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We can work on Gender/race/ethnic Minority person in history from the 1700s through 2000s
Throughout each era in history, there have been people who have impacted the course of history. These people have been remembered and studied and are now part of the narrative of our countryâs story. Many of the people that have shaped our history are less known and not studied in traditional U.S. history classes. This course has highlighted some lesser-known minorities (The less-known notables) throughout the weekâs lessons. ⢠Find a gender/race/ethnic Minority person in history from the 1700s through 2000s that has made contributions in the United States but is not studied in U.S. history courses. ⢠Investigate a person who has had a significant influence in shaping America, but has not been amply studied. For example, Martin Delany was Fredrick Douglassâs contemporary but has not been studied as much as Douglass has been. We are now studying the contributions of Cesar Chavez but we do not study his contemporaries such as Dolores Huerta and Cruz Reynoso, which also worked, tirelessly for farm workerâs rights. ⢠Create an argument as to why you believe the person youâve chosen should be studied in U.S. history courses. Argue the reasons why you think their contribution to America should be noted, studied and even celebrated.
Sample Solution
Drugs has been known to induce structural plasticity of dendrites since 1997 (Robinson & Kolb, 2004; Russo et al., 2009; Dietz et al., 2009; Russo et al. 2010). Since then, researches on various drugs of abuse have shown to induce a structural change in the brainâs reward circuitry such as opiates decreasing number of NAc medium spiny neurons (MSN) in contrast to stimulants which increases NAc MSN numbers. Early withdrawal after exposure to chronic cocaine induces expression of N-methyl-D-aspartate (NMDA) glutamate receptors at MSN surface causing silent synapse formation and long-term depression (LTD). Prolonged withdrawal will cause retraction of the NMDA receptors to be replaces by α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) glutamate receptors changing structure of the spine to become mushroom shaped and promoting long-term potentiation (LTP). This change however can be reversed easily by a challenge dose of cocaine (Figure 2) (Russo et al.,2010). Figure 2. Cocaine-induced synaptic and structural plasticity (Russo et al., 2010) At a molecular level, this is caused by regulation of actin cytoskeleton via scaffolding proteins as well as GTPases and they are activated by transcription factor ÎFosB and cyclic AMP response element binding protein (CREB) which induces spinogenesis (Heiman et al., 2008; Kim et al., 2009). On the other hand, ÎFosB also regulates cyclin dependent kinase 5 (Cdk5) (Kumar et al., 2005) as well as nuclear factor κB (NFκB) (Russo et al., 2009) where both molecules play a role in cocaine-induced spine formation showing the major role of ÎFosB in cocaine-induced structural changes. The only paradox here is that both opiates and cocaine induce similar behavioural phenotypes (Russo et al., 2010) as well as drug administration and withdrawal symptoms although they have completely opposite effect on the NAc MSNs. A few possible hypothesises include changes in synaptic plasticity having a bidirectional property where a change in both directions result in similar behavioural phenotypes, decrease in neuronal complexity in one brain area is compensated by a strength>
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Drugs has been known to induce structural plasticity of dendrites since 1997 (Robinson & Kolb, 2004; Russo et al., 2009; Dietz et al., 2009; Russo et al. 2010). Since then, researches on various drugs of abuse have shown to induce a structural change in the brainâs reward circuitry such as opiates decreasing number of NAc medium spiny neurons (MSN) in contrast to stimulants which increases NAc MSN numbers. Early withdrawal after exposure to chronic cocaine induces expression of N-methyl-D-aspartate (NMDA) glutamate receptors at MSN surface causing silent synapse formation and long-term depression (LTD). Prolonged withdrawal will cause retraction of the NMDA receptors to be replaces by α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) glutamate receptors changing structure of the spine to become mushroom shaped and promoting long-term potentiation (LTP). This change however can be reversed easily by a challenge dose of cocaine (Figure 2) (Russo et al.,2010). Figure 2. Cocaine-induced synaptic and structural plasticity (Russo et al., 2010) At a molecular level, this is caused by regulation of actin cytoskeleton via scaffolding proteins as well as GTPases and they are activated by transcription factor ÎFosB and cyclic AMP response element binding protein (CREB) which induces spinogenesis (Heiman et al., 2008; Kim et al., 2009). On the other hand, ÎFosB also regulates cyclin dependent kinase 5 (Cdk5) (Kumar et al., 2005) as well as nuclear factor κB (NFκB) (Russo et al., 2009) where both molecules play a role in cocaine-induced spine formation showing the major role of ÎFosB in cocaine-induced structural changes. The only paradox here is that both opiates and cocaine induce similar behavioural phenotypes (Russo et al., 2010) as well as drug administration and withdrawal symptoms although they have completely opposite effect on the NAc MSNs. A few possible hypothesises include changes in synaptic plasticity having a bidirectional property where a change in both directions result in similar behavioural phenotypes, decrease in neuronal complexity in one brain area is compensated by a strength>
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