HSC BIO GUIDE 3: THE SEARCH FOR BETTER HEALTH

[teodora.simic]

1.What is a healthy organism?

1.a) Difficulties of defining the term ‘health’ and disease’

Main issues are:
-many different types of ‘health’ e.g. physical, mental, social and many types of ‘disease.’
-concept of ‘health’ is highly subjective – what you may think is healthy, I may not.

1.b) How the function of genes, mitosis, cell differentiation and specialisation assist in the maintenance of health

Always define each concept first, and then explain how it helps!

Gene

•   Section of DNA that codes for a particular polypeptide and thus a particular trait/characteristic.
•   Without it, gene malfunction would occur → the normal metabolic pathway of an organism would be unable to function.

Mitosis

•   Cell division in which identical cells are produced.
•   Needed for growth + repair → without it, millions of dead cells would not be replaced and the organism would be unable to function.

Cell differentiation + specialisation

•   During development in embryo somatic cells differentiate into specialised cells (e.g. muscle cells, epithelial cells etc).
-specific genes are ‘switched on’ so the cells can carry out particular functions in body.
•   Without this, specific functions wouldn’t be allocated to specific tissues, so complex functions of the organism couldn’t be carried out.
•   E.g. B cells (type of white blood cells) differentiate into plasma cells in response to infection → specialised to fight infection by producing antibodies.

SPECIFIC EXAMPLE: GENE MUTATION (causing cystic fibrosis) (i.e. showing how genes maintain health by showing health damaging effects of genes not working properly)
•   Normally, CFTR protein controls chloride ion transport across cell membranes → regulates bodily fluid secretion e.g. sweat, mucous, enzymes.
•   CF affects the exocrine glands → increased, thicker secretions → disrupts normal functioning of sweat glands, lungs + pancreas.

1. c) Links between gene expression and maintenance and repair of body tissues

What is gene expression?
•   For a gene that is ‘switched on,’ the DNA code is converted into polypeptides which control functions of cell.
How body tissues are repaired + maintained…
•   IF DNA is damaged (but can be repaired)
-variety of enzymes produced that can repair damaged DNA e.g. some cut out damaged DNA + make new DNA to replace it.
•   IF cell exposed to very high temp
-gene ‘switched on’ to produce ‘heat shock proteins’ → stabilise other proteins in cell → protects cell so can keep functioning.
•   Some enzymes ‘proofread’ – prevent copying errors when DNA is replicated
-e.g. when cells are replaced e.g. those lining intestines (bc too damaged by digestion to be repaired).
Genes which control cell division (and growth + repair):

1.Proto-oncogenes: speed up cell division

•   Code for proteins involved in promoting cell division + differentiation.
•   If mutation occurs in this gene it becomes an ‘oncogene’ → normal maintenance + repair of body tissues disrupted → can lead to uncontrolled cell division → tumours + cancer (usually mutation in tumour suppressor genes ALSO required to cause cancer).

2.Tumour suppressor genes: slow down/restrict cell division

•   Code for proteins that slow cell growth.
•   If mutation occurs in this gene → normal maintenance + repair of body tissues disrupted → uncontrolled cell division can no longer be restrained (as genes which would normally be ‘switched off’ are now expressed) → cancer may result.
•   E.g. in colon cancer: tumour suppressor gene functions normally to control cell division BUT mutation leading to deactivation of this gene leads to increased cell division → formation of colon polyps.

2.   History of cleanliness in food, water and personal hygiene

2. a) Distinguish between infectious and non-infectious disease

•   Disease: any change to normal bodily function that impairs, producing specific signs + symptoms.

Infectious disease

•   Caused by macro + microscopic pathogens *THIS IS VERY IMPORTANT! (live on host organism or invade its tissues → interfere w normal bodily functions) → can be transmitted from one organism to another or via a vector.
•   Pathogens found in water, soil, air and contaminated food + wastes.
•   E.g. bacteria causes cholera, virus causes influenza.

