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Faculty
K.J.S. ('Sunny') Anand , MBBS, D.Phil.
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Title
Dr. Anand has moved his laboratory to the University of Tennessee Health Science Center in Memphis, TN. Click to find his new address.
Medical School
M.B.B.S., Mahatma Gandhi Memorial Medical College, University of Indore, Indore, India
PhD
D.Phil., Jesus College, University of Oxford, UK; F.A.A.P., American Academy of Pediatrics, Elk Grove Village IL
Residency
Research Fellow, University Department of Paediatrics, University of Oxford, Oxford, U.K.;
Research Fellow in Anesthesia, Harvard Medical School, Boston, MA;
Clinical Fellow in Pediatrics, Harvard Medical School, Boston, MA
Fellowship
Clinical Fellow, Neonatal and Pediatric Intensive Care Units, Massachusetts General Hospital, Boston, Massachusetts
Post Doctoral Training
Intern, Maharaja Yeshwantrao Hospital, Indore, India; Intern, Hindu Rao
Board Certification(s)
1981, Registered Medical Practitioner, Madhya Pradesh Board, Bhopal, India; 1991, Board Certification in Pediatrics, American Board of Pediatrics; 1994, Board Certification in Pediatric Critical Care, American Board of Pediatrics; 1997, Arkansas State Medical Board, Little Rock, Arkansas
Major Interests
Neurobiology and behavioral effects of neonatal pain.
Research Interests
Dr. Anand's research interests are focused on mechanisms of cell death during critical periods for human or rodent brain development, primarily including:
(a) NMDA receptor-mediated excitotoxicity resulting from repetitive pain and (b) enhanced naturally occurring neuronal apoptosis during early development due to maternal separation. The pattern and magnitude of cellular changes depend on genetic variability as well as the timing, intensity, and duration of adverse environmental experiences:
1. Diverse developmental inputs during infancy cause activation and increased cell death in specific areas during the first postnatal week. These data suggest that early enrichment may allow the increased survival of neurons during cortical development.
2. Acute pain causes uncoupling of opioid receptors in the forebrain, leading to a decreased tonic inhibition of foci associated with pain processing in the brain-stem and spinal cord. This novel mechanism explains why tissue injury leads to prolonged periods of hyperalgesia.
3. Inflammatory pain occurring in the right forelimb leads to the bilateral activation of somatosensory and other cortical areas, as well as multiple foci in the limbic system, thalamus, and hypothalamus. Supraspinal pain processing shifts from subcortical areas in rat pups to cortical areas by two weeks after birth. Near-infra red spectroscopy in the human neonate showed similar patterns with bilateral activation of the somatosensory cortex following a unilateral painful stimulus (venipuncture).
4. Inflammatory pain increases neurodegenerative changes in newborn rat pups with specific regional changes noted in the first week after birth. Thus, repetitive pain may explain the poor cognitive outcomes of ex-preterm children.
5. Pre-emptive continuous morphine analgesia does not alter the incidence of early intraventricular hemorrhage or periventricular leukomalacia, but intermittent morphine boluses may increase the vulnerability of preterm neonates to develop these lesions.
Thus, converging lines of investigation, including clinical studies and basic neuroscience research, are focused on investigating the role and mechanisms of neuronal cell death caused by repetitive or prolonged pain. These changes may help to explain the behavioral abnormalities and poor cognitive outcomes noted from follow-up studies of ex-preterm neonates during their childhood and adolescence.
Email: kanand@utmem.edu
Address: K.J.S. Anand, MBBS, D. Phil., FAAP, FCCM, FRCPCH.
Division Chief of Pediatric Critical Care Medicine
University of Tennessee at Memphis
Department of Pediatrics
50 North Dunlap St.
Memphis, TN 38103
Phone: 901-287-6132
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| Selected Publications |
| 1. Anand KJS, Hall RW. Love, pain, and neonatal care. Pediatrics (in press), 2008. 2. Hall RW, Wallace T, Anand KJS, Skinner RM, Garcia-Rill E. Long-term deficits of preterm birth: Evidence for arousal and attentional disturbances. Clinical Neurophysiology (in press), 2008. 3. Stroud MH, Moss MM, Prodhan P, Anand KJS. Application of the Golden Hour to pediatric transport. Pediatric Critical Care Medicine (in press), 2008. 4. Meert KL, Eggly S, Pollack M, Anand KJS, et al., and the NICHD CPCCRN Network. Parents’ perspectives on physician-parent communication near the time of a child’s death in the pediatric intensive care unit. Pediatric Critical Care Medicine 9(1): 2–7, 2008. 5. Anand KJS, Garg S, Rovnaghi CR, Narsinghani U, Bhutta AT, Hall RW. Ketamine reduces the cell death following inflammatory pain in newborn rat brain. Pediatric Research 62(3): 283-290, 2007. 6. Anand KJS. Anesthetic neurotoxicity in newborns: Should we change clinical practice? Anesthesiology 107(1): 2-4, 2007. 7. Bhutta AT, Venkatesan AK, Rovnaghi CR, Anand KJS. Anaesthetic neurotoxicity in rodents: is the Ketamine controversy real? Acta Paediatrica 96(11): 1553-1555, 2007. 8. Anand KJS. Consciousness, cortical function, and pain perception in non-verbal humans. Behavioral & Brain Sciences, 30: 82-83, 2007. 9. Meert KL, Eggly S, Pollack M, Anand KJS, Zimmerman J, Carcillo J, Newth CJ, Dean JM, Willson DF, Nicholson C; NICHD Collaborative Pediatric Critical Care Research Network.. Parents' perspectives regarding a physician-parent conference after their child's death in the pediatric intensive care unit. Journal of Pediatrics, 151(1): 50-55, 55.e1-2, 2007. 10. Anand KJS. Pain assessment in preterm neonates. Pediatrics, 119(3): 605-7, 2007. |
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