Supply Chain Case Study Example | Topics and Well Written Essays - 2500 words

Supply Chain - Case Study Example It is the world’s largest apparel retail store having chain stores in many countries. It is famous that the production, operations and then the supply chain activities are so well managed at Zara that it takes just two weeks to manufacture a new product and then launch at a display store. Whereas other competitors working in the Apparel industry take minimum of six months for manufacturing and then launching a new product in the market. This developed structure is really a source of competitive advantage for the Company Zara (Bhagwat 2011). Benetton is another Italian based Clothing Company, working globally regardless of the geographical boundaries. Benetton is famous for its dual supply chain system. The production is usually based on the quantity demanded from the stores themselves. This is also sometimes known as pull driven strategy. In addition, the last one, H & M is Swedish based Apparel Company working successfully in the market. The full name of H & M is Hennes and M auritz. The products are famous for its reasonable prices and the availability of variety of stocks within no time. It is famous that no single item remains on shop shelves more than a month duration. At Zara, the efficient operational activities and the processes are the real cause or the source of gaining competitive advantage as compare to many other competitor firms operating in the industry. The managers at Zara Company continue the research process throughout the whole season and not just in the end. For this reason, they are successful in the provision of new products within no time. The lower prices as compare to many other competitors may also give a positive impact to strengthen the competitive advantage of the company. Anyone can imagine the work efficiency at Zara Company that the product stay at distribution centre is only three days and after that, workers dispatch it to different retail stores. Another innovative thinking of marketing managers at Zara

CDA analysis Essay Example | Topics and Well Written Essays - 750 words

CDA analysis - Essay Example Thus, the selected element is a discourse, and its analysis has three dimension: as a text, sentence-by-sentence, and the words and phrases evaluation. Firstly, the text as a whole is close to the genre of political speech, since its content is mostly based on the speech made by Michelle Obama. In this context, it has her direct quotations both in the text and in the video. However, the content and the comments on the speech make this discourse resemble the slice of life genre with casual style of writing, which means that the Guardian presented the speech itself with its subjective reflection on it. On the frames, the exact concepts that unite text are two main identities – on the one hand, it discusses â€Å"ethnicity,† â€Å"black race,† and â€Å"African Americans† (it refers to both the speaker and to Tuskegee University students); on another hand, the family values appear in the text as â€Å"my husband’s chances,† â€Å"my girls,† and â€Å"kids and families.† Moreover, these two identities are in different position in terms of foregrounding and backgrounding, because i n the end of the text there appears the conclusion that â€Å"folks like you and me† (meaning the race) must believe in their potential (meaning realization in family life). On the cases of omission within the text, it does not mention any justification of first lady’s words with the facts from her biography; in other words, readers have nothing but to fall under emotional impression in what is given in the text. In addition, the voice of white public is neglected by this discourse, as the African American first lady speaks to the â€Å"mainly black graduates.† Although, the text includes horizontal intertextuality, as it has two direct quotations from other famous people on the same topic. Even though they have opposite opinions, the article does not reveal any support to them and provides only brief information on their

Personal Finance Essay Example for Free

Personal Finance Essay Personal finance refers to the principal that is applied to the monetary decisions of an individual or a family unit. It addresses issues such as the ways in which the individuals or families obtain finance, budget, save and spend the monetary resources of a company over a given period of time while at the same time taking in account the financial risks and the future life events that are related to the businesses activities. The profits or loss of a company are derived by determining the incomes of a company and the expenses that are incurred by a company. If the incomes are more than the expenses the company generates profit for the company. If the expenses of the company are more than the incomes then the company incurs losses in the financial period of a company. Assumptions The income of Donna Terrell is estimated to be $3333 per month since it is assumed that he earns a salary that is equally distributed throughout the year. The expenses of Donna Terrell are also assumed to be evenly distributed throughout the year except in the months where Donna Terrell specified that the expenses were incurred in those months. After Sherman acquisition of his new job on June 2003 and his decision to assist Donna Terrell was a positive move since after the month of June the Donna’s business started to earn profits since in the previous months the business was incurring losses, but after June 2003 the company started to generate profits for the company, thus was in a position to run it affairs effectively (http://64. 233. 169. 104/search? q=cache:DmCJZy7zP6kJ) It is also assumed that Sherman would earn a salary that would be $1500 per the month that followed the month of June up to December 2003. In the first quarter of the year Donna business had been incurring losses from January to May 2008 since the amount of losses have been increasing rapidly since the expenses of the business were more than the incomes of the business. After Mr. Sherman decision to assist Mr. Donna in giving him financial assistance the business started to improve in its performance. The business incomes was greater than the expenses as from July to December of the Year 2003 and this contributed to the increased profits of the business as it continued with its operation until December 2003. As at December 2003 the Company had profits that were over $13000. The management of companies can run their activities if they ask for financial assistances from friends and also financial institutions since after the Mr. Sherman decision to assist Mr. Donna the performance of the company started to improve. The instances where the management of companies runs other business activities that generate revenue to a company this can contribute to the profitability of the company since the additional income increases the companies working capital that enables the company to generate as much revenue to the company hence its increased returns and finally this leads to the growth of the company. The management of companies should also plan their finances properly so as to avoid budget deficits as this can affect the performance of the company and also its reputation as this can result to reduce sales volume for a company hence in some cases due to the poor management of the companies finances the company go into liquidation that can lead to the closure of the company.

