`2n^2 > (n + 1)^2, n >=3` Use mathematical induction to prove the inequality for the indicated values of n.

You need to use mathematical induction to prove the formula for every positive integer n, hence, you need to perform the two steps of the method, such that:

Step 1: Basis: Show that the statement P(n) hold for n = 3, such that:

`2*3^2 > (3+1)^2 => 18>16`

Step 2: Inductive step: Show that if P(k) holds, then also P(k + 1) holds:

`P(k):2k^2 >(k+1)^2`

`holds `

`P(k+1):2(k+1)^2 >(k+2)^2` 

You need to use induction hypothesis that P(k) holds, hence, you need to re-write the left side, such that:

`2*2k^2 >  (k+2)^2`

`4k^2 > k^2 + 4k + 4`

`k^2 + k^2 + k^2 + k^2 > k^2 + 4k + 4`

` k^2 + k^2 + k^2 > 4k + 4`

`k^2 > 4k and 2k^2 > 4 => k^2 > 2`

Notice that P(k+1) holds.

Hence, since both the basis and the inductive step have been verified, by mathematical induction, the statement `P(n):2n^2 >(n+1)^2`   holds for all positive integers n.

What is psoriasis?

Causes and Symptoms

Psoriasis is a common skin problem that afflicts approximately two of every hundred people, affecting males and females with relatively equal frequency. Although it affects all races, it is most prevalent among northern Europeans. This stubborn, chronic, and as yet incurable disease most commonly appears in one’s teens or twenties, although it can appear in early childhood. While 70 percent of those who develop psoriasis do so by the age of twenty, there is another common danger period in the fifties and sixties, with a large number of patients developing their first symptoms at that time.

There are several different types of psoriasis, making diagnosis difficult. By far the most widespread is the plaque type; because it accounts for 95 percent of all cases, this type is also called common psoriasis. Plaque-type psoriasis gets its name from the appearance of the patches of affected skin. Each patch resembles a plaque or small disk stuck to the body’s surface. These dull, wine-colored patches of abnormal skin are often rounded or oval; they may be very irregular in shape when several nearby patches join together. The surface of each thickened patch is rough and scaly, with the scales ranging in color from red to white to the most typical silvery gray. These psoriatic plaques can be small (the size of coins) or become palm-sized and larger. Whatever their final size, they generally begin as purple or reddened areas the size of a pinhead. The original areas expand in size, usually for a few weeks, until they reach a stable phase and stop expanding. The average size of a plaque in the stable phase is between two and three inches. A patch of stable psoriasis may eventually grow pale, become less scaly, and disappear completely, or it may begin to enlarge for no apparent reason. Even those plaques that have disappeared may be reactivated and reappear in the same place at some later time.

Certain parts of the body seem most prone to psoriatic
lesions, namely the elbows, the knees, the scalp, and the lower back. The patches may appear elsewhere, including the genitals and the buttocks, but the face, hands, and feet are rarely affected. Severe cases may cover the entire chest or back. In a few cases, psoriasis is symmetrical, appearing in the same area on the left and right sides of the body simultaneously. The patches are, however, more likely to develop in a random, scattered manner. Almost 50 percent of patients with psoriasis have lesions on their scalps. When these plaques are very large and widespread, they are difficult to treat and very difficult to hide. Although very uncomfortable, scalp psoriasis does not affect the growth of hair or cause baldness. It can cause a temporary thinning of the hair, but the hair grows normally again once the disease is controlled by medication. About one-third of psoriasis patients have affected fingernails and toenails. The diseased nails show pits or pinpoint indentations, loosening, thickening, and a yellowish discoloration. Surprisingly, in some people the condition remains on the nails alone, never developing elsewhere.

In addition to psoriasis of the nails, there are several rare and unusual types of psoriasis that are quite different from the common or plaque type. These include flexural or inverse, guttate, pustular, and erythrodermic psoriasis. Flexural psoriasis appears in folds and creases on the body and is often found on people who are particularly overweight and who are in their mid-forties or older. The patches tend to be very moist rather than scaly and are particularly sore and uncomfortable. Guttable psoriasis consists of an enormous number of highly scattered but minute plaques. It is extremely rare and occurs between the ages of eight and sixteen. Although the spots usually clear up in a few weeks, they sometimes recur or change into the large lesions of common psoriasis. Pustular psoriasis is the only form of the disease that occurs on the palms of the hands or the soles of the feet. It was named for the yellow or white pus-filled spots that form on the skin and eventually drop off. These spots form when enormous numbers of white blood cells invade the skin even though there is no infection present and, therefore, no need for these infection-killing cells. Erythrodermic psoriasis literally means “red skin.” This very rare condition is so named because the entire body is covered by flaming red patches that do not turn scaly. Since the extensive nature of this condition makes internal temperature control very difficult and dehydration inevitable, it can be very dangerous and may require hospitalization.

Common psoriasis, by comparison, is not dangerous or life-threatening. It is usually not painful and does not even cause itching in most patients. It is, however, very annoying because of its unsightly appearance and its tendency to flare up repeatedly. Once the disease has appeared, it stays with the person for life, improving or worsening periodically. After periods of relative quiet, during which the skin may appear quite normal, patients with psoriasis experience new eruptions and scaling for no apparent reason. Plaques continue to form for an unpredictable amount of time, until the condition spontaneously quiets down again.

The source of the plaques is a failure in the mechanism by which normal skin renews itself. Ordinarily, the cells at the base of the epidermis reproduce themselves at a slow and steady rate. They then move upward in about twenty-eight days, changing chemically, dying, and detaching from the surface, the stratum corneum. In psoriatic skin, however, there is a huge increase in the number of basal cells in the epidermis, which reproduce so rapidly that they push upward to the surface in only four days, forming thick disks of sticky, abnormal cells. Below the epidermis, the dermis of a patient with psoriasis is also abnormal. Its normally fine blood vessels are wide and extremely twisted, which results in the red appearance of the plaques and causes bleeding to occur easily when the skin is bumped or scratched. An unusually high number of the white blood cells called neutrophils and T lymphocytes are also present. They move up into the epidermis, creating inflammation and swelling within the plaques.

Long before modern dermatology discovered these disturbing facts about the structure and the functioning of psoriatic skin, it was noted that the disease does seem to run in families. If one parent has the problem, there is a one-in-three chance that a child will eventually be afflicted; if both parents have the disease, the risk for their offspring is one in two. With nonidentical twins, there is a 70 percent chance that if one has psoriasis, they both will; with identical twins, the figure can be as high as 90 percent, according to some studies. Investigators suspect that psoriasis is not handed down by a simple pattern, such as with eye color inheritance. It seems more likely that the condition results from a combination of several genetic factors from each parent, much like the manner in which height and intelligence are inherited.

Treatment and Therapy

More than 90 percent of psoriasis patients can be cleared significantly of their lesions or even made lesion-free by the medicines and methods developed by modern technology. For minor outbreaks, limited to a small area of the body, the first choice for treatment is a corticosteroid cream or ointment applied directly to the plaques.
Corticosteroids are hormones, produced by the adrenal glands, that are able to reduce inflammation. Corticosteroids are produced in the laboratory and combined with other chemicals to reduce inflammation even more effectively by decreasing blood flow to the psoriatic lesions. Dermatologists have a large variety of such preparations ranging from mild to extremely potent. They must find one that is strong enough to suppress the inflammation but not so strong that it causes unwanted side effects.

There are two major undesirable side effects of corticosteroid therapy. Psoriatic skin absorbs all substances more easily than normal skin; the excess hormones enter the bloodstream and can change the output of hormones by the pituitary and adrenal glands, dangerously altering the body’s chemical balance. The other danger is to the skin itself, which becomes abnormally thin, easily damaged, and prone to infections. Another drawback to the use of corticosteroids is the tendency for the psoriatic plaques to reappear soon after the creams or ointments are discontinued.

Many patients find relief from a completely different class of medications, those which contain tar. This thick, black, oily liquid is produced from coal. It contains thousands of chemical substances, and biochemists do not know which of those substances actually help to heal the skin. Tar-containing ointments, creams, gels, shampoos, and bath additives are useful for removing the scales without worrisome side effects. A major drawback, however, is their tendency to stain clothing, bedding, bathroom tiles, and bathtubs. Some staining can be avoided by covering the treated skin area with bandages, cotton underwear, or a shower cap. In addition to the staining, many patients find the tar odor quite unpleasant; pharmaceutical companies are constantly trying to improve this aspect of these quite effective products.

A third type of preparation is particularly effective for removing very thick scales. These medications contain a compound called salicylic acid. Like the corticosteroids, salicylic acid ointments and gels are most effective when they are in contact with the plaques for a long period of time. After treatment, it is often recommended that patients cover their lesions with plastic gloves, plastic bags (for the feet), or taped-down plastic wrap for four to eight hours.

