Deals with the Devil Essay Example for Free

Deals with the D malefic EssayThe goliath is portrayed in legion(predicate) ways and throughout many different types of literature, movies, and music. The most iconic image of the devil is a red beast with horns, a pointed tail, and a pitchfork in his hand. This famous image depicts an evil monster that is in the depths of hell where he rules everyplace the other evil beings of the world. This is only one image of many that you quite a little adjust in a vast amount of literature and media both past and presend. In The Devil and Tom Walker, the devil is described as a black woodsman, human in form nevertheless with red eyes. Similarly in The Devil and Daniel Webster, the Devil is described as a dark-dressed stranger, who is soft spoken but has an evil smile.In these descriptions you still get a sense of evil from the Devil but he is in human form. So what or who is the Devil? From early stories in Christianity, Lucifer commonly cognize as Satan or the Devil is origin ever y last(predicate)y an archangel created in the image of idol. He is the highest form of an angel, but challenges God and is cast down to rule the pits of hell. Can someone created in the image of God as Christianity suggests be a dark stranger or a red beast? The Devil can be depicted in many ways, but what the Devil really represents is the existence greed and moral depravity in society. Regardless of the imagery, the Devil plays a similar role throughout literature and media both past and present.One of the earliest stories of a man making a pact with the Devil is a character named Faust, from an old German legend. Faust was a brilliant scholar but always wanted more knowledge. The Devil comes to him one night and promises him infinite wisdom for a certain amount of time after which Fausts soul would be owned by the Devil. Faust quick agrees and signs a contract with the Devil. Faust lives with his infinite knowledge until the year comes when the Devil comes to collect his soul . Faust is then taken by the Devil and spends the rest of eternity in hell. This figment maybe one of the original stories of the Devil making a deal with a man for his soul. The Devil knows and uses the mans greatest desire to come-on him into signing a contract to get his soul. Man is easily corruptible when promised his deepest desire and choses instant gratification without fully understanding or thinking of the repercussions.In Anne Rices novel Memnoch the Devil, the Devil begins to stalk Lestate until one evening he appears to him and takes him on a voyage. Lestate is a very old and powerful Vampire, known to only look out himself and his own needs. The Devil takes Lestate to Heaven and Hell where he tells Lestate the story of the beginning of time when God created the world and human beings. Memnoch, or the Devil, spent a lot of time on Earth admiring Gods creation, but begins to notice the suffering and pain of human beings and the souls of deceased that argon stuck in bet ween Heaven and Earth. He describes God as uncaring of the evil in the world he created and begs God to do something to help the human being that are suffering on Earth and Sheol, which is the afterlife. Memnoch claims that he is not evil in fact he was an archangel created in Gods image, but because he questioned God several times about why he is letting humans suffer God gets angry.God casts him out of Heaven to find all the lost souls on earth and Sheol that he thinks deserves to be in the Kingdom of Heaven, before Memnoch can return. This turns out to be a daunting labour and he enlists Lestate to be his partner and adversary of God. This journey throws Lestate to question everything he has ever known about God and the Devil, sfor he has lived centuries and had dismissed such whimsey that Heaven and Hell exist. Lestate ends up running from the Devil and when he returns to Earth he steals a biblical artifact, Veronicas Veil, he reveals the artifact to the world. In the end it is revealed that the Devil was only using Lestate by allowing him to return with an artifact that would renew faith in God and therefore limit the amount of souls sent to Hell. In this story the Devil is manipulative and cunning though he claims he is not evil. Although Lestate never made a deal with the Devil, the Devil won by using Lestates narcissism for his own purposes.In the darkness of the Opera, a popular Broadway show, one can view the Devil as the office of the masked phantom in the opera house. The young understudy Christine hears a beautiful verbalise calling to her when she arrives at the opera house. She had heard stories of an Angel of music who could give her a more powerful and beautiful voice and readily begins to sing with the Devil. A series of mysterious accidents forces the lead singer to lose her voice therefore losing the star role in the opera. Christine is the given then given the lead role after her voice improves drastically while practicing with the Devil. The Angel of medicine takes Christine to the depths of the opera house tunnels against her will. Christine is in love with another man, who searches for her in the tunnels of the opera house.The Devil captures Christines love and tells her he will kill him if she doesnt repose with him. This story is similar to the short stories of The Devil and Tom Walker and The Devil and Daniel Webster, in that the characters make a deal with the Devil to improve some looking of their lives but when the Devil wants to collect on their deal none of the characters want to go willingly. One noticeable difference between the stories is that in the end of The Phantom of the Opera Christine shows kindness to the Angel of Music and he lets her go and he disappears forever leaving only his mask behind. Overall mankind has shown a ensample of making deals with the devil for their desires to their own detriment.From the short stories of, The Devil and Daniel Webster and The Devil and Tom Walker, to the legend of Faust, and the Phantom of the Opera musical you can see similarities in all the characters desiring something unattainable. The Devil then comes to them and promises to deliver their wishes for a small price, merely their souls for the rest of eternity. The Devil feeds on the lack of moral integrity and uses this to gain power over these characters souls. On the other hand, in Memnoch the Devil, Anne Rice changes the deal with the devil theme because Lestate never actually bargains with the devil, none the less the Devil gets what he desires. As you can see, literature and other mediums have adapted the story of making a pact with the Devil in many ways.Works CitedFaust. (n.d.). Retrieved 10 8, 2012, from Wikipeadia http//en.wikipedia.org/wiki/Faust Rice, A. (1995). Memnoch the Devil. Knopf.The Phantom of the Opera. (n.d.). Retrieved 10 8, 2012, from Wikipedia http//en.wikipedia.org/wiki/The_Phantom_of_the_Opera

Airline Reservation System Essay Example for Free

Airline Reservation System EssayAirlines search results are presented in an easy-to-use ground substance that displays a vast array of travel options for you. When customers prefer a specific travel itinerary, they offer the widest range of flight options and fares. Users privacy is very important to us at Arabian Travels. With that in mind, we have established and implemented information handling practices for that we believe are consistent with the highest standards and best practices of organizations doing business.SEA Airlines have watchful a detailed privacy policy because they believe users should know as much as possible about our practices so that they can make an sensible decision about the extent of our firm. 1. 2ABOUT THE PROJECT SEA Airlines is a site, which helps the flight travelers. Its mission is to offer flexible leisure travelers a quick and easy air to get better deals on airline tickets. Through partnerships with leading travel companies, it can negotiat e special prices that cant be found anywhere else. The working of the project is as follows. The first page provides several links.The Home link contains several informations about the site it provides a link to the login page. In the Login link a user have to login before ordering for tickets. An already registered user can simply type in -hisher valid username and password, and then click the Login button. But those visitors who are not registered have to go to the registration page before they login. In that page user have to enter First name, Last name, Address, Postal Code, City, holler number, Username and password. About Us Link contains some information regarding SEA Airlines and its developers.After registration user can reserve the seats in particular flights by using the flights date and time. The user can enter the number of seats required and the details of the passengers by specifying adult or child.

