Assistant Professor
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 4255
Office Phone: 513-558-8679
chellakn@ucmail.uc.edu

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Description of Research:
Dr. Chella Krishnan's major research focus is to understand the role of sex differences and mitochondrial (dys)function in the pathophysiology of non-alcoholic fatty liver disease (NAFLD).

One of the major complications of obesity affecting the liver, in the absence of alcohol, is NAFLD. It is estimated that 20-30% of the population worldwide are affected by NAFLD and is more prevalent in men than women, with men exhibiting severe NAFLD symptoms. Work in the K Lab is focused on understanding how host genetic background and sex differences influence the mitochondrial (dys)function and increases the susceptibility to NAFLD, and other cardiometabolic diseases such as obesity and diabetes.

The approaches we use include

1. a population-based ‘systems genetics' approach to integrate information on natural genetic variations (host genetics) with molecular phenotypes (such as gene expression, proteomics, etc.) and clinical phenotypes, with a targeted focus on sex differences and mitochondria, to identify candidate genes
2. characterizing the candidate genes in genetically modified mouse models and/or eukaryotic cell lines
3. characterizing the mitochondrial functions using a Seahorse Bioanalyzer
4. characterizing the molecular functions using RNA-Sequencing and Single Cell Genomics.

Keywords: mitochondria, sex differences, metabolism, metabolic diseases, system genetics, population genetics, fatty liver disease, obesity, atherosclerosis, hypercholesterolemia, cardiovascular diseases

Professor
Dept of Pharmacology, Physiology, and Neurobiology
Cardiovascular Research Center 5939
Office Phone: 513-558-1392
k.drosatos@uc.edu

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Description of Research:
Our research investigates transcriptional regulation mechanisms that link cardiac stress with altered myocardial fatty acid and glucose metabolism. Our long-term goal pertains to the application of interventions that can improve cardiac function by modulating fatty acid oxidation and energy production.

We are interested in the role of Kruppel-like factors (KLFs) and particularly, KLF5 and its role in the regulation of cardiac fatty acid oxidation during diabetes, myocardial ischemia, ischemia/reperfusion and aging. We also investigate the role of cardiomyocyte KLF5 in regulating systemic metabolism via an undiscovered cross-talk mechanism between the heart and the adipose tissue.

Furthermore, we study the role of the cellular energetic machinery in the alleviation of cardiomyopathy in sepsis.

Keywords: metabolism, heart failure, systems biology, diabetes, ischemia, sepsis

Professor
Dept of Pharmacology, Physiology, and Neurobiology
Cardiovascular Research Center 5923
Office Phone: 513-558-2340
fangg@ucmail.uc.edu

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Description of Research: 
Our group investigates the molecular and cellular mechanisms underlying stress- and disease-induced cardiovascular remodeling. More specifically, our work focuses on macrophage function in ischemia/reperfusion-triggered heart failure, sepsis-caused cardiovascular leakage, diabetes-induced microvascular rarefaction and cardiac dysfunction. The lab uses in vivo transgenic and knockout animal models as well as in vitro primary cell culture to identify and validate novel therapeutic targets in cardiovascular disease. In addition, multiple state-of-art techniques (i.e., adenovirus-mediated gene transfer, single-cell/bulk RNA sequencing, cell sorting, flow cytometry, Co-IP, co-immunostaining, and bioinformatics) are employed to analyze the associated molecular/cellular mechanisms.

Among possible lines of investigations, we chose to focus primarily on macrophage-associated proteins (i.e., Sectm1a, Lcn10)  and extracellular membrane vesicles (collected from mammalian cells or gut bacteria) in the regulation of macrophage phagocytosis, efferocytosis and polarization, endothelial permeability and cardiac contractile function, because both acute and long-term inflammation are major culprits to cardiovascular disease.

Keywords: cardiac inflammation, myocardial ischemia-reperfusion injury, vascular leakage, sepsis-induced cardiomyopathy, efferocytosis, macrophage phagocytosis, cardiac protection, cell death, endothelial cells, cardiovascular disease

Assistant Professor
Dept of Pharmacology, Physiology, and Neurobiology
Cardiovascular Research Center 5935
Office Phone: 513-558-2562
gaoc3@ucmail.uc.edu

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Description of Research:
The Gao Lab is focused on uncovering novel molecular mechanisms for the pathogenesis of cardiac diseases, including cardiac hypertrophy, remodeling, and dysfunction.  The lab utilizes state-of-the-art molecular, genomic, and genetic tools to discover and interrogate key molecules involved in the understudied post-transcriptional processes in RNA metabolism in cardiac tissues under physiological and pathological states.  Ultimately, the lab aims to develop novel therapeutic and diagnostic strategies for heart failure and cardiometabolic diseases.

Keywords: cardiovascular disease, RNA metabolism, mouse models, molecular biology, cardiometabolic disorder, branched-chain amino acid, high-throughput sequencing, RNA splicing, RNA degradation

Professor
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 4204
Office Phone: 513-558-3115
Heinyja@ucmail.uc.edu

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Description of Research:
Our laboratory conducts basic research on muscle physiology at the molecular and cellular levels. Recent research projects have focused on:

• The physiological roles and regulation of the Na, K-ATPase α isoforms in skeletal muscle
• Development of new technologies, based on Inductively Coupled Plasma-Mass Spectroscopy (ICP-MS) for measuring ion and nutrient transport in biological samples, including cultured cells, skeletal muscle single fibers and intact muscles
• Klf2, in the inflammatory response to injury

Our current research focuses on the question: How do contracting skeletal muscles take up glucose by a mechanism that does not require insulin? This study is motivated by the fact that contraction-induced glucose uptake, which does not require insulin, can exceed insulin-dependent glucose uptake by 50- to 100-fold and, therefore, is critical for maintaining glucose homeostasis in disorders of insulin-dependent glucose uptake (diabetes).  These studies represent an ongoing collaboration between my laboratory and the laboratory of Dr. Julio Landero-Figuero, Dept. of Chemistry, Univ. of Cincinnati.

We use a range of experimental approaches to address this question, including:  in vitro measurement of glucose uptake in isolated contracting mouse skeletal muscles of WT and TG mice; simultaneous measurement of multiple ions (K/Rb, Ca, Na, et al.) and carbon-based molecules (13C-glucose et al.) that are potentially co-transported during contraction; and immunohistochemistry assays and functional measurements of muscle force in situ and in vivo.

Keywords: skeletal muscle, K-ATPase, gastrocnemius muscle, injury, mice, muscle injury, K-ATPase α1, cell function, dihydropyridine receptor, knockout mice

Departmental Chair & Professor
Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 5259/ Reading Campus, Building A-145 
Office Phone: 513-558-5636
hermanjs@ucmail.uc.edu

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Description of Research:
My major research interests explore structural, functional and molecular biological principles underlying stress integration, with an emphasis on delineating mechanisms linking stress with mental illness and cognitive disorders. The organismal ‘stress response’ represents an integrated physiological process whose primary goal is to redistribute energy to meet a real or perceived challenge.  As a consequence, stress engages a variety of physiological and neural processes with the ultimate objective of achieving optimal survival value, including the hypothalamo-pituitary-adrenocortical axis, the autonomic nervous system, and brain stress regulatory pathways that coordinate the behavior of the organism to fit desired outcomes. While initially adaptive, prolonged stress causes aberrant neuroplastic events in brain that have a long-term negative impact on physiology and behavior. My research is geared toward understanding the mechanisms underlying initiation of these neuroplastic events and their consequences on the individual. We have developed chronic stress paradigms that model physiological, metabolic and behavioral symptoms of depression (e.g., glucocorticoid dyshomeostasis; helplessness; anhedonia; cardiovascular pathology; visceral obesity) and PTSD (late-emerging, long-lasting potentiation of conditioned fear; late-emerging metabolic pathologies). We exploit these models to discover neurocircuit mechanisms mediating the deleterious effects of stress on neuroplasticity and behavior, focusing on corticolimbic pathways. Our work employs a broad spectrum of methods, including region/tissue-specific knockout in mice and rats; viral vector gene knockdown/ overexpression/CRISPR to modify gene expression in discrete brain regions; chemogenetic/optogenetic methods to modify brain activation in a site and projection specific manner; genomic approaches to understanding gene and epigenetic (microRNA) expression patterns in identified cell populations; mathematical modeling and bioinformatics; and state-of-the-art neuroanatomical approaches.

Keywords: stress neurobiology, behavioral neuroscience, CNS neurocircuitry: signaling mechanisms, prefrontal cortex, neurobiology of disease, computational neuroscience, multi-omics, neuropharmacology, neurophysiology, stress and cardiovascular disease

Assistant Professor - Educator
Dept of Pharmacology, Physiology, and Neurobiology
Medical Science Building 4203
Office Phone: 513-558-4159
katie.hobbing@uc.edu

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Graduate Director: 
Applied Pharmacology & Drug Toxicology Master's Degree Program

Interim Graduate Director: 
Special Master's Program (SMP) in Physiology

Keywords: educator, pharmacology, physiology, safety pharmacology, drug toxicology, drug development, career development, graduate education 

Associate Professor
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 4201
Office Phone: 513-558-5093
hongca@ucmail.uc.edu

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Description of Research:
Our long-term goal is to utilize temporal information from the circadian clock and its connections with other cellular processes (e.g. cell cycle, metabolism, etc.) to improve human health. Circadian rhythms are periodic physiological events that recur about every 24 hours. Disruption of circadian rhythms exacerbate progression of numerous diseases ranging from metabolic disorders to cancer. Despite the critical importance of circadian rhythms in human disease progression and treatments, roles of circadian rhythms in complex human diseases remain largely unknown. To achieve our goal, we seek to understand molecular mechanisms of circadian rhythms and their interconnected network with other cellular processes such as cell cycle, DNA damage response, and metabolism in order to design novel therapeutic regimens. These complex biological modules are intertwined by molecular components that communicate and adapt to various external environments to optimize the survival of an organism. We employ mathematical modeling to navigate complex dynamics of molecular networks, and use genetics and molecular biology to validate model-driven hypotheses.

Keywords: circadian clock, metabolism, cell cycle, DNA damage response, mathematical modeling, organoids, fungi, small intestine

Professor
Dept of Pharmacology, Physiology, and Neurobiology
Cardiovascular Research Center 5926
Office Phone: 513-558-2353
kirleytl@ucmail.uc.edu

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Description of Research:

Our research involves the following:

• Antibody Utilization, Characterization, Fragmentation, and Structure.
• Purinergic Signaling, Extracellular Nucleotides and Nucleotidases.
• Enzyme Analysis and Structure, Enzyme Inhibitors.
• Protein Expression and Refolding, Protein Engineering.
• Cysteine and Disulfide Chemistry and Analysis.
• Ligand Binding Techniques and Applications.

