Nurse Anesthetists Essay Example for Free

Nurse Anesthetists Essay In a career in nursing, one must possess a need to help people, as well as the scientific and educational knowledge to perform the duties required. As I complete the final years of my high school education, I realize that I must focus on my goals and interests in order to make intelligent college curriculum decisions. I have always been considering a career in health, but the opportunities and diversification in the health field have perplexed me. I have always thought the job of a nurse anesthetist was extremely interesting, and it would be a great way to contribute to helping the lives of others. In the United States, a Certified Registered Nurse Anesthetist (CRNA) is simply an advanced practice registered nurse (APRN) who has acquired graduate-level education and board certification in anesthesia and they are the oldest nurse specialty group in the U. S. However, their job isn’t that simple. Anesthesia describes drugs and gases that help to block sensation, and they keep patients unconscious while in surgery. The main goal of the CRNA (Certified Registered Nurse Anesthetist), which is extremely important, is to have the patient awake free of pain. CRNAs, or Nurse Anesthetists, are responsible for administering, supervising, and monitoring anesthesia related care for those patients undergoing surgical procedures. Before the surgery, the CRNA obtains information regarding the patient’s medical history, evaluates the patient’s anesthesia needs, and develops a treatment plan with the goal of a risk-free and uncomplicated surgery. CRNA then explains the planned procedure to the patient, and answers any question that they may have. However, there are big steps that you have to take to become a CRNA. According to the American Association of Nurse Anesthetists (AANA), here is what you need to do to become a nurse anesthetist. All would-be nurse anesthetists must have an active registered nurse (RN) license, which requires a minimum of two years of study. Applicants to nurse anesthetist programs should have at least one year of work experience as an RN working in acute care, such as an intensive care unit. Once admitted to the Anesthesia program, the registered nurse must complete twenty-four to thirty-six months of classroom and clinical experience. A bachelors degree is the minimum required educational credential for certification as a nurse anesthetist. Many training programs are structured as masters degree programs, which always require a bachelors degree. Accredited Training Programs is the most important requirement to become a nurse anesthetist. Different programs have different specific requirements for application. Upon completion of the training program, prospective nurse anesthetists need to pass the certification examination offered by the Counsel on Certification of Nurse Anesthetists, and then maintain certification by regularly taking continuing educational units. Nurse anesthetists must obtain the appropriate licenses to practice in their state by contacting the state board of nursing for more information.

Moral Decisions In Daily Life

Moral Decisions In Daily Life Moral decision making is something every human does on a daily basis, modifying their behavior to obey standards of society which are based upon a shared system of values. In its most simplistic form, moral decision making is done with ethical motives in mind, concerned with the distinction between right and wrong by each individual. Moral decision making models and theories provide specific guides and rules to help individuals unravel their moral deliberations. Two of the most well-known moral decision making models in philosophy are consequentialism and deontological theory, both of which have strengths and weaknesses. The two models do share some commonality but there are many issues at which they stand at opposition. All of this must be taken into consideration before choosing which moral decision making model best fits an individual. The consequentialist moral decision making theory states that an action is considered morally right provided that the consequences which result are more positive than negative. A good aphorism for describing the backbone of consequentialism is that the ends justify the means. Provided that a good outcome results from an act, that act is considered morally just. Consequentialism can be agent-neutral or agent-focused and the two approaches are worth discussing to better understand the moral decision making model. Agent-Neutral consequentialism ignores the specific affect an action has for any certain individual and instead focuses on the consequences benefitting all. Agent-Focused consequentialism, on the other hand, is when the results of the moral decision are concentrated on the needs of the decision maker. This means that the moral actor makes their decision so that consequences resulting better themselves and the welfare of those they care about and not just the general welfare of society. The deontological moral decision making theory is a different form of moral reasoning than consequentialism for a variety of reasons. As opposed to consequentialism, deontological moral theory states that the rightness of an action or decision is not solely dependent upon maximizing the good of society. Instead, deontological theory defines the morally rightness or wrongness of an action from the behavior of the action itself, not the behavior of the outcome. Deontological moral decision making provides distinct guidelines for morally right and wrong behavior for individuals to use when making day to day choices. This deontological moral guide places a higher value on the individual than on maximizing the good for society. In fact, deontology actually has constraints to stop an individual from maximizing the good if it hinders following the moral standards of the guideline. Deontology is more open to interpretation than consequentialism, however, because it remains flexible for self- interpretation. Consequentialism possesses strengths as a moral model that deontology does not. One of the strongest points in favor of consequentialism is actually another theory which resulted from it known as utilitarianism. Utilitarianism was founded by Jeremy Bentham, an English philosopher, who believed that the best moral action would result in the greatest good for the largest amount of people. Following it allows for relaxed tensions in society ensuring that the most people feel pleasure, rather than a large amount of individuals on edge or in pain. However, consequentialism possesses weaknesses in its moral decision making too. Consequentialism causes irresolvable morality dilemmas as it requires correlating principles which cannot be compared against one another on the same scale. A resulting weakness of utilitarianism is that it is so focused on the interest of all that it overlooks the rights of the individual which can lead to injustice. The most unavoidable weakness of consequentialis m is that is does not provide any direction to its followers for which actions are right or wrong, morally. The wrongness of the action can only be determined by its consequences and by that time its too late to change the decision. Deontological moral theory also possesses its own unique strengths and weaknesses. One of the advantages of deontological morality is that it allows the individual to take into account their families, friends, and personalized plans when making ethical decisions, as opposed to consequentialism which tends to be alienating in its decision making module. By putting more stress on the self-worth and personal capital of the individual deontology results in a less flawed moral theory. Immanuel Kant, a well-known deontological philosopher, and his Kantian ethics are a strength of deontology as well because he stated that its not the consequences of the actions that are right or wrong but rather the motives of the person doing the action. This forces the agent to take responsibility for all parts of their moral decision making, not only the results. However, the biggest weakness of deontology is that it categorizes actions as right or wrong, black or white, leaving no room for any gray area despite the obvious existence of many moral gray areas. Deontology is also hard to follow because its stringency leaves its followers feeling unguided by their morals which lack prioritizing, ultimately causing confusion. These are only two moral decision making models in philosophy and neither are necessarily the ideal. It is my belief that the ideal moral decision making process must combine the strengths of consequentialism and deontology while attempting to compensate for their errors. The best decision making process must involve an individuals own moral beliefs combined with the knowledge that can be gained from studying a large amount of moral theories and opinions. Morals are subjective, meaning that each person or group of people may possess their own set which differs from those of others. This is why the ideal process must be personalized to meet the needs of the individual following it. This compensates for deontologys inadequate claim of unchanging principles known as universal law. However, it should include the aspect of deontology that forces a person to be morally responsible for their own actions as this is its best idea. By forcing an individual to take into account how their decisi on will affect them and their own rather than society, leads, I believe, to better moral decisions being made. This combination decision making theory will also make use of the principle of utility, the best idea of Jeremy Bentham, which teaches individuals to do the greatest amount of good for the greatest amount of people. This combined with deontologys focus on the individuals rights dissipates the danger of consequentialism justifying genocide, torture or violence as necessary means to a morally right end. The ideal moral decision making process is difficult to pinpoint, as morals vary by individual and are subjective to different opinions from one person to the next. However, there are aspects of modern philosophical theories, consequentialism and deontology, which can be studied and used to help create an ideal guideline. Consequentialism is important because it focuses on the results of an action for the good of humanity, something which cannot be overlooked in an increasingly globalized world. Deontology forces the moral agent to take responsibility for their own actions instead of relying on someone else to care, just as important to maintaining moral societal standards. Together the two create checks and balances, which, when combined with an individuals beliefs, allow for moral decision making to occur with limited room for error.

