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Assistant Professor Dept of Pharmacology and Systems Physiology Medical Sciences Building 4255 Office Phone: 513-558-8679 chellakn@ucmail.uc.edu Publications CV in UC Research Directory Lab Home Page 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
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
Office Phone: 513-558-2340 fangg@ucmail.uc.edu Publications CV in UC Research Directory Lab Home Page 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
Office Phone: 513-558-2562 gaoc3@ucmail.uc.edu Publications CV in UC Research Directory Lab Home Page 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 Publications CV in UC Research Directory Lab Home Page Description of Research: Our laboratory conducts basic research on muscle physiology at the molecular and cellular levels. Recent research projects have focused on:
Office Phone: 513-558-5636 hermanjs@ucmail.uc.edu Publications CV in UC Research Directory Lab Home Page 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
Medical Sciences Building 4201 Office Phone: 513-558-5093 hongca@ucmail.uc.edu Publications CV in UC Research Directory Lab Home Page 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
Our research involves the following:
Office Phone: 513-558-3097 lorenzjn@ucmail.uc.edu Publications CV in UC Research Directory Lab Home Page 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 Publications CV in UC Research Directory 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
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.
Cardiovascular Research Center 5938 Office Phone: 513-558-6654 normanab@ucmail.uc.edu
Publications CV in UC Research Directory Lab Home Page
Publications CV in UC Research Directory Lab Home Page 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.
pixleysk@ucmail.uc.edu CV in UC Research Directory Lab Home Page 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
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.
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!
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
ulrichym@ucmail.uc.edu Publications CV in UC Research Directory Lab Home Page 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
wanghs@ucmail.uc.edu CV in UC Research Directory Lab Home Page 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.
wohlebes@ucmail.uc.edu Publications CV in UC Research Directory Lab Home Page 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
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
zhangtl@ucmail.uc.edu Publications CV in UC Research Directory 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
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231 Albert Sabin WayMSB 4261Cincinnati, OH 45267-0576
Mail Location: 0576Phone: 513-558-3102Email:jeannie.cummins@uc.edu