Andrew Qian

IM6/11AP
Compiled Annotations

Chen, Y., Won, S. J., Xu, Y., & Swanson, R. A. (2014). Targeting Microglial Activation in
Stroke
Therapy: Pharmacological Tools and Gender Effects. Current Medicinal Chemistry,
21(19), 2146–2155.

This source discusses the activation of microglia, and how that immune response can
actually prove to be detrimental after stroke. Additionally, it discusses various methods that have
been considered to control microglial activation after stroke to limit inflammation. After injury,
microglia have an innate immune response in which they produce various neural factors such as
reactive oxygen species, cytokines, and proteases that may kill neighboring cells. This response
was thought to have evolved as a first line of defense against infection; this response, however, is
actually detrimental to neural health after stroke. Therefore, it is only logical that treatments
should seek to inhibit this cytotoxic immune response. Previously, studies have been done which
examine the various signaling pathways which lead to microglia activation and possible cell
death. However, the sheer number of these pathways prevent those methods from having and real
effects. As such, an alternative approach has been proposed which involves targeting gene
expression changes which stimulate microglial activation.
This source is important because of the fact that it discusses the area where this
researcher hopes go develop his project. This article gives valuable information on how other
researchers have targeted microglia gene expression, which provides a foundation for this
researcher to build his project on.

Deb, P., Sharma, S., & Hassan, K. (n.d.). Pathophysiologic mechanisms of acute ischemic stroke:
An overview with emphasis on therapeutic significance beyond thrombolysis -
Pathophysiology. Retrieved September 10, 2018, from
https://www.pathophysiologyjournal.com/article/S0928-4680(09)00136-9/

This source focuses primarily on the pathology of stroke, discussing the various causes as
well as mechanisms of ischemic stroke. As a result of thrombus (blood clot in an artery to the
brain), the brain becomes much more vulnerable to ischemia, an inadequate blood supply to a
vital organ. As a result of this ischemia, part of the brain parenchyma will immediately succumb
to death, while other less affected parts may only be partially injured, with potential to recover.
At the cellular level, ischemia will to lead to the ischemic cascade, which leads to depletion of
valuable compounds, such as adenosine-triphosphate (ATP). A lack of these vital energy
compounds will generally lead to severe cell injury and eventually cell death. Additionally, the
neuron requires a large of amount of oxygen and glucose in order to perform its role in impulse
transmission. However, this makes it particularly susceptible to hypoxic changes, meaning that
thrombus can be highly detrimental to neurons as well.
This source is highly valuable as understanding of the pathology of an injury is vital for
developing a possible treatment method. For example, by understanding the fact that ischemia is
the main reason for cell death, researchers can focus on methods in order to artificially supply
oxygen while reducing the artery blockage.
Dostovic, Z., Dostovic, E., Smajlovic, D., Ibrahimagic, O. C., & Avdic, L. (2016). Brain Edema
After Ischaemic Stroke. Medical Archives, 70(5), 339–341.
https://doi.org/10.5455/medarh.2016.70.339-341

This source discusses the primary effects of brain edema, which is the abnormal
collection of fluid within the brain. Brain edema typically develops in the first 24-48 hours after
stroke, reaching its peak approximately 3-5 days after injury. This edema typically results in
deterioration of the brain, and in extreme cases, death. Generally, cerebral edema results from
tissue necrosis in the brain, which can lead to the breaking down of the blood brain barrier
(BBB). This allows for the transfer of various proteins from the blood vessels to the brain, a
disturbance which can lead to increased fluid levels in the tissues.
This source is valuable as it explains the development and causes of brain edema, one of
the major contributing factors to severe damage and death after stroke. Greater understanding of
brain edema allows this researcher to connect the pro-recovery actions of the microglia and
macrophages to the damage in the brain.

