We have been cleaning carpet since 1985. With 30 years experience and 1000's of homes cleaned, we have just the right tool in our tool box of experience to provide you with the most though cleaning available.
Our professional deep cleaning services have expanded beyond carpet cleaning over the years to furniture cleaning, tile and grout cleaning, hardwood, laminate, Auto, RV and commercial carpet cleaning. Using the latest technology in Truck Mounted Steam Cleaning and Rotary Jet Extraction we have been able to nearly eliminate the problems of the past like the same spots reappearing after the carpet has dried.
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WHY CHOOSE CLEAN IT RIGHT CARPET CARE?
When you choose us for your Carpet cleaning, Furniture cleaning or Tile and grout cleaning you can be assured that you will receive the best cleaning available. We learned long ago that it is much easier to keep your customers than it is to always be looking for new ones. We do this by providing the utmost respect to you and your home. We arrive at your home knowing that you have many choices and you have chosen us. We enter your home with an attitude of gratitude.
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Back Beat Seattle hosts our first showcase with The Redwood Plan, What What Now and THEESatisfaction on Friday, August 14th at the historic Blue Moon. Show starts at 10pm and is $5.
We're proud of this lineup as it features three amazing local bands, whose sounds range from hip-hop to hard rock to rock with synthesizer flavor. It will also be one of THEESatisfaction's last Seattle shows before the sci-fi ladies move to San Francisco. We've seen What What Now and The Redwood Plan numerous times among the Back Beat staffers and know that they, as THEESatisfaction, will show you a good time.
Written by: Dagmar on 08/10/2009.


Illusion of Joy is the duo of musicians Seth Warren and Maresa Whitehead. Initially conceived as a solo recording project of Seth Warren's during the Summer of 2000 in the small village of Potsdam, New York, Illusion of Joy has been based out of Pittsburgh, Pennsylvania since early 2003. Maresa Whitehead joined both recording and for live performances in the summer of 2016. Influenced by a plethora of alternative 1980s musicians including The Cure, Public Image Ltd. and The Bolshoi, the retro aesthetic of Illusion of Joy is balanced by lyrics that alternate between contemporary and timeless. Live, Illusion of Joy has shared stages with acts like Christian Death, The Dark Clan, ThouShaltNot and Wax Idols.
Illusion of Joy began as the musical project of keyboardist, vocalist and songwriter Seth Warren in Potsdam, a village located in Northern New York. During Warren's time at college there in the late 1990s, often spent playing at a local coffeehouse and the open-mic night on the SUNY Potsdam campus, he was approached by Claude Aldous, head of Jetpack Records, to do some recordings for a reasonable rate. In the summer of 2000, thirteen hours were spent in a studio located on one of the back roads outside of Potsdam recording Crystalline, an EP of four songs.
Crystalline was well-received enough locally that people were dropping by Warren's dorm room to buy copies. The EP was released through Anhedonia Records, a "label" made up of a five-way partnership between members of As Yet Untitled, a band based out of Albany and Seth Warren. The label was perpetually in the red and releases consisted of CD-Rs and home-printed booklets. As such, the label did about as well as could be expected when one has little capital to draw upon but a dogged determination to put out some sort of product. During the existence of Anhedonia, it was able to put out three total releases: The aforementioned Crystalline and two albums by As Yet Untitled.
Live performances continued in the form of the solo and open-mic shows as the musical project pressed on. Bitter Illusion of Joy's debut LP came about as a result of Warren's participation in a music class entitled "Recording Studio Techniques." John Junklaus, whose main area of expertise lies in the remastering of jazz records, was the class instuctor. While Illusion of Joy bears little resemblance to Charlie Barnett, Junklaus was so impressed by the music and Warren's drive in the class, that he allowed the recording of Bitter over several months of extracurricular sessions.
The album was initially released via the now defunct MP3.com (at the time, an early social networking site for musicians). Unfortunately Bitter was widely ignored, despite containing the open-mic hits "Billie Jo" and "Ebony." It and Crystalline went out of print, when the site closed in December of 2003. There are currently no plans to reissue either release.
In early 2003, Seth Warren moved to Pittsburgh after his college career ended in a less than stellar manner. This move also brought about the dissolution of Anhedonia Records.
In the beginning stages of laying down new roots and acclimating to a new locale, Warren pushed forward and began recording another album. Sound waves were laid down at Masochist Monkey Studios, also known as the recording room at Joe Stacy's apartment. Stacey had moved to the city a year prior and was continually working on his own musical project, Masochist Monkey Circus. The new Illusion of Joy album was titled Division and released in April of 2004 on HPL Laboratories.
During the time that Division was being recorded, illusionofjoy.net marked the return of the musical project to the internet. A presence on several social networking sites would soon follow (subsequently, Facebook and Twitter would eclipse them all).
Early in 2005, Seth Warren's personal and professional relationship with Joe Stacey ended on very unfavourable terms. Neither one has spoken to the other since then. As access to Stacey's studio was closed, Warren had just finished building a studio of his own in the form of a custom-made computer with multi-tracking software and a high-end sound card. In a twist of luck, the master files for Division were rescued from Stacey's possession hours before the falling-out.
It was during the summer of 2005 that work began on another album. Titled The Forever Syndrome, the album was released in September of 2006. Prior to that, a single from the disc – 'A Place Outside' – was released in November of 2005, marking Illusion of Joy's departure from HPL Laboratories and move to Randy's Alternative Music, where the project resided until 2011. At present, Illusion of Joy is fully independent – a label unto itself – and the intention is for things to stay as such from here on out.
November 2005 also saw the opening of an online kiosk where purchasing Illusion of Joy CDs was finally as easy as entering a credit card number (or debit card, or PayPal account). 'A Place Outside' marked the first item ever available for purchase from illusionofjoy.net. A re-release of Division followed not long after as did the official release of The Forever Syndrome and 'Michelle,' a single which came out in early 2007. That humble "kiosk" was re-dubbed "The Virtual Merch Table" before being shut down entirely in 2015 as it is, quite frankly, easier to enlist third-parties to sell merchandise online.
In late 2007, Illusion of Joy was brought to the stage for the first time since Seth Warren had made his new home in Pittsburgh. However, in the grand tradition of being unconventional, said performances were few and far-between and all outside of Warren's adopted hometown. It would not be until 2008 that Illusion of Joy would début live locally in Pittsburgh with a handful of performances during the Spring and Summer.