The key steps of the implantation

The key steps of the implantation IMPLANTATION The life journey of a conceptus consists of many stages right from the point of conception to the point of birth which is one of natures wonders. However, an essential stage in this journey is the process of implantation. Implantation is generally defined as an event in which an embryo becomes progressively attached to the wall of the uterus during early pregnancy. This process is pivotal to the events that occur later in pregnancy. According to Makrigiannakis (2005), implantation is an active process in which a blastocyst apposes, attaches and progressively invades into the endometrium to establish the placenta (Figure 5). From this definition, we can deduce that the embryo undergoes the process of implantation at the blastocyst stage (Figure 1). Implantation is a process that occurs in mammals and it takes places in the endometrial lining of the uterus. IMPORTANCE OF IMPLANTATION Implantation is a key event in the reproductive physiology of mammals as it is a pre-requisite for further embryonic development. It is the first stage in the process of placental formation which is in turn is a crucial component of fetal development as it serves as a medium for nutrient absorption, gaseous exchange and waste disposal. Physiological defects in humans and other mammals have gone further to emphasize the importance of the implantation process. Implantation defects have been associated with non-chromosomal early pregnancy loss and infertility (Makrigiannakis, 2005). Many complications that show up late in pregnancy such as pre-eclampsia and preterm labour appear to have originated early in pregnancy with abnormalities in the process of implantation and placental development (Norwitz, 2006). Another implantation defect is a phenomenon known as ectopic pregnancy. In this case, the blastocyst implants outside the uterine cavity usually in the fallopian tubes although ectop ic implantation could also occur in the cervix, abdomen and ovaries. A good understanding of the steps involved in the process of implantation and the factors controlling these steps are necessary in order to be able to influence clinical outcomes in humans such as reduction of recurrent miscarriages and improvement of implantation rates in both natural and assisted reproduction. This will also be beneficial to the use of animals in the area of research and agriculture. A greater detail of the events that take place before and during the process implantation shall be discussed herein. PRE-IMPLANTATION DEVELOPMENT The developmental events that take place between the fertilization of the ovum and the implantation of the blastocyst are important in order to understand the process of implantation. Following fertilization, a process known as cleavage occurs (Figure 1). Cleavage is the mitotic division of the cells of the resulting embryo without any growth. This starts from the time the embryo is at the 2-cell stage and each cell continues to divide up to the morula stage. At this point the embryo is a solid ball of 16 or more cells. In humans, this stage is normally observed at about 4 days after fertilization. In continuation of development, the morula undergoes a process known as compaction. Here, the embryonic cells begin to change shape and gap junctions start to form between adjacent cells. The inner cells of the embryo then start to differentiate from the outer cells as different genes are being expressed in the inner and the outer cells. Blastocyst formation follows shortly after and the i nner cells give rise to the inner cell mass whilst the outer cells give rise to the trophoblast cells (Figure 1). A vast knowledge of the structure of the blastocyst is important as each of its structural components play an important role in the process of implantation. The inner cell mass of a blastocyst gives rise to the embryo proper while the trophoblast gives rise to the fetal component of the placenta (Schoenwolf et al., 2009). The process of implantation is generally known to take place a few days after fertilization and the uterine wall is ready to accept the implanting blastocyst during a limited period of time outside of which it may not optimally support the implantation of the embryo. This period of time is known as the ‘window of implantation (Psychoyos et al., 1995; Klentzeris, 1997). THE BLASTOCYST AND THE UTERUS BEFORE IMPLANTATION In the build up to the implantation process following pre-implantation development, there are a number of necessary events that take place. First of all, there has to be a receptive and hormonally primed uterus present. The uterus is composed of 3 layers namely the endometrium, perimetrium and myometrium (Figure 2). The endometrium which is the most important uterine tissue involved in implantation consists of the luminal epithelium, the stroma and the germinal basalis (Yoon et al., 2004). The hormone progesterone, which is secreted by the corpus luteum, is actively involved here as it makes the already thickened endometrial lining of the uterus more favourable for the implantation of the blastocyst. The thickening of the endometrium is due to the effect of estrogens (Norwitz, 2006). The blastocyst is then transported to the uterus via signalling mechanisms and arrives there at about 5 to 7 days after fertilization (Bischof and Campana, 1996). After the blastocyst arrives in the uter us, it begins to move towards the endometrium with the inner cell mass positioned towards the endometrial lining (Bischof and Campana, 1996). Before any further interaction with the endometrium, the blastocyst must undergo a process known as hatching. This simply involves the blastocyst boring a hole through the zona pellucida with the aid of enzymes and squeezing out. It is a general school of thought that serine proteases are responsible for this process although the mechanisms behind its action are not clearly understood (OSullivan et al., 2002). After hatching, the blastocyst is naked of all its original investments and can interact directly with the endometrium (Schoenwolf et al., 2009). At this time, blastocystis also known to secrete moleculesthat affect the activity of the ovary, fallopian tube and the endometrium (Norwitz, 2006). Shortly before the blastocyst comes in contact with the endometrium, thetrophoblastdifferentiates intotwo different cell masses, which are the inn er cytotrophoblast and the outer syncytiotrophoblast which is formed as a result of the fusion of cytotrophoblast cells. PATTERNS OF IMPLANTATION There are three known patterns of implantation which are centric, eccentric and interstitial (Wimsatt, 1975). Centric implantation occurs when the embryo expands and increases in size before implantation, then stays in the centre of the uterus (Lee and DeMayo, 2004). Examples of animals that undergo this pattern of implantation include rabbits, dogs, cows, pigs, sheep, horses and a number of marsupials. Eccentric implantation occurs when the embryo is small in size and implants inside the endometrium usually taking place on the side of the uterus, opposite to the mesometrium (Lee and DeMayo, 2004). Examples of animals that show this pattern of implantation include rats, mice and hamsters. In Interstitial implantation, the embryo is also small and it invades through the endometrial epithelium into the subepithelial connective tissue (Lee and DeMayo, 2004). Examples of animals under this category include guinea pigs and humans (Wimsatt, 1975). KEY STEPS OF THE IMPLANTATION PROCESS There are three key steps in the process implantation namely apposition, attachment and invasion. Apposition This is the first major step of the implantation process following the hatching of the blastocyst. During apposition, the blastocyst comes in slight contact forming a weak bond with the uterine luminal epithelium. Microvilli on the apical surface of the cytotrophoblasts interlock with microprotrusions called pinopodes (Figure 3) which are present on the apical surface of the endometrial epithelium (Norwitz et al., 2001). This interaction involves changes in the expression of cell adhesion molecules and extracellular matrix (ECM) proteins (Nagaoka et al., 2003). Pinopodes are progesterone-dependent organelles, and they have been suggested to be indicators of endometrial receptivity (Nikas, 1999). In humans, they are usually visible on days 20-21 of the menstrual cycle prior to the time of implantation (Nikas, 1999). They could facilitate implantation by preventing the blastocyst