Patients with psoriasis have noted for years that exposure to the sun is very helpful in clearing their lesions. Daily sunlight exposure is effective for as many as 80 percent of patients. This treatment is relatively accessible for at least part of the year and inexpensive compared to the various medications available. Given the increased risk of skin cancer, it is strongly recommended that patients have repeated but brief sun exposures and avoid sunburn by using creams and lotions. Although sun exposure is helpful to most patients with common psoriasis, it rarely helps and can even worsen the pustulate and erythrodermic types. Since too much exposure to sunlight will damage rather than help any skin, even plaque-type patients are advised to stop their sun exposure once the psoriasis has improved.

For patients in many climates, sunbathing is possible for only a few months of the year. The development of sunlamps for use at home or in a dermatologist’s office, hospital, psoriasis care center, or tanning parlor has made this therapy possible all year round. Because of the danger of severe sunburns, sunlamp treatments remain controversial. To reduce their danger, a dermatologist must carefully determine the amount of time of each treatment, the precise distance from the lamp, and the appropriate frequency of treatments for each individual patient to achieve maximal and safe results.

The curative effect of sunlight depends on the presence of the very short wavelength part of the light, called ultraviolet. It is ultraviolet B (UVB) waves that help heal psoriasis, possibly by slowing down the high growth rate of cells in the epidermis. Both natural sunlight and sunlamps contain UVB and, therefore, have the potential to help psoriasis. They also have the potential, however, to burn the skin.

Patients with severe psoriasis may require the use of ultraviolet A (UVA) waves from a special kind of sunlamp. The patient is given a dose of a psoralen, a substance that makes the skin more light-sensitive, and is then exposed to UVA inside a full-body light cabinet. Thirty treatments may be required to completely clear the skin. The psoralen is often given in tablet form, although some patients suffer fewer side effects if it is painted onto the skin or if they bathe in it. The early side effects of PUVA (psoralen plus UVA) treatment include nausea, itching, colored blotches on the skin, and occasional worsening of the psoriasis. More worrisome are the possible later side effects: skin cancer and the development of cataracts in the eyes. The danger of developing cataracts also exists from natural sunlight and UVB sunlamps; patients using any light therapy must use excellent sunglasses that block out all rays harmful to the eyes.

For the patient with widespread psoriasis who is not responsive to corticosteroids, tar preparations, or the various light therapies, the drug methotrexate is effective in more than 80 percent of patients. This powerful drug was originally developed to treat various kinds of cancer because it slows down the process of cell multiplication. Thus the psoriatic epidermal cells are prevented from reproducing and forming the scaly plaques. Often methotrexate must be taken for six months or a year, in pill form or by injection, to have a significant impact on an extensive case. Such a dosage poses a risk of numerous and serious side effects, including persistent feelings of sickness, indigestion, and diarrhea. Frequent tests are necessary to monitor the condition of the blood, since methotrexate can interfere with the bone marrow’s production of normal blood cells. Most important, periodic liver biopsies, the removal of sample liver cells by means of a special needle, are necessary because methotrexate can cause irreversible damage to this crucial organ. It is very important that a pregnant woman never take methotrexate or that a woman never
become pregnant while taking it. The drug’s ability to interfere with cell growth can cause many abnormalities in a developing embryo or fetus. Similar fetal abnormalities can be caused by the drugs called retinoids.

For patients with pustular and erythrodermic psoriasis, the retinoids etretinate and acitretin can be very useful, if side effects are carefully monitored. Some dermatologists have been especially successful combining PUVA and etretinate therapies; the improvement in the psoriasis is greater than with either alone, while the lower dosage of each minimizes risk and side effects.

Another medication effective in treating severe psoriasis is cyclosporine. It has brought dramatic improvement to patients with lifelong disabling symptoms. Many people, however, can tolerate the drug only for short periods. Because of its potential to cause high blood pressure and kidney damage, as well as an increased risk of cancer, this medicine is prescribed only with extreme caution.

All the many therapies described can bring partial or total clearing of lesions and even result in the remission of the disease for a period of time. Until the cause of psoriasis is completely understood, however, it is likely that no permanent cure will be developed.

Perspective and Prospects

Descriptions of psoriasis are found in the records of the earliest known civilizations. The term “psora” comes from the ancient Greek language. Psoriasis was considered a form of leprosy in biblical times. Despite this ancient history and extensive modern research, however, the exact cause of psoriasis is still unknown. Unlike many human diseases, psoriasis does not afflict any animals; therefore, it cannot be studied through controlled laboratory testing.

Early work on psoriasis by dermatologists centered on differential diagnosis. This is the ability to distinguish psoriasis from various rashes caused by fungi, such as ringworm, and from the many forms of eczema or dermatitis caused by allergies. Skin biopsies developed by oncologists can now determine that the condition is not a cancer; the portion of skin removed, when placed under a microscope, will clearly show the dermal and epidermal appearance characteristic of psoriatic skin.

While skin scientists have proven that psoriasis is not contagious, it has been known since the 1930s that many cases develop soon after strep throat and other upper respiratory infections. The bacteria involved are not the cause of the psoriasis, however, but rather a trigger for the development of a condition for which the patient is genetically predisposed. Another trigger, excessive scratching or rubbing of the skin, can precipitate outbreaks in susceptible people; this is named the Koebner phenomenon, for its discoverer. With the help of neurologists and psychologists, it has been proven that the disease is not caused by “nerves,” yet stress of all kinds is definitely able to make its symptoms worse, and patients must be helped to lower their stress levels if they are to keep the disease under control.

Nutritionists have searched for ways to use diet to help psoriatics, but to no avail. Although no particular foods either help or hinder the course of the disease, most dermatologists now recognize that drinking alcohol can both precipitate and aggravate the disfiguring plaques.

Immunologists have been very involved in the study of psoriasis even though it is not an allergic reaction to any substance in one’s environment. In the late twentieth century, they pursued many possible connections between the streptococci bacteria that cause strep throat, the white blood cells called T lymphocytes that seek to destroy them, and the development of psoriasis. They believe that, in predisposed people, chemicals from the bacteria cause the T lymphocytes to give off substances that trigger the skin’s uncontrolled and excessive production of epidermal cells.

Geneticists have been searching diligently for the source of the predisposition to psoriasis. Among the genes children receive from their parents are those that build particular proteins on their white blood cells called human leukocyte antigens (HLAs). Out of the hundreds of different HLAs that one can possibly inherit, those who develop psoriasis always seem to possess similar combinations. The identification of the genes responsible for HLAs and the role of those genes in precipitating psoriasis may bring about major improvements in the treatment and possibly a cure for this disease afflicting millions of people throughout the world.

Bibliography

"An Overview of Psoriasis and Psoriatic Arthritis." National Psoriasis Foundation, Feb. 2011.

"About Psoriasis." National Psoriasis Foundation, 2013.

Camisa, Charles. Handbook of Psoriasis. 2d ed. Hoboken, N.J.: John Wiley & Sons, 2004.

Cram, David L. Coping with Psoriasis: A Patient’s Guide to Treatment. Omaha, Nebr.: Addicus Books, 2000.

Freinkel, Ruth K., and David T. Woodley. Biology of the Skin. New York: Parthenon, 2001.

Mackie, Rona M. Clinical Dermatology. 5th ed. New York: Oxford University Press, 2003.

Marks, Ronald. Psoriasis. 2d rev. ed. London: Sheldon Press, 1994.

Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Psoriasis. San Diego, Calif.: Icon Health, 2004.

"Psoriasis." MedlinePlus, May 6, 2013.

Shuman, Jill, and Purvee S. Shah. "Psoriasis." Health Library, Feb. 25, 2013.

Turkington, Carol, and Jeffrey S. Dover. The Encyclopedia of Skin and Skin Disorders. 3d ed. New York: Facts On File, 2007.

Weedon, David. Skin Pathology. 3d ed. New York: Churchill Livingstone/Elsevier, 2010.

"What Is Psoriasis?" National Institute of Arthritis and Musculoskeletal and Skin Diseases, Sept. 2009.

`(-1/2 + sqrt(3)/2 i )^3` Use the Binomial Theorem to expand the complex number, then simplify the result.

The expansion of `(x+y)^n` is,

`_nC_0x^n+_nC_1x^(n-1)y^1+_nC_2x^(n-2)y^2+.......+_nC_ny^n`

`=x^n+nx^(n-1)y+(n!)/(2!(n-2)!)x^(n-2)y^2+......+y^n`

`:.(-1/2+sqrt(3)/2i)^3)=(-1/2)^3+3(-1/2)^(3-1)*(sqrt(3)/2i)+_3C_2*(-1/2)^(3-2)*(sqrt(3)/2i)^2+(sqrt(3)/2i)^3`

`=-1/8+3(-1/2)^2*(sqrt(3)/2i)+(3!)/(2!(3-2)!)*(-1/2)^1*(sqrt(3)/2i)^2+(sqrt(3)/2i)^3`

`=-1/8+((3sqrt(3))/8)i-3/2*((3i^2)/4)+(3sqrt(3)i^3)/8`

`=-1/8+(3sqrt(3)i)/8-9/8i^2+(3sqrt(3)i^3)/8`

plug in `i^2=-1 `

`=-1/8+(3sqrt(3)i)/8-9/8(-1)+(3sqrt(3)(-i))/8`

`=-1/8+(3sqrt(3)i)/8+9/8-(3sqrt(3)i)/8`

`=-1/8+9/8`

`=(-1+9)/8`

`=8/8`

`=1`

How does Toni Cade Bambara create authentic voice in the narrative of Squeaky?

