Friday, September 30, 2011

Which bacteria are anaerobic?

Anaerobes, in general, are organisms that survive without the need for oxygen. Hence, anaerobic bacteria are bacteria that thrive and survive in environments without oxygen. These bacteria will have different metabolic processes and requirements than their aerobic counterparts. Most anaerobic organisms will not survive in the presence of oxygen. Some are killed by oxygen, some do not use oxygen but tolerate it, and others survive without oxygen but will use it if it is available. 


In humans, these types of bacteria reside in the gastrointestinal tract and cause various diseases, including appendicitis and diverticulitis.


Other examples of such bacteria include the following:


Bacteroides - gram negative, cause intra-abdominal infections


Porphyromonas - gram-negative, cause aspiration pneumonia


Clostridia - family of gram-positive bacteria responsible for botulism, food poisoning, and certain colitis.


Energy metabolism of anaerobes is referred to as anaerobic respiration, a form of respiration that does not involve oxygen.

In "My Financial Career" by Stephen Leacock, what is the transaction made by the narrator in the bank like?

Stephen Leacock intended to make a very simple transaction at the bank, but he had never had any previous experience with banking and made a hash of it. He asked for a private interview with the manager of a large, imposing bank and then revealed that he only wanted to open a very small account. The manager, of course, assumed that Leacock was there on an important mission.



"You are one of Pinkerton's men, I presume," he said.


He had gathered from my mysterious manner that I was a detective. I knew what he was thinking and it made me worse.



Leacock explained his intended transaction in one simple line of dialogue.



“I propose to deposit fifty-six dollars now, and fifty dollars a month regularly.”



Leacock for many years was the most popular English-speaking writer in the world. One of the reasons for his popularity was his simplicity. It can be noted that "My Financial Career" is full of very short paragraphs and that the language is all conversational English. Another famous humorist, Robert Benchley, was so inspired by Leacock's writing that he once said he had written everything Leacock had ever written--not "read" but "written." In other words he had written on every topic covered by Leacock. Both men were obviously inspired by the great Mark Twain, an earlier author who wrote many humorous stories and essays characterized by wild exaggeration.


"My Financial Career" was published in 1914. Even in those days, fifty dollars was not a large sum of money--although it seemed large to Leacock. The manager turns him over to a clerk, who shows him how to open an account and how to write a check. In those days there was no distinction between savings accounts and checking accounts. A check could be written on any personal account. 


Leacock is so flustered by this point that he mistakenly writes a check for fifty-six dollars, although he had only intended to withdraw six dollars for present personal expenses. For some reason it didn't occur to him that he could simply keep six dollars of his cash and deposit fifty. The clerk is astonished.



“What! Are you drawing it all out again?”


An idiot hope struck me that they might think something had insulted me while I was writing the check and that I had changed my mind. I made a wretched attempt to look like a man with a fearfully quick temper.



This, Leacock claims, was his last experience with banking. As the title of the story suggests, it was the whole extent of his "financial career." Leacock, characteristically, is exaggerating wildly. He was a professor of Political Economy and chairman of the Department of Economics and Political Science at McGill University in Montreal, Quebec. However, he concludes his story as follows:



As the big doors swung behind me I caught the echo of a roar of laughter that went up to the ceiling of the bank. Since then I bank no more. I keep my money in cash in my trousers pocket, and my savings in silver dollars in a sock.


How do behavioral addictions affect parenting?


Parental Influence on Behavioral Addiction

Parents have three potential mechanisms by which they influence the development of behavioral addictions in their children. However, none of these mechanisms directly causes behavioral addictions.




The first and most fundamental parental mechanism is genetic inheritability. Addiction is promoted through a neuronal reward system in which the pleasure areas of the brain are stimulated and the behavior that brought the pleasurable experience is identified and repeated. A well-known example is the endorphin release or rush experienced by runners, cyclists, and other extreme athletes. At some point during the activity, the physical expenditure of energy triggers a release of brain chemicals (neurotransmitters), most notably endorphin, which the athlete experiences as pleasurable.


While this pleasurable response to vigorous exercise is almost universal and can be brought about by any number of strenuous physical activities, individual sensitivity is primarily genetically inherited. If it takes a lot of exercise before a parent experiences the pleasure of endorphin release, it is likely that his or her children will require much exercise before they experience the endorphin rush. What a parent contributes here is his or her child’s sensitivity to having the pleasure centers of the brain stimulated.


In the example of the runners’ high, just how much running has to occur before endorphins are released will vary among individuals, with most of the variation accounted for by how much exercise their parents would have had to do before their own endorphins were released. Largely determined by what was true for one’s parents is how much activity one has to engage in to bring on the pleasurable experience, how intense (and thus addictive) is that experience, and how long that experience lasts.


Parents’ genetic contributions influence their children’s addictive sensitivity, pleasurable intensity (which corresponds to addictive potential with the more the intensity, the greater the potential), and duration. Duration involves the length of the experience and how much behavior was required to result in the reward. Parents pass down a tendency toward or a tendency away from pleasurable addiction; they do not pass down specific behavioral addictions like pornography or kleptomania. The more excitable the parents’ brains, the more excitable the children’s brains are likely to be.


The second mechanism through which parents influence the development of behavioral addiction is through imitative, behavioral, and social learning. Parents who are addicted to exercise, gambling, social networking, or shopping, for instance, show their children that these behaviors are within the range of what this family will accept. Most behavioral addictions are merely extreme examples of normally encountered and readily observed behaviors that all individuals exhibit. When parents are addicted to any of these behaviors, children are exposed to the idea that the behaviors are acceptable or normal to some degree; the parents legitimate the behaviors through their actions. For example, most children will not see a spotlessly clean home as normal unless they are raised in an environment in which compulsive cleaning is the norm.


The third and most common mechanism for parents to influence and sustain behavioral addictions in their children is enabling. The cycle begins with children engaging in a commonly accepted behavior, such as video gaming. There also is a good chance that children have participated with their parents in that activity. It is common for parents, for example, to play video games with their children. However, because the threshold between normal, daily activity and driven addiction is more nuanced and not well defined, it usually takes a substantial period of time to go from family entertainment to individual addiction.


The behavior crosses the threshold into addiction when it directly or indirectly harms the child, interferes with other health- and growth-promoting activities (such as school work, socializing with friends, participating in family functions), and becomes the major focus or prime motivation for how the child allocates his or her time. Addicted children, like their adult counterparts, are on a quest to satiate urges and avoid the anxiety they will feel when those urges are not met. The addict’s focus is on how soon he or she will be able to satisfy the next urge.


Even with the foregoing conditions as a guideline, it still can be difficult to distinguish passion and dedication from compulsion and absorption. For example, when does excessive football practice become exercise addiction? Addiction is usually difficult to determine until the addiction is well established; at this point parents are at risk of knowingly or unknowingly promoting the addiction by sustaining the addictive behavior of the child.


The behavior that is troubling to parents and harmful to their children is allowed to continue because of parents’ uncertainty, unreliability, and hesitation about how they should respond to their child and his or her problem. Parents have ultimate authority and influence over their children’s lives; they provide life’s essentials—food, clothing, shelter, and security. They also provide life’s social essentials—identity, belonging, and support for a life outside the home through financial and material means.


Helping children is generally natural for parents. This predisposition becomes problematic when children begin to manipulate parents and other family members to fulfill their addictive cravings. When parents minimize or deny that their child’s behavior, such as excessive shopping or compulsive eating, is a problem, they enable the child to engage in these behaviors without having to identify that they have a problem.


Subconsciously, children study parental behavior and learn from it. This behavior cues children about what is allowable, what will be confronted, what will be ignored, and what will or will not be tolerated. By failing to identify the behavior and its impact on children and family as a problem, parents subconsciously influence how children see the addictive behavior. The addiction becomes something that is acceptable, “a phase,” or something that the child will outgrow.


Placed between the emotionally difficult situation of loving and supporting their children without unnecessarily challenging them, parents often take responsibility for the actions and behaviors of their children. This allows the child to dismiss responsibility for the consequences of their behaviors. This feeds the addiction because the child is never forced to look at the harmful consequences of his or her behavior.



Children with behavioral addictions often display both an alarming lack of concern for those they affect and a disarming, narcissistic, self-concern. In the jargon of addiction treatment, this behavior becomes an example of “It’s not the person but the addiction speaking.” At this stage, children have learned to manipulate their parents’ confusion and concern. Parents’ attempts to control children’s environments are vigorously opposed or cleverly bypassed. Children may lie, steal, and mislead to overcome the obstacles. The home environment becomes hostile, discordant, and conflict-ridden.


To establish stability, calm, and peace, parents begin to second guess how they should act around their addicted children, what they should or should not say, and what feelings they should share or keep to themselves. The relationship between parents and the addicted child may feel strained, forced, uncomfortable, and unfamiliar.


