How does the identity of Maycomb, Alabama, change throughout the course of Harper Lee's To Kill a Mockingbird?

In the opening chapter of Harper Lee's To Kill a Mockingbird, Scout, the narrator, describes Maycomb as a sleepy, "tired old town." It was particularly sleepy and tired due to the Great Depression. As a result of financial distress, "People moved slowly then" because "there was nowhere to go, nothing to buy and no money to buy it with" (Ch. 1). Yet Scout also describes it as an optimistic town. In general, she depicts a classically relaxed, Southern town with upbeat spirits.

As the novel progresses, racial tensions due to Tom Robinson's trial bring out the town's aggression and hatred. At one point in the story, Atticus tells Jem that there have never been mobs or gangs in Maycomb. Plus, he states that the only time the Ku Klux Klan was present was in 1920, but "they couldn't find anybody to scare," so they quickly dispersed (Ch. 15). However, immediately after making these statements, Atticus must face a lynch mob in front of Maycomb's jailhouse. After Robinson loses his trial, he is shot to death with 17 bullets, a ghastly and unjustified number of bullets, while trying to escape prison. Both the lynch mob and his death signify that Maycomb has changed from a relaxed, lazy town to a town overruled by its racist hatred and is growing violent as a result. The book even ends with violence when the town's most violent member, Bob Ewell, attacks Atticus's children with the intention of killing them.

Yet despite the change from a calm atmosphere to a violent one, hope still remains in Maycomb. Hope is particularly expressed in Miss Maudie's comment to the children after the trial that Atticus is the "only man in these parts who can keep a jury out so long in a case like that"; she further notes that the town is making a "baby-step" towards creating a more just society (Ch. 22).

Hence, all in all, the town changes from a relaxed town to a violent town, while some of its members hold on to hope for change.

What is inflammation?

Causes and Symptoms

In inflammation, the following changes are seen locally: redness, swelling, heat, pain, and loss of function. These changes are chemically mediated. Inflammation may be caused by microbial infection; physical agents such as trauma, radiation, and burns; chemical toxins; caustic substances such as strong acids or bases; decomposing or necrotic tissue; and reactions of the immune system. Acute inflammation is of relatively short duration (from a few minutes to a day), while chronic inflammation lasts longer. The local changes associated with inflammation include the outflow of fluid into the spaces between cells and the inflow or migration of white blood cells (leukocytes) to the area of injury. Chronic inflammation is characterized by the presence of leukocytes and macrophages, as well as by the proliferation of new blood vessels and connective tissue.

Inflammation is a protective mechanism for the body. Redness is attributable to increased blood flow to the injured area. Swelling is caused by the flow of fluid into the spaces between cells. Heat is produced by a combination of increased blood flow and chemical reactions in the local area. Pain results from the presence of two main chemicals found in the bloodstream: prostaglandins and bradykinin. Loss of function is a result of pain (the body limits movement to reduce discomfort) and swelling (interstitial fluid limits movement).

Acute inflammation. Many chemicals are involved in acute inflammation. Mediators of inflammation originate from blood plasma and from both damaged and normal cells. Vasoactive amines are a class of chemicals that increase the permeability of blood vessel and cell walls. The most well studied of these are histamine and serotonin. Histamine is stored in granules in mast cells that are found in both tissue and basophils, the latter being a type of cell found in the blood. Serotonin is found in mast cells and platelets; it is another type of cell found in the bloodstream. These substances cause vasodilation (expansion of the walls of blood vessels) and increased vascular permeability (leakage through the walls of small vessels, especially veins). Histamine and serotonin can be released by traumaor exposure to cold. Other chemicals that circulate in the blood can release histamine. Two of these are part of the complement system; another is called interleukin-1. The effects of histamine diminish after approximately one hour.

Plasma proteases comprise three interrelated systems that explain much that is known about inflammation: the complement, kinin, and clotting systems. The complement system is composed of twenty different proteins involved in reactions against microbial agents that invade the body. The various chemicals act in a cascade, similar to falling dominoes: Each one sets off another in sequence. The result of these chemical actions is to increase vascular permeability, promote chemotaxis (the attraction of living cells to specific chemicals), engulf invading microorganisms, and destroy pathogens through a process called lysis.

