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Incessant Fed flip-flopping from hawkish to dovish (6x in 8 months!?) is simply insane. What will they do at Wednesday's FOMC meeting? Tell us what you think by casting your vote in our Poll of the Day here.
In this excerpt from The Macro Show, Hedgeye Internet & Media analyst Hesham Shaaban lays out our Best Idea Long call on Expedia and why the company's HomeAway acquisition is a "considerable opportunity" relative to Wall Street's expectations.
(Don't worry. We don't bite)
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Takeaway: After hitting a post-recession high, S&P 500 company share buybacks fell -6.8% y-o-y in the second quarter.
is the tide turning?
Consider this. After hitting a post-recession high in 2Q16, FactSet reports today that S&P 500 buyback activity tumbled -6.8% year-over-year in 2Q16.
Here's the key excerpt and chart from the FactSet data:
"Companies in the S&P 500 spent $125.1 billion on share buybacks during the second quarter, which marked the smallest quarterly total since Q3 2013. This comes after a first quarter that saw buybacks for the index hit a new post-recession high. Aggregate buybacks in Q2 represented a 6.8% decline from the year-ago quarter, which was the largest year-over-year decrease since Q1 2015. This Q2 decline came during a quarter that saw the S&P 500 index hit record-high price levels. On a trailing twelve-month basis, shareholder buybacks amounted to $592.9 billion at the end of the second quarter. This was a 6.8% increase from the same time period a year ago. The TTM buyback total at the end of Q2 marked the fourth largest amount going back to the start of 2005, despite this quarter's decline."
This dour question mark is a far cry from the headlines we saw just two months ago when the buyback boom was cited as justification for why the S&P 500 was hitting all-time highs. Indeed, as the Wall Street Journal wrote, "There's No Need To Fear the Buyback-Boosted Stock Market."
We advised otherwise, here. (Note: The S&P 500 is down -0.9% since then.)
***To understand why we think buybacks, corporate profits, consumer confidence, the labor market etc, etc, etc, are all past peak and U.S. growth continues to slow, watch this 6-second animated clip Hedgeye CEO Keith McCullough in "An Animated History of U.S. #GrowthSlowing" below.
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Takeaway: The BOJ is monetizing over half of annual JGB issuance but has still failed to energize economic growth.
Editor's Note: Below is an excerpt from a research note written by Hedgeye Senior Macro analyst Darius Dale. To access our institutional research email email@example.com.
That Japan's failure to launch
...is occurring at a time when the Bank of Japan (BoJ) is expanding its balance sheet at a near +25% annual clip speaks volumes about the inefficacy of the BoJ's existing monetary easing platform.
And while market participants have yet to defend critical ratios with respect to the size of the BoJ's balance sheet or the pace of its accumulation of JGBs, the seemingly egregious nature of both is worth flagging.
- The BoJ's balance sheet is nearly three times the size of the next closest G4 counterpart when adjusted for the size of the respective economies.
- When assessed as a ratio to total nonfinancial sector credit (a good proxy to evaluate where LSAP programs may face frictional resistance), the BoJ's balance sheet is twice the size of the next closest G4 counterpart.
- Prior to the start of Abenomics, the BoJ was a fairly distant third with respect to JGB ownership at 12% of the float. It's now far and away the #1 holder at 33.9% of the total. Monetizing over half of annual JGB issuance has a tendency to do that for you.
All told, the purpose of this note isn't to speculate on what the BoJ will or won't do tomorrow. For all I care, Kuroda could tightrope across the towers of the Tokyo Metropolitan Government Building wearing nothing but whitey tightys and I would be largely unfazed.
While there's no doubt the BoJ has the potential to shock global bond markets for a TRADE, there's also no doubt that nothing they do tomorrow or in the not-too-distant future will outweigh economic gravity in the pricing of interest rates over the long term. How they plan to achieve the aggressive growth and inflation targets as mandated by Abenomics remains well beyond our purview – and likely theirs too (hence the stench of desperation and policy fatigue).
See the forest, not the trees. The central planning #BeliefSystem continues to break down right before your very eyes.
Takeaway: What do you think? Cast your vote. Let us know.
Editor's Note: Below is a complimentary research note written over the weekend by Hedgeye Potomac National Security analyst LTG Dan Christman USA Ret. To access our institutional research email email@example.com.
With Russian foreign minister Sergei Lavrov at his side, Secretary John Kerry a week ago announced a Syrian cease-fire deal that could lead to coordinated U.S.-Russian air operations against Syria-based jihadists; Kerry also posited that the deal could provide an eventual path to a negotiated political settlement to replace the Assad regime in Damascus.
- Unfortunately, based on previous efforts to secure a pause in the fighting alongside Moscow, this will likely prove to be a classic triumph of hope over experience.
- Syria is already on a long path to repeat Europe's 17th Century 30 Years War - one that laid waste to much of what is today's Germany. Syria will never again be the pre-2011 unified state it was before the onset of the current anti-Assad fighting. Sadly, this latest Kerry deal will probably do nothing to alleviate the horrific suffering of the Syrian population or even begin the process of putting the Syrian "Humpty-Dumpty" back together.
Consider the deal itself:
- In its essence, it requires a cease fire, effective last Monday, in which all parties - the Assad government as well as the opposition - stop air and ground attacks; humanitarian corridors would be opened to relieve suffering in the city of Aleppo in particular; and IF the cease fire is effective for seven continuous days, then and only then would the US and Russia work to establish a Joint Implementation Center (JIC) to coordinate air attacks against ISIS and the principal al Qaeda affiliate in the area, "Syria Conquest" (formerly al Nusra).
- But who seriously believes that the dozens of opposition groups battling Assad (many closely intertwined with Syria Conquest) or the Damascus regime will adhere to this? The "support" for the deal from Russia, Iran, Damascus, and Hezbollah is beyond cynical. Because of "facts on the ground," each now holds the military advantage; there's no incentive for them to change anything.
- Numerous cease fire violations of the accord this week have confirmed the worst; yet, so far, the deal has gotten off the ground – but barely; sadly, like the "cessation of hostilities" accord from last February, an agonizing death for this deal probably awaits.
Many have talked about what might be needed to change the "facts on the ground" in Syria. Here's one answer:
- First, because nearly all of the civilian casualties in major population centers like Aleppo, Homs, and Hama - and the refugees flows from these areas - are caused by barrel bombs, cluster bombs, and chlorine gas dropped from Syrian aircraft and helicopters, Washington needs to bluntly warn Assad, in simplest terms: "NO More!"
- Then, if Assad uses those systems, after a one hour notice to the Russians (the notice they gave us before they launched their first air combat sorties in Syria), the U.S. should send cruise missiles, drones, rockets, and stealth aircraft to target every Syrian fixed wing asset, every helicopter, and all of Assad's personal aircraft. If a restrike is necessary after a bomb damage assessment (BDA), we should execute it immediately.
- The U.S. should then say to Assad, "Don't do this again." This becomes a "no-fly" zone, but vigorously enforced from the outset.
- The Russians would howl; but Washington would have their attention, and in the end, their cooperation.
