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How can cancer be targeted without killing healthy cells?
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How can cancer be targeted without killing healthy cells?

Targeted Therapy: a tremendous solution

Abstract: Targeted therapy is a relatively new method of curing cancer that uses drugs to attack targets on which cancer cells’ growth closely depend. [1] By attacking the proteins or enzymes responsible for their abnormal growth, its effects are amplified. Targeted therapy is successful in curing many cancer patients, it has fewer effects on healthy cells and causes fewer long-term conditions or complications than other chemotherapy treatments [1]; although the side effects it can cause, such as hand-foot syndrome, are very complicated. [2]

Tracing Targeted Therapy

Targeted Therapy is a new way of curing cancer by using drugs that target specific proteins or enzymes in addition to blocking signals that help the cancer cells to grow and spread through the body’s systems. Targeted therapy has fewer side effects on the normal dividing cells and causes fewer long-term conditions than other chemotherapies. A significant factor in the functioning of other cancer treatments, like radiotherapy, is cytotoxicity, meaning they function to slow the spreading of or to kill the cancerous cells. This impacts the cells’ dividing routine: the cell cycle. [1]

Figure 2

The Cell Cycle

The cell cycle is the normal growth routine of cells. It has 5 phases [1] (as seen in Figure 2):

Cells in the G0 phase are not dividing nor preparing for dividing, and are in an inactive state. This stage can lasts for a few hours or for years depending on the cell type.

Specific signalling will allow progression to G1. In this stage normal metabolic processes occur (e.g. respiration and protein synthesis) and cells are preparing to progress to the next phase.

Next is stage S: now DNA is being replicated for the daughter cells that will form. There is then a second G phase (G2), before finally mitosis (the cell division) in stage M. [1]

Radiotherapy has been successful in targeting actively dividing cells (those not in G0) but has led to killing healthy cells as well. To avoid killing healthy cells, a new solution was needed: a cytostatic(meaning stopping tumor cells’ proliferation), targeted therapy. [3]

Targeted therapy differs from standard chemotherapy in several ways, including:

• Most standard chemotherapies act on all dividing cells, while targeted therapies act on specific molecular targets associated with cancer.

• Targeted therapies are designed to interact or change something involving the genes within cancer cells that causes further growth to be inhibited. Thus the tumour stays the same size and they are cytostatic. However many chemotherapies kill cells to decrease the size of tumours and therefore are cytotoxic. [1][2]

Targeted therapy can cause different reactions inside the cell such as:

• Preparing and developing immune systems to kill the cancer cells

• Carrying a toxin to the cancer cell to kill it without harming normal cells [4]

• Blocking or turning off the signals that tell cancer cells to grow and divide

• Keeping cells from living longer than normal [4.1]

• Changing proteins within the cancer cells so the cells die

• Stopping to make new blood vessels to feed the cancer cells [4.2]

Different cancers propagate through the body differently. Identifying the target of the targeted therapy is one of the most important factors in using this kind of method to cure cancer, as each type of cancer has its own target that needs to be identified to have a successful treatment.

Detailed Action of certain types of Targeted Therapy

Enzyme Inhibitors

One of the main goals of targeted therapy is the slowing down of the infected cells’ growth and spread, which can be targeted through enzyme inhibitors. In the human body, there are many enzymes that function to keep the body normal and some of these are enzymes give “spreading” and “growing” signals to infected cancer cells. Some targeted therapies block these signals, which results in the interruption of the infected cells’ cell cycles. However it does not distinguish cancerous cells from normal cells. [2]

In new research published on 21 March 2016 by Cornell researchers from Ithaca and Weil Cornell Medicine campuses, a promising new inhibitor which showed effectiveness most noticeably against several types of difficult and complicated cancer types, such as leukemia, breast and colorectal cancer was described. “This started from basic science, and the basic study led us to this path, which looks very promising. We have high hope that in a few years, we can develop an effective anti-cancer drug,” said co-lead author Hening Lin, professor of chemistry and chemical biology in the College of Arts and Sciences and a Howard Hughes Medical Institute investigator. [5] An important role in the survival of several types of cancer, and one of the major factors in this research was played by the oncoprotein c-Myc, which is found in almost half of all human tumors and on the enzyme SIRT2. Experimenting on a laboratory breast cancer mouse model, the tumor growth in the breast cancer was inhibited by the group of researchers in addition to inhibiting SIRT2 and decreasing the c-Myc protein level by using a compound known as TM, which is a thiomyristoyl lysine compound. [5]

Apoptosis-inducing drugs

Many cancer treatments, including radiotherapy, cause changes in cells which lead to apoptosis (programmed cell death). Targeted therapy drugs in this treatment, apoptosis-inducing drugs, cause the cancer cells to die. In some situations, the “signals” for cell death do not work properly and drugs such as Olaparib (Lynparza) try to restore them in addition to:

• Blocking poly ADP-ribose polymerase (PARP) enzymes so that the cancer cells’ DNA cannot be repaired, causing the cells to die [6]

• Making the cells more easily destroyed

• Blocking BCL2 which promotes cancer call survival resulting in more sensitivity to anti cancer drugs [1] [6]

