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PubMed1998

Theoretical note: tests of synergy in sweetener mixtures.

Some methods for examining the additivity of sweeteners, and their synergy in mixtures depend upon setting component concentrations on the basis of sweetness equivalence, usually to a sucrose reference. These methods may under- or over-predict the sweetness of a mixture, leading to spurious claims of synergy or mixture suppression. This paper points out one problem with one such popular method, in that the method can lead to a conclusion that a substance would synergize with itself. To the extent that self-synergy is an illogical conclusion for a mixture comparison, such a method should be avoided in tests of synergy. The sweetness equivalence approach is contrasted with a simpler approach based on concentrations that does not lead to conclusions of self-synergy.

Drug Synergism↗

PubMed1988

Ceftazidime combined with mecillinam: serum bactericidal titres compared with in-vitro synergy against gram-negative bacilli.

In a study of the possible interaction between mecillinam and ceftazidime against Gram-negative bacilli, ten volunteers received on separate days: ceftazidime 20 mg/kg iv in 15 min, mecillinam 10 mg/kg iv in 15 min, or the combination. Blood samples were obtained before and 1 and 6 h after the end of the infusion. Ten strains each of Klebsiella pneumoniae, Serratia marcescens, Citrobacter freundii, Salmonella spp. and Yersinia spp. and nine strains each of Acinetobacter spp., and Pseudomonas aeruginosa were selected. Most of the strains were resistant to ampicillin and cefazolin. Serum levels of ceftazidime and mecillinam were measured by bioassay. Serum bacteriostatic (SBS) and bactericidal (SBA) titration was done in microtitre plates in cation supplemented Mueller-Hinton broth and 50% human serum. Chequerboard titration was also studied to assess in-vitro synergy between ceftazidime and mecillinam in Mueller-Hinton broth with or without 50% serum. The mean serum concentrations (SD) were for mecillinam: 6.1 (1.7) at 1 h, and less than 0.3 at 6 h and for ceftazidime: 36.3 (5.5) at 1 h and less than 5 at 6 h. Identical concentrations were measured for the combination. By chequerboard titration, no synergy occurred for Acinetobacter spp. and Ps. aeruginosa, whereas it was observed in 37/60 (FIC) and 33/60 (FBC) of the strains of other species in Mueller-Hinton; from the strains showing synergy, 28/37 (FIC) and 30/33 (FBC) showed also synergy in Mueller-Hinton with 50% human serum. In SBS and SBA, on the other hand, the combination of mecillinam with ceftazidime showed an additive effect against most Enterobacteriaceae tested, synergy being shown for only 10-35% of tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Amdinocillin↗

PubMed2000

Biochemical characterisation of cap-poly(A) synergy in rabbit reticulocyte lysates: the eIF4G-PABP interaction increases the functional affinity of eIF4E for the capped mRNA 5'-end.

The 5' cap and 3' poly(A) tail of eukaryotic mRNAs cooperate to synergistically stimulate translation initiation in vivo. We recently described mammalian cytoplasmic extracts which, following ultracentrifugation to partially deplete them of ribosomes and associated initiation factors, reproduce cap-poly(A) synergy in vitro. Using these systems, we demonstrate that synergy requires interaction between the poly(A)-binding protein (PABP) and the eukaryotic initiation factor (eIF) 4F holoenzyme complex, which recognises the 5' cap. Here we further characterise the requirements and constraints of cap-poly(A) synergy in reticulocyte lysates by evaluating the effects of different parameters on synergy. The extent of extract depletion and the amounts of different initiation factors in depleted extracts were examined, as well as the effects of varying the concentrations of KCl, MgCl(2) and programming mRNA and of adding a cap analogue. The results presented demonstrate that maximal cap-poly(A) synergy requires: (i) limiting concentrations of ribosome-associated initiation factors; (ii) precise ratios of mRNA to translation machinery (low concentrations of ribosome-associated initiation factors and low, non-saturating mRNA concentrations); (iii) physiological concentrations of added KCl and MgCl(2). Additionally, we show that the eIF4G-PABP interaction on mRNAs which are capped and polyadenylated significantly increases the affinity of eIF4E for the 5' cap.

