Vortex Dynamics at the transition to the normal state in YBCO films

We propose a description of the vortex dynamics in YBCO films from the critical to the normal states. This description supposes that the vortex motion is thermally activated along the twin boundaries of the films. The discontinuity observed in the current-voltage curves at the transition to the normal state is explained by the sudden increase in the dissipated power rate due to vortex depinning. However, near the critical temperature, this phenomenon does not occur because the vortex activation energy is near zero. We also show how the current at the transition to the normal state can be computed from the current-voltage curves measured at low currents. The predictions of this description are compared to the data published by Gonzalez et al. [Phys.Rev.B68,054514 (2003)]

The carboxy-terminal fragment of α1A calcium channel preferentially aggregates in the cytoplasm of human spinocerebellar ataxia type 6 Purkinje cells

Spinocerebellar ataxia type 6 (SCA6) is an autosomal dominant neurodegenerative disease caused by a small polyglutamine (polyQ) expansion (control: 4–20Q; SCA6: 20–33Q) in the carboxyl(C)-terminal cytoplasmic domain of the α1A voltage-dependent calcium channel (Cav2.1). Although a 75–85-kDa Cav2.1 C-terminal fragment (CTF) is toxic in cultured cells, its existence in human brains and its role in SCA6 pathogenesis remains unknown. Here, we investigated whether the small polyQ expansion alters the expression pattern and intracellular distribution of Cav2.1 in human SCA6 brains. New antibodies against the Cav2.1 C-terminus were used in immunoblotting and immunohistochemistry. In the cerebella of six control individuals, the CTF was detected in sucrose- and SDS-soluble cytosolic fractions; in the cerebella of two SCA6 patients, it was additionally detected in SDS-insoluble cytosolic and sucrose-soluble nuclear fractions. In contrast, however, the CTF was not detected either in the nuclear fraction or in the SDS-insoluble cytosolic fraction of SCA6 extracerebellar tissues, indicating that the CTF being insoluble in the cytoplasm or mislocalized to the nucleus only in the SCA6 cerebellum. Immunohistochemistry revealed abundant aggregates in cell bodies and dendrites of SCA6 Purkinje cells (seven patients) but not in controls (n = 6). Recombinant CTF with a small polyQ expansion (rCTF-Q28) aggregated in cultured PC12 cells, but neither rCTF-Q13 (normal-length polyQ) nor full-length Cav2.1 with Q28 did. We conclude that SCA6 pathogenesis may be associated with the CTF, normally found in the cytoplasm, being aggregated in the cytoplasm and additionally distributed in the nucleus

Oki Electric Industry: Description of the Oki System as Used for MUC-7

This paper describes the Oki Information Extraction system as used for MUC-7 evaluation [1][2]. The tasks we have conducted are Named Entity, Co-reference, Template Element and Template Relation. Each module is implemented using MT system modules and pattern recognition modules. Our purposes to participate MUC-7 evaluation are to evaluate how MT system modules are e ectiv

Supplementary Material for: Nutritional Status and Changes in Body Weight in Patients with Multiple System Atrophy

<i>Introduction:</i> The importance of nutritional management in neurodegenerative diseases is increasingly recognized in the clinical setting. However, few reports have examined the nutritional intake in patients with multiple system atrophy (MSA). Here, we investigated changes in daily caloric intake, body mass index (BMI) and nutritional status during the disease course of MSA. <i>Methods:</i> We performed a single-hospital study of 82 consecutive patients with probable MSA according to the consensus criteria. We determined daily caloric intake, the level of activities of daily living (ADL; independent, wheelchair-bound or bedridden) and BMI at the time of admission. Nutritional status was also evaluated using biochemical nutritional markers including serum albumin, total cholesterol and lymphocyte count. <i>Results:</i> Although daily caloric intake decreased with ADL level deterioration (p < 0.01), no significant differences were observed in BMI among ADL levels. Serum albumin also decreased with ADL deterioration (p < 0.01); however, no significant differences were observed for serum total cholesterol or lymphocyte count with respect to ADL level. <i>Conclusion:</i> We demonstrated that patients with advanced stage MSA may develop malnutrition in the absence of a decrease in BMI. Moreover, serum albumin level may be useful for evaluating nutritional changes in MSA patients