The Great Depression Essay Example for Free

The Great Depression Essay In 1932, the USA was in an economic depression. The Great Depression. President Hoover introduced the â€Å"Old Deal† to protect American industries by aiming to prevent the price of imported goods from being lower than the price of local goods. He felt it was up to individual Americans to sort out their own economic problems. With the failure of the Old Deal, Franklin D. Roosevelt offered a â€Å"New Deal† for America. The Democratic Party nominated Roosevelt to stand for president in 1932. Being more flexible and more willing to experiment the Hoover, Roosevelt won the 1932 elections, have more the 60% of the votes. Roosevelt’s New Deal focused on three things: Relief, Recovery and Reform. These aims were to bring relief to the poor, help the country recover to industry and agriculture, and to prevent another depression by introducing social reforms. The New Deal was not a set plan or strategy, but rather a series of improvisations and experiments to survive the depression and preserve capitalism. During the Great Depression, many banks had failed, wiping out families savings. People had lost confidence in the banks. To restore this confidence, on his second day of office, Roosevelt declared a four-day â€Å"Banking Holiday†, where he closed all the banks in order to re-organise themselves. Congress passed the Emergency Banking Relief Act, which only allowed banks with enough money and properly managed accounts to re-open. Roosevelt explained the complexities of the banking problem to the public in his first â€Å"fire-side chat†. This restored the people’s confidence in the banks. The Depression also made the level of unemployment sky-rocket. To fix this problem, Roosevelt launched many new agencies with the Works Progress Administration (WPA), which created four million new jobs during the 1930’s. Some of these agencies were the AAA, CCC, SEC, FERA and the SSA. The Agricultural Adjustment Administration (AAA) made the government pay farmers not to work. This caused prices to rise and halted overproduction. The Federal Emergency Relief Administration (FERA) gave direct relief ($) to those who needed it. The Social Securities Act (SSA) was established to provide old-age pensions for workers, survivor’s benefits for victims of industrial accidents, unemployment insurance and aid for dependent mothers and children, the blind and physically disabled. The SSA received its funds from government taxes. Although Roosevelt was victoriously re-elected in 1936, his reform programme slowed. Factors, such as his failure to re-organise the Supreme Court to get more support for his policies, led to more opposition to government spending and taxes. This was his greatest mistake. Some of the positive out-comes of the New Deal was that it restored optimism and hope to American’s and provided the necessary relief to many. But, there were negative out-comes as well. Of these was that it did not really fix the depression and it left the nation with much debt. It also left people too dependent on the government.

Fibroblast Growth Factors (FGFs) in Neural Induction

Fibroblast Growth Factors (FGFs) in Neural Induction Abstract Neural induction represents the first stage in the formation of the vertebrate nervous system from embryonic ectoderm. Fibroblast Growth Factors (FGFs), initially identified for their mitogenic and angiogenic roles in bovine brain extracts, are now known to have many developmental roles in particular that of neural induction, comprising of a family of 22 FGFs. Spemann and Mangold (1924) pioneered the study of neural induction through the identification of the organizer. Early work in amphibians suggested that neural fate was instructed by signals from Spemanns organiser or dorsal mesoderm. Over a decade ago, the default model proposed that neural induction was the direct consequence from inhibition of bone morphogenetic proteins (BMPs) found in Xenopus laevis, not taking into consideration neural induction in avian embryos. Consequently many experimental studies, in the chick, subsequent to this finding conflicted the idea that BMP inhibition was the only necessary step required suggesting that FGFs were required at an earlier stage prior to BMP inhibition. Much controversy has surrounded the role of FGFs in neural induction but now it is widely accepted to have a role in both amphibians and amniotes. Fibroblast Growth Factors in neural induction Structure and Function: FGFs broken down Fibroblast Growth Factors (FGFs) regulate a vast array of developmental processes, including, limb development, neural induction and neural development (Bà ¶ttcher and Niehrs, 2005). FGFs play an important role in development of an organism by regulating cellular differentiation, proliferation and migration and are involved in tissue-injury repair (Itoh and Ornitz, 2004). The early FGFs, FGF1 and FGF2 (also known as acidic and basic FGF, respectively) were first discovered from bovine brain and pituitary extracts and identified for their mitogenic and angiogenic activities (Gospodarowicz et al., 1974). Additionally, a number of family members were found revealing a total of 22 FGFs in humans ranging from 17 to 34 kDa in molecular mass in vertebrates. The nomenclature extends to FGF23 but in humans FGF19 is the equivalent to mouse Fgf15 (Ornitz and Itoh, 2001). Also the FGFs have been organised into seven subfamilies based on sequence comparisons. FGFs show conservation through species, especially across the vertebrate species in gene structure and amino-acid sequence. FGF sequences are yet to be found in unicellular organisms such as yeast (Saccharomyces cerevisiae) and bacteria (Escherichia Coli) (Itoh and Ornitz, 2004). Interestingly, an Fgf-like gene has been encoded in the nuclear polyhedrosis virus