Photoassisted selective catalytic reduction of NO with ammonia (photo-SCR) at low temperature over irradiated TiO2 in a flow reactor was confirmed to proceed efficiently and the adsorbed ammonia reacted with NO under irradiation of TiO2.

Background/Aims: Strongyloidiasis, which is caused by Strongyloides stercoralis, is one of the prevalent infections in the tropical and subtropical regions worldwide. The larvae mainly infect the small intestine and cause serious disseminated strongyloidiasis. Although upper gastrointestinal features in strongyloidiasis are well known, colonoscopic evaluation has not been established yet. The aim of this study is to clarify the characteristic findings on colonic lesions in strongyloidiasis. Method: From January 2005 to December 2009, 10 cases with strongyloidiasis underwent colonoscopy at a single center on an endemic island of Japan. The clinical and colonoscopic findings were analyzed retrospectively. Results: Six (60%) cases had an immunocompromised condition, including human T lymphotropic virus type 1 infection, corticosteroids, and chemotherapy. Hyperinfection or disseminated strongyloidiasis was not presented. Endoscopic features included yellowish-white nodules, erythema, and loss of vascular pattern, which were mainly observed in the right colon. Pathological examination revealed the filariform Strongyloides larvae and the eosinophilic infiltration of the lamina propria. Conclusion: This study demonstrates that colonoscopic observation and biopsies are very useful to diagnose strongyloidiasis. Asymptomatic cases with strongyloidiasis can have colonic involvement. Yellowish-white nodules may be a characteristic finding of colonic lesions in strongyloidiasis and can be a cautious marker to prevent fatal disseminated strongyloidiasis in endemic regions.

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common non-skin cancer worldwide. Despite improvement in therapeutic strategies, the prognosis of advanced HNSCC remains poor. The extacellular lipid mediators known as lysophosphatidic acids (LPAs) have been implicated in tumorigenesis of HNSCC. LPAs activate G-protein-coupled receptors not only in the endothelial differentiation gene (Edg) family (LPA1, LPA2, LPA3) but also in the phylogenetically distant non-Edg family (LPA4, LPA5, LPA6). The distinct roles of these receptor isoforms in HNSCC tumorigenesis have not been clarified. In the present study, we investigated the effect of ectopic expression of LPA4 in SQ-20B, an HNSCC cell line, expressing a trivial level of endogenous LPA4. LPA (18:1) stimulated proliferation of SQ-20B cells, but did not affect proliferation of HEp-2, an SCC cell line expressing higher levels of LPA4, comparable to those of with LPA1. LPA-stimulated proliferation of SQ-20B cells was attenuated by Ki16425 and Rac1 inhibitor, but not by Y-27632. Infection with doxycycline-regulatable adenovirus vector expressing green fluorescent protein-tagged LPA4 (AdvLPA4G) abolished LPA-stimulated proliferation in SQ-20B cells with the accumulation of G2/M-phasic cells. Ectopic LPA4 induction further downregulated proliferation of Ki16425-treated SQ-20B cells, of which downregulation was partially recovered by LPA. Ectopic LPA4 induction also downregulated proliferation of Rac1 inhibitor-treated SQ-20B cells, however, LPA no longer recovered it. Finally, LPA-induced cell motility was suppressed by ectopic LPA4 expression as well as by Ki16425, Rac1 inhibitor or Y-27632. Our data suggest that LPA4 signaling potentially modulates malignant behavior of SQ-20B cells. LPA signaling, which is mediated by both Edg and non-Edg receptors, may be a determinant of malignant behavior of HNSCC and could therefore be a promising therapeutic target.

Marked differences have been reported in the prevalence of glutamic acid decarboxylase (GAD) antibodies between Caucasian (63–84 %) and Japanese (30–50 %) or Asian (5–50 %) IDDM patients. Using a new immunoprecipitation assay based on 125 l‐labelled recombinant human GAD65 , we have reassessed prevalence of GAD65 antibodies in Japanese patients. We also assessed prevalence of IA‐2 antibodies. GAD65 antibodies were detected in 83.3 % of sera taken within 1 year of onset, comparable to the prevalence reported in Caucasian patients. Positivity decreased to 66.7 % after 2 to 3 years and to 54.3 % after 3 years from onset, still higher than previously reported Asian prevalence. Except in one patient, high antibody levels persisted chronically, up to 12 years. There was no difference in the prevalence of GAD65 antibodies between Japanese IDDM patients with and without autoimmune thyroid disease (AITD). IA‐2 antibodies were detected in 64.7 % of sera taken within 1 year of onset. Prevalence of IA‐2 antibodies was lower than that of GAD65 antibodies. The difference in positivity in Asian IDDM patients between present and previous reports arose from the sensitivity of our assay for GAD65 antibodies. Additionally, the patients we studied had classic IDDM with a well‐defined onset. We conclude that prevalence of GAD65 antibodies in Japanese IDDM patients is comparable to that in Western studies. There was no relationship of GAD65 antibody positivity to coexistence of AITD. Our results suggest that autoimmunity is the most significant cause of Japanese IDDM. © 1997 by John Wiley & Sons, Ltd.

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