Friday, July 31, 2020

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?

Friday, May 22, 2020

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.

Sunday, May 10, 2020

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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Wednesday, May 6, 2020

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

Wednesday, April 29, 2020

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.

Friday, March 20, 2020

Pope Urban Ii Essays - Crusades, Christianization, Invasions

Pope Urban Ii Essays - Crusades, Christianization, Invasions Pope Urban Ii Pope Urban II had called the Christians to join him in a Holy War to reclaim the Holy Lands as an act of Christianity, but there were many activities that took place that werent characteristics of Christianity. The Crusades were a smokescreen for Popes craving for power and control. The Crusades were the idea of Pope Urban II, a wise Frenchman. On November 18, 1095 AD, Pope Urban II opened the Council of Clermont. Nine days later, the Pope made a very important speech just outside the French city of Clermont-Ferrand. In his speech, he asked the people to help the Christians effort to restore peace to the East. The Crusades had originally been to help the Churches in the East, but the now it was to reclaim the Holy Land, especially Jerusalem from the Muslims. Pope Urban II stayed in France until September 1096 in hopes of providing leadership for the First Crusaders. Urban had originally hoped for the crusading army to be composed of mostly knights and other warriors, but his speech had already began spreading throughout the west, and many people of different social classes started joining the crusading army. (Foss, Michael. pg. 23) Because of this Urban lost all control of the army, which led to the slaughter of Jews in northern France. These poor people also caused strain on the armies supplies and discipline. They were never trained and they were poor, so they couldnt bring anything and were poorly disciplined(Foss, Michael. pg. 24). The entire crusading army had planned on reaching the city of Constantinople, but because of their lack of supplies and training the vast majority of them were slaughtered before they got there. The few troops that did reach Constantinople split up into two groups. One group tried to capture Nicaea, a key city that blocked the road of their supply routes. This group was unsuccessful. The other group was attacked near the city of Civetot in October. The few survivors retreated to Constantinople and joined the second wave of Crusaders. (Phillips, Jonathan. pg. 59) Religious beliefs were a major motive of the crusaders. In Urbans speech to the people of Clermont-Ferrand, Urban guaranteed the complete forgiveness of all sins to any crusader that lost his life in the name of the Crusades. Urban also proclaimed It is necessary that you bring to your brothers in the East the help so often promised and so urgently needed. They have been attacked, as many of you know, by Turks and Arabs... Churches have been destroyed and the countryside laid waste. If you do not make a stand against the enemy now, the