Keywords: pharmacology, anti-cocaine antibody, binding thermodynamics, ligand binding, pharmacokinetics, protein

Professor
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 4259
Office Phone: 513-558-3097
lorenzjn@ucmail.uc.edu

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Description of Research:
My research has two facets.  First, I am director of the Murine Physiology Core Facility in the University of Cincinnati College of Medicine.  The facility is dedicated to the functional analysis of cardiovascular and renal phenotypes in mutant mice and rats. We employ a wide variety of approaches to interrogate the effects of genetic modifications in mice including acute in vivo and ex vivo diagnostic techniques as well as chronic models of cardiac hypertrophy, ischemic injury and systemic hypertension. This facility is well recognized and heavily utilized by investigators at the University of Cincinnati and elsewhere.

Second, my lab is currently engaged in research to examine the autonomic cardiovascular effects of traumatic brain injury (TBI).  The ANS governs homeostatic control over different organs in the body, and is comprised of sympathetic and the parasympathetic pathways working in concert with the endocrine system to regulate cardiac, renal, adrenal, homoeothermic, and enteric function.  Autonomic dysfunction can occur when there is an imbalance in the regulation or function of the parasympathetic and sympathetic pathways, resulting in cardiovascular dysfunction and failure.  Thus, the overall goal of these studies is to examine the effects of TBI on the autonomic control of cardiovascular and renal function.

Keywords: cardiovascular physiology, small animal and organ physiology, functional assessment in genetic mouse models, cardiac muscle function, regulation of blood pressure, renal function, telemetric measurement of ECG/blood pressure, autonomic control, traumatic brain injury, baroreceptor function

Professor
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 4257A
Office Phone: 513-558-3627
mackenb@ucmail.uc.edu

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Description of Research:
Our research program is focused on the molecular physiology of iron transporters and their roles in iron homeostasis and iron disorders.

Keywords: iron transport, iron homeostasis, molecular physiology, membrane transport, intestinal iron absorption, iron disorders, Xenopus oocyte expression system, genetically modified mouse models, structure-function, voltage clamp

Associate Professor
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 4200
Office Phone: 513-558-0667
maclenaj@ucmail.uc.edu

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Keywords: neurophysiology, motor neuron, ciliary neurotrophic factor, CNTF, mouse model, nerve lesion

Assistant Professor
Dept. of Pharmacology, Physiology, and Neurobiology
Reading Campus, Building A-141
Office Phone: 513-558-6893
mcreynje@ucmail.uc.edu

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Description of Research:
Our lab studies how stress facilitates or exacerbates pathological brain states and behavior, such as substance use disorder. While acute, mild stress can be beneficial for cognition and behavior, traumatic and chronic stress have deleterious effects and influence the development or severity of many neuropsychiatric disorders. This is why our lab is focused on understanding how stress can increase vulnerability in the development or severity of substance use disorders using rodent pre-clinical models of drug self-administration. We are interested in understanding how repeated stress can drive drug use and increase susceptibility for drug-seeking behavior in abstinent animals. We are focusing on the circuit-specific cellular and synaptic mechanisms that underlie this influence of stress on addiction-related behaviors. We investigate these research questions on multiple levels using complex behavioral models, such as drug self-administration, viral-mediated chemogenetic approaches, pharmacological manipulations, molecular and biochemical techniques, and neuroimaging of in vivo calcium and neurotransmitter biosensors using fiber photometry.

Keywords: neuroscience, stress, substance use disorder, addiction, mouse models, neuropsychiatric disorders

Professor
Dept of Pharmacology, Physiology, Neurobiology
Cardiovascular Research Center 5938
Office Phone: 513-558-6654
normanab@ucmail.uc.edu

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Description of Research:
The focus of the Norman Laboratory is translational research to develop medications for the treatment of cocaine abuse.

Drug self-administration by animals is a valid model of human addictive behavior. It has long been considered axiomatic that drugs of abuse are self-administered because of their pleasurable (hedonic or euphoric) effects, which in turn makes these drugs positively reinforcing. Unfortunately, these assumptions result in well-known paradoxes and the idea that reinforcement plays any significant role in maintained self-administration behavior is of limited utility.

The Norman laboratory has developed a quantitative pharmacological theory of self-administration behavior in which cocaine-induced responding occurs only while drug concentrations are within a specific range. The core of our model of the maintenance phase of drug self-administration is the equation: T=ln(1+DU/DST)·t1/2/ln2, which defines the inter-injection intervals (T) in terms of only three parameters: the unit dose of cocaine (DU), the elimination half-life of cocaine (t1/2) and the satiety threshold (DST). This latter parameter is defined as the highest concentration of drug at which self-administration occurs. This simple model is the first to successfully define a seemingly complex behavior in terms of purely physical parameters.

This pharmacological paradigm represents a scientifically rigorous foundation for generating testable hypotheses about the biological basis of addictive behavior.  More importantly, it provides a rational basis for the development of medications for drug addiction. To this end an active collaboration with Dr. Jim Ball has developed a human anti-cocaine monoclonal antibody as a pharmacokinetic antagonist of cocaine, which is intended as an immunotherapy to prevent relapse in cocaine abusers.

The Norman lab is also using drug self-administration behavior as a bioassay system to measure the absolute pharmacodynamic and pharmacokinetic potencies of receptor antagonists as a basis for developing antagonist based pharmacotherapies.

Keywords: pharmacology, cocaine disorder, addiction, satiety threshold, self-administration behavior, anti-cocaine antibody

Associate Professor
Dept of Pharmacology, Physiology, and Neurobiology
Reading Campus, Building A-123
Office Phone: 513-558-8658
pereztdo@ucmail.uc.edu

    
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Description of Research:
Our laboratory focuses on understanding the mechanisms involved in the neuroendocrine control of energy balance. We investigate how afferent endocrine signals, such as GLP-1, ghrelin and leptin, interact with neural circuits, specifically the melanocortin system, to regulate metabolism, and how those interactions are influenced by nutrient and environmental status. We also work on identifying the specific efferent mechanisms whereby those neural circuits in the brain control metabolism in peripheral tissues. Our technical approach is focused in the in vivo and ex vivo analysis of glucose and lipid metabolism, energy intake and energy expenditure in rodent models.  In addition, we collaborate with the pharmaceutical industry to develop new therapies to treat obesity and diabetes.

Keywords: physiology, metabolism, energy balance, neuroendocrinology, melanocortin system, obesity, diabetes, ghrelin

Professor
Dept of Pharmacology, Physiology, Neurobiology
Reading Campus, Building A-129
Office Phone: 513-558-4338
reyesta@ucmail.uc.edu

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Description of Research:
Dr. Teresa Reyes examines the effects of early-life adversity on behavior and cognition in mice, with a focus neural-immune interactions. Current projects in the lab investigate (1) the mechanism by which chemotherapy leads to cognitive deficits in survivors of childhood leukemia, (2) how maternal opioid use affects cognition and behavior in exposed offspring, and (3) how diet shapes brain development. Advanced operant testing is used to assess executive function (e.g., attention, impulsive behavior, cognitive flexibility) and the lab is also interested in examination of sex differences.

Keywords: neuroscience, neurodevelopment, behavior, cognition, mouse model, neuron-glia interactions, transcriptomics, adverse early life, sex differences

Professor
Dept of Pharmacology, Physiology, and Neurobiology
Reading Campus, Building A-133
Office Phone: 513-558-5129
sahr@ucmail.uc.edu

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Description of Research:
The Sah laboratory is interested in understanding mechanisms that promote vulnerability to psychiatric disorders. We are focusing on threat and fear associated conditions such as posttraumatic stress disorder (PTSD) and panic disorder (PD). The prevalence of these disorders is on the rise due to an increase in life traumas ranging from combat to COVID.

As humans, we consistently encounter traumatic experiences, some of which may signal a threat to survival. Fear, a normal adaptive response to threat can become maladaptive in certain individuals resulting in abnormal threat detection and persistent fear memories promoting symptoms of panic and PTSD. We are interested in finding out “what” promotes abnormal fear regulation and “why” some individuals have deficits in processing fear. We use translationally relevant rodent models and translational approaches aligned with the National Institute of Mental Health RDoC criteria (https://www.nimh.nih.gov/research/research-funded-by-nimh/rdoc/about-rdoc). Although our research is fear-centered, we also investigate stress, anxiety, learning-memory and depression relevant behaviors in our models.

In the past several years the Sah group has made several seminal discoveries on novel target proteins and mechanisms that signal threat sensing and generation of fear. We established the relevance of stress resiliency neuropeptides in PTSD as well as an unprecedented role of immune signaling in panic genesis. Over the years, our lab focus has moved from being “brain-centric” to appreciating the “body and the brain”. A primary interest centers on understanding how peripheral signals can regulate threat responding and fear. As an example, we are trying to understand how chronic inflammation associated with asthma can regulate fear processing to other traumatic experiences. We are also exploring specialized brain areas located near the ventricles in body-to-brain signaling of threat and fear generation.

The immediate goals for these projects are to a) understand fear genesis to both external triggers as well as homeostatic “within the body” signals, b) identify novel targets that regulate fear learning and memory of relevance to PTSD and PD, and c) understand pre-trauma predisposition factors that promote susceptibility to psychiatric illness. The long-term goal is to identify novel and effective therapeutic targets and predictive biomarkers for PTSD and PD.

If you are interested in our research, please contact us (sahr@uc.edu). We welcome motivated, curious, and hard-working individuals in our group!

Keywords: PTSD, panic disorder, abnormal fear, stress resiliency neuropeptides, neuroendocrinology, body-to-brain signaling, rodent models

Associate Professor
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 5157
Office Phone: 513-558-9754
schuljo@ucmail.uc.edu

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Graduate Director: Molecular, Cellular, & Biochemical Pharmacology PhD Degree Program and System Biology and Physiology PhD Degree Program

Description of Research: 
The interests of my research program are to elucidate the signaling mechanisms involved in cardiac pathophysiology, especially in relation to cardioprotection (heart protecting itself against injury due to ischemia) and heart failure. Our approach involves the utilization of transgenic and gene-targeted mice with pertubations of specific receptors, endogenous factors, and signal transduction cascades in the heart. This allows us to relate changes in the action of single gene products with specific alterations of cardiac biochemistry, physiology and pathophysiology in vivo. Both in vivo and in vitro physiological approaches are utilized in my lab to elucidate the contribution of the opioid and growth factor receptor systems to cardiac pathophysiology. We routinely employ echocardiography, work-performing and Langendorff whole heart preparations, in vivo hemodynamic measurements, and isolation and analysis of cardiomyocytes. In addition, a number of surgical techniques (aortic banding, coronary artery ligation, catheterizations) are used in my laboratory. Throughout these studies, pharmacological, histological, biochemical, and state-of-the art molecular biology assays are employed, and include PCR for mouse genotype determination, Northern blot and quantitative real-time PCR analysis of mRNA expression, and protein analysis via Western blot, ELISA and immunostaining. Genomic and proteomic tools, including DNA microarrays, will be implemented in the lab to further characterize or identify known and novel mechanism(s) of opioid- and growth factor-mediated cardiovascular physiology and pathology.

