My Triple Threat free essay sample

We look in the mirror together with beaming smiles on our faces. Holding back tears of laughter, Steve says, â€Å"Playboy?† Ten minutes later, we’re on the beach. I can feel the eyes piercing my skin, my self—esteem holding on by threads. I transfer the laser-like energy into a positive vibe as I strut by the sporadic crowd. The snickers come and go, but some people actually think we are for real. I welcome the spectators. The sun beats down on my unprotected thighs and shoulders, making me sweat more than I already am. We walk to the volleyball courts, pull up two lounge chairs, throw on the shades, and soak up the sun— we focus on getting perfect tan lines. Next thing I know, I’m in a photo shoot with three different cameras flashing at me. â€Å"We must look good,† I say to Steve. He responds with a seductive pose and a dramatic, â€Å"Smile with the eyes. We will write a custom essay sample on My Triple Threat or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page † Two hours later, I hang my pink leopard print delight on the railing for everyone to see. I shower, change, and go back out to the hub of the hotel. I am no longer Michael—I am now sexy pink, leopard print Speedo Man. Humor. The white walls close on me, just like how my entire world collapses on me. The blank walls share the same expression as my mind. Blank. I don’t know what to think, what to do, what to say. I can’t cry. That would make me feel sorry for myself. I can’t scream. Nobody else did anything wrong. But me. And I can’t talk. I have no one to talk to. I hear the footsteps closing in on the door that separates me in my isolated box in hell, from the disappointed authorities that wait on the other side. The door opens. I walk through the light into what I know is my own funeral, but I own my actions and step forward. I turn into a conference room and swell up, even though I knew what was going to be in front of me. My mom’s tears don’t cleanse me like water does. The tears are sharp and painful. They pierce my skin and attack my heart. A police officer enters the room. â€Å"Have you been drinking alcohol tonight?† He interrogated. â€Å"Yes sir.† I cracked out. Minutes later, I blew double zeroes on the breathalyzer. I could have lied and been free from the trouble and the pain. But I chose the high road. Honesty. â€Å"Have you thought about schools, Mike?† I shrugged my shoulders. Judy, my boss, is sitting across from me at a table in a small Hartland coffee shop talking about my future. â€Å"All I know is what I want to go into.† She nods and leans back, her mind working. I sit and focus intently on every word, every gesture, and every facial expression. After all, she is my ticket to the next level. If I ever want to complete my dream of being an anchor and a writer for ESPN, she is going to get me there. After our meeting, I stop in the school parking lot and t ake out a notebook. I write everything down. Everything she said. I study the words on the paper and close my eyes and hear the faint ESPN jingle, â€Å"Deh neh neh, deh neh neh.† I hear the voice over say, â€Å"This is Sports Center.† And I hear my voice—â€Å"Hi, I’m Mike. Welcome to Sports Center.† Ambition. Humor. Honesty. Ambition. Humor helps keep me rolling through tough situations. Honesty keeps my conscience clean and helps me stay positive on a personal level with myself. And ambition gives me the drive to do the improbable. Humor. Honesty. Ambition. My triple threat

Cashless Society1 essays

Cashless Society1 essays One article that caught my attention recently was one presented in the November 21, 1998 issue of The Economist. The article was about a cashless society and how well alternative forms of tender were catching on. According to the article, some forms of the "smart card" haven't caught on as well as expected. Smart cards have information embedded in them, essentially allowing a consumer to purchase things quickly and conveniently. It was the hope that these cards would supplant paper and coin money forever. However, that has not been the case. Smart cards do exits, however. In the article, it is mentioned that smart cards with chips embedded in them allowed a customer to quickly swipe the card through the reader. Thirty-two cents is then deducted. Simple and easy, right? Well, it hasn't caught on. One of the main reasons that smart cards have struggled a bit is that it has competition in the form of current debit cards. People can purchase anything they desire with these cards already. Therefore, there wouldn't be any added value of having a debit card. A survey of 2,400 North Americans by Smart Card Forum gives some interesting results. According to the survey, more than three-quarters would have liked to have a card that stored vital medical and car-related information. Less than half wanted a card that they could use to purchase things with. Another problem facing smart cards is compatibility. Current smart cards utilize only on a small range of readers. For example, a smart card for parking meters in Boston would not work for ones in New York. And since local governments control those areas of jurisdiction, it has to take a national effort to make it work. This means that the U.S. government must implement and lead the way. When this happens, then we will truly see the fall of paper and coin money. ...

