37.3: Regulation of Body Processes
Skills to Develop
- Explain how hormones regulate the excretory system
- Discuss the role of hormones in the reproductive system
- Describe how hormones regulate metabolism
- Explain the role of hormones in different diseases
Hormones have a wide range of effects and modulate many different body processes. The key regulatory processes that will be examined here are those affecting the excretory system, the reproductive system, metabolism, blood calcium concentrations, growth, and the stress response.
Hormonal Regulation of the Excretory System
Maintaining a proper water balance in the body is important to avoid dehydration or over-hydration (hyponatremia). The water concentration of the body is monitored by osmoreceptors in the hypothalamus, which detect the concentration of electrolytes in the extracellular fluid. The concentration of electrolytes in the blood rises when there is water loss caused by excessive perspiration, inadequate water intake, or low blood volume due to blood loss. An increase in blood electrolyte levels results in a neuronal signal being sent from the osmoreceptors in hypothalamic nuclei. The pituitary gland has two components: anterior and posterior. The anterior pituitary is composed of glandular cells that secrete protein hormones. The posterior pituitary is an extension of the hypothalamus. It is composed largely of neurons that are continuous with the hypothalamus.
The hypothalamus produces a polypeptide hormone known as antidiuretic hormone (ADH) , which is transported to and released from the posterior pituitary gland. The principal action of ADH is to regulate the amount of water excreted by the kidneys. As ADH (which is also known as vasopressin) causes direct water reabsorption from the kidney tubules, salts and wastes are concentrated in what will eventually be excreted as urine. The hypothalamus controls the mechanisms of ADH secretion, either by regulating blood volume or the concentration of water in the blood. Dehydration or physiological stress can cause an increase of osmolarity above 300 mOsm/L, which in turn, raises ADH secretion and water will be retained, causing an increase in blood pressure. ADH travels in the bloodstream to the kidneys. Once at the kidneys, ADH changes the kidneys to become more permeable to water by temporarily inserting water channels, aquaporins, into the kidney tubules. Water moves out of the kidney tubules through the aquaporins, reducing urine volume. The water is reabsorbed into the capillaries lowering blood osmolarity back toward normal. As blood osmolarity decreases, a negative feedback mechanism reduces osmoreceptor activity in the hypothalamus, and ADH secretion is reduced. ADH release can be reduced by certain substances, including alcohol, which can cause increased urine production and dehydration.
Chronic underproduction of ADH or a mutation in the ADH receptor results in diabetes insipidus . If the posterior pituitary does not release enough ADH, water cannot be retained by the kidneys and is lost as urine. This causes increased thirst, but water taken in is lost again and must be continually consumed. If the condition is not severe, dehydration may not occur, but severe cases can lead to electrolyte imbalances due to dehydration.
Another hormone responsible for maintaining electrolyte concentrations in extracellular fluids is aldosterone , a steroid hormone that is produced by the adrenal cortex. In contrast to ADH, which promotes the reabsorption of water to maintain proper water balance, aldosterone maintains proper water balance by enhancing Na + reabsorption and K + secretion from extracellular fluid of the cells in kidney tubules. Because it is produced in the cortex of the adrenal gland and affects the concentrations of minerals Na + and K + , aldosterone is referred to as a mineralocorticoid , a corticosteroid that affects ion and water balance. Aldosterone release is stimulated by a decrease in blood sodium levels, blood volume, or blood pressure, or an increase in blood potassium levels. It also prevents the loss of Na + from sweat, saliva, and gastric juice. The reabsorption of Na + also results in the osmotic reabsorption of water, which alters blood volume and blood pressure.
Aldosterone production can be stimulated by low blood pressure, which triggers a sequence of chemical release, as illustrated in Figure \(\PageIndex{1}\). When blood pressure drops, the renin-angiotensin-aldosterone system (RAAS) is activated. Cells in the juxtaglomerular apparatus, which regulates the functions of the nephrons of the kidney, detect this and release renin . Renin, an enzyme, circulates in the blood and reacts with a plasma protein produced by the liver called angiotensinogen. When angiotensinogen is cleaved by renin, it produces angiotensin I, which is then converted into angiotensin II in the lungs. Angiotensin II functions as a hormone and then causes the release of the hormone aldosterone by the adrenal cortex, resulting in increased Na + reabsorption, water retention, and an increase in blood pressure. Angiotensin II in addition to being a potent vasoconstrictor also causes an increase in ADH and increased thirst, both of which help to raise blood pressure.
Hormonal Regulation of the Reproductive System
Regulation of the reproductive system is a process that requires the action of hormones from the pituitary gland, the adrenal cortex, and the gonads. During puberty in both males and females, the hypothalamus produces gonadotropin-releasing hormone (GnRH), which stimulates the production and release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland. These hormones regulate the gonads (testes in males and ovaries in females) and therefore are called gonadotropins . In both males and females, FSH stimulates gamete production and LH stimulates production of hormones by the gonads. An increase in gonad hormone levels inhibits GnRH production through a negative feedback loop.
Regulation of the Male Reproductive System
In males, FSH stimulates the maturation of sperm cells. FSH production is inhibited by the hormone inhibin, which is released by the testes. LH stimulates production of the sex hormones ( androgens ) by the interstitial cells of the testes and therefore is also called interstitial cell-stimulating hormone. The most widely known androgen in males is testosterone . Testosterone promotes the production of sperm and masculine characteristics. The adrenal cortex also produces small amounts of testosterone precursor, although the role of this additional hormone production is not fully understood.
Everyday Connection: The Dangers of Synthetic Hormones
Some athletes attempt to boost their performance by using artificial hormones that enhance muscle performance.  Steroids are used to help build muscle mass. Other hormones that are used to enhance athletic performance include erythropoietin , which triggers the production of red blood cells, and human growth hormone, which can help in building muscle mass. Most performance enhancing drugs are illegal for non-medical purposes. They are also banned by national and international governing bodies including the International Olympic Committee, the U.S. Olympic Committee, the National Collegiate Athletic Association, the Major League Baseball, and the National Football League.
The side effects of synthetic hormones are often significant and non-reversible, and in some cases, fatal. Androgens produce several complications such as liver dysfunctions and liver tumors, prostate gland enlargement, difficulty urinating, premature closure of epiphyseal cartilages, testicular atrophy, infertility, and immune system depression. The physiological strain caused by these substances is often greater than what the body can handle, leading to unpredictable and dangerous effects and linking their use to heart attacks, strokes, and impaired cardiac function.
Regulation of the Female Reproductive System
In females, FSH stimulates development of egg cells, called ova, which develop in structures called follicles. Follicle cells produce the hormone inhibin, which inhibits FSH production. LH also plays a role in the development of ova, induction of ovulation, and stimulation of estradiol and progesterone production by the ovaries, as illustrated in Figure \(\PageIndex{3}\). Estradiol and progesterone are steroid hormones that prepare the body for pregnancy. Estradiol produces secondary sex characteristics in females, while both estradiol and progesterone regulate the menstrual cycle.
In addition to producing FSH and LH, the anterior portion of the pituitary gland also produces the hormone prolactin (PRL) in females. Prolactin stimulates the production of milk by the mammary glands following childbirth. Prolactin levels are regulated by the hypothalamic hormones prolactin-releasing hormone (PRH) and prolactin-inhibiting hormone (PIH) , which is now known to be dopamine. PRH stimulates the release of prolactin and PIH inhibits it.
The posterior pituitary releases the hormone oxytocin , which stimulates uterine contractions during childbirth. The uterine smooth muscles are not very sensitive to oxytocin until late in pregnancy when the number of oxytocin receptors in the uterus peaks. Stretching of tissues in the uterus and cervix stimulates oxytocin release during childbirth. Contractions increase in intensity as blood levels of oxytocin rise via a positive feedback mechanism until the birth is complete. Oxytocin also stimulates the contraction of myoepithelial cells around the milk-producing mammary glands. As these cells contract, milk is forced from the secretory alveoli into milk ducts and is ejected from the breasts in milk ejection (“let-down”) reflex. Oxytocin release is stimulated by the suckling of an infant, which triggers the synthesis of oxytocin in the hypothalamus and its release into circulation at the posterior pituitary.
Hormonal Regulation of Metabolism
Blood glucose levels vary widely over the course of a day as periods of food consumption alternate with periods of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining homeostasis of blood glucose levels. Additional regulation is mediated by the thyroid hormones.
Regulation of Blood Glucose Levels by Insulin and Glucagon
Cells of the body require nutrients in order to function, and these nutrients are obtained through feeding. In order to manage nutrient intake, storing excess intake and utilizing reserves when necessary, the body uses hormones to moderate energy stores. Insulin is produced by the beta cells of the pancreas, which are stimulated to release insulin as blood glucose levels rise (for example, after a meal is consumed). Insulin lowers blood glucose levels by enhancing the rate of glucose uptake and utilization by target cells, which use glucose for ATP production. It also stimulates the liver to convert glucose to glycogen, which is then stored by cells for later use. Insulin also increases glucose transport into certain cells, such as muscle cells and the liver. This results from an insulin-mediated increase in the number of glucose transporter proteins in cell membranes, which remove glucose from circulation by facilitated diffusion. As insulin binds to its target cell via insulin receptors and signal transduction, it triggers the cell to incorporate glucose transport proteins into its membrane. This allows glucose to enter the cell, where it can be used as an energy source. However, this does not occur in all cells: some cells, including those in the kidneys and brain, can access glucose without the use of insulin. Insulin also stimulates the conversion of glucose to fat in adipocytes and the synthesis of proteins. These actions mediated by insulin cause blood glucose concentrations to fall, called a hypoglycemic “low sugar” effect, which inhibits further insulin release from beta cells through a negative feedback loop.