The U.S. is currently not a country that believes in changing "facts on the ground" in the Middle East, even "facts" that have produced over 400,000, largely civilian, deaths. But an action like the one outlined above may be about the only way to get the attention - and the respect - of Vladimir Putin. And it can also help move us to the ultimate goal: a political solution in this fractured country - one that is the only way to end the Syrian version of Europe's 30 Years War.
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Bios are funny aren't they? I feel like names are irrelevant too. But if you'd like to indulge in my fractal experience of life, I'm a cliche California girl. But I'm no poser. I actually rip in the ocean, own a Jeep Cherokee named Old Blue, and am currently becoming a bonafide yoga instructor. So indulge in my musical preference if you like!
Member since Dec 2011
With Love
207 8 27 tracks
CHVRCHES//DIPLO//MARVIN GAYE - I hope this music inspires you to love unconditionally
Ride the Wave.
150 11 20 tracks
TEMPER TRAP//LADYHAWKE//CHROMATICS It's time to shimmy on your surfboard or pretend like you're out ...
Into the Unknown
135 3 23 tracks
TAME IMPALA//PURITY RING//THE XX - Music tends to expound upon current events and emotionally project...
Peeing Your Pants is Cool
201 9 25 tracks
If you possess a golden ticket to Coachella this mix may induce an overactive bladder
Divinity in Everything
154 12 22 tracks
The difference between time and space seems to be slipping away

subset: commoncrawl


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I will do 35 Canada and USA local citation for your business
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Go Radio Comes to an End
rip in peace
Mayday Parade is way better anyways
I wouldn't say way better. Go Radio's 2 LP's were really good.
Too bad. They released some great tunes.
Digging: Emilie Nicolas - Like I'm a Warrior
Mayday Parade is way better anyways
maybe when Lancaster was in it
Nah. Mp is/was better by their 3rd LP.
Bummer, they were pretty good
though I think I know a few friends of mine that are going to be especially crushed by this news
Digging: Ulcerate - Everything Is Fire
Too bad. I Enjoyed Lucky Street by these guys, never listened to their latest.
Sucks, especially since the last Mayday Parade record wasn't too good.
its a shame, their first LP was pretty great. but true mayday parade is better anyway
Mayday started going downhill for me after Lancaster left, was rather happy when he started Go Radio and most of their songs were pretty neat. Their last release wasn't that great, but Lucky Street featured, like stated before, some pretty good material.
Digging: Push Over - Demo
rip im sad godammit
It's a shame, cause new mayday parade blows
wel im gonna love new mayday parade regardless because i love mayday parade but lucky street was some next level shit
New mayday is great
I saw them live once. Had no idea the guy from Mayday Parade was in it until now.
Really shocked Andcas didn't report this but then again he's probably gunning for the latest hot piece of juicy TNZ gossip.
Digging: Fishtank Ensemble - Woman in Sin
I don't I just get my kicks in Andcasing everything that seems Andcasable.
Close The Distance doesn't get enough love on this site. Also that Adele cover they did was great too.
• Michael Gira Accused of Rape• R.I.P. David Bowie• R.I.P. Lemmy• The Story So Far's vocalist dropk..• Scott Weiland dead at 48 • Brand new Brand New Single• Killswitch Engage debut new single• Rush drummer retires• Deftones stream new single• Riverside guitarist dies
• Doomocracy post new song• Crystal Fairy stream debut LP• Epic leaves Crazy Town• New All Time Low Song• Volumes promote new single, album• New Demon Hunter video• Incubus Share New Track• Emmure premiere new single, video• No Lives Matter to Body Count• 2017 Applications Open• New Once Human video• Benighted Stream New Album• Echo Tail is Building a Myth• Sorority Noise drop 2nd single• Papa Roach release new song» see all news
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Suggestive, but not conclusive, studies implicate many genetic variants in oral cleft etiology. We used a large, ethnically homogenous study population to test whether reported associations between nonsyndromic oral clefts and 12 genes (CLPTM1, CRISPLD2, FGFR2, GABRB3, GLI2, IRF6, PTCH1, RARA, RYK, SATB2, SUMO1, TGFA) could be confirmed.
Thirty-one single nucleotide polymorphisms (SNPs) in exons, splice sites, and conserved non-coding regions were studied in 509 patients with cleft lip with or without cleft palate (CLP), 383 with cleft palate only (CP), 838 mothers and 719 fathers of patients with oral clefts, and 902 controls from Ireland. Case-control and family-based statistical tests were performed using isolated oral clefts for the main analyses.
In case-control comparisons, the minor allele of PTCH1 A562A (rs2066836) was associated with reduced odds of CLP (OR: 0.29, 95% CI: 0.13–0.64 for homozygotes) whereas the minor allele of PTCH1 L1315P (rs357564) was associated with increased odds of CLP (OR: 1.36, 95% CI: 1.07–1.74 for heterozygotes and OR: 1.56, 95% CI: 1.09–2.24 for homozygotes). The minor allele of one SUMO1 SNP, rs3769817 located in intron 2, was associated with increased odds of CP (OR: 1.45, 95% CI: 1.06–1.99 for heterozygotes). Transmission disequilibrium was observed for the minor allele of TGFA V159V (rs2166975) which was over-transmitted to CP cases (P=0.041).
For 10 of the 12 genes, this is the largest candidate gene study of nonsyndromic oral clefts to date. The findings provide further evidence that PTCH1, SUMO1, and TGFA contribute to nonsyndromic oral clefts.
Oral clefts are among the most common birth defects. Population-based estimates of the prevalence of nonsyndromic cleft lip with or without cleft palate (CLP) and cleft palate only (CP) are 4–13/10,000 births and 2–5/10,000 births, respectively, with worldwide estimates varying by ethnicity and geographic region (Hashmi et al., 2005). Research suggests that multiple genes are involved in oral clefts etiology (Schliekelman and Slatkin, 2002) and that various signaling pathways are important in lip and palate development (Marazita and Mooney, 2004), but the specific genes in these pathways that play a role in causing oral clefts in humans remain unknown. There have been consistent findings of an association with nonsyndromic oral clefts for only one gene, interferon regulatory factor 6 (IRF6), however this gene does not account for the majority of the genetic contribution to nonsyndromic oral clefts and more genes remain to be identified. Studies using a variety of approaches have produced inconclusive or conflicting results, possibly because of inadequate power and population diversity. To address these limitations we have assembled a large, ethnically homogenous study population in Ireland to examine genetic risk factors for oral clefts. The intent of the current study was to follow-up on previously published reports of genes examined for an association with oral clefts in humans and to confirm whether an association was present in an independent study population. Therefore, we performed case-control and trio-based analyses to examine whether selected SNPs in genes that were previously suggested to be risk factors for oral clefts were associated with nonsyndromic CLP and CP.
