Sunday 31 May 2015

Why does Bill and Sam's plan backfire in "The Ransom of Red Chief"?

O. Henry's "The Ransom of Red Chief" is the perfect short story to find examples of irony. Irony is when the opposite of what is expected to happen, happens. For example, when two grown men decide to kidnap a young boy of ten, it is they, not him, who should have the upper hand. The kidnappers should strike fear into the boy and the boy's family in order to be taken seriously and obtain the...

O. Henry's "The Ransom of Red Chief" is the perfect short story to find examples of irony. Irony is when the opposite of what is expected to happen, happens. For example, when two grown men decide to kidnap a young boy of ten, it is they, not him, who should have the upper hand. The kidnappers should strike fear into the boy and the boy's family in order to be taken seriously and obtain the ransom they want. None of these things occur. In fact, Johnny Dorset strikes fear into Bill and Sam by threatening to scalp Bill and to burn Sam at the stake by daybreak. Johnny inflicts other acts of terror on the kidnappers while his father, Ebenezer, does the unexpected as well.


Ebenezer Dorset does not accommodate the kidnappers' demands for ransom. He knows his son for who he is and therefore knows that Johnny can take care of himself in any crisis. Two kidnappers are nothing compared to his son. This attitude is ironic because no one would expect a father to be calm in a situation like the kidnapping of his son. All the father has to do is wait until the kidnappers have had enough of Johnny and they will more than likely pay him to give back his son. Ebenezer is right because he sends them an offer to pay him $250 to take Johnny off their hands. Bill and Sam comply because they need their sleep and a chance to get out of town before something worse happens. Therefore, Bill and Sam's kidnapping plan to get some "quick" money for their next con backfires because of the above-mentioned, unexpected events that occur.

Saturday 30 May 2015

What are learning disorders? |


Introduction

Learning disorders (LD) is a general term for clinical conditions that meet four diagnostic criteria, as specified by the fifth edition of the
Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published in 2013 by the American Psychiatric Association. Those criteria include an individual displays symptoms of a learning disorder for more than six months, despite efforts to provide additional or specifically targeted instruction; the person's achievement in an academic domain (such as reading) is substantially below that expected given his or her age, schooling, and level of intelligence, and this learning disturbance interferes significantly with academic achievement or activities of daily living that require specific academic skills; the symptoms manifest during the individual's school-age years or young adulthood; and intellectual disorders, sensory problems, adverse learning conditions, and other potential causes have been ruled out. Earlier editions of the DSM listed four subcategories of learning disorders: reading disorder, mathematics disorder, disorder of written expression, and learning disorder not otherwise specified (NOS). However, the DSM-5 groups all learning disorders under the category of specific learning disorder. Specific learning disorder encompasses all varieties of learning disorders, including problems in reading, writing, and mathematics.





A variety of statistical approaches are used to produce an operational definition of academic achievement that is “substantially below” expected levels. Despite some controversy about its appropriateness, the most frequently used approach defines “substantially below” as a discrepancy between achievement and intelligence quotient (IQ) of more than two standard deviations (SD). In cases where an individual’s performance on an IQ test may have been compromised by an associated disorder in linguistic or information processing, an associated mental disorder, a general medical condition, or the individual’s ethnic or cultural background, a smaller discrepancy (between one and two SDs) may be acceptable. In general, the DSM-5 has moved somewhat away from the use of IQ tests in diagnosis, instead encouraging a greater focus on assessments that take environmental and other factors into account.


Differential diagnosis involves differentiating learning disorders from normal variations in academic achievement; scholastic difficulties due to lack of opportunity, poor teaching, or cultural factors; and learning difficulties associated with a sensory deficit. In cases of autism spectrum disorder, communication disorders, or mild intellectual disability, an additional diagnosis of learning disorder is given if the individual’s academic achievement is substantially below the expected level given the individual’s schooling and intelligence.


The term learning disorders was first applied to a clinical condition meeting these three criteria in the DSM-IV, published in 1994. Earlier editions of the DSM used other labels such as learning disturbance, a subcategory within special symptom reactions in DSM-II (1968). In DSM-III (1980) and DSM-III-R (1987), the condition was labeled academic skills disorders and listed under specific developmental disorders; furthermore, the diagnosis was based only on academic achievement substantially below the norm. The LD condition is also known by names other than those used in the psychiatric nomenclature, most frequently as learning disabilities, which may manifest in an imperfect ability to listen, think, speak, read, write, spell, or do mathematical calculations in children whose learning problems are not primarily the result of visual, hearing, or motor handicaps, mental retardation, emotional disturbance, or environmental, cultural, or economic disadvantage. Specific learning disorders are also commonly referred to by other names, such as dyslexia
(reading disorder), dyscalculia
(mathematics disorder), or dysgraphia (disorder of written expression). Empirical evidence about prevalence, etiology, course of the disorder, and intervention comes mainly from subjects identified as having dyslexia or learning disabilities.




Prevalence

Prevalence rates for learning disorders vary, depending on the definitions and methods of determining the achievement-intelligence discrepancy. According to a 2014 report by the National Center for Learning Disabilities (NCLD), approximately 5 percent of public school students in the United States have been diagnosed with a learning disorder; in addition, other children who fit the DSM-5's criteria may not yet have been officially diagnosed. The prevalence rate for specific subsets of specific learning disorder is more difficult to establish because many studies simply report the total number of learning disorders without separating them according to subcategory. According to the NCLD report, specific learning disorder with impairment in reading is the most common, followed by impairment in mathematics. Disorder of written expression alone is rare; it is usually associated with the other categories of specific learning disorder.


The NCLD report further states that male students are significantly more likely to be diagnosed with a learning disability than female students; as of 2014, two-thirds of diagnosed students were male. LD often coexists with another disorder, usually language disorders, communication disorders, or attention-deficit hyperactivity disorder (ADHD).




Etiology

There is strong empirical support for a genetic basis of reading disorders or dyslexia from behavior genetic studies. John C. DeFries and his colleagues indicate that heredity can account for as much as 60 percent of the variance in reading disorders or dyslexia. As for the exact mode of genetic transmission, Lon R. Cardon and his collaborators, in two behavior genetic studies, identified chromosome 6 as a possible quantitative trait locus for a predisposition to develop reading disorder. The possibility that transmission occurs through a subtle brain dysfunction rather than autosomal dominance has been explored by Bruce Pennington and others.


The neurophysiological basis of reading disorders has been explored in studies of central nervous dysfunction or faulty development of cerebral dominance. The hypothesized role of central nervous dysfunction has been difficult to verify despite observations that many children with learning disorders had a history of prenatal and perinatal complications, neurological soft signs, and electroencephalograph abnormalities. In 1925, neurologist Samuel T. Orton hypothesized that reading disorder or dyslexia results from failure to establish hemispheric dominance between the two halves of the brain. Research has yielded inconsistent support for Orton’s hypothesis and its reformulation, the progressive lateralization hypothesis. However, autopsy findings of cellular abnormalities in the left hemisphere of dyslexics that were confirmed in brain-imaging studies of live human subjects have reinvigorated researchers. These new directions are pursued in studies using sophisticated brain-imaging technology.


Genetic and neurophysiological factors do not directly cause problems in learning the academic skills. Rather, they affect development of neuropsychological, information-processing, linguistic, or communication abilities, producing difficulties or deficits that lead to learning problems. The most promising finding from research on process and ability deficits concerns phonological processing—the ability to use phonological information (the phonemes or speech sounds of one’s language)—in processing oral and written language. Two types of phonological processing, phonological awareness and phonological memory (encoding or retrieval), have been studied extensively. Based on correlational and experimental data, there is an emerging consensus that a deficit in phonological processing is the basis of reading disorder in a majority of cases.




Assessment

Assessment refers to the gathering of information to attain a goal. Assessment tools vary with the goal. If the goal is to establish the diagnosis, assessment involves the individualized administration of standardized tests of academic achievement and intelligence that have norms for the child’s age and, preferably, social class and ethnicity. To verify that the learning disturbance is interfering with a child’s academic achievement or social functioning, information is collected from parents and teachers through interviews and standardized measures such as rating scales. Behavioral observations of the child may be used to supplement parent-teacher reports. If there is a visual, hearing, or other sensory impairment, it must be determined that the learning deficit is in excess of that usually associated with it. The child’s developmental, medical, and educational histories and the family history are also obtained and used in establishing the differential diagnosis and clarifying etiology.


If LD is present, then the next goal is a detailed description of the learning disorder to guide treatment. Tools will depend on the specific type of learning disorder. For example, in the case of dyslexia, E. Wilcutt and Pennington suggest that the achievement test given to establish the achievement-intelligence discrepancy be supplemented by others such as the Gray Oral Reading Test, a timed measure of reading fluency as well as of reading comprehension. Still another assessment goal is to identify the neuropsychological, linguistic, emotional, and behavioral correlates of the learning disorder and any associated disorders. A variety of measures exist for this purpose. Instrument selection should be guided by the clinician’s hypotheses, based on what has been learned about the child and the disorder. Information about correlates and associated disorders is relevant to setting targets for intervention, understanding the etiology, and estimating the child’s potential response to intervention and prognosis.


