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G.K -Parts of a plant
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SYI-1.D: Describe the structure and/ or function of subcellular components and organelles. ★ SYI-1.E: Explain how subcellular components and organelles contribute to the function of the cell. ★ SYI-1.F: Describe the structural features of a cell that allow organisms to capture, store, and use energy. ★ ENE-1.B: Explain the effect of surface area-to-volume ratios on the exchange of materials between cells or organisms and the environment. ★ ENE-1.C: Explain how specialized structures and strategies are used for the efficient exchange of molecules to the environment. ★ ENE-2.A: Describe the roles of each of the components of the cell membrane in maintaining the internal environment of the cell. ★ ENE-2.B: Describe the Fluid Mosaic Model of cell membranes. ★ ENE-2.C: Explain how the structure of biological membranes influences selective permeability. ★ ENE-2.D: Describe the role of the cell wall in maintaining cell structure and function. ★ ENE-2.E: Describe the mechanisms that organisms use to maintain solute and water balance. ★ ENE-2.F: Describe the mechanisms that organisms use to transport large molecules across the plasma membrane. ★ ENE-2.G: Explain how the structure of a molecule affects its ability to pass through the plasma membrane. ★ ENE-2.H: Explain how concentration gradients affect the ★ movement of molecules across membranes. ★ ENE-2.I: Explain how osmoregulatory mechanisms contribute to the health and survival of organisms. ★ ENE-2.J: Describe the processes that allow ions and other molecules to move across membranes. ★ ENE-2.K: Describe the membrane-bound structures of the eukaryotic cell. ★ ENE-2.L: Explain how internal membranes and membrane- bound organelles contribute to compartmentalization of eukaryotic cell functions. ★ EVO-1.A: Describe similarities and/or differences in compartmentalization between prokaryotic and eukaryotic cells. ★ EVO-1.B: Describe the relationship between the functions of endosymbiotic organelles and their free-living ancestral counterpartsCovalent Molecules and Compounds Just as an atom is the simplest unit that has the fundamental chemical properties of an element, a molecule is the simplest unit that has the fundamental chemical properties of a covalent compound. Some pure elements exist as covalent molecules. Hydrogen, nitrogen, oxygen, and the halogens occur naturally as the diatomic (“two atoms”) molecules H2, N2, O2, F2, Cl2, Br2, and I2 (part (a) in Figure 3.1.1). Similarly, a few pure elements exist as polyatomic (“many atoms”) molecules, such as elemental phosphorus and sulfur, which occur as P4 and S8 (part (b) in Figure 3.1.1). Each covalent compound is represented by a molecular formula, which gives the atomic symbol for each component element, in a prescribed order, accompanied by a subscript indicating the number of atoms of that element in the molecule. The subscript is written only if the number of atoms is greater than 1. For example, water, with two hydrogen atoms and one oxygen atom per molecule, is written as H2O. Similarly, carbon dioxide, which contains one carbon atom and two oxygen atoms in each molecule, is written as CO2. Covalent compounds that predominantly contain carbon and hydrogen are called organic compounds. The convention for representing the formulas of organic compounds is to write carbon first, followed by hydrogen and then any other elements in alphabetical order (e.g., CH4O is methyl alcohol, a fuel). Compounds that consist primarily of elements other than carbon and hydrogen are called inorganic compounds; they include both covalent and ionic compounds. In inorganic compounds, the component elements are listed beginning with the one farthest to the left in the periodic table, as in CO2 or SF6. Those in the same group are listed beginning with the lower element and working up, as in ClF. By convention, however, when an inorganic compound contains both hydrogen and an element from groups 13–15, hydrogen is usually listed last in the formula. Examples are ammonia (NH3) and silane (SiH4). Compounds such as water, whose compositions were established long before this convention was adopted, are always written with hydrogen first: Water is always written as H2O, not OH2. The conventions for inorganic acids, such as hydrochloric acid (HCl) and sulfuric acid (H2SO4), are described elswhere. Note! For organic compounds: write C first, then H, and then the other elements in alphabetical order. For molecular inorganic compounds: start with the element at far left in the periodic table; list elements in same group beginning with the lower element and working up. Write the molecular formula of each compound. a. The phosphorus-sulfur compound that is responsible for the ignition of so-called strike anywhere matches has 4 phosphorus atoms and 3 sulfur atoms per molecule. b. Ethyl alcohol, the alcohol of alcoholic beverages, has 1 oxygen atom, 2 carbon atoms, and 6 hydrogen atoms per molecule. c. Freon-11, once widely used in automobile air conditioners and implicated in damage to the ozone layer, has 1 carbon atom, 3 chlorine atoms, and 1 fluorine atom per molecule. Solution: a. • A The molecule has 4 phosphorus atoms and 3 sulfur atoms. Because the compound does not contain mostly carbon and hydrogen, it is inorganic. • B Phosphorus is in group 15, and sulfur is in group 16. Because phosphorus is to the left of sulfur, it is written first. • C Writing the number of each kind of atom as a right-hand subscript gives P4S3 as the molecular formula. b. • A Ethyl alcohol contains predominantly carbon and hydrogen, so it is an organic compound. • B The formula for an organic compound is written with the number of carbon atoms first, the number of hydrogen atoms next, and the other atoms in alphabetical order: CHO. • C Adding subscripts gives the molecular formula C2H6O. c. • A Freon-11 contains carbon, chlorine, and fluorine. It can be viewed as either an inorganic compound or an organic compound (in which fluorine has replaced hydrogen). The formula for Freon-11 can therefore be written using either of the two conventions. • B According to the convention for inorganic compounds, carbon is written first because it is farther left in the periodic table. Fluorine and chlorine are in the same group, so they are listed beginning with the lower element and working up: CClF. Adding subscripts gives the molecular formula CCl3F. • C We obtain the same formula for Freon-11 using the convention for organic compounds. The number of carbon atoms is written first, followed by the number of hydrogen atoms (zero) and then the other elements in alphabetical order, also giving CCl3F. Write the molecular formula for each compound. a. Nitrous oxide, also called “laughing gas,” has 2 nitrogen atoms and 1 oxygen atom per molecule. Nitrous oxide is used as a mild anesthetic for minor surgery and as the propellant in cans of whipped cream. b. Sucrose, also known as cane sugar, has 12 carbon atoms, 11 oxygen atoms, and 22 hydrogen atoms. c. Sulfur hexafluoride, a gas used to pressurize “unpressurized” tennis balls and as a coolant in nuclear reactors, has 6 fluorine atoms and 1 sulfur atom per molecule. Answer: a. N2O b. C12H22O11 c. SF6. Ionic Compounds The substances described in the preceding discussion are composed of