What is a summary of "A Child's Thought" by Robert Louis Stevenson?

In his poem “A Child’s Thought,” Robert Louis Stevenson captures the musings of a seven-year child as he drifts off to his sleepy dreams. In the second stanza, he describes the child’s room as it sits the next morning.  The poem is written in couplets which provide a quick, child-like rhyming pattern.

The first stanza describes the young child’s dreams. The child sees castles, gardens, heroic horsemen, and ladies who need rescuing. There are “magic fruits” in the lush, imaginary land a seven-year conjures in his sleepy head.  

In the second stanza, Stephenson, describes how the child seeks that enchanted dreamland when he awakes. The child’s room is just as it should be with chairs, carpet, bath, and boots all in place. There are no gallant horsemen or damsels in distress.  It is the room of seven-year-old, not of his dreams.

What is Addison's disease? |

Causes and Symptoms

Anything that results in damage to the adrenal gland
has the potential to cause the development of Addison's disease. Most commonly, the disorder is the result of an autoimmune malfunction, in which the body begins to react against its own tissue. The disorder may also result from adrenal cancers or infections. The prevalence rate is approximately 1 per 100,000 people.

The specific cause of the adrenal insufficiency may be either primary or secondary. In the case of primary adrenal insufficiency, the disorder arises directly within the outer region of the adrenal gland, called the adrenal cortex. Most of the time, the disorder is associated with an autoimmune dysfunction in which the body produces antibodies against adrenal tissue. Over time, the adrenal cortex is destroyed and the secretion of glucorticoid, mineralocorticoid, and adrenogenic hormones, the products of the adrenal cortex, ceases. Another cause of primary adrenal insufficiency is bacterial infections, particularly those associated with tuberculosis. The first identification of the disease, described by Thomas Addison in 1855, was associated with a tuberculosis
infection in his patient. Other less common causes include fungal infections and malignancies.

Secondary adrenal insufficiency does not originate with the adrenal glands but rather is associated with abnormal regulation of adrenal hormone production, a function of the pituitary gland. Among the hormones produced within the pituitary gland is adrenocorticotropic hormone (ACTH), which stimulates glucocorticoid production by the adrenal cortex. Insufficient ACTH production results in a decrease in corticoid secretion. Any damage to the pituitary (or the hypothalamus, which actually regulates ACTH production by the pituitary) has the potential to affect ACTH production indirectly.

With Addison’s disease, the onset of symptoms is gradual and can easily be overlooked or misdiagnosed during the early stages of the disease. Initially, the person may exhibit extreme fatigue, low blood pressure, and loss of appetite. The person may faint upon standing. Severe diarrhea and vomiting are also common. As a result of salt loss, the person may crave salty foods. Severe expression of such symptoms is referred to as an Addisonian crisis; if untreated, it may be life-threatening. Because the production of ACTH itself is regulated by corticosteroid production in a feedback mechanism, reduced adrenal function results in increased levels of ACTH. This in turn can produce skin changes, particularly a darkening which mimics that of deep tanning. The presence of darkening equally over both exposed and unexposed skin can be indicative of Addison’s disease, particularly if other symptoms are also present.

A definitive diagnosis of Addison's disease is based upon a series of blood and urine tests. Patients may exhibit abnormally high levels of potassium, a potentially life-threatening situation, or a low level of sodium. More definitive tests measure the concentration of corticol hormones in the urine. Because ACTH production is controlled by corticosteroid concentrations, an increase in blood ACTH may also be observed. The definitive test begins with the intravenous injection of ACTH. Cortisol levels in the blood are then measured over a one-hour period. If cortisol levels do not change, this result is indicative of a likely adrenal insufficiency.

Treatment and Therapy

The treatment of Addison's disease generally involves replacing the hormones that the adrenal cortex is no longer manufacturing. Oral medication is available for most of these hormones, though dietary changes may also be necessary. For example, if the mineralocorticoid aldosterone is insufficient, resulting in a salt imbalance, then patients taking aldosterone supplements may also be advised to increase the salt content of their food.

Other forms of treatment may be symptomatic. If the patient suffers from low blood pressure or severe salt imbalances, conditions that are potentially life-threatening, then intravenous medication may be necessary.

As the monitoring of potassium and sodium levels is critical, it is generally recommended that patients routinely visit their physicians. It is important that a patient exhibiting symptoms of an Addisonian crisis (vomiting, diarrhea) receive immediate salt replacement and probably hydrocortisone as well.

Because secondary adrenal deficiency most often originates in the pituitary gland, the primary result is a decrease in ACTH production. In turn, the adrenal cortex is deficient only in the production of cortisol. Treatment generally involves the oral replacement of cortisol, often in the form of synthetic prednisone.

Perspective and Prospects

Addison's disease is a lifelong, chronic condition. While in the past it was often a life-threatening disorder, proper monitoring and hormone replacement can allow most people with the disease to live relatively normal lives with no restrictions. Because in most individuals the immediate cause is an autoimmune disorder, it is possible that eventually stem cell research, along with improved methods of controlling autoimmune phenomena, will provide a means for replacing adrenal tissue.

Bibliography:

Bar, Robert, ed. Early Diagnosis and Treatment of Endocrine Disorders. Totowa, N.J.: Humana Press, 2003.

Besser, G. Michael, and Michael Thorner, eds. Clinical Endocrinology. 2d ed. St. Louis, Mo.: Gower-Mosby, 1994.

Greenspan, Francis S., Dolores M. Shoback, and David G. Gardner, eds. Greenspan’s Basic and Clinical Endocrinology. 8th ed. New York: McGraw-Hill, 2007.

Kronenberg, Henry M., et al., eds. Williams Textbook of Endocrinology. 11th ed. Philadelphia: Saunders/Elsevier, 2008.

MedlinePlus. "Addison Disease." MedlinePlus, Apr. 8, 2013 (reviewed May 2, 2012)..

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

Rennert, Nancy J., MD. "Addison's Disease." MedlinePlus, Dec. 11, 2011.

How did Anne Frank describe herself?

Anne Frank described herself as "a bundle of contradictions." In her last diary entry from Tuesday, August 1, 1944, she states that she rejects other people's opinions of her and that she often feels like she knows best and must have the last word in a conversation or fight; she recognizes that these are antagonistic and unpleasant characteristics. That being said, Anne also recognizes that she has many good qualities, including a sense of cheerfulness,...

Anne Frank described herself as "a bundle of contradictions." In her last diary entry from Tuesday, August 1, 1944, she states that she rejects other people's opinions of her and that she often feels like she knows best and must have the last word in a conversation or fight; she recognizes that these are antagonistic and unpleasant characteristics. That being said, Anne also recognizes that she has many good qualities, including a sense of cheerfulness, the ability to find joy in the world around her, and an appreciation for humor and lightness.

Anne sees these contradictions as rivaling components of herself and is fearful that she will be rejected or labeled as "ridiculous and sentimental" if she shows the world her vulnerability and sensitivity. Anne has a reputation of "being boy-crazy as well as a flirt, a smart aleck and a reader of romances," who "laughs, gives a flippant reply, shrugs her shoulders and pretends she doesn't give a darn." She thinks of her inner self as deeper, purer, but also weaker; the nice Anne has "never made a single appearance, though she almost always takes the stage when [she is] alone." 

Anne describes this back-and-forth best as follows:

If I'm being completely honest, I'll have to admit that it does matter to me, that I am trying very hard to change myself, but that I'm always up against a more powerful enemy.

This enemy is Anne's public persona: the girl who rivals the sensitive and thoughtful young woman who is revealed in her diary. 

Who is Dr. Webster Civit in The Great Gatsby?

In chapter seven, Tom and Daisy join Nick and Jordan at a party at Gatsby's home.  They gather at "a particularly tipsy table" where a guest, Miss Baedecker, is so drunk that she tries to slump against Nick's shoulder.  She had apparently been yelling, and some of the guests had ducked her head in Gatsby's swimming pool to try to sober her up.  Doc Civet, also a guest at the party, is summoned.  He suggests...

In chapter seven, Tom and Daisy join Nick and Jordan at a party at Gatsby's home.  They gather at "a particularly tipsy table" where a guest, Miss Baedecker, is so drunk that she tries to slump against Nick's shoulder.  She had apparently been yelling, and some of the guests had ducked her head in Gatsby's swimming pool to try to sober her up.  Doc Civet, also a guest at the party, is summoned.  He suggests to Miss Baedecker "you ought to leave it alone," meaning that she should stop drinking.  She rudely tells the doctor "Speak for yourself! Your hand shakes. I wouldn't let you operate on me!"  Earlier, in chapter four, Nick recalls that Doctor Webster Civet "drowned last summer up in Maine", which presumably was later this same summer of 1922.

Shortly thereafter, Nick observes "it was like that" to understate that the party was full of unsavory behavior and antics that ultimately appall and offend Daisy.

In Rand's Anthem, what resolution does Equality make after he and Liberty finally speak for the first time?

Equality and Liberty make eye contact for days before they are able to speak to each other. When they finally do speak, Equality asks how old Liberty is. When she tells him that she is seventeen, he feels relieved and possessive at the same time. He first feels relief because this means that she has not gone to the Palace of Mating, yet. Next, he becomes possessive because he wants Liberty all to himself. He...

