Search

Purpose: To define based on expert opinion and practical experience using a systematic and scientific approach, (1) the perceived most effective exercise-based strategies to prevent muscle injury in elite footballers; and, (2) when and how these exercise programs are prescribed based on the number of days between games i.e. implementation strategy. Methods: A Delphi survey obtained opinions and assessed for agreement. Delphi respondents consisted of 21 experienced sports practitioners (12 ± 5.3 years in elite football and with an academic background) belonging to 18 teams from the Big-5 European football leagues; England, France, Germany, Italy, Spain. Three teams were represented collaboratively by two experts. The Delphi process involves sequential rounds each evolving based on the responses from the previous. The number of rounds is not pre-defined and continues until an agreement is either achieved or it is clear that no agreement will be reached. Frequency of responses was recorded where the agreement was sought (i.e. in closed questions) and an agreement was achieved if ≥ 13/18 (70%) respondents agreed. For open-ended questions, a qualitative content analysis was performed to identify recurring themes and when themes were specified by ≥ 13 (70%), these were also considered as reaching an agreement. Practitioners had the opportunity to raise concerns if they disagreed with the 'agreement from recurrent themes'. Results: There were four Delphi rounds (100% response for each round). Sprinting and High-Speed Running (HSR) focused exercises were agreed as most effective (perceived) to prevent muscle injuries. Eccentric exercise was perceived as the next most effective. It was agreed that sprinting and HSR be integrated into coaches training, and target 100% of players worst-case match scenario (e.g. volume, intensity) based on individual maximum speeds. Eccentric exercise was recommended to be implemented according to the context of the main football session and planned/actual sprinting and HSR content. It was agreed that eccentrics can be performed before or after training, context dependent. The day to perform specific sprinting and HSR or eccentric exercises depended on the proximity of previous and upcoming matches. Other exercises reaching agreement as 'somewhat effective' included concentric and isometric, horizontal and vertical plyometrics, coordination, core and dynamic flexibility in addition to core stability. No agreement was reached for multi-joint, resisted sprinting, kicking or agility exercises nor simultaneous single-leg strength and stability. Finally, no agreement was reached regarding programming variables e.g. sets, repetitions as deemed too contextual. Conclusion: Regarding exercise-based strategies, particular importance agreed by the Delphi expert group was to focus on sprinting, HSR and eccentric exercises, integrated with a variety of other exercise modes which also carry some level of effectiveness in a multidimensional programme. Context was agreed to be key and decision-making about when to undertake/ how to prescribe exercise strategies to be made according to the content of normal football training and the proximity of matches. [ABSTRACT FROM AUTHOR]

The purpose of this study was to explore the potential modulation of equine neutrophil oxidative burst by a series of classical NSAIDs which was subsequently monitored by the luminol or lucigenin-enhanced chemiluminescence (CL) technique. A significant dose-dependent inhibition of the luminol CL was observed with the majority of investigated drugs. This inhibition was very significant for phenylbutazone and Indomethacin; while for aspirin, a higher concentration is required. The action of Ketoprofen was significant during the first 5 min and only when the concentration was above 1 mM. Indomethacin and acetylsalicylic acid result in an inhibition dose-dependent of luminol CL. On the other hand, the phenylbutazone showed an inhibiting effect when used either luminol or lucigenin though luminol is slightly better. When the ketoprofen is considered, an inhibiting effect of luminal CL was observed but less significant than the other NSAIDs investigated. The flunixin meglumine enhances strongly the CL. [ABSTRACT FROM AUTHOR]

