The effects of a Jewish primary school education in England on the religious observance and practice of less or non-observant parents of the pupils

The main aim of this research is to determine whether or not there has been any noticeable change in the level of religious observance and practice of less or non-observant parents which directly or indirectly can be attributed to the influence of their children and the Jewish primary school they attend. There is a frequently voiced assumption amongst those involved in Jewish education that parents, whose children attend a Jewish primary school, have increased their level of observance due to the influence of their children and the school. However, no previous research has been carried out in the United Kingdom in order to examine the basis of this premise. The purpose ofmy own research is to test this assumption in a thorough and rigorous manner by means of both questionnaires and in-depth interviews with parents of pupils attending three Jewish primary schools in England. In addition, there are two further specific areas that will be investigated as supplementary parts ofthe main research: [i] To compare the extent of similarities and differences of any such changes in religious observance between those Jewish families in England who formed part ofmy study, and those in the USA whose children attend Jewish day schools, who have also been the subject of separate research in the USA. [ii] To determine whether within the data of this research study, there is any correlation with previous research in the field of social psychology regarding causes and effects of social conformity and deviation. The data from this specific area of research will be used to focus on the effects of a crucial inter-connection between parents, children and the school. The thesis includes an examination of previous allied research and its implications relating to the nature of religious identity and changes in parental behaviour attributed to the influence of their children's Jewish education. It also contains chapters outlining the historical and social background which led to a weakening ofJewish religious observance in the UK during the zo" century and a study of the changing role of the traditional Jewish family and its effect on the levels of religious observance in Anglo-Jewry. The data from questionnaires and interviews are analysed in a thorough manner. The results and conclusions of this thesis should be of benefit to those planning and administering Jewish primary schools in the UK

Time series of CH₄ and CO concentrations for 2010 and 2011.

<p>(a) Variability in XCH₄ concentrations (ppb) in the southern Amazon region (dark green circles), central South America region (light green circles), and background region (ocean area between 0°–20°S and 20°–50°W; red line). Daily data of the background region were constructed from discrete XCH₄ data using a Humming window with a window-width of 80 days. The standard errors (one sigma) of XCH₄ data are given by the gray boundary. The discontinuity at the background region for May 22–June 20 in 2011 reflects a lack of XCH₄ data. (b) Monthly variability in XCH₄ values (ppb) with the background subtracted (ΔXCH₄) in the southern Amazon region (dark green box-and-whiskers) and the central South America region (light green box-and-whiskers). Upper and lower values of the boxes are monthly quartiles of ΔXCH₄, bars through the boxes are medians, and whiskers represent the range of the 10^th and 90^th percentiles (data are not shown for months in which the number of data points was <25). (c) Same as (b), but showing surface CO concentrations (ppb) from the MOPITT L3 product.</p

Total annual CH₄ flux (upper) and relative contributions of anthropogenic (magenta), natural (blue), and biomass-burning (red) fluxes (lower) in the southern Amazon region (left) and central South America region (right) for 2010 and 2011 (in Tg CH₄ region⁻¹ yr⁻¹).

<p>Error bars represent flux uncertainties.</p

Data_Sheet_1_Progression of Pulmonary Emphysema and Continued Increase in Ectodomain Shedding of Cell Adhesion Molecule 1 After Cessation of Cigarette Smoke Exposure in Mice.pdf

<p>Pulmonary emphysema usually arises in cigarette smokers, and often progresses after smoking cessation and even in ex-smokers. Lung-epithelial cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member, is extracellularly shed to produce a proapoptotic C-terminal fragment (CTF) within the cell and contribute to the development of emphysema. Here, we made an ex-smoker model using C57BL/6 mice; mice (6-week-old; 5 mice per group) were exposed to passive smoke of eight cigarettes twice a day 5 days a week until 18 weeks of age, and were then left untreated until 30 weeks of age. We calculated the mean linear intercept (Lm) and the alveolar septal thickness in the lung histologic sections to estimate the alveolar space dilatation. At 18 weeks of age, Lm was marginally enlarged (P = 0.023) with a marked increase in the septal thickness (P < 0.001) in comparison with age-matched control mice (5 mice per group), while at 30 weeks, the increase in Lm was much more prominent (P = 0.006) and the septal thickness was normalized, suggesting that emphysema progressed with septal remodeling during smoking cessation. Western blot analyses of the lungs were performed for CADM1, a possible CADM1 sheddase ADAM10, an epithelial marker pan-cytokeratin, and a myofibroblastic marker α-smooth muscle actin to estimate the expression levels of CTF and ADAM10 per epithelial cell and the levels of pan-cytokeratin and αSMA per tissue. CADM1 shedding was increased in the treated mice than in control mice at both ages, in association with an increase in the CTF level at 30 weeks (P = 0.021). In total of the treated and control mice of 30 weeks of age, Lm was positively correlated with the CTF and ADAM10 levels, and pan-cytokeratin was negatively correlated with CTF, suggesting an involvement of CADM1 shedding in emphysema progression. Positive correlations were also found between CTF and ADAM10, and between ADAM10 and αSMA, suggesting that increased septal myofibroblasts might be involved in increased CADM1 shedding. Taken together, persisting increase in ectodomain shedding of CADM1 appeared to contribute to the progression of emphysema in ex-smokers, and might be accounted for by alveolar septal remodeling.</p

Additional file 1: Figure S1. of The intracellular domain of cell adhesion molecule 1 is present in emphysematous lungs and induces lung epithelial cell apoptosis

Synthesis of the cell adhesion molecule 1 intracellular domain (C-ICD) and the mutated cell adhesion molecule 1 intracellular domain (C-ICDmut) peptides. High-performance liquid chromatography data of the synthesized peptides. The C-ICD (upper) and C-ICDmut (lower) peptides were detected at 5657.09 (theoretical value 5657.78) and 5127.55 (theoretical value 5126.57) m/z, respectively. (TIFF 356 kb

Subcellular localization of endogenous and exogenous αCTF in MIN6-m9 cells.

