What do you think Ray Bradbury wanted his readers to think about when they finished reading his story "All Summer in A Day"?

Bradbury likely hopes that people will take bullying seriously.

This is a story about a group of children on Venus who behave in much the same way some children do on Earth.  They target a girl different than themselves, and make fun of her.  Margot has been to Earth and remembers the sun, and for this reason the other children do not like her.

Margot keeps herself apart from the other children.  The way they treat her is a combination of the fact that she is different and the fact that she holds herself apart from them.

Margot stood apart from them, from these children who could ever remember a time when there wasn’t rain and rain and rain. They were all nine years old, and if there had been a day, seven years ago, when the sun came out for an hour and showed its face to the stunned world, they could not recall.

The other children resent Margot for remembering the sun.  They have been on Venus all of their lives, and the last time the sun came out they were toddlers.  For this reason, they bully Margot.  They get irritated when she claims to remember the sun.

When the other children bully Margot, the teacher barely intervenes.

That was Margot’s poem, read in a quiet voice in the still classroom while the rain was falling outside. "Aw, you didn’t write that!" protested one of the boys.

"I did," said Margot. "I did."

"William!" said the teacher.

This is the same teacher who leaves the children alone when the sun comes out.  It is because she left them alone and did not stop them from bullying Margot beforehand that they bully her now.  The teacher’s neglect leads the children to their final cruel act of locking Margot in the closet so that she misses the sun.

Bradbury’s message is that all adults (and children) need to take bullying seriously.  It is not just fun and games.  Bullying can have disastrous consequences on both the bullied and the bullies.  After the children lock Margot in the closet, they are horrified at their own actions.  This is an incident that every child will remember for the rest of his or her life.

`(x + 1)^6` Use the Binomial Theorem to expand and simplify the expression.

We have to expand the expression using the Binomial Theorem. So use the binomial formula,

`(a+b)^n=sum_(k=0)^n((n),(k))a^(n-k)b^k`

`:.(x+1)^6=((6),(0))x^(6-0)*1^0+((6),(1))x^(6-1)*1^(1)+((6),(2))x^(6-2)*1^2+((6),(3))x^(6-3)*1^3+((6),(4))x^(6-4)*1^4+((6),(5))x^(6-5)*1^5+((6),(6))x^(6-6)*1^6`

`=x^6+(6!)/(1!(6-1)!)x^5+(6!)/(2!(6-2)!)x^4+(6!)/(3!(6-3)!)x^3+(6!)/(4!(6-4)!)x^2+(6!)/(5!(6-5)!)x^1+1`

`=x^6+(6*5!)/(5!)x^5+(6*5*4!)/(2*1*4!)x^4+(6*5*4*3!)/(3*2*1*3!)x^3+(6*5*4!)/(4!*2*1)x^2+(6*5!)/(5!)x+1`

`=x^6+6x^5+15x^4+20x^3+15x^2+6x+1`

What is septicemia?

Causes and Symptoms

The rapid multiplication of bacteria and the presence of their toxins in the blood is a condition commonly known as blood poisoning, septicemia, or bacteremia. It is always an extremely serious condition and represents a medical emergency that requires the prompt medical intervention. A person in whom septicemia develops suddenly becomes seriously ill with a high fever, chills, rapid breathing, headache, and often clouding of consciousness. Skin
rashes or
jaundice may occur, and sometimes the hands are unusually warm. In many cases, especially when large amounts of toxins are produced by the circulating bacteria, the person passes into a state of septic shock, which is life-threatening.

Bacteria in the bloodstream can produce two different types of complications: microbiologic and inflammatory. The microbiologic complications result from the local and systemic proliferation and seeding of the bacterial causative organism, which causes direct tissue or organ damage. The inflammatory complications are produced locally and can result in tissue or organ destruction independent of the toxic factors produced by the causative organism. Bacteremia triggers intravascular activation of the same inflammatory systems that are protective within tissues. These systems, which combine with stress-generated endocrine responses, produce a sequence of metabolic events, the end stage of which is the systemic vascular collapse traditionally called septic shock.

Shock symptoms vary with the extent and site of major tissue damage. They are similar to those for septicemia, with additional symptoms including cold hands and feet, often with blue-purple coloration caused by poor blood flow; a weak, rapid pulse; and markedly reduced blood pressure. There may be vomiting and diarrhea, and a poor output of urine may indicate that damage to the kidneys is occurring and that there is risk of renal failure. Heart failure and abnormal bleeding may also occur.

Septic shock is a dangerous condition in which there is tissue damage and a dramatic drop in blood pressure as a result of septicemia. Septic shock is usually preceded by signs of severe infection, often of the genitourinary or gastrointestinal systems. Fever, tachycardia, increased respiration, and confusion or coma may occur during shock. The classic septic shock
syndrome results primarily from the sequence of events triggered by bacteremia, during which the bacterial toxins activate compounds that impair the functioning of surrounding cells in several ways. In many cases, the bacterial toxins are the main cause of trouble because they can cause damage to cells and tissues throughout the body and promote clotting of blood in the smallest blood vessels, seriously interfering with circulation. Consequently, damage occurs especially to tissues in the kidneys, heart, and lungs. The bacterial toxins may cause leakage of fluid from blood vessels and a reduction of the ability of the vessels to constrict, leading to a severe drop in blood pressure. Therefore, septic shock is a systematic vascular collapse, in which the systolic blood pressure of the patient is less than 90 millimeters of mercury. In septic shock, the low blood pressure has become unresponsive to adequate volume replacement. Morbidity and mortality associated with septic shock are high: About two-thirds of patients die.

Septicemia and septic shock can precipitate multiple organ failure. As the patient becomes hypermetabolic and febrile with progressive failure of one or more organs, the mortality rate can be as high as 90 percent. Septicemia is most common in people hospitalized with major disorders such as diabetes mellitus, cancer, or cirrhosis and who have a focus of infection somewhere in the body (often the intestines or urinary tract). Progression to septic shock is especially likely for people who have immunodeficiency disorders or are taking immunosuppressant drugs for cancer or an inappropriate antibiotic treatment. Newborn infants are also particularly at risk if septicemia develops.

Treatment and Therapy

A presumptive diagnosis of septicemia is often made on the basis of historical, physical, and laboratory data even in the absence of proof. The setting in which the episode is occurring should be evaluated promptly. Crucial to appropriate initial decision-making are the background history, which may help to define the type of host-defense defect present, and prior blood culture data, which might predict the infecting organism. The physical examination should be quick and thorough, searching for the septic source as well as signs that might indicate progression to shock.

A diagnosis can be confirmed and the infective bacteria identified by growing a culture of the organisms from a blood sample. Several laboratory tests are often helpful in the evaluation of a potentially septic patient. In general, patients with fever should be considered septic until proved otherwise, and therapy should always be initiated for high-risk febrile patients in advance of a microbiologic confirmation of septicemia.

Common microorganisms that enter the bloodstream when the body’s defenses break down include staphylococci from boils, abscesses, and wounds; streptococci from the tonsils, throat, or cuts; and pneumococci from the lungs. Other invaders of the bloodstream include the gonococci, the typhoid bacilli in typhoid fever, and Escherichia coli (E. coli) in bowel infections. All these bacteria may be detected by taking a blood culture.

Antibacterial therapy should be started as soon as septicemia is suspected. It is normally started by intravenous infusion of antibiotic drugs and glucose and/or saline solution. The focal site of infection is sought immediately and may be surgically removed. Surgical debridement (removal) and drainage of septic foci are especially important, and all severe localized infections should be widely debrided and drained. If the infection is recognized and treated promptly, there is usually a full recovery.

Broad antibacterial coverage is required in patients with severe septicemia. It is best to initiate therapy with a combination of
antibiotics when the infecting organism is unknown. When cultures define the causative microbe(s) or other data point to a specific organism, therapy can then be tailored to the most appropriate, most specific, least toxic, and least expensive single antibiotic. Penicillin is usually used to combat staphylococcic, streptococcic, pneumococcic, and gonococcic infections; chloramphenicol and ampicillin are used against typhoid and paratyphoid infections; and neomycin is used against E. coli infections. Extreme care must be taken with the administration of chloramphenicol and neomycin because of their toxic side effects.

Antibiotics limit the microbiological complications of bacteremia, but other metabolic events, whether initiated by or independent of bacterial proliferation, may still produce substantial morbidity and mortality. Therefore, therapy in addition to antibiotics is recommended to counter this metabolic sequence.

Septic shock requires immediate treatment, including the use of antibiotics and surgery, rapid fluid replacement by infusion, and the maintenance of urine flow to prevent the effects of renal failure. Other measures must also be taken to raise the blood pressure and to promote a better supply of important nutrients to tissues, such as through intravenous infusion and oxygen therapy. The use of anti-inflammatory drugs is under active investigation.

Perspective and Prospects

Most febrile patients lacking other signs of severe septicemia will usually do well. Such patients usually respond quickly to fluid administration, antibacterial therapy, and drainage of the primary focus of infection. The presence of septic shock, however, dramatically increases morbidity and mortality. Even when the inciting infection is localized, shock is associated with at least 50 percent mortality. Full-blown septic shock has greater than 70 percent mortality. A favorable outcome in a patient in severe shock depends on the skill of management in the intensive care unit. Early diagnosis and therapy of severely septic patients will greatly decrease the morbidity and mortality of these individuals. The best means of preventing bacteremia is the proper care of burns and wounds and prompt application of antiseptic tinctures or preparations to ordinary cuts and tears.

