Enhanced OLSR Routing Protocol Using Link-Break Prediction Mechanism for WSN

Jaggi, Sukhleen,Wasson, Er. Vikas Korean Institute of Industrial Engineers 2016 Industrial Engineeering & Management Systems Vol.15 No.3

In Wireless Sensor Network, various routing protocols were employed by our Research and Development community to improve the energy efficiency of a network as well as to control the traffic by considering the terms, i.e. Packet delivery rate, the average end-to-end delay, network routing load, average throughput, and total energy consumption. While maintaining network connectivity for a long-term duration, it's necessary that routing protocol must perform in an efficient way. As we discussed Optimized Link State Routing protocol between all of them, we find out that this protocol performs well in the large and dense networks, but with the decrease in network size then scalability of the network decreases. Whenever a link breakage is encountered, OLSR is not able to periodically update its routing table which may create a redundancy problem. To resolve this issue in the OLSR problem of redundancy and predict link breakage, an enhanced protocol, i.e. S-OLSR (More Scalable OLSR) protocol has been proposed. At the end, a comparison among different existing protocols, i.e. DSR, AODV, OLSR with the proposed protocol, i.e. S-OLSR is drawn by using the NS-2 simulator.

Enhanced OLSR Routing Protocol Using Link-Break Prediction Mechanism for WSN

Sukhleen Jaggi,Er. Vikas Wasson 대한산업공학회 2016 Industrial Engineeering & Management Systems Vol.15 No.3

In Wireless Sensor Network, various routing protocols were employed by our Research and Development community to improve the energy efficiency of a network as well as to control the traffic by considering the terms, i.e. Packet delivery rate, the average end-to-end delay, network routing load, average throughput, and total energy consumption. While maintaining network connectivity for a long-term duration, it’s necessary that routing protocol must perform in an efficient way. As we discussed Optimized Link State Routing protocol between all of them, we find out that this protocol performs well in the large and dense networks, but with the decrease in network size then scalability of the network decreases. Whenever a link breakage is encountered, OLSR is not able to periodically update its routing table which may create a redundancy problem. To resolve this issue in the OLSR problem of redundancy and predict link breakage, an enhanced protocol, i.e. S-OLSR (More Scalable OLSR) protocol has been proposed. At the end, a comparison among different existing protocols, i.e. DSR, AODV, OLSR with the proposed protocol, i.e. S-OLSR is drawn by using the NS-2 simulator.

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Kumar, Rohit,Jaggi, Amteshwar Singh,Singh, Nirmal The Korean Society of Pharmacology 2010 The Korean Journal of Physiology & Pharmacology Vol.14 No.5

The present study was undertaken to explore the potential of erythropoietin in memory deficits of mice. Memory impairment was produced by scopolamine (0.5 mg/kg, $i.p.$) and intracerebroventricular streptozotocin (i.c.v STZ, 3 mg/kg, $10{\mu}l$, $1^{st}$ and $3^{rd}$ day) in separate groups of animals. Morris water-maze test was employed to assess learning and memory. The levels of brain thio-barbituric acid reactive species (TBARS) and reduced glutathione (GSH) were estimated to assess degree of oxidative stress. Brain acetylcholinesterase enzyme (AChE) activity was also measured. Scopolamine/streptozotocin administration induced significant impairment of learning and memory in mice as indicated by marked decrease in Morris water-maze performance. Scopolamine/streptozotocin administration also produced a significant enhancement of brain AChE activity and brain oxidative stress (an increase in TBARS and a decrease in GSH) levels. Treatment of erythropoietin (500 and 1,000 IU/Kg i.p.) significantly reversed scopolamine- as well as streptozotocin-induced learning and memory deficits along with attenuation of those-induced rise in brain AChE activity and brain oxidative stress levels. It may be concluded that erythropoietin exerts a beneficial effect in memory deficits of mice possibly through its multiple actions including potential anti-oxidative effect.