Link to Learning
This animation describes the role of insulin and the pancreas in diabetes.
Impaired insulin function can lead to a condition called diabetes mellitus , the main symptoms of which are illustrated in Figure \(\PageIndex{4}\). This can be caused by low levels of insulin production by the beta cells of the pancreas, or by reduced sensitivity of tissue cells to insulin. This prevents glucose from being absorbed by cells, causing high levels of blood glucose, or hyperglycemia (high sugar). High blood glucose levels make it difficult for the kidneys to recover all the glucose from nascent urine, resulting in glucose being lost in urine. High glucose levels also result in less water being reabsorbed by the kidneys, causing high amounts of urine to be produced; this may result in dehydration. Over time, high blood glucose levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system. Oversecretion of insulin can cause hypoglycemia , low blood glucose levels. This causes insufficient glucose availability to cells, often leading to muscle weakness, and can sometimes cause unconsciousness or death if left untreated.
When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized rapidly during exercise, the hormone glucagon is released from the alpha cells of the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect, by stimulating the breakdown of glycogen to glucose in skeletal muscle cells and liver cells in a process called glycogenolysis . Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells. Glucagon also stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose. This process of glucose synthesis is called gluconeogenesis . Glucagon also stimulates adipose cells to release fatty acids into the blood. These actions mediated by glucagon result in an increase in blood glucose levels to normal homeostatic levels. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in Figure \(\PageIndex{5}\).
Exercise
Pancreatic tumors may cause excess secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin. Which of the following statement about these two conditions is true?
- A pancreatic tumor and type I diabetes will have the opposite effects on blood sugar levels.
- A pancreatic tumor and type I diabetes will both cause hyperglycemia.
- A pancreatic tumor and type I diabetes will both cause hypoglycemia.
- Both pancreatic tumors and type I diabetes result in the inability of cells to take up glucose.
- Answer
-
B
Regulation of Blood Glucose Levels by Thyroid Hormones
The basal metabolic rate, which is the amount of calories required by the body at rest, is determined by two hormones produced by the thyroid gland: thyroxine , also known as tetraiodothyronine or T 4 , and triiodothyronine , also known as T 3 . These hormones affect nearly every cell in the body except for the adult brain, uterus, testes, blood cells, and spleen. They are transported across the plasma membrane of target cells and bind to receptors on the mitochondria resulting in increased ATP production. In the nucleus, T 3 and T 4 activate genes involved in energy production and glucose oxidation. This results in increased rates of metabolism and body heat production, which is known as the hormone’s calorigenic effect.
T 3 and T 4 release from the thyroid gland is stimulated by thyroid-stimulating hormone (TSH) , which is produced by the anterior pituitary. TSH binding at the receptors of the follicle of the thyroid triggers the production of T 3 and T 4 from a glycoprotein called thyroglobulin . Thyroglobulin is present in the follicles of the thyroid, and is converted into thyroid hormones with the addition of iodine. Iodine is formed from iodide ions that are actively transported into the thyroid follicle from the bloodstream. A peroxidase enzyme then attaches the iodine to the tyrosine amino acid found in thyroglobulin. T 3 has three iodine ions attached, while T 4 has four iodine ions attached. T 3 and T 4 are then released into the bloodstream, with T 4 being released in much greater amounts than T 3 . As T 3 is more active than T 4 and is responsible for most of the effects of thyroid hormones, tissues of the body convert T 4 to T 3 by the removal of an iodine ion. Most of the released T 3 and T 4 becomes attached to transport proteins in the bloodstream and is unable to cross the plasma membrane of cells. These protein-bound molecules are only released when blood levels of the unattached hormone begin to decline. In this way, a week’s worth of reserve hormone is maintained in the blood. Increased T 3 and T 4 levels in the blood inhibit the release of TSH, which results in lower T 3 and T 4 release from the thyroid.
The follicular cells of the thyroid require iodides (anions of iodine) in order to synthesize T 3 and T 4 . Iodides obtained from the diet are actively transported into follicle cells resulting in a concentration that is approximately 30 times higher than in blood. The typical diet in North America provides more iodine than required due to the addition of iodide to table salt. Inadequate iodine intake, which occurs in many developing countries, results in an inability to synthesize T 3 and T 4 hormones. The thyroid gland enlarges in a condition called goiter , which is caused by overproduction of TSH without the formation of thyroid hormone. Thyroglobulin is contained in a fluid called colloid, and TSH stimulation results in higher levels of colloid accumulation in the thyroid. In the absence of iodine, this is not converted to thyroid hormone, and colloid begins to accumulate more and more in the thyroid gland, leading to goiter.
Disorders can arise from both the underproduction and overproduction of thyroid hormones. Hypothyroidism , underproduction of the thyroid hormones, can cause a low metabolic rate leading to weight gain, sensitivity to cold, and reduced mental activity, among other symptoms. In children, hypothyroidism can cause cretinism, which can lead to mental retardation and growth defects. Hyperthyroidism , the overproduction of thyroid hormones, can lead to an increased metabolic rate and its effects: weight loss, excess heat production, sweating, and an increased heart rate. Graves’ disease is one example of a hyperthyroid condition.
Hormonal Control of Blood Calcium Levels
Regulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive. If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms can result.
Blood calcium levels are regulated by parathyroid hormone (PTH) , which is produced by the parathyroid glands, as illustrated in Figure \(\PageIndex{6}\). PTH is released in response to low blood Ca 2+ levels. PTH increases Ca 2+ levels by targeting the skeleton, the kidneys, and the intestine. In the skeleton, PTH stimulates osteoclasts, which causes bone to be reabsorbed, releasing Ca 2+ from bone into the blood. PTH also inhibits osteoblasts, reducing Ca 2+ deposition in bone. In the intestines, PTH increases dietary Ca 2+ absorption, and in the kidneys, PTH stimulates reabsorption of the CA 2+ . While PTH acts directly on the kidneys to increase Ca 2+ reabsorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels.
Hyperparathyroidism results from an overproduction of parathyroid hormone. This results in excessive calcium being removed from bones and introduced into blood circulation, producing structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany (severe sustained muscle contraction).
The hormone calcitonin , which is produced by the parafollicular or C cells of the thyroid, has the opposite effect on blood calcium levels as does PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy nonpregnant, unstarved adults, the role of calcitonin is unclear.
Hormonal Regulation of Growth
Hormonal regulation is required for the growth and replication of most cells in the body. Growth hormone (GH) , produced by the anterior portion of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bones. Growth hormone has direct and indirect mechanisms of action. The first direct action of GH is stimulation of triglyceride breakdown (lipolysis) and release into the blood by adipocytes. This results in a switch by most tissues from utilizing glucose as an energy source to utilizing fatty acids. This process is called a glucose-sparing effect . In another direct mechanism, GH stimulates glycogen breakdown in the liver; the glycogen is then released into the blood as glucose. Blood glucose levels increase as most tissues are utilizing fatty acids instead of glucose for their energy needs. The GH mediated increase in blood glucose levels is called a diabetogenic effect because it is similar to the high blood glucose levels seen in diabetes mellitus.
The indirect mechanism of GH action is mediated by insulin-like growth factors (IGFs) or somatomedins, which are a family of growth-promoting proteins produced by the liver, which stimulates tissue growth. IGFs stimulate the uptake of amino acids from the blood, allowing the formation of new proteins, particularly in skeletal muscle cells, cartilage cells, and other target cells, as shown in Figure \(\PageIndex{7}\). This is especially important after a meal, when glucose and amino acid concentration levels are high in the blood. GH levels are regulated by two hormones produced by the hypothalamus. GH release is stimulated by growth hormone-releasing hormone (GHRH) and is inhibited by growth hormone-inhibiting hormone (GHIH) , also called somatostatin.
A balanced production of growth hormone is critical for proper development. Underproduction of GH in adults does not appear to cause any abnormalities, but in children it can result in pituitary dwarfism , in which growth is reduced. Pituitary dwarfism is characterized by symmetric body formation. In some cases, individuals are under 30 inches in height. Oversecretion of growth hormone can lead to gigantism in children, causing excessive growth. In some documented cases, individuals can reach heights of over eight feet. In adults, excessive GH can lead to acromegaly , a condition in which there is enlargement of bones in the face, hands, and feet that are still capable of growth.
Hormonal Regulation of Stress
When a threat or danger is perceived, the body responds by releasing hormones that will ready it for the “fight-or-flight” response. The effects of this response are familiar to anyone who has been in a stressful situation: increased heart rate, dry mouth, and hair standing up.
Evolution Connection: Fight-or-Flight Response
Interactions of the endocrine hormones have evolved to ensure the body’s internal environment remains stable. Stressors are stimuli that disrupt homeostasis. The sympathetic division of the vertebrate autonomic nervous system has evolved the fight-or-flight response to counter stress-induced disruptions of homeostasis. In the initial alarm phase, the sympathetic nervous system stimulates an increase in energy levels through increased blood glucose levels. This prepares the body for physical activity that may be required to respond to stress: to either fight for survival or to flee from danger.