In an environment of indecision, addicted children will continue to accept that all is well; they will do this until parents express concern or confrontation. Children then often respond in the extreme. Pleading, promises, punishment, coercion, and reward have lost their effectiveness at this point. Even if both parents and child do not want a discordant climate, they lack the language and direction to make sustainable changes for the better. However, in any family that is understood to function as a system, it takes only one member to effect change in the rest of the family and to prompt the family toward a healthier direction. Knowing what type of help to get, and where to get it, is critical to family recovery.



Parenting as a Cure

At the most basic level, parents must acknowledge how their responses may have made the addiction worse and treatment more difficult. Going against better judgment; not standing their ground; and punishing, bribing, and codependently watching and reacting to their troubled child have all made the family system less functional, trustworthy, and effective.


The first step in treating the addict and his or her family is for parents to accept how they may have helped sustain an addiction in their child. Parents can rarely control their children’s harmful behaviors, but they can control their responses to those behaviors. They can begin to control their dysfunctional responses.


Parents must educate themselves about addiction in general and the specific behavioral addiction of their child. This will include demonstrating healthier behaviors for the child. Parents should understand that they may do whatever they can to help their child but do nothing that supports the addiction.


Parents did not create the addiction, and they cannot control or cure it. Parents who educate themselves about healthy actions, rather than reactions, can begin to support their addicted child.


Progress is likely to be uneven. Parents can make great strides in recovery while the child seems to regress, or the reverse can occur. Critical to this stage of recovery is accepting that recovery from addiction involves a long-term commitment to practicing healthy behaviors. As long as one side incorporates even some positive behavioral changes, the entire family system will improve and the relationship between child and parents will begin to mend.


While these behavioral modifications are critical first steps toward a healthier, addiction-free life, they are not usually enough to address all aspects of the addiction. Routinely, parents’ and children’s recoveries will involve multidimensional treatment, often with a specially trained clinician and with group support. Some addicts will need to enroll in a treatment facility to facilitate their recovery.


It is vital that parents and the child work separately at modifying their behaviors first. The best place to start is with a counselor who is trained to work with addicts and their parents. The counselor will be able to set up a proper treatment plan and refer the patients to the right resources.


Parents should seek professional help and support groups for themselves too. Self-help groups such as Al-Anon, Alateen, and Co-Dependents Anonymous also are available for parents and other family members to receive additional support.



American Academy of Child and Adolescent Psychiatry. “Facts for Families.” Washington, DC: AACAP, 2011. PDF file.


Sadock, B. J., and V. A. Sadock, eds. Kaplan and Sadock’s Comprehensive Textbook of Psychiatry. Philadelphia: Lippincott, 2000. Print.

What is the structure of the atomic nucleus?

The atomic nucleus is the center of an atom, and is composed of protons and neutrons.


Protons and neutrons are composite particles, meaning they are made of something even smaller. Both are made of quarks, which behave in ways that don't really conform to our normal expectations for particles. There are several varieties of quark, but the ones found in protons and neutrons are the "up" quark, which has a charge of +2/3, and the "down" quark, which has a charge of -1/3. 


The proton is made of two ups and a down, which mathematically works out to a charge of 1. The neutron is made of one up and two downs, which works out to a charge of 0. Their charge is the reason for their names.


An atom is defined as belonging to a particular element based on the number of protons found in the nucleus. This is primarily because the number of neutrons in the nucleus can change without affecting the atom's ability to attract electrons, and atoms regularly do end up having different numbers of neutrons with a certain number of protons. These variations in the number of neutrons are called isotopes, and they contribute to the stability of the atom; atoms that are said to be radioactive are ones that are, basically, too large for the forces holding them together, and they tend to split apart into smaller atoms in relatively predictable ways.


Despite the way it's typically depicted in diagrams as a relatively large structure, the nucleus is in fact extremely small compared to the electron orbits, and most of the atom is composed of empty space. 

What is the theme of "Bilingual" by Rhina P. Espaillat, and how does it connect it to "Girl" by Jamaica Kincaid?

A primary theme of Espaillat's poem "Bilingual/Bilingüe" is straddling two cultures creates conflicts. This is certainly the case for the speaker's father, who wants the speaker to be able to navigate the English-speaking world well, but still remember her culture and heritage by speaking Spanish at home. Even as a famous writer, the speaker says of her father:



"even when, 
proud (orgulloso) of his daughter’s pen, 




he stood outside mis versos, half in fear 
of words he loved but wanted not to hear" (lines 15-18)



The speaker is saying that her father is conflicted between pride of her talent at writing poetry and dismay at the way she has blended Spanish and English, and the two cultures these represent. The speaker herself is conflicted as well, describing reading English in the house to practice, against the father's wishes:




"I hoarded secret syllables I read 




until my tongue (mi lengua) learned to run 


where his stumbled" (lines 12-14).



The speaker understands the importance of learning English well, but in order to do so, she needs to break her father's rule. Also, it separates her from him in a meaningful way; she can speak English well, while he cannot. 



The theme of straddling two cultures creates conflicts is relevant in Kincaid's "Girl" as well. "Girl" takes place in the Caribbean Islands, where European colonization has a firm influence. In the mother's monologue of advice to her daughter, she teaches her ways in which her native Antiguan culture needs to stay separate from her British culture:



"Is it true that you sing benna in Sunday School? [...] don't sing benna in Sunday school"



Benna is a calypso-like style of music that was used as a way to spread scandalous information and rumors, and often also had a sexual double meaning. It definitely wasn't appropriate for a religious setting and probably not for the ears of the white folks who would presumably be presiding over Sunday school. This quote shows the mother encouraging the girl to keep these cultures separate. 



There could also be a conflict through the girl's faith. The girl goes to Sunday school, but the mother also teaches her the traditional religion Obeah, saying things like



"Don't throw stones at blackbirds because it might not be a blackbird at all,"



which demonstrate the Obeah beliefs she still holds. The perils of navigating two cultures, especially two with an uneven power dynamic, create some conflict and confusion in the adolescent girl, as well as in the mother, who is exasperated with her daughter and fearful of her failure.


Wednesday, September 28, 2011

What does "organs of government propaganda" mean?

Organs of government propaganda are the means by which government disseminates its propaganda, meaning methods of communication designed to persuade people to its stance or point of view.  "Propaganda" is perceived almost universally as a negative term, but what is or is not propaganda depends largely on one's perspective, as a few examples should make clear.  There are many "organs" of propaganda, and governments at one time or another have taken advantage of all of them.


Two common organs of government propaganda are television and radio. In some countries, these are actually owned and operated by the government, and viewers and listeners are subject to whatever the government wants them to hear, all promoting that government's agenda.  I imagine that North Korea, for instance, has no television or radio station that is not government owned.  And there are other countries in which the television and radio stations are not owned and operated by the government, but are subject to strict government control and forced to air ads or other content that promotes the government's agenda.


Newspapers can be state-owned or controlled as well, in a similar fashion.  And even in a society with a free press, newspapers can be organs of government propaganda.  For example, if the administration wishes to garner support for its doings, it will often "plant" stories in newspapers, which the newspapers have a tendency to go along with, possibly as a quid pro quo for gaining more cooperation from the government in interviews.


Another organ is the pamphlet drop.  During World War II, the United States dropped thousands of pamphlets to people in Europe and in the Pacific front, to persuade them of the United States' point of view and efforts in the war.  These were always in the language of the people whom the drops were aimed at. My father brought home a number of these from the war, in German and in French. 


I would say that generally, governments that are repressive tend not to use social media such as Facebook to communicate propaganda because these are governments that can ill-afford to allow their citizens to use such social media. This would allow citizens to see other perspectives and thus ruin the value of the propaganda.


In short, any way that a government can communicate with people to persuade people of its point of view can be viewed as an organ of government propaganda.  Whether one thinks that communication is propaganda or simply friendly information depends on one's perspective. 

Tuesday, September 27, 2011

What are some important quotes from Act 5, scene 3 of Shakespeare's play Macbeth?

When Macbeth is alone on stage, he delivers a soliloquy that reveals his innermost feelings at this point in the play.  He says,



My way of life
Is fall'n into the sere, the yellow leaf,
And that which should accompany old age,
As honor, love, obedience, troops of friends, 
I must not look to have, but in their stead
Curses, not loud but deep, mouth-honor, breath
Which the poor heart would fain deny and dare not.  (5.3.26-32)



He means that he has begun to age, and all the things that typically come with old age such as good friends, respect, and love, he doesn't have.  Instead, he is cursed by others, not loudly (because they fear him) but deeply (from their hearts), and the only honor he gets is from people's mouths rather than their hearts because no one is loyal to him.  People would want to speak against him from their hearts if they were not so afraid to do so.  In other words, we see some regret here, a little remorse that Macbeth's reign, and life, have not turned out the way he thought they would.