Study subject enrollment and data collection have been described in detail previously (Mills et al., 2008). Subjects with CLP or CP were identified by one of two methods. First, patients at the Dublin Cleft Centre which treats most patients with oral clefts (80%) in Ireland, were recruited. The attending surgeons examined all patients, reported a diagnosis of CLP or CP, and confirmed the presence or absence of other birth defects. Second, patients were identified through membership in the Cleft Lip and Palate Association of Ireland, a patient support group. Medical record data on the diagnosis of oral clefts were available for 87% of all patients. Recruited case-parent trios gave either blood or buccal samples. Study participants, or in the case of minors, their parents, provided written informed consent. The Research Ethics Committees of the Health Research Board of Ireland, the participating hospitals, and the Institutional Review Board of the National Human Genome Research Institute gave ethical approval for the study.
Blood samples had previously been collected from 56,049 pregnant women who had attended any of the three main maternity hospitals in Dublin between 1986 and 1990. These hospitals deliver approximately 90% of Dublin births and about one-third of all Irish births occur in Dublin. Controls were a random sample (N=926) from this group. Women were not eligible to be controls if they had delivered a child with a known birth defect or if they had previously had a child with a neural tube defect. All the genes selected for this study are located on autosomes and, among the controls, allele frequencies for genes on the autosomes reflect those of the underlying Irish population (Parle-McDermott et al., 2003; Kirke et al., 2004).
We selected 11 candidate genes that have been implicated in previous studies that produced suggestive, but not conclusive, evidence that they were associated with nonsyndromic oral clefts. We attempted to focus on genes that did not have a large body of published literature concerning their association with oral clefts as well as genes with previous controversial findings related to oral clefts. Genes were chosen if there were a) any reports of mutations or chromosomal breakage within the gene in patients with oral clefts; b) expression or gene-knockout data from animal studies linking the gene to oral clefts; or c) previous conflicting reports concerning their associations with oral clefts. Also, either the gene or the chromosomal region in which it is located had to have been examined in at least one human study. The selected genes were cleft lip and palate associated transmembrane protein 1 (CLPTM1), cysteine-rich secretory protein LCCL domain containing 2 (CRISPLD2), fibroblast growth factor receptor 2 (FGFR2), gamma-aminobutyric acid A receptor, beta 3 (GABRB3), GLI-Kruppel family member GLI2 (GLI2), patched homolog 1 (Drosophila) (PTCH1), retinoic acid receptor alpha (RARA), RYK receptor-like tyrosine kinase (RYK), SATB homeobox 2 (SATB2), SMT3 suppressor of mif two 3 homolog 1 (Saccharomyces cerevisiae) (SUMO1), and transforming growth factor alpha (TGFA). In addition to the 11 genes, IRF6 was also included in this study to investigate gene-gene interactions and because the gene has not been examined in the Irish population.
SNPs were selected for study based on published reports and/or their locations in the genes. Our aim was to target SNPs that might affect function rather than to SNP-tag or examine all the SNPs within these genes. Thirty-one SNPs were selected located in exons, splice sites, or conserved non-coding regions, locations in which nucleotide changes could have functional consequences. SNPs in conserved regions were identified from multi-species alignments of DNA sequences using the University of California at Santa Cruz Genome Browser (http://genome.ucsc.edu/).
Genomic DNA was extracted from blood or buccal samples using a QIAamp DNA Blood Mini Kit (Qiagen, Sussex, UK). KBiosciences (Herts, United Kingdom) performed SNP genotyping using a competitive allele-specific PCR genotyping system. Quality control measures included the use of blank wells, the repetition of one human DNA sample across multiple plates, and repeat genotyping for approximately 4% of study subjects. Fifteen of the 31 SNPs were called successfully >95% of the time, 14 were called successfully 93–95% of the time, and the remaining two SNPs, CRISPLD2 S105G (rs12051468) and SATB2 Intron 9 T>G (rs4675475), were called successfully 91% and 90% of the time, respectively. Tests of Hardy-Weinberg Equilibrium (HWE) were carried out for all SNPs (independently for cases, case-mothers, case-fathers, and controls). The level of agreement for repeat genotyping was >96% for all SNPs.
Of the 1,088 cases recruited, 196 were excluded from analyses for the following reasons (number of cases in parenthesis): maternal diabetes (5), maternal epilepsy (12), maternal teratogenic drug exposure (27), chromosomal abnormalities (9), known syndromes (49), type of cleft could not be classified (3), possible non-Mendelian inheritance (8), having two or more SNPs with discordant results upon repeat genotyping (1), and samples could not be genotyped (82). Among the 926 controls, two that had two or more SNPs with discordant results upon repeat genotyping and 22 that had samples that could not be genotyped were excluded from the analysis.
Patients with isolated oral clefts (absence of other non-cleft defects) were used for the main analysis and were categorized into isolated CLP and isolated CP case groups. We also divided the CLP case group into cleft lip only and cleft lip with cleft palate, and performed separate analyses for these subgroups, because epidemiological and molecular data indicate that these could be distinct conditions (Harville et al., 2005; Rahimov et al., 2008; Genisca et al., 2009). Analyses were repeated adding cases with multiple defects (presence of other non-cleft defects) to determine if they influenced the results. Tests of HWE were performed using a chi-squared test for genotype proportions. Allele frequencies were compared between cases and controls using a chi-squared test. Case-control comparisons of genotype frequency were performed using logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for each SNP. Effect estimates were reported separately for being heterozygous and homozygous for the minor allele, with homozygosity for the major allele as the reference category. We also used the multiplicative disease model in logistic regression analyses to generate P-values for the overall effect of minor allele copy number on the association. The transmission disequilibrium test (TDT) was used to assess allele transmission distortion among case-parent trios. Adjustment for multiple comparisons was done using permutation (N=99,999), separately by gene, because the associations between oral clefts and each gene were considered to be distinct a priori hypotheses derived from the literature. Multivariate permuting of the trios for the TDT was performed by treating the test as a one-sample test, and permuting the allele of interest. Permutations of cases and controls were independent of permutations of trios, and the results combined by Bonferroni adjustment so that the resulting adjusted P-values accounted for all comparisons on that gene while controlling the probability of any false-positives (family-wise error rate). Gene-gene interactions were examined between IRF6 SNPs and those in genes associated with oral clefts in individual analyses. A disease inheritance model for each SNP was estimated from the OR and 95% CI for heterozygotes and homozygotes in individual analyses and was then used in logistic regression analysis to test gene-gene interaction.
Measures of linkage disequilibrium (LD) were estimated using Haploview (http://www.broad.mit.edu/mpg/haploview/) (Barrett et al., 2005). LD measures were based on genotypes of control samples (N=902) from this study or publicly available data (www.hapmap.org) as indicated in Results and discussion.
There were 892 cases (765 of them isolated), 838 case-mothers, 719 case-fathers, and 902 controls included in the analysis (Table 1). The birth year of the cases ranged from 1931–2004. The proportion of case-mothers who reported smoking and alcohol use during the affected pregnancy was 38% and 55%, respectively. There was a positive family history of oral clefts among first-degree relatives for 7.5% (67/892) of cases.
The selected SNPs and their minor allele frequencies among controls and patients with isolated CLP or CP are presented in Table 2. Genotype distributions among study groups were in HWE with one exception: PTCH1 N555N (rs1805155) among controls (P=9×10−14). This could have been due to genotyping error; therefore, we did not report any results for this SNP. Quality control results indicated that genotyping was performed satisfactorily on the other two PTCH1 SNPs.
