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PubMed1989

[Receptor-effector relations in the effect of adosterone on mononuclear leukocytes: validation and application to various water and electrolyte imbalances in humans].

Mineralocorticoid receptors were found in cells from extrarenal tissues such as spleen, hippocampus, smooth muscle, heart, hypophysis and mammary gland. Recently, mineralocorticoid receptors and effects of aldosterone on intracellular sodium and potassium have been described for human mononuclear leukocytes (HML). Both intracellular sodium and potassium concentrations decreased when HML from normal subjects were incubated for 1 h in a medium without aldosterone. In the presence of 1.4 nM aldosterone this loss of intracellular sodium and potassium from HML was absent, with values similar to those found in freshly prepared cells before incubation. The clinical significance of this model was underlined by the demonstration of absent or a decreased number of mineralocorticoid receptors and the lack of electrolyte response to aldosterone in HML of patients with pseudohypoaldosteronism. For patients with primary and secondary aldosteronism a reduced number of mineralocorticoid receptors has been shown on HML, thus indicating a "down-regulation" in response to chronically elevated serum levels of aldosterone. Additionally, an abnormal effector mechanism could be demonstrated in HML from these patients. These studies are the first to demonstrate the significance of extrarenal, nonepithelial mineralocorticoid receptors and the related effector mechanism for different disorders of the water- and electrolyte-balance in man.

Aldosterone↗

PubMed1992

Hierarchy of in vitro sensitivity and resistance of tumor cells to cytotoxic effector cells, cytokines, drugs and toxins.

Drug resistance of tumor cells has led to the development of other therapeutic modalities including biological response modifiers, lymphokine-activated killer cells (LAK), and cytokines alone and in combination. The premise of these alternative modalities is that drug resistance can be overcome by other cytotoxic agents or cytotoxic effector cells. However, the relationship between tumor cell sensitivity to these different agents and the cytotoxicity caused by drugs is not known or well understood. Thus, understanding the relationship between these different systems of tumor cell cytotoxicity is essential for optimal therapeutic intervention. To this end, we compared the tumor cell cytotoxicity mediated by recombinant tumor necrosis factor (rTNF), cytotoxic effector cells (natural killer cells, monocytes, LAK cells), chemotherapeutic drugs, and microbial toxins. Human tumor cell lines sensitive and resistant to rTNF or drugs were used to evaluate the effectiveness of the other cytotoxic modalities. Sensitivity was considered as tumor cell cytotoxicity above 15% while resistance refers to that below 10%. Cell lines tested consisted of several histological types such as brain, lung, colon and ovarian tumors. In our experiments, cell lines made resistant to rTNF by coculture were also relatively resistant to unactivated monocytes and their supernatants. These lines were sensitive to all other methods tested including activated monocytes, natural killer and LAK cells, drugs, and toxins. The tumor lines naturally resistant to rTNF were found to have various degrees of sensitivity and resistance to these other systems. Upon the analysis of our data, a pattern emerged that suggested a hierarchy of sensitivity and resistance of the tumor cells to the cytotoxic mechanisms explored. From a majority of cell lines resistant to rTNF to a minority of lines resistant to LAK, we found an interesting gradation of sensitivity and/or resistance to the other cytotoxic modalities employed. The hypothesis of an underlying common mechanism of action within these systems is discussed.

Bacterial Toxins↗

PubMed1992

Comparative efficiencies of bispecific F(ab'gamma)2 and chimeric mouse/human IgG antibodies in recruiting cellular effectors for cytotoxicity via Fc gamma receptors.

