xplain the main reason(s) why these are the three factors that you feel need to be considered.

Part 1: Hypothesis/Answer (~150 characters)

List the three ‘factors’ you think need to be considered in the analysis based on the initial set of data in order to improve this organization’s ability to study how pollution influences the development of allergic diseases, such as asthma.

Part 2: Main Reason(s) (~450 characters)

Explain the main reason(s) why these are the three factors that you feel need to be considered. You can simply list a main reason for each factor, or if 2-3 of the factors connect with a common theme, you can also address it this way. Think very deeply about these factors to ensure they are unique to you in some way.

Part 3: Supporting Arguments(~550 characters)

Explain the main reason(s) why these are the three factors that you feel need to be considered. You can simply list a main reason for each factor, or if 2-3 of the factors connect with a common theme, you can also address it this way. Think very deeply about these factors to ensure they are unique to you in

Part 5: So What? (~350 characters)

Relate it back to the overarching purpose/goal of this study (in your opinion) and why looking at these factors will not only support this, but also help guide the future of this research in the right direction.

Discuss one important discovery that has involved the use of E. coli.

1. Discuss one important discovery that has involved the use of E. coli.
2. Discuss two reasons why E. coli is so commonly used in biomedical research.
3. Table 1 lists several databases involving E. coli. Choose one, visit the site, and report what you have found.
4. Define a bacterial plasmid. How is this different from the chromosomal DNA?
5. One example of genomic studies to E. coli is the Keio collection, which has mutated all E. coli genes. This study found that 4288 could be deleted without killing the bacteria. How many of these genes were essential for E. coli to survive and function? How many of them have unknown functions?
6.Describe an example of how E. coli could be used as a biosensor. Discuss what the molecule would be that the E. coli is sensing and how the bacteria would respond after binding to the molecule.
7. What is synthetic biology? What is the source of synthesized DNA?
8. How has the use of synthetically modified E. coli been beneficial to the perfume industry?

Describe the work in Coopey 2008 and discuss the implications of this study on work in Coopey 2007.

Description

Consider Coopey et al’s 2007[1] & 2008[2] papers. Write a series of paragraphs addressing the following points:

1) What is the question being addressed by the modellers in Coopey 2007 & what is their hypothesis?

2) How do the equations in the paper enable the group to address their question? Give a general description of the model. Then describe the meaning of each term in equations (1) and (2).

3) Why are there two phases in the model? Describe the biological motivation for the phases and explain how they are realised in the model.

4) Why were partial differential equations chosen instead of Boolean networks?

5) What prediction did the model make about the biological system and how could this be tested experimentally?

6) Describe the work in Coopey 2008 and discuss the implications of this study on work in Coopey 2007.

[1] Coppey, M. et al. (2007) Modeling the bicoid gradient: Diffusion and reversible nuclear trapping of a stable

protein. Developmental Biology 312. DOI 10.1016/j.ydbio.2007.09.058

[2] Coppey, M. et al. (2008) Nuclear Trapping Shapes the Terminal Gradient in the Drosophila Embryo. Current

Biology 18. DOI 10.1016/j.cub.2008.05.03

Describe the principles of the ‘maquette’ approach to de novo protein design.

Description

Instructions

Questions to be answered

Question 1. Describe in detail the pathways for engineering functional CO2 -concentrating mechanisms into plant chloroplasts.

Question 2. This question is in two parts, each carrying equal marks.

(a) The formal definitions for metabolite identifications have been defined by the Metabolite Standards Initiative.  With particular reference to the identification of tryptophan using GC-MS discuss how Level 2 identification is achieved and how this can be improved to Level 1.

(b) Now that you know you can detect tryptophan with GC-MS; how can its level in a yeast culture be quantified?

Question 3. This question involves genetic engineering and is in three parts, each carrying equal

marks.

(a) Describe the principles of the ‘maquette’ approach to de novo protein design.

(b) Describe in vitro compartmentalisation used in directed evolution experiments. What are the advantages of using this technique over in vivo experiments?

(c) What is the difference between non-homologous end-joining and homology-directed repair of a nuclease-induced double-strand break? How can each be used in genome editing to introduce mutations?

Question 5. This question involves genetic modification and is in three parts, each

carrying equal marks.