Toni Cade Bambara creates authentic voice for Squeaky as she narrates “Raymond’s Run” by using colloquialisms and language that is appropriate for a child of Squeaky’s age. Hazel Elizabeth Deborah Parker, also known as Squeaky, is the first person narrator of the story, which provides the reader with her point of view. As Squeaky relates the story she uses words such as cause in place of because, and ain’t instead of are not. This is common in children her age, but it is also common in one whose education is incomplete. In addition, Squeaky uses the colloquial language of the streets of her Harlem neighborhood. All of these techniques engage the reader in Squeaky's world and identify her personality.

But now, if anybody has anything to say to Raymond, anything to say about his big head, they have to come by me. And I don’t play the dozens or believe in standing around with somebody in my face doing a lot of talking. I much rather just knock you down and take my chances even if I am a little girl with skinny arms and a squeaky voice, which is how I got the name Squeaky.

Squeaky’s language is a window into her personality. She is brash, straight forward, and a bit irreverent, but she is insecure with her identity.

So I’m strolling down Broadway breathing out and breathing in on counts of seven, which is my lucky number, and here comes Gretchen and her sidekicks: Mary Louise, who used to be a friend of mine when she first moved to Harlem from Baltimore and got beat up by everybody till I took up for her on account of her mother and my mother used to sing in the same choir when they were young girls, but people ain’t grateful, so now she hangs out with the new girl Gretchen and talks about me like a dog; and Rosie, who is as fat as I am skinny and has a big mouth where Raymond is concerned and is too stupid to know that there is not a big deal of difference between herself and Raymond and that she can’t afford to throw stones.

By providing the reader with Squeaky’s internal dialogue, the thoughts that are developing in her mind, the reader comes to know the little girl as she has a revelation about her character and self-worth.

Was the New Deal a success or a failure?

The New Deal was Franklin D. Roosevelt’s program to deal with the effects of the Great Depression. While it didn’t get us out of the Great Depression, it did help alleviate the harsh effects it had on many Americans. It also created some programs that we still have today. Thus, it is fair to say the New Deal was fairly successful.

When President Roosevelt took office, our financial system was in ruins, and nearly 25% of our people were unemployed. President Roosevelt took steps to strengthen the banking system and to increase the confidence our people had in it. The Emergency Banking Relief Act closed all banks until the federal government could inspect them. Then, only the strongest banks were allowed to reopen. President Roosevelt also told the American people they needed to have confidence in our banks as a result of the actions the government took. President Roosevelt also helped the Glass-Steagall Act become law. This law prevented commercial banks from investing in the stock market. It also created the Federal Deposit Insurance Corporation, which provided insurance for savings accounts. We still have the Federal Deposit Insurance Corporation today. The Securities Act required companies to provide truthful information to investors. It also created the Security and Exchange Commission to regulate the stock market and to prevent fraud. We still have this agency today.

There were several job programs created to get people back to work. The Civilian Conservation Corps provided jobs for young men who worked on conservation projects in the West. The Public Works Administration provided money to hire workers to work on construction projects such as roads, bridges, and schools. The Civil Works Administration did the same thing. As a result of these programs, unemployment dropped as more people were working.

The Social Security program was created by the New Deal. The program provided a pension to those people who were at least 65 years old. It also provided aid to the unemployed and helped those who were disabled. This program is very important today. Many people depend on this program as part of their retirement income.

The New Deal was created to deal with the effects of the Great Depression. It also tried to provide safeguards to prevent another Great Depression from occurring. While unemployment wasn’t reduced to a normal level by the New Deal, it did get people back to work and provided some safeguards to prevent another Great Depression from occurring. We have not had another Great Depression. We have programs from the New Deal that impact us today. Thus, it can be said that the New Deal was generally a success.

How is the periodic table divided into metals and nonmetals?

The periodic table of elements is an arrangement of chemical elements in rows and columns, according to certain characteristics. The different rows are called periods, while the columns are called groups. The elements are arranged according to the atomic numbers, electronic configurations and chemical characteristics. The elements with fully filled configurations (the noble gases) constitute the last group (on the right side) of the periodic table. As we move across a row, from left to right, one electron is added to every subsequent element. This means that elements on the left side of the periodic table will have a higher tendency to donate electrons, while the ones close to the noble gases will have a higher tendency to accept electrons. Thus, the metals are on the left side of the table, while non-metals are towards the right side of the table. 

Since there are many more metals than non-metals, most of the table is occupied by metals. In fact, metals occupy the left two groups, the entire central section (transition metals) and parts of the groups on the right sides, apart from the two bottom rows (actinides and lanthanides). 

Hope this helps. 

What is Osgood-Schlatter disease?

Causes and Symptoms

Osgood-Schlatter disease is most frequently found in young athletes during their years of rapid growth. It is more common in boys, who are typically affected between the ages of thirteen and fourteen. Girls usually are affected at younger ages, ten to eleven. However, children are at risk between the ages of ten and eighteen, especially during their rapid skeletal growth years. Children who play sports that involve running or repetitive jumping have the highest risk.

The most common symptom of Osgood-Schlatter disease is pain below the kneecap. There is usually a swollen, bony bump in that area. Pain is often felt when the bump is touched or when the knee is bent or fully extended in activities such as running, jumping, kneeling, squatting, or lifting weights. As the child matures, Osgood-Schlatter disease will usually go away. When children stop growing, the patellar tendon is stronger and the pain and swelling disappear. Very seldom does the disease continue after rapid growth stops.

If the pain persists, then the child should see a pediatrician or orthopedist. The physician will examine the knee area and the location of pain in order to make a diagnosis. If the source of the pain is unclear, then an x-ray will be taken of the knee to verify Osgood-Schlatter disease.

Treatment and Therapy

The best treatment for Osgood-Schlatter disease is simply rest. Depending on the severity of the condition, the child may have to decrease activity levels or stop playing sports for several months. Deep knee bending and jumping should be minimized, and running may need to be limited. To treat the pain, the knee should get more rest, and ice should be applied for twenty minutes three times per day. Elastic bandages should be used to compress the knee area, and the leg should be elevated when possible. Over-the-counter pain relievers can be taken. In extreme cases, a brace or cast may be used.

After recovery from the pain, the child can slowly return to previous activity levels. Additionally, a physical therapist can prescribe exercises that will help strengthen the leg muscles around the knee to minimize the chances of a recurrence.

There is no surgical procedure for Osgood-Schlatter disease unless the patellar tendon is fully torn from the tibia. This should not happen if the patient gets proper rest, in which case Osgood-Schlatter disease will resolve itself.

Bibliography

Dunn, J. F., Jr. “Osgood-Schlatter Disease.” American Family Physician 41, no. 4 (1990): 173.

Globus, S. “Osgood-Schlatter: More than Growing Pains.” Current Health 2 28, no. 4 (2002): 20.

Kaneshiro, Neil K. "Osgood-Schlatter Disease." MedlinePlus, November 12, 2012.

Lackey, E., and R. Sutton. “Rest Is Best for Common Knee Swelling.” GP: General Practitioner 1c (2003): 75.

Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Osgood-Schlatter Disease. San Diego, Calif.: Icon Health, 2002.

Woodward, A. H. “Osgood-Schlatter Disease.” Pediatrics for Parents 11, no. 1 (1990): 11.

Why does Half Arrow watch quietly while the guard binds True Son's arms?

True Son is being marched back to white civilization in chapter four after the Indians agree to a treaty which will release the whites who had been taken captive. True Son has lived with the Lenne Lenapi or Delaware tribe for eleven years. He is accompanied for much of the journey by his Indian cousin Half Arrow and he is being guarded by Del Hardy, a white soldier who speaks the Indian language.

Right before they cross the river (probably the Ohio or Allegheny) into Fort Pitt, Del informs Half Arrow and Little Crane, who is accompanying his wife, that they can go no further into white territory. Half Arrow ignores this and continues to march side by side with True Son until they get to the ford in the river. When Dell pushes Half Arrow out of the way, True Son retaliates and attacks the guard. He is quickly restrained by a group of guards who then tie his arms. Half Arrow stands by passively. He knows that to resist would be to commit suicide.

Appropriately, Half Arrow's last words to True Son before they part company is a message from True Son's Indian father about patience and waiting for the right moment to escape. He tells True Son to bear "his hardship with patience and cheerfulness." He advises him to look for the proper time to act. Being impatient or foolish will lead to certain death. It is better to stay alive and go along with the white man until the time is "ripe" to overtake his captor.

In Walt Whitman's "When I Heard the Learn'd Astronomer," what does the astronomer's lecture represent? What does the "moist night-air" represent?

