What is the value of computerized medical records for patient care Essay

What is the value of computerized medical records for patient care - Essay Example In this regard, it is claimed that computerized medical health records reduce the costs as well as the time associated with maintaining paper records (Rozenbluma et al., 2013). In addition, it is claimed that computerized medical records streamline workflow process, promotes the quality of patients’ care as well as patients’ safety (GE Healthcare, 2011; Rosen, 2010). Caffrey & Park-Lee, (2013) propagated that computerized medical records provide a significant advantage in the overall â€Å"implementation and evaluation processes† of patient health, which is the major pitfall in the traditional system (Caffrey & Park-Lee, 2013). In addition, computerized medical records are advocated to ensure more reliable and complete medical records, which in turn increases the reliability of health care delivered to the patients. Besides, data that are stored in the form of computerized medical records can be retrieved quickly, which further supports the clinical decision maki ng. Precisely stating, the benefits associated with computerized medical records are argued to be substantial to patients, clinic practices, physicians and health care service providers in the current health care industry (Healthcare IT News, 2005; Wang et al., 2003). Rozenbluma, R., Donzà ©, J., Hockey, P. M., Guzdar, E., Labuzettaa, M. A., Zimlichmana, E., & Batesa, D. W. (2013). The impact of medical informatics on patient satisfaction: A USA-based literature review. International Journal of Medical Informatics, 82(3), 141-158. Wang, S. J., Middleton, B., Prosser, L. A., Bardon, C. G., Spurr, C. D., Carchidi, P. J., Kittler, A. F., Goldszer, R. C., Fairchild, D. J., Sussman, A. J., Kuperman, G. J., & Bates, D. W. (2003). A cost-benefit analysis of electronic medical records in primary care. The American Journal of Medicine, 114,

Inanna vs. Oedipus Rex Essay Example for Free

Inanna vs. Oedipus Rex Essay She wondered: How long will it be until I have a shinning throne to sit upon? How long will it be until I have a shinning bed to lie upon? The huluppu-tree is a metaphor of Inanna herself. The trees growth symbolizes Inannas growth in her own life. When she mentions that she wants to make a thrown and bed for herself, she is foreshadowing her destiny of becoming a queen. This was her first test in becoming a leader. A leader needs to know how to be responsible for something or someone. They need to show that they care and can put forth tremendous effort toward what is important. In many instances through out the story, Inanna showed responsibility and maturity, but this was her first sight of it. After a couple years of waiting for the bark to split so that she can build her thrown and bed, A serpent who could not be charmed made its nest in the roots of the huluppu-tree. The Anzu-bird set his young in the branches of the tree. And the dark maid Lilith built her home in the trunk. (Pg. 6;Lines 1-4) The three things that built their home in the tree was the next test that he needed to overcome so that she can start her life in becoming a woman. When these struggles started in her life, she knew that she couldnt do it alone, so she asked for help. She first asked her brother Utu, The Sun God. He would not help her. So she then asked her other brother, Gilgamesh who agreed to help. He put on his armor and grabbed his bronze ax and entered Inannas holy garden. He struck the serpent and then the Anzubirds flew away. Finally the Lilth smashed her home and fled. Gilgamash then carved a throne and bed for Inanna using the tree trunk. This portrays a strong leadership quality in Inanna, which is openness. A leader needs to be able to listen to new ideas, even if they do not conform to the usual way of thinking. They need to be able to know that sometimes they might not be right, and have to listen to someone else. Inanna knew she couldnt do it on her own, and she needed help. Asking for help was a learning step for her in maturing her leadership qualities. Oedipus showed different leadership qualities as Inanna, which were determination and integrity. When the plague hit the town the second time, Oedipus as determined to end it. Just as he did when he first entered the town and solved the riddle. He sent many men out to find who killed