Foreign policy and globalization theory: The case of Israel

Since the early 1990s, international relations has witnessed a stimulating debate on globalization. This debate laid the foundations for globalization theory (GT), providing the tools for an empirical examination of the globalization of multiple activities: from politics and organized violence, to finance, trade and production, through culture and environmental degradation. However, examination of what appear to be the best-known works on globalization reveals that foreign policy has been virtually excluded from GT. In this context, based on what is described here as a synergistic transformationalist approach (STA) to globalization, I provide a critique of GT. The critique is geared towards examining why foreign policy hitherto has been overlooked by contemporary GT. I expose the problems this generates and address them by exploring how STA enables GT to incorporate foreign policy. I use the case of Israel heuristically to elicit how incorporating foreign policy into GT may provide a better understanding of the relationship between foreign policy and globalization. Three themes are highlighted: the role of foreign policy in inducing and reproducing globalization; determining the mutually constitutive relationship between globalization and the state; and shaping the interfacing between international politics and globalization

‘Medusa head ataxia’: the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 3: Anti-Yo/CDR2, anti-Nb/AP3B2, PCA-2, anti-Tr/DNER, other antibodies, diagnostic pitfalls, summary and outlook

Serological testing for anti-neural autoantibodies is important in patients presenting with idiopathic cerebellar ataxia, since these autoantibodies may indicate cancer, determine treatment and predict prognosis. While some of them target nuclear antigens present in all or most CNS neurons (e.g. anti-Hu, anti-Ri), others more specifically target antigens present in the cytoplasm or plasma membrane of Purkinje cells (PC). In this series of articles, we provide a detailed review of the clinical and paraclinical features, oncological, therapeutic and prognostic implications, pathogenetic relevance, and differential laboratory diagnosis of the 12 most common PC autoantibodies (often referred to as ‘Medusa head antibodies’ due to their characteristic somatodendritic binding pattern when tested by immunohistochemistry). To assist immunologists and neurologists in diagnosing these disorders, typical high-resolution immunohistochemical images of all 12 reactivities are presented, diagnostic pitfalls discussed and all currently available assays reviewed. Of note, most of these antibodies target antigens involved in the mGluR1/calcium pathway essential for PC function and survival. Many of the antigens also play a role in spinocerebellar ataxia. Part 1 focuses on anti-metabotropic glutamate receptor 1-, anti-Homer protein homolog 3-, anti-Sj/inositol 1,4,5-trisphosphate receptor- and anti-carbonic anhydrase-related protein VIII-associated autoimmune cerebellar ataxia (ACA); part 2 covers anti-protein kinase C gamma-, anti-glutamate receptor delta-2-, anti-Ca/RhoGTPase-activating protein 26- and anti-voltage-gated calcium channel-associated ACA; and part 3 reviews the current knowledge on anti-Tr/delta notch-like epidermal growth factor-related receptor-, anti-Nb/AP3B2-, anti-Yo/cerebellar degeneration-related protein 2- and Purkinje cell antibody 2-associated ACA, discusses differential diagnostic aspects and provides a summary and outlook

Peripheral T-lymphocytes express WNT7A and its restoration in leukemia-derived lymphoblasts inhibits cell proliferation

<p>Abstract</p> <p>Background</p> <p>WNT7a, a member of the Wnt ligand family implicated in several developmental processes, has also been reported to be dysregulated in some types of tumors; however, its function and implication in oncogenesis is poorly understood. Moreover, the expression of this gene and the role that it plays in the biology of blood cells remains unclear. In addition to determining the expression of the <it>WNT7A </it>gene in blood cells, in leukemia-derived cell lines, and in samples of patients with leukemia, the aim of this study was to seek the effect of this gene in proliferation.</p> <p>Methods</p> <p>We analyzed peripheral blood mononuclear cells, sorted CD3 and CD19 cells, four leukemia-derived cell lines, and blood samples from 14 patients with Acute lymphoblastic leukemia (ALL), and 19 clinically healthy subjects. Reverse transcription followed by quantitative Real-time Polymerase chain reaction (qRT-PCR) analysis were performed to determine relative <it>WNT7A </it>expression. Restoration of WNT7a was done employing a lentiviral system and by using a recombinant human protein. Cell proliferation was measured by addition of WST-1 to cell cultures.</p> <p>Results</p> <p>WNT7a is mainly produced by CD3 T-lymphocytes, its expression decreases upon activation, and it is severely reduced in leukemia-derived cell lines, as well as in the blood samples of patients with ALL when compared with healthy controls (<it>p </it>≤0.001). By restoring <it>WNT7A </it>expression in leukemia-derived cells, we were able to demonstrate that WNT7a inhibits cell growth. A similar effect was observed when a recombinant human WNT7a protein was used. Interestingly, restoration of <it>WNT7A </it>expression in Jurkat cells did not activate the canonical Wnt/β-catenin pathway.</p> <p>Conclusions</p> <p>To our knowledge, this is the first report evidencing quantitatively decreased <it>WNT7A </it>levels in leukemia-derived cells and that <it>WNT7A </it>restoration in T-lymphocytes inhibits cell proliferation. In addition, our results also support the possible function of <it>WNT7A </it>as a tumor suppressor gene as well as a therapeutic tool.</p

