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32.5: Bibliography - Biology

32.5: Bibliography - Biology


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[1] Peter A. Nature biotechnology, 27(12):1151–1162, December 2009.

[2] G. M. The Personal Genome Project. Molecular Systems Biology, 1(1):msb4100040–E1– msb4100040–E3, December 2005.

[3] G. Church and W. Gilbert. Genomic sequencing. Proceedings of the National Academy of Sciences of the United States of America, 81(7):1991–1995, April 1984.


Nomenclature

Nomenclature ( UK: / n ə ˈ m ɛ ŋ k l ə ˌ tʃ ər / , US: / ˈ n oʊ m ə n ˌ k l eɪ tʃ ər / ) [1] [2] is a system of names or terms, or the rules for forming these terms in a particular field of arts or sciences. [3] The principles of naming vary from the relatively informal conventions of everyday speech to the internationally agreed principles, rules and recommendations that govern the formation and use of the specialist terms used in scientific and any other disciplines. [4]

Naming "things" is a part of general human communication using words and language: it is an aspect of everyday taxonomy as people distinguish the objects of their experience, together with their similarities and differences, which observers identify, name and classify. The use of names, as the many different kinds of nouns embedded in different languages, connects nomenclature to theoretical linguistics, while the way humans mentally structure the world in relation to word meanings and experience relates to the philosophy of language.

Onomastics, the study of proper names and their origins, includes: anthroponymy (concerned with human names, including personal names, surnames and nicknames) toponymy (the study of place names) and etymology (the derivation, history and use of names) as revealed through comparative and descriptive linguistics.

The scientific need for simple, stable and internationally accepted systems for naming objects of the natural world has generated many formal nomenclatural systems. [ citation needed ] Probably the best known of these nomenclatural systems are the five codes of biological nomenclature that govern the Latinized scientific names of organisms.


Chapter Summary

Solute concentrations across a semi-permeable membranes influence the movement of water and solutes across the membrane. It is the number of solute molecules and not the molecular size that is important in osmosis. Osmoregulation and osmotic balance are important bodily functions, resulting in water and salt balance. Not all solutes can pass through a semi-permeable membrane. Osmosis is the movement of water across the membrane. Osmosis occurs to equalize the number of solute molecules across a semi-permeable membrane by the movement of water to the side of higher solute concentration. Facilitated diffusion utilizes protein channels to move solute molecules from areas of higher to lower concentration while active transport mechanisms are required to move solutes against concentration gradients. Osmolarity is measured in units of milliequivalents or milliosmoles, both of which take into consideration the number of solute particles and the charge on them. Fish that live in fresh water or saltwater adapt by being osmoregulators or osmoconformers.

32.2 The Kidneys and Osmoregulatory Organs

The kidneys are the main osmoregulatory organs in mammalian systems they function to filter blood and maintain the osmolarity of body fluids at 300 mOsm. They are surrounded by three layers and are made up internally of three distinct regions—the cortex, medulla, and pelvis.

The blood vessels that transport blood into and out of the kidneys arise from and merge with the aorta and inferior vena cava, respectively. The renal arteries branch out from the aorta and enter the kidney where they further divide into segmental, interlobar, arcuate, and cortical radiate arteries.

The nephron is the functional unit of the kidney, which actively filters blood and generates urine. The nephron is made up of the renal corpuscle and renal tubule. Cortical nephrons are found in the renal cortex, while juxtamedullary nephrons are found in the renal cortex close to the renal medulla. The nephron filters and exchanges water and solutes with two sets of blood vessels and the tissue fluid in the kidneys.

There are three steps in the formation of urine: glomerular filtration, which occurs in the glomerulus tubular reabsorption, which occurs in the renal tubules and tubular secretion, which also occurs in the renal tubules.

32.3 Excretion Systems

Many systems have evolved for excreting wastes that are simpler than the kidney and urinary systems of vertebrate animals. The simplest system is that of contractile vacuoles present in microorganisms. Flame cells and nephridia in worms perform excretory functions and maintain osmotic balance. Some insects have evolved Malpighian tubules to excrete wastes and maintain osmotic balance.

32.4 Nitrogenous Wastes

Ammonia is the waste produced by metabolism of nitrogen-containing compounds like proteins and nucleic acids. While aquatic animals can easily excrete ammonia into their watery surroundings, terrestrial animals have evolved special mechanisms to eliminate the toxic ammonia from their systems. Urea is the major byproduct of ammonia metabolism in vertebrate animals. Uric acid is the major byproduct of ammonia metabolism in birds, terrestrial arthropods, and reptiles.

