Seasonal Variations in Vegetation Indices derived from in situ Type Vegetation Monitoring System at typical landcovers in Japan : From the Observation Results in PGLIERC and Lake Biwa Project

研究概要:本研究では光学センサー搭載衛星データの検証及び地表面フラックスとの対応関係を調べるために簡易式の地上設置型植生モニタリングシステムを日本を代表する土地被覆上(草地,水田,アカマツ林,落葉広葉樹)に設置し,それぞれの土地被覆から得られる植生指標の季節変化について示した.その結果,以下の知見が得られた;1.草原系(草地・水田)では各植生の季節変化特性を良好にモニターすることが可能である,2.森林系(アカマツ林・落葉広葉樹)ではセンサーとキャノピーの距離が近すぎるため,思うような結果を得ることが出来なかった.3.ただし全般としては各土地被覆特性を示す連続したデータを取得することができ,システムの妥当性を示すことができた

Additional file 8: Table S5. of Male-specific association between MT-ND4 11719 A/G polymorphism and ulcerative colitis: a mitochondria-wide genetic association study

Results for nuclear SNPs with p value < 1·10−04 for interaction with rs2853495 in the subgroup of males, sorted by chromosomal positions. (DOC 78 kb

Carboxypeptidase E Modulates Intestinal Immune Homeostasis and Protects against Experimental Colitis in Mice

<div><p>Enteroendocrine cells (EEC) produce neuropeptides, which are crucially involved in the maintenance of the intestinal barrier. Hence, EEC dysfunction is suggested to be involved in the complex pathophysiology of inflammatory bowel disease (IBD), which is characterized by decreased intestinal barrier function. However, the underlying mechanisms for EEC dysfunction are not clear and suitable models for a better understanding are lacking. Here, we demonstrate that Carboxypeptidase E (CPE) is specifically expressed in EEC of the murine colon and ileum and that its deficiency is associated with reduced intestinal levels of Neuropeptide Y (NPY) and Peptide YY (PYY), which are both produced by EEC. Moreover, <i>cpe^−/−</i> mice exhibit an aggravated course of DSS-induced chronic colitis compared to wildtype littermates. In addition, we observed elevated mucosal IL-6 and KC transcript levels already at baseline conditions in <i>cpe^−/−</i> mice. Moreover, supernatants obtained from isolated intestinal crypts of <i>cpe^−/−</i> mice lead to increased IL-6 and KC expression in MODE-K cells in the presence of LPS. This effect was reversible by co-administration of recombinant NPY, suggesting a CPE mediated immunosuppressive effect in the intestines by influencing the processing of specific neuropeptides. In this context, the chemotaxis of bone marrow derived macrophages towards respective supernatants was enhanced. In conclusion, our data point to an anti-inflammatory role of CPE in the intestine by influencing local cytokine levels and thus regulating the migration of myeloid immune cells into the mucosa. These findings highlight the importance of EEC for intestinal homeostasis and propose EEC as potential therapeutic targets in IBD.</p></div

Additional file 9: of Male-specific association between MT-ND4 11719 A/G polymorphism and ulcerative colitis: a mitochondria-wide genetic association study

Data in aggregate form. (XLSX 16 kb

Proinflammatory properties of colonic crypt supernatants of CPE-deficient mice.

<p>(A) Experimental set-up for the acquirement and utilization of forskolin-stimulated supernatants of isolated colonic crypts. (B–C) Determination of KC (B) and IL-6 (C) transcript levels produced in MODE-K cells after incubation with LPS (50 ng/ml) and forskolin-stimulated supernatants of <i>cpe</i>^+/+ and <i>cpe</i>^−/− colonic crypts via RT-PCR. (D). KC transcript levels produced in MODE-K cells after incubation with forskolin-stimulated supernatants of of <i>cpe</i>^+/+ and <i>cpe</i>^−/− mice and LPS together with recombinant NPY +/− PYY (1 µM/ml). KC expression levels are expressed in percent of the Mean of <i>cpe^+/+</i>. (E–F) BMDM migration via Boyden chamber assay. Representative pictures of migrated BMDM (E) and quantification (F) of BMDM migration towards supernatants of forskolin-stimulated colonic crypts of <i>cpe</i>^+/+ and <i>cpe</i>^−/− mice. *p<0.05, **p<0.01, ***p<0.001 by t-test.</p

CPE deficiency aggravates experimental chronic colitis.

<p>(A) Calculation of the disease activity index (DAI) by determining clinical parameters of inflammation (body weight development, stool consistency, rectal bleeding) through 30 days of experimental colitis. n = 9 (<i>cpe</i>^+/+), n = 8 (<i>cpe</i>^−/−). (B-C) Determination of macroscopic colitis severity via mouse endoscopy. Representative endoluminal pictures of the distal colon on day 30 of experimental colitis (B) and calculation of the murine endoscopic index of colitis severity (MEICS) by analyzing mucosal morphology, stool consistency and shape of the vascular pattern via mouse endoscopy (C). n = 9 (<i>cpe</i>^+/+), n = 8 (<i>cpe</i>^−/−). (D–E) Determination of microscopic colitis severity via histology. Representative histological pictures of the distal colon on day 30 of experimental colitis (D) and calculation of the histology score by analyzing mucosal architecture and infiltration of immune cells (E). n = 8 per genotype. (F) Determination of expression level of TNF-α, IL-6 and KC in colonic punch biopsies by real time RT-PCR after 30 days of experimental colitis and at baseline. n = 8 per genotype. *p<0.05, **p<0.01, ***p<0.001 by t-test.</p

Laboratory values in patients without evidence of hemolytic uremic syndrome (HUS) at first presentation to health care center.

*<p>Mann-Whitney U test.</p

Specificity and sensitivity of the risk score.

<p>Specificity and sensitivity of the risk score.</p

Receiver operating characteristic (ROC) curve indicating specificity and sensitivity of the risk score (Numbers indicate score-cutoffs).

<p>Receiver operating characteristic (ROC) curve indicating specificity and sensitivity of the risk score (Numbers indicate score-cutoffs).</p

Multivariable logistic regression model analyzing risk factors for hemolytic uremic syndrome and risk score to predict development of HUS in patients with proven STEC infection (add points to get total risk score).

*<p>vs. <75 years.</p