Twenty-Four Years of Mondays

The former Disney darling has come a long way since her days on the set of Sonny With a Chance. After her sixth studio album, Tell Me You Love Me, was.

Free download. Book file PDF easily for everyone and every device. You can download and read online Brief an einen Verleger: Text (Fischer Klassik Plus 193) (German Edition) file PDF Book only if you are registered here. And also you can download or read online all Book PDF file that related with Brief an einen Verleger: Text (Fischer Klassik Plus 193) (German Edition) book. Happy reading Brief an einen Verleger: Text (Fischer Klassik Plus 193) (German Edition) Bookeveryone. Download file Free Book PDF Brief an einen Verleger: Text (Fischer Klassik Plus 193) (German Edition) at Complete PDF Library. This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats. Here is The CompletePDF Book Library. It's free to register here to get Book file PDF Brief an einen Verleger: Text (Fischer Klassik Plus 193) (German Edition) Pocket Guide.

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Buy with confidence excellent customer service! Good Plus condition Hardcover 12mo with no dust jacket. About 75 pages. Binding and book are great interior is excellent. Small orange and black design on thin stiff boards. Minor shelf wear to exterior. This book has hardback covers. In good all round condition. Used; Acceptable. Used; Good. New edition.

First Thus. First Edition. First Printing. New translation of the author's novel. One of the greatest novels of the 20th century. The First Hardcover Edition. Precedes and should not be confused with all other subsequent editions. Published in a small and limited first print run as a hardcover original only and as part of the now-legendary Schocken Library Series.


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The First Edition is now scarce. Presents Franz Kafka's "Das Schloss" in what is widely regarded as the definitive translation in English. Amended corrected and realized seventy-two years after its publication in the original German Published at the end of the 20th century Mark Harman's translation is an achievement of the highest order and honors Kafka in our chaotic confused time. Such poets as Rilke or such novelists as Thomas Mann are dwarfs or plaster saints in comparison with him" Vladimir Nabokov.

An absolute "must-have" title for Franz Kafka collectors. Please note: Copies available online have serious flaws or are subsequent printings which feature a different DJ. A scarce copy thus. A fine copy. ISBN Perfect Paperback. May not contain Access Codes or Supplements. May be ex-library. Retrospective collection of the author's writings plus critical responses. One of the most valuable books on Robert Walser ever published in the 20th century.

The first appearance of the title in English and in the United States. Published in a small and limited first print run as a hardcover original only by a University Press. One of the earliest and most important publications in English of the great writer's work the precursor to the remarkable and welcome publishing cottage industry that has now seen a significant chunk of Walser's writings translated into English.

Marks the very first appearance of "Cinderella" and "Snowwhite" two so-called "anti-fairy tales" that are still written as fairy tales rather than literary criticism hence their genius. As such Walser may yet hit the readers Hermann Hesse wished for him and for the good of Mankind. Scattered elsewhere the pieces are gathered in this volume with cumulative effect. A succinct description of the discovery and experience of the Walserian universe: "The reader is in the presence of a mind-bending genius but one characterized by a wry buoyant voice as apparently cheerful as it is disturbing.


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One of the twentieth century's great Modern Masters" Publisher's blurb. A truly wonderful heartbreaking writer" Susan Sontag. An absolute "must-have" title for Robert Walser collectors. Please note: Copies available online are former library copies or have serious flaws. This is surely an accessible and lovely alternative. A rare copy thus. New Ed. Ships next day.

Book is in very good shape no tears scribbles highlighting or underlining a little general wear from a smoke-free environment.

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London England: Trolley Books Retrospective collection of color photographs presented as an Artist Book. One of Nick Waplington's best books. Limited Edition of numbered and signed copies. The first and only edition. Canine hip dysplasia is a common, non-congenital, complex and hereditary disorder. It can inflict severe pain via secondary osteoarthritis and lead to euthanasia. An analogous disorder exists in humans. The genetic background of hip dysplasia in both species has remained ambiguous despite rigorous studies.

