麻豆传媒

Degree: Ph.D., Colorado State University, 1989

My research interests are in the area of animal physiological ecology and evolutionary physiology.  More specifically, I am interested in how anatomical and physiological capacities meet environmental demands.  For instance: when an animal is confronted by a greater energetic or physiological demand (cold temperatures, hypoxic conditions) can it compensate for that demand by increasing (or decreasing) physiological processing capacity?

Animals often meet changes in demand with changes in the size of organs and organ capacity.   I am most interested in learning how these load/capacity relationships are reflected in an animal's life history.  This approach demands an appreciation of both mechanistic physiology and ecology, and requires both field and laboratory research.  In addition, I study animals at all stages of development, concentrating on the effects of environmental demands in utero and during adulthood.  At present I work primarily in desert and montane systems, using rodents as study species.

Recent and current projects of my students, my colleagues, and myself:

The interplay between physiological acclimation and genetic adaptation to hypoxia in deer mice. 
Limits to metabolic energy output elicited by lactation, cold exposure, and exercise in laboratory mice, house mice and deer mice. 
Effects of sub-lethal parasites on host physiology during lactation, cold exposure and food restriction in mice. 
The correlation between organ size and aerobic performance in junglefowl
Changes in organ size and function in deer mice (Peromyscus maniculatus) along an altitudinal gradient. 

Department of Cell & Developmental Biology

Research Interests:
Define the Molecular Mechanisms Responsible for Tissue Protection and Reversible Metabolic Depression in Hibernation by using High-Throughput-omics Analyses

What we do: We answer both applied and basic questions about how the nervous system helps animals survive in their environments. On the applied side, we study animals that evolved ways to avoid damage to the nervous system. We focus most of our efforts on challenges to the nervous system that tend to be big problems in many human diseases. These include inactivity of neuromuscular systems (think, 鈥渋f you don鈥檛 use it you lose it鈥�) and impaired oxygen transport (think, brain damage in stroke and cardiac arrest). By learning from animals that already 鈥渒now鈥� how to get around these problems, we up our chances of finding new solutions. On the basic side, we use this approach to make new discoveries about how nervous systems use plasticity to help animals adapt to their environments. To do this, we take fundamental concepts about plasticity that were developed outside of real-life contexts (e.g., cell culture, lab settings, modeling, etc.) and test how they work in situations where animals may need them to survive. This allows us to put together new ideas about how these processes are important for behavior and why they may have evolved.

How we do it: We tend to ask questions using the neural system that regulates breathing in amphibians for two reasons. First, breathing is a tractable, rhythmic behavior that is easily studied across scales of organization (genes to proteins to cells to networks to behavior) compared to other behaviors like learning and memory. Second, amphibians have interesting life history traits that allow us to ask questions about how different forms of plasticity have adaptive importance in nature. On the technical side, we use an integrative approach that spans whole animal behavior down to the molecular biology of single neurons. We use a range of tools that include patch-clamp electrophysiology to study electrical properties of neurons, single-cell quantitative PCR and RNA sequencing to assess gene expression in individual neurons, in vivo measurements of behavior (measurements of breathing and EMG to record muscle activity), extracellular recording to measure circuit activity, and fluorescence imaging microscopy.

Interests
Cellular neuroscience, comparative neurobiology, electrophysiology

Education
Ph.D., Wright State University


Research:
What we do: We answer both applied and basic questions about how the nervous system helps animals survive in their environments. On the applied side, we study animals that evolved ways to avoid damage to the nervous system. We focus most of our efforts on challenges to the nervous system that tend to be big problems in many human diseases. These include inactivity of neuromuscular systems (think, 鈥渋f you don鈥檛 use it you lose it鈥�) and impaired oxygen transport (think, brain damage in stroke and cardiac arrest). By learning from animals that already 鈥渒now鈥� how to get around these problems, we up our chances of finding new solutions. On the basic side, we use this approach to make new discoveries about how nervous systems use plasticity to help animals adapt to their environments. To do this, we take fundamental concepts about plasticity that were developed outside of real-life contexts (e.g., cell culture, lab settings, modeling, etc.) and test how they work in situations where animals may need them to survive. This allows us to put together new ideas about how these processes are important for behavior and why they may have evolved.

