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It worked! Thanks for the recipe.
View Instructable »Great, I have been trying to make naan bread a few times, but It never worked. I'll try this and see how Iir turns out. Thanks for the Instructable.
View Instructable »Awesome! By the way what is the name of the game displayed on the table in the first picture?
Thanks man, I'll check it out!
By the way, have you heard of the game called chicken foot. It is a game you play with a huge pack of dominos ( 1to 16).
Yes, it appears to be the same game but with a bit more glamour. Have you ever played axis and allies. It is a war strategy game for ww1 or ww2. The ww2 global edition is SO BIG. I think it will be able to fit on you table though.
View Instructable »That is awesome! Great job! ?
View Instructable »


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Parents and family members were likely offering their 18-year-olds plenty of last-minute advice yesterday as they helped the students move into dorm rooms and prepare for their first year of college. At the same time, family members were not spared nuggets of wisdom offered by people very familiar with the Bowdoin experience.
Relatives of incoming students gathered in Kanbar Auditorium/Studzinski Recital Hall for two different sessions to listen to members of Bowdoin's administration speak about what incoming students might experience in the coming four years. These experts (many of whom have sent their own kids off to college) also offered a bit of advice to parents.

subset: commoncrawl


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Nordic Iron Greaves wrong weight class "T_Nor_Iron_Greaves_01" are Medium Armor while the rest of the set is Heavy. Should be fixed by raising the weight. Read more about Nordic Iron Greaves wrong weight classLog in or register to post comments
Bleeding Kreshweed Flora_kreshweed_03 with targetID "060353bc" is bleeding into terrain_rock_wg_17 with targetID "060353f" in Mephalan Vales (35, -18) Read more about Bleeding KreshweedLog in or register to post comments
topic overriding I think topic "running an errand" may hide standard "errand" topic making impossible to go on with http://www.uesp.net/wiki/Morrowind:Sharn_gra-Muzgob (link is external) without addtopic errand by console possible fix: addtopic errand in the same greeting introducing the "running an errand" topic e.g. addtopic "running an errand" ; safety addtopic "errand" ; fix for main quest Journal "EB_Express" 10 Choice "I'll deliver it for you." 1 "I can't help you." 2 Read more about topic overriding2 commentsLog in or register to post comments
Velk Sound Gen Problem The sound "T_SndCrea_VelkScream" has been added to Sound Gen without a designated creature. As a result, the sound is treated as a default scream by the engine and is used frequently by other creatures, especially mod-added ones. Serious compatability issue. Read more about Velk Sound Gen Problem1 commentLog in or register to post comments
bugtracker: bugtracker has no category button The bugtracker is missing a category button where one could/would have to choose the context of the bug. It would be far easier to find issues related to certain things if there were one. Suggestions for categories: general/unspecific, scripting, meshes&placement, quest, OpenMW, CS IDs,… By the way: we don't "Create A Bug", we state them, so the headline ought to be changed into "Report a Bug" Read more about bugtracker: bugtracker has no category buttonLog in or register to post comments
Necrom, warning list for missing idles (OpenMW) As reported on Discord by zhakaron. Read more about Necrom, warning list for missing idles (OpenMW)Log in or register to post comments
Mainland Ghostfence replies As filed on Discord by zhakaron. All Ghostfence replies are filtered off this NPC, but if they know that, they probably should have a generic reply. Read more about Mainland Ghostfence repliesLog in or register to post comments
Old Ebonheart, Mages Guild: Fire Hazard As filed on Discord by zhakaron. rot-edit: Same convention is used everywhere in OE, Mainland and vanilla – in fact I can't find a single placement that does use a plate. Will just have to assume that the wicks stop before the bottom. Read more about Old Ebonheart, Mages Guild: Fire HazardLog in or register to post comments
TR_m1_q_RR_MQ_FinalShowdown Script TR_m1_q_RR_MQ_FinalShowdown has possibly some critical bug, I needed to use console and type "enableplayermovement", because script lacks this part and I couldn't move after it ends. It's a script connected to Master Mithras questline. Read more about TR_m1_q_RR_MQ_FinalShowdown1 commentLog in or register to post comments
tr_dres_bug_small_vo.nif, tr_swampfly_vo.nif tr_dres_bug_small_vo.nif bounding box should be smaller/resized. tr_swampfly_vo.nif tends to disappear under the Bal Oyra fort floor, making impossible to kill it and finish the related quest (e.g. if paralyzed, this happens every time if a MCA guard is near) . Possible things I'd try is changing the Bounding Box to be more similar to the one used e.g. with CliffRacer.nif, covering the flying creature legs and a little below. and/or put some collision box under the fort floor Read more about tr_dres_bug_small_vo.nif, tr_swampfly_vo.nifLog in or register to post comments


