A Structure–Conduct–Performance Perspective of How Strategic Supply Chain Integration Affects Firm Performance

There are several factors that affect a firm\u27s ability to successfully integrate internally and externally for organizational improvement. This study seeks to understand the relationship between a firm\u27s strategy, its supply chain integration efforts, and firm performance. Leveraging the theoretical lens of structure–conduct–performance from the industrial organization economics literature, and utilizing both archival and survey data, we describe how firms may align their internal and external supply chain integration strategies with customers and suppliers. In doing so, these internal and external integration strategies affect the firm\u27s ability to respond to customer demand, which then impacts operational and financial performance. Our work provides theoretical and empirical evidence of these relationships and thus extends prior strategic supply chain integration literature

Influence of Tap Water Quality and Household Water Use Activities on Indoor Air and Internal Dose Levels of Trihalomethanes

Individual exposure to trihalomethanes (THMs) in tap water can occur through ingestion, inhalation, or dermal exposure. Studies indicate that activities associated with inhaled or dermal exposure routes result in a greater increase in blood THM concentration than does ingestion. We measured blood and exhaled air concentrations of THM as biomarkers of exposure to participants conducting 14 common household water use activities, including ingestion of hot and cold tap water beverages, showering, clothes washing, hand washing, bathing, dish washing, and indirect shower exposure. We conducted our study at a single residence in each of two water utility service areas, one with relatively high and the other low total THM in the residence tap water. To maintain a consistent exposure environment for seven participants, we controlled water use activities, exposure time, air exchange, water flow and temperature, and nonstudy THM sources to the indoor air. We collected reference samples for water supply and air (pre–water use activity), as well as tap water and ambient air samples. We collected blood samples before and after each activity and exhaled breath samples at baseline and postactivity. All hot water use activities yielded a 2-fold increase in blood or breath THM concentrations for at least one individual. The greatest observed increase in blood and exhaled breath THM concentration in any participant was due to showering (direct and indirect), bathing, and hand dishwashing. Average increase in blood THM concentration ranged from 57 to 358 pg/mL due to these activities. More research is needed to determine whether acute and frequent exposures to THM at these concentrations have public health implications. Further research is also needed in designing epidemiologic studies that minimize data collection burden yet maximize accuracy in classification of dermal and inhalation THM exposure during hot water use activities

Sestrin2 is a leucine sensor for the mTORC1 pathway

Leucine is a proteogenic amino acid that also regulates many aspects of mammalian physiology, in large part by activating the mTOR complex 1 (mTORC1) protein kinase, a master growth controller. Amino acids signal to mTORC1 through the Rag guanosine triphosphatases (GTPases). Several factors regulate the Rags, including GATOR1, aGTPase-activating protein; GATOR2, a positive regulator of unknown function; and Sestrin2, a GATOR2-interacting protein that inhibits mTORC1 signaling. We find that leucine, but not arginine, disrupts the Sestrin2-GATOR2 interaction by binding to Sestrin2 with a dissociation constant of 20 micromolar, which is the leucine concentration that half-maximally activates mTORC1. The leucine-binding capacity of Sestrin2 is required for leucine to activate mTORC1 in cells. These results indicate that Sestrin2 is a leucine sensor for the mTORC1 pathway.United States. National Institutes of Health (R01CA103866)United States. National Institutes of Health (AI47389)United States. Department of Defense (W81XWH-07-0448)United States. National Institutes of Health (T32 GM007753)United States. National Institutes of Health (F30 CA189333)United States. National Institutes of Health (F31 CA180271

The future of human nature: a symposium on the promises and challenges of the revolutions in genomics and computer science, April 10, 11, and 12, 2003

This repository item contains a single issue of the Pardee Conference Series, a publication series that began publishing in 2006 by the Boston University Frederick S. Pardee Center for the Study of the Longer-Range Future. This was the Center's Symposium on the Promises and Challenges of the Revolutions in Genomics and Computer Science took place during April 10, 11, and 12, 2003. Co-organized by Charles DeLisi and Kenneth Lewes; sponsored by Boston University, the Frederick S. Pardee Center for the Study of the Longer-Range Future.This conference focused on scientific and technological advances in genetics, computer science, and their convergence during the next 35 to 250 years. In particular, it focused on directed evolution, the futures it allows, the shape of society in those futures, and the robustness of human nature against technological change at the level of individuals, groups, and societies. It is taken as a premise that biotechnology and computer science will mature and will reinforce one another. During the period of interest, human cloning, germ-line genetic engineering, and an array of reproductive technologies will become feasible and safe. Early in this period, we can reasonably expect the processing power of a laptop computer to exceed the collective processing power of every human brain on the planet; later in the period human/machine interfaces will begin to emerge. Whether such technologies will take hold is not known. But if they do, human evolution is likely to proceed at a greatly accelerated rate; human nature as we know it may change markedly, if it does not disappear altogether, and new intelligent species may well be created

The future of human nature: a symposium on the promises and challenges of the revolutions in genomics and computer science, April 10, 11, and 12, 2003