from being swept away by uterine cilia (Stavreus-Evers, 2005). It has been identified that high molecular w eight mucin glycoproteins particularly MUC1, are dominant inhibitors of embryo apposition and attachment (Thathiah and Carson, 2002). However, a decrease in the expression of MUC1 at the time of implantation could facilitate blastocyst apposition (Thathiah and Carson, 2002). During apposition, soluble mediators such as chemokines e.g. CX3CL1, CCL7, CCL14 and CCL4 have been found to establish a dialogue between the maternal cells and those of the blastocyst (Hannan and Salamonsen, 2007). Chemokines are a large family of chemotactic cytokines, well known for their functions in leucocyte recruitment and activation (Dominguez et al., 2003). They have a wide range of functions and have been implicated to play a role in implantation (Dominguez et al., 2003). Chemokines have been localized in areas of inflammation and they are suggested to be potential mediators of inflammation (Feng, 2000). This could be the reason why blastocysts tend to implant on scar tissue from caesarean sections which is an area of inflammation (Dominguez et al., 2005). The dialogue between the maternal and blastocyst cells has important influences on the development of the implanting blastocyst and maintenance of endometrial receptivity (Hannan and Salamonsen, 2007). It also results in the expression of a unique array of adhesion molecules on the surface of both fetal and maternal cells, promoting the attachment of the trophoblast cells to the endometrial epithelium (Hannan and Salamonsen, 2007). Attachment Following apposition, the next step in the process of implantation is known as attachment or adhesion. This is characterized by increased physical contact between the blastocyst and the uterine epithelium (Norwitz et al., 2001). At this point the blastocyst can no longer be dislodged. A ligand carbohydrate known as trophinin has been identified as an adhesion molecule that mediates the initial step of attachment of the blastocyst to the endometrial epithelium (Fukuda and Sugihara, 2008). Trophinin mediates cell adhesion by homophilic Trophinin-Trophinin binding (Fukuda and Sugihara, 2008). A carbohydrate-binding protein known as L-selectin which is expressed in the blastocyst, has also been discovered to play a role in human embryo attachment (Genbacev et al., 2003). Interaction between L-selectin on the blastocyst and L-selectin ligands on the endometrial surface allows for loose attachment and rolling of blastocyst to its implantation site ((Fukuda and Sugihara, 2008). The human Ch orionic Gonadotrophin (HCG) produced by the blastocyst up regulates trophinin expression on pinopodes and down regulates MUC1 expression (Fukuda and Sugihara, 2008). The blastocyst then adheres to the pinopodes by trophinin-trophinin interaction (Figure 4). A substance known as Heparin Binding Epidermal Growth Factor (HB EGF) has also been implicated in blastocyst attachment (Lim and Dey, 2008). This growth factor is expressed by the endometrium whilst its receptors are present on the blastocyst. This interaction also helps in facilitating the attachment of the blastocyst. Figure 4: Proposed role of L-selectin and trophinin in human embryo implantation. Source: Fukuda and Sugihara, 2008. (a) A human blastocyst entering the uterine cavity is prevented from attaching to the endometrial epithelia by MUC1, except for epithelia that express the L-selectin ligand (T). The human blastocyst expresses L-selectin (L), and ‘rolls on the surface of the endometrium covered by glycocalyx. (b) The blastocyst feebly interacts with the glycocalyx. Here, human chorionic gonadotropin (hCG) which is secreted from the blastocyst, acts locally on endometrial epithelia to induce trophinin expression. (c) Trophinin expressed by endometrial epithelia is enriched in the pinopodes, the structure extended above the glycocalyx. MUC1, which carries the L-selectin ligand, is down-regulated from the endometrial epithelia underneath the blastocyst, allowing direct contact and attachment of blastocyst trophectoderm cells and pinopodes via trophinin-trophinin binding. Invasion The next step which is critical to the implantation of the blastocyst is known as invasion. As the term implies, this involves the infiltration of the endometrium by the cytotrophoblast cells of the blastocyst. This starts with the progression of the trophoblast cells between the adjacent endometrial epithelial cells to reach the underlying basement membrane. This membrane is destroyed, allowing the trophoblast cells to reach the stromal compartment (Bischof and Campana, 1996). The syncytiotrophoblast undergoes proliferation and invades the endometrial stroma. The progressive invasion of the blastocyst into the endometrium continues until the blastocyst is completely embedded in subepithelial stromal tissue and the uterine epithelium grows to cover the implantation site (Norwitz, 2006). The syncytiotrophoblast cells continue to develop quickly and surround the blastocyst until it has completely embedded itself in the endometrial stroma. In the syncytiotrophoblast, fluid-filled spaces known as lacunae are formed as a result of the fusion of syncytiotrophoblast cells. The lacunae are separated by trabeculae and they transform the syncytiotrophoblast into a sponge-like material (Bischof and Campana, 1996). The trabeculae are arranged radially, and cytotrophoblastic cells divide within the trabeculae, leading to the formation of primary chorionic villi (Bischof and Campana, 1996). Following this event, the primary villi grow and branch into secondary and tertiary villi (Bischof and Campana, 1996). This process is known as placentation. A wide range of factors e.g. cytokines, integrins, matrix metalloproteinases (MMPs), Leukaemia Inhibiting Factor (LIF) e.t.c have been found to play a role in the invasion process (Makrigiannakis, 2005; Norwitz, 2006). The role of these c omponents in the process of implantation shall be discussed shortly under the factors that regulate implantation. Figure 5: Implantation of the human blastocyst step by step. Source: Bischof and Campana, 1996. (1): Transport. The blastocyst arrives in the uterus after fertilization. (2) Orientation: The inner cell mass is positioned towards the endometrial lining. (3) Hatching: The zona pellucida is perforated making way for the release of the blastocyst. (4) Apposition: The blastocyst is now in close contact with the endometrial lining but no connections have been established. (5) Adhesion: Connections are established between the embryo and the endometrial epithelium. (6) Invasion: Thin folds of trophectodermal cells intrude between the endometrial epithelial cells. (7) Syncytialization: Some trophectodermal cells fuse to form syncytia which proliferate and invade the endometrial stroma. (8) Villous formation: The cytotrophoblastic cells migrate between the syncytia followed by the fetal stroma. This will lead to the formation of the placental villi. The cells of the endometrial stroma react to the presence of the blastocyst and the secretion of progesterone by differentiating into metabolically active, secretory cells called decidual cells (Schoenwolf et al., 2009). This response is known as the decidual reaction or decidualization. In humans, this begins in the secretory phase of the menstrual cycle. The decidua is also known as the maternal portion of the placenta (Gilbert, 2006) and it is believed to provide an element of control of trophoblast invasion during implantation (Loke and King, 1995). The decidualized stroma cells have been found to secrete prolactin and Insulin-like Growth Factor Binding Protein-1(IGFBPI) which are held to function in complex gene networks that function in the regulation of trophoblast invasion as well as many other endocrine and paracrine factors (Bazer et al., 2010). This regulatory function is required for the optimal implantation of the blastocyst as the invasion of the cytotrophoblast to the proper depth is a major factor in determining pregnancy outcome (Norwitz, 2006). Excessive invasion resulting from the inability of the decidua to control the invading cytotrophoblast cells could lead to an unusually strong attachment of the placenta to the myometrium (placenta accreta), extension into the myometrium (placenta increta), or invasion through the myometrium into adjacent organs also known as placenta percreta (Norwitz, 2006). Insufficient cytotrophoblast invasion has also been associated with pre-eclampsia (Lyall, 2006; Lee et al., 