Animals↗

PubMed1995

Pit-1 binding to specific DNA sites as a monomer or dimer determines gene-specific use of a tyrosine-dependent synergy domain.

Transcriptional activation of the prolactin and growth hormone genes, occurring in a cell-specific fashion, requires short-range synergistic interactions between the pituitary-specific POU domain factor Pit-1 and other transcription factors, particularly nuclear receptors. Unexpectedly, we find that these events involve the gene-specific use of alternative Pit-1 synergy domains. Synergistic activation of the prolactin gene by Pit-1 and the estrogen receptor requires a Pit-1 amino-terminal 25-amino-acid domain that is not required for analogous synergistic activation of the growth hormone promoter. The action of this Pit-1 synergy domain is dependent on the presence of two of three tyrosine residues spaced by 6 amino acids and can be replaced by a comparable tyrosine-dependent trans-activation domain of an unrelated transcription factor (hLEF). The gene-specific utilization of this tyrosine-dependent synergy domain is conferred by specific Pit-1 DNA-binding sites that determine whether Pit-1 binds as a monomer or a dimer. Thus, the critical DNA site in the prolactin enhancer, where this domain is required, binds Pit-1 as a monomer, whereas the Pit-1 sites in the growth hormone gene, which do not utilize this synergy domain, bind Pit-1 as a dimer. The finding that the sequence of specific DNA sites dictates alternative Pit-1 synergy domain utilization based on monomeric or dimeric binding suggests an additional regulatory strategy for differential target gene activation in distinct cell types.

Amino Acid Sequence↗

PubMed2002

alpha(2C)-Adrenergic receptors mediate spinal analgesia and adrenergic-opioid synergy.

The alpha(2A)-adrenergic receptor (AR) subtype mediates antinociception induced by the alpha(2)AR agonists clonidine, dexmedetomidine, norepinephrine, and 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine (UK-14,304) as well as antinociceptive synergy of UK-14,304 with opioid agonists [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin and deltorphin II. Differential localization of alpha(2)-adrenergic (alpha(2A)-, alpha(2B)-(,) alpha(2C)-) and opioid (mu-, delta-, kappa-) subtypes suggests differential involvement of subtype pairs in opioid-adrenergic analgesic synergy. The present study applies a novel imidazoline(1)/alpha(2)-adrenergic receptor analgesic, moxonidine, to test for involvement of alpha(2B)- and alpha(2C)ARs in antinociception and antinociceptive synergy, because spinal antinociceptive activity of moxonidine shows minimal dependence on alpha(2A)AR. Intrathecal administration of moxonidine produced similar (2-3-fold) decreases in both mutant mice with a functional knockout of alpha(2A)AR (D79N-alpha(2A)AR) and alpha(2C)AR knockout (KO) mice. The potency of moxonidine was not altered in alpha(2B)KO mice, indicating that this subtype does not participate in moxonidine-induced spinal antinociception. Moxonidine-mediated antinociception was dose dependently inhibited by the selective alpha(2)-receptor antagonist SK&F 86466 in both D79N-alpha(2A) mice and alpha(2C)KO mice, indicating that alpha(2)AR activation is required in the absence of either alpha(2A)- or alpha(2C)AR. Spinal administration of antisense oligodeoxynucleotides directed against the alpha(2C)AR decreased both alpha(2C)AR immunoreactivity and the antinociceptive potency of moxonidine. Isobolographic analysis demonstrates that moxonidine-deltorphin antinociceptive synergy is present in the D79N-alpha(2A) mice but not in the alpha(2C)AR-KO mice. These results confirm that the alpha(2C)AR subtype contributes to spinal antinociception and synergy with opioids.

Adrenergic alpha-Agonists↗

PubMed2003

Growth and DNA damage-inducible transcription factor 153 mediates apoptosis in response to fenretinide but not synergy between fenretinide and chemotherapeutic drugs in neuroblastoma.