Recent Publications:
Adams, S., Zubov, T., Bueschke, N., & Santin, J. M. Neuromodulation or energy failure? Metabolic limitations silence network output in the hypoxic amphibian brainstem. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2020. In press. doi.org/10.1152/ajpregu.00209.2020

Burton, M. T., & Santin, J.M. A direct excitatory action of lactate ions in the central respiratory network. 2020. Journal of Experimental Biology. In press. doi: 10.1242/jeb.235705
Northcutt, N.J., Kick, D.R., Otopalik, A.G., Goetz, B.M., Harris, R.M., Santin, J.M., Hoffman, H.A., Marder, E., Schulz, D.J. Molecular profiling of single neurons of known identity in two ganglia from the crab Cancer borealis. Proceedings of the National Academy of Sciences. 2019. doi: https://doi.org/10.1073/pnas.1911413116

Santin, J.M. Motor inactivity in hibernating frogs: Linking plasticity that stabilizes neuronal function to behavior in the natural environment. Developmental Neurobiology. 2019, in press doi: https://doi.org/10.1002/dneu.22721

Cassondra鈥檚 work focuses on understanding baseline physiology in diving animals and how physiological responses are altered from natural or anthropogenic disturbances. Her past work includes investigating cardiovascular responses to routine and anthropogenic disturbances in loggerhead marine turtles and freshwater turtles. Her current research with northern elephant seals investigates muscle and cardiovascular physiology during routine diving and in response to natural disturbances.

Cassondra Williams received her PhD from Scripps Institution of Oceanography for research on the diving physiology of emperor penguins in Antarctica. 

Overview
Dr. Matthay's overall focus is on improving clinical care of patients with acute respiratory failure from the acute respiratory distress syndrome and from sepsis. His research and clinical trials groups are very well funded by grants from the National Institute of Health. He also spends considerable time mentoring physicians and young faculty in career development and academic medicine.

Education and Training
Harvard University	A.B.	1969	English
University of Pennsylvania	M.D.	1973	School of Medicine
University of Colorado Medical Center	Internship and Residency	1976	Internal Medicine
University of California, San Francisco	Fellowship	1978	Pulmonary DIvision
University of California, San Francisco	Fellowship	1979	Cardiovascular Research Institute
 Awards and Honors
American Thoracic Society	2014		Edward Livingston Trudeau Medal
University of California, San Francisco	2013		Lifetime Achievement in Mentoring Award
University of Paris	2011		Honora Causa
American Physiologic Society	2009		Julius Comroe, Jr. Award
New York State Thoracic Society	2009		Trudeau Award

Research Goal
Our ultimate goal is to develop effective therapies that simultaneously target metabolic and vascular dysfunction in obesity and diabetes.

Current Research
Our research focuses on studies of the metabolic and vascular actions of insulin and how these actions are impaired in insulin-resistant states such as obesity, diabetes, and cardiovascular disease. Insulin-mediated microvascular recruitment plays an important role in glucose disposal and is frequently impaired in people with obesity and diabetes. We perform clinical studies that seek to understand how therapeutic interventions modulate biological actions of insulin and the molecular mechanisms of insulin resistance that play a role in coupling metabolic and vascular dysfunction in obesity and diabetes. Our research is also directed toward understanding the physiologic basis for the higher prevalence of cardiovascular dysfunction and insulin resistance in ethnic minorities such as African-Americans, Hispanic/Latinos, and Asians.

Professional Experience
Fellowship, State University of New York (SUNY), 2001鈥�2004
Residency, Wayne State University Program, 1998鈥�2001
Ph.D., Wayne State University, 1999
M.D., Bangalore Medical College, 1991

Dr. Sadis Matalon is the founding director of the Pulmonary Injury and Repair Center in the School of Medicine. He has been continuously funded by the NIH since 1978, and he is currently the principal investigator of two U01 grants and an industry grant. 

Research and Clinical Interests
Lung Injury and Repair, RSV Induced Injury to Vectorial Alveolar Na+ Transport, Chlorine Injury to the Lung, RONS and Ion Channels

Education
Graduate
University of Minnesota, Ph.D.

