Analysis of the Circus Film Essay Example | Topics and Well Written Essays - 750 words

Analysis of the Circus Film - Essay Example As the paper highlights Tramp is then made aware of the opportunity at the circus availed by the ringmaster for him to show his talent. At this point, Tramp discovers that his comic or hilarious bits only happen unintentionally. Replacing the circus apple with a banana from his pocket is particularly very funny. The scene is important as it reveals more characters such as Merna and the Circus Ringmaster and Proprietor.From this paper it is clear that  it is important to focus on the shot angles. Medium shot overwhelms the scene with the ordeal between Tramp and Merna ‘fighting’ over the bread, which sends Tramp sitting on the fire he lit to make his food. The medium shot features from 17:35 to 19: 45 capturing the conversation between Tramp and the lady. This is followed by a long shot showing Tramp give Merna the egg then runs off to catch up with the Circus Ringmaster and Proprietor. The long shot continues in Tramp’s circus tryout, covering all the characters present in the event. Basically, the scene represents an alteration between medium shot and long shot, with the medium shots majorly utilized to show conversations or actions between two characters and the long shot used in showing a bigger audience of characters such as that at the Tramp’s circus try out.  The eye level shots have been overwhelmingly used in the circus tryout, with low shots essentially used together with the medium shots in conversations between two characters, such as the instance between Merna and Tramp.  

Private sector bank Essay Example for Free

Private sector bank Essay 1. Difference of recruitment Public sector banks recruit mainly through bank exams and public notices. Private banks, on the other hand, prefer campus placements and referrals. For entry level jobs too, private banks usually go through campus placements. You would seldom find a public notice issued by a private bank for recruitments. 2. Difference of vacancies Public sector banks go by the vacancy rules laid by the government. There is a certain portion of vacancies reserved for OBCs and SC/STs. There are no reservations in private sector banks. The reservations make it harder to find a job in a public sector bank. 3. Difference in growth One of the banes of public sector banks is slow growth. If you get recruited at the entry level in a public sector bank, you would take forever to reach the higher levels. There are certain rules for promotion and salary is fixed according the level you are working at. Promotions in public sector banks are usually not done on merit, but other criteria laid down by the government. On the other hand, growth can be fast and robust in a private sector bank job. In the private sector, you get promotions on merit, and if you are good, sky is the limit for you. 4. Difference in working environment Largely, the working environment of private and public sector banks is the same. However, private sector banks are largely more competitive than the public sector banks, although that situation is changing fast. In a private sector bank, you usually have to meet tough targets, and adhere to the deadlines. You could be working longer hours very often in private sector banks in order to meet your targets and deadlines. The environment is more relaxed in a public sector bank, but that by no means implies you do not have work in the public sector. 5. Difference in pay scale Largely, the pay scale in private and public sector banks is the same. However, according to recent studies done on the field, it has been seen that public sector banks pay more compared to private sector banks, when the working hours are taken into consideration. However, since the growth in public sector banks can be slow, the advantage of higher pay scale is usually negated. As for the question, whether to work in a private sector or a public sector bank, the difference between both the sectors is fast diminishing. If you have a choice, go for a bank that offers opportunities for growth, which could be a public sector bank or a private sector bank too.

Cardiac Muscle Structure and Function

Cardiac Muscle Structure and Function The structure of cardiac muscle The capacity for cells to utilize biochemical energy to generate both mechanical force and movement of the human body is a dominant feature found in muscle cells. There exist three distinct categories of muscle tissue, each differing by specific structural and functional properties. These categories include smooth muscles, skeletal muscles and cardiac muscles. Smooth muscles are involuntarily contracting, non-striated muscles that surround the inside walls of hollow organs such as the urinary bladder, reproductive organs, and both the gastrointestinal and respiratory tracts. Its contraction enables and regulates the progression of liquid content, such as food, urine and blood, along the internal passageways. Skeletal muscles are voluntarily contracting, striated muscles that attach to bones of the skeleton. The contraction of skeletal muscle is primarily responsible for the movement of the skeleton, but also has roles in heat production and protection of internal organs. Cardiac musc les are an involuntarily contracting, striated muscle found exclusively in the walls of the heart, more specifically in the myocardium. Contraction of cardiac muscles propel oxygenated blood into the circulatory system to deliver oxygen to the body, as well as regulates blood pressure (Martini et al., 2009). Cardiac muscle tissue is composed of a network of individual cardiac muscle cells, called cardiomyocytes. Cardiomyocytes are small in size, averaging 10-20ÃŽ ¼m in diameter and 50-100ÃŽ ¼m in length, have a single centrally positioned nucleus and connect to adjacent cells in a branched manner through specialized sites known as intercalated discs (Martini et al., 2009). Two structures that are found within the intercalated discs are  desmosomes and gap junctions. Desmosomes are specialized structures involved in cell-to-cell adhesion and gap junctions are intercellular channels that connect the cytoplasm of adjacent cells, allowing the free passage of molecules, ions and electrical signals. Within the cytoplasm of striated muscle cells are long, cylindrical organelles termed myofibrils. With a diameter of 1 to 2ÃŽ ¼m and numbering between hundreds to thousands in a cell, myofibrils are enveloped and grouped together by connective tissue called the fasciculus, which forms bundles of myofibrils that spans the length of the cell (Widmaier et al., 2006). Individual myofibrils can be further divided into two types of contractile filaments: thin filaments and thick filaments. These filaments are composed primarily of actin and myosin proteins, respectfully. The thin and thick filaments are aligned in a manner where they form repeating structural units along the length of the myofibril. Among these structures is the sarcomere, which is a Ca2+-dependent contractile unit responsible for muscle contraction and relaxation (Widmaier et al., 2006). An increase in cytoplasmic Ca2+ influx causes the thin and thick filaments to overlap each other, causing a shortening of the sarcomere, leading to a muscle contraction. Alternatively, a decrease in cytoplasmic Ca2+ levels causes the thin and thick filaments to pull away from each other, leading to relaxation of the myofilaments. The specific arrangement of the thin and thick myofilaments is responsible for the striated appearance of both skeletal and cardiac muscle tissue. Electrical stimuli, called action potentials, are required for striated muscle cell contraction. In skeletal muscles, action potentials are derived from neurons in the brain and spinal cord that transmits