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|Half Baths
|Property type
|chateau / country house
|Minimum Stay
|3 nights
NEW DATES MADE AVAILABLE FOR SUMMER 2016. Very unique and architecturally significant Gentleman's Farm unlike anything else in Harbor Country. Country retreat on 7 acres only 10 minutes from Lake Michigan beaches but 'million miles from Monday.' Turn down private lane past horse paddock to galvanized aluminum-wrapped Main House featuring open layout with Chef's Kitchen, screened-in porch, fireplace, TV room and stone shower. Separate bunkhouse situated over horse stables with own bathroom sleeps 6. Large lawn perfect for family games of football, kickball, lacrosse or croquet. Horseshoe pit. Spectacular walk-in pool surrounded by loungers and outdoor dining areas. Tennis and golf nearby. No Smoking. No Pets. There is no a better way - or more memorable place - to spend your Harbor Country getaway.
Weekly rentals from Friday afternoon to Friday morning. 3 night weekend rentals.
Keywords: horse farm, farmhouse, country retreat, country getaway
We are an active outdoor family of four from Chicago who work hard during the week and like to relax and have fun on the weekends
Our home is only 1.5 hours from Chicago. In Sawyer, we get the best of both worlds - the beaches are 10 minutes away and yet the country side makes us feel like we are a million miles away from the stresses of our work week. This is the perfect place for us to get away from it all and relax and recharge.
We booked this house because we were looking for a nice family getaway with plenty of room for the four of us to sleep, hang out, and relax without feeling cramped and it was perfect!
The house is set on a few acres which allowed us to feel disconnected without having to contend with neighbors, traffic, or shared spaces like at hotels or condos. A driveway sets the adorable house well off the street. There is a nice front porch looking out toward the street but on an open field. The back porch is screened with great couches and chairs looking out at the private pool and more fields.
The house is so impeccably decorated you truly feel like you're staying at a good friend's house where all of the colors and decoration are whimsical, warm, and happy. It's clear that the owners have spent a lot of time making this place their home away from home. There is plenty of living, dining, and sleeping space...enough that you never feel cramped or on top of each other.
We were there for a few days and had great meals at Greenbush, Clean Plate Club, and the Greenbush Annex but still chose to cook a number of meals in the cooks kitchen that had every cooking implement, pot, pan, plate, bowl, or cup we ever needed.
And finally, the pool! The pool was an amazing luxury. We went to the Warren Dunes one day but then spent the entire next day at the pool in the back yard. We brought a few inflatables with us for our kids 10 and 8 and just never got around or had reason to leave the pool. It was plenty warm outside but the pool also had a heater so we were never chilled even in the morning or evening. This heated outdoor pool would make for a great fall/winter/spring destination too. The pool reminded us of Italy; so peaceful and serene!
The Greenbush Brewery, Clean Plate Club, Greenbush Annex, cute shops, grocery store, and farm market are all a 4 minute drive...very close. Warren Dunes is about 10 minutes away. FYI that there is a great beer selection at Greenbush and the market but there is a better wine selection at the Farm market behind Greenbush Brewery. If driving and you're a wine fan I might suggest bringing your favorites from home as the larger grocery store is further away...or hit the grocery on the way in.
We loved Gentleman's Farm!
This is a nice farmhouse with a very nice pool. The kitchen is nice and the property is nicely decorated. There are just two bedrooms in the main house, however, and the barn sleeping arrangements are VERY rustic. 12 people will not be comfortable sleeping for an extended period of time at this property, but 4-6 adults will, unless the others are willing to sleep in the upstairs, semi-finished barn (the barn accommodations are just barely "okay.")
While the property boasts a very large green space and visible horse area, the grass around the home is so tall that it was not particularly fun playing with the kids in the grass area. Our kids enjoyed watching and interacting with the two horses that visited the fenced area just about every day.
Lack of wi-fi is disappointing. Downtown Sawyer is really cool and the main grocery/market about 5 minutes down the road is excellent, with lots of fancy/gourmet foods and an impressive gift shop.
Overall, we had a nice stay, but the adults that spent a week sleeping in the upstairs of the barn were not especially comfortable. Not worth the nightly/weekly price point.
Blueberry farms, wineries, apple orchards, state parks
|Rate Period
|Weekend Night
My Standard Rate
3 night minimum stay
Please call/email for Memorial Day, Fourth of July and Labor Day availability and rates.
At least 1/2 of payment due at time of booking to confirm reservation. Balance due prior to check-in.


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Land plots - commercial, Sale, Myjava, Slovakia
5.999,00 €
Land plots - commercial, Sale, Myjava, Num. ZR-283923
We sell land kept as a garden for Moravské Kopanice area of 763 m2, suitable for building huts. Beautiful surroundings of the forest with a beautiful view, great possibilities hiking, biking, fishing and skiing options. Maintained year round road, electricity directly on the site, MY 8 km, PN 25 km Bratislava 105 km. If interested contact: Renata Szikhartová 0904504108th
more information
Listing summary
763 m²
personal property
Real Estate Agency 80 offers
Remi reality s. r. o.
Moravská 991/1
Myjava 90701
0904 504 108
Real Estate Agent 80 offers
Renáta Szikhartová
0904 504 108
Your Listing seems interesting, please contact me.
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subset: commoncrawl


text:
|"...Although mold is a naturally existing substance, it can be harmful to humans. When airborne mold spores are
present in large quantities, they can cause allergic reactions, asthma episodes, infections, and other respiratory
problems. Continued exposure to mold may result in nasal or sinus congestion, eye, nose, or throat irritations, and
adverse effects to the nervous system..."
Source FEMA
Mold: A Health Hazard
Release Date: November 8, 2005
Release Number: 1605-096
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Pet Hair Removal.
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NOTE: This is just my opinion. I'm not trying to further bum the Creddiers' joy. This was just based on a point that was made on that Creddie Vent blog that caused so much excitement. As always, feel free to disagree.
This is just a simple blog explaining why I don't think that Carly is acting OOC in iLMM by being happy for Sam and Freddie.