Using Kanamycin Resistance Bacteria Essay Example for Free

Using Kanamycin Resistance Bacteria EssayKanamycin is a common anti bacteriuml that interferes with bacterial growth, by inhibiting protein synthesis, and causing the mistranslation of mRNA. Kanamycin is commonly engaged in chicken feed to keep harmful bacteria from getting into the eggs and producing healthier chickens. Recently reports of unappeasable gastroenteritis nurture been linked to eating raw or undercooked eggs. This has led to the FDA to look for possible radicals of contamination. Scientists have now isolated bacteria from batches of eggs know to cause the illness, and they found that the bacteria ar resistant to kanamycin. The contaminated eggs were found to have come from three diverse chicken farms, Acme, full-grown ALs, and Cluckys chicken farm, that are geographic tout ensembley separate, and are in different states. The scientists also know that in that respect are three different genes responsible for kanamycin resistance, and that these different gene s graves for a certain enzyme that alters the kanamycin molecule differently. The enzymes are located between the inner and outer bacterial membranes, and act on the kanamycin after it passes through the outer membrane.The modification of the kanamycin molecule prevents it from being taken up by the inner membrane, preventing it from r from from each one oneing the ribosomes. Therefore if any bacteria fork over has one of the three genes for kanamycin resistance, than kanamycin wont prevent bacterial contamination (Hass C. , Woodward D. , and Ward A. , 2010. ). The purpose of this lab was to determine if there was a shared offset of contamination for the three chicken farms, and to make recommendations for gradations to prevent further outbreaks. The hypothesis is that all the chicken farms shared the same source of contamination.The guiding questions for the lab are what is the concentration of viable bacteria in the fender samples from the three chicken farms? And what is t he frequency of resistant bacteria in the original samples? Methods and Materials This lab is broken up into four different incisions. To begin part one of this lab you need to make sure that your lab area is stereotypic so that there is no contamination of the bacteria. because each group gets a bacteria sample, and the letter represents which chicken farm the sample came from. nigh each group should obtain sextet plates.Three have kanamycin, and are labeled with a K, and three unlabeled plates. Each group should because put the label of the groups member s, date, lab section number, letter of bacteria sample, and label one of each of the three sets of plates, K versus non K, 10-2, 10-4, and 10-6. Then label three, empty, sterile, microtubules with the dilutions, 10-2, 10-4, and 10-6 that will be made. Next using sterile techniques add 990 microliters of water into each microtubule. Afterward mix the bacterial suspension by gently flicking the microtubule, as shown by your TA.Then for each dilution factor, use 10 microliters of the bacterial suspension, and use this as the starting sample to make three-fold serial dilutions. For each dilution factor make sure to keep the bacteria well suspended by flicking the tube before removing each sample, and make sure that a fresh pipet tip is used for each dilution. Then use sterile glass beads to distribute the bacteria evenly on the agar surface of the 10-6 plate by gently swirling the beads in a circular motion. Then using the same set of beads for each plate transfer the beads from 10-6 to 10-4, accordingly 10-2.Each group should then flip the dishes upside down and stack the three dishes together. finally tape the stacks together, and label the tape with your group member names, and section number. The plates should be incubated for around 24 hours, and then placed in a cold storage room until you are ready to cipher the colonies (Hass C. , Woodward D. , and Ward A. , 2010. ) For section two of this la b each group will be working as one group with the other groups at your lab bench. To begin you will collect the petri dishes that you fain before. Remove the tape from the stacks and examine your plates for colonies.Each lab bench will have six tubes containing PCR mix. The orange, blue, and yellow tubes will have primers only, and will have some colonies added to them. The red, green, and pink tubes will have primers with the control plasmid so no colonies will be added to these tubes, as they will be used as positive controls. Second identify and number the antibiotic resistant plates labeled K which have colonies growing on them. Third, use a white pipette tip and dip it into a colony on the plate labeled number one, and dip that into the orange tube, and close the cap.In turn repeat this step using a new pipette tip each time for colonies two and three, in the blue tube, and the yellow tube respectively. Finally load all six tubes into the PCR machine, and you TA will help you associate them. While the PCR machine is running each group can begin working on section three of the lab. To begin with each group will look at the bacteria plates, and count the number of colonies. If the colonies are distributed evenly in the plate then you can divide the plate into four quadrants and just count one quadrant and multiply that number by four. However if they are non, you must count all of the colonies.If there is more than 800 colonies on a plate record the number as lawn growth. Finally record the number of colonies for each plate and use these numbers to calculate the concentration of viable bacteria in the original sample, and the frequency of antibiotic resistant bacteria in the sample. In the last section for the lab each group will be using gel dielectrolysis to run their bacteria DNA. Each lab bench will make, and run one gel electrophoresis per table. once the gel is ready to be loaded, load five microliters of PCR DNA ladder into the first well, as a standard. This should be found in a tube in and ice bucket.Next add two microliters of 6x loading dye into the six sample tubes. The dye should be mixed in thoroughly by gently pipetting up and down after adding the dye. Following that you should load fifteen microliters of each sample into the following six wells. Since lane one will have the DNA ladder lane two starts the samples using the orange tube, then the blue, yellow, red, green, and pink tubes go into lanes three, four, five, six, and seven respectively. Once all the samples are loaded turn on the electrophoresis machine, and wait until the bromophenol blue tracking dye has migrated at least half the length of the gel.Lastly using gloves carefully remove the gel and carry it to the UV light box to view, and photograph the gel (Hass C. , Woodward D. , and Ward A. , 2010. ). Results The results of this experiment show that the farms do not share the same plasmid that carries the antibiotic resistance gene. hedge one shows the individual group data for the concentration and frequency of the antibiotic resistant bacteria. Table two shows the overall frequency