Equality and Liberty make eye contact for days before they are able to speak to each other. When they finally do speak, Equality asks how old Liberty is. When she tells him that she is seventeen, he feels relieved and possessive at the same time. He first feels relief because this means that she has not gone to the Palace of Mating, yet. Next, he becomes possessive because he wants Liberty all to himself. He can't stand the thought of someone else touching the woman he wants. Finally, he experiences confusion because he doesn't understand these new feelings. He has been taught throughout his life not to feel any emotional connection with other people; thus, he isn't sure what to do next. What he does think is explained in the following passage:

"And we thought that we would not let the Golden One be sent to the Palace. How to prevent it, how to bar the will of the Councils, we knew not, but we knew suddenly that we would" (44).

Therefore, Equality resolves to stop the Council from forcing Liberty to go to the Palace of Mating when she turns eighteen. This resolution is significant because it is the motivation he needs to rebel against the government. Equality winds up fighting for the freedom to explore his own educational interests, the freedom to love whom he wants, and the freedom to live the life he chooses. 

What is angioplasty? |

Indications and Procedures

Angioplasty, particularly balloon angioplasty, may be performed on any blocked or narrowed blood vessel, such as in the legs, but it is most commonly used to open heart vessels blocked by coronary artery disease.

Worldwide, an estimated seventeen million people die each year from cardiovascular disease, a condition often signaled by chest pain known as angina pectoris. Other symptoms include shortness of breath, heart palpitations, or an actual heart attack. Probable causes of heart disease can be diagnosed by stress tests and angiography
. If the cause is blockage of the coronary arteries, the cardiologist may order angioplasty to open the blocked vessels and restore a better blood flow to the heart.

The patient cannot eat or drink anything after midnight the day before the procedure is to be performed. A mild sedative may be given. The site for insertion of the catheter, often the inside of the elbow or the groin, is shaved and is cleaned with an antiseptic solution. A local anesthetic is injected at the insertion site, but the patient remains awake during the procedure. The surgeon makes a small opening in the skin at the insertion site, inserts the catheter into an artery, watches the progress of the catheter on an x-ray monitor, and guides the tip into the blocked arteries.

In balloon angioplasty, the most common type, the tube is equipped with a balloon. Once the tip is in place in the blocked area, the balloon is inflated and deflated several times in order to compress the fatty material (plaque) and increase blood flow through the artery. The catheter then is slowly withdrawn.

If the arm site was used, the small incision is stitched closed. If the groin site was used, the puncture opening is closed with pressure. A dressing is applied to the insertion site. Barring any complications, the patient may return home later the same day or the next day.

Uses and Complications

The cardiac catheters used in angioplasty can also remove plaque with special cutting or laser tips. The balloon tip may be used to place a stent, a metal mesh tube that is placed permanently in the coronary artery to keep it open. Blood thinning medication may be prescribed to keep blood from clotting on the stent and closing it.

About 80 percent of the angioplasty treatments are successful, with the patient being able to resume a reasonably normal lifestyle and enjoy a good quality of life. Complications of coronary artery angioplasty seldom occur, but they may include bleeding or clotting, an abnormal heartbeat, perforation of the heart muscle or artery, and, rarely, a heart attack, stroke, or even death.

Bibliography

American Heart Association. AHA Focus Series: Arteriosclerosis. Washington, D.C.: American Heart Association, 1988.

"Angioplasty and Stent Placement—Heart." Medline Plus, August 24, 2012.

"Coronary Angioplasty." Health Library, February 7, 2013.

McGoon, M. The Mayo Clinic Heart Book. 2d ed. New York: William Morrow, 2000.

Ohman, Magnus, Gail Folger Cox, and Victoria K. Folger. So You’re Having a Heart Cath and Angioplasty. Hoboken, N.J.: John Wiley & Sons, 2003.

Rutherford, Robert B., ed. Vascular Surgery. 7th ed. Philadelphia: Saunders/Elsevier, 2010.

Tcheng, James E. Primary Angioplasty in Acute Myocardial Infarction. Totowa, N.J.: Humana Press, 2002.

"What Is Coronary Angioplasty?" National Heart, Lung, and Blood Institute, February 1, 2012.

What is a mastectomy, and what is a lumpectomy?

Indications and Procedures

The early indications of breast cancer are often quite subtle, although in this stage it may be revealed by routine mammograms. In some cases, no overt symptoms exist until the cancer is well advanced. Women between forty and fifty years of age without risk factors are advised to have a mammogram every two years. Women over fifty or in the high-risk category because of a family history of breast cancer should have a mammogram once every year. If palpation of the breast reveals a lump, then immediate mammography is indicated.

It is necessary to be constantly vigilant for any sign that an abnormality exists in the breast. Clear indications of possible breast cancer include lumps or thickening of the tissue in the breast or in the area under the arms. Symptoms such as discoloration of the breasts or dimpling, thickening, scaling, or puckering of one or both breasts may also arouse suspicion of breast cancer. A significant change in the shape of the breast or a swelling of it are also symptomatic. A bloody discharge from the nipple, scaly skin on the nipple or surrounding area, inversion of the nipple, or discoloration of the area surrounding the nipple may presage the presence of breast cancer.

Monthly palpation of the breasts, preferably seven or eight days after menstruation, may reveal lumps that could be harmless growths but that might be cancerous. This procedure is referred to as breast self-examination (BSE). Because the female breast contains many glands, it is not uncommon in some women for lumps to appear regularly—often profusely—particularly in the week prior to menstruation. Women with notably lumpy breasts are said to have fibrocystic breasts. Often, the lumps diminish in size in the week following menstruation. If they do not recede, however, then these lumps should be regarded with suspicion and the patient should be examined by a physician, preferably a surgeon, gynecologist, or oncologist.

Once a problem is detected, a number of procedures must be considered for dealing with it. The initial procedure in treating suspected breast cancer usually involves a mammogram to reveal irregularities in the breast. If the results of the mammogram are negative and the patient is still convinced that there is a lump in the breast, an ultrasound or sonographic examination may be indicated. In such tests, harmless sound waves are focused on the breast. These sound waves are reflected so that they create an image of formations within the breast. Although ultrasound cannot definitively indicate whether a lump is cancerous, it can at least verify whether a lump exists. It can also show whether the lump is hollow and filled with fluid, in which case it is usually a benign cyst rather than a cancerous growth.

If a growth is detected, the next, least-invasive means of determining whether it is cancerous is through a needle biopsy.
In this procedure, the patient, under local anesthetic, has a hollow needle inserted into the growth. Fluids and cells are then harvested from it. If the growth is a cyst,
a clear or light yellow fluid will be withdrawn, causing the cyst to collapse. This may be all the treatment required. In all cases, however, the substances withdrawn from the growth are examined by a pathologist for the presence of cancer cells.

Not all growths are so positioned that needle biopsies are possible. In such cases, a surgical biopsy is probably necessary. If the lump is small, then a lumpectomy, or the removal of the entire lump, may occur. Larger lumps often cannot be removed at this stage, so portions are excised for pathological examination. A pathologist carefully studies the tissue removed to determine whether it contains cancer cells.

In the past, biopsies often occurred while patients were anesthetized and, if the pathological report was positive for cancer, then a radical mastectomy was performed immediately while the patient was still under anesthetic. Since the late twentieth century, however, a two-step procedure has usually replaced this one-step method. If cancer is detected, then surgery is delayed, giving physicians the opportunity to consult with their patients about the treatments available to them.

The major decision in such cases usually is whether a total mastectomy or a partial mastectomy, commonly referred to as a lumpectomy, should be performed. Total mastectomy involves the total removal of the breast and the surrounding lymph nodes.

A radical mastectomy, done under general anesthetic, involves making a large, elliptical incision on the breast, including the nipple and often the entire breast. The incision normally extends into the armpit. All the breast tissue is excised, including the skin and the fat down to the chest
muscles. The incision extends into the armpit to remove as much of the breast tissue as possible, including the lymph nodes, which may be cancerous. Once the bleeding has been controlled, a drainage tube is inserted and the incision is closed with sutures, clips, or adhesive substances.

This drastic form of treatment can be traumatic both physically and psychologically to patients. Many women fear the disfigurement that follows it. Some women, especially those with a family history of breast cancer, may decide that the total removal of the breast is their safest option. In some cases, to prevent future threats of breast cancer, they demand the removal of both breasts.

A lumpectomy, usually performed under local anesthetic, involves the removal only of cancerous tissue. The incision is made under the breast, and the lump, with surrounding tissue, is removed. The appearance of the breast remains much the same as it was before the surgery. In some cases, physicians recommend a quadrantectomy, which involves the removal of the cancerous tissue as well as significant amounts of the surrounding tissue. Quite often, the lymph nodes are removed as well. When this treatment is used, the breast will appear slightly smaller than it previously was, but it can be enhanced through plastic surgery.

Subcutaneous mastectomy is frequently indicated in situations in which the tumor is small. In this procedure, the surgeon makes an incision under the breast. Most of the skin and the nipple remain intact, although the milk ducts that lead into the nipple are cut. Following the surgery, sometimes immediately, a breast implant can be inserted, restoring the breast to its normal appearance. Mastectomy and lumpectomy are routinely followed by a course of radiation and/or chemotherapy designed to kill any fugitive cancer cells that the surgery has missed.

While the goal of mastectomy is to create as little scarring as possible, considerable scarring may occur, particularly with radical mastectomy, and the absence of one or both breasts usually requires significant psychological adjustments on the part of women who have undergone the procedure. The breast reconstruction performed by a plastic surgeon following a mastectomy is often accompanied by treatment from a psychologist or psychiatrist.

Some women with family histories of breast cancer, particularly if the disease has occurred in first-level relatives (mother or sisters), may opt for a mastectomy rather than a lumpectomy to relieve themselves of the fear of contracting the disease, although most oncologists make such women fully aware of other, less drastic procedures available to them.