The three forms of Fc gamma receptor carried by monocytes (Fc gamma RI, II) and natural killer (NK) cells (Fc gamma RIII) are all capable of mediating cell lysis. Here we compare the use of F(ab'gamma)2 bispecific antibodies, specifically targetting individual Fc gamma R, and chimeric IgG mouse/human antibodies which are capable of targetting all Fc gamma R, for their ability to mediate target cell destruction. The derivatives are prepared by linking hinge sulphydryl residues via tandem thioether bonds, using a bismaleimide crosslinker: Fab' from an anti-Fc gamma R mAb linked to Fab' from a common anti-target mAb (BsAb), or Fab' from the common anti-target mouse antibody linked to human Fc gamma (FabFc or bisFabFc). All the derivatives targetting chick red blood cells gave efficient lysis, although different effector cell donors yielded differences in both the lytic levels achieved and the comparative efficiencies of derivatives. In contrast, significant lysis of the guinea pig lymphoblastic leukaemia, L2C, regularly resulted only via the anti-Fc gamma RIII BsAb and the chimeric derivatives. These results suggest that the chimeric, Fc-containing derivatives mediate tumour cell lysis principally through Fc gamma RIII on NK cells. This is in contrast to the situation with the chick red blood cells where the chimeric derivatives appear capable of lysing erythrocytes by utilizing either monocytes or NK cells, because significant (approximately 50%) lysis occurred with effector cell populations magnetically depleted through either Fc gamma RII or Fc gamma RIII. A major difference between these two types of antibody derivative was their ability to function in the presence of high concentrations of normal human Fc gamma. The lysis mediated by BsAb reactive with Fc gamma RI or II was unaffected by the presence of human Fc gamma at 2.5 mg/ml (a concentration comparable with that yielded by IgG in plasma) whereas the BsAb recognizing Fc gamma RIII and all the Fc-containing derivatives were completely inhibited.

Animals↗

PubMed1990

Characterization of effector cells of graft vs leukemia following allogeneic bone marrow transplantation in mice inoculated with murine B-cell leukemia.

It is now widely accepted that immunocompetent lymphocytes in allogeneic bone marrow grafts exert an antileukemic effect that contributes to the cure of leukemia. Graft vs leukemia (GVL) effects independent of graft vs host disease were investigated in allogeneic bone marrow chimeras tolerant of host and donor alloantigens. The role of Thy1.2, L3T4 and Lyt2 T lymphocytes as effector cells of GVL were investigated in (BALB/c x C57BL/6)F1 mice inoculated with murine B-cell leukemia and subsequently conditioned with total lymphoid irradiation and cyclophosphamide (200 mg/kg). Mice were reconstituted with C57BL/6 bone marrow cells depleted of well-defined T-cell subsets or enriched for stem cells by the soybean agglutination method. Detection of residual tumor cells, an indicator for efficacy of GVL, was carried out by adoptive transfer of peripheral blood or spleen cells obtained from treated chimeras into secondary naive BALB/c recipients at different time intervals following bone marrow transplantation. Treatment of the primary marrow inoculum with monoclonal anti-Thy1.2 or anti-Lyt2 abolished the GVL effects and all secondary BALB/c recipients developed leukemia within 60 days. On the other hand, the treatment with monoclonal anti-L3T4 did not influence the effect of GVL and all treated recipients remained without leukemia. The data suggest that T cells may mediate GVL effects in the absence of graft vs host disease and in circumstances where tolerance to conventional alloantigens is elicited. Effector cells of GVL across the major histocompatibility complex (MHC) in the murine B-cell leukemia tumor model system appear to be Thy1.2+ Lyt2+ L3T4-. Induction of GVL effects by allogeneic cells tolerant of host MHC suggests that these effects may be independent of graft vs host disease.

Agglutinins↗

PubMed1994

Th1 type CD4+ T cells may be a potent effector against poorly immunogenic syngeneic tumors.

