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Event Date: 13/06/2018
The HPRA hosted an information day on veterinary medicines on Wednesday 13th June 2018. The meeting took place in the Hilton Hotel Dublin Airport, so as to facilitate those travelling. The purpose of this information day was;
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This event was timely and important given the major developments taking place across the regulatory environment for veterinary medicines.
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6 Tips to Ease Back-to-School Anxiety
Anxious feelings triggered by transitions are normal and expected, but with one out of eight children presenting with an anxiety disorder, back-to-school anxiety can be even more problematic for some.
As a child psychologist, I hear about a wide range of anxious thinking among my patients: What if I don't have any friends in my class? I heard this grade is tough, what if I don't do well? If I don't do well, I won't get into a good college and then I won't get a good job. What if there will be class presentations or the teacher calls on me? What if I have no one to sit with at lunch? I can't go. I won't go.
School anxiety takes many forms. Students can experience increased irritability and sad moods. They can be more argumentative at home or clingy and fearful to separate from parents. Some anxious children experience somatic symptoms, including bellyaches and headaches, and more traditional panic symptoms like shaking, increased heart rate, shortness of breath and dizziness. Sleep disruptions are also common.
Even for children who are excited to return to school, there are a number of things that parents can do to help ease the transition.
Below are some ideas that many parents and children – from anxious to eager and all points in between – may find helpful.
- Be prepared and organized. A successful return to school begins well before the first bell rings. Gather school supplies. Talk about your child's school lunch preferences. Plan outfits. Review school and bus schedules. Also, consider taking advantage of opportunities to help your child become more familiar with the school's setting. Many schools offer private tours, open houses, and social events before the first day.
- Return to a back-to-school sleep schedule. It is recommended that you return to a school-appropriate bedtime schedule two weeks before returning to school. Adolescents in particular may need additional parent prompting so that they develop a healthy sleep schedule. The American Academy of Pediatrics reports that the average adolescent in the U.S. is chronically sleep-deprived and pathologically sleepy. Teens certainly have a variety of distractions competing for their attention in the evening hours and they may not fully understand how sleep impacts attention, school performance and emotional well-being. If your child is finding it difficult to fall asleep earlier, try unplugging from electronics. The blue light emitted from electronic devices has been shown to suppress the sleep hormone melatonin and subsequently delay sleeping. Create a consistent bedtime routine which includes calm, soothing activities (bath, reading, music) and avoid talking about emotionally-laden topics before bed.
- Validate your child's emotions. Encourage your child to express their thoughts and emotions. Use reflective statements — paraphrasing and mirroring your child's speech. This can help you and them understand what they are anxious about. It is important that parents listen empathetically and without judgment. Avoid asking leading questions or providing excessive reassurances.
- Engage in problem-solving approaches and prompt healthy coping. Help your child identify and label anxious thoughts. With repeated practice, your child can learn how to challenge and replace anxious thinking with more realistic and helpful thoughts. For example, consider the fact that when anxious, we often overestimate the likelihood that something bad is going to happen. Guide your child through a series of logical questions – e.g., how likely is this to happen, has this happened before, is there a more helpful way of thinking about this? With younger children, develop a list of calm and brave thoughts. Encourage your child to think of a brave character (like Poppy from Trolls) and how that character might handle tough situations.
- Avoid avoidance. It is natural to want to avoid anxiety-provoking situations. The problem is that when we avoid anxious situations, we contribute to a negative cycle of avoidance and strengthen anxious beliefs. Avoidance makes it increasingly difficult for your child to manage their anxiety in the future. It is important to encourage your child to tolerate anxiousness and face their fears in manageable steps. We know that anxiety can decrease with recurrent exposure to situations, so the school anxiety they feel in October is likely to be less intense than the nervousness they feel in the month of September.
- Seek professional guidance. Become familiar with school resources. Guidance counselors and school adjustment counselors offer a variety of support for children. Talk with your pediatrician or behavioral health clinician if your child is experiencing significant symptoms of anxiety and/or if your child is refusing to attend school. Early identification and intervention for school refusal behaviors is crucial because the longer your child avoids school, the more difficult reentry is. A behavioral health clinician can help you generate a school reentry plan and provide coping skills for your child's anxiety.
By taking some small steps now, you can make the transition back to school easier on an anxious child.
Learn more about mental health services for your child through Youth Health Connection.


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Intel iGPU (6xx series) crashesFixed drivers available!Instructions here
Engine and extra tuning for the Pessima.
uploaded an outdated file
What's new in this update:
Clean & smooth trunk
New licenseplate placement (EU and US):
New config - High Rev Hillclimb AWD:
Updated the configs to have the new parts.
This update adds 2 new configs;
High Rev Rally AWD:
High Rev Track AWD:
Adjusted the Custom Dual Exhaust 2. It now splits off right after the header/turbo.
Yes, it does clip through the transmission/engine, but who cares. No one is going to look down there anyway, right?
New thumbnails
Some engine value changes.
Hope you enjoy!
I forgot to add the new spoiler to the Sleeper AWD config..
This update adds a new spoiler and some lowered looking front and rear bumpers, both normal and widebody versions!
Sleeper AWD has the new spoiler and widebody lowered bumpers
Turbo AWD has the new normal lowered bumpers


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This drill works on defense contolling the puck while in transition and then having to adjust to a quick turnover turnover in the neutral zone.The drill starts when D1 skates up to center ice and calls for a pass from F1. F1 makes the pass to D2 and skates up to center ice and around the center ice circle looking for a pass back from D1. D1 should receive the pass skating backwards as in transition. D1 should control the puck and tranistion to forwards to create a good passing angle to F1. F1 receives the pass from D1 and goes in for a shot on net. Right when F1 receives the pass F2 takes on D1 in a one on one in the opposite direction.
$14 per month
Billed $14.00 every month


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Sex determination in fish is a labile character in evolutionary terms. The sex-determining (SD) master gene can differ even between closely related fish species. This group is an interesting model for studying the evolution of the SD region and the gonadal differentiation pathway. The turbot (Scophthalmus maximus) is a flatfish of great commercial value, where a strong sexual dimorphism exists for growth rate. Following a QTL and marker association approach in five families and a natural population, we identified the main SD region of turbot at the proximal end of linkage group (LG) 5, close to the SmaUSC-E30 marker. The refined map of this region suggested that this marker would be 2.6 cM and 1.4 Mb from the putative SD gene. This region appeared mostly undifferentiated between males and females, and no relevant recombination frequency differences were detected between sexes. Comparative genomics of LG5 marker sequences against five model species showed no similarity of this chromosome to the sex chromosomes of medaka, stickleback, and fugu, but suggested a similarity to a sex-associated QTL from Oreochromis spp. The segregation analysis of the closest markers to the SD region demonstrated a ZW/ZZ model of sex determination in turbot. A small proportion of families did not fit perfectly with this model, which suggests that other minor genetic and/or environmental factors are involved in sex determination in this species.
SEX ratio is a central demographic parameter directly related to the reproductive potential of individuals and populations (Penman and Piferrer 2008). The phenotypic sex depends on the processes of both sex determination and sex differentiation. Exogenous factors, such as temperature, hormones, or social behavior, can modify the gonad development pathway in fish (Baroiller and D'Cotta 2001; Piferrer and Guiguen 2008). Both genetic (GSD) and environmental sex determination has been reported in this group (Devlin and Nagahama 2002; Penman and Piferrer 2008), although primary sex determination is genetic in most species (Valenzuela et al. 2003). Among GSD, single, multiple, or polygenic sex-determining (SD) gene systems have been documented (Kallman 1984; Matsuda et al. 2002; Lee et al. 2004; Vandeputte et al. 2007).