molecules that are electrically neutral; that is, the number of positively-charged protons in the nucleus is equal to the number of negatively-charged electrons. In contrast, ions are atoms or assemblies of atoms that have a net electrical charge. Ions that contain fewer electrons than protons have a net positive charge and are called cations. Conversely, ions that contain more electrons than protons have a net negative charge and are called anions. Ionic compounds contain both cations and anions in a ratio that results in no net electrical charge. Note! Ionic compounds contain both cations and anions in a ratio that results in zero electrical charge.An ionic compound that contains only two elements, one present as a cation and one as an anion, is called a binary ionic compound. One example is MgCl2, a coagulant used in the preparation of tofu from soybeans. For binary ionic compounds, the subscripts in the empirical formula can also be obtained by crossing charges: use the absolute value of the charge on one ion as the subscript for the other ion. This method is shown schematically as follows: Crossing charges. One method for obtaining subscripts in the empirical formula is by crossing charges. When crossing charges, it is sometimes necessary to reduce the subscripts to their simplest ratio to write the empirical formula. Consider, for example, the compound formed by Mg2+ and O2−. Using the absolute values of the charges on the ions as subscripts gives the formula Mg2O2:Polyatomic Ions Polyatomic ions are groups of atoms that bear net electrical charges, although the atoms in a polyatomic ion are held together by the same covalent bonds that hold atoms together in molecules. Just as there are many more kinds of molecules than simple elements, there are many more kinds of polyatomic ions than monatomic ions. Two examples of polyatomic cations are the ammonium (NH4+) and the methylammonium (CH3NH3+) ions. P. The method used to predict the empirical formulas for ionic compounds that contain monatomic ions can also be used for compounds that contain polyatomic ions. The overall charge on the cations must balance the overall charge on the anions in the formula unit. Thus, K+ and NO3− ions combine in a 1:1 ratio to form KNO3 (potassium nitrate or saltpeter), a major ingredient in black gunpowder. Similarly, Ca2+ and SO42− form CaSO4 (calcium sulfate), which combines with varying amounts of water to form gypsum and plaster of Paris. The polyatomic ions NH4+ and NO3− form NH4NO3 (ammonium nitrate), a widely used fertilizer and, in the wrong hands, an explosive. One example of a compound in which the ions have charges of different magnitudes is calcium phosphate, which is composed of Ca2+ and PO43− ions; it is a major component of bones. The compound is electrically neutral because the ions combine in a ratio of three Ca2+ ions [3(+2) = +6] for every two ions [2(−3) = −6], giving an empirical formula of Ca3(PO4)2; the parentheses around PO4 in the empirical formula indicate that it is a polyatomic ion. Writing the formula for calcium phosphate as Ca3P2O8 gives the correct number of each atom in the formula unit, but it obscures the fact that the compound contains readily identifiable PO43− ions.Summary • There are two fundamentally different kinds of chemical bonds (covalent and ionic) that cause substances to have very different properties. • The composition of a compound is represented by an empirical or molecular formula, each consisting of at least one formula unit.Contributors The atoms in chemical compounds are held together by attractive electrostatic interactions known as chemical bonds. Ionic compounds contain positively and negatively charged ions in a ratio that results in an overall charge of zero. The ions are held together in a regular spatial arrangement by electrostatic forces. Most covalent compounds consist of molecules, groups of atoms in which one or more pairs of electrons are shared by at least two atoms to form a covalent bond. The atoms in molecules are held together by the electrostatic attraction between the positively charged nuclei of the bonded atoms and the negatively charged electrons shared by the nuclei. The molecular formula of a covalent compound gives the types and numbers of atoms present. Compounds that contain predominantly carbon and hydrogen are called organic compounds, whereas compounds that consist primarily of elements other than carbon and hydrogen are inorganic compounds. Diatomic molecules contain two atoms, and polyatomic molecules contain more than two. A structural formula indicates the composition and approximate structure and shape of a molecule. Single bonds, double bonds, and triple bonds are covalent bonds in which one, two, and three pairs of electrons, respectively, are shared between two bonded atoms. Atoms or groups of atoms that possess a net electrical charge are called ions; they can have either a positive charge (cations) or a negative charge (anions). Ions can consist of one atom (monatomic ions) or several (polyatomic ions). The charges on monatomic ions of most main group elements can be predicted from the location of the element in the periodic table. Ionic compounds usually form hard crystalline solids with high melting points. Covalent molecular compounds, in contrast, consist of discrete molecules held together by weak intermolecular forces and can be gases, liquids, or solids at room temperature and pressure. An empirical formula gives the relative numbers of atoms of the elements in a compound, reduced to the lowest whole numbers. The formula unit is the absolute grouping represented by the empirical formula of a compound, either ionic or covalent. Empirical formulas are particularly useful for describing the composition of ionic compounds, which do not contain readily identifiable molecules. Some ionic compounds occur as hydrates, which contain specific ratios of loosely bound water molecules called waters of hydration.What is Electric Force? Electric force is just one of many types of forces in the world of physics. Forces are how and why things move, and can be explained by Newton's Laws of Motion. On the smallest scale, electric force is the resulting interaction between two charged particles. These charges can be either positive or negative. Larger objects can be charged by having an abundance of either of these particles, and therefore can create an electric force on a larger scale. Electric force is the reason why hair will sometimes stand up on its own and is also why we have electricity, allowing us to live in the modern world with lights and technology. Even out in nature electric force is present, as electric force causes lightning to strike. Electric force is fundamental to our everyday way of living. Reviewing Newton's Laws of Motion Newton's Laws of motion are the basic principles or ground rules that are applied all across physics. They describe how objects move and can be used to describe the interaction of charges. They are the following: An object in motion will stay in motion unless an external force is applied The force exerted on an object is equal to the mass times the acceleration of the object. ( ) Every force has an equal and opposite force Newton's laws explain how and why charged particles move. Since there is a force involved (e.g. electric force), particles will move around, which is explained by