Post-primary education in West Ham, 1918-39.

This thesis is concerned with post-primary education in West Ham 1918-39, with particular reference to secondary education. The realities of local educational experience are set against a background of educational acts an economies. The economic difficulties of the 1920s and the Depression of the 1930s were keenly felt in West Ham despite the efforts of the predominantly Labour council to mitigate poverty. A gap sometimes existed between the educational opportunities Labour councillors wished to provide and those they were able to provide. Generally a pragmatic approach was taken and certainly a secondary education was not seen as essential for all. Chapter One outlines West Ham's pre-1918 history and growth with reference to local politics and immigrant and religious groupings. West Ham's interwar history is told in greater detail. Chapter Two relates the difficulties encountered by the West Ham Education Committee in its decision to establish compulsory continuation schools, not least from the parents of West Ham. West Ham was one of the few areas in the country which succeeded in implementing compulsory continuation education albeit for a limited period. A section on technical education is also included in this chapter, although detailed treatment is hampered by a scarcity of records. Chapter Three examines West Ham's secondary school scholarships in the context of the national situation. West Ham's higher elementary/central school scholarships are subjected to the same scrutiny. Each of West Ham's secondary schools shared a broadly similar curriculum and ethos. Chapter Four highlights these similarities but also points out differences. Of the five interwar secondary schools, two catered for girls, one for boys and two were mixed. Two of the secondary schools were Catholic institutions, although both accepted non-Catholic pupils. Three of the schools were aided and two municipal. A section is included on West Ham's higher elementary/central schools but records are less full than those for the secondary schools. Chapter Five compares and contrasts West Ham's interwar secondary school system with that in East Ham, its sister borough. Chapter Six discusses both the economic and cultural factors underlying local attitudes to post-compulsory schooling. The main conclusions drawn relate to these attitudes which militated against any easy acceptance of such education as necessarily beneficial

Additional file 1: of High-resolution manometry in patients with and without globus pharyngeus and/or symptoms of laryngopharyngeal reflux

The reflux symptom idex. (DOCX 68 kb

XRCC5 interacting with p300 to co-regulate COX-2 expression in colon cancer cells.

<p>(A) Immunofluorescence and confocal microscopy of XRCC5 and p300 in RKO and LoVo cells. XRCC5 is stained by TRITC-conjugated secondary antibodies (red), p300 is stained by FITC-conjugated secondary antibodies (green), and nuclei are stained with DAPI (blue). (B) Co-immunoprecipitation assay of p300 and XRCC5 in RKO, LoVo and SW480 cells.Left: Immunoprecipitation assay (IP) of p300 and XRCC5. Right: Western blot (WB) of XRCC5 and p300. (C) Bottom: The design of the flag-tagged plasmids with different domains of p300. Left: The interaction between XRCC5 and the different domains of p300 detected by immunoprecipitation assay and Western blot. (D)Western blot of XRCC5 with the nuclear extractsimmunoprecipitated by an anti-acetylation antibody in RKO, LoVo and SW480 cells. (E) Western blot of XRCC5 with the nuclear extracts immunoprecipitated by an anti-acetylation antibody in LoVo cells. (F) Western blot of XRCC5 and COX-2 in LoVo cells. (G) MTS cell viability assay in LoVo cells (Left) and RKO cells (Right). Cells treated with liposome negative control is used for data alignment. Data are presented as the meanen.D. (*<i>P</i><0.05). lacZ represents negative control vector, p300WT represents wild type p300 overexpression, Δp300 represents histone acetyltransferase (HAT) domain deletion mutant p300, C646 represents p300 HAT inhibitor C646, and siXRCC5 represents knockdown of XRCC5 with siRNAs.</p

Additional file 2: of High-resolution manometry in patients with and without globus pharyngeus and/or symptoms of laryngopharyngeal reflux

Life exposure factors questionnaire. (ZIP 45 kb

XRCC5 regulating COX-2 promoter activation and protein expression in colon cancer cells.