However, some stresses, such as illness or injury, can last for a long time. Glycogen reserves, which provide energy in the short-term response to stress, are exhausted after several hours and cannot meet long-term energy needs. If glycogen reserves were the only energy source available, neural functioning could not be maintained once the reserves became depleted due to the nervous system’s high requirement for glucose. In this situation, the body has evolved a response to counter long-term stress through the actions of the glucocorticoids, which ensure that long-term energy requirements can be met. The glucocorticoids mobilize lipid and protein reserves, stimulate gluconeogenesis, conserve glucose for use by neural tissue, and stimulate the conservation of salts and water. The mechanisms to maintain homeostasis that are described here are those observed in the human body. However, the fight-or-flight response exists in some form in all vertebrates.
The sympathetic nervous system regulates the stress response via the hypothalamus. Stressful stimuli cause the hypothalamus to signal the adrenal medulla (which mediates short-term stress responses) via nerve impulses, and the adrenal cortex, which mediates long-term stress responses, via the hormone adrenocorticotropic hormone (ACTH) , which is produced by the anterior pituitary.
Short-term Stress Response
When presented with a stressful situation, the body responds by calling for the release of hormones that provide a burst of energy. The hormones epinephrine (also known as adrenaline) and norepinephrine (also known as noradrenaline) are released by the adrenal medulla. How do these hormones provide a burst of energy? Epinephrine and norepinephrine increase blood glucose levels by stimulating the liver and skeletal muscles to break down glycogen and by stimulating glucose release by liver cells. Additionally, these hormones increase oxygen availability to cells by increasing the heart rate and dilating the bronchioles. The hormones also prioritize body function by increasing blood supply to essential organs such as the heart, brain, and skeletal muscles, while restricting blood flow to organs not in immediate need, such as the skin, digestive system, and kidneys. Epinephrine and norepinephrine are collectively called catecholamines.
Link to Learning
Watch this Discovery Channel animation describing the flight-or-flight response.
Long-term Stress Response
Long-term stress response differs from short-term stress response. The body cannot sustain the bursts of energy mediated by epinephrine and norepinephrine for long times. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. The adrenal cortex is stimulated by ACTH to release steroid hormones called corticosteroids . Corticosteroids turn on transcription of certain genes in the nuclei of target cells. They change enzyme concentrations in the cytoplasm and affect cellular metabolism. There are two main corticosteroids: glucocorticoids such as cortisol , and mineralocorticoids such as aldosterone. These hormones target the breakdown of fat into fatty acids in the adipose tissue. The fatty acids are released into the bloodstream for other tissues to use for ATP production. The glucocorticoids primarily affect glucose metabolism by stimulating glucose synthesis. Glucocorticoids also have anti-inflammatory properties through inhibition of the immune system. For example, cortisone is used as an anti-inflammatory medication; however, it cannot be used long term as it increases susceptibility to disease due to its immune-suppressing effects.
Mineralocorticoids function to regulate ion and water balance of the body. The hormone aldosterone stimulates the reabsorption of water and sodium ions in the kidney, which results in increased blood pressure and volume.
Hypersecretion of glucocorticoids can cause a condition known as Cushing’s disease , characterized by a shifting of fat storage areas of the body. This can cause the accumulation of adipose tissue in the face and neck, and excessive glucose in the blood. Hyposecretion of the corticosteroids can cause Addison’s disease , which may result in bronzing of the skin, hypoglycemia, and low electrolyte levels in the blood.
Summary
Water levels in the body are controlled by antidiuretic hormone (ADH), which is produced in the hypothalamus and triggers the reabsorption of water by the kidneys. Underproduction of ADH can cause diabetes insipidus. Aldosterone, a hormone produced by the adrenal cortex of the kidneys, enhances Na + reabsorption from the extracellular fluids and subsequent water reabsorption by diffusion. The renin-angiotensin-aldosterone system is one way that aldosterone release is controlled.
The reproductive system is controlled by the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which are produced by the pituitary gland. Gonadotropin release is controlled by the hypothalamic hormone gonadotropin-releasing hormone (GnRH). FSH stimulates the maturation of sperm cells in males and is inhibited by the hormone inhibin, while LH stimulates the production of the androgen testosterone. FSH stimulates egg maturation in females, while LH stimulates the production of estrogens and progesterone. Estrogens are a group of steroid hormones produced by the ovaries that trigger the development of secondary sex characteristics in females as well as control the maturation of the ova. In females, the pituitary also produces prolactin, which stimulates milk production after childbirth, and oxytocin, which stimulates uterine contraction during childbirth and milk let-down during suckling.
Insulin is produced by the pancreas in response to rising blood glucose levels and allows cells to utilize blood glucose and store excess glucose for later use. Diabetes mellitus is caused by reduced insulin activity and causes high blood glucose levels, or hyperglycemia. Glucagon is released by the pancreas in response to low blood glucose levels and stimulates the breakdown of glycogen into glucose, which can be used by the body. The body’s basal metabolic rate is controlled by the thyroid hormones thyroxine (T 4 ) and triiodothyronine (T 3 ). The anterior pituitary produces thyroid stimulating hormone (TSH), which controls the release of T 3 and T 4 from the thyroid gland. Iodine is necessary in the production of thyroid hormone, and the lack of iodine can lead to a condition called goiter.
Parathyroid hormone (PTH) is produced by the parathyroid glands in response to low blood Ca 2+ levels. The parafollicular cells of the thyroid produce calcitonin, which reduces blood Ca 2+ levels. Growth hormone (GH) is produced by the anterior pituitary and controls the growth rate of muscle and bone. GH action is indirectly mediated by insulin-like growth factors (IGFs). Short-term stress causes the hypothalamus to trigger the adrenal medulla to release epinephrine and norepinephrine, which trigger the fight or flight response. Long-term stress causes the hypothalamus to trigger the anterior pituitary to release adrenocorticotropic hormone (ACTH), which causes the release of corticosteroids, glucocorticoids, and mineralocorticoids, from the adrenal cortex.
Glossary
- acromegaly
- condition caused by overproduction of GH in adults
- Addison’s disease
- disorder caused by the hyposecretion of corticosteroids
- adrenocorticotropic hormone (ACTH)
- hormone released by the anterior pituitary, which stimulates the adrenal cortex to release corticosteroids during the long-term stress response
- aldosterone
- steroid hormone produced by the adrenal cortex that stimulates the reabsorption of Na + from extracellular fluids and secretion of K + .
- androgen
- male sex hormone such as testosterone
- antidiuretic hormone (ADH)
- hormone produced by the hypothalamus and released by the posterior pituitary that increases water reabsorption by the kidneys
- calcitonin
- hormone produced by the parafollicular cells of the thyroid gland that functions to lower blood Ca 2+ levels and promote bone growth
- corticosteroid
- hormone released by the adrenal cortex in response to long-term stress
- cortisol
- glucocorticoid produced in response to stress
- Cushing’s disease
- disorder caused by the hypersecretion of glucocorticoids
- diabetes insipidus
- disorder caused by underproduction of ADH
- diabetes mellitus
- disorder caused by low levels of insulin activity
- diabetogenic effect
- effect of GH that causes blood glucose levels to rise similar to diabetes mellitus
- epinephrine
- hormone released by the adrenal medulla in response to a short term stress
- estrogens
- - a group of steroid hormones, including estradiol and several others, that are produced by the ovaries and elicit secondary sex characteristics in females as well as control the maturation of the ova
- follicle-stimulating hormone (FSH)
- hormone produced by the anterior pituitary that stimulates gamete production
- gigantism
- condition caused by overproduction of GH in children
- glucagon
- hormone produced by the alpha cells of the pancreas in response to low blood sugar; functions to raise blood sugar levels
- glucocorticoid
- corticosteroid that affects glucose metabolism
- gluconeogenesis
- synthesis of glucose from amino acids
- glucose-sparing effect
- effect of GH that causes tissues to use fatty acids instead of glucose as an energy source
- glycogenolysis
- breakdown of glycogen into glucose
- goiter
- enlargement of the thyroid gland caused by insufficient dietary iodine levels
- gonadotropin
- hormone that regulates the gonads, including FSH and LH
- growth hormone (GH)
- hormone produced by the anterior pituitary that promotes protein synthesis and body growth
- growth hormone-inhibiting hormone (GHIH)
- hormone produced by the hypothalamus that inhibits growth hormone production, also called somatostatin
- growth hormone-releasing hormone (GHRH)
- hormone released by the hypothalamus that triggers the release of GH
- hyperglycemia
- high blood sugar level
- hyperthyroidism
- overactivity of the thyroid gland
- hypoglycemia
- low blood sugar level
- hypothyroidism
- underactivity of the thyroid gland
- insulin
- hormone produced by the beta cells of the pancreas in response to high blood glucose levels; functions to lower blood glucose levels
- insulin-like growth factor (IGF)
- growth-promoting protein produced by the liver
- mineralocorticoid
- corticosteroid that affects ion and water balance
- norepinephrine
- hormone released by the adrenal medulla in response to a short-term stress hormone production by the gonads
- osmoreceptor
- receptor in the hypothalamus that monitors the concentration of electrolytes in the blood
- oxytocin
- hormone released by the posterior pituitary to stimulate uterine contractions during childbirth and milk let-down in the mammary glands
- parathyroid hormone (PTH)
- hormone produced by the parathyroid glands in response to low blood Ca 2+ levels; functions to raise blood Ca 2+ levels
- pituitary dwarfism
- condition caused by underproduction of GH in children
- prolactin (PRL)
- hormone produced by the anterior pituitary that stimulates milk production
- prolactin-inhibiting hormone
- hormone produced by the hypothalamus that inhibits the release of prolactin
- prolactin-releasing hormone
- hormone produced by the hypothalamus that stimulates the release of prolactin
- renin
- enzyme produced by the juxtaglomerular apparatus of the kidneys that reacts with angiotensinogen to cause the release of aldosterone
- thyroglobulin
- glycoprotein found in the thyroid that is converted into thyroid hormone
- thyroid-stimulating hormone (TSH)
- hormone produced by the anterior pituitary that controls the release of T 3 and T 4 from the thyroid gland
- thyroxine (tetraiodothyronine, T 4 )
- thyroid hormone that controls the basal metabolic rate
- triiodothyronine (T 3 )
- thyroid hormone that controls the basal metabolic rate


5.3: Fractures- Bone Repair
A fracture is a broken bone. It will heal whether or not a physician resets it in its anatomical position. If the bone is not reset correctly, the healing process will keep the bone in its deformed position.