In Walt Whitman's "When I Heard the Learn'd Astronomer," the lecture is clearly some type of presentation. The narrator gives us clues by describing what else is present at the lecture. There are "proofs," "figures," "charts," and "diagrams" mentioned on lines 2 and 3. Initially this may come across as some type of classroom, however, further details indicate this is more likely a lecture presenting some new findings regarding the state of the universe. The lecturer is an astronomer, rather than a teacher, by trade, and the narrator mentions that there was "much applause," which also suggests that this is not a student-filled classroom but a special presentation. People are there to listen and applaud as some mysterious phenomena is explained through charts and graphs. This lecture, with its new findings, represents the idea that the quest for knowledge can take away from the beauty of the natural world.

Conversely, the "moist night-air" represents everything that the lecture hall is not. It is the natural world, filled with wonder and unexplained majesty. While the poem begins in the lecture-room, the narrator soon grows weary of the facts and figures, stating "[h]ow soon, unaccountable, I became tired and sick" (6). At this point the narrator leaves and wanders outside, leaving the crowds and the stuffiness of the lecture-room behind. They find themself out of doors, where they "[l]ook'd up in perfect silence at the stars."  The description of the night-air as "mystical" lends itself to the above juxtaposition. To Whitman's narrator, and to Whitman himself, the wonders become less wonderful the more they are explained. Like the universe, the "mystical moist night-air" needs no explanation; it simply needs to be.

What type of personality does Sylvia have in "A White Heron"? What in the story lets the reader know?

Sylvia feels especially alive in the natural setting and could never seem to thrive and grow when she lived in the city.  Listening to thrushes near her grandmother's farm, her "heart [...] beat fast with pleasure."  She is incredibly comfortable in the company of animals, and even more uncomfortable with people.  When she first hears the hunter's whistle, she is "horror-stricken" and associates the sound with an "enemy," an impression that makes it clear just how intuitive and accurate she is (the hunter is very much the enemy of the creatures to whom she feels such a kinship). 

The comparison of her to several different natural creatures alerts us to her fragility as well as her strength.  When the hunter starts to follow her home, "she hung her head as if the stem of it were broken"; here, she is compared to a broken flower, its stem snapped.  However, climbing the big pine tree, her "bare feet and fingers [...] pinched and held like bird's claws"; in this scene, she is compared to a bird, another creature that, perhaps, seems fragile but can really be quite strong and tough and resilient.  In the end, Sylvia is extremely loyal to the nature she loves so much, and she refuses to give the heron's secret away. 

What is a summary of the play 'night, Mother by Marsha Norman?

The two main characters in ‘night, Mother are Jessie Cates and her mother Thelma, whom Jesse calls “Mama.” Jesse is middle-aged and lives with Mama, taking care of all the details of her mother’s life. They live in a small house on a lonely country road, and the onstage action occurs in the living room and kitchen area. At the beginning of the play, Jesse matter-of-factly tells her mother that she is going to kill herself that night.

After she announces this, she begins preparing to commit suicide, including gathering old towels to minimize the mess and writing lists of things that need to be tended to after she is gone. At first Mama refuses to believe her, but as the drama progresses, Mama realizes Jessie does intend to shoot herself and tries to talk her daughter out of it.

We learn that Jesse has epilepsy. This means she cannot keep a steady job and must have someone around at all times. She is divorced after being married to a man who never loved her. Her son from the marriage is a small-time thief and general "loser." Jesse has had severe depression for a long time.

Jesse sees her life as stagnant, with no hope of ever changing. There is little in her life that she can control, but she can certainly control her death. The play ends as she goes into her bedroom and locks the door. A moment later, we hear the sound of a gunshot.

Are foreign citizens counted in the calculation of GDP?

I assume that you are asking whether the income of a foreign citizen in a given country (for example, a Chinese citizen in the United States) would be counted as part of the GDP of the host country (the US).  If this is what you are asking, the answer is yes.  GDP (gross domestic product) does not take into account who makes goods or services or who owns the factories that make them.  It only takes into account where they are made.

When GDP is computed, every new good or service produced within the borders of a country is counted in that country’s GDP.  It does not matter who made the product or who owned the company that made it.  For example, Toyota, which is a company owned by Japanese people, has a factory in Kentucky.  All the money paid to workers in that factory counts towards US GDP.  It does not matter if the workers are from Kentucky or if they are managers who have come from Japan.

Thus, the income of a foreign citizen is counted in the GDP of the country where that person lives and works.

What is the theme of "Winter Dreams"?

Ambition is one prevalent theme in "Winter Dreams" by F. Scott Fitzgerald.

Dexter Green dreams of breaking free of his humble origins and becoming a part of the society of those who frequent the Sherry Island Golf Club, where he works as a caddy. In fact, it is his encounter with the imperious upper class young girl, Judy Jones, which precipitates this decision to follow the dictates of his "winter dreams," his ill-fated ambitions for the future.

After he quits his subservient job as a caddy in rebellion against his station in life, Dexter also declines a business course at the state university and goes instead to the East. There, at a prestigious university, Dexter entertains the hope of attaining social rank by his association with "glittering things and glittering people." After college, Dexter succeeds in becoming financially successful in the laundry business. However, he desires more in his ambition; so, before he reaches the age of twenty-seven, Dexter sells his business and moves to New York.

But, a couple of years before he sells his business, back in Minnesota Dexter accompanies the men for whom he once caddied in a round of golf at the Sherry Island Golf Club. While on the course, he again encounters the rich girl, whose "passionate quality of her eyes" and her imperious demeanor captivate Dexter. Now she is a young woman of arresting beauty and "passionate vitality." Indeed, Dexter perceives Judy as the embodiment of all that he envies. Therefore, his ambition now becomes the goal of capturing her. For, in doing so, Dexter feels that he will validate his claim as a member of the upper class.

However, this "Winter Dream," like the dream of wealth, proves itself false and costly as the selfish Judy later discards Dexter. For, wealth and social status are hollow dreams that cannot substitute for genuine relationships with people and genuine values that truly bring happiness and fulfillment to a person's life. Thus, Dexter Green's ambitions have been hollow ones. 

What is pick's disease?

Causes and Symptoms

Pick’s disease, also called frontotemporal dementia
(FTD), is similar to, but much rarer than, Alzheimer’s disease. The current designation of the syndrome groups together Pick’s disease, primary progressive aphasia, and semantic dementia. Some medical researchers believe that corticobasal degeneration and progressive supranuclear palsy should be added to FTD, which would then be called Pick complex. The differing terms reflect different theoretical models of the disease, and specialists are likely to continue to debate these models.

An autosomal dominant genetic trait is speculated as a specific cause in some cases of FTD. In these cases, there is a family history of someone showing symptoms of a frontal lobe dementia. Pick's disease is often inherited, though in many cases there is no evident family (genetic) history and the cause is unknown.

Onset is slow and insidious. Tissues shrink (atrophy) in the frontal and temporal brain lobes. FTD also causes some brain
cells to develop abnormal fibers called Pick’s bodies. The cells in these bodies have an abnormal amount of a protein called tau. Tau appears throughout the body’s cells but exists in abnormally high amounts in Pick’s bodies and in Pick cells that exist inside normal brain cells (neurons). These form elsewhere in the brain and are not limited to the frontotemporal regions. These fibers are generally straight and single, as compared to Alzheimer’s neurofibrillary tangles, which tend to be paired and helical.

Though Pick’s disease varies greatly in how it affects individuals, it has a common core or clusters of symptoms. Some or all may be present at different stages of the disease. Since the frontal lobes involve emotional and social functioning, the first notable cluster of symptoms usually causes behavioral and affective changes such as impulsivity, compulsive overeating or only eating one type of food, drinking alcohol to excess (when not a prior problem), rudeness, impatience, aggressiveness, social withdrawal, poor social interaction, inability to hold a job, inattention to personal hygiene, sexual exhibitionism, promiscuity, abrupt mood changes, emotional aloofness, environmental indifference, marked distractibility, decreased interest in daily activities, and being unaware of these changes (lack of insight). Deterioration in personality usually occurs before dementia itself is evident—that is, before there is evident memory loss. This is one way that specialists diagnose it as distinct from Alzheimer’s disease, in which the early symptoms involve memory loss.

Changes in physical mobility and coordination (apraxia) can also appear as early symptoms. They can include increased muscle rigidity or stiffness, difficulty getting around, worsening coordination, generalized weakness, and urinary incontinence.

Another characteristic cluster of symptoms relates to worsening language, including reduced-quality speech, shrinking vocabulary, word-finding problems, difficulty understanding speech (receptive aphasia) or producing understandable speech (expressive aphasia), repeating words and phrases others use (echolalia), progressive loss of reading and writing, and possibly complete loss of speech (mutism).

Treatment and Therapy

At present, there are no medications that can effectively treat FTD, although several can help treat many of its symptoms. Medications used in Alzheimer’s disease are not routinely prescribed because they often increase aggression in Pick’s disease patients.

