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Sheng-Xing Ma, MD, PhD
Sheng-Xing Ma is a Professor and Director of Integrated Medicine Research Laboratories at Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center. He was recruited to UCLA as an Assistant Professor in 1996, and he received a promotion to Associate Professor in 2003 and Professor in 2008 in the Department of Obstetrics and Gynecology at UCLA David Geffen School of Medicine and Harbor-UCLA Medical Center. Dr. Ma has been engaged in the studies of nitrate pharmacology, biochemistry and physiological effects of nitric oxide (NO) for the past 20 years. He has demonstrated that nitroglycerin modifies neuronal excitability, increases norepinephrine release/synthesis in heart and brain, and stimulates noradrenergic activation in the posterior hypothalamus, which contributes to nitrate tolerance and central cardiovascular effects of the drug. Results from his group have found that NO mediates acupuncture-induced cardiovascular and analgesic effects through a novel pathway, the dorsal medullar-thalamic tract. Another novel discovery is that NO-cGMP related biomolecules contribute to biochemical physiological changes in acupoints associated with meridian practices and diseases. He has developed a painless, non-invasive device to biocapture NO, cGMP, and nitrotyrosine from skin surface of acupoints and meridians for studies of signal transduction molecules during physiological and pathological changes, and therapies such as acupuncture, moxibustion, and meditation/Qi Gon.
1124 West Carson Street Building RB-1, Room 208 Torrance CA 90502
Mark Mandelkern, MD, PhD
Juan Carlos Marvizon, PhD
Dr. Juan Carlos Marvizón is Assistant Professor at the Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at UCLA.Dr. Marvizón was born in 1957 in Rome, Italy. He majored in Biochemistry and Molecular Biology at the Autonomous University of Madrid (Spain). He received his Ph.D. in 1985 for his work on the glycine receptor at the Severo Ochoa Center of Molecular Biology in Madrid. During 1985, he worked as a research scientist at Pharmuka Laboratoires, a pharmaceutical company in Paris, France, investigating peripheral benzodiazepine receptors. He was then awarded a Fulbright Fellowship to work at the National Institutes of Health (NIH) in Bethesda, Maryland, where he studied the biochemistry of glycine and GABA receptors in relation to stress, and later became interested in NMDA receptors. From 1989 to 1991, he was faculty at the Autonomous University of Madrid (Spain). Prior to coming to UCLA, he was Research Assistant Professor at the University of Southern California, in Los Angeles, where he worked with Dr. Michel Baudry on the role of NMDA receptors in learning and memory. Dr. Marvizón came to UCLA in 1994. His current research focuses on the role of NMDA, substance P and opioid receptors in pain. He is the principal investigators of a grant from the NIH to study the release of substance P and opioids in the spinal cord.
Selected References:
Marvizon JCG, Grady EF, Stefani E, Bunnett NW, Mayer EA. Substance P release in the dorsal horn assessed by receptor internalization: NMDA receptors counteract a tonic inhibition by GABAB receptors. Eur. J. Neurosci. 11:417-426, 1999.
Marvizon JCG, Wang X, Matsuka Y, Neubert JK and Spigelman I. Relationship between capsaicin-evoked substance P release and NK1 receptor internalization in the rat dorsal horn. Neuroscience 118: 535-545, 2003.
Lao LJ., Song B and Marvizon JCG. Neurokinin release produced by capsaicin acting on the central terminals and axons of primary afferents: relationship with NMDA and GABAB receptors. Neuroscience 121: 667-680, 2003.
Song B and Marvizon JCG. Peptidases prevent m-opioid receptor internalization in dorsal horn neurons by endogenously released opioids. J. Neurosci. 23: 1847-1858, 2003.
Song B and Marvizón JCG. Dorsal horn neurons firing at high frequency, but not primary afferents, release opioid peptides that produce m-opioid receptor internalization in the rat spinal cord. J. Neurosci. 23: 9171-9184, 2003.
