Do you consider Mr and Mrs Bennet to be good parents? Essay

I don't believe Mr or Mrs Bennet to be acceptable guardians. Jane Austen doesn't present them in an ideal light and I think any individual who peruses this novel would get the feeling that they are bad guardians. An obligation of fathers in the public eye in Austen’s day was to give monetarily to his kids so they have secure prospects. Be that as it may, Mr Bennet doesn't do this. He pays little idea to the girls’ fates and is by all accounts a man who doesn't generally consider anything genuinely. We know this since Austen lets us know, after Lydia had fled and Mr Bennet trusts himself in the obligation of Mr Gardiner, that Mr Bennet had regularly wanted that he had spared a yearly entirety for the â€Å"better arrangement of his kids, and of his wife† and that now he â€Å"wished it more than ever.† This gives us he is unthoughtful and settles on silly choices, which later on he laments. Mr Bennet doesn't pay attention to anything or converses with Mrs Bennet with deference or earnestness. This implies the young ladies don't experience childhood in an extremely cheerful or secure home. The parents’ marriage has not worked out positively and Mr Bennet just wedded Mrs Bennet by virtue of her â€Å"youth and great humour†. We learn of his absence of regard for her as he delineates for her, subsequent to hearing her grumble about her nerves, that he regards her nerves and says, ‘They are my old companions. I have heard you notice them with thought these twenty years at least’. He appreciates prodding his significant other and imagines that he hasn’t visited Bingley †just to see the stun on his wife’s face when he lets them know. He is in reality brutal to Mrs Bennet, as she doesn't comprehend his snide mind. This absence of comprehension is reflected in Lydia, who has grown up to accept that jokes, even brutal ones, are the best approach to carry on, gratitude to her father’s conduct and impact. In her letter recounting her elopement as she kept in touch with Mrs Forster, she sys that she will chuckle and ‘what a decent joke it will be’. A mother in Austen’s day ought to be liable for helping her girls discover spouses. This is by all accounts Mrs Bennet’s solid point yet she appears to let this target dominate. As opposed to thinking about their current state, she is continually contemplating the future and is set up to humiliate her young ladies so as to allow them to wed well. For instance, on page 27, Mrs Bennet makes Jane ride on a pony with the expectation that it may rain so she would turn out to be sick and ‘stay all night’ in Bingley’s house. Austen composes that Mrs Bennet was ‘delighted’ when a deluge began. This shows inconsideration, minimal nurturing love and that Mrs Bennet is fixated on Bingley wedding Jane. Jane could have been paid attention to sick. This doesn't show that Mrs Bennet is a decent parent. Another obligation of the mother was to raise her kids in a very much reared way. I will clarify in the accompanying sections how obviously Mrs Bennet doesn't do this. Mrs Bennet is a consideration searcher. This is appeared in her nonstop disappointed grumblings about her ‘poor nerves’. After Lydia has fled she tells anyone who will listen that she is ‘frightened out of my wit†¦such fits in my side, and agonies in my mind, and beatings on the most fundamental level that I can get no rest†¦Ã¢â‚¬â„¢ She likewise predicts her future in such a sad route as to pick up consideration †she says to the Gardiners that Mr Bennet will bite the dust in a battle with Wichkam and the Collinses will turn her out of her home. She feels frustrated about herself and states ‘but I was over-controlled, as I generally am’. This is coming about because of the absence of regard Mr Bennet shows her. We can see this reflected in Mary at the Netherfield ball, where she gets up to sing and play the piano. She is looking for consideration and is glad for her achievements, in spite of the fact that Austen reveals to us her voice is ‘weak’. At the Netherfield ball, Mrs Bennet humiliates Lizzy by talking boisterously close to Darcy about Jane and Bingley and the Lucases. When implored by Lizzy to quieten down, she answers, ‘I am certain we owe him (Darcy) no such specific consideration as to be obliged to state nothing that he dislike to hear’. In Austen’s day this conduct would have been totally unsuitable and looked on with scorn as Mrs Bennet shows sick rearing. This urges the young ladies to be tattles, uncouth and impolite. Mrs Bennet does nothing all through the novel to educate and train her five young ladies of how to carry on in the public arena, that is, aside from how to discover spouses. Mrs Bennet has brutal emotional episodes. At the point when she previously knew about Lydia’s elopement she was in ‘hysterics’ and whined of ‘tremblings†¦spasms in my side and torments in my head’ and said Mr Bennet would be executed and they would be turned out of their home. At the point when she heard that Lydia and Wickham were to be hitched, she quickly overlooked her agonies and distresses and told everybody ‘I knew how it would be’. Mrs Bennet likewise doesn't show appreciation †a terrible effect on her girls. When evidently Mr Gardiner pays Wickham to wed Lydia, she says that ‘who else ought to do it yet her own uncle’. This quality is reflected in Lydia, who is never appreciative for anything. We can likewise take a gander at the manner in which the parent treat their little girls legitimately, just as unpretentiously impacting them. The two guardians show partiality. Mr Bennet to Lizzy as a result of her sense and mind, Mrs Bennet to Lydia for being such as herself, and furthermore to Jane for her excellence. Mr Bennet additionally affronts his kids, rather than delicately putting them on the correct way. He discloses to them they are ‘silly’, particularly Lydia and Kitty †‘you must be two of the silliest young ladies in the country’. Mr Bennet doesn't appear to attempt all at being a