30, 60, 90 Day Branch Plan Essay Example | Topics and Well Written Essays - 750 words

30, 60, 90 Day Branch Plan - Essay Example The plan will be demarcated into distinct categories so as to accommodate the several sections of the comprehensive plan in initiating the processes that will symbolize the development and expansion of the branch and its activities. The new branch will not involve several officials on the grounds that being a novel venture it has been considered unfit to have several positions that may not only be costly for the corporation but also unnecessary. As a result, the composition will be a Branch Manager, approximately 2-3 Personal Banking Advisers and possibly 1 customer service adviser. The branch manager will play overall duties in the branch including the supervision of the other officials who will directly report to him. The minimum number of positions created will make it simple for the operations of the branch to begin pending further expansion of the branch as situations necessitate. The branch will be based on the University site where all products will be sold. The education inst itution will be the major centre for the branch as the target market along with core operations of the branch will be based on the university premises. Accordingly, focus will be on personal customers from the student and staff population implying that the market for the branch’s services and products will directly emanate from the university; both staff and student. A brand new branch would operate basing on the location whereby the university will provide the required market and focus for the business. The daily function of a branch manager will be to oversee the basic operations of the new branch including supervision of the staff, coordination of activities as well as interaction with the staff. The initial 30 day plan to implement growing business, staffing and development will be based on two primary parameters namely, product introduction and marketing through which the branch will engage in a process of making itself known to the potential clients. Under this program, the branch will develop a comprehensive product introduction scheme that will attract the clients most of whom will be drawn from the staff and students of the university to develop interests and demand in the products offered (Nieman & Pretorius, 2007, 24). Such a process will be inherently involving since the products must be relevant to needs and requirements as well as tastes of the potential clients. As a result, prior to the product development and introduction procedure, the branch will research and analyse the potential clients and their requirements. This will inform both the marketing and product introduction processes that will be of core importance in the initial thirty days of the implementation of the plan. Subsequently, marketing will be of prime importance in the initial phases of the implementation of the plan. Through marketing, the branch will seek to establish a niche in the wide mart by focusing on the target market that constitutes the staff and students of th e university. Through the marketing endeavour, the branch will attempt to popularize itself along with its activities, services and products to the potential customers (Ericson, 2007, 74). This will be an important step towards initializing the implementation of the entire plan. The subsequent step in the plan to implement growing business, staffing and development will involve staffing and development which constitute a crucial stage in the entire plan. Staffing will take pre-eminence owing to the fact that any commercial entity operates through its staff and the human resources of any entity determine its entire operation and stature. As a new venture, the

Electronic Waste Speech or Presentation Example | Topics and Well Written Essays - 750 words