Maximizing quality of life is the key treatment, and many of the more disturbing behaviors respond well to medication, including aggression and agitation. In addition to adding medications for symptom control, discontinuation of medications that promote confusion or that are not essential to the care of the person may improve cognitive function. It is common for anticholinergics, analgesics, and central nervous system depressants to be discontinued. Because many of the functions that FTD affects are also affected by low levels of thiamine, thiamine supplementation is often recommended.

Behavior modification is often the treatment of choice in controlling unacceptable or dangerous behaviors. Rewarding and reinforcing appropriate, positive behaviors while ignoring inappropriate, negative behaviors (within the bounds of safety) can significantly influence how patients act and interact. Formal psychotherapy is seldom effective because it overloads patients’ limited cognitive resources. Reality orientation, with repeated reinforcement of environmental and other cues, can reduce disorientation and agitation. Sensory functions, often overlooked, should be evaluated and augmented as needed, including hearing
aids, eyeglasses, and cataract surgery.

In addition, good nursing and caregiving, guided occupation activities, and participation in support groups all can improve the management of this type of dementia. Family counseling and family psychoeducation often go a long way in fostering adaptive changes that are necessary to care for patients at home. It is also important for families of Pick’s disease patients to obtain support to help them cope with a disease that is likely to have a prolonged, ever-demanding course. Visiting nurses or aides, volunteer services, adult protective services, and other community resources may be helpful in caring for the person. Legal advice may be appropriate early in the course of the disorder. Advance directives, power of attorney, health care proxy, and “do not resuscitate” orders can make dealing with the later stages of the disease easier.

Perspective and Prospects

Pick’s disease affects about 1 out of 100,000 people, accounting for 0.4 percent to 2.0 percent of all cases of dementia. More common in women then men, it typically has an onset between ages forty and sixty, with a modal age of fifty-four, but it has been known to affect patients as young as twenty. A family history of FTD is considered a risk factor, although most Pick’s patients have no family history of the disease.

The first description of the disease was published in 1892 by Arnold Pick. Until recently, it was thought that Pick’s disease could not be distinguished from Alzheimer’s disease during life. In accordance with major research criteria of German neuropsychiatry, Pick’s atrophy was constructed as a full-blown disease entity in the 1920s. This concept gained acceptance in the German and Anglo-American scientific community and was the starting point for further investigations in the 1950s and 1960s.

Initial diagnosis is mostly based on history and symptoms, signs, and tests and by ruling out other causes of dementia, especially those with metabolic causes. The development of neuropsychological assessment procedures and the use of electroencephalograms (EEGs), computed tomography (CT) scans, and magnetic resonance imaging (MRI) scans are generally necessary in the prediagnostic workup of the disease. Functional brain imaging, such as single photon emission computed tomography (SPECT) or positron emission tomography (PET) scans, are often appropriate in some patients.

Patients with FTD or Pick’s disease will show a progressive decline. Rapidly progressing forms may be fatal in two years; slower forms may take ten. The cause of death is often opportunistic infection or, less commonly, the general failure of total body systems.

Recent identification of pathogenic mutations in Alzheimer’s disease and frontotemporal dementia has improved understanding of these dementias and is guiding the investigations that use animal and tissue culture models. Eventually, it is hoped that this research will result in developing medications that can treat, stop, and reverse these diseases.

Bibliography:

Carson-DeWitt, Rosalyn, and Rimas Lukas. "Dementia." Health Library, Sept. 27, 2012.

Frederick, Justin, “Pick Disease: A Brief Overview.” Archives of Pathology and Laboratory Medicine 130 (July, 2006): 1063–1066.

"Frontotemporal Disorders: Information for Patients, Families, and Caregivers." National Institute on Aging, Mar. 13, 2013

Kertesz, Andrew, and David G. Munoz, “Frontotemporal Dementia.” Medical Clinics of North America 86 (2002): 501–518.

Jasmin, Luc, and David Zieve. "Pick's Disease." MedlinePlus, Feb. 16, 2012.

"NINDS Frontotemporal Dementia Information Page." National Institute of Neurological Disorders and Stroke, Mar. 20, 2013.

“Non-Alzheimer’s Forms of Dementia.” In The Mayo Clinic Guide to Alzheimer’s Disease: The Essential Resource for Treatment, Coping, and Caregiving. Rochester, Minn.: Mayo Clinic, 2005.

In "There Will Come Soft Rains," what conclusion can you draw from the text about what happened to the rest of the houses in the town?

The main house in "There Will Come Soft Rains" is the last functioning home in the city after a nuclear war.  This is evidenced both by the absence of people and by the revelation, at ten-fifteen, of silhouettes left in the charcoal dust on the side of the house.  At last, due to a storm, fire breaks out and consumes the house as there is no one left to fight the blaze.

Based on this example, it is reasonable to assume that other houses continued to function well, until some event that required human intervention occurred.

Also, though there is nothing left of the house save one wall and a lone voice, there are hints that the fire may have spread before dying down.  Towards the beginning of the scene, Bradbury writes, “It had sent flames outside the house” and, then, at the end, “A great quantity of smoke,” as though the fire still burned somewhere and would make its way to the other houses of the town.

We can conclude that without humans to stop, or repair damage from storms, fires, and malfunctions, the other houses will die, too.

How does a focus on the role of “chess players,” (America’s financial elite), alter the standard narrative of American history? What events...

There are a number of examples of decisions that were made in American history that were done to protect the elite class.  Howard Zinn dedicates an entire book on this very topic (A People's History of the United States.)  He begins his narrative with the birth of the United States and how the establishment instigated the conflict with Great Britain in an effort to create more wealth for themselves.  Most of the middling and lower classes in the colonies had very little to gain from independence from England.  They were essentially trading one elite group for the other.  For this reason, there was draft violence throughout the colonies as the lower classes were forced to fight this conflict.  He examines every American conflict in the same way:  they are fought to protect the interests of the powerful.  

The use of the American military throughout history to protect the interests of the wealthy needs be discussed when altering the standard narrative. History textbooks generally discuss American wars being fought to protect democracy and freedom around the world.  If you think about American involvement in World War I, it can be stated that American forces were sent to Europe to protect the interests of banks and munitions dealers that were creditors to the Allied Powers.  Congress itself drew the same conclusion in the 1920's (Nye Committee.)  The United States would commit to the same action a generation later in World War II when it instigated Japan to war in an effort to protect financial efforts in China.  The narrative continues into the Cold War and more recently with the War on Terror.  When you examine the acts of the United States through the lens of who benefits from different actions, the answer is usually the "chess players" that you reference in your question.  

**The link to the study guide below provides chapter summaries of the book that I have referenced.  There are countless examples of what you are looking for there.  

Where does Nick Carraway move to when he finds a job in his chosen profession?

In Chapter 1, Nick talks about learning the bond business in New York because, when he came back from World War I, he was "restless." Not knowing what to do or where to go (except away from the Midwest), Nick moves East, settling finally in West Egg, New York, the "less fashionable" of the two peninsulas jutting out into the bay. Nick admits "the practical thing was to find rooms in the city," but for some reason, West Egg calls to him, perhaps because it resembles more the countryside from whence he came. This location puts him in direct contact with Jay Gatbsy, his next-door neighbor on West Egg. Daisy Buchanan, Nick's cousin, lives across the bay with her husband Tom. Thus sets the scene for The Great Gatbsy.

In "The Devil and Tom Walker," Tom saw a man in the swamp. What did this man like most about Tom?

The man in the swamp probably likes Tom for having a fearless, tough attitude.

This happens near the beginning of the story. Tom is taking "an ill-chosen shortcut" through a dark and creepy patch of woods, so readers definitely know that something sinister is about to happen. As Tom meets the devil there--without fully realizing just yet who he is--he talks with him openly and in a relaxed manner.

As they talk, Tom realizes who the man is, and they make a deal. The narrator tells us that the devil has "conceived an especial kindness for him," meaning he has taken a special liking to Tom. Why?

The narrator never explains why, exactly, but we can make a good guess (an inference) based on this sentence from the text:

One would think that to meet with such a singular personage in this wild, lonely place would have shaken any man's nerves; but Tom was a hard-minded fellow, not easily daunted, and he had lived so long with a termagant wife that he did not even fear the devil.

So, what we know is that most people would be really freaked out if they suddenly met the devil. But Tom is so "hard-minded," so hard to scare, that he just chats with the devil as if he were an equal or a friend. His attitude seems to impress the devil enough for him to offer the deal--that is, the devil will tell Tom how to get incredible wealth, and in exchange, Tom will give the devil his soul.

What is dracunculiasis?

Definition

Dracunculiasis, or guinea worm disease (GWD), is caused by
the parasitic guinea worm, a long, thin worm that can grow inside humans.
Dracunculiasis affects people living in certain parts of rural Africa who drink
water contaminated by guinea worm larvae. GWD is one of the few diseases
specifically mentioned in the Bible, where it is called dracunculiasis
medinensis, or “fiery serpents.” An adult female worm can reach up to
three feet long.

