Mazhar Husain

Effect of Sowing Date and Cultivars on Aphid Infestation in Wheat with Climate Change Adaptation Perspective

Four field experiments, two experiments each during winter season of 2012–2013 and 2013–2014, were conducted to evaluate effect of sowing time and four wheat cultivars on population of wheat aphids. Wheat crop was found infested with Rhopalosiphum padi and Sitobion avenae in various proportions in different experiments. During vegetative crop phase, December (late) sown crop had in general higher aphid population than November (timely) sown crop, while during reproductive crop stage, timely sown crop harboured more aphids on ear heads than late planted one. October (early) and January (very late) sown crop evaded aphid attack on ear heads. Significant differences in peak aphid populations among different plantings indicated that alteration of sowing time might disturb phenological synchrony between aphids and wheat crop, affecting pest population. Aphid population was positively influenced by the temperature. Sowing dates were also found to significantly affect the crop yield. Among varieties, WR-544 was observed to have lower number of aphids than other cultivars during vegetative crop stage. Because alteration in sowing time is deemed to be one of the adaptation strategies to sustain agricultural productivity under climate change, effect of sowing time on aphid population is the need to be heeded while formulating such strategy for effective crop management.

The 10,000-Fold-Effect-Retrograde Neurotransmission-a Newer Concept for Paraplegia's Physiological Revival-use of Intrathecal Sodium Nitroprusside in 100 Cases-A Priliminary Report

Background Methylprednisolone has shown level-1-benefit (20%) in traumatic paraplegia cases (but within-8hrs) yet disproved by many studies. Patients wait long for physiological recovery. Intrathecal-Sodium-Nitroprusside (ITSNP) has been used in literature to relieve vasospasm-due-to-subarachnoid-hemorrhage. ITSNP has been studied here for physiological recovery in paraplegia cases of various etiologies in a wide-window-period-range. Two mechanisms for acute-cases and one-mechanism for chronic-cases, which are interrelated, are being proposed for physiological recovery. (a) Retrograde-Neurotransmission (acute-cases). 1. During Normal excitatory impulse: at synaptic-level, glutamate activates NMDA-receptors, having Nitric-Oxide-Synthetase(NOS) on postsynaptic-membrane, for further propagation by calcium-calmodulin-complex. Nitric-Oxide (NO produced by NOS) travels backward across chemical synapse, binding to axon terminal (NO-receptor/sGC) of presynaptic-neuron, regulating-Anterograde-Neurotransmission (ANT) called Retrograde-Neurotransmission (RNT). The-haem is the ligand binding site of NO receptor/sGC. The affinity of haem exhibits 10,000-fold excess for NO than Oxygen (THE=10,000-FOLD effect) completes in 20msec. 2. In Pathological conditions: normal-ANT, synaptic-activity including-RNT is-absent. NO-donor(SNP) release NO from NOS at postsynaptic-region. NO travels backward across a chemical-synapse to bind to the haem of NO-receptor at axon-terminal of a presynaptic-neuron, generates-impulse, as in normal-condition. (b) Vasospasm (acute-cases). Perforators show vasospastic activity. NO vasodilates the perforators by NO cAMP pathway. (c) Long Term Potentiation (LTP) (chronic-cases). NO–cGMP-pathway plays a role in LTP at many synapses throughout the CNS, and at neuromuscular junction. The LTP has been reviewed both generally and with respect to specific brain regions for memory/learning. LTP plays an important factor for relief from paraplegia in chronic cases. Aims/Study Design: Principle of “generation-of-impulses from presynaptic-region to postsynaptic-region by-RNT, vasodilatation of arteriolar-perforators and LTP is the basis-of-authors” hypothesis to treat-acute-and-chronic-paraplegia-cases. Case-control-prospective-study. Material/Methods: 200 paraplegia patients {100 patients taken as control (50 with no superfusion and 50 with dextrose 5% superfusion) and 100 patients taken as in ITSNP-group} were studied here. The mean time for superfusion was 14.11 days. ITSNP administered at a dosage of 0.2 mg/kg bo wt at L3/4 level by 24 G LP needle. Pre and post ITSNP was monitored by SSEP/MEP. Results AFTER-2-HOURS in ITSNP-group MEAN-CHANGE-FROM-BASELINE-ASIA MOTOR/SENSORY-SCORE 13.84%/13.10%, after-24 hours MOTOR-1.27-points decrease(3.77%) and SENSORY 10.5 points-increase(6.22%)as compared with Control-group no-change noted upto 24 hours, At-7days ITSNP motor/sensory;11.56%/6.22% as compared with Control-group 7.60/4.48%, At-2months in ITSNP 27.69%/6.22% as compared with Control-group 16.02/4.5%. SSEP/MEP-documented-improvements-noted. Conclusions ITSNP, a-swift-acting-drug in treatment-of-paraplegia, is effective within-two-hours (mean-change-MOTOR-13.84%andSENSORY-13.10%) on-mean14.11th postparaplegia-day with a small-detrimental-response after-24 hours which-recovers-fast