decent dad. He disregards every one of his youngsters however Lizzy. Mrs Bennet doesn't appear to possess energy for her girls with the exception of Lydia and Jane. We can likewise take a gander at the Mr Bennet’s response to Lydia escaping with Wickham. He censures himself for he let Lydia go to Brighton in spite of the fact that Lizzy cautioned him against it. Indeed, even in his blame, Mr Bennet is snide by advising Lizzy to permit him to feel remorseful for once and afterward says, ‘I am not terrified of being overwhelmed by the impression. It will die soon enough’. At that point he reveals to Kitty that she can't leave the house until she has demonstrated herself to be reasonable †and Kitty blasts unto tears at this. Beforehand, I have taken a gander at what the Bennet guardians resemble to perceive how great guardians they are, however on the off chance that we take a gander at the Bennet sisters, we can perceive how they have been raised, and the parents’ characteristics will reflect in the girls. Lydia is a tease, has no mindfulness and is extremely youthful. We see this in the manner she argues to go to Brighton so she can blend in with the officials there. At the point when she is welcomed, Austen lets us know in her creative mind, Lydia sees herself â€Å"seated underneath a tent, softly playing with in any event six officials all at once†. Mrs Bennet supports Lydia by advising her of her own youth teases †â€Å"I sobbed for two days when Colonel Millar’s regiment left. I figured I ought to have broke my heart!† In Austen’s day being a tease would have been viewed as inadmissible conduct. Also, Lydia is fifteen, which is a lot to youthful to go to Brighton with the officials and this is demonstrated by her juvenile elopement. Kitty has an exceptionally frail character coming about because of an absence of instructing and control from the Bennet guardians. We see this in the manner she continually follows and duplicates Lydia. She backs her up when contending about going to Brighton, and just when she is totally isolated from Lydia does she improve. Austen lets us know †â€Å"removed from the impact of Lydia’s model, she became, by appropriate consideration and the board, less fractious, less oblivious, and less insipid†. Just two out of the five young ladies are actually an a good representative for Mr and Mrs Bennet †Jane and Lizzy. Jane is exceptionally mindful and consistently observes the best in individuals. In any event, when she knows Wickham’s genuine character she alludes to him as â€Å"Poor Wickham!† Towards the center of the novel, Lizzy is starting to see her family in a similar light as untouchables would and gets mindful of their numerous failings. She additionally grows progressively mindfulness, which her folks didn't educate her. Lizzy shows one of her father’s qualities †her diversion. Lizzy makes a joke out of the hurt Darcy brought about by ‘slighting her’. Austen composes, ‘she had an enthusiastic, fun loving attitude, which thoroughly enjoyed anything ridiculous’. This is appeared in her dad at the Netherfield ball, where Mr Collins humiliates the family and Austen composes, ‘no one looked more interested than Mr Bennet himself’. To finish up, from Austen’s utilization of language and the impression she gives, I trust Mr and Mrs Bennet are bad guardians.

Comparing Language and Identity in Pygmalion and Educating Rita :: comparison compare contrast essays

Pygmalion and Educating Rita:â Language and Identityâ â â â â â â â This exposition depends on the perusing of two scholarly plays, George Bernard Shaw’s Pygmalion and Willy Russell’s Educating Rita. Language and character are two articulations that should be clarified. English is the official language in a few nations; Chinese is the language verbally expressed by Chinese individuals and Danish is the manner by which Danes talk. Be that as it may, dialects could likewise be portrayed as various methods of talking because of social foundation, instruction, calling, age and sex. A person’s language is associated with his social circumstance. Eliza, the cockney bloom young lady from the canal doesn't communicate in a similar language as teacher Higgins, regardless of whether English is their normal primary language. They talk distinctively on the grounds that they have a place with various social universes. Personality can imply the exceptional trait of an individual, something that causes him to vary from others. Training AND IDENTITY CHANGES Eliza and Rita, the chief characters of the two plays are the two objects of personality change over the span of the accounts. Are these progressions indistinguishable or would we be able to discover contrasts? The two young ladies initially originate from mentally poor circles. Eliza is a youthful bloom young lady who communicates in a canal language. She talks in the accompanying manner: Aint no call to intrude with me, he aint. (1) Her habits are rough, and her cockney emphasize leaves her inclination as though she is a peasant. She is dealt with that way. In any case, she is by all accounts pleased with herself, I’m a decent young lady, I am. (2) Rita is a twenty-six-year-old, reckless, hearty beautician, wedded to a Liverpudlian beerdrinker who requests her to have kids and to be a decent spouse. She feels unsatisfied with her marriage. At the hairdressing salon where she works, she becomes weary of the every day tuning in to ladies who ramble without saying any significant. They never tell y’things that issue. (3) The narrative of the two plays tells how the instruction of the ladies transforms them. There are wonderful advances in their examinations and the outcome is a conspicuous difference in their lives. Inner AND EXTERNAL CHANGES I would figure that numerous perusers and observers of the two plays view them as about a similar story. Actually, they are most certainly not. There is in any event one significant distinction. The progressions are not the equivalent. One of them is outer while the other is inside.