of antibiotic resistant bacteria for label A which was taken from Acme Farm, for the section.Table three shows the section data for the overall frequency of antibiotic resistant bacteria, for all three farms, and which plasmid corresponds to that bacteria code. The results showed that for code A which was Acme farm, their resistant bacteria carried plasmid A. For code B, Big Als, and code C Cluckys chicken farm, their resistant bacteria carried plasmids B, and C respectively. Figure A shows the gel electrophoresis picture for the bacteria code A. This figure shows that code A does in fact carry the plasmid A.DiscussionBased on our data we can conclude that the three farms had different sources of contamination because the three farms all had different strands of resistant bacteria, as shown by the gel electrophoresis pictures from each farm. Fig ure one shows the plasmid that correlates to bacteria code A which came from Acme Farm. Based on the results shown in table 3 we learn that our hypothesis that all three farms shared a contamination source was wrong. The three farms each carry a different plasmid that is resistant to the antibiotic so their contamination sources must be different.The overall trends from this data are that there was an overwhelming amount of bacteria in almost every case for the 10-2 dilution factor, and the frequencies of viable resistant bacteria were low so that means there was not a lot of resistant bacteria. Some possible sources of error were the DNA samples were not placed properly in the gel so the electrophoresis was not as reliable, or a fresh pipette tip was not used for each dilution which would have messed up the dilutions. Additional experiments that can be done are use three different farms from the previous experiment and see if the same results are obtained.Our research was significa nt because it showed that there was not a common source of bacteria for the farms, and that bacteria can have multiple strands of DNA that could be resistant to an antibiotic. The significance of the guiding questions was to give practice reason the concentrations and frequencies of bacteria. Doing these calculations also gave us an indication of how reliable or data could be based on the amount of viable specimen. Recommendations for the farms would be to figure out where the bacteria is coming from and find a way to keep it from the chickens, or to use a different antibiotic that has less resistant strands.

Coordination Compounds and Ligands

Coordination Compounds and LigandsIn order to explain the framingulae and structures of the Gordian increases, or daedales, create by transition alloy salts with molecular species such as ammonia, Werner coined the terms primary valence and secondary valence, as explained in Chapter 1. These concepts remain valid straight off except that the term oxidation state has replaced primary valence and the term coordination cast has replaced secondary valence. Werner had recognized that a transition surface salt could form a intricate compound in which the alloy ion became bonded to a number of groups which need not necessarily be the counter anions originally present in the salt. The orientations in space of these alloylic element-bound groups would lead to the complex having a particular geometric structure. In this chapter the structures of transition element complexes are examined in more than detail and any(prenominal) definitions of key terms are provided.One definition o f a metallic element complex or coordination compound is a compound formed from a Lewis acidic and a Brnsted base, a Lewis acid being an electron pair acceptor and a Brnsted base a proton acceptor. Thus the interaction of the Lewis acid metal centre in Ni(ClO4)2 with the Brnsted base ammonia to form a complex according to equation 4.1 Ni(ClO4)2 + 6NH3 Ni(NH3)6(ClO4)2 (4.1) provides an example of the formation of a coordination compound. In piece the formulae of metal complexes it is conventional to include the complete coordination complex within square brackets, an example being provided by Co(NH3)5ClCl2, in which the coordination complex is Co(NH3)5Cl2+ with two chloride counterions. The Brnsted bases attach to the metal ion in such compounds are called ligands. These may be simple ions such as Cl-, small molecules such as H2O or NH3, astronomical molecules such as H2NCH2CH2NH2 or N(CH2CH2NH2)3, or even macromolecules, such as proteins. The coordination number (CN) of a meta l ion in a complex do-nothing be defined as the number of ligand donor atoms to which the metal is directly bonded. In the case of Co(NH3)5Cl2+ this will be 6, the sum of one(a) chloride and five ammonia ligands for each one donating an electron pair. Although this definition usually works well for coordination compounds, it is not always appropriate for organometallic compounds. An alternative definition of CN would be the number of electron pairs arising from the ligand donor atoms to which the metal is directly bonded. To apply this definition, it is necessary to assume an ionic formulation and a particular oxidation state for the metal ion, so that charges can be designate to the ligands as appropriate and the number of electron pairs determined.Types of LigandWhere a ligand is bound to a metal ion through a single donor atom, as with Cl-, H2O or NH3, the ligand is give tongue to to be unidentate (the ligand binds to the metal through a single point of attachment as if it h ad onetooth). Where two donor atoms can be apply to bind to a metal ion, as with H2NCH2CH2NH2, the ligand is said to be bidentate, and where several donor atoms are present in a single ligand as with N(CH2CH2NH2)3, the ligand is said to be polydentate. When a bi- or polydentate ligand uses two or more donor atoms to bind to a single metal ion, it is said to form a chelate complex (from the Greek for claw). Such complexes tip to be more stable than similar complexes containing unidentate ligands. A huge variety of ligands appear in coordination complexes, Any of a variety of elements may function as donor atoms towards metal ions, alone the more or less commonly encountered are probably nitrogen, phosphorus, oxygen, sulfur and the halides. In addition, a large number of compounds are known which contain carbon donor atoms these are known as organometallic compounds. Bidentate ligands may be classified according to the number of atoms in the ligand which separate the donor atoms a nd hence the size of the chelate abut formed with the metal ion. Thus 1,1-ligands form a four-membered chelate ring when bound to a metal ion, 1,2-ligands a five membered ring, and so on. Cyclic compounds which contain donor atoms oriented so that they can bind to a metal ion and which are large enough to encircle it are known as macrocyclic proligands. Bicyclic proligands are also known which can completely capsulise a metal ion. Some of these systems subscribe to given the constructs cryptand or sepulchrate, Certain polydentate ligands are particularly good at linking together several metal ions and are refered to as polynucleating ligands.GeometryIn coordination