Mechanisms drug resistance to cancer chemotherapy

Mechanisms drug resistance to cancer chemotherapy Introduction Cancer is one of the major causes of death in the developed world and statistics show that one in three people will be diagnosed with cancer during their lifetime [1]. Cancers are malignant tumours and can be distinguished from normal cells by four characteristics; uncontrolled proliferation, dedifferentiation and loss of function, invasiveness, and ability to metastasise [2]. These characteristics are caused by altered gene expression, as a result of genetic mutations that inactivate tumour suppressor genes and / or activate oncogenes. Most cancer chemotherapeutic drugs affect only one characteristic aspect, which is uncontrolled proliferation [3]. In many cases the antiproloferation action is caused by damage to DNA, which initiates apoptosis and cell death [4]. As their main target is cell division, they affect all rapidly dividing cells, including normal cells. This produces general toxic effects, such as myelosuppression, alopecia, damage to gastrointestinal epithelium, sterility and severe nausea and vomiting. Besides the toxic effects of chemotherapy, another major problem is chemoresistance [5]. Resistance to chemotherapy is when the cancer cells do not respond to the drugs. It can be inherented, as a genetic mutation, or it can be acquired, as a cellular response to drug exposure. Mechanisms of resistance include: increased efflux or decreased influx of cytotoxic drugs; insufficient activation of the drug; increased inactivation of the drug; increased concentration of target enzyme; rapid repair of DNA lesions; or mutations in various genes. When patients develop resistance, multiple drugs with different pathways of entry and different cellular targets are used. However, cancer cells can become multidrug resistant, a phenomenon due to cells expressing mechanisms that cause simultaneous resistance to many different, structurally and functionally, unrelated drugs [6]. Multidrug resistance, generally, results from over expression of ATP-dependent efflux pumps [5]. These pumps have broad drug specificity and belong to a family of ATP-binding cassette (ABC) transporters, of which P-glycoprotein (PGP) is one of the most important members. Increased drug efflux, via these transporters, lowers intracellular drug concentration, allowing cancer cells to escape the toxic effects of the drugs. PGP inhibitors are being developed to overcome multidrug resistance and two that have reached clinical trials are varapamil, a calcium channel blocker, and cyclosporin A, an immunosuppressant [7]. The remainder of this review will focus on the different chemotherapeutic agents currently being used for the treatment of cancer and their mechanism of action. Also the main mechanism of resistance to these drugs will be explored, particularly focusing on the role of P-glycoprotein and how it can be modulated to reverse drug resistance. Drugs used in cancer chemotherapy Drugs used in the treatment of cancer are summarised in table 2. They are grouped into: cytotoxic drugs, which preferentially but not exclusively target rapidly dividing cancer cells; hormone therapy, which is a more specific form of treatment used for tumours derived from hormone sensitive tissues; and miscellaneous agents, which include a number of recently developed drugs such as monoclonal antibodies. Cytotoxic drugs Cytotoxic drugs can be further divided into the following; alkylating agents, which act by forming covalent bonds with DNA and impeding replication; antimetabolites, which block one or more of the metabolic pathways involved in DNA synthesis; cytotoxic antibiotics, which are of microbial origin and prevent cell division by directly acting on DNA; and plant derivertives, which affect microtubule function and hence the formation of the mitotic spindle. Alkylating agents Alkylating agents form carbonium ions, which are highly reactive and interact instantaneously with nucleophilic sites such as N7 of guanine in DNA [8]. They are bifunctional, which means they have two alkylating groups, and can cause intra- or inter-chain cross-linking between DNA strands. This prevents strand separation for DNA synthesis or transcription. They can also cause base mispairing between strands, which interferes with the progression of the replication fork [3]. These actions block DNA synthesis, causing a block at G2 phase and subsequently apoptotic cell death. Alkylating agents currently being used in chemotherapy primarily belong to the following families: nitrogen mustards (Cyclophosphamide, Chlorambucil, Melphalan, Ifosfamide, Busulfan); nitrosoureas (Carmustine, Lomustine, Fotemustine); aziridines (Thiotepa); Dacarbazine and platinum compounds (Cisplatin, Carboplatin, Oxaliplatin) [9]. Nitrogen mustards, nitrosoureas and aziridines are believed to kill tumour cells by inducing DNA inter-strand cross-links, while platinum compounds induce intra- and inter-strand cross-links, as well as DNA-protein cross-links under certain circumstances [8]. Resistance to these drugs can develop as a result of cancer cells rapidly repairing drug induced lesions [10], which will be discussed in detail later. Antimetabolites Antimetabolites interfere with the metabolic pathways involved in DNA synthesis. An example of an antimetabolite is Methotrexate, which is a folate antagonist [11]. Folates are essential for the synthesis of purine nucleotides and thymidylate, which in turn are essential for DNA synthesis and cell division. Folates are actively taken up into cells by the reduced folate carrier (RFC), where they are converted to polyglutamates. Polyglutamate folates are then reduced to tetrahydrofolate (FH4) by the enzyme dihydrofolate reductase (DHFR). Methotrexate exerts its action by being taken up into cells by the follate carrier, and like folate being converted to the polyglutamate form. It has a higher affinity for DHFR than the endogenous folate and thus inhibits the enzyme, depleting intracellular FH4, and therefore hindering DNA synthesis. Another example of an antimetabolite is Fluorouracil, which is a pyrimidine analogue [12]. It interferes with DTMP synthesis by forming a ternary complex with thymidylate synthetase (TS); the enzyme that produces DTMP. DTMP is required for the synthesis of DNA and purines, so the irreversible inhibition of the enzyme by fluorouracil results in is inhibition of DNA but not RNA or protein synthesis. Fludarabine is a purine analogue, which is another group of antimetabolites [13]. It is metabolised to its triphosphate form, which inhibits DNA polymerase. As well as the general side effects associated with chemotherapy, patients may develop resistance to antimetabolites; due to a decreased amount of drug uptake [14] or altered concentration of target enzymes [15], which will be discussed later. Cytotoxic antibiotics Cytotoxic antibiotics, such as the anthracyclines (Doxorubicin, Idarubicin, Daunorubicin, Epirubicin, Aclarubicin, Mitoxantrone) bind to DNA and inhibit both DNA and RNA synthesis [16]. Their main cytotoxic action is mediated through an inhibitory effect on topoisomerase II, the activity of which is markedly increased in proliferating cells. During DNA replication, reversible swivelling needs to take