the king and promised the town that he would find this man and end the plague. Ironically, who he was looking for was himself. He was the murderer of the king and the husband of his mother. When his guilt, no longer see those they should never seen, nor see, unseeing, those he had longed to see, henceforth seeing nothing but night To this wild tune he pierced his eyeballs time and tie again, till bloody tears ran down his beard. (Pg. 1 ;Lines 7-12) Oedipus was a very strong leader. He put an exceptional amount of effort and responsibility towards the people of the city. He was determined to end the plague for his people of Thebes. When he found out that he was the man he was looking for, he punished himself. Instead of killing himself, he pierced his eyes out so he has to live the rest of his life knowing that all of his answers were right in front of him, but he couldnt see it. This is why he was a great leader. He had the most power in the whole city and could have easily accused someone else. Yet he punishes himself Just as would if it was another man. This shows a great amount of integrity. He never veered from his inner values, even when it was expeditious to do so. I think that Inanna has better leadership skills than Oedipus because she is more experienced. Oedipus has natural leadership qualities. Inanna was tested throughout her life, which made her a stronger leader. The one part of her life that made her a better leader than Oedipus was when she decented herself to the underworld. My Lady abandoned heaven and earth to decened to the underworld. Inanna abandoned heaven and earth to decened to the underworld. She abandoned her office of holy priestess to decened to the underworld. (pg. 52;Lines 4-6) This shows great leadership qualities. She was striving so much to be great, she never experienced the difficulties of life. So she descended herself so that she can experience the other side of life. This was the biggest step into making her the leader that she was. Oedipus is nothing like Inanna in the sense of leadership. Through out the story of Inanna, she works to achieve royality, experience both sides of life and doesnt help nyone but herself on the way..

What Does The Author Of Sir Ga :: essays research papers

The author of the book Sir Gawain and the Green Knight teaches the reader many different things about facing challenges such as how they come unexpecteantly and how they must be faced. Throughout the ballad there are numerous refernces to the challenges that Sir Gawain and the different ways that he must deal with them.   Ã‚  Ã‚  Ã‚  Ã‚  The author shows that people have to face a challenge straight on. You cannot run away and hope that the problem will go away. One reason for this is that challenges, unless dealt with, will follow you forever. An expample of this is the challenge that the Green Knight bestows upon Sir Gawain. He must find the Green Knight in a year and a day to have the Green Knight hit him with a weapon of his choosing. The author shows through the description of chivarly that if Sir Gawain were not hold up his end of the deal, the knights and the people of Camalot would be forever shamed by his presence. The author shows that challenges cannot be lefy alone, they must be faced straight on and dealt with.   Ã‚  Ã‚  Ã‚  Ã‚  In the Ballad the author also shows that challenges can come from unexpected sources and that these also cannot be ignored. That is shown in the ballad through the example of the challenge that arose from the Green Knight. The challenge is aimed at King Authorm but is spontaneously taken on by Sir Gawain. Sir Gawain has no time to prepare for the challenge and only took it to protect his king. With a little forethought and knowledge, he might have concluded that the challenge was not woth the risks. There are other examples of unexpected challenges, such as the problems he had during his travel for the court of King Arthur to the Green Chapel. These challenges came up as he was traveling and he had no choice about taking them on, it was that or for him to die. The other main challenge was from the lady of the house. This challenge was totally unexpected; Sir Gawain did not even know that it was a challenge until his talk with the Green Knight right at the end. Sir Gawain did not know that the Green Knight was testing the young knight to see how strong his sense of chivalry really is.