genome (Ayres et al., 1994). In protostomes, there are far fewer FGFs in contrast to vertebrates, as two (let-756 and egl-17) have been found in Caenorhabditis elegans and three (branchless, pyramus and thisbe) in Drosophila (Mason, 2007). Most FGFs have amino-terminal signal peptides (Fig. 1 (a)) and are secreted from cells. FGFs 9, 16 and 20 lack this signal peptide but nevertheless are still secreted (Ornitz and Itoh, 2001). FGF1 and FGF2 lack these signal sequences and are secreted by non-canonical pathways, however they can be found on the cell surface and within the extracellular matrix. Golfarb (2005) suggests that FGFs 11-14 do not interact with FGF receptors (FGFRs) and are not secreted but instead localise to the cell nucleus. Fig. 1 (above) illustrates the structural features of the FGF polypeptide (a). A signal sequence (shaded grey) can be seen here within the amino terminus and is present in most FGFs. All FGFs contain a core region (Fig. 1 (a)) containing around 120 amino acids of which 6 are identical amino acids residues and 28 are highly conserved (Goldfarb, 1996). The black boxes (numbered 1 to 12) represent the location of ÃŽ ² strands within the core. The three dimensional structure of FGF2 (b) can also be seen where the heparin binding region (yellow) includes residues between ÃŽ ²1 and ÃŽ ²2 strands and in ÃŽ ²10 and ÃŽ ²11 strands. FGFs have a high affinity for heparan sulfate proteoglycans (HSPG) and require heparan sulphate to activate one of four transmembrane receptor tyrosine kinases (FGFR1-4) in all vertebrates. FGFR5 has been identified recently, however most action is mediated via FGFR1-4 (Powers et al., 2000). FGFRs are membrane associated class IV receptor tyrosine kinases (RTKs). The FGFR tyrosine kinase receptors (Fig. 2 B) include 3 immunoglobulin (Ig) domains and a heparin binding sequence which requires heparan sulphate to be activated (McKeehan et al., 1998). HSPG are low affinity receptors that are unable to transmit a biological signal but act as co-factors for activation and regulation of an interaction between FGFs and FGFRs. Fig. 2 (above) illustrates a two dimensional generic FGF (A) and a FGFR (B) protein. The structure of a FGF (A) coincides with that of Fig. 1, containing a signal sequence in the amino-terminus and the conserved core region containing HSPG and receptor-binding sites. The main features of FGFRs (B) include 3-Immunoglobulin domains, an acidic box (AB) which lies between IgI and IgII, heparin-binding domain, Cell Adhesion Molecule (CAM)-homology domain, transmembrane domain and a split tyrosine kinase enzyme domain for catalytic activity and binding of adaptor proteins. The Ig domains in the extracellular region of a FGFR are required for FGF binding and regulate binding affinity and ligand specificity. Multiple alternative splicing that generates a range of FGFR1-4 receptor isoforms with transformed ligand binding properties provides diversity (Olsen et al., 2006). For example, FGF2 interacts with all four receptors FGFR1-4 whereas FGF7 only interacts with the FGFR2 IIIb isoform (a splice variant of FGF2; expressed in epithelial cells). Ligand-receptor binding specificity is affected by alternative splicing particularly in the C-terminal region of the third immunoglobulin loop in FGFR1-3 which produces IIIb or IIIc isoforms (Mason, 2007). Table 1 (below) illustrates the specificity of the FGF ligands for particular FGFR isoforms. This table is useful yet evidence from in vitro may appear misleading as in vivo involves influence from co-factors such as HSPG (Mohammadi et al., 2005). Table 1 (above) shows there are seven FGFR isoforms (FGFR1b; FGFR1c; FGFR2b; FGFR2c; FGFR3b; FGFR3c and FGFR4) that FGF1 through to FGF23 variously bind. Alternative mRNA splicing of FGFR1-3, particularly in the carboxy-terminal half of the third extracellular immunoglobulin loop (Ig-domain III), derives the b and c isoforms. HSPGs are necessary co-factors in activation of FGFRs by FGFs and evidence has found the ternary complex to comprise of FGF-FGFR-HSPG in a 2:2:1 ratio (Mohammadi et al., 2005). The co-binding of HSPG prevents proteolysis and thermal denaturation (Itoh and Ornitz, 2004). HSPG binding of FGF induces dimerization of FGFR, followed by transphosphorylation of receptor subunits, initiating an intracellular signalling cascade. FGF signalling: Its a cellular game Following formation of the FGF-HSPG-FGFR complex several downstream signalling pathways are activated (Fig. 3 below). This includes three pathways, the Ras/Mitogen-activated protein kinase (MAPK) pathway, Phosphoinositide 3-kinase (PI3K)/ Akt pathway and phospholipase C- (PLC )/ Ca2+/ protein kinase C (PKC) pathway. These pathways are mediated via docking proteins (such as FGF receptor substrate (FRS) and Grb2 in the Ras/MAPK pathway) that recruit downstream enzymes. The Ras/MAPK pathway (Fig. 3) is initiated via Grb2 (a docking protein) where its SH2 domain binds to the tyrosine phosphorylated FRS2 in response to activation of the FGFR receptor (Kouhara et al., 1997). Grb2 binds to SOS (son of sevenless; a guanine nucleotide exchange factor) via a SH3 domain on the Grb2 molecule. This Grb2-SOS complex activates SOS which promotes the dissociation of GDP from Ras so it is able to bind GTP for its activation. Activated Ras activates RAF (MAPKKK) which is normally held in a closed conf ormation by the 14-3-3 protein. Once activated, RAF phosphorylates and activates mitogen-activated and extracellular signal-regulated kinase (MEK (MAPKK)) which in turn phosphorylates ERK1/2 (MAPK). MAPK then translocates into the nucleus to phosphorylate specific transcription factors of the Ets family which in turn activate expression of FGF target genes. In addition, it is also evident from Fig. 3 that active ERK itself can antagonise FRS activity. Activation