Student Research

Faculty Advisors

Photo of Lawrence Dall, M.D.
Lawrence Dall, M.D.
Assistant Dean of Medical Student Research Clinical Professor of Medicine & Infectious DiseasesInternal Medicine
  • Medical School: Medical College of Wisconsin
  • Residency: Rutger Medical School
  • Fellowship: Hospitalist Leaders – University of California-San Francisco, Infectious Diseases – University of California-San Francisco
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Photo of Agostino Molteni, M.D., Ph.D., F.A.C.C.B.
Agostino Molteni, M.D., Ph.D., F.A.C.C.B.
Director of Student Research UMKC School of Medicine
  • Professor of Pathology & Pharmacology – UMKC School of Medicine
  • Professor Emeritus of Pathology – Northwestern University
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Research Interests

Dr. Molteni’s main research interest is the study of development of interstitial pulmonary fibrosis (IPF) in several models of experimental lung injury: exposure to radiation and hypoxia, administration of bleomycin and fat embolism syndrome. Also studied is the role played by the renin angiotensin system in the development of fibrosis and the antifibrotic protection of angiotensin converting inhibitors or angiotensin II receptor blockers.

His projects are conducted in cooperation with Dr. Betty Herndon (UMKC SOM); Dr. T. McIff, Dept. of Orthopedic Surgery and Dr. A. Poisner, Dept. of Pharmacology, University of Kansas Medical Center, Dr. B. Uhal, Dept. of Physiology, Michigan State University, Dr. R. Baybutt, Dept. of Health Sciences, Wheaton College, Wheaton, IL., Dr. G Van Den Heuvel, Dept. of Physiology, Eastern Michigan University, Kalamazoo, MI.

Research Career Development Award, National Institutes of Health, 1972
Albert E. Lasker Award, 1980, to NHLBI sharing as principal investigator, Central Laboratory Hypertension Detection and Follow-up Program
Meritorious Service Award, Chicago Heart Association,1982
Clinical Chemists Recognition Award, 1983

Recent research includes the evaluation of exenatide in a rodent model of non-alcoholic liver steatosis, and in particular, the drug’s effect on the pancreas and the thyroid of these animals. This study was performed in cooperation with Dr. Herndon, Dr. Laura Alba, and others of the Dept. of Medicine, in the UMKC SOM. An additional study is the evaluation of pulmonary and cardiac damage in a model of Cux-1 mice expressing the cyclin kinase inhibitors P21 and P27 (Drs Baybutt and Van Den Heuvel).

Selected Publications

Has published more than 200 articles and book chapters and more than 370 presentations at national and international scientific meetings.

Curcumin Effects on Hepatic Steatosis and Histopathology in an Obese Mouse Model. British Journal of Medicine and Medical Research: 5(8): 1017-1023, 2015. Article no BJMMP.2015.112

Fat Embolism sensitizes rats to a “second hit” with LPS: an animal model of Pulmonary Fibrosis: Journal of Trauma and Acute Surgical Care; 783:552-557, 2015

Fat Embolism Syndrome following caesarean section in an obese patient and it’s similarity to an animal model of the same syndrome: a case report. Case reports in Clinical Pathology: Published online 3-3-2015, D01110.5430/crcp.vnp

NF-KB controls Resistance of Human Salivary Gland (HSG) Cells to apoptosis in an in vitro model of Sjögren syndrome. Open Journal of Rheumatology and Auto immune Diseases (OJRA): Vol 4 #3; ID: 2040 128, 2014

Mitigating effect of Captopril and Losartan on Lung Histopathology in a rat model of Fat Embolism. The Journal of Trauma 70 (5):1186-1191; 2011

Biochemical and Histological Effects of Exendin 4 (exenatide) in the rat pancreas. Diabetologia53(1):153-159; 2010

“Persistent and progressive fibrotic changes in a model of fat embolism.” Journal of Trauma 72 (h) 992-998, 2012

“Dietary flaxseed oil protects against bleomycin-induced pulmonary fibrosis in rats.” Pulmonary Medicine, published on line, June 2012 10457031 doi 0.1155/2012/457031

“Urease and Helicobacter spp. Antigens in Pulmonary Granuloma” Journal of Comparative Pathology(2012)