Further, when Macbeth speaks to the doctor about his wife, he asks,



Canst thou not minister to a mind diseased,
Pluck from the memory a rooted sorrow,
Raze out the written troubles of the brain,
And with some sweet oblivious antidote
Cleanse the stuffed bosom of that perilous stuff
Which weighs upon the heart? (5.3.50-55)



By this, he means that he's surprised the doctor can do nothing to help his wife.  He knows that she's tormented by her guilt, and so he tells the doctor to find a way to get inside Lady Macbeth's brain and get rid of the memory that bothers her.  He wants the doctor to unburden her somehow, but that is not what medicine does (as the doctor tells him).  This quote really helps to show how distant Macbeth and his wife have become, especially given that they thought of each other as "partner[s]" before they committed the murder of Duncan together.  Now Macbeth can hardly be bothered with her and her regret.

In The Westing Game by Ellen Raskin, what do the other heirs think when Turtle is caught with exploding fireworks in the elevator?

Judge Ford thinks that Turtle set off the fireworks to divert suspicion from the real bomber, Angela. 


Turtle set off the fireworks in the elevator to protect her sister, Angela.  Theo called Turtle and told her that he saw Angela at the hospital.  Then he told her to let him have her bike.  The implication was obvious.  He was blackmailing her. 



Turtle hung up the phone. If Theo knew, others knew.  Angela had set off those fireworks wanting to get caught, but it was different now. Now she was confused, now she was just plain scared. They could force a confession out of her in no time, the guilt was right there staring out of those big blue eyes. (Ch. 21) 



Turtle's solution was dangerous, but she was desperate.  When the police come to investigate the “bombing” they find Turtle still in the hallway.  The police assure her mother that it was just a childish prank.  Turtle's mother is clueless about what both her daughters are up to.  The policeman found Turtle’s essay in the elevator, on the back of a sign that said, “THE BOMBER STRIKES AGAIN!!!” 


The police do not want the paperwork of taking Turtle in, so they take her to Judge Ford instead.  Judge Ford thinks she knows why Turtle would set off explosives in an elevator. 



She was protecting someone. She had set off the fireworks in the elevator to divert suspicion from the real bomber. But who was the real bomber? Nothing to do but drag it out of her, name by name, starting with the least likely. “Are you protecting Angela? (Ch. 21) 



Judge Ford is surprised at the empathic denial she gets from that suggestion.  It seems unlikely that someone like Angela would be the bomber, after all. She seems harmless.  Realizing she has underestimated Angela, as everyone else has, Judge Ford makes Turtle promise not to set off fireworks again.

I need help writing a critical appreciation of the poem "My Last Duchess".

A critical appreciation focuses on the literary qualities of the poem rather than simply being a summary.


Your introduction might mention that the poem was written by Robert Browning and first published in 1842. It is an historical poem, being set in Renaissance Italy rather than England of the Victorian era.


Next, you might discuss meter. The poem consists of 28 heroic couplets meaning that the lines are written in iambic pentameter and have the rhyme scheme AABBCC, etc. It has no stanza breaks. Browning's frequent use of enjambment, in which syntactical breaks do not coincide with line breaks but rather sentences run unbroken from one line to the next, make the poem flow in almost a pattern of ordinary speech, unlike, say, the work of Alexander Pope in which the lines are end-stopped and rhymes emphasized often for humorous effect. 


The genre of the poem is a dramatic monologue, in which we overhear the speaker talking to a messenger. As the speaker talks, he reveals elements of his character which gradually undermine his credibility, revealing himself as selfish, cruel, jealous, paranoid, and perhaps a murderer. 


A theme this poem has in common with many others by Browning is that of the "collector", a character who is obsessed with collecting, owning, and possessing, and who treats people as possessions. 

How did Macbeth destroy Scotland?

Macbeth destroys Scotland, first, by killing the country's compassionate and noble king, Duncan. Under Duncan's rule, people were rewarded for their good services, and the country seemed to prosper, even seizing victory in two wars at once. After Macbeth takes over, however, people are made desperate by fear, hunger, and poverty, presumably because Macbeth hoards everything good for himself. The Lord with whom Lennox speaks in Act 3, scene 6, says that, with Malcolm's help, people might once "again / Give to [their] tables meat, sleep to [their] nights, and / Free from [their] feasts and banquets bloody knives, / Do faithful homage, and receive free honors, / All which we pine for now" (3.6.37-41). Therefore, we can understand that Macbeth's rule has devastated Scotland and her people in myriad ways.


Ross says something similar when he speaks with Lady Macbeth in Act 4, scene 2: "cruel are the times when we are traitors / And do not know ourselves; when we hold rumor / From what we fear, yet know not what we fear, / But float upon a wild and violent sea / Each way and move [...]" (4.2.22-26). He says that men are accused of treason and do not even know why, that so many rumors circulate that one knows not what to fear nor what is even true, and that the country feels adrift in every way. This was not so during Duncan's reign, and so Macbeth's corruption, greed, and paranoia appear to have devastated Scotland.

Monday, September 26, 2011

What is a good thesis statement about medieval knights? I have written that knights emerged to help local nobles control their world.

You could write about the societal influence of knights and their clash with religious tradition during that time. Knighthood is an interesting outlet through which to explore medieval values, especially in reference to the Christian church's role among the population (as Christians dominated the religious environment of Western Europe during that time). During the medieval era, there were two types of "heroes": knights and saints—but one couldn’t necessarily be both. The notion of sainthood is in many ways oxymoronic in concurrence with knighthood. Saints were chaste; knights married and had children to carry on their legacy. Saints were expected to live in poverty, but the public understood poverty to be a direct threat to the preservation of a knight’s honor. While saints prayed and read scripture, knights went into battle alongside kings and helped eliminate the enemy by any means necessary. There was one thing saints and knights did have in common, however. They were both meant to serve as exemplary individuals, but in different capacities.


This all presented a challenge to the church, as Christianity was confronted with balancing tradition and scripture with an unstoppable progression of culture among the populace. Considering this context, one may wonder how a knight or a warrior could be a “good” Christian, or perhaps whether it was possible for them to be eligible for canonization as a saint (although to date, there are no canonized knights). Potential answers to this theoretical question depended largely on the medieval church’s attitude towards chivalry. In particular, it is important to consider the church’s reaction to warriors, tournaments, and the general notion of competitive glory.


Throughout this period, the church found ways to justify violence in the context of fighting to preserve Christian authority. For instance, the Crusades and the Knights Templar were outlets for people to exhibit their aggression and satiate their competitive appetite, while also remaining “good” in the eyes of the church.


Aside from the Crusades and the Knights Templar, some good specific examples you could use in this exploration are William Marshal, St. Louis (or King Louis IX), St. Joan of Arc, and St. Francis of Assisi. While William Marshal was never canonized, the cases of Joan of Arc, Louis IX, and even Francis d’Assisi (before his spiritual awakening) demonstrate that engaging in violence did not prevent one from being a saint.

What is Addison's disease?


Causes and Symptoms

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




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


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


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


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




Treatment and Therapy

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


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


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


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




Perspective and Prospects

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




Bibliography:


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



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



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



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



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



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



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

Sunday, September 25, 2011

What are the form and figurative language of Stephen Spender's poem, "My Parents kept me away from children who were rough?"

Stephen Spender's "My Parents kept me from children who were rough" is a poem written in free verse. That means it is unrhymed and has no specific meter. However, we can confirm by counting that the lines range from 10-12 syllables each, and many of the "feet" of the poem are anapests (two unstressed syllables followed by a stressed one, such as in the line "and who threw" where the stress is placed on the word "threw").


The poem is filled with similes:


"words like stones"


"I feared more than tigers their muscles like iron"


"they sprang out behind hedges / Like dogs to bark at our world"


The words within these similes help contribute to our understanding of the "rough children." The words "stones," "tigers," "iron," and "dogs" all carry the rough connotation that the author is trying to convey.


Another device that has the same effect is metaphor. The poet says, "I feared the salt coarse pointing of those boys." Thus, the pointing of the boys is compared to coarse salt - not a pleasant feeling!


The tone of the poem is most strongly conveyed through the device anthesis. This device uses contrast in order to prove a point. So in this poem, the speaker discusses all of the things that the rough children are, and by doing so he also tells us everything he is NOT. He tells us all the horrible things the other kids do, which emphasizes his position as a victim.


The speaker also seems envious of how free the other children are, even though he resents their bullying. We can see this in the title and first line, where he states that his parents keep him away from the others, implying that it is not his own decision to avoid them.


Hope this helps! 

How can classical conditioning be used to explain the development of phobias?