the first law. The second law describes how acceleration of charges can be calculated once the electric force is known. The third law explains how attractive and repulsive forces between charged objects are equal and opposite. Electric Force Examples and Types of Charge As previously mentioned, there are only two types of charges; positive and negative. Two like charges will repel (or move away from) each other, and two opposite charges will attract (or move towards) each other. In other words, two positive or two negative charges will repel, while a positive and a negative charge will attract. Opposite charges will attract while like charges will repel. Attraction versus Repelling Forces Notice how the forces acting upon each other are equal and opposite, as Newton's third law states. Both charges are exerting forces onto each other. Charges in Atoms An atom is made up of three types of particles; protons, neutrons, and electrons. Protons have a positive charge, neutrons have no charge, and electrons have a negative charge. There are no positive or negative charges smaller than protons and electrons. Objects on a larger scale result in an overall positive or negative charged due to an uneven distribution of protons to electrons. An atom consisting of more protons than electrons would be considered positive, and an atom with more electrons than protons would be considered negative. Protons are held close to the nucleus and are tightly bound to an atom, so it's difficult for protons to escape an atom. Electrons, on the other hand, are much further away from the nucleus of an atom. This makes it much easier for them to be removed from an atom. Electrons can leave or join atoms, making them positive or negative depending on the amount of protons. Similarly, for the bigger picture, overall materials and objects with more electrons than protons would be considered negative, and vice versa. Electric Force Examples Hair standing up: When hair is brushed, the hairbrush can strip electrons from hair strands, resulting in the hair being positively charged. This addition of electrons to the hairbrush in turn makes the hairbrush negatively charged. Since the hair is now positively charged, and like forces repel, hair strands will move away from each other, resulting in the hair standing up. Current electricity: All of our everyday technology is powered through current electricity, which is the consistent flow of electrons through conductive materials. This flow is caused by the electric force, as the electrons flow from a negative source to a positive source. Lightning: During a storm, it is common for an abundance of electrons to build up on the bottom of a cloud, making that part of the cloud negatively charged. Positive charges in the ground start to gather on the surface or even on tall objects such as trees as they are attracted towards the negatively charged undersides of clouds. Lightning strikes as a result of these charges becoming extremely built up. Lightning is caused by electric force Lightning Electric Force Equation: Coulomb's Law The magnitude of the electric force, or the amount of force in which objects repel or attract, depends on the distance between the two charged objects and the amount of charge each object carries. The electric force is stronger the closer together the two charges are, and weaker as the two charges move apart. Electric force is also stronger with more charge, and weaker with less charge. This effect on electric force is predictable, and is known as Coulomb's Law. It can be calculated using a mathematical equation, and the resulting magnitude of electric force is measured in Newtons. Coulomb's Law Electric force can be calculated using the following equation known as Coulomb's Law: In this equation, F is the electric force measured in newtons, K is a constant known as the electrostatic constant, and are charges one and two measured in coulombs, and is the radial distance in meters between the two charges. Since the distance is squared and on the denominator, the electric force drops off exponentially as charges move away from each other. This means that the Electric force is inversely proportional to distance. As charges move away from each other, the electric force between them gets smaller and smaller, until the force is negligible. The amount of charges are in the numerator of this equation, making the magnitude of the force larger with more charge. This means that the force is directly proportional to the amount of charge. When the charges are smaller, the amount of force will be smaller. When there is a lot of charge, the force will be much greater. When calculating the electric force using Coulomb's law, the resulting answer only gives the magnitude of the force and not the direction. In order to know the direction, you must know the types of charges. Once again, like forces repel, and unlike forces attract. It helps to draw a visual representation, or a free-body diagram, of the charges and forces acting upon them in order to understand the resulting force direction. Electric Field versus Electric Force An electric field is a direct result of an electric force. Its pure definition is electric force per unit charge, and can be thought of as a mapping of the force vectors. An electric field is present anytime there is an electric force. Therefore, when there are two or more charged particles, there is a surrounding electric field. The direction of the electric field is the direction a positive charge would flow if it were placed within the field. The electric field moves out from a positive charge and goes into a negative charge. Particles with unlike charges move towards each other, and their corresponding electric field lines move out from the positive charge and into the negative charge. The strength of the force at any given point can be seen through the spacing of the electric field lines. The electric force is strongest where the electric field lines are closest together, and weaker as these lines move apart. Like Coulomb's law expresses, electric field lines show how the electric force is strongest with a minimum distance between the two charges. Unlike charges will result in a repelling force, and the resulting electric field is a visual representation of this effect. Electric fields of two positive charges have the electric field moving out away from both of them. As with two negative charges, the field lines move in towards each negative. Lesson Summary An electric force is created when there are two or more charged particles or objects. These charges can be either positive or negative. Like charges will attract (move towards each other) while unlike charges will repel (move away from each other). As Newton's third law suggests, the forces acting upon each other are both equal and opposite. Electrons and protons within an atom are the two smallest types of charges there are. Electrons carry a negative charge while protons carry a positive charge. Electrons can be easily removed or added to atoms, making the overall charge positive or negative. Objects with more electrons than protons are negatively charged. Electric force is strengthened with increased charge and a shorter distance between the charges. This effect is known as Coulomb's law and can be calculated with the Coulomb's law equation. The magnitude of the force is measured in Newtons, and