Three-Dimensional Conformation of Folded Polymers in Single Crystals.

The chain-folding mechanism and structure of semicrystalline polymers have long been controversial. Solid-state NMR was applied to determine the chain trajectory of (13)C CH3-labeled isotactic poly(1-butene) (iPB1) in form III chiral single crystals blended with nonlabeled iPB1 crystallized in dilute solutions under low supercooling. An advanced (13)C-(13)C double-quantum NMR technique probing the spatial proximity pattern of labeled (13)C nuclei revealed that the chains adopt a three-dimensional (3D) conformation in single crystals.

Human epididymis protein 4 is up-regulated in gastric and pancreatic adenocarcinomas.

Upper gastrointestinal neoplasia in the esophagus, stomach, and pancreas is associated with the formation of preneoplastic metaplasias. We have previously reported the up-regulation of human epididymis protein 4 (HE4) in all metaplasias in the stomach of humans and mice. We have now sought to evaluate the expression of HE4 in metaplasias/preneoplastic precursors and cancers of the human stomach, pancreas, and esophagus.

Guidelines for the management of cutaneous lymphomas (2011): a consensus statement by the Japanese Skin Cancer Society - Lymphoma Study Group.

In 2010, the first Japanese edition of guidelines for the management of cutaneous lymphoma was published jointly by the Japanese Dermatological Association (JDA) and the Japanese Skin Cancer Society (JSCS) - Lymphoma Study Group. Because the guidelines were revised in 2011 based on the most recent data, we summarized the revised guidelines in English for two reasons: (i) to inform overseas clinicians about our way of managing common types of cutaneous lymphomas such as mycosis fungoides/Sézary syndrome; and (ii) to introduce Japanese guidelines for lymphomas peculiar to Asia, such as adult T-cell leukemia/lymphoma and extranodal natural killer/T-cell lymphoma, nasal type. References that provide scientific evidence for these guidelines have been selected by the JSCS - Lymphoma Study Group.

Alterations in gastric mucosal lineages before or after acute oxyntic atrophy in gastrin receptor and H2 histamine receptor-deficient mice.

Spasmolytic polypeptide (SP/TFF2)-expressing metaplasia (SPEM) is induced by oxyntic atrophy and is known as a precancerous or paracancerous lesion. We seek to determine whether the gastrin receptor or H(2) histamine receptor influence the development of SPEM. DMP-777 was administered to gastrin receptor and/or H(2) receptor-deficient mice and wild-type mice.

Surfactant gel extraction of gold(III), palladium(II), platinum(II), and lead(II) as thiourea-complexes.

Anionic surfactant solutions of sodium dodecylbenzenesulfonate (SDBS) and sodium dodecylsulfate (SDS) separate into two phases through cooling of the solution and the addition of salts. Thiourea (TU) reacts with many metals to form cationic complexes of [M(TU)(n)](m+); some of them extract into the SDBS phase. The separation was examined for lead and tin in commercially purchased solders.

Altered gastric chief cell lineage differentiation in histamine-deficient mice.

The orderly differentiation of cell lineages within gastric glands is regulated by a complicated interplay of local mucosal growth factors and hormones. Histamine secreted from enterochromaffin-like cells plays an important role in not only stimulated gastric acid secretion but also coordination of intramucosal growth and lineage differentiation. We have examined histidine-decarboxylase (HDC)-deficient mice, which lack endogenous histamine synthesis, to evaluate the influence of histamine on differentiation of fundic mucosal lineages and the development of metaplasia following induction of acute oxyntic atrophy.

Development of carcinoid tumors of the glandular stomach and effects of eradication in Helicobacter pylori-infected Mongolian gerbils.

The relation between Helicobacter pylori (Hp) eradication and prevention of stomach carcinoid development has hitherto remained unclear. We therefore examined this problem using an Hp-infected and Hp-eradicated Mongolian gerbil (MG) model. Enterochromaffin-like (ECL) lesions (hyperplasia/dysplasia and carcinoid) were histopathologically evaluated in the glandular stomachs of Hp-infected and Hp-eradicated MGs.

A molecular signature of gastric metaplasia arising in response to acute parietal cell loss.

Background & Aims: Loss of gastric parietal cells is a critical precursor to gastric metaplasia and neoplasia. However, the origin of metaplasia remains obscure. Acute parietal cell loss in gastrin-deficient mice treated with DMP-777 leads to the rapid emergence of spasmolytic polypeptide/trefoil factor family 2 (TFF2)-expressing metaplasia (SPEM) from the bases of fundic glands.

Molecular simulation of crystallization in n-alkane ultrathin films: effects of film thickness and substrate attraction.

Crystallization in n-alkane ultrathin films supported by solid substrates is investigated by molecular dynamics simulation. We consider a relatively short n-alkane, undecane C11H24, on a flat substrate of varied degree of attraction. By the use of the united atom model for n-alkane, we reveal several characteristics of the thin film crystallization.

Intestinal phenotypes of stomach cancers arising after Helicobacter pylori eradication in carcinogen-treated Mongolian gerbils.

Aims: We have previously demonstrated the importance of gastric and intestinal phenotypic expression for the histogenesis of stomach cancer. However, the phenotypes of stomach cancers arising after Helicobacter pylori (Hp) eradication have hitherto remained unclear. We therefore examined a series of lesions occurring after Hp eradication in the Mongolian gerbil (MG) model.