First of all, I know that Freddie was technically the one who broke up with Carly, and I'm not going to lie, she did look pretty hurt and upset. However, I do believe she moved on from it quickly. How do I know this? Well, just look at all the guys she's dated and has claimed to love, since then. There was Adam, and Steven, and even Cort, if you would want to count him.
Now, I know what you're thinking: Carly might just be dating all these guys to get over the pain of losing Freddie.
And you may be right. Nevertheless, that doesn't necessarily mean that it's out-of-character for her to be happy for her friends. Remember, Carly is a nice person. She's not going to hate on her best friend for dating her ex-boyfriend, even if it does secretly bother her.
Plus, she already freaked out when she first heard that they kissed. Since then, she has probably accepted the fact that Sam and Freddie may like eachother.
Also, remember that these are Dan's characters and that he can do whatever he wants with them. I could understand why people were upset about iSPT because that wasn't written by Dan; therefore, it's fair to say that it was out-of-character. On the other hand, with episodes like iKiss and iOMG, these are purely Dan's ideas because he wrote them.
Whether or not you agree with these ideas is another issue, but my point is, I don't think Carly is acting OOC in this particular instance.
Thoughts? Comments? Please discuss! xD


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Hotplug lets you plug in new devices and use them immediately. That means that users won't need to learn so much system administration, since the Linux system will at least partially autoconfigure itself. Initially, hotplug included support for USB and PCI (Cardbus) devices, and could automatically configure some common network interfaces. Updated versions include IEEE 1394 (Firewire/i.Link) support and can download firmware to USB devices that need it.
Noca is a shared library that prevents the page cache from filling with data that we know we only need once. It hooks read, lseek, and close. If some conditions are met, they trigger an fadvise call so that the memory is freed. An example of its use could be to limit the page cache of a "tar zxvf" operation to a specified size, no matter how big the archive is.
The Ad hoc Protocol Evaluation testbed is a small Linux distribution intended for the analysis of ad hoc networking environments. It is self-contained and pre-configured, and contains tools for data gathering at both the IP and ethernet level. It also has a scenario scripting system, which enables APE test runs to use movement choreography, with instructions to participants.
VIA High Speed Serial is a little kernel module (1 KB) which enables high speed serial port modes of VIA VT82C686A or VT82C686B southbridge-equipped motherboards. Basically, this is developed for ISDN-TAs, which at least in europe are constrained by the normal serial port speed of 115200 bit/s. With this module, you can use the serial port at 230400 bit/s so that you can get the full 128000 bit/s from ISDN-TA. The module has been tested with both 686A and 686B chipsets. Functionality is the same as with SHSMOD patches, but you don't have to patch the serial port driver.
Fullscreen display of a short text.
A PHP class to decode email messages.


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Game On! bloggers Reid Cherner and Tom Weir are bidding goodbye to 2010 with their list of the Top 100 Sports Personalities of the Year. These are the people who, for better or worse, drove our traffic. Today's list is Nos. 71-80.
No. 80: Aroldis Chapman. He's lefthanded. He throws the ball 105 miles an hour. How could he not be on this list?
No. 79: Landon Donovan. His World Cup goal against Algeria (video here. "You could not write a script like this") in stoppage time was one of the those "I remember where I was" moments in sports. We also like that he gave a shout-out to his ex-wife, actress Bianca Kajlich after his World Cup goal.
No. 78: Erica Blasberg. The suicide of the LPGA player was one of the saddest stories of the year. The details of her final hours are still a bit of a mystery.
No. 77: Yeardley Love. The death of the University of Virginia lacrosse star was the worst nightmare for every parent who sends their child off to school.
No. 76: Gilbert Arenas. Injuries. Suspension. Fake injuries. Trade out of town. Is this anyway for a $111 million man to act?
No. 75: Tony Parker and Eva Longoria: Nobody knows what goes on inside a marriage and this is Exhibit 1. Whatever happened, no one is talking about it unless they are denying the latest rumor.
No. 74: Frank and Jamie McCourt. They have paid $20 million to lawyers to try to get a divorce. It is one of the few marriages that, depending on the outcome, will have to get approval from a majority of the owners of Major League Baseball. It is tough to be a Dodger fan these days.
No. 73: John Isner and Nicolas Mahut. Their 11-hour match at Wimbledon was one for the record books and divided fans as to whether they had seen the greatest match ever or whether the folks in London need to change their rules.
No. 72: San Franciso Giants. Tim Lincecum. Cody Ross. Buster Posey. Fear the Beard. Wine country. The Giants won a World Series that we all (excluding Rangers fans) could appreciate.
No. 71: Greg Oden. We would love to remember the Funny or Die audition or the excitement of his coming to Ohio State, but sadly he is being remembered for a man whose body continued to betray him year-after-year. We can only hope 2011 finds a miracle cure.
Click here for Nos. 81-90.
Click here for Nos. 91-100.
Reid Cherner has been with USA TODAY since 1982 and written Game On! since March 2008.
He has covered everything from high schools to horse racing to the college and the pros. The only thing he likes more than his own voice is the sound of readers telling him when he's right and wrong.
Michael Hiestand has covered sports media and marketing for USA TODAY, tackling the sports biz ranging from what's behind mega-events such as the Olympics and Super Bowl to the sometimes-hidden numbers behind the sports world's bottom line.


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Rare variants in >30 genes have been shown to cause idiopathic or familial dilated cardiomyopathy (IDC/FDC), but the frequency of genetic causation remains poorly understood. We have previously resequenced 9 genes in a cohort of IDC/FDC probands for rare variants, and now report resequencing results for 5 more genes with established relationships to DCM.
Blood samples were collected and DNA prepared from 312 patients, 181 with FDC and 131 with IDC. Genomic DNA underwent bidirectional sequencing and DNA of additional family members underwent analysis when a rare variant was identified. We identified rare variants in 34 probands (10.9% overall), including 29 unique protein-altering rare variants and 2 splicing variants that were absent in 246 control subjects (492 chromosomes). These included 12 myosin binding protein C (MYBPC3) variants in 13 (4.2%) probands, 8 alpha myosin heavy chain (MYH6) variants in 10 (3.2%) probands, six tropomyosin (TPM1) variants in six (1.9%) probands, four cardiac troponin C (TNNC1) variants in four (1.3%) probands, and one cardiac troponin I (TNNI3) variant in two (0.6%) probands. Variants were classified as likely or possibly disease-causing in 13 and 20 probands, respectively (33, 10.6% overall). One MYH6 variant was classified as unlikely to be disease-causing.
