Road Rage Menace: A Cross-sectional Study to Assess Driver Anger Level in Public Motor Vehicle Drivers in a City in Central India

Introduction: Road rage and aggressive driving is a prevalent condition in today’s society due to motorists’ frustrations during heavy traffic volumes. Objective: This study was done to assess the level of anger amongst the drivers of public transport vehicles in Indore, using Driving Anger Scale (DAS by Deffenbacher et. al.) and various factors affecting it. Material and Methods: A cross-sectional study was conducted among 135 drivers of Public transport vehicle drivers (Star bus, City-van and star cab drivers) in Indore to assess their anger level using Driving Anger Scale. The participants were required to record the amount of anger they would experience in response to each item in the scale (1=not at all angry, 2=a little angry, 3=some anger, 4=much anger, 5=very much angry). Results: The mean DAS score in Indore was found to be 3.013 and in the three organizations namely Star bus drivers, City van drivers and Star cab drivers was 2.92, 3.08 and 3.04 respectively. The DAS score of drivers with respect to the 6 sub-scales were: hostile gestures (Star bus -3.42,City van -3.67,Star cab -3.38), slow driving (Star bus -2.73,City van driv-2.78,Star cab-3.17), traffic obstructions (Star bus-2.85,City van -3.25,Star cab-3.18), discourtesy (Star bus -3.23,City van-3.33,Star cab -3.25)and police presence (Star bus -2.15,City van -1.99,Star cab -2.78), illegal driving (Star bus -3.04,City van -3.14,Star cab -2.89). The DAS scores of the drivers did not vary significantly with age group, experience, and educational qualification. Conclusion: Though DAS scores did not vary between the three groups of drivers, however average level anger for various given circumstances commonly found in the Indian traffic scenario was on the higher side

Activation of Anthocyanin Biosynthesis in Gerbera hybrida (Asteraceae) Suggests Conserved Protein-Protein and Protein-Promoter Interactions between the Anciently Diverged Monocots and Eudicots

We have identified an R2R3-type MYB factor, GMYB10, from Gerbera hybrida (Asteraceae) that shares high sequence homology to and is phylogenetically grouped together with the previously characterized regulators of anthocyanin pigmentation in petunia (Petunia hybrida) and Arabidopsis. GMYB10 is able to induce anthocyanin pigmentation in transgenic tobacco (Nicotiana tabacum), especially in vegetative parts and anthers. In G. hybrida, GMYB10 is involved in activation of anthocyanin biosynthesis in leaves, floral stems, and flowers. In flowers, its expression is restricted to petal epidermal cell layers in correlation with the anthocyanin accumulation pattern. We have shown, using yeast (Saccharomyces cerevisiae) two-hybrid assay, that GMYB10 interacts with the previously isolated bHLH factor GMYC1. Particle bombardment analysis was used to show that GMYB10 is required for activation of a late anthocyanin biosynthetic gene promoter, PGDFR2. cis-Analysis of the target PGDFR2 revealed a sequence element with a key role in activation by GMYB10/GMYC1. This element shares high homology with the anthocyanin regulatory elements characterized in maize (Zea mays) anthocyanin promoters, suggesting that the regulatory mechanisms involved in activation of anthocyanin biosynthesis have been conserved for over 125 million years not only at the level of transcriptional regulators but also at the level of the biosynthetic gene promoters

The Crohn's disease risk factor IRGM limits NLRP3 inflammasome activation by impeding its assembly and by mediating its selective autophagy

Several large-scale genome-wide association studies genetically linked IRGM to Crohn’s disease and other inflammatory disorders in which the IRGM appears to have a protective function. However, the mechanism by which IRGM accomplishes this anti-inflammatory role remains unclear. Here, we reveal that IRGM/Irgm1 is a negative regulator of the NLRP3 inflammasome activation. We show that IRGM expression, which is increased by PAMPs, DAMPs, and microbes, can suppress the pro-inflammatory responses provoked by the same stimuli. IRGM/Irgm1 negatively regulates IL-1β maturation by suppressing the activation of the NLRP3 inflammasome. Mechanistically, we show that IRGM interacts with NLRP3 and ASC and hinders inflammasome assembly by blocking their oligomerization. Further, IRGM mediates selective autophagic degradation of NLRP3 and ASC. By suppressing inflammasome activation, IRGM/Irgm1 protects from pyroptosis and gut inflammation in a Crohn’s disease experimental mouse model. This study for the first time identifies the mechanism by which IRGM is protective against inflammatory disorders