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Background {#Sec1} ========== The American Academy of Pediatrics recommends participation in family meals as a childhood obesity prevention strategy due to the literature demonstrating a protective effect of participation in healthy mealtime routines on child diet and weight \[[@CR1]\]. However, the current evidence linking family meals with improved child dietary intake (increased fruit and vegetable intake, decreased sugar-sweetened beverage (SSB) intake) and weight status (decreased body mass index (BMI; (weight (kg)/height (m)^2^)) z-score) has significant limitations. The majority of the family meals literature -- specifically in the area of childhood obesity prevention -- represents observational studies, demonstrating only an associative relationship of family meals with child diet and weight status \[[@CR2]--[@CR5]\]. What's more, racial and ethnic differences have been highly understudied; given that the segment of the United States (US) child population with high prevalence of obesity is racial and ethnic minorities \[[@CR6]\], it has been suggested that this is an area in which additional research is needed. Similarly, the existing family meals intervention research (i.e., studies designed specifically to examine the cause and effect relationship between family meals and child diet and weight status), while strong with regard to study design, is limited and primarily targets non-Hispanic White children (8 to 12 years old), particularly from well-educated families \[[@CR7], [@CR8]\]. In addition, the majority of the current research fails to examine the child health impact of family meals beyond BMI (e.g., central adiposity and blood pressure (BP)), with only a small number of studies including additional outcomes (e.g., disordered eating) \[[@CR9]--[@CR12]\]. Given the ongoing childhood obesity public health crisis \[[@CR13]\] and the potential protective effect of family meals, there is need for additional family meals research, specifically experimental studies with expanded health outcomes that focus on the at-risk populations in highest need of intervention. Future research, specifically intervention work, would also benefit from an expansion of the target age range to include younger children (4--7 year olds), who are laying the foundation of their eating patterns \[[@CR14]\], and are capable of participating in family meal preparations \[[@CR15]\]. The purpose of this paper is to address this gap in the literature by presenting the objectives and research methods of a 10-week multi-component family meals intervention study, Simple Suppers, aimed at eliciting positive changes in child dietary intake and weight status. The Simple Suppers study is a two group quasi-experimental trial with staggered cohort design that targets underserved families with elementary school age children (4--10 years) and includes an examination of health outcomes beyond weight status. Methods {#Sec2} ======= Objectives and hypotheses {#Sec3} ------------------------- The objectives of this study with related hypotheses will be as follows:Assess the impact of Simple Suppers on children and caregivers of participating families relative to children and caregivers of families in the control group.Hypothesis 1.1.Diet quality, BMI z-scores and BMI, waist circumference (WC) z-scores and WC, and BP z-scores and BP will improve more from baseline to post-intervention among children and caregivers, respectively, participating in the intervention than in the controls.Hypothesis 1.2.Diet quality, BMI z-scores and BMI, WC z-scores and WC, and BP z-scores and BP improvements will be maintained during the follow-up period among children and caregivers, respectively, participating in the intervention. Objective 2.Assess the impact of Simple Suppers on the family meals environment of participating families relative to the controls.Hypothesis 2.1.Frequency of family meals (breakfast and dinner), TV viewing during meals, and eating family meals in a dining area will improve more from baseline to post-intervention among families participating in the intervention than in the controls.Hypothesis 2.2.Frequency of family meals (breakfast and dinner), TV viewing during the meals, and eating family meals in a dining area improvements will be maintained during the follow-up period among families participating in the intervention. Study design {#Sec4} ------------ The study will be implemented over 12-months as a two-group (intervention; waitlist control) quasi-experimental trial using a staggered cohort design (Table [1](#Tab1){ref-type="table"}). At each of three time periods, separated by 10 weeks, a cohort of 20 families will be recruited. Each cohort will be divided into an intervention and waitlist control group (10 families in each). Consequently, a total of 60 families (30 in the intervention group and 30 in the waitlist control group) will be enrolled. Upon confirmation of study eligibility, a baseline data collection appointment will be scheduled at the participating family's home or the community center during the two weeks preceding intervention commencement. Data will be collected on the primary food preparing caregiver and all children 4--10 years old. Written caregiver consent and child assent will be obtained. Data will be collected on all outcomes via direct measure and questionnaires at baseline (time point 0, T0), 10-week post-test (time point 1, T1), and 10-week follow-up (time point 2, T2). Repeatability of the intervention (replication) will be evaluated by assessing measures on the waitlist control group at T1 and T2. Assessments will last up to 90 min. A team of trained research staff, blinded from group assignment, will facilitate data collection. Caregiver participants will receive a \$25 grocery store gift card at each data collection point for their participation in the research. All study materials and procedures have been approved by the Institutional Review Board at Ohio State University.Table 1Simple Suppers Intervention Study Design: Two-Group, Staggered Cohort Quasi-Experimental Design Following baseline data collection, families will decide whether to enroll in either the upcoming 10-week session of Simple Suppers (intervention group) or to wait for 10-weeks (waitlist control group) after which time they would begin the Simple Suppers program. Randomization of families is not feasible because of scheduling conflicts with participating families, the desire of families to participate in the program with families they know, and the need to establish trust with the site/participating families; thus, to preserve sample size and establish trust with the site/participating families, the personal preference of participating families will determine group membership. Setting {#Sec5} ------- A faith-based community center will serve as the setting for the Simple Suppers intervention. The question of "who is my neighbor?" is central to the mission and ministries of the center, which has approximately 10,000 visits per month for programming. The most recent service area census tracts demonstrate the following statistics in the center's immediately surrounding neighborhoods: median household income is \$32,307 to \$58,490, compared to \$51,890 in the broader county; number of families falling below the poverty line ranges from 10.7% to 24.9%, compared to 13.2% in the broader county; higher percentage of racial and ethnic minorities than the county as a whole, with 41.8% being Black compared to 21.2 in the county; and a high percentage of households that are families (58.7%). Participants {#Sec6} ------------ Participants will be recruited in-person at community center events, center newsletter advertisements, and posters displayed in center. Information on recruitment materials will direct interested families to contact the research team for a screening evaluation to determine study eligibility. To be eligible for inclusion, caregivers should be the primary food preparer in the home; be responsible for at least one child 4--10 years of age; speak English as the primary language in the home; and have lived in the U.S. for at least one year. Families with one or more family members following a restrictive or therapeutic diet will be excluded. Intervention {#Sec7} ------------ The Intervention Mapping protocol was utilized in the development of the Simple Suppers intervention \[[@CR16], [@CR17]\]. Formulation of proximal program objectives occurred as the first step in the mapping process. Based on the current evidence linking family meals with improved child diet and weight status \[[@CR2]--[@CR5]\], the following program objectives were formulated: 1) 'Increase frequency of family meals prepared in the home (≥5 days/week)' and 2) 'Improve child diet quality (significantly increase Healthy Eating Index (HEI) score (p \< 0.05); increase servings of fruits and vegetables to meet Dietary Guidelines recommendations; significantly decrease daily servings of sugar sweetened beverages (p \< 0.05)' (Table [2](#Tab2){ref-type="table"}).Table 2Overview of formulated program objectives at each level of interventionProgram objectiveLevel of InterventionTarget groupPerformance Objectives1. Increase frequency of family meals prepared in the home (≥5 days/week)^a^IndividualChildPO1. Children participate in cooking activitiesInterpersonalCaregiverPO2. Caregivers identify health benefits of regular family meals prepared in the home\ PO3. Caregivers plan well-balanced weekly dinner menus that include ≥1 svg from 3 of the 5 food groups\ PO4. Caregivers plan when and where family meals will be served in the home\ PO5. Caregivers use list for grocery shopping\ PO6. Caregivers use cost-saving strategies for family meals in the home\ PO7. Caregivers use time-saving strategies for family meals in the home2. Improve child diet quality (significantly increase HEI score (p \< 0.05); increase daily svgs of fruits, vegetables to Dietary Guidelines recommendations;^b^ significantly decrease daily svgs of: SSBs (p \< 0.05 decrease)^c^IndividualChildPO1. Children know health benefits of eating well-balanced meals and snacks\ PO2. Children participate in planning/preparing well-balanced family meals ≥2x/weekInterpersonalCaregiverPO3. Caregivers know benefits of serving well-balanced meals/snacks\ PO4. Caregivers serve family meal in the home that include ≥1 svg from 3 of the 5 food groups ≥1x/week\ PO5. Caregivers serve ≥3 snacks/week that include ≥1 serving from 2 food groups\ PO6. Caregivers buy food for planned meals/snacks at grocery storePO: Performance objective HEI: Healthy Eating Index SSB: Sugar sweetened beverage Svg: Serving^a^Measured by asking the question, "During the past 7 days, how many times did all or most, of your family eat dinner together?"\[[@CR7]\]^b^U.S. Departments of Agriculture and Health and Human Services. Dietary Guidelines for Americans, 2010. 7th ed., Washington, DC. December, 2010 \[[@CR18]\]^c^Measured by 24-h dietary recall \[[@CR29]\] Matrices containing the behavioral performance objectives relating to each program objective were created for each level of intervention: individual (child) and interpersonal (caregiver) (Table [2](#Tab2){ref-type="table"}). Development of the performance objectives were guided by the evidence-based 2010 Dietary Guidelines for Americans guidelines for families and children \[[@CR18]\]. For example, under program objective 1) (family meals), the performance objective at the individual (child) level was 'Children participate in cooking activities' and at the interpersonal (caregiver) level, 'Caregivers identify health benefits of regular family meals prepared in the home'. After formulation of performance objectives, a list of personal determinants for each performance objective was generated based on the theoretical foundation of the Simple Suppers program -- the Social Cognitive Theory, which posits that behavior change is a function of a reciprocal relationship between personal (e.g., behavioral capabilities and cognitive factors, such as self-efficacy and self-evaluation) and environmental (e.g., norms, modeling, and reinforcement) factors \[[@CR19], [@CR20]\]. Next, personal determinants were selected for children at the individual level and caregivers at the interpersonal level based on importance (i.e., strength of the association of the determinant with the behavior) and changeability (i.e., likelihood that the intervention may impact the determinant) \[[@CR16]\]. The personal determinants included: behavioral capability; self-efficacy; self-evaluation; and norms, modeling, and reinforcement (Table [3](#Tab3){ref-type="table"}). The performance objectives were then crossed with the selected determinants, which resulted in matrices of change objectives (Tables [3](#Tab3){ref-type="table"} and [4](#Tab4){ref-type="table"}). The change objectives stated precisely what needs to change in the determinants' behavioral outcomes in order to accomplish the performance objectives. They were developed using action words and followed by a statement of what is expected to result from the intervention \[[@CR16], [@CR17]\]. Because two target groups were selected, two difference matrices of change were developed under each program objective. For example, for program objective 1) (family meals), on the individual (child) level, the performance objective for children that stated 'Children participate in meal preparation activities' was crossed with the determinant 'behavioral capability', which resulted in the change objective that 'children practice cooking skills during Simple Suppers and at home'. An example on the interpersonal (caregiver) level, also for program objective 1) (family meals), is as follows: the performance objective for caregivers that stated 'Caregivers identify health benefits of regular family meals prepared in the home' was crossed with the determinant 'behavioral capability', which resulted in the change objective that 'Caregivers know benefits of regular family meals prepared at home.'Table 3Matrix of change objectives by level of intervention for program objective 1 of the simple suppers interventionProgram objective 1: Increase frequency of family meals prepared in the home (≥5 days/week)^a^Level of interventionPerformance objectivesPersonal determinantsBehavioral capabilitySelf-efficacySelf-evaluationNorms, modeling, reinforcementIndividual (child)PO1. Children participate in meal preparation activitiesCO1.1.1 Children practice cooking skills during Simple Suppers and at home\ CO1.1.2 Children are able to participate in age-appropriate cooking activities at Simple Suppers and at homeCO2.1 Children express confidence in participating in cooking activitiesCO3.1 Children are able to determine if they meet their weekly goal for participating in cooking at homeCO4.1.1 Children participate in cooking activities at Simple Suppers family meals 1x/week\ CO4.1.2 Children increase their participation in cooking at home to ≥1x/week in the homeInterpersonal (caregiver)PO2. Caregivers identify health benefits of regular family meals prepared in the homeCO1.2.1 Caregivers identify barriers to family meals at home\ CO1.2.2 Caregivers know benefits of regular family meals prepared at homePO3. Caregivers plan well-balanced weekly dinner menus that include ≥1 svg from 3 of the 5 food groupsCO1.3.1 Caregivers know importance of planning/serving well-balanced dinner menus\ CO1.3.2 Caregivers know how to plan/serve well-balanced family meals at homeCO2.3 Caregivers express confidence in planning/serving well-balanced family mealsCO3.3 Caregivers are able to determine if they meet their weekly goal for planning/serving well-balanced family meals at homeCO4.3.1 Caregivers learn to plan, prepare and serve well-balanced family meals from Simple Suppers Educators\ CO4.3.2 Caregivers plan, prepare and serve ≥1 well-balanced family meal at home each weekPO4. Caregivers plan when and where family meals will be served at homeCO1.4.1 Caregivers know importance of mealtime routines\ CO1.4.2 Caregivers know strategies to minimize mealtime distractions\ CO1.4.3 Caregivers plan/establish family mealtime routinesCO2.4.1 Caregiver expresses confidence in establishing mealtime routines at home\ CO2.4.2 Caregiver expresses confidence in minimizing mealtime distractionsCO3.4.1 Caregivers able to determine if family mealtime routines are being established\ CO3.4.2 Caregivers able to determine if mealtime distractions are minimizedCO4.4 Caregivers guided by Simple Suppers Educators in establishing family mealtime routines during Simple Suppers group family mealsPO5. Caregivers use list for grocery shoppingCO1.5.1 Caregivers know benefits of using a grocery list\ CO1.5.2 Caregivers know how to develop grocery list using planned family mealsCO2.5.1 Caregivers express confidence about developing grocery list\ CO2.5.2 Caregivers express confidence in using list for grocery shoppingCO3.5 Caregivers able to determine if they meet their goal to develop and use a list for grocery shoppingCO4.5 Caregivers develop weekly grocery list for planned family mealsPO6. Caregivers use cost-saving strategies for family meals at homeCO1.6 Caregivers know how to use cost-saving strategies to plan/prepare family meals at homeCO2.6 Caregivers express confidence in preparing and serving family meals at home on a budgetPO7. Caregivers use time-saving strategies for family meals at homeCO1.7 Caregivers know how to use time-saving strategies to plan/prepare family meals at homeCO2.7 Caregivers express confidence in preparing and servings family meals at home when time is limitedPO performance objective, CO change objective, HEI healthy eating index, Svg serving, SSB sugar sweetened beverage^a^Measured by asking the question, "During the past 7 days, how many times did all or most, of your family eat dinner together?"\[[@CR7]\] Table 4Matrix of Change Objectives by Level of Intervention for Program Objective 2 of the Simple Suppers InterventionProgram objective: Improve child diet quality (significantly increase HEI score (p \< 0.05); increase daily svgs of fruits, vegetables to Dietary Guidelines recommendations; significantly decrease daily svgs of: SSBs (p \< 0.05 decrease)^a^Level of interventionPerformance objectivesPersonal determinantsBehavioral capabilitySelf-efficacySelf-evaluationNorms, modeling, reinforcementIndividual (child)PO1. Children know health benefits of eating well-balanced meals/snacksCO1.1 Children know health benefits of eating a variety of nutritious foodsCO2.1 Children express confidence in knowing health benefits of eating well-balanced meals/snacksPO2. Children participate in planning/preparing well-balanced family meals/snacks ≥2x/weekCO1.2.1 Children can identify food group sources in meals/snacks\ CO1.2.2 Children are able to perform age-appropriate coking skillsCO2.2 Children express confidence in participating in meal/snack planning/preparationCO3.2 Children are able to determine if they meet their weekly goal for participating in family meal/snack preparationCO4.2.1 Children participate in cooking a well-balanced family meal/snack with peers of the same age 1x/week during Simple Suppers\ CO4.2.2 Children participate in cooking well-balanced family meals/snacks at home ≥1x/weekInterpersonal (caregiver)PO3. Caregivers know benefits of serving well-balanced meals/snacksCO1.3.1 Caregivers identify barriers to offering well-balanced meals/snacks and know strategies to overcome identified barriers\ CO1.3.2 Caregivers know short- and long-term consequences of not serving well-balanced meals/snacksCO2.3 Caregivers express confidence in knowing benefits of serving well-balanced meals/snacksPO4. Caregivers serve a family meal that includes ≥1 serving from 3 of the 5 food groups ≥1x/weekCO1.4.1 Caregivers know importance of including a variety of foods in meals\ CO1.4.2 Caregivers know ≥2 strategies to incorporate foods from 3 food groups into family mealsCO2.4 Caregivers express confidence in planning/preparing well-balanced family meals\ CO2.4.2 Caregivers express confidence in eating/serving well-balanced family mealsCO3.4.1 Caregivers set goal to serve a family meal that includes ≥1 serving from 3 of the 5 food groups ≥1x/week\ CO3.4.2 Caregivers monitor goal progress and determine if meeting established goalCO4.4 Caregivers plan ≥1 family meal/week that includes ≥1 serving from 3 of the 5 food groupsPO5. Caregivers serve ≥3 snacks/week that include ≥1 serving from 2 food groupsCO1.5.1 Caregivers know importance of eating/serving well-balanced snacks\ CO1.5.2 Caregivers are able to plan ≥3 snacks/week that include ≥1 serving from 2 food groupsCO2.5.1 Caregivers express confidence in planning well-balanced snacks\ CO2.5.2 Caregivers express confidence in eating/serving well-balanced snacksCO3.5.1 Caregivers set goal to serve ≥3 snacks/week that include ≥1 serving from 2 food groups\ CO3.5.2 Caregivers monitor goal progress and determine if meeting established goalCO4.5 Caregivers plan ≥3 snacks/week that include ≥1 serving from 2 food groupsPO6. Caregivers buy food for planned meals/snacks at grocery storeCO1.6.1 Caregivers plan well-balanced family meals and snacks\ CO1.6.2 Caregivers prepare grocery list using planned meals/snacksCO2.6.1 Caregivers express confidence in developing grocery list\ CO2.6.2 Caregivers express confidence in using list for grocery shoppingCO3.6.1 Caregivers set goal to develop and use list for grocery shopping each week\ CO3.6.2 Caregivers monitor goal progress and determine if meeting established goalCO4.6 Using list for grocery shopping becomes norm for caregiversPO Performance objective, CO Change objective, HEI Healthy Eating Index, Svg Serving, SSB Sugar sweetened beverage^a^U.S. Departments of Agriculture and Health and Human Services. Dietary Guidelines for Americans, 2010. 7th ed., Washington, DC. December, 2010 \[[@CR18]\] Next, theory-based methods to influence change in the determinants at the individual (child) and interpersonal (caregiver) level were selected based on the theoretical framework of the intervention (Social Cognitive Theory) \[[@CR19], [@CR21]\] and in reference to methods described by Bartholomew et al. \[[@CR16], [@CR17]\]. For identifying theory-based methods to influence determinants at the interpersonal (caregiver) level, the Adult Learning Theory, which purports that adult learning is most effective when a collaborative, problem-based approach was also referenced \[[@CR22], [@CR23]\]. A list of all change objectives that were linked with a specific determinant was made, and the theoretical methods were then matched with the corresponding determinant (Table [5](#Tab5){ref-type="table"}). Finally, practical strategies were designed to put the theoretical methods into practice (Table [5](#Tab5){ref-type="table"}). For example, under the family meals program objective, on the individual (child) level, the result of crossing the performance objective 'children participate in meal preparation activities' with the determinant 'behavioral capability' was the change objective 'children are able to participate in age-appropriate cooking skills'. The selected theory-based method that corresponded to the determinant 'behavioral capability' in order to achieve the change objective was facilitation. This theory-based method was then translated into a practical strategy. In this case, a practical strategy that was chosen for the method facilitation was to 'Learn age appropriate cooking skills at each Simple Suppers lesson'. An example on the interpersonal (caregiver) level, also under the family meals program objective, (caregiver) level is as follows: the result of crossing the performance objective 'Caregivers identify health benefits of regular family meals prepared in the home' with the determinant behavioral capability was the change objective 'Caregivers know benefits of regular family meals prepared at home'. The selected theory-based method that corresponded to the determinant behavioral capability in order to achieve the change objective was active learning. This theory-based method was then translated into a practical strategy. In this case, a practical strategy that was chosen for the method active learning was: 'Educators use the 4A method (participants think about their experience with a topic (Anchor), learn new information (Add), reinforce learning through hands-on activities (Apply), and set goals to utilize new knowledge at home (Away)) to lead weekly caregiver discussions \[[@CR23], [@CR24]\].Table 5Theory-based methods and practical strategies to achieve the change objectives for selected program objectives of the simple suppers interventionProgram objectiveLevel of interventionDeterminantChange objectiveTheory-based methodTheoryPractical strategy1. Increase frequency of family meals prepared in the home (≥5 days/week)^a^Individual (child)Behavioral capabilityCO1.1.1, CO1.1.2• Facilitation• SCT• Learn new age-appropriate cooking skills at each Simple Suppers lesson\ • Discuss food safety and cleanup with EducatorsCO1.1.1, CO1.1.2• Vicarious learning• SCT• Children divided into three age groups (4--5 years olds; 6--8 years olds; 9--10 year olds) for nutrition education & engagement in food preparationCO1.1.1, CO1.1.2• Mastery experience• SCT• Learned food prep skills accrued/practiced over lessonsSelf-efficacyCO2.1• Facilitation• SCT• Educators provide guidance & feedback as children learn/practice food prep skillsCO2.1• Vicarious learning• SCT• Participate in cooking activities with peers of the same ageCO2.1• Mastery experience• SCT• Practice cooking skills learned during Simple Suppers at homeSelf-evaluationCO3.1• Self-monitoring• SCT• Establish weekly goal during Simple Suppers to practice newly learned cooking skill at home\ • Weekly goals are reinforced by sharing goal with caregivers during Simple Suppers family mealCO3.1• Feedback• SCT• Discuss cooking skills used at home during past week with Educators and peers during Simple SuppersNorms, modeling, reinforcementCO4.1.1, CO4.1.2• Facilitation• SCT• Engage in family meal cooking activities with peers and Educators during Simple Suppers\ • Decorate/wear aprons for food prep during Simple Suppers and at home\ • Share cooking skills learned each week with caregivers at start of Simple Suppers group family meals\ • Lead cleanup at Simple Suppers family meals\ • Families receive take-home cooking utensil during each Simple Suppers lessonCO4.1.1, CO4.1.2• Mastery experience• SCT• Repeated engagement in family meal cooking during Simple Suppers\ • Weekly goal established to engage in family meal food prep at homeInterpersonal (caregiver)Behavioral capabilityCO1.2.1, CO1.2.2, CO1.3.1, CO1.3.2, CO1.4.1, CO1.4.2, CO1.4.3, CO1.5.1, CO1.5.2, CO1.6, CO1.7• Active learning• ALT• Educators use 4A method to lead weekly caregiver discussions\ • Educators engage caregivers in games, meal planning & goal-setting related to weekly lesson topicsCO1.3.2, CO1.4.2, CO1.4.3, CO1.5.2, CO1.6, CO1.7• Facilitation• SCT• Educators provide resources (e.g., recipe book, coupons, store ads) to plan family meals using skills learned at each lessonCO1.2.1, CO1.2.2, CO1.3.2, CO1.4.2, CO1.4.3, CO1.5.2, CO1.6, CO1.7• Problem solving• ALT• Caregivers set weekly goals & discuss successes/challenges with meeting goals with Educators & other caregivers\ • Educators & caregivers provide suggestions to help peer caregivers overcome challenges preventing them from reaching their goalsCO1.2.1, CO1.2.2, CO1.3.1, CO1.3.2, CO1.4.1, CO1.4.2, CO1.4.3, CO1.5.1, CO1.5.2, CO1.6, CO1.7• Vicarious learning• SCT• Caregivers acquire new knowledge through peer discussions\ • Caregivers participate in games, goal-setting & menu planning with peer caregiversCO1.3.2, CO1.4.3, CO1.5.2, CO1.6, CO1.7• Mastery experience• SCT• Caregivers plan ≥1 family meal using skills learned each week to practice skills at homeSelf-efficacyCO2.3, CO2.4.1, CO2.4.2, CO2.5.1, CO2.5.2, CO2.6, CO2.7• Feedback• SCT• Discuss challenges and successes with weekly family meals goal.\ • Problem solve with peers to overcome challengesCO2.3, CO2.4.1, CO2.4.2, CO2.5.1, CO2.5.2, CO2.6, CO2.7• Social support• SCT• Post goal successes and challenges throughout week on Simple Suppers Facebook page. Peers and Educators provide praise/support/encouragementCO2.3, CO2.4.1, CO2.4.2• Modeling• SCT• Caregivers plan family meals for upcoming week with peer caregivers during weekly lessons\ • Caregivers observe Educators facilitating group family meal during weekly lessonsCO2.3, CO2.4.1, CO2.4.2,• Mastery experience• SCT• Caregivers participate in group family meals during weekly lessons\ • Caregivers plan and set weekly goals to have family meals at homeSelf-evaluationCO3.3, CO3.4.1, CO3.4.2, CO3.5• Self-monitoring• SCT• Set individualized weekly SMART goals aligned with lesson topicsCO3.3, CO3.4.1, CO3.4.2, CO3.5• Feedback• SCT• Goals are reinforced by caregivers sharing their weekly goals\ • Educators and peers provide feedback/assure appropriateness\ • Discuss previous week's goal successes and challenges at beginning of each lesson. Caregivers problem solve together to overcome challengesNorms, modeling, reinforcementCO4.3.1, CO4.3.2, CO4.4, CO4.5• Facilitation• SCT• Simple Suppers group family meals follow routine/establish norm for family meals\ • Provide weekly take-home cooking utensil to facilitate cooking at homeCO4.4• Mastery experience• SCT• Educators guide caregivers in establishing mealtime routine during Simple Suppers and at homeImprove child diet quality (significantly increase HEI score (p \< 0.05); increase daily svgs of fruits, vegetables to Dietary Guidelines recommendations; significantly decrease daily svgs of: SSBs (p \< 0.05 decrease)^b^Individual (child)Behavioral capabilityCO1.2.1• Facilitation• SCT• Before Simple Suppers family meals, children name foods from each food group in the upcoming family mealCO1.1, CO1.2.2• Vicarious learning• SCT• Discuss food groups and benefits of healthy eating with Educators and peers at Simple Suppers\ • Learn to cook a variety of foods with peersCO1.1, CO1.2.2• Mastery experience• SCT• Children learn food prep skills & become familiar with a variety of food while helping prepare Simple Suppers family mealsSelf-efficacyCO2.1, CO2.2• Facilitation• SCT• Learn health benefits of foods through interactive discussions & food prep\ • Engage in planning/preparing well-balanced meals/snacks during Simple Suppers and at home ≥2x/weekCO2.2• Vicarious learning• SCT• Engage in food prep with peers of the same age\ • Eat Simple Suppers group family meals with peersSelf-evaluationCO3.2• Self-monitoring• SCT• Establish weekly goal during Simple Suppers to try a new food at home\ • Weekly goal reinforced by sharing goal with caregivers during Simple Suppers family mealCO3.2• Feedback• SCT• Discuss new foods tried at home during past week with Educators and peers during weekly Simple Suppers lessonNorms, modeling, reinforcementCO4.2.1, CO4.2.2• Facilitation• SCT• Foods from ≥3 food groups served at Simple Suppers family meals\ • Eat Simple Suppers family meals with family and peers\ • Children & caregivers establish weekly goal to engage in preparing well-balanced meals at home ≥1x/weekInterpersonal (caregiver)Behavioral capabilityCO1.3.1, CO1.3.2, CO1.4.1, CO1.4.2, CO1.5.1, CO1.5.2, CO1.6.1, CO1.6.2• Active learning• ALT• Educators use 4A method to lead caregiver discussions\ • Caregivers learn skills to serve nutritious meals/snacks through discussions, problem solving, games, meal planning, goal settingCO1.4.2, CO1.5.2• Facilitation• SCT• Caregivers plan\ • Caregivers provided with take-home recipe book of nutritious recipes\ • Families receive take-home cooking utensil during each lessonCO1.3.1, CO1.3.2, CO1.4.1, CO1.4.2, CO1.6.1• Problem solving• ALT• Discuss challenges and successes with serving well-balanced meals/snacks\ • Problem solve with peers to overcome challengesCO1.4.2, CO1.5.2, CO1.6.1• Vicarious learning• SCT• Simple Suppers group family meals contain ≥1 svg from all 5 food groups\ • Caregivers observe Educators serving/engaging children in preparing well-balanced family mealsCO1.4.2, CO1.5.2, CO1.6.1, CO1.6.2• Mastery experience• SCT• Caregivers plan ≥1 well-balanced (contains ≥1 svg from 3 food groups) family meal per week during each Simple Suppers lesson using skills acquired each lesson\ • Learned skills repeated in caregiver family meal planningSelf-efficacyCO2.3, CO2.4.1, CO2.4.2,, CO2.5.1, CO2.5.2, CO2.6.1, CO2.6.2,• Feedback• SCT• Discuss challenges and successes with serving well-balanced meals/snacks.\ • Problem solve as a group to overcome challengesCO2.4.1, CO2.4.2, CO2.5.1, CO2.5.2, CO2.6.1• Social support• SCT• Plan weekly family meals with peers during Simple Suppers lessons\ • Post weekly successes and challenges on Simple Suppers Facebook page. Peers and Educators provide praise/support/encouragementCO2.3, CO2.4.1, CO2.4.2• Modeling• SCT• Educators serve Simple Suppers group family meals with ≥1 svg from all 5 food groups\ • Simple Suppers group family meals eaten with Educators and peersCO2.3, CO2.4.1, CO2.4.2• Mastery experience• SCT• Families eat a well-balanced family meal during Simple Suppers group family meals\ • Caregivers plan ≥1 family meal ≥1 svg from 3 food groups each lesson for upcoming weekSelf-evaluationCO3.4.1, CO3.4.2, CO3.5.1, CO3.5.2, CO3.6.1, CO3.6.2,• Self-monitoring• SCT• Set individualized weekly SMART goal to serve set number of family meals at home with ≥1 svg from ≥3 food groups\ • Caregivers plan menus for the number of family meals they made their goal for the upcoming week during Simple Suppers\ • Goals are reinforced by sharing weekly goal and planned menus during Simple Suppers each week. Educators and peers provide feedback/assure appropriatenessCO3.4.2, CO3.5.2, CO3.6.2• Feedback• SCT• Discuss previous week's goal successes and challenges at beginning of each Simple Suppers lesson. Caregivers problem solve together to overcome challengesNorms, modeling, reinforcementCO4.4, CO4.5, CO4.6• Facilitation• SCT• All Simple Suppers group family meals contain ≥1 svg from all 5 food groups\ • Receive Simple Suppers cookbook with kid-friendly, well-balanced mealsPO performance objective, CO change objective, HEI healthy eating index, Svg serving, SSB sugar sweetened beverageALT adult learning theory, SCT social cognitive theory^a^Measured by asking the question, "During the past 7 days, how many times did all or most, of your family eat dinner together?"\[[@CR7]\]^b^U.S. Departments of Agriculture and Health and Human Services. Dietary Guidelines for Americans, 2010. 7th ed., Washington, DC. December, 2010 \[[@CR18]\] The next step was to develop the Simple Suppers curriculum in direct reference to the results produced from the aforementioned Intervention Mapping (Table [6](#Tab6){ref-type="table"}). The initial draft was reviewed by field experts using a nutrition education curriculum assessment tool \[[@CR25]\]. Curriculum modifications were then made using reviewer feedback (e.g., incorporating additional hands-on learning activities in the caregiver component to enhance interactive nature of curriculum), after which additional pilot testing occurred and subsequent curricular revisions were made \[[@CR26]\].Table 6Simple Suppers Topics and Goals by Weekly LessonLessonTopicBroad goal for upcoming week1Making family mealtime fun!Play 1 family meal-friendly game during mealtime at 2 family meal occasions2Planning family meals on a budgetUse 1 cost-saving strategy to plan and serve 1 well-balanced family meal at 1 family meal occasion3Timesaving strategies for family mealsUse 1 timesaving strategy to plan and serve 1 well-balanced family meal at 1 family meal occasion4Connecting with your child through family mealsInvolve child in 1 mealtime activity at 2 family meal occasions5Planning well-balanced family mealsServe a family meal with 1 serving of whole grains, vegetables, and protein at 1 family meal occasion6Rethink your drinkServe 1 well-balanced family meal with low-fat/no sugar added beverages7Making healthy cooking tasty & easyUse 1 healthy cooking method to plan and serve 1 well-balanced family meal at 1 family meal occasion8Serving & eating healthy portionsServe 1 well-balanced family meal with healthy portion sizes at 1 family meal occasion9Eating healthy when eating away-from-homeEat 1 well-balanced, nutritious meal away-from-home at 1 family meal occasion10Planning fun & healthy snacksServe 2 planned, pre-portioned, well-balanced snacks to your child Finally, the Simple Suppers program design was developed with feedback from program adopters (faith-based community center staff), implementers, and the target population \[[@CR27]\] (e.g., utilizing two (versus one) educators for the caregiver component and incorporating site-based staff into the staffing structure). Each 90-min lesson is delivered weekly over the dinner hour. Session components include: a) interactive group discussion and goal setting with caregivers; b) hands-on activities with children; and c) group family meal with caregivers and children. Outcome measures {#Sec8} ---------------- ### Children and caregivers {#Sec9} #### Diet quality {#FPar1} Dietary intake will be assessed by conducting three, nonconsecutive (two weekdays, one weekend day) 24-h (24 h) dietary recalls using USDA's 5-step multi-pass dietary recall method \[[@CR28]\]. At each data collection time point, the first dietary recall will be conducted during the in-person data collection visit, the remaining two will be conducted via telephone within two weeks of the initial in-person recall. For the child dietary recalls, caregivers will provide assistance, as caregiver-assisted 24 h recalls, collected in this way (i.e., relying on three days and utilizing the multi-pass method), provide the most accurate estimate of dietary intake among children 4 to 11 years of age \[[@CR29]\]. Caregiver 24 h dietary recalls will be conducted independently following the child recall(s). Typical daily dietary intake will be determined by averaging dietary intake across the three recalls at each time point to determine daily servings of fruit, vegetables, and SSB. Diet quality will be assessed at each point by calculating a Healthy Eating Index 2010 score using the three 24 h dietary recalls collected \[[@CR30]\]. #### Anthropometric assessments {#FPar2} Standardized procedures will be used to assess height and weight on all participating children and caregivers via calibrated stadiometers (Hopkins portable road rod stadiometer) and scales (BFHA-B400SV digital scale), respectively \[[@CR31], [@CR32]\]. Body mass index will be calculated using measured heights and weights. Centers for Disease Control and Prevention (CDC) age- and sex-adjusted BMI growth charts will be used to determine BMI z-scores for children to adjust for expected healthy growth and weight gain \[[@CR31], [@CR33]\]. Waist circumference will be measured on all participating children and caregivers with a tape measure at the uppermost lateral border of the hip crest (ilium) \[[@CR31]\]. To adjust for expected growth among child participants, child WC z-scores will be determined using CDC age- and sex-specific growth charts \[[@CR34]\]. #### Blood pressure {#FPar3} Blood pressure will be assessed on all participating children and caregivers via automated, calibrated BP monitors (Panasonic EW3109W). Age-, sex-, and height-adjusted National Heart, Lung, and Blood Institute (NHLBI) charts will be used to appropriately classify child BP \[[@CR35]\]. #### Personal determinants {#FPar4} We will also assess immediate intervention targets relating to behavioral capabilities. For child participants, food preparation skills and frequency of involvement will be assessed at each data collection point by caregiver completion of an age-appropriate food preparation skills questionnaire designed to assess both skill ability and frequency of involvement in practicing the skill. Working from an existing validated questionnaire designed to assess child food preparation skills (ability) among 8--10 year olds \[[@CR7]\], three versions of the questionnaire (4--5 year old questionnaire; 6--8 year old questionnaire; 9--10 year old questionnaire) were developed to accurately assess child food preparation skills (ability) according to age appropriateness. Assessment of frequency of involvement in practicing each food preparation skill was added to these modified questionnaires. The resulting questionnaires assessing a child's ability to participate (8 items; 4-point scale; strongly agree to strongly disagree) and frequency of participation (8 items; 5-point scale; 0 times to 7+ times) in age-appropriate food preparation skills (during the past 30 days) included 16 items. Among caregiver participants, menu planning skills and frequency will be assessed at each data collection point by caregiver completion of an existing menu planning questionnaire \[[@CR36]\] to evaluate immediate intervention targets relating to behavioral capabilities. The 9-item menu planning questionnaire, which has demonstrated adequate internal consistency (α = 0.68) and high test-retest reliability (Pearson test-retest = 0.89), asks respondents to rate statements regarding menu planning, meal decision-making, and grocery shopping using a 4-point scale ('never,' 'sometimes,' 'often,' 'always'). A key affective variable - caregiver self-efficacy for healthy dietary practices related to family meals - will be assessed using an existing 12-item, 10-point scalar (0 = not at all confident; 10 = extremely confident) questionnaire \[[@CR37]\]. The caregiver self-efficacy questionnaire, which will be completed by caregiver participants at each data collection point, has demonstrated high internal consistency (α = 0.88) among a sample of caregivers of 4--6 year old children. Tests of internal consistency will be run on all of the aforementioned questionnaires. Caregivers will also complete a brief food security questionnaire at each data collection point (6-item Short Form of the USDA Home Food Security Survey) \[[@CR38]\] and a demographics questionnaire to assess key participant characteristics (age, race/ethnicity, education, employment, income) at baseline. ### Home environment {#Sec10} #### Family meals {#FPar5} Weekly frequency of shared family dinners, shared family breakfasts, television viewing during family meals, and eating family meals in a dining area will be assessed via caregiver reports with 4, 5-point scalar (0 = never; 5 = 7 times) items from previous family meals research \[[@CR39], [@CR40]\]. Process measures {#Sec11} ---------------- Feasibility (program dose and fidelity) and acceptability will be assessed prospectively throughout the study as process outcomes. Program dose will be assessed by collecting weekly attendance (family and individual level) and tracking presence of caregiver/child dyads at each weekly lesson. Participants who demonstrate irregular attendance and/or discontinue participation will be contacted to learn underlying reasons for absence. To determine program fidelity, a trained observer will complete a program specific fidelity tool at the end of each weekly lesson, which will include a checklist of key program components, activities, and leader characteristics. Acceptability of the program will be measured with a caregiver-completed 5-item satisfaction survey administered at the end of the 10-week program \[[@CR41]\]. At the end of programming, interviews will be conducted with a subset of caregivers to learn their perceptions of program strengths and weaknesses. Sample size and data analysis {#Sec12} ----------------------------- Sample size was determined by examining the power of the test for comparing increases in frequency of family meals (day per week) of the intervention and waitlist control group. The data used to estimate power come from a previous pilot study, in which the main outcome of interest was the change in frequency of family dinners prepared and eaten at home together (weekly basis) from baseline to post-intervention \[[@CR42]\]. Change in frequency of family dinners was used to power the current study because there is strong evidence that it has a downstream effect on the outcome of interest, child BMI \[[@CR3], [@CR42]--[@CR44]\], and there are no previous studies that show a causal effect of family dinners on BMI. Based on these data, assuming 20% attrition \[[@CR42]\], with an expected effect size of 0.7071, there will be 80% power to detect a difference in frequency of family dinners of 3 days per week with 30 families per group for a total sample size of 60 families at α = 0.05. Because the sample size in the previous pilot study was small and uncertainty about estimated effect size was large, we used a conservative estimate of effect size (i.e., the lower bound of a 95% confidence interval) for the power calculation. Data from each of the three cohorts will be pooled and the intervention tested by comparing change (T1-T0) in diet quality, anthropometric measures, and blood pressure of child and caregiver participants in the intervention compared to participants in the waitlist control (hypotheses 1.1 and 2.1). Multiple regression models will be used to determine the association between the difference in the response variables of interest between the intervention and control group, controlling for potential confounders (race/ethnicity, income, cohort, intervention dose), from baseline (T0) to 10-week post-test(T1) and 10-week follow-up (T2). For families in which data will be collected on multiple children, the effect of family will also be controlled by including a random effect for family. Sustainability of intervention effects will be tested by pooling intervention group data from each of the three cohorts, comparing change (T2-T1) in diet quality, anthropometric measures, and blood pressure among intervention group participants at the end of the 10-week follow-up period (hypothesis 1.2 and 2.2). Intervention replication will be assessed by pooling waitlist control group data from each of the three cohorts, comparing post-program change in diet quality, anthropometric measures, and blood pressure among waitlist control participants (T2-T1) to intervention participants (T1-T0). Significance will be set at p \< 0.05. Discussion {#Sec13} ========== We may encounter challenges engaging and developing trust with the target population, an issue that is common to intervention research with economically disadvantaged families \[[@CR45]--[@CR47]\]. However, this study was designed to minimize this potential barrier by implementing the intervention at a local faith-based community center, which has established relationships with the target population. In addition, this study will engage current staff from the faith-based community centers to serve as educators in delivering the intervention. Grounding the caregiver component in Adult Learning Theory will further enhance our abilities to engage with families, as this approach is designed to present new information in a non-threatening, approachable way. Another limitation is the lack of randomization study design. Randomization was not appropriate for this study because preserving sample size and developing trust with the site/participating families was paramount \[[@CR47]--[@CR49]\]. We will overcome this limitation by assessing potential between- group differences at baseline and, if identified, will be controlled for in the analyses. We thank our community collaborator Vineyard Community Center (VCC) and VCC staff, Mr. Daniel Nathan (Executive Director) and Ms. Maria Broeckel (Director of Program Development). Funding {#FPar6} ======= Cardinal Health Foundation. Availability of data and material {#FPar7} ================================= Not applicable. Authors' contributions {#FPar8} ====================== CG led the conceptual development of the study with input from CR, SSA, JSD, TFH, CH, CKM, and KJP. CG and CR led intervention preparations with assistance from SSA, CH, CKM, and KJP. CG and CR took primary responsibility for writing the manuscript. SSA, JSD, TFH, CH, CKM, and KJP contributed to editing the manuscript. CG, CR, SSA, JSD, TFH, CH, CKM, and KJP read and approved the final manuscript. Competing interests {#FPar9} =================== The authors declare that they have no competing interests. Consent for publication {#FPar10} ======================= Not applicable. Ethics approval and consent to participate {#FPar11} ========================================== This study is approved by The Ohio State University Behavioral and Social Sciences Institutional Review Board. Parent consent and parent permission, as well as child assent will be received from participants prior to study enrollment.
Casino gambling deepens inequality, study finds State-sponsored casino gambling is a growing scourge masquerading as a harmless source of entertainment and government revenue, argues a new report by a group of scholars and community leaders. The report entitled "Why Casino's Matter" was spearheaded by the Institute for American Values in New York City and vetted and endorsed by 33 scholars and civic leaders from across the political spectrum. The study grew out of an earlier report that addressed predatory lending institutions, said Barbara Dafoe Whitehead, the researcher at the Institute for American values who spearheaded the report. Among its key contentions is that casino gambling preys on poor communities and exacerbates inequality. The authors focus on the rapid expansion of casino gambling, which until recently was legal only in Nevada and Atlantic City, New Jersey. Casinos, the study notes, are “popping up across the nation, near a shopping mall or a river dock near you, with the full support and sponsorship of the very state governments that only yesterday had outlawed them.” The rapid growth of state-sponsored gambling, the authors argue, is “affecting our health, our economics, our politics, our ideas and social values, and perhaps even who we are as a people and what obligations we have toward one another.” The gaming industry sees little new or convincing in the “Why Casinos Matter” report. "Basically they have just taken out of mothballs a lot of long-discredited arguments against casinos that have been made by gambling opponents for decades," said Judy Patterson, executive director of the American Gaming Association. "Many of the researchers cited in the report have a tendency to cite each other's research in a very circular fashion.” A commission unheeded "This all began with the National Gambling Impact Commission," Patterson said, referring to a 1999 report commissioned by Congress to investigate the impact of a massive expansion of legalized gambling. Congress commissioned the study in 1996 — not coincidentally, the same year the industry established the National Center for Responsible Gaming. The commission was spurred by concerns that a social shift had occurred with little attention to its possible impacts. The commission noted that in 1975 just 10 percent of Americans reported playing at a casino, jumping to 24 percent by 1998. Twenty-four percent bought a lottery ticket in 1975. In 1998, 52 percent did. The commission recommended the rapid expansion of gaming be curtailed, urging that the National Institutes of Health, the Justice Department, the Department of Labor, and the Substance Abuse and Mental Health Services Administration all be asked to open relevant lines of data and research centered on gambling. The 1999 Commission held that too little research had been done on critical questions, including the impact of gambling on local communities, economics, savings and investment, and possible sociological impact of pathological gambling on families and communities. "There are surprisingly few independent studies that have addressed issues such as these," the 1999 report stated, "And as for the impact on the national economy, efforts to estimate the net impact of gambling on national statistics such as investment, savings, economic growth, and so forth, break down in the face of our limited knowledge." Industry responds Beginning in 1996, the gaming industry decided to get out in front of gaming addiction issues, founding the National Center for Responsible Gaming. The industry has funneled more that $22 million into research, using careful firewall protocols modeled on the National Institutes of Health model, with an independent science advisory board. The NCRG does not play any role in deciding which research projects to fund, and never sees them until after they are published. In contrast to tobacco executives, who as recently as 1994 infamously testified before Congress that tobacco was not addictive, AGA president Frank Fahrenkopf has openly asserted that gambling is addictive and can "affect brain chemistry in ways that are similar to substance abuse," as he put it in a 2009 address. But the gaming industry argues that only one percent of the adult population has been found to be vulnerable to damaging behavior. Industry research has focused efforts on identifying and containing those problem gamblers. Whitehead acknowledges the gaming industry-supported research has been of high quality and that the firewalls have been adequate. But she argues that the resulting research has focused narrowly on individual pathological gambling, sidestepping some critical questions. "The danger is greater than one percent, and it is increasing as casinos become more accessible," Whitehead said. An 80/20 problem A key contention in the “Why Casinos Matter” report is that 40 to 60 percent of casino revenue comes from problem, i.e. addicted, gamblers. It's a classic 80/20 problem, with 80 percent of the payoff being driven by 20 percent of the clientele, critics of the industry argue. In an appendix, the report points to 11 different sources for this data, including peer-reviewed studies and government reports from Canada and Australia. The one percent problem gambler figure is an adult population estimate, Patterson said. She said she is not aware of any data on the percentage of casino customers who fit that profile, nor the percentage of revenue that is driven by problem gamblers. Unanswered questions Fifteen years later, the commission’s report had little impact, and little has changed on the research front, with the exception that industry-funded research through NCRG has produced substantial information about the psychology and treatment of individual gaming addiction. The larger sociological and economic questions remain largely unasked and unanswered, Whitehead said. That may explain why the new report by the Council of Casinos offers more questions than answers, and sometimes slips into generalization rather than offering data and footnotes. To Judy Patterson and the gaming industry, this lack of hard data coming from critics is a symptom of weakness in their arguments. And yet, Patterson likewise had no data to offer on one key question pressed by Whitehead, namely, the ratio of casino revenue that comes from problem gamblers. That data would be difficult to collect, Patterson protested, because it would involve intrusive customer surveys.
Liverpool 5-1 Oldham Athletic: 5 goal Reds advance A 5 goal showing from Liverpool downed League One visitors Oldham Athletic Friday night at Anfield in the third round of the FA Cup. Kenny Dalglish made 8 changes to his side from the 3-0 defeat at Manchester City midweek, with only Pepe Reina, Dirk Kuyt, and Jay Spearing retaining starting positions. Captain Steven Gerrard made his first start since a 1-1 draw against Norwich City in October, while oft-injured LB Fabio Aurelio got his first 60 minutes of the season. The Lactics got off to a quick start against the Premiership side, taking advantage of a shaky Liverpool back four and going close on numerous occasions. The League One side almost went ahead in the 14th minute when a header from Tom Adeyemi just went over the bar. Oldham were rewarded with a goal in the 28th minute from Robbie Simpson, who hit a screaming, dipping volley past Reina. Oldham’s lead was short lived, however, as 66 seconds after Simpson’s goal saw Liverpool equalize at the Anfield Road end. A shot from Jonjo Shelvey deflected off Craig Bellamy for the Welshman’s sixth goal in all competitions. Oldham’s goal woke the Reds up, as the Liverpool controlled most of the match from there on out, including Bellamy’s deflection in. Bellamy could have had a second a few minutes later, but a ball played over the top by Maxi Rodriguez was just inches out of his reach. A cross from Gerrard into the box saw Rodriguez tumbled over by Adeyemi in the 44th minute, resulting in a penalty kick. Gerrard stepped up to the spot, fired to his right and clipped the underside of the crossbar to give the Reds a 2-1 lead at halftime. The second half got off to an entertaining start, as Oldham continued their fearless play with Jean Yves Mvoto shooting just wide for the visitors before Bellamy drilled over the bar from a clever flick on from Kuyt. Liverpool got their insurance goal in the 68th minute on a cross from Bellamy. Bellamy, who’s overall play earned him Man of the Match honors, fired in a cross that was met by Shelvey for the 19-year-old’s first career Liverpool goal. Substitute Andy Carroll one-timed a volley in the 86th minute from outside the area to give Liverpool a 4-1 lead. Stewart Downing, also starting the game from the bench, joined Shelvey in opening his Liverpool account by netting a rebound in stoppage time. Sadly, there was an incident of alleged racial abuse towards Tom Adeyemi from a fan sitting in the Kop which overshadowed the occasion. Adeyemi was running along the byline for a goal kick when he stopped, turned around and ran back pointing to someone in the Kop. The on-loan midfielder from Norwich was very visibly upset at the incident, and had to be calmed down by the official, Oldham players, and Kuyt and Gerrard. Man of the Match: Craig Bellamy. Bellamy was excellent all game, finding space, using his explosive pace, and playing in great crosses. One of the few Liverpool players who actually played well on the night that resulted in a goal and an assist for the Welshman. Needs to do better: Dirk Kuyt. Kuyt had a very good season last campaign, but this season something doesn’t quite seem right with the Netherlands international. His performance against Oldham, while putting in his usual great effort, was mediocre, particularly in comparison to his performances last season. Player to keep an eye on: Jay Spearing. Filling in for the injured Lucas Leiva is no easy task, but Spearing has done well already. How he continues to play going forward in the season is worth keeping an eye on. Side note: The play-by-play man for Setanta Ireland quipped, “No matter how bad Carroll has been for Liverpool, he’s still been better than Torres,” in reference to their respective Jan. 2011 moves. Welcome to Off The Mark! My name is Jeremy Mikula, a graduate journalism student at DePaul University. I'm the former Online Editor of The DePaulia, but after 2 years, I've returned to being a writer/reporter. This blog features general assignments as well as stories and opinions on the world of football (soccer).
Q: Java: Interface generic of a superclass Imagine the following code: class A {} class B extends A {} interface IA extends Iterable<A> {} interface IB extends Iterable<B> {} Ideally, I would like the interface IB to be able to also extend IA because it does in fact allow you to retrieve As. interface IB extends Iterable<B>, IA {} or even interface IB extends Iterable<B> implements IA {} However, the compiler really dislikes both of those and it would make my code much better if this was allowed as conceptually B can be used as A without up-casting everywhere What solutions are available for me to solve this problem? A: The non-covariance of generics means that what you want isn't viable (at least not in the general case). However, perhaps wildcards would solve your specific problem? e.g. void methodThatOperatesOnA(Iterable<? extends A> it) { ... } This will allow you to extract elements from it as if they were As, but the compiler will prevent you from inserting objects,* because it can't guarantee that invariants would be maintained. * other than null and a few other wacky cases A: A type cannot have two super types G<X> and G<Y> where X!=Y - probably due to erasure. One way to solve your problem is to use a type parameter for the type to be iterated interface IA<X extends A> extends Iterable<X> { @Override Iterator<X> iterator(); } interface IB extends IA<B> { @Override Iterator<B> iterator(); } I'd usually avoid that, it's just more complexity. In your example, extending Iterable<A> is probably not a good idea in the first place. For example class Team implements Iterable<Member> { public Iterator<Member> iterator() { ... } } for(Member member : team) ... but a team concept probably is broader than just a collection of members. It might be clearer to class Team { Iterable<Member> members() { ... } } for(Member member : team.members()) ... In that case, your types can be designed as interface IA { Iterable<? extends A> members(); } interface IB extends IA { @Override Iterable<? extends B> members(); } One can also question whether Iterable should have been more relaxing, instead of public interface Iterable<T> Iterator<T> iterator(); would it be better to public interface Iterable<T> Iterator<? extends T> iterator();
If this is your first visit, be sure to check out the FAQ by clicking the link above. You may have to register before you can post: click the register link above to proceed. To start viewing messages, select the forum that you want to visit from the selection below. Keenan allen/Jonathan Hankins and Knile davis are all my favorites. If we can get our hands on one of these guys I would be extremely happy. Tyrann Mathieu in the late 6th-UDFA would also make me happy, I know i am taking a big flyer on him but at best a special teams guy, gunner, punt returner or nickle guy for depth; too much talent just too much. Could u imagine a Eddie Lacy/ David Wilson DUO backfield? That'd be TIKI/JACOBS Esque... I would love David Wilson's chances to be a big time player if he had a guy like Eddie Lacy to take some of the load off his shoulders.. Could u imagine a Eddie Lacy/ David Wilson DUO backfield? That'd be TIKI/JACOBS Esque... I would love David Wilson's chances to be a big time player if he had a guy like Eddie Lacy to take some of the load off his shoulders.. I have tossed around the Lacy pick myself and really like the idea. Another guy later in draft is leveon bell Michigan st. The main reason i didnt' like the Wilson pick.. I knew we'd end up liking the idea of a Bell or Lacy guy being drafted, which u shoulden't be thinking about when u just drafted a 1st rd RB the yr before... I agree In a way but it a 2 back league now. It very few an far between to find a every down back coming out of college. College football has changed with the spread and more of a passing nfl league. I think people would be surprised that Wilson can carry the load but another back allows flexibility. Throughout the league teams have two backs. I'll be the first to say I wanted Glenn but Wilson will be a breakout back. Having a bigger back Ala lacy/bell makes too much sense and adds to offense.
Silicone breast prostheses implantation and explanation. Breast implants have been used for augmentation and reconstruction for a 30-year period. Standard techniques have been used for the successful placement of mammary prostheses to enhance or replace breast tissue. All breast implants are surrounded by a capsule. The most common complication of breast implant surgery is hardening and contracture of the capsule. Explanation of implants is indicated for implant rupture, infection, extrusion, siliconoma, breast pain, painful capsular contracture, malposition, significant patient fear, and systemic symptoms thought secondary to implants. A number of alternatives are available for postexplant reconstruction, including myocutaneous flaps and free tissue transfers.
51 F.3d 1044 Marzov.Straine NO. 94-41094 United States Court of Appeals,Fifth Circuit. Mar 23, 1995 Appeal From: E.D.Tex., No. 6:92-CV-77 1 DISMISSED. Conference Calendar
Injustice at the Intersection Injustice at the Intersection How America’s suburbs are engineered against the walking poor Georgia pedestrians (Stephen Lee Davis / Transportation for America) On April 10, 2010, four-year-old A.J. Newman was killed just steps from his home. Along with his mother and two sisters, he was trying to get back to his apartment building from a bus stop on the far side of a five-lane highway. As they waited on a narrow concrete median, A.J. broke loose from Raquel Nelson’s hand, following the lead of his older sister, who took advantage of a short break in traffic to dash across the road. A drunk driver struck him dead before his mother’s eyes. Raquel Nelson’s troubles didn’t end there. In the wake of her son’s death, she was charged with vehicular homicide because, with three young children and an armful of groceries, she chose not to walk a third of a mile to the nearest marked crosswalk. A jury whose members never ride local buses found Nelson guilty of a crime whose true perpetrators were poverty and traffic engineering. She nearly went to jail, but after a national outcry, the judge reversed her conviction. She ultimately paid a $200 fine for jaywalking. The death of another young black man this summer has made the setting of these events familiar. Like Ferguson, Missouri, the run-down corner of Cobb County, Georgia, where A.J. Newman was killed is a declining inner suburb. When created in the middle years of the last century, these were places for middle-class white homeowners to get away from urban poverty. Their builders envisioned an endless future of affluent isolation. Circumstances have changed, but landscape and governance endure, bequeathing a legacy of institutionalized injustice to today’s residents. When Michael Brown encountered officer Darren Wilson on August 9, 2014, his suburban environment disadvantaged him triply. It wasn’t just that he was poor and black. Like Raquel Nelson, he was using his two feet for transportation in a place designed to be traveled by car. Carless Ferguson residents often seek out rides to the convenience store a few blocks away, a neighbor of Brown’s told the New York Times, just to avoid police harassment. The pretext Darren Wilson used to stop Michael Brown was jaywalking, the same offense for which Raquel Nelson nearly went to jail. Jaywalking, as Peter Norton shows in his landmark history Fighting Traffic, is an invented crime. It was the product of a massive publicity campaign orchestrated by automobile companies and allied motoring interests in the 1920s. Ostensibly aimed to promote safety, the real purpose of this effort was to push pedestrians off the street so that cars would move faster and be easier to sell. Along with their invention of jaywalking, the automakers exerted a controlling influence over the nascent discipline of traffic engineering. Industry-funded experts denied that speed was to blame for an epidemic of pedestrian crashes. They designed new roadways with the overriding objective of moving cars faster. As the years went by, engineering practices evolved to place those on foot at ever-greater disadvantage. Sidewalks disappeared, first on residential streets and then on main roads. Suburbs laid out to funnel traffic onto main arteries sent anyone who walked on long detours. Street corners were reconfigured to promote high-speed turns by cars. Highways widened and signage moved overhead, inviting freeway-speed movement on local roads. Midway through the 1920s, car ownership was still largely confined to the rich, and the public saw pedestrians hit by motorists as victims of irresponsible behavior by a privileged elite. As car ownership spread to the masses, however, the class aspect of road design faded into the background. Seen through the windshield, the highway was a place where all were equal—even more so with the opening of the toll-free interstates in the 1960s and ‘70s. Not everyone could afford a car, of course, even at the peak of postwar mass prosperity. But in the mid-twentieth century, the walking poor were shielded from the worst effects of the new road designs. Urban decay meant that their homes were still concentrated in old city neighborhoods, where they walked on streets laid out before the advent of traffic engineering. Today’s suburban poor lack that scant protection. The full weight of ninety years of car-first engineering bears down as they make their way to and from decaying apartment complexes and aging tract houses. Long walks to the main road, unprotected dashes across wide highways, and perilous waits at bus stops on unpaved shoulders are a daily routine. A landscape created for affluent motorists becomes an oppressive burden in its decline. In wealthier areas, street designs have begun to change. Roadways where it’s hard to walk bother city-dwellers. Even worse, they impede real estate development: under prevalent engineering standards, new construction cannot reproduce the inviting, narrow streets of the old urban neighborhoods homebuyers covet. Cities like New York, Washington, and Chicago, where people of all economic classes share the sidewalks, are starting to reclaim pavement once abandoned to fast-moving vehicles. But elsewhere, especially in poorer suburbs, the automobile still rules the road. Beneath a veneer of scientific neutrality, traffic engineering operates to the prejudice of anyone on foot. The objective is to move motor vehicles; those who walk, whether they do so by choice or by necessity, are little more than obstacles. Dissidents within the traffic engineering profession have begun to challenge this philosophy, but innovation, even when it revives the practices of a century ago, encounters fierce resistance from highway traditionalists. An elaborate body of doctrine maintains and justifies the status quo. Federal Highway Administration manuals lay out hundreds of pages of specifications that engineers rigidly apply. State highway bureaucrats, strongly inclined to maintain the primacy of automobile movement, dominate the committees that write these documents. The highway agencies, which can reallocate street construction funds and squeeze businesses seeking access to the roadway, have vast leverage over local politicians who might challenge them. Backing them up when needed is the political clout of auto and trucking interests. Hence the perilous highway crossing imposed on Raquel Nelson and her children. The builders of a five-lane road with a speed limit of 45 miles per hour did not furnish her bus stop with a traffic light or even mark a crosswalk with stripes on the pavement. Why such conditions are not just tolerated but actually mandated deserves a closer look. The rules for pedestrian crossings nationwide are set out in the Manual of Uniform Traffic Control Devices, known to specialists as the MUTCD. Chapter 4C specifies when red lights can be installed. One rule concerns vehicle traffic that approaches busy highways from a side street. It takes 240 cars in four hours to justify a traffic signal. Under the same conditions, at least 300 people must walk across the main road before a red light can be installed. A pedestrian, in other words, counts for four-fifths of a driver.* Even then, no signal is allowed if there is another light within 300 feet. This distance is considered a short enough detour to impose on pedestrians, even though, at a steady pace, a 600-foot round trip on foot takes two-and-a-half minutes. Drivers’ time is valued quite differently: engineers classify an intersection as “failing” if an average car is delayed in rush hour by a minute twenty seconds. If pedestrians don’t use the crossing because it is unsafe, moreover, no light may be installed. Determining where to install traffic lights by counting people who step onto a dangerous highway, critics point out, is like deciding whether a bridge is needed by observing how many people swim across the river. Absent a traffic light, might Cobb County at least paint simple crosswalk stripes at the Nelsons’ bus stop? No, it may not. The 2009 revision of the MUTCD banned new crosswalk markings on roads where heavy traffic moves faster than 40 miles per hour—just the sort of environment where the only people likely to walk are those who cannot afford a car. The ostensible rationale for this edict rests on a little known and less enforced provision of traffic law. In most states, a pedestrian crossing the road at an intersection with no traffic signal always has the right of way, whether or not there are stripes on the pavement. Pedestrians, therefore, should need no help getting across the street. In theory, markings exist only to prevent collisions by warning drivers of the need to stop. But in a massive federal study, researchers observed that, in practice, “very few motorists stopped or yielded to pedestrians either before or after marked crosswalks were installed” at intersections with no traffic light. This much, surely, was already obvious to anyone who’s ever navigated the suburbs on foot. But the study’s conclusion was somewhat more surprising: on roads with four or more lanes, pedestrians were more likely to be hit by drivers in a marked crosswalk than when crossing at a corner without crosswalk markings. There were many possible explanations for this finding. Engineers, trying to minimize congestion, often put stripes where pedestrians will interfere least with car traffic. On occasion, public pressure gets crosswalk markings at particularly dangerous points. In either case, pedestrians concerned for their own safety might well select crossing points safer than those chosen for them by others. But the investigators ignored such possibilities and seized on a more congenial interpretation, one that reinforced traffic engineers’ long-standing dislike of crosswalk markings. They concluded that the absence of stripes makes it safer to walk across wide roads. Not only does this defy common sense, but the highway officials’ own behavior contradicts it. Their safety campaigns never advise pedestrians to avoid striped crosswalks and cross at unmarked intersections. Only a traffic engineer could think this is the best way to cross East-West Highway in Chillum, Maryland. A driver killed a pedestrian here last month, and there was a critical injury in 2012. Google Earth photo. By banning pavement stripes, the revised 2009 MUTCD did more than make it harder to get to the other side of the road. Those who step onto unstriped asphalt lose in practice what meager protection the law by its letter affords. Outside a marked crosswalk, police are more likely to ticket the pedestrian who has the legal right of way than the driver who fails to yield. In collisions, officers and courts absolve motorists of blame unless they are drunk or flee the scene. The victim, held to have caused the crash by jaywalking, has little chance of collecting from the driver’s insurance. The edict against marked crosswalks did not go through without controversy, and advocates of walking won a concession. The MUTCD still allows the stripes at locations where twenty people an hour already cross, if special pushbutton-operated flashing lights are placed overhead. New crossings with these signals are starting to appear here and there, but they are vanishingly rare in the declining inner suburbs where the need is greatest. Even when cash-strapped local governments can afford the cost—the installations run some $100,000 each—people too poor to own cars rarely have enough political clout to overcome the traffic engineers’ resistance. A secure walk across the street, something that should be taken for granted anywhere, has been made into a luxury good. To be sure, the case of four-year-old A.J. Newman did prompt Georgia authorities to action. Within months, officials examined the site of the crash. Nothing could be done, they said, because there wasn’t enough money for a flashing light. But the state transportation department, like many such agencies, is slowly growing more attentive to those on foot. In May 2013, it had a sixteen-person team reexamine the entire highway. The study concluded that the bus stop should move a short distance for better visibility and its users should be helped across the road with pavement stripes, pushbutton, and flashing light. This recommendation has not yet been carried out. Almost five years after A.J. Newman’s passing, there is still no marked crosswalk where he died. Benjamin Ross is a transit activist in Maryland. His new book, Dead End, is about the politics of urbanism and transit. *Correction: This article previously stated that, in the MUTCD, a pedestrian counts for “just under three-fifths” or a driver. But a (reformist) traffic engineer points out a section of the MUTCD that allows a red light for 300 pedestrians under conditions similar to the conditions that allow them for 240 cars. A pedestrian counts, for this purpose, as four-fifths of a driver rather than three-fifths. We regret the error.
