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A study compared five dierent methods for teaching

OpenIntro Statistics | 3rd Edition | ISBN: 9781943450039 | Authors: David M Diez; Christopher D Barr; Mine Çetinkaya-Rundel ISBN: 9781943450039 86

Solution for problem 5.44 Chapter 5

OpenIntro Statistics | 3rd Edition

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OpenIntro Statistics | 3rd Edition | ISBN: 9781943450039 | Authors: David M Diez; Christopher D Barr; Mine Çetinkaya-Rundel

OpenIntro Statistics | 3rd Edition

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Problem 5.44

A study compared five dierent methods for teaching descriptive statistics. The five methods were traditional lecture and discussion, programmed textbook instruction, programmed text with lectures, computer instruction, and computer instruction with lectures. 45 students were randomly assigned, 9 to each method. After completing the course, students took a 1-hour exam. (a) What are the hypotheses for evaluating if the average test scores are dierent for the dierent teaching methods? (b) What are the degrees of freedom associated with the F-test for evaluating these hypotheses? (c) Suppose the p-value for this test is 0.0168. What is the conclusion?

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CHAPTER 11 NOTES NOT REQUIRED: Figures 11­3 and 11­5; parts of Table 11­1 that are not covered in class. Not required to know detailed chemical structures of any hormone. We will not cover gonadal hormones, so you are not required for any text that is associated with them EXCEPT to know the general properties of them that are mentioned in lecture. Anatomy of bone (Section 11.17 including figures 11­26 and 11­27) not required even though lectured briefly on it in class. SECTION F NOT REQUIRED but know material on parathyroid hormone and 1,25­ (OH) ­D 2 from lecture 11.1 – Hormones and Endocrine Glands  Endocrine gland: ductless, release hormones into blood (contains all organs that secrete hormones, including heart and hypothalamus) o Compared to exocrine: products are secreted into ducts  Each cell type can only secrete one hormone; glands that secrete multiple hormones have multiple cell types (few exceptions) o Some hormones double as neurotransmitters or paracrine/autocrine substances  Know Table 1 hormones that were covered in class (adrenal glands, gonads ­ general, some hypothalamus, kidneys, liver, pancreas, parathyroid glands, pituitary, thyroid) 11.2 – Hormone Structures and Synthesis (don’t need to know detailed structures)  Amine hormones o Derivatives of amino acid tyrosine o Includes thyroid hormones (thyroid gland), epinephrine, norepinephrine (both adrenal medulla), dopamine (hypothalamus) o Adrenal glands located above each kidney contain adrenal medulla and surrounding adrenal cortex  Epinephrine expressed 4x more than norepinephrine due to PNMT enzyme that catalyzes conversion from norepi to epi o Dopamine is released into special circulatory system (portal system) to inhibit hormonal activity in pituitary endocrine cells  Peptide hormones o Initially synthesized on ribosomes of endocrine cells as preprohormones  then cleaved into prohormones in rough ER  then cleaved again into active hormone in Golgi (posttranslational processing)  Pieces of prohormone cleaved from active hormone may have hormonal effects (ex: insulin and C­peptide originally attached to insulin both cause effects)  Steroid hormones o Produced by adrenal cortex, gonads, and placenta o Vitamin D  converted into steroid 1,25­dihydroxyvitamin D (1,25­(OH) D) in2 liver and kidneys o All derived from cholesterol, which is taken up from extracellular fluid by cells or synthesized by intracellular enzymes  Steroid product depends on cell type and types/amounts of expressed enzymes o Not highly soluble in blood (hydrophobic nature)  must be reversibly bound in plasma to carrier proteins (albumin, etc.) o Hormones of adrenal cortex  Aldosterone: mineralocorticoid, effects kidney’s ability to handle sodium, + potassium, and H ions; synthesis controlled by angiotensin II (hormone that activates inositol triphosphate 2 ­messenger pathway in adrenal cortex) + + +  Stimulates Na and H 2 retention, K and H excretion in urine  Cortisol (a glucocorticoid along with corticosterone): effects on organic metabolism, facilitates body’s responses to stress and regulates immune system  Androgens: includes testosterone (major male sex hormone produced in testes) o Adrenal cortex is composed of three distinct layers  Zona glomerulosa: synthesizes corticosterone and aldosterone  Zona fasciculata and zona reticularis: synthesizes cortisol and androgens o Certain diseases may be caused by