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Conceived and designed the experiments: RH MKK AL KT HP MO TV JCM SAM LP LJM AP MH. Performed the experiments: RH MKK BPC JP. Analyzed the data: RH MKK AL TV BPC JP SAM LJM AP. Contributed reagents/materials/analysis tools: LJM MH. Wrote the paper: RH MKK. Contributed in recruiting patients: KT HP. Contributed in obtaining patient data and DNA: HP. Contributed in obtaining the DNA array: LP. Contributed in writing the paper: AP MH. Served as a liaison between the investigators: MH.
Preterm birth is the major cause of neonatal death and serious morbidity. Most preterm births are due to spontaneous onset of labor without a known cause or effective prevention. Both maternal and fetal genomes influence the predisposition to spontaneous preterm birth (SPTB), but the susceptibility loci remain to be defined. We utilized a combination of unique population structures, family-based linkage analysis, and subsequent case-control association to identify a susceptibility haplotype for SPTB. Clinically well-characterized SPTB families from northern Finland, a subisolate founded by a relatively small founder population that has subsequently experienced a number of bottlenecks, were selected for the initial discovery sample. Genome-wide linkage analysis using a high-density single-nucleotide polymorphism (SNP) array in seven large northern Finnish non-consanginous families identified a locus on 15q26.3 (HLOD 4.68). This region contains the IGF1R gene, which encodes the type 1 insulin-like growth factor receptor IGF-1R. Haplotype segregation analysis revealed that a 55 kb 12-SNP core segment within the IGF1R gene was shared identical-by-state (IBS) in five families. A follow-up case-control study in an independent sample representing the more general Finnish population showed an association of a 6-SNP IGF1R haplotype with SPTB in the fetuses, providing further evidence for IGF1R as a SPTB predisposition gene (frequency in cases versus controls 0.11 versus 0.05, P=0.001, odds ratio 2.3). This study demonstrates the identification of a predisposing, low-frequency haplotype in a multifactorial trait using a well-characterized population and a combination of family and case-control designs. Our findings support the identification of the novel susceptibility gene IGF1R for predisposition by the fetal genome to being born preterm.
Preterm birth is the major cause of infant deaths and life-long neurologic and cardiopulmonary morbidity. More than 10% of births in the United States occur prematurely, and the rate is increasing without known effective prevention. Previous premature birth increases the risk 3-fold in subsequent pregnancies. We report here, for the first time to our knowledge, a genome-wide study on susceptibility to spontaneous preterm birth in singleton pregnancies. To detect novel regions of the genome associated with preterm birth, we performed linkage analysis on seven carefully selected large families with recurrent spontaneous premature births. When we studied the fetuses, evidence was found for linkage of a region on chromosome 15 with spontaneous preterm birth, with the highest linkage signals occurring within a single gene, IGF1R. Evidence of the involvement of this gene in the etiology of preterm birth was further strengthened by subsequent haplotype segregation analysis and case-control analysis of an independent patient population. The IGF1R gene encodes insulin-like growth factor receptor 1 (IGF-1R), an important protein that potentially regulates signaling cascades involved in the onset of labor. Our analyses are unique in providing evidence that fetal IGF1R influences the risk of spontaneous preterm labor, leading to preterm birth.
Preterm birth, defined as birth before 37 wk of gestation, accounts for an estimated 2 million annual deaths worldwide and is the major cause of serious morbidity in infants born preterm. Currently, approximately 12% of all births in the United States are premature. The serious acute diseases of prematurely born infants are principally caused by functional immaturity. Common life-long diseases that result in deteriorating quality of life among individuals born preterm include a chronic respiratory disease called bronchopulmonary dysplasia; retinopathy of prematurity, which is the most common cause of blindness in infants; cerebral palsy; and cognitive disorders [1]. The majority of preterm births (approximately 70%) occur after spontaneous onset of labor; nearly 50% of these cases are preceded by rupture of fetal membranes. Apart from excessive uterine distension in multiple pregnancies or certain fetal malformations, and severe maternal diseases such as sepsis and abdominal trauma, no obvious environmental risk factors can be identified in most preterm births. Activation of spontaneous preterm labor and preterm birth is thought to result from the action of multiple pathways and mechanisms, including endocrine dysfunction or ascending intrauterine infection and inflammation that can lead to the induction of labor-producing mediators [2]. Despite ongoing research efforts, there is no effective medication for the prevention of spontaneous preterm birth (SPTB).
A history of SPTB of a single fetus is a strong predictor of its recurrence in families [3]. Approximately 20% of mothers with a preterm delivery have another baby born preterm [4], suggesting that factors that are stable over time, such as genetics, affect birth timing [5]. Mothers and daughters [6] and sisters [7] share the risk of delivering preterm. Twin studies suggest a heritability estimate of about 30% [8]–[10]. Both the fetal and maternal genome, as well as gene–gene and gene–environment interactions are likely to influence predisposition to SPTB. Several studies using fetal or maternal DNA have reported associations of individual gene polymorphisms [11]. These studies have focused on genes involved in infection, inflammation, and innate immunity; e.g. those encoding the cytokines tumor necrosis factor alpha and interleukins 4, 6, and 10, and mannose-binding lectin [12]–[21]. However, most of these associations were not replicated in subsequent studies and across populations. So far, only case-control candidate gene studies have been conducted for SPTB. Genome-wide methods of identifying genes a priori may reveal genes not considered to be obvious candidates, which are potentially important unexplored sources of variability in preterm birth. These studies may contribute to defining the risk of SPTB and developing potential preventive interventions.
The overall aim of the present approach was to define major genes that influence the susceptibility to SPTB. In this first report, we describe a SNP-based genome-wide linkage and haplotype segregation analysis of recurrent familial SPTB using a strictly defined phenotype and carefully selected families, followed by case-control association analysis of a study population independent of the subjects used for the linkage scan. The linkage scan was performed with seven large families originating from northern Finland, where the population is characterized by genetic homogeneity, making it advantageous for gene-mapping studies [22]. With the phenotype defined as being born preterm, significant linkage signals (HLODmax=4.68) were obtained for chromosome locus 15q26.3 in a region harboring IGF1R (MIM *147370), the gene encoding insulin-like growth factor receptor 1 (IGF-1R). Haplotype segregation analysis performed for markers encompassing the IGF1R gene revealed prominent identical-by-descent (IBD) within-family and identical-by-state (IBS) between-family haplotype sharing among affected relatives. Evidence of the involvement of IGF1R in the etiology of SPTB was further strengthened by case-control analysis of an independent cohort located in northern and southern Finland, with a 6-SNP IGF1R haplotype overrepresented in SPTB infants. In summary, evidence from our linkage, haplotype sharing, and association analyses implicated IGF1R as a candidate gene for susceptibility to SPTB.
The overall study design is illustrated in Figure 1.
We selected the families for the linkage analysis from a total 120,000 births that took place in a single regional hospital in northern Finland; this region is characterized by a homogeneous and stable population with a low prevalence of prematurity (approximately 5.5–6.5% of all births). We chose mothers with recurrent SPTB using very stringent criteria, with known risk factors for SPTB and elective preterm births without labor among the exclusion criteria. We identified 120 mothers with at least two spontaneous singleton preterm deliveries. Family interviews revealed 20 large families with multiple relatives affected by SPTB. According to a genealogical study, these families were non-consanginous. Finally, families with apparent maternal inheritance of SPTB were chosen for the analysis.
We conducted parametric linkage analysis using seven large northern Finnish families with recurrent SPTB. Because genetic factors acting either on the fetus or the mother may influence SPTB, we used two settings in this study: affected fetus or infant phenotype (being spontaneously born preterm as the phenotype, n=41) and affected mother phenotype (giving spontaneous preterm birth as the phenotype, n=21). The pedigrees of the families are shown in Figure S1.
Before the analysis, markers were linkage-disequilibrium (LD) pruned to exclude high-LD SNPs, leaving 6377 markers with an average distance of 0.43 Mb between consecutive markers. We considered a heterogeneity logarithm of odds (HLOD) score of >2 as an initial signal of linkage. When we studied the affected fetus phenotype, analysis of the pruned marker set revealed HLOD scores of >2 on six autosomes, as depicted in Figure 2. The maximum HLOD score (HLODmax) of 2.59 was detected for SNP rs2715416 on chromosome locus 15q26.3 (θ=0.04, α=1.00). Figure 2 also shows the linkage signals for mother-based analysis, with an HLODmax of 1.53 at rs11167102 on chromosome locus 8q24.3 (θ=0.00, α=1.00).
For the affected fetus phenotype, we performed fine mapping using the unpruned marker set on the regions flanking (approximately 5 Mb) the six initial linkage signals. We considered an HLOD of >3 as a further sign of linkage. Table 1 reveals that the three markers with an HLOD of >3 were all on the same chromosome locus 15q26.3 and shows the HLOD scores in the fine-scale analysis for each of the seven families with recurrent SPTB. The HLODmax of 4.68 was obtained at rs2684811. Because one preterm infant not fulfilling the stringent criteria of SPTB (preterm infant from a twin pregnancy) was included among the premature births, we repeated the linkage analyses while excluding this infant from the affected individuals, with little effect on the results. All three markers with the highest HLOD scores are located within a single gene IGF1R. Interestingly, the markers that yielded the second- and third-highest HLOD scores in the mother-based analysis (SNPs rs329292 and rs11247268 with HLOD scores of 1.51 and 1.48 respectively; Figure 2) were located on the same chromosomal region (15q26.3) as the marker with HLODmax in the infants, with a distance of approximately 2.2 Mb between the markers. Because of the colocalized linkage signals in both the fetal- and mother-based analysis in the region including IGF1R, we chose to explore this gene in greater detail.
We performed haplotype segregation analysis using the SNPs flanking the highest linkage peak within IGF1R in the six linked families 24, 70, 126, 150, 185 and 253. Family 210 did not undergo haplotype segregation analysis due to an absence of linkage in this family (Table 1). The analysis was performed for 30 SNPs covering a 330 kb region encompassing the entire IGF1R gene. We aimed to resolve whether one or more distinguishable haplotype segments inferred from these SNPs cosegregated with SPTB. While not suitable as such for statistical evaluation, segregation analysis is a useful tool for an empirical hypothesis-generating approach [23]. The model used for the segregation analysis was initially designed to be best-fit to the mode of inheritance (MOI) used in the linkage analysis (dominant MOI, allowing for the presence of healthy carriers as transmitters of a disease-cosegregating haplotype). However, haplotype-sharing analysis offers the advantage over parametric linkage analysis of dissecting the genetic data regardless of true MOI.
IGF1R haplotypes for family 70 with the highest linkage signal are represented in Figure 3, and Figure S2 shows these haplotypes for all of the linked families, including family 70. In all six families, and considering the haplotypes comprising 30 SNPs spanning the entire IGF1R gene, we observed prominent IBD within-family haplotype sharing among the affected relatives (Figure 3 and Figure S2). A single disease-cosegregating haplotype was shared IBD within family in families 70, 126, 253 and 185. In the remaining two families, 24 and 150, an IBD-shared haplotype was identified in a subset of members of each family, and a second haplotype derived from another carrier was identified in a different subset of members. On the whole, the segregation analysis supported the assumed model very precisely, because it predicted the carriership of a disease-cosegregating haplotype in 34 out of all 38 affected individuals (absent from individuals 70-2, 150-15, 150-19 and 150-24), whereas only six nonaffected family members were deemed to be carriers of a disease-cosegregating haplotype (present in individuals 24-1, 24-5, 24-11, 24-9, 150-8, and 150-26) (Figure 3 and Figure S2). The recombinations that we observed, particularly that in the unaffected male 253-5, also fit the segregation model well. Three of the families (126, 253, and 185) showed a complete haplotype-disease cosegregation (Figure S2). However, unexpected male carriers were identified in four families (spouses of females 24-2 and 70-1, and males 253-1 and 150-3). Families 24 and 150 were consistent with a mixed maternal-paternal bilineal transmission pattern, and family 70 exhibited nearly complete penetrance with mixed unilineal maternal–paternal transmission. The segregation patterns were consistent with complete penetrance in families 126, 253, and 185; with 100% maternal transmission in families 126 and 185; and unexpected 100% paternal transmission in family 253.
An attempt to identify a similar IBD- or IBS-shared chromosomal segment among families led us to discover two core haplotypes with overlapping locations (illustrated in Figure S2). A 55-kb 12-SNP haplotype, CAGACGATACTC (core I, comprising the interval between SNPs rs1879612–rs2715416), was shared IBS among five families: all of families 24, 70, 126 and 253 and part of 150. Another 79-kb 11-SNP core haplotype, ATGTGTAATGT (core II, SNPs rs2684761–rs3743259), was shared IBS between part of family 150 and the whole of family 185. The disease-segregating chromosomes with the core II haplotype were maternal in 100% of preterm-born individuals carrying these chromosomes, while haplotypes with core I were maternal in only about half (47%) of the cases.
All of the linked families shared one of the core haplotype segments, I or II. To demonstrate further the relevance of these haplotypes, we compared the haplotype frequencies in the affected and unaffected members of the linked families with those of an independent Finnish reference population from the Nordic Database Lund-Malmö dataset [24]. These Finnish reference samples (referred to as Nordic–Finn, n=955) are derived from a region in Bothnia in which there is evidence of western late settlement. The people in this region are genetically close to those in the region of western early settlement representing the origin of the linkage families [22]. Thus, these samples represented a good control and were also better matched with our study population than HapMap CEU individuals (CEPH; Utah residents with ancestry from northern and western Europe). Frequencies of haplotype core segments I and II were 0.30 and 0.33, respectively, in the affected members of the linkage families. Frequencies of core I and II haplotypes were 0.17 and 0.12, respectively, in the unaffected members of the linkage families, and 0.18 and 0.06 in the Nordic–Finn population. Thus, frequencies of the core haplotypes in the reference population were close to those of the unaffected members of the linkage families, while these frequencies were increased in the affected members of the linkage families. The higher frequency of haplotype core II in the unaffected members of the linkage families compared to Nordic–Finn individuals is explained by the high overall incidence of this haplotype in the largest linked family (Family 150; Figure S2). In terms of the LD patterns (Figure S3) in the unaffected individuals, the genetic profile of our study population was representative of the Nordic–Finn reference population. Furthermore, there was a short two-SNP major-allele haplotype AT at rs11630259–rs1357112 shared IBS between core segments I and II in 100% of the affected inviduals (n=38) and predicted carriers (n=18) (Figure S2), whereas the same haplotype was present in only 62% of the unaffected family members (n=37) and 72% of the Nordic-Finn individuals. Whether this particular segment sharing reflected the critical location of disease predisposition or arose by chance, could not be statistically evaluated in the current setting. Unfortunately, these two SNPs, which are not in LD with the surrounding region SNPs (Figure S3) and thus could not be imputed from other SNPs, failed to settle in the Sequenom iPLEX association platform and therefore could not be included in the following case-control association study.
We additionally performed a post hoc linkage analysis in which we used the transmission information obtained from the segregation analysis model, with both unaffected carriers and individuals born preterm defined as affected (naffected=55). An overall increase in the HLOD scores was observed within IGF1R, with an HLODmax of 3.81 at rs2715416 after pruning and an HLODmax of 5.15 at rs2684811 without pruning, further supporting the view that this genomic region may harbor a true susceptibility gene.
To validate the potential linkage and association between IGF1R and SPTB, we enrolled a new Finnish population comprising cases originating from the northern (Oulu) and southern (Helsinki) regions of the country; these cases were independent of the families used for the linkage analysis. Tagging SNPs covering the entire IGF1R gene were determined using HapMap data from the CEU population. Among the 20 SNPs studied, two (rs7165181 and rs4966038) showed a weak association (P<0.05) in the infants but not in the mothers (Table 2). Even so, a 55-kb region of six SNPs in LD (Figure 4) spanning these two SNPs and extending to rs2715416 (which yielded the original linkage signal) showed statistically significant haplotype association with SPTB in the infants exclusively (Table 3). Similar associations were evident in both recurrent and sporadic SPTB. The signals obtained from independent sets of study populations using linkage, segregation and association approaches were colocalized within the same region of IGF1R (Figure 5 and Table S1) and were consistently observed in the infants but not the mothers; i.e., when the affected phenotype was being born preterm instead of giving birth to preterm infant(s). The birthweights and gestational ages of preterm infants carrying the associating haplotype (n=71; 2,025±626 g; 32.6±3.0 wk; mean ± standard deviation) did not differ significantly from those of preterm infants without this haplotype (n=263; 2,105±616 g; 32.3±2.9 wk; P values of 0.64 and 0.35, respectively). Similar to our control population, the predicted frequency of the associating haplotype was 0.052 in the HapMap CEU population. In HapMap CHB (Han Chinese in Beijing, China) and JPT (Japanese in Tokyo, Japan) populations, allele and haplotype distibutions were completely different from our controls, as well as from the HapMap CEU population. The CHB and JPT populations completely lacked the associating haplotype. We were not able to estimate the frequency of this haplotype in the rest of the HapMap populations, including YRI (Yoruba in Ibadan, Nigeria), due to unavailable genotype data for part of the SNPs in these populations.
According to epidemiological studies, there is evidence for a heritable predisposition to preterm birth with both maternal and fetal contribution [11]. To our knowledge, the present report describes the first genome-wide investigation and the first linkage study to identify genomic regions associated with SPTB. We detected significant parametric HLOD scores in the infants for three intronic markers (rs1521480, HLOD=3.63; rs4966936, HLOD=3.63; and rs2684811, HLOD=4.68) on chromosome 15q26.3 within a single candidate gene, IGF1R, encoding the type 1 insulin-like growth factor receptor IGF-1R (Table 1).
We identified one major disease-cosegregating haplotype (core I) in all but one of the six linked families (Figure 3 and Figure S2). Rather than IBD, this sharing is likely to be IBS, because of the high frequency of this haplotype in the population, a view consistent with the genealogical survey, which suggested no common ancestry among the linked families. The occurrence of an alternative shared haplotype segment (core II) in all of family 185 and part of family 150 may reflect allelic heterogeneity or absence of true linkage in this subgroup, which would be typical of complex phenotypes even in an isolated population [25]. Taken together, our data on linkage and disease segregation of IGF1R SNPs are consistent with a role for this genomic region in SPTB under dominant MOI with incomplete penetrance allowing for healthy carriers or disease transmitters under etiological heterogeneity (the existence of phenocopies). However, because the segregation pattern supports the model of disease-cosegregating IGF1R haplotype transmission via both healthy male and female carriers, our initial MOI based on pure unilineal maternal transmission is likely to be oversimplified.