Causes

People get dracunculiasis by drinking contaminated water infested with water fleas
that have ingested the guinea worm larvae. The guinea worms, usually female, move
through the body, and about one year later, protrude through the skin, usually on
the lower leg or feet, causing immense pain. At the site of protrusion, there is a
blister or an ulcer, and the worm can be seen emerging. Some people seek
relief by placing the infected area in open water (such as a pond, lake, or river)
that is used for drinking, which allows the female worms to release larvae into
the water and repeat the process of infestation.

Risk Factors

This disease tends to affect people living in rural or poorer communities in certain countries in Africa, where water sources are scarce and where drinking water most often comes from open, and exposed,sources.

Symptoms

Symptoms do not appear until about one year after a person has become infected
with dracunculiasis. When the guinea worm prepares to emerge from the
body, a person usually experiences intense pain and itching or burning, often
followed by nausea, vomiting, and fever. A blister forms at the site of where the
worm will emerge, leaving the person virtually incapacitated, sometimes for many
months, as the worm is gently pulled from the body and removed.

Screening and Diagnosis

There is no screening for dracunculiasis. A person does not know he or she has the disease until the worm begins to exit the body, about one year after contaminated water has been ingested.

Treatment and Therapy

Once the worm emerges at the site of the blister, it is pulled out in a slow and painful process; the infection is then cleaned. The only treatment for the infection is to help alleviate symptoms once the worm emerges.

Prevention and Outcomes

Preventive methods against dracunculiasis include using a cloth filter to remove water fleas from drinking water and to drink water from protected (closed) sources. Persons already infected with a dracunculiasis blister should not enter any water source that is used for drinking.

Although this disease was once widespread throughout Asia and Africa, public health experts and others are getting closer to eradicating the disease, aided by disease education and the use of chemicals to treat potentially unsafe drinking water.

Bibliography

Berger, Stephen A., and John S. Marr. Human Parasitic Diseases Sourcebook. Sudbury, Mass.: Jones and Bartlett, 2006.

Centers for Disease Control and Prevention. “Progress Toward Global Eradication of Dracunculiasis, January, 2008-June, 2009.” Morbidity and Mortality Weekly Report 58, no. 40 (2009): 1123-1125.

Muller, Ralph. Worms and Human Disease. 2d ed. New York: CABI, 2002.

Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Dracunculiasis: A Revised and Updated Directory for the Internet Age. San Diego, Calif.: Icon Health, 2002.

Roberts, Larry S., and John Janovy, Jr. Gerald D. Schmidt and Larry S. Roberts’ Foundations of Parasitology. 8th ed. Boston: McGraw-Hill, 2009.

Weedon, David. Skin Pathology. 3d ed. New York: Churchill Livingstone/Elsevier, 2010.

What is cysticercosis?

Definition

Cysticercosis is an infectious disease caused by the parasite
Taenia solium, which is a pork tapeworm.
This parasite invades the central nervous system and causes cysts to form
in various parts of the body, including the eyes, muscles, brain, and nervous
system. Cysticercosis is a major cause of epileptic seizures, especially in the developing world. Although the
prognosis is usually good, cysticercosis can lead to serious consequences,
including blindness, brain damage, and heart failure.

Causes

Cysticercosis is caused by ingestion of T. solium eggs, which are found in foods that have been contaminated or cooked improperly. Once consumed, the eggs hatch and their embryos penetrate the intestinal wall and enter the bloodstream.

Risk Factors

Risk factors for cysticercosis include eating meats, vegetables, or fruits that are contaminated with T. solium. Such contamination can occur if foods are not washed or cooked properly.

Symptoms

In many cases, cysticercosis does not produce symptoms. If the parasite invades
muscle tissue, lumps may be visible beneath the skin. If the eyes are involved,
symptoms may include blurred vision and detachment or swelling of the retina. If
the disease invades the nervous system, it is often accompanied
by seizures, headaches, brain swelling, and problems with balance.

Screening and Diagnosis

Establishing the diagnosis of cysticercosis can be challenging and requires
various tests. Blood tests can be used to detect antibodies to
T. solium. Imaging studies such as X rays, computed
tomography, ultrasonography, and magnetic resonance imaging can aid in visualizing
the cysts. Biopsies can be performed on infected tissue. Electroencephalographs
are useful if seizures are present. A spinal tap (lumbar puncture) may be
appropriate for some persons.

Treatment and Therapy

Consultation with an infectious disease specialist is highly recommended.
Treatment should be tailored to each patient, based on multiple factors, including
the symptoms, the stage of cyst development, and the site and quantity of cysts.
Treatment may involve corticosteroids, anticonvulsant
medications, and antiparasitic agents. Although antiparasitic agents are effective
for expelling parasites, they may produce a reactive localized inflammation.
Multiple courses of treatment may be needed to fully eliminate the cysts. If
seizures are present, referral to a neurologist is helpful for determining
appropriate therapy. In some cases, surgery or shunting may
be needed.

Prevention and Outcomes

Public education is extremely important for preventing cysticercosis. One should properly handle and cook food; fruits and vegetables should be washed thoroughly. One should not consume raw or undercooked pork. The risk of person-to-person transmission can be reduced by exercising good personal hygiene, including frequent handwashing. No vaccine against T. solium infection is available.

Bibliography

Garcia, H. H., et al. “Taenia solium Cysticercosis.” The Lancet 16 (2003): 547-556.

Icon Group. Cysticercosis: Webster’s Timeline History,1909-2007. San Diego, Calif.: Author, 2009.

Penrith, M. L. “Cysticercosis Working Group in Eastern and Southern Africa.” Journal of the South African Veterinary Association 80 (2009): 206-207.

Roberts, Larry S., and John Janovy, Jr. Gerald D. Schmidt and Larry S. Roberts’ Foundations of Parasitology. 8th ed. Boston: McGraw-Hill, 2009.

Singh, Gagandeep, and Sudesh Prabhakar. “Taenia solium.” Cysticercosis: From Basic to Clinical Science. Cambridge, Mass.: CAB International North America, 2002.

World Health Organization. “Taeniasis/Cysticercosis.” Available at http://www.who.int/zoonoses/diseases/ taeniasis.

Compare the Cretan and Mycenaean civilizations.

Two of the earliest civilizations in Europe existed in and around Greece. The Cretan or Minoan Civilization was probably the first European civilization. Archaeological remains point to a utopian-like civilization in which the socio-economic lines were blurred and warfare was not common. There was a high degree of sophistication in art and architecture on Crete during this period.

The Mycenaeans were from mainland Greece. They based their society on strict class lines and warfare. While the Minoans relied on a seaborne trade network for wealth, the Mycenaeans depended on their military and conquest. The city-states of mainland Greece were under constant threat of attack to the extent that they built their palaces inside a citadel with thick and high walls. There is very little evidence of this degree of warfare in the archaeological record of Crete. The two civilizations developed a linear script for keeping records. Both civilizations were dramatically impacted by earthquakes which led to their ultimate demise.

How would you compare Ekwefi's behavior when Ezinma is ill with Okonkwo's when Ikemefuna goes on his final journey?

In Chinua Achebe’s Things Fall Apart, Achebe portrays the disparate ways that Ekwefi and Okonkwo suffer in an interesting way that illustrates their singular personalities. Ekwefi is openly distressed when Ezinma falls ill and is on the verge of death. Out of ten pregnancies, Ezinma is Ekwefi’s only surviving child. Thus, she cherishes her child, and is terrified to find Ezinma violently ill:

“'Ezinma is dying,' came her voice, and all the tragedy and sorrow of her life were packed in those words” (76).

Similarly, Okonkwo suffers a great deal when he discovers that his adoptive son Ikemefuna has been condemned to die. However, he pushes aside these feelings, fearing that they are feminine and weak, and actually takes part in murdering the young man. Indeed, it is Okonkwo who lands the blow that kills Ikemefuna. After he has murdered Ikemefuna, Okonkwo falls into a deep depression. He questions why he feels this way:

“When did you become a shivering old woman... you, who are known in all the nine villages for your valor in war? How can a man who has killed five men in battle fall to pieces because he has added a boy to their number? Okonkwo, you have become a woman indeed” (65).

Thus, Achebe shows that Ekwefi is more willing to embrace her feelings than Okonkwo. Okonkwo is agonized by Ikemefuna’s death, but he believes that any emotion other than anger is a sign of weakness, so he pushes his feelings aside.

What is Caenorhabditis elegans?

The Organism

The nematode Caenorhabditis elegans (C. elegans) has been the subject of intense analysis by biologists around the world. Nematodes, or roundworms, are simple metazoan animals that have cells specialized to form tissues and organs such as nerve tissue and digestive tissue. Analysis of genetic control of the events that lead to the formation of the tissues in C. elegans has revealed biological mechanisms that also control the differentiation of tissues and organs in more complex organisms such as humans.