32.5 Hormonal Control of Osmoregulatory Functions

Hormonal cues help the kidneys synchronize the osmotic needs of the body. Hormones like epinephrine, norepinephrine, renin-angiotensin, aldosterone, anti-diuretic hormone, and atrial natriuretic peptide help regulate the needs of the body as well as the communication between the different organ systems.

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    32.5 Hormonal Control of Osmoregulatory Functions

    In this section, you will explore the following questions:

    • How do hormonal cures help the kidneys synchronize the osmotic needs of the body?
    • How do hormones and other chemical messengers including epinephrine, norepinephrine, rennin-angiotensin, aldosterone, antidiuretic hormone, and atrial natriuretic peptide help regulate waste elimination, maintain correct osmolarity, and perform other osmoregulatory functions?

    Connection for AP ® Courses

    As we learned in an earlier section, the excretory system works with the circulatory and endocrine systems to maintain osmotic balance, eliminate wastes, and maintain blood pressure. For AP ® , you do not need to memorize the list of hormones that control osmoregulatory functions or their specific function(s). However, information in this section applies to concepts previously explored.

    The kidneys synchronize with hormonal cues. As you recall from our study of the endocrine system, hormones are small messenger molecules that travel in the bloodstream to affect a target cell. Different regions of the nephron have specialized cells with receptors to respond to chemical messengers and hormones. Table 32.1 summarizes the hormones that control the osmoregulatory functions. For example, the flight/flight hormones epinephrine and norepinephrine, released by the adrenal medulla and nervous subsystem, respectively, halt kidney function temporarily when the body is under extreme stress and much of the body’s energy is used to combat imminent danger. Another example is the rennin-angiotensin-aldosterone system that increases blood pressure and volume primarily by constricting blood vessels. Another hormone, antidiuretic hormone (ADH) increases membrane permeability to water in the collecting ducts of the nephron by adding aquaporins, causing more water to be reabsorbed. You’ve experienced the effects of ADH when it’s hot outside and you’re running around the athletic field since you’re losing water by sweating and breathing hard, ADH prevents you from losing more water in urine and risking dehydration.

    Information presented and the examples highlighted in the section support concepts outlined in Big Idea 3 of the AP ® Biology Curriculum Framework. The AP ® Learning Objectives listed in the Curriculum Framework provide a transparent foundation for the AP ® Biology course, an inquiry-based laboratory experience, instructional activities, and AP ® exam questions. A learning objective merges required content with one or more of the seven science practices.

    Big Idea 3 Living systems store, retrieve, transmit and respond to information essential to life processes.
    Enduring Understanding 3.D Cells communicate by generating, transmitting and receiving chemical signals.
    Essential Knowledge 3.D.2 Cells communicate with each other through direct contact with other cells or from a distance via chemical signaling.
    Science Practice 6.2 The student can construct explanations of phenomena based on evidence produced through scientific practices.
    Learning Objective 3.34 The student is able to construct explanations of cell communication through cell-to-cell direct contact or through chemical signaling.
    Essential Knowledge 3.D.2 Cells communicate with each other through direct contact with other cells or from a distance via chemical signaling.
    Science Practice 1.1 The student can create representations and models of natural or man-made phenomena and systems in the domain.
    Learning Objective 3.35 The student is able to create representation(s) that depict how cell-to-cell communication occurs by direct contact or from a distance through chemical signaling.
    Hormone Where produced Function
    Epinephrine and Norepinephrine Adrenal medulla Can decrease kidney function temporarily by vasoconstriction
    Renin Kidney nephrons Increases blood pressure by acting on angiotensinogen
    Angiotensin Liver Angiotensin II affects multiple processes and increases blood pressure
    Aldosterone Adrenal cortex Prevents loss of sodium and water
    Anti-diuretic hormone (vasopressin) Hypothalamus (stored in the posterior pituitary) Prevents water loss
    Atrial natriuretic peptide Heart atrium Decreases blood pressure by acting as a vasodilator and increasing glomerular filtration rate decreases sodium reabsorption in kidneys

    Epinephrine and Norepinephrine

    Epinephrine and norepinephrine are released by the adrenal medulla and nervous system respectively. They are the flight/fight hormones that are released when the body is under extreme stress. During stress, much of the body’s energy is used to combat imminent danger. Kidney function is halted temporarily by epinephrine and norepinephrine. These hormones function by acting directly on the smooth muscles of blood vessels to constrict them. Once the afferent arterioles are constricted, blood flow into the nephrons stops. These hormones go one step further and trigger the renin-angiotensin-aldosterone system.