When a broken bone is manipulated and set into its natural position without surgery, the procedure is called a closed reduction . Open reduction requires surgery to expose the fracture and reset the bone. While some fractures can be minor, others are quite severe and result in grave complications. For example, a fractured diaphysis of the femur has the potential to release fat globules into the bloodstream. These can become lodged in the capillary beds of the lungs, leading to respiratory distress and if not treated quickly, death.
Types of Fractures
Fractures are classified by their complexity, location, and other features (Figure 5.20). Table 5.4 outlines common types of fractures. Some fractures may be described using more than one term because it may have the features of more than one type (e.g., an open transverse fracture).
| Types of Fractures | |
|---|---|
| Type of fracture | Description |
| Transverse | Occurs straight across the long axis of the bone |
| Oblique | Occurs at an angle that is not 90 degrees |
| Spiral | Bone segments are pulled apart as a result of a twisting motion |
| Comminuted | Several breaks result in many small pieces between two large segments |
| Impacted | One fragment is driven into the other, usually as a result of compression |
| Greenstick | A partial fracture in which only one side of the bone is broken |
| Open (or compound) | A fracture in which at least one end of the broken bone tears through the skin; carries a high risk of infection |
| Closed (or simple) | A fracture in which the skin remains intact |
Bone Repair
When a bone breaks, blood flows from any vessel torn by the fracture. These vessels could be in the periosteum, osteons, and/or medullary cavity. The blood begins to clot, and about six to eight hours after the fracture, the clotting blood has formed a fracture hematoma (Figure 5.21 a ). The disruption of blood flow to the bone results in the death of bone cells around the fracture.
Within about 48 hours after the fracture, chondrocytes from the endosteum have created an internal callus (plural = calli) by secreting a fibrocartilaginous matrix between the two ends of the broken bone, while the periosteal chondrocytes and osteoblasts create an external callus of hyaline cartilage and bone, respectively, around the outside of the break (Figure 5.21 b ). This stabilizes the fracture.
Over the next several weeks, osteoclasts resorb the dead bone; osteogenic cells become active, divide, and differentiate into osteoblasts. The cartilage in the calli is replaced by trabecular bone via endochondral ossification (Figure 5.21 c ).
Eventually, the internal and external calli unite, compact bone replaces spongy bone at the outer margins of the fracture, and healing is complete. A slight swelling may remain on the outer surface of the bone, but quite often, that region undergoes remodeling (Figure 5.21 d ), and no external evidence of the fracture remains.
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4: The Prokaryotic Cell - Bacteria
Despite sharing certain characteristics, cells may vary significantly. The two main types of cells are prokaryotic cells (lacking a nucleus) and eukaryotic cells (containing a well-organized, membrane-bound nucleus). Each type of cell exhibits remarkable variety in structure, function, and metabolic activity. This chapter will focus on the historical discoveries that have shaped our current understanding of microbes, including their origins and their role in human disease. We will then explore the distinguishing structures found in prokaryotic and eukaryotic cells.
-
- 4.1: Spontaneous Generation
- The theory of spontaneous generation states that life arose from nonliving matter. It was a long-held belief dating back to Aristotle and the ancient Greeks. Experimentation by Francesco Redi in the 17th century presented the first significant evidence refuting spontaneous generation by showing that flies must have access to meat for maggots to develop on the meat. Louis Pasteur is credited with conclusively disproving the theory and proposed that “life only comes from life.”
-
- 4.2: Foundations of Modern Cell Theory
- Although cells were first observed in the 1660s by Robert Hooke, cell theory was not well accepted for another 200 years. The work of scientists such as Schleiden, Schwann, Remak, and Virchow contributed to its acceptance. Endosymbiotic theory states that mitochondria and chloroplasts, organelles found in many types of organisms, have their origins in bacteria. Significant structural and genetic information support this theory. The miasma theory was widely accepted until the 19th century.
-
- 4.3: Unique Characteristics of Prokaryotic Cells
- Prokaryotic cells differ from eukaryotic cells in that their genetic material is contained in a nucleoid rather than a membrane-bound nucleus. In addition, prokaryotic cells generally lack membrane-bound organelles. Prokaryotic cells of the same species typically share a similar cell morphology and cellular arrangement. Most prokaryotic cells have a cell wall that helps the organism maintain cellular morphology and protects it against changes in osmotic pressure.


17.4.1: Transgenic Animals
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A transgenic animal is one that carries a foreign gene that has been deliberately inserted into its genome. The foreign gene is constructed using recombinant DNA methodology. In addition to the gene itself, the DNA usually includes other sequences to enable it to be incorporated into the DNA of the host and to be expressed correctly by the cells of the host. Transgenic sheep and goats have been produced that express foreign proteins in their milk. Transgenic chickens are now able to synthesize human proteins in the "white" of their eggs. These animals should eventually prove to be valuable sources of proteins for human therapy.
Note
In July 2000, researchers from the team that produced Dolly reported success in producing transgenic lambs in which the transgene had been inserted at a specific site in the genome and functioned well.
Transgenic mice have provided the tools for exploring many biological questions.
Example
Normal mice cannot be infected with polio virus. They lack the cell-surface molecule that, in humans, serves as the receptor for the virus. So normal mice cannot serve as an inexpensive, easily-manipulated model for studying the disease. However, transgenic mice expressing the human gene for the polio virus receptor
- can be infected by polio virus and even
- develop paralysis and other pathological changes characteristic of the disease in humans.
Two methods of producing transgenic mice are widely used:
- transforming embryonic stem cells ( ES cells) growing in tissue culture with the desired DNA
- injecting the desired gene into the pronucleus of a fertilized mouse egg
Fig.11.4.1 Methods to produce Transgenic mice
The Embryonic Stem Cell Method - Method 1
Embryonic stem cells ( ES cells) are harvested from the inner cell mass (ICM) of mouse blastocysts. They can be grown in culture and retain their full potential to produce all the cells of the mature animal, including its gametes .
1. Make your DNA
Using recombinant DNA methods, build molecules of DNA containing- the gene you desire (e.g., the insulin gene)
- vector DNA to enable the molecules to be inserted into host DNA molecules
- promoter and enhancer sequences to enable the gene to be expressed by host cells
2. Transform ES cells in culture
Expose the cultured cells to the DNA so that some will incorporate it.3. Select for successfully transformed cells
4. Inject these cells into the inner cell mass (ICM) of mouse blastocysts.
5. Embryo transfer
- Prepare a pseudopregnant mouse (by mating a female mouse with a vasectomized male). The stimulus of mating elicits the hormonal changes needed to make her uterus receptive.
- Transfer the embryos into her uterus.
- Hope that they implant successfully and develop into healthy pups (no more than one-third will).
6. Test her offspring
- Remove a small piece of tissue from the tail and examine its DNA for the desired gene. No more than 10–20% will have it, and they will be heterozygous for the gene.
7. Establish a transgenic strain
- Mate two heterozygous mice and screen their offspring for the 1 in 4 that will be homozygous for the transgene.
- Mating these will found the transgenic strain.
The Pronucleus Method - Method 2
1. Prepare your DNA as in Method 1
2. Transform fertilized eggs
- Harvest freshly fertilized eggs before the sperm head has become a pronucleus.
- Inject the male pronucleus with your DNA.
- When the pronuclei have fused to form the diploid zygote nucleus, allow the zygote to divide by mitosis to form a 2-cell embryo.
3. Implant the embryos in a pseudopregnant foster mother and proceed as in Method 1.
Example
This image (courtesy of R. L. Brinster and R. E. Hammer) shows a transgenic mouse (right) with a normal littermate (left). The giant mouse developed from a fertilized egg transformed with a recombinant DNA molecule containing:
- the gene for human growth hormone
- a strong mouse gene promoter
The levels of growth hormone in the serum of some of the transgenic mice were several hundred times higher than in control mice.
Random vs. Targeted Gene Insertion
The early vectors used for gene insertion could, and did, place the gene (from one to 200 copies of it) anywhere in the genome. However, if you know some of the DNA sequence flanking a particular gene, it is possible to design vectors that replace that gene. The replacement gene can be one that- restores function in a mutant animal or
- knocks out the function of a particular locus.