Fenretinide induces apoptosis of neuroblastoma cells in vitro and interacts synergistically with the chemotherapeutic drugs cisplatin and etoposide. The stress-inducible transcription factor known as growth and DNA damage (GADD)-inducible transcription factor 153 is induced in response to fenretinide and in other cell types modulates apoptosis via pro- and antiapoptotic members of the BCL2 family. Because BCL2-family proteins are important in apoptosis induced by chemotherapeutic drugs, GADD153 may be a key mediator of synergy between fenretinide and chemotherapeutic drugs. To investigate this, GADD153 cDNA in sense and antisense orientations was stably transfected into SH-SY5Y neuroblastoma cells using a tetracycline-inducible vector. Increased expression of GADD153 raised the background level of apoptosis and increased apoptosis induced by fenretinide or the chemotherapeutic drugs cisplatin and etoposide. However, there was no increase in synergy between fenretinide and chemotherapeutic drugs. Conversely, expression of antisense-GADD153 virtually abolished the induction of apoptosis in response to fenretinide but overall had no significant effect on apoptosis induced by chemotherapeutic drugs. The effect of antisense-GADD153 on synergy between chemotherapeutic drugs and fenretinide varied with the drug used: there was no effect on synergy between fenretinide and cisplatin, but the combination of fenretinide with etoposide became antagonistic. These results suggest that mechanisms mediating synergy between fenretinide and chemotherapeutic drugs lie upstream of GADD153.

Antineoplastic Agents↗

PubMed1976

Synergy of mecillinam, a beta-amidinopenicillanic acid derivative, combined with beta-lactam antibiotics.

Mecillinam, a beta-amidinopenicillanic acid derivative, was combined with ampicillin, amoxicillin, carbenicillin, cephalothin, cefamandole, and cefoxitin and tested against most members of the Enterobacteriaceae and Pseudomonas. Synergy was demonstrated with selected isolates of most of the organisms tested. Isolates highly susceptible to mecillinam (minimum inhibitory concentration, <0.8 mug/ml) were not synergistically inhibited by addition of another beta-lactam antibiotic. Synergy of mecillinam and a beta-lactamase-resistant penicillin, cloxacillin, was demonstrated. In media of osmolality >10 mOsm or of conductivity >6 mS, mecillinam and beta-lactam antibiotics showed synergy in most instances, whereas at low osmolality and conductivity the activity of mecillinam is so great that synergy cannot be demonstrated. The proportion of mecillinam to beta-lactam antibiotic that will be synergistic ranged from 100:1 to 1:1 to 1:100. Mecillinam did not increase the activity, minimum inhibitory concentration or minimum bactericidal concentration values, of beta-lactam compounds against streptococci, staphylococci, clostridia, listeria, or bacteroides. Synergy was not demonstrated with combinations of mecillinam and aminoglycosides (kanamycin, gentamicin, tobramycin, amikacin), chloramphenicol, tetracycline, or polymyxins.

Azepines↗

PubMed1992

Synergy of itraconazole with macrophages in killing Blastomyces dermatitidis.

We examined in vitro interaction between the azole antifungal agents itraconazole and ketoconazole and macrophages and their activities against Blastomyces dermatitidis. Fungistatic and fungicidal concentrations for B. dermatitidis in vitro were assessed in a microculture system in which fungistasis was measured as inhibition of multiplication and fungicidal activity was measured as reduction of inoculum CFU. Resident peritoneal murine macrophages, which surround but do not phagocytize the fungus, were not fungicidal for B. dermatitidis isolates but were fungistatic for some isolates studied. Synergy was demonstrated when fungistatic concentrations (e.g., 0.01 micrograms/ml) of itraconazole, which limited growth 55% compared with that of controls, were cocultured with macrophages; this resulted in fungicidal activity (85% killing) against B. dermatitidis (ATCC 26199) in 72-h assays. This synergy could occur even if itraconazole was added after the macrophages had surrounded the fungus. Ketoconazole at fungistatic concentrations did not act synergistically with macrophages to kill B. dermatitidis. Lymph node lymphocytes could not substitute for macrophages in synergy with itraconazole to kill B. dermatitidis. When B. dermatitidis was separated by a filter from macrophages in Transwell cultures, fungicidal synergy with itraconazole was less efficient. Pretreatment of B. dermatitidis with itraconazole for 24 h did not render the fungus susceptible to killing by macrophages in the absence of itraconazole, whereas pretreatment of nonfungistatic macrophages with itraconazole rendered them fungistatic in a dose-dependent manner. Three other isolates were killed by otherwise fungistatic concentrations of itraconazole when the isolates were cocultured with macrophages. These findings indicate that one basis for the efficacy of itraconazole versus ketoconazole in treating blastomycosis could be synergy of a fungistatic concentration of itraconazole with macrophages in killing of B. dermatitidis.

