Determination of CoCl2·6H2O via Spectrophotometry

 

Determination of CoCl2·6H2O via Spectrophotometry and Titration lab report, need you to organize the data, write us calculation/result portion, discussion and conclusion

Observations and Data:

Organize all your observations and data in a way that is the most appropriate.

Calculations/Results:

Determine the molarity concentration of cobalt in your unknown solution. Show every calculation you had to perform in the experiment. Make sure that your calculations are clearly labeled and organized. If you have multiple calcluations of the same type, you may show one complete calculation and summarize the rest in a table. Calculate the average and standard deviation of your determination. Clearly indicate your final result for the unknown concentration of cobalt. Report your final result as average molarity ± standard deviation, ¯x ± σ. A significant portion of your grade for this experiment (10%) will be related to the accuracy and precision of your result.

Discussion:

Write an appropriate discussion for this experiment.

Sample Solution

inflammatory cytokine that plays a role in the development and regulation of the immune system and generation of T-cells (Stubgen, 2007). It has been implicated in neurological disorders, such as Guillain-Barre syndrome. TNF has been shown to damage peripheral nerve, Schwann cells and myelin sheaths, and prevent action potential transmission (Stubgen, 2007). TNF is up-regulated in the first hours following a traumatic brain injury but returns to normal gene expression levels within 24 hours (Bennett et al., 2016). Knockout studies have suggested that this up-regulation may have neuroprotective properties (Scherbel et al., 1999). Short-term, mice that lacked TNF were found to have less cognitive impairments compared to mice with the gene. However, long-term, the mice without TNF had more motor deficits and cortical tissue loss compared to mice with TNF (Scherbel et al., 1999). This suggests that while TNF has initial adverse neuronal effects, it can positively influence future repair after brain injury. Interleukin-1 (IL-1) is another pro-inflammatory cytokine associated with brain injuries. By working with TNF, cytokines in this family can increase inflammation and body temperature after a brain injury (Bennett et al., 2016). Studies have demonstrated that not only do IL-1 increase following brain injury but that it is also associated with severity, with high IL-1 levels being associated with more severe brain injuries (Bennett et al., 2016). However, other studies have also reported that IL-6 may lend neuronal benefits as higher levels of IL-6 resulted in better outcomes and recovery in patients with brain injuries (Bennett et al., 2016). Apolipoprotein E (APOE) is a gene that is associated with neuronal growth and repair, synaptodendritic connection maintenance, and inflammation (Bennett et al., 2016). Following stress and injury, APOE is produced by astrocytes and microglia and may have negative effects on cognition (Bennett et al., 2016). Lastly, human brain-derived growth factor (BDNF) is a gene that is involved in synaptic connectivity, plasticity, neuronal growt

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