    Renin-Angiotensin-Aldosterone

    The renin-angiotensin-aldosterone system, illustrated in Figure 32.16 proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone (ADH) from the hypothalamus, leading to water retention in the kidneys. It acts directly on the nephrons and decreases glomerular filtration rate. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).

    Mineralocorticoids

    Mineralocorticoids are hormones synthesized by the adrenal cortex that affect osmotic balance. Aldosterone is a mineralocorticoid that regulates sodium levels in the blood. Almost all of the sodium in the blood is reclaimed by the renal tubules under the influence of aldosterone. Because sodium is always reabsorbed by active transport and water follows sodium to maintain osmotic balance, aldosterone manages not only sodium levels but also the water levels in body fluids. In contrast, the aldosterone also stimulates potassium secretion concurrently with sodium reabsorption. In contrast, absence of aldosterone means that no sodium gets reabsorbed in the renal tubules and all of it gets excreted in the urine. In addition, the daily dietary potassium load is not secreted and the retention of K + can cause a dangerous increase in plasma K + concentration. Patients who have Addison's disease have a failing adrenal cortex and cannot produce aldosterone. They lose sodium in their urine constantly, and if the supply is not replenished, the consequences can be fatal.

    Antidiurectic Hormone

    As previously discussed, antidiuretic hormone or ADH (also called vasopressin), as the name suggests, helps the body conserve water when body fluid volume, especially that of blood, is low. It is formed by the hypothalamus and is stored and released from the posterior pituitary. It acts by inserting aquaporins in the collecting ducts and promotes reabsorption of water. ADH also acts as a vasoconstrictor and increases blood pressure during hemorrhaging.

    Atrial Natriuretic Peptide Hormone

    The atrial natriuretic peptide (ANP) lowers blood pressure by acting as a vasodilator. It is released by cells in the atrium of the heart in response to high blood pressure and in patients with sleep apnea. ANP affects salt release, and because water passively follows salt to maintain osmotic balance, it also has a diuretic effect. ANP also prevents sodium reabsorption by the renal tubules, decreasing water reabsorption (thus acting as a diuretic) and lowering blood pressure. Its actions suppress the actions of aldosterone, ADH, and renin.

    Science Practice Connection for AP® Courses

    Think About It

    Create a diagram to show an example of a hormone and how the hormone works in regulating an osmoregulatory process such as maintaining blood pressure and blood volume and altering kidney function to reduce the amount of water eliminated in urine.

    Teacher Support

    The question is an application of AP ® Learning Objective 3.35 and Science Practice 1.1 because students are creating a diagram to depict how cell communication can occur via hormonal signaling, altering body physiology.

    Renin is made by ________.

    Patients with Addison's disease ________.

    Which hormone elicits the “fight or flight” response?

    Describe how hormones regulate blood pressure, blood volume, and kidney function.

    Hormones are small molecules that act as messengers within the body. Different regions of the nephron bear specialized cells, which have receptors to respond to chemical messengers and hormones. The hormones carry messages to the kidney. These hormonal cues help the kidneys synchronize the osmotic needs of the body. Hormones like epinephrine, norepinephrine, renin-angiotensin, aldosterone, anti-diuretic hormone, and atrial natriuretic peptide help regulate the needs of the body as well as the communication between the different organ systems.

    How does the renin-angiotensin-aldosterone mechanism function? Why is it controlled by the kidneys?

    The renin-angiotensin-aldosterone system acts through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I. ACE (angiotensin converting enzyme) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It triggers the release of aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone from the hypothalamus, which leads to water retention. It acts directly on the nephrons and decreases GFR.

    As an Amazon Associate we earn from qualifying purchases.

    Want to cite, share, or modify this book? This book is Creative Commons Attribution License 4.0 and you must attribute OpenStax.

      If you are redistributing all or part of this book in a print format, then you must include on every physical page the following attribution:

    • Use the information below to generate a citation. We recommend using a citation tool such as this one.
      • Authors: Julianne Zedalis, John Eggebrecht
      • Publisher/website: OpenStax
      • Book title: Biology for AP® Courses
      • Publication date: Mar 8, 2018
      • Location: Houston, Texas
      • Book URL: https://openstax.org/books/biology-ap-courses/pages/1-introduction
      • Section URL: https://openstax.org/books/biology-ap-courses/pages/32-5-hormonal-control-of-osmoregulatory-functions

      © Jan 12, 2021 OpenStax. Textbook content produced by OpenStax is licensed under a Creative Commons Attribution License 4.0 license. The OpenStax name, OpenStax logo, OpenStax book covers, OpenStax CNX name, and OpenStax CNX logo are not subject to the Creative Commons license and may not be reproduced without the prior and express written consent of Rice University.