Animals↗

PubMed1996

In vitro synergy testing of macrolide-quinolone combinations against 41 clinical isolates of Legionella.

Combination antimicrobial therapy against Legionella species has not been well studied. Several quinolones have activity against Legionella strains, which prompted this in vitro search for a synergistic combination with the macrolides. By a checkerboard assay, erythromycin, clarithromycin, and azithromycin, each in combination with ciprofloxacin and levofloxacin, were tested for synergy against 46 isolates of Legionella. The agar dilution method was employed using buffered charcoal-yeast extract media. A final inoculum of 10(4) CFU per spot was prepared from 24-h growth of each isolate. Plates were incubated at 35 degrees C for 48 h. Synergy, partial synergy, additive effect, or indifference was observed for all combinations of antibiotics tested. There was no antagonism observed. Synergy occurred to a significantly greater extent for the clarithromycin-levofloxacin (P = 0.0001) and azithromycin-levofloxacin (P = 0.003) combinations versus erythromycin-levofloxacin. The azithromycin-ciprofloxacin combination demonstrated significantly greater synergy than did either erythromycin-ciprofloxacin (P = 0.003) or clarithromycin-ciprofloxacin (P = 0.001). The newer macrolides clarithromycin and azithromycin may be more active in combination with a fluoroquinolone than is erythromycin.

Anti-Bacterial Agents↗

PubMed1988

High-content aminoglycoside disks for determining aminoglycoside-penicillin synergy against Enterococcus faecalis.

We investigated the use of high-content aminoglycoside disks for determining Enterococcus faecalis susceptibility to aminoglycoside-penicillin synergy. The susceptibility of the organisms to synergy was established by 24-h time-kill studies performed with streptomycin, kanamycin, amikacin, gentamicin, and tobramycin, alone and in combination with penicillin. A total of 20 isolates that were susceptible to all drug combinations and 20 strains that were resistant to each aminoglycoside-penicillin combination were selected for testing against high-content disks. Disk-agar diffusion was performed on Mueller-Hinton agar, with and without 5% sheep blood, by using disks that contained either 300 or 2,000 micrograms of streptomycin and either 120 or 2,000 micrograms of kanamycin, amikacin, tobramycin, or gentamicin. Zone size results obtained for each aminoglycoside, except amikacin, could be used to differentiate between synergy-susceptible and -resistant isolates. No overlap occurred between the zone sizes of susceptible and resistant strains. Susceptibility to amikacin-penicillin synergy could reliably be tested with kanamycin, but not amikacin, disks. When the disks containing 120 micrograms were tested, a narrow zone size range of 6 to 7 mm could be used to identify all resistant strains. In contrast, when the disks containing 2,000 micrograms were used, the zone size ranges for resistant isolates varied widely with the aminoglycoside being tested. The presence of blood in the medium did not appreciably affect the disk test results. To detect resistance to every aminoglycoside-penicillin combination that may be considered for therapy, E. faecalis isolates need to be tested against a maximum of three different high-content disks (i.e., streptomycin, gentamicin, kanamycin). The disk-agar diffusion test performed with high-content aminoglycoside disks can provide laboratories with a convenient and reliable method for detecting E. faecalis isolates that are resistant to aminoglycoside-penicillin synergy.