In schools, identification of LD involves a multidisciplinary evaluation team, including the classroom teacher, a psychologist, and a special education teacher or specialist in the child’s academic skill deficit (such as reading). As needed, input may be sought from the child’s pediatrician, a speech therapist, an audiologist, a language specialist, or a psychiatrist. A thorough assessment should provide a good description of the child’s strengths as well as weaknesses that will be the basis of effective and comprehensive treatment plans for both the child and the family. In school settings, these are called, respectively, an Individualized Education Plan (IEP) and an Individual Family Service Plan (IFSP).




Treatment

Most children with LD require special education. Depending on the disorder’s severity, they may learn best in a one-to-one setting, small group, special class, or regular classroom plus resource room tutoring.


Treatment of LD should address both the disorder and associated conditions or correlates. Furthermore, it should include assisting the family and school in becoming more facilitative contexts for development of the child with LD. Using neuropsychological training, psychoeducational methods, behavioral or cognitive behavioral therapies, or cognitive instruction, singly or in combination, specific interventions have targeted the psychological process dysfunction or deficit assumed to underlie the specific learning disorder; a specific academic skill such as word attack; or an associated feature or correlate such as social skills. Process-oriented approaches that rose to prominence in the 1990s are linguistic models aimed at remediating deficits in phonological awareness and phonological memory and cognitive models that teach specific cognitive strategies that enable the child to become a more efficient learner. Overall, treatment or intervention studies during the last two decades of the twentieth century and at the beginning of the twenty-first century are more theory-driven, built on prior research, and rigorous in methodology. Many studies have shown significant gains in target behaviors. Transfer of training, however, remains elusive. Generalization of learned skills and strategies is still the major challenge for future treatment research, and LD remains a persistent or chronic disorder.




Bibliography


American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-5. Washington: American Psychiatric Association, 2013. Print.



American Psychiatric Association. "Specific Learning Disorder." American Psychiatric Association. APA, 2013. Web. 5 June 2014.



Brown, F. R., H. L. Aylward, and B. K. Keogh, eds. Diagnosis and Management of Learning Disabilities. San Diego: Singular, 1996. Print.



Harwell, Joan M., and Rebecca Williams Jackson. The Complete Learning Disabilities Handbook . 3rd ed. San Francisco: Jossey-Bass, 2008. Print.



Lerner, Janet W., and Beverley Johns. Learning Disabilities and Related Mild Disabilities: Characteristics, Teaching Strategies, and New Directions . Boston: Houghton, 2009. Print.



Lyon, G. Reid. “Treatment of Learning Disabilities.” Treatment of Childhood Disorders. Ed. E. J. Mash and L. C. Terdal. New York: Guilford, 1998. Print.



National Center for Learning Disabilities. The State of Learning Disabilities. New York: NCLD, 2014. Print.



Sternberg, Robert J., and Louise Spear-Swerling, eds. Perspectives on Learning Disabilities. Boulder: Westview, 1999. Print.

How does the structure of Maya Angelou's poem "Still I Rise" affect the meaning?

Maya Angelou’s poem “Still I Rise,” published in 1978, expresses the empowering message to rise above hate and pain.


The poem has many repeated structures. For example, the poem begins with addressing a “You” who commits acts of hate against the narrator. This “you” is never specifically defined and can be interpreted as an individual or a collective group. There is a repeated list of actions this “you” may commit against the speaker—tell lies about...

Maya Angelou’s poem “Still I Rise,” published in 1978, expresses the empowering message to rise above hate and pain.


The poem has many repeated structures. For example, the poem begins with addressing a “You” who commits acts of hate against the narrator. This “you” is never specifically defined and can be interpreted as an individual or a collective group. There is a repeated list of actions this “you” may commit against the speaker—tell lies about her, step on her, look at her with contempt, even “kill me with your hatefulness.” The poem twice uses the word “history,” showing the struggle to rise above hate is not just personal but collective, reflecting Angelou’s African American heritage.


The poem also uses a structure of repeated questions directed against “you” who the speaker defies with her boldness. Rather than shrinking back in the face of hate, she flaunts her “sassiness,” “haughtiness,” and “sexiness.” Thus, along with the racial themes of the poem, these moments reveal feminist ideas too. The female speaker is proud to “dance like I’ve got diamonds / At the meeting of my thighs.”


The poem’s repeated refrain, “I rise,” underpins the structure of the poem. Including the title, the phrase is repeated eleven times. This repetition emphasizes the speaker’s audacious determination, not to be pushed down, but to rise up against hate, pain, lies, and fear. 


To especially notice the sound effects created by the structure of the poem, hear Angelou's reading of the poem here: 

Which was not a cause of civil unrest in the United States in the 1960s? A. Black citizens were still fighting against...

There were many factors that led to civil unrest in the 1960s. The lack of civil rights for African-Americans was a big factor. African-Americans had been protesting peacefully for an end to discrimination and segregation. However, progress was very slow, and some people believed a more aggressive policy was needed than Dr. King’s non-violent methods. When people saw how non-violent protestors were treated, such as with the Selma March, more people became upset and demanded...

There were many factors that led to civil unrest in the 1960s. The lack of civil rights for African-Americans was a big factor. African-Americans had been protesting peacefully for an end to discrimination and segregation. However, progress was very slow, and some people believed a more aggressive policy was needed than Dr. King’s non-violent methods. When people saw how non-violent protestors were treated, such as with the Selma March, more people became upset and demanded action.


The opposition to the Vietnam War grew in the 1960s. Many Americans, especially young Americans, were opposed to this war. They didn’t believe this was a conflict in which we should be involved. There were many anti-war protests, and some of them became violent.


Women were upset that they weren’t being treated fairly. They made less than men made for the same kind of work. Women also found it hard to break into male-dominated professions. The National Organization for Women formed to protest the lack of equal treatment and the lack of opportunities for women.


The correct answer to this question is answer D. It is not an accurate statement to say that most people in the cities were rich. Some of the violence in the cities occurred because there were many poor people living there. For various reasons, including discrimination, it was very hard for some people living in the cities to break away from poverty. It is not accurate to say most people living in the cities were rich.


The correct answer to your question is answer D.

What is von Willebrand disease?


Causes and Symptoms

Von Willebrand disease (vWD) is a genetic disorder affecting the normal clotting
function of platelets in the blood. There are three types of vWD that run in families, all due to inheriting a gene mutation. The pattern of inheritance may be autosomal dominant or autosomal recessive, although with either, both males and females are affected equally; some persons could be carriers of the defective gene without exhibiting any symptoms. There is another form of vWD called acquired von Willebrand syndrome. This disease is not caused by inheriting a gene mutation, and thus does not run in families. This disease is characterized by the qualitative or quantitative deficiency of von Willebrand factor
(vWF). This glycoprotein, present in platelets and the endothelium of blood vessels, facilitates the adhesion of platelets to one another to form a stable clot when there has been injury to a blood vessel. Therefore, patients with vWD exhibit the signs and symptoms of blood clotting abnormality.





Three types of vWD are recognized: type I vWD, with decreased levels of the protein vWF; type II vWD, with normal levels but decreased activity of vWF; and type III vWD, the most severe form of the disease, with a nearly complete deficiency of vWF.


Patients with mild or moderate vWD (type I or type II) can become symptomatic at any age and usually exhibit one or more of the following symptoms: easy bruisability, bleeding gums, frequent nosebleeds, bleeding points under the skin (subcutaneous hemorrhages), prolonged bleeding after injury or surgery of any kind, and, in women, menorrhagia, or excessive bleeding during menstrual periods. Patients with severe type III vWD become symptomatic at an early age and exhibit symptoms similar to hemophilia, with bleeding into and pain in the joints (hemathrosis), spontaneous bleeding into the gastrointestinal tract and from the mucous membranes that is potentially life-threatening, and painful bleeding into the muscles (hematomas). Some patients with type III disease also have multiple episodes of acute gastrointestinal bleeding and are often misdiagnosed. Some patients also have decreased factor VIII, which is deficient in hemophilia. The symptoms of vWD appear to decrease with advancing age, and they are milder in pregnancy, when factor VIII levels
are high. Typically, bleeding time is prolonged in all patients with vWD.


The disease is diagnosed in the laboratory using specialized blood tests, such as the von Willebrand factor antigen (which measures the amount of vWF in blood), Ristocetin cofactor (which measures the function of vWF in blood), vWF multimers, and factor VIII levels. A careful family history of the disease should help distinguish it from the rarer hemophilia. A correlation of family history, laboratory findings, and clinical findings may be needed in order to diagnose the condition in mild cases of vWD, in which diagnosis is difficult.


A few cases of acquired vWD have been identified, with antibodies against vWF being present. Such persons may be otherwise healthy or may also exhibit other immune-mediated diseases.




Treatment and Therapy

The aim of therapy for vWD is to stop the bleeding and to prevent further episodes. Both goals can be met by increasing vWF and/or factor VIII levels in the blood. This result can be achieved by many methods, the most common being the administration of the drug DDAVP (desmopressin acetate) by a nasal or intravenous route. This drug does not seem to have a beneficial effect in type III disease, and these patients may need intravenous infusions of concentrates of factor VIII and vWF. For women with heavy menstrual bleeding, estrogen therapy in the form of oral contraceptive (birth control) pills is a good alternative, as it has been observed that estrogen increases the levels of vWF in the blood. Local antifibrinolytic drugs, which delay the dissolution of the clot, are useful in milder presentations of the disease (such as nosebleeds) or following dental procedures.