Certainly a consideration in reaching a decision about whether to have a lumpectomy or the more drastic mastectomy must include many factors. High on the list of such factors is heredity. In many patients who suffer from this disease, BRCA1
and BRCA2, mutated genes, are an early indication that breast cancer may eventually occur. The BRCA gene is frequently present in the female members of families with histories of breast cancer and ovarian cancer. About 85 percent of women with the BRCA gene will develop breast cancer if they live a normal life span. Women who have the BRCA gene may decide to have a prophylactic mastectomy before symptoms occur, although many women in this situation prefer treatment with tamoxifen, which appears to hold breast cancer at bay.

Advances in treating cancers of all kinds progressed rapidly during the last half of the twentieth century, and even greater impetus characterizes current advances. The four major treatments—often used in combination with each other—are surgery, radiation therapy, chemotherapy, and hormonal therapy. In the treatment of breast cancer, radiation may be used initially to shrink existing tumors that, once reduced in size, will be removed surgically. However, when surgeons remove cancerous tumors, they also remove large numbers of surrounding cells that might be affected; such a procedure is usually followed by additional radiation aimed at killing any lingering cancer cells the surgery has missed.

Uses and Complications

The salient use of surgery in cases of breast cancer is to remove its source, not only clearing away any tumors that may be found but also removing additional cancerous tissue as well as lymph nodes that might be affected.

Cancer cells can exist either in the breast’s lobules, which contain the cells that produce milk, or in the ducts that carry the milk to the nipples. Cancer cells in either of these locations can be of two types, invasive or noninvasive (also called in situ). The major complication with invasive cancer is that it can and usually does metastasize, spreading often to the lymph nodes, into the lungs and to other parts of the body. In such cases, a radical mastectomy is indicated. It must be performed as quickly as possible and followed by a strenuous course that typically includes radiation or chemotherapy. Noninvasive cancer is less likely to metastasize, although it sometimes does. Lumpectomy or quadrantectomy is often used to treat such cancers, but these procedures must be followed by close monitoring over the rest of the patient’s life and by radiation or chemotherapy following surgery.

Chemotherapy is used less often than radiation in the postsurgical treatment of breast cancer but is occasionally used along with it. Some physicians use anticancer drugs to reduce the possibility of recurrence. This treatment, as well as hormone treatment, is designed to kill any fugitive cancer cells that have strayed from the immediate site of the cancer that has been removed. Whereas surgery and radiation are local, affecting only the part of the body being focused upon, chemotherapy is systemic: the drugs used in chemotherapy travel through the bloodstream to all parts of the body. The disadvantage of chemotherapy is that it nearly always has significant side effects. In rare cases, complications are so extreme that they result in death. Usually, chemotherapy is indicated only for women who have not yet undergone the menopause and whose tumors are an inch or larger in size. It may also be employed in cases in which the patient’s tumor shows signs of growing rapidly and aggressively invading and attacking other parts of the body.

Related to chemotherapy is hormonal therapy.
Hormones
are chemicals produced by the body for various purposes. For example, when one is under sudden, undue stress, the body produces adrenaline, which provides a rush of energy and causes the heartbeat to accelerate. In women, the body produces estrogen every month during the menstrual cycle. Estrogen causes the cells in the milk ducts and lobules to grow in preparation for pregnancy. This chemical stimulates the growth of normal cells but can also stimulate the growth of cancer cells. Hormonal therapy is systemic. It involves introducing into the bloodstream a synthetic chemical, usually tamoxifen, which makes it impossible for the body’s natural estrogen to find its way to cancer cells that would be nourished by it. A complete biopsy report can determine whether hormonal therapy is appropriate in individual cases.

Perspective and Prospects

Until the middle of the twentieth century, a diagnosis of cancer, particularly of breast cancer, was viewed as a death sentence. Diagnosis generally occurred after the cancer had metastasized. In the first half of the century, general practitioners were much more prevalent than the specialists who, working as a team, are now generally mustered to provide cancer treatment once a diagnosis is made.

With the proliferation of sophisticated medical equipment, including the highly sensitive X-ray machines used in mammography and the various forms of ultrasound and sonograph equipment that are part of nearly every hospital’s arsenal of diagnostic equipment, an increasing number of cancers are discovered before they become symptomatic, so that they can be treated with considerable success.

Historically, mastectomies have been performed for centuries. President John Adams’s daughter underwent this excruciating surgery early in the nineteenth century, enduring this procedure without the benefit of anesthesia. As was usually true in such cases, the surgery extended her life for only a little while because her cancer was discovered in an advanced stage and had metastasized.

By the late nineteenth and early twentieth centuries, accepted treatment for breast cancer was a radical mastectomy that involved the removal of the affected breast and of as many surrounding cancer cells and lymph nodes as possible. William Halsted, a pioneer in the field of breast cancer surgery and a professor of surgery at the highly respected Johns Hopkins University Medical School, championed the cause of the radical mastectomy, which he viewed as a procedure that could extend substantially the survival of his patients. Little was said about curing breast cancer patients of their cancers. The radical surgery that physicians across the country performed following Halsted’s lead was viewed simply as a means of adding months or years to the life of the cancer patient. Until 1970, about 70 percent of women in the United States who had breast cancer were subjected to radical mastectomy.

Several factors brought about a major change in the treatment of breast cancer during the 1960s and 1970s, when social activism was very much in the forefront of American life. Feminists pointed out that most of the surgeons treating breast cancer were men. As an increasing number of women entered medical schools and eventually established medical practices, greater attention was paid to treating breast cancer in less disfiguring ways than had been common earlier.

Along with this change came advances in medical technology that made early diagnosis and more focused treatment a reality. As the chemical treatment of all cancers came to be better understood and more widely employed, the focus was more on preventing and curing cancer than on merely prolonging the lives of those who suffered from it.

Laboratory tests for detecting a woman’s predisposition for breast cancer have become increasingly sophisticated and accurate. Where the BRCA1 or BRCA2 gene is present, the possibility of developing breast cancer is greatly increased; women shown to possess this gene have been made more vigilant than ever before in monitoring their conditions and in seeking immediate medical intervention if even the slightest symptom appears.

Shortly after the end of World War II, some oncologists rejected Halsted’s emphasis on radical mastectomy. Surgeon Jerome Urban garnered numerous followers in his call for superradical surgeries in cancer cases. His procedures involved the removal of ribs, various internal organs, and even limbs in order to find and destroy every cancer cell. Surgeon Bernard Fisher stood in opposition to Urban, championing the effectiveness of smaller surgeries, such as the simple mastectomy, which involved the removal of one breast but not of all the lymph nodes and, in some cases, the lumpectomy, involving the removal only of the tumor and its surrounding cells.

The lumpectomy has gained acceptance through the intervening years. It is less disfiguring than either the radical or the simple mastectomy, leaving only a small scar on the underside of the breast. In cases where lumpectomy is viewed as a viable option, survival rates and cure rates are comparable to those of patients who have undergone more radical surgery.

Advances in medical science are accelerating substantially. Stem cell research offers great promise in the treatment and cure of diseases such as breast cancer. Researchers appear to be on the threshold of developing cells designed to destroy specific errant cells, such as those that cause cancer, while leaving healthy cells intact.

Bibliography

Abouzied, Mohei. "Lumpectomy." Health Library, Nov. 26, 2012.

"Breast Cancer." MedlinePlus, June 12, 2013.

Chisholm, Andrea. "Mastectomy." Health Library, Oct. 31, 2012.

Fowble, Barbara, et al. Breast Cancer Treatment: A Comprehensive Guide to Management. St. Louis: Mosby Year Book, 1991.

Friedewald, Vincent, and Aman U. Buzdar, with Michael Bokulich. Ask the Doctor: Breast Cancer. Kansas City, Mo.: Andrews McMeel, 1997.

Hirshaut, Yashar, and Peter I. Pressman. Breast Cancer: The Complete Guide. 5th ed. New York: Bantam Books, 2008.

Lange, Vladimir. Be a Survivor: Your Guide to Breast Cancer Treatment. 5th rev. ed. Los Angeles: Lange Productions, 2010.

Lerner, Barron H. The Breast Cancer Wars: Hope, Fear, and the Pursuit of a Cure in Twentieth-Century America. New York: Oxford University Press, 2001.

Link, John S. The Breast Cancer Survival Manual: A Step-by-Step Guide. 5th ed. New York: Henry Holt, 2012.

"Mastectomy." MedlinePlus, May 24, 2013.

Mayer, Musa. Examining Myself. London: Faber & Faber, 1994.

Morris, Peter J., and William C. Wood, eds. Oxford Textbook of Surgery. 2d ed. New York: Oxford University Press, 2000.

Phippen, Mark L., and Maryann Papanier Wells, eds. Patient Care During Operative and Invasive Procedures. Philadelphia: W. B. Saunders, 2000.

Sproul, Amy, ed. A Breast Cancer Journey: Your Personal Guidebook. 2d ed. Atlanta: American Cancer Society, 2004.

"Surgery for Breast Cancer." American Cancer Society, Feb. 26, 2013.

Sutton, Amy L., ed. Breast Cancer Sourcebook: Basic Consumer Health Information About Breast Cancer. 4th ed. Detroit: Omnigraphics, 2012.

How does Shakespeare's Macbeth show us a true leader should not resort to the misuse of power?

Shakespeare's Macbeth shows us the beginning and end of Macbeth's downfall once he embraces evil. 