We examined the possibility that Th1 type CD4+ T cells may be an effector against three kinds of syngeneic tumors such as highly immunogenic B16 melanoma (B16) and two poorly immunogenic lines of MCA fibrosarcoma (MCA) and 3LL carcinoma (3LL). In a proliferation assay, the Th1 type CD4+ T cell clone (MH2) recognized the purified protein derivatives (PPD) derived from Mycobacterium tuberculosis. In a tumor-neutralizing assay, MH2 showed anti-tumor activity against both B16 and MCA. In a model of pulmonary metastasis, MH2 also showed anti-tumor activity against both B16 and 3LL. In an assay of cytolysis, MH2 showed a moderate level of tumor necrosis factor-dependent cytolytic activity only against MCA. In a cytostasis assay, MH2 showed a high level of interferon gamma-dependent cytostatic activity against the three tumors in the presence of macrophages. The anti-tumor activity of MH2 against B16 and 3LL was suggested to be, at least in part, attributable to the augmented natural killer activity. Taken together, these findings suggest that we may potentially be able to utilize Th1 type CD4+ T cells as an effector for immunotherapy against poorly immunogenic tumors.

Animals↗

PubMed1985

Immunologic regulator and effector mechanisms in myocarditis and perimyocarditis.

The diagnosis and etiology of myocarditis and perimyocarditis are often difficult to ascertain. We therefore investigated regulator and humoral and cellular effector mechanisms in patients with viral heart disease (Coxsackie B3, influenza, EBV, mumps). In acute carditis, OKIA1-positive cells were increased and no significant alteration in suppressor cell activity was observed in our patients in contrast to others reports. The characteristic immunofluorescent pattern is the presence of antimyolemmal antibodies (AMLA) with rat and human collagenase-pretreated intact cardiocytes (in titers of 1:40-1:320) as antigens. The pattern is indistinguishable on cardiocytes from antibodies against cytoskeletal antigens (microtubules, intermediate filaments--tubulin/vemitin) when associated with antibodies directed against the Z-bands. In contrast, only anti-interfibrillary antibodies are present in cytomegalovirus myocarditis. The antimyolemmal fluorescence can be absorbed with the respective causative virus, indicating that the antibodies are cross-reactive. AMLA-positive sera induce cytolysis of vital rat cardiocytes in vitro, indicating that the antibodies are of pathogenetic relevance. Cytolytic serum activity could be absorbed out with the respective virus. Immunohistologic specimens obtained from patients with carditis demonstrate the fixation of IgG-type antibodies to the sarcolemma that also fix complement. In the acute phase of carditis, circulating immune complexes were also measured, thus monitoring immunoreactivity. Cellular effector mechanisms against vital cardiocytes were maintained or even slightly enhanced; in vitro NK-cell activity against K 562, however, was decreased. This is compatible with a more target-specific cytotoxicity in carditis but reduced NK-cell activity in peripheral blood cells.

Acute Disease↗

PubMed1996

Effectors of the mammalian plasma membrane NADH-oxidoreductase system. Short-chain ubiquinone analogues as potent stimulators.

In the presence of effectors variations in the two recognized activities of the plasma membrane NADH-oxidoreductase system were studied in separate, specific in vitro assays. We report here that ubiquinone analogues that contain a short, less hydrophobic side chain than coenzyme Q-10 dramatically stimulate the NADH-oxidase activity of isolated rat liver plasma membranes whereas they show no effect on the reductase activity of isolated membranes. If measured in assays of the NADH:ferricyanide reductase of living cultured cells these compounds have only a limited effect; the oxidase activity of whole cells is not measurable in our hands. We have furthermore identified selective inhibitors of both enzyme activities. In particular, the NADH-oxidase activity can be significantly inhibited by structural analogues of ubiquinone, such as capsaicin and resiniferatoxin. The NADH:ferricyanide reductase, on the other hand, is particularly sensitive to pCMBS, indicating the presence of a sulfhydryl group of groups at its active site. The identification of these specific effectors of the different enzyme activities of the PMOR yields further insights into the function of this system.

Animals↗

PubMed1989

The "double grafted tumor system", proposed to find effector cells in the analyses of antitumor effect of BRMs.

