Supplemental Income: British newspaper colour supplements in the 1960s

The introduction of colour supplements by three ‘quality’ newspapers during the 1960s was a key development in the British press during the decade, and was described by the editor of the Sunday Times as ‘perhaps the most successful single innovation in post-war journalism’. This article provides an overview of the advent of the colour supplements, explaining why they emerged when they did and developed in the manner they did, and exploring some of the difficulties and issues that attended their arrival. The article also demonstrates that sections of the British press were capable of taking advantage of changes in print and advertising culture brought about by the arrival of the post-war consumer society. However, the term ‘colour supplement’ became pejorative shorthand for the perceived vacuity of this new society, in part because of the tension that existed between the editorial and advertising content of these modish new publications. Consequently, the success of the colour supplement experiment was not universally celebrated

The Consolidation of the White Southern Congressional Vote

This article explores the initial desertion and continued realignment of about one-sixth of the white voters in the South who, until 1994, stood by Democratic congressional candidates even as they voted for Republican presidential nominees. Prior to 1994, a sizable share of the white electorate distinguished between Democratic congressional and presidential candidates; since 1994 that distinction has been swept away. In 1992, a majority of white southern voters was casting their ballot for the Democratic House nominee; by 1994, the situation was reversed and 64 percent cast their ballot for the Republican. Virtually all categories of voters increased their support of Republican congressional candidates in 1994 and the following elections further cement GOP congressional support in the South. Subsequent elections are largely exercises in partisanship, as the congressional votes mirror party preferences. Republicans pull nearly all GOP identifiers, most independents, and a sizeable minority of Democratic identifiers. Democrats running for Congress no longer convince voters that they are different from their party’s presidential standard bearers—a group that has consistently been judged unacceptable to overwhelming proportions of the southern white electorate.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition

Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk

The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project-imputed genotype data in up to similar to 370,000 women, we identify 389 independent signals (P <5 x 10(-8)) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain similar to 7.4% of the population variance in age at menarche, corresponding to similar to 25% of the estimated heritability. We implicate similar to 250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility

Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk

The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project–imputed genotype data in up to ~370,000 women, we identify 389 independent signals (P < 5 × 10$^{−8}$) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain ~7.4% of the population variance in age at menarche, corresponding to ~25% of the estimated heritability. We implicate ~250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility

Molecular signal processing by eukaryotic elongation factor 2 kinase (eEF-2K)

Translation of mRNA to protein is essential to all life, and is carried out by the ribosome with the assistance of various initiation and elongation factors. The rate and location at which translation occurs is subject to regulation by an intricate network of positive and negative signaling mechanisms. Such regulation allows the cell to respond to changes in external conditions, such as a sudden drop in nutrient availability. In higher eukaryotes, a key component of this regulation is the phosphorylation of elongation factor 2 (eEF-2) - the enzyme which catalyzes ribosome translocation along the mRNA - by eEF-2 kinase (eEF-2K) on Thr56. This event impedes the affinity of eEF-2 for the ribosome and therefore lowers the rate of protein synthesis. The activity of eEF-2K is tightly regulated by upstream signals, including Ca²⁺-calmodulin and post-translational modification. Aberrant regulation of the eEF-2K axis is known in various disease states, including cancer and depression, yet the molecular mechanisms by which eEF-2K processes the multiple signals that communicate with it are poorly defined. This gap in knowledge precludes the rational design of eEF-2Ktargeting treatments which may be effective at treating such diseases. Here, three broad topics are discussed. First, an overview of what is currently known about the structure, function, and regulation of eEF-2K is presented. Second, we elucidate the mechanisms by which eEF-2K integrates signals at the nutrient-sensitive signaling node. Finally, we characterize a highly active form of eEF-2K which provides insight into the potential structure-function relationship of key portions of the enzyme. Taken together, this work is an important step towards a complete description of the biochemical mechanisms by which eEF-2K is regulated by diverse inputsPharmaceutical Science

MS 9

Harold Giles was born in March 1890 at Springvale Station in the Northern Territory, the third of four children of Alfred Giles and Mary Augusta. Four years after Harold?s birth the family moved to Bonrook Station homestead just out of Pine Creek. This diary is a childhood account of life in the Northern Territory in the Federation period. Soon after this was written, Giles, like his brothers before him, would be sent away to boarding school in Adelaide. Growing up in the bush, Harold was a good shot and excellent bushman. He became a policeman and enlisted in the First World War, although was found to be medically unfit and he rejoined the police force. When posted to Maranboy, Harold met and fell in love with a young nurse from the Maranboy Inland Mission Hospital. They married in 1924 and went on to have three children. He retired to Queensland in 1954 after managing Elsey Station and eventually died in Brisbane in 1960. This diary offers a rare opportunity to read a first-hand account of a child?s life on a pastoral station in the Territory at the beginning of the twentieth century. An account of daily life by a Top End schoolboy at the turn of the century, 1900-1901. Harold Giles notes daily events where trips to Pine Creek and Bonrook Station are mentioned frequently. Cradling for gold is also a common occurrence, with young Harold telling of his discoveries. The diary is in exercise book format and is handwritten in ink. The diary is in a fragile condition but has been transcribed.1. Original Diary -- 2. Typed transcript of diary -- 3. Handwritten transcript of diary -- 4. Hand drawn colour picture by Harold Stanage aged 10 years in dated 1903 -- 5. 3 page handwritten letter dated 6 July 1932 addressed to Harold by his mother M.A. Giles

Letter, 1935 June 10, New Jersey, to Mrs. Putnam, New York

Letter, Harold G. Hoffman, Governor of New Jersey, inviting Earhart to judge an air derby, June 10, 193

Letter, 1935 June 5, Sea Girt, N.J., to Mrs. Putnam

Letter, Harold Hoffman, Governor of New Jersey, to Amelia Earhart, invitation to an event, June 5, 193