of the PI3K/Akt pathway (Fig. 3) is by binding of Gab1 (Grb2-associated-binding protein 1) to FRS2 indirectly via Grb2. In the presence of Gab1, activation of PI3K stimulates the Akt pathway which suggests FGFs have anti-apoptotic effects in the developing nervous system (Mason, 2007). In addition, PI3K can bind to a phosphorylated tyrosine residue of FGFR directly. The third way in which the PI3K/Akt pathway is activated is by activated Ras inducing membrane localisation of the PI3K catalytic subunit. PLC- /Ca2+/PKC pathway is also activated when a tyrosine residue is autophosphorylated in the carboxy terminal of the FGFR. PLC- hydrolyses phosphatidylinositol to produce inositol trisphosphate (IP3) and diacylglycerol (DAG) which stimulates calcium release and activates PKC, respectively. PKC has also been found to activate the Ras/MAPK pathway independent of Ras but dependent on c-Raf (Ueda et al., 1996). Fig. 3 also indicated that the final activated components, of the three signalling pathways mentioned, translocate into the nucleus to activate specific transcription factors of the Ets family (particularly Ets1, Pea3, and Erm) which activate expression of FGF target genes and in turn these feedback (Fig, 4) to regulate intracellular signalling (Dailey et al., 2005). Most of the proteins produced function as feedback inhibitors (as seen in Fig. 4), including Sprouty (Spry), Sef and MAP Kinase phosphatase 3 (MKP3) which modulate particularly the Ras/Erk pathway at different levels (Mason, 2007). In contrast, stimulation of the fibronectin leucine-rich transmembrane type III (XFLRT3) protein causes FGF signalling to be positively regulated (Bà ¶ttcher et al., 2003). Sprouty (Spry) was one of the first identified feedback regulators of the FGF pathway. Thisse and Thisse (2005) found Spry to antagonise FGF Signalling by gain and/or loss of function experiments in mouse. Spry acts at the level of Raf and/or Grb2 (Fig. 4). Gain and/or loss of function experiments in zebrafish demonstrated that Sef antagonises FGF signalling (Fig. 4) acting at level of MEK and ERK (Tsang et al., 2002). Mouse studies have suggested that FGFR signalling is required for Dusp6 transcription which codes for MKP3 (Ekerot et al., 2008). From this study it was also found that MKP3 acts as a negative regulator of ERK activity (as seen in Fig. 4). Sef and XFLRT3 are located at the membrane (Fig. 4) and carry out antagonising actions with FGFR directly. FGF signalling can be regulated at different levels, from the membrane all the way down to the level of phosphorylation of MAPK and it is important also to know that FGFs have been detected in the nucleus (Mason, 2007). Most of the downstream target genes as described earlier are feedback inhibitors (Spry, Sef and MKP3) but FGF signals are also known to interact with many other important pathways such as transforming growth factor-ÃŽ ² (TGF-ÃŽ ²), Hedgehog (HH), Notch and Wnt (Gerhart, 1999). Therefore, in conjunction with these, FGFs are responsible for development of most organs of the vertebrate body. In the nervous system, FGFs have been implicated to play a role in early developmental processes, such as neural induction, patterning and proliferation (Umemori, 2009). Neural induction: The Default Model Spemann and Mangold (1924) pioneered the study of neural induction, which is defined as the process by which naive ectodermal cells aquire a neural fate. Their work involved demonstrating that tissue from the dorsal lip of the frog Xenopus laevis blastopore could induce a second ectopic nervous system (Fig. 5 above left) when implanted onto the ventral side of a host gastrula embryo. The second ectopic nervous system was host derived indicating that the graft was important in determining cell fate. This region, located on the dorsal side of an amphibian embryo, was named the Spemann organizer as it could direct the neighbouring ectodermal cells to form nervous system instead of epidermis. Although the organizer (group of dorsal mesodermal cells) was found to be present in many species (Hamburger, 1988) it was the Xenopus laevis which gave an insight into the molecular events involved in neural induction in vertebrates (Hemmati-Brivanlou et al., 1994). This was particularly because amphibians were found to be ideal experimental models for the study of neural induction as neurulation initiated within twelve hours after fertilisation (Weinstein and Hemmati-Brivanlou, 1997). It was implied that signals from the organizer provide instructions to the ectoderm to form neural tissue therefore for many decades the view was that the default state of the ectoderm was to produce epidermis. The first challenges to this model came from studies making use of dissociated cell cultures (Sato and Sargent, 1989). It was found that when animal caps were cultured intact that epidermis formed but neural tissue arose from animal caps that had been dissociated for prolonged periods (as seen in Fig. 6 below). This led to the idea that intact tissue may block the formation of neural tissue by presence of neural inhibitors which are diluted out when the tissue is dissociated. Recent research has found that the default nature of the ectoderm is to produce neural tissue that requires inhibition of a neural inhibitor from the ectoderm. Before considering the process of neural induction I would like to take a step back and describe the three germ layers of the embryo. Following fertilisation, the zygote undergoes stages of cleavage to eventually form a gastrula with three germ layers (in triploblastic animals) usually only visible in vertebrate animals. The Germ layers will eventually give rise to all of the animals organs through a process known as organogenesis. The three layers include, the ectoderm (outermost), endoderm (innermost) and mesoderm (which is