- the desired gene
- neo r , a gene that encodes an enzyme that inactivates the antibiotic neomycin and its relatives, like the drug G418, which is lethal to mammalian cells
- tk , a gene that encodes thymidine kinase , an enzyme that phosphorylates the nucleoside analog ganciclovir . DNA polymerase fails to discriminate against the resulting nucleotide and inserts this nonfunctional nucleotide into freshly-replicating DNA. So ganciclovir kills cells that contain the tk gene
Step 1
Treat culture of ES cells with preparation of vector DNA.Results:
- Most cells fail to take up the vector; these cells will be killed if exposed to G418.
- In a few cells : the vector is inserted randomly in the genome. In random insertion, the entire vector, including the tk gene, is inserted into host DNA. These cells are resistant to G418 but killed by gancyclovir.
- In still fewer cells : homologous recombination occurs. Stretches of DNA sequence in the vector find the homologous sequences in the host genome, and the region between these homologous sequences replaces the equivalent region in the host DNA.
Step 2
Culture the mixture of cells in medium containing both G418 and ganciclovir.- The cells (the majority) that failed to take up the vector are killed by G418.
- The cells in which the vector was inserted randomly are killed by gancyclovir (because they contain the tk gene).
- This leaves a population of cells transformed by homologous recombination (enriched several thousand fold).
Step 3
Inject these into the inner cell mass of mouse blastocysts.
Knockout Mice: What do they teach us?
If the replacement gene ( A* in the diagram) is nonfunctional (a "null" allele), mating of the heterozygous transgenic mice will produce a strain of " knockout mice " homozygous for the nonfunctional gene (both copies of the gene at that locus have been "knocked out"). Knockout mice are valuable tools for discovering the function(s) of genes for which mutant strains were not previously available. Two generalizations have emerged from examining knockout mice:
- Knockout mice are often surprisingly unaffected by their deficiency. Many genes turn out not to be indispensable. The mouse genome appears to have sufficient redundancy to compensate for a single missing pair of alleles.
- Most genes are pleiotropic . They are expressed in different tissues in different ways and at different times in development.
Tissue-Specific Knockout Mice
While "housekeeping" genes are expressed in all types of cells at all stages of development, other genes are normally expressed in only certain types of cells when turned on by the appropriate signals (e.g. the arrival of a hormone).
To study such genes, one might expect that the methods described above would work. However, it turns out that genes that are only expressed in certain adult tissues may nonetheless be vital during embryonic development. In such cases, the animals do not survive long enough for their knockout gene to be studied. Fortunately, there are now techniques with which transgenic mice can be made where a particular gene gets knocked out in only one type of cell.
The Cre/ loxP System
One of the bacteriophages that infects E. coli, called P1, produces an enzyme — designated Cre — that cuts its DNA into lengths suitable for packaging into fresh virus particles. Cre cuts the viral DNA wherever it encounters a pair of sequences designated loxP . All the DNA between the two loxP sites is removed, and the remaining DNA ligated together again (so the enzyme is a recombinase). Using "Method 1" above, mice can be made transgenic for
- the gene encoding Cre attached to a promoter that will be activated only when it is bound by the same transcription factors that turn on the other genes required for the unique function(s) of that type of cell;
- a "target" gene, the one whose function is to be studied, flanked by loxP sequences.
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those cells that
- receive signals (e.g., the arrival of a hormone or cytokine)
- to turn on production of the transcription factors needed
- to activate the promoters of the genes whose products are needed by that particular kind of cell
- All other cells will lack the transcription factors needed to bind to the Cre promoter (and/or any enhancers) so the target gene remains intact.
The result: a mouse with a particular gene knocked out in only certain cells.
Knock-in Mice
The Cre/ loxP system can also be used to
- remove DNA sequences that block gene transcription. The "target" gene can then be turned on in certain cells or at certain times as the experimenter wishes.
- replace one of the mouse's own genes with a new gene that the investigator wishes to study.
Such transgenic mice are called "knock-in" mice.
Transgenic Sheep and Goats
Until recently, the transgenes introduced into sheep inserted randomly in the genome and often worked poorly. However, in July 2000, success at inserting a transgene into a specific gene locus was reported. The gene was the human gene for alpha1-antitrypsin , and two of the animals expressed large quantities of the human protein in their milk.
This is how it was done.
Sheep fibroblasts (connective tissue cells) growing in tissue culture were treated with a vector that contained these segments of DNA:
-
2 regions homologous to the sheep
COL1A1
gene. This gene encodes Type 1 collagen. (Its absence in humans causes the inherited disease osteogenesis imperfecta.)
This locus was chosen because fibroblasts secrete large amounts of collagen and thus one would expect the gene to be easily accessible in the chromatin.
- A neomycin-resistance gene to aid in isolating those cells that successfully incorporated the vector.
-
The human gene encoding alpha1-antitrypsin.
Some people inherit two non- or poorly-functioning genes for this protein. Its resulting low level or absence produces the disease Alpha1-Antitrypsin Deficiency ( A1AD or Alpha1 ). The main symptoms are damage to the lungs (and sometimes to the liver).
- Promoter sites from the beta-lactoglobulin gene. These promote hormone-driven gene expression in milk-producing cells.
- Binding sites for ribosomes for efficient translation of the beta-lactoglobulin mRNAs.
- Fused with enucleated sheep eggs and implanted in the uterus of a ewe (female sheep)
- Several embryos survived until their birth, and two young lambs lived over a year.
- When treated with hormones, these two lambs secreted milk containing large amounts of alpha1-antitrypsin (650 µg/ml; 50 times higher than previous results using random insertion of the transgene).
On June 18, 2003, the company doing this work abandoned it because of the great expense of building a facility for purifying the protein from sheep's milk. Purification is important because even when 99.9% pure, human patients can develop antibodies against the tiny amounts of sheep proteins that remain.
However, another company, GTC Biotherapeutics, has persevered and in June of 2006 won preliminary approval to market a human protein, antithrombin, in Europe. Their protein — the first made in a transgenic animal to receive regulatory approval for human therapy — was secreted in the milk of transgenic goats.Transgenic Chickens
Chickens grow faster than sheep and goats and large numbers can be grown in close quarters. They also synthesize several grams of protein in the "white" of their eggs.Two methods have succeeded in producing chickens carrying and expressing foreign genes.
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Infecting embryos with a viral vector carrying
- the human gene for a therapeutic protein
- promoter sequences that will respond to the signals for making proteins (e.g. lysozyme) in egg white
- Transforming rooster sperm with a human gene and the appropriate promoters and checking for any transgenic offspring.
Preliminary results from both methods indicate that it may be possible for chickens to produce as much as 0.1 g of human protein in each egg that they lay.
Not only should this cost less than producing therapeutic proteins in culture vessels, but chickens will probably add the correct sugars to glycosylated proteins — something that E. coli cannot do.
Transgenic Pigs
Transgenic pigs have also been produced by fertilizing normal eggs with sperm cells that have incorporated foreign DNA. This procedure, called sperm-mediated gene transfer (SMGT) may someday be able to produce transgenic pigs that can serve as a source of transplanted organs for humans.
Transgenic Primates
In the 28 May 2009 issue of Nature , Japanese scientists reported success in creating transgenic marmosets. Marmosets are primates and thus our closest relatives (so far) to be genetically engineered. In some cases, the transgene (for green fluorescent protein) was incorporated into the germline and passed on to the animal's offspring. The hope is that these transgenic animals will provide the best model yet for studying human disease and possible therapies.


14: Excavations
“Safety isn’t expensive, it’s priceless.” – Author Unknown
Overview
Most construction starts with ground preparation and grading. Excavations are man made depressions and removal of soil and considered a part of ground preparation. A special type of excavation, the trench, a deep and narrow excavation is often needed for placement of underground utilities, electrical cables and pipe for water mains and gas lines. The removal of large amounts of soil that leaves a trench vulnerable to cave in is what makes them extremely hazardous. A cubic meter of soil can weigh as much as a small vehicle and without proper trench protection will crush, suffocate and trap a worker if the sides of trench walls fail. This chapter will discuss the importance of various protective systems needed to keep workers safe when performing excavation work and especially while working in trenches.
Chapter Objective:
- Determine how to Identify Soil Types.
- Identify the Hazards Associated with Excavations & Trenching.
- Understand the Responsibilities of the Competent Person.
- Select the Proper Method of Protection for Workers in Excavations.
- Properly Prepare for Excavation Work.
Learning Outcome:
- List the five most critical excavations hazards.
- Apply the hierarchy of controls to Subpart P.
Standards: 1926 Subpart P-Excavations
Key Terms:
Cohesive, fissure, shoring, surface encumbrance, unconfined compressive strength
Mini-Lecture: Excavations
Topic Required Time: 1 hrs; Independent Study and reflection 3/4 hour.
Thumbnail: Chinese transcontinental railroad workers, public domain


7.6: Ageism
In the 1960s, Robert Butler coined the phrase ageism, which he defined as:
A process of systematic stereotyping of and discrimination against people because they are old, just as racism and sexism accomplish this with skin color and gender. Old people are categorized as senile, rigid in thought and manner, old-fashioned in morality and skills. . . . Ageism allows the younger generations to see older people as different from themselves; thus they subtly cease to identify with their elders as human beings.
