O poema//processo de Wlademir Dias-Pino: entre escritura e visualidade

O presente artigo apresenta o movimento do poema//processo, criado pelo poeta mato-grossense Wlademir Dias-Pino em 1967, que envolveu uma série de poetas e artistas e marcou uma passagem importante na história das vanguardas da literatura e da arte brasileiras. A partir dos principais conceitos do movimento, trataremos das imbricações entre poesia e artes visuais utilizando três abordagens inter-relacionadas na poesia de Dias-Pino: a separação entre as ideias de estrutura e de processo; a separação entre as ideias de língua e de linguagem; e a recusa radical à escrita alfabética. Também serão marcados os aspectos que aproximam e que separam o poema//processo da chamada poesia visual e da Poesia Concreta de Haroldo e Augusto de Campos e de Décio Pignatari

Correlation of DNA methylation of DNMT3A and TET2 with oral squamous cell carcinoma

Abstract Oral squamous cell carcinoma (OSCC) is the sixth most common malignancy worldwide. Abnormal epigenetic modifications, including DNA methylation, are hallmarks of cancer and implicated in the development of various tumors. DNA methylation is catalyzed by the DNA methyltransferase and ten-eleven translocation dioxygenase families, with DNMT3A and TET2 being the most widely studied members, respectively. The correlation of methylation β values and clinical features was conducted in patients with OSCC in The Cancer Genome Atlas database. DNA methylation and protein expression levels of DNMT3A and TET2 in tissues were analyzed with methylation-specific polymerase chain reaction (MSP) and western blotting. To evaluate the effects of DNMT3A and TET2 on the biological characteristics of OSCC, cell proliferation was assessed with 5-ethynyl-2'-deoxyuridine, and cell migration capacity was quantified with wound healing and transwell assays. A survival analysis was performed with the Kaplan–Meier approach. The correlation between different methylation β values and clinical features was revealed. MSP revealed varying methylation degrees of DNMT3A and TET2 in OSCC tissues. Furthermore, western blotting showed that the protein expression levels were significantly different in cancer and surrounding healthy tissue samples. In vitro experiments demonstrated that DNMT3A knockdown and TET2 overexpression could inhibit the proliferation and migration of OSCC. Survival analysis revealed that patients with high DNMT3A methylation levels showed higher survival rates

Human Umbilical Cord Mesenchymal Stem Cells Suppress Systemic Lupus Erythematosus Lesions by Rebalancing CD4+/CD8+ Cell Population

Despite considerable advances in the treatment for systemic lupus erythematosus (SLE), there is still an unmet need to develop novel therapeutic approaches with improved efficacy and lower side effects. Here we explore human umbilical cord-derived mesenchymal stem cells (hUCMSCs) as a promising treatment for SLE induced by concanavalin A-activated spleno-lymphocyte in BALB/c mice. The isolated hUCMSCs,&nbsp; carrying specific MSC cell surface markers (CD105, CD73 and CD90), exhibited the potential to&nbsp; differentiate into osteogenic and adipogenic lineages. In mice with SLE, transplantation of hUCMSCs&nbsp; improved disease symptoms by decreasing the levels of serum autoantibody (antidsDNA and anti- nuclear) and cytokines (TNF-α and IFN-γ). The cell therapy significantly alleviated renal lesions by&nbsp; lowering serum urea nitrogen, creatine and uric acid, and increasing albumin. Using immunohistochemical staining, we found that that hUCMSCs decreased endocapillary hypercellularity, glomerular degeneration,&nbsp; and complement C3 immune complex deposition in the kidney. Mechanically, the therapy with hUCMSCs&nbsp; decreased CD4+/CD8+ cell ratio in animals. These data suggest that hUCMSCs may modulate&nbsp;&nbsp; autoimmunity in SLE mice by rebalancing CD4+/CD8+ cell population. Transplantation of hUCMSCs may&nbsp; be explored as a promising alternative approach in the treatmentof human lupus.</p

Genetic damage and potential mechanism exploration under different air pollution patterns by multi-omics

Ambient air pollution was classified as carcinogenic to humans (Group 1) for lung cancer. DNA damage was an important first step in the process of carcinogenesis, and could also be induced by air pollution. In this study, intratracheal instillation and real-time air exposure system were combined to establish SHP (short-term high-level PM2.5) and LLPO (long-term low-level PM2.5 and O3) exposure patterns, respectively. Hierarchical levels of genetic biomarkers were analyzed to explore DNA damage effects in rats. Representative DNA repair genes from different repair pathways were selected to explore the relative expression levels. The methylation level of differentially expressed repair genes were also determined. Besides, miRNA sequencing and non-targeted metabolomic analysis were performed in rat lungs. KEGG and multi-omics analysis were used to explore the potential mechanism of genetic damage under different air pollution patterns. We found that LLPO exposure induced DSBs and chromosome damage. SHP exposure could induce DSBs and DNA oxidative damage, and the effects of genetic damage under this pollution pattern could be repaired by natural repair. Repair genes involved in two pattern were different. SHP exposure could induce higher methylation levels of RAD51, which might be a potential epigenetic mechanism for high-level PM2.5 induced down-regulated expression of RAD51 and DSBs. Besides, 29 overlapped alterations in metabolic pathways were identified by metabolomic and miRNA sequencing, including purine metabolism and pyrimidine metabolism after LLPO exposure. Differential miRNAs expression in lung tissue were associated with apoptosis, DNA damage and damage repair. We concluded that under different air pollution patterns, DNA damage biomarkers and activated targets of DNA damage repair network were both different. The genetic damage effects caused by high-level short-term PM2.5 can be alleviated by natural repair. We provided possible mechanisms by multi-omics which could explain the increased carcinogenic risk caused by air pollution