The kinin system is responsible for releasing bradykinin, a chemical substance that causes contraction of smooth muscle tissue, dilation of blood vessels, and pain. The duration of action for bradykinin is brief because it is inactivated by the enzyme kininase. Bradykinin does not promote chemotaxis.

The clotting system is made up of a series of chemicals that result in the formation of a solid mass. The most commonly encountered example is the scab that forms at the site of a cut in the skin. Like the complement system, the clotting system is a cascade of thirteen different chemicals. In addition to producing a solid mass, the clotting system increases vascular permeability and promotes chemotaxis for white blood cells.

Other substances are involved in acute inflammation. Among the most important of these is a class called prostaglandins. Several different prostaglandin molecules have been isolated; they are derived from the membranes of most cells. Prostaglandins cause pain, vasodilation, and fever. Aspirin counteracts the effects of prostaglandins, which explains the antipyretic (fever-reducing) and analgesic (pain-reducing) properties of the drug.

Another group of substances involved in acute inflammation are leukotrienes. The primary sources for these molecules are leukocytes, and some leukotrienes are found in mast cells. This group promotes vascular leakage but not chemotaxis. They also cause vasoconstriction (a decrease in the diameter of blood vessels) and bronchoconstriction (a decrease in the diameter of air passageways in the lungs). The effect of these leukotrienes is to slow blood flow and restrict air intake and outflow. A different type of leukotriene is found only in leukocytes. This type enhances chemotaxis but does not contribute to vascular leakage. In addition, leukotrienes cause white blood cells to stick to damaged tissues, speeding the removal of bacteria and promoting healing.

Other chemical substances are known to be involved with inflammation: platelet-activating factor, tumor necrosis factor, interleukin-1, cationic (positively charged) proteins, neutral proteases (enzymes that break down proteins), and oxygen metabolites (molecules resulting from reactions with oxygen). The sources of these are generally leukocytes, although some are derived from macrophages. They reinforce the effects of prostaglandins and leukotrienes.

There are four different outcomes for acute inflammation. There may be complete resolution in which the injured site is restored to normal; this outcome usually follows a mild injury or limited trauma where there has been only minor tissue destruction. Healing with scarring may occur, in which injured tissue is replaced with scar tissue that is rich in collagen, giving it strength but at the cost of normal function; this outcome follows more severe injury or extensive destruction of tissue. There may be the formation of an abscess, which is characterized by pus and which follows injuries that become infected with pyogenic (pus-forming) organisms. The fourth outcome is chronic inflammation.

Chronic inflammation. Acute inflammation may be followed by chronic inflammation. This reaction occurs when the organism, factor, or agent responsible for the acute inflammation is not removed or when the normal processes of healing fail to occur. Repeated episodes of acute inflammation may also lead to chronic inflammation, in which the stages of acute inflammation seem to remain for long periods of time. In addition, chronic inflammation may begin insidiously, such as with a low-grade infection or other process that does not display the usual signs of acute inflammation; tuberculosis, rheumatoid arthritis, and chronic lung disease are examples of this third alternative.

Chronic inflammation typically occurs in one of the following conditions: prolonged exposure to potentially toxic substances such as asbestos, coal dust, and silica that are nondegradable; immune reactions against one’s own tissue (autoimmune diseases such as lupus and rheumatoid arthritis); and persistent infection by an organism that is either resistant to drug therapy or insufficiently toxic to cause an immune reaction (such as viruses, tuberculosis, and leprosy). The characteristics of chronic inflammation are similar to those of acute inflammation but are less dramatic and more protracted.

Bibliography

Challem, Jack. The Inflammation Syndrome: Your Nutritional Plan for Great Health, Weight Loss, and Pain-Free Living. Rev. ed. Hoboken: Wiley, 2010. Print.

Dartt, Darlene A. Immunology, Inflammation and Diseases of the Eye. Boston: Academic, 2011. Print.

Gallin, John I., and Ralph Snyderman, eds. Inflammation: Basic Principles and Clinical Correlates. 3rd ed. New York: Raven, 1999. Print.

Górski, Andrzej, Hubert Krotkiewski, and Michał Zimecki, eds. Inflammation. Boston: Kluwer, 2001. Print.

Guha, Sushovan, Sunil Krishnan, and Bharat B. Aggarwal. Inflammation, Lifestyle, and Chronic Disease: The Silent Link. Boca Raton: CRC, 2012. Print.