—R. Butler, Why Survive? Being Old in America , 1975
While some advocates for elders suggest that ageism is a cause of elder abuse, neglect, and exploitation, we do not have enough valid research into the attitudes of known perpetrators of elder mistreatment to be able to definitively make that statement. However, as the following references indicate, ageism contributes to conditions that disadvantage and marginalize older individuals in society.
Inequitable treatment occurring in the workplace, in the health care sector, and in the legal arena appears to be based, at least in part, on age discrimination. Even efforts to offer protection may be based upon compassionate ageism that may lead to disempowerment. Ageist beliefs and policies categorize seniors as a homogenous group, ignoring diversity issues and individual needs. Furthermore, it appears that aging individuals are not only subjected to ageist beliefs by others; they internalize these beliefs as well. Age discrimination can impact elders in tangible ways by contributing to reduced financial security and poorer health outcomes, but also appears to a have subtler, though perhaps more pervasive impact, by contributing to social isolation (a risk factor for mistreatment), lower self-esteem and poorer quality of life. When combined with other prejudices, such as sexism, racism and biases against the disabled (known as “ableism”), the health and well-being of elders is further jeopardized.
Take the Implicit Association Test (IAT) on aging and reflect on your results then ask someone else to take the IAT and interview that person about the results.
- How might the results may impact your attitudes?
Consequences of Attributing Illness to Old Age
Stereotypic beliefs about older adults and the aging process have led to endorsement of the myth that “to be old is to be ill.” A study on older adults’ beliefs about the causes of their chronic illness (i.e., heart disease, cancer, diabetes, etc.), found that attributing an illness to “old age” is associated with negative health outcomes. ‘Old age’ attributions were associated with more frequent perceived health symptoms, poorer health maintenance behaviors and a greater likelihood of mortality. The probability of death was more than double among those who strongly attributed illness symptoms to “old age” as compared to those who did not. [1]
Sources
Source: Ageism, NCEA, AOA, www.ncea.aoa.gov/main_site/library/cane/CANE_Series/CANE_ageism.aspx
- Stewart TL , Chipperfield JG , Perry RP , Weiner B . (2011). Attributing illness to 'old age:' Consequences of a self-directed stereotype for health and mortality . Psychol Health. http://www.ncbi.nlm.nih.gov/pubmed/22149693 ↵


3.8B: Intercellular Junctions
Intercellular junctions provide plant and animal cells with the ability to communicate through direct contact.
- Describe the purpose of intercellular junctions in the structure of cells
Key Points
- Plasmodesmata are intercellular junctions between plant cells that enable the transportation of materials between cells.
- A tight junction is a watertight seal between two adjacent animal cells, which prevents materials from leaking out of cells.
- Desmosomes connect adjacent cells when cadherins in the plasma membrane connect to intermediate filaments.
- Similar to plasmodesmata, gap junctions are channels between adjacent cells that allow for the transport of ions, nutrients, and other substances.
Key Terms
- plasmodesma : A microscopic channel traversing the cell walls of plant cells and some algal cells, enabling transport and communication between them.
- connexon : An assembly of six connexins forming a bridge called a gap junction between the cytoplasms of two adjacent cells.
- occludin : Together with the claudin group of proteins, it is the main component of the tight junctions.
Intercellular Junctions
The extracellular matrix allows cellular communication within tissues through conformational changes that induce chemical signals, which ultimately transform activities within the cell. However, cells are also capable of communicating with each other via direct contact through intercellular junctions.
There are some differences in the ways that plant and animal cells communicate directly. Plasmodesmata are junctions between plant cells, whereas animal cell contacts are carried out through tight junctions, gap junctions, and desmosomes.
Junctions in Plant Cells
In general, long stretches of the plasma membranes of neighboring plant cells cannot touch one another because they are separated by the cell wall that surrounds each cell. How then can a plant transfer water and other soil nutrients from its roots, through its stems, and to its leaves? This transport primarily uses the vascular tissues (xylem and phloem); however, there are also structural modifications called plasmodesmata (singular: plasmodesma) that facilitate direct communication in plant cells. Plasmodesmata are numerous channels that pass between cell walls of adjacent plant cells and connect their cytoplasm; thereby, enabling materials to be transported from cell to cell, and thus throughout the plant.
Plasmodesmata : A plasmodesma is a channel between the cell walls of two adjacent plant cells. Plasmodesmata allow materials to pass from the cytoplasm of one plant cell to the cytoplasm of an adjacent cell.
Junctions in Animal Cells
Communication between animal cells can be carried out through three types of junctions. The first, a tight junction, is a watertight seal between two adjacent animal cells. The cells are held tightly against each other by proteins (predominantly two proteins called claudins and occludins). This tight adherence prevents materials from leaking between the cells. These junctions are typically found in epithelial tissues that line internal organs and cavities and comprise most of the skin. For example, the tight junctions of the epithelial cells lining your urinary bladder prevent urine from leaking out into the extracellular space.
Tight Junctions : Tight junctions form watertight connections between adjacent animal cells. Proteins create tight junction adherence.
Also found only in animal cells are desmosomes, the second type of intercellular junctions in these cell types. Desmosomes act like spot welds between adjacent epithelial cells, connecting them. Short proteins called cadherins in the plasma membrane connect to intermediate filaments to create desmosomes. The cadherins join two adjacent cells together and maintain the cells in a sheet-like formation in organs and tissues that stretch, such as the skin, heart, and muscles.
Desmosomes : A desmosome forms a very strong spot weld between cells. It is created by the linkage of cadherins and intermediate filaments.
Lastly, similar to plasmodesmata in plant cells, gap junctions are the third type of direct junction found within animal cells. These junctions are channels between adjacent cells that allow for the transport of ions, nutrients, and other substances that enable cells to communicate. Structurally, however, gap junctions and plasmodesmata differ. Gap junctions develop when a set of six proteins (called connexins) in the plasma membrane arrange themselves in an elongated doughnut-like configuration called a connexon. When the pores (“doughnut holes”) of connexons in adjacent animal cells align, a channel between the two cells forms. Gap junctions are particularly important in cardiac muscle. The electrical signal for the muscle to contract is passed efficiently through gap junctions, which allows the heart muscle cells to contract in tandem.
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1.47: Friedel's law
Friedel's law, or rule, states that the intensities of the h , k , l and \({\bar h}, {\bar k}, {\bar l}\) reflections are equal. This is true either if the crystal is centrosymmetric or if no resonant scattering is present. It is in that case not possible to tell by diffraction whether an inversion center is present or not. The apparent symmetry of the crystal is then one of the eleven Laue classes .
The reason for Friedel's rule is that the diffracted intensity is proportional to the square of the modulus of the structure factor, | F h | 2 , according to the geometrical, or kinematical theory of diffraction. It depends similarly on the modulus of the structure factor according to the dynamical theory of diffraction. The structure factor is given by:
\(F_h = \Sigma_j f_j {\rm exp - 2 \pi i} {\bold h} . {\bold r_j}\)
where f j is the atomic scattering factor of atom j , h the reflection vector and \({\bold r_j}\) the position vector of atom j . There comes:
\(|F_h|^2 = F_h F_h^* = F_h F_{\bar h} = |F_{\bar h}|^2 \)
if the atomic scattering factor, f j , is real. The intensities of the h , k , l and \({\bar h}, {\bar k}, {\bar l}\) reflections are then equal. If the crystal is absorbing, however, due to resonant scattering , the atomic scattering factor is complex and
\(F_{\bar h} \ne F_h^*\)
The reflections h , k , l and \({\bar h}, {\bar k}, {\bar l}\) are called a Friedel pair . They are used in the resolution of the phase problem for the solution of crystal structures and in the determination of absolute structure.
History
Friedel's law was stated by G. Friedel (1865-1933) in 1913 (Friedel G., 1913, Sur les symétries cristallines que peut révéler la diffraction des rayons X. , C.R. Acad. Sci. Paris , 157 , 1533-1536.


Section 05: Rules for identity
The identity predicate is not part of QL, but we add it when we need to symbolize certain sentences. For proofs involving identity, we add two rules of proof.
Suppose you know that many things that are true of \(a\) are also true of \(b\). For example: \(Aa\)&\(Ab\), \(Ba\)&\(Bb\), ¬\(Ca\)&¬\(Cb\), \(Da\)&\(Db\), ¬\(Ea\)&¬\(Eb\), and so on. This would not be enough to justify the conclusion \(a\) = \(b\). (See p. 89.) In general, there are no sentences that do not already contain the identity predicate that could justify the conclusion \(a\) = \(b\). This means that the identity introduction rule will not justify \(a\) = \(b\) or any other identity claim containing two different constants.
However, it is always true that \(a\) = \(a\). In general, no premises are required in order to conclude that something is identical to itself. So this will be the identity introduction rule, abbreviated =I:
Notice that the =I rule does not require referring to any prior lines of the proof. For any constant \(\mathcal{c}\), you can write \(\mathcal{c}\) = \(\mathcal{c}\) on any point with only the =I rule as justification.
If you have shown that \(a\) = \(b\), then anything that is true of \(a\) must also be true of \(b\). For any sentence with \(a\) in it, you can replace some or all of the occurrences of \(a\) with \(b\) and produce an equivalent sentence. For example, if you already know \(Raa\), then you are justified in concluding \(Rab\), \(Rba\), \(Rbb\).
The identity elimination rule (=E) allows us to do this. It justifies replacing terms with other terms that are identical to it.