Book Review: Streaming Culture: Subscription Platforms and the Unending Consumption of Culture

Mishra, Mudita,Jaggi, Ruchi Kher Center for Asian Public Opinion ResearchCollaborat 2022 Asian journal for public opinion research Vol.10 No.3

Effect of Neurosteroid Modulation on Global Ischaemia-Reperfusion-Induced Cerebral Injury in Mice

Grewal, Amarjot Kaur,Jaggi, Amteshwar Singh,Rana, Avtar Chand,Singh, Nirmal The Korean Society of Pharmacology 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.6

The present study was designed to investigate the putative effect of neurosteroid modulation on global ischaemia-reperfusion-induced cerebral injury in mice. Bilateral carotid artery occlusion followed by reperfusion, produced a significant rise in cerebral infarct size along with impairment of grip strength and motor coordination in Swiss albino mice. Administration of carbamazepine (16 mg/kg, i.p.) before global cerebral ischaemia significantly attenuated cerebral infarct size and improved the motor performance. However, administration of indomethacin (100 mg/kg, i.p.) attenuated the neuroprotective effect of carbamazepine. Mexiletine (50 mg/kg, i.p.) did not produce significant neuroprotective effect. It may be concluded that the neuroprotective effect of carbamazepine may be due to increase in synthesis of neurosteroids perhaps by activating enzyme ($3{\alpha}$ HSD) as indomethacin attenuated the neuroprotective effect of carbamazepine. The sodium channel blocking effect of carbamazepine may not be involved in neuroprotection as mexiletine, a sodium channel blocker, did not produce significant neuroprotective effect.

Pharmacological Preconditioning by Milrinone: Memory Preserving and Neuroprotective Effect in Ischemia-Reperfusion Injury in Mice

Reetu Saklani,Amteshwar Jaggi,Nirmal Singh 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.7

We tested the neuroprotective effect of milrinone, a phosphodiesterase III inhibitor, in pharmacological preconditioning. Bilateral carotid artery occlusion for 12 min followed by reperfusion for 24 h produced ischemia-reperfusion (I/R) cerebral injury in male Swiss albino mice. Cerebral infarct size was measured using triphenyltetrazolium chloride staining. Memory was assessed using the Morris water maze test, and motor coordination was evaluated using the inclined beam walking test, rota-rod test, and lateral push test. Milrinone (50 μg/kg & 100 μg/kg i.v.) was administered 24 h before surgery in a separate group of animals to induce pharmacological preconditioning. I/R increased cerebral infarct size and impaired memory and motor coordination. Milrinone treatment significantly decreased cerebral infarct size and reversed I/R-induced impairments in memory and motor coordination. This neuroprotective effect was blocked by ruthenium red (3 mg/kg, s.c.), an intracellular ryanodine receptor blocker. These findings indicate that milrinone preconditioning exerts a marked neuroprotective effect on the ischemic brain, putatively due to increased intracellular calcium levels activating calcium-sensitive signal transduction cascades.

Ameliorative Effect of a Selective Endothelin $ET_A$ Receptor Antagonist in Rat Model of L-Methionine-induced Vascular Dementia

Mangat, Gautamjeet S.,Jaggi, Amteshwar S.,Singh, Nirmal The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.3

The present study was designed to investigate the efficacy of selective $ET_A$ receptor antagonist, ambrisentan on hyperhomocysteinemia-induced experimental vascular dementia. L-methionine was administered for 8 weeks to induce hyperhomocysteinemia and associated vascular dementia in male rats. Ambrisentan was administered to L-methionine-treated effect rats for 4 weeks (starting from $5^{th}$ to $8^{th}$ week of L-methionine treatment). On $52^{nd}$ day onward, the animals were exposed to the Morris water maze (MWM) for testing their learning and memory abilities. Vascular endothelial function, serum nitrite/nitrate levels, brain thiobarbituric acid reactive species (TBARS), brain reduced glutathione (GSH) levels, and brain acetylcholinesterase (AChE) activity were also measured. L-methionine-treated animals showed significant learning and memory impairment, endothelial dysfunction, decrease in/serum nitrite/nitrate and brain GSH levels along with an increase in brain TBARS levels and AChE activity. Ambrisentan significantly improved hyperhomocysteinemia-induced impairment of learning, memory, endothelial dysfunction, and changes in various biochemical parameters. These effects were comparable to that of donepezil serving as positive control. It is concluded that ambrisentan, a selective $ET_A$ receptor antagonist may be considered as a potential pharmacological agent for the management of hyperhomocysteinemia-induced vascular dementia.