Big Questions and Small Scientists

Big Questions and Small Scientists I was five years old the first time someone accused me of witchcraft. I was taking a bath (not really sure why this detail sticks in mind) and it was close to Halloween: my birthday. My little sister poked her head in. Lisa: Anna, does being born on Halloween mean that youre a witch? Me [exhibiting how to irresponsibly wield ones older sibling powers]: Yes. Lisa: REALLY? Me: Yes. Lisa: Woah! The second time someone accused me of witchcraft, I was a sophomore in High School, tutoring a seven-year-old a short bus ride away. One day, while I was explaining how to add double-digit numbers, she interrupted to ask whether I was Hermione Granger, from Harry Potter. Flattered, I tried to imagine that it was because of my towering intellect and spirit, and not the combination of bushy brown hair and big front teeth. The third time was a little more peculiar. I was getting a tuberculosis skin test, which I needed in order to start volunteering at a local hospital. Nurse: Birth date? Me: 31 October, 1992. Nurse: WOAH! Youre a HALLOWEEN BABY! Me: yep. Nurse: I KNEW you looked like a witch! Me: .. The fourth time was a couple of weeks ago, at the elementary school where I volunteer on Tuesday afternoons. My partner and I were supposed to teach a group of kids (ages 6-8ish) about gases and liquids, using Alka Seltzer. I was disappointed by the first step in the lesson plan it said to drop the tablets in the water, and watch them fizz, which I thought would go down in history as The Most Boring Demonstration Ever. Fire is  cool. Rockets are cool. Kids dont want to see fizzing water. They can drink soda for that. Feeling a little guilty for bringing such a lame demonstration,  I filled up a film canister at the sink, and carried it over to the table. Silence fell as the tablet plopped into the water. The fizzing began, and so did the chaos. I thought someone had broken a leg, because the kids started  screaming.  They grabbed my arms, and screamed. They leaned into my ears, and screamed. They jumped up and down and grabbed each other and tried to climb on the table. They hollared and howled and flapped their arms, screaming:  ITS EXPLODING!!!!!!!!!!!!! I glanced down. Foam bubbled feebly over the sides of the canister and formed a little puddle on the table. The kids continued to celebrate as though a rocket had been launched. ITS EXPLODING!!!!! I was stunned. One kid sidled up next to me, and gazed up in awe through big round glasses. Are you he began. Are youare you a wizard? Have you ever had a conversation with a child? If you havent, go find one. He or she will remind you how exciting the world can be, when youre curious about everything and can see the magic in fizzing Alka Seltzer. In High School, I tutored and babysat a second grader who told me that he was going to become king of the planet, so that he could force everyone to recycle. To encourage him do his math homework, we pretended that his pencil was a rocket and the pencil sharpener a refuelling station: when he did enough problems to run out of lead, he could navigate the pencil over to the sharpener, which I held high up in orbit. This kid also drew detailed diagrams of helicopters and told me that he was going to build robots a thousand kilometers wide. He had a beautiful imagination. On Sundays, I volunteer on a pediatrics floor for infants and toddlers (what I needed that TB skin test for.) I disinfect toys and deliver movies and games to rooms, but more than anything I love playing with the kids. These kids are not extraordinary. Whats extraordinary is that they manage to remain so ordinary. Ive seen a baby giggling and babbling (as babies do) with my pinky in a vice grip while being fed through a tube up her nose. Ive seen a girl toddle into the playroom, and sit down at the table to paint some flowers while connected to an enormous trolley of tubes and bags of liquid, which she wheeled in and parked next to her seat.  One little boy cooked me an eight-course meal at the plastic stove; when I asked for dessert, he handed me a toy shark, and explained that the shark ate some Reeses pieces, which were now in its stomach: by eating the shark I could eat the Reeses too. Another boy  grabbed my ID badge, and held it up to his ear, looking very serious. Hello? he said, into the ID badge. Hello? Yes. Yes, thank you. Thank you. Good bye. He hung up, and the ID-badge-phone flopped back against my chest. I had a fight with another kid over which of us was actually Iron Man. He won. These kids at the hospital manage to remain as sparkly and creative as those at the elementary school, and the little boy I used to tutor. They remain children: they still see the world as a place where Iron Man exists and Alka Seltzer is magic and ID badges are phones and pencils are rocket ships. Theyre sick and exhausted but they still want to get up and run around and play pretend and have adventures. I find that inspiring. Has a child ever asked you a question? If not, maybe youre unfamiliar with the fact that little kids ask wonderful questions that they, in Neil deGrasse Tysons words (quoted recently by Emad), are born scientists. The Cambridge Science Festival runs an annual Curiosity Challenge, which accepts submissions from children who have some questions about how the world works. A woman who helps organize the festival (an MIT alum!) showed me the results while I chatted with her about volunteering opportunities, and I knew from Page 1 that I had to have that book. She let me keep it. Pictures of some (of the many!) submissions are below I would post all of them, but Im pretty sure that would break the Internet. How does your brain use your eyebrows? How many cells are in a panda? I am curious about TVs. Are there little people inside when youre watching?   I wonder why junk food is made if it is unhealthy? Arent these magical?