At the beginning of the play, Macbeth is a loyal and valiant warrior, praised by everyone, including the king of Scotland. He is given honors for his honesty and bravery, and our first impression is that things could not go better for Macbeth. 

Once we examine Macbeth more closely in his soliloquies, however, we begin to understand he harbors some...

Shakespeare's Macbeth shows us the beginning and end of Macbeth's downfall once he embraces evil. 

At the beginning of the play, Macbeth is a loyal and valiant warrior, praised by everyone, including the king of Scotland. He is given honors for his honesty and bravery, and our first impression is that things could not go better for Macbeth. 

Once we examine Macbeth more closely in his soliloquies, however, we begin to understand he harbors some perilous ambitions which could change his life for good. His tragic flaw is his unrestrained ambition because he is ready to cast aside all the true values for the sake of gratifying his needs. He knows that in order to become the king, he must resort to the most illegal means—he must kill Duncan. 

When Macbeth murders the king with his manipulative wife's help, his life begins to change for the worse. He manages to fulfill his ambition of taking the throne, but he loses other people's support and his own inner peace, stability, and compassion. He turns into an evil murderer, ready to have anyone assassinated if doing so will ensure his security.

Macbeth's abuse of power leads to his own downfall. Macbeth is anything but powerful; he becomes obsessed with protecting himself because he knows he took the throne illegally. His conscience begins to haunt him because of all the misdeeds he committed.  

Once he accepts evil, Macbeth voluntarily deprives himself of the opportunity to lead a meaningful life. Not only is Macbeth defeated at the end of the play, he also realizes his life has become "a tale told by an idiot, full of sound and fury, signifying nothing."

What is mitral valve prolapse?

Causes and Symptoms

The mitral valve connects the heart’s left ventricle and left atrium. The oxygenated blood, having already passed through the right heart chambers and the lungs, arrives in the left atrium through the pulmonary
veins and then passes through the mitral valve into the left ventricle. Compression of the left ventricle pumps the blood into the aorta and on to the rest of the body. A properly functioning mitral valve closes and prevents regurgitation or backflow into the left atrium. Mitral valve prolapse occurs when the two leaves of the mitral valve close imperfectly, allowing leakage. This condition, known also as mitral valve insufficiency prolapse, is the most common cardiac syndrome. Found in all segments of society, it is most common in young adult women.

Mitral valve prolapse has several possible causes including rheumatic fever, inflammation of the heart lining (endocarditis), cardiac tumors, or most often, genetic error. Its symptoms are undue fatigue after exercise, shortness of breath, and chest pain. Other common complaints are anxiety, depression, and panic, all related to stress. The number of diagnosed cases in Western countries is rising markedly and may be the result of more sophisticated diagnostic techniques or the increasing stress in modern society.

Perspective and Prospects

Until the 1960s, the detection of mitral valve prolapse was through a characteristic “click” heard by the physician when the mitral leaves attempted to close. Now the use of echocardiograms, allowing ultrasound images of the beating heart and blood flow, is standard practice.

People with mitral valve prolapse lead a normal life, and many are unaware that they have the condition. Repeated irregularity in breathing or an inexplicable shortness of breath is a sign to see one’s physician. Regular exercise and good eating habits are recommended for this mild condition. Only in severe cases is mitral valve prolapse treated surgically or considered life-threatening.

Bibliography

Alpert, Joseph S., James E. Dalen, and Shahbudin H. Rahimtoola, eds. Valvular Heart Disease. 3d ed. Philadelphia: Lippincott Williams & Wilkins, 2000.

Badash, Michelle. "Mitral Valve Prolapse." Health Library, May 9, 2013.

Boudoulas, Harisios, and Charles F. Wooley, eds. Mitral Valve: Floppy Mitral Valve, Mitral Valve Prolapse, Mitral Valvular Regurgitation. 2d ed. Armonk, N.Y.: Futura, 2000.

Crawford, Michael, ed. Current Diagnosis and Treatment—Cardiology. 3rd ed. New York: McGraw-Hill Medical, 2009.

Eagle, Kim A., and Ragavendra R. Baliga, eds. Practical Cardiology: Evaluation and Treatment of Common Cardiovascular Disorders. 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2009.

Frederickson, Lyn. Confronting Mitral Valve Prolapse Syndrome. New York: Warner Books, 1992.

Gersh, Bernard J., ed. The Mayo Clinic Heart Book. 2d ed. New York: William Morrow, 2000.

"Mitral Valve Prolapse." Mayo Clinic, April 21, 2011.

"What Is Mitral Valve Prolapse?" National Heart, Lung, and Blood Institute, July 1, 2011.

What business does Gatsby tell Nick and Daisy he was in?

In chapter five while Gatsby and Nick wait for Daisy outside Nick's bungalow prior to touring Gatsby's house, Gatsby casually observes "It took me just three years to earn the money that bought it."  Realizing that he has contradicted his earlier claim that he had inherited his wealth, he quickly tells Nick "I was in the drug business and then I was in the oil business."  

In chapter six, Daisy tells Tom that Gatsby...

In chapter five while Gatsby and Nick wait for Daisy outside Nick's bungalow prior to touring Gatsby's house, Gatsby casually observes "It took me just three years to earn the money that bought it."  Realizing that he has contradicted his earlier claim that he had inherited his wealth, he quickly tells Nick "I was in the drug business and then I was in the oil business."  

In chapter six, Daisy tells Tom that Gatsby "owned some drug-stores, a lot of drug-stores. He built them up himself." Readers assume that Gatsby has told her this in private, since Nick, the novel's narrator, does not witness the conversation and Daisy does not hear Gatsby's remarks in chapter five.

When Tom confronts Gatsby in chapter seven, he reveals to Daisy, Nick, and Jordan that a private investigator he has hired has discovered that Gatsby and Meyer Wolfsheim had bought drug-stores in Chicago "and sold grain alcohol over the counter."  Gatsby does not deny bootlegging.   

Fitzgerald, F. Scott. The Great Gatsby.  Charles Scribner's Sons, 1925.

What are aphasia and dysphasia?

Causes and Symptoms

Dysphasias are usually associated with cerebrovascular accident (CVA), or stroke, involving the middle cerebral artery or one of its many branches. Language disorders
may arise, however, from a variety of injuries and diseases: vascular, neoplastic, traumatic, degenerative, metabolic, or infectious.

Dysphasia results from dysfunction in the left cerebral hemisphere, most commonly in the frontotemporal region of the brain and particularly around the insula. Most language disorders are attributable to acute processes that either resolve or cause a chronic residual deficit, while others result from degenerative disorders that cause the dysfunction to be progressive.

Dysphasias have been classified both anatomically and functionally. Other classifications are linguistic and describe the fluency, volume, or quantity of speech. Pure forms of any language dysfunction, however, are very rare. Expressive dysphasias are primarily characterized by expressive deficits, but a verbal comprehension deficit may be present. Receptive dysphasias have expressive deficits. Transcortical dysphasias involve the ability to repeat and to recite. Speech is fluent but with striking paraphrases. The individual is unable to read and write, and comprehension is impaired.

Transcortical dysphasias are caused by hypoxia
(oxygen deficiency) from prolonged hypotension (low blood pressure), carbon monoxide poisoning, or other mechanisms that destroy the border zone between the anterior, middle, and posterior cerebral arteries. Blood supply is marginal in this region. Hypoxia in this area may occasionally isolate the posterior speech areas or all the speech areas from the remainder of the cortex, although both areas remain intact. The sensory and motor speech areas are, therefore, functional, but connections with other sensory or motor areas are impaired. Information from the remaining areas of the cortex cannot be transmitted to be transformed into language.

Aphasias can be classified into Broca’s, Wernicke’s, anomic, or global aphasias. Aphasia reflects damage to one or more of the brain’s primary language centers, which, in most persons, are located in the left hemisphere. Broca’s area lies next to the region of the motor cortex that controls the muscles necessary for speech, and presumably coordinates their movement. Wernicke’s area, which helps control the content of speech and affects its auditory and visual comprehension, lies between Heschl’s gyrus, the primary receiver of auditory stimuli, and the angular gyrus, a “way station” between the auditory and visual regions. Connecting Wernicke’s and Broca’s areas is a large nerve bundle, the arcuate fasciculus, which also helps control the content of speech and enables repetition.

The left hemisphere is dominant for language in all right-handed people and in the majority of left-handed people. When a stroke occurs in the dominant hemisphere, the patient may experience dysphasia or aphasia. Language disorders involve the expression and comprehension of written or spoken words. When the lesion involves Wernicke’s area of the brain, the patient experiences receptive aphasia; neither the sounds of speech nor its meaning can be distinguished, and comprehension of both written and spoken language is impaired. The lesion causing expressive aphasia affects Broca’s area, the motor area for speech. The patient has difficulty speaking and writing. Aphasias may be classified as either nonfluent or fluent. In nonfluent aphasia, the patient speaks very little and produces speech slowly and with obvious effort. In fluent aphasia, the patient may speak, but the phrases have little meaning because of impaired comprehension. Conduction aphasia is a type of
fluent aphasia in which the lesion is in the pathway between Broca’s and Wernicke’s areas. Most aphasias are mixed, with some impairment of both expression and understanding. A massive lesion may result in global aphasia, in which virtually all language function is lost.

Stroke is the most common cause of aphasia. Associated findings usually include decreased level of consciousness, right-sided hemiparesis, and paresthesia. Another communication problem experienced by many stroke patients is dysarthria, or slurred speech. Dysarthria results from a disturbance in muscular control and produces impairment of pronunciation, articulation, and phonation. Dysarthria does not result in any disturbance of language function itself. However, an occasional stroke patient may be unfortunate enough to have both aphasia and dysarthria.