Infections most commonly occur in the hospital setting, where many infected patients become bacteremic. About 5 percent of all hospital patients either are admitted with or develop an infection during hospitalization. This means that the number of patients at risk of developing septic shock is large. The clinician must be familiar with the manifestations and differential diagnosis of the patient who appears to suffer from septic shock and must have in mind rapid, comprehensive diagnostic and therapeutic plans of action. It is important to develop the concept of a preshock phase of septic shock predicated on identifying a subgroup of infected patients more likely than others to develop shock. In such patients, fluids should be administered and broad antibiotic coverage started early. Treatment before shock develops undoubtedly prevents some of the morbidity and mortality associated with septicemia.

Bibliography

Goldman, Lee, and Dennis Ausiello, eds. Cecil Textbook of Medicine. 23d ed. Philadelphia: Saunders/Elsevier, 2007.

Litin, Scott C., ed. Mayo Clinic Family Health Book. 4th ed. New York: HarperResource, 2009.

Mosby’s Medical Dictionary. 9th ed. St. Louis, Mo.: Mosby/Elsevier, 2012.

Rodak, Bernadette, ed. Hematology: Clinical Principles and Applications. 4th ed. St. Louis, Mo.: Saunders/Elsevier, 2011.

"Sepsis." Mayo Clinic, January 26, 2013.

"Septicemia." Medline Plus, August 24, 2011.

Strand, Calvin L., and Jonas A. Shulman. Bloodstream Infections: Laboratory Detection and Clinical Considerations. Chicago: American Society of Clinical Pathologists, 1988.

Wilson, Michael, Brian Henderson, and Rod McNab. Bacterial Disease Mechanisms: An Introduction to Cellular Microbiology. New York: Cambridge University Press, 2002.

Wood, Debra. "Blood Poisoning." Health Library, October 31, 2012.

Zucker-Franklin, D., et al. Atlas of Blood Cells: Function and Pathology. 3d ed. Philadelphia: Lea & Febiger, 2003.

What is LSD?

History of Use

LSD was synthesized in 1938 by Albert Hoffman, of Sandoz Laboratories in Basel, Switzerland, as part of a research program seeking new medicines. LSD did not seem to offer such promise, but in 1943 Hoffman accidentally ingested a dose, experienced its psychoactive effects, and described these effects as being surprisingly transformational.

For the next twenty years, Sandoz Laboratories marketed LSD for research purposes. Among early research was that by the US Central Intelligence Agency from the 1950s through the 1970s, in an attempt to discover whether LSD could be used for mind-control purposes. Mostly, however, psychiatry and psychology became involved, initially because LSD seemed to simulate a “model psychosis.”

The perceptual distortions induced by LSD, however, are not experienced as hallucinations in the sense of something that is not there; rather, they transform what is given in the perceptual field. This distinction led Canadian psychiatrists Humphry Osmond, Abram Hoffer, and Duncan Blewett to use LSD as a treatment for psychosis. LSD was also studied as an adjunct in psychotherapy, especially by Stanislav Grof in Czechoslovakia. Before its criminalization, more than forty thousand patients were treated with LSD psychotherapy. Notable results occurred in alcoholics, felons, and the terminally ill, persons who normally are resistant to successful therapeutic outcomes.

In the United States, research was conducted at Harvard University by Timothy Leary, Ralph Metzner, and Richard Alpert (who later became Ram Dass). The trio’s 1964 book The Psychedelic Experience popularized the view that LSD could be useful in enhancing human potential. Leary, in particular, became a public advocate for LSD with his slogan to “turn on, tune in, drop out.”

Soon writers such as Aldous Huxley and Ken Kesey and musicians, most famously the Beatles, also reflected a view of LSD’s possibilities. Cary Grant, a major film star, attributed a “new assessment of life” to his experience on LSD. By the 1960s, LSD had become a common drug for American youth, especially in California, where it spread among the burgeoning counterculture. Owsley Stanley, who made and distributed a large amount of LSD in San Francisco in the mid-1960s, is known for fueling the upsurge of interest there. Largely because of this sense that LSD contributed to a rejection of mainstream values, the drug became intensely controversial and the subject of much negative publicity. The manufacture and sale of LSD was made a crime in 1965 and possession was criminalized in 1966.

According to the US Substance Abuse and Mental Health Services Administration, LSD use peaked in the early 1970s, fell slowly to a low in 2003, and has been increasing since. The National Household Survey on Drug Abuse indicated that 20.2 million Americans age twelve years and older used LSD at least once in their lifetime. The most common age of first-time users is eighteen years.

Effects and Potential Risks

The effects of LSD become noticeable within thirty to sixty minutes and last six to eight hours or more. The threshold dose is 25 micrograms (mcg), and 100 to 250 mcg is typical; beyond 400 mcg no further change seems to occur. A feature of LSD is how widely its effects vary. Researchers quickly realized the keys to this variability are the mental set (or state) of the user and the setting in which the drug is used.

The physiological effects of LSD include changes to the pulse rate, muscular tension, blood pressure, constriction of arteries in the periphery, and pupil dilation. These effects tend to be mild and do not last beyond the psychoactive period. Longer term effects have been reported, most spectacularly chromosome breakage, but these claims have not survived rigorous research.

Negative experiential effects of LSD are cognitive and emotional. Judgment is impaired such that the user is not as concerned with safety. Emotionally, a user can become so disoriented as to feel anxiety or panic, a reaction augmented if the setting were conducive to disorientation. A rare longer-term negative effect is the unwelcome vivid memory of an emotionally charged moment from the LSD event, known as a flashback.

The experiential effects of LSD include positive aesthetic, psychological, and spiritual transformations. Aesthetically, the effects center on perceptual changes, especially to the visual field, which is intensely enhanced with greater mobility, colorfulness, transiency, luminosity, energy, swelling, vividness, and synesthesia. Psychologically, the effects of LSD include mood changes, particularly feelings of well-being and euphoria; a new and greater awareness of the world and of self; a deeper understanding of human relationships; a transcendence of time and space; and a sense of ineffability. Spiritually, the effects of LSD include a sense of rebirth; a sense of encounters with divinity; a sense of the world as sacred; and a sense of communion, unity, and nonduality.

These effects tend to be experienced as an inward journey; they are remembered and are felt by the user to be of lasting benefit. The effects are so unmistakable that blinded research studies are impossible. For this reason too, substances other than LSD are rarely sold as LSD.

LSD is not addictive. A tolerance is built up after a few days if used daily, but the tolerance is diminished quickly following cessation of use. Studies of lethal overdose levels in animals indicate it would require an extremely huge amount for humans, and no lethal overdoses have been shown in humans.

Bibliography

Dobkin de Rios, Marlene, and Oscar Janiger. LSD, Spirituality, and the Creative Process. Rochester, VT: Park Street, 2003. A research collection examining the impact of LSD on creativity before LSD was made illegal.

Grof, Stanislav. LSD: Doorway to the Numinous. Rochester, VT: Park Street, 2009. A good summary of the clinical research on LSD up to the point it was made illegal. Originally published in 1975.

Hoffman, Albert. LSD: My Problem Child. San Francisco: MAPS, 2005. The synthesizer of LSD reflects on its science and mysticism.

Websites of Interest

Multidisciplinary Association for Psychedelic Research

http://www.maps.org

National Institute on Drug Abuse

http://www.drugabuse.gov/infofacts/hallucinogens.html

What mental state might the inability to sleep reflect?

An inability to fall asleep or stay asleep might be caused by high anxiety or stress.

Emotional or mental distress puts the brain and body on a sort of "high alert." For this reason, people may have a difficult time falling asleep when they are anxious. Even if someone wants to relax and go to sleep, high levels of cortisol and adrenaline caused by stress can make this difficult. Adrenaline in particular, sometimes called the "fight or flight" hormone, primes our body and mind to act quickly in stressful situations.

A vicious cycle develops when stress interferes with someone's ability to sleep. First, the anxiety makes it difficult for someone to wind down and rest. A lack of rest then puts more stress on the mind and body, driving up those levels of hormones I mentioned before. Poor sleep creates more stress, which creates worse sleep! 

When someone finds that stress is interfering with their sleep, they should take action to try to break the cycle. Avoiding caffeine late in the day, creating a bed time "ritual" to train the brain to relax, and developing effective coping strategies can help to remedy this problem. 

Do you think that Farquhar's dream made it easier for him to face death? Why?

I think that sounds like a romantic attitude--and Ambrose Bierce was certainly not a romanticist. Far from it. He was noted for being a realist, a cynic, a pessimist. If Farquhar thought he was dying for a noble cause, it didn't prevent him from having all sorts of regrets and concerns about self-preservation. In what he thought were his last moments, he was thinking about escaping and getting back to the heaven on earth represented by his beautiful wife and his lush, sunny plantation. He must have also regretted his stupidity in allowing himself to walk right into a trap with his big can of kerosene and  pocketful of kitchen matches. 