<p>MIN6-m9 cells were untreated (−), treated with PMA (200 nM) and trypsin (0.025% w/v), or transfected with pCX4bsr-SP-αCTF. After 45 min of treatment and 2 days of transfection, CADM1 levels were assessed in western blot (<b>a</b>) and immunofluorescence (<b>b</b>) analyses using a CADM1 antibody. In <b>a</b>, arrowheads indicate full-length CADM and αCTF. The blot was reprobed with an anti-β-actin antibody to show the protein loading. In <b>b</b>, cells were double stained with CADM1 antibody (green; top) and MitoTracker (red; middle). Merged images are also shown (bottom). Data are representative of three independent experiments. Bar  = 10 µm.</p

Characteristics of the patient groups^a.

a<p>Data for individual patients are presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0100988#pone.0100988.s005" target="_blank">Table S1</a>.</p>b<p>Data are expressed as the mean ± SE.</p>c<p>Control, n = 3; T2DM, n = 10.</p

Increased Ectodomain Shedding of Cell Adhesion Molecule 1 from Pancreatic Islets in Type 2 Diabetic Pancreata: Correlation with Hemoglobin A1c Levels

<div><p>Pulmonary emphysema and type 2 diabetes mellitus (T2DM), both caused by lifestyle factors, frequently concur. Respectively, the diseases affect lung alveolar and pancreatic islet cells, which express cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member. Protease-mediated ectodomain shedding of full-length CADM1 produces C-terminal fragments (CTFs) with proapoptotic activity. In emphysematous lungs, the CADM1 shedding rate and thus the level of CTFs in alveolar cells increase. In this study, CADM1 expression in islet cells was examined by western blotting. Protein was extracted from formalin-fixed, paraffin-embedded sections of pancreata isolated from patients with T2DM (n = 12) or from patients without pancreatic disease (n = 8) at autopsy. After adjusting for the number of islet cells present in the adjacent section, we found that full-length CADM1 decreased in T2DM islets, while ectodomain shedding increased. Hemoglobin A1c levels, measured when patients were alive, correlated inversely with full-length CADM1 levels (<i>P</i> = 0.041) and positively with ectodomain shedding rates (<i>P</i> = 0.001). In immunofluorescence images of T2DM islet cells, CADM1 was detected in the cytoplasm, but not on the cell membrane. Consistently, when MIN6-m9 mouse beta cells were treated with phorbol ester and trypsin to induce shedding, CADM1 immunostaining was diffuse in the cytoplasm. When a form of CTFs was exogenously expressed in MIN6-m9 cells, it localized diffusely in the cytoplasm and increased the number of apoptotic cells. These results suggest that increased CADM1 ectodomain shedding contributes to blood glucose dysregulation in T2DM by decreasing full-length CADM1 and producing CTFs that accumulate in the cytoplasm and promote apoptosis of beta cells. Thus, this study has identified a molecular alteration shared by pulmonary emphysema and T2DM.</p></div

Increased ectodomain shedding of CADM1 in T2DM pancreata.

<p>(<b>a</b>) Western blot analysis of CADM1 expression in control and T2DM pancreata. Cases are numbered as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0100988#pone.0100988.s005" target="_blank">Table S1</a>. Arrowheads indicate bands corresponding to the full-length, αCTF, and βCTF forms of CADM1. The blot was reprobed with an anti-β-actin antibody to show protein loading. (<b>b</b>) CADM1 expression per islet cell in each patient sample. For each lane in <b>a</b>, the intensities of the full-length CADM1, αCTF, βCTF, and β-actin bands were quantified, and CADM1 levels were expressed relative to β-actin and the islet cell count (/cm² of tissue). Statistical significance was analyzed with the Mann-Whitney <i>U</i>-test. <i>P</i>-values are shown. (<b>c</b>) CADM1 ectodomain shedding rates (relative amounts of CTFs to the full-length CADM1). Statistical significance was analyzed with the Mann-Whitney <i>U</i>-test. <i>P</i>-values are shown. (<b>d</b>) Correlation of HbA1c levels with full-length CADM1 expression per islet cell (left) or the CADM1 shedding rate (αCTF/full-length; right). In each graph, the dot distribution approximated a linear function (dotted lines). Correlations and statistical significance were analyzed with Spearman’s rank test. <i>R²</i> and <i>P</i>-values are shown.</p

Representative photomicrographs of CADM1 immunofluorescence in pancreatic islets.

<p>Pancreatic sections from control (case 7; left) and T2DM (case 3; right) patients were double stained with antibodies against CADM1 (red) and glucagon (green; top) or insulin (green; bottom) and then counterstained with DAPI (blue). Merged images are shown. Bar  = 50 µm.</p