LEVENTE KAPÁS, MD, PhD
- PhD in theoretical medicine, Albert Szent-Györgyi Medical and Pharmaceutical Center,Faculty of Medicine, University of Szeged, Hungary
- MD, summa cum laude, Albert Szent-Györgyi Medical and Pharmaceutical Center,Faculty of Medicine, University of Szeged, Hungary
Dr. Levente Kapás is an associate professor and researcher affiliated with the medical education program at WSU Spokane and the Neuroscience Graduate Program. He also gives lectures about the nervous system, sleep and gut-brain communication.
Kapás graduated from medical school in his native Hungary, where he started his research career. In 1989, Kapás started his postdoctoral training at the University of Tennessee, Memphis. In 1996, he established his independent research at Fordham University in New York City before coming to Spokane in 2009. Dr Kapás research interest is the regulation of sleep, body temperature and feeding. He focuses on the role of systemic, peripheral signals in sleep regulation and mechanisms that integrate metabolic and immune signals with core sleep circuits of the brain.
Szentirmai, É., N.S. Millican, A. R. Massie, and L. Kapás. Butyrate, a metabolite of intestinal bacteria, enhances sleep. Scientific Reports, 9:7035. doi: 10.1038/s41598-019-43502-1, 2019.
Szentirmai, É. and L. Kapás. Sleep and body temperature in TNFα knockout mice: the effects of sleep deprivation, β3-AR stimulation and exogenous TNFα, Brain Behav. Immun. doi: 10.1016/j.bbi.2019.06.022, 2019.
Szentirmai, É. and L. Kapás. Nicotinic acid promotes sleep through prostaglandin synthesis in mice. Scientific Reports, 9:17084. doi: 10.1038/s41598-019-53648-7, 2019.
Szentirmai, É. and L. Kapás. Brown adipose tissue plays a central role in systemic inflammation-induced sleep responses. PLOS One. 13(5): e0197409, doi: 10.1371/journal.pone.0197409, 2018.
Massie, A., E. Boland, L. Kapás, and É Szentirmai. Mice lacking alternatively activated (M2) macrophages show impairments in restorative sleep after sleep loss and in cold environment. Scientific Reports, 8:8625. doi: 10.1038/s41598-018-26758-x, 2018.
Szentirmai, É. and L. Kapás. Interactive regulation of sleep and feeding. In: Kryger, M. H. (Ed.), Atlas of Clinical Sleep Medicine, Philadelphia: Saunders Elsevier, 2nd Edition, 2014, pp. 56–58.
Szentirmai, É. and L. Kapás. Ghrelin and sleep regulation. In: Portelli, J. and Smolders, I. (Eds.), Central Function of Ghrelin Receptors, The Receptors 25, New York, NY: Springer, 2014, pp. 153–165.
Szentirmai, É., L. Kapás, Y. Sun, R.G. Smith, and J.M. Krueger. The preproghrelin gene is required for normal integration of thermoregulation and sleep in mice. Proc. Natl. Acad. Sci. USA, 106:14069–14074, 2009.
Kapás, L., S. G. Bohnet, J. A. Majde, É. Szentirmai, P. Magrath, P. Taishi and J. M. Krueger. Spontaneous and influenza virus–induced sleep are altered in TNF–α double–receptor deficient mice. J. Appl. Physiol., 105:1187–1198, 2008.
Kapás, L. and É. Szentirmai. Sleep regulatory factors. In: Monti, J., Sinton, C. and Pandi-Perumal, S.R. (Eds.), The Neurochemistry of Sleep and Wakefulness. Cambridge University Press, UK, 2008, pp. 315-336.
Ribeiro, A.C. and L. Kapás. The effects of intracerebroventricular application of 8-Br-cGMP and LY-83,583, a guanylyl cyclase inhibitor, on sleep–wake activity in rats. Brain Res., 1049:25-33, 2005.
Shemyakin, A. and L. Kapás. L-364,718, a cholecystokinin-A receptor antagonist, suppresses feeding-induced sleep in rats. Am. J. Physiol., 280:R1420-R1426, 2001.
Kapás, L., M. K. Hansen, H.–Y. Chang, and J. M. Krueger. Vagotomy attenuates but does not prevent the somnogenic and febrile effects of lipopolysaccharide in rats, Am. J. Physiol., 274: R406–R411, 1998.
Kapás, L., M. Shibata, M. Kimura, and J.M. Krueger. Inhibition of nitric oxide synthesis suppresses sleep in rabbits. Am. J. Physiol. 266: R151-157, 1994.
Kapás, L., F. Obál, Jr., P. Alföldi, G. Rubicsek, B. Penke, and F. Obál. Effects of nocturnal intraperitoneal administration of cholecystokinin in rats: simultaneous increase in sleep, increase in EEG slow–wave activity, reduction of motor activity, suppression of eating, and decrease in brain temperature. Brain Res. 438: 155–164, 1988.