the signal through the nervous system and innervates muscle fibers, causing contraction. However, unlike skeletal muscles, the contraction of cardiac muscles occurs without neural stimulation, a property called automaticity (Martini et al., 2009). This is because the heart contains pacemaker cells, which are specialized cells that have no contractile function; rather having the ability to initiate and conduct action potentials to neighboring cardiomyocytes. The cardiac action potential propagates across cardiomyocytes through gap junctions, allowing the cells to contract in tandem, which enables the heart to contract as one muscle. Cells which have pacemaker activity constitute 1% of cardiac muscle cells, whereas the other 99% are contractile cells (Sherwood, 2006). The conversion of an electrical stimulus into a mechanical response is performed through a physiological process known as the excitation-contracting coupling or the ECC. This phenomenon has a critical role in muscle cells as it allows a propagating action potential to cause shortening of the sarcomere, leading to muscle cell contraction. When action potentials are produced by pacemaker cells, they conduct across the heart by traveling along the length of the myofibril on the muscle sarcolemma. An action potential will transmit on the sarcolemma until it reaches a transverse-tubule (T-tubule). T-tubules are defined as deep invaginations into the sarcolemma that contact the cisternae of the sarcoplasmic reticulum (SR), an organelle that functions as a Ca2+ storing body. Upon penetrating the T-tubules, the action potential will cause a depolarization of the membrane voltage potential, leading to an increased influx of Ca2+ into the cytoplasm. Resting within the T-tubules are many ion tr ansporters such voltage-gated L-type Ca2+ channels and Na+ / Ca2+ exchangers (D. Bers, 2002). These Ca2+-transporters are opened/activated when stimulated by action potentials, prompting the entry of extracellular Ca2+ into specific microdomains in the cytosol (Berridge, 2006). An elevation of cytoplasmic Ca2+ levels will trigger the opening of ryanodine receptors (RyR), which are intracellular Ca2+ channels present on the membrane of the SR, allowing stored Ca2+ to exit the SR and enter the cytosol. The mechanism of how Ca2+ ions triggers Ca2+ release from the SR was identified by several groups in the 1960s, and appropriately termed Ca2+-induced- Ca2+-release (Endo et al., 1968; Ford et al., 1968). An overall increase in intracellular Ca2+ level causes Ca2+ to bind and cause a conformational change in Troponin C, a protein present on actin filaments. This conformational change causes a displacement of Tropomyosin, which prevents the interaction of myosin protein with actin filaments, thereby allowing myosin to contact actin, which promotes sarcomeric contraction. Alternatively, Ca2+ sequestration from myofilaments and cytoplasmic depletion prompts a relaxation of the sarcomere. Such a decrease of cytoplasmic Ca2+ occurs by either by re-entering the lumen of organelles, such as the SR and mitochondria, or cellular export by Ca2+ pumps and Na+/ Ca2+ exchangers on the sarcolemma (D. Bers, 2002). The efficiency of muscle contraction is partly depicted by the type of myosin heavy chain (MyHC) that the cell expresses. MyHC are enzymes, found on the head of myosin proteins, which catalyze the hydrolysis of ATP. The rate at which MyHC can hydrolyze ATP ultimately depicts the speed at which the myofilaments contract, as well as the overall energy efficiency of that cell. In cardiomyocytes, two types of MyHC proteins are expressed: ÃŽ ±-MyHC and ÃŽ ²-MyHC. The following table represents the distinguishing features of the cells that express either ÃŽ ±-MyHC or ÃŽ ²-MyHC: Similar to skeletal muscles, cardiomyocytes are categorized into two distinct classes, based on the type of myosin heavy chain (MyHC) that is expressed. Those who predominantly express ÃŽ ±-MyHC are found in adult hearts, contract in a more energy inefficient manner and are quicker to fatigue. In contrast, cardiomyocytes that express more ÃŽ ²-MyHC are present in developing hearts, have a more energy efficient contraction and are more resistant to fatigue. Cardiovascular diseases and pathological cardiac hypertrophy Cardiovascular diseases are disorders that prevent the proper function of the heart and blood vessels, causing abnormalities of the cardiovascular system, which lead to defects in the brain, kidneys, lungs and other parts of the body (Public Health Agency of Canada, 2009). According to the World Health Organization, cardiovascular diseases accounted for 29% of global deaths in 2004, making it the leading cause of death in the world (World Health Organization, 2009). Furthermore, with an aging population, the number of patients diagnosed with heart disease in America is expected to double within the next 30 years, from 5 million to 10 million (Hobbs, 2004). In Canada, this disease was responsible for 31% (or >70,000) of total deaths in 2005 (Statistics Canada, 2009). Amongst the numerous categories of cardiovascular diseases, heart failure is the most prevalent, with the fastest spreading rate and the highest mortality rate over the past decade (Heineke et al., 2006). Heart failure is defined by defects in cardiomyocyte structure, function, rhythm or conduction, which prevents the heart to pump adequate amounts of oxygenated blood and nutrients to meet the bodys demands (McMurray et al., 2005). Individuals living with a failing heart suffer from severe coughing, shortness of breath and edema, leading to a decreased tolerance to exercise and an overall diminishment in physical and mental health. As the disease progresses, patients may develop further pathophysiologies due to detrimental effects on the function of vital organs, ultimately resulting in death. A common abnormality that precedes heart failure is the pathological enlargement of the heart, a condition known as cardiac hypertrophy. Cardiac hypertrophy is induced by the release of hormones, cytokines, chemokines and peptide growth factors, which act on cardiomyocytes in an endocrine, paracrine and autocrine manner (Heineke et al., 2006). The release of these factors occurs in response to increased cardiac workload, myocardial injury or defects in the contractibility of cardiomyocytes (J. Molkentin, 2000). The initial stage leading to cardiac hypertrophy is increased size and cell volume of cardiomyocytes in order to sustain the increased cardiac output demanded by the hypertrophied heart. Such a process is referred to as compensatory hypertrophy. At later stages of cardiac hypertrophy, the hypertrophied heart can no longer keep up with the increased workload, which subjects patients to heart failure, cardiac arrhythmias and sudden death (Berenji et al., 2005). It should be noted physiological cardiac hypertrophy, which occurs during pregnancy, adolescence growth and aerobic training, does not share the same detrimental consequences on cardiomyocytes as pathophysiological heart growth (Oakley, 2001). A characteristic of pathologically hypertrophied hearts is cardiomyocyte disarray, which is a disorder of heart cells. Misaligned cardiomyocytes prompts a disruption in the conduction of action potentials across cells, leading to compromised intracellular Ca2+ kinetics and decreased shortening of the sarcomere, which ultimately compromises the contractions of the heart. The molecular signaling pathways, responsible for cardiac hypertrophy, are being extensively studied by researchers with the hopes of developing therapies to treat cardiac hypertrophy. Calcineurin-NFAT signaling pathway The availability of intracellular calcium (Ca2+) in mammalian cells is critical for their existence and proper function. In addition to its role in muscle cell