IS BRAIN DEATH REVERSAL POSSIBLE IN NEAR FUTURE: INTRATHECAL SODIUM NITROPRUSSIDE (SNP) SUPERFUSION IN BRAIN DEATH PATIENTS = THE 10,000 FOLD EFFECT

BACKGROUND: Primary or secondary brain death is accompanied with vasospasm of the perforators & further exaggerating the anoxic damage, in the form of neuropraxia. In normal conditions the excitatory impulse propagates as anterograde neurotransmission (ANT) and at the level of synapse, glutamate activates NMDA receptors on postsynaptic membrane. Nitric oxide (NO) is produced by Nitric oxide Synthetase (NOS) in postsynaptic dendride or cell body and travels backwards across a chemical synapse to bind to the axon terminal of a presynaptic neuron for regulation of ANT this process is called as the retrograde neurotransmission (RNT). Thus the primary function of NO is RNT and the purpose of RNT is regulation of chemical neurotransmission at synapse. For this reason, RNT allows neural circuits to create feedback loops. The haem is the ligand binding site of NO receptor (sGC) at presynaptic membrane. The affinity of haem exhibits >10, 000- fold excess for NO than Oxygen (THE 10, 000 FOLD EFFECT). In pathological conditions ANT, normal synaptic activity including RNT is absent. NO donors like sodium nitroprusside (SNP) releases NO by activating NOS at the level of postsynaptic area. NO now travels backwards across a chemical synapse to bind to the haem of NO receptor at axon terminal of a presynaptic neuron as in normal condition. NO now acts as impulse generator (at presynaptic membrane) thus bypasses the normal ANT. Also the arteriolar perforators are having Nitric Oxide Synthetase (NOS) at the adventitial side (outer border) on which sodium nitroprusside (SNP) acts; causing release of Nitric Oxide (NO) which vasodilates the perforators causing gush of blood in brains tissue and reversal of brain death. OBJECTIVE: In brain death cases we only think for various transplantations but this study being a pilot study reverses some criteria of brain death by vasodilating the arteriolar perforators. To study the effect of intrathecal sodium nitroprusside (IT SNP) in cases of brain death in which: Retrograde transmission = assessed by the hyperacute timings of reversal. The arteriolar perforator vasodilatation caused by NO and the maintenance of reversal of brain death reversal. METHODS: 35 year old male, who became brain death after head injury and has not shown any signs of improvement after every maneuver for 6 hours, a single superfusion done by SNP via transoptic canal route for quadrigeminal cistern and cisternal puncture for IV ventricular with SNP done. RESULTS: He showed spontaneous respiration (7 bouts) with TCD studies showing start of pulsations of various branches of common carotid arteries. CONCLUSIONS: In future we can give this SNP via transoptic canal route and in IV ventricle before declaring the body to be utilized for transplantations or dead or in broader way we can say that in near future it is possible to revert back from brain death or we