Anti-Americanism: recent sources

Anti-American sentiment has, it would seem, increased in the wake of the election of George Bush, jr. and the US&rsquo;s response to the events ofSeptember 11. Commentators within the US, and globally, have analysed the recent variants of a long-standing condition. Below is a review of recent coverage of the phenomenon. The entries for the print sources are divided into:(1) analyses of anti-Americanism written in the US,(2) accounts of international expressions of anti-Americanism.<br /

Chromatin structure and gene expression: from the TMAC complex to the dREAM complex

Multi-subunit complexes such as the testis-specific meiotic arrest complex (TMAC) and the dREAM complex are context specific gene regulators, controlling genes involved in spermatogenesis and the G2/M transition respectively. The TMAC and dREAM complexes largely consist of subunits that are the same or paralogous to one another. One shared subunit, chromatin assembly factor 1, is also a component of the nucleosome remodelling factor complex, which has a similar testis gene expression phenotype to a TMAC mutant when its testis specific isoform, NURF301, is mutated. Therefore both complexes are thought to control gene expression, at least in part, through modifying chromatin either directly or through associations with chromatin remodellers. To investigate this further I have employed an unbiased approach for determining the positions of DNA bound proteins in vivo called Chromatin Particle Spectrum Analysis (CPSA) which involves micrococcal nuclease digestion of native chromatin and paired-end mode Illumina sequencing. Strikingly, in the cells which have many genes activated by TMAC, the spermatocytes, the transcriptional start sites of TMAC target genes lack coherent nucleosome positioning, which is a robust indicator of high gene expression in somatic cells. Disruption of TMAC does not decidedly alter this structure, suggesting that TMAC does not influence nucleosome positioning surrounding testis specific transcriptional start sites. In contrast, when analysing dREAM subunit deficient S2R+ cells, dREAM is found to contribute to the depletion of a nucleosome sized particle at the mid-point between divergently transcribed genes. This phenotype is linked with the involvement of dREAM in both enhancer blocking between proximal genes and its interaction with the nucleosome remodelling and deacetylase complex. Overall, I uncover the unique chromatin structure of highly expressed genes in spermatocytes, and implicate dREAM as being involved in nucleosome removal between divergent gene pairs

Chromatin structure and gene expression: from the TMAC complex to the dREAM complex

Multi-subunit complexes such as the testis-specific meiotic arrest complex (TMAC) and the dREAM complex are context specific gene regulators, controlling genes involved in spermatogenesis and the G2/M transition respectively. The TMAC and dREAM complexes largely consist of subunits that are the same or paralogous to one another. One shared subunit, chromatin assembly factor 1, is also a component of the nucleosome remodelling factor complex, which has a similar testis gene expression phenotype to a TMAC mutant when its testis specific isoform, NURF301, is mutated. Therefore both complexes are thought to control gene expression, at least in part, through modifying chromatin either directly or through associations with chromatin remodellers. To investigate this further I have employed an unbiased approach for determining the positions of DNA bound proteins in vivo called Chromatin Particle Spectrum Analysis (CPSA) which involves micrococcal nuclease digestion of native chromatin and paired-end mode Illumina sequencing. Strikingly, in the cells which have many genes activated by TMAC, the spermatocytes, the transcriptional start sites of TMAC target genes lack coherent nucleosome positioning, which is a robust indicator of high gene expression in somatic cells. Disruption of TMAC does not decidedly alter this structure, suggesting that TMAC does not influence nucleosome positioning surrounding testis specific transcriptional start sites. In contrast, when analysing dREAM subunit deficient S2R+ cells, dREAM is found to contribute to the depletion of a nucleosome sized particle at the mid-point between divergently transcribed genes. This phenotype is linked with the involvement of dREAM in both enhancer blocking between proximal genes and its interaction with the nucleosome remodelling and deacetylase complex. Overall, I uncover the unique chromatin structure of highly expressed genes in spermatocytes, and implicate dREAM as being involved in nucleosome removal between divergent gene pairs

Rings graded equivalent to the Weyl algebra

We consider the first Weyl algebra, A, in the Euler gradation, and completely classify graded rings B that are graded equivalent to A: that is, the categories gr-A and gr-B are equivalent. This includes some surprising examples: in particular, we show that A is graded equivalent to an idealizer in a localization of A. We obtain this classification as an application of a general Morita-type characterization of equivalences of graded module categories.Comment: 38 pages; minor changes to final published versio

Differential effects of nutritional folic acid deficiency and moderate hyperhomocysteinemia on aortic plaque formation and genome-wide DNA methylation in vascular tissue from ApoE-/- mice