Electronic Waste - Speech or Presentation Example Developed nations have made several steps towards ensuring e-waste management. On the other hand, developing nations lag behind and so far policies enacted as not fully implemented. In most developed nations, there are no policies that govern the disposal of electronic materials (Karpus, 1). This, therefore, implies that e-waste is posing several challenges in many nations.   Electronic wastes are made up different materials that are extremely toxic. Some of these materials cannot be decomposed or decompose at a unusually slow rate (Toothman & Elizabeth, 1). Toxic Components of E-Waste  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚   Smoke alarms contained in many electronic devices are made up of americium or carcinogen. This two materials are radioactive and take a very long to decompose. Mercury is used to make tilt switches, fluorescent tubes, flat screen monitors and thermostats. If mercury is absorbed into the environment, it results into serious health eff ects such as dermatitis, sensory impairment, general muscle weakness, and memory loss in human beings and reduced fertility, death, slower rate of growth and development in animals (Karpus, 1). Lead acid batteries are made up of particularly harmful chemical called sulphur. If absorbed into an individual’s body it causes adverse effects such as kidney damage, throat and eye irritation, and heart damage. When allowed to reach the clouds, it reacts with vapor.... o serious health effects such as dermatitis, sensory impairment, general muscle weakness, and memory loss in human beings and reduced fertility, death, slower rate of growth and development in animals (Karpus, 1). Lead acid batteries are made up of particularly harmful chemical called sulphur. If absorbed into an individual’s body it causes adverse effects such as kidney damage, throat and eye irritation, and heart damage. When allowed to reach the clouds, it reacts with vapor to form sulphuric acid (Toothman & Elizabeth, 1). BFR is used in most electronics as flame retardants. It is made up of other several chemicals, which when allowed to the environment causes several health complications. These include liver problems, thyroid problems, and impaired nervous system development both in animals and human beings (Grossman, 1). Cadmium is used to make light sensitive resistors and nickel cadmium rechargeable batteries used in electronic devices. Cadmium has adverse effects if ex posed to the environment. If inhaled, it causes permanent damage to the lungs as well as causing kidney diseases. Due to its adverse effects, it was banned in Europe except for medical purposes (Toothman & Elizabeth, 1). Lead is a vital component of most electronic devices including monitors, solders, lead-acid batteries, cathode ray tubes and PVC. Lead if allowed into the soil will encourage leaching and destroy natural habitats for many micro-organisms. Beryllium is used as filler in thermal materials. These include thermal grease that is used in CPUs and heat sinks, X-rays ceramic windows, vacuum tubes, and gas lasers (James, 13). If all of these harmful chemicals are released into the environment then our future generations are threatened. Most animals will get extinct the generations that

Face Recognition Technology Research Paper Example | Topics and Well Written Essays - 1000 words

Face Recognition Technology - Research Paper Example Availability of ‘biometrics’ technology provides controls for verifying true identity of an individual. These controls are automated processes that recognize physiological characteristics such as fingerprints, face, eyes, DNA etc. of a living person which are not easy to forge as they are attributes of an individual gifted by nature. There are also automated processes that recognize individual behaviors such as handwriting style, key stroke patterns etc. (Lin, 2000) Physiological controls are more stable when compared with behavioral controls. The main reason is that the features of physiological controls are non-alterable unless some serious injury is inflicted on a living being. On the other hand the patterns of behavior controls fluctuate with the mood and activities of an individual. In real-life, it is found that verification of physiological attributes is although very accurate, yet it is far more intrusive than the behavior attributes (Lin, 2000) One of the few biometrics controls that have the merits of both low intrusiveness and high accuracy is the Face Recognition technology. Researches in the field of image processing, security and psychology were attracted towards the concepts of computer vision which led to the designing of face recognition technology. (Lin, 2000) The real-world image has only size in inches or centimeters. The capturing device such as camera or scanners uses digitization process through which it stores the number of pixels that contains in an image. It is called Resolution which is of two types; Spatial Resolution and Colour Resolution (JISC Digital Media, 2006) The capturing device in Spatial Resolution is concerned with the frequency at which samples are taken from the real-world object or art-work. Frequency is mostly expressed as samples per inch (spi) when scanning and pixels per inch (ppi) when processing the digital image. The resolution to use for capturing an image is dependent mostly on its ‘end-use’.