Mutation-based molecular diagnostics of autosomal dominant polycystic kidney disease (ADPKD) is complicated by genetic and allelic heterogeneity, large multi-exon genes, duplication of PKD1, and a high level of unclassified variants (UCV). Present mutation detection levels are 60 to 70%, and PKD1 and PKD2 UCV have not been systematically classified. This study analyzed the uniquely characterized Consortium for Radiologic Imaging Study of PKD (CRISP) ADPKD population by molecular analysis. A cohort of 202 probands was screened by denaturing HPLC, followed by direct sequencing using a clinical test of 121 with no definite mutation (plus controls). A subset was also screened for larger deletions, and reverse transcription–PCR was used to test abnormal splicing. Definite mutations were identified in 127 (62.9%) probands, and all UCV were assessed for their potential pathogenicity. The Grantham Matrix Score was used to score the significance of the substitution and the conservation of the residue in orthologs and defined domains. The likelihood for aberrant splicing and contextual information about the UCV within the patient (including segregation analysis) was used in combination to define a variant score. From this analysis, 44 missense plus two atypical splicing and seven small in-frame changes were defined as probably pathogenic and assigned to a mutation group. Mutations were thus defined in 180 (89.1%) probands: 153 (85.0%) PKD1 and 27 (15.0%) PKD2. The majority were unique to a single family, but recurrent mutations accounted for 30.0% of the total. A total of 190 polymorphic variants were identified in PKD1 (average of 10.1 per patient) and eight in PKD2. Although nondefinite mutation data must be treated with care in the clinical setting, this study shows the potential for molecular diagnostics in ADPKD that is likely to become increasingly important as therapies become available.
PKD1 has 46 exons and a coding region of approximately 13 kb; the area that contains exons 1 to 33 is duplicated six times more proximally on chromosome 16 (the HG loci).1,2 Because of the high level of homology between PKD1 and the HG, protocols for locus-specific amplification of PKD1 are required for analysis.17 PKD2 has 15 exons and a coding region of approximately 3 kb. Because of these complications, few complete screens of both genes have been described, and detection levels are at 60 to 70%.17 A total of 270 different PKD1 and 73 PKD2 mutations are described in the Human Gene Mutation Database (HGMD), illustrating the high level of allelic heterogeneity; most mutations are unique to a single family.17–19 The majority of changes are predicted to truncate the proteins, although a significant number of missense changes have been described.
DNA for mutation screening was available from 202 families who had at least one individual enrolled in CRISP. Thirty-two families were multiplexed within CRISP, giving a total of 239 patients. The initial PKD1 and PKD2 screening of the 202 probands by denaturing HPLC (DHPLC) identified 81 definite mutations (nonsense, frame-shifting deletions or insertions, typical splicing, or in-frame changes of five or more amino acids [aa]); defined as mutation group (MG) = A in Table IA). A second round of screening by direct sequencing (DS) of both genes in all patients in whom no definite mutation was detected, plus 29 control subjects (a total of 150), revealed an additional 37 definite mutations. In addition, analysis of a subset by field inversion gel electrophoresis (FIGE) and visualization of PKD1 long-range PCR (LR-PCR) products revealed four large deletion mutations, giving 122 probands with MG = A (Table IA).
In four atypical splicing cases, RNA was available to test the splicing predictions, and in a fifth, IVS43+14del20, skipping of exon 43 had been previously demonstrated.28 In two patients, substitutions close to the end of IVS15 generated novel AG dinucleotides predicted to form novel splice acceptors and cause frame-shifting mutations. Reverse transcription–PCR (RT-PCR) and sequencing confirmed this abnormal splicing (Figure 1A). A similar mutation, IVS37-10C→A, was predicted to abolish the normal acceptor site by weakening the poly-pyrimidine tract (Figure 1B) and RT-PCR showed skipping of exon 38, plus a product that included the final 180 bp of IVS37. In the final case, PKD2 IVS4+3delAAGT, the splice donor site was predicted to be destroyed (Figure 1C). No abnormality was seen with RT-PCR across the region, but amplification with a primer in IVS4 showed that all or part of IVS4 is incorporated into the sequence. These mutations were therefore classed as MG = A, giving a total of 127 families with definite mutations.
Examples of atypical splicing events in PKD1 (A and B) and PKD2 (C). (A, top) Diagram of wild-type and mutant cDNA sequence illustrating the effects of two IVS15 substitutions. Novel sequence included in the transcript is boxed in red. (Bottom) Genomic sequence from these cases. Exonic sequence is in boldface, intron/exon boundaries are indicated with vertical lines, and polypyrimidine tracts are underlined. Substituted nucleotides are in red, and novel acceptor sites and polypyrimidine tracts are shown with red vertical and horizontal lines, respectively. Novel exonic sequence is in blue boldface. (B) Wild-type and mutated sequence of IVS37-10C→A. This substitution weakens the normal polypyrimidine tract (7/10; dashed black line) and eliminates the normal acceptor site. Reverse transcription–PCR (bottom right: M, mutant; N, normal) shows that exon 38 is skipped (the skipped product is also found at a low level normally) and a product including part of IVS37 is also seen. A diagram shows the wild-type and mutant transcripts (bottom left); the genomic sequence of the novel donor site in IVS37 is in red. (C) Diagram of the wild-type and mutant sequence of the PKD2 mutant IVS4+3del4 (top) and mutant cDNA sequence (bottom). This deletion destroys the normal donor site (underlined), and cDNA sequence (bottom) shows that a product including part of IVS4 is present in the mutant.
All UCV that were not previously described as polymorphisms were analyzed and evaluated as possible disease-associated mutations. Those variants that ultimately were scored as probably pathogenic are summarized in Table II. The detailed scoring of UCV is shown in Table II (probably pathogenic), Table III (indeterminate), and Table IV (likely neutral polymorphisms). The algorithm that was used to evaluate the UCV is described in detail in the Materials and Methods section. To illustrate how this algorithm works, two examples are provided here. The PKD1 change G381S is moderately conservative but at a highly conserved site, giving a GD/GV score of +5. The change is not in a conserved domain, and no abnormal splicing was predicted (+0). This change was found in three different families, two of which had no other likely mutation and one had the indeterminate variant R3063C (+5). Segregation was demonstrated in one family with nine affected individuals (+4); and another mutation, G381C, has been described at this residue (+1) giving a variant score (VS) = +15. This is a high score (MG = B) reflecting the recurrent nature of the change, demonstrated segregation, and highly conserved residue that is mutated. In contrast, the same substitution at another site, G3651S, is less clearly pathogenic. The GD/GV score is the same (+5), but it is not in a conserved domain, it is not predicted to change splicing, and segregation has not been demonstrated (+0). No other variant was found in this individual (+2), giving a VS = +7 (MG = C). This lower level of certainty reflects that the substitution is relatively conservative and that the mutation is novel.
As a result of this analysis, 44 missense, two atypical splicing, and seven small in-frame deletions were defined as probably pathogenic, giving a total 180 (89.1%) of 202 with a probable mutation characterized. In 37 probands, a highly likely mutation (MG = B) was defined, with a likely mutation (MG = C) in another 16 (Table II). The pathologic significance of 22 additional variants was not clear, and they were defined as indeterminate (I; Table III). The remainder of novel variants were defined as likely neutral polymorphisms and are shown in Table IV.
The most important factor in determining whether a missense change was likely pathogenic was the degree to which it was conserved in orthologs and in other proteins with the same domain, with the GD almost always substantially greater than the GV (Table II). This contrasted with the 48 newly described neutral variants (Table IV), where the residue was rarely conserved and the GV was often higher than the GD. Recurrence of a variant in two or more patients with no other clear mutation also strongly supported a pathogenic likelihood. A factor that was important in excluding UCV as likely pathogenic was the finding of a more likely mutation in the same patient (Table IV). Four PKD1 UCV that previously were described as mutations were defined as indeterminate, R1340W and R4276W, or neutral polymorphisms, R324L and R2200C (Tables III and IV). The most interesting polymorphism was a 3-aa deletion (PKD1: 2894delANS) that did not segregate with the disease in a family with a segregating PKD2 missense change, R325Q. Analysis of orthologs in this area (Figure 2A) shows that this region is present only in the human sequence, not in the HG pseudogenes or other mammals. The presence of these three residues is, therefore, the result of a recent duplication in the human sequence. Segregation analysis also helped to identify likely mutations; for instance, in case 380166, two possible changes were found (F3168L and R2477C), but only the former segregated with the disease.
Multisequence alignment illustrating how comparative analysis can inform about the likely pathogenicity of variants. (A) Polycystin (PC1) sequence from CRISP case 187456 (pedigree 120010), mammalian orthologs, as indicated, and an example of the HG sequence, showing the position of the 2894delANS variant. This 3–amino acid region is present just in the human sequence. (B) Alignment of human polycystin-1 PC1 and PC2 homologs and sea urchin REJ sequences, as indicated, in the region of the polycystin-A motif (PC-A).29 Four missense mutations, two PC1 (red; R3753W and R3753Q) and two PC2 (blue; R322W and R325Q), affect highly conserved basic residues in this motif. (C) C-type lectin domains of human PC1, low-affinity Ig epsilon Fc receptor (FCER2), macrophage mannose receptor 1 (MRC1), asialoglycoprotein receptor 2 (ASGR2), and C-lectin consensus (Pfam). Mutations are shown in red (A432V, C436Y, and C508R), and indeterminate changes are shown in green (V466L and V466M). (D) Alignment of the PKD repeats of human PC1. The position of pathogenic changes are shown in red (W967R, Y1412D, G1503R, N1870H, G1999S, and G1999V), indeterminate changes are shown in green (N970K, H1093D, R1340W, S1352N, R1411C, and R1698W), and neutral changes are shown in blue (S903G, N10345, H1093Y, L1106V, V1339M, R1351W, A1422T, A1516T, H1777P, A1790V, E1811D, and A1871T). The position of the residue changed is shown colored.
Mutation analysis of the CRISP population defined 85.0% as PKD1 and 15.0% as PKD2. These values correspond closely to previous studies,5,6 although these are the first data that are based on mutation detection. The breakdown of mutation type in the two genes is summarized in Table 1. Overall, >70% of mutations were predicted to truncate the protein, >80% in PKD2. Although the majority of mutations were novel, 27 had previously been described and seven others were seen more than once in the study; 30% of families had a recurrent mutation (Table 1). The most common mutation in the study was 5014delAG (five [2.5%] families), followed by Q2556X (four [2.0%] families); two truncating and two missense changes were found three times, and six mutations were found twice (see Table I for details).
The large number of missense changes identified several residues or regions that were disrupted more than once, suggesting particular functional significances. In the PC-A domain (in the first extracellular loop of PC2 and third extracellular loop of PC129), two basic residues were substituted a total of four times (two PC1 and two PC2; Figure 2B) and four additional times in the literature (see Table I). Several mutations were also seen in the C-type lectin with three highly conserved residues substituted with a nonconservative or, in one case, a relatively conservative change (Figure 2C). Two other interesting substitutions, L4137P and L4139P, are predicted to disrupt the helical structure of the G-protein binding region.30 A clear indication of how conservation within a domain helped determine whether a substitution is likely pathogenic is shown in the PKD repeats (Figure 2D). Likely pathogenic changes were usually nonconservative in nature and at well-conserved residues, whereas the likely neutral or indeterminate changes were most often found at nonconserved residues and were often conservative changes (in some cases matching the residue found in other PKD repeats).
Mutations were spread throughout both the PKD1 and PKD2 genes with at least three mutations found in each 5% interval across PKD1 (except one with a single event) and at least one in each 12.5% interval across PKD2 (Figure 3). Of the 46 PKD1 exons (including immediate flanking regions), 40 harbored mutations, as did nine of the 15 in PKD2. Analysis of the distributions show that they were NS differently from uniform in PKD1 (P > 0.05) or PKD2 (P > 0.10). The median mutation position in PKD1 was 6873nt (median gene position 6454.5nt) with 55.6% of mutation in the 3′ half of the gene. Missense changes were relatively evenly distributed in PKD1 (P > 0.10), but truncating changes were nonuniform (P < 0.01; Figure 3A). In particular, there was a cluster of truncations at the end of exon 15 to exon 19, corresponding to the junction of the PKD repeats and the REJ domain. This clustering was not due to recurrent mutations (Table I). IVS21 has previously been suggested as a possible hotspot for mutations as a result of a long polypyrimidine tract,31 and although this could be a factor, the peak did not correspond precisely to that region. Too few missense changes were seen in PKD2 to determine the significance of the distribution (Figure 3B).
Positions of mutations in PKD1 (A) and PKD2 (B). Graph of number of mutations, truncating (light blue) or in-frame (dark blue), in intervals of the genes (PKD1, 10 divisions; PKD2, eight divisions). Corresponding exonic regions of the transcript are shown below each graph (PKD1, green; PKD2, red) with exon number indicated. Protein structures with domain regions indicated are shown above the graphs for PC1 (A) and PC2 (B). Only truncating mutations in PKD1 were distributed significantly differently from uniform (expected per interval 10.7 mutations).