The narrator tells us in Part I what is going through Farquhar's mind:

He closed his eyes in order to fix his last thoughts upon his wife and children.

He unclosed his eyes and saw again the water below him. "If I could free my hands," he thought, "I might throw off the noose and spring into the stream. By diving I could evade the bullets and, swimming vigorously, reach the bank, take to the woods and get away home. 

As these thoughts, which have here to be set down in words, were flashed into the doomed man's brain rather than evolved from it the captain nodded to the sergeant. The sergeant stepped aside.

Farquhar is not thinking about dying for a noble cause. He is thinking about his wife and children and wishing it were only possible for him somehow to escape from this horrible situation. The last words of Part I are intended to set the reader up to believe for most of the rest of the story that what Farquhar was wishing really happened. The rope broke and he landed in the swift waters of Owl Creek. It took the soldiers some time to get organized and start firing. He managed to free himself. The reader is completely engaged in Farquhar's hopes and problems because it is natural to identify with any character when we are held in his point of view and share his motivation, which in this case is simply self-preservation, a feeling we all have all our lives. Even though we may not sympathize with Farquhar's politics and ideals, we identify with his desire to stay alive and to get back home.

He is not thinking about dying for a noble cause but about saving his life and getting back to what he has sacrificed for an idea. Ambrose Bierce, the cynic, the realist, has us believing that Farquhar has almost made it into the outstretched of his beautiful, loving wife--and then:

As he is about to clasp her he feels a stunning blow upon the back of the neck; a blinding white light blazes all about him with a sound like the shock of a cannon--then all is darkness and silence!

Peyton Farquhar was dead; his body, with a broken neck, swung gently from side to side beneath the timbers of the Owl Creek bridge.

Ambrose 

In She's Come Undone, what age was Dolores when she was raped?

The 1992 novel She's Come Undone, written by author Wally Lamb, tells the story of Dolores Price and her journey to recovery after a traumatic childhood. Dolores' parents fought often until her father left, causing her mother to have a nervous breakdown. While her mother is in the mental hospital, Dolores stays with her grandmother. A handsome and charming man named Jack Speight moves into the same apartment as Dolores, her grandmother, and her now-recovered mother. Dolores develops a crush on Speight, and even though she is just thirteen years old, he recognizes her affections and takes advantage of her. After being assaulted, Dolores feels it was her own fault. Her mother tries to ease her suffering by keeping Dolores stocked up on her favorite junk foods, but this means of coping doesn't serve to actually heal her trauma. Dolores becomes obese and struggles with her weight, her identity, and her sexuality for the rest of the book.

What is the relationship between marginal costs and variable costs?

The relationship between these two kinds of costs is that the change in variable costs creates the change in marginal costs.  Therefore, the slope of the total variable cost curve is the marginal cost of the product.  Let us see why this is so.

First, remember that variable costs are the costs that change as output changes.  We can distinguish these from fixed costs, which do not change when you make more or less of a product.  Imagine that you are running a motel.  You have already built the motel and the cost of the building is your fixed cost.  That cost remains the same whether you rent out all the rooms or none of the rooms.  However, you also have variable costs.  If you rent out more rooms, you have to pay more for housekeeping staff.  You have to pay for the internet that the guests use.  You have to pay for the water and the detergent used to wash the bedding after they leave.  You have to pay for the food for the continental breakfast that you provide.  All of these costs change as you rent more or fewer rooms.

Now let us think about what marginal costs are.  The marginal cost of renting out a room is the amount that your total costs rise when you rent out that room.  If you think about it, you will see that this cost has to be made up of variable costs.  When you go to rent out that room, your fixed costs do not change.  If the cost of renting (for example) 51 rooms is greater than the cost of renting (for example) 50 rooms, those costs have to be variable costs.  They come from the housekeeping, the water and detergent, the internet, and the breakfast. 

Because of this, your variable costs and your marginal costs have to be the same thing.  If all your costs are fixed, you will have no marginal costs.  The change in your total variable costs is the same thing as your marginal cost.

What is mechanoreception?

Introduction

The human body is supplied with an abundance of sensory receptors that detect touch and pressure. These receptors are members of a larger group called mechanoreceptors; they are able to detect energy in mechanical form and convert it to the energy of nerve impulses. Mechanoreceptors occur both on body surfaces and in the interior, and they detect mechanical stimuli throughout the body. Touch receptors are located over the entire body surface; pressure receptors are located only under the skin and in the body interior. The two sensations are closely related. A very light pressure on the body surface is sensed by receptors in the skin and is felt as touch. As the pressure increases, mechanoreceptors in and immediately below the skin and at deeper levels are stimulated, and the sensation is felt as pressure.

Types of Mechanoreceptors

Several different types of mechanoreceptors are located in the skin and primarily detect touch. One type, known as free nerve endings, consists simply of branched nerve endings without associated structures. Although located primarily in the skin, some mechanoreceptors of this type are also found to a limited extent in deeper tissues, where they detect pressure.

A second mechanoreceptor type, termed Meissner’s corpuscles, consists of a ball of nerve endings enclosed within a capsulelike layer of cells. These mechanoreceptors, which are exquisitely sensitive to the lightest pressure, occur in nonhairy regions of the skin, such as the lips and fingertips.

A third mechanoreceptor type, the expanded-tip tactile receptor, occurs in the same nonhairy regions as Meissner’s corpuscles and, in smaller numbers, in parts of the skin that are covered with hair. These mechanoreceptors often occur in clusters that are served by branches of the same sensory nerve cell. Meissner’s corpuscles and the expanded-tip tactile receptors, working together in regions such as the fingertips, are primarily responsible for a person’s ability to determine the size, surface texture, and other tactile features of objects touched.

A fourth type of mechanoreceptor consists of a network of nerve endings surrounding the root of a hair. The combined nerve-hair root structure, called a hair end organ, is stimulated when body hairs are displaced. These mechanoreceptors, because hairs extend from the body surface, give an early warning that the skin of a haired region of the body is about to make contact with an object. The remaining mechanoreceptors of this group are located in deeper regions of the body; because of their location, they detect pressure rather than touch.

Pacinian corpuscles, which occur just under the skin and in deeper regions of the body, consist of a single sensory nerve ending buried inside a fluid-filled capsule. The capsule is formed by many layers of connective tissue cells, which surround the nerve ending in concentric layers, much like the successive layers of an onion. Pressure displaces the capsule and deforms its shape; the deforming pressure is transmitted through the capsule fluid to the surface of the sensory nerve ending. In response, the sensory nerve generates nerve impulses.

The remaining type of pressure receptor, Ruffini’s end organ, consists of a highly branched group of nerve endings enclosed in a capsule. These mechanoreceptors occur below the skin, in deeper tissues, and in the connective tissue capsules surrounding the joints. They detect heavy pressures on the body that are transmitted to deeper layers, and, through their locations in the joints, contribute to proprioception
—the sense of the position of the body’s limbs.

The various types of mechanoreceptors are believed to convert mechanical energy into the electrical energy of nerve impulses by essentially the same mechanism. In some manner, as yet incompletely understood, the mechanical forces deforming the cell membranes of sensory nerve endings open channels in the membranes to the flow of ions. The ions, which are electrically charged particles, produce the electrical effects responsible for generating nerve impulses.

Mechanoreceptor Adaptation

The different mechanoreceptor types exhibit the phenomenon of adaptation to varying degrees. In adaptation, the number of nerve impulses generated by a sensory receptor drops off with time if the stimulus remains constant. In the Pacinian corpuscle, for example, which is highly adaptive, adaptation results from flow of the capsule fluid. If pressure against the corpuscle is held at steady levels, deforming the capsule in one direction, the fluids inside the capsule flow in response to relieve the pressure. The new fluid distribution compensates for the applied pressure, and the nerve impulses generated by the Pacinian corpuscle drop in frequency. Any change in the pressure, however, is transmitted through the fluid to the sensory nerve ending before the fluid has a chance to shift in response. As a result, a new volley of nerve impulses is fired by the sensory neuron on a change of pressure until the fluid in the corpuscle shifts again to compensate for the new pressure. In Pacinian corpuscles, compensating movements of the fluid take place within hundredths or even thousandths of a second. Meissner’s corpuscles and the hair end organs also adapt quickly.

The expanded-tip tactile receptors and Ruffini’s end organs adapt significantly more slowly than the other mechanoreceptors. Expanded-tip tactile receptors adapt initially to a steady touch or pressure but reach a base level at which they continue to generate nerve impulses under steady pressure. The Ruffini’s end organs adapt only to a limited extent. The continuing nerve impulses arriving from these mechanoreceptors provide continuous monitoring of a constant stimulus. Thus, some of the mechanoreceptors are specialized to detect changes in touch or pressure and some to keep track of constant stimuli.

Mechanosensory Abilities

The combined effects of touch and pressure receptors, along with the varying degrees of adaptation of different receptor types, allow the detection of a range of stimuli, varying from the lightest, most delicate, glancing touch, through moderate pressures, to heavy pressures that stimulate both the body surfaces and interior. People can explore the surface, texture, and shape of objects and can interpret the various levels of touch and pressure so well that they can reconstruct a mental image of objects touched by the fingers with their eyes closed.