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

Blue Hotel :: essays research papers

The Blue Hotel Steven Crane is not one of the most liked authors in the world. He tends to become to engulfed in the scenery around the action that is taking place rather than the action itself. When watching the movie, cannot experience this description since it is given to them. Details are very important for the readers because if the reader cannot see the same thing that the writer sees then the reader might lose interest in the story. In the story â€Å"The Blue Hotel,† Crane uses his excellent setting and character description along with the physical, emotional, and intellectual responses of people under extreme pressure and the betrayal and guilt he shows between the characters to help the reader better understand the story or poem. Crane shows these characteristics in almost everything he writes. In â€Å"The Blue Hotel,† Crane does an excellent job of describing the setting to you in every way possible. For example in the beginning of the story â€Å"The Blue Hotel,† he says â€Å"the hotel was painted a light blue, a shade that is on the legs of a kind of heron, causing the bird to declare its position against any background.† He does this type of depiction on every single thing he describes. Then in paragraph three he says, â€Å"A little Irishman wore a heavy fur cap squeezed tightly down on his head. It caused his two red ears to stick out stiffly, as if they were made of tin.† In the movie you are left with no dialogue and all you can do is witness what is being presented. In the end Crane even goes into an in depth description of the bitter cold snow outside. From his description the reader can imagine more chilling scenery than that one that can be created by Hollywood. Crane also does a good job of establishing his characters through one of his major themes; the physical, emotional, and intellectual responses of people under extreme pressure. Crane shows this in his characters to help the reader better understand what the character is going through. One example of this is when the Swede accuses Johnny of cheating in a card game. This offends Johnny and his emotional and physical reaction is to challenge the Swede to a fight. Crane stories consist of that moment when the characters confront the inescapable impasse of their situation, they are caught and boxed in by fate, and then nothing happens.

Human Embryonic Stem Cells

Human embryonic stem (hES) cells have the unique capability of differentiating into all cell types, leading to the development of an entire organism. As the integrity of ES cells is critical for the developing embryo, these cells have likely evolved mechanisms that detect and respond rapidly to adverse stimuli. Indeed, hES cells have been shown to be highly sensitive to DNA damage, but the molecular mechanisms underlying this rapid death remain unclear. Caspases are critical mediators of apoptosis in mammalian cells, and a key protein that controls their activation is Bax, a proapoptotic member of the Bcl-2 family. While the main components of the apoptotic pathway have been identified, exactly how this pathway is regulated in various primary cells remains unclear. Here, we examined the apoptotic pathway in hES cells and report a unique mechanism engaged by hES cells that can prime them to undergo rapid apoptosis inresponse to genotoxic damage.To visualize GFP-tagged Bax, 3-day colonies of hES cells were transfected with 2 mg of hBaxC3-EGFP (Addgene) with FuGENE HD transfection reagent. The process of introducing nucleic acids into eukaryotic cells by nonviral methods is defined as transfection. Using various chemical, lipid or physical methods, this gene transfer technology is a powerful tool to study gene function and protein expression in the context of a cell. Development of reporter gene systems and selection methods for stable maintenance and expression of transferred DNA have greatly expanded the applications for transfection. Assay-based reporter technology, together with the availability of transfection reagents, provides the foundation to study mammalian promoter and enhancer sequences, trans-acting proteins such as transcription factors, mRNA processing, protein:protein interactions, translation and recombination events (Groskreutz and Schenborn, 1997). Transfection is a method that neutralizes or obviates the issue of introducing negatively charged molecules (e.g., phosphate backbones of DNA and RNA) into cells with a negatively charged membrane. Chemicals like calcium phosphate and DEAE-dextran or cationic lipid-based reagents coat the DNA, neutralizing or even creating an overall positive charge to the molecule. This makes it easier for the DNA:transfection reagent complex to cross the membrane, especially for lipids that have a â€Å"fusogenic† component, which enhances fusion with the lipid bilayer. Physical methods like microinjection or electroporation simply punch through the membrane and introduce DNA directly into the cytoplasm. Here we describe the striking observation that healthy undifferentiated hES cells maintain Bax in its preactivated state at the Golgi. This is in contrast to other cell types in which Bax is typically present in an inactive form in the cytosol. Our results also highlight the fact that the apoptotic machinery undergoes dynamic changes even at early stages of differentiation.While undifferentiated hES cells have constitutively active Bax and undergo rapid apoptosis in response to DNA damage, just 2 days of differentiation induced significant changes suchthat Bax was no longer active, and the cells were no longer highly sensitive to DNA damage. This could be manifested with even greater complexity in vivo as cells during early embryogenesis undergo rapid proliferation and differentiation.