Twenty-two families did not have a probable mutation defined (Table V). In 10 of these, no variants other than known polymorphisms were detected, whereas in five others, only a single unique synonymous change was detected, which was not predicted to change splicing significantly. Two cases had a substitution of the same residue, V466, suggesting significance; however, both changes (to leucine or methionine) were highly conservative, and this residue is not well conserved (leucine in frog) and variable in the C-type lectin (Figure 2C). The unique change S1352N was similarly not scored as a mutation, because the substitution matched that found in fish, whereas another, L2696P, was rejected because of the highly nonconservative nature of this site in orthologs (see Table IIIA). Two cases, 103227 (V609G and N970K) and 118641 (V690G and R1340W), had two indeterminate changes, and a third had a single such change (476972; H1093D). V690G is at a residue previously described as the site of a pathogenic change (V690D), whereas H1093D is a nonconservative change at the site of a likely polymorphism (H1093Y). Although these both are suggestive of pathogenic changes, they did not meet the threshold that we set in this article (Table IIIA). Some cases may have larger deletions because not all were screened by FIGE, and, indeed, suggestive changes (dosage or possible aberrant fragments) or regions of apparent homozygosity (hemizygosity?) were seen in four cases, but the DNA changes have not been characterized (Table V).
We describe here a scheme for comprehensive mutation analysis in ADPKD. A definite mutation was detected in 62.9% of cases; in an additional 26.2%, a UCV was found to be probably mutagenic, giving a total detection level of 89.1%. These values compare favorably with previous mutation studies using DHPLC, with a mutation detection level of approximately 67%,17 or other screenings that found PKD1 truncating mutations in <50% of cases.18 The higher detection level was achieved because of DS; DHPLC alone detected mutations in 63.9% (similar to previous studies), but DS identified an additional 51 mutations, 28.3% of the total cases. These variants did not generate abnormal DHPLC profiles under the conditions used or mimicked one of the many polymorphisms in PKD1 and so were not characterized.34 Although the majority of missed mutations were to PKD1, seven were to PKD2. It is worth noting, however, that two control mutations were not found by DS, and one other required specific re-analysis. In two additional cases, changes were initially seen as homozygous but later shown as heterozygous with different primers. These findings illustrate the complexity of mutation analysis in ADPKD, especially in PKD1 with locus-specific LR-PCR, and suggest that allele dropout can be a problem, even with carefully designed primers.
Screening for larger deletions revealed four mutations (2.0% of the total), consistent with the level (1 to 3%) detected in other studies,1,35 with suggestions that some missed mutations may also be larger rearrangements (Table V). However, FIGE is time-consuming, and a rapid screening method, such as multiplex ligation probe-dependent amplification,36 is required to detect these mutations, although the duplicated area of PKD1 will prove a challenge to establishing multiplex ligation probe-dependent amplification at this locus.
A major factor in achieving this high detection level was establishing a framework for scoring UCV. Building on experience gained in analysis of the BRCA1 and 2 genes,22,25 we used a combination of scoring the potential detrimental effect of the change with contextual information about the variant. Although it would be ideal to test the functional significance of UCV, this is impractical for large, complex proteins such as PC1 and PC2 in a routine diagnostic setting (and at least for PC1, no such functional test is yet available). However, data obtained in the research setting—for instance, channel activity of a PC2 mutant,37 or effect on GPS cleavage of a PC1 mutant,38—may be useful to include in calculations of likely pathogenicity.
The value of an ADPKD molecular test depends on the reliability to which the pathogenicity of UCV can be determined. Factors that were found critical were to include distant related vertebrates (chicken, frog, and fish) in the comparative analysis and to analyze conservation in domain structures. There is scope to improve these predictions as more three-dimensional structures become available.24 Contextual information was gained by complete analysis of both genes; when a UCV was the only variant, it was a strong candidate to be pathogenic. No patient was found in this study with two definitely pathogenic mutations. One previous example has been described of a PKD1 patient with two nonsense mutations in cis17 (either occurring simultaneously or a second mutation on an already mutant allele), and rare similar examples have been described in other diseases. However, because these cases are rare, the finding of a UCV in a patient with a definite mutation is highly suggestive that the change is not pathogenic. Data regarding the contextual finding of variants are enhanced by accumulated knowledge on disease-associated and neutral variants being collected in ADPKD databases (HGMD and ADPKD Mutation Database).
The high level of novel variants limits the number of cases in which previous data are useful, but additional information can be obtained by segregation analysis (lack of segregation proves that it is not pathogenic). In this study population, segregation analysis was limited by the family samples that were available, although segregation of 20 UCV was demonstrated (Table II). Furthermore, segregation was crucial for showing that some PKD1 changes (R2477C and 2894delANS) were not pathogenic (Figure 2A and Table IV). Some variants were classed indeterminate, with a possibility that they may be pathogenic; segregation analysis would be helpful to define their status, especially in families with more than one such variant. When possible, the family should be the unit of analysis for molecular diagnostics in ADPKD.
From this study, approximately 11% of cases had no probable mutation defined. Further analysis is needed to screen for larger DNA rearrangements (see Discussion). Studies of other large, multi-exon genes have illustrated how exonic and intronic variants can have unpredicted consequences on splicing by influencing the normal splice junction or branch point or by creating a cryptic site39; our RT-PCR data have illustrated some examples in ADPKD. A category of changes that have not been analyzed in this study are those that alter splice enhancer and silencing sites.40 These are difficult to predict because the consensus sequences are short and not highly conserved41; RT-PCR analysis in patients in whom no mutation has been defined is likely to be productive and may also identify mutations that are embedded deep within introns that can influence splicing.42 Other possible sites of missed mutations are the promoter regions.43 Once this next level of mutation analysis has been completed, it will be possible to assess the representation of unlinked "PKD3" families in this cohort. The level of such families is likely to be low (certainly <10%), but they cannot be excluded altogether at this stage.
Recurrent mutations account for 30% of the families and have diagnostic implications because prescreening regions that contain these changes may simplify molecular diagnostics; ultimately, a focused approach that uses a DNA array may be productive. The most common mutation, 5014delAG (also the most commonly described in the literature; Table I), is not flanked by sequences that are likely to promote recurrent deletion and raises the possibility that it is an ancestral change. Haplotype analysis would be helpful to determine whether a common origin is likely. Of the other five mutations found at least three times in this study, three have been described elsewhere (see Table I for details) and two represent C→T (or A→G) changes at CpG dinucleotides (PKD1:E2771K and PKD2:R872X), suggesting that they may be recurrent.44 Others may be population specific; all three 3814delG cases were identified at the same center and may reflect unknown relatedness. The finding of some missense changes multiple times, notably E2771K (seven times in total), giving it a high VS, and to a lesser extent G381S (three times), suggests that a group of missense changes with almost certain pathogenicity will be defined over time.
Our studies have important implications for molecular diagnostics of ADPKD. Sequencing is the most reliable means to identify base-pair variants, but screens for larger changes have revealed mutations in a few additional cases. Definite truncating mutations can be determined in 60 to 65% of cases, and careful evaluation of UCV in the remainder can push the level of detection of probable mutations to approximately 90%. It is particularly important that the pathogenic potential of all UCV be assessed and explained in a mutation report so that the likely significance of the described variants can be judged. Although using the mutation information on the majority of patients with definite mutations in the clinical arena should be straightforward, caution is still required when using information from MG = B or C patients in the setting of transplantation decisions or starting therapy. ADPKD mutation databases will be a guide for those previously described UCV, but many novel changes can be expected so that analysis of a family, especially if large enough to determine the gene responsible, will allow the use of more nondefinite mutations in the clinic. It is likely that improved mutation screening will become an increasingly important part of obtaining a firm diagnosis in the patient with ADPKD.
The CRISP study cohort consists of 239 patients who have ADPKD, are aged 15 to 46 yr, and have a GFR of >70 ml/mm at enrollment.15,16 For each proband, a blood sample was obtained for DNA extraction, and Epstein Barr virus (EBV)-transformed lymphoblast cell lines were established. Samples are stored at the National Institute of Diabetes and Digestive and Kidney Disease Center for Genetic Studies.
DS was performed on a fee-for-service basis using a commercial diagnostic test (Athena Diagnostics, Worcester, MA), and a subset were analyzed at Emory for PKD2. This sequence data are now stored at the CRISP web site.
All likely pathogenic changes were double-checked in a different aliquot of the same sample, and, when samples were available, the segregation of variants was tested by DS. A subset of samples were also analyzed for large genomic rearrangements using FIGE, as described previously.1 The precise mutation in these cases was determined by amplifying across the deletion and sequencing the aberrant product. The designation of all variants in both genes was numbered from their translational start. The PKD1 sequence also included the alternatively spliced codon at the start of exon 32 so that the total length of the protein was 4303 aa.
RNA was isolated from lymphoblast cell lines using TRizol (Invitrogen, Carlsbad, CA), and cDNA was generated with the Superscript III cDNA synthesis kit (Invitrogen). For the IVS15 variants, LR-RT-PCR was performed with the SPEC-4 primers,18 followed by nested PCR with primers in exons 15 and 18. The IVS37 mutation was analyzed with primers in exons 36 and 39, and the PKD2 IVS4 mutation was analyzed with primers in exons 3, 7, and IVS4 (primer sequences available on request). All PCR products were sequenced by standard methods.
The GMS20 was used to determine the GD of each substitution. An MSA was generated using the software ClustalW (MacVector Inc, Cary, NC) of PC1 orthologs from human, rat, mouse, chicken, frog (Xenopus tropicalis), and fish (Fugu rubripes). Other fish species, Tetraodon nigroviridis and Danio rerio, were also used in some cases. For PC2, human, dog, mouse, chicken, Danio, and Fugu were used, plus in some cases Drosophila melanogaster, sea urchin, and Caenorhabditis elegans. Sequences were obtained from NCBI or Ensembl. Predicted sequences for chicken, frog, and fish species were edited as necessary. The GV was determined as the largest GMS between vertebrate orthologs. Conservation within defined motifs used published MSA: WSC46; PKD repeat2,3,47; REJ domain48; GPS38,46; PLAT domain49; and polycystin motifs, PC-A and B29; plus MSA of PC1 and PC2 homologs (PC1L1, PC1L2, PC1L3, PKDREJ, PC2L1, and PC2L2) and sea urchin REJ1 to 4 homologs. Changes within transmembrane regions and the G-protein binding region were also assessed for disruption of secondary structure. Predicted splicing changes were scored using the Splicing Predictor by Neural Network (http://www.fruitfly.org/seq_tools/splice.html).50 Details of previous descriptions of the UCV were obtained from the HGMD (http://www.hgmd-cf.ac.uk) and/or the ADPKD Mutation Database (http:/pkdb.mayo.edu).
For all of the UVC, a VS was calculated. A matrix comparing the GD and GV was used with the GMS divided into six groups (0, 1 to 35, 36 to 80, 81 to 130, 131 to 179, and >180) and scores from +8 (e.g., GD >131, GV <35) to −4 (e.g., GD <35, GV >81) given. An additional −4 was allotted when the substitution matched the residue in an ortholog. Conservation of the reside in a domain scored +2 to +4 (highly conserved to invariant) with −2 when substitution matched the residue in an ortholog. Splicing changes were scored from +20 when an abnormal splice product was demonstrated by RT-PCR to −5 when an intronic change was not predicted to alter splicing. Additional points were given when a variant segregated in siblings or a family (+2 to +4); failure to segregate = −20. Other descriptions of the change as a mutation added +2 per time described. If another likely mutation (groups A through C) or an indeterminate (I) change was found with the variant, −5 (A) to −1 (I) was subtracted; otherwise +2 was added. The sum of these scores gave the VS. VS ≥11 were classed very likely mutations (MG = B); 5 to 10 as likely mutations (MG = C); −4 to 4 as variants of indeterminate (I) pathogenicity; and ≤5 as neutral polymorphisms (P). The χ2 test was used to examine whether the mutation location in each gene was uniform.
The study was supported by National Institute of Diabetes and Digestive and Kidney Diseases cooperative agreements (DK56934, DK56956, DK56957, and DK56961), with additional support from an ancillary study for genetic analysis (DK56957-S1) and grant DK58816.
The study coordinators who collected samples are thanked: Jody Mahan, Beth Stafford, Lorna Stevens, Kristin Cornwell, Vickie Kubly, Diane Watkins, Sharon Langley, and Pam Trull. We also thank Mary Virginia Gaines for management support. Jim Calvet is thanked for discussions of specific mutations. John McAuliffe, William Seltzer, Lynne Leclair, and Mark Smith at Athena Diagnostics are thanked for assistance in the fee-for-service DS mutation analysis.