We introduce quantized Chebyshev polynomials as deformations of generalized Chebyshev polynomials previously introduced by the author in the context of acyclic coefficient-free cluster algebras. We prove that these quantized polynomials arise in cluster algebras with principal coefficients associated to acyclic quivers of infinite representation types and equioriented Dynkin quivers of type $\mathbb{A}$ . We also study their interactions with bases and especially canonically positive bases in affine cluster algebras. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the mechanisms of action underlying the anti-inflammatory action of aceclofenac in vivo, we studied in vitro the effect of aceclofenac and its main metabolite, 4′-hydroxyaceclofenac, in comparison with diclofenac, another metabolite, on cyclooxygenases activity as well as interleukin-1 β, -6 and -8, nitric oxide, and prostaglandin E2 production by human osteoarthritic and normal articular chondrocytes. Methods: Enzymatically isolated human chondrocytes were cultured for 72 h in the absence or presence of interleukin-1 β (IL-1 β) or lipopolysacharride (LPS) and with or without increased amounts (1 to 30 μM) of aceclofenac or metabolites. The production of different cytokines was measured by Enzyme Amplified Sensitivity Immunoassays (EASIA). Prostaglandin E2 was quantified by a specific radioimmunoassay. Nitrite and nitrate concentrations in the culture supernatants were determined by spectrophotometric method based upon the Griess reaction. Cyclooxygenase-2, inducible NO synthase and IL-1 β gene expression were quantified by reverse transcription of mRNA followed by real time and quantitative polymerase chain reaction. Finally, cyclooxygenase inhibitory potency of the drugs was also tested in both a cell-free system using purified ovine cyclooxygenase-1 and -2 (COX-1 and COX-2) and at a cellular level using human whole blood assay. Results: We have demonstrated that aceclofenac, 4′-hydroxyaceclofenac and diclofenac significantly decreased interleukin-6 production at concentrations ranged among 1 to 30 μM and fully blocked prostaglandin E2 synthesis by IL-1 β- or LPS-stimulated human chondrocytes. Aceclofenac and diclofenac had no effect on interleukin-8 production while 4′-hydroxyaceclofenac slightly decreased this parameter at the highest dose (30 μM). Aceclofenac was without effect on IL-1 β- or LPS-stimulated nitric oxide production. At 30 μM, 4′-hydroxyaceclofenac inhibited both IL-1 β or LPS-stimulated nitric oxide production while diclofenac inhibited only the LPS-stimulated production. Finally, at 30 μM, the three drugs significantly decreased IL-1 β mRNA. In the whole blood test, aceclofenac and 4′-hydroxyaceclofenac weakly inhibited COX-1 with IC50 values superior to 100 μM, but decreased by 50% COX-2 activity at the concentration of 0.77 and 36 μM, respectively. Diclofenac strongly inhibited both COX-1 and COX-2 with IC50 values of 0.6 and 0.04 μM, respectively. On the other hand, aceclofenac and diclofenac weakly inhibited purified ovine cyclooxygenases with IC50 values superior to 100 μM, whereas 4′-hydroxyaceclofenac was without effect. Conclusions: These results suggest that aceclofenac actions are multifactorial and that metabolites could contribute to its anti-inflammatory actions. [ABSTRACT FROM AUTHOR]

Objective and Design: Because high concentrations of histamine are locally released in inflammation, we investigated the effects of supraphysiological doses of histamine on the production of reactive oxygen species (ROS) by neutrophils. ¶ Materials and Methods: Isolated equine neutrophils were activated by 10-4 to 5 × 10-3 M histamine. The production of ROS and free radicals was estimated by luminol-enhanced chemiluminescence (CL) and electron spin resonance (ESR) with spin trapping technique. In this model of histamine-stimulated neutrophils, we tested the antagonists of H1 and H2 histamine receptors, the role of Ca2+ and Mg2+, the role of staurosporine and pertussis toxin (inhibitors of protein kinase C and proteins G) and the effects of superoxide dismutase, catalase, hydroxyl radical scavengers (phenylalanine and mannitol) and NG-monomethyl-L-arginine (L-NMMA), inhibitor of NO-synthase. ¶ Results: Histamine (from 10-5 to 10-3 M) stimulated neutrophils to produce CL and ESR signals characterized by spin adducts of superoxide anion and/or hydroxyl radicals. The CL response was inhibited by 10-4 and 10-3 M H1 receptor antagonists (promethazine, pyrilamine, and diphenhydramine), by Ca2+ and Mg2+ depletion and by 10 nmoles staurosporine. CL was partially inhibited by pertussis toxin (4 μg/ mL). The ESR signals were practically suppressed by pyrilamine (an H1 receptor antagonist) and superoxide dismutase, and partially inhibited by catalase, hydroxyl radical scavengers and L-NMMA (respectively 59, ± 30% and 68% inhibition). ¶ Conclusions: High concentrations of histamine stimulated the neutrophils to product ROS and free radicals via H1 receptors and the NADPH-oxidase pathway. [ABSTRACT FROM AUTHOR]

