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Search Results: 1 - 10 of 355481 matches for " Emilio G de la Concha "
Evidence for the association of the SLC22A4 and SLC22A5 genes with Type 1 Diabetes: a case control study
Jose Santiago, Alfonso Martínez, Hermenegildo de la Calle, Miguel Fernández-Arquero, M ángeles Figueredo, Emilio G de la Concha, Elena Urcelay
BMC Medical Genetics , 2006, DOI: 10.1186/1471-2350-7-54
Abstract: A case-control study was performed in the Spanish population with 295 T1D patients and 508 healthy control subjects. Maximum-likelihood haplotype frequencies were estimated by applying the Expectation-Maximization (EM) algorithm implemented by the Arlequin software.When independently analyzed, one of the tested polymorphisms in the SLC22A4 gene at 1672 showed significant association with T1D in our Spanish cohort. The overall comparison of the inferred haplotypes was significantly different between patients and controls (χ2 = 10.43; p = 0.034) with one of the haplotypes showing a protective effect for T1D (rs3792876/rs1050152/rs2631367/rs274559, CCGA: OR = 0.62 (0.41–0.93); p = 0.02).The haplotype distribution in the carnitine transporter locus seems to be significantly different between T1D patients and controls; however, additional studies in independent populations would allow to confirm the role of these genes in T1D risk.Type 1 diabetes (T1D) is a multifactorial autoimmune T-cell-mediated disease resulting from selective destruction of the insulin producing β cells in the pancreatic islets, leading to an absolute insulin deficiency. The risk of developing T1D is determined by a complex interaction between multiple genetic and environmental factors. Although susceptibility to disease is strongly associated with alleles in the major histocompatibility complex (MHC) [1,2], there are more than 20 putative T1D susceptibility regions identified by linkage and association studies [3,4]. At present, several non-MHC susceptibility loci with modest genetic effects have been clearly defined. However, it is well known that many non-MHC loci predisposing to T1D remain as yet undefined [5].Type 1 diabetes is a chronic degenerative disease, with altered metabolism characterized by hyperglycemia and ketoacidosis and T1D patients depend on exogenous insulin to sustain life. The role of the carnitine system in cell metabolism is mainly known in the mitochondria, where the intera
Susceptibility to type 1 diabetes conferred by the PTPN22 C1858T polymorphism in the Spanish population
Abstract: A case-control was performed with 316 Spanish white T1D patients consecutively recruited and 554 healthy controls, all of them from the Madrid area. The PTPN22 C1858T SNP was genotyped in both patients and controls using a TaqMan Assay in a 7900 HT Fast Real-Time PCR System.We replicated for the first time in a Spanish population the association of the 1858T allele with an increased risk for developing T1D [carriers of allele T vs. CC: OR (95%) = 1.73 (1.17–2.54); p = 0.004]. Furthermore, this allele showed a significant association in female patients with diabetes onset before age 16 years [carriers of allele T vs. CC: OR (95%) = 2.95 (1.45–6.01), female patients vs female controls p = 0.0009]. No other association in specific subgroups stratified for gender, HLA susceptibility or age at onset were observed.Our results provide evidence that the PTPN22 1858T allele is a T1D susceptibility factor also in the Spanish population and it might play a different role in susceptibility to T1D according to gender in early-onset T1D patients.Type 1 diabetes (T1D) is an autoimmune disorder resulting from destruction of the insulin-producing β cells of the pancreas. T1D is a complex trait with both genetic and environmental factors contributing to the etiology of this disease. Several susceptibility loci involved in disease development have been identified and were consistently replicated in independent populations [1]. These efforts contribute to a better definition of the molecular pathways leading to increased T1D risk and this knowledge, in turn, may help in understanding the genetic basis of the disease. The MHC class II, the CTLA4 and the PTPN22 loci have all been proved important in the pathogenesis of autoimmunity globally considered, whereas the insulin gene is a disease-specific T1D predisposition locus. Most of the new general susceptibility loci identified in the past few years have a clear role in the modulation of T cell development and activation, indicating that
Early B-cell Factor gene association with multiple sclerosis in the Spanish population
Alfonso Martínez, Ana Mas, Virginia de las Heras, Rafael Arroyo, Miguel Fernández-Arquero, Emilio G de la Concha, Elena Urcelay
BMC Neurology , 2005, DOI: 10.1186/1471-2377-5-19
Abstract: The role of the EBF1 gene in multiple sclerosis susceptibility was analyzed by performing a case-control study with 356 multiple sclerosis patients and 540 ethnically matched controls comparing the EBF1 polymorphism rs1368297 and the microsatellite D5S2038.Significant association of an EBF1-intronic polymorphism (rs1368297, A vs. T: p = 0.02; OR = 1.26 and AA vs. [TA+TT]: p = 0.02; OR = 1.39) was discovered. This association was even stronger after stratification for the well-established risk factor of multiple sclerosis in the Major Histocompatibility Complex, DRB1*1501 (AA vs. [TA+TT]: p = 0.005; OR = 1.78). A trend for association in the case-control study of another EBF1 marker, the allele 5 of the very informative microsatellite D5S2038, was corroborated by Transmission Disequilibrium Test of 53 trios (p = 0.03).Our data support EBF1 gene association with MS pathogenesis in the Spanish white population. Two genetic markers within the EBF1 gene have been found associated with this neurological disease, indicative either of their causative role or that of some other polymorphism in linkage disequilibrium with them.Multiple sclerosis (MS) is one of the most common neurological diseases of young adults in Europe and North America [1]. Similarly to other common complex diseases, the interplay of genome and environment as MS susceptibility factors seems to determine the final outcome. Its precise etiology is at present unknown, even though the first genetic association with the MHC was published more than thirty years ago [2]. Genomic screens support the hypothesis that susceptibility to develop MS is determined by multiple genes with small individual contributions. To decipher those combinations of genes resulting in MS is a major goal of research. Association of MS with the HLA-DRB1*1501-DQB1*0602 haplotype has been unambiguously demonstrated [3]. The diversity of the predisposition genes is evident if we consider that the major risk allele HLA-DRB1*1501 is present
Interleukin-10 polymorphisms in Spanish IgA deficiency patients: a case-control and family study
Javier Ortiz, Miguel Fernández-Arquero, Elena Urcelay, Raquel López-Mejías, Antonio Ferreira, Gumersindo Fontán, Emilio G de la Concha, Alfonso Martínez
Abstract: We genotyped 278 patients with IgAD and 573 ethnically matched controls for the microsatellites IL-10R and IL-10G and for three single nucleotide polymorphisms at positions -1082, -819 and -592 in the proximal promoter of the gene. We also included in this study the parents of 194 patients in order to study the IL-10 haplotypes transmitted and not transmitted to the affected offspring.The only allele where a significant difference was observed in the comparison between IgA deficiency patients and controls was the IL-10G12 allele (OR = 1.58 and p = 0.021). However, this p value could not withstand a Bonferroni correction. None of the IL-10R or promoter SNP alleles was found at a different frequency when patients were compared with controls.Our data do not show any significant difference in IL-10 polymorphism frequencies between control and IgAD patient samples. Their haplotype distribution among patients and controls was also equivalent and therefore these microsatellites and SNPs do not seem to influence IgAD susceptibility.IgA deficiency (IgAD) is the most common primary immunodeficiency in Caucasians and is sometimes associated with deficiency of IgG2, IgG3, IgG4 and IgE [1]. Genetic studies indicate that IgAD may have an inherited component and the disease is associated with certain susceptibility genes located in the major histocompatibility complex region [2,3]. Celiac disease and selective IgA deficiency are frequently associated, and share a similar genetic background [4,5]. Environmental factors also play a role in the occurrence of IgAD. The most usual consequence of this disease is an increased susceptibility to infection [6].Although the basic immunologic defect that underlies IgAD is unknown, a number of in vitro immunological alterations have been identified: arrest in the B cell differentiation pathway [7], and a decrease in T helper lymphocyte function [8,9].IL-10 is a regulatory cytokine that has several functions; it is a potent stimulator of NK cel
Interleukin-10 haplotypes in Celiac Disease in the Spanish population
Concepción Nú?ez, Diana Alecsandru, Jezabel Varadé, Isabel Polanco, Carlos Maluenda, Miguel Fernández-Arquero, Emilio G de la Concha, Elena Urcelay, Alfonso Martínez
Abstract: A case-control and a familial study were performed. Positions -1082, -819 and -592 of the IL-10 promoter were typed by TaqMan and allele specific PCR. IL10R and IL10G microsatellites were amplified with labelled primers, and they were subsequently run on an automatic sequencer. In this study 446 patients and 573 controls were included, all of them white Spaniards. Extended haplotypes encompassing microsatellites and SNPs were obtained in families and estimated in controls by the Expectation-Maximization algorithm.No significant associations after Bonferroni correction were observed in the SNPs or any of the microsatellites. Stratification by HLA-DQ2 (DQA1*0501-DQB1*02) status did not alter the results. When extended haplotypes were analyzed, no differences were apparent either.The IL-10 polymorphisms studied are not associated with celiac disease. Our data suggest that the IL-10 alteration seen in patients may be more consequence than cause of the disease.Celiac disease (CD) is a chronic inflammatory disorder characterized by a pathological response after exposure to gluten in genetically susceptible individuals [1]. HLA class II genes, mainly the alleles DQA1*0501 and DQB1*02 (HLA-DQ2) but also DQA1*0301 and DQB1*0302 (HLA-DQ8), have been found to play an important role in the development of celiac disease. However, HLA genes do not explain the totality of CD cases detected and other genes must be involved in CD onset. In fact, the sibling familial risk attributed to HLA is approximately half of the sibling risk for CD [2].The histological lesions typical of CD seem to be associated with a predominant T helper type 1 (Th1) cell response. Thus, cytokines characteristic of a Th1 inflammatory response as interferon gamma, are produced by lamina propria T cells isolated from the intestine of CD patients after gluten stimulation [3]. The complex homeostatic regulation of immune processes involves numerous interacting cells and molecules. The prototypic regulatory cytoki