Kumar, Vinay, Abul K. Abbas, and Nelson Fausto, eds. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Philadelphia: Saunders/Elsevier, 2015.

McPherson, R. "Inflammation and Coronary Artery Disease: Insights from Genetic Studies." The Canadian Journal of Cardiology 28.6 (2012): 662–66. Print.

Meggs, William Joel, and Carol Svec. The Inflammation Cure. Chicago: Contemporary, 2004. Print.

Preddy, Victor R., and Ronald R. Watson. Bioactive Food as Interventions and Related Inflammatory Diseases. Boston: Elsevier, 2013. Print.

Yian, Gu, and Nikolas Scarmeas. "Dietary Inflammation Factor Rating System and Risk of Alzheimer Disease in Elder." Alzheimer Disease and Associated Disorders 25.2 (2011): 149–54. Print.

Zimmerli, Werner. Bone and Joint Infections: From Microbiology to Diagnostics and Treatment. Hoboken: Wiley, 2015. Print.

How has Behrman proven himself a source of new life to Johnsy in "The Last Leaf"?

Behrman has at long last painted his "masterpiece," a painting that gives rebirth to Johnsy's spirit and will to live.

A poignant tale, O. Henry's "The Last Leaf" relates the story of two young aspiring artists who have come from Maine and California in May to the quaint Greenwich Village where they establish themselves in a studio. But, when the New York winter besets the Village, Johnsy, who is from warm, sunny California, is not acclimated to such weather. Consequently, she is stricken with pneumonia.

Despite the efforts of the physician and the tender care of her dear friend Sue, Johnsy continues to weaken and the frail young woman begins to despair of getting well. In fact, she tells Sue that she has been watching the leaves fall off the ivy outside her window: "When the last one falls I must go, too. I've known that for three days. Didn't the doctor tell you?"

Sue will not hear such despairing talk:

"Don't be a goosey. Why, the doctor told me this morning that your chances for getting well real soon were...ten to one!"

In truth, Sue is really worried, so she goes to Mr. Behrman, who lives on the ground floor and asks him what they can do to make Johnsy more positive. He accompanies Sue upstairs, and they find Johnsy sleeping. But, when they look out at the ivy vine, they stare at each other holding their breaths; then, Sue pulls down the window shade. Later on, after posing as a model for Sue, Behrman departs.

The next morning when Johnsy awakens, she asks Sue to roll up the shade. Reluctantly, Sue does so; however, despite the cold rain and wind of the previous night, one leaf yet clings to the window. Johnsy has a conversion from her despairing thoughts of dying:

"I've been a bad girl, Sudie," said Johnsy. "Something has made that last leaf stay there to show me how wicked I was.  It is a sin to want to die. You may bring me a little broth now, and some milk with a little port in it, ...."

When the doctor comes in the afternoon, he sees promise that Johnsy will get well. The next day Johnsy's condition is, indeed, much improved.

Unfortunately, however, Mr. Behrman died of pneumonia because on the night of the cold rain, he dragged a ladder outside, climbed it, and painted an ivy leaf onto the window. He then fell ill, and lay all night in his wet clothes. By the time the janitor found him, it was too late. 

Although Mr. Behrman's death was unfortunate, he had painted a masterpiece because, like all great art, it inspired the viewer: Johnsy. As a result, Johnsy's spirit felt a rebirth with the sight of it and she regained the will to live.

What is nephrostomy?

Cancers treated:
Ovarian cancer, cervical cancer, colorectal cancer, and other cancers of the pelvic area

Why performed: Tumors may cause a blockage of one or both of the ureters, the tubes that normally carry urine from the kidneys to the bladder. The blockage causes a backup of urine into the kidneys, creating a great risk of infection and kidney damage that cannot be repaired. The insertion of nephrostomy tubes prevents the backup of urine. Nephrostomy tubes may also be placed during a diagnostic procedure called an antegrade pyelogram, which is done to determine the location of the blockage. In some cases, the nephrostomy tubes are inserted to allow the placement of anticancer drugs directly into the kidney. Nephrostomy tubes are also used for other conditions that affect the urinary tract.