decreased/increased secretion of steroids  Ex) congenital adrenal hyperplasia (CAH): excess androgen causes virilization of genitalia in female fetuses o Gonad hormones  Estrogens: including estradiol and estrone (androgen  estrogen)  Progesterone: important for uterine maturation and maintaining a pregnancy 11.3 – Hormone Transport in the Blood  Most hormones are water (and therefore blood) soluble  simply dissolve into plasma o Steroid and thyroid hormones attach to plasma proteins; however exist in equilibrium of free hormone + binding protein ↔ hormone­protein complex  Right shift when endocrine gland secretes more free hormone  Left shift when hormone dissociates from binding protein to move into a cell  Only free hormone can diffuse across membranes 11.4 – Hormone Metabolism and Excretion  Concentration of hormone returns to normal once activity is no longer needed (prolonged increased concentrations can have harmful effects)  Concentration depends on: o Rate of secretion by endocrine gland o Rate of removal from blood (via excretion or metabolic transformation, majorly controlled by liver and kidneys)  Endocytosis of hormone­receptor complexes on plasma membranes allows cells to remove peptide hormones from their surfaces and catabolize  Enzymes in tissues/blood also break down catecholamine and peptide hormones (exist only briefly when needed) o Protein­bound hormones are protected from enzymes  removal of steroid and thyroid hormones takes longer  Metabolism of some hormones is activating rather than inactivating o Ex) thyroxine is inactive until metabolized by target cell  Figure 11.8 11.5 – Mechanisms of Hormone Action  Ability of a cell to respond to hormone depends on presence of specific receptors on target cells  highly specific o Catecholamines and peptide hormones: receptors in plasma membranes o Lipid­soluble chemical messengers (steroids, thyroid hormones): receptors located inside target cell  Up­regulation: increase in number of hormone’s receptors in cell; occurs after prolonged exposure to low concentrations  Down­regulation: decrease in receptor number; occurs after high concentrations of given hormone (prevents overstimulation) o Hormones can up/down­regulate their own receptors and other hormones’ receptors  Permissiveness: hormone B will only work in presence of hormone A (needed for up­regulation)  Ex) thyroid hormone must be present for epinephrine to cause a large release of fatty acids from adipose tissue (because it stimulates synthesis of beta­adrenergic receptors needed)  Effects of peptide hormones and catecholamines o Bound receptors trigger one or more signal transduction pathways  Directly influence receptor­associated enzyme activity/activity of cytoplasmic janus kinases/G proteins coupled to secondary messengers o Changes in enzyme activity are very rapid o Can lead to activation/inhibition of genes  affects synthesis of proteins (slower)  Effects of steroid and thyroid hormones o Activation/inhibition of particular gene transcriptions, causing change in synthesis rate of encoded protein o Ultimate result of changes in the concentrations of proteins is an enhancement or inhibition of particular processes carried out by cell or change in cell’s rate of protein excretion  Pharmacological effects of hormones o Hormones often used in large doses as therapeutic agents o Ex) prednisone (potent synthetic form of cortisol) used to treat allergic and inflammatory reactions 11.6 – Inputs That Control Hormone Secretion  Changes in plasma concentrations of mineral ions or organic nutrients o Typically due to function of hormone as negative feedback regulator o Ex) insulin: stimulated by increased concentration of glucose to return glucose levels back to normal o Ex) parathyroid hormone (PTH) regulates Ca concentrations: stimulated when concentration is low  Neurotransmitters released from neurons ending on the endocrine cell o Adrenal medulla is modified sympathetic ganglion; stimulated by sympathetic preganglionic fibers o Parasympathetic and sympathetic inputs can both excite and inhibit endocrine cells o Ex) parasympathetic system stimulates insulin production, sympathetic system inhibits  Another hormone (or paracrine substance) acting on the endocrine cell o Tropic hormone: hormone that stimulates secretion of another hormone (typically also stimulates growth of stimulated gland) o Hormones can also inhibit secretion of other hormones  More than one input may affect hormone secretion at once o Ex) insulin secretion: stimulated by extracellular concentrations of glucose and also stimulated/inhibited by autonomic NS o Resulting output of hormone depends on ratio of stimulatory to inhibitory inputs 11.7 – Types of