Non-infectious disease

•   Not caused by a pathogen → apart from inherited, cannot be transmitted from one organism to another.
•   Can be caused by heredity, environment, poor nutrition.
•   E.g. Down’s Syndrome is genetic, skin cancer is environmental.

2.b) Explain why cleanliness in food, water and personal hygiene practices assist in control of disease

•   Infectious diseases can be passed on via contaminated food (e.g. cholera), water (e.g. giardia) + inadequate personal hygiene
→ therefore, controlling these can reduce exposure to disease carrying microbes by reducing conditions in which they can rapidly multiply → controls spread of infectious disease.

Food
•   Food handlers must follow guidelines for storing, preparing + serving food:
-Washing hands before preparing + eating food.
-Thoroughly cooking food (e.g. no uncooked meat).
-When working with food, hair + skin lesions should be covered. 
•   Prevent conditions for ideal growth of pathogens (higher temp, high moisture etc).

Water
•   Most developed countries have basic legal requirements to ensure domestic water is filtered + chlorinated by licensed companies (→ not contaminated).
•   Can be issue in developing countries BUT many have legislation requiring use of ‘safe water system’ for safe disposal of sewage + wastes (e.g. not just dumping it into waterways used for drinking or cleaning).
•   Minimises risk of pathogens multiplying → reduces risk of transmission + disease e.g. cholera, giardia.

Personal hygiene
•   Can spread disease through inhalation of infective droplets by direct contact OR other bad practices relating to personal hygiene e.g. influenza + pneumonia transferred by inhaling infective droplets from a ‘sneeze.’

Good hygiene practices:
Personal:
-Proper hand washing with soap + water (hands carry millions of microbes – many harmless but some can cause disease).
-Keeping body, hair + teeth regularly clean to prevent pathogen build up (esp bacteria).
-Covering nose + mouth when sneezing – preventing transmission of pathogens.
Community wise:
-disposal of sewage + other wastes → reduces pathogen growth.
-sterilisation of equipment in surgeries, hospitals → reduces risk of pathogen transmission.
-city planning → reduces chances of overcrowding + spread of disease.

2.c) Identify the conditions under which an organism is described as a pathogen

What is a pathogen?

•   Parasite or infective agent that lives in or on a host – MUST be able to cause disease (needs right conditions to multiply + be transmitted) e.g. bacteria, virus. 

2.d) Ways in which drinking water can be treated + how this reduces the risk of infection from pathogens

Generally how drinking water can be treated:

1. Water chlorination (part of Sydney Water treatment – chlorine gas injected in water to kill pathogens e.g. bacteria, viruses → reduces chances of infection).
2. Boiling water for a few minutes → kills microbes → reduces chances of infection
-only used on small samples (not mass purification of water like 1.)

How Sydney Water treats drinking water
•   This method achieves removal/reduction of pathogens to a safe level for consumption → minimised spread of infectious disease via pathogens.
Once water flows into the catchment area from creeks + streams it enters Sydney Water’s filtration plants…
1.   Coagulation
-chemicals added → microbes, dirt + suspended solids stick together.
2.   Flocculation
-water flows through paddles →these particles now clump together.
3.   Sedimentation
-by gravitational forces, the clumps settle to the bottom → removes most particles.
4.   Filtration
-removal of finer particles.
5.   Disinfection
-chlorine gas added → kills pathogens (enough added that remains in water when goes through     pipes to reach public → ensures water remains disinfected).

*Fluoridation
-adding fluoride ions for dental health (prevents tooth decay – not part of purification).

Important variables tested for by Sydney Water + why
•   Coliforms (i.e. bacteria) e.g. E-coli associated with faecal contamination)
-indicates cleanliness of drinking water – presence of coliforms indicates other disease-causing pathogens also present.
-chlorine kills such bacteria.
•   Trace elements
-naturally occur in low levels e.g. aluminium, iron → may cause problems of staining + taste.
•   Turbidity (clarity)
-measure of suspended particles in water (may appear murky) → could hold pathogens.