We examined the gene encoding IGF-1R in a separate investigation with a Finnish population originating from two regions of the country, which revealed an association of a fetal IGF1R haplotype with SPTB (Table 3 and Figure 5). Both the pattern of maximal haplotype sharing in the linked families and the region of association observed in the case-control study independently placed SPTB susceptibility on the same segment within IGF1R. As a whole, these analyses provide evidence that the fetal IGF1R influences the risk of spontaneous preterm labor leading to preterm birth.
IGF-1R is a heterotetramer composed of two extracellular alpha subunits containing a ligand-binding site for IGFs and two membrane-spanning beta subunits harboring intracellular tyrosine kinase activity involved in a variety of cellular functions [26], [27]. Upon activation by IGF-1 or IGF-2, IGF-1R participates in regulation of the cell cycle. Accordingly, certain IGF1R mutations result in intrauterine growth restriction, whereas polymorphisms of this ubiquitously expressed gene may not influence fetal growth [28]–[32]. The roles of IGF-1R in normal and pathological growth and differentiation and aging involve interactions with the ubiquitous growth factors, hormones, and proinflammatory cytokines that are considered to be mediators of the labor process [33]–[35]. Several IGF-binding proteins that regulate IGF-1R–dependent signaling cascades have been studied in the context of SPTB, and some of them have been implicated in preterm labor [36]–[38]. However, these studies did not involve IGF1R and thus the extension of studies involving IGF-1R (particularly the ligand-binding alpha subunit encoded by exons 1–10) to the process of labor, with special consideration of fetal involvement in the endocrine and paracrine control of the preterm labor process, is clearly indicated. The range of regulatory roles performed by the IGF system is consistent with our view that IGF1R influences susceptibility to SPTB. Furthermore, a recent study revealed a parent-of-origin-specific methylated site within intron 2 of IGF1R [39], which localizes to the same region that was identified in our haplotype segregation and case-control association analyses. This site was predominantly methylated on the maternally derived chromosome and may be involved in the imprinting process. This finding suggests a possible epigenetic mechanism through which IGF1R may be involved in the preterm labor process. In our linkage families, the core II IGF1R haplotype was maternally transmitted to the individuals born preterm, whereas the core I haplotype had a mixed transmission. This is an important aspect to consider in future studies involving IGF1R and preterm birth.
In the present study, we obtained no clear linkage or association signals when the outcome phenotype was giving preterm birth (affected mother phenotype). Because the number of affected mothers was small (n=21), the power to detect regions of linkage was limited. Although the maternal HLODmax was <2, which we considered to be below an initial threshold suggesting linkage in this study, we identified the regions yielding the highest maternal linkage signals (HLODs of 1.53 and 1.51 for markers rs11167102 and rs329292 on chromosomes 8q24.3 and 15q26.3 respectively). An interesting finding was that the SNP with the maternal HLOD score of 1.51 was located on the same region as the one with the HLODmax obtained from the infants, separated by 2 Mb (Figure 5). To conclude, the lack of association in the mothers and the observation of both maternal and paternal transmission in the segregation analysis unexpectedly did not support a major maternal contribution in IGF1R-mediated genetic susceptibility to SPTB. Our discovery of a fetal gene was unforeseen, but does not exclude the role of maternal effects via other susceptibility genes. Interestingly, a recent study suggested that the fetal genome plays a more significant role than the maternal genome in individuals of European ancestry [40]. However, other studies have pointed out the importance of the maternal genome in genetic predisposition to SPTB [41], [42].
Our study has several strengths compared to previous genetic studies of preterm birth. These candidate gene studies have been limited in several respects, such as small or mixed populations that may represent only the mother or the fetus, lack of replication, inconsistencies in phenotype definitions and incomplete coverage of variation within a gene [11]. In contrast, our study first focused on detecting novel genes involved in SPTB using a nonhypothesis-driven genome-wide approach. We evaluated both the maternal and fetal contribution. Additionally, careful attention was paid to selection of the families for the linkage analysis to ensure a precise phenotype definition. Lastly, we replicated the finding of a linked and disease-cosegregating region in an independent case-control cohort covering a large part of the entire country. The effect size we observed in the infants fell within the range of power calculations described in Materials and Methods. Although the Finnish population represents a higher genetic similarity than most populations, a clear substructure caused by population history is known to exist within the country [22]. However, the linkage and segregation analyses were performed using a relatively homogenous study population, which is amenable to using a search for shared genomic segments [25]. Our case-control cohort comprised two regions (northern Finland and southern Finland/Helsinki) known to represent slightly distinct patterns of genetic variation; the Helsinki region is known to be representative of a genetically more diverse population [22], [43]. The fact that the association was observed across these two subpopulations gives further credence to our findings.
Our results constitute proof of principle for using a genome-wide SNP linkage scan to elucidate a complex heterogenic trait via stringent initial selection of a limited set of individuals. Despite the important strengths mentioned above, our study has some limitations. The result remains yet to be confirmed and extended by independent case-control analyses in populations with larger sample sizes than in the current study, and by studying additional SNPs covering the large gene more extensively. It is possible that while the ethnically homogenous nature of our Finnish linkage families can facilitate detection of genetic factors, the relatively high degree of genetic similarity among the Finnish population compared to others may mean that this finding cannot be generalized to more outbred populations. The frequency of the associating IGF1R haplotype in the HapMap CEU population was similar (0.052) to the frequency of controls in our case-control analysis (Table 3), while this haplotype was completely lacking from HapMap CHB and JPT populations, reflecting population-specific variation within this genomic segment. In the current setting, it cannot be evaluated whether the observed association was due to a haplotypic effect or another linked polymorphic site that was not analyzed in the current study. Therefore, this region needs to be more thoroughly investigated to find the causative sequence variant(s) and also to determine whether other populations may have an IGF1R-mediated risk of SPTB. Furthermore, although we discussed here only regions with an HLOD of >3, other regions with initial linkage signals on chromosomes 2, 4, 10, 12, and 13 should not be ignored as candidates for the risk of spontaneous preterm labor leading to preterm birth.
In conclusion, our genetic linkage and haplotype segregation analysis mapped the novel fetal SPTB susceptibility gene IGF1R on chromosome 15q26.3; this was further confirmed by association in an independent case-control population replicate. This result was unexpected, because the studies on the etiology of SPTB have been focused on cytokine-mediated inflammatory signaling as a possible route of predisposition by the maternal genome. Future clarification of the molecular mechanism of a growth factor pathway with considerable influence on the heritable proportion of the risk of spontaneous premature labor and birth is likely to open up a new potential avenue for preventive therapies.
Written informed consent was obtained from the participants and the study was approved separately by the Ethics Committee of Oulu University Hospital and that of Helsinki University Central Hospital.
We selected families for the linkage analysis from among the population born in the Oulu University Hospital region. We selected mothers with recurrent SPTB from approximately 120,000 birth diaries between 1975–2005 (prospectively from 2002). To avoid misclassification bias at borderline gestational ages, we defined SPTB as spontaneous onset of labor and birth before 36 (rather than ≤37) completed weeks of gestation. Both labors initiated with intact membranes and those following premature rupture of fetal membranes (PROM, defined as leakage of amniotic fluid as the presenting symptom before the onset of contractions) were included among the SPTBs. Additional exclusion criteria were known risk factors for SPTB (multiple gestation, polyhydramnios, septic infection or chronic disease of the mother, narcotic or alcohol abuse, accidents, and fetuses with congenital anomalies) and all elective preterm births without labor (preeclampsia, intrauterine growth restriction, and placental abruption). Only families of Finnish origin were included. We identified 120 families altogether, with at least two spontaneous singleton preterm births. The family interview revealed that 20 of them were actually large families with multiple relatives affected by SPTB. To search for potential consanguinity, we performed a genealogical study in accordance with the published criteria [44], tracing ancestors from the Finnish Population Registries and scrutinizing microfiche copies available in the provincial and national archives of Finland. The genealogical survey showed that most of the large families originated from Northern Ostrobothnia. However, neither close consanguinity nor the common residence of ancestors dating from the 17th century was apparent. Because prior evidence suggests that a maternal family history of preterm birth may have a greater influence on this disorder, we selected families with apparent maternal inheritance of predisposition to preterm birth, excluding families with seemingly paternal or mixed transmission of the preterm birth phenotype. Using these criteria, seven families were selected. Whole-blood DNA samples (n=89) were taken from both affected and unaffected family members. The pedigrees of the families appear in Figure S1. Six of the mothers who gave preterm birth were themselves born preterm.
We selected mothers with a history of at least one SPTB and their preterm infants from singleton pregnancies from the regions of Oulu (northern Finland) and Helsinki (southern Finland) University Hospitals for an association study using the same phenotypic criteria as for the linkage analysis, resulting in a case population of 348 mothers (244 from Oulu and 104 from Helsinki) and 334 infants (238 from Oulu and 96 from Helsinki). One infant per family was included using the criteria described [45]. One hundred and forty-six (42.6%) of the mothers gave birth following PROM and 197 (57.4%) had labor initiated with intact membranes, while 128 (39.5%) of the infants were born following PROM and 196 (60.5%) without PROM. For five mothers and ten infants, there was no information concerning the occurrence of PROM. The control population consisted of 143 mothers and 197 newborn singleton infants who were prospectively recruited from Oulu University Hospital in 2004–2005 among mothers who had at least three exclusively term deliveries with no pregnancy- or labor-associated complications. It is of note that this part of the study was not restricted to familial SPTB, because it included mothers with both recurrent (n=79) and sporadic (n=265) SPTB and their preterm infants (recurrent n=76 and sporadic n=258). All of the individuals from the families included in the linkage analysis and their relatives were excluded from the association study.
DNA was prepared from whole blood specimens (n=89) by standard methods. DNA samples were genotyped in the Broad Institute Center for Genotyping and Analysis (CGA) using the Affymetrix Genome-Wide Human SNP Array 5.0Kb consisting of 500,568 SNP markers.
Whole blood (n=797) and buccal cell samples (n=305) were used for DNA extraction. Buccal DNA was extracted using Chelex 100 (Bio-Rad, Hercules, CA, USA), after which it was were whole-genome amplified (WGA) in duplicate reactions using the Illustra GenomiPhi V2 DNA Amplification kit (GE Healthcare Sciences, Cardiff, UK), followed by pooling of the duplicates and purification with Illustra Microspin G-50 columns (GE Healthcare Sciences). The quality and quantity of the WGA samples was confirmed with ethidium bromide–stained agarose gels and UV absorbance measurements, and by including nontemplate reactions to control for DNA contamination. In the set-up stage, we genotyped the WGA products in parallel with the corresponding unamplified DNA for a set of test SNPs, yielding >99% consistent genotypes. IGF1R SNP genotyping was performed at the Institute for Molecular Medicine Finland FIMM Technology Centre using the Sequenom iPLEX Gold assay on the MassARRAY Platform for user-defined SNP sets.
We processed the Affymetrix array data files using PLINK, v. 1.02 [46]. We used a 1 Mb-to-1 cM converted map, as justified in [47]. Before linkage analysis, the markers were pruned using a linkage disequilibrium (LD) r2 threshold of 0.35 with PLINK. Markers with either minor allele frequency (MAF)<0.08, genotyping failure >0.1 or Mendelian errors were excluded, as well as those violating the Hardy–Weinberg equilibrium (HWE, P<0.001). Data processing after removal of the high-LD SNPs yielded a selection of 6,377 autosomal SNPs for the genome-wide linkage analysis. We rechecked the genotype data for any Mendelian inconsistencies using PedCheck [48] before proceeding to linkage analysis.
We studied two main outcome phenotypes for SPTB: (1) being spontaneously born preterm (affected fetus/infant, naffected=41), and (2) giving spontaneous preterm birth (affected mother, naffected=21) (pedigrees in Figure S1). A parametric two-point linkage analysis of SPTB as a dichotomous trait was performed with ANALYZE, v. 1.9.3 BETA, which is a linkage and LD analysis package that uses FASTLINK 4.1P to calculate the pedigree likelihoods and is capable of managing both extended pedigrees and large numbers of markers [49]. We used a dominant low-penetrance model, assuming a disease allele frequency of 0.001 and penetrances of 0.001, 0.001, and 0 for the homozygotes, heterozygotes and wild-type homozygotes, respectively. This kind of model is nearly convergent with a model-free analysis, because it minimizes the effect of misspecifying the true MOI while retaining the highest power of a parametric analysis to detect linkage [50], [51]. Parametric linkage in the presence of heterogeneity was assessed using heterogeneity LOD (HLOD) scores and their accompanying estimates of the proportion of linked families (α) and recombination fraction (θ).
We applied two-point linkage analysis to avoid bias that could result in multipoint analyses due to missing parental genotypes and markers residing in LD [52]. Our linkage analysis strategy was to perform an analysis with an LD-pruned marker set and then to screen regions with initial linkage signals (HLOD>2) with a denser marker map including all markers with MAF>0.08 on the region. Using high-density SNPs in linkage analysis has the advantages of a low error rate, high per-marker call rates, and higher information content when compared to microsatellites [53]. In two-point analysis, LD does not increase type 1 error [54].
When a marker showed HLOD>2 (six positions), we selected the genomic region for further analysis. This fine-scale linkage analysis was performed using the unpruned marker set on the flanking region (~5 Mb) of each of the initial linkage signals with the same parametric model as the original scan. We considered an HLOD score of >3 as a signal of linkage.
We used PedPhase version 2.0 utilizing integer linear programming (ILP) to find the minimum-recombinant haplotype configuration in the linked families 24, 70, 126, 150, 185 and 253 for the SNPs flanking the best linkage peak [55]. Deceased or untyped individuals were also included if their haplotypes could be reconstructed from their relatives. The potential presence of disease-cosegregating haplotypes ("affected haplotypes", affected fetus phenotype) was evaluated using a model compatible with the assumption of maternal unilineal inheritance with incomplete penetrance, utilizing the scheme of the most likely segregation pattern to search for a minimum number of affected haplotypes. The model assumed dominant MOI, allowing for the presence of healthy carriers as transmitters of an affected haplotype.
We used an independent Finnish reference population of the Nordic Database Lund-Malmö dataset [24]. These samples (referred to as Nordic–Finn, n=955) are derived from a region in Bothnia in which there is evidence of western late settlement. We used Beagle 3.1 [56] to infer the haplotype phases for unrelated individuals in the Nordic–Finn samples.
IGF1R is a large, >300 kb gene with nearly 2,000 SNPs (NCBI B36 assembly dbSNP b126), but little frequent exonic variation; it has relatively weak intragenic LD and is not readily divided into discrete blocks of limited haplotype diversity. Using HapMap data (release 23a/phaseII) from the CEU population to determine tagging SNPs (tSNPs) covering the entire IGF1R gene (chr15: 97,004,502–97,329,396), we obtained a list of 100 tSNPs (pairwise tagging, r2 cutoff 0.8, MAF>0.1). Given the number of individuals available for the study and the power to detect associations, it was reasonable to set up a single iPLEX set, which can include up to approximately 30 compatible SNPs. To select SNPs, we visualized the gene region's LD pattern in the HapMap CEU population in the Haploview program v. 4.1 [57] and selected one SNP with the highest MAF from each haplotype block designated by this program. We also included the coding SNP rs2229765 (Glu1043Glu, also referred to as 3174 G>A) because individuals carrying at least one A allele are reported to have lower levels of free plasma IGF-1 than GG homozygotes [58], suggesting that this polymorphism may have a functional effect. After testing and validation, a selection of 20 SNPs (listed in Table 2 and details in Table S1) remained for the case-control association study.
We performed statistical tests using Haploview v. 4.1 [57]. We took multiple testing into account by performing permutations with 10,000 replicates and considered a corrected P value of <0.05 to be statistically significant. For analysis of haplotypes with birthweight and gestational age, we inferred phased IGF1R haplotypes from unphased data using Beagle 3.2 [56]. To analyze potential associations between haplotypes and birthweight or gestational age, the nonparametric Mann-Whitney U-test was used with Predictive Analytics SoftWare (PASW) statistics, version 17.0.3 (IBM SPSS, Inc.). Power consideration of the case-control study: the sample size provides 80% power (alpha=0.0025, allowing for multiple testing of 20 SNPs) to detect the risk allele carrier relative risks of approximately 2.1–2.7 in the infants and 2.4–3.1 in the mothers for allele frequencies ranging from 0.2 down to 0.05, considering SPTB as a discrete trait, assuming causal SNP, a prevalence of 0.05, and using the allelic 1 df test [59].
All of the chromosomal positions refer to NCBI Build 36 of the human genome.
International HapMap Project: http://www.hapmap.org
National Center for Biotechnology: http://www.ncbi.nlm.nih.gov
Nordic Database: http://www.nordicdb.org
Genetic Power Calculator: http://pngu.mgh.harvard.edu/~purcell/gpc
Pedigrees of the seven families with recurrent SPTB included in the linkage analysis.
IGF1R haplotype segragation in the linked families.
Pairwise marker linkage disequilibrium (LD) in the unaffected members of the linked families and the reference population.
Combined results of IGF1R SNPs in fine-scale linkage analysis and association analysis with the affected fetus phenotype.
We thank Maarit Haarala, Outi Kajula, Mirkka Ovaska, and Riitta Vikeväinen for sample collection and technical assistance and Tero Hiekkalinna and Joseph Terwilliger for helpful scientific advice in linkage analysis.
The authors have declared that no competing interests exist.
This research was supported by the Academy of Finland (grant number 105734 to RH, 126662 and 125911 to MH), the Sigrid Juselius Foundation (MH), the Foundation of Pediatric Research in Finland (RH) and University of Oulu Faculty of Medicine (RH). Oulu University Hospital was supported by the Ministry of Social Affairs and Health (MH), the Wellcome Trust (grant number WTO89062 to AP), the Academy of Finland Center of Excellence for Complex Disease Genetics 200923 (AP), and by grants from the March of Dimes, the Children's Discovery Institute at Washington University School of Medicine, and St. Louis Children's Hospital awarded to LJM. The Broad Institute Center for Genotyping and Analysis was supported by grant U54 RR020278 from the National Center for Research Resources. The Malmo-Lund study was supported by Novartis Pharmaceuticals, the Sigrid Juselius Foundation, the Folkhalsan Research Foundation, and a Swedish Research Council Linne grant; and the data source was funded by the Nordic Center of Excellence in Disease Genetics based on samples regionally selected from Finland and Sweden. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers. |


