Design of Standard Operating Procedures for Concrete Delivery and Pour Data Collection and Analysis

Webcor Concrete Group (WCG) is a self-perform subsidiary of Webcor Builders, a large general contractor in the state of California. Inefficiencies plague the construction industry, resulting in Webcor reaching out to the Cal Poly Industrial and Manufacturing Department and its students for help. The opportunity addressed in this report centers on a lack of concrete pour data collection. This gap results in a struggle to defend against, or pursue, backcharges with their concrete suppliers regarding additional labor costs or wasted material. The project objective is to provide WCG with a baseline data collection system and procedure, leading to increased back-charge accounting, future project justification, and root cause analyses of inefficiencies. The authors first researched automated GPS and RFID truck tracking systems, but ultimately used an iterative design process to create a manual data collection software solution. With the assistance of current Webcor Project Engineers, the authors were able to view several concrete pours, determining specific and measurable metrics to be collected for the data collection application. After researching software alternatives on the market, the authors pursued a solution that utilized Microsoft Excel and its formulas, charts, and coding language. The Excel workbook underwent several revisions, each building upon the last with project sponsor feedback and recommendations. Once the final design was completed, the Excel workbook was distributed throughout WCG for Project Engineer use and Project Manager review. This feedback was used to conclude that the design met all project objectives; however, recommendations for additional functionality show that this design can be extended further. It can also be concluded that Industrial Engineering tools and methodology are applicable and beneficial to the construction industry, i.e. ‘Lean Construction.’ Long term implementation of the workbook will ultimately verify the success of the solution. As a result of the workbook being developed free of cost by the authors, it is recommended that Webcor implement the tool and standard procedures, as there are no economic barriers, but only potential gains. The biggest impacts associated with the design implementation are organizational. In the short term, Project Engineers will dedicate additional time to data collection and input, but could potentially save time if redundant procedures are eliminated. The design also increases accountability of all parties in the concrete construction supply chain, provides a means of tracking long term Project Engineer performance and project progress, and can be used to justify future process improvement projects. Moving forward, it is recommended that an automated GPS or RFID truck tracking system be pursued and that efforts be made to turn the desktop application into a cloud-based one for increased collaboration and data visibility

Obesity mediated dysregulation in the expression and action of myostatin

Background: Obesity is often associated with impaired sensitivity to the effects of insulin (insulin resistance) and dietary protein (anabolic resistance) and may exacerbate the age-related decline of skeletal muscle (sarcopenia). Myostatin is a protein that negatively regulates skeletal muscle growth but its inhibition in rodents also improves insulin sensitivity. In humans, myostatin appears to be upregulated by obesity and associated with insulin resistance, but observations are confounded by lifestyle factors and ageing. Aims: To delineate between the effects of obesity and ageing on myostatin expression in human skeletal muscle; to investigate the underlying causes of these effects; and to establish the functional significance and interconnectivity of modulating insulin sensitivity and myostatin expression in human skeletal muscle cells. Methods: In Chapter 3 a cross-sectional analysis of skeletal muscle gene expression was undertaken, in conjunction with correlation analyses between serum myostatin and descriptive characteristics, to isolate the effects of obesity and ageing per se on myostatin expression and abundance. In Chapters 4 and 5, in vitro and ex vivo techniques were employed using human primary myotubes to investigate the potential involvement of lipid-induced insulin and anabolic resistance and secretory cross-talk between subcutaneous adipose tissue and muscle, in the obesity-mediated upregulation of myostatin and the associated impairment of insulin and anabolic sensitivity. In Chapter 6, the novel polyphenol metabolite Urolithin A was applied to human myotubes and a model of adipocytes, to investigate its therapeutic potential to enhance insulin and anabolic sensitivity and to suppress myostatin expression. Results: In Chapter 3 it was revealed that muscle myostatin expression is uniquely upregulated by obesity with ageing, but not by ageing in the absence of obesity, and occurs concurrently with insulin resistance and abnormal regulation of pathways involved in the maintenance of skeletal muscle mass. This association was corroborated by positive correlations between serum myostatin and multiple indices of adiposity, but not age. In Chapters 4 and 5 it was demonstrated that neither acutely elevated fatty acid availability (which induced insulin and anabolic resistance), nor chronic exposure to obese subcutaneous adipose tissue conditioned medium (which did not induce insulin or anabolic resistance but altered the expression of genes involved in myogenesis and muscle protein breakdown) recapitulated the obesity-mediated upregulation of myostatin expression. In Chapter 6 it was demonstrated for the first time that Urolithin A suppresses myostatin expression and enhances glucose transport in human myotubes (and 3T3-L1 adipocytes), the latter of which was associated with an upregulation of GLUT4 expression. Conclusions: Skeletal muscle myostatin expression is uniquely upregulated by obesity per se, but this does not appear to be mediated by lipid-induced insulin resistance, nor by the secretory milieux of obese subcutaneous adipose tissue. Nevertheless, both models perturbed factors involved in myogenesis and muscle protein breakdown, independent of an upregulation of myostatin. Thus, the factors responsible for the obesity-mediated upregulation of myostatin remain to be elucidated and future work to establish such causality is required. Furthermore, translational research to investigate the potential of Urolithin A to enhance glucose handling in peripheral tissues and to repress myostatin’s inhibitory effects on muscle growth is warranted in humans and could be of particular benefit in conditions such as sarcopenic obesity