Angiogenesis inhibitors

Tumors and cancer cells need blood and nutrients to grow and spread– if they get insufficient amounts of nutrients they will not be able to grow. Angiogenesis is the process of making new blood vessels, which is a healthy and normal process; it may not be much needed for healthy adults but is very useful and important in remaking blood vessels when injured for example. So, one way of stopping the growth of cancer tumors is stopping the supply of nutrients needed for their growth. Cancerous cells use VEGF, vascular endothelial growth factor, which is a family of protein growth factors made by some tumors: the VEGF proteins attach to their receptors in blood vessel cells and cause new blood vessels to form around the tumor, allowing it to become more massive. Some angiogenesis inhibitors work to block VEGF. [1]

Figure 3: Man-made targeted antibody drugs

Figure 4: Small-molecule drugs for inner cell treatments.

 

Types of Targeted Therapy Drugs:

Most targeted therapy drugs are divided into two main types:

•Antibody drugs: Man-made versions of immune system proteins (as seen in Figure 3) called antibodies that have been designed to attack certain targets on cancer cells, mostly around the surface of infected cells as they are more massive than others drugs. Normally the body itself makes antibodies to fight harmful microbial attackers.

• Small-molecule drugs: Such drugs are smaller and can easily go inside cells and therefore are assigned to do tasks inside cancer cells and that can be noticed in Figure 4. [2]

Some drugs that have noticeably great usage today:

Gleevec: There are many different kinds and types of targeted therapy drugs, one of the first to be used to cure cancer was Gleevec (imatinib mesylate) which is usually used to treat gastrointestinal  stromal tumor, a rare type of cancer in the gastrointestinal area known as GIST, and specific kinds of leukemia. This drug, imatinib, is a tyrosine kinase inhibitor meaning it targets tyrosine kinase proteins that are used for growth signaling of cells [7] and a type of small molecular drug that normally targets abnormal proteins or enzymes that form on and inside cancer cells and provide the key to the uncontrolled growth of dividing cells. Blocking these enzymes inhibit the growth of these cells, that is one of the main goals of targeted therapy. [2]

Iressa (gefitinib): One way to treat advanced non-small cell lung cancer is the targeting of epidermal growth factor receptors– (EGFR) which are found on the surface of many normal cells, but specific cancer cells have an abnormally high number of them on their surface which helps in giving more signals to the infected cells to grow and spread. Using gefitinib to stop the signals by blocking them  results in slowing or stopping of abnormal cell growth [2].

Sutent: One of the multi-functioning targeted therapy drugs available for treating both advanced kidney cancer and some gastrointestinal stromal tumors (GIST), which is very useful and impressive, is Sutent (sunnitinib). It is considered as a multi-targeted kinase inhibitor as it is a kind of vascular endothelial growth factor receptor inhibitor and an angiogenesis inhibitor. It stops the source of nutrients for cancer tumors, in addition to blocking the well-known tyrosine kinase enzyme. By succeeding in performing all these tasks, this useful drug not only slows cancer growth but it keeps tumors from making their own blood vessels to help the growth of them throughout the body. [2]

Velcade (bortezomib): This kind of drug, which is a small molecular drug, is necessary to treat multiple myeloma when other drugs have not responded to previous treatments. This proteasome inhibitor, bortezomib, stops the proteasome (which is a complex of enzymes that helps destroy proteins no longer necessary to the cell, including those regulating cell function and growth) from breaking down these proteins which in turn causes cancer cells to die. [2] Velcade has been used to treat an estimated number of 550000 atients worldwide which is very hopeful for a brighter future. [8]

Figure 5: Different kinds of side effects from targeted therapy, such as hand-foot syndrome (shown in the bottom-centre image)

Targeted Therapy Side Effects

One of the main benefits of targeted therapy is that it has fewer side effects on the body than other standard chemo treatments, although it can have side effects that are deeply dependent on the target that the drugs are used to attack. [2] Some drugs have more targets on cancer cells but also some on healthy cells that can cause negative impacts. The side effects increase in severity as the number of drug targets increase, especially drugs that play an important role in angiogenesis inhibition, as that affects new blood vessel formation all over the body, not just those near the infected cancer cells and tumors, meaning they can lead to complications, such as those seen in Figure 5.

Some people get few, if any side effects and it really depends on the person that uses the drugs; even the severity of the effects varies greatly from person to person and how long the drug was used. The side effects usually are not long-term as most side effects go slowly after treatment and the healthy cells recover however it really depends on the patient’s overall health conditions and the consumed drugs’ specifications. [2]  Some types of medicines may be given to the patient to control the side effects after or even before the medication. These are some of the most common side effects of targeted therapy:

Skin problems:

The most common skin problem after the treatment is rash: more than half of patients who chose this type of treatment are affected by it. Its severity depends on the type of cancer and the dose used to treat it, although it is mild for most people. It is often similar to acne but without blackheads as seen in Figure 6, and usually appears on the scalp, face, neck, chest and upper back by about the fourth week of the treatment, when the skin usually crusts and gets very dry and red (dryness of the skin which can even crack open is another side effect which is more difficult to handle than rash) and after that, flat or raised spots appear on the skin which can itch, burn, sting and may even be painful to touch (some patients may be needed to use drugs such as diphenhydramine to get relief); the rash usually should completely go away about after a month of the treatment [9].