A transient ischemic attack (TIA) can produce any type of aphasia. Usually, the aphasia occurs suddenly and resolves within twenty-four hours of the TIA. Brain abscess may result in any type of aphasia. Usually, the aphasia develops insidiously and may be accompanied by hemiparesis, ataxia, facial weakness, and signs of increased intracranial pressure. A brain tumor may cause anomic aphasia, which may be an early sign of the condition. Encephalitis
(brain inflammation) usually produces transient aphasia. Its earlier signs include fever, headache, and vomiting. Accompanying the aphasia may be convulsions, confusion, stupor or coma, hemiparesis, asymmetrical deep tendon reflexes, positive Babinski’s reflex, ataxia, myoclonus, nystagmus, ocular palsies, and facial weakness. Head trauma may cause any type of aphasia. Typically, aphasia resulting from severe
trauma occurs suddenly and may be transient or permanent, depending on the extent of brain damage. Anomic aphasia may begin insidiously and then progress; associated signs include behavioral changes, memory loss, poor judgment, restlessness, myoclonus, and muscle rigidity. Alzheimer’s disease, a degenerative dementia, may also cause aphasia. Drug abuse, particularly heroin overdose, can cause any type of aphasia.

Depending on its severity, aphasia may impede communication slightly or may make it impossible. Anomic aphasia eventually resolves in more than 50 percent of patients, but global aphasia is irreversible.

In the pediatric population, aphasia is sometimes mistakenly attributed to children who fail to develop normal language skills but who are not considered mentally retarded or developmentally delayed. Aphasia refers solely to loss of previously developed communication skills, however, and should not be used in this context. Brain damage associated with aphasia in children most commonly follows anoxia (oxygen deprivation), the result of near-drowning or airway obstruction.

Treatment and Therapy

If a person suddenly develops aphasia, a physician should be notified immediately. The patient is assessed quickly for signs of increased intracranial pressure, such as papillary changes, decreased level of consciousness, vomiting, seizures, bradycardia (slow heart rate), widening pulse pressure, and irregular respirations. If signs are detected related to increased intracranial pressure, appropriate medications are administered to decrease cerebral edema. Emergency resuscitation equipment may be used to support respiratory and cardiac function, if necessary. Emergency surgery may be indicated.

If the patient does not display signs of increased intracranial pressure, or if the aphasia has developed gradually, then a thorough neurologic
assessment is performed, starting with the patient history. Information may be obtained from the patient’s family or companion because of the patient’s impairment. The staff member assigned to the patient’s care will ask about a history of headaches, hypertension, or seizure disorders, as well as about any drug use. The patient’s ability to communicate and to perform routine activities before the aphasia began is assessed. The patient is checked for obvious signs of neurologic deficit, such as ptosis or fluid leakage from the nose and ears. The patient’s vital signs are taken and level of consciousness assessed. Assessing the level of consciousness is often difficult, however, because the patient’s verbal responses may be unreliable. In addition, dysarthria or speech apraxia (the inability to control voluntarily the muscles of speech) may accompany aphasia. The patient should be allowed ample time to
respond and should be spoken to slowly. Assessment of pupil response, eye movements, and motor function, especially mouth and tongue movement and swallowing, is conducted. To best assess motor function, the care provider will first demonstrate and then have the patient imitate responses, rather than merely providing verbal directions.

Immediately after aphasia develops, the patient may become confused or disoriented. The care provider can help restore a sense of reality by frequently telling the patient what has happened, where he or she is and why, and the date. The patient needs careful explanation of diagnostic tests, such as computed tomography (CT) scans, angiography, and Electroencephalography (EEG). Later, periods of depression are expected as the patient recognizes the handicap. The patient can be aided in attempts at communication through a relaxed, accepting environment with a minimum of distracting stimuli. When speaking to the patient, the staff assigned to care cannot assume that he or she understands. The patient may simply be interpreting subtle clues to meaning, such as social context, facial expressions, and gestures. To help avoid misunderstanding, care providers should speak in simple phrases and use demonstration to clarify verbal directions. Because aphasia is a language disorder, not an emotional or auditory one, a normal tone of voice should be used when speaking to the patient. Necessary aids, such as eyeglasses or dentures, should be provided to facilitate communication. Referrals to speech
pathologists early in the development of the problem will help the patient cope with aphasia.

Aminoff, Michael J., David A. Greenberg, and Roger P. Simon. Clinical Neurology. 7th ed. New York: McGraw-Hill Medical, 2009.

Rowland, Lewis P., ed. Merritt’s Textbook of Neurology. 12th ed. Philadelphia: Lippincott Williams & Wilkins, 2010.

Samuels, Martin A., ed. Manual of Neurologic Therapeutics. 7th ed. New York: Lippincott Williams & Wilkins, 2004.

Victor, Maurice, and Allan H. Ropper. Adams and Victor’s Principles of Neurology. 9th ed. New York: McGraw-Hill, 2009.

What is the Progressive opportunity?

The Progressive opportunity was a period of time when the country was ready to make various social and political changes. Around 1900, muckrakers began to write about problems in various areas of our society. People were concerned about some of the issues that existed and were supportive of making reforms.

Upton Sinclair wrote a book called The Jungle. The book described the unhealthy and the unsanitary conditions in the meat industry. This led to...

The Progressive opportunity was a period of time when the country was ready to make various social and political changes. Around 1900, muckrakers began to write about problems in various areas of our society. People were concerned about some of the issues that existed and were supportive of making reforms.

Upton Sinclair wrote a book called The Jungle. The book described the unhealthy and the unsanitary conditions in the meat industry. This led to the passage of the Meat Inspection Act. This law required meat to be inspected by the federal government before it could be sold. The Pure Food and Drug Act also was passed when people realized companies were falsely labeling foods and medicines in order to make more money.

John Spargo’s book called The Bitter Cry of Children led to changes in laws regarding workers. Laws were passed that outlawed child labor in certain industries and required children to attend school. When people realized that kids were being exploited, they were ready to make changes to fix the problem.

Lincoln Steffens wrote in his book called The Shame of the Cities about how money was influencing politics. This led to many political changes. These included the direct election of U.S. Senators, the development of the initiative, the referendum, and the recall, and the granting of the right to vote to women. It also led to new forms of local government such as the development of the commission plan of government.

People were concerned about the actions of big businesses. Many people believed big businesses exploited the common person. Several government agencies were developed to regulate big businesses, and some big businesses were ordered to dissolve. The Northern Securities Company was one example of a big business that was broken up by court action.

The Progressives seized upon the opportunities that presented themselves in the early 1900s. Other groups such as the Populists had previously discussed some of the ideas that the Progressives were now supporting, but these ideas weren’t enacted. The Progressives took advantage of a supportive environment that allowed for many changes to be made to reform our society.

What is S-adenosylmethionine (SAMe) as a nutritional supplement?

Overview

The chemical structure and name of S-adenosylmethionine, usually called SAMe, are derived from two materials: methionine, a sulfur-containing amino acid, and adenosine triphosphate (ATP), the body’s main energy molecule. SAMe was discovered in Italy in 1952. It was first investigated as a treatment for depression, but along the way it was accidentally noted to improve arthritis symptoms–a kind of positive side effect.

Sources

The body makes all the SAMe it needs, so there is no dietary requirement. However, deficiencies in methionine, folate, or vitamin B12 can reduce SAMe levels. SAMe is not found in appreciable quantities in foods, so it must be taken as a supplement. It has been suggested that the supplement trimethylglycine might indirectly increase SAMe levels and provide similar benefits, but this effect has not been proven.

Therapeutic Dosages

A typical full dosage of SAMe is 400 milligrams (mg) taken three to four times per day. As little as 200 mg twice daily may suffice to keep a person feeling better once the full dosage has “broken through” the symptoms.

However, some people develop mild stomach distress if they start full dosages of SAMe at once. To avoid this side effect, one may need to start low and work up to the full dosage gradually.

SAMe is on the market in the United States at a recommended dosage of 200 mg twice daily. This dosage labeling makes SAMe appear more affordable, but it is unlikely that SAMe will actually work when taken at such a low dosage.

Therapeutic Uses

A substantial amount of evidence suggests that SAMe can be an effective treatment for osteoarthritis, the “wear and tear” type of arthritis that many people develop as they get older. Also, a moderate amount of evidence suggests that SAMe might be helpful for depression.

Weak and inconsistent evidence hints that SAMe might be helpful for a variety of liver conditions such as cirrhosis, chronic viral hepatitis, pregnancy-related jaundice, and Gilbert’s syndrome. SAMe also may help the chronic, painful muscle condition known as fibromyalgia.

SAMe has undergone some investigation as a possible supportive treatment for Parkinson’s disease. One study suggests that it may reduce the depression so commonly associated with the disease. In addition, the drug levodopa, used for Parkinson’s disease, depletes the body of SAMe. This suggests that taking extra SAMe might be helpful. However, it is also possible that SAMe could interfere with the effect of levodopa, requiring an increase in dosage. Finally, preliminary evidence suggests that SAMe can protect the stomach against damage caused by alcohol.

Scientific Evidence

Osteoarthritis. A substantial body of scientific evidence supports the use of SAMe to treat osteoarthritis. Double-blind studies involving a total of more than one thousand participants suggest that SAMe is about as effective as standard anti-inflammatory drugs. In addition, evidence from studies of animals suggests that SAMe may help protect cartilage from damage.