Sex determination in fish can evolve very rapidly (Woram et al. 2003; Peichel et al. 2004; Ross et al. 2009). Different sex determination mechanisms have been reported between congeneric species and even between populations of the same species (Almeida-Toledo and Foresti 2001; Lee et al. 2004; Mank et al. 2006). The evolution of sex chromosomes involves the suppression of recombination between homologous chromosomes probably to maintain sex-related coadapted gene blocks (Charlesworth et al. 2005; Tripathi et al. 2009). The sex determination pathway appears to be less conserved than other developmental processes (Penman and Piferrer 2008). However, differences are more related to the top of the hierarchy in the developmental pathway, while downstream genes are more conserved (Wilkins 1995; Marín and Baker 1998). As a consequence, the SD master gene in fish can vary among related species (Kondo et al. 2003; Tanaka et al. 2007; Alfaqih et al. 2009). In this sense, fish represent an attractive model for studying the evolution of SD mechanisms and sex chromosomes (Peichel et al. 2004; Kikuchi et al. 2007).
A low proportion of fish species have demonstrated sex-associated chromosome heteromorphisms (Almeida-Toledo and Foresti 2001; Devlin and Nagahama 2002; Penman and Piferrer 2008). This is congruent with the rapid evolution of the SD region in fish, and thus in most species the male and female version of this chromosome region appears largely undifferentiated. In spite of this, indirect clues related to progenies of sex/chromosome-manipulated individuals or to segregation of morphologic/molecular sex-associated markers indicate that mechanisms of sex determination in fish are similar to other vertebrates (Penman and Piferrer 2008). With the arrival of genomics, large amounts of different genetic markers and genomic information are available for scanning genomes to look for their association with sex determination. Quantitative trait loci (QTL) (Cnaani et al. 2004; Peichel et al. 2004) or marker association (Felip et al. 2005; Chen et al. 2007) approaches have been used to identify the SD regions in some fish species. Also, microarrays constructed from gonadal ESTs have been applied to detect differentially expressed genes in the process of gonadal differentiation (Baron et al. 2005). Further, the increased genomic resources in model and aquaculture species have allowed the development of both comparative genomics (Woram et al. 2003; Kikuchi et al. 2007; Tripathi et al. 2009) and candidate gene (Shirak et al. 2006; Alfaqih et al. 2009) strategies to identify and characterize the SD region in fish. This has permitted the identification of the SD region in eight fish, including both model and aquaculture species (reviewed in Penman and Piferrer 2008).
The turbot is a highly appreciated European aquaculture species, whose harvest is expected to increase from the current 9000 tons to >15,000 tons in 2012 (S. Cabaleiro, personal communication). Females of this species reach commercial size 4–6 months before males do, explaining the interest of the industry in obtaining all-female populations. Although some differences between families can be observed in the production process at farms, sex ratio is usually balanced at ∼1:1. Neither mitotic nor meiotic chromosomes have shown sex-associated heteromorphisms in turbot (Bouza et al. 1994; Cuñado et al. 2001). The proportion of sexes observed in triploid and especially gynogenetic progenies moved Cal et al. (2006a,b) to suggest an XX/XY mechanism in turbot with some additional, either environmental or genetic, factor involved. However, Haffray et al. (2009) have recently claimed a ZZ/ZW mechanism on the basis of the analysis of a large number of progenies from steroid-treated parents. These authors also suggested some (albeit low) influence of temperature in distorting sex proportions after the larval period. Finally, hybridizations between brill (Scophthalmus rhombus) and turbot render monosex progenies, depending on the direction of the cross performed, which suggests different SD mechanisms in these congeneric species (Purdom and ThaCker 1980).
In this study, we used the turbot genetic map (Bouza et al. 2007, 2008; Martínez et al. 2008) to look for sex-associated QTL in this species. The identification of a major QTL in a specific linkage group (LG) in the five families analyzed prompted us to refine the genetic map at this LG and to perform a comparative genomics approach against model fish species for a precise location and characterization of the putative SD region. Also, sex-associated QTL markers were screened in a large natural population to provide additional support to our findings and to obtain population parameters at sex-related markers that could aid in interpreting the evolution of this genomic region.
Biological material
The five families used to search for sex-associated QTL (Qfam) and to evaluate the association of specific markers with sex (Afam) were obtained from the genetic breeding program of the Stolt Sea Farm SA (SSF), a specialized turbot company located in northwestern Spain. Families were obtained following a three-generation scheme starting from unrelated grandparents coming from natural populations of the Atlantic Ocean. Two families were used for QTL identification using a large number of markers: Qfam1 (the DF reference family in Bouza et al. 2007) constituted 85 individuals (49 females and 36 males) and Qfam2 constituted 38 individuals (20 females and 18 males). Three additional families were used to confirm the QTL detected in Qfamilies by checking the association of the closest QTL markers to sex: Afam1 (39 individuals: 28 females and 11 males), Afam2 (30 individuals: 17 females and 13 males), and Afam3 (73 individuals: 36 females and 37 males).
A total of 145 sexed breeders (50 females and 95 males) of the SSF broodstock were used to search for association of the closest QTL markers to sex at the population level. These breeders were collected in the Atlantic Ocean where very low or no significant genetic differentiation was previously reported in turbot (Bouza et al. 2002).
Sexing and DNA sampling:
Qfamilies and Afamilies were selected depending on the suitability of the crosses and the availability of sexing information in progenies, respectively. Qfamilies were sexed at 8 months of age (∼100 g and 18 cm) at Cluster de Acuicultura de Galicia facilities as soon as male and female gonads could be discriminated with confidence. Sex was recorded by examining gonad morphology after biopsy. Afamilies were constituted by 3-year-old fish, and sex could be determined by abdominal palpation at maturation time (an unambiguous procedure routinely practiced in turbot farms). A small piece of the caudal fin of each individual was cut and stored in absolute ethanol for DNA extraction.
Microsatellite genome scan:
A total of 98 homogeneously distributed microsatellite markers previously described (Bouza et al. 2007, 2008) were analyzed in Qfam2. Average distances between these markers are 18.4 and 13.8 cM according to the total and framework turbot genetic map lengths, respectively (supporting information, Table S1). This panel of markers is currently being used for identification of QTL related to productive traits in turbot. Qfam1 was one of the reference families for turbot mapping, and therefore 177 markers covering all LGs had been previously analyzed. Of these, 148 were anonymous (Bouza et al. 2007) and 29 were EST linked (Bouza et al. 2008). In this family, the 26 LGs reported in the turbot map were covered with at least 2 markers/LG and a mean of 6.5 markers/LG (Bouza et al. 2007). After QTL analysis, two additional microsatellite loci closely linked to the QTL detected were genotyped in Qfamilies to provide additional statistical support. Also, the 2–3 of the closest sex-associated QTL markers were analyzed in Afamilies and in the SSF broodstock to confirm QTL location and to look for association at the population level, respectively.
DNA was extracted from caudal fin clippings using standard phenol–chloroform protocols. Microsatellite PCR amplifications were carried out as previously reported (Pardo et al. 2006). Genotyping was conducted on an ABI 3730 DNA sequencer and analyzed using the Genemapper, version 3.7 software (Applied Biosystems, Foster City, CA). The complete cDNA sequence of the closest EST-linked microsatellite to the major sex-associated QTL was obtained following the ABI Prism BigDye Terminator v3.1 cycle sequencing kit protocol on an ABI 3730 DNA sequencer (Applied Biosystems).