Herpes Simplex Virus

Herpes Simplex Virus Type 1 Infection at the Molecular Level Research Paper Virology 24 November 2008 Abstract Herpes simplex virus type 1 (HSV-1) infection is widespread and causes significant disease in humans. The structure, epidemiology, pathogensis and immune response are examined in this review, as well as specific ways to reduce and eliminate pathology and related diseases. The virus naturally infects mucosal areas and begins the search for its target host cell. Upon binding to the host cell membrane via teams of glycoproteins, the virion is then phagocytosed.Soon the nucleus is seized and all regular host cell mechanisms are shut off. Replication of HSV-1 is specific encoding immediate early, early and late genes. Once the virus replication process is complete the virus exits epithelial cells near the site of infection through a process known as cell lysis. Sensory neurons are the specific target of HSV-1, where it can then travel to the trigeminal ganglia (TG) stoma via neur onal microtubular networks. Both innate and adaptive immune systems respond to the infection with various antibodies, interleukins and interferons.Once the virion reaches the nervous system, the immune responses are unable to detect it although they try to contain it as best they can. HSV-1 enters a latent stage, usually via latent associated transcripts, not causing pathogenesis but unable to fight off by means of the host immune system. Following a stressful situation or similarly UV activation, HSV-1 travels back down nerve fibers to re-infect cells near the original site of infection. This process is known to continue throughout the lifespan of the infected individual, normally without fatalities.When the host immune response is unable to contain the virus in the TG, several associated diseases such as encephalitis and keratits result. Genes involved with virus replication and host genes, to eliminate the virus, have been maneuvered to cause reverse effects and are currently use d as antivirals. Although no vaccine has been approved for use against HSV-1, various attempts have been made. This research paper defines the virus infection at a molecular level as well as demonstrates modifications of the virus genes to cause reverse effects and investigates just a few of the diseases connected with HSV-1.Introduction Herpes simplex viruses type 1 and 2 are well known members of the family Herpesviridae, subfamily Alphaherpesvirinae, which cause lifelong, latent infection in humans. Herpes simplex virus type 1 (HSV-1) typically remains the cause of cold sores, gingivostomatitis, and skin lesions in the orofacial area, as well as many rare but fatal conditions (1). Herpes simplex virus type 2 (HSV-2) is primarily associated with genital area infection. Worldwide, approximately one third of people display clinical manifestations of HSV-1 infection (2).HSV-1 is neurotropic, infecting multiple cell types but establishing latency in the trigeminal ganglia (TG). HSV-1 reactivates, in response to certain stimuli such as emotional or physical stress or UV light, and is transported along nerve fibers to mucosal or cutaneous regions (1). Infected cells show signs of the nucleus changing shape and nucleolus displacement with a formation of multinucleated giant cells. Cells degenerate, lyse and vesicles of fluid containing the virus locate between the epidermis and dermal layer of the skin forming a lesion (2).Although HSV-1 infects a large percentage of the population, few actually show symptoms of disease. HSV Structure and Genome HSV-1 is an enveloped double stranded DNA (dsDNA) virus consisting of four elements. First, an outer envelope with glycoprotein spikes on its surface. Second, a tegument layer including several viral proteins important during HSV-1 infection. Third, an iscosahedral capsid surrounding the last compartment, the electron opaque core containing the dsDNA genome wrapped as a spool. The envelope is made up of 13 different viral g lycoproteins embedded in a lipid bilayer.The viral genome of 152 kb, encode the majority of the proteins of the mature virion. Covalently linked L (long) and S (short) components are broken down into unique long (Ul), flanked by ab and b’a’ repeated segments, and