Copyright of Intensivmedizin und Notfallmedizin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Arachidonic acid cyclooxygenase metabolites, thromboxane B (TXB), prostaglandin E (PGE) and 6-keto-prostaglandin F (6-keto-PGF) were measured in horses where anaesthesia was maintained with halothane. Two horses suffering from postanaesthetic myositis were compared with four normal horses. TXB and PGE levels were higher in mixed venous blood drawn from the myopathic horses. An increase of TXB and PGE levels appeared when myopathic horses were rolled into dorsal recumbency after a prolonged period of lateral recumbency. One hour after the end of anaesthesia, TXB had continued to increase whereas PGE decreased. By measurements on blood samples drawn from the brachial vein, we have shown that the rising level of TXB in mixed venous blood is mainly due to the increase of TXB in blood draining the dependent leg. The origin of the rise in PGE is not demonstrated in this study. 6-keto-PGF did not change during anaesthesia. An explanation of this imbalance between TXB and 6-keto-PGF production is considered. [ABSTRACT FROM AUTHOR]

In order to obtain a radioimmunoassay (RIA) technique for the measurement of human plasma myeloperoxidase (MPO), we purified the enzyme from polymorphonuclear granulocytes (neutrophils), and compared three methods of labeling it withIodine: chloramine T, lactoperoxidase, and an original technique of 'self labeling' based on the ability of the enzyme to oxidize and bindI in the presence of HO. The chloramine T technique produced a degraded protein, as well shown by a high non-specific binding of tracer to antibody. The lactoperoxidase technique did not succeed in labeling MPO with an adequate specific activity. In contrast, the self-labeling method gave a stable tracer with a specific activity of 23 μCi/gmg MPO (85 MBq), a satisfactory level of immunoreactivity, and a low-specific binding (≤3%). After labeling, purification of tracer was achieved by gel filtration chromatography in phosphate buffer (0.05 M; pH7) to which 0.1% poly-L-lysine was added. The labeled molecule remained stable for 40 days and could be used for RIA with a polyclonal antibody raised in rabbits. [ABSTRACT FROM AUTHOR]

An increasing body of data suggest that strenuous exercise triggers an inflammatory response having some similarity with those occurring in sepsis. Indices of this inflammatory response to exercise (IRE) especially include leukocytosis, release of inflammatory mediators and acute phase reactants, tissue damage, priming of various white blood cell lines, production of free radicals; activation of complement, coagulation and fibrinolytic cascades. Inflammatory responses to strenuous exercise and sepsis could in part be due to the release of endotoxin in blood as common triggering factor, but it seems that tissue damage and/or contact system activation are more important triggering mechanisms in exercising subjects. While the magnitude and duration of cellular and humoral changes associated with IRE are quite different from those observed in sepsis, recent human studies suggested that chronic and/or excessive IRE could have adverse effects. Among the possible consequences of acute and chronic IRE are delayed onset muscular soreness and loss of force, cardiovascular complications, intravascular hemolysis, hypoferraemia and increased susceptibility to infection. [ABSTRACT FROM AUTHOR]

