Groin pain in sportsmen is not always musculotendinous in origin.
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Abdominal Abscess↗
Biomedical subjects
R Dawson
Publications and source records attributed to R Dawson.
Dietary taurine manipulations in aged male Fischer 344 rat tissue: taurine concentration, taurine biosynthesis, and oxidative markers.
Taurine (TAU) is a ubiquitous sulfur-containing amino acid that has been proposed to be an antioxidant. The concentration of TAU decreases during aging, which may increase susceptibility to oxidative stress. Our study attempted to elucidate the mechanism for the age-dependent decrease in TAU content by examining TAU biosynthesis in aged rats. We also examined the effects of dietary TAU manipulations on TAU content and oxidative markers in aged male Fischer 344 (F344) rats. Adult (9 months) and aged (26 months) rats fed control diets, aged rats fed control diet and TAU-supplemented (1.5%) water, and aged rats fed a TAU-deficient diet were used. We observed a significant age-related decrease in TAU content in liver, kidney, and cerebellum. Dietary TAU supplementation increased tissue TAU content, whereas dietary TAU restriction had no effect. Enzyme-dependent TAU synthesis showed an age-dependent reduction in liver that was decreased further by TAU supplementation. Protein carbonyl content was elevated in the cerebral cortex and kidney of aged rats and was attenuated by TAU supplementation. A trend for a decrease in protein and acid-soluble thiol contents in hepatic tissue of aged rats was observed, and this was attenuated with dietary TAU supplementation. Our data show that a decrease in hepatic TAU biosynthesis may cause, in part, the observed decline in tissue TAU content in aged F344 rats, and TAU supplementation can restore TAU levels. Our study indicates that a decline in TAU content may exacerbate oxidative stress in aged rats, which can be reversed by dietary TAU supplementation.
Aging↗
Provisional stenting for symptomatic intracranial stenosis using a multidisciplinary approach: acute results, unexpected benefit, and one-year outcome.
Percutaneous techniques have dramatically changed our approach to coronary and peripheral revascularization. Intracranial atherosclerosis is a highly morbid disease; however, techniques for revascularization are still in evolution. The authors comprise a multidisciplinary team of neurologists, neuroradiologists, and interventional cardiologists who have collaborated in treating fifteen patients with symptomatic intracranial stenosis who have failed medical therapy. The acute success rate (100%) and one-year freedom from death and stroke (93.4%) using balloon angioplasty and provisional stenting are encouraging. A surprising observation in this patient cohort was that 53% of patients had improvement or resolution of a deficit that was chronic and presumed to be permanent and irreversible. This type of chronic but reversible deficit is termed "brain angina". The background, rationale for a multidisciplinary team, techniques, and preliminary results of intracranial angioplasty with provisional stenting are presented.
Aged↗
Taurine is a weak scavenger of peroxynitrite and does not attenuate sodium nitroprusside toxicity to cells in culture.
Many studies have suggested an antioxidant role for taurine, but few studies have directly measured its free radical scavenging activity. The aim of the present study was to directly determine the action of taurine and taurine analogs to inhibit peroxynitrite-mediated oxidation of dihydrorhodamine 123 (DHR) to rhodamine. Taurine was also tested to determine if it could attenuate the toxicity of sodium nitroprusside (SNP) to neuronal cultures. Taurine at concentrations above 30 mM had a modest ability to inhibit peroxynitrite formation derived from SIN-1. Hypotaurine could inhibit peroxynitrite formation from both SIN-1 (decrease 75%) and SNP (decrease 50%) at 10 mM. Other taurine analogs (homotaurine, beta-alanine & isethionic acid) slightly potentiated DHR oxidation by SIN-1. Short-term (1-hour) treatment of PC12 cultures with either SNP (1-2mM) or taurine (20-40 mM) appeared to induce cellular proliferation. In contrast, 24-hour treatment with SNP (1 mM) induced cell death. Combination treatments with taurine and SNP appeared to interact in an additive fashion for both cell proliferation and neurotoxic actions. It appears unlikely that taurine is a major endogenous scavenger of peroxynitrite.