“Effect of exendin (exenatide) on the thyroid and parathyroid gland in a rat model.” Eur. J., of Pharmacology 2012 

Photo of Paula Monaghan-Nichols, Ph.D.
Paula Monaghan-Nichols, Ph.D.
Associate Dean for Research, Chair and Professor Biomedical Sciences Biomedical Sciences Home M3-C02 Work Phone: (816) 235-6663
  • Trinity College, Dublin, Ireland, BA (Genetics)
  • Medical Research Council, Edinburgh, Scotland, Ph.D. (Genetic Engineering and Molecular Biology)
  • Medical Research Council, Human Genetics Unit, Edinburgh, Scotland, Post-Graduate (Molecular Genetics and Development)
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Research and Professional Experience

Postdoctoral Fellow/Research Associate, Molecular Biology of the Cell 1, German Cancer Research Centre, Heidelberg, Germany.

Assistant Professor, Department of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA

 Associate Professor, Department of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA

Research Interest

Molecular Genetic Analysis of the Developmental Basis of Neuropsychiatric Disorders

Research Summary

My laboratory focuses on understanding the molecular and developmental basis of emotional and cognitive behavior and psychiatric illness. The long-term goal of my research is to identify both intrinsic and environmental factors that specifically alter the development of areas in the brain that are essential for emotion and cognition.  My laboratory has identified a number of transcriptional repressors (Tlx, Sall1, Sall2, Sall3 and Sall4) that are expressed in the developing forebrain. This research has shown that these genes are express in stem and progenitor cells in the cerebral cortex, and are required to regulate the rate of stem/progenitor cell proliferation and neuronal differentiation.  Using both conditional and classical knockout experiments and in-utero electroporation studies in mice, my laboratory has shown that altering the levels of these proteins during development leads to emotional, behavioral and cognitive abnormalities in adult animals.  Our most recent studies focus on identifying the cellular and biochemical targets of glucocorticoid action on the developing brain in-utero. Synthetic glucocorticoids are administered to mothers at risk for pre-term labor, to stimulate lung maturation and to reduce the risk of intraventricular hemorrhage and necrotizing enterocolitis. Clinical follow up studies indicate that children exposed to steroid in-utero have cognitive abnormalities and an altered stress response. My laboratory is using a combination of molecular, cellular, proteomic, RNA-Seq. and genome wide DNase hypersensitive site mapping to identify the cellular targets of steroid action. These studies have shown that prenatal exposure to glucocorticoids leads to changes in neuronal number and density in the cerebral cortex at birth coupled to long-term alterations in neurite complexity in the prefrontal cortex and hippocampus in adolescents. These anatomical abnormalities are associated with changes in anxiety and depressive like behaviors in adults. Follow up studies include validating our identified targets in human brain and in umbilical cord blood cells.  These findings will for a framework for modifying current clinical dosing regiments in preterm labor to reduce the adverse consequences of premature exposure to corticosteroids in-utero.

Current Research Project(s)

This project examines the developmental basis of neurological abnormalities. Several approaches are used to investigate how environmental or genetic factors influence neural stem cell behavior and how perturbing these processes leads to anatomical and behavioral abnormalities. We are particularly interested in environmental factors that act in-utero such as steroid use, cannabinoids, hypothermia etc. Specific techniques include mouse transgenics, molecular and cellular biology, biochemistry, tissue culture, human umbilical cord blood cell, single nucleotide polymorphism, RNA seq and genetic databases.

Selected Publications

Research Resource: The Dexamethasone Transcriptome in Hypothalamic Embryonic Neural Stem Cells.Frahm KA, Peffer ME, Zhang JY, Luthra S, Chakka AB, Couger MB, Chandran UR, Monaghan AP, DeFranco DB. Mol Endocrinol. 2016 Jan;30(1):144-54.

Genome-wide transcript profiling reveals novel breast cancer-associated intronic sense RNAs.Kim SW, Fishilevich E, Arango-Argoty G, Lin Y, Liu G, Li Z, Monaghan AP, Nichols M, John B. PLoS One. 2015 Mar 23;10(3):e0120296..

Caveolin-1 regulates genomic action of the glucocorticoid receptor in neural stem cells.Peffer ME, Chandran UR, Luthra S, Volonte D, Galbiati F, Garabedian MJ, Monaghan AP, DeFranco DB. Mol Cell Biol. 2014 Jul;34(14):2611-23.

