U26318 PERSONAL DEVELOPMENT PLANNING 1
SCIENCE DIARY ENTRY
STUDENT NUMBER: 882228 DATE: 13/02/19
1. What is the name of the news story you chose and who is the author?
‘Simple drug combination creates new neurons from neighbouring cells’- Team of researchers from Penn state
2. In your own words, provide a brief synopsis of the report
In this article the authors highlight how a simple combination of 3-4 molecules can help convert cells that neighbour damaged neurons into functioning new neurons which could possibly be used to treat Alzheimer’s, Strokes and brain injuries. The researchers believe that turning glial cells that are neighbours of the damaged neurons into new neurons is probably the best way to restore the lost neurons. The scientists disclose that the previously developed combination of 9 molecules to convert human foetal astrocytes into neurons isn’t a clinically applicable. They also demonstrate the modulation of the 3-4 signalling pathways important to change an astrocyte to a neuron. "By using four molecules that modulate four critical signalling pathways in human astrocytes, we can efficiently turn human astrocytes -- as many as 70 percent -- into functional neurons." Said Jiu-Chao Yin, a graduate student in biology at Penn State who identified the ideal combination of small molecules. The following chemically converted neurons can survive more than 7 months in the culture dish in lab; are able to form neuronal networks and send chemical and electrical signals like other neurons inside the brain.
3. State one or two points that would help you to understand the topic better:
1. what is the neuroinhibitory effect of glial scarring
2. Benefits of this new approach
4. Briefly explain what your research from point 3 showed.
1. Further research into glial scarring showed that although glia can repair damaged areas of the nervous tissue by proliferating (dividing) and form scar tissues which fill the gaps between degenerated neurons in order to protect neighbouring tissues from further damage, the continuous presence of glial scar inhibits neuronal growth and synaptic transmission, forming barriers which prevents the physical and functional recovery of the CNS after injury or diseases such as Alzheimer’s.
2. The scientists had developed a gene therapy technology to convert astrocytes to neurons but due to the therapy being too expensive for patients, the new approach is far more economically achievable for patients. Also the delivery system of the gene therapy is very complex as it requires injecting viral molecules into the body whereas the new 3-4 molecule combination in the new method can be packaged into a pill which is a simpler drug delivery system, and can be available to people even in rural areas.
5. Reference sources (reported in Vancouver format). [Please consult: http://referencing.port.ac.uk/ for g.
1. Brain Basics: The Life and Death of a Neuron | National Institute of Neurological Disorders and Stroke [Internet]. [cited 2019 Jan 7];Available from: https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Life-and-Death-Neuron
2. Fawcett JW, Asher R. The glial scar and central nervous system repair. Brain Res Bull [Internet] 1999 [cited 2019 Feb 7];49(6):377–91. Available from: https://www.sciencedirect.com/science/article/abs/pii/S0361923099000726
3. Fitch MT, Silver J. CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure. Exp Neurol [Internet] 2008 [cited 2019 Feb 7];209(2):294–301. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17617407
4. Penn State. Simple drug combination creates new neurons from neighboring cells -- ScienceDaily [Internet]. [cited 2019 Jan 7];Available from: https://www.sciencedaily.com/releases/2019/02/190207173226.htm
5. Yin J-C, Zhang L, Ma N-X, Wang Y, Lee G, Hou X-Y, et al. Chemical Conversion of Human Fetal Astrocytes into Neurons through Modulation of Multiple Signaling Pathways. Stem cell reports [Internet] 2019 [cited 2019 Jan 7];0(0). Available from: http://www.ncbi.nlm.nih.gov/pubmed/30745031
U26318 PERSONAL DEVELOPMENT PLANNING 1
SCIENCE DIARY ENTRY
STUDENT NUMBER: 882228 DATE: 01/12/18
1. What is the name of the news story you chose and who is the author?
A Zombie LIF Gene in Elephants Is Upregulated by TP53 to Induce Apoptosis in Response to DNA Damage. An article written by Article written by Juan Manuel Vazquez et al
2. In your own words, provide a brief synopsis of the report
In this article Vazquez et al, the researchers who investigated the resistance to cancer in elephants, report that there is a specific gene in elephants which acts as a detector to those mutated genes and takes further action to remove them from the body. The researchers point out how theoretically large organisms should be more prone to developing cancer than smaller organisms, however, there is no correlation between the size of organisms and their risk of getting cancer which is also called ‘‘Peto’s paradox’’. The researchers point out that less than 5% of elephants in captivity die from cancer compared to the 25% of people. Vazquez et al. provide evidence that there is an elephant specific gene Leukaemia inhibitory factor 6 a (LIF6) which is regulated by TP53 gene when DNA damage is detected and triggers apoptosis. The researchers further state that elephants reduced their risk of getting cancer by evolving excess cancer suppressor gene.
3. State one or two points that would help you to understand the topic better:
1. How do the LIF and TP53 work together to inhibit cancerous cells from forming?
2. What experiments were carried out to test whether the function of LIF6 is elephant specific only?
4. Briefly explain what your research from point 3 showed.
1. The researchers in the article state that elephants have around 20 copies of the tumour suppressor protein P53 whereas humans only have 1, and like TP53 they have many copies of LIF pseudogenes but have somehow found a way to activate one of the genes, LIF6, which produces a transcript. The TP53 protein regulates cell division and keeps the cell from dividing and growing at too quick of a rate or in an uncontrolled way and when DNA damage is detected then LIF6 is transcriptionally upregulated by TP53 in response to DNA damage and translocate to the mitochondria where it induces apoptosis which destroys the cells completely and any genetic defects that are caused by cancer.
