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Platos Laches - 1027 Words

During his lifetime Socrates’ various interactions with his fellow Athenians left his intentions debatable. Popular belief in Athens seemed to be that, â€Å"he [Socrates] was an evildoer, and a curious person, who searches into things under the earth and in heaven ¸ and makes the worse appear the better cause† (Plato, pg. 5) as stated by the unofficial charges against him in The Apology. After discussions, his interlocutor’s were left confused in a state of aporia, with no conclusion. And so while negative views of Socrates became increasing popular in Athens right up until his death, Socrates was, on the contrary, serving as Athens’s benefactor, opening up their eyes to the truth of world in which they lived in. In Plato’s Laches, Socrates†¦show more content†¦However, other Athenians eventually grew tired of Socrates’ extensive questioning and can be seen in The Apology putting Socrates on trial for it. Instead of taking Socrate s’ conversations for what they were worth, they labeled him as argumentative and a man who was corrupting the youth of the city. By breaking down his interlocutors’ various thoughts, ideas, and theses, Socrates was trying to reveal to them that they were not in fact wise and that the knowledge they thought they possessed was not true knowledge. Socrates himself was only considered wiser than his fellow Athenians because he considered his one piece of knowledge to be that he didn’t know anything. By breaking down, piece by piece, the arguments of those he conversed with, he intended for them to realize that their knowledge was relative and therefore meaningless in the grander scheme of things. By recognizing this, only then could they begin living a life in search of finding true meaning. In searching for meaningful things they would have to learn to question things. While he is on trial in The Apology, Socrates tells the jury that, â€Å"The unexamined life is not worth living† (Plato pg. 24) Living life without asking questions, and without inquiry, is not living life at all, and is ther eforeShow MoreRelatedHow Xenophon’s Oeconomicus is a Response to Aristophanes’ Clouds1043 Words   |  5 Pagespresents much of his thought in a manner that requires readers to constantly keep in mind Plato’s thought but also diligently strive to discern Xenophon’s voice. We can easily recognize the relation of Xenophon’s Apology of Socrates to the Jury to Plato’s Apology of Socrates and Xenophon’s Symposium to Plato’s Symposium, and recently it has been proposed that Xenophon’s Education of Cyrus is a direct response to Plato’s Republic exploring grave difficulties Xenophon has with the best regime.1 We may thusRead MoreSocrates s Philosophy And Critical Analysis1138 Words   |  5 PagesDialogues via Plato’s words Socratic dialogues are manifestations of discussions between Socrates and notable men of Athens. These involve a sequel of different questions on themes such as friendship, piety, courage etc. These dialogues serve to be indirect in nature and thus leave the reader to undergo through a catharsis and analyze the beliefs of Socrates. Laches (Courage) This is a dialogue based on strife of two fathers,Lysimachus and Melesias, along with Nicias, Laches, Stesilaus andRead More Plato Essay example1737 Words   |  7 PagesCritias, was the leader of the Thirty Tyrants who were installed in power by the victorious Spartans. One means of perpetuating themselves in power was to implicate as many Athenians as possible in their atrocious acts. Thus Socrates, as we learn in Platos Apology, was ordered to arrest a man and bring him to Athens from Salamis for execution. When the great teacher refused, his life was in jeopardy, and he was probably saved only by the overthrow of the Thirty and the reestablishment of the democracyRead More A life sketch of Plato and his works Essays891 Words   |  4 Pageshis broad shoulders. Plato was born in Athens, Greece to one of the oldest and most distinguished families in the city. He lived with his mother, Perictione, and his father, Ariston (Until Ariston died.) Born in an aristocratic and rich family, Plato’s childhood was indulged within luxury. But his life changed when he came across Socrates. Socrates, a Greek philosopher who lived from 470-399 BC. He devoted all his time with young citizens discussing philosophy and questioning their confidence inRead MorePlato s Views On The Virtue Of The Virtues Essay1256 Words   |  6 Pages(Republic 354c) Plato presents Socrates as believing in the unity of the virtues, skeptical of those who, like Meno, wish to treat the virtues