unique short (Us), flanked by ac and c’a’ repeated segments. Homologous recombination between terminal repeats results in four linear isomers at equimolar concentrations (see figure 1). All four isomers, including P (prototype), IL (inversion of the L component), IS (inversion of the S component) and ISL (inversion of both the S and the L component), encode 90 unique transcription genes essential for viral replication (3).HSV Replication Infection is first initialted by the attachment to the host cell glucosaminoglycans, usually heparin sulphate and chondroiton sulphate, with viral glycoprotein C (gC). This bond results in at least five glycoprtoeins, gB, gC, gD, gH and gL, binding to other cell surface receptors, such as Herpesvirus entry mediator or nectin 1? or ? (4). Fusion of the viral envelope follows, and the de-enveloped tegument capsid is transported to the nuclear pores via the microtubular network, where DNA is released into the nucleus.Nuclear pore complex accepts the viral DNA from the capsid, minimizing the diffusion of DNA to the cytoplasm, and the transfer is completed by nuclear pore proteins (5). The viral genome circularizes upon entering the nucleus, and transcription of the five immediate early genes (IE) is done by the host RNA polymerase II. Among the IE genes are ICP0, ICP4, ICP22, ICP27 and ICP47. Host transcription, RNA splicing and transport are inhibited during replication, known as host cell shut off. Early (E) viral genes encode enzymes in nucleotide metabolism and viral DNA replication and require the presence of IE genes.Viral E gene products, including viral DNA polymerase, single-stranded DNA-binding protein, origin binding protein and DNA helicase-primase, assemble on the parental viral DNA and start DNA synthesis in replication compartments. Three DNA replication origins bind by viral origin-binding protein, separate the DNA strands and initiate viral DNA synthesis. Expression of the late (L) genes begins and produces structural components of the virion. Capsid assembly occurs in the cytoplasm and the associated proteins are then transported to the nucleus.Progeny DNA concatamers are cleaved into monomers and are inserted into the capsid. Cleavage and packing of HSV-1 genome requires two cis-acting elements, pac1 and pac2. Next the nucleocapsid matures and egress by passing through the Golgi apparatus with the tegument layer and the virion envelope. (3) HSV Latency After infection of the mucosa or epithelial abrasion, HSV-1 enters sensory neurons near the site of infection and the tegument and nucleocapsid travel by retrograde axonal transport to cell neuronal soma releasing viral DNA and VP16, when the virus may en ter lytic replication or the latent state.Lytic replication results in neuronal cell death as described above. (2,3) During latency the genome circularizes and enters a heavily chromatinated state where no infectious virus is produced and the majority of viral gene expression is silenced. Latency associated transcripts (LAT), mRNA genes, are the only transcripts found in latent neurons (6). Expression of LATs is not absolutely required for maintenance of latency. Reactivation triggers the virus to be transported in the opposite direction, antrograde, and re-infection occurs at the initial site of infection. HSV and the Immune SystemThe immune response to HSV-1 includes both innate and adaptive immune responses. Innate immunity is the first line of defense including natural killer (NK) cells, macrophages, dendritic cells, and various cytokines and complement proteins. Initial response involves secreted proteins, such as defensins and complement proteins. Complement proteins bind HSV antigens resulting in the cleavage of complement molecules. This, followed by the formation of the membrane attack complex, destroys the virus. HSV gC blocks the complement cascade, counteracting the effects of complement.The adaptive immune response is triggered with B cell memory enhanced in response to the virus. An antiviral state is induced by infected epithelial cells and resident interferon producing cells (IPCs), secreting interferon ? and ? , priming the surrounding cells for apoptosis. Tumor necrosis factors ? (TNF-? ) is also produced by IPCs and acts as an