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Follow-up of recurrences of limb soft tissue sarcomas in patients with localized disease: performance of ultrasound. To evaluate diagnostic performance of ultrasound in the detection of local recurrences in patients with localized soft tissue sarcomas of the limb. An analysis of patients treated for soft tissue sarcomas between 2005 and April 2014 was performed. Sixty-eight patients (men/women, 36:32; age range, 18-84 years) were evaluated. Sensitivity, specificity with 95% confidence intervals (CIs), positive predictive value (PPV), pre-test probability (the prevalence), negative predictive value (NPV), likelihood ratio for positive results (LH+), accuracy and post-test probability (post-P) of ultrasound were reported on a per patient basis using surgical findings and clinical follow-up as reference standard. Effects of independent variables (US equipment, age and sex, body mass index, radiologist) were considered. Comparison with MR was also performed. The overall sensitivity and specificity were 0.88 (0.60-0.94) and 0.94 (0.86-0.98). PPV, pre-test probability, NPV, LH+, accuracy and post-P: 0.83/0.25/0.96/14.9/0.92/0.83. There were two false negative cases both graded as G3 and deeply located and three false positive US cases. Diagnostic accuracy was not dependent by US machine (p = 0.08), age and sex (p = 0.16), body mass index (p = 0.07) and radiologists (p = 0.07). Diagnostic accuracy of ultrasound was relatively high. Negative US results excluded the presence of a local recurrence with acceptable accuracy. • US accuracy is relatively high in sarcoma follow-up. • Negative US results exclude the presence of local recurrence with acceptable accuracy. • US may miss a small proportion of lesions. • False positive US cases are rare.
Background {#Sec1} ========== Admission to the intensive care unit (ICU) with critical illness is typically associated with significant morbidity for survivors, including profound impairment in physical strength and functional performance. These symptoms contribute to the 'post-intensive care syndrome' evident in survivors of critical illness \[[@CR1]\] and have been shown to persist up to 5 years following resolution of the original illness \[[@CR2]--[@CR7]\]. Peripheral skeletal muscle wasting and dysfunction that occurs early and rapidly during critical illness \[[@CR8]\] contributes to the development of intensive care unit-acquired weakness (ICU-AW) and these physical sequelae. Physical rehabilitation interventions are advocated to address physical and functional deficits associated with ICU-AW, and delivery is advocated across the continuum of the patient pathway commencing in the ICU, following transfer to the ward and beyond hospital discharge into the community \[[@CR9]\]. Typically, early mobilisation of patients in the ICU represents a hierarchical progression of increasingly functional activities such as active-assisted bed exercises, sitting on the edge of the bed, standing, marching-on-the-spot and walking \[[@CR10]\], with use of adjunctive technologies including electrical muscle stimulation \[[@CR11]\], interactive video games \[[@CR12]\] and passive cycle ergometry \[[@CR13]\]. On ICU discharge to the ward, the emphasis of physical rehabilitation for post-critical illness patients is directed towards the necessary level of functional mobility required to expedite hospital discharge, which can be supplemented by input from generic rehabilitation assistants \[[@CR14], [@CR15]\]. Following hospital discharge, physical rehabilitation has been evident in the delivery of either home- or hospital-based exercise rehabilitation programmes including combined strength, cardiovascular and functional components \[[@CR16]--[@CR19]\]. As the profile of physical rehabilitation for critical illness patients has increased and the volume of published data exploring the effectiveness of interventions has grown, multiple systematic reviews have been reported aiming to synthesise available evidence and draw conclusions on the most beneficial therapeutic options. A number of these have focused on interventions delivered within the ICU, e.g. Kayambu et al. \[[@CR20]\], Calvo-Ayala et al. \[[@CR21]\], Li et al. \[[@CR22]\] and Stiller \[[@CR23]\], albeit the stages of recovery following ICU discharge are also being evaluated \[[@CR24], [@CR25]\]. These systematic reviews are valuable for summarising findings from clinical trials at discrete time points along the recovery trajectory, involving particular types of physical rehabilitation strategies, in defined ICU populations and evaluating impact on select outcomes. However, this specificity of focus fails to provide a broader overview of the existing evidence base for physical rehabilitation during recovery from critical illness spanning the acute to chronic phases, to elucidate patient cohorts that may respond to interventions at different time points, and temporal variation in intervention effectiveness. In addition, variability in individual review methodology and quality appears evident which can influence robustness and clinical applicability of findings. Objectives of this overview {#Sec2} --------------------------- We will carry out an overview of existing Systematic review (SR) evaluating physical rehabilitation interventions for adult patients with critical illness patients across the continuum of recovery. Variability in the review question and population, intervention, comparator and outcome components across the large body of currently available reviews is a limiting factor to the overall synthesis of their findings and translation into clinical practice. An overview of SR offers a logical and appropriate step allowing comparison and contrast of individual reviews to be made and providing a precis of evidence at these different levels \[[@CR26]\]. Undertaking an overview of existing reviews is a novel approach within the field of physical rehabilitation following critical illness. Adopting this strategy, our aim is to summarise and appraise the best available evidence for the use of physical rehabilitation interventions across the continuum of recovery following critical illness, to address the following questions:At which stage of the post-critical illness recovery continuum (within the ICU, following ICU discharge on the ward and post-hospital discharge) do physical rehabilitation interventions have the most effect?Do particular patient populations gain more benefit from post-critical illness physical rehabilitation interventions than others?Which type of physical rehabilitation interventions produce benefits (short- and long-term) for post-critical illness patients?What adverse events or harmful effects are experienced from receipt of any physical rehabilitation interventions? Methods/design {#Sec3} ============== Protocol and registration {#Sec4} ------------------------- Our protocol has been written using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocol (PRISMA-P) \[[@CR27]\] and is registered on PROSPERO ([CRD42015001068](http://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42015001068)). Data sources and search strategy {#Sec5} -------------------------------- We will search the Cochrane Systematic Review Database, Database of Abstracts of Reviews of Effectiveness, Cochrane Central Register of Controlled Trials (CENTRAL), Ovid SP MEDLINE, Ovid SP Excerpta Medica Database (EMBASE) and Cumulative Index to Nursing and Allied Health Literature (CINAHL) via EBSCO host. All authors contributed to devising the search strategies for each database using a combination of subject headings and free-text keywords to describe critical illness, physical rehabilitation interventions and the different stages of the recovery continuum. Table [1](#Tab1){ref-type="table"} presents the search strategy for use in Ovid SP MEDLINE. No date or language restrictions will be applied to the initial searches.Table 1Example search strategy for Ovid SP MEDLINE1. ((intensive or critical) adj1 care unit).mp. \[mp=title, abstract, original title, name of substance word, subject heading word, keyword heading word, protocol supplementary concept word, rare disease supplementary concept word, unique identifier\]2. ((intensive or critical) adj1 care).mp. \[mp=title, abstract, original title, name of substance word, subject heading word, keyword heading word, protocol supplementary concept word, rare disease supplementary concept word, unique identifier\]3. exp Intensive Care Units/ or exp Intensive Care/ or ICU.mp. or exp Critical Care/4. critical illness.mp. or exp Critical Illness/5. mechanical ventilation.mp. or exp Respiration, Artificial/6. 1 or 2 or 3 or 4 or 57. exp Exercise Therapy/ or exercise.mp. or exp Exercise/8. ((exercise or physical) adj2 rehabilitation).mp. \[mp=title, abstract, original title, name of substance word, subject heading word, keyword heading word, protocol supplementary concept word, rare disease supplementary concept word, unique identifier\]9. physiotherapy.mp.10. physical therapy.mp.11. exp Early Ambulation/ or early mobilisation.mp.12. early mobilization.mp.13. physical fitness.mp. or exp Physical Fitness/14. muscle strength.mp. or exp Muscle Strength/15. cycling.mp.16. cycle ergometry.mp.17. exp Electric Stimulation Therapy/ or electrical muscle stimulation.mp.18. neuromuscular stimulation.mp.19. NMES.mp.20. 7 or 8 or 9 or 10 or 11 or 12 or 13 or 14 or 15 or 16 or 17 or 18 or 1921. randomized controlled trial.pt.22. controlled clinical trial.pt.23. randomized.ab.24. placebo.ab.25. randomly.ab.26. trial.ab.27. groups.ab.28. 21 or 22 or 23 or 24 or 25 or 26 or 2729. exp animals/ not humans.sh.30. 28 not 2931. Meta-Analysis as Topic/32. meta analy\$.tw.33. metaanaly\$.tw.34. Meta-Analysis/35. (systematic adj (review\$1 or overview\$1)).tw.36. exp Review Literature as Topic/37. or/31-3638. cochrane.ab.39. embase.ab.40. (cinahl or cinhal).ab.41. science citation index.ab.42. or/38-4143. reference list\$.ab.44. bibliograph\$.ab.45. hand-search\$.ab.46. relevant journals.ab.47. manual search\$.ab.48. or/43-4749. selection criteria.ab.50. data extraction.ab.51. 49 or 5052. Review/53. 51 and 5254. Comment/55. Letter/56. Editorial/57. animal/58. human/59. 57 not (57 and 58)60. or/54-56,5961. 37 or 42 or 48 or 5362. 61 not 6063. 6 and 20 and 3064. 6 and 20 and 62 Selection of reviews {#Sec6} -------------------- Following initial removal of duplicate and non-relevant material, two review authors will independently screen search results (based on abstract and title) against inclusion criteria (see below) for full-text review (BC and LS initial searches; BC and BO'N for updated searches). Full-text papers will then be further screened for eligibility. A bespoke assessment of study eligibility form will be used for documentation. In the absence of consensus, arbitration by a third author (KM) will be sought. References will be managed in Endnote v7.0 (Thomson Reuters). Types of reviews {#Sec7} ---------------- We will include systematic reviews of randomised controlled trials (RCTs) investigating the effect of any physical rehabilitation interventions following critical illness at any stage of the recovery continuum. If a review includes quasi-RCTs in addition to RCTs, we will also include these. Where non-RCTS are included in the review, the review will be included only if the RCTs are reported separately. Types of participants {#Sec8} --------------------- Participants will be adult patients who have been admitted to the ICU with critical illness, irrespective of causal diagnosis. We will exclude systematic reviews that only include studies of short-stay post-operative management (less than 48-h length of stay in the ICU). This is to focus the review content on patients considered most likely to develop intensive care unit-acquired weakness and go on to experience the physical consequences of critical illness and require physical rehabilitation interventions. Data extraction will include details of the populations included in each eligible systematic review, and these can be discussed and interpreted accordingly. Types of intervention {#Sec9} --------------------- We will include all types of physical rehabilitation interventions including exercise-based treatments and adjunctive strategies such as electrical muscle stimulation or cycling. These interventions can either be compared to control interventions (standard or usual care) or an alternative physical rehabilitation. We will exclude reviews including studies of composite interventions such as combined physical and cognitive rehabilitation and reviews including studies where the comparator was the same intervention but delivered at a different level of intensity. Types of outcomes {#Sec10} ----------------- ### Primary outcomes {#Sec11} Primary outcomes of interest are findings reflecting the recovery of any aspect of physical function, long-term measures of physical function or its surrogates. Where applicable, these outcomes will be summarised according to type of physical rehabilitation intervention, e.g. exercise-based rehabilitation programmes or electrical stimulation, and time point of assessment and duration of follow-up (such as 1, 3 or 12 months post-ICU discharge). ### Secondary outcomes {#Sec12} Secondary outcomes will include the following: structure, content and format of physical rehabilitation interventions according to recovery continuum stage; details on specific patient populations examined in each included review; reported rates of adverse events or harmful effects associated with interventions; and effect on other domains of outcome such as health-related quality of life where examined and reported. Data extraction and analysis {#Sec13} ---------------------------- Data extraction and analysis will be conducted in line with guidance from the Cochrane Handbook of Systematic Reviews of Interventions. Full texts of included reviews will be retrieved. Two review authors (LS and BO'N) will independently extract descriptive and outcome data from each included review. A third review author (KM) will arbitrate in the event that discrepancies cannot be resolved by consensus. A bespoke data extraction form will be designed, piloted and used to record review features including the aims and rationale, types of studies included, population(s), intervention(s), comparator(s), outcomes (including beneficial and harmful effects and reported adverse events) and date of last search and methods of assessing quality of studies. In the event that we include more than one review containing the same studies, we will examine the review question and comparisons explored, the date of the last search and key aspects of methodological quality (e.g. types of studies included and risk of bias assessment) and will list the individual studies included in each of the review. In this way, we will enable identification of trials included in one review but not another. Using these data, we will determine which of the reviews should contribute data to the results based on the review with the more current search strategy and more recent trials. Assessment of methodological quality of included reviews {#Sec14} -------------------------------------------------------- Two review authors (BC and BB) will independently assess the quality of reporting and the methodological quality of included reviews using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) \[[@CR28]\] checklist and the Assessment of Multiple Systematic Reviews (AMSTAR) tool \[[@CR29]\], respectively. We will report the proportion of PRISMA quality (number of items reported/27 checklist items\100 %). We will deem systematic reviews achieving an AMSTAR score of 8 to 11 of high methodological quality, 4 to 7 of medium quality and 0 to 3 as low quality \[[@CR30]\]. We will use the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach \[[@CR31]\] to assess the overall quality of evidence within, and across, the systematic reviews for each outcome. Disagreement will be resolved through consensus, and where this is not achieved, arbitration by a third review author (KM) will be sought. Dealing with missing data {#Sec15} ------------------------- Reasons for missing data will be recorded as reported by the original reviews. If the original reviews included this detail, we will report the number of studies that performed intention-to-treat or per protocol analyses. Data synthesis and reporting {#Sec16} ---------------------------- Data will be presented as a narrative synthesis, with textual commentary supplemented with use of summary tables and figures to enhance clarity of reporting \[[@CR26]\]. We will document primary and secondary outcomes of each intervention comparison in an included review, as well as the number of studies and number of participants included in the comparison, and (when reported in reviews) the mean difference (or standardised mean difference), 95 % confidence intervals and I^2^ statistic for heterogeneity \[[@CR32]\]. We will synthesise key information pertaining to the quality of evidence, and documented eligibility criteria, study characteristics and the primary outcome of each review. As previously described, we will also use the GRADE approach to determine overall quality of evidence and methodological checklist items for standardised evaluation of reporting and quality appraisal \[[@CR28], [@CR29]\]. Flow diagrams will be used to summarise the study selection process. Finally, reasons for excluding reviews will be reported. Sensitivity analysis {#Sec17} -------------------- If applicable, we will conduct sensitivity analysis in relation to studies of differing methodological quality. Sub-group analysis {#Sec18} ------------------ Depending on sufficiency of reviews, we plan to analyse the main functional outcomes according to patient population (e.g. age and causal diagnosis), intervention (i.e. type of physical intervention) and setting (i.e. within ICU, within the ward, post-hospital discharge). Discussion {#Sec19} ========== Expected significance of the study {#Sec20} ---------------------------------- The findings of this overview of systematic reviews of physical rehabilitation for adult patients with critical illness across the continuum of recovery will potentially have implications for clinical practice, research and future guideline development and update. It is intended that our results provide greater clarity and synthesis of available evidence on the most effective physical rehabilitation interventions to deliver according to the stage of recovery following critical illness. This is likely to have impact on existing and planned resource allocation in the clinical environment, inform the direction of future research including randomised controlled trials of intervention effectiveness and underpin guideline recommendations. Conclusions from this overview will highlight which, if any, physical rehabilitation interventions demonstrate clear benefit and those for which there is no clear evidence at which, if any, stage in the continuum of recovery. If sufficient data are available, our findings may also add clarity to the 'dose' of physical rehabilitation intervention, i.e. type, timing, intensity, duration and also circumstances under which any adverse effects of harm was caused as a result of the intervention. Potential limitations of overview design {#Sec21} ---------------------------------------- We plan to follow the approach outlined by the Cochrane Collaboration for undertaking an overview \[[@CR33]\]. As such, including individual studies that have not previously been included in a systematic review is beyond the scope of an overview although this could be considered a limitation if any new evidence exists. We will note when included systematic reviews are out of date and identify any relevant new studies that have been published subsequent to the date of the last reported systematic review search although we will not formally undertake a new systematic review within our overview framework \[[@CR33]\]. Our discussion will focus on the current state of the systematic review evidence for physical rehabilitation interventions for adults with critical illness, albeit we will comment on the volume of outstanding evidence identified as awaiting inclusion in systematic review. Conclusion {#Sec22} ---------- It is intended that this overview will provide insight regarding considerations for the design and conduct of future interventional trials of physical rehabilitation intervention in the post-critical illness population, acknowledged to be complex studies \[[@CR34]\]. AMSTAR : Assessment of Multiple Systematic Reviews GRADE : Grading of Recommendations Assessment, Development and Evaluation ICU : Intensive care unit ICU-AW : Intensive care unit-acquired weakness PRISMA : Preferred Reporting Items for Systematic Reviews and Meta-Analyses RCT : Randomised controlled trial Competing interests* The authors declare that they have no competing interests. Authors' contributions BC contributed to conception and design of the overview, development of search strategies and construction of PROSPERO review registration. BC drafted and revised the current protocol manuscript and will perform the searches, conduct quality appraisal on included reviews and draft and revise the manuscript for the final review. BO'N contributed to conception and design of the overview, development of search strategies and construction of the PROSPERO review registration and contributed to manuscript revision of the current protocol manuscript. BO'N will conduct data extraction on included reviews and contribute to manuscript revision for the final review. LS contributed to conception and design of the overview, development of search strategies and construction of the PROSPERO review registration and contributed to manuscript revision of the current protocol manuscript. LS will conduct data extraction on included reviews and contribute to manuscript revision for the final review. KM contributed to conception and design of the overview, development of search strategies and construction of the PROSPERO review registration. KM will act as arbitrator for data extraction and quality appraisal where required and contribute to manuscript revision for the final review. BB contributed to conception and design of the overview, development of search strategies and construction of the PROSPERO review registration and contributed to manuscript revision of the current protocol manuscript. BB also prepared and submitted the PROSPERO registration. BB will conduct quality appraisal on included reviews and draft and revise the manuscript for the final review. All authors read and approved the final manuscript for the current review protocol and will agree and act as joint guarantors for the final review manuscript. We did not receive any dedicated funding for this manuscript. BC salary is funded by the Lane Fox Respiratory Unit Patient Association (LFRUPA), Guy's and St. Thomas' NHS Foundation Trust. LFRUPA was not involved in any aspect of the design of this protocol or the systematic review to which it relates and in addition will have no input on the interpretation or publication of results. BC is supported by the National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. The Enhanced Recovery After Critical Illness Programme Group additionally includes the following: Nicholas Hart, Michael Grocott, Stephen Brett, Timothy Walsh, David Griffith, Stephen Shepherd, Judith Merriweather, Nazir Lone, Simon Baudouin, Stephen Bonner, Kathryn McDowell, Dorothy Wade, Natalie Pattison, Danielle Bear, Sallie Lamb, Rebecca Cusack, Daniel F McAuley, Robert Hatch, David Parkin, Mark Foster, Laura Price, Liesl Wandrag and Pamela Ramsay.
Dutch industrial paints and chemicals company AkzoNobel on Monday rejected a third unsolicited takeover bid from American rival PPG Industries, worth $28.8 billion, saying it was not in the interests of shareholders. "The PPG proposal undervalues AkzoNobel, contains significant risks and uncertainties, makes no substantive commitments to stakeholders and demonstrates a lack of cultural understanding," AkzoNobel CEO Ton Buchner said in a statement. Advertisement AkzoNobel said that its own plan, announced last month, to spin off its Specialty Chemicals unit within 12 months to boost growth "offers a superior route to growth and long-term value creation and is in the best interests of shareholders and all other stakeholders." AkzoNobel announced the shakeup after rejecting two earlier PPG bids, saying they undervalued the company. Last month, PPG Industries upped the ante again with a third bid for AkzoNobel; a cash-and-stock deal valued at about $28.8 billion. AkzoNobel said it rejected the latest offer after "considerable in-depth analysis" including talks with PPG's CEO, Michael McGarry. PPG said in a statement posted on its website that it was disappointed by the latest rejection and added that the talks, held on Saturday in Rotterdam, lasted less than 90 minutes. PPG said that Buchner and AkzoNobel's supervisory board chairman Antony Burgmans opened the meeting by saying "that they did not have the intent nor the authority to negotiate" and refused to discuss AkzoNobel's restructuring plan. PPG said it believes that its bid "is vastly superior in shareholder value creation and provides more certainty to employees and pensioners than AkzoNobel's recently announced new standalone plan." AkzoNobel's share price was down 2.4 percent at 77.50 euros ($84.82) late Monday morning compared to its previous close, but had edged up by 0.6 percent since the Amsterdam stock exchange opened.
Q: What is a product ID in USB and do I need to buy it for my project? I am trying to develop a portable device that will allow me to transfer data from one USB storage device to another without a using PC/Laptop. I was reading the developers guide by Jan Axelson where I came across a section that said that one must buy a USB vendor ID/product ID in order to make any USB device. I read the same on the USB Implementers Forum. I am unsure of the importance of this product ID in my project. Is it something like a MAC address for computers/laptops and will I need it? Is it something required only for developing peripheral devices and not devices like what I wish to implement(which I guess is more like a host)? A: I am not sure what exactly you want to make, but if it is a host device you indeed don't need an USB VID/PID. The USB VID/PID of a slave device is used by the host to identify the driver(s) to be used for the slave device. A host device does not need to identify itself to the slave, hence it does not need a VID/PID. A: Only devices need a VID and PID not hosts. The Vendor ID or VID is a 16-bit number which you have to buy from the USB Foundation. If you want to make USB device (and fully play by the rules) the VID identifies your organisation. The Product ID or PID is also a 16-bit number but is under your control. When you purchase a VID you have the right to use that with every possible PID so this gives you 65536 possible VID:PID combinations. The intention is that a VID:PID combination should uniquely identify a particular poduct globally. This guarantees that no PC can ever see two different devices with the same VID and PID as the PC uses these to identify the device otherwise a conflict could occur. Note: Unlike a MAC-ID the purpose of a VID:PID combination is to uniquely identify a device type to the extent that the operating system knows what drivers to use it's not always necessary to be able to distinguish between two identical devices. For example two USB memory sticks has the computer not only knows what the device is it knows which port its plugged into. When you plug a USB device in the OS asks the device for its VID and PID and gives the device an address which it will continue to use until the device is removed (or the computer switched off). Once the PC knows the VID and PID it checks to see if it knows these already. If it does it loads the correct drivers for it; if not you are given the opportunity to install any relevant drivers. This process is called enumeration. On the other hand a MAC-ID does not in its self provide any information about what a device is (computer, printer, router, etc.) but does uniquely identify a device: two identical PCs will have different MAC-IDs as if they both get plugged into the same Ethernet network it wont work correctly. Two identical USB memory sticks however will have identical VID and PID. If I want to make and sell 1 million identical USB devices I only need to buy one VID. If I want to make and sell 1 million Ethernet devices I have to buy 1 million MAC-IDs
Q: C union - please explain As far as I understand a union in C can hold only 1 value at a time and I don't really understand how this code in C makes sense since event.window cannot be populated at the same time as event.type? while(SDL_PollEvent(&event)) { switch(event.type) { case SDL_WINDOWEVENT: switch(event.window.event) The event is defined as: typedef union SDL_Event { Uint32 type; /*< Event type, shared with all events / SDL_CommonEvent common; /*< Common event data / SDL_WindowEvent window; /*< Window event data / SDL_KeyboardEvent key; /*< Keyboard event data / SDL_TextEditingEvent edit; /*< Text editing event data / SDL_TextInputEvent text; /*< Text input event data / SDL_MouseMotionEvent motion; /*< Mouse motion event data / SDL_MouseButtonEvent button; /*< Mouse button event data / SDL_MouseWheelEvent wheel; /*< Mouse wheel event data / SDL_JoyAxisEvent jaxis; /*< Joystick axis event data / SDL_JoyBallEvent jball; /*< Joystick ball event data / SDL_JoyHatEvent jhat; /*< Joystick hat event data / SDL_JoyButtonEvent jbutton; /*< Joystick button event data / SDL_JoyDeviceEvent jdevice; /*< Joystick device change event data / SDL_ControllerAxisEvent caxis; /*< Game Controller axis event data / SDL_ControllerButtonEvent cbutton; /*< Game Controller button event data / SDL_ControllerDeviceEvent cdevice; /*< Game Controller device event data / SDL_QuitEvent quit; /*< Quit request event data / SDL_UserEvent user; /*< Custom event data / SDL_SysWMEvent syswm; /*< System dependent window event data / SDL_TouchFingerEvent tfinger; /*< Touch finger event data / SDL_MultiGestureEvent mgesture; /*< Gesture event data / SDL_DollarGestureEvent dgesture; /*< Gesture event data / SDL_DropEvent drop; /*< Drag and drop event data / /* This is necessary for ABI compatibility between Visual C++ and GCC Visual C++ will respect the push pack pragma and use 52 bytes for this structure, and GCC will use the alignment of the largest datatype within the union, which is 8 bytes. So... we'll add padding to force the size to be 56 bytes for both. */ Uint8 padding[56]; } SDL_Event; A: Every aggregate (structs probably) member SDL_CommonEvent common;, SDL_WindowEvent window;, SDL_KeyboardEvent key; etc... of the union SDL_Event is starting with some Uint32 field giving the type and that common type field has the same address and size in every union member. So while indeed a union carries only one field at once in memory (in other words, all union members have the same address), each of them starts with a type and the event.type makes sense; it fetches that type. Such an idiom is a common way in C to implement tagged unions. A: Every member of the SDL_Event union starts with the same two members, Uint32 type and Uint32 timestamp. The C standard specifically says that if a union is currently holding a value of one struct type, but read as another struct type whose first members match the other struct type, it's okay to read those matching members.
CFS Shelburne Canadian Forces Station Shelburne, also known as CFS Shelburne, is a former Canadian Forces Station located in Shelburne County, Nova Scotia. The facility operated from two locations within the Municipality of the District of Shelburne: The original facility opened during World War II and was located on the eastern shore of Shelburne Harbour in the community of Sandy Point, immediately south of the boundary for the town of Shelburne. This facility included a deepwater port and shore facilities including barracks and residences. The newer facility opened during the Cold War (part of the original Sandy Point facility was reactivated as well) and was located in the community of Lower Sandy Point, approximately south of the town of Shelburne, on Government Point at the southern tip of a peninsula separating Shelburne Harbour from Jordan Bay. HMCS Shelburne (1941–1946) In December 1941 the Royal Canadian Navy opened a naval station in the community of Sandy Point named HMCS Shelburne on the eastern shore of Shelburne Harbour immediately south of the town of Shelburne. Located at the mouth of the Roseway River, this station consisted of a deepwater pier and associated shore facilities, including barracks and residences. It was connected by Canadian National Railways via a short spur from the government wharf spur off its Yarmouth to Halifax main line. On May 13, 1945, the commanding officer of U-889, Kapitänleutnant Friedrich Braeucker formally surrendered to the RCN at HMCS Shelburne after being escorted there from Bay Bulls, Newfoundland, on May 10 by and . On May 14 U-889 was taken by the RCN to Halifax. HMCS Shelburne was closed in 1946 as part of the RCN's post-World War II budget cuts and force draw-down. The facility was converted into an industrial park with buildings sold for private use. Approximately of the Sandy Point property was purchased by the Government of Nova Scotia in 1948 for construction of the "Nova Scotia School for Boys" – a modern penal facility to replace the "Halifax Industrial School for Boys", a penal facility that had closed in 1947. The Nova Scotia School for Boys (later called the Shelburne Youth Centre) would close in 1988 upon the opening of the Nova Scotia Youth Centre in Waterville, NS RCAF Station Shelburne (1942–1944) Throughout the winter of 1942 during the months following the Attack on Pearl Harbor, the Royal Canadian Air Force constructed a seaplane base in Sandy Point, immediately south of HMCS Shelburne. It was intended for operational use by the United States Navy for conducting anti-submarine patrols off southern Nova Scotia for the shipping lanes to Boston and the Gulf of Maine as part of the Battle of the Atlantic. The USN decided against using the facility prior to its completion, thus it was commissioned as RCAF Station Shelburne and opened in June 1942 as a training base that saw occasional operational use. RCAF Station Shelburne hosted the No. 3 Operational Training Unit using the PBY-5A Canso with No. 116 Squadron RCAF being the first to train at the facility. In June 1943 No. 116 Squadron deployed to RCAF Station Botwood. Throughout the rest of 1943 the station was used occasionally by No. 117 Squadron RCAF and the No. 6 Coast Artillery Co-operation Detachment. In March 1944 the station was taken over by the Royal Canadian Navy and consolidated into the adjacent HMCS Shelburne. HMCS Shelburne (1955–1968) The creation of NATO in 1949 coincided with the development of the SOSUS network (SOund SUrveillance System) by the United States Navy and later other NATO navies for monitoring submarines of Warsaw Pact navies. The research and development phase of SOSUS ended with success and it began to be operationally deployed in 1952, beginning with the creation of 6 arrays in the North Atlantic basin. Deployment of SOSUS and the larger Integrated Undersea Surveillance System (IUSS) was likely spurred by development of ballistic missile submarines and associated missile technology in the Soviet Union during the mid-1950s. Each array required a shore-based facility to be constructed, which the USN termed a "Naval Facility" (NAVFAC). The first NAVFAC built under the "Caesar Program" was commissioned in September 1954 at Ramey Air Force Base, Puerto Rico. Similar stations were established that year at Grand Turk Island (Turks and Caicos) and San Salvador Island (Bahamas). One of the original 6 SOSUS arrays in the Atlantic basin was deployed off Nova Scotia and northern New England, requiring a NAVFAC to be constructed in southern Nova Scotia. As a result, the RCN reactivated HMCS Shelburne as a lodger unit on April 1, 1955. The RCN reacquired 23 of its former buildings in the industrial park at the original HMCS Shelburne in Sandy Point and constructed several new buildings including residences. Additionally, a new property was acquired to the south in Lower Sandy Point on a headland named Government Point where the NAVFAC was constructed as a joint RCN/USN "Oceanographic Research Station" – a cover for what would become the first SOSUS station in Canada (Naval Station Argentia would become the second). HMCS Shelburne became operational on August 14, 1955, with the commanding officer of HMCS Shelburne being appointed the officer-in-charge of the Oceanographic Research Station (aka the NAVFAC). As such, HMCS Shelburne was also the first SOSUS station to not fall under direct command of the USN. HMCS Shelburne would undergo numerous changes during the remainder of the 1950s and through the 1960s as the World War II-era quonset huts were replaced with modern facilities. One of the most notable events involving HMCS Shelburne was a reported UFO crash on October 4, 1967, that was witnessed in the waters off Shag Harbour, Nova Scotia, a fishing community in western Shelburne County approximately southwest of the military facilities at Shelburne Harbour. What would come to be called the Shag Harbour UFO incident reportedly also involved a coordinated military operation by the RCN and USN in the waters off the Shelburne NAVFAC at Government Point in the days following this incident. CFS Shelburne (1968–1995) On February 1, 1968, the RCN merged with the RCAF and the Canadian Army to form the Canadian Armed Forces. As part of the unification, HMCS Shelburne was renamed to Canadian Forces Station Shelburne, or CFS Shelburne. CFS Shelburne continued operations much as before, supporting the NAVFAC and the SOSUS array as part of IUSS; in fact CFS Shelburne was the smallest NAVFAC in the Atlantic basin. CFS Shelburne was placed under control of Maritime Command (MARCOM) which was the new name for naval forces in Canada. Operationally, CFS Shelburne was part of Maritime Forces Atlantic (MARLANT) which operated the Atlantic Fleet and associated support facilities. The reunification of Germany and dissolution of the Soviet Union led to the end of the Cold War, resulting in numerous defence budget cutbacks in NATO nations, including Canada and the United States. This period also coincided with numerous technological changes that made remote operation of sensor systems such as SOSUS possible from further distances. The IUSS underwent significant changes in 1994 when Commander Undersea Surveillance Atlantic and Pacific consolidated into a single command located in Dam Neck, Virginia, leading to remote operation of the SOSUS arrays and closure of associated NAVFACs. In support of this process, the Canadian Forces established the Canadian Forces IUSS Centre or CFIC which was housed in a new lodger unit named located at CFB Halifax. CFIC was created to operate the two SOSUS arrays at NAVFAC Shelburne (located at CFS Shelburne) and NAVFAC Argentia (located at Naval Station Argentia). NAVFAC Shelburne's monitoring operations for its SOSUS array was transferred to the CFIC/HMCS Trinity by remote operation in summer 1994 with NAVFAC Argentia following that fall. On August 1, 1994, the NAVFAC at CFS Shelburne was disestablished with USN personnel departing. The station itself was decommissioned entirely as a military facility by the Canadian Forces on March 13, 1995. Civilian use (1995–present) After its decommissioning, the properties comprising the former CFS Shelburne were transferred by the Government of Canada to the Government of Nova Scotia which in turn transferred them to the Shelburne Park Development Agency, who operated them as Shelburne Park. In 1997, responding to plans of the Shelburne Park Development Agency to develop Shelburne Park as a land-based aquaculture park, Ocean Produce International Ltd. (OPI) purchased 8 acres of "Government Point" at the southern tip of the former CFS Shelburne from the Shelburne Park Development Agency. In May 1997, Ocean Produce International Ltd. constructed a land-based seaweed research and development facility for two dwarf seaweed mutations with a salt-water greenhouse, production and processing facilities, microbiology, wet and dry labs and refrigeration rooms as well as office facilities. For the next ten years, OPI was involved in selling and winning culinary awards for their fresh and dried seaweed to culinary markets in Canada, the United States, Europe and Asia. OPI also developed raw materials for nutritional and cosmetics markets in North America. For its part, OPI also extracted a rare excitatory amino acid (kainic acid) and marketed it to some 300 neurological labs, universities and pharmaceutical companies in over 40 countries over the next decade. Shortly after the construction of OPI's facilities, the Shelburne Park Development Agency announced that it had abandoned its plans to develop the former base as a land-based aquaculture park adopting a plan to develop a sound stage instead. Ocean Produce International Ltd. is today reviewing the potential for re-purposing and re-development of its 8-acre property at Government Point, which could include high volume saltwater wells and potential wind-turbines at the entrance to Shelburne Harbour and at the tip of the peninsula between the harbour and Jordan Bay. The Shelburne Park Development Agency was made a subsidiary of the Shelburne Area Industrial Commission, which has since been merged with the Yarmouth Area Industrial Commission and Clare Area Industrial Commission to form the South West Shore Development Authority (SWSDA). Shelburne Park is operated by SWSDA as a business park from the two former military facilities at Sandy Point and Lower Sandy Point. Several of the buildings at the Lower Sandy Point road location (the former NAVFAC) have been transformed into the Shelburne Film Production Centre, which opened on 9 July 2000. It was listed for sale by the SWSDA for $5 million and sold in 2008 to Seacoast Entertainment Arts Inc. for development as a film production studio. In late November 2011, the facility was sold to Tri-County Construction, a marine construction contracting company, for $125,000, plus $48,442.58 in back taxes, as well as undisclosed sales taxes and a municipal deed transfer tax. Shortly after the purchase, the buyer said he had no immediate plans for the property. Reportedly numerous buildings at the former NAVFAC sit in derelict condition open to the elements. References Category:Canadian Forces bases in Nova Scotia Category:Canadian Forces bases in Canada (closed) Category:Buildings and structures in Shelburne County, Nova Scotia Category:Royal Canadian Navy bases
Image via Twitter Last Thursday, the Hurricanes officially announced that owner Peter Karmanos had sold a majority stake in the franchise to Thomas Dundon. Dundon bought 61 percent of the team, paid a reported $420 million, and has the option to buy the rest of the franchise in three years. He’s boys with Tony Romo and Mark Cuban and he’s 43 years old. So, where did he make all his money? Lost in all the typical bluster that occurs whenever a team gets a young new owner—“He loves business! He works hard! He’s gonna shake things up around here!”—is the fact that Dundon could afford to buy the team because he made a fortune ripping off vulnerable people. Here’s a paragraph from a recent, adulatory Raleigh News & Observer profile that is somehow presented as a reason to trust Dundon: He started over as a back-room finance associate at a used-car dealership, quickly figuring out that there was more money to be made in financing used cars than selling them – especially to people with bad credit. They could be charged high interest rates, but they’d still do whatever they could to make the payments, because if their cars were repossessed, they’d often lose their jobs. That kept default rates down. Dundon made millions. Dundon founded a subprime auto loan company in 1992 and sold it to Santander Bank in 2006. The sole purpose of Dundon’s company, in its various iterations, was to provide loans to customers with bad credit so that they could buy cars. According to regulatory filings, they’d offer loans with interest rates as high as 29 percent to customers the company knew would have a hard time repaying their debts. Because of the necessity for even the most vulnerable Americans to own a car in order to work, Drive Financial and Santander were able to take advantage of their customers’ desperation and lock them into predatory loans, the same sort that led to economic collapse a decade ago. As Jalopnik’s Ryan Felton noted this summer, they knew exactly what they were doing: Santander recognized a high rate of Massachusetts consumers had loan applications that contained inflated incomes, but still continued to fund the loans, according to the settlement document. Santander estimated that 42 percent of subprime loans created in Massachusetts between 2009-2014 have already defaulted or will end in default, the document says. While Dundon was enriching himself, his company’s aggressive hawking of dangerous loans was driving desperate customers to financial ruin. As of the third quarter of 2017, Americans owed a total of $1.21 trillion in auto loan debt, and Santander is the biggest player in the market. Dundon resigned from Santander in 2015 as the bank faced intense regulatory scrutiny over its subprime lending practices, and last March, Santander reached a $22 million settlement with the state of Massachusetts “for its role in facilitating unfair, high-rate auto loans for thousands of Massachusetts car buyers.” Dundon got an exit deal from Santander last November and his cashout was $713 million.
Ghrelin and cardiovascular health. Ghrelin and its receptor are widely distributed in cardiovascular tissues, and there is no doubt that the effects of ghrelin in the cardiovascular system are mediated not only via its growth-hormone-releasing effect but also by direct effects on the heart. Indeed, new pharmacological approaches with animal and cell models using elegant study designs have described new functions of ghrelin, providing new potential therapeutic opportunities for ghrelin in cardiovascular medicine.
Q: Setting JPanel layout (Say) I've created a JPanel with three buttons. I want to place the buttons as follows (I've done this using netbeans GUI editor. But I need to write the whole GUI manually). Can some one show me a way to achieve this. (In words, I need to place some buttons right aligned, some other left aligned.) A: I guess you want the Configure button to be as far to the left as possible, and the ok and cancel grouped together to the right. If so, I would suggest using a BorderLayout and place the Configure button in WEST, and a flow-layout for Ok, Cancel and place that panel in the EAST. Another option would be to use GridBagLayout and make use of the GridBagConstrant.anchor attribute. Since you're taking the time to avoid the NetBeans GUI editor, here's a nice example for you :-) Code below: import java.awt.BorderLayout; import javax.swing.*; public class FrameTestBase { public static void main(String args[]) { // Will be left-aligned. JPanel configurePanel = new JPanel(); configurePanel.add(new JButton("Configure")); // Will be right-aligned. JPanel okCancelPanel = new JPanel(); okCancelPanel.add(new JButton("Ok")); okCancelPanel.add(new JButton("Cancel")); // The full panel. JPanel buttonPanel = new JPanel(new BorderLayout()); buttonPanel.add(configurePanel, BorderLayout.WEST); buttonPanel.add(okCancelPanel, BorderLayout.EAST); // Show it. JFrame t = new JFrame("Button Layout Demo"); t.setContentPane(buttonPanel); t.setDefaultCloseOperation(JFrame.EXIT_ON_CLOSE); t.setSize(400, 65); t.setVisible(true); } }
Q: Android timer problem I am using timer in my application for the background process and the timer runs successfully. But the problem is that i have to stop timer when logout button is clicked , the logout button is in different Activity. i have used timer.cancel() but As the Both Activity different it does't work. so give some hint to stop timer. A: Declare your Timer as public static Timer timer; and you will be able to access it in any Activity or class using Acitivity_name.timer.cancel(); Thanks...
[Determination of cytomegalo-, herpes simplex- and rubellavirus-antibodies resp. during perinatal period by Elisa-technique (author's transl)]. Cytomegalovirus (CMV)-infections attract increased attention among viral infections in the pre- und perinatal period resp. The decreasing cell mediated immunity by the end of pregnancy may favour conditions for primary infections or reactivations with CMV. With the Elisa-technique we looked for CMV-specific antibody status in the perinatal period with special respect to striking titers. The same serum samples were screened for antibody status to Herpes simplex virus (HSV) type 1 specific IgG and rubellavirus specific IgG resp. 67% were positive for CMV-IgG, 90% for HSV-type 1-IgG and 93.5% for rubellavirus IgG. CMV-specific IgM antibodies were found in 3.6% but only 1.5% were suspicious for recent CMV-infections according to higher CMV specific IgM titers.
# Runtime models and parameters All files specifying parameters and models loaded at runtime are consolidated here. This includes empirical variant scoring models and default indel error parameters.