Figure 6: Rash is the most common side effect of this therapy

These problems usually develop slowly over days to weeks and are not the signs of drugs allergy – which includes serious symptoms such as dizziness, trouble in breathing, tightness in the chest and throat, swelling of lips or tongue, intense itching or hives that usually becomes noticeable suddenly a few minutes to hours after taking the drug– but problems like lack of skin moisture, which is the result of some of the specialized drugs that target the epidermal growth factor receptor (EGFR) protein which sends growth and division signals to cancer cells, like Iressa (geftinib); as explained above, it affects the normal skin cells which do have a lot of EGFR on their surfaces making it harder to maintain skin moisture [10].

Figure 7: Hand-Foot syndrome can result in swelling of the soles and hands.

Other problems that are a result include the hand-foot syndrome –its cause is not known yet but is probably because of the damage to the tiny blood vessels in the hands and feet or the drugs themselves leaking out from the blood vessels and into tissues, leading to tissue damage that targets proteins such as the vascular endothelial growth factor (VEGF) which helps tumors build and maintain a blood supply. Some patients who reach severe levels of pain both in the hands and feet may be given medicine for relief as it can cause swelling in the palms of the hands and soles of the feet, which can be seen in Figure 7, redness which may even blister and open up and become painful sores and can even affect the ability to walk and doing normal activities. Scientists have reached the conclusion that patients getting radiotherapy, as well as targeted therapy, have more skin problems in the area where the radiotherapy treatment has been focused on as well. [2]

Another side effect caused by some targeted therapies is swollen, red, open and painful skin sores around fingernails and toenails which can superficially look like an infection or an ingrown nail as can be seen in Figure 5 (bottom right image). It happens mostly to the big toes and thumbs and may get infected, brittle and grow slowly.

Other types of side effect include changes in hair growth, affecting both men and women, can be noticed including the hair becoming thin, dry, curly and even brittle. Bold patches or complete loss of scalp hair may as well be observed when using targeted therapy for a long time. Some drugs may even affect the colour of the hair, in addition to a change of the skin colour; the skin usually tends to turn to a yellowish shade and in rare situations hair becomes darker. These effects usually fade away as the treatment ends.

Targeted therapy may even cause damage to the clear part of the eye, which can result in injury, pain, or infection as in few people the eyelids may turn inwards or outwards as seen in Figure 5, get tender, swollen or inflamed and crusts may be seen in the eyelashes. [2] The eye itself can become dry and red and burn painfully. Problems with wound healing like the opening up of old wounds and new ones not closing, perforations, which are holes opening up in the digestive system organs, can also be observed.

Complications with bleeding and clotting because of angiogenesis inhibitors’ interference in the formation of new blood vessels can occur and result in bruising. Throwing up blood may also be a sign that the patient is facing inner bleeding in the intestines and stomach, which is very severe. These drugs may even cause clots in the lungs and legs, heart attacks and strokes – of which  symptoms include sudden swelling, pain, or tenderness in the arm or leg. These symptoms should always be reported immediately to a doctor as they may lead to death. [2]

In conclusion, targeted therapy is a very useful treatment for many types of cancer, with fewer side effects on normal, healthy cells than other therapies. [1]  Specific drugs can attack their targets in many different ways to decrease the number of cancerous cells in the body, but inevitably do lead to complications (such as blood clots). The difficulties a patient may go through because of their treatments can include rare but possibly long-term diseases [3]; however, because these techniques are still young compared with other chemo treatments, there are still many more studies to be done and improvements to be made. The very best is wished to all victims of cancer, a deadly killer, in the hope of the best use of targeted therapy to cure them.

 

By Anne-Rosa Bilal

 

 

References:

Figure 1. (Edited image with two pictures)

Shutterstock Original Image: https://www.shutterstock.com/image-illustration/medical-medicinegoal-

health-care-success-629989916?src=mgg0dfYNVRvSEBsmKh645w-1-38

ABC Australia: http://www.abc.net.au/news/2016-05-06/lymphoblast-cells/7390420

1. National Cancer Institute. “Targeted Cancer Therapies.” National Cancer Institute. April 15,

2014: https://www.cancer.gov/about-cancer/treatment/types/targeted-therapies/targeted-therapiesfact-

sheet

2. American Cancer Society. “Targeted Therapy”, 2013. Last accessed at: https://old.cancer.org/acs/

groups/cid/documents/webcontent/003024-pdf.pdf

3. The American Cancer Society medical and editorial content team. “How does radiation work to

treat cancer?” American Cancer Society. October 27, 2014. http://www.cancer.org/treatment/

treatmentsandsideeffects/treatmenttypes/radiation/radiationtherapyprinciples/radiation-therapyprinciples-

how-does-radiation-work

4. The American Cancer Society medical and editorial content team. “What is targeted therapy?”

American Cancer Society. June 6, 2016: http://www.cancer.org/treatment/treatmentsandsideeffects/

treatmenttypes/targetedtherapy/targeted-therapy-what-is

4.1. American Society of Clinical Oncology. Understanding Targeted Therapy. 10/2015:

www.cancer.net/navigating-cancer-care/how-cancer-treated/personalized-and-targeted-therapies/

understanding-targeted-therapy on May 10, 2016.

