If this sounds like a fairytale, that's because it is.
It's also a love story. And a comedy. Some might find its diversity of styles to be a confusing flaw, but a few episodes in, you'll find that this show is undeniably soapy and dare I say magical? The eco-pocalypse will come via rain, spreading its zombie infection within seconds of being hit by droplets. That's the future Netflix's The Rain posits, anyway.
Unlike other post-apocalyptic fictions, the survivors we're following are teenagers navigating the push-and-pull of their emotional stress, fast and forced maturation, cliquiness even in the end days, and teen horniness to stay alive. Most food TV emphasizes anxiety over pleasure: the pressure to innovate, the terror of the ticking clock, and the sound of Gordon Ramsay's braying voice all make viewers sweat instead of salivate.
Samurai Gourmet , a fictional Japanese show about retired businessman Takeshi Kasumi Naoto Takenaka exploring the culinary world around him, is as relaxing as Top Chef is stressful. Plus, at less than 25 minutes, the episodes are mercifully shorter. It's an invigorating riposte to the intensity of the cable cooking trends, presenting a vision of eating that's rooted in the joy of drinking a midday beer, the adventure of testing a new ramen place, and the teenage memories conjured by eating dried mackerel. It's like a refreshing nap you can stream.
Netflix has become flush with scripted and reality Korean TV, but this latecomer is worth investing in. Bouncing somewhere between supernatural drama and rom-com, and altogether breaking the expectations of superhero shows, Strong Girl Bong-Soon sports a charming quirkiness and a darker-than-expected plotline following the lead, Bong-Soon Do, search for love and follow her dreams to be a game designer while being impossibly strong.
In other words: This is not the next Archer. A Very Secret Service 's mannered "hmm mm mm" comedy style mirrors the bespoke suits and mod locations on display, making it one of the more sophisticated comedies on Netflix. Your browser does not support the video tag. Share on Facebook Tweet this article Pin it Email. Share on Facebook Pin it.
Atelier Japan The Japanese drama, Atelier , can best be compared to The Devil Wears Prada -- complete with the Anna Wintour business matriarch type and her ambitious mentee -- stripped of the meanness and petty cruelty stereotypically depicted in the fashion world and replaced with an earnest drive to work really hard and succeed within reason. France Think of this as a French version of Entourage , but instead of a faction of bros' Hollywood misadventures, this spastic and funny series has a Parisian cadre of agents attempting to save their flailing business while confronting realities like sexism, ageism, and the gender pay gap in movies and TV.
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This study aimed to identify predisposing loci in patients with these disorders.
Linkage analysis, exome and whole-genome sequencing were performed in a family affected by microsatellite stable CRCs. Gene expression was assessed at the mRNA and protein level. Homozygosity mapping revealed a disease-associated region at 1q This includes a region previously associated with risk of CRC. Sequencing identified the p. In both cases and controls the population frequency was 0.
Furthermore, immunohistochemistry revealed increased expression of MIA3 in adenomatous tissues. Taken together, our two independent strategies associate genetic variations in chromosome 1q loci and predisposition to familial CRC and polyps, which warrants further investigation. Family history is a major risk factor in colorectal cancer CRC aetiology. It is generally accepted that a substantial proportion of CRC incidence is due to predisposition to non-malignant CRC lesions e. Indeed, first-degree relatives of patients with colorectal adenomas have an increased risk of developing colorectal adenocarcinomas Johns and Houlston, ; Tuohy et al, In support of this, linkage studies in CRC families have identified disease-associated chromosomal areas where predisposing genes have not yet been identified Wiesner et al, ; Kemp et al, ; Neklason et al, ; Middeldorp et al, Similarly, some regions, such as chromosome 1q41 rs, rs and rs , identified in genome-wide association studies GWAS still have not led to the identification of functional CRC variants Houlston et al, ; Spain et al, ; Zhang et al, Furthermore, one study measuring runs of homozygosity in search for recessive disease-causing loci, did not identify novel CRC predisposing loci Spain et al, In recent years, advances in sequencing technologies have made it possible to identify germline susceptibility loci that were previously not encountered in linkage and association studies.
In this study, we searched for germline variants involved in colorectal neoplasm susceptibility using two independent genomic strategies. Homozygosity mapping analysis was conducted in a cohort of index patients with various colorectal neoplasms, ranging from few to hundreds of polyps and controls. In parallel, a combination of linkage analysis and sequencing was performed in individuals from a large family with an extensive history of microsatellite stable CRC.
Both strategies identified an association of chromosome 1q loci with these diseases. Informed consent was given for further research at initial blood withdrawal for the homozygosity mapping cohort, family 68 and the MIA3 genotyping cohorts. The clinical characteristics of the cohort are presented in Supplementary Table 1. For controls we used genotypes of individuals from the LifeLines cohort study Stolk et al, ; Dolmans et al, The quality control procedure is described in Supplementary Methods.