between the ectoderm and endoderm) layers. The Endoderm gives rise to the lung, thyroid and pancreas. The mesoderm forms the skeleton, skeletal muscle, the urogenital system, heart and blood. The outermost layer, the ectoderm which is of concern here, gives rise to the epidermis and nervous system. It is at gastrulation that the vertebrate ectoderm is competent to differentiate into neural tissue or epidermis. Unless told otherwise, the default nature of the ect oderm is to produce neural tissue and this was outlined as the default model. The Default model of vertebrate neural induction, discovered over a decade ago in Xenopus, proposed that in the presence of bone morphogenetic protein (BMP), a signalling molecule of the TGF-ÃŽ ² superfamily, causes the ectoderm to give rise to an epidermal cell fate (Stern, 2006; Muà ±oz-Sanjuan and Brivanlou, 2002). In support of this model, consistent with the idea that BMP activity inhibits neural fates, animal caps which had been injected with RNA encoding effectors of BMP4 (Smad 1/5 or Msx1) neuralization did not occur. Conversely, it was found that inhibition of BMP activity in the ectoderm is essential for a neural fate which forms the basis of the default model of neural induction. Inhibition of BMP is achieved through direct binding of BMP antagonists emitted from the organizer (Wilson and Hemmati-Brivanlou, 1997). These BMP antagonists include chordin (Sasai et al., 1995), noggin (Lamb et al., 1993) and follistatin (Hemmati-Brivanlou et al., 1994) which bind to BMPs extra cellularly to prevent its interaction with its own receptor (Hemmati-Brivanlou and Melton, 1997). These molecules have direct neural activity which means they induce formation of neural tissue in the ectoderm without forming mesoderm. It was initially believed that these molecules acted as ligands to bring about neural tissue formation. Experiments found that there was conservation through species, identifying that chordin was homologous to the short gastrulation (sog) gene found in Drosophila which has been shown to antagonize the BMP homologue decapentaplegic (dpp) (Wharton et al., 1993), suggesting that these molecules might act as inhibitors rather than inducers and that these inhibitory mechanisms have been conserved from arthropods through to vertebrates. It was experiments (Fig. 6) showing that dissociated ectodermal explants would become neural tissue in absence of inducing signals from the organizer (Sato and Sargent, 1989). Evidence found that neural induction resulted from inhibition of the TGF-ÃŽ ² pathway as expression of dominant-negative activin receptor gave rise to neural fates in amphibian ectoderms (Hemmati-Brivanlou and Melton, 1994). It was found that chordin, noggin, follistatin and molecules such as Cerberus and Xnr3 (Xenopus nodal related 3) bound to BMP in the extracellular space inhibiting its action (Hemmati-Brivanlou and Melton, 1997) leading to the much debated default model of neural induction. Neural Induction: FGFs get it started Support for the default model still remains, mainly in Xenopus, but other work (especially in chick and mouse) suggests a more complex mechanism (Streit et al., 1998). It has been established that the BMP pathway is involved in determining ectodermal cell fate (Wilson and Hemmati-Brivanlou, 1997) but it still remains to be proved conclusive if BMP inhibition is required for neural induction alone or if other pathways act separately or with BMP inhibition. In the chick embryo it has been found that naive epiblast cells do not respond to BMP antagonists until previous exposure to organizer signals for five hours (Streit et al., 1998). Striet et al. (2000) grafted an organizer to observe the genes induced in the epiblast within this time period. A gene ERNI (early response to neural induction) was identified as a coiled coil domain with a tyrosine phosphorylation site and found to be expressed throughout the region that later contributes to the nervous system at pre-primitive streak stages (Hatada and Stern, 1994). Striet et al. (2000) findings made ERNI the earliest known marker after a response to organizer signals, prior to even Sox3 (induced by the node in 3 hours (Streit and Stern, 1999)). FGFs are becoming more evident that they have a major role in neural induction as it has been shown to begin before gastrulation, before BMP antagonists even appear (Wilson et al., 2000). In the chick, it has been found that FGFs have the role of blocking BMP signalling and promoting neural differentiation (Wilson et al., 2000). In ascidians, FGF signalling is the main mechanism of neural induction with BMP antagonism playing a role in later development (Lemaire et al., 2002). In frogs and fish, in contrast, FGFs do not have a certain role in neural induction and is believed their primary role is BMP inhibition (Pera et al., 2003). Exposure of the chick epiblast to an implanted organiser for around 5 hours induces Sox3 (an early neural plate marker) (Stern, 2005). After removal of the implanted organiser, chordin can be used to stabilise it (Striet et al., 1998) which implies that before the ectoderm can respond to BMP antagonists it must be exposed to 5 hours of signals from the organizer. During these 5 hours, several genes become activated such as, ERNI (early response to neural induction) which becomes active after 1 hour (Streit et al., 2000) and Churchill (Chch) after about 4 hours (Sheng et al., 2003). These are both induced by FGF and not BMP inhibition, indicating the importance of FGFs in early neural induction. Churchill which is expressed in the neural plate inhibits brachyury, a transcription factor, which as a result suppresses mesoderm formation by preventing cell ingression. In the chick, FGF8 is expressed in the hypoblast, prior to gastrulation before Hensens node appears (the chick equivalent to the organizer) indicating that neural induction is in fact able to begin before gastrulation. This is important because ERNI and Sox3 mark neural induction and require FGF signalling (Stern, 2005). Streit et al. (2000) found that FGF8 coated beads induce ERNI as efficiently as the node within 1-2 h without inducing brachury and also the expression of Sox3. These results indicate FGFs to be possible early signals in neural induction. It is FGF8 which has been identified as the best candidate because it is expressed in the anterior part of the str