Rare variants in these five genes likely or possibly caused 10.6% of DCM in this cohort. When combined with our prior resequencing reports, approximately 27% of DCM probands have had possible or likely disease-causing variants identified.
Enormous progress has recently been made to understand the genetic basis of dilated cardiomyopathy (DCM). Most of this effort has been devoted to identifying genetic cause of DCM in families, termed familial dilated cardiomyopathy (FDC). While mutations in more than 30 genes have been described as causative of DCM,1, 2 determining the frequency of mutations in any one gene in a cohort of patients with DCM has been complicated by this dramatic locus heterogeneity. Also, identified mutations are usually unique ('private') to that family, and this allelic heterogeneity demands that, minimally, all coding exons and intron/exon junctions of any gene under study be examined to exclude variants relevant for disease. Furthermore, some of the genes that harbor DCM mutations are very large. Hence, examining coding sequence for variations in multiple genes has been costly and labor intensive.
Despite these experimental issues, gaining knowledge of the identities, character and frequencies of mutations in known DCM genes is essential to understand this phenotype that underlies a great deal of heart failure morbidity and mortality. Such knowledge is critical to the emerging practice of cardiovascular genetic medicine,3 as well as to the design of DCM genetic epidemiology studies.
To begin to address this problem, we recently resequenced exonic and intron/exon junctions of 6 DCM genes (MYH7, TNNT2, SCN5A, CSRP3, LDB3, and TCAP) in 313 DCM probands4 with support from the NHLBI's Resequencing and Genotyping Service (RS&G) (Table 1).4–6 We found 32 variants (10.2%) not identified in 253 control DNAs.4 Even though the reference (wildtype) sequence has been established for these DCM genes, determining if a newly identified variant is disease-causing is challenging. In discovery studies, confirming that a candidate gene indeed harbors a causative mutation is usually resolved by a combination of a significant lod score, segregation of a variant with the disease phenotype in one or more large families, and/or definitive functional studies. However, such approaches, especially functional studies, exceeded the scope of our prior gene survey study and were not included in the initial publication (although some functional studies, e.g., for TNNT27 and LMNA8 have been published and others are underway). Hence, we developed conservative standards to classify these variants as 'possibly' or 'likely' disease causing.4
To extend these findings, we have now performed bidirectional sequencing of five additional genes in the same cohort, again with RS&G support. These five genes included myosin binding protein C (MYBPC3), α-myosin heavy chain (MYH6), tropomyosin 1 (TPM1), troponin C (TNNC1) and cardiac troponin I (TNNI3). Using the same approach, we present here the variants identified in this study thought to be possibly or likely disease-causing.
Written, informed consent was obtained from all subjects, and the Institutional Review Board at the Oregon Health & Science University approved the project. The study included 312 probands (311 subjects from the prior cohort4 and one additional DCM case), 290 Caucasians, of whom seven were of Hispanic descent; 16 African-Americans, three Asians and three Native Americans/Alaskan Natives, and used methods of clinical categorization of FDC versus IDC as previously described.9 These 312 probands included 298 of the 304 previously described9 in detail. Families with confirmed and probable histories of familial disease were classified as having FDC; those with histories consistent with possible FDC or a negative family history were classified as having IDC.4, 9 In cases classified as confirmed FDC, the patient and at least one closely related relative had IDC, defined as left ventricular enlargement (LVE) accompanied by systolic dysfunction upon exclusion of other detectable causes of DCM, as previously described.4, 9
The 5 genes reported herein were chosen following the same selection and analysis strategy described in our 6 gene resequencing report.4 Briefly, using the published FDC literature available in early 2005, we estimated the number of exons needed to be sequenced in order to find a single mutation in each gene, based upon the numbers of exons in that gene and an estimate of the frequency of that gene in DCM, in an effort to conserve resequencing resources at the NHLBI.4 We selected genes in that study with a threshold of sequencing up to 1000 exons to identify one putative disease-causing variant (as shown in Table 1 of that report).4 The prior estimates for TNNC110 (1500 exons), TNNI311 (1600 exons) 11 and TPM112 (1667 exons), were used for this study's gene selection, as previously reported,4 as well as estimates from single studies for MYH613 (estimated at 907 exons), and MYBPC314 (estimated at 1591 exons).
Genomic DNA was extracted from whole blood as previously reported.4 Bidirectional sequencing was conducted for the following five genes: MYBPC3, myosin binding protein C, NM_000256.3, chr11:47,309,533-47,330,829, MYH6, α-myosin heavy chain, NM_002471.2, chr14:22,921,039-22,947,322, TPM1, tropomyosin 1, NM_001018004.1, NM_001018005.1, NM_001018006.1, NM_001018007.1, NM_001018008.1, NM_001018020.1, spanning chr15:61121891–61151166, TNNC1, troponin C, NM_003280.1, chr3:52,460,158-52,463,098, and TNNI3, cardiac troponin I, NM_000363.3, chr19:60,354,948-60,360,912. All exons and intron/exon boundaries were PCR amplified by standard methods at SeattleSNPs under contract with the NHLBI resequencing service.
Samples from probands identified by the resequencing service as carriers of protein-altering variants, as well as any available samples from their relatives were sequenced in our laboratory for confirmation and segregation analysis. Nucleotide changes were only evaluated if they were absent from all 246 (186 Caucasian, 23 Yoruban, 19 Asian and 18 Hispanic) control samples analyzed at the resequencing center. Any possibly disease-causing nucleotide alterations identified in African-American samples were further evaluated in an additional 167 control African-American DNA samples in our laboratory, for a total of 190 controls of African descent (380 chromosomes). As per our prior report,4 nucleotide changes were considered possibly disease-causing if they predicted a change in a conserved amino acid, a frameshift, a premature truncation, or a mis-splicing event and were absent in ethnically matched normal controls. Nucleotide changes were considered likely disease-causing if they met the above criteria and also segregated with disease in multiple affected individuals within a family or were identified in multiple unrelated probands, or had previously been reported as causative of DCM. Nucleotide changes that did not segregate with disease were considered unlikely to be associated with IDC or FDC.
