text:
Caisson failure induced by wave action
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Data publicació2015-08-29
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In 2001 a storm induced the failure of four caissons recently built for the construction of a dyke in a new entrance to the Barcelona Harbor. Understanding the failure required the analysis of the construction history and the wave action. The caissons were founded on a thick layer of soft silty clays potentially liquefactable. The main properties of foundation soils are discussed based on laboratory and field data. A back-analysis of the failure is developed using an analytical and a numerical procedure. The analytical procedure is based on well-known solutions and concepts in Soil Mechanics. It involves the calculation of pore water pressure distributions on the foundation, its dissipation, the induced increase of the undrained strength, and the caisson stability during construction stages. An analysis of liquefaction, which explains the collapse observed, is also described. The problem is also solved numerically using a commercial finite difference code. This second analysis allowed a cross-checking of the analytical solution and the quantification of some simplifications introduced that can be properly accounted for in the numerical analysis. In the final part of the paper an alternative stable design of the caisson dyke is presented.
CitacióAlonso, E., Pinyol, N.M., Fernández, P. Caisson failure induced by wave action. A: "Forensic geotechnical engineering". 2015, p. 45-93.
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text: I noticed an interesting thread in the Droid X forum about useful Build.prop edits and wonder why there is not one here? For example (some listed from LexusBrian400 thread): To save battery by decreasing the amount of time Wifi looks for an access point, I changed wifi.supplicant_scan_interval = 60 to wifi.supplicant_scan_interval = 90 Now wifi will scan once every 1.5 minutes when not around a known location instead of once every minute which will save battery. Or not so useful, but possible for fun.. change your Build Number ro.build.display.id=FRG01B to ro.build.display.id=FRG01B blah blah now see something more personalized in the settings > about phone > Build Number. Mine says FRG01B Locked & Loaded To make the phone ring faster when dialing out ro.telephony.call_ring.delay=3000 to ro.telephony.call_ring.delay=1000 Now the phone rings pretty much instantly when dialing out.

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Hello, SORRY NOT INVOLVED WITH PERSONAL CHECKS. SORRY I DO NOT SHIP TO ALASKA, HAWAII OR CANADA EITHER!!!!!!. Up for Auction this evening is a Lot of 124 Pieces from Lego Company. These are Original Duplo Size Lego Blocks along with and Original Lego Lap Table.. This is a mixture of all sizes of blocks, These are very Clean and All Original Lego Brand Duplo Size Blocks. Also Original Lego Brand Lap Table, The only thing wrong with the table is the Lego Sticker pealed off by kids on both sides see last pics. Nice Clean Green Board with storage on both sides, Also Included is the Storage Lego Bin which you can see is full with the 124 Pieces. Various Sizes and shapes with one person. Very Nice Super Large Lot. Actual Items in Picture. Smoke Free Home. PLEASE E-MAIL ME WITH ANY REQUESTS OR QUESTIONS. I WILL TRY TO ANSWER THEM. I'm starting the bidding out LOW at $30.00. Shipping Cost will be $16.95 Parcel Select Shipping in a Box or Fed Ex Ground depending on Location. Shipping. Insurance optional at end of Auction. If not Insured seller is not responsible for shipping problems. Pay Pal payments only. Will ship within 2 Business Days. When Shipped That evening I will send you a tracking # for you to trace on . SAVE ON MULTIPLE AUCTION WINS WITH SHIPPING. WHEN USING PAY-PAL ON MULTIPLE WINS MAKE SURE ONLY TO CHECK OUT 1 TIME AND COMBINE... read more


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WTF, as far as any of us can tell, remains blissfully unaware of any other meanings of this infamous three letter expression. Or perhaps some folks just don't want to listen or change their style. In fact, Wisdom, Tenacity, and Focus are all extremely important. However, humility and purpose are equally crucial. Also, trying not to be arrogant by attacking those who don't always agree with you.
W- George W Bush's Presidency was full of lies and he had an especially peculiar run, to say the least. W was President during Gulf War and 911. Anyone ready to give his a pass in his image remake has got to stop and think.
T- Donald J Trump Some say Trump's self-proclaimed leadership skills need to show lots more compassion and much less ego and the desire to help the rich, including himself. The jury is still out and investigators are busy.
F - Fateful meeting at the tarmac William Jefferson Clinton's less than presidential actions is what got him impeached but his fateful outreach at the tarmac to US Attorney General Loretta Lynch may have caused his wife Hillary Rodham Clinton the election, which she could have won as she easily received the popular vote.
The character of an individual has much to do with who they are and what you'll do once given the opportunity to lead or crash and burn.
We now have The Rock hinting that he may run to be President of The United States of America http://www.cbsnews.com/news/dwayne-johnson-for-president-committee-files... Kid Rock has announced he is running for The US Senate http://www.newyorker.com/humor/daily-shouts/im-kid-rock-and-i-approve-th... and we have a president who was once a wannabe international playboy and a reality NBC TV celebrity. https://www.washingtonpost.com/blogs/plum-line/wp/2017/07/14/this-nbc-ne...
Everyone knows that all improves with diversity and most intelligent people would agree, but seriously?
Enough with the George W. Bush nostalgia http://www.salon.com/2017/07/13/enough-with-the-george-w-bush-nostalgia/...
Even the most painfully ignorant #Trump supporters will have this sad fact staring them in the face before too long... Screw America, it's all about ME, MYSELF AND I
I love that song, Me, Myself, and I. The one that sampled George Clinton, you know Im talkin about. Love from Jersey. Peace
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Pigs on livestock farm. Pig farming.
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Keywords: eat, eating, family, farm, farming, fauna, feeding, growth, hungry, kids, life, little, pet, pink, young.


text: Now that I've got my Stihl, I'm attacking logs too large to lift onto the sawbuck. Fun! Yowza, that saw rips! But Ive learned on this forum that you should never let your saw blade touch the earth or it'll dull the cutters in an instant. So what's the best way to buck a log laying flat on the ground? Bring the sawblade through the wood almost to the ground then roll the log over to finish the cut? Or roll the log onto a small wedge or something to get it an inch off the ground?