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text:
John Hodger Laurinaitis (* 31. Juli 1962 in Philadelphia, Pennsylvania) ist ein ehemaliger US-amerikanischer Wrestler, der zurzeit bei der WWE unter Vertrag steht.

Laurinaitis' Bruder Joseph war ebenfalls Wrestler und wurde unter seinem Ringnamen Road Warrior Animal, als Teil des Tag Teams Road Warriors, bekannt. Sein Neffe James spielte 2009 bis 2015 bei den St. Louis Rams in der NFL American Football.

Karriere

Aktives Wrestling
Laurinaitis begann seine Karriere in der National Wrestling Alliance, wo er 1986 unter dem Namen Johnny Ace debütierte. Ab 1988 trat er auch in Japan bei All Japan Pro Wrestling auf. Dort nahm er mit dem Wrestler Dan Spivey an der Real World Tag League teil. 1989 kehrte er in die USA zurück und trat fortan in der NWA World Championship Wrestling an. Dort bildete er mit dem späteren Shane Douglas das Tag Team The Dynamic Dudes. Mit diesem gewann Laurinaitis 1989 zwei Mal die NWA Florida Tag Team Championship. 1990 kehrte er wieder nach Japan zu AJPW zurück. 1990 und 1991 gewann Laurinaitis zusammen mit Kenta Kobashi zwei Mal die AJPW All Asia Tag Team Championship. 1993 trat er zweimal in der WCW auf, die zwischenzeitlich die NWA verlassen hatte.

Im Jahr 1996 gewann Laurinaitis zusammen mit Steve Williams die AJPW World Tag Team Championship. Von 1997 bis 1999 errang er den Titel drei weitere Male (zweimal mit Kenta Kobashi und einmal mit Mike Barton). Am 9. Juni 2000 beendete Laurinaitis seine aktive Karriere, kehrte 2004 jedoch für ein Match bei Ohio Valley Wrestling zurück.

Zeit nach dem aktiven Wrestling
Nachdem Laurinaitis 2000 seine aktive Karriere beendet hatte, wurde er noch im selben Jahr als Booker bei der WCW verpflichtet. Nach dem Ende der WCW im Jahr 2001 wurde Laurinaitis von der damaligen WWF übernommen. Dort wurde er jedoch nicht als Booker, sondern als Road Agent eingesetzt. 2004 trat er die Nachfolge von Jim Ross als Vizepräsident der Talent-Relations-Abteilung an und war bis Juni 2012 Leiter dieser Abteilung, ehe er diese Aufgaben an Paul Levesque abtreten musste.

Seit dem 17. Juli 2011, dem Money in the Bank-PPV der WWE, ist er regelmäßig im WWE-TV zu sehen. Dabei war er ab dem 10. Oktober 2011 Interim General Manager von RAW. Bei WrestleMania 28 am 1. April 2012 gewann ein von ihm aufgestelltes Team gegen eines des SmackDown-General Manager Theodore Long. Dadurch war er dauerhafter General Manager von RAW und SmackDown, ehe am 17. Juni 2012 bei der Großveranstaltung No Way Out Big Show ein Match gegen John Cena verlor und Laurinaitis daraufhin gemäß Storyline entlassen wurde.

Erfolge

Titel
 All Japan Pro Wrestling
 4 × AJPW World Tag Team Champion 2× mit Kenta Kobashi und je 1× mit Mike Barton und Steve Williams
 2 × All Asia Tag Team Champion mit Kenta Kobashi

 National Wrestling Alliance
 2 × NWA Florida Tag Team Champion mit The Terminator

Auszeichnungen
 Wrestling Observer
 Match Of The Year 1996 mit Steve Williams gegen Jun Akiyama und Mitsuharu Misawa

Weblinks

 WWE-Profil (englisch)
 WWE-Profil (deutsch)
 Profil bei Cagematch.de
 Profil bei Genickbruch.com

Einzelnachweise

Wrestler (Vereinigte Staaten)
US-Amerikaner
Geboren 1962
Mann
AJPW World Tag Team Champion

redpajama_set_name: RedPajamaWikipedia


text:
Translation: Trouw 25th May 2018
Trouw – 25th May 2018
De geslotenheid van Jehovah's Getuigen staat de aanpak van misbruik in de weg
The closed nature of Jehovah's Witnesses stands in the way of abuse
When the cesspool of sexual abuse in the Roman Catholic Church in the Netherlands finally opened in the spring of 2010, it was a matter of weeks: the Dutch bishops set up an external, independent committee to map out the abuse in the church. bring.
Now there is still a lot to be said about the approach to sexual abuse in the Roman Catholic Church, but the Dutch Jehovah's Witnesses can take an example to the urgency with which this committee of inquiry was set up.
After this newspaper reported last year, it has become clear that the sexual abuse within the Jehovah's and the way in which that community deals with it is a big and serious problem. At the victim organization that was established in the autumn, nearly three hundred people have reported themselves.
The Jehovah's use an internal legal system that they deem to be higher than the judicial system. This approach works traumatizing for victims, perpetrators get away with mild punishments or are kept out of the wind, according to the stories of abuse victims.
The pressure on the Jehovah's Witnesses to have an external commission investigate is considerable. But the Jehovahs do not care about that. We have already done enough to protect minors against abuse, so is the defense. That is very unsatisfactory, first and foremost for the victims, and it gives the impression of a cover-up.
Minister Dekker is investigating whether the obligation to declare for third parties should be extended in cases of sexual abuse, because the Jehovah's can not be forced to conduct an independent investigation. And because he finds it undesirable that sexual offenses are only dealt with internally by movements like the Jehovah's Witnesses. This could mean that organizations (all organizations, not just the Jehovah's Witnesses) are obliged to report it to the police if they know about child abuse.
That the minister is looking for ways to free the victims of sexual abuse from the Jehovah's Witnesses is obviously to be welcomed. But there are quite a few hooks and eyes on the extension of the declaration obligation. There are many organizations where combating and tackling abuse seems to be reasonably well organized.
Expansion of the declaration obligation could create new problems there and it will not be able to break open the closed world of the Jehovah's. It would be good if Dekker continues to increase the pressure on the Jehovah's Witnesses to institute research. Not that with such an investigation all the problems are from the world, but it can be a first important step to turn the inward-looking attitude for victims into such a difficult situation.
In the comments you read the opinion of the newspaper, expressed by members of the editors and senior editors, all comments can be found in this file.
Also read: Abuse is handled indoors
Trouw did a long time research into sexual abuse at Jehovah's Witnesses in the Netherlands. Interviews with victims and (former) members and internal documents show that cases are handled indoors and abuse is almost never done. Read all articles on this subject here.

redpajama_set_name: RedPajamaCommonCrawl


text:
James Hamilton, 2nd Marquess of Hamilton and 4th Earl of Arran KG PC (1589 – 2 March 1625), styled Lord Aven from 1599 to 1604, was a Scottish politician. He was the son of John Hamilton, 1st Marquess of Hamilton and Margaret Lyon.

Career
Hamilton inherited his father's titles and estates in 1604. King James granted him the property and lands of Arbroath Abbey, or  "Aberbrothwick", and on 5 May 1608 created him Lord Aberbrothwick. In 1609, Aberbrothwick inherited the earldom of Arran from his insane and childless uncle James Hamilton.

He moved to England with King James, and invested in the Somers Isles Company, an offshoot of the Virginia company, buying the shares of Lucy Harrington, Countess of Bedford. The Parish of Hamilton in the Somers Isles (alias Bermuda) is named for him. He was created Earl of Cambridge and Baron of Innerdale in the peerage of England on 16 June 1619. In 1621 he served as Lord High Commissioner to the Parliament of Scotland, the King's representative in the Parliament of Scotland.

Marriage and children

In 1603, he married Lady Ann Cunningham, a daughter of James Cunningham, 7th Earl of Glencairn and they had five children:
Lady Anne Hamilton, married Hugh Montgomerie, 7th Earl of Eglinton and had issue
Lady Margaret Hamilton, married John Lindsay, 17th Earl of Crawford, 1st Earl of Lindsay and had issue
Lady Mary Hamilton (died 1633), married James Douglas, 2nd Earl of Queensberry, no issue
James Hamilton, 1st Duke of Hamilton (1606–1649)
William Hamilton, 2nd Duke of Hamilton (1616–1651)

He also had an illegitimate daughter, Margaret (who married John Hamilton, 1st Lord Belhaven and Stenton and had issue) by Anne Stewart, a daughter of Walter Stewart, 1st Lord Blantyre.

Hamilton died on 2 March 1625 at Whitehall, London, from a fever and was buried in the family mausoleum at Hamilton, on 2 September of that year.