Endocrine Disorders  Hyposecretion – too little hormone o Primary hyposecretion: hyposecretion due to gland not functioning normally  Due to partial destruction of gland (decreased secretion)  Enzyme deficiency (decreased synthesis)  Dietary deficiency of iodine  specific to thyroid hormones  Infections, toxic chemical exposure o Secondary hyposecretion: hyposecretion due to gland receiving too little stimulation by tropic hormone  Reversible o Concentration of tropic hormone is distinguishing factor between primary and secondary (increased concentration: primary; decreased/no change: secondary) o Treated by administering missing hormone (pill/cream/injection/spray)  Hypersecretion – too much hormone o Primary hypersecretion: gland secretes too much hormone on its own o Secondary hypersecretion: excessive stimulation of gland by tropic hormone o Both may be caused by hormone­secreting, endocrine­cell tumors o Treated by removal/destruction (via radiation) of gland or drugs that inhibit hormone synthesis or that are receptor antagonists  Hyporesponsiveness and hyperresponsiveness o Target cells do not respond normally to hormone o Ex) type 2 diabetes mellitus: target cells of insulin are hyporesponsive o Hyporesponsiveness: caused by decrease/loss of hormone receptor or malfunction in proceeding signaling event or deficiency in enzymes needed to catalyze metabolic activation of hormones o Hyperresponsiveness: can be caused by hypersecretion of up­regulating hormones 11.8 – Control Systems Involving the Hypothalamus and Pituitary Gland  Pituitary gland: lies in pocket below hypothalamus, connected to it via the infundibulum o Composed of anterior pituitary gland and posterior pituitary (not a gland, just extension of neural components of hypothalamus) o 2 major hypothalamic neurons pass through infundibulum and end in posterior pituitary; terminals end directly on capillaries for hormone release  No important neural connections exist between hypothalamus and anterior pituitary o Median eminence: junction of hypothalamus and infundibulum where capillaries recombine to form the hypothalamo­hypophyseal portal vessels (portal veins: veins that connect two sets of capillaries)  Provides mechanism for hormones synthesized in cell bodies in hypothalamus to directly alter activity of cells in anterior pituitary gland (bypasses general circulation for efficiency/specificity in hormone release)  Posterior pituitary hormones o Hormones are actually synthesized in hypothalamus  Hormone is transported down 2 major axons down infundibulum and ends up in posterior pituitary  Various stimuli activate input to the neurons, causing action potentials  trigger release of stored hormone via exocytosis  hormone enters blood o Oxytocin: stimulates contraction of smooth muscle cells in breasts (milk production) and stimulates contraction of smooth muscle cells in uterine for birth  Suggested to also be involved in pair bonding, maternal behavior, emotions like love (present in both males and females) o Vasopressin: causes contraction of smooth muscle cells around blood vessels, causing increased blood pressure  Involved in response to decreased blood pressure due to blood loss  Also acts within kidneys to decrease water excretion in urine/maintain blood volume  Also known as antidiuretic hormone (ADH)  Anterior pituitary gland hormones and hypothalamus o Hypophysiotropic hormones: hypothalamic hormones that regulate anterior pituitary gland function  3­hormone sequence followed by all hypophysiotropic hormones except dopamine: (1) controls secretion of (2) an anterior pituitary gland hormone, which controls the secretion of (3) a hormone from some other endocrine gland  action on target cell  Sequences permit a variety of types of important hormonal feedback and amplification of hypothalamic neuronal response into a large peripheral hormonal signal o Follicle­stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH, somatotropin), prolactin, thyroid­stimulating hormone (TSH, thyrotropin), adrenocorticotropic hormone (ACTH, corticotropin)  FSH and LH are gonadotropic hormones, secreted by same cell  Everything else secreted by own type of cell  All peptide hormones o Beta­lipotropin and beta­endorphin are derived from same prohormone as ACTH but physiological functions are not known o See Figure 11.15  TSH  secretion of thyroxine and triiodothyronine  ACTH  secretion of cortisol o GH  insulin­like growth factor 1 (IGF­1) by liver  Hypophysiotropic hormones o Originate in discrete nuclei of hypothalamus and terminate in median eminence of hypothalamo­hypophyseal portal vessels (hormones are released in response to action potential in neurons) o Diffuse out of anterior pituitary