Thoracic duct drainage (TDD) may be of value for removing toxic substances released by the inflamed pancreas and which are responsible for lung damage. We have prospectively assessed the efficacy of TDD in improving pulmonary gas exchange in 12 patients with severe acute pancreatitis (SAP) complicated by persistent respiratory failure despite standard conservative treatment including peritoneal dialysis in 8 patients. In group A were 6 patients (mean Ranson score = 7.3) with adult respiratory distress syndrome (ARDS) and in group B were 6 hypoxemic patients (mean Ranson score = 6.6) judged to be at risk of developing ARDS. The duration of TDD ranged from 3 to 10 days and the total amount of drained lymph (L) varied from 770 to 15,600 ml. Immunoreactive trypsin levels were significantly higher in L when compared to blood in both groups. Leukocyte myeloperoxidases in L (normal value less than than 332 +/- 82 ng/ml in plasma) were increased in 5 of 5 group A patients (830 +/- 317 ng/ml) and in 3 of 6 patients in group B (671 +/- 467 ng/ml). After TDD pulmonary gas exchange as measured by median PaO2/FiO2 (mmHg) improved from 148 +/- 60 to 285 +/- 42 in group A and from 192 +/- 37 to 330 +/- 42 in group B (p less than 0.05). All patients were weaned after ventilation for a mean of 8 days in group A and 4 days in group B. All patients survived apart from 1 group B patient who died of sepsis on day 34.(ABSTRACT TRUNCATED AT 250 WORDS) [ABSTRACT FROM AUTHOR]

Plasma thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured in 84 patients at risk of developing adult respiratory distress syndrome (ARDS) (44 patients following multiple trauma, 29 patients following abdominal surgery and 11 patients with acute pancreatitis). Forty-nine of these 84 patients developed an ARDS. High (greater than 140 pg/ml plasma) TXB2 values were found in 52/84 patients. The median values of TXB2 were: 360 pg/ml in multiple injured, 250 pg/ml in abdominal surgery and 410 pg/ml in acute pancreatitis patients. The median TXB2 value was 575 pg/ml in patients developing ARDS and 140 pg/ml in those without this complication: this difference was statistically significant (p less than 0.05). The median values of 6-keto-PGF1 alpha were 55 pg/ml in multiple injured, 25 pg/ml in abdominal surgery and 120 pg/ml in acute pancreatitis patients. The median 6-keto-PGF1 alpha value was 122 pg/ml in ARDS patients and 25 pg/ml in non-ARDS patients (statistically significant: p less than 0.05). High TXB2 and 6-keto-PGF1 alpha values were particularly related to sepsis in abdominal surgery patients (p less than 0.05) and in multiple injured patients (p less than 0.01). No relation could be established between abnormal TXB2 or 6-keto-PGF1 alpha values and death. High TXB2 values often persisted for several days and were observed particularly at the time ARDS diagnostic criteria were fulfilled.(ABSTRACT TRUNCATED AT 250 WORDS) [ABSTRACT FROM AUTHOR]

With the purpose of studying the role of proteinases in the development of ARDS, plasma levels of immunoreactive trypsin (IRT) and amylase were measured in 43 intensive care patients at risk of developing ARDS (22 polytrauma, seven abdominal surgery, four burns, two DIC and eight pancreatitis). Twenty four of these 43 patients developed ARDS and 31 presented abnormal IRT values (above 70 micrograms/L). Twenty-one of these 31 patients had ARDS; a significant correlation thus appeared between ARDS and abnormal IRT values. In nine patients, IRT values were higher than 800 micrograms/L and remained high for 3 to 4 days. A statistically significant correlation also appeared between abnormal IRT and septic phenomena: 20 patients with high IRT values presented septic problems. When IRT values were high, amylase values were often also abnormal: 12 of 23 patients with high IRT had abnormal amylase levels (the eight patients with documented pancreatitis were excluded); no other clinical signs or symptoms of pancreatitis were present in these patients. IRT could be one of the mediators of ARDS in septic patients. It is not clear that the pancreas is the origin of IRT in all cases. [ABSTRACT FROM AUTHOR]

Divergent results have been reported on the effects of lipopolysaccharides (LPS) on the activation of equine polymorphonuclear leukocytes (PMN). We therefore attempted to determine whether LPS alone can stimulate equine PMN or whether plasma factors are necessary. PMN were isolated from citrated blood on a discontinuous density gradient of Percoll. The luminol (10-3 mol/L)-enhanced chemiluminescence (CL) of 1.25 x 106 cells was measured after addition of Escherichia coli LPS (0.001-10 µg/ml) alone or after incubation in autologous plasma (1 h, 37°C). After direct stimulation with LPS, there were random variations of CL in 16 horses that were not reproducible from one sample to the next for the same horse. LPS which had been incubated in plasma gave a dose-dependent stimulation of the CL of the PMN, which did not occur if the plasma had been heat inactivated (1 h, 56°C). These results indicated a role for plasma factors, which were unlikely to be cytokines, as there were no monocytes or lymphocytes in the plasma incubated with LPS, but might have been complement fragments or LPS ligands, such as LPS binding protein. Studies using specific antibodies against these factors are needed to clarify this question. [ABSTRACT FROM AUTHOR]

