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  1. Home
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Browsing by Author "S. Patnaik"

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    PublicationConference Paper
    Antibodies to dynorphin A (1-17) attenuate closed head injury induced blood-brain barrier disruption, brain edema formation and brain pathology in the rat
    (Springer-Verlag Wien, 2009) H.S. Sharma; R. Patnaik; S. Patnaik; A. Sharma; S. Mohanty; P. Vannemreddy
    The potential neuroprotective efficacy of dynorphin A antiserum on BBB dysfunction, edema formation and brain pathology was examined in a closed head injury (CHI) model in the rat. The CHI was produced by an impact of 0.224 N on the right parietal bone under anesthesia by dropping a weight of 114.6 g on the skull from a height of 20 cm through a guide tube. This concussive brain injury resulted in profound BBB disruption as evidenced by leakage of Evans blue and radioiodine in the brain. Edema formation and swelling at 5 h were most pronounced in the contralateral cerebral hemisphere. Pretreatment with dynorphin A antiserum (1:20, monoclonal) infused into the left lateral cerebral ventricle (30 μL in PBS) either 30 min before or 30 min after CHI significantly attenuated BBB dysfunction, brain edema formation, volume swelling and brain pathology. However, no reduction in brain edema, BBB permeability or improved brain pathology was seen when the antiserum was given 60 min post-CHI. These observations are the first to suggest that antiserum to dynorphin when administered into the CSF during early phase of CHI is neuroprotective. Our work further indicates that dynorphin is actively involved in the cellular and molecular mechanisms of edema formation and BBB breakdown in CHI. © 2009 Springer-Verlag Vienna.
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    Antibodies to serotonin attenuate closed head injury induced blood-brain barrier disruption and brain pathology
    (Blackwell Publishing Inc., 2007) H.S. Sharma; R. Patnaik; S. Patnaik; S. Mohanty; A. Sharma; P. Vannemreddy
    Closed head injury (CHI) often results in profound brain swelling and instant death of the victims due to compression of the vital centers. However, the neurochemical basis of edema formation in CHI is still obscure. Previous studies from our laboratory show that blockade of serotonin synthesis prior to CHI in a rat model attenuates brain edema, indicating a prominent role for serotonin in head injury. Thus, neutralization of endogenous serotonin activity and/or blocking of its receptors will induce neuroprotection in CHI. Since serotonin has more than 14 receptors and selective serotonin antagonists are still not available, we used serotonin antiserum to neutralize its in vivo effects before or after CHI in a rat model. CHI was produced by an impact of 0.224 N on the right parietal skull bone under Equithesin anesthesia by dropping a weight of 114.6 g from a height of 20 cm through a guide tube. This concussive brain injury resulted in blood-brain barrier (BBB) disruption, brain edema formation, and volume swelling at 5 h that were most pronounced in the contralateral cerebral hemisphere. The plasma and brain serotonin levels were increased several-fold at this time. Intracerebroventricular administration of serotonin antiserum (1:20, monoclonal) into the left lateral cerebral ventricle (30 μL in PBS) 30 min before or 30 min (but not 60 min) after CHI significantly attenuated BBB disruption, brain edema formation, volume swelling, and brain pathology. The plasma and brain serotonin levels continued to remain high. These observations are the first to suggest that antiserum to serotonin when administered into the CSF during the early phase of CHI are capable of inducing neuroprotection. © 2007 New York Academy of Sciences.
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    PublicationArticle
    Antimicrobial assay and genetic screening of selected freshwater Cyanobacteria and identification of a biomolecule dihydro-2H-pyran-2-one derivative
    (2017) A. Srivastava; V.K. Singh; S. Patnaik; J. Tripathi; P. Singh; G. Nath; R.K. Asthana
    Aims: Explorations of freshwater Cyanobacteria as antimicrobial (bacteria, fungi and methicillin-resistant Staphylococcus aureus (MRSA) strains) drug resource using bioassay, NRPS (non-ribosomal polypeptide synthetase) and PKS (polyketide synthase) genes, as well as in silico approach. Methods and Results: We have bioassayed the extracts of Phormidium CCC727, Geitlerinema CCC728, Arthrospira CCC729, Leptolyngbya CCC732, Phormidium CCC730, Phormidium CCC731 against six pathogenic bacteria comprising Gram (+ve): S. aureus including seven clinical MRSA and Enterococcus faecalis, Gram (−ve): Escherichia coli, Salmonella Typhimurium, Klebsiella pneumoniae and Shigella boydii along with non-pathogenic Enterobacter aerogenes as well as fungal strains (Cryptococcus neoformans and Candida albicans, C. krusei, C. tropicalis and Aspergillus niger) exhibiting antimicrobial potential. The NRPS and PKS genes of the target strains were also amplified and sequenced. The putative protein structures were predicted using bioinformatics approach. Conclusion: PKS gene expression indicated β keto-acyl synthase as one of the important active domains in the biomolecules related to antitumour and antifungal group. The simultaneous identification of the biomolecule (dihydro-2H-pyran-2-one derivative) was also inferred spectroscopically. Significance and Impact of the Study: Freshwater Cyanobacteria are prolific producers of secondary metabolite(s) that may act as the antimicrobial drug resource in addition to their much explored marine counterpart. © 2016 The Society for Applied Microbiology
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    Effect of dilution of both A-and B-sites on the multiferroic properties of spinal Mott insulators
    (Institute of Physics Publishing, 2015) Prashant Shahi; Rahul K. Singh; Rajesh K. Singh; Shiv Kumar; A. Tiwari; A. Tripathi; J. Saha; S. Patnaik; A.K. Ghosh; Sandip Chatterjee
    The structural, magnetic, electrical and transport properties of FeV2O4, by doping Li and Cr ions in A and B sites, respectively, have been studied. Dilution of the A site by Li doping decreases the V-V distances which in effect increases the A-V coupling. This increased coupling enhances the ferrimagnetic ordering temperature and reduces the ferroelectric transition temperature. Furthermore, since Li is non-magnetic the A-V coupling is also decreased. The increase in A-V coupling dominates over the decrease in A-V coupling with Li doping. On the other hand, Cr doping increases the ferrimagnetic ordering temperature but does not alter the ferroelectric transition temperature, which is due to the fact that the polarization originates from the presence of almost non-substituted regions. © 2015 IOP Publishing Ltd.