Haplotype analysis was performed with the program Cocaphase15 for variants identified in multiple subjects to rule out founder effects. All individuals with the mutations in question were of Caucasian origin, thus haplotype estimation was carried out on Caucasian samples only. Markers at each gene locus with minor allele frequencies >0.1 in the whole sample were selected for analysis.
The bidirectional sequencing of five genes known to cause DCM was completed for DNA specimens from 312 unrelated probands with IDC or FDC. Protein-altering variants, none of which were present in 246 control specimens, were identified in 34 of 312 probands (10.9%) (Table 2). Most unique variants were missense mutations (29/31; 94%) and altered highly conserved amino acids; two were predicted to affect splicing. Some had previously been reported with DCM or hypertrophic cardiomyopathy (HCM) (Table 2).16–21
Of the five genes examined, the most rare variants were identified in the gene encoding myosin binding protein C (MYBPC3), with variants identified in 13 of the 312 probands (4.2%). All MYBPC3 variants were considered possibly or likely disease-causing (Table 2). One mutation (Ala833Thr; A.8), which was observed to segregate with disease, was also found in two additional families in our cohort (A.7 and A.9), none of whom were known to be related and who were geographically remote to one another; haplotype sharing was identified near to the mutation, suggesting that this may be a founder mutation. This same variant had been previously reported in an individual with familial HCM.19 In that report, the variant was identified in the proband with HCM as well as in his brother and father, both who had mild cardiac hypertrophy. Two probands (A.11 and A.12) had novel, possibly disease-causing splicing variants. Tissue samples were not available from either proband to assess the impact of these variants on mRNA splicing. One of the subjects with a splicing variant (A.12) also carried a MYBPC3 Gly1260Asp variant in trans (A.13). DNA from relatives was not available in either case with splicing variants and therefore segregation could not be assessed. The Gly5Arg variant (A.1) was previously reported in a patient with early onset HCM harboring this and another MYBPC3 variant;16 however, segregation was not assessed in that report. DNA from other affected relatives was not available to assess segregation, and we therefore classified the Gly5Arg variant as possibly disease-causing. The Arg272Cys variant (A.3) was considered possibly disease-causing due to lack of segregation data. The Gly490Arg variant (A.4), which has been reported with HCM,16, 18 was considered possibly disease causing, as segregation with DCM could not be assessed.
Eight unique α-myosin heavy chain (MYH6) variants were identified in 10 probands (Table 2). Six of the probands carried three likely disease-causing variants (Ala1004Ser, Ala1440Pro and Asp1826Asn). The Ala1004Ser variant (B.3, B.4 and B.5) occurred at a highly conserved site, was previously reported in a sporadic DCM case20 and was therefore considered likely disease-causing. The likely disease-causing Ala1440Pro (B.7) occurred at a highly conserved amino acid and segregated with DCM. The Asp1826Asn variant (B.9 and B.10), caused by two G>A substitutions in cis at positions 25743 and 25744, were identified in two probands. The affected sister of one of these probands was found to carry the same alteration, and thus the variant (B.9) was classified as likely disease-causing. The second proband, who also carries the Asp1826Asn variant (B.10), has sporadic DCM, and was also reported to have an in-frame G474_D475insQ LMNA variant (family R in Parks et al.)5 and a TCAP Pro141Ala variant (denoted as D.3 and categorized as unlikely to be disease causing in Hershberger 2008)4. Two MYH6 variants (B.1 and B.8) were identified in the same individual, a female diagnosed with DCM at 8 years old who was previously reported as carrying the disease-causing TNNT2 Lys210del mutation (B.7 in Hershberger 2009)7. The remaining MYH6 nucleotide variants were considered possibly disease-causing (B.2, B.6), or unlikely to be disease-causing because of lack of segregation (B.11).
We screened the exons from seven different transcripts at the TPM1 locus, encoding the tropomyosin 1 gene. Six different novel protein-altering variants were identified among six probands (Table 1), and all of the nucleotide changes were considered possibly or likely disease-causing. With the exception of Ser16Ile, all of the TPM1 variants were located in exons found to be present in the TPM1κ isoform22, which unlike other TPM1 isoforms has been reported to be expressed uniquely in cardiac tissue. Two novel variants, Lys15Asn and Ile92Thr, (C.1 and C.4) segregated with DCM in the respective families of each proband and were considered likely disease-causing. The Ala277Val variant (C.6), was identified in a severely affected IDC patient requiring transplant at age 13. This proband was previously reported as carrying a likely disease-causing Glu244Asp TNNT2 variant shown to cause decreased calcium sensitivity.7 Segregation could not be assessed in this family; thus the Ala277Val TPM1 variant was considered possibly disease-causing.
Four private protein-altering variants were identified in TNNC1 encoding troponin C, in four probands. One of the variants identified (D.2) occurred at a conserved site, segregated with disease and was considered likely disease-causing. The Tyr5His variant (D.1) occurred in an individual with early onset DCM known to carry a possibly disease-causing Arg1045Cys variant in MYH7.4 Segregation could not be assessed and therefore the Tyr5His variant has been categorized as possibly disease-causing. The individual with variant D.3 (also found to carry MYBPC3 Pro910Thr denoted as A.10), carries a TNNC1 Asp145Glu variant previously reported in a male with a family history of HCM. This variant was shown to increase Ca2+ sensitivity of force recovery.21 The Asp145Glu variant is novel for DCM and segregation data is lacking for this individual; therefore, we categorized this case as possibly disease-causing.
The Asp180Gly nucleotide alteration was identified in TNNI3, encoding cardiac troponin I, in two unrelated probands (variants denoted E.1 and E.2). The variant was predicted to change a highly conserved amino acid; however, no family DNA specimens were available in either case, and the variant was therefore considered possibly disease-causing.