Much of this mechanosensory ability depends on the degree to which the different receptor types adapt. The rapid adaptation of Meissner’s corpuscles and the hair end organs explains why, if a steady, light to moderate pressure (not heavy enough to cause pain) is maintained on the body surface, the sensation of pressure quickly diminishes. If the pressure is heavy enough to cause pain, a person continues to be aware of the painful sensation, because pain receptors are very slow to adapt. If the degree or location of the pressure is altered, a person again becomes acutely aware of the pressure.

Awareness of continued touch depends primarily on the expanded-tip tactile receptors, which initially adapt but then continue to send nerve impulses when a light surface pressure is held constant. This allows a person to continue to be aware, for example, that some part of the body surface is touching an object. The limited adaptation of Ruffini’s corpuscles keeps a person aware of stronger pressures that are felt deeply in the body. Through their locations in joints, these slow-adapting mechanoreceptors also help keep a person continually aware of the positions of the limbs.

The sensory effects of the fast- and slow-adapting mechanoreceptors can be demonstrated by a simple exercise such as pinching the skin on the back of the hand with a steady pressure strong enough to cause only slight pain. The feeling of pressure dissipates rapidly; however, one remains aware of the touch and pain. The rapid dissipation of the sensation of pressure is caused by the fast adaptation of Meissner’s corpuscles and any Pacinian corpuscles that may have been stimulated. Some degree of touch sensation is maintained, however, by residual levels of nerve impulses sent by the expanded-tip tactile receptors. The sensation of pain continues at almost steady levels because, in contrast to most of the mechanoreceptors, pain receptors adapt very little. If the pressure is released, the pain stops, and another intense sensation of pressure is felt as all the receptor types fire off a burst of nerve impulses in response to the change.

Mechanoreceptors located at deeper levels keep a person constantly aware of the positions of body parts and the degree of extension of the limbs with respect to the trunk. Ruffini’s and Pacinian corpuscles located within the connective tissue layers covering the bones, and within the capsules surrounding the joints, keep track of the angles made by the bones as they are pulled to different positions by the muscles. Ruffini’s and Pacinian corpuscles are among the most important mechanoreceptors keeping track of these movements.

Muscle Spindles and Golgi Tendon Organs

Touch and pressure receptors represent only a part of the body’s array of mechanoreceptors. Other mechanoreceptors located more deeply in the body help monitor the position of body parts and detect the degree of stretch of body cavities.

In addition to the Ruffini’s and Pacinian corpuscles detecting the positions of the bones and joints, two further types of mechanoreceptors constantly track the tension developed by the muscles moving the limbs. One is buried within the muscle itself, and one is in the tendons connecting the muscles to the bones. The mechanoreceptors buried within muscles, called muscle spindles, consist of a specialized bundle of five to twelve small muscle cells enclosed within a capsule of connective tissue. Sensory nerve endings surround the muscle cells in a spiral at the midpoint of the capsule and also form branched endings among the muscle cells of the capsule. Because of their position within the muscle spindle, the nerve endings are stretched, and generate nerve impulses, when the surrounding muscle tissue contracts.

The mechanoreceptors of tendons, called Golgi tendon organs, are formed by nerve endings that branch within the fibrous connective tissue cells forming a tendon. The nerve endings of Golgi tendon organs detect both stretch and compression of the tendon as the muscles connected to them move and place tension on the limbs. The combined activities of the deeply located mechanoreceptors keep a person aware of posture, stance, and positions of the limbs. They also allow a person to perform feats such as bringing the thumbs or fingers together behind the back or touching the tip of the nose with the forefinger with the eyes closed.

Somatic Senses

Mechanoreceptors are one of five different types of sensory receptors that also include thermoreceptors, which detect changes in the flow of heat to or from the body; nociceptors, which detect tissue damage and whose nerve impulses are integrated and perceived in the brain as pain; chemoreceptors, which detect chemicals in locations such as the tongue, where they are responsible for the sense of taste, and in the nasal cavity, where they contribute to the sense of smell; and photoreceptors, which detect light. The mechanoreceptors, thermoreceptors, and nociceptors together form what are known as the somatic or body senses.

Sensory nerve tracts originating from mechanoreceptors, particularly those arising from the body surfaces, and their connecting neurons within the spinal cord and the brain are held in highly organized register with one another. Sensory fibers and their connecting nerves originating from the hand, for example, are located in a position near those originating from the wrist. In the cerebral cortex, the organization is retained, so that there is a projection of the body parts over a part of the cerebrum called the somatic sensory cortex. In this region, which occupies a band running from the top to the lower sides of the brain along anterior segments of the parietal lobes, segments corresponding to major body parts trace out a distorted image of the body from the top of the brain to the sides, with the genitalia, feet, and legs at the top, the arms and hands at the middle region, and the head, lips, tongue, and teeth at the bottom. Sensory information from the right side of the body is received and integrated in the somatic sensory cortex on the left side of the brain, and information from the left side of the body is received and integrated on the right side of the brain. The area of the somatic sensory cortex integrating signals from various body regions depends on the numbers of touch and other sensory receptors in the body regions. The lips and fingers, for example, which are generously supplied with sensory receptors, are represented by much larger areas in the somatic sensory cortex than the arms and legs. Reception and integration of signals in the somatic sensory cortex are partly under conscious control; a person can direct attention to one body part or another and concentrate on the signals arriving from the selected region. The activities of touch, pressure, and other sensory receptors, integrated and interpreted in the somatic sensory cortex, supply people’s link to the world around them and supply the information people require to survive and interact with the environment.

Bibliography

Berne, Robert M., and Matthew N. Levy, eds. Physiology. 5th ed. St. Louis: Mosby, 2004. Print.

Coren, Stanley. Sensation and Perception. 6th ed. Hoboken: Wiley, 2004. Print.

Guyton, Arthur C., and John E. Hall. Textbook of Medical Physiology. 11th ed. Philadelphia: Elsevier, 2006. Print.

Hertenstein, Matthew J., and Sandra Jean Weiss. The Handbook of Touch: Neuroscience, Behavioral, and Health Perspectives. New York: Springer, 2011. Print.

Schmidt-Nielsen, Knut. Animal Physiology: Adaptation and Environment. 5th ed. New York: Cambridge UP, 1998. Print.

What is genetic screening?

Newborn Screening

The most widespread use of genetic screening is the testing of newborn babies. The purpose of newborn screening is to provide immediate treatment after birth to affected infants so that the symptoms of a disease can be lessened or prevented.

Screening for phenylketonuria (PKU) began in the 1960s and is one of the oldest and best-known newborn screening programs. Blood samples are taken from the heels of newborn babies in the hospital nursery, placed on filter papers as dried spots, and sent off to appropriate laboratories for analysis. Newborns with elevated phenylalanine levels can be effectively treated with a diet low in phenylalanine (low-protein foods). If treatment is not initiated within the first two months of life, mental retardation will occur. Individuals with PKU lack the enzyme phenylalanine hydroxylase (PAH), which converts the essential amino acid phenylalanine into the amino acid tyrosine. The lack of the enzyme PAH leads to the accumulation of phenylalanine in the body, which causes irreversible brain damage.

In addition to PKU, the newborn screen can test for other metabolic disorders, endocrine disorders (such as congenital hypothyroidism),
blood conditions, deafness, and some acquired perinatal infections. In the United States, differences exist between states in terms of what conditions are screened for on the newborn panel. In 2005, the median number of tests on the newborn screen in each state was twenty-two. Only screening for PKU and congenital hypothyroidism is mandatory in all states.

Carrier Screening

Carrier screening is the voluntary testing of healthy individuals of reproductive age who may be carriers for an autosomal recessive disorder. Autosomal recessive disorders occur when an individual inherits a nonworking gene, or mutation, from both of their parents. The parents are called “carriers” because they have one working copy of the gene and one nonworking copy of the gene. Carriers do not exhibit any symptoms of the genetic condition. However, with each pregnancy, two carrier parents have a 25 percent chance for the offspring to inherit the genetic condition.

The risk of being a carrier for an autosomal recessive disorder is often dependent upon one’s ancestry. For example, individuals of African descent have an increased risk of being a carrier for sickle-cell anemia, which is a blood disorder associated with a change in the shape of the red blood cells that can lead to difficulty transporting oxygen around the body. Individuals of Ashkenazi Jewish heritage are at increased risk of being carriers of at least ten genetic conditions. Tay-Sachs disease, which is a progressive neurological condition associated with death in infancy, is one of the best-known conditions for which Ashkenazi Jewish individuals are offered screening.

Historically, people were not always given a choice to have carrier screening. In the early 1970s, mandatory, large-scale screening of African American couples and some schoolchildren was implemented in an effort to identify carriers of the gene for sickle-cell anemia. Screening results were not kept in strictest confidence; consequently, many healthy African Americans who were carriers for sickle-cell disease were stigmatized and discriminated against in terms of employment and insurance coverage. There were also charges of racial discrimination because carriers were advised against bearing children. The laws mandating screening were later repealed. Today, carrier screening programs are very different from newborn screening programs because individuals are able to choose whether they want testing.