Amikacin↗

PubMed1994

HLA class I heavy-chain gene promoter elements mediating synergy between tumor necrosis factor and interferons.

The cytokines tumor necrosis factor (TNF), beta interferon (IFN-beta), and IFN-gamma increase major histocompatibility complex class I molecule expression. A greater than additive (i.e., synergistic) induction of class I heavy-chain mRNA is observed in HeLa cells treated with TNF in combination with either type of IFN. To define the cis-acting elements mediating cytokine synergy, the promoter of a human major histocompatibility complex class I heavy-chain gene (HLA-B7) was placed in front of a reporter gene and transfected into HeLa cells. Deletion analysis mapped the elements required for synergy to a 40-bp region containing a kappa B-like element, which is necessary for the response to TNF, and an interferon consensus sequence (ICS), which is necessary for the responses to IFNs. When the orientation of these elements was reversed or their normal 20-bp spacing was reduced by 5 or 10 bp, i.e., one half or one full turn of the DNA helix, essentially equivalent responses were obtained, suggesting that these parameters are not critical. In electromobility shift assays, a p50-containing NF-kappa B nuclear factor from TNF-treated cells binds kappa B-containing probes, and ISGF-2 from IFN-gamma-treated cells binds ICS-containing probes. A probe containing both the kappa B and ICS elements (kappa B-ICS) forms a novel complex with nuclear factors isolated from cells treated with both TNF and IFN-gamma; this complex also forms when nuclear factors from individually cytokine-treated cells are mixed in vitro. The natural variant ICS found in HLA-A responds to IFN-gamma and can mediate synergy with TNF. However, the variant kappa B found in HLA-C does not respond to TNF, nor can it mediate synergy between TNF and IFN-gamma. These observations suggest that synergy between TNF and IFNs in the induction of HLA class I gene expression results from the sum of individual interactions of cytokine-activated enhancer-binding factors with the transcription initiation complex.

Base Sequence↗

PubMed1988

The spectrum of Escherichia coli--Bacteroides fragilis pathogenic synergy in an intraabdominal infection model.

Pathogenic synergy between Escherichia coli and Bacteroides fragilis was investigated in an intraabdominal infection model. Defined inocula of E. coli and B. fragilis, alone or in combination, were enmeshed within a fibrin clot and surgically implanted into the peritoneal cavity of rats. A spectrum of bacterial synergy ranging from synergistic abscess formation to synergistic lethality was demonstrated using this model. The type of synergy exhibited was dependent upon the initial E. coli inoculum. When combined with B. fragilis, high inocula of E. coli (greater than 10(8) cfu/clot) produced synergistic lethality while low inocula (2 x 10(2) to 2 x 10(7) cfu/clot) resulted in synergistic abscess formation. With respect to abscess formation, there was reciprocal synergy between E. coli and B. fragilis. Abscesses resulting from mixed inocula were larger and had significantly higher numbers of E. coli and B. fragilis than abscesses initiated by monomicrobial inocula. These studies define a clinically relevant model of bacterial interactions in the setting of intraabdominal infection and suggest that conclusions drawn from experimental models of bacterial synergy should consider the type of model examined, the strains of bacteria studied, and the number of bacteria inoculated.

Abscess↗

PubMed2006

Control of fast-reaching movements by muscle synergy combinations.

How the CNS selects the appropriate muscle patterns to achieve a behavioral goal is an open question. To gain insight into this process, we characterized the spatiotemporal organization of the muscle patterns for fast-reaching movements. We recorded electromyographic activity from up to 19 shoulder and arm muscles during point-to-point movements between a central location and 8 peripheral targets in each of 2 vertical planes. We used an optimization algorithm to identify a set of time-varying muscle synergies, i.e., the coordinated activations of groups of muscles with specific time-varying profiles. For each one of nine subjects, we extracted four or five synergies whose combinations, after scaling in amplitude and shifting in time each synergy independently for each movement condition, explained 73-82% of the data variation. We then tested whether these synergies could reconstruct the muscle patterns for point-to-point movements with different loads or forearm postures and for reversal and via-point movements. We found that reconstruction accuracy remained high, indicating generalization across these conditions. Finally, the synergy amplitude coefficients were directionally tuned according to a cosine function with a preferred direction that showed a smaller variability with changes of load, posture, and endpoint than the preferred direction of individual muscles. Thus the complex spatiotemporal characteristics of the muscles patterns for reaching were captured by the combinations of a small number of components, suggesting that the mechanisms involved in the generation of the muscle patterns exploit this low dimensionality to simplify control.