as distinct objects of inquiry in dialogues such as Laches, Protagoras, Meno, the Republic, and Euthyphro. These dialogues provide good reason to deny that Plato’s Socrates believed in the numerical identity of the virtues. I shall argue that in the various virtues is one essence (or ‘virtue’), as revealed in a conceptual search for definitional clarity andRead MoreCan Virtue Be Acquired? An Examination of the Laches, Meno and Protagoras2955 Words   |  12 PagesCan Virtue be Acquired? An Examination of the Laches, Meno, and Protagoras In the Socratic dialogues of Plato, Socrates often argues against the pretence of knowledge in his interlocutors. In the case of the Laches, Meno, and Protagoras dialogues, the pretence is the knowledge of virtue, among other things. The Laches seeks a definition of arà ªte (virtue), the Meno examines the teaching of virtue, and the Protagoras offers a known expert the chance to defend that virtue can, indeed, be taught. UsingRead MoreThe Republic Essay1514 Words   |  7 Pagesboth Solon and Pisistratus. Platos parents were Ariston and Perictone, his older brothers were Adeimantus and Glaucon, and his younger sister was Potone. In keeping with his family heritage, Plato was destined for the political life. But the Peloponnesian War, which began a couple of years before he was born and continued until well after he was twenty, led to the decline of the Athenian Empire. The war was followed by religious movement that led to the execution of Platos mentor, Socrates. TogetherRead Mor e Sport, Education, and the Meaning of Victory Essay examples3416 Words   |  14 Pagessummed up in a word: winning. Is this a sign that we have lost touch with the age-old rationale for including sport in education? I argue that it need not be by showing that we value winning precisely for the virtues associated with it. I then take Platos traditional parts of aretà ª: piety, sophrosunà ª, courage and justice and show how they are manifest in modern athletic ideals of self-knowledge, discipline, courage and justice. To the extent that scholastic athletic programs develop these virtues,Read More Plato on Education as the Development of Reason Essay3512 Words   |  15 Pagesa person never falters to the end of life, this is no more than moral luck. One is still guilty on the level of the logos, and liable to blame and punishment not for what one does, but for what one could have done. The unexamined life, says Platos Socrates, is not worth living for men (Apology 38a5). Two central ideas of Western philosophy came together in this saying, and also a third, Socrates own great innovation. The novelty was not his turning towards man; in this he was but a childRead MoreGreek Philosophers Bible On The Ancient World And English I2969 Words   |  12 Pages Socrates enrolled in the army, fulfilling the position of a hoplite, a type of Greek soldier. He served in Athens military during the Peloponnesian War. Several accounts describe Socrates’ service in the war including writings from Alcibiades, Laches, and Socrates himself. Alcibiades describes how Socrates saved his life in the battle of Potidaea. The trial of Socrates was one of the most controversial trials in the ancient world. Socrates praised Sparta, Athens rival, because of their government

Herpes Simplex Virus Free Essays

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. We will write a custom essay sample on Herpes Simplex Virus or any similar topic only for you Order Now 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 neuronal 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 used 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 glycoproteins 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 enter 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 System The 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 Associated Diseases Occasionally 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 associated 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 viral genes, including LATs, and is inducible by viral proteins. Erg-1 increases viral replication in infe cted 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 blood 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 showed 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. )Shen, 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"Glucocorticoid 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 s implex 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 . How to cite Herpes Simplex Virus, Papers

Psychodelic Drugs Essay Example For Students