place around the replication fork in order to prevent the daughter DNA molecule becoming inextricably entangled during mitotic segregation [17]. The swivel is produced by topoisomerase II, which nicks both DNA strands and subsequently reseals the breaks. Doxorubicin intercalates in the DNA, and its effect is in essence, to stabilise the DNA-topoisomerase II complex after the strands have been nicked, thus halting the process at this point [18]. Dactinomycin is also a cytotoxic antibiotic, which intercalates in the minor groove of DNA, interfering with the movement of RNA polymerase along the gene and thus preventing transcription [19]. Bleomycins are a group of metal-chelating glycopeptide antibiotics that degrade preformed DNA, causing chain fragmentation and release of free bases [20]. This action is thought to involve chelation of ferrous iron and interaction with oxygen, resulting in the oxidation of iron and generation of superoxide and/or hydroxyl radicals. They are most effective in the G2 phase of the cell cycle and mitosis, but are also active against non-dividing cells, that is cells in the G0 phase. This class of drugs cause resistance by altered activity of topoisomerase II, aswell as reduced uptake of the drugs [21]. Plant derivatives One sub group of plant derivatives is the vinca alkaloids, which includes Vincristine, Vinblastine, Vindesine and Vinorelbine [22]. They bind to tubulin and inhibit its polymerisation into microtubules. This prevents spindle formation in dividing cells, which causes arrest at metaphase. They also inhibit other cellular activities that involve microtubules, such as leucocyte phagocytosis, chemotaxis and axonal transport in neurons. They are relatively non-toxic in comparison to the previously mentioned cytotoxic drugs. Another group of plant derivatives is the taxanes, which include Paclitaxel and Docetaxel [23]. They act on microtubules by stabilising them, in effect freezing them in the polymerised state, which achieves a similar effect to that of the vinca alkaloids. Campothecins is another group of plant derivatives and include Irinotecan and Topotecan [24]. They bind to and inhibit topoisomerase I; high levels of which occur throughout the cell cycle. Hormone therapy Tumours derived from hormone sensitive tissues may be hormone dependent [25]. This is due to the presence of steroid receptors in the malignant cells. Their growth can be inhibited by agents with apposing actions, hormone antagonists or drugs that inhibit the endogenous hormone synthesis. The most important group of drugs used to treat cancer are the steroids, namely the glucocorticoids (Prednisolone and Dexamethasone), oestrogens (Diethylstilbestrol and Ethinyloestradiol) and gonadotrophin-releasing hormone analogues (Octreotide and Lanreotide), as well as agents that antagonise hormone action (Tamoxifen, Toremifene and Fulvestrant). Such drugs rarely act as a cure but do mitigate the symptoms of the cancer and thus play an important part in the clinical management of sex-hormone-dependant tumours. Miscellaneous agents Crisantaspase Crisantaspase is a preparation of the enzyme asparaginase and therefore, like asparaginase, can break down asparagine to aspartic acid and ammonia [26]. It is active against tumour cells, such as those of acute lymphoblastic leukaemia, which have lost the capacity to synthesise asparagine and therefore require an exogenous source. As most normal body cells are able to synthesise asparagine, the drug has a fairly selective action and very little suppressive effect on the bone marrow, the mucosa of the gastrointestinal tract or hair follicles. Monoclonal Antibodies Antibodies are immunoglobulins that react with defined target proteins expressed on cancer cells. This activates the hosts immune response, which kills cancer cells by complement-mediated lysis or by killer cells. Monoclonal antibodies can also attach to and activate growth factor receptors on cancer cells, thus inhibiting the survival pathway and promoting apoptosis. Rituximab is a monoclonal antibody that is licensed (in combination with other chemotherapeutic agents) for treatment of certain types of lymphomas [27]. It lysis B lymphocytes by binding to the calcium- channel forming CD20 protein and activating completment. It also sensitises resistant cells to other chemotherapeutic drugs. Trastuzumab (Herceptin) is a humanised murine monoclonal antibody that binds to a protein termed HER2 (the human epithelial growth factor receptor 2); a receptor with integral tyrosine kinase activity [28]. It induces the host immune response as well as inducing the cell cycle inhibitors p21 and p27. Imatinib Mesylate Imatinib is an inhibitor of signalling pathway kinases [29]. It inhibits the platelet-derived growth factor (PDGF); a receptor tyrosine kinase, and the Bcr/Abl kinase; a cytoplasmic kinase. These are considered to be unique factors in the pathogenesis of chronic myeloid leukaemias. Imatinib is licensed for the treatment of this tumour when it has proved to be resistant to other therapeutic strategies, as well as for the treatment of some gastrointestinal tumours that are not susceptible to surgery. Resistance to Anticancer Drugs As mentioned previously patients can develop resistance to many chemotherapeutic agents. This can be caused by a number of mechanisms, which are summarised in figure 1. A decrease in the amount of drug taken up by the cell Resistance can develop as a result of decreased drug uptake. This can be due to the loss of transporter function, for example RFC [30]. Decreased influx of Methotrexate in tumour cells has been widely associated with decreased RFC gene expression. Down-regulation of the transporter protein is due to alterations in the transcription and translation factors. Transcriptional factors, such as the Sp1 family, CREB (cyclic AMP-response element binding protein) and p53, regulate RFC gene expression [31]. Therefore loss of function of these transcription factors cause silencing of the RFC gene, which results in reduced protein level. Also post-translational modifications of transcription factors alter phosphorylation patterns, which abolishes Sp1 and CREB function thereby resulting in loss of RFC gene expression and subsequently resistance [32]. Mutations in the human RFC gene can also decrease drug influx. Jensen et al (1998) have reported a mutation that causes marked changes in the kinetic properties of RFC mediated transport of folates [14]. The structurally altered RFC was functionally characterized by a 9- and 31-fold increased affinity for transport of reduced folate cofactors and folic acid, respectively. This allowed the accumulation of intracellular folates, which sustained cell growth and DNA replication, allowing cancer cells to escape the cytotoxic effects of antifolate drugs. Altered concentration of target enzyme Increased expression of target enzyme is a common mechanism of acquired resistance. For example Methotrexate resistance can develop as a result of DHFR gene amplification and subsequent enzyme overexpression [15]. Gene amplification is thought to occur as a consequent of antifolate inhibitors binding to DHFR, which causes a conformational change that alters the translational autoregulatary negative feedback mechanism, wherein DHFR protein