Guruswamy, R., & ElAli, A. (2017). Complex Roles of Microglial Cells in Ischemic Stroke
Pathobiology: New Insights and Future Directions. International Journal of Molecular
Sciences, 18(3). https://a.org/10.3390/ijms18030496

This source focuses primarily on the role that microglia cells play after Ischemic
Stroke. Microglia have always been considered as a major target as a point of interest after
experimentation revealed that neuroinflammation played a major role in Ischemic Stroke
pathobiology. Microglia act as the primary immune cells in the brain, and can stimulate the
activation of the neural immune system as a whole. After injury, microglia become activated
which stimulates the circulation of other macrophages and immune cells as with any immune
response. The functions of microglia cells are mainly controlled by its surface molecules and the
signaling pathways that they respond to. These pathways allow microglia cells to have a much
larger role in regulating the surrounding environment. Additionally, microglia play a role in
elimination of neural cell debris after injury via phagocytosis as well as release anti-
inflammatory cytokines in order to promote regeneration and repair.
This source is valuable because it provides detailed information on the impacts that
microglia have after ischemic stroke, specifically the role that they play in signal and protein
release. By understanding the various pathological process the microglia control, researchers are
able to better develop experimentation to discern the potential of microglia in developing novel
therapeutic treatments for stroke.

Han, X., Lan, X., Li, Q., Gao, Y., Zhu, W., Cheng, T., … Wang, J. (2016). Inhibition of
prostaglandin E2 receptor EP3 mitigates thrombin-induced brain injury. Journal of
Cerebral Blood Flow & Metabolism, 36(6), 1059–1074.
https://doi.org/10.1177/0271678X15606462

This source discusses the role of the prostaglandin E2 receptor EP3 after thrombin-
induced brain injury. Thrombin induced blood injury occurs when a blood clot reduces flow of
blood to the brain; thrombin is an enzyme in blood plasma that causes the clotting of blood by
converting fibrinogen to fibrin, hence the name. In the study, analysis in vitro and vivo revealed
that inhibition of the EP3 receptor, which is expressed by astrocytes and microglia, actually
decreased lesion volume in the brain, less overall neuronal cell death, less neurologic deficit, and
increased amounts of Ym-1+M2 microglia, anti-inflammatory microglia. Reactivation of the Ep3
receptor, however, increased RhoA-Rho kinase expression. These results suggest that the EP3
receptor actually contributes to thrombin-induced brain damage via Rho-Rho kinase–mediated
cytotoxicity and proinflammatory responses.
This source is important because of its relationship with the topic that this researcher has
chosen. While this article does not explicitly link to what this researcher has been reading about
over the past few days. It still connects back to the topic of microglial receptor mediated
responses, investigating which ones can lead to damaging responses and which ones can mitigate
the damages, which is what this researcher is studying.

Hata, A. N., & Breyer, R. M. (2004). Pharmacology and signaling of prostaglandin receptors:
multiple roles in inflammation and immune modulation. Pharmacology & Therapeutics,
103(2), 147–166. https://doi.org/10.1016/j.pharmthera.2004.06.003

This source discusses what prostaglandins are, and the role that they plan in the brain. Past
Experimentation has revealed that prostaglandins play a major role in the modulation of many
physiological systems, such as the CNS, cardiovascular, gastrointestinal, genitourinary,
endocrine, respiratory, and immune systems. Additionally, they also are involved in many
diseases, such as cancer, inflammation, cardiovascular disease, and hypertension. Prostaglandins
take their effect on the brain through activation of rhodopsin-like seven transmembrane spanning
G protein-coupled receptors (GPCRs), a form of reception that is very common throughout the
body. A key attribute of prostaglandins is the fact that different classes can have
opposite/contrasting effects on the body. This is especially true in terms of inflammation, as
some prostaglandins are pro-inflammatory mediators, while other have anti-inflammatory
properties.
This source is important because it describes the central focus of the paper that his
researcher will be writing. Specifically, it focuses on the role that prostaglandins can play in the
physiological process of inflammation, a key aspect of what causes neuronal damage after
intracerebral hemorrhage.

Heindl, S., Gesierich, B., Benakis, C., Llovera, G., Duering, M., & Liesz, A. (2018). Automated
Morphological Analysis of Microglia After Stroke. Frontiers in Cellular Neuroscience,
12, 106. http://doi.org/10.3389/fncel.2018.00106

This source provides an analysis on the morphological change or microglia after injury,
more specifically, stroke. It is now common knowledge that brain tissue injury induces a local
inflammatory response which includes a gradual morphological transformation among activated
microglia. When the brain is healthy, microglia are observed to be consisting of small soma and
large tails. In this state, they are often referred to as “surveilling microglia”, screening the brain
parenchyma for pathogens or damage associated molecular patterns (DAMP’s). In the presence
of DAMPS, microglia are able to initiate a rapid morphological transformation, morphing into a
more amoebalike form which allows them to quickly migrate to the site of an injury. The
morphological nature of microglia, is not simply limited to those two forms. Rather, it has been
determined that microglia have a whole range of morphological changes. This is important as
microglia morphology can now be used to determine the level of microglia activation and
function after stroke.
This source is important because it provides additional information on a valuable aspect
of microglia: their morphology. By understanding more about what the morphology means for
the function and activation of microglia, this researcher can better determine the main functions
of microglia after injury and the best method to utilize them.

