Sphingosine 1-Phosphate Receptor 1 (S1P1) plays a critical role in lymphocyte recirculation and is a clinical target for treatment of multiple sclerosis. By generating a short-duration S1P1 agonist and mice where fluorescently tagged S1P1 replaces wild-type receptor, we elucidate physiological and agonist-perturbed changes in expression of S1P1 at a subcellular level in vivo. We demonstrate differential downregulation of S1P1 on lymphocytes and endothelia following agonist treatment.

Using a mixture of cetyltrimethylammonium bromide and carboxylate anionic surfactant (C n H2 n +1COONa, n = 11, 13, 15, 17) as templates, siliceous MCM-48 is synthesized with low molar ratio (0.168:1) of mixed surfactants to silica and low concentration (5 wt %) of mixed surfactants.

The epithelial-mesenchymal transition (EMT) induced by EGF promotes cervical cancer progression; however, the mechanisms underlying the EGF-induced EMT remain unclear. In this study, we reported that miR155 overexpression suppressed EGF-induced EMT, decreased migration/invasion capacities, inhibited cell proliferation and increased the chemo-sensitivity to DDP in human Caski cervical cancer cells. Further, the overexpression of miR155 increased TP53 expression but reduced SMAD2, and CCND1 expression levels. These data suggest that miR155 negatively regulates EGF-induced EMT. We conclude that miR155 does not act as an oncogene but as a tumour suppressor in Caski cells.

ObjectivesThis investigation was undertaken in response to an outbreak of suspected shellfish poisoning in Zhejiang Province, China. The objectives of this project were to confirm the outbreak and to identify the aetiology, source and mode of transmission.MethodsA probable case was defined as an individual with diarrhea (≥3 times/day) plus at least one of the following symptoms: fever (≥37.5°C), vomiting, or abdominal pain after consuming seafood between May 23rd and May 28th, 2011. Using a case-control study design, we compared exposures to suspected seafood items and cooking methods between 61 probable cases and 61 controls.ResultsOver 220 suspected or probable cases of diarrhetic shellfish poisoning (DSP) were identified (incidence of 18 cases per 100,000). The case control study revealed that 100% of cases and 18% of controls had eaten mussels during the exposure period (OR = ∞, χ2 = 84.72,P = 0.000). The number of mussels consumed was related to DSP risk (P = 0.004, χ2 test for trend). Consumption of other seafood items was not associated with disease. The frequency of diarrhea and vomiting were positively correlated with the number of mussels consumed (r = 0.424 and r = 0.562, respectively). The frequency of vomiting and the incubation period were significantly correlated with the total time the mussels were boiled (r = 0.594 and r = −0.336, respectively). Mussels from 3 food markets and one family contained Okadaic acid (OA) and Dinophysistoxin-1 (DTX-1).ConclusionsThis outbreak was attributed to the consumption of mussels contaminated by DSP-toxins (OA and DTX-1) which are produced by different species of dinoflagellates (toxic microalgae) from the genus Dinophysis or Prorocentrum. Suspension of mussel sales and early public announcements were highly effective in controlling the outbreak, although oversight of seafood quality should be a priority to prevent future contamination and outbreaks.

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