specifically interacts with its own mRNA and negatively controls translational efficiency. The drug concentration will be limited to the dose administered, which will not be able to block the additional enzyme that is synthesised, resulting in cancer cells overcoming the inhibitory effect of the drug. Insufficient activation of the drug Some drugs require metabolic activation to manifest their antitumour activity for example Cytarabine has to undergo catalytic conversion, by the action of deoxycytidine kinase, to an active form [33]. So under expression or mutation of this drug-metabolising enzyme can reduce drug efficacy and cause resistance. Another example of resistance due to insufficient activation of the drug is Mercaptopurine, which is a prodrug [34]. Mercaptopurine is activated by hypoxanthine guanine phosphoribosyl transferase (HGPRT) and mutations that reduce the activity of this enzyme will allow the cancer cells to escape the toxic effects of the drug. Increase in inactivation Resistant to Mercatopurine can also develop as a result of increased inactivation of the drug [35]. The mechanism behind this is thiopurine s-methyltransferase (TPMT), which inactivates Mercaptopurine and thereby prevents the formation of the active drug. Mutations in the TPMT gene will alter its activity and may cause resistance. Rapid repair of drug-induced lesions Patients can develop resistance as a result of cancer cells recognizing DNA lesions and rapidly initiating repair pathways [9]. This is the main cause of resistance to alkylating agents as their mechanism of action is DNA damage There are several repair pathways and include the Direct Repair (DR) pathway, Base Excision Repair (BER) pathway, Nucleotide Excision Repair (NER) pathway, Homologous Recombination (HR) pathway and Non-Homologous End Joining (NHEJ) pathway. The DR pathway is mainly mediated by the DNA repair protein: O6-alkylguanine DNA alkyltransferase (AGT) [36]. AGT transfers the alkyl adducts from the nucleotides to the cysteine residue within its active site, independently from other proteins and without causing DNA strand breaks. The BER pathway recognizes and accurately removes bases that have been damaged by alkylation [37]. A damaged base is removed by a damage-specific DNA glycosylase, leading to the formation of a potentially cytotoxic apurinic or apirimidinic site intermediate. This is then processed by an AP endonuclease (APE1), which generates a strand break that is further processed by Poly ADP-Ribose Polymerase (PARP), DNA polymerase b (Polb) and ligase III to restore the damage. The NER pathway deals with the repair of bulky DNA lesions formed by DNA-alkylating agents such as Cisplatin, which distort the DNA double helix and block DNA replication and transcription [38]. Two major mechanisms of DNA repair have been recognized in this pathway: the transcription-coupled repair, which specifically targets at and removes lesions that block the progression of RNA polymerase II, and the global genome repair, which deals with lesions in the rest of the genome. Generally, nucleotide repair is a complex multi-step process that sequentially deploys a group of proteins to reorganize the lesion, remove the damage, and support new DNA synthesis. The HR and NHEJ pathways are involved in the repair of DNA double strand breaks, commonly considered to be the most lethal of all DNA lesions. Double strand breaks are induced by chemotherapeutic agents such Bleomycin, and Etoposide. In the HR pathway, ATM (ataxia talagiectasia mutated kinase) and its related ATR proteins sense the severe DNA lesions, and are mobilized to phosphorylate a wide range of substrate proteins [39]. Also a number of regulatory proteins, including BRCA1, BRCA2 and p53, are recruited to coordinate the DNA repair. The NHEJ pathway involves the alignment of the broken ends followed by recruitment and activation of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and DNA ligase IV to complete the ligation step [40]. Mutations Mutations in various genes can give rise to resistant target molecules, for example the p53 gene [41]. The p53 protein is an important regulator of the cell cycle and is sensitive to any DNA damage caused during replication. Following DNA damage it will normally induce G1 arrest and/or apoptosis to prevent the production of defective cells. Mutations in this gene will cause the loss of p53 function, which will allow cells with damaged DNA to continue replicating, resulting in resistance to DNA damaging drugs. Other genes, such as h-ras and bcl-2/bax, involved in the apoptotic pathway, have also been implicated in resistance [42]. Resistance due to mutations in genes will affect a wide range of anticancer drugs as all cells contain the same genetic material. It also potentially increases the proportion of surviving mutant cells, which leads to greater tumour heterogeneity. Increased expression of efflux pumps Resistance to natural hydrophobic drugs, such as vinca alkaloids and taxanes, as well as the cytotoxic antibiotics, such as anthracyclines and Dactinomycin, occurs due to the over expression of ATP-dependent efflux pumps in cancer cells [5]. These pumps belong to a family of ATP-binding cassette (ABC) transporters, which are divided into eight distinct subfamilies, shown in table 1. Of these subfamilies PGP, also known as MDR1, has a broad drug specificity, which explains the cross-resistance to several chemically unrelated compounds. It is a multidrug efflux pump that has 12 transmembrane regions, which bind hydrophobic drug substrates that are either neutral or positively charged [6]. It also has two ATP-binding sites, as hydrolysis of two ATP molecules are needed for the transport one drug molecule [43]. Binding of substrate to the transmembrane regions stimulates the ATPase activity of PGP, causing a conformational change that releases substrate to the extracellular space. Hydrol ysis at the second ATP site is required to re-set the transporter so that it can bind substrate again, completing one catalytic cycle. Increased expression of the PGP transporter in cancer cells increases the amount of catalytic cycles that occur, which increases the amount of drug effluxed [5]. This lowers the intracellular drug concentration below a cell-killing threshold, which results in resistance. Not all multidrug-resistant cancer cells express PGP. Resistance in these cells was discovered to be linked with the expression of the multidrug-resistance-associated protein 1 (MRP1) [44]. MRP1 is similar to PGP in structure (table 1) but, unlike PGP, it recognizes neutral and negatively charged hydrophobic natural products, and transports glutathione and other conjugates of these drugs, or, in some cases, such as for Vincristine, co-transports unconjugated glutathione. Some anticancer drugs, such as Mitoxantrone, are poor substrates for PGP and MRP1. Mitoxantrone resistance is due to a more distant member of the ABC transporter family, MXR (Mitoxantrone-resistance gene) [45]. This transporter is thought to be a homodimer of two half-transporters, each containing an ATP-binding domain at the amino-terminal end of the molecule and six transmembrane segments (table 1). Resistance can also develop as a result of increased expression of ABC transporters in the apical membrane