Advanced Glycation End Products and Diabetic Complications

Singh, Varun Parkash,Bali, Anjana,Singh, Nirmal,Jaggi, Amteshwar Singh The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.1

During long standing hyperglycaemic state in diabetes mellitus, glucose forms covalent adducts with the plasma proteins through a non-enzymatic process known as glycation. Protein glycation and formation of advanced glycation end products (AGEs) play an important role in the pathogenesis of diabetic complications like retinopathy, nephropathy, neuropathy, cardiomyopathy along with some other diseases such as rheumatoid arthritis, osteoporosis and aging. Glycation of proteins interferes with their normal functions by disrupting molecular conformation, altering enzymatic activity, and interfering with receptor functioning. AGEs form intra- and extracellular cross linking not only with proteins, but with some other endogenous key molecules including lipids and nucleic acids to contribute in the development of diabetic complications. Recent studies suggest that AGEs interact with plasma membrane localized receptors for AGEs (RAGE) to alter intracellular signaling, gene expression, release of pro-inflammatory molecules and free radicals. The present review discusses the glycation of plasma proteins such as albumin, fibrinogen, globulins and collagen to form different types of AGEs. Furthermore, the role of AGEs in the pathogenesis of diabetic complications including retinopathy, cataract, neuropathy, nephropathy and cardiomyopathy is also discussed.

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

Puneet Kaur Randhawa,Kavinder Singh,Amteshwar Singh Jaggi 대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.4

Ulcerative colitis and Crohn’s disease are a set of chronic, idiopathic, immunological and relapsinginflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, developmentof various animal models provides new insights to unveil the onset and the progression of IBD. Variouschemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closelymimic morphological, histopathological and symptomatical features of human IBD. Among thechemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazoloneinduced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBSelicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response ofTh-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. Thepresent review discusses the methodology and rationale of using various chemical-induced colitismodels for evaluating the pathogenesis of IBD.

Ameliorative Effect of a Selective Endothelin ETA Receptor Antagonist in Rat Model of L-Methionine-induced Vascular Dementia

Gautamjeet S Mangat,Amteshwar S. Jaggi,Nirmal Singh 대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.3

The present study was designed to investigate the efficacy of selective ETA receptor antagonist, ambrisentanon hyperhomocysteinemia-induced experimental vascular dementia. L-methionine was administeredfor 8 weeks to induce hyperhomocysteinemia and associated vascular dementia in male rats. Ambrisentan was administered to L-methionine-treated effect rats for 4 weeks (starting from 5th to8th week of L-methionine treatment). On 52nd day onward, the animals were exposed to the Morriswater maze (MWM) for testing their learning and memory abilities. Vascular endothelial function,serum nitrite/nitrate levels, brain thiobarbituric acid reactive species (TBARS), brain reduced glutathione(GSH) levels, and brain acetylcholinesterase (AChE) activity were also measured. L-methionine-treated animals showed significant learning and memory impairment, endothelial dysfunction,decrease in/serum nitrite/nitrate and brain GSH levels along with an increase in brain TBARS levelsand AChE activity. Ambrisentan significantly improved hyperhomocysteinemia-induced impairment oflearning, memory, endothelial dysfunction, and changes in various biochemical parameters. Theseeffects were comparable to that of donepezil serving as positive control. It is concluded that ambrisentan,a selective ETA receptor antagonist may be considered as a potential pharmacological agentfor the management of hyperhomocysteinemia-induced vascular dementia.