The antitumor effects of three biological response modifiers (BRMs; PSK, IFN alpha A/D and OK432) and two chemotherapeutics (Mitomycin C and Neocarzinostatin) in a new experimental mouse model, the "double grafted tumor system," were evaluated. BALB/c mice received simultaneous inoculations of Meth A fibrosarcoma cells on right flank (1 x 10(6) cells) and left flank (2 x 10(5) cells) on day 0, and drugs were given intratumorally into the right-flank tumor on day 3. The growth of the left-flank tumor was the real target for the evaluation of a given drug after 21 days. All tested five agents successfully cured the drug-injected right tumor with a pre-determined optimum dose. In addition, PSK, OK432, IFN alpha A/D and MMC among the five, inhibited the left-flank tumor, whereas no inhibition was observed when treated with NCS. To understand the mechanism by which the antitumor effect of the above four agents is able to influence the growth of tumor on the other side, tumor cells (2 x 10(5) cells) inoculated only into the left flank were treated with drugs given subcutaneously to the right flank (single tumor system). Among the four, MMC exhibited an effect similar to that obtained in the double tumor system, and IFN alpha A/D showed a less pronounced but still definite antitumor effect. However, PSK and OK432 failed to express anti-tumor effect in the single tumor system. These results obtained with PSK, OK432 and IFN alpha A/D suggest that the effect of the drug on the left-tumor may be mediated by certain effector cells, which are specifically induced by injection of the drug, in the right-tumor tissues. When effector cell analysis was conducted with spleen cells obtained after PSK treatment by means of intratumoral adoptive transfer into 3-day Meth A bearing recipients, these cells were shown to be Lyt-1+2(-)-T and L3T4(+)-T cell.

Animals↗

PubMed1992

5-HT1A receptor-effector system responsivity in panic disorder.

To explore 5-HT1A receptor responsivity in panic disorder (PD), hypothermic, neuroendocrine and behavioral responses to the selective partial 5-HT1A receptor agonist ipsapirone (IPS) were investigated in patients with primary PD and healthy controls. Fourteen patients and matched controls received a single oral dose of 0.3 mg/kg IPS or placebo under double-blind, random-assignment conditions. IPS induced hypothermia and corticotropin (ACTH)/cortisol release but had only minimal effects on behavior. Compared with controls, the patients with PD exhibited significantly attenuated thermoregulatory and neuroendocrine responses to IPS. Although the healthy subjects reported increased drowsiness and the PD patients rated themselves more nervous and less calm following administration of IPS, no consistent changes in ratings of anxiety or panic symptoms were recorded. The impaired hypothermic and ACTH/cortisol responses following 5-HT1A receptor activation reflects subsensitivity of both the pre- and post-synaptic 5-HT1A receptor-effector system, thus supporting the hypothesis that a 5-HT1A receptor-related serotonergic dysfunction may be linked to the pathophysiology of PD. Future studies of 5-HT1A receptor-effector complex function in conjunction with assessment of the responsivity of other subtypes (e.g. 5-HT2, 5-HT3) should promote the evaluation of 5-HT system integrity in anxiety disorders and its involvement in anxiolytic drug effects.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Overexpression of rho effector rhotekin confers increased survival in gastric adenocarcinoma.

Like many epithelial-derived cancers, gastric cancer (GC) results from a multistep tumorigenic process. However, the detailed mechanisms involved in GC formation are poorly characterized. Using an ordered differential display method, we have identified rhotekin (RTKN), the gene coding for the Rho effector, RTKN, as one of the genes differentially expressed in human GC. Northern analysis using human multiple tissue blots showed that RTKN is predominantly expressed in the kidney and spinal cord, and, to a lesser degree, in the thyroid, tongue, liver, brain, prostate, trachea, and stomach. RT-PCR analysis confirmed that RTKN was overexpressed in most (5/7; 71%) GC examined. By analyzing the Stanford Microarray Database for the expression profiles of gastric tissues, we also found a progressional increase in RTKN expression in nonneoplastic mucosa, GC, and then lymph node metastases (p < 0.005 by Jonckheere-Terpstra test), suggesting that RTKN expression correlates with GC progression. The role of RTKN in the pathogenic development of GC was investigated by transfection and expression of RTKN in AGS gastric cells, which express endogenous RTKN at a low basal level. Flow-cytometric analysis showed that RTKN-transfected AGS cells were significantly more resistant than vector-transfected cells to apoptosis upon treatment with sodium butyrate. To explore the mechanisms underlying RTKN-mediated cell survival, a reporter assay was performed. Since the NF-kappaB activation is known to promote cell survival and Rho GTPase may lead to NF-kappaB activation, we transfected AGS cells with the RTKN expression vector along with a pNF-kappaB-Luc reporter plasmid. Our results showed that overexpression of RTKN induced robust activation of NF-kappaB, and RTKN-mediated NF-kappaB activation was suppressed significantly by C3 transferase, an inhibitor of the small GTPase Rho. We conclude that Rho/RTKN-mediated NF-kappaB activation leading to cell survival may play a key role in gastric tumorigenesis. This study provides original documentation for the overrepresentation of the Rho GTPase effector rhotekin in human cancer and its links to cancer formation.