Classical conditioning refers to the pairing of two kinds of external stimuli to cultivate the same response to both. This can be used to develop phobias by simultaneously exposing a subject to one kind of stimuli that doesn't cause a fear response and to another stimuli that does, so that the fear response will eventually emerge with the second stimulus alone. An example of classical conditioning used to develop fear in humans is an experiment performed on a 9-month-old baby by researchers Watson and Rayner in 1920. The researchers exposed the baby to various types of animals and masks and recorded no fear response to any of them. The stimulus that did cause the baby to express distress was the sound of a hammer hitting a steel bar behind him. To classically condition a phobia of the animals, the doctors showed the baby a rat while making the sound that he was afraid of. In response, the child showed signs later in life of having a phobia of rats and animals that shared characteristics with rats.

Saturday, September 24, 2011

Use the Nernst Equation to calculate the cell potential when the concentrations are [Zn^2+] =0.1M and [Cu^2+]=0.001M +1.04v +1.10v +1.16v 0.00v...

For `Zn(s) + Cu^(2+)(aq) -> Zn^(2+)(aq) + Cu(s)` E(st.cell) = +1.10V.


E(st.cell) here is the standard potential. Given the concentrations for the ions of copper and zinc as 0.001M and 0.1M respectively, the Nernst equation can be used to calculate E as follows:


`E = E(st.cell) - ((RT)/(nF))ln(Q)` where n is the number of electrons transferred, and in this case is 2, and Q is the reaction quotient, or the ratio of concentrations of ion products to ion reactants. In this case, Q will be [Zn2+]/[Cu2+] = 0.1/0.001 = 100.


R is the universal gas constant: 8.314 J/molK


F is Faraday's constant: 96, 485 C/mol


T is temperature in kelvin.


No temperature is given, but I will assume that this is STP so that temperature is 25C or 298K.


Then,


`E = +1.10 - ((8.314 * 298)/(2 * 96485))* ln(100) = +1.04V` .


Therefore, the cell potential is +1.04V.


Note that I assumed the temperature to be 298K. If the temperature is different, simply change the temperature, but the entire process remains the same.

I need questions for a Macbeth interview, and it should be based on Act I Scene II (where the soldier tells the King about Macbeth's bravery when...

Often, when people conduct interviews, they are less interested in factual events and more interested in the humanity of the person they interview, how that person felt when they accomplished something, what prompted them to act how they did, and so on.  Therefore, you could consider questions you might put to Macbeth that would satisfy the kind of "human interest" aspect of an interview.


Macdonwald was formerly thought to be loyal, and he has turned traitor against the Scottish crown, an action that would likely be quite shocking to Macbeth at this early stage.  Therefore, you might ask Macbeth if he knew Macdonwald well, and if he was surprised when he learned that Macdonwald had been revealed as a traitor.  


Then, the captain continues, as soon as Macbeth had defeated Macdonwald's troops, he turns around to find fresh Norwegian troops ready to fight him.  You might ask Macbeth how he was feeling in that moment.  He must have been exhausted and yet he somehow managed to carry on.  What gave him the strength he needed to win yet another battle?


You might also ask about the relationship between Macbeth and Banquo.  They seem quite close during the early scenes of the play, and it stands to reason that they were a huge support to one another during these battles.  You might ask Macbeth to describe how important that support was.

Friday, September 23, 2011

How does the electronegativity of elements depend on atomic size?

Electronegativity can be thought of as the ability of an atom to pull the bonding pair of electrons towards itself. The more electronegative an atom is, the closer the bonding pair will be to it. Metals generally have low electronegativity, while non-metals have higher values of electronegativity. When the electronegativity difference between the bonding atoms is high, we get an ionic bond. When the bonding atoms have similar electronegativity, we get a non-polar covalent bond.


Electronegativity is dependent upon the size of the atom, since the attraction for electrons falls rapidly as the distance from the nucleus increases. The larger the atom gets, the more distant electrons become from the nucleus and hence have lesser attraction to the atom. That is why electronegativity decreases as we go down a group in the periodic table. This is because between each successive group member (as we go down), an extra electron shell is added to the atom and the bonding electrons become more distant from the nucleus. However, when we move across a period in the periodic table, electronegativity increases, since the atomic size decreases across a period.


Hope this helps.

What part does Romeo inadvertently play in Mercutio's death?

When Tybalt comes to challenge Romeo the day after Romeo and his friends crashed the Capulets' party, Romeo has just come from his own secret wedding to Juliet, Tybalt's cousin. As a result, Romeo refuses to fight Tybalt, stating that he has reasons to love Tybalt that Tybalt cannot possible understand. Mercutio views Romeo's unwillingness to fight and his peaceful, loving words as a "dishonorable, vile submission," and he steps in to fight Tybalt on Romeo's behalf. As Mercutio and Tybalt fight, Romeo begs them to stop, put their swords down, and walk away peacefully, but they only continue. Finally, Romeo physically comes between them, and, when he does so, Tybalt stabs Mercutio under Romeo's arm, mortally wounding him. Mercutio dies moments later, cursing both the house of Capulet and the house of Montague.

Wednesday, September 21, 2011

Did Christianity spread through trade?

There is historical and archaeological evidence that suggests trade was influential in the spread of Christianity. Early on, the official means for spreading the "good news" was through missionaries. Men like Paul of Tarsus went out into the world to preach publicly and inspire Jewish and non-Abrahamic peoples to convert. Initially, Christianity was a sect of Judaism, but Paul was significant in permanently separating the two faiths. Many early missionaries thought people should convert to Judaism and then to Christianity as a sect of Judaism, but Paul thought (and taught) this double conversion was unnecessary.


After Paul's journeys throughout the Mediterranean, the next biggest conversion to Christianity was when Emperor Constatine issued the Edict of Milan, which decriminalized Christianity. Constantine is upheld as the first Christian Roman Emperor, and he made it safe for people to practice Christianity in the Roman Empire without fear of death or punishment. 


Between Paul's time in the 1st century CE and Constantine's Edict of Milan in in 313 CE, Christianity was booming in the Roman Empire but had to be practiced almost entirely in secret. Trade played some part in the spread of Christianity, as the entire Roman Empire was connected by trade routes. The only people really likely to be traveling were involved in trade or were intentional missionaries. By the 9th century, Christianity spread as far north as Scandinavia. In Anders Winroth's The Age of the Vikingshe describes graves found in Scandinavia where people were buried with crosses that originated as far away as Turkey or Greece. Even after the fall of the Roman Empire in the west, trade routes connected Europe and exposed people to Christianity.


During the second millennium CE, trade expanded globally, with ships regularly sailing from Europe to Africa to Asia and even to the New World. Though the primary purpose of far-distance international trade and New World exploration was to acquire valuable goods, there was a significant secondary effect of evangelization. Especially in relations with East Asia, evangelization was on par with trade in terms of importance. With Europeans claiming territory in the New World, they could declare the land as belonging to a Christian nation and officially make anyone who lived there a Christian. By the time the Americas were colonized, Europeans came to see it as a duty to convert the native peoples to Christianity.


Christianity really flourished in the context of a world that was connected by trade, so much so that conversion has almost replaced trade interests in more recent centuries.

Tuesday, September 20, 2011

What are some similarities and differences between Shakespeare's Sonnet 18 and the balcony scene in Romeo and Juliet?

For starters, both Sonnet 18 and Romeo and Juliet were written by William Shakespeare! Though this fact makes further similarities and differences all the more interesting. Let's consider some differences, first.


While Sonnet 18 is a piece of standalone poetry, the balcony scene of Romeo and Juliet is but one part of a greater play. What's more, Sonnet 18 is written from the perspective of the speaker to an unknown reader. In this way, it is like a love letter. We have the perspective of the speaker, but not the recipient-subject. The balcony scene of Romeo and Juliet may be considered to consist of parallel monologues until the two characters actually speak to one another. It differs from the Sonnet because we hear both characters' perspectives, and each is the recipient-subject of the other's speech.


What do these two pieces of text have in common? Both are declarations of love! They also bear similarities in their content. Comparisons of beauty and nature are in both, evoking images of beautiful summer flowers. One can easily understand what Shakespeare found beautiful in nature as well as in a person by reading and comparing these two texts.

What are noncoding RNA molecules?


