Pushpendra Kumar

Steroidogenic alterations in testes and sera of rats exposed to formulated Fenvalerate by inhalation.

Fenvalerate (Fen) is a synthetic pyrethroid, which is commonly used for destroying a variety of insect pests damaging several vegetable, fruit, and cotton crops. This insecticide is also used to mitigate household insects like flies, cockroaches, mosquitoes, and so forth. Human beings are exposed to formulated Fen preparations mostly by inhalation during spraying in fields for crop protection, for control of household insects, and also during handling and packaging at manufacturing plants. Limited online information is available regarding toxic effects of formulated Fen exposure on mammalian reproductive system. The present study has been undertaken to investigate male reproductive toxic effects of a formulated preparation of Fen (20% EC) particularly in relation to steroidogenic alterations in testes and sera of rats exposed by nose-only inhalation for (4 hours/day and five days a week) for three months. The results indicate significant reduction in the weight of testes, epididymal sperm counts, and sperm motility, along with decrease in marker testicular enzymes for testosterone biosynthesis viz. 17-b-hydroxy steroid dehydrogenase (17-b-HSD) and glucose-6-phosphate dehydrogenase (G6PDH), leading to net decrease in serum testosterone concentration in group of rats exposed to onefifth LC50 of Fen (20% EC) by inhalation (4 hours/day, five days a week) subchronically for three months. These results for the first time indicate the role of testosterone in Fen (20% EC)-induced male reproductive toxicity of rats subchronically exposed by inhalation probably due to neuroendocrine-mediated phenomenon and hormone-disrupting property of the insecticide.

Association of Tuberculous Endometritis with Infertility and Other Gynecological Complaints of Women in India

ABSTRACT Endometrial biopsy samples derived from 393 patients with assorted gynecological complaints were investigated for mycobacterial infection. By employment of four different techniques, mycobacterial pathogens were detected irrespective of the nature/type of clinical complaint. Mycobacterium tuberculosis was the predominant pathogen detected among the samples investigated.

Pre-seismic, co-seismic and post-seismic displacements associated with the Bhuj 2001 earthquake derived from recent and historic geodetic data

The 26th January 2001 Bhuj earthquake occurred in the Kachchh Rift Basin which has a long history of major earthquakes. Great Triangulation Survey points (GTS) were first installed in the area in 1856–60 and some of these were measured using Global Positioning System (GPS) in the months of February and July 2001. Despite uncertainties associated with repairs and possible reconstruction of points in the past century, the re-measurements reveal pre-seismic, co-seismic and post-seismic deformation related to Bhuj earthquake. More than 25 Μ-strain contraction north of the epicenter appears to have occurred in the past 140 years corresponding to a linear convergence rate of approximately 10 mm/yr across the Rann of Kachchh. Motion of a single point at Jamnagar 150 km south of the epicenter in the 4 years prior to the earthquake, and GTS-GPS displacements in Kathiawar suggests that pre-seismic strain south of the epicenter was small and differs insignificantly from that measured elsewhere in India. Of the 20 points measured within 150 km of the epicenter, 12 were made at existing GTS points which revealed epicentral displacements of up to 1 m, and strain changes exceeding 30 Μ-strain. Observed displacements are consistent with reverse co-seismic slip. Re-measurements in July 2001 of one GTS point (Hathria) and eight new points established in February reveal post-seismic deformation consistent with continued slip on the Bhuj rupture zone.

Effect of the M 9.3 Sumatra-Andaman islands earthquake of 26 December 2004 at several permanent and campaign GPS stations in the Indian continent

The effect of the 26 December 2004 Sumatra–Andaman earthquake on the Indian continent has been estimated from the analysis of GPS data from permanent and campaign GPS sites in the Indian continent. Co‐seismic displacements at these sites have been determined for 11 permanent GPS stations of the national network, five campaign sites in southern India, and four campaign sites in Andaman and Nicobar Islands. The results indicate co‐seismic eastward displacements of 12–20 mm in southern India almost directly west of Andaman, 1.8–6 mm in Central India and insignificant displacement in the Himalayas. Permanent sites in north‐east India which lie almost towards the northward extension of the rupture plane show smaller co‐seismic displacements ranging from 5 to 10 mm southward. Four campaign sites in the Andaman and Nicobar Islands show large horizontal co‐seismic displacements of 1.6–6.49 m WSW and SW. Vertical displacement varies from an uplift of 0.6 m in north Andaman to 1.1 m subsidence at Car Nicobar. The observed GPS displacements are modelled using coulomb 2.6, and the slip on the four segments of the rupture plane (450 km×175 km; 250 km×140 km; 250 km×100 km; 150 km×100 km) that best fits both the far and near field displacements is estimated to be predominantly 12 m reverse in the southernmost segment, which slowly translates to an oblique slip of 7 m in the northernmost segment of the rupture plane. The seismic moment of the Sumatra–Andaman earthquake for the above rupture plane and slip is M o = 5.21×1022 Nm, which corresponds to a moment magnitude of M w = 9.1.

Diisopropylphosphorofluoridate-induced depression of compound action potential of frog sciatic nerve in vitro is mediated through the inhibition of cholinesterase activity

Effect of diisopropylphosphorofluoridate (DFP), an irreversible cholinesterase (ChE) inhibitor, on compound action potential (CAP) of sciatic nerve in vitro was examined. Further, the role of cholinesterase reactivator (1 acetyl‐4‐hydroxy imino methyl pyridinium bromide; SPK‐3) in reversing DFP‐induced changes was also evaluated. Diisopropylphosphorofluoridate produced a dose‐dependent depression of the CAP. A concentration as low as 0.01u2009μM DFP produced a 5% depression (Pu2009<u20090.05) and the maximal depression (30% of control) was observed with 1u2009μM. The SPK‐3 (up to 10u2009μM) had no effect on the CAP; SPK‐3 (10u2009μM) antagonized the DFP‐induced depression of the CAP partially but not after 1u2009μM DFP. However, the inhibitory concentration of DFP to produce 50% of the maximal depression (ic50) was 0.38u2009±u20090.025u2009μM in the presence of SPK‐3 (10u2009μM; nu2009=u20094), against 0.15u2009±u20090.05u2009μM for DFP alone (nu2009=u20097).These ic50 values were significantly different (Pu2009<u20090.05, Students t‐test). The DFP decreased nerve ChE activity by 41% in t he absence of SPK‐3 and by 31% in the presence of SPK‐3. Although SPK‐3 could not completely reactivate the inhibited enzyme, it seems reasonable to conclude that the DFP‐induced depression of the action potential of sciatic nerve was mediated by inhibiting the ChE activity.