Patient preparation: Nephrostomy is usually performed on hospitalized patients. Some patients may have the procedure done without admission to a hospital. Preparation for the procedure may vary depending on the patient’s condition, the physician’s practice, and the facility. Generally, the patient must not have anything to eat or any opaque fluids to drink for six to eight hours before the procedure; clear, nonalcoholic fluids may be consumed up until a few hours ahead. The physician may ask the patient to temporarily stop or adjust the dose of some medications, including aspirin, blood thinners, and diabetes medications. Laboratory tests such as a complete blood count (CBC), coagulation tests, urinalysis, and urine culture for bacteria may be done before the procedure. The physician discusses the procedure, including the type of local anesthetic used, sedation, risks, and aftercare. The patient gives the physician permission to perform the procedure by reading and signing a consent form. Before signing the form, the patient may ask the physician questions to clarify anything that the doctor has said or any part of the consent form that the patient does not understand.

Steps of the procedure: An intravenous (IV) line is inserted, usually in the patient’s arm or hand, to provide fluids, antibiotics, pain medication, and sedation. Nephrostomy is generally performed in the interventional radiology department by an interventional radiologist or urologist. The patient lies on the stomach and remains awake, although medication is given that may cause drowsiness. Monitoring of blood pressure, heart rate, and oxygen level is done throughout the procedure. Imaging procedures, such as ultrasound, computed tomography (CT), or fluoroscopy, are used to visualize the area. These procedures are done before and during insertion of the nephrostomy tube to guide the physician in placing the tube.

The site where the tube will be inserted is sterilized. A medication such as lidocaine (Xylocaine) is given to numb the skin and tissues. A small incision is made, and a needle is inserted into the kidney. Contrast dye is injected for visualization, and the nephrostomy tube is inserted. The needle is removed. A dressing is placed over the site, and the nephrostomy tube is connected to a drainage bag. The tube site is on the right or left side of the back near the waistline, depending on which kidney is blocked. If both kidneys are blocked, then the physician will insert tubes for each kidney.

After the procedure: The patient is taken to the recovery room or back to the hospital room. A nurse will monitor the patient for any changes in blood pressure, heart rate, or breathing. The nurse monitors the urine output by measuring the urine collected in the bag. The bag may be attached to the patient’s leg by use of straps that are provided. Before discharge, the physician and/or a nurse will give the patient instructions on caring for the nephrostomy site, emptying the bag, monitoring the urine output, and noting signs of complications. Patients may need others to assist them in caring for the site and emptying the bag once they are home. In addition to the urine drained through the nephrostomy tube, the patient will still need to urinate. If only one tube is placed but the other kidney works normally, then the urine from that kidney still passes into the bladder. If nephrostomy tubes are placed in both kidneys, then there may still be drainage of some urine into the bladder.

Risks: The risks of nephrostomy include bleeding, infection, blood clots in the nephrostomy tube or bladder, and dislodgement of the nephrostomy tube. Pain at the catheter site may also occur.

Results: The placement of nephrostomy tubes will alleviate the backup of urine in the kidneys or allow treatment to be given. Although their use is normally for a short time, in some cases the blockage cannot be removed and the nephrostomy tubes remain in use permanently. In these cases, the tubes are replaced periodically.

Berman, Joel. Understanding Surgery: A Comprehensive Guide for Every Family. Wellesley: Branden, 2001. Print.

Clinical Center, Natl. Inst. of Health. Patient Education: Caring for Your Percutaneous Nephrostomy Tube. Bethesda: Natl. Inst. of Health Clinical Center, n.d. Digital file.

Hashim, Hashim, et al., eds. Urological Emergencies in Clinical Practice. London: Springer-Verlag, 2013. Print.

Kellicker, Patricia Griffin. "Nephrostomy." Health Library. EBSCO Information Services, Mar. 2014. Web. 4 Nov. 2014.

Nurse’s Five-Minute Consult: Treatments. Philadelphia: Lippincott, 2007. Print.

"Urinary Diversion." National Kidney and Urologic Diseases Information Clearinghouse. Natl. Inst. of Diabetes and Digestive and Kidney Diseases, Natl. Inst. of Health, 18 Sept. 2013. Web. 4 Nov. 2014.

What is Marfan syndrome?

Causes and Symptoms

Studies have located the gene that causes the inherited form of Marfan syndrome. About 25 percent of Marfan syndrome cases result from spontaneous mutation. While this knowledge promises better future recognition of the condition, the range and severity of the condition is so variable that diagnosis remains difficult.