Statistical procedures
QTL and sex-associated marker analysis:
QTL analyses were performed using the software GridQTL 1.3.2 (Seaton et al. 2006) that considers the linkage phase between markers according to pedigree information. As each family arose from a single couple with a known genotype, the chosen module was the sib pair. The trait considered was sex (coded as a binary character: females—0; males—1), and no other fixed factor or covariate was included in the model. A single QTL was assumed at each linkage group. The default-solving method in the Grid QTL software (Haseman-Elston) was applied. Genomewide and LG-wide significant thresholds (for those linkage groups with a LOD score >2) were estimated by implementing a bootstrapping method at P = 0.05 and 0.01, respectively. The number of iterations was set to 1000. The Pearson χ2 test was conducted to search for genotypic and allelic association between specific microsatellite markers and sex both in the families and in the SSF broodstock. Bonferroni correction was considered for multiple tests.
Genetic map refinement:
The turbot genetic map (Bouza et al. 2007, 2008; Martínez et al. 2008) was reanalyzed at LG5, where the main sex-associated QTL was located (see results). Previous mapping data in the reference haploid (HF) and diploid (DF = Qfam1) families (Bouza et al. 2007) were revised, and missing data were supplied. Also, segregation data from Qfam2 and Afamilies, and from the other four diploid F2 families currently used to look for QTL for tolerance to Aeromonas salmonicida, were used for map refinement at LG5. The order of adjacent triplets of markers was repeatedly tested using Joinmap 3.0 through an optimized algorithm to ensure marker order. The data files were screened for putative double recombinants, which were verified or corrected by reexamining genotypic data. A LOD threshold >3.0 and a recombination threshold <0.40 were used to obtain the framework map. The remaining markers were ordered by lowering the LOD threshold until they were included (in all cases the LOD was ≥2). Once the most likely order was obtained, genetic distances were estimated by applying the Kosambi mapping function (Kosambi 1944). The graphic maps were generated using MapChart 2.1 (Voorrips 2002). Genetic maps were constructed for each sex (averaging across the different families within sex), so recombination frequencies could be compared between male and female maps. A consensus LG5 map was constructed by using all segregation data with Joinmap 3.0 and by following the methodology previously reported (Bouza et al. 2007).
The position of the putative turbot sex-determining gene (SDg) was estimated by assuming that this was the only SD locus in the genome and that the trait showed full penetrance. For this, SDg genotypes of females and males were coded as heterozygotes and homozygotes, respectively, according to the ZW/ZZ model demonstrated in our study (see results). The mapping methodology outlined previously (Bouza et al. 2007) was applied.
The position of the centromere at LG5 was reanalyzed using previous data and new information obtained after genotyping 96 individuals of the reference diploid gynogenetic family (Martínez et al. 2008) with the closest informative centromere markers. Complete interference was used for estimating locus–centromere distances, and joint segregation analysis was applied to order the group of closely linked markers and the centromere (Thorgaard et al. 1983).
Comparative genomics of LG5:
BLAST/Autofact searches of the SmaUSC-E30 sequence were performed against public databases for gene annotation. Additionally, unique sequences of the turbot genomic clones containing the microsatellite loci at LG5 were compared by NCBI-BLAST against model fish genomes downloaded from ftp://ftp.ensembl.org: Tetraodon nigroviridis, Takifugu rubripes, Danio rerio, Oryzias latipes, and Gasterosteus aculeatus. Hits were considered significant using a threshold of E < 10−5 (Stemshorn et al. 2005).
Population analysis:
The SSF broodstock was split by sex for analyzing population parameters at microsatellite loci. These were estimated in the whole population and in the male and female subsamples. In addition to the sex-associated QTL microsatellites analyzed in this work, previous data on 11 mapped microsatellites in the same population (Castro et al. 2004) were reanalyzed by sex to complete a panel of 20 microsatellites. These 11 microsatellites are essentially unlinked, and only Smax-02 and Sma3-129INRA map in the same LG at 34.8 cM. Expected heterozygosity (He) and the mean number of alleles per locus (A) were computed to estimate genetic diversity. Departure from Hardy–Weinberg proportions (HW) was checked by exact tests. The magnitude and sign of deviations at each locus were estimated by FIS statistic. Genetic differentiation between male and female subsamples was estimated by using the relative coefficient of genetic differentiation (FST) and tested by using exact probability homogeneity tests. All these analyses were implemented using the default options of Genepop 3.1 (Raymond and Rousset 1995).
Sex-related QTL:
All 177 microsatellites analyzed in Qfam1 were informative because this family had been used for mapping (Bouza et al. 2007, 2008). Among the 98 microsatellites analyzed in Qfam2, 79 were informative. Four QTL were detected in Qfam1 (qSD1, qSD2, qSD3, and qSD4) and only one in Qfam2 (qSD1) after a first analysis with 177 and 79 markers, respectively. The associations were maintained in a second-round analysis after including 2 additional closely linked microsatellites at all LGs where QTL had been detected (Table 1; Figure 1). A major highly significant QTL (qSD1) was detected close to the SmaUSC-E30 microsatellite at LG5 in both families. The association, although highly significant in both cases, was much higher in Qfam1 (LOD = 1697.1; F = 7815.6) than in Qfam2 (LOD = 18.0; F = 83.0). The SmaUSC-E30 marker correctly sexed 96.5% and 84.2% of individuals in Qfam1 and Qfam2, respectively. Additionally, three suggestive QTL were detected in Qfam1 at LG6 (qSD2), LG8 (qSD3), and LG21 (qSD4), which were close to Sma-USC110, Sma-USC59, and Sma-USC231 microsatellite loci, respectively. Their association to sex was significant only within the LG-significant threshold, but nonsignificant after correction for multiple tests. No additional QTL other than qSD1 were detected at Qfam2.
Association of sex-related QTL markers in Afamilies:
Association of the four aforementioned QTL with sex was additionally checked in three families (Afam) using the two to three closest QTL-linked markers: SmaUSC-E30, Sma-USC270, and Sma-USC65 at qSD1; Sma-USC188 and Sma-USC110 at qSD2; Sma-USC194 and Sma-USC59 at qSD3; and Sma-USC117 and Sma-USC231 at qSD4. Association with qSD1 was detected in at least one of the tested markers in all families at both genotypic (g) [P(χ2)g = 0] and allelic (a) [P(χ2)a = 0] levels. This association was detected only with markers segregating in the mother (Table 2). Sma-USC270 in Qfam2 and Afam2 and Sma-USC65 in Afam1 and Afam3 did not show association with sex when segregation occurred only in the father. Markers showed significant association even at long distances from qSD1, such as Sma-USC225 in Qfam1 [35.8 cM; P(χ2)g = 0; P(χ2)a = 0]. Association probabilities were much low at all other sex-associated QTL from Qfam1, where only the closest markers were significant. No sex association was detected with the closest markers to qSD2, qSD3, and qSD4 in the other four families analyzed (Qfam2, Afam1, Afam2, and Afam3).