Wu P1, Teot L, Murdoch GH, Monaghan-Nichols P, McFadden K.  Neuropathology of 22q11 Deletion Syndrome in an Infant. Pediatr Dev Pathol. 2014 17(5):386-92.

An in-depth map of polyadenylation sites in cancer. Lin Y, Li Z, Ozsolak F, Kim SW, Arango-Argoty G, Liu TT, Tenenbaum SA, Bailey T, Monaghan AP, Milos PM, John B. Nucleic Acids Res. 2012 Sep 1;40(17):8460-71.

Sall1 regulates cortical neurogenesis and laminar fate specification in mice: implications for neural abnormalities in Townes-Brocks syndrome. Harrison SJ, Nishinakamura R, Jones KR, Monaghan AP. Dis Model Mech. 2012 May;5(3):351-65.

 Comprehensive polyadenylation site maps in yeast and human reveal pervasive alternative polyadenylation. Ozsolak F, Kapranov P, Foissac S, Kim SW, Fishilevich E, Monaghan AP, John B, Milos PM. Cell. 2010 Dec 10;143(6):1018-29. doi: 10.1016/j.cell.

New class of gene-termini-associated human RNAs suggests a novel RNA copying mechanism.Kapranov P, Ozsolak F, Kim SW, Foissac S, Lipson D, Hart C, Roels S, Borel C, Antonarakis SE, Monaghan AP, John B, Milos PM. Nature. 2010 Jul 29;466(7306):642-6. doi: 10.1038/nature09190.

Sall3 is required for the terminal maturation of olfactory glomerular interneurons.Harrison SJ, Parrish M, Monaghan AP. J Comp Neurol. 2008 Apr 10;507(5):1780-94.

Sall1 regulates mitral cell development and olfactory nerve extension in the developing olfactory bulb. Harrison SJ, Nishinakamura R, Monaghan AP. Cereb Cortex. 2008 Jul;18(7):1604-17.

Abnormal development of zinc-containing cortical circuits in the absence of the transcription factor Tailless. Land PW, Monaghan AP. Brain Res Dev Brain Res. 2005 Aug 8;158(1-2):97-101.

The Tlx gene regulates the timing of neurogenesis in the cortex. Roy K, Kuznicki K, Wu Q, Sun Z, Bock D, Schutz G, Vranich N, Monaghan AP. J Neurosci. 2004 Sep 22;24(38):8333-45.

Loss of the Sall3 gene leads to palate deficiency, abnormalities in cranial nerves, and perinatal lethality. Parrish M, Ott T, Lance-Jones C, Schuetz G, Schwaeger-Nickolenko A, Monaghan AP. Mol Cell Biol. 2004 Aug;24(16):7102-12.

Expression of the transcription factor, tailless, is required for formation of superficial cortical layers. Land PW, Monaghan AP. Cereb Cortex. 2003 Sep;13(9):921-31.

Loss of the tailless gene affects forebrain development and emotional behavior. Roy K, Thiels E, Monaghan AP. Physiol Behav. 2002 Dec;77(4-5):595-600.

A new member of the spalt like zinc finger protein family, Msal-3, is expressed in the CNS and sites of epithelial/mesenchymal interaction. Ott T, Parrish M, Bond K, Schwaeger-Nickolenko A, Monaghan AP.= Mech Dev. 2001 Mar;101(1-2):203-7.

Defective limbic system in mice lacking the tailless gene. Monaghan AP, Bock D, Gass P, Schwäger A, Wolfer DP, Lipp HP, Schütz G. Nature. 1997 Dec 4;390(6659):515-7.