The choice to have carrier screening is a personal one. If both parents are found to be carriers of the same genetic condition, during a pregnancy the family is offered prenatal diagnosis via amniocentesis or chorionic villus sampling (CVS). Both procedures carry a small risk of miscarriage. Some families elect to have prenatal diagnosis so that they can prepare for the birth of a child with a medical condition. Other families may consider adoption or termination of the pregnancy if the fetus is found to have a genetic condition. Some families prefer to find out about such conditions at birth. If a couple learns that they are both carriers of a genetic condition prior to pregnancy, then their options include conceiving a pregnancy and considering prenatal diagnosis, egg or sperm donation, adoption, no pregnancy, or a fairly new technique called preimplantation genetic diagnosis. Religion, socioeconomic status, and emotions all play a role in these decisions. Genetic counselors often meet with individuals to help them decide if they want testing.

Prenatal Screening

All pregnant women are routinely offered screening tests for chromosome abnormalities such as Down syndrome, the most common chromosome condition. Individuals with Down syndrome have an extra copy of chromosome number 21 that leads to a distinctive appearance, mild-to-moderate mental retardation, and sometimes other medical issues such as heart defects or digestive system problems. The risk of having a baby with Down syndrome increases with a woman’s age, but all women have some risk. Blood and ultrasound tests are routinely offered to all women to determine if the pregnancy is at increased risk for Down syndrome. Women in the high-risk category are offered diagnostic testing such as a CVS or amniocentesis.

Impact and Applications

With the completion of the Human Genome Project, the number of genetic screening options has grown exponentially. In 2003, the American College of Obstetricians and Gynecologists recommended that providers offer all couples who are pregnant or planning a pregnancy carrier screening for cystic fibrosis, an autosomal recessive multisystem disorder that can affect the lungs, digestive system, and urogenital tract. Most states now also offer newborn screening for cystic fibrosis. In 2008, the American College of Medical Genetics issued a practice guideline stating that providers should offer all couples carrier screening for spinal muscular atrophy, an autosomal recessive neurological disorder. Some experts are advocates for population-based carrier screening for fragile X syndrome, a relatively common genetic form of mental retardation in males that can be carried by females and inherited by their sons. The technology to detect fetal cells in the maternal bloodstream is rapidly evolving, and soon pregnant woman may be able to learn if their fetus has Down syndrome with a simple blood draw.

As new tests are added to routine screening protocols and further tests are considered for population screening, society is faced with the ethical dilemma of deciding what makes a disease a candidate for genetic screening. In order for a disease to be considered for a population screening program, certain factors must exist. Some are concrete entities, such as a reliable test, infrastructure to carry out a screening program, and a high frequency of the particular disorder. Other factors are more subjective, such as the definition of the disease as “serious.”

The source of contention is that the population differs on what makes a disease “serious.” For example, many individuals involved with the Down syndrome community are opposed to the idea of offering prenatal screening because they do not see individuals with Down syndrome as very different from the rest of the population. Individuals with Down syndrome can go to school, participate in hobbies, and have meaningful interactions with their families. Similarly, some individuals who have cystic fibrosis do not see the disease as an impediment to accomplishing their life goals.

As the technology for genetic testing improves, medical professionals and lay people will both be confronted with even more ethical dilemmas about genetic screening. Where does one draw the line on what defines a disease? Is a disease simply a variation thought to be undesirable by the majority of the population? These questions are quickly becoming real issues for society to reckon with rather than something characters deal with in the world of science fiction.

Key terms



amniocentesis

:

invasive procedure performed during the second trimester of pregnancy that involves the removal of a small amount of amniotic fluid with a needle to perform genetic testing on cells from the fetus




chorionic villus sampling

:

invasive procedure performed during the first trimester of pregnancy that involves the removal of a small amount of the tissue that will form the placenta for genetic testing




genetic counselor

:

professional trained in genetics and counseling who provides individuals with information about genetic testing and facilitates decision making




preimplantation genetic diagnosis

:

in this process, embryos are conceived via in vitro fertilization, and genetic testing for a particular condition is performed on the embryos prior to implantation in the uterus; only unaffected embryos are implanted





Bibliography

Chadwick, Ruth, et al., eds. The Ethics of Genetic Screening. Boston: Kluwer Academic, 1999. Print.

Evans, Mark I., ed. Metabolic and Genetic Screening. Philadelphia: Saunders, 2001. Print.

Heyman, Bob, and Mette Henriksen. Risk, Age, and Pregnancy: A Case Study of Prenatal Genetic Screening and Testing. New York: Palgrave, 2001. Print.

Juth, Niklas, and Christian Munthe. The Ethics of Screening in Health Care and Medicine: Serving Society or Serving the Patient? Dordrecht: Springer, 2012. Print.

Milunsky, Aubrey, and Jeff M. Milunsky. Genetic Disorders and the Fetus: Diagnosis, Prevention, and Treatment. 6th ed. Chichester: Wiley, 2010. Print.

Nussbaum, Robert, et al. Genetics in Medicine. 6th ed. Rev. reprint. Philadelphia: Thompson, 2004. Print.

Pierce, Benjamin A. The Family Genetic Sourcebook. New York: Wiley, 1990. Print.

Shannon, Joyce Brennfleck, ed. Medical Tests Sourcebook. Detroit: Omnigraphics, 1999. Print.

Teichler-Zallen, Doris. To Test or Not to Test: A Guide to Genetic Screening and Risk. Piscataway: Rutgers UP, 2008. Print.

Timmermans, Stefan, and Mara Buchbinder. Saving Babies?: The Consequences of Newborn Genetic Screening. Chicago: U of Chicago P, 2013. Print.

What is the relationship between philosophy and psychology?

Introduction

The relationship between philosophy and psychology is complex. Psychology has its origins in philosophy, and until the mid-twentieth century, psychology was part of the philosophy department at universities. Psychology is often held to have split off from philosophy in 1879, with the founding of Wilhelm Wundt’s experimental psychology laboratory in Leipzig, Germany. To recognize the split is to define psychology as an empirical science, as many have done. However, psychology and philosophy address many of the same questions, questions that have puzzled people since time immemorial and that have been addressed not only by psychology and philosophy but also by religion, anthropology, political science, and other social sciences and humanistic disciplines. Not all those questions can be or have been addressed empirically, and the empirical work of psychology has raised many philosophical questions in its own right. The concerns addressed by both disciplines include questions of metaphysics (including ontology), epistemology, and moral philosophy (ethics), although the distinctions between these areas often blur, and other topics have also been addressed by both disciplines (such as phenomenology and hermeneutics).

Philosophical Origins of Psychology

Many trace the origin of psychology to the ancient Greek philosophers, particularly Socrates, Plato, and Aristotle. Certainly, topics such as the ones favored by the philosophers were being addressed long before psychology developed a disciplinary identity. Throughout the Middle Ages, philosophers and theologians such as Peter Abelard, Thomas Aquinas, Saint Bonaventure, and William Ockham explored the realm of human knowing, thinking, feeling, and sensing, although without the extensive empirical investigation of these states that came to characterize the psychological method. From the time of the Renaissance, philosophers such as René Descartes, Thomas Hobbes, John Locke, George Berkeley, David Hume, James Mill, John Stuart Mill, and Immanuel Kant debated the topics that have come to be central to the discipline of psychology.

Metaphysics

Metaphysics is the branch of philosophy that addresses questions regarding the nature of reality and the sorts of things that exist in the world. In modern philosophical usage, this branch includes questions of ontology, including the philosophy of mind. Both psychology and philosophy are concerned with the philosophy of mind. The philosophy of mind traces its origins to the ancient Greek philosophers, as well as Franz Brentano, William James, and John Dewey, among others. The philosophy of mind has primarily been concerned with three questions: the meaning of intentionality, the mind-body problem, and the problem of free will versus determinism.

Philosophers have asked what it means to have intentionality. Some have asserted that mental states, such as wishing, believing, and thinking, are necessarily about something, which is termed the “intentional object” of the mental state. (For example, I think that it is almost time for dinner; I wish that my homework were done; I believe I can succeed.) However, this raises the question of whether intentions “cause” actions, in a strict philosophical sense. This line of thought has been pursued by the philosophers Ludwig Wittgenstein, Donald Davidson, and Derek Parfit.

The philosophy of mind also looks at the relationship between the mind and the body (the mind-body problem) and asks: If all mental acts arise from physical states, what claims are left for the realm of the purely mental, rather than physical? The mind-body problem is related directly to questions regarding idealism versus materialism (whether the world is reducible to ideas or to the material world) and indirectly to questions of free will versus determinism. It is also related to questions of dualism versus monism (for example, the question of whether there are two sorts of things in the world or one). Under dualism, if the brain and mind (or body and mind) are wholly separable, questions arise concerning how the two are linked and how something that has no physical properties might be related to, communicate with, or affect something that has exclusively physical properties. These types of questions have been addressed by research in cognitive neuroscience by scientists such as Paul Churchland and Patricia Churchland and by philosophers such as Davidson and Thomas Nagel. However, if mind and brain are assumed to be the same (monism), other questions arise. For example, if mental states are wholly determined by physical changes in the brain, in what sense is it possible to claim that human beings have free will?