Spanish Verbs of Happening

Spanish has at least three verbs that can mean to happen, and all three of them — pasar, ocurrir and suceder — are fairly common. Although pasar is the most common and can be used in both formal and informal contexts, many times the three verbs are interchangeable. Pasar Uses and Examples As indicated in the lesson on pasar, pasar has a variety of meanings, including to pass in various senses. Here are some examples of where it can be translated as to happen:  ¿Quà © ha pasado con el robo de datos en PlayStation Network? What has happened with the data theft on the PlayStation network?Lo que pasà ³, pasà ³. What happened, happened.Yo no sà © lo que me pasà ³. I dont know what happened to me.Tememos lo que pasarà ¡ a nuestro alrededor. We fear what will be happening to our vicinity.Es el lugar donde nunca pasa en tiempo. Its the place where nothing happens on time. OcurrirUses and Examples Ocurrir is a cognate of the English to occur and has much the same meaning, although the synonym to happen is a more common translation. Some examples: Esto nunca ocurrirà ¡. This will never happen.Espero que ocurra lo que les dice el horà ³scopo de hoy. I hope what todays horoscope is telling you happens. ¿Quà © ocurrià ³ en el accidente del Challenger? What happened in the Challenger accident?Lo mejor que puede ocurrir es que tengo mi dà ­a en corte. The best that can happen is that I have my day in court.Me ocurrià ³ un problema similar. A similar problem happened to me. SucederUses and Examples Suceder also is often used to mean to happen. Note that while suceder is related to the English verb to succeed, it never has the meaning of to have success, although it can mean succeed in the sense of to take the place of as in suceder al trono, to succeed to the throne. Here are some examples of where it means happen: It Happened One Night es conocida en castellano como Sucedià ³ una noche. It Happened One Night is known in Spanish as Sucedià ³ una noche.No debo pensar que a mi nunca me sucederà ¡ algo malo. I shouldnt think that nothing bad will ever happen to me.Hay diez cosas que seguro que nos sucedieron a todos. There are 10 things Im sure have happened to all of us. ¿Quà © sucede con Fernando? Whats happening with Fernando?En el camino de la vida, muchas cosas suceden. On the road of life, many things happen. Etymology Pasar comes from the Latin verb passare, to pass. Occurir is from the Latin occurrere, to occur. In addition to the meaning of to happen, in the reflexive form ocurrirse can, like occur, also mean to bring to mind: Nunca se me ocurrià ³ que iba a ser actor. It never occurred to me that I was going to become an actor. Suceder comes from the Latin succedere, to follow or to take the place of. Suceder has come to mean to happen in the same way that English speakers give the same meaning to to take place. The shift in English of succeed to mean having success occurred after the verbs meaning was established in Spanish.

Depression as a Physiological Disorder Essay - 1376 Words

Depression as a Physiological Disorder When researching the above statement, I have taken into account what I consider to be some of the main physiological and biological arguments regarding depression as a physical illness, as well as several psychodynamic and behavioural theories in order to attempt to compare the two and result in understanding how true the above statement is. When looking at the physiological view, it can be useful to look at the biological explanation that depression is caused by a disturbance of hormones and brain chemistry. The Endocrine system can seriously affect the behaviours of a person. This system produces hormones that have an effect on many behaviours such as†¦show more content†¦When contemplating the above idea, it would be exceedingly difficult to understand why depression is more frequent during periods of great hormonal change such as menstruation and childbirth, if hormones did not affect the onset of depression. Although there is a great deal of research to support this, it is difficult to prove as often during times like this, there is also social change occurring (pregnancy etc,). The levels of Cortisol that have recently been mentioned are seen by some researchers to have a great effect on depression and mood. Barlow and Durand (1995) discovered that levels of Cortisol seem to be lower in that of depressed patients in comparison to ‘normal’ people. Carroll et al (1980) also looked into this and found that by using dexamethasone to suppress Cortisol, the amount present in an individual could be measured. It was found that in ‘normals’ about 50% would be suppressed, however in those people suffering from depression, very little suppression was shown. This could indicate that the level of Cortisol could be causing depression, it could however be that the high level of Cortisol is the result of the depression rather than the cause. 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Molecular Mechanisms, Symptoms and Treatment of Cystic Fibrosis Free Essays

string(27) " a problem in CF patients\." Abstract Cystic fibrosis (CF) is a genetic disease that causes a dysfunctional cystic fibrosis transmembrane conductance regulator protein (CFTR) to be produced. This essay firstly will focus on the mutations of this defective protein and the intracellular effects. It will then consider the symptoms of the disease that can be observed including pulmonary, gastrointestinal, endocrine and reproductive problems. We will write a custom essay sample on Molecular Mechanisms, Symptoms and Treatment of Cystic Fibrosis or any similar topic only for you Order Now Then focus will be on the current treatment methods which target the consequences of the CFTR dysfunction such as phlegm retention and infection and the new treatment methods which treat the underlying CFTR defect such as targeting the trafficking of the protein. Introduction Cystic fibrosis is an autosomal recessive inherited disease caused by a gene defect on chromosome seven that is responsible for the