Caenorhabditis elegans is a microscopic, 1-millimeter-long roundworm that lives in soils and eats bacteria from decaying materials. It belongs to the phylum Nematoda (the roundworms), which includes many significant plant and animal parasites. Caenorhabditis elegans, however, is free-living (nonparasitic) and does not cause any human diseases. It exists as two sexes, males (containing a single X chromosome) and hermaphrodites
(containing two X chromosomes). Both male and hermaphrodite worms have five pairs of autosomal (non-sex) chromosomes. The hermaphrodites are self-fertile. They produce sperm first, which they store, and later “switch” gonads to begin producing eggs. These eggs may be fertilized by the hermaphrodite’s own sperm, or if the hermaphrodite mates with a male, sperm from the male will fertilize the eggs. A hermaphrodite that is not mated will lay approximately three hundred fertilized eggs in the first four days of adulthood; hermaphrodites that mate with males will continue to lay eggs as long as sperm are present.

Caenorhabditis elegans eggs begin development within the uterus. They hatch as small L1 larvae and molt four times as they proceed through the easily recognizable larval stages of L2, L3, L4, and adult. The adult hermaphrodite is a little larger than the adult male and can be distinguished by the presence of fertilized eggs lined up in the uterus. The smaller males have specialized tails that contain structures for mating called copulatory spicules.

A Model Organism

Because of its small size and simple diet (bacteria), C. elegans is easily adapted to laboratory culture conditions. The worms are grown on small agar-filled petri plates that are seeded with E. coli. The worms live comfortably at room temperature, but elevating or lowering the temperature can speed up or slow down development, and changes in temperatures can even reveal conditional phenotypes of some genetic mutations.

One unmated hermaphrodite will produce three hundred progeny over the first four days of adulthood. Additionally, C. elegans has a short generation time of approximately three weeks. Obtaining large numbers of progeny allows thorough statistical analysis of the way a mutation is segregated within a population. Because researchers can screen large numbers of worms in a short period of time, extremely rare mutations are likely to be revealed. Genetically “pure” strains are also quickly produced.

Hermaphrodite genetics also provides advantages. Because hermaphrodites are self-fertile, getting homozygous mutations is not difficult. A hermaphrodite that is heterozygous for a given mutation (has one wild-type copy of a gene and one mutated copy of a gene) will produce progeny, one-fourth containing two mutated copies of the gene (homozygotes). Additionally, for researchers studying mutations that affect reproduction or mating behavior, having self-fertile hermaphrodites allows them to maintain mutations that affect processes such as sperm production. A hermaphrodite that cannot make its own sperm can be mated to a wild-type male, and the mutation causing the defect can be maintained. This is not possible in organisms that are strictly male/female or that are strictly hermaphroditic.

Another strength of C. elegans is that the genetic strains can be frozen in liquid nitrogen and maintained indefinitely. Even fruit flies have to be constantly mated or “passaged” to maintain the genetic stocks for a laboratory. Caenorhabditis elegans strains are maintained in a central location, giving all scientists access to the same well-characterized genetic stocks.

Caenorhabditis elegans is a transparent worm, ideally suited for microscopic analysis. The origin and ultimate fate of every cell in the worm (the cell lineage) has been mapped and traced microscopically. Adult hermaphrodites have 959 somatic (non-sex) cell nuclei, and males have 1,021. Because the entire cell lineage for the worm is known and the worm is transparent, researchers can use a laser to destroy a single, specific cell and observe how loss of one cell affects development of the worm. These kinds of studies have contributed to the understanding of how neurons find target cells and how one cell can direct the fate of another.

Embryonic Development: Asymmetric Divisions

Research on C. elegans has revealed how programmed genetic factors (autonomous development) and cell-cell interactions guide development of an organism from egg to adult. The very first division of the fertilized egg (zygote) in C. elegans is asymmetric (uneven) and creates the first difference in the cells of the organism that is reflected in the adult. This division produces two daughter cells called P and AB. AB is a large cell that gives rise to tissues such as muscle and digestive tract. P is a much smaller cell that ultimately produces the cells that become the gonads (sex cell-producing tissues). The difference in P and AB is determined by the segregation of small P granules in the cell. The location of these granules and the asymmetry of this initial division are determined by the point of entry of the sperm. Until the eight-cell stage, there is no genetic activity by the embryo; the first few divisions are directed by the maternal gene products. This is one example of how maternal gene products can influence the early development of an embryo.

Neural Development

One of the areas of later development that is particularly well understood in C. elegans is the development of the nervous system. The nervous system has been completely reconstructed with serial electron micrographs that reveal precisely how one neuron connects to another. Some neurons migrate to assume their final cell fate and function. These migrations are easily studied in the worm because of its transparency, and a single neuron can be visualized by marking it with green fluorescent protein. Many genes and their encoded proteins that have been identified as important for directing the growth, connectivity, and migration of C. elegans neurons are highly conserved in evolution and control axon guidance in the vertebrate spinal cord.

Apoptosis: Programmed Cell Death

The 2002 Nobel Prize in Physiology or Medicine was awarded to Sydney Brenner,
H. Robert Horvitz, and John E. Sulston for research describing the regulation of organ development and programmed cell death. Cell death is an important part of development in plants and animals. For instance, human embryos have webbing between fingers and toes. This webbing is composed of cells that die in the course of normal development before a human baby is born. The death of these cells occurs because of a genetic program in the cells, apoptosis. The genes that control apoptosis are highly conserved throughout evolution. Apoptosis also plays a role in cancer. Often cancer is thought of as resulting from uncontrolled proliferation of cells, but it can also result when cells that should die during development fail to die. Scientists are looking at ways to specifically activate apoptosis in tumor cells in order to kill tumors. The clues for what genes to target for such treatments come, in part, from studies of the apoptosis pathway in organisms such as C. elegans.

A Molecular Tool

The first metazoan genome
that was sequenced was C. elegans. Many of the technologies (automated machines, chemistries for isolating and preparing DNA) that were developed in the course of the C. elegans genome-sequencing project were directly applied to the human genome sequencing project, and many of the scientists involved in sequencing the C. elegans genome contributed expertise to the Human Genome Project as well.

In 2008, Osamu Shimomura,
Martin Chalfie, and Roger Y. Tsien were awarded the Nobel Prize in Chemistry for the discovery and development of the green fluorescent protein (GFP). GFP is a protein originally isolated from jellyfish that glows bright green under ultraviolet light. Once the gene for GPP was isolated and cloned, researchers began using it as a “marker” to trace specific cell types. Chalfie first used this protein to identify six specific cells in C. elegans. GFP is now used in experiments to follow specific cells, such as migrating neurons during development, and in experiments that trace the transport or localization of proteins within cells. Researchers also have used GFP to “mark” tumor cells to trace their spread within an organism.

RNA interference (RNAi)
allows eukaryotic cells to degrade foreign RNA molecules, such as double-stranded RNA molecules from infecting viruses. The RNA molecule is cleaved into small fragments (approximately 23 nucleotide pairs), which can then bind to complementary RNA sequences within the cell and disrupt their expression. In 2006, C. elegans researchers Andrew Fire and Craig Mello were awarded the Nobel Prize in Physiology or Medicine for their work describing the mechanism of RNAi and showing that cleavage of the foreign double-stranded RNA could lead to specific suppression of gene expression. In the research laboratory, RNAi is used to specifically knock out expression of a target gene. This technique is useful for researchers working with human or other mammal cell culture systems because it does not require laborious cloning work. RNAi may also have therapeutic uses in knocking out expression of specific cancer-related genes in tumor cells.

Caenorhabditis elegans research identified the first presenilin, a class of proteins later implicated in Alzheimer’s disease. Research on the worm has led to a greater understanding of certain proteins that are involved in cellular aging. Studies in C. elegans are even contributing to a better understanding of learning and behavior. Most C. elegans scientists are studying the worm because it provides a tool for answering many of the hows and whys of biology that cannot be answered easily in more complex systems. The answers to seemingly esoteric questions, such as how C. elegans sperm move, will shed light on fundamental biological processes shared by all organisms.

Key Terms



apoptosis

:

a genetically programmed series of events that results in the death of a cell without affecting or damaging the surrounding cells and tissue; apoptosis can be triggered by events such as DNA damage or can be part of the normal development of an organ or tissue




cell differentiation

:

a process during which a cell specifically expresses certain genes, ultimately adopting its final cell fate to become a specific type of cell, such as a neuron, or undergoing programmed cell death (apoptosis)




model organism

:

an organism well suited for genetic research because it has a well-known genetic history, a short life cycle, and genetic variation between individuals in the population




RNA interference

:

a specialized type of RNA degradation in which foreign double-stranded RNA molecules stimulate the activity of an enzyme complex containing RNAse, which cleaves the RNA molecule into small fragments that can then bind to complementary RNA sequences and disrupt expression of specific genes





Bibliography

Alberts, B., et al. Molecular Biology of the Cell. 5th ed. New York: Garland Science, 2007. Print.

Bernards, R. “Exploring Uses of RNAi–Gene Knockdown and the Nobel Prize.” New England Journal of Medicine 355.23 (2006): 2391–3. Print.

Chang, K. “Three Chemists Win Nobel Prize.” New York Times. New York Times, 8 Oct. 2008. Web. 16 July 2014.

Lewin, Benjamin. Genes VII. New York: Oxford UP, 2001. Print.