2010) which is a medical complication that presents itself late in pregnancy. During implantation, a process known as angiogenesis has been identified to be important (Sherer and Abulafia, 2001). Angiogenesis is the growth of new capillaries from pre-existing blood vessels. In this case, it occurs in the endometrium and takes place throughout the implantation period. Endometrial angiogenesis starts with the degradation of the capillary vessel membrane, creating a means through which migrating endothelial cells proliferate to create a new lumen and further vessel maturation (Sherer and Abulafia, 2001). This vascularization functions to maintain endometrial structure and receptivity. Angiogenesis is known to be mediated by some factors present in the endometrium such as fibroblast growth factor, vascular endothelial growth factor and platelet activating factors (Norwitz 2006; Sherer and Abulafia, 2001). FACTORS THAT REGULATE IMPLANTATION The regulation of implantation and early development is dependent on a wide range of factors. Although the molecular and cellular mechanisms behind implantation are not well understood, it is apparent that multiple factors (including maternal and fetal) are needed to synchronize blastocyst maturation and uterine receptivity up to the point of initiation of implantation and through the process of implantation (Norwitz, 2006). A closer look will now be taken at some of the important factors associated with implantation and early pregnancy maintenance. Maternal factors Starting with the uterine (maternal) side, there are a lot of components to consider. Cytokines and growth factors have been shown by different studies to be important to the maternal role in implantation. These include interleukin-1 (Sheth et al., 1991; Simon et al., 1996; Stewart and Cullinan, 1997; Huang et al., 1998), Interleukin-2 (Stewart and Cullinan, 1997), Insulin-like growth factor I and II (Stewart and Cullinan, 1997; Giudice and Irwin, 1999), transforming growth factor a and (Slowey et al., 1994; Stewart and Cullinan, 1997; Godkin and Dore, 1998), vascular endothelial growth factor (Athanassiades et al., 1998) and leukemia inhibitory factor (Cullinan et al., 1996; Stewart and Cullinan, 1997). The mode of function of the leukemia inhibitory factor is not well understood but has been established as a critical factor in the process of implantation (Stewart et al., 1992; Cheng et al. 2002). These cytokines and growth factors all work towards facilitating the communication bet ween the blastocyst and the uterus whilst promoting endometrial proliferation and differentiation (Norwitz, 2006). They have also been found to regulate endometrial angiogenesis and vascular permeability (Norwitz, 2006). As mentioned earlier, some steroid hormones such as Progesterone (Peyron et al., 1993) and Oestradiol-17 (Miller, 1988) have also been found to be important. They function in the proliferation of uterine epithelial cells and endometrial stromal cells (Norwitz, 2006). Some changes in the uterine luminal epithelium such as the expression of pinopodes (Nikas, 1999) and MUC 1 (Thathiah and Carson, 2002) have been suggested to be important for blastocyst recognition and attachment. Transcription factors such as the peroxisome proliferator activated receptor-s (Lim et al., 1999; Barak et al., 1999) have been identified to function in defining the molecular mechanisms by which the regulatory factors exert their effects at a cellular level (Norwitz, 2006). Studies have shown the relevance of some other components such as homeobox genes Hoxa-10 and 11 which have been found to regulate the responsiveness of stromal cells to progesterone (Benson et al., 1996; Taylor et al., 1997; Lim et al., 19 99), Cyclooxy-genase-2 which regulates prostaglandin production (Norwitz and Wilson 2000) and oxygen tension (Genbacev et al., 1997) which has been found to promote trophoblast vascular mimicry by initiating integrin expression. Also, proteins such as Rac1 and RhoA which are found in stromal cells have been implicated in trophoblast invasion (Grewal et al., 2008). Fetal factors Evaluations of the blastocyst (fetal) factors also reveal that present here, are some of the groups of factors present on the maternal side of implantation as they possess some overlapping functions. Cytokines and growth factors, in addition to facilitating communication between the blastocyst and uterus, could also enhance trophoblast differentiation and invasion. These include Interleukin-1, Interleukin-6 (Stewart and Cullinan, 1997), leukemia inhibiting factor, transforming growth factor a and , insulin-like growth factor II and colony stimulating factor-1 (Stewart and Cullinan, 1997, Cohen et al., 1997). Some trophoblast proteinases and inhibitors such as the matrix metalloproteinases (Makrigiannakis, 2005) and cathepsin B and L (Afonso et al., 1997) have also been found to regulate trophoblast invasion. The expression of some adhesion molecules e.g. integrins have been identified in the enhancement of trophoblast invasion. Some of them include integrin a64, integrin a11 and E-ca dherin (Lessey, 1998; Lessey and Arnold, 1998; Damsky and Fisher, 1998). Some other important factors include prostaglandin E2 which aids the process of endometrial apoptosis and platelet-activating factor which stimulates uterine prostaglandin production (Norwitz, 2006). Immunological factors The immunological interactions between the blastocyst and the uterine decidua are essential in the regulation of the implantation process. Implantation is of immunological significance because the blastocyst contains half of its paternal genes hence it is immunologically foreign to its mother. Despite this fact, blastocyst implantation still turns out to be a successful process and the blastocyst is not rejected by the maternal immune system during normal implantation. This is down to the action of immunological factors. These factors are a combination of elements expressed by both the blastocyst and the uterus and they act together to ensure fetal survival. On the maternal side such factors include Interleukin-10 (Roth et al., 1996; Roth and fisher, 1999) which plays an important role in immunosuppression thus reducing the activity of the maternal immune system against the foetus (Norwitz, 2006). Another factor is 2, 3-dioxygenase (Kamimura et al., 1991; Munn et al., 1998) which has been found to be responsible for macrophage action during implantation (Norwitz, 2006). Uterine natural killer cells found in the stroma also play a role here as they produce cytokine, chemokines and angiogenic factors which all promote and regulate trophoblast invasion (King and Loke, 1997). On the fetal side, factors such as histocompatibility antigen, class I, G (HLA-G) have been found to be involved in preventing the maternal immune rejection of the semi-allogenic foetus (Lanier, 1999; Norwitz, 2006). Coordination of the regulatory factors within the window of implantation The window of implantation as defined earlier is characterized by the perfect synchrony of all the components that play a role in the implantation process. These include the endometrium, the blastocyst and the factors regulating the process of implantation. Figure 6 below illustrates how all these factors are coordinated during the implantation window. This shows that within the window of implantation, the endometrium is highly influenced by steroid hormones (oestrogen and progesterone) and the interaction between the blastocyst and the endometrium is as a result of stage-specific actions of different implantation factors. Figure 6: Events that take place within the implantation window. Source: Achache and Revel, 2006 (A) Endometrium proliferates under the enhancement of estrogen. (B) Progesterone from follicles that have been luteinized leads to endometrial differentiation. (C) The blastocyst makes its way to the uterus via the ostia and rolls freely over the endometrium with the aid of L-selectin signals. (D) MUC-1 repels the blastocyst and prevents it from adhering to areas on the endometrium with poor chances of implantation. (E) Cytokines and chemokines attract the blastocyst to the optimal implantation spot. (F) Adhesion molecules (e.g. integrins and cadherins) attach the blastocyst firmly to the endometrial pinopodes to ensure successful implantation. The functions of all the factors mentioned earlier further emphasize the importance of these components to the process of implantation. A lot of studies have also been carried out on some of these molecules to