Anti-CALCA polyclonal antibody

INTRODUCTION Early detection of diabetic retinopathy (DR) is crucial for preventing irreversible blindness. Recent studies identified some of the genetic factors involved in the pathology of DR, although their precise underlying mechanisms remain unclear. OBJECTIVES This pilot study aimed to determine genetic predictors of DR among patients with type 2 diabetes (T2D) and diabetic foot (DF) based on pathogenetic pathways. PATIENTS AND METHODS The study included 114 patients with T2D and DF (64 with DR, 50 without DR). Genetic analysis was performed for each patient and the following alterations were analyzed: rs759853 (AKR1B1), rs1800469 (TGFB1), rs2073618 and rs3134069 (TNFRSF11B), rs6330 and rs11466112 (NGF), rs1801133 (MTHFR), rs8192678 (PPARGC1A), rs1799983 (NOS3), rs1553005 (CALCA), and rs121917832 (CDKN1B). RESULTS Correlations with DR were identified for the following single nucleotide variants (SNVs): rs759853, rs2073618, and rs3134069. Carriers of the G allele of the rs759853 variant had a higher risk of DR in the dominant model (odds ratio [OR], 3.0; 95% confidence interval [CI], 1.15-7.81; P = 0.02). We analyzed 2 SNVs of the osteoprotegerin gene (rs3134069 and rs2073618), and found that the A allele of the rs3134069 variant decreased the risk of DR in both the recessive and additive models (OR, 3.33; 95% CI, 1.07-10.3; P = 0.04). Conversely, there were fewer carriers of the C allele of the rs2073618 variant in patients with DR in the dominant model (OR, 0.28; 95% CI, 0.09-0.92; P = 0.04). CONCLUSIONS The results of our study suggest that the SNVs rs759853, rs3134069, and rs2073618 may be involved in the development of DR in patients with T2D and DF.

BACKGROUND. Aberrant DNA methylation of the CpG islands for cancer-related genes is among the earliest and most frequent alterations in cancer and may be useful for diagnosing cancer or evaluating recurrent disease. METHODS. In this study, a 3-dimensional (3-D), polyacrylamide gel-based DNA microarray coupled with linker-polymerase chain reaction (PCR) was developed to detect hypermethylation of CpG islands in multiple genes from a large group of different samples. The authors determined the frequency of aberrant promoter methylation of 15 genes in 28 resected primary nonsmall cell lung cancers (NSCLCs) and in 12 corresponding nonmalignant lung tissues. RESULTS. Methylation frequencies in the tumor samples were detected in 18% of samples for the breast cancer 1 gene BRCA1, in 43% of samples for the tissue inhibitor of metalloproteinase 3 gene TIMP-3, in 38% of samples for the cyclin-dependent kinase inhibitor 4A gene p16INK4a, in 54% of samples for the cadherin 13 gene CDH13, in 50% of samples for the death-associated protein kinase gene DAPK, in 11% of samples for the E-cadherin gene ECAD, in 25% of samples for the insulin-like growth factor binding protein 7 gene IGFBP7, in 18% of samples for the Ras association domain family 1 gene RASSF1, in 68% of samples for the adenomatous polyposis coli gene APC, in 7% of samples for the cyclin-dependent kinase inhibitor gene p15, in 18% of samples for the CD44 cell adhesion molecule gene, in 29% of samples for the human Mut-L homolog gene hMLH, in 32% of samples for the human telomerase reverse transcriptase gene hTERT, in 64% of samples for the calcitonin gene-related polypeptide 0. gene CALCA, and in 54% of samples for the estrogen receptor gene ER; however, methylation was not observed in the majority of corresponding nonmalignant tissues. Six samples in from 28 tumors had > 6 genes methylated, and 1 sample had 13 genes methylated. Methylation of these genes was correlated with some clinicopathologic patient characteristics. CONCLUSIONS. This study demonstrated that a 3-D microarray could be used to detect DNA hypermethylation and provided a high-throughput platform for DNA hypermethylation analysis.