chemistry, a structure is first described by its coordination number, the number of ligands attached to the metal (more specifically, the number of -type bonds between ligand(s) and the central atom). ordinarily one can count the ligands attached, but sometimes even the counting can become ambiguous. Coordination nu mbers are normally between two and nine, but large numbers of ligands are not uncommon for the lanthanides and actinides. The number of bonds depends on the size, charge, and electron configu proportionalityn of the metal ion and the ligands. Metal ions may have more than one coordination number.Typically the chemistry of complexes is dominated by interactions between s and p molecular orbitals of the ligands and the d orbitals of the metal ions. The s, p, and d orbitals of the metal can accommodate 18 electrons (see 18-Electron rule for f-block elements, this extends to 32 electrons). The maximum coordination number for a certain metal is thus related to the electronic configuration of the metal ion (more specifically, the number of empty orbitals) and to the ratio of the size of the ligands and the metal ion. Large metals and small ligands lead to high coordination numbers, e.g. Mo(CN)84-. Small metals with large ligands lead to low coordination numbers, e.g. PtP(CMe3)2. Due to th eir large size, lanthanides, actinides, and early transition metals tend to have high coordination numbers.Different ligand geomorphological arrangements result from the coordination number. Most structures follow the points-on-a-sphere pattern (or, as if the central atom were in the middle of a polyhedron where the corners of that square off are the locations of the ligands), where orbital overlap (between ligand and metal orbitals) and ligand-ligand repulsions tend to lead to certain regular geometries. The most observed geometries are listed below, but there are legion(predicate) cases which deviate from a regular geometry, e.g. due to the use of ligands of different types (which results in irregular bond lengths the coordination atoms do not follow a points-on-a-sphere pattern), due to the size of ligands, or due to electronic effects (see e.g. Jahn-Teller distortion)Linear for two-coordination,Trigonal planar for tether-coordination,Tetrahedral or square planar for four-co ordinationTrigonal bipyramidal or square pyramidal for five-coordination,Octahedral (orthogonal) or trigonal prismatic for six-coordination,Pentagonal bipyramidal for seven-coordination,Square antiprismatic for eight-coordination, andTri-capped trigonal prismatic (Triaugmented triangular prism) for nine coordination.Some exceptions and provisions should be notedThe idealized descriptions of 5-, 7-, 8-, and 9- coordination are a good deal indistinct geometrically from alternative structures with slightly different L-M-L (ligand-metal-ligand) angles. The classic example of this is the difference between square pyramidal and trigonal bipyramidal structures.Due to special electronic effects such as (second-order) Jahn-Teller stabilization, certain geometries are stabilized relative to the other possibilities, e.g. for some compounds the trigonal prismatic geometry is stabilized relative to octahedral structures for six-coordination.IsomerismThe arrangement of the ligands is stiff for a given complex, but in some cases it is mutable by a reaction that forms another stable isomer.There exist many kinds of isomerism in coordination complexes, just as in many other compounds.StereoisomerismStereoisomerism occurs with the same bonds in different orientations relative to one another. Stereoisomerism can be further classified intoCis-trans isomerism and facial-meridional isomerismCis-trans isomerism occurs in octahedral and square planar complexes (but not tetrahedral). When two ligands are mutually adjacent they are said to be cis, when opposite each other, trans. When three identical ligands fulfill one face of an octahedron, the isomer is said to be facial, or fac. In a fac isomer, any two identical ligands are adjacent or cis to each other. If these three ligands and the metal ion are in one plane, the isomer is said to be meridional, or mer. A mer isomer can be considered as a combination of a trans and a cis, since it contains both trans and cis pairs of identic al ligands.Optical isomerismOptical isomerism occurs when the mirror image of a compound is not superimposable with the original compound. It is so called because such isomers are optically active, that is, they turn off the plane of polarized light. The symbol (lambda) is apply as a prefix to describe the left-handed propeller twist formed by three bidentate ligands, as shown. Similarly, the symbol (delta) is used as a prefix for the right-handed propeller twist.7Structural isomerismStructural isomerism occurs when the bonds are themselves different. Linkage isomerism is only one of several types of structural isomerism in coordination complexes (as well as other classes of chemical compounds). Linkage isomerism occurs with ambidentate ligands which can bind in more than one place. For example, NO2 is an ambidentate ligand it can bind to a metal at either the N atom or at an O atom. http//t2.gstatic.com/images?q=tbnANd9GcRKxYHqV_eczrlInNE3ZAbZOBh-Q1JBpMbyWoRehkKI8y1KEukt=1usg=_ _PClvZyGR5yoOsiA5HEgW1Zjyvko=Naming Coordination CompoundsA complex is a substance in which a metal atom or ion is associated with a group of neutral molecules or anions called ligands. Coordination compounds are neutral substances (i.e. uncharged) in which at least one ion is present as a complex. You will learn more about coordination compounds in the lab lectures of experiment 4 in this course.The coordination compounds are named in the following way. (At the end of this tutorial we have some examples to show you how coordination compounds are named.)A. To name a coordination compound, no matter whether the complex ion is the cation or the anion, always name the cation before the anion. (This is just handle naming an ionic compound.)B. In naming the complex ion1. Name the ligands first, in alphabetical order, then the metal atom or ion. Note The metal atom or ion is written before the ligands in the chemical formula.2. The names of some common ligands are listed in Table 1.For anionic ligands end in -o for anions that end in -ide(e.g. chloride), -ate (e.g. sulfate, nitrate), and -ite (e.g. nirite), change the endings as follows -ide http//www.chemistry.wustl.edu/edudev/LabTutorials/arrow.jpg-o -ate http//www.chemistry.wustl.edu/edudev/LabTutorials/arrow.jpg-ato -ite http//www.chemistry.wustl.edu/edudev/LabTutorials/arrow.jpg-itoFor neutral ligands, the common name of the molecule is used e.g. H2NCH2CH2NH2 (ethylenediamine). Important exceptions water is called aqua, ammonia is called ammine, carbon monoxide is called carbonyl, and the N2 and O2 are called dinitrogen and dioxygen.3. Greek prefixes are used to designate the number of each type of ligand in the complex ion, e.g. di-, tri- and tetra-. If the ligand already contains a Greek prefix (e.g. ethylenediamine) or if it is polydentate ligands (ie. can