"Our father, who art in heaven, hallowed be thy name." "Thy kingdom come, thy will be done on earth as it is in heaven." "Give us this day our daily bread, and forgive us our trespasses, as we forgive those who trespass against us." "Lead us not into temptation, but deliver us from evil." "For the kingdom, the power, and the glory are yours, now and forever." "Amen." "Looking at mostly cloudy skies and with lows in the upper 20s." "There will likely be some refreeze on some of the roads." "So, slick spots are possible tonight in isolated lo" "You know the most important thing your granddad ever taught me?" "Hmm?" "Be ready." "Hurricane, flood, whatever it ends up being." "No more food gets delivered to the grocery store, gas stations dry up." "People just turn on each other, and, uh..." "All of a sudden, all that stands between you and being dead is you." "I'm proud of you, son." "It was a nice shot." "Hey, come on, hon." "Wait, wait, wait." "I forgot something." "Hold on a second, Anna!" "Ralph, you have the venison?" "Yup." "I forgot the pie." "Are we taking the truck?" "We're going up the street, you dope." "Come on." "Hey, wait for your mother, please." "Give me a ride." "Here." "Oh, you're gettin' heavy." "Um, Danny's dad said he'd sell me their old car." "I got half of what I need saved from the summer." "I thought maybe you'd -- forget it." "I can barely get enough carpentry work to keep up with the mortgage." "Well, why don't you rent out grandpa's old apartment house?" "Like I keep telling your mother, it's an old building, and it'll cost a fortune to fix it up." "Okay, okay." "They're here!" "Hello." "Happy Thanksgiving." "Happy Thanksgiving." "Anna, wait until we're invited." "Oh, for God's sake, Keller." "Get the hell in here." "Aah!" "Keller, you got the deer you shot?" "This one's Ralph's." "Well, you killed it, you take it into the kitchen." "All right." "Thank you." "Mwah." "Happy Thanksgiving." " Happy Thanksgiving." " There he is." "Thank you." "Happy t-day." "All right." "Joy." "Joy, three times." "Joy, get your dolls off the table." "Y'all missing the game." " Anna!" "Anna!" " Hi." "How are you?" "Hey." "Happy Thanksgiving." "Anna, come here." "We wait until we're invited." "You understand?" "You're in charge of this." "Us veterinarians make lousy butchers." "No problem." "Can I go outside with joy?" "Uh, convince your brother to go with you, and you can." "All right." "And wear a hat, please." "You're just getting over a cold." "Joy, you wear a hat, too." "Did you feel bad for that deer when you shot it?" "Do you feel bad for cows when you go into McDonald's?" "That's -- that's what my dad says." "And the deer, if they have too many babies, then the babies starve anyway." "You gotta keep the population down." "Right." "Your dad say that, too?" "Pull harder." "Hey, hey!" "Get away from that thing!" "Let me see that." "Come on, let's go." "No." "I said let's go!" "Hey, hey, hey, hey, hey." "Stop." "You can't just take somebody's stuff like that." "No!" "Let's go!" "Come on." "Come on, come on, come on." "Wait." "Shh." "You hear that?" "Somebody's in there." "All right, I don't feel like getting yelled at." "Let's go." "Not on Thanksgiving, okay?" "Now the school board's telling me there's no money for new marching-band uniforms." "These kids are wearin' the same uniforms they had when we went there, and they were old then." "I mean, marching' right out of 1979." "Why isn't he speaking to me?" "He doesn't speak." "Cutie pie." "Mm-hmm." "Oh, my gosh!" "He's fast, too." "He's so quick." "Is that a slide?" "Thank you, all." "Thank you, all." "Got a surprise." "Ohh." "And I am taking requests." "Yes!" "No." "You gotta listen out for it, 'cause this is not easy." "Mom." "Mommy, can I take joy to our house?" "Why?" "My red whistle." "She's gonna help me look for it." "Oh, my sweetheart, I think that red whistle is long gone." "What whistle?" "The emergency whistle daddy gave me." "I lost it 133 days ago." "Well, if you want to find a whistle, you have to whistle for it." "So we'll do "jingle bells" to find it." "Yay!" "Okay!" "Okay!" "You can go, all right?" "Just make sure eliza and Ralph go with you, please." " No looking in the basement." " I won't." "Y'all eardrums are just startin' to grow." "I don't want to damage them yet." "But I am taking requests from you, Keller." "From me?" "Your day, your request." "Oh." "Uh, the piano." "No." "No, no, no." "So all set?" "Wait, listen, he used to love -- he used to dress like Springsteen." "Really?" "I still love Springsteen." ""The river," "Jersey girl."" "Well, I ain't white, and I like him too much" "And I'm too drunk to cover the boss." "Thank you." "Honey?" "What else?" "Nothing comes to mind." "Nothing." "Oh, I know." "What?" "He actually loves "the star-spangled banner."" "I know." "Sings it in the shower." "I do not." " Yes, you do!" " I got you." "Where are your sisters?" "I can't find them." "You, uh, you go to the house with them?" "No." "What are you talking about?" "Earlier?" "No." "What?" "They were supposed to come down earlier and get you." "They didn't come get you?" "No." "We haven't seen them since we ate." "It's all right." "All right." "They're probably at our house." "Anna?" "Joy?" "Anna?" "Girls?" "Who put these dishes in here?" "Get outta here." "They weren't outside." "It's starting to rain." "Did you check over by Maria's swing?" "Yeah." "Well, they're gettin' whupped when they get here." "Sorry, grace." "I whup kids." "So they weren't there either?" "They must be at home." "Are they here?" "No." "They're not here." "They weren't there?" "No, they're not at our house." "No, they're not there." "I checked the entire house." "They're not here." "The -- the -- the rv." "What rv?" "Dad, there was this rv, and they were playing on it." "We thought there was someone inside." "Where?" "Where was it?" "Show me." "You wait here." "I'm gonna gonna over the house again." "Relax." "Relax." "Go that way." "I'll meet you on the other side." "Anna?" "!" "Joy!" "Roger, you seen my daughter walk by here?" "No." "Is there a problem?" "Anna?" "Here!" "Dad, it was parked right here." "Anna?" "Anna?" "Hello, hello!" "Did you see 'em?" "No!" "Hello!" "I couldn't find 'em!" "Were you messing around in this house?" "No." "I told you not to come here." "We weren't." "They were just on the rv, and we got them off of it." "Tell me everything you remember about that rv." "Everything." "A-a ladder on the back." "Police, police." "Happy Thanksgiving." "Thanks." "Hey, you have any of those, um, fortune-cookie things?" "My boss told me cops don't like fortune cookies." "What year were you born?" "Are you a dragon or a snake or a horse?" "I'm a monkey." "Oh, you're a monkey." "You're very intelligent." "You have an ability to influence people." "Think maybe you could influence your boss to lower the check a little bit?" "No." "I cannot." "My boss is a rooster." "Silly, selfish, and eccentric." "That's..." "All units, all units, an rv was reported matching the description." "The vehicle is parked at a rest stop off of route 46, northbound, past exit 17." "Any available units?" "This is 12-12 responding." "10-80 responding." "This is 13-40." "I'm five minutes out." "I'll meet the responding units." "12-12 standing by." "10-80 standing by." "13-40." "I'm on scene." "Be advised, we're moving in." "Whoa!" "Hey, don't move!" "Hey!" "Whoa, whoa, watch out!" "Hey, don't shoot!" "Don't shoot!" "Don't shoot!" "All right, Sloan, take the right!" "Clear!" "Clear!" "Wait, wait, wait, wait, wait!" "I got this." "Gimme that." "Hey." "Hey." "I see you in there." "Show me both your hands right now." "Hey, I see you in there!" "Show me your hands!" "Both hands right now!" "That's it." "Slow." "Slow." "Slow!" "Slow." "Slowly." "Both hands." "Both fuckin' hands!" "Walk!" "Walk!" "Hey!" "Walk!" "Get up!" "Get up!" "Get up!" "Show me those girls!" "Show me where you put those girls, huh?" "Where are those girls?" "Hey, give me the flashlight." "Sir." "Show me where those girls -- they in the woods?" "You put them in the woods?" "Where did you put those girls?" "You hear me?" "!" "What the fuck is this guy on?" "He's high on something." "Put this fucking guy in the car." "Get him in the car." "Put him in the fucking car!" "Walk!" "Let's go." "Hey, call psp, tell 'em to send their scent dogs." "And seal off the whole area." "The entrance, all of it." "Right." "You, come with me." "No, they weren't playing on your rv?" "No." "Okay, take a look at 'em again." "Don't recognize these girls?" "I didn't see them." "May I sit down?" "What do you do in the rv?" "Answer my question." "Sleep there." "You sleep in there?" "You were sleeping out there?" "In the day?" "Why was the rv parked outside the house?" "Hmm." "I went for a drive?" "You went for a drive?" "You weren't driving." "I know for a fact those girls were playing outside your rv." "You weren't driving." "It was parked." "Was it a special day?" "Were you planning on taking two little girls?" "No." "Have you done that before?" "No." "Did you ask them to come inside?" "No." "You ask them to come inside the RV and then you take them away?" "No." "Did you put those girls somewhere?" "May I sit down?" "Come on." "Did you put those girls somewhere?" "Please don't touch me." "I know you put those girls somewhere." "You hide 'em?" "No." "How did you hide 'em?" "Do you tie 'em up?" "Mnh-mnh." "Do you tie 'em up?" "Mnh-mnh-mnh." "Huh?" "Hey." "Hey." "Hey." "Look, I know you're a good guy, all right?" "I know you're a decent guy." "I'm not tryin' to tell you you're doing anything bad." "I'm just tryin' to get the right answers out of you, okay?" "The real ones." "That's all I want." "Where do you usually park your rv, Alex?" "My aunt's house." "Your aunt's house?" "She lets me park it in the backyard." "The grass don't grow back there anyway." "It was my husband's." "For sale, if you want it." "No, thanks." "Well, would you tell me what you're doin' on my property then?" "I'm just glad to know where he is." "He's always home before dark, and..." "I just don't understand." "That boy has never been in trouble, not a day in his life." "Uh, in the summertime, he sleeps out in the camper some, but..." "This time of year, he sleeps in here on the sofa bed." "That -- that's my husband." "We had a fight, jeez, five years ago." "Walked out, didn't come back." "Alex loved him like a father." "Where are Alex's real parents?" "My husband's brother and his girlfriend, they died in a car accident when Alex was about 6." "Sorry to hear that." "He doesn't have much." "What have you got?" "Well, this thing's clean." "I mean, it's filthy as shit, but we didn't find anything." "We didn't find any, uh, wool fibers, anything like that?" "The girls could be wearing some wool gloves or wool hat." "No cotton fibers?" "Well, if he was just usin' this thing to transport 'em," "I might buy that." "But if there had been a struggle," "I would have found something." "I'd start lookin' in the woods by the rest stop." "Yeah." "Half the uniformed cops in the state are doin' that right now." "When you're done with this thing, can you send a crew over to the aunt's house?" "Anna!" "Anna?" "!" "Thanks for comin'." "Franklin birch." "My wife's in here." "Honey?" "Her name's Nancy." "Detective loki is -- honey?" "These photos are better than the ones my husband gave you." "You can see her eyes more clearly." "So, did we pass?" "I'm sorry, what did you say?" "The poly thing." "The lie detector we took this morning." "Did we pass?" "Oh, yeah, yeah." "Sorry." "Yes, we appreciate your cooperation." "It's embarrassing, all the -- all this fuss." "Everyone's gonna think we're crazy when those two come out of hiding, wherever they are." "Do you have some reason to believe they ran away?" "No." "They're happy." "They must have run away." "I think they must have run away." "Right?" "Um, your police captain told me that you've solved every case that you've ever been assigned." "Is that right?" "Sorry." "I am so sorry." "Do you -- do you have children, detective?" "I'm gonna find your daughter." "We believe that they came back here after they left you at the birches' yesterday." "They were looking for Anna's red whistle." "Right." "I read your statement." "I'm detective loki." "I'm heading up the investigation into your daughter's disappearance." "Please sit down." "Uh, uh, m-my son already told you that the guy was inside the rv just watchin' 'em, right?" "We haven't found any physical evidence inside the rv." "Or his aunt's house where he lives." "Nothing?" "Alex Jones unfortunately has the I.Q. Of a 10-year-old." "There is no way that someone with the I.Q. Of a 10-year-old could abduct two girls in broad daylight and then..." "Somehow make them disappear." "Uh, well, how can he drive an rv?" "If he can't answer a question..." "Well, he has a legal Pennsylvania license." "And he ran, right?" "They said he tried to run away." "Why -- why..." "Why would he run?" "I've just spent 10 hours questioning this boy." "Okay?" "I hear what you're saying." "Uh..." "Did -- did you give him a lie detector?" "You gave us a lie detector." "Did you give him one?" "Sir, I understand what you're asking me." "Yes, we did." "We gave him a lie detector, and there is no way of " "A lie detector doesn't work if you don't understand the questions." "Well, maybe he wasn't on his own." "How could he drive an rv if he has an I.Q. Of a 10-year-old?" "Hey, we're considering all possibilities." "I don't think you are considering all possibilities." "I-I hear what you're saying." "Sir -- sir -- you listen to me." "Just shut the fuck up for a fucking second!" "This is what I'm gonna need you to do for me." "I need you to calm down." "I'm sorry." "I'm sorry." "Please listen to me for a second." "Mr. Dover, I understand this is an incredibly hard time." "But I have every uniformed police officer in this state looking for Anna." "I don't understand what any of this means." "They said he ran." "They said he tried to get away." "I don't understand why he would try to run away." "We're considering all possibilities, Mr. Dover." "I hear what you're saying." "I'm not crossing anybody off my list." "Just..." "Let me do my job." "Hey!" "Detective!" "Oh, shit." "Hey!" "He stays in custody until my daughter's found, right?" "Right?" "We have a 48-hour hold on him that ends tomorrow unless we bring charges." "Well, charge him with something." "Charge him." "Mr. Dover, I understand what you're -- detective, detective, two little girls have got to be worth whatever little rule you've got to break to keep that asshole in custody." "Now, I know you can't promise me anything." "I understand that." "But I'm asking you to be 100% sure." "Thank you." "I appreciate it." "So you're positive he's innocent, but you want to keep holding him?" "Anna Dover's father was on my ass this morning." "I-I get it." "I understand." "But it's not gonna happen." "I was asking for one more day." "Fuck you." "No, no." "You find his daughter, he'll forgive you." "You don't, he's gonna hate you anyway." "So what's next?" "I'm knockin' on doors all night." "Yeah, well, you're comin' up on 24 hours missing, and you have exactly shit." "No, I've got nine level-three sex offenders living within a 10-mile radius of Fairmont circle." "So if you don't mind..." "Then go." "Yeah." "Go." "It's right here." "Look, I-I'm staying straight, okay?" "Well, hey, look." "Look, I know you're -- you like yourself some German porn, huh?" "Look, I was..." "Father!" "Open up!" "It's the police!" "Father!" "Father." "You mind if I take a look around?" "Fuckin' drunk." "What the fuck?" "Whoa." "Fuck." "Aye." "Fuck." "Oh!" "Please, God!" "God!" "What's the name of your buddy down there, huh?" "What's the name, huh?" "I don't know his name." "You don't know his name?" "I don't know his name." "Hey, you know what?" "I spent six years in huntington boys' home, father." "You know the huntington boys' home, right?" "Huh?" "Hurting a fuck like you'd be a real treat for me." "Why don't you tell me his fuckin' name?" "He didn't tell me his name." "He came to me for confession." "He said he'd killed 16 children." "He bragged about it." "I convinced him to come back here." "He said he'd kill more." "16 children, huh?" "Let's go, you fucking chicken-hawk!" "Hey." "They're letting him go." "What?" "The man." "The police said they're letting him go today." "O-okay." "I'll take care of it." "Dad?" "Keep searching." "Where are you goin'?" "!" "He wants you to write your whole name." "That's good." "Mm-hmm." "Good job." "Now you give it to the man." "All right." "Come on." "I don't want you minding these people out here." "Don't talk to them." "You've got nothing to say to them." "Come on." "Come on, Alex." "You took those kids, didn't you?" "Sir -- I just want to talk." "He's a free man, I'm a free man!" "Hey!" "Tell me what you did with them!" "Tell me!" "They didn't cry until I left them." "What did you say?" "What did you say?" "!" "Whoa, no, no!" "Fuckin' get off him!" "God!" "Get up!" "Get him down!" "Get him down!" "Move back!" "Please, just let us go." "Thanks for nothing." "We're fine." "Thank you." "Now, I know your dad was a guard at graterford." "And I've got a daughter of my own, so we're gonna pretend this never happened." "And as for Alex Jones, he has orders not to leave the commonwealth." "What?" "Sir, I need you to go home." "All right?" "I need you to go home to your family." "What about what I just fucking told you?" "Why aren't you sending someone out to go arrest this guy?" "Tell detective loki what you just told me, and he'll definitely look into it." "Go ahead." "That asshole you promised me you'd keep in custody, right?" "And you didn't." "And right now when I grabbed him in the parking lot, he said right to my fucking face," ""they didn't cry until I left them."" "Right to my fucking face." "He -- he said that to you in the parking lot just now?" "Right now, yeah." "What did I just say?" "In the parking lot." "Before you grabbed me off him." "Did anyone else hear it besides you?" "I don't know." "It was quiet." "He -- he said it to me." "He wanted me to know." "Are you sure he said that?" "What?" "Are you sure that's what he said?" "Jesus Christ, you think I'm makin' this up?" "No." "Why would I make this up?" "Hey, hey, hey, whoa, whoa." "No, think about it." "Why would I make this up?" "I'm not saying that to you." "I'm just asking you a couple questions." "I will talk to him." "No, don't talk to him!" "Mr. Dover -- arrest him!" "What did I fuckin' tell you?" "What'd I tell you?" "One more day." "You sure you didn't say anything to Mr. Dover in the parking lot today?" "Anything he could have misinterpreted or...?" "I was right there." "They didn't say anything to each other." "Man just attacked the boy." "Nothing like "get away from me" or "help" or..." "Anything like that?" "No." "Can I speak to Alex alone for a minute?" "It's all right, sweetie." "I'll be right in the next room." "You love your aunt, don't you, Alex?" "Yes." "You know if you know something you're not telling us that she could go to jail for a very long time." "Do you want that for her?" "After everything she's done for you?" "No." "Mr. Dover, this is detective loki." "Have you arrested him?" "Yeah, look, I just came from Alex Jones, and he said he didn't say anything to you in the parking lot." "I pushed him pretty hard, and he didn't budge." "So, look, we can't waste any more time on this guy." "All right?" "You're gonna have to trust me." "I'll let you know if I have anything new, all right, for the -- fuckin' "a."" "The zipper on her coat was broken, and I told her it didn't matter 'cause we were just gonna go right down the street." "No, no." "Why hasn't she come home?" "It's been three days." "Why can't you make her come home?" "I don't understand." "I don't understand." "It's been too long." "Please make her come home." "Please make her..." "How many of these?" "How many of these?" "How many of these?" "I don't know!" "It's okay." "It's all right." "Just take one." "Here." "No." "I just want to sleep." "I just want to go to sleep." "You..." "You made me feel so safe." "You told us that you could protect us from everything." "Oh, God..." "I'm gonna go out and help the police." "Just keep an eye on your mother." "Your sister needs us to be brave for her." "Be brave for her." "Be a grown-up for me, okay?" "Can you do that?" "Can you do that?" "I know you're scared." "Look at me." "Come here." "I know you're scared." "It's gonna be okay." "The former is a reason why we should be very patient." "The latter why we should be very penitent when we are afflicted." "He reminds him that trouble and affliction are what we have all reason to expect in this world." "Man is brought into trouble, not as man, but as sinful man, who was in transgression." "Man born in sin and therefore born to trouble." "Come on." "Come on, Tucker." "That song." "Where did you hear those words?" "Hmm?" "Did you bring a change of clothes like I told you?" "Yeah." "You gonna tell me why?" "It's better if I just show you." "Show me what?" "Didn't you used to live here?" "Mm-hmm." "Close the door." "Lock it." "Wow." "Oh, my God." "What -- what did you do?" "Keller, what the hell...?" "I heard him singing the same song they were singing on Thanksgiving." "Swear to God, Franklin." "The same fucking song." "And I told you what he said in the parking lot." "Then we take him to the police -- no, no, no." "The police won't do shit." "He'll just clam up and act crazy like he did last time." "Someone has to make him talk." "Someone." "Shit, man." "This -- this ain't right." "I mean, what if you're wrong?" "I'm not wrong." "But what if you are?" "What if you only heard what you wanted to hear?" "What if..." "Man, I want my daughter back as much as you do, but it ain't right." "Franklin!" "Franklin!" "We hurt him until he talks, or they're gonna die." "This ain't -- no!" "No!" "We hurt him until he talks or they're gonna die." "That's the choice." "That's the choice you have to make." "I've made my choice." "I know what I heard." "He's not a person anymore." "No, he stopped being a person when he took our daughters." "I need your help." "This is your last chance." "I know you're scared." "And I know you wanna go home." "And I don't -- I don't want to hurt you." "I don't." "I'm gonna take the tape off, and I want you to tell me where they are." "Mnh!" "Hey." "Come on." "Did you see my glasses?" "What?" "I can't see." "If you're not gonna talk, Alex, I'm gonna have to hurt you." "Tell me where they are." "Where are they?" "Tell me where they are!" "Yeah, I'm out here at a house on Fairmont circle, the house the rv was parked in front of." "It's only been on the market a couple of months." "I'm gonna track the owners down, see if they know anything." "You got any new info on that corpse we found in the priest's basement?" "No DNA, dental, or fingerprint matches." "Nothing." "Priest is sticking to the story, too." "All right." "Same person who took him took those girls." "I'm sure of it." "Wearing out the tape, I guess." "I watch it every day after breakfast." "It's the only video I have of him." "It was before your time." "26 years ago, August 19th." "I took a nap in the afternoon, and when I woke up, Barry was gone." "No one could ever tell me what happened to him." "He was playing in the front yard, just a few feet from where they say that rv was parked." "What do you think that means?" "I'm more interested in what you think that means." "I don't think we'll ever know." "It's just like Barry." "No one took them." "Nothing happened." "They're just gone." "How you doin', father?" "I'm..." "I'm -- gettin' better." "So detective chemelinski tells me that you have some specifics about the crime you claim that guy committed." "The abductor." "He was..." "Waging a war against God." "Great." "That's great." "I thought you said he had something specific." "Tell him how he took the kids." "He said he took them in daylight." "Sometimes..." "More than one child at a time." "He said that?" "Yeah." "Did he say he was with anybody?" "He did it alone?" "He..." "He said he had a family." "That's it?" "All right." "Informative." "You said they cried when you left them." "Look at me." "You said they cried when you left them!" "You said they cried when you left them!" "Now tell me!" "Where is she?" "Hmm?" "Hmm?" "Tell me where they are!" "Just tell me." "Just tell me and I'll stop." "I'll stop as soon as you tell me." "Just..." "Just tell me where they are." "Why won't you tell me?" "Huh?" "Why won't you just fuckin' tell us?" "He knows." "He knows." "I can see it in his eyes." "He fucking knows." "I know you know!" "Why aren't you fucking telling me?" "!" "Why?" "!" "Fine." "Get him up." "Get him up." "Get up." "Get up." "Get up." "Get up!" "You gonna make me use this?" "You gonna tell us?" "If you don't, I'm gonna use this." "Fine." "You're doing this to yourself." "Just tell us." "Tell me." "Tell me!" "Tell me!" "Tell me!" "Tell me!" "Where's my daughter?" "!" "Where's..." "My..." "Daughter?" "!" "Four days have passed since Anna Dover and joy birch were last seen by their families." "The two girls, aged 6 and 7, are believed to have been playing on this street when they disappeared without a trace." "As you can see, despite the cold, a lot of people have turned out tonight to show their support." "Police are asking that anyone with any information on the girls' whereabouts..." "Where have you been?" "I was searching for her in the woods." "I'm okay." "I'm okay." "Franklin." "Franklin, what is it?" "I just need a minute." "What the fuck?" "Hey!" "Get offa me!" "Hey!" "Hey!" "Okay." "And this is who police are saying is a person of interest in the investigation of the two missing girls." "Now, this unidentified man, who was last seen at last night's candlelight vigil, fled on foot when the investigating detective attempted to question him." "Police caution the public not to approach this man, but to call police immediately if they do see him." "Thanks, John, for that update." "And now for the weather." "We should expect heavy rain into the weekend and " "Look, Keller, I mean, just think about it." "Why would the police be lookin' for this man if they didn't think that he did it in the first place?" "They did it together." "They know each other." "Listen, I fuckin' told you, all right?" "Jones looked me in the eye and he said," ""they only cried when I left them."" "He left 'em with someone, and he knows where this guy is." "Holly Jones' dog got hit on southward street." "Apparently Alex Jones took the dog for a walk the night before last -- they never came home." "And his aunt didn't want to tell us about the dog when we called her about it this morning." "She said that she thought it would get him into trouble or some shit." "I thought you said you would keep him under surveillance." "Yeah, and I thought you said the guy was innocent." "And I thought the guy from last night you said was our guy." "Look, I don't have money in the budget for watching innocent people." "You said to me that you'd put him under surveillance." "What do you want me to say?" "You gonna keep your word?" "You could have just given me a call, because I would have been there all night." "I would have stayed up all night." "I would know where he was now." "I need to know where everybody is." "All right, point made." "All right?" "Point made." "If you can be clear with me, then I'll be clear with you." "I need to know where everybody is." "If you're gonna do something different, please tell me." "Tell me about your rv." "What do you do in your rv?" "It's where I go..." "To be alone." "What music do you listen to in your rv when you're alone?" "Radio, tape..." "The rv was parked over on Fairmont circle?" "No." "Is my aunt coming?" "Have you seen these girls?" "No." "Take a look at 'em." "You seen these girls?" "No." "Did you participate in any way in the abduction of those girls?" "No." "Loki!" "You got a call." "All right." "I called as soon as I saw the sketch on TV." "He comes in here every week almost and buys kids' clothes, but he's always buying stuff in different sizes." "Caught him messing around with the mannequins once." "What did he pay with?" "Cash." "All right, you give me a call if you hear anything." "Okay." "It's been five days." "Maybe five days since they had a drink of water." "This could be the last night that matters." "Look, I'll call you after Nancy goes to sleep, all right?" "I promise." "Where have you been all this time?" "What the hell were you thinking?" "You tell anyone?" "Did you?" "I wanna see him." "Oh..." "Please help me." "Could you help me find my little girl?" "Got a picture." "See?" "This my baby." "You see her?" "Her name is joy." "And, um..." "This is..." "A stuffed animal we got her when she was 2 because she's afraid to sleep by herself." "Please..." "Tell me where my little girl is." "Please tell me where my little girl..." "I know you're gonna tell me." "I know you're gonna tell me." "I know." "Help me." "Help me." "Franklin, did you close the door to the " "Nancy!" "What the fuck you doin'?" "God damn it!" "Damn!" "Let it go!" "Let it go!" "You untied him?" "Huh?" "That was close." "What is it?" "What happened?" "Get Franklin." "I need to show you something." "Did he say anything new?" "He will soon." "You'll see." "No light gets in." "There's barely enough room to sit down inside." "Shower still works, but we control it from out here." "And I rigged the water heater so it either comes out scalding or freezing." "And, uh, you talk to him through this." "It's to remind us..." "In case we start feeling sorry for him." "My God." "I can't hurt him any more without killing him, so this is the only way." "Have you lost your mind, Keller?" "Do you have a better idea, Franklin?" "Do you?" "Go ahead." "Let him out, if you want." "I'm not gonna stop you." "If that's what you really want, you go ahead." "You think someone's lookin' out for our girls the way you're lookin' out for him?" "I hope." "It's been five days now, man." "We're runnin' out of time." "You don't even know it's him." "Yeah, I do." "No, you don't." "I do." "I know you." "You don't." "Look, I want my baby back..." "As much as you miss Anna." "And despite what you think about me," "I would die for my daughter." "But this ain't right." "This has to stop." "Well, then, you better get to work." "You can start with that wall there." "Franklin." "Stop." "Franklin..." "Think of joy." "I need to get out of this place, Ralph." "Everything in this house just makes me want to throw up." "Your dad's building?" "There is no way I'm staying in that crackhouse." "It's disgusting." "Yeah, okay." "We're not gonna help Keller, but we won't stop him, either." "Let him do what he needs to." "We don't know about it anymore." "Eliza?" "Eliza?" "Excuse me." "Eliza?" "Eliza, open the door!" "Eliza?" "Is she in there?" "Honey?" "Get out of the way!" "Get out of the way!" "Yeah, fuck you both!" "Next time you plan on leaving me here alone, maybe you could try at least telling me where you're going!" "Ralph?" "Anna?" "Anna?" "Anna?" "Anna?" "Anna?" "Mom?" "Mom?" "Anna." "Anna was here." "Mom, it's freezing in here." "Mom!" "Hey, mom, mom, mom, please sit down." "Stop." "Calm down." "I'm gonna close the window." "And she wasn't here." "And then I heard a sound from my room, and I..." "I came in and the window was open." "And -- and it wasn't open before." "And then -- and then Ralph, he -- he came in..." "And he looked and -- and, um..." "And then..." "Then I don't know." "Aren't you gonna write this down?" "The basement." "I didn't check the basement." "We need to check the basement." "I-I'll show you." "I'll show you." "The kids know they're not allowed down here." "They're not supposed to come down here, but I-I don't know." "My husband likes to be prepared for emergencies." "Where is your husband, Mrs. Dover?" "I was gonna ask you." "He's been out searching with the police for Anna." "Which you should be doing right now." "Does he always stay out this late?" "Yes, he stays out this late when he's looking for my daughter, since my daughter has been gone -- yes!" "Shit." "Hey, go aro-- go around." "Fuck." "Come on, Mr. Dover." "Shit." "Why are you following me?" "Get in the car." "Why are you following me?" "Where did you go just now?" "I parked at a liquor store." "I have a bottle of liquor." "You're the shit-hot detective." "Work it out." "I actually meant before that." "You were walking in the opposite direction across the parking lot." "Towards campello street." "Yeah, well..." "I haven't had a drink in nine-and-a-half years." "I figured if I walked around the parking lot for a while, by the time they opened, I'd stop wanting it that bad." "And then -- then I saw you." "Sorta helped me make up my mind." "There's a bag of lye in your basement that's half-empty." "Your wife thinks you've been helpin' us..." "But we both know that's not true." "I used the lye to bury our dog last year." "And "helping the cops" sounds better than "I've been driving aimlessly in my truck 'cause I don't know what the fuck else to do."" "Is that what you were doing last Saturday night?" "Probably." "Am I a suspect?" "No, I'm only asking " "I'm only asking 'cause you assaulted a man who's now missing." "I heard about that." "What happened to him?" "Thought you had him under surveillance." "I'm " " I'm gonna assume you're asking me because you have no idea." "Well, I didn't think it was something I could get away with." "It's not." "Yeah, well, it couldn't be that he skipped town 'cause the asshole is guilty." "Couldn't be that, right?" "'Cause that would mean it would be your fault, right?" "Mr. Dover?" "Mr. Dover?" "What?" "You need to take care of yourself and your wife." "That's the best thing you can do right now." "That little girl is gonna need you when she comes home." "Kids gone for more than a week have half as good a chance of being found, and after a month, almost none are." "Not alive." "All right?" "So forgive me for doing everything I can -- you know what?" "It hasn't been a fucking week." "You're right." "It's day fucking six!" "Day six!" "And every day she's wondering why" "I'm not there to fucking rescue her!" "All right." "Do you understand that?" "!" "Me!" "Not you!" "Not you!" "But me!" "Every day!" "All right." "So forgive me for not going home to have a good night's rest!" "Now, why don't you look for my fucking daughter rather than fighting -- hey, hey, hey, hey, hey, hey." "Don't follow me." "Hey, hey." "Mr. Dover." "Mr. Dover." "You don't think I'm gonna let you get behind the wheel after you've been drinkin', do you?" "I'm gonna walk." "You look for my daughter." "Daddy." "Daddy." "Look, daddy, we found it." "Anna..." "Where was it?" "I'm not Alex." "I'm not Alex." "What -- what are you saying?" "What?" "What?" "I'm..." "Not..." "Alex." "Wait a minute." "You're not Alex?" "What?" "I'm not Alex." "Just a second." "I don't understand." "Just -- just talk to me." "I waited, and he never came." "Come on." "No more riddles." "Just fuckin' tell me." "I'll let you go home to your aunt if you tell me where they are." "I just wanted to play." "Don't make me do this again." "And he never came." "Don't make me do it." "He never came." "I just wanted to -- why are you making me do this?" "Help me, God." "Relying on your almighty power and infinite mercies and promises," "I hope to obtain pardon for my sins." "Fuck me." "No -- no noise." "You shut up." "You make any noise, I'm gonna turn on that tap." "Hey, rise and shine." "I'm not gonna find two girls here, am I?" "Fuck you." "What about Alex Jones?" "What about him?" "I came here to drink." "I don't want to drink in front of my wife." "Look..." "My father left me this building, all right?" "You mind giving me a tour?" "Why didn't you tell me about this place?" "I didn't think it mattered." "Everything matters." "It's all pretty much like this." "I'm gonna renovate soon." "Yeah." "Not as organized as your basement, huh?" "What's up with all the survivor gear in there?" "Pray for the best, prepare for the worst." "Guess we agree there, yeah?" "Come on, hurry up." "Shit." "Hello?" "The guy that you were looking for was just here." "He saw me watching him and ran." "You get a plate?" "Yeah." "Yeah." "Yeah." "Go home, Mr. Dover." "Hi." "Mornin'." "Why'd you run away from me the other night, man?" "I've never seen you before." "You sure you have the right house?" "You doin' some shopping at the value mall lately?" "Yeah." "Why?" "Is it a crime to shop there?" "I can't afford to buy suits from Brooks brothers." "Yeah, I know." "You bought children's clothes." "Did I?" "Must've been in a hurry." "Mm-hmm." "Do -- do you have children?" "No." "I don't..." "Have..." "Have anything -- come on!" "Christ!" "Give me your fucking hand." "Hey." "If you move, I'll put a bullet through your fuckin' head." "This is 13-40." "I need additional unit for search." "437 Carrol street." "Possible kidnapping victims on the premises." "Anna?" "Fuckin'..." "Anna?" "Joy?" "Fuck." "Fuck." "Ah!" "Fuck." "Ah." "Ah." "Fuck." "Ah." "So we've taken photographs of some of the clothing we found in the suspect's house." "Mr. Dover." "Mr. Dover, is your wife here?" "She's not coming." "Well, if you can't make a positive I.D." "On any of these photographs" "I'm gonna need her to come in and take a look at them." "Have a seat." "So he confessed?" "He said he killed them?" "We were hoping he was lying, but..." "We haven't even found any bodies, Mr. Dover, but the birches positively identified two pieces of clothing." "I'm gonna need you " "I'm gonna need you to tell me if you recognize anything." "No." "Uh..." "I'm not sure." "I don't know." "Okay." "No." "No." "That..." "That's her..." "That's her sock." "You..." "You wasted time." "You wasted time following me." "You let this happen." "Don't talk to them." "Eliza told me they're dead." "Is it true?" "No." "She said they found their bloody clothes -- don't you tell your mother that." "Don't you dare tell your mother that." "You understand me?" "Now, I need you to listen to me." "I need you to stay around the house for a couple of days, and you make sure she does not watch the news, and when the paper comes, you just throw it the fuck away -- listen to me!" "We do not give up on your sister!" "We do not!" "I'm gonna find her." "I'm gonna bring her home." "We do not give up." "You're gonna bring her home?" "She's dead." "You can't do anything." "You've been leavin' me and mom here while you -- you've been goin' out and getting fuckin' drunk!" "You think I can't smell it on you?" "!" "Shut..." "Up!" "How long has this Bob Taylor been workin' on this map?" "Three-and-a-half hours." "And you think this is gonna lead you to the bodies?" "'Cause I sure as shit don't." "Do me a favor, captain." "Go fuck yourself." "We weren't getting anywhere questioning him." "That looks more like a maze than a map." "He's got a thing for mazes." "I'm goin' home." "Call me if somethin' happens." "Give me that card, Johnny." "The key card." "All right, it's done now." "Tell me what you're drawing." "You said you were drawing a map." "That looks like a fucking puzzle." "You tell me what you're drawing." "Tell me what you're drawing." "I can't!" "Yes, you can!" "Yes, you can!" "Oh, shit!" "Shit!" "Yes, you can!" "Yes, you can!" "Take him!" "Come on!" "Yes, you can!" "Yes, he can!" "Oh, shit!" "Gun!" "Gun!" "Gun!" "Bob, don't!" "Put the gun down!" "Bob." "Bob." "Put the gun down!" "Bob, Bob, Bob, Bob, Bob, no!" "No, no, no!" "No, no, no!" "Fuck." "Go call a fuckin' r.A.!" "Our father who art in heaven, hallowed be thy name." "Thy kingdom come, thy will be done, on earth as it is in heaven." "Give us this day our daily bread, and forgive us our trespasses..." "As we " "As we for" "He explain this before he ate the bullet?" "I'm sorry." "Fuck you're sorry." "Save it for the girls' parents." "I don't know what to do, Alex." "I don't know what to do anymore." "And what's completely fucked up about all this is I know you know where they are." "I think we're done." "They're in the maze." "That's where you'll find them." "What?" "What did you say?" "In the maze." "What -- what -- maze?" "Where is it?" "Where is the maze?" "Where do I find it?" "Alex?" "Alex, Alex, listen to me." "I'm gonna get you out of here, okay?" "Just tell me where the maze is." "That's it." "Just tell me, man." "Where is the maze?" "Come on, tell me." "Just tell me where the maze is, okay?" "Come on, don't fuck with me." "Don't fuck with me now." "Tell me, God damn it!" "Tell me where they are!" "Tell me!" "Tell me!" "Tell me!" "Something's gonna get to you, man." "Something's gonna get to you!" "Something's gonna get to you!" "Just a minute!" "Can I help you?" "Morning, ma'am." "Um..." "I'm Keller Dover." "Uh, my little girl was abducted with a friend." "What do you want?" "Uh..." "I-I guess I haven't thought this through too good, huh?" "I..." "I've been thinkin' a lot about what happened to your nephew." "And I know I scared him the other day at the police station, and -- and..." "What I'm tryin' to say is" "I kind of feel responsible for him running away." "You wanna come on in?" "Yeah." "My husband and I were..." "Very devout at one time." "Spent our summers driving around in that camper with our son..." "Handin' out pamphlets..." "Spreadin' the good word." "After our son died of cancer..." "We started seein' things differently." "Adopting Alex helped..." "But we never got over it." "I'm sorry." "You look very tired." "Yeah, I don't sleep much." "I, uh..." "I keep dreaming about being lost in a maze." "I'm sorry." "Alex never talks very much, so..." "When people come over here, I hardly know what to say." "He doesn't talk much?" "Well, he talks, you know." ""Good morning," "good night" -- that sort of thing." "Hard to get too much more than that out of him." "He had an accident when he was little." "After that, he started choosing his words a little too carefully." "What, uh, what kind of accident did he..." "Oh." "My husband kept snakes." "It wasn't that bad what happened, but Alex had a fear of them and..." "That's not my favorite memory." "I'm sorry." "It's none -- none of my business." "Oh, it's..." "Can I get you a cup of tea, Mr. Dover?" "Oh." "Oh, I'm so sorry." "I thought you had known about that already." "I say it's better this way." "You know, that awful man, he would have spent years on death row just watchin' TV and gettin' fat." "Well, least I don't have to worry about losing you to psp." "When forensics is finished with the guy's place, we're gonna deploy the cadaver dogs." "Look, kid, we can't always save the day." "All right?" "We're just cops, janitors." "So you lost this one, all right?" "Look, you want fulfillment, you need to find a girl, you know, start a family, have some kids." "Let it go." "Right." "Yeah?" "Hey, it's rich." "We found somethin'." "Guys, let us have a look." "Two kid-sized department store mannequins, with their heads caved in." "I just talked to our lab guys, and they told me that all the blood that we sampled from the plastic containers -- pig's blood." "All right, you guys, let's get this covered up." "It's supposed to snow soon." "Hurry up, okay?" "It's like he's play-acting." "I mean, case in point." "Except for the few items I.D.'D by the dovers and the birches, all the kids' clothes that we found still had the tags on them." "And that maze book that we found, he made it." "Photocopies, pictures from this book that we found in the attic." "Ex-f.B.I. Agent wrote that." ""Finding the invisible man."" "Yeah, it's about a theoretical suspect that he believed was responsible for a bunch of child abductions." "It's totally discredited, I guess, but I read some of it." "Taylor " " Taylor was abducted when he was a kid." "He ran away after three weeks." "And the captor drugged him on some sort of lsd/ketamine cocktail." "He never remembered." "They never caught the guy." "Okay, so..." "He read the book and decided he was taken by the invisible man." "Now he's doing his best imitation, right?" "Yeah, he was doing his best imitation." "He killed himself last night." "How did he do that?" "I thought he was in custody." "Hey." "Taylor drew this." "It's a map to the bodies." "It's a map to the bodies." "And we found the same design on a pendant that we pulled off that corpse the other day." "There's a connection." "Okay?" "The connection is that it's the last maze in the book." "I did it." "It's unsolvable." "There's no way out." "Your corpse is another wannabe who read the book." "What are you saying to me, rich?" "What are you saying to me?" "What are you saying?" "That -- that -- that this guy is a fake?" "You're saying that the girls -- the girls are still out there somewhere?" "How did Bob Taylor get those clothes?" "How did -- how did -- how did the parents..." "Positively I.D. Those clothes?" "!" "That I can't reconcile." "You can't reconcile that?" "Just keep knockin' on doors, look in the windows." "Hey, why is that there?" "Bag that." "Will do, sir." "Right away." "Yes?" "Um, yeah." "This is she." "What?" "Oh, my God!" "Uh, wait." "Is she...?" "Ralph!" "Keller!" "Keller!" "We need to go to the hospital!" "They found joy, but not Anna!" "What?" "They didn't find Anna!" "Maybe she'll know where Anna is!" "Please, we have to go!" "Keller!" "Eliza's not picking up." "You should text her." "Yeah." "Nobody gets beyond this point." "Don't touch me." "Miss!" "Wait a minute -- it's okay." "Nancy." "Grace." "They'll find Anna." "I know they will." "I know they will." "I know." "How is she?" "Is she awake?" "Joy, were you far from our street?" "How far from the street were you, joy?" "Joy?" "You can't be doing this now." "How long did it take you to get there?" "Just let me ask a question!" "Please." "Keller!" "The detective will be back in just a minute." "You need to wait." "She's been drugged." "Joy." "Sweetheart..." "Just let us know she's alive, okay?" "Can you just nod your head, baby?" "Just nod your head?" "Baby?" "Can you give us a nod?" "Can you nod your head for us, please?" "Joy?" "Joy?" "You were there." "What?" "I was " " I was where?" "It put tape on our mouths." "Shhh." "It's okay." "It's okay, baby." "It's okay." "It's okay." "Mommy and daddy are here now, okay?" "You're all right." "Excuse me." "You're all right now." "I said nobody's allowed in that room but her family." "Hey!" "Where you goin'?" "Keller?" "Hey!" "Where's he goin'?" "I don't know." "Hey!" "Call downstairs." "Don't let him go." "Hey!" "Hey!" "Block off the exits." "Hey!" "Stop that car!" "Get his truck!" "Stop it!" "Hey!" "Hey!" "I've got you, you fucker." "I know where you're goin'." "I know where you're goin'." "Hello again." "Hey." "I was hoping you'd, uh, you'd let me do some penance." "For what?" "For scaring you the other day at the, uh, the police station." "You already apologized for that." "I know." "I was -- you know, I thought maybe you, uh..." "You could use some, uh, help around the -- you know, I noticed your door here needs fixing, so I brought my tools and, uh..." "Oh." "I see." "I burned myself." "Feel a little icky today." "But I'm glad you want to talk some more." "No need to make excuses." "You come on in and make me a cup of tea." "Come on in." "I don't want to have to hurt you." "I know they were here." "Put your hands on your head and turn around." "Do it." "I'm just gonna go." "Don't touch that bag." "Put your hands on your head." "Come over here to this counter." "Come on!" "Top drawer." "Open it." "Mm-hmm." "Put them on." "You don't know me, Mr. Dover." "But believe me when I tell you, I won't let you go." "You don't have to drink all of it." "About a third should do for a man your size." "Something to make you more manageable." "Forget it." "Drink it, Mr. Dover, or I'll kill you right here in my kitchen and bring your daughter in here and have her scrub your brains off the floor -- where is she?" "Drink." "Just let me see her." "You want to see her?" "Yes!" "That's your ticket to your daughter right there." "A little more, Mr. Dover." "Little more." "Good, isn't it?" "That's my darlin' husband's recipe." "Now go on out back." "Let me see her." "Take it out of your pocket." "Put it in the sink." "Put it in the disposal." "Put your car keys on the table." "Put your car keys on the table." "That's right." "Over to the trans am over there." "The car over there." "Come on, move it." "Get over there." "The look on your face." "My husband used to have the very same look..." "Till we took Alex." "He was the first kid we ever took." "His name was Jimmy." "Or Barry." "Can't remember." "Doubt he can, either." "So many names." "Forgot all about Bobby Taylor till I read about him in the paper." "Get in the driver's seat." "Open the door and get in the car." "Making children disappear is the war we wage with God." "Makes people lose their faith." "Turns them into demons like you." "Had to slow down since my husband disappeared." "But I do what I can." "Start the car." "Start the car." "Keep tryin'." "Back up." "Slowly." "Come on." "Back up." "Come on." "Stop." "Turn it off." "Turn it off!" "Get out." "Think you should know." "Alex never laid a hand on those girls." "Just wanted to take 'em for a ride in the camper." "I was the one who decided they should stay." "Take a look." "Maybe your daughter's under there." "You never know." "Anna." "Anna!" "Anna?" "Anna." "Anna!" "Anna!" "Anna?" "!" "I had the girls down there when the police came poking' around." "Should have left 'em down there." "I was so lonely without Alex." "Now get in there." "What?" "Get in." "You want me to get in there, you're gonna have to shoot me." "I'm not gonna get in there just 'cause you asked." "God!" "Oh!" "God!" "Go on." "Get in there." "That's right." "Ah!" "Make yourself a tourniquet." "Just might last 24 hours." "I'd love for you to still be alive when I dump your daughter's body down there." "Wait!" "No, wait, wait, wait!" "Wait!" "No." "No." "Hey." "I need you to go over to holly Jones'." "She needs to be notified." "No." "I need to find Dover." "Come on." "You're done with Dover, okay?" "Please?" "You want me to go to holly Jones'?" "I want you to go to holly Jones' and notify her, please." "Oh, God." "Almighty God..." "Protect my girl." "Mrs. Jones?" "Mrs. Jones?" "Show me your hands right now." "Don't move and show me your fuckin' hands right now." "Stop!" "Right now!" "Show me your fuckin' hands." "Do not move and show me your hands." "Make sure they cremate me." "I sure as hell don't want to be buried in some box." "Both hands!" "Right now!" "Right now!" "Fuck!" "Anna." "Oh, my God." "Oh, God." "Anna." "Oh, shit." "Come on." "Come on." "Anna." "Anna." "Come on." "Stay with me, Anna." "Anna, stay with me, huh?" "Stay with me, Anna!" "Stay with me, Anna!" "It's all right!" "It's all right!" "Come on!" "Go, move, move, move, move!" "Don't die, don't die." "It's okay, it's okay." "Honey." "You're okay." "Hey." "Hey." "Hey!" "Help!" "Help!" "Help!" "Help!" "Help!" "Uh, detective loki?" "I hope we're not intruding." "No." "She's doing real good." "She's gonna be up and around in a few days, aren't you, buddy?" "She just wanted to come and say thank you and hi to her hero." "Hello." "Uh, would you mind giving me a minute?" "Yeah." "Thank you." "Say goodbye, joy." "Bye." "I'll be out in a minute." "All right?" "Say goodbye, Anna." "She found her whistle?" "Uh, no." "She keeps insisting that joy helped her find it on Thanksgiving before they were taken." "But I think she's just confused." "I got her a new one." "He hasn't contacted me." "I know you don't..." "I know you probably don't believe that, but he hasn't." "I-I believe you." "Do you think you're gonna find him?" "Yeah." "And he'll go to jail." "Probably." "Anyway..." "Thank you for everything." "Oh, God." "I miss him." "He..." "He did what he had to do to find Anna, and I thank God for that." "He's a good man." "Bye." "That's it." "Let's pack it up." "You all done for the night?" "Yeah, the ground's frozen solid." "It's gonna take weeks to excavate the entire property." "Just found some dead snakes and shit." "Pray for the best, prepare for the worst, yeah?" "Night." "Night." "Shut her down."
A new study appears to shed more light on the harmful effects of smoking while pregnant using 4D ultrasound scans to detect the tiny movements made by foetus in the womb. By monitoring the growing babies, scientists believe that they can flag potential problems by examining the minute movements foetuses make in the womb. It is hoped that the research can be used to encourage more mothers to give up the habit while pregnant. The top set of images show the baby in a womb of a smoking mother, compared to one whose mother was not a smoker (PA) Dr Nadja Reissland studied the moving 4D ultrasound scans of 20 expectant mothers, four of whom were smokers, recording thousands of tiny movements as the foetuses developed at 24, 28, 32 and 36 weeks. Her study, conducted at the James Cook University Hospital in Middlesbrough, found that the unborn babies of the four smoking mothers touched their faces more frequently. Foetuses usually move their mouths and touch themselves as they develop and gain control over their limbs. Dr Reissland’s results – which she hopes to replicate across a far larger sample size – indicates that mothers who smoke may delay the development of their babies’ central nervous systems. “A larger study is needed to confirm these results and to investigate specific effects, including the interaction of maternal stress and smoking,” Dr Reissland said. Although the number of women smoking during pregnancy has fallen to an all-time low, according to figures gathered last year, 12 per cent of expectant mothers continue smoking. However, figures vary across the country. In 2013-2014, 28 per cent of pregnant women who attended the NHS Blackpool smoked, while in central London only two per cent of expectant mothers smoked. Research has found that pregnant mothers who smoke risk damaging their unborn children’s hearts and can also increase the risk of miscarriage and premature births. The scans show differences in movement ebtween foetuses of smoking and non-smoking mothers (PA) The pilot study, conducted by Durham and Lancaster Universities, was published in the medical journal Acta Paediatrica. Dr Reissland, who specialises in foetal development, called for women to be offered more help in giving up, rather than demonising those mothers who smoke. "I'm really grateful, they did a good thing," she said. "These are special people and they overcame the stigma to help others."
1949–50 Western Football League The 1949–50 season was the 48th in the history of the Western Football League. This was the first and only season in the history of the Western League in which it consisted of three divisions. Division Three was created largely from reserve sides of existing members, but was abandoned at the end of the season. The champions for the first time in their history were Wells City, and the winners of Division Two were new club Barnstaple Town. Bideford Town won Division Three, only dropping one point. Final tables Division One Division One remained at eighteen members with two clubs promoted to replace Clevedon and Bristol City Colts, who were relegated to Division Two. Weymouth had moved up to the Southern League and were replaced in Division One by their Reserves. Cheltenham Town Reserves, runners-up in Division Two Chippenham United, champions of Division Two Division Two Division Two remained at eighteen clubs, after Cheltenham Town Reserves and Chippenham United were promoted to Division One, and RAF Melksham left the league. Three new clubs joined: Bridgwater Town Bristol City Colts, relegated from Division One. Clevedon, relegated from Division One. Swindon Town replaced their Reserves with their Colts. Division Three Division Three consisted of eleven clubs, all of which were new to the Western League except Bristol Rovers "A", this side rejoining the league having left in 1939. Seven of the other ten clubs were Reserve sides of clubs in Divisions One and Two. References 1949-50 4
Q: Why do we need torque separately from force? I'm studying physics for a couple of month now and and I am currently finding it a bit unsatisfying how the basic physical concepts are presented, meaning often times we only get a formula ($\tau=r \times F$, for example) without much discussion or any derivation. So I was trying to build up a bit of background knowledge and intuition from the Feynman lectures. From what I understand he derived torque (firstly without vectors) simply by inserting angular coordinates into the displacement in the work formula and rearranged it: \begin{equation} \Delta W=F_x\,\Delta x+F_y\,\Delta y. \end{equation} angular coordinates ("angular displacement"?): \begin{equation} \Delta x=-PQ\sin\theta=-r\,\Delta\theta\cdot(y/r)=-y\,\Delta\theta. \end{equation} \begin{equation} \Delta y=+x\,\Delta\theta. \end{equation} inserted: \begin{equation} \Delta W=(xF_y-yF_x)\Delta\theta. \end{equation} He then calls the part without the angle "torque". So isn't the torque just a special kind of force, one that acts on a circular displacement? Why do we treat force and torque so seperately when torque just seems to emerge when we work with angular coordinates? Isn't this just a special case, why can't we not use just force all the time (and not separate force/momentum/... and torque/angular momentum/... so strictly)? Obviously I'm thinking about it the wrong way and have some major misunderstandings regarding the concept of torque and thus angular momentum etc. Are there any "better"/other derivations of this concept? After weeks of frustration I signed up here, maybe you have a better way of getting some intuition with torque. Thanks. A: That derivation of Feynman's is one of the best around. As you have worked out yourself, in principle you can think of everything in terms of force as long as you also know the position vector where the force acts. This is actually more information - often a great deal more - than you need to compute the dynamics and statics of a rigid body: you can slide a force vector along the straight line with its same direction and passing through its tail, and the effect of that force on a rigid body's dynamics is the same (although where the force acts is important for working out internal stresses on a body). The sum of forces acting at the centre of mass and the nett torque about the centre of mass is all the information you need to compute rigid body statics and dynamics. This is in general a great deal less information (three vectors: force, torque and position of centre of mass) than a specification of all the individual forces and their positions of action. So, if you like, this is an instance of data compression to make a description of dynamics more wieldy. Another way of thinking of the split between force and torque is that they correspond to the natural, intuitive split between the Euclidean isometries of translation and rotation. Feynman's work calculation is splitting the work done by a system of forces into the resulting translational kinetic energy that results and the kinetic energy associated with rotation about the centre of mass. Ultimately you will meet the notion of Lagrangian dynamics and Noether's Theorem. Feynman from memory touches on these notions in his famous lectures in a "Symmetry In Physics" chapter. From Noether's Theorem we understand that the conservation of various quantities arises because our description of physics does not change if we impart continuous transformations on our co-ordinate systems: because most physics does not change if we shift our time co-ordinate origin, we conclude through Noether's theorem that there is a conserved quantity which we call energy. Conservation of momentum arises because our physics is invariant with respect to translations of our co-ordinate systems (one component of momentum conservation for each component of co-ordinate translation) and conservation of angular momentum arises because our physics is invariant with respect to co-ordinate translations. So again we see a split of conserved quantities between those to do with translation (momentum) and those to do with rotation (angular momentum). The split thus arises very neatly and naturally from the notions of Eucledean isometries.
Jiang Zhuyun Jiang Zhuyun (; 20 August 1920 – 14 November 1949) was a Chinese communist resistance fighter and revolutionary martyr. She is the basis of the character of Jiang Xueqin, or "Sister Jiang" () in the semi-fictional novel Red Crag. Life She was born Jiang Zhujun () in Jiangjiawan, Dashanpu, Zigong, Sichuan province. She moved after a drought struck their area and her mother asked for help from her brother who lived in Chongqing. When her grandmother died they were able to move out of her uncle's house. He was well off, whilst her family had difficulty living on her father's wage and her mother's job. Her father sent money home as he was a sailor, Jiang attended a church school and in 1939 started to attend university. She joined the communist party. She was assigned an undercover role where she was required to appear as the wife of Peng Pongwu. He already had a wife called Tan Zhenglun and because of this they were unsuccessfully in keeping their relationship professional. In 1944 the Communist party arranged for her to attend Sichuan University. There she worked secretly and she not only studied Russian but she read Russian media and books. She was allowed to marry Peng Pongwu in 1945. The following year their son was born. Peng was leading a group of guerrillas when he was killed in 1948 and she took on his role. She left her son with Peng's first wife and led the group. Another revolutionary was captured and gave her name to her captors. She was arrested in Wanxian and then imprisoned in Zhazidong Concentration Camp. She was tortured but she kept all her knowledge secret. She did manage to send out a letter, which is now at the Three Gorges Museum in Chongqing. A quote from it says "Tortures are too small tasks for the Communists. Bamboo sticks are made of bamboo, but the will of the Communists is made of iron and steel". The letter is said to have inspired many to make generous donations to the Communist Party of China. Literary and artistic representations 'Sister Jiang', a key character in the popular novel Red Crag (1961), is based on Jiang Zhuyun. The character also features in many adaptations of the novel, including: Sister Jiang (1964), a Chinese-language western-style opera Life in Eternal Flame (1965), a film directed by Shui Hua Sister Jiang (2010), a CCTV-1 television series References Category:1920 births Category:1949 deaths Category:People from Zigong Category:People executed by the Republic of China Category:Chinese communists
Building employee resilience through wellbeing in organisations Building employee resilience through wellbeing in organisations Karen Tonkins University of Canterbury, Masters Thesis, 2015 Abstract An untested assumption is that ‘a resilient organisation comprises of resilient employees’. Under the guidance of the Employee Resilience Research Group, this research used quantitative surveys to investigate how resilience at an individual, employee and organisational level interact. Secondly, to investigate the role that the workplace plays in the resilience and wellbeing of its employees, participants took part in the Mental Health Foundation’s ‘Wellbeing Game’, a free online game in which players engage in some or all of the ‘Five Ways to Wellbeing’ (Give, Connect, Take Notice, Keep Learning, Be Active). These five actions have been scientifically shown to improve mental wellbeing. The results showed that individual, employee and organisational resilience are indeed related. Not only that, our participants reported feeling more resilient at work than outside of the workplace. Following playing the Game, levels of Employee Resilience (not individual or organisational resilience) increased. As expected, participants also reported positive increases in mental wellbeing. These results indicate that resilience is contextual, employee resilience can be developed, and a resilient organisation is indeed comprised of resilient employees.
Paul Ryan Filibusters His Own Town Hall Meeting April 28, 2011 Fears that GOP Representative Paul Ryan is planning to end Medicare as Americans know it are now spreading outside the beltway. Joining Ed Schultz on MSNBC’s The Ed Show, The Nation‘s John Nichols said that citizens at town hall meetings in Wisconsin are starting to fight back against the severe cuts that are central to Ryan’s budget plan. In Kenosha, those in attendance challenged Ryan on most of what he was arguing, citing government agency reports and other materials that show that Ryan’s plan is built on falsehoods. Nichols reports that "Ryan was kept on his toes," and Kenosha citizens were as charged as he’s ever seen them because they really are afraid of Ryan’s plan and what it might do to Medicare.
Direct observation of the formation of surfactant micelles under nonisothermal conditions by synchrotron SAXS. Self-assembly of amphiphilic molecules into micelles occurs on very short times scales of typically some milliseconds, and the structural evolution is therefore very challenging to observe experimentally. While rate constants of surfactant micelle kinetics have been accessed by spectroscopic techniques for decades, so far no experiments providing detailed information on the structural evolution of surfactant micelles during their formation process have been reported. In this work we show that by applying synchrotron small-angle X-ray scattering (SAXS) in combination with the stopped-flow mixing technique, the entire micelle formation process from single surfactants to equilibrium micelles can be followed in situ. Using a sugar-based surfactant system of dodecyl maltoside (DDM) in dimethylformamide (DMF), micelle formation can be induced simply by adding water, and this can be followed in situ by SAXS. Mixing of water and DMF is an exothermic process where the micelle formation process occurs under nonisothermal conditions with a temperature gradient relaxing from about 40 to 20 °C. A kinetic nucleation and growth mechanism model describing micelle formation by insertion/expulsion of single molecules under nonisothermal conditions was developed and shown to describe the data very well.
Civil Rights Groups Split Over NCLB Accountability Provisions Stirring Heated Debate Leading national civil rights groups and advocates are increasingly divided over whether the No Child Left Behind Act will improve the academic achievement of poor and minority students, a rift that is generating conversation and concern among a circle of people accustomed to working together. The differences of opinion range from qualified support to harsh criticism, leaving some longtime civil rights activists on opposing sides for the first time. “Unity is always best,” said John H. Jackson, the national director of education for the NAACP, which has joined forces with those seeking major changes to the nearly 4-year-old federal law. “But a little of what everyone is saying is correct. Each side is presenting a voice that needs to be heard.” The divisions are deep enough that last year, two civil rights groups joined forces with a prominent business organization to form the Achievement Alliance, a coalition that counters attacks on the law. Few civil rights advocates disagree with the law’s overarching goal: bringing all U.S. students’ state test scores in reading and mathematics to the proficient level by 2013-14. Because that goal requires closing gaps between African-American and Hispanic students and their white peers, most support the law’s mandate to break down performance data for racial, ethnic, economic, and other subgroups to hold schools and districts accountable for their progress. But the law’s sanctions for failing to make adequate yearly progress toward its goals have some in the civil rights community claiming it penalizes and stigmatizes struggling districts and schools without giving them the resources needed to improve. Others believe the law is the best tool available to pressure schools and districts to ensure that all students receive a high-quality education. The NCLB law, the centerpiece of President Bush’s agenda for schools, passed Congress in 2001 with large bipartisan majorities. The debate came into sharp focus this summer, when the Civil Rights Project at Harvard University released a report examining district-level accountability under the federal law in six states. It concluded that districts facing sanctions, such as student transfers, serve large numbers of poor and minority students. The report, which characterized the law as having a “racially disproportionate impact,” also contended that federally approved changes to some states’ accountability standards are letting predominantly white suburban districts off the hook. Accountability at Issue Gary Orfield, the director of the Civil Rights Project, said some civil rights leaders who were “very involved” in writing the law believe in demanding a level of academic achievement from schools and districts and setting deadlines to get the job done. But that approach is not founded in any research or understanding of effective ways of improving education, he argued. Assessing the No Child Left Behind Act Raul Gonzalez Legislative Director, National Council of La Raza "For the most part, civil rights groups all have the same goal in mind. Given the breadth of NCLB, it shouldn't be a surprise that there are some differences of opinion." Gary Orfield Director, Civil Rights Project, Harvard University Civil rights leaders are "absolutely committed to racial justice. It's a matter of understanding how to get there." Reg Weaver President, National Education Association "There's a growing chorus of dissatisfaction with the implementation of NCLB that can't be swept under the rug." The “adequate yearly progress” requirements and sanctions in the law were “misconceived in serious ways by people who had the best of intentions,” Mr. Orfield said. He added that the measures have resulted in “unanticipated, deep consequences” that are undermining efforts to improve schools. “The fact that students in larger, more diverse districts are being paid attention to and given extra help is a welcome change in an education system that routinely shortchanges such students,” the statement said. “This additional support should not be characterized as punishment.” The Achievement Alliance is made up of the Citizens’ Commission on Civil Rights, a national watchdog group; the National Council of La Raza, a leading Hispanic advocacy group; the Education Trust, a research and advocacy group that promotes high achievement for poor and minority students; the Business Roundtable, an association of chief executives of major corporations; and the National Center for Educational Accountability, an Austin, Texas-based nonprofit organization that promotes the use of data to improve learning. The other groups are located in Washington. “Kids were getting punished before this,” said William L. Taylor, the chairman of the Citizens’ Commission, who helped write the education law. “Even if they’re not held back in school, they are coming out of school without having learned what’s necessary to be effective participants in society.” Mr. Taylor, a veteran desegregation lawyer and longtime activist, characterized the split within the civil rights community as harmful to achieving the law’s goals. “It’s a war on the whole idea of reform. Gary [Orfield] wasn’t opposed to sanctions when it came to dealing with segregated schools,” he said. “When public officials are not carrying out their duties, you sanction them.” Observers say that civil rights advocates have differed on the No Child Left Behind law since its inception, but that those differences have been overshadowed by the National Education Association’s April lawsuit challenging the act and by widely publicized examples of state resistance to the legislation. Monty Neill, the co-executive director of the National Center for Fair & Open Testing, or FairTest, a Cambridge, Mass.-based group critical of standardized tests, said most civil rights groups have found “serious flaws” with the law, including an over-emphasis on testing and a lack of adequate funding. Calling for Changes Mr. Neill helped write a joint statement last fall that calls for substantial changes to the law, which is due for renewal by Congress in 2007. More than 50 groups support the continuing effort, including the National Association for the Advancement of Colored People, the League of United Latin American Citizens, the Asian American Legal Defense and Educational Fund, the NEA, and the National School Boards Association. “You can’t just outline these requirements and sanction students and teachers without also providing the resources to do it,” said Mr. Jackson of the NAACP. Reg Weaver, the president of the 2.7 million-member NEA, said some critics are erroneously portraying the union as anti-No Child Left Behind to drive a wedge between it and civil rights groups. In fact, Mr. Weaver argues there are few differences in their positions, because the union supports standards, accountability, and elimination of achievement gaps. “All we’re talking about is fixing it and funding it,” he said of the law. “I think it’s a cruel hoax to have the data disaggregated and find out what you need, but in many instances not have the needs of the students met.” Civil rights advocates do share common criticisms of several provisions under the law, including concerns about the quality of testing for English-language learners and a wish to extend the law’s transfer option to allow students to move to better schools in neighboring districts, not just their home districts. Raul Gonzalez, the legislative director for the National Council of La Raza, believes that cohesiveness proves that views of the law are not that far apart. “I believe that the civil rights community, at the end of the day, will come up with some principles that we can all rally behind,” he said. 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--- abstract: 'Zigzag graphene nanoribbons have spin-polarized edges, anti-ferromagnetically coupled in the ground state with total spin zero. Customarily, these ribbons are made ferromagnetic by producing an imbalance between the two sublattices. Here we show that zigzag ribbons can be ferromagnetic due to the presence of reconstructed divacancies near one edge. This effect takes place despite the divacancies are produced by removing two atoms from opposite sublattices, being balanced before reconstruction to 5-8-5 defects. We demonstrate that there is a strong interaction between the defect-localized and edge bands which mix and split away from the Fermi level. This splitting is asymmetric, yielding a net edge spin-polarization. Therefore, the formation of reconstructed divacancies close to the edges of the nanoribbons can be a practical way to make them partially ferromagnetic.' author: - 'W. Jaskólski' - Leonor Chico - 'A. Ayuela' title: ' Divacancy-induced Ferromagnetism in Graphene Nanoribbons ' --- Introduction ============ Magnetism in zigzag graphene nanoribbons (ZGNR) is related to edge-localized states, which appear as two flat bands at the Fermi energy ($E_F$) in a simple noninteracting model. In fact, the electron interaction splits these bands, so the edges are antiferromagnetically coupled with total spin zero [@son_nature; @son_prl2006]. This magnetic behavior is rather general, because similar localized bands are also present in any non-armchair graphene ribbon [@fujita; @nakada; @our_prb2011]. When the edges of the nanoribbon are identical, all the bands remain spin-degenerate. For dissimilar edges with sublattice balance, the spin splitting may be different for each edge [@our_ssc_2014], but the ribbons have total spin zero. In order to exploit spin effects in ZGNRs for applications, spin degeneracy should be lifted, so uncompensated spin channels are obtained. Such splitting can be achieved under a strong external electric field [@son_nature; @mananes] or by chemical attack [@hod]. In general, one way to attain ferromagnetic graphene nanostructures is to impose sublattice imbalance. According to Lieb’s theorem, a bipartite lattice has a total spin moment proportional to the difference of the number of atoms belonging to the two sublattices [@lieb]. For instance, ZGNRs with one decorated edge of Klein-type atoms [@klein; @book_CBM], triangular graphene nanoislands [@jfr_palacios_prl2007], and graphene systems with vacancies that remove a different number of nodes from each sublattice [@palacios_jfr_prb2008; @palacios_jfr_bry_fertig_sst2010; @cnr; @lps] have a non-zero spin due to the imbalance. In this work we show another way of producing a net magnetic moment in zigzag graphene nanoribbons by including reconstructed divacancies. We consider divacancies produced by the removal of two neighbor carbon atoms, so that the two sublattices are balanced. They rebuild into the so-called 5-8-5 defects, composed of an octagon and a pair of pentagons which mix the two sublattices. Divacancies may naturally appear as stable defects during growth or can be created on purpose by electron or ion irradiation [@hashimoto_nature2004; @kotakoski_prl2011; @kim_prb2011; @robertson_nc2012; @ugeda_prl2012; @ugeda2]. They are the source of defect-localized states with energies close to $E_F$, as it was recently shown for the case of semiconducting armchair ribbons [@our_app2013]. Since divacancies do not introduce sublattice imbalance, they have not been regarded to this date as possible sources of magnetization in graphene. However, we show here that when these defects are present in zigzag nanoribbons, they give rise to localized states which may interact with those originated from the zigzag edges, so they can lead to spin effects and ribbon magnetization. Two previous calculations for 5-8-5 defects in ZGNRs presented results in apparent contradiction, showing either zero spin polarization [@topsakal_prb2008], or spin-polarized transport in ribbons with narrow widths [@oeiras_prb2009]. The issue of whether these defective nanoribbons are ferromagnetic or not was not addressed in those works. In principle, one could interpret that spin polarization arose in narrow ribbons because of size effects. In order to clarify this point, in this work we perform a systematic study of the magnetic behavior of ZGNRs with reconstructed divacancies. We have found that, although these divacancies arise from lattice-balanced defects, can nevertheless produce a net magnetic moment in zigzag nanoribbons. This happens when they are located close to the zigzag ribbon edge. We attribute the appearance of a nonzero spin to the strong interaction between edge and divacancy states. ![\[fig:fig1\] (Color online) (a) Divacancies in ZGNRs. The position of the defect in the ribbon is given by the integer $N$. (b) Schematic drawing of the periodically placed defects along the ribbon forming a superlattice. The translation period $T$ spans the length of the unit cell. ](fig1_nt.pdf){width="5.5cm"} We have examined systematically how the magnetic properties of ZGNR depend on the position of 5-8-5 defects. We show that when defects are centrally located in wide ZGNRs, the ribbons have zero net magnetic moment. However, when they are placed close to one of the zigzag edges, the defect-localized and the nearby edge bands interact, so they mix and split in energy. The zero energy band corresponding to the other edge situated farther from the defect remains unmixed. The inclusion of electron-electron interaction results in the spin splitting of all these bands. The aforementioned unmixed band is symmetrically split around $E_F$, while the hybridized defect-edge bands are asymmetrically split, yielding a non-zero net magnetization. We propose that the production of reconstructed divacancies by techniques such as ion bombardment may produce magnetic ribbons. As the one of the most abundant defects in ZGNRs are divacancies [@wang], which are preferentially found at the edges [@oeiras_prb2009], this defect engineering could be a feasible way to produce spin-polarized ZGNRs. Model and systems studied ========================= We study reconstructed divacancies in wide zigzag graphene nanoribbons. The ribbon width $W$ is defined [@nakada_fujita] as the number of carbon dimers across the ZGNR. The divacancies are located at different positions $N$, measured in units of two carbon dimers from the edge of the ribbon, as shown in Fig. \[fig:fig1\] (a). The 5-8-5 defects are periodically situated in an infinite ZGNR, as schematically depicted in Fig. \[fig:fig1\] (b). The translation period $T$ of the ribbon is defined as the number of zigzag edge nodes in the unit cell. The electronic properties are calculated with a one $\pi$-orbital tight-binding (TB) model. The electron-electron interaction is considered within a Hubbard model solved in the mean-field approximation. We choose this approach in order to calculate large unit cells, which are not feasible with first-principles methods. We assume all hoppings $t$ to be equal throughout the ribbon. We previously tested this approach for the study of the magnetic properties in graphene with topological defects using the hopping parameter $t=-2.7$ eV and the Coulomb interaction term $U=3$ eV [@our_prb2013; @our_ssc_2014]. Results ======= We first consider centrally located 5-8-5 defects, periodically placed along a wide ribbon with $W=19$ and $T=3$. It is the smallest periodicity of a ZGNR with horizontally placed defects separated by at least one hexagon. Note that for $T=2$ the consecutive octagon-pentagon pair defects form a defect line, which was studied elsewhere [@our_prb2013; @Song2012; @Jiang2012; @Kan2012; @Hu2012]. The energy spectra calculated within the TB approximation and the Hubbard model are presented in Figs. \[fig:fig2\](a) and (b), respectively. The spectra are not symmetric with respect to $E=0$ because of the electron-hole symmetry breaking induced by the pentagons. The insets show the band structure of a ZGNR with $T=3$, i.e., the three times folded spectrum of the pure (1,0) ZGNR with the Dirac point at $k=0$. It has a pair of zero-energy bands extending in the entire zone in the TB approximation (Fig. \[fig:fig2\] (a)), which are split when the electron-electron interaction is included (Fig. \[fig:fig2\] (b)) [@son_prl2006]. The 5-8-5 defects introduce divacancy-localized states, which in the TB approximation form a flat band exactly at $E=0$, as shown in Fig. \[fig:fig2\] (a) [@our_app2013]. When the Coulomb interaction is considered, as in Fig. \[fig:fig2\] (b), the two edge localized bands are spin-split in the same way as in the pristine ZGNR. The unoccupied defect-localized band remains spin-degenerate. As the defect is symmetric about the center of the ribbon, the ground state remains anti-ferromagnetic. ![\[fig:fig2\] (Color online) Bands of a ZGNR with $W=19$ and $T=3$ with 5-8-5 defects located at the center of the ribbon, calculated in (a) the TB approximation and (b) the Hubbard model. For comparison, the corresponding spectra of pure ZGNR folded three times ($T=3$) are included as insets. The Fermi level lies at $E=0$. Notice that in (b) the zero energy edge bands are spin-split, but they remain spin degenerate with no spin polarization; the defect band is spin-degenerate. ](fig2_nt.pdf){width="8.5cm"} More interesting is when we move the 5-8-5 defect close ($N=1$) to one of the edges of the ribbon, e.g., the upper one. The energy spectra calculated in the TB and Hubbard models are shown in Figs. \[fig:fig3\] (a) and (b), respectively. In the TB approximation the flat band at $E=0$ is localized at the lower edge, and it remains unaffected by divacancies. However, the states localized at the upper edge strongly interact with the defect-localized states; they hybridize and split. The bonding combination of these states is the band below $E=0$, while the anti-bonding combination is unoccupied. All the bands are spin-degenerate. The inclusion of electron-electron interaction lifts the spin degeneracy and significantly modifies the spectrum, as it can be seen in Fig. \[fig:fig3\] (b). The bands localized at the lower edge are marked in Fig. \[fig:fig3\] (b) by arrows. The spin-down polarized states are almost fully occupied. The bonding and anti-bonding combinations between the upper-edge and defect-localized bands also spin-split. However, their splitting is weaker because of the defect-edge mixing. The spin-split pairs are marked with ellipses. In the TB approximation the bonding combination is situated closer to $E_F$ than its anti-bonding counterpart. Now, when the Hubbard term is included, spin-up and spin-down bands cross the Fermi level at different $k$-values. This produces a non-zero final spin polarization, about $ 0.2$ $\mu_B$. Note that this result does not contradict Lieb’s theorem: although the lattice was balanced before reconstruction, the mixing of sublattices produced by the topological defects makes the theorem inapplicable to this case. Significantly, ZGNRs on one hand and 5-8-5 defects on the other hand have a total spin zero. However, when the defect is placed close to one of the edges, a net spin appears due to the asymmetrical band splitting produced by the defect-edge interaction. ![\[fig:fig3\] (Color online) Bands of a ZGNR with $W=19$ and 5-8-5 defects placed close to the upper edge ($N=1$) and separated by the translation vector $T=3$, calculated in the TB (a) and Hubbard (b) models. Spin-down bands are denoted by dotted lines, spin-up by solid lines. Arrows mark the up and down spin bands localized at the lower edge. Ellipses mark the spin-split bands of the bonding and anti-bonding combinations between the upper edge and the defect-localized states. ](fig3_nt.pdf){width="9cm"} Figure \[fig:fig4\] (a) shows how the spin polarization depends on the position of the defect with respect to the edge of the ribbon. We consider a ribbon with $T=6$ and $W=39$, which is wide enough to have the defect in several sites between the center of the ribbon and its edge. When the defect is situated close to the edge, i.e. $N=1$, the spin polarization is $ 1.3$ $\mu_B$. Moving the defect towards the center makes the polarization decrease rapidly to zero. This may explain why no magnetization was reported in the study presented in Ref. for ZGNR with slightly off-center divacancies. Another work [@oeiras_prb2009] gives an example of a very narrow ribbon, not large enough to distinguish the magnetic polarization effect induced by such defects from that caused by the edges themselves. We have systematically studied how the spin polarization depends on the translation period $T$ for the ribbon of width $W=39$, as shown in Fig. \[fig:fig4\] (b). When $T$ increases, the ribbon polarization also increases (albeit non monotonically), and saturates for large $T$ at $2$ $\mu_B$. ![\[fig:fig4\] Dependence of spin polarization on (a) the position $N$ of defects with respect to the edge of the ribbon, and (b) the translation period $T$, for a wide ribbon of $W=39$. ](fig4_nt.pdf){width="8.5cm"} In order to understand the values of spin polarization presented above, we have also studied in more detail the energy spectra of ZGNR with larger $T$. When the defects are situated at the center of the ribbon, no spin polarization is observed for any $T$. In order to compare the results with those with $T=3$ presented above, in which the Dirac point is at $k=0$, we choose $T$ to be a multiple of three. The smallest translation period for which the polarization converges to $2$ $\mu_B$ is $T=9$. The TB energy spectrum of a pure ZGNR (9,0) has 6 flat bands at $E=0$ [@our_prb2011]. Three of them are localized at the lower edge, and another trio is at the upper edge. ![image](fig5_nt.pdf){width="14cm"} When the 5-8-5 defects are close to the upper edge, defect and upper-edge bands interact, so they mix and split. Fig. \[fig:fig5\] shows the TB energy bands for the $W=19$ and $T=9$ ZGNRs with a 5-8-5 defect close to the edge. There are four flat bands near to the Fermi level. Three bands are localized at the lower edge (LE) and one at the upper edge (UE). These states are mostly localized at the edge nodes and have a negligible overlap with the defect atoms. The two remaining upper edge bands hybridize with the defect band, yielding three bands (UE+D) of mixed upper edge-defect character, with only one occupied and all away from $E_F$. A diagram showing how these bands spin-split when the Coulomb interaction is taken into account is presented in Fig. \[fig:fig5\] (b). The LE bands (blue) are strongly split so they are fully spin-polarized; we take the occupied spin as the down projection. The unperturbed $E=0$ UE band (green) is split with a spin opposite to the LE bands, as expected. The UE+D bands are spin-split more weakly because of the sublattice mixing at the defect. Consequently, we have four spin-down and two spin-up occupied states, summing up to $2$ $\mu_B$. Calculations employing the Hubbard model confirm this picture, as displayed by the energy bands in Fig. \[fig:fig5\] (c). We have checked that our results are robust, i.e., independent on the Coulomb term for a wide range of $U$ values. ![\[fig:fig6\] (Color online) (a) Schematic energy diagram showing how the defect-localized state mixes with two upper-edge localized states. The TB levels are shown in black; filled and half-filled dots indicate that the state is fully or half-occupied, respectively. Electron interaction splits these levels; colors indicate their localization as in Fig. 5 (b). Occupied states are represented with an arrow indicating the spin direction. (b) Diagram illustrating the final distribution of occupied spin states due to divacancy placed close to the edge.](fig6_nt.pdf){width="8.5cm"} The energy and spatial schemes presented in Fig. \[fig:fig6\] describe these edge-defect interactions in detail. The edge bands of the pure ZGNR (1,0), which extend from $k=2\pi/3$ to $k=\pi$, contribute in average with one electron for every three edge nodes. For $T=9$ this band folds into three edge bands. For the divacancy close to the upper edge, the defect band hybridizes with two edge bands, giving three bands away from $E_F$, as shown in Fig. \[fig:fig6\] (a). The defect does not mix with the remaining upper edge band (green), because it stems from the states close to $k=\pi$ of the unfolded edge band of the ZGNR (1,0): as it is mostly localized at the edge atoms, it has a small overlap with the defect. Likewise, the lower edge discrete states (blue) are also unaffected by the divacancy due to the spatial separation. These unchanged states are spin-split as for a pure ZGNR. However, the spin splitting of the hybridized states (red) is much weaker, with a state below $E_F$ occupied for both spin polarizations. For even larger $T$, the spins of the extra occupied upper edge states far from the defect cancel with the spins of the occupied lower edge states. Thus, an isolated straight divacancy in an infinite ZGNR has a total spin polarization equal to $ 2$ $\mu_B$. We have also checked that tilted vacancies have a similar behavior, although the total magnetic moments tend to be reduced. This divacancy-induced magnetism at the edge of zigzag ribbons is now brought into contact with experiments. We propose that ion irradiation of zigzag ribbons could be employed to create divacancies. This technique is used nowadays to produce vacancies in graphene [@ugeda_prl2012]. In fact, vacancies are mobile and cluster in the form of divacancies [@ugeda2]. Note that for nanoribbons, it is more energetically favorable for these vacancies to move close to the edge because of its lower coordination, where they can coalesce in the more stable and abundant divacancies [@wang]. Conclusions =========== In summary, we have studied the electronic and magnetic properties of ZGNRs with reconstructed divacancies, which can be viewed as the removal of two neighbor carbon atoms from different sublattices before reconstruction to 5-8-5 defects. Although 5-8-5 defects stem from lattice-balanced vacancies, they can give rise to a net spin magnetic moment. We have shown that a nonzero magnetization arises when the defect is located close to the edges of the zigzag ribbon. The 5-8-5 defects introduce localized states with energies close to $E_F$. When they are located at the center of the ribbon, the total spin polarization is zero, keeping the magnetic edge configuration of pristine ribbons. However, when the defects are placed closer to one of the edges of the ribbon, the defect band interacts with the edge-localized band, so they hybridize and split asymmetrically from $E_F$. States localized at the other edge remain strongly spin-split, leading to a net spin polarization and spontaneous magnetization of the ribbon, despite they are derived from systems with balanced sublattices before reconstruction. The total magnetic moment saturates for large periods to a value of 2 $\mu_B$. Finally, we have also clarified the apparent contradiction between previous works, namely, the absence of spin polarization shown for some defective ribbons, in contrast with the obtention of spin-polarized currents in similar systems [@oeiras_prb2009; @topsakal_prb2008]. In narrow ribbons, divacancies are naturally close to edges, so a spin-polarized current may arise. In wider ribbons, divacancies situated at the central region of the ribbon do not produce such spin polarization. Our findings indicate that it is possible to design spin-transport devices based on graphene nanoribbons by introducing divacancies close to its edges by means of electron or ion irradiation. This work was supported by the Polish National Science Center (Grant DEC-2011/03/B/ST3/00091), the Basque Government through the NANOMATERIALS project (Grant IE05-151) under the ETORTEK Program [iNanogune]{}, the Spanish Ministry of Economy and Competitiveness MINECO (Grants FIS2013-48286-C2-1-P and FIS2012-33521), and the University of the Basque Country (Grant No. IT-366-07). WJ and LC acknowledge the DIPC for its generous hospitality. Y. W. Son, M. L. Cohen, and S. G. Louie, Nature (London) [444]{}, 347 (2006). Y.-W. Son, M. L. Cohen, and S. G. Louie, Phys. Rev. Lett. [97]{}, 216803 (2006). M. Fujita, K. Wakabayashi, K. Nakada, and K. Kusakabe, J. Phys. Soc. Jpn. [65]{}, 1920 (1996). K. Nakada, M. Fujita, G. Dresselhaus, and M. S. Dresselhaus, Phys. Rev. B [54]{}, 17954 (1996). W. Jaskólski, A. Ayuela, M. Pelc, H. Santos, and L. Chico, Phys. Rev. B [83]{}, 235424 (2011). W. Jaskólski and A. Ayuela, Solid State Comm., [196]{}, 1 (2014). A. Mañanes, F. Duque, A. Ayuela, M. J. 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Study on the correlation between pore morphology of porous calcium silicate and high-capacity formaldehyde adsorption. A novel porous calcium silicate (PCS) material with unique pore structure prepared from coal fly ash (CFA) was reported. The microstructure was investigated through X-ray diffraction, Fourier transform infrared spectroscopy, scanning electron microscopy, transmission electron microscopy, nuclear magnetic resonance cryoporometry, and Brunauer-Emmett-Teller method. Model describing the nanostructure of the prepared PCS was proposed in this work. Results show that the prepared PCS has open pores, a high specific surface area, and multi-peak pore size distributions (macro-, meso-, and micropores). The unique conical pore structure and interconnected micro-, meso-, and macropores are favourable to the reduction of the diffusion resistance of gas molecules. Benefiting from such a valuable structure, PCS exhibits excellent gas adsorption properties. Used in formaldehyde (HCHO) adsorption experiment, PCS shows excellent properties, including high storage capacity and endurance. The saturated adsorption capacity of the prepared PCS is 2.056 mg/g, which is enhanced by fourfold compared with that of active carbon commercially used for formaldehyde adsorption. This work provides a new, efficient, and rational way to utilize CFA. The prepared material can be used as an efficient and cost-effective adsorbent of HCHO under ambient conditions. Furthermore, the microstructure and the correlation between pore morphology and gas adsorption properties of the prepared PCS are revealed.