further establish their importance. A notable one amongst these molecules is the leukemia inhibitory factor. As mentioned earlier, this molecule has been identified to be critical to the process of implantation. Studies revealed that implantation did not occur in female transgenic mice that were homozygous for the deficiency of the gene responsible for the leukemia inhibitory factor (Aghajanova, 2004). It was further proven that the lack of implantation was not caused by faults in the embryo because the implantation of the same embryos occurred when they were transferred to pseudopregnant recipients. The addition of exogenous LIF to the females with this defective gene throughout the period of normal implantation restored implantation sites and allowed proper attachments of the blastocysts (Aghajanova, 2004). LIF and LIF mRNA has also been shown to be expressed throughout the menstrual cycle of women with proven fertility (Arici et al., 1995; Charnock-Jones et al., 1994). This was associated with peaks in the mid and late secretory phase, and in early pregnancy (Aghajanova, 2004). Leukemia inhibitory factor has also been found to be present in uterine flushings within the implantation window in fertile women. This characterized by gradually increasing concentrations from 7 days to 12 days after the LH surge (Laird et al., 1997). In future, the evidence and information obtained from similar studies may be applied clinically through a well regimented administration of LIF in a pharmaceutical form to improve implantation rates in both natural and assisted reproduction. IMPLANTATION AND ASSISTED REPRODUCTIVE TECHNOLOGY (ART) Successful pregnancy outcomes from assisted reproductive techniques such as in vitro fertilization (IVF) have largely depended on the process of implantation. The advances in ART techniques have not had a significant effect on implantation rates (Donaghay and Lessey, 2007) hence a lot of measures have been taken by ART units over the years in an attempt to optimize implantation rates. Assisted hatching (Cohen, 1991) is a well known procedure carried out in this regard. This involves the manual perforation of a blastocysts zona pellucida in order to separate the blastocyst from the zona pellucida just as it would have occurred during natural hatching. This may increase implantation and pregnancy rates in IVF cycles (Chao et al., 1997). The function of regulatory factors in the process of implantation indicates that a number of biomarkers can be adapted from these to determine the ideal period of endometrial receptivity which can be traced and monitored during IVF cycles (Haouzi et al. , 2009). These may include the detection and monitoring of some of the molecules and steroid hormones involved in implantation by making use of samples obtained from IVF treatment cycles such as follicular fluids and embryo culture supernatants. Fluorescent markers can also be used to highlight proteins and any other key component in the blastocyst involved in implantation. Continuous studies are being performed with the aim of discovering techniques that would improve implantation rates during ART treatments. CONCLUSION Over the years, the research carried out on implantation and the factors that control implantation has been done making use of mostly animal models with the exception of some that have employed the use of in vitro human systems. The use of animals in the study of implantation has many benefits as many factors and regulatory mechanisms are being discovered. However, it is difficult to precisely extrapolate results obtained from animal data into human cases. This is one of the problems being encountered by implantation studies as the difficulty and ethical significance associated with research using humans make scientists resort to the use of animal models. The process of implantation occurs with the uterus and the blastocyst in synchrony. It has been clearly shown that a lot of factors are responsible but the complete framework of the regulation of implantation has not yet been understood. With continuous research and more human-based studies, a better understanding of the process and regulation of implantation may be achieved in the future. REFERENCES Achache, H. and Revel, A., 2006. Endometrial receptivity markers, the journey to successful embryo implantation. Hum. Reprod. Update. 12(6), 731-746. Afonso, S., Romagnano, L. and Babiarz, B., 1997. The expression and function of cystatin C and cathepsin B and cathepsin L during mouse embryo implantation and placentation. Development. 124, 3415-3425. Aghajanova, L., 2004. Leukemia inhibitory factor and human embryo implantation. Ann. NY. Acad. Sci.1034, 176-183. Arici, A., Engin, O., Attar, E. And Olive, D.L., 1995. Modulation of leukaemia inhibitory factor gene expression and protein biosynthesis in human endometrium. J. Clin. Endocr. Metab. 80, 1908-1915 Athanassiades, A., Hamilton, G.S., Lala, P.K., 1998. Vascular endothelial growth factor stimulates proliferation but not migration or invasiveness in human extravillous trophoblast. Biol. Reprod. 59, 643-654. Barak, Y., Nelson, M.C., Ong, E.S. et al., 1999. PPAR gamma is required for placental, cardiac, and adipose tissue development. Molecular Cell 4, 585-595. Bazer, F.W., Wu, G., Spencer, T.E., Johnson, G.A., Burghardt, R.C. and Bayless, K., 2010. Novel pathways for implantation and establishment and maintenance of pregnancy in mammals. Mol. Hum. Reprod 16(3), 135-152. Benson, G.V., Lim, H., Paria, B.C. et al., 1996. Mechanisms of reduced fertility in Hoxa-10 mutant mice: uterine homeostasis and loss of maternal Hoxa-10 expression. Development. 122, 2687-2696. Bischof, P. and Campana, A., 1996. A model for implantation of the human blastocyst and early placentation. Hum. Reprod. Update. 2(3), 262-270. Chao, K., Wu, M., Chen, S., Yang, Y., Chen, H. and Ho, H., 1997. Assisted hatching increases the implantation and pregnancy rate of in vitro fertilization (IVF)-embryo transfer (ET), but not that of IVF-tubal ET in patients with repeated IVF failures. Fertil. Steril. 67(5), 904-908 Charnock-Jones, D.S., Sharkey, A.M., Fenwick, P. and Smith, S.K., 1994. Leukemia inhibitory factor mRNA concentration peaks in human endometrium at the time of implantation and the blastocyst contains mRNA for the rec

Humorous Wedding Speech by an Old Roomate (Flatmate) :: Wedding Toasts Roasts Speeches

Humorous Wedding Speech by an Old Roomate (Flatmate) Well, congratulations to Herman and Connie. I assume that you are now expecting me to have a bit of fun at Herman's expense. Well, the only trouble is, Herman's expenses have been so high today that I’m not sure how much more he can take. Herman and I have been great friends (mates) for a long time now, and inevitably we've shared many things over the years: football; college; my driving license when Herman didn't have one - and now, a wedding table. Who'd have thought it? We also shared an apartment (a flat) for a short time. Not long after finding a place together I realised his biggest hate in life – housework! And why? Because you have to make the beds and do the dishes. Then six months later you have to start all over again. But we had a good understanding and split everything down the middle. It was my job to get the take-out, Herman’s job to get the beer, my job to clean the bath room, Herman’s job to clean the kitchen. And I’m not joking, when Herman was done with the kitchen you could eat of that floor †¦ there was lots of food still down there. On the whole, though, living with Herman was a pleasurable experience. Having said that, there weren’t any books in our flat, so when the Satellite dish stopped working we actually had to talk to each other. Now, I'd like to think I taught Herman a thing or two before he got a place of his own, especially about women. Imagine the shock I got when out of the blue he called me to say that he had got engaged, the things that go through a best friend’s mind. Mostly about mail order brides, one-way tickets from Thailand and subscriptions to Gay Connections Monthly. Then when I heard that it was Connie, I was filled with much relief and happiness. Because when it came to finding a wife, Herman couldn't have been luckier. Connie is a fantastic person and, as I'm sure you will all agree, looks stunning today. I have a great deal of respect and admiration for her. And, being a nurse, she has the added bonus of already being familiar with dealing with incontinence and impotence on a daily basis. Since Herman met Connie, I have seen a change in him.