For writing the rule, we will introduce a new bit of symbolism. For a sentence \(\mathcal{A}\) and constants \(\mathcal{c}\) and \(\mathcal{d}\), \(\mathcal{Ac}\)↺\(\mathcal{d}\) is a sentence produced by replacing some or all instances of \(\mathcal{c}\) in \(\mathcal{A}\) with \(\mathcal{d}\) or replacing instances of \(\mathcal{d}\) with \(\mathcal{c}\). This is not the same as a substitution instance, because one constant need not replace every occurrence of the other (although it may).
We can now concisely write =E in this way:
To see the rules in action, consider this proof:


5.2.5: Alternatives to Bankruptcy
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Learning Objectives
By the end of this section, you will be able to:
- Understand that there are nonbankruptcy alternatives for debtors who cannot pay their bills in a timely way: assignment for benefit of creditors, compositions, and receiverships.
- Recognize the reasons why these alternatives might not work.
Alternatives to Bankruptcy: Overview
Bankruptcy is a necessary thing in a capitalist economic system. As already noted, without it, few people would be willing to take business risks, and the economy would necessarily operate at a lower level (something some people might not think so bad overall). But bankruptcy, however “enlightened” society may have become about it since Victorian days, still carries a stigma. Bankruptcy filings are public information; the lists of people and businesses who declare bankruptcy are regularly published in monthly business journals. Bankruptcy is expensive, too, and both debtors and creditors become enmeshed in significantly complex federal law. For these reasons, among others, both parties frequently determine it is in their best interest to find an alternative to bankruptcy. Here we take up briefly three common alternatives.
In other parts of this book, other nonbankruptcy creditors’ rights are discussed: under the Uniform Commercial Code (UCC), creditors have rights to reclaim goods sold and delivered but not paid for; under the UCC, too, creditors have a right to repossess personal property that has been put up as collateral for the debtor’s loan or extension of credit; and mortgagees have the right to repossess real estate without judicial assistance in many circumstances. These nonbankruptcy remedies are governed mostly by state law.
The nonbankruptcy alternatives discussed here are governed by state law also.
Assignment for Benefit of Creditors; Compositions; Receivership
Benefit of Creditors
Under a common-law assignment for the benefit of creditors, the debtor transfers some or all of his assets to a trustee—usually someone appointed by the adjustment bureau of a local credit managers’ association—who sells the assets and apportions the proceeds in some agreed manner, usually pro rata, to the creditors. Of course, not every creditor need agree with such a distribution. Strictly speaking, the common-law assignment does not discharge the balance of the debt. Many state statutes attempt to address this problem either by prohibiting creditors who accept a partial payment of debt under an assignment from claiming the balance or by permitting debtors to demand a release from creditors who accept partial payment.
Composition
A composition is simply an agreement by creditors to accept less than the full amount of the debt and to discharge the debtor from further liability. As a contract, composition requires consideration; the mutual agreement among creditors to accept a pro rata share of the proceeds is held to be sufficient consideration to support the discharge. The essential difference between assignment and composition lies in the creditors’ agreement: an assignment implies no agreement among the creditors, whereas a composition does. Not all creditors of the particular debtor need agree to the composition for it to be valid. A creditor who does not agree to the composition remains free to attempt to collect the full sum owed; in particular, a creditor not inclined to compose the debt could attach the debtor’s assets while other creditors are bargaining over the details of the composition agreement.
One advantage of the assignment over the composition is that in the former the debtor’s assets—having been assigned—are protected from attachment by hungry creditors. Also, the assignment does not require creditors’ consent. However, an advantage to the debtor of the assignment (compared with the composition) is that in the composition creditors cannot go after the debtor for any deficiency (because they agreed not to).
Receivership
A creditor may petition the court to appoint a receiver; receivership is a long-established procedure in equity whereby the receiver takes over the debtor’s property under instructions from the court. The receiver may liquidate the property, continue to operate the business, or preserve the assets without operating the business until the court finally determines how to dispose of the debtor’s property.
The difficulty with most of the alternatives to bankruptcy lies in their voluntary character: a creditor who refuses to go along with an agreement to discharge the debtor can usually manage to thwart the debtor and her fellow creditors because, at the end of the day, the US Constitution forbids the states from impairing private citizens’ contractual obligations. The only final protection, therefore, is to be found in the federal bankruptcy law.
Key Takeaway
Bankruptcy is expensive and frequently convoluted. Nonbankruptcy alternatives include assignment for the benefit of creditors (the debtor’s assets are assigned to a trustee who manages or disposes of them for creditors), compositions (agreements by creditors to accept less than they are owed and to discharge the debtor from further liability), and receivership (a type of court-supervised assignment).
Exercises
- What is an assignment for benefit of creditors?
- What is a composition?
- What is a receivership?
- Why are these alternatives to bankruptcy often unsatisfactory?


9.2: Trans-Neptunian objects, the Kuiper Belt, and the Oort Cloud
Trans-Neptunian objects (TNO) are any solar system minor planet that orbits the sun at a greater average distance than Neptune. Pluto is now considered a TNO, as is Eris. As of July 2014, over 1,500 trans-Neptunian objects have been cataloged and of these, some 200 have been designated as dwarf planets. From Earth, astronomers study TNO heat emissions, colors, and spectra. The Kuiper Belt is a region beyond the orbit of Neptune at 30 Astronomical Units (AU) to about 50 AU from the sun. It is sometimes called the Edgeworth–Kuiper Belt . The Kuiper Belt is much larger than the Asteroid Belt. It’s about twenty times as wide and twenty to two hundred times as massive. Kuiper Belt objects, called KBOs , are composed of rock and metal, like the asteroids, but also frozen ices like ammonia, methane, and water. Trans-Neptunian objects are Kuiper Belt objects (KBOs), but KBOs are not TNOs because the distance range of KBOs from the sun is much farther out in the solar system.
At least two moons – Saturn’s Phoebe and Neptune’s Triton – are believed to be captured KBOs. To date, over 1,000 KBOs have been discovered and around 100,000 KBOs are suspected to exist.
KBOs are fragments from the original solar system’s protoplanetary disc that did not combine to form the more-massive and larger bodies. Astronomers believe that belts of fragments like the solar system’s Kuiper Belt are present around other stellar systems being studied.


18.3A: Venules
Venules are small blood vessels in the microcirculation that connect capillary beds to veins.
- Describe the venules of the venous system
Key Points
- Many venules unite to form a vein.
- Venule walls have three layers: an inner endothelium composed of squamous endothelial cells that act as a membrane, a middle layer of muscle and elastic tissue, and an outer layer of fibrous connective tissue.
- High-endothelial venules are specialized post- capillary venous swellings characterized by plump endothelial cells, in contrast with the thinner endothelial cells found in regular venules.
Key Terms
- high endothelial venule : A specialized post-capillary venous swelling of the lymphatic system that allows lymphocytes (white blood cells) to easily exit the circulatory system.
- venule : A small blood vessel in the microcirculation that allows deoxygenated blood to return from capillary beds to veins.
A venule is a small blood vessel in the microcirculation that allows deoxygenated blood to return from capillary beds to larger blood vessels called veins. Venules range from 8 to 100μm in diameter and are formed when capillaries come together. Many venules unite to form a vein.
Venule : Venules form when capillaries come together and converging venules form a vein.
Venule walls have three layers: an inner endothelium composed of squamous endothelial cells that act as a membrane, a middle layer of muscle and elastic tissue, and an outer layer of fibrous connective tissue. The middle layer is poorly developed so that venules have thinner walls than arterioles. Venules are extremely porous so that fluid and blood cells can move easily from the bloodstream through their walls.
In contrast to regular venules, high-endothelial venules (HEV) are specialized post-capillary venous swellings. They are characterized by plump endothelial cells as opposed to the usual thinner endothelial cells found in regular venules. HEVs enable lymphocytes (white blood cells) circulating in the blood to directly enter a lymph node by crossing through the HEV.


11.1A: Overview of the Spinal Cord
The spinal cord runs along the inside of the vertebral column and serves as the signaling conduit between the brain and the periphery.
- Describe the features of the spinal cord
Key Points
- The spinal cord extends from the occipital bone of the skull until it terminates near the second lumbar vertebra.
- The spinal cord is protected by three layers of meninges: the dura mater, the arachnoid mater, and the pia mater.
 The area between the arachnoid space and the pia mater contains cerebral spinal fluid (CSF).
- The spinal cord is divided into 31 segments that send nerve rootlets out into the body through intervertebral foramen.
- Each segment of the spinal cord is associated with a pair of ganglia called dorsal root ganglia, which are situated just outside of the spinal cord and contain cell bodies of sensory neurons. These neurons travel into the spinal cord via the dorsal roots.
- Ventral roots consist of axons from motor neurons, which bring information to the periphery from cell bodies within the CNS. Dorsal roots and ventral roots come together and exit the intervertebral foramina as they become spinal nerves.
Key Terms
- peripheral nervous system : The part of the nervous system that consists of the nerves and ganglia on the outside of the brain and spinal cord.
- efferent : The conduction of impulses outward from the brain or spinal cord.
- afferent : The conduction of impulses inwards to the brain or spinal cord.
- cauda equina : A bundle of nerve roots at the base of the spinal column.
- spinal cord : A thick, whitish cord of nerve tissue which is a major part of the vertebrate central nervous system. It extends from the brain stem down through the spine, with nerves branching off to various parts of the body.