Refinement of LG5 genetic map:
The location of the putative SDg of turbot close to SmaUSC-E30 at LG5 moved us to refine the genetic map and to compare recombination frequencies between male and female genetic maps at this LG. The reanalysis of the mapping reference families (HF and DF; Bouza et al. 2007) and the increase of data from eight additional families (Qfam2, Afamilies, and four families used to identify QTL for tolerance to A. salmonicida) enabled us to obtain a more consistent order of markers at this LG (Figure 2). The number of framework markers increased from 8 to 11, but a much better definition was achieved especially at the extremes of this LG. The four closest markers to qSD1 (Sma-USC254, Sma-USC65, SmaUSC-E30, and Sma-USC270) are now framework markers. The length of this LG was reduced from 79.4 cM (Bouza et al. 2007) to 66.5 cM. Common pairs of segregating markers for comparison of recombination in male and female maps were available at four of the five closest markers to qSD1 (Sma-USC247, Sma-USC65, SmaUSC-E30, and Sma-USC270) in six families. No relevant recombination differences were detected between sexes. The only remarkable difference involved the SmaUSC-E30 and Sma-USC247 loci in Qfam2 (0.306 vs. 0.171 recombination frequency in female and male maps, respectively). Remarkably, the consensus map of Qfam2 suggested an inversion between the closest markers to SDg (Sma-USC270 and SmaUSC-E30).
A second goal within LG5 map refinement was to locate the positions of the putative SDg and the centromere. As shown in Table 2, the closest marker to SDg (SmaUSC-E30) appeared farther apart in Qfam2 (r = 15.8) than in the other four families (mean r = 1.7). The aforementioned inversion at Qfam2 could explain this observation. So to map SDg, we decided to exclude this family and to estimate the position of SDg using all informative markers of Qfam1 and the three Afamilies. For this, sex was considered a single-gene fully penetrant character, and SDg genotypes in females and males were coded as heterozygotes and homozygotes, respectively, according to the ZW/ZZ model demonstrated in this species. SDg was positioned at 32.2 cM from the centromere between SmaUSC-E30 and Sma-USC65 (Figure 2).
A more accurate location of centromere at LG5 was determined by analyzing a large sample (96 individuals) in the reference diploid gynogenetic family with the two closest informative markers to the centromere, Sma-USC270 and Sma-USC65 (Martínez et al. 2008). An accurate centromere position could aid both in interpreting recombination frequencies in terms of physical distances in its vicinity and in explaining previous sex ratios observed in turbot gynogenetic and triploid progenies (Cal et al. 2006a,b). In Figure 3, the joint segregation analysis for both markers and the two alternative centromere locations—I (Martínez et al. 2008) and II (present data) in Figure 3—is presented. Joint segregation evidenced the necessity of 25 double recombinants to explain the data under hypothesis I, while only 1 double recombinant would be necessary under hypothesis II.
Comparative genomics of LG5 microsatellites:
The closest sex-associated microsatellite (SmaUSC-E30) was obtained from a 389-bp EST from a turbot EST database related to immune tissues (Pardo et al. 2008). The closeness of this EST to the putative SD region recommended its complete sequencing and subsequent bioinformatic analysis for gene annotation and for comparative genomics with related fish species (updated GenBank accession no. FE946656). No significant hits (E-value <10−5) could be obtained either against public DNA, protein, and EST databases or against PROSITE (protein motifs) database.
BLASTn matches of 13 microsatellite sequences at LG5 against the Tetraodon nigroviridis (Tni), Takifugu rubripes (Tru), Gasterosteus aculeatus (Gac), Oryzias latipes (Ola), and Danio rerio (Dre) genomes revealed putative syntenic patterns with respect to these model fish species (Table 3). Matches appeared highly congruent because they involved the same microsatellites across different species following a decreasing homology from Gac to Dre. Nearly half of the turbot sequences compared showed significant homology against the Gac genome, four against the Tni and the Tru genomes (30%), two against the Ola genome (15%), and only one (8%) against the Dre genome. Significant matches (E < 10−5) were due to small, highly conserved sequences between 22 and 252 bp (average 94 bp) in length and with 83 to 100% sequence similarities. Most matches were at the 20-cM distal region of turbot LG5 and represented putative syntenies of specific chromosomes (Tni LG1, Ola LG4, and Gac LG8) or chromosome regions (Tru scaffold-25) of the species compared. Among the query sequences of the LG5 proximal region, only the closest marker to SDg (Sma-USCE30) showed significant homology. This was achieved against the Gac genome (51 pb; 92% identity).
Sex association of markers in the natural population:
The availability of a large sexed turbot population from the Atlantic Ocean allowed us to check the association of QTL markers with sex in a natural population and to estimate population parameters to analyze the evolution of the SD region. The existence of previous putatively neutral microsatellite data in the same sample (Castro et al. 2004) represented an appropriate material to be used as background for these analyses. Only 1 locus of 20 analyzed showed deviation from HW proportions after Bonferroni correction in the male (Sma3-129INRA) and female (Sma1-125INRA) subsamples and only 3 loci in the whole sample (Sma5-111INRA, Sma3-129INRA, and Sma-USC110) showed deviation (Table S2). Null alleles had been previously reported at the Sma3-129INRA locus after a detailed family analysis (Castro et al. 2004); this represents the most probable cause of positive deviations at this locus (FIS = 0.083 and 0.053 in the male subsample and the whole population, respectively). Accordingly, only 3 of 60 tests (5%) deviated from the null hypothesis of HW proportions.
SmaUSC-E30, the closest to SDg, was the only locus among the 20 analyzed that showed significant sex association at genotypic [P(χ2)g = 0.033] and allelic [P(χ2)a = 0.005] levels, although not after Bonferroni correction (Table S2). This locus also was among the least diverse (He = 0.663; number of alleles = 5; mean He and A for all loci = 0.771 and 11.4, respectively; Figure 4, top; Table S2) and showed a significantly larger genetic differentiation between female and male subsamples (FST = 0.0409, P = 0.008) than the remaining loci (mean FST = 0.0019, P = 0.427) (Figure 4, bottom). Another two close microsatellites to SDg (Sma-USC270 and Sma-USC65) were among the least variable loci (Figure 4, top).
The major SD region of turbot:
In our study, a single major sex-associated QTL (qSD1) was detected in turbot at the proximal end of LG5. The association was highly significant even at very long distances (35.8 cM), and the closest marker to this QTL (SmaUSC-E30) correctly classified 98.4% offspring in four of five families analyzed. Another three minor sex-associated QTL were suggested at LG6, LG8, and LG21 in our analysis, but only in a single family and with low statistical support. SmaUSC-E30 also showed significant association with sex in the panmictic natural turbot sample from the Atlantic Ocean. This was also the only locus where a significant differentiation between male and female subsamples was detected in this population. The FST value (4.1%) is close to that previously estimated among populations in the natural distribution of turbot, including the Atlantic Ocean and Mediterranean Sea areas (5–7%; Blanquer et al. 1992; Bouza et al. 1997). These observations support the close vicinity of the SmaUSC-E30 marker to the SDg in turbot, considering that the break in association between a pair of loci is directly related to the recombination frequency. Under a fully penetrant single-locus hypothesis, the turbot SDg was estimated to be 2.6 cM from the SmaUSC-E30 marker. This genetic distance would be even lower if other minor genetic and/or environmental factors were involved in turbot sex determination. This means that the SDg would be <1.4 Mb, considering the average relationship between physical and genetic distance in the turbot genome (0.53 Mb/cM; Bouza et al. 2007). In summary, our data strongly suggest that a major SDg is located at LG5 in turbot very close to the SmaUSC-E30 marker. Since this species has a simple ZW/ZZ sex-determination type (Haffray et al. 2009; this study), our data suggest that this gene is most likely the master SDg of turbot.