electrophysiology and contraction, Ca2+ acts as a secondary messenger in many signal transduction pathways, involved in physiological processes such as fertilization, memory, apoptosis, membrane trafficking and cell division (D. M. Bers, 2008). Furthermore, at the molecular level, Ca2+ has been implicated in regulation of gene transcription, DNA replication, DNA repair and both protein synthesis and degradation. A common question in muscle cell biology is that, with its numerous downstream targets, how does Ca2+ specify and activate a particular signaling pathway. It is generally understood that Ca2+ influxes into the cytoplasm through Ca2+ transporters on the sarcolemma as waves of Ca2+. In the 1990s, researchers have identified that depending on the amplitude and frequency at which Ca2+ waves penetrate the cell, different Ca2+-dependent signaling pathways are activated, which also affects gene expression and cell differentiation (Berridge, 1997; Dolmetsch et al., 1997; Dolmetsch et al., 1998). However, the exact molecular mechanisms in which specific Ca2+-dependent pathways in contracting cardiomyocytes are regulated remains disputed due to the highly specialized rhythmic cycling of Ca2+ involved in the hearts ECC. Molkentins group have postulated the existence of Ca2+ microdomains in the cytoplasm, which are relatively independent of the Ca2+ involved in the ECC. Within these microdomains , Ca2+ is locally regulated and can activate protein signaling pathways in that particular region (Houser et al., 2008). Many proteins that require Ca2+ to be active cannot readily bind Ca2+, thus use Calmodulin (CaM), a high affinity Ca2+-binding protein, as a Ca2+ sensor and signal transducer. Expressed in all eukaryotic cells, CaM is a 17kDa protein composed of four EF-hand motifs, each capable of binding a single Ca2+ ion. The affinity to which Ca2+ binds CaM depends on changes in intracellular Ca2+ concentrations. When cytoplasmic Ca2+ level are low, CaM exists in a closed conformation, where the EF-hand motifs are packed together, hiding the Ca2+ binding sites. Alternatively, when intracellular Ca2+ level are high, Ca2+ ions bind to the EF hand motifs on CaM, causing a conformational change that allow Ca2+ to bind more readily to the other motifs, allowing CaM to attain an open configuration (Chin et al., 2000). Because CaM is a small, flexible molecule with numerous targets, such conformational changes are required to expose specific hydrophobic regions on each domain, which allow the Ca2+-CaM c omplex to bind and activate specific proteins (Al-Shanti et al., 2009). One of the most recognized signaling pathways that require the Ca2+-CaM complex to be activated is the Calcineurin Nuclear Factor of Activated T-Cells cascade. Calcineurin (Cn), also referred to as protein phosphatase 2B (PP2B), is a Ca2+-dependent serine/threonine phosphatase that was first discovered in 1979 as a CaM binding protein in brain extracts (Klee et al., 1979). Further research by Schreibers group identified that Cn played a prominent role in the immune system, where the addition of immunosuppressive drugs, cyclosporine A (CsA) and FK506, decreased Cns activity (Liu et al., 1991). Cn is ubiquitously expressed in all cells and the gene that encodes the Cn protein is conserved from yeast to mammals, suggesting a common mode of regulation (Al-Shanti et al., 2009; Rusnak et al., 2000). Once active, Cn can de-phosphorylate a number of transcription factors such as myocyte enhancer factor 2 (MEF2), nuclear factor kappa-light-chain-enhancer of activated B cells (NFÃŽ ºB) and nuclear factor of activated T-cells (NFAT) (Alzuherri et al., 2003; Blaeser et al., 2000; Jain et al., 1993; Michel et al., 2004). In addition to transcription factors, Cn has been identified as a direct regulator of the pro-apoptotic factor, Bcl-2 (Wang et al., 1999). The most characterized downstream target of Cn is the family of NFAT transcription factors. In the heart, the role of the Cn-NFAT signaling pathway in mediating pathological cardiac hypertrophy in vitro and in vivo has been extensively studied (Bueno et al., 2002; De Windt et al., 2001; Hill et al., 2002; Molkentin et al., 1998; Sussman et al., 1998; Zou et al., 2001). Once de-phosphorylated, NFAT transcription factors translocate to the nucleus and dimerize with other transcription factors to re-activate cardiac fetal genes, leadin g to hypertrophy of the adult heart. The structure of Calcineurin Human Cn was first crystallized in 1995 by the Villafranca group (Kissinger et al., 1995). Although it shares similar sequence homology to other serine/threonine protein phosphatases, PP1 and PP2A, the structure of Cn was found to be unque due to its dependence on Ca2+ for optimal activity (Griffith et al., 1995; Kincaid et al., 1988; Klee et al., 1988). From its structure, it was discovered that Cn exists as a heterodimeric protein, consisting of two subunits: the 59kDa catalytic subunit, calcineurin A (CnA), and the 19kDa regulatory subunit, calcineurin B (CnB) (Kissinger et al., 1995). The structure of CnA consists of two domains: a catalytic region which is found on the N-terminal and the regulatory domain which is present on the C-terminal region (Al-Shanti et al., 2009). The regulatory domain of CnA consists of three sub-domains: a CnB binding domain), a CaM binding domain) and an autoinhibitory domain (AI) as depicted in Figure 1.4 (Ke et al., 2003; Klee et al., 1998). Alternatively, the structure of CnB shares a 35% sequence identity to CaM and contains four EF-hand motifs, allowing it to bind Ca2+ ions in a similar mechanism as CaM (Klee et al., 1988; Kretsinger et al., 1973). In non-stimulated muscle cells, Cn is present in its inactive conformation, in the cytoplasm, where the autoinhibitory domain sterically blocks CnAs catalytic domain, rendering the phosphatase inactive. Upon stimulation, cytoplasmic Ca2+ will bind CnB, causing a conformational change, which exposes the CaM binding domain on CnA. Once the Ca2+-CaM complex docks onto its respective binding domain, another conformation change occurs which displaces the autoinhibitory domain from the catalytic domain, enabling the enzyme to be active. The crystal structure of full length human Cn was solved with a resolution of 2.1Ç º. The globular structure of CnA consists of 521 residues, where residues 14-342 form the catalytic domain and residues 343-373 form the CnB binding helical domain (Kissinger et al., 1995). Residues 374-468 and 487-521 are not visible in the crystal structure because they are presumed to exist in a random conformation(Ke et al., 2003). The AI domain is represented by a segment of 18 residues (Ser469-Arg486) that lie over the substrate-binding cleft on the C-terminus of CnA. The AI domain consists of two conserved short ÃŽ ±-helical domains, with five additional residues in its extended form. The residues of the AI domain that have the strongest interactions with the substrate-binding cleft of CnA were identified as Glu481-Arg-Met-Pro484, where Glu481 hydrogen-bonds with water molecules bound to the dimetal site in Cns active site (Kissinger et al., 1995). Residues 343-373 form an extended amphipathic ÃŽ ±-helical region that interacts with hydrophobic residues within the CnB binding cleft. In mammals, CnA is encoded by three genes (CnAÃŽ ±, CnAÃŽ ², CnAÃŽ ³) and CnB by two genes (CnB1, CnB2). Yet in the heart, only CnAÃŽ ±, CnAÃŽ ² and CnB1 are expressed (J. Molkentin, 2000). NFAT proteins NFAT transcription factors were first identified by the Crabtree group where, similar to Cn, NFAT played an important role in the regulation of early T-cell activation genes (Shaw et al., 1988). Since its discovery, researchers have provided evidence that the role of NFAT proteins was not restricted to T-cells, having been implicated in the central