How to Write a Lab Proposal | Synonym. (n.d.). Retrieved October 1, 2018, from
https://classroom.synonym.com/write-lab-proposal-7738594.html

This source discusses how a researcher would go about creating a lab proposal. A lab
proposal is an integral step in performing a project as a good lab proposal can help acquire
confirmation from the lab supervisor/mentor for the project. Additionally, writing a good lab
proposal makes experimentation much easier once that step is arrived at. First off, a good lab
report needs a provoking introduction which explains to the audience why this project is so
important. This will increase the credibility of the project in the eyes of the audience. Next
should be the materials and procedure section. By detailing what specifically will be done during
the experiment, the researcher is able to explain to both himself as well as his audience what is
required for this proposed research project. This allows for analysis of the techniques used by the
researcher in order to ensure that the methods used are both efficient and proper. Finally, a good
project proposal requires an effective conclusion in which future plans and implications of this
research should be detailed. This helps emphasize the significance of the research conducted and
gives meaning to the work.
This source is important as knowing how to write a good lab proposal is essential to
actually developing one’s own experiment. This researcher helps to use the information found in
this article, as well as in various other areas, to develop an effective lab proposal that he hopes to
present to his mentor for overview and hopefully confirmation.

Kanazawa, M., Ninomiya, I., Hatakeyama, M., Takahashi, T., & Shimohata, T. (2017).
Microglia
and Monocytes/Macrophages Polarization Reveal Novel Therapeutic Mechanism against
Stroke. International Journal of Molecular Sciences, 18(10).
https://doi.org/10.3390/ijms18102135

This source discusses the potential of macroglia and macrophage polarization in the
development of a new therapeutic method for the treatment of stroke. With microglia and
macrophages, the differing polarization states can have both positive and negative effects after
stroke, acting as a “double edged sword”. Originally, macrophages and microglia were thought
to merely accelerate inflammation as cultured neurons would die in the presence of activated
microglia after the administration of pro-inflammatory factors. However, it was also discovered
that microglia and macrophages can also play a protective role in the acute/chronic phases of
stroke as they help promote neurological recovery by clearing neural debris and promoting the
healing of brain tissue.
 This article is important in helping combat stroke as it introduces new evidence which
indicates that both macrophages and microglia have functional role in suppressing inflammation
and promoting tissue recovery within the brain. Further experimentation could be done to
determine any possible treatments that could be developed from this evidence.

Kim, E., & Cho, S. (2016). Microglia and Monocyte-Derived Macrophages in Stroke.
Neurotherapeutics, 13(4), 702–718. https://doi.org/10.1007/s13311-016-0463-1

This source discusses the role that microglia and macrophages play when the brain
experiences a stroke. Primarily, it focuses on the inflammatory response, and the benefits and
harms that can come from it. Originally, it was widely believed that post ischemic inflammation
had only negative effects on the brain. Experimentation showed that stroke-induced immune
responses were often excessive, leading to immunosuppression in patients with stroke, increasing
the risk of secondary infections and increasing the probability of death. However, it was later
discovered that immune-mediated responses, including inflammation, were vital to Central
Nervous System (CNS) recovery. Additionally, these immune cells potentially playa major roles
in reducing dangerous inflammation as well, as studies have shown that decreased presence of
microglia has led to increased neural inflammation and subsequent injury.
This source is valuable as it provides evidence to support the argument that macrophages
and microglia play a vital role in supporting neural repair after stroke through modulation of
inflammation within the brain. It helps to support the line of reasoning that microglia and
macrophages are important areas of study for the development of a novel therapeutic treatment
for stroke.