Keywords: cardiovascular, growth factors, opioids and opiates, ischemia, vascular growth, heart failure

Assistant Professor
Dept of Pharmacology, Physiology, and Neurobiology
Reading Campus, Building A-143
Office Phone: 513-558-2709
timmens@ucmail.uc.edu

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Description of Research:
Research in our laboratory is focused on understanding the neural computations underlying decision-making and how they malfunction. Specifically, we are most interested in understanding the causes of aversion-resistant alcohol drinking and finding treatments for this key component of alcohol use disorder (AUD, “alcoholism”). People who suffer from AUD frequently drink alcohol despite negative consequences. Our lab seeks to identify and repair alterations in the neural circuits that govern the decision to drink which produce this behavior.

In pursuit of these goals, we employ pre-clinical rodent models and in vivo electrophysiology to examine neural computations during decision-making. We also utilize advanced data analysis techniques, including machine learning and computational models to analyze the data. We also utilize optogenetic and chemogenetic techniques to modify neural behavior.

In the future, we will expand our studies to include the roll stress plays in aversion-resistant drinking, we will examine other types of addiction (both addictions with (e.g., opioids) and without (e.g., gambling) exogenous pharmacological elements), and we will pursue more advanced computational modelling approaches to improve treatment predictions.

Keywords: prefrontal cortex, alcohol drinking, alcohol use disorder, medial prefrontal cortex, neural activity, aversion-resistant drinking, brain regions, cortex, information theory, negative consequences

Professor 
Dept of Pharmacology, Physiology, and Neurobiology
Reading Campus, Building A-143
Office Phone: 513-558-6118
ulrichym@ucmail.uc.edu

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Description of Research:
Our research goal is to identify the neural and hormonal substrates that are responsible for the interactions among diet, obesity, and stress. Obesity is a major health problem affecting 30% of adults in the United States. Despite public health efforts to combat obesity, it continues to rapidly increase in incidence, along with obesity-related diseases and health costs. Similarly, stress-related psychiatric disorders, including depression and anxiety, affect large segments of the population and place a substantial toll on patients, families, and communities. Notably, there is a high co-morbidity between obesity/metabolic disorders and stress-related psychiatric disorders, supporting the idea that there are complex interactions among stress, obesity, and diet. For instance, stress generally increases the intake of palatable ‘comfort’ foods (which can promote obesity), and the ingestion of these foods improves mood and decreases emotional and behavioral responses to stress. However, the mechanisms underlying these interactions among are unknown, and this knowledge is needed to identify novel therapeutic targets for the prevention and treatment of obesity, as well as other stress-related disorders.

Keywords: behavior, stress, obesity, diet, reward, brain, hormones, metabolism, neural circuits, corticosterone

Professor
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 5151A
Office Phone: 513-558-2379
wanghs@ucmail.uc.edu

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Description of Research:
Our lab studies the cardiovascular system. We are interested in how normal cardiac physiology is governed by various cardiac ion channels, and how cardiac electrical properties are altered in disease conditions or by environmental chemicals. In particular, we are interested in how a group of environmental chemicals called “endocrine disrupting chemicals” may alter the normal electrical and mechanical properties of the heart. Our past studies systematically examined the impact of a common environmental chemical, bisphenol A or BPA, and its related analogs, on the heart, and showed that these chemicals can increase the risk of cardiac arrythmias. Further, we elucidated the signaling, receptor, molecular and pharmacokinetic mechanisms underlying the actions of these chemicals. Currently we are examining the cardiovascular toxicity of a broader range of environmental chemicals using animals models, human stem cell-derived cardiac myocytes, and human cohort biosamples. We also study cardiac ion channels and cardiac electrical properties. A current focus is how a type of proton channels contributes to acid extrusion and pH regulation in the heart.

Keywords: cardiovascular system, ion channels, bisphenol A, arrythmias, cardiac myocytes, pH regulation

Associate Professor
Dept of Pharmacology, Physiology, and Neurobiology
Reading Campus, Building A-121
Office Phone: 513-558-6870
wohlebes@ucmail.uc.edu

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Description of Research:
Our research group studies how neuroimmune systems shape synaptic function and behavior in pathological and physiological conditions. To this end, we use multi-disciplinary approaches, including flow cytometry and cell sorting, cell type-specific molecular analyses (RNA-Seq), viral-mediated genetic and pharmacological manipulations, and imaging techniques to study pathways mediating neuro-immune interactions.

We strive for scientific excellence and integrity; and we value a supportive work environment that fosters provocative ideas and collective efforts to achieve goals.

Keywords: microglia, neuroplasticity, stress, psychoneuroimmunology, DNA breaks, neuropharmacology, electrophysiology, glia

Professor - Educator
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 4251
Office Phone: 513-558-6489
worrelrt@ucmail.uc.edu

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Graduate Director: Systems Biology and Physiology PhD Degree Program

Description of Research:
My research focuses on understanding the factors influencing epithelial transport, particularly in the GI track.

Keywords: physiology, epithelium, transport, Ussing chamber, chloride, educator, mucus, intestine

Associate Professor                                      
Dept of Pharmacology, Physiology, and Neurobiology
Medical Sciences Building 4260
Office Phone: 513-558-6156
zhangtl@ucmail.uc.edu

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Description of Research:
Cells, working machines in our body, respond to environmental signals (e.g. food, hormone, and infection, etc.) and make critical decisions such as proliferation, differentiation, defense, or even death.

The decision makings of cells are carried out by their molecular control networks. Although no single molecule is directing the cellular behaviors by itself, the dynamical properties emerging from the interaction between the control molecules serve as clear commands to the cells.

As we know more about the molecular control networks, they are getting more complex. These networks often include feedbacks, crosstalk, context-dependent changes, and time-dependent changes. Mathematical modeling is a powerful tool to handle such complexities.

In my research, I combine biological intuition with mathematical modeling to make clear the seemingly confusing networks. My biological intuition is on cell cycle, apoptosis, p53 pathway and NF-κB pathway. My modeling expertise is on positive feedbacks, negative feedbacks, switches, and oscillations.

Interested students are encouraged to send me CVs and discuss opportunities in my group.

Keywords: quantitative systems pharmacology, machine learning, neural network, artificial intelligence, model informed drug development, digital twins, matlab, python, nonlinear dynamics, computational biology

Assistant Professor
Dept of Pediatrics
Children's Hospital Building S10
Phone: 513-636-4200
sandra.andorf@cchmc.org

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Description of Research:
The Andorf Lab primarily focuses on computational approaches in the intersection of immunological and clinical research to study underlying causes and novel approaches for the prevention, diagnosis and treatment of disease. Most of our research is in the field of food allergy. However, we also study other immune-mediated disorders. Our projects often involve the analysis of single-cell data from assays such as flow cytometry (FCM) or mass cytometry (CyTOF), and much of our work is collaborative with experimental biologists, clinicians and biostatisticians.

A secondary focus of the Andorf Lab is the reuse of individual-level clinical study data. For this research, we leverage data that are available in the immunology database and analysis portal (ImmPort) and other similar resources.

Professor
Dept of Pediatrics - Biomedical Informatics
Children's Hospital Building R
Office Phone: 513-636-4865
bruce.aronow@cchmc.org

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Description of Research:
The Aronow Lab focuses on collaborative research projects and the development of informatics systems that leverage multiple disciplines of knowledge, expertise and diverse data. The goal is to improve our collective ability to formulate high-impact inferences, hypotheses and next-stage experiments that could have the highest overall impact for biomedical research. We currently focus on finding or supporting efforts to solve problems relevant to genomic medicine by developing, both independently and collaboratively, new algorithms, tools and methodologies in translational bioinformatics. To this effect, we deal with several aspects of bioinformatics, ranging from gene regulatory networks to systems biology of normal and perturbed states.

Professor
Dept of Anesthesiology
Medical Sciences Building 3412
Office Phone: 513-558-5037
bacceiml@ucmail.uc.edu

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Description of Research:
Although infants and children experience pain as the result of injury, disease, surgery or intensive care therapy, pediatric pain remains undertreated and poorly understood. Efforts to design new, evidence-based treatments for chronic pediatric pain have been hampered by a lack of information regarding how neonatal pain circuits respond at a cellular and molecular level to tissue damage or other forms of early life adversity.  My lab is currently characterizing the short- and long-term effects of early life adversity on developing sensory neurons and synaptic networks located within the superficial dorsal horn of the spinal cord, which serves as an important relay station in the pain pathway.  Experimental approaches include ex vivo electrophysiology in rodent dorsal root ganglia and spinal cord slices, 3D confocal microscopy, immunohistochemistry, in situ hybridization, RNA-sequencing, and behavioral measurements of pain sensitivity. It is our hope that by identifying age-specific changes in the functional organization of pain networks under pathological conditions, this work will yield new insight into the underlying basis for hyperalgesia during the early postnatal period and also help explain why neonatal tissue damage appears capable of altering pain perception throughout life.

Associate Professor
Dept of Pediatrics - Allergy
Children's Hospital Building S6.409
Office Phone: 513-636-1851
artem.barski@cchmc.org

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Description of Research:
The Barski Lab researches epigenomics with a primary focus on the immune system. Our main research projects are designed to investigate epigenomic regulation of T-cell differentiation, activation and memory.

To support these projects, we run a complete “-omics” kitchen, including both wet lab “-omics” biotechnology and dry lab data analysis. Our expertise in both areas has led to multiple collaborative papers and grant applications on topics ranging from the epigenomics of spermatogenesis to the epigenomics of atopic disease to epigenomics of lung development.  Dr. Barski is also a co-founder of a startup, Datirium, LLC, which developed Scientific Data Analysis Platform, SciDAP is used for analysis of various NGS data including bulk and single cell transcriptomics and epigenomics data.

Professor
Dept of Chemistry
Crosley 1301
Office Phone: 513-556-4886
becktl@ucmail.uc.edu

CV

Description of Research:

• Theory and computer simulations of liquids.
• Development of multiscale methods for electronic structure.
• Electron transport in molecular electronics
• Modeling of biological ion channels.
• Fundamental studies of ion hydration and specific ion effects.
• Solvation Science,
• Statistical Mechanics.
• The Energy Sciences.

Professor
Dept of Biological Sciences
A&S Biological Sciences Room 711D
Office Phone: 513-556-9714
benoitja@ucmail.uc.edu

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Description of Research:
Mechanisms underlying insect stress tolerance, reproductive physiology, regulation of metabolism and aging are the encompassing themes of my research, with the goal of integrating these topics under whole system studies that use molecular-, organismal- and population-based approaches. The emphasis of my lab is on producing broadly-trained biologists that have knowledge and experience in a variety of techniques, allowing proficiency in bioinformatics, laboratory techniques and field research.  Although individuals within my lab are not limited to a specific insect system, there is a slant toward medically-important insects/arthropods such as mosquitoes, tsetse flies and ticks.