      A molecular cell biology of lithium

      R. Williams, W.J. Ryves, E.C. Dalton, B. Eickholt, G. Shaltiel, G. Agam, A.J. Harwood A molecular cell biology of lithium. Biochem Soc Trans 1 November 2004 32 (5): 799–802. doi: https://doi.org/10.1042/BST0320799

      Lithium (Li + ), a mood stabilizer, has profound effects on cultured neurons, offering an opportunity to investigate its cellular biological effects. Here we consider the effect of Li + and other psychotropic drugs on growth cone morphology and chemotaxis. Li + inhibits GSK-3 (glycogen synthase kinase-3) at a therapeutically relevant concentration. Treated cells show a number of features that arise due to GSK-3 inhibition, such as altered microtubule dynamics, axonal branching and loss of semaphorin 3A-mediated growth cone collapse. Li + also causes growth cones to spread however, a similar effect is seen with two other mood stabilizers, valproic acid and carbamazepine, but without changes in microtubules or axon branching. This common effect of mood stabilizers is mediated by changes in inositol phosphate signalling, not GSK-3 activity. Given the presence of neurogenesis in the adult brain, we speculate that changes in growth cone behaviour could also occur during treatment of mental disorders.


      Human Biologists confront the COVID-19 pandemic

      The COVID-19 pandemic stands as the defining global health crisis of our age, transforming human societies and exacerbating long-standing social and health inequalities. As a field that integrates across the biological and social sciences, human biology is uniquely positioned to offer important insights on nature and differential impact of the pandemic. In this special issue of the American Journal of Human Biology, I have invited a diverse group of scholars to provide Commentaries on the COVID-19 pandemic from the perspective their research. These 14 Commentaries highlight the impressive scope of work being undertaken in our field to address this pandemic. All of these contributions are freely-accessible and are also posted on Wiley's Covid-19 Resource Center (https://novel-coronavirus.onlinelibrary.wiley.com/).

      The Commentaries by McDade & Sancilio ( 2020 ), Jones, Hazel, & Almquist ( 2020 ) and Moya et al. ( 2020 ) showcase the methodological and analytical innovations that human biologists are making in advancing testing, diagnostics, and modelling the spread of the virus. Thom McDade & Amelia Sancilio (2020) discuss how the field-based research approaches developed and used by human biologists can play a critical role in advancing community-based COVID-19 research. In particular, McDade et al.' ( 2020 ) recently-developed technique for measuring SARS coronavirus-2 (SARS-CoV-2) IgG antibodies in dried blood spot samples offers an important tool for assessing variation in the impact of the pandemic in diverse populations around the globe.

      James Jones et al. ( 2020 ) provide an overview of the application of transmission-dynamic models for understanding the impact of the COVID-19 pandemic. Such models were critically important in helping epidemiologists estimate the size and scope of the early stages of the epidemic in China (Li et al., 2020 ). More recent studies have used transmission-dynamic models to explore postpandemic conditions such as the potential for seasonality in SARS-CoV-2 outbreaks and the need for prolonged or intermittent social distancing (Kissler et al., 2020 ).

      Cristina Moya et al. ( 2020 ) explore the challenges associated with promoting behavioral change that will reduce the impact of the pandemic. They suggest that models and insights from evolutionary biology may be help to improve public health strategies for effecting such change.

      Theodore Schurr ( 2020 ) examines the potential genetic risk factors for SARS-CoV-2 infection. He notes that most of the genes currently identified likely have a relatively limited impact on infection risk. These findings suggest that social factors and other health risks and comorbidities are having a much stronger hand in shaping the disparities in the impact of the virus across communities and populations.

      Commentaries by Gildner & Thayer ( 2020 ), Palmquist, Asiodu, & Quinn ( 2020 ), and Bogin & Varea ( 2020 ) examine the potential transgenerational effects of the pandemic through its impacts on maternal-child health. Theresa Gildner & Zane Thayer (2020) nicely summarize several ongoing studies by human biologists that are exploring the consequences of the pandemic for different dimensions of mother-infant well-being (eg, immune function, psychosocial stress, infant feeding). Aunchalee Palmquist et al. ( 2020 ), in turn, provide a critical evaluation of the wave of recent studies designed to understand whether SARS-CoV-2 can be transmitted to an infant through breastmilk. They discuss both the difficulties in conducting such research under pandemic conditions as well as the challenges in translating these findings into relevant clinical and public health recommendations. Palmquist and colleagues underscore the importance of the comparative, anthropological/evolutionary perspective in providing the necessary context for understanding the how the COVID-19 pandemic is shaping maternal-child health.