Usually, Marfan syndrome is discovered through a detailed family history. The observation that a person is tall and slender and has unusually long fingers or arms is often an early clue. The presence of loose joints with great suppleness is characteristic of the disease. Manifestations of this condition may occur in any part of the body, but the heart, eyes, and spinal column are the most common.

Treatment and Therapy

Because a variety of organs may be involved in Marfan syndrome, it is essential that several specialists form a team to evaluate and monitor the patient during his or her lifetime. The most serious, and most common, problem area is the heart. Mitral valve problems may lead to leakage or regurgitation of blood. The aortic valve can develop a backflow into the heart.

In the eyes, a characteristic sign is the dislocation of the lens. This symptom is difficult to detect and, like many others, can vary widely in intensity. Cataracts are also associated with this condition.

Other characteristics are found in the skeleton. Spinal curvature, or scoliosis, and a breastbone that either protrudes or indents are observed. Crowded teeth and an arched palate are not uncommon.

Any of these symptoms can lead to serious consequences and should be discovered as early as possible. Regular examinations by specialists in cardiology, ophthalmology, and orthopedics are essential. Most of the possible progressive aspects of the condition can be treated effectively.

Bibliography:

Alan, Rick. "Marfan Syndrome." Health Library, March 15, 2013.

Hetzer, R., P. Gehle, and J. Ennker, eds. Cardiovascular Aspects of Marfan Syndrome. New York: Springer, 1995.

"Learning about Marfan Syndrome." National Human Genome Research Institute, November 14, 2012.

"Marfan Syndrome." Genetics Home Reference, March 2012.

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

Pyeritz, Reed E., and Julia Conant. Marfan Syndrome. 5th ed. Port Washington, N.Y.: National Marfan Foundation, 2001.

Robinson, Peter N., and Maurice Godfrey, eds. Marfan Syndrome: A Primer for Clinicians and Scientists. New York: Kluwer Academic/Plenum, 2004.

What is the best information on Ben Franklin?

Benjamin Franklin was born in 1704 in Boston and died in 1790. He is remembered as a scientist, inventor, author, and diplomat. Depending on what kind of information you find interesting or worth knowing about someone, it is difficult for me to tell you what the "best" thing about Ben Franklin was. Here I can share with you some widely-valued facts about Franklin, as well as some of my own favorite anecdotes.

Franklin was fond of writing and had an active mind- which he would build a career on later in life. When he was just sixteen, he was struggling to find anyone who would publish his writings. He came up with the pseudonym Mrs. Silence Dogood and wrote a fictitious memoir about her, and "sent" the memoir by way of letters to his brother's newspaper, where they were published. Later in life he wrote and published Poor Richard's Almanac- an annual text which advised on weather and crop planting, as well as including witty sayings and advice on life.

Franklin was passionate about inventing and developed the first bifocal glasses for distance sight as well as reading. He is also remembered for his interest in electricity and his experiments thereupon. Maybe you are familiar with the story that Franklin tied a key to a kite during a thunderstorm to conduct the electricity of lightning. 

In his work as a politician and diplomat, Benjamin Franklin signed numerous official documents, including the United States Declaration of Independence and Constitution.

My favorite tidbit concerning Benjamin Franklin is that he believed in the benefits of "wind bathing-" alternately called an "air bath." This involved standing nude in the open air, or in front of a window, and allowing the winds to "cleanse" the body. Franklin apparently made it a habit to regularly sit in the nude in front of an open window to air himself!

How did Hitler violate the Versailles Treaty?

Adolf Hitler violated the Versailles Treaty in several ways. The Versailles Treaty required that Germany would dismantle its military and have only a military with defensive capabilities. Hitler began to build up the German military so that it could have offensive capabilities. He also began to draft soldiers, which was a violation of the terms of the Versailles Treaty. He felt Germany was mistreated by the terms of the Versailles Treaty. He wanted to build up the military as part of his plan to restore German nationalism and to help stimulate the economy that was in a depression.

Hitler also moved his military into the Rhineland in 1936. This region, which borders Germany and France, was supposed to be a demilitarized area according to the terms of the Versailles Treaty.

Hitler also began to invade other countries. In 1938, he annexed Austria, and he wanted to take over part of Czechoslovakia where many Germans lived. He was able to get this land, called the Sudetenland, as a result of the Munich Pact. In 1939, he invaded the rest of Czechoslovakia.

Adolf Hitler violated the Versailles Treaty in many ways.