For example, a double-blind, placebo-controlled Italian study tracked 732 people taking SAMe, naproxen (a standard anti-inflammatory drug), or placebo. After four weeks, participants taking SAMe or naproxen showed about the same level of benefit compared with each other and a superior level of benefit compared with those in the placebo group.

A later double-blind study compared SAMe with celecoxib (Celebrex), a member of the newest class of nonsteroidal anti-inflammatory drugs. Celecoxib produced more rapid effects than SAMe, but over time, SAMe appeared to catch up. However, the lack of a placebo group makes these results less than fully reliable.

Another double-blind study compared SAMe with the anti-inflammatory drug piroxicam. Forty-five people were followed for eighty-four days. The two treatments proved equally effective. However, the SAMe-treated persons maintained their improvement long after the treatment was stopped, whereas those on piroxicam quickly started to hurt again.

Similarly long-lasting results have been seen with glucosamine and chondroitin. This pattern of response suggests that these treatments are somehow making a deeper impact on osteoarthritis than simply relieving symptoms. However, while there is some direct evidence that glucosamine and chondroitin can slow the progression of osteoarthritis, the evidence regarding SAMe is more hypothetical. In other double-blind studies, oral SAMe has shown benefits equivalent to those of various doses of indomethacin, ibuprofen, and naproxen.

Depression. The evidence for SAMe for the treatment of depression is provocative but far from definitive. Several double-blind, placebo-controlled studies have found SAMe effective in relieving depression, but most were small and poorly reported, and many used an injected form of the supplement. Furthermore, a late trial, a double-blind, placebo-controlled study of 133 people with depression, failed to find intravenous SAMe more effective than placebo. (Researchers resorted to questionable statistical manipulation of the data to show benefit.)

Other trials compared SAMe to standard antidepressants rather than to placebo. The best of these trials was a six-week, double-blind trial of 281 people with mild depression that compared oral SAMe to imipramine. The results indicated that the two treatments were about equally effective. However, the absence of a placebo group makes this study less than fully definitive.

Other studies have also compared the benefits of oral or intravenous SAMe to those of tricyclic antidepressants and have also found generally equivalent results; however, again, poor reporting and inadequacies of study design (such as too limited a treatment interval) mar the meaningfulness of the reported outcomes.

Fibromyalgia. Four double-blind trials have studied the use of SAMe for fibromyalgia, three of them finding it to be helpful. Most of these studies, however, used SAMe given either intravenously or as an injection into the muscles, sometimes in combination with oral doses. Injected medication has effects that can be quite different from those of the same medications taken orally. For this reason, these studies are of questionable relevance.

Nonetheless, the one double-blind study that used only oral SAMe did find positive results. In this trial, forty-four people with fibromyalgia took 800 mg of SAMe or placebo for six weeks. Compared with the group taking placebo, those taking SAMe had improvements in disease activity, pain at rest, fatigue, and morning stiffness, and in one measurement of mood. In other respects, such as the amount of tenderness in their tender points, the group taking SAMe did no better than those taking the placebo. It is not clear whether SAMe is helping fibromyalgia through its antidepressant effects or by some other mechanism.

Parkinson’s disease. Evidence suggests that levodopa (the drug used to treat Parkinson’s disease) can reduce brain levels of SAMe. This depletion may contribute to the side effects of levodopa treatment and to the depression sometimes seen with Parkinson’s disease. One study found that SAMe taken orally improved depression without changing the effectiveness of levodopa. However, it is also possible that over time, taking extra SAMe could interfere with levodopa’s effectiveness.

Safety Issues

SAMe appears to be quite safe, according to both human and animal studies. The most common side effect is mild digestive distress. However, SAMe does not actually damage the stomach.

Like other substances with antidepressant activity, SAMe might trigger a manic episode in those with bipolar disease. Also, safety in young children, pregnant or nursing women, or those with severe liver or kidney disease has not been established.

SAMe might interfere with the action of the Parkinson’s drug levodopa. In addition, there may be risks involved in combining SAMe with standard antidepressants. For this reason, one should not try either combination without physician supervision.

Important Interactions

One should not take SAMe except on a physician’s advice if already taking standard antidepressants, including monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and tricyclics. Also, SAMe might help relieve the side effects of levodopa for Parkinson’s disease. However, it might also reduce levodopa’s effectiveness over time.

Bibliography

Fava, M. “Using Complementary and Alternative Medicines for Depression.” Journal of Clinical Psychiatry 71 (2010): e24.

Hosea Blewett, H. J. “Exploring the Mechanisms Behind S-adenosylmethionine (SAMe) in the Treatment of Osteoarthritis.” Clinical Reviews in Food Science and Nutrition 48 (2008): 458-463.

Najm, W. I., et al. “S-adenosyl Methionine (SAMe) Versus Celecoxib for the Treatment of Osteoarthritis Symptoms.” BMC Musculoskeletal Disorders 5 (2004): 6.

Porter, N. S., et al. “Alternative Medical Interventions Used in the Treatment and Management of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Fibromyalgia.” Journal of Alternative and Complementary Medicine 16 (2010): 235-249.

In “Birches,” why do the birch trees remind the speaker of childhood games?

"When I see birches bend to left and right

Across the lines of straighter darker trees,

I like to think some boy’s been swinging them.

But swinging doesn’t bend them down to stay

As ice storms do."

As you can see here in the opening lines of the poem, the birch trees remind the speaker of the childhood game of swinging on the branches of those same birch trees, or similar ones. It's because heavy...

"When I see birches bend to left and right

Across the lines of straighter darker trees,

I like to think some boy’s been swinging them.

But swinging doesn’t bend them down to stay

As ice storms do."

As you can see here in the opening lines of the poem, the birch trees remind the speaker of the childhood game of swinging on the branches of those same birch trees, or similar ones. It's because heavy ice from a storm has built up on the branches so much that they are actually bent downward, much like the speaker himself would bend those branches as a child when he played on them and his weight caused them to bend downward. However, the difference, as the speaker notes here, is that the ice has caused the branches to stay bent permanently, while when he played on the branches as a kid, the speaker only temporarily caused the branches to be bent.

This difference doesn't matter too much, though, because as soon as the poet has made that connection between ice-laden branches and his childhood adventures on similar trees, a bud of memories has appeared, and the poem unfurls from there. The speaker goes on to talk about how thrilling it was to leap from the trunk of the tree onto a branch, and he considers that activity in retrospect, with a thoughtful adult's ability to analyze that childhood activity and what it reveals about life.

You can understand this poem's structure, then, by noticing that it follows a common pattern: the speaker sees something, it reminds him of something from the past, and he goes on to juxtapose past and present and thereby discover new insights.

What are some of Tom Robinson's quotes, from Harper Lee's novel To Kill a Mockingbird, that depict courage?

It is very courageous of Tom Robinson to even testify in court, as he is in a racist southern town in the 1930s. It wasn't customary at this time for African-Americans to think that they could defend themselves, as many were harmed or even lynched when they tried to stand up for themselves.

In Chapter 19, Tom tells the story of what happened between him and Mayella Ewell when he is testifying in court. He...

It is very courageous of Tom Robinson to even testify in court, as he is in a racist southern town in the 1930s. It wasn't customary at this time for African-Americans to think that they could defend themselves, as many were harmed or even lynched when they tried to stand up for themselves.

In Chapter 19, Tom tells the story of what happened between him and Mayella Ewell when he is testifying in court. He says, "She reached up an‘ kissed me ’side of th‘ face. She says she never kissed a grown man... She says what her papa do to her don’t count" (page numbers vary by edition). This statement is very daring on several counts. First, Tom admits that a white woman tried to kiss him. Physical contact between whites and African-American people was highly charged in the south at this time, and it was strictly forbidden. The truth is very dangerous for the jury to hear, but Tom tells it anyway, knowing that it will likely mean he is convicted. In making this statement, he also reveals that Mayella's father has been abusing her. It was not customary at this time for people to speak about sexual or physical abuse, and it was even more daring for an African-American person to accuse a white man of abusing his daughter. Therefore, this statement is courageous for several reasons.

Later, when the prosecutor is asking Tom Robinson why he helped Mayella Ewell, Tom says, “I felt right sorry for her, she seemed to try more’n the rest of ‘em—” (page numbers vary by edition). It is courageous of Tom to admit that he felt pity for a white woman, as it was almost forbidden for an African-American person to admit to feeling sorry for a white person at that time. 

What is connective tissue? |

Structure and Function

Cells, the structural and functional units of life, are organized into tissue, a group of different types of cells and their nonliving intracellular matrix, or glue, that performs a specialized function. The four groups of tissues are epithelial (covering and lining tissue; also glands); connective (adipose, blood, bone, cartilage, ligament, and tendon); muscle (skeletal, cardiac, and smooth); and nervous (brain and spinal cord).

Connective tissue typically has cells widely scattered throughout a large amount of intracellular matrix (that is, a substance in which the cells are embedded), unlike epithelial tissue that typically has cells arranged in an orderly manner and has a limited amount of intracellular matrix.

Connective tissues are categorized as loose (areolar), dense, and specialized. Some connective tissues are difficult to classify, with the distinction between “loose” and “dense” not clearly defined. Also, dense connective tissue may be called fibrous connective tissue because of the large amount of collagen or elastin fibers contained.