University of Minnesota, M.S.

Secondary Roles
Professor of Cell Biology, Physiology and Biophysics & Microbiology
Professor of Environment Health Sciences, UAB School of Public Health
Editor-in-Chief, American Journal of Physiology鈥擫ung Cellular and Molecular Physiology

My  research focuses on epithelial injury and repair, transepithelial ion transport, and ENaC-related signal pathways. We perform mechanistic preclinical and clinical studies on ALI/ARDS, COPD, asthma, and IPF.    

The laboratory of Michael J. Joyner, M.D., is interested in how humans respond to various forms of physical and mental stress during activities such as exercise, hypoxia, standing up and blood loss.

Dr. Joyner and his team study how the nervous system regulates blood pressure, heart rate and metabolism in response to these forms of stress. They are also interested in how blood flow to muscle and skin responds to these stressors. These responses are studied in young healthy subjects, healthy older subjects and people with conditions such as heart failure.

Finally, Dr. Joyner is personally interested in the role of integrative approaches in science as a powerful tool to integrate and critique data from reductionist approaches.

Focus areas
Convalescent plasma. Dr. Joyner is leading a national program sponsored by the U.S. Government to coordinate the collection and distribution of COVID-19 convalescent plasma for the treatment of individuals with severe or life-threatening disease.

Blood flow during exercise. Blood flow to exercising skeletal muscle can increase 50 to 100 times above resting values. Dr. Joyner's group is interested in the mechanisms that drive this increase in flow.

Blood pressure regulation. Blood pressure is regulated by complex interactions among the nervous system, heart and blood vessels. Dr. Joyner's group is interested in how these interactions are affected by the sex and age of the subject.

Blood glucose regulation. Glucose levels in the blood are tightly regulated to guard against hypoglycemia. Dr. Joyner and his collaborators are studying the novel idea that sensors in the body that respond to hypoxia also control blood glucose.

Breathing in heart failure. In heart failure, breathing during exercise can be excessive. Dr. Joyner and his collaborators have novel data suggesting that signals from the exercising muscle are driving ventilation in heart failure.

Physiology of elite athletes. Elite athletic performances are experiments in nature on the limits of human physiology. Dr. Joyner uses data from real-world competitions to understand the limits of human physiology.

Cognitive impairment and heart disease. Cognitive impairment is associated with risk factors for cardiovascular disease. Dr. Joyner and his collaborators are studying how aging and fitness influence brain blood vessels in humans.

The research in my lab is primarily concerned with understanding the effects of dietary genistein and other nutriceuticals (and exercise) on intestinal function.

Genistein is an isoflavonic phytoestrogen found naturally in soy, and a known activator of the CFTR chloride channel. Cystic fibrosis (CF) is an inherited disease in which epithelia are adversely affected by loss of proper CFTR function (i.e. sweat duct, pancreas, vas deferens, airway and intestine). \We have shown that consuming dietary genistein increases basal and cAMP-mediated chloride secretion in female wild-type (Wt) murine jejuna and in the well established DeltaF508-CF mouse dietary genistein eliminates the dependence of CF mice for laxatives.  Current work is aimed to evaluate how genistein mediates  benficial effect on survival and weight gain in CF mice.   We have shown that diabetic/obese ob/ob mice have significantly reduced jejunal basal chloride secretion, and furthermore, we demonstrate that consuming genistein-diet will rescue this deficit in basal secretion via influences on intestinal ion transporters.  Recent work in my lab is aimed to evaluate the influence of genistein and exercise in mice fed a high-fat/high-sugar (HFHS) diet, a model of diet-induced diabetic obesity, known to lead to Alzheimer's like pathology. In this model we are examining the gut brain axis.

Current studies in the lab are aimed at determining the mechanism(s) of action of genistein on intestinal function in Wt, CF, ob/ob and HFHS-fed mice, and importantly understanding the sex-dependent differences observed.

My research program is focused on the cell biology of recently deorphanized receptors and their cognate peptides as well as structural cues for cellular function. Specifically I am focused on these interactions at the interface of the retinal pigmented epithelium and underlying Bruch鈥檚 membrane of the eye. In addition, I direct the Research Microscopy and Histology Core at Saint Louis University School of Medicine.