of the gastrointestinal tract [46]. ABC transporters play a key physiological role, where they extrude toxins thus forming a protective mechanism and a first line of defense. Increased expression of these transporters decreases drug uptake and therefore decrease drug bioavailability. Examples of chemotherapeutic agents that develop resistance by this mechanism include antimetabolites, such as Methotrexate and Fluorouracil, and alkylating agents, such as Cisplatin. Also water-soluble drugs that piggyback on transporters and carriers or enter by means of endocytosis can fail to accumulate as they will not be able to enter the body. Additionally, PGP actively secretes intravenously administered drugs into the gastrointestinal tract [47]. Resistance due to increased levels of PGP transporters in the gastrointestinal tract is illustrated by MDR1a/MDR1b-knockout mice, which have shown to have increased tissue concentrations of PGP substrates. Studies have also shown increased tissue absorption of PGP substrates, following oral administration, when co-administered with a PGP inhibitor. Reversal of drug resistance in cancer Ways to overcome multidrug resistance due to the over expression of ABC transporters are being researched. Some of the main approaches include developing PGP inhibitors, antibodies against the PGP transporter, antisense oligonucleotides and liposome-encapsulated drugs. Drugs that can reverse multidrug resistance, such as PGP inhibitors, could be useful interventions to improve bioavailability, by increasing oral uptake of anticancer drugs and decreasing drug excretion, thereby reducing dosing requirements [7]. Two inhibitors that are used in the laboratory and in clinical trials that attempted to reverse drug resistance are the calcium channel blocker, verapamil and, the immunosuppressant, cyclosporin A. Another method that can be used to inhibit PGP is by competitive inhibition [48]. PGP binds many different hydrophobic compounds so any drug that interacts with the substrate-binding region is likely to be a competitive inhibitor of other drugs. Thus, two drugs that are transported by PGP will compete for this transport, resulting in increased oral absorption of both, decreased excretion, and redistribution. This kind of drug interaction can be used to inhibit the multidrug transporter, when the inhibitor drug has little or no other pharmacologic e ffect. Monoclonal antibodies (MAbs) against PGP have been used to kill multidrug resistant cells [49]. MAbs are of therapeutic use as they can activate the immune response, which results in complement mediated lysis or antibody dependent cellular cytotoxicity of the cells. An example of a MAb is MRK-16, which has shown selective toxicity towards tumours that are over expressing PGP. Molecules, which are normally involved in signal transduction on T and B cells can also be targeted for antibody therapy [50]. Such molecules include CD19, which is a membrane receptor involved in signal transduction and potentiates the response of B cells to antigens. MAbs directed against CD19 can induce cell-cycle arrest due to negative growth signals that cross-link immunoglobulin M and CD19. Antisense drugs work by down regulating gene expression [51]. This occurs by sequence-specific blinding of either DNA or RNA, which inhibits transcription or translation, respectively. Different antisense-oligodeoxynucleotides have been reported to chemosensitize resistant tumour cells to anticancer drugs through down regulation of PGP expression and thus increasing the intracellular accumulation of anticancer drugs in the cancer cells. The efficiency of a synthetic oligodeoxynucleotide (ODN) in regulating gene expression in living cells depends on its thermodynamic stability, resistance toward nucleases and cellular uptake [52]. A number of studies indicate that a synthetic ODN coupled with a DNA intercalator such as acridine, naphthyl imide, psoralen or pyrene might act to increase stability. Novel drug delivery systems such as liposome-encapsulated drugs have also been developed to overcome multidrug resistance [53]. Liposome formulations contain a small fraction of polyethylene glycol (PEG)-derivatised phospholipid, which has been shown to dramatically alter the pharmacokinetic properties of certain anticancer drugs. These pharmacokinetic alterations include long elimination half-life and small volume of distribution. Another formulation developed to bypass PGP transporters is anionic liposomes, which are internalised by certain cells and are able to provide drug release in intracellular compartments. Conclusion Cancer is prevalent in the western world and much research is dedicated to produce effective chemotherapy. Current chemotherapy includes alkylating agents, antimetabolites, cytotoxic antibiotics, plant derivertives, hormone therapy and monoclonal antibodies. However the efficacy of these chemptherapeutic agents is limited to patients developing multidrug resistance. This is mainly due to the over expression of ABC transporters, particularly the PGP transporter, as they have broad drug specificity so can bind many structurally unrelated drugs [5]. Techniques to reverse multidrug resistance are being developed and include co-administration of PGP inhibitors, which prevent the binding of anticancer drugs the transporter [7], the use of antibodies, which kill cells over expressing the PGP transporter [49], antisense oligonucleotides that down regulate PGP expression [51] and liposome-encapsulated drugs, which alter the pharmacokinetic properties of anticancer drugs [53]. A better understanding of the mechanism by which ABC transporters efflux chemotherapy and further analysis, in clinical trials, of known mechanisms of multidrug resistance would increase the development of agents that reverse multidrug resistance. Also improved imaging techniques used in clinic to screen cancer cells would enhance the ability of practitioners to prescribe individualised treatment according to the patients level of resistance. One approach that can be developed is to produce fluorescent antibodies against all 48 human ABC transporters and use them in conjunction with a specialised fluorescent microscope to monitor the levels of ABC transporters in cancer cells. References Office for National Statistics (2005) Cancer Statistics registrations: registrations of cancer diagnosed in 2006, England. http://www.statistics.gov.uk/downloads/theme_health/MB1-37/MB1_37_2006.pdf [accessed December 2009] Weinberg RA (1996) How Cancer Arises. Scientific American; 275: 42-48 Lawley PD and Phillips DH (1996) DNA adducts from chemotherapeutic agents. Mutation Research; 355: 13-40 This article is not included in your organizations subscription. However, you may be able to access this article under your organizations agreement with ELowenthal RM and Eaton K (1996) Toxicity of Chemotherapy. Hematology/Oncology Clinics of North America; 10: 967-990 Gottesman MM (2002) Mechanisms of cancer drug resistance. Annual Review of Medicine; 53: 615-627 Ambudkar SV, Dey S, Hrycyna CA, Ramachandra M, Pastan I and Gottesman MM (1999) Biochemical, cellular, and pharmacological aspects of the multidrug transporter. Annual Review of Pharmacology and Toxicology; 39: 361-398 Ferry DR, Traunecker H and Kerr DJ (1996) Clinical trials of P-glycoprotein reversal in solid tumours. European Journal of Cancer ; 32A: 1070-1081 Lawley PD and Brookes P (1967) Interstrand cross-linking of DNA by difunctional alkylating agents. Journal of Molecular Biology; 25: 143-160 Zhu Y, Hub J, Hu Y and Liu W (2009) Anti-Tumour Treatment Targeting DNA repair pathways: A novel approach to reduce cancer therapeutic resistance. Cancer Treatment Reviews; 35: 590-596 Bouziane M, Miao F, Ye N, Holmquist G, Chyzak G and OConnor TR (1998) Repair of DNA alkylation damage. Acta Biochim Pol; 45:191-202 Schweitzer BI, Dicker AP and Bertino JR (1990) Dihydrofolate reductase as a therapeutic target. FASEB Journal; 4: 2441-2452 Spiegelman S, Nayaak R, Sawyer R, Stolfi R and Martin D (1980) Potentiation of the antitumor activity of 5-FU by thymidine and its correlation with the formation of (5-FU)RNA. Cancer; 45: 1129-1134 Nabhan C, Gartenhaus RB and Tallman MS (2004) Purine nucleoside analogues and combination therapies in B-cell chronic lymphocytic leukemia: dawn of a new era. Leukemia Research; 28: 429-442 Jansen G, Mauritz R, Drori S, Sprecher H, KathmannI, Bunni M, Priest DG, Noordhuis P, Schornagel JH, Pinedo HM, Peters GJ and Assaraf YG (1998). A structurally altered human reduced folate carrier with increased folic acid transport mediates a novel mechanism of antifolate resistance. Journal of Biological Chemistry; 273: 30189-30198 Tai N, Schmitz JC, Chen TM and Chu E (2004) Characterization of cis-acting regulatory element in the proteincoding region of human dihydrofolate reductase mRNA. Biochemical Journal; 378: 999-1006 Zunino F and Capranico G (1990) DNA topoisomerase II as the primary target of antitumor anthracyclines. Anti-Cancer Drug Design; 5: 307-317 Wang JC (1996) DNA Topoisomerases. Annual Review of Biochemistry; 65: 635-692 Kasahara K, Fujiwara Y, Sugimoto Y, Nishio K, Tamura T, Matsuda T and Saijo N (1992) Determinants of Response to the DNA Topoisomerase II Inhibitors Doxorubicin and Etoposide in Human Lung Cancer Cell Lines. Journal of the National Cancer Institute; 84: 113-118 Chen AY, Yu C, Gatto B, and Liu LF (1993) DNA minor groove-binding ligands: A different class of mammalian DNA topoisomerase I inhibitors. Procedings of the National Academy of Sciences of the USA; 90: 8131-8135 Povirk LF (1996) DNA damage and mutagenesis by radiomimetic DNA-cleaving agents: bleomycin, neocarzi

Education and the Digital Divide :: essays papers

Education and the Digital Divide Closing the digital divide involves many components, starting with the education program and teachers. While schools are integrating new technologies into their programs, teachers are supposed to keep up with the latest technologies and use them in their curriculum to teach students. According to a U.S. Department of Education Report (1999), only 24 percent of new teachers felt sufficiently prepared to integrate technology into the curriculum they were using (Brogan, 2000). The problem is, many teachers did not grow up with computers and are not receiving the training they need to operate them (Brogan, 2000). Starting work as early as 7 a.m. and leaving school as late as 5 p.m. to go home and do even more work, leaves teachers lacking the time to learn new technological skills. Many schools offer training programs for teachers. For example, the Palm Beach County, Florida school district teaches Web basics for teachers at middle schools and magnet schools (Brogan, 2000). This i s a great idea because it is giving teachers the opportunity to learn about technology and it is showing that the school district is interested in helping its employees become better at what they do. Andy Carvin states â€Å" internet access in schools isn’t worth a hill of beans if teachers aren’t prepared to take full advantage of technology† (2000). Schools spend a lot of money on computer hardware and software as well as other technologies without realizing that many of their employees are unprepared to include them in their teaching and use them to their advantages. Educators often use technology as a classroom management tool rather than an educational one, allowing computer time as a reward for good behavior (Clark & Gorski, 2001). The problem with this is that students learn to use the computer for games and such because it is their reward instead of using it on their own time for educational purposes. This is teaching them the wrong idea. Margaret Honey, director of the Center for Children and Technology in NYC said it best, â€Å"The bottom line is, you don’t just put technology into schools or into homes and expect miracles to happen. The technology is only as good as the program that surrounds it† (Meyer, 2002, p.2). â€Å"Education is probably the most important issue that affects the ability to benefit from technology.

More Purchase Instead of Less Essay -- Human Rights

In recent years, people in Europe and America have been clearly aware that the general commodity price in their markets had dropped dramatically. A lovely Barbie doll which, In the old days, used to cost them more than ten dollars or eight euros, now, values costs less than half of the original price. But as we all know, there must be someone who would pay for such a good bargain. So what on earth is the trigger that lead to the remarkable decline? And what is the most influential factor that rewrote the numbers on hundreds of thousand of price tags? When our curiosities drive us to keep on questioning, and to trace the unusual economic phenomenon, some mysterious burgeoning factories emerge in our sights. These factories are prevalent in a world scope because of the incredibly cheap price, while, on the other hand, they are also infamous for their poor working conditions, unbelievably low salaries, threatening devices, and abusing of labors. For reasons above, those factories are c alled sweatshops. And most of the sweatshops are located in Asia, such as China, South Korea, Indonesia, Vietnam and so on. From the beginning, there were only a small group of people who paid attention to those sweatshops. But with more and more grievous news unveiled, a huge growing number of people start to keep a watchful eye on the livelihood of those workers in sweatshops. To their surprise, those poor workers were bearing that unequal contracts, that long working hours, and that potential risks of their lives everyday How could those Americans and Europeans who have been high-fed and spoiled in the last century, imagine a twelve-hour day, seven days per week, no paid holiday in the foreseeable future job with an skinny income which was only en... ...ss Studies Vol. 31, No. 3 (3rd Qtr., 2000), pp. 367-385, Palgrave Macmillan Journals. Jean-Paul Sajhau, ‘Business ethics in the textile, clothing and footwear (TCF) industries: Codes of Conduct’, ILO Bulletin, no. II-9, (June, 1997). Stephen Frenkel, ‘Globalization, athletic footwear commodity chains and employment relations in China’, Organization Studies, issue 4 (2001). Nicholas D. Kristof and Sheryl WuDunn. â€Å"Two Cheers for Sweatshops.† New York Times 24 September 2000. 5 May 2012. Doug Guthrie, Dragon in a Three-Piece Suit (Princeton, New Jersey: Princeton University Press, 1999). Pun Ngai. The China Journal No. 54 (Jul., 2005), pp. 101-113. The University of Chicago Press.