EXAMPLES
- A lumbar puncture (spinal tap) is an example of a medical procedure that directly targets the spinal cord.
- The birth defect spina bifida is a failure of the vertebral arch to close, exposing the spinal cord.
The spinal cord is a long, thin, tubular bundle of nervous tissue and support cells that extends from the medulla oblongata of the brain to the level of the lumbar region. The brain and spinal cord together make up the central nervous system (CNS). The spinal cord, protected by the vertebral column, begins at the occipital bone and extends down to the space between the first and second lumbar vertebrae. The spinal cord has a varying width, ranging from 0.5 inch thick in the cervical and lumbar regions to 0.25 inch thick in the thoracic area. The length of the spinal cord is approximately 45 cm (18 in) in men and about 43 cm (17 in) long in women.
Spinal Cord and Vertebrae.png : Relationship between the spinal cord and vertebral column, delineating the cervical, thoracic, and lumbar sections.
Layers and Regions of the Spinal Cord
The spinal cord is protected by three layers of tissue called meninges and divided into three regions.
Spinal Cord Tissue Layers
The dura mater is the outermost layer of spinal cord tissue, forming a tough protective coating. The space between the dura mater and the surrounding bone of the vertebrae is called the epidural space. The epidural space is filled with adipose tissue and contains a network of blood vessels. The middle layer is called the arachnoid mater. The pia mater is the innermost protective layer and is tightly associated with the surface of the spinal cord. The space between the arachnoid and pia maters is called the subarachnoid space and is where the CSF is located. It is from this location at the level of the lumbar region that CSF fluid is obtained in a spinal tap.
Spinal Cord Regions
In cross-section, the peripheral region of the cord displays neuronal white matter tracts containing sensory and motor neurons. Internal to this peripheral region is the gray, butterfly-shaped central region made up of nerve cell bodies. This central region surrounds the central canal, which is an anatomic extension of the spaces in the brain known as the ventricles and like the ventricles, contains cerebrospinal fluid.
Spinal Cord Regions : Cross-sectional perspective of the spinal cord regions
The spinal cord is divided into cervical, thoracic, and lumbar regions. The cervical region is divided into eight levels that are related to different motor and sensory functions in the neck and the arms. The spinal nerves of the thoracic region supply the thorax and abdomen. The nerves of the lumbosacral spinal cord supply the pelvic region, legs, and feet.
Spinal Cord Nerve Branches
Thirty-one pairs of spinal nerves (sensory and motor) branch from the human spinal cord. Each spinal nerve is formed from the combination of nerve fibers from its posterior and anterior roots. The posterior root is the sensory (afferent) root that carries sensory information to the brain from other areas of the body. The anterior root is the motor (efferent) root that carries motor information to the body from the brain.
The spinal nerve emerges from the spinal column through the opening (intervertebral foramen) between adjacent vertebrae. An exception is the first spinal nerve pair (C1), which emerges between the occipital bone and the atlas (the first vertebra). The swelling found in the posterior root is the posterior (dorsal) root ganglion, which contains the cell bodies of sensory neurons. The anterior (ventral) root contains axons of motor neurons that conduct nerve impulses from the CNS to other parts of the body such as the muscles.
The cauda equina (“horse’s tail”) is the name for the collection of nerves in the vertebral column that extends beyond the cord. The nerves that compose the cauda equina supply the pelvic organs and lower limbs, including motor innervation for the hips, knees, ankles, feet, and internal and external anal sphincters. In addition, the cauda equina extends to sensory innervation of the perineum.
Primary Spinal Cord Function
The spinal cord functions primarily in the transmission of neural signals between the brain and the rest of the body, but it also contains neural circuits that can independently control numerous reflexes and central pattern generators. The three major functions of the spinal cord are the conduction of motor information traveling down the spinal cord, the conduction of sensory information in the reverse direction, and acting as the center for conducting certain reflexes. The spinal cord is the main pathway for information connecting the brain and peripheral nervous system.


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1.2: The Cautionary Tale of Simpson’s Paradox
The following is a true story (I think…). In 1973, the University of California, Berkeley had some worries about the admissions of students into their postgraduate courses. Specifically, the thing that caused the problem was that the gender breakdown of their admissions, which looked like this…
| Number of applicants | Percent admitted | |
|---|---|---|
| Males | 8442 | 46% |
| Females | 4321 | 35% |
…and the were worried about being sued. 4 Given that there were nearly 13,000 applicants, a difference of 9% in admission rates between males and females is just way too big to be a coincidence. Pretty compelling data, right? And if I were to say to you that these data actually reflect a weak bias in favour of women (sort of!), you’d probably think that I was either crazy or sexist.
Oddly, it’s actually sort of true …when people started looking more carefully at the admissions data (Bickel, Hammel, and O’Connell 1975) they told a rather different story. Specifically, when they looked at it on a department by department basis, it turned out that most of the departments actually had a slightly higher success rate for female applicants than for male applicants. Table 1.1 shows the admission figures for the six largest departments (with the names of the departments removed for privacy reasons):
Table 1.1: Admission figures for the six largest departments by gender
| Department | Male Applicants | Male Percent Admitted | Female Applicants | Female Percent admitted |
|---|---|---|---|---|
| A | 825 | 62% | 108 | 82% |
| B | 560 | 63% | 25 | 68% |
| C | 325 | 37% | 593 | 34% |
| D | 417 | 33% | 375 | 35% |
| E | 191 | 28% | 393 | 24% |
| F | 272 | 6% | 341 | 7% |
Remarkably, most departments had a higher rate of admissions for females than for males! Yet the overall rate of admission across the university for females was lower than for males. How can this be? How can both of these statements be true at the same time?
Here’s what’s going on. Firstly, notice that the departments are not equal to one another in terms of their admission percentages: some departments (e.g., engineering, chemistry) tended to admit a high percentage of the qualified applicants, whereas others (e.g., English) tended to reject most of the candidates, even if they were high quality. So, among the six departments shown above, notice that department A is the most generous, followed by B, C, D, E and F in that order. Next, notice that males and females tended to apply to different departments. If we rank the departments in terms of the total number of male applicants, we get A > B >D>C>F>E (the “easy” departments are in bold). On the whole, males tended to apply to the departments that had high admission rates. Now compare this to how the female applicants distributed themselves. Ranking the departments in terms of the total number of female applicants produces a quite different ordering C>E>D>F> A > B . In other words, what these data seem to be suggesting is that the female applicants tended to apply to “harder” departments. And in fact, if we look at all Figure 1.1 we see that this trend is systematic, and quite striking. This effect is known as Simpson’s paradox. It’s not common, but it does happen in real life, and most people are very surprised by it when they first encounter it, and many people refuse to even believe that it’s real. It is very real. And while there are lots of very subtle statistical lessons buried in there, I want to use it to make a much more important point …doing research is hard, and there are lots of subtle, counterintuitive traps lying in wait for the unwary. That’s reason #2 why scientists love statistics, and why we teach research methods. Because science is hard, and the truth is sometimes cunningly hidden in the nooks and crannies of complicated data.
Before leaving this topic entirely, I want to point out something else really critical that is often overlooked in a research methods class. Statistics only solves part of the problem. Remember that we started all this with the concern that Berkeley’s admissions processes might be unfairly biased against female applicants. When we looked at the “aggregated” data, it did seem like the university was discriminating against women, but when we “disaggregate” and looked at the individual behaviour of all the departments, it turned out that the actual departments were, if anything, slightly biased in favour of women. The gender bias in total admissions was caused by the fact that women tended to self-select for harder departments. From a legal perspective, that would probably put the university in the clear. Postgraduate admissions are determined at the level of the individual department (and there are good reasons to do that), and at the level of individual departments, the decisions are more or less unbiased (the weak bias in favour of females at that level is small, and not consistent across departments). Since the university can’t dictate which departments people choose to apply to, and the decision making takes place at the level of the department it can hardly be held accountable for any biases that those choices produce.
That was the basis for my somewhat glib remarks earlier, but that’s not exactly the whole story, is it? After all, if we’re interested in this from a more sociological and psychological perspective, we might want to ask why there are such strong gender differences in applications. Why do males tend to apply to engineering more often than females, and why is this reversed for the English department? And why is it it the case that the departments that tend to have a female-application bias tend to have lower overall admission rates than those departments that have a male-application bias? Might this not still reflect a gender bias, even though every single department is itself unbiased? It might. Suppose, hypothetically, that males preferred to apply to “hard sciences” and females prefer “humanities”. And suppose further that the reason for why the humanities departments have low admission rates is because the government doesn’t want to fund the humanities (Ph.D. places, for instance, are often tied to government funded research projects). Does that constitute a gender bias? Or just an unenlightened view of the value of the humanities? What if someone at a high level in the government cut the humanities funds because they felt that the humanities are “useless chick stuff”. That seems pretty blatantly gender biased. None of this falls within the purview of statistics, but it matters to the research project. If you’re interested in the overall structural effects of subtle gender biases, then you probably want to look at both the aggregated and disaggregated data. If you’re interested in the decision making process at Berkeley itself then you’re probably only interested in the disaggregated data.
In short there are a lot of critical questions that you can’t answer with statistics, but the answers to those questions will have a huge impact on how you analyze and interpret data. And this is the reason why you should always think of statistics as a tool to help you learn about your data, no more and no less. It’s a powerful tool to that end, but there’s no substitute for careful thought.