autocrine signal stimulating differentiation of ICPs to dendritic cells. They can travel to the lymph nodes to stimulate CD4+ T cells to produce IFN-? and interleukin 10 (IL-10). After infection and replication, HSV-1 destroys infected cells and travels to sensory neurons.Polymorphonuclear leukocytes, macrophages, NK and TCR+ T cells infiltrate the TG, control the infection and prevent the spread of the virus to rear by cells, including the brain. The adaptive immune response is driven by the innate immune response. Antigen presenting cells migrate from the site of infection to the regional lymph node to present CD4+ and CD8+ T cells and B cells. Deficient complement cascades leads to less vigorous memory response to HSV-1. Antibodies against gD and the gH-gL complex are found to protect against HSV-1 and are observed as cross reactive to other strains of HSV.Macrophages engulf viral proteins and cell particles from lysed cells and also secrete cytokines favoring the T helper (Th) cell CD4+ response. CD8+ cytoxic T lymphocytes (CTL) are produced and they react with epitopes displayed on infected cells, which are then targeted for apoptosis. See figure 2. The IE protein ICP 27 contains potent CTL epitopes. The efficacy of gB to induce a CTL response suggests gB is the immunodominant antigen of HSV-1. (2) Beneficial Modifications of Genes Associated with Herpes Simplex Virus type 1 and Relative As sociated DiseasesOccasionally the immune system is unable to prevent HSV-1 from spreading to surrounding structures such as the eye. Ocular HSV-1 infection is termed herpetic keratitis, tissue destruction of the eye, and is currently treated with trifluridine or valacyclovir to inhibit HSV-1 DNA polymerase and terminate synthesis of the sugar backbone of viral DNA. The current antiviral compounds require phosphorylation by the infected cell, meaning the antiviral activity cannot take place until the infection has progressed to the point where specific viral thymidine kinase is synthesized.A new idea involves helicase-primase inhibitors acting to prevent the unwinding of the double-stranded DNA and the initiation of the new strand synthesis necessary for viral production. Kleymann et al. found a compound, BAY 57-1293, more potent and more effective than valacyclovir and unassociated with systemic toxicity to initiate the described mechanism. (7) A similar study explored the lesion as sociated with the tissue destruction of the cornea, specifically angiogenesis of stromal keratits (SK).The fibroblast growth factor 2 (FGF-2), a molecule known to stimulate cell growth to contribute to wound healing, was targeted to observe the antiviral activity via its effect on HSV-1 cell entry. FGF-2 inhibits HSV-1 from binding to heparin sulfate, thus hindering entrance into the host cell. Results of this study suggest severity and clinical SK could be significantly diminished by daily treatment of lesions with FGF-2 protein, due to accelerated epithelial wound healing. (8) Similarly, HSV-1 can surpass the immune response and travel to the brain. HSV-1 encephalitis is the most devastating consequence of HSV and the most ommon cause of fetal encephalitis. Early growth response 1 (Erg-1) is a zinc finger transcription factor expressed in neural tissue, and is induced during stress. It regulates growth, apoptosis, angiogenesis and development. Erg-1 is known to regulate several vi ral genes, including LATs, and is inducible by viral proteins. Erg-1 increases viral replication in infected cells and mortality in infected mice. Knockout of Erg-1 expression was shown to reduce the mortality by decreasing the viral loads to tissues in a study conducted by Shis-Heng Chen et al. 9) It has been demonstrated HSV-1 can induce increased activity of central norepinephrine or serotonin neurons, by activating the cell bodies located in the brain stem, following encephalitis. Increased brain stem activity of these neurotransmitters can impair glucocorticoids (GC) negative feedback receptors, activating cytokines IL-1 and TNF? , reducing the binding capacity of said GC receptors. Impaired control of the GC negative feedback regulation upon the hypothalamo-pituitary adrenal axis has been suggested as an important aspect in major depression. (10)Thrombin