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Andrew McKnight EPK
"With a voice reminiscent of Don McLean, McKnight traverses from old-time Appalachian tunes to contemporary folk and blues, all backed up by his dead-on guitar playing" - The Boston Globe
connect at andrewmcknight.net • 540/338-3233
Scroll down for paragraph bios, solo concert videos, a full streaming concert audio, and credits/career highlights.
Reviews | Print-quality (hi-res) Photos | Publicity Tools
Tech Requirements | Andrew McKnight & Beyond Borders site
ABOUT: Since permanently leaving his corporate environmental engineering career in 1996, award-winning folk/Americana artist Andrew McKnight's musical journey has traced nearly a million miles of blue highways, and earned him a wealth of critical acclaim and enthusiastic fans for his captivating performances and seven recordings. Andrew's powerful and entertaining show is like one man theatre, delivered with warmth and down-home comfort. His finely crafted songs are woven together with humorous stories and poetic drama, while the musical soundscape traverses influences from Appalachia, tasteful slide and jazzy blues, feisty anthems, rustic folk, and even a little fancy flatpicking on a Carter Family tune. While his skillful guitar work provides a tasteful foundation, the touches of native American cedar flute, resonator guitar, djembe (African hand drum) and even mandolin add delightful and mesmerizing embellishments to the show.
Andrew has performed at many prestigious venues like the Kennedy Center, the International Storytelling Center and the Atlanta Olympics, has been part of the Rocky Mountain, South Florida, Boston and Delmarva Folk Festival lineups, and a guest on NPR's "Art of the Song" and "River City Folk" shows.
[Full length biography] | [1-sentence bios/description]
RECOMMENDED IF YOU LIKE: Darrell Scott, John McCutcheon, Richard Shindell
HEAR A FULL CONCERT: Enjoy streaming audio of Andrew's November 2015 live radio concert on WVBR "Bound for Glory". There are 16 songs and separately indexed stories and introductions; use the player controls to move between tracks.
Credits & Accolades
Over his 20-year career he has enjoyed many accolades within the folk music world; a Formal Showcase Artist at Folk Alliance International (FAI), Southeast (SERFA) and Northeast Regional Folk Alliance (NERFA) conferences, a Performing Songwriter Top 12 DIY selection, and finalist in the Rocky Mountain Folks Festival Songwriter Showcase, Kerrville New Folk and Falcon Ridge Emerging Artist competitions. His album Something Worth Standing For was one of five Finalists for the 2008 Washington Area Music Awards Album of the Year (overall). His "Good Things Matter" is a past Great American Song Contest Winner (Folk) and has been used in several anti-bullying campaigns.
Jamband Great American Taxi regularly performs his song "Made by Hand", co-written with current bandmate Les Thompson (Nitty Gritty Dirt Band) and Chance McCoy (Old Crow Medicine Show) about mountaintop mining in West Virginia's Coal River Valley, including on the NPR Woodsongs Old-Time Radio Hour. Originally released along with songs from Kathy Mattea and the Del McCoury Band on the acclaimed 2009 compilation Still Moving Mountains, the song also appears in Low Coal, a documentary about conflicts over mountaintop mining in West Virginia's Coal River Valley.
Andrew has produced or performed on recordings by many different artists, been a contributing writer for Blue Ridge Country and Americana Rhythm magazines, and is a sought-after clinician and panelist for songwriting and music business workshops. His article "Real Money" appears in Killing it in the Streaming Age, published by NPR's "Art of the Song" in late 2014. He enjoys an Artist Endorsement with Fairbuilt Guitars and since 2002 with Elixir Strings, and is a member of the prestigious Virginia Commission for the Arts Touring Artist Program.
Since 2014 Andrew has been the featured guest musician for Friends and Family Week at the Ferry Beach Conference Center in Saco Maine, where he selects music and leads a pickup choir in a short interfaith service each morning, teaches workshops for kids and adults, and arranges music for a variety of folk and jazz performances.
Select Performance Highlights
- Amazing Things Art Center, Framingham MA
- Anderson Fair, Houston
- Atlanta Summer Olympic Games
- Austin Acoustical Cafe, Austin
- Baltimore Artscape Festival
- Boston Folk Festival
- The Birchmere/WFMA, Washington DC
- Brewery Arts Center, Carson City NV
- Bristol Historical Society, Bristol CT
- Chattanooga Riverbend Festival
- Chesapeake Arts Center, Baltimore MD
- Chesapeake Maritime Museum, St. Michaels MD
- Court Square Theater, Harrisonburg VA
- Delmarva Folk Festival
- The Fret House, Los Angeles
- International Storytelling Ctr, Jonesborough TN
- John F. Kennedy Center, Washington DC
- Katharine Hepburn Theater, Old Saybrook CT
- Mountain Spirit Coffeehouse, Asheville NC
- Mountain Stage NewSongFestival, WV
- Museum of Shenandoah Valley, Winchester VA
- Narrows Center for the Arts, Fall River MA
- Off Square Music Festival, Woodstock IL
- Palace Theatre, Canton OH
- Rocky Mountain Folks Festival
- South Florida Folk Festival
- Susquahanna Music & Arts Festival, Havre de Grace MD
- Swallow Hill Music Association, Denver
- Toadstone Theater, Helena MT
- Uncle Calvin's Coffeehouse, Dallas TX
- Vanilla Bean Cafe, Pomfret CT
- Virginia Highlands Festival
- Westhaven Center for the Arts, Trinidad CA