We aimed to investigate the genetic causes of this disorder in one of the high-risk breeds, the German Shepherd. We performed genetic analyses with carefully phenotyped case-control cohorts comprising German Shepherds. In our genome-wide association studies we identified four suggestive loci on chromosomes 1 and 9.

Targeted resequencing of the two loci on chromosome 9 from 24 affected and 24 control German Shepherds revealed deletions of variable sizes in a putative enhancer element of the NOG gene. NOG encodes for noggin, a well-described bone morphogenetic protein inhibitor affecting multiple developmental processes, including joint development. The deletion was associated with the healthy controls and mildly dysplastic dogs suggesting a protective role against canine hip dysplasia. Two enhancer variants displayed a decreased activity in a dual luciferase reporter assay. Our study identifies novel loci and candidate genes for canine hip dysplasia, with potential regulatory variants in the NOG gene.

Further research is warranted to elucidate how the identified variants affect the expression of noggin in canine hips, and what the potential effects of the other identified loci are.

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Hip dysplasia is a common orthopedic disorder in dogs and humans. It can pose a serious welfare problem with severe pain. The genetic background of this disorder remains inconclusive even after years of arduous research. We used the genotypes of German Shepherds with carefully determined hip scores to identify genomic regions potentially harboring genetic risk factors for the disorder.

We found four regions on chromosomes 1 and 9 exhibiting suggestive association with the disorder phenotypes. Further analysis of the identified loci on chromosome 9 by sequencing 48 dogs revealed deletions in a potential regulatory region of NOG - the gene encoding noggin, a known regulator of joint development in mice and in humans.

Using a reporter assay, we demonstrated that the deletions decrease the enhancer activity of the regulatory region and could therefore affect the expression of NOG in hips. The deletions significantly differentiate the healthy and the mild phenotypes from the moderate-to-severe phenotypes. Therefore, our results suggest that the deletion protects against hip dysplasia. Future research should focus on how these regulatory variants affect the expression of noggin in canine hips, and what the roles of noggin and the other revealed loci are in canine hip dysplasia.

"Der Brief" von Friedrich Schütter - gesprochen von Reinhard Wiegand

Many hereditary disorders appear in both humans and dogs with gene variants from common ancestral genes affecting the disease [ 1 ]. Canine hip dysplasia CHD is a non-congenital disease, causing skeletal abnormalities in growing dogs, the first signs appearing at the age of three to four months [ 2 ].

CHD is defined as the laxity of the joint, resulting in instability and subluxation [ 2 , 3 ]. The femoral head is not completely covered by the acetabulum, which then leads to increased force over smaller surface area due to incongruence of the coxofemoral joint [ 2 , 3 ]. This in turn causes microfractures in the acetabulum and the femoral head [ 2 , 3 ], detrition of the articular cartilage, inflammation of the synovial membrane and secondary osteoarthritis OA [ 3 ].

CHD can be painful up to a point where it poses a serious welfare problem. Hip dysplasia appears in humans in divergent forms from infancy to adolescence and to adulthood [ 4 ]. Of these, the adolescent hip dysplasia is clinically and developmentally closest to CHD [ 5 ]. The scoring is based on the following features: level of congruence between the femoral head and the acetabulum, degree of subluxation of the joint, Norberg angle, shape of the femoral head and neck, shape and depth of the acetabulum, and signs of secondary OA [ 6 , 7 ].

Other traits also add into hip morphology, but they are not routinely evaluated [ 8 ]. In the end, only the categorical score for each hip joint is recorded and made available for later use. The severity of CHD depends on environmental and genetic factors [ 2 , 3 , 9 — 23 ]. The heritability h 2 estimates for the hip score are generally moderate across breeds 0.

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In a Finnish German Shepherd population the estimates were 0. In earlier studies the h 2 estimates for the traits determining the hip score e. Some evidence of major genes affecting CHD exist from studies utilizing variance estimates and Bayesian modeling [ 16 , 18 , 26 , 27 ].