4.2. National Cancer Institute. Targeted Cancer Therapies. 2014: www.cancer.gov/cancertopics/

factsheet/Therapy/targeted on May 4, 2016.

5. Fleischman, Tom. “Enzyme inhibitor looks promising against cancer.” Cornell University. March

21, 2016. http://www.news.cornell.edu/stories/2016/03/enzyme-inhibitor-looks-promising-againstcancer

6. Canadian Cancer Society, “Targeted Therapy”: http://www.cancer.ca/en/cancer-information/

diagnosis-and-treatment/chemotherapy-and-other-drug-therapies/targeted-therapy/?region=sk

7. Science Magazine: “The protein kinase family: conserved features and deduced phylogeny of the

catalytic domains” (1 July 1998): http://science.sciencemag.org/content/241/4861/42

8. VELCADE® (bortezomib). “How VELCADE® (bortezomib) works.” VELCADE®

(bortezomib) http://www.velcade.com/understanding-velcade/about-velcade

9. Esper P, Gale D, Muehlbauer P: “What kind of rash is it? Deciphering the dermatologic toxicities

ofbiologic and targeted therapies.” Clinical Journal of Oncology Nursing. 2007:

https://cjon.ons.org/cjon/11/5/what-kind-rash-it-deciphering-dermatologic-toxicities-biologic-andtargeted-

therapies

10. Burtness B, Anadkat M, Basti S, et al. NCCN Task Force Report: “Management of

Dermatologic and Other Toxicities Associated With EGFR Inhibition in Patients With Cancer.”

Journal of National Comprehensive Cancer Network. 2009: http://www.jnccn.org/content/7/

Suppl_1/S-5.abstract

Figure 2. The American Cancer Society medical and editorial team. 2014. Cell cycle: http://

www.cancer.org/treatment/treatmentsandsideeffects/treatmenttypes/radiation/

radiationtherapyprinciples/radiation-therapy- principles-how-does-radiation-work

Figure 3. Lonza ADC Experts. Antibody Drug Conjugates: http://www.lonza.com/custommanufacturing/

chemical- manufacturing/antibody-drug-conjugates-adcs.aspx

Figure 4. Expert. Small Molecule Targeted Therapy Market Lead in 2016! 2016. http://emergingmarket-

trends.blogspot.com/2016/01/small-molecule-targeted-cancer-therapy.html

Figure 5. Conway, Jia. Prevention and management of hand-foot syndromes. 2010.: http://

www.oncologynurseadvisor.com/ce-courses/prevention-and-management-of-hand-foot-syndromes/

article/ 174390/

Figure 6. Scowcroft, Henry. “The quest to unravel the side effects of cancer drugs” 2013: http://

www.scienceblog.cancerresearchuk.org/2013/09/05/the-quest-to-unravel-the-side-effects-of-cancerdrugs/

 

 

Does Classical Music Improve Short Term Memory?
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Does Classical Music Improve Short Term Memory?

A study by Zurafa Sakel.

 

Abstract

The aim of this study is to explore whether classical music can improve short term memory in healthy volunteers. This may help learning of healthy people. It may also have a positive impact on communication and interaction as well as reducing agitation in dementia patients. This standardised prospective experiment involved using ‘Digit Span Test’ as the primary outcome measure. Digit span is used to determine the memory’s capacity for the storage of numbers. The subjects were presented with a series of numbers and were asked to repeat them in correct sequence. If successful, the list was increased by one digit. This was done similarly with the backward digit span task, where the subject had to repeat the numbers in reverse order. All subjects then repeated these tests in silence without any music on. This task exercises verbal working memory. Verbal working memory is involved in everyday tasks eg. remembering a phone number or understanding long and difficult sentences. I used descriptive statistics to analyse the results. The results did not show any correlation to suggest that classical music improves short term memory in healthy volunteers. More research is needed with a larger sample, taking into account the inherent musicality of people.

Background

Short term memory (STM) is like the mind’s ‘post it’ note.1 STM is the ability to hold small amounts of information in our mind for a short period of time. It requires a registration and retrieval system for information when it is needed. STM is a key requirement for long term memory and working memory which is essential for learning. In the ever increasing busy nature of modern life a person has to undertake many tasks which require STM, e.g. remembering a phone number or understanding long and difficult sentences. STM may be affected by factors like attention, ‘chunking’ (reducing long strings of information into shorter easier to remember chunks) and concentration.