nervous system, blood vessels, heart, kidney, bone, skeletal muscle and haematopoietic stem cells (Crabtree et al., 2002; Graef et al., 2001; Hogan et al., 2003; Kiani et al., 2004; Macian, 2005). NFAT proteins are part of the Rel-family of transcription factors. The molecular mass of NFAT ranges from 70-200kDa, which is due to alternative splicing of genes resulting in varying protein sizes and differential phosphorylation states (van Rooij et al., 2002). The primary structure of NFAT consists of a moderately conserved N-homology region (NHR), a conserved Rel-homology region (RHR) and a non-conserved C-terminal domain (CTD). Firstly, the NHR (residues 1-407) contains a transactivation domain (TAD), a Cn docking site, a nuclear localization signal (NLS), a nuclear export signal (NES), serine-rich regions (SRR) and Ser-Pro-X-X-repeating motifs (SP), where X denotes any amino acid. The TAD is required for NFAT to bind the promoter region of genes to initiate transcriptional events. The Cn docking domain contains a SPRIEIT sequence, a variant of PxIxIT, which allows Cn to bind to NFAT and de-phosphorylate serine residues, mediating the nuclear shuttling of NFAT. Secondly, the RHR (residues 408-677), which is conserved among all Rel proteins, confers to a shared DNA binding specificity (L. Chen et al., 1998). The C-terminus of the RHR contains a DNA binding motif, which permit Rel-proteins to bind the 5-GGAAA-3 consensus sequence (Rao, 1994). The N-terminus of the RHR contains a domain that allows NFAT to interact with other transcription factors in the nucleus. Such molecular partners include the leucine zipper protein activator protein-1 (Fos, Jun), the Zn-finger protein GATA-4, the MADS box protein MEF2 and many others (L. Chen et al., 1998; Crabtree et al., 2002; Hogan et al., 2003; Molkentin et al., 1998). Lastly, although the exact role of the CTD (residues 678-928) remains ill defined, due to the differences in the length of the CTD between NFAT isoforms, it is possible that the CTD is responsible for the different transcriptional activity of the NFAT isoforms, as shown by several groups (Calabria et al., 2009; Rinne et al., 2010). NFAT transcription factors are ubiquitously expressed and consists of five isoforms: NFATc1, NFATc2, NFATc3, NFATc4 and NFAT5 (also known as tonicity-responsive enhancer-binding protein or TonEBP) (Mancini et al., 2009). Of the five NFAT proteins, only NFATc1, NFATc2, NFATc3 and NFATc4 are regulated by Ca2+-Cn signaling and are have known roles in skeletal and cardiac muscles (Calabria et al., 2009; van Rooij et al., 2002). NFAT5 cannot interact with Cn due to the absence of a SPRIEIT domain and is therefore insensitive to Ca2+-Cn signaling (Lopez-Rodriguez et al., 1999). Rather, NFAT5 is regulated by osmotic stress and is known to control the expression of cytokines, such as tumor-necrosis factor (TNF) and lymphotoxin-ÃŽ ², in lymphocytes (Lopez-Rodriguez et al., 2001; Macian, 2005). Due to its insensitivity of Cn and unclear roles in muscle cells, for the remainder of this thesis, the focus will be on the Ca2+-Cn regulated NFAT isoforms: NFATc1, NFATc2, NFATc3 and NFATc4. The cellular localization of NFAT proteins depend on the phosphorylation state of approximately 14 serine residues on the NHR. Okamura et al. identified that of these residues, 13 phosphoserines are targeted by Cn and are located in motifs SRR1, SP2 and SP3 (Macian, 2005; Okamura et al., 2000). Upon de-phosphorylation, the NLS sequence of NFAT is exposed and the NES is masked, prompting nuclear entry. NFAT kinases are regulators of NFAT transcription factors, which can interact with NFAT and reversibly phosphorylate the same serine residues that are targeted by Cn. Known NFAT kinases include casein kinase-1 (CK-1), glycogen-synthase 3ÃŽ ² (GSK3-ÃŽ ²), p38 and JUN-N-terminal kinase (JNK) (Beals, Sheridan et al., 1997; Chow et al., 1997; Gomez del Arco et al., 2000; Zhu et al., 1998). Upon re-phosphorylation, the NES sequence is re-exposed whereas the NLS sequence is hidden, prompting cytoplasmic retention of NFAT (Okamura et al., 2000). These kinases can either be classified as mainte nance kinases, which phosphorylate NFAT in the cytosol to prevent nuclear import or export kinases, which target NFAT in the nucleus to promote nuclear export. Each kinase can phosphorylates serine residues on specific motifs. CK-1 acts as both an export and maintenance kinase on SRR1 of NFATc2 (Okamura et al., 2004). GSK3-ÃŽ ² functions as an export kinase on both SP2 and SP3 of NFATc1 and SP2 on NFATc2 (Beals, Clipstone et al., 1997; Macian, 2005). The mitogen activated protein kinase (MAPK) family consists of p38, JNK and extracellular-regulate-signal kinases (ERK) and can phosphorylate the first serine of SRR1 on different NFAT isoforms. JNK phosphorylates NFATc1, whereas p38 targets NFATc2 (Chow et al., 1997; Gomez del Arco et al., 2000). CK1 may be responsible for phosphorylating the remaining serines on SRR1 (Macian, 2005). Although a cell may have the potential to translate different NFAT isoforms, depending on which NFAT kinase is expressed, only certain NFATs may be nuclea r localized. Cn-NFAT signaling in cardiac hypertrophy Cn-NFAT signaling is described as a multifunctional regulator, where its function depends on the cell type in which this pathway is active. In the brain, Cn-NFAT signaling mediates numerous processes, which include memory, brain strokes, ischemic injury, Parkinson and Alzheimers disease and the regulation of the cAMP-response-element binding protein (CREB) (Shibasaki et al., 2002). In the lungs, Cn-NFAT signaling has been implicated in the perinatal lung maturation and function, and regulating genes involved in the homeostasis of pulmonary surfactant, which is required for proper breathing (Dave et al., 2006). In skeletal muscles, this pathway is required for functional-overload induced skeletal muscle hypertrophy and for mediating skeletal muscle-fiber type conversions from fast muscle fiber type to slow muscle fiber type (Dunn et al., 1999; Michel et al., 2004). In the cardiovascular system, Cn is required for the early development of the heart, specifically the cardiac septum and valves (de la Pompa et al., 1998; Ranger et al., 1998). During heart disease, Cn-NFAT signaling promotes the reactivation of cardiac fetal genes, which are responsible for cardiac growth during development. The reactivation of these genes in the adult heart is responsible for the pathological growth of the heart, and not physiological growth (Wilkins et al., 2004). In 1998, Molkentin et al. first reported the novel role that Cn-NFAT signaling played in mediating pathological cardiac hypertrophy (Molkentin et al., 1998). Among the major findings of this report was that Cn-induced the de-phosphorylation of NFATc4, prompting its nuclear entry and allowed NFATc4 to interact with the GATA-4 transcription factor, leading to cardiac hypertrophy. In addition, cultured cardiomyocytes, treated with Cn inhibitors CsA and FK-506 immunosuppressive drugs, blocked chemical-induced cardiac hypertrophy. To support their in vitro findings, transgenic mice that expressed a cardiac-specific constitutively active form of CnA were generated. The hearts of CnA overexpressing transgenic mice, compared to the hearts of wild-type counterparts, displayed a 2-to-3 fold increase in heart weight-to-body weight ratio, a thickening of the left ventricular wall and intraventicular septum, a 2-fold increase in cross-sectional area of cardiomyocytes and extensive fibrosis. Furth ermore, CnA overexpressing mice had a greater increased susceptibility to sudden death, mimicking the effects of heart failure in humans. Upon treatment with the Cn inhibitor, CsA, the hearts of CnA transgenic mice returned to normal size. Many genes and proteins that are