Photo of Michael Wacker, Ph.D.
Michael Wacker, Ph.D.
Assistant Dean of Medical Student Research Associate Teaching Professor, Vice-chair Biomedical SciencePhysiology, Biomedical Sciences Work Phone: (816) 235-6069
  • University of Kansas – Ph.D. (2003)
  • Texas Christian University – B.S. (1997)
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Dr. Wacker joined the Department of Basic Medical Science in the School of Medicine in 2007. He currently teaches physiology in the Human Structure Function series taught to the medical school students, as well as physiology courses in the Anesthesiologist Assistant program and the Physician Assistant program. Dr. Wacker is a member of the Muscle Biology Group at UMKC with expertise in cardiac muscle physiology. The interests in his laboratory focus on agents that alter cardiac muscle function and calcium homeostasis in cardiac myocytes. Acutely, changes in calcium homeostasis can lead to arrhythmias and alteration of cardiac muscle contractility. More chronic alterations in calcium, however, can lead to remodeling of the heart as observed in cardiac hypertrophy and heart failure. Specifically, Dr. Wacker is interested in endocrine/paracrine agents which may directly alter calcium changes in cardiac myocytes via signaling mediated by membrane receptors. Recently, Dr. Wacker and the Muscle Biology Group have worked in collaboration with the UMKC Bone Biology Group on a NIH-funded project exploring mechanisms of bone-muscle crosstalk. Dr. Wacker’s laboratory has concentrated on a hormone, FGF23, released by bone cells that may play a role in directly altering cardiac function during chronic kidney disease. Additional interests in the laboratory focus on how thromboxane A2, intracellular phosphoinositide signaling, and fibrate drugs may directly alter cardiac muscle function.

Research Interests

My laboratory is interested in agents that alter cardiac muscle function and calcium homeostasis in cardiac myocytes. I am specifically interested in endocrine/paracrine agents which may directly alter cardiac function. One main area of focus currently in the lab is on hormones/toxins (e.g. FGF23) that are elevated during chronic kidney disease that may cause heart disease. Typical experiments in the lab center around measuring cardiac contractility/ function, Langendorf perfusion of isolated hearts, calcium imaging of cardiac myocytes, cardiac gene/protein changes, exploring cardiac myocyte signal transduction mechanisms like IP3 signaling, and blood vessel function.


Recent Publications

Gallagher PM, Touchberry CD, Teson K, McCabe E, Tehel M, Wacker MJ. Effects of an acute bout of resistance exercise on fiber-type specific GLUT4 and IGF-1R expression. Applied Physiology, Nutrition, and Metabolism. 38 (5): 581-586, 2013. PMID: 23668768

Touchberry CD, Green TM, Tchikrizov V, Mannix JE, Mao TF, Carney BW, Girgis M, Vincent RJ, Wetmore LA, Dawn B, Bonewald L, Stubbs JR, Wacker MJ. FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy. American Journal of Physiology: Endocrinology and Metabolism. 304 (8): E863-873. 2013. PMID: 23443925

Bonewald LF, Wacker MJ. FGF23 Production by Osteocytes. Pediatric Nephrology. 28 (4): 563-568. 2013. PMID: 22983423

Silswal N, Parelkar NK, Wacker MJ, Badr M, Andresen J.   PPARa-Independent Arterial Smooth Muscle Relaxant Effects of PPARa Agonists. PPAR Research. 302495. 2012. PMID: 23008696

Wacker MJ, Tevis O, Hanke J, Howard T, Gilbert W, Orr JA. Characterization of thromboxane A2 receptor and TRPV1 mRNA in cultured sensory neurons. Neuroscience Letters. 515(1):12-7. 2012. PMID: 22425716

Silswal N, Parelkar N, Wacker MJ, Brotto M, Andresen J. Phosphatidylinositol 3,5-bisphosphate increases intracellular free calcium in arterial smooth muscle cells and elicits vasocontraction. American Journal of Physiology: Heart and Circulatory Physiology. 300 (6): H2016-26. 2011. PMID: 21421826

Touchberry CD, Elmore CJ, Nguyen TM, Andresen JJ, Zhao X, Orange M, Weisleder N, Brotto M, Claycomb WC, Wacker MJ. Store-Operated Calcium Entry is Present in HL-1 Cardiomyocytes and Contributes to Resting Calcium. Biochemical and Biophysical Research Communications. 416 (1-2): 45-50. 2011. PMID: 22079292

Touchberry CD, Bales IK, Stone JK, Rohrberg TJ, Parelkar NK, Nguyen T, Fuentes O, Liu X, Qu CK, Andresen JJ, Valdivia HH, Brotto M, Wacker MJ. Phosphatidylinositol 3,5-Bisphosphate (PI(3,5)P2) Potentiates Cardiac Contractility Via Activation of the Ryanodine Receptor. Journal of Biological Chemistry. 285 (51): 40312-21. 2010. PMID: 20947503