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#SaxoStratsUS president Donald Trump backed himself to get the deal over the line but was find wanting at the decisive moment. If he was unable to get his healthcare bill through, what does it say about tax cuts and other reforms he needs to deliver his $1 trillion stimulus package pledge?21hIt seems like the market is writing a new narrative here post Trump's defeat. Negative sentiment in key risky asset classes with S&P 500 (cash) down 0.8%...20hCrude oil has hit new lows for the day as the risk off sentiment in stocks has triggered additional long liquidation. Both Brent and WTI are holding... -
Article / Yesterday at 7:00 GMT
Morning Markets: Stocks retreat after Trump's Obamacare defeat
Asia-Pacific equities retreated on Monday following losses by US stocks on Friday after the Trump administration was dealt a blow by failure in Congress to repeal the Affordable Care Act, known as Obamacare. Bonds and gold rose in a flight to safety. Oil prices fell after a meeting of Opec and non-Opec producers in Kuwait caused confusion by leaving it to an expert committee to decide on a possible extension of production cuts.Read the article -
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The author is a Forbes contributor. The opinions expressed are those of the writer.
Consumers may not be overly familiar with their name, but travel industry people know . They were spun off from American Airlines, owners of Travelocity, they process about 1 billion travel transactions daily, and more than 300 million people purchase airline tickets through Sabre's travel network each year.
Their travel's version of Andre The Giant -- a man of few words -- minus the French dialect, of course. And with the immense popularity of mobile apps -- the Yankee Group reports that mobile app users worldwide will surpass 2 billion in 2016 -- Sabre is now reinventing its rather practical travel organizing app know as TripCase.
Just this week Sabre's TripCase released a campaign that asks what #ShouldBEaThing (ShouldBEaThing.com), inviting people to create photo memes of other things that #ShouldBEaThing. You know -- flying cars, new homes that come with a bacon scent, socks to walk through airport security, Mr. T masks in every gym locker, or maybe high chairs in airports.
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Beyond the overall popularity of apps, the vertical in particular is crowded with the likes of TripIt, FlightTrack, WorldMate, Travelplan and others dotting the landscape. But what I like about Sabre's TripCase campaign is that the marketing of the product is different -- it stands out -- which is always a nice reminder to CMOs satisfied with the status quo.
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Here's an amusing video they created to kick things off featuring Chicago music and performance act The Flavor Savers.