is a result of the generation of sequential proteolytic enzymes activating circular precursor enzymes and cofactors for bloo d clotting. HSV-1, HSV-2 and cytomegalovirus have been shown to avoid cellular control of coagulation initiation through the constitutive expression of procoagulant phospholipids and tissue factor. This allows the unregulated generation of thrombin because tissue factor can bind ciruculating factor VIIa, forming a cofactor-enzyme complex directly on the virus. ‘Tenase’ activity has been credited to HSV-1 encoded gC, which accelerates the FVIIa-dependent activation of FX.FXa associates with its cofactor V to convert prothrombin to thrombin. Assembly of FX and FV leading to thrombin generation has been demonstrated on the virus surface. Herpes virus genomic material has been associated with atherosclerosis plaque, thrombosis and atherosclerosis due to the unregulated production of thrombin. (11) It is well known NK cells aid in the fight against HSV-1 infection. Severe herpetic infections have been seen in NK -deficient patients, as well as early infiltrations of herpetic lesions by NK cells. This due to damage of HLA class 1 expression by HSV-1 and the lysis of HSV-1 infected targets by NK cells.E. Estefania et al. presented a study suggesting clinical symptoms of HSV-1 infection being more likely to happen among humans expressing the NK cell receptors KIR2DL2 and KIR2DS2. The genes encoding the receptors appear to increase the risk of recurrent infection, where the lack of the receptors is shown to protect from the disease. (1) Conclusion HSV-1 can cause severe recurrent disease in humans and establish lifelong infection in their hosts. Several antiviral approaches have been considered to counteract the effects of HSV-1 throughout the body yet no vaccine, to cure the infection from its host, has been accepted.Acyclovir, and its ester derivative valacyclovir, as well as penciclovir and its prodrug famciclovir, are the latest approved antiviral medications to battle HSV-1 infection. Several other strategies are currently under investigation such as potential therapeutic vaccines, cidofovir, and aqueous extracts in Africa. Past attempts of vaccines have utilized viral vectors, DNA vaccination, recombinant bacteria, cytokines to manipulate the immune response, novel adjuvants, innovative delivery systems and different routes of inoculation. Most of which have been successful in lab mice but none have been approved for human use.Therapeutic vaccines target symptomatic individuals, using DNA vaccines encoding various cytokines used to intentionally bias the immune system toward Th1 or Th2 responses. Different boosts with different cytokine adjuvants may be used to induce proper immune response. (2) Extracts from the eastern cape of Africa, Aloe ferox and Withania somnifera, confirmed morphological changes indicative of cytopathic effects that retard the replication and spread of HSV-1. (12) Furthermore, a hematopoietic stem cell transplant recipient developed mucosal HSV-1 infection, and while under acyclovir treatment, later show ed resistance to the antiviral.After developing hemorrhagic cystitis due to polyomavirus BK, cidofovir was prescribed and the patient profited from the broad spectrum anti-DNA virus activity with the disappearance of HSV-1 lesions. (13) In conclusion, as described above the mechanisms by which HSV-1 hijacks and hides out in its host, have been studied to great detail and are routinely manipulated. The particularly complex structure, as well as detailed means by which each gene in the large genome is activated and carries out its genes products, intrigue many scientists which continue to investigate and attempt a formidable vaccine against the virus.Studies among mice have proven effective, although HSV-1 is a very host specific infection, thus making trials of acceptable anitvirals and vaccines extremely difficult. The only slightly acceptable element of HSV-1 infection is, in rare cases where no reoccurrences is shown, and moreover there are many instances of asymptomatic carriers. Devastating incidence such as transferring HSV-1 to a neonate during delivery and schizophrenics showing decreased prefrontal grey matter due to HSV-1, are just a pinch of the terrifying effects of this virus, remaining in host TG until a stressful situation comes along. 