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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Autism comprises a spectrum of behavioral and cognitive disturbances of childhood development and is known to be highly heritable. Although numerous approaches have been used to identify genes implicated in the development of autism, less than 10% of autism cases have been attributed to single gene disorders.
We describe the use of high-resolution genome-wide tilepath microarrays and comparative genomic hybridization to identify copy number variants within 119 probands from multiplex autism families. We next carried out DNA methylation analysis by bisulfite sequencing in a proband and his family, expanding this analysis to methylation analysis of peripheral blood and temporal cortex DNA of autism cases and matched controls from independent datasets. We also assessed oxytocin receptor (OXTR) gene expression within the temporal cortex tissue by quantitative real-time polymerase chain reaction (PCR).
Our analysis revealed a genomic deletion containing the oxytocin receptor gene, OXTR (MIM accession no.: 167055), previously implicated in autism, was present in an autism proband and his mother who exhibits symptoms of obsessive-compulsive disorder. The proband's affected sibling did not harbor this deletion but instead may exhibit epigenetic misregulation of this gene through aberrant gene silencing by DNA methylation. Further DNA methylation analysis of the CpG island known to regulate OXTR expression identified several CpG dinucleotides that show independent statistically significant increases in the DNA methylation status in the peripheral blood cells and temporal cortex in independent datasets of individuals with autism as compared to control samples. Associated with the increase in methylation of these CpG dinucleotides is our finding that OXTR mRNA showed decreased expression in the temporal cortex tissue of autism cases matched for age and sex compared to controls.
Together, these data provide further evidence for the role of OXTR and the oxytocin signaling pathway in the etiology of autism and, for the first time, implicate the epigenetic regulation of OXTR in the development of the disorder.
See the related commentary by Gurrieri and Neri: http://www.biomedcentral.com/1741-7015/7/63
Classic autism comprises a spectrum of behavioral and cognitive disturbances of childhood development. The core autism phenotype includes deficits in social interaction, language development and patterns of repetitive behaviors and/or restricted interests. The population prevalence of the spectrum of autism disorders is estimated to range between 1/300 [1] to 1/100 http://www.nschdata.org/, with a male: female ratio of 4:1 [2,3]. The disorder has been shown to be highly heritable with the relative risk for siblings being approximately 2% to 8%, much higher than that of the general population [4]. To date, only a small percentage of autism cases (<10%) have been ascribed to single gene disorders such as fragile X syndrome, tuberous sclerosis [5] and Rett syndrome [6]. Numerous approaches including genetic linkage, genome-wide association, candidate gene association and gene expression analysis have been used to identify the additional genes implicated in the development of autism [7,8]. However, the heterogeneous nature of autism and autism spectrum disorders has limited their success.
An additional approach to identify genes involved in autism is to characterize copy number variants (CNVs), that is, chromosomal deletions and duplications, that are known to be present within at least 5% of individuals with idiopathic autism [9]. Autism CNVs have been shown to involve almost all chromosomes [10,11], with the most frequently observed alteration localizing to chromosome 15q11-13 [12-23]. A number of different methods have been used to characterize autism related CNVs, including but not limited to, cytogenetic G-banding [14,23,24], metaphase fluorescence in situ hybridization (FISH) [22], Southern blotting [18], loss of heterozygosity (LOH) analysis [15-17,19], quantitative polymerase chain reaction (PCR) [25] and, more recently, genotyping and representational oligonucleotide microarray analysis (ROMA) [26].
Here we describe the use of genome-wide tilepath microarrays and array comparative genomic hybridization (CGH) to identify CNVs in a dataset of 119 unrelated probands from multiplex autism families [27]. The genomic profiles of our autism dataset were compared to the array CGH profiles of 54 phenotypically normal individuals, to previously published CNVs present within the database of genomic variants [28] and to the Autism Chromosome Rearrangement Database http://projects.tcag.ca/autism/. The most significant finding thus far from our analysis is a heterozygous deletion of the oxytocin receptor gene (OXTR) (MIM accession no.: 167055) in an individual with autism and his mother with putative obsessive-compulsive disorder (OCD). We further investigated the relationship between OXTR and autism by carrying out epigenetic analysis of the promoter region of OXTR. We show that the gene is hypermethylated in independent cohorts with autism as compared to controls, in both peripheral blood mononuclear cells (PBMCs) and the temporal cortex. Additionally, our analysis of expression levels of OXTR in the temporal cortex shows decreased levels of expression in individuals with autism as compared to controls matched for age and sex.
These data suggest that OXTR and the oxytocin signaling pathway play an important role in the etiology of autism and autism spectrum disorders and implicate epigenetic misregulation of OXTR in this complex disease.
Research diagnostic classification entailed the collection of detailed family, developmental, and medical history and systematic screening of each child with autism before proceeding with clinical assessments. The clinical diagnosis of autism was confirmed by standardized diagnostic assessments once a family had completed the screening process and was considered eligible. For research classification, a clinical diagnosis that conforms to Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria was made based on all available medical, clinical, and behavioral data. The clinical diagnosis was established as a research diagnosis on the basis of scores that exceed established cut-offs for autism on the Autism Diagnostic Interview-Revised (ADI-R) [29,30]. In addition, all individuals demonstrated a minimum IQ equivalent of 35 or Vineland Adaptive Behavior Scale age equivalent of 18 months. This ensured a sufficient developmental level for reliable classification on diagnostic measures. All instruments were administered by clinical staff that had been formally trained on all measures and, as appropriate, had demonstrated reliability within the research group as well as at clinical centers. All individuals are qualified only after review of materials by a licensed child psychologist (MC). Parents/caregivers were informed of the purposes, risks, and benefits of participating in this project and provided informed consent.
All aspects of the research study were approved by the Institutional Review Boards of the participating centers. DNA for copy number and methylation analyses was obtained from the peripheral blood of autism probands from multiplex families, the extended family of the proband with the OXTR deletion, and phenotypically normal controls. Genomic DNA was extracted from whole blood using the Pure Gene method and standard protocols, as described previously [31]. DNA for the methylation analysis was collected from 20 autism cases and controls, all individuals were Caucasian, and the male to female ratio was 1:1.
Postmortem studies were performed using frozen brain tissue samples dissected from the superior temporal gyrus (BA 41/42) of eight patient-control pairs, obtained through the Autism Tissue Program from the Maryland National Institute of Child Health and Human Development (NICHD) Brain Tissue Center and the Harvard Brain Tissue Resource Center (Table (Table1).1). This neocortical region was chosen because it hosts well documented structural and functional abnormalities in autism [32-35]. These tissue samples largely overlap with those employed in our recent studies of the MET and PRKCB1 genes [36,37]. Clinical and demographic information, family history, and autopsy reports were obtained from the Autism Tissue Program web site http://www.atpportal.org and are summarized in Table Table1.1. The presence of mental retardation was defined on the basis of a full-scale IQ <70. Autism spectrum disorder cases fulfill DSM-IV diagnostic criteria [38], confirmed using the ADI-R [29,30]. Although the methylation study was not planned according to a matched design, all controls were selected to match patients on sex, age (± 2 years, wherever possible) and postmortem interval (PMI), where possible (Table (Table11).
High-resolution genome tilepath microarrays were constructed using large bacterial clones (bacterial artificial chromosome (BAC) clones) as previously described [39]. Briefly, BAC DNA was purified by alkaline lysis and used as the template for three different, degenerate oligonucleotide primed PCR reactions, prior to a second round of amino linking PCR and printing onto Codelink slides (GE Bioscience, Piscataway, NJ, USA) using a Genetix Qarray2 (Genetix, Boston, MA, USA). A total of 450 ng of autism proband and control DNA, from peripheral blood, were differentially labeled with Cy3-CTP and Cy5-CTP (BioPrime Labeling Kit; Invitrogen, Carlsbad, CA, USA), purified (Qiagen, Hilden, Germany) and hybridized to the tilepath arrays using the MAUI hybridization station (BioMicro Systems Inc, Salt Lake City, UT, USA). Image capture of the hybridized arrays for fluorescent intensity extraction was performed using a Genepix 4100A scanner (Molecular Devices, Sunnyvale, CA, USA) and Bluefuse microarray software (BlueGnome http://www.cambridgebluegnome.com/bluefuse_micro) was used for data processing of the scanned images prior to porting into Nexus (BioDiscovery http://www.biodiscovery.com/index/nexus) for analysis.
Microarray data was preprocessed in Nexus by removing poor quality flagged spots (confidence <0.3 as defined by Bluefuse software), removing background by Lowess correction before normalization of log2 ratios and combining BAC replicates. BioDiscovery's rank segmentation algorithm (RSA), which is similar to circular binary segmentation (CBS) [40], was used to identify genomic rearrangements. Briefly, the algorithm uses a normal distribution function for testing for change points as opposed to the non-parametric permutation based statistics used in the original CBS algorithm. It also uses the log ratio rank of each probe as oppose the log ratio value itself. The calling algorithm used cluster values and defined log2 thresholds of ± 1.4 and 0.38 for two and one copy gain/loss, respectively. We applied a conservative cut-off of three BAC clones showing the same copy number change trend to define genomic deletion or duplication with the significance threshold set at 0.005. Array CGH dye-swap experiments were carried out on 21 samples to confirm 21 genomic changes, including novel and known CNVs within the database of genomic variants.
DNA copy number was validated using the Applied Biosystems 7900 HT Fast Real-Time PCR System (Applied Biosystems, Foster City, CA, USA). Primers and probes were designed to a region spanning exon 2 in OXTR: forward 5'-GCTGAACATCCCGAGGAACTG-3' and reverse 5'-GCAAATGAGCGGGAATCCTCTA-3'. DNA samples from autistic probands and their family members were used to determine if the CNV was familial or de novo. DNA isolated from tumor samples with known deletions at the regions containing OXTR were used as 1 × copy number controls and an unaffected individual identified in our normal-normal CGH experiment served as our 2 × copy number control at these loci. A primer and probe set designed to the single copy gene that encodes the RNA moiety for the RNase P enzyme, RPPH1 (MIM accession no.: 608513), a region of stable copy number (2 ×), was used to normalize each sample for equal input. Copy number was assessed in quadruplicate for each sample and the 2-ΔΔCT method was used for analysis [41].
Microsatellite markers were analyzed in the family carrying the deletion of OXTR to determine maternal or paternal contributions. Five markers on chromosome 3 (D3S1489, D3S18, D3S4539, D3S4163, D3S3691) were fluorescently labeled using PCR (primers indicated in Additional file 1) and size fractionated on an Applied Biosystems 3730 capillary sequencer (Applied Biosystems, Foster City, CA, USA). Then, 1 μl of the PCR product was diluted 1/70 and run on an agarose gel to confirm amplification, and 1 μl of the diluted PCR product was added to 19 μl of HiDye Formamide/LIZ 500 Standard solution and loaded on to the capillary sequencer and analyzed using standard software.
DNA isolated from blood or brain samples was bisulfite converted using a methylSEQr Bisulfite Conversion Kit (Applied Biosystems, Foster City, CA, USA). Primers were designed to bisulfite-converted regions of CpG islands in the promoter region of the OXTR gene and in the third intron that had previously been shown to exhibit different patterns of methylation among individuals [42] (Additional file 2). PCR was performed on bisulfite treated DNA using the following reaction conditions, 1 cycle: 95°C for 3 min, 55 cycles: 95°C for 1 min followed by 56.8°C for 1 min followed by 72°C for 3 min, and a final extension at 72°C for 5 min. The reaction was run on an agarose gel and the bands were gel extracted (Qiagen, Valencia, CA, USA) and TOPO TA cloned (Invitrogen, Carlsbad, CA, USA). Single clones were isolated and plasmids purified (Qiagen, Valencia, CA, USA). Sequencing was performed using the M13 forward primer provided with the TOPO TA cloning kit. On average, 10 individual clones were sequenced per amplicon in order to calculate percentage methylation at each of the CpG sites (note: 8 clones were used in OXTR family analysis). Bisulfite conversion was verified for each clone by assessing the C to T conversion of non-CpG sites. The average methylation level (%) was determined for each individual and these values were used to generate an average percentage methylation for each group, autism cases and normal controls, respectively (Additional file 1). The Welch-Satterthwaite t test was employed to adjust for unequal variances between groups and to compare the mean methylation level (%) at each site between the autism cases versus control groups. A nominal significance of P ≤ 0.05 indicated a significant change in the methylation state between the two groups. The direction of the change was determined by comparing the average methylation level at each site between the two groups.
Total RNA was extracted from four case-control pairs matched for age, sex and PMI (see Table Table1)1) using the TRIzol reagent (Invitrogen, Carlsbad, CA, USA) according to standard methods, and RNA quality was checked using a Bioanalyzer (Agilent, Santa Clara, CA, USA). Reverse transcription was performed with the QuantiTect Reverse Transcription kit (Qiagen, Valencia, CA, USA), using random hexamers as primers and a starting RNA quantity of 1 μg in a 20 μl final volume. OXTR cDNA was quantified using an iQ5 Multicolour Real-time PCR Apparatus (Bio-Rad, Hercules, CA, USA), according to a standard ΔΔCt Syber Green protocol [43]. PPIA (MIM accession no.: 123840) cDNA was measured in parallel and used as a standard for normalization. Due to relatively low neocortical OXTR gene expression levels compared to PPIA, PCR reactions were performed using 1:5 and 1:25 cDNA dilutions, respectively. OXTR primers were targeted to exon 2, which is shared by all four alternative mRNA transcripts, and designed as follows: F2, 5'-CTGAACATCCCGAGGAACTG-3', and R2, 5'-CTCTGAGCCACTGCAAATGA-3'. To ensure specificity, PCR products were initially sequenced using a CEQ8000 DNA sequencer (Beckman-Coulter, Fullerton, CA, USA), and afterwards checked by running a melting curve at the end of each experiment. Analysis was performed using the 2-ΔΔCT method [41] and expression level from the group of cases and the group of controls were compared using a one-tailed paired t test.
Array CGH data was generated for 54 phenotypically normal individuals in 27 sex-mismatched hybridizations to establish the performance of our large insert bacterial clones on the genomic tilepath microarray. Sex mismatching was used to establish the baseline of heterozygous loss using the X chromosome as a reference. Analysis of the 27 normal-normal array CGH experiments identified 12 CNVs within 2 or more of the array CGH hybridizations. In all, 10 CNVs were contained within previously published CNVs from the database of genomic variants [28], while 2 CNVs extended the size of the known CNV regions (Additional file 3).
The genomic profiles of 119 idiopathic autism probands (93 male and 26 female) were generated by sex-mismatch array CGH experiments using controls from our normal-normal analysis. A total of 113 loci within 111 autistic individuals contained at least 1 genomic deletion or duplication, with a range of 1-6 CNVs per individual (Additional file 3). Approximately half of these, 52, were wholly contained within known copy number variants from the Database of Genomic Variants [28], 57 loci overlapped with 1 or more known CNVs regardless of size (CNV regions), and 5 were novel regions of loss (n = 2) or gain (n = 3) that contained 21 genes (Additional file 3). According to Fable http://fable.chop.edu/ only one gene within these novel regions, ring finger protein 19A (RNF19A, also known as p38) in a 0.6 Mb deletion on chromosome 8q22.2, has been previously implicated in autism spectrum disorders (ASDs) via an observation in Rett syndrome [44], and none fell within previous regions of linkage (as reviewed in [7]). We chose to focus on 19 of the 113 putative deletions or duplications identified in the first screen to validate by array CGH dye swap experiments using select individuals (Additional file 3, top) or, in the case of the OXTR deletion described below, by microsatellite and quantitative real-time PCR analysis. Genomic rearrangements of note included a 12.5 Mb deletion within 2q24.1-2q24.3, a region previously linked to autism [45,46] and containing 41 known genes; a 4.6 Mb duplication and a 3.4 Mb deletion within 15q11-13 that contains a complex arrangement of CNVs and has previously been associated with autism by numerous genetic linkage [47-49] and genome copy number studies [12-23]; and a 0.7 Mb deletion in 3p25.3 that contains 5 genes: Lim and cysteine-rich domains 1, LMCD1 (MIM accession no.: 604859); C3orf32; Caveolin 3, CAV3 (MIM accession no.: 601253); oxytocin receptor, OXTR (MIM accession no.: 167055); and RAD18 (MIM accession no.: 605256) (Figure (Figure1).1). Though this region contains known smaller copy number variants, none of these correspond to a deletion of 0.7 Mb identified by this study or contain the genes mentioned above. Additionally, OXTR is a candidate autism gene whose levels may be important for social development of offspring [50].