cystic fibrosis transmembrane conductance regulator protein (CFTR). This is found in the apical plasma membrane of epithelial cells in the lungs, sweat glands, pancreas amongst other tissues. This causes dysfunctional CFTR to be produced leading to a thick sticky mucus causing a recurrent cough, frequent lung infections by bacteria such as Psuedomonas aeruginosa and digestive problems. More than 1,500 mutations have been found including DF508 which is the most common, caused by a deletion of phenylalanine. The mutant allele was first isolated in 1989 and since then life expectancy has improved greatly to between 31 and 37 years old and is still increasing today. Numerous mutations have been identified which are classed differently (class I – VI) depending on how the dysfunctional protein is handled within the cell. Molecular Mechanisms Cystic fibrosis is an autosomal recessive disease which means both parents must be heterozygous carriers of the CF allele in order for the offspring to have a 25% chance of inheriting the disease, or 50% of being a carrier (figure 1). There are over 1,500 observed mutations of the CFTR protein but the majority of these are rare. The most common mutation is caused by a deletion of phenyl-alanine in position 508 (DF508) which accounts for 66% of CF cases.[1] The CF mutations are grouped into 6 classes depending on their functional consequences within the cell (table 1)[2]and the DF508 belongs to class II. Classes I III are more common and often have associated pancreatic insufficiency though class IV-VI are more rare and these patients are normally pancreatic sufficient.[1] The DF508 for example produces a misfolded CFTR and is recognised within the cell endoplasmic reticulum as an abnormal protein, leading to it being proteolytically degraded in the proteasome. This results in only small amounts of CFTR reaching the plasma membrane but this has a short half life leading to an insufficiency of chloride transport. The misfolded CFTR leads to a protein trafficking problem, hence new drugs that aim to rescue the protein from ER degradation could be therapeutic strategies to re-develop intracellular protein movement.[2] Since different mutations lead to different problems with the CTFR protein, certain treatment strategies may only work on a small proportion of patients. Table 1: Different classes of CFTR mutations and the effects of each intracellularly – adapted from O’Sullivan, B.P. Freedman, S.D. (2009) Cystic Fibrosis. Lancet 373: 1891-904 There are several hypotheses as to how this CFTR mutation causes the disease known as cystic fibrosis. The first is the low-volume hypothesis. The loss of inhibition of sodium channels causes excess sodium and water reabsorption causing dehydration of airway surface materials and lack of a compensatory mechanism. This lower water volume causes inhibition of normal ciliary and cough clearance of the mucus and plaques form that harbour bacteria. Secondly, the salt hypothesis believes excess sodium and chloride are retained in airway surface liquid and the increased concentration of chloride disrupts the innate antibiotic molecules so bacteria persist. Thirdly, it is hypothesised disease is due to the dysregulation of host inflammatory response which is backed up by the abnormally high concentration of inflammatory mediators found in children as young as 4 weeks who appear disease free. Finally, the increased presence of asialo-GM1 receptors in apical membranes allow increased binding o f P. aeruginosa and S. aureus without the rapid self-limiting innate immune response since in normal patients it is believed the binding of bacteria to functioning CFTR generates an innate immune response which would not function in CF patients. This is made worse by the combination of increased bacterial binding. The CFTR gene defect causes absent or malfunctioning CTFR protein causing abnormal chloride conductance on apical membrane of epithelial cells in the lungs. [1] CFTR belongs to a family of transmembrane proteins called adenosine triphosphate binding cassette transporters and is a chloride channel.[2] It also has several other functions such as inhibition of sodium transport through sodium channels in the epithelium, regulation of ATP channels, regulation of intracellular vesicle transport, acidification of intracellular organelles and inhibition of endogenous calcium activated chloride channels. In the lungs, this dysfunctional CFTR causes airway surface liquid depletion leading to decreased ciliary stability and ciliary collapse with decreased mucociliary transport causing phlegm retention, infection and inflammation of the airways. Increased cAMP levels leads to phosphorylation of CFTR causing chloride transport but since this is not functioning in CF patients the chloride channel fails to open and respond to cAMP (a second messenger). This causes a decreased secretion of Cl? into the lumen airway so excessive water and sodium is absorbed. This cannot cross the epithelial membrane due to the osmotic gradient created leading to increased viscosity of mucus. Local mediators that are secreted onto airway surface liquid help regulate the surface liquid volume as they induce CFTR dependent and independent chloride secretion. The alternative chloride channel mediates chloride secretion since the P2Y receptor is activated by ATP in both CF and non CF epithelium which is triggered by movement. Respiratory syncytical viruses that may infect the airways have increased ATPase activity so more ATP is broken down; the loss of this compensatory mechanism that would activate the alternative chloride channel has a negative effect on airway clearance becoming a problem in CF patients. You read "Molecular Mechanisms, Symptoms and Treatment of Cystic Fibrosis" in category "Essay examples" Symptoms Cystic fibrosis can be diagnosed at different stages of a child’s life; newborn testing occurs as standard since all babies are tested by a heel-prick blood sample as part of the Guthrie test and antenatal testing is carried out on women considered to be high risk