<?php /* * @copyright 2014 Mautic Contributors. All rights reserved * @author Mautic * * @link http://mautic.org * * @license GNU/GPLv3 http://www.gnu.org/licenses/gpl-3.0.html / namespace Mautic\CoreBundle\Form\Type; use Symfony\Component\Form\Extension\Core\Type\TextType; use Symfony\Component\Form\FormBuilderInterface; /* * Class SlotImageCaptionType. / class SlotImageCaptionType extends SlotType { public function buildForm(FormBuilderInterface $builder, array $options) { $builder->add( 'caption', TextType::class, [ 'label' => 'mautic.core.image.caption', 'label_attr' => ['class' => 'control-label'], 'required' => false, 'attr' => [ 'class' => 'form-control', 'data-slot-param' => 'caption', ], ] ); $builder->add( 'align', ButtonGroupType::class, [ 'label' => 'mautic.core.image.position', 'label_attr' => ['class' => 'control-label'], 'required' => false, 'attr' => [ 'class' => 'form-control', 'data-slot-param' => 'align', ], 'choices' => [ 'mautic.core.left' => 0, 'mautic.core.center' => 1, 'mautic.core.right' => 2, ], ] ); $builder->add( 'text-align', ButtonGroupType::class, [ 'label' => 'mautic.core.caption.position', 'label_attr' => ['class' => 'control-label'], 'required' => false, 'attr' => [ 'class' => 'form-control', 'data-slot-param' => 'text-align', ], 'choices' => [ 'mautic.core.left' => 0, 'mautic.core.center' => 1, 'mautic.core.right' => 2, ], ] ); $builder->add( 'color', TextType::class, [ 'label' => 'mautic.core.text.color', 'label_attr' => ['class' => 'control-label'], 'required' => false, 'attr' => [ 'class' => 'form-control', 'data-slot-param' => 'color', 'data-toggle' => 'color', ], ] ); parent::buildForm($builder, $options); } /* * @return string */ public function getBlockPrefix() { return 'slot_imagecaption'; } }
l) be the third derivative of l4/24 + l2. Give i(f(w)). 22w Let w(i) = -i2 + 78i - 4. Let p(r) = 2r2. What is w(p(j))? -4j*4 + 156j*2 - 4 Let c(r) = 9r - 5. Let u(d) = -13d + 7. Let n(j) = 7c(j) + 5u(j). Let k(x) = -2x + 5x - 2x. Give n(k(b)). -2b Let p(s) = -4s. Let j(f) = 4f2 - 2f. Calculate j(p(t)). 64t2 + 8t Suppose 0 = a + a. Suppose a = -h + 6h - 10. Let f(o) = 1 - ho*2 - 1. Let n(b) = -b. Give f(n(z)). -2z2 Let j(c) be the second derivative of -c4/6 + c. Let o(f) = 2f - 4. Let d(w) be the first derivative of -w - 1. Let p(x) = 4d(x) - o(x). Calculate p(j(n)). 4n2 Let v(w) = 3. Let z(g) = -g2 - 2. Let a(t) = 2v(t) + 3z(t). Let u(b) = 6b*2. Calculate u(a(r)). 54r*4 Let u(c) = -4c*2. Let m(w) = -2w - 1. Let r(d) = 22d + 7. Let o(y) = -14m(y) - 2r(y). Determine o(u(g)). 64g*2 Let l(b) = 2b*2. Let p be -4(-3 - (-15)/6). Let n(v) be the second derivative of -3v + 0v*p - 1/2v*3 + 0. What is l(n(k))? 18k*2 Let k(f) be the second derivative of 35f*3/6 + 35f. Let q(l) = -l. Calculate k(q(v)). -35v Let p(c) = -2c. Let l(u) = -2u - 5u - 3u + 3u. Determine l(p(z)). 14z Let d(s) = 2s. Suppose 5w = -0w - 25. Let a(c) = 3c. Let r(q) = -4q. Let h = 6 + -14. Let x(u) = ha(u) + wr(u). Give x(d(j)). -8j Let g(j) = -22j2. Let o(l) be the first derivative of -l2 - 10. Calculate o(g(h)). 44h2 Let s(k) = k2. Let m(t) = 13t. Let n(z) = 144z. Let y(d) = 45m(d) - 4n(d). Give s(y(g)). 81g*2 Let j(w) = -2w*2. Let s(y) = 18y + 21. Suppose 0 = -m - 2t - 8, 0m - 5m = 3t + 5. Let f(l) = -l - 1. Let c(r) = ms(r) + 42f(r). What is j(c(b))? -72b2 Suppose 11 - 3 = 4c. Let t(j) = 3j2 - j2 - 3jc - j2. Let b(k) = 0k - k + 0k. Give b(t(l)). 2l2 Let j(o) be the second derivative of o3/6 + o. Let n(z) = z - 6. Let m be n(9). Let t(g) = -mg - 2g + 4g + 3g. What is t(j(u))? 2u Let f(y) = -7y2. Let a(i) be the second derivative of -i4/6 - 4i. Calculate f(a(m)). -28m4 Let p(z) = -2z*2. Let w = -227 - -155. Let j be w/(-30) - (-2)/(-5). Let m(h) = h + 3h - jh. What is p(m(y))? -8y*2 Let q(b) = -22b. Let f(y) = -122y. What is q(f(k))? 2684k Let z(q) = 7q. Let t(c) = -6c. Let k(u) = 5t(u) + 4z(u). Let o(w) = 4 - 3w - 4. Give o(k(b)). 6b Let r(h) = 0h - 5h + 3h. Suppose 2 = 3y - y. Let f(t) = 4t2 - y + 1. Calculate r(f(i)). -8i*2 Let z(n) be the second derivative of -5n*3/6 - 5n. Suppose -8 = -3b - 2. Let r(m) = -5m2 + mb + 6m2. Give z(r(k)). -10k2 Let o(p) be the second derivative of -p3/6 + 6p. Let i(l) = -3l. Calculate i(o(m)). 3m Let k(m) = -4m - 2m + 0m + 7. Let b(v) = -5v + 6. Let u(n) = -7b(n) + 6k(n). Let o(s) = -2s. Give o(u(i)). 2i Let d be (42/9)/(2/3). Let t(q) be the first derivative of 5 + 3q*3 - 2q*3 - d. Let h(z) = z. What is h(t(j))? 3j*2 Let u(t) = 3t - 5. Let h(i) = 3i - 5. Let c(r) = -5h(r) + 6u(r). Let a(w) = -3w + 4. Let k(m) = -5a(m) - 4c(m). Let v(l) = l*2. Calculate k(v(d)). 3d*2 Let a(x) be the first derivative of -2x3 - 56. Let v(j) be the second derivative of j4/12 - j. Calculate a(v(c)). -6c4 Let c(f) = 1. Let h(j) = -12j + 2. Suppose -3m = -4m - 5, 3d - 19 = 5m. Let s(o) = dc(o) + h(o). Let a(p) = -p. Give a(s(r)). 12r Let n(k) = -15k2 - 7. Let p(r) = 8r*2 + 4. Let o(j) = -4n(j) - 7p(j). Let g(h) = -h2. Determine g(o(u)). -16u*4 Let k(g) be the third derivative of -37g*5/60 - 23g*2. Let m(s) = 2s. Determine m(k(i)). -74i2 Let h(u) = -4u. Let v(r) = -10r2 - 2r. Give h(v(a)). 40a2 + 8a Let j(d) be the first derivative of d*3 + 8. Let o(b) = -b. What is o(j(f))? -3f*2 Let m(r) = 2r. Let g(i) = -4i - 1. Let v be g(-1). Let b be -2(0 + 3 + -4). Let d(c) = bc + 4c - vc. Calculate m(d(y)). 6y Let c(a) = -a*2. Let n(s) = -158s - 9s2 + 158s. Determine c(n(m)). -81m4 Let w(q) = q. Suppose 2y - 5f + f = -12, 2y + f = 13. Let c = 6 - 4. Let v(b) = -6b2 + yb2 + bc. Determine w(v(t)). -t*2 Let n(t) = 5t - 11t + 2t. Let o(q) = 2q2. What is o(n(v))? 32v*2 Let x(i) = -2081i*2. Let f(r) = 13r. Determine f(x(q)). -27053q2 Let d(w) = -32w*2. Let q(y) = -10y - 1. Give q(d(f)). 320f2 - 1 Let j(k) = -306k. Let p(f) = -2f. What is j(p(m))? 612m Let m(p) = -16p + 26p + 17p - 48p*2. Let s(g) = -7g*2 + 4g. Let u(t) = -4m(t) + 27s(t). Let k(h) = 2h2. What is u(k(o))? 12o*4 Let b(z) = -z. Let c(p) = -4p + 41. Determine c(b(y)). 4y + 41 Let t(s) = 8s*2 - 8s. Let f(p) = -17p2. Determine t(f(q)). 2312q*4 + 136q*2 Let i(o) = 5o + 33. Let a(m) = 17m. What is a(i(g))? 85g + 561 Let y(d) = -d + 1. Let l(c) = 2c + 1. Let q(t) = -l(t) + y(t). Let z(x) = -x - 4 + 4. Determine q(z(n)). 3n Let b(i) = i + i + 4 + 2. Let l(c) = c + 5. Let a(s) = 5b(s) - 6l(s). Let h(z) = 2z. What is a(h(g))? 8g Let s(p) = -2463p. Let b(j) = -2j*2. What is b(s(w))? -12132738w*2 Let f(a) = 6a*2. Let y(d) = 3d + 5. Let u(v) = 10v + 16. Let i(t) = -5u(t) + 16y(t). Calculate f(i(k)). 24k*2 Let m(d) = -3d. Let u(i) = 6i2. Let h(w) = w2. Let g(k) = -5h(k) + u(k). Calculate m(g(t)). -3t2 Let w(y) = 2y. Let t(h) = -2h2 - 5h + 5. Suppose 5z - 16 = 9. Let l(v) = -2v*2 - 6v + 6. Let a(i) = zl(i) - 6t(i). Determine w(a(n)). 4n2 Let b(k) = 724k. Let x(c) = -c*2. Give b(x(z)). -724z*2 Let g(q) be the second derivative of -2q*3/3 + 2q. Let o(d) be the third derivative of -d4/12 - d2. Calculate o(g(h)). 8h Let u(z) be the first derivative of z2 + 1. Let v(h) = -2h*2. Let y(p) = -5p*2. Let q(o) = 5v(o) - y(o). Calculate u(q(x)). -10x2 Let h(m) = 3m. Suppose 2t = -3 + 5. Suppose 2y = -t + 7. Let i(v) = -y - v*2 + 3. Give h(i(f)). -3f2 Let r(i) be the second derivative of i3/6 + 3i. Let t(a) = 10a. What is t(r(k))? 10k Let v(a) = 2a*2. Let t(g) = -29g*2 + 2. Determine v(t(y)). 1682y*4 - 232y*2 + 8 Let w(j) = 169j*2. Let y(g) = 28g. Give y(w(f)). 4732f2 Let r(j) = 55j*2 - 85. Let l(f) = -4f*2 + 6. Let u(i) = -85l(i) - 6r(i). Let o(s) = 2 + 2s - 2 + 0s. What is u(o(w))? 40w*2 Let w be 2/(-4)(-5 - -1). Let z(o) = -3o2 + 2o*w + 2o*2. Let i(l) = 2l*2. Determine z(i(p)). 4p*4 Let b(c) = 127c*2. Let j(o) = -6o*2. Determine j(b(i)). -96774i*4 Let t(m) = 2m*2. Let q(x) = -6x - 9x + 2 + 1. Give q(t(p)). -30p*2 + 3 Let z = -2 - 1. Let p(b) = 2b*2 + 3b + 3. Let m(j) = -4j2 - j2 - 3j - 7 - 4j. Let o(n) = zm(n) - 7p(n). Let s(r) = -3r. Determine s(o(w)). -3w2 Let m(c) = 2c. Let z(g) = 3g2 - 41 + 41. Determine m(z(k)). 6k*2 Let a(z) = -2z. Let d(r) = -658r2 - 1. Determine d(a(x)). -2632x*2 - 1 Suppose 3l = -0 + 6. Let t(w) = 4w2 - 3w*l + 4w*2. Let m(f) = f. What is m(t(j))? 5j*2 Let b(n) = 0n*2 + 0n2 - n2 - 4n2. Let o(x) = 2x2 - 67 - x2 + 67. Calculate o(b(i)). 25i4 Let p(v) be the third derivative of 0v*4 + 0 + 0v - v*2 + 0v*3 + 1/60v*5. Let x(n) = -3n. What is p(x(l))? 9l2 Let l(h) = h. Let w(r) = 5r. Let u(b) = -6l(b) + w(b). Let n(x) be the first derivative of 2x*3/3 + 1. Give n(u(v)). 2v*2 Let n(b) = 10b - 18b - 8b - 14b. Let t(x) = 3x*2. Give n(t(j)). -90j2 Let y(m) be the first derivative of m3/3 + 12. Let x(c) = 13c2. Calculate x(y(k)). 13k*4 Suppose -2q = -3d - 13, q + q - 15 = 5d. Let n(s) = -6s + qs + 9s. Let f(c) = 3c - 4c + 0c. Give f(n(g)). -8g Let u(p) be the third derivative of 13p*5/60 + 40p*2. Let m(d) = -d. Determine u(m(o)). 13o*2 Let d(j) = 70j*2 - 5. Let x(g) = -176g*2 + 12. Let p(t) = 12d(t) + 5x(t). Let f(q) = q2. Calculate f(p(n)). 1600n*4 Let q(a) = -a. Let i(h) = 4h. Let p(z) = -i(z) - 5q(z). Let r(u) = -2u*2 - 2 + 4 - 2. Give p(r(b)). -2b*2 Let l(d) = 171d*2. Let t(f) = -2f. Calculate t(l(g)). -342g2 Let r(k) = 3k*2 + 196. Let i(m) = -11m*2. Calculate r(i(q)). 363q*4 + 196 Let w(c) = -98c. Let m(t) be the first derivative of -2t3/3 + 24. Determine m(w(q)). -19208q2 Let h(y) = y2 + 3y + 1. Let v = 9 - 13. Let r be h(v). Let l(m) = m + 2m - rm + m. Let u(g) = 2g*2. Determine u(l(d)). 2d*2 Let f(w) = 2w. Let j be
I’m back from my first visit to Milan and Italy. The impressions I’m left with it that I have to go back and that I have to have more time. The city, the shopping, the food was simply an amazing experience. Here are some of my thoughts and recommendations: Eat: As the pasta addict I am, I was very excited about visiting Milan and Italy for the first time and trying out all their famous pasta cousins. Below I’ve listed some of the dinning places I visited during my stay and my experiences with them. The Kitchen (Via Scarlatti, 7) Good: Tasty and inexpensive food in a family friendly venue with free Wi-Fi. I think we ended up paying 25 euros for bread and tomatoes, two main dishes, a wine carafe (500ml for 5 euros – a bargain for Norwegians!) and some sweets for dessert.Bad: Nothing really, but might be a little “touristy” as we ended up next to two Swedish backpackers and several English speaking families. Papermoon (Via Bagutta, 1) Good: Tasty first course and dessert.Bad: Unfriendly staff ( I got the feeling they did not like drop-in tourists, even if the venue was less than half full the whole evening) that didn’t give more than the minimum of attention required. As this was a somewhat expensive place, I expected that waiter would present the menu and the dishes and recommend wine but that did not happen. Obika Mozzarella Bar (Piazza del Duomo, 3) Good: Rich menu, affordable prices and with its location, on the top of the department store La Rinascente, it gives you a perfect overview of the magnificent Milan Cathedral (Duomo di Milano). The taste-of-three dessert (Ricotta di Bufala Mousse, Tiramisù Chocolate and Almond Cake) is delicious!Bad: I expect this is a very crowded place in the tourist season, but for an off-season visit it was great. Also quite “touristy”, the couple at the table next to us were Norwegians as well. Shopping: Where to go shopping in Milan? I have to say – EVERYWHERE! I found that almost everywhere I turned there was a shopping street, a mall or at least one shop I had to check out. La Rinascente, Piazza del Duomo, 3 ( Subway stop: Duomo) Large (8 floors) department store located right next to Milan Cathedral (Duomo di Milano). High-end brands and designers mostly. Nice food court on the top floor. Galleria Vittorio Emanuele II ( Subway stop: Duomo) To be fair, I did not do much shopping here ( my shopping budget did not contain a big post for goodies from Gucci, Prada and Louis Vuitton), but just admiring the stores, the high sealing, golden decor and mosaic floor makes it worth visiting. Excelsior, Galleria del Corso, 4 (Subway stop: Duomo or San Babila) Free Wi-Fi, a big gadgets department on the first floor, a coctail bar, modern art on the walls and shoes from Manolo Blahnik and Christian Louboutin makes this my favourite department store in Milan. A visit here is highly recommended! Corso Buenos Aires (Subway stop: Porta Venezia, Lima or Loreto) If you’re tired of the high end stores (or, like me, have a modest shopping budget), check out Corso Buenos Aires. It’s one of the biggest shopping streets in Milan, and was very conveniently located just a few minutes’ walk from my hotel, contains most mainstream brands and stores such as H&M, Footlocker and Nike and a lot of Italian brands as well. I recommend a visit to Kiko Make Up Milan (located close to the Porta Venezia Subway stop), for nail polish in every color thinkable at 3,60 euro. Outlets: With all the high-end designers, stores and brands present, Milan is also known for its many factory outlets and discount stores. Many of them are even located within the city center, close to the main shopping areas. Here is a list of some of the outlets I visited: Brands I spotted: Marc Jacobs, Jimmy Choo, D&G, Stella McCartney, Prada, and many more at 30% to 70% off. A big selection of shoes. Small venue, so it gets crowded! KiloFascion, Via Bagetta (Subway stop: San Babila) At KiloFascion the weight of the item determines its price (the items are categorized as either good- better – best and this also effects the prices). I was quite fascinated by the concept at first, but after a closer look I found that I preferred set prices over constantly going back and forth to the weights and checking the items up against their category and weight. See: Looking back at my Milan visit, I’m sad to say I did not manage to see many great sights (shopping and dining took up most of my time it seems). The only sightseeing was done while walking around looking for shops, outlets and dining places. I did manage to get a close look at Milan Cathedral (Duomo di Milano) and buy my standard souvenir ( a snow globe with famous sights from the city), but next time (I’ll be back for sure) I also want to visit the Brera Art Gallery and Santa Maria delle Grazie, see a AC Milan match ( they were out of town this time) and take a trip to one of the many lakes located right outside the city. Some practicalities: – Free Wi-Fi is offered on several café’s and stores (giving me some sweet Foursquare points😉 ) – Credit card is accepted throughout the city (I did not come across any places that didn’t accept card payment) – The subway is a great means of transportation within the city centre, with frequent departures and information in English. – English: Everyone I meet understood and spoke English quite well ( I mainly talked to people working in the service- and tourist industry though). Please bare in mind that this is my personal experience and opinion based on only a couple of days in Milan. I’m sure I missed MANY great places, and would be very grateful for other recommendations. Have you been to Milan? What did you see and do? Where would you recommend dining for the most authentic Italian taste and atmosphere? On April 1st I’m going to Milan for the first time (in fact, first visit to Italy at all). This is a place I’ve been wanting to go for some time now, so I’m super excited! Before going some place new I like to plan ahead, get really in to all the sites, must-sees, and activities offered. Usually this means buying a travel book and searching online, this time it also includes Pinterest. Yesterday I started a board for Milan and begun the pinning – buildings – food – people on the streets of Milan (or at least what I believe to be Milan😉 ) and so on was pinned to this board: Thanks to Pinterest and its users, I was able to get a glance at people’s own vacation pictures from Milan and pictures taken by people living there, and from the looks of it – Milan is a very beautiful city!🙂 I’m still on the look-out for must-see spots and most-do activities in Milan. Have you been there? Let me know what you think, what you did and what I cannot miss!
November 18, 2011 — Chiropractor and New Mexico Military Institute (NMMI) alumnus Mary Beth Larsen has been inducted into NMMI’s Alumni Hall of Fame, in Roswell, N.M. Larsen, chiropractic relations manager for Standard Process Inc., was one of four 2011 inductees recognized for their successes after attending NMMI. The inductees were honored in a ceremony during the school’s annual homecoming event held last month. NMMI selected Larsen for its “eminence in a chosen field of endeavor” honor based on her notable achievements in the sport of modern pentathlon. The sport tests skill level in five disciplines: Pistol shooting Fencing Swimming Equestrian show jumping Running “Dr. Larsen is a gifted individual who approaches all aspects of her life, both as a professional and an athlete, with the determination to succeed,” said John Nab, DC, director of professional development at Standard Process. “Standard Process and I are pleased to see Dr. Larsen receive this honor from her alma mater.” During her first year at NMMI, Larsen started competing in modern pentathlons. Her commitment to the sport ultimately resulted in two Summer Olympic appearances, and features in multiple publications, including the cover of Esquire magazine, ESPN The Magazine, and Sports Illustrated. Larsen won a 1999 Pan American Games gold medal in the pentathlon. Her first trip to the Olympics was in 2000, the first year women competed in the modern pentathlon. She placed fourth in her inaugural appearance at the games held in Sydney, Australia. In 2004 Larsen participated in the Olympic Games in Athens, Greece, placing 15th overall. During her acceptance speech, Larsen thanked the alumni association and NMMI for the “incredible honor and for providing a firm foundation from which I was able to launch my dreams.” Larsen, a 1994 graduate of NMMI, graduated as First Class salutatorian for the junior college division with an associate of arts degree. Larsen received her chiropractic degree from Logan College of Chiropractic, graduating in 2001. She joins other noted NMMI alumni in the hall of fame including Sam Donaldson, Jr., former ABC News anchor.
<% # Copyright (C) 2012 - present Instructure, Inc. # # This file is part of Canvas. # # Canvas is free software: you can redistribute it and/or modify it under # the terms of the GNU Affero General Public License as published by the Free # Software Foundation, version 3 of the License. # # Canvas is distributed in the hope that it will be useful, but WITHOUT ANY # WARRANTY; without even the implied warranty of MERCHANTABILITY or FITNESS FOR # A PARTICULAR PURPOSE. See the GNU Affero General Public License for more # details. # # You should have received a copy of the GNU Affero General Public License along # with this program. If not, see <http://www.gnu.org/licenses/>. %> <fieldset> <legend><%= t :select_quizzes, "Select Quizzes to Export" %></legend> <div style="overflow: auto; max-height: 200px"> <%= check_box :copy, :all_quizzes, :class => "copy_all", :checked => true %><%= label :copy, :all_quizzes, t('labels.all_quizzes', "All Quizzes") %> <ul class="unstyled_list" style="margin-<%= direction('left') %>: 20px;"> <% global_ids = @context.content_exports.temp_record.can_use_global_identifiers? %> <% @context.quizzes.active.each do \|quiz\| %> <li> <%= check_box "copy[quizzes]", mig_id(quiz, global: global_ids), :class => 'quiz_item', :checked => true %> <%= label "copy[quizzes]", mig_id(quiz, global: global_ids), quiz.title %> </li> <% end %> </ul> </div> </fieldset>
Integrative Therapists in Austin, TX 78731 "As a psychotherapist I strive to assist my clients in the process of becoming more whole in all aspects of their lives. My primary training is as an art therapist and I use an integrative approach to promote healing. I find that enhancing talk therapy with experiential methods gives my clients the freedom to express their deepest selves. Within the therapeutic relationship we can find the existing internal nuances and textures that make us all unique and valuable. My work includes seeing individuals, adolescents and adults, who have depression/anxiety, past trauma, addiction related issues and middle-aged challenges." "As a psychotherapist I strive to assist my clients in the process of becoming more whole in all aspects of their lives. My primary training is as an art therapist and I use an integrative approach to promote healing. I find that enhancing talk therapy with experiential methods gives my clients the freedom to express their deepest selves. Within the therapeutic relationship we can find the existing internal nuances and textures that make us all unique and valuable. My work includes seeing individuals, adolescents and adults, who have depression/anxiety, past trauma, addiction related issues and middle-aged challenges." "I help my clients find their spark and fall back in love with life. I specialize in helping those who are stuck in a long-standing depression, and I have a strong understanding of the issues of trauma, anxiety, and grief and loss that can reinforce it. Many people live lives weighed down by old issues and stuck patterns. If you can envision a better version of yourself and a fuller life, now is the time to start figuring out how to get there---and we can all get there." "I help my clients find their spark and fall back in love with life. I specialize in helping those who are stuck in a long-standing depression, and I have a strong understanding of the issues of trauma, anxiety, and grief and loss that can reinforce it. Many people live lives weighed down by old issues and stuck patterns. If you can envision a better version of yourself and a fuller life, now is the time to start figuring out how to get there---and we can all get there." "It can be difficult to find the right therapist and finding a good fit is very important. With that in mind, I will spend time getting to know and understand your personal beliefs, characteristics, and history to create a safe, contained and trusting environment where you feel at ease to share your concerns and experiences. I work interactively, offering genuine compassion and sensitivity. We will work together to make sure therapy feels comfortable and effective. Sometimes it is a matter of seeking another perspective that opens the door to new ideas in order to uncover solutions." "It can be difficult to find the right therapist and finding a good fit is very important. With that in mind, I will spend time getting to know and understand your personal beliefs, characteristics, and history to create a safe, contained and trusting environment where you feel at ease to share your concerns and experiences. I work interactively, offering genuine compassion and sensitivity. We will work together to make sure therapy feels comfortable and effective. Sometimes it is a matter of seeking another perspective that opens the door to new ideas in order to uncover solutions." "You listen to NPR and think deeply about the world. Lately, you suffer from sleep, mood and relationship disturbances that overwhelm and exasperate your ability to calm and ground yourself. You are certain you need help yet uncertain it will really work for you, after mixed results with other therapists. If you are goal-oriented and desperate for effective help, I am your informed voice of clarity and insight for individual or couples work together." "You listen to NPR and think deeply about the world. Lately, you suffer from sleep, mood and relationship disturbances that overwhelm and exasperate your ability to calm and ground yourself. You are certain you need help yet uncertain it will really work for you, after mixed results with other therapists. If you are goal-oriented and desperate for effective help, I am your informed voice of clarity and insight for individual or couples work together." "We all have a story. Want to tweak yours so it feels better?You're frustrated with family challenges...Play therapy for your child and parent coaching can make things better. You're feeling disconnected....Counseling can help you rebuild your relationship or gently let it go. Distressing thoughts, emotions or behaviors are wreaking havoc on your life and sabotaging success and happiness....EMDR can help resolve past trauma or disturbing events that might be subconsciously driving your current functioning. These are all things I can help you with." "We all have a story. Want to tweak yours so it feels better?You're frustrated with family challenges...Play therapy for your child and parent coaching can make things better. You're feeling disconnected....Counseling can help you rebuild your relationship or gently let it go. Distressing thoughts, emotions or behaviors are wreaking havoc on your life and sabotaging success and happiness....EMDR can help resolve past trauma or disturbing events that might be subconsciously driving your current functioning. These are all things I can help you with." "Any crisis or symptom can be much more than just a problem to be solved. Whether your soul aches, you feel alone and confused in a dark and difficult time, or you hunger to live a more passionate and satisfying life... these difficulties can become doorways, allowing you to come more fully into heartfelt contact with your unique life's journey, its particular challenges and gifts, and the courage to heal from the inside out." "Any crisis or symptom can be much more than just a problem to be solved. Whether your soul aches, you feel alone and confused in a dark and difficult time, or you hunger to live a more passionate and satisfying life... these difficulties can become doorways, allowing you to come more fully into heartfelt contact with your unique life's journey, its particular challenges and gifts, and the courage to heal from the inside out." "My mission is to connect with other people in order to help them learn and grow on their path to healing. I believe that therapy should be a place of warmth, acceptance and growth. My motivation for being a therapist today is based on the awe and amazement I experience from working with my remarkable and resilient clients. I work with adolescents, teens and adults." "My mission is to connect with other people in order to help them learn and grow on their path to healing. I believe that therapy should be a place of warmth, acceptance and growth. My motivation for being a therapist today is based on the awe and amazement I experience from working with my remarkable and resilient clients. I work with adolescents, teens and adults." "Your 20s and 30s are an important time of self-determination. If you're feeling stuck or lost, I can help you develop the tools and insights you need to enjoy this time of your life. With individuals, I specialize in helping young professionals and grad students with academic and workplace adjustment, anxiety, burnout and stress management, multicultural stressors, and relationship and sexual issues (low desire, pain & orgasm difficulty). With couples, I have expertise in helping partners improve communication and conflict skills and manage sexual issues (differences in desire, enhancing intimacy)." "Your 20s and 30s are an important time of self-determination. If you're feeling stuck or lost, I can help you develop the tools and insights you need to enjoy this time of your life. With individuals, I specialize in helping young professionals and grad students with academic and workplace adjustment, anxiety, burnout and stress management, multicultural stressors, and relationship and sexual issues (low desire, pain & orgasm difficulty). With couples, I have expertise in helping partners improve communication and conflict skills and manage sexual issues (differences in desire, enhancing intimacy)." "I welcome diversity, including relationships and families of every kind. I offer a safe place to talk (at your own pace) about challenges that may feel impossible to discuss anywhere else. Focus areas include relationship difficulties, loss, interpersonal challenges, LGBTQ+/queer concerns, divorce support, stress, pre-teen and adolescent challenges, anxiety, depression, a general sense of feeling unhappy, parenting and more. If you're having a hard time you do not need to be alone. I offer weekend hours and work with individuals, relationships, families and groups." "I welcome diversity, including relationships and families of every kind. I offer a safe place to talk (at your own pace) about challenges that may feel impossible to discuss anywhere else. Focus areas include relationship difficulties, loss, interpersonal challenges, LGBTQ+/queer concerns, divorce support, stress, pre-teen and adolescent challenges, anxiety, depression, a general sense of feeling unhappy, parenting and more. If you're having a hard time you do not need to be alone. I offer weekend hours and work with individuals, relationships, families and groups." "Do you feel like your life is a series of incomplete sentences? Are you homesick for a place you aren't even sure exists? Adulting is like folding a fitted sheet. No one really knows how to do it. Growth is painful. Change is painful. But nothing is as painful as staying stuck somewhere you don't belong. Decisions sometimes prove to be the hardest to make, especially when it's a choice between where you are and where you really wanted to be." "Do you feel like your life is a series of incomplete sentences? Are you homesick for a place you aren't even sure exists? Adulting is like folding a fitted sheet. No one really knows how to do it. Growth is painful. Change is painful. But nothing is as painful as staying stuck somewhere you don't belong. Decisions sometimes prove to be the hardest to make, especially when it's a choice between where you are and where you really wanted to be." "My goal is to create a safe and comfortable space where clients can articulate their inner experience through both words and symbols. Deeper and clearer understanding unfolds as we engage in the therapeutic process with both a playful curiosity and a nonjudgmental attitude. I listen deeply and empathize with clients, while simultaneously encouraging them to confront the unhealthy roles, ineffective patterns and behaviors, and difficult emotions that are keeping them stuck in their lives. I believe that psychotherapeutic work profoundly transforms our inner worlds. It is truly a gift to be witness, partner, and guide on this journey." "My goal is to create a safe and comfortable space where clients can articulate their inner experience through both words and symbols. Deeper and clearer understanding unfolds as we engage in the therapeutic process with both a playful curiosity and a nonjudgmental attitude. I listen deeply and empathize with clients, while simultaneously encouraging them to confront the unhealthy roles, ineffective patterns and behaviors, and difficult emotions that are keeping them stuck in their lives. I believe that psychotherapeutic work profoundly transforms our inner worlds. It is truly a gift to be witness, partner, and guide on this journey." "Most of us live from problem to problem. As soon as one ends, another pops up. It seems we are always on high alert; always switched on, with stress running the show. Research is discovering new ways of regulating our brains and leading us out of stress mode. My approach to psychotherapy goes beyond traditional talk therapy and offers a gentle, life-affirming way to work with painful life experiences, and tools to help you access the inner resources you need to live life more fully: EMDR, mindfulness, cognitive restructuring, and positive psychology." "Most of us live from problem to problem. As soon as one ends, another pops up. It seems we are always on high alert; always switched on, with stress running the show. Research is discovering new ways of regulating our brains and leading us out of stress mode. My approach to psychotherapy goes beyond traditional talk therapy and offers a gentle, life-affirming way to work with painful life experiences, and tools to help you access the inner resources you need to live life more fully: EMDR, mindfulness, cognitive restructuring, and positive psychology." "I have 20 years of experience and specialize in: counseling for boys and teen males; adult psychotherapy for depression, anxiety, trauma, grief and loss, men's issues; family counseling and parenting skills. I help my clients to identify and tap their inner strengths. I am described by clients as calm, caring, supportive and highly effective. I will work with you to establish a safe, trusting relationship as the foundation for our work towards your personal goals. I offer a free initial consultation and evening appointments are available." "I have 20 years of experience and specialize in: counseling for boys and teen males; adult psychotherapy for depression, anxiety, trauma, grief and loss, men's issues; family counseling and parenting skills. I help my clients to identify and tap their inner strengths. I am described by clients as calm, caring, supportive and highly effective. I will work with you to establish a safe, trusting relationship as the foundation for our work towards your personal goals. I offer a free initial consultation and evening appointments are available." "I work with couples and individuals, both in and out of relationships. I provide a safe environment that makes painful feelings and thoughts more manageable. I blend warmth, regard, sensitivity and support with playfulness, curiosity and humor to build an open therapeutic relationship conducive to long-term deep work. I work with you to relieve feelings of shame, fear, anxiety, anger, self-loathing and isolation stemming from physical and emotional trauma. Over time, I can help you find greater satisfaction in relationships, improve your self-esteem and lead a richer, fuller more self-assured life." "I work with couples and individuals, both in and out of relationships. I provide a safe environment that makes painful feelings and thoughts more manageable. I blend warmth, regard, sensitivity and support with playfulness, curiosity and humor to build an open therapeutic relationship conducive to long-term deep work. I work with you to relieve feelings of shame, fear, anxiety, anger, self-loathing and isolation stemming from physical and emotional trauma. Over time, I can help you find greater satisfaction in relationships, improve your self-esteem and lead a richer, fuller more self-assured life." "The majority of the clients I see are women experiencing a transition in life. Sometimes this looks like the end of a relationship, feeling stuck in a career, or not really being sure where to go next but knowing it is time to make a change. I specialize in working with women who are experiencing change within the context of reproductive health. I see women struggling with infertility, experiencing the grief of miscarriage or other perinatal loss, and transitioning into the phase of pregnancy, postpartum, and parenting. I love supporting women during these times of their lives that feel so vulnerable." "The majority of the clients I see are women experiencing a transition in life. Sometimes this looks like the end of a relationship, feeling stuck in a career, or not really being sure where to go next but knowing it is time to make a change. I specialize in working with women who are experiencing change within the context of reproductive health. I see women struggling with infertility, experiencing the grief of miscarriage or other perinatal loss, and transitioning into the phase of pregnancy, postpartum, and parenting. I love supporting women during these times of their lives that feel so vulnerable." "I offer individual and couples therapy with an expertise in trauma recovery. I use a variety of methods including Somatic Experiencing, AEDP, Pia Mellody's Post Induction Therapy, and Mindfuness, Interpersonal Neurobiology, Attachment Theory, Shame Resilience Theory, and Sandtray Therapy for adults. My therapeutic approach is to provide support and practical feedback to help clients effectively address personal life challenges. I also facilitate groups, workshops, and intensive weekend retreats based on the research of Dr. Brene' Brown. NOTE: I offer early morning appointments at my Onion Creek office for the convenience of NE Hays and SE Travis County residents" "I offer individual and couples therapy with an expertise in trauma recovery. I use a variety of methods including Somatic Experiencing, AEDP, Pia Mellody's Post Induction Therapy, and Mindfuness, Interpersonal Neurobiology, Attachment Theory, Shame Resilience Theory, and Sandtray Therapy for adults. My therapeutic approach is to provide support and practical feedback to help clients effectively address personal life challenges. I also facilitate groups, workshops, and intensive weekend retreats based on the research of Dr. Brene' Brown. NOTE: I offer early morning appointments at my Onion Creek office for the convenience of NE Hays and SE Travis County residents" "I believe we can become ashamed of events in our lives, or carry past regrets. Without addressing these issues, we might come to believe these problems are a part of us, and become negative toward ourselves and others. We may begin to experience and internalize pain and suffering which can affect our daily living and relationships. Through counseling, you can experience freedom, confidence and kindness toward yourself and others. Working collaboratively, I will support you in developing the tools, skills and insight to create positive change." "I believe we can become ashamed of events in our lives, or carry past regrets. Without addressing these issues, we might come to believe these problems are a part of us, and become negative toward ourselves and others. We may begin to experience and internalize pain and suffering which can affect our daily living and relationships. Through counseling, you can experience freedom, confidence and kindness toward yourself and others. Working collaboratively, I will support you in developing the tools, skills and insight to create positive change." "Currently, I am on maternity leave until January 2018 and am not taking new clients. As a therapist, I focus on helping my clients recognize and develop the strengths they may not realize they already have. I am a child, adolescent, and family psychologist who has experience working with a variety of issues such as anxiety (including selective mutism), depression, anger, noncompliance, defiance, impulsive behavior, trauma, parenting, and family relationships. I respect the time and effort that families put into participating in therapy, and I support them in identifying and achieving realistic goals." "Currently, I am on maternity leave until January 2018 and am not taking new clients. As a therapist, I focus on helping my clients recognize and develop the strengths they may not realize they already have. I am a child, adolescent, and family psychologist who has experience working with a variety of issues such as anxiety (including selective mutism), depression, anger, noncompliance, defiance, impulsive behavior, trauma, parenting, and family relationships. I respect the time and effort that families put into participating in therapy, and I support them in identifying and achieving realistic goals." "In my role as Clinical Director and Therapist at Innovation360, I specialize in helping young people and adults who have become stuck, adrift or immobilized. I work with many people who struggle to actualize or even identify what their goals for progress may be. Anxiety, insecurity, substance abuse, mood disorders and challenges in relating to others are frequent obstacles that my clients face and develop the capacity to overcome. As part of a team that values the involvement of family, partners and specialized professionals, we strive to involve and support members of our clients' support system as well." "In my role as Clinical Director and Therapist at Innovation360, I specialize in helping young people and adults who have become stuck, adrift or immobilized. I work with many people who struggle to actualize or even identify what their goals for progress may be. Anxiety, insecurity, substance abuse, mood disorders and challenges in relating to others are frequent obstacles that my clients face and develop the capacity to overcome. As part of a team that values the involvement of family, partners and specialized professionals, we strive to involve and support members of our clients' support system as well." Online Therapy See Nearest Integrative TherapistsIntegrative therapy in 78731 refers to therapy in which elements from different types of therapy may be used. Therapists 'integrate' two or more therapeutic styles (e.g. Cognitive and Family Systems) to bring about a personalized and practical approach to healing. These 78731 integrative therapy Therapists practice an integrative therapy style. Integrative therapy (with a small 'i') may also refer to the process of 'integrating' the personality by taking disowned or unresolved aspects of the self and making them part of a cohesive personality whole. It reduces the use of defense mechanisms that inhibit spontaneity and allows flexibility in solving emotional problems. How can I tell if a therapist is right for me? Therapists in Austin 78731 are able to work with a wide range of issues. Email Don't be shy. Our therapists are here to help you and are pleased to hear from you. 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Francis Basin Francis Basin LdH CdeG MBE (1903 -1975) was a French secret agent of the Special Operations Executive during the Second World War. Early life François Marcel Basin was born on 6 August 1903 in Grasse, the son of Antoine Basin, a railway employee, and Élise née Vernin. Wartime activities In August 1940, he enlisted in the British army on the advice of Colonel Massip to whom he was secretary and who was close to General de Gaulle. Incorporated as a private soldier with thirty other Frenchmen, he undertook all the classes without thinking of becoming a secret agent. He attended the Liaison Officer course at Wanborough Manor (Guildford) and took the exam on 27 December 1940. He was then visited by the commander Nicolas Bodington, director of Section F prior to Maurice Buckmaster. Bodington offered him special training to go to France on a dangerous mission. "Think about it," he advised. "You will give me your answer tomorrow." Basin replied: "I prefer to say ‘yes’ straight away. If I think, I will deflate." He was one of the first recruits of the SOE. On 14 July 1941, he was promoted to Lieutenant. Mission in France He was head of the URCHIN network on the Côte d'Azur, working under the nom de guerre of "Olive". On 28 August 1941, he sailed from England to Gibraltar in HMS Fidelity in Operation AUTOGYRO and on the night of 19/20 September 1941 landed by submarine at Le Barcarès near Perpignan with Robert Leroy "Louis", Raymond Roche "François", and Georges Duboudin "Alain". The day after his arrival, Basin was arrested by the police at his hotel in Cannes and held in Fort Saint-Nicolas of Marseille. The investigating judge recognised his good faith and released him on 5 October 1941. Then for more than ten months until his arrest in August 1942 he developed the URCHIN network. He made contact with Élie Lévy, whose house in Antibes became a reception centre for many agents in transit. Lévy put him in touch with André Girard, head of the CARTE network. He established his headquarters in Cannes, in the Villa Isabelle. Baron Henri Ravel of Malval "Antoine", whom he knew at the beginning of the war and whom he met by chance in Cannes, put his house at his disposal. There, Basin received SOE agents landed on the Côte d'Azur. It formed 31 cells covering several departments: Bouches-du-Rhône, Var, Basses-Alpes, Alpes-Maritimes, of which seven cells were assigned to propaganda. He was in regular contact with American SOE agent Virginia Hall "Marie", based in Lyon. Together, they prepared reports for London. On 15 January 1942 Peter Churchill arrived by submarine to evaluate his network, provide him with Fr.400,000 and revised guidelines. He established contact with the leaders of resistance movements and supported them financially: Henri Frenay (FREEDOM, which became COMBAT), General de La Laurencie (LIBERATION NATIONAL), Emmanuel d'Astier de la Vigerie "Bernard" (LIBERATION). He was in contact with London, first by reports sent by the Swiss diplomatic bag, then also by radio from 20 April 1942 after the arrival of Isidore Newman "Julien", the radio operator assigned to him. Impressed by the possibilities of contact with London that Basin could assure, André Girard agreed to send one of his officers to England, and chose Henri Frager, his second in command. Taking advantage of the departure of Max Hymans "Frédéric" for London, Basin sent a report on his relations with the MAP network. Unfortunately, Max Hymans was interned for three months in Spain, and the report arrived in London only on 12 August 1942. Arrest On 18 August 1942 Basin was arrested in Cannes by the Security Service, having been given away by a Swiss diplomatic courier, Jean Cogniat, who was arrested at the Swiss border in possession of secret reports of Basin. On the night of 27/ 28 August 1942 Peter Churchill returned to the south of France to take over the URCHIN network in the Midi under the name of SPINDLE. Churchill planned to rescue Basin but this attempt was called off, apparently at Basin's request. On 4 September 1942 there was a failed attempt by the MAP network to rescue Basin in a train taking him to Montluc prison in Lyon. Release On 29 November 1942 Basin was released from Montluc prison with false provisional liberty papers. The Germans, who had invaded the free zone, were searching for him. He was weak and in need of medical care, but had to disappear quickly. With the help of Lazare Rachline (VIC escape network), Virginia Hall took him to Mont-Dore and placed him in a safe house in Auvergne. He then went to Nîmes where a plane came to fetch him, but he broke his leg in an accident on the ground. On 20 August 1943 he was flown back to London in a Hudson in Operation DYER, organized by Henri Déricourt. Accompanying him were Peter Deman "Paul" from section DF; Marie-Thérèse Le Chêne, Tony Brooks (SOE) "Alphonse", Robert Boiteux "Nicolas", Octave Simon, Joseph Marchand, Victor Gerson, Robert Benoist, Raymonde Mennessier, Jean-Louis de Ganay. Basin remained in London until the end of the war, firstly as an instructor at the Beaulieu Special Training School, then at the headquarters of Section F in London. Finally, he was reinstated in the French services (BCRA), staff FFI on 19 September 1944. Post-war He testified about his wartime experiences on 18 March 1947 with Miss Patrimonio, and on 3 November 1971 with André Gillois. He died in Paris on 20 October 1975. Awards United Kingdom: Member of the Order of the British Empire (MBE), France: Croix de Guerre 1939-1945, Médaille de la Résistance, Légion d'honneur (1946), Officer of the Légion d'honneur(1951). References External sources Basin's profile in Special Forces Roll of Honor. Chronology of SOE operations with the resistance in France during World War II , Lt. Col. EG Boxshall, 1960, typed document (copy from the Pearl Witherington-Pearlioley Library), available at Valençay. See sheet 17, DONKEYMAN CIRCUIT . Le réseau carte : Histoire d'un réseau de la Résistance antiallemand, antigaulliste, anticommuniste et anticollaborationniste, Perrin, 2008, 398 p. () The spy: Virginia Hall, an American in the war. Vincent Nouzille, Fayard, Paris. The uncertain adventure Claude Bourdet. Category:Special Operations Executive personnel Category:Members of the Order of the British Empire Category:People from Grasse Category:Recipients of the Croix de Guerre 1939–1945 (France) Category:1903 births Category:1975 deaths Category:Officiers of the Légion d'honneur Category:Recipients of the Resistance Medal
Definitions of infertility and recurrent pregnancy loss. The American Society for Reproductive Medicine has recently revised its definitions of infertility and recurrent pregnancy loss.
Wing shape-mediated carry-over effects of a heat wave during the larval stage on post-metamorphic locomotor ability. Two key insights to better assess the ecological impact of global warming have been poorly investigated to date: global warming effects on the integrated life cycle and effects of heat waves. We tested the effect of a simulated mild (25 °C) and severe (30 °C) heat wave experienced during the larval stage on the flight ability of the damselfly Ischnura elegans. To get a mechanistic understanding of how heat stress may translate into reduced post-metamorphic flight ability, we evaluated the hypothesized mediatory role of adult size-related traits, and also tested alternative pathways operating through changes in wing shape and two flight-related traits (both relative fat and flight muscle contents). Exposure to a heat wave, and particularly the severe one, shortened the larval stage, reduced adult size-related traits and modified the wing shape but did not significantly affect emergence success, relative fat content and relative flight muscle mass. Notably, the heat wave negatively affected all components of flight ability. Unexpectedly, the heat wave did not reduce flight ability through reducing size. Instead, we identified a novel size-independent mechanism bridging metamorphosis to link larval environment and adult flight ability in males: through affecting wing shape. The present study advances mechanistic insights in the still poorly understood coupling of life stages across metamorphosis. Additionally, our results underscore the need for integrative studies across life stages to understand the impact of global warming.
Social relations and depressive symptoms in older adults with knee osteoarthritis. Depressive symptoms often occur as a comorbid condition in the context of chronic illnesses such as arthritis. However, the role of both social support and social strain in relation to depressive symptoms has not been adequately explored. This study investigates the association of support and strain with depressive symptoms among a sample of older men and women in the USA (N = 298, mean age 71 years) who have knee osteoarthritis (OA). Data were collected from a survey mailed to residents who had previously participated in the Osteoarthritis Study in Seniors (OASIS), a longitudinal observational study of OA progression (survey response rate was 77%). Hierarchical regression analyses revealed significant associations of both support and strain with depressive symptoms, while statistically controlling for a variety of demographic, psychosocial and disease-related variables. In addition, social support significantly buffered the relation between social strain and depressive symptoms. The interaction effect was not significantly different for women and men, nor were the individual associations of support and strain with depressive symptoms conditioned by participant gender. The results add to the ongoing discussion regarding gender and social relations as well as highlight the role of both positive (social support) and negative (social strain) aspects of social interactions in relation to the psychological functioning of older adults coping with a chronic illness.