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I recently was involved in two seperate support cases for Civil 3D, where the software users asked for assistance with alignment using surface elevations. I decided to create this blog post as a quick reference on this design issue, as well as provide the same information in Spanish.
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Tagged with Spanish, Tech Support, Infrastructure, Civil 3D, Alignment, AutoCAD Civil 3D, surface elevations
In the current release of InfraWorks 2015, there are NO Cul-De-Sac or Roundabout options, not even within the Roadway module. Autodesk is working on the Roundabout feature, but it is unclear when this will be released, we hope it will be later this year.
For now, take a look at the pictures below, 3 styles were created by copying the existing style and making some modifications.
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Tagged with Civil 3D 2015, AEC, Infrastructure, Civil 3D, Autodesk Infraworks, Road, Highways, Roundabouts, Cul-De-Sacs
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Tagged with Technical Support, Download, Tech Support, downloads, Advanced Solutions, Software, Support, Autodesk, Autodesk Virtual Agent, Autodesk Software, Software Installation, Software Download
This article was written by ASI Technical Specialist, Anthony Chiles, for The Industry.
The ASI Technical Support line is always receiveing calls from new and existing software users for guidance in downloading Autodesk software. I've created a quick and easy two-part reference guide to downloading software, that is quick and easy... Just follow the steps:
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The question of how to show Existing and Proposed design on a cross section has come up in the past couple of my custom classes. I've always assumed it could be done, but finally decided to put my thoughts to the test and create a write up.
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Tagged with Technical Support, Tech Support, Corridors, Infrastructure, Code Set Styles, AutoCAD Civil 3D, Software, Autodesk, Proposed Conditions, Assemblies, Existing Conditions
Look no further... Autodesk is hosting a monthly construction focused webcast series called, Construction Innovation & Productivity!
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Tagged with innovation, productivity, webinar, AEC, BIM, News & Events, construction, Autodesk
Advanced Solutions is now offering "After Hours" PILOT classes for select classes. You spoke and we listened...
Don't try to cram classes into your busy daily schedule! We now have three afternoon/evening classes, beginning June 15th, starting at 1pm, 2pm, and 4pm EDT:
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Tagged with Training, AEC, educational series, Infrastructure, CEUs, PILOT, Revit, Civil 3D, AutoCAD, Manufacturing, Software, News & Events, education, Revit Architecture
A little know fact... As an Advanced Solutions (ASI) CAD Club member, you have access to exclusive member benefits. One of the most recent to be unveiled is the NEW CAD Club Tech Talks.
CAD Club Tech Talks are "lunch and learns" hosted by ASI PILOT Instructors. This ongoing educational series began on May 29th. There are 21 CAD Club Tech Talks scheduled from June to December, on a wide variety of topics for the architecture, engineering, construction, infrastructure and manufacturing industries. Here is a list of the upcoming Talks:
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Tagged with DFM, Autodesk Vehicle Tracking, CAD Club, AEC, Infrastructure, 3ds Max, PILOT, BIM, Revit, Civil 3D, Manufacturing, Simulation, News & Events, Moldflow, TechTalks, Revit Structure
Can you see the Future?
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Tagged with product design, product development, Technology, Advanced Solutions, digital prototyping, Manufacturing, 3D Digital Modeling, Software, News & Events, Autodesk, The Future of Making Things, Rapid Prototyping
The Future Shock with Autodesk 2016 Software virtual event will begin on Tuesday, June 23, 2015 and run through Wednesday, June 24, 2015. Through the registration link, participants will be directed to a dynamic landing page with detailed descriptions of each session, event highlights, presenter biographies, a full agenda, and frequently asked questions.
Once the registration is closed and the event opens, event attendees will enter the virtual conference hall and gain access to:
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Tagged with Autodesk 3ds Max, Autodesk Revit, Autodesk Design Suite, Autodesk Inventor, AEC, architecture, Infrastructure, BIM, Autodesk 2016, AutoCAD, AutoCAD Civil 3D, Autodesk Vault, digital prototyping, Manufacturing, Simulation, Autodesk Infraworks, News & Events, construction, Autodesk, engineering, A360
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The headline and subheader tells us what you're offering, and the form header closes the deal. Over here you can explain why your offer is so great it's worth filling out a form for.
- Bullets are great
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I really like the double farm sink, the island, and the cabinetry. Everything except the window treatment and perhaps the floor.
I would put a colorful runner in front of this busy work area and that would help the coldness of the floor. The whole room needs to be accessorized to make it warmer. I have a really busy day ahead of me and I'm trying to keep my head on straight to get everything done in an orderly fashion. See you later. xo
Thursday, August 21, 2014
3 comments:
- Mama Pea said...
The owners must need the drapes on the window for privacy at night. But it does give the window a very "dated" look, doesn't it?
Hope your day goes smoothly! - August 21, 2014 at 10:16 AM
- Catherine said...
I agree with everything you said. I will add the modern hardware on the cabinets to the list. I would not have used that on them.
- August 21, 2014 at 10:44 AM
- The Queen Vee said...
I agree with you. I think that stone floors are a hard surface to stand on for any length of time altho I suppose if you live in a very warm climate it would help in cooling a room down.
- August 22, 2014 at 10:08 PM
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Rush Limbaugh
9:00am - 12:00pm
Listen Live
Posted: 2011-02-25 10:27:00 by julia2
Bend Police along with the Oregon Attorney General's Office are warning the public this morning about door to door sales tactics. Door to door sales companies usually arrive in Central Oregon in the spring and summer. Aand at this time, law enforcement gets a lot of complaints and calls about what the public rights are when confronted with these aggressive sales tactics. Remember: a legitimate sale person will immediately provide to you: their identification, the purpose of the call, a simple description of goods or services offered and they must ask you if you are interested in hearing their sales presentation. If you indicate "no" then the sales person must discontinue. Click here for a website from the Department of Justice where you can file a complaint.