Because a tissue is defined as a collection of different cells, several types of cells may be found in various types of connective tissue: fibroblasts, which secrete collagen and other elements of the extracellular matrix, thereby creating and maintaining the matrix; adipocytes, which store excess caloric energy in the form of fat; and mast cells, macrophages, leukocytes, and plasma cells, which have immune functions and, therefore, an active role in inflammation. The components of the matrix are different in the various types of connective tissue and may include fibers, amorphous ground substances (glycoproteins, proteins, and proteoglycans), and tissue fluid. Each type of connective tissue has a characteristic pattern of cells and a distinctive amount and type of matrix. For example, bone matrix includes minerals, while blood has plasma for a matrix.

Loose connective tissue is the most common type of connective tissue; it holds organs in place and attaches epithelial tissue to underlying tissues. Loose connective tissue can be further categorized based on the type of fibers and how the fibers are arranged: collagenous fibers, which are composed of collagen and are arranged as coils; elastic fibers, which are composed of elastin and are able to stretch; and reticular fibers, which join connective tissue to other tissues. Loose connective tissue has a relatively large amount of cells, matrix, or both, and a relatively small amount of fibers. Loose connective tissue is found in the hypodermis and fascia (the connective tissue that loosely binds structures to one another).

Dense connective tissue is identified by the high density of fibers in the tissue and a low density of cells and matrix. The type of fiber that predominates determines the type of dense connective tissue. Dense collagenous connective tissue, for example, contains an abundance of collagen fibers and is found in structures where tensile strength is needed, such as the sclera (white) of the eye, tendons, and ligaments. Dense elastic connective tissue contains an abundance of elastin fibers and is found in structures where elasticity is needed (for example, the aorta).

Specialized connective tissues include adipose tissue, cartilage, bone, and blood. Adipose tissue is a form of loose connective tissue that stores fat. It is found in the fatty layer around the abdomen, in bone marrow, and around the kidneys. Cartilage is a form of fibrous connective tissue. It is composed of closely packed collagenous fibers embedded in a gelatinous intracellular matrix called chondrin. While the skeleton of human embryos are composed of cartilage, cartilage does not become bone but rather is replaced by bone. The replacement is not universal; cartilage provides flexible support for ears (external pinnae), nose, and trachea. Bone is a type of mineralized connective tissue, and it contains collagen and calcium phosphate. Cells found in bone include osteoblasts, which form new bone for growth, repair, or remodeling, and osteoclasts, which break down bone for growth and remodeling. The living cells are found in spaces in the calcified matrix. These spaces are called lacunae and are interconnected by small channels called canaliculi that eventually join up with blood vessels in the bone organ. Thus, even in a solidified matrix, living cells are able to obtain nutrients and expel wastes.>

Blood too is a type of specialized connective tissue. Blood may seem to be an unlikely connective tissue, but it fits the definition: different cells widely dispersed in intracellular matrix, working together to perform a specific function. Unlike other connective tissues, blood has no fibers. Blood does have several types of cells: red blood cells or erythrocytes, white blood cells or leukocytes (with subdivisions of monocytes, macrophages, eosinophils, lymphocytes, neutrophils, and basophils), and platelets or thrombocytes. The matrix is liquid and contains enzymes, hormones, proteins, carbohydrates, and fats.

Disorders and Diseases

Connective tissue, like any other tissue, is subject to disorders and diseases. Some disorders are inherited (passed from one generation to the next by means of DNA in chromosomes), while other disorders are related to environmental factors (such as a lack of specific nutrients).

Some inherited connective tissue disorders are Marfan syndrome and osteogenesis imperfecta. In Marfan syndrome, connective tissue grows outside the cell, having deleterious effects on the lungs, heart valves, aorta, eyes, central nervous system, and skeletal system. People with Marfan syndrome are often unusually tall with long, slender arms, legs, and fingers. In osteogenesis imperfecta, or brittle bone disease, the quantity and quality of collagen is insufficient to produce healthy bones. People with this disorder have multiple spontaneous bone breaks. Other connective tissue diseases are environmental, such as scurvy, which is caused by a lack of vitamin C required for the production and maintenance of collagen. Without sufficient vitamin C in the diet, and subsequent lack of collagen, the patient will develop spots on the skin, particularly the legs and thighs; will be tired and depressed; and may lose teeth. Osteoporosis has many factors, but lack of vitamin D and calcium in the diet will lead to a thinning of the bone, subjecting the patient to fractures, primarily of the hip, spine, and wrist.

Connective tissue diseases may also be classified as systemic autoimmune disease and may have both genetic and environmental causes. In these situations, the immune system is spontaneously overactivated and extra antibodies are produced. Examples of systemic autoimmune diseases include systemic lupus erythematosus and rheumatoid arthritis. Systemic lupus erythematosus can damage the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. More woman than men are diagnosed with lupus, and more black women than other groups. Rheumatoid arthritis is caused when immune cells attack the membrane around joints and destroys the cartilage of the joint; it can also affect the heart and lungs and interfere with vision.

Bibliography

Gordon, Caroline, and Wolfgang Gross. Connective Tissue Diseases: An Atlas of Investigation and Management. Oxford: Clinical Publishing, 2011.

Lundon, Katie. Orthopedic Rehabilitation Science: Principles for Clinical Management of Nonmineralized Connective Tissue. Boston: Butterworth-Heinemann, 2003.

"Mixed Connective Tissue Disease." Mayo Clinic, May 30, 2012.

Price, Sylvia Anderson, and Lorraine McCarty Wilson, eds. Pathophysiology: Clinical Concepts of Disease Processes. St. Louis: Mosby, 2003.

"Questions and Answers about Heritable Disorders of Connective Tissue." National Institute of Arthritis and Musculoskeletal and Skin Diseases, October 2011.

Royce, Peter M., and Beat Steinmann, eds. Connective Tissue and Its Heritable Disorders: Molecular, Genetic, and Medical Aspects. New York: Wiley-Liss, 2002.

What is the esophagus? |

Structure and Function

The esophagus lies between the spine and the trachea and is part of the digestive system. The esophagus, however, does not produce or secrete any digestive enzymes, and absorption of nutrients in this part of the digestive system is almost nil. The esophagus pierces the diaphragm as it moves through the thoracic cavity and into the abdominopelvic cavity, where it joins with the stomach.

All parts of the digestive system have four tunics (tissues): from superficial to deep, tunica serosa, tunica muscularis, tunica submucosa, and tunica mucosa. Tunica serosa anchors the esophagus in the mesentery. Tunica muscularis is composed of smooth muscle fibers arranged in circular and longitudinal fibers. These two layers of muscles are important as they are able to squeeze the food bolus (chewed mass of food) and move it down toward the stomach. The muscles are involuntary and perform peristaltic contractions behind the bolus, pushing it downward, as if a tennis ball were being pushed through a leg of panty hose. Tunica submucosa is a layer of loose connective tissue; blood vessels and nerves, including the important submucosa plexus, are found in this layer. The innermost layer, tunica mucosa, is comprised of epithelial cells and is the layer in contact with the bolus. Of all the tunics, tunica mucosa is the most variable along the length of the digestive system. The epithelium here is stratified squamous
epithelial tissue to protect the esophagus from sharp or dangerous food items, such as bones, hot pizza, or insufficiently chewed carrots.

The esophagus has an upper and a lower sphincter. When one swallows, the upper sphincter relaxes. In a coordinated effort, the larynx pulls forward and the epiglottis clamps down to cover this opening into the respiratory system (lungs). Glands produce mucus to lubricate food as it passes along the lumen. The lower sphincter closes once the bolus has passed into the stomach. Failure to do so would allow stomach acids to leak up into the esophagus, causing what is commonly called heartburn or acid indigestion, more properly known as gastroesophageal reflux disease.

Disorders and Diseases

The most common medical problem with the esophagus is gastroesophageal reflux disease (GERD), which is caused when the lower sphincter fails to close properly. Stomach contents, which are acidic, then leak into the esophagus and irritate it. Left untreated, GERD can damage the esophagus.

Barrett’s esophagus is a disease often is found in patients with GERD. In Barrett’s esophagus, the tissue that lines the esophagus, tunica mucosa, is replaced by tissue that is more similar to tissue lining the intestines. The process is called intestinal metaplasia. Barrett’s esophagus may lead to the development of esophageal cancer,
but this is a rare event. It should be emphasized that not all patients with GERD develop Barrett’s esophagus and that very few people with Barrett’s esophagus develop cancer. The cause of Barrett’s esophagus is unknown, as is the cause of esophageal cancer.

Bibliography

"Digestive System." MedlinePlus, January 14, 2013.

"Esophagus Disorders." MedlinePlus, June 12, 2013.

Johnson, Leonard R., ed. Gastrointestinal Physiology. 7th ed. Philadelphia: Mosby/Elsevier, 2007.

Mayo Clinic. Mayo Clinic on Digestive Health: Enjoy Better Digestion with Answers to More than Twelve Common Conditions. 2d ed. Rochester, Minn.: Author, 2004.

Scanlon, Valerie, and Tina Sanders. Essentials of Anatomy and Physiology. 6th ed. Philadelphia: F. A. Davis, 2012.

Wood, Debra, Daus Mahnke, and Brian Randall. "Heartburn—Overview." Health Library, March 18, 2013.

What is dwarfism? What role do genetics play?

Risk Factors

Having a parent with a form of dwarfism, such as achondroplasia, a parent who carries a mutated FGFR3 gene, or parents of advanced age can increase the risk of inheriting dwarfism. Other abnormalities such as damage or conditions of the pituitary gland, hormonal disorders, problems with absorption, malnutrition, kidney disease, or extreme emotional distress can increase the risk of developing dwarfism.

Etiology and Genetics

Dwarfism, of which there are several hundred forms, occurs in approximately one in every ten thousand births. Approximately 85 percent of little people are born to parents of average height. The most common type of dwarfism, achondroplasia, is an autosomal dominant trait, but in 80 percent of cases it appears in children born to normal parents as a result of mutations in the sperm or egg.