Polymorphisms in the selenoprotein S gene: lack of association with autoimmune inflammatory diseases
Alfonso Martínez, Jose Santiago, Jezabel Varadé, Ana Márquez, José Lamas, Juan Mendoza, Hermenegildo de la Calle, Manuel Díaz-Rubio, Emilio G de la Concha, Benjamín Fernández-Gutiérrez, Elena Urcelay
BMC Genomics , 2008, DOI: 10.1186/1471-2164-9-329
Abstract: Six polymorphisms distributed through the SEPS1 gene (rs11327127, rs28665122, rs4965814, rs12917258, rs4965373 and rs2101171) were genotyped in more than two thousand patients suffering from type 1 diabetes, rheumatoid arthritis or inflammatory bowel diseases and 550 healthy controls included in the case-control study.Lack of association of SEPS1 polymorphisms or haplotypes precludes a major role of this gene increasing predisposition to these inflammatory diseases.The human gene SEPS1, located on chromosome 15q26.3, encodes selenoprotein S which participates in the retro-translocation of misfolded proteins from the endoplasmic reticulum (ER) to the cytosol for their degradation [1]. This ER membrane protein functions in stress responses to prevent the deleterious consequences of accumulation of misfolded proteins, accumulation that has been linked to immune and inflammatory processes [2]. A study identified the strong association of the proximal promoter SEPS1 polymorphism at -105G/A with circulating levels of three pro-inflammatory cytokines, interleukin (IL)-6, IL-1β and TNF-α [3]. Moreover, these authors reported that the mutant variant significantly reduced the promoter activity of the SEPS1 gene in stressed HepG2 cells and that the suppression of this gene by short interfering RNA increased the release of pro-inflammatory cytokines in a macrophage cell line. A regulatory loop has been recently proposed whereby cytokines stimulate the expression of SEPS1, which in turn diminishes cytokine production [4].The murine homolog gene of the human SEPS1 is the Tanis gene, which encodes a serum amyloid A receptor [5]. Acute phase serum amyloid A proteins (SAAs) are multifunctional apolipoproteins produced in large amounts during the acute phase of inflammation and also during the development of chronic inflammatory diseases. SAAs are involved in the pathogenesis of several chronic inflammatory diseases, such as rheumatoid arthritis (RA) [6-9], multiple sclerosis (MS)[10
Type 1 Diabetes in the Spanish Population: additional factors to Class II HLA-DR3 and -DR4
Elena Urcelay, José L Santiago, Hermenegildo de la Calle, Alfonso Martínez, Julián Méndez, José M Ibarra, Carlos Maluenda, Miguel Fernández-Arquero, Emilio G de la Concha
BMC Genomics , 2005, DOI: 10.1186/1471-2164-6-56
Abstract: Genetic MHC markers were analysed in a case-control study with 302 T1D patients and 529 ethnically matched controls. DR3-TNFa1b5 carrier rate was significantly higher in DR3-positive heterozygous T1D patients than in DR3-positive heterozygous controls (p = 0.0019; odds ratio OR [95% confidence interval CI] = 2.26 [1.3–3.93]). This data was confirmed analysing the allelic frequency, which includes the information corresponding to the DR3-homozygous individuals (p = 0.001; OR = 2.09) and by using the Arlequin software to check the DR3-positive haplotypes (p = 0.004;OR = 1.93). The present results provide strong evidence of a second susceptibility region in the ancestral haplotype 18.2 in the Spanish population.Moreover, we searched for T1D susceptibility factors in addition to the MHC classical ones, within the DR2-DQ6/DR3-DQ2/DR4-DQ8 negative population. Several genetic markers in both MHC class II (DQA1*0101-DQB1*0501 [p = 0.007;OR = 2.81], DQA1*0201-DQB1*0202 [p = 0.03; OR = 2.35]) and III (TNFa2b1 [p = 0.01 OR = 2.74], BAT-2*2 [p = 0.004; OR = 3.19]) were found. These different alleles associated with T1D were not independent and we observed linkage disequilibrium among them leading us to describe two new risk haplotypes (DQA1*0101-DQB1*0501-TNFa2b1 and DQA1*0201-DQB1*0202- BAT-2*2). Finally, we studied a T1D susceptibility/protection marker located in extended class I, D6S2223; however, no association was observed in our population.Our results suggest that other associated MHC haplotypes might present susceptibility factors in loci different from HLA-class II and that the class II molecules are not necessarily the universal etiologic factor in every MHC haplotype.Type 1 diabetes is a multifactorial autoimmune disease characterised by insulin deficiency, due to the T cell mediated destruction of pancreatic β-cells [1]. Among the genetic determinants of susceptibility, with more than 18 putative loci identified to date, a region in chromosome 6p21 (IDDM1) containin
CD209 in inflammatory bowel disease: a case-control study in the Spanish population
Concepción Nú?ez, Javier Oliver, Juan Mendoza, María Gómez-García, Carlos Taxonera, Luis M Gómez, Miguel A López-Nevot, Emilio G de la Concha, Elena Urcelay, Alfonso Martínez, Javier Martín
Abstract: We performed a case-control study with 515 CD patients, 497 UC patients and 731 healthy controls, all of them white Spaniards. Samples were typed for the CD209 single nucleotide polymorphism (SNP) rs4804803 by TaqMan technology. Frequency comparisons were performed using χ2 tests.No association between CD209 and UC or CD was observed initially. However, stratification of UC patients by HLA-DR3 status, a strong protective allele, showed that carriage of the CD209_G allele could increase susceptibility in the subgroup of HLA-DR3-positive individuals (p = 0.03 OR = 1.77 95% CI 1.04–3.02, vs. controls).A functional variant in the CD209 gene, rs4804803, does not seem to be influencing Crohn's disease susceptibility. However, it could be involved in the etiology or pathology of Ulcerative Colitis in HLA-DR3-positive individuals but further studies are necessary.Inflammatory bowel diseases comprise two distinct entities, Crohn's disease (CD) and Ulcerative Colitis (UC). Both forms are characterized by a chronic inflammation of the intestine, but several clinical and immunological profiles differ between them. IBD is a multifactorial disease: environmental factors seem to be involved in disease onset in genetically susceptible individuals. Common susceptibility genetic components exist for both diseases as evidenced apparently by the higher risk of developing UC in relatives of patients with CD or vice versa, but also specific genes seem to play an important role in the development or course of each disease. For CD, CARD15 mutations are the main susceptibility factors described in Caucasian populations [1]. On the other hand, HLA genes show stronger effects on UC in our population, specifically HLA-DR3 seems to have a protective role in the development of this disease [2]. However, a complex genetic contribution exists in both diseases and new etiological genes remain to be discovered.DC-SIGN (dendritic cell-specific ICAM3-grabbing non-integrin), also named CD209, is a type
DRB1*03:01 Haplotypes: Differential Contribution to Multiple Sclerosis Risk and Specific Association with the Presence of Intrathecal IgM Bands
Emilio G. de la Concha, María L. Cavanillas, M. Carmen Cénit, Elena Urcelay, Rafael Arroyo, óscar Fernández, José C. álvarez-Cerme?o, Laura Leyva, Luisa M. Villar, Concepción Nú?ez
Abstract: Background Multiple sclerosis (MS) is a multifactorial disease with a genetic basis. The strongest associations with the disease lie in the Human Leukocyte Antigen (HLA) region. However, except for the DRB1*15:01 allele, the main risk factor associated to MS so far, no consistent effect has been described for any other variant. One example is HLA-DRB1*03:01, with a heterogeneous effect across populations and studies. We postulate that those discrepancies could be due to differences in the diverse haplotypes bearing that allele. Thus, we aimed at studying the association of DRB1*03:01 with MS susceptibility considering this allele globally and stratified by haplotypes. We also evaluated the association with the presence of oligoclonal IgM bands against myelin lipids (OCMB) in cerebrospinal fluid. Methods Genotyping of HLA-B, -DRB1 and -DQA1 was performed in 1068 MS patients and 624 ethnically matched healthy controls. One hundred and thirty-nine MS patients were classified according to the presence (M+, 58 patients)/absence (M?, 81 patients) of OCMB. Comparisons between groups (MS patients vs. controls and M+ vs. M?) were performed with the chi-square test or the Fisher exact test. Results Association of DRB1*03:01 with MS susceptibility was observed but with different haplotypic contribution, being the ancestral haplotype (AH) 18.2 the one causing the highest risk. Comparisons between M+, M? and controls showed that the AH 18.2 was affecting only M+ individuals, conferring a risk similar to that caused by DRB1*15:01. Conclusions The diverse DRB1*03:01-containing haplotypes contribute with different risk to MS susceptibility. The AH 18.2 causes the highest risk and affects only to individuals showing OCMB.
A functional PTPN22 polymorphism associated with several autoimmune diseases is not associated with IgA deficiency in the Spanish population
Concepción Nú?ez, Raquel López-Mejías, Alfonso Martínez, M Cruz García-Rodríguez, Miguel Fernández-Arquero, Emilio G de la Concha, Elena Urcelay
Abstract: A total of 259 IgAD patients and 455 unrelated matched controls, and 128 families were used for each approach. Comparisons were performed using Chi-Square tests or Fisher's exact test when necessary.No association between the PTPN22 1858C/T SNP and IgA deficiency was found in any case (allelic frequencies 8% vs. 6% in patients and controls, respectively, OR= 1.14 (0.72–1.79), p= 0.56; TDT p = 0.08).The result obtained seems to reinforce the consideration of IgA deficiency as a primary immunodeficiency rather than an autoimmune disease.Selective IgA deficiency (IgAD) is the most prevalent primary immunodeficiency in white populations, with values around one out of 600 [1]. This disease is characterized by a severe deficiency or total absence of IgA class immunoglobulins in the serum and secretions. Their clinical symptoms are very variable, and thus some IgAD patients are relatively healthy while others show significant illness, mainly a higher susceptibility to infections, autoimmune diseases and allergies. IgAD shows a multifactorial origin, with genetic and environmental factors involved. Class II and class III HLA genes have been implicated in the origin of this disease (see [2] and references therein). However, these HLA genetic components can not explain the totality of the genetic influence in this disease.The molecular bases underlying the origin of IgAD are not completely understood. Although it has been recently shown that a mutation in TACI is involved in the origin of the disease in some patients [3], other genetic and environmental factors remain to be discovered. Despite IgAD has been traditionally considered as an immunodeficiency, some authors [4] have pointed out that it could be an autoimmune disease.Recently, a single-nucleotide polymorphism (SNP) of the PTPN22 (protein tyrosine phosphatase, non-receptor type 22) gene, 1858C/T, has been found associated with many autoimmune diseases [5,6]. This gene, located on chromosome 1p13, encodes a lymphoid p