Case-control comparisons of genotype frequency indicated statistically significant associations between PTCH1 SNPs and CLP (Table 3). The PTCH1 A562A (rs2066836) minor allele was associated with reduced odds of CLP among homozygotes (OR: 0.29, 95% CI: 0.13–0.64; corrected P=0.038) which is equivalent to the major allele increasing the odds of CLP (OR: 3.51, 95% CI: 1.56–7.87). The PTCH1 P1315L (rs357564) minor allele was associated with increased odds of CLP (OR: 1.36, 95% CI: 1.07–1.74 for heterozygotes and OR: 1.56, 95% CI: 1.09–2.24 for homozygotes; corrected P=0.023). There was little linkage disequilibrium between these two PTCH1 SNPs (r2 = 0.10). The minor allele of the SUMO1 intron 2 G>A SNP (rs3769817) was associated with increased odds of CP among heterozygotes (OR: 1.45, 95% CI: 1.06–1.99; corrected P=0.038) but among homozygotes the confidence interval included the null (OR: 1.62, 95% CI: 0.65–4.03) (Table 4). The minor allele of the other SUMO1 SNP tested (intron 1 G>A, rs12470401) had a similar OR estimate for CP that was of borderline significance (OR = 1.44, 95% CI = 1.05–1.97 for heterozygotes; corrected P=0.056); it was in strong LD (r2= 0.98) with rs3769817. Based on the TDT, there was no transmission distortion of PTCH1 SNPs to CLP cases or of SUMO1 SNPs to CP cases (Table 4). TDT results indicated that the TGFA V159V (rs2166975) minor allele was over-transmitted to CP cases (corrected P=0.041) (Table 4). SNPs in the other nine genes were not associated with CLP or CP. When the CLP case group was divided into isolated cleft lip only and isolated cleft lip with cleft palate, the only statistically significant finding was for the association of the PTCH1 P1315L (rs357564) minor allele with cleft lip and palate in case-control comparisons (OR = 1.67, 95% CI = 1.13–2.49 for homozygotes; corrected P=0.040) (Table 5). Repeating the analyses after adding patients with multiple birth defects to the case groups produced no important changes in the results. The numbers of cases and controls in Table 1 are different to those in Table 3 due to the numbers of subjects with genotype data available. IRF6 S153S (rs2013162) was used in tests of gene-gene interaction because it was the only IRF6 SNP to show an association with CLP, based on its uncorrected P-value (P=0.046). There was no evidence of gene-gene interaction between this SNP and those in PTCH1, SUMO1, and TGFA.
In a large, ethnically homogenous study population, we tested 12 genes that previously were suggested to be risk factors for oral clefts and found that SNPs in three genes had statistically significant associations with oral clefts, after adjusting for multiple comparisons. PTCH1 A562A (rs2066836) and P1315L (rs357564) were associated with CLP while a SUMO1 non-coding SNP (rs3769817) and TGFA V159V (rs2166975) were associated with CP. When the cleft lip only and cleft lip with cleft palate subgroups were examined separately, it was found that PTCH1 P1315L was associated with cleft lip with cleft palate.
PTCH1 is a receptor for sonic hedgehog (SHH), an important regulator of craniofacial morphogenesis and an etiologic factor in holoprosencephaly, a phenotype that often includes oral clefts (Cohen Jr., 2006). PTCH1 mutations have been identified in patients with holoprosencephaly, some with oral clefts (Ming et al., 2002). PTCH1 mutations also cause nevoid basal cell carcinoma syndrome, a condition in which approximately 3–5% of affected patients have oral clefts (Kimonis et al., 1997), a prevalence that is 30–50 times greater than in the general population. A study of CLP and CP cases combined observed that PTCH1 P1315L (rs357564) was associated with nonsyndromic oral clefts in Caucasians (71 cases, 66 controls) but not in Filipinos (84 cases, 414 controls) (Mansilla et al., 2006). PTCH1 A562A (rs2066836) was not tested in that study but based on analyses in 220 Filipino families it also found an association between oral clefts and a haplotype composed of two PTCH1 SNPs, C89T (rs2297088) and T86C (rs2236407), that was of borderline significance. The larger sample size in the current study permitted separate analyses to be conducted for CLP and CP and the results confirmed the association of CLP with PTCH1 P1315L observed previously among Caucasians.
Reports of SUMO1 haploinsufficiency (Alkuraya et al., 2006) and deletion (Shi et al., 2009) in patients with oral clefts implicate this gene in nonsyndromic oral clefts. SUMO1 participates in the post-translational modification of many target proteins including the products of genes with evidence of a role in oral clefts in humans: msh homeobox1 (MSX1) (Lee et al., 2006); SATB2 (Dobreva et al., 2003); T-box 22 (TBX22) (Andreou et al., 2007); and tumor protein 63 (TP63) (Ghioni et al., 2005). A study of 181 cases and 162 controls from China that examined four SUMO1 SNPs found an association with CLP for one haplotype but not for any individual SNPs (Song et al., 2008). HapMap data from a Caucasian population shows that one of the haplotype SNPs from that study (rs6761131) is in perfect LD (D′ = r2 = 1) with the two SUMO1 SNPs that we tested.
A number of studies have examined whether TGFA polymorphisms are related to oral clefts in humans but have produced conflicting results. However, these studies varied according to the type of study population, study design, sample size, and TGFA variants used (Vieira, 2006). The authors of a meta-analysis stated that the evidence concerning TGFA polymorphisms and oral clefts was inconclusive, and suggested that the different study outcomes could be due to variations in the clinical characteristics of cases and in the proportion of cases with a positive family history (Mitchell, 1997). TGFA V159V (rs2166975) was associated with CP in a study of 94 CLP trios and 18 CP trios from Lithuania (Morkuniene et al., 2007). The association with CP was confirmed by the current study in which the analysis was based on a larger sample size from another European population: 133 informative CP trios. Based on HapMap data for Caucasians, TGFA V159V was not in strong LD with two TGFA variants that have previously been examined for an association with oral clefts: the BamHI polymorphism (rs11466297; r2 = 0.253) and the T3851C polymorphism of Marker H2A (rs11466285; r2 = 0.021). Other TGFA variants that have been examined in studies of oral clefts, including the TaqI polymorphism, were not found in the HapMap database.
The V274I (rs2235371) variant and other SNPs in IRF6 have been shown to be associated with nonsyndromic CLP, and although the European populations studied were rarely polymorphic for V274I, there was a suggestive positive association between the V allele and CLP in these populations (Zucchero et al., 2004). Less than 3% of our study population had the I allele of the V274I variant, resulting in too few informative subjects. IRF6 S153S (rs2013162) has also been associated with nonsyndromic CLP in previous reports (Scapoli et al., 2005). In our study, case-control and TDT association tests for IRF6 S153S produced uncorrected P-values <0.05 for isolated CLP; however, the results were not statistically significant after adjustment for multiple comparisons. HapMap data for Caucasians indicated that the four IRF6 SNPs we tested were not in strong LD with IRF6 rs642961 (rs2235371, r2 = 0.014; rs2013162, r2 = 0.203; rs7552506, r2 = 0.171; rs2235377, r2 = 0.010), a common polymorphism (minor allele frequency in Europeans = 0.25) which is associated with cleft lip only and cleft lip with cleft palate in Europeans (Rahimov et al., 2008).