Adenocarcinoma↗

PubMed1996

Untranslated sequence upstream of MarA in the multiple antibiotic resistance locus of Escherichia coli is related to the effector-binding domain of the XylS transcriptional activator.

MarA, the 129-amino-acid (aa) protein which plays a crucial role in the multiple antibiotic resistance (Mar) phenotype in Escherichia coli, shows homology to members of the XylS/AraC family of transcriptional regulators. Although these proteins vary in size from around 100 to 350 aa they all contain a DNA-binding domain with a helix-turn-helix motif. The larger ones, e.g., XylS, AraC, and Rob, contain an additional domain either at their amino- or at their carboxyterminus. This domain is important for effector-binding or dimerization or of unknown function. MarA consists only of the DNA-binding component. Nevertheless, a sequence with a coding potential of 141 aa upstream of its ATG start-codon showed 20.5-26.9% aa identity with the corresponding section within the effector-binding domain of XylS from the TOL plasmid of Pseudomonas putida when translated in the same reading frame as MarA. However, the reading frame was interrupted by 11 translational stops. In another frame, this upstream sequence actually codes for a real protein, MarR, that is completely unrelated to XylS. Implications for the putative evolution of regulatory proteins through translocation of domains followed by adaptation are discussed.

Amino Acid Sequence↗

PubMed1999

Human CD4+ T cell differentiation and effector function: implications for autoimmunity.

Human CD4+ memory T cells progress through stages of postthymic differentiation that have been characterized by distinct phenotypes. We have investigated the factors regulating cytokine production, and the correlation between phenotype and effector function in normal and autoimmune individuals. These studies suggest that antigen-induced proliferation in the periphery drives CD4+ T cells through successive stages of differentiation that culminate in optimal effector function and resistance to external modulatory influences. Moreover, these studies support the concept that in autoimmune individuals, the chronic accumulation of differentiated proinflammatory T cells perpetuate the inflammatory response resulting in aggressive disease.

Arthritis, Rheumatoid↗

PubMed1997

Effects of lidocaine on cytosolic pH regulation and stimulus-induced effector functions in alveolar macrophages.

Local anesthetics influence a variety of stimulus-induced effector functions in leukocytes. The present study determined the effects of lidocaine on intracellular pH (pHi) regulation, superoxide production, and tumor necrosis factor-alpha (TNF-alpha) release in alveolar macrophages (m phi). Resident m phi were obtained by bronchoalveolar lavage of rabbits. The cells were subjected to an intracellular acid load, and subsequent pHi recovery was followed in the presence or absence of bafilomycin A1, a specific inhibitor of V-type H(+)-translocating ATPase (V-ATPase) or amiloride, an inhibitor of Na+/H+ exchange. Lidocaine slowed pHi recovery in a dose-dependent manner. Pretreatment (1 h) with 2.5 mM lidocaine abolished Na+/H+ exchange and reduced the V-ATPase-mediated component of pHi recovery. Lidocaine also significantly depressed the superoxide production induced by phorbol ester. TNF-alpha release induced by endotoxin was not affected significantly by the local anesthetic. Macrophage viability (trypan blue exclusion) and cellular ATP concentration were unaffected. These results indicate that lidocaine inhibits pHi regulatory mechanisms in alveolar m phi. This disruption of pHi regulation could contribute to inhibitory actions of lidocaine on m phi effector functions.