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Q: Custom Rectangle Class Not Drawing import pygame

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redpajama_set_name: RedPajamaStackExchange


Ferguson Mann Architects has taken the wraps off its restoration of Castle House in Bridgwater, which is one of the world's earliest surviving examples of the use of prefabriated concrete and constructional post-tensioning.
The grade II*-listed Somerset property was built in 1851 as both a family home and as a show house for John Board – a pioneer of concrete construction. It features gothic window frames and pre-cast architectural detailing, while the top floor has concrete vaults supporting the roof.
But the building was disused for many years and gutted by fire. It even featured on the BBC 2 programme Restoration before work began on Ferguson Mann's exterior revamp in 2009, driven by Save Trust and supported by funding from English Heritage and power firm EDF.


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Meet the 12 Southern Tier athletes going to the world's 'biggest wrestling tournament'
Twelve top wrestlers from Section 4 will help what is perhaps the biggest junior event in the country celebrate 50 years.
The USA Wrestling U.S. Marine Crops Junior and 16-under National Championships return to the Fargodome in Fargo, North Dakota, from July 17 to 23 after a one-year hiatus caused by the COVID-19 pandemic.
Wrestlers will compete in men's freestyle, Greco-Roman and women's freestyle competition. Junior competition is open to wrestlers 18-and-under.
The Southern Tier contingent includes six Tioga wrestlers: Gianni Silvestri, Levi Bellis, Caden Bellis, Mason Welch, Donavan Smith and Ousmane Duncanson.
The other qualifiers from Section 4 schools were Chenango Forks' Logan Gumble and Tyler Ferrara, Horseheads' Zach Levey, Corning's Charles Loucks, Windsor's Gabe Monroe and Bainbridge-Guilford/Harpursville/Afton's Darren Florence.
For subscribers:How Team Gumble handles uncertain wrestling season at Chenango Forks and in STAC
Rick Gumble, a state leader who is heading up the Southern Tier contingent along with coach Kris Harrington of Tioga, estimates 120 boys and girls from New York state will compete.
"It's a weeklong festival," said Gumble, recently retired after 27 years coaching Chenango Forks. "It is arguably the biggest wrestling tournament in the history of the planet. In terms of numbers to size of mats, it's the biggest wrestling tournament in the world."
Five things to know about this year's event:
'Nothing like it'
Some of the top wrestlers in United States history have competed at this national tournament, which moved to its longtime home in Fargo in 1993. It got its start in Iowa City, Iowa, in 1971 and was also held in Cedar Falls, Iowa; Warrensburg, Missouri; and St. Paul, Minnesota.
High-profile names such as Penn State coach Cael Sanderson, Oklahoma State coach John Smith and two-time Lansing High state champion and four-time Cornell University national champ Kyle Dake, a Tokyo Olympics qualifier this year, have competed at USA Nationals. Troy Nickerson, a five-time state champ at Chenango Forks, was a five-time national champ in Fargo before becoming a four-time All-American at Cornell.
Preliminaries include 23 to 24 wrestling mats at one time, while finals take place on a single mat under the bright lights of the Fargodome, which is the home of North Dakota State football.
"I don't think there's a state tournament like it in any other high school division," Gumble said. "Imagine an all-star basketball tournament where New York state sends its best high school basketball team to a tournament where almost all 50 states are represented. There's nothing like it in any other sport."
Dake recalled the hot dorm rooms during what was otherwise an "exciting" time in his life.
"It was a fun time," he said. "Kind of a bonding moment between all the kids on the team, staying in one spot. I really enjoyed going out to Fargo and competing."
Top competition again for area wrestlers
Section 4 wrestlers had a season this school year, but it was heavily modified and did not include sectional or state tournaments. Some of the dual meets held did not include team scoring, with a focus on individual opportunities during a condensed season.
Add to that the lack of a 2020 national championship meet and this event gains added significance for the competitors, especially with some weight classes including more than 100 wrestlers.
Gumble coached at Maine-Endwell and Johnson City before coming to Forks. He said all of the state champions he coached trained in freestyle and Greco-Roman for nationals. That includes Lucas Scott, who did not compete in Fargo because he was focused on football. He is entering his freshman year at West Point, where he will play for Army's football team.
"The fact that they train for this competition or participate in this competition is the key reason they've been very, very successful in Section 4 wrestling," said Gumble, who pointed out Section 4 ranks behind only Long Island's Section 11 in scholastic state titles in New York.
For underclassmen, this event provides an ideal opportunity to make an impression on a college coach.
"The NCAA Division I wrestling tournament is the only tournament in the college season that goes three consecutive days. This is the only tournament at the high school level that you wrestle that much wrestling in a week," Rick Gumble said. "One reason college coaches like this event is they can see if a kid can handle that kind of pressure over a course of several days."
Generosity on display
In March of 2018, the Jeff Reese Foundation and Mark Stephens Foundation announced they were pooling their resources to help wrestlers in the Elmira area and throughout Section 4.
This event is a prime example of the significance of their efforts. Each wrestler from the Southern Tier will be provided $400 from their fund to help with expenses related to the tournament.
Jeff Reese was a state champion at Elmira Southside who died in December of 1997 while trying to make weight for a match while at the University of Michigan. Mark Stephens won a state title for Southside in 1966 and went on to become a coach and highly respected wrestling official. He died in December of 2013 at age 65.
Jeff's dad, Ed Reese, has teamed with Mike Stephens, Mark's brother, to keep the legacies of Jeff and Mark going while helping a sport that meant so much to both.
"Mike Stephens and Ed Reese, what they've done to make this affordable for these kids, especially in this COVID year, that level of generosity is unbelievable," Rick Gumble said.
Q&A: From state champ to NCAA official, Johnson City native stays connected to wrestling
COVID impact still felt
Rick Gumble estimated the last 15 qualifiers for this event had been held in Broome County at sites such as Johnson City High School, Binghamton University's West Gym and the Broome Community College ice rink. Because of the pandemic, this year's state qualifier was held in the Pocono Mountains region of Pennsylvania.
Top-three state finishers qualified for nationals, with regional championships also offering a path to Fargo.
The pandemic has led to separate travel plans for the 12 Southern Tier athletes, who ordinarily would have gone out together on a rented bus or by airplane. Because of protocols, athletes have to make their own travel arrangements this year.
A central training camp gave way to satellite camps across the state. COVID protocols will also be in place in Fargo.
Farewell opportunities
Levey and Logan Gumble both just graduated from high school, making this their farewell event at the high school level. Both won Section 4 titles in 2019.
Levey, this year's recipient of the Dan Manganaro Memorial Scholarship from Horseheads, will wrestle at SUNY Brockport. Gumble will stay close to home and compete for Binghamton University.
For Rick Gumble, this will represent two goodbyes in one.
"It's sort of romantic for me as a coach retiring," Rick said. "This is the last event that I'll coach my son in. It's a life that's gone full circle. My brother (Mark Gumble) wrestled in this event back in the '80s and I started my coaching career and my coaching career is ending with my son wrestling in this event."
Follow Andrew Legare on Twitter: @SGAndrewLegare. You can also reach him at alegare@gannett.com. To get unlimited access to the latest news, please subscribe or activate your digital account today.