Community Service Essay -- Humanitarian Organizations Essays

Community Service People complain everyday about the problems in this world. One of my complaints is about people who complain! I have a high respect for those who take actions to try to solve these problems. One major group which has to solve problems this is internationally recognized is Rotary International. Another group with similar goals is The Ruritan Foundation. Both of these groups have a website used by people all over the world to communicate information about their organization and how people can get involved. Ruritan focuses on the loval community and serving on a much smaller scale than Rotary. For Rotary, an overall emphasis is made on international service needs and diversity among people, as well as advancing global awareness about issues. There are more ignorant people out there than you may think. According to the main website, www.rotary.org., "Rotary International is an organization of business and professional leaders united worldwide who provide humanitarian service, encourage high ehtical standards in all vocations, and help huild good will and peace in the world." Rotarians devote their lives so much to humanity that its motto is "Service before Self,"by service and helping others and ultimately, in a utopian world, accomplishing peace, in daily personal lives as well as while working on Rotary-specific projects (About Rotary). You may be asking what types of concerns this association cares about. According to the "About Rotary" section of the website, they address many of today's most critical issues, such as children at risk, poverty and hunger, the environment, illiteracu, and violence, to name a few. Getting involved in a particular area of concern would not be a s... ...s website in that it contains a list of links on the left side to investigate differnt aspects of the organization. The webpage is not as formal as that of Rotary International, but still is not necessary that it is. The differences between Ruritan Foundation and Rotary International actually complement each other. while Ruritan focuses on the local community and serving its needs, Rotary has world-wide perspective on similar issues. Information for prospective members is also a crucial objective of these websites since they are target readers. People who are too stagnate to follow through with their altruistic desires can at least donate money to the people who take action on their calling to kindness. The Rotary and Ruritan organizations relate to almost all people in this world, whether a member, donating, or receiving care; everyone can benefit.

No Accidents in Jack Londons To Build a Fire Essays -- London To Buil

As the title implies, Jack London's 1908 short story contains within its narrative a literal set of sequential directions on how "To Build a Fire." London extends this sequential conceit to his fatidic vision of the universe. Unlike the dog in the story, who can rely on its pure-bred arctic instinct as it navigates through the dangerous tundra, the anonymous man possesses a duller, myopic instinct which is unable foresee the consequentiality of the environment. This instinctual flaw in mankind (relative to that of a husky) is a given, but the man fails to compensate by integrating intellectuality into his journey. Were he to use all his resources efficiently, as the dog does, the man could anticipate the chain of events that leads to his demise, and then alter his literal and figurative course. Such a deconstruction of a pre-ordained universe is possible, London suggests, since the reader is made aware - through parallelism, choice wording, and other stylistic and suspen seful devices - of the subtle ways in which seemingly disconnected events are causally-linked. London prompts an investigation into the motifs of linkage in the first two sentences by crafting a landscape of connections, layers, and progression: Day had broken cold and gray, exceedingly cold and gray, when the man turned aside from the main Yukon trail and climbed the high-earth bank, where a dim and little-travelled trail led eastward through the fat spruce timberland. It was a steep bank, and he paused for breath at the top, excusing the act to himself by looking at his watch. (462) The care which London takes to produce a conjunctive atmosphere is delicate but insistent. The adverbial and prepositional clauses - "when the m... ...ight, old hoss; you were right'" (477). He certainly was right. Works Cited and Consulted "Existentialism." The American Heritage Dictionary. 3rd ed. New York: Dell, 1994. Hendricks, King. Jack London: Master Craftsman of the Short Story. Logan: Utah State U P, 1966. Rpt. In Jack London: Essays in Criticism. Ed. Ray Wilson Ownbey. Santa Barbara:Â   Peregrine, 1978. 13-30. Labor, Earle. Jack London. New York: Twayne, 1974. London, Jack. "To Build a Fire." Literature: An Introduction to Fiction, Poetry and Drama. 6th ed. Ed. X. J. Kennedy and Dana Gioia. New York: Harper Collins, 1995. 118-29. McElroy, Davis Dunbar. Existentialism and Modern Literature. Westport: Greenwood, 1968. Perry, John. Jack London: An American Myth. Chicago: Nelson-Hall, 1981. Walcutt, Charles Child. Jack London. Minneapolis: U of Minnesota P, 1966.

