Patiala, India
Patiala, India

Punjabi University is a higher education institute located in Patiala, Punjab, India. Punjabi University teaches and researches in science, engineering and technology, humanities, social science, performing arts and sports.It was established on the 30 April 1962, and is only the second university in the world to be named after a language, after Hebrew University of Israel. Originally it was conceived as a unitary multi-faculty teaching and research university, primarily meant for the development and enrichment of Punjabi language and culture, but alive to the social and education requirements of the state. Wikipedia.

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Dsingh A.,Punjabi University
Smart Innovation, Systems and Technologies | Year: 2017

Children spend long hours inside their classrooms which require them to continuously sit on the classroom furniture provided to them. 400 boys and girls school going children ranging in age from 4 to 14 years of government and private sponsored schools in Punjab were randomly selected for the study. A structured questionnaire was used for evaluating Musculoskeletal and other health problems of school children. The Faces Pain Scale—Revised and Visual analogue scale were used to measure pain intensity. The percentage of musculoskeletal pain and discomfort complained by subjects were Neck Pain 11%, Upper Back Pain 17.5%, Low Back Pain 14.75%, Upper Limb Pain 31%, Lower Limb Pain 33.25%, Sleep/dozy in classroom 14.25%, General Body Fatigue 35% and Any other discomfort 26%. Study concluded that classroom Furniture has significant impact on wellbeing of school children. This in order will help overcome the growing problems of poor posture found frequently among present day young generation. © Springer Nature Singapore Pte Ltd. 2017.

Bali A.,Punjabi University | Randhawa P.K.,Punjabi University | Jaggi A.S.,Punjabi University
Neuroscience and Biobehavioral Reviews | Year: 2014

Research studies have defined the important role of endogenous opioids in modulating stress-associated behavior. The release of β-endorphins in the amygdala in response to stress helps to cope with a stressor by inhibiting the over-activation of HPA axis. Administration of mu opioid agonists reduces the risk of developing post-traumatic stress disorder (PTSD) following a traumatic event by inhibiting fear-related memory consolidation. Similarly, the release of endogenous enkephalin and nociceptin in the basolateral amygdala and the nucleus accumbens tends to produce the anti-stress effects. An increase in dynorphin levels during prolonged exposure to stress may produce learned helplessness, dysphoria and depression. Stress also influences morphine-induced conditioned place preference (CPP) depending upon the intensity and duration of the stressor. Acute stress inhibits morphine CPP, while chronic stress potentiates CPP. The development of dysphoria due to increased dynorphin levels may contribute to chronic stress-induced potentiation of morphine CPP. The activation of ERK/cyclic AMP responsive element-binding (CREB) signaling in the mesocorticolimbic area, glucocorticoid receptors in the basolateral amygdala, and norepinephrine and galanin system in the nucleus accumbens may decrease the acute stress-induced inhibition of morphine CPP. The increase in dopamine levels in the nucleus accumbens and augmentation of GABAergic transmission in the median prefrontal cortex may contribute in potentiating morphine CPP. Stress exposure reinstates the extinct morphine CPP by activating the orexin receptors in the nucleus accumbens, decreasing the oxytocin levels in the lateral septum and amygdala, and altering the GABAergic transmission (activation of GABAA and inactivation of GABAB receptors). The present review describes these varied interactions between opioids and stress along with the possible mechanism. © 2015 Elsevier Ltd. All rights reserved.

Jaggi A.S.,Punjabi University | Singh N.,Punjabi University
Brain Research | Year: 2011

Neuropathic pain has been described as the "most terrible of all tortures which a nerve wound may inflict" and arises as a consequence of nerve injury either of the peripheral or central nervous system. Following peripheral nerve injury, a cascade of events in the primary afferents leads to peripheral sensitization resulting in spontaneous nociceptor activity, decreased threshold and increased response to supra-threshold stimuli. A series of molecular changes in spinal cord and brain centers are associated with central sensitization which is responsible for the pain to non-injured extra-territory regions (extraterritorial pain) and contralateral parts (mirror-image pain). The peripheral nerve injury has been reported to induce neuroplastic changes in different brain regions including the anterior cingulate cortex, insular cortex, ventrolateral orbitofrontal area, amygdala, striatum, thalamus, hypothalamus, rostral ventromedial medulla, periaqueductal gray, pons (locus coeruleus), red nucleus, and medulla oblongata. The present review article discusses the involvement of these different brain areas in the development of peripheral nerve injury-induced neuropathic pain. © 2011 Elsevier B.V. All rights reserved.