re-employed in response to heart disease have prominent functions in embryonic and fetal heart development. For example, cardiac fetal genes are active during the physiological growth in developing hearts. This family of genes consists of atrial natriuretic factor (ANF), b-type natriuretic peptide (BNP), ÃŽ ±-myosin heavy chain (ÃŽ ±-MHC), ÃŽ ²-myosin heavy chain (ÃŽ ²-MHC), and many others (Oka et al., 2007). When the heart has fully matured into an adult heart, the expression of these genes becomes dormant. During heart disease, hypertrophic stimuli re-activate the expression of these genes in the adult heart, which enables the heart to grow to a pathological state. One of the most studied transcription factor that interacts with NFAT to initiate cardiac hypertrophy are GATA proteins. GATA transcription factors consist of two conserved zinc fingers that are required to bind to the consensus DNA sequence 5-(A/T)GATA(A/G)-3, as well as domains that allow GATA to interact with transcriptional cofactors (Ko et al., 1993; Merika et al., 1993; Oka et al., 2007). Of the six members of the GATA family (GATA-1 to GATA-6), GATA-4, GATA-5 and GATA-6 are expressed in the heart (J. D. Molkentin, 2000). Among the GATA proteins expressed in the heart, GATA-4 has been associated with embryonic cardiogenesis, such as heart tube formation, and pathological growth of the adult heart (Molkentin et al., 1997; Pikkarainen et al., 2004). In addition, GATA-4 is a known regulator of the expression of cardiac structural genes during development. GATA-4 gene targeted mice were embryonic lethal at E7-9.5 due to structural and functional defects of the heart (Molkentin et al., 1997). Alternatively, cultured cardiomyocytes overexpression of GATA-4 caused a 2-fold increase in cell surface area, whereas GATA-4 overexpressing transgenic mice lead to increased heart-weight-to-body weight ratio, cardiomyopathy features of the cells and upregulation in the expression of cardiac fetal genes (Liang, De Windt et al., 2001). The regulation of GATA-4 occurs post-translationally, where such modifications affect its DNA binding ability, transcriptional activity and cellular localization. A number of chemical stimuli that induce cardiac hypertrophy have been associated with the phosphorylation of GATA-4, which increases both its DNA binding and transcriptional activity (Oka et al., 2007; Pikkarainen et al., 2004). Molkentins group identified that phosphorylation of Ser105 on GATA-4 by the ERK1/2 and p38 MAPK was responsible for GATA-4 increased DNA binding affinity and transactivation during heart failure (Charron et al., 2001; Liang, Wiese et al., 2001). Another kinase that targets GATA-4 is GSK3-ÃŽ ², a known negative regulator of cardiac hypertrophy (Haq et al., 2000). GSK3-ÃŽ ²-mediated phosphorylation of GATA-4 prompts its export from the nucleus, rescuing Cn-mediated cardiac hypertrophy (Morisco et al., 2001). A second family of transcription factor that is re-activated during heart disease is the myocyte enhancer factor 2 (MEF2). There are four members of the MEF2 family expressed in vertebrates: MEF2A, MEF2B, MEF2C and MEF2D. MEF2 proteins can either homodimerize or heterodimerize with other transcription factors such as NFAT and GATA, which can then bind to the DNA sequence 5-CTA(A/T)4TAG-3 to carry out transcriptional events (Blaeser et al., 2000; McKinsey et al., 2002; Morin et al., 2000; Oka et al., 2007). Although the MEF2 proteins are expressed in most cell types, their transcriptional activity is restricted to the immune system, neurons and contractile muscle cells (Akazawa et al., 2003). In the heart, MEF2 have critical roles in cardiac differentiation. MEF2C null mice were embryonic lethal, due to cardiac looping defects, an absence of a right ventricle and a downregulation of cardiac structural genes (Bi et al., 1999; Lin et al., 1997; Oka et al., 2007). The majority of MEF2A null mice died 2-10 days after birth because of defects in conduction and architecture of the heart. Surviving MEF2A null mice displayed reduced mitochondrial content and a less efficient conductive system. (Naya et al., 2002). In addition, transgenic mice that express a dominant negative MEF2 died shortly after birth because of cardiomyocyte hypoplasia, thinning of the ventricular walls and heart chamber dilation (Kolodziejczyk et al., 1999; Oka et al., 2007). A greater workload imposed on the heart, a phenotype of cardiac hypertrophy, has been associated with increased MEF2-DNA binding (Molkentin et al., 1993; Nadruz et al., 2003). In cultured cardiomyocytes, adenoviral-mediated overexpression of MEF2A or MEF2C caused sarcomeric degeneration and cell elongation, both of which indicate cardiac dilatation. The hearts of transgenic mice overexpressing MEF2A or MEF2C were subject to contractile defects, ventricular dilation and were more readily hypertrophied when pressure overload stimulation was induced. However, when cells of the transgenic hearts were isolated, rather than having a greater cross-sectional area, the cardiomyocytes were more elliptical in shape, suggesting that MEF2 did not d

Existence of Reality in Christopher Durangs Beyond Therapy and Edward

Existence of Reality in Christopher Durang's Beyond Therapy and Edward Albee's Who's afraid of Virginia Woolf? Growing up, I always assumed that my parents would grow old together. I fantasized about introducing my future children to their still-married grandparents and attending, if not personally planning, my parent’s fiftieth anniversary celebration. Although my parents fought and struggled with areas of perpetual disagreement, somehow things always worked out and in my naivety, I believed they always would. However, as time progressed, the unresolved, and in some cases unspoken, issues that had plagued my parent’s marriage since its conception festered and ultimately reached intractable proportions. As a messy divorce loomed, each parent explained his version of the events and â€Å"irreconcilable differences† engendering a separation. Although the facts presented in each account matched, my parent’s respective interpretations of the facts differed greatly. As I listened to my parent’s rationalize their inability to get along, I realized that although my parent’s stories did not match, neither party was actually lying. Each parent simply presented to me his or her version of the reasons for divorce. I knew that somewhere hidden in the subtext of my parent’s explanations laid the truth. As I sifted through the slightly convoluted information, I began to wonder, â€Å"Is reality a relative concept?† After reviewing my personal experience, Christopher Durang’s play Beyond Therapy, and Edward Albee’s Who’s afraid of Virginia Woolf?, I reached the conclusion that, as inherently paradoxical as it seems, reality exists as a relative concept. Ostensibly, in the complexities of a divorce, the true reasons necessitating a permanent... ...xtremes of denial and testifies to the true relativity of reality depending upon mindset. After overcoming her denial and admitting that no son exists, Martha lies prostrate as George asks her, â€Å"Who’s afraid of Virginia Woolf?†(242). Martha wearily replies, â€Å"I†¦am†¦George†¦.I†¦am†¦Ã¢â‚¬ (242). In other words, â€Å"Who’s afraid of the truth?† My parents, Stuart of Christopher Durang’s Beyond Therapy, and Martha and George from Thomas Albee’s â€Å"Who’s Afraid of Virginia Woolf?†. Ceasing to rationalize reality to suit one’s needs entails dealing with the truth and experiencing pain. Therefore, it stands to reason that many smart, reasonable people fall victim to the allure of denial. However, as Martha demonstrates, the walls crumble eventually, and one feels the pain as acutely as ever. So, who’s afraid of the truth? The more appropriate question is who’s not afraid of the truth?