Women in Space - Female Astronauts and Cosmonauts

Women in Space - Female Astronauts and Cosmonauts 1959 - Jerrie Cobb selected for testing for the Mercury astronaut training program. 1962 - Though Jerrie Cobb and 12 other women (the Mercury 13) passed astronaut admission tests, NASA decides not to select any women. Congressional hearings include testimony by Cobb and others, including Senator Philip Hart, husband of one of the Mercury 13. 1962 - The Soviet Union recruited five women to become cosmonauts. 1963 - June - Valentina Tereshkova, cosmonaut from the USSR, becomes the first woman in space. She flew Vostok 6, orbiting the earth 48 times, and was in space nearly three day. 1978 - Six women chosen as astronaut candidates by NASA: Rhea Seddon, Kathryn Sullivan, Judith Resnik, Sally Ride, Anna Fisher and Shannon Lucid.   Lucid, already a mother, is questioned about the effect of her work on her children. 1982 -  Svetlana Savitskaya,  USSR  cosmonaut, becomes the second woman in space, flying aboard the Soyuz T-7. 1983 - June - Sally Ride, American astronaut, becomes the first American woman in space, the third woman in space. She was a member of the crew on STS-7, space shuttle  Challenger. 1984 - July - Svetlana Savitskaya, USSR cosmonaut, becomes first woman to walk in space and the first woman to fly in space two times. 1984 - August - Judith Resnik becomes the first Jewish American in space. 1984 - October - Kathryn Sullivan, American astronaut, becomes first American woman to walk in space. 1984 - August - Anna Fisher becomes the first person to retrieve a malfunctioning satellite, using the orbiter remote manipulator arm. She was also the first human mother to travel in space. 1985 - October - Bonnie J. Dunbar made her first of five flights on a space shuttle. She flew again in 1990, 1992, 1995 and 1998. 1985 - November - Mary L. Cleave made her first flight of two into space (the other was in 1989). 1986 - January - Judith Resnik and Christa McAuliffe were the women among the crew of seven to die on the space shuttle Challenger when it exploded.   Christa McAuliffe, a schoolteacher, was the first non-government civilian to fly on the space shuttle. 1989: October - Ellen S. Baker flew on STS-34, her first flight. She also flew on STS-50 in 1992 and STS-71 in 1995. 1990 - January - Marsha Ivins makes her first of five space shuttle flights. 1991 - April - Linda M. Godwin makes her first of four flights on the space shuttle. 1991 - May - Helen Sharman became the first British citizen to walk in space and the second woman aboard a space station (Mir). 1991 - June - Tamara Jernigan makes her first of five flights in space.   Millie Hughes-Fulford becomes the first female payload specialist. 1992 - January - Roberta Bondar becomes the first Canadian woman in space, flying on U.S. space shuttle mission STS-42. 1992 - May - Kathryn Thornton, the second woman to walk in space, was also the first woman to make multiple walks in space (May 1992, and twice in 1993). 1992 - June/July - Bonnie Dunbar and Ellen Baker are among the first American crew to dock with the Russian space station. 1992 - September STS-47 - Mae Jemison becomes first African American woman in space.   Jan Davis, on her first flight, with her husband, Mark Lee, become the first married couple to flly in space together. 1993 - January  - Susan J. Helms flew on the first of her five space shuttle missions. 1993 - April - Ellen Ochoa becomes first Hispanic American woman in space. She flew three more missions. 1993 - June - Janice E. Voss flew her first of five missions.   Nancy J. Currie flew her first of four missions. 1994 - July - Chiaki Mukai becomes the first Japanese woman in space, on U.S. space shuttle mission STS-65. She flew again in 1998 on STS-95. 1994 - October - Yelena Kondakova flew her first of two missions to the Mir Space Station. 1995 - February - Eileen Collins becomes the  first woman to pilot a space shuttle. She flew three more missions, in 1997, 1999 and 2005. 1995 - March - Wendy Lawrence  flew the first of four missions on the space shuttle. 1995  - July - Mary Weber flew the first of two space shuttle missions. 1995  - October - Cahterine Coleman flew her first of three missions, two on the U.S. space shuttle and, in 2010, one on Soyuz. 1996 - March - Linda M. Godwin becomes the fourth woman to walk in space, making another walk later in 2001. 1996 - August - Claudie Haignerà © Claudie Haignerà ©the first French woman in space. She flew two missions on Soyuz, the second in 2001. 1996 - September - Shannon Lucid returns from her six months on Mir, the Russian space station, with a record for the time in space for women and for Americans she is also the first woman to be awarded the Congressional Space Medal of Honor. She was the first American woman to fly on a space station. She was the first woman to make three, four and five space flights. 1997 - April - Susan Still Kilrain became the second female shuttle pilot.   She also flew in July 1997. 1997 - May -  Yelena Kondakova becomes  the first Russian woman to travel on the U.S. space shuttle. 1997 - November - Kalpana Chawla becomes the first Indian American woman in space. 1998 - April - Kathryn P. Hire flew her first of two missions. 1998 - May - Nearly 2/3 of the flight control team for STS-95 were women, including the launch commentator, Lisa Malone, the ascent commentator, Eileen Hawley, the flight directory, Linda Harm, and the communicator between crew and mission control, Susan Still. 1998 - December - Nancy Currie completes the first task in assembling the International Space Station. 1999 - May - Tamara Jernigan, on her fifth space flight, becomes the fifth woman to walk in space. 1999 - July - Eileen Collins becomes the first woman to command a space shuttle. 2001 - March - Susan J. Helms becomes the sixth woman to walk in space. 2003 - January - Kalpana Chawla and Laurel B. Clark die among the crew in the Columbia disaster aboard STS-107.   It was Clarks first mission. 2006 - September - Anousheh Ansara, on board for a Soyuz mission, becomes the first Iranian in space and the first female space tourist. 2007 - When Tracy Caldwell Dyson flies her first US space shuttle mission in August, she becomes the first astronaut in space who was born after the Apollo 11 flight.   She flew in 2010 on the Soyuz, becoming the 11th woman to walk in space. 2008 - Yi So-yeon becomes the first Korean in space. 2012 - Chinas first female astronaut, Liu Yang, flies in space.   Wang Yaping becomes the second the following year. 2014 - Valentina Tereshkova, the first woman in space, carried an Olympic flag in the Winter Olympics. 2014  -   Yelena Serova becomes the first woman cosmonaut to visit the International Space Station. Samantha Cristoforetti becomes the first Italian woman in space and the first Italian woman on the International Space Station. This timeline  © Jone Johnson Lewis.