Q: Jquery - Setting form select-field "selected" value only works after refresh I want to use a form select-field for users to select their country of residence, which shows the IP based country as default value (plus the IP address next to it); Location info (ipinfodb.com) is working. I'm passing "country" and "ip" to the function, which should modify select-field and ip adress Problem: IP adress works, but the select-field only updates after I hit refresh. Can someone tell me why? Here is the code: HTML <select name="setup_changeCountry" id="setup_changeCountry"> <option value="AL-Albania">Albanien</option> <option value="AD-Andorra">Andorra</option> <option value="AM-Armenia">Armenien</option> <option value="AU-Australia">Australien</option> ... </select> <div class="setup_IPInfo"> <span>Your IP</span> <span class="ipAdress"> -- ip --</span> </div> Javascript/Jquery function morph(country,ip) >> passed from function, called on DOMContentLoaded { var ipAdress = ip; $('.ipAdress').text(ipAdress); var countryForm = country; $('#setup_changeCountry option').each(function() { if ($(this).val().substr(0,2) == countryForm) { $(this).attr('selected', "true"); } }); } Thanks for any clues on how to fix this. Frequent A: you can simplify your loop immensely and let jQuery do the work: $("#setup_changeCountry option[value$='" + country + "']").attr('selected', true); make sure: the case matches (your country must then also begin with a capital letter) you execute this code after the DOM's loaded, otherwise you might be trying to select an option that doesnt exist yet
package org.scilab.forge.jlatexmath.examples.basic; import java.awt.Dimension; import javax.swing.BorderFactory; import javax.swing.JFrame; import javax.swing.JLabel; import org.scilab.forge.jlatexmath.TeXConstants; import org.scilab.forge.jlatexmath.TeXFormula; import org.scilab.forge.jlatexmath.TeXIcon; public class ExampleSwing2 { public static void main(String[] args) { String latex = "\\text{hello world}"; TeXFormula formula = new TeXFormula(latex); TeXIcon icon = formula.new TeXIconBuilder().setStyle(TeXConstants.STYLE_DISPLAY) .setSize(16) .setWidth(TeXConstants.UNIT_PIXEL, 256f, TeXConstants.ALIGN_CENTER) .setIsMaxWidth(true).setInterLineSpacing(TeXConstants.UNIT_PIXEL, 20f) .build(); JFrame frame = new JFrame(); final JLabel label = new JLabel(icon); label.setMaximumSize(new Dimension(100,300)); label.setBorder(BorderFactory.createEmptyBorder(10,10,10,10)); frame.getContentPane().add(label); frame.setDefaultCloseOperation(JFrame.EXIT_ON_CLOSE); frame.pack(); frame.setVisible(true); } }
1. Introduction {#sec1-ijms-19-03642} =============== The three layers of skin contain the human dermal fibroblasts (HDFs), epidermal keratinocytes, immune cells, nerves, and intradermal adipocytes \[[@B1-ijms-19-03642],[@B2-ijms-19-03642],[@B3-ijms-19-03642]\]. The constant communication between the different cellular constituents of various compartments of the skin and its extracellular matrix (ECM) plays a critical role in maintaining physiological homeostasis of the body \[[@B4-ijms-19-03642],[@B5-ijms-19-03642],[@B6-ijms-19-03642]\]. The most essential resident cell of the dermis is HDF which is involved in wound healing through the production of ECM \[[@B4-ijms-19-03642],[@B5-ijms-19-03642]\]. HDFs communicate with each other and with other cell types, including keratinocytes, immune cells, and adipocytes, thus playing a crucial role in regulating skin physiology and tissue repair \[[@B2-ijms-19-03642],[@B7-ijms-19-03642]\]. Tissue repair immediately starts after the skin gets damaged. Wound repair is a tightly regulated complex process, which includes hemostasis, inflammation, proliferation, and re-epithelialization \[[@B8-ijms-19-03642],[@B9-ijms-19-03642]\]. During wound healing, proliferation and migration of resident HDFs into the damaged area results in the recovery of skin wounds \[[@B10-ijms-19-03642],[@B11-ijms-19-03642]\]. Visfatin, also known as pre-B cell colony-enhancing factor (PBEF) or nicotinamide phosphoribosyl-transferase (NAMPT), was originally cloned from activated peripheral blood lymphocytes in 1994, as a highly conserved intracellular and extracellular 52 kDa adipokine \[[@B12-ijms-19-03642],[@B13-ijms-19-03642],[@B14-ijms-19-03642],[@B15-ijms-19-03642],[@B16-ijms-19-03642]\]. Visfatin is released from various cell types and tissues of higher organisms, including peripheral-blood monocytes, lymphocytes, dendritic cells, macrophages, adipose tissues, in particular visceral adipose tissue and is expressed in various malignant tumors, including colon, stomach, pancreas, liver, prostate, and breast cancers \[[@B13-ijms-19-03642],[@B15-ijms-19-03642],[@B17-ijms-19-03642],[@B18-ijms-19-03642],[@B19-ijms-19-03642],[@B20-ijms-19-03642],[@B21-ijms-19-03642],[@B22-ijms-19-03642],[@B23-ijms-19-03642],[@B24-ijms-19-03642]\]. To date, two forms of visfatin have been identified: intracellular and extracellular. Intracellular visfatin plays a key role in maintaining the activity of nicotinamide adenine dinucleotide (NAD)-dependent enzymes and is implicated in the regulation of cellular metabolism. A recent study has reported that both intracellular and extracellular visfatin have been shown to be involved in tumor development \[[@B25-ijms-19-03642]\]. Additionally, many studies have demonstrated that visfatin promotes angiogenesis by enhancing the proliferation, migration, formation of functional neovessels, and invasion of vascular endothelial cells in vitro and in vivo \[[@B26-ijms-19-03642],[@B27-ijms-19-03642],[@B28-ijms-19-03642],[@B29-ijms-19-03642]\]. Further, visfatin has been shown to exhibit anti-apoptotic and proinflammatory properties \[[@B30-ijms-19-03642]\]. Previous studies have reported the potential effects of visfatin on the proliferation and collagen synthesis in rat cardiac tissue and on induction of vascular smooth muscle cells \[[@B31-ijms-19-03642]\]. Vascular endothelial cell growth factor (VEGF) is an angiogenic factor and the most important regulator of cell proliferation, migration, and permeabilization \[[@B32-ijms-19-03642],[@B33-ijms-19-03642],[@B34-ijms-19-03642],[@B35-ijms-19-03642]\]. Many studies have reported that VEGF plays a critical role in wound healing through the induction of vascular permeability \[[@B32-ijms-19-03642],[@B36-ijms-19-03642]\]. VEGF is produced in many cell types, including tumor cells and healthy cells, such as epidermal cells of the skin, including keratinocytes and fibroblasts \[[@B32-ijms-19-03642],[@B37-ijms-19-03642],[@B38-ijms-19-03642]\]. A recent study has suggested that visfatin-induced proliferation of endothelial cells relies on the synthesis and secretion of VEGF \[[@B39-ijms-19-03642]\], a key regulator of cell proliferation and angiogenesis. Moreover, visfatin has been shown to up-regulate the VEGF receptor 2, which mediates the angiogenic actions of VEGF \[[@B27-ijms-19-03642],[@B39-ijms-19-03642]\]. Visfatin has been reported to regulate the expression of VEGF through activation of several pathways, including phosphatidylinositol 3-kinase (PI3K)/Akt, the mitogen-activated protein kinases (MAPK) extracellular signal-regulated kinases 1 and 2 (ERK1/2), and p38 signaling pathways \[[@B26-ijms-19-03642],[@B27-ijms-19-03642],[@B39-ijms-19-03642],[@B40-ijms-19-03642],[@B41-ijms-19-03642]\]. Thus, we hypothesized that visfatin might induce wound healing through the induction of proliferation and migration. However, to date, there is poor evidence on the functions and direct effect of visfatin on wound healing in vitro and in vivo. In the present study, we aimed to evaluate the effect of visfatin on cell proliferation and migration. 2. Results {#sec2-ijms-19-03642} ========== 2.1. Visfatin Enhances the Proliferation and Migration of HDFs {#sec2dot1-ijms-19-03642} -------------------------------------------------------------- The proliferation and migration of skin dermal fibroblasts play an important role in wound repair. HDFs express numerous genes in response to epidermal growth factor (EGF) stimulus. We hypothesized that EGF-induced genes are directly or indirectly involved in the enhancement of cell proliferation and migration in wound repair. Thus, in this study, we performed a cDNA microarray to characterize the wound-related genes and investigate the role of these genes in wound healing in vitro and in vivo. According to cDNA microarray analysis, out of a total number of genes analyzed (36,079), expression of 1210 genes (3.35%) was up- or down-regulated more than 2-fold in EGF-stimulated HDFs, compared with the untreated control. As shown in [Figure 1](#ijms-19-03642-f001){ref-type="fig"}A, as previous studies reported, we also found the up-regulated wound healing-related genes such as prostaglandin synthase 2 (PTGS2), intracellular adhesion molecule 1 (ICAM-1), matrix metalloproteinase 1 (MMP1), MMP3, hyaluronan synthase 2 (HAS2), and chemokines including interleukin-1 (IL-1), chemokine (C-X-C motif) ligand-1 (CXCL-1), chemokine (C-C motif) ligand 2 (CCL2), CXCL-5, CCL11 and CXCL10 in EGF-stimulated HDFs. Notably, EGF markedly increased the expression of visfatin in a dose-dependent manner in HDFs ([Figure 1](#ijms-19-03642-f001){ref-type="fig"}A,B). Based on several previous studies suggesting that visfatin promotes cell proliferation, migration and angiogenesis \[[@B26-ijms-19-03642],[@B27-ijms-19-03642],[@B28-ijms-19-03642],[@B29-ijms-19-03642]\], we have selected a gene that visfatin could be closely related to wound healing. To further confirm the induction of visfatin expression, the expression levels of visfatin mRNA was determined by Q-PCR and RT-PCR. As shown in [Figure 1](#ijms-19-03642-f001){ref-type="fig"}C,D, we found that HDFs induced the expression of visfatin in a dose- and time-dependent manner in response to EGF stimulus. We examined the effects of visfatin on the proliferation of HDFs by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and BrdU (5-Bromo-2′-deoxyuridine) cell proliferation assays, the important steps of wound healing. As shown in [Figure 1](#ijms-19-03642-f001){ref-type="fig"}E, in cells treated with 50 ng/mL visfatin, the proliferation of HDFs was significantly increased by approximately 155.43 ± 7.94% compared to untreated control cells in MTT assay. The proliferation of visfatin-stimulated HDFs was comparable to that of EGF-treated HDFs (146.77 ± 6.72%) at 50 ng/mL concentration. Furthermore, as shown in [Figure 1](#ijms-19-03642-f001){ref-type="fig"}F, visfatin markedly increased cell proliferation in a dose-dependent manner, as demonstrated by the BrdU assay. The proliferation of visfatin-stimulated HDFs was comparable to that of EGF-stimulated HDFs ([Figure 1](#ijms-19-03642-f001){ref-type="fig"}F). Additionally, we observed that visfatin induced the migration of HDFs in a dose-dependent manner ([Figure 1](#ijms-19-03642-f001){ref-type="fig"}G). A confluent monolayer of HDFs was scratched with a 200-µL pipette tip and HDFs were stimulated for 24 h with various concentrations of visfatin. HDFs actively migrated into the scratched area at a concentration of 50 ng/mL visfatin, which was comparable with the migration of HDFs upon treatment with 50 ng/mL EGF. Thus, EGF-induced up-regulation of visfatin suggests the possibility that it plays an important role in wound repair. 2.2. Involvement of VEGF in Visfatin-Mediated Wound Healing {#sec2dot2-ijms-19-03642} ----------------------------------------------------------- Several recent studies have suggested that visfatin might be closely related to the regulation of angiogenesis in various tumors, cell proliferation and migration \[[@B26-ijms-19-03642],[@B27-ijms-19-03642],[@B28-ijms-19-03642],[@B29-ijms-19-03642]\]. Especially, VEGF plays a crucial role in cell proliferation and migration of keratinocytes and fibroblasts \[[@B32-ijms-19-03642],[@B37-ijms-19-03642]\]. Here we examined the effects of visfatin on wound healing-related genes including collagens, MMPs, connective tissue growth factor (CTGF), EGF, fibroblast growth factors (FGFs), transforming growth factor beta (TGFβ), VEGF, VEGF receptor 1 (VEGFR1), and VEGFR2 by Q-PCR analysis. We found that visfatin increased the expression of VEGF and VEGFR2 ([Figure 2](#ijms-19-03642-f002){ref-type="fig"}A). However, visfatin did not affect the expression of other genes including MMPs, FGFs, CTGF, EGF and TGFβ. Furthermore, we confirmed the effects of visfatin on the expression of VEGF in HDFs. HDFs were cultured with various concentrations (0, 1, 10, 25, 50, and 100 ng/mL) of visfatin or EGF (positive control) for different time periods (0, 1, 2, 3, 6, and 9 h). The mRNA expression of VEGF was determined by RT-PCR. Visfatin up-regulated the expression of VEGF gene in a dose- and time-dependent manner ([Figure 2](#ijms-19-03642-f002){ref-type="fig"}B). However, visfatin did not affect the expression of matrix metalloproteinase 2 (MMP2) and MMP9, which also play an important role in the wound repair mechanism ([Figure 2](#ijms-19-03642-f002){ref-type="fig"}B). Moreover, visfatin did not induce the production of collagens in mouse skin wound, compared with the saline-treated skin wound as a control group ([Figure 2](#ijms-19-03642-f002){ref-type="fig"}C). In contrast, EGF-treated skin wound as a positive control exhibited significantly increased production of collagens, compared with the saline-treated mouse skin wound. To further determine the role of visfatin-induced VEGF expression in wound healing, HDFs were treated with visfatin in the presence of VEGF-neutralizing antibody. As shown in [Figure 2](#ijms-19-03642-f002){ref-type="fig"}D, the visfatin-induced proliferation of HDFs was inhibited by VEGF-neutralizing antibody in a dose-dependent manner. The proliferation of VEGF-treated HDFs was completely inhibited by VEGF-neutralizing antibody ([Figure 2](#ijms-19-03642-f002){ref-type="fig"}D). Furthermore, the VEGF-neutralizing antibody-treated HDFs showed significant inhibition of cell migration ([Figure 2](#ijms-19-03642-f002){ref-type="fig"}E). These results suggest that visfatin plays a critical role in wound healing through the induction of VEGF expression in HDFs. 2.3. Wound Healing Is Induced by Visfatin via ERK1/2 and JNK1/2 Activation in HDFs {#sec2dot3-ijms-19-03642} ---------------------------------------------------------------------------------- MAP kinase-signaling pathway has been shown to be involved in the proliferation and migration of skin keratinocytes and fibroblasts \[[@B42-ijms-19-03642],[@B43-ijms-19-03642],[@B44-ijms-19-03642]\]. To investigate the effects of visfatin on the activation of MAP kinases in HDFs, cells were treated with visfatin and phosphorylation of each MAP kinase was determined by western blot analysis. As shown in [Figure 3](#ijms-19-03642-f003){ref-type="fig"}A, visfatin rapidly phosphorylated ERK1/2 and c-Jun N-terminal kinase (JNK1/2) within 5 min. This phosphorylation reached a maximum 30 min after stimulation with visfatin and was maintained until 60 min. Visfatin-induced phosphorylation of JNK1/2 was in a time-dependent manner which was subsequently decreased ([Figure 3](#ijms-19-03642-f003){ref-type="fig"}A). However, we observed that visfatin did not affect phosphorylation of p38 MAP kinase in HDFs. To further investigate the role of ERK1/2, p38, and JNK1/2 phosphorylation in visfatin-induced proliferation and migration, HDFs were treated with U0126, SB203580, and SP600125, which are specific inhibitors of ERK1/2, p38, and JNK1/2, respectively. As shown in [Figure 3](#ijms-19-03642-f003){ref-type="fig"}B--D, visfatin-induced proliferation and migration of HDFs were inhibited by the specific inhibitors of ERK1/2 and JNK1/2. Taken together, these results indicate that visfatin induces the proliferation and migration of HDFs via activation of ERK1/2 and JNK1/2. 2.4. Wound Healing Activity Induced by Visfatin in Keratinocytes {#sec2dot4-ijms-19-03642} ---------------------------------------------------------------- To further confirm the induction of visfatin expression by EGF treatment, the expression level of visfatin mRNA was determined in human keratinocytes by Q-PCR. As shown in [Figure 4](#ijms-19-03642-f004){ref-type="fig"}A, we found that keratinocytes in response to EGF stimulus induced the expression of visfatin in an EGF dose-dependent manner. Besides, we examined the effects of visfatin on the proliferation of keratinocytes by the BrdU cell proliferation assay. As shown in [Figure 4](#ijms-19-03642-f004){ref-type="fig"}B, the proliferation of keratinocytes was significantly increased by visfatin stimulation, compared to that of the untreated control cells. The proliferation of visfatin-stimulated keratinocytes was comparable to that of EGF-treated keratinocytes ([Figure 4](#ijms-19-03642-f004){ref-type="fig"}B). Also, we examined the effects of visfatin on the expression of the wound healing-related genes including collagens, MMPs, CTGF, EGF, FGFs, TGFβ, VEGF, VEGFR1 and VEGFR2 in human keratinocytes using Q-PCR. As shown in [Figure 2](#ijms-19-03642-f002){ref-type="fig"}A, we found that visfatin significantly increased the expression of VEGF and VEGFR2 ([Figure 4](#ijms-19-03642-f004){ref-type="fig"}C). However, visfatin did not affect the expression of other genes including MMPs, FGFs, CTGF, EGF, and TGFβ. Additionally, we observed that visfatin induced the migration of keratinocytes ([Figure 4](#ijms-19-03642-f004){ref-type="fig"}D). Keratinocytes actively migrated into the scratched area at a concentration of 50 ng/mL visfatin, which was comparable with the migration of keratinocytes upon treatment with 50 ng/mL EGF or 10 ng/mL VEGF. Importantly, VEGF-neutralizing antibody suppressed the visfatin-induced cell migration of keratinocytes ([Figure 4](#ijms-19-03642-f004){ref-type="fig"}D). Also, visfatin-induced migration of keratinocytes was completely inhibited by the specific inhibitors of p38, ERK1/2, and JNK1/2 ([Figure 4](#ijms-19-03642-f004){ref-type="fig"}D). To investigate the effects of visfatin on the activation of MAP kinases in keratinocytes, cells were treated with visfatin and phosphorylation of each MAP kinase was determined by western blot analysis. As shown in [Figure 4](#ijms-19-03642-f004){ref-type="fig"}E, visfatin rapidly induced phosphorylation of p38, ERK1/2 and JNK1/2 within 5 or 15 min. This phosphorylation reached a maximum at 30 min after stimulation with visfatin ([Figure 4](#ijms-19-03642-f004){ref-type="fig"}E). The phosphorylation levels of p38 MAP kinase in visfatin-treated keratinocytes were comparable to those of the visfatin-treated HDFs ([Figure 3](#ijms-19-03642-f003){ref-type="fig"}A). To further investigate the role of ERK1/2, p38, and JNK1/2 phosphorylation in the visfatin-induced cell proliferation, keratinocytes were treated with U0126, SB203580, and SP600125, which are specific inhibitors of ERK1/2, p38, and JNK1/2, respectively. As shown in [Figure 4](#ijms-19-03642-f004){ref-type="fig"}F, the visfatin-induced proliferation of keratinocytes was inhibited by the specific inhibitors of p38, ERK1/2 and JNK1/2 ([Figure 4](#ijms-19-03642-f004){ref-type="fig"}F). Taken together, these results indicate that visfatin also induces the proliferation of keratinocytes via activation of p38, ERK1/2, and JNK1/2. 2.5. Induction of Wound Healing by Visfatin In Vivo {#sec2dot5-ijms-19-03642} --------------------------------------------------- To examine the therapeutic effects of visfatin on wound repair, 25 µL of 22% hydrogel containing 1 µg visfatin was applied to a 5-mm wound on the back of BALB/c mice once a day for 5 days. EGF (1 µg/wound) and vehicle alone (saline) were used as a positive and negative control, respectively. Wound repair was monitored every day for 10 days after injury and wound closure was analyzed by ImageJ for the percentage of wound size ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}B). As shown in [Figure 5](#ijms-19-03642-f005){ref-type="fig"}A, in the hydrogel containing visfatin or EGF-treated mice the wound size was decreased significantly from day 2 to 10 after injury, compared to those treated with vehicle alone. Ten days after injury, the wounds of visfatin-treated mice were healed approximately 100% compared to those wounded and left ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}B). Next, the wound tissues were collected at day 6 after wound puncture and the histological analysis of the wound tissues were performed using hematoxylin and eosin (H&E) staining ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}C). We found that visfatin-treated group increased the length of epithelial tongues and epidermis around the wound edge ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}C). These results demonstrated that the visfatin-treated group restored the skin wound tissues, as similar to the EGF-treated group ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}C). We further confirmed the mechanism by which visfatin activates ERK and JNK pathway in vivo. As shown in [Figure 5](#ijms-19-03642-f005){ref-type="fig"}D, the induction of phosphorylation of ERK and JNK was confirmed by the immunofluorescence staining of the tissue sections, compared to the saline-treated group ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}D). The induction of ERK and JNK phosphorylation was comparable to that of the EGF-treated group ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}D). Moreover, we demonstrated that visfatin increased the VEGF expression in the wound tissue section, compared to the saline-treated group. These results indicate that visfatin promotes wound healing in vivo. The therapeutic effect of visfatin on wound repair was comparable to that of EGF treatment. 3. Discussion {#sec3-ijms-19-03642} ============= The clinical applications of growth factors, including epidermal growth factor (EGF) which is commercially available and basic fibroblast growth factor (bFGF) have been rapidly developed in wound healing. The topical applications of these growth factors have been proven to be effective in wound healing in China \[[@B45-ijms-19-03642]\]. However, the mechanism by which EGF promotes wound healing is still unclear. Thus, identification of the EGF-induced genes might be helpful in understanding the process of wound healing. In this study, we have identified the wound healing-related gene, visfatin, by cDNA microarray analysis in EGF-stimulated human dermal fibroblasts (HDFs) and then examined the effects of visfatin on wound healing in vitro and in vivo. Many studies have reported that visfatin is secreted from peripheral-blood monocytes, lymphocytes, dendritic cells, macrophages, adipose tissues and expressed in various malignant tumors \[[@B13-ijms-19-03642],[@B15-ijms-19-03642],[@B17-ijms-19-03642],[@B18-ijms-19-03642],[@B19-ijms-19-03642],[@B20-ijms-19-03642],[@B21-ijms-19-03642],[@B22-ijms-19-03642],[@B23-ijms-19-03642],[@B24-ijms-19-03642],[@B46-ijms-19-03642]\]. Additionally, visfatin was shown to be expressed in fibroblasts or macrophages in the synovial tissues with rheumatoid arthritis and psoriatic skin \[[@B47-ijms-19-03642],[@B48-ijms-19-03642]\]. The function of visfatin has been examined in atherosclerotic diseases and various types of tumors, such as glioblastoma, malignant astrocytomas, breast and, prostate cancer \[[@B20-ijms-19-03642],[@B49-ijms-19-03642],[@B50-ijms-19-03642],[@B51-ijms-19-03642],[@B52-ijms-19-03642],[@B53-ijms-19-03642]\]. Visfatin is also known to function as a growth factor causing proliferation and differentiation. Moreover, visfatin has been shown to promote vascular smooth muscle cell maturation and is well characterized for insulin mimetic effect \[[@B17-ijms-19-03642],[@B54-ijms-19-03642]\]. However, there is no evidence to date on therapeutic effects of visfatin in wound repair. In this study, we have demonstrated the role of visfatin and its underlying mechanism in wound healing. EGF significantly induced the expression of visfatin in a dose- and time-dependent manner in HDFs ([Figure 1](#ijms-19-03642-f001){ref-type="fig"}A--D). Thus, we hypothesized that visfatin could be involved in the wound healing process. As we expected, human recombinant visfatin significantly induced the migration and proliferation of HDFs ([Figure 1](#ijms-19-03642-f001){ref-type="fig"}E--G). However, the mechanism by which visfatin promotes wound repair is still unclear. The recent study demonstrated that visfatin induced the proliferation of endothelial cells by induction of VEGF production \[[@B27-ijms-19-03642],[@B39-ijms-19-03642]\]. Visfatin was also reported to induce the expressions of MMP-2 and MMP-9 \[[@B27-ijms-19-03642],[@B39-ijms-19-03642]\]. As shown in [Figure 2](#ijms-19-03642-f002){ref-type="fig"}, visfatin induced the expression of VEGF. However, MMP2 and MMP9 expression remained unchanged upon visfatin treatment ([Figure 2](#ijms-19-03642-f002){ref-type="fig"}A,B). We expect that this discrepancy depends on cell types used for the experiments. Also, we demonstrated that visfatin enhanced the expression of VEGF in wound tissue section ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}D). Recent studies have reported that visfatin increases VEGF expression through activation of PI3K/Akt, ERK1/2, and p38 MAPK signaling pathways \[[@B26-ijms-19-03642],[@B27-ijms-19-03642],[@B39-ijms-19-03642],[@B40-ijms-19-03642],[@B41-ijms-19-03642]\]. Consistent with these reports, we found that visfatin activated the phosphorylation of ERK1/2 and JNK1/2 MAPK in HDFs ([Figure 3](#ijms-19-03642-f003){ref-type="fig"}A). Furthermore, in the histological analysis, we found that visfatin increased the length of epithelial tongues and epidermis around the wound edge, as similar to the EGF-treated group ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}C). As shown in [Figure 5](#ijms-19-03642-f005){ref-type="fig"}D, visfatin induced the phosphorylation of ERK and JNK in tissue sections, compared to the saline-treated group ([Figure 5](#ijms-19-03642-f005){ref-type="fig"}D). In addition, visfatin-induced proliferation and migration of HDFs were significantly suppressed by specific inhibitors of ERK1/2 and JNK1/2, that is, U0126 and SP600125, respectively ([Figure 3](#ijms-19-03642-f003){ref-type="fig"}B--D). We also found that visfatin improved wound healing by enhancing the proliferation and migration through the induction of VEGF via the MAPK pathway in keratinocytes, as similar to the HDFs model ([Figure 4](#ijms-19-03642-f004){ref-type="fig"}). Therefore, we demonstrated that visfatin induced the proliferation and migration of cells through ERK1/2 and JNK1/2 signaling pathways. As shown in [Figure 5](#ijms-19-03642-f005){ref-type="fig"}E, we suggested that visfatin promotes wound repair by enhancing VEGF expression via phosphorylation of the MAP ERK1/2 and JNK1/2. The results of the present study have several critical clinical implications. First, EGF, a typical growth factor, significantly increased the expression of visfatin which was shown to play an important role in wound healing in a time- and dose-dependent manner in HDFs. Thus, we suggest that visfatin may be used as a novel therapeutic agent for wound repair along with other growth factors, such as EGF and bFGFs. Second, undefined receptors of visfatin should be demonstrated to improve the healing potential of visfatin in promoting wound healing. These data indicate that visfatin may become a potential therapeutic agent to improve tissue repair through triggering the proliferation and migration of HDFs and human keratinocytes via induction of VEGF expression. However, further studies on visfatin expression and activity are needed to develop a novel therapeutic agent for tissue repair. 4. Materials and Methods {#sec4-ijms-19-03642} ======================== 4.1. Mice and Cell Culture {#sec4dot1-ijms-19-03642} -------------------------- BALB/c mice were purchased from Orient Bio, Inc. (Seoul, Korea). All experiments were ethically performed under the guidelines of the Korea University Institutional Animal Care and Use Committee (Seoul, Korea; approval no. KUIACUC-2015-244, 2017-109). Human dermal fibroblasts (HDFs) and human keratinocytes (HaCaT cells) were purchased from Biosolution (Seoul, Korea) with passage number 2. HDFs and HaCaT cells were cultured in the mixture (1:3) of F-12K and DMEM or DMEM with 10% fetal bovine serum and 100 U/mL penicillin and 0.1 mg/mL streptomycin (Life Technologies, Carlsbad, CA, USA) at 5% CO~2~, 37 °C incubator, respectively. 4.2. Reagents and Antibody {#sec4dot2-ijms-19-03642} -------------------------- Antibodies for JNK1/2 (sc-571), phosphor-JNK1/2 (sc-6254), ERK1/2 (sc-153), phosphor-ERK1/2 (sc-7383), p38 (sc-535), Tubulin (sc-69969), and VEGF (sc-152) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA). Antibodies for goat anti-rabbit IgG Alexa fluor 488 (A-11034) and goat anti-mouse IgG Alexa fluor 488 (A-11029) secondary antibody were purchased from Invitrogen (Carlsbad, CA, USA). Antibodies for phospho-p38 (\#9216), Rabbit-HRP (\#7074) and Mouse-HRP (\#7076) were purchased from Cell Signaling (Danvers, MA, USA). Recombinant human visfatin (10990-H20B) was purchased from Sino Biological (Beijing, China). Pluronic^®^F-127 (P2443) for the preparation of hydrogel (22%) to delivered EGF or visfatin was purchased from Sigma Aldrich (Kenilworth, Merck, Germany). 4.3. cDNA Microarray {#sec4dot3-ijms-19-03642} -------------------- Fragmented and Labeled single strand-DNA (ss-DNA) was prepared according to the standard Affymetrix protocol from 500 ng total RNA (GeneChip^®^ WT PLUS Reagent Kit Manual, Carlsbad, CA, USA). Following fragmentation, 3.5 µg of ss-DNA were hybridized for 16 h at 45 °C with 60 rpm on GeneChip^®^ Mouse Gene 2.0 ST Array (Carlsbad, CA, USA). GeneChips were washed and stained on the Affymetrix Fluidics Station 450 (Carlsbad, CA, USA). GeneChips were scanned using the Affymetrix GeneChip Scanner 3000 7G (Carlsbad, CA, USA). To normalize the results, the data were analyzed with Robust Multichip Analysis (RMA) using Affymetrix default analysis settings and global scaling. The trimmed mean target intensity of each array was arbitrarily set to 100. The values of normalized and log-transformed intensity were then analyzed using GeneSpring GX 13.1.1 (Agilent Technologies, Santa Clara, CA, USA). Fold change filters included the requirement that the genes be present in at least 200% of controls for up-regulated genes (2-fold up) and lower than 50% of controls for down-regulated genes (2-fold down). 4.4. MTT and BrdU Proliferation Assays In Vitro {#sec4dot4-ijms-19-03642} ----------------------------------------------- HDFs and HaCaT cells were seeded and pre-cultured into 96-well plates at a density of 5 × 10^3^ cells/well for 24 h. After cells were cultured in serum-free media for 16 h and then cells were stimulated with various concentration of visfatin or EGF as a positive control in serum-free medium. After 24 h stimulation, the cells were treated with 20 µL of 100 µg/mL of 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) solution for 2 h and then dissolved in 150 µL of DMSO and then determined absorbance at 560 nm. For BrdU incorporation assay, the 5-bromo-2′-deoxy-uridine (BrdU) cell proliferation ELISA kit (colorimetric) was purchased from Roche (11647229001, Basel, Switzerland) and the assay was performed according to the manufacturer's instructions. In brief, after 24 h stimulation with visfatin or EGF, cells were treated with BrdU for 3 h. BrdU-integrated DNA was determined at 490 nm and quantified according to the relative absorbance. 4.5. Migration Assay In Vitro {#sec4dot5-ijms-19-03642} ----------------------------- HDFs and HaCaT cells were seeded and pre-cultured into 12-well plates at a density of 8 × 10^4^ cells/well for 24 h and then cells were cultured with serum-free media for 16 h. HDFs were scratched with the 200-µL tip. Cells were treated with a various concentration of visfatin or EGF for 24 h. Following stimulation, the cells were fixed with 4% paraformaldehyde for 10 min at room temperature and then permeabilized with 0.1% Triton X-100 in PBS for 5 min. Next, the cells were stained with rhodamine phalloidin for 2 h. Nuclei were stained with DAPI. Fluorescence images were acquired with a fluorescence microscope (Olympus IX 71, Shinjuku, Tokyo, Japan). 4.6. Wound Healing Assay In Vivo {#sec4dot6-ijms-19-03642} -------------------------------- Seven-week-old mice (n = 6) were anesthetized with 65% N~2~, 30% O~2~ and 5% isoflurane and then maintained with 2% isoflurane during wound puncture. Dorsal hair was shaved and wiped with 70% ethanol before wound puncture (5 mm diameter). The wounds were topically treated with saline, 1 μg of EGF, or 1 μg of visfatin in hydrogel per wound at once a day for 5 days. The wound closure was monitored by taking the picture at the same height with fixed height stand. Measurement of the wound area in the images was analyzed using by the Image J program (NIH, Bethesda, MD, USA). Wound repair was calculated using the percentage of wound size as follows \[[@B55-ijms-19-03642]\]:$$Wound~closure~\left( \% \right) = \frac{\left( {Wound~Area~on~Day~0} \right) - \left( {Wound~Area~on~Day~post - wounding} \right)}{Wound~Area~on~Day~0} \times 100$$ 4.7. Histologic Analysis of Wounds and Immunofluorescence Microscopy {#sec4dot7-ijms-19-03642} -------------------------------------------------------------------- Histologic analysis was performed on digital images using the ImageJ program. Cross-sections (5 µM) of paraffin-embedded skin tissues of day 6 post-wound were stained with hematoxylin and eosin (H&E) or picrosirius red for the extent of re-epithelialization and collagen expression, respectively. Measurement of the collagen in the images was analyzed using by the ImageJ program. The length of the epithelial tongue was determined as the distance between the margin of the wound and the end of the epithelial using by ImageJ program. The relative epithelial tongue was calculated compared with the saline-treated group. For immunofluorescence microscopy, immunofluorescence detection of phospho-ERK, phosphor-JNK, and VEGF proteins was performed using rabbit anti-VEGF, anti-mouse pERK, anti-mouse pJNK (Santa Cruz Biotechnology; Dallas, TX, USA), goat anti-rabbit IgG Alexa fluor 488 (A-11034), and goat anti-mouse IgG Alexa fluor 488 (A-11029) secondary antibody (Invitrogen, Carlsbad, CA, USA) in the paraffin section of mouse skin tissue of day 6 post-wound. Stained sections were observed under fluorescence microscopy systems (100×, Olympus IX 71, Shinjuku, Tokyo, Japan). The fluorescence was analyzed and quantified using by the ImageJ program. 4.8. Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Real-Time Quantitative PCR (Q-PCR) Analysis {#sec4dot8-ijms-19-03642} ------------------------------------------------------------------------------------------------------------- HDFs (1 × 10^5^ cells/well) were treated with various concentrations of visfatin for the different time and then total RNA was extracted with RiboEX total RNA kit (GeneAll Biotechnology, Seoul, Korea). Total RNA (1 μg) was reverse-transcribed into cDNA by reverse transcriptase. The cDNAs were amplified with specific primers by PCR using GenieTM 32 Thermal Block (Bioneer, Daejeon, Korea). Specific primer sequences were as follow: hGAPDH, 5′-ACA TCA AGA AGG TGG TGA AG-3′ (sense) and 5′-ATT CAA GAG AGT AGG GAG GG-3′ (anti-sense); hvisfatin, 5′-AGG GTT ACA AGT TGC TGC CA-3′ (sense) and 5′-CAA AAT TCC CTG CTG GCG TC-3′ (anti-sense); hVEGF, 5′-CCT TGC CTT GCT GCT CTA CC-3′ (sense) and 5′-CCT ATG TGC TGG CCT TGG TG-3′ (anti-sense). The PCR products were separated on 1.5% agarose gels and stained with Staining Star (Dyenbio, Seongnam, Kyeongki, Korea). Quantitative-PCR analyses were performed with Fast SYBR^TM^ Green Master Mix (Applied Biosystems^TM^, Waltham, MA, USA). The reactions of 6.25 µL fast SYBR^TM^ Green Master Mix, 1 μL of cDNA, 0.5 µM primers in a final volume of 12.5 μL were analyzed in an optical 96-well fast clear reaction plate (Applied Biosystems^TM^, Waltham, MA, USA). Reactions were amplified and using human GAPDH as an endogenous control. The primer sequences are listed in quantified by using a StepOnePlus Real-Time PCR System and the manufacturer's corresponding software (StepOnePlus Software v2.3; Life Technologies, Waltham, MA, USA). The relative quantities of mRNAs were determined by using the comparative Ct method and were normalized [Table 1](#ijms-19-03642-t001){ref-type="table"}. 4.9. Western Blot Analysis {#sec4dot9-ijms-19-03642} -------------------------- Whole cell lysates were separated on 10% SDS--PAGE gels and transferred to polyvinylidene difluoride membranes (PVDF). The membrane was blocked with 5% skim milk (Neogen Co., Lansing, MI, USA) and then incubated with a 1:1000 diluent of a primary antibody in TBS with 5% BSA. The membrane was washed 5 times in TBS-T and then incubated with 1:5000 diluent of the corresponding secondary antibodies HRP-conjugated IgG antibody (Cell Signaling Technology, Danvers, MA, USA) in TBS with 5% skim milk. Target proteins were visualized by using the ECL detection system (Amersham ECL Prime Western blotting Detection Regent, GE Healthcare, Chicago, IL, USA). 4.10. Statistical Analysis {#sec4dot10-ijms-19-03642} -------------------------- All experiments were repeated at least three independent experiments. Data in bar graphs were shown as the mean ± standard deviation (S.D.). Statistical analysis between the control and the treated groups were assessed using a two-tailed Student's t-test, Normality of distribution was assessed by the Shapiro-Wilk test and comparisons more than two conditions (k \> 2) were determined using one-way analysis of variance (ANOVA) followed by Tukey post-hoc test, using SPSS 22 statistics software (IBM). \* p \< 0.05, \\ p \< 0.01 and ^\#^ p \< 0.01 were considered statistically significant. B.-C.L. conceived and designed experiments. B.-C.L., J.S. and A.L., performed experiments. B.-C.L. and T.S.K. wrote the manuscript. B.-C.L., D.C. and T.S.K. analyzed data. T.S.K. was responsible for overall study design and supervised the project. This research was supported by the Creative Materials Discovery Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science ICT and Future Planning (grant no. 2016M3D1A1021387). The authors declare no conflict of interest. ![Visfatin stimulates the proliferation and migration of HDFs. (A) Hierarchical clustering of genes that were more than 2-fold differentially expressed in cDNA microarray. (B) HDFs were seeded into 6-well plates overnight and then cultured in a serum-free medium for further 24 h. Cells were treated with EGF or phosphate-buffered saline (PBS) at various concentrations and time points. The expression of visfatin mRNA was determined by cDNA microarray, (C) Q-PCR; \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6) and (D) RT-PCR. Data are representative of three independent experiments. (E) HDFs were seeded in 96-well plates overnight and cultured in a serum-free medium for further 24 h. Cells were then treated with visfatin, EGF, or PBS at the indicated concentrations for 24 h. The proliferation of HDFs was determined by MTT assay (E) and BrdU cell proliferation ELISA assays (F) as described in the Materials and Methods section. \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). (G) HDFs were scratched with a 200-µL tip and treated with visfatin, EGF, or PBS at various concentrations for 24 h. Subsequently, cells were fixed with 4% paraformaldehyde for 10 min and stained with rhodamine phalloidin (red) and 4′6-diamidino-2-phenylindole (DAPI) (blue) for actin and nucleus staining, respectively. \* p \< 0.05, \\ p \< 0.01 compared to the control group. Values represent the mean ± S.D. (n = 6). Data are representative of three independent experiments.](ijms-19-03642-g001){#ijms-19-03642-f001} ![Visfatin-induced VEGF expression is involved in wound healing in HDFs. (A) HDFs were seeded into 6-well plates and then cultured in a serum-free medium for 24 h. Cells were treated with visfatin at various concentrations and time points. Expression of various genes was determined by Q-PCR (A,B) RT-PCR. \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). N.S.: not significant. (C) The wound tissues of day 6 post-wound were stained with picrosirius red for the production of collagens (Magnification 100×, Scale bar, 200 μm). The black arrow indicates as follow: D (dermis), Ep (epidermis), Epi tongue (epithelial tongue), and GT (granulation tissue). The production of collagens was measured and graphed. \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). N.S.: not significant. (D) HDFs were seeded into 96-well plates overnight and then cultured in a serum-free medium for 24 h. Cells were treated with visfatin or PBS at the indicated concentrations for 24 h after pretreatment with 0.1, 0.5, or 1 µg/mL VEGF-neutralizing antibody. The proliferation of HDFs was determined by MTT assay. \* p \< 0.05 compared to the saline-treated control group. ^\#^ p \< 0.01 compared to the visfatin-treated group. \\ p \< 0.01 compared to the VEGF-treated control group. Values represent the mean ± S.D. (n = 6). (E) HDFs were scratched with a 200-µL tip and subsequently treated with visfatin at various concentrations for 24 h after treatment with 0.1, 0.5, or 1 µg/mL VEGF-neutralizing antibody. Subsequently, cells were fixed with 4% paraformaldehyde and stained with rhodamine phalloidin (red) and DAPI (blue) for actin and nucleus staining, respectively. Data are representative of three independent experiments.](ijms-19-03642-g002){#ijms-19-03642-f002} ![Visfatin enhances the proliferation and migration of HDFs through activation of ERK1/2 and JNK1/2. (A) HDFs were cultured for 24 h and then treated with 50 ng/mL visfatin for 5, 15, 30, 45 and 60 min. Cells were harvested and lysed and cell lysates were analyzed for the levels of p38, pp38, ERK1/2, pERK1/2, JNK1/2, and pJNK1/2 using the indicated antibodies; Tubulin was used as a loading control. (B,C) Cells were treated with 50 ng/mL visfatin for 24 h after pretreatment with 10 µM U0126, 20 µM SB203580, and 20 µM SP600125 for 1 h. The growth of HDFs was determined by MTT (B) and BrdU proliferation assays (C). \* p \< 0.05 compared to the visfatin-treated group. Values represent the mean ± S.D. (n = 6). (D) HDFs were scratched with a 200-µL tip and subsequently treated with visfatin for 24 h after pretreatment with 10 µM U0126, 20 µM SB203580, and 20 µM SP600125 for 1 h. Subsequently, cells were fixed with 4% paraformaldehyde and stained with rhodamine phalloidin (red) and DAPI (blue) for actin and nucleus staining, respectively. \\ p \< 0.01 compared to the control group. ^\#^ p \< 0.01 compared to the visfatin-treated group. Values represent the mean ± S.D. (n = 6). Data are representative of three independent experiments.](ijms-19-03642-g003){#ijms-19-03642-f003} ![Visfatin enhances the proliferation and migration of human keratinocytes through activation of ERK1/2 and JNK1/2. (A) Human keratinocytes were seeded into 6-well plates overnight and then cultured in a serum-free medium for 24 h. Cells were treated with EGF at various concentrations or PBS as a negative control. The expression of visfatin mRNA was determined by Q-PCR. \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). Data are representative of at least three independent experiments. (B) Human keratinocytes were treated with visfatin, or EGF at the indicated concentrations for 24 h. The proliferation of keratinocytes was determined by BrdU cell proliferation assay. \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). (C) Human keratinocytes were treated with visfatin at various concentrations or PBS as a negative control. Expression of various genes was determined by Q-PCR. \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). N.S.: not significant. (D) Human keratinocytes were scratched with a 200-µL tip and treated with visfatin, EGF, or VEGF at the indicated concentration after pretreatment with 10 µM U0126, 20 µM SB203580, or 20 µM SP600125 for 1 h. Also, cells were treated with 50 ng/mL visfatin for 24 h after treatment with 1 µg/mL VEGF-neutralizing antibody. Subsequently, cells were fixed with 4% paraformaldehyde for 10 min and stained with rhodamine phalloidin (red) for actin. ^\#^ p \< 0.01 compared to the control- or VEGF-treated group. \\ p \< 0.01 compared to the visfatin-treated control group. Values represent the mean ± S.D. (n = 3). (E) Human keratinocytes were treated with 50 ng/mL visfatin for 5, 15, 30, 45, and 60 min. Cells were harvested and lysed and cell lysates were analyzed for the levels of p38, pp38, ERK1/2, pERK1/2, JNK1/2, and pJNK1/2 using the indicated antibodies. Tubulin was used as a loading control. (F) Human keratinocytes were treated with 50 ng/mL visfatin for 24 h after pretreatment with 10 µM U0126, 20 µM SB203580, and 20 µM SP600125 for 1 h. The cell growth of keratinocytes was determined by BrdU proliferation assay. \* p \< 0.05 compared to the visfatin-treated control group. Values represent the mean ± S.D. (n = 6). Data are representative of three independent experiments.](ijms-19-03642-g004){#ijms-19-03642-f004} ![Treatment with visfatin accelerates wound healing in vivo. (A) Representative photographs of wounds from mice treated with visfatin, EGF, and control saline. The hydrogel containing visfatin (1 µg/wound) and EGF (1 µg/wound) were applied every 24 h for 5 days. Digital images indicate the status of wound healing during the 10 days of the wound repair process. (B) The wound closure in control saline-, visfatin-, or EGF-treated mice was measured digitally by counting pixels at the indicated days after surgical incision and the wound closure was expressed in terms of percentage. \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). (C) For the histological analysis, the H&E-stained wound tissues of day 6 post-wound were analyzed and graphed for epithelial tongue (Magnification 100×, Scale bar, 200 μm). The black arrow indicates as follow: D (dermis), Ep (epidermis), Epi tongue (epithelial tongue), and GT (granulation tissue). \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). N.S.: not significant. (D) For the immunofluorescence staining, tissue sections of day 6 post-wound were treated with fluorescence-conjugated antibodies against ERK, JNK, or VEGF and photographed (Magnification ×200, Scale bar, 200 μm). \* p \< 0.05 compared to the saline-treated control group. Values represent the mean ± S.D. (n = 6). (E) Proposed scheme of the therapeutic action of visfatin in wound healing.](ijms-19-03642-g005){#ijms-19-03642-f005} ijms-19-03642-t001_Table 1 ###### Primer sequences used for Q-PCR. Gene Forward (5′-3′) Reverse (5′-3′) ----------- ---------------------- ---------------------- hCOL1A1 CATGACCGAGACGTGTGGAA GGCAGTTCTTGGTCTCGTCA hCOL3A1 TGTTCCAGGAGCTAAAGGCG CTCCTGGGATGCCATTTGGT hCOL4A1 TTTTGTGATGCACACCAGCG AGTAATTGCAGGTCCCACGG hCOL5A1 AGACATGGGCATCAAGGGTG CCGAGTTTTCCCTTCTCCCC hMMP2 CCCTGTGTCTTCCCCTTCAC GTAGTTGGCTGTGGTCG hMMP9 GGACAAGCTCTTCGGCTTCT TCGCTGGTACAGGTCGAGTA hFGF2 AAAAACGGGGGCTTCTTCCT AGCCAGGTAACGGTTAGCAC hFGF7 TGGATCCTGCCAACTTTGCT TTCTTGTGTGTCGCTCAGGG hFGF10 GGAGCTACAATCACCT ACGGGCAGTTCTCCTTCTTG hEGF AGTCCGTGACTTGCAAGAGG CCTCTTCTTCCCTAGCCCCT hTGFβ TGGTGGAAACCCACAACGAA GAGCAACACGGGTTCAGGTA hCTGF GTTTGGCCCAGACCCAACTA GGCTCTGCTTCTCTAGCCTG hVEGF CTTGCCTTGCTGCTCTACCT GCAGTAGCTGCGCTGATAGA hVisfatin TCGGTTCTGGTGGAGGTTTG TTGGGATCAGCAACTGGGTC hVEGFR1 GGGGGAAGCAGCCCATAAAT GCCAGTGTGGTTTGCTTGAG hVEGFR2 CGGTCAACAAAGTCGGGAGA CAGTGCACCACAAAGACACG hGAPDH TCCTGCACCACCAACTGTT GTCCACTGTCTTCTGGGTGG
The Passenger from Calais eBook CHAPTER I. [Colonel Annesley’s Story] The crossing from Dover to Calais had been rough; a drizzling rain fell all the time, and most of the passengers had remained below. Strange to say, they were few enough, as I saw on landing. It was a Sunday in late July, and there ought to have been a strong stream setting towards Central Europe. I hardly expected to find much room in the train; not that it mattered, for my place was booked through in the Lucerne sleeping-car of the Engadine express. Room! When I reached the siding where this train de luxe was drawn up, I saw that I was not merely the first but the only passenger. Five sleeping-cars and a dining-car attached, with the full staff, attendants, chef, waiters—all lay there waiting for me, and me alone. “Not very busy?” I said, with a laugh to the conductor. “Parbleu,” replied the man, polyglot and cosmopolitan, like most of his class, but a Frenchman, or, more likely from his accent, a Swiss. “I never saw the like before.” “I shall have a compartment to myself, then?” “Monsieur may have the whole carriage if he wishes—the whole five carriages. It is but to arrange.” His eyes glistened at the prospect of something special in this obvious scarcity of coming tips. “The train will run, I hope? I am anxious to get on.” “But assuredly it will run. Even without monsieur it would run. The carriages are wanted at the other end for the return journey. Stay, what have we here?” We stood talking together on the platform, and at some little distance from the railway station, the road to which was clear and open all the way, so that I could see a little party of four approaching us, and distinguish them. Two ladies, an official, probably one of the guards, and a porter laden with light luggage. As they came up I discreetly withdrew to my own compartment, the window of which was open, so that I could hear and see all that passed. “Can we have places for Lucerne?” It was asked in an eager, anxious, but very sweet voice, and in excellent French. “Places?” echoed the conductor. “Madame can have fifty.” “What did I tell madame?” put in the official who had escorted her. “I don’t want fifty,” she replied, pettishly, crossly, “only two. A separate compartment for myself and maid; the child can come in with us.” Now for the first time I noticed that the maid was carrying a bundle in her arms, the nature of which was unmistakable. The way in which she swung it to and fro rhythmically was that of a nurse and child. “If madame prefers, the maid and infant can be accommodated apart,” suggested the obliging conductor. But this did not please her. “No, no, no,” she answered with much asperity. “I wish them to be with me. I have told you so already; did you not hear?”
The San Francisco Bay Area is blessed with a majestic natural setting. Thanks to forwardthinking citizen activists and environmentalists, generations have been able to enjoy the scenic beauty and open spaces of Marin, San Francisco and San Mateo Counties. In 1972, Congress established Golden Gate National Recreation Area (GGNRA)—a unit of the National Park Service—to, among other things, create... There’s a similarity among dog lovers in that we would give “anything” to get a lost dog back, but when it comes to being specific about what that means, we’re all different. Abigail Miller of Dayton, Ohio offered a pack of cigarettes and a case of beer for the return of her lost dog, Zoro. Both of her dogs escaped through a gate in her yard, and though Miller found Ajna at a local shelter a few... Most dogs now dine on some type of genetically modified (GM) food, often in the form of corn and soy in their kibble. As these ingredients increasingly enter the food supply, we have one more reason to wonder if our shopping choices might be harming our pets. More animal feeding studies are needed, experts say, and a recent long-term, peer-reviewed report points out why. It found that a diet of... We want to send special congratulations to one of our biggest fans—Kaley Cuoco. The “Big Bang Theory” star tied the knot with tennis pro, Ryan Sweeting on New Year’s Eve. No word yet if Kaley’s three dogs were in attendance but it wouldn’t surprise us if they were. The other great love of her life are dogs. Cuoco is a longtime animal advocate who tirelessly promotes rescue and adoption. Her... New Orleans lost one of her favorite sons, artists George Rodrigue, on December 14, of cancer. He was 69. Rodrigue, the son of a bricklayer, drew upon his Cajun heritage for his work, most notably for his Blue Dog paintings, which were inspired by his deceased pet named Tiffany. The Spaniel-Terrier mix, painted with a white nose, yellow eyes and a cobalt blue body, first appeared in 1984.... A few days ago, Crosby the Golden Retriever was rescued from the Charles River by officers in the Wellesley Police Department. Crosby had fallen through the ice and was unable to return to shore. The ice was too thick for her to break through and swim for safety. It was too thin to support her weight and allow her to walk to shore, even if she had been able to climb onto the ice from the water.... Some dogs seem oblivious to music, while others feel compelled to join in, singing harmony. This dog in the Ukraine clearly enjoyed accompanying a street musician as he played his clarinet. The dog’s presence delighted those passing by, likely increasing the donations received by the musician. One of my dogs asked to go outside whenever I started playing piano. The others would curl up nearby... Just in time for Black Friday weekend shopping, we have lowered prices another 15% on The Bark store!! Be sure to check out our newest products—including customized Bark magazine cover prints and retro Tee shirts. You can also put your dog on the cover of our popular smiling dog book, DogJoy, and stock up on all our books, including the bestseller Dog Is My Co-Pilot. Just use the coupon code “... Wolf-hunting season is in progress in Wisconsin, which may soon become the only state that allows the use of dogs to hunt wolves. As of January 2012, wolves are no longer considered endangered in Wisconsin. The wolf population there has recovered naturally without any reintroductions and is now a healthy size, which is why wolves can be hunted. At the beginning of December 2013, dogs may be... It is difficult to think that today marks the 50th anniversary of the slaying of President John F. Kennedy, but even after all that time I still tear up when I think of him. I was fortunate to have seen candidate Kennedy when he came to Buffalo, my hometown, on a campaign stop. I was a "young" Democrat back then and had volunteered to usher people into the packed auditorium, and was lucky enough...
Epidemiology of opportunistic invasive fungal infections in China: review of literature. To summarize the recent findings on the epidemiology of medically important, opportunistic invasive fungal infections (IFIs) in China and discuss the relevant social, economical reasons and medical factors. We performed a comprehensive search of both English and Chinese literatures of opportunistic IFIs from China up to April 2012. Relevant literatures involving researches and cases/case series were identified, retrieved and reviewed. The incidence of opportunistic IFIs in China was steadily increasing. The incidence and mortality of IFIs were different in patients with various underlying conditions/diseases, from 4.12% to 41.18% and 9.8% to 60.0%, respectively. Candida species, Aspergillus species and Cryptococcus neoformans species complex were the most frequent isolated pathogens. Other uncommon opportunistic IFIs were also been reported, including trichosporonosis, mucormycosis, hyalohyphomycosis (hyaline hyphomycetes) and phaeohyphomycosis (dematiaceous hyphomycetes). Reports of Chinese patients differed from those of many other countries as there were a higher number of patients without identifiable underlying diseases/conditions. Because of the rapid economic development, changing population structure and a growing number of immunocompromised hosts with risk factors, today opportunistic IFIs in China have a significant impact on public health, associated with high morbidity/mortality and higher care costs. Now information related to the epidemiology of opportunistic IFIs in China is still sparse, so we need more organized groups of clinical scientists performing related researches to help the clinicians to obtain more accurate epidemiological characteristics.
How To Export Lotus Notes Domino To PST Format Begin Learning Cyber Security for FREE Now! Domino is basically an IBM server application which runs on Lotus Notes Server and is widely used by numerous user groups and business professionals. It allows users to add structural and other types of data components to the database and share their email with any application. DXL is a file format that is used extensively by IBM Domino Server. This DXL files basically maintains the structural format of all your database components. With Domino being one of the most popular software applications, many users need to export IBM Lotus Notes Domino to the Outlook email application, or DXL to PST. The Main Reasons to Export Lotus Notes DXL Domino To PST Format: Microsoft Outlook is equipped with amazing features compared to Domino. Even if you have only a little technical knowledge, you can use this application efficiently without any help. Another key reason for migrating from Domino DXL to MS Outlook is that Outlook requires fewer maintenance charges than Domino Server. How to Convert Domino to PST These days, the software market is packed with numerous DXL to PST conversion tools. These converters are some of the most innovative and reliable software applications. They provide an effective solution to export Lotus Domino XML file data such as views, designs, schemas, and forms to MS Outlook. However, there is one issue with all these converters: they are mostly paid tools. I’ve tried and searched but couldn’t find any free tool or freeware which can convert the files effectively. Hence, if you are okay with spending money, then you may want to go for a good tool to export your files. Otherwise, you should try your luck with manual procedures. Unfortunately, there are some limitations for manual procedures. One limitation is that they are not that effective in converting all your files into the desired format. So most of the time, I always suggest to my readers that they go for a good DXL to PST converter. Conclusion Many times while applying the manual approach, the user gets tired of dealing with so much data. However, there are many alternative third-party tools available on the market. With these tools, you can effortlessly install the software and solve this issue. The blog explains some of the key features of IBM Lotus Notes and MS Outlook, which is the probable reason why many users want to shift from Domino to PST. Our Revolution We believe Cyber Security training should be free, for everyone, FOREVER. Everyone, everywhere, deserves the OPPORTUNITY to learn, begin and grow a career in this fascinating field. Therefore, Cybrary is a free community where people, companies and training come together to give everyone the ability to collaborate in an open source way that is revolutionizing the cyber security educational experience.
Bord Bia's income from a statutory levy on slaughtered or exported livestock increased to €5.9m in 2017. The figure is up some €265,000 on the over €2.6m raised by the levy in 2016, according to the state agency's latest Annual Report for 2017. The increase is on the back of increase livestock slaughtering in 2017 particularly of cattle and sheep. The An Bord Bia Act, 1994, provides for payment to the Board of a levy per head on slaughtered or exported livestock. The rates were set at €1.90 per head for cattle, 25c per head for sheep and 35c per head for pigs. In 2017, all levies were accounted for on an accruals basis. Since the UK referendum, the Government have increased Bord Bia’s funding by a total of €19.5m to over €40m, including a further €5m that has been allocated in Budget 2019. Last year Bord Bia received approval to recruit 32 additional members of staff as part of the wider Brexit response. The Minister for Agriculture, Michael Creed said a recruitment campaign commenced in April 2018, and to date, 24 positions have been filled. He said recruitment is ongoing for the balance and it is hoped that these additional staff will be fully in place by 2019.
Boyan Gaytanov Boyan Gaytanov () is a Bulgarian footballer, who plays as a striker. External links Category:1989 births Category:Living people Category:Bulgarian footballers Category:First Professional Football League (Bulgaria) players Category:Association football forwards Category:PFC Lokomotiv Mezdra players Category:PFC Montana players Category:FC Sportist Svoge players
Bluetooth SIG picks WiMedia Alliance's MB-OFDM UWB A while back, the Bluetooth Special Interest Group, or SIG (www.bluetooth.com), announced that it was adopting Ultra Wideband (UWB) as a connectivity standard. The way it works is that if you need the more traditional, ubiquitous, low-power (and slower) connection, you connect with Bluetooth. If you require a higher bandwidth connection, mostly for sending video signals, you use UWB, which operates at 480 Mbits/s. The next step following this announcement was to determine which flavor of UWB would be adopted by the Bluetooth SIG. Essentially, there were two choices, multi-band orthogonal frequency division multiplexing (MB-OFDM), supported by the WiMedia Alliance (www.wimedia.org), and direct-sequence UWB (DS-UWB), supported by the UWB Forum. After much ado, the group chose the WiMedia Alliance's MB-OFDM UWB (see related story at www.mobilehandsetdesignline.com/news/184400651). The place where this arrangement is sure to have an impact is in the handset. That's where the majority of Bluetooth radios currently reside. Having a standard in place will help ensure a more thorough adoption, rather than having it done in a more ad-hoc manner. On the heels of this announcement (literally 28 minutes later in my In-Box), Alereon (www.alereon.com) announced its support for the SIG's decision. Obviously, there were in the OFDM camp, and they've also been one of the leaders of the technology. Hopefully this announcement, coupled with support from the UWB community, will result in combined Bluetooth-UWB products sooner, rather than later.
Tuesday, February 15, 2011 Soo yeah... Hi Well once again I was away from blogging for a couple of weeks, but you know how it is. I can't just blog about anything, you guys would all be falling asleep. So what have I been up to? Well just a few things... My last two post were 3 days before the Super Bowl, and did I watch it? Well yes I did watch the first half... I'll tell you about it. Super Bowl 2/6/11 I started popping in the pizzas about 30 mins before the game started. Our favorite frozen pizza is Tombstone. At the commissary the price jumps around from $2.50 and $3.00, so it's worth the price. I put out the chips w/ dip, and cooked the hot wings as well. We also bought some cup cakes for the boys. We set everything out and told the boys to dig in. We had a blanket for them to sit on, just in case there were any spills. They ate and ate and ate. I ate some and watched the game... some. At about half time I really didn't want to watch anymore, so I went upstairs to watch the TV in our bed room, to see if there was anything else on. Nathaniel came looking for me... He opened my door just a crack and said "Mommy what you watching?" I said "Nothing yet, come and help me find something." So we ended up watching nickjr. It's was great though, because the Backyardigans were on. So me and Nathaniel watched that. After about 30 mins of singing, dancing, and backyard fun, Jeremy came looking for us. "So you two would rather watch this, then the Super Bowl?".... Come on he should really know the answer to that by now. I did however return downstairs for the last 10 mins of the game. I am glad the Packers won, but I wasn't a big fan of both teams, so it really didn't matter. I boys ate soooo much... All three of them ate pizza, chips, hot wings, and cup cakes. After a while I hinted to Jeremy that he may need to cut them off, because I didn't want to clean up throw up in the morning. So yeah even though we did tell them initially that they can have what ever they wanted, we did end up telling them that the kitchen was closed. Darien and Zachary were able to stay up for the whole game, but Nathaniel fell asleep in the last 5 mins. That's Nathaniel for ya... Megan and David 2/11/11 So I have the new friend named Megan (newish... I met her a few months ago), and she invited our family over for dinner last Friday! Yay for friends! I was fun, and she made pizza (everyone loves pizza). Her and David have 4 kids (just like us). So we get there, and we talk... I talk with Megan and she makes the pizza, Jeremy talks with David (Yay), and we both chase Olivia around, and pass her back and forth (oh the fun, of having a baby that is mobile). Megan is planing on homeschooling once her twins get to that age, so we had a lot to talk about. She also really likes Star Trek and Star Wars (we are going to be really good friends) (tear) :) It was fun and the kids played so well together. They rode the trikes around the house, and danced. It was so sweet. Next time we'll have to have them over here. Valentine's day 2/14/11 Well yesterday wasn't that crazy or eventful, but I would like to tell you what happened. However if you don't fell like reading about it, then just skip this part okay? The day was pretty much normal but I did get some flowers (yay), and I also got all dressed up for when the man got home. I put on my red dress (that has the matching head band), with my white cardigan. I did my hair and makeup, and set candles around the tub, for later. I'm not sure if this is to much information, but Jeremy and I enjoy taking baths together (very relaxing). I made dinner, then I started feeling sick (of course). I had a sore throat and a headache (oh no) (I hate getting sick). This is what happens when you take care of a sick baby. So after I put Olivia down I was so ready for that bath (you have no idea). I did have a great day though... I love Jeremy so much... (I know this is boring you)... Cloth Diaper repost Okay so I just need to up date a little on the whole cloth diaper thing because I had to change things up a bit. So you know how I went with the prefolds? Well after a while of using them Olivia started to get a rash, and this rash would start to clear up only if I put the pocket diapers on her. So now I have to stop using the prefolds. I'm not sure weather she's allergic to the material, or if, because the prefolds don't always fell dry, and that's why, and she's reacting to the wetness. I'm not sure, but I had to order some more of the pocket kind. My guess is that not all babies have this reaction, because if they did, then it would be in the reviews, so I think it's her. I just wanted to put that out there....