Psychodelic Drugs Essay Psychodelic Drugs AlcoholAlcohol is one of the most widely used drugs in this society. It isaccepted as a part of social life. Its use is widely promoted via sponsorship ofsporting events. Advertising infers that drinking is the path to happiness,success, romance, etc. There are references to alcohol and its effects fromearliest known writings. Alcohol is consumed in the beverage form and soldlegally in this state to persons over 21. Alcohol is absorbed directly into the bloodstream through the stomachand small intestine. It is distributed by the blood throughout the body,affecting literally every organ it touches in a matter of minutes. Enzymes inthe liver metabolize alcohol at a rate of 10-15 ml (less than one half ounce)per hour. Hence, only time can sober someone up. Coffee, cold showers, orexercise do not work. The warm glow of disinhibition, letting go is a major desired effectof alcohol. People feel more sociable and talkative with small amounts of thedrug. Alcohol is a relaxant, so many people drink to unwind from the demands oflife. Because alcohol has been around for so long, its effects are well-known. Two key concepts to understand in dealing with alcohol use and abuse areimpairment and tolerance. They are both problems in themselves and signals ofpossible additional difficulties. IMPAIRMENT refers to the deficits in performance, judgment, memory, andmotor skills which occur because of alcohol consumption. Impairment becomesnoticeable at blood levels of 0.05%, which can occur when as few as two drinksare consumed in an hour by a 160 pound person. The deceptive part aboutimpairment is that, by definition, impaired judgment cannot recognize its ownimpairment. The individual thinks he or she is functioning well, when actuallys/he is not. Later, there is impaired memory of the impaired performance. TOLERANCE means that a drug loses some of its effect with repeated use,and that higher and higher doses are needed. It is the bodys way of adapting tohaving a foreign substance in the system. People develop a high tolerance to alcohol when they drink a great dealover an extended length of time. WHILE TOLERANCE MAY SEEM TO SOME TO BE ADESIRABLE STATE, IT SIGNIFICANTLY INCREASES THE RISK OF ALCOHOLISM AND LONG-TERMHEALTH AND SOCIAL PROBLEMS. For example, a heavy drinker could still be lucidat 0.25%, whereas the average person would barely be able to function. Even so,the heavy drinker would be extremely dangerous on the highway. Thirteen percent of male and five percent of female college studentsnationwide are alcoholic. Persons are considered alcoholic if they exhibit threeor more of the following symptoms for more than one month, or if the symptomsget repeated over a longer period of time:1.Alcohol is consumed in greater quantities or for longer periods oftime than the person intended; 2.The individual has a persistent desire tocontrol or eliminate drinking, or has made one or more unsuccessful efforts todo this (for example, there are resolutions to cut down, but these effortsdisappear after a period of time); 3.Considerable time is spent in obtaining,using, or recovering from alcohol and its effects; 4.Intoxication or itsaftereffects (e.g., hangovers) frequently occur at times when the person isexpected to fulfill work, family or school obligations; or there is physicallyhazardous use (e.g., while driving); 5.The individual gives up or reduces social,recreational or job-related activities because of alco hol use; 6.Drinkingcontinues despite the knowledge that alcohol causes the person to have social,psychological or medical problems; 7.Significantly increased tolerance hasdeveloped; 8.Withdrawal symptoms occur when initially attempting abstinence(e.g., flu-like symptoms, headaches, gastrointestinal distress, sweatiness, moodswings, irritability, anxiety); 9.Alcohol or other drugs are used to ward offthe withdrawal. Other long-term medical problems include high blood pressure, increasedrisk of heart attack, pancreatitis, various cancers, cirrhosis of the liver. Chronic heavy drinking in men is associated with testicular atrophy and breastenlargement. In women, as little as one drink a day greatly increases the riskof breast cancer. Drinking during pregnancy can cause birth defects and mentalretardation. Alcohol is also fattening. One glass of wine daily added to the diet canresult in a weight gain of ten pounds a year. Cocaine and CrackCocaine is an alkaloid extracted from the leaves of the coca plant. Itis a stimulant and euphoric substance that has powerful effects on the humanbrain. The practice of sniffing (snorting) cocaine actually dates back to thebeginning of this century as knowledge spread about cocaines ability to inducefeelings of