Previous reports have implicated a role in oral clefts for the other eight genes that we tested: CLPTM1 (Yoshiura et al., 1998); CRISPLD2 (Chiquet et al., 2007); FGFR2 (Riley et al., 2007); GABRB3 (Scapoli et al., 2002; Inoue et al., 2008; Vieira et al., 2008); GLI2 (Roessler et al., 2003); RARA (Chenevix-Trench et al., 1992; Maestri et al., 1997); RYK (Watanabe et al., 2006); and SATB2 (Fitzpatrick et al., 2003; Beaty et al., 2006). In contrast, several studies did not find strong evidence of an association between oral clefts and variants in some of these genes. A study of Japanese patients found no association between CLPTM1 and oral clefts (Ichikawa et al., 2006). Two FGFR2 SNPs showed no association with nonsyndromic CLP in 294 Filipino families (Riley et al., 2007). There was only a suggestive association between GABRB3 SNPs and CP for patients from Iowa (Vieira et al., 2008) and between SATB2 variants and oral clefts based on another Iowa study population (Vieira et al., 2005). Some studies observed no association between RARA polymorphisms and oral clefts (Kanno et al., 2002; Mitchell et al., 2003). Most of these findings were reported after adjustment for multiple comparisons and it is possible that some true positive associations became statistically non-significant in an attempt to reduce false-positive reports. We found no evidence of an association with oral clefts among the SNPs that we selected for testing in these eight genes however other variants in these genes should be examined for a possible role in oral clefts.
With the exception of CRISPLD2, the genes we selected were also included in a recent report that examined 357 candidate genes in two European study populations (Jugessur et al., 2009). There were only two SNPs in common between the two studies: IRF6 rs2013162 and RYK rs1131262. Their study found that IRF6 was one of seven genes associated with CLP. The other six genes found to be associated with CLP were not among the genes that we selected. Another recent study that examined SNPs in or near a number of candidate genes found that IRF6 rs2013162 was associated with cleft lip only and that forkhead box E1 (FOXE1) was associated with cleft lip with cleft palate (Marazita et al., 2009). These reports provide further evidence that IRF6 is involved in nonsyndromic oral clefts but, along with the results of our study, also implicate a role for other genes. Other recent reports include the first genome-wide association studies of oral clefts. Two such studies in people with European ancestry found that a SNP in the chromosome 8q24 region (rs987525) is associated with CLP, although the SNP is not located near any known genes (Birnbaum et al., 2009; Grant et al., 2009).
An advantage of our study was the large number of CLP and CP cases and parents available from an ethnically homogenous study population. A limitation of our study was that only one or a few SNPs were tested in each gene. Many haplotype blocks were not examined in the genes we selected because we did not use haplotype-tagging SNPs. Therefore, failure to find an association for SNPs in some of the genes studied does not provide conclusive evidence about whether the genes play a role in oral clefts. Within each gene, we considered whether SNPs in different LD blocks could represent separate a priori hypotheses regarding an association between possible functional effects of the SNP on the gene and oral clefts. Had we adjusted for multiple comparisons separately for SNPs in different LD blocks, without accounting for the other SNPs examined in the same gene, then the only altered finding would be that CRISPLD2 rs4783099 would be associated with cleft lip with cleft palate. We chose to be more conservative when adjusting for multiple comparisons and therefore, within each gene, adjusted for all comparisons performed on the SNPs selected for the gene. This was done to limit the possibility of a false-positive finding in our study. We used a permutation procedure to control the probability of a false-positive association at 5%, separately for each gene. Therefore it was expected that the chance of a Type I error would be small. It is difficult to determine whether our adjustment was over-conservative. Another shortcoming was that most of the SNPs (in PTCH1, SUMO1, TGFA) associated with clefts in this report alter codons but do not result in an amino acid change. However, synonymous changes can have a direct impact on gene function (that is, via splicing, altering translation rates). It is also possible that other variants in these genes are associated with oral clefts and were missed by our study.
Our control group was comprised of women only whereas the case group included both males and females. If the allele frequencies in the control group were not representative of those in the source population that gave rise to the cases then this would produce bias in the results. However, we had no reason to expect that genotype frequencies would differ by sex because the genes we selected were located on autosomes and not sex chromosomes. We compared the case-control and TDT results for SNPs in PTCH1, SUMO1, and TGFA to determine whether the findings based on use of our control group were in agreement with another test of association. The effect estimates for the association between the TGFA SNP (rs2166975) and CP were similar using the case-control and TDT methods, although the result from the case-control method was not statistically significant after adjustment for multiple comparisons. This similarity suggests that the use of our control group did not result in biased estimates of effect.
For 10 of the 12 candidate genes, ours was the largest study to have examined associations between SNPs and nonsyndromic oral clefts. We observed associations with SNPs in PTCH1, SUMO1, and TGFA. PTCH1 A562A (rs2066836) is located in the protein's sterol-sensing domain and P1315L (rs357564) is in the C-terminal domain; both domains are required for transduction of the SHH signal (Johnson et al., 2000; Martin et al., 2001). P1315L alters the third non-conserved amino acid in a motif, PPxY, that is a potential target for Nedd4 ubiquitin ligases, proteins that regulate the trafficking of intracellular cargo (Ingham et al., 2004). Mutation studies of the PPxY motif suggest that it is important for the regulation of PTCH1 turnover (Lu et al., 2006). TGFA V159V (rs2166975) encodes a terminal valine in the TGFA precursor protein and this residue is required for glycosylation leading to mature protein and for TGFA localization to the cell surface (Briley et al., 1997). The work reported here suggests that most of the 31 SNPs we examined do not play a role in oral clefts but that three genes, PTCH1, SUMO1, and TGFA, warrant further investigation as risk factors for oral clefts. We recommend that future research investigates whether the SNPs that showed positive associations with oral clefts in this study actually alter gene function.
This work was supported by the Intramural Research Programs of the National Institutes of Health, Eunice Kennedy Shriver National Institute of Child Health and Human Development and the National Human Genome Research Institute.
The authors gratefully acknowledge the patients and families who participated in the study, the Cleft Lip and Palate Association of Ireland, and the Dublin Cleft Center team.
Presented in poster form at the 22nd annual meeting of the Society for Pediatric and Perinatal Epidemiologic Research, June 22–23, 2009, Anaheim, California.
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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Helping children manage distress in the aftermath of a tragedy
California State PTA offers its condolences and deepest sympathy to the families and school community for the tragic loss today in Newtown, Connecticut. Our hearts go out to all for this terrible loss. At this time of tragedy, children throughout our country may be struggling with their thoughts and feelings about the stories and images and they may turn to adults for help and guidance. PTA has many resources available to assist students, families, schools and PTAs in coping with school violence. Additional resources regarding media exposure and traumatic events may be found online.