Biography
Dr. Tessem received his Bachelors degree in Microbiology from Brigham Young University in 2001 and his Ph.D. in Biochemistry and Molecular Biology from the University of Colorado Health Sciences Center in 2007. Dr. Tessem completed a post-doctoral fellowship with Christopher Newgard at the Duke University Medical Center's Sarah W. Stedman Center for Nutrition and Metabolism Research.

Research Interests
Both Type 1 (T1D) and Type 2 diabetes (T2D) are caused by a relative insufficiency in functional 尾-cell mass. Current therapeutic options for diabetes include daily insulin injections to maintain normoglycemia, pharmacological agents to stimulate 尾-cell function and enhance insulin sensitivity, or islet transplantation. A major obstacle to greater application of islet transplantation therapy is the scarcity of human islets. Thus, new methods for expansion of 尾-cell mass, applied in vitro to generate the large numbers of human islet cells needed for transplantation, or in situ to induce expansion of the patients remaining 尾-cells, could have broad therapeutic implications for this disease. To this end, our lab is interested in delineating the molecular pathways that increase 尾-cell proliferation, enhance glucose stimulated insulin secretion, and protect against 尾-cell death.

Teaching Interests
My teaching interests focus on nutrient metabolism and biochemistry. I am interested in the metabolic disorders that cause human diseases.

The goal of my laboratory is to understand the molecular determinants of musculoskeletal development and the role of exercise in improving health and performance. To achieve this goal, we work on muscle, tendon, and ligaments from 2- and 3-dimensional tissue culture, in vivo wild type and genetically modified animals, and humans. Of particular interest are: 1) the interplay between nutrition and exercise and the mammalian target of rapamycin complex 1 (mTORC1) in the maintenance of muscle mass; 2) the role of the amino acid transceptor LAT1 in the activation of protein synthesis and maintenance of muscle mass; 3) the mechanism of ER stress-induced loss of protein synthesis and how this leads to anabolic resistance in muscle; and 4) the role of growth factors and loading on the activation of the Egr-1 transcription factor and the development and mechanics of ligaments. Our laboratory discovered that mTORC1 was activated by resistance exercise and that this correlates with the degree of skeletal muscle hypertrophy. Since then, we have focused on mTORC1 and its regulation by loading and nutrients. We have shown that: 1) mTORC1 is activated directly by load in a growth factor-independent manner; 2) a1-AMPK regulates mTORC1 activity during overload; 3) following a high fat diet the unfolded protein response, through inhibition of PKB, can attenuate mTORC1 activation; and 4) muscle signaling and protein synthesis after exercise are modified by nutritional interventions that are rich in leucine. Our laboratory has also developed a number of 2- and 3-dimensional tissue culture assays that can be used to study the effects of genes and nutrients on muscle, tendon, and ligament function. These studies have a direct clinical application and we work closely with colleagues in orthopedics, internal medicine, and the cancer center to develop resistance exercise, nutritional, and novel small molecule interventions that prevent muscle wasting from cachexia and sarcopenia and improve muscle function and quality of life.

I am currently conducting research aimed at improving our understanding of the regulation of the adenine nucleotide pool (ATP, ADP, AMP) in skeletal muscle and its effects on cellular energetics, muscle atrophy, and adaptive capacity.