The Marzano Information Processing Programme (2)

The Marzano Information Processing Programme (2)

The part of the brain that involves STM includes the hippocampus (temporal part of the brain) which is the first part of the brain to be primarily affected by Alzheimer’s disease.3 Alzheimer’s is the most common type of dementia.4 Studies have shown that Alzheimer’s patients undertaking memory tests were able to learn more lyrics with music in the background, compared to if the lyrics were just spoken.5 Music stimulates the cortical and subcortical areas of the brain. It has been said that using music therapy could help patients with their well-being and independence and may enhance the functionality of memory impaired patients with Alzheimer’s. I observed a positive impact on communication, interaction and agitation in dementia patients whilst I undertook my work experience at a dementia care home. This is what triggered my idea for this study.

The aim of this study is to see if classical music can improve short term memory in healthy volunteers through a standardised experiment. My objective was to seek an appropriate assessment tool to assess STM in healthy subjects, analyse the data and review the outcomes.

Methodology

This investigation involves the use of the ‘Digit Span Test’.7 I have decided on this particular test as it is quick and easy to use and produces more reliable results than alternative tests. Other tests that have been used in other studies to assess STM include memorising as many items/objects from a picture or tray in 30 seconds or memorising a list of words. However, the Digit Span Test is the recommended tool for short term memory assessment in neuropsychology.

In psychology and neuroscience, memory span is the longest list of items that a person can repeat back in correct order immediately after having seen it.8  When numbers are used it is called digit span. Digit span is used to determine the memory’s capacity for the storage of numbers. The subjects will be presented with a series of numbers (e.g. 1,8, 4) and has to repeat them back. If successful, the list increases by one digit. This is done similarly with the backward digit span task except the subject has to repeat the numbers in reverse order. The total number of digits remembered is noted for each test and individual. The average number of items a person remembers in their short term memory is between 5 and 9 objects.

This task exercises verbal working memory. Verbal working memory is involved in everyday tasks e.g. remembering a phone number or understanding long and difficult sentences. It is thought to be one of the key elements associated with intelligence, therefore making the digit span task a common part of many IQ tests and the Wechsler Adult Intelligence Scale (WAIS). The performance on the digit span task is linked to language learning abilities.9

After the subject is tested initially they will be tested again but with classical music (in this case Mozart’s Violin Concerto No.3,  2nd Movement) in the background. The order of the silent and music tests were chosen randomly to avoid bias. There are some factors that have to be taken into consideration with this test:

  • The rate of the presentation of numbers is important; experimental investigations show that the speed of presenting the digits affects the score.10 In this test numbers were presented one word per second.
  • The time required to respond- subjects are advised not to wait too long after the last digit in the sequence is presented.
  • Any distractions – the more distractions there are, the worse the recall of information.11 The tests were carried out in a quiet room with no interruptions.
  • Sample size – it was decided to recruit a minimum of 20 volunteers to improve accuracy, precision and reliability.
  • Volume of music- this was adjusted so that it was not too loud and distracting. All subjects were checked to ensure there were no hearing impairments.
  • Visual acuity- vision was checked so that all subjects could read the numbers. The same distance was kept between the investigator (myself) and each of the subjects.
  • Memory impairment-none of the subjects in this study had a diagnosis of memory impairment.
  • Incomplete tests- A few tests were disregarded as the subjects were unable to complete all 4 of the tests.
  • Recruitment of volunteers – Volunteers were chosen from friends and family, ranging from the age of 9 to 81 years old

Undertaking each test using the same controlled conditions (mentioned above) by the same investigator ensures a fair test and thus improving reliability.

The demography (ages, ethnicity and educational attainment) of each participant was also recorded. Educational attainment refers to the highest degree of education an individual completed.

Results

Table 1 shows each individual score (number of digits recalled correctly) from each test for each subject.

Table 1

Table 1

Table 2 and the chart below shows the mean score for each individual test.

Mean Scores

Mean Scores

The following graph and table demonstrate the mean scores of participants according to their highest level of educational attainment, and the demography of the sample.

Relationship between Highest Level of Education and Mean Score

Relationship between Highest Level of Education and Mean Score

Conclusions and Implications

  • Looking at the overall results for the scores for silence and music, there is no conclusive evidence that classical music improves short term memory in healthy volunteers.
  • There is no correlation between the ages of the subjects and the scores.
  • There is no correlation between the genders of the subjects and the scores.
  • The participants of secondary school age had the highest overall mean scores and those with a high school degree had the lowest scores. This may indicate a positive correlation between IQ/ intelligence and mean score as most of the secondary school children who participated in the study attend a selective grammar school. However, we have to take into consideration that the sample size for those with a high school degree was small (2 participants), indicating that the mean score may not be reliable.
  • Some subjects commented that it took some time for them to adjust to the format of the tests which may have affected their score.

If this project was to be developed in the future, I would recommend the following changes:

  • Increase the sample size.
  • Allow more time for each individual test by incorporating a practice test (forwards and backwards) to ensure that each subject understands the format of testing.
  • Allow more time for the whole project in order to arrange for recruitment of volunteers to be carried out on a much bigger scale.
  • The musicality of each subject could be measured to see what impact this would have on the scores.

