胃黄斑瘤的研究进展

胃黄斑瘤常被认为是胃部的良性病变,是组织细胞或巨噬细胞吞噬大量脂质后堆积在固有层而形成的.然而,最近研究发现胃黄斑瘤可能与胃部的癌前病变和胃癌相关,内镜下需与胃印戒细胞癌和胃透明细胞癌加以鉴别.

Effects of Elevated CO_2 on Growth, Carbon Assimilation, Photosynthate Accumulation and Related Enzymes in Rice Leaves during Sink-Source Transition

To study the effects of growing rice （Oryza sativa L.） leaves under the treatment of the short-term elevated CO2 during the period of sink-source transition, several physiological processes such as dynamic changes in photosynthesis, photosynthate accumulation, enzyme activities （sucrose phosphate synthase （SPS）, and sucrose synthase （SS））, and their specific gene （spsl and RSusl） expressions in both mature and developing leaf were measured. Rice seedlings with fully expanded sixth leaf （marked as the source leaf, L6） were kept in elevated （700 μmol/mol） and ambient （350 mol/L） CO2 until the 7th leaf （marked as the sink leaf, L7） fully expanded. The results demonstrated that elevated CO2 significantly increased the rate of leaf elongation and biomass accumulation of L7 during the treatment without affecting the growth of L6. However, in both developing and mature leaves, net photosynthetic assimilation rate （A）, all kinds of photosynthate contents such as starch, sucrose and hexose, activities of SPS and SS and transcript levels of spsl and RSusl were significantly increased under elevated CO2 condition. Results suggested that the elevated CO2 had facilitated photosynthate assimilation, and increased photosynthate supplies from the source leaf to the sink leaf, which accelerated the growth and sink-source transition in new developing sink leaves. The mechanisms of SPS regulation by the elevated CO2 was also discussed.

Targeting GATA1 and p2x7r Locus Binding in Spinal Astrocytes Suppresses Chronic Visceral Pain by Promoting DNA Demethylation

Irritable bowel syndrome is a gastrointestinal disorder of unknown etiology characterized by widespread,chronic abdominal pain associated with altered bowel movements.Increasing amounts of evidence indicate that injury and inflammation during the neonatal period have long-term effects on tissue structure and function in the adult that may predispose to gastrointestinal diseases.In this study we aimed to investigate how the epigenetic regulation of DNA demethylation of the p2x7r locus guided by the transcription factor GATA binding protein 1(GATA1)in spinal astrocytes affects chronic visceral pain in adult rats with neonatal colonic inflammation(NCI).The spinal GATA1 targeting to DNA demethylation of p2x7r locus in these rats was assessed by assessing GATA1 function with luciferase assay,chromatin immunoprecipitation,patch clamp,and interference in vitro and in vivo.In addition,a decoy oligodeoxynucleotide was designed and applied to determine the influence of GATA1 on the DNA methylation of a p2x7r CpG island.We showed that NCI caused the induction of GATA1,Ten-eleven translocation 3(TET3),and purinergic receptors(P2X7Rs)in astrocytes of the spinal dorsal horn,and demonstrated that inhibiting these molecules markedly increased the pain threshold,inhibited the activation of astrocytes,and decreased the spinal sEPSC frequency.NCI also markedly demethylated the p2x7r locus in a manner dependent on the enhancement of both a GATA1–TET3 physical interaction and GATA1 binding at the p2x7r promoter.Importantly,we showed that demethylation of the p2x7r locus(and the attendant increase in P2X7R expression)was reversed upon knockdown of GATA1 or TET3 expression,and demonstrated that a decoy oligodeoxynucleotide that selectively blocked the GATA1 binding site increased the methylation of a CpG island in the p2x7r promoter.These results demonstrate that chronic visceral pain is mediated synergistically by GATA1 and TET3 via a DNA-demethylation mechanism that controls p2x7r transcription in spinal dorsal horn astrocytes,and provide a potential therapeutic strategy by targeting GATA1 and p2x7r locus binding.