Twenty-one of 181 (11.6%) probands categorized as having FDC and 12 of 131 (9.2%) probands categorized as having IDC carried possibly or likely disease-causing variants.
Haplotype analysis was consistent with a possible founder effect in the shared mutations for the MYBPC3 Ala833Thr and MYH6 Asp1826Asn variants, where haplotype sharing was present. However, the high degree of linkage disequilibrium between the observed variations at the MYBPC3 locus makes it difficult with this limited dataset to decipher if this is a potential founder effect or a chance finding.
This study, when combined with our prior reports,4–6 provides the most extensive resequencing data to date in one of the largest and most well characterized cohorts of probands with DCM.9 We used Sanger-based sequencing, still the gold-standard for sequencing sensitivity and specificity, and have now established approximately 27% of putative genetic cause within this cohort of DCM patients: 10.6% from the current study of five genes (MYBPC3, MYH6, TPM1, TNNC1, TNNI3), 10.2% from the prior resequencing study of six other genes4 (MYH7, TNNT2, SCN5A, CSRP3, LDB3, and TCAP) (Table 1), 5.9% from a study of the LMNA gene5 encoding lamins A and C, and 1.0% from a resequencing study of PSEN1 and PSEN2,6 encoding presenilins 1 and 2. Approximately 3% of these probands have been found to carry multiple variants in the same or different DCM genes.
The genetics of DCM vary significantly from that of other genetic cardiomyopathies, most strikingly with >30 genes reported to be involved, but with each accounting for only a small fraction of our cohort (0.3% – 5.9%), as shown in this and our prior resequencing studies (Table 1). In contrast, mutations in 2 genes, MYH7 and MYBPC3, collectively account for approximately 40–45% of HCM (or 80–90% of detectable genetic cause when a genetic cause can be identified, which has estimated to occur in 42%23 to 65%24 of HCM cases). Similarly, 3 genes, PKP2 (plakophilin 2), DSP (desmoplakin), and DSG2 (desmoglein 2) account for 40–50% of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C).25 Further, while HCM and ARVD/C are largely genetic disorders of genes encoding sarcomeric or desmosomal proteins, respectively, genes encoding proteins of exceedingly diverse function have been implicated to cause genetic DCM. For example, LMNA, to date the most frequent genetic contributor of DCM, encodes a structural protein of the inner nuclear membrane with as yet undefined disease pathways. Other genes implicated to cause DCM range from sarcomeric proteins, transcription factors, Z-disc proteins, channel proteins (including Na+, Ca++, and K+), and most recently a protein of the RNA spliceosome.26
These findings have several implications. One key insight is that despite the large number and variety of genes involved, a unitary, homogenous DCM phenotype results. Careful phenotyping by our group and others has distinguished 'DCM with prominent conduction system disease' as the only sub-phenotype of non-syndromic DCM, observed principally with mutations in LMNA and SCN5A in a small fraction of cases.1, 2 Very few other Mendelian conditions show this degree of locus heterogeneity while manifesting one homogeneous phenotype. Examples include retinitis pigmentosa or hereditary deafness, encompassing >40 genes each.27
Furthermore, how this homogeneous DCM phenotype occurs from such a broad array of genetic cause remains largely unexplained. While our colleagues have suggested a 'final common pathway' for DCM,28 we suggest that the DCM phenotype results from several different genetic injury pathways. This multi-locus pathway hypothesis resulting in a final DCM phenotype will need to have the gene network injury pathways and their respective injury mechanisms elucidated to lay this important question to rest.
Our nomenclature of likely or possibly disease-causing implies that the variant alone causes or could cause disease, reflecting common usage in rare-variant classical Mendelian disease. An alternative descriptor would be disease-associated, a term more commonly used to describe risk alleles in genome association studies aimed to determine genetic cause in multifactorial, polygenic disease. For a genetically heterogeneous Mendelian disease such as DCM, we favor the disease-causing nomenclature even though we recognize that our emerging data suggests that two (or more) nonsynonymous rare variants appear to be causative of DCM, suggesting a more complex genetic model in some cases. Also, even though we sequenced 246 control DNAs (492 chromosomes), it is possible that some of the variants reported herein as possibly disease-causing may still be rare benign or neutral mutations that do not directly account for disease. For that reason we have taken a conservative approach to categorizing these variants as 'possibly' disease-causing. Conversely, we also recognize that variants excluded from this analysis because they were identified at low frequency in control DNAs could still be relevant for DCM pathogenesis. Further, some variants had been previously identified as disease-causing HCM mutations that were identified in this study in probands with DCM. Considerable locus and allelic heterogeneity of sarcomeric genes for DCM and HCM has been reported previously, (see29 for review). For example, one mutation in TNNT2 identified in our prior study in a DCM proband and previously reported in HCM4 had a mixed picture at functional studies7. Another report showed DCM, HCM and restrictive phenotypes with the same sarcomeric variant in one large family, although the mechanisms, whether genetic or environmental, of this phenotypic variability remain to be discovered.30
Assessing the significance of a novel nonsynonymous rare variant in a patient with DCM but no affected family members presents special challenges. This is because the most powerful clinical genetics finding to establish that a specific rare variant is disease-causing is the segregation of that variant with the disease phenotype in multiple affected family members (and ideally, in multiple families), accompanied by the absence of the variant in multiple unaffected family members. This is a stringent but critical standard for resequencing data to be translated into clinical care. Determining which of the variants reported herein might be useful for genetic counseling of probands and/or family members regarding DCM risk is particularly challenging. While specific criteria for diagnostic molecular genetics laboratories vary, most diagnostic standards would follow the general outline of our approach to categorize variants: rare, nonsynonymous variants identified in genes established to have mutations that cause DCM would be considered at least as possibly disease-causing, and in the absence of segregation, prior reports, or other supporting data, predictive testing of family members would usually not be recommended. However, if one of these possibly disease-causing variants reported herein would be observed in additional DCM probands undergoing diagnostic testing, in most cases the variants would be assigned as likely disease-causing. Functional studies of the variant in gene targeting experiments in animals or in heterologous cell systems could also increase the evidence that a rare variant is disease-causing, but such approaches have not been conducted by diagnostic molecular genetics laboratories for DCM-associated genes. Hence, all of these issues will need to be resolved with research-based resequencing studies of much larger cohorts of DCM patients and their family members, regardless of whether they appear to have familial or sporadic DCM. These studies should also include longitudinal follow up, accompanied by large numbers of reference DNAs and combined with functional studies.