Definition

Noncoding RNAs (ncRNAs) include any RNA that is not messenger RNA (mRNA), ribosomal RNA (rRNA), or transfer RNA (tRNA). The discovery of the first ncRNAs in the 1960s occurred because they were expressed in such high numbers. At the time, RNA was considered to function only as a means to express a gene, with all three of the main types of RNA being intimately involved in this process. Many of the ncRNAs discovered over the next twenty years were also discovered fortuitously, before any speculation about their possible functions was even considered. Once transcription and processing of mRNAs was elucidated, many of the ncRNAs were considered leftover fragments representing the introns that had been cut out of pre-mRNAs. At the same time it was discovered that some of the ncRNAs were involved in the process of intron removal and exon splicing. Systematic searches for ncRNAs did not begin until the later 1990s and, once undertaken, revealed a veritable universe of ncRNAs, ranging from very short sequences of less than 100 nucleotides to some around 100,000 nucleotides, and possibly more. Researchers have now identified ncRNAs in essentially all organisms, from bacteria to humans. For a system considered so well understood, the entry of so many new players has added a whole new layer of complexity to the study of genetics.













ncRNAs Involved in RNA Processing and Modification

In almost all eukaryotic genes the coding sequence is interrupted by intervening sequences, called introns,. Therefore when an mRNA is transcribed it cannot be translated without first removing the introns and the joining together (splicing) of the remaining fragments. These remaining fragments, which contain the coding sequence of the gene, are termed exons because they exit into the cytoplasm of the cell, unlike the introns, which are eventually degraded in the nucleus. The cellular “machine” that removes the introns and joins together the exons is the spliceosome. It is a complex assemblage of proteins and several particles called small nuclear ribonucleoproteins (snRNPs, pronounced “snurps” by geneticists). Each snRNP is made up of one or more small nuclear RNAs (snRNAs), the most common ones being U1, U2, and U4/U5/U6 snRNAs, and a characteristic set of proteins bound to the snRNA.


Polyadenylation, another mRNA processing event, is the addition of adenine nucleotides to the 3′ end of mRNAs to make what is called a poly-A tail. A complex made up of several proteins is responsible for recognizing the polyadenylation signals in the mRNA transcript and adding the adenine nucleotides. Replication-dependent histone mRNAs are not polyadenylated, but instead a specific snRNP, and thus an snRNA called U7, are involved in forming a unique stem-loop structure at the 3′ end of the mRNA.


The three rRNAs found in eukaryotic ribosomes (28S, 5.8S, and 18S) are cleaved from a long 45S primary transcript. About half of the original transcript is removed in processing, mature rRNAs have some of their ribose sugars methylated, and some uracil nucleotides in rRNA are converted to pseudouracil (a modified nucleotide), in a process called pseudouridylation. The specific sites for modification and cleavage of the rRNA are determined by small nucleolar RNAs (snoRNAs) acting as guide RNAs. The snoRNAs bind transiently to rRNA in regions where they have complementary base sequences and direct methylation (C/D snoRNPs), pseudouridylation (H/ACA snoRNPs), or cleavage (U3, U8, U22 and MRP snoRNPs in vertebrates) at a set distance on the rRNA from the binding site of the snoRNA. For example, Cbf5 is the pseudouridine synthase enzyme in H/ACA snoRNPs, which is recruited to the site of rRNA modification because it is in the complex with the guide snRNA in the snoRNP. SnoRNA homologs (a homolog is a molecule that is similar to another) have been found in Archaea, but in Bacteria rRNA modifications do not appear to involve guide RNAs.


A complex related to snRNPs was first found in bacteria and has now been found in all groups of organisms. It contains proteins and RNA and is called ribonuclease P (RNase P); it is involved in the processing of tRNA and some rRNAs. Experiments have shown that the RNA component can catalyze the required reactions, even without the protein component, making it the first clear-cut “ribozyme,” an RNA with catalytic properties. Several types of ncRNA are now known to act as ribozymes, and this ability prompted the evolutionary community to propose that early “life” was RNA-based rather than protein and DNA-based.


Another type of ncRNA is involved in RNA editing. These are guide RNAs (gRNAs), discovered in some protists. They guide the insertion or deletion of uracil nucleotides in mitochondrial genes. The details of the process are not well understood, but the mechanism involves complementary base pairing between the rRNA and a gRNA, much like that seen with snoRNAs. RNA editing was found in other organisms and with rRNA and tRNA as well.


Finally, like mRNA, rRNA and tRNA contain introns as well, but their removal and splicing together of the remaining fragments does not rely on the spliceosome machine. Instead, some contain self-splicing introns, that is the introns catalyze their own removal (self-splicing introns are also found in some protein-coding genes in mitochondria). The splicing of tRNA introns is by yet another mechanism, which does not involve ncRNAs.




Small ncRNAs in RNA Interference

One of the most exciting discoveries in the area of ncRNAs was the realization that short (20-30 nucleotides) double-stranded RNAs (dsRNAs) trigger RNA silencing, a previously unknown but ubiquitous mechanism of controlling gene expression. The 2006 Nobel Prize in Physiology or Medicine was awarded to Andrew Fire and Craig Mello for their discovery of this phenomenon termed RNA interference or RNAi. The intensive and ongoing research effort that followed this initial discovery identified two major groups of small RNAs involved in RNA silencing: small interfering RNAs (siRNAs). and microRNA (miRNAs). Both originate from long double-stranded RNAs, which can be thousands of base pairs long in the case of siRNAs, but are usually a 70-base-pair long RNA hairpin structure for an miRNA. The 20-30 nucleotides long small RNAs are cleaved from their dsRNA precursors by an enzyme called Dicer, which is a ribonuclease. The small RNAs generated by Dicer bind to the RNA-induced silencing complex (RISC). A nuclear form of RISC is called RITS, for RNA-induced transcriptional silencing. At the core of each complex is a protein called Argonaute, which binds to the small RNA. RISC or RITS are targeted to a particular mRNA by the small RNA bound to Argonaute serving as a guide, since it has a base sequence complementary to the coding, or “sense,” region of an mRNA. When “guided” to an mRNA by the bound siRNA or miRNA, Argonaute stops translation by sequestering or cleaving the target mRNA.


Another type of sRNA is PIWI-interacting RNA (piRNA); it is involved mainly in protection of the genome from parasitic DNA elements, and is thought to work through complexes similar to RISC and RITS.


RNAi was initially thought to exert a type of genetic control called post-transcriptional gene silencing, whereby silencing occurs by targeting mRNA translation or stability. Control of gene expression at the earlier stage of transcription is determined in part by the state of the DNA in the transcribed region. Heterochromatin is a more tightly packed form of DNA associated with repressed transcription and subsequent silencing of gene expression. To a large extent modifications of histones around which the DNA is wrapped determine the packing state of the DNA and subsequently the level of gene expression. Increasing evidence points to RNA silencing acting during transcription as well, and even linking to alterations in DNA packing through interactions with histone modifying agents, as well as affecting DNA methylation, which is also associated with transcriptional silencing.


In bacteria, sRNAs (generally 100 nucleotides long) also target specific mRNAs for degradation, but a protein called Hfq, which is of a different type from Argonaute, plays the role of mediator and effector in the sRNA and target mRNA interaction. Other sRNAs in bacteria activate certain mRNAs by preventing formation of an inhibitory structure in the mRNA. Another ncRNA, simply called OxyS RNA, represses translation by interfering with ribosome binding.




Other Specialized ncRNAs

A variety of other ncRNAs carry out more specialized functions, some just beginning to be understood. Gene silencing is a very important component of normal development. As cells become differentiated and specialized, they must express certain genes, and the remaining genes must be silenced. A form of silencing different from RNAi is called imprinting, whereby certain alleles from an allele pair are silenced, often those received from only one sex. A large ncRNA (a little longer than 100,000 nucleotides) called Air is responsible for silencing the paternal alleles in a small autosomal gene cluster. The mechanism underlying Air RNA action is beginning to be elucidated, and involves interaction with the DNA at the region to be silenced and recruitment of histone-modifying activities, leading to transcriptional silencing of the DNA in that region.


In human females, one of the X chromosomes (females have two) must be inactivated so the genes on it will not be expressed. This inactivation, called Lyonization after the discoverer of the phenomenon, Mary Lyon, occurs during development on a random basis in each cell, so that the X chromosome subjected to deactivation is randomly determined. An ncRNA called XIST plays a central part in this process. It is a large RNA of 16,500 nucleotides and it is initially transcribed from genes on both X chromosomes. When X inactivation begins, the active X chromosome ceases to express XIST, whereas the future inactive X chromosome has increased XIST expression and the XIST transcript binds all over the inactivated X chromosome. The X chromosome that gets coated with XIST is then silenced, and the only gene it transcribes thereafter is the XIST gene.


A type of ncRNA called transfer messenger RNA (tmRNA) is involved in resuming translation at ribosomes that have stalled. When a stalled ribosome is encountered, a tmRNA first acts as a tRNA charged with the amino acid alanine. The stalled polypeptide is transferred to the alanine on the tmRNA. Then translation continues, but now the tmRNA acts as the mRNA, instead of the mRNA the ribosome was initially translating. A termination codon is soon reached and the amino acids that were added based on the tmRNA code act as a tag for enzymes in the cytoplasm to break it down. This allows those ribosomes that would normally remain tied up with an mRNA they cannot complete translating to be recycled for translating another mRNA.


Telomerase is an enzyme responsible for maintaining the ends of chromosomes called telomeres. It is a large RNP containing the TER RNA, which is a few hundred (and in some species more than a thousand) base pairs long. TER contains a template sequence used to synthesize the repeat sequences normally found in telomeres.