Insect reproductive physiology. Insect reproduction varies from oviparity (egg production) to viviparity (birth of live young).  The main point of this research is on factors that influence egg production (mosquitoes, bed bugs) and production of live young (tsetse flies, cockroaches). Research on tsetse flies and cockroaches focuses on the mobilization of maternal nutrients from stores to feed developing progeny within the mother, a process known as insect lactation.  The goal of these studies are to identify reproductive bottlenecks that could be used as targets for control of pestiferous insects.  Individuals focusing on this topic will have a broad understanding of the molecular mechanisms of reproductive physiology.

Mechanisms of stress tolerance in insects. The ability of an organism to tolerate and respond to stress is critical to its establishment and persistence in specific localities.  The objectives of this research are to identify mechanisms utilized at multiple biological levels (molecular to population) by insects to prevent and recover from stress.  Projects investigating these responses range from direct measurement of insect stress tolerance to functional genomics and metabolomic analyses. When possible field studies will be integrated into these projects to assess if mechanisms identified in the laboratory can be confirmed in natural populations.  Individuals working on these projects will have extensive knowledge of molecular mechanisms utilized by insect to prevent stress-induced damage and techniques necessary to investigate these mechanisms.

Regulation of nutrient storage and breakdown. Maintenance of nutrient levels is critical for organisms to maintain adequate body mass so they can function properly.  This research focuses on the role of insulin and other hormones in relation to the regulation of nutrient levels during progeny production, stress and starvation.  Projects involve the utilization of basic techniques of insect endocrinology and expand to the determination of large-scale transcript and proteome changes.  Two specific goals for this research: 1. determine the role of nutrient homeostasis during insect reproduction to reduce the fecundity of pest insects, and 2. identify factors that are similar among animals to promote insects as models for metabolic diseases.

Aging. Aging and death are processes that affect every organism.  The process of aging is influenced by a multitude of factors including the genotype, stress exposure and reproduction.  The encompassing goal of the research topic is to determine how stress and reproduction alter longevity and fecundity. Specific topics include mechanisms by which individuals prevent damage at the molecular and organismal levels.

Assistant Professor
Dept of Pediatrics-Dev Biology
Children's Hospital Building R
Office Phone: 513-636-4200
cristina.cebrian@cchmc.org

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Description of Research:
My laboratory studies the cellular and molecular mechanisms driving kidney development; the mechanisms that, when they go awry, can cause Congenital Anomalies of the Kidney and the Urinary Tract (CAKUT). These anomalies, that range from common defects such as vesicoureteral reflux to severe malformations such as renal agenesis, represent about 30% of all prenatally diagnosed malformations. Our overarching goal is to identify the mechanisms that drive renal progenitor cell self-renewal and differentiation and the pathological outcomes of disrupting these processes.

In addition, we are unraveling the earliest events leading to cystogenesis in Autosomal Dominant Polycystic Kidney Disease (ADPKD). This is the most common monogenic disease leading to kidney insufficiency and affects 12.5 million people worldwide. Our research aims at understanding the cellular behavior of mutant cells at the inception of cyst development, with the ultimate goal of identifying early therapeutic interventions.

We use both mouse models and human pluripotent stem cell lines that we differentiate into kidney organoids to answer these questions. Among our most common tools, we use transcriptomics and advanced imaging including whole kidney clearing and time-lapse confocal imaging.

Professor
Dept of Internal Medicine - Nephrology & Hypertension
Medical Sciences Building 6115
Office Phone: 513-558-5471
conforl@ucmail.uc.edu

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Description of Research:
My laboratory specializes in immune cell function and the mechanisms that control the ability of T and NK cells to perform effector functions in the context of cancer and autoimmunity. Our research focuses on ion channels and the membrane mechanisms that regulate the activation and function of these cells. Ion channels, located on the membrane of immune cells, regulate calcium homeostasis and associated effector functions and gene expression.

Our main focus areas are: 

1. Role of ion channels in immune surveillance and the response to immunotherapies in cancer patients. This research focuses on the role of the tumor microenvironment (TME) in cancer immune escape and the resistance to immunotherapies. We have discovered that ion channels control the anti-tumor capabilities of cytotoxic T cells and mediate the immunosuppressive effects of hypoxia, adenosine, PDL1 in the TME. We recently discovered that these channels are involved in the resistance to immune checkpoint therapies.  These studies have contributed to establishing ion channels as new elements of immunosuppression in cancer and have opened new venues for investigation targeted toward developing novel cancer immunotherapies. Lately, we have expanded our research interest to exosomes, important immune suppressive mediators of the TME.

2. Role of ion channels in human T lymphocyte dysfunction in autoimmunity and infectious diseases. Systemic Lupus Erythematosus (SLE) is an autoimmune disease that affects predominantly women and is characterized by a broad variety of clinical symptoms such as glomerulonephritis and central nervous system impairment. We have shown that human T lymphocytes of SLE patients present with a characteristic defect in potassium channel behavior. Recently, we have extended our studies to COVID-19, where an exaggerated T cell function is associated with the cytokine storm, an excessive production of proinflammatory cytokines that contributes to acute lung damage and death. We discovered that T cells of severe COVID-19 patients have an increased expression of Kv1.3 channels and that dexamethasone’s beneficial effects in COVID-19 can be in part ascribed to its ability to suppress T cell function via Kv1.3 channel inhibition. These studies emphasize the therapeutic potentials of ion channel blockers in autoimmunity and COVID-19.

3. Development of nanoparticle-based targeted therapy in autoimmunity and cancer. Our ultimate goal is to develop new therapeutics that suppress the activity of T cells in autoimmunity and increase the activity of T cells in cancer. To this end, we have developed a novel therapy for SLE that selectively inhibits memory T cells by knock-down of Kv1.3 channels. We have fabricated functionalized lipid nanovesicles for siRNA delivery. We showed that these nanoparticles effectively prevented the development of lupus nephritis in a humanized mouse model of the disease. We are now applying a similar approach to cancer with the fabrication of lipid nanovesicles for mRNA delivery in adaptive immune cells that can block the immune suppressive effects of the TME via ion channel upregulation.

Associate Professor
Dept of Neurosurgery
Children's Hospital Building S3.421
Office Phone: 513-803-9275
steven.crone@cchmc.org

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Description of Research:
The Crone Lab investigates how neural circuits that control breathing are altered by disease and injury. A variety of approaches are used to study the control of breathing in transgenic mice at the level of the whole animal (plethysmography, electromyography), neural circuit (synaptic tracing, 3D imaging, chemogenetics) and individual molecules (RNA sequencing).

We are working to develop new approaches to repair or enhance the function of respiratory circuits to improve breathing in patients with spinal cord injury, epilepsy, and neuromuscular diseases such as amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA) and muscular dystrophy.

Our lab is also actively involved in the Neuromuscular Development Group. Our collaborations aim to accelerate research in the development and diseases of the neuromuscular system.

Professor
Dept of Cancer & Cell Biology
Vontz Center 3304
Office Phone: 513-558-1957
czyzykm@ucmail.uc.edu

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Description of Research:
Kidney cancer affects annually 300,000 worldwide and 65,000 in USA, with 100,000 and 14,000 deaths respectively. Clear cell renal cell carcinoma (ccRCC) is the most common type of renal cancer. ccRCC is characterized by mutations in several tumor suppressors positioned on the short arm of chromosome 3 (3p), including VHL, PBRM1, BAP1 and SETD2. Our laboratory has been working in the field of ccRCC and VHL for the past several years. We are investigating three important areas in ccRCC pathobiology: (1) Using metallomics and metabolomics as well as molecular and biochemical approaches we investigate the role of copper in metabolic reprogramming during progression of ccRCC. (2) Using molecular and biochemical approaches we interrogate mechanisms of tumor promoting and tumor suppressing autophagy and connections between autophagy and cancer metabolism. (3) Using systems biology approaches we investigate genomic, transcriptomic, metabolomic subtypes of ccRCC and the role of environmental factors such as metals and tobacco smoking in the etiology of these subtypes.

Associate Professor
Dept of Pediatrics
Children's Hospital Building R
Office Phone: 513-636-0286
senad.divonovic@cchmc.org

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Description of Research:
The overall goal of my research program is to define the fundamental processes, mechanisms and immune pathways underlying disease pathogenesis, with an ultimate goal of translational exploitation of such insights for eliminating/reducing burdens of inflammatory/metabolic/infectious diseases.

My research interests are directly coupled to my expertise in various pathways that regulate immune responses— developed via reductive analysis of both innate and adaptive immune responses (e.g., TLR, BAFF, type I IFN, IL-17 signaling) in animal models of standard and thermoneutral housing and various infections— have positioned our group ideally to examine cellular and molecular processes that regulate immunopathogenesis of various disease. Further, our experimental model findings are supported by established and ever developing platforms of primary human samples/tissues from individuals clinically stratified into respective disease categories (collaborations with physicians/clinical scientist).

Specifically, the current focus of my laboratory is to exploit novel immune pathways underlying: (i) maternal obesity associated vertical transmission of adverse offspring health outcomes; (ii) infection/inflammation driven regulation of parturition; (iii) metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis; (iv) obesity development and adipocyte-immune like behavior; and (v) obesity-associated infectious insult and asthma susceptibility.

Professor
Dept of Pediatrics
Children's Hospital Building R
Office Phone: 513-636-4200
john.hogenesch@cchmc.org

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Description of Research:
John Hogenesch, PhD, is a genome and circadian biologist focusing on the genetics of circadian timing in mammals.

He discovered Bmal1, the master regulator of the mammalian clock, but also its paralog Bmal2, its partner Npas2, and the positive loop of the clock (Hogenesch et al., JBC, 1997; Hogenesch et al., PNAS, 1998; Hogenesch et al., J. Neurosci, 2000).

Later, his lab characterized Rora/Rorb/Roc as key regulators of Bmal1 and circadian function (Sato et al., Neuron, 2004), discovered Chrono as a non-canonical repressor of Bmal1/Clock (Anafi et al., PLoS Biology, 2014), and Kpnb1 as a required transporter of the PER/CRY complex (Lee et al., Elife, 2015).

The Hogenesch lab studies transcriptional outputs of the clock in animal models and humans (Panda et al., Cell, 2002, Hughes et al., PLoS Genetics, 2009, Zhang et al., PNAS, 2014; Anafi et al., PNAS, 2017; Ruben et al., Science Translational Medicine, 2018). This work is leading to a wealth of new opportunities in circadian medicine and has spurred community contributions, such as the public databases the Gene Atlas and Gene Wiki, CircaDB, and algorithms, including JTK, PSEA, MetaCycle, and CYCLOPS (Su et al., PNAS, 2004; Huss et al., NAR, 2010; Hughes et al., JBR, 2010; Pizarro et al., NAR, 2013; Zhang et al., JBR, 2014; and Wu et al., Bioinformatics, 2016; Anafi et al., PNAS, 2017).

