Search Results - "Ajaib, S"

Synergistic activity of interleukin-17 and tumor necrosis factor-α enhances oxidative stress-mediated oligodendrocyte apoptosis by Paintlia, Manjeet K, Paintlia, Ajaib S, Singh, Avtar K, Singh, Inderjit

“…J. Neurochem. (2011) 116, 508-521. ABSTRACT: Th1 cytokine-induced loss of oligodendrocytes (OLs) is associated with axonal loss in CNS demyelinating diseases…”
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AMP-Activated Protein Kinase Signaling Protects Oligodendrocytes that Restore Central Nervous System Functions in an Experimental Autoimmune Encephalomyelitis Model by Paintlia, Ajaib S, Paintlia, Manjeet K, Mohan, Sarumathi, Singh, Avtar K, Singh, Inderjit

“…AMP-activated protein kinase (AMPK) signaling is reported to protect neurons under pathologic conditions; however, its effect on oligodendrocytes (OLs) remains…”
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Modulation of Rho-Rock signaling pathway protects oligodendrocytes against cytokine toxicity via PPAR-[alpha]-dependent mechanism by Paintlia, Ajaib S, Paintlia, Manjeet K, Singh, Avtar K, Singh, Inderjit

“…We earlier documented that lovastatin (LOV)-mediated inhibition of small Rho GTPases activity protects vulnerable oligodendrocytes (OLs) in mixed glial cell…”
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Modulation of Rho-Rock signaling pathway protects oligodendrocytes against cytokine toxicity via PPAR-α-dependent mechanism by Paintlia, Ajaib S., Paintlia, Manjeet K., Singh, Avtar K., Singh, Inderjit

“…We earlier documented that lovastatin (LOV)‐mediated inhibition of small Rho GTPases activity protects vulnerable oligodendrocytes (OLs) in mixed glial cell…”
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S-Nitrosoglutathione Induces Ciliary Neurotrophic Factor Expression in Astrocytes, Which Has Implications to Protect the Central Nervous System under Pathological Conditions by Paintlia, Manjeet K., Paintlia, Ajaib S., Singh, Avtar K., Singh, Inderjit

“…Accumulating evidence suggests that reactive astrogliosis has beneficial and detrimental outcomes in various CNS disorders, but the mechanism behind this…”
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Lipopolysaccharide-induced peroxisomal dysfunction exacerbates cerebral white matter injury: Attenuation by N-acetyl cysteine by Paintlia, Manjeet K., Paintlia, Ajaib S., Contreras, Miguel A., Singh, Inderjit, Singh, Avtar K.

“…Cerebral white matter injury during prenatal maternal infection characterized as periventricular leukomalacia is the main substrate for cerebral palsy (CP) in…”
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Differential CpG DNA methylation in peripheral naïve CD4 + T-cells in early rheumatoid arthritis patients by Pitaksalee, R, Burska, A N, Ajaib, S, Rogers, J, Parmar, R, Mydlova, K, Xie, X, Droop, A, Nijjar, J S, Chambers, P, Emery, P, Hodgett, R, McInnes, I B, Ponchel, F

“…The genetic risk associated with rheumatoid arthritis (RA) includes genes regulating DNA methylation, one of the hallmarks of epigenetic re-programing, as well…”
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N-acetylcysteine prevents endotoxin-induced degeneration of oligodendrocyte progenitors and hypomyelination in developing rat brain by Paintlia, Manjeet K., Paintlia, Ajaib S., Barbosa, Ernest, Singh, Inderjit, Singh, Avtar K.

“…Periventricular leukomalacia (PVL), the dominant form of brain injury in premature infants, is characterized by diffuse white matter injury and is associated…”
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Activation of PPAR-γ and PTEN cascade participates in lovastatin-mediated accelerated differentiation of oligodendrocyte progenitor cells by Paintlia, Ajaib S., Paintlia, Manjeet K., Singh, Avtar K., Orak, John K., Singh, Inderjit

“…Previously, we and others documented that statins including‐lovastatin (LOV) promote the differentiation of oligodendrocyte progenitor cells (OPCs) and…”
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HMG-CoA reductase inhibitor augments survival and differentiation of oligodendrocyte progenitors in animal model of multiple sclerosis by Paintlia, Ajaib S, Paintlia, Manjeet K, Khan, Mushfiquddin, Vollmer, Timothy, Singh, Avtar K, Singh, Inderjit

“…Impaired remyelination due to degeneration of both postmitotic oligodendrocytes and oligodendrocyte progenitors (OPs) is the major hallmark of inflammatory…”
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IL-4-Induced Peroxisome Proliferator-Activated Receptor γ Activation Inhibits NF-κB Trans Activation in Central Nervous System (CNS) Glial Cells and Protects Oligodendrocyte Progenitors under Neuroinflammatory Disease Conditions: Implication for CNS-Demyelinating Diseases by Paintlia, Ajaib S., Paintlia, Manjeet K., Singh, Inderjit, Singh, Avtar K.