Border Security essays

Border Security essays The terrorist attacks on the World Trade Center in September 11, 2001 or commonly known as 9/11 made America join the ranks of countries that suffered from the effects of terrorism for decades such as the France, United Kingdom, Germany and Italy. Americas innocence was since this terrorist incident is of greater enormity compared to other terrorist events that occurred and in terms of the socio-political impact, the message was brought home that no one is safe and it was time to close ranks and protect the homeland from future incidents such as 9/11. The U.S. governments initial response to 9/11was the rapid implementation of the Patriot Act of 2001 or completely known as Uniting and Strengthening America by Providing Appropriate Tools Required to Intercept and Obstruct Terrorism Act of 2001. The legislation contains sections that defines and effects controls and measures in the fight against terrorism such as (Senate and House of Representatives of the United States of America, 2001): Enhanced domestic security against terrorism; Abatement of international money laundering and anti-terrorist financing; Removal of obstacles to investigating terrorism; Provision for victims of terrorism, public safety officers and their families; Increased information sharing for critical infrastructure protection; Strengthening the criminal laws against terrorism; and Aside from the enactment of the Patriot Act, the Department of Homeland Security (DHS) was stood up through House Resolution 5005 Homeland Security Act of 2002. The primary mandate of the Department of Homeland Security or DHS is to prevent terrorist attacks within and reduce the vulnerability to terrorism of the United States (Senate and House of Representatives of the United States of America, 2002). By being the focal point of the U.S. response to terrorism, the DHS absorbed some major government agencies ...