the direction can be determined by knowing whether the charges are attracting or repelling each other. An electric field is present wherever there is an electric force. The direction of this electric field is the direction a positive charge would flow if it where to be dropped in the field, which is from the positive to the negative. Received: 26 November 2019 Revised: 10 January 2020 Accepted: 19 January 2020 DOI: 10.1111/obr.13005 PEDIATRICS/PHYSIOLOGY Adipokines: A gear shift in puberty Desirée Nieuwenhuis | Natàlia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-α alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- α and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-α 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-α, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-α and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. The majority of the studies examining boys with obesity indicate an early onset of puberty, while not all reported an earlier onset of puberty. In detail, high leptin, TNF-α, and IL-6 levels combined with low adiponectin levels stimulate the activation of the HPG axis in girls and boys with obesity, and 5, 45, 50, 51 REFERENCES 1. Kumar S, Kelly AS. Review of childhood obesity: from epidemiology, etiology, and comorbidities to clinical assessment and treatment. May- o Clin Proc. 2017;92(2):251-265. 2. Reinehr T, Roth CL. Is there a causal relationship between obesity and puberty? The Lancet Child & adolescent health. 2019;3(1):44-54. 3. WorldHealthOrganization. Facts and figures on childhood obesity. 2017. 4. Guglielmi V, Sbraccia P. Obesity phenotypes: depot-differences in adipose tissue and their clinical implications. Eat Weight Disord. 2018; 23(1):3-14. 5. Gomez-Hernandez A, Beneit N, Diaz-Castroverde S. Escribano O. 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FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including ‘onset of puberty and adiposity/obesity’, ‘onset of puberty’, ‘children with obesity’, ‘adipose tissue’, ‘childhood obesity’, ‘adiposity’, ‘obesity’, ‘adipokine(s)’, ‘HPG axis’, ‘adipokines ovary/ova- ries’, or ‘adipokines testes’, either alone or in combination. 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The relationship between obesity and body compositions with respect to the timing of puberty in Chongqing adolescents: a cross-sectional study. BMC Pub- lic Health. 2017;17:664-673. 81. Ishikawa T, Fujioka H, Ishimura T, Takenaka A, Fujisawa M. Expres- sion of leptin and leptin receptor in the testis of fertile and infertile patients. Andrologia. 2007;39(1):22-27. 82. Martins AD, Moreira AC, Sa R, et al. Leptin modulates human Sertoli cells acetate production and glycolytic profile: a novel mechanism of obesity-induced male infertility? Biochim Biophys Acta. 1852;2015: 1824-1832. 83. Morash BA, Willkinson D, Ur E, Wilkinson M. Resistin expression and regulation in mouse pituitary. FEBS Lett. 2002;526(1-3):26-30. 84. Cabrera SM, Bright GM, Frane JW, Blethen SL, Lee PA. Age of thelarche and menarche in contemporary US females: a cross- sectional analysis. Journal of pediatric endocrinology & metabolism: JPEM. 2014;27(1-2):47-51. 85. Herman-Giddens ME, Steffes J, Harris D, et al. Secondary sexual characteristics in boys: data from the Pediatric Research in Office Settings Network. Pediatrics. 2012;130(5):e1058-e1068. 86. WHO. Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. World Health Organ Tech Rep Ser. 1995;854:1-452. 87. Akin I, Tolg R, Hochadel M, et al. No evidence of “obesity paradox” after treatment with drug-eluting stents in a routine clinical practice: results from the prospective multicenter German DES.DE (German Drug-Eluting Stent) Registry. JACC Cardiovasc Interv. 2012;5(2): 162-169. 88. Marcovecchio ML, Chiarelli F. Obesity and growth during childhood and puberty. World Rev Nutr Diet. 2013;106:135-141. How to cite this article: Nieuwenhuis D, Pujol-Gualdo N, Arnoldussen IAC, Kiliaan AJ. Adipokines: A gear shift in puberty. Obesity Reviews. 2020;21:e13005. https://doi.org/ 10.1111/obr.13005 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are goverCan you create an evaluation using this information PHONETICS VS. PHONOLOGY Whereas phonetics is the study of sounds that occur in language, phonology is the study of how these sounds are organized and how they function in language. It uses the classifications of sounds derived from phonetics to describe and analyze how sounds occur in speech. STRUCTURALIST PHONEMICS STRUCTURALIST PHONEMICS As linguists began to study sounds in fine detail, they recognized increasingly complex aspects of phonetic organization. For example, the sound /p/ appears in different varieties in English. STRUCTURALIST PHONEMICS One of the varieties of /p/ is indicated by [ph]. This sound is produced with an accompanying puff of air called aspiration, as in the words “pill,” and “peace.” Another sound, indicated by [p•], is produced when there is little or no aspiration; this sound occurs in a word like “spill.” A third major variety for the /p/ sound is the unreleased [p– ], which may occur at the end of a word like “stop.” To deal with these variations for the /p/ sound, the structuralists suggested the existence of an abstract unit which they termed a phoneme. STRUCTURALIST PHONEMICS A phoneme was defined by the structuralists as an abstract phonological unit that represents a class of real sounds, termed the allophones of a phoneme. The phoneme /p/ in English, then, is represented by the allophones [ph], [p•], and [p– ]. STRUCTURALISTS: MINIMAL PAIRS How do we know what these abstract units of sound called phonemes are? In order to find the phonemes of a language, the structuralists developed the concept of the minimal pair, defined as any two words that: a) Contain the same number of segments b) Differ in meaning c) Exhibit only one phonetic difference. STRUCTURALISTS: MINIMAL PAIRS In practical terms, phonemes distinguish meanings; and a phoneme can also be defined as the smallest meaning-distinguishing unit of sound. For instance, the words “pin” /pɪn/ and “bin” /bɪn/ mean different things, and the only one difference in these words occurs in the initial sounds. STRUCTURALISTS: MINIMAL PAIRS By using the concept of a minimal pair, we can determine that the three variations of the /p/ sound do not represent three phonemes. Certainly, it is possible to pronounce the word cap with either an aspirated [ph ] or unreleased [p– ]; however, the two forms [kæph ] and [kæp– ] are not a minimal pair, even though they involve different sounds, because they are identical in meaning. STRUCTURALISTS: FREE VARIATION The two forms [kæph ] and [kæp– ] are, therefore, said to exhibit free variation: that is, the pronunciation may vary without signifying a change in meaning. In other words, we may conclude that the unreleased [p– ] and the aspirated [ph ] are not representations of different phonemes in English; they are, in fact, allophones of one phoneme, /p/. STRUCTURALISTS: COMPLEMENTARY DISTRIBUTION When phonemes have more than one allophone in a language, the allophones are said to be in complementary distribution. Complementary distribution means that the allophones of a phoneme occur in different phonetic environments (that is, with different sounds surrounding them). TRANSFORMATIONAL- GENERATIVE PHONOLOGY TRANSFORMATIONAL-GENERATIVE PHONOLOGY Transformational-generative