Obesity mediated dysregulation in the expression and action of myostatin

Background: Obesity is often associated with impaired sensitivity to the effects of insulin (insulin resistance) and dietary protein (anabolic resistance) and may exacerbate the age-related decline of skeletal muscle (sarcopenia). Myostatin is a protein that negatively regulates skeletal muscle growth but its inhibition in rodents also improves insulin sensitivity. In humans, myostatin appears to be upregulated by obesity and associated with insulin resistance, but observations are confounded by lifestyle factors and ageing. Aims: To delineate between the effects of obesity and ageing on myostatin expression in human skeletal muscle; to investigate the underlying causes of these effects; and to establish the functional significance and interconnectivity of modulating insulin sensitivity and myostatin expression in human skeletal muscle cells. Methods: In Chapter 3 a cross-sectional analysis of skeletal muscle gene expression was undertaken, in conjunction with correlation analyses between serum myostatin and descriptive characteristics, to isolate the effects of obesity and ageing per se on myostatin expression and abundance. In Chapters 4 and 5, in vitro and ex vivo techniques were employed using human primary myotubes to investigate the potential involvement of lipid-induced insulin and anabolic resistance and secretory cross-talk between subcutaneous adipose tissue and muscle, in the obesity-mediated upregulation of myostatin and the associated impairment of insulin and anabolic sensitivity. In Chapter 6, the novel polyphenol metabolite Urolithin A was applied to human myotubes and a model of adipocytes, to investigate its therapeutic potential to enhance insulin and anabolic sensitivity and to suppress myostatin expression. Results: In Chapter 3 it was revealed that muscle myostatin expression is uniquely upregulated by obesity with ageing, but not by ageing in the absence of obesity, and occurs concurrently with insulin resistance and abnormal regulation of pathways involved in the maintenance of skeletal muscle mass. This association was corroborated by positive correlations between serum myostatin and multiple indices of adiposity, but not age. In Chapters 4 and 5 it was demonstrated that neither acutely elevated fatty acid availability (which induced insulin and anabolic resistance), nor chronic exposure to obese subcutaneous adipose tissue conditioned medium (which did not induce insulin or anabolic resistance but altered the expression of genes involved in myogenesis and muscle protein breakdown) recapitulated the obesity-mediated upregulation of myostatin expression. In Chapter 6 it was demonstrated for the first time that Urolithin A suppresses myostatin expression and enhances glucose transport in human myotubes (and 3T3-L1 adipocytes), the latter of which was associated with an upregulation of GLUT4 expression. Conclusions: Skeletal muscle myostatin expression is uniquely upregulated by obesity per se, but this does not appear to be mediated by lipid-induced insulin resistance, nor by the secretory milieux of obese subcutaneous adipose tissue. Nevertheless, both models perturbed factors involved in myogenesis and muscle protein breakdown, independent of an upregulation of myostatin. Thus, the factors responsible for the obesity-mediated upregulation of myostatin remain to be elucidated and future work to establish such causality is required. Furthermore, translational research to investigate the potential of Urolithin A to enhance glucose handling in peripheral tissues and to repress myostatin’s inhibitory effects on muscle growth is warranted in humans and could be of particular benefit in conditions such as sarcopenic obesity

Chronic effects of high intensity interval training on postprandial lipaemia in healthy individuals

BACKGROUND: Dyslipidaemia is associated with atherosclerosis and subsequent cardiovascular disease. Acute high intensity interval exercise (HIIT) is a time-efficient means to improve postprandial lipaemia (PPL), but little is known about its cumulative effects. AIM: To investigate the chronic effects of HIIT on PPL and metabolic health in healthy young individuals. METHODS: Following ethical approval, 8 recreationally active males (mean ± SD: 22 ± 3years, 1.77 ± 0.07m, 67.7 ± 6.2kg) undertook two 6h mixed-meal tolerance tests, before the first session and ≥72h after the final session of four weeks of HIIT (16 sessions; 10x60s bouts of cycling at 90%VO2max, interspersed by 60s intervals at 45%VO2max). A vastus lateralis muscle sample was taken in the fasted state before and after training. Regular arterialised and deep venous blood samples across the forearm, brachial artery blood flow measurements, and whole body indirect calorimetry data were obtained before, and at regular intervals for 6h after consumption of the mixed-meal tolerance test before and after training. RESULTS: VO2max (mean ± SEM) increased from 47.30 ± 5.46 to 51.80 ± 3.41mLO2∙kg-1∙min-1 (P < 0.01), without changes in body mass. Neither fasting circulating triglyceride (TAG) concentrations and postprandial responses, nor skeletal muscle protein content of lipolytic enzymes were altered with training. Free fatty acid (FFA) forearm uptake and fractional extraction significantly increased after training (ANOVA main effects; P = 0.03 and P = 0.048, respectively), with a strong trend towards increased blood flow in the latter half of the tolerance test (P = 0.07). CONCLUSIONS: Four weeks of HIIT increases cardiovascular fitness and the postprandial uptake and extraction of FFA across the forearm but has no chronic effect on circulating TAG. Our findings suggest the frequently observed exercise-induced reduction in postprandial TAG is a transient effect of the last exercise bout, and highlight the importance of regular exercise for the maintenance of training-induced benefits to postprandial lipaemia