“…Th2 phenotype cytokine, IL-4, plays an important role in the regulation of Th1 cell responses and spontaneous remission of inflammatory CNS demyelinating…”
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Combination therapy of lovastatin and rolipram provides neuroprotection and promotes neurorepair in inflammatory demyelination model of multiple sclerosis by Paintlia, Ajaib S., Paintlia, Manjeet K., Singh, Inderjit, Skoff, Robert B., Singh, Avtar K.

“…Drug combination therapies for central nervous system (CNS) demyelinating diseases including multiple sclerosis (MS) are gaining momentum over monotherapy…”
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Attenuation of Lipopolysaccharide-Induced Inflammatory Response and Phospholipids Metabolism at the Feto-Maternal Interface by N-Acetyl Cysteine by Paintlia, Manjeet K, Paintlia, Ajaib S, Singh, Avtar K, Singh, Inderjit

“…Maternal microbial infections cause adverse fetal developmental outcomes including embryonic resorption, intrauterine fetal death, and preterm labor. Recent…”
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Combined medication of lovastatin with rolipram suppresses severity of experimental autoimmune encephalomyelitis by Paintlia, Ajaib S., Paintlia, Manjeet K., Singh, Inderjit, Singh, Avtar K.

“…Combinations of new medications or existing therapies are gaining momentum over monotherapy to treat central nervous system (CNS) demyelinating diseases…”
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A Systematic Approach To Decipher the Microstructure of Methyl Hydrosiloxane Copolymers and Its Impact on Their Reactivity Trends by Saxena, Anubhav, Markanday, Meghna, Sarkar, Alok, Yadav, Vinod K, Brar, Ajaib S

“…A thorough comprehensive microstructure analysis of poly(dimethylsiloxane-co-hydromethylsiloxane) copolymers (PDMS-co-PHMS) was achieved using high resolution…”
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Immunomodulatory Effect of Combination Therapy with Lovastatin and 5-Aminoimidazole-4-Carboxamide-1-β- d-Ribofuranoside Alleviates Neurodegeneration in Experimental Autoimmune Encephalomyelitis by Paintlia, Ajaib S., Paintlia, Manjeet K., Singh, Inderjit, Singh, Avtar K.

“…Combination therapy with multiple sclerosis (MS) therapeutics is gaining momentum over monotherapy for improving MS. Lovastatin, an HMG-CoA reductase inhibitor…”
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Modulation of peroxisome proliferator-activated receptor-α activity by N-acetyl cysteine attenuates inhibition of oligodendrocyte development in lipopolysaccharide stimulated mixed glial cultures by Paintlia, Manjeet K, Paintlia, Ajaib S, Khan, Mushfiquddin, Singh, Inderjit, Singh, Avtar K

“…Glial cells secrete proinflammatory mediators in the brain in response to exogenous stimuli such as infection and injury. Previously, we documented that…”
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Increased Plp1 gene expression leads to massive microglial cell activation and inflammation throughout the brain by Tatar, Carrie L, Appikatla, Sunita, Bessert, Denise A, Paintlia, Ajaib S, Singh, Inderjit, Skoff, Robert P

“…PMD (Pelizaeus-Merzbacher disease) is a rare neurodegenerative disorder that impairs motor and cognitive functions and is associated with a shortened lifespan…”
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Interference with RhoA–ROCK Signaling Mechanism in Autoreactive CD4+ T Cells Enhances the Bioavailability of 1,25-Dihydroxyvitamin D3 in Experimental Autoimmune Encephalomyelitis by Paintlia, Ajaib S, Paintlia, Manjeet K, Hollis, Bruce W, Singh, Avtar K, Singh, Inderjit

“…Vitamin D deficiency is a major risk factor for central nervous system (CNS) demyelinating diseases including multiple sclerosis (MS) and its animal model,…”
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Impaired peroxisomal function in the central nervous system with inflammatory disease of experimental autoimmune encephalomyelitis animals and protection by lovastatin treatment by Singh, Inderjit, Paintlia, Ajaib S., Khan, Mushfiquddin, Stanislaus, Romesh, Paintlia, Manjeet K., Haq, Ehtishamul, Singh, Avtar K., Contreras, Miguel A.

“…Peroxisomes are ubiquitous subcellular organelles and abnormality in their biogenesis and specific gene defects leads to fatal demyelinating disorders. We…”
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