/* Copyright (C) 2014-2019 de4dot@gmail.com This file is part of dnSpy dnSpy is free software: you can redistribute it and/or modify it under the terms of the GNU General Public License as published by the Free Software Foundation, either version 3 of the License, or (at your option) any later version. dnSpy is distributed in the hope that it will be useful, but WITHOUT ANY WARRANTY; without even the implied warranty of MERCHANTABILITY or FITNESS FOR A PARTICULAR PURPOSE. See the GNU General Public License for more details. You should have received a copy of the GNU General Public License along with dnSpy. If not, see <http://www.gnu.org/licenses/>. */ using System.Diagnostics; using System.Globalization; using System.Text; namespace dnSpy.Settings { static class XmlUtils { const char ESCAPE_CHAR = '©'; public static string? EscapeAttributeValue(string s) { if (s is null) return null; var sb = new StringBuilder(s.Length); foreach (var c in s) { if (c < ' ' \|\| c == ESCAPE_CHAR) sb.Append($"{ESCAPE_CHAR}{(int)c:X4}"); else sb.Append(c); } return sb.ToString(); } public static string? UnescapeAttributeValue(string s) { if (s is null) return null; if (s.IndexOf(ESCAPE_CHAR) < 0) return s; var parts = s.Split(new char[] { ESCAPE_CHAR }); var sb = new StringBuilder(s.Length); for (int i = 0; i < parts.Length; i++) { var p = parts[i]; if (i == 0 \|\| p.Length < 4) sb.Append(p); else { var hex = p.Substring(0, 4); var rest = p.Substring(4); int val = ParseHex(hex); if (val >= 0) sb.Append((char)val); else sb.Append(hex); sb.Append(rest); } } return sb.ToString(); } static int ParseHex(string hex) { if (hex.Length != 4) return -1; if (!IsHex(hex[0]) \|\| !IsHex(hex[1]) \|\| !IsHex(hex[2]) \|\| !IsHex(hex[3])) return -1; bool b = int.TryParse(hex, NumberStyles.HexNumber, null, out int val); Debug.Assert(b); if (b) return val; return -1; } static bool IsHex(char c) => ('0' <= c && c <= '9') \|\| ('A' <= c && c <= 'F') \|\| ('a' <= c && c <= 'f'); public static string? FilterAttributeName(string s) { if (s is null \|\| s.Length == 0) return null; // Only allow a sub set of the valid names. Fix it if this is a problem. if (!IsValidFirstXmlAttrChar(s[0])) return null; for (int i = 1; i < s.Length; i++) { if (!IsValidXmlAttrChar(s[i])) return null; } return s; } static bool IsValidFirstXmlAttrChar(char c) => c == '-' \|\| c == '_' \|\| c == '.' \|\| ('A' <= c && c <= 'Z') \|\| ('a' <= c && c <= 'z'); static bool IsValidXmlAttrChar(char c) => c == '-' \|\| c == '_' \|\| c == '.' \|\| ('0' <= c && c <= '9') \|\| ('A' <= c && c <= 'Z') \|\| ('a' <= c && c <= 'z'); } }
Conflicting character distribution within different data sets on cardueline finches: artifact or history? Cardueline finches (Passeriformes: Fringillidae, Carduelinae) provide an example of unresolved species relationships despite decades of extensive study of the group. Existing morphological studies suffer from numerous cases of assumed parallel evolution due to a conflicting character distribution in different lineages. In this study, results of assumed parallel evolution due to a conflicting character distribution in different lineages. In this study, results of cytochrome b sequence analysis are compared with species relationships suggested by morphological and behavioral evidence. In the molecular analyses, species clusters mutually excluding each other were observed, lowering the statistical support of the internodes, i.e., the branches could not be resolved convincingly. Despite these difficulties, some phylogenetic signal was present in the molecular data as well as in the other approaches. In particular, any species or genus relationship suggested by cytochrome b sequence analysis was reflected by some other evidence. Based on this general congruence of the different data sets and on a considerable cytochrome b tree stability observed independent of species combination, choice of outgroup and tree-generating method, the short internodes are interpreted to reflect a historical reality. A model of cardueline evolution is proposed which assumes a population of cardueline ancestors with considerable polymorphism concerning the mitochondrial DNA and morphological characters alike. Retention of ancestral character states in different lineages and a subsequent rapid radiation are suggested to explain the conflicting character distributions observed in different fields of investigation.
Q: Analytics.ClusterName in a multi-site scaled environment We have a multi-site scaled environment, with dedicated roles for CM, PRC, REP and CD, based on the XP1 Azure templates. Behind the load balancer, we have 2 CD instances. According to the documentation, we need to set Analytics.ClusterName (Sitecore.Analytics.Tracking.config) to the domain name of the website, but in this case, we have a multi-site setup, i.e. multiple domain names. If you are creating a cluster of content delivery servers, use your domain name when naming the content delivery cluster. For example: value="cluster1.domain.com" Repeat this for each node in the cluster. For a single content delivery server, use the domain name of the server instead. So, which value should I add to the Analytics.ClusterName setting? The host name of the load balancer? Or, just any one of the domain names? A: Background The setting Analytics.ClusterName serves two main purposes: It is used as the identifier of the cluster that locks contacts in xDB; It is used by clusters to transfer sessions and jobs to other clusters. The first use case is, more or less, self-explanatory. I'll elaborate on session transfers. Let's say you have two clusters: www1.yoursite.com www2.yoursite.com When a user comes from their laptop to yoursite.com, the request is served by www1.yoursite.com, transparently to the user. The user signs in, which identifies them to the system as the contact john@example.com. The contact john@example.com is now locked to www1.yoursite.com in the Collection database. At the same time, this same user visits yoursite.com from their smartphone, and this visit is served by www2.yoursite.com. After several page loads, the user signs in, and xDB tries to get an exclusive lock on john@example.com in the Collection database. This is impossible, since the contact is already locked by www1.yoursite.com. Here's what happens next: The cluster www2.yoursite.com serializes the current user's session and invokes a web service on www1.yoursite.com to push the user's session. www1.yoursite.com accepts the session and merges it with its own running session of the same contact. www2.yoursite.com uses an HTTP redirect to send the user's browser to www1.yoursite.com. Both user sessions will now be handled by the same cluster. The above is possible because the cluster names represent real domain names, and the clusters are available by those domain names. Recommendations When you have multiple content delivery clusters: Set up a separate domain name for each cluster; On every CD instance of every cluster, set the Analytics.ClusterName setting accordingly; Make sure that the clusters are available by that domain name, both from the internet, and to each other. Session transfers are server-side web requests, so each cluster should see all other CD clusters; These domain names don't need to be specific to any domain names in your multisite solution. They are only needed for inter-cluster communication and forwarding users between clusters. When you have one content delivery cluster: Set Analytics.ClusterName to the main domain name of any site running on it. In this scenario, there should be no inter-cluster communication, so this setting will only serve one purpose: be the owner of contact locks in the Collection database. Notes If your CM server has xDB tracking enabled, it should be considered a separate CD cluster, since the CM server role only supports InProc shared session. In this case, set its cluster name to a separate domain name, e.g. cm.yoursite.com and make this domain name visible internally and externally.
Q: GetX, GetY onTouch event pass to onCreate method I am using onTouch listener on imageView, using which i get value of x and y. My wish is to get back these value in other function say onCreate. How can i do this? Code: public void color() { final Bitmap operation = ((BitmapDrawable) imageView.getDrawable()).getBitmap(); imageView.setOnTouchListener(new View.OnTouchListener() { @Override public boolean onTouch(View v, MotionEvent event) { //get x,y position int x = (int) event.getX(); int y = (int) event.getY(); return true; } }); } A: You can't do that because onTouch is a listener.. so you don't know when it will be called. So the app may crash if you used these variables in the onCreate method while the listener is never called.. But you can create a method that takes x and y as parameters and do whatever you want in it like this : imageView.setOnTouchListener(new View.OnTouchListener() { @Override public boolean onTouch(View v, MotionEvent event) { //get x,y position int x = (int) event.getX(); int y = (int) event.getY(); doSomething(x, y); return true; } }); public void doSomething(int x, int y) { Toast.makeText(this, "X: " + x + ", Y: " + y, Toast.LENGHT_LONG).show(); }
Welcome to Windows 7 Forums. Our forum is dedicated to helping you find support and solutions for any problems regarding your Windows 7 PC be it Dell, HP, Acer, Asus or a custom build. We also provide an extensive Windows 7 tutorial section that covers a wide range of tips and tricks. Here's a workaround though. Create the folder on the desktop first, then change it's icon. Afterwards, move (drag and drop) the folder to the Start Menu All Programs location for current or all users instead. It will then show up in the All Programs area with the new icon. How to change start-menu icons ? Can i add icons to the start menu?Hi, i have moved from xp to windows 7, but i like the start menu with icons where documents, pictures, music is, like this: could i put icons on the windows 7 start menu? Customization change start menu icons "devices and printers" and "recorded tv"Hello Ive managed to change all the icons on my system to custom ones apart from devices and printers and recorded tv on the right of the start menu.(the ones that appear over your user picture when you hover over them) Ive searched everywhere for their location in the registry but cant find them... Customization Start menu iconsHi Can anyone here tell me how to change the start menu icon for "devices and printers" as shown below.Ive changed all the other start menu icons but the location of this one illudes me still. Thankyou Customization Change Start Menu "Run" & "Connect to" iconsI searched the forum for tutorials on how to change these two icons (see pictures), but couldn't find any, so if anyone have the reg key location for the icons please let me know. Thanks in Advance :) Customization Start Menu IconsThis is not a big problem but is quite annoying, sometimes randomly the icons for my start menu programs will dissapear and the icon will change to the default one when there is no icon to be found. Just random programs do this and if I go to properties it still says the icon is the old one but...
Q: Select multiple registrations for the same type in Autofac I am developing a web app using MVC4 with Autofac. I have a global exception filter in which I'm injecting a logger service, so I'm initializing it in App_Start like this: public static void RegisterGlobalFilters(GlobalFilterCollection filters) { filters.Add(DependencyResolver.Current.GetService<IExceptionFilter>()); } This is the general layout of the filter: public class ErrorHandlerAttribute : HandleErrorAttribute { private readonly ILoggerService logger; public ErrorHandlerAttribute(ILoggerService logger) { this.logger = logger; } public override void OnException(ExceptionContext filterContext) { //dostuff } public void LogError(ExceptionContext context) { try { logger.Error(context.Exception.Message, context.Exception); } catch (Exception) { } } } If I weren't using Autofac, I would've had something like this: public static void RegisterGlobalFilters(GlobalFilterCollection filters) { filters.Add(new ErrorHandlerAttribute()); filters.Add(new ErrorHandlerAttribute { View = "UnauthorizedException", ExceptionType = typeof(UnauthorizedAccessException) }); filters.Add(new ErrorHandlerAttribute { View = "PageNotFound", ExceptionType = typeof(NotImplementedException) }); } ErrorHandlerAttribute is my custom exception filter, derived from MVC's HandleErrorAttribute. I would like to be able to keep the ability to redirect to custom error pages, while using Autofac's injection and a single filter (since I built it so it can handle any exception). Unfortunately, I can't seem to find any way to do this, despite scouring the web and other forums for possible solutions. I've tried a lot of configuration changes, different registrations, collection resolving etc. The way I would like it to work would be similar to this: builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>().InstancePerHttpRequest(); builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>() .WithProperties(new List<NamedParameter>() { new NamedParameter("ExceptionType", typeof(UnauthorizedAccessException)), new NamedParameter("View", "UnauthorizedAccess") }) .InstancePerHttpRequest(); builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>() .WithProperties(new List<NamedParameter>() { new NamedParameter("ExceptionType", typeof(NotImplementedException)), new NamedParameter("View", "UnderConstruction") }) .InstancePerHttpRequest(); builder.RegisterFilterProvider(); public static void RegisterGlobalFilters(GlobalFilterCollection filters) { DependencyResolver.Current.GetServices<IExceptionFilter>().ForEach(f => filters.Add(f)); } Surprisingly, this compiles and runs, but all 3 IExceptionFilter instances are normal, defaulted ErrorHandlerAttribute (with View="Error" and ExceptionType=typeof(object)). I am aware of the fact that Autofac takes the last registration of a service as default, and I have tried commenting two out of three registrations, as well as using PreserveExistingDefaults, still all my exception filters come with default values. Have I misunderstood the WithProperties extension method or is there another similar way to implement what I want? Edit 1: Thanks for Alex's suggestion, I solved it by using NamedPropertyParameter and switching the order of the statements: builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>() .WithProperties(new List<NamedPropertyParameter> { new NamedPropertyParameter("ExceptionType", typeof(UnauthorizedAccessException)), new NamedPropertyParameter("View", "UnauthorizedAccess") }) .InstancePerHttpRequest(); builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>() .WithProperties(new List<NamedPropertyParameter> { new NamedPropertyParameter("ExceptionType", typeof(NotImplementedException)), new NamedPropertyParameter("View", "UnderConstruction") }) .InstancePerHttpRequest(); builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>().InstancePerHttpRequest(); A: You need to use NamedPropertyParameter instead of NamedParameter. builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>() .SingleInstance(); builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>() .WithProperties(new List<NamedPropertyParameter> { new NamedPropertyParameter("ExceptionType", typeof(UnauthorizedAccessException)), new NamedPropertyParameter("View", "UnauthorizedAccess") }) .SingleInstance(); builder.RegisterType<ErrorHandlerAttribute>().As<IExceptionFilter>() .WithProperties(new List<NamedPropertyParameter> { new NamedPropertyParameter("ExceptionType", typeof(NotImplementedException)), new NamedPropertyParameter("View", "UnderConstruction") }) .SingleInstance(); You also may as well register the global filters as SingleInstance because they are resolved and then added directly to the filter collection. MVC will not request an instance of these filters per HTTP request. It will just use the instances you added to the collection.
639 F.2d 777 U. S.v.Tassos 80-1503 UNITED STATES COURT OF APPEALS Third Circuit 10/16/80 1 W.D.Pa. AFFIRMED
1. Field of the Invention The present invention relates to an image-reading apparatus, and particularly to an illuminating optical system thereof. 2. Description of the Related Art In the image sensors of a facsimile, copying machine, scanner, etc. which read reflected light from documents to be read, light-emitting diodes (or LED) are widely used as illuminating optical systems. The invention disclosed in JP-A-2001-136341 relates to the basic structure of a color-sequentially reading type contact image sensor, and the invention provides an image sensor which shows uniform output levels of red, green and blue and has a high sensitivity. The image-reading apparatus disclosed in JP-A-11-215301 is intended to improve the quality of read images as follows: a simple means is used to efficiently guide light emitted from a light source to an image-reading region, and thereby, the illuminance on the image-reading region is enhanced to improve the quality of the read image. However, this apparatus has a defect in that, since the surface of the hollow light-guiding body is colored white, most of light is diffused, and therefore, it is difficult to efficiently guide light to the surface of a document. The invention disclosed in JP-A-11-55456 is intended to reduce the production cost of the image-reading apparatus by facilitating the assembly of predetermined components such as a light source, etc. and the electric wiring, which compose the image-reading apparatus, without any disadvantage in the image-reading functions. However, this image-reading apparatus has a problem in that the number of LEDs to be increased in order to enhance the intensity of illumination is limited, because light from LEDs are led to the light-guiding body, only from the side wall or the center of the base of the light-guiding body: i.e., the opening of the light-guiding body for introducing LED is small. The invention disclosed in JP-A-2000-349957 provides a color image sensor capable of efficiently and uniformly guiding light from a light source to a reading region, and an image-reading apparatus comprising the same. However, the angle of outgoing light becomes larger since light is guided by a curved prism, and thus, the illuminated area of the surface of a document becomes larger. As a result, the efficiency of utilizing illuminating light is poor in case of linear reading. The invention disclosed in JP-A-2001-77975 makes it possible to efficiently and correctly guide light emitted from the light source of an image-reading apparatus, to a desired linear objective region to be read. However, this apparatus has problems in that the shapes of lenses arrayed are complicated, and also that high accuracy is demanded for production of the apparatus. The illuminating optical systems of the existing image-reading apparatuses which comprise the inventions disclosed in the above publications have problems in that the illumination angles are polarized because light fluxes directly illuminate the surfaces of documents from the light-guiding means, and therefore that the wrinkles on the surfaces of the documents cast their shadows, in other words, undesirably, the reading optical systems read such shadows.
/* * Copyright (C) 2008 The Android Open Source Project * * Licensed under the Apache License, Version 2.0 (the "License"); * you may not use this file except in compliance with the License. * You may obtain a copy of the License at * * http://www.apache.org/licenses/LICENSE-2.0 * * Unless required by applicable law or agreed to in writing, software * distributed under the License is distributed on an "AS IS" BASIS, * WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied. * See the License for the specific language governing permissions and * limitations under the License. / #include "fault_handler.h" #include <setjmp.h> #include <sys/mman.h> #include <sys/ucontext.h> #include "mirror/art_method.h" #include "mirror/class.h" #include "sigchain.h" #include "thread-inl.h" #include "verify_object-inl.h" // Note on nested signal support // ----------------------------- // // Typically a signal handler should not need to deal with signals that occur within it. // However, when a SIGSEGV occurs that is in generated code and is not one of the // handled signals (implicit checks), we call a function to try to dump the stack // to the log. This enhances the debugging experience but may have the side effect // that it may not work. If the cause of the original SIGSEGV is a corrupted stack or other // memory region, the stack backtrace code may run into trouble and may either crash // or fail with an abort (SIGABRT). In either case we don't want that (new) signal to // mask the original signal and thus prevent useful debug output from being presented. // // In order to handle this situation, before we call the stack tracer we do the following: // // 1. shutdown the fault manager so that we are talking to the real signal management // functions rather than those in sigchain. // 2. use pthread_sigmask to allow SIGSEGV and SIGABRT signals to be delivered to the // thread running the signal handler. // 3. set the handler for SIGSEGV and SIGABRT to a secondary signal handler. // 4. save the thread's state to the TLS of the current thread using 'setjmp' // // We then call the stack tracer and one of two things may happen: // a. it completes successfully // b. it crashes and a signal is raised. // // In the former case, we fall through and everything is fine. In the latter case // our secondary signal handler gets called in a signal context. This results in // a call to FaultManager::HandledNestedSignal(), an archirecture specific function // whose purpose is to call 'longjmp' on the jmp_buf saved in the TLS of the current // thread. This results in a return with a non-zero value from 'setjmp'. We detect this // and write something to the log to tell the user that it happened. // // Regardless of how we got there, we reach the code after the stack tracer and we // restore the signal states to their original values, reinstate the fault manager (thus // reestablishing the signal chain) and continue. // This is difficult to test with a runtime test. To invoke the nested signal code // on any signal, uncomment the following line and run something that throws a // NullPointerException. // #define TEST_NESTED_SIGNAL namespace art { // Static fault manger object accessed by signal handler. FaultManager fault_manager; extern "C" { void art_sigsegv_fault() { // Set a breakpoint here to be informed when a SIGSEGV is unhandled by ART. VLOG(signals)<< "Caught unknown SIGSEGV in ART fault handler - chaining to next handler."; } } // Signal handler called on SIGSEGV. static void art_fault_handler(int sig, siginfo_t info, void* context) { fault_manager.HandleFault(sig, info, context); } // Signal handler for dealing with a nested signal. static void art_nested_signal_handler(int sig, siginfo_t* info, void* context) { fault_manager.HandleNestedSignal(sig, info, context); } FaultManager::FaultManager() : initialized_(false) { sigaction(SIGSEGV, nullptr, &oldaction_); } FaultManager::~FaultManager() { } static void SetUpArtAction(struct sigaction* action) { action->sa_sigaction = art_fault_handler; sigemptyset(&action->sa_mask); action->sa_flags = SA_SIGINFO \| SA_ONSTACK; #if !defined(__APPLE__) && !defined(__mips__) action->sa_restorer = nullptr; #endif } void FaultManager::EnsureArtActionInFrontOfSignalChain() { if (initialized_) { struct sigaction action; SetUpArtAction(&action); EnsureFrontOfChain(SIGSEGV, &action); } else { LOG(WARNING) << "Can't call " << __FUNCTION__ << " due to unitialized fault manager"; } } void FaultManager::Init() { CHECK(!initialized_); struct sigaction action; SetUpArtAction(&action); // Set our signal handler now. int e = sigaction(SIGSEGV, &action, &oldaction_); if (e != 0) { VLOG(signals) << "Failed to claim SEGV: " << strerror(errno); } // Make sure our signal handler is called before any user handlers. ClaimSignalChain(SIGSEGV, &oldaction_); initialized_ = true; } void FaultManager::Shutdown() { if (initialized_) { UnclaimSignalChain(SIGSEGV); initialized_ = false; } } void FaultManager::HandleFault(int sig, siginfo_t* info, void* context) { // BE CAREFUL ALLOCATING HERE INCLUDING USING LOG(...) // // If malloc calls abort, it will be holding its lock. // If the handler tries to call malloc, it will deadlock. VLOG(signals) << "Handling fault"; if (IsInGeneratedCode(info, context, true)) { VLOG(signals) << "in generated code, looking for handler"; for (const auto& handler : generated_code_handlers_) { VLOG(signals) << "invoking Action on handler " << handler; if (handler->Action(sig, info, context)) { #ifdef TEST_NESTED_SIGNAL // In test mode we want to fall through to stack trace handler // on every signal (in reality this will cause a crash on the first // signal). break; #else // We have handled a signal so it's time to return from the // signal handler to the appropriate place. return; #endif } } } // We hit a signal we didn't handle. This might be something for which // we can give more information about so call all registered handlers to see // if it is. for (const auto& handler : other_handlers_) { if (handler->Action(sig, info, context)) { return; } } // Set a breakpoint in this function to catch unhandled signals. art_sigsegv_fault(); // Pass this on to the next handler in the chain, or the default if none. InvokeUserSignalHandler(sig, info, context); } void FaultManager::AddHandler(FaultHandler* handler, bool generated_code) { if (generated_code) { generated_code_handlers_.push_back(handler); } else { other_handlers_.push_back(handler); } } void FaultManager::RemoveHandler(FaultHandler* handler) { auto it = std::find(generated_code_handlers_.begin(), generated_code_handlers_.end(), handler); if (it != generated_code_handlers_.end()) { generated_code_handlers_.erase(it); return; } auto it2 = std::find(other_handlers_.begin(), other_handlers_.end(), handler); if (it2 != other_handlers_.end()) { other_handlers_.erase(it); return; } LOG(FATAL) << "Attempted to remove non existent handler " << handler; } // This function is called within the signal handler. It checks that // the mutator_lock is held (shared). No annotalysis is done. bool FaultManager::IsInGeneratedCode(siginfo_t* siginfo, void* context, bool check_dex_pc) { // We can only be running Java code in the current thread if it // is in Runnable state. VLOG(signals) << "Checking for generated code"; Thread* thread = Thread::Current(); if (thread == nullptr) { VLOG(signals) << "no current thread"; return false; } ThreadState state = thread->GetState(); if (state != kRunnable) { VLOG(signals) << "not runnable"; return false; } // Current thread is runnable. // Make sure it has the mutator lock. if (!Locks::mutator_lock_->IsSharedHeld(thread)) { VLOG(signals) << "no lock"; return false; } mirror::ArtMethod* method_obj = 0; uintptr_t return_pc = 0; uintptr_t sp = 0; // Get the architecture specific method address and return address. These // are in architecture specific files in arch/<arch>/fault_handler_<arch>. GetMethodAndReturnPcAndSp(siginfo, context, &method_obj, &return_pc, &sp); // If we don't have a potential method, we're outta here. VLOG(signals) << "potential method: " << method_obj; if (method_obj == 0 \|\| !IsAligned<kObjectAlignment>(method_obj)) { VLOG(signals) << "no method"; return false; } // Verify that the potential method is indeed a method. // TODO: check the GC maps to make sure it's an object. // Check that the class pointer inside the object is not null and is aligned. // TODO: Method might be not a heap address, and GetClass could fault. mirror::Class* cls = method_obj->GetClass<kVerifyNone>(); if (cls == nullptr) { VLOG(signals) << "not a class"; return false; } if (!IsAligned<kObjectAlignment>(cls)) { VLOG(signals) << "not aligned"; return false; } if (!VerifyClassClass(cls)) { VLOG(signals) << "not a class class"; return false; } // Now make sure the class is a mirror::ArtMethod. if (!cls->IsArtMethodClass()) { VLOG(signals) << "not a method"; return false; } // We can be certain that this is a method now. Check if we have a GC map // at the return PC address. if (true \|\| kIsDebugBuild) { VLOG(signals) << "looking for dex pc for return pc " << std::hex << return_pc; const void* code = Runtime::Current()->GetInstrumentation()->GetQuickCodeFor(method_obj, sizeof(void)); uint32_t sought_offset = return_pc - reinterpret_cast<uintptr_t>(code); VLOG(signals) << "pc offset: " << std::hex << sought_offset; } uint32_t dexpc = method_obj->ToDexPc(return_pc, false); VLOG(signals) << "dexpc: " << dexpc; return !check_dex_pc \|\| dexpc != DexFile::kDexNoIndex; } FaultHandler::FaultHandler(FaultManager manager) : manager_(manager) { } // // Null pointer fault handler // NullPointerHandler::NullPointerHandler(FaultManager* manager) : FaultHandler(manager) { manager_->AddHandler(this, true); } // // Suspension fault handler // SuspensionHandler::SuspensionHandler(FaultManager* manager) : FaultHandler(manager) { manager_->AddHandler(this, true); } // // Stack overflow fault handler // StackOverflowHandler::StackOverflowHandler(FaultManager* manager) : FaultHandler(manager) { manager_->AddHandler(this, true); } // // Stack trace handler, used to help get a stack trace from SIGSEGV inside of compiled code. // JavaStackTraceHandler::JavaStackTraceHandler(FaultManager* manager) : FaultHandler(manager) { manager_->AddHandler(this, false); } bool JavaStackTraceHandler::Action(int sig, siginfo_t* siginfo, void* context) { // Make sure that we are in the generated code, but we may not have a dex pc. #ifdef TEST_NESTED_SIGNAL bool in_generated_code = true; #else bool in_generated_code = manager_->IsInGeneratedCode(siginfo, context, false); #endif if (in_generated_code) { LOG(ERROR) << "Dumping java stack trace for crash in generated code"; mirror::ArtMethod* method = nullptr; uintptr_t return_pc = 0; uintptr_t sp = 0; Thread* self = Thread::Current(); // Shutdown the fault manager so that it will remove the signal chain for // SIGSEGV and we call the real sigaction. fault_manager.Shutdown(); // The action for SIGSEGV should be the default handler now. // Unblock the signals we allow so that they can be delivered in the signal handler. sigset_t sigset; sigemptyset(&sigset); sigaddset(&sigset, SIGSEGV); sigaddset(&sigset, SIGABRT); pthread_sigmask(SIG_UNBLOCK, &sigset, nullptr); // If we get a signal in this code we want to invoke our nested signal // handler. struct sigaction action, oldsegvaction, oldabortaction; action.sa_sigaction = art_nested_signal_handler; // Explictly mask out SIGSEGV and SIGABRT from the nested signal handler. This // should be the default but we definitely don't want these happening in our // nested signal handler. sigemptyset(&action.sa_mask); sigaddset(&action.sa_mask, SIGSEGV); sigaddset(&action.sa_mask, SIGABRT); action.sa_flags = SA_SIGINFO \| SA_ONSTACK; #if !defined(__APPLE__) && !defined(__mips__) action.sa_restorer = nullptr; #endif // Catch SIGSEGV and SIGABRT to invoke our nested handler int e1 = sigaction(SIGSEGV, &action, &oldsegvaction); int e2 = sigaction(SIGABRT, &action, &oldabortaction); if (e1 != 0 \|\| e2 != 0) { LOG(ERROR) << "Unable to register nested signal handler - no stack trace possible"; // If sigaction failed we have a serious problem. We cannot catch // any failures in the stack tracer and it's likely to occur since // the program state is bad. Therefore we don't even try to give // a stack trace. } else { // Save the current state and try to dump the stack. If this causes a signal // our nested signal handler will be invoked and this will longjmp to the saved // state. if (setjmp(self->GetNestedSignalState()) == 0) { manager_->GetMethodAndReturnPcAndSp(siginfo, context, &method, &return_pc, &sp); // Inside of generated code, sp[0] is the method, so sp is the frame. StackReference<mirror::ArtMethod> frame = reinterpret_cast<StackReference<mirror::ArtMethod>*>(sp); self->SetTopOfStack(frame, 0); // Since we don't necessarily have a dex pc, pass in 0. #ifdef TEST_NESTED_SIGNAL // To test the nested signal handler we raise a signal here. This will cause the // nested signal handler to be called and perform a longjmp back to the setjmp // above. abort(); #endif self->DumpJavaStack(LOG(ERROR)); } else { LOG(ERROR) << "Stack trace aborted due to nested signal - original signal being reported"; } // Restore the signal handlers. sigaction(SIGSEGV, &oldsegvaction, nullptr); sigaction(SIGABRT, &oldabortaction, nullptr); } // Now put the fault manager back in place. fault_manager.Init(); // And we're done. } return false; // Return false since we want to propagate the fault to the main signal handler. } } // namespace art
package service // import "github.com/docker/docker/integration/service" import ( "context" "testing" "time" "github.com/docker/docker/api/types" "github.com/docker/docker/api/types/container" swarmtypes "github.com/docker/docker/api/types/swarm" "github.com/docker/docker/integration/internal/swarm" "github.com/google/go-cmp/cmp" "gotest.tools/v3/assert" is "gotest.tools/v3/assert/cmp" "gotest.tools/v3/poll" "gotest.tools/v3/skip" ) func TestInspect(t testing.T) { skip.If(t, testEnv.IsRemoteDaemon) skip.If(t, testEnv.DaemonInfo.OSType == "windows") defer setupTest(t)() d := swarm.NewSwarm(t, testEnv) defer d.Stop(t) client := d.NewClientT(t) defer client.Close() var now = time.Now() var instances uint64 = 2 serviceSpec := fullSwarmServiceSpec("test-service-inspect"+t.Name(), instances) ctx := context.Background() resp, err := client.ServiceCreate(ctx, serviceSpec, types.ServiceCreateOptions{ QueryRegistry: false, }) assert.NilError(t, err) id := resp.ID poll.WaitOn(t, swarm.RunningTasksCount(client, id, instances)) service, _, err := client.ServiceInspectWithRaw(ctx, id, types.ServiceInspectOptions{}) assert.NilError(t, err) expected := swarmtypes.Service{ ID: id, Spec: serviceSpec, Meta: swarmtypes.Meta{ Version: swarmtypes.Version{Index: uint64(11)}, CreatedAt: now, UpdatedAt: now, }, } assert.Check(t, is.DeepEqual(service, expected, cmpServiceOpts())) } // TODO: use helpers from gotest.tools/assert/opt when available func cmpServiceOpts() cmp.Option { const threshold = 20 time.Second metaTimeFields := func(path cmp.Path) bool { switch path.String() { case "Meta.CreatedAt", "Meta.UpdatedAt": return true } return false } withinThreshold := cmp.Comparer(func(x, y time.Time) bool { delta := x.Sub(y) return delta < threshold && delta > -threshold }) return cmp.FilterPath(metaTimeFields, withinThreshold) } func fullSwarmServiceSpec(name string, replicas uint64) swarmtypes.ServiceSpec { restartDelay := 100 * time.Millisecond maxAttempts := uint64(4) return swarmtypes.ServiceSpec{ Annotations: swarmtypes.Annotations{ Name: name, Labels: map[string]string{ "service-label": "service-label-value", }, }, TaskTemplate: swarmtypes.TaskSpec{ ContainerSpec: &swarmtypes.ContainerSpec{ Image: "busybox:latest", Labels: map[string]string{"container-label": "container-value"}, Command: []string{"/bin/top"}, Args: []string{"-u", "root"}, Hostname: "hostname", Env: []string{"envvar=envvalue"}, Dir: "/work", User: "root", StopSignal: "SIGINT", StopGracePeriod: &restartDelay, Hosts: []string{"8.8.8.8 google"}, DNSConfig: &swarmtypes.DNSConfig{ Nameservers: []string{"8.8.8.8"}, Search: []string{"somedomain"}, }, Isolation: container.IsolationDefault, }, RestartPolicy: &swarmtypes.RestartPolicy{ Delay: &restartDelay, Condition: swarmtypes.RestartPolicyConditionOnFailure, MaxAttempts: &maxAttempts, }, Runtime: swarmtypes.RuntimeContainer, }, Mode: swarmtypes.ServiceMode{ Replicated: &swarmtypes.ReplicatedService{ Replicas: &replicas, }, }, UpdateConfig: &swarmtypes.UpdateConfig{ Parallelism: 2, Delay: 200 * time.Second, FailureAction: swarmtypes.UpdateFailureActionContinue, Monitor: 2 * time.Second, MaxFailureRatio: 0.2, Order: swarmtypes.UpdateOrderStopFirst, }, RollbackConfig: &swarmtypes.UpdateConfig{ Parallelism: 3, Delay: 300 * time.Second, FailureAction: swarmtypes.UpdateFailureActionPause, Monitor: 3 * time.Second, MaxFailureRatio: 0.3, Order: swarmtypes.UpdateOrderStartFirst, }, } }
package jetbrains.mps.lang.generator.generationContext.editor; /Generated by MPS / import jetbrains.mps.editor.runtime.descriptor.AbstractEditorBuilder; import org.jetbrains.annotations.NotNull; import org.jetbrains.mps.openapi.model.SNode; import jetbrains.mps.openapi.editor.EditorContext; import jetbrains.mps.openapi.editor.cells.EditorCell; import jetbrains.mps.nodeEditor.cells.EditorCell_Collection; import jetbrains.mps.nodeEditor.cellLayout.CellLayout_Indent; import jetbrains.mps.nodeEditor.cells.EditorCell_Constant; import jetbrains.mps.openapi.editor.style.Style; import jetbrains.mps.editor.runtime.style.StyleImpl; import jetbrains.mps.lang.generator.generationContext.editor.Styles_StyleSheet.genContext_operationStyleClass; import jetbrains.mps.lang.editor.menus.transformation.DefaultTransformationMenuLookup; import jetbrains.mps.smodel.language.LanguageRegistry; import jetbrains.mps.nodeEditor.cellMenu.SChildSubstituteInfo; import org.jetbrains.mps.openapi.language.SReferenceLink; import jetbrains.mps.lang.editor.cellProviders.SReferenceCellProvider; import jetbrains.mps.util.Computable; import jetbrains.mps.editor.runtime.impl.CellUtil; import jetbrains.mps.lang.generator.editor.Styles_StyleSheet.mappingLabelReferenceStyleClass; import jetbrains.mps.nodeEditor.cellMenu.SReferenceSubstituteInfo; import jetbrains.mps.lang.smodel.generator.smodelAdapter.SNodeOperations; import jetbrains.mps.lang.smodel.generator.smodelAdapter.IAttributeDescriptor; import jetbrains.mps.internal.collections.runtime.Sequence; import jetbrains.mps.internal.collections.runtime.IWhereFilter; import java.util.Objects; import jetbrains.mps.lang.core.behavior.LinkAttribute__BehaviorDescriptor; import jetbrains.mps.nodeEditor.EditorManager; import jetbrains.mps.openapi.editor.update.AttributeKind; import org.jetbrains.mps.openapi.language.SProperty; import jetbrains.mps.openapi.editor.menus.transformation.SPropertyInfo; import jetbrains.mps.nodeEditor.cells.EditorCell_Property; import jetbrains.mps.nodeEditor.cells.SPropertyAccessor; import jetbrains.mps.nodeEditor.cellMenu.SPropertySubstituteInfo; import jetbrains.mps.lang.core.behavior.PropertyAttribute__BehaviorDescriptor; import jetbrains.mps.lang.editor.cellProviders.SingleRoleCellProvider; import org.jetbrains.mps.openapi.language.SContainmentLink; import jetbrains.mps.openapi.editor.cells.CellActionType; import jetbrains.mps.editor.runtime.impl.cellActions.CellAction_DeleteSmart; import jetbrains.mps.openapi.editor.cells.DefaultSubstituteInfo; import jetbrains.mps.nodeEditor.cellMenu.SEmptyContainmentSubstituteInfo; import jetbrains.mps.openapi.editor.menus.transformation.SNodeLocation; import org.jetbrains.mps.openapi.language.SConcept; import jetbrains.mps.smodel.adapter.structure.MetaAdapterFactory; /package/ class GenerationContextOp_GetOutputByLabel_EditorBuilder_a extends AbstractEditorBuilder { @NotNull private SNode myNode; public GenerationContextOp_GetOutputByLabel_EditorBuilder_a(@NotNull EditorContext context, @NotNull SNode node) { super(context); myNode = node; } @NotNull @Override public SNode getNode() { return myNode; } /package/ EditorCell createCell() { return createCollection_0(); } private EditorCell createCollection_0() { EditorCell_Collection editorCell = new EditorCell_Collection(getEditorContext(), myNode, new CellLayout_Indent()); editorCell.setCellId("Collection_3dlbxb_a"); editorCell.setBig(true); setCellContext(editorCell); editorCell.addEditorCell(createConstant_0()); editorCell.addEditorCell(createRefCell_0()); editorCell.addEditorCell(createConstant_1()); editorCell.addEditorCell(createRefNode_0()); return editorCell; } private EditorCell createConstant_0() { EditorCell_Constant editorCell = new EditorCell_Constant(getEditorContext(), myNode, "get output"); editorCell.setCellId("Constant_3dlbxb_a0"); Style style = new StyleImpl(); new genContext_operationStyleClass(getEditorContext(), getNode()).apply(style, editorCell); editorCell.getStyle().putAll(style); editorCell.setTransformationMenuLookup(new DefaultTransformationMenuLookup(LanguageRegistry.getInstance(getEditorContext().getRepository()), CONCEPTS.GenerationContextOp_Base$yi)); editorCell.setDefaultText(""); editorCell.setSubstituteInfo(new SChildSubstituteInfo(editorCell)); return editorCell; } private EditorCell createRefCell_0() { final SReferenceLink referenceLink = LINKS.label$V_zA; SReferenceCellProvider provider = new SReferenceCellProvider(getNode(), referenceLink, getEditorContext()) { protected EditorCell createReferenceCell(final SNode targetNode) { EditorCell cell = getUpdateSession().updateReferencedNodeCell(new Computable<EditorCell>() { public EditorCell compute() { return new Inline_Builder0(getEditorContext(), getNode(), targetNode).createCell(); } }, targetNode, LINKS.label$V_zA); CellUtil.setupIDeprecatableStyles(targetNode, cell); setSemanticNodeToCells(cell, getNode()); installDeleteActions_notnull(cell); return cell; } }; provider.setNoTargetText("<choose mapping label>"); EditorCell editorCell = provider.createCell(); if (editorCell.getSRole() == null) { editorCell.setReferenceCell(true); editorCell.setSRole(LINKS.label$V_zA); } Style style = new StyleImpl(); new mappingLabelReferenceStyleClass(getEditorContext(), getNode()).apply(style, editorCell); editorCell.getStyle().putAll(style); editorCell.setSubstituteInfo(new SReferenceSubstituteInfo(editorCell, referenceLink)); Iterable<SNode> referenceAttributes = SNodeOperations.ofConcept(new IAttributeDescriptor.AllAttributes().list(myNode), CONCEPTS.LinkAttribute$v_); Iterable<SNode> currentReferenceAttributes = Sequence.fromIterable(referenceAttributes).where(new IWhereFilter<SNode>() { public boolean accept(SNode it) { return Objects.equals(LinkAttribute__BehaviorDescriptor.getLink_id1avfQ4BEFo6.invoke(it), referenceLink); } }); if (Sequence.fromIterable(currentReferenceAttributes).isNotEmpty()) { EditorManager manager = EditorManager.getInstanceFromContext(getEditorContext()); return manager.createNodeRoleAttributeCell(Sequence.fromIterable(currentReferenceAttributes).first(), AttributeKind.REFERENCE, editorCell); } else return editorCell; } /package/ static class Inline_Builder0 extends AbstractEditorBuilder { @NotNull private SNode myNode; private SNode myReferencingNode; /package/ Inline_Builder0(@NotNull EditorContext context, SNode referencingNode, @NotNull SNode node) { super(context); myReferencingNode = referencingNode; myNode = node; } /package/ EditorCell createCell() { return createProperty_0(); } @NotNull @Override public SNode getNode() { return myNode; } private EditorCell createProperty_0() { getCellFactory().pushCellContext(); try { final SProperty property = PROPS.name$MnvL; getCellFactory().setPropertyInfo(new SPropertyInfo(myNode, property)); EditorCell_Property editorCell = EditorCell_Property.create(getEditorContext(), new SPropertyAccessor(myNode, property, true, false), myNode); editorCell.setDefaultText("<no name>"); editorCell.setCellId("property_name"); editorCell.setSubstituteInfo(new SPropertySubstituteInfo(editorCell, property)); setCellContext(editorCell); Iterable<SNode> propertyAttributes = SNodeOperations.ofConcept(new IAttributeDescriptor.AllAttributes().list(myNode), CONCEPTS.PropertyAttribute$Gb); Iterable<SNode> currentPropertyAttributes = Sequence.fromIterable(propertyAttributes).where(new IWhereFilter<SNode>() { public boolean accept(SNode it) { return Objects.equals(PropertyAttribute__BehaviorDescriptor.getProperty_id1avfQ4BBzOo.invoke(it), property); } }); if (Sequence.fromIterable(currentPropertyAttributes).isNotEmpty()) { EditorManager manager = EditorManager.getInstanceFromContext(getEditorContext()); return manager.createNodeRoleAttributeCell(Sequence.fromIterable(currentPropertyAttributes).first(), AttributeKind.PROPERTY, editorCell); } else return editorCell; } finally { getCellFactory().popCellContext(); } } } private EditorCell createConstant_1() { EditorCell_Constant editorCell = new EditorCell_Constant(getEditorContext(), myNode, "for model"); editorCell.setCellId("Constant_3dlbxb_c0"); editorCell.setDefaultText(""); return editorCell; } private EditorCell createRefNode_0() { SingleRoleCellProvider provider = new forModelSingleRoleHandler_3dlbxb_d0(myNode, LINKS.forModel$QAM2, getEditorContext()); return provider.createCell(); } private static class forModelSingleRoleHandler_3dlbxb_d0 extends SingleRoleCellProvider { @NotNull private SNode myNode; public forModelSingleRoleHandler_3dlbxb_d0(SNode ownerNode, SContainmentLink containmentLink, EditorContext context) { super(containmentLink, context); myNode = ownerNode; } @Override @NotNull public SNode getNode() { return myNode; } protected EditorCell createChildCell(SNode child) { EditorCell editorCell = getUpdateSession().updateChildNodeCell(child); editorCell.setAction(CellActionType.DELETE, new CellAction_DeleteSmart(getNode(), LINKS.forModel$QAM2, child)); editorCell.setAction(CellActionType.BACKSPACE, new CellAction_DeleteSmart(getNode(), LINKS.forModel$QAM2, child)); installCellInfo(child, editorCell, false); return editorCell; } private void installCellInfo(SNode child, EditorCell editorCell, boolean isEmpty) { if (editorCell.getSubstituteInfo() == null \|\| editorCell.getSubstituteInfo() instanceof DefaultSubstituteInfo) { editorCell.setSubstituteInfo((isEmpty ? new SEmptyContainmentSubstituteInfo(editorCell) : new SChildSubstituteInfo(editorCell))); } if (editorCell.getSRole() == null) { editorCell.setSRole(LINKS.forModel$QAM2); } } @Override protected EditorCell createEmptyCell() { getCellFactory().pushCellContext(); getCellFactory().setNodeLocation(new SNodeLocation.FromParentAndLink(getNode(), LINKS.forModel$QAM2)); try { EditorCell editorCell = super.createEmptyCell(); editorCell.setCellId("empty_forModel"); installCellInfo(null, editorCell, true); setCellContext(editorCell); return editorCell; } finally { getCellFactory().popCellContext(); } } protected String getNoTargetText() { return "<current>"; } } private static final class CONCEPTS { /package/ static final SConcept GenerationContextOp_Base$yi = MetaAdapterFactory.getConcept(0xd7706f639be2479cL, 0xa3daae92af1e64d5L, 0x11b5282d0d3L, "jetbrains.mps.lang.generator.generationContext.structure.GenerationContextOp_Base"); /package/ static final SConcept LinkAttribute$v_ = MetaAdapterFactory.getConcept(0xceab519525ea4f22L, 0x9b92103b95ca8c0cL, 0x2eb1ad060897da51L, "jetbrains.mps.lang.core.structure.LinkAttribute"); /package/ static final SConcept PropertyAttribute$Gb = MetaAdapterFactory.getConcept(0xceab519525ea4f22L, 0x9b92103b95ca8c0cL, 0x2eb1ad060897da56L, "jetbrains.mps.lang.core.structure.PropertyAttribute"); } private static final class LINKS { /package/ static final SReferenceLink label$V_zA = MetaAdapterFactory.getReferenceLink(0xd7706f639be2479cL, 0xa3daae92af1e64d5L, 0x11b5282d0d6L, 0x11b5282d0d7L, "label"); /package/ static final SContainmentLink forModel$QAM2 = MetaAdapterFactory.getContainmentLink(0xd7706f639be2479cL, 0xa3daae92af1e64d5L, 0x11b5282d0d6L, 0x5f171e4376fc8e82L, "forModel"); } private static final class PROPS { /package/ static final SProperty name$MnvL = MetaAdapterFactory.getProperty(0xceab519525ea4f22L, 0x9b92103b95ca8c0cL, 0x110396eaaa4L, 0x110396ec041L, "name"); } }
Run for the Roses We’re in a race for our Country, for victory over the dark forces of Satan, of the dementia of our captured politicians. Soon millions will descend on our nation’s capital, and simply escort the scoundrels to jail. It will be like the Gideon moment. 156 Responses to “Run for the Roses” Thursday night at midnight we had an eq–slight around 3.5 but never reported–this is the 2nd one that woke me up with the gound rumbling and the bed shaking. No reports at all–so of course I called the local radio station early the next morning to report it and asked for them to research it but again, no news on it. There are just to many weather and earth movement going on and not being reported and not our weather patterns. Haarp has the ability to move the gulf stream causing these storms and once they do this they activate more fly overs with their chemtrails making it more severe. Thursday early evening we had a severe breakout of thunder storms sucking the humidity out of the air so quick it went from 100 degrees to 79 in a flash–and I stepped outside to look at the sky and that sucking of the air must have sucked the air out of me, I suddenly could not breath at all…i immediately went in to be able to catch some breaths. That was frightening to say the least. That same storm ended up being a microburst and took out 2 dozen telephone poles in the Tulsa city limits along of course with trees and quick flooding. This storm came in quick and left as quick—very very strange. Wow. Thanks for this, as my dearly departed Grandfather was a Marine Raider. The first Special Forces in the military. He was in Maikin Island then went on to Iwo Jima. Never realized why he was so strict yet silent until I viewed his secret ‘war chest’ full of photos and memorabilia…what they endured…Bless his heart. Just saying “hello” after a 3 week stent at my Mom’s house. Unfortunately I’m her live in care-giver for now. She has a pinched nerve in her leg and can’t walk…this caused a fall and broken wrist. She’s confined to a wheelchair for now and I’m the only daughter so you guessed it…it’s all on me. And no, she has no internet service & I can’t get a wireless connection there so I’m net-less there. At home tonight for a brief break so I’m trying to play catch-up. Hi Ann! thank you for checking in…hope your Mom is really ok…took care of mine for several months before she passed at 96…worrisome, no rest (!), but glad to be with her and I’m glad you are with your Mom…thanks always for reading and commenting here! Obama tells CBS’ “Sunday Morning” that there’s no doubt that he underestimated how much “politics trump problem-solving.” Yeah his politics trumps everything. There he goes blaming everyone else for his failed economy (while he gutted the treasury but no one is talking about that.) All he’s worried about is his kids growing up and leaving an empty nest. No kidding. One Big Assed Mistake America! America gets a POS for president disguised as a mixed breed. I’m with Condi but we need to organize. And Electro Magnetic Fields? Don’t get me started. The recent stroms and blackouts was just a test run. Same going on in Russia. So Barry Hussein Oblama. The MoFo who never had the MoJo he claims to have. We have had weird storms. The thunder is odd. Short loud booms for about 3-minutes, spaced 1-sec apart, now we have real rolling thunder. The short booms almost sounded like something was jump starting what came later?? Jan–we have had the same here–its almost like created thunder and my sister on the east coast is saying the same. These are forced storms and easily distingished as man made. At least for people like us they are–and the second I hear a clap or a boom I am up and listening and watching to see what horror they are dumping on us. I don’t post on her much, but read your site drkate almost everyday. I was so angry after hearing what ob said yesterday in VA. He said, “If you’ve got a business, you didn’t build that…somebody else made that happen.” What kind of an idiot would crush the hope of thousands of young graduates seeking to build a business? He has to go …… I saw a sound bite of that but was on my way out the door. What’s that about? Pelosi is involved with that train of thought too? “you used our highways to transport your goods, (even though our taxes pay for it) and you use our kids to hire whom were educated in our schools, (even though our property taxes pay for that) and you you you….didn’t build that business on your own.” The freak I didn’t ? You fuggin fool. If I didn’t then who did? He is still taliking bullchit and in simple riddles. former Secretary of State Condoleezza Rice said: “It is a narrative that is being pushed by our current president, that ‘I’m doing poorly because you’re doing well,’” she said. “That has never been the American narrative. Ours has never been a narrative of aggrievement and ours has never been a narrative of entitlement. It is time for all of us, in any way we can, to mobilize, get our act together, and storm Washington D.C.” Been gone for a bit and got behind in my reading—picking up on the bit about the “paralegals” and the “corpseman”—I don’t think these are slips of the tongue, these are true manifestations of bho’s non-American background. He was very well trained and indoctrinated but they didn’t get all of America into his basic functioning. It is very often the small things that become the tip-offs. During the Big War, the Dutch used the local pronunciation of a popular resort town to expose German agents who would fail to use the proper Dutch version of the name. The current occupant of our White House ain’t an American !! I’m listening now but a good part is already past, check tomorrow for the archives listen to the archives for 7-15-12, second part of show is on chem trails. This lady is good and has done a ton of research. THE COMMON SENSE SHOW w/ Dave Hodgeshttp://www.republicbroadcasting.org/ O/T, How is Terry?…..He’s been kinda scarce around here lately….If I know him like I think I do, I’d be willing to bet that he is looking out for his loved ones and spending a lot of time prepping for the “Great Collapse”. He’s a very logical and resourceful man that knows when it’s time for preventative action. I’ll take that as a compliment, especially coming from you Troy, thanks. God has provided some opportunity for me and I have been working every waking minute taking advantage of it. And yes, using it to prepare to the extent possible. Really like working two full time jobs right now. Also passed a kidney stone over the weekend…I now know what child birth is like. Didn’t want to go to ER at first, but when the pain makes you nauseous, all that John Wayne crap goes out the window. Learned a few things about dehydration and watching what you drink. Pop is bad stuff, with or without Aspartame. Obama cites “national security” in this EO. I guess Obama sees ANY excuse for declaring a national security emergency will appear better than taking over the nation’s communications assets by force Want more examples of what Obama is doing? •EO 10990 allows the Government to take over all modes of transportation and control of highways and seaports. •EO 10997 allows the government to take over all electrical power, gas, petroleum, fuels, and minerals. •EO 11000 allows the government to mobilize civilians into work brigades under government supervision •EO 11002 designates the Postmaster General to operate a national registration of all persons. •EO 11003 allows the government to take over all airports and aircraft, including commercial aircraft. •EO 11004 allows the Housing and Finance Authority to relocate and establish new locations for populations. •EO 11005 allows the government to take over railroads, inland waterways, and public storage facilities. Are we beginning to see a pattern here? We’re being prepared for a national emergency. Then there’s taking control. I personally think that what Obama is doing goes way beyond being prepared. North Carolina governor Beverly Perdue (Democrat), on September 28, 2011, suggested that perhaps elections should be suspended for two years by canceling, until the economy recovers, the 2012 elections. After that remark got the reception it deserved, Pardue’s staff tried to pass it off as a joke. Well, tomorrow is suppose to be the day that Arpaio and Zullo “lower the boom” on Barry, the communist usurper…..I pray to God that it is so devastating that there is no way in hell that it can be ignored by the MSM government propaganda machine – that includes you too, O’Really and the rest of the Faux News operatives…..I want to see Beck have to publicly eat a giant dookie sammich!!!…..Yummy, yummy Beck, ya freakin’ TURD!!!! “And while we’re at it Sheriff Joe in Arizona – f— you you f—ing puto. How about that? F— you. You fat motherf—er. F— you. I said I was going to talk some s—. F— you Sheriff Joe you f—ing puto. F— you. F— you.” The special ran on HBO Saturday night – with no F-bombs censored. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ I didn’t realize Arpaio was 80 years old…..He looks really good for his age…..I’d love to see him stomp Lopez’s ass into a little puddle of oozing wetback slime on the ground……If Lopez was any kind of a man at all he’d meet Arpaio’s challange and show up, but I’m sure the balless Lopez is packing a vagina down there instead of balls…..Freakin’ punk!!!! if they aired those f bombs then it was deliberate as usual when it comes to anyone opposing barry soetoro……my take is all of hollywood has been told they will never work again, they will lose their lives and families, and their assets will be stolen! there are only a handful of stars that speak against barry and his merry band of thugs………those a true patriots………i refuse to go to movies and i watch 2 shows on tv — i wouldnt give any of them the opportunity of growing their ratings! God forgive me, for I aim to wish no man (or woman) ill will. So, suffice it to say that Lopez has already had a kidney transplant. God only gave us two. Just sayin’. Please forgive me, God for my unkind thought. dr. kate —– i’m all for this big assualt on d. c. to arrest all these criminals but , where did you get that information and where are all these millions of people coming from ? it seems just wishful thinking to me . i cannot get 5 people organized to move on anybody . Is there an icon for a blow hole? Some may try to make that a vulgar term, but my whale friends will appreciate it. Yes, I’m doing the jackass in a hail storm trick…sometimes you just gotta hunker down and take the flack. If my family isn’t taken care of, none of my other efforts will mean much, so I’m storing up nuts while the gathering is available so I can live to fight when the onslaught is peaking. Haven’t missed the smoke screen much. Been doing some soul searching too…we are all caught up on that hampster wheel. The controlled opposition is even more intense than we want to admit. We get bent by things we should take as a grain of salt and work more to see the extent of the lies. God wants us existing in the present…and the father of lies wants us worrying about tomorrow or yesterday or a political party or, or, or anything trivial to distract us from the present. We find God in the present. Ah, so my educated guess was and is correct in regards to your limited presence lately…..I figured you were prepping for the storm…..It’s a comin’ and soon!….Your priorities are in the proper order as i knew they would be.😉 According to the latest rumors (or news) the decision making chain goes directly to Hillary. Frankly I don’t understand that because the SS would not be in that chain of command. Also, there is not much love lost between Hill and O, so why would O protect her (by refusing to release the docs), while he is ready throw anyone under the bus who is the slightest way inconvenient to his goals. Could this be an intentional misleading leak to divert attention from the top decision maker. Orly Taitz on Hagmann & Hagmann, listen to the archives (7-16-12). She has a case in CA for voter fraud, other cases against obama but the best one soon is the obama Tax case. All Muslims will be exempt (7-million of them) the illegals will get free coverage-expempt from taxes, so we will pay. She has a good suit going. this is very dangerous for us, they can manipulate our fico scores, our credit histories, any and all judgements and/or leins. Please everyone go to annualcreditreport.com and pull all 3 and save them for the following yr. you can get them all for free—but scores are a fee. you are entitled to a free report from all 3 once a yr. creep—why can’t he speak as eloquently as romney–he is nothing but a street thug who couldnt fight his way out of a paper bag–instead he sends in his thugs to take out those that are a threat to him and he talks like a street thug………just listen to him. He destroys the english language…what a pos. boortz had dick morris on this am about the sea treaty and the gun treaty and he said that all they have to do is not bring it up for a floor vote and let it hang and it stays alive and thats exactly what they will do. like i said above, we won this time, but be on guard for this to come up again. Heather, I wrote Dick Morris this morning as he is really ticking me off. He just put out an article pushing Rubio for Romney’s VP. I gave him a pretty good earful and hope everyone else will do the same. I told him I understand that he was either threatened or paid off but just because obat was the illegal usurper does not mean we can tollerate another one, along with a few other choice statements. Jan–I know–I did the same and when I signed his petition today I wrote in my own comments in that section. I said that everyone in DC is a traitor and all need to be arrested for the treason and terror that barry and co have done to the American people and the gutting of our financial system into his pocket to redistribute to his cronies. Of course I went on and on and thats a good thing, because they will all be read one way or another and sent on to each of our on senators and congressmen. I had written Rush about 6 mos ago for pushing Rubio and he hasnt brought him up except when he is reporting on who is. These talking heads need to know that WE THE PEOPLE all know their tricks and evilness. hello dr. kate —— i thought you had blown me off permanently . i remember you taking a small platoon to d. c. a couple years back to support lt. col. lakin and to meet with republican members of congress concerning the usurper . the only time i remember 1 or 2 million was the tea party protest more than 2 years back . the protest was against the usurper policies and in the speeches not one word was mentioned about obama ineligibility to be potus . that was a totally wasted effort by the tea party . there were only a very few signs asking about the birth certificate . even at that time i was saying that both parties were complicit in the fraud and we could not rely on the republicans to do anything about the usurper when they got control of congress . i even urged everybody not to wait on the republicans but to go after the democrats then . having said that , if you go back to arrest these criminals with enough people to get the job done , i intend to be there with you . MSM trying to smear Arpaio. Of course they don’t care about Obama wasting money on cvampaigning fraudulently on the taxpayer dime, and employing legions of lawyers to thwart any contest of his appearance on state ballots. I know that all of us here want RP as potus and we all know that isnt going to happen. So what we need to do is rally behind the pic we have–Romney….After listening to him and watching him I have to admit that he is a pure gentleman, with ethics, and morals and love for America. Now i know some of you will disappointed in what I am saying and thats ok because we all have our own opinions and wants, but I want barry out so bad that I will stand behind Romney. Again, he isnt my fav or my pic, but he is who we have and if we want barry and co gone, we have to stand with this man. He is articulate, presidential – has class, and I don’t believe he is evil. He would never bow to another leader, never bad mouth America, never give our resources away to enemies and I don’t believe he would steal our wealth, what we have left, to redistribute to his buddies. Romney is what we have. I hope you’re right QL–and I take your words seriously and I continue to pray for RP to elected–wouldnt that be a miracle for all of us to see and this country needs to being God back in and stop these atheists from destroying him and pushing him out. The Most Im[ortant Thing Heather IS PUTTING UP AUDIT THE FED. The problem will still go on,with Rich corrupt Romney or Rich traitor Treason in america OBAMA.We have to deal with the truth the Elitist,banksters,goverment,Ron Paul is the one who speaks of this.endfinancialfraud.org just look at this—this is deliberate…haarp is activated and causing this–global warming is man made alright–they are creating this heat again. It’s been 100+ here since the beginning of June, a few 90+ mostly over 100 with no rain–at all. We had a rain storm last week and that was the first since May. Another summer of this heat-like last yr where nothing grew because of it. The chemtrails are different this time, they are there in full force but are being sprayed differently. They are not whiting the skys out completely from the sun, they are making corkscrew trails now where they adhere to the real clouds and the sun still shines. They have changed their patterns since the end of May, to meet with the growing season. Oh how they must think we are stupid! DITTO–somethings causing these solar flare ups–and my opinion is haarp. We only know what this weapon of mass destruction does here, what does it do in the solar system? hmmm—-yep, all things point back to haarp. So, $9600 to go to HI to find out there are two boxes on the forged BC that should be empty but are not. Are there no Congressmen from AZ that have the balls to take this to Issa? I agree there should be a grand jury called. Can Sheriff Joe call for one? Let me say this regarding the person Rinos have picked as the presumptive candidate. I have to answer to God first because I am a born again Christian. No person on this earth can save the United States from its sure path to intrusive government slavery and it certainly won’t be Romney who is big gov’ all over the place! Do you see any republicans in the house, senate, judiciary with a shred of honor? Do you? You think they will change their stripes and get courage with a Romney as president? They whimper and cower in corners under the usurper! Mormons are NOT Christians and are cultists. I cannot and will not vote for a cultist who has supplanted the Bible with a book by a charlatan and who calls Jesus and Satan brothers!! What shall I say to God? Hey, the devil made me do it? I have heard certain preachers say it ok to vote for Romney if you are an evangelical because Mormons support a moral climate. Really Mr. preacher?? It is moral to call God a liar and distort his truths?? Really???? Romney lies when he calls himself a Christian, just like Obama. I should support a liar to lead the country? Not MY brand of morality!! Stuff it. How much better it would be if Mittens said “ya know what…I am not a Christian and my beliefs are strange and outside of biblical christianity and I won’t lie to you.” I will never vote for man that has peed on scripture and Jesus the way mormons do and call themselves Christians. The US won’t solve its problems by further turning against God and His word. The bible is clear that the world IS going to hell…and turning to some fake Christian to right this country…is wrong. Do not be deceived. I tip my hat to Sheriff Joe and his Posse for their press conference today, their courage in the face of insults and mocking and death threats. True Patriots, in the deepest sense of the word. I had hoped to also hear some info on the SS # issue, but perhaps next time. It is frustrating and demoralizing to confront the realization that most people simply do not care about America, her history, the heroism and wisdom and blessings that flowed from the muskets and pens of our Founders and generations who sacrificed and died. To our right and left we see neighbors and co-workers who do not yearn for Truth, or Justice or value Freedom. We try as we might to engage in various manners, gently, more forcefully, with humor, with subtlety and fail to persuade more often than we care to admit. There are powers at play far more influential than our logic or wit or appeal to Righteousness. My greatest disappointment has been in the clergy. Absolutely gutless wonders. For the sake of preserving a non-profit tax exemption they have completely sold their soul to Satan. Wow, it hurts to say that. As disappointing as all that is, our allegiance is to our Lord, our families and America. We will be judged based upon our acceptance of our Savior and hopefully appreciated for our loving service to guide and raise our families properly, to spread the Gospel and work to preserve our Free Land. Warren, thank you for your comments, God Bless You. Sheriff Joe stated today that there are several issues surrounding obama, however they decided to pick one and stick with it and so far, they are staying focused. The newspeople were down right rude and obnoxious, pray for them. Heard on local radio today that GOP is NOT letting Ron Paul speak at the GOP Convention. They are trying to keep him out of the convention. GOP scumbags are really afraid of RP winning the nomination!! Just follow copyright law and nobody gets hurt! The contents of this blog are protected under U.S. Copyright Law, United States Code, Title 17. Requests for use of active and archived articles in this blog must be presented in writing in the comment section, and proper attribution is expected. 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Cairn UK to offload 8% stake in Indian arm to raise $940 mn Cairn Energy is selling an 8 percent stake in India-focused oil explorer Cairn India in a deal that could raise up to $940 million, in a deal that could be worth around $1billion. Reuters Cairn Energy is selling nearly 153 million shares of Cairn India for between Rs 317.90 and Rs 328.30 per share, said the source, declining to named as he was not authorised to speak to the media. Post the sale, the UK-based energy firm, which was the majority holder in Cairn India before it sold over 50% controlling stake to the Vedanta group in December 2011, will hold 10.3% in the Indian company. Cairn has appointed Citigroup as sole book runner for the transaction. The block deal is expected to be done on Tuesday across stock exchanges. .According to a Bloomberg report, Cairn has pledged to sell down its remaining stake in Cairn India to free up cash for new projects after spending $1 billion on a two-year exploration campaign in Greenland that failed to find oil and gas
Definition of Paraffin dip Paraffin dip: A treatment for the symptoms of joint and muscle conditions, such as arthritis, that involves applying melted mineral wax derived from petroleum to a body area. Paraffin dips can be especially helpful in relieving the pain and stiffness of arthritis involving the small joints of the hands. The hands are repeatedly dipped into the melted, warm wax, and the wax is allowed to cool and harden around the sore joints. The paraffin is then peeled off and can be remelted in the bath for repeated use. Also known as wax dip.