SNP selection and homozygosity mapping analysis is described in Supplementary Methods. A quantile—quantile Q—Q plot of the observed and expected P -values indicated differential genotyping between cases and controls. Multiple test correction was done using false discovery rate estimation Benjamini and Yekutieli, Peripheral blood was collected from 16 members of family DNA was extracted using standard techniques. Data was previously described Middeldorp et al, A total of SNPs had a valid annotation.
Genotypes incompatible with the family relations were removed using pedcheck. Patients diagnosed with CRC before 60 years or with colorectal polyps before 55 years were considered affected. Other family members were classified as unaffected. For the analysis of the exome sequencing data, we selected variants predicted to be coding or affecting splice-sites.
In the whole-genome analysis, we prioritised the non-coding variants which were present within the linkage peak based on regions under strong negative selection, as previously described Khurana et al, The MIA3 c. AspGlu variant was validated by standard bidirectional Sanger sequencing.
Leucocyte or normal colon tissue derived DNA was screened of CRC patients, polyposis patients and population-based controls anonymous blood donors from The Netherlands and CRC patients and healthy controls from the Czech Republic Pardini et al, All carriers were validated by Sanger sequencing and the existence of a common ancestor was excluded using STR profiling Supplementary Methods. AspGlu carriers and both carriers identified with screening were screened for second hits in the MIA3 gene. For comparison, the somatic mutation data from colorectal adenocarcinoma exomes Muzny et al, ; Seshagiri et al, ; Giannakis et al, was retrieved from The cancer genome atlas TCGA using cBioPortal Cerami et al, ; Gao et al, Formalin-fixed, paraffin-embedded tissue blocks of MIA3 p.
AspGlu carriers were collected caecum carcinoma and normal tissue; two serrated lesions, two adenomas and normal colon tissue. Paired DNA was analysed to determine baseline amplification differences between the two alleles. Using the Cq values obtained for both alleles, the allelic dosage was calculated similarly to the Pfaffl method for relative gene expression Pfaffl, Formalin-fixed, paraffin-embedded tissues blocks were available of 82 patients from the FACTS study Hennink et al, which included 18 serrated lesions and 97 adenomas with low-grade dysplasia and a series of 15 anonymous colorectal adenocarcinomas.
Formalin-fixed, paraffin-embedded and fresh frozen tissue sections of MIA3 p. AspGlu carriers were stained. MIA3 immunohistochemistry was performed as described in Supplementary Methods. The intensity of MIA3 cytoplasmic staining was classified as negative-weak or moderate-strong. Normal mucosa was analysed when present in the tissue sections. MIA3 gradient expression was scored: maximal staining at the base of the crypts and decreasing towards the lumen top-down , maximal staining at the lumen and decreasing toward the base of the crypts down-top or homogeneous staining across lumen and crypt no gradient.
We genotyped germline DNA samples from index patients affected with colorectal neoplasms ranging from few to hundreds of polyps polyposis , with and without CRC. Per individual a similar number of runs of homozygosity On chromosome region 1q Overrepresentation of runs of homozygosity located on chromosome 1q A Frequency of the runs of homozygosity on chromosome 1; cases blue and controls pink. Overrepresented homozygosity in cases is indicated with a red box. B Overlapping runs of homozygosity of six cases blue bars at chromosomal locus 1q In parallel to the homozygosity mapping analysis we performed linkage analysis in a family not included in the homozygosity mapping cohort.
Updated clinical follow-up information warranted the reanalysis of a previously described Amsterdam criteria I fulfilling family affected with microsatellite stable CRCs without a known causative mutation Middeldorp et al, All affected family members developed less than 10 polyps. The clinical presentation of the late-onset patients included the diagnosis of CRC in an elderly patient at 88 years of age and the identification of 1—2 adenomas during periodic colonoscopy screenings in three relatives, aged 56—60 years , and Furthermore, the linkage analysis included one family member without a history of polyps or cancer at 59 years of age and one unaffected spouse.
The linkage region spans Pedigree of family Filled symbol, colorectal cancer. Grey, late-onset colorectal neoplasms. Numbers indicate individuals whose DNA was available. Non-parametric linkage analysis in family Logarithm of odds scores of chromosome 1 in centiMorgan of the non-parametric linkage analysis of 15 individuals using the exponential model.
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To further investigate the chr1q loci identified with homozygosity mapping and linkage analysis, we focussed on the largest region, the linkage region in family In search of disease-associated variants, exome sequencing was performed on DNA from five affected family members , , , and Exonic or predicted splice-site variants with a maximum population frequency below 0. Three variants were shared amongst these five individuals Table 1 , of which only one was located within the linkage peak; the c.
Additional variants identified within the linkage peak were not shared between the individuals Supplementary Table 6. Segregation analysis, using Sanger sequencing, showed that all family members presenting with early-onset colorectal neoplasms were carriers of the MIA3 p. AspGlu variant, whereas one unaffected relative , one patient with a single polyp at 60 years of age and one unaffected spouse were non-carriers.
The MIA3 variant was present in three late-onset patients , ,