Endogenous retrovirus-K promoter: a landing strip for inflammatory transcription factors?

Humans are symbiotic organisms; our genome is populated with a substantial number of endogenous retroviruses (ERVs), some remarkably intact, while others are remnants of their former selves. Current research indicates that not all ERVs remain silent passengers within our genomes; re-activation of ERVs is often associated with inflammatory diseases. ERVK is the most recently endogenized and transcriptionally active ERV in humans, and as such may potentially contribute to the pathology of inflammatory disease. Here, we showcase the transcriptional regulation of ERVK. Expression of ERVs is regulated in part by epigenetic mechanisms, but also depends on transcriptional regulatory elements present within retroviral long terminal repeats (LTRs). These LTRs are responsive to both viral and cellular transcription factors; and we are just beginning to appreciate the full complexity of transcription factor interaction with the viral promoter. In this review, an exploration into the inflammatory transcription factor sites within the ERVK LTR will highlight the possible mechanisms by which ERVK is induced in inflammatory diseases

No evidence against Sketch Reinstatement of context, verbal labels or the use of registered intermediaries for children with Autism Spectrum Disorder: response to Henry et al. (2017)

Recently, Henry et al. (2017) found no evidence for the use of Verbal labels, Sketch Reinstatement of Context and Registered Intermediaries by forensic practitioners when interviewing children with a diagnosis of Autism Spectrum Disorder. We consider their claims, noting the limited ecological validity of the experimental paradigm, the impacts of repeated interviewing where retrieval support is not provided at first retrieval, question the interviewer/intermediary training and their population relevant experience, and comment on the suppression of population variances. We submit that rejecting these techniques on the basis of this study is completely unwarranted and potentially damaging, particularly if used in legal proceedings to undermine the value of testimony from children with ASD, who continually struggle to gain access to justice

The penetrating potential of autoantibodies into live cells in vitro coincides with the in vivo staining of epidermal nuclei

We have previously demonstrated that IgG autoantibodies derived from SLE patients are capable of penetrating into nuclei of living COLO-16 cells, in vitro. To address the possible correlation in Lupus Erythematosus (LE) between the in vivo ANA binding to nuclei of epidermal cells and the presence of intranuclear penetrating antibodies in sera of those patients, 25 consecutive patients were studied. Out of 25 skin biopsies, 11 specimens (8 of SLE and 3 of DLE) showed by immunofluorescent microscopy extensive in vivo presence of IgG in epidermal nuclei, whereas all sera of these patients stained nuclei of living COLO-16 cells, in vitro. Such penetration was also observed in additional 6/25 sera of patients, but with in vivo negative biopsies. This in vitro nuclear binding, which was unrelated to clinical symptoms of patients or their serological autoantibody profile and titer, was reproduced following cross-linking of intracellular protein by PLP fixation. Likewise, western blotting (immunoblotting) analysis, demonstrated the intranuclear presence of IgG in all in vitro intranuclear IgG staining sera. Furthermore, this in vitro presence, which neither affects cell viability nor DNA synthesis, is time-dependent and of a transient nature: nuclear staining disappears within 48 h following removal of the penetrating sera from medium. In conclusion, since the COLO-16 in vitro assay mirrors exactly the in vivo situation, and because of its higher sensitivity, it provides an excellent tool for the study of non-degraded autoantibody penetration into the nuclei of living cells.</jats:p