In the Marketplace simulation this week, you will be assessing strategies for hiring and compensating employees to support your growth plans. According to the Conrad-Bradshaw (2022) employers are struggling to fill open jobs. Job seekers may also have struggles finding the jobs they want (Zahn, 2018). Understanding the causes of this problem can alleviate the gap between employer talent shortage and candidate success in the search effort, increasing company success in a world economy that is experiencing a talent shortage.
For this discussion topic, you will:
Main Response
Using the readings and videos for this unit as a base, along with other sources you uncover in your research, provide a synopsis of the points that stand out for you on the gap discussed above.
Use the 6-step problem-solving process from Unit 2 to complete a diagnosis on the problem(s) as you see it/them. Use Steps 1â5 and explain how you would incorporate Step 6, Follow Up & Evaluate Progress.
Post the results of this diagnosis, including how you used integrative thinking in the completion of the diagnosis.
If given the opportunity, how would you use this information to increase hiring and retention success in the simulation?
Example Responses to Peers to Increase Discussion Success
Provide additional research to support or refute the information that peers have posted.
Include personal examples of how your company (if applicable) may be overcoming the talent shortage.
Talk about how this could be included in simulation game play or in the work you do every day.
Provide a personal example of how this has happened to you in the past and the outcome.
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>