of having a child with CF. Carrier testing is a mouthwash test to establish if each parent is a carrier and a genetic test via a swab on the inside of the cheek probes for 40 of the most common CF mutations which correctly diagnoses 90% of cases. One further test is to test the sweat on the skin of babies or children since patients with CF have a high salt concentration in the sweat and CF can be diagnosed if the salt concentration is above 60 mmol/L – this is because CFTR resorbes chlorine into cells of sweat glands and if this is dysfunctional this cannot occur. General symptoms that lead to a diagnosis include a family history, salty-skin, clubbing of the toes and fingers, a cough with sputum production, mucoid Pseudomonas aeruginosa isolated – repeated chest infections, diarrhoea and poor weight gain. The further symptoms can be grouped into the organ they affect from pulmonary to gastrointestinal, digestive system, endocrine and reproductive symptoms. Pulmonary symptoms are perhaps the most obvious and commonly associated with the disease. A thick secretion of high levels of mucus into the lungs occurs which leads to frequent bronchial infections and a recurrent cough. Pseudomonas aeruginosa and Staphylococcus aureus are the most commonly isolated bacteria and can be found at high affinities in CF lungs. It is the failure of the mucosal defence system to clear these organisms that is the issue. Early studies suggested P. aeruginosa binds to CF epithelial cells at higher density than normal individuals due to more asialo-GM1 receptors in CF patients, however other theories hypothesised CFTR itself is a receptor for the bacteria that mediates intracellular uptake of the bacteria and killing of it that would be absent in patients with defective CFTR protein. Current studies however suggest the bacteria are present on the mucus layer on respiratory epithelial cells rather than the cell membranes making it unlikely this is the case. It was hypothesised salt-sensitive cationic antimicrobial peptides called defensins could not function in CF patients if the luminal side of the epithelium has an increased sodium chloride concentration. This seems unlikely though as not all defensins are salt sensitive. It is now thought dehydration of the airway surface liquid impairs cilia functioning and mucociliary clearance so inhaled bacteria colonise. Furthermore CF sputum has below normal oxygen levels that switch P. aeruginosa from non-mucoid to mucoid form that is resistant to host defences.[3] â€Å"The persistence of chronic P. aeruginosa infections in cystic fibrosis patients is due to biofilm growing mucoid strains.† [4] These biofilms exhibit increased tolerance to antibiotics and resist phagocytosis as well as parts of the innate and adaptive immune system. This leads to complex-mediated chronic inflammation which can cause lung damage. The bacteria are also so persistent as the mutate and have low metabolic ra tes and increased doubling times.[5] In the gastrointestinal tract, several problems occur throughout life. At the newborn stage, some babies may need an operation to remove mucus that is obstructing the bowel – a condition known as meconium ileus. Pancreatic insufficiency is also seen causing symptoms such as greasy stools, flatulence, abdominal bloating, poor weight gain and fat soluble vitamin deficiency with malnutrition. Since it is hard to digest food, malnutrition can occur which causes poor growth, physical weakness and delayed puberty. This requires a pancreatic enzyme therapy with high calorie intake to manage. Older patients’ may develop an intestinal obstruction and the lack of absorption of vitamins A, D, E and K can lead to conditions such as anaemia, neuropathy and osteoporosis. The endocrine system can sometimes be affected in later life due to obstruction of the pancreatic ducts due to thickened secretions. As pancreatic disease develops the proportion of islet cells declines leading to a lack of insulin production where the blood sugar cannot be controlled which is then diagnosed as CF related diabetes mellitus, with symptoms such as constant thirst, hunger, weight loss and urination, however CF diabetes is not the same as type 1 and 2 diabetes. The reproductive system in women patients does not seem to be affected and they still produce healthy eggs, in men however the sperm ducts are blocked leading to male infertility. Some other symptoms include frequent sinusitis and hay fever that requires nasal spray or antibiotics and adults may develop nasal polyps. Incontinence can sometimes develop and in some patients bile ducts in the liver become blocked by mucus and the patient may require a liver transplant. Treatment Current Treatment of cystic fibrosis currently focuses on the consequences of the CFTR dysfunction such as phlegm retention, infection and inflammation though new strategies target the underlying gene defect. Currently, physiotherapy is one main treatment strategy used in combination with other management techniques. The thick sticky mucus secretions that block the airway in CF patients causing infections and coughing can be dislodged either by mechanical chest thumps or autogenic drainage and positive expiratory pressure. Physiotherapy is needed every day from between 15 and 50 minutes depending on the level of mucus present. Physical activity is also important as it prevents deterioration of the lungs and increases bulk and strength. Medication is used to treat cystic fibrosis such as lung medication including bronchiodilator drugs to open airways by relaxing the surrounding muscles, relieving tightness and shortening of breath and can be taken by being inhaled in nebulisers, taken orally or intravenously. Other medication includes antibiotics to treat persistent pulmonary infections, steroids to reduce inflammation of the airways and DNase to break down the mucus making it easier for the body to digest. Repeated pulmonary infections and thick mucus secretions can become so severe that the patient may need a lung transplant and possibly a heart or liver