Insights on the turbot SD region from comparative genomics:
Syntenies among species represent the bridge to complementing the initial QTL experiments with candidate gene approaches from homologous chromosomal locations identified in related model organisms (Erickson et al. 2004). In agreement with phylogenetic data, the comparative mapping of the 13 mostly anonymous turbot sequences at LG5 against model fish genomes showed higher similarities with other Acantopterygians such as T. nigroviridis (Tni), T. rubripes (Tru), G. aculeatus (Gac), and O. latipes (Ola) than with D. rerio (Ostariophysi; Miya et al. 2003; Li et al. 2008). The highest homology was observed with Gac, where homologous markers covered most of the LG5 length and included SmaUSC-E30, the SDg closest marker. Our data suggest the synteny of the turbot LG5 distal interval with Ola LG4, Gac LG8, and Tni LG1. The lack of homology of turbot LG5 markers with the sex chromosomes of medaka (LG1; Matsuda et al. 2002), stickleback (LG19; Peichel et al. 2004), or fugu (scaffolds anchored to LG19; Kikuchi et al. 2007) suggests that the sex chromosome of turbot evolved independently from that of these three model species. Nevertheless, turbot LG5 markers could be indirectly linked to the Oreochromis spp. LG23, where a sex-associated QTL was detected (Shirak et al. 2006) from a previous comparative homology demonstrated between Oreochromis spp. LG23 and stickleback LG8 (Sarropoulou et al. 2008). Amh and Dmrta2 genes, involved in the gonadal differentiation pathway, map in the vicinity of the SD QTL at Oreochromis spp. LG23 (Shirak et al. 2006). These two genes also co-map to Gac LG8 (http://ensemble.org/index.html) and are physically located at ∼10–13 Mb from the stickleback homologous sequence to the turbot Sma-USCE30, the closest turbot marker to SDg. These observations suggest a putative role of these genes in turbot sex determination and strongly recommend their mapping.
Comparison of sex determination with other Pleuronectiformes:
Previous data in flatfish (Pleuronectiformes) suggest that a single genomic region is involved in sex determination, such as in turbot. This information was obtained mainly from sex ratios in progenies of meiogynogenetics and triploids, and both XX/XY and ZZ/ZW mechanisms have been reported (Purdom 1972; Tabata 1991; Howell et al. 1995; Tvedt et al. 2006; Chen et al. 2009). Environmental factors, such as temperature, do (Tabata 1995; Goto et al. 1999; Luckenbach et al. 2005) or do not affect (Hughes et al. 2008) gonad differentiation in flatfish, but this appears not to be a primary factor in sex determination in this group (Ospina-Alvarez and Piferrer 2008). Segregation patterns of the closest markers to the SD region in turbot support a ZZ/ZW mechanism in the five families analyzed. Our results are greatly in accordance with those reported by Haffray et al. (2009), who reported a ZZ/ZW mechanism in most turbot families obtained from androgen- and estrogen-treated parents crossed with normal females and males, respectively. Also, this mechanism would fit well with sex ratios of most triploid and meiogynogenetic families reported by Cal et al. (2006a,b). According to the fine mapping of the SD region obtained in our study, SDg would be at 32.2 cM from the centromere. This would render 82.2% female:17.8% male in meiogynogenetic (females: 64.4% ZW, 17.8% WW; males: 17.8% ZZ) and triploid (females: 64.4% ZZW, 17.8% ZWW; males: 17.8% ZZZ) progenies, assuming the dominance of the W chromosome and the normal viability of WW individuals. These proportions are very similar to those reported by Cal et al. (2006a,b). Cal et al. (2006b) invoked a primary XX/XY chromosome determinism in turbot on the basis of 100% all-female offspring obtained in a single meiogynogenetic family. However, as suggested by Haffray et al. (2009), this result also could be explained by a ZZ/ZW model that considers the presence of lethal genes associated with the SD region, as previously reported by Martínez et al. (2008).
Sex-associated heteromorphisms previously had not been detected either in mitotic or in the >11-fold longer meiotic chromosomes of turbot (Bouza et al. 1994; Cuñado et al. 2001). As in most fish species (Almeida-Toledo and Foresti 2001), this observation shows the primitive evolutionary condition of sex chromosomes in this species. In accordance with this observation, no consistent recombination differences were detected between males and females around the SD region in our study. However, these could be occurring at a finer scale as the significant genetic differentiation (FST = 4.1%) at SmaUSC-E30 between males and females suggests. The brill (S. rhombus), a close related species according to genetic data (Blanquer et al. 1992; Pardo et al. 2001; Bouza et al. 2002), did not show any chromosome heteromorphism, and its mitotic karyotype was not distinguishable from that of turbot (Pardo et al. 2001). Remarkably, hybrid crosses between female brill × male turbot produce nearly all-male populations (Purdom and Thacker 1980). This could be explained by opposite sex determination mechanisms in both species (female XX × male ZZ). If so, a transition in the SD mechanism between these closely related species could have occurred recently. A similar situation has been suggested in tilapia species (Lee et al. 2004).
Other minor factors in turbot sex determination:
The results discussed thus far explain most observations of sex determination reported to date in turbot. However, both in our study and in that by Haffray et al. (2009) some families did not conform exactly to the model proposed. In our work, SmaUSC-E30 did not predict the sex of individuals in Qfam2 as accurately as in the other families. The inversion suggested in the consensus map of Qfam2 could explain this discrepancy. Chromosome reorganizations in the SD regions in different species have been suggested as a way to suppress recombination to maintain sex-associated coadapted gene blocks (Peichel et al. 2004). Haffray et al. (2009) also reported some turbot families that did not conform to the ZZ/ZW model. An excess of males was observed in most of these families, with proportions close to 2 males to 1 female. Minor genetic or environmental factors could be necessary to explain these proportions. In this sense, a more detailed analysis of temperature during the most sensitive larval period could be undertaken in turbot for a better comprehension of the possible influence of temperature on sex ratios. Also, a QTL and marker association analysis in the atypical families reported by Haffray et al. (2009) could shed some light on this point.
We thank Lucía Insua, María Portela, Sonia Gómez, Susana Sánchez, María López, and Mónica Otero for technical assistance. This study was supported by the Consellería de Pesca e Asuntos Marítimos and the Dirección Xeral de I+D-Xunta de Galicia project (2004/CP480) and by the Spanish government (Consolider Ingenio Aquagenomics: CSD200700002) project.
Supporting information is available online at http://www.genetics.org/cgi/content/full/genetics.109.107979/DC1.
Communicating editor: D. Charlesworth
- Received July 31, 2009.
- Accepted September 17, 2009.
- Copyright © 2009 by the Genetics Society of America


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Oct 25, 2010 - 8:38 pm
From Science Daily News a very interesting article on the use of aspirin for lowering recurrance of PC:
There is also a good article on the benefits of proton therapy:
Oct 25, 2010 - 9:10 pm
Thanks Trew for sharing...Who knows but my Oncologist had it on the list of things he wanted me to do... I have posted these items a few times since Dec 09.... I guess it will not hurt...Peace
Oct 25, 2010 - 9:36 pm
I miss a lot, but the aspirin is new to me. S0, back to taking the baby aspirin once a day.
Oct 26, 2010 - 10:22 am
Trew, thanks for the post. Like some of the others who have posted, I've been on aspirin for quite a while. I'd been taking the aspirin for a number of years before my PCa was diagnosed. In my case the aspirin doesn't seem to have stoped the beginning of PCA; however, maybe it slowed the growth (?).
After reading the article I thought that those guys doing AS might want to consider taking aspirin if they are't taking it already.
Oct 26, 2010 - 8:55 pm
The article doesn't say how much aspirin the study participants took. Is it the same as recommended to avert heart disease (80-160 mg/daily) or some other quantity? Anyone know?
