Authors:P. R. Nambiar, V. R. Pai Verneker, and S. R. Jain
The explosive sensitivity of methylammonium perchlorates has been investigated by differential thermal analysis, thermogravimetric analysis, mass spectrometry and explosion delay experiments. The decomposition temperature of these compounds increases in the order CH3NH3ClO4>(CH3)2NH2ClO4>(CH3)3NHClO4. The activation energy shows the reverse order, indicating thereby that the stability increases with increasing substitution. Mass spectrometric investigation, however, suggests an increasing reactivity with increasing substitution. A possible explanation for such behaviour is proposed. It appears that explosion delay is correlated with thermal decomposition and impact sensitivity.
Authors:H. Dang, D. Jaiswal, K. Murthy, R. Sharma, P. Nambiar, and C. Sunta
This paper compares the urinary excretion levels of Th obtained in bio-assay monitoring using the neutron activation technique with those predicted by applying the ICRP metabolic model to the measured Th activity in chest and total body of a group of Thorium plant workers. The results indicated much lower urinary Th excretion as compared to what was expected on the basis of the ICRP model. Lower urinary excretion in occupational subjects is explained in terms of negligible contribution of skeleton and soft tissue to the activity excreted in urine. It is suggested that the existing model should be modified to enable it to be applicable to the bio-assay monitoring of occupational workers.
Authors:Peethambaran Arun, Manojkumar Valiyaveettil, Lionel Biggemann, Yonas Alamneh, Yanling Wei, Samuel Oguntayo, Ying Wang, Joseph B. Long, and Madhusoodana P. Nambiar
Emerging studies show that blast exposure causes traumatic brain injury (TBI) and auditory dysfunction without rupture of tympanic membrane, suggesting central auditory processing impairment after blast exposure. There is limited information on the mechanisms of blast-induced TBI and associated peripheral and central auditory processing impairments. We utilized a repetitive blast exposure mouse model to unravel the mechanisms of blast TBI and auditory impairment. C57BL/6J mice were exposed to three repeated blasts (20.6 psi) using a shock tube, and the cerebellum was subjected to proteomic analysis. The data showed that calretinin and parvalbumin, two major calcium buffering proteins, were significantly up-regulated after repeated blast exposures, and this was confirmed by Western blotting. Since these proteins are reportedly involved in auditory dysfunction, we examined the inner ear and found both calretinin and parvalbumin were up-regulated, suggesting that modulation of these proteins plays a role in blast-induced peripheral and central auditory processing impairments. Expression of cleaved caspase-3 was also up-regulated in both regions indicating ongoing cellular apoptosis, possibly due to altered calcium homeostasis. These results provide a molecular basis for changes in central and peripheral auditory processing involving abnormal calcium homeostasis resulting in hearing impairment after blast exposure.