Based on the strength of the novel deletion of OXTR and the previous data implicating OXTR in the development of autism [51-53], we focused further copy number analysis on the 3p25.3 deletion by screening other members of the proband's family. Quantitative real-time PCR (qRT-PCR) analysis confirmed that the deletion containing OXTR was not a de novo event (Figure (Figure2a)2a) and microsatellite analysis confirmed that the deletion was inherited from the mother (Figure (Figure2b),2b), who has possible OCD (not clinically evaluated). OCD cases have been reported to be more common among first-degree relatives of autistic probands, which may hint at a common genetic mechanism or pathway shared between these two disorders [54,55]. Curiously, the proband's affected brother did not inherit the allele containing the genomic deletion (Figure (Figure2).2). Microsatellite analysis of the deletion revealed that the proband's alternative allele was inherited from the father, therefore excluding the prospect of uniparental disomy at the OXTR locus contributing to the phenotype (Figure (Figure22).
Based on the CNV data within the OXTR deletion family, we hypothesized that a hemizygous deletion of OXTR may result in a reduction in the available levels of OXTR in utero and during development, ultimately leading to the development of autism. However, if this is true, it is unclear how this deletion confers autism in the proband when the proband's affected sibling does not carry the deletion. To investigate the possibility that a mechanism other than a genomic deletion may play a role in decreasing OXTR levels in the affected sibling we investigated the DNA methylation status, a form of epigenetic silencing, of two regions of OXTR previously shown to be methylated and associated with differential expression of the gene in liver and myometrium [56,57]. We carried out bisulfite sequencing (BSS) analysis of cloned alleles of two OXTR CpG islands in the peripheral blood mononuclear cells (PBMCs) of all four family members (Figure (Figure3).3). The first CpG island overlaps exons 1, 2, and 3 of OXTR and is located on chromosome 3 at 8,783,962-8,786,280 base pairs (Ensembl Homo sapiens version 54.36p, NCBI36). Kusui et al. had shown that the methylation status of a specific 405 base-pair fragment of this CpG island (termed 'MT2' by Kusui et al.) is important for tissue-specific expression of OXTR (Figure (Figure33 depicts MT2 position). The second CpG island is located within the third intron of OXTR on chromosome 3 at 8,775,160-8,776,624 base pairs (Ensembl Homo sapiens version 54.36p, NCBI36). This island has previously been experimentally defined as an EcoRI-KpnI fragment that was less methylated in myometrial DNA than in the DNA from peripheral blood leukocytes [42]. All CpG dinucleotides tested within the intron 3 CpG island were heavily methylated in all family members (data not shown). However, several of the 33 CpG dinucleotides tested within the region overlapping exons 1, 2, and 3 of OXTR differed in methylation level between family members. Specifically, CpG dinucleotides at positions -959, -934, -924, -901 and -860 (relative to translation start site) showed the most dramatic differences in methylation status, with the proband's affected sibling being heavily methylated at sites -934, -924 and -901. These specific residues fall within the critical region (MT2) in the CpG island of OXTR shown by Kusui et al. to regulate the expression of OXTR in liver [56]. Importantly, in keeping with the hypothesis that increases in DNA methylation (hypermethylation) lead to gene silencing, CpG sites -934 and -924 showed the largest increase in methylation, 37.5%, between the autistic sibling and the non-autistic father (62.5% methylated versus 25% methylated, 100% methylated versus 62.5% methylated, respectively), both lacking the OXTR deletion. The 100% methylation of a specific CpG could indicate maintenance of an aberrant methylation mark, making this a more dramatic change.
Given the data observed within the OXTR deletion family, we hypothesized that DNA methylation of residues found within the critical region of OXTR regulation may extend beyond this family and represent a more general epigenetic contribution to autism spectrum disorders. We extended our BSS analysis of the 5 differentiallly methylated CpG dinucleotides to PBMCs from 20 phenotypically normal control individuals (10 males and 10 females) and 20 individuals with autism (10 males and 10 females). BSS data showed significantly increased methylation in the PBMCs of CpG -860 (P = 0.0009), -934 (P = 0.0081) and -959 (P = 0.0026) in individuals with autism compared to controls (Table (Table2).2). When the data are stratified by sex, the associated significance of -860 and -934 can be ascribed only to males (Table (Table3)3) and that of -959 to females (Additional file 4).
To determine if differential methylation of the five putative regulatory OXTR CpG dinucleotides may be important in a tissue implicated in the etiology of autism, we analyzed temporal cortex tissue from eight individuals with autism and eight controls matched for age and sex (see clinical data in Table Table1),1), six male and two female. The BSS results in the cortex again showed statistically significant hypermethylation in the autism cases versus normal controls. There was significant increased methylation at CpG -860 (P = 0.0251), CpG -901 (P = 0.0149), CpG -924 (P = 0.0448) and CpG -934 (P = 0.0233) between autism cortex tissue compared to the normal cortex controls (Additional file 5). We performed a stratified analysis to increase the homogeneity within the sample using six male samples matched for age and sex, and to validate our sex-specific findings in blood. This analysis reproduced the significance at sites -924 and -934 (Table (Table33).
To functionally correlate DNA methylation levels within the temporal cortex DNA and expression of OXTR from which the DNA was derived, we carried out quantitative PCR analysis of mRNA levels from the cortex tissue of four autism cases matched for age and sex and four controls. Assays were designed to exon 2 of the gene. Although OXTR expression levels were low, we detected a sex-specific decrease in expression of OXTR for each of the autistic male control pairs tested (Figure (Figure4a),4a), and in two of the three cases expression levels correlated with an increase in methylation at site -934. As a group, autistic males showed a 20% decrease in expression compared to controls that was significant at P = 0.0389 (Figure (Figure4b).4b). These data suggest that increased methylation of the promoter in OXTR correlates with decreased expression of the gene in a tissue type relevant to the development of autism.
For several years the characterization of CNVs in autism patients has identified genes that potentially contribute to the etiology of the disorder [9,58-60]. In this study we used high-resolution genomic tilepath arrays with comparative genomic hybridization to identify 113 CNVs within 119 unrelated autistic individuals. Of note were five novel CNVs that do not map to prior regions of linkage and which, according to Fable http://fable.chop.edu/, contain only one gene in 8q22.2 (RNF19A) that has previously been implicated in autism spectrum disorders [44]. CNVs observed in known autism regions included a 12.5 Mb deletion within 2q24.1-2q24.3 [45,46], two rearrangements in 15q11-13 [12-23,47-49], and a 0.7 Mb deletion in 3p25.3. We chose to focus on the deletion in chromosome 3p25.3 because of previous reported linkage to the region [61,62], association data implicating the oxytocin receptor (OXTR) that is contained within the deletion to the etiology of autism [51-53]. More recently, the DECIPHER database https://decipher.sanger.ac.uk/ has had copy number data deposited from a syndromic patient who has developmental delay and cognitive impairment presumably emanating from a novel 1.1 Mb deletion that contains OXTR, amongst other genes. Detailed DNA methylation analysis of the promoter region of OXTR, prompted by the observation that the proband's autistic brother did not carry the novel deletion, identified a single CpG dinucleotide within a known OXTR control region [56] that, independently, showed a statistically significant increase in methylation in PBMCs and the temporal cortex tissue of autism cases compared to controls. The identification of similar methylation profiles in the temporal cortex and peripheral blood may be indicative of an early developmental event during which these profiles are differentially established, prior to germ layer specification. If this locus is epigenetically labile, then it might be vulnerable to (unknown) exposures in utero during the first few weeks of pregnancy that lead to shifts in methylation status of OXTR. Similar influences have been seen in IGF2 methylation based on in utero exposures such as smoking and folic acid intake in humans [63]. Since epigenetic profiles undergo reprogramming during very early gestation (fertilization to implantation), it is not surprising that the profiles in these two disparate tissue types of ectodermal and mesodermal origin are similar and furthermore provides a potential means for detection in multiple, more accessible tissues.
The impact of this epigenetic mark on OXTR expression was supported by analysis of the corresponding mRNA from the temporal cortex of autism cases matched for age and sex and controls. As one would hypothesize given their increased methylation of OXTR, the autism cases also showed statistically lower transcript levels of OXTR expression compared to the normal controls. Because deletions encompassing OXTR have not been observed in other studies characterizing structural variation in autism [58,64,65] such events appear to be rare. At the same time our findings suggest that the hypermethylated status of OXTR in autism, resulting in a decrease in OXTR expression, may more commonly contribute to the disorder. While the mechanism for the development of autism from a germ line deletion of OXTR versus epigenetic silencing of the gene in the temporal cortex may clearly be different, the effect on oxytocin signaling could be the same. Together, these data provide strong evidence for the role of OXTR and oxytocin signaling pathway in the etiology of autism and, for the first time, show that the epigenetic regulation of OXTR may be an important factor in the development of the disorder.
Epigenetic control of autism susceptibility is a recent concept and most certainly a topic of great interest in the field. Over the past decade, researchers have uncovered suggestive links between epigenetics and autism, for example, autism is associated with duplications of 15q11-13 (especially maternally inherited), an imprinted region in the genome where DNA methylation status has been linked to Prader-Willi syndrome (PWS) and Angelman syndrome (AS) [66]; mutation within a gene that encodes a methyl-DNA-binding protein (MECP2, (MIM accession no.: 300005)) is the causative agent of Rett syndrome [67]; and mutation of this same gene has been associated with both autism and AS populations [55]. Nagarajan et al have shown that 79% of autism cases have a decrease in MECP2 expression in the frontal cortex and that an increase in aberrant DNA methylation correlates with this decrease in MECP2 expression [68]. These data implicate epigenetic dysregulation as a mechanism for the development of autism and justify the examination of DNA methylation of autism candidate genes, such as OXTR identified in this study.
The oxytocin receptor, OXTR, is spatially and temporally regulated by a complex combination of sex hormones, inflammatory cytokines, oxytocin (OXT) feedback and epigenetic mechanisms [56,57]. It is a high affinity G-protein coupled receptor for OXT, a nine amino acid hormone that has important and complex roles in animal physiology and behavior [69], including parturition and neurotransmission. A putative role for OXT in the development of ASDs was first highlighted by Insel and colleagues [70] who showed that signaling of oxytocin and the closely related molecule vasopressin play important 'prosocial' roles influencing social behavior and cognitive function in a species-specific manner [71-73]. Subsequent studies in mice revealed that Oxt [74] and Oxtr [75] knockouts largely resulted in normal parturition, however, social memory was impaired. Recently, Lee and colleagues [76] showed that only male mice with a targeted forebrain knock out of Oxtr exhibited social impairment by failure to recognize individuals of their own species. It has been suggested that the normal social behavior of the female knockout mice may be attributed to the compensatory function of vasopressin or developmental compensation [69,77]. In an excellent review by Carter [50] that describes the complex sexually dimorphic roles of vasopressin and oxytocin in brain function and behavior, it is apparent that aberrant oxytocin and/or vasopressin signaling is likely to elicit sex-specific outcomes, which is of particular relevance to autism because of disproportionate number of affected males. Our family analysis identified an OXTR deletion in the mother who does not present with autism. Sex-specific effects of OXTR function from animal models, together with statistical data that suggest dominantly acting de novo mutations may have reduced penetrance in females [78], may explain why the heterozygous deletion of OXTR in the mother from our study does not result in autism while the male proband displays the disorder.
We identified a single CpG dinucleotide within a predicted CpG island that showed statistically significant hypermethylation in PBMCs and the temporal cortex of individuals with autism compared to controls. Although the dominant paradigm for regulation of transcription by DNA methylation suggests that clusters of CpGs are necessary for silencing, recent evidence has indicated that methylation of single CpG dinucleotides may also lead to transcriptional changes via interference of transcription factor binding or recruitment of silencing factors [79]. This is the most likely explanation for the findings presented here as CpG site -934 falls within a predicted c-Rel, ZHX2, and LGALS4 binding domains (T. Wang, personal communication). However, further molecular work is required to dissect the likely complex transcriptional regulation of OXTR.
In this study, we focused on the temporal cortex (Brodmann areas 41/42 and 22) because studies have shown that localized temporal dysfunction is linked with clinical symptoms in autism, such as perceptive, emotional and cognitive deficits [32-35]. Although we were not able to determine the methylation status of cortex tissue from the family in which we observed the OXTR deletion, the data we collected from the affected sibling shows hypermethylation of the CpG dinucleotide (-934) in the predicted CpG island upstream of OXTR. Given our results suggesting that DNA methylation of OXTR in PBMCs may be a marker of methylation status in the temporal cortex, it follows that the affected sibling may also exhibit a decrease in OXTR expression due to methylation instead of deletion; thus implicating two separate mechanisms of transcriptional regulation with the same outcome. These results suggest that because the methylation status of site -934 is significantly different in the temporal cortex and PBMCs between autism cases and controls, measuring the methylation status of OXTR from the blood for autism cases could act as a surrogate for methylation status in the temporal cortex and be diagnostic of affection status, together with traditional diagnostic criteria.
In summary, the data presented suggest that genomic deletion or aberrant methylation of OXTR may contribute to the development of autism. We acknowledge that screening for these genomic changes in a large, well controlled autism sample is necessary to determine the prevalence of these changes and their relationship to the disease. However, regardless of the sample size, we provide strong evidence that the epigenetic regulation of OXTR may be an important factor in the development of the disorder and suggest that further studies begin to focus on this regulatory event and its relationship to disease.
The authors declare that they have no competing interests.
SGG conceived the experimental design and wrote the paper; JJC assisted with experimental design, carried out experiments and wrote the paper; AT, JJ, DB, DB, CM and CL carried out the experiments; RKA, HHW, GW ascertained autism families for the paper; PE and CFL assisted with experimental design, SKM assisted with the writing of the paper; MLC helped ascertain autism families and assisted with clinical assessment of the study population; AP and MAP-V assisted with experimental design and in the writing of the paper.
The pre-publication history for this paper can be accessed here:
Cloned bisulfite sequencing results for each peripheral blood mononuclear cell (PBMC) sample.
Primer pairs used for this study.
Genomic duplication and deletion events within 54 control and 119 autistic individuals identified by whole genome tilepath array comparative genomic hybridization (CGH).
OXTR promoter CpG methylation status in peripheral blood mononuclear cells (PBMCs) of 10 autistic females and 10 age-matched controls.
OXTR promoter CpG methylation status in the cortex of eight autism cases and controls matched for age and sex.
We thank all the patients and families who generously participated in this study, including the donors and their families of the cortex tissue, and the collaborating clinics and physicians for referring individuals to the study. We would also like to thank Joshua Virgadamo, Christina Sheedy and Rachel Cote for their laboratory assistance, Dr Elizabeth Hauser for evaluating our statistical techniques, Dr Ty Wang for transcription factor binding analysis, and Sarah Nelson for comments on the draft of this manuscript. This research was supported by the JP Hussman Foundation and National Institutes of Health grants P01-NS026630 and R01-NIH080647, and by MIUR PRIN 2006058195 (AMP). We also gratefully acknowledge the Autism Tissue Program, the Maryland NICHD Brain Tissue Center and the Harvard Brain Tissue Resource Center for providing brain tissues for this study (SGG and AMP).
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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I miss Lollapalooza being at Shoreline! I remember the first one there, with Jane's Addiction and Nine Inch Nails and Rollins and…anyway.
It's all Chicago all the time now, so… not so much for us, unless we wanna hellz Road Trip. Which is why I basically just You-Tubed anybody I wanted to see (like The 1975 and Ellie Goulding)
…and then my friend sent me this clip and I couldn't stop watching it. It's X Ambassadors doing the.most.amazing.version. of "Unsteady"…. x Jayn