Skeletal muscle myostatin mRNA expression is upregulated in aged human adults with excess adiposity, but is not associated with insulin resistance and ageing

Myostatin negatively regulates skeletal muscle growth and appears upregulated in human obesity and associated with insulin resistance. However, observations are confounded by ageing, and the mechanisms responsible are unknown. The aim of this study was to delineate between the effects of excess adiposity, insulin resistance and ageing on myostatin mRNA expression in human skeletal muscle and to investigate causative factors using in vitro models. An in vivo cross-sectional analysis of human skeletal muscle was undertaken to isolate effects of excess adiposity and ageing per se on myostatin expression. In vitro studies employed human primary myotubes to investigate the potential involvement of cross-talk between subcutaneous adipose tissue (SAT) and skeletal muscle, and lipid-induced insulin resistance. Skeletal muscle myostatin mRNA expression was greater in aged adults with excess adiposity than age-matched adults with normal adiposity (2.0-fold higher; P &lt; 0.05) and occurred concurrently with altered expression of genes involved in the maintenance of muscle mass but did not differ between younger and aged adults with normal adiposity. Neither chronic exposure to obese SAT secretome nor acute elevation of fatty acid availability (which induced insulin resistance) replicated the obesity-mediated upregulation of myostatin mRNA expression in vitro. In conclusion, skeletal muscle myostatin mRNA expression is uniquely upregulated in aged adults with excess adiposity and insulin resistance but not by ageing alone. This does not appear to be mediated by the SAT secretome or by lipid-induced insulin resistance. Thus, factors intrinsic to skeletal muscle may be responsible for the obesity-mediated upregulation of myostatin, and future work to establish causality is required

Chronic effects of high-intensity interval training on postprandial lipemia in healthy men

The aim of this study was to determine thechronic (≥72h post-exercise) effects of high intensity interval training (HIIT) on postprandial lipaemia and metabolic markers in healthy volunteers. Eight physically active young males (Mean ± SD: age 22 ± 3years, height 1.77 ± 0.07m, body mass 67.7 ± 6.2kg) underwent two 6h mixed-meal tolerance tests and resting vastus lateralis muscle biopsies, before the first- and ≥72h after the final-session of four weeks of HIIT (16 sessions in total; 10x60s bouts of cycling at 90% maximal oxygen uptake [V̇O2max], interspersed by 60s intervals at 45% V̇O2max). Arterialised and deep venous blood samples across the forearm, brachial artery blood flow measurements, and whole-body indirect calorimetry data were obtained before, and at regular intervals for 6h after, consumption of a standardised mixed-meal. The main findings revealed that, when assessed ≥72h post-exercise, postprandial free fatty acid (FFA) uptake across the forearm was increased in response to exercise training (P= 0.025). However, four weeks of HIIT did not alter fasting or postprandial circulating triglyceride (TAG) concentrations, or their tissue uptake, despite a 10.2 ± 7.7% improvement in V̇O2max(P= 0.004). Protein content of adipose triglyceride lipase (ATGL) in the vastus lateralis at rest was reduced by 25 ± 21% (P= 0.01). Collectively, these findings suggest that 4 weeks of HITT enhances postprandial clearance of FFA, when assessed ≥72h post-exercise, but does not confer persisting (training) adaptations in postprandial triglyceridaemia

Predictors of vitamin D status and its association with parathyroid hormone in young New Zealand children.

BACKGROUND: Despite increased awareness of the adverse health effects of low vitamin D status, few studies have evaluated 25-hydroxyvitamin D [25(OH)D] status in young children. OBJECTIVES: We aimed to assess vitamin D status on the basis of 25(OH)D and its relation with parathyroid hormone (PTH) and to identify possible predictors of 25(OH)D status in young children living in a country with minimal vitamin D fortification. DESIGN: Serum 25(OH)D and PTH concentrations were measured in a cross-sectional sample of children aged 12-22 mo [n = 193 for 25(OH)D, n = 144 for PTH] living in Dunedin, New Zealand (latitude: 45 degrees S). Anthropometric, dietary, and sociodemographic data were collected. RESULTS: The majority of children sampled in the summer (94%; 47 of 50) had 25(OH)D >50 nmol/L; however, nearly 80% of children sampled in the winter (43 of 55) had serum concentrations 60-65 nmol/L, a plateau in PTH was evident. CONCLUSIONS: Seasonal variation in 25(OH)D concentration implies that postsummer vitamin D stores were insufficient to maintain status >50 nmol/L year-round. Examination of the predictors of 25(OH)D in our model shows few modifiable risk factors, and thus effective dietary strategies may be required if future research determines that children with 25(OH)D concentrations <50 nmol/L are at significant health risk. This trial was registered at www.actr.org.au as ACTRN12605000487617