The Future of ncRNA Research

Most of the ncRNAs described above were unknown until the 1980s, and some of them were only discovered in the 1990s. What appeared to be a relatively simple picture of genetic control in cells has now gained many, previously hidden, layers involving all manner of RNAs, ranging from a mere 20 nucleotides to 100,000 nucleotides or so in length. Some are suggesting that this glimpse is just the tip of the iceberg and that continued research will reap increasingly complex interactions among RNAs and between RNAs and proteins. Genomics, the study of the DNA sequence of genomes, has been a hot field for some time, and is now often focused on discovery of ncRNAs.


Initially, cDNA libraries were surveyed for ncRNA sequences, especially some of the smaller ones that were long thought merely to be leftover scraps from other processes. For example, one study in 2001, which included a survey of a mouse-brain cDNA library, revealed 201 potential novel, small ncRNAs. In a 2003 survey of a cDNA library from
Drosophila melanogaster
(fruit fly), sixty-six potential novel ncRNAs were discovered. Judging by the large numbers of candidate ncRNAs showing up in what are essentially first-time surveys, many more may remain to be found, and methods for generating small RNA libraries are continually improving. There could potentially be thousands of ncRNA genes. What is surprising is that many of these ncRNA genes are being found in spacer regions and introns, places that were once considered useless junk. With so much now being found in these regions, many geneticists have become ever more cautious in calling any DNA sequence junk DNA.


Because the field of ncRNAs is in its infancy and the functions of many of the ncRNAs are just barely understood, it may be premature to predict specific medical applications, but certainly the potential is there. The population of ncRNAs in a cell, in some sense, resembles a complex set of switches that turn genes on and off—before they are transcribed, while they are being transcribed, or even once translation has begun. Once these switches are better understood, researchers may be able to exploit the system with artificially produced RNAs. Geneticists will probably also discover that a number of diseases that appeared to have unexplained genetic behavior will find the solutions in ncRNA.




Key terms



cDNA library

:

a collection of clones produced from all the RNA molecules in the cells of a particular organism, often from a single tissue




clone

:

a culture of bacteria, usually Escherichia coli, whose cells contain a recombinant plasmid




codon

:

a three-letter nucleotide sequence in RNA or DNA that codes for a specific amino acid; a gene is composed of a long string of codons




intron

:

an intervening sequence in a eukaryotic gene (generally there are several to many per gene) that must be removed when it is transcribed into messenger RNA (mRNA); introns are assumed to have no function and therefore mutations in them are often considered neutral




spliceosome

:

a complex assemblage of proteins and RNA in the nucleus of cells that cuts out introns and splices the exons of a maturing mRNA





Bibliography


Bass, Brenda L. “The Short Answer.” Nature 411 (2001): 428–29. Print.



Castel, Stephane E., and Robert A. Martienssen. “RNA Interference in the Nucleus: Roles for Small RNAs in Transcription, Epigenetics and Beyond.” Nature Reviews Genetics 14.2 (2013): 100–12. Print.



Gesteland, Raymond F., Thomas R. Cech, and John F. Atkins, eds. The RNA World. 3rd ed. New York: Cold Spring Harbor Laboratory P, 2005. Print.



Ghildiyal, Megha, and Phillip D. Zamore. “Small Silencing RNAs: An Expanding Universe.” Nature Reviews Genetics 10 (2009): 94–108. Print.



Grosshans, Helge, and Frank J. Slack. “Micro-RNAs: Small Is Plentiful.” The Journal of Cell Biology 156.1 (2002): 17–21. Print.



Hentze, Matthias W., Elisa Izaurralde, and Bertrand Séraphin. “A New Era for the RNA World.” EMBO Reports 1.5 (2000): 394–98. Print.



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



Morris, Kevin V. Non-Coding RNAs and Epigenetic Regulation of Gene Expression: Drivers of Natural Selection. Norfolk: Caister Academic, 2012. Print.



Storz, Gisela. “An Expanding Universe of Noncoding RNAs.” Science 296 (2002): 1260–263. Print.



Zhang, A. T., et al. “Dynamic Interaction of Y RNAs with Chromatin and Initiation Proteins during Human DNA Replication.” Journal of Cell Science 124.12 (2011): 2058–069. Print.

Monday, September 19, 2011

What is the theme of the poem "Still I Rise?"

This poem is about resilience and determination when facing oppression. This is a general theme but Angelou is also specifically talking about the historical oppression of African-Americans. In the poem, she shows a determination to resist being a victim of this oppression. No matter how she (the speaker) is portrayed in history books, she will "rise" (live, fight, resist). Even if she is forced to live a poor life, she will act as though she is rich ("oil wells"). She will "rise" with the certainty that the sun and moon both rise. 


She challenges those who would oppress or hold her down. Rather than acting defeated, with "bowed head and lowered eyes," she will laugh and even be haughty or sassy. This is in defiance of the oppressors. 


She ends the poem with



"I am the dream and the hope of the slave. / I rise / I rise / I rise."



Although no longer a slave, she still faces racism and oppression. Instead of wallowing in frustration resulting from this oppression, she endeavors to defy it and live a happy life. The penultimate stanza notes the difficult history her ancestors had to endure. She responds to that past with that same empowering refrain of rising. 



Out of the huts of history's shame 


I rise 


Up from a past that's rooted in pain 


I rise 


I'm a black ocean, leaping and wide 


Welling and swelling I bear in the tide. 


What does the detainment of Friar John due to his possible contact with a deadly plague suggest in the text? Could this act as another instance...

Friar John's detainment as a result of his possible contact with a terrible disease seems to be just one more way that fate is working against Romeo and Juliet.  Friar Lawrence's plan for Juliet to fake her death and thereby escape her marriage to the County Paris is relatively sound; it just depends on this one thing: Romeo receiving the letter that acquaints him with the details of the plan. However, as early as the Prologue, the Chorus says that Romeo and Juliet are "star-crossed lovers" who are "misadventured"; thus, we know that fate will work against them in the play, and an unexpected and previously unheard of "pestilence" is just another example of a terribly unlucky, unpredictable thing that could happen. 


Just as no one could have predicted that Tybalt would challenge Romeo just hours after he married Tybalt's cousin, or that Tybalt would kill Mercutio when Romeo came between them (an action that should have protected Mercutio rather than led to his death), or that Romeo would slay Tybalt, some random disease is just an unfortunate and arbitrary event.  Therefore, Friar John's quarantine seems like just one more symbol that fate will intervene to prevent Romeo and Juliet from being together, at least in this life.

What are spinal cord disorders?


Causes and Symptoms

Most people take certain basic tasks for granted, such as walking up a flight of stairs, brushing their teeth, or using a personal computer. Motor neurons in the
spinal cord control the hundreds of muscle fibers that are involved in each of these activities. At the same time, other neurons of the spinal cord serve as part of the sensory pathways that provide information regarding body position and motion, which contributes to the coordination of these activities. In amyotrophic lateral sclerosis (ALS)
, also known as Lou Gehrig’s disease, the motor neurons in the spinal cord die, leaving patients without control of their muscles. This example of a spinal disorder serves to emphasize the important role that the spinal cord plays as it serves as an interface (input-output system) between the brain and the body.


Similarly, most people have experienced pain in the hand, which is followed by an instantaneous, automatic movement of the hand away from the object causing that pain. Such reflexes represent the simplest of movements, yet they still require the integrative and relay action of neurons of the spinal cord to cause immediate hand withdrawal without requiring the individual to think about the act consciously. Only after the reflex has occurred does the spinal cord activity “inform” the brain that something happened. Therefore, in addition to sensory and motor interface functions for the brain, the spinal cord performs basic integration tasks as it controls reflexes, contributes to the coordination of movement between the left and right sides of the body, and prevents opposing muscle groups from trying to move a joint in opposite directions at the same time. As with any other vital organ of the body, spinal cord damage or defects have serious consequences for the health and well-being of humans.


In the medical research laboratory,
paralysis results from complete or partial transection of the spinal cord. In the real world, a fracture or dislocation of vertebrae or damage done by a bullet can cause paralysis in the same fashion. Acute transection of the spinal cord can also result from an inflammatory condition or from any situation in which the spinal cord is compressed, such as by a tumor. The spinal cord is contained within the vertebral column, which is divided into the cervical, thoracic, lumbar, and sacral regions, each of which is associated with a specific set of functions. Transection typically results in the loss of sensory and motor functions below the level of the lesion.


Spinal cord injuries and defects are the result of three basic types of pathological conditions. The first of these conditions is traumatic physical injury to spinal cord tissue, such as the severing of the spinal cord during a car accident. The second condition is a congenital or inherited genetic problem with spinal cord development and function, as illustrated by spina bifida. The third is an acquired condition, such as damage caused by a viral or bacterial infection. In each case, the severity of the pathological condition is dependent upon the location and extent of the resultant spinal cord lesion. In the clinical setting, physicians utilize information regarding all aspects of spinal cord function, such as sensory, motor, reflex, and coordination functions, as well as information from a variety of imaging techniques to diagnose pathological conditions and select appropriate treatments.