Publications (17)
Increased Adenine Nucleotide Degradation in Skeletal Muscle Atrophy
Article
Full-text available
Dec 2019
Spencer G. Miller
Paul Hafen
Jeffrey J Brault
Adenine nucleotides (AdNs: ATP, ADP, AMP) are essential biological compounds that facilitate many necessary cellular processes by providing chemical energy, mediating intracellular signaling, and regulating protein metabolism and solubilization. A dramatic reduction in total AdNs is observed in atrophic skeletal muscle across numerous disease state...
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Accumulation of Skeletal Muscle T Cells and the Repeated Bout Effect in Rats
Article
Dec 2019
Michael R. Deyhle
Meghan Carlisle
Jacob Sorensen[...]
Robert D Hyldahl
Purpose: The purpose of this investigation was to characterize skeletal muscle T-cell accumulation following contraction-induced muscle damage, and test the hypothesis that T-cells contribute to post-damage muscle protection (i.e., the repeated bout effect) in a way reminiscent of their role in adaptive immunity. Methods: In vivo lengthening con...
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An altered response in macrophage phenotype following damage in aged human skeletal muscle: implications for skeletal muscle repair
Article
Jun 2019
Jacob Sorensen
Jamie P. Kaluhiokalani
Paul Hafen[...]
Robert D Hyldahl
The purpose of this study was to test the hypothesis that macrophage polarization is altered in old compared to young skeletal muscle, possibly contributing to the poor satellite cell response observed in older muscle tissue. Muscle biopsies were collected prior to and at 3, 24, and 72 h following a muscle-damaging exercise in young and old individ...
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Daily heat treatment maintains mitochondrial function and attenuates atrophy in human skeletal muscle subjected to immobilization

Kim Henige received her B.A. in Physical Education (emphasis in Exercise Science) and her M.A. in Physical Education (emphasis Exercise Physiology) from CSU Northridge and her Ed.D. in Education (emphasis Learning & Instruction/Exercise Physiology) from the University of Southern California. 

Dr. Henige is a Certified Strength & Conditioning Specialist (National Strength and Conditioning Association) and a Certified Exercise Physiologist (American College of Sports Medicine). Dr. Henige is an active member of the American Physiological Society (APS) and regular reviewer for Advances in Physiology Education. She is also an active member of the American College of Sports Medicine (ACSM).

At CSUN, Dr. Henige supervises the Peer Learning Facilitator Program for exercise physiology courses within the department. In addition, she supervises Commit to be Fit, a fitness program on campus for staff, faculty, students, and the local CSUN community.

Her research interests are in the area of science education, specifically improving the cognitive and affective domains of the learning experience for students in exercise physiology.

Dr Tamara Hew-Butler is a podiatric physician and associate professor of Exercise and Sports Science at Wayne State University in Detroit, Michigan. She obtained her BS in Kinesiology at the University of California at Los Angeles, CA; Doctor of Podiatric Medicine (DPM) at Temple University in Philadelphia, PA; and Philosophy Doctor (PhD) at the University of Cape Town, South Africa. Dr Hew-Butler is a Fellow of the American College of Sports Medicine (FACSM) and specializes in both sports medicine and exercise physiology. Her expertise is in exercise-associated hyponatremia and the endocrine regulation of water and sodium balance. Her scientific work has been highlighted on radio shows (Science Friday, National Public Radio), television (The Weather Channel), podcasts (CJSM), newspapers (New York Times, Washington Post, CNN), a comic strip (xkcd) and reality television show (Adam Ruins Everything).

Dr Hew-Butler is an avid runner and sports fan. She enjoys spending time with her husband, Bill, and pet ducks on their 10-acre hobby farm.

Kim Huey, professor of health sciences and 2017 Troyer Research Fellow in the Drake University College of Pharmacy and Health Sciences, was recently named a fellow of the American Physiological Society (APS).

APS is a global multidisciplinary community of nearly 10,000 scientists and educators solving the major issues affecting life and health. Members are advancing treatment and cures for a wide variety of conditions from heart disease and cancer, to addiction and obesity.

The rank of fellow in the American Physiological Society is an elite member status meant to honor prominent leaders who have demonstrated excellence in science, have made significant contributions to physiological sciences and related professions, and have served the Society. Huey has been a student or professional member of the APS for more than 20 years.

At Drake, Huey teaches a number of physiology courses to pharmacy and health sciences students while maintaining an active research program that investigates muscle function on both the basic science and applied levels.

In a recent research project, Huey led a team of undergraduate students, one of which received an American Physiological Society Undergraduate Summer Research Fellowship, investigating the effects of statin treatment on muscle function and cardiorespiratory endurance in response to treadmill training in mice with high cholesterol.  These experiments have important implications in the design of exercise training programs for individuals undergoing statin treatment.

