Anatomy

We study how neuronal axons and their terminals respond to stress and damage, and how the molecules activated by stress and damage execute decisions about whether to repair themselves or self-destruct. We hope to identify target molecules that could be used to prevent axon and nerve terminal loss in diseases ranging from diabetic neuropathy to Alzheimer's disease.

We investigate how the chemicals in our daily lives interact with the female reproductive system and influence fertility. We hope that our discoveries will help reduce the incidence of infertility and improve women's health.

Approximately 795,000 Americans suffer a stroke each year, and 400,000 will experience long-term disability. The number of stroke survivors in the population is expected to double by 2025. Currently, treatments for stroke patients are limited to tissue plasminogen activator (TPA), but its use is limited to the first few hours after stroke. Therefore, the goal of our research is to develop new therapeutics that can promote repair and recovery in this rapidly growing population.

I examine the molecular functions of the different cells found in the tissues and organs of plants and animals and how they combine these functions to optimize the health and vigor of the organism.

The Garcia laboratory works to understand the molecular mechanisms of lung inflammatory processes, particularly those producing lung edema or vascular leak. The laboratory focus is to investigate gene discovery, protein function assessment, SNP discovery, genetic manipulation, in vivo testing, and candidate gene and biomarker identification, working to translate basic research into potential novel clinical therapies.

Scott Going is an expert in models and methods for assessment of changes in body composition during growth, and with aging, and is currently investigating the effects of chronic exercise versus hormone replacement therapy on bone, soft tissue composition and muscle strength in postmenopausal women, as well as the role of exercise in obesity prevention in children.

Our lab has a new treatment for heart failure. We have a biodegradable graft seeded with adult human cells that we put on the surface of the heart. The potential is to regenerate new heart muscle

Our research is focused on elucidating the structure and function of titin and nebulin, two large filamentous proteins found in muscle. We use a range of model systems with a major focus on KO and TG mouse models. The techniques that we use range from single molecule mechanics, (immuno) electron microscopy, exon microarray analysis, in vitro motility assays, low angle X-ray diffraction, cell physiology (including calcium imaging), muscle mechanics, and isolated heart physiology.

The research in my laboratory is focused on identifying the components and molecular mechanisms regulating actin architecture in cardiac and skeletal muscle during normal development and disease. Control of actin filament lengths and dynamics is important for cell motility and architecture and is regulated in part by capping proteins that block elongation and depolymerization at both the fast-growing (barbed) and slow-growing (pointed) ends of the filaments.

The long-term goal of research in my lab is to understand the molecular mechanisms of muscle contraction. I am especially interested in how contractile proteins of muscle sarcomeres regulate the force and speed of contraction in the heart. The question is important from both basic science and clinical perspectives because mutations in sarcomere proteins of muscle are a leading cause of hypertrophic cardiomyopathy (HCM), the most common cause of sudden cardiac death in the young and a prevalent cause of heart failure in adults. Myosin binding protein-C (MyBP-C) is a muscle regulatory protein that speeds actomyosin cycling kinetics in response to adrenaline (b-adrenergic stimuli) and is one of the two most commonly affected proteins linked to HCM. Currently, the major research focus in my lab is understanding the mechanisms by which cMyBP-C regulates contractile speed and mechanisms by which mutations in cMyBP-C cause disease.

Our lab is focused on the development of novel peptides to inhibit this inflammatory cascade and improve brain blood flow. These peptides are designed to significantly improve serum half-life and penetrate the blood-brain-barrier. These peptides act to inhibit the inflammatory pathways at both the level of brain blood vessels and the brain itself.

https://www.engr.arizona.edu/~klaksari/

Jonathan Lifshitz's research questions primarily investigate traumatic brain injury as a disease process that dismantles, repairs and regenerates circuits in the brain. The underlying principle is that adaptive repair and regeneration fail, leaving a miswired brain and neurological impairments that decrease quality of life.

Kirsten Limesand's research program has its foundation in radiation-induced salivary gland dysfunction; mechanisms of damage, clinical prevention measures, and restoration therapies. They utilize a number of techniques including: genetically engineered mouse models, real-time RT/PCR, immunoblotting, immunohistochemistry, primary cultures, siRNA transfections, and procedures to quantitate salivary gland physiology and integrate this information in order to understand the complete system.

Our current research program use an integrative approach at the whole animal, isolated organ, cellular and molecular levels to investigate developmental adaptations in pancreatic β-cells and insulin sensitivity that result from early life risk factors, such as intrauterine growth restriction, and increase risk of glucose intolerance and Diabetes in later life.

The kidney plays a critical role in clearing the body of potentially harmful compounds, including many commonly prescribed drugs. Unfortunately, this also sets the kidney up as a site where multiple drugs can interact in unwanted ways. We study the cellular transport processes responsible for renal drug clearance with the intent of developing predictive models that can assist clinicians, drug companies, and the Food & Drug Administration in their efforts to increase patient safety.

We are working to uncover the molecular mechanisms of aging and neurodegenerative diseases using a combination of genetic, computational and pharmacological tools, and a diverse array of experimental models. We also seek to develop therapies for ALS and related neurodegenerative diseases.