Assistant Professor
Dept of Pharmacology and Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
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 and Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology

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 & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
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.

The McReynolds Lab is committed to maintaining and promoting a diverse and inclusive environment and is an advocate of positive mental health.

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

Professor
Dept of Pharmacology & Systems Physiology

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 & Systems Physiology
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.

Associate Professor
Dept of Pharmacology & Systems Physiology
Medical Sciences Building 4206A
Office Phone: 513-558-6086

pixleysk@ucmail.uc.edu

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Description of Research:
Dr. Pixley’s lab coordinates with an interdisciplinary group that spans UC colleges, US universities, international partners and industrial partners. For over 10 years, this work has been part of an NSF Engineering Research Center (ERC) funding mechanism. This ERC was entitled Revolutionizing Metallic Biomaterials. Three US universities, several industrial partners and an international partner were involved. The Pixley lab focus has been on novel applications of metallic biomaterials, particularly to repair damaged nervous tissues. The particular application pursued to date has been peripheral nerve regeneration. While the ERC funding has now ended, the lab continues its partnership with engineers to advance biomedical repairs. Our most recent partnership is with an engineering team in Israel.

When substantial injuries occur that result in complete loss of peripheral nerve segments, surgical intervention is required. A scaffold is used to replace the lost segments and reconnect the two cut nerve endings. We seek to develop “man-made” or biomaterial scaffolds to avoid the hazards and dangers of using autografts (nerves from the same patient). In particular, we are interested in using a unique material, biodegradable metals (magnesium (Mg) and zinc (Zn)) as part of scaffolds. These metals have promise to provide a physical pathway to safely guide and support regenerating cells as they cross an injury gap in a nerve and regenerate a nerve segment.

Our research has shown that Mg and now Zn metal, in microfilament forms, have great promise to provide this type of contact guidance.  Our goals now are to continue to refine the use of these biomaterials, as well as to develop a better understanding of the mechanisms by which nerve regeneration adapts to these unusual biomaterials, as a means to understand nerve regeneration and nerve repair in general.

Techniques used in the lab involve animal surgery, behavioral studies and then histological analyses. We also use cell culture to study the cellular responses to the metals, their ions and other degradation products.

Keywords: tissue regeneration after injury, peripheral nerve regeneration, skin wound healing, biodegradable metals, nerve repair scaffolds, tissue implants and engineering, foreign body tissue responses, Schwann cells, rodent cell culture and in vivo experiments, tissue implants and engineering

Professor
Dept of Pharmacology & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
Medical Sciences Building 5157
Office Phone: 513-558-9754
schuljo@ucmail.uc.edu

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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 & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
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 & Systems Physiology
Medical Sciences Building 4251
Office Phone: 513-558-6489
worrelrt@ucmail.uc.edu

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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 & Systems Physiology
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