Wednesday, March 4, 2020

How to Add Resource Files in Delphi Executables

How to Add Resource Files in Delphi Executables Games and other types of applications which use multimedia files like sounds and animations must either distribute the extra multimedia files along with the application or embed the files within the executable. Rather than distribute separate files for your applications use, you can add the raw data to your application as a resource. You can then retrieve the data from your application when it is needed. This technique is generally more desirable because it can keep others from manipulating those add-in files. This article will show you how to embed (and use) sound files, video clips, animations and more generally any kind of binary files in a Delphi executable. For the most general purpose, youll see how to put an MP3 file inside a Delphi exe. Resource Files (.RES) In the Resource Files Made Easy article you were presented with several examples of the use of bitmaps, icons, and cursors from resources. As stated in that article we can use the Image Editor to create and edit resources that consist of such types of files. Now, when we are interested in storing various types of (binary) files inside a Delphi executable well have to deal with resource script files (.rc), the Borland Resource Compiler tool and other. Including several binary files in your executable consists of 5 steps: Create and/or collect all the files you wish to put in an exe.Create a resource script file (.rc) that describes those resources used by your application,Compile the resource script file (.rc) file to create a resource file (.res),Link the compiled resource file into the application’s executable file,Use individual resource element. The first step should be simple, simply decide what types of files you would like to store in your executable. For example, we will store two .wav songs, one .ani animations and one .mp3 song. Before we move on, here are a few important statements concerning limitations when working with resources: Loading and unloading resources is not a time-consuming operation. Resources are part of the applications executable file and are loaded at the same time the application runs.All the (free) memory can be used when loading/unloading resources. In other words, there are no limits on the number of resources loaded at the same time.Of course, resource files do double the size of an executable. If you want smaller executables, consider placing resources and parts of your project in a dynamic link library (DLL) or its more specialized variation. Lets now see how to create a file that describes resources. Creating a Resource Script File (.RC) A resource script file is a just a simple text file with the extension .rc that lists resources. The script file is in this format: ResName1 ResTYPE1 ResFileName1ResName2 ResTYPE2 ResFileName2...ResNameX ResTYPEX ResFileNameX... RexName specifies either a unique name or an integer value (ID) that identifies the resource. ResType describes the type of resource and the ResFileName is the full path and file name to the individual resource file. To create a new resource script file, simply do the following: Create a new text file in your projects directory.Rename it to AboutDelphi.rc. In the AboutDelphi.rc file, have the following lines: Clock WAVE c:\mysounds\projects\clock.wavMailBeep WAVE c:\windows\media\newmail.wavCool AVI cool.aviIntro RCDATA introsong.mp3 The script file simply defines resources. Following the given format the AboutDelphi.rc script lists two .wav files, one .avi animation, and one .mp3 song. All statements in a .rc file associate an identifying name, type and file name for a given resource. There are about a dozen predefined resource types. These include icons, bitmaps, cursors, animations, songs, etc. The RCDATA defines generic data resources. RCDATA let you include a raw data resource for an application. Raw data resources permit the inclusion of binary data directly in the executable file. For example, the RCDATA statement above names the application’s binary resource Intro and specifies the file introsong.mp3, which contains the song for that MP3 file. Note: make sure you have all the resources you list in your .rc file available. If the files are inside your projects directory you dont have to include the full file name. In my .rc file .wav songs are located *somewhere* on the disk and both the animation and MP3 song are located in the projects directory. Creating a Resource File (.RES) To use the resources defined in the resource script file, we must compile it to a .res file with the Borlands Resource Compiler. The resource compiler creates a new file based on the contents of the resource script file. This file usually has an .res extension. The Delphi linker will later reformat the .res file into a resource object file and then link it to the executable file of an application. The Borlands Resource Compiler command line tool is located in the Delphi Bin directory. The name is BRCC32.exe. Simply go to the command prompt and type brcc32 then press Enter. Since the Delphi\Bin directory is in your Path the Brcc32 compiler is invoked and displays the usage help (since it was called with no parameters). To compile the AboutDelphi.rc file to a .res file execute this command at the command prompt (in the projects directory): BRCC32 AboutDelphi.RC By default, when compiling resources, BRCC32 names the compiled resource (.RES) file with the base name of the .RC file and places it in the same directory as the .RC file. You can name the resource file anything you want, as long as it has the extension .RES and the filename without the extension is not the same as any unit or project filename. This is important because, by default, each Delphi project that compiles into an application has a resource file with the same name as the project file, but with the extension .RES. Its best to save the file to the same directory as your project file. Including (Linking/Embedding) Resources to Executables After the .RES file is linked to the executable file, the application can load its resources at run time as needed. To actually use the resource, youll have to make a few Windows API calls. In order to follow the article, youll need a new Delphi project with a blank form (the default new project). Of course add the {$R AboutDelphi.RES} directive to the main forms unit. Its finally time to see how to use resources in a Delphi application. As mentioned above, in order to use resources stored inside an exe file we have to deal with API. However, several methods can be found in the Delphi help files that are resource enabled. For example, take a look at the LoadFromResourceName method of a TBitmap object. This method extracts the specified bitmap resource and assigns it TBitmap object. This is *exactly* what LoadBitmap API call does. As always Delphi has improved an API function call to suit your needs better. Now, add the TMediaPlayer component to a form (name: MediaPlayer1) and add a TButton (Button2). Let the OnClick event look like: One minor *problem* is that the application creates an MP3 song on a user machine. You could add a code that deletes that file before the application is terminated. Extracting *. Of course, every other type of a binary file can be stored as a RCDATA type. The TRsourceStream is designed specially to help us extract such file from an executable. The possibilities are endless: HTML in an exe, EXE in exe, empty database in an exe, and so and so forth.