The mechanism of ascorbate oxidation by metal-binding proteins (ceruloplasmin, albumin and transferrin) was investigated in vitro and in isolated plasma by the measurement of the ascorbyl free radicals (AFR) by electron spin resonance (ESR). In plasma of 13 healthy volunteers, a spontaneous and variable pro-duction of AFR was detected, which was increased by a 10 M ascorbate overloading; however, this increase was not correlated to the intensity of the spontaneous AFR signal. The addition of Cu and ceruloplasmin to plasma increased the ESR signal, while the addition of transferrin decreased the signal intensity in a dose-dependent manner. In vitro, we demonstrated that ascorbate was oxidized by human serum albumin and by ceruloplasmin, and that this oxidase-like activity was lost by trypsin or heat treatment of these proteins. These two proteins positively interacted in the oxidation of ascorbate, since addition of crude albumin to a solution of ascorbate and ceruloplasmin increased the intensity of ESR signal in a dose-dependent manner. The treatment of albumin by a metal chelator (DDTC) abolished these positive inter-actions. The respective roles of copper and iron in ascorbate oxidation were studied and showed a dose-dependent effect of these ions on ascorbate oxidation. The role of iron was confirmed by the inhibiting effect of metal-free transferrin on iron-dependent ascorbate oxidation. Concerted actions between iron carrying albumin and copper carrying ceruloplasmin appear responsible for the production of AFR in vitro and in vivo. © Rapid Science 1998 [ABSTRACT FROM AUTHOR]

To examine whether endotoxaemia accompanying long-term, strenuous physical exercise is involved in exercise-induced increase in plasma tumour necrosis factor alpha (TNF-α) concentration and polymorphonuclear neutrophil (PMN) activation, 14 male recreational athletes [mean age 28 (SEM 1) years] were studied. Exercise consisted of a 1.5-km river swim, a 40-km bicycle race, and a 10-km road race. Mean time to complete the race was 149.8 (SEM 4.8) min. The plasma concentrations of granulocyte myeloperoxidase (MPO) and TNF-α were significantly higher than baseline values immediately and 1 h after exercise ( P < 0.001). Both variables returned to pre-race levels the day after exercise. Marked, transient decreases in plasma concentrations of anti-lipopolysaccharide (LPS) immunoglobulin G (IgG) and immunoglobulin M (IgM) antibodies directed against a panel of selected smooth gram-negative LPS were observed after the race, reaching in most cases minimal values in the blood sample drawn immediately following the completion of the triathlon. There was no significant correlation between the magnitude of PMN activation, as assessed by the increase in plasma concentrations of MPO, and the humoral markers of endotoxaemia and TNF-α. An inverse, highly significant relationship between the increase in plasma TNF-α concentrations and the changes in circulating anti-LPS IgM antibodies concentrations was observed ( r = −0.7; P < 0.01). These findings suggest that exercise-induced endotoxaemia was involved in the release of TNF-α, that the magnitude of the TNF-α response to exercise was down-regulated by anti-LPS antibodies of the IgM class, and that the production of TNF-α and endotoxaemia did not seem to play a role in the activation of circulating PMN in the exercising subjects. [ABSTRACT FROM AUTHOR]