The Collapse of the Tacoma Narrows Bridge Essay -- Bridges Engineering

The Collapse of the Tacoma Narrows Bridge The Tacoma Narrows Bridge is perhaps the most notorious failure in the world of engineering. It collapsed on November 7, 1940 just months after its opening on July 1, 1940. It was designed by Leon Moisseiff and at its time it was the third largest suspension bridge in the world with a center span of over half a mile long. The bridge was very narrow and sleek giving it a look of grace, but this design made it very flexible in the wind. Nicknamed the "Galloping Gertie," because of its undulating behavior, the Tacoma Narrows Bridge drew the attention of motorists seeking a cheap thrill. Drivers felt that they were driving on a roller coaster, as they would disappear from sight in the trough of the wave. On the last day of the bridge's existence it gave fair warning that its destruction was eminent. Not only did it oscillate up and down, but twisted side to side in a cork screw motion. After hours of this violent motion with wind speeds reaching forty and fifty miles per hour, the bridge collapsed. With such a catastrophic failure, many people ask why such an apparently well thought out plan could have failed so badly?(This rhetorical question clearly sets up a position of inquiry-which iniates all research.) The reason for the collapse of the Tacoma Narrows Bridge is still controversial, but three theories reveal the basis of an engineering explanation. (Jason then directly asserts what he found to be a possible answer to his question.) The bridge was designed at a time when America was moving toward streamline products, this included the design of bridges. The Tacoma Narrows Bridge was a sleek, graceful looking suspension bridge. Suspension bridges consist of many cables anchored... ... suspension bridges (pp. 13-102). Seattle: University of Washington Press French, C. & Lorentz, T. (1995). Corrosion of reinforcing steel in concrete: Effects of materials, mix composition, and cracking. ACI Materials Journal, 92, 181-190. Koughan,J. (1996, August 1). The collapse of the Tacoma Narrows Bridge, evaluation of its demise, and the effects of the disaster of succeeding bridge designs [Online] Available: http://www.me.utexas.edu/~uer/papers/paper_jk.html O'Connor, C. (1971). Designs of superstructures. New York: Wiley and Sons Petroski, H. (1992). To engineer is human. New York: Vintage Books Troitsky, M. S. (1994). Planning and design of bridges. New York: Wiley and Sons Washington State Department of Transportation. (1999). A short history of "galloping gertie" [Online]. Available: http://www.wsdot.wa.gov/solve16/history.html The Collapse of the Tacoma Narrows Bridge Essay -- Bridges Engineering The Collapse of the Tacoma Narrows Bridge The Tacoma Narrows Bridge is perhaps the most notorious failure in the world of engineering. It collapsed on November 7, 1940 just months after its opening on July 1, 1940. It was designed by Leon Moisseiff and at its time it was the third largest suspension bridge in the world with a center span of over half a mile long. The bridge was very narrow and sleek giving it a look of grace, but this design made it very flexible in the wind. Nicknamed the "Galloping Gertie," because of its undulating behavior, the Tacoma Narrows Bridge drew the attention of motorists seeking a cheap thrill. Drivers felt that they were driving on a roller coaster, as they would disappear from sight in the trough of the wave. On the last day of the bridge's existence it gave fair warning that its destruction was eminent. Not only did it oscillate up and down, but twisted side to side in a cork screw motion. After hours of this violent motion with wind speeds reaching forty and fifty miles per hour, the bridge collapsed. With such a catastrophic failure, many people ask why such an apparently well thought out plan could have failed so badly?(This rhetorical question clearly sets up a position of inquiry-which iniates all research.) The reason for the collapse of the Tacoma Narrows Bridge is still controversial, but three theories reveal the basis of an engineering explanation. (Jason then directly asserts what he found to be a possible answer to his question.) The bridge was designed at a time when America was moving toward streamline products, this included the design of bridges. The Tacoma Narrows Bridge was a sleek, graceful looking suspension bridge. Suspension bridges consist of many cables anchored... ... suspension bridges (pp. 13-102). Seattle: University of Washington Press French, C. & Lorentz, T. (1995). Corrosion of reinforcing steel in concrete: Effects of materials, mix composition, and cracking. ACI Materials Journal, 92, 181-190. Koughan,J. (1996, August 1). The collapse of the Tacoma Narrows Bridge, evaluation of its demise, and the effects of the disaster of succeeding bridge designs [Online] Available: http://www.me.utexas.edu/~uer/papers/paper_jk.html O'Connor, C. (1971). Designs of superstructures. New York: Wiley and Sons Petroski, H. (1992). To engineer is human. New York: Vintage Books Troitsky, M. S. (1994). Planning and design of bridges. New York: Wiley and Sons Washington State Department of Transportation. (1999). A short history of "galloping gertie" [Online]. Available: http://www.wsdot.wa.gov/solve16/history.html

Intellectual Auto Biography Essay

Unlike many of my colleagues or others who have majored in history before, my intellectual background has been influenced by two major cultures in the world. As a twenty three years old student living in America but originally from Japan, the foundation of my intellectual being was shaped by the Japanese culture and education since the first 18 years of my life and schooling took place in Tokyo Japan. Later I moved to America, California where I have been under taking my degree course, majoring in History. This does not mean that my intellectual story is different or unique but I have to admit that, it is somehow interesting since many people and many things have played a part in it. From the time I started schooling, I have always had an interest in history. Just like America, Japan is really rich in history which is somehow different from the American one. The curiosity and the thirst to know more about my native country and the world at large formed the basis of my interest in history. In other words, I know why I am pursing history and sometimes I think taking this course of study was inevitable since it has really shaped my life. It is a well known fact that Buddhism is one of the major religions in the world especially in Japan and from a historical point of view; the religion has come to be identified with the country. It has shaped its culture, economy and political aspects. I am a self confessed Buddhist brought up by Buddhist parents and the whole of my life has been characterized by Buddhist doctrines. My beliefs and how I view life can only be attributed to the religion. As a history major, I believe one of the