The Effects of Flooding on Shirakawa Delta Morphology

Floods can significantly alter the morphology of a delta, from inputting increased volumes of sediments to modifying the reach of incoming waves, currents, and other gravity-driven forces occurring within the near shore. Kumamoto experienced flooding in July 2012. This flood event altered the equilibrium profile of the intertidal flat area of the Shirakawa River. This research looks at these modifications and attempts to explain their long-term implications on the overall delta morphology. Data collected over a 30-year period was analyzed and profiles were generated to better analyze and assess the trend in delta morphological changes. Numerical predictions on delta morphology in the presence of gravitydriven sediment transport were applied to investigate the morphological changes related to the flood event. The slope of equilibrium profile is lower and steeper offshore, helping to explain the models created before and after the flood occurred

Artificially Induced Epithelial-Mesenchymal Transition in Surgical Subjects: Its Implications in Clinical and Basic Cancer Research

BACKGROUND: Surgical samples have long been used as important subjects for cancer research. In accordance with an increase of neoadjuvant therapy, biopsy samples have recently become imperative for cancer transcriptome. On the other hand, both biopsy and surgical samples are available for expression profiling for predicting clinical outcome by adjuvant therapy; however, it is still unclear whether surgical sample expression profiles are useful for prediction via biopsy samples, because little has been done about comparative gene expression profiling between the two kinds of samples. METHODOLOGY AND FINDINGS: A total of 166 samples (77 biopsy and 89 surgical) of normal and malignant lesions of the esophagus were analyzed by microarrays. Gene expression profiles were compared between biopsy and surgical samples. Artificially induced epithelial-mesenchymal transition (aiEMT) was found in the surgical samples, and also occurred in mouse esophageal epithelial cell layers under an ischemic condition. Identification of clinically significant subgroups was thought to be disrupted by the disorder of the expression profile through this aiEMT. CONCLUSION AND SIGNIFICANCE: This study will evoke the fundamental misinterpretation including underestimation of the prognostic evaluation power of markers by overestimation of EMT IN past cancer research, and will furnish some advice for the near future as follows: 1) Understanding how long the tissues were under an ischemic condition. 2) Prevalence of biopsy samples for in vivo expression profiling with low biases on basic and clinical research. 3) Checking cancer cell contents and normal- or necrotic-tissue contamination in biopsy samples for prevalence

The collagen-binding protein of Streptococcus mutans is involved in haemorrhagic stroke.

Although several risk factors for stroke have been identified, one-third remain unexplained. Here we show that infection with Streptococcus mutans expressing collagen-binding protein (CBP) is a potential risk factor for haemorrhagic stroke. Infection with serotype k S. mutans, but not a standard strain, aggravates cerebral haemorrhage in mice. Serotype k S. mutans accumulates in the damaged, but not the contralateral hemisphere, indicating an interaction of bacteria with injured blood vessels. The most important factor for high-virulence is expression of CBP, which is a common property of most serotype k strains. The detection frequency of CBP-expressing S. mutans in haemorrhagic stroke patients is significantly higher than in control subjects. Strains isolated from haemorrhagic stroke patients aggravate haemorrhage in a mouse model, indicating that they are haemorrhagic stroke-associated. Administration of recombinant CBP causes aggravation of haemorrhage. Our data suggest that CBP of S. mutans is directly involved in haemorrhagic stroke

Involvement of a periodontal pathogen, <it>Porphyromonas gingivalis </it>on the pathogenesis of non-alcoholic fatty liver disease

<p>Abstract</p> <p>Background</p> <p>Non-alcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome that is closely associated with multiple factors such as obesity, hyperlipidemia and type 2 diabetes mellitus. However, other risk factors for the development of NAFLD are unclear. With the association between periodontal disease and the development of systemic diseases receiving increasing attention recently, we conducted this study to investigate the relationship between NAFLD and infection with <it>Porphyromonas gingivalis </it>(<it>P. gingivalis</it>), a major causative agent of periodontitis.</p> <p>Methods</p> <p>The detection frequencies of periodontal bacteria in oral samples collected from 150 biopsy-proven NAFLD patients (102 with non-alcoholic steatohepatitis (NASH) and 48 with non-alcoholic fatty liver (NAFL) patients) and 60 non-NAFLD control subjects were determined. Detection of <it>P. gingivalis </it>and other periodontopathic bacteria were detected by PCR assay. In addition, effect of <it>P. gingivalis</it>-infection on mouse NAFLD model was investigated. To clarify the exact contribution of <it>P. gingivalis</it>-induced periodontitis, non-surgical periodontal treatments were also undertaken for 3 months in 10 NAFLD patients with periodontitis.</p> <p>Results</p> <p>The detection frequency of <it>P. gingivalis </it>in NAFLD patients was significantly higher than that in the non-NAFLD control subjects (46.7% vs. 21.7%, odds ratio: 3.16). In addition, the detection frequency of <it>P. gingivalis </it>in NASH patients was markedly higher than that in the non-NAFLD subjects (52.0%, odds ratio: 3.91). Most of the <it>P. gingivalis </it>fimbria detected in the NAFLD patients was of invasive genotypes, especially type II (50.0%). Infection of type II <it>P. gingivalis </it>on NAFLD model of mice accelerated the NAFLD progression. The non-surgical periodontal treatments on NAFLD patients carried out for 3 months ameliorated the liver function parameters, such as the serum levels of AST and ALT.</p> <p>Conclusions</p> <p>Infection with high-virulence <it>P. gingivalis </it>might be an additional risk factor for the development/progression of NAFLD/NASH.</p