attach at more than one binding site) the prefixes bis-, tris-, tetrakis-, pentakis-, are used instead. (See examples 3 and 4.) The numerical prefixes a re listed in Table 2.4. After naming the ligands, name the central metal. If the complex ion is a cation, the metal is named same as the element. For example, Co in a complex cation is call cobalt and Pt is called platinum. (See examples 1-4). If the complex ion is an anion, the name of the metal ends with the suffix -ate. (See examples 5 and 6.). For example, Co in a complex anion is called cobaltate and Pt is called platinate. For some metals, the Latin names are used in the complex anions e.g. Fe is called ferrate (not compressate).5. Following the name of the metal, the oxidation state of the metal in the complex is given as a Roman numeral in parentheses.C. To name a neutral complex molecule, follow the rules of naming a complex cation. Remember Name the (possibly complex) cation BEFORE the (possibly complex) anion.See examples 7 and 8.For historic reasons, some coordination compounds are called by their common names. For example, Fe(CN)63 and Fe(CN)64 are named ferricyanide a nd ferrocyanide respectively, and Fe(CO)5 is called iron carbonyl.Examples Give the systematic names for the following coordination compounds1. Cr(NH3)3(H2O)3Cl3Answer triamminetriaquachromium(III) chlorideSolution The complex ion is inside the parentheses, which is a cation.The ammine ligands are named before the aqua ligands according to alphabetical order.Since there are three chlorides binding with the complex ion, the charge on the complex ion must be +3 ( since the compound is electrically neutral).From the charge on the complex ion and the charge on the ligands, we can calculate the oxidation number of the metal. In this example, all the ligands are neutral molecules. Therefore, the oxidation number of chromium must be same as the charge of the complex ion, +3.K4Fe(CN)6Answer potassium hexacyanoferrate(II)Solution potassium is the cation and the complex ion is the anion.Since there are 4 K+ binding with a complex ion, the charge on the complex ion must be 4.Since each ligand carries -1 charge, the oxidation number of Fe must be +2.The common name of this compound is potassium ferrocyanide.Applications of Co-ordination Compounds(1) Estimation of hardness in water, as Ca++ and Mg2+ ions form complexes with EDTA.(2) Animal and plant world e.g. chlorophyll is a complex of Mg2+ and haemoglobin is a complex of Fe2+ vitamin B12 is a complex of Co2+.(3) Electroplating of metals involves the use of complex salt as electrolytes e.g. KAg(CN)2 in silver plating.(4) Extraction of metals e.g. Ag and Au are extracted from ores by dissolving in NaCN to form complexes.(5) Estimation and detection of metal ions e.g. Ni2+ ion is estimated using dimethyl glyoxime.(6) Medicines e.g. cis-platin i.e. cis PtCl2(NH3)2 is used in sermon in cancerImportance and Applications of Coordination CompoundsImportance and applications of coordination compounds follow use in many qualitative and quantitative chemical analyses. The familiar color reactions given by metal ions with number of ligands. Similarly purification of metal can be achieved through formation and sub sequence decomposition of their coordination compounds.Inflexibility of water is predictable by simple titration with Na2EDTA.the Ca2+ and Mg2+ ions form stable complex with EDTA. The selective estimation of these ions can be done due to difference in the stability constants of calcium and magnesium complexes. Some important extraction processes of metals like those of silver and gold, make use of complex formation.Importance and applications of coordination compounds are of great importance in biological system. The pigment responsible for photosynthesis chlorophyll is a interrelated compound of magnesium. Haemoglobin, the red pigment of blood which acts as oxygen carrier is a coordination compound of iron. Coordination compounds are used as catalysts for many industrial processes.Applications of articles can be electroplating with the silver and gold much more smoothly and evenly from the solut ion of the complexes. In black and white photography, the developed film is fixed by washing with hypo solution which dissolves the unrecompensed AgBr to from a complex ion Ag9S2O3)23-There is growing interest in the user of chelate therapy in medicinal chemistry. An example is the treatment of problem caused by the presence of metal in toxic proportion in plant and animal. Thus, excess of copper and iron are removed by chelating ligands D-penicillamine and desferrioxime B via the formation of the coordination compounds. EDTA is use in the conduct of guide poisoning. Some coordination compounds of platinum effectively inhibit the growth of tumours.Sonochemical Asymmetric Hydrogenation with PalladiumEnantioselective hydrogenation is one of the most versatile methods of asymmetric synthesis, with heterogeneous catalysis, using chiral modifiers, rapidly becoming an alternative to the .traditional. homogeneous methods. The role of modifiers in asymmetric hydrogenations is to enhance cat alysis, with the bonding mode and geometry of adsorption being important, as well as the modifier concentration and the type and position of the substituent groups in the aromatic ring. Ultrasonic irradiation (sonication) is known to be dear in catalytic asymmetric hydrogenations. Sonication removes catalyst surface impurities, and gives raise adsorption to the chiral modifiers. Now a team from Michigan Technological University, Houghton, U.S.A. (S. C. Mhadgut, I.Bucsi, M. Trk and B. Trk, Chem. Commun., 2004, (8), 984-985 DOI 10.1039/b315244h) has revisited the Pd-catalysed, proline-modified, asymmetric hydrogenation of isophorone (3,3,5-trimethyl-2-cyclohexen-1-one (with a C=C bond)). They examined the catalyst, the modifier and the effects of sonication. Pd/Al2O3 was found to give a better, thoughlow, enantiomeric excess (ee) than Pd/C. Prolineand its derivatives (isomeric hydroxyl-prolines, prolinols and proline esters) were tested as chiralmodifiers for Pd/Al2O3. Proline was th e best modifier, and both enantiomers gave ee 35%. Presonication was found to enhance the enantioselectivity when both the Pd/Al2O3 catalyst and the proline modifier were present. .Modifier-free. presonication and the presence of substratum during pretreatment decreased the enantioselectivity. The reaction was performed at 50 bar closet and 25C. Presonication for 20 minutes gave the highest optical yields, and increased optical yields across all the H2 pressure range. Maximum ee occurred at a 12 isophoroneproline ratio, and with optimised conditions and presonication, the ee for the Pd/Al2O3-(S)-proline catalytic system was 85%. Ultrasonic cleaning of the catalyst enhanced both the adsorption of the modifier and the modifier- induced surface restructuring of the Pd. The high ee was due to proline adsorption on the Pd surface. New catalysts that can strongly adsorb proline could thus become important in heterogeneous catalysis for C=C double bond hydrogenation of a,b-unsaturated c arbonyl compounds.

