Magnetic reversal dynamics of NiFe-based artificial spin ice: Effect of Nb layer in normal and superconducting state

Square arrays of artificial spin ice (ASI) constituting weakly interacting NiFe nano-islands, with length similar to 312 nm, width similar to 125 nm, thickness similar to 20 nm, and lattice constant similar to 570 nm, were fabricated on Nb thin film and on thermally grown 300 nm SiO2 on silicon. Detailed investigations of magnetic force microscopy (MFM) at room temperature, and magnetization M(H) loops and relaxation of remanent magnetization (M-r) at various temperatures were carried out in two in-plane field geometries, namely, parallel ("P"-parallel to the square lattice) and diagonal ("D"-45 degrees to the square lattice). The magnetic response of the ASI samples shows striking difference for insulating (SiO2), metallic (Nb, T > 6.6 K) and superconducting (Nb, T 6.6 K), (1) in "P" geometry the M(H) loops are found to be more "S" shaped in comparison with that for SiO2 base; (2) the ratio of magnetic vertex population of Type II to Type III vertices extracted from MFM studies in "P"("D") geometry is similar to 1:1.1(1.2:1) that changed for the SiO2 base to similar to 2.1:1 (4:1). However, the NiFe-ASI on both metallic Nb and SiO2 bases exhibit a highly athermal decay of magnetization, and the % change in Mr in about two hours at T = 10K (300 K) lies in a range of similar to 1.07-1.80 (0.25-0.62). With Nb base in superconducting state (T < 6.6 K), the M(H) loops not only look radically different from those with SiO2 and metallic Nb as bases but also show significant difference in "P" and "D" geometries. These results are discussed in terms of inter-island magnetostatic energy as influenced by field geometry, presence of metallic Nb base and competing vortex pinning energy of superconducting Nb base

Atypical NK-cell proliferation of the gastrointestinal tract in a patient with antigliadin antibodies but not celiac disease

We describe a unique case of atypical natural killer (NK)-cell proliferation likely related to gluten sensitivity, mimicking NK-cell lymphoma. The patient, a 32-year-old man, has had persistent multiple erythematous bull-eye lesions in the stomach, small bowel, and large bowel for 3 years. Histologically, the lesions were well circumscribed and relatively superficial, composed of atypical medium-sized to large-sized lymphocytes with slightly irregular nuclear contours, a dispersed chromatin pattern, and clear cytoplasm. Immunohistochemistry and flow cytometry showed that the cells were NK cells expressing CD56 (aberrantly bright), T-cell intracellular antigen (TIA)-1, cytoplasmic CD3, and CD94, but not surface CD3, with bright aberrant expression of CD7 and a lack of other NK cell-associated markers. Polymerase chain reaction for rearrangement of the T-cell receptor-γ chain gene showed no evidence of a clonal T-cell population, and in situ hybridization for Epstein-Barr virus encoded RNA was negative. There was no evidence of the involvement of peripheral blood or bone marrow. Although a diagnosis of extranodal NK/T-cell lymphoma was considered because of the atypical morphology and immunophenotypic aberrancy, no chemotherapy was given because of the relatively superficial nature of the infiltrates, lack of significant symptoms, and negativity for Epstein-Barr virus. Two years after initial presentation, the patient was found to have high titers of antigliadin antibodies with no other evidence of celiac disease. After instituting a gluten-free diet, many of the lesions regressed, suggesting that this atypical NK-cell proliferation may be driven by an anomalous immune response. Awareness of this case may prevent pathologists from misdiagnosing similar lesions as NK/T-cell lymphomas. It is as yet unknown whether this process occurs more commonly in patients with gluten sensitivity, or in other settings, and the pathogenesis is as yet undetermined. Copyright © 2006 by Lippincott Williams & Wilkins

Relationship between dysplasia, p53 protein accumulation, DNA ploidy, and Glut1 overexpression in Barrett metaplasia

Background: There is a need for molecular markers of malignant progression in Barrett metaplasia (BM). The aim of this study is to determine the relationship between dysplasia, p53 protein accumulation, DNA ploidy, and Glut1 in BM. Methods: Sections of esophageal biopsy specimens from 120 patients with BM were evaluated for dysplasia, p53 protein, and Glut1 expression by immunohistochemistry, and DNA ploidy by Feulgen stain and image analysis. In cases with diploid DNA histograms, the percentage cells in the G0G1 and G2M phases of the cell cycle were determined. Results: Of 108 diploid cases 19 (28%) of 69 cases with G0G1 ≥ 90% or G2M ≥ 8.33% were p53- positive, in contrast to only 1 (3%) of 39 cases with lower G0G1 or G2M (P = 0.0008). Of 32 p53-positive cases 11 (32%) were aneuploid, in contrast to none (0%) of 88 p53-negative cases (P \u3c 0.0001). Ten (91%) of 11 aneuploid cases were high-grade dysplasia/adenocarcinoma (HGD/CA), compared with only 1 (1%) of 109 diploid cases (P \u3c 0.0001). Five (45%) of 11 cases with HGD/CA were Glut1-positive, in contrast to none (0%) of 109 cases without HGD/CA (P \u3c 0.0001). Conclusions: Our data strongly suggest that in BM, after oxidative DNA damage, as a result of gastroesophageal reflux, there is an increase in the percentage of cells in the G0G1 or G2M phases of the cell cycle to enable repair of damaged DNA; in some of these cases this is followed sequentially by p53 gene mutation and protein accumulation, DNA aneuploidy, HGD, and CA with or without Glut1 overexpression. These events can be detected in routinely processed biopsy samples