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Lisak, robert

Joyce A Benjamins, Liljana Nedelkoska, Robert P Lisak
ACTH, a melanocortin peptide used to treat multiple sclerosis (MS) relapses, acts by stimulating adrenal corticosteroid (CS) production via melanocortin receptor 2 (MC2R), but it may also exert a therapeutic effect independent of CS by stimulating other melanocortin receptors (MCR) distributed in many tissues, including the brain. We reported that oligodendroglia (OL) and oligodendroglial precursor cells (OPC) express MC4R, and that ACTH 1-39 protects OL and OPC in vitro from cell death induced by mechanisms likely involved in white matter damage in MS...
September 6, 2017: Journal of Neuroscience Research
Robert P Lisak, Joyce A Benjamins
The melanocortins and their receptors have been extensively investigated for their roles in the hypothalamo-pituitary-adrenal axis, but to a lesser extent in immune cells and in the nervous system outside the hypothalamic axis. This review discusses corticosteroid dependent and independent effects of melanocortins on the peripheral immune system, central nervous system (CNS) effects mediated through neuronal regulation of immune system function, and direct effects on endogenous cells in the CNS. We have focused on the expression and function of melanocortin receptors in oligodendroglia (OL), the myelin producing cells of the CNS, with the goal of identifying new therapeutic approaches to decrease CNS damage in multiple sclerosis as well as to promote repair...
August 14, 2017: Brain Sciences
Robert P Lisak, Liljana Nedelkoska, Joyce A Benjamins, Dana Schalk, Beverly Bealmear, Hanane Touil, Rui Li, Gillian Muirhead, Amit Bar-Or
B cells mediate multiple sclerosis (MS) pathogenesis by mechanisms unrelated to immunoglobulin (Ig). We reported that supernatants (Sup) from cultured B cells from blood of relapsing remitting MS (RRMS) patients, but not normal controls (NC), were cytotoxic to rat oligodendrocytes (OL). We now show that RRMS blood B cells, not stimulated in vitro, secrete factor/s toxic to rat and human neurons. Cytotoxicity is independent of Ig and multiple cytokines, not complement-mediated, and involves apoptosis. The factor/s have an apparent mw of >300kDa...
August 15, 2017: Journal of Neuroimmunology
Deepak K Kaushik, Heather Y F Yong, Jennifer N Hahn, Claudia Silva, Steven Casha, R John Hurlbert, Francois H Jacques, Robert Lisak, Omar Khan, Carolina Ionete, Catherine Larochelle, Alex Prat, Amit Bar-Or, V Wee Yong
Extracellular matrix metalloproteinase inducer (EMMPRIN, CD147) is an inducer of matrix metalloproteinases and has roles in leukocyte activation and migration. We reported previously that in MS and its animal model, experimental autoimmune encephalomyelitis, cell surface-associated EMMPRIN was significantly elevated in leukocytes around inflammatory perivascular cuffs in the CNS. In this study we report that activated T-cells can secrete soluble form of EMMPRIN (sEMMPRIN) upon activation. As sEMMPRIN is also present in biological fluids, we determined whether sEMMPRIN is altered in the CSF and sera of MS subjects...
2016: PloS One
Robert P Lisak, Suhayl Dhib-Jalbut
No abstract text is available yet for this article.
October 2016: Multiple Sclerosis: Clinical and Laboratory Research
Robert P Lisak
No abstract text is available yet for this article.
November 1, 2016: JAMA Neurology
Robert P Lisak, Beverly Bealmear, Joyce A Benjamins
Interferon-gamma (IFN-γ) upregulates major histocompatibility complex class II (MHC class II) antigens and intercellular adhesion molecule-1 (ICAM-1) on Schwann cells (SC) in vitro, but in nerves of animals and patients MHC class II is primarily expressed on inflammatory cells. We investigated whether SC maturation influences their expression. IFN-γ induced MHC class II and upregulated ICAM-1; the axolemma-like signal 8-bromo cyclic adenosine monophosphate (8 Br cAMP) with IFN-γ inhibited expression. Delaying addition of 8 Br cAMP to SC already exposed to IFN-γ inhibited ongoing expression; addition of IFN-γ to SC already exposed to 8 Br cAMP resulted in minimal expression...
June 15, 2016: Journal of Neuroimmunology
Elliot M Frohman, Olaf Stüve, Teresa C Frohman, Robert Lisak
No abstract text is available yet for this article.
April 2016: JAMA Neurology
Robert P Lisak, Liljana Nedelkoska, Joyce A Benjamins
Damage to myelin and oligodendroglia (OL) in multiple sclerosis (MS) results from a wide array of mechanisms including excitotoxicity, neuroinflammation and oxidative stress. We previously showed that ACTH 1-39, a melanocortin, protects OL in mixed glial cultures and enriched OL cultures, inhibiting OL death induced by staurosporine, ionotropic glutamate receptors, quinolinic acid or reactive oxygen species (ROS), but not nitric oxide (NO) or kynurenic acid. OL express melanocortin receptor 4 (MC4R), suggesting a direct protective effect of ACTH 1-39 on OL...
March 15, 2016: Journal of the Neurological Sciences
Robert P Lisak, Liljana Nedelkoska, Beverly Bealmear, Joyce A Benjamins
Patients with relapsing-remitting multiple sclerosis (RRMS) are commonly treated with high doses of intravenous corticosteroids (CS). ACTH 1-39, a member of the melanocortin family, stimulates production of CS by the adrenals, but melanocortin receptors are also found in the central nervous system (CNS) and on immune cells. ACTH is produced within the CNS and may have direct protective effects on glia and neurons independent of CS. We previously reported that ACTH 1-39 protected oligodendroglia (OL) and their progenitors (OPC) from a panel of excitotoxic and inflammation-related agents...