*tests daily for 2 main ORGANISMS as well: cryptosporidium & giardia.


3. During the second half of the nineteenth century, the work of Pasteur and Koch and other scientists stimulated the search for microbes as causes of disease

3.a) Describe the contribution of Pasteur and Koch to our understanding of infectious diseases

Pasteur (19th C) – created ‘science of microbiology’

•   Helped disprove the theory of spontaneous generation:
-idea that living cells can be spontaneously produced from non-living cells e.g. in old meat, flies ‘appeared’ from meat cells (not true).
•   Did this by putting forward the “germ theory of disease” which established relationship bw microorganisms + disease – idea that ‘germs’ are present in the air + these lead to infection (modern understanding of infectious disease based on this idea).
-As specific bacteria became associated with specific disease, the “germ theory of disease” became more accepted and spontaneous generation was less widely supported (shows how scientific theories change over time with new tech + therefore new evidence).
•   Evidence for this:
-Studied fermentation to show such germs could cause the souring of alcohol + vinegar (led to development of pasteurisation process – widely used today to rid of these microbes).
-HOWEVER, most famously supported by his ‘swan-necked’ flask experiments (explained below).
•   Also established the principle of immunity + developed an effective way to prevent infectious disease (via vaccines):
-developed vaccine for chicken cholera
-used Koch’s work on anthrax to develop vaccine to prevent the disease.

The ‘swan-necked’ flask experiments…
•   Had identical flasks with long, drawn out necks (like swans) – they were not sealed.
•   Filled them with equal amounts of broth + sterilised broth within by boiling.
•   As broth cooled:
-air drawn in from outside BUT any microorganisms present in air couldn’t reach broth (trapped in narrow, curved neck) → no bacterial or fungal growth observed.
-BUT, for those flasks which he broke off ‘swan neck,’ bacterial growth occurred (bc contents of flask exposed to air + microbes in it) → showed microbes which contaminated the broth MUST be carried in air, not spontaneously generated (otherwise BOTH flasks would have had growth).
•   Significance reflected in Pasteur’s swan-necked flasks still on display in Paris museum (after nearly 150 years, broth still free of bacterial growth).
Variables
•   Independent: shape of flask tubing (straight or swan-necked)
•   Dependent: observed microbial growth (evident with cloudiness)
•   Controlled:
-type + amount of broth
-same sterilisation process (boiling) → ensured microbes could only enter via AIR and nothing else
-length of tubing

•   *NOTE: technically, the control is the STRAIGHT NECK flask, bc CURVED one = ALTERED SHAPE to see how microbes can affect it.

Koch (also 19th C) – expert on bacteriological techniques

Koch’s postulates
•   Developed a series of steps to determine if a particular microorganism is responsible for causing a disease – known as ‘Koch’s postulates’ (still in use today):
1. Observe blood of all diseased organisms under a microscope – same pathogen must be present in all.
2. Isolate pathogen from host + culture (grow) pure sample in lab.
3. When pure sample of pathogen is cultured, this is inoculated into a health host – if they develop the same symptoms as original host (i.e. become infected), this must be the microorganism causing disease.
4. The pathogen is isolated from this new host, cultured again and identified as the same as the original species.

Limitations of these postulates

•   Some pathogens (e.g. viruses, prions) cannot be grown in a lab dish bc they are not living cells.
-e.g. for virus can be viewed with EM microscope to learn more about it.
•   Tests usually done on animals (not ethical to do on humans) → not necessarily true that if a pathogen doesn’t infect an animal it won’t infect humans.


Therefore, both Pasteur and Koch’s work has influenced modern understanding of infectious disease which is based off their ideas, and has led to a further understanding of how disease arises and how it can be prevented/treated (shows positives of scientific collaboration also).