transplant also. Due to the nutritional problems associated with the disease, enzyme pills are taken with every meal and snack to replace pancreatic enzymes so more energy is gained from the food since there is a lack of digestive enzymes hence less nutrients can be absorbed from the food. These problems occur due to blocking of the small channels carrying digestive juices by mucus causing enzymes to build up in the pancreas that damages it over time. Nutritional supplements may also be given such as high energy drinks, and insulin may be necessary if the patient develops CF related diabetes mellitus. A suitable diet that is high in calories is also required to ensure adequate energy is gained. The lack of mineral absorption can lead to osteoporosis – weakening of the bones – which can be treated with bisphosphonates. Future There are a variety of new treatment possibilities targeting the underlying gene defect in the transmembrane receptor rather than downstream effects. Anti inflammatory drugs are one option due to persistent endobronchial inflammation in patients. The first main possibility is CF transmembrane regulator replacement therapy. This has already been tested using a variety of vectors such as adneoviruses, adeno-associated viruses and cationic lipids to transfect the functioning gene into epithelial cells. Some successful gene transfer has been seen into airway epithelial cells however it was short-lived CFTR expression and was hard to prove the link between improvement in CFTR function and clinical manifestations. The issue is it is yet unknown how much improvement in CTFR function is needed in order to make a big difference. The current research now focuses on the correct vector to use to minimise adverse effects and increase expression time – this is difficult as viral vectors hav e good transfection rates but more adverse effects and as multi dose therapy would be needed, virus-specific immune responses would devleop whereas liposomal vectors have less negative effects but worse transfection rates. [6] A second option being researched currently is CFTR pharmacotherapy involving drugs with affect intracellular trafficking of CFTR. This would not work for all patients due to the specific classes of mutations so it is of limited benefit. Class I mutations are stop mutations that decrease or eliminate production of CFTR. Aminoglycosides induce read through of premature stop codons so would produce a full length functioning CFTR protein, these can be topically applied and an improvement in CFTR functioning has been seen however the concentration needed is high and adverse effects mean they are not clinically suitable. An alternative to this includes PTC 124 – premature termination codon – which acts in a similar way but lacks toxicity. Class II mutations have misfolded CFTR and the trafficking of these is impaired due to proteosomic degradation; this CFTR does have chloride transport function however it is prematurely degraded and most does not reach the membrane. This giv es a new target – drugs which reduce degradation of the misfolded protein and increase trafficking to the membrane – and libraries of chemical agents are being screened for applicants. Class III mutations have a reduced probability of opening the CFTR channel but these are rarer. Compounds which activate CFTR would aid class III mutations such as VX770 (a potentiator) that is being used in trials for patients with the G551D mutation that could show improvements in function of the CFTR as well as reduced sweat chloride concentration. However effects in class II may also be seen if used in combination with a corrector compound that brings CFTR to the surface and then the potentiator can activate it. [7] Option three involves opening alternative chloride channels to compensate for the lack of function of the CFTR channel. CFTR is not the only chloride transport channel in a membrane, a calcium-dependent chloride channel also secretes chloride in epithelial cells and increasing the activity of this may be an option so enough chloride transport occurs in the cell. Two drugs have shown to have an ability to do this via the P2Y receptor. First of these is denufusol, which bypasses the defective channel and activates the alternative chloride transporter – â€Å"This activation results in an increase in airway surface epithelial hydration, and through these actions and effects on cilia beat frequency, increases mucociliary clearance†[8] and has been shown to be an early intervention strategy when inhaled. The second of these drugs is lacovutide (Moli990) increases intracellular calcium level and activates alternative chloride channels, it does not bind with receptors but inst ead interacts with phospholipids on the plasma membrane. The CFTR protein has several functions – chloride transport, inhibiting sodium transport as well as regulation of ATP channels. Inhibition of sodium absorption was hypothesised as a treatment option however amiloride (an epithelial sodium channel blocker with a short half life) was shown to have no clinical benefit and a tendency to decreased lung function. Studies on mice have shown when given as an early intervention the disease progression was prevented, however there is little evidence to show this in humans. An improvement may be seen in a blocker with a longer half life. Finally, airway surface liquid rehydration could improve the inadequate water content of the surface liquid by increasing the airway fluid layer with an inhaled osmotic agent. Hypertonic saline was found to have a positive effect on mucociliary transport and lung function due to induction of coughing and hydrating the mucus and new evidence has shown it also increased depth of the airway surface liquid. Inhaled powdered mannitol is an alternative. Effectiveness is limited to those with established lung disease but again, early intervention may prove more effective. [9] Conclusion Cystic fibrosis is a lifelong eventually fatal disease caused by a genetic defect in the CFTR protein. How this protein functions and which factor