Low folate intake is associated with vascular disease. Causality has been attributed to hyperhomocysteinemia. However, human intervention trials have failed to show the benefit of homocysteine-lowering therapies. Alternatively, low folate may promote vascular disease by deregulating DNA methylation. We investigated whether folate could alter DNA methylation and atherosclerosis in ApoE null mice. Mice were fed one of six diets (n = 20 per group) for 16 weeks. Basal diets were either control (C; 4% lard) or high fat (HF; 21% lard and cholesterol, 0.15%) with different B-vitamin compositions: (1) folic acid and B-vitamin replete, (2) folic acid deficient (−F), (3) folic acid, B6 and B12 deficient (−F−B). −F diets decreased plasma (up to 85%; P < 0.05), whole blood (up to 70%; P < 0.05), and liver folate (up to 65%; P < 0.05) and hepatic SAM/SAH (up to 80%; P < 0.05). −F−B diets reduced plasma (up to 76%; P < 0.05), whole blood (up to 72%; P < 0.05), and liver B12 (up to 39%; P < 0.05) and hepatic SAM/SAH (up to 90%; P < 0.05). −F increased homocysteine 2-fold, while −F−B increased homocysteine 3.6- and 6.8-fold in the C and HF groups (P < 0.05). Plaque formation was increased 2-fold (P < 0.0001) in mice fed a HF diet. Feeding a HF–F diet increased lesion formation by 17% (P < 0.05). There was no change in 5-methyldeoxycytidine in liver or vascular tissue (aorta, periadventitial tissue and heart). These data suggest that atherogenesis is not associated with genome-wide epigenetic changes in this animal model

The relationships between bone mineral density in the spine, hip, distal femur and proximal tibia and medial minimum joint space width in the knees of healthy females

SummaryObjectiveTo investigate the relationships between bone mineral density (BMD) in the hip, spine, distal femur and proximal tibia and minimum joint space width (mJSW) in the knees of healthy women.MethodsWomen 22–68 years old without a history of knee pain, bone or joint disease or injury underwent a single, fixed-flexion knee X-ray. Radiographs were graded according to the Kellgren–Lawrence scale and analyzed for mJSW using a computer algorithm. Dual X-ray absorptiometry scans of the spine, hip, distal femur and proximal tibia were also acquired for each participant. Femur and tibia scans were acquired and analyzed using a modified version of the lumbar spine software.ResultsForty-five females, mean [standard deviation (SD)] age and body mass index (BMI) of 40.1 (13.9) years and 24.6 (4.5)kg/m2, respectively, participated. The mean (SD) mJSW was 4.64 (0.68)mm. Linear regression analyses controlling for age and BMI revealed that BMD in the femoral trochanter and the central two regions of the tibia (T2 and T3) was significantly related to mJSW in the knee. A backwards regression analysis performed to determine which region of interest is most significantly related to mJSW revealed that femoral trochanter BMD (β-value=0.416) is the most significant.ConclusionsIn contrast to the suggestion that BMD is negatively correlated with mJSW in the knees of osteoarthritic individuals, these results suggest that increasing BMD in the femoral trochanter and tibia is significantly associated with increasing mJSW in healthy females. Further investigation of this relationship is warranted

Cumulative mutagenesis of the basic residues in the 201-218 region of insulin-like growth factor (IGF)-binding protein-5 results in progressive loss of both IGF-I binding and inhibition of IGF-I biological action

We have reported previously that mutation of two conserved nonbasic amino acids (G203 and Q209) within the highly basic 201–218 region in the C-terminal domain of IGF-binding protein-5 (IGFBP-5) decreases binding to IGFs. This study reveals that cumulative mutagenesis of the 10 basic residues in this region, to create the C-Term series of mutants, ultimately results in a 15-fold decrease in the affinity for IGF-I and a major loss in heparin binding. We examined the ability of mutants to inhibit IGF-mediated survival of MCF-7 cells and were able to demonstrate that this depended not only upon the affinity for IGF-I, but also the kinetics of this interaction, because IGFBP-5 mutants with similar affinity constants (KD) values, but with different association (Ka) and dissociation (Kd) rate values, had markedly different inhibitory properties. In contrast, the affinity for IGF-I provided no predictive value in terms of the ability of these mutants to enhance IGF action when bound to the substratum. Instead, these C-Term mutants appeared to enhance the actions of IGF-I by a combination of increased dissociation of IGF-IGFBP complexes from the substratum, together with dissociation of IGF-I from IGFBP-5 bound to the substratum. These effects of the IGFBPs were dependent upon binding to IGF-I, because a non-IGF binding mutant (N-Term) was unable to inhibit or enhance the actions of IGF-I. These results emphasize the importance of the kinetics of association/dissociation in determining the enhancing or inhibiting effects of IGFBP-5 and demonstrate the ability to generate an IGFBP-5 mutant with exclusively IGF-enhancing activity

CD90 is not constitutively expressed in functional innate lymphoid cells

Huge progress has been made in understanding the biology of innate lymphoid cells (ILC) by adopting several well-known concepts in T cell biology. As such, flow cytometry gating strategies and markers, such as CD90, have been applied to indentify ILC. Here, we report that most non-NK intestinal ILC have a high expression of CD90 as expected, but surprisingly a sub-population of cells exhibit low or even no expression of this marker. CD90-negative and CD90-low CD127+ ILC were present amongst all ILC subsets in the gut. The frequency of CD90-negative and CD90-low CD127+ ILC was dependent on stimulatory cues in vitro and enhanced by dysbiosis in vivo. CD90-negative and CD90-low CD127+ ILC were a potential source of IL-13, IFNγ and IL-17A at steady state and upon dysbiosis- and dextran sulphate sodium-elicited colitis. Hence, this study reveals that, contrary to expectations, CD90 is not constitutively expressed by functional ILC in the gut