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Want to donate more than your checkbook says you can? Anyone can turn the donation dial from "whippet" to "mastiff." Here are 3 ways to give your donation more muscle:
- Tell a friend about PA IPL, about your deep concerns about climate change and about your path, and invite your friend to donate, too. (Ahead in 2014: a new program initiative will tap into our one-to-one relationships!)
- Involve your congregation. We'll help. A generous 2014 matching grant from the national IPL will effectively double congregational contributions. The challenge is good both for direct contributions, and for directed donations by congregants (does your congregation call these "second collections"?). We'll only get the grant if we raise the match!
- Help expand our successful Bike Trip program with a local solidarity ride of any length. These will connect riders with congregations and elected leaders, supporting the efforts of our annual trip from State College to Washington, DC – and all contributions will be matched! We're actively looking for someone (or a group of someones) who will help organize local rides. The rides are fun, and hopeful, and we want to give more individuals, congregations, and communities the chance to participate. Do help us connect with the right people to make it happen!


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Phoenix man identified as 2016 serial street shooting suspect
PHOENIX (KSAZ) - Phoenix Police announced that the suspect in 2016's serial street shooting incidents has been identified.
According to police officials, Aaron Saucedo, 23, has been identified as a suspect in connection with the shootings. The announcement was made, during a news conference Monday afternoon that was attended by many public officials, including Phoenix Mayor Greg Stanton.
"Our officers did not rest," said Stanton. "Investigators worked every lead ,followed the evidence thorough, had a mission bring this killer to justice and get it right."
The announcement on Monday came, after police received 3,300 tips from members of the public, and Silent Witness will pay $75,000 in reward money.
>>VIDEO: Accused 'Serial Street Shooter' Aaron Saucedo proclaims his innocence during initial court appearance
(Can't see this Facebook video? Click here)
The shootings happened in 2016, and according to a Phoenix Police update posted on the department's verified Facebook page on August 3, 2016, at least 9 incidents are allegedly related to the serial street shooter. During the news conference, officials also linked a fatal shooting on New Year's Day in 2016 to the investigation.
According to a statement released by Phoenix Police after the news conference, Saucedo was booked for a total of 12 incidents between August 2015, and July of 2016. With the new addition, the total number of deaths from the serial street shootings now stand at nine.
(Can't see this Facebook post? Click here)
On April 25, Phoenix Police Chief Jeri Williams responded to reports that a "person of interest" was identified in the case, and said the department "cannot allow the release of unconfirmed information to jeopardize justice for anyone."
(Can't see this Facebook post? Click here)
At the time, sources told FOX 10 Phoenix that a man in custody for a previous murder incident is being looked at as a person of interest in the unsolved shootings, and that there are several coincidences between Saucedo and the serial shooting suspect. At the time, Saucedo was accused of murdering his mother's boyfriend, Paul Romero, in 2015.
Neighborhood residents react to Saucedo's Arrest
Monday's announcement of Saucedo's arrest and linking to the serial street shootings was news that not only the victims' families have been waiting for, but also people who live in the neighborhoods where the shootings took place.
FOX 10 Phoenix spoke with the family members of a 22-year-old man who was shot to death on New Year's Day 2016, whose case is now linked to the serial street shootings. Up until Monday, the case was unsolved.
The victim's family said the man was possibly shot in a drive-by shooting, when he was walking back from feeding the homeless that night.
"There's nothing we can do. We can't bring my brother back," said Hosanna Lopez, who is the victim's sister. "We can prevent it from happening to another family, because it can be anybody else's family also."
People in the neighborhood where the 22-year-old man was shot said they are happy that hard police work have paid off, and that they can rest easy, knowing the person who is allegedly responsible is now behind bars.