Microglial function in the Healthy Brain. (n.d.). Retrieved September 17, 2018, from
https://faculty.sites.uci.edu/kimgreen/bio/microglia-in-the-healthy-brain/

This source gives background information on what microglia are, and their function in
the healthy adult brain. It describes the process by which they become activated in response to
pathogens and injury. During activation, microglia rapidly change their morphology before
migrating to the location of the injury in order to destroy pathogens as well as phagocytose dead
cells. Additionally, this source describes the role of microglia in the inflammatory response as
they are a major producer of anti-inflammatory cytokines, indicating that they play a major role
in the immune response. Finally, microglia have also been studied extensively for their role in
neurodegenerative disease such as alzheimer's, parkinson's, ischemic injuries, and traumatic
brain injuries.
This source is important because of the fact that it is always necessary to have
background information about the topic that one is studying. The information provided in this
article will enable this researcher to build a foundation upon which he can make connections to
the various evidence that he will find throughout his research.

McCullough, L., Wu, L., Haughey, N., Liang, X., Hand, T., Wang, Q., … Andreasson, K.
(2004).
Neuroprotective Function of the PGE2 EP2 Receptor in Cerebral Ischemia. Journal of
Neuroscience, 24(1), 257–268. https://doi.org/10.1523/JNEUROSCI.4485-03.2004
 This source describes the method by which the PGE2 EP2 receptor is able to play a
beneficial role in the brain after cerebral ischemia. Prostaglandin receptors are receptors that play
an important role in brain, as they are able to control many physiological factors through G-
protein coupled receptor (GCPR) signaling. The EP2 receptor, specifically, is highly abundant in
the cerebral cortex, striatum, and the hippocampus. This receptor is also known to be positively
coupled to cAMP production. From this study, the researchers discovered that the EP2 receptor
actually had a neuroprotective role against NMDA toxicity and oxygen glucose deprivation.
This source is important because it describes the specific topic of this researcher in the
role of prostaglandin reception after stroke. It detailed the beneficial effect that this type of
signaling can have, allowing this researcher to build a stronger base for his thesis that controlling
prostaglandin signaling is key to developing a new therapeutic treatment for ICH.

Mohan, S., Narumiya, S., & Dore, S. (n.d.). Neuroprotective Role of Prostaglandin PGE2 EP2
Receptor in Hemin-mediated Toxicity. Retrieved January 6, 2019, from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681391/

This source describes another neuroprotective role of prostaglandin receptors, specifically

that of the EP2 receptor. In this study, the researchers analyzed the role of the EP2 receptor in
defending against hemin-mediated toxicity. Heme and hemin, the prosthetic group of
hemoprotein, are cytotoxic due to their ability to contribute to the production of reactive oxygen
species, increased intracellular calcium levels and stimulate glutamate mediated-excitotoxicity.
The damage that hemin related toxicity can cause well documented, and clearly shown in
examples such as sickle cell disease and thalassemia, where release of heme from hemoglobin
following lysis of red blood cells is known to cause stress and ultimately cell death. Additionally,
the oxidative state of iron within heme can lead to oxidative stress, initiate proteins and lipids
oxidation, and damage RNA and DNA, leading to neuronal death. In the study, researchers
discovered that activation of the Ep2 receptor actually minimized neuronal damage and played a
protective role against hemin neurotoxicity.
This source is important because it describes the potential of the EP2 receptor in
developing a novel therapeutic treatment for stroke. While the article does not specifically focus
on stroke, it describes the overall neuroprotective benefits that PGE2 EP2 signaling can bring,
building onto the foundation that this researcher is writing his paper on.

Overview of Immunohistochemistry - US. (n.d.). Retrieved September 22, 2018, from

https://www.thermofisher.com/us/en/home/life-science/protein-biology/protein-biology-l
earning-center/protein-biology-resource-library/pierce-protein-methods/overview-immun
ohistochemistry.html

This source gives background information on what encompasses the technique known as
Immunohistochemistry. Immunohistochemistry, otherwise known as IHC, is a process by which
scientists are able to produce images of specific components in cell tissue. This enables
researchers to visualize certain cellular components, which makes studying microscopic
processes and environments much easier. Primarily, IHC is used for disease diagnosis, biological
research, and drug development. In regards to diagnosis, IHC can be used to determine whether a
tumor is malignant or benign as well as to identify the site of the origin of the tumor. In research,
IHC is used to study tissue and organ development, pathological processes, cell death and repair,
etc. Finally, IHC can be used during drug development in order to test the efficacy of a
developed drug by detecting activity of disease markers in order to determine whether or not the
drug is having its anticipated effects in the target tissue. Overall, IHC has many invaluable uses
in practically every field of science and medicine.
This source is valuable to this researcher because it describes a technique that this
researcher hopes to use throughout his project. IHC is a process that is constantly used
throughout research. By gaining a better understanding of this technique, it enables this
researcher to develop a better project plan.