(a) What are the differences between rational design and directed evolution approaches to protein design?

(b) You want to introduce an indel into a gene encoding a eukaryotic protein of known structure to disrupt the gene’s function. Where in the gene sequence should you target, and why?

(c) How does off-target nuclease activity with CRISPR-Cas9 occur? Why is this a problem? How is this most-commonly minimised?

Describe where and how the termination of Polymerase II takes place across the genome at the molecular level.

Description

With reference to the research article from Nojima et al., Cell 2015 [1], discuss the relevant data and write a series of paragraphs addressing the following points:

a. Briefly describe the mNET-seq technique and explain two advantages and two disadvantages compared to

i) RNA Pol II ChIP-seq method and ii) PRO-seq assays. (30%)

b. Describe where and how the termination of Polymerase II takes place across the genome at the molecular level. Explain the biological significance of the regulation of transcription termination in regard to gene expression. (40%)

c. With reference to the paper, explain how Polymerase pausing proximally to promoters and at the transcription termination site (TES) are linked to mechanisms of transcription termination. What was the phosphorylation status of the CTD of Pol II molecules found by the authors to be associated with promoter-proximal pausing, splicing sites and the TES? How, in your opinion, can differential phosphorylation of the CTD dictate and control the different co-transcriptional activities of transcriptional termination and splicing that take place across the gene? (30%)

Reference: Nojima, T. et al. Mammalian NET-Seq Reveals Genome-wide Nascent Transcription Coupled to RNA Processing. Cell 161, 526-540, doi:10.1016/j.cell.2015.03.027 (2015).

 

What are the physiological, pathophysiological and therapeutic implications of this study?

Description

Structured evaluative piece of writing based on this research paper: UCHL1 provides diagnostic and antimetastatic strategies due to its deubiquitinating effect on HIF-1α Goto, Y., Zeng, L., Yeom, C. et al. UCHL1 provides diagnostic and antimetastatic strategies due to its deubiquitinating effect on HIF-1α. Nat Commun 6, 6153 (2015).

Questions to be answered;

1. Briefly summarise the main findings described in this paper

(Indicative length approx. 150 words)

2. In Figure 1C the authors use siRNA to reduce UCHL1 levels in cells. Briefly describe how

siRNA can reduce UCHL1 expression and suggest two alternative approaches the authors could

have used, outlining how they work, their benefits and their limitations.

(Indicative length approx. 250 words)

3. Pick the figure (relates to an entire figure (e.g Fig 1 or Fig 2 etc) and not the individual panels (e.g 1A, 1B or 1C etc)) that you think is the most important. Describe the results, the experimental

approach(es) used and why you think that it is the key figure in the paper.

(Indicative length approx. 300 words).

4. Draw and briefly discuss the signalling pathway delineated in this study and how this adds to

what was previously known about HIF regulation.

(Indicative length: Figure plus approx. 300 words)

5. What are the physiological, pathophysiological and therapeutic implications of this study?

(Indicative length approx. 300 words)

Instructions

– Answer the five questions separately.

– When writing your answers for the 5 separate questions, it is important to ensure that each individual answer is well structured, coherent and well-argued. This may involve including short introductory or concluding statements in some answers, but this will likely not be necessary for all of the questions. Indeed, having an introduction and conclusion for each question would probably result in a lot of unnecessary repetition.

Describe the mesolimbic and mesocortical dopamine systems and their role in reward and addiction.

ADHD and nervous system

Learning outcomes for Topic 5

Module learning outcomes are given in brackets.

By the end of this topic you will be able to:

5.1  Define and use in context, or recognise, definitions and applications of each of the terms in bold in the text and defined in the glossary (KU1, KU2, KU3, KU4).
5.2  Describe key characteristics of addiction and how they are used in diagnosis (KU3).
5.3  Describe the mesolimbic and mesocortical dopamine systems and their role in reward and addiction (KU2, KU3).
5.4  Describe the biomedical incentive sensitisation theory of addiction (KU1, KU3).
5.5  Discuss the biological, psychological and social risk factors that are associated with developing an addiction (KU2, KU3, CS3).
5.6  Outline key approaches to managing addiction, including the evidence base for management (KU3, CS2).