extracted with EDTA) to total primary production (TPP) were rneasured using "C-tracer to estirnate the ratio for each fraction of organic carbon photosynthetically produced by microphytobenthos and phytoplankton. TEOC for rn.icrophytobenthos ranged frorn 4 2 to 73% of TPP and was rnade up mostly of 14C-Colloidal-OC The TEOC/TPP for phytoplankton ranged frorn 1.5 to 220,). The ratio of I4C-EPS to I4C-CoUoidal-OC for rnicrophytobenthos was 41 to 53%, and for phytoplankton was 4.4 to 24%. Algal species in the transitional phase were used for experiments because microphytobenthos Nitzschia hybridaeformis most abundantly produced TEOC and EPS in the transitional phase during growth in experirnents studying the effect of the growth phase. By using EDTA for the extraction of extraceUular organic matter, it beComes clear that excretion of colloidal organic matter by rnicrophytobenthos has always been underestimated. These results suggest that the large arnount of TEOC containing EPS produced by microphytobenthos plays a more mportant role than secretion of phytoplankton as a source of organic carbon for heterotrophic organisms in the intertidal-flat ecosystem.

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Whole Fusobacterium species, but not F. nucleatum, are common in UC patients and have a role in persistence of colonic inflammation in UC. However, Fusobacterium infection is associated with rather mild clinical phenotypes of UC.

Background. Gastric cancer is discovered even after successful eradication of H. pylori. We investigated clinic pathological features of early gastric cancers after H. pylori eradication. Methods. 51 early gastric cancers (EGCs) from 44 patients diagnosed after successful H. pylori eradication were included as eradication group. The clinic-pathological features were compared with that of 131 EGCs from 120 patients who did not have a history of H. pylori eradication (control group). Results. Compared with control group, clinic-pathological features of eradication group were characterized as depressed (p < 0.0001), reddish (p = 0.0001), and smaller (p = 0.0095) lesions, which was also confirmed in the comparison of six metachronous lesions diagnosed after initial ESD and subsequent successful H. pylori eradication. Prevalence of both SM2 (submucosal invasion greater than 500 μm) and unexpected SM2 cases tended to be higher in eradication group (p = 0.077, 0.0867, resp.). Prevalence of inconclusive diagnosis of gastric cancer during pretreatment biopsy was also higher in the same group (26.0% versus 1.6%, p < 0.0001). Conclusions. Informative clinic pathological features of EGC after H. pylori eradication are depressed, reddish appearances, which should be treated as a caution because histological diagnosis of cancerous tissue is sometimes difficult by endoscopic biopsy.

On 11 March 2011, a massive tsunami generated by a mega‐earthquake with a moment magnitude of 9.0 hit a wide area of Pacific coast of northeast Japan. We observed and analyzed the effects of the earthquake and tsunami event on populations of the abalone Haliotis discus hannai and sea urchin Strongylocentrotus nudus at Tomarihama in Miyagi, where we have carried out regular surveys since January 2008. Before the event, algal forests dominated by the brown macroalga Eisenia bicyclis had developed in the survey area shallower than 5 m in depth, where adult abalone >50 mm in shell length (SL) inhabited. Juvenile abalone <20 mm SL and juvenile and adult urchins inhabited the deeper area dominated by crustose coralline algae (CCA). After the event, although no apparent decrease was observed in the brown macroalgal population, the mean density of adult abalone >50 mm SL, mainly inhabiting the algal forests, was reduced by more than half. The impact of the tsunami was more profound in the CCA area than in the macroalgal forest. Juvenile abalone and urchins largely decreased to 14 and 5% of the densities just before the event, respectively. The distribution pattern of juvenile abalone and urchins could be a cause of the marked decrease, because most of these animals inhabited the CCA area where the disturbance by the massive water movement was not reduced by the effects of the macroalgal forest.

Background and aimTP53 gene is frequently mutated in gastric cancer (GC), but the relationship with clinicopathological features and prognosis is conflicting. Here, we screened TP53 mutation spectrum of 214 GC patients in relation to their clinicopathological features and prognosis.ResultsTP53 nonsilent mutations were detected in 80 cases (37.4%), being frequently occurred as C:G to T:A single nucleotide transitions at 5′-CpG-3′ sites. TP53 mutations occurred more frequently in differentiated histologic type than in undifferentiated type in the early stage (48.6% vs. 7%, P=0.0006), while the mutations correlated with venous invasion among advanced stage (47.7% vs. 20.7%, P=0.04). Subset of GC with TP53 hot spot mutations (R175, G245, R248, R273, R282) presented significantly worse overall survival and recurrence free survival compared to others (both P=0.001).MethodsMatched biopsies from GC and adjacent tissues from 214 patients were used for the experiment. All coding regions of TP53 gene (exon2 to exon11) were examined using Sanger sequencing.ConclusionOur data suggest that GC with TP53 mutations seems to develop as differentiated histologic type and show aggressive biological behavior such as venous invasion. Moreover, our data emphasizes the importance of discriminating TP53 hot spot mutations (R175, G245, R248, R273, R282) to predict worse overall survival and recurrence free survival of GC patients.

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BackgroundTelomere length shortening in Helicobacter pylori (H. pylori) infected gastric mucosa constitutes the earliest steps toward neoplastic transformation. In addition to this genotoxic changes, epigenetic changes such as promoter CpG island (PCGI) methylation are frequently occurred in H. pylori infected gastric mucosa. The aim of this study was to investigate a potential link between H. pylori related PCGI methylation and telomere length shortening in the human gastric mucosa.MethodsTelomere length was measured in non-neoplastic gastric mucosa from 106 cancer-free subjects. To identify H. pylori related PCGI methylation, bisulfite pyrosequencing was used to quantify the methylation of 49 PCGIs from 47 genes and LINE1 repetitive elementResultsWe identified five PCGIs (IGF2, SLC16A12, SOX11, P2RX7 and MYOD1), which the methylation is closely associated with H. pylori infection. Hypermethylation of all these PCGIs was associated with development of pathological state from normal to mild, active, and atrophic gastritis (P<0.001) and lower pepsinogen I/II ratio (P<0.05), an indicator for gastric mucosal atrophy. Telomere shortening was significantly associated with mean Z score methylation of five PCGIs (R=−0.39, P<0.0001) and four of these locus (IGF2: R=−0.35, P=0.0003, SLC16A12: R=−0.35, P=0.0002, P2RX7: R=−0.29, P=0.003, and MYOD1: R=−0.33, P=0.0005). Multivariate analysis revealed that telomere shortening held an increased risk for hypermethylation (odds ratio: 1.71, 95% confidence interval: 1.11-2.63, P=0.016).ConclusionPotential link between H. pylori related PCGI methylation and telomere shortening emphasize the importance of genotoxic-epigenetic interaction in the pathological state of H. pylori infected gastric mucosa.