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Yaaa Yaa, I know Lubber is doing that video thing again!
This one has been around for a while but I still think it's cool...
Friday, June 02, 2006
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"It is of great use to the sailor to know the length of his line, though he cannot with it fathom all the depths of the ocean." --- John Locke ---


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Visitor's Center and Museum
The Visitor's Center and Museum renovation is complete! Regular operating hours of Tuesday through Saturday 10 a.m. to 4 p.m. will resume after the holiday break on Tuesday, January 3rd!
The Visitor's Center is located at the top of the first gravel driveway, overlooking the site grounds. This facility is wheelchair accessible with an access ramp adjacent to the paved designated parking.
Museum Exhibit:
The 800 square-foot museum exhibit highlights Arcadia's unique story by exploring the historical and archaeological aspects of the site through interpretive panels and artifacts on display.
Museum Store:
The exhibit space includes a museum store that is a wonderful source of books and gifts relating to local history and culture.
The classroom is used as an educational station for scheduled tours, lecture and program facility, and as a meeting room available for local non-profit organizations and groups. If you are interested in using the classroom as a meeting space, please contact the Education Staff at 850-626-3084 or firstname.lastname@example.com.
Restroom Facilities:
Accessible restrooms and a water fountain are available inside the Visitor's Center, which is the only location on site for such facilities.
Administrative Offices:
The administrative offices of the site manager and museum educator are also located inside the Visitor's Center.
Little Free Library:
The Visitor's Center porch features a Little Free Library, Charter #35132, built by a local Pensacolian. Visitors of all ages are encouraged to participate through the motto, "Take a Book, Return a Book."
Guests are encouraged to stop by the Visitor's Center to view the museum exhibit; pick up our brochure with a site map; obtain information about other local destinations; and request a guided tour, if desired. Free guided tours are available Tuesday through Saturday during business hours, with the last tour leaving at 3:15 p.m. The Visitor's Center also features a wide porch with rocking chairs, so stop by for a while!


