Utilizing Knowledge Transfer to Promote Management of Countervailing Risks in Value Stream Analysis

Organizations are frequently faced with the challenges of modifying and streamlining their processes by utilizing the latest process improvement techniques such as Lean Thinking. They use these techniques to allow them to better perform their organizational purposes through the elimination of waste and non-value added steps. Personnel performing these modifications need to account for potential outcomes and risks when streamlining processes. An association of knowledge transfer and experience to the identification and handling of these countervailing or alternative risks when performing Lean Thinking value stream analysis is investigated. The elements of risk management, Lean Thinking and knowledge transfer are described. This dissertation presents the results of a non-experimental examination to identify knowledge transfer as a means to promote management of countervailing risks that may arise when performing Value Stream Analysis and provides a foundation for future research. A research model was formulated, and a survey instrument developed with data collected from Department of the Navy personnel during Lean Thinking events. Quantitative data analysis supported the research question and showed an association between a decision-maker\u27s knowledge from other projects and the identification and handling of countervailing risks that arise during Value Stream Analysis

Determination of the Impact of a Human Capital Decision Cost Model on the Economic Performance Measures of a Technical Services Company

Human Capital has a major impact on cash flow management decisions in a Technical Services company. Decisions to hire or terminate employees to meet contract requirements affect the company\u27s economic value. The objective of this research is to develop a model that assists management in establishing a starting point in making, as efficiently as possible, those decisions that impact employees\u27 lives. To understand that impact, the operations and economic parameters of a Technical Services company are compared with those of a manufacturing company. This analysis establishes two · essential points for Technical Services organizations; first, that the capital investment decision is one of human capital skills and that cost is critical for an organization\u27s financial success. Building on this conceptual base, the research develops a starting point for managerial decisions associated with human capital using two parallel decision models. First, the Quality Function Deployment (QFD) technique is applied to map service industry business objectives with employee skill sets. This determines which job classifications are most critical. A weighting factor is then developed to identify skill importance. Concurrently, a linear programming model determines the impact of hiring and termination on costs. This approach provides a quantitative methodology that supports service industry managers in understanding both the strategic and tactical (bottom line) financial value of their Human Capital decisions. Armed with that knowledge, they can begin an employment decision process based on the quantitative information provided by these models and that integrates with other subjective and system based factors that must also be a part of a comprehensive human resources plan

AvrRpm1 Missense Mutations Weakly Activate RPS2-Mediated Immune Response in <em>Arabidopsis thaliana</em>

<div><p>Plants recognize microbes via specific pattern recognition receptors that are activated by microbe-associated molecular patterns (MAMPs), resulting in MAMP-triggered immunity (MTI). Successful pathogens bypass MTI in genetically diverse hosts via deployment of effectors (virulence factors) that inhibit MTI responses, leading to pathogen proliferation. Plant pathogenic bacteria like <em>Pseudomonas syringae</em> utilize a type III secretion system to deliver effectors into cells. These effectors can contribute to pathogen virulence or elicit disease resistance, depending upon the host plant genotype. In disease resistant genotypes, intracellular immune receptors, typically belonging to the nucleotide binding leucine-rich repeat family of proteins, perceive bacterial effector(s) and initiate downstream defense responses (effector triggered immunity) that include the hypersensitive response, and transcriptional re-programming leading to various cellular outputs that collectively halt pathogen growth. Nucleotide binding leucine-rich repeat sensors can be indirectly activated via perturbation of a host protein acting as an effector target. AvrRpm1 is a <em>P. syringae</em> type III effector. Upon secretion into the host cell, AvrRpm1 is acylated by host enzymes and directed to the plasma membrane, where it contributes to virulence. This is correlated with phosphorylation of Arabidopsis RIN4 <em>in vivo</em>. RIN4 is a negative regulator of MAMP-triggered immunity, and its modification in the presence of four diverse type III effectors, including AvrRpm1, likely enhances this RIN4 regulatory function. The RPM1 nucleotide binding leucine-rich repeat sensor perceives RIN4 perturbation in disease resistant plants, leading to a successful immune response. Here, demonstrate that AvrRpm1 has a fold homologous to the catalytic domain of poly(ADP-ribosyl) polymerase. Site-directed mutagenesis of each residue in the putative catalytic triad, His63-Tyr122-Asp185 of AvrRpm1, results in loss of both AvrRpm1-dependent virulence and AvrRpm1-mediated activation of RPM1, but, surprisingly, causes a gain of function: the ability to activate the RPS2 nucleotide binding leucine-rich repeat sensor.</p> </div

Missense mutants of AvrRpm1 do not elicit an RPM1-mediated hypersensitive response, but can be translocated.

