Redox control in arsenic accumulation with organic matter derived from a varved lacustrine deposit in the Jurassic accretionary complexes.

Oxidation states and distribution of arsenic (As) in annually laminated (varved) lacustrine deposits were analyzed with a seasonal resolution. This deposit was formed in the mid-Holocene landslide-dammed paleolake in the upper reaches of the Ane River, central Japan and the paleolake watershed consists of the Jurassic accretionary complexes (Mino-Tamba belt) including sedimentary and igneous rocks. In the outcrop, centimeter-to-decimeter-scale silty clay layers alternating with laminated layers are well developed.

CC-chemokine ligand 17 gene therapy induces tumor regression through augmentation of tumor-infiltrating immune cells in a murine model of preexisting CT26 colon carcinoma.

Chemokines, which regulate leukocyte trafficking and infiltration of local sites, are attractive candidates for improving the efficacy of cancer immunotherapy by enhancing the accumulation of immune cells in tumor tissue. Herein, we evaluated the antitumor effects of intratumoral injection of RGD fiber-mutant adenoviral vectors (AdRGDs) encoding the chemokines CCL17, CCL19, CCL20, CCL21, CCL22, CCL27, XCL1 or CX3CL1 in a murine model of preexisting CT26 colon carcinoma. Among these 8 chemokine-expressing AdRGDs, injection of AdRGD-CCL17 most effectively induced tumor regression and generated specific immunity in rechallenge experiments.

Anti-tumor activity of chemokine is affected by both kinds of tumors and the activation state of the host's immune system: implications for chemokine-based cancer immunotherapy.

In this study, we screened the anti-tumor activity of murine chemokines including CCL17, CCL19, CCL20, CCL21, CCL22, CCL27, XCL1, and CX3CL1 by inoculating murine B16BL6, CT26, or OV-HM tumor cells, all of which were transfected with chemokine-expressing fiber-mutant adenovirus vector, into immunocompetent mice. A tumor-suppressive effect was observed in mice inoculated with CCL19/B16BL6 and XCL1/B16BL6, and CCL22/OV-HM showed considerable retardation in tumor growth. In the cured mice inoculated with CCL22/OV-HM, a long-term specific immune protection against parental tumor was developed.