Publications by Colleges and Departments (MSU - Bozeman)
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Item A Novel Method for Curvefitting the Stretched Exponential Function to Experimental Data(2013-12) June, Ronald K.; Cunningham, J. P.; Fyhrie, D. P.The stretched exponential function has many applications in modeling numerous types of experimental relaxation data. However, problems arise when using standard algorithms to fit this function: we have observed that different initializations result in distinct fitted parameters. To avoid this problem, we developed a novel algorithm for fitting the stretched exponential model to relaxation data. This method is advantageous both because it requires only a single adjustable parameter and because it does not require initialization in the solution space. We tested this method on simulated data and experimental stress-relaxation data from bone and cartilage and found favorable results compared to a commonly-used Quasi-Newton method. For the simulated data, strong correlations were found between the simulated and fitted parameters suggesting that this method can accurately determine stretched exponential parameters. When this method was tested on experimental data, high quality fits were observed for both bone and cartilage stress-relaxation data that were significantly better than those determined with the Quasi-Newton algorithm.Item IgG Endopeptidase SeMac does not Inhibit Opsonophagocytosis of Streptococcus equi Subspecies equi by Horse PolymorphonuclearLeukocytes(2010-08) Liu, Mengyao; Lei, BenfangThe secreted Mac protein made by group A Streptococcus (GAS) inhibits opsonophagocytosis of GAS by human polymorphonuclear leukocytes (PMNs). This protein also has the endopeptidase activity against human immunoglobulin G (IgG), and the Cys94, His262 and Asp284 are critical for the enzymatic activity. The horse pathogen Streptococcus equi subspecies equi produces a homologue of Mac (SeMac). SeMac was characterized to determine whether SeMac has IgG endopeptidase activity and inhibits opsonophagocytosis of S. equi by horse PMNs. The gene was cloned and recombinant SeMac was overexpressed in Escherichia coli and purified to homogeneity. Mice with experimental S. equi infection and horses with strangles caused by S. equi seroconverted to SeMac, indicating that SeMac is produced in vivo during infection. SeMac has endopeptidase activity against human IgG. However, the protein just cleaves a small fraction, which may be IgG1 only, of horse IgG. Replacement of Cys102 with Ser or His272 with Ala abolishes the enzymatic activity of SeMac, and the Asp294Ala mutation greatly decreases the enzymatic activity. SeMac does not inhibit opsonophagocytosis of S. equi by horse PMNs but opsonophagocytosis of GAS by human PMNs. Thus, SeMac is a cysteine endopeptidase with a limited activity against horse IgG and must have other function.Item Group A Streptococcus Secreted Esterase Hydrolyzes Platelet-Activating Factor to Impede Neutrophil Recruitment and Facilitate InnateImmune Evasion(2012-04) Liu, Mengyao; Zhu, Hui; Li, Jinquan; Garcia, C. C.; Feng, Wenchao; Kirpotina, Liliya N.; Hilmer, Jonathan K.; Tavares, L. P.; Layton, A. W.; Quinn, Mark T.; Bothner, Brian; Teixeira, M. M.; Lei, BenfangThe innate immune system is the first line of host defense against invading organisms. Thus, pathogens have developed virulence mechanisms to evade the innate immune system. Here, we report a novel means for inhibition of neutrophil recruitment by Group A Streptococcus (GAS). Deletion of the secreted esterase gene (designated sse) in M1T1 GAS strains with (MGAS5005) and without (MGAS2221) a null covS mutation enhances neutrophil ingress to infection sites in the skin of mice. In trans expression of SsE in MGAS2221 reduces neutrophil recruitment and enhances skin invasion. The sse deletion mutant of MGAS5005 (ΔsseMGAS5005) is more efficiently cleared from skin than the parent strain. SsE hydrolyzes the sn-2 ester bond of platelet-activating factor (PAF), converting biologically active PAF into inactive lyso-PAF. KM and kcat of SsE for hydrolysis of 2-thio-PAF were similar to those of the human plasma PAF acetylhydrolase. Treatment of PAF with SsE abolishes the capacity of PAF to induce activation and chemotaxis of human neutrophils. More importantly, PAF receptor-deficient mice significantly reduce neutrophil infiltration to the site of ΔsseMGAS5005 infection. These findings identify the first secreted PAF acetylhydrolase of bacterial pathogens and support a novel GAS evasion mechanism that reduces phagocyte recruitment to sites of infection by inactivating PAF, providing a new paradigm for bacterial evasion of neutrophil responses.Item The Chronic Kidney Disease Model: A General Purpose Model of Disease Progression and Treatment.