Oct 27, 2010 - 10:13 am
Not sure that I would go along with the "aspirin is a cure" bandwagon just yet but there have been a number of studies that show a relationship between low-dose aspirin use and reduced risk of prostate cancer. The one below highlights a common thread in most of the reports I have read:
"Use of aspirin and other nonsteroidal antiinflammatory medications in relation to prostate cancer risk - Abstract
Wednesday, 25 August 2010
In a population-based case-control study designed to investigate the relation between these medications and prostate cancer risk, detailed exposure data were analyzed from 1,001 cases diagnosed with prostate cancer between January 1, 2002, and December 31, 2005, and 942 age-matched controls from King County, Washington. A significant 21% reduction in the risk of prostate cancer was observed among current users of aspirin compared with nonusers (95% confidence interval (CI): 0.65, 0.96). Long-term use of aspirin (> 5 years: odds ratio = 0.76, 95% CI: 0.61, 0.96) and daily use of low-dose aspirin (odds ratio = 0.71, 95% CI: 0.56, 0.90) were also associated with decreased risk. There was no evidence that the association with aspirin use varied by disease aggressiveness, but there was effect modification (P(interaction) = 0.02) with a genetic variant in prostaglandin-endoperoxide synthase 2 (PTGS2) (rs12042763). Prostate cancer risk was not related to use of either nonaspirin NSAIDs or acetaminophen. These results contribute further evidence that aspirin may have chemopreventive activity against prostate cancer and highlight the need for additional research."
I have also read studies that suggest tha aspirin is associated with reduced PSA but interestingly, not PSA velocity, causing some researchers to opine that perhaps we ought not to take aspirin for a few days before our PSA draw.
For several years the benefits of low dose aspirn from a cardiology aspecxt for men in their 50s and older has been fairly well documented. Having it also potentially be a guard against PCa seems to be icing on the cake.
Unless there was some other medical reason that overrode those advantages, why not take it?
Oct 27, 2010 - 12:02 pm
Thanks, Kongo, but I still don't see any mention of the exact dosage of aspirin used in the abstract you posted.
Have you seen a dosage number mentioned anywhere in the studies or abstracts for the use of aspirin for PCa that you've read or are we just to "assume" that they're talking about 81mg aspirin (1/4 of the normal aspirin tablet and the dosage normally used for the prevention of heart disease) when they say "low dose"?
FWIW, I take a lot of supplements already and, if Dr. Oz and other media docs are to be believed, there are many, many more that I should take as well.
I'm now using up a supply of saw palmetto, pomegranate and cranberry that I bought for frequent urination associated w/PCa (which I'll probably stop taking after the supply is exhausted) and I'm taking (and have been for several years) a multi-vitamin, calcium, glucosamine and fish oil pill daily for other things.
I'm not convinced that low dose aspirin is a wonder drug either, but my family has a history of cancer as well as heart disease. I haven't taken low dose aspirin for heart disease yet but may do so if there's also a possible side benefit to suppress the spread or growth of PCa following treatment.
It would just help to know if these PCa-aspirin studies are talking about 81mg or some other dosage of aspirin.
Oct 27, 2010 - 12:36 pm
I was assuming that the "low dose" is the 81 mg tablet that they sell but I did see a study in the UK at about the same time that used a 75 mg dosage each day.
I looked into saw palmetto but decided not to do it as the reports I read at the time indicated that it took two or three years for it to have much effect, although others swear by it. I got the impression that it was masking the PSA rather than actually lowering it. I drink a lot of pomegranate juice but don't take the supplements. I've grown to like it. Cranberry juice is supposed to do a good job of neutralizing uric acid which causes the burning at urination.
Oct 27, 2010 - 9:43 pm
Maybe I should, ah, start taking it now? LOL!
Oct 29, 2010 - 12:27 am
If it can help prevent heart disease and maybe even help prevent the spread of PCa, why not? I just bought a bottle that'll last me a year and 1/2 and started taking 'em today.
Oct 29, 2010 - 8:34 am
A friend was diagnosed with PCa 20(?)years ago. He and his wife were ex-hippies, but were still into natural foods and cures big time (grew their own food, dried their fruit, etc.). He decided to take saw palmetto and other herbs. Lowered his PSA considerably (I am not sure if he had a biopsy ... at that time I was too ignorant of PCa to ask).
With time (5years?) the PSA began to increase and he was treated with brachy. He died of PCa about five years ago.
I am of the opinion that the saw palmetto (and other herbs masked his PSA), and that he might have been better off being treated when the PSA first increased. I know this is anecdotal ... but it did impact my decision making on what to do and when to do it.
I did try saw palmetto for about a year when I was diagnosed with an enlarged prostate. It didn't do much for me (I still had to get up at night), so I quite taking it ... maybe I should have taken it longer. I don't know if it had any impact on my PSA (my PSA was low at the time).
Oct 29, 2010 - 11:08 am
From what I have read, saw palmetto is used commonly in Europe to treat BPH as it has been shown to reduce the size of the prostate similar to the commonly prescribed drug finasteride here in tghe United States. As I understand it, saw palmetto inhibits certain enzymes in the prostate that interact with dihydrotestosterone (DHT) that enables interaction at the molecular level with prostate cell receptors, having an impact on the "true" PSA reading. In other words, the cancer is still there but the PSA shows a lower level than might otherwise be indicated.
I suppose this is most important for the early detection of prostate cancer where PSA screening gives us an early clue that the might be something abnormal going on. If our PSA was actually 6, for example, but long time use of saw palmetto showed that it was only a 3, then a man might not be advised to have a biopsy or other tests to determine the rise cause of the elevated PSA. Because of this I believe that saw palmetto only acts to lower the PSA reading, not reduce or reverse PCa.
While saw palmetto may be a less expensive way to reduce prostate volume in men who suffer from BPH, I would think it would be prudent to have a "baseline" PSA reading before taking it or finasteride, and that a man's doctor should be aware of the use of the drug as he made evaluations based on PSA readings.
I don't know the dosage levels of saw palmetto that should be administered to reduce BPH but I would encourage any man considering taking this herb to discuss it with his doctor first and weigh the pros and cons of using that, finasteride, or some other procedure to treat BPH but not reduce the ability to early detect PCa.
Oct 29, 2010 - 8:19 pm
I'm well aware of the PSA masking issue but once you know you have PCa, what does it matter?
I already knew I had PCa when I started taking saw palmetto (which made the masking effect irrelevant) and only started taking it after I already took 3 prescription drugs (Hytrin - huge headaches, Ditropan - no noticeable effect and Flowmax -- dried up ejaculate) which did not solve the problem which originally led to my PCa diagnosis -- namely, frequent urination at night.
I bought and started to use saw palmetto (standardized extract - 160mg) twice daily (morning and night) and it worked for me BEFORE treatment. Don't know if it reduced the size of my prostate which was slightly enlarged at 43ccs, but I stopped urinating as frequently as before AND it did not have any noticeable effect on my PSA. In fact, my PSA spiked frighteningly while I was taking saw palmetto, which my doctors attributed to the biopsy. My PSA level subsequently dropped (almost but not quite back to pre-biospy level before I was treated w/CK) but I don't know whether the drop was due to saw palmetto use or not but, based on my experience, my guess is not.
I've also been taking cranberry (standardized extract - 250mg) and pomegranate (standardized extract - 150mg)twice daily along w/saw palmetto for no good reason other than the fact that they are considered good anti-oxidants which are believed to also have cancer preventative benefits. Since I have already been treated, the only possible benefit to taking them for me is to reduce the potential spread of the cancer, which they also are believed to do. Their use is also associated with a drop in PSA.
After CK treatment, I am urinating more frequently than I had been before treatment, which was an anticipated result. My radiation oncologist suggested Flomax but I refuse to take it because of the way it dries up my ejaculate. I am still taking the supply of saw palmetto and cranberry/pomegranate extract that I have on hand and I don't plan to buy any more.