Animals↗
Simulation of acid-base condition and copper speciation in the fish gill microenvironment.
pH, alkalinity, and mucus content in the fish gill microenvironment of carp (Cyprinus carpio) were measured by exposing fish to copper at various water pH levels using an apparatus which separates inspired and expired water. The relationship between pH levels inside and outside of the gill microenvironment, between pH and alkalinity, and between mucus secretion, pH, and copper exposure concentration were modeled. Copper speciation in the surrounding water and in the fish gill microenvironment was simulated using MINTEQA2 chemical equilibrium calculation software. The results of the modeling for pH, alkalinity, and mucus calculation were then adopted as inputs for purposes of parameter identification in the speciation modeling. The differences observed in the copper species distribution between that of the fish gill microenvironment and the surrounding water were based on the speciation modeling. The change in copper bioavailability for fish uptake was also examined. The results indicate the presence of an experimental pH balance point at 6.9, where the pH in the fish gill microenvironment is identical to that of the surrounding water. The observed deviation range in pH levels between that found at the gills and that of the surrounding water varied from -0.4 to 0.8 units. A sinusoidal model was developed for calculation of gill pH based on the pH of the surrounding water. Models calculating alkalinity either in the gill microenvironment or in the surrounding water and for estimating mucus secretion were also developed. The results of the chemical equilibrium calculations demonstrate that, within a pH range of 6-9, the dominant species of copper in bulk solution shifted from free ions to that of the hydroxo complex. With respect to the fish gill microenvironment, the dominant species found under acidic conditions were the mucus copper complex and free ions. Because of the influence of mucus complexation and pH change, bioavailable copper species in the fish gill microenvironment were significantly lower than that in the bulk solution, especially under acidic conditions.
Acid-Base Equilibrium↗
Palliative radiotherapy of bone metastases: an evaluation of outcome measures.
The objective of this study was to identify and evaluate important patient-based outcomes that are specific to the palliative radiotherapy of bone metastases. We first conducted a literature review to identify and evaluate outcomes that are currently in use. To identify outcomes that are important to patients, in-depth patient interviews were conducted. Finally, issues identified through the interviews were quantified through a prospective survey, in which patients completed a questionnaire prior to commencing radiotherapy and again after 6 weeks. In our literature review, we found that there was no standardized definition of either response to radiotherapy or assessment of pain relief. Pain measurement in many studies was undertaken using very simple measures, which could possibly yield inaccurate results. The vast majority of studies did not include quality of life as an endpoint. The patient interviews and survey showed that chronic pain and associated limitation of movement were the disease symptoms causing the most concern. Having a clear, alert mind and being able in self-care were the aspects of daily living given the highest priority. Sustained pain relief and minimizing the risk of future complications were the main priorities relating to radiotherapy treatment. The practical aspects of treatment (travelling distance, remaining at home and brevity of treatment) were of least importance. This study indicates the complexity of evaluating the outcomes of palliative interventions, and confirms the deficiencies of pain relief as the primary end-point. The patient's quality of life is affected by many factors other than pain (such as limited mobility, reduced performance, side effects and impaired role functioning); hence a wider range of end-points is required. Greater sensitivity is required than in currently used end-points. Concurrent diseases as well as concurrent therapies can make it difficult to attribute effects with precision. Unless such factors are considered in research design, the results may prove unreliable.
Analgesics↗
QSAR modeling of bioconcentration factors in fish based on fragment constants and structural correction factors.
The quantitative structure-activity relationship between the BCF and fragment constant of organic chemicals was studied using a database containing 337 experimental BCF values. The database covered a large variety of chemicals ranging from the very hydrophobic to the very hydrophilic with logKow values between 0.39 and 8.60. The structural features affecting the BCFs were identified and evaluated during a preliminary modeling. A final linear multivariate regression model was derived that was able to account for as much as 98.0% of the variation in the experimental BCF values. The mean absolute error for the final model was 0.315 log-units. In addition, the predictability and robustness of the model was also evaluated.
Animals↗
'Fast track' carotid duplex scanning in a district general hospital.
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Carotid Stenosis↗
Post-traumatic stress disorder in extremely poor women: implications for health care clinicians.
