Assessment of factors influencing the olfactory bulb volume in patients with post-viral olfactory dysfunction.

PURPOSE: To investigate the factors influencing the volume of the olfactory bulb (OB) in patients with post-viral olfactory dysfunction (PVOD). METHODS: We collected 92 olfactory bulb volumes from patients with PVOD who underwent a sinus computed tomographic and magnetic resonance imaging (MRI) scan of the head and collected clinical information including gender, age, disease course, minimal cross-sectional area, nasal airway resistance, and olfactory function. OB volume was measured in MRI and the scans were evaluated according to the Lund-Mackay (LM) scoring system. RESULTS: Male patients with PVOD had a larger OB volume (ß = 0.284, P < 0.05). OB volume was smaller in patients with a longer course of olfactory dysfunction (ß = - 0.254, P < 0.05). According to the LM scoring system, patients with a higher anterior ethmoidal sinus score had smaller OB volume (ß = - 0.476, P < 0.05). CONCLUSIONS: The study revealed that gender, disease course, and the score of anterior ethmoidal sinusitis can affect the OB volume in patients with PVOD.

Assessment of gustatory function in aging people using event-related potentials.

Gustatory dysfunctions are more frequent than other chemosensory dysfunctions in aging people. Gustatory event-related potentials (ERPs) has been suggested as a reliable and effective approach for assessing gustatory functions in young and middle subjects, but has rarely been investigated in aging people, leaving influencing factors of ERPs in that population not completely understood. In this study, we analyzed gustatory ERPs results of aging participants and characterized potential impacting factors, including age, sex, BMI, drinking, smoking, hypertension, diabetes, cognition and psychophysical test scores of gustation and olfaction. Our results revealed three components (P1, N1 and P2) in gustatory ERPs upon salty stimulation. Significant differences between responses collected from different recording electrodes were observed: minimum latencies and maximum amplitudes of P1 were detected at frontal electrode, and maximum amplitudes of N1 and P2 were detected at central and centro-parietal electrodes, respectively. Major cortical sources of components P1, N1 and P2 were located at bilateral insula, frontal operculum, and orbitofrontal cortex. Diabetes was positively associated with latencies of P1. Sex was positively associated with amplitudes of P1, N1 and P2. Hypertension was negatively associated with amplitudes of P1 and P2. In conclusion, gustatory ERPs in aging people exhibited a specific topographical distribution, represented by sex-related differences and negative impacts of diabetes and hypertension.

Genetic predisposition to lung cancer: comprehensive literature integration, meta-analysis, and multiple evidence assessment of candidate-gene association studies.

More than 1000 candidate-gene association studies on genetic susceptibility to lung cancer have been published over the last two decades but with few consensuses for the likely culprits. We conducted a comprehensive review, meta-analysis and evidence strength evaluation of published candidate-gene association studies in lung cancer up to November 1, 2015. The epidemiological credibility of cumulative evidence was assessed using the Venice criteria. A total of 1018 publications with 2910 genetic variants in 754 different genes or chromosomal loci were eligible for inclusion. Main meta-analyses were performed on 246 variants in 138 different genes. Twenty-two variants from 21 genes (APEX1 rs1130409 and rs1760944, ATM rs664677, AXIN2 rs2240308, CHRNA3 rs6495309, CHRNA5 rs16969968, CLPTM1L rs402710, CXCR2 rs1126579, CYP1A1 rs4646903, CYP2E1 rs6413432, ERCC1 rs11615, ERCC2 rs13181, FGFR4 rs351855, HYKK rs931794, MIR146A rs2910164, MIR196A2 rs11614913, OGG1 rs1052133, PON1 rs662, REV3L rs462779, SOD2 rs4880, TERT rs2736098, and TP53 rs1042522) showed significant associations with lung cancer susceptibility with strong cumulative epidemiological evidence. No significant associations with lung cancer risk were found for other 150 variants in 98 genes; however, seven variants demonstrated strong cumulative evidence. Our findings provided the most updated summary of genetic risk effects on lung cancer and would help inform future research direction.