phonology is a relatively recent development in linguistic theory. Chomsky launched Transformational-Generative Grammar in 1957, but the earliest studies within this framework were largely concerned with syntax. A decade later, the first comprehensive transformational-generative treatment of English phonology appeared: Chomsky and Halle’s The Sound Pattern of English (1968). TRANSFORMATIONAL-GENERATIVE PHONOLOGY Transformational-generative phonologists strongly oppose the structuralists’ phonemic level. They replace this level by a series of rules that directly relate underlying representations to observed phonetic representations. The central mechanisms in transformational-generative phonology, then, are underlying representations and phonological rules. PHONOLOGICAL RULES A rule is an operational statement in which some linguistic entity is modified, resulting in a new linguistic entity. Rules may add elements, remove elements, or change elements. By using phonological rules, linguists attempt to demonstrate that there is order in linguistic phenomena and that linguistic patterns are systematic. PHONOLOGICAL DERIVATION A phonological derivation is an operation that begins with an underlying representation and, through the application of a set of specific rules, yields the actual sound the speaker produces. The representation of a phonological rule has the following general appearance. /A/ → [B] / C “A” changes to “B” under condition “C” PHONOLOGICAL RULE – EXAMPLE In most Southern dialects, the word ten is pronounced like the word tin. This is not an isolated fact, for den is pronounced like din and Ben is pronounced like bin, and so on. This very general fact can be represented by the phonological rule: /ɛ/ → [I] / ___ [n] den /dɛn/ → /dIn/ Ben /bɛn/ → /bIn/ ten /tɛn/ → /tIn/ /ɛ/ → [I] / ___ [n] - high - low - tense + front + high - tense + front + sonorant + anterior + coronal - continuant NOTATIONAL DEVICES IN PHONOLOGICAL RULES The statement of phonological rules can be complex, and linguists have developed several notational devices for writing them. Often, the following symbols will be necessary for stating the conditions under which rules apply: # indicates a word boundary + indicates an intraword boundary $ indicates a syllable boundary UNDERLYING REPRESENTATIONS AND RELATED ISSUES The transformational-generative description of phonology relates underlying representations to phonetic representations by rules. This can be represented in a simple example: In English, there are certain pairs of words like sign / signature, and malign / malignant that exhibit a regular alternation in their phonetic representations: [g] is present in the second member of the pairs but absent in the first member. UNDERLYING REPRESENTATIONS AND RELATED ISSUES To explain the relatedness of words such as sign / signature, we could claim that the underlying representation of the segment in all such pairs is /g/ and that a rule operates to delete /g/ before syllable-final nasals. Thus, the rule “/g/ is deleted before syllable-final nasal” would appear formally as: + voice - anterior →∅ ____ [+ nasal] $ - coronal UNDERLYING REPRESENTATIONS AND RELATED ISSUES On the left-hand side of the arrow, we place the features needed to uniquely specify /g/ among the consonants; that is, no other consonant has the features [+ voice], [- anterior], and [- coronal]. The symbols → mean that the sound /g/ changes to nothing or more properly “/g/ is deleted.” The horizontal line following the slash mark refers to the position of /g/ - namely, before a segment that is [+nasal]. Finally, this [+nasal] segment occurs before a syllable boundary, as indicated by $. A less formal way of writing this rule would be: /g/ → / _ [+nasal] $ Notice that this rule also helps describe such alternations as phlegm/phlegmatic and paradigm/paradigmatic. Application Activity: Think of other words in which this rule can be applied. Write the sound segments to prove /g/ is deleted. Another example is the process through which the prefix meaning “not” is added to words. This prefix alternates among the forms /Im/, /In/, and /Iŋ/, depending on the point of articulation of the initial segment of the following word. -If the segment begins in the extreme front part of the mouth (labials), the form is /Im/, as in improper. -If the segment begins in the extreme back part of the mouth (velars), the form is /Iŋ/, as in incomplete. -If the segment begins in the mid-region of the mouth (all other sounds), the form is /In/, as in indecent. *Exceptions:Words beginning with /r/ or /l/. Analyze the Word “in + complete,” for example. /n/ → [ŋ] / __ [k] - continuant - continuant - continuant + sonorant → + sonorant - sonorant + anterior - anterior - strident + coronal - coronal - coronal + tense THE VELAR SOFTENING RULE Still another example of alternation in English is found in pairs of words like “electric / electricity,” in which the segments /k/ and /s/ alternate. /k/ changes to [s] only before non- low, front vowels. THE VELAR SOFTENING RULE /k/ → [s] / __ - continuant + continuant - strident → - sonorant V - anterior + anterior - low - coronal + coronal - backChapter 22 Antihypertensive Drugs Hypertension Defined (JNC-8) Pharmacology Overview 7 main categories of drugs to treat HTN Adrenergic drugs (old friend) Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers (ARBs) Calcium channel blockers (CCBs) Diuretics Vasodilators Direct renin inhibitors A. Adrenergic Drugs: 5 Subcategories and where they act A1. Adrenergic neuron blockers (central and peripheral)- we won’t talk about this A2. Alpha1 receptor blockers (peripheral) A3. Alpha2 receptor agonists (central) A4. Beta receptor blockers (peripheral) A5. Combined α and β receptor blockers (peripheral) A2. Peripherally Acting Adrenergic Drug Alpha1 Blockers (we’ve met these) Doxazosin, prazosin, alfuzosin Block alpha1-receptors which causes BP to decrease Reduces peripheral vascular resistance and BP by dilating both arterial and venous blood vessels Main Use: benign prostatic hyperplasia (BPH) Alpha1 Blockers REMEMBER Tamsulosin (Flomax)* is an α1 blocker BUT *Tamsulosin is not used to control BP, just for BPH. A3. Centrally Acting Adrenergic Drugs Alpha 2 agonist Clonidine and methyldopa 1- Stimulate alpha2-adrenergic receptors. in the brain Decreases sympathetic outflow from the CNS which decreases NE production 2. Stimulate alpha2-adrenergic receptors in kidneys remember alpha 2 opposes alpha 1 Dilates peripheral blood vessels → lowers peripheral resistance → Results in decreased BP So ….Clonidine (Catapres) Used primarily for its ability to decrease blood pressure in an urgent setting Also use in opioid withdrawal as previously discussed Oral (multiple times a day), and topical patch formulations Do not stop abruptly as it may lead to rebound hypertension In reality, Clonidine and methyldopa Not prescribed as first-line home antiHTN drugs High incidence of unwanted adverse effects: orthostatic hypotension, fatigue, and dizziness MIGHT be uses as adjunct drugs after other drugs have failed, in conjunction with other antiHTN such as diuretics A4. Adrenergic Drugs Selective Beta 1 Blockers Metoprolol, Atenolol Reduction of HR through β1 receptor blockade (remember adrenergic blocking of this receptor???) HR results in BP Cause reduced secretion of renin = BP A4. Adrenergic Drugs Selective Beta1 