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MOVIE SYNOPSIS [ General Audiences ] With production of Germany, this 2012 film was directed by Eric Hordes. You can watch Der Gründer online on TV cable or theaters with original audio in German at different dates. This film premiered in theaters in 2012.
Rating: 5 by 22 users./
Runtime: 108 minutes
Helmut Krauss, Vera Göpfert, Santiago Ziesmer, Uwe Karpa, Pierre Kiwitt, Julie Trappett, Cecilia Pillado, Ingo Frischeisen, Ades Zabel, Rainer König, Julia Kratz, Michael Schumacher, Volkmar Leif Gilbert, Susanne Menner and Wolfgang Völz.
Comedy, Science fiction.
108-minute film (full movie) directed by Eric Hordes.
The original audio of Der Gründer has dialogues in or German, it was produced in Germany.
It premiered in cinemas or television in 2012.
Screenplay written by Eric Hordes.
Jakob Fritz.
This film was produced and / or financed by Hordes Film.
Composed by Florian Linckus and Eric Hordes.
Turbine Medien GmbH.
Without commercial breaks, the full movie Der Gründer has a duration of 108 minutes; the official trailer can be watched in streaming on the Internet. You can watch this full movie free in English or German in movie TV channels, renting the DVD or with VoD services (Video On Demand player, Hulu) and PPV (Pay Per View, Netflix).
See the page of this full movie, Der Gründer in FULLTV Movies.


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A Year of Cool Comic Book Moments – Day 81
Here is the latest cool comic book moment in our year-long look at one cool comic book moment a day (in no particular order whatsoever)! Here's the archive of the moments posted so far!
Today we look at the classic conclusion of the FF tale, "This Man, This Monster"!
The basic set-up of this Jack Kirby/Stan Lee tale is that a jealous (unnamed) scientist decides to get his revenge on Reed Richards by switching places with the Thing.
He, of course, is shocked by the goodness of the Fantastic Four, and, well, read on…
Perhaps a bit over the top, but overall, and excellent representation of the humanity of Lee/Kirby's Fantastic Four. And this was the NEXT issue after the Galactus trilogy!!
And NEXT issue introduces the Black Panther!
And this is only eight or so issues after the introduction of the Inhumans!!
What a heady time for a comic book!
As for "the" moment, I'm torn between the actual sacrifice and Reed's epitaph. I guess I'll go with the former.
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Your Career Services Team
Career Services is comprised of two teams: Career Coaching and Employer Relations. Collectively, we are dedicated to each student's personal growth and career development.
Brenda Fabian and Matt Soroka, the Career Services team, provide you with one-on-one assistance in meeting the goals communicated above. They can serve as guides, facilitators, and instructors. While you are expected to take personal ownership of your career and job search, Brenda and Matt collectively have years of experience to share and are committed to supporting you along the way.
Paul Poissant, Carol Lockard and Kim Kneas, on the Employer Relations side of the house, will strive to give you access to job and internship opportunities through bringing myriad employers right here to campus. Their resources and knowledge are extensive but are meant to represent one piece of the job search pie. The bulk of your job search success will depend on your personal networking skills, your planning, and your persistence.


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Short Story: Usually we had like 5 kids for youth group. I told some kids that we were going to Paintball Arena and all of a sudden hoards of kids showed up.
Pros: You get to...
All reviews seem positive
This Field Is the Product of Over 20yrs Experience in the Spot
Booking a private field at Paintball Arena allows you and your group to play the game on your own, with the assistance of you own head referee. Other customers will be present but will not play with your group. If you are a beginner group and want to play the game at your own pace, or have decided to play paintball to develop specific team-building and planning skills that will improve your workplace, or maybe you're having a friendly face-off between fire departments or stores... booking a private party is the way to go.Paintball is becoming the hot item for birthday and bachelor parties, and is perfect for an outing that is different from the usual get-together's. We adjust the equipment to best accommodate beginners, and we're ready to get into the spirit of things to make your party a day or night to remember!Special treatment for the bachelor or birthday-girl We sell refreshments, and we offer packages that include pizza and ice cream cakeTwo Playing Fields:* Featuring the Latest Ultimate Air & Supair Bunkers* Fields Can Combine To One Extreme Megafield* Large Staging Area* Nitro Tippmann Rentals* Padded, Sure-Grip Sports Turf Flooring* Professionally Trained Refs* Superb Lighting. On the Nassau/Suffolk County border,Paintball Arena at 400 Patton Avenue,West Babylon,Long Island NY is the Island's closest indoor field to New York City and is the closest playing field for Nassau County residents. Patton Avenue is in a small industrial area surrounded by the Pine Lawn National Cemetery,off Wellwood Avenue. Two minutes from Paintball Arena is Airport Plaza,offering a Multiplex Cinema and lots of choices for shopping and dining. Beyond are more shopping,dining,and entertainment opportunities on Route 110 in Farmingdale.The Arena staging area is comfortable and decorative. Soak up the Roman Coliseum gladiator theme,check out our paintball history wall,or watch games from behind the safety of two layers of anti-paintball netting,plenty of space and plenty of tables and chairs. Remember,this is indoor paintball! Real restrooms,cushioned carpet,paint,air refills,and paintball gear for purchase are spaced out to reduce long lines.What Is A Private Paintball Party?* Bachelor Parties or Any Reason* Birthdays* Enjoy a 2 Or 3 Hour Session with Your Own Group of Friends * Group Rates save You Money * Special Occasions
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The Most Outrageous Outfits At Bonnaroo, A 4-Day Hippy Fest In Tennessee
Alyson Shontell/Business InsiderBonnaroo is a 4-day music festival in the middle of nowhere Tennessee, 70-miles outside of Nashville.
It ended yesterday after 90,000 people enjoyed music performances by Billy Idol, Tom Petty, Paul McCartney, The Lumineers, R. Kelly and more.
If you've never attended Bonnaroo, then the attire worn by attendees may surprise you. Judgement-free hippies wear next to nothing to stay cool during the 95-degree days and camp in tents at night.
How strange were the outfits, exactly? We took lots of pictures. Prepare to be startled.
Check out the intesting attire at the nation's largest hippy fest, Bonnaroo 2013 > »
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They wanted desperately for things to work out, but they faced an insurmountable obstacle – the Indian government.
That's not a plot from an abandoned Barbara Cartland novel, rather news that Allen & Overy (A&O) and Indian firm Trilegal have called time on their referral relationship after giving up hope that India will liberalise its legal market any time soon (see story).
The pair first linked up in January 2008, when it seemed that liberalisation was just around the corner, and even extended the tie-up indefinitely last year because things were going so well (8 February 2011). Some 18 months later, alas, it has become a different story.
As India's economy continued to expand, the tie-up became more of a hindrance, since the firms weren't free to exploit the increase in legal work from other sources.
Other UK firms have split from their Indian best friends recently, too. In January 2011 Clifford Chance and AZB & Partners ended their tie-up (21 January 2011) and a few months later Clyde & Co ended its relationship with ALMT (27 April 2011).
With that in mind, you might consider that A&O and Trilegal did well to stick things out as long as they did, though at just under five years they still fell short of the seven-year itch.
Also on TheLawyer.com
Banking partner Helen Hancock joins Simmons & Simmons' burgeoning Bristol office from Burges Salmon, marking her second return to the firm – what is it about the place?;
The Bar Council has teamed up with Barclays to launch a third-party client money account to make payment easier in the growing number of situations where clients want to instruct a barrister directly;
And, former editor of The Sun Kelvin MacKenzie hires Rosenblatt Solicitors senior partner Ian Rosenblatt to help extract an apology from South Yorkshire Police for supplying the information that led to his infamous Hillsborough front page.