is responsible for all the symptoms seen in CF patients is not yet confirmed though it is clear the dehydration if airway surface liquid causing the thick mucus that is hard to dislodge and harbours biofilms of bacteria leading to frequent infection is a major factor. Current treatment strategies target the downstream effects of CF such as the phlegm retention and make the disease manageable. The new development of drugs targeting the underlying defect is occurring with some in clinical trials though the benefit to each patient is unknown. This is because of the diversity of mutations and varying symptoms within each patient making this a difficult disease to treat. References O’Sullivan, B.P. Freedman, S.D. (2009) Cystic Fibrosis. Lancet 373: 1891-904 Ratjen, F. (2009) Cystic Fibrosis: Pathogenesis and Future Treatment Strategies. Respiratory Care 54: 595-605 http://www.cftrust.org.uk/aboutcf/whatiscf/CF trust Kellerman D, Rossi Mospan A, Engels J, Schaberg A, Gorden J, Smiley L, Denufosol: a review of studies with inhaled P2Y(2) agonists that led to Phase 3.( Pulm Pharmacol Therapeutics. 2008 Aug;21(4):600-7. Epub 2007 Dec 31) Development, Inspire Pharmaceuticals, Inc., 4222 Emperor Blvd, Suite 200, Durham, NC, USA. [email protected] http://www.ncbi.nlm.nih.gov/pubmed/18276176 Hoiby N, Ciofu O, Bjarnsholt T, Pseudomonas aeruginosa biofilms in cystic fibrosis, (Future Microbiology 2010 Nov;5(11):1663-74) Department of Clinical Microbiology 9301, Rigshospitalet, University of Copenhagen, Juliane Maries Vej 22, Copenhagen, Denmark. [email protected] http://www.ncbi.nlm.nih.gov/pubmed/21133688 Stryer, Berg, Tymoczko, Biochemistry, 6th edition, Freeman Griffiths, Wessler, Lewonitin, Carroll, Introduction to Genetic Analysis, 9th edition, Freeman Pocock and Richards, Human Physiology, 3rd edition, Oxford Publishing How to cite Molecular Mechanisms, Symptoms and Treatment of Cystic Fibrosis, Essay examples

The mysteries of God and a Human Being

This discussion can be better started with a question that is related to the most important issues in theology and philosophy. Namely what are the mysteries of God and what is the place of a human being?Advertising We will write a custom essay sample on The mysteries of God and a Human Being specifically for you for only $16.05 $11/page Learn More Moreover, it is important to find out what famous philosophers and theologians such as Karl Rahner, Brian Swimme, Saint Augustine, and Bernard Lonergan can tell about these issues. This paper is aimed at discussing the works of these thinkers and their conception of God and an individual. Overall, these authors recognize the limits of human intelligence and cognition; therefore, the mysteries of God and the universe are not fully knowable. In his work The Universe is a Green Dragon Brian Swimme expresses very interesting ideas on God, the universe and a person. This author compares the universe to a green drago n or a creature that cannot be fully understood by a human being. God is the creator of the universe, but the language of this Supreme Being is not comprehensible to people. In turn, human beings strive to understand their place in the universe, but they cannot do it yet, even despite scientific and technological advances. Apart from that, people have to accept that they are only an infinitesimally small part of the universe. In turn, St. Augustine gives a slightly different of interpretation of God. In St. Augustine’s view, this Supreme Being is the paragon of goodness and perfection. The task of a person is to learn how to see this goodness in the things that he/she likes. These are the first steps that people should take in order to reach a higher moral level.Advertising Looking for essay on religion theology? Let's see if we can help you! Get your first paper with 15% OFF Learn More Brian Swimme emphasizes the cognition of a human being, while St. Augustine focuses on the person’s ability to recognize beauty and goodness. This is the main distinction between these theologians. A slightly different interpretation of God and human beings is offered by Karl Rahner in his book Foundations of Christian Faith. This theologian strives to reconcile the theory of evolution with the main tenets of Christianity. In Rahner’s view, one should not see the existence of nature and living beings just as a blind accident. This philosopher believes that lack of human understanding does not necessarily imply that the universe is driven by randomness. In his view, the idea of evolution and Christian faith are compatible with one another. In turn, one should mention Bernard Lonergan’s ideas and his views on theology. This philosopher strives to develop ways in which people can understand God and the universe. One of his arguments is that a person cannot understand God and universe individually. The intelligence of a separate person is capable of collecting and analyzing every piece of evidence regarding the laws of the universe. The author does argue that the mysteries of God are unknowable, but this task cannot be done by a single individual. On the whole, there are several ideas that Karl Rahner, Brian Swimme, Saint Augustine, and Bernard Lonergan might have supported. These philosophers may agree on the idea that the cognition of a human being is limited. Moreover, people have to recognize the limitations of their intelligence in order to understand the mysteries of God.Advertising We will write a custom essay sample on The mysteries of God and a Human Being specifically for you for only $16.05 $11/page Learn More Secondly, they can accept the premise that God is the creator of the universe, but people should learn to see the presence of this Supreme Being. These are the main issues that one can identify in their works. This essay on The mysteries of God and a Human Being was written and submitted by user Brayden Meadows to help you with your own studies. You are free to use it for research and reference purposes in order to write your own paper; however, you must cite it accordingly. You can donate your paper here.