UCLA Department of Medicine Box 951792 Los Angeles CA 90095-1792
Emeran A. Mayer, MD
Emeran Mayer is the director of the G Oppenheimer Center for the Neurobiology of Stress and Resilience (CNSR) at UCLA and co-director of the P30 funded CURE Digestive Diseases Research Center at UCLA. The CNSR is a NIH-funded, interdisciplinary and translational research center focused on brain gut microbiome interactions in 4 areas: Functional GI Disorders, Inflammatory Bowel Disorders, Ingestive Behavior/Eating Disorders, Chronic Visceral Pain Disorders. Within the CNSR, he has been the PI of a P50 SCOR grant from ORWH/NIDDK on sex-related differences in brain gut interactions with an emphasis on the effects of early adverse life effects on adult stress responsiveness and related brain circuits for the past 15 years. This grant has been successfully renewed over a total of three 5 year funding cycles under hisleadership. He is also the Co-PI of a UO1 grant focused on studying mechanisms of chronic pelvic pain (MAPP), now in its third 5 year funding cycle, and he leads the neuroimaging efforts within the consortium. Under his leadership, CNSR investigators have done pioneering work in applying psychophysiological and advanced brain imaging techniques to study the response of the brain to visceral stimuli in rodent models and human subjects with persistent visceral pain disorders, including IBS, IBD, IC/PBS and vulvodynia, to identify sex related differences in these brain responses, and to evaluate the effectiveness of pharmacologic and mind-based (including cognitive behavioral therapy) therapeutic approaches to some of these disorders. During the last 5 years, they have expanded their research efforts into the role of the gut microbiome in bidirectional brain gut interactions. They have pursued studies looking at the effect of altered autonomic nervous system output to the gut in altering gut microbial composition and function, and have been testing the hypothesis that gut microbial metabolites and inflammatory mediators in vulnerable patients can lead to neuroplastic changes in the central nervous system manifesting in persistent visceral hypersensitivity, cognitive decline and symptoms of autism spectrum disorders.
Publications:
http://www.ncbi.nlm.nih.gov/sites/myncbi/emeran.mayer.1/bibliograpahy/40552943/public
10833 Le Conte Avenue Center for Health Sciences 42-210 Los Angeles CA 90095 United States
John Mazziotta, MD, PhD
Dr. John C. Mazziotta assumed the position of Vice Chancellor of UCLA Health Sciences and Dean of the David Geffen School of Medicine at UCLA on March 1, 2015. Dr. Mazziotta has been a member of the UCLA faculty since 1983. Before his appointment as Vice Chancellor and Dean, he served as Associate Vice Chancellor for health sciences and Executive Vice Dean of the school of medicine. Dr. Mazziotta also has been chair Department of Neurology and director of the Ahmanson-Lovelace Brain Mapping Center, of which he was the founder.
Dr. Mazziotta earned his MD and PhD in neuroanatomy and computer science from Georgetown University. Following an internship at Georgetown, he completed neurology and nuclear medicine training at UCLA.
Dr. Mazziotta has published more than 260 research papers and eight texts. He has received numerous awards and honors, including the Oldendorf Award from the American Society of Neuroimaging, the S. Weir Mitchell Award and the Wartenberg Prize of the American Academy of Neurology, and the Von Hevesy Prize from the International Society of Nuclear Medicine. Dr. Mazziotta also has been elected to the Institute of Medicine of the National Academy of Sciences and he is a member of the Royal College of Physicians.
Practice Location 300 UCLA Medical Plaza, Suite B200 Los Angeles CA 90095
John McDonald, MD
Dr. John McDonald received his M.D. from the University of Iowa in 1964. He completed internship at the University of Oregon in 1965. He completed an Ob/Gyn residency at the University of Iowa in 1968. He completed his second residency in Anesthesiology at the University of Washington in 1970.
His first academic position was at LAC/USC from 1970-1977 as Assistant Professor of Anesthesiology and Obstetrics and Gynecology. He co-founded the first neonatal intensive care unit at LAC/USC and was also director of anesthesiology and Respiratory Therapy at Women’s Hospital.
His second academic position was the University of Colorado as Professor and Vice Chairman of Anesthesiology and Professor of Obstetrics and Gynecology 1977-1978.
His third academic appointment was at The Ohio State University as Professor and Chairman of Anesthesiology and Professor of Obstetrics and Gynecology 1978-1998. He was also appointed as faculty at the Ohio Super-Computer Center 1988.
His fourth academic appointment is at Los Angeles where he is Professor and Chairman of Anesthesiology and Professor of Obstetrics and Gynecology both at Harbor-UCLA Medical Center and David Geffen School of Medicine at the University of California at Los Angeles.
Dr. McDonald was recruited by founder of the Ohio Supercomputer Center, Dr. Charlie Bender; who believed his presence as faculty would stimulate ideas from the medical viewpoint that would be fresh projects for research and development of new viewpoints of model formulation. This became reality within the next few years with the development of the model of “Virtual Reality Lumbar Epidural”. This provided Dr. McDonald and colleague Don Stredney’s development of an end product that later precipitated their receiving a Smithsonian Award at the 1966 annual Washington D.C. ceremony.
Recent research efforts have focused on development of a unique research group composed of a total of five M.D.s and Ph.D.s. Our work continues to be centered about the confocal scope with the academic focus on pain messaging systems of the rat pelvis bladder, uterus, and colon. Our group has published 4 peer review papers in the past five year period.
Our current focus is development of unraveling of the mystery of pain as it concerns the “intracellular mechanisms”. We believe some of the quandary of inconsistent relief of pelvic pain lies in this medium and we plan to continue our search for some means of understanding this enigmatic major pain problem.