Trauma. The neurons of the spinal cord carry out their functions by way of their long nerve processes (axons), which extend to form synapses with, and control, target cells (muscles and other neurons). Some of these nerve processes extend out of the spinal cord to the body, others extend either up to or down from higher-brain regions, and yet others extend from one side of the spinal cord to another. Trauma mainly damages the nerve process of cells and in this fashion disrupts their function in controlling target neurons and muscles. Often, after nerve processes have been damaged, the neuron itself will die because of loss of neurotrophic influences from their target cells. It has been estimated that every year, between ten thousand and twelve thousand people in the United States are disabled by some degree of paralysis resulting from traumatic injury to the spinal cord. The spinal cord can be also damaged by blocked blood flow to the cord, blood accumulation (hematoma) in or near the cord, or the presence of a ruptured or herniated disk, all of which can be caused by trauma.



Congenital defects. Spinal cord defects are not the result of trauma but rather are generally attributed to abnormal events during
embryonic development. In particular, most major spinal cord defects arise around the third week of development. During this time, the flattened neural plate is beginning to fold upward as its lateral edges come together and fuse to form the top margin (dorsal aspect) of the neural tube. If this process is incomplete, then the spinal cord remains open and exposed along the embryo’s back, as the vertebral bones fail to surround the spinal cord tissue completely. This condition is referred to as spina bifida. Often, rather than simply being exposed, some normal contents of the vertebral canal, including spinal cord tissue, protrude out of the back as a bulge. Spina bifida is most common in the lower lumbar and upper sacral regions of the spine, but more severe cases may involve the cervical and thoracic regions.


Depending on the level and extent of the defect, the clinical symptoms of spinal abnormalities range from mild impairment to fatality. The type of neural tube defect seen in spina bifida often causes some degree of motor and sensory handicap. The cerebrospinal fluid is continuous from the ventricles of the brain to the central canal of the spinal cord. If the spinal defect impairs the normal flow of cerebrospinal fluid, other problems may occur, such as retardation resulting from
hydrocephalus (fluid on the brain). Although there is still much to learn about the causes of spinal cord defects, in many cases scientific evidence points the finger at genetic problems (mutations) and the disruptive action of teratogens such as environmental pollutants and drugs.



Infections. Acquired spinal cord lesions are related to such conditions as tumor development and viral or bacterial infections. In general, invasion of the spinal cord by viruses or bacteria can produce inflammation known as myelitis.
Multiple sclerosis (MS) and ALS are the two most common nontraumatic disorders of the spinal cord. Many of the nerve fibers of the central nervous system are covered by a myelin sheath produced by neuroglia cells, known as oligodendrocytes. This sheath contributes to the speed and efficiency of the nerve cells as they carry electrical information. MS involves the destruction of this important myelin sheath, which leads to the disruption of motor and sensory nerve pathway functions, manifested by such symptoms as abnormal sensations, paralysis, and exaggerated reflexes. Although its cause is not clearly understood, researchers believe that viral infections are involved in some cases, while in others the individual’s own immune system might be mistakenly destroying normal myelin tissue (an autoimmune disorder). ALS is a fatal condition that is restricted to the loss of motor neurons. As with MS, there is much speculation regarding the causes of ALS. Acquired immunodeficiency syndrome (AIDS) is a viral infection that can involve the disruption of spinal cord neuron function.


Other infections that can cause spinal cord lesions include tabes dorsalis,
poliomyelitis, meningitis, and syringomyelia. Tabes dorsalis involves the degeneration of sensory neurons from the dorsal region of the spinal cord as a result of the invasion of the syphilis spirochete bacterium. The polio virus infects and kills spinal motor neurons in a disease called poliomyelitis; if the disease destroys the brain-stem neurons that control respiration and heart rate, then this condition is fatal. Meningitis is a bacterial inflammation of the layers of cells that cover the spinal cord (collectively referred to as meninges), producing high fever and sometimes inducing a comatose state that can lead to death.




Tumors and cysts
. Growths within the spinal cord can also disrupt normal spinal cord function. Syringomyelia is such a condition, in which fluid-filled cysts develop among the neurons of the spinal cord. Cancerous tumors are often the result of uncontrolled growth of the neuroglia cells, which can damage neurons and nerve fiber pathways.




Treatment and Therapy

Spinal cord defects, either congenital or hereditary, pose serious challenges for the medical community. Surgical intervention is the only option in mild cases of spina bifida; in severe cases, there is no effective treatment. The advent of intrauterine surgery prior to the birth of the baby for the correction of minor cases of spina bifida is a major step toward alleviating serious problems. It is believed that better prenatal care may reduce the risk of spinal cord defects. For example, consumption of the vitamin folic acid in pregnancy greatly reduces the incidence of spina bifida. Numerous other causative factors have been implicated in spinal cord defects, including alcoholism, drug use, and even environmental pollution. In some cases, genetic screening may provide a method to reduce certain types of defects, while in other cases reduced exposure to risk elements is the most effective preventive action.


Treatments for acquired spinal cord injury involve antiviral and antibacterial drugs that combat infection and, in so doing, reduce inflammation and cell damage. It is clear that early detection and intervention is an important factor in being able to save as many neurons as possible and limit the extent of the lesion. Neurotrophic factors are likely to be important therapeutic agents as doctors try to stimulate the maximum recovery of neuronal function. In cases in which the immune system itself may be damaging healthy neurons, as is suspected in some cases of MS, drugs are used to suppress immune function.




Perspective and Prospects

Medical researchers are taking numerous approaches to understanding spinal cord development and function in the hope of utilizing that information to develop new therapies to prevent or treat these clinical conditions. One interesting aspect of the problem is that, unlike most other organ systems, the adult
nervous system appears to retain only a few selected stem cell populations after embryonic development. Stem cell populations are groups of cells that divide to produce cells for the growth and regeneration of tissues and organs.


It was previously believed that human babies were born with all the neurons in their central nervous system that they would ever have, meaning that no new neurons would be produced. Recent work in rodents and nonhuman primates, however, has unequivocally demonstrated that neural stem cells exist in the adult mammalian brain and give rise to millions of new neurons during an individual’s life span. This process generates new neurons predominantly in two areas of the brain—the olfactory bulb, which controls the sense of smell, and the hippocampus, a memory center—but not to any appreciable extent in other brain areas. Scientists are beginning to identify stem cells in other brain regions, but there appear to be only a few, and those lack the ability to repair spinal cord injuries. Many laboratories are working on harnessing the potential of stem cells for cell replacement therapies, which hold significant promise for brain repair. As an individual ages, the nervous system becomes more efficient in processing information as neural networks are modified. This modification involves changes in nerve cell connections (plasticity) and new neuron generation (neurogenesis), but only in a few areas of the adult brain. Researchers hope to utilize information about the biological basis of normal plasticity to help repair damaged or impaired nervous systems.


Modern neuroscience research quickly vanquished the long-held belief that it is impossible to repair neurons damaged by trauma or disease. Experiments with animals and in tissue culture have demonstrated that damaged neurons can survive, regrow nerve processes, and once again carry electrical impulses. In fact, neurons from human spinal cords have been grown in tissue culture under conditions that stimulated them to regrow their axonal process. One of the most important aspects of understanding nervous system development is the fact that the cells communicate with one another not only with neurotransmitters but also with neurotrophic factors. Basic research and clinical trials are being done on neurotrophic factors with the expectation that they will become important parts of therapeutic treatments to stimulate the repair and regeneration of damaged neurons. These neurotrophic factors hold such promise because they are important in stimulating normal cell differentiation during embryonic development and for the subsequent survival of neurons after birth into adulthood. Therefore, clinical treatments are being designed to recreate the embryonic conditions that contributed to normal development. In addition, it is believed that one of the major factors in the lack of a regeneration response in damaged spinal cords is that the neuroglia cells, known as astrocytes, form scar tissue that is not conducive to nerve fiber regeneration. Therefore, medical researchers are looking at treatments that, in addition to prolonging the life of neurons, reduce the formation of scar tissue.




Bibliography


Carey, Joseph, ed. Brain Facts: A Primer on the Brain and Nervous System. 6th ed. Washington, D.C.: Society for Neuroscience, 2008.



Carlson, Bruce M. Human Embryology and Developmental Biology. 4th ed. Philadelphia: Mosby/Elsevier, 2009.



Kandel, Eric R., James H. Schwartz, and Thomas M. Jessell, eds. Principles of Neural Science. 5th ed. Norwalk, Conn.: Appleton and Lange, 2006.



Larsen, William J. Human Embryology. Edited by Lawrence S. Sherman, S. Steven Potter, and William J. Scott. 3d ed. New York: Churchill Livingstone, 2001.



