dynamics, in particular with regard to the competition that exists between the neurons. Competitive interactions predominate at low GmaxK, while coactivation predominates at high GmaxK. We suggest that the former dynamic governs reciprocal inhibition of antagonistic muscles, while the latter governs cocontraction and rigidity. The model offers insights into the control of striatal neurodynamics by GmaxK which establish closer links between dopaminergic actions in the striatum and the mechanism of Parkinsonian rigidity. A prediction of the model is that acetylcholine should increase GKmax in striatal output neurons.

Acetylcholine↗
PubMed2005

Inhibitory coupling specifically generates emergent gamma oscillations in diverse cell types.

Networks of inhibitory neurons regulate synchrony during many physiological and pathological oscillations. To explore how these effects depend on cellular, network, and synaptic factors, we developed and validated a semisynthetic inhibitory network that approximates simultaneous activity in multiple neurons by using consecutive responses from single cells. We recorded from three types of neurons, each of which forms interconnected networks in vivo, but has unique intrinsic properties. In all three cell types, fast inhibitory coupling generated emergent gamma oscillations. By contrast, inhibitory coupling desynchronized slower, spindle-frequency responses specifically in thalamic reticular neurons. The emergent gamma-frequency synchronization was also specific to tonic input and did not occur during responses to phasic inputs. These results illustrate how particular features of inhibitory networks (e.g., cell or input type) contribute to their synchronizing or desynchronizing functions. They also demonstrate phenomena (emergent gamma oscillations) that occur robustly in multiple cell types and may thus be a generic feature of inhibitory networks throughout the brain.

Animals↗
PubMed2005

Where are we in genomics?

Genomic studies provide scientists with methods to quickly analyse genes and their products en masse. The first high-throughput techniques to be developed were sequencing methods. A great number of genomes from different organisms have thus been sequenced. Genomics is now shifting to the study of gene expression and function. In the past 5-10 years genomics, proteomics and high-throughput microarray technologies have fundamentally changed our ability to study the molecular basis of cells and tissues in health and diseases, giving a new comprehensive view. For example, in cancer research we have seen new diagnostic opportunities for tumour classification, and prognostication. A new exciting development is metabolomics and lab-on-a-chip techniques (which combine miniaturization and automation) for metabolic studies. However, to interpret the large amount of data, extensive computational development is required. In the coming years, we will see the study of biological networks dominating the scene in Physiology. The great accumulation of genomics information will be used in computer programs to simulate biologic processes. Originally developed for genome analysis, bioinformatics now encompasses a wide range of fields in biology from gene studies to integrated biology (i.e. combination of different data sets from genes to metabolites). This is systems biology which aims to study biological organisms as a whole. In medicine, scientific results and applied biotechnologies arising from genomics will be used for effective prediction of diseases and risk associated with drugs. Preventive medicine and medical therapy will be personalized. Widespread applications of genomics for personalized medicine will require associations of gene expression pattern with diagnoses, treatment and clinical data. This will help in the discovery and development of drugs. In agriculture and animal science, the outcomes of genomics will include improvement in food safety, in crop yield, in traceability and in quality of animal products (dairy products and meat) through increased efficiency in breeding and better knowledge of animal physiology. Genomics and integrated biology are huge tasks and no single lab can pursue this alone. We are probably at the end of the beginning rather than at the beginning of the end because Genomics will probably change Biology to a greater extent than previously forecasted. In addition, there is a great need for more information and better understanding of genomics before complete public acceptance.

Animals↗
PubMed2002

Canine mesenteric artery and vein convey no difference in the content of major contractile proteins.

BACKGROUND: Mesenteric arteries and veins are composed of tonic smooth muscles and serve distinct functions in the peripheral circulation. However, the basis for the functional disparity of the resistive and capacitative parts of the mesenteric circulation is poorly understood. We studied potential differences in the expression levels of six contractile proteins in secondary and tertiary branches of the inferior mesenteric artery and vein along with differences in the vessel wall morphology. RESULTS: Bright field and electron microscopy showed that both vessel walls had the same major structural elements. The arterial walls, however, had greater number, and more tightly assembled, smooth muscle cell layers compared to vein walls. The content of actin, myosin heavy chain, myosin light chain, and calponin was similar in the two blood vessels. The artery expressed higher amount of the actin-binding protein caldesmon than the vein (41.86 +/- 2.33 and 30.13 +/- 3.37 microg/mg respectively, n = 12). Although the total tropomyosin content was almost identical in both blood vessels, the alpha isoform dominated in the artery, while the beta isoform prevailed in the vein. CONCLUSIONS: Canine mesenteric artery and vein differ in vessel wall morphology but do not convey differences in the expression levels of actin, myosin light chain, myosin heavy chain and calponin. The two vascular networks express distinct amounts of caldesmon and tropomyosin, which might contribute to the fine tuning of the contractile machinery in a manner consistent with the physiological functions of the two vascular networks.