Harbor/UCLA Medical Center, Department of Anesthesiology 1000 West Carson Street Torrance CA 90502
James McRoberts, PhD
Dr. McRoberts’ research focuses on the mechanisms involved in visceral pain, particularly that associated with the GI tract. He uses in vitro biological approaches to examine neurons and neurotransmission at the cellular and molecular level. He also examines behavioral responses to various visceral pain paradigms with an emphasis on stress modulation of pain perception. The specific goal of Dr. McRoberts’ project is to determine the role of peripheral N-methyl-D-aspartate-type glutamate receptors (NMDARs) expressed on extrinsic primary afferent nerves in visceral and somatic pain transmission and in the development of peripheral and central sensitization. Using various molecular techniques and whole cell patch clamp methodology, he has identified the NMDAR subunits expressed by different subtypes of dorsal root ganglia (DRG) neurons, characterized the functional and pharmacological properties of these receptors, identified their role in modulating afferent sensitivity to mechanical distension of the colon, demonstrated that NMDARs in DRG neurons regulate voltage-dependent calcium channels through PKC activation, and shown that colonic inflammation leads to persistent up-regulation in NMDAR channels with altered pharmacological properties . He has also developed mice with tissue specific knock out of NMDARs in DRG neurons and shown that these mice have diminished nociceptive responses during phase 2 of the formalin test, thus demonstrating that these receptors participate in the process of central sensitization. The long-term goal of this research is find better means to control pain of visceral origin in order to help patients with functional bowel diseases such as IBS.
Paul Micevych, PhD
The reproductive hormones estradiol and progesterone bathe our internal organs. They have profound influence over the central and peripheral nervous system. While these steroids have been studied for many years, recent advances indicate that many actions of estradiol in the nervous system are mediated by receptors located on the cell membrane, suggesting more of a neurotransmitter than a hormonal role. My lab is working to understand the multiple mechanisms and circuits through which estrogen and progesterone affect cell types in different systems to affect reproduction, behavior, pain transmission and neuroprotection.
Research efforts in the Micevych laboratory involve understanding the cellular and molecular events underlying estrogen action on neurons and glial cells. Estrogen has profound effects on cognitive function and neuroprotection, as well as, reproductive functions. Estrogen affects the expression and activity of various neuropeptides and sex steroids. In particular they have focused on regulation mu-opioid and nociceptin receptors in the CNS regulation of sexual behavior. Recent experiments have demonstrated the synthesis of progesterone in the brain, its regulation by estrogen and physiologic functions of neuroprogesterone. RT-PCR and calcium imaging experiments in neurons and astrocytes have been used to elucidate the mechanisms of estrogen rapid signaling in both glial cells and neurons. The Micevych laboratory has demonstrated that estrogen can modulate nociceptive signaling through rapid actions on primary sensory neurons demonstrating a novel mechanism of estrogen modulation of pain. Additionally, the Micevych Laboratory has been studying the neuroprotective action of estrogen in the nigrostriatal dopamine system. Estrogen activates the insulin-like growth factor-1 (IGF-1) to ameliorate a hallmark of ParkinsonA?s disease A? the neurodegeneration of dopamine neurons. Significantly, estrogen or IGF-1 is efficacious after either central or peripheral administration. Together these experiments underscore the broad range of estrogen signaling influencing both physiology and pathology.
Holly Middlekauff, MD
My research is focused on the derangements of the autonomic nervous system, especially the sympathetic nervous system, in humans with heart failure. I am currently studying the abnormal reflex responses to exercise in heart failure patients, and how these contribute to the overall exercise limitation in heart failure. We are testing the hypothesis that exaggerated sympatho-excitatory responses to exercise in heart failure are mediated by muscle mechanoreceptor sensory nerves, which have been sensitized by ischemic metabolites. A secondary focus of my research is on the effects of acupuncture on the autonomic nervous system.
200 UCLA Medical Plaza Suite C365 Los Angeles CA 90095
Million Mulugeta, DVM, PhD
Dr. Mulugeta focuses on the role of CRF2 receptors (CRF2R) in stress-related alteration of colonic function and visceral pain. His research program tests the hypothesis that CRFR2 activation modulates stress-related neuroenteric physiology, lower gut motor function alterations and stress-related visceral pain of colonic origin. Short term goals are 1) identification of enteric neuron, neuroendocrine and spinal cells expressing the CRF2R and its ligand/s and 2) understanding of the interaction of CRF2R and CRF1R activation during stress. Long-term goals include defining the cellular and molecular mechanisms involved in the coping response, homeostasis, of the gastrointestinal tract during stress.
Dr Mulugeta has published several papers on the brain-gut interaction and stress related gastrointestinal motility, pain and inflammatory responses. He serves as a peer-reviewer for numerous medical journals, and is on the editorial boards for the Digestive Diseases & Science and the World Journal of Gastroenterology. Dr Mulugeta is recipient of several awards including the 2011 International Foundation for Functional Gastrointestinal Disorders award in basic sciences. Dr Mulugeta’s research is supported by NIH and industry grants.