gland capillaries into interstitial fluid and stimulate/inhibit secretion of anterior pituitary gland hormones (different than posterior pituitary hormones that enter into general circulation) o Benefits of portal veins:  Small amounts of hypophysiotropic hormones in few veins with low blood flow = concentration can change rapidly for larger amplification  Total amount of hormone entering general circulation is low = minimizes unintended side effects o Corticotropin­releasing hormone (CRH)  ACH; growth hormone­releasing hormone (GHRH)  GH; thyrotropin­releasing hormone (TRH)  thyrotropin; gonadotropin­releasing hormone (GnRH)  luteinizing/follicle­ stimulating hormones o Somatostatin (SST) INHIBITS secretion of GH; dopamine (DA) INHIBITS secretion of prolactin  Neural control of hypophysiotropic hormones o Controlled by neurotransmitters (catecholamines, serotonin), o Strong circadian influence (neural inputs linked to parts of hypothalamus that respond to presence/absence of light)  Ex) CRH (affected by night/day) secretion affects ACTH and cortisol concentrations  Hormonal feedback control of the hypothalamus and anterior pituitary gland o Long­loop negative feedback: hormone secreted by a third endocrine gland in a sequence exerts a negative feedback over anterior pituitary gland and/or hypothalamus  Ex) stressful stimulus causes CRH  ACTH  cortisol; increased cortisol concentration inhibits CRH­secreting cells in anterior pituitary gland  Does not exist for prolactin because it does not have a 3­hormone sequence (still has short­loop negative feedback)  “Non­sequence hormones” exist and still have effects on secretion of hypophysiotropic or anterior pituitary gland hormones in a sequence o Ex) estradiol enhances secretion of prolactin even though they are not connected in a sequence 11.9 – Synthesis of Thyroid Hormone  Thyroid gland  thyroxine (T ) a4d triiodothyronine (T ) 3 o Most T is converted into T  T is major hormone; T acts as a reservoir 4 3 3 4  Thyroid gland contains numerous follicles: an enclosed sphere of epithelial cells surrounding a core filled with colloid (protein­rich material)  Figure 11.21 o Iodide trapping: first step in synthesis of T , 4odide is actively cotransported with + Na cells across basolateral membranes of epithelial cells o Iodide ions diffuse across membrane and are transported into colloid by integral membrane protein pendrin o Iodide is oxidized to iodine and is attached to phenolic rings of tyrosine within thyroglobulin by enzyme thyroid peroxidase  Monoiodotyrosine (MIT) or diiodotyrosine (DIT) o MIT or DIT is coupled to DIT on thyroglobulin molecule  DIT + DIT = T ; MIT + DIT = T 4 3 o Endocytosis of thyroglobulin containing T and 3 4 o Proteolysis of thyroglobulin to release T an3 T af4er coming in contact with lysosomes; hormones diffuse into blood 11.10 – Control of Thyroid Function  TRH  TSH  negative feedback on action of T and T3 on th4 anterior pituitary gland and hypothalamus  TSH also increases protein synthesis in follicular epithelial cells, increases DNA replication and cell division, and increases the amount of rough ER and other cellular machinery required for protein synthesis  Hypertrophy: increase in size of thyroid cells due to increase in amount of TSH o Leads to a goiter: enlarged thyroid gland 11.11 – Actions of Thyroid Hormone  Thyroid hormone receptors are present in nuclei of most cells o T a3ts by inducing gene transcription and protein synthesis  Metabolic actions o Stimulates carbohydrate absorption in small intestine and increases fatty acid release from adipocytes o Helps maintain metabolism at high rates to support Na /K ­ATPases  ATP concentrations controlled by negative feedback system  Contributes to body temperature homeostasis (heat production)  Permissive actions o Upregulates beta­adrenergic receptors (binds to catecholamines) notably in heart and nervous system o Anxiety, nervousness, “racing heart” may be experienced with increased T due t3 potentiation of epinephrine/norepinephrine (sympathetic NS); treated with beta­ adrenergic receptor blockers  Growth and development o T 3GH (low T = d3creased growth) o Important developmental hormone for nervous system – formation of axon terminals, production of synapses, growth of dendrites/dendritic extensions, formation of myelin o Congenital hypothyroidism: absence of T ; char3cterized by poorly developed NS and mental retardation (reversible if caught early/prenatally)  Mostly caused by lack of iodine in mother’s diet (rare in US) o Also required for proper nerve/muscle reflexes and normal cognition 11.12 – Hypothyroidism and Hyperthyroidism  Hypothyroidism: chronically low concentrations of thyroid hormones o 