Relativism vs. Objectivism in Aesthetic Evaluation Essay

Relativism vs. Objectivism in Aesthetic Evaluation - Essay Example In accordance with Young (2003) ‘the aesthetic value can be objective or subjective, being influenced by the criteria used for evaluating a specific event/ object’ (Young 2003 p.117). On the other hand, it should be made clear that a work of art is considered as having no value when the specific work of art has no effect on people. Moreover, the evaluation of a work of art should be primarily based on the potential benefits that the specific piece would secure for the public (Young 2003). In any case, when no reference is made to the pleasure that a particular work of art can offer to the public, then the evaluation of the specific work of art can be characterized as invalid. The identification of the influence of objectivism and relativism on the aesthetic evaluation is a difficult task. In terms of its nature, aesthetic value is a concept used for explaining the value of an object based on its characteristics. In accordance with Bunnin and Yu (2004) the aesthetic value can be described as ‘the properties rendering a work of art good or successful, such as balance, charm and elegance’ (Bunnin and Yu 17). Aesthetic value, in the above sense, can be focus on different characteristics of a work of art, such as its colour or its significance for the society’ (Bunnin and Yu 17). ... Then, their role in aesthetic evaluation would be made clear. It should be noted that the existing theory on relativism and objectivism, especially regarding the aesthetic evaluation, is based on different approaches, mostly because of the extensive use of these concepts in explaining the response of individuals to their external environment. It should be noted that the relevant views will be presented and analyzed, as possible, especially in regard to their relation to aesthetic evaluation. In accordance with Baghramian (2004) relativism can have three different forms; it can be characterized as subjective, social and conceptual (Baghramian 7). Subjective relativism is based on the view that ‘aesthetic evaluations are depended on the beliefs of individual thinkers’ (Baghramian 7). The above type of relativism is differentiated from social relativism, which highlights the importance of social conditions as a criterion for the development of aesthetic evaluation. Moreover , conceptual relativism is highly based on ‘ontology and scientific paradigms’ (Baghramian 7), which can be used every time that an object or an event has to be evaluated in terms of its aesthetic status or quality (Baghramian 7). Among the three forms of relativism presented above, the one that most reflects the role of relativism in aesthetic evaluation is the first one, the subjective relativism. This form of relativism is clearly opposed to objectivism, as a concept also reviewed in this paper, especially as of its use in aesthetic evaluation. At the same time, relativism can result to the different evaluation of aesthetic properties. More specifically, in the context

Migration and Sexual Health Essay Example | Topics and Well Written Essays - 3000 words

Migration and Sexual Health - Essay Example stion, the report has established that MSM are more prone to acquiring STIs than their heterosexual partners because unprotected anal intercourse presents more chances of acquire STIs than virginal intercourse. On the third question, it has been conclusively noted that the sexual and reproductive health of African migrants is gendered in its effects because men have more powers and privileges over the sexuality and reproduction of their female partners. This present report is primarily based on the topics of migration and sexual health. In the context of the report, the term ‘migration’ will be used to refer to the movement of people from one region to another while the term ‘sexual health’ will be used to refer to the â€Å"state of mental, physical, emotional, and social well-being of a person in terms of sexuality (Rutter and Schwartz, 2012) and (Crooks and Baur, 2014). In order to broaden the understanding of the topic area it is important to note that the term ‘sexuality’ refers to the sexual habits and desires of a person. The study on migration and sexual health cuts across as unique in the field of academics because not so many studies have been dedicated to look into the relation of migration and sexual health. In particular, this present study will look at the migration of Africans from various African countries into the United Kingdom. It is important to note that over the past years dating back to the late part of the 20th century, there has been a continued increase of African migrants drawn from various countries into the United Kingdom. According to Spencer (2010), this trend of migration has been promoted by the fact that UK is perceived to be a greener pasture for the African migrants who believe they can easily secure well paying jobs in the country, and gain access to quality education. However, Arthur et al. (2012) added that some African migrants opted to migrate to the UK as asylum seekers in order to evade the hostile political