Preventive care should be taken by all persons suspected of having vWD. Adequate care and treatment taken prior to any dental procedure or surgical intervention should prevent the excessive loss of blood. Children with the disease are advised against engaging in rough and vigorous sports activities with a high potential for injury. Patients should also be cautioned against the excessive intake of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), as they worsen the symptoms of vWD.




Perspective and Prospects

In 1925, Finnish physician Erik von Willebrand identified a bleeding disorder in the natives of the Aland Islands and named it after himself. Later, it was found that the disease was caused by a defect in one of the clotting factors, and the factor was also named after the brilliant physician. Today, vWD is recognized as the most common inherited bleeding disorder; it is thought to affect 1 to 3 percent of the population, with an equal distribution between the two sexes. It is important to distinguish this condition from the better-known hemophilia. The diagnosis of vWD in women is significant, as it is a popular misconception that bleeding disorders occur only in men.


The present drug therapy available to combat the disease is quite effective in reducing the bleeding that occurs. Modern-day medicine has reduced the problems of blood infections associated with the administration of cryoprecipitates. Further research is being conducted to develop an effective recombinant vWF.




Bibliography


Fauci, Anthony S., et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill, 2012.



Gersten, Todd, Linda J. Vorvick, and David Zieve. "Von Willebrand Disease." MedlinePlus, Feb. 16, 2012.



Greer, John, et al., eds. Wintrobe’s Clinical Hematology. 12th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2009.



Judd, Sandra J., ed. Genetic Disorders Sourcebook: Basic Consumer Information About Hereditable Disorders. 4th ed. Detroit, Mich.: Omnigraphics, 2010.



"Platelet Disorders." MedlinePlus, May 22, 2013.



Rosenblum, Laurie, and Michael Woods. "Von Willebrand Disease." Health Library, Nov. 26, 2012.



Ruggeri, Zaverio M., ed. Von Willebrand Factor and the Mechanisms of Platelet Function. New York: Springer, 1998.



Westphal, Robert G., and Dennis M. Smith, Jr., eds. Treatment of Hemophilia and Von Willebrand’s Disease: New Developments. Arlington, Va.: American Association of Blood Banks, 1990.



"What Is von Willebrand Disease?" National Heart, Lung, and Blood Institute, June 1, 2011.

Friday 29 May 2015

How would one describe nine-year-old Scout Finch based on the Old Sarum bunch mob scene in Harper Lee's To Kill a Mockingbird?

As the children approach and observe the mob scene unfold, Scout, being young, does not share the same fears Jem does. In fact, she's not certain exactly why Jem is afraid that Atticus may be in danger. Hence, when Atticus responds, "Do you really think so?" to one of the mob member's statement that the sheriff being off in the woods on a wild-goose chase changes Atticus's ability and need to defend Tom Robinson...

As the children approach and observe the mob scene unfold, Scout, being young, does not share the same fears Jem does. In fact, she's not certain exactly why Jem is afraid that Atticus may be in danger. Hence, when Atticus responds, "Do you really think so?" to one of the mob member's statement that the sheriff being off in the woods on a wild-goose chase changes Atticus's ability and need to defend Tom Robinson from the mob, Scout thinks he is playing some sort of game of whits and happily bounds out of hiding to greet him. Scout phrases her young line of thinking in the following:



This was the second time I heard Atticus ask that question in two days, and it meant somebody's man would get jumped. This was too good to miss. I broke away from Jem and ran as fast as I could to Atticus. (Ch. 15)



Even once she is in the midst of the mob, Scout still doesn't feel Jem's fear; instead, she only feels embarrassed to find herself in the midst of a crowd of strangers, not in the midst of the same crowd of friends who had gathered in Atticus's lawn the night before. Scout's brave actions that serve to break up the mob stem from a combination of her youthful embarrassment and her efforts to show politeness.

Standing on the steps of the jail, Scout searched the mob until she found a familiar face, that of Walter Cunningham. She instantly greets him and asks him, "How's your entailment gettin' along?" because she knows it's the polite thing to do. When he doesn't respond, she introduces herself and reminds him that his son, Walter Cunningham Jr. is in her class, asking Mr. Cunningham to say "hey" for Walter for her. When he still doesn't respond, she goes back to talking about his entailment, saying, "Entailments are bad," because she remembers Atticus once told her it is polite to "talk to people about what they were interested in, not about what you were interested in." She continues forth to remind Mr. Cunningham that Atticus had once promised he and Mr. Cunningham would "ride [his entailment] out together." All of these attempts at conversation are simply Scout's way of being polite, not realizing the extent of the imminent danger.

Scout's youthful, naive attempt at making polite conversation with Mr. Cunningham inadvertently serves to break up the mob. Scout inadvertently breaks up the mob by reminding Mr. Cunningham of his humanity, first by being polite, second by empathizing with his plight due to his entailment, and third by reminding him of the amount of respect he has for Atticus. Scout's actions before the mob show us just how much childlike innocence can accomplish, especially when such innocence reflects polite and empathetic behavior.

Identify the low pressure area, the air masses, the one cold front, and one warm front in the weather map. There are also two air masses to...

On this map, the low pressure area can found near where South Carolina and Georgia meet on the coast. By reading the barometric pressures (the black numbers) we can find this area has the lowest air pressures on the map. Towards the NW into Tennessee is a high pressure system, the numbers beginning with 0's are actually 1000 numbers, however standard practice is to drop the one to save space. 


All air wants to move...

On this map, the low pressure area can found near where South Carolina and Georgia meet on the coast. By reading the barometric pressures (the black numbers) we can find this area has the lowest air pressures on the map. Towards the NW into Tennessee is a high pressure system, the numbers beginning with 0's are actually 1000 numbers, however standard practice is to drop the one to save space. 


All air wants to move from higher to lower pressures, and we can see that on this chart. The flags pointing out from each of the different air port weather stations point in the direction air is coming from. This shows all the wind is moving towards the low pressure area as we would expect. 


One air mass (a mass of air with similar temperature and humidity throughout) is moving in from over the ocean and will bring warm humid weather. This is a Maritime Tropical air mass because it starts in a warmer climate over a large body of water. Another is moving from the NW and is carrying much drier and colder air. This is a Continental Polar air mass, cold and dry from having started over a land mass. 


Where an air mass meets another we refer to this as a front. As the MT and CP air masses converge on the low pressure area they bring moving air and weather patterns. The MT, being warmer than the air it is approaching, will be moving slowly and without much of a storm presence. This makes a warm front which bring warmer air and a smattering of rain for a day or two. The CP however is being led by a cold front. This will be much more dense, cold, and usually pushes a storm on its front. The low pressure area will probably have a thunderstorm and a cold night followed by a slow warming with slightly rainy/cloudy skies for a couple of days. 


In the picture I tried to show where everything would be however Paint can only do so much. I hope this helps! 

Thursday 28 May 2015

What are prevention methods for addiction? What does research tell us?


Prevention Program Efficacy

Of the three levels of prevention, primary prevention receives most of the funding and attention, as it is often more effective and less costly than secondary or tertiary prevention. However, the effectiveness of a prevention program is difficult to determine without expensive, long-term studies. As a consequence, a large number of programs are in use in the United States that may not be effective. For example, an estimated 80 percent of youths age twelve to seventeen years were exposed to some form of education about drugs or alcohol in 2004, but only 20 percent were exposed to effective prevention programs.


Research on prevention methods may take the form of a randomized-controlled trial (RCT) or observational study or may use more informal evaluation methods. The most rigorous design tests the program’s effects on a group that receives the intervention and compares results with a second group that did not receive the intervention (a control group).


One of the drawbacks of most of the studies conducted to evaluate prevention programs is that substance abuse is usually self-reported, and so studies may overestimate the benefits of the intervention because of underreporting by participants. In addition, short-term follow-up, lack of randomization, lack of blinding, and failure to control for confounders are all common in the research literature in this area and may cause results to appear more or less significant than if higher-quality research methods had been used.


Another method that is sometimes used to assess interventions is cost-effectiveness research, which includes an assessment of the cost of providing the program and the costs or losses prevented by the program. Taking both costs and benefits into account enables policymakers and communities to choose programs that not only are effective but also are efficient in the use of resources. However, cost-effectiveness is not often evaluated, and there are no requirements that a program be cost-effective for it to be used.


One notable feature of most of the research on substance abuse prevention is that the effect sizes are generally quite small. Therefore, to prevent substance abuse and its adverse consequences, a comprehensive program of intervention strategies is required. No single intervention can reduce the problem enough on its own.




Alcohol Abuse

Prevention of alcohol abuse is a major public health goal, as alcohol abuse is the most costly substance abuse disorder and the consequences are severe. A number of laws and policies have proven effective in preventing alcohol-related problems.


Well supported in the research literature as both effective and cost-effective are alcohol excise taxes of up to 20 percent of the pretax selling price, a minimum legal drinking age of twenty-one years, and a curfew for novice drivers. Laws against serving patrons who are intoxicated and ensuring that servers are trained to recognize impairment are more costly to implement and enforce, and so may not be as cost-effective in the long run. Implementation of stringent drunk driving laws (such as lower blood-alcohol concentration laws, minimum legal drinking-age laws, and sobriety checkpoints) has been credited with reducing the number of alcohol-attributable traffic deaths in the United States since about 1970.