redpajama_set_name: RedPajamaCommonCrawl


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Q: JLabel's text is in the middle of the hitbox I have created a JLabel and draw a long String on it. But, the problem is, however long is the content, the content always display at the middle of the label's box! I want to push the text to the top of the box.
How can I fix it? Thank you so much!

Font times = new Font("Times New Roman", Font.CENTER_BASELINE, 13);
JLabel mess = new JLabel();
mess.setFont(times);
mess.setLocation(300, 125);
mess.setSize(250, 200);
mess.setText(message);
mess.setForeground(Color.WHITE);
getContentPane().add(mess);


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Q: Calligra words: what syntax is used in ~/.kde/share/config/wordsrc? I have Calligra Words, Version 2.9.7, Using KDE Development Platform 4.14.22 from the standard repo of Kubuntu 16.04.
I was looking at ~/.kde/share/config/wordsrc and saw an entry like this:
ko_geometry=AdnQywABAAD////6AAAANQAABRAAAALLAAAAAAAAAFoAAAUKAAACxQAAAAAAAA==
The next line relates to ko_windowstate and is much longer but similar to the stuff that follows ko_geometry= in the code above.

ko_windowstate=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

What sort of information is contained in such strings?

A: KDE configuration files
Earlier AskUubntu: Configuration files in a KDE application
Now KDE Frameworks KConfig: https://api.kde.org/frameworks/kconfig/html/
Calligra 2.9.7
...calligra-2.9.7/libs/main/KoMainWindow.cpp line 444:
KConfigGroup cfg(KGlobal::config(), "MainWindow");
cfg.writeEntry("ko_geometry", saveGeometry().toBase64());
cfg.writeEntry("ko_windowstate", saveState().toBase64());

The Calligra is saving the window geometry and the window state (what widgets are open and where they are etc...) to the rc files as base 64: https://en.wikipedia.org/wiki/Base64 .
Deconding your ko_windowstate snippet - https://www.base64decode.org:


text:
More Than Alternative
FM90 Blog
KAABOO 2019
Yellow City Sounds Music Festival
YCSMF – Photos & Video
Blues Festival 2019
The Deltaz Pop-Up Show at Six Car Pub & Brewery
The Deltaz Pop-Up Show – Photos & Videos
Fox Tracks Pop-Up Show at Golden Light Cantina
Foxtrax Pop-Up Show – Video
Body & Soul Pop-Up Show
Body & Soul Pop-Up Show Interviews
Queen V
BlxxzyFYH
Jrew Retro
King Slim Soul
Sabii, Fish Lips & Ugly Chulo
Vinylthon 2018
Vinylthon 2018 – Photos & Video
Indie Show
Top 9 at 9
Inside Skullcap's Closet
Inside Skullcap's Closet – #001
The Adventures of Abraham Steadfast
#001 Summer Reading Lists
#002 You'll Need Therapy
#003 Where is the Love?
#004 The Defenders
#005 The Peeples' Choice
#006 Drink The Kool-Aid
#007 The Kids Are Alright
#008 Long-Term Relationships
#009 The Book is Always Better
#010 Scary Monsters and Super Creeps
#011 And The Winners Are…
#012 Scout's Honor
Summer is upon us! The smell of fresh cut grass, grills, and chlorine fill the air. FM90 has you covered in the Summer Music department. We add new music every week, plus we still have our normal lineup of specialty shows through the summer.
Two new shows are on Tuesday nights: The Golden Hour, hosted by Stevi, and Brown, hosted by Waste. Times vary based on the June Jazz schedule. The Golden Hour will be running from 6-7PM on Tuesdays through July 9th and will be back to its normal time of 7-8PM on July 16th. Brown will be back on July 16th at 8 PM.
The Golden Hour features Americana artists like Jason Isbell, Brandi Carlile, The Deltaz, Shakey Graves, and many more. Stevi plays your favorites and new tunes from the genre as well, plus she takes requests.
Brown features the weird and wacky side of music with artists like Frank Zappa, Ween, The Butthole Surfers, The Greenskeepers and more. Waste will also be taking your requests.
FM90 wants to thank everyone for listening during the summer while most of our students are enjoying their time off before school starts again in August.
Amy Presley
FM90 Program Director
FM90 Blog – Vinylthon 2019
FM90 is getting ready for our second year of Vinylthon! On Saturday, April 13th we'll be playing 5 hours of nothing but vinyl. This year we are excited to have support from Spinning Jenny's House of Music in Shamrock. We'll have some videos of my recent visit to the store coming soon.
Vinylthon is not only great to participate in because it's fun, but it's also a day of learning for our students. They get to witness the "old days" of radio and how DJs before them had to change records every 2 ½ minutes. The students are encouraged to bring their own vinyl and share stories about why it's important to them. Last year our students brought everything from Zack Brown to Van Halen, even some Frank Sinatra and Dean Martin.
For the first time we'll be including the first two hours of Body and Soul into Vinylthon. Brian Frank and I will be spinning our favorite "Old School Jams".
We're can't wait for another chance to celebrate records and their importance in the history of radio. FM90 and Vinylthon can be heard on 89.9 FM and online right here at kacvfm.org.
FM90 Blog – Brevet Show
It's a Monday morning and I'm feeling grateful (a rare and unnatural occurrence for a Monday). I spent the weekend with The Brevet, who blew the roof off the GoldenLight Cantina on Saturday night.
The band, who hails from California, played for the first time in Amarillo to a full capacity crowd. Playing songs from their entire catalog, but focusing on songs from their latest album, 'LEGS'. The crowd was prompted by lead singer Aric Chase Damm to clap and sing along. It was a tall order for a band that didn't have an opening act, but after the first song, no one seemed to remember they walked out on a cold stage.
People danced, clapped, and sang along to songs, specifically "Gateway Drug", which Damm exclaimed afterwards, "I didn't know you guys knew that one." The band finished out their set with "So Long", another FM90 favorite.
The merch line was packed, and I myself waited over an hour to say goodnight to the band before they made the trek back to California that night.
Thank you again to the GoldenLight for their hospitality and hard work putting this show together. Of course, a huge thank you to The Brevet for the music, energy, and love you poured out to the crowd. And, thank you to all of the FM90 listeners who have been by our side for so many years. Our students learn what REAL radio is because of you!
KACV-FM
amy.presley21@actx.edu
Posted on November 9, 2018 April 9, 2019
FM90 is excited to present The Brevet to the GoldenLight Cantina on Saturday, February 23rd.
I recently did an interview with Aric Chase Damm, the lead singer for The Brevet and he is excited to play Amarillo for the first time ever. The band will be supporting their newest album 'LEGS'. FM90 has had a great response to the two latest singles from the album, "So Long" and "Gateway Drug".
The Brevet hails from California and pride themselves on the energy they bring to their live shows. With Damm's commanding voice leading the charge, the songs have instantly recognizable hooks that will have you singing along before the end.
FM90 is giving away tickets to the show, autographed merch, and dinner with the band. We'll have chances to get qualified before the February 20th drawing.
Tickets for the show are on sale now: https://www.brownpapertickets.com/event/3918678
FM90 Presents: The Brevet at Golden Light Cantina
The Brevet performs live in Amarillo at the Golden Light Cantina
www.brownpapertickets.com
We can't wait to see everyone on the 23rd!
Site created by Sad Monkey Media	| KACV-FM Public File