95% due to primary defects (damage/loss of functional thyroid tissue or low iodine) o Low iodine = compromised TH synthesis = hypothalamus and anterior pituitary gland aren’t subject to negative feedback = increase in TRH without negative feedback = goiters  Can be reversed with iodine added into diet o Autoimmune thyroiditis: autoimmune; results from things such as Hashimoto’s disease (immune system attacks thyroid) = increase TSH concentrations = goiter  Treated with daily T 4pill (stimulates negative feedback for TSH) o Secondary hypothyroidism: caused by inadequate release of TSH from anterior pituitary gland o Can lead to cold intolerance, weight gain, fatigue, changes in skin tone/hair/appetite/GI function/neurological function  Myxedema: puffiness of face/body due to accumulation of glycosaminoglycans (T u3ually suppresses accumulation)  Hyperthyroidism: thyrotoxicosis o Caused by hormone­secreting tumors or autoimmune disease Graves’ disease: production of antibodies that bind to and activate TSH receptors, leading to overstimulation o Can lead to heat intolerance, weight loss, increased appetite, increased sympathetic NS activity (anxiety, tremors, jumpiness, increased HR) o Treated with drugs that inhibit thyroid hormone synthesis, surgical removal of gland, radioactive iodine to destroy part of gland 11.13 – Physiological Functions of Cortisol  Always produced by adrenal cortex; effects mainly seen during times of stress  Permissive actions on responsiveness to epinephrine and norepinephrine of smooth muscle cells surrounding lumens of blood vessels (ex: arterioles) o Maintains normal BP (low BP without cortisol)  Maintains cellular concentrations of certain enzymes involved in metabolic homeostasis o Enzymes expressed in liver  increase hepatic glucose production between meals to maintain normal glucose levels always  Systemic actions o Anti­inflammatory  Inhibits leukotrienes and prostaglandins o Anti­immune – prevents overreaction to minor infections/etc.  Stabilizes lysosomal membranes in damaged cells to prevent release of proteolytic contents  Decrease capillary permeability in injured areas to decrease fluid leakage into interstitium (suppresses growth/function of immune cells)  Developmental hormone in fetal/neonatal stages  differentiation of parts of brain, adrenal medulla, intestine, lungs; production of surfactant (substance in lungs) 11.14 – Functions of Cortisol in Stress  Table 11.3 summarizes major effects  Mobilizes energy sources for increased plasma concentrations of amino acids (used to repair tissues or in hepatic gluconeogenesis for energy), glucose, glycerol, free fatty acids o Medical implications  Patients that are ill/need surgery will catabolize large quantities of body protein  Diabetes mellitus sufferers with an infection will need more insulin  Children subjected to severe stress may have decreased growth rates  Increases ability of vascular smooth muscle to contract in response to norepinephrine to improve cardiovascular performance  Anti­inflammatory effects protect body from possible damage against excess inflammation during stress o Certain cytokines (immune cell secretions)  ACTH  cortisol; negative feedback system o Dampens fevers caused by infections  Too much cortisol (too much stress, even emotional) over time can be damaging o Chronic suppression of immune system o Worsen symptoms of diabetes (continual increased glucose levels) o Possible increased death rate of neurons in brain o Decreased reproductive fertility, delayed puberty, suppressed childhood growth  Absence of cortisol is fatal  Use of synthetic analogs to cortisol o Treatment of allergies, arthritis, other inflammatory diseases 11.15 – Adrenal Insufficiency and Cushing’s Syndrome  Adrenal insufficiency: general term describing chronically low concentrations of plasma cortisol o Typically results in fatigue, weakness, loss of appetite and weight, low blood pressure (hypotension), low blood sugar o Primary adrenal insufficiency: due to loss of adrenocortical function, also known as Addison’s disease  Results in decreased cortisol and increased ACTH concentrations (no negative feedback system without cortisol)  May be due to tuberculosis or other infectious diseases/tumors/ autoimmune diseases that destroy adrenal glands +  Al+o results in decreased aldosterone concentrations  imbalance in Na , K , and water in blood  Treat with daily administration of glucocorticoids and mineralocorticoids, monitor Na and K intakes o Secondary adrenal insufficiency: inadequate ACTH secretion  May arise from pituitary disease  Often less dramatic symptoms as aldosterone is still produced (does not rely on ACTH)  Cushing’s syndrome o Excess cortisol in