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11 Strangest Medical Conditions That Will Blow Your Mind!
A type of paranoia, people suffering believe that different people around him are not real, they are in-fact the same person in disguise, this delusion is one of the common delusion in sufferers of brain delusions.[Ref]
Natalie Adler is a women with a strange medical condition, her eyes are closed for every 3 consecutive days. She cannot open her eyes no matter how hard she tries to when they are shut, when its over she finally can open and close her eyes at will. She is the only person known to have this condition. The cause is unknown. This first happened right before her exams, it was thought to be because of a sinus but later it became recurring and she had live every consecutive 3 days in complete darkness, even though she has a perfect eyesight.
The color of the blood is not always red, it can be green or blue. In humans a rare condition known as sulfhemoglobinemia makes the blood green. It occurs due to overdose of a few medications containing sulfur compounds that bond with iron in the blood and changes its color.
Blue blood is seen in some spiders, lobsters and snails as their blood contains hemocyanin(a copper compound) instead of hemoglobin to carry oxygen.
An uncontrollable genital arousal, occurring throughout the life, unrelated to any sexual desire. The first ever documented case was in 2001. The disorder only occur in female patients, although a very similar condition in men has also been reported a few times recently.
There have been several reported cases, all were caused by either a stroke, trauma or brain injury. Despite of the popular belief, in no case the sufferer's accent actually improved.
A man developed a star shaped cataract due to 14000V Electric shock on his shoulder. There have been 2 cases like this, one caused by a shock and the other by severe punch in one eye, leaving star shaped figure developed in the eye, along with blurred vision. The star-shape is known as stellate cataract.
One of the twins was carrying her own sibling when she was born, according to a child care news report.
Alien hand syndrome can be caused by an infection, stroke or brain surgery, it is relatively a rare disorder, more common in the left hand, the hand moves without any voluntary control over it, and yes it might try to kill!!
Gabby Gingras feels no pain, she had several injuries due to this disorder, there are only a few people in the world suffering from the disorder congenital insensitivity to pain with anhidrosis, they are incapable of feeling anything, they have no neural network that gives them the feeling of pain.


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It's official - economy has bottomed out
For those who have their money and/or retirement in a mutual fund, more than likely you've lost half your money in the past year-and-a-half (even more when you figure inflation). Don't take my word for it, check this Feb. 23, 2009 story:
By TIM PARADIS, AP Business Writer
"The Dow Jones industrial average tumbled 251 points to its lowest close since Oct. 28, 1997
"According to preliminary calculations, the Dow dropped 250.89, or 3.41 percent, to 7,114.78. It last closed this low on Oct. 28, 1997 when it finished at 6,971.32. The Dow hasn't traded below the 7,000 mark since October 1997."
Admittedly, I have several mutual funds because you don't put all your eggs in one basket. My mid-cap is doing well. If you need to know what a "mid-cap" is, call a broker and remember they're called "broker" for a reason. Ask them where they invest their money – surprise, they don't or it's in tobacco and liquids – in other words wine and cigarettes. If you're a "broker" right now, you need those. Or you could spend a couple hours a week educating yourself.
I wish I could say I'm all wise and created all this information myself. Go back to the previous paragraph. If you want to keep your money, you educate yourself.
Wish I was as wise as chartingstocks.net. The first day of 2007, it had a blog "The Coming Stock Market Crash of 2007." Pretty accurate prophecy of what has been going on the past two years.
Oct. 9, 2007 baby-boomers and fools leaped for joy. Dow went over 14,000. In 1984, I remember watching it with the son of the owner of Crow Publishing. We were betting on 2,000, which it hit in 1985. Wonder if it will hit that level again this year? The good thing if it does, homes averaged $75,000 that year and interest rates were at 15 percent. If you purchased one of those $225,000 or higher average priced homes, not so good for you.
Now for today's lesson: Where the economy is going.
You find wisdom everywhere if you look for it. This past weekend I was freaking out because gold is near or over $1,000. I remember when owning gold became legal and it was like $250 an ounce. To have gold at $1,000 was surely the death knoll for the U.S. dollar, I thought. Until I spoke to a customer service rep at Godaddy.com.
This wise expert, probably making $13 per hour compared to those million-dollars a year stock brokers you consult, wisely said, "What about the other precious metals?" Wise, wise, wise!
Looking at silver, it is down about a third of where it was a year ago, but double what it was five years ago – a good indicator that I will explain in a moment.
A look at platinum reveals it is down 250 percent from a year ago, at about the same price it was five years ago. Another good indicator.
Then you look at gold. It is higher than it was when gas was nearly $5 a gallon (which I predicted in a summer, 2007 story in the Arizona Republic). Looking at the five year history for gold bullion, you see it is up 250%.
These precious metals tell a story. Silver and platinum are indicators that the depression has bottomed out and now would be an EXCELLENT time to do your homework and find some worthy investments – I recommend real estate.
The rise in gold tells me something else. The fool investors who drove up home and stock market prices to a level beyond their value have been listening to those "buy gold" pitches on the radio.
The economy isn't about to fall – only for those fools who rush from one trend invesmentt to another, purchase SUVs and Krispy Kreme donuts and think In-n-Out burgers are any different than McDonald's or Burger King . These fools are driving up gold prices and will get burned like they did in both the stock market and buying those rental homes to flip. Good luck on that. It doesn't work. It's okay, though. The taxpayer will be there again to pay for these investors' stupidity.
Do your homework and invest wisely. Listen to those lowly customer service peons you want to ignore. They're probably smarter than you. I KNOW they're smarter than me.


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Irelia Build Guide by impike
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Ability Sequence
Not Updated For Current Season
The masteries shown here are not yet updated for the current season, the guide author needs to set up the new masteries. As such, they will be different than the masteries you see in-game.
Ranked Play
Just Farm and wait for gank!Try to dont die!In mid game after Aegis of the Legion and Spirit Visage u can be a litle bit agressive.After Warmog u can tank all and go in midle of the fight everywhere.Remember u're the tank u must tank all fights.When u can gat the last 2 items u sure win the game:)(In fights always focus Ad carry and mid lane!<-- When u get this 2 u win the fight!


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Researchers experiment with medical alert systems
Jasmine Phu
June 9, 2011
Technology has brought us a lot of things. The internet, better cars, cellphones and digital cameras, just to name a few, but there has been a surprising lack of innovation when it comes to helping seniors age at home.
That's all changing now as the 78 million members of the baby boomer generation get ready for their retirement years and look to technological advances to help keep them safe. One product that is already on the market is a medical alert system, which enables users to immediately sound a medical alarm if they suffer an unexpected injury at home.
In Seattle, researchers are also studying the way that sensors can help older adults stay safe, according to HealthCanal.com. The main goal of the initiative is to learn how technology can be applied to safe and independent aging.
"It's a tragedy when a crisis comes up that families didn't plan for or anticipate," Lee Burnside, the medical director of retirement home Horizon House, told the news provider. "It's very difficult for everyone, and our hope is that the stress can somehow be eased a bit. This kind of situation touches everyone."