Severity of gastritis determines glandular stomach carcinogenesis in Helicobacter pylori-infected Mongolian gerbils.

Helicobacter pylori (H. pylori) infection causes chronic gastritis and is also related to gastric carcinoma. The present study focused on severity of H.

Helicobacter pylori-negative / API2-MALT1 translocation-negative low-grade MALT lymphoma.

A 71-year-old man with a Helicobacter pylori infection-negative and API2-MALT1 translocation-negative extranodal marginal-zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) type of the stomach has been followed conservatively for over 5 years. The lesion has shown no major morphological changes or malignant progression into a diffuse large-cell type during the time course. The absence of genetic translocation of API2-MALT1 was confirmed with fluorescence in situ hybridization (FISH).

Efficacy of triple therapy plus cetraxate for the Helicobacter pylori eradication in partial gastrectomy patients.

In the present study, we aimed to establish an additional standardized protocol with a higher H. pylori eradication rate in the remnant stomach. Fifty-five H.

Helicobacter pylori-dependent NF-kappa B activation in newly established Mongolian gerbil gastric cancer cell lines.

Mongolian gerbils are an ideal animal model to explore the role of H. pylori on cancer development. However, there have been no established adenocarcinoma cell lines from this model animal.

Ethanol production from cellulosic materials by genetically engineered Zymomonas mobilis.

To confer the ability to ferment cello-oligosaccharides on the ethanol-producing bacterium, Zymomonas mobilis, the beta-glucosidase gene from Ruminococcus albus, tagged at its N-terminal with the 53-amino acid Tat signal peptide from the periplasmic enzyme glucose-fructose oxidoreductase from Z. mobilis, was introduced into the strain. The tag enabled 61% of the beta-glucosidase activity to be transported through the cytoplasmic membrane of the recombinant strain which then produced 0.

Eradication of Helicobacter pylori induces apoptosis and inhibits proliferation of heterotopic proliferative glands in infected Mongolian gerbils.

Mongolian gerbils infected with Helicobacter pylori (H. pylori ) develop heterotopic proliferative glands (HPGs) in the glandular stomach submucosa. To investigate the effects of H.

Beta-catenin gene alteration in glandular stomach adenocarcinomas in N-methyl-N-nitrosourea-treated and Helicobacter pylori-infected Mongolian gerbils.

The goal of this study was to elucidate whether beta-catenin gene mutations might contribute to glandular stomach carcinogenesis in Helicobacter pylori (H.pylori)-infected Mongolian gerbils. Firstly, exon 3 of gerbil beta-catenin cDNA, a mutation hot spot, was cloned and sequenced and found to have 89.

beta-Catenin mutations and nuclear accumulation during progression of rat stomach adenocarcinomas.

Aberrant Wnt/beta-catenin signaling caused by mutations in exon 3 of the beta-catenin gene has been identified in a number of human malignancies, including stomach cancer. However, studies of mutation frequency have yielded conflicting results, and timing during progression remains largely unknown. In this study, we utilized an animal model to address this question.

Expression of the intestine-specific transcription factors, Cdx1 and Cdx2, correlates shift to an intestinal phenotype in gastric cancer cells.

Purpose: It is well known that gastric cancers (GCs) at early stages, independent of the histological type, mainly consist of gastric phenotype malignant cells, while those at advanced stage tend to have a more intestinal phenotype with progression. However, the connection between this shift and expression of homeobox genes, which are important factors to maintain tissue character, has remained unclear. We therefore evaluated the expression of Cdx1/2 in relation to the phenotype of GCs.

Effect of early eradication on Helicobacter pylori-related gastric carcinogenesis in Mongolian gerbils.

Helicobacter pylori (Hp) infection and gastric carcinogenesis are known to have a close relationship, but the effect of eradication of Hp on Hp-related gastric carcinogenesis has not been fully studied experimentally. To evaluate the effect of eradication in gastric carcinogenesis, an experimental model with eradication in the early, middle or late period was studied using Hp-infected and N-methyl-N-nitrosourea (MNU)-treated Mongolian gerbils. The animals were divided into seven groups: group A (MNU + Hp + eradication at 15 w), group B (MNU + Hp + eradication at 35 w), group C (MNU + Hp + eradication at 55 w), group D (MNU + Hp), group E (MNU), group F (Hp) and group G (control).

Helicobacter pylori infection and gastric carcinogenesis in animal models.

The effects of helicobacter pylori infection on gastric disorders have been proven by many epidemiological and experimental studies. To explore the relationships between h. Pylori infection and gastric carcinogenesis, many factors, including host responses, environmental status, and the virulence factors of the bacteria should be taken into account.

[Mechanism of Helicobacter pylori induced stomach carcinogenesis--analysis using animal models].

Helicobacter pylori is known to infect a half of the world's population and has been closely linked to an increased risk of the development of gastric adenocarcinoma, making it a pathogen of potentially great significance. The IARC/WHO in 1994 designated H. pylori a class I carcinogen based on epidemiological evidence.

[Effect of high salt diet and Helicobacter pylori infection on gastric carcinogenesis].

Helicobacter pylori(Hp) infection and a high salt diet are considered important enhancing factors in gastric carcinogenesis. A high salt diet is considered to cause temporary tissue damage, alteration of the viscosity of the protective mucous barrier, and to facilitate colonization of Hp, resulting in gastric tumor progression. The high prevalence of Hp infection and high salt diets might have greatly affected the rates of gastric carcinogenesis, especially in Japan.