Ancestry

References

Biography

Hamilton, James Hamilton, 2nd Marquess of
Hamilton, James Hamilton, 2nd Marquess of
Hamilton, James Hamilton, 2nd Marquess of
17th-century Scottish peers
Hamilton, James Hamilton, 2nd Marquess of
Members of the Parliament of Scotland 1612
Members of the Convention of the Estates of Scotland 1617
Members of the Parliament of Scotland 1617
Members of the Parliament of Scotland 1621
James
Earls of Cambridge
James
Earls of Arran


text:
Washington to Redirect $200Mln in West Bank, Gaza Aid Funding to Other Projects
© AFP 2019 / ABBAS MOMANI
https://sputniknews.com/middleeast/201808241067455971-washington-redirect-gasa-funding/
WASHINGTON (Sputnik) - US President Donald Trump ordered the State Department to redirect $200 million in funding away from programs targeting the West Bank and Gaza, the Department said in a press release on Friday.
"At the direction of President Trump, we have undertaken a review of US assistance to the Palestinian Authority and in the West Bank and Gaza to ensure these funds are spent in accordance with U.S. national interests and provide value to the U.S. taxpayer," the release said.
Previously, US senators reportedly passed a bill which is paving the way for military aid to Israel that may exceed 3.8 billion dollars.
READ MORE: UN Urges Israel to Halt Plans to Demolish West Bank Bedouin Camp
Since late March, the tensions between the Israelis and the Palestinians near the Gaza border have been growing as the Palestinian protest campaign against Israel, dubbed the Great March of Return began. Over 160 Palestinians were killed in clashes since that time. Israel accuses Hamas of using the protests to covering attacks along the country's border with Gaza.
Netanyahu Had Secret Meeting With Egyptian President on Gaza Riots - Minister
Majority of Israelis Dissatisfied With Netanyahu Policy on Gaza - Poll
Israeli Jets Attack Over 140 Targets in Gaza, Israel Defense Forces Report
Gaza Militants Fire Scores of Rockets at Israel, IDF Reports
Third Palestinian Dies After Friday's Clashes With IDF - Gaza Health Ministry
Israel, United States, West Bank, Gaza Strip


text:
Ohio State rides Justin Fields' toughness, leadership to championship game
Steve Hummer, The Atlanta Journal-Constitution
FILE - Ohio State quarterback Justin Fields throws a pass against Indiana during the first half of an NCAA college football game in Columbus, Ohio, in this Saturday, Nov. 21, 2020, file photo. Fields threw a Sugar Bowl-record six touchdown passes and accumulated 385 yards passing in the third-ranked Buckeyes' 49-28 College Football Playoff semifinal victory over No. 2 Clemson.
Jay LaPrete
Immediately after Clemson's James Skalski speared Justin Fields on New Year's Day – we dress it up as "targeting" these days – Pablo Fields took a phone call.
A friend of the family, a doctor, was reaching out to Fields' father, bearing a scrap of cold comfort.
"She said he should be fine, the spleen is on the other side," Pablo recalled.
Plenty of other internal parts were still in play, though. Who knew for sure what damage had been done by the kind of hit that reaches through the flat screen and knocks the breath out of a viewer? What was later revealed, after Justin emerged from the sideline M.A.S.H. tent where pain goes to be numbed, was that between grimaces the Ohio State quarterback remained capable of something special. His first pass back, maybe his wobbliest ever, was for a touchdown. Others would be much prettier. Count that as one of his six touchdown passes in a 49-28 playoff semifinals victory over the Tigers.
Flipping the script from a season ago, the quarterback from Kennesaw prevailed this time over the quarterback from Cartersville (Clemson's Trevor Lawrence). In most gripping fashion.
"I'll never forget that night. ... He's just tough," Ohio State coach Ryan Day said Thursday.
But at the time:
"I was a linebacker (at Eastern Kentucky), and I've folded up some guys like that when they didn't have the rib protectors on. And Justin doesn't wear the biggest rib protector in the world. Seeing your kid flipping around out there like a fish out of water, you can't do anything but close your eyes and pray," Pablo said.
It seems as if this entire jury-rigged football season has been one long leadership course for Fields. That the Buckeyes have gone from not playing the season by Big Ten decree, to piecing together a half-dozen games between COVID-19 cancellations to Monday's College Football Playoff Championship game against Alabama speaks to just how he has crushed that required course.
If they can skirt the virus and make it to Monday's game, Fields' fitness will be the dominant question. How that hit still echoes through his rib cage will be key.
So, dad, will your boy be anywhere near functional in his likely last college game? "We'll see. We'll see," Pablo said.
"I'll be good on Monday night," Justin said Thursday. On this subject, they're all cagey around the Ohio State program.
Fields' old coach at Harrison High, Matt Dickman, expects his competitive nature to override all else. "He obviously made it through the last game. And barring any other things that occur during the week, I have no doubt he'll be out there on the field," Dickman said.
"He doesn't want to let anybody down. You always love coaching kids who are thinking about their teammates first instead of themselves," he added.
Maybe when Fields transferred from Georgia to Ohio State at the start of 2019, he initially held back a little. Leaving home, being such a high-profile transfer with such scant experience at Georgia, going to a locker room of strangers, it was only natural that he'd quietly study the new landscape.
But by the time the page turned to 2020, Fields was making it clear that he was in charge. Early, when the Buckeyes were picking their way through spring workouts during the first stages of the pandemic, offensive coordinator Kevin Wilson noticed one guy who seemed to be pushing all the others. "I just think (Fields) has doing a really good job of being a little bit more of what you think that quarterback's going to be as a strong leader," he said at the time.
At spring break, Fields came home to Kennesaw and never let up. He changed his diet, joining his father's plant-based approach. He worked out maniacally. Pablo could remember when Justin was in high school how he would load a bag of balls into his pickup in the morning to work on his throwing at Harrison before class. But now this offseason he began to wonder if his son wasn't throwing too much.
If there was anything left for a father to learn about his 21-year-old son, it was this: "He works," Pablo said. "You may know the glory, but you got to see the story. He works physically. He works mentally. He works on what he eats, how he carries himself. It's all a package. I didn't know he worked that hard."
Which made the Big Ten's announcement in August that it was scraping the season because of the coronavirus all the more soul-crushing for Fields. All that work lost in the maze of football bureaucracy.
He couldn't understand the rush to cancel. Coming from the south and the SEC, he couldn't help but notice how that conference was pressing on.
Fields had two choices:
Accept the Big Ten's decision and quietly begin training for the NFL draft.
Or, step out front of a hash-tag movement – #WeWantToPlay – and advocate for the player's right to determine whether to play.
(A third choice, one posited by some Georgia fans after Fields was spotted taking in a Bulldogs scrimmage, was that he'd transfer back to Athens. It was never going to happen, his father said. He was just in town to visit his sister, Jaiden, a UGA student and softball player. He merely was a football player who wanted to see a little football, dad said.)
Fields chose the second option. He took to social media with a call to give this season a chance. He started an online petition for the Big Ten to reconsider that drew more than 300,000 signatures.
He now was an official face of the game, who along with Lawrence spoke for the players' desire to play. While it's debatable exactly how much influence any player – even the most noted – wields in college football, Fields efforts didn't go unnoticed by his teammates.
"He's grown a lot," said Ohio State running back Trey Sermon, who played his high school football at Marietta's Sprayberry. "He took on that role and he spoke out, and he was trying to do whatever he could just to make sure we had the opportunity to play. That just shows what type of guy he is."
Of course, then came the obligation of backing up his position of leadership with performances to match. On that score, it's worth nothing that Fields' thus-far signature game as a Buckeye in the national semifinal came just two weeks after his worst one. Against Northwestern in the Big Ten Championship game, he passed for just 114 yards, completing just 12 of 27 passes while throwing a pair of interceptions. Hardly the stuff of a player expected to be taken in the first handful of picks during the next NFL draft.
"I think that again shows his competitiveness," Day said. "You started to hear some rumblings about the fact that he didn't play very well (against Northwestern), and I know that bothered him. It took a couple days to recover from."
Now having vented his undamaged spleen at Clemson, there remains one more collegiate challenge, the biggest one out there, in Alabama. Time to show the Crimson Tide he's a little bit more than the guy they last saw, when the Bulldogs ran him in during a disastrous fourth-and-11 fake-punt attempt in the 2018 SEC Championship game. ("All I remember is I went in for the punt and everyone was yelling my name, and the punt didn't go the way we wanted to," he said Thursday when asked about it by an Alabama-based writer.)
Mindful of any SEC trademark infringement here, but can there be any doubt that from where Fields has come this season, being here just means more?
"At one point, you're standing on the tiptoes of anticipation about this season and your legs get cut out from under you. No season. No football," Pablo said. "To get to this point, it's great."
"It's definitely more meaningful because this is where we wanted to be before the season even started and when the season got canceled," Justin said. "All the stuff we've done in the past – all the workouts, getting the games canceled, saying we're not playing, saying we're playing that messes with your mental. All the stuff this team has been through, the big sacrifices, have been for this moment."
Ldcjd
Alabama wins college football title. Are you surprised? Get a recap
Top-ranked Alabama beat No. 3 Ohio State 52-24 to win its sixth national championship under coach Nick Saban. Here are the highlights in photos.
Despite all the hurdles, CFP title game has arrived with No. 1 Alabama taking on No. 3 OSU in Miami
There was a point in August where having a season appeared to be greatly at risk, let alone reaching the College Football Playoff national championship game.
Chip Scoggins: 'It's time': College Football Playoff should expand to 8-team field
College football will crown a new national champion Monday night, as the strangest and most tenuous season on record ended in a familiar place.
DeVonta Smith caps his Heisman season by leading Alabama to yet another national title
DeVonta Smith ran into the end zone at Hard Rock Stadium untouched — again — and pointed his right index finger toward the sky.
Shannon Ryan: A complicated college football season — filled with exasperation and exhilaration — is over. Was it all worth it?
The most pressing questions heading into the 2020 college football season was whether the season would start at all and, if it did, would it be able to finish.
Mac Engel: Why Texas' hiring of Steve Sarkisian should depress every minority coaching candidate
Few people in college athletics believe in a second, third, fourth or 9,999th chance more than Texas athletic director Chris Del Conte, and the one he granted Steve Sarkisian will be the chance that defines his tenure in Austin.
Paul Sullivan: A college football bowl season like no other includes the usual suspects in the playoffs and the Rose Bowl in ... Texas?
The Big Four made it to the Final Four of the college football season, as expected, ending one chapter of the most contentious, controversial and unpredictable years in the history of the sport. The College Football Playoff selection committee avoided chaos Sunday, pitting No. 1 Alabama against No. 4 Notre Dame in one semifinal game and No. 2 Clemson vs. No. 3 Ohio State in the other. The ...


