Nasal Masses: A Report of Two Rare Cases, from Benign to Malignant.

Medical practitioners in peripheral remote areas face challenges in treating patients, that are much different from those who are working in an institute or accessible regions. We are discussing two cases, which were clinically diagnosed at our centre and were biopsy proven at a tertiary care institute. First case is of a benign adnexal neoplasm while the second is dreaded midline granuloma. Both the patients received satisfactory consultation and management.

Acquired resistance to oxaliplatin is not directly associated with increased resistance to DNA damage in SK-N-ASrOXALI4000, a newly established oxaliplatin-resistant sub-line of the neuroblastoma cell line SK-N-AS.

The formation of acquired drug resistance is a major reason for the failure of anti-cancer therapies after initial response. Here, we introduce a novel model of acquired oxaliplatin resistance, a sub-line of the non-MYCN-amplified neuroblastoma cell line SK-N-AS that was adapted to growth in the presence of 4000 ng/mL oxaliplatin (SK-N-ASrOXALI4000). SK-N-ASrOXALI4000 cells displayed enhanced chromosomal aberrations compared to SK-N-AS, as indicated by 24-chromosome fluorescence in situ hybridisation. Moreover, SK-N-ASrOXALI4000 cells were resistant not only to oxaliplatin but also to the two other commonly used anti-cancer platinum agents cisplatin and carboplatin. SK-N-ASrOXALI4000 cells exhibited a stable resistance phenotype that was not affected by culturing the cells for 10 weeks in the absence of oxaliplatin. Interestingly, SK-N-ASrOXALI4000 cells showed no cross resistance to gemcitabine and increased sensitivity to doxorubicin and UVC radiation, alternative treatments that like platinum drugs target DNA integrity. Notably, UVC-induced DNA damage is thought to be predominantly repaired by nucleotide excision repair and nucleotide excision repair has been described as the main oxaliplatin-induced DNA damage repair system. SK-N-ASrOXALI4000 cells were also more sensitive to lysis by influenza A virus, a candidate for oncolytic therapy, than SK-N-AS cells. In conclusion, we introduce a novel oxaliplatin resistance model. The oxaliplatin resistance mechanisms in SK-N-ASrOXALI4000 cells appear to be complex and not to directly depend on enhanced DNA repair capacity. Models of oxaliplatin resistance are of particular relevance since research on platinum drugs has so far predominantly focused on cisplatin and carboplatin.

Evaluation of glycated albumin and microalbuminuria as early risk markers of nephropathy in type 2 diabetes mellitus.

INTRODUCTION: Since Glycated Albumin (GA) reflects short term variations and glycated protein shows degrees of hyperglycaemia, the objective of this study was to find GA and microalbuminuria as a early risk markers along with the duration of Uncontrolled Diabetes Mellitus in type 2 diabetic nephropathy. MATERIAL AND METHODS: The present cross-sectional study included randomly selected Uncontrolled Type 2DM (n = 75), controlled Type 2DM (n = 75) and healthy controls (n = 75). Their fasting venous blood samples were obtained for GA and serum creatinine, while their morning urine samples were obtained for detection of microalbuminuria. Statistical analysis was done by using SPSS, version 16.0. One-Way ANOVA was performed. All p-values which were ≤ 0.05 were considered as statistically significant. RESULTS: The mean GA, microalbuminuria and serum creatinine were the highest in Uncontrolled DM as compared to those in Controlled DM respectively. Microalbuminuria and GA had a significant correlation with the duration of diabetes (p<0.0001). CONCLUSION: The present study identified that the risk of microalbuminuria increased with a poor glycaemic control. A persistent increase in GA and microalbuminuria may be considered as risk markers in diabetic nephropathy. Therefore, a regular screening for microalbuminuria and estimation of GA can help in the clinical management, to prevent complications.