A number of programs aimed at young people have been identified as effective in reducing alcohol abuse in the long term. These programs include Botvin’s LifeSkills Training (LST) and the family-based Strengthening Families Program (SFP). The LST program was designed to be delivered to students in seventh through ninth grades by trained teachers. It has two main goals: developing personal decision-making skills (competence-enhancement) and developing social skills to help students resist peer pressure to smoke, drink, and use drugs. In one RCT, students who attended more than 60 percent of the studied LST training sessions reported significantly lower prevalence rates for weekly drinking, heavy drinking, and problem drinking six years after the initial intervention.


Some LST programs have been specially designed for high-risk youth. In one such study, drinking frequency and drinking amount were significantly lower in students who received LST or a culturally focused intervention compared with students who received information only. In another study, students who received LST reported significantly fewer occasions of binge drinking compared with students who did not. Another variation of the LST program, which incorporated American Indian values, legends, and stories and was delivered to American Indian students in grades three through five, also reported positive long-term effects.


SFP, developed in the early 1980s, is a fourteen-session skills-training program aimed at preventing alcohol, tobacco, and drug abuse among high-risk families. More than fifteen independent studies have found similar positive results with families.


Secondary and tertiary alcohol-abuse prevention programs include screening and brief counseling interventions in primary care settings, employee assistance and skills-training programs in the workplace, and peer interventions and support groups. Brief interventions by clinicians have been shown to reduce alcohol consumption in men, but the evidence is less clear for women. However, heavy drinkers who received a brief (fifteen-to-twenty-minute) intervention have been shown to be twice as likely to decrease their alcohol consumption in the medium term (six to twelve months after an intervention) compared with drinkers receiving no intervention.


Minimal research exists on the effectiveness of workplace prevention programs. The effectiveness of skills training to reduce consumption among college students also has not been proven, although there is weak evidence of some effects. Also, peer-led programs may be more effective than teacher-led programs among young people.




Tobacco Use

As with alcohol, a number of laws and policies have been used to prevent underage smoking and to encourage smokers to quit. Indoor and workplace smoking bans, enforcement of prohibitions on underage purchase, and increased taxes on tobacco products have all been shown to be effective in preventing smoking.


A strong relationship exists between increased taxes on tobacco products and rates of smoking among people of all ages. For example, after an increase of $1.25 in New York State’s excise tax on cigarettes in 2008, the adult smoking rate dropped by 12 percent. Every 10 percent increase in the price of cigarettes reduces youth smoking by about 7 percent.


Going beyond smoke-free workplace policies, some employers have even instituted policies against hiring smokers, although the evidence base is limited in terms of the effectiveness of such policies in preventing smoking; about twenty-nine states have passed laws protecting smokers who smoke on their own time as of 2015.


The We Card Program, established by the Coalition for Responsible Retailing in 1995, “is a youth-smoking prevention” program in the United States. The program primarily involves tobacco sales training and education, which includes the display of graphical materials in retail locations that sell tobacco products. The program’s effectiveness has been questioned in terms of preventing sales of tobacco products to minors. Some critics have argued that the program was intended to enhance positive perceptions of tobacco companies and to reduce law enforcement “stings” of retail establishments. The campaign may even be perceived by some high-risk youths as encouragement to smoke upon turning eighteen.


School-based programs for primary prevention of smoking include information campaigns, skills-training programs, and community interventions. School-based programs that simply provide information have not proven effective in preventing smoking. Although studies of programs that used a skills-training approach have found short-term effects in preventing youth smoking, the highest quality and longest trial (the Hutchinson Smoking Prevention Project, a fifteen-year randomized trial) found no long-term effects. Programs that teach social resistance skills (the ability to resist peer pressure) can reduce the proportion of youth who initiate smoking by about one-third relative to controls, although the effects of the intervention dissipate by about three years after the program ends.


Groups that have been the targets of a number of secondary interventions aimed at preventing smoking in users include pregnant women, persons with heart disease, and persons who have had surgery. The most effective programs for these adults appear to be brief interventions delivered by clinicians. Brief smoking-cessation counseling offered at the first prenatal visit results in more women quitting than no intervention or in an education-only intervention. Full insurance coverage (removing copayments or coinsurance) for smoking cessation therapy, including nicotine replacement (such as nicotine gum or patches) or pharmaceutical products such as Zyban and Chantix, also is effective and cost-effective in reducing tobacco use in current smokers.




Illicit and Nonmedical Pharmaceutical Drugs

Laws and policies designed to prevent drug use are often more severe than those aimed at alcohol and tobacco. In an era of mandatory minimum sentencing and zero tolerance laws, about one-half of all prisoners in US prisons were incarcerated for nonviolent drug offenses in 2015, and the United States has the highest per-capita prison population in the world. Although the Office of National Drug Control Policy (ONDCP) has asserted that prevention is the most cost-effective approach to the drug problem, funding for prevention programs makes up only a small portion of the ONDCP budget; the majority of spending is on law enforcement and interdiction activities.


Many employers require drug testing of employees, particularly those in transportation and security services. Research on the effectiveness of drug testing policies on preventing drug abuse is scarce, but some evidence suggests that productivity is actually lower in firms that have drug testing policies.


Another policy that has recently become more common is mandatory and random student drug testing (MRSDT), often required for student athletes and others who wish to participate in afterschool or other extracurricular activities. The effectiveness of such policies, in terms of their ability to prevent drug abuse, is not clear. A large study funded by the National Institute on Drug Abuse, called Monitoring the Future, has found that schools with MRSDT had virtually identical drug use rates as schools without drug testing.


Many of the same approaches that are used in primary prevention programs for alcohol are also used in programs that aim to prevent drug use. Also, many programs aimed at youths are intended to prevent substance abuse of all types. However, since the 1980s, the emphasis of these programs, including the “Just Say No” national campaign, has typically been on illicit drugs such as marijuana, cocaine, and heroin. More recently, the nonmedical use of pharmaceutical drugs, such as painkillers and stimulants (such as Ritalin), has become a focus of concern.


One of the most commonly used educational programs has long been Drug Abuse Resistance Education (D.A.R.E.)
. In a comparison study in the mid-1990s and in a follow-up study about five years later, schools that used the D.A.R.E. program had no significant reductions in drug use relative to control schools. More broadly, much research has shown that education-only programs are not sufficient to change behavior, although they may be effective in changing knowledge or attitudes.


Programs that can be effective in changing behaviors are usually derived from psychosocial theories and focus on minimizing the risk factors for, and on enhancing the protective factors against, substance abuse initiation. Multiple evaluations since the early 1990s have found that a combination of social resistance skills-training and competence enhancement are among the most effective approaches. Programs that use these approaches and that have shown positive results in RCTs include LST and SFP and the programs Lions Quest Skills for Adolescence, Project ALERT, CASASTART, and Project STAR.


Mass media campaigns appear to have little effect on drug use rates. Billions of dollars have been appropriated by the US Congress since 1998 for the National Youth Anti-Drug Media Campaign, yet evaluations have found no evidence that the campaign had a positive effect on teen drug use and some indications of a negative effect. Although the program was retooled and refocused specifically to address marijuana use in the early 2000s, further evaluations found that the campaign has had no effect on youth marijuana-use rates.




Bibliography


McGrath, Yuko, et al. Drug Use Prevention among Young People: A Review of Reviews. London: Natl. Inst. for Health and Clinical Excellence, 2006. PDF file.



Miller, Ted R., and Delia Hendrie. Substance Abuse Prevention Dollars and Cents: A Cost-Benefit Analysis. Rockville: Center for Substance Abuse Prevention, 2008. PDF file.



National Institute on Drug Abuse. Preventing Drug Use among Children and Adolescents: A Research-Based Guide for Parents, Educators, and Community Leaders. 2nd ed. Bethesda: NIDA, 2003. PDF file.



O’Connell, Mary Ellen, Thomas Boat, and Kenneth E. Warner. Preventing Mental, Emotional, and Behavioral Disorders among Young People: Progress and Possibilities. Washington, DC: Natl. Academies, 2009. PDF file.



Robinson, Matthew B., and Renee G. Scherlen. Lies, Damned Lies, and Drug War Statistics: A Critical Analysis of Claims Made by the Office of National Drug Control Policy. Albany: State U of New York P, 2007. Print.

In "The Devil and Tom Walker," what does the devil think of the whites? Why?

Because the white religions condemn him, the "black woodsman" or "old scratch" seems to revel in the persecution of whites. He notes that the Indians, who first settled the woods where he lives, would sometimes burn a white man as a "sweet-smelling sacrifice." He's also proud of persecuting Quakers and Anabaptists. He calls the whites savages. Since he is the devil, however, he does not reserve his evil just for religious whites, but is also...

Because the white religions condemn him, the "black woodsman" or "old scratch" seems to revel in the persecution of whites. He notes that the Indians, who first settled the woods where he lives, would sometimes burn a white man as a "sweet-smelling sacrifice." He's also proud of persecuting Quakers and Anabaptists. He calls the whites savages. Since he is the devil, however, he does not reserve his evil just for religious whites, but is also linked with slave dealers who oppress blacks and as a "grandmaster" who sat in judgement at the Salem witch trials. The fact that he is described as a "black man" does not mean he is African. He is black because that is a color associated with evil. At the end Tom Walker is taken away by a black man on a black horse. That whites are now the predominant population in the area around his woods makes them his prime target. He lures white men such as Deacon Peabody and Tom Walker into a pact whereby they exchange their souls for great wealth. He does seem to have some kinship with the Native Americans in the area who "consecrated" the woods in his name. Of course, the Native Americans have all been "exterminated" by the whites, another deed that he probably had a hand in.  