Blockers Nebivolol (Bystolic) Uses: hypertension and HF Action: blocks β1 receptors and produces vasodilatation, which results in a decrease in SVR High doses loses selectivity and blocks both β1 and β2 Less sexual dysfunction All BB- Do not stop abruptly; must be tapered over 1 to 2 weeks A4. Adrenergic Drugs NONSelective Beta Blockers Propranolol Acts equally on β1 and β2 Other uses include situational anxiety associated with public speaking, test taking As mentioned on previous slide, nebivolol at high doses becomes beta nonselective A5. Dual-Action Adrenergic Drugs α1 and β Receptor Blockers Dual antihypertensive effects of reduction in heart rate (beta1 receptor blockade) and vasodilation (alpha1 receptor blockade) Examples are carvedilol (common) and labetalol (not as common) A5. Dual-Action Adrenergic Drugs α1 and β Receptor Blockers Carvedilol (Coreg) Widely used drug that is well tolerated Uses: HTN, mild to moderate HF in conjunction with digoxin, diuretics, and ACE inhibitors Contraindications: severe bradycardia or unstable HF, bronchospastic conditions such as asthma, and various cardiac conduction problems Adrenergic Drugs Indications - HTN But also for Glaucoma (topical) BPH: doxazosin, prazosin, and terazosin (2 for 1) Management of severe HF when used with cardiac glycosides and diuretics Contraindications Acute HF- have to stabilize first MOAIs- yeah doesn’t everything interact with MAOIs? Peptic ulcers Severe liver/kidney disease Asthma (with beta blockers) Adrenergic Drugs: Adverse Effects Orthostatic hypotension 1st-dose syncope Rebound hypertension with abrupt discontinuation Most common: Dry mouth, drowsiness, constipation, sedation Interactions- always check for specific drug interactions Can cause additive CNS depression with alcohol, benzodiazepines, opioids Question #1 When administering an alpha-adrenergic drug for hypertension, it is most important for the nurse to assess the patient for the development of what response? Hypotension Hyperkalemia Oliguria Respiratory distress Answer A Hypotension This is a key point in patient education These drugs have strong vasodilating properties and may cause severe hypotension, especially at the beginning of therapy. B. Angiotensin-Converting Enzyme Inhibitors aka ACE Inhibitors or ACEi Large group of safe and effective drugs Currently are 10 ACEi Often used as first-line drugs for HF and hypertension May be combined with a thiazide diuretic, loop diuretic, or Calcium Channel Blocker (CCB) You need to understand the basics ACE Inhibitors: Review RAAS ACE converts angiotensin I, formed through the action of renin, to angiotensin II Angiotensin 2 is a potent vasoconstrictor and also induces aldosterone secretion by the adrenal glands Aldosterone stimulates sodium resorption (H20 follows Na Both act to raise BP which causes kidneys to reduce renin production ACEi= Great drug to treat HTN BUT contraindicated in pregnancy (2nd,3rd trimester due to fetal renal damage) and breastfeeding first few weeks after birth B. ACE Inhibitors - PRIL Lisinopril (Prinivil) super common, often the 1st drug Enalapril (Vasotec) also common Captopril (Capoten) great if liver disease present Benazepril (Lotensin) Fosinopril (Monopril) Perindopril (Aceon) Quinapril (Accupril) Ramipril (Altace) Trandolapril (Mavik) Primary Effects of the ACE Inhibitors Prevent Na (and H2O) resorption by inhibiting aldosterone secretion (volume reduction) (GO BACK TO RAAS DIAGRAM) blood volume decreases work of the heart preload, or the left ventricular end-diastolic volume which is important in HF ACE SUMMARY OF ACTIVITY 1) Prevent vasoconstriction caused by angiotensin 2 (2) Prevent aldosterone secretion less sodium and water resorption Cardioprotective Effects of ACEi They slow progression of left ventricular hypertrophy (ventricular remodeling) after MI so considered cardioprotective ACE inhibitors have been shown to decrease morbidity and mortality in patients with HF Renal Protective Effects of ACEi ACE inhibitors: reduce glomerular filtration pressure by volume reduction Cardiovascular drug of choice for patients with diabetes since it helps protect kidneys by reducing pressure. Sometimes used low dose for kidney protection with DM without HTN B. ACEi Enalapril (Vasotec) Only ACEi available in both oral and IV Enalapril IV does not require cardiac monitoring Oral enalapril: prodrug (metabolized in liver) Improves patient’s chances of survival after an MI Reduces the incidence of HF B. ACEi Captopril (Capoten) Uses: prevention of ventricular remodeling after MI; reduce the risk of HF after MI Shortest half-life Must be administered multiple times throughout the day so this limits its use Not a prodrug so good for patient with liver disease Question #2 A patient with diabetes has a new prescription for the ACE inhibitor lisinopril. She questions this order because her provider has never told her that she has hypertension. What is the best explanation for this order? The doctor knows best The patient is confused This medication has cardioprotective properties This medication has a protective effect on the kidneys for patients with diabetes Answer D ACE inhibitors have been shown to have a protective effect on the kidneys because they reduce glomerular filtration pressure. This property makes them the cardiovascular drug of choice for patients with diabetes. Question #3 A patient with a history of pancreatitis and cirrhosis is also being treated for hypertension. Which drug will most likely be ordered for this patient? Clonidine Prazosin Diltiazem Captopril Answer D Captopril Captopril is not a prodrug; therefore, it does not need to be metabolized by the liver to be effective. This is an advantage in patients with liver disease. ACE Inhibitors: Adverse Effects *Dry, nonproductive cough, which reverses when therapy is stopped. This is a class effect Dizziness- Note: First-dose hypotensive effect may occur Headache & Fatigue Possible hyperkalemia ** Angioedema: rare but potentially fatal Not safe in pregnancy-are contraindicated during the second and third trimesters of pregnancy because of increased risk of fetal renal damage C. Angiotensin II Receptor Blockers (ARB) Considered an alternative to ACEi Less likely to cause a dry cough and hyper K+ that is common with ACE inhibitors Angiotensin II Receptor Blockers: Mechanism of Action Go back to RAAS diagram! ARBs affect primarily 2 places 1. Vascular smooth muscle - blocks vasoconstriction 2. Adrenal gland -Selectively blocks the binding of Ang 2 to certain Ang 2 receptors inhibiting secretion of aldosterone Lowers volume retention and BP Angiotensin II Receptor Blockers -ARTAN Losartan (Cozaar)- very common Eprosartan (Teveten) Valsartan (Diovan) Irbesartan (Avapro) Candesartan (Atacand) Olmesartan (Benicar) Telmisartan (Micardis) Azilsartan (Edarbi) C. ARB Losartan (Cozaar) Beneficial in patients with HTN and HF Used with caution in patients with kidney or liver dysfunction and in patients with renal artery stenosis ***Not safe for breastfeeding women and should not be used in pregnancy (Cat C 1st trimester, Cat D 2nd-3rd trimester), potential fetal toxicity Appear to be equally effective for the treatment of hypertension and well tolerated ARBs less likely to cause cough and hyperK+ but can still happen Evidence that ARBs are associated with lower mortality after MI than ACE inhibitors Never take ACEi and ARBs