Vitamin A Inhibits Development of Dextran Sulfate Sodium-Induced Colitis and Colon Cancer in a Mouse Model.

Vitamin A is essential to mucosal immunity and cell differentiation. The fact that lack of it might involve chronic inflammation and increased risk of cancer has been reported. Little is known about the mechanism of vitamin A deficiency in the development of colitis and its influence on development of colorectal cancer. To determine the influence of vitamin A deficiency on colitis and colorectal cancer development, an experimental study using a colitis mouse model was performed. Dextran sulfate sodium (DSS) colitis was induced in vitamin A-deficient and vitamin A-supplemented mice. Further, colorectal carcinoma was induced by a combination of azoxymethane preinjection and DSS colitis. Results were compared between the two groups mainly by immunohistochemical analysis. Colitis was more severe and recovery from colitis was slower in vitamin A-deficient mice than in vitamin A-supplemented mice. Compared with vitamin A-supplemented mice, vitamin A-deficient mice had decreases in colonic subepithelial myofibroblasts and the ratio of mucosal IgA(+)/IgG(+) cells, increases in CD11c(+) dendritic cells, and a higher rate of development of colorectal carcinoma with colitis following azoxymethane. Vitamin A lipid droplets in subepithelial myofibroblasts were decreased in vitamin A-deficient mice, suggesting alterations in colonic crypt niche function. Thus, vitamin A inhibited colitis and the development of colorectal cancer.

Silicone intraocular lens surface calcification in a patient with asteroid hyalosis.

PURPOSE: To confirm a substance presence on the posterior intraocular lens (IOL) surface in a patient with asteroid hyalosis. METHODS: An 80-year-old man had IOLs for approximately 12 years. Opacities and neodymium-doped yttrium aluminum garnet pits were observed on the posterior surface of the right IOL. Asteroid hyalosis and an epiretinal membrane were observed OD. An IOL exchange was performed on 24 March 2008, and the explanted IOL was analyzed using a light microscope and a transmission electron microscope with a scanning electron micrograph and an energy-dispersive X-ray spectrometer for elemental analysis. To confirm asteroid hyalosis, asteroid bodies were examined with the ionic liquid (EtMeIm+ BF4-) method using a field emission scanning electron microscope (FE-SEM) with digital beam control RGB mapping. RESULTS: X-ray spectrometry of the deposits revealed high calcium and phosphorus peaks. Spectrometry revealed that the posterior IOL surface opacity was due to a calcium-phosphorus compound. Examination of the asteroid bodies using FE-SEM with digital beam control RGB mapping confirmed calcium and phosphorus as the main components. CONCLUSIONS: Calcium hydrogen phosphate dihydrate deposits were probably responsible for the posterior IOL surface opacity. Furthermore, analysis of the asteroid bodies demonstrated that calcium and phosphorus were its main components.

Identification of a chromosomal breakpoint and detection of a novel form of an MLL-AF17 fusion transcript in acute monocytic leukemia with t(11;17)(q23;q21).

More than 40 genes have been reported as translocation partners of the mixed lineage leukemia gene (MLL) in hematologic malignancies. AF17 was identified earlier than most other MLL translocation partners. On the other hand, there is only 1 report of an MLL-AF17 fusion transcript in acute myeloid leukemia (AML). Here we describe a 40-year-old man with a diagnosis of AML involving t(11;17)(q23;q21). We identified a chromosomal breakpoint for t(11;17)(q23;q21) at MLL intron 6 and AF17 intron 8. Although the previously reported form of the MLL-AF17 fusion transcript was not detected by reverse transcriptase-polymerase chain reaction (PCR) analysis, a novel form of an MLL-AF17 fusion transcript joining MLL exon 6 to AF17 exon 9 was detected by complementary DNA panhandle PCR. The fact that 2 forms of MLL-AF17 retain the leucine zipper domain of AF17 suggests that the dimerization domain of AF17 is critical for leukemogenesis by the MLL-AF17 fusion gene.