Please provide some examples of a reversal of values in Act 5 for Lady Macbeth and explain how the values have been distorted by her.

In Act 5, Scene 1, we can see how Lady Macbeth's guilty conscience has become more than she can bear.  Earlier in the play, she had valued ruthlessness and remorselessness, and she'd even prayed to evil spirits to help her become more ruthless and remorseless than she already was.  Now, however, she laments Macbeth's ruthlessness when she asks, "The Thane of Fife had a wife.  Where is / she now?" (5.1.44-45).  Macbeth had brutally murdered...

In Act 5, Scene 1, we can see how Lady Macbeth's guilty conscience has become more than she can bear.  Earlier in the play, she had valued ruthlessness and remorselessness, and she'd even prayed to evil spirits to help her become more ruthless and remorseless than she already was.  Now, however, she laments Macbeth's ruthlessness when she asks, "The Thane of Fife had a wife.  Where is / she now?" (5.1.44-45).  Macbeth had brutally murdered Lady Macduff and her children when he realized that Macduff had escaped him by fleeing to England.  Including Lady Macbeth is clearly now no longer part of his plans, and she is sad for Macduff's wife and her own husband's terrible and purposeless brutality.


Further, she had earlier suggested that a little water would clear them of the deed of killing Duncan, implying that regret would never play a role in the way the Macbeths seized power.  However, now she feels that she cannot get the smell of the blood off her hands and cries that "All the perfumes of Arabia will not sweeten this little hand" (5.1.53-54).  In the end, although she formerly valued remorselessness and ambition and brutality and power, Lady Macbeth now seems to understand the emotional and mental toll taken on her by her earlier priorities, and she cries, pitifully and alone.  Guilt has distorted her previous ideas about which qualities are best.

Wednesday 27 May 2015

In "The Crucible" Act II, what are the possible new character traits of John Proctor and Elizabeth Proctor? In addition, is there any textual...

Act Two shows us John and Elizabeth Proctor at home, and thus we can assume that they are relatively comfortable and not attempting to conceal anything from one another.  We certainly get a sense of John's bitterness and guilt, something we hadn't seen in Act One, when he raises his voice to his wife, saying, "You forget nothin' and forgive nothin'.  Learn charity, woman."  He is angry at his wife for continuing to hold a...

Act Two shows us John and Elizabeth Proctor at home, and thus we can assume that they are relatively comfortable and not attempting to conceal anything from one another.  We certainly get a sense of John's bitterness and guilt, something we hadn't seen in Act One, when he raises his voice to his wife, saying, "You forget nothin' and forgive nothin'.  Learn charity, woman."  He is angry at his wife for continuing to hold a grudge against him due to his infidelity with their former servant, Abigail Williams.  Elizabeth does continue to have her suspicions about him.  When John says that he spoke to Abigail alone, his story doesn't match the first one he told her, and she claims, "John, you are not open with me.  You saw her with a crowd you said."  His continuing guilt and resentment due to her continued suspicion of him drive a wedge between them. 


We also learn that the Proctors' are very pious people, though they have a spotty record of attending Sunday services of late.  They know their commandments (excepting that John has trouble with the one), John helped to build the church, and so forth.  Their "soft record" has everything to do with John's dislike of the Reverend Parris, an antagonism we saw in Act One.  Though the Proctors are pious, they are not not perfect, and their failure to believe in witches does make them somewhat unusual for their era.


Finally, we see how much John really does love his wife, and she him, when she is threatened by an accusation from the court.  Suddenly, all of their bad feelings seem to vanish, and their love for one another takes center stage.  Proctor claims that he will "fall like an ocean on that court" in order to save her.  We might have thought that John's feelings for Abigail were being put to the side only because he felt an obligation to his wife (from the conversation between John and Abigail in Act One), but Act Two makes it quite clear that -- even though he may have some feelings remaining for Abigail -- it is his wife that means the most to him.

What is syphilis? |


Causes and Symptoms


Syphilis is a sexually transmitted disease (STD) resulting from infection by Treponema palladum. The history of the disease is unclear. Evidence exists that its origin may have been linked with a disease, yaws, found in the Western Hemisphere at the time of explorer Christopher Columbus (1451–1506). Yaws is a relatively mild disease generally transmitted through contaminated objects or open skin
lesions, but not generally through sexual transmission; it results from infection by a subspecies of Treponema called T. palladum ssp. pertenue. The theory suggests that this may have been the form of the disease brought back to Europe on one of Columbus’s ships. Mutation and sexual transmission in the population of Europe may have produced the more serious form of the disease.



The disease is characterized by several distinct stages. Initial exposure to the organism during sexual intercourse results in formation of a painless skin lesion called a chancre at the site of infection (primary syphilis), developing anywhere from a week to months after infection. Spirochete
bacteria may be isolated from the lesion, as well as being found live inside white blood cells (macrophages and neutrophils) that infiltrate the area. The white cells may be a mechanism for systemic spread of the organism. The lesion generally heals spontaneously, leaving the impression that the disease has been eliminated.


During the weeks after formation of the chancre, the spirochetes multiply to large numbers and become disseminated throughout the body. A second stage (secondary syphilis) often appears within two months following regression of the chancre. Symptoms are often described as flu-like, with malaise, headache, fever, and joint aches. A skin rash often appears, covering most of the body. Sores may develop in the mouth and throat and on many of the mucous membranes in the body. The organism is highly transmissible during this period. The rash and other symptoms generally fade over a period of weeks.


Approximately 10 percent of untreated cases develop a third, or tertiary, stage of syphilis. The organism can infiltrate any organ or system in the body, resulting in soft tumors (gummas) in the eyes, lungs, bone, brain, or other organs. Symptoms are characteristic of the organ infected. For example, infection of the brain or other areas of the central nervous system are described as neurosyphilis or syphilitic dementia, characterized by memory loss, personality changes, and neurodegeneration. Even if tertiary syphilis is treated, prognosis for the patient at this stage is often poor.



Treponema has the ability to cross the placenta, and the infection of a pregnant woman may result in congenital syphilis, or infection of her unborn child. Infection may kill the fetus or cause it to be born with obvious deformities such as blindness or physical abnormalities. The infant may also be asymptomatic. An undiagnosed infection will likely progress, with symptoms appearing within weeks after birth. It is common for a rash to appear, with evidence of tertiary stage neurosyphilis or cardiovascular syphilis.


A diagnosis of syphilis can be made through microscopic examination of lesion exudates, noting the presence of spirochetes. However, Treponema is notoriously unstable, and the test must be made shortly after obtaining the specimen. More commonly, diagnosis is based upon serological testing for serum antibodies against the organism or tissue lipids released from infected or damaged cells.




Treatment and Therapy

Penicillin is the preferred method of treatment for both primary and secondary syphilis. If the disease has progressed to the tertiary stage, then antibiotic treatment will still eliminate the organism, but it will not reverse organ damage that may have occurred. Treatment for related organ involvement is symptomatic.


Alternative antibiotics include erythromycin, tetracyclines, and chloramphenicol, if necessary. However, only penicillin is effective during the tertiary stage or for use in pregnant women.




Perspective and Prospects

Despite the long-time existence of effective therapy, penicillin or alternative antibiotics, and the absence of any reservoir for T. palladum other than humans, syphilis remains the third most common sexually transmitted bacterial disease in the West. Only gonorrhea and chlamydia are more common.


As a result of effective therapy and the generally obvious symptoms of the disease, tertiary syphilis has largely disappeared. However, sexual practices continue to sustain spread of the disease. The Centers for Disease Control and Prevention estimate that 55,400 people acquire new syphilis infections each year in the United States. Three factors are primary contributors to the resurgence of the disease: prostitution, the increase in riskier sexual practices among homosexual men, and general apathy toward a disease that is relatively easy to treat in its early stages. An increase in congenital syphilis also reflects the presence of the disease in women of childbearing years. In the absence of condom use, both unwanted pregnancy and the spread of STDs such as syphilis may result.


No vaccine currently exists for syphilis. The inability to culture the organism in the laboratory has made research related to Treponema difficult, and the organism does not infect animals other than humans to act as a method of vaccine production. However, genetic engineering has resulted in the cloning of several bacterial gene products related to surface proteins and virulence factors, allowing the possibility for a vaccine in the future. For now, the best means of controlling syphilis remains the prevention of its spread through education and safer-sex practices, as well as early treatment of those infected.




Bibliography


Centers for Disease Control and Prevention. The National Plan to Eliminate Syphilis from the United States. Atlanta: U.S. Department of Health and Human Services, 2006.



Centers for Disease Control and Prevention. "Syphilis—CDC Fact Sheet." Centers for Disease Control and Prevention: Sexually Transmitted Diseases (STDs), February 11, 2013.



Mandell, Gerald L., John E. Bennett, and Raphael Dolin, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 7th ed. New York: Churchill Livingstone/Elsevier, 2010.



Murray, Patrick R., Ken S. Rosenthal, and Michael A. Pfaller. Medical Microbiology. 7th ed. Philadelphia: Elsevier/Saunders, 2013.



Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Syphilis. ICON Group, 2009.



Scholten, Amy. "Syphilis." Health Library, May 16, 2013.



Quetel, Claude. The History of Syphilis. Baltimore: Johns Hopkins University Press, 1990.



Sutton, Amy L., ed. Sexually Transmitted Diseases Sourcebook. 3d ed. Detroit, Mich.: Omnigraphics, 2006.

Tuesday 26 May 2015

What made the Industrial Revolution possible?

The Industrial Revolution took place between 1760 and 1840.  It started in Europe and gradually moved to the United States.  It is a time period in history that is characterized by the transition from small scale at home production of goods by people who were self-employed to large scale production of goods in factories that employed many workers.  


The primary thing that made the Industrial Revolution possible was the invention of machines that could...

The Industrial Revolution took place between 1760 and 1840.  It started in Europe and gradually moved to the United States.  It is a time period in history that is characterized by the transition from small scale at home production of goods by people who were self-employed to large scale production of goods in factories that employed many workers.  


The primary thing that made the Industrial Revolution possible was the invention of machines that could do work that was previously done by hand. This allowed production to shift from inside the home into factories.  


During the time of the industrial revolution new inventions were plentiful and helped to 'revolutionize' the way in which people lived.  


Furthermore, manufacturing processes were invented following the invention of machines.  These manufacturing processes enabled the speed of the production of goods to accelerate.


In addition, the use of steam to power machines allow made the Industrial Revolution possible.  


What are tumors? |


Causes and Symptoms


Tumors, also called neoplasms, are caused by a variety of factors—including mutations, improper hormonal signaling, viruses, and environmental influences—which cause certain normal body cells to deviate from a genetically determined developmental pattern for that particular organism. Tumors arise in all multicellular eukaryotic organisms, such as animals, plants, and fungi, where colonies of cells are intricately connected and are dependent on one another.



A tumor arises when a mistake is made in the cellular expression of a given gene. At a certain point in the cell’s development, a gene may be activated when it should not produce protein, or it may be inactivated when it should be producing protein. In either case, a cascade of subsequent developmental changes within the cell may be initiated. The cell may function inefficiently, die, or start to grow and divide at a faster rate than normal. In this latter scenario, the cell has become tumorous.


Many developmental biologists view the tumorous state as a throwback to the early embryonic development of the organism, when cells are undifferentiated and do not reveal the effects of specific hormonal genetic controls. Therefore, tumors reflect a dedifferentiated state of the cell. Tumors may be benign or malignant. A benign tumor grows as an enlarged tissue region without spreading elsewhere; often, it is only an inconvenience or irritant to the organism without harming the individual. A malignant tumor is invasive, spreading rapidly throughout many tissues, draining the organism of various resources, and eventually destroying key tissues and killing the individual. The breaking off and rapid spread of malignant tumors is termed metastasis.


The changes within genes and the subsequent gene expression or cellular dedifferentiation associated with tumors are brought about by mutations, changes within the nucleotide sequence (the genetic code) of the genes. Mutations can be caused by a number of agents called mutagens. Two major classes of mutagens are chemical mutagens (including benzene, carbon tetrachloride, and diethylstilbestrol) and radiation such as ultraviolet light, X radiation, and gamma radiation. Some mutagens also are carcinogens, causing malignant tumors. Not all mutagens, however, are also carcinogens. Caffeine, for example, is mutagenic but not carcinogenic.


Tumors can arise within cells of any of the five principal tissue types: epithelia, endothelia, connective tissue, nerve, and muscle. Epithelial tissue lines the organs outside and inside the body, including the skin, exocrine glands (such as oil and sweat glands), the digestive tract, and the reproductive organs. Endothelial tissue includes blood cells, blood vessels, and lymph nodes and glands. Connective tissue includes bone, fat cells, and cartilage. Nerve tissue includes the billions of nerves that compose the brain, spinal cord, and peripheral sensory and motor nerves. Muscle tissue includes the heart, more than six hundred skeletal muscles, and tens of thousands of smooth muscles.


Epithelial tissue cancers collectively are called carcinomas; they include adenocarcinomas, basal cell carcinomas, melanomas, malignant melanomas, squamous cell carcinomas, cervical cancer, uterine cancer, prostate cancer, colorectal cancer, and lung cancer. Whereas benign tumors of the skin such as freckles, moles, and warts are not serious, cancers of the skin and internal organ membranes can be fatal. Adenocarcinomas affect glands. Basal cell carcinomas, melanomas, and squamous cell carcinomas are serious cancers of the skin that can arise from prolonged sun exposure. Malignant
melanoma is a rapidly invasive skin cancer that can penetrate other body tissues and cause death within two or three months. Cervical and uterine cancers are serious tumors of the female reproductive tract. Prostate cancer is prevalent among males and is a leading cause of cancer deaths. Colon and rectal cancers, believed to be triggered by the lack of roughage in diets, are also relatively common. Lung cancer may result from exposure of lung tissue to cigarette smoke and air pollution.


Endothelial tissue cancers include leukemias, which affect blood cells, and lymphomas, which affect lymphatic tissue. Most leukemias affect the immune system’s white blood cells (leukocytes) or the stem cells from which they are derived. Leukemias include acute lymphoblastic leukemia, acute myeloblastic leukemia, acute monoblastic leukemia, chronic lymphocytic leukemia, and chronic granulocytic leukemia. Lymphatic cancers attack the lymph nodes and glands that serve as blood reservoirs for the circulatory system. Lymphatic cancers include lymphosarcomas, Hodgkin disease, and
Burkitt lymphoma, which is induced by the Epstein-Barr virus.


Connective tissue tumors include benign varieties such as osteomas and osteochondromas affecting bone, chondromas affecting cartilage, and lipomas affecting adipose (fat) tissue. Connective tissue cancers are called sarcomas. Chondrosarcomas are cartilaginous tissue cancers affecting joints. Osteosarcomas are bone cancers. Liposarcomas are fatty tissue cancers that attack a variety of bodily regions. Fibrosarcomas are cancers of the dense, fibrous tissue that holds together many bodily structures, including the skin.


Benign muscle tissue tumors are called myomas, whereas malignant muscle cancers are called myosarcomas. Leiomyosarcoma is a malignancy of smooth, visceral muscle. Rhabdomyosarcoma is a malignancy of cardiac and skeletal muscle.


Benign tumors of the central nervous system are called neuromas and neurofibromas. They include multiple neurofibroma, a condition in which numerous nerve tumors develop throughout the body, thereby causing a severely distorted physical appearance; multiple neurofibroma (or
neurofibromatosis) is also known as the “Elephant Man” syndrome after the term used to describe Joseph Merrick, a nineteenth-century Englishman who suffered from this disease. Nervous system cancers include brain cancer and neurogenic sarcoma, glioblastoma, neuroblastoma, and malignant meningioma.


The formation of tumors is probably triggered by many factors. For example, the stress associated with living in a fast-paced technological society causes severe disturbances to the normal homeostatic balance within the body, particularly with reference to the nervous and endocrine systems. The nervous system activates many organ systems and tissues throughout the body. Even more potent in its effects is the endocrine system, which directly controls gene expression in various body cells and tissues via chemical messengers called hormones. When these hormones are hyperactivated by stress, they may activate or inactivate certain genes and their protein products at the wrong time in an individual’s development, thereby causing drastic changes in cellular functioning, often accompanied by abnormal growth of tissue into a tumor.


Virus infections may also result in cancer. In 1908, cell-free extracts prepared from leukemia in mice were shown to transmit the disease. In 1910, Peyton Rous discovered that a similar filterable agent would transmit a solid tumor, a sarcoma, in chickens. However, it was felt at the time that cancers in animals represented special circumstances, and that the work was not directly applicable to human cancer. The existence of the Rous sarcoma virus (RSV) was corroborated later by other researchers, culminating in the awarding of the 1966 Nobel Prize in Physiology and Medicine to Rous. Most human cancers are of endogenous (genetic) origin and not associated with viral infection, but there are a number of notable exceptions. Hepatitis B virus infection is associated with a hepatocarcinoma, or cancer of the liver. The Epstein-Barr virus, the etiological agent of infectious mononucleosis, is associated with both Burkitt lymphoma and nasopharyngeal
carcinoma.




Treatment and Therapy

Oncologists and other medical researchers study both benign and malignant tumors. Studies are devoted to the occurrence of these tumors, improved means of diagnosis, and the development of effective treatments. Cancer is the second-leading cause of death in many Western nations. Stress, viruses, pollution, and an individual’s everyday exposure to hazardous materials increase the chance of developing tumors.


Regardless of a tumor’s cause, it is important that it be identified and treated. The American Cancer Society’s seven warning signs for cancer serve as an important model for tumor and cancer prevention. The warning signs are a sore that does not heal, persistent coughing, a lump anywhere on the body, unusual bleeding, a change in a wart or mole, a change in bladder or bowel movements, and difficulty swallowing.


Tumors may be benign or malignant. Benign tumors are less severe in most cases because they continue to grow within a localized region without invading other tissue regions. Benign tumors may press on critical organs and cause discomfort, however, thereby necessitating their surgical removal or inactivation using lasers, freezing, cytotoxic chemicals, or radiation. Warts represent a good example of a benign tumor. Warts are caused by a papillomavirus that infects skin cells of the dermis and enters a lysogenic phase, where it lays dormant in the host cell DNA but accelerates cell growth into a small tumor. A person can contract a papillomavirus merely by shaking an infected individual’s hand. Some warts may become malignant.