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Apartments Stan?i? offers accommodation in Lopar. The air-conditioned unit is 16 km from Baška.
The kitchen is fitted with a dishwasher, an oven and a microwave, as well as a coffee machine. Towels and bed linen are provided in this self-catering accommodation. There is a private bathroom with a bath.
Crikvenica is 38 km from Apartments Stan?i?, while Novalja is 33 km away. The nearest airport is Rijeka Airport, 45 km from the property....
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Smidge & Pinch expanding Powell party store
"It's your party and you don't want to throw it?" Then, head to Smidge & Pinch for cool party supplies. Want to do a Buckeye theme? No problem. How about a farm party with cow balloons?
Theresa Crawford and Sue Nevett started the business in Teresa's basement and then moved to a storefront in Powell. They searched for the best items, bought them in bulk and then packaged goods in smaller lots. Just about every color, pattern and character can be found for a birthday or party day.
A new addition is Celebrations by Smidge & Pinch in space next to the current location. It can hold 30 people for parties which can be planned by Crawford and Nevett or the customer. They also plan to hold cake decorating and craft workshops in the space. Celebrations is expected to open Nov. 1. Dates are available for reservations now at this Powell party destination at 343 W. Olentangy St. Click on the slideshow to see the store's fun party supplies. Click here to visit the company's website.


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The Ways You Unwind After Work
We asked you: What's your favorite way to relax after a hard day at work? 500 of our Facebook fans responded with their routine. Most of you are exhausted and want to just eat then fall into bed while listening to music. Read on to see what everyone else is doing at the end of the day:
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Im confused as to when do waves cancel out and why does it happen. Also, I don't understand what stationary waves are, do they not move since no energy is transferred?? and how can they be demonstrated on string??
Im so confused
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Company Overview of ID Analytics, LLC
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ID Analytics, LLC announced that Peng Leong has joined the company as vice president of finance. He reports directly to CEO Scott Carter and is responsible for managing the company's financial strategy. Leong brings more than 20 years of executive leadership experience in finance, reporting, management consulting and risk analytics to ID Analytics. He joins the company after a successful 11-year career at CoreLogic, where he played a key role as the senior director of finance for its Credit Information and Verification Services business.
ID Analytics announced Eric Lindeen as the new vice president of marketing, reporting directly to ID Analytics CEO Scott Carter. Lindeen is responsible for the company's overall marketing and communications strategy as well as its brand and demand generation program. He will lead strategic marketing efforts to expand market presence and visibility around ID Analytics credit and identity risk solutions. Lindeen brings more than 25 years of marketing and technology experience to his role, with expertise working directly with financial institutions as well as the financial services and lending markets. Prior to joining ID Analytics, he was vice president of solution marketing for Zoot Enterprises, where he helped lenders develop and deploy complex solutions for credit originations.
ID Analytics, LLC announced ID Connect, which helps businesses provide an easy, effective and safe way for consumers to complete the digital enrollment or new account application process. A highly configurable, software-as-a-service solution, ID Connect is designed to help businesses from financial services to telecommunications companies and more, streamline their digital application and enrollment process, ensuring a frictionless consumer experience with two key features, ID Connect Resolution and ID Connect Photo. ID Connect allows businesses to grow safely by increasing conversion rates while verifying the individuals identity and managing against fraud risk.
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Queensland Handwriting Made Easy Book 5
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Not all bras, and other intimate apparel, are machine washable due to delicate fabric, laces and embellishments. Always read the care instructions on the tag inside your garment carefully.
To maintain the condition of your purchase and keep it looking its best, we recommend the following care instructions;
Hand washing – We recommend washing by hand using cold water. This guarantees your lingerie won't become tangled or damaged by a washing machine. Cold water helps the elastic retain its stretch and shape, whereas hot water damages elastic, making it hard to maintain the original shape. Larger cup sizes are also best hand washed as the underwire can be put under stress when machine washed (even if it's in a wash bag).
Wash bags – If you choose to machine wash, place your lingerie in a wash bag and always use a delicate cycle. We recommend hooking your bra together before placing it in the wash bag.
Drying your lingerie – We recommend drying your lingerie in the shade. This prevents it from being stretched or sun bleached. Don't place your lingerie in dryers - exposure to heat may damage them.


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Howitzer, Delta Nove, Major Lingo, The Father Figures, and Cory Branan This Weekend
Sometimes you see a press photo of a band and laugh. Is one guy staring artfully away from the others? Are they pressed against a brick wall? Are they all making the goofy face?
Phoenix-based metal band Howitzer isn't having any of that. Seriously -- look at these guys. They look ready to haul off and kick some ass. We're betting that will be the case at Martini Ranch tonight, where they are scheduled to perform with Play for Blood Until Chaos, Ti22, Lost in Lies, and Grudghold. It'll be loud -- way loud -- which is the perfect way to celebrate 11-11-11, or as we like to call it, Nigel Tufnel Day.
Read through to see our other four picks, and to catch a video of Howitzer in action.
Friday, November 11:
Howitzer is scheduled to perform at Martini Ranch in Scottsdale.
Upcoming Events
The Australian Bee Gees Show
TicketsFri., Mar. 3, 8:00pm
Isaiah Rashad
TicketsSat., Mar. 4, 7:30pm
Dueling Chicago Quartets
TicketsWed., Mar. 8, 7:30pm
Dave Stamey
TicketsFri., Mar. 10, 7:30pm
Art Garfunkel
TicketsSat., Mar. 11, 7:30pm
California jazz-funkers Delta Nove hit the Sail Inn, which local support by Dry River Yacht Club.
Saturday, November 12:
Classic Arizona band Major Lingo is scheduled to perform at Hollywood Alley.
Post punks The Father Figures bring their angular sound to the George & Dragon Pub.
Sunday, November 13:
Singer/songwriter Cory Branan brings his Americana jams to The Rhythm Room, with locals Matthew Reveles, JD Stooks,and The Worrymen.
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Keep your thumb on the local music scene each week with music news, trends, artist interviews and concert listings. We'll also send you special ticket offers and music deals.
In Case You Missed It
Upcoming Events
Born of Osiris
TicketsWed., Mar. 1, 6:30pm
Ugly God & Wintertime
TicketsThu., Mar. 2, 9:00pm
L.A. Vation
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SAN CLEMENTE, Calif., May 2, 2011 – Surfline has predicted "excellent conditions" for the start of the Association of Surfing Professionals (ASP) PRIME Nike 6.0 Lowers Pro and ASP 5-Star Oakley Pro Junior holding period (May 3-7) at San Onofre State Beach – Lower Trestles, San Clemente, Calif.
According to the official forecaster, a small mix of south and southwest swells will prevail for the first couple of days of the contest, with a small southwest swell building in for the last couple of days. The surf will generally be in the three-to-four foot range on the sets (around waist to shoulder high). Wind and weather conditions look excellent to start out the event as well, with sunny skies and morning offshore flow. For the last couple of days of the event, there will be cooler weather, cloudy skies and potential for some onshore flow.