Even though the results of this study were inconclusive, future projects could be developed:

  • Different genre of music could be used for this test. It may be that younger subjects could perform better with contemporary music.
  • Future studies could be done concentrating on an older population (over 65 year olds) and comparing results between those with and without memory impairment. This would give a better indication of the effect of classical music on dementia patients.
  • Further studies could also be done to look at the effect of classical music on the well-being and quality of life of dementia patients.

 

By Zurafa Sakel

 

Acknowledgements

I would like to thank the following for providing advice and guidance on psychological memory assessment tools and the Digit Span Test:

  1. Laura Smith, Research PHD student & Associate Lecturer, School of Psychology, University of Kent.
  2. Dr Melanie George, Principal Clinical Neuropsychologist, Kent & Medway NHS Trust

I would also like to thank the Neurorehabilitation Team at Kent & Canterbury Hospital for providing resources on the function of the brain and the neuroscience of memory.

Finally, I would like to thank all the volunteers for making time to participate in this project.

References

  1. (2010) Mastin Luke Short term (working) memory
  2. (1998) Marzano Information Processing Model
  3. Koch Sarah- Neena Subcortical Brain Structures
  4. (2014) Krishnan Mani What is Alzheimers Disease?
  5. (2010) Seligson Susan Music boosts memory in Alzheimers
  6. (2012) Parikh Nina Therapeutic effects of personalised music
  7. (2009) Mcleod S.A. Short term memory
  8. (1938) Blankenship Albert B. The psychological bulletin, Vol. 35, No. 1, 2-3
  9. Medical Research Council. About this test: Improve your digit span performance by ‘chunking’
  10. (2015) Ricklaman. Memory Span
  11. (1934) Lumiley, F. H., and Calhoon, S. W. Memory Span for Words Presented Auditorially. Appl. Psychol., 18, 773-784

 

Are you interested in animal biology? Why not enter ZSL’s competition for young scientists?
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Are you interested in animal biology? Why not enter ZSL’s competition for young scientists?

The Zoological Society of London (ZSL) is keen to encourage students to see biology as an inspiring and exciting field of study. Linda DaVolls tells us about ZSL’s annual Prince Philip Award and Marsh Prize!

zsl-logo

If you are reading this then it’s probably safe to assume that you have more than a passing interest in science and are curious about the natural world. At ZSL we want to inspire students to take the step from learning about wildlife to investigating it.  ZSL runs an annual competition for the Prince Philip Award and Marsh Prize, which is presented to a sixth-form student for the best project on animal biology. The aim is not to ‘discover everything’ about the species being studied but to focus on one or two simple questions about its ecology, behaviour or physiology, which can be explored through practical work.  Recent winners have studied the effect of lemon peel on the behaviour of worms in a wormery, or assessed factors that affect the distribution of ground beetles in Scotland or devised an experiment to investigate whether the common garden snail can see in colour.

Full guidelines for entering the completion can be found here http://www.zsl.org/science/zsl-awards

Each project should be about 3000 words and include photos, tables and graphs. You will need to explain the aims of the study and include a testable hypothesis, as well as select the best methods and statistical analysis to interpret your results. The experiments should be described in sufficient detail to allow the study to be replicated. If possible, you should include a description of how the variables are controlled to produce reliable results. Your conclusions and a discussion should describe any limitations of the study and highlight areas for further research.  Large data sets can be added as appendices, and don’t forget to include a bibliography to demonstrate the background reading and references you used to research your topic.

To enter you must be under 19 years of age on 1 January in the competition year and must be/have been a pupil at a school or college in Great Britain or Northern Ireland. A project may be the work of one student or a joint project from not more than two students.

Projects are judged by a panel of scientists and education officers, and marked on accuracy of observations, planning, interpretation, significance of conclusions, writing style and neatness of presentation.

The prize is £600 for you, while your school or college receives a medal. You will also have an opportunity to publish a summary of your project in YSJ.  What better way to start your career in science?

A Prince Philip Medal

A Prince Philip Medal

The closing date is 30 November 2016. Please submit your project to Linda DaVolls, Zoological Society of London, Regent’s Park, London NW1 4RY.

I look forward to receiving your project!

stewart
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Mitochondrial Donation now deemed 'safe'

Why does this procedure exist? 

Mitochondria provide energy to nearly every cell in the body. Mitochondria is transferred from mother to the baby, but if there is a problem with the mitochondria inherited to the baby, then this can result in severe mitochondrial diseases. One in every 6,500 babies born have severe mitochondrial disease which can include muscle weakness, blindness, deafness, fatal heart failure, liver failure, learning disability and diabetes and can lead to death in early infancy.

In March 2015, MP’s in the UK voted to allow mitochondrial donation. This resulted in the United Kingdom being the first country to legalize the procedure. Experts from the Human Fertilisation and Embryology Authority (HFEA) stated that they would require more evidence that the procedure was safe before the end of the year, before they could consider issuing a license for doctors to perform the procedure.

Professor Turnball from Newcastle University

Professor Turnbull from Newcastle University.