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Nurse leads UConn to 94-64 rout of Syracuse as streak runs to 109
The Hartford Courant — By Paul Doyle The Hartford CourantMarch 20-- STORRS, Conn.-She pumped her first or raised her arms or unleashed a primal scream, bouncing back on defense after a series of long-range jump shots.
Kia Nurse could not miss and she could not hide the joy. As the first half was ending Monday night, the UConn junior guard was grinning after dropping 3-pointers on consecutive possessions.
The best backcourt in the country? The UConn guards were reminded that Syracuse's guards were on record as declaring that about themselves this season.
But in a second round meeting in the NCAA Tournament, it wasn't close. Nurse was the best backcourt player on the Gampel Pavilion floor.
Nurse had 29 points, including 26 in the first half, to propel UConn to the Sweet 16 with 94-64 victory of Syracuse in front of a raucous crowd at Gampel Monday night.
The Huskies (34-0) won their 109th consecutive game and advanced to the regional semifinals for the 24th consecutive season. UConn will play at Webster Bank Arena in Bridgeport, Conn., on Saturday.
And UConn is four wins away from its 12th NCAA title and fifth in a row.
Nurse has been part of the past two titles as a starter. As UConn's most seasoned player entering the season, she figured to play a prominent role for a young team.
But as the games get more meaningful, Nurse is emerging a force. She had 24 points and was 6-for-7 on 3-pointers in a win over Albany in the first round.
Against Syracuse and its ballyhooed backcourt, Nurse was unstoppable. As UConn ran to a 57-29 first-half lead, she converted 8-of-10 3-point attempts and displayed unbridled excitement as one shot after another landed in the net.
UConn has productive inside scorers and the Huskies were getting points in the paint (20 in the first half) as Gabby Williams scored 15 points. But the Orange (22-11) were allowing Nurse to roam free on the arc and she was responding with baskets.
Syracuse guard Alexis Peterson had 16 points in the first half and finished with 25. Backcourt mate Brittney Sykes scored 15.
Neither was nearly as good as Nurse. Her ninth three-pointer came in the third quarter and tied an NCAA Tournament record for 3-pointers in a game, matching Purdue's Courtney Moses (2012).
When she connected on No. 9 from the left corner, she smiled and flapped her hands as if they were wings. She seemed almost bewildered by her night.
Nurse was averaging 12.6 points before Monday and was often the team's third scoring option behind Katie Lou Samuelson, Napheesa Collier and Williams. But after starting the season as an erratic outside shooter, she steadily evolved into a reliable 3-point threat.
Perhaps inspired by the challenge of facing a boastful pair of guards, Nurse became the go-to scorer for UConn. At least while the Huskies ran away in the first half.
As the third quarter ended, she lined up for yet another three-point attempt. Instead of shooting, she tossed the ball into the paint. Collier gathered the pass and converted a layup just before the buzzer.
Geno Auriemma raised both fists to the air as the quarter expired. It was UConn's 30th assist on its 31st basket.
Williams and Samuelson had 23 points each. Williams was 10-for-13 from the floor with six rebounds and five assists, Samuelson 11-for-13 from the free throw line with five rebounds and four assists. Collier added 17 points and seven rebounds.
Nurse also had six assists and Saniya Chong seven.
(c)2017 The Hartford Courant (Hartford, Conn.)
Visit The Hartford Courant (Hartford, Conn.) at www.courant.com
Distributed by Tribune Content Agency, LLC.


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Curiosity is perfectly natural, but don't let it make you a bystander. We invite you to come and participate fully in your first class as a 100% free trial. You'll receive a special visitor's packet after class which will include a Kindermusik instrument for your child to take home, and we'd be thrilled to have you enroll right there on the spot—or at home, after you've given it some thought.
The free class offer is valid for all new-to-Kindermusik families, and is available for any one of our weekly classes. (Not the playdates, because of the goodies we give out—click here for more info.)
To request a free trial class, fill out the form below, and someone will get back to you within 24 hours.
You're never a stranger at Kindermusik, but we completely understand those first-timer questions. What's it like? Will my child enjoy it? What exactly goes on in the 40 minutes of class?
We are located at


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ミクリッツ病と全身性IgG4関連疾患 : 当科における systemic IgG4-related plasmacytic syndrome (SIPS) 40例の臨床的検討から Mikulicz's disease and systemic IgG4-related plasmacytic syndrome (SIPS)
ミクリッツ病は涙腺・唾液腺腫脹を,自己免疫性膵炎は膵のびまん性腫脹を呈し,ともに腺組織中へのIgG4陽性形質細胞浸潤を特徴とする疾患である.私たちは,当科における全身性IgG4関連疾患(systemic IgG4-related plasmacytic syndrome ; SIPS)40例の臨床的特徴(腺分泌機能,血清学的評価,合併症,治療および予後)を解析した.男性は11例,女性は29例で,診断時の平均年齢は58.9歳であった.疾患の内訳は,ミクリッツ病33例,キュッツナー腫瘍3例,IgG4関連涙腺炎4例であった.涙腺・唾液腺分泌低下は,約6割の症例にみられたが,軽度であった.抗核抗体陽性率は15%,抗SS-A抗体陽性は1例のみ,低補体血症は30%に認められた.また自己免疫性膵炎,間質性腎炎,後腹膜線維症,前立腺炎などの合併を認めた.治療は,臓器障害を有する症例で治療開始時のステロイド量が多く,観察期間は最長16年のうち,臓器障害の有無に関わらず3例で再燃を認めた.ミクリッツ病をはじめとするSIPSの現時点における問題点と今後の展望について述べてみたい.

Mikulicz's disease represents persistent enlargement of the lacrimal and salivary glands, and autoimmune pancreatitis is shown with diffuse pancreatic swelling. Both diseases are characterized with elevated IgG4 concentrations in the serum and prominent infiltration by plasmacytes expressing IgG4 in the glands. Clinical analyses were performed in 40 patients with systemic IgG4-related plasmacytic syndrome (SIPS) who consulted the doctors in Sapporo Medical University Hospital. Our patients were mainly middle-aged or elderly females. The average age was 58.9 years. The diagnosis was following ; 33 cases with Mikulicz's disease, 3 cases with Küttner's tumor, and 4 cases with IgG4-related dacryoadenitis. Slight dysfunction of lacrimal and salivary gland was observed in about 60% of them. Antinuclear antibodies were detected in only 15% of the cases with SIPS. Almost all, except one case, did not have anti-SS-A or anti-SS-B antibodies. Interestingly, hypocomplementemia was revealed in 30% of them. The complications of SIPS include autoimmune pancreatitis, tubulointerstitial nephritis, retroperitoneal fibrosis, prostatitis, and so on. SIPS is mainly treated by the administration of steroids. We started to prescribe much quantity of prednisolone to the patients with organ failure. The recurrence was admitted in the 3 patients for the followed 16 years. We present here the problems and prospects in SIPS.

- 日本臨床免疫学会会誌 = Japanese journal of clinical immunology
日本臨床免疫学会会誌 = Japanese journal of clinical immunology 31(1), 1-8, 2008-02-28
The Japan Society for Clinical Immunology


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Industrial hygiene equipment and technologies in Nevada
Found: 122 products← Back to category "Industrial ecological equipment"
Place of washing of footwear. Brush, the dosed water supply
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Place of washing of footwear. Brush, the dosed water supply. Material - stainless steel. The purpose of creation of the company - release of the high-quality equipment in the market of Ukraine. Quali Read more
Verified partner for over 8 years
Delivery to Nevada from
UkraineThis company replies on the enquiry during 24 hours
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Vacuum cleaner
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Pilosos 449 The system to start-up for p_dklyuchennya elektro_nstrument potuzhn_styu to 2000 W is automaticFor vology that dry pribirannyaZsistema f_ltrats і ї: paperoviya m_shechok-f_ltr, dvosharovi Read more
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SRF 100/2000 noise suppressor
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You can buy goods SRF 100/2000 Noise suppressor here!Application The noise suppressor is applied to absorption of the noise arising during the work of the ventilating equipment and extending on air du Read more
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DeWalt DC500 2 Gallon Cordless or Corded Wet/Dry Vacuum
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Brand: DeWALT. Description: Dewalt DC500 Specifications: • Tank Size: 2 Gallons • Hose Diameter: 1-1/4" • Hose Length: 5' • Voltage (DC Operation): 12-18 V • Blower Read more
USA, Las Vegas
Bun Warmer Bidet
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Quick Overview Buy any Biffy bidet and receive the second Biffy at 1/2 off the original price. Plus enjoy FREE shipping too! Choose between the *New CHROME metal Biffy. It's Smooth, Beauti Read more
USA, Boulder City
Industrial hygiene equipment and technologies in other regions
Trading platform Allbiz offers to see the catalog Industrial hygiene equipment and technologies which contains 122 products offers from 2 companies and enterprises. Don't know what Industrial hygiene equipment and technologies to buy? You can clarify the specifications, see photos Industrial hygiene equipment and technologies and choose the best seller and supplier. Buy Industrial hygiene equipment and technologies trough online ! On Allbiz — You can just place your order right on the site.