<p>(A) Left: Western blot of XRCC5 and COX-2 in LoVo cells. Right: Western blot of XRCC5 and COX-2 in RKO cells. (B) Luciferase reporter assay of the activity of COX-2 promoter in LoVo cells. Protein weight is used to adjust relative luciferase activity (RLU), and cells treated with BPS negative control are also used for data alignment. Data in the figure are presented as the meanmoter i<i>P</i><0.05). (C) Luciferase reporter assay of the activity of COX-2 promoter in RKO cells. Protein weight is used to adjust relative luciferase activity (RLU). Data are presented as the meanve pro<i>P</i><0.05).(D) MTS cell viability assay of RKO cells. Cells treated with LacZ is used for data alignment. Data are presented as the mean±SD. (*<i>P</i><0.05). Si1, Si2 and Si3 represent three sequences of siRNAs of XRCC5, Sictr represents negative control siRNA of XRCC5, LacZ represents negative vector control, LPS represents lipopolysaccharides, PBS represents PBS negative control, XRCC5 represents overexpression of XRCC5, and CB represents celecoxib.</p

XRCC5 regulating colon cancer cell proliferation <i>in vitro</i>.

<p>(A) MTS cell viability assay of LoVo cells. Cells treated with BPS negative control are used for data alignment. Data are presented as the meaen.D. (*<i>P</i><0.05). (B) MTS cell viability assay of RKO cells. Cells treated with PBS negative control are used for data alignment. Data are presented as the meannt.D. (*<i>P</i><0.05). (C) Morphology observation of LoVo cells. (D) Colony formation assay of LoVo cells. Si1, Si2 and Si3 represent three sequences of siRNAs of XRCC5, Sictr represents negative control siRNA of XRCC5, PBS represents PBS negative control, XRCC5 represents overexpression of XRCC5, and LacZ represents negative control vector.</p

Additional file 5: Figure S3. of Bipartite structure of the inactive mouse X chromosome

Mapping of the hinge region. Contact maps at the hinge region in F1 brain and Patski cells. Data are shown at a 100 kb resolution for a region of chrX:70,000,000–75,099,999 (left) and at a 40 kb resolution for chrX:70,000,000–75,039,999 (right). The estimated boundaries of the superdomains 1 and 2 (at 100 kb or 40 kb) are marked by dotted red lines and the hinge region located in between the superdomains contains the least number of contacts. (PDF 825 kb

Additional file 1: Table S1. of Bipartite structure of the inactive mouse X chromosome

Summary of allele-specific contacts. (XLSX 10 kb

Additional file 8: Figure S5. of Bipartite structure of the inactive mouse X chromosome

Intrachromosomal contacts at Kcnk9 and at imprinted genes, excluding those located on chromosome 7. a Significant contacts are detected at the maternally expressed gene Kcnk9 on the maternal allele (Mat). Allelic mRNA-seq profiles show expression on the maternal allele at imprinted genes Kcnk9, Trappc9, Chrac1 and Ago2, and on the paternal allele (Pat) at Peg13, in agreement with a previous study [62]. Allelic CTCF profiles show absence of binding to the differentially methylated region (DMR) on the maternal allele (arrow) presumably facilitating the formation of contacts between the Kcnk9 promoter region and an unidentified distant enhancer, similar to the situation in human [62]. The needle plot of contact counts between a 40 kb window that overlaps Kcnk9 (grey bar) and other regions shows more interactions on the maternal (pink) than the paternal allele (blue). Genes with maternal or paternal expression are colored pink or blue, non-imprinted genes black, and non-expressed genes grey, respectively. Contact regions showing significant allelic biases are marked by asterisks. b Distribution of maternal-to-paternal allelic contacts at autosomal genes and X-linked genes determined by DNase Hi-C at 40 kb resolution in F1 brain in which the paternal chromosomes are from spretus. c Violin plots show the distribution of maternal-to-paternal allelic contacts at maternally and paternally imprinted genes at 40 kb resolution in F1 brain, after removing genes located on chromosome 7, which changes the shape of the distribution, due to fewer genes showing a low maternal-to-paternal contact ratio (see also Fig. 7). Dotted line indicates median ratios of maternal-to-paternal contacts at autosomal genes. (PDF 1263 kb

Additional file 3: Figure S1. of Bipartite structure of the inactive mouse X chromosome

Allelic differences between contact maps for the X chromosomes are not seen for homologous autosomes. Allelic intrachromosomal chromatin contact heatmaps of chromosome 1 homologs based on SNP reads at 1 Mb resolution obtained by DNase Hi-C and in situ DNase Hi-C in F1 brain and in Patski cells. Contact maps for chromosomes 1 appear remarkably similar between maternal (BL6) and paternal (spretus) chromosomes. See Fig. 1a for comparison with contacts maps obtained for the Xa and Xi, which demonstrate striking differences. (PDF 1178 kb