The process of Mitochondrial Donation

A team of scientists led by Dr Mary Herbert and Professor Doug Turnbull from Newcastle Univeristy have been the pioneers behind the technique. There are several, different processes that can be used for mitochondrial transfer. Scientists at Newcastle University published results on one form of mitochondrial donation called Pronuclear Transfer (PNT). This is when the mothers egg is fertilised with the fathers sperm using standard IVF procedures. Before the egg has a chance to divide into two, the parents’ chromosomes are removed and placed into a fertlised egg from a healthy donor, which has had it’s own own chromosomes removed.

Pronuclear transfer

The scientists concluded that healthy embryos created from mitochondrial transfer were likely to produce normal pregnancies. While this was positive, follow-up studies urged some caution. When cells were taken from PNT embryos in the lab, some showed rising levels of mutated mitochondrial DNA. Although small amounts are carried over, the faulty DNA came back. The scientists suggested they could screen PNT embryos for high levels of mutated mitochondria before deciding which to implant. Professor Turnball states “This procedure could potentially help 150 women who carry Mitochondrial Diseases in the UK each year. But many may choose alternatives to avoid passing the mutated DNA such as adoption or IVF with donor eggs.”

The Negative Outcry

Although the donor egg is said to only contibute 0.1% of the genetic make up of the child, when examining the genetic material of these children there are still three identifiable genetic parents. This is due to the fact that the donor egg usually comes from a non-maternal relative. For the child to have only two identifiable genetic parents, the donor egg must have to come from a paternal relative because mitochondrial DNA (mtDNA) is inherited maternally, maternal relatives will, have identical mitochondrial DNA, barring random mutations. Scientists have yet to explore the prospect of mitochondrial donation from paternal relatives. This means that currently any child born from this procedure would have three parents. However, the new proposed laws state that the identity of ‘the second mother’ would remain anonymous. This has raised some backlash because egg and sperm donators by law cannot remain anonymous as the child has a legal right to know where they came from. But, the mitochondrial donor has contributed DNA to the creation of the child, they are another parent so why are they not treated the same as egg and sperm donors.

The Council of Europe’s Convention on Human Rights and Biomedicine and the World Health Organisation stated that they are opposed to anything that alters genes across generations. But the result from parliaments vote showed that the benefits that mitochondrial donation can give to carriers of mitochondrial disease outweighs the ethical arguments against the procedure.

Transfer

The Telegraph- Tim Stanley- www.telegraph.co.uk/news/health/11380784/Three-parent-babies-unethical-scary-and-wrong.html

BBC News- James Gallagher- www.bbc.co.uk/news/health-26367220

The Guardian- Ian Sample- https://www.theguardian.com/science/2016/jun/08/doctors-edge-closer-to-creating-babies-with-dna-from-three-people

https://en.m.wikipedia.org/wiki/Mitochondrial_donation

BBC News- Fergus Walsh- www.bbc.co.uk/news/health-36481452

http://www.mitochondrialncg.nhs.uk/research.html

www.geneticsandsociety.org- CGS 3 person IVF

http://www.bbc.co.uk/news/health-36499807

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Mitochondrial Donation now deemed ‘safe’

Why does this procedure exist? 

Mitochondria provide energy to nearly every cell in the body. Mitochondria is transferred from mother to the baby, but if there is a problem with the mitochondria inherited to the baby, then this can result in severe mitochondrial diseases. One in every 6,500 babies born have severe mitochondrial disease which can include muscle weakness, blindness, deafness, fatal heart failure, liver failure, learning disability and diabetes and can lead to death in early infancy.

In March 2015, MP’s in the UK voted to allow mitochondrial donation. This resulted in the United Kingdom being the first country to legalize the procedure. Experts from the Human Fertilisation and Embryology Authority (HFEA) stated that they would require more evidence that the procedure was safe before the end of the year, before they could consider issuing a license for doctors to perform the procedure.

Professor Turnball from Newcastle University

Professor Turnbull from Newcastle University.

The process of Mitochondrial Donation

A team of scientists led by Dr Mary Herbert and Professor Doug Turnbull from Newcastle Univeristy have been the pioneers behind the technique. There are several, different processes that can be used for mitochondrial transfer. Scientists at Newcastle University published results on one form of mitochondrial donation called Pronuclear Transfer (PNT). This is when the mothers egg is fertilised with the fathers sperm using standard IVF procedures. Before the egg has a chance to divide into two, the parents’ chromosomes are removed and placed into a fertlised egg from a healthy donor, which has had it’s own own chromosomes removed.

Pronuclear transfer

The scientists concluded that healthy embryos created from mitochondrial transfer were likely to produce normal pregnancies. While this was positive, follow-up studies urged some caution. When cells were taken from PNT embryos in the lab, some showed rising levels of mutated mitochondrial DNA. Although small amounts are carried over, the faulty DNA came back. The scientists suggested they could screen PNT embryos for high levels of mutated mitochondria before deciding which to implant. Professor Turnball states “This procedure could potentially help 150 women who carry Mitochondrial Diseases in the UK each year. But many may choose alternatives to avoid passing the mutated DNA such as adoption or IVF with donor eggs.”