OBJECTIVES: To identify childhood antecedents for lifetime post-traumatic stress disorder (PTSD) and to determine how this diagnosis relates to health and service use among extremely poor women. METHODS: We conducted a secondary data analysis of 425 women in the Worcester Family Research Project, a case-control longitudinal study of 220 sheltered homeless and 216 extremely poor housed (never homeless) women in Worcester, Massachusetts. RESULTS: We found that extremely poor women with lifetime PTSD were more likely to have grown up in family environments of violence, threat, and anger than those without PTSD. The strongest risk factor for PTSD was childhood sexual abuse with threat. Low-income women with lifetime PTSD had more bodily pain, even when controlling for other health and demographic factors. Women with PTSD experienced more chronic health conditions and had more problematic relationships with their health care providers and perceived more barriers to care. CONCLUSION: Many low-income women have difficulty using medical care appropriately because of childhood histories of physical and sexual abuse, the subsequent development of post-trauma responses, and structural barriers to care. Given these factors, it is critical that health care clinicians routinely screen for histories of violence and PTSD and develop treatment plans that ensure safety, link current symptoms with prior experiences, and provide support as necessary. A team approach coordinated by a case manager may be the best strategy. Without routine screening for PTSD and sensitive treatment, many extremely poor women will receive compromised health care and may even be retraumatized.
Adult↗
Omeprazole in oesophageal reflux disease.
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Anti-Ulcer Agents↗
Flexible treatment strategies in chronic disease: clinical and research implications.
Multiple treatments are available for nearly all the mood disorders. This range of treatment options adds a new dimension of choice to clinical decision making. In addition to prescribing the best initial treatment, clinicians should have an algorithm for deciding if and when to make subsequent changes in treatment to take advantage of second-line treatment options when necessary. This article aims to 1) show that a wide variety of clinical decisions can be framed as choices among adaptive (within-patient) threshold-based strategies or algorithms, illustrating the generality of the concept; 2) illustrate two ways to design randomized clinical trials to compare treatment strategies with each other to decide which strategy is best; and 3) discuss some of the advantages offered by these designs, in terms of both patient acceptability and adherence to experimental protocols.
Algorithms↗
Induction or suppression of a B cell-specific response to self antigen in vivo is dependent upon dendritic cell activation via the TNF-alpha receptor at the time of antigen uptake.
In this study we show that the retinal autoantigen, S-antigen, contains a functional TNF-alpha homologous domain which stimulates maturation and differentiation of cultured dendritic cells (DC) or tissue DC via the p55 TNF-alpha receptor. Tissue DC became more dendritiform in shape, and migrated into culture supernatant. S-antigen also stimulated accumulation of cell surface MHC class II antigen with a corresponding loss of acidic intracellular vesicles, and induced IL-1beta and IL-12 mRNA expression in cultured bone marrow-derived DC. In addition, cultured splenic DC primed immune responses to S-antigen in vivo in the absence of other, exogenous cytokine sources. DC pulsed with either retinal S-antigen or another retinal autoantigen, interphotoreceptor retinoid binding protein (IRBP), were able to stimulate naive T cell proliferation in vitro, but only S-antigen-pulsed DC were able to induce an immune response in vivo and initiate antibody class switching. In contrast, IRBP-pulsed DC had no detectable in vivo priming effect and IgG antibody levels remained suppressed even after immunization with IRBP in complete Freund's adjuvant. These results indicate that DC from the same precursor population can either induce or suppress a B cell-specific response to self antigen in vivo, the outcome being dependent upon DC activation at the time of antigen uptake and presentation.
Animals↗
The influence of mucus on copper speciation in the gill microenvironment of carp (Cyprinus carpio).
pH and mucus (as total organic carbon) in the gill microenvironment of carp, Cyprinus carpio, exposed to various concentrations of total copper were measured in an exposure experiment using Playle's apparatus. The activities of free copper ions in both inspired and expired waters were determined using a copper ion selective electrode. A trial-and-error procedure of coupling species distribution calculations (MINEQA2) with single-site complexation modeling (mucus-copper) was proposed for computation of both copper speciation and complexation capacity of gill mucus for copper in an interactive loop. The method was demonstrated to be valid in calculating the metal speciation in this study. It was found that pH and alkalinity in the gill microenvironment were slightly higher than in the surrounding water of pH 6.7. The rates of excretion of CO(2), HCO(-)(3), and mucus at the gills increased, either linearly or nonlinearly with increases in the total copper concentration in the surrounding water. The conditional complexation stability constant of the mucus was calculated as log k=5.32, while the complexation stability equivalent concentration of the mucus was derived as 0.95 mmolCu/mgC. As a consequence of changes in pH and alkalinity, in conjunction with occurrence of mucus, copper speciation in the gill microenvironment is significantly different from that in the surrounding water, with 3-20% of the copper complexed by the gill mucus. The sequence of species domination also shifted from CuCO(0)(3), Cu(2+), CuHCO(+)(3), and Cu(OH)(0)(2) in the surrounding water to CuCO(0)(3), Cu(2+), Cu(OH)(0)(2), CuHCO(+)(3), and mucus-Cu in the gill microenvironment.