most interesting topics in history is religion and how it shapes people’s lives. I have always taken myself as an example, trying to analyze how it has really affected my life and my views about everything. I tend to agree that Buddhism is a philosophy more than religion because it defines lives of those who believe in it. Philosophers have defined the word philosophy as ‘the love of wisdom and Buddhism propagates that. I myself love wisdom and that is why I chose to do history in the first place; just to know almost everything that has shaped this world from the time it came into existence. Another thing I believe in is honesty. For me it is a very important virtue and has a major role to play in this world in regards to morality. Honesty, according to my understanding and beliefs can only be achieved the moment one is true to himself and to God/gods, depending on whom one worships or believes in. Being true to oneself forms the basis of honesty which will be followed by other forms of honesty for example, being honest to others and to God/gods. Those who are familiar with Buddhism religion will agree that, this view has somehow been influenced by the religion and that is why I began by saying that Buddhism is part of my life. As a Buddhist, I am supposed to be aware of my thoughts before I do anything. This also applies to actions. Before undertaking any action, one is supposed to be aware of it and to have wisdom and understanding on how to go about it . When all these are combined, they all add up to being true to oneself and that is what I call honesty in other words. This belief has really shaped my life especially in regards to my relationships with others. The moment one adopts this view of honesty, it is very difficult to fall out with anyone since one will always be open-minded. Being true to oneself will only mean that, you will do what you believe is true and it will be very difficult to be pressurized maybe by the peers into doing something against your will. When it comes to handling others, it will be very easy. For example, if one sees a friend doing something one is not comfortable with and maybe that friend wants you to join him/her, since you are true to yourself, you will be able to express your concerns and at the end of the day, that friend will see that your concern is actually genuine since it is coming from deep within you. It is not forced, not a pretence or expression of fear but your true self expressed in words. This will actually be felt by another person and it will eventually influence his thinking. I remember mentioning earlier that I am Buddhist and some may question whether I believe in one God or gods. I know in the modern days there are those Buddhists who believe in one God and there are others who do not for they believe in many gods. The question always poses some problems to me especially when it comes to explaining to others, especially my friends. They have always known the religion that I profess and what it says about the issue of God and gods but they are never sure about my stand. First I have to clarify something, Buddhism is a way of life and that is what makes it different from other religions. It emphasizes so much on how people are supposed to live and as a Buddhist; there is that kind of life that I am supposed to live. There is no mention in my religion that Buddha worshipped or believed in any one God. That does not mean we are atheists in fact there are so many Buddhists who believe in that one God of the Jews, we call Him, ‘the God of the desert. ’ Personally, I don’t have problems with those Buddhist who profess a kind of God in their lives even though it is not in Buddhism doctrines. Sometimes I tend to think that I will head there someday. Right now, from what I have read and seen, I tend to think that, there is a supernatural power that is in control of the world. I have been skeptical about the issue for a very long time and sometimes I do not want to talk about it. I have read so much regarding the matter, I have been exposed to so many religions and I have even been following what is happening in this world and to some extent, I think there could be actually a supernatural hand behind it all. Can I be regarded as an atheist then? I leave that judgment to ones discretion but as I said earlier, I am true to myself and what I believe in, but maybe one day I may change my mind; no one knows. I believe that Buddhism is a well organized religion. In fact, it has never been heard before that Buddhists have fought with any religion over religious matters and that is what I love most about the religion. Foundation is the most interesting part of the religion as far as I am concerned. Buddha was born in an affluent family but he decided to leave all that to suffer. He manly focused on suffering. The religion is not about God but suffering as a way of life and that God has no solution to suffering. The only thing can bring sufferings to an end is the teachings of Buddha whereby only wisdom and compassion can end one’s problems. I really believe in these concepts which continue to shape my life. Wisdom has always been a driving force behind everything that I do. The course that I am pursuing is my way of becoming wise especially of the things of his world coupled with other ways for example meditation which is a requirement of my religion. One has to accept everything that comes in the way. That is how I mainly live my life and this has really helped me to come to terms with my problems. The pains that we go through as human beings can only be solved the moment we accept them. Some people have always misunderstood Buddhism as a religion, some of them claiming that we worship a human being. I don’t blame them because they are acting out of ignorance. Even though we really hold Buddha with high esteem that does not mean that we worship him. In fact I have so much respect for him and this should not be misquoted that I worship him. I have always tried to apply his principles in my life and so far I do not have any complaints. Another thing that interests me about Buddha’s teachings is that, he says that moral and ethical uprightness will end suffering forever. Many will definitely differ on the definition of the phrase ‘morally uprightness’ because the word ‘morally’ is relative depending on one’s culture and background. However, according to me, being true to oneself constitutes moral uprightness. Sometimes it is argued that ones life is predestined and I find myself asking, since human life is characterized by so much suffering, were we predestined to suffer? If that is so, why then do we have to struggle to improve life? Is there anything like free will? In the course of my study, I have come across so many stories and events that have characterized human beings from the time they came into existence and one thing we can agree on is that life has not been smooth sailing for human beings. It has always been about diseases, wars and rumors of wars, poverty