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    Hidden transition in multiferroic and magnetodielectric CuCrO2 evidenced by ac-susceptibility
    (Institute of Physics Publishing, 2017) Kaushak K. Shukla; Arkadeb Pal; Abhishek Singh; Rahul Singh; J. Saha; A.K. Sinha; A.K. Ghosh; S. Patnaik; A.M. Awasthi; Sandip Chatterjee
    Ferroelectric polarization, magnetic-field dependence of the dielectric constant and ac and dc magnetizations of frustrated CuCrO2 have been measured. A new spin freezing transition below 32 K is observed which is thermally driven. The nature of the spin freezing is to be a single-ion process. Dilution by the replacements of Cr ions by magnetic Mn ions showed suppression of the spin freezing transition suggesting it to be fundamentally a single-ion freezing process. The observed freezing, which is seemingly associated to geometrical spin frustration, represents a novel form of magnetic glassy behavior. © CopyrightEPLA, 2017.
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    Histamine receptors influence blood-spinal cord barrier permeability, edema formation, and spinal cord blood flow following trauma to the rat spinal cord
    (Springer-Verlag Wien, 2006) H.S. Sharma; P. Vannemreddy; R. Patnaik; S. Patnaik; S. Mohanty
    The role of histamine in edema formation, blood-spinal cord barrier (BSCB) permeability, and spinal cord blood flow (SCBF) following spinal cord injury (SCI) was examined using modulation of histamine H1, H2, and H3 receptors in the rat. Focal trauma to the spinal cord at the T10-11 level significantly increased spinal cord edema formation, BSCB permeability to protein tracers and SCBF reduction in the T9 and T12 segments. Pretreatment with histamine H1 receptor antagonist mepyramine (1 mg, 5 mg, and 10 mg/kg, i.p.) did not attenuate spinal pathophysiology following SCI. Blockade of histamine H2 receptors with cimetidine or ranitidine (1 mg, 5 mg, or 10 mg/kg 30 minutes before injury) significantly reduced early pathophysiological events in a dose dependent manner. The effects of ranitidine were far superior to cimetidine in identical doses. Pretreatment with a histamine H3 receptor agonist α-methylhistamine (1 mg and 2 mg/kg/i.p.), that inhibits histamine synthesis and release in the CNS, thwarted edema formation, BSCB breakdown, and SCBF disturbances after SCI. The lowest dose of histamine H3 agonist was most effective. Blockade of histamine H3 receptors with thioperamide (1 mg, 5 mg/kg, i.p.) exacerbated spinal cord pathology. These observations suggest that stimulation of histamine H3 receptors and blockade of histamine H2 receptors is neuroprotective in SCI. © 2006 Springer-Verlag.
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    Zinc protoporphyrin IX attenuates closed head injury-induced edema formation, blood-brain barrier disruption, and serotonin levels in the rat
    (Springer-Verlag Wien, 2006) P. Vannemreddy; A.K. Ray; R. Patnaik; S. Patnaik; S. Mohanty; H.S. Sharma
    The role of heme oxygenase (HO) in closed head injury (CHI) was examined using a potent HO and guanylyl cyclase inhibitor, zinc protoporphyrin (Zn-PP) in the rat. Blood-brain barrier (BBB) permeability to Evans blue and radioiodine, edema formation, and plasma and brain levels of serotonin were measured in control, CHI, and Zn-PP-treated CHI rats. CHI was produced by an impact of 0.224 N on the right parietal bone by dropping 114.6 g weight from a height of 20 cm in anesthetized rats. This concussive injury resulted in edema formation and brain swelling 5 hours after insult that was most pronounced in the contralateral hemisphere. The whole brain was edematous and remained in a semi-fluid state. Microvascular permeability disturbances to protein tracers were prominent in both cerebral hemispheres and the underlying cerebral structures. Plasma and brain serotonin showed pronounced increases and correlated with edema formation. Pretreatment with Zn-PP (10 mg/ kg, i.p) 30 minutes before or after CHI attenuated edema formation, brain swelling, plasma and brain serotonin levels, and microvascular permeability at 5 hours. Brain edema, BBB permeability, and serotonin levels were not attenuated when the compound was administered 60 minutes post-CHI suggesting that HO is involved in cellular and molecular mechanisms of edema formation and BBB breakdown early after CHI. © 2006 Springer-Verlag.
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