As in our prior study,4 the fraction of likely and possibly disease-causing mutations was similar for probands whether categorized as FDC or IDC. This finding, although preliminary in nature, again suggests that a significant proportion of what has been categorized as idiopathic DCM may rather have a rare variant genetic basis. If replicated in much larger cohorts of patients with IDC, that is, apparently sporadic DCM, this finding would impact our approach to determining DCM etiology in a fundamental way, bringing diagnostic molecular genetics to the clinic for thousands of patients with DCM of unknown cause.3
Family data was not available in 19 of the 34 cases so we were unable to assess segregation of the variant with disease. We have not sequenced two very large DCM genes (titin and dystrophin) in order to apply our resequencing resources to greater numbers of smaller genes; however, dystrophin (DMD) resides on the X chromosome and family history information in our DCM cohort supports autosomal inheritance in most cases.9 We have sequenced only a fraction of DCM genes. However, based on the available literature, we selected genes for study thought more likely to be represented in genetic DCM. Less expensive screening methods (D-HPLC, SSCP) that might have screened greater numbers of genes with equivalent resources are less sensitive and may have missed gene variation relevant to DCM that could be identified with Sanger-based sequencing methods. We also note that we only examined coding sequences and intron/exon boundaries for variation, and hence additional genetic variation including copy number variants, or variation in regulatory areas (promoters, 5' and 3' untranslated regions) or introns of these five genes would not have been detected. The difficulties of assessing variants in sporadic DCM have been noted above.
The nonsynonymous rare variants identified in these five genes implicated in FDC and IDC account for only a small fraction of the underlying genetic cause. Taken with prior data from this cohort and others, the genetic landscape of DCM is distinctive from that of other known genetic cardiomyopathies. Future studies in larger cohorts, ideally with family members screened for disease, with many genes sequenced and accompanied by functional studies, will be needed to confirm and extend these findings.
We thank the many families and referring physicians for their participation in the Familial Dilated Cardiomyopathy Research Project, without whom these studies would not have been possible.
Funding Sources:
This work was supported by NIH awards RO1-HL58626 (Dr Hershberger) and 5 M01 RR000334. Resequencing services were provided by the University of Washington, Department of Genome Sciences, under U.S. Federal Government contract number N01-HV-48194 from the National Heart, Lung, and Blood Institute.
Journal Subject Codes: Genetics of cardiovascular disease; clinical genetics; myocardial cardiomyopathy disease
Conflict of Interest Disclosure: No conflicts.
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.


text:
Crime Victims' Ombudsman
The mission of the Office of the Crime Victims' Ombudsman (CVO) is to ensure that victims of crime are served justly, equitably and fairly by the South Carolina Criminal Justice System and its victim service organizations. Additionally, the Office of the Crime Victims' Ombudsman through its Office of Victim Services and Education (OVSEC) provides oversight of training, education and certification for victim service providers.
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Running Time: 108 minutes
Released: 07/2007
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text:
|By Heroic Firebender
|More from Heroic Firebender
|G (all ages)
|No update page
|New Friend, New Foe
|Chapter information
|Written by
|Last chapter
Southern Air Temple
Aang and On Ji's home.
"Happy Birthday!"
Today was the day. Aang and On Ji's new baby turned one. They, finally, get to find out whether he's an Airbender or a Firebender. It's also the day they get to name the baby. For a whole year it was nameless. Aang and On Ji promised to wait until they found out what kind of bender he was. If he was an Airbender, he'd be named Gyatso. If he was a Firebender, he'd be named Kuzon.
"Today's a great day, On Ji."
"I know, Aang," She said as she hugged him.
Earth Kingdom
Near Zuko's Ferry
Lee was wearing all black clothing with an uncomfortable mask covering his face. He held a bow-and-arrow in his left hand while he climbed through a window. There was darkness everywhere aside from where Lee was looking. He was now in an empty kitchen. Suddenly, he winced and looked down at his feet. Lee's right hand wiped the sweat off his forehead. After a few seconds, he pulled himself together. He walked out of the messy kitchen and entered a hallway that led to where he needed to go. Silently, Lee unobtrusively entered a bedroom. There was only a slight sound made when Lee retrieved and arrow from his sheath. The arrow, now readily in place, was pointed toward his target. Something wasn't right, however. He quickly glanced at where he had just entered moments ago. Standing, with a typical brown teddy bear, was a little girl. It only took a matter of moments for girl drop her teddy bear and scream.
The scream echoed through Lee's head and he violently shook himself awake. He took quick breaths in rapid succession in an attempt to stabilize his breathing. Sweat trickled down from his temple. He sensed somebody else's presence and quickly stood up, forming a defensive position. However, he came to realize it was only a girl – a beautiful girl. He immediately felt something come over him. He didn't know what it was, however. Hopelessly, he tried to search for something to say...or even think. He only managed a mutter.
"Feeling better?"
"Uhhh...I-I don't know."
"I'm Jin. You're the hero who saved Iroh in the Jasmine Dragon."
"What- wait. How do you know...I feel dizzy."
Lee collapsed into Jin's arms.
Fire Nation Palace
Zuko's quarter's.
Zuko had the same dream he always had. The dream that always haunted him. It was of his mother leaving him. He used to wake up to it in a cold sweat, panting. Now, he calmly opened his eyes. Zuko was all too used to it. He hand with being held by somebody. He wasn't surprised to see it was Katara. She had fallen asleep by his beside their bed. As silent as possible, Zuko slipped out of bed. He didn't want to wake Katara. She was probably up for as long as she could, desperately waiting for him to wake, for all he knew. She deserved a rest. There was a slight echo as Zuko walked to see his officials. He had no sense of what time it was, but he suspected it to be very early in the morning. Out of the darkness further down the hallway emerged a figure.