Sun, D. (2014). The potential of endogenous neurogenesis for brain repair and
regeneration following traumatic brain injury. Neural Regeneration Research, 9(7), 688–
692. https://doi.org/10.4103/1673-5374.131567

This paper focuses on the potential of neurogenesis as a neuronal process that would
allow for further healing in the brain after traumatic brain injury. In this article, it overviews how
continuous NSPC differentiation would the brain could allow the brain to recover from the
effects of traumatic brain injury. It has been shown from experimentation that the brain, after
experiencing traumatic brain injury, will induce a heightened rate of differentiation by neuronal
stem cell and progenitor cells. This allows for the conclusion to be made that the brain has
inerent methods for recovery from Traumatic brain injury, so if it were possible to manually
induce this response, then it would be possible to develop an effective treatment method to help
people recover from the effects of traumatic brain injury. Currently, research has shown that
changes in the environment, as well as other physical stimuli, leads to an increase in NSPC
differentiation.
This paper discusses many of the points that this researcher hopes to address in his paper.
It discusses the possibility of neurogenesis as a possible area of focus for developing better
treatment methods. Using background knowledge, then, a link can be created between the
communicability factor of astrocytes and the role that it plays in modulating neurogenesis. The
information in this source can be combined with other information to develop the argument that
astrocytes play an essential role in the development and healing response in the brain, making it
a prime target for research.

Wang, N., Liang, H., & Zen, K. (2014). Molecular Mechanisms That Influence the Macrophage
M1–M2 Polarization Balance. Frontiers in Immunology, 5.
https://doi.org/10.3389/fimmu.2014.00614

This source discusses the molecules that can influence the polarization of macrophages
between the M1 and M2 phases. One molecule that stimulates M1 polarization is IRF/STAT
signaling. Experimentation has revealed that toll-like receptor signaling, particularly TLR4
stimulated by lipopolysaccharide (LPS) and other microbial ligands will often result in M1
polarization of macrophages. Additionally, as M1 polarization often results in an inflammatory
response, the downstream signaling pathway results in activation of the transcription factor, NF-
κB, which ins turn regulates the expression of a large number of inflammatory genes such as
TNFα, IL1B, cyclooxygenase 2 (COX2), IL-6, and IL12p40. In contrast, other stimuli like IL-4,
IL-13, and IL-10 have been shown to cause M2 polarization of macrophages through activation
of certain transcription factors such as STAT6 through the IL-4 receptor alpha (IL-4Rα).
 This source is important because of the fact that it provides examples of molecules that
can result in stimuli of polarization to certain forms of macrophages. In knowing these
molecules, it enables this researcher to focus his studies on increased release of certain molecules
to reduce M1 polarization and therefore improve survivability after stroke.

Wu, H., Wu, T., Hua, W., Dong, X., Gao, Y., Zhao, X., … Wang, J. (2015). PGE2 receptor
agonist misoprostol protects brain against intracerebral hemorrhage in mice.
Neurobiology of Aging, 36(3), 1439–1450.
https://doi.org/10.1016/j.neurobiolaging.2014.12.029

This source describes the ability of misoprostol to act as a PGE2 receptor agonist in
protecting the brain against intracerebral hemorrhage. Misoprostol, a synthetic prostaglandin, has
been shown to reduce cerebral ischemia. In this experiment, the researchers showed that
misoprostol post treatment led to decreased brain lesion volumes, edema, and brain atrophy, as
well as lower levels of inflammation, Src kinase activity, interleukin-1β expression, and
oxidative death. Misoprostol treatment was also found to reduce high-mobility group box 1
(HMGB1) expression. Additionally, separate inhibition of the HMGB1 receptor led to decreased
neuronal death, decreased Src kinase activity, gelatinolytic activity, and brain lesion volume as
well. These results suggest that misoprostol protects the brain against ICH injury through
mechanisms that may involve the HMGB1 signaling pathway.
This source is valuable to this researcher because it provides an example of certain types
of receptors and signaling pathways that are responsible for some of the damaging effects that an
immune response can have on the brain. Additionally, the detailed layout of the experiment
found in this article will be useful for helping the researcher design his own project.