text:
Red Hot Chili Peppers - One Hot Minute
One Hot Minute is an album by the Red Hot Chili Peppers. Released on September 12, 1995 by Warner Brothers Records, this is the only RHCP album to feature Dave Navarro as the band's guitarist.
Stephen Perkins appears on this album, performing on the track One Big Mob. A recording of Dave's younger half-brother Gabriel James Navarro crying also appears on One Big Mob.
Aside from the standard version of this album, there is an advance/promo version, and a Japanese import with the bonus track Melancholy Mechanics. There is also a "tour pack" edition that comes with a bonus disc including an interview from a July 1995 appearance on Australia's JJJ Radio. There is also a version with a holographic 3D cover, and a sampler cassette.
On May 15, 2012, Warner Brothers released a remastered version of One Hot Minute. This limited edition double 12″ red vinyl version comes with a "lenticular 3D" cover, and was remastered by Bernie Grundman.
Deep Kick
One Big Mob
One Hot Minute
Shallow Be Thy Game
Release Date: 09/12/1995, 5/15/2012 (Red Vinyl)
Released By: Warner Brothers Records
ID Number(s): 45733 (Album), PRO-CD-7878-R (Promo)
Medium(s): CD, Cassette, iTunes AAC, Amazon MP3, 2x 12″ Red Vinyl
Time: 61:16 (Album)
U-Card Inside
3D Cover
3D Cover U-Card
3D Cover Disc
Russian Cover
Russian Back
Promo Cassette Cover
Promo Cassette Tape


text:
Robert P. Murphy
Research Assistant Professor
Free Market Institute at Texas Tech University
Robert.P.Murphy@ttu.edu
Ph.D. Economics, New York University, Spring 2003
B.A. Economics, Hillsdale College, Magna Cum Laude, 1998
Research Assistant Professor, Free Market Institute at Texas Tech, August 2015 –.
Senior Economist, Institute for Energy Research, May 2007 – April 2010, September 2010 –.
Senior Fellow, Fraser Institute, July 2013 –.
Senior Fellow, Mises Institute, October 2017 –.
Research Fellow, Independent Institute, August 2012 –.
Senior Fellow, Bus. & Econ. Studies, Pacific Research Institute, Sept. 2007 – August 2011.
Research Analyst, Laffer Associates, September 2006 – June 2007.
Visiting Scholar, New York University, June 2006 – August 2006.
Visiting Assistant Professor of Economics, Hillsdale College, August 2003 – May 2006.
Murphy, Robert P. (2018) "Inequality and the Gold Standard." [Chapter in collection of essays on inequality published through Troy University, forthcoming.]
Manish, G.P. and Robert P. Murphy. (2018) "Monetary Misperception, Rational Expectations, and the Austrian Theory of the Business Cycle." Journal of Private Enterprise, Vol. XXXIII, No. 2, Summer 2018, pp. 83-96.
Murphy, Robert P. (2018) "Removing the 1970s Crude Oil Price Controls: Lessons for Free Market Reform." Journal of Private Enterprise, Vol. XXXIII, No. 1, Spring 2018, pp. 63-78.
Murphy, Robert P. (2018) "The Connection Between Entrepreneurship and Economic Prosperity: Theory and Evidence," Chapter 1 in Demographics and Entrepreneurship: Mitigating the Effects of an Aging Population (Fraser Institute), May 2018.
Murphy, Robert P. (2017) "Is Garrison's Notion of 'Secular Growth' Compatible With the Solow Growth Literature?" Quarterly Journal of Austrian Economics, Vol. 20, No. 4, pp. 336-353.
Murphy, Robert P. (2017) "Libertarian Law and Military Defense." Libertarian Papers, Vol. 9, No. 2, pp. 213-232.
Murphy, Robert P. (2017) "Conclusion," chapter in Robert M. Whaples, ed., Pope Francis and the Caring Society, Independent Institute, pp. 199-220.
Knappenberger, Paul, Pat Michaels, and Robert P. Murphy. (2016) "The Case Against a Carbon Tax." Cato Policy Analysis #801, October 17, 2016.
Murphy, Robert P. (2016) "Review of The Midas Paradox: Financial Markets, Government Policy Shocks, and the Great Depression by Scott Sumner." Quarterly Journal of Austrian Economics, Vol. 19, No. 1 (Spring 2016), pp. 101-111.
Magness, Phillip and Robert P. Murphy. (2015) "Challenging the Empirical Contribution of Thomas Piketty's Capital in the Twenty-First Century." Journal of Private Enterprise, 2015 Vol. 30 (Issue 1), Spring.
Murphy, Robert P. (2014) "The Carbon Tax Win-Win: Too Good to Be True? The Tax Interaction Effect and Political Realities." Macdonald-Laurier Institute (MLI) Report, October 2014, pp. 1-19.
Murphy, Robert P. (2013) "Energy Conservation Program for Consumer Products: Energy Conservation Standards for Residential Furnace Fans." Mercatus Center Public Interest Comment submitted to Department of Energy, Office of Energy Efficiency and Renewable Energy, December 2013, pp. 1-9.
Clemens, Jason, Robert P. Murphy, and Niels Veldhuis. (2013) "The Economic Costs of Increased Marginal Tax Rates in Canada." Fraser Institute, Studies in Budget and Tax Policy, October 2013, pp. 1-46.
Clemens, Jason and Robert P. Murphy. (2013) "Reforming Alberta's Heritage Fund: Lessons from Alaska and Norway." Fraser Institute, Alberta Prosperity Initiative, March 2013, pp. 1-42.
Murphy, Robert P. (2012) "Carbon 'Tax Swap' Deals: A Review and Critique." Institute for Energy Research, November 2012, pp. 1-47.
Crowley, Brian Lee and Robert P. Murphy. (2012) "No Dutch Treat: Oil and Gas Benefits All Canadians" (with Brian Lee Crowley). MLI Commentary, No. 1 in the High Dollar Series of commentaries, May 2012, pp. 1-13.
Murphy, Robert P. (2010) "Coordination: A Critique of Daniel Klein." Journal of Private Enterprise, Vol. 25, No. 2, Spring 2010, pp. 117-127.
Wutscher, Robert, Robert P. Murphy, and Walter E. Block. (2010) "Mathematics in Economics: An Austrian Methdological Critique." Philosophical Investigations, Vol. 33, No. 1, January 2010, pp. 44-66.
Michaels, Robert and Robert P. Murphy. (2009) "Green Jobs: Fact or Fiction? An Assessment of the Literature." Institute for Energy Research, January 2009, pp. 1-19.
Barnett II, William, Walter Block, and Robert P. Murphy. (2009) "Testing Austrian Business Cycle Theory? A Rejoinder to Andrew T. Young." Journal of Business and Economic Perspectives, Vol. XXXV, No. 2, Fall/Winter 2009.
Murphy, Robert P. (2009) "Rolling the DICE: Nordhaus' Dubious Case for a Carbon Tax." The Independent Review, Vol. 14, No. 2 (Fall 2009), pp. 197-217.
McQuillan, Lawrence J. and Robert P. Murphy. (2009) "The Sizzle of Economic Freedom: How Economic Freedom Helps You and Why You Should Demand More." Pacific Research Institute, January 2009, pp. 1-30.
Bundt, Thomas and Robert P. Murphy. (2008) "Are Residual Economic Relationships Normally Distributed? Testing an Assumption of Neoclassical Economics." The Review of Austrian Economics, Vol. 21, No. 4 (December 2008), pp. 329-340.
Murphy, Robert P. (2008) "Oil Speculators: Bad or Good" EconLib Featured Article, August 4, 2008.
Westley, Christopher, Robert P. Murphy, and William L. Anderson. (2008) "Institutions, Incentives, and Disaster Relief: The Case of the Federal Emergency Management Agency Following Hurricane Katrina." International Journal of Social Economics, Vol. 35, No. 7, pp. 501-511, Summer 2008.
Murphy, Robert P. (2008) "Ending the Revenue Rollercoaster: The Benefits of a 3% Flat Income Tax for California." Pacific Research Institute, May 2008, pp. 1-61.
Murphy, Robert P. (2008) "Oil Prices." EconLib Featured Article, April 7, 2008.
Murphy, Robert P. (2007) "Interest and the Marginal Product of Capital: A Critique of Samuelson." Journal of the History of Economic Thought, Vol. 29, No. 4, pp. 453-464.
Murphy, Robert P. (2006) "Cantor's Diagonal Argument: An Extension to the Socialist Calculation Debate." The Quarterly Journal of Austrian Economics, Vol. 9, No. 2 (Summer 2006), pp. 3-11.
Murphy, Robert P. (2006) "A Note on Walter Block's Defending the Undefendable: The Case of the 'Heroic' Counterfeiter." American Journal of Economics and Sociology, Vol. 65, Issue 2 (April 2006), pp. 463-467.
Murphy, Robert P. (2005) "Dangers of the One-Good Model: Böhm-Bawerk's Critique of the 'Naïve Productivity Theory' of Interest." Journal of the History of Economic Thought, Vol. 27, No. 4 (December 2005), pp. 375-382.
SELECT WORKING PAPERS
Murphy, Robert P. "More Than Quibbles: Problems With Fractional Reserve Free Banking." Under review at the Quarterly Journal of Austrian Economics.
Murphy, Robert P. "Is Fractional Reserve Banking Necessary to Prevent Monetary Disequilibrium?"
Murphy, Robert P. "Physical Capital and Financial Capital Are Different Things, and Why It Matters." (Presented at the 2018 APEE meeting.)
Murphy, Robert P. and Michael Makovi. "How the Solow Model Misleads Economists in Cross-Country Comparisons."
Murphy, Robert P. and Ryan Griggs. "The Inverted Yield Curve, Austrian Business Cycle Theory, and the Austrian 'True Money Supply.'"
Murphy, Robert P. and Ryan Griggs. "Americans' Choice of Assets Over Time."
Murphy, Robert P. "Why Does an Inverted Yield Curve 'Predict' a Recession? Hayek vs. Harvey." (To be presented at the 2018 SDAE meeting.)
Murphy, Robert P. "Secular Growth and 'Real Liquidity': Bridging Garrison and Salerno."
Murphy, Robert P. and Gonzalo Macera. "Pitfalls in the 'New' Minimum Wage Literature: A Simulation Approach." (Presented at 2016 SEA meeting.)
Murphy, Robert P. "A General Equilibrium Illustration of the 'Tax Interaction Effect' with a Carbon Tax." (Presented at 2016 SEA meeting.)
SELECT BOOKS
Murphy, Robert P. and Doug McDuff, M.D. (2015). The Primal Prescription: Surviving the "Sick Care" Sinkhole. Primal Publishing, September 2015.
Murphy, Robert P. (2015). Choice: Cooperation, Enterprise, and Human Action. The Independent Institute, May 2015.
Murphy, Robert P., Jason Clemens, Milagros Palacios, and Niels Velduis. (2014) Economic Principles for Prosperity. Fraser Institute.
Murphy, Robert P. (2009) The Politically Incorrect to the Great Depression and the New Deal. Regnery, 2009.
Murphy, Robert P. (2007) The Politically Incorrect Guide to Capitalism. Regnery, 2007.
Murphy, Robert P. (2017) "Federal Energy Related Tax Policy and Its Effects on Markets, Prices, and Consumers." Testimony submitted before the House Committee on Energy and Commerce, Subcommittee on Energy, March 29, 2017.
Murphy, Robert P. (2013) "The 'Social Cost of Carbon': Some Surprising Facts." Testimony submitted before the Senate Committee on Environment and Public Works, July 18, 2013.
Murphy, Robert P. (2011) "How Federal Reserve Policies Add to Hard Times at the Pump." Testimony submitted before the Subcommittee on Regulatory Affairs, Stimulus Oversight, and Government Spending, May 25, 2011.
Murphy, Robert P. (2008) Testimony submitted at House Financial Services Committee hearing entitled, "Implications of a Weaker Dollar for Oil Prices and the U.S. Economy," July 24, 2008.
SELECT COMMENTARY FOR INSTITUTE FOR ENERGY RESEARCH (IER)
Murphy, Robert P. (2015) "New Study on 'Unburnable' Energy Belies Carbon Tax Rhetoric." IER post, January 9, 2015.
Murphy, Robert P. (2014) "Prices Are Dropping, But Gas Is Still Historically Expensive." IER post, December 17, 2014.
Murphy, Robert P. (2014) "The Oil Export Ban: Time to Unleash American Producers." IER post, December 10, 2014.
Murphy, Robert P. (2014) "The Case for a Carbon Tax Is Much Weaker Than You Think." IER post, December 1, 2014.
Murphy, Robert P. (2014) "Milton Friedman and Climate Change." IER post, October 14, 2014.
Murphy, Robert P. (2014) "Australians Repeal Carbon Tax and CASE for Carbon Tax." IER post, July 17, 2014.
Murphy, Robert P. (2014) "Power Plant Rule Fails Administration's Own Cost/Benefit Test." IER post, June 2, 2014.
Murphy, Robert P. (2014) "Are Climate Change Mitigation Policies a Form of Insurance?" IER post, April 17, 2014.
…plus 170+ articles at http://instituteforenergyresearch.org/about/people/robert-murphy/articles/.
SELECT POPULAR PUBLICATIONS
Murphy, Robert P. (2016) "The Economics of Brexit." Daily Caller, July 5, 2016.
Crowley, Brian Lee and Robert P. Murphy. (2012) "Compared to Canada, It's a Fiscal Dip, Not Cliff." Huffington Post Canada, December 29, 2012.
Murphy, Robert P. (2011) "The Tea Party should hold fast on debt ceiling." Wall Street Journal's MarketWatch, May 3, 2011.
Murphy, Robert P. (2010) "An ironic twist in fiscal policy." Reuters, September 27, 2010.
Murphy, Robert P. (2010) "Double dip looks doubly certain." MarketWatch, July 20, 2010.
Murphy, Robert P. (2010) "There's no defense for the estate tax." L.A. Times, July 14, 2010.
Murphy, Robert P. (2010 "Artificially low interest rates bad for the economy." Detroit News, May 11, 2010.
Murphy, Robert P. (2010) "Setting the stage for stagflation." The Washington Times, February 19, 2010.
Murphy, Robert P. (2008) "Designing the Market's Mechanisms." Barron's, May 12, 2008.
Hoskins, Lee and Robert P. Murphy. (2008) "Memo to the Fed: Stop Those Rate Cuts." Forbes.com, March 17, 2008.
Murphy, Robert P. (2007) "Socialized Oil Can't Replace Market Sense." Investor's Business Daily, December 13, 2007.
Murphy, Robert P. (2007) "Can Free Markets Be Designed?" Forbes.com, November 15, 2007.
Principles of Microeconomics / Macroeconomics
Intermediate Microeconomics
History of Economic Thought I and II