Together with collaborators at Cincinnati Children's ( David Smith, MD, PhD,  Thomas Dye, MD,  Kelly Byars, PsyD,  Danielle Graef, PhD and Carlos Prada, MD), the Hogenesch lab is also characterizing genetic variation in syndromic and non-syndromic children with circadian sleep disorders. 

Professor
Department of Internal Medicine - Cardiology
Cardiovascular Research Center Room 3935
Office Phone: 513-558-5675
hollanck@ucmail.uc.edu

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Description of Research:

• Bioeffects of Diagnostic and Therapeutic Ultrasound
• Acoustic Cavitation
• New Diagnostic imaging Techniques for the Early Detection of Vascular Disease and Ischemic Injury to Brain

Professor
Department of Pediatrics - Hematology
Children's Hospital Building R
Office Phone: 513-636-0989
theodosia.kalfa@cchmc.org

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Description of Research:
Our laboratory is studying signaling within the erythroid progenitor and precursor cells during erythropoiesis, as well as in mature red blood cells. We specifically focus on signals conducted by Rac GTPases, which are members of the Rho family and Ras superfamily. They switch between the inactive GDP-bound form and the active GTP-bound form to regulate a wide spectrum of cellular functions. They have been shown to play unique and overlapping roles in hematopoietic and blood cells (Mulloyet al., Blood. 115:936–947. 2010). They control actin cytoskeleton, cell motility, vesicular transport pathways, reactive oxygen species production, as well as cell adhesion and migration, proliferation and survival.

We explore the role of Rac GTPases in erythropoiesis and mature RBCs in gene-targeted mice where Rac1 and Rac2 GTPases have been deleted from the hematopoietic cells. We also study the role of Rac GTPases in generation of reactive oxygen species (ROS) within human erythrocytes from patients with sickle-cell disease. 

Professor
Department of Pediatrics
Children's Hospital Building R
Office Phone: 513-636-4259
jennifer.kaplan@cchmc.org

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Description of Research:
Sepsis is a response to infection that can lead to a massive and dysregulated systemic inflammatory response resulting in multiple organ dysfunction and death. Although treatment with antibiotics treats the underlying infection, it does not reverse the cascade of signaling events activating the inflammatory responses. There are few interventional trials demonstrating clinical benefit in patients with sepsis. The Kaplan Laboratory is dedicated to understanding and treating the inflammatory responses in sepsis by using a basic, translational and clinical research approach.

Our research focuses on three main areas:

1. The Role of PPAR gamma in Sepsis. 
2. The Increased Susceptibility of Diet-Induced Obesity to Sepsis. 
3. Phase 1 Clinical Trial of Pioglitazone in Pediatric Sepsis.

Associate Professor
Department of Immunobiology
Children's Hospital Building R
Office phone 513-636-3999
ian.lewkowich@cchmc.org

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Description of Research:
The research in Lewkowich lab focuses on identifying the mechanisms through which a variety of conditions or exposures can alter the development and/or severity of allergic asthma. Many of the factors the lab are interested in are those that are present primarily in early life, and  have a long-lasting effect on asthma outcomes, even later in life. These include things like early life exposure to allergens (even exposure of the mother, or the father, prior to conception), or dysbiosis induced by maternal exposure to antibiotics. The lab has also recently developing a unique model of  asthma in obese mice that recapitulates many of the features of the “obese asthma” endotype observed in humans (including more severe asthma, a shift away from the normal “Th2-dominated” inflammatory profile to a “mixed Th2/Th17 inflammatory profile”, and a marked female bias). We are currently exploring the mechanistic underpinning of how these exposures modify the immune responses underlying asthma, with a hope to identify therapeutic targets that can be used to mitigate, or reverse the impact of these exposures. Work is also being done to identify how factors uniquely associated with each of these exposures/conditions alters the “normal” asthma pathways, and contributes to the development of more severe asthma.

Research in the lab uses a combination of in vitro approaches and in vivo animals models, and seeks to apply findings from these models to samples collected from pediatric donors with asthma complicated by a variety of conditions.”

Professor
Department of Mathematical Sciences
4199 French Hall West 
Office Phone: 513.556.4127
limsg@ucmail.uc.edu

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Description of Research:
My expertise centers on mathematical modeling, computer simulations, numerical algorithm development, and dynamical process analysis, particularly within biological and physical realms. Currently, my research is primarily focused on investigating bacterial swimming mechanisms, nonlinear dynamics within coupled biological systems, and tumor growth and invasion patterns in brain and breast cancer. I work on advancing mathematical models, validating them through biological experiments, and proposing avenues for further experimental exploration.

Professor
Department of Environmental Health
Kettering Lab Complex 110
Office Phone: 513-558-8564
medvedm@ucmail.uc.edu

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Description of Research:
The research focus of the laboratory is the development of statistical and bioinformatics methods for learning from diverse genomics data types, and the application of such methods through interdisciplinary biomedical efforts. The laboratory leads the LINCS-BD2K Data Coordination Center and Integration Center, which is NIH funded U54 Center jointly funded by the BD2K (Big Data To Knowledge) and LINCS (Library of Integrated Network Based Signatures) programs. Members of the laboratory are also developing protocols for comprehensive data management and the bioinformatics analysis of microarray and next-gen sequencing data generated by the University of Cincinnati Genomics Core. The lab also leads the Bioinformatics Core of the Center for Environmental Genetics (CEG)  and participates in several other collaborative biomedical projects.

Professor
Department of Pediatrics - Asthma Research
Children's Hospital Building R 236
Office Phone: 513-803-2766
tesfaye.mersha@cchmc.org

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Description of Research:
Prof. Mersha leads the Population Genetics, Ancestry and Bioinformatics Laboratory (pGAB). His research combines genetic ancestry, bioinformatics, and statistical and functional genomics to unravel genetic and non-genetic contributions to complex diseases in human populations, particularly in allergic disorders. Dr. Mersha's lab long-term goals are to understand and dissect the role of genetic and genetic-modifying causes of asthma and reduce health disparities in children. Current research interests/ approaches of the Mersha Lab include 1.) Ancestry Analysis and Admixture Mapping, 2.) Genome-wide Association Analysis, 3.) RNA-seq Analysis, 4.) Biological Pathways / Networks Analysis, 5.) Multi-Omics Data Integration.

Professor
Department of Molecular Genetics
Medical Sciences Building 2206
Office Phone: 513-558-0866
millerwe@ucmail.uc.edu

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Description of Research:
The Miller laboratory is interested in the mechanisms by which viral pathogens manipulate host cell signal transduction pathways. We are primarily using cytomegaloviruses to examine how the pathogens alter signaling pathways directed by G-protein coupled receptors (GPCRs) to facilitate robust replication in tissues important for host-host dissemination.

Associate Professor
Department of Pediatrics - Immunobiology
Children's Hospital Building R
COM Pediatrics Immunobiology - 0054
Office Phone: 513-636-4200
emily.miraldi@cchmc.org

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Description of Research:
The Miraldi lab’s focus is mathematical modeling of the immune system from high-dimensional genomics measurements. In close collaboration with experimental immunologists, we seek to learn how diverse immune cells sense and respond to their environment in both health and disease. Our studies leverage new biotechnologies (e.g., chromatin accessibility, single-cell genomics measurements) and often require development of new computational methods. The resulting genome-scale models provide unbiased, experimentally testable hypotheses. Long-term, we would like to use these models to re-engineer immune-cell behavior in the context of autoimmunity, cancer and other diseases.

Associate Professor
Department of Pediatrics - Translational and Clinical Pharmacology
Children's Hospital Building S2.610
Office Phone: 513-636-0912
tomoyuki.mizuno@cchmc.org

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Description of Research:
The Mizuno Lab at Cincinnati Children’s utilizes quantitative modeling and simulations, pharmacometrics, pharmacogenetics, and systems pharmacology approaches to develop and implement personalized precision dosing strategies in children and adults.

Most medications on the market come with dosage recommendations for the average patient. However, the optimal dose varies among patients due to substantial variability and complex interactions in patient physiology, drug response, and disease characteristics. Our overarching goal is to optimize drug dosing strategies by predicting drug behaviors, therapeutic efficacy, and disease profiles by using computational models at both population and individual levels.

Professor
Department of Pediatrics - Molecular Cardiovascular Biology
Children's Hospital Building R 
Office Phone: 513-636-3557
jeff.molkentin@cchmc.org

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Description of Research:
Our laboratory investigates a range of focus areas, all of which center on understanding the molecular mechanisms of heart and skeletal muscle disease. Toward this end we study the basic machinery that underlies cell death, with a special interest in mitochondrial-dependent mechanisms of nonapoptotic death (such as cellular necrosis). Prominent diseases of both heart and skeletal muscle are affected by cellular necrosis, so identifying the genes that control this process could have a substantial effect on our treatment of these types of diseases.

We are also interested in characterizing the intracellular signaling pathways that control cellular growth, differentiation and replication in cardiac and skeletal muscle. A better understanding of the signaling pathways that control these processes, coupled with the identification of novel genes, could suggest new treatment strategies for human diseases. Similarly, we are examining the transcriptional regulatory factors and epigenetic mechanisms that regulate cardiac and skeletal muscle differentiation, growth, death and replication, in order to suggest additional targets for treating human disease.

Our laboratory is also actively engaged in identifying novel secreted protein factors in the heart (cytokines, growth factors, chemokines) that might control disease responsiveness. We study the cardiac fibroblast and how it functions during disease to alter the extracellular matrix, which affects heart remodeling. And we are investigating the basic mechanisms of intracellular calcium handling in cardiac and skeletal muscle to further understand the paradigms of excitation-transcription coupling and excitation-signaling coupling.

Associate Professor
Department of Pediatrics - Endocrinology
Children's Hospital Building R 609
Office Phone: 513-803-9230
Takahisa.Nakamura@cchmc.org

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Description of Research:
Our lab’s primary interest is the pathogenesis of obesity and metabolic diseases such as type 2 diabetes and non-alcoholic fatty liver disease (NAFLD). We are specifically interested in molecular mechanisms by which alternations in cellular and circulating RNA networks disrupt systemic glucose and lipid metabolism in the development and progression of these diseases. We have established a variety of mouse and cell culture models to study glucose and lipid metabolism, and miRNA-regulatory machinery in the pathogenesis of obesity. Our goal is to find novel therapeutic approaches targeting RNA networks for treating such diseases.