24/10/2016 · Read a free sample or buy 2017 NFHS Baseball Rules Book by NFHS. You can read this book with Apple Books on your iPhone, iPad, iPod touch, or Mac. You can read this book with Apple Books on your iPhone, iPad, iPod touch, or Mac.


text:
Sonic Youth Gossip > Non-Sonic Sounds
louder's hip-hop café VI
Page 3 of 52 < 1 2 3 4 5 6 13 > »
01.11.2017, 11:33 AM #41
invito al cielo
^^ THAT SAID... There's nothing on A Seat at the Table that comes close to the perfection of "All Night," which is without question Lemonade's highlight (as I've been saying since the album came out.) "All Night" is a tremendous, powerful, soulful pop song with a timeless quality to it that transcends trends and topical references. It's almost like a "Let it Be," or a "You Can't Always Get What You Want" in that sense.
It's classy, it's happy, it's sad, there's a universality to it that isn't present on most of Lemonade's songs. It throws back to Motwown, to Phil Spectre, to Tina Turner, to fucking Outkast for christ's sake! It's the most perfect pop song of 2016. Funny (and infuriating) that out of all the tracks on the album, it has probably received the least attention.
I don't think I've read any reviews of Lemonade that even mention "All Night" specifically, except to note how the album ends on a reconciliatory note. Meanwhile, "Hold Up" and "Formation" and "Freedom" are fucking everywhere. That's sad, and it kinda posses me off. I feel like you'd be an idiot not to think "All Night" was the high point of Lemonade, and yet the rest of the world barely seems to have noticed the song even exists.
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AAAAAnyway. I'm not pissed that Lemonade got more attention than A Seat... Solange was selected as NPR's album of the year, and was at or near the top of pretty much every list, right next to her sister. They're very different albums, but I'm not attached enough to either of them to be mad about which one gets more attention.
Ultimately, both records are really just timepieces for modern R&B production and songwriting teams. Neither Beyoncé nor Solange was the primary artistic force behind their respective albums. They were just the face, the voice, and provided inspiration for the storytellers. When it comes to music like that, music that is so removed or detached from the "artist," I can only get so attached. Here's nothing wrong with letting other people produce, record, engineer and mostly write your songs... but it results in a less personal form of music. I would hesitate to attribute any of ASATT's observations directly to Solange Knowles, and it's not super appropriate to treat her as the source of the intellectual properties of the music. To say "Solange made a protest album" is only partially accurate. In truth, Solange participated in the creation of a "protest" product, which she put her name on.
Sorry to be that guy, but there is a certain part of the artistic puzzle that is missing from BOTH releases. This is not John Lennon sitting at a piano writing "Imagine" here. It's something much different. I'm not saying that what it is is BAD... as long as the music sounds good to you/me/us, who cares, right? But I will say that its missing a layer of from-the-gut, personal artistic expression.
01.11.2017, 01:40 PM #43
Originally Posted by noisereductions
Black Star is fantastic. So is Black On Both Sides.
Honestly, so is The Ecstatic. That was a major turnaround after The New Danger and True Magic. I barely remember those albums really, but I feel the urge to hear Ecstatic fairly regularly. I never put that one on the shelf like I did with Black Star and BOBS.
If I remember correctly it was, like, my #3 Album of '09? No present access to my list archives (lol) but I'm fairly sure it was too 5.
Fuckin' "Auditorium" y'all!
noisereductions
people hated The New Danger and True Magic, but I seriously listened to the heck out of those albums. I mean - kind of gimmicky. TND was like his "rock" album. (Basically what Weezy did w/ Rebirth) And TM was basically just a major label mixtape. But I dare say I loved them both at the time, and at least still like them a lot. They were kind of ballsy moves at the time. Even if they weren't classics.
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Also, fucking "Priority."
I bought and played both of them to death too. Honestly, I thought the New Danger was good at the time. True Magic I don't remember much, but I would not have played it if I didn't like it.
It was kind of weird though that these two albums were distributed so heavily. At the time you had to go to a well-stocked Best Buy AT LEAST to find Black Star or BOBS, but there were copies of TNG and TM at, like, Fred Meyer and shit. I thoight that was odd. Anyway, I haven't listened to either album in forever, but I doubt they deserve the bad rap they generally received.
TheDom
expwy. to yr skull
Location: Nashville.
Re: Black Star - that album is a fucking masterpiece and it's a shame they didn't do more albums like that. The beats and their flows compliment each other so perfectly. Verse after verse I'm always like "there'a no way the other one can follow that" but they always do. They were hungry as fuck. Thieves in the Night is my favorite track by far. Every time it's on I have no choice but to sit and listen to what they have to say.
Re: Beyoncé and Solange - I was in love with Lemonade at first but it didn't hold up (lol) for me. I watched the video once and haven't thought about it since. There are a batch of songs (The country one, the one with The Weeknd, the jack white song, sorry I'm bad with names) that I can't get all the way through any more. I agree with whoever said the anger was "theatrical" and honestly it's a little hard to take seriously sometime.
Another difference between the two is I feel Solange's album comes straight from her. It sounds like she's singing to you and not at you like a lot of Lemonade. When I hear Lemonade I hear a great pop record but it's not coming from a singular voice. It really does sound like an album a lot of people worked on, which of course it is, and it leaves me feeling like I'm being tRicked in a way (I'm not sure if that makes any sense i hope y'all can see where I'm getting at). Solange's album sounds a lot more honest to me, like I'm hearing someone creating music from their heart and telling the truth. I think a look at songwriting credits for the Solange record proves that. Also her performance on SNL was the shit.
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pepper_green
Anthony Fantano reviewed Trout Mask Replica! couldn't tell if he liked or loved it. somewhere inbetween. don't no why im posting this. maybe because he reviews a lot of modern hip hop and then he throws something like this in the mix. what a great way to turn ignorant people on to the Captain. TMR is one of the best albums ever. of fucking course. Safe as Milk and Lick is close behind.
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still absorbing Black Star. like it but hasn't quite soaked in. it's classic material no doubt. very 90's very Nas like.
Originally Posted by pepper_green
Glad you're enjoying it.
I thought I recommended this to you years ago, when you were using a different username. It's weird, but all along I was sure you knew of and liked this record. Kind of a trip to learn I was mistaken.
oh yea dawg. it grooves and bangs like a classic. should have came across that I was still absorbing the lyrics. the hooks and catchiness gets me first then i play catch up with the rhymes. but, yea enjoying it.
Yeah, catchy as hell.
"One, two, three! Mos Def and Talib Kweli! Black star shine eternally! Best alliance in hip-hop, right ooooon"
http://www.complex.com/music/2017/01/kendrick-lamar-kanye-west-so-appalled-throwback-video-freestyle
New Lupe Fiasco album, DROGAS Light coming out Feb. 10.
It's Lupe, so I will buy. Loved Tetsuo & Youth. Here's hoping it doesn't suck.
Rob Instigator
Location: In the land of the Instigator
RXTT's Intellectual Journey - my new blog where I talk about all the books I read.
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Originally Posted by Severian
He did a freestyle over "Monster" too. Kendrick really loved this album I guess. Can't blame him.
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Anderson .Paak announced an album of his band (The Free Nationals) in 2017. I guess it's gonna be an "Anderson .Paak & the Free Nationals" project, in the same vein as "Bob Marley & the Wailers" and "Prince & the Revolution". Excited.
He's gonna be featured on Flying Lotus' upcoming album too. And him and Pharrell said they're planning to get in the studio together. This year is gonna be huge for the dude, happy for him.
New Sampha and Syd (of The Internet) albums in February 3rd. And Big Sean is dropping the same day too.
Listen to Syd's dope lead single: https://www.youtube.com/watch?v=ZNIOrsxsa0A
Syd wrote and produced Fin, which also features production from MeLo-X (who worked on Lemonade), Hit-Boy, Haze, Rahki, and the Internet's Steve Lacy (on "All About Me").
New SZA single is finally here too (listen on Apple Music),
Loved it. She seems to have progressed a lot since 'Z'.
13 > »


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text:
Katherine Faith Macky ( — ), également connue sous le nom de Willow Macky, est une auteur-compositeur néo-zélandaise. Elle a souvent collaboré avec Dorothea Franchi.

Lors des  de 2006 Macky a reçu la  pour services rendus à la communauté.