Introduction ============ Gaucher disease (GD) is an autosomal recessive lysosomal storage disorder that, with the exception of rare patients with saposin C deficiency, is caused by mutations in the glucocerebrosidase gene, GBA1\[[@B1]\]. Deficient glucocerebrosidase activity leads to accumulation of the enzyme's substrate, glucocerebroside (glucosylceramide), in tissue macrophages primarily in the liver, spleen and bone marrow. Subject to genotype, other genetic modifiers \[[@B2],[@B3]\] and undefined genetic, epigenetic and environmental factors, untreated patients with GD may be asymptomatic with few signs of disease or present with combinations of hematologic abnormalities, hepatosplenomegaly, skeletal disease, growth retardation, and decreased health-related quality of life \[[@B1]\]. GD type 1 (GD1), found in approximately 90% of known GD patients worldwide, is differentiated from GD type 2 and GD type 3 by the absence of overt, early onset neurological signs and symptoms. However, distinct late onset neurological symptoms such as peripheral neuropathy and Parkinson disease may occur in GD1 \[[@B4]\]. The incidence of GD1is estimated at 1/50,000-75,000 live births in non-Jewish populations in North America, Europe and Australia \[[@B5],[@B6]\]. Of more than 350 GBA1 variant alleles that are associated with GD, 6 mutations account for 98% of those found in the Ashkenazi Jewish population in which GD1 is especially prevalent \[[@B7]\]. One in 10--15 Ashkenazi Jews is a carrier for a GBA1 mutation projecting a disease incidence of 1/600 live births \[[@B8]\]. However, the observed disease prevalence among North American Ashkenazi Jews is substantially lower than predicted. In South Florida, home to an estimated 500,000 Ashkenazi Jews \[[@B9]\], only approximately 100 Ashkenazi Jews with GD1 have been identified over a 20 year period (NJW, personal observation). This lower than expected prevalence is comparable to other US metropolitan areas with large Ashkenazi Jewish populations \[[@B10],[@B11]\]. The difference between observed and predicted cases with GD1 may be readily explained by the highly variable penetrance resulting in large numbers of asymptomatic individuals who never come to medical attention although missed diagnoses cannot be excluded \[[@B12]\]. Among western non-Jewish populations, the prevalence of GD1 is also less than predicted: 1/150,000-300,000 in French and Spanish national registries \[[@B13],[@B14]\]. It is unclear to what extent phenotypic heterogeneity contributes to this finding in light of evidence that the GD1 clinical phenotype tends to be more severe in non-Jewish patients compared to Ashkenazi Jews \[[@B15]\]. Here, we present a demographic and genotypic profile for 93 GD1 patients who live in South Florida and are enrolled in the ICGG Gaucher Registry and correlate genotype with validated severity scores and hematologic, visceral and skeletal therapeutic outcomes. Methods ======= Patient population ------------------ The ICGG Gaucher Registry was launched in 1991 to track the clinical, demographic, genetic, biochemical and therapeutic characteristics of patients with GD throughout the world, irrespective of disease severity, treatment status or treatment choice \[[@B16]\]. Governance and scientific direction is provided by an international group of physician experts in GD, with operational support from Genzyme, a Sanofi company (Cambridge, Massachusetts). For this report, we independently analyzed the medical records of all patients with Type 1 GD at the University Research Foundation for Lysosomal Storage Diseases South Florida site who enrolled patients into the ICGG Gaucher Registry from 1991-June 2011. All participating patients gave informed consent to participate in the ICCG Registry using forms approved at the time of their enrollment by the Western Institutional Review Board. Genotype -------- Genotype was obtained for most patients by PCR specific oligonucleotide screening for 5 common mutations prevalent in the Ashkenazi Jewish population (N370S, L444P, 84GG, IVS2 + 1, R496H; Genzyme Genetics, acquired by Laboratory Corporation of America in May 2010). Samples from some patients with unidentified alleles were referred to the ICGG Registry Genotyping Service at the laboratory of H. Ronald Scott, MD, PhD at the University of Washington, Seattle, WA, USA for whole gene sequencing. Gaucher disease severity scoring -------------------------------- Patients were categorized based on a validated DS3 disease severity scoring system \[[@B17]\], performed according to instructions in Figure [1](#F1){ref-type="fig"} and evaluated per instructions in Table [1](#T1){ref-type="table"}. For treated patients, baseline DS3 scores were calculated just prior to or at the time of initiation of enzyme replacement therapy (ERT). For patients never treated with ERT, the DS3 score was calculated at the most recent follow up point for which complete data was available. ![GD-DS3.](1750-1172-9-45-1){#F1} ###### Gaucher disease type 1 DS3 scoring General instructions --------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- -------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- 1\. Record date of assessment 2\. For each assessment, determine the GD1 DS3 score of the patient at the time of evaluation (See notes below regarding specific assessments). a\. If current data are not available for all assessments when the DS3 score is calculated, data from previous evaluations may be used if the patient's overall clinical status has remained stable and assessments were collected within the following period of time prior to the current date: • Bone imaging 12--24 months • Hematological 12--24 months • Visceral imaging 12--24 months b\. If bone marrow infiltration and/or bone mineral density data are not available at the time of assessment or from previous evaluations, the GD1 has been optimized to be accurate and consistent without these parameters. c\. All other assessment scores within the time frames described above are required. DS3 score calculation 1\. First calculate the average Disease Domain Scores by adding the assessment scores for each domain (bone, haematological, visceral) and dividing by the number of assessment scores completed. Do not include assessments that were marked "not available" (NA) 2\. The total GD1 DS3 score is the sum of the three Disease Domain Scores. Maximum possible DS3 score 1\. The maximum possible DS3 score is 19. 2\. In initial validation testing using 20 patient cases scored at 2 different time points, no patient received a score higher than 13 and scores above 9 correlated with an expert assessment of "severe disease". Interpretation of GD1 DS3 scores 1\. 0-3 Borderline to mild disease 2\. 3--6 Moderate disease 3\. 6--9 Marked disease 4\. \>9 Severe disease Notes regarding specific assessments 1\. Lytic lesions, AVN or pathologic fracture "present" means any new occurrence in the past 12 months. 2\. Bone marrow infiltration may be reported either semi-quantitatively (BMB score) or qualitatively (mild, moderate, marked to severe. 3\. For bleeding, an assessment of moderate (no transfusions) or severe (transfusion needed) should be based on bleeding considered by the assessor to be related to GD, whether due to low platelet count, other hemostatic disorders or vascular disease such as portal hypertension. 4\. Assessment of bone pain should be based on severity in the absence of analgesics and should consider only pain resulting from GD rather than pain attributable to other concurrent musculoskeletal diseases. Therapeutic goals ----------------- In 2008, an ICGG Registry benchmark analysis evaluated the attainment of six previously suggested therapeutic goals (for hemoglobin concentration, platelet count, spleen volume, liver volume, bone pain, and bone crisis) in 195 non-splenectomized patients with type I GD after 4 years of imiglucerase treatment \[[@B18]\]. Here, we present therapeutic outcomes relative to the same therapeutic goals for our cohort of patients treated with enzyme replacement therapy for a minimum of 3 years. Results are reported for the date of latest follow up and separately for patients with a history of pre-treatment splenectomy. Statistical analyses -------------------- Demographic analyses used standard descriptive statistics (frequencies and percentages). DS3 scores are summarized using means and standard deviations. ANOVA testing was performed using a 2 tailed T test (Excel, Microsoft Corporation). Results ======= Demographics and genotype ------------------------- 93 individuals (mean age 62.1 years; range 25--91) were initially eligible. 57 (61.2%) were women. The mean (SD) age at first assessment was 49.9 years (SD 19, range: 4.2 to 83.6y). 75 patients (80.6%) reported Ashkenazi Jewish ethnicity. Five lacked genotype information. There were 4 sibling pairs. Of 84 unrelated patients with genotype data, 52 (61.9%) were homozygous for the N370S allele and 29 (34.5%) carried one N370S allele (Table [2](#T2){ref-type="table"}). Among patients of Ashkenazi Jewish ethnicity, 51 of 71 with known genotypes were N370S homozygous (71.8%) while only 2 of 17 non-Jewish patients (11.8%) were homozygous for N370S. ###### GBA genotypes and ethnicity of South Florida patients with GD1 GBA genotype Ashkenazi Jewish Non-Ashkenazi Jewish: Hispanic Non-Ashkenazi Jewish: Caucasian -------------------- ---------------------- ------------------------------------ ------------------------------------- N370S/N370S 51\* 2 N370S/V394L 5\* N370S/84GG 4 N370S/IVS^2+1^ 2 N370S/L444P 2 2 7\* N370S/other 5\* 5 Other/other 2 1 Unknown 4 1 \Includes 1 sibling pair. For the 88 patients with known genotypes, sufficient information to calculate baseline DS3 scores was available for 81 patients. DS3 scores in N370S homozygous patients (N = 48) were highly variable but generally in the mild to moderate range (Table [3](#T3){ref-type="table"}). Because of small numbers of patients in each sub-group, the only genotype with a statistically significant difference in DS3 score from N370S/N370S was N370S/L444P (N = 10) in which severity was generally severe. Severity was also significantly higher when N370S/84GG patients (N = 4) are grouped with the N370S/L444P patients. The broad range of genotypes and disease severity in South Florida patients is shown is shown in Figure [2](#F2){ref-type="fig"} which emphasizes the highly variable severity scores in N370S homozygous patients with approximately half the patients falling within the moderate to marked severity range. ###### South Florida GD1 patients: Mean DS3 scores per genotype category Genotype* Mean DS3 score (SD) 95%CI *P value (Ttest)* --------------------------------------------------------- ------------------------- --------------- ----------------------- N370S/N370S (N = 48) 3.86 (2.31) 3.21-4.51 Reference N370S/84 GG compound heterozygote (N = 4) 6.98 (1.85) 5.17-8.79 NS N370S/L444P (N = 10) 6.82 (1.08) 6.15-7.49 0.018 N370S/unidentified (N = 5) 4.30 (2.20) 2.37-6.23 NS N370S/V394L (N = 5) 4.80 (2.29) 2.79-6.81 NS N370S/L444P or 84GG compound heterozygotes and (N = 14) 6.86 (1.26 5.60-8.12 0.021 N370S/Y212H (N = 2 sisters) 9.33; 4.17 N370S/IVS2 + 1 (N = 2) 8.93; 2.33 N370S/F216Y (N = 1) 1.83 N370S/RecNCI1 (N = 1) 10.17 N370S/Y135X (N = 1) 8.00 R463C/K198 (N = 1) 5.08 L444P/unidentified (N = 1) 2.50 Statistical comparison is for the N370S/N370S genotype versus the other genotypes identified. ![DS3 scores (Y axis) per GBA genotypes in 89 South Florida patients with GD1.](1750-1172-9-45-2){#F2} Treatment status (93 patients) ------------------------------ Fifteen patients have not received disease-specific treatment primarily because comprehensive initial and serial assessments (NJW) indicated a clinically mild phenotype. ERT access was not problematical. One patient with symptomatic bone disease declined ERT and SRT. Until the imiglucerase shortage/interruption beginning in June 2009, virtually all patients who required treatment received imiglucerase. Two patients of unknown genotype who died prior to 1995 received alglucerase 60 U/kg every 2 weeks. They are excluded from the genotype and response analyses . At last evaluation through June 2011, 49 patients were receiving imiglucerase of whom 1 was infused weekly, 33 every two weeks, 2 every three weeks and 13 every four weeks (Table [4](#T4){ref-type="table"}). Doses ranged from 20--120 U/kg but most received 30--60 U/kg. Ten patients received velaglucerase alfa mostly every 2 weeks at 60 U/kg. Four patients were treated with oral miglustat 100 mg three times daily. 13 patients had treatment interruptions-- 3 for infusion reactions prior to 2009 and 10 due to the imiglucerase shortage. One has been stable since splenectomy in 1997 and the other 12 are clinically stable. ###### Treatment Status of 91 South Florida GD1 patients as of the most recent evaluation through June 2011\* No. of pts ERT dose (Units/kg) ----------------------------------------------- ---------------- ------------------------- ----------- ----------- ---------- Treatment status \<30 30-45 46-60 \>60 Never treated 15 Imiglucerase (total) 49 Q1W 1 Q2W 3 14 16 Q3W 2 Q4W 1 9 3 Velaglucerase alfa (total 10 Q2W 2 6 Q3W 1 Q4W 1 Miglustat 100 mg po TID 4 Treatment interrupted and not resumed (total) 13 Severe infusion reactions 3 Treatment shortage 10 \Two patients with unknown genotypes who were treated solely with alglucerase prior to 1994 are excluded from this analysis. Treatment outcomes and attainment of therapeutic goals ------------------------------------------------------ Of the initial 93 patients, 61 are included in this analysis. Fifteen untreated patients, 12 patients treated for less than 3 years, and 5 patients with insufficient data were excluded. The median treatment duration at the time of analysis is 12 years (Range: 3-19y; Mid-quartile range: 6.6-16.5y). Fifteen patients (24.5%) had splenectomy prior to treatment initiation. 17 patients are deceased of whom 4 had undergone splenectomy. The mean age (SD) at death was 71.9 (15.4) years; median age at death (range): 71.5 years (28y-92y); interquartile range: 64.5y-83.8y. The genotypes of deceased patients were 13 - N370S/N370S, 2 N370S/L444P and 1 N370S/V394L. The causes of death are shown in Table [5](#T5){ref-type="table"}. The mean pre-treatment DS3 score for the 13 N370S homozygous deceased patients is 5.50 (SD 1.79) compared to 3.22 (SD 2.05) for the treated N370S homozygous patients who remain alive (p = 0.002). The mean age (SD) at which ERT was initiated was 66.0 (SD 10.6) years for the deceased N370S homozygous patients and 52.1 (SD 14.4) years for the still surviving N370S homozygous patients (p = 0.006). ###### Causes of death in 17 deceased South Florida treated GD1 patients * Cause of death Total number of pts Number of pts with splenectomy** ----------------------------------------------------------- ------------------------- ------------------------------------ Parkinsonism\* 3 2 Chronic kidney disease 3 Acute myeloid leukemia and/or myelodysplasia 3 1 Dementia without Parkinsonism 2 Non-Hodgkin's lymphoma 1 1 Lung cancer, metastatic 1 Cerebrovascular accident 1 Congestive heart failure 1 Bronchiolitis obliterans and auto-immune hemolytic anemia 1 Air embolism associated with illicit IV drug use 1 \Age at Parkinson disease diagnosis: 45, 54, and 63 years respectively. As shown in Table [6](#T6){ref-type="table"}, 26 concurrent malignancies developed in 24 of 93 patients (25.8%). Two patients had 2 cancers (cutaneous melanoma and localized breast CA; cutaneous squamous cell CA and cervical CA in situ). Four patients have a significant monoclonal gammopathy but none has yet developed overt multiple myeloma. Cancers were diagnosed at a median age of 67 years (47--83 y). Of the 24 patients with concurrent malignancies, 5 have never been treated definitively for GD1 (Table [4](#T4){ref-type="table"}). ###### Concurrent malignancies in 93 South Florida patients with GD1 * Malignancy No of patients Ages at CA Dx (y) Mean age at CA Dx (y)** ---------------------------- -------------------- ------------------------- --------------------------- Monoclonal gammopathy 4 54, 68, 70^\#^, 82^\#^ 68.5 Cutaneous Squamous CA 5 59, 66, 66, 77, 80 69.6 Myelodysplasia, AML 3 51\, 63\, 72\* 62.0 Non-Hodgkin's lymphoma 3 59, 74\, 83 72.0 Breast carcinoma 3 47^\#^, 72^\#,^ 75 64.7 Cutaneous Melanoma 2 57, 71 64.0 Prostate carcinoma 2 65, 75 70.0 Bladder carcinoma 1 80 80.0 Lung cancer 1 62\ 62.0 Fallopian tube carcinoma 1 49^§\#^ 49.0 Cervical carcinoma in situ 1 53 53.0 \Cause of death. ^§^BRCA2 mutation. ^\#^Never treated with ERT or SSIT. After a median 12 treatment years, South Florida patients matched or exceeded the ICCG 4 year therapeutic goal achievement for platelet count (85.4% vs. 79.6% success), spleen volume (93.3% vs. 78.0% success), liver volume (93.4% vs. 90.6% success), and bone crises (100% vs. 99% success). Nevertheless, fewer patients with intact spleens had sustained achievement of all 6 therapeutic goals (30.4% versus 41.4%) and only 40% of the splenectomy patients sustained achievement of 5/5 possible goals (Table [7](#T7){ref-type="table"}). Of 6 South Florida patients who "failed" therapeutic goal criteria for hemoglobin concentration, 5 had concurrent hematological diagnoses: auto-immune hemolytic anemia \[[@B1]\], acute myelocytic leukemia \[[@B1]\], myelodysplasia \[[@B1]\], chronic kidney disease \[[@B2]\]. ###### Attainment of therapeutic goals: South Florida patients with GD1 and the ICCG benchmark cohort\[[@B18]\] * Therapeutic goal South Florida GD1 patients (Median treatment:12 years minimum treatment: 3 years) ICGG cohort (N-195) (evaluated after 4 years of ERT)** --------------------------------- --------------------------------------------------------------------------------------- ---------------------------------------------------------- Bone pain (N = 61) 45.3%^\#^ 70.2%^\#^ Hemoglobin (N = 61) 90.6%\* 91.6% ^§^Platelets (N = 46) 85.4% 79.6% ^§^Spleen volume (N = 46) 93.3% 78.0% Liver volume (N = 61) 93.4% 90.6% Bone crises (N = 61) 100% 99.9% ^§^Attained 6/6 goals (N = 46) 30.4% 41.4% ^§§^Attained 5/5 goals (N = 15) 40.0% Not applicable ^§^Intact spleen patients only. ^§§^Splenectomy patients. ^\#^63% of the ICGG patient cohort had no reported bone pain prior to initiation of treatment. 73.4% of the South Florida patients reported bone pain prior to initiation of treatment; bone pain was scaled as moderate or worse in 59.6%. \In 5/6 patients, Hb was depressed because of concurrent illnesses at evaluation point (auto-immune hemolytic anemia, acute myeloid leukemia, myelodysplasia, chronic kidney disease \[[@B2]\]). 54.7% of the intact spleen patients (and 53.3% of the splenectomy patients, for whom there is no comparison group) continued to have bone pain vs. 29.8% in ICCG. On average, there was no age difference between patients with residual bone pain and those free of pain. Of note, only 37% of the ICGG patient cohort had bone pain prior to initiation of treatment compared to 73.4% of the South Florida patients (moderate or severe pain in 59.6%). Of 28 patients with baseline bone pain scaled as moderate or worse, 20 (71.4%) failed to realize the therapeutic goal for bone pain at their most recent evaluation. Of 35 patients who initially reported either no bone pain or pain no worse than mild, 15 (42.8%) had bone pain at their most recent evaluation. Age at inception of ERT was not significantly associated either with severity of pre-treatment bone pain or with therapeutic goal "failure" due to persistent bone pain. However, of the 61 patients included in the therapeutic goal analysis, only 9 patients were younger than 30 years of age when ERT was begun and only 4 were younger than 18 years. Regardless of age at inception of treatment, severity of pre-treatment bone pain was a key predictor for persistent bone pain. Age at commencement of ERT also did not appear to be a significant determinant of failure to achieve therapeutic goals other than bone pain. Among our patients, poor compliance with treatment schedules was not a contributory factor to poor therapeutic responses. The initial total DS3 bone domain score, although including heavily weighted information about avascular necrosis, lytic lesions, fractures, bone marrow infiltration and bone density, was less likely to predict pain outcomes than the bone pain score itself. There also was no significant association between the baseline DS3 bone domain score and composite attainment of therapeutic goals in either patients with intact spleens or in those with splenectomy (Table [8](#T8){ref-type="table"}). Likewise, neither the total pre-treatment DS3 score nor the GBA genotype was predictive of outcome in terms of achievement of the 6 therapeutic goals that were examined. ###### Lack of association between the baseline DS3 bone domain score and composite attainment of therapeutic goals Therapeutic goals attained* Number of patients Mean DS3 score (SD) 95%Confidence interval ANOVA P value -------------------------------- ------------------------ ------------------------- ---------------------------- ------------------- Intact spleen pts (N = 45) 0.508 6 of 6 14 2.70 (1.60) 1.86\--3.54 5 of 6 21 3.01 (1.71) 2.28\--3.74 4 of 6 10 2.23 (1.97) 1.01\--4.20 Splenectomy pts (N = 15) 0.282 5 of 5 6 4.26 (2.33) 2.40\--6.12 4 of 5 5 5.82 (1.03) 4.92\--6.72 3 of 5 3 6.08 (1.28) 4.63\--7.53 Discussion ========== To our best estimate, the 93 patients included in this report constitute at least 75% of known GD1 patients living in South Florida during a 22 year period. During that time, a 1990 population of 3.5 million in which 57% were non-Hispanic White has grown to 5.5 million with only 41% being non-Hispanic White \[[@B19]\]. There are approximately 2.3 million Hispanic or Latino South Floridians of any race and 1.1 million of Black-American ethnicity. 37% of the region's population is foreign-born and 32% were born elsewhere in the United States. Nevertheless, our patients with GD1 continue to be genotypically and phenotypically different from patient populations that have been reported from various European and Latin American countries and much closer in characteristics to other patients with GD1 living primarily in the northeastern United States, California and in Israel (Table [9](#T9){ref-type="table"}). ###### GD1 Genotypes in different world populations Country or Region N370S/N370S (%) N370S/L444P (%) N370S/other (%) Total N370S (%) ----------------------------------------------- --------------------- --------------------- --------------------- --------------------- Spain and Portugal (N = 370) 16.8 31.6 43.2 91.6 France\* (N = 203) 19.2 20.2 60.6 ? Netherlands (N = 40 unrelated) 2.5 40.0 45.0 87.5 Italy (N = 106 unrelated) 12.3 25.4 49.1 86.8 UK and Ireland (N = 30) 30.3 3.3 40.0 73.6 Turkey (N = 32) 31.2 18.8 25.0 75.0 Latin America (N = 431) 11.7 29.3 52.0 93.0 World ICGG Registry 1998 (N = 680) 24.0 18.1 46.7 88.8 Jewish: USA and Israel (N = 545 unrelated)^§^ 45.0 8.8 34.1 87.9 AZ CT NJ NY, USA (N = 403) 53.6 13.4 33.0 100.0 South Florida, USA (N = 84 unrelated) 61.9 11.9 22.6 96.4 \*Restricted to GD1 patients with at least one N370S allele. ^§^From Boot RG et al. Human Mutation. 10:348:1997. Compared to the GD1 patients from the Northeast United States described by Taddei et al. \[[@B11]\], somewhat fewer South Florida patients were Ashkenazi Jews, were N370S homozygous, and had a history of splenectomy. Our patients were significantly older when initially assessed (mean age 49.9 years (SD 19.0) versus 39.2 years (SD 18.8), p \< 0.0001). The difference in age and increased years at risk may explain why the occurrence of malignancy was greater in our patient group (24/93 (25.8%) versus 46/367 (12.0%)). Among our patients with cancers, hematological malignancies were the most prevalent. However, despite strong evidence for a substantial increased risk for this malignancy in older patients with GD1 \[[@B20]-[@B23]\], none of our patients have yet developed myeloma although four have monoclonal gammopathy of uncertain significance. Our experience does not suggest that patients with GD1 have a greater risk for developing the most common solid tumors (lung, breast, prostate, colorectal, pancreatic) than unaffected individuals in the general population. With the exception of N370S/N370S, the number of our patients in each GBA1 genotype sub-set is small. Nevertheless, the DS3 scores are consistent with the consensus perception of "severity" of GD1 genotypes and our results complement the validity testing of the DS3 instrument \[[@B17]\]. In most western non-Jewish populations, 20-30% of patients with GD1 are N370S/L444P and moderately to severely affected prior to starting treatment. The mean DS3 score for our N370S/L444P patients (6.82) is consistent with this experience. No N370S/L444P patient in our study had a pre-treatment DS3 score in the mild range. There was more DS3 score heterogeneity among other N370S heteroallele genotypes including N370S/V394L (generally associated with mild phenotypes) \[[@B24]\] and N370S/IVS^2+1^ (generally associated with clinically more severe disease \[[@B25]\]. As expected, there was substantial variability in the severity scores among N370S homozygous patients \[[@B26]\]. Although the lowest DS3 scores (\<2.00) were confined to the N370S/N370S patients, half of the N370S homozygous patients had DS3 scores that were in the moderate range or higher. Skeletal disease, as measured with the Hermann score and Zimran Severity Score Index (SSI) is reported to worsen with age in untreated, non-splenectomized homozygous GD1 patients \[[@B11]\]. However, in similar patients, we did not find a significant correlation between patient age at first assessment and either bone domain DS3 score (ρ = 0.21) or total DS3 score (ρ = 0.25). As regards treatment response, pending completion of a larger, multicenter study designed to examine serial changes in DS3 scores in both treated and untreated patients (Clinicaltrials.gov; NCT01136304), we elected to evaluate our patients in terms of achievement of therapeutic goals for hemoglobin concentration, platelet count, spleen and liver enlargement, bone pain and bone crises. These short term goals are not necessarily disease specific over an extended period of observation and they are an incomplete representation of all the elements that are integral to capturing the essence of clinical response to treatment for life long chronic illnesses such as GD1. Nevertheless, regulatory approvals of new therapy for GD1 and most reports of 4--10 year treatment outcomes have relied heavily, and sometimes exclusively on these six parameters \[[@B18],[@B27]\], and sustained cumulative maintenance of these specific therapeutic goals has been proposed as a benchmark for therapeutic efficacy and as a basis for treatment comparisons \[[@B28]\]. Although assessment of achievement of multiple therapeutic goals is very useful for individualized case management, our results demonstrate the limitations and pitfalls of such applications to studies of patient populations that are not matched in terms of pre-treatment characteristics and potentially confounding concurrent or emerging medical events. Although the percentages of our patients completely at therapeutic goal after a median 12 years of GD1 treatment was less than that reported by ICCG after 4 years of treatment, the clinical circumstances suggested that many "failures" were probably not attributable to "breakthrough" manifestations of GD1. In fact, with the longer duration of treatment, as predicted by the 10 year imiglucerase experience \[[@B27]\], improvement in thrombocytopenia and regression of hepatosplenomegaly exceeded that observed in the ICGG study. Recurrent anemia was associated with onset of concurrent illnesses including renal insufficiency, GI bleeding, or hematologic malignancy and risk of death was clearly associated with aging and cumulative co-morbidities. Persistent bone pain, the greatest cause for failure to achieve all therapeutic goals, is difficult to interpret objectively. Although chronic pre-treatment bone pain was often persistent, we found that there was little correlation with the presence of objective evidence of bone damage such as infarction, osteonecrosis or prior fractures, with severity of bone marrow infiltration and osteopenia, or with overall DS3 severity score. As patients age, it becomes more difficult to distinguish between Gaucher bone pain and that attributable to other musculoskeletal diagnoses. Unresponsive pain in young individuals is sometimes associated with drug-seeking behaviors not necessarily related to severity of GD1 based on objective measurements. In a scientific study, can an investigator legitimately dismiss positive patient pain reports of uncertain relevance, without introducing the possibility of bias? If not, are the resultant aggregate "report cards" an accurate measure of outcome? The contextual relevance of bone pain reports would be enhanced by accompanying assessments of duration and constancy of pain, effects on activities of daily living including school and work performance and fluctuations in the use of adjuvant analgesic medications. The clinical outcomes research field is increasingly emphasizing the centrality of patient-reported input and value-based medicine (the ability of an intervention to produce a clinical benefit in actual practice) as a necessary accompaniment to classical efficacy and safety studies with physician-conceived endpoints (evidence-based medicine) \[[@B29],[@B30]\]. Rare, chronic, phenotypically heterogeneous diseases such as GD1 for which treatment, when indicated, is generally lifelong and very expensive, are prime targets for value-based research studies that are applicable not only to individual patient care choices but also to justification of societal health care priorities. Our experiences with the medical complexity of a "simple Mendelian hereditary disease" population \[[@B31]\], with the confounding effects of age-acquired co-morbidities on even precisely defined and measured end points such as hemoglobin concentration and with the difficulties in contextual interpretation of patient-reported symptoms such as bone pain highlight the need for expert guidance when implementing patient-centered outcomes research \[[@B32]\]. Although such studies strive to maximize patient creativity and freedom of expression, they nonetheless require careful design and annotation of patient characteristics, clear objectives, defined nomenclature, and formulation of focused and unambiguous questions that are meaningful and important to the participants but whose answers will be internally consistent and amenable to rigorous analysis. Competing interests =================== Neal J Weinreb receives honoraria and expense reimbursement for serving on a Board of Advisors of the ICGG Gaucher Registry; travel reimbursements and/or honoraria and/or research support from Genzyme-a Sanofi Company, Shire, Pfizer Corporation, and Actelion Corporation. Olaf A Bodamer is member of the Speaker Bureau for Shire and Genzyme-Sanofi, receives research support from Shire and is on the US Advisory Board for Gaucher Disease for Shire. Authors' contributions ====================== MO participated in data analysis and helped to draft and to revise the manuscript. DB participated in the study design and data analysis and helped revise the manuscript. OAF helped to review and revise the manuscript. NJW conceived of the study, participated in the study design, data analysis and statistical analysis, and helped to draft and to revise the manuscript. All the authors read and approved the final manuscript. Funding sources =============== This investigation was supported in part by a research grant (Independent Sponsored Study Grant to NJW) from Genzyme-a Sanofi Company, Cambridge, MA, USA.
A teenager was in custody Wednesday after a fight outside of K Sandwiches in Linda Vista led to a shooting. San Diego police say the 17-year-old suspect fired at least five shots into the restaurant at someone he had been in a fist fight with just before. SDPD said the altercation involved students of Kearny High School and Mesa College. Customers were inside the restaurant at the time of the shooting but no one was injured by the gunfire, police said. "The amount of people who could have been injured in this shooting was incomprehensible," said Coedy Gilbert who lives in an apartment complex nearby. "It didn't matter if the crosswalk was off or on. They were running, they were bolting across the street. They had to get to safety. They were running through my complex they were running all up and down the streets." Police say the teenager was found with a handgun in his possession and was arrested. SDPD said the altercation does not appear to be gang-related.
Q: Remove history entry in Jquery Address When for example a customer adds an item to the cart I set the address through Jquery Address to /cart/23432 (productid). After the item has been added to the cart and the cart details have been shown, i want to change the url to /cart/. In that way when the customer refreshes the page, the product is not added again. However, now there will be two history entries 1. /cart/23432 2. /cart/ When i change the address to /cart/, how do i delete the previous entry (/cart/23432)? A: You can try this approach $.address.history(false); $.address.value(yoururl); $.address.history(true); This will replace the last history entry with the new url
Q: How to create an addin with a toolbar in it I am struggling to find a solution to my problem. I designed several UserForms and wrote many functions in a Workbook, and I added a new toolbar with buttons that call those functions. Now what I want is to save this Workbook as an add-in so that when I add the add-in on another PC the toolbars appear. But the toolbars does not appear. I could save the Workbook as an add-in with all the functions and the UserForms, but I couldn't get the toolbar. Any suggestions? A: By no means a solution, but maybe the following provides a starting point: From what you say I assume you managed to activate your .xlam add-in on another pc you could access all it's vba-code and userforms you could not access it's CustomUI-ribbon Check if your final .xlam still has the toolbar the toolbar in it when you deploy it: make a backup of your ready-to-deploy add-in file (*.xlam). open the file, either by changing it's file extension to .zip. (There is no need to rename it if you're using a file archiver like 7-zip) the contents of the file \customUI\customUI.xml should roughly resemble the following. Example XML: <customUI xmlns="http://schemas.microsoft.com/office/2006/01/customui" xmlns:shared="sharedNamespace" onLoad="onLoadRibbonDB" > <ribbon> <tabs> <tab idQ="shared:tabControls" label="AddIn_Beispiele" > <group id="grpA" label="Buttons"> <button id="buttonA" label="Button_large" image="bunny2" onAction="buttonA_Click" size="large"/> </group> </tab> </tabs> </ribbon> </customUI> Note that Excel won't show the ribbon if there are even minor errors in it. For testing, exclude anything that could result in an error, then re-introduce your ribbon controls step by step. If found the following the most common: id's are not distinct (e.g. used in other ribbons / add-ins) custom icons are not formatted correctly custom icons are not referenced correctly Off-topic: if you plan to deploy the file across numerous PCs, a simple macro like the following could work for you: Sub InstallAddIn() On Error GoTo skpError Dim path as String path = "L:\SQL_AddIn\SQL_AddIn_V1.0.xlam" name = "SQL_AddIn_V1.0" ' Copy the file With New FileSystemObject .CopyFile _ path _ , "C:\Users\" & Environ("USERNAME") & "\AppData\Roaming\Microsoft\AddIns\" End With ' Add-In Aktivieren AddIns(name).Installed = True MsgBox ws1.Cells(1, 2).Value & " installiert.", vbInformation Exit Sub skpError: MsgBox "Fehler #" & Err & vbNewLine & Error End Sub
Repairing tree bark? When the builder of our new house was clearing land he damaged the bark on two rather large oak trees. Is there a way I can prevent the trees from further damage by repairing or protecting the bark? In both cases the damaged areas are approximately 1 sq ft in size. Someone I know suggested putting roofing cement over the damaged areas to prevent water from getting under the bark and causing more damage. I normally don't read this news group, so please send mail to me directly. I'll post a summary if necessary. Thanks, Marty marty at sw.stratus.com
Caco-2 cell permeability and stability of two d-glucopyranuronamide conjugates of thyrotropin-releasing hormone. Caco-2 cell permeability and stability assays were used as an in vitro model to study the intestinal epithelial transport and stability of two analogues of thyrotropin-releasing hormone (TRH; Pyr-His-Pro-NH2). Peptide 1 (Pyr-His-Pro-D-glucopyranuronamide) was more permeable across the Caco-2 cell monolayer compared with the permeability of the parent TRH peptide (Papp=5.10+/-1.89x10(-6) cm/s c.f. Papp=0.147+/-0.0474x10(-6) cm/s respectively). The permeability of peptide 1 was improved threefold by attaching a 2-aminooctanoic acid moiety to the N-terminus to form peptide 2 (2-aminooctanoic acid-Gln-His-Pro-D-glucopyranuronamide) (Papp=16.3+/-2.47x10(-6) cm/s). The half-life for both peptide 1 and peptide 2 was approximately 20 min in a homogenate of Caco-2 cells compared with the half-life of TRH which is approximately 3 min. It was concluded that the permeability of peptides 1 and 2 was enhanced because of their increased stability, while the higher permeability of peptide 2 compared with peptide 1 may be attributed to its increased lipophilicity which results in enhanced passive diffusion.
WATCH: Brazilian Charity Has Cartoons Going Bald In Support Of Children With Cancer Warning: Grab a tissue (or the whole box) before you watch this video. A Brazilian charity is using Charlie Brown, Snoopy, Garfield, Hello Kitty, and more animated characters to show children with cancer that bald is beautiful. GRAACC collaborated with animators to create Bald Cartoons, a project that aims to empower children with cancer to feel less afraid and self-conscious about losing their hair. In a heartbreaking moment, several children with cancer spoke about the stares and looks they receive from people on the street. "I wanted people to understand that we are not sick because we want to [be]," one child says. If you're crying now, just you wait. The video cuts to a screen that reads, "A child with cancer deserves to be seen just like any other child." Next, it launches into a series of clips showing off some well-known cartoon characters -- all without their locks of hair! The children begin to smile as they see characters on screen that look like them. The response to the heartwarming project was overwhelmingly positive. 120 million people were impacted, and over 91% of social media users supported the endeavor, including the President of Brazil, DilmaRousseff, who tweeted her support. And what about the children? Well, they loved it. "I think it will be more normal to see a bald child," says one of the children. "Because everyone will see on TV, everyone in Brazil will see on TV." A teenager chimes in, "You have to be proud of each and every bald kid you see, because this person is fighting for life. And I think this is pretty dignifying." Latina Media Ventures, LLC is a participant in the Amazon Service LLC Associate Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to amazon.com, and is also a Linkshare, ShareaSale, and CJ affiliate. Our decisions to feature and recommend products is guided by our editorial decisions.
Q: Dimension of sum of subspaces Let $V$ be a vector space of dimension $29$ over the field $\mathbb{F}$. Suppose that $U$ and $W$ are subspaces of $V$ with $\dim (U) = 24$ and $\dim(W)=15$. What are the possible values of $\dim (U \cap W)$ and $\dim (U+W)$? I know that $\dim(U+W) = \dim (U) + \dim (W) - \dim (U\cap W) = 39 - \dim(U\cap W)$. How would I find the range of the dimension of $U+W$ and dimension of $U\cap W$? A: The dimension of $U \cap W$ can be no more than the dimension of $U$ nor more than the dimension of $W$. So there is the dimension of $U \cap W$ is at most $15$. Since both $U$ and $W$ are subspaces of $V$, which has dimension $29$, the dimension of $U+V$ is at most $29$. Putting these two together, we see that: \begin{align} 10 &\leq \dim (U \cap V) \leq 15 \\ 24 &\leq \dim (U + V) \leq 29 \end{align} I like to think of it as $29$ degrees of freedom available in $V$ and $U+W$ has at least the degrees of freedom occupied by $U$, which is $24$, and cannot surpass $29$. $U \cap W$ can do no more than $W$, which has $15$ degrees of freedom, and, trying to minimize the intersection with $U$, which has already occupied $24$ degrees of freedom, there are only $5$ left in $V$ for $W$, meaning it is forced to share at least $10$ with $U$.
Turkey sandwich, soup and coffee! Author Message GuestGuest Subject: Turkey sandwich, soup and coffee! Fri Apr 20, 2012 2:07 am I scrubbed at my tired eyes, taking a sip of my coffee as I sat in the booth. I had been working 12 hours straight and I was so tired I felt like passing out right here. The damn table looked comfortable. However I still had a few more patients to attend to before I could truly go home. I was lucky enough that I could drag myself away for some... lunch? I think it was lunch time. It was light on. "Turkey sandwich, cream of broccoli soup and a refill on this," I said, showing her my mug. "That's it." I leaned my face in my hands, closing my eyes as the waitress walked away. I loved and hated my job. I mostly hated it. It took time from my family, and it was so exhausting sometimes I wasn't sure how the hell I didn't faint damn near daily.. but the money was a huge perk, as was saving lives. I guess somewhere down the road I'd have to decide what was more important. Money or my life. But for now I worked till I was ready to drop and missing my family like crazy. I needed to pick up some groceries and a few other necessities that we still needed, but I needed something to eat. Sometimes I forgot to eat, so I was ready to eat something. I knew I didn't have breakfast, and it was getting on close to two o'clock. I walked into the cafe, intending only to get a sandwich to go, but I saw Dante about ready to pass out in one of the booths. The hostess asked if I'd like a table and I shook my head. "My friend is here. I'll sit with him." She nodded and I walked over to slide into the booth with Dante. "Long day getting you down, D?" I pulled my head back, a smile creeping across my lips when I saw Bianca. "You could say that. But it's nice to see you. So this helps." I smiled. "What are you doing all the way over here by the hospital? Everything's okay, right?" I laughed, nodding my head. "Just out shopping. Jackie's Mustang came in on the transport today, so I thought while the kids were at school and he was working on it, I'd run out and do some errands. So I caught a cab and came down." The waitress came over and asked what I'd like. "Turkey on rye and an ice tea." The waitress nodded and left us alone again. "So, how was A's ultra sound? Still too early to tell if it's a boy or girl, right?" I rubbed at my tired eyes again and stopped dead, my hand slowly falling down on the table. "Her what?" I thought hard, trying to remember what today was. "Tuesday. It's Tuesday... Oh God... It's Tuesday isn't it?" I let my head fall back against the booth. "Damn it, I'm scum!" I can't believe I forgot all about her appointment. I bit my lip, wincing slightly. "Oh, D. I'm sorry. I thought you'd gone." I felt horrible for bringing it up when he had forgotten all about it. "I bet she got a recording of it?" Wincing again, I reached across the table, taking his hand. "I know that doesn't make you feel any better. You could bring some flowers to her on your way home. Chocolates too, maybe? I know it doesn't make up for anything, but at least she knows you're sorry." I glanced down at her hand in mine before placing my other one over hers. "That's really great advice... but..." I sighed, "she's going to hate me. She practically begged me everyday last week not to forget and what did I do? Work a few hours and forget." I sighed. "Flowers and chocolates won't fix a boo boo this big." I nodded my head softly, looking down at his hand on mine, mine on his. It was strange how close both Jackie and I felt to both A and Dante. I mean, it wasn't a bad strange. It was good. It felt good to have people in my life I could depend on. For so long it was just Jackie, but now it was A and Dante as well. "She loves you, Dante. She will forgive you. She might be hurt right now, but I know it won't be the end of the world. Trust me." "I wanna trust you and I usually would but I know Abby and I know how she's going to feel. She's probably crying her eyes out right now." I pulled my hands from hers, rubbing at my face and holding my face there. "I really fucked this up. This one thing. It's all she asked of me." "You'll get through it, Dante. Tell you something about us women?" The waitress brought our food over and left us alone again. I picked up my ice tea, looking across the table at Dante. "Thing about us, we always forgive the men love. Sooner or later, and a lot of the time, no matter how upset we are, it's usually sooner rather than later." "Forgive, yes," I told him after sipping some of my tea. "Forgetting, that's another story. Jackie can really fuck up at times." I blushed, looking down at my sandwich. "Sorry. I don't usually curse like that, but Jackson can be really infuriating at times." I tossed enough money down for my lunch and Bianca's as well, also some tip and leaned over to give her a hug. "Thank you for your help." I pulled back. "Seriously. I'd be unprepared if it wasn't for you." I gave her a smile and walked out the door. I crossed the street, told them I was heading home and did just that.
Q: Problem creating type with Reflection I got a following base class: public class ValidationItem { public ObservableCollection<object> GetFilteredValues( ObservableCollection<object> values) { return new ObservableCollection<object>(); // nothing here yet } } I create a type which inherits this base type and I create a getter which is going to return a base class GetFilteredValues method result. This is how a new property should look like: public ObservableCollection<object> Values { get { return GetFilteredValues(_values); } set { _values = value; } } This is what I do: Type pType = typeof(ObservableCollection<object>); FieldBuilder fieldBuilder = tb.DefineField("_" + propertyName, pType, FieldAttributes.Private); PropertyBuilder propertyBuilder = tb.DefineProperty( propertyName, PropertyAttributes.HasDefault, pType, null); MethodBuilder getPropMthdBldr = tb.DefineMethod("get_" + propertyName, MethodAttributes.Public \| MethodAttributes.SpecialName \| MethodAttributes.HideBySig, pType, Type.EmptyTypes); getPropMthdBldr.SetReturnType(typeof(ObservableCollection<>).MakeGenericType(typeof(object))); ILGenerator getIL = getPropMthdBldr.GetILGenerator(); MethodInfo minfo = typeof(ValidationItem).GetMethod("GetFilteredValues", new[] { typeof(ObservableCollection<object>) }); // it's not null so everything is ok here getIL.Emit(OpCodes.Ldarg_0); getIL.Emit(OpCodes.Ldfld, fieldBuilder); getIL.EmitCall(OpCodes.Callvirt, minfo, Type.EmptyTypes); getIL.Emit(OpCodes.Ret); propertyBuilder.SetGetMethod(getPropMthdBldr); But each time I run an app and use this created type, I get an error "Common Language Runtime detected an invalid program". What am I doing wrong? Thanks in advance. A: When you call GetFilteredValues, the only thing on the stack is the ObservableCollection<object>. Since GetFilteredValues is an instance method, you also need to push this. Add a second Ldarg_0 before the existing one so that you push it on the stack before _values: getIL.Emit(OpCodes.Ldarg_0); getIL.Emit(OpCodes.Ldarg_0); getIL.Emit(OpCodes.Ldfld, fieldBuilder); getIL.EmitCall(OpCodes.Callvirt, minfo, Type.EmptyTypes); getIL.Emit(OpCodes.Ret); A: As per documentation to Ldfld, stack transition is the following An object reference (or pointer) is pushed onto the stack. The object reference (or pointer) is popped from the stack; the value of the specified field in the object is found. The value stored in the field is pushed onto the stack. So after executing getIL.Emit(OpCodes.Ldarg_0); getIL.Emit(OpCodes.Ldfld, fieldBuilder); you will have only field reference on the evaluation stack (without 'this'). To fix, duplicate arg_0 getIL.Emit(OpCodes.Ldarg_0); getIL.Emit(OpCodes.Dup); getIL.Emit(OpCodes.Ldfld, fieldBuilder); getIL.EmitCall(OpCodes.Callvirt, minfo, Type.EmptyTypes); getIL.Emit(OpCodes.Ret); This should help.
PESHAWAR: The Khyber Pakhtunkhwa (KP) government on Friday appointed the first woman as a deputy superintendent of police (DSP) in the Counter Terrorism Department (CTD). Hamida Bano, who is a grade 17 officer,… Khyber Pakhtunkhwa (KP) is finalising arrangements to introduce regular policing in all seven tribal districts and is working to establish about one hundred police stations across the tribal districts. A spokesman of… Senior minister directs authorities to take action over violation of Archeology Act 2016 PESHAWAR: Khyber Pakhtunkhwa Police has lodged an FIR over demolition of a historical house in Peshawar city, charging owner and… The authority of Khyber Pakhtunkhwa (KP) Police has been extended to tribal areas of Pakistan in the light of the Federally Administered Tribal Areas (FATA) Reforms. The government has already made laws… PESHAWAR: Khyber Pakhtunkhwa Police has devised a systematic and professional approach to apprehend criminals through introduction of Criminal Record Verification System (CRVS). According to a press release issued here Friday, Inspector General of… PESHAWAR: Khyber Pakhtunkhwa (KP) police on Saturday arrested two culprits involved in torturing, killing and making the video on an animal in Bannu. A video emerged online showing a man shooting dead a… MARDAN: An anti-terrorism court (ATC) on Monday convicted the suspect in the rape and murder case of four-year-old Aasma in Mardan, Muhammad Nabi, and handed him life imprisonment. The court also imposed… MARDAN: An eight-year-old girl with hearing impairment was raped in Bakshally area of Mardan, family and Khyber Pakhtunkhwa (KP) police said on Tuesday. Police stated that a case has been registered and nominated suspect… PESHAWAR: Students from the Federally Administered Tribal Areas (FATA) on Monday took out a protest rally against the alleged biased behaviour of the provincial police force. “The police force is being used…
Local ND Oil, Freight Shipments Detour Amtrak Trains Related Tags: BISMARCK, N.D. (AP) — The ice fishing in northeast North Dakota is the best it’s been in two decades, but some anglers can’t make it because trains handling freight and crude from the state’s oil patch are displacing Amtrak passenger service. Steve Dahl, owner of the Perch Patrol guide service, said he spent the past week calling hundreds of customers who had made reservations to fish at Devils Lake and stay in its namesake city. “The conditions are perfect but I’ve had to explain to them about this dumb train thing,” Dahl said. “For some of them who had their heart set on this, I would have rather told them I ran over their dog.” The federally funded rail corporation, which uses BNSF Railway Co. lines, said the “severe freight train interference” is causing long delays along its Chicago-to-Pacific Northwest Empire Builder route. In North Dakota, Amtrak trains are bypassing the cities of Grand Forks, Devils Lake and Rugby. Passengers in those cities are being bused to either Minot or to Fargo to reconnect to westbound or eastbound trains. The detours are expected to continue through February, said Amtrak spokesman Marc Magliari. Devils Lake Mayor Dick Johnson said the track congestion hurts the city’s economy and residents’ ability to travel, especially the elderly who routinely take trains to hospitals in Minnesota. The city of about 7,500 has no scheduled bus or flight service. “We depend on Amtrak as a key part of our public transportation service. We are crippled and landlocked without it,” Johnson said. “But oil and freight is taking priority over people, that’s pretty much a given.” BNSF said in a statement it has been “disappointed in our service” but that oil trains are not solely responsible for the delays because other freight volumes also have been increasing. Severe winter weather also “has significantly impacted our efforts to make service improvements for both Amtrak and all freight customers.” Fort Worth, Texas-based BNSF is part of Warren Buffett’s Omaha, Neb.-based Berkshire Hathaway Inc. Magliari said Amtrak has an operating agreement in place with BNSF that sets rates Amtrak must pay and incentives for BNSF to ensure Amtrak’s “on-time delivery of trains.” “The single, largest thing is trains’ punctuality,” Magliari said. “The mix of traffic volume is affecting our ability to run reliably in North Dakota.” BNSF is the biggest player the rich oil fields of Montana and North Dakota, hauling the bulk of the crude out of the region and the inbound freight that supports oil drilling. “There are oil trains, grain trains, trains hauling automobiles and lumber and a lot of each of them,” said Dale Niewoehner, who owns a funeral home in Rugby and is a former mayor of the city that bills itself as the geographical center of North America. He and Stephanie Armstrong, a funeral director in Devils Lake, said the lack of Amtrak service not only is hurting passenger service but also the ability to move human remains by rail. The funeral homes typically use Amtrak to ship bodies because of the convenience and low cost. “We shouldn’t be so naive to think that oil from the western part of the state isn’t going to affect us here too,” Armstrong said. Scores of workers moving to and from North Dakota’s rich oil fields have made the Empire Builder route one of Amtrak’s most popular long-distance overnight trains. It runs from Chicago to Portland, Ore., and Seattle. The number of people getting on and off the trains at the route’s seven stations in North Dakota has jumped from 111,000 in fiscal 2011 to 154,800 in fiscal 2013. Oil from North Dakota began being shipped by trains in 2008 when the state reached capacity for pipeline shipments. The state is now the nation’s No. 2 oil producer, behind Texas. BNSF said it plans to invest $5 billion in its railroad this year, including $900 million to expand capacity where crude oil shipments are surging. Its 2014 spending plan is about $1 billion more than last year. “The good news is that there is nothing systemically wrong with the system that cannot be corrected,” the railroad said in a statement. That’s of hardly a salve for Kelly Arnoldink of Allendale, Mich., who along with three of his buddies recently cancelled their ice fishing trip to Devils Lake because of the lack of train service. The drive was too far and the plane ride was too expensive, he said. Fishing for jumbo perch, walleyes, and northern pike in the bitter cold and on the frozen ice of Devils Lake was a dream vacation, he said. “I’d been planning it for more than a year and hopefully I can come back,” he said. “But what’s going up there now is just ridiculous.”
Athletics at the 2016 Summer Paralympics – Women's 5000 metres The Women's 5000m athletics event for the 2016 Summer Paralympics took place at the Estádio Olímpico João Havelange from September 14 to September 15, 2016. A single event was contested over this distance for the T54 classifications. Schedule Medal summary T54 References Category:Athletics at the 2016 Summer Paralympics
Q: Obtain Java 11 for macOS? I know in recent years the Java development cadence has changed, becoming much more rapid and more predictably scheduled. New plans were announced for regular Long-Term Support (LTS) releases. And I have heard Oracle changed their licensing terms for their Oracle-branded releases. All of this has left me confused as to how and where I can obtain Java 11 or later for my Mac. Can someone give some general overview of my options? A: tl;dr If you are an end-user needing a free-of-cost JVM to run a Java app on your Mac (rather than a developer), my personal recommendation is to download an .pkg file from AdoptOpenJDK. Open that file to run a macOS installer. You will then find a JVM installed in /Library/Java/JavaVirtualMachines. Later, you can upgrade in the same manner, deleting the old JVM from that folder. Details Yes, there have been several major changes to the evolution of Java in recent years, and they can be a bit confusing. Multiple vendors, both free and paid First, know that there are new options available for those wishing to pay for commercially supported implementations of Java. And know that Java is still available freely without cost. For both a summary as well as the gory details, read this white paper published by major figures in the Java community: Java Is Still Free OpenJDK Secondly, know that all releases for Java 11 and later for macOS are based on the same codebase, the open-source project known as OpenJDK. Apple contributes Mac-specific code to this project, and has staff working on this to make sure that Java continues to work well on macOS. IBM, Oracle, and many other companies have contributed code and testing as well. Oracle has recently announced their intention to reach feature-parity between their own Oracle-branded Java releases and the OpenJDK product; this even included the donation of some of their previously-commercial tools such as Flight Recorder to OpenJDK. The upshot is that you should see very similar behavior and features across the various sources of Java for macOS. JVM bundled within desktop apps If you make desktop apps to run locally on a Mac or other computer, you may continue to do so, and keep on using Swing and/or JavaFX as always. But the delivery of your app will change. Java Applet and Java Web Start technologies are being phased out. Oracle will no longer encourage end-users to have a JVM by itself installed. Instead, Oracle advises building your app as a standalone executable with a JVM bundled inside. This has already been commonly done on Macs, especially so if delivering an app through the Apple App Store. That approach is the new normal, to be done across all platforms including macOS, Windows, Linux, etc. The new Java Modularization technology that began with Java 9, including the jlink and jpackage tools, make it easier than ever to bundle a down-sized JVM with your app. For more info, see the white paper Java Client Roadmap Update of 2018-03. So, for the purpose of bundling with your app, you will need to consider redistribution/deployment rights when choosing a JVM vendor and product. Choosing a vendor Some major vendors of Java to consider for Java 11 and later: Azul SystemsOffering two product lines, Zulu based directly on OpenJDK with possibly a few tweaks, and Zing a specially-enhanced version of the Java platform. OracleOffering their own commercial product Oracle JDK and the quite-similar free-of-cost and GPL-licensed jdk.java.net. AdoptOpenJDK.netOffering free-of-cost builds of Java based on OpenJDK. Choose between with the usual HotSpot engine (just-in-time compiler & optimizer) or the OpenJ9 engine from Eclipse (previously from IBM). Here is a diagram chart that may help guide your decision-making. This chart is not necessarily complete or accurate. It is simply meant to help get you oriented. You should research further your options. A: If you want to have the simplest life possible, install homebrew and then install java with brew cask install java.