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Make this your preferred store
1602 State Rd 50
Bourbonnais, IL 60914
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Please call this store for service hours and to make sure that we can repair your specific carry-in item.
If you're looking for great deals on top-notch products, look no further than the Bourbonnais Sears on State Road 50. Whether you're looking for clothes, automotive tools, outdoor furniture or anything else, you're sure to find something you love here. Make sure to take advantage of our auto and optical centers while you're here to get a few extra errands completed. You can drop off your car for maintenance or stop by for a quick eye exam, all without having to make an extra trip.
If you work somewhere that requires a special uniform, check out our selection of workwear and uniforms. You're sure to find a comfortable and durable solution here at Sears. We have uniforms for automotive workers, construction workers, medical workers and more.
Taking care of your health is important. If you have a cold, a cut, a headache or anything else that leaves you feeling less than your best, check out our health and wellness department for a selection of products that can help you feel better. Look for cold medicine, vitamins, first-aid kits and more here at Sears.
We're located just off IL-50 in Bourbonnais. To find us, just take exit 315 off I-57. We're about a quarter of a mile north on IL-50. Give us a call at 815-937-8427 if you need any help with directions.
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A public interest lawyer whose firm represented homeowners in a controversial case regarding eminent domain 10 years ago told lawmakers that the U.S. Supreme Court has left private property owners with "very little protection" if a city wants to take their residences for developmental purposes.
Dan Alban, an attorney for the Institute for Justice, a firm that represents people whose rights, the outfit determines, are being violated by the government, appeared before the Senate Subcommittee on the Constitution to say what he characterized as the "infamous" Kelo v. City of New London case can be used to "transfer perfectly fine private property to a private developer based simply on the mere promise of increased tax revenue."
The court, Alban said, determined that it is "acceptable to use the power of eminent domain when there is a mere possibility that something else could make more money than the homes or small businesses that currently occupy the land."
In her dissent in Kelo, Alban noted, Justice Sandra Day O'Connor wrote, "The specter of condemnation hangs over all property. Nothing is to prevent the State from replacing any Motel 6 with a Ritz-Carlton, any home with a shopping center, or any farm with a factory."
"Eminent domain sounds like an abstract issue but it affects real people," Alban told the panel. "Real people lose the homes they love and watch as they are replaced with luxury condominiums. Real people lose the businesses they count on to put food on the table and watch as they are replaced with shopping malls. And all this happens because local governments prefer the taxes generated by condos and malls to modest homes and small businesses."
Federal law currently allows expending federal funds to support condemnations for the benefit of private developers. By doing so, Alban said, the government "encourages this abuse."
"Using eminent domain so that another richer, better-connected person may live or work on the land you used to own tells Americans that their hopes, dreams and hard work do not matter as much as money and political influence," Alban said. "The use of eminent domain for private development has no place in a country built on traditions of independence, hard work and the protection of property rights."


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On a busy London street, a young woman is attacked in broad daylight and left bleeding to death on the pavement. Among the eyewitnesses are DI Simon Fenchurch and his wife.
Fenchurch pursues the attacker through a warren of backstreets and eventually arrests a young hoodie with a cache of stolen phones - an 'Apple picker' on the make. The case should be closed but something feels off...Was this really just about a smartphone? Why did the victim look nervous before she was targeted? And why don't the prints on the murder weapon match the young man in custody?
Before Fenchurch can probe further, his superiors remove him from the case, convinced he has let the real culprit run free. But Fenchurch is determined to get to the truth and, before long, uncovers a conspiracy that reaches high above the street gangs of London.
©2016 Ed James. (P)2016 Brilliance Audio, all rights reserved.
Intricate play on current social climate regarding race, immigrants, marginalization and violence The author uses insight on violence as a means to illicit emotional trauma and the toll that it takes on interpersonal relationships.
Book two is a marked improvement on book one. I look forward to the next installment.
"Very mediocre police procedural"
The lead cop is not very bright and not very likeable. He is plagued--did we really need to know it?--with acid reflux and, endlessly, by a drumming in his ears. Then there are the caricature rastas. My recommendation is: Skip it.
"Another great one!"
I am hooked on Fenchurch... I am looking forward to his next adventure. Hurry please:)
"Carbon Copy"
James needs to stop the repetitive plot line of kidnapped children who are later exploited. In his first book it was interesting, in this one it became redundant.
"A new favorite author"
Another good police procedural by Ed James. Fenchurch is in the wrong place a few times in this book. At least his personal life seems to be working out. His obsession about finding their daughter seems to have been managed and then...stuff happens to bring it back to him.
The story kept me quite interested and up way too late at night. The narration is first rate. I'm ready to download book 3 now. Good work!
"Deplorables Are Not Welcome......."
Fine Job.
Members of the Tory Party, UKIP and all of those who support Brexit are shallow, greedy people who are responsible for all of London's woes. Woe to the Deplorables !
"Good "
Enjoy reading this book, I have read the three books over the past nine days, when you start one you can't wait to start the next...
i found the portrayal of black people really stereotypical. i have yet to meet someone who says man every 2 seconds like every black man in this book they lie, steal and are dishonest. i think listening to the postscript the authors anger is clear. he vents in this book. The voice.overs were also lazy caricatures.
"strangely gripping"
a brilliantly gripping story that just creeps up on you and won't let you put it down
"Great book"
Brilliant story. Excellent listen. Emotion. Passion, and desire are all expressed in this excellent story.
"can't wait for the next one"
i love how this story carries on from the last one without any long tedious explanations. The plot is intriguing and kept me interested throughout the story.
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- Attorney Resource Center
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2D. Understanding and Improving Local Voucher Utilization and Success Rates
Advocates are all too aware that even after waiting years to obtain a voucher, many families are forced to return their voucher because they can't find a place to live before the expiration of the search term. As a result, PHAs experience low "success" rates (or, high "turn-back" rates). Some of these PHAs, however, have high "voucher utilization" rates, as published by HUD. How can we reconcile these two concepts and how are they related? How can advocates encourage PHAs to improve both utilization and success rates and why is this important? In what ways are PHAs' goals aligned with tenant advocates? This workshop aims to answer these questions and deepen participants' understanding of utilization and success rates including obtaining and interpreting data for each. Panelists will focus on PHA incentives to improve utilization and success rates as well as practical strategies for advocating with your local PHA.
01 Voucher Utilization Presentation
02 Housing Choice Voucher Data Available on CBPP Website
03 How to Use CBPP HCV data
04 Get Ready Letter 2016 HCVP
05 Chart on Payment Standard Section 8 Vouchers


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Most spend a third of their life sleeping. I spend a third of my life in my wardrobe.
Well, not actually in my wardrobe (that would be weird) but in the room where my wardrobe lives. I hang the pile of clothes I regretfully left on the floor the night before. I see how many T-shirts I can fit on one hanger before I go and buy another set of hangers. I sit on the floor in my knickers and stare at my clothes for 20 minutes waiting for a cute outfit to hit me, before I actually start trying things on. I find new, creative ways to store my stuff so I don't have to get rid of anything. And I experiment with ways to clean things, because I'm clumsy and wear my good white shoes to festivals and also like saucy foods.
Anyway, my point is this: I'm a wardrobe expert. Storing, cleaning, wearing, you name it, I can do it… but not without these hacks. They have made my life as a hoarding, messy, sad person who's addicted to clothes, much, much easier.
Now it's time to pass them onto you.
1. Cleaning your shoes
We're all familiar with the White Magic Eraser Sponge. It's returned to us many a real estate bond, even after we've left foundation smudges on light switches and weird, scratchy marks on walls throughout the house.
Well, grab your shades, because it turns out the White Magic Eraser Sponge is bloody amazing at turning the white of your sneakers from a suspicious grey to blinding white again.
If you're more of a fancy-pants patent leather wearing type and you also want to make your shoes sparkle, that's cool too. A little dab of Vaseline does the trick when buffing out scuff marks.
2. Hanging your earrings
If you're taking part in the Great Statement Earring Trend of 2017, you've probably noticed how they're taking up all the room on your dresser/desk/bathroom sink. But by leaving them just lying about the place, not only are you compromising on space, you're also dancing with fire. Let me ask you: how many earrings have you lost so far?
To combat this, buy a small canvas from a craft shop. If you're especially creative, you can paint or decorate the canvas first. If not, channel your inner voodoo and get straight to pinning the earrings across the board, before hanging on the wall or balancing on a shelf. #ART.
3. Clearing out your closet
This is a trick used by stylists everywhere, and for good reason.
It's pretty simple: pick up all of the clothes hanging in your wardrobe and hang them the opposite way. Every time you wear something, you can return it to the wardrobe the *normal* way. Anything left hanging the opposite way in 6-12 months should be donated, because you don't wear it and here is the cold, hard proof. Once you've donated your clothes to charity, go and buy yourself something nice.
4. Making the most of space
If you're a minimalist that lives in one of those tiny houses like on the Netflix doco, or you just spend all your money on smashed avo and live in a tiny apartment, it's likely you're dealing with a very small wardrobe space.
So, rather than hanging five things on one hanger and stretching all the collars of your tees (ahem) use one of these tricks.
The first involves a chain. Grab any old chain from Bunnings or your dad's garage and loop it over your hanger. Instantly, you've got about 10 more holes from which you can hang more hangers – vertically.
For an even more povvo version of this, you can loop a soft drink can tab over your hanger, and use the extra hole on the tab for one more item of clothing. You're welcome.
5. Grouping your annoying clothes
Hands up if you have about one billion plain singlets floating around your draws? Well, those singlets are taking up valuable space that could be much better used on winter coats and jeans.
By throwing them wherever the f*ck you want, it's also really hard to find your singlets when it's 5am and 8 degrees and you're trying to get dressed in the dark.
Instead, use a tie rack to group together all of your singlets, and hang it on the far side of your wardrobe.
6. Planning tomorrow's outfit
Ever see those people in movies that have time to sit down and eat a hot breakfast before heading off for work? That could be you. All you have to do is place a hook on the inside of your wardrobe door, and use it each night to prepare tomorrow's outfit.
At first, it will be like a fun game and you'll actually use it for a while, allowing you to eat a sit-down breakfast and making you earlier to work and probably getting you a promotion. It's a win-win.
7. Freshening your denim
Any denim lover will tell you NOT to wash your jeans – it's basically murder. But if you're like me and also enjoy saucy foods, sometimes you have accidents. For these moments, spot cleaning is your friend.
When the time comes to give them an all-over freshen up, pop them into a canvas bag (rather than plastic, so it can breathe) and throw them straight in the freezer.
Keep in mind this doesn't actually kill the bacteria (it just freezes it until the denim warms up again). But it's a handy little trick for eliminating odour and feeling fresh as a daisy in your newly-thawed jeans, without committing denim murder.
8. Avoiding the dreaded hosiery ladder
It's winter, it's freakin' cold and tights are on high rotation. But sometimes, our tights get a snag.
Rather than giving up completely and throwing them out, stop the snag becoming a full-blown ladder by dabbing a teeny amount of clear nail polish on the hole. This will harden and stop the fabric from tearing further.
Obviously, this only works if you have one of those cute little holes. If you happen to be eating something saucy, drop it, then burn a hole in your tights the size of your palm, well, you're on your own.
Illustration by Twylamae.