Broken Rites in Hamlet

In order to understand the role of the rites in Hamlet, one must conceptualize the ritual. The rites in Hamlet concern mainly marriage, mourning and funeral. It is crucial to distinguish their specific nature to detect how they participate in the tragedy. Arnold van Gennep identified and elaborated in his works that birth, puberty, marriage and death are the principal changes in life of an individual and that of the society. He defined and qualified them in the book of the same name as The Rites of Passage (Van Geppen).Every passage understands the successive phases of separation, liminality and re-corporation in order to allow the emotional adaptation of an individual to the transition. The transition can be particulary dangerous for the concord of the social life as its cataclysmal habitual order. Since the rites of passage are designed to avoid the possible disturbance when regulating each changing in the society, the broken rites of passage concieve the impetus for the desintegra tion.In the course of this effort to disclose the extent of the broken rites in Hamlet of how it can affect on disjonction in the play, I will analyse them as the very motor of the tragic in the play. The investigation of the broken rites in Hamlet as those that became infallible when taking in consideration the socio-cultural pecularities of the historical period of the 16th and early 17th centuries. The Plague and also the Protestant movement resulted in the abolishment of the funeral rites that could be the last and only possible defence against the all powerful, inexorable death.In the sequel, the deep and extreme human anxiety before the death rose. In the work of Michael Neil, The Issues of Death: Mortality and Identity in English Renaissance Tragedy, he made apparent how the loss of the ritual is connected with the loss of the identity. In these terms, the investigation of the broken rites is particularly relevant for the reconsideration of Hamlet because many inerpreters of the work have focused on Hamlet's character as the central axis of the tragedy (Coyle). In choosing to focus on rites, one gets a more complex understanding on what occurs in the play and how theproblematical interaction between cultural expectations and individual tendencies are tragically intertwined. Exploring the substance of the broken rites in Hamlet which explicitly stands for unmasking and accusation of the order based on the lies throw the new light upon the mechanism of the tragedy. PART I: Broken Rites as the Starting Point of the Tragic Impulse. The play is obsessed with death. Its very exposition is marked by mortal events: the old King of Denmark kills the old King of Norway, the majesty of buried Denmark (1. I. I.48) appears as a Ghost. However, the starting point of the tragic impulse is asserted by the broken rites of the funeral and marriage. The mirth in funeral and dierge in mariage/In equal scale weighing delight and dole (2. I. 2. 12). It is consequentially imp ortant to conceive that these two broken rites serve for the determinant in the inner disintegration of Hamlet. The dead King, Old Hamlet did not receive the proper mourning, due to him, hence the narration chain of his memory is broken. Especially when in a very short time, his wife marries his brother.Two months dead-nay not so much, not two A little month, or ere those shoes were old, With which she followed my poor father's body†¦ a beast that wants discourse of reason Would have mourned longer-married with my uncle My father's brother†¦ the salt of most unrighteous tears†¦ incestuous sheets!(I. 2. 138-154) â€Å"No windy suspiration of forced breath, /No, nor the fritful river in the eye, /Nor the dejected havior of the visage†( I. 2. 79-81). Hamlet is alone to â€Å"give these mourning duties to your father† ( I. 2. 88) and to be dressed in black, while the rest of the court-including the queen-are already in the â€Å"remembrance of ourselvesâ₠¬  ( I. 2. 7 ) by admitting with pleasure the changes of hierarchy and moral behavior that Claudius institutes: â€Å"The funeral baked meats/Did coldly furnish forth th emarriage tables† ( I. 2. 180-181).The origin of the tragic must be detected properly. To do this, it is helpful to refer to Steiner's definition of tragedy which is defined as â€Å"the tragic personage is broken by forces which can neither be fully understood, nor overcome by rational prudence†¦ Tragedy is irreparable† (Dollimore). The irreparable begins with the irreparably broken rites of the funeral and marriage of Hamlet’s parents, the King and Queen of Denmark that Hamlet assumes on his own. Therefore before learning the truth from the Ghost, which will turn the tragedy into a revenge, the tragedy is set already.Before learning the truth , the hero's self is disjointed : O that this too too solid flesh would melt, /thaw and resolve itself into a dew,/Or that the Everlasting had not fixed/His canon ‘gainst self-slaughter†¦ ( I. 2. 129-133). Some historical facts are necessary to evoke in order to understand the whole picture of the tragedy. Funeral and mourning rites were substantial in the Elizabethan period maingly in order to maintain the social order and the psychological defense against mortality (Tylliard).The Plague had brought in the brutal abolishment of funeral rites wherein the mass burials of all classes have no distinction in common pits without any hierarchy. The denial of the purgatory by Protestants resulted into â€Å"a painfully private apocalypse,† placing the deceased â€Å"beyond our help† (Neil). The tormenting thoughts that death strikes anyone at any moment and that â€Å"a king may go a progress through the guts of beggar† (4. 3. 30) roused extreme anxiety on the issues of death. This anxiety has developed into a profound meditation on mortality and identity.That is why the melancholic character Hamlet ha d always â€Å"his eyes turned into his very soul. † The certitude of anything, the balance were beyond any human power or will and hence any change seemed even more tormenting. The marriage to a deceased husband's brother was forbidden by the Church, whether Catholic or Protestant (Shakespear). Claudius introduces the unnatural marriage by the shift from our â€Å"sometimes sister† to â€Å"wife† ( I. 2. 8-14). Therefore it is an already irreparably broken marriage rite before learning that Gertrude was seduced and then committed adultery in the sacred marriage.The role of the rites of passage is to guarantee the smooth adaptation to change. But Hamlet was stuck in the phase of limination even before learning the truth from the Ghost. His limination phase was his mourning. He was between the live and the death, where the death was the material category. The impossibility of his passage out of mourning was reinforced by the fact that he already mentioned that he is the only mourned, hence twicely isolated. The phase of re-incorporation to the world of the dead is the most significant in the funeral rite (Van Geppen 210).Assurance was not given to Old Hamlet, as there was no separation and liminality. Separation: he was honored no relief, no purification: â€Å"Cut off even in the blossoms of my sin,/Unhouseled, dis-appointed, unaneled, /No reckoning made, but sent to my account/With all my imperfections on my head. † Limination: no proper mourning. In the sequel, The King Hamlet was not re-incorporated and that is why he appears as a Ghost. He is ineffectual to reach â€Å"the country from wich nor traveller returns†( 3. 1. 80-81).Horatio's words about the Ghost seem unrelevant at first reading but in reality they are important for the perception of the tragedy structure. â€Å"What if it tempt you toward the flood, my lord,/Or to the dreadful summit of cliff†¦ Which might deprive your soveregnty of reson/and draw you i nto madness? †( 1. 4. 48-53) The individuals that were not accorded with the proper funeral rites could never integrate into the world of the dead. This kind of dead was particularly dangerous as they were trying to penetrate there at the expense of the living beings. Usually they were marked by the desire of vengeance (Van Geppen 229-230).The passage out the liminality is possible only through the successful re-incorporation (Van Geppen 211). Can King Hamlet be re-incorporated if Hamlet revenges? Or does the chase to repair forever broken store the true mousetrap for the hero himself? The same the re-incorporation phase of mariage is never re-incorporated by Hamlet. His mother not only reintegrated in the social life, but she lives her new marriage in the amplitude of plaesures. Having been re-incorporated by others, the rite of marriage does not concern the court as it concerns Hamlet.The latter has not passed through the phases and that is why he finds himself ruptured from society. To reconstitute the inverted natural order of things, Hamlet must restore the broken chain of narration. His father must be remembered and Claudius must be punished. PART II Sleeping Dog But what restoring the memory that is restoring the broking rites inserts for the hero? Is his invocation for a retribution a possibility to reahibilitate the former natural order or is it a course towards an inevitable tragic end? One of the hero's attempts to restore the memory is the introducing of the Moustrap.The broken rites' great instigation of the unnatural is contrasting with the situation in the speech on Priam's slaughter. He maternity†¦ and for a robe,/About her lank and fall o'er-teemed loins, A blanket in th'alarum†¦ (2. 