Starting this fall, Huey and two undergraduate students who received research fellowships from the Iowa Space Grant Consortium will study if Vitamin D supplementation improves the muscular and cardiorespiratory adaptations to endurance training or combined endurance and strength training in mice.  

BIOGRAPHICAL INFORMATION
Dr. Kerksick is currently an associate professor of exercise science in the Exercise Science Department in the School of Health Sciences at Lindenwood University. He currently serves as the director of the Exercise and Performance Nutrition Laboratory (www.lindenwood.edu/epnl) and the Master of Science in Health Sciences program at Lindenwood University. His primary research interests include sport nutrition as well as the biochemical, cellular, and molecular adaptations relative to various forms of exercise and nutrition interventions, primarily those that promote muscle hypertrophy, prevent muscle atrophy, and promote health and recovery in healthy as well as clinical populations.

ACADEMIC INTERESTS
Dietary Supplements
Obesity
Performance Nutrition
Protein
Recovery
Research
Skeletal Muscle
RESEARCH INTERESTS
Examining the impact of exercise and nutritional interventions on changes in health, performance, and recovery of active and clinical populations.

COURSES TAUGHT
Exercise Physiology
Independent Research
Nutrition for Performance
Research Methods and Data Interpretation
Research Internship
Sport Nutrition
Thesis
PUBLICATIONS
Complete Bibliography

This is a selected list of publications since the start of Dr. Kerksick鈥檚 faculty appointment with Lindenwood University (Jan. 2015).

Harty PS, Zabriskie HA, Stecker RA, Currier BS, Moon JM, Richmond S, Jagim A, Kerksick CM鈥�. Position-specific body composition norms in female collegiate rugby union athletes.  J Strength Cond Res, Acceptance date: June 18, 2019. PMID: 31403573.
J盲ger R, Purpura M, Kerksick CM. Curcumin attenuates performance decrements following muscle damaging exercise. Nutrients. Acceptance date: July 18, 2019. PMID: 31340534.
Harty PS, Zabriskie HA, Stecker RA, Currier B, Moon JM, Jagim AR, Kerksick CM鈥�. Upper and lower thresholds of fat-free mass index in a large cohort of female collegiate athletes. J Sports Sci. 2019 Jun 25:1-8. PMID: 31238804.
Currier B, Harty PS, Zabriskie HA, Stecker RA, Moon JM, Jagim AR, Kerksick CM鈥�. Fat-free mass index in a diverse sample of male collegiate athletes. J Strength Cond Res, Acceptance Date: March 3rd, 2019. PMID: 30985525.
Zabriskie HA, Currier BS, Harty PS, Stecker RA, Jagim AR, Kerksick CM鈥�. Body composition and energy status across a women鈥檚 lacrosse season. Nutrients. 2019 Feb 23;11(2). Pii: E470.  PMID: 20813399.

RESEARCH INTERESTS
Examine the physiological mechanisms and overall health benefits related to optimal hydration, physical activity, and heat exposure.

EDUCATION
Ph.D. University of Connecticut (2014)

M.A. University of Connecticut (2008)

B.A. George Washington University (2004)

TEACHING
KIN 4900, Drugs & Exercise Performance
KIN 3021, Physiology of Exercise
KIN 5586, Advanced Exercise Physiology

Research Interests
Dr. Markofski's overarching research question is How do exercise and nutrition encourage healthy aging? We know that people who are physically active have a lower risk of chronic diseases and decreased mortality, but what are the mechanisms for this benefit? Dr. Markofski is primarily interested in the contribution of the immune system and skeletal muscle to healthy aging, but acknowledges that these systems are influenced by other physiological processes.

Many of the diseases typically associated with aging may not be related to aging per se, but rather an age-associated decrease in physical activity and increase in sedentary time. These changes in physical activity cause numerous changes to physiology, including to the immune system, adipose tissue, and skeletal muscle鈥攁nd cause an increase in the risk for developing chronic diseases. Dr. Markofski approaches her research questions by studying the acute and chronic effects of exercise and nutrition on skeletal muscle and immune function. She is an exercise physiologist with a research agenda in exercise immunology. Her current projects encompass healthy research participants, cancer patients and survivors, and health disparities.