at the same time* 5. Calcium Channel Blockers (CCB) Primary use: HTN, angina, some dysrhythmias Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction Results in: Relaxed blood vessels to the heart Decreased peripheral smooth muscle tone Decreased SVResistance Decreased BP E. Diuretics First-line antiHTN in JNC 8 guidelines Decreases fluid volume The results from diuresis: preload, Peripheral resistance Overall effect Decreased workload of the heart and decreased BP Thiazide diuretics are the most commonly used diuretics for HTN Ie hydrochlorothiazide (HCTZ), chlorthalidone We will discuss diuretics further in the chapter on diuretics F. Vasodilators Directly relax arterial or venous smooth muscle (or both) Results in: Decreased SVR Decreased afterload Peripheral vasodilation Indicated for treatment of HTN May be used in combination with other drugs F. Vasodilators Hydralazine (Apresoline) Orally: routine cases of essential hypertension Injectable: hypertensive emergencies BiDil: specifically indicated as an adjunct for treatment of HF in African-American patients F. Vasodilators Sodium Nitroprusside (Nitropress) *Sodium nitroprusside and IV diazoxide are reserved for the management of hypertensive emergencies. Contraindications: severe HF, known inadequate cerebral perfusion (especially during neurosurgical procedures) F. Vasodilators Adverse Effects Hydralazine: dizziness, headache, tachycardia, edema, dyspnea, N/V/D, vitamin B6 deficiency, rash Sodium nitroprusside: hypotension, bradycardia, decreased platelet aggregation, rash G. Direct Renin Inhibitors Aliskirin (Tekturna) Blocks the RAS pathway at the point of activation. Inhibiting renin production prevents the downstream production of Ang II (potent vasoconstrictor) Adverse effects: N/V, severe hypotension, hyponatremia, hyperkalemia… Contraindicated in patients with DM taking ACEi or ARB Miscellaneous Antihypertensives Eplerenone (Inspra) Newer class of drugs called selective aldosterone blockers (remember RAAS?) Reduces BP by blocking the actions of aldosterone at its corresponding receptors in the kidney, heart, blood vessels, and brain Indications: routine treatment of hypertension and for post-MI HF Contraindicated if serum potassium levels are high (above 5.6 mEq/L) A Special Form of HTN Treatment of Pulmonary Hypertension Sildenafil and Tadalafil Commonly used for erectile dysfunction Used for pulmonary hypertension but with different trade names Sildenafil: Revatio* (Viagra for ED) Tadalafil: Adcirca* (Cialis for ED)Gd`ëôGF≥ e`™ Gdª`æõd«á Gdª`¡ÉQI GdãÉdã`á : J¡ªæ» e©∏ƒeÉä : e©∏ƒeÉä J¡ªæ» : Gdμ¡ôHÉF» , hGT°à©É∫ GdæÉQ ´ eù°ÑÉä GdëôGF≥ Gdªæõd«á eÉ H«ø GdàªÉS¢ GdæÉJè eø Jàæƒ q Gdõjƒä , GC hd∏à©Éeπ MógªÉ hbÉ F» LÉfÑÉ¿ : GC Gdªæõd«á GdëôGF≥ e™ hG’BN`ô Gdƒb`ÉF» g`æÉd∂ Gdé`ÉfÖ , aØ`» Y`ÓL» Gdù° ˘ ∏ƒc« ˘ Éä Gdü° ˘ ë`« ˘ ë ˘ á J ˘ é`É√ Gd ˘ à ˘ ©Ée ˘ π e™ eãπ G’CL¡õI hbƒ´ J∏∂ a» Jàù°ÑÖ bó Gdà» hG’COhGä Gdë`ƒGOç eæ`¡É : b`ôGAI Gdà©∏«ªÉä Gd `ƒGQOI Y∏≈ ± G’CL¡õI jªμø Gdëójå Gdà» Jõhjó G’CL¡õI , J©ô q Gd ˘ ª ˘ Ñ ˘ Éf ˘ » H ˘ ¡ ˘ É ’c˘àû°˘É± GC … N˘∏˘π c˘¡˘ô H˘ÉF˘», GC h hL˘ƒO k Gdû°μπ : eã∏å )3( GdæÉQ . É : «ø GC j †° Môj≥ . GC eÉ GdéÉfÖ Gd©ÓL» aæéó GC ¿ d¬ T°≤ s S° ˘ ∏ƒc» cù° ˘ ôY ˘ á Gd ˘ à ˘ Ñ ˘ ∏ ˘ « ˘ ≠ ’EW ˘ Ø`ÉA Gd˘ë`ôj˘≥ , he˘¡˘ÉQ… ± G’CL¡õI GdîÉU°á ’MàƒGA GdμÉQKá GC h cÉS°àîóGΩ e£Ø ÉC I Gdëôj≥ , HÉ’EV°Éaá GEd≈ J©ô q Gdù°«£ôI Y∏«¡É . h Gd¨ÉR ; eªÉ bó jƒDO… GEd≈ cƒGQç Y¶«ªá a» G’CQhGì hGdªà∏μÉä . ± eà≈ G’Efù°É¿ jëÉh∫ Gdù°«£ôI heø Gdæü°ÉFí Gdª¡ªá Gdªà©∏≤á H¡òG G’Ceô J©ô q ’ Hó Y∏≈ YÉeá eø aÉE¿ gæÉd∂ bƒGYó . dòG j£∏Ö Gdªù°ÉYóI , heà≈ ≥ HæØù°¬ Gdëôj eôGYÉJ¡É … fƒ´ eø GdëôGF≥ eæ¡É : Yæó Móhç GC É a» GS°àóYÉA GdóaÉ´ Gdªóf» Mà≈ hGE¿ GEPG dº Jàªμø eø GEWØÉA Gdëôj≥ aÓ JàôO e£∏≤ k GC ¿ HÉEeμÉf∂ GEWØÉA√ bÑπ hU°ƒ∫ QLÉ∫ eμÉaëá G , hGYà≤óä HóG Gdëôj≥ U°¨«ô k 62 Gdëôj≥. hY∏«∂ Gd≤«ÉΩ HÉdàÉd» : - Gd«≤¶á hG’S°à©óGO dÓS°àéÉHá Hû°μπ S°ôj™ hMμ«º. - aü°π Yø Gdμ¡ôHÉF» eü°óQ√. Gdà«ÉQ - hV°™ eæójπ eÑ∏π Y Cf ∏≈ Gdغ hG’ ∞ hGdõM∞ Y∏≈ G’CQV¢ HÉJéÉ√ eîôê Gd£ƒGQÇ 9 a» MÉ∫ hLƒO ONÉ¿ cã«∞. eîÉQê Gd£ƒGQÇ - S°ôYá GENÓA GdªμÉ¿ Yø Wôj≥ G’Beæá, eƒb™ GEd≈ Gdëôj≥ GdôL`ƒ´ eë`Éhdá hY`óΩ É. ’CNò GC … T°»A Mà≈ hdƒ cÉ¿ Kª«æ k OGN∏`» , fû°Ö a«¡É M`ôj≥ hH¡`É Mª`ÉΩ - a» M`Édá GfëÑ`ÉS°∂ OGN`π Z`ôaá jªμæ∂ aàí MæØ«Éä GdªÉA dàÑ∏«π GC QV°«á Gd¨ôaá hGdªù°à∏õeÉä Gdæù°«é«á a«¡É. - G’Jü°É∫ Gdôbº Y∏≈ ) 9 ( . Gdªóf» HÉdóaÉ´ Jòcô GC ¿ GC a†°π GdàóGH«ô GdƒbÉF«á eø GdëôGF≥ g» Hμπ Hù°ÉWá : - eæ™ fû°ƒH¡É. - J£Ñ«≥ GEQT°ÉOGä Gdù°Óeá GdªæÉS°Ñá. ± G’CL¡õI GS°àîóGe¡É, hJ©∏º hWô¥ Gdëójãá heø gæÉ GC Ló eø G’Cgª«á HªμÉ¿ J©ô q GC H ù°§ G’CS°Éd«Ö Gdà» J©«æ» a» GMàƒGA fû°ƒÜ Môj≥ ’ S°ªí Gd∏¬ a» eæõd» GC h eæõ∫ GC Mó L«ôGf». H©ó GC¿ GCfà¡» eø JæØ«ò GCfû°£á gò√ Gdª¡ÉQI , jàƒb™ eæ» GC¿ : GT°à©É∫ eø GdæÉJè Gdëôj≥ ± Wô¥ e™ Gdà©Éeπ Gdõjƒä . - GCJ ©ô q - GC càû°∞ Jù°ôÜ Gd¨ÉR H£ôj≤á U°ë«ëá . GT°à©É∫ eø GdæÉJè GdÑù°«§ G dëôj≥ cÉaí Gdõjƒä . - GC GC Y» - GC Gdëμ«º Yæó Móhç Gdëôj≥ hJù°ôÜ Gd¨ÉR . gª«á Gdàü°ô± Gdù°ôj™ 72 GT°à©É∫ eø GdæÉJè GdÑù°«§ GMàƒGA Gdëôj≥ Gdõjƒä . fû°É• ) 1 ( : : GCV°«∞ GCV°«∞ e©∏ƒeÉJ» GEd≈ GEd≈ e©∏ƒeÉJ» : GE¿ GS°à©ªÉ∫ Gdõjƒä GEd≈ GEeÉ Hû°μπ eÑÉT°ô JôL™ Gd£©ÉΩ Yø W¡» GdæÉLªá GdëôGF≥ e©¶º GC GdªÓHù¢ GC GEd≈ eÓeù°á h aƒ• Gdª£Ñï d∏æÉQ . hbó Jàù°ÑÖ h Gdógƒ¿ Hü°ƒQI NÉWÄá , hGEeÉ GEU°ÉHÉä N£«ôI Gd eø HÉd©ójó GEdëÉ¥ Gd†°ôQ a» gò√ GdëôGF≥ ªæÉR∫ , hbƒ´ ha«Éä . h’MàƒGA Gdëôj≥ GdÑù°«§ , hHü°ƒQI S°ôj©á jªμø GJÑÉ´ Wôj≤á J¨£«á G’EfÉA Gdëôj≥ cªÉ a» Gdû°μπ )4( , GC Gdªû°à©π H¨£ÉA GC cÑô eæ¬ , GC h H£Éf«á h J¨£«à¬ GC ¿ J≤∏π eø H؃Wá eÑ∏á. hgò√ Gd£ô¥ e ø T° ÉC f ¡É GC Of≈ Mó GEd≈ d∏ëôj≥ GdØôO aôU¢ J©ôV¢ eªμø, aÉdਣ«á J©ªπ Y∏≈ eæ™ ONƒ∫ Gd¡ƒGA . Gdû°μπ : H£Éf«á )4( Gdëôj≥ . : GCJæ`Ѭ GCJæ`Ѭ GEd`≈ GEd`≈ : Gd«≤¶á hG’S°à©óGO dÓS°àéÉHá Hû°μπ S°ôj™ hMμ«º . YóΩ GS°àîóGΩ GdªÉA ’EWØÉA Gdõjâ Gdªû°à©π ; ’ Cf ¬ jù°ÉYó Y∏ ≈ RjÉOI G’T°à©É∫, HÉ’EV°Éaá GEd≈ GC ¿ GdªÉA jàù°ÑÖ a» G ’C¿ Gdõjâ Gfàû°ÉQ Gd∏¡Ö aƒ¥ Gdõjâ Gdªëàô¥ . hf¶ô k GC N ∞ eø GdªÉA aÉEf¬ S°ƒ± j£Øƒ Y∏≈ S°£í GdªÉA ; eªÉ 82 jƒDO… GEd≈ J£Éjô Gdõjâ Gdù°ÉNø hJæÉKô Gdù°ÉFπ Gdª∏à¡Ö Y∏≈ Gdû°îü¢ hY∏≈ LƒGfÖ Gdª£Ñï . Gdæ«ôG¿ É ’fó’´ a» Gdªû°à©∏á hGdóa™ H¡É YóΩ Jëôj∂ Gdª≤ÓI GEd≈ NÉQê Gdªæõ∫ JØÉOjk GdªæÉW≥ eø G’CNôi Gdªæõ∫ . É eø Pd∂ , Hë«å ’ jƒDO… Gd∏éƒA GEd≈ GEWØÉA Gdëôj≥ a» MÉdá GEPG cÉ¿ Gdû°îü¢ eàªμæ k fØù°¬ GC b«Ée¬ Hª¡ªá G’EWØÉA GEd≈ GEjòGA h RjÉOI G’T°à©É∫ . a`ƒ¥ Gdª≤`ÓI ’EWØÉA eÑ`ÉT°ôI Oa©á hGM`óI YóΩ hV°™ Gd¨£ÉA Gdõjâ Gdª`û°à©π ; É dàƒL¬ fëƒ GdæÉQ Gdû°îü¢ . JéæÑ`k h Gdóg`ƒ¿ GC Gdõjƒä eø cÑ«ôI e≤ÉOjô GS°àîóGΩ Yæó eù°£ëá e≤ÓI YóΩ GS°à©ªÉ∫ a» k eø eõhOI Yª«≤á H¨£ÉA. e≤ÓI Pd∂ Jù°à©ªπ Gd£¡» , hHó’ YóΩ Jù°î«ø Gdõjƒä GC h Gdógƒ¿ GC cãô eªÉ jæѨ» ; Pd∂ ’ Cf ¡É JÑó GC a» Gdàëƒ∫ GEd≈ ONÉ¿ Yæ`óeÉ Jü°π OQL`á MôGQJ¡`É GEd≈ fëƒ 402OQL`Éä S°«∏«õjá , hjªμø GC ¿ Jû°à©`π H©ó dë ¶Éä eø GfÑ©Éç GdóNÉ¿. 92 GCM`àÉê GEd`≈ GCM`àÉê GEd`≈ - GEfÉA W¡» , Z£ÉA GC - aƒWá . cÑô eø Méº G’EfÉA . e¡ÉQGä eà†°ªæá : - G’YàªÉO GdòGä Y∏≈ hJëªπ Gdªù°ƒDhd«á . - GJîÉP Gd≤ôGQ . - S°ôYá Gdàü°ô± . HÉ’BJ`» GCb`ƒΩ : GCb`ƒΩ HÉ’BJ`» : GCJóQÜ Gdëôj≥ GdæÉJè GEWØÉA Y∏≈ HÉdàªã«π eø Rjâ eû°à©π eàÑ© k É GdàÉd» : - GEWØÉA eü°óQ GdëôGQI. - J¨£«á GdƒYÉA Gdò… H¬ Rjâ eû°à©π HƒYÉA GB Nô GC cÑô eæ¬ dëéÖ Gd¡ƒGA Yæ¬ , G Yø Gdéù°º f¡Éjà¡É GEd≈ É eø Gdª≤ÓI HóGjá H©«ó k Hë«å GC L© ∏¬ jæõd≥ JóQjé« v É . h JÑ∏«π aƒWá hYü°ôgÉ a» MÉdá YóΩ hLƒO GC Mà≈ Jμàªπ Gdਣ«á JªÉe k hGJÑÉ´ GdàÉd» : Z£ÉA , - e`ù°∂ Gd`؃Wá Gd`ªÑà∏á GC h H`£Éf«á Gd`ëôj≥ H`ë«å GC Mª» Gd«ójø e`ø Gd`æÉQ , c`ªÉ a`» Gdû°μπ ) 5( . - hV°™ Gd؃Wá Hôa≥ Y∏≈ G’EfÉA Gdªû°à©π , hYóΩ Jëôjμ¡É Mà≈ Gdà ÉC có GdàÉΩ eø Gf£ØÉA GdæÉQ. GCbØπ GCS°£ƒGfá Gd¨ÉR . - Gdû°μπ ) 5( : Wôj≤á G’EWØÉAEff..rs of ott.