text:
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Who Was Georgetown Named After?
Book a Guided Walking Tour
Have you ever heard that Georgetown was named for George Washington (or another famous George)? Find out if that is true or not on this week's Should Have Asked A Tour Guide.
Check us out on YouTube - Top Things To Do DC - for our weekly series, Should Have Asked A Tour Guide, every Tuesday at 230pm.
Is the Capitol the Tallest Building in DC?
Was DC Designed to Confuse Invaders?
Do the Hooves on an Equestrian Statue Show How the Rider Died?
Can you Explain the Layout of DC?
Did Taft really get Stuck in a Bathtub?
All About the Statues in Lafayette Square
Canden: Hey, guys. Canden here with-
Becca: -Becca, hi.
Canden: We are part of free tours by foot and top things to do DC with another episode of-
Becca and Canden: Should Have Asked A Tour Guide.
Canden: Thank you for getting that. We didn't even practice that.
Becca: Not even rehearsed.
Canden: I am back from New Orleans. Florence did not come with me. We thought we'd do another episode for you guys this week.
We are here in Georgetown which is my favorite part of Washington DC. Shameless plug, I have had two books published on the history of Georgetown.
Becca: She literally wrote the book on Georgetown.
Canden: The only Canden on Amazon. It's really easy to find me. We thought we'd go over some of the common questions that we get about Georgetown.
Now, so we're in Georgetown, which means we are not in Washington DC anymore?
Becca: No, we're definitely still in Washington DC. Sometimes people think Georgetown is a separate part of DC, which is not true today, but has its roots in some truth. If you've watched some of our other videos, you might know this.
In 1790 Congress passes something called the Residence Act, which establishes a federal district to become the new capital city. George Washington is going to plan out and map out our nation's capital.
Georgetown had already existed. By the time 1790 rolls around, Georgetown had been a bustling tobacco port for more than 50 years.
Okay, Canden. So we're in Georgetown. Who is Georgetown named for?
Canden: George in the 1700s was a very popular name. There are many options and there are a few that haven't passed around throughout the years. We know some of them are not true. The town of George is not named after George Clooney, unfortunately-
Becca: [laughs]
Canden: -though I would name a town after him. It is not named after George Washington. George Washington was like 19 years old when the town of George was founded. That's basically middle age in the 18th century.
There are plenty of well-accomplished 19 year olds at that time, but George Washington was not one of them. It's probably named after King of England. Maryland was a colony at the time. So it's King George II, who was grandfather of King George the III who would we would later rebel against. This point we're fine. We are still naming things after British royalty.
It could also be named after the two men who owned this land first- They either willingly or forcibly sold their land to kind of create this port town of George. That was George Gordon and George Bell. It is definitely named after a George. We just don't know which one.
Becca: If you visit Georgetown today, it does feel a part from Washington in some ways and so much of that is rooted in the fact that it was its own established town long before the District of Columbia was established.
Canden: Visiting Georgetown is something we highly recommended. Becca and I are in Georgetown regularly. We offer three tours of the neighborhood.
There's the historic Georgetown tour, the ghost of Georgetown tour and an adults-only wicked Georgetown tour. If you guys have any more questions about Georgetown, let us know in the comments below. Tag us on social media @topthingstodo#shouldhaveaskedatourguide or sign up for a tour and ask us in person.
Becca: Come visit Georgetown yourself.
[00:03:43] [END OF AUDIO]
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Canden Arciniega
Canden is a historian and tour guide in Washington DC with 4 published books about the city. She has written for HuffPost Travel and has been featured in the Washington Post, WTOP, and numerous other DC papers. She's also been interviewed by the BBC, NPR, Travel Channel and Discovery Family Channel. Canden is the producer of our podcast, Tour Guide Tell All With a M.A. in History from University College London and a B.A. in History from Elon University, she is an authority on D.C. history, and has led tours in the city for over 10 years. She currently resides in DC, but has also lived in London and South Korea, and has travelled to 28 countries. Her two children (both under the age of 4) have their passports and own frequent flier accounts.
Updated: January 17th, 2023
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text:
Q: Inner join in LINQ? How to convert below inner join SQL statement into LINQ statement
 SELECT ca.[CUS_ADDRESS_ID]
  ,ca.MASTER_CUSTOMER_ID
  ,ca.[ADDRESS_1]
  ,[CITY]
  ,[STATE]
  ,COUNTRY_CODE
  ,cad.ADDRESS_TYPE_CODE
  ,cad.ADDRESS_STATUS_CODE
   inner join [CUS_ADDRESS_DETAIL] cad on ca.CUS_ADDRESS_ID = cad.CUS_ADDRESS_ID and cad.PRIORITY_SEQ = 0
  where ca.CUSTOMER_ID = '0000026'