The saw palmetto doesn't seem to be working as well post-treatment as it did pre-treatment, but it's not a major problem. I also am not worried that the taking of these supplements may "mask" a recurrence of my PCa following treatment; if the treatment is working it should be readily apparent regardless of the effect of these supplements. My doctor knows that I'm taking these supplements and does not think otherwise because he (and other doctors) really don't believe that they have any significant medical benefit (or detriment, for that matter).
Oct 29, 2010 - 5:30 pm
Thanks for a great explanation ... as usual, very interesting.


text:
HR Onboarding: Drive Organizational Success Going Into 2020
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Practice is held on Tuesday, Thursday and Saturday. Our students participated in the Circuit Meet, Zonal Meet, Western Province Meet, Sir John Tarbet Meet Schools National Meet and the ?Saints Quadrangular Meet?.
We were placed 1st in the Circuit Meet, 3rd in the Zonal Meet, and 4th in the Sir John Tarbet Meet. Master Damindu Darshana was the Best Athlete in the Zonal Meet. Master Chamath was placed 1st in the 400Meters Hurdles in the Schools National Meet. Kavindu Navaratne was placed 1st in the Long Jump and Triple Jump events at the Sir John Tarbet meet


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Private lessons at Hillcrest
Individual, Group Lessons with Hillcrest Teaching Professionals
We have a highly experienced and knowledgeable certified coaching staff that will help you grow your game step-by-step and gain more enjoyment from this great game! Give us a call today (610-779-7900) for an individual lesson, group lesson, or for available clinics.
Individual and Group Lessons with Peter Heckler
|Lesson Rate (1/2 hour)
|Lesson Rate (1 hour)
|*Guest fee of an additional $5/hour lesson.
|Book of 8 1-hour lessons
|Book of 8 1 1/2-hour lessons
|*Guest fee of an additional $30/guest.
Individual and Group Lessons with Kim Cubero, Will Hill and Paul McDonough
|Lesson Rate (1/2 hour)
|Lesson Rate (1 hour)
|*Guest fee of an additional $5/hour lesson.
|Book of 8 1-hour lessons
|Book of 8 1 1/2-hour lessons
|*Guest fee of an additional $30/guest.
Peter Heckler, USPTA
Peter is a certified USPTA Elite Professional with over thirty years teaching experience extending from the development of 10 & Under Tennis Programs to the coaching of senior USTA leagues and teams. Peter has coached over forty juniors for a minimum of three years who have continued on to Division I Tennis Scholarships.
Involved with the game of tennis for over 43 years, Peter grew up in the Philadelphia suburbs and competed at a high level in Middle States, representing them nationally in Juniors and went on to play Division I Collegiate Tennis on scholarship at the University of Florida.
Peter currently lives in Ft. Washington, PA with his wife Robyn and their two children, Campbell and Penelope.
Kim Cubero, USPTR
Kim is USPTR Certified and has over 20 years experience teaching at Country Clubs and Racquet Clubs in the Philadelphia and New Jersey area. She has taught at Hillcrest for over 10 years. She has certification from the USPTR in 10 and Under Tennis and Etcheberry Certification for strength and conditioning in tennis.
Kim grew up with tennis and was a top ranked Middle States player as a junior. As a teacher, she has experience with all levels, priding herself in clear, simple communication to help players learn a strong foundation to accelerate development and stay involved with the "sport of a lifetime."
Kim is passionate about teaching and believes that when you enjoy what you do, you never work a day in your life. In addition, she believes in continual learning as a teacher so she is better able to help her students. She loves the social aspect of the game, running many of our social events and encourages members and guest to share ideas with her.
William Hill, USPTR
Will graduated from Davis & Elkins College with degrees in Criminology, Physical Education, Psychology and Management. As a player Will received a full athletic scholarship and helped lead the Davis & Elkins team to their first Conference Championship playing at positions one through four, received the MVP award, Most Dedicated Player award, and was an All-Conference player.
As a coach, Will is a USPTR Certified Professional Coach of High Performance. He comes to the club with seven years of experience as a coach of high performance tennis training, as well as three years personal training and fitness coordinator for a quality NCAA intercollegiate athletic program in the Great Midwest Atlantic Conference through Davis & Elkins College. He has shown a successful track record for improving players, managing athletic programs, and developing talent at the high school, junior, and collegiate levels. He has placed young players in Division 1 and 2 programs such as Temple, University of Arkansas, and Fairmont State.
Will has had one core Philosophy that drives both him and his students towards reaching their potential. "There may be others with more skill than you, there may be those who started sooner, but there should never be anyone who works harder than you. I'm the only person that will work harder on your game than you."
Paul McDonough, USPTA, USPTR
Paul has been teaching at Hillcrest for over 25 years. He has the distinction of being both USPTA and USPTR certified, and is a graduate of Tyler Junior College's nationally recognized program for tennis instruction.
He has enjoyed playing USTA Team Tennis for over 20 years, qualifying for sectionals 17 times and Nationals 5 times as well as achieving 3rd place at Nationals in 2006 and 1st in 2014. Paul has also previously served as President of the Berks County Tennis Association.
Paul loves instructing all levels of play. He runs many of our drill sessions, offers instruction for our junior programs, gives private lessons and coaches some of our USTA teams. In 2011, Paul was voted USTA Teaching Professional of the Year for both the Eastern PA District and for the entire Middle States.


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Meet Laura | Pradaxa® Patient Profiles | Boehringer Ingelheim
Meet Laura
- 79 years old
- Active grandmother…
6 grandchildren keep her busy!
- Recently diagnosed with nonvalvular
atrial fibrillation (NVAF). Her cousin takes apixaban
but Laura wants to know more about all of her
treatment options
How will you counsel Laura
on her options?
find out
Laura is interested in discussing a
lower risk of bleeding
In a real-world, observational analysis, Pradaxa® 110 mg had a lower risk of
any bleeding vs warfarin while apixaban 2.5 mg and rivaroxaban 15 mg were
associated with a similar risk vs warfarin (n=55,644)1
Not a head-to-head study; this was a real-world, observational analysis comparing the effectiveness and safety of Pradaxa® 110 mg, rivaroxaban 15 mg, and apixaban 2.5 mg vs warfarin.
Hazard ratios for additional bleeding outcomes: major bleeding=Pradaxa® 0.87 (0.75 to 1.10), apixaban 1.04 (0.76 to 1.43), rivaroxaban 1.17 (0.94 to 1.45); haemorrhagic
stroke=Pradaxa® 0.46 (0.29 to 0.72), apixaban 0.59 (0.34 to 1.02), rivaroxaban 0.68 (0.30 to 1.53).
Laura will thank you for prescribing the
most studied low-dose NOAC
Pradaxa® 110 mg has been studied in more patients than
both rivaroxaban and apixaban
Life Happens
If Laura ever needs it, Praxbind® provides the reassurance of specific, immediate, and complete reversal of Pradaxa®
Dual indication—for life-threatening or uncontrolled bleeding and emergency surgery/urgent procedures5
Specific binding allows for immediate and complete reversal of Pradaxa® with no procoagulant effects5
Easy to use—1 ready-to-use dose for ALL Pradaxa® patients5
Widely available—8,300+ sites in 48 countries6
- References:
- 1. Nielsen PB et al. BMJ. 2017;356:j510.
- 2. Connolly SJ et al. N Engl J Med. 2009;361(12):1139-1151.
- 3. Fox KAA et al. Eur Heart J. 2011;32(19):2387-2394.