Animals↗
Uptake of cadmium adsorbed on particulates by gills of goldfish (Carassius auratus).
Goldfish (Carassius auratus) were exposed to mixtures of constant dissolved cadmium (0.01 mg/L) and cadmium adsorbed on gibbsite particles at concentrations of 0, 0.025, 0.050, 0.075, and 0.100 mg/L. The gills of the fish were excised after a 5-day exposure experiment and both cadmium and aluminum in the gills were measured. The gills were also examined with a light microscope for surface adherence of the particles after the exposure. The evidence collected demonstrated that the concentration of cadmium in the gills increased with increased concentration of particulate cadmium during the exposure while the dissolved cadmium remained constant. The ratio of cadmium to aluminum in the gills was apparently higher than that in the solution, indicating the stripping and translocation of cadmium from the particles. A multistep uptake process is proposed and the bioavailability of particulate cadmium to fish gills is discussed.
Adsorption↗
Attenuation of oxidative damage to DNA by taurine and taurine analogs.
Taurine has been suggested to have cytoprotective actions via a number of different mechanisms. The role of taurine in protecting DNA from oxidative damage has received only limited attention. The aim of the present studies was to test the hypothesis that taurine might act to attenuate oxidative damage to DNA caused by free radicals generated by iron-stimulated catecholamine oxidation in the presence of H2O2. Calf thymus DNA (100 microg/tube) was exposed to a reaction mixture containing: ferric chloride (60 microM), H2O2 (2.8 mM) and L-dopa (100 microM). Taurine and taurine analogs were added simultaneously to determine their effects to prevent oxidative damage to DNA. The reaction was carried out for 1 hour at 37 degrees C and terminated by rapid freezing in an ethanol/dry ice bath. The DNA was precipitated with ethanol and subsequently hydrolyzed with formic acid under vacuum. The hydroxylated bases were separated by HPLC and detected electrochemically. All experiments were replicated a minimum of 5 times. Taurine (20 mM) was found to reduce (p<0.05) damage to DNA as indexed by reductions in the formation of 5-OH-uracil (49% decrease), 8-OH adenine (37% decrease), and 8-OH guanine (21% decrease). Taurine had minimal effects to reduce the formation of 5-OH cytosine (<7% decrease). Taurine (20 mM) also increased total DNA recovery after damage 36-40% and increased total undamaged guanine approximately 32%. 5-OH Uracil formation could be reduced (p<0.05) by 1 mM taurine and 8-OH-adenine formation was reduced (p<0.05) by 5 mM taurine. Studies were conducted with various amino acid analogs and total base adduct formation was reduced by 20 mM beta-alanine (30% decrease), lysine (58% decrease) and glutathione (88% decrease). When tested at 20 mM, both hypotaurine and homotaurine provided greater protection against DNA damage than taurine, whereas isethionic acid provided a similar level of protection as taurine. Using identical conditions as the assays for base hydroxylation, we tested whether inhibition of quinone formation could account for taurine's mechanism of action. Taurine (49% decrease), homotaurine (24% decrease) and hypotaurine (79% decrease) all reduced quinone formation. Thus, inhibition of quinone formation could account for part of taurine's mechanism of action to inhibit oxidative damage, but it could not account for homotaurine's greater efficacy in preventing DNA damage. Overall, these studies show that taurine at concentrations normally found in cells can inhibit oxidative damage to DNA.
Adenine↗
Cytoprotective effect of taurine against hypochlorous acid toxicity to PC12 cells.