This repository item contains a single issue of the Pardee Conference Series, a publication series that began publishing in 2006 by the Boston University Frederick S. Pardee Center for the Study of the Longer-Range Future. This was the Center's Symposium on the Promises and Challenges of the Revolutions in Genomics and Computer Science took place during April 10, 11, and 12, 2003. Co-organized by Charles DeLisi and Kenneth Lewes; sponsored by Boston University, the Frederick S. Pardee Center for the Study of the Longer-Range Future.This conference focused on scientific and technological advances in genetics, computer science, and their convergence during the next 35 to 250 years. In particular, it focused on directed evolution, the futures it allows, the shape of society in those futures, and the robustness of human nature against technological change at the level of individuals, groups, and societies. It is taken as a premise that biotechnology and computer science will mature and will reinforce one another. During the period of interest, human cloning, germ-line genetic engineering, and an array of reproductive technologies will become feasible and safe. Early in this period, we can reasonably expect the processing power of a laptop computer to exceed the collective processing power of every human brain on the planet; later in the period human/machine interfaces will begin to emerge. Whether such technologies will take hold is not known. But if they do, human evolution is likely to proceed at a greatly accelerated rate; human nature as we know it may change markedly, if it does not disappear altogether, and new intelligent species may well be created

Changes in Breath Trihalomethane Levels Resulting from Household Water-Use Activities

Common household water-use activities such as showering, bathing, drinking, and washing clothes or dishes are potentially important contributors to individual exposure to trihalomethanes (THMs), the major class of disinfection by-products of water treated with chlorine. Previous studies have focused on showering or bathing activities. In this study, we selected 12 common water-use activities and determined which may lead to the greatest THM exposures and result in the greatest increase in the internal dose. Seven subjects performed the various water-use activities in two residences served by water utilities with relatively high and moderate total THM levels. To maintain a consistent exposure environment, the activities, exposure times, air exchange rates, water flows, water temperatures, and extraneous THM emissions to the indoor air were carefully controlled. Water, indoor air, blood, and exhaled-breath samples were collected during each exposure session for each activity, in accordance with a strict, well-defined protocol. Although showering (for 10 min) and bathing (for 14 min), as well as machine washing of clothes and opening mechanical dishwashers at the end of the cycle, resulted in substantial increases in indoor air chloroform concentrations, only showering and bathing caused significant increases in the breath chloroform levels. In the case of bromodichloromethane (BDCM), only bathing yielded a significantly higher air level in relation to the preexposure concentration. For chloroform from showering, strong correlations were observed for indoor air and exhaled breath, blood and exhaled breath, indoor air and blood, and tap water and blood. Only water and breath, and blood and breath were significantly associated for chloroform from bathing. For BDCM, significant correlations were obtained for blood and air, and blood and water from showering. Neither dibromochloromethane nor bromoform gave measurable breath concentrations for any of the activities investigated because of their much lower tap-water concentrations. Future studies will address the effects that changes in these common water-use activities may have on exposure

Genetics Analysis Workshop 20: Methods and Strategies for the New Frontiers of Epigenetics and Pharmacogenomics

GAW20 provided a platform for developing and evaluating statistical methods to analyze human lipid-related phenotypes, DNA methylation, and single-nucleotide markers in a study involving a pharmaceutical intervention. In this article, we present an overview of the data sets and the contributions analyzing these data. The data, donated by the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) investigators, included data from 188 families (N = 1105) which included genome-wide DNA methylation data before and after a 3-week treatment with fenofibrate, single-nucleotide polymorphisms, metabolic syndrome components before and after treatment, and a variety of covariates. The contributions from individual research groups were extensively discussed prior, during, and after the Workshop in groups based on discussion themes, before being submitted for publication

Phosphorylation of LXRα impacts atherosclerosis regression by modulating monocyte trafficking

LXRα activation in macrophages enhances regression of atherosclerotic plaques in mice by regulating genes crucial for cholesterol efflux, cell motility and inflammation. Diabetes, however, impairs plaque regression in mice. LXRα is phosphorylated at serine 198 (pS198), which affects the expression of genes controlling inflammation, lipid metabolism and cell movement. We hypothesize that LXRα function is affected by hyperglycemia through changes in LXRα pS198. Indeed, macrophages cultured in diabetes relevant high glucose versus normal glucose display alterations in LXR-dependent gene expression and increased LXRα pS198. We therefore examined the consequence of disrupting LXRα phosphorylation (S196A in mouse LXRα) during regression of atherosclerosis in normal and diabetic mice. We find that phosphorylation deficient LXRα S196A reduces macrophage retention in plaques in diabetes, which is predicted to be anti-atherogenic and enhance plaque regression. However, this favorable effect on regression is masked by increased monocyte infiltration in the plaque attributed to leukocytosis in LXRα S196A mice. RNA-seq of plaque macrophages from diabetic S196A mice shows increased expression of chemotaxis and decreased expression of cell adhesion genes, consistent with reduced macrophage retention by LXRα S196A. Thus, the non-phosphorylated form of LXRα precludes macrophage retention in the plaque. Our study provides the first evidence for a physiological role of LXRα phosphorylation in modulating atherosclerosis regression. Compounds that prevent LXRα phosphorylation or ligands that induce the conformation of non-phosphorylated LXRα may selectively enhance macrophage emigration from atherosclerotic plaques

Bankruptcy Reform

Presentation materials from the Bankruptcy Reform Course held by UK/CLE in December 1994