and assign to
 public class Location
{
    public string CustomerNumber { get; set; }
    public string City { get; set; }
    public string State { get; set; }
    public string Country { get; set; }
    public string AddressLocCode { get; set; }
    public string AddressStatus { get; set; }
}

A: The query would wind up looking something like this (keep in mind, though, that you'll have to change your field names to match since they look a little mangled):
var locations = from c in Customers
                join ca in CustomerAddresses
                on new { c.CustomerAddressId, 0 }
                    equals new { ca.CustomerAddressId, ca.PrioritySeq }
                select new Location
                {
                    CustomerNumber = c.MasterCustomerId,
                    City = ca.City,
                    State = ca.State,
                    Country = ca.Country,
                    AddressLocCode = ca.AddressLocCode,
                    AddressStatus = ca.AddressStatus
                };


text:
Q: Measuring link load time asynchronously with ajax New to ajax and stackoverflow--how can I determine how long it will take to load links on my page using ajax in a Chrome extension? Currently, I'm running a function each time a url on my page is successfully reached, but I don't believe the start time accurately reflects when the page starts loading. Is there a way I can remedy this? How would I be able to effectively calculate the time it takes for a link to fully load?
var col = new Array();
chrome.runtime.onMessage.addListener(
 function(request, sender, sendResponse) {
if( request.message === "clicked_browser_action" ) {
    $("a").each(function(){
    var temp = $(this).not("#next").attr("href");
    var xhttp = new XMLHttpRequest();
    if(temp===undefined){
        return;
    }
    col.push(temp);
    var start = 0;
    $.ajax({
    url:$(this).attr("href"),
    beforeSend: function (request, settings) {
    start = Date.now();
    },
    success: function () {
        var end = Date.now();
        console.log(temp);
        console.log(start)
    },
    error: function (jqXHR, status, er) {
        if (jqXHR.status === 404) {
        console.log(temp);
            console.log("connection failed");
        }
  }
});
}
)}}
);

Many thanks.


HEH. LA OSS BARE SI AT JEG ER EN SVÆRT RIK OG MEKTIG MANN SOM GJØR DET DE FLESTE RIKE OG MEKTIGE MENN GJØR.
BARE AT JEG KREVER FÆRRE LIVVAKTER.
NEI. JEG ER GLAD FOR AT DU IKKE FORTSATT DRIVER OG RANER BANKER OG SÅNT.
SÅ…DA DU FIKK KREFTENE DINE, ØH, GJORDE DU DET?
LOT MOBBERNE BETALE FOR DET DE GJORDE?
NÅR JEG SER TILBAKE PÅ DET, INNSER JEG AT DE BARE VAR UNGER OG JEG – JA, JEG SKADET DEM VELDIG, VELDIG MYE.
JEG ANTAR AT DET VAR ET DEFINERENDE ØYEBLIKK.
HEH. DIGAMOS QUE SOLO SOY UN HOMBRE MUY RICO Y PODEROSO QUE ACTÚA COMO MUCHOS HOMBRES MUY RICOS Y PODEROSOS.
YO SIMPLEMENTE NECESITO MENOS GUARDAESPALDAS.
NO. ME ALEGRO QUE NO SIGAS ROBANDO BANCOS Y COSAS POR EL ESTILO.
ASÍ QUE… UNA VEZ QUE OBTUVISTE TUS PODERES, LO, UH, HICISTE?
EN RETROSPECTIVA, ME DOY CUENTA DE QUE ERAS SOLO UNOS NIÑOS SIENDO NIÑOS Y YO — BUENO, YO LOS LASTIME MUCHO, GRAVEMENTE.
FUE UN MOMENTO DECISIVO, SUPONGO.
A)Duncan: He. Vamos dizer apenas que sou um homem muito rico e poderoso que age como a maioria dos homens muito ricos e poderosos agem.
B)Duncan: Eu simplesmente preciso de um pouco menos de guardacostas.
D)Kyle: Não. Eu estou feliz porque você não continua roubando bancos e coisas assim.
E)Kyle: Então… uma vez que você conseguiu seus poderes você, anh, fez aquilo?
F)Kyle: Fez os valentões pagarem?
H)Duncan: Olhando pra trás, agora, eu percebo que eram apenas crianças sendo crianças e eu– bem, eu os machuquei muito, muito mesmo.
I)Duncan: Foi um momento de definição, eu suponho.
HEH. SAGEN WIR EINFACH ICH BIN EIN SEHR REICHER UND MÄCHTIGER MANN DER SICH VERHÄLT, WIE ES DIE MEISTEN SEHR REICHEN UND MÄCHTIGEN MÄNNER TUN.
ICH BENÖTIGE BLOß WENIGER BODYGUARDS.
NEIN. ICH BIN FROH, DASS DU NICHT IMMERNOCH BANKEN AUSRAUBST UND SO.
ALSO… ALS DU DANN DEINE KRÄFTE HATTEST, HAST DU, ÄHM, ES GETAN?
WENN ICH NUN SO ZURÜCKBLICKE ERKENNE ICH, DASS SIE BLOß KINDER WAREN, DIE SICH WIE KINDER BENAHMEN UND ICH – NUN, ICH HABE IHNEN SEHR, SEHR GROßES LEID ZUGEFÜGT.
ICH SCHÄTZE, DAS WAR EIN ENTSCHEIDENDER MOMENT.
Heh. Disons juste que je suis un homme très riche et puisssant qui agit comme la plupart des hommes très riches et puissants.
J'ai simplement besoin de moins de gardes du corps.
Non. Je suis content que vous ne voliez plus de banques et ce genre de trucs.
Et donc… Une fois que vous avez eu vos pouvoirs, vous, hum, l'avez fait ?
Faire payer les brutes ?
En y repensant maintenant, je réalise que c'étaient juste des enfants agissant comme le font les enfants et je — et bien, je les ai blessés très, très sérieusement.
C'était un moment clé, je suppose.
HEH. LET'S JUST SAY I'M A VERY RICH AND POWERFUL MAN WHO ACTS AS MOST VERY RICH AND POWERFUL MEN DO.
I SIMPLY REQUIRE FEWER BODYGUARDS.
NO. I'M GLAD YOU'RE NOT STILL ROBBING BANKS AND STUFF.
SO… ONCE YOU GOT YOUR POWERS, DID YOU, UH, DO IT?
LOOKING BACK NOW, I REALIZE THEY WERE JUST KIDS BEING KIDS AND I — WELL, I HURT THEM VERY, VERY BADLY.
IT WAS A DEFINING MOMENT, I SUPPOSE.
We're blasted past $75,000 with The Young Protectors Volume One Kickstarter Project which means that all backers are going to get a 5-15 page TRUTH OR DARE BONUS COMIC PDF where the The Young Protectors team will be playing a game of Truth or Dare and backers will be able to create and vote on what questions/dares will be asked to which character!
And Kickstarter backers are now geting a whole stack of stuff! In addition to a gorgeous softcover book of the Prologue, Chapter One and Interlude One, what other goodies are backers going to get?
Any of that sound like stuff you'd like? Want to participate in future votes where you'll get to decide who's going to be featured in bonus art prints and whether those art prints will be Not Safe For Work?
Become a backer of The Young Protectors Volume One Kickstarter right now and it's all yours, my friend!
We had our tenth bonus page on Wednesday and look below! We're already at $298 towards the next bonus page!
Special thanks go out to long-time supporters Liz S. (who makes their second generous donation to The Young Protectors!), Corinna K. (who makes their fourth generous donation to The Young Protectors!) & Saxon B. (who makes their twenty-ninth [!!!] generous donation to The Young Protectors!) and a warm welcome and grateful bow go out to new supporters Kori H., Stephanie C., David C. & Albert L. for their generous donations over the last few days!
Big hugs go out to long-time friend of The Young Protectors Robert B. & joshua G. for their super-generous $25 donations! And this makes both Robert's and joshua's nineteenth super-generous donations to this comic! You two are on a roll! Thank you so, so much, Robert and joshua!
Thank you all so much for your generous support! Almost $80,000 pledged to our first The Young Protectors Kickstarter and we're very close to our next bonus page! You all ROCK!
So! It's just been revealed that The Annihilator began doing questionable things at a tender age. How will Kyle react to this revelation? And what other things will The Annihilator reveal?
DING! DING! DING! DING! DING! DING! DING! Edit 6/15/13 12:20 AM: You've done it again! Thanks to your generous donations, you've yet again blown past the target on the donation bar! So that means that in addition to our regular update next Saturday (page 8!), there will be a BONUS UPDATE this Wednesday, June 19th (page 7)! You TOTALLY ROCK! Thank you so much!