Adult↗

PubMed2006

Synergies in health and disease: relations to adaptive changes in motor coordination.

This article describes an approach to motor synergies that allows them to be quantified in people with atypical movement patterns during exercise or practice. Within this approach, motor variability may be classified with respect to a task-specific performance variable as "good" (not affecting the variable) or "bad" (changing the variable). The authors review studies of motor synergies in people with typical movement patterns, in people with Down syndrome, in patients after stroke, and in elderly people. Two stages of practice effects on motor synergies are described as being characterized by different changes in the synergy index: an increase followed by a drop in the index. Synergy changes with practice may be accompanied by plastic changes in both descending projections from the primary cortex and interhemispheric projections. The authors emphasize the importance--for practitioners in the area of motor disorders and rehabilitation--of being aware of the latest progress in motor control and coordination.

Adaptation, Physiological↗

PubMed1989

Sequence and schedule-dependent synergy of trimetrexate in combination with 5-fluorouracil in vitro and in mice.

The purpose of this study was to determine the conditions for optimum synergistic efficacy of the two-drug combination of trimetrexate and 5-fluorouracil. Synergistic cell killing of Chinese hamster ovary cells in these clonogenic survival assays was observed only when the cells had been exposed to trimetrexate (25 microM) for 2 to 4 h prior to 5-fluorouracil exposure (either 125 or 250 microM). The schedule dependence of the observed synergy in vitro was closely linked to trimetrexate-induced changes in cellular 5-phosphoribosyl 1-pyrophosphate (PRPP) pools. Exposure to 25 microM trimetrexate induced increases in PRPP pools to 398% and 761% of control values at 2 and 4 h, respectively. Methotrexate (20 microM) also increased Chinese hamster ovary cell PRPP content in a time-dependent fashion to values of 280 and 511% of control after 2 and 4 h of drug exposure. Previous in vivo studies demonstrated a modest degree of therapeutic synergy between trimetrexate and 5-fluorouracil against P388 leukemia. Our in vitro results suggested that the degree of synergy seen in vivo could be increased with appropriate schedule changes. Mice were implanted i.p. with 10(6) P388 leukemia cells on Day 0 and were treated with trimetrexate (every 3 h for eight injections; Days 1, 5, and 9) and 5-fluorouracil (Days 1, 5, and 9) as single agents or in combination on one of two schedules; 5-fluorouracil was administered with either the first or the last of the eight trimetrexate doses on Days 1, 5, and 9. Both treatment regimens demonstrated therapeutic synergy but, as predicted from the in vitro data, the "5-fluorouracil last" was superior to the "5-fluorouracil first" sequence. Treatment with the optimal doses on the "5-fluorouracil last" sequence (trimetrexate, 31; 5-fluorouracil, 33 mg/kg/injection) produced an increased life span of 183% and a net reduction in tumor cell burden of 6.7 logs compared with a 111% increased life span (net reduction in tumor burden of 2.6 logs) produced by the most active of the single agents, 5-fluorouracil. Thus the efficacy of the combination of trimetrexate with 5-fluorouracil was sequence and time dependent both in vitro and in vivo. The synergy, observed in vitro and probably in vivo, was linked to a trimetrexate-induced elevation of intracellular PRPP, thus facilitating the production of 5-fluoropyrimidine nucleotides. These data are similar to the sequence and schedule dependency of the methotrexate/5-fluorouracil combination with important differences.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Synergy of tumor necrosis factor and interleukin 2 in the activation of human cytotoxic lymphocytes: effect of tumor necrosis factor alpha and interleukin 2 in the generation of human lymphokine-activated killer cell cytotoxicity.