Bansal Y.,Punjabi University | Silakari O.,Punjabi University
European Journal of Medicinal Chemistry | Year: 2014

Multifunctional compounds (MFCs) are designed broadly as hybrid or conjugated drugs or as chimeric drugs from two or more pharmacophores/drugs having specific pharmacological activities. These are capable of eliciting multiple pharmacological actions and have emerged as magic bullets in treatment of multifactorial diseases. Many research articles disclosing the development of such compounds for treatment of multifactorial diseases are published during last 7 years. Some successful MFC candidates for multifactorial CNS disorders include ziprasidone, duloxetine, ladostigil and M-30 whereas sunitinib, lapatinib and synthetic oleandane triterpinoids are the successful MFC candidates for various cancers. Many more compounds derived from berberine, tacrine, artemisnin, quinine, NSAIDs, pralidoxine, donepezil, rivastigmine, curcumin and various antioxidants are under investigations for exploration of their multifunctional potential. In general, MFCs possess the advantages of reduced molecularity, no drug-drug interactions and improved pharmacokinetics and pharmacodynamics. A MFC derived from two or more different pharmacophores exerts its activities by interacting with respective receptors of its constituent pharmacophores. It may also exhibit additional binding interactions with the receptor sites that may be responsible for significantly improved or additional activities. The present review discusses various MFCs developed for specific class of disorders with an aim to provide an insight into the strategies in medicinal chemistry for development of such compounds. © 2014 Published by Elsevier Masson SAS.

Involvement of vascular pathology has been suggested in hypertension as well as vascular dementia (VaD), which also have a very high degree of co-occurrence in ageing population. We have recently reported that experimental diabetes as well as hyperhomocystenemia induces VaD. In the present research work, for the first time we are reporting the genesis of VaD by deoxycorticosterone acetate (DOCA)-salt induced experimental hypertension. Furthermore, we have also investigated the beneficial effect of telmisartan, an angiotensin II type 1 receptor blocker (ARB) and donepezil, an acetylcholinesterase inhibitor (AChEI), on DOCA-salt hypertension induced VaD in rats. DOCA-salt hypertensive rats performed poorly on Morris water maze, reflecting impairment in their learning and memory. Furthermore, DOCA-salt treatment has shown a significant impairment of vascular endothelial function (DOCA attenuated acetylcholine induced endothelium dependent relaxation), with a significant reduction in serum nitrite/nitrate levels, along with increased aortic, serum and brain oxidative stress levels (aortic superoxide anion, serum and brain thiobarbituric acid reactive species, brain glutathione) and brain acetylcholinesterase activity. Treatments of telmisartan as well as donepezil significantly attenuated DOCA-salt hypertension induced learning and memory deficits, endothelial dysfunction, and changes in various biochemical parameters. It may be concluded that DOCA-salt hypertension induces VaD in rats. ARBs and AChEIs may be considered as potential pharmacological agents for the management of hypertension induced VaD. © 2012 Elsevier Inc. All rights reserved.

Anand P.,Punjabi University | Singh B.,Punjabi University
Archives of Pharmacal Research | Year: 2013

Alzheimer's disease (AD), a progressive neurodegenerative disorder, is characterized by the deficits in the cholinergic system and deposition of beta amyloid (Aβ) in the form of neurofibrillary tangles and amyloid plaques. Since the cholinergic system plays an important role in the regulation of learning and memory processes, it has been targetted for the design of anti-Alzheimer's drugs. Cholinesterase inhibitors enhance cholinergic transmission directly by inhibiting the enzyme acetylcholinesterase (AChE) which hydrolyses acetylcholine. Furthermore, it has been also demonstrated that both acetylcholinesterase and butrylcholinesterase (BuChE) play an important role in Aβ-aggregation during the early stages of senile plaque formation. Therefore, AChE and BuChE inhibition have been documented as critical targets for the effective management of AD by an increase in the availability of acetylcholine in the brain regions and decrease in the Aβ deposition. This review discusses the different classes of cholinesterase inhibitors including tacrine, donepezil, rivastigmine, galantamine, xanthostigmine, para-aminobenzoic acid, coumarin, flavonoid, and pyrrolo-isoxazole analogues developed for the treatment of AD. © 2013 The Pharmaceutical Society of Korea.