Acid-Base Equilibrium↗

PubMed1998

Fibroblasts as target and effector cells in Japanese patients with sarcoidosis.

Fibroblasts play a crucial role in progressive lung fibrosis, acting not only as target cells but also as effector cells. To clarify these functions in sarcoidosis, lung fibroblasts from Japanese sarcoid patients were studied for their proliferative capacity and cytokine productivity. Fibroblasts were cultured from transbronchial lung biopsy specimens from seven patients with sarcoidosis. As a comparison, fibroblasts from open lung biopsy specimens of four patients with idiopathic pulmonary fibrosis (IPF) were studied. For controls, fibroblasts were cultured from specimens of normal resected lung tissue of five patients with localized lung cancer. The proliferative activity of cultured fibroblasts from patients with sarcoidosis was highest among the three groups (p < 0.05). However, the proliferative capacity in all groups was suppressed when fibroblasts were cultured with interleukin-1beta (IL-1beta). No significant differences were noted in the degree of inhibition among the three groups. Addition of interferon-gamma (IFN-gamma) also resulted in inhibition of fibroblast growth in all groups, but the degree of inhibition was significantly greater in both the sarcoid and IPF groups than in controls (p < 0.05). The amount of interleukin-6 (IL-6) in the culture supernatants from sarcoid fibroblasts cocultured with IL-1beta was significantly higher than in controls. Sarcoid fibroblasts are not only proliferatively active but also possess effector cell function to produce cytokines. IL-6 may enhance the immunologic reaction to sarcoidosis and cause the disease to become chronic. IFN-gamma suppresses proliferation of sarcoid fibroblasts and may prevent fibrotic changes of the lungs in the Japanese sarcoid patients.

Adult↗

PubMed2006

Anti-tumoral capabilities of effector cells after IFN-alpha or CpG-motif treatment of cocultured dendritic cells.

INTRODUCTION: Ex vivo expansion of monocyte-derived dendritic cells (mDCs) and subsequent coculture with autologous cytokine-induced killer (CIK) cells is an established system to create specific and non-specific anti-tumoral immunity. mDCs constitute the most frequently applied DC subset in clinical studies. One recently published approach to optimize the immunological functions of the DC/CIK cell system is the replacement of interleukin (IL)-4 by interferon (IFN)-alpha in the maturation process of the DCs. MATERIALS AND METHODS: The expressions of relevant surface antigens of IL-4-DCs and IFNalpha-DCs by flow cytometry and the anti-tumoral activation of effector cells cocultured with both types of DCs using cytotoxicity assays were compared. In addition, short-term coculture experiments with both types of DCs and IFNgamma-LAK effector cells were performed and compared with standard CIK cell coculture experiments. RESULTS: Regarding the expressions of functionally relevant surface markers, no differences could be detected for CD80, CD83, and HLA-DR between IFNalpha-DCs and IL-4-DCs, whereas the mean fluorescence intensities of CD40, CD86, CD54, and HLA-ABC were decreased and the expression of CD14 was increased for IFNgamma-DCs. Moreover, no enhancement of cytotoxicity of cocultured CIK cells against tumor cell lines (A498 and SW480) was detected by the use of IFNalpha-DCs. Additionally, coculture experiments with IFNgamma-LAK cells were performed and unexpectedly higher lysis rates in comparison with the established IL-4-DC/CIK coculture model was observed. Early incubation of the mDCs with several CpG-ODNs failed to increase the anti-tumoral cytotoxicity of the cocultured IFNgamma-LAK cells. CONCLUSIONS: These results demonstrate that in the mDC/CIK cell system, IFNalpha-DCs are not superior in inducing anti-tumoral cytotoxicity and even moderately inferior regarding the expression of functionally relevant surface markers compared with IL-4-DCs.