Roles of MicroRNAs in the Cell Cycle

Roles of MicroRNAs in the Cell CycleEvaluate the roles of microRNAs in the stall wheel around and explain the consequences of disruption to microRNA use in named diseasesIntroductionThe presence and activity of various proteins atomic number 18 required in the booth cycle progression.(1) The regulation of these protein levels is vital for the understanding of the carrell cycle control and its dysregulation. The dysregulation results elementtic mutation tie in diseases. For instance, over preparation of cyclins or the elimination of CDK inhibitors or pRB out-of-pocket to genetic mutation are common cause in humanity cancer.(2) Therefore, the proper control of protein levels is crucial for the cell cycle.MicroRNAs are 22-25 nucleotide non-coding RNAs.(3) It is post- transcriptional repressor of mRNA control the stability and translation of protein-coding mRNAs. (1, 3). MiRNAs bind the 3 untranslated region (3UTR) of butt mRNAs. The binding of miRNA- protein complexes to mRNA causes translation curtailment or destabilisation of target transcripts.(1) This is resulting in the peckregulation of the protein encoded by mRNA.Figure 1 microRNA as post-transcription inhibitor in protein encoding (4)MicroRNAs control the levels of numerous cell cycle regulators that controls cell proliferation.(1) The alternation of protein levels of minute oncogenes or tumour suppressor genes, which causes by miRNAs deregulation may also lead to proliferative diseases such as cancer. MiRNAs that linked to human cancers, known as oncomirs. These are divided into two group, those miRNAs that are upregulated in cancer which are liable(predicate) to be acting as oncogenes and those downregulated in cancer which are samely to be acting as tumour suppressors.(5)Approximately 30-60 % of the human genome, regulated by miRNAs. As a consequence, any modulations of the target transcript manifestation, miRNAs can discover various signalling pathways and cellular process such as a poptosis, proliferation or diverseiation. Therefore, miRNAs could consider as cancer targets.Besides cancer, some miRNAs genes cause or contribute in many inherited and genetic based diseases. For instance, miR-26b upregulated in Alzerimers disease, (6) miR 96 causes nonsyndromic progressive audition loss (7) and miR -184 causes Familial Keratoconus with Cataract.(8)Nevertheless(prenominal), some miRNAs genes are beneficial give away antiproliferative properties.(1) For example, the down-regulation of miR15s and miR 16 1 in chronic lymphocytic leukaemia, prostate cancer and pituitary tumours, leading to the inhibition of tumour growth and induce cell cycle arrest at the G1 pattern by target cell cycle regulators ( cyclin D1, cyclin E1, cyclin D3 and CDK6). (9)As miRNAs proposed to control the expression up to atomic number 53 third of all genes and by chance utilised as diagnostic and prognostic marker for many genetic based diseases.(10) Therefore, it is important to evalu ate its role in the cell cycle and its dysregulation.The different roles of MicroRNAs in the cell cycleThe understanding of miRNA has increased over the past 10 years, and particularly the involvement of miRNAs in cancer. Nowadays, cancer is a common disease, which occurs to one third of the population. There are lots of cancer treatments available, however to identify an effective treatment is still challenging.(9) Therefore, it is important to develop a new treatments with less side effect are greatly demanded. A greater understanding of miRNA could possibly lead to better diagnostic and treatment of cancer.(9)Let-7 Let-7 has an essential role in cell cycle and the differentiation of cell cycle terminals. Let-7 is coded by 12 genes these are produced from the eight genomic loci. These 12 genes are located at a region, which is oftentimes deleted in cancer. Throughout the lung cancer examination, it has been showed that a low level of let-7 relates to the poor prognosis. The expre ssion of let-7 induces the crushing growth of cell and human tumour cell lines.(12) Over-expression of let-7 in lung cancer causes the lowered cell division and stopped the progression of cell cycle. Ras, Caspase-3 and HMGA2 genes are targeted by let-7 for controlling tumour growth. Furthermore, let-7 represses number of cell cycle regulator gene cyclin D1, cyclin A, cyclin D3, CDK4 and CCNA2, CDK6, CDC25A and CDK8. (13)MiR-15a/16 Chromosome 13q14 region is frequently deleted in more than 50% of the B-cell chronic lymphocytic leukaemia (CLL). This region of the chromosome includes the expression of miR-15a/16 cluster. Further studies have set that miR-15a/16 is located at the 30 kb region of the loss chromosome in CLL. (14) In CCL patients, about 70% of the patients have miR-15a and miR-16 either deleted or down regulated same applies to gastric cancer and pituitary adenomas cell lines. The miR-15a and miR-16 target cell cycle regulators such as cyclin D1, cyclin D3, cyclin E1 and CDK6, this causes the cell cycle arrest during the G1 phase.(13) miR-15 and miR-16 in colon cancer cell lines presented with a high level of down-regulated transcripts for gene related to cell-cycle progression. Moreover, the high expression of miR16 which leads to increase G0 and G2 phase accumulation through down-regulating the gene expression of cell cycle, CARD10, CDK6 and CDC27. These conclusiond the miR15a and miR16 associated with complex gene expression.(12)Figure 2 Cell cycle and proteins that are involved in the cycle. (11)MiR-17/20 The miR-17/20 induces suppression of tumour growth in the breast cancer and human B-cell line it encodes 6 mature miRs in a 1 kb region. MiR-17/20 target several cell cycle regulators, including E2F, Rb, c-myc and cyclin D1, for the time control of cell cycle. At G1 phase (figure 2) , Cyclin D1 and c-myc are induced and inactivation of E2F1 when bind to Rb. The transition of G1 to S phase of the cell cycle requires the miR-17/20 cluster.