2. 498-99), wouild have made milch the burning eyes (2. 2. 508) is opposed to Gertrude's adulltry unrighteous tears( 1. 2. 155). Hecube mourning was so intense that the death or the Fortune's Wheel would treason have pronounced (2. 2. 502). It stre ssed the potent power of the rite. When the rite is devoutly respected, it can accomplish the miracles.After his successful attempt to reveal the truth, Hamlet does not kill Claudious during his attempt to pray because he must ensure the bad phase of separation for him and not to â€Å"send him to heaven. † He must be killed in â€Å"the blossom of his sin† as Old Hamlet to get stuck in the tormenting limination phase. Trying to resrore the irrepareble broken rites by restoring the memory of his father, the hero has desperately condemened to the tragic end. The atonement of the obscure past is impossible without the occurence of new tragic events. As a consequence, the individual crisis of Hamlet was becoming more contradictive and more tormenting.The successive broken rites were reperpetuted throughout the play: the Rosencrantz and Guildenstern deaths, the â€Å"hugger-mugger† way of Polonius burial which causes the disjunction in the minds of his children. It is relevant here to mark that Ophelia suffered quite the similar inner disintegration issued from the broken rites than that of Hamlet. Her father's death was insultingly dishonorable. The marriage that she prepared was abolished and hence, she can only be analyzed as stuck in the phase of the liminality. The songs in her madness speak out: â€Å"Larded with sweet flowers, /Which bewept to the grave did not go /With true-love showers.† â€Å"You promised me to wed†¦. Stricktly speaking, the death of innocent Ohelia is provoked by these two broken rites introducing a new variotion on â€Å"mirth in funeal and dierge in marriage:† â€Å"I thought thy bridebed to have decked, sweet maid† (5. 1. 154). The inexorable insistence on the irreparable collapse caused by the broken rites works up the tragedy. So considering Ophelia's death â€Å"doubtful,† the priest deprieves her from the correct obsequious rites: â€Å"Yet here she is allowed her virgin rit es†¦ †( 5. 1. 222); Hamlet: â€Å"And such maimed rites? This doth betoken/ The corpse they follow did with desp'rate hand† ( 5. 1. 209-210).Moreover, one of the Clown concludes that â€Å"if this had not been a gentlewoman, she have been buried out of Christian burial† (5. 1. 23-24). Ophelia's tragic accompined by the tokens of floral innocence end seems to be one of the most dramatic and the ambigues quarrel of Hamlet and Laertes on her coffin only exacerbates the task of restoring the rememberance. Claudious is speculating on the rite of mourning, when inciting Laertes agaings Hamlet. Was your father dear to you? /Or are you like the painting of sorrow,/A face without a heart? ( 4. 7. 95-96). The rite stakes in the sort: â€Å"To cut his throat i'th'church† ( 4. 7. 103).PART III: The effect on the identity or how the broken rites change the perception of life Exploring the anxieties and in particular the anxieties concerning the funeral and mournin g rites, the play is imminently influenced by the memento mori traditions. Making apparent the similitude of the skulls in the scene with the grave-diggers, Hamlet broods on the subject of death. The tragic emphasis intensified when unwillingly but opportunately the grief of Ophelia's death was fractured by the joking with the Yourick skull: â€Å"Now get you to my lady's chamber, and tell her, let her paint and inch thick, to this favor she must come.Make her laugh at that†( 5. 1. 184-185). And accordingly if addressed to the living this joke would have brought rather melancholy than joy. Melancholy emerges with the awareness of the loss of a geocentric and athropocentric universe, the loss of the centre. In this mesh, â€Å"the melancholic finds the opportunity to re-centre himself† (Curti 156-157). Hamlet is trying to reconstitute himself through the restoration of the rememeberance which became his obsession. In the last scenes of the play, Hamlet was getting more and more aware of the imporance of the a good death also for himself.The issue of the suicide was left aside in the first two acts. Hamlet percieved that the good end may be guaranteed by noone, but oneself. â€Å"Readiness is all† (5. 2. 169). This equivocal statement accounts also for the excuses that Hamlet presents to Laertes before his possible end. â€Å"The soldiers' music and the rites of war/ Speak loudly for him† (5. 2. 352-53) can not truely be appease the initial disjointing of time and state. Even if the solemn obsequious march that ends the play indemnify on a certain level the lack of the accomplished rite, Fortinbras is a foreigner and the former enemy who had taken the rule in his hands.The cost of this â€Å"truly delivered† ( 5. 2. 338) restoration of a piece of memory is the tragic end of the whole kindom. Conlcusion Exploring the role of the broken rites in Hamlet as the motor of the tragic in the play cannot be a delusion, but is a broad fi eld of research of the precision in the approaches of the understanding of the tragedy. Alternatively, from the very broken cemectries of Caesar's Rome and to the groteskly solemn funeral rites on Hamlet's honor, the broken rites are confirmed to possessan an eldritch power to affect on the social as well as on the individual.Proving their susceptibility to unremitting reproduction of the new broken rites that bind us towards a more sophisticated account of the mechanism of the emergence of the successive tragic impulses in the play, the critical reading of the play from the broken rites axis. Bearing in mind the social and cultural context of the 16 th and early 17th centuries and in particular the memento mori and the arts of death traditions, the play does not impend the remorseless broken rites to gratify the tragedy. Works Cited Coyle, Martin. Hamlet. UK: Palgrave Macmillan, 1992.Curti, Lidia. Female Stories, Female Bodies. Narrative identity and Representation. New York: Macmi llan Press, 1998. Dollimore, Jonathan. Radical Tragedy: Religion, Ideology and Power in the Drama of Shakespeare and his Contemporaries. New York: Harvester Wheatsheaf, 1984. Neil, Michael. Issues of Death: Mortality and Identity in English Renaissance Tragedy. Oxford: Clarendon Press, 1998. Shakespeare, William. Hamlet. Ed. G. R. Hibbard. Oxford: Oxford UP, 1987. Tylliard, Eustace M. W. The Elizabethan World Picture. US: Penguin, 1990. Van Geppen, Arnold. Les Rites de Passage.

Effect of concentration on Nacl solution Essay

In this assignment we will be focusing on one property, which influences the electrical conductance of an ionic solution. Compounds can be held by a covalent or ionic bond, which depends on the nature of the bonds. In case of ionic compounds (we also call them electrolytes), the force of attraction is present between the ions, which have opposite charge. One of the ions has a positive charge, which is called a cation, and the other has a negative charge, which is called an anion. This attraction is called an ionic bond. Ionic compounds1 form crystals in which anions and cations are held together with force of attraction. Ionic compounds are also known as salts mostly. They are usually hard and brittle. They are solid at room temperature and they have high melting and boiling points. They conduct electricity in solution because they dissociate into ions when dissolved in water, which are free to move. These ions carry the electrical charge from the anode to the cathode. Properties of salt solutions, which influence their electric conductance:2 The temperature of the solution. The magnitude of the charge on the ions. The concentration of the ions in the solution. The liquid used to dissolve the ionic substances in. The size of the ions. I would like to investigate that how the concentration of the ions in the solution affects the electric conductance of the solution. Aim Our aim is to figure out the answer of the research question through this experiment Research question What is the relationship between the conductivity of the ionic solution and concentration of the ionic compound (electrolyte)? Hypothesis When an ionic compound dissolves in water, the ions usually break apart and diffuse throughout the whole solution. Ions conduct electricity because they are mobile and carry charge with them. In this case, the ionic compound (NaCl) will be dissolved in water, this causes the ions (Na+ and Cl-) to diffuse in the solution and resulting in them conducting electricity. It happens because the sodium holds one excess electron and Chlorine is in need of one electron, resulting in sodium giving one electron to Chlorine when they get separated. As a result of this, the Chlorine becomes electrically negative and the Sodium becomes positive. This is the chemical reaction which occurs- NaCl(s) ? à ¯Ã‚ ¿Ã‚ ½ ? Na+(aq) + Cl-(aq) When we put electrodes in the solution, the positive ions (Na) will migrate to negative electrode and negative ions (Cl) towards the positive electrode that’s how electric current will flow. The conductivity of a solution depends on the concentration of the solution. In water, it is the ions that pass electricity from one to the next. This means that the more Na+ and Cl- contained in water the more electricity is carried, and the higher the conductivity. If the solution of water and NaCl is