November 2015: Experimental Neurology
Dusanka S Skundric, William W Cruikshank, Paul C Montgomery, Robert P Lisak, Harley Y Tse
Cytokines are pleiotropic soluble mediators of cellular functions. Cytokines are critical in immune pathogenesis of human diseases, including autoimmune CD4(+) T cell mediated chronic inflammatory, demyelinating and neurodegenerative diseases of the central nervous system (CNS), multiple sclerosis (MS). In MS and its experimental model, experimental autoimmune encephalomyelitis (EAE), chronic persistence and/or reoccurrence of inflammation in the CNS causes chronic progressive or relapsing disease, accompanied with demyelination and damage to axons and oligodendrocytes, which ultimately leads to paralysis and disability...
October 2015: Cytokine
Robert P Lisak, Lisa Barcellos
No abstract text is available yet for this article.
April 2015: JAMA Neurology
(no author information available yet)
No abstract text is available yet for this article.
October 15, 2013: Journal of the Neurological Sciences
Joyce A Benjamins, Liljana Nedelkoska, Robert P Lisak
Oligodendroglia (OL) are highly susceptible to damage and, like neurons, are terminally differentiated. It is important to protect OL precursors (OPC) because they are reservoirs of differentiating cells capable of myelination following perinatal insult and remyelination in white matter diseases, including multiple sclerosis (MS). Patients with relapsing-remitting MS are commonly treated with high-dose corticosteroids (CS) when experiencing an exacerbation. Adrenocorticotropin hormone (ACTH), a primary component of another approved MS exacerbation treatment, is a melanocortin peptide that stimulates production of CS by the adrenals...
October 2014: Journal of Neuroscience Research
Michelle Figueroa, Yong Guo, Alexandros Tselis, Sean J Pittock, Vanda A Lennon, Claudia F Lucchinetti, Robert P Lisak
IMPORTANCE: Reports of neuromyelitis optica spectrum disorder (NMOSD) occurring in the setting of neoplasia suggest that aquaporin-4 autoimmunity may in some cases have a paraneoplastic basis. OBSERVATIONS: In this case report, we describe a patient with NMOSD whose test results were seropositive for aquaporin-4 IgG and who had a hepatic metastasis from a small-bowel neuroendocrine tumor. The tumor cells expressed aquaporin-4 immunoreactivity. She presented to the Neurology Department at Wayne State University with bilateral leg weakness, ascending paresthesias, and decreased sensation...
April 2014: JAMA Neurology
Bin Zhang, Chengyong Shen, Beverly Bealmear, Samia Ragheb, Wen-Cheng Xiong, Richard A Lewis, Robert P Lisak, Lin Mei
To determine if patients with myasthenia gravis (MG) have antibodies to agrin, a proteoglycan released by motor neurons and is critical for neuromuscular junction (NMJ) formation, we collected serum samples from 93 patients with MG with known status of antibodies to acetylcholine receptor (AChR), muscle specific kinase (MuSK) and lipoprotein-related 4 (LRP4) and samples from control subjects (healthy individuals and individuals with other diseases). Sera were assayed for antibodies to agrin. We found antibodies to agrin in 7 serum samples of MG patients...
2014: PloS One
Robert P Lisak, Liljana Nedelkoska, Joyce A Benjamins
Dextromethorphan (DM), a sigma receptor agonist and NMDA receptor antagonist, protects neurons from glutamate excitotoxicity, hypoxia and ischemia, and inhibits microglial activation, but its effects on differentiation and protection of cells in the oligodendroglial lineage are unknown. It is important to protect oligodendroglia (OL) to prevent demyelination and preserve axons, and to protect oligodendroglial progenitors (OPC) to optimize myelination during development and remyelination following damage. Enriched glial cultures from newborn rat brain were used 1-2 days or 6-8 days after shakeoff for OPC or mature OL...
May 2014: Glia
Stuart D Cook, Suhayl Dhib-Jalbut, Peter Dowling, Luca Durelli, Corey Ford, Gavin Giovannoni, June Halper, Colleen Harris, Joseph Herbert, David Li, John A Lincoln, Robert Lisak, Fred D Lublin, Claudia F Lucchinetti, Wayne Moore, Robert T Naismith, Carlos Oehninger, Jack Simon, Maria Pia Sormani
It has recently been suggested that the Lublin-Reingold clinical classification of multiple sclerosis (MS) be modified to include the use of magnetic resonance imaging (MRI). An international consensus conference sponsored by the Consortium of Multiple Sclerosis Centers (CMSC) was held from March 5 to 7, 2010, to review the available evidence on the need for such modification of the Lublin-Reingold criteria and whether the addition of MRI or other biomarkers might lead to a better understanding of MS pathophysiology and disease course over time...
2012: International Journal of MS Care
Robert P Lisak
No abstract text is available yet for this article.
January 14, 2014: Neurology
Richard A Lewis
Over the past 40 years Dr. Robert Lisak has made important contributions to our understanding of the pathophysiology and therapy of myasthenia gravis. This review will touch upon some of his work as it discusses current therapies and the potential for new treatments based on the evolving knowledge of the underlying basis of the disease. The recognition of different immune mechanisms that can cause the phenotype that we acknowledge as myasthenia gravis coincides with the introduction of monoclonal antibodies and other new therapies that can target specific aspects of the disease...
October 15, 2013: Journal of the Neurological Sciences
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