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



National Institute of Neurological Disorders and Stroke. http://www.ninds.nih.gov.



Nicholls, John G., A. Robert Martin, and Bruce G. Wallace. From Neuron to Brain. 5th ed. Sunderland, Mass.: Sinauer, 2012.



Palmer, Sara, Kay Harris Kriegsman, and Jeffrey B. Palmer. Spinal Cord Injury: A Guide for Living. 2d ed. Baltimore: Johns Hopkins University Press, 2008.



Salter, Robert Bruce. Textbook of Disorders and Injuries of the Musculoskeletal System. 3d ed. Baltimore: Williams & Wilkins, 1999.



“Spinal Cord Diseases.” MedlinePlus, January 7, 2013.



“Spinal Cord Injuries.” MedlinePlus, May 9, 2013.

Define "bread line." During what time period were these common in America?

Bread lines were lines on which people waited to receive free bread, usually given out by a church or other religious institution or a charity. Bread lines and soup kitchens were common during the Great Depression, which started with the stock market crash of 1929 and lasted until about 1939. By 1933, one quarter of Americans were unemployed, and the federal government had not yet stepped in, as it would under Franklin D. Roosevelt starting in that year, to help provide jobs and money to Americans. People were largely reliant on private charities to dispense free food, such as on bread lines or in soup kitchens. Asking for public charity was a new experience for most Americans at that time, and one that many people found deeply shaming, though it was necessary. Many wanted jobs but could not find any. 

A man has $100 and decides to invest it in a bank for 6 years. The bank gives him two choices, annual rate of interest 2%, compounded annually,...

Since the bank is paying compound interest , we have to use the formula for compound interest for calculating the amount.


The formula is,


`A_t=P(1+r/n)^(nt)`  


where ,


`A_t`  is the amount at the end of t years of investment


P is the principal


r is the annual rate of interest, 


n is the number of compounding periods per year


Case 1


Given P=$100, t= 6 years , n=1 as interest is compounded annually, r=2%


Now plug in the given values in the formula to calculate the amount at the end of 6 years of investment,


So, `A_6=100(1+2/100)^6`


`A_6=100(1+1/50)^6`


`=100(51/50)^6`


`=100(1.02)^6`


`=112.6162419`


`~~112.62`


Case 2 


Given: P=$100 , r=1.8% , n=4 ( as interest is compounded quarterly ) , t=6 years


Now plug the given values in the formula to calculate the amount at the end of 6 years,


`A_6=100(1+1.8/(4*100))^(4*6)`


`=100(1.0045)^24`


`=111.3777874`


`~~111.38`


So the first option is better with annual rate of interest 2% compounded annually, as the amount received after 6 years of investment is more than the second option.

What does RNA stand for?

RNA stands for ribonucleic acid. It is a molecule that is linear in shape and is similar to DNA, which RNA is synthesized and created from. RNA differs from DNA in that RNA is single stranded. RNA also contains four different nucleotide bases. These bases consist of adenine, guanine, cytosine, and uracil. It is created from DNA by molecules known as RNA polymerases, and can come in three different types. These types are known as transfer RNA, messenger RNA, and ribosomal RNA, with each having a slightly different function in the cell. There is also snRNA (small nuclear RNA), but the other three are the primary types.


Following transcription, ribosomes in the cell use RNA to create proteins that are important for cellular function. This process, known as translation, is what regulates the amount and type of proteins being produced in the cell that are vital for cell survival.


Hope this helps!

Sunday, September 18, 2011

For most critics, Hamlet is, first and foremost, a revenge tragedy. How does this view ignore the philosophical aspects of the play?

To limit an assessment of Hamlet as a revenge tragedy is indeed short-sighted. Throughout the play, Hamlet struggles to understand himself and the meaning of life, thus a more thoughtful theme of existentialism emerges.  In his examination of life and death, Hamlet observes that man ultimately becomes food for worms, and he delivers this insight in a witty and punishing remark to Claudius to remind him of death's equalizing power.  Yet in the same act (Four), Hamlet considers the idea that God wouldn't give man profound intellect and powers if He didn't intend for man to make profound use of them.  Hamlet wonders what happens after death; the unknowable nature of the afterlife prevents him from killing Claudius when he catches him in prayer and stays his own hand when he contemplates suicide in the play's most famous "to be or not to be" soliloquy in Act Three.  

Saturday, September 17, 2011

What percentage of starch digestion occurs in mouth?

Altogether, about 5% of starch digestion happens in the mouth. However, it will vary a bit depending on how long you chew, how much moisture there is in the mouth, and how much moisture the starch can absorb.


The digestion of starch occurs due to the combined effects of chewing (mastication) and the enzyme, salivary amylase. This enzyme is produced by your salivary glands. It coats the food particles in your mouth, and breaks the bonds that link together the monomeric sugar units that make up a starch molecule. This chemical breakdown process is called starch hydrolysis; its end products are smaller sugar chains, including maltose, maltotriose, and dextrins. When you chew on a piece of whole grain bread, and find it becoming sweeter as you continue to chew, it's because you are converting starch into these sugars.


Hydrolysis depends on the presence of water, so food particles that absorb more water may get digested faster. Moreover, the more you chew the more saliva you produce. Thus, chewing is responsible for more than mechanical breakdown -- it also triggers the release of more amylase and water.


In one experiment (see last link below), researchers asked volunteers to chew mouthfuls of either bread or spaghetti. Then the researchers compared how much starch digestion had occurred before swallowing. The bread was broken down into smaller particles, and mixed with much larger amounts of saliva. And starch hydrolysis -- or the digestion of starch in the mouth -- was "twice as high for bread as for spaghetti."

What is a splenectomy?


Indications and Procedures


Splenectomy is often performed after trauma to the upper left abdominal cavity that results in injury to the spleen. When the spleen is damaged in such cases, life-threatening intra-abdominal hemorrhage may occur. Surgical repair of the damaged spleen is sometimes difficult, but the lack of a spleen has relatively few ill effects, as other organs such as the liver and tissues of the lymphatic system compensate for its absence. Therefore, splenectomy is usually the indicated treatment for damage to the spleen.



Patients undergoing splenectomy are first anesthetized by an anesthesiologist. Surgical assistants then prepare the patient by scrubbing the upper abdomen to rid the skin of pathogens. The surgeon than makes an incision in the upper left abdomen or along the midline of the abdomen. He or she will then expose the spleen and tie off blood vessels to the spleen with sutures. The surgeon then cuts the attachments that anchor the spleen in the abdomen and removes the organ. This procedure takes approximately one hour to complete, provided that there are no complications. Most patients are allowed to leave the hospital after about one week or less. Although surgical infections are rare, they may require the patient to remain hospitalized for a few more days.




Uses and Complications

Splenectomy is also performed to treat patients with certain types of anemia and hypersplenism. Since the normal function of the spleen is to destroy aged or nonfunctional red blood cells and platelets, overactivity of the spleen in hypersplenism results in excessive destruction of these blood cells and leads to anemia and blood-clotting disorders.


Even though splenectomy has few long-term adverse effects, some adult patients have a slightly increased risk of contracting infections. Splenectomy in children, however, results in greater susceptibility, particularly to pneumococcal pneumonia. Physicians often recommend that children who have undergone splenectomy be immunized against this bacterial pneumonia, and many of these patients even receive long-term prophylactic antibiotic therapy to prevent the disease.




Bibliography


Daller, John A. "Spleen Removal." MedlinePlus, January 29, 2013.



Griffith, H. Winter. Complete Guide to Symptoms, Illness, and Surgery. Rev. 6th ed. New York: Perigee, 2012.



Health Library. "Splenectomy." Health Library, September 10, 2012.



Hiatt, J. R., E. H. Phillips, L. Morgenstern, eds. Surgical Diseases of the Spleen. New York: Springer, 1997.



Kasper, Dennis L., et al., eds. Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw-Hill, 2005.



Mayo Clinic. "Splenectomy." Mayo Clinic, July 12, 2012.



Schwartz, Seymour I., James T. Adams, and Arthur W. Bauman. Splenectomy for Hematologic Disorders. Chicago: Year Book Medical, 1971.



Society of American Gastrointestinal and Endoscopic Surgeons. "Patient Information for Laparoscopic Spleen Removal (Splenectomy) from SAGES." SAGES: Society of American Gastrointestinal and Endoscopic Surgeons, 2013.



Wilkins, Bridget, and Dennis H. Wright. Illustrated Pathology of the Spleen. New York: Cambridge University Press, 2000.



Zollinger, Robert M., Jr., and Robert M. Zollinger, Sr. Zollinger’s Atlas of Surgical Operations. 9th ed. New York: McGraw-Hill, 2011.

What are hearing tests?

Indications and Procedures Hearing tests are done to establish the presence, type, and sever...