2. The researchers introduced the LIF6 gene into a Chinese hamster which don’t normally have this gene and witnessed the same response to any DNA damage and induction of apoptosis.
5. Reference sources (reported in Vancouver format). [Please consult: http://referencing.port.ac.uk/ for guidance].
1.Vazquez JM, Sulak M, Chigurupati S, Lynch Correspondence VJ, Manuel Vazquez J, Lynch VJ. A Zombie LIF Gene in Elephants Is Upregulated by TP53 to Induce Apoptosis in Response to DNA Damage. Cell Rep [Internet]. 2018 [cited 2018 Oct 21]. Available from: https://doi.org/10.1016/j.celrep.2018.07.042
2.Patterson PH. Commentary Leukaemia inhibitory factor, a cytokine at the interface between neurobiology and immunology [Internet]. Vol. 91, Proc. Nati. Acad. Sci. USA. 1994 [cited 2018 Oct 21]. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC44497/pdf/pnas01139-0010.pdf
3.Elephants’ low cancer rates explained - BBC News [Internet]. [cited 2018 Oct 21]. Available from: https://www.bbc.co.uk/news/health-34466220
4.Killer ‘zombie gene’ protects elephants from cancer | Irish Examiner [Internet]. [cited 2018 Oct 23]. Available from: https://www.irishexaminer.com/breakingnews/world/killer-zombie-gene-protects-elephants-from-cancer-862186.html
5.Zilfou JT, Lowe SW. Tumor suppressive functions of p53. Cold Spring Harb Perspect Biol [Internet]. Cold Spring Harbor Laboratory Press; 2009 Nov [cited 2018 Oct 23]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20066118
6.Primary information of p53 gene [Internet]. [cited 2018 Oct 23]. Available from: http://www.bioinformatics.org/p53/introduction.html
U26318 PERSONAL DEVELOPMENT PLANNING 1
SCIENCE DIARY ENTRY
STUDENT NUMBER:882228 DATE:13/02/19
1. What is the name of the news story you chose and who is the author?
Platelet 'decoys' outsmart both clots and cancer- Article by Lindsay Brownell WYSS institute
2. In your own words, provide a brief synopsis of the report
The a
The article reports that the platelet decoys created by the researchers at the WYSS institute of Harvard university inhibit thrombosis and prevent the formation of metastatic tumours. The article points out that although platelets play a key role in homeostasis they also contribute to various disorders such as cancers and other cardiac diseases. the article further talks about the irreversibility of the effects of antiplatelet drugs that are currently used to treat platelet related disorders, to address these concerns the group of researchers created this reversible antiplatelet therapy using the deactivated decoy platelets which is smaller than normal platelets but consist of most of the adhesive proteins without the inner contents of normal platelets. The decoys still use the surface molecules to bind to other cells but are unable to activate the clotting process which inhibits the aggregation and adhesion of platelets on thrombogenic (clotting) surfaces and also hinder the normal platelets’ ability to bind. Furthermore the decoys’ inhibition can be reversed by adding more fresh platelets to the channels.
3. State one or two points that would help you to understand the topic better:
1. How can the immune system be prevented from attacking the decoy platelets?
2. How will decoys prevent cancer?
4. Briefly explain what your research from point 3 showed.
1. The researchers state that it is possible to create decoys by using the platelets removed from the same patient to minimize the immune response.
2. Further research showed how platelets bind to cancer cells and protect them from the immune system therefore helping them form metastatic tumours. The researchers injected mice with normal cells along with the decoys with humans breast cancer cells; they were able to prevent the platelets from binding to cancer cells completely suggesting that they could prevent the formation of new tumour cells.
This diagram shows that when platelets are exposed to platelet simulating molecules they send out long tendrils and clump together forming clots (left) however when the decoys were exposed to the same molecules they failed to activate and stayed in the resting state (right)
5. Reference sources (reported in Vancouver format). [Please consult: http://referencing.port.ac.uk/ for guidance].
1. How Blood Clots - Blood Disorders - MSD Manual Consumer Version [Internet]. [cited 2019 Feb 15];Available from: https://www.msdmanuals.com/en-gb/home/blood-disorders/blood-clotting-process/how-blood-clots
2. Decoy platelets could prevent clots and cancer spread [Internet]. [cited 2019 Feb 15];Available from: https://www.pharmaceutical-technology.com/news/decoy-platelets-clots-cancer-spread/
3. Research & Development - OSE Immunotherapeutics [Internet]. [cited 2019 Feb 15];Available from: https://ose-immuno.com/en/research-development/
4. Platelet “Decoys” Outsmart Both Clots and Cancer [Internet]. [cited 2019 Feb 15];Available from: https://wyss.harvard.edu/platelet-decoys-outsmart-both-clots-and-cancer/
5. How Blood Clots - Blood Disorders - MSD Manual Consumer Version [Internet]. [cited 2019 Feb 15];Available from: https://www.msdmanuals.com/en-gb/home/blood-disorders/blood-clotting-process/how-blood-clots
