ABSTRACT
Purpose: This study aimed to assess and compare the changes in peripapillary retinal nerve fiber layer (RNFL) thickness in nondiabetics and diabetics with various stages of diabetic retinopathy (DR). Methods: The study subjects were divided into four groups based on their diabetic status and findings, namely, controls (normal subjects without diabetes [NDM]), diabetics without retinopathy (NDR), nonproliferative DR (NPDR), and proliferative DR (PDR). Peripapillary RNFL thickness was assessed using optical coherence tomography. One?way analysis of variance (ANOVA) with the post?Tukey HSD test was done to compare RNFL thickness in different groups. The Pearson coefficient was used to determine the correlation. Results: There was statistically significant difference in measured average RNFL (F = 14.8000, P < 0.05), superior RNFL (F = 11.7768, P < 0.05), inferior RNFL (F = 12.9639, P < 0.05), nasal RNFL (F = 12.2134, P < 0.05), and temporal RNFL (F = 4.2668, P < 0.05) across the different study groups. Pairwise comparison showed that there was a statistically significant difference in RNFL measured (average and all quadrants) in patients with DR (NPDR and PDR) and the NDM control group (P < 0.05). In diabetics without retinopathy, the RNFL measured was reduced compared to controls, but it was statistically significant only in the superior quadrant (P < 0.05). Average RNFL and RNFL in all quadrants showed a small negative correlation with the severity of DR and it was statistically significant (P < 0.001). Conclusion: In our study, peripapillary RNFL thickness was reduced in diabetic retinopathy compared to normal controls and the thinning increased with the severity of DR. This was evident in the superior quadrant even before the fundus signs of DR set in
ABSTRACT
Background: The coexistence of obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) is termed “Overlap syndrome (OS).” Objectives: The present study aimed at estimating the prevalence of OS among patients diagnosed with OSA. Methods: It was a prospective observational study conducted on patients presenting to respiratory medicine outpatient department (sleep clinic) with symptoms of sleep-disordered breathing and was found to have OSA by overnight polysomnography. These patients were then subjected to spirometry to diagnose COPD. Results: The prevalence of OS in the study population was found to be 41.3%. Excessive daytime sleepiness was found to be higher in overlap group patients (P = 0.033), the difference was statistically significant. The mean age (59.9 ± 9.6 years) was found to be high in the OS group compared to those without the same. The mean forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and FEV1/FVC (pre? and postbronchodilator) spirometry parameters were found to be lower in patients with OS. Conclusion: The study showed that the prevalence of OS in the present study was 41.3%. Excessive daytime sleepiness and age >60 years were risk factors for OS in a patient with OSA. OS patients had lower pulmonary function values.
ABSTRACT
A new hallmark of cancer involves acquisition of a lipogenic phenotype which promotes tumorigenesis. Little is known about lipid metabolism in melanomas. Therefore, we used BRB (Biometrics Research Branch) class comparison tool with multivariate analysis to identify differentially expressed genes in human cutaneous melanomas, compared with benign nevi and normal skin derived from the microarray dataset (GDS1375). The methods were validated by identifying known melanoma biomarkers (CITED1, FGFR2, PTPRF, LICAM, SPP1 and PHACTR1) in our results. Eighteen genes regulating metabolism of fatty acids, lipid second messengers and gangliosides were 2-9 fold upregulated in melanomas of GDS-1375. Out of the 18 genes, 13 were confirmed by KEGG pathway analysis and 10 were also significantly upregulated in human melanoma cell lines of NCI-60 Cell Miner database. Results showed that melanomas upregulated PPARGC1A transcription factor and its target genes regulating synthesis of fatty acids (SCD) and complex lipids (FABP3 and ACSL3). Melanoma also upregulated genes which prevented lipotoxicity (CPT2 and ACOT7) and regulated lipid second messengers, such as phosphatidic acid (AGPAT-4, PLD3) and inositol triphosphate (ITPKB, ITPR3). Genes for synthesis of pro-tumorigenic GM3 and GD3 gangliosides (UGCG, HEXA, ST3GAL5 and ST8SIA1) were also upregulated in melanoma. Overall, the microarray analysis of GDS-1375 dataset indicated that melanomas can become lipogenic by upregulating genes, leading to increase in fatty acid metabolism, metabolism of specific lipid second messengers, and ganglioside synthesis.