(2011-06) Orlando, L. A.; Belasco, Eric J.; Patel, U. D.; Matcher, D. B.Background: Chronic kidney disease (CKD) is the focus of recent national policy efforts; however, decision makers must account for multiple therapeutic options, comorbidities and complications. The objective of the Chronic Kidney Disease model is to provide guidance to decision makers. We describe this model and give an example of how it can inform clinical and policy decisions. Methods: Monte Carlo simulation of CKD natural history and treatment. Health states include myocardial infarction, stroke with and without disability, congestive heart failure, CKD stages 1-5, bone disease, dialysis, transplant and death. Each cycle is 1 month. Projections account for race, age, gender, diabetes, proteinuria, hypertension, cardiac disease, and CKD stage. Treatment strategies include hypertension control, diabetes control, use of HMG-CoA reductase inhibitors, use of angiotensin converting enzyme inhibitors, nephrology specialty care, CKD screening, and a combination of these. The model architecture is flexible permitting updates as new data become available. The primary outcome is quality adjusted life years (QALYs). Secondary outcomes include health state events and CKD progression rate. Results: The model was validated for GFR change/year -3.0 ± 1.9 vs. -1.7 ± 3.4 (in the AASK trial), and annual myocardial infarction and mortality rates 3.6 ± 0.9% and 1.6 ± 0.5% vs. 4.4% and 1.6% in the Go study. To illustrate the model's utility we estimated lifetime impact of a hypothetical treatment for primary prevention of vascular disease. As vascular risk declined, QALY improved but risk of dialysis increased. At baseline, 20% and 60% reduction: QALYs = 17.6, 18.2, and 19.0 and dialysis = 7.7%, 8.1%, and 10.4%, respectively. Conclusions: The CKD Model is a valid, general purpose model intended as a resource to inform clinical and policy decisions improving CKD care. Its value as a tool is illustrated in our example which projects a relationship between decreasing cardiac disease and increasing ESRD.Item Production, Characterization, and Flocculation Mechanism of Cation Independent, pH Tolerant, and Thermally Stable Bioflocculant from Enterobacter sp. ETH-2(2014-12) Tang, Wei; Song, Liyan; Li, Dou; Qiao, Jing; Zhao, Tiantao; Zhao, Heping; Lei, BenfangSynthetic high polymer flocculants, frequently utilized for flocculating efficiency and low cost, recently have been discovered as producing increased risk to human health and the environment. Development of a more efficient and environmentally sound alternative flocculant agent is investigated in this paper. Bioflocculants are produced by microorganisms and may exhibit a high rate of flocculation activity. The bioflocculant ETH-2, with high flocculating activity (2849 mg Kaolin particle/mg ETH-2), produced by strain Enterobacter sp. isolated from activated sludge, was systematically investigated with regard to its production, characterization, and flocculation mechanism. Analyses of microscopic observation, zeta potential and ETH-2 structure demonstrates the bridging mechanism, as opposed to charge neutralization, was responsible for flocculation of the ETH-2. ETH-2 retains high molecular weight (603 to 1820 kDa) and multi-functional groups (hydroxyl, amide and carboxyl) that contributed to flocculation. Polysaccharides mainly composed of mannose, glucose, and galactose, with a molar ratio of 1:2.9:9.8 were identified as the active constituents in bioflocculant. The structure of the long backbone with active sites of polysaccharides was determined as a primary basis for the high flocculation activity. Bioflocculant ETH-2 is cation independent, pH tolerant, and thermally stable, suggesting a potential fit for industrial application.Item Carbohydrates for physical activity: A strategy to avoid undesirable health consequences(2012-03) Miles, MaryIntake of carbohydrates above the dietary guidelines to support performance of physical activity is common but may be unnecessary and counterproductive. Sports nutrition guidelines have not been designed to incorporate characteristics that may make high carbohydrate consumption a source of metabolic stress that may increase oxidative stress, inflammation, and