Stained Glass Windows :: Art Architecture

Stained glass windows Stained glass windows used to be only referred to Cathedral windows but it has now moderated into a wide variety of different things. Many people think stained glass is just work on windows but it can also be three dimensional structures and sculptures. Stained glass is still widely used for different things. There was a time when stained glass was deceased but then it later got revived. Stained glass is sometimes difficult to make but if the artist is skilled enough they will produce beautiful designs. Origin of stained glass Colored glass is not something that started just recently. In fact history has it that there were colored windows around since ancient times. The Egyptians and the Romans both produced colored objects. The early Christians during the 4th and 5th century had wooden window frames that contained some omate patterns of alabaster that gave it a colored glass effect. These effects were also done by Muslim architects and others in southern Asia. Then later in the 8th century a Muslim alchemist scientifically describe 46 different colored glass. Destruction of stained glass In England many stained glass windows were being torn down and plain windows would replace them. All this happened during the dissolution of the monasteries under Henry the VIII. This caused thousands of windows to be destroyed since the dissolution of the monasteries gave Henry the right to confiscate the property of the monasteries, and to do whatever he wanted with it. Then later the traditional method of making stained glass was also destroyed and they would not be revived until early 19th century. Stained glass now Lots of stained glass windows were worked on, because there were many churches that had had their windows destroyed during World War II. The German artists were the once that set the tone to restart the restoration. Many artists have transformed stained glass into an art form. Artists now use slab glass and concrete as an innovation to the older era of stained glass. The United States also has a 100-year-old trade organization called the stain glass association of America.

Bond and Market Capitalization Rate

330-s2013-prac9 1. An American put option gives its holder the right to _________. A. buy the underlying asset at the exercise price on or before the expiration date B. buy the underlying asset at the exercise price only at the expiration date C. sell the underlying asset at the exercise price on or before the expiration date D. sell the underlying asset at the exercise price only at the expiration date 2. An American call option gives the buyer the right to _________. A. buy the underlying asset at the exercise price on or before the expiration date B. buy the underlying asset at the exercise price only at the expiration date C. ell the underlying asset at the exercise price on or before the expiration date D. sell the underlying asset at the exercise price only at the expiration date 3. A European call option gives the buyer the right to _________. A. buy the underlying asset at the exercise price on or before the expiration date B. buy the underlying asset at the exercise price on ly at the expiration date C. sell the underlying asset at the exercise price on or before the expiration date D. sell the underlying asset at the exercise price only at the expiration date 4. You purchase one IBM July 120 call contract for a premium of $5.You hold the option until the expiration date when IBM stock sells for $123 per share. You will realize a ______ on the investment. A. $200 profit B. $200 loss C. $300 profit D. $300 loss 5. At contract maturity the value of a call option is ___________ where X equals the option's strike price and ST is the stock price at contract expiration. A. Max(0, ST – X) B. Min(0, ST – X) C. Max(0, X – ST) D. Min(0, X – ST) 1 1. C 2. A 3. B 4. B 5. A Long Call Profit = Max[0,($123 – $120)(100)] – $500 = -$200 1. A firm that has an ROE of 12% is considering cutting its dividend payout.The stockholders of the firm desire a dividend yield of 4% and a capital gain yield of 9%. Given this information which of the following statement(s) is/are correct? I. All else equal the firm's growth rate will accelerate after the payout change II. All else equal the firm's stock price will go up after the payout change III. All else equal the firm's P/E ratio will increase after the payout change A. I onlyB. I and II onlyC. II and III onlyD. I, II and III 2. A firm cuts its dividend payout ratio. As a result you know that the firm's _______. A. return on assets will increaseB. arnings retention ratio will increase C. earnings growth rate will fallD. stock price will fall 3. An underpriced stock provides an expected return which is ____________ the required return based on the capital asset pricing model (CAPM). A. less thanB. equal toC. greater thanD. greater than or equal to 4. Stockholders of Dog's R Us Pet Supply expect a 12% rate of return on their stock. Management has consistently been generating a ROE of 15% over the last 5 years but now believes that ROE will be 12% for the next five year s. Given this the firm's optimal dividend payout ratio is now ______.A. 0%B. 100%C. between 0% and 50%D. between 50% and 100% 5. The constant growth dividend discount model (DDM) can be used only when the ___________. A. growth rate is less than or equal to the required returnB. growth rate is greater than or equal to the required return C. growth rate is less than the required returnD. growth rate is greater than the required return 6. Suppose that in 2009 the expected dividends of the stocks in a broad market index equaled $240 million when the discount rate was 8% and the expected growth rate of the dividends equaled 6%.Using the constant growth formula for valuation, if interest rates increase to 9% the value of the market will change by _____. A. -10%B. -20%C. -25%D. -33% 7. You are considering acquiring a common share of Sahali Shopping Center Corporation that you would like to hold for one year. You expect to receive both $1. 25 in dividends and $35 from the sale of the share at the end of the year. The maximum price you would pay for a share today is __________ if you wanted to earn a 12% return. A. $31. 25B. $32. 37C. $38. 47D. $41. 32 8. Eagle Brand Arrowheads has expected earnings of $1. 5 per share and a market capitalization rate of 12%. Earnings are expected to grow at 5% per year indefinitely. The firm has a 40% plowback ratio. By how much does the firm's ROE exceed the market capitalization rate? A. 0. 5%B. 1. 0%C. 1. 5%D. 2. 0% 9. A preferred share of Coquihalla Corporation will pay a dividend of $8. 00 in the upcoming year, and every year thereafter, i. e. , dividends are not expected to grow. You require a return of 7% on this stock. Using the constant growth DDM to calculate the intrinsic value, a preferred share of Coquihalla Corporation is worth _________. A. $13. 50B. $45. 50C. $91. 0D. $114. 29 10. Brevik Builders has an expected ROE of 25%. Its dividend growth rate will be __________ if it follows a policy of paying 30% of earning in t he form of dividends. A. 5. 0%B. 15. 0%C. 17. 5%D. 45. 0% 11. Cache Creek Manufacturing Company is expected to pay a dividend of $3. 36 in the upcoming year. Dividends are expected to grow at 8% per year. The riskfree rate of return is 4% and the expected return on the market portfolio is 14%. Investors use the CAPM to compute the market capitalization rate, and the constant growth DDM to determine the value of the stock. The stock's current price is $84. 