well-being and increased energy. At that time, cocaine was alsoavailable in over-the-counter tonics and potions. Crack is cocaine that has been processed so that it can be smoked. It isgenerally sold in small quantities and distributed in small glass vials or smallplastic bags. When crack is smoked, it produces an immediate, short-lived effect. Intravenous use (shooting up) also results in rapid onset of effects, whilethe effects of sniffing are delayed several minutes. The onset of the high, or rush, from cocaine and crack is reported byusers to be intense and pleasurable. Some users have called the rush an orgasmof the brain. The rush lasts only a few seconds, followed by a 20 minute high. Individuals report an increased sense of well-being and self-confidence, alongwith a decrease in fatigue and hunger. Some people report that they experiencecocaine as an aphrodisiac. There is a social aspect to cocaine use as well, ascocaine is frequently obtained from friends and consumed in small get-togethers. Cocaine (and in particular crack) is one of the most addictive drugsknown to humankind. Laboratory studies have shown that animals, when offered theoption to self-administer cocaine, will continue to administer the drug untilthey die, ignoring their needs for food and water. It is reported that as many as one out of every three crack users becomeaddicted to cocaine. There is no scientific way to predict who will becomeaddicted. However, there has been a good deal of news media attention given tostories of successful people who have lost themselves, their jobs, fortunes, andfamilies because of their involvement with cocaine. The problems cocaine causesin peoples lives are so severe and the pull to use the drug again is so strongthat it generally takes people two years of rehabilitation to recover from acocaine addiction, once they seek treatment. Crack is a very rapidly addicting form of cocaine, with addiction oftenbecoming apparent within a matter of weeks. Some users have reported becomingaddicted after their first experience with this form of cocaine. Thus crack isan especially dangerous form of the drug. Food Processing And Preservation EssayRepeated use of the drug produces tolerance (that is, the drug becomesineffective), and it can produce a crash. A recent study found that one of the by-products created when Ecstasy ismetabolized is a toxic substance harmful to nerve endings. This seems to causeParkinsons disease-like symptoms in persons as young as 30 years of age. Thesesymptoms do not appear immediately, but may occur after a period of time. Theyare apparently non-reversible. MushroomsThere are a number of plant materials which have LSD-like effects andwhich come under the heading of mushrooms or shrooms as they are often called. These include the psilocybe mexicana and several other species which have theactive ingredient psilocybin. Mushrooms are generally dried and then eaten. Mescaline originally came form the buttons which grow on the top of peyotecactus. Several varieties of psilocybin mushrooms grow and are illegallymarketed in the Northwest. The initial effects of psilocybin are experienced in 30 minutes and thehigh generally lasts several hours. Small doses can reportedly produce feelingsof physical and mental relaxation and pleasant changes in mood and perception. Larger doses can produce marked changes in perception, with the userexperiencing effects similar to those found with LSD. With mescaline, the effects appear slowly and last from 10-18 hours. Commonly reported effects include euphoria, heightened sensory perception,visual hallucinations, alterations in body image, and some muscular relaxation. With regard to perceptual processes, the unpleasant effects of thesedrugs are similar to those found with LSD. In addition, psilocybin can causedizziness, light-headedness, abdominal discomfort, numbness in the mouth, nausea,vomiting, shivering, facial flushing, sweating, and fatigue. With mescaline,nausea and vomiting frequently occur, and high doses can produce low bloodpressure, cardiac depression, slowed respiration, and headache. These sideeffects have the potential to be medically serious. Both psilocybin and mescaline can be manufactured in the laboratory. MarijuanaMarijuana consists of the dried leaves and flowering tops of the hempplant (cannabis sativa). The plants principal psychoactive ingredient is delta-9 THC (tetrahydrocannabinol). Hashish or hash is the dried resin from the topsand leaves of the female plant. It contains a higher concentration of the THCand is therefore more potent. Both marijuana and hash are usually smoked. When smoked, the effects of