      Barry Bogin and Carlos Varea (2020) explore how the pandemic may be contributing to maternal stress, low birth weights, and later-life health outcomes. Drawing on previous analyses of changes in birth weight in Spain in response to the 2008 financial crisis (see Terán et al., 2020 ), Bogin & Varea offer predictions on how COVID-19 will impact birth weight and infant health in the next generation. They suggest that it may take two or more generations to fully evaluate the consequences of the pandemic on human health across the life cycle.

      Peter Katzmarzyk, J. Michael Salbaum, & Steven Heymsfield ( 2020 ) consider the role of obesity and other chronic health problems in increasing the risk of severe COVID-19 complications. Recent work from the UK indicates that even modest levels of excess weight are associated with greater risk of hospitalization due to COVID-19 (Hamer et al., 2020 ). While the mechanisms responsible for these interactions have not yet been determined, it is clear that this dynamic between chronic health problems and SARS-CoV-2 infection is further exacerbating long-standing social and ethnic health disparities.

      Contributions by Brewis, Wutich & Mahdavi ( 2020 ), Bentley ( 2020 ), Gibb et al. ( 2020 ) and Gravlee ( 2020 ) evaluate dimensions of social and ethnic disparities in the impact of COVID-19. Alexandra Brewis and colleagues draw on insights from their previous research (eg, Brewis & Wutich, 2019 ) to offer predictions on the role of stigma in promoting disparities in the effects of COVID-19. They highlight the powerful and long-lasting effect that the stigma associated with SARS-CoV-2 infection is likely to have, along with the outlining the mechanisms through which stigma leverages inequalities in both mental and physical health.

      Gillian Bentley ( 2020 ) considers the influence of structural inequalities on producing ethnic disparities in the impact of the pandemic. The model presented by Bentley nicely complements the Commentary by Katzmarzyk and colleagues in showing how larger structural inequalities over the life course contribute to cardiometabolic health problems that increase susceptibility to COVID-19.

      James Gibb et al. ( 2020 ) address the differential impact of COVID-19 on sexual and gender minority (SGM) health. They note that the pandemic has further exacerbated the structural and interpersonal stigma and discrimination that SGM people have long experienced. Gibb and colleagues underscore the important role that human biologists can play in shaping policies and recommendations to promote more equitable responses to this health crisis.

      Lance Gravlee ( 2020 ) broadens the lens on health disparities by using a syndemics framework to explore the interaction of COVID-19 with systemic racism and chronic health problems. The syndemics concept, developed and advanced by Merrill Singer and colleagues (eg, Singer, 2009 Mendenhall & Singer, 2020 ), highlights the roles of social and political-economic forces in promoting and sustaining synergistic interactions among co-occurring disease epidemics. Gravlee offers a detailed syndemic model, articulating the pathways through which conditions of systemic racism and social distress contribute to the rising and interacting disparities in the impact of cardiometabolic diseases and COVID-19.

      Andrew Kim ( 2020 ) provides his insights on strategies for addressing the mental health consequences of the COVID-19 pandemic from his ongoing research in Soweto, South Africa. His commentary offers ethnographic accounts of COVID-19 from his fieldwork on trauma and mental health. In addition, Kim discusses the measures that he and his colleagues have implemented to the safeguard the mental health of research staff, study participants, and their communities.

      Cara Ocobock and Christopher Lynn ( 2020 ) conclude this special issue by discussing the critical importance of effective science communication on the pandemic. They offer a range of recommendations for increasing the impact and exposure (eg, blogs, podcasts, local events, multimedia formats) of our work. As the Social Media Editors for the AJHB, Ocobock and Lynn will also be doing a Sausage of Science podcast (https://www.humbio.org/podcasts/) with the contributing authors to this special issue to further highlight the distinctive approaches and perspectives that human biologists are using to understand and address the pandemic.

      I sincerely thank all the authors for their thoughtful and timely contributions to this special COVID-19 issue of the journal. I hope and expect that these Commentaries will help stimulate further research and collaboration to better understand and address the biosocial dimensions of this pandemic. The AJHB will continue to be an important venue for publishing original research, reviews, and commentary on COVID-19.


      Watch the video: Lecture4 Part1 HowGenesWork BIO110 (October 2022).