among others. Sometimes I ask myself, if we use the concept of predestination to explain this, does that mean that we were predestined to go through all these? If we agree on this, then that means we have no control whatsoever and the actions that we carry out are also predestined. Then why does human being try to look for solutions to solve these problems or prevent them from repeating themselves in the future? If we believe that everything is predestined, then nothing matters because it means we are not in control of anything. I have read about almost all the wars that have characterized the world right from world wars and major civil wars and some countries have justified some of these wars, giving so many reasons. Let’s consider two wars; World War II and the Vietnam War. These two wars have been surrounded by controversies right from the start, and some have argued that, they were not to happen in the first place. The US has been regretting of its decision of going to war with Vietnam for so many years and if we adopt the concept of predestination, it will only mean that, they do not have a reason to regret because everything was predestined. The war had to happen and they had no control over it. Why then should they blame themselves? Even though the world has been trying to prevent another World War, then its efforts are meaningless because if it is predestined to happen, then no one can prevent it. The concept of predestination will only mean that, we are not answerable for the mistakes that we do and we owe no one an apology. If we believe that everything in the world is pre-designed, then, that means we are just existing to fulfill our purposes in life and not living our lives the way we would want. So does that mean that free will is at work and not predestination? The more I tend to think about these two concepts, the more I get confused. If we say that free will is at work, then as human beings we are to blame for everything that we go through because the power of making free choices is in our hands. Every thought that we harbor in our heads and every action that we undertake, will be determined by us. Should we blame ourselves for all those wars that took place? Sometimes I tend to think that free will and predestination are both at work. There are some areas of our lives which have been predestined for example death and birth of children. No one wants to die any day but at one point we will all have to die. When I was young, still in primary school, I wondered what brought about twins. After learning some biology I understood but I used to ask myself why I was not born with a twin sister or brother and the only answer I could think of is predestination. I was destined to be born alone. Where does free will come in then? I believe that human beings can choose to live their lives the way they want to live, for example, one can choose to be successful or to be a failure, one can choose to pass exams or not, marry or not to marry, have children or not among others. Even though I believe this to some extent, I think that free will and predestination are both at work. I am always left with so many questions regarding the two concepts and thus I agree with those who propose that, free will and predestination are two concepts that can never be understood and are not conclusive enough. I am well aware of the concept of predestination according to Buddhism religion; that every human being’s destiny is determined by ones personal actions. This means that, one’s thoughts and words will determine what he will become in the future. I do not dispute that; in fact, it forms the foundation of my faith. However, I also believe that human beings have a choice to make when it comes to the actions they decide to carry out. In other words, if one chooses to do wrong actions, that will determine his or her destiny, and that is why I believe that free will and predestination work together.

How Does the Writer Tell the Story in the Road Pages 24-7 Essay

The narrative in Pages 24-7 is based on the main character taking his son to see the old house he lived in. It consists of generally a sad tone because he is reminiscing his past and how he has lost it all. This part of the novel begins neutrally, but with an apocalyptic atmosphere to it, which is demonstrated through the use of no punctuation. McCarthy also uses short sentences through these pages, which gives a robotic sense – ‘The man stopped.’ This idea is also reflected in the title ‘The Road’; almost as if the journey is just on one set path. This takes us away from the blur of the novel and brings us to a stark reality, The climax in this part of the novel is when McCarthy describes the character’s bedroom, in which he uses detailed description – ‘In the nights in their thousands to dream the dreams of a child’s imaginings’, and then goes on to open the closet door. Again, we are brought back to reality when he expects to see his childhood things and instead is faced with ‘raw cold daylight’. The page ends circling back to the beginning ‘We shouldn’t have come’, which is what the b oy said at the beginning. Therefore, there is a sense of resolution. The form of these pages is retrospective narrative punctuated by flashbacks over a period of 40 years. As the narrative is from 3rd person perspective, the anonymity of ‘the man’ prevents a connection being made between the reader and the character. This also suggests that, because his name is never mentioned, a sense of being lost is portrayed. Additionally, the constant flashbacks used contribute to the idea that the days are blurring together. Again, this adds to the apocalyptic theme because there is no sense of prediction due to the only clear parts of the novel are the moments of reality when we are brought back from the flashbacks. McCarthy does this as an effective way of showing the character’s thought process. The main use of language McCarthy uses is to set the negative tone of being in a lost, almost sad and lonely world. Again, he does this by using short, snappy sentences and a lot of the dialogue used includes questioning. This could refer to the boy’s confusion of the situation, as he seems quite young and naà ¯ve – ‘We should go Papa, can we go?’ Moreover, this suggests that he needs reassurance, and perhaps that there is a glimmer of hope in the situation, which perhaps could foreshadow to what could happen later on in the novel. We can also learn that the man doesn’t want to return from his old home as he agrees to leave but then doesn’t, which connotes that he misses how things used to be in his old home. The rhythm in this part of the novel goes on and on through McCarthy’s use of short sentences and questions, which almost leaves the reader feeling out of breath and as if ‘The Road’ and its journey is ongoing. In conclusion, McCarthy uses a range of techniques to tell the story from Pages 24-27 to generally contribute to the main themes within the novel, such as death and the ‘end of the world’.