Our Research interests include:

• Analyzing roles of hepatic miRNA regulatory machinery in the regulation of metabolism in obesity
• Determining endogenous pathogenic dsRNA pathways in chronic inflammation
• Identifying mitochondrial RNA regulating glucose and lipid metabolism
• Investigating circulating RNA that impacts systemic glucose metabolism

Associate Professor
Department of Biomedical Engineering
College of Engineering and Applied Science
850 ERC
Office Phone: 513-556-3997
narmond@ucmail.uc.edu

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Description of Research:
Our laboratory is focused on engineering vascularized tissues through manipulation of the process of angiogenesis, i.e. formation of capillaries.

Potential applications of this research include different areas where therapeutic angiogenesis can be of benefit, including wound healing, heart remodeling and regeneration following myocardial infarction, and repair of ischaemic tissues.

Professor
Department of Cancer & Cell Biology
Vontz Center 3312
Office Phone: 513-558-7245
plasd@ucmail.uc.edu

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Description of Research:
Our group investigates the effects of oncogenic signal transduction on tumor cell metabolism and apoptosis control. In PTEN-deficient cancer cells, signal transduction activates the protein kinase S6K1, which in turn primes cell metabolism to growth and survival in cancer cells. By counteracting oncogenic signal transduction and cancer cell metabolism, we aim to restore normal cell death control in cancer cells.

The lab uses genetic and biochemical approaches to identify and validate novel therapeutic targets in brain cancers and leukemia. We join with outstanding clinical and research colleagues to pursue answers for the biggest obstacles in cancer therapy.

Professor
Department of Surgery
Division Chief of General Surgery
Medical Sciences Building SRU Room 1577
Office Phone: 513-558-8467
prittsta@ucmail.uc.edu

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Description of Research:
General Surgery, Gastrointestinal Surgery, Surgical Critical Care, Trauma Surgery, Sepsis, Inflammation.

Assistant Professor
Department of Pediatrics
Children's Hospital Building R
COM Pediatrics Mol. Cardio. Biology - 0054
Office Phone: 513-517-1221
mattia.quattrocelli@cchmc.org

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Description of Research:
The Mattia Quattrocelli Lab investigates molecular mechanisms and translatable biomarkers in dysfunction and rescue of striated muscles. The lab aims at combining genetics, epigenetics, and metabolism to garner a deeper understanding of muscle physiology and pharmacology.

An important focus of the lab centers on “precision dosing” for glucocorticoid steroids in heart and muscle regulation. Glucocorticoids (dexamethasone, prednisone, deflazacort) are widely used immunosuppressants and they have a pervasive yet overlooked impact on metabolic homeostasis and striated muscle function. We are currently investigating how repetitive versus pulsatile regimens of these drugs remodel energy production and performance in several contexts of disease, including obesity, unhealthy aging, and heart failure. Moreover, we are leveraging the newly-discovered pharmacological mechanisms to expand the concept of precision dosing for these drugs to “chrono-pharmacology”. In this line of investigation, we are asking what are the circadian and molecular mechanisms governing steroid pharmacology and physiological response in striated muscles.

The overarching goal of the lab is to advance mechanistic understanding and applicable pharmacology to improve the health of heart and muscle.

Professor
Department of Computer Science
Old Chemistry Building 819B
CEAS - Computer Science - 0030
Office Phone: 513-556-4752
ralescal@ucmail.uc.edu

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Description of Research:
My research centers mainly around machine learning theory and applications.  It includes development of algorithms for learning from imbalanced data, context dependent computing, supervised and unsupervised learning, feature selection, support vector machines, quantum computing and learning.  At the application level I am interested in image understanding, brain computer interface, and malware detection.

Professor
Department of Internal Medicine
Cardiovascular Research Center 3926
Office Phone: 513-558-3062
rubinsjk@ucmail.uc.edu

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Description of Research:
The Rubinstein laboratory has been at the forefront of understanding the roles of the TRPV channels in regulating cardiac function with specific attention to TRPV2 channels in modulating contractility and TRPV1 channels in ischemic preconditioning. The laboratory has also worked on several translational science projects with basic researchers.

Associate Professor
Department of Pediatrics
Children's Hospital Building R
Office phone 513-556-3642
nathan.salomonis@cchmc.org

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Description of Research:
The role of alternative splicing in mammalian development and disease is profound. Unique alternative mRNA isoforms dictate opposing transcriptional, signaling, and cell survival responses. These molecular switches can drive differentiation into new lineages or modulate the effectiveness of chemotherapy. While the research community has made significant strides understanding the role of isoform regulation in diseases such as cancer, its broader impact on lineage decisions, tumor survival, and immune responses remains largely undefined.

The Salomonis lab is pioneering the use of artificial intelligence (AI) to investigate tumor evolution and normal cell development at an unprecedented scale. Our work aims to define the precise role of RNA isoform regulation in cancer, understand which cells and how these programs emerge and to exploit such findings for the creation of new therapies. To address these challenges, our team has developed advanced software ecosystems, cell atlases and web platforms to enable new discoveries. Our tools include the highly used AltAnalyze workflow for alternative splicing and single-cell analysis, scTriangulate to automate cell atlas creation from diverse single-cell modalities or prior knowledge and Splicing Neoantigen Finder (SNAF) to define new shared targets for cancer therapy. Our approaches leverage exciting new advances in long-read single-cell analysis, spatial transcriptomics, deep learning, Bayesian modeling and rigorous experimental validation with our collaborative partners. With these approaches in hand, we aim create new cellular and immunotherapies, characterize disease-specific cell states, and unravel the complexities of clonal evolution.

Professor
Department of Radiation Oncology
UC Barrett Cancer Center
3151 Bellevue Avenue
Cincinnati, OH 45219
Office Phone: 513-584-5668
vinita.takiar@uchealth.com

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Description of Research:
The Takiar and Wise-Draper co-led laboratory is interested in mechanisms of resistance to various anti-cancer therapy. Dr. Wise-Draper is a medical oncologist focused on experimental therapeutics for the treatment of head and neck cancer and other solid tumor malignancies. Dr. Takiar is a radiation oncologist with a clinical focus on treating patients with head and neck cancer. As such, the Takiar & Wise-Draper group uses head and neck cancer as a model system to better understand how tumors may respond to treatment including chemotherapy,immunotherapy, and radiation therapy, and the mechanisms by which tumors recur despite aggressive treatment. The laboratory also participates in the translational elements of clinical trials in order to better understand the basic biology behind the outcomes being observed in the clinic.

The overall goal of the laboratory is to better understand how tumor cells evade or resist cell death by anti-cancer therapy. If these mechanisms were better understood, then potentially clinical treatment could be better tailored to each patient.

One focus of the laboratory is on identifying mechanisms of adaptive resistance to radiation therapy. For this project, we use Reverse Phase Protein Microarray Analysis (RPPA) as well as cellular and mouse models to try and replicate the human host. Select therapies are then tested alone and in combination with ionizing radiation in a strategic manner to identify new combinations of treatment that may be more effective than those currently available.

Another focus of the laboratory is on better understanding the mechanisms underlying resistance to immunotherapy, including T-cell dysfunction, and the potential role of NK cells and the microenvironment. Currently, immunotherapy is indicated for patients in the recurrent or metastatic setting for head and neck cancer, and although those who respond to treatment have terrific outcomes, the majority of patients do not respond. The goals of this project are to be able to better identify patients most likely to respond to treatment and to understand how to turn a non-responder into a responder to potentially design subsequent human trials that will improve immunotherapy effectiveness.

Assistant Professor
Department of Pediatrics - Division of Translational and Clinical Pharmacology
Children's Hospital
Office Phone: 513-373-0238
zachary.taylor@cchmc.org

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Description of Research:
My work focuses on developing and implementing personalized drug dosing strategies for pediatric patients. The scope of my research includes understanding and applying pharmacokinetic (PK), pharmacodynamic (PD), pharmacometric (PMx) and pharmacogenetic (PGx) approaches to develop and implement model-informed precision dosing (MIPD).

Through my research, I seek to describe a drug's metabolism and response through quantitative methods, creating translational tools that enable optimized drug dosing strategies and improve therapeutic outcomes for pediatric patients.

Professor
Department of Molecular Genetics
Medical Sciences Building 2204
Office Phone: 513-558-6246
thompstb@ucmail.uc.edu

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Description of Research:
Cues to direct cellular programs are executed by protein signaling molecules such as that of the Transforming Growth Factor b family. Disruption of these programs are a leading cause of numerous human pathologies including cancer and fibrosis. Thus, efforts are aimed at rebalancing signaling programs can offer therapeutic opportunities for treatment. By using a combination of structural biology (E.g. cryoEM and X-ray crystallography), artificial intelligence and bioengineering we are making the next generation of therapeutics that can modulate ligands of the TGF-b family.

Professor
Department of Pediatrics - Neurology
Children's Hospital Bldg R
COM Pediatrics Neurology - 0054
Lubov.Timchenko@cchmc.org

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Description of Research:
Molecular pathobiology and development of therapies for adult and congenital forms of neuro-muscular disease myotonic dystrophy type 1 and myotonic dystrophy type 2; the role of toxic RNAs containing long repeats in regulation of gene expression; skeletal muscle.

Professor
Department of Cancer & Cell Biology
Vontz Center 2328
Office Phone: 513-558-8675
waltzse@ucmail.uc.edu

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Description of Research:
The Waltz laboratory is interested in the molecular mechanisms by which cell-surface receptor tyrosine kinases and growth factors control human disease processes, with a special emphasis on mechanisms regulating cancer growth and metastasis, and inflammation. The Waltz group has made several seminal discoveries related to the Ron receptor tyrosine kinase in both breast and prostate cancers. In particular, the laboratory has shown that Ron overexpression specific to the breast epithelium is sufficient to induce aggressive breast cancers that are highly metastatic. In addition, the Waltz group has found that Ron is an important contributing factor controlling the growth of prostate cancers through the regulation of tumor angiogenesis (blood vessel formation). The immediate goals for these projects are to understand the physiological signaling pathways that control the aggressive tumor phenotype downstream of Ron signaling. Future studies will involve the utilization of in vivo gene-targeted murine models to study disease progression as well as the isolation and analysis of primary epithelial and stromal cells from the breast and prostate environments. In addition, the laboratory plans to use orthotopic transplantation of gene-modified cell lines into syngeneic models to explore these signaling pathways in detail.

With respect to control of cellular inflammation, the Waltz laboratory has also shown that Ron is expressed on select macrophage populations, and that signaling through this receptor negatively regulates the balance of cytokine and chemokine production during acute tissue injury in vivo. This critical balance of immune mediators is essential to control the body's response to injury, wounding, and infection. To analyze the mechanisms responsible for the Ron-dependent regulation of cytokine/chemokine production, the laboratory utilizes co-culture systems composed of primary tissue macrophages and epithelial cells from select gene knockout animals to dissect the role of macrophages in tissue injury.

