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• W2935703100 abstract "Physiology in PerspectivePhysiology in Perspective: Physiology is EverywhereGary C. Sieck Gary C. SieckMayo Clinic, Rochester, Minnesota Editor-in-ChiefPublished Online:10 Apr 2019https://doi.org/10.1152/physiol.00006.2019MoreSectionsPDF (47 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat A few years ago, I visited Turkey and toured the ancient Hittite ruins in central Anatolia where I was re-introduced to the Epic of Gilgamesh, the Sumerian king of the city of Uruk located in present-day Iraq. This epic tale represents the world's oldest surviving poetry written ~4,000–6,000 years ago. The story of Gilgamesh was passed on from the Sumerians to the Babylonians and then to the Hittites, and later to the Greeks, where it influenced the epic tales of Homer. The story of Gilgamesh reflects the timeless concerns of all humans about life, death, wisdom, and immortality, undoubtedly motivated by the author’s consideration of our place as humans in the vast universe. I thought of this epic tale when I was in northern Norway about 4 weeks ago, where I had traveled to visit a colleague. His “summer” house is almost 300 miles above the arctic circle, needless to say in a very remote location, but one that affords a fantastic view of the fjords, mountains, sky, and vast universe. As I viewed the wonder around me, but particularly the sky above, my memories brought back the view of Earth sent back from Neil Armstrong’s first step for mankind during the lunar landing 50 years ago in July. As he noted at the time, this was a giant leap for mankind, and, as a fledgling undergraduate zoologist, I was in awe of the view of Earth projected back to us. However, at the time, I could not help but think how fragile life is on our small planet. Since then, I have been able to travel the world and see the diversity of life. Physiology is everywhere I look; in forests and deserts, in mountains and valleys, in lakes and oceans, in the sky above. Just as in ancient times, curiosity in this life and how it works drives human discovery, and I am so happy to be a small part of this exploration. As Pearl S. Buck, author of the novel The Good Earth, said in an interview, “Like Confucius of old, I am so absorbed in the wonder of Earth and the life upon it that I cannot think of heaven and angels” (1939). In this issue of Physiology, the review articles explore different aspects of ongoing discoveries in our wonderous life on earth.The discovery that cells selectively secrete extracellular vesicles (exosomes from multivesicular bodies and microvesicles from the plasma membrane) opened a new frontier in our understanding of cell-cell communication. Extracellular vesicles contain functional molecules, including genetic material, that allow targeted communication between cells and likely serve an important role in physiological homeostasis in multicellular organisms. In their review, Stahl and Raposo (5) explore how cells use intracellular trafficking pathways to package “informational” molecules into newly formed extracellular vesicles. Through this process, cells share metabolites and survival factors with other cells—a process called commingling. In this way, cells and tissues communicate with each other by dispatching messages in extracellular vesicles that are targeted to recipient cells, contributing to overall homeostasis. Understanding the details of extracellular vesicle-mediated communication is important to fully understand normal physiological systems. It is also important to understand how disrupted extracellular vesicle-mediated communication may play a role in the pathophysiology underlying diseases such as diabetes and cancer, among others. Finally, one of the most promising and exciting new directions of research is the consideration of pharmacological/therapeutic applications of extracellular vesicles. The “magic bullet” concept that Paul Ehrlich presented over a century ago may actually come to pass should we learn how extracellular vesicles can target specific tissues as part of their normal physiological role.Hypertension is the most important risk factor for cardiovascular disease morbidity and mortality. More women die from cardiovascular disease than men, and more than 70% of women over the age of 70 yr are hypertensive, often uncontrolled. Thus it is imperative that we explore the causes for hypertension in women so that precision therapeutic options can be tailored to protect women and reduce morbidity and mortality. However, most research to date has focused on men. In male animal models, numerous studies have shown that interventions that reduce or increase oxidative stress also reduce or increase blood pressure. However, similar interventions in females have no effect on blood pressure. Accordingly, research is needed to explore the underlying basis for sex differences in responses to oxidative stress: what type of reactive oxidants are produced (reactive oxygen, nitrogen species, or peroxides), what downstream mediators are affected (vasodilators or vasoconstrictors), and what role endogenous antioxidants play to determine how oxidative stress contributes to control of blood pressure. Yet the role that oxidative stress may play in mediating hypertension in women is virtually unknown. In their review, Reckelhoff and colleagues (4) highlight the lack of sufficient research on whether oxidative stress contributes to hypertension in females as it does in males. If the mechanisms for hypertension can be identified specifically for women and therapeutic options can be made available, there should be a reduction in cardiovascular disease risk, with reductions in morbidity and mortality that would improve the quality of life for women as they age.The kidneys play a key role in fluid and electrolyte