-PoFllat i What woLrld hoppen ro our colnrry i, it is ovetsp.pulored? When our counrry is ov€.-populdted, re @ €xp€ri.nce rh€ foll.wirg: Food is our bdsic h@d. Wh€n th€.Cs an ih.re.se ir populdtion it neans thar hore ,@d is iealed. It rheds ho .naJgh food, rrtrple irll srruggle wirh eddr oth€r in ordeLro €!'r- As o l!fllr, lhde rill be o f@d -- , ond ou, now]nert of on ihdiyiduol fron d c..tair - the move$eni o, on individudl our of o cerrain pla.e which help r€duce ihe populotion of th6t fr Arcih€. b.sic ned is w.ra. Wde. shorroge ocu.s when there is on ircreare of hu,nber of p@ple ro be $pptied. rn owr-popur.t d ore.s, woler is rdior€d, Ir rEB rhoi supplies like ti,tWSS ond ,IWSI can'i $pply enoish worer. Do you hdve enough supply of sai.. in your oreo? Aside f.om food alld worer, shelier is olso ohe o, our inportant heeds. As the populoiion ihcre.!e!, building n.w hoLr!€s or rhelt€r is limit.i. To find solulion to this prcbl€n, some goverihent og.ncies dnd orhs non{ov€Ihrehl offi.iofs (N6O) .onvefied sot@ ti.elields, du,np site. dnd nountcirlr inlo flbdivisions dnd relidentiols. Sut whot uould be ths effect o{ coMrtiig .i@fields to .6id€nri6l uits in our food supply? z , 2 Z Z :'", becouse there ore no enough space for prcpex garbage dkposol. ^s o r€sulr, sore peoPle lend to ihrow'their gorbdge onywh.f€. oorbdge baones brc{niry ond rursing ground of iEecrs and onidols ihot @se horm ro pe.ple. Dec.yiry garboge olso produces r,hpleaiant odor ard ehen burn if pmduces pois.nour qds @lled nelhohe As ihe populdtion incr€a3*, the 9d6.9e dso incraes. nris is T't ,,8 T H Wha you de living in on oa-populdi.d pla@, you moy oqaiae halrh prcblerns. Ir is be@@. the woi.r srpply is limit.d ihct will l..d you to poor hygi.ni. hobirs. In plo.4 like rhis, the surrouhdiigs naybe uniidy. o focrorthoi @uld oko cfFe.t your h4l'th. The common oilments rhot yd @uld oc$rire in ovesfDpllar€d ploces ore bEnchil is, o5l hnq. diqrrha and rube.culosis. 7,\ ,\\ \1" 6. Lnck of Herlrh sarvice llosi Pelple in 6n oM-populci€d 6ra 90 ro rubli. heilrh @trtas ond governhent hospirols be6u.e ii prcvides fr@ @Eulrorion oid los @sr rEdicdrions. A3 a ..suli, lh€s€ gow.nnenr dg€rciB b.@ne itud.4$re in mcetiig ihe n eds b..ou!€ df ihsrffici€nr funds. Lock of medicol personnel ,o odmaiisi€I is also s problen in mosr hosptols ev€n rhere or. od.audtc supply of hedicire!. 7_ Do you how wlry rhe crim€ roi€ hexs ih becdur€ fiDre pe.ple o.e fnJrrct€d d@ ro sLffici€.i naE io supp.rr their forniliG. ouf country inclY{ses? If is uh.mploym€ni dnd hdve no arinet .re u$dv gr€{rer ia dn dq-popltdled ra whq. tl, , a, v, tlr I E. Air ard Wat€r Pollutioh How dir be.o'nes pollut€d? I11€ dir b@'n€s p.llurn be.4ne of rhe hormfolgoees thot ser. produ.4 by the fdciori€s and vehicles. Itete {octories ond whi.l6 @ fuel ro run nochiB ond .JBin6. In ,h€ prc.ess, they give our Cdrboh Dioxide ond other ho.6ful gars.r such 6 Nittugei Oxide, Corbon l oioxide dnd Le.d iiio the oir. Do you know whot .ontdbute io ihe incr€asing number of whides qnd foctories? It is ihe inc.6e o, populdtion. As whdt I hove dis.!sse!, wirh a lihired sra.e 9@bd9e disposalie one of the problens thot .o!ld ise i, dh o!er-pop!,.t€d ploce. exn,jple ot thie orc rhos€ pelpl€ livi,rg oh the raverside teid 'ro ,hrou, lheir gEr&ge Hde you seen 'th. P6si9 river or the Tulyahan river? Did you {ind it Whdr do you think i! ihe eff€.t of ihis ih the.re4iures sho lives ih Ahothd f6do.s thal could.on rlbule to wdtd pollutioh dre oil s?ills, gorbqg€ fro,n boa, or ships ahd som€ ihdust.iol wosre. 9. Ite l@96f p4.enroge group. Individuols who orc this grclp. of olr popllarioh is compos.n of the working @pobla of s'rpporting ,heir fomilies nok !-up Though rhas group hol& the lojgeei percenroge of d. populaiion, rhis olso becomer one o{ oveFpopulored probl€]ns b€4use there ore rc jobs awildble fo. oll of iha10. Erergy Shortdge ltere will be on energy shortdge iJ ihe populdtion incre63"l be.dise rhe d.,nand i. €le.iriciry is high. Why is thai wh.n th. PoPqldion inclE.g, rhe d4ord in el4tricity is high? Ir B be.ouse there $,ould be 8to.e hdsat dnd blildirys to lighr ond nore el?riric oPPliohces ro run. rt.6rcznho!3.Ef+ed Whor is rhe grernho@ eff€.r? In whoi say il c.uld offect c2 6re.hhG. effed is rhe wdrniltg of rhe drltlosphee. lvhen the 5un worft rhe.nrrh s1jrf.@, sone of rhe h@r go€J bo.k ro rhe ornos?herc. Air an the dtnDsphere which is C@boi Dioxid. ,rops ihe heot 6hd it mok6 the a.th very worm. As ihe populdtion coniinuou!|,l gtol4 , the gt@rl$use etfe.t b@res no.e visible. Ir is becaosu ,hera ore mo.e focrories snd whicl.s iha, produce wdst€s ond fuma5 which cduses more C{.bo. Diodde ir the ormosphere. As a rcsutt, ,herc eiould be nore h4, ,rop in the ornosphere uhich osk6 th. @ih nuch wornerIf this will hoppen continuously, ,h€ fish ih th€ ocah *ill di€, ricerields/f@mlands will dry too due to lh€ wcm clitnole 12. Destruction of rhe Ozone Loyer A5 whot you hove l@med lrheh you de in v5-6, rhot the qzore ldver is 'the proiecrive loy€. of the olnosPhd€. ft protects us {rom the homful effects of ultrdviolei rays of the su. Do you khow ,hot our Ozore lol€t q4. dQ4tt\!ci.d? Il olreadY hod holes lhai dllow the ulrroviolet rdys to .4dt ihe @rrh. How do6 this hdpPei? Does th. in rc$e of poPuldioh h@€ sonething 'to do tr,lh ir? Yes, rhe I6i grov/irts PoPuldiion .odribuied o lot be@use 6 th' populotion incre3es, rhe u5e of refrigerd'tors, d€rosol lProvs 6nd pl4srics 6bo ihcre&s6. The sid producls coiiojn chemicol called Chlorofluorocdrbons (CFCS) which is mix wafh ihe dir in ihe ormosPher€. As o resulr. ihe hcrmfirl chernicol r€oches the Prolectiw ldver dnd lhrowh. hole in {hid ult@iolzi cahders aid cai4.ct3 ,F.*Y.iis hi!586$q€9.7,- Ho$ doas dcid rdin form? Is cid roii hdmful ro rEn? In the prcvious dis.ussions, yodt€ t.on€d rhd more vel .1e3 dnd fdctori€s or€ necded fo het the iii:.e.siry number o{ P@Pla. Lefs now fihd af hd f@tot.i€s dnd vehicle! .ontribure in the forrEtion of ocid When foctories 6nd whi.ler give off woste gd..3 ,hot will ,nix on lhe noisture i. rhe oir, it will ihen Produ.e sulPhu.i. ocld dnd Nitri. o.id. 'Ihe clol,Jd folb will ,h€h obsorb rhese ccids ond ehei ihe clold f.lls os .oin, ih. ccid is ahady Pdrr of itU/ha d.id ftin falls oh lok"!, ,46 or ocan ih€ fish sill die d.d if h fdlls oh fopnlonds,lhe pldni. together oith the soil B desrroyed. When you inhole dir with Niiric acid, your blood will los. irs @pobilily io fonspori Oxyg€h to your diff€.ai bodY Po.i3. ScieniisB include other rorns oJ dcidic pr€cipiigrion. Thes€ drc nisi, Do you krcw ihot Nuclerr power slotionr Use .adiodctive ,ndie.ials in producirE fuels, yet, rhey do and those .odioactiw rndlqlotE gi\e otf radio'ting en.rgy thoi is harmrul 'to livirq thilEs. wlren rodiotion enlert ihe body ot living things it {ill srq rhere for o lorg ,eriod of ri'ne. Exonple fhe rodiqtion vG srilled to the c.m. Then rhe @rn will be aie by rhe chicken, the .odiotion o the c.rn 'rill also 'tronsf€r to the chi.k€n. Wha on individuol als ihe nat of the chickeh sith mdiarion, helshe rill .ko oblorb ihe rodi@.tirc mtaid that will destrcy hB/her .€lls ond ruket hnn/hd si.r. Over-populoiion .on leld to food shoridg€, wdter shorroqe, housiB probl€ms, qdrbog€ probl€rs, lock of halrh sdi.e. tisa ol clit@ rote, oir ond woi€r pollution, uhanpl6ynat, eiergy 5horr69e, grenhoq3€ efreci, desrruction o( th. ozo@ lat/e?, rci.l roi. olld e.l€d. watta