lipogenesis. This metabolic stress is linked to the physiology underlying the development of insulin resistance, type 2 diabetes mellitus, and cardiovascular diseases. This review describes research-based evidence to aid in bridging the gap between dietary guidelines for overall health and those to support physical activity. Characteristics that increase the likelihood of metabolic stress resulting from carbohydrate intake include overweight and obesity, central/visceral adiposity, older age, sedentary lifestyle, and caloric state. Carbohydrate-based foods that provide the most health benefits are whole grains, beans and legumes, fruits, and vegetables. Carbohydrate-based foods that most readily elicit metabolic stress are those with added sugars and refined grains or that have a high glycemic index. A checklist that incorporates both the number of these characteristics and prevailing guidelines for nutrition and physical activity is presented. This may be useful in determining whether additional carbohydrates are needed to support the physical activity level of the individual.Item Low-dose creatine supplementation enhances fatigue resistance in the absence of weight gain(Elsevier, 2011-04) Miles, Mary; Rawson, E.S.; Stech, M.J.; Frederickson, Sara J.Objective: We examined the effects of 6 wk of low-dose creatine supplementation on body composition, muscle function, and body creatine retention. Methods: Twenty healthy men and women (21 ± 2 y old) were randomized to receive creatine (0.03 g • kg -1 • d-1; n=10, 4 women) for 6 wk in a double-blind placebo-controlled fashion. Participants were tested on two occasions before supplementation to establish a reliable baseline, and then were retested after supplementation. Testing included body composition, maximal strength (three-repetition maximal concentric knee extension at 180 degrees/s), muscle fatigue (five sets of 30 concentric knee extensions at 180 degrees/s), and plasma creatine concentration. Results: There were no significant differences in body mass, fat-free mass, fat mass, body fat percentage, total body water, or maximal strength in either group from before to after supple-mentation (all P > 0.05). After supplementation, plasma creatine increased significantly in the creatine group (+182%, P = 0.03), with no difference in the placebo group. Compared with baseline values, creatine-supplemented volunteers were more resistant to fatigue during sets 2 (7%), 3 (9%), 4 (9%), and 5 (11%) (all P < 0.05). In placebo-supplemented participants, there was no improvement in fatigue resistance during sets 2 (0%), 3 (1%), 4 (0%), and 5 (1%) (all P > 0.05). Conclusion: Ingesting a low dose (2.3 g/d) of creatine for 6 wk significantly increased plasma creatine concentration and enhanced resistance to fatigue during repeated bouts of high-intensity contractions.Item Creatine supplementation does not reduce muscle damage or enhance recovery from resistance exercise(2007-11) Rawson, E.S.; Conti, M.P.; Miles, MaryPrevious studies have shown that creatine supplementation reduces muscle damage and inflammation following running but not following high-force, eccentric exercise. Although the mechanical strain placed on muscle fibers during high-force, eccentric exercise may be too overwhelming for creatine to exert any protective effect, creatine supplementation may protect skeletal muscle stressed by a resistance training challenge that is more hypoxic in nature. The purpose of this study was to examine the effects of short-term creatine supplementation on markers of muscle damage (i.e., strength, range of motion, muscle soreness, muscle serum protein activity, C-reactive protein) to determine whether creatine supplementation offers protective effects on skeletal muscle following a hypoxic resistance exercise test. Twenty-two healthy, weight-trained men (19–27 years) ingested either creatine or a placebo for 10 days. Following 5 days of supplementation, subjects performed a squat exercise protocol (5 sets of 15–20 repetitions at 50% of 1 repetition maximum [1RM]). Assessments of creatine kinase (CK) and lactate dehydrogenase activity, high-sensitivity C-reactive protein, maximal strength, range of motion (ROM), and muscle soreness (SOR) with movement and palpation were conducted pre-exercise and during a 5-day follow up. Following the exercise test, maximal strength and ROM decreased, whereas SOR and CK increased. Creatine and placebo-supplemented subjects experienced significant decreases in maximal strength (creatine: 13.4 kg, placebo: 17.5 kg) and ROM (creatine: 2.4°, placebo: 3.0°) immediately postexercise, with no difference be-tween groups. Following the exercise test, there were significant increases in SOR with movement and palpation (p < 0.05 at 24, 48, and 72 hours postexercise), and CK activity (p < 0.05 at 24 and 48 hours postexercise), with no differences between groups at any time. These data suggest that oral creatine supplementation does not reduce skeletal muscle damage or enhance recovery following a hypoxic resistance exercise challenge.Item Apolipoprotein A1 genotype affects the change in high density lipoprotein cholesterol subfractions with exercise training.