Malignant tumors are invasive cancers that multiply rapidly, break off into the bloodstream, and colonize other body regions, where they destroy tissues, organs, and sometimes the entire organism. Malignant cancer cells are immortal in the sense that they reproduce without any developmental barriers. Many malignant colonies can manipulate available blood supplies away from normal tissue, thereby promoting their own growth. Malignant cancers are classified according to tissue type. Any tissue is subject to cancerous growth, given the appropriate stimuli.


Genetic and biochemical research focuses heavily on the study of neoplastic cellular transformation. The prime emphasis is upon gene regulation, the ultimate control point that determines whether a cell will function properly. Mutations in gene regulatory regions, improper hormonal signaling, or viral interference via lysogeny may contribute to abnormalities in cellular growth.


Benign and malignant tumors can be induced and studied in laboratory animals. The application of a chemical mutagen to a localized tissue region in a mouse usually gives rise to a tumor. Female mice infected with the mouse mammary tumor virus pass the virus to their young via milk during suckling; this virus generates grotesquely large tumors that are often as big as the mouse itself. Tumors or sections of tumors removed from humans are studied by biopsy and subsequent biochemical analysis. Human cells are grown in tissue culture in flasks and roller bottles containing fetal calf serum so that medical researchers can study the nature of the neoplastic tumorous cells.




Perspective and Prospects

The study of tumors is of critical importance to medicine because tumor formation is a major cause of illness in millions of people yearly. An understanding of the genetic mechanisms underlying tumor formation is directly applicable to both the study of cancer and the understanding of mechanisms that regulate cell growth in general.


Critical to understanding the genetic basis of cancer was the discovery of retroviruses, RNA viruses that replicate using a DNA intermediate. These viruses were discovered to carry oncogenes, cancer-causing genes that the viruses originally acquired from the cells they infected. It was discovered that oncogenes actually encode a variety of proteins that regulate cell growth, including growth factors and DNA regulatory proteins. The genetic basis behind most human cancers seems to involve mutations in these genes. The study of the mechanism by which these proteins function may eventually lead to a fuller understanding of how cancers develop.


Since most cancers have a genetic origin, the ability to screen for certain genetic patterns allows clinicians to observe patients most at risk for the disease. For example, women who carry certain forms of the genes BRCA1 and BRCA2 are at greater risk for developing ovarian or breast cancer.


Developing cancers in certain tissues may also secrete unique forms of proteins, allowing for detection of the disease at an early stage. For example, prostate tumors, the leading form of cancer in men (other than skin cancer), secrete a prostate specific antigen (PSA); elevated levels of PSA in the blood suggest a possible tumor in the prostate.


Oncofetal proteins, normally found on fetal cells, may also be reexpressed by certain tumors. Elevated levels of alpha-fetoprotein and carcinoembryonic antigen in serum may indicate liver or colorectal cancer. The increasing sensitivity of such screening methods holds out the prospect that the most common forms of cancer may be detected in a “curable” stage.




Bibliography


Alberts, Bruce, et al. Molecular Biology of the Cell. 5th ed. New York: Garland, 2008.



"Benign Tumors." MedlinePlus, May 9, 2013.



"Cancer." MedlinePlus, May 28, 2013.



Chiras, Daniel D. Biology: The Web of Life. St. Paul, Minn.: West, 1993.



Dollinger, Malin, et al. Everyone’s Guide to Cancer Therapy. Rev. 5th ed. Kansas City, Mo.: Andrews McMeel, 2008.



Eyre, Harmon J., Dianne Partie Lange, and Lois B. Morris. Informed Decisions: The Complete Book of Cancer Diagnosis, Treatment, and Recovery. 2d ed. Atlanta: American Cancer Society, 2002.



Janes-Hodder, Honna, and Nancy Keene. Childhood Cancer: A Parent’s Guide to Solid Tumor Cancers. 2d ed. Cambridge, Mass.: O’Reilly, 2002.



Kindt, Thomas J., Richard A. Goldsby, and Barbara A. Osborne. Kuby Immunology. 6th ed. New York: W. H. Freeman, 2007.



"Learn about Cancer." American Cancer Society, Feb. 6, 2013.



Ross, Michael H., and Wojciech Pawlina. Histology: A Text and Atlas. 6th ed. Baltimore: Lippincott Williams & Wilkins, 2011.



Stark-Vance, Virginia, and M. L. Dubay. One Hundred Questions and Answers About Brain Tumors. 2d ed. Sudbury, Mass.: Jones and Bartlett, 2011.



"Understanding Cancer Series: Cancer." National Cancer Institute, Sept. 30, 2009.



Varmus, Harold, and Robert Weinberg. Genes and the Biology of Cancer. New York: W. H. Freeman, 1993.

Monday 25 May 2015

What does Friar Laurence say will happen when Juliet drinks the potion in Romeo and Juliet?

Friar Laurence says that the potion Juliet drinks will mimic death. 


Juliet married Romeo in secret.  When he got himself banished for brawling in the streets and killing Tybalt, she would have been forced to marry another man.  Since she did not want to marry Paris, she went to Friar Laurence for help.  He knew her situation because he had secretly married her to Romeo. 


She told him she wanted to kill himself, but...

Friar Laurence says that the potion Juliet drinks will mimic death. 


Juliet married Romeo in secret.  When he got himself banished for brawling in the streets and killing Tybalt, she would have been forced to marry another man.  Since she did not want to marry Paris, she went to Friar Laurence for help.  He knew her situation because he had secretly married her to Romeo. 


She told him she wanted to kill himself, but he had other ideas.  He told her that he would give her a special "vial" to save the day.



When presently through all thy veins shall run
A cold and drowsy humour, for no pulse
Shall keep his native progress, but surcease:
No warmth, no breath, shall testify thou livest;
The roses in thy lips and cheeks shall fade
To paly ashes, thy eyes' windows fall,
Like death, when he shuts up the day of life … (Act 4, Scene 1)



Friar Laurence was gifted with herbs and potions, and knew just the trick.  He had developed a special potion which had the qualities to mimic death. If Juliet drank it, everyone would think she was dead and she would be buried in her family’s tomb.  Later, she could be reunited with Romeo. 


The problem was that Friar Laurence was also supposed to get word to Romeo, but a plague delayed the letter.  Romeo killed himself after thinking she was dead, right there in her tomb.  She awoke to that.  Seeing he had taken poison, she stabbed herself.


After Juliet died for real, Friar Laurence explained to her parents and Romeo’s parents what happened.



Then gave I her, so tutor'd by my art,
A sleeping potion; which so took effect
As I intended, for it wrought on her
The form of death: meantime I writ to Romeo,
That he should hither come as this dire night,
To help to take her from her borrow'd grave,
Being the time the potion's force should cease. (Act 5, Scene 3)



Friar Laurence took full responsibility, but the Capulets and Montagues forgave him.  They were devastated by the loss of their children, but they realized their part in their deaths.  With their children's deaths, they buried their feud.


What is a visual system?


Introduction

The visual system is one of the primary means by which humans are aware of and monitor their environment. The visual system provides information on the form, color, size, movement, and distance of any object in sight range. Its importance is seen in the fact that sight loss (blindness) is much more debilitating than any other sensory deprivation.






The anatomy of the eye is quite complex. Each eye sits in a protective, bony skull cavity, an eye socket. The human eye is roughly spherical and about one inch in diameter. Six muscles, attached at one end to the eyeball and at the other end to the eye socket, control the directional movements of each eye.


The semiliquid eyeball interior is surrounded by three tissue layers. Outermost is the tough and protective sclera, made up of fibrous tissue. The sclera, or “white of the eye,” has at its front a circular cornea. This sclera segment is modified to allow light rays to enter the eye and to aid in the focusing of light reflected from objects seen. At the front of each eye, paired eyelids protect the sclera’s outer surface, removing dirt and lubricating with tears by blinking. The eyelids also close reflexively for protection when an object comes close to an eye.


The middle and inner tissue layers of the eye are the choroid and the retina. The choroid holds all the blood vessels that feed the eye and a muscular ciliary body that alters the shape of the eye lens to help to focus light. The retina lines most of the eyeball interior, except at its front. Retinal tissue converts light energy to nerve impulses carried to the brain. Choroidal blood vessels extend throughout the retina, except at its front. There, a hole, the pupil, allows light entry into the eye. A circular iris around the pupil gives each eye its color.


The retina translates light energy into nerve impulses, using rod cells, cone cells, bipolar cells, and ganglion cells. Rods and cones are light-sensitive, yielding nerve impulses when they are struck by light. Bipolar cells transfer the acquired information to the brain via ganglion cell fibers in the optic nerve at the rear of the eye. The rods, sensitive to tiny amounts of light, enable dim light vision. Cones enable the perception of color and detail. Rods and cones hold the pigment rhodopsin (RO, or visual purple). When it interacts with light, RO decomposes to a protein (opsin) and a form of vitamin A called retinol1. More RO must be made before a rod’s next operation. Unless the diet provides vitamin A (as retinol1) in amounts enabling this, an afflicted person has night blindness (nyctalopia). Nyctalopics cannot see well in dim light.