homeostasis, acid base balance, and the excretion of endogenous and exogenous compounds. Nephrons are the functional units of the kidney, and all of these kidney functions are impaired with nephron loss. The number of nephrons can be reduced due to a low nephron number at birth, kidney donation, or kidney injury. In particular, acute kidney injury and chronic kidney disease are associated with high morbidity and mortality. In their review, Fattah and colleagues (2) integrate data obtained from previous animal and human studies to provide insight into how kidneys respond and adapt to nephron loss. These adaptations include a compensatory hyperfunction of the remaining nephrons, with an increase in single nephron glomerular filtration rate and tubular hypertrophy. These changes can help to preserve kidney function but may facilitate further nephron loss in some conditions. A better understanding of the adaptations to nephron loss and their pathophysiological relevance can provide new therapeutic strategies.The incidence of Type 2 diabetes is reaching epidemic proportions worldwide. Despite the introduction of several new anti-diabetes medications, safe and effective insulin sensitizers are lacking, and insulin resistance is still a major unmet medical need. Understanding the pathophysiology of insulin resistance is key to identifying new therapeutic targets that would enable us to develop novel anti-diabetes treatments. In their review, Najjar and Perdomo (3) discuss current research that shows considerable promise in identifying new approaches to develop more efficacious insulin sensitizers. To understand how insulin resistance develops, investigators have endeavored to generate animal models that recapitulate different aspects of the disease. Without such models, it remains difficult to untangle cause-and-effect relationships in humans. Most clinical studies have shown that, as a compensatory mechanism to insulin resistance, insulin clearance is impaired together with increased insulin secretion. However, in animal models in which expression of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is altered, the resulting impairment of hepatic insulin clearance causes a secondary insulin resistance that is not simply a consequence of insulin clearance. Thus research exploring the role of CEACAM1 may provide novel insight into the etiology of insulin resistance.Spastic cerebral palsy is the most common motor disability that occurs in childhood, yet a full understanding of the underlying etiology of cerebral palsy remains elusive. Clinical diagnosis of cerebral palsy is primarily based on motor symptoms that appear early in childhood. Despite the name, cerebral palsy is not consistently identifiable or predictable by the presence of specific brain lesions. Instead, clinical research has focused on identifying risk factors for cerebral palsy such as premature birth or fetal hypoxic exposure. Following up on these clinical findings, most current animal models focus on mimicking risk factors for cerebral palsy. However, few animal models reproduce the symptoms of cerebral palsy that are required to diagnose this disorder (i.e., the animals do not actually display cerebral palsy). In their review, Brandenburg and colleagues (1) discuss the evolution of our understanding of spastic cerebral palsy from the early description of symptoms by William John Little in 1862 to more modern consensus clinical definitions of cerebral palsy that focus on risk factors but fail to highlight the role of the spinal cord and motor neurons in the symptoms of cerebral palsy. Thus, to advance our understanding of the mechanisms contributing to the motor impairment and spasticity in cerebral palsy, animal models must advance beyond modeling risk factors for cerebral palsy and instead model the symptoms. To this end, the spinal cord and motor neurons should be considered the final common pathway for both spasticity and altered motor control in cerebral palsy. To dissect potential underlying spinal cord mechanisms for the spasticity and motor dysfunction observed in cerebral palsy, animal models must display the developmental onset and progression of symptoms observed clinically.No conflicts of interest, financial or otherwise, are declared by the author(s).References1. Brandenburg JE, Fogarty MJ, Sieck GC. A critical evaluation of current concepts in cerebral palsy. Physiology (Bethesda) 34: 216–229, 2019. doi:10.1152/physiol.00054.2018.Link | ISI | Google Scholar2. Fattah H, Layton A, Vallon V. How do kidneys adapt to a deficit or loss in nephron number? Physiology (Bethesda) 34: 189–197, 2019. doi:10.1152/physiol.00052.2018.Link | ISI | Google Scholar3. Najjar SM, Perdomo G. Hepatic insulin clearance: mechanism and physiology. Physiology (Bethesda) 34: 198–215, 2019. doi:10.1152/physiol.00048.2018.Link | ISI | Google Scholar4. Reckelhoff JF, Romero DG, Yanes Cardozo LL. Sex, oxidative stress, and hypertension: insights from animal models. Physiology (Bethesda) 34: 178–188, 2019. doi:10.1152/physiol.00035.2018.Link | ISI | Google Scholar5. Stahl PD, Raposo G. Extracellular vesicles: exosomes and microvesicles, integrators of homeostasis. Physiology (Bethesda) 34: 169–177, 2019. doi:10.1152/physiol.00045.2018.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByA survey of multiscale modeling: Foundations, historical milestones, current status, and future prospects18 September 2020 | AIChE Journal, Vol. 1 More from this issue > Volume 34Issue 3May 2019Pages 167-168 Copyright & PermissionsCopyright © 2019 Int. Union Physiol. Sci./Am. Physiol. Soc.https://doi.org/10.1152/physiol.00006.2019PubMed30968752History Received 28 February 2019 Accepted 28 February 2019 Published online 10 April 2019 Published in print 1 May 2019 Metrics" @default.
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