The Negative Outcry

Although the donor egg is said to only contibute 0.1% of the genetic make up of the child, when examining the genetic material of these children there are still three identifiable genetic parents. This is due to the fact that the donor egg usually comes from a non-maternal relative. For the child to have only two identifiable genetic parents, the donor egg must have to come from a paternal relative because mitochondrial DNA (mtDNA) is inherited maternally, maternal relatives will, have identical mitochondrial DNA, barring random mutations. Scientists have yet to explore the prospect of mitochondrial donation from paternal relatives. This means that currently any child born from this procedure would have three parents. However, the new proposed laws state that the identity of ‘the second mother’ would remain anonymous. This has raised some backlash because egg and sperm donators by law cannot remain anonymous as the child has a legal right to know where they came from. But, the mitochondrial donor has contributed DNA to the creation of the child, they are another parent so why are they not treated the same as egg and sperm donors.

The Council of Europe’s Convention on Human Rights and Biomedicine and the World Health Organisation stated that they are opposed to anything that alters genes across generations. But the result from parliaments vote showed that the benefits that mitochondrial donation can give to carriers of mitochondrial disease outweighs the ethical arguments against the procedure.

Transfer

The Telegraph- Tim Stanley- www.telegraph.co.uk/news/health/11380784/Three-parent-babies-unethical-scary-and-wrong.html

BBC News- James Gallagher- www.bbc.co.uk/news/health-26367220

The Guardian- Ian Sample- https://www.theguardian.com/science/2016/jun/08/doctors-edge-closer-to-creating-babies-with-dna-from-three-people

https://en.m.wikipedia.org/wiki/Mitochondrial_donation

BBC News- Fergus Walsh- www.bbc.co.uk/news/health-36481452

http://www.mitochondrialncg.nhs.uk/research.html

www.geneticsandsociety.org- CGS 3 person IVF

http://www.bbc.co.uk/news/health-36499807

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Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)

Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)
This new revolutionary genome editing tool will enable the elimination of many genetic diseases. It could also be used to modify crops, screen for cancer genes, eradicate virus’ and for genome engineering. This has sparked debate on whether ethically, this could lead to a slippery slope on what grounds can a genome be edited?

Crispr potential

CRISPR’s ability range to edit DNA organisms. Illustrated by: Davide Bonazzi

How exactly does this technique work? 

CRISPR editing is a process whereby scientists can rewrite the genetic code of an organism by cutting out and replacing the individual components of DNA. This can prevent many genetic diseases such as Huntington’s Disease or Cystic Fibrosis.

If we look at the way bacteria work, we can use CRISPR using the Cas-9 bacterial enzyme to our advantage. The stages explained are:

  1. When bacteria encounter an invading source of DNA, such as from a virus, they can copy and incorporate segments of the foreign DNA into their genome as “spacers” between the short DNA repeats in CRISPR.
  2. These spacers enhance the bacteria’s immune response by providing a template for RNA molecules to quickly identify and target the same DNA sequence in the event of future viral infections.
  3. If the RNA molecules recognize an incoming sequence of foreign DNA, they guide the CRISPR complex to that sequence. There, the bacteria’s Cas proteins, which are specialized for cutting DNA, cut out and disable the invading gene.

Crispr in action

The CRISPR/Cas system. (From E. Pennisi, Science, 341:833-6, 2013. Credit: K. Sutliff/Science)

Professor Jennifer Doudna, is credited with developing the gene-editing technology using the bacterial enzyme Cas-9. She explains CRISPR by comparing it to a film editor. “Think about a film strip, you see a particular segment of the film that you want to replace. And if you had a film splicer, you would go in and literally cut it out and piece it back together, maybe with a new clip. Imagine being able to do that in the genetic code, the code of life,” Doudna added. “You could go in and snip out a piece and replace it with something that corrects a mutation that would cause disease.”

It is believed that with more research and development CRISPR could also be a cure for HIV. It would be used to cut the DNA of the inactive phase of the virus out of an infected cell. However more research is required because of the difficulty scientists have to target the specific area of the genome that the virus lives in, especially because HIV can remain dormant in the body for many years. Scientists need to understand where the virus lives and what it needs to survive before they carry out the technique. If they cut in the wrong area of the genome then this can produce more damaging effects.

Doudna states “We can expect to see clinical applications of CRISPR within the next few years.” But with CRISPR’s potential comes some fears of what embryo-editing leads to. Doudna goes on to say “We’re talking about something that would affect human evolution.”

Genome editing

http://blogs.discovermagazine.com/crux/files/2015/11/DNA_edits.jpg

http://www.umassmed.edu/news/news-archives/2015/04/editing-hiv-out-of-our-genome-with-crispr/

http://www.cbsnews.com/news/crispr-jennifer-doudna-gene-editing-technology-diseases-dangers-ethics/

http://motherboard.vice.com/read/what-is-crisprcas9-and-why-is-it-suddenly-everywhere

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Is Altitude Training the best way to legally improve sporting performance?

Please follow the link below to view my Biology AS Coursework looking at the effectiveness of Altitude training on Elite Performers. Also explores the effectiveness of Performance Enhancing Energy Drinks and Ice Baths as a recovery method.

Is altitude training the best way to legally improve sporting performance?