marijuana produces a feeling of euphoriawhich gives rise to a tendency to talk and laugh more than usual. Color, sound,and taste, touch and/or smell may be enhanced and experienced as pleasant andfascinating. Muscular relaxation may occur, as well as a sense of well-being andrelief from tension. Cannabis impairs the ability to perform complex motor tasks such asdriving a car. It also impairs short-term memory and logical thinking. At veryhigh doses, effects can be similar to those of hallucinogens, and the user canexperience confusion, restlessness, hallucination, paranoia, and anxiety orpanic. These problems have become more noted in recent years, as the strains ofmarijuana now available are many times more potent than the marijuana of theearly 1970s. Heavy use appears to interfere with brain cell functioning, producingproblems with sequencing ability, time sense, depth perception, memory storage,and recall. Chronic heavy users sometime demonstrate apathy, loss of energy,confusion, and memory problems. Long-term use of THC is also associated with lower sperm counts in malesand alterations in sperm shape and mobility. In women, irregularities inmenstruation and ovulation occur. Pregnant women who are heavy marijuana smokershave higher levels of miscarriages, still-births and genetic disorders. Marijuana smoke contains more cancer-causing agents than tobacco smoke. Laboratory studies have shown pre-cancerous cellular changes in the lung tissueof long term users. Warning SignalsSigns That The Chemical Has Taken ControlThe following symptoms and behaviors, when related to chemical use(including alcohol, of course), indicate that a person has seriouslyoverindulged. Beyond this, these symptoms could indicate a more serious problemor addiction: MEDICALAccidents or injuries Nausea and vomiting Mysterious bruises Gastritis Blackouts (cannot remember something while drinking) Passing out(unconsciousness) Emergency room visitsACADEMIC/EMPLOYMENTAcademic failure/poor work performance Missing classes/absenteeism from work Not living up to ones potential Difficulties with deadlines or procrastination SEXUALImpotence Sexual assault Inability to resist unwanted sexual advance Engaging in sexual activities that are contrary to valuesSOCIAL/PSYCHOLOGICALLoss of self-respect Mood swings Panic and unexplained fears Depression Property damage Paranoia Fights and arguments Social isolation and withdrawalProblems with legal or college authorities Causing emotion al pain to friendsor loved onesDRINKING/USING BEHAVIORSneaking drinks or drugs or using alone Hiding bottles/drugs Consuming morethan intended Inability to predict how much one will consume Using again rightafter sobering up Using to relieve anxiety, insomnia, pain or depression Usingto feel more confident in social situations Spending substantial amounts ofmoney on alcohol and drugs Preoccupation with next high Centering onesrecreational activities around chemicals Family members or friends expressingconcern about ones drinking or other drug use Feeling annoyed or angry whenones chemical use is discussed Inability to carry out an intention to cutdownState LawsThe following chart describes the penalties for POSSESSION of key drugs(the schedules are more inclusive) according to the Federal Drug Schedules:Max. Prison Time Max .Fine SCHEDULE #ClassHeroin, LSD, other hallucinogens marijuana, others 10 years$100,000 SCHEDULE II Class C Felony Methadone, morphine, amphetamines cocaine,PCP 5 years $100,000 SCHEDULE II Class A MisdemeanorsNon-amphetamine stimulants,1 year$2,500SCHEDULE IV Class CMisdemeanors some depressants1 Valium-type tranquilizers, some less potentdepressants 30 days $500SCHEDULE VViolation Dilutemixtures, compounds with small amounts of controlled drugsNone $1,000Delivery of less than five grams or possession or less than one ounce ofmarijuana is a violation. established mandatory evaluation, education andtreatment services for those under 18 years old. If services are successfullycompleted, the charge will be dropped. Alcohol is an illegal drug for those under 21 years of age. For a driverunder 18 ANY detectable amount of alcohol (above .00 BAC) is grounds for losingthe license. That pretty much sums it up for psychodelic drugs. I hope this proved toyou that if you use a psychodelic drug that you should stop, unless it is alcholbecause it is not as bad as LSD, pcp, or anything you have to inject or snort. So I sign out with I hope you learned something, I mean you had to you couldenthave know all of this information. BiblyographyName Year TypeMicrosoft Encarta96EncyclopediaDartmouth collage95Brochure White House97InternetSocial Issues