Torsion homology growth and cycle complexity of arithmetic manifolds

Let M be an arithmetic hyperbolic 3-manifold, such as a Bianchi manifold. We conjecture that there is a basis for the second homology of M, where each basis element is represented by a surface of ‘low’ genus, and give evidence for this. We explain the relationship between this conjecture and the study of torsion homology growth

Glycans in Sera of Amyotrophic Lateral Sclerosis Patients and Their Role in Killing Neuronal Cells

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by degeneration of upper and lower motor neurons. To date, glycosylation patterns of glycoproteins in fluids of ALS patients have not been described. Moreover, the aberrant glycosylation related to the pathogenesis of other neurodegenerative diseases encouraged us to explore the glycome of ALS patient sera. We found high levels of sialylated glycans and low levels of core fucosylated glycans in serum-derived N-glycans of patients with ALS, compared to healthy volunteer sera. Based on these results, we analyzed the IgG Fc N297-glycans, as IgG are major serum glycoproteins affected by sialylation or core fucosylation and are found in the motor cortex of ALS patients. The analyses revealed a distinct glycan, A2BG2, in IgG derived from ALS patient sera (ALS-IgG). This glycan increases the affinity of IgG to CD16 on effector cells, consequently enhancing Antibody-Dependent Cellular Cytotoxicity (ADCC). Therefore, we explore whether the Fc-N297-glycans of IgG may be involved in ALS disease. Immunostaining of brain and spinal cord tissues revealed over-expression of CD16 and co-localization of intact ALS-IgG with CD16 and in brain with activated microglia of G93A-SOD1 mice. Intact ALS-IgG enhanced effector cell activation and ADCC reaction in comparison to sugar-depleted or control IgG. ALS-IgG were localized in the synapse between brain microglia and neurons of G93A-SOD1 mice, manifesting a promising in vivo ADCC reaction. Therefore, glycans of ALS-IgG may serve as a biomarker for the disease and may be involved in neuronal damage

Clinical use of the bcr/abl probe test in the evaluation of chronic myeloid leukemia patients

CML is characterized by a reciprocal translocation between the abl and bcr genes on chromosomes 9 and 22 and is usually diagnosed by the presence of the Philadelphia (Ph-1) chromosome. However, the translocation may also occur without the appearance of the Ph-1 chromosome, In this study the diagnostic efficiency of the molecular hybridization assay was investigated in 227 patients using a probe specific for the bcr region of the gene, Gene rearrangements were observed in 96% of Ph-1-positive cases and in 92% of the patients in whom no Ph-1 chromosome could be detected by karyotype analysis. By using peripheral blood the assay is easy to perform and superior in sensitivity. Thus, it is recommended that this assay should be routinely used as anadjunct to classical cytogenetics