Taurine has been shown to be an effective scavenger of hypochlorous acid (HOCl). The role of HOCl is well established in tissue damage associated with reperfusion injury mediated by neutrophils. The role of HOCl in CNS injury and inflammatory reactions has not been well established. Myeloperoxidase activity is present in the CNS and it has been associated with ischemic injury. The aim of the present study was to determine the cytotoxicity of HOCl in a neuronal cell line (PC12) and the ability of taurine to prevent or reverse neurotoxicity. PC12 cells were grown in 96 well plates at a plating density of approximately 100,000 cells per well. HOCl was made up fresh from NaOCl for each experiment and the concentration verified spectrophotometrically. PC12 cells were exposed to HOCl for 1 hour in phosphate-buffered saline. Taurine was added at the time of HOCl treatment and in some experiments a post-treatment with taurine was performed by adding 1 or 10 mM taurine to the culture media (RPMI 1640). The cells were allowed 24 hours to recover and viability was determined using a tetrazolium-based (MTT) assay. The first series of experiments evaluated the toxicity of HOCl and the efficacy of taurine to protect PC12 cells. HOCl at 50 microM reduced PC12 cell viability by 50% and 150 microM reduced viability to <25% of control levels. Taurine (0.5-20 mM) was tested for cytoprotection against 150 microM HOCl and PC12 cells treated with 0.5 mM taurine exhibited only a 20% reduction in viability compared to untreated controls. Taurine concentrations of 1 mM or higher provided nearly 100% protection against HOCl. A second study was performed comparing taurine to beta-alanine, glutathione and isethionic acid. HOCl (100 microM) reduced viability to 25 +/- 1% of controls and taurine, beta-alanine and glutathione at 1 mM provided nearly complete protection. In contrast, isethionic acid, which lacks an amino group, failed to provide protection. Taurine (1 or 10 mM) added after 50 microM HOCl treatment did not provide any protection and PC12 cell viability was reduced to <39% of controls. In contrast, if taurine (50 microM) was present during the HOCl treatment and 1 mM taurine was added after the treatment, PC12 cell viability was 80 +/- 5% of controls. A combination of 250 microM taurine during the HOCl treatment and 1 mM taurine post-treatment produced 100% protection. These results clearly show that taurine is an efficient scavenger of HOCl and can prevent neuronal damage caused by HOCl. Since myeloperoxidase expression in the CNS is increased by ischemia, one function of taurine released during an ischemic event may be to scavenge HOCl and provide neuroprotection.
Animals↗
Taurine inhibition of metal-stimulated catecholamine oxidation.
Taurine is an abundant amino acid found in mammalian tissues and it has been suggested to have cytoprotective functions. The aim of the present study was to determine if taurine had the potential to reduce oxidative stress associated with metal-stimulated catecholamine oxidation. Taurine and structural analogs of taurine were tested for their ability to inhibit metal-stimulated quinone formation from dopamine or L-dopa. Oxidative damage to proteins and lipids were also assessed in vitro and the effects of taurine were determined. Taurine (20 mM) was found to decrease significantly ferric iron (50-500 microM)- and manganese (10 microM)-stimulated L-dopa or dopamine oxidation. Taurine had no effect on zinc-induced dopamine oxidation and slightly potentiated copper- and NaIO(4)-stimulated quinone formation. Ferric iron-stimulated lipid peroxidation was not affected by taurine (1-20 mM). Protein carbonyl formation induced by ferric iron (500 microM) and L-dopa (500 microM) was significantly reduced by 10 mM taurine. The cytotoxicity of L-dopa (250 microM) and ferric chloride (75 microM) to LLC-PK(1) cells was attenuated by 10 mM taurine or hypotaurine. Homotaurine alone stimulated L-dopa oxidation and potentiated the cytotoxic effects of ferric iron. Homotaurine was found to be cytotoxic when combined with L-dopa or L-dopa/iron. In contrast, hypotaurine inhibited quinone formation and protected LLC-PK(1) cells. These studies suggest that taurine may exhibit cytoprotective effects against the oxidation products of catecholamines by acting as a scavenger for free radicals and cytotoxic quinones.
Journal Article↗
Bioavailability of apparent fulvic acid complexed copper to fish gills.
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Animals↗