blood always  May be primary defect (ex: cortisol­secreting tumor) or secondary (Cushing’s disease, usually due to ACTH­secreting tumor) o Results in uncontrolled catabolism of bone, muscle, skin, organs  Can lead to osteoporosis (loss of bone mass), weak muscles, thin/easily bruised skin  Loss of fat around extremities, redistribution in trunk/face/back of neck  Increased appetite  obesity o Constantly high glucose levels in blood similar to diabetes mellitus o Possible immunosuppression and hypertension (high blood pressure) o Treatment usually involves surgical removal of pituitary tumor if Cushing’s disease, or depends on case­by­case basis 11.16 – Other Hormones Released During Stress  Aldosterone & vasopressin: retain water and Na to prevent dehydration, hemorrhage, sweating  GH, glucagon, decreased insulin: increase plasma concentration of glucose  Beta­endorphin (co­released from anterior pituitary gland with ACTH): painkilling effects  Activation of sympathetic NS (fight or flight response, epinephrine) SKIP 11.17 11.18 – Environmental Factors Influencing Growth  Maternal malnutrition  growth retardation in fetus o Low birth weight, increased infant mortality, adult disease  Malnutrition during infancy/childhood  inters with intellectual development and total­ body growth  Proper nutrition/recovery from illness can lead to catch­up growth that brings child back within expected ranges for growth 11.19 – Hormonal Influences on Growth  Hormones/growth factors are present in different amounts at different stages throughout life  Growth hormone and insulin­like growth factors o GH (anterior pituitary gland) is most important hormone for ages 1­2, concentration decreases with age; promotes bone­lengthening (maturation and division in epiphyseal plates)  Has mitogenic effects indirectly through mediation of IGF­1  released from liver and other types of cells (bone) to function as a hormone, autocrine, and paracrine substance o GH stimulates chondrocyte precursor cells in bone  cells secrete IGF­1 and become responsive to it  IGF­1 stimulates cell division o Short stature: can be caused by decreased GH production or decreased IGF­1 production/failed response to it  Growth hormone­insensitivity syndrome: failure to produce IGF­1 in response to GH, causes decreased growth rate in child  DNA technology allows for treatment of short stature children with GH o IGF­1 secretion/activity affected by nutrition and other non­GH hormones  Malnutrition can prevent IGF­1 production even in presence of GH  Essential for development of fetal nervous system (produced by placenta) o GH stimulates protein synthesis by increasing amino acid uptake and synthesis/activity of ribosomes  Facilitates ability of tissues/organs to enlarge o GH is involved in energy homeostasis  Breaks down triglycerides stored in adipose cells to release fatty acids in blood  Stimulates gluconeogenesis in liver, inhibits insulin/glucose transport into cells  Increased exercise/stress/fasting causes increased GH concentrations o Insulin­like growth factor (IGF­2): closely related to IGF­1; secretion is independent of GH  Crucial mitogen during prenatal stage; postnatal function unknown  Thyroid hormone o Essential for normal growth  facilitates synthesis of T 3 o Stimulates chondrocyte differentiation, growth of new blood vessels in new bone, and responsiveness of bone cells to other growth factors o Hypothyroidism = slower growth rates  Insulin o Anabolic hormone, promotes transport of glucose/amino acids from extracellular fluid to adipose tissue, skeletal/cardiac muscle cells o Stimulates storage of fat, inhibits protein degradation o Growth­promoting effects on cell differentiation/division in fetal life  Sex steroids o Increased production between 8­10 years old, pubertal growth spurt occurs o Stimulates secretion of GH and IGF­1  Ultimately helps stop bone growth by inducing epiphyseal closure (rapid growth spurt then same height for rest of life) o Testosterone: anabolic effects on protein synthesis (boys develop more muscle mass than girls)  Anabolic steroids: androgens used in attempt to increase muscle mass/strength (testosterone, DHEA, androstenedione, synthetics); toxic effects on liver, fertility, behavior/emotions, etc.  Cortisol o Can have antigrowth effects when present in high concentrations  Inhibits DNA synthesis, bone growth, secretion of GH and IGF­1, stimulates protein/bone catabolism

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Textbook: OpenIntro Statistics
Edition: 3
Author: David M Diez; Christopher D Barr; Mine Çetinkaya-Rundel
ISBN: 9781943450039

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A study compared five dierent methods for teaching