Notes et références

Auteur-compositeur néo-zélandais
Naissance en juin 1921
Naissance en Nouvelle-Zélande
Décès en décembre 2006
Décès à 85 ans


text:
"Wayne D. Overholser is one of the greatest western novelists in American history. Every one of his books were researched for historical accuracy and realism. His books are a treasure." ~ Dick Symonds
Spur Awards
Wayne's Books
Stephen Overholser
Partial List of Wayne's Books
Buckaroo's Code (1947)
West of the Rimrock (1949)
Draw or Drag (1950)
The Snake Stomper (1951) writing as Joseph Wayne
Law Man (1953) writing as Lee Leighton[1]
Steel to the South (1953)
The Violent Land (1954)
Fabulous Gunman (1954)
The Nester (1954) writing as John S. Daniels
Beyond the Pass (1956) writing as Lee Leighton
The Lone Deputy (1960)
The Killer Marshal (1961)
Standoff at the River (1961)
War in Sandoval County (1961)
The Bitter Night (1962)
The Judas Gun (1962)
The Trial of Billy Peale (1963)
A Gun for Johnny Deere (1964)
To the Far Mountains (1964)
Day of Judgement (1965) aka Colorado Incident
Big Ugly (1966) writing as Lee Leighton
Ride Into Danger (1967)
Summer of the Sioux (1967)
Hanging at Pulpit Rock (1967) writing as Lee Leighton
North to Deadwood (1968) published in German as Dakota Jones (1969)
The Meeker Massacre (1969) writing as Lewis B Patten
You'll never hang me (1971) writing as Lee Leighton
The Noose (1972)
The Long Trail North (1973)
Brand 99 (1974)
Diablo Ghost (1978)
The Trouble Kid (1978)
The Cattle Queen Feud (1979)
Cassidy (1980) writing as Lee Leighton
Sun on the Wall (1981)
Mason County War (1981)
Dangerous Patrol (1982)
The Long Wind (1986)
Bunch Grass (1986)
Gunplay Valley: The Sweet And Bitter Land (1987)
Return of the Kid (1987)
By Gun and Spur (1987)
Red Snow (1988)
The Dry Gulcher (1988)
Gunlock (1988)
Red Is the Valley (1988)
Land of Promises (1989)Proud Journey (1989)
Valley of Guns (1991)
Cast a Long Shadow (1991)
Desperate Man (1992)
Hearn's Valley (1992)
Tough Hand (1992)
The Hunted (1994)
The Patriarch of Gunsight Flat (1996)
They Hanged Wild Bill Murphy (1996)
Nightmare in Broken Bow (1997)
Nugget City (1997)
War Party (1997) writing as John S. Daniels
The Violent Men (1997)
Riders of the Sundowns (1997)
Buckskin Man (1998)
The Petticoat Brigade (1998)
Oregon Trunk (1998)
Chumley's Gold (1999)
Ride the Red Trail (2000)
Tales of the West (2000)
Gunflame (2000)
The Outlaws (2000)
Gateway House (2001)
Revenge in Crow City (2001)
Rainbow Rider (2001)
The Day the Killers Came (2002)
The Three Sons of Adam Jones (2003)
The Bad Man (2003)
Wild Horse River (2003)
The Law at Miles City (2004)
Bitter Wind (2006)
Fight for the Valley (2007) writing as Lee Leighton
Tomahawk (2009) writing as Lee Leighton
Pass Creek Valley (2009)
Shadow on the Land (2009)
Law at Angel's Landing (2010)
The Man from Yesterday (2010)
Death of a Cattle King (2011)
Ten Mile Valley (2012)
The Waiting Gun (2013)
Swampland Empire (2013)
The Best Western Stories of Wayne D. Overholser (1984) aka The Best Western Stories
Overholser was also referred to in Stephen King's "Wolves of the Calla" in the Dark Tower Series. Not only was he referred to as a writer but Overholser was also the name of a character in the town of Calla Bryn Sturgis (a town in "Wolves of the Calla).
© 2013-14, WDO Enterprises


These are some of the tough but critical questions we've been asked over the years regarding purchasing point of sale systems. Request this FREE publication and be better prepared to save thousands of dollars when making YOUR next point of sale system purchase.
Do you want to increase your sales? Control inventory shrinkage?
Improve relationships with your customers or patrons?
Then I urge you to pick up the phone right now, dial 1 (800) 896-4022 and talk to us about helping you acquire a profitable Point-Of-Sale (POS) solution for your business. Here's why.
Contrary to popular belief, a POS system is more than just "a cash register". A POS system is a major focal point in your business.
My friend, a cash register can only show your cash flow for the day. That's it. Nothing else. "I made [insert any number here] dollars in sales today." So what? This tells you NOTHING about the state of your business.
Excellent question. Let's review a few ways how a POS solution by P Hardy Technologies can help you financially, shall we?
A POS solution by P Hardy Technologies can provide insight into profit… instantly.
Why do you want this benefit? Well, do you want to stay in business? The only way you are going to know if you can afford to stay in business is if you know how profitable you are. Duh.
A POS system by P Hardy Technologies can provide [more accurate] insight into inventory.
Take the money you would have spent on counting inventory and go make a bank deposit.
Something tells me you prefer option B. This is what a POS solution by P Hardy Technologies allows you to do. It's all about dollars and cents, my friend. Dollars and cents.
A POS solution by P Hardy Technologies can help you improve customer relationships.
To operate a sustainable business, you don't want shoppers or window gazers, you want customers, patrons or who we sometimes refer to as preferred guests.
A POS solution by P Hardy Technologies will allow your employees to spend more time on the floor helping your preferred guests and less time behind the counter or standing around doing nothing. Your preferred guests will appreciate the discounts, gift cards and/or extra services you can provide to them for their loyalty and in return, you'll enjoy the new and recurring business (read: guaranteed revenue) you'll receive. When you know who your preferred guests are, what they're buying, and when, you can create effective marketing campaigns that target the right guests with the right incentives.
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Are you tired of trying to manage the IT side of your store or restaurant? Conerned about PCI? Worried about the last time you backed up your data? (You did back it up, right?) Is it 100% guaranteed to be reliable in the event of data loss or corruption? How do you know?
We can help! Check out our technical support and managed services section for more information.
Please contact us for store and restaurant relocation solutions.


text:
Q: Space is Worspace name is causing java.net.URISyntaxException I am working on a Selenium Project where the Workspace name I was using had a space because of which I was getting following error:
Exception in thread "main" java.lang.IllegalArgumentException: C:/Users/xyz/eclipse-workspace ValveAware/TestProject/src/test/resources/features/Administration/Export.feature is not valid. Try URI[:LINE]*
    at io.cucumber.core.model.FeatureWithLines.parse(FeatureWithLines.java:56)
    at cucumber.runtime.RuntimeOptions.parse(RuntimeOptions.java:189)
    at cucumber.runtime.RuntimeOptions.<init>(RuntimeOptions.java:107)
    at cucumber.runtime.RuntimeOptions.<init>(RuntimeOptions.java:100)
    at cucumber.runtime.RuntimeOptions.<init>(RuntimeOptions.java:96)
    at cucumber.runtime.Runtime$Builder.withArgs(Runtime.java:131)
    at cucumber.runtime.Runtime$Builder.withArgs(Runtime.java:127)
    at cucumber.api.cli.Main.run(Main.java:22)
    at cucumber.api.cli.Main.main(Main.java:8)
Caused by: java.lang.IllegalArgumentException: Illegal character in path at index 36: C:/Users/xyz/eclipse-workspace ValveAware/TestProject/src/test/resources/features/Administration/Export.feature
    at java.base/java.net.URI.create(URI.java:883)
    at io.cucumber.core.model.FeaturePath.parseProbableURI(FeaturePath.java:44)
    at io.cucumber.core.model.FeaturePath.parse(FeaturePath.java:37)
    at io.cucumber.core.model.FeatureWithLines.parseFeaturePath(FeatureWithLines.java:77)
    at io.cucumber.core.model.FeatureWithLines.parse(FeatureWithLines.java:53)
    ... 8 more
Caused by: java.net.URISyntaxException: Illegal character in path at index 36: C:/Users/xyz/eclipse-workspace ValveAware/TestProject/src/test/resources/features/Administration/Export.feature
    at java.base/java.net.URI$Parser.fail(URI.java:2915)
    at java.base/java.net.URI$Parser.checkChars(URI.java:3086)
    at java.base/java.net.URI$Parser.parseHierarchical(URI.java:3168)
    at java.base/java.net.URI$Parser.parse(URI.java:3116)
    at java.base/java.net.URI.<init>(URI.java:600)
    at java.base/java.net.URI.create(URI.java:881)
    ... 12 more

I changed the name of the workspace and removed the space. I checked the path of the file Export.feature and the space is not there. But when I execute this file, I am still getting the same error.
Runner File:
package valveAware.port.localhost.tests;

import cucumber.api.CucumberOptions;
import cucumber.api.testng.AbstractTestNGCucumberTests;

@CucumberOptions(
        features = { "src/test/resources/features/Administration/Export.feature" },
        monochrome = true,
        plugin = { "pretty","html:target/Destination" },
        glue = { "valveAware.port.localhost.tests" }
        )

public class ValveAwareRunnerTest extends AbstractTestNGCucumberTests{

}

A: I created a new workspace and imported the projects, then it worked

redpajama_set_name: RedPajamaStackExchange


HFT is pleased to announce the newest member of our family – Delta Lab. Guitar slayer Rude Jude Gold is now endorsed by Delta Lab. Check them out at your nearest Guitar Center!
You can see Jude at the NAMM Show 2011 with HOT FOR TEACHER this Friday night at midnight in Anaheim, CA.