Actins↗
PubMed1997

Implementation of intussusceptive microvascular growth in the chicken chorioallantoic membrane (CAM).

Intussusceptive microvascular growth (IMG) is a new mechanism of capillary growth: The vascular network expands by insertion of newly formed columns of interstitial tissue (interstitial tissue structures) into the vascular lumen called tissue pillars or posts (diameter: 0.5-2.5 microm). IMG has so far been described during organ development and growth and in tumor angiogenesis. Different modes of its implementation could be demonstrated in the rat lung and the chicken chorioallantoic membrane (CAM). In the present investigation a further mechanism of IMG is reported in the chicken CAM: tissue pillars form by splitting of larger interstitial tissue structures and intercapillary walls located between neighboring capillary segments which will consecutively fuse. Splitting is dependent on the existence of a pillar's core composed of a bundle of collagen fibrils ensheathed by extensions of endothelial-like cells inside these structures. Pillar cores thus represent the smallest unit of interstitial tissue around which the vascular lumen might expand. This mode of IMG is obviously connected to physiological remodeling of the capillary network and appears to be dominant during later stages of CAM development.

Actin Cytoskeleton↗
PubMed1987

Calcium control of macrophage cytoplasmic gelation: evidence for the involvement of the 70,000 Mr actin-bundling protein.

Under appropriate conditions macrophage cytosolic extracts can form a three-dimensional gel network of cross-linked actin filaments. These cytoplasmic gels are mainly composed of actin, filamin, alpha-actinin, and two new proteins of about 70,000 and 55,000 Mr (70 and 55 K). The behaviour of 70 K protein was found to be remarkably affected by Ca2+. Ca2+ treatment of isolated cytoplasmic gels led to the selective solubilization of the 70 K protein along with a 17 K polypeptide. Half-maximal recovery in the supernatant fraction was obtained from about 0.15 microM free Ca2+. The cytoplasmic gel constituents solubilized in high ionic strength buffer were able to re-assemble into an insoluble actin network when returned to near physiological ionic conditions. However, the inclusion of micromolar Ca2+ prevented the re-association of 70 K protein with actin in these complexes. As compared to the 70 K protein, alpha-actinin was fully resistant to any variations in Ca2+ concentrations. On the other hand, purified 70 K protein displayed the property of assembling actin filaments into bundles at low Ca2+ concentrations (less than 0.15 microM). However, the bundling activity decreased progressively at higher Ca2+, as detected by co-sedimentation and electron microscopy of the 70 K protein-actin mixtures. Half-maximal inhibition was observed at about 0.3 microM free Ca2+. Re-assembly of actin filaments into bundles occurred after chelation of Ca2+ by EGTA, indicating that the inhibitory effect of Ca2+ was reversible. Severing of actin filaments by 70 K protein was not observed in any of the solution conditions used. The Ca2+-dependent inhibition of the ability of 70 K protein to interact with actin networks resulted in a marked distortion of the overall organization of actin filaments, as revealed by thin-section electron microscopy of cytoplasmic gels formed in the presence and absence of Ca2+. Large zones of oriented bundles of filaments were replaced by a looser mesh. When the actin gel constituents were re-assembled in the presence of Ca2+ and exogenous gelsolin, it was also observed that the filament bundles (essentially generated by alpha-actinin) collapsed into dense aggregates. Furthermore, gelsolin did not significantly affect the ability of actin to re-combine with other proteins. The data presented here and previously led us to suspect that the Ca2+ control of the functional state of 70 K protein might be one of the prime factors in the triggering of rapid assembly and disassembly of microfilaments within macrophages.

Actins↗
PubMed1993

Model experiments on measuring flow in microvessels using tracers.