Human lymphocytes can respond to interleukin 2 (IL-2) under serum-free conditions with generation of major histocompatibility locus-unrestricted oncolytic activity. This function has been named lymphokine activated killing (LAK). Although IL-2 is sufficient for the development of LAK, this function can be regulated positively by the addition of tumor necrosis factor alpha or beta (TNF-alpha or -beta). The cytotoxic synergy observed with TNF enables production of optimal LAK function at a 10-fold lower IL-2 concentration. Neither TNF-alpha nor -beta is able to induce LAK function in the absence of IL-2. Using TNF-alpha as a model, we demonstrate that (a) the cytotoxic synergy occurs with both fresh human tumors and cell lines; (b) the degree of IL-2/TNF-alpha synergy, for most peripheral blood lymphocyte donors, is dependent upon the IL-2 concentration used for activation with the most striking synergy observed at lower IL-2 doses; (c) synergy is specific for TNF-alpha and can be abrogated by neutralizing antibody against this cytokine; (d) addition of high-dose neutralizing antibody to IL-2 alone-stimulated peripheral blood lymphocytes can reduce the cytotoxicity capacity of these effectors suggesting an immunoregulatory role for endogenous TNF-alpha; and (e) TNF-alpha addition to IL-2-stimulated peripheral blood lymphocytes does not increase proliferation or cell recovery but does result in enhanced IL-2 receptor expression. Collectively, our results suggest that TNF-alpha (and -beta) have immunopotentiating roles in the amplification of non-major histocompatibility locus-restricted lymphocyte effector function.

Cell Line↗

PubMed1986

Muscular synergies during different conditions of postural activity.

With the view to studying the muscular synergies in maintaining of upright posture EMG activity of soleus (SOL), tibialis anterior (TA), peroneus longus (PL), biceps femoris (BF), vastus lateralis (VL) and gluteus medius (GM) muscles during easy standing, voluntary leaning and induced body oscillations in frontal and sagital plane were recorded. The data showed that during easy standing and during small external disturbances the vertical posture was maintained mainly by the activity of SOL (triceps surae muscle) which was modulated by the modification of the external force field. TA remained silent. PL muscle was slightly active as a synergist of SOL. The pattern of muscular synergies during fast voluntary leaning and induced body oscillations differed as compared to the muscular synergies at easy standing. The activity of all muscles studied increased and became continuous with exception of that of the TA. The latter was silent but was involved earlier when gravity center passed behind its projection. VL being a synergist of TA during slow sway became continuously active as a synergist of SOL during the fast sway. Typical changes in muscular synergies appeared when induced body oscillations were imposed during horizontal and rotational movements of the platform. The various patterns of muscular synergies during pronation and supination of the foot depended on the knee joint angle. The amplitude of body leaning forward and backward and its variability as well as the plane of the lateral sway depended on the biomechanical variables and related motor programs for postural control.

Electromyography↗

PubMed1987

Electromyographic gait assessment, Part 2: Preliminary assessment of hemiparetic synergy patterns.

The electromyographic (EMG) gait patterns of both lower limbs in 12 hemiparetic patients were studied during the early and late recovery periods. The linear envelopes of surface EMG were ensemble averaged to represent performance. The patients' stride parameters and EMG envelopes were compared to those of normal individuals measured at very-slow walking speeds. Both limbs could have normal or abnormal synergies. The abnormal synergy exhibited by the contralateral limb was almost always a cocontraction. Three different groups of synergies were defined depending on the change in synergy type exhibited by the contralateral limb. Patients who walked at less than a normal very-slow speed during the early recovery period never achieved a normal synergy in either limb. Seventy-five percent of the patients whose walking speed was at least 0.6 meters per second during the early recovery period improved or maintained their gait performance for at least one year.

Cerebrovascular Disorders↗