text:
GET NEWS AND ARTICLES IN YOUR INBOXPrint
Home | Wire | How the Postal Service Loses So Much Money
How the Postal Service Loses So Much Money
Tags Monopoly and Competition
04/14/2018Justin Murray
Lately, when he isn't trying to blame China on America's competitiveness woes, President Donald Trump has become obsessed with the online retailer Amazon. While there's speculation that Trump is using the reins of government to carry out a personal grudge because Jeff Bezos, Amazon CEO, also owns The Washington Post, the more recent obsession is based on his belief that the United States Postal Service is subsidizing Amazon's activity. The claim is that, based on a cost-plus method of pricing, Amazon is being subsidized $1.47 per package delivered by the USPS as a last-mile carrier. With an estimated 608 million boxes shipped by the online retailer in 2017, Trump is implying that Amazon has shorted the postal service by $893 million. Considering the USPS lost $2.7 billion, this further implies that Amazon is a key reason why the USPS is struggling financially. Trump goes on to state that Amazon should fork over the entire $2.7 billion to cover the difference.
A key problem here is the assumption that businesses operate on a cost-plus basis. This kind of thinking is a result of how warped government operations are, which frequently engage in cost-plus kinds of contracts. Cost-plus contracts are where the government agrees to cover all the applicable costs of performing the work plus a guaranteed profit. These forms of contracts are relatively unusual in the private business sector, where bidding on price are the primary form of activity. Because of the nature of cost-plus, and how they will frequently go over-budget because there is little incentive to control costs of performance, companies generally don't engage in them. This means, in the world outside of tax-funded activity, the USPS has to compete with other package carriers like UPS and FedEx and doesn't have the luxury of guaranteeing itself a profit on every activity.
When it comes to the USPS, the organization has significant fixed costs. In business planning, prices are usually lower-bound by the variable cost of activity. Any revenues that are collected above and beyond the variable costs are able to contribute toward fixed expenses. This is referred to as the contribution margin. Because the fixed component exists whether the product or service is sold or not, companies will be pressured to lower prices until they reach this contribution margin is exhausted. Companies then hope to generate sufficient volume at this margin to cover the fixed expenses. If the choice is between no sale and a sale below an optimal price with some contribution margin, the organization will usually go with the lower than optimal price to at least slow the resource deterioration.
The reason the USPS is in trouble and is struggling to cover its estimated $29 billion in fixed costs is because of its status as a partial legal monopoly. From the own words of the USPS, Congress has granted, with criminal penalty, the USPS total monopoly over the delivery of letters, with some carve-out exceptions (such as urgent or free of charge). Like most monopolies, the USPS had little incentive to keep costs controlled. In 1999, the USPS even went so far as to shrug off the burgeoning Internet, e-mail in particular, as some fad and engaged in sorting facility expansions with the expectation that letter volume would continue to grow. Since peaking in 2001, the number of letters delivered by the USPS has since collapsed to nearly half as much in 2017. The USPS costs, however, continued to increase, from $62 billion in 2000 to $72.3 billion in 2017, despite the collapse of business volume. The USPS was only able to remain solvent by leveraging its monopoly status by driving up the price of stamps from $0.34 for a first class stamp in 1999 to $0.50 later this year. But even this is running into limitations as the decline in mail volume accelerates.
This monopoly, however, doesn't cover package delivery, putting the USPS in a strange position of having a legal monopoly on only part of its business. This creates the impression that the package business is subsidized by the letter business since the prices on the letter side aren't limited by a competitive force. This then creates the further impression that the expenses, which were never controlled because of the historical reliance on letter delivery, should be evenly applied to package delivery as well. Thus the assumption there is a subsidy at all when in reality the costs are grossly overinflated due to a lack of market discipline.
When a private business is threatened by decreased volume, they usually have to trim operations to adjust their size to meet the new market demands. The USPS, on the other hand, does not do this. The organization continues to operate on the assumption it must make daily deliveries, six days a week, to every address in the nation. Even the old rural excuse has become weakened as the nation becomes more urban (assuming it was ever justified to tax city residents to provide city amenities to those who elected to live in remote places). Not that rural residents need a monopoly organization to deliver junk mail.
Repeal the Postal Service's Monopoly
So what's the answer to the failings of the USPS? Repeal the Private Express Statutes and let the USPS loose to manage its own affairs without Congressional interference in its operations. As Lysander Spooner famously proved back in 1844 with the American Letter Mail Company, the private sector can not only deliver the mail, it can deliver the mail profitably for a fraction of the cost of the postal service. This solves two problems:
The appearance that Amazon is subsidized through the USPS is eliminated
Profitable, stable delivery organizations can come into play
Repealing the private express statutes and getting government out of the mail delivery business may also very well save the USPS as not only can the USPS get out from under populist mandates, such as the overly generous retirement program and maintaining an absurd number of postal service locations; the USPS maintains over twice as many postal stops as McDonald's has restaurants. It will also open up the market to more competition and competition breeds superior operations for competing members as creative methods of operation are more likely to be identified and can be mimicked, leading to superior operations for all players.
In the end, the "problem" with Amazon is self-inflicted by the government insisting it operates a monopoly letter carrier. Trump can fix the problem with one fell swoop by pressuring Congress not to pass laws imposing higher rates on Amazon delivered packages, which will only accelerate the failure of the USPS since Amazon would just pick an alternate carrier, but to open up unrestricted competition in mail delivery and cut the USPS loose from the government tether. It certainly worked out well in New Zealand.
Justin Murray received his MBA in 2014 from the University of St. Gallen in Switzerland.
Note: The views expressed on Mises.org are not necessarily those of the Mises Institute.
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Justin Murray
Justin Murray received his MBA in 2014 from the University of St. Gallen in Switzerland....
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Per Bylund
Per Bylund is assistant professor of entrepreneurship & Records-Johnston Professor of Free Enterprise in the...


Over the past few years, several commercial vendors have started providing Personal Health Record (PHR) services. The PHR has been developed to be consumer-centric such that the consumer has all the control and not the health care provider. PHRs can be created, accessed and shared by a patient with authorized persons with the help of Health cloud based services provided by vendors like Microsoft HealthVault and Google Health. However, there is no formalized semantics that encourage users to share their data with prospective research facilities and drug companies. Creating an environment that allows users to manage how their personal health information is used will encourage them to share data that will improve the way healthcare is delivered due to the many advantages of secondary usage of data. This thesis presents a proof of concept with the implementation of an agent based framework that allows users to negotiate and trade medical data by the application of usage management of records and payment schemes.


Hematologic Neoplasms: Neoplasms located in the blood and blood-forming tissue (the bone marrow and lymphatic tissue). The commonest forms are the various types of LEUKEMIA, of LYMPHOMA, and of the progressive, life-threatening forms of the MYELODYSPLASTIC SYNDROMES.Leukemia: A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)Pancreatic Neoplasms: Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.


This is a wonderful time of year to bicycle out to Grimes Farm to see all the flowers in bloom in the patches of prairie surrounding the wetlands just east of the Nature Center. Here you'll find all sorts of goodies in bloom at the moment (early August)–from the spare little "Rattlesnake master" to the more showy stands of Purple Coneflowers, Prairie Clover, and Wild Bergamot. It's beautiful to look at, and it also shows what a really healthy stand of native Iowa prairie might have looked like to the Native Americans and the first settlers. A true native prairie is a complex ecosystem that we can only approximate in our modern plantings, but the richness of the flora and fauna certainly show something of the possibilities.
For more information, we might recommend a little booklet from Iowa State called "Introduction to Native Iowa Prairie Plants" (a free download if you just click the title). As the title suggests, this nicely illustrated document will give you a very good foundation in the plants and grasses that make up a native Iowa prairie.
One sad fact: the Queen Anne's Lace that many visitors to Grimes Farm find so attractive is not a native species, and, in fact, the USDA lists it as a "noxious weed" and treats it as an invasive species. This seems like harsh treatment for a plant whose other name is "wild carrot" and from which our domestic carrots have originated!


When we stepped off the bus at Camp our first year, we didn't know what to expect. When we stepped off the bus our second year, it felt like we were home. Camp Poyntelle has become our summer home where we feel safe, comfortable and welcomed. We've learned so many lessons here about competition and sportsmanship to Jewish values. Some how we're having so much fun while doing this is all happening. There is always so much to do at Camp, sports like baseball, soccer, flag football and tennis. There's drama, arts and crafts and best water park! Friday nights celebrating Shabbat as a whole Camp is one of the highlights of the week. Each day we get to pick electives too. This way you can focus on one area that you really like. Camp Poyntelle gives you the courage to try new things and be yourself. We both were actually in the play for the first time ever! We will never forget the memories made at Camp Poyntelle. The friends, the counselors.. the best summers ever!
Camp Poyntelle was incredible for me. It taught me leadership, how to be a better person, and gave me lifelong memories.


text:
Home News Kelsie Kimberlin Proves That Home Is Where The Heart Is With Her Latest Single "Cosmopolitan Girl."
Kelsie Kimberlin Proves That Home Is Where The Heart Is With Her Latest Single "Cosmopolitan Girl."
Posted By: Rick JammPosted date: September 07, 2022 in: NewsNo Comments
Following hot on the string of successes that solo artist Kelsie Kimberlin has created through her music over the past two years that has seen her songs/videos like "Lobotomy," "American Guns," "Right Place Wrong Time," "Masterpiece" and more, soar into hundreds of thousands/millions of clicks and views from around the world – it was perfectly fitting that her latest single "Cosmopolitan Girl" has her going global!
Set in the heart of cities all around the world, the Ukrainian-American singer/songwriter makes stops all over the map in her brand-new video for "Cosmopolitan Girl." Taking her music straight into the streets of Paris, New York, Kyiv, Seoul, Cairo, Tokyo, London, Shanghai, and Dubai – Kelsie goes international to unite the world through her latest single and prove that the concept of 'home' resides wherever we are.
With her intense love and respect for every culture, the unique diversity of different languages, her true passion for international travel, and undeniably visionary talent, Kelsie has combined her many interests and influences from far and wide to create a moment in time guaranteed to connect everyone together.
By visually revealing how our cultural differences create joy within us all, and how they are spectacularly special and to be celebrated by each & every one of us – "Cosmopolitan Girl" is a genuine reminder of all there is to learn from each other, and how our souls immensely benefit from the experiences we share.
Paired with a stunningly stylistic Pop song that echoes the spirit and inspiration for the music video within her words, Kelsie takes listeners on a vivid tour to all corners of the map through the irresistible hooks and relentless charm of "Cosmopolitan Girl."
Allowing listeners and viewers a once in a lifetime opportunity to see the world from her own perspective, and hear about the many pleasures of her travels as she makes her way around the globe – Kelsie takes the entire audience along with her for the ride in the ultimate trip of a lifetime.
By showcasing her own authentic interests and confident individuality, Kelsie becomes even closer to her worldwide fans than ever before, highlighting exactly how much we have in common. A humanitarian at her core, Kelsie is a world-citizen that has sincere love for everyone, everywhere.
By creating "Cosmopolitan Girl," she's able to give back to the many hearts and minds that have opened their doors to her all over the world by expanding the horizons of her legions of fans with a fully cross-cultural experience they'll never forget.
Available online worldwide this September 4th, 2022 – join Kelsie for the release of her brand-new single "Cosmopolitan Girl" this year as she continues to rise up the charts both locally and internationally with another extraordinary chapter of her story, and achievements as an artist. Excited as ever to share her latest song with every one of YOU listening in from around the globe – view the world from Kelsie's beautiful perspective, and help celebrate our uniqueness and diversity, together.
OFFICIAL LINKS: Homepage – Facebook – Instagram – Twitter – Spotify – Apple Music – YouTube – Soundcloud
Tags: Cosmopolitan GirlKelsie Kimberlinpopsinger songwriterUkrainian-American
Doug Cash – "Child Alone" tackles the epidemic of child abuse head on!
T-Ray Da Don brings his glossy Trapcentric sound to the table!