Dwarfisms in which body proportions are normal usually result from metabolic or hormonal disorders in infancy or childhood. Chromosomal abnormalities, pituitary gland disorders, problems with absorption, malnutrition, kidney disease, and extreme emotional distress can also interfere with normal growth. When body parts are disproportioned, the dwarfism is usually due to a genetic defect.

Skeletal dysplasias
are the most common causes of dwarfism and are the major cause of disproportionate types of dwarfism. More than five hundred skeletal dysplasias have been identified. Chondrodystrophic dwarfism occurs when cartilage cells do not grow and divide as they should and cause defective cartilage cells. Most chondrodystrophic little people have abnormal body proportions. The defective cells occur only in the spine or only in the arms and legs. Short-limb dwarfism includes individuals with achondroplasia, diastropic dysplasia, and Hunter-Thompson chondrodysplasia.

Achondroplasia is the most common skeletal dysplasia and affects more than 70 percent of all dwarfs. It occurs in every 26,000 to 40,000 babies born of all races and ethnicities. Achondroplasia is caused by an autosomal dominant allele and is identified by a disproportionate short stature consisting of a long trunk and short upper arms and legs. Eighty percent of all cases of achondroplasia result from a mutation on chromosome 4 in a gene that codes for a fibroblast growth factor receptor. Achondroplasia is seen in both males and females, occurs in all races, and affects approximately one in every twenty thousand births. If one parent has achondroplasia and the other does not, then a child born to them would have a 50-percent chance of inheriting achondroplasia. On the other hand, if both parents have achondroplasia, their offspring have a 50 percent chance of inheriting achondroplasia, a 25-percent chance of being normal, and a 25-percent chance of inheriting the abnormal allele from each parent and suffering often fatal skeletal abnormalities. Children who do not inherit the defective gene will never have achondroplasia and cannot pass it on to their offspring, unless a mutation occurs in the sperm or egg of the parents. Geneticists have observed that fathers who are forty years of age or older are more likely to have children with achondroplasia as a result of mutations in their sperm.

Diastrophic dysplasia
is a relatively common form of short-limb dwarfism that occurs in approximately one in 100,000 births and is identified by the presence of short arms and calves, clubfeet, and short, broad fingers with a thumb that has a hitchhiker type appearance. Infant mortality can be high as a result of respiratory complications, but if they survive infancy, short-limbed dwarfs have a normal life span. Orthopedic dislocations of joints are common. Scoliosis is seen especially in the early teens, and progressive cervical kyphosis and partial dislocation of the cervical spine eventually cause compression of the spinal cord. Diastrophic dysplasia is an inherited autosomal recessive condition linked to chromosome 5. Parents have a 25-percent chance that each additional child will get diastrophic dysplasia.

Short-trunk dwarfism includes individuals with spondyloepiphyseal dysplasia, which results from abnormal growth in the spine and long bones that leads to a shortened trunk. It occurs in one of every 95,000 births. In spondyloepiphyseal dysplasia tarda, the lack of growth may not be recognized until five to ten years of age. Those affected have progressive joint and back pain and eventually develop osteoarthritis. Spondyloepiphyseal dysplasia congenita is caused by autosomal dominant gene mutations and is evidenced by a short neck and trunk, and barrel chest at birth. It is not uncommon for cleft palate, hearing loss, myopia, and retinal detachment to be present.

Morquio syndrome, which was first described in 1929, is classified as a mucopolysaccharidosis (MPS) disease caused by the body’s inability to produce enzymes that help to break down and recycle dead cells. Consequently, wastes are stored in the body’s cells.

Hunter-Thompson chondrodysplasia is a form of dwarfism caused by a mutation in growth factor genes. Affected individuals have shortened and misshapened bones in the lower arms, the legs, and the joints of the hands and feet. Fingers are shortened and toes are ball-shaped.

Growth hormone, a protein that is produced by the pituitary (“master”) gland, is vital for normal growth. Hypopituitarism results in a deficiency of growth hormone and afflicts between ten thousand and fifteen thousand children in the United States. In panhypopituitarism, the gland does not produce any hormones. The pituitary gland shuts down and growth is stunted.

Turner syndrome
affects one in every two thousand female infants and is characterized by the absence of or damage to one of the X chromosomes in most of the cells in the body. Short stature and the failure to develop sexually are hallmarks of Turner syndrome. Learning difficulties, skeletal abnormalities, heart and kidney problems, infertility, and thyroid dysfunction may also occur. Turner syndrome can be treated with human growth hormones and by replacing sex hormones.

Symptoms

For inherited disorders at birth, a long trunk and shortened limbs will be noticeable. A child born with dwarfism may go on to exhibit delayed gross motor development and skills, breathing and neurologic problems, hydrocephalus (water on the brain), increased susceptibility to ear infections and hearing loss, weight problems, curvature of the spine (scoliosis), bowed legs, stiff arms, joint and back pain or numbness, and crowding of teeth. Portions of the face may be underdeveloped. Sleep apnea can develop as a result of compression of the spine. Adult height will be stunted (usually reaching 42-52 inches). Seeking proper medical care can help to relieve some of these symptoms and complications.

Screening and Diagnosis

Close monitoring by parents and doctors is necessary to record the constellation of symptoms for each unique case of dwarfism. Often an initial diagnosis can be made by observing physical characteristics. Magnetic resonance imaging (MRI) and computed tomography (CT) scans can illustrate spinal and other structural abnormalities before serious complications arise. Imaging techniques can also help to determine the type of dwarfism present. Molecular genetic testing can be done to detect a FGFR3 mutation. Genetic testing is 99-percent sensitive and available in clinical laboratories. The Human Genome Project continues to investigate genetic links to dwarfism. Prenatal counseling and screening for traits of dwarfism, along with genetic counseling and support groups, are avenues to pursue for family and individual physical, psychological, and social well-being and to make informed choices.

Treatment and Therapy

Some forms of dwarfism can be treated through state-of-the-art surgical and medical interventions such as bone-lengthening procedures, reconstructive surgery, and growth and sex hormone replacement.

Short stature is the one quality all people with dwarfism have in common. After that, each of the many conditions that cause dwarfism has its own set of characteristics and possible complications. Fortunately, many of these complications are treatable, so that people of short stature can lead healthy, active lives. Continued follow-up with the physician team is essential.

For example, some babies with achondroplasia may experience hydrocephalus (excess fluid around the brain). They may also have a greater risk of developing sleep apnea—a temporary stop in breathing during sleep—because of abnormally small or misshapen airways or, more likely, because of airway obstruction by the adenoids or the tonsils. Occasionally, a part of the brain or spinal cord is compressed. With close monitoring by doctors, however, these potentially serious problems can be detected early and surgically corrected.

Prevention and Outcomes

Genetic counseling as well as family and public education regarding dwarfism and growth problems can bring greater awareness of dwarfism to communities and allow parents to make good choices. Inherited dwarfism is not preventable, but some cases caused by malnutrition, injury, absorption, or kidney conditions may be prevented.

The type, symptoms, and severity of complications vary from person to person, but most little people have an average life span. With a sense of support, self-esteem, and independence, a person with dwarfism can lead a very satisfying and productive life.

Bibliography

Ablon, J. Living with Difference: Families with Dwarf Children. Westport: Greenwood, 1988. Print.

Alan, Rick. "Achondroplasia." Health Library. EBSCO Information Services, 11 May 2013. Web. 21 July 2014.

Apajasalo, M., et al. “Health-Related Quality of Life of Patients with Genetic Skeletal Dysplasias.” European Journal of Pediatrics 157.2 (1998): 114–21. Print.

"Diseases and Conditions: Dwarfism." Mayo Clinic. Mayo Foundation, 27 Aug. 2011. Web. 21 July 2014.

"Dwarfism." MedlinePlus. US Natl. Lib. of Medicine, 20 June 2014. Web. 21 July 2014.

Krakow, D., et al. “Use of Three-Dimensional Ultrasound Imaging in the Diagnosis of Prenatal-Onset Skeletal Dysplasias.” Ultrasound in Obstetrics and Gynecology 21.5 (2003): 4676–78. Print.

Page, Nick. Lord Minimus: The Extraordinary Life of Britain’s Smallest Man. New York: St. Martin’s, 2002. Print.

Ranke, M., and G. Gilli. Growth Standards, Bone Maturation, and Idiopathic Short Stature. Farmington: Karger, 1996. Print.

Richardson, John H. In the Little World: A True Story of Dwarfs, Love, and Trouble. San Francisco: HarperCollins, 2001. Print.

Thorner, M., and R. Smith. Human Growth Hormone: Research and Clinical Practice. Vol. 19. Totowa: Humana, 1999. Print.

Ulijaszek, J. S., Francis E. Johnston, and Michael A. Preece. Cambridge Encyclopedia of Human Growth and Development. New York: Cambridge UP, 1998. Print.

Vajo, Zoltan, Clair A. Francomano, and Douglas J. Wilkin. “The Molecular and Genetic Basis of Fibroblast Growth Factor Receptor 3 Disorders: The Achondroplasia Family of Skeletal Dysplasias, Muenke Craniosynostosis, and Crouzon Syndrome with Acanthosis Nigricans.” Endocrine Reviews 21.1 (2000): 23–39. Print.

Zelzer, Elazar, and Bjorn R. Olsen. “The Genetic Basis for Skeletal Diseases.” Nature 15 May 2003): 343–8. Print.