(13) The miR-17 family might involve in inhibit or promote cellular proliferation. In a low level of mitogenic stimulation, miR-17 thinkable involves in the E2F signalling maintenance to be at a level below threshold for proliferation. Furthermore, the missing miR-17-19 cluster has been identified in many malignancies, and disruption of miR-17 expression possible reduces the proliferation of certain breast cancer cell lines. The suppression of irregularly high E2F activation, the apoptosis response might be eliminated by the miR-17-92 cluster, then this run as an oncogene. Subsequently, in various solid and haematopoietic malignancies are found to have amplificated and over-expressed miR-17 family. These have indicated that miR-17/20 play a essential role in cellular proliferation and progression of malignancies. (12)MiR-221/222The regulation of cell cycle by miR-221/222, which it targets the CDK inhibitors. The miR-221 and miR-222 ectopic expression initiate CDK2, aiding the transitio n of G1 to S phase of cell cycle and p27kip2 and p57kip2 are negatively regulated which lead to increase tumour growth. This is frequently identified in human breast cancer tissues.(13) In addition, miR-221 and miR-222 act as a direct regulator of p27. The over-expression of this cluster increases cellular proliferation and allowed anchorage growth independently. The suppression of miR221 and miR-222 initiated G1 phase arrest in breast cancer cell lines. It is found that miR-221/222 is over-expressed in several human tumors. (12)Table 1 miRNA genes and clusters that target cell cycle regulators and its deregulation in cancer. (1)MiRNA related diseasesChronic Lymphocytic LeukaemiaChronic Lymphocytic Leukaemia (CLL) occurs due to the homozygous or heterozygous deletion of the chromosomal region 13q14.3. MiR 15a and miR -16-1 are located in this region as shown in Calin et als study.(9, 15) This provided evidence that miRNAs might be involved in the pathogenesis of CLL and other human cancers.(9) These genes were found to be deleted in 68 % of CLL patients.(15) MiR-15a and miR-16-1 leads to the inhibition of tumour growth by negatively regulate BCL2 anti-apoptotic gene.(9) They also induce cell cycle arrest at the G1 phase by targeting cell cycle regulators cyclin D1, cycline D3, cyline E1 abd CDK6.(9) The deletion of miR-15a and miR-16-1 associated with CLL patients phenotypes the loss of these two genes accelerates B- lymphocytes proliferation by modulating genes expression controlling cell-cycle progression.(9) As consequences, CLL clinical features occurs.Breast cancerbreast cancer is oestrogen hormone dependant disease. Breast cancer occurs when the number of oestrogen receptors (ER) increase abnormally. Alb1 genes are oncogenes in breast cancer. It enhances the transcriptional activity of the ER and E2F1 and other transcription factors. (16) Alb1 is a rate-limiting factor for oestrogen. (16) E2F1 is involving in growth hormonesignalling pathway and media te breast cancer cells growth. (16) From the Hossain et als study, mir-17-5p play a role of tumour suppressor, which controls the cell proliferation of breast cancer cells. (16) In cell culture experiment, AlB1 expression was downregulated by mir-17-5p through translational inhibition. This resulted in decreased ER and cancer cellsproliferation. As mir-17-5p binds to the cyclin D1 3UTR in the MCF-7 breast cancer cells . It inhibits cyclin D1 expression, resulting in suppressed cell proliferation and cell cycle arrest.(9)ConclusionMicroRNAs are crucial in the cell cycle. The Mitchell et als study has shown that miRNAs displayed high stability in tissue from human plasma. (17) It is possible that miRNA might be useful biomarker to indicate disease state. Moreover, the demonstration of miRNA profiles are potential for distinguishing a development of tumours origin and miRNA that acts like tumour suppressor in cancer.(18) From Lu et als study, they have demonstrated that there are lower miRNA expression in poorly secern as compared to highly differentiate tumour which is very interesting fact and provide evidence to shoe that possibility that miRNA could utilised in disease diagnostics. (19) Therefore, shape up researches should carry out to gain more understandings and invent more effective treatment.References1. Bueno J, Mara., Malumbres M. MicroRNAs and the cell cycle. 20111812(5)592601.2. Malumbres M, Barbacid M. To cycle or not to cycle a critical decision in cancer. Nat Rev malignant neoplastic disease. 20011(3)222-31.3. Carleton MC, A., Michele. Linsley,S.,Peter. MicroRNAs and Cell Cycle Regulation. Cell cycle. 2007 September 16(17)2127-32.4. The image of microRNA image on the internet. 2013 cited 2014 February 4. open from http//www.fireflybio.com/introduction_to_microRNA.5. Johnson CD, Esquela-Kerscher A, Stefani G, Byrom M, Kelnar K, Ovcharenko D, et al. The let-7 microRNA represses cell proliferation pathways in human cells. Cancer Res. 200767(16)77 13-22.6. Absalon S, Kochanek DM, Raghavan V, Krichevsky AM. MiR-26b, upregulated in Alzheimers disease, activates cell cycle entry, tau-phosphorylation, and apoptosis in postmitotic neurons. J Neurosci. 201333(37)14645-59.7. Menca ea. Mutations in the seed region of human miR-96 are responsible for nonsyndromic progressive hearing loss. Nature Genetics. 200941(5)609-13.8. Hughes AE, Bradley DT, Campbell M, Lechner J, Dash DP, Simpson DA, et al. Mutation Altering the miR-184 Seed Region Causes Familial Keratoconus with Cataract. The American Journal of Human Genetics. 