more concentrated (NaCl in large amount), its electric conductance will be more than if the solution is less concentrated (NaCl in a smaller amount). Therefore in my opinion, the greater the concentration of the ions, the more the conductivity of the solution will be. Variables: Controlled variables: temperature, voltage applied (in this case 10 volts), the electrolyte (Nacl) used with water to make a solution. Independent variables: The concentration of NaCl solution and volume of water. Dependant variables: Electric conductance measured by an ammeter. Plan for experiment In this experiment we will be using NaCl solution as the ionic compound (electrolyte). We will be placing the electrolyte in water as to create a concentrated solution. Different amounts of NaCl and water shall be mixed to prepare the solutions, which have different concentrations so we can compare the electric conductance in different cases. This giving us an idea of how the electric conductance of the solution would change when the concentration of the solution is increased or decreased. So then from the experiment we can draw a conclusion on how the concentration of a solution affects the conductivity of an ionic solution. Two electrodes are placed and a potential is applied across the electrodes. Then electric current is measured, which passes through the solution. The electric conductance facilitates by the charge on ions. So we can say that the conductivity of the solution is directly proportional to the concentration of its ions. Materials: Goggles Electrodes made of copper Lab coat ( 2 sizes available small and large) 5 beakers Tissue paper Demineralized water – 425 ml in a washbottle as to make it easier to be more accurate while pouring water in the beakers NaCl – 75 ml Ammeter Voltage Power supply Stirring Spoon Measuring Cylinder Experimental set-up Diagram Steps of the experiment: Safety precautions 1. Wear lab coat to prevent clothes from any damage, which can be caused. 2. Wear goggles for safety measures. Checking materials 1. Make sure all the materials are present. 2. Take out 4 glass beakers and set them out on the table. Solutions preparation The solution chosen is NaCl. In the five different beakers, there will be different amounts of water and different amount of concentrations of NaCl will be added. The amount of water will decrease with the increase of concentration as to keep the same volume of the solution, which is 100 ml in total for all 5 cases. These 5 solutions are prepared in 5 different beakers. We use a measuring cylinder to measure the amount of water and measuring beaker for NaCl solution. 1. 1st solution -Take 95ml water in a beaker and then add 5ml of NaCl solution. 2. 2nd solution – Take 90 ml water and then add 10ml of NaCl Solution. 3. 3rd solution – Take 85 ml of water and then add 15 ml of NaCl Solution. 4. 4th solution – Take 80ml water and then add 20 ml of NaCl solution. 5. 5th solution – Take 75 ml of water and then add 25 ml of NaCl solution. Measuring the conductivity / amount of electricity created 1.To measure the electric conductance, we need to first create a circuit by using a pair of copper electrodes. The electrodes are supposed to be placed on an electrode holder, and tightened with clamps. 2. Connect the electrodes with a wire to the ammeter and also with the power supply. 3. Immerse the electrodes in the beaker. Note: Keep the electrodes as far apart as possible (2 – 3 inches), don’t let them touch or the power module will be damaged.3 4. Now turn on the voltage power supply and make sure to put the current limitation to maximum so that there is no interference at all with the result. Note: Do not touch the electrodes after the power supply is turned on. 5. To control the amount of voltage turn the button to 10 volts, it doesn’t matter how many volts are applied as long as the value is kept the consistent throughout the whole experiment. 6. Monitor the conductivity of the solution for 4-5 seconds on the ammeter until it become stable. Making observations: 1. Record the conductivity value in your data table. 2.Make sure to clean the electrodes after taking measurement. 3. Then place the electrodes into 2nd, 3rd and 4th and 5th solutions respectively and record the conductivity in the table for each case. Cleanup: 1. Empty all the beakers in the sink then wash and dry them. 2.Remove ammeter from the electrodes. 3.Dry up the electrodes with tissue. 4.Place all materials back into the cupboards. Data and Observations Amount of NaCl (in ml) Conductance (in amperes) Amount of water (in ml) The graph shows the relationship between the amount of Nacl and the conductance. Conclusion The line represents the conductance. Results: I’ve presented all my data in form of a graph, it will show the co-relation between the conductivity4 and concentration 5of salt solution. On the horizontal axis I have placed the Nacl concentration and on the vertical axis the conductivity of the solution. We can then draw a conclusion after looking at it. After doing the experiment, I can conclude that if an electrolyte is dissolved in water, it completely dissociates into ions and the electrolyte would contribute to conduction of electricity to the solution. In this experiment, NaCl dissociates into Na+ and Cl- ions, which made it possible for water to conduct electricity. The conductivity of the solution depends on the concentration of the electrolyte and behaves differently for different concentration of the electrolyte. As we can see by the graph, if we start increasing the concentration of the electrolyte (NaCl), the electric conduction will be increasing accordingly. So we can get to the conclusion that the conductivity of the solution is directly proportional to the concentration of the electrolyte solution. Evaluation: In overall I find that this experiment went very well. My hypothesis turned out to be as I had assumed it would, as the conductance did increase with the increase of concentration. Although there was mistake we did at first, which was creating the wrong circuit by connection the wrong wires which caused the conductance on the ammeter to be show in negative. However we soon figured out our mistake and then re did the circuit after which we got successful results. My results are reliable up to an extent as we tried to make our experiment as accurate as possible. We made sure that no extra solution was left on the electrode holder whiles taking measurements by cleaning them so that the conductance wouldn’t be affected. Also we applied the same amount of energy to each solution so that it wouldn’t contribute to the conductance. During measuring the amount of water we took a considerably accurate account and tried to make sure that there wasn’t a big difference. However there were a few things we could have done better to get even more reliable results. We could have taken an average of the readings of the solutions whose conductance kept changing and wouldn’t become stable. Also a larger gap could have been taken between the amount of concentrations such that to assist in making conclusions in a much easier way. We tried to consume as less time as possible and were able to finish our experiment in sufficient time. In my view we were also extremely organized in the experiment as we knew exactly what we had to do , and any small mistakes which we made we were able to solve them. Fair testing: There should be reasonable difference in the concentrations of the NaCl solutions used for the experiment to get more reliable result. Keep electrodes for sometime in each solution, and as soon as the reading is stable, note it down on your table. Stir the solutions properly before putting electrodes into it to make sure that NaCl has mixed properly with water in each case. Clean and dry electrodes before putting them into different solutions. The amount of the voltage applied should be the same in each case. Follow up Experiment: We are investigating on the various factors that influence the conductance of an ionic solution. In this experiment we concentrated on how the concentration of a solution affected the conductance. So the follow up experiment should be focusing on another influential factor, which in my view should be how temperature influences the conduction of an ionic solution. I also find this a really interesting topic to continue investigation on. This experiment will give us an even better understanding of conductance and electrolytes. References 1. â€Å"All about ionic compounds.† Web. 13 Dec. 2009. . 2. â€Å"Concentration -.† Wikipedia, the free encyclopedia. Web. 13 Dec. 2009. . 3. â€Å"Conductivity of Electrolytic Solutions.† UCS Home. Web. 13 Dec. 2009. . 4. â€Å"Experiments in Electrochemistry.† Fun Science Gallery – Scientific Experiments for Amateur Scientists and Schools. Web. 13 Dec. 2009. . 5. â€Å"Factors Affecting Electrolytic Conductance † Web. 13 Dec. 2009. . 6. â€Å"The HiddenCures G-2 Water Ionizer User Instructions.† Google. Web. 13 Dec. 2009. . 7. â€Å"Ionic compound -.† Wikipedia, the free encyclopedia. Web. 13 Dec. 2009. . 1 â€Å"Ionic compound -.† Wikipedia, the free encyclopedia. Web. 13 Dec. 2009. . 2 â€Å"Factors Affecting Electrolytic Conductance † Web. 13 Dec. 2009. . 3 â€Å"The HiddenCures G-2 Water Ionizer User Instructions.† Google. Web. 13 Dec. 2009. . 4 â€Å"Conductivity of Electrolytic Solutions.† UCS Home. Web. 13 Dec. 2009. . 5 â€Å"Concentration -.† Wikipedia, the free encyclopedia. Web. 13 Dec. 2009. .