Rothman, Joel H., and Andrew Singson. Caenorhabditis elegans: Cell Biology and Physiology. 2nd ed. Waltham: Academic, 2012. Print.

Schedl, Tim. Germ Cell Development in C. elegans. New York: Springer, 2013. Print.

Topper, Stephen, et al. "Alcohol Disinhibition of Behaviors in C. elegans." PLoS ONE 9.3 (2014): 1–9. Print.

Wood, W. B., et al. The Nematode “Caenorhabditis elegans.” Cold Spring Harbor: Cold Spring Harbor Laboratory, 1988. Print.

What shows the direction of energy transfer?

Energy can be in a multitude of forms and transferred in many ways, but for the purpose of this answer, I will focus on a main way that energy is transferred-- as heat.

The direction of energy transfer is always from objects that are hotter to objects that are colder.

There are three types of energy transfer:

• 
  Radiation: Radiation is the transmission of energy through empty space. Example: Energy from the sun is transferred by radiation.

• 
  Conduction: Conduction occurs when energy is transferred by collisions between particles. Materials that are good at transferring energy by conduction are called conductors. Example: Energy is transferred in copper metal through contact between individual copper atoms.

• 
  Convection: In convection, heat is transferred by the movement of mass within a fluid. The fluid can be a gas or a liquid. Example: In the atmosphere, warm air rises and cold air sinks.

When energy is transferred to an object, it becomes warmer. In order for an object to cool, energy must be removed.

What is digeorge syndrome?

Causes and Symptoms

Chromosomes possess two parts. The upper arms are called “p” arms and the lower arms are called “q” arms. Patients with DiGeorge syndrome are missing a tiny interstitial piece inside the long arm of chromosome 22. The specific region inside the long “q” arm is labeled 11.2. Thus, DiGeorge syndrome is also referred to as 22q11.2 deletion syndrome or chromosome 22 interstitial deletion.

Most microdeletions such as these cannot be observed under a microscope because they are so tiny. A molecular cytogenetic test known as fluorescence in situ hybridization (FISH) is used. It includes the use of deoxyribonucleic acid (DNA) probes made from the DiGeorge chromosomal region (DGCR). A green fluorescent probe is used to identify chromosome 22, while a red probe is specific to the DGCR. In DiGeorge syndrome, one of the chromosomes will lack the red fluorescence.

About 93 percent of patients have a spontaneous (de novo) deletion of a 22q11.2, and 7 percent have inherited the deletion from a parent. The very high de novo rate indicates that the deletion recurs with a high frequency as a result of new mutations occurring in the population. This deletion is inherited in an autosomal dominant manner. The offspring of persons with the deletion have a 50 percent chance of inheriting it. This interstitial deletion encompasses about three million base pairs of DNA in the majority of patients. About 90 percent of patients have the same three million base pair deletion, while 10 percent have a 1.5 million base pair deletion. Therefore, the deletion is large enough to contain nearly one hundred genes.

DiGeorge syndrome is initiated by defective embryonic development of the third and fourth pharyngeal pouches during the fifth week of development. These pouches normally become the thymus and the parathyroid glands. In the absence of a thymus, T lymphocyte maturation is stopped at the precell stage. DiGeorge syndrome is one of the most severe forms of deficient T cell immunity. Children with DiGeorge syndrome develop recurrent viral infections and have abnormal cellular immunity, as characterized by severely reduced or absent T lymphocytes. They also have defects in T cell–dependent antibody production. A spectrum of abnormal phenotypes may develop. These defects arise from the absence of key genes that are not available for normal development when a 22q microdeletion is present. Infants with this disease may suffer from congenital heart disease of various types, palatal abnormalities (such as cleft palate), and learning difficulties.

Treatment and Therapy

Children with a 22q11.2 deletion may exhibit a wide spectrum of problems and much variation in the severity of symptoms. A patient with DiGeorge syndrome may have several organs or systems affected. DiGeorge syndrome may result in problems in different body systems, such as the heart or palate, and in cognition, such as learning style. Consequently, a multidisciplinary approach is needed for management of a specific patient.

In the neonatal period, the following clinical and laboratory studies are pursued. The serum is tested for calcium; a low concentration points to the need for supplementation. The lymphocytes are measured; a low absolute count means referral to an immunologist, who will look at T and B cell subsets. A renal ultrasound examination should be performed because of the high incidence of structural renal abnormalities. A chest X-ray is needed to identify thoracic vertebral anomalies. A cardiac evaluation is recommended for all patients with DiGeorge syndrome because possible malformations may include tetralogy of Fallot, ventricular septal defect, interrupted aortic arch, or truncus arteriosus. Pediatric cardiologists are necessary for the treatment and therapy that is needed. An endocrinologist could follow up possible growth hormone deficiencies. Since there is a high incidence of speech and language delay, speech therapy and early educational intervention are highly recommended. All children with the 22q deletion should be seen by a cleft palate team to diagnose problems and schedule surgery if necessary.

Other medical needs of children are met through evaluation by a feeding specialist, especially in the newborn period; a neurologist, for possible seizure disorders or problems with balance; a urologist, for possible kidney problems; and an otorhinolaryngologist (ear, nose, and throat doctor) for problems in this region.

Perspective and Prospects

DiGeorge syndrome is relatively frequent, occurring with a frequency of one in four thousand live births. Therefore, this disorder is a significant health concern in the general population. Since the phenotype associated with it is broad and variable, many types of clinical and laboratory specialists are needed. The medical geneticist is the most likely person to have an overview of the diagnosis. A yearly genetics evaluation is beneficial in answering questions. Parents should be tested to determine their chromosomal status. Genetic counseling could provide individuals and families with information on the nature, inheritance, and implications of DiGeorge syndrome to help them make informed medical and personal decisions. Current and future research using model organisms may help to explain the problems of phenotypic variability in DiGeorge syndrome.

Bibliography:

American Academy of Allergy Asthma & Immunology. "DiGeorge Syndrome (DGS)." AAAAI, 2013.

Emanuel, Beverly S., et al. “The 22q11.2 Deletion Syndrome.” Advances in Pediatrics 48 (2001): 33–73.

King, Richard A., Jerome I. Rotter, and Arno G. Motulsky, eds. The Genetic Basis of Common Diseases. 2d ed. New York: Oxford UP, 2002.

Maroni, Gustavo. Molecular and Genetic Analysis of Human Traits. Malden, Mass.: Blackwell, 2001.

McCoy, Krisha. "DiGeorge Syndrome." Health Library, Dec. 11, 2012.

Rimoin, David L., et al., eds. Emery and Rimoin’s Principles and Practice of Medical Genetics. 5th ed. Philadelphia: Churchill, 2007.

Stocker, J. Thomas, and Louis P. Dehner, eds. Pediatric Pathology. 2d ed. Philadelphia: Lippincott, 2001.

Turnpenny, Peter, and Sian Ellard. Emery’s Elements of Medical Genetics. 13th ed. New York: Churchill, 2007.

How can I find the motivation behind the sponsors of the Keeping Children and Families Safe Act of 2003? I've scoured money trails, committee...

If you have a Westlaw account or know someone who will let you borrow theirs you might be successful in finding what you are looking for.  A local public library or a law school library is another good place to ask for permission to use their Westlaw account.  If you have any friends in law school, law students get free accounts with Westlaw and/or Lexis Nexis.  

I went to law school and many times when I was doing legal research for the purposes of interpreting a statute, simply reading the cases interpreting the statute wasn't enough, especially with newer statutes that had not yet been the subject of litigation.  WestlawNext allows you to research legislative history, which often contains meeting minutes of legislative bodies.  Their debate and discussion when they were creating the law can be very helpful in discerning its intent or motivation.  Although it is not binding precedent, many attorneys will refer to legislative history of a law in order to persuade the court that a certain interpretation of the law is correct and judges will often consider the "legislative intent" (e.g., the motivation) when making their ruling.

Hope this helps! 

What does Howard Zinn mean by the American "image in American high-school history textbooks, but not its record in world affairs?"

This question refers to Howard Zinn's influential book A People's History of the United States. Zinn suggests that American history books portray World War II as a "people's war" because of the overwhelming popular support that the war garnered. The quote you reference is from the beginning of Chapter Sixteen:

For the United States to step forward as a defender of helpless countries matched its image in American high school history textbooks, but not its record in world affairs.

Zinn believes that American textbooks attempt to portray the United States as the defender of freedom and democracy and the protector of weaker countries. The author feels that the true historical record of the United States has not always reflected what is depicted in the history books. The chapter gives a number of examples to demonstrate this disconnect.

• The United States government did not support the revolution in Haiti against the oppressive French imperialists.


• The Mexican-American War was instigated by the United States against a weaker power which resulted in Mexico losing significant land.


• America's imperial aims in the Pacific after the Spanish-American War including a war to acquire the Philippines.


• America's intervention in Cuba against the Spanish was meant to look like aid, but in reality the United States dominated the island until the 1950's.

These examples prove the United States does not always advocate for freedom and does not always protect weaker countries.  This is a stark contrast to the image of the United States that is forwarded by traditional American history textbooks.