14,15) Herpes Simplex Virus type 1 Genome (Figure 1) 00 Herpes Simplex Virus Type 1 Infection (Figure 2) Works Cited 1. )Estefania, E, et al. â€Å"Influence of KIR gene diversity on the course of HSV-1 infection: resistance to the disease is associated with the absence of KIR2DL2 and KIR2DS2. † Tissue Antigens 70. 1 (July 2007): 34-41. MEDLINE. EBSCO. [Library name], [City], [State abbreviation]. 19 Nov. 2008 . 2. )Ferenczy, Michael W. â€Å"Prophylactic Vaccine Strategies and the Potential of Therapeutic Vaccines Against Herpes Simplex Virus. † Current Pharmaceutical Design 13. 9 July 2007): 1975-1988. Academic Search Premier. EBSCO. [Library name], [City], [State abbreviation]. 19 Nov. 2008 . 3. )S hen, Y, and J Nemunaitis.. â€Å"Herpes simplex virus 1 (HSV-1) for cancer treatment. † Cancer Gene Therapy 13. 11 (07 Nov. 2006): 975-992. MEDLINE. EBSCO. [Library name], [City], [State abbreviation]. 19 Nov. 2008 . 4. )Clement, Christian, et al. â€Å"A novel role for phagocytosis-like uptake in herpes simplex virus entry. † Journal of Cell Biology 174. 7 (25 Sep. 2006): 1009-1021. Academic Search Premier. EBSCO. [Library name], [City], [State abbreviation]. 4 Sep. 2008 . 5. )Newcomb, William W, Frank P Booy, and Jay C Brown. â€Å"Uncoating the herpes simplex virus genome. † Journal Of Molecular Biology 370. 4 (20 July 2007): 633-642. MEDLINE. EBSCO. [Library name], [City], [State abbreviation]. 3 Sep. 2008 . 6. )Ramachandran, Srividya, and Paul R Kinchington.. â€Å"Potential prophylactic and therapeutic vaccines for HSV infections. † Current Pharmaceutical Design 13. 19 (2007): 1965-1973. MEDLINE. EBSCO. [Library name], [City], [State abbreviation]. 22 Nov. 2008 . 7. )Kaufman, Herbert E, et al. Efficacy of a helicase-primase inhibitor in animal models of ocular herpes simplex virus type 1 infection. † Journal Of Ocular Pharmacology And Therapeutics: The Official Journal Of The Association For Ocular Pharmacology And Therapeutics 24. 1 (Feb. 2008): 34-42. MEDLINE. EBSCO. [Library name], [City], [State abbreviation]. 19 Nov. 2008 . 8. )Kim, Bumseok, et al. â€Å"Application of FGF-2 to Modulate Herpetic Stromal Keratitis. † Current Eye Research 31. 12 (Dec. 2006): 1021-1028. Academic Search Premier. EBSCO. [Library name], [City], [State abbreviation]. 19 Nov. 2008 . 9. )Chen S, Yao H, Chen I, Shieh B, Li C, Chen S.Suppression of transcription factor early growth response 1 reduces herpes simplex virus lethality in mice. Journal of Clinical Investigation [serial online]. October 2008;118(10):3470-3477. Available from: Academic Search Premier, Ipswich, MA. Accessed November 22, 2008. 10. )Bener, Dafna, et al. â€Å"Gl ucocorticoid Resistance following Herpes Simplex-1 Infection: Role of Hippocampal Glucocorticoid Receptors. † Neuroendocrinology 85. 4 (Apr. 2007): 207-215. Academic Search Premier. EBSCO. [Library name], [City], [State abbreviation]. 19 Nov. 2008 . 11. )Thrombin paper 12. )Kambizi, L. , et al. Anti-viral effects of aqueous extracts of Aloe Xerox and Withania somnifera on herpes simplex virus type 1 in cell culture. † South African Journal of Science 103. 9/10 (Sep. 2007): 359-360. Academic Search Premier. EBSCO. [Library name], [City], [State abbreviation]. 10 Sep. 2008 . 13. )Andrei, G, et al. â€Å"Dual infection with polyomavirus BK and acyclovir-resistant herpes simplex virus successfully treated with cidofovir in a bone marrow transplant recipient. † Transplant Infectious Disease: An Official Journal Of The Transplantation Society 9. 2 (June 2007): 126-131. MEDLINE. EBSCO. Library name], [City], [State abbreviation]. 19 Nov. 2008 . 14. )Brown, Elizabeth L. , et al. â€Å"Effect of maternal herpes simplex virus (HSV) serostatus and HSV type on risk of neonatal herpes. † Acta Obstetricia & Gynecologica Scandinavica 86. 5 (May 2007): 523-529. Academic Search Premier. EBSCO. [Library name], [City], [State abbreviation]. 17 Sep. 2008 . 15. )Prasad, K. M. R. , et al. â€Å"Brain morphological changes associated with exposure to HSV1 in first-episode schizophrenia. † Molecular Psychiatry 12. 1 (Jan. 2007): 105-113. Academic Search Premier. EBSCO. [Library name], [City], [State abbreviation]. 1 Oct. 2008 .