Wu, H., Wu, T., Hua, W., Dong, X., Gao, Y., Zhao, X., … Wang, J. (2015). PGE2 receptor
agonist misoprostol protects brain against intracerebral hemorrhage in mice.
Neurobiology of Aging, 36(3), 1439–1450.
https://doi.org/10.1016/j.neurobiolaging.2014.12.029

Intracerebral Hemorrhage (ICH), otherwise known as Hemorrhagic stroke, accounts for

approximately 15% of all strokes. In this form of stroke, high blood pressure or external brain
trauma causes thin walled arteries in the brain to tear, resulting in a ruptured artery within the
brain. As blood spills into the brain, the area that the artery originally circulated is deprived of
oxygen-rich blood, leading to neuronal death. This damage is only furthered by the release of
toxic molecules by microglia and other brain cells. Prostaglandin E1 and Prostaglandin E2 are
lipid ligands found predominantly in the brain that helps mediate neuroinflammation, usually
through the release of matrix metalloproteins from macrophages. Misoprostol is a synthetic
PGE1 analog, meaning that it is similar in structure to PGE1, but different in chemical
composition. Past experimentation has revealed that misoprostol has beneficial impacts on the
brain, but a
This source is valuable to this researcher because it provides an example of certain
ligands that are responsible for some vital signaling pathways that are present in the brain. Once
again, this source provides an example of a molecule that has beneficial effects on the brain.

Zhao, S., Ma, L., Chu, Z., Xu, H., Wu, W., & Liu, F. (2017). Regulation of microglial activation
 in stroke. Acta Pharmacologica Sinica, 38(4), 445–458. \
https://doi.org/10.1038/aps.2016.162

This source discusses the various stimulants of microglia which could lead to microglial
activation after stroke. This activation can have various detrimental effects on the health of the
brain as microglia produce both detrimental and neuroprotective mediators which would likely
exacerbate the issue. Primarily, it has been found that M1 microglia are involved in the
proinflammatory response. Several signaling pathways have been found which are believed to
contribute to the activation of M1 microglia. Interferon secreted by T helper 1 cells are key to
inducing the polarization of M1 microglia; experimentation has revealed that Interferon activates
transducer and activator of transcription 1 (STAT1) factor and increases the production of pro-
inflammatory cytokines, such as tumor necrosis factor α (TNFα), interleukin (IL)-23, IL-1β, IL-
12, chemotactic factors, reactive oxygen species, and nitrogen monoxide (NO). Therefore, it can
be concluded that modulation of these signaling pathways could help reduce levels of
inflammation in patients and subsequently improve chances of survival.
This source is valuable as it provides detailed information on the various responses to
ischemic stroke that this researcher is planning to focus on for his research. This researcher
hopes to choose some of the signaling pathways discussed to incorporate into his project in
which he hopes to analyze therapeutic methods which could decrease inflammation in ischemic
stroke patients after injury.

Zhao, X., Wu, T., Chang, C.-F., Wu, H., Han, X., Li, Q., … Wang, J. (2015). Toxic Role of
Prostaglandin E2 Receptor Ep1 After Intracerebral Hemorrhage in Mice. Brain,
Behavior,
and Immunity, 46, 293–310. https://doi.org/10.1016/j.bbi.2015.02.011

This source discusses the Ep2 receptor Ep1 after intracerebral hemorrhage. Intracerebral
Hemorrhage (ICH), otherwise known as Hemorrhagic stroke, accounts for approximately 15% of
all strokes. In this form of stroke, high blood pressure or external brain trauma causes thin walled
arteries in the brain to tear, resulting in a ruptured artery within the brain. As blood spills into the
brain, the area that the artery originally circulated is deprived of oxygen-rich blood, leading to
neuronal death. This damage is only furthered by the release of toxic molecules by microglia and
other brain cells. Initial impacts of stroke, however, are nearly impossible to target as a result of
the time frame efficacy of the drugs that target those specific responses. Therefore, it is only
logical to develop treatment methods which focus on inhibition of the signaling pathways that
induce the secondary injuries from stroke. An example of that is Ep2, a receptor which has been
found to have toxic effects after stroke.
This source is valuable to this researcher because it provides an example of certain types
of receptors and signaling pathways that are responsible for some of the damaging effects that an
immune response can have on the brain. It helps to build a foundation of the paper that this
researcher hopes to write.