The relative antioxidant effect of ampicillin, ceftazidime, ceftriaxone, and cefuroxime on oxygenreactive species was examined in vitro using stimulated human polymorphonuclear neutrophils. There was no evidence that any of the β-lactam agents tested had an effect on superoxide or H2O2 generation. In contrast, all of the β-lactam agents prevented hypochlorous acid (HOCl) chlorination of 1,1-dimethyl-4-chloro-3,5-cyclo-hexanedione in a cell-free system at concentrations of <10 μg/ml. Furthermore, all antibiotics provided dose-dependent protection against HOCl cytotoxicity to 16HBE140 bronchial epithelial cells. Taken together, these data indicate a possible therapeutic role for β-lactam agents in protecting host tissues from HOCl-induced oxidative damage. [ABSTRACT FROM AUTHOR]

Myeloperoxidase (MPO) is an enzyme located within polymorphonuclear neutrophils capable of producting cytotoxic oxidant species that are particularly active against bacteria with polysaccharide capsules. Pseudomonas aeruginosa (10 bacteria per 1 ml) are killed within 1 h in vitro by a MPO/HO/Cl system (48 mU=132 ng of MPO). The question arose as to whether human macrophages would acquire cytotoxic activity when loaded with this enzyme. Monocytes were therefore isolated from human blood and cultured for up to ten days to induce maturation to macrophages. These cells lost endogenous MPO within five days while HO production in response to stimulation by phorbol myristate acetate (10M) decreased to 23% within ten days. On the other hand, their capacity to take up exogenous MPO increased fourfold from day three to day ten. Human macrophages cultured from eight days (when both HO production and MPO uptake were sufficient) were therefore used to study the effects of MPO uptake on cytocidal activity against Pseudomonas aeruginosa. After a 1 h MPO loading period, macrophages (5×10 cells per ml) were incubated in the presence of bacteria (0.5 to 2×10 bacteria per ml) for 2 h at 37°C. At a bacteria/macrophage ratio of 1, only 34.8±7.0% of bacteria survived (compared to killing by non-loaded macrophages), while 74.4±9.3% survived at a ratio of 4. From these results, we conclude that loading macrophages with exogenous MPO could enhance their microbicidal activity, suggesting a potentially useful therapeutic application. [ABSTRACT FROM AUTHOR]

Lidocaine, which was recently demonstrated to be a good pro-lipoperoxidant, was tested on in vitro PGs biosynthesis, and on arachidonate-induced arterial hypotension, in the rabbit. In the in vitro experiments, lidocaine alone was a poor stimulant of cyclo-oxygenase, but it enhanced significantly the cyclo-oxygenase activation of uric acid. In the rabbit, lidocaine lowered the i.v. arachidonate dose necessary to obtain a significant drop of blood pressure. [ABSTRACT FROM AUTHOR]

Evaluation of lipoperoxidation is performed by 2 methods, the first one measuring the amount of peroxyfunction (−OOH) at a given time, and the second one measuring the accumulation of a degradation product against time. The combination of the 2 methods allows us to investigate the kinetics of lipoperoxidation and to demonstrate, for example, the accelerating effect of lidocaine on autoxidation processes. [ABSTRACT FROM AUTHOR]

Dry blood spot immunoreactive trypsin was measured by radioimmunoassay in 84 preterm babies and in 65 full-term newborns studied daily from the first to the fifth day of life. In a control group of 3858 full-term newborns, trypsin concentrations at days 4-6 of life exhibited a log-normal pattern distribution, the geometric mean being 18 ng/ml serum. Immunoreactive trypsin concentrations did not change significantly between days 1, 2, 3, 4 and 5 after birth. Immunoreactive trypsin was found to be significantly lower (geometric mean 9 ng/ml, P less than 0.01) in preterm newborns before 32 weeks of gestation. In hypotrophic newborns of 34 weeks gestational age, immunoreactive trypsin values were higher than those observed at 31 weeks of gestation in eutrophic newborns, the mean birth weight not being different between both groups. These data suggest that trypsin production by the pancreas is dependent on maturity but does not seem related to intrauterine nutritional status. Immunoreactive trypsin concentrations do not change after 32 weeks gestational age and during the first postnatal week. [ABSTRACT FROM AUTHOR]

Uric acid enhances cyclo-oxygenase activity, in in vitro and in vivo experiments. It appears to be a potent hydroxyl radical scavenger; by this property, uric acid may prolong the life of cyclo-oxygenase. [ABSTRACT FROM AUTHOR]