Free will versus determinism is the third question addressed by the philosophy of mind. Although this issue is not completely separate from religious questions treated by philosophers and theologists, the question has taken a different form in psychology. Psychologists as varied as the American behaviorist B. F. Skinner and the Viennese psychoanalyst Sigmund Freud have held that human behavior is determined, either by conscious or unconscious forces, while the early American psychologist William James and the American founder of person-centered therapy Carl R. Rogers, as well as other humanistic and existential psychologists, have held that humans have free will. However, if humans have free will and therefore can make choices that are independent of antecedent conditions, the question arises of whether psychology is a science in the sense of being a discipline that can make reliable predictions that can be tested and produce results that can be replicated by others.

Epistemology

Epistemology is the branch of philosophy devoted to the question of how people know what they know. This includes questions regarding the nature, scope, and possibility of any knowledge, and psychological knowledge. Both psychology and philosophy have wrestled with such epistemological questions as the nature of consciousness, the possibility of intersubjectivity (how people know others’ minds), and how people know their own minds.

The nature of consciousness has been a central question of both psychology and philosophy. This topic has been explored phenomenologically, including by Freud, and also through an attempt to identify the neural correlates of consciousness, a method pursued by cognitive neuroscientists as well as the philosopher John Searle. Questions regarding consciousness have become increasingly intriguing with the discovery of functional magnetic resonance imaging (fMRI), which permits correlation of the structures of the brain with the functions that they are performing in real time. Included in the study of consciousness are questions regarding sensation and perception, which raise philosophical problems, including whether the sensation of the object is separate from the perception of it, the knowledge of it, or both.

The problem of other minds, or intersubjectivity, has been of concern in both psychology and philosophy. It has taken many forms, including questions regarding how people know that others have minds and how they can have knowledge of others’ mental states. Philosophers Daniel Dennett and Davidson in particular have addressed this question. In psychology, this question is central to both clinical practice and research methodology, insofar as both depend on understanding the minds of those whom psychologists are studying and treating.

The question of how well people can know others’ minds leads directly to a third question, namely, how people can know their own minds and whether introspection is possible and by what means. Philosophers have asked how people can be sure about the contents of their own minds and on what authority they issue claims about their self-knowledge. They also ask what the relationship is between people’s claims of self-knowledge and the language they use to express them, as well as how to validate what people say about themselves. These questions have been pursued by the philosophers Wittgenstein and Davidson and the cognitive scientist Jerry Fodor. Such questions have clear implications for introspective (talk) psychotherapies, which rely heavily on first-person assertions by clients regarding their mental states.

Philosophy of Science

The philosophy of science is primarily concerned with the question of whether and to what extent the claims made by empirical psychology can be justified; that is, whether psychology is in fact a science like chemistry and physics. This critique has its origin in the work of the philosopher of science Thomas Kuhn, who pointed out that sciences move forward through a process of paradigm shifts, in which previously inchoate data or anomalous data become organized by a new explanatory rubric that better accounts for them than the previous theory did. By such standards, many have concluded that psychology is a preparadigmatic science. The work of philosophers Karl Popper and Paul Feyerabend is related to this topic.

Psychoanalysis in particular has been concerned with questions of whether its findings are best judged by scientific criteria (a correspondence theory of truth) or by hermeneutic or aesthetic criteria (coherence or parsimony). This debate has gained force because the status of psychoanalysis as a medical, and therefore presumably scientific, treatment rests on data obtained through the methods of free association and recollection, which raise unique philosophical problems. This debate has often taken the form of whether psychoanalysis is a hermeneutic pursuit, with the philosopher of science Adolf Grunbaum and the American psychoanalysts Donald Spence, Arnold Modell, and Roy Shafer weighing in on the matter.

Moral Philosophy

Moral philosophy is the branch of philosophy that concerns ethics. Although ethics has been a major topic in philosophy, psychology’s concern with ethics has been largely restricted to questions regarding the treatment of human and animal subjects in experiments and patients in clinical practice. Less attention has been devoted to broader questions of the place of values in human life, and such work has rarely drawn on the related work in moral philosophy.

Phenomenology

Phenomenology is a branch of philosophy that studies people’s conscious experiences of the world. Its premise is that reality is based on how objects and events are perceived or understood by the human consciousness and not on anything independent of human consciousness. Its philosophical origins are to be found in the works of Martin Heidegger, Edmund Husserl, Maurice Merleau-Ponty, Paul Ricoeur, and other twentieth century European philosophers. Its concern with first-person subjective mental states made phenomenology a natural fit for the emerging discipline of psychology, and existential and humanistic psychology in particular have conducted research to test phenemonological assertions as a guide to effective treatment. The work of the American person-centered psychologists Carl R. Rogers and Eugene Gendlin and the existential Swiss psychiatrists Ludwig Binswanger and Medard Boss have been influential among clinicians interested in phenomenology. The Society for Theoretical and Philosophical Psychology has served as one intellectual home for those interested in such topics.

Bibliography

Honderich, Ted, ed. The Oxford Guide to Philosophy. New York: Oxford University Press, 2005. Print.

Leahey, Thomas. A History of Psychology: Main Currents in Psychological Thought. 7th ed. Englewood Cliffs, N.J.: Prentice Hall, 2007. Print.

MacLeod, Robert B. The Persistent Problems of Psychology. Pittsburgh: Duquesne University Press, 1975. Print.

McLaughlin, Brian P., et al. The Oxford Handbook of Philosophy of Mind. New York: Oxford UP, 2011. Print.

Messer, Stanley, Louis Sass, and Robert Woolfolk, eds. Hermeneutics and Psychological Theory: Interpretive Perspectives on Personality, Psychotherapy, and Psychopathology. New Brunswick, N.J.: Rutgers University Press, 1990. Print.

Presbey, Gail, Karsten Struhl, and Richard Olsen. The Philosophical Quest: A Cross-Cultural Reader. 2d ed. New York: McGraw-Hill, 2000. Print.

Schellekens, Elisabeth, and Peter Goldie. The Aesthetic Mind: Philosophy and Psychology. New York: Oxford UP, 2014. Print.

Sneddon, Andrew. Like Minded: Externalism and Moral Psychology. Cambridge: MIT P, 2011. Print.

What is the smallpox vaccine?

Definition

The development of a smallpox vaccine began with variolation, which was the practice
of removing material from the scabbing pustules of infected people and
administering that material to healthy people to induce a milder form of smallpox
and subsequent immunity. Smallpox, caused by the Variola
major virus, is thought to have arisen as many as ten thousand years
ago in northern Africa and spread to the rest of the world by the seventeenth
century, leaving millions dead in its wake.

Although used in Asia and the Middle East as early as the eleventh century, variolation was not in widespread use in Europe until the late eighteenth century. Although variolation was often fatal, the total number of smallpox cases was significantly reduced because of the technique.

Vaccine Development

In 1774, an English farmer made the observation that milkmaids who became
infected with cowpox, a mild disease caused by the vaccinia virus, seldom
became infected with smallpox. The farmer immunized his family against smallpox by
infecting them with cowpox taken from a cow’s udder.

Edward
Jenner, an English physician, is credited with developing the
smallpox vaccine. In 1796, Jenner removed fluid from a cowpox pustule of a
milkmaid and inoculated an eight-year-old boy. The boy was exposed to material
taken from a fresh smallpox lesion six weeks later but did not develop smallpox.
By the early to mid-nineteenth century, inoculation with cowpox replaced
variolation. Jenner referred to his preparation as a vaccine
because the material came from a cow (vacca, in Latin).

The modern vaccine uses an attenuated vaccinia strain. After administration, a pustule develops, eventually scabs over, and falls off. For a few days after vaccination, the patient may have mild symptoms. Rarely do serious side effects develop. Vaccination within three to seven days of exposure to the smallpox virus can result in a significant reduction in the severity of the symptoms.

In 1982, after smallpox had been eradicated and the United States terminated
its mandatory vaccination program, production of the smallpox vaccine ceased. In
2007, the U.S. Food and Drug Administration authorized the production of a
newer and safer vaccine to be placed in the Strategic National Stockpile to be
used in the event of national emergency by the Centers for Disease Control and
Prevention.

Impact

The development of the smallpox vaccine led to the eventual eradication of the
disease. Although smallpox had been virtually eradicated from developed countries
by the 1950’s, epidemics continued in developing countries. In 1967, the
World Health
Organization (WHO) began a worldwide eradication campaign
that led to the last endemic case of smallpox, which was reported in 1977. In
1980, WHO announced that the world was free of smallpox.

Bibliography

Baciu, Alina, et al., eds. The Smallpox Vaccination Program: Public Health in an Age of Terrorism. Washington, D.C.: National Academies Press, 2005.

Henderson, D. A., and Richard Preston. Smallpox: The Death of a Disease—The Inside Story of Eradicating a Worldwide Killer. Amherst, N.Y.: Prometheus Books, 2009.

Hildreth, C. “Smallpox.” Journal of the American Medical Association 301 (2009): 1086.

Hopkins, Donald R. The Greatest Killer: Smallpox in History. Chicago: University of Chicago Press, 2002.

Koplow, David A. Smallpox: The Fight to Eradicate a Global Scourge. Berkeley: University of California Press, 2003.