1.Overview of aging and COPD ============================ Chronic Obstructive Pulmonary Disease (COPD) is a common public health problem associated with high morbidity and mortality. Worldwide, the Global Burden of Disease study in 2015 estimated that 174.5 million adults had prevalent COPD \[[@b1-ad-11-1-129]\], and spirometry-defined COPD suggested as many as 384 million adults were affected \[[@b2-ad-11-1-129]\]. The China Pulmonary Health (CPH) study revealed the spirometry-defined overall prevalence of COPD was 8.6%, which accounted for 99.9 million Chinese adults aged 20 years or older \[[@b3-ad-11-1-129]\]. Globally, COPD is a major burden to current societies and economies. By 2030, COPD is expected to be the fourth leading cause of death \[[@b4-ad-11-1-129], [@b5-ad-11-1-129]\]. With regard to aging of the population, the CPH study showed that among people aged 40 years or more, the incidence of COPD was much higher, at 13.7% \[[@b3-ad-11-1-129]\]. COPD surveillance in United States showed the prevalence of COPD increased with advancing age at 6.6% for those aged 45-54 years, 9.2% for those aged 55-64 years, and 12.1% for those aged 65-74 years \[[@b6-ad-11-1-129]\]. Similarly, the mortality attributable to COPD increased with age \[[@b7-ad-11-1-129]\]. Impaired tissue growth and organ dysfunction are characteristics of aging, and aging is the greatest risk factor for chronic, non-communicable diseases \[[@b8-ad-11-1-129], [@b9-ad-11-1-129]\]. During aging, chronic, sterile, low-grade inflammation, called inflammaging, develops and this contributes to the pathogenesis of COPD \[[@b10-ad-11-1-129]\]. Current treatment measures for COPD such as bronchiectasis, anti-inflammaging drugs and anti-oxidants only relieve symptoms, or reduce the occurrence of acute exacerbations, but they do not delay or prevent the progression of the disease \[[@b11-ad-11-1-129]\]. To date, there are no effective countermeasures to the deterioration of lung function and disease progression in elderly COPD patients. Aging functions include mitochondrial dysfunction, cell-to-cell information exchange, protein homeostasis and extracellular matrix dysregulation, all of which are also closely associated with chronic inflammatory response and oxidant-antioxidant imbalance in the pathogenesis of COPD. COPD displays other characteristics of aging such as stem cell exhaustion, oxidative stress, cellular senescence, abnormal extracellular matrix and a reduction in endogenous anti-aging molecules. Recent studies show oxidative stress accelerates aging, and a consequence is that stem cell populations are depleted, antioxidant defenses are reduced, and there is defective mitochondrial function, all of which generate additional oxidative stress \[[@b12-ad-11-1-129]\]. Since COPD and inflammaging share similar characteristics, it is imperative for a better understanding of the development of COPD to identify and elucidate the mechanisms of oxidative stress, inflammaging and lung mesenchymal stem cell function. This is especially important in elderly COPD patients. In this review, we conducted an extensive literature appraisal of inflammaging-related studies associated with COPD. The aim was to assess our knowledge of the specific mechanisms operating in COPD that are responsible for oxidative stress, inflammaging and abnormal lung mesenchymal stem cell function, and their interactions. In addition, we used this knowledge to explore potential new treatment strategies aimed at delaying or preventing the progression of COPD. 2. Oxidative stress and COPD ============================ 2.1 Oxidation-antioxidant imbalance is involved in the development of COPD -------------------------------------------------------------------------- Several mechanisms associated with aging including oxidative stress, shortened telomere length and cellular senescence, are potentially involved in the pathogenesis of COPD \[[@b13-ad-11-1-129]\]. Previous studies showed that increased levels of biomarkers of oxidative stress (8oxodG, NT, F2-IsoPs and AGEs) were strongly correlated with the severity of airflow limitation in COPD elderly patients \[[@b14-ad-11-1-129]\]. Decreased levels of sRAGE and esRAGE have been detected in COPD elderly patients (i.e. with a mean age of 63 years), and their reduced levels have a significant association with forced expiratory volume in 1 second (FEV1) and FEV1/ forced vital capacity (FVC), and age demonstrated a covariation of sRAGE \[[@b15-ad-11-1-129]\]. Oxidant-antioxidant imbalance plays a crucial role in the development of COPD. Oxidative stress caused by smoking and environmental pollution can lead to extensive tissue damage and COPD exacerbation in patients at about 63 years of age \[[@b16-ad-11-1-129], [@b17-ad-11-1-129]\]. Some markers, such as MDA in sputum, appear to be useful for monitoring exacerbation-associated oxidative stress in COPD \[[@b18-ad-11-1-129]\]. Oxidative stress is a consequence of the action of reactive oxygen species (ROS). Exacerbation of COPD patients showed markedly increased ROS production in sputum neutrophils \[[@b19-ad-11-1-129]\]. ROS are mainly comprised of the superoxide radical O~2~^-^ and hydrogen peroxide (H~2~O~2~). ROS molecules such as O~2~^-^, ONOO^-^, H~2~O~2~, and OH^-^ cause damage to the integrity of airway epithelial cells. Nrf2 (nuclear factor-E2-related factor 2) is the major transcription factor that controls antioxidant responses. The expression level of Nrf2 decreases in the chronic obstructive lung, thereby unbalancing the oxidant-antioxidant levels. \[[@b20-ad-11-1-129]\]. Activation of NADPH oxidase 2 (Nox2) in neutrophils, macrophages and epithelial cells may produce the superoxide radical O~2~^-^. O~2~^-^ either forms a peroxynitrite ONOO- with nitric oxide (NO) or rapidly forms hydrogen peroxide (H~2~O~2~) under the action of superoxide dismutase (SOD). Under normal conditions, H~2~O~2~ is metabolized into water and oxygen by glutathione peroxidase (Gpxs), catalase (Cat) and Prdx6. However, in elderly patients with COPD, the levels of Gpxs and Cat decrease severely, which leads to a further increase of H~2~O~2~. Previous studies found that the plasma oxidative stress marker lipid peroxide MDA (malondialdehyde) was significantly elevated in patients with COPD. The MDA level in patients with severe COPD was significantly higher than in patients with mild to moderate COPD. There is a negative correlation between MDA level and forced expiratory volume in one second (FEV1)% (P \< 0.001) \[[@b21-ad-11-1-129], [@b22-ad-11-1-129]\]. The concentration of H~2~O~2~ in the exhaled breath of patients with smoking-induced COPD was significantly higher than in patients with non-smoking COPD. H~2~O~2~ was further elevated when the condition worsened. H~2~O~2~ levels are elevated in elderly patients with COPD due to various aging factors, which exacerbates oxidative stress. The above data indicate that the oxidant-antioxidant imbalance is manifested by abnormal oxidative free radical scavenging, and it induces DNA damage and premature senescence \[[@b23-ad-11-1-129]\]. This imbalance is a key factor involved in the development and progression of COPD, which is more severe in elderly patients with COPD. 2.2 Abnormalities in CFTR/pendrin transport and redox products of ion channel regulation, are involved in oxidative stress imbalance in COPD -------------------------------------------------------------------------------------------------------------------------------------------- CFTR (cystic fibrosis transmembrane conductance regulator) is the main ion channel for the secretion of fluid from the airway epithelial cells. There are two NBD (nucleotide binding site) active sites in the cytoplasm. Phosphorylation of NBD1 in combination with ATP initiates the opening of the CFTR channel, whereas ATP dephosphorylation into ADP, combined with NBD-2, closes the CFTR channel \[[@b24-ad-11-1-129]\]. After activation of CFTR, the channel is open, and chloride ions are transported from inside to the outside of cell in order to maintain the stability of the airway surface liquid (ASL) \[[@b25-ad-11-1-129]\]. In addition to transporting chloride ions, CFTR transports glutathione (GSH). GSH has a reducing function, which maintains a relatively high reduction state of ASL. GSH reduces the cross-linking reaction of mucin, and reduces the production of free radicals, leading to an anti-oxidative stress and anti-inflammaging state. A recent study showed that COPD emphysema pathogenesis is alleviated by treatment with a potent anti-oxidant with CFTR/autophagy-augmenting properties \[[@b26-ad-11-1-129]\]. Another study showed that reduced β-adrenergic sweat rate, which reflecting acquired CFTR dysfunction and sweat chloride are associated with COPD severity and clinical symptoms, and univariate analysis revealed a significant relationship with age \[[@b27-ad-11-1-129]\]. The CFTR M470V gene variant may be a potential modifier of COPD severity \[[@b28-ad-11-1-129]\]. Our studies and related studies found that CFTR down-regulation or inhibition causes the following changes: (1) ASL thickness is reduced by 30%; (2) ASL viscosity is increased 5 fold if accompanied by up-regulation of epithelial cell Na^+^ channel ENaC function; (3) CFTR inhibits inflammation, and the ability of epithelial cells to release inflammatory factors is enhanced after CFTR inhibition; (4) CFTR affects cell migration and post-injury repair; (5) since CFTR can transport GSH, inhibition of CFTR increases oxidative stress response of epithelial cells and the removal of sulfhydryl groups on mucins, and increases the viscosity of cross-linked aggravated mucus \[[@b29-ad-11-1-129]-[@b32-ad-11-1-129]\]. The studies described above suggest that CFTR plays an important role in chronic inflammation of the airways and in balancing oxidative/antioxidants. If CFTR is down regulated or inhibited, it affects airway mucus clearance and aggravates both the inflammatory response and epithelial oxidative stress. Studies show that CFTR on the cell membrane is significantly decreased in epithelial cells exposed to cigarette extracts, resulting in decreased thickness of the air layer of the respiratory epithelium \[[@b33-ad-11-1-129]\]. In vitro, CFTR, MRP2, or BCRP inhibition decreases GSH efflux after exposure to cigarette smoke extract. In a murine model, CFTR-, BCRP-, or MRP2-deficient mice were exposed to either air or acute CS. Only CFTR-deficient mice had reduced basal and CS-induced GSH in the epithelial lining fluid (ELF). BCRP- or MRP2-deficiency showed no effect on ELF, GSH basal or CS-exposed levels \[[@b34-ad-11-1-129]\]. Reduced CFTR expression decreases the transport of GSH, increases the viscosity of secretions, and leads to decreased respiratory dysfunction and decreased antioxidant capacity. Therefore, up-regulating CFTR channel function or increasing its cell membrane expression may be a novel strategy for intervention in COPD. Pendrin (SLC26A4) is an important member of SLC26 family of proteins, is expressed on the surface of airway epithelial cells, and participates in Cl^-^/HCO3^-^transportation. Pendrin is mainly involved in thickness regulation of ASL, and the expression of mucin. In addition to the above effects, pendrin transports thiocyanate (SNC^-^) to ASL and participates in the production of the antibacterial molecule OSCN^-^ \[[@b35-ad-11-1-129]\]. CFTR interacts with pendrin, and the R region of CFTR is phosphorylated by PKA to bind to pendrin\'s STAS (sulfate transporter and anti-sigma factor antagonist domain), which activates pendrin \[[@b36-ad-11-1-129]-[@b38-ad-11-1-129]\]. A recent study showed that pendrin mediates bicarbonate secretion and enhances CFTR function in airway surface epithelia \[[@b39-ad-11-1-129]\]. Whether pendrin is synergistic with CFTR transport of GSH is still unclear. Further studies should focus on employing inhibitors and activators of CFTR, inhibitors of pendrin, and highly specific small molecule compounds obtained by high-throughput screening, to regulate the function of these channels and provide important information for improving respiratory tract function ([Fig. 1](#F1-ad-11-1-129){ref-type="fig"}). To summarize, oxidative stress adversely affects the microenvironment of respiratory epithelial cells and impairs epithelial integrity. CFTR maintains a stable and reduced oxidative stress state in the respiratory epithelial microenvironment, participates in the migration and repair of respiratory epithelial cells and contributes to anti-inflammaging and anti-oxidative responses. CFTR interacts with pendrin to maintain the stability of the respiratory epithelial microenvironment. Manipulating the expression of CFTR/pendrin in epithelial cells, developing effective channel inhibitors and activators to regulate anti-oxidative function and efficacy are strategies that have potential clinical significance in treating elderly patients with COPD. Figure 1.Oxidative stress interacts with airway epithelial cells to participate in the development of COPD. Activators of CFTR, such as pendrin (SLC26A4), SLC26A8 and Ivacaftor, may improve respiratory tract function and delay the process of COPD. 3. Inflammaging and COPD ======================== 3.1 Inflammaging is the key cause of lung damage and the development COPD in elderly patients --------------------------------------------------------------------------------------------- The main features of inflammaging are chronic progressive elevation of the pro-inflammatory state and age-related chronic inflammatory processes, which are low, uncontrollable, asymptomatic, chronic, and systemic. Our research and that of others suggests that inflammaging is closely related to geriatric diseases and is the underlying cause of COPD \[[@b40-ad-11-1-129]-[@b42-ad-11-1-129]\]. Inflammaging is a key link in the conversion of inflammation to COPD \[[@b43-ad-11-1-129]-[@b45-ad-11-1-129]\]. A study in a population aged about 70 years showed that the decrease in growth differentiation factor 11 (GDF11), an anti-ageing factor, may be involved in the cellular senescence observed in COPD \[[@b46-ad-11-1-129]\]. The decline and onset of COPD in the elderly is closely related to systemic low-grade chronic inflammation, the so-called inflamm-ageing (also called inflammaging) hypothesis, and this might add to the burden of COPD in the elderly \[[@b47-ad-11-1-129]\]. A meta-analysis showed that the pathogenesis of COPD is closely related to the increase of serum leukocytes, IL-6, IL-8, C-reactive protein (CRP) and fibrinogen \[[@b48-ad-11-1-129]\]. Cell senescence is an important factor in the induction of chronic obstructive pulmonary inflammation. Aging eventually leads to the recruitment and colonization of lung neutrophils, macrophages and T cells in patients with COPD caused by smoking. Once inflammation is triggered, it causes a series of permanent inflammations and damages the lung parenchyma, which eventually results in the development of COPD. Therefore, intervention in aging may be an important breakthrough in the prevention, delaying or treatment of lung disease. Most important is that the elderly population can present with diminished lung function but without the presence of clinical COPD. Therefore, a confident clinical diagnosis of COPD needs to be made \[[@b49-ad-11-1-129]\]. There are many theories about the mechanism of inflammaging. The theory of oxidation-inflammaging and the theory of stem cell aging are particularly important. Based on the close association between oxidative stress, inflammation, and aging, De la Fuente M et al. \[[@b50-ad-11-1-129]\] proposed the oxidation-inflammation theory of aging. The theory holds that oxidative stress leads to inflammaging. Glucocorticoid resistance, sympathetic nervous system function changes, and parasympathetic nervous system function changes during chronic stress may be the mechanism of stress-induced inflammation \[[@b51-ad-11-1-129], [@b52-ad-11-1-129]\]. Inflammaging is closely related to stem cell aging. Chronic inflammation induces stem cell senescence during pathological processes of inflammaging. Studies show that mutation of the WRN gene in human stem cells produces features of premature aging, which include slowing of growth, increased DNA damage response, and secretion of a large number of inflammatory factors. Moreover, these mutant stem cells also exhibit accelerated loss of heterochromatin, which decreases heterochromatin stability, and in turn induces cellular senescence \[[@b53-ad-11-1-129]\]. Another study found that AU-rich-binding factor 1 (AUF1) controls both aging and inflammatory processes, not only by controlling inflammatory responses, but also by repairing telomerase to restore the length of telomeres at the ends of chromosomes and thereby prevent the acceleration of aging \[[@b54-ad-11-1-129]\]. Clearly, it is very important to determine the connections and interactions between aging, inflammation, oxidative stress, stem cells, and COPD. We propose that a better understanding of the above pathophysiological mechanisms and stem cell functions is needed. This will provide the foundation for novel strategies to simultaneously control oxidative stress, inflammation, and aging, which will delay the aging process in lungs and thereby prevent and/or treat COPD. 3.2 SIRT6 slows down the process of COPD by inhibiting the inflammaging pathway ------------------------------------------------------------------------------- Sirtuin 6 (SIRT6) is a member of the sirtuin family of NAD-dependent enzymes and is one of the few genes that regulates longevity and aging. SIRT6 plays a role in DNA repair, telomerase function, genome stability and cell senescence \[[@b55-ad-11-1-129]\]. In SIRT6-deficient mice, loss of the single-strand DNA damage repair function leads to genomic instability \[[@b56-ad-11-1-129]\]. Our previous study reported that icariin (ICA) up-regulates SIRT6 protein expression, inhibits NF-κB (p65) protein expression and reduces the expression of downstream inflammatory cytokines in aged mice. ICA down-regulates target genes (i.e.TNF-α, ICAM-1, IL-2, IL-6 and NF-κB) by acting directly or indirectly on SIRT6 \[[@b57-ad-11-1-129]\]. Takasaka et al \[[@b58-ad-11-1-129]\] found that SIRT6 expression was decreased in lungs of patients with COPD, whereas overexpression of SIRT6 inhibited smoking-induced senescence of human bronchial epithelial cells. Therefore, the properties of SIRT6 in delaying aging, and its anti-inflammaging action, make it a new target for the treatment of COPD. Further studies should explore the expression of SIRT6 in elderly patients with COPD, and the effect of SIRT6 on chronic obstructive pulmonary airway inflammation. 3.3 SIRT6 controls the pathophysiological mechanism of COPD by regulating PAI-1 ------------------------------------------------------------------------------- Plasminogen activator inhibitor-1 (PAI-1) is expressed by inflammatory cells such as monocytes, neutrophils, mast cells, and activated T lymphocytes. PAI-1 also affects the migration and activation of these inflammatory cells. PAI-1 levels are significantly elevated in various senescent cells (e.g. fibroblasts and endothelial cells). Klotho (kl/kl) deficient mice are used as an aging model and show significantly higher levels of PAI-1 in plasma and tissues than normal mice \[[@b59-ad-11-1-129]\]. Plasma PAI-1 concentrations are above the upper limit of normal in patients with the hereditary premature aging Werner syndrome \[[@b60-ad-11-1-129]\]. Therefore, PAI-1, is considered to be a marker molecule for aging and is widely used in aging-related studies both in vitro and in vivo. PAI-1 affects inflammatory factor levels and cell migration processes. Studies show increased levels of PAI-1 in patients with COPD and this is associated with oxidative stress-induced activation of NF-κB \[[@b61-ad-11-1-129]\]. A previous study reported that the concentration of PAI-1 in alveolar lavage fluid correlated with mortality in patients with compromised host defense mechanisms \[[@b62-ad-11-1-129]\]. We used the mouse PAI-1 knockout model and found that PAI-1 is a key regulator of early lung inflammation, which affects the recruitment of neutrophils in the lung when knocked out \[[@b63-ad-11-1-129]\]. The pivotal role of PAI-1 in the development of inflammation in the lungs, its mode of activation (which is dependent on the NF-κB pathway), and particularly its negative effects on aging, suggest PAI-1 may be a downstream target of the SIRT6 pathway ([Fig. 2](#F2-ad-11-1-129){ref-type="fig"}). Actively exploring the role and mechanism of action of inflammaging in COPD and using this information to delay the development of COPD through anti-inflammaging and anti-aging treatments, is a new direction and new strategy for the prevention and treatment of COPD. Figure 2.Effect of SIRT6 and PAI-1 on smoking-induced pulmonary inflammation. 4. Inflammaging and oxidative stress affect mesenchymal stem cells during the development of COPD ================================================================================================= Mesenchymal stem cells have the ability to self-renew and have multipotent differentiation potential. These cells play an important role in tissue damage repair, homeostasis maintenance and immune regulation \[[@b64-ad-11-1-129], [@b65-ad-11-1-129]\]. In the lung, stem and progenitor cells are the main regenerative cells, which maintain the steady state and repair damage to lung epithelial cells. Current studies identify a variety of lung-derived stem/progenitor cells with self-renewal and differentiation potential, which include basal cells from the airway, secretory rod-like cells and alveolar type II epithelial cells from the alveoli, and mesenchymal stem cells from the pulmonary stroma \[[@b66-ad-11-1-129]\]. Direct delivery of FGF-10 in the lungs of rats increases lung resident-MSCs in the treated lungs, which suggests that the protective effect of FGF-10 could be mediated, at least in part, by mobilizing lung resident-MSCs \[[@b67-ad-11-1-129]\]. MSC therapy is an important tool for regenerative medicine. Many studies have confirmed that MSCs have obvious therapeutic effects in various acute and chronic lung diseases \[[@b66-ad-11-1-129]\]. A previous study showed that MSCs can treat lipopolysaccharide induced acute lung injury and ischemia-reperfusion induced lung injury \[[@b68-ad-11-1-129]\]. 4.1 Application of MSC therapy for COPD --------------------------------------- In a COPD animal model, exogenous MSCs reduced the destruction of emphysema and pulmonary function caused by cigarette smoke \[[@b69-ad-11-1-129], [@b70-ad-11-1-129]\]. MSCs increased the expression of vascular endothelial growth factor (VEGF), VEGF receptors and TGF-beta 1, reduced lung cell apoptosis, inhibited the inflammatory cytokines TNF alpha, IL-1 beta, MCP-1, as well as reducing the secretion of IL-6 \[[@b69-ad-11-1-129]\]. Clinical trials based on MSC therapy for COPD are underway, these trials use MSCs in different ways to obtain a therapeutic outcome. A placebo-controlled, randomized trial of MSCs in COPD in patients around 68 years old suggested there were no significant differences in pulmonary function tests or quality-of-life indicators following MSC administration. However an early, significant decrease in levels of circulating C-reactive protein (CRP) was observed, and MSC administration appears to be safe in patients with moderate to severe COPD \[[@b71-ad-11-1-129]\]. Another study using one-way endobronchial valves (EBV) together with MSC administration, provided evidence of decreased levels of circulating CRP, BODE (Body mass index, airway obstruction, dyspnea, and exercise index) and MMRC (Modified Medical Research Council) scores \[[@b72-ad-11-1-129]\]. Systemic MSC infusion may be useful in the attenuation of inflammation in COPD patients \[[@b73-ad-11-1-129]\] . Other studies verified that autologous MSC treatment in severe emphysema is feasible and safe \[[@b74-ad-11-1-129]\]. From the above research, we propose that current clinical trials on patients with COPD support that MSC therapy improves inflammatory responses in patients with COPD, but the improvement of pulmonary function is not obvious \[[@b75-ad-11-1-129]\]. Thus, the efficacy of MSCs in the treatment of COPD remains controversial. From the perspective of treatment, a one-time administration of MSCs can alleviate the inflammatory reactions in the airway and lung through a paracrine effect, but whether this permanently improves the airway reconstruction is more important and will most likely rely on the number and activity of endogenous MSCs in bodily tissues. COPD is a disease that accelerates aging of the lungs and is closely associated with other aging effects \[[@b76-ad-11-1-129]\]. Aging leads to a decrease in the number and activity of stem cells in the trachea tissue and a consequence is a significant decrease in the ability to repair tissue \[[@b77-ad-11-1-129]\]. Elderly patients with COPD have significantly reduced stem cell numbers and activity. Therefore, it is important to understand the effects of senescence, oxidative stress and chronic inflammation on both endogenous MSCs in the lungs of COPD patients, and on exogenous, administered MSCs used to treat COPD. 4.2 Inflammaging and oxidative stress associated with COPD lead to an abnormal microenvironment for endogenous MSCs ------------------------------------------------------------------------------------------------------------------- Studies have found that compared with young mice, the number of alveolar type I and type II epithelial cells in elderly mice is generally decreased, and the regeneration capacity of alveolar type II epithelial cells is weakened \[[@b78-ad-11-1-129]\]. Senescence of alveolar type II epithelial cells was also found in lung tissues of patients with COPD \[[@b79-ad-11-1-129]\]. Bone marrow MSCs from elderly patients show increased levels of intracellular reactive oxygen species, DNA methylation changes, telomere shortening and increased aging-related protein expression of the beta-galactose glucoside enzyme, all of which contribute to inhibiting the differentiation of MSCs \[[@b80-ad-11-1-129]\]. Moreover, bone marrow MSCs showed reduced proliferation, migration and altered immune response \[[@b81-ad-11-1-129]\]. Gene expression profile studies found aging human MSCs show aging-related phenotypes, and contain a variety of highly expressed factors that promote inflammation \[[@b82-ad-11-1-129]\]. Extracellular matrix (ECM) also plays an important role in lung stem cell injury repair. In aging connective tissue, type I collagen is increased while type III collagen, and proteoglycan expression is decreased \[[@b80-ad-11-1-129]\]. Matrix composition changes with age and this affects adhesion, proliferation and migration of stem cells in the lung. In patients with COPD, alveolar structure is often damaged, which leads to the failure of endogenous lung stem/progenitor cells to reconstruct the functional lung structure. The lungs of COPD patients are more exposed to tobacco smoke, airborne particulate matter and pollutants, which cause an oxidant-antioxidant imbalance in the lungs, resulting in increased ROS production in the extracellular matrix. ROS cause cell DNA damage, promote the release of inflammatory cytokines, inhibit cell proliferation, promote apoptosis, and decompose extracellular matrix \[[@b83-ad-11-1-129]\], which hinder the repair by lung stem cells. We propose that the combination of abnormal stem cells malfunctioning in the hostile microenvironment of the lungs in patients with COPD, particularly in the elderly patients with COPD, contributes to the destruction of lung tissue and the irreversible decline in lung function. Methods to improve the activity of endogenous MSCs or supplement/replace their activity by the use of exogenous stem cells are needed. Moreover, treatments that provide a more conducive microenvironment for enhanced stem cell repair of damaged lungs in elderly patients with COPD are also required. Oxidative stress and chronic inflammation accelerate the progression of stem cell aging and COPD through the following mechanisms. In COPD patients, excessive ROS lead to an increase in senescent cells, and the senescence-associated secretory phenotype (commonly referred to as SASP) further stimulates inflammation, alveolar structural destruction and endothelial dysfunction. ROS also leads to loss of stem cell self-renewal capacity and stem cell depletion \[[@b84-ad-11-1-129]\]. ROS mediated phosphorylation of p53 via p38 MAPK, induces the expression of the cell cycle inhibitor p21, thereby inhibiting cell proliferation \[[@b85-ad-11-1-129]\]. In human endothelial cell-derived MSCs, oxidative stress causes rapid phosphorylation of the adaptor protein 53BP1, activating DNA damage responses and causing irreversible arrest of the cell cycle in the G0/G1 phase. DNA damage response activates p53, which up-regulates p21 and thereby inhibits pRb protein, leading to senescence growth inhibition \[[@b86-ad-11-1-129]\]. The use of glutathione synthetase inhibitors to induce increased expression of ROS in stem cells aggravates DNA damage and leads to increased expression of cell cycle inhibitors p16, p14 and p21 \[[@b87-ad-11-1-129]\]. In addition, senescent cells up-regulate the expression of the cell cycle inhibitor p16, which plays an important regulatory role in oxidative stress-induced stem cell senescence and proliferation inhibition. Up-regulation of p16 is also closely related to p53 expression and telomere shortening. Studies show ROS regulate the epigenetic process of stem cells, promote their DNA methylation and acetylation, thereby inhibiting stem cell proliferation and differentiation \[[@b88-ad-11-1-129]\]. Elevated ROS inhibits the expression of the deacetylase SIRT1 during COPD and aging. Spontaneous alveolar cavity enlargement occurred in SIRT1+/- mice, and activation of FOXO3-related pathways by cigarette smoke further aggravates alveolar cavity enlargement and cell senescence \[[@b89-ad-11-1-129]\]. Studies in a murine model, implicated the ROS-producing enzyme NOX2 in the pathogenesis of human emphysema. In mice, macrophage-specific NOX2 contributed to elastase-induced emphysema via SIRT1/MMP-9 pathways \[[@b90-ad-11-1-129]\]. In patients with COPD, SIRT1 expression is decreased, which in turn promotes the release of the inflammatory factor IL-8. At present, oxidative stress and chronic inflammation have a well-established role in the development and progression of COPD, however simple antioxidant and/or anti-inflammaging treatments cannot control or reverse the clinical symptoms of COPD, especially in the elderly. Lung tissue destruction and lung function decline in patients with lung obstruction. Improving the stem cell microenvironment and restoring the repair function of endogenous stem cells is crucial in the treatment of chronic obstructive pulmonary disease, especially in elderly patients with chronic obstructive pulmonary disease. Other recent studies demonstrated that KGF-2 repairs alveolar epithelium and vascular endothelium by promoting proliferation of lung MSCs \[[@b91-ad-11-1-129]\]. Figure 3.A new strategy for treatment of elderly patients with COPD; combining antioxidants and anti-inflammaging drugs with improved endogenous/exogenous MSC function. 5. Possible therapeutic direction in elderly patients with COPD =============================================================== MSCs have the characteristics of multipotent differentiation potential, immune regulation and self-replication. In addition to ROS-dependent depletion of MSCs, ROS also interacts with inflammatory aging, which causes an increase in senescent cell numbers and alters the microenvironment of MSCs in the lungs of COPD. Based on the results of the studies described above, inflammaging, oxidative stress and stem cell dysfunction are involved in the development of COPD. Therefore, in addition to anti-inflammaging drugs and antioxidants, improving the microenvironment and repair function of MSCs is key to the treatment of chronic obstructive pulmonary disease([Figure 3](#F3-ad-11-1-129){ref-type="fig"}). In this article, we reviewed the interaction between oxidative stress, inflammaging and stem cell dysfunction. On one hand, oxidative stress and inflammaging increases the aging-related phenotype, induces and aggravates the inflammatory response in the airway, and thus changes the microenvironment of stem cells with regard to their proliferation and differentiation. Moreover, oxidative stress and inflammaging leads to MSC exhaustion. Our research on COPD now focusses on the mechanism of oxidative stress and inflammaging, and the involvement of these mechanisms in MSC exhaustion. Employing a combination of antioxidants, anti-inflammatories and MSC treatment, is a possible therapeutic strategy for treating elderly patients with COPD. This study was supported by the National Natural Science Foundation of China (81870044 and 81600056) and National Key R&D Program of China (2018YFC2000 301). Conflict of interests The authors have no competing interests to declare. [^1]: These authors contributed equally to this work.
Sen. Tom Coburn (R-OK) argued Monday that the notion the United States will default if Congress doesn’t raise the debt ceiling is pure “rumor.” “Look, the debt ceiling and the [continuing resolution] are the same thing,” Coburn said on “CBS This Morning.” “There is no such thing as a debt ceiling in this country because it’s never been not increased and that’s why we’re $17 trillion in debt.” “And I would dispel the rumor that’s going around that you hear on every newscast that if we don’t raise the debt ceiling, we’ll default on our debt. We won’t,” he continued. “We’ll continue to pay our interest, we’ll continue to redeem bonds and we’ll issue new bonds to replace those. So it’s not entirely accurate.” Republicans are considering merging re-opening the federal government with the upcoming fight to raise the debt ceiling. Both President Barack Obama and Treasury Secretary Jack Lew have warned of potential dire consequences on the country’s economy if the debt ceiling is not lifted by the Oct. 17 deadline. [h/t Huffington Post]
189 F.2d 708 LIPSCOMBv.TENNESSEE COAL, IRON & R. CO.TENNESSEE COAL, IRON & R. CO.v.LIPSCOMB. No. 13441. United States Court of Appeals Fifth Circuit. June 25, 1951. William L. Hogue, Asst. U. S. Atty., John D. Hill, U. S. Atty., Birmingham, Ala., for appellant. Andrew J. Thomas, Birmingham, Ala., for appellee. Before HUTCHESON, Chief Judge, and BORAH and STRUM, Circuit Judges. JOSEPH C. HUTCHESON, Chief Judge. 1 Brought to recover $3301.20, the difference between the pay of the position he was assigned to on his return from the service and the one he claims he was entitled to have been placed on, this is another in the long catalogue of suits which have been brought in vindication of the rights accorded returned veterans by the Selective Training and Service Act of 1940, as amended.1 2 The claim in substance was: that on his re-employment by the defendant in February, 1946, after a leave of absence on military service since October, 1943, he should have been assigned to the position of lathe machine operator rough, or of roughing lathe helper; that instead, defendant reemployed him as crane operator, the same position he had had when he left; and that in doing so, it had, in violation of his rights under the act, deprived him of his seniority rights in favor of one Elrod who had succeeded him as craneman and had then been successively promoted to roughing lathe helper and machine operator. 3 While there were other defenses, the one relied on mainly below and entirely here is: that the re-employment of plaintiff in February, 1946, in his former position was not in derogation of, but in compliance with, the act;2 that however, by virtue of a written agreement of date June 10, 1946, between defendant and the United Steel Workers Union, the recognized bargaining agent, plaintiff became entitled, within fifteen days thereafter, to be placed in the position of roughing lathe helper with seniority in such position from November 21, 1943, and, because he was not assigned to that position until February 20, 1948, which position he now holds, he was entitled to recover wages lost by the delay in assigning him to it in a sum of which was agreed to as $119.87, less payroll deductions. 4 The case was tried to the court without a jury, and, the evidence all in, the district judge, on full findings of fact and of law, held: that plaintiff, upon his return was not, and would not have been except after six months' experience as roughing lathe helper, qualified to perform the duties, and he was, therefore, not entitled to be then employed as roughing lathe operator; but that he was qualified however, to perform, and should have been assigned to the job of, roughing lathe helper with seniority on that job from November, 1943, and was entitled to recover the agreed wages lost by not being earlier assigned to that job. He found, too: that, under the practice and custom recognized by the defendant and its employees and prevailing in that part of the defendant's plant where plaintiff was employed, seniority as to both promotion and increase or decrease in forces operated on the individual and separate job positions or levels in the line of promotion; that because by the time plaintiff could have qualified as a roughing lathe operator, Byron Elrod, during the period after plaintiff's return, acquired age on the job as roughing lathe operator, which gave Elrod job seniority as roughing lathe operator, before plaintiff could have qualified as roughing lathe operator; and that plaintiff was, therefore, not entitled to seniority over Elrod as to that position. 5 He, therefore, entered a judgment for plaintiff: (1) that plaintiff recover the sum of $115.25, less $15.59; (2) that the defendant be, and it is hereby required to maintain plaintiff's seniority as a roughing lathe helper ahead of and superior to that of Byron V. Elrod insofar as said seniority concerns increase or decrease in forces, but the defendant is not required to maintain plaintiff's seniority with respect to promotion to the position of roughing lathe operator ahead of, or superior to, that of Byron V. Elrod. 6 Plaintiff is here appealing from the part of the judgment denying him seniority over Elrod as to the position of lathe operator and a recovery of lost wages accordingly. 7 Defendant, while not complaining of the effect of the judgment either as to the seniority adjudged or as to the amount of back pay awarded, has cross appealed in complaint of some of the findings of the court and of the court's failure to amend and add to its findings as requested by defendant. 8 Matching plaintiff's complaint of the judgment with defendant's, the matter before us comes down to this: Was the district judge wrong in denying plaintiff seniority over Elrod as to the position of lathe operator? Appellant insists that he was because he was either entitled upon his return to be assigned to the position of lathe operator or, if he was not so entitled but only to be assigned to the position of roughing lathe helper with seniority as to that position, he was nevertheless entitled to maintain that seniority not only as to that position but as to the next position in line of promotion, lathe operator. 9 Urging upon us that it is illogical to hold, as the trial court did, that plaintiff was entitled to seniority over Elrod as roughing lathe helper but was not entitled to it as to lathe operator, a position which Elrod got by first serving as roughing lathe helper, appellant insists that the judgment must be reversed. 10 Appellee, on its part, urges: that when plaintiff went into the service, it was under the protection of an act which entitled him not to a promotion during his absence but a return to the same position;3 that since when he went into the service he had no contract entitling him to such promotion on seniority alone, and no contract, as in Armstrong's case, 73 F.Supp. 329, relied on by appellant, was made while he was in the service which enlarged his rights, he was not entitled on his return to promotion on seniority alone; that by virtue of the contract of June 10, 1946, he became entitled to be employed as of his return in a position which he was qualified to fill on his return that would result in a promotion with seniority as to that position; and that it was because of that contract alone and not because of any requirement of the act that he was so entitled to the position of roughing lathe helper which he was able to fill on his return. 11 It further points out that, under the contracts and practices existing between defendant and the bargaining agent for the employees, and as found by the district judge, it was established that a seniority acquired as to a particular job or position may not be made to give way to a general seniority; and that, under the unpear on either the appeal or the cross ap-disputed facts and as found by the court, plaintiff was not entitled on his return to the position of lathe operator, and, while he was getting the necessary experience, Elrod had already acquired seniority in that position. 12 So pointing, it urges upon us that, notwithstanding the erroneous finding of the court that plaintiff was entitled to reemployment as a roughing lathe helper from the time of his return, the judgment must, nevertheless be affirmed. This is because plaintiff was entitled from and after the making of, and under, the contract in June, 1946, to receive the position of roughing lathe helper with seniority and defendant therefore owes plaintiff the amount awarded him the difference in pay between the position of craneman and roughing lathe helper from the time of his return. 13 We agree with appellee, and, agreeing, affirm the judgment. A careful reading as a whole of the findings of fact and of law of the district judge, in the light of the evidence and the judgment, leaves us in no doubt: that the amounts agreed to be due plaintiff were stipulated as due from June, 1946, to February, 1948, and not as inadvertently stated by the court from February, 1946, to February, 1948; and that the finding and the conclusion of law that plaintiff was entitled to recover for that period were erroneous. It convinces us, too, that, though erroneous, they were inadvertent and also without bearing or effect upon the substance of the findings and judgment. The findings and conclusions as a whole particularly fact findings 13 and 14, and the judgment, make it quite clear that the district judge understood and gave full effect to the contract of June 10, 1946, and that in finding and deciding as he did, no conflict or inconsistency was intended or occurred between the decision in this case and those in the other cases from the Northern District of Alabama cited and relied on.4 14 No reversible error being made to appeal, the judgment as to both appeals is 15 Affirmed. Notes: 1 50 U.S.C.A. Appendix, §§ 308 and 357 2 Fishgold v. Sullivan Drydock & Repair Corp., 328 U.S. 275, 66 S.Ct. 1105, 90 L. Ed. 1230; Aeronautical Industrial Dist. Lodge 727 v. Campbell, 337 U.S. 521, 69 S.Ct. 1287, 93 L.Ed. 1513; Meehan v. Nat'l Supply Co., 10 Cir., 160 F.2d 346; Hewitt v. System Federation No. 152, 7 Cir., 161 F.2d 545; Harvey v. Braniff International Airways, 5 Cir., 164 F. 2d 521; Raulins v. Memphis Un. Station Co., 6 Cir., 168 F.2d 466; Oil Workers Int. v. Sinclair, 5 Cir., 171 F.2d 192; Special Service Co. v. Delaney, 5 Cir., 172 F.2d 16; Bond v. Tennessee Coal, Iron & R. Co., D.C., 73 F.Supp. 333 3 See authorities cited in note 2, supra 4 Armstrong v. Tennessee Coal, Iron & R. Co., D.C., 73 F.Supp. 329; Bond v. Tennessee Coal, Iron & R. Co., D.C., 73 F.Supp. 333
A case of severe MAGIC syndrome treated successfully with the tumor necrosis factor-alpha inhibitor infliximab. We report a patient with an overlap of relapsing polychondritis and Behcet disease whose cartilaginous inflammation and genital lesions were refractory to corticosteroids and immunosuppressants, but fully remitted with the tumor necrosis factor-alpha inhibitor, infliximab. We believe this case represents the first report of a response to a tumor necrosis factor inhibitor in a patient with mouth and genital ulcerations with inflamed cartilage syndrome.
Any reasonable Game of Thrones fan has given "The Battle of the Bastards" repeated viewings throughout the last week. It's the grandest and most tastefully filmed fight scene ever put on the small screen. The showrunners put in days of work, hundreds of extras, blood, sweat, and tears into making it happen. HBO spared no expense. But, did they overlook one small detail? That Jon Snow's sword should be made of metal? You decide. Matt Miller Culture Editor Matt is the Culture Editor at Esquire where he covers music, movies, books, and TV—with an emphasis on all things Star Wars, Marvel, and Game of Thrones. This content is created and maintained by a third party, and imported onto this page to help users provide their email addresses. You may be able to find more information about this and similar content at piano.io
The wear plates on this bucket were obviously worn. The way the wear bars were installed from the factory was not the best way. When the bars are installed parallel with the flow of the material they do not protect bucket well. We removed the damaged wear bars and installed new wear bars perpendicular to the flow of material. The reason this configuration is better is the dirt (in this case) will get caught between the the bars and protect the bucket bottom. The material then is wearing against the hardened wear bars and dirt. We could do this kind of work all day, we really enjoy working with pipe. Pipe fabrication takes a different set of skills than structural fabrication and we thrive in the challenge. A couple of wyes and a spool We welded the pipe using a dual shield wire – E71T-1 – one of the easiest wires to use in a shop setting. It is termed “dual shield” because it uses both a shielding gas and flux which is inside the tubular wire. This is the base of one of the legs of a three legged tower we worked on in May, 2012. This tower is in Fortuna, CA just south of Eureka. The weather was very nice for working when I was there, overcast and cool. However, when Dan was there they couldn’t work one of the days due to rain and wind. All the welding was done using flux core wire, E70T-8. I repaired this “Remu” type excavator bucket for BlueIron, Inc. They had a job in Santa Cruz so I traveled there to work on the bucket. The blade was obviously worn, I cut it off and replaced with a new one. The grinders were also worn and I hardfaced using tungsten powder. Hardfacing is the overlaying of a harder material than the parent metal to help the existing metal last longer. There are several types of hardfacing. Some are designed to withstand abrasion which you would use in an application where the piece was subject to constant wear from dirt, sand, or gravel, etc. Others are designed for impact resistance which would be used in applications where the piece is used in crushing or chipping. The product I used is designed for high wear applications, it is a very specialized type of hardfacing and provides for excellent wearability.
Course Title: Determine maintenance strategy Part A: Course Overview Program: C5194 Course Title: Determine maintenance strategy Portfolio: BUS Nominal Hours: 30.0 Regardless of the mode of delivery, represent a guide to the relative teaching time and student effort required to successfully achieve a particular competency/module. This may include not only scheduled classes or workplace visits but also the amount of effort required to undertake, evaluate and complete all assessment requirements, including any non-classroom activities. This course defines the competency required to determine and operationalise maintenance strategies and supporting processes to achieve continuity of IT operations and business functions. If you are undertaking this course in Melbourne from semester 2, 2012 onwards your teacher will advise you if you require access to a computer for the course. It is recommended that you have access to a mobile computing device to allow greater flexibility in terms of where you can work on campus outside class times. Students must demonstrate an understanding of all elements of competency to be deemed competent. A range of assessment methods are used to assess practical skills and knowledge, for example: • direct questioning combined with review of portfolios of evidence and third party workplace reports of on-the-job performance by the candidate • review of authenticated documents from the workplace or training environment • demonstration of techniques
1. Field of the Invention This invention relates to a portable circular hand held power saw base plate. This base plate has the capability of engaging a system to preform a precision perpendicular cut to the longitudinal axis of the material being cut. This base plate is not an add on saw guide to a hand help circular power saw, but rather, a new type of base plate that can be manufactured with the saw or as a retro--fit precision saw base replacement for existing circular saws. This base plate can be used like any presently manufactured circular saw base plate but has the capability of engaging the precision cut mechanism. 2. Description of the Prior Art A review of the art in the field reveals a number of devices designed to guide a circular saw blade perpendicularly across a longitudinal axis. Examples include: U.S. Pat. No. 4,777,726 issued to randy flowers which describes a guide for portable hand help power circular saws. The primary drawbacks to this invention are the limitation on the width of the material being cut when the guide is in the operating position. From the vertical center axis of the saw blade to the stop positions of the saw guide there is a very limited space for cutting the desired product. Also the coil springs used for resistance to the forward movement of the saw itself, and for the return of the slide plate, are a poor choice of springs as this type of spring offers varying degrees of resistance and a varying degree of force for the slide plate return. PA1 U.S. Pat. No. 4,602,435 issued to Jim Z. Nishioka which describes an aligning mechanism for power hand saws. The primary drawbacks to this invention are the use of a coil spring, which once again, offers varying degrees of resistance and a varying degree of force for the aligning device return, also the aligning device is to the far left of the main force of the forward movement of the saw, thus, this is awkward to hold without getting a pivotal action against the aligning device, which would mis-align a true perpendicular cut. PA1 U.S. Pat. No. 5,279,037 issued to Alfred R. Leatherman which describes a guide for a portable sae. This invention is limited to sheet material and longitudinal cuts as the trailing pin described would not engage normal widths of material before they are already cut. U.S. Pat. No. 4,619,170 issued to Peter Maier which describes a guide for a hand power tool. The primary draeback for this device id than it requires the clamping of an external guide strip to the work to be cut and an attachment affixed to the saw base to be guided along the strip. A review of the prior art reveals that the previous inventions are very limited in use and scope. That is, they are limited in the width of the product to be cut, or not refined in design by the type of springs used or require clamping an external guide on the work to be cut.
--- title: Contributing to Gatsby.js description: Learn about contributing to one of the most welcoming communities helping develop the future of the web disableTableOfContents: true --- Thanks for being interested in contributing! We're so glad you want to help! Below you'll find guides on the Gatsby community, code of conduct, and how to get started contributing: - [Community](/contributing/community/): Learn why you should contribute to Gatsby, the most effective ways to do so, and all about the benefits (did we mention the free swag?) - [Code of Conduct](/contributing/code-of-conduct/): Read about what we expect from everyone participating in Gatsby to make it the most friendly and welcoming community - [Gatsby Style Guide](/contributing/gatsby-style-guide/): The art of contributing to Gatsby, a.k.a. the detailed requirements that will make it more likely your contribution is accepted with minimal changes - [How to Contribute](/contributing/how-to-contribute/): How to get the most out of your Gatsby contributing experience, including GitHub management tips, setup instructions for docs and code contributions, and more - [RFC process](/contributing/rfc-process): Learn how the Gatsby team manages bigger changes, by way of a “Request-for-comment” process on GitHub <EmailCaptureForm signupMessage="Want to keep up with the latest tips & tricks? Subscribe to our newsletter!" />
Caught on camera https://creativecommons.org/licenses/by-nc-sa/3.0/ Computers are playing spot the difference in the Serengeti. An image-recognition algorithm that can identify different species could make it easier to track animals in the wild. Using a database of 3.2 million photos taken by hidden camera traps in the Serengeti National Park in Tanzania, Jeff Clune at the University of Wyoming in Laramie and his colleagues trained the deep-learning system to distinguish between 48 animal species, such as elephants, giraffes and gazelles. In tests, it correctly identified the species present in an image 92 per cent of the time. Camera traps automatically take pictures of passing animals when triggered by heat and motion. This produces thousands or millions of photographs for ecologists to study, but people usually have to go through and label what each picture shows by hand, says Ali Swanson, who worked on the project while at the University of Oxford. If an algorithm could categorise at least some of the images, it could save a lot of time. In 2010, Swanson set up 225 camera traps in the Serengeti, inviting an army of 70,000 online volunteers to help label the images. When Clune heard about this, he saw a perfect opportunity for deep learning – so he and Swanson arranged to team up on the project. “Right now in AI and deep learning, one of the hardest things to come by is a very good, large labelled dataset,” says Clune. His team started by teaching a neural network to recognise whether an image contained an animal, which 75 per cent of the Serengeti images lack. The researchers then trained it to differentiate between species. Better ID The system is much better at identifying the most common animals in the data set, such as wildebeest, says Clune. It has trouble with more rare species like the zorilla, a type of polecat that only appears in the images a few dozen times. Clune says the system could be used to classify most of the photographs and researchers could work on any it wasn’t sure about. It could then be further trained on these hand-labelled images to get better at recognising rarer species. The team also plans to test whether the system can identify animal behaviour in images. “This is very exciting,” says Chris Carbone at the Zoological Society of London. Automatic species recognition could help us learn more about the distribution of species and get a better idea of the impact humans are having on them, he says. An ideal system would provide live tracking information about animals as they pass traps, says Swanson. But the challenge would be transmitting the data from the device in real time for the system to analyse, rather than the current method of using an SD card to store the data on the device until a researcher comes along to collect it. One difficulty is that hyenas and elephants have a habit of damaging the cameras, which are thus kept in heavy-duty plastic cases with no space for an antenna that can transmit data. “And if you do put an antenna on a camera, it won’t last very long at all,” says Swanson. “Something will come along and chew it off pretty quick.” Reference: arxiv.org/abs/1703.05830
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Oh, the Places I’ll Go Now That my Feet are Back! For the first time three months, I’m not sporting a bandage on my foot. It began early last year when I bought what I considered to be the softest and most comfortable pair of shoes I could find (that happened to be the most expensive I’ve ever bought) just so my tootsies wouldn’t hurt. But it didn’t help. The shoes that felt like butter on my feet when I bought them, hurt so much the first time I wore them, I had to buy another pair as soon as I got to work. You see, like almost half of the women in the U.S., I have a bunion, a deformity of the bone at the base of my big toe. Actually, I have one on each foot and they made it painful to wear regular shoes. Forget anything with heels higher than an inch or two. And pointed toes? Well, you get the idea. I was relegated to wearing shoes not even my mother would wear and I was beginning to feel older than my years. So when I told my friend, Connie, that I was going to give away my new soft, comfortable and expensive pair of shoes (and several others) because they were too painful to wear, she told me I should see her podiatrist, Dr. Bernard F. Martin, who had just performed her bunionectomy. I had two questions for Dr. Martin: would it hurt and would I be able to wear my beautiful shoes after surgery. He reassured me it wouldn’t, as long as I followed his instructions and yes, I would be able to wear my fancy shoes. Though minor, my bunions had begun to curve in and push my second toe out of alignment. Dr. Martin explained that he would shave the bone and put a pin in my toe to realign it. Dr. Martin spent about an hour describing my options and told me think about them. I didn’t have to think, I knew what I had to do. My first surgery was at the end of October. The procedure itself was not painful – I was under local anesthesia. I was back home that night and and two days after, I was off all pain medication. I hobbled around in this attractive looking number for the first three weeks after. Globoped But I was feeling so good, I was up and down the apartment. As soon as Dr. Martin saw my foot at my next appointment, he knew and reminded me that continued swelling would slow down my recovery. So I kept my foot elevated and iced and when I did, the swelling. I was thrilled when I graduated to the next show – a designer look that was the rage on all the runways in Paris last season. My designer shoes I was able to walk better and a little faster and after three more weeks, I moved into my own running shoes. Most people wait a few months or more between surgeries – I didn’t. I had a personal deadline and needed to have both surgeries completed by December, 2010.
Photochemotherapy For Psoriasis with Psoralen and Sunlight. A double blind study with systemic psoralen and sunlight exposure therapy in psoralen and is reported. Evaluation was done on the basis of clinical features, patients subjective improvement, severity of scores and histopathology. 66.7% of patients on systemic psoralen and sunlight responded with complete clearance of lesions in 21 to 56 days and 33.3% of patients showed moderate improvement. This study shows that systemic psoralen and direct sunlight elwsure is a safe and effective line of t reatment for psoriasis. We feel, this method of treatment can be recomended as a routine in psoriatic patients in our country.
Culture Street Food Lemon drizzle cake is without question my favourite. I love its upfront lemon zing. This is my version. Half afternoon tea at your gran’s and half mint tea at the souk. I use ground almonds here, which keeps the cake moist and lovely and also has more to offer nutritionally than straight-up flour. Instead of loading this cake with butter and sugar, I use yoghurt in place of butter – it means the cake doesn’t dry out and is a bit lighter too. Honey sweetens it instead of sugar. Limes can be used instead of lemons – just use 1½ limes to each lemon in the recipe. Honey is a completely natural sugar. I love the variations of flavour you get with honey and the way you can taste the flowers the bees have taken the pollen from. Sure, it’s still a sugar, but it’s not been messed around with in the way refined sugar has. I think orange blossom honey works really well here if you can get it. In summer I mix a teaspoon of local Hackney honey into my morning hot water – a little honey from your local area is supposed to help with allergies like hay fever. For the syrup1 unwaxed lemons100ml honeyseeds from 8 cardamom pods, crushed to a powder in a pestle and mortar First preheat your oven to 180°C/fan 160°C/gas 4. Put the eggs into a mixing bowl and whisk until they have fluffed up a bit. Fold in the yoghurt, honey and olive oil, then grate in the zest of both lemons. Now put all your dry ingredients into another bowl and mix well. Gently beat this dry mixture into the yoghurt mix. Grease a 20cm springform cake tin with olive oil, then line the base with baking paper. Pour the cake mixture into the tin and level out the top with the back of a spoon. Bake in the oven for 30 minutes, until golden on top. Test with a skewer – if it comes out clean it’s ready. Meanwhile, make the syrup for the drizzle. Peel the zest from the lemon with a vegetable peeler. Squeeze the juice into a pan and add the zest and the honey. Add the ground cardamom seeds. Place on a medium heat and simmer for 15–20 minutes, until the syrup has slightly thickened and the zest has candied. You’ll know that is has candied when the strips havebecome shiny and translucent, and have curled up a little at the edges. Remove the cake from the oven and leave to cool until you can safely take it out of the tin. Transfer to a cooling rack, then place a large plate underneath to catch any drips. While the cake is still warm, skewer it all over and slowly pour the warm syrup all over the cake, making sure you go right to the edges.
It’s been nearly a year since the Tigers gave Inge his unconditional release. He signed with Oakland on April 30 and hit .226 in 74 games while battling a groin and shoulder injury that eventually ended his season in September. Brandon Inge of Indianapolis signals to the infield players. Inge got Indianapolis on the board in the first with an RBI double. “Going to Oakland was a lot of fun,” he said. “They appreciate me over there, and we did well. We played with some heart, had some fun, and made the post-season.” The 35-year-old Inge signed a minor-league contract with the Pirates this off-season, but his chances of making that club were ruined when he was hit by a fastball in spring training and fractured his scapula. “I played through it for a week, and then I realized there was nothing I could do about it,” he said. “Now I’m trying to get to a point where I can help them in Pittsburgh. “This is basically my spring training. I’m trying to get some at-bats and play in games consistently, and when I’m ready I should be back up.” Indianapolis manager Dean Treanor said he’s just happy to have the versatile Inge — he played left field Monday, and already has played both second and third base — on his team’s roster. “It’s good for our guys to have that veteran presence in the clubhouse,” Treanor said of Inge. “He’s been up there [in the major leagues] and done that, he has playoff experience, and it’s only going to help our guys be around somebody like that.” Inge got the Indians on the board in the first when, with Josh Harrison on second, he slammed a pitch high off the left-field fence for an RBI double. Toledo got a big hit from Ben Guez in the third to take the lead. With the bases loaded and two outs, Guez — who came into the game batting just .167 — lined a bases-clearing double. “It took me a little longer to get my timing and rhythm down than I would have hoped,” said Guez, who added a single and a walk. “But I found it, it clicked and it worked. “I knew, with the bases loaded, that he had to throw a strike. I didn’t want to expand the [strike] zone and get away with throwing a ball, and luckily I got a good pitch to hit — and I drove it.” Indianapolis scored a run in the fifth that the Hens got back in the sixth. But the Indians rallied for three runs in the eighth to post the come-from-behind win. Toledo reliever Evan Reed gave up two singles and a walk to load the bases, and Indy’s Matt Hague greeted reliever Bruce Rondon with a two-run single through the hole at short to tie the game. Jerry Sands then brought home the winning run with a single up the middle. “The only thing I didn’t like about that inning was the walk,” Toledo manager Phil Nevin said. “You can’t walk guys late in the game. Those always come back to haunt you. “Rondon came in and did his job. If the ball had been hit a foot to the right, he’s probably out of the inning [with a double play].”
@available(watchOS 20000, ) class HMRoom : NSObject { var name: String { get } var accessories: [HMAccessory] { get } @available(watchOS 2.0, ) @NSCopying var uniqueIdentifier: NSUUID { get } }
Q: Could not override FOSUserBundle default register form I'm new to symfony, I'm using symfony 2.8. I installed FOSUserBundle and it works just fine, the problem is that i want to add a field to the registration form I followed the steps in FOSUserBundle documentation But nothing has changed and I don't get an error. I don't know what exactly am I missing. This is my User entity: <?php // src/AppBundle/Entity/User.php namespace AppBundle\Entity; use FOS\UserBundle\Entity\User as BaseUser; use Doctrine\ORM\Mapping as ORM; use Symfony\Component\Validator\Constraints as Assert; /** * @ORM\Entity * @ORM\Table(name="fos_user") / class User extends BaseUser { /* * @ORM\Id * @ORM\Column(type="integer") * @ORM\GeneratedValue(strategy="AUTO") / protected $id; /* * @ORM\Column(type="string", length=255) * * @Assert\NotBlank(message="Please enter your name.", groups={"Registration", "Profile"}) * @Assert\Length( * min=3, * max=255, * minMessage="The name is too short.", * maxMessage="The name is too long.", * groups={"Registration", "Profile"} * ) / protected $name; public function __construct() { parent::__construct(); // your own logic } } This is the RegistrationType.php : <?php // src/AppBundle/Form/RegistrationType.php namespace AppBundle\Form; use Symfony\Component\Form\AbstractType; use Symfony\Component\Form\FormBuilderInterface; class RegistrationType extends AbstractType { public function buildForm(FormBuilderInterface $builder, array $options) { $builder->add('name'); } public function getParent() { return 'fos_user_registration'; } public function getName() { return 'app_user_registration'; } } The app/config/services.yml file: parameters: #parameter_name: value services: app.form.registration: class: AppBundle\Form\RegistrationType tags: - { name: form.type, alias: app_user_registration } And this is the section related to FOSUserBundle in app/config/config.yml: fos_user: db_driver: orm # other valid values are 'mongodb', 'couchdb' and 'propel' firewall_name: main user_class: AppBundle\Entity\User registration: form: name: app_user_registration I couldn't find what I'm missing. Thank you. A: Add to you form: /* * @param OptionsResolverInterface $resolver */ public function setDefaultOptions(OptionsResolverInterface $resolver) { $resolver->setDefaults(array( 'data_class' => 'AppBundle\Entity\User' )); } if you are using Symfony < 2.8 # app/config/config.yml fos_user: # ... registration: form: type: AppBundle\Form\RegistrationType if you are using Symfony > 2.8 # app/config/config.yml fos_user: # ... registration: form: name: AppBundle\Form\RegistrationType
Mumbai: Exploring The Best Of The Best In The City Mumbai- the city of many hoping hearts and eyes full of dreams! Apart from the fact that thousands of people relocate to Mumbai every year for such of better job prospects from around the country, Mumbai itself is a famous tourist destination. There are various places to see and enjoy when in Mumbai, which has both a telling past and not to mention a dynamic present. Mumbai is a city that is best discovered when roaming on the streets and living here. However, if you are dropping by for a short time here, then there are a few places that you can visit for a nice time and to get know this city better. Come let’s take a look at the most interesting places that Mumbai can offer its tourists: Gateway of India: Head out to the Colaba region to experience this wonder with your own eyes. This is one of the finest and most crowd pulling locations of Mumbai, where tourists and locals both flock to almost on a regular basis. Film and photo shoots are also often held here for its natural beauty and old Mumbai charm which is hard to miss once you visit this place. This is one of the first places that you ought to visit on reaching Mumbai. Marine Drive: Book a cab or rent a car and take long drive on the famous Marine Drive of Mumbai. Let the cab go at some point and walk along the Arabian Sea with the waves lashing at the rocks. This is one of the most beautiful places in the city where you can enjoy a leisurely time all by yourself or with a pleasant company. Quiet yet crowded, Mumbai’s Marine drive is a wonder in itself. The Haji Ali Mosque: You cannot leave Mumbai without visiting the Haji Ali Mosque which was built by a Sufi Saint. You will be able to see this mosque from the Marine Drive itself since it is located smack in the Arabian Sea. There is a long road on the sea leading up to the mosque. It is famed to be one of the most auspicious and meditative places in the country. BandraKurla Complex: Mumbai is developing everyday in leaps and bounds and if you are staying in any one the hotels near bandra kurla complex, then you should definitely visit the BandraKurla Complex since this is a piece of modern day architectural brilliance which needs to be appreciated and admired. Elephanta Caves: Take a ferry from Gateway of India and travel to the Elephanta Caves. You will find numerous rock cut carvings and paintings in the Elephanta caves that will take you back to the days of rock painting. It is a very popular tourist destination and if history is what interests you then a visit to this series of caves is a must for all! Apart from these Mumbai harbours many pleasant and local treasures that is best explored on your own!

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