The overall goal of the Waltz laboratory is to examine the Ron signaling pathway as a novel therapeutic target in the regulation of a variety of human diseases.

Professor
Department of Pathology & Laboratory Med
Cardiovascular Research Center 1933
COM Pathology Wang Lab - 0529
Office Phone: 513-558-5798
wanyy@ucmail.uc.edu

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Description of Research:
Dr. Wang's research over the past two decades has focused on cardiovascular pathophysiology and therapies, with three primary areas of concentration: 1) studying the impact of various additive agents in cardioplegic solutions on functional cardiac restoration, 2) investigating ischemic preconditioning as a protective mechanism against ischemia/reperfusion injury, including its molecular mechanisms and signaling pathways, and 3) advancing progenitor/stem cell-based therapy for treating myocardial infarction.

Currently, Dr. Wang's research team delves into progenitor/stem cell biology, with a particular emphasis on pluripotency, differentiation, proliferation, and survival. Their aim is to enhance the regenerative potential of adult heart tissue following myocardial infarction (MI). Through innovative CRISPR-induced cell manipulation techniques, they have successfully generated cardiovascular progenitor cells (CPCs) exhibiting clonality, self-renewal, and cardiac tri-potentiality. These CPCs have shown promising results in improving heart function and reducing scar formation in MI mice upon transplantation. Dr. Wang's team is also developing a viral or non-viral CRISPR approach to activate endogenous genes for CPC generation from fibroblasts, with a focus on identifying long non-coding RNAs (lncRNAs) crucial for epigenetic remodeling during cell reprogramming. Additionally, their research explores the roles of transcription factors, microRNAs, and growth factors in optimizing conditions for cardiomyocyte regeneration. Notably, they have identified microRNA-128 as a pivotal regulator of cardiomyocyte proliferation, offering a novel therapeutic avenue for heart repair. Dr. Wang's research has gained notable recognition in esteemed cardiovascular journals, underscoring their substantial expertise in cardiovascular research and previous experience as a cardiovascular and thoracic surgeon. This wealth of knowledge, combined with adeptness in both animal models and human surgeries, uniquely equips Dr. Wang to pioneer advancements in myocardial repair strategies through progenitor/stem cell-based therapy in ischemic environments.

Professor
Department of Pediatrics
Children's Hospital Building R
COM Pediatrics Hematology - 0054
Office Phone: 513-803-4597
russell.ware@cchmc.org

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The Ware Lab team focuses on translational hematology research to improve our overall understanding of sickle cell disease with the long-term goal of improving the lives of affected children. Specific areas of laboratory focus include the identification and validation of genetic modifiers, optimizing the use of hydroxyurea, investigating the safety of long-term hydroxyurea treatment, and elucidating the phenotypic variability of drug responses through investigation of the pharmacokinetics, pharmacodynamics and pharmacogenomics of hydroxyurea. The lab performs a wide variety of laboratory techniques including genetic / genomic studies, gene expression profiling and functional analyses. DNA, serum / plasma and urine samples are analyzed from multiple clinical trials, including ones conducted in the United States as well as in the global arena.

Russell E. Ware, MD, PhD, has a strong interest in global health and especially for children with sickle cell disease who live in developing countries within the Caribbean and sub-Saharan Africa. He has designed and completed collaborative surveillance programs for sickle cell disease in Angola, Uganda, Tanzania and Malawi. He has conducted clinical trials in Jamaica (EXTEND) and in the Dominican Republic (SACRED) evaluating the effectiveness of therapies used for children who have sickle cell disease coupled with factors indicating a higher stroke risk. Additionally, Dr. Ware has established studies designed to safely introduce hydroxyurea into sub-Saharan Africa: Realizing Effectiveness Across Continents with Hydroxyurea (REACH), Novel use Of Hydroxyurea in an African Region with Malaria (NOHARM), and Prospective Identification of Variables as Outcomes for Treatment (PIVOT).

Professor
Department of Pediatrics
CCHMC S Building
Molecular Cardiovascular Biology
Office Phone: 513-636-7232
joshua.waxman@cchmc.org

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Congenital heart defects are among the most common birth defects. Thus, understanding the underlying molecular nature of these defects is a major priority in cardiac research. Our lab investigates the selection of progenitor cells, a developmental process that establishes the heart’s size.

The ultimate fate of organ progenitors depends upon a balance of both inductive and restrictive signals. Because the same signals affecting the formation of cardiac progenitors in embryos are used by cardiac stem cells, our studies will have implications for understanding stem cell differentiation and cardiac regeneration.

Ultimately, we think that our elucidation of the mechanisms restricting cardiac progenitors will lead to a greater understanding of congenital heart defects, and will also have the potential to positively affect our ability to develop novel therapies aimed at healing injured hearts in children and adults.

Professor
Department of Pediatrics
Children's Hospital Building R
Office Phone: 513-803-9078
matthew.weirauch@cchmc.org

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The control of when and where genes are utilized is a major component driving phenotypic differences between organisms and individuals. In our lab, we use computational methods to study how, when, where, and why genes are “turned on and off”. To this end, we study transcription factors, which interact with the genome by binding to short sequences proximal to the genes they control. Humans have 1500 different transcription factors, each of which recognizes different short sequences, or “motifs”, within the genome. We develop methods for determining transcription factor motifs, integrating these motifs with other information to predict transcription factor binding, and understanding the regulatory mechanisms underlying human diseases.

Professor
Department of Internal Medicine - Pulmonary
Medical Sciences Building
Room 7165
231 Albert Sabin Way
Office Phone: 513-558-6246
yuj9@ucmail.uc.edu

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I lead a research laboratory focusing on investigation of the role of tumor suppressor proteins tuberin (TSC2) and hamartin (TSC1) in steroid action, cell survival, cellular metabolism, tumorigenesis and metastasis, and signaling transduction pathways. My laboratory also develops animal models to test the efficacy of FDA approved drugs on the progression and metastasis of mTORC1 hyperactive cells, lung inflammation and injury. Current studies include determining the role of estrogen in the progression of lymphangioleiomyomatosis (LAM), a female predominant rare lung disease, from the alteration of signaling pathways, to the integrity of alveolar epithelium and microenvironment in the lung, and to the pulmonary functions. We are also investigating the potential application of using bloodbased biomarkers in LAM. Our research has been funded by NIH/the National Heart, Lung and Blood Institute, the National Institute of Diabetes and Digestive and Kidney Diseases, the Department of Defense and the LAM Foundation. My laboratory developed the first LAM-associated, patient-derived primary cell line and the first metastatic model of LAM. We also have identified mTORC1-independent but mTORC2-mediated activation of prostaglandin biosynthesis in TSC and LAM, and used metabolomics profiling to identify dysregulation of glucose metabolism and pentose phosphate pathway addiction in TSC2-deficient cells.

Professor
Department of Anesthesiology 
Medical Sciences Building 3413
Office Phone: 513-558-2427
zhangj4@ucmail.uc.edu

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Description of Research:
Chronic pain conditions such as neuropathic pain are very common and can last a lifetime, persisting long after the initial damage to the nerve has healed. Chronic pain conditions involve complex, orchestrated changes in the sensory neurons and their synaptic targets. These changes include abnormal electrical activity, alterations in ion channels and transmitters, and sensitization of the pain pathways in the spinal cord and brain. We are currently investigating the role of cytokines in pain. We have developed new animal models involving compression and/or inflammation of the sensory ganglia. These models are particularly relevant to understanding low back pain. We have found that several inflammatory cytokines are upregulated in these models, with a time course that parallels the development of pain behaviors. Our aim is to understand the possible causal roles of these cytokines in abnormal pain states, with the ultimate goal of identifying new therapeutic targets for chronic pain. We use a number of techniques, including electrophysiology, animal behavior, microscopy, and biochemical and molecular methods. In a related project, we are also investigating the role and causes of the abnormal sympathetic sprouting into the sensory ganglia that exacerbates many chronic pain states and how sympathetic regulate local immune/inflammatory responses.  Recently, we have started several new projects: 1) determine how  microvascular responses in the dorsal root ganglia triggers neuropathic spontaneous pain; 2) relationship between nerve injury initiated regeneration and the persistence of neuropathic pain; 3) how steroid receptors change under pathological conditions and how such changes may affect therapeutic efficacy of steroids used for managing inflammatory pain conditions.  Lastly, we have initiated several clinical studies to translate preclinical findings to clinical practice.  Specifically, we are interested in whether extended nerve block provides additional benefit for patients with traumatic injury in lowing the risk of chronic pain; and how to improve efficacy of epidural steroids for managing low back pain.

Professor
Department of Pediatrics - Critical Care

Children's Hospital Building R 033
Office Phone: 513-636-8704
basilia.zingarelli@cchmc.org

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Description of Research:
The Zingarelli Laboratory is focused on the investigation of the pathophysiologic mechanisms of sepsis, trauma and hemorrhagic shock, which are leading causes of morbidity and mortality in intensive care units. A particular goal of her research has been to define the mechanisms of metabolic recovery and innate immune responses mediated by the nuclear hormone receptors peroxisome proliferator activated receptors (PPARs) and by the AMP activated protein kinase (AMPK), which are major regulators of the glucose and lipid metabolism. In dissecting the dysmetabolic mechanisms of organ injury, the Zingarelli laboratory has discovered that key molecules of the mitochondrial retrograde signaling, such as humanin, may contribute to the regulation of metabolic recovery of damaged organs. Research efforts also focus on understanding the role of aging on the clinical course of infections, severe hemorrhage and trauma. The laboratory employs a multidisciplinary approach combining in vivo and in vitro experimental models in genetically modified rodents and cell lines. These models are also utilized as a translational research platform to screen novel pharmacological compounds that can modulate the molecular mechanisms of organ function. The goal is to identify specific therapeutic interventions for pediatric, adult and elderly patients.

The Zingarelli Laboratory is also collaborating with several basic science and translational studies at Cincinnati Children’s Hospital. In collaboration with Takahisa Nakamura, PhD of the Division of Endocrinology and Jennifer Kaplan, MD, MS, of the Division of Critical Care Medicine, the Zingarelli Laboratory explores critical pathways of cell signaling and reprogramming of innate immune responses through release of extracellular vesicles in obesity and sepsis.

Ongoing projects are primarily funded by multiple grants from the National Institutes of Health.

Associate Professor
Dept of Anesthesia
S6.622, CCHMC
Office Phone: 513-636-3397
sascha.alles@cchmc.org

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Description of Research:
The Alles Lab's area of study is on nociception and chronic pain mechanisms with a primary focus on the physiology of sensory neurons. Our main goal is to contribute to the development of novel non-opioid treatments by investigating and gaining new insights into the molecular and cellular mechanisms of nociception and chronic pain using pre-clinical mouse and human models.