"Zuko? Is that you?"
It was one of his advisors.
"How are you feeling? You were out for quite some time. I was just about to check on you."
"I'm fine. What has happened since I was out? The insurgents must have done something."
"I- well..."
"Spit it out."
"It's your uncle, again. I am sorry, but he's been kidnapped."
Southern Air Nomad
Outside the oasis.
Their newest son was either going to become the second Airbender in the world...or another Firebender. Aang couldn't hide the fact that he wanted it to be an Airbender. However, no matter what he was, Aang knew he'd always love their child. He knew they could always try again and have another baby.
Aang left the oasis and met up with On Ji.
"On Ji, would you like to hold...Kuzon?"
Earth Kingdom
Near Zuko's Ferry.
Lee finally had a clear head. He had finally emerged from the darkness and was fully operational.
"My healing abilities have brought you back to good health."
"Thank you. I really appreciate it," Lee said while he stared at her. She seemed so familiar.
"Why are you staring? Is their something on my face?" Jin said with a chuckle.
"You seem familiar. Have we met before?"
"Yes, do you not remember our previous conversation?"
"No, I don't think I do."
"Well, I'm Jin. I was the Waterbender who helped you after you saved Iroh from-"
"Iroh! Where is he?" Maybe he wasn't as aware as he thought. How could he have forgot about Iroh?
"What do you mean?"
"I was traveling with Iroh. He was with me back at the village...there was a fight. What happened? If you were in Ba Sing Se, how did you end up here?!" Lee started to panic.
"Calm down, Lee-"
"How do you know my name? How do I know I can trust you?! I need to get to the Fire Nation, right now!"
Fire Nation Capitol Prison
Phoenix King Ozai's cell room.
"Sir, Zuko saved Katara. They planted the explosives but she managed to elude them with Zuko's help. They say he was injured, but we don't know how extensive."
"Why am I not surprised? You cannot rely on anybody these days..."
"Sir, if I may add, an Insurgent group came across Iroh. They successfully captured him. He was traveling with Lee. The one who had-"
"I know who he is. Contact Hide. I want him dead!"
"Aye, sir. What do you want to do with your brother?"
Ozai grinned viciously.
Fire Nation Palace
Hallway outside of Zuko's quarter's.
"I'm enacting the lockdown protocol. All government personnel and their families will be staying here. Nobody in, nobody out. Everything we do, everywhere we go puts us in danger. This way, we can limit government casualties. I need all of you and I don't want anything to happen to their families. This unrest needs to stop. I'm going to put together a team-"
"You're not thinking-"
"That's exactly what I'm thinking. You know what to do. Put it together..."
Fire Nation Guard Post
Outskirts of Fire Nation Palace
"So, I there's rumors going around that the explosion injured the Fire Lord. Guess he's not such a big deal after all."
"Shut up! You wouldn't know respect if it hit you right in the face."
"Hey, don't get mad at me, I'm just saying..."
"You're an immature fool-"
"Who the hell is that? Wait-"
"What it is?"
"I don't know. Look for yourself."
The guard peered over the wall. There were three figures. None of them could be seen clearly. However, it did appear that two of the figures were carrying the third one. "Hey! Who's there?! You're not authorized to be here. Any step close and you're finished!" They stopped dead in their tracks. Two of the figures threw the third on the ground with no care, whatsoever. Then, disappeared. "Quick, you fool, get down there!" The two guards quickly went to investigate. One of them made a fireball to light the way. Once they got to the body, it was bloody. There were obvious and severe wounds. Torture wasn't a far fetched conclusion of what happened to the man. Without hesitation, the guards turned the body over. Luckily, he was still alive. But, who was it? They wiped the blood of his face and moved the hair out of his eyes.
"Is this who I think it is?"
"Quick, contact the Fire Lord! It's the Dragon of the West!"
Author's Note
Hello, everybody. I am back to the livin', as Sokka would say. My prologue and first chapter got some great feedback and I look forward to what people think of the new chapter. I will continue this, hopefully, on a regular basis. Please, tell me what you think about it. Thanks. ~Heroic Firebender 17:32, June 30, 2011 (UTC)
See more
For the collective works of the author, go here.


text:
Vote now - Team of the Hinrunde #BLTOTH
Durée: 1min 14sec Vues: 81 Soumis: 6 mois Ajouté par:
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Sous-catégories: Championnat Allemand


text:
Let us know when your receive great advice so we can thank our lawyers and point others with similar questions in the right direction.Got it!
Two juveniles stole my girlfriends car at gunpoint and blew out the transmission which cost me over $1200 to repair and other visible damage. The state found them guilty and put them on probation. Doesn't seem like any justice is done when the victims are ending up paying the repair bills as well as the emotional effects.
This is a victim's rights issue. There are two ways to do this. One way is to seek restitution through the criminal action, which is usually ordered during the sentencing phase. In most states, you can recoup money from parents up to a certain amount - in Arizona it is $10,000. The second way is to sue them civilly. Be sure to include the parents as civil law also provides for including the parents under certain circumstances. A lawyer can be helpful for either or both of those issues.
This answer does not establish a lawyer-client relationship and is meant as general information only. A reliable, specific answer depends on a full meeting and your specific case facts.Ask a similar question
The Texas Crime Victims Compensation Fund might be able to assist you. It helps victims of violent crime, and aggravated robbery with a deadly weapon should qualify. Contact the DA'S office and the juvenile probation department. Both should have victims' advocates who can help you with the paperwork. Good luck. Oh, and they should pay for counseling too if you're needing it to cope.Ask a similar question
Normally part of a sentence is the restitution component. You can check with both the prosecutor's office and/or the probation department to see if such an order was made.Ask a similar question
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Full service grocery store and active lease with USPS for additional bldg. Deli/Cafe with indoor seating. 100KW Fired Diesel Generator
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Est. Mortgage: $/month
Federal 30-year interest rate: 4.03% last updated on 2017-05-25
This product uses the FRED® API but is not endorsed or certified by the Federal Reserve Bank of St. Louis.


