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The past few years have seen the issue of refugees rise in prominence, particularly in Europe but also in other parts of the world. It has been almost seven decades since the United Nations High Commissioner for Refugees was set up and the first international treaty regulating the issue of refugees signed. This article examines the international legal framework governing the issue of refugees and argues that it is ineffectual because refugees are inherently a matter of high politics -- refugees are fundamentally a political issue subject to the vicissitudes of politics. The moral and economic justifications for the international refugee regime are also highly contested, and this contestation plays out in the political realm. The international refugee regime and legal regulation of the issue is unlikely to be effective for as long as the nation-state continues to be the primary actor in the international world order. This is because the international refugee regime requires enforcement by states to be effective -- however, political, moral and economic vicissitudes across the states involved impede its ability to function in its ideal conception. [ABSTRACT FROM AUTHOR]

Globalisation has radically transformed the world in many ways, one of which is the unprecedented numbers of people migrating across international borders. Starting from the end of the Cold War, there were scholarly predictions that the forces of globalisation would eventually render international borders irrelevant, leading to a borderless world. Migration, however, appears to be an area where the importance of international borders remains strong. Contemporary developments across the world suggest that real and/or perceived negative effects of international migration often lead to international borders becoming strengthened, disrupting migration flows. This paper examines both sides of the debate about whether we are becoming a borderless world in relation to migration today, in light of contemporary events and developments. [ABSTRACT FROM AUTHOR]

A case study of 11‑year‑old female is presented with poor appetite and progressive weight loss of 10 kg over a period of 6 months and also a case study of 14‑month‑old male had been followed up for feeding difficulties and failure to thrive for 4 months. Topics include examines diencephalic syndrome denotes the association of failure to thrive in infants and children with the presence of a neoplastic disease in the central part of the brain.

Background: Cell surface sialylation is associated with tumor cell invasiveness in many cancers. Glioblastoma is the most malignant primary brain tumor and is highly infiltrative. ST3GAL1 sialyltransferase gene is amplified in a subclass of glioblastomas, and its role in tumor cell self-renewal remains unexplored. Methods: Self-renewal of patient glioma cells was evaluated using clonogenic, viability, and invasiveness assays. ST3GAL1 was identified from differentially expressed genes in Peanut Agglutinin-stained cells and validated in REMBRANDT (n = 390) and Gravendeel (n = 276) clinical databases. Gene set enrichment analysis revealed upstream processes. TGFβ signaling on ST3GAL1 transcription was assessed using chromatin immunoprecipitation. Transcriptome analysis of ST3GAL1 knockdown cells was done to identify downstream pathways. A constitutively active FoxM1 mutant lacking critical anaphase-promoting complex/cyclosome ([APC/C]-Cdh1) binding sites was used to evaluate ST3Gal1-mediated regulation of FoxM1 protein. Finally, the prognostic role of ST3Gal1 was determined using an orthotopic xenograft model (3 mice groups comprising nontargeting and 2 clones of ST3GAL1 knockdown in NNI-11 [8 per group] and NNI-21 [6 per group]), and the correlation with patient clinical information. All statistical tests on patients' data were two-sided; other P values below are one-sided. Results: High ST3GAL1 expression defines an invasive subfraction with self-renewal capacity; its loss of function prolongs survival in a mouse model established from mesenchymal NNI-11 (P < .001; groups of 8 in 3 arms: nontargeting, C1, and C2 clones of ST3GAL1 knockdown). ST3GAL1 transcriptomic program stratifies patient survival (hazard ratio [HR] = 2.47, 95% confidence interval [CI] = 1.72 to 3.55, REMBRANDT P = 1.92 x 10⁻⁸; HR = 2.89, 95% CI = 1.94 to 4.30, Gravendeel P = 1.05 x 10⁻¹¹), independent of age and histology, and associates with higher tumor grade and T2 volume (P = 1.46 x 10⁻⁴). TGFβ signaling, elevated in mesenchymal patients, correlates with high ST3GAL1 (REMBRANDT gliomacor = 0.31, P = 2.29 x 10⁻¹⁰; Gravendeel gliomacor = 0.50, P = 3.63 x 10⁻²⁰). The transcriptomic program upon ST3GAL1 knockdown enriches for mitotic cell cycle processes. FoxM1 was identified as a statistically significantly modulated gene (P = 2.25 x 10⁻⁵) and mediates ST3Gal1 signaling via the (APC/C)-Cdh1 complex. Conclusions: The ST3GAL1-associated transcriptomic program portends poor prognosis in glioma patients and enriches for higher tumor grades of the mesenchymal molecular classification. We show that ST3Gal1-regulated self-renewal traits are crucial to the sustenance of glioblastoma multiforme growth. [ABSTRACT FROM AUTHOR]

This retrospective study analyses the outcome of posterior inferior cerebellar artery aneurysms treated surgically. Thirteen consecutive ruptured and unruptured PICA aneurysm patients from January 1998 to January 2004 were reviewed retrospectively. The mean age was 49.1 ± 7.4 years. Three were unruptured aneurysms and ten presented with acute subarachnoid haemorrahge. Surgery was performed immediately after completed 4 vessel angiograms using the far lateral approach. Eight were fusiform while five were saccular aneurysms. The saccular aneurysms were clipped. Treatment of the fusiform aneurysms included 3 trappings and three proximal clippings. One patient refused surgery and had endovascular occlusion of a giant PICA aneurysm. Eight out of ten (80%) operated patients needed CSF shunting for hydrocephalus. All check angiograms during follow up demonstrated adequate exclusion of the aneurysms from the circulation. None developed the PICA syndrome clinically or showed infarction on brain scans. All good grade patients recovered without neurological deficits. Our experience showed that early surgery for ruptured PICA aneurysm carries a good prognosis with low morbidity. In aneurysms that cannot be clipped, sacrifice of the PICA without revascularisation procedures in proximally located PICA aneurysms may still be feasible if the occlusion is done distal to the perforators. [ABSTRACT FROM AUTHOR]