Society and the Roles We Play/Zimbardo and the Hoax

Psych 333: Social Psychology Society and the Roles We Play/Zimbardo and the Hoax As social human beings we encounter the powerful effects of roles every day. Whether you’re an experienced doctor or a propane truck driver, your roles are much more than just a small piece of a big picture. Our roles are in nature a social element that when used correctly can slightly or completely alter another’s. When used maliciously our roles can not only psychologically damage an individual or a handful of people, but also the masses.Adolf Hitler’s role as a chancellor changed the roles of normal German soldiers to genocidal henchmen which in turn changed the Jews’ roles as a race of beautiful people to what seemed like verminous animals needing extermination. The dynamics of social roles are not always this drastic but when they are, our life as we know it changes. To see how similar a real life tragedy and a staged study are with damaging effects of roles, it is import ant to analyze the Stanford Prison Experiment and a very horrible real life tragedy comparatively.In order to explain such a socially fascinating phenomenon as the Stanford Prison Experiment led by Zimbardo, we must first see what social psychological factors were at play. First it is important to know that all participants in this experiment including the prisoners, the guards, and the confederates gave their full consent to participate. This is important because the main method of this experiment would make the participants take on different roles. This method helped determine the purpose of this experiment which is whether or not the participants’ would perceive their roles as pretending or reality.This perception was shown through behavior from both prisoners and guards as a self-fulfilling prophecy. This is evident because the reciprocal behaviors expressed by the prisoner participants and the guard participants would amplify each other’s behavior. An increase of aggression causes an increase in submissiveness which in turn amplifies aggression and continuous into a vicious cycle. The experiment has been argued to have been unsuccessful; however the experiment contained a high amount of experimental realism. Although the experiment was unethical it yielded fascinating results from both the prisoners and the guards.First I believe it is important to analyze the behavior exhibited by the participants in the experiment. Prior to the experiment, the participants were in fact informed about the nature of the experiment and the moment they were arrested they would assume their roles as prisoners. A majority of the experiment was done inside of the prison. It was during this time that the prisoners displayed many social psychological behaviors that result from playing a submissive role. The progression of the experiment’s time also caused some of these interesting behaviors to amplify.It is important to understand that the underlining qualit y that the prisoners in this study exhibited was learned helplessness. This is predominantly evident when the prisoners’ acts of rebellion toward the guards diminish. This leaved the prisoners with an overall sense of helplessness. They were more likely to submit to the hostile and aggressive demands of the guards. Although some of the demands of the guards such as doing countless numbers of pushups would seem unethical in a real prison, even a participant assuming a false role as a prisoner follows such preposterous demands.What is more perplexing about this study was the fact that these participants in fact knew that they were not really guilty of any crime but as the experiment progressed and the guards became more aggressive the inmates displayed very passive behavior because they knew that their behaviors could not change the current predicament that they were in. Another remarkable concept that helped reinforce the participants’ roles as prisoners was the Saying- Becomes-Believing Effect. In one instance the participant known as prisoner 8612 would either rebel or would show what would be seen as undesirable behaviors in the guards’ eyes.After doing this the guards would have the inmates punished and also have them chant â€Å"Prisoner 8612 was bad†. The prisoners seemed to show a certain degree of animosity towards prisoner 8612 and eventually led to his outright emotional breakdown and made him to truly believe that he was a bad prisoner. This again shows the strength of learned helplessness in social cognition. Prisoner 8612 believed he was a bad prisoner; therefore he became a bad prisoner. The only thing more fascinating than the growing submission of the prisoners had to be the increasing aggression by the prisoners.It is a confounding concept that in most prisons, the idea that prison guards act more harshly towards an inmate because they are in fact psychologically feeding off of the prisoners’ submissiveness. Th e guards in the study were introduced exactly as the prisoners were to the study’s nature just as different roles. Their roles would begin the moment they arrested the prisoners. Upon arriving to the prison however, the guards would assume an entirely different role than a prisoner.These soon-to-be tyrants would use one of the most powerful social psychological weapons in their armory: deception. The Stanford Prison guards used deception in a number of ways during this study. In the experiment they introduced the privilege cell and the penalty box to the prisoners. The privilege cell was a much nicer cell than the ones given to the rest of the prisoners. When the guards put certain prisoners in the privilege cell this deceived the other prisoners into believing that this prisoner was good which in turn caused the prisoners to be more behaved.The same deception was used in punishing the prisoner with the penalty box which was a small broom closet sized room which would be used to keep the prisoners when they were bad. Another method of deception that the guards inflicted was towards the family of the prisoners. The guards forced the prisoners to write to their families constantly that everything was going well in the prison. Along with these letters the prisoners would also force the prisoners to identify themselves as their assigned numbers rather than their actual names.I confounding factor that also helped in the amplifying aggression of the guards towards the prisoners was their act of justification. It is rather odd that regular people who for the most part did not assume any kind of authoritative role use authority in such a severe way. When questioning the severity of their actions towards the prisoners justified their actions by telling themselves that they are being told to be this way towards the prisoners and also that the prisoners’ behaviors caused them to bring the consequences upon themselves. The experiment seemed so real that it c ould not even complete the full desired duration.This experiment will always be remembered as one of the biggest contributions to social psychology because it showed the powerful effects of submissiveness vs. authority. It was because of this experiment also question and reevaluate what is and isn’t ethical in social psychology experiments. It also shows us how people whether they are in positions of authority or not can manipulate this powerful psychological element against others causing not only psychological and emotional ramifications, but also legal ones as well. This was seen in one of the cruelest hoaxes ever played.The hoax that I am describing was one that went from what seemed to be a mean prank call, to dozens of legal repercussions and countless victims of emotional and psychological distress. These calls were made by David R. Stewart. Although Stewart seemed like a man of average intelligence, it wouldn’t be unfair to consider him to be a social psycholog ical genius. Stewart’s calls as a person in a position of authority not only manipulated his victims but also tormented them with a number of social psychological weapons but also used the psychological factors of his victims against themselves.He was sometimes able to take two innocent people and make one a victim of sexual assault and the other a victim in a single phone call. In order to analyze how Stewart was able to succeed at this