0. Using the constant growth DDM, the market capitalization rate is _________. A. 9%B. 12%C. 14%D. 18% 12. Ace Ventura, Inc. has expected earnings of $5 per share for next year. The firm's ROE is 15% and its earnings retention ratio is 40%. If the firm's market capitalization rate is 10%, what is the present value of its growth opportunities? A. $25B. $50C. $75D. $100 13. Flanders, Inc. has expected earnings of $4 per share for next year. The firm's ROE is 8% and its earnings retention ratio is 40%. If the firm's market capitalizat ion rate is 15%, what is the present value of its growth opportunities?A. -$6. 33B. $0C. $20. 34D. $26. 67 14. Cache Creek Manufacturing Company is expected to pay a dividend of $4. 20 in the upcoming year. Dividends are expected to grow at the rate of 8% per year. The riskfree rate of return is 4% and the expected return on the market portfolio is 14%. Investors use the CAPM to compute the market capitalization rate on the stock, and the constant growth DDM to determine the intrinsic value of the stock. The stock is trading in the market today at $84. 00. Using the constant growth DDM and the CAPM, the beta of the stock is _________. A. 1. 4B. 0. 9C. 0. 8D. 0. 5 15.Westsyde Tool Company is expected to pay a dividend of $2. 00 in the upcoming year. The risk-free rate of return is 6% and the expected return on the market portfolio is 12%. Analysts expect the price of Westsyde Tool Company shares to be $29 a year from now. The beta of Westsyde Tool Company's stock is 1. 20. Using a on eperiod valuation model, the intrinsic value of Westsyde Tool Company stock today is _________. A. $24. 29B. $27. 39C. $31. 13D. $34. 52 16. Todd Mountain development Corporation is expected to pay a dividend of $2. 50 in the upcoming year. Dividends are expected to grow at the rate of 8% per year.The risk-free rate of return is 5% and the expected return on the market portfolio is 12%. The stock of Todd Mountain Development Corporation has a beta of 0. 75. Using the CAPM, the return you should require on the stock is _________. A. 7. 25%B. 10. 25%C. 14. 75%D. 21. 00% 17. Interior Airline is expected to pay a dividend of $3 in the upcoming year. Dividends are expected to grow at the rate of 10% per year. The risk-free rate of return is 4% and the expected return on the market portfolio is 13%. The stock of Interior Airline has a beta of 4. 00. Using the constant growth DDM, the intrinsic value of the stock is _________.A. $10. 00B. $22. 73C. $27. 78D. $41. 67 18. Everything equal, w hich variable is negatively related to intrinsic value of a company? A. D1B. D0C. gD. k 19. A common stock pays an annual dividend per share of $1. 80. The risk-free rate is 5 percent and the risk premium for this stock is 4 percent. If the annual dividend is expected to remain at $1. 80 per share, what is the value of the stock? A. $17. 78B. $20. 00C. $40. 00D. None of the above 20. A stock is priced at $45 per share. The stock has earnings per share of $3. 00 and a market capitalization rate of 14%. What is the stock's PVGO?A. $23. 57B. $15. 00C. $19. 78D. $21. 34 21. If a firm has a free cash flow equal to $50 million and that cash flow is expected to grow at 3% forever, what is the total firm value given a WACC of 9. 5%? A. $679 millionB. $715 millionC. $769 millionD. $803 million 22. Next year's earnings are estimated to be $5. 00. The company plans to reinvest 20% of its earnings at 15%. If the cost of equity is 9%, what is the present value of growth opportunities? A. $9. 09B . $10. 10C. $11. 11D. $12. 21 1. A2. B3. C4. B5. C6. D7. B8. A9. D10. C11. B12. A13. A14. B15. B16. B17. A18. D19. B20. A21. C22.C 1. Consider two bonds, A and B. Both bonds presently are selling at their par value of $1,000. Each pay interest of $120 annually. Bond A will mature in 5 years while bond B will mature in 6 years. If the yields to maturity on the two bonds change from 12% to 14%, _________. A. both bonds will increase in value but bond A will increase more than bond B B. both bonds will increase in value but bond B will increase more than bond A C. both bonds will decrease in value but bond A will decrease more than bond B D. both bonds will decrease in value but bond B will decrease more than bond A 2.Everything else equal the __________ the maturity of a bond and the __________ the coupon the greater the sensitivity of the bond's price to interest rate changes. A. longer; higher B. longer; lower C. shorter; higher D. shorter; lower 3. A __________ bond is a bond where the issuer has an option to retire the bond before maturity at a specific price after a specific date. A. callable B. coupon C. puttable D. treasury 4. In an era of particularly low interest rates, which of the following bonds is most likely to be called? A. Zero coupon bonds B. Coupon bonds selling at a discount C. Coupon bonds selling at a premium D.Floating rate bonds 5. A coupon bond which pays interest of 4% annually, has a par value of $1,000, matures in 5 years, and is selling today at $785. The actual yield to maturity on this bond is _________. A. 7. 2% B. 8. 8% C. 9. 1% D. 9. 6% 6. A coupon bond which pays interest of $60 annually, has a par value of $1,000, matures in 5 years, and is selling today at a $75. 25 discount from par value. The current yield on this bond is _________. A. 6. 00% B. 6. 49% C. 6. 73% D. 7. 00% 7. A coupon bond which pays interest semi-annually has a par value of $1,000, matures in 8 years, and has a yield to maturity of 6%.If the coupon rate is 7 %, the intrinsic value of the bond today will be __________ (to the nearest dollar). A. $1,000 B. $1,063 C. $1,081 D. $1,100 8. A treasury bond due in one year has a yield of 6. 3% while a treasury bond due in 5 years has a yield of 8. 8%. A bond due in 5 years issued by High Country Marketing Corporation has a yield of 9. 6% while a bond due in one year issued by High Country Marketing Corporation has a yield of 6. 8%. The default risk premiums on the one-year and 5-year bonds issued by High Country Marketing Corp. are respectively __________ and _________. A. 0. 4%, 0. 3% B. 0. 4%, 0. % C. 0. 5%, 0. 5% D. 0. 5%, 0. 8% 9. A zero-coupon bond has a yield to maturity of 5% and a par value of $1,000. If the bond matures in 16 years, it should sell for a price of __________ today. A. $458. 00 B. $641. 00 C. $789. 00 D. $1,100. 00 10. You can be sure that a bond will sell at a premium to par when _________. A. its coupon rate is greater than its yield to maturity B. its coupon rate is le ss than its yield to maturity C. its coupon rate equal to its yield to maturity D. its coupon rate is less than its conversion value 11. Consider a 7-year bond with a 9% coupon and a yield to maturity of 12%.If interest rates remain constant, one year from now the price of this bond will be _________. A. higher B. lower C. the same D. indeterminate 12. The yield to maturity on a bond is ________. I. above the coupon rate when the bond sells at a discount, and below the coupon rate when the bond sells at a premium II. the discount rate that will set the present value of the payments equal to the bond price III. equal to the true compound return on investment only if all interest payments received are reinvested at the yield to maturity A. I only B. II only C. I and II only D. I, II and III 13.Assuming semiannual compounding, a 20-year zero coupon bond with a par value of $1,000 and a required return of 12% would be priced at _________. A. $97 B. $104 C. $364 D. $732 14. The yield to maturity of an 10-year zero coupon bond, with a par value of $1,000 and a market price of $625, is _____. A. 4. 8% B. 6. 1% C. 7. 7% D. 10. 4% 15. If the quote for a Treasury bond is listed in the newspaper as 98:09 bid, 98:13 ask, the actual price for you to purchase this bond given a $10,000 par value is _____________. A. $9,828. 12 B. $9,809. 38 C. $9,840. 62 D. $9,813. 42 16. The price on a treasury bond is 104:21 with a yield to maturity of 3. 5%. The price on a comparable maturity corporate bond is 103:11 with a yield to maturity of 4. 