(2006-03) Ruaño, G.; Seip, R.L.; Windemuth, Andreas; Zöllner, S.; Tsongalis, Gregory J.; Otvos, J.; Ordovas, J.M.; Bilbie, C.; Miles, Mary; Zoeller, Robert F.; Visich, Paul S.; Gordon, P.M.; Angelopoulos, T.J.; Pescatello, Linda S.; Moyna, Niall M.; Thompson, P.D.High density lipoprotein cholesterol (HDL-C) is a primary risk factor for cardiovascular disease. Apolipoprotein A-1 (apoA1) is the major HDL-associated apolipoprotein. The −75 G/A single nucleotide polymorphism (SNP) in the apolipoprotein A1 gene (APOA1) promoter has been reported to be associated with HDL-C concentrations as well as HDL-C response to dietary changes in polyunsaturated fat intake. We examined the effect of this APOA1 SNP on exercise-induced changes in HDL subfraction distribution. From a cohort of healthy normolipidemic adults who volunteered for 6 months of supervised aerobic exercise, 75 subjects were genotyped for the −75 G/A SNP. Of these, 53 subjects were G homozygotes (G/G) and 22 were A carriers (A/G and A/A). HDL subfractions were measured by nuclear magnetic resonance (NMR) spectroscopy by adding categories HDL-C 1 + 2 for the small subfraction, and HDL-C 3 + 4 + 5 for the large. The change in total HDL-C after exercise was 0.8 ± 7.2 mg/dL (+1.7%), and was not statistically significant. HDL subfraction amounts also did not significantly change with exercise training in the total cohort or in G homozygotes or A carriers. The amount of the large HDL subfraction increased in the G homozygotes and decreased in the A carriers (mean ± S.E.M., 1.8 ± 6.6 mg/dL versus −6.1 ± 2.3 mg/dL, p < 0.0005). In contrast, the amount of the small HDL subfraction decreased in G homozygotes and increased in A carriers (−1.3 ± 6.6 mg/dL versus 4.7 ± 1.2 mg/dL, p < 0.005). These results show that genetic variation at the APOA1 gene promoter is associated with HDL subfraction redistribution resulting from exercise training.Item Basal, diurnal, and acute inflammation in normal versus overweight men.(Lippincott Williams & Wilkins, 2012-12) Miles, Mary; Keller, J.M.; Kordick, L.K.; Kidd, J.R.Increased inflammation is present in obese compared with normal weight individuals, but inflammation characteristics of nonobese, overweight individuals are less clear. Purpose: The objective of this study was to determine whether basal, circadian, and posteccentric exercise inflammation levels differ between normal and overweight men. Methods: Men (18–35 yr old) classified as normal weight (body mass index ≤2 5 kg·m-2, n = 20) and overweight (body mass index = 25–30 kg·m-2 conditions in random order. Maximal voluntary effort and eccentric actions (3 X 15) using the elbow flexor muscles of one arm were performed, and blood was collected preexercise and 4, 8, 12, and 24 h postexercise at 7:00 a.m., 12:00 p.m., 4:00 p.m., 8:00 p.m., and 7:00 a.m. Blood was collected on a time-matched schedule without exercise for CON. Soluble tumor necrosis factor receptor-1, interleukin-6, C-reactive protein (CRP), and cortisol responses (EX value j time-matched CON value) were measured. Results: Basal CRP was higher in the overweight compared with normal weight group (mean ± SD, 0.542 ± 0.578 vs 1.395 ± 1.041 mg·L-1). Soluble tumor necrosis factor receptor-1 increased (P < 0.05) 8 h postexercise in both groups, and the response was greater 12 and 24 h postexercise in the overweight compared with normal weight groups. Interleukin-6 increased (P < 0.05) 8 h postexercise, with a trend (P = 0.09) to be greater in the overweight group. CRP and cortisol responses were not detected. Conclusions: The low-grade inflammation state in overweight compared with normal weight men includes both higher basal CRP concentrations and enhanced acute inflammation, but not in changes to the circadian patterns of cortisol and inflammation variables.
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