Acts 9 has two segments. In the first, Saul  is stricken with blindness as he tries to hunt down Jesus's followers, is taken to Damascus , is healed by a follower of Jesus by the laying on of hands, and immediately turns around and preaches the gospel as passionately as he persecuted it. In the second segment, Peter heals a paralytic and raises a woman from the dead.
This chapter provides us with an exposition on religious experience and some guidance on what it means to be a member of the body of Christ. Saul initially is "breathing out murderous threats" but appears to be acting under the authority of the high priest to arrest followers of the Way. Jesus appears to him as a blinding light and Saul falls to the ground. In attacking Jesus' disciples, Saul has attacked Jesus Himself . His companions hear "the sound," presumably of Jesus speaking, but they see nothing. In Damascus, Saul sat in blindness in the house of Judas on Straight Street  for three days, until Jesus directed Ananias  to lay hands on Saul. God says that He will show Saul how much he has to suffer. Ananias tells Saul that not only will he heal him but that Saul will be filled with the Spirit. Something like scales fall from Paul's eyes, he is baptized, and begins preaching in favor of Jesus. The Damascus Jews conspire to kill Saul, but he is lowered in a basket outside the walls, and goes to Jerusalem. Barnabas takes him to the apostles and tells them Saul's story . Saul starts preaching to the Grecian Jews, who try to kill him, so the apostles dispatch Saul to Tarsus via the port of Caesarea . The church had peace and grew stronger in all of Israel.
In the second part of the chapter, Peter goes to Lydda and performs a miracle much like Jesus' . He tells a bedridden Aeneas to pick up his mat and walk, that Jesus has healed him. This miracle converted both Lydda and Sharon. In Joppa, Peter also raises a dead Tabitha/Dorcas  from the dead. Before he does so, the widows show Peter all the clothes that Tabitha/Dorcas made, presumably for them as a good work. Joppa was converted. Peter stayed with a tanner named Simon.
1. Saul means "desired." The name occurs in Genesis 36 as an Edomite king, but more centrally was the name of the first king of Israel, a king the Lord rejected.
2. Damascus occurs many times in the Old Testament. It generally symbolizes foreign, pagan power. In Genesis 14, Abram pursues the four kings as far as Damascus. In 2 Samuel 8, David conquers as far as Damascus. In 2 Kings 8, Elisha goes to Damascus to encourage rebellion against the king.
3. Followers are as cells in Jesus's body.
5. Ananias means "whom Jehovah has graciously given." In Acts, it has an ominous overtone, since Ananias and Sapphira were slain by the Lord for lying to the Holy Spirit. Ananias is also the high priest of Acts 24 who denounces Paul.
6. Barnabas means "Son of Consolation" or "Son of Exhortation". It's unclear why Barnabas tells Saul's story. Perhaps the church elders would be disinclined to believe Saul.
7. Caesarea was built by Herod for Caesar Augustus. It was a town always associated with paganism, having begun as a Phoenician port.
8. Joppa is the port from which the prophet Jonah's hoped to flee to Tarshish. In Mathew 12, Matthew 16, and Luke 11, Jesus says that this generation will not get a miraculous sign, but only "the sign of Jonah," presumably the miracle of seeing the dead rise. And through Peter, Joppa receives the sign of Jonah.
 Tabitha/Dorcas means "gazelle," the first in Hebrew, the second in Greek. Peter calls her "Tabitha." The widows call her "Dorcas." Presumably this means that the widows she had been tending were Greek, but that she was a Jew.
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Iron Stamper – Two Quick Cards Today!
Tomorrow will be my last post in this series and will feature an Easter card that will knock your socks off! Be sure to check back!!
Before I get started I just want to remind you that SALE-A-BRATION ENDS TODAY AT 10:59PM PST!!! Get your orders in to me for your last chance to earn free products this year. Check out the brochure to see all the great products you can earn for free by clicking the ad on the side bar to your right. To see what is available in the Occasions Mini or the 2011-2012 Idea Book and Catalogue click on the links – remember a $60 order (pre-tax etc) earns you ONE FREE PRODUCT from the Sale-a-Bration brochure.
Okay, on to today's cards. These are SUPER simple cards featuring the Spring Fever Simply Scrappin' kit in the Occasions Mini.
What did I tell you? Super simple, right? But fun and something I'd be happy to receive. What about you?
I started with my Daffodil Delight card base. I trimmed about a 1/2″ off one side and then used my Scallop Trim Border punch on that shortened side. I then backed it with a piece of Whisper White. The banner is one of the border stickers from the kit – cut down to fit. I dressed it up with some of the smallest sized Paper Daisies and a Basic Pearl Jewel accent. To colour the paper daisies (they come in white only) I simply placed them on my ink pad (I think I used Blushing Bride but I can't remember now – oops!) and used my tweezers to push them into the pad until they were saturated with colour. Allow them to dry thoroughly before trying to glue them to the card OR the pearls to them!!
A simple sentiment (this one is from my absolute favourite stamp set from Sale-a-Bration – Elementary Elegance) stamped in Chocolate chip and your card is finished.
Next up, an Easter inspired card.
I started with a base of Daffodil Delight again but this time I made a 5″ square card. I layered a piece of the patterned paper from the Spring Fever Simply Scrappin' kit over top. Then a 3″ circle of the Melon Mambo textured card stock from the kit which I cut out using my 3″ Circle Originals Die and my Big Shot. The rest of the card is made up of various stickers from the kit simply layered on top of each other in a pleasing manner.
The middle one I popped up with Dimensionals for some added interest.
There you are. Two cards which took me probably 15 minutes to make … total!! Sometimes it's not so much the level of detail or the amount of product you put onto the card but the act of actually sending or giving a card that matters. So having an arsenal of quick and easy cards to pull out when the occasion calls for it is priceless!


text:
Q: dnSpy doesn't decompile async/await method as it has been written dbSpy v6.1.8
asp .net core app on .net5
In dnSpy's settings there is option Decompile async methods (async/await).
I assumed this option influence on how async methods should be decompiled. In one case it should be something like this:
public static Task Main(string[] args)
{
    Program.<Main>d__6 <Main>d__ = new Program.<Main>d__6();
    <Main>d__.<>t__builder = AsyncTaskMethodBuilder.Create();
    <Main>d__.args = args;
    <Main>d__.<>1__state = -1;
    <Main>d__.<>t__builder.Start<Program.<Main>d__6>(ref <Main>d__);
    return <Main>d__.<>t__builder.Task;
}

In other something like this:
public static async Task Main(string[] args)
{
    CreateHostBuilder(args).Build().Run();
}

But despite value of this option it always shows method like in first example. I tried relaunch dnSpy, clear all assemblies and reload them, but all in vain.
Is it possible to force dbSpy shows method similar to second example?