Most techniques for measuring plasma or red cell flow velocity within microvessels rely on determining the transit time of a tracer to transverse the distance between two monitoring sites within a vessel. In principle, proper transit time determinations require flow-weighted sampling of the tracer at monitoring sites. In practical application of the tracer technique, however, trace sampling at monitoring sites is not flow-weighted but is area-weighted, and hence elapsed transient time can only be estimated from tracer data. We previously showed theoretically (Microvasc. Res. 40, 394-411, 1990) that the flow velocity determined under these conditions can differ appreciably from the actual mean flow velocity of the carrier fluid within the microvessel. Nevertheless, trace mean flow velocity does approach that of the fluid when tracer velocity is measured past a finite distance from the microvessel entrance. In this study, we examined the tracer measurement of flow experimentally using a physical model. We perfused single glass microvessels and simple fabricated microvessel networks with distilled water at physiological flow rates. Mean tracer velocity (Vd) was determined at several axial locations within the microvessels using injected Evans blue dye. At each location Vd was determined in a manner consistent with usual application of the tracer flow measurement technique. Actual mean flow velocity (Va) was determined from the measured effluent flow rates discharged from each microvessel. Our experimental results confirm the existence of an appreciable velocity measurement error (VME) associated with the tracer technique. The VME behavior was consistent with our original theoretical analysis. Vd was significantly smaller than Va within a finite length of vessel near the entrance, but approached and became equal to Va past this length. Furthermore, even under conditions where the VME was negligible at the end of a parent microvessel, a new and appreciable VME arose within the connecting downstream daughter microvessels. These results underscore that tracer mean flow velocity as obtained in normal implementation of the tracer technique can differ from that for the fluid itself within a microvascular network.

Blood Flow Velocity↗
PubMedDate not supplied

Digital vision theory: Boolean logic model.

Guild (1932) stated the general requirements for processing signals in color vision system and a digital format of his paradigm is developed in this paper. The disk structure generates the digital receptor pulse. The input modalities form sets, linked by intersections, joins, and complement junctions. The synapses are elements in these junctions. Complex synapses form complex junctions to create Boolean logic processing. A computer program using these Boolean logic functions calculates: Light and dark adaptation responses; Color matching and spectral coordinate functions; Chromatic adaptation and color shift responses; and dynamic neural responses. These calculations compare favorably with the experimental data.

Adaptation, Physiological↗
PubMed1994

Acquisition of color opponent representation by a three-layered neural network model.

This paper discusses color representation in the visual system by analysis of a three-layered neural network model. The model incorporates physiological knowledge of color representation at the sensor level (broad-band trichromatic representation by cones) and the higher level (narrow-band color representation by color-coded cells in V4). We trained the model to perform a mapping between these color representations by the back propagation algorithm and analyzed the acquired characteristics of the hidden units. It turned out that the hidden units learned characteristics similar to those of the color opponent cells found in the visual system. It was concluded that the R-G and Y-B color opponent representations reflect the efficiency of the color representation in the visual system from investigations on the efficiency of color representation in the hidden layer and on the capability of the color recognition task of the model.

Color Perception↗
PubMed1998

Effect of zinc ions on fibrin network structure.

In addition to calcium, other physiologically important divalent cations (magnesium and zinc) are known to influence fibrin formation and structure. We have studied the effect of different concentrations (0-20 micromol/l) of zinc ions (Zn2+) in the absence and presence of calcium on the gel structure formed in purified fibrinogen-enzyme systems. For that purpose, we used turbidity measurement, liquid permeation and confocal three-dimensional microscopy of the gel as well as sodium dodecyl sulphate (SDS)-gel electrophoresis. The results of turbidity measurements indicated that the clotting time decreased with increasing concentrations of Zn2+. The fiber mass: length ratio (mu) values showed that the porosity of the gels increased in a concentration-dependent manner, i.e. at higher concentrations of Zn2+, larger pores with thicker fibrin fibers were formed. Three-dimensional microscopy data of the gels were in good agreement with the mu data. On SDS-gel electrophores of reduced fibrin, no cross-linking was observed in the presence of zinc ions only (without the addition of calcium ions), nor were D-D dimer bands observed in non-reduced plasmin digested fibrin samples in the presence of zinc ions only. The above results show that zinc changes the fibrin gel structure and that this effect appears to be independent of calcium.

Calcium↗