Randhawa P.K.,Punjabi University | Jaggi A.S.,Punjabi University
European Journal of Pharmacology | Year: 2015

Besides the involvement of TRPV channels in exhibiting various cellular functions including thermoregulation, pain perception, maintenance of bone homeostasis and gastrointestinal function; certain studies have also implicated the putative role of these channels in mediating ischemic conditioning-induced cardioprotection. The potential role of TRPV1 channels in different forms of ischemic conditioning (pre/post/remote)-induced cardioprotection has been described by employing TRPV1 knockout mice and various pharmacological modulators. The cardioprotective effects of TRPV1 activation during ischemic conditioning have been linked with increased CGRP, substance P release and augmented ALOX expression. Furthermore, the role of TRPV4 channels in mediating preconditioning-induced preservation of vascular function in terms restoring NO- and further improving EDH(F)-mediated endothelial relaxation has been described. The present review discusses the putative role of TRPV1 and TRPV4 channels in mediating different forms of conditioning (pre/post/remote)-induced cardioprotection along with the possible mechanisms. Future perspectives have also been described to fully understand the cascade of signaling and contribution of TRPV channel activation during myocardial ischemic conditioning. © 2014 Elsevier B.V. All rights reserved.

Bansal Y.,Punjabi University | Silakari O.,Punjabi University
Bioorganic and Medicinal Chemistry | Year: 2012

Presence of benzimidazole nucleus in numerous categories of therapeutic agents such as antimicrobials, antivirals, antiparasites, anticancer, anti-inflammatory, antioxidants, proton pump inhibitors, antihypertensives, anticoagulants, immunomodulators, hormone modulators, CNS stimulants as well as depressants, lipid level modulators, antidiabetics, etc. has made it an indispensable anchor for development of new therapeutic agents. Varied substitutents around the benzimidazole nucleus have provided a wide spectrum of biological activities. Importance of this nucleus in some activities like, Angiotensin I (AT1) receptor antagonism and proton-pump inhibition is reviewed separately in literature. Even some very short reviews on biological importance of this nucleus are also known in literature. However, owing to fast development of new drugs possessing benzimidazole nucleus many research reports are generated in short span of time. So, there is a need to couple the latest information with the earlier information to understand the current status of benzimidazole nucleus in medicinal chemistry research. In the present review, various derivatives of benzimidazole with different pharmacological activities are described on the basis of substitution pattern around the nucleus with an aim to help medicinal chemists for developing an SAR on benzimidazole derived compounds for each activity. This discussion will further help in the development of novel benzimidazole compounds. © 2012 Elsevier Ltd. All rights reserved.

Sharma N.,Punjabi University
Physical Review D - Particles, Fields, Gravitation and Cosmology | Year: 2010

Two-body hadronic weak decays of Bc meson involving tensor meson in the final state are studied by using the Isgur-Scora-Grinstein-Wise II model. Decay amplitudes are obtained using the factorization scheme in the spectator quark model. Branching ratios for the charm changing and bottom changing decay modes are predicted. © 2010 The American Physical Society.

In our previous study, the saponin-rich fraction (SRF) of adventitious root extract of Ficus religiosa L. (Moraceae) was shown to have an anticonvulsant effect in acute animal models of convulsions. The present study was envisaged to study the effect of SRF in the pentylenetetrazol (PTZ) kindling mouse model and its associated depression and cognition deficit. Treatment with the SRF (1, 2 and 4 mg/kg; i.p.) for 15 days in kindled mice significantly decreased seizure severity on days 5, 10 and 15 when challenged with PTZ (35 mg/kg; i.p.). Marked protection against kindling-associated depression was also observed on days 10 and 15 in the SRF-treated groups when tested using the tail-suspension test. However, the SRF treatment failed to protect kindling-associated learning and memory impairments in the passive shock avoidance paradigm. The observed behavioral effects were corroborated with modulation in the levels of noradrenaline, dopamine, serotonin, GABA and glutamate in discrete brain regions. Copyright © 2012 Elsevier Inc. All rights reserved.

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