Antigens, Surface↗

PubMed2005

Mucosal effector memory T cells: the other side of the coin.

Immunological memory allows for rapid and effective protective immunity to previously encountered pathogens. New insights in understanding specific memory differentiation and function have now indicated that in addition to providing enhanced immunity, an important purpose of immunological memory is to provide immediate protection at all sites of the body, including non-lymphoid tissues. Effector memory CD8 T cells have the capacity to reside long-term at epithelial surfaces, where they allow for rapid containment of the invading pathogens at the local entry site and prevent systemic spreading and excessive immune responses. The accumulation of tissue-specific memory T cell subsets, together with cross-reactivity of these antigen-experienced T cells even to unrelated pathogens, provides flexibility and expansion of their specificity repertoire that over time greatly surpasses that of the declining naïve T cell populations. This review will discuss new insights into T cell memory. We will focus in particular on the generation and function of effector memory CD8 T cells at the intestinal mucosa, which represents one of the largest entry sites for pathogens.

Animals↗

PubMed2005

Motor variability within a multi-effector system: experimental and analytical studies of multi-finger production of quick force pulses.

The purpose of the study was to develop a model of force variability for a fast action performed by a multi-effector system and to verify it for multi-finger quick force production. The experiments involved quick isometric contractions to different target force levels using different finger combinations. Force variance calculated over sets of trials for a multi-finger force production task showed non-monotonic single-peak profiles of force variance with a peak at a time between the times of the maxima of the force rate and of the total force. When analyzed in the four-dimensional space of finger forces, the variance peak was mostly expressed in the direction of the force rate, and was absent in the directions orthogonal to it. The non-monotonic time profile of the force variance could be reproduced by a model of force production, which assumes that each finger force profile is based on a template function scaled in duration and magnitude with two parameters assigned prior to each trial with some variability. The model allows decomposition of the force variance into two fractions related to variability in setting the magnitude and duration scaling parameters. The former fraction changes monotonically with time, while the latter shows a transient peak in the middle of the action. The model was able to reproduce experimental variance time profiles across conditions with the total error of under 8%. The results demonstrate, in particular, that fast multi-finger actions may show transient changes in motor variability in certain directions of the finger force space, particularly in the direction of the first force derivative, without any task-specific coordinating action by the controller. These findings require a reconsideration of some of the conclusions drawn in recent studies on the structure of motor variability in redundant multi-effector systems.

Adult↗

PubMed2000

Movement-related potentials are task or end-effector dependent: evidence from a multifinger experiment.

In a number of recent studies, the specific sensitivity of movement-related EEG potentials toward experimental manipulations of motor tasks using the index finger as a primary end-effector is well documented. The major question in this study was whether different movement-related EEG components are primarily end-effector or task dependent. Accordingly, the experimental task (i.e., the rate of force development - a ratio of peak force to time-to-peak force) was systematically manipulated and the effects of this manipulation on movement-related potentials were examined while subjects used either the index, middle, ring or little finger. Significant effects observed in this study were due mainly to the sensitivity of movement-related potentials preceding movement onset (Bereit shafts potential and motor potential) toward the specific finger performing the task and the sensitivity of components accompanying the task (movement-monitoring potential) toward the rate of force development. In addition, both movement-related potentials preceding and accompanying movement significantly changed as a function of the finger performing the slow task (lower rate of force development) with maximum values observed for the ring finger and minimal values observed for the index finger. Behaviorally subjects were less accurate during slow tasks regardless of the finger performing the task. In contrast, the amplitude of neither early nor late components of movement-related potentials changed as a function of the finger performing the fast task (higher rate of force development). Overall, our results are consistent with the notion that the whole complex of movement-related EEG potentials reflect a combination of factors including the selection of corresponding general motor programs as reflected in the amplitude of potentials preceding movement and specific elements of the task including rate of force development as reflected in the amplitude of potentials accompanying movement execution.

Adult↗