A novel update rule of HALS algorithm for nonnegative matrix factorization and Zangwill’s global convergence

Nonnegative Matrix Factorization (NMF) has attracted a great deal of attention as an effective technique for dimensionality reduction of large-scale nonnegative data. Given a nonnegative matrix, NMF aims to obtain two low-rank nonnegative factor matrices by solving a constrained optimization problem. The Hierarchical Alternating Least Squares (HALS) algorithm is a well-known and widely-used iterative method for solving such optimization problems. However, the original update rule used in the HALS algorithm is not well defined. In this paper, we propose a novel well-defined update rule of the HALS algorithm, and prove its global convergence in the sense of Zangwill. Unlike conventional globally-convergent update rules, the proposed one allows variables to take the value of zero and hence can obtain sparse factor matrices. We also present two stopping conditions that guarantee the finite termination of the HALS algorithm. The practical usefulness of the proposed update rule is shown through experiments using real-world datasets

Free-bound excitation and predissociation of ytterbium dimers near the ¹S₀-¹P₁ atomic transition

A continuous excitation band of a free-bound photoassociation transition of ytterbium atoms is observed as a red wing of the ¹S₀-¹P₁ atomic line at 399 nm for a hot thermal vapor. The excitation to the 0u⁺ molecular state is observed by monitoring fluorescence from the ³P₁ state atoms, which allows us to detect the production of Yb₂ molecules with high sensitivity. The photoassociation is characterized in comparison with transitions to atomic Rydberg states. The time profile of the fluorescence signal suggests that the 0u⁺ molecular state predissociates with states correlating to the ¹S₀+³D₂ atomic states

全身性強皮症の病態における上皮細胞での転写因子Fli1の発現低下の意義についての検討

学位の種別: 課程博士審査委員会委員 : (主査)東京大学教授 田中 栄, 東京大学教授 山本 一彦, 東京大学准教授 菅谷 誠, 東京大学講師 近藤 健二, 東京大学講師 藤尾 圭志University of Tokyo(東京大学

Oligonucleotide Microarray Analysis of Dietary-Induced Hyperlipidemia Gene Expression Profiles in Miniature Pigs

BACKGROUND: Hyperlipidemia animal models have been established, but complete gene expression profiles of the transition from normal lipid levels have not been obtained. Miniature pigs are useful model animals for gene expression studies on dietary-induced hyperlipidemia because they have a similar anatomy and digestive physiology to humans, and blood samples can be obtained from them repeatedly. METHODOLOGY: Two typical dietary treatments were used for dietary-induced hyperlipidemia models, by using specific pathogen-free (SPF) Clawn miniature pigs. One was a high-fat and high-cholesterol diet (HFCD) and the other was a high-fat, high-cholesterol, and high-sucrose diet (HFCSD). Microarray analyses were conducted from whole blood samples during the dietary period and from white blood cells at the end of the dietary period to evaluate the transition of expression profiles of the two dietary models. PRINCIPAL FINDINGS: Variations in whole blood gene expression intensity within the HFCD or the HFCSD group were in the same range as the controls provide with normal diet at all periods. This indicates uniformity of dietary-induced hyperlipidemia for our dietary protocols. Gene ontology- (GO) based functional analyses revealed that characteristics of the common changes between HFCD and HFCSD were involved in inflammatory responses and reproduction. The correlation coefficient between whole blood and white blood cell expression profiles at 27 weeks with the HFCSD diet was significantly lower than that of the control and HFCD diet groups. This may be due to the effects of RNA originating from the tissues and/or organs. CONCLUSIONS: No statistically significant differences in fasting plasma lipids and glucose levels between the HFCD and HFCSD groups were observed. However, blood RNA analyses revealed different characteristics corresponding to the dietary protocols. In this study, whole blood RNA analyses proved to be a useful tool to evaluate transitions in dietary-induced hyperlipidemia gene expression profiles in miniature pigs

Appendiceal Orifice Inflammation in Ulcerative Colitis Mimicking Mucosa-Associated Lymphoid Tissue Lymphoma in the Cecum

A 55-year-old Japanese woman, who had been diagnosed with ulcerative colitis at 18 years of age, underwent screening endoscopy examinations. Esophagogastroduodenoscopy revealed an extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) of the stomach. Colonoscopy showed a slightly elevated reddish lesion with dilated microvessels but no erosions or ulcers. Although MALT lymphoma in the cecum was endoscopically suspected, flow cytometry and pathological analyses led to the diagnosis of appendiceal orifice inflammation in ulcerative colitis. This case highlights the diversity of the endoscopic appearance of appendiceal orifice inflammation in ulcerative colitis

Elevated expression of CD30 in adult T-cell leukemia cell lines: possible role in constitutive NF-κB activation

BACKGROUND: Human T-cell leukemia virus type 1 (HTLV-1) is associated with the development of adult T-cell leukemia (ATL). HTLV-1 encoded Tax1 oncoprotein activates the transcription of genes involved in cell growth and anti-apoptosis through the NF-κB pathway, and is thought to play a critical role in the pathogenesis of ATL. While Tax1 expression is usually lost or minimal in ATL cells, these cells still show high constitutive NF-κB activity, indicating that genetic or epigenetic changes in ATL cells induce activation independent of Tax1. The aim of this study was to identify the molecules responsible for the constitutive activation of NF-κB in ATL cells using a retroviral functional cloning strategy. RESULTS: Using enhanced green fluorescent protein (EGFP) expression and blasticidin-resistance as selection markers, several retroviral cDNA clones exhibiting constitutive NF-κB activity in Rat-1 cells, including full-length CD30, were obtained from an ATL cell line. Exogenous stable expression of CD30 in Rat-1 cells constitutively activated NF-κB. Elevated expression of CD30 was identified in all ATL lines examined, and primary ATL cells from a small number of patients (8 out of 66 cases). CONCLUSION: Elevated CD30 expression is considered one of the causes of constitutive NF-κB activation in ATL cells, and may be involved in ATL development