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Near the end of the book the author shows the children finally accepting others as they are not for whom they want them to be. In â€Å"To Kill a Mockingbird†, there are many influential figures that help Scout and Gem mature over the course of the story as they overcome daily obstacles. During the story, Gem and Scout lose their innocence and develop a sense of maturity as time goes on. When Scout arrives at school, her teachers Mrs.. Caroline Is frustrated because she already knows how to read. Scout learns that ‘It Is not always proper to say bluntly what the truth is† (Lee, 20).As the chapter continued on, Scout realizes that Miss Caroline did to mean to offend her. Throughout the story characters are Judged based on their actions. Attic's lecture's Scout on how she needs to learn how people are and not who she wants them to be. The story takes place during a time of racial discrimination. Harper Lee wrote â€Å"There is nothing wrong with defending a black ma n† (30). Prejudice Is a common problem during the early quarter of the twentieth century. After Scours tantrum with Cecil Jacobs, Attic's says to Scout â€Å"Remember It's a sin to kill a mockingbird. â€Å"(Lee, 89).Since Scout couldn't comprehend what this meant, she had a talk with Mrs.. Maude. â€Å"Your father's right,† she said. â€Å"Mockingbirds don't do one thing but make music for us to enjoy †¦ But sing their hearts out for us. That's why It's a sin to kill a 50). Boo Rudely, the mysterious neighbor, Is an example of prejudice. On page 9 In â€Å"To Kill a Mockingbird† it says â€Å"Boo Rudely Is an example of prejudice, he Is not accepted to society because he Is different from others, and he is an erratic 9). In the beginning of the novel Scout, Gem, and Dill all see Boo as a bizarre man who never came out of his house.As the story continued on, Scout starts to realize who he really is as she matures. She finally became aware of all the wond erful things he has done. When Scout and Gem were playing outside, Scout discovers items in a tree. The whole time this was Boo Rudely showing compassion. On page 101 it shares â€Å"The court takes a white man's word over a black mans. The Judge convicted him guilty before he even read the case. â€Å"(Lee, 101). Attic's explains to Scout that no matter what color, size, or ethnicity a person is, everyone deserves to be treated with equality.Scout matures wrought the book by finally realizing that no one or creature should be harmed for causing peace or Joy. She finally understand how society really is. The theme of prejudice opens the eyes of many characters and changes their opinion on society. Some who provide love with no limits in this novel. Overtime Scout and Gem both learn how to love people. On page 22 Scout says, â€Å"Neighbors bring food with death and flowers with sickness and little things in between. Boo was our neighbor. He gave us two soap dolls, a broken watch and chain, a pair of good-luck pennies, and our lives.But neighbors give in return. We never put back into the tree what we took out of it: we had given him nothing, and it made me sad. â€Å"(Lee, 2) This quote is in the beginning of the book when they both Judged Boo Rudely. After he gave them all of these wonderful items they finally start to realize he is a compassionate man. He is beyond lonely and Just wants someone to accept him for who he is, not what others see him as. â€Å"One time Attic's said you never really knew a man until you stood in his shoes and walked around in them; Just standing' on the Rudely porch was enough.The summer that had begun so long ago had ended, and another summer had taken its place, and a fall, and Boo Rudely had come out. Said Scout. â€Å"(Lee, 40). Scout is talking about how as she grew older she finally starts to realize what it really means to show others what it means to care. It also shows that she is learning to accept a man who is kn own to be erotic. On the last few pages of the novel, Boo and Scout are walking home. It states â€Å"l started to see another life through Boob's eyes. This quote is beyond important for how the children mature throughout the story.