A small region in the retina’s center, the fovea centralis, contains cones but no rods, and cone number per unit of retinal area decreases as the front edge of the retina—near the pupil—is approached from the fovea. In contrast, the relative number of rods increases as the number of cones diminishes. Humans see most clearly in daylight, using the fovea almost exclusively. At night, vision is accomplished mostly by using a retina region at the side of each eye.


A blind spot in the visual field occurs when objects cast images on the retina’s optic disk. This disk, the point where the optic nerve leaves the eye, lacks both rods and cones. The optic nerves from the two eyes pass through the optic chiasma. Fibers from the inner half of each retina cross to the opposite side of the brain. Those from the outer half remain on the same side of the brain. This causes the right visual field, which stimulates the left half of each retina to activate the left half of the thalamus and visual cortex. The left visual field affects the right half of the brain, a situation similar to that of the other human sensory systems.


The visual cortex includes the occipital lobe of each cortical hemisphere, and there is a point-for-point correspondence between the retinas and the cortex. This yields a “map,” whose every point represents a point on the retina and visual space seen by each eye. Vision simultaneously depicts object color, shape, location, movement, and orientation in space. Seeking a model to explain the overall brain action in vision, neurophysiologists have identified various cortical cell types, each involved selectively in these features. Retinal maps from each eye merge in a cortical projection area, which allows images from the two eyes to yield stereoscopic vision. Other brain regions also participate in vision; for instance, the cortex appears to be involved in perceiving form and movement.




Lenses and Vision Types

Just behind the cornea, a transparent, elastic lens is attached to a ligament that controls its shape. Lens shape focuses light reflected from an object and forms on the retina the sharpest possible visual image. The eyes regulate the amount of light reaching retinal rods and cones by contracting or expanding the pupil by means of the iris. These involuntary responses are controlled by brain reflex pathways. The lens also divides the eye into two compartments. The small compartment in front of the lens holds watery aqueous humor. The much larger rear compartment between lens and retina is full of jelly-like vitreous humor. This humor maintains the eye’s shape.


Usable visible (380- to 730- nanometer) light enters the eye through the pupil and excites color sensations by interacting with retinal cones. Light reflected from an object passes through the lens to form a focused retinal image, similar to what a camera forms on film. Focusing a visual image also requires regulation of the amount of light passing through the pupil by making the iris larger or smaller. The eye lens produces an inverted retinal image, interpreted in the brain right-side-up. Binocular vision enables accurate depth perception
. Each eye gets a slightly different view of any object, and the two retina images are interpreted by the brain as a three-dimensional view.


Nocturnal animals see in low-light environments with black-and-white (scotopic) vision. Diurnal (day-living) animals have photopic vision, which needs much more light to perceive colors and textures. Humans have both photopic and scotopic vision. Scotopic vision uses the rods as well as photosensitive RO. RO is bleached by bright light, so scotopic animals are almost blind by day. Humans suffer brief blindness on walking indoors on bright days. Then, by dark adaptation, scotopic vision quickly begins to function. Faulty dark adaptation (night blindness) occurs in humans who lack rods or are vitamin A deficient. Afflicted individuals cannot find their way around at night without artificial light. Photopic vision mostly uses the fovea, so it is due to cones, the only foveal visual cells. In the central fovea there are approximately 100,000 cones per square millimeter of retinal surface. Each cone associates with nerve cells that process the incoming visual data, convey them to the brain cortex, and provide detailed information on objects whose images fall in the fovea.


Peripheral vision occurs outside of the fovea, as may be seen by looking directly at one letter on a page. That letter and a few others nearby look very sharp and black because they are seen by foveal vision. The rest of the page, seen by peripheral vision, blurs. The clarity of foveal vision versus peripheral vision is due to the increasing scarcity of cones in retinal areas farther and farther from the fovea. Also, the nerve connections in the retinal periphery result in each optic nerve fiber being activated by hundreds of rods. This shared action is useful in detecting large or dim objects at night. However, it prevents color vision, which requires the brain to differentiate among many signals.




Visual Defects and Their Symptoms

Human eyes can have numerous vision defects. The most common of these defects are small, opaque bodies (floaters) in the eye humors. Usually, floaters are only an inconvenience. Much more serious are lens opacities called cataracts. They develop for several reasons, including advancing age and diabetes. Opacity of the cornea can also cause obscured vision. It can be repaired through the transplantation of a section of clear cornea from another person. Three very dangerous eye diseases that can cause blindness are detached retinas (retina rips), glaucoma (eye pressure buildup due to blocked tear ducts), and macular degeneration (destruction of the retinal areas responsible for sight).


Six serious, but relatively easily treated, vision problems are myopia, hyperopia, presbyopia, astigmatism, diplopia, and strabismus. They are due to incorrect eyeball length, to lens defects, or to external eye muscle weakness. In myopia (nearsightedness) the eyeball is too long. Light from nearby objects will focus well on the retina. Distant rays focus before it, yielding blurry images. Conversely, farsightedness (hyperopia) occurs because the eyeball is too short. As a result, the light from distant objects focuses on the retina, but that from nearby objects focuses behind it and makes them blurry. An eye can also lose the ability to adapt quickly from far vision to near vision. This problem, presbyopia, usually happens after age forty. In an astigmatism, uneven curvature of an eye lens causes retinal images to be made up of short lines, not sharp points. Weakness or paralysis of external eyeball muscles may cause diplopia (double vision) and strabismus (crossed eyes).



Blindness, the most serious vision problem, is much more debilitating than any other sensory deprivation. It occurs in many forms. Some are temporary, mild, and readily treated. Others are severe and untreatable. Color blindness is an incurable lack of some or all color vision. This congenital form of blindness is attributed to genetic defects in the retina or some part of the optic tract. It is mild, causing, at worst, no color perception and a life spent in a black-and-white world. Amblyopia, weak vision without apparent structural eye damage, is another type of acquired blindness, due to toxic drugs, alcoholism, or hysteria. Blindness may also be caused by diseases such as iritis and trachoma.


Blindness varies in extent, from inability to distinguish light from darkness (total blindness) to inability to see well enough to do any job requiring use of the eyes (economic blindness) to vocational and educational blindness: inability to work in a job done before becoming blind, and inability to become educated by methods commonly used in school, respectively. Most severe blindness is permanent and incurable. There are about two blind people per thousand in industrialized nations and two per hundred in underdeveloped countries. The causes of blindness include genetic abnormalities of components of the eye or brain, pressure on the optic nerve from a brain tumor, detachment of the retina from the choroid, damage to the eyes or brain by excess light, or severe head trauma.




Treatment Options for Vision Problems

Visual defects are most often identified by ophthalmologists who prescribe eye treatments such as the use of eyeglasses, contact lenses, or surgery. Detached retinas and glaucoma can both be repaired by surgery, and most night blindness is cured by adding sufficient vitamin A to the diet to allow optimal cone and rod operation. Amblyopia is treated by psychologists or psychiatrists who identify its basis and work with afflicted individuals to reassure them or apply pharmacological treatment of the problem. Some kinds of structurally based blindness may be cured by surgery (such as removing brain tumors). However, in a great many cases the blindness is incurable. When blindness is acquired by sighted people (adventitious blindness), it can be important to receive the help of a mental health professional to gain the ability to live with it successfully. This is most crucial early in the adventitious blindness, when afflicted individuals are least likely to be able to cope with being cut off from a major source of their contact with the world.


The adjustments that must be made on occurrence of adventitious blindness are so extensive that the blind person eventually becomes a different individual from the sighted person he or she once was. Usually, the initial response to adventitious blindness is apathy and severe depression. These symptoms are followed by the return of interest in living and coping with the practical problems caused by blindness. The function of a psychologist or a psychiatrist is the careful combination of psychotherapy and pharmacological treatment—varied, individually, in its length and scope—to ready each afflicted individual to function well in a sighted world. After an adventitiously blind individual is capable of coping well with being blind, there are several federal and private agencies aimed at teaching such individuals to operate well and to engage in training so as to allow them to reachieve gainful employment.




Bibliography


Chalkley, Thomas. Your Eyes. 4th ed. Springfield: Thomas, 2000. Print.



De Valois, Karen K., ed. Seeing. 2d ed. San Diego: Academic, 2000. Print.



Hollins, Mark. Understanding Blindness: An Integrative Approach. Hillsdale: Erlbaum, 1989. Print.



Heller, Morton A., and Edouard Gentaz. Psychology of Touch and Blindness. Hoboken: Taylor, 2013. Digital file.



Hubel, David H. Eye, Brain, and Vision. New York: Freeman, 1995. Print.



Livingstone, Margaret, and David H. Hubel. Vision and Art: The Biology of Seeing. Rev. ed. New York: Abrams, 2014.



MedlinePlus. "Vision Impairment and Blindness." MedlinePlus. MedlinePlus, 9 July 2014. Web. 14 July 2014.



Remington, Lee Ann. Clinical Anatomy and Physiology of the Visual System. 3d ed. St. Louis: Elsevier, 2012. Digital file.



Rodieck, Robert W. The First Steps in Seeing. Sunderland: Sinauer, 1998. Print.



Schwartz, Steven H. Visual Perception: A Clinical Orientation. 4th ed. New York: McGraw, 2010. Print.



Tovée, Martin J. An Introduction to the Visual System. 2d ed. New York: Cambridge UP, 2009. Print.

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