The Nike 6.0 Lowers Pro will feature 26 of the World's Top 34 surfers including 10-time defending World Champion and current #1 Kelly Slater, as well as the world's best juniors in the Oakley Pro Junior. The combination of contestable swell, a world-class wave, major points and elite athletes will ensure fierce competition at the famed Southern California surf break.
According to Surfline, the forecast will break down as follows:
TUESDAY 3rd: Small mix of mid period S swell (185-195) and longer period SW swell (205) with 2-3' occasional 4' surf (waist up to shoulder high sets). Sunny skies, warm weather and light to moderate offshore/ENE flow in the morning. Moderate westerly flow develops in the afternoon.
WEDNESDAY 4th: Small mix of S and SW swell continues with more 2-4' faces (waist up to shoulder high). Slightly cooler, but plenty of sunshine still possible with weak offshore flow in the morning. Light to moderate W wind builds for the afternoon.
THURSDAY 5th: Small, long period SW swell (200-215) will build through the day as old S swell fades. Surf continues in the 2-3' occasional 4' range (waist-shoulder high sets). Light S wind in the morning with overcast skies and a little morning sickness possible. Light SW/W wind for the afternoon and a possible clean up.
FRIDAY 6th: Continued small SW swell (200-215) with more waves in the 2-3' occasional 4' range (waist up to shoulder high sets). Light S wind in the morning with overcast skies. Light SW/W wind builds for the afternoon.
SATURDAY 7th: Small SW swell continues with 3-4' faces on the larger sets (waist-shoulder high). Light S wind in the morning with overcast skies. Light SW/W wind builds for the afternoon.
Both the Nike 6.0 Lowers Pro and Oakley Pro Junior will feature an HD webcast with live video coverage and scoring for all five days of competition with announcers Sal Masekela, Mark Fewell, Dino Andino, Saxon Boucher, Chris Mauro, Brad Gerlach and Jodie Nelson.
The Nike 6.0 Lowers Pro will be televised live and in its entirety in Hawaii on Oceanic Time Warner Cable's Oceanic SURF Channel 250 and 1250HD.
For more information about the Nike 6.0 Lowers Pro, visit nike6lowerspro.com. For more about the Oakley Pro Junior, visit oakleyprojunior.com.
The Nike 6.0 Lowers Pro and Oakley Pro Junior wouldn't be possible without the generous support of sponsors. A special thank you goes out to presenting sponsors Nike 6.0 and Oakley, co-sponsors Red Bull and Sierra Nevada, media sponsor SURFER Magazine (Surfermag.com) and official forecaster Surfline.com.


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News & Politics, Society & Culture, HistoryFollow
|Society & Culture
The best of BBC World Service documentaries and other factual programmes.
April 2nd, 2011
Episode 51 of 1421 episodes
Great Expectations follows the lives of people who live in the diverse ethnic mix of east London, on the doorstep of the 2012 Olympic Games. It looks at their view of the changes and money being spent around them from where they live - in a deprived part of the inner city, in dense blocks of flats and social housing - known as an estate in the UK. The BBC's Nina Robinson reports in the first of two programmes on the incidence of poverty in the area and how this is reflected in the lives of residents.
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Welcome to the daily audio workout for your head.


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Avail Cheap locksmith in Canberra
Category : Repair Posted : 23/03/2015 Price : Check with seller Location : Canberra(ACT)
Jeanette started career as a Professional Spiritual reader. Numerology, Colour Interpretations and Feng Shui got added to my repertoire and I began to run Meditation and Psychic Development classes, conducted courses on several topics, and facilitated regular monthly Angel Gatherings. (as I am also an Angel Intuitive, having attended Doreen Virtue's seminars from 2002 to 2005)And of course I was continually giving readings, consulting with many people who went on to become dear friends. Finally, we returned to Australia in the early 1990's moving from Perth to Melbourne , to Sydney and back to Melbourne and in 2005, we decided to make our final move to Brisbane.


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Energy Infrastructure India Limited
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Job title: Technician Experience: 2-3 years Salary: 12-15,000/- per month Qualification : Graduate/Diploma. Key Skills: Good Communication skills Technical Skills: Knowledge of unix and linux Job Responsibilities: - Must be proficient in ope...
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Love of the week
Marni Fall/Winter 2011/2012
The reason why
Sport chic
Marni's Fall/Winter 2011/2012 fringed jacket it can be bought in all maison boutique.
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Vittoria Mentasti - Dead Sea
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Menswear and womenswear collections will walk together and will be on sale right after the show. These are the news from Burberry but the evolution is generalized: runway shows are changing


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Park St. Penthouse E.- Downtown, Payette Lake View
From $150 / night
balance of due
Description from the owner
Description from the owner
Bedrooms: 3/
Bathrooms: 2/
Sleeps: 12/
Type: Apt. / Condo
Book this 3 bedroom, 2 bathroom apt. / condo in McCall today! A total of 12 people can sleep here comfortably.
Guests can enjoy a outdoor grill, air conditioning, and parking space among other amenities offered by this rental.
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A University of Florida study of married couples released on Wednesday shows that self-delusion may actually be a more accurate indicator of a successful marriage than good communication or truthful, open relationships.
Benjamin Karney, a psychology professor at the University of Florida, studied several hundred couples and found that the satisfied ones often remembered the past as worse than it was to make the present seem better by comparison. Couples in the study were interviewed every six months for four years.
''The advice to husbands and wives to communicate better puts a lot of pressure and blame on couples,'' Professor Karney said. ''It says, 'If only you communicated better, you'd be happy.' I don't think that's true, nor does the research show it to be true.''
His team studied couples in the Los Angeles area and found that people most likely to say they were happy in their marriages were those who used their memories selectively to feel good about their pasts.Continue reading the main story


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By: Shannon Ralph
I have a dream.
My dream is not as lofty or historic as Dr. King's dream. It is a small dream. A simple dream. A seemingly easy dream to attain.
I dream of going home.
I am a Southern girl born and bred. I grew up right below the Mason-Dixon line in Owensboro, Kentucky. Though right across the Ohio River from Indiana—practically Midwestern in locale—Kentuckians are one hundred percent Southern in their sensibilities. Kentuckians cherish nothing more than family, God, honor, and fried chicken. We are nothing if not devoted to one another. Those of you not raised in the South may look down upon those who were. You may make jokes about bare feet and wedded cousins. Hillbillies and stupid rednecks. Southern Belles and illiterate moon-shiners. You do not get it. And we forgive you for that. We even pity you a little bit, bless your heart.
There is something special about the South. Yes, we have an ugly history. I do not deny that in any way. We have ugly politics and uglier politicians. We are far from perfect. We have our faults, for sure. We are not always willing to change. We value tradition and change scares us. It's not that we think our way of life is better than your way of life, necessarily. It's just all we've ever known. So we cling to it out of fear. We are changing, but like a cool autumn day after a long steamy summer, change comes slow in the South.