<p>(<b>A</b>) Four week old Col-0 plants were hand inoculated with 5×10⁷ cfu/mL <i>Pto</i> DC3000 carrying either an empty vector or <i>avrRpm1</i> with missense mutations eliminating localization to the membrane (G2A) <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042633#pone.0042633-Nimchuk1" target="_blank">[11]</a>, to the putative catalytic triad (H63A, Y122A, and D185A) and a double mutant (G2A D185A) and assayed for the ability to promote electrolyte leakage via RPM1-mediated hypersensitive response (HR) (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042633#s2" target="_blank">Methods</a>). Error bars represent 2× SEM. (<b>B</b>) Five week old <i>rpm1 RPS2</i> plants were infiltrated with 5×10⁷ cfu/mL <i>Pto</i> DC3000 carrying missense mutations of <i>avrRpm1</i> cloned to produce fusion proteins with Δ79<i>avrRpt2</i>. The ability to elicit an RPS2-mediated hypersensitive response was assayed at 20 hours post inoculation (HPI). Leaf counts (HR positive/total inoculated) are displayed under representative leaves.</p

AvrRpm1 exhibits structural homology to the catalytic domain of Poly-ADP-ribosyl polymerase (PARP).

<p>(<b>A</b>) Sequence alignment of DT family ADP-ribosylating proteins <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042633#pone.0042633-Yates1" target="_blank">[35]</a> and the four AvrRpm1 family proteins illustrating key regions of conservation. Secondary structure for each region is shown above. Highly conserved residues are highlighted in blue. Red carets denote the catalytic triad of PARP. (<b>B</b>) Homology model of the AvrRpm1 reference allele (copper) from <i>P. syringae</i> pv. <i>maculicola</i> M6 (<i>Psm</i> M6) with the catalytic domain of Poly-ADP-ribosyl polymerase 1 (PARP-1; PDB ID: 3GJW) (silver). The side chains for residues highlighted in (<b>A</b>) are denoted by dark blue (AvrRpm1) and light blue (PARP-1). Residues in the catalytic triad are labeled according to AvrRpm1. “N” and “C” represent the amino- and carboxy-terminus of the protein respectively. Independent homology models for the remaining three AvrRpm1 family members from (<b>B</b>) <i>P. syringae</i> pvs. <i>syringae</i> B728a (<i>Psy</i> B728a), (<b>C</b>), <i>pisi</i> race 6 (<i>Ppi</i> race 6) (<b>D</b>), and <i>phaseolicola</i> 2708 (<i>Psp</i> 2708).</p

Putative catalytic triad residues are required for AvrRpm1 virulence that is inhibited via weak activation of RPS2-mediated disease resistance.

<p>(<b>A–C</b>) Growth of <i>Psm</i> CR299, a derivative of <i>Psm</i> M2 that carries an insertion in <i>avrRpm1 </i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042633#pone.0042633-Ritter1" target="_blank">[13]</a> was complemented in <i>trans</i> with plasmids expressing wild type AvrRpm1 and missense mutations as noted. Four week old <i>rpm1</i> (<b>A</b>), <i>rpm1 rps2</i> (<b>B</b>) or <i>rpm1 rps2 rin4</i> (<b>C</b>) plants were inoculated with 10⁶ cfu/mL and samples were collected on day 0 and day 3. Error bars represent 2× SEM. An analysis of variance (ANOVA) was performed among the day 3 samples followed by Tukey's post-hoc analysis (α = 0.05) with significance groups indicated by letters on the graph. (<b>D</b>) Immunoblot assay for accumulation of the wild type and mutant AvrRpm1 proteins at 3 days post inoculation for strains used in (<b>B</b>) and (<b>C</b>).</p

Thigh-length compression stockings and DVT after stroke

Controversy exists as to whether neoadjuvant chemotherapy improves survival in patients with invasive bladder cancer, despite randomised controlled trials of more than 3000 patients. We undertook a systematic review and meta-analysis to assess the effect of such treatment on survival in patients with this disease

Genetic heterogeneity in LEOPARD syndrome: two families with no mutations in PTPN11

LEOPARD syndrome (lentigines, electrocardiographic conduction abnormalities, ocular hypertelorism, pulmonary stenosis, abnormal genitalia, retardation of growth, and sensorineural deafness) is an autosomal dominant condition. The main clinical features include multiple lentigines, cardiovascular defects, and facial anomalies, some of which are shared with Noonan syndrome (NS). Recent reports have shown that LEOPARD syndrome can be caused by mutations in PTPN11, the gene in which mutations can produce NS. Here we report the findings of mutation screening and linkage analysis of PTPN11 in three families with LEOPARD syndrome. We identified a novel mutation in one family. The mutation (1529A&gt;C) substitutes proline for glutamine at amino acid 510 (Gln510Pro). No variations in sequence were observed in the other two families, and negative LOD scores excluded linkage to the PTPN11 locus, showing that LEOPARD syndrome is genetically heterogeneous

Food reinforcement, energy intake, and macronutrient choice123

Background: Food is a powerful reinforcer that motivates people to eat. The relative reinforcing value of food (RRVfood) is associated with obesity and energy intake and interacts with impulsivity to predict energy intake