201189(5)628-33.9. MicroRNA in Cancer Spinger Science and Business Media Dordrecht 2013 cited 2014 February 2. Available from http//books.google.co.uk/books/about/MicroRNA_in_Cancer.html?id=RS8qLrSkdkgC.10.Yang MM, Joerg. Discovery, biology and therapeutic potential of RNA interference, microRNA and antagomirs. 2008117(1)94104.11. Cohen B. The image of cell cycle image on the internet. 2013 cited 2014 February 4. Availa ble from http//www.studyblue.com/notes/note/n/neoplasia-vii-cancer-critical-genes-and-familial-cancer-syndromes/deck/6316935.12. Chivukula R, Raghu. Mendell,T., Joshua. rotary reasoning microRNAs and cell-cycle control. October 200833(10)474-81.13. Yu Z, Baserga R, Chen L, Wang C, Lisanti MP, Pestell RG. microRNA, Cell Cycle, and Human Breast Cancer. American Journal of Pathology, The. 2010176(3)1058-64.14. Cho WC. OncomiRs the discovery and progress of microRNAs in cancers. Molecular Cancer Internet. 2007 2007-09-25 cited 2014 Febuary 5 6(1)60 p.. Available from http//www.molecular-cancer.com/content/6/1/60.15. Calin GA, Dumitru CD, Shimizu M, Bichi R, Zupo S, Noch E, et al. Frequent deletions and down-regulation of micro- RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia. 200299(24).16. Hossain A, Kuo MT, Saunders GF. Mir-17-5p Regulates Breast Cancer Cell Proliferation by Inhibiting Translation of AIB1 mRNA. Molecular and Cellular Biology. Novemble 200626(20).1 7. Mitchell PS, Parkin RK, Kroh EM, Fritz BR, Wyman SK, Pogosova-Agadjanyan EL, et al. spread microRNAs as stable blood-based markers for cancer detection. Proc Natl Acad Sci U S A. 2008105(30)10513-8.18. Hydbring PV-B, Gayane. Clinical applications of microRNAs F1000Research. 2014.19. Lu J, Getz G, Miska EA, Alvarez-Saavedra E, Lamb J, Peck D, et al. MicroRNA expression profiles classify human cancers. Nature. 2005435(7043)834-8.

Terra-Cotta Girl :: essays research papers

Terra Cotta GirlThe poem has clear, wide-open drama while managing ambiguity and open-endedness. A sort of modern local color piece tinted with gray elements, it nevertheless makes its characters real and sympathetic, treats important themes that are both topical and general, and offers an apt objective relationship with universal implications.Technically a lyric, the poem filled with story and drama an off-the-farm college misfire, a Southerner, and perhaps a Georgian like Sellers herself, has fallen in love with a quiet girl down the hall (9). The girls conservative mother has seen to (10) having her daughter seek for an expert help. Ungraceful, conflicted inwardly, and beset outwardly by parental pressure, the girl now waits to see a counselor. No character speaks, provided the role of each is well defined. At least five characters, perhaps six, come into play ii girls, their two mothers, and one or maybe two counselors. Onstage is the terra cotta girl (1)--and maybe her mot her as well. The other, quiet (9) daughter and her mother, along with a counselor (perhaps the same one), running a parallel to the scene we are witnessing.Although the poem shows us the girls as living down the hall (9) from each other in their college dormitory, it also suggests another verifying possibility that, at the very moment of the present action, this other girl, the quiet one, is just down the hall waiting to see another counselor during two parallel sessions that the mothers have seen to (10). Perhaps, the other girls mother is with her, too. The other girl may be quiet precisely because the narrator chooses not to run her a separate story. If this is the case, her terra cotta lover stands in as her delegate. The phrase quiet girl draws the image of a shy character, who may be less subject to handle her current torture, and not as strong as terra cotta girl.Formally, the poem has thirteen short lines with different numbers of syllables and accents. The poem is unrhym ed but engages such alliterations as flat farm feet (2) / furrows (3), soil has seen (10), and weep for the waste (12). All of the alliterated sounds are voiceless, which projects the current situation of the girls. The thirteen breath units of the poem drainage basin into two clear sentences. With no stanza break in the poem, these sentences establish the language of the drama.

Abortion: The Wrong Choice Essay -- The Truth about Abortion

Abortion? Is it the right or wrong thing to do? In this paper I will try to usher why I believe that it is wrong to have an abortion. Why have an abortion when you can have the baby and ordinate it up for adoption after birth? When you have an abortion, you ar committing manslaughter, murder. Some people may not think so, but they are. If the woman does not ask to have a baby, then why did she take the risk by having sex? I believe that once you have name out that you are pregnant you should continue the process and see the pregnancy through to birth.The entire complex issue comes down to one question Is the fetus a soulfulness?(Gilbert,Intro-2). This question is the most important one to ask yourself before deciding whether or not to have an abortion. Some people ask doctors the same question, and their resolution would be to define life. After a discussion in 1981, the U.S. Senate decided that biological life starts at implantation. Many of the Pro-abortionists, however cou ld not found one expert to prove that life starts at any other time than implantation. They were able to however to show an alternative viewpoint.It considers the continuum to run from sperm and egg, to single-cell zygote, to multi-cell blastocyst, to embryo, to fetus, to newborn, etcetera This view is attractive because it supports the right of each mother and doctor to individually choose when in the continuum the fetus becomes a person(Gilbert,Med-2).This view though did not prove the ...