Spherical Cap Studs: A novel speed bump alternative to reduce discomfort with effective speed reduction.

OBJECTIVE: The aim of this study is to assess the potential of Spherical Cap Studs (SCS) as a substitute for conventional speed bumps, with a focus on limiting two wheeler speed while minimizing discomfort to riders by comparing the speed reduction capabilities and discomfort levels associated with SCS and speed bumps. METHODS: The study uses experimental approach to compare the speed limiting ability and discomfort caused to rider by the proposed SCS and a standard speed bump. Speed profiles were developed for two wheelers passing over both SCS and speed bump. The parameter employed to compare speed profiles is the Mean Absolute Percentage Difference (MAPD), offering valuable insights into how effectively the two traffic calming measures reduce two wheeler speeds. To compare discomfort, the study calculates the 'Vibration Dose Value' (VDV) experienced by riders when traversing both speed bump and SCS. Additionally, 'Static Compressive Stress' (Se) applied to the spinal cord is also calculated in both scenarios. RESULTS: The analysis of speed profiles reveals an MAPD value of 13.70% indicating that SCS exhibits speed reduction capabilities comparable to traditional speed bump. In terms of discomfort, the VDV for two wheelers passing over a speed bump is measured at 5.92 m/s1.75, whereas the VDV for SCS is found to be 5.16 m/s1.75. Similarly, the Static Compressive Stress (Se) experienced at a speed bump is 0.60 MPa, in contrast to the 0.33 MPa recorded for SCS. This data underscores a noteworthy 12.8% reduction in VDV and a substantial 45.57% reduction in Se. CONCLUSION: The study's findings support the potential adoption of SCS as an effective alternative to conventional speed bumps for controlling two wheeler speeds. SCS demonstrate a speed reduction capability similar to that of traditional speed bumps while significantly alleviating discomfort for riders. SCS is expected to be a promising solution for traffic calming purposes in various settings, such as markets, residential areas, institutional campuses, and parking lots.

Aluminium induced oxidative stress and DNA damage in root cells of Allium cepa L.

Aluminium (Al) was evaluated for induction of oxidative stress and DNA damage employing the growing roots of Allium cepa L. as the assay system. Intact roots of A. cepa were treated with different concentrations, 0, 1, 10, 50, 100, or 200 microM of aluminium chloride, at pH 4.5 for 4 h (or 2 h for comet assay) at room temperature, 25+/-1 degrees C. Following treatment the parameters investigated in root tissue were Al-uptake, cell death, extra cellular generation of reactive oxygen intermediates (ROI), viz. O(2)(*-), H(2)O(2) and (*)OH, lipid peroxidation, protein oxidation, activities of antioxidant enzymes namely catalase (CAT), superoxide dismutase (SOD), guaiacol peroxidase (GPX), ascorbate peroxidase (APX); and DNA damage, assessed by comet assay. The findings indicated that Al triggered generation of extra-cellular ROI following a dose-response. Through application of specific enzyme inhibitors it was demonstrated that extra-cellular generation of ROI was primarily due to the activity of cell wall bound NADH-PX. Generation of ROI in root tissue as well as cell death was better correlated to the levels of root Al-uptake rather than to the concentrations of Al in ambient experimental solutions. Induction of lipid peroxidation and protein oxidation by Al were statistically significant. Whereas Al inhibited CAT activity, enhanced SOD, GPX and APX activities significantly; that followed dose-response. Comet assay provided evidence that Al induced DNA damage in a range of concentrations 50-200 microM, which was comparable to that induced by ethylmethane sulfonate (EMS), an alkylating mutagen served as the positive control. The findings provided evidence that Al comparable to biotic stress induced oxidative burst at the cell surface through up- or down-regulation of some of the key enzymes of oxidative metabolism ultimately resulting in oxidative stress leading to DNA damage and cell death in root cells of A. cepa.