59%. What is the approximate percentage value of the credit risk of the corporate bond? A. 1. 14% B. 3. 45% C. 4. 59% D. 8. 04% 17. You buy an 8 year $1000 par value bond today that has a 6% yield and a 6% annual payment coupon. In one year promised yields have risen to 7%. Your one year holding period return was ___. A. 0. 61% B. -5. 39% C. 1. 28% D. -3. 25% 18. If the coupon rate on a bond is 4. 50% and the bond is selling at a premium, which of the following is the most likely yield to maturity on the bond?A. 4. 30% B. 4. 50% C. 5. 20% D. 5. 50% 19. All other things equal, which of the following has the longest duration? A. A 30 year bond with a 10% coupon B. A 20 year bond with a 9% coupon C. A 20 year bond with a 7% coupon D. A 10 year zero coupon bond 20. All other things equal, which of the following has the shortest duration? A. A 30 year bond with a 10% coupon B. A 20 year bond with a 9% coupon C. A 20 year bond with a 7% coupon D. A 10 year zero coupon bond 21. (Challenge question) A pension fund must pay out $1 million next year, $2 million the following year and then $3 million the year after that.If the discount rate is 8% what is the duration of this set of payments? A. 2. 00 years B. 2. 15 years C. 2. 29 years D. 2. 53 years 22. All other things equal, which of the following has the longest duration? A. A 20 year bond with a 10% coupon yielding 10% B. A 20 year bond with a 10% coupon yielding 11% C. A 20 yea r zero coupon bond yielding 10% D. A 20 year zero coupon bond yielding 11% 23. Because of convexity, when interest rates change the actual bond price will ____________ the bond price predicted by duration. A. always be higher than B. sometimes be higher than C. always be lower than D. ometimes be lower than 24. Duration is a concept that is useful in assessing a bond's _________. A. credit risk B. liquidity risk C. price volatility D. convexity risk 25. A pension fund has an average duration of its liabilities equal to 15 years. The fund is looking at 5 year maturity zero coupon bonds and 4% yield perpetuities to immunize its interest rate risk. How much of its portfolio should it allocate to the zero coupon bonds to immunize if there are no other assets funding the plan? A. 52% B. 48% C. 33% D. 25% 26. You own a bond that has a duration of 6 years. Interest rates are urrently 7% but you believe the Fed is about to increase interest rates by 25 basis points. Your predicted price cha nge on this bond is ________. A. +1. 40% B. -1. 40% C. -2. 51% D. +2. 51% 27. A bank has an average duration of its liabilities equal to 2 years. The bank's average duration of its assets is 3. 5 years. The bank's market value of equity is at risk if _______________________. A. interest rates fall B. credit spreads fall C. interest rates rise D. the price of all fixed income securities rises 28. Banks and other financial institutions can best manage interest rate risk by _____________. A. aximizing the duration of assets and minimizing the duration of liabilities B. minimizing the duration of assets and maximizing the duration of liabilities C. matching the durations of their assets and liabilities D. matching the maturities of their assets and liabilities 29. The duration of a portfolio of bonds can be calculated as _______________. A. the coupon weighted average of the durations of the individual bonds in the portfolio B. the yield weighted average of the durations of the individu al bonds in the portfolio C. the value weighed average of the durations of the individual bonds in the portfolio D. verages of the durations of the longest and shortest duration bonds in the portfolio 30. Rank the interest sensitivity of the following from most sensitive to an interest rate change to the least sensitive. I. 8% coupon, noncallable 20 year maturity, par bond II. 9% coupon, currently callable 20 year maturity, premium bond III. Zero coupon, 30 year maturity bond A. I, II, III B. II, III, I C. III, I, II D. III, II, I 31. A bank has $50 million in assets, $47 million in liabilities and $3 million in shareholders' equity. If the duration of its liabilities are 1. and the bank wants to immunize its net worth against interest rate risk and thus set the duration of equity equal to zero, it should select assets with an average duration of _________. A. 1. 22 B. 1. 50 C. 1. 60 D. 2. 00 A bond pays annual interest. Its coupon rate is 9%. Its value at maturity is $1,000. It mat ures in four years. Its yield to maturity is currently 6%. 32. The duration of this bond is _______ years. A. 2. 44 B. 3. 23 C. 3. 56 D. 4. 10 33. The modified duration of this bond is ______ years. A. 4. 00 B. 3. 56 C. 3. 36 D. 3. 05 34. A bond with a 9-year duration is worth $1,080. 0 and its yield to maturity is 8%. If the yield to maturity falls to 7. 84%, you would predict that the new value of the bond will be _________. A. $1,035 B. $1,036 C. $1,094 D. $1,124 35. When interest rates increase, the duration of a 20-year bond selling at a premium _________. A. increases B. decreases C. remains the same D. increases at first, then declines 36. Duration facilitates the comparison of bonds with differing ___________ A. default risk B. conversion ratios C. maturities D. yields to maturity 37. The historical yield spread between the AA bond and the AAA bond has been 25 basis points.Currently the spread is only 9 basis points. If you believe the spread will soon return to its historic al levels you should ________________________. A. buy the AA and short the AAA B. buy both the AA and the AAA C. buy the AAA and short the AA D. short both the AA and the AAA 38. The duration of a bond normally increases with an increase in _________. I. term-to-maturity II. yield-to-maturity. III. coupon rate A. I only B. I and II only C. II and III only D. I, II and III 39. Compute the modified duration of a 9% coupon, 3-year corporate bond with a yield to maturity of 12%. A. 2. 45 B. 2. 75 C. 2. 88 D. 3. 00 40.An 8%, 30-year bond has a yield-to-maturity of 10% and a modified duration of 8. 0 years. If the market yield drops by 15 basis points, there will be a __________ in the bond's price. A. 1. 15% decrease B. 1. 20% increase C. 1. 53% increase D. 2. 43% decrease 41. To create a portfolio with a duration of 4 years using a 5 year zero-coupon bond and a 3 year 8% annual coupon bond with a yield to maturity of 10%, one would have to invest ________ of the portfolio value in the z ero-coupon bond. A. 50% B. 55% C. 60% D. 75% 42. Which of the following set of conditions will result in a bond with the greatest price volatility?A. A high coupon and a short maturity. B. A high coupon and a long maturity. C. A low coupon and a short maturity. D. A low coupon and a long maturity. 43. An investor who expects declining interest rates would maximize their capital gain by purchasing a bond that has a ___ coupon and a ___ term to maturity. A. low; long B. high; short C. high; long D. zero; long 44. A zero coupon bond is selling at a deep discount price of $430. 00. It matures in 13 years. If the yield to maturity of the bond is 6. 7%, what is the duration of the bond? A. 6. 7 years B. 8. 0 years C. 10 years D. 13 years 45.Convexity implies that duration predictions _______. I. underestimate the % increase in bond price when the yield falls II. underestimate the % decrease in bond price when the yield rises III. overestimates the % increase in bond price when the yield f alls IV. overestimates the % decrease in bond price when the yield rises A. I and III only B. II and IV only C. I and IV only D. II and III only 1. D2. B3. A4. C5. D6. B7. B8. D9. A10. A11. A12. D13. A14. A15. C16. A17. A18. A19. A20. D21. C22. C23. A24. C25. A27. C28. C29. C30. C31. A32. C33. C34. C35. B36. C37. C38. A39. A40. B41. B42. D43. D44. D45. C