- 4. Granger CB et al. N Engl J Med. 2011;365(11):981-992.
- 5. Praxbind® (idarucizumab) Summary of Product Characteristics. 2018.
- 6. Data on file, Boehringer Ingelheim.


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[1.15.2] New SoundType - Registry Object not present
Corgam, in Modder Support
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By urbanxx001 · PostedChoonster thank you! That's so much simpler, I had no idea about helper functions. Draco thank you as well, I didn't realize the events were clashing like that. I'll credit you all in the toml file.
The ENTIRE point is that you use the game directory option in the launcher and split your configs/worlds/whatever. It is kinda annoying that you also split your resource packs, as those typically arnt damaging if you apply the wrong version. But it's a happy cost for the benefit of not screwing up your worlds.
Hello! I've got 2 questions about to different things. The first is about filling a capability and the second about particles. 1. So I've got a working capabilities for projectile entities and I want to fill it with data from its source. I also got other capabilities, where I use the AttachCapabilitiesEvent to fill them (I use data, that I loaded from json). Now in the case for the projectile entity I wanted to use func_234616_v_(), which should return the shooter of my projectile. But this functions always returns null, mostly likely because the shooter hasn't be set yet. Should I use an other event or is there some other way to get the shooter, that I'm not aware of? 2. I have 4 particles, which are all working as intended. But I also have a lot of code duplication going on, because all 4 particles behave the same, except the texture and when they are supposed to be displayed. What would be the better solution, than copying the code 4 times like I did? Just in case you want to look at my code, here is my repository. The code for the particles is here and they are getting generated here. Trying to get the shooter of a particle can be found here.
So I'm trying to make a block that when I right click on with a certain item it spawn a portal of the end arround the block. The problem is even though the end block appears, it doesn't do anything so I don't know if the way I did it is wrong or if I'm missing something but I can't figure out why the end block doesn't teleport to the end. btw I'm a beginer so if you have some documentations that I should read to help me it would be awesome
Thank you Draco, I was being stupid.
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Stairs are a connection of walls with gradual height difference. A maximum length of 5 tiles can be drawn, however they can be shorter. Stairs can connect walls with the ground, however they can do so with walls with different height (e.g. low walls and normal walls).
Just like walls, stairs can be damaged with rocks. Segments can either lower in height or disappear, restricting access between their two endpoints. Stairs can only attach to walls, but not to gatehouses and towers. They can host braziers.
Considering normal elevations, a unit will only get height advantage, if it stands on the highest end of the stairs.
Community content is available under CC-BY-SA unless otherwise noted.


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Price: $1,850.00
Quantity: 1 available
Book Condition: Fine
Cambridge: Riverside Press. Fine. 1892. Hardcover. Early rebinding in brown cloth with black morocco labels in what appears to be a nineteenth century replacement for the publisher's fugitive ooze calf. Moire end papers, TEG. Unaccountably uncommon. Not in BAL. Two volumes. ; 8vo ; All shipments through USPS insured Priority Mail. .
Title: Uncle Tom's Cabin or Life Among the Lowly. Large Paper Anniversary Edition Number 88 of but 250 copies.
Categories: Americana,
Publisher: Cambridge, Riverside Press: 1892
Binding: Hardcover
Book Condition: Fine
Item: 1.00 Item
Seller ID: 1384
Keywords: Americana


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"If these sorts of things really did happen on such large scales we would expect a myriad of eye witness testimonies and outside biblical reports around that time frame, but outside the bible, we don't find any."
I believe Dr. Gary Habermas and Mike Licona offer a satisfactory answer to this point in their book The Case for the Resurrection:
"In the first century, people did not have access to all of our convenient ways to record and preserve the facts about events. Further, we know that much of what was recorded in the past has been lost. New Testament Scholar Craig Blomberg , who served as an editor for and contributor to a large scholarly work on the Gospels, provides four reasons why more was not written on Jesus in his time: "the humble beginnings of Christianity, the remote location of Palestine on the eastern frontiers of the Roman empire, the small percentage of the works of ancient Graeco-Roman historians which have survived, and the lack of attention paid by those which are extant to Jewish figures in general." We know that about half of what the Roman historian Tacitus wrote is no longer available. Only a fragment of what Thallus wrote in the first century about ancient Mediterranean history has survived. Suetonius is aware of the writings of Asclepiades of Mendes, yet, his writings are no longer available. Herod the Great's secretary. Nicholas of Damascus, wrote Universal History in 144 books, none of which have survived. Livy, the great Roman historian, has suffered a similar fate. Only his early books and excerpts of the rest survive.
We also know of several early Christian writings that are no longer available. For example, an influential church leader of the early part of the second century named Papias wrote five books that are quoted by several early church fathers. However, none of these books have survived. Only a few citations and slight summary information remain. Quadratus was a Christian leader who wrote a defense of the Christian faith to the Roman Emperor Hadrain around 125. However, if Eusebius had not quoted a paragraph and mentioned his work, we would be totally unaware of its composition. The five books of Recollections, written by Hegesippus in the second century, have likewise been lost. Only fragments have been preserved, mostly by Eusebius.
What we have concerning Jesus actually is impressive. We can start with approximately nine traditional authors of the New Testament. If we consider the critical thesis that other authors wrote the pastoral letters and such letters as Ephesians and 2 Thessalonians, we'd have an even larger number. Another twenty early Christian authors and four heretical writings mention Jesus within 15o years of his death on the cross. Moreover, nine secular, non-Christian sources mention Jesus with the 150 years: Josephus, the Jewish historian; Tacitus, the Roman historian; Pliny the Younger, a politician of Rome; Phlegon, a freed slave who wrote histories; Lucian, the Greek satirist; Celsus, a Roman Philosopher; and probably the historians Suetonius and Thallus, as well as the prisoner Mara Bar-Serapion. In all, at least forty-two authors, nine of them secular, mention Jesus within 150 years of his death.
In comparison, let's take a look at Julius Caesar, one of Rome's most prominent figures. Caesar is well know for his military conquests. After his Gallic Wars, he made the famous statement, "I came, I saw, I conquered." Only five sources report his military conquests: writings by Caesar himself, Cicero, Livy, the Salona Decree, and Appian. If Julius Caesar really made a profound inpact on Roman society, why didn't more writers of antiquity mention his great military accomplishments? No one questions whether Julius did make a tremendous impact on the Roman Empire. It is evident that he did. Yet in those 150 years after his death, more non-Christian authors alone comment on Jesus than all of the sources who mentioned Julius Caesar's great military conquests within 150 years of his death.
Let's look at an even better example, a contemporary of Jesus. Tiberius Caesar was the Roman emperor at the time of Jesus' ministry and execution. Tiberius is mentioned by ten sources within 150 years of his death: Tacitus, Suetonius, Velleius Paterculus, Plutarch, Pliny the Elder, Strabo, Seneca, Valerius Maximus, Josephus, and Luke. Compare that to Jesus' forty-two total sources in the same length of time. That's more than four times the number of total sources who mention the Roman emperor during roughly the same period. If we only considered the number of secular non-Christian sources who mention Jesus and Tiberius within 150 years of their lives, we arrive at a tie of nine each." [1]
So, the historical data we actually do have, especially after one considers other examples from antiquity, is actually impressive.
Finally, I would also like to add that I believe it to be mistaken to adopt the attitude that the gospels are not a reliable source of history.
For an exhaustive treatment of this question, see here or visit our Old and New Testament research page located here.
Courage and Godspeed,
1. Gary Habermas and Mike Licona, The Case for the Resurrection, p. 127-128.