We utilize a combination of techniques in our research, including electrophysiology, imaging, behavioral, bioinformatics, and molecular biology, particularly studying the neuronal function in the peripheral nervous system, spinal cord, and brain. We collaborate with clinical colleagues and institutions such as New York University, the University of Florida, the University of Kansas Medical Center and University of New Mexico, using these partnerships to inform and guide our studies. Dr. Alles's expertise in the pain field has led him to serve as a reviewer for grant review panels at the National Institutes of Health (NIH), Department of Defense (DoD), and Veterans Affairs (VA), as well as an editorial board member for the Journal of Pain.

Keywords: neuroscience, pain, nociception, sensory neurons, ion channels, electrophysiology, human tissue, hiPSCs

Associate Professor
Dept of Pathology and Laboratory Medicine
CVC 1925
Office Phone: 513-558-0135
nives.zimmermann@UC.edu

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Description of Research:
The Zimmermann Lab's research centers on three main areas: eosinophilic diseases, mast cell-mediated disease, and cancer immunology, all within the field of pathology and allergy/immunology specialty. Regarding eosinophilic diseases, our goal is to understand and investigate the damage they can cause. While eosinophils may be present in some tissues without harmful effects, there are instances where they can cause serious damage. Eosinophilic diseases include allergic conditions such as asthma, parasitic infestation, eosinophilic gastrointestinal diseases and rare eosinophilic leukemias.

We also conduct translational studies on mast cell-mediated diseases, including the analysis of pathology samples from patients experiencing unexplained gastrointestinal symptoms and/or dysautonomia, such as fainting, headaches, 'brain fog'. Our cancer immunology research is conducted in clinical settings and involves a large collaborative team of basic scientists, medical oncologists, and radiation oncologists.

Dr. Zimmermann has received several awards throughout her career, including the Woman Physician in Allergy Junior Faculty Development Award; the ARTrust™ and Donald Y. M. Leung, MD, PhD Lectureship; the Pathology Department’s Disciplined Developer Award at the University of Cincinnati; and the Resident of the Year Award.

Assistant Professor
Dept of Pediatrics
Childrens Hospital Bldg R
Office Phone: 513-636-4200
ziyuan.guo@cchmc.org

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Description of Research:
The Guo Lab focuses on neuroscience and regenerative medicine, with a core mission to understand and model neurodevelopmental and neurodegenerative disorders. The lab leverages a versatile toolkit that combines cutting-edge stem cell technologies (iPSCs, organoids, trans-differentiation) with engineering approaches to study disease etiology in genetically relevant human systems.

A key contribution from Dr. Guo’s earlier work was a pioneering study demonstrating that reactive glial cells could be directly reprogrammed into functional neurons in vivo. This was achieved in the adult mouse brain through the targeted overexpression of a single neural transcription factor, NeuroD1.

Dr. Guo is the recipient of numerous awards in recognition of his research, including the Cincinnati Children's Trustee Award, the Maryland Stem Cell Research Fund Postdoctoral Fellowship Award, and the Penn State University Alumni Association Dissertation Award and J. Ben and Helen D. Hill Memorial Fund Award.

Keywords: Stem cell biology, iPSCs, organoids, trans-differentiation, neurodevelopment, neurodegeneration, organ-on-a-chip, blood-brain barrier (BBB), microfluidic engineering, gene editing (CRISPR/Cas9), electrophysiology, Amyotrophic Lateral Sclerosis (ALS), autism, fragile x syndrome, Alzheimer's disease, gene therapy, single-cell RNA sequencing (scRNA-seq), spatial transcriptomics

Assistant Professor
Division of Pediatric Ophthalmology - Science of Light Center
CCHMC – R2.455
Office Phone: 513-558-5151
diego.fernandez@cchmc.org

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Description of Research:
The Fernandez Lab's research focuses on understanding how the body and brain coordinate physiology and behavior in a timely manner in response to environmental stimuli, such as daily changes in light and feeding patterns. Our goal is to uncover relevant explanations for how neuronal bases of disorders are connected to deleterious environmental stressors, such as light pollution and circadian disruptors. Through this approach, we also aim to expand opportunities to develop innovative therapeutics strategies. In particular, understanding how artificial light affects physiology can guide the design of better lighting conditions to improve human health and reduce environmental impact.

Keywords: Sensory neuroscience, light-driven behavior, retina-brain communication, sleep-wake regulation, circadian biology, neural circuits

Associate Professor
Dept of Environmental Health - Division of Biomedical Informatics
Children's TCHRF-C 8509
Office Phone: 513-636-2056
jmeller@cchmc.org

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Description of Research:
The Meller Lab's area of research centers in the fields of structural bioinformatics, computational genomics and systems biology. Our lab develops and applies computational approaches for mining, analyzing, and interpreting biomedical data. One of our Lab's goals is to develop improved data mining methods to predict the activity of environmental factors and other small molecules by incorporating docking simulations, chemical similarity and toxicogenomics. Our lab has successfully achieved in developing new methods that analyze and predict protein interactions, including those for membrane proteins and for model quality assessment. The methods we develop are applied in collaborative projects and in the development of bioinformatic tools to analyze the structures and functional purposes of proteins, including their complexes. Our tools, including SABLE, SPPIDER and POLYVIEW-3D are being widely used by research in many countries and is available to the community as web servers.

Keywords: bioinformatics, biomedical informatics, computational biology, prediction methods, predictive fingerprints of disease states, protein structure and function, membrane proteins, gene finding and annotation, bioinformatics and computational biology courses

Associate Professor
Dept of Pediatrics - Division of Experimental Hematology & Cancer Biology
Childrens Hospital Bldg R
Office Phone: 513-636-6597
nicolas.nassar@cchmc.org

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Description of Research:
The Nassar Lab's research is based both on basic and translational methods, with a particular focus on drug development and signaling, primarily involving small GTPases. Our lab's main goal is to find ways to inhibit hyperactivation in leukemia by understanding the regulation of Rac and its role in cancer. Additionally, we aim to investigate the mechanism of the Vav3-inhibitor's action.

We incorporate several methodologies in our research work, including protein crystallography, biophysical and biochemical studies, cellular functional assays, and the identification of small molecule modulators of GTPase signaling using in vivo cancer models. An innovative finding from our lab is the identification of a small molecule inhibitor of Vav3, a Rac activator. The Nassar Lab has reached a significant milestone with the submission of our small molecule technology to the US Patent Office.

Keywords: small GTPases, Rac regulation, Vav3 inhibitor, leukemia, drug development, GTPase signaling, small molecule inhibitor

Assistant Professor
College of Pharmacy
Medical Sciences Building 3005M
Office Phone: 513-558-7749
timothy.phoenix@cchmc.org

Publications
CV in UC Research Directory

Description of Research:
Phoenix lab's area of expertise centers on developmental neurobiology, genomics, and tumor microenvironment interactions. While Phoenix lab focuses on multiple areas of research, our main focus is on brain tumors, which are now the leading cause of cancer-related deaths in children.

Some of the projects we work on in our lab include developing novel animal models that mimic pediatric brain tumors in preclinical settings and using these platforms to investigate the function and mechanisms of emerging oncogenes that are identified in patient samples. Additionally, we leverage our research expertise to describe mechanisms that regulate vascular and blood-brain barrier heterogeneity in pediatric brain tumors.

Keywords: developmental neurobiology, genomics, tumor microenvironment, pediatric brain tumors, oncogenes, animal models, blood-brain barrier

Professor
Dept of Pediatrics - Division of Translational and Clinical Pharmacology
bhagwat.prasad@cchmc.org

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Description of Research:
Prasad Lab's research focuses on investigating the biological and molecular determinants of drug response. Specifically, we aim to identify biomarkers for drug pharmacokinetics, toxicity, and efficacy, as well as to understand how inter-individual and developmental variability impacts drug disposition and response. Additionally, we focus on developing translational tools that further strengthen precision medicine for children and other underrepresented populations.

Our research stems from a passion to improve and predict drug safety, efficacy and disease progression in populations typically underrepresented in clinical trials, often children. Our lab utilizes several innovative, predictive and noninvasive research methods to achieve these goals, including multi-omics technologies to build advanced computational models such as physiologically based pharmacokinetic (PBPK) and quantitative systems pharmacology (QSP) models. Dr. Prasad's expertise in this field has led him to serve as Chair-Elect of the Drug Metabolism and Disposition Division of ASPET, Chair of Transporter Focus Group of ISSX and Vice-Chair of the 2025 Gordon Research Conference on Drug Metabolism.

Keywords: drug response, biomarkers, pharmacokinetics, drug toxicity and efficacy, precision medicine, multi-omics, PBPK models, QSP models

Associate Professor
Dept of Internal Medicine
Medical Sciences Building 7063
Office Phone: 513-558-4437
jason.winnick@uc.edu

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Description of Research:
Winnick Lab's primary research revolves around the regulation of hepatic glucose metabolism in both healthy and diseased states. Additionally, our work expands into areas such as hypoglycemic counter-regulation, investigating whole body mechanisms responsible for improvements related to hepatic glucose production (HGP) and blood glucose homeostasis, and exploring how intrahepatic pathways contribute to HGP responses to lifestyle modifications.

With growing evidence that Roux-en-Y gastric bypass (RYGB) surgery improves glucose homeostasis in individuals with type 2 diabetes, we are also interested in understanding the mechanisms by which post-RYGB surgery leads to reduced HGP and enhances insulin responsiveness in the liver.

Keywords: hepatic glucose metabolism, glucose homeostasis, hypoglycemic counter-regulation, type 2 diabetes, Roux-en-Y gastric bypass, RYGB, insulin responsiveness

Professor
Dept of Cancer Biology
Vontz Center for Molecular Studies 3326
Office Phone: 513-558-0114
jun-lin.guan@uc.edu

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CV in UC Research Directory
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Description of Research:
The Guan Lab's research is centered on understanding the fundamental principles of cell signaling and how the disruption of these pathways can lead to diseases such as cancer. Our goal is to uncover the mechanisms of cancer metastasis, dormancy and relapse, which are major contributors to cancer-related mortality. We approach this by studying the critical role of autophagy and its cross-talk with kinase signaling pathways.

Our lab has made multiple innovative contributions to this area of research. For example, we identified focal adhesion kinase (FAK) as a key component of integrin signaling that is also regulated by oncogenic transformation and discovered FIP200 (FAK-Family Interacting Protein of 200 kDa) as a component of the ULK1/Atg13/FIP200 complex, which is essential for autophagy induction. Another key finding is that autophagy may play a pro-tumorigenic role in animals with an intact immune system.

Our team also uncovered how FAK signaling promotes breast cancer growth and metastasis by regulating breast cancer stem cells. Additionally, we developed a novel mouse model that closely mimics human lymphangiosarcoma, which allowed us to demonstrate that sustained mTORC1 activation and VEGF autocrine signaling are critical for tumor growth and maintenance.

Keywords: cell signaling, cancer metastasis, kinase signaling pathways, autophagy, oncogenes