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Discussion in 'Proxies' started by bigdog67, Nov 3, 2013.
I need a socks 4 or 5 French proxy that does not appear to be proxy. Will pay.
How many do you need, if you only need 1 or 2 I'll just give em to ya.
Separate names with a comma.


text:
This property is no longer available.Search for Available Property.
13 acres in Bullard
Land adjoins Eagles Bluff Golf Course. Great 13 acre wooded tract in the Bullard School District! Level land and ready to build in a great location.
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NOTE: The information contained herein is provided as general information only and has been obtained from sources deemed reliable. It is provided without any guaranty, warranty or representation, expressed or implied, made by Lands of America, or any related entity, as to the accuracy or completeness of the information. The information is presented subject to errors, omissions, change of price or conditions, prior sale or withdrawal without notice. Prospective purchasers should make their own investigations, projections and conclusions concerning the information.


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Reviewed By Frankie K (SAN JOSE, CA) Reviewed for a 2016 Toyota Tundra —5/20/2017 4:09 AM
Installation was easy. Truck runs great but throttle still has soft touch and delay.
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14750 Laplaisance, Monroe, Michigan 48161 - High Visibility Plaza. Located just west of the I-75 exit 11. Bring your business here. Office, Retail, Light Manufacturing, Distribution. You name it. 2,000 to 30,000 square feet. Gross Lease. All utilities. Fire Suppression. Parking for hundreds of cars. Less than a minute to I-75. Strategic Located between Toledo and Detroit area. Special Rent Prices for a limited time. Act now.
Listing Courtesy of Coldwell Banker Haynes R.E.


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One of the benefits of trail running is that, compared to road running, the trail offers a greater variation in surfaces so you work your body differently with nearly every footstep.
For the same reason running in different pairs of shoes regularly may decrease overuse injuries, so can trail running - Different shoes, different terrains, etc all load the legs slightly differently. This spreads out the loading and impact forces to a wider range of body structures rather than hitting the same spot over and over again. Read More


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International Fetish Day is a day supporting the BDSM community. It originated in the United Kingdom as "National Fetish Day" and was first held on 21 January 2008.[1] The first International Fetish Day is to be held on 16 January 2009.[2] The main purpose of International Fetish Day is to increase awareness and support of the fetish community, whilst also opposing pornography laws. It is also designed to encourage members of the community to be more open about their sexuality.[1]
National Fetish DayEdit
National Fetish Day was first celebrated in the United Kingdom on 21 January, 2008. However, International Fetish Day has taken over from it.[3]
Perverts Wear PurpleEdit
On National Fetish Day, one of the main aspects is that members of the community wear an item of purple clothing as a sign that they are a member, in an event known as "Perverts Wear Purple". The main benefit of this act is that it indicates that someone is a member of the community whilst being "Vanilla" at the same time. Purple is a colour widely used in BDSM circles.[4] The main website says that, "By joining this fun 'National Fetish Day – Perverts Wear Purple' event, you as an individual will be joined by fellow community people all over the country in saying 'It's ok to enjoy what I enjoy' without damaging your 'vanilla' identity or integrity."[1] There has been contention around the slogan 'Perverts Wear Purple' primarily to do with the fact that many in the BDSM community distance themselves from the 'pervert' label. Others in the community feel that using the word 'Pervert' is a useful reclaiming.[3]
Ronnie Campbell MPEdit
The Labour Member of Parliament for Blyth Valley, Ronnie Campbell, accidentally gave his support to National Fetish Day, because he misunderstood the word "Fetish" and was not aware of the "Perverts Wear Purple" slogan.[5][6] A local newspaper, the Sunday Sun interviewed Campbell about his supposed support for the event by wearing purple. Campbell said, "I thought a fetish was a worry, like worrying about backing the right horse."[7]
Pierced Knight, one of the people publicised National Fetish Day claimed that,
"I received an email from Carol Delaney, the secretary to Ronnie Campbell, Labour MP for Blyth Valley. She confirmed that Mr Campbell will be supporting this national day of awareness on 21st January. Using the tag line of 'Perverts Wear Purple' those that support this day will be wearing about their person something that is purple, like a shirt, a tie, a skirt, a hair band."[7]
Campbell wrote a letter of complaint to the Sunday Sun, claiming that they had been making him look stupid by "twisting and turning" the meaning of what he had been saying. He wrote that, "I would never have agreed to support anything that had the title 'Perverts wear Purple' and I do not imagine any other Member of Parliament would either."[8]
The Sunday Sun published a response saying,
"If you hadn't misunderstood the word 'fetish' and backed National Fetish Day in the first place, we wouldn't have had a story. We did not twist anything and contacted you four times to clarify certain points. In fact, you were still backing National Fetish Day — saying you would wear your purple tie or shirt — until our final call when we pointed out the event slogan was 'perverts wear purple'. Imagine the story we could have written if we hadn't done this? This paper respects you as a Labour MP with an independent voice. However, this doesn't stop us writing stories when you drop yourself in it."[8]
- ↑ 1.0 1.1 1.2 NFD Statement. National Fetish Day. Retrieved on 2008-01-29.
- ↑ Homepage. International Fetish Day. Retrieved on 2008-01-29.
- ↑ 3.0 3.1 Home. National Fetish Day. Retrieved on 2008-01-29.
- ↑ "MP confesses to horse fetish", Metro, 2008-01-20. Retrieved on 2008-01-25.
- ↑ Oglaza, Glen (2008-01-21). MP Is In A Bind Over National Fetish Day. Sky News. Retrieved on 2008-01-25.
- ↑ Template:Cite episode
- ↑ 7.0 7.1 Robson, Ian. "North MP hot under collar at fetish mistake", Sunday Sun, 2008-01-20. Retrieved on 2008-01-25.
- ↑ 8.0 8.1 Smith, Caroline; Campbell, Ronnie (2008-01-27). Ronnie Campbell MP complains about fetish story. Sunday Sun. Retrieved on 2008-01-28.