Plotkin, Stanley A., Walter A. Orenstein, and Paul A. Offit. Vaccines. 5th ed. Philadelphia: Saunders/Elsevier, 2008.

Tucker, Jonathan B. Scourge: The Once and Future Threat of Smallpox. New York: Atlantic Monthly Press, 2001.

Williams, Gareth. Angel of Death: The Story of Smallpox. New York: Palgrave Macmillan, 2010.

What is pneumothorax?

Causes and Symptoms

Pneumothorax is the result of anything that causes air or fluid, such as blood, to leak into the space between the two layers of pleura, which line the chest wall (parietal) and the lung tissue (visceral). For normal lung function there is negative pressure in this space. When air enters, the negative pressure is disrupted, and the atmospheric pressure presses on the lung tissue, deflating it. A pneumothorax can be mild and self-limiting, but a severe pneumothorax can collapse the whole lung and cause a shift in the location of the heart and great vessels. This is a life-threatening situation.

Pneumothorax is caused by trauma to the lung, medical procedures performed on the lungs, infant prematurity, existing lung disease, endometriosis in the chest, and bullae. Trauma includes anything that penetrates the chest wall, such as a stabbing, gunshot wound, or excessive blunt trauma to the chest. Medical procedures such as a bronchoscopy, cardiopulmonary resuscitation (CPR), liver or lung biopsy, chest surgery, and the insertion of chest tubes can cause a pneumothorax. Premature infants or infants who swallow meconium, newborn stool, can rupture their lungs attempting to breathe despite lung tissue that is sticking together. The presence of existing lung disease can increase the risk of developing a pneumothorax. These diseases include emphysema, asthma, chronic infections, tuberculosis, cystic fibrosis, cancer, and chronic obstructive pulmonary disease (COPD). An unusual cause of pneumothorax is the presence of endometriosis in the chest. This condition causes pneumothorax at the time of the menstrual
cycle, when the endometrial tissue bleeds. Bullae develop due to local weakness in the lung tissue and can rupture with changes in atmospheric pressure, such as when scuba diving, flying, and mountain climbing. Most often bullae rupture for no apparent reason. Bullae are more common in cigarette smokers.

The symptoms of pneumothorax are shortness of breath, sharp pain in the chest, a feeling of tightness, cyanosis, dry cough, rapid heart rate, subcutaneous emphysema, and the sound of air moving through a penetrating chest wound. A primary pneumothorax is diagnosed by the symptoms; pulse oximetry, which measures oxygen saturation of the blood; auscultation, or listening to the lobes of the lungs through a stethoscope; and chest x-ray. A traumatic pneumothorax is related to a traumatic injury and a postmedical pneumothorax to a medical procedure.

Treatment and Therapy

A small pneumothorax will resolve on its own. It is treated with watchful waiting and repeated chest x-rays. If there is shortness of breath, then oxygen can be administered. If a pneumothorax does not resolve on its own, then a needle can be inserted through the chest wall into the pneumothorax (thoracentesis), and the air or fluid can be extracted. Another common treatment is the insertion of a chest tube with its tip in the intrapleural space. An airtight dressing is placed around the tube and the tube is drained into a system that includes a water seal in order to prevent the reintroduction of air. Gentle suction may be used to remove the air or any drainage present. Usually, the pneumothorax will resolve within two to three days, and then the tube can be removed. If the pneumothorax reoccurs after the suction is removed from the chest tube, then there is a more portable system called a Heimlich valve that can be used to continue chest drainage. This valve permits air or fluid to leave the interpleural space without permitting air to reenter.

If the pneumothorax does not improve, or if it reoccurs, then surgery may be required. Pleurodesis may be performed, particularly for ruptured bullae. In this procedure, a chemical irritant is used to create scar tissue to heal weakened spots in the lung. Surgery in the form of video-assisted thoracic surgery (VATS) can be performed to close the lung with staples. Open chest surgery is less commonly used to treat pneumothoraces.

In an emergency, a sucking or traumatic chest wound should be treated with an occlusive dressing to prevent the introduction of additional air into the chest. Ideally, this dressing should be sterile and have either petroleum jelly gauze or plastic to seal the wound.

Perspective and Prospects

Pneumothorax was first identified by Jean Marc Gaspard Itard, a student of Rene Laennec, in 1803. Laennec, himself, described the clinical picture of pneumothorax, in 1819. The first treatment of pneumothorax was thoracentesis. Both thoracentesis and chest tubes generally led to empyema, an infection in the pleural space because of the absence of aseptic technique. After the discovery of germ theory and aseptic technique by Ignaz Semmelweiss (1818–1865), Louis Pasteur
(1822–1895), and Joseph Lister
(1827–1912), pneumothorax could be treated with aseptic thoracentesis, or with surgery. Semmelweis discovered that hand washing between patients could limit the spread of infection after childbirth. Pasteur tested germ theory, and wrote about the microscopic germs that cause infection, both in the presence of air and in anaerobic tissue. Lister is referred to as the father of surgery because he introduced the use of chemicals to sterilize surgical instruments and to clean wounds. In 1875, G. E. Playfair developed water seal drainage for removing fluids from the chest, and in 1876, F. Cresswell Hewett used water seal drainage with chest tubes.

Tuberculosis was a scourge in the nineteenth century, and it frequently created a pneumothorax by eating through the lung. There were no antibiotics at this time, so treatment was limited, and most persons who developed tuberculosis died from it. In 1882, Italian physician Carlo Forlanini began to use pneumothorax for treatment of tuberculosis in an effort to rest the lung. This treatment was continued into the early twentieth century.

Bibliography

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What is Hodgkin disease?

Causes and Symptoms

Malignant lymphomas are neoplasms of lymphoid tissues and are of two general categories: those related to Hodgkin (also known as Hodgkin’s) disease and others that are collectively called non-Hodgkin lymphomas. The lymphoid tissues represent the structural expressions of the immune system, which defends the body against microbes. This system is widely spread throughout the body, is highly complex, and interacts closely with other physiologic systems of the body—especially the mucosa that lines the airways and digestive tract, where there is direct exposure to environmental microbes and other foreign substances. The components of this system are aggregations of lymphocytes in the mucosal linings (such as tonsils and adenoids), lymph nodes, and the spleen. The components of the lymphatic system connect with one another via small lymphatic vessels. The lymph nodes, which are situated in anatomical regions all over the body, interconnect and drain centrally toward the great veins of the body. The cellular components of the immune system are the lymphocytes, also called immunocytes. These account for about 20 percent of blood cells; lymphocytes make up the bulk of the lymphoid tissue that makes up the lymphatic system. The blood cells have a finite life and are disposed of in the spleen, which is the largest lymphoid organ in the body.

There are two major functional immunologic classes of lymphocytes and several other subclasses. Nevertheless, all share similar morphologic appearance, being small round cells almost completely occupied by a round nucleus. The B lymphocyte (the B refers to its bone marrow derivation) can, under proper antigenic stimulation, transform and mature into a plasma cell, which is the cell in charge of producing antibodies. Antibodies are the protein products of the immune system that act by capturing and removing foreign substances, called antigens. The other major class of lymphocytes is the T lymphocyte (the T refers to its thymus derivation). T lymphocytes are of at least two major functional subclasses, which either help or suppress the B lymphocytes in their transformation into plasma cells; thus they are termed helper and suppressor T cells, respectively. Other cellular
components of the immune system, cellular monocytes and macrophages, play an important role in carrying and transferring specific immunologic information between the various cellular components of the immune-lymphatic system. This, then, is a highly organized and complex system, with positive and negative biofeedback that maintains optimal, balanced proportions of all the cellular components that make up the system.

Hodgkin disease is a neoplasm of the lymphoid tissues that usually arises in lymph nodes, often in the neck, and has a varied histologic appearance characterized by the presence of Reed-Sternberg cells. The Reed-Sternberg cell is a giant cell having two nuclei that are situated in a mirror-image fashion. Treatment and prognosis in Hodgkin disease are determined by two parameters: the histopathologic classification, whereby the morphologic appearance is evaluated by the pathologist, and the clinical staging classification, whereby the extent of spread of the disease and its localization are determined by clinical studies. The pathology is studied by reviewing thinly cut sections of diseased lymph nodes removed from the patient. This study is most important for establishing a diagnosis of Hodgkin disease and ruling out other conditions that may closely simulate its clinical and/or pathologic features. At times, peer consultations are used to confirm the diagnosis.

Reed-Sternberg cells have a characteristic appearance and must be identified to make a diagnosis of Hodgkin disease. The pathologic classification of this disease, based on microscopic study, recognizes four different types, each with its own clinical implications regarding survival and prognosis. The classification is based on the relative dominance of lymphocytes when compared to the number of the neoplastic Reed-Sternberg cells. In the most favorable type, the lymphocytes predominate and Reed-Sternberg cells are sparse; this type is called lymphocyte predominance. In the worst type, the lymphocytes are very sparse and there are many more Reed-Sternberg cells and their variants; this type is called lymphocyte depletion. In between these two extremes are the mixed-cellularity type, in which there is an even mixture of lymphocytes and Reed-Sternberg cells, and nodular sclerosis, which forms nodules of fibrous scar tissue that surround the mixture of lymphocytes and Reed-Sternberg cells.