it is important to see what psychological factors were in play both in the mind of Stewart and his victims. First, Stewart assumed a role of authority as a police officer, corporate employee, or federal officer. This role helped Stewart claim legitimacy to his victims. Although this would seem like enough to control his victims he also used a factor that was possessed not by him but by his victims.Stewart attacked those who worked in the food industry. This may seem odd but it is fact a very intelligent group of people to attack because peopl e in the food industry are trained to be more obedient than others traditionally would. Society’s schema of the food industry portrays it in such a fashion that the number one priority of the industry’s employees is customer satisfaction. In order to achieve customer satisfaction the employees must obey the customer’s wishes. When the employee is on this type of a mindset it isn’t unfair to say that their vulnerability to authority would also heighten.The heightened obedience to authority also arises from another social schema of law enforcement. We tend to live in the illusion that because law enforcement has a higher authority than civilians do, we must do everything they tell us to. This schema is also the reason police often get a confession or information leading to a confession from people because although individuals have the right to remain silent, police use authority to trick them into confessing. The perplexing aspect of this event is not just the acts themselves that were performed, but the fact that the acts grew more and more sexually perverse.Although the act of the hoax itself was perplexing, it is even more fascinating on how the public criticized the whole phenomenon. This alone had so many interesting psychological happenings. Even news broadcasters like Fox-TV called the â€Å"victims† of this hoax were â€Å"colossally stupid†. Another made a statement quoting â€Å"They had the critical ability to decide whether to carry out their orders†. Statements like these show both a hindsight bias and a self-serving bias. People claim that they would never perform perverse and lewd acts on another because an authoritative figure told them to do so.The self-serving bias is the fact that they believe they would personally behave more favorably and the hindsight bias is the fact they claim they would have behaved differently after they heard of the incident. Although people harshly criticized the victim s Stewart did in fact con two thirds of the people he called. This proves an interesting argument because people who read this story will most likely claim that they will never behave in such the fashion the victims did, but because of these social biases it is impossible to know if one would truly fall for a hoax like that.Many look at Zimbardo’s and Milgram’s studies and see the obvious social psychological connection between both. What is interesting is how this real world hoax and the two above studies have very predominant similarities. Both instances involve two different groups of normal people assuming a role and watch how their roles completely change their lives. In both situations people who would never normally behave to the roles they were given behave exactly to their roles. In both situations the submissiveness of one person amplifies the aggression and authority of another.In both situations the victims’ roles caused long term psychological and e motional distress. It shows us a society full of schemas that is naturally obedient in following orders whether we believe them to be right or wrong. So in essence these incidents are very relevant to each other and also to social psychology as a field. It is relevant to how we think, how we behave, and how we interact with others. The average person would say that Zimbardo’s study was obviously unethical. This is true because it is unethical.The American Psychological Association provides the Institutional Review Boards to keep experiments ethical and protect the participants in this study. The fact that participants in the study underwent emotional distress proves that the study was unethical. In hindsight, if Stewart’s hoax was indeed replicated it would be terribly unethical to say the least. It is because Zimbardo’s study being so similar to the hoax that roles become psychological damaging. In Zimbardo’s experiment, the participants felt the effects of a six day role long after the study.In Stewart’s hoax, just a few minutes or hours changed some of the victims involved for the rest of their lives. Although it is fair to challenge ourselves as psychologist, experiments with the psychological severity of the Stanford prison experiment are not needed because we know the social psychological implications of role playing. This analysis fits very well with the social psychological perspective. Roles, schemas, and biases show the dynamic of the human’s psychological potential.You do not have to be a PhD psychologist to manipulate more than sixty average people to perform sexual or lewd acts on other innocent people. It also does not take a PhD psychologist to give average people a role that is unordinary to them and watch them change as a person. What seems like simple terms in social psychology can be used as powerful and manipulative weapons in psychological warfare. These concepts also help realize the importance of the roles that we play every day and how they can change the social world as we know it.

The Handphone Influences People’s Behaviour

The handphone influences people’s behaviour Behaviour is not be formed by a thing constantly, but it is formed by many things continously. Because, everything what people saw, listened, and said forms his behaviour. One of them is one of media of communication, which is called handphone. Hand phone is one of the tool of communication between a person with others. Today, it is used by both adult or child, rich or poor, and because of necessery or style in our society. But, their behaviour is influenced unconsious by using it. The phone gives the big role to influence people’s behavior.First, it neglects the user. Usually it is happened in the users who can not control their self such as the students. For examples, when the teacher is teaching in the class they are busy by playing the game or texting a message to their friends. They are serious in their doing, sometimes they are laught and smile by theirself. Moreover, the the teacher does not give the rule or punishment for them. So, they will get nothing in the class. Besides, if the parents do not control, they also do not study or do homework. Second, disturbs the childen’s development or maturity.Because, there are many things in the phone. Such as camera, games, pictures, and others. Which changes the student’s attention and concentretion, both in the class or in the home. Moreover, it gives dishonest way. Exmple, in the examination they should cheat with others by sending message or searching the material about etc. In addition, by using handphone lets the students to send or receive everything is not good and educated. So, if we let them to use it free without controling, they will be the educated of technology, but not educated of knowledge or attitude.Third, it contibutes the people to be arrogant. Because, everyperson is different personality. Basicly, the phone is used for communication with others. But, some person are use it not only for communication but also for style. As we know, today are many merks and types of phone. Such as BlackBerry, Android, Nokia, Samsung etc. Some of us compete to buy the more expensive, exis and newer. Sometimes, they more emphasize to buy the new phone than other things. Example, the students able to buy the new phone, but do not able to buy the book.This is very bad to their maturity, which compete in the extravagance. Overall, the phone gives many good function for us. There are to communicate with others, save the things as a memorial, share information etc. But, we have to release that phone is same as another technology also has the negative effects should influence the people behaviour. Forthat, we have to be wise in using it, control and tell our family, student and society the positive and negative effects. Because the phone influence the people’s behaviour.