Our way of life is slow, as well, but that does not mean that our intellect is. We like the simple things in life, but we are far from simpleminded. We are witty. We are intelligent. We are well-read. Some of our greatest American writers wrote with a Southern sensibility. We are charming. We still believe in saying "yes, ma'am" and "no, sir." We respect our elders. We hang out on front porches. We love nothing more than a good barbecue. We endure stifling heat to say "hey, y'all" to our neighbors. We call strangers "honey" and "sugar." We show our love and affection with homemade biscuits and fried catfish and peach cobbler. We don't take ourselves too seriously. We are ridiculous at times, but we know it. We look you in the eye when we walk past you.
Despite everything I love about the great northland—and there are many things I love—my heart belongs in the South. The blood that runs through my veins is decidedly Southern. My heart beats to the rhythm of Stephen Foster's "My Old Kentucky Home."
I want to go home.
I don't want my children to grow up as Midwesterners. I have nothing against Midwesterners, of course. Some of my very best friends in the world are Minnesotans. But my children have the Southland in their souls. In their roots. In their very core. They just don't know it yet.
I want to go home.
Ruanita and I have had several conversations recently about moving south. We have been in Minneapolis for fifteen years. In that time, we have enjoyed one hundred percent complete and total acceptance as a lesbian couple. I have been out in every job I have ever had here. I have been out to all of my children's teachers. I have been out at the YMCA. I have been out at the zoo. I have been out to all my neighbors. I have been out to my mailman. And my realtor. And my insurance agent. And my doctor. And my hairdresser. My kids' pediatrician. I have been out to my daughter's Girl Scout troop. I have been out to all my children's friends and their parents. In essence, there is not a single soul in my life who does not know that I am a lesbian mom in a loving long-term relationship. Why in the world would I want to mess with that?
Because I want to go home.
Perhaps it is selfish to even consider such a move. Yes, I want to live in the South, but what about my children? Currently, we know numerous families like our own right here in Minneapolis. My children have never had to endure another child telling them their family is weird. Or wrong. Or an abomination. They have never been teased for who their parents are. They are oblivious to the fact that we are any different from any other family. They live in this incredibly safe little bubble of complete acceptance. And they are happy there. They are content.
Louisville, Kentucky is by no means a backward town. There are progressives who live in Louisville. There are numerous raging liberals, many of whom are my good friends from college. There are lesbian and gay families. There are neighborhoods where gay families are safe. There are schools with Gay-Straight Alliances. There exists the possibility to create a new bubble. Our own safety zone. Surrounded by friends and family who adore us.
Ruanita's mother is aging. She is not well. And Ruanita just recently reconnected with her father, who made a strong impression on my sons. They want to know their grandfather—their only grandfather. My extended family and many wonderful friends from my childhood and college years are in Kentucky. We have people there who will help us create a new bubble. So why am I so hesitant?
Because maybe I don't want to live in a bubble.
Maybe I don't want to have to worry about being outed in the wrong mall or the wrong line in the grocery store or the wrong PTA meeting. Maybe I am afraid I will not be able to protect my children from everyone who exists outside of our little bubble. Maybe I am afraid of my children discovering that we are not like everyone else. We are different. What would I say to them then?
Life in Minneapolis is comfortable. It is pleasant. It is easy. But easy doesn't change the world. Easy doesn't change hearts and minds. Easy will not make this country a better place for my children and my grandchildren. Perhaps it is going to take those of us who are different making the rest of you feel a little uneasy for the world to get better. Perhaps that's the only way minorities attain the rights they deserve. If we don't make you see us, it's easier to pretend we don't exist. It's easier to deny us rights when we aren't in your own neighborhoods. In your own schools. In your own grocery stores and church pews and Little League bleachers. Maybe things are only going to change when we pop the bubbles and make our presence known.
I don't pretend to know the answers. I just know that I want to go home.
The post I Want to Go Home appeared first on The Next Family.
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Originally published on The Seattle Lesbian
By Laura King
Life can get busy. With work, kids, family commitments, friends, chores, and the general chaos of everyday life, it can be near impossible at times to sit down for a cup of tea, let alone squeeze in an hour of exercise regularly. However, all things are possible if you set your mind to them. Those that prioritize their fitness nearly...
With the passage of marriage equality last year, laws have been quickly changing across the United States. LGBT couples with or without children weren't just given the right of marriage, they were provided new protections and benefits within their families. All of a sudden, LGBT couples and families had to figure out how to file jointly when it came to taxes, how to add...
By Alex Temblador
I recently wrote an article for The Next Family called, "Family-Friendly Films That Feature Adoption and Foster Care," that shared wonderful family films with adoption or foster care story lines. My reasoning behind doing so was because every family deserves a chance to see similar families like theirs represented in various forms of entertainment.
The same can be said of other...


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And one more thing on snow fences:
Well, maybe I should have said in Wyoming they are slightly tilted
aeay from the thing, object or whatever the builder is hoping to protect..
Maybe they are built that way or maybe the wind does it. The wind blows all
the time in the part of Wyoming I am from,and everything is slanted. The
trees, the people, the building (grin) everything.
At any rate I have never seen a farmer, rancher or road person out
there with a right angle, measuring to be sure they are perpendicular to the
ground. Of course I have been a little busy to make a real study of the
snow fence building art. I so know that ranchers and farmers do a lot of
work they would rather not be doing. It is a fact of most of our lives.
The distance between the poles are standard or near it, on all fences, and I
believe the slats are cut to a standard length. They are not slanted/
tilted because of sloppy work, there is a reason for the tilt. In these 3
states, to the best of my knowledge, the fences are never taken down, but
stay there until they either won't do the job anymore and are replaced or
they fall down. Most of the new ones in Wyoming are metal I am informed and
still have openings so the wind doesn't destroy them quite so quickly.
Having lived in New Hamshire and often visited New York state I
don't think Carolyn understands the hundreds of open miles the wind blows
absolutly unhindered and the terrific force it builds to. The "wide open
spaces" of New York state are nothing like the "wide open spaces" of the west.
Snow fences were a mute point anyway, when I was teaching in Idaho
because the snow was so deep by Dec. 15 that we couldn't see the tops of our
cars, and by Jan. 15 the slide was covered. I imagine that they use
snowmobiles now to get around. We used snow planes if we wanted to go
anywhere. The snow planes are another story.
I guess different snow fences for different parts of the country.
And there Amy is more than you ever wanted to know about snow fences. If
you ever get to Wyoming think of me. I was born and raised in Casper which
is smack dab in the middle of the state. Unless you are going there
particularly, not many people go through it. My mother and son and his
family still live there.
Who started this topic anyway?
>One more thing on snow fences:
>So they are slanted (not perpendicular to the ground)? And slanted
>towards whatever they are to protect, or slanted away from prevailing
>wind, or slanted towards either or the above? Are the openings to keep
>the wind from blowing the fence down?
>If the fences are NOT perpendicular to the ground, it is because they are
>cheep, put up by guys who would rather be doing something else with their
>lives, andn/or who didn't put enough fence posts to hold the fence up, or
>the wind has blown it down. The openings are to conserve wood, I'm sure,
>as well as to allow some wind to blow through so the fence won't completely
>The snow fence SHOULD be perpendicular to the ground, don't you think,
>experts?? I'm sure this is less an art than a science in the hands of
>day workers.
>Carolyn Schaffner


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