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Gaza blast setback for opening territory
Fri., May 23, 2008
GAZA CITY, Gaza Strip – A Palestinian detonated a powerful truck bomb at the main pedestrian crossing between Israel and the Gaza Strip on Thursday, causing extensive damage that dealt a serious blow to Gazans' hopes of opening up their sealed-off territory.
Although the bomber killed only himself, the magnitude of the explosion – which shook buildings for miles – raised fears that Palestinians are adopting tactics used by al-Qaida, Hezbollah and other extremist groups.
The attack at the Erez crossing also reinforced skepticism about Egyptian-led efforts to bring a truce to the violence-wracked area and hurt international efforts to ease the Israeli-led blockade of Gaza, imposed after Hamas militants seized control of the coastal territory almost a year ago.
Later, at the Karni cargo crossing some 5 miles away, a protest against the blockade turned violent, with Palestinians accusing Israeli troops of firing into the crowd of thousands, killing a 22-year-old man and wounding 16 other people.
In chaotic scenes, swarms of people darted along a narrow road near the crossing, fleeing tear gas and live bullets as Israeli tanks rumbled into Gaza from Israel. The military said soldiers opened fire after spotting armed men in the crowd, including one carrying an anti-tank missile, and that the gunmen returned fire.
"Zionists, death is coming," loudspeakers blared. "You will fall, your corrupt state will fall," the crowd chanted – reflecting the intensity of Gazans' bottled up frustration a year into Hamas' turbulent rule, a period in which 80 percent of Gaza's adult population has descended into poverty, according to the United Nations.
The violence at Gaza's border crossings came as Egyptian mediation efforts to forge an Israeli-Hamas cease-fire ran into trouble, with several Hamas leaders claiming the truce talks had failed. The leaders, who spoke on the condition of anonymity because the group had not made an official statement, blamed the breakdown on Israel's failure to accept a six-month truce.
Israeli military officials, who also spoke on the condition of anonymity citing the lack of a formal announcement, confirmed that Amos Gilad, a senior Israeli defense official, will travel to Egypt on Sunday for more talks – a sign the truce remains on the table.


text: Be Resorts - Mactan is just 4.6 mi (7.5 km) from the airport and offers a shuttle for PHP 700 per vehicle one way. After splashing around at the outdoor pool, you can grab a bite to eat at the restaurant or unwind with a drink at the bar/lounge. A beach bar and a children's pool are other highlights, and rooms at this Art Deco resort offer flat-screen TVs and refrigerators.


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Conor McGregor's striking skills continue to draw praise, but following his loss to Nate Diaz at UFC 196, the questions regarding his ground game haven't gone away.
The Irish star put his big left hand to use against Diaz earlier this month, and bloodied up the veteran fighter. Diaz, however, kept coming, and put an end to McGregor's undefeated UFC run in round two with a rear-naked-choke,
Well, the two are expected to rematch on July 9th at UFC 200, and recently Joe Rogan weighed-in on the match-up during his podcast. While doing so, Rogan, who is a black belt in Brazilian Jiu-Jitsu, had this to say (quote via MMA Fighting.com):
"A guy like Conor, if you've been tapped before by Joe Duffy just a few years ago with an arm triangle … to get caught like that, you've got a lot to learn and I don't know if you've learned it all in time. You've got to be obsessed with jiu jitsu. You've got to be in there every day training and I didn't think he did [for UFC 196]. I thought it was more about movement and striking and all that stuff. I know he was doing some jiu jitsu but it's not like the primary focus. So I felt like, 'That's a big f**king deep end jump.'"
"He might knock [Diaz] out," Rogan added. "Conor can knock out anybody. But he didn't. So now that he didn't and now that Nate knows he didn't, now they're going to go into the second fight and Nate's going to have a full training camp. Good luck."
Now you know McGregor boosters and others will argue that the featherweight champ was tired and or rocked when Diaz submitted him. Further, McGregor did hit a nice roll out earlier in the fight when the action hit the mat.
But, against Chad Mendes last July, McGregor didn't appear to have many answers against "Money's" top game. So, now that he was quickly subbed by Diaz at UFC 196, Rogan isn't the only person who's questioning whether McGregor can hang with top tier grapplers on the floor. If you can't, staying at the top of one division, much less two, is pretty, pretty difficult.
UFC 200 will take place on July 9th in Las Vegas.


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Management Team
Gabi joined BVT in September 2014 as CEO & President. Previously, she was Senior Vice President of Technology & Development and a founding officer of ENTrigue Surgical, Inc. Gabi was also on the management team of Concept to Market Medical. Gabi's research and development expertise has been critical to the successful acquisitions of three medical device companies where she also led regulatory, quality, clinical and intellectual property functions. At OsteoBiologics, her team developed a suite of sports medicine products while actively participating in raising $20 million in funding. The company sold to Smith&Nephew for more than $72 million in 2006. Concept to Market Medical developed a unique shoulder anchor, which was acquired by Tornier. At ENTrigue Surgical, her team developed commercially viable products for otolaryntology. The company was acquired in 2013 for $45 million by ArthroCare Corporation, which was subsequently purchased by Smith&Nephew.
Gabi has more than 25 years of experience in the development and commercialization of medical technologies. Her research has led to over 20 peer-reviewed articles and numerous presentations/abstracts. Gabi is also a co-inventor on nine patents and seven applications for devices and methods used in orthopedic surgery, tissue engineering and ENT procedures. She serves on the advisory boards of several medical/biotech companies (Bio2 Technologies, PuraCath Medical, StemBioSys, and Cardiovate). Gabi completed a Post-Doc in the Orthopaedic Biomechanics Laboratory at UTHSCSA. She earned a PhD in Biomedical Engineering and a MS in Materials Science and Biomedical Engineering from Iowa State University, and a Bachelor of Science degree in Ceramic Engineering from Clemson University.
Lex joined BVT as Director of Research & Development in September 2012 to lead product development and commercialization of current and new products. Lex brings more than 25 years of experience in medical device engineering specializing in minimally invasive device development. Prior to joining BVT, Lex held engineering leadership roles at Avantis Medical, Vertos Medical, SpineView, Kyphon and Boston Scientific where he developed a variety of novel devices to treat cardiology, neurology and spinal conditions. With over 30 issued and pending patents, Lex has successfully commercialized cardio, neuro, spine, surgery and dental products. Lex holds a mechanical engineering degree from The Hague, Netherlands, and a BS in Technical Management from the Wentworth Institute, Boston MA.


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Pandhayam Trailer (2008)
19 September 2008 Action, Thriller, Romance 145 mins
A local thug and criminal who kills people like mosquitoes Masanam (Prakash Raj) slowly rises up the ranks to be a Minister. We have Shakthivel (Nithin Sathya) a die-hard fan of actor Vijay who studies in a city college. He falls in love with the wicked minister's sister Thulasi (Sindhu Tolani) and challenges him (he has a reason for that) and a cat and mouse game ensues. What follows is a series of incidents between the two that leads to a melodramatic climax.
Watch the official Pandhayam 2008 trailer in HD below or find more Pandhayam videos on Vidimovie.


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|Vin De Syrah Spirit and Wine Parlor
Design by Michael Soriano
Monday, June 27, 2011
Go ask Alice...when she's ten feet tall
So I'm in the process of trying to plan my sister's bachelorette party down in San Diego. It poses a few difficulties trying to pick a venue that is a few hundred miles away that I've never been to before. I found this super cool spot on Yelp called Vin De Syrah, that from the looks of it, if I lived in San Diego I would totally be there every weekend. It's like an Alice in Wonderland acid trip but with the sophistication of wine and cheese tastings! The saturated colors, foliage on the walls, and rustic wood accents...I would probably just stare at all the details all night! Unfortunately it doesn't meet our requirements of a private room for this particular event, and from the looks of the Yelp reviews is more of a loud club scene at night, but if I'm ever down in San Diego any other time, I'd totally love to sip some Pinot down in the rabbit hole!
Posted by Victoria at 2:00 PM
Labels: Decor, Inspiration, Interiors
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