This classification has important prognostic implications. It correctly presumes that the neoplastic cells are the Reed-Sternberg cells and their variants, and that the lymphocytes are induced by the immune system to multiply and to fight the spread of the neoplastic cells. It follows that the more the process is successful, the better is the prognosis. Hence lymphocyte predominance carries a more favorable outlook than lymphocyte depletion, with mixed-cellularity types somewhere in between. Nodular sclerosis also carries a good prognosis. Other inflammatory cells are invariably mixed with the lymphocytes and Reed-Sternberg cells; these cells are also part of the body’s immune response against cancer cells.

The clinical staging classification of Hodgkin disease was formulated by a group of experts who met at a workshop in Ann Arbor, Michigan, in 1971. It is based on the proposition that the disease begins in a single group of lymph nodes (usually in the neck) and then spreads to the next adjacent group of lymph nodes, on the same side, before it crosses over to the other side of the body. The disease then advances farther across the diaphragm muscle, which separates the thorax from the abdominal cavity, and finally disseminates into the blood to involve the bone marrow and other distant sites. In this schema, stage I represents early stage, with involvement of only a single lymph node region, and stage II is the condition in which two or more such regions are involved on the same side of the diaphragm (that is, either above or below the diaphragm).

In the United States, Hodgkin disease is an uncommon neoplasm accounting for an estimated 9,000 cases. As of 2013, the disease accounts for approximately 1,300 deaths annually, according to American Cancer Society statistics. The incidence in the United States is slightly higher in males than females, and in whites than blacks. As of 2010, approximately 94,000 men and 88,000 women were alive who had histories of Hodgkin disease.

Hodgkin disease can occur at any age, although the highest peak incidence occurs in adolescents and young adults, and smaller peaks occur in the fifth and sixth decades of life. Most patients come to clinical attention because of painless, nontender, enlarged lymph nodes in the neck or armpits (above the diaphragm) or, less commonly, in the groin. In the young adult or adolescent, a mass in the chest may press against the airways to produce a dry, hacking cough and shortness of breath, which may be the patient’s first symptoms. Some patients may have anemia or severe itching. At times, especially when the disease is aggressive and extensive, the patient may have a fever, which may run for a few days and then disappear, only to recur after a week or two; there can also be night sweats and weight loss. These symptoms—fever, night sweats, and weight loss—indicate a less favorable prognosis. Younger patients and those with lymphocyte predominance and nodular sclerosis histologic types (favorable histologic types) tend to have limited disease—that is, stages I and II—found primarily above the diaphragm. Older patients and those with mixed-cellularity or lymphocyte depletion types are more likely to have extensive disease involving lymph nodes on both sides of the diaphragm (stage III) or even involving the liver, spleen, and bone marrow (stage IV).

When a patient with persistent lymph node enlargement seeks medical attention, a lymph node biopsy is usually made to make sure of the diagnosis. Other cancers that may simulate Hodgkin disease must be excluded, as well as a long list of benign conditions such as infectious mononucleosis and tuberculosis. A series of blood tests, x-ray and other imaging studies, and a bone marrow biopsy are done in order to evaluate the spread of disease and to assign the proper clinical stage. At times, even surgical exploration of the abdomen, with biopsies of abdominal lymph nodes, the liver, and the spleen, is done to assign an accurate stage of Hodgkin disease; this procedure is called staging laparotomy.

Treatment and Therapy

Modern cancer therapy has achieved its greatest triumph in the treatment of Hodgkin disease. The advent of a generally acceptable histopathologic classification, accurate staging, improved radiotherapy, effective chemotherapy, and supportive care, such as antibiotics and the transfusion of platelets, have contributed to the impressive 80 percent overall cure rate. The therapy is enhanced by an effective teamwork of medical experts in oncology, radiation therapy, surgery, pathology, and diagnostic radiology.

Because Hodgkin disease spreads in an orderly fashion through adjacent lymph node groups, effective high-dose radiation can be directed at affected lymph nodes and at their neighboring, uninvolved nodes. Irradiation, with a full dose of 3,500 to 4,000 rads in three to four weeks, can eradicate Hodgkin disease in involved nodes within the treatment field more than 95 percent of the time. In addition, extended-field irradiation of the adjacent uninvolved nodes is a standard practice used to eradicate minimal or early disease in these lymph nodes.

Stages I and II can be treated with radiotherapy alone by an extended field to include all areas above the diaphragm bearing lymph nodes (the axilla, neck, and chest), and in most cases the lymph nodes in the abdomen. Such treatment cures about 90 percent of patients. For patients in which the disease is found extensively in the chest, chemotherapy is added to the radiotherapy and results in prolonged, relapse-free survival in 85 percent of patients.

A variety of cytotoxic drugs (those that kill cells) are available to treat Hodgkin disease. Such drugs are similar to nitrogen mustard (which was once used in war) and are toxic to the body. It has been found that when more than one drug is used, each in a smaller dose, the toxicity can be reduced without diminishing effectiveness. Thus, combination chemotherapy has evolved. There are many effective regimens of combination chemotherapy that are called by the initials of the individual components; the most widely used is MOPP (mechlorethamine, Oncovin, procarbazine, and prednisone). In stage III, chemotherapy with or without radiotherapy is used, depending upon specific variations within the stage, with cure rates achieved in 80 percent of patients. Even in stage IV disease, combination chemotherapy (particularly with MOPP) has produced a complete remission in about 65 percent of patients, with a cure rate of more than 50 percent.

Bone marrow transplantation

, which is the intravenous infusion of normal marrow cells into the patient shortly after treatment in order to protect the patient from toxicity, has permitted the use of much higher doses of certain drugs. It allows the therapist to irradiate all the patient’s bone marrow, eradicating both “good” and “bad” cells, with the hope that the normal marrow cells that are infused will populate the bone marrow and grow there. Bone marrow transplantation has been successfully used mainly in young patients who were resistant to conventional chemotherapy.

Perspective and Prospects

Thomas Hodgkin of Guy’s Hospital in London was the first to recognize the disease that would bear his name. In 1832, he described the autopsy findings and clinical features of seven patients who had simultaneous enlargement of grossly diseased lymph nodes and spleens, and he considered the condition to be a primary affliction of these organs. This condition, he himself records, was vaguely outlined by Marcello Malpighi in 1665. Four years earlier than Hodgkin, David Craige had described the autopsy findings of a similar case. Subsequent histologic examination of tissues from Hodgkin’s original cases confirmed the disease in three of them. In 1865, Sir Samuel Wilks elaborated on the autopsy studies of similar cases and published the findings on fifteen patients, calling the condition Hodgkin disease.

Important histopathologic observations were contributed by William Greenfield in 1878 and E. Goldman in 1892. George Sternberg described the giant cells but believed the condition to be a peculiar form of tuberculosis. The recognition that these cells were an integral part of the disease awaited the careful pathologic observation of Dorothy Reed of Johns Hopkins Hospital in Baltimore. These cells, appropriately named Reed-Sternberg cells, are the hallmark of Hodgkin disease.

Controversy as to the nature of this disease led early investigators to study infectious agents as possible etiologic causes, especially the tuberculosis bacillus, but to no avail. More recent studies have examined the roles of other viral infectious agents, especially the agent of infectious mononucleosis, but with no consistent results. At present, the condition is accepted as neoplastic, probably triggered by some unknown environmental agent or agents.

Between 1930 and 1950, major advances included the recognition of meaningful histologic subtypes of Hodgkin disease correlating with prognosis, and the development by Vera Peters of a clinical staging system. Impressive responses to X-ray therapy were reported at the beginning of the twentieth century, and treatment with megavoltage therapy was further developed. By World War II, it became realistic to speak of curing some patients with early Hodgkin disease. The potential for a cure meant that accurate histologic diagnosis and estimation of the extent and localization of disease were imperative in planning treatment; a multidisciplinary approach to diagnosis and treatment was developed. Modern concepts of histologic classification became codified at a conference held in Rye, New York, in 1965, and the clinical staging system was refined into its present form at a workshop held at Ann Arbor, Michigan, in 1971.

Modern effective chemotherapy was developed concurrently with these advances in classification, staging, and radiotherapy. The alkylating agents, created as an outgrowth of studies on nitrogen mustard gas during World War II, provided the first drugs to produce impressive shrinkage of the tumor and significant palliation of the disease. The subsequent developments in modern pharmacology and therapeutics enabled Vince DeVita and his coworkers, in 1970, to design the first effective combination chemotherapy regimen, MOPP.

Today, many more such regimens are being tested; the possibility for cure has become a realistic hope for every patient with Hodgkin disease. This is the case because of the refinement of ancillary therapies with antibiotics (for infections that may occur during the necessary phases of suppression of the immune system by these powerful toxic drugs) and platelet transfusion technology.
Bone marrow transplantation technology also offers strong hope of curing patients with advanced cases who are resistant. The bone marrow is harvested and then reintroduced into a patient whose marrow has been effectively disabled. Immunotherapy is also being investigated. It can boost the patient’s ability to combat disease by modulating the body’s responses. The drawback to aggressive combinations of chemotherapy and radiotherapy, however, is the emergence of therapy-related leukemia and leukemia-like malignancies several years after the completion of successful therapy for Hodgkin disease.

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