3.b) Distinguish between:
-prions
-viruses
-bacteria
-protozoans
-fungi
-macro-parasites
and name one example of a disease caused by each type of pathogen













3.c) The historical development for our understanding of the cause and prevention of malaria

Basic info about malaria
•   CAUSE: protozoan transferred via mosquito vector

Developments in understanding the CAUSE   
Developments in understanding PREVENTION

2000 years ago
•   Greeks described symptoms of the disease + called in malaria BUT didn’t know it was transferred via mosquito vector - thought it was linked to stagnant water → developed water systems to take away this water (& so prevent the disease).

1800s
•   Scientist Laveran examined blood of those with disease and without it → common microbe in blood of all sufferers (Koch’s 1st postulate) → discovered the malaria causing pathogen.
•   Scientist Ross was convinced of a link bw malaria + mosquitoes as a vector
-compared microbes present in mosquitoes which had bitten malaria sufferers with those of mosquitoes which had bitten non-sufferers → common microbe in those that had bitten sufferers (partially satisfied Koch’s 2nd postulate by growing in pure culture) → discovered main steps in transmission of malaria (+ its life cycle) and identified certain type of mosquito as vector.
•   Scientist Grassi showed mosquitoes which had bitten sufferers could pass pathogen onto non-sufferers (Koch’s 3rd p bc isolated pathogen could cause the disease in a healthy host when given it).
Such developments in 1800s relating to cause led to many developments in prevention later on…

Early 1900s
•   Anti-malarial drugs (discontinued due to side effects).
•   WHO implemented program attempting to eradicate malaria. Involved DDT spraying, biological control of mosquitoes (e.g. sterilising M or F so couldn’t breed) → measures not greatly successful (reflected in malaria as a worsening problem → currently threatens lives of 40% of world’s population).
Late 1900s
•   Start of development of malaria vaccine

CURRENT – 2014
•   Now know malaria parasite multiplies in liver + invades RBCs, spreading its proteins across these BUT there is only 1 pathway via which this can occur – scientists attempting to block this pathway and so kill parasite:
-achieved already in mice
-being furthered through genetically modified parasites in which gene responsible for protein transfer can be ‘switched off.’

3.d) Describe 1 infection disease in terms of:
-cause
-transmission
-host response
-major symptoms
-treatment
-prevention
-control

Cause
•   Pathogen (bacteria): Vibrio cholera (scientific name)

Transmission
•   Bacteria ingested in contaminated food or water (sewage infected)
-TOXIN produced by the bacteria infects bowel of human and also enters their faeces (→ can be further passed on from flies carrying the bacteria on their feet, unwashed hands etc).

Host response
•   This toxin causes production of antibodies (HOWEVER, usually not enough are produced → continued symptoms).

Major symptoms
•   Diarrhoea + vomiting → dehydration
•   Stomach cramps

Treatment
•   ORS mixture (oral rehydration solution – an electrolyte) → replacement of salts + fluids (lost in diarrhoea + vomiting).
•   Glucose intake (helps patients reabsorb fluid).

Prevention
•   Cholera vaccine (effective for 6 months).
•   Extra care: avoiding drinking unsterilised water/eating contaminated food e.g. boiling water or adding chlorine drops to water + waiting half an hour (both to kill cholera).

Control (big picture things)
PARTICULARLY IN DEVELOPING COUNTRIES
•   Vaccination programs
•   Effective sewerage systems (so doesn’t enter waterways used for drinking + washing)
•   Education e.g. proper hand washing

3.e) Identify the role of antibiotics in the management of infectious disease

What are antibiotics?

•   Chemicals made by microbes with a toxic effect on bacteria (and sometimes fungi) – inhibits growth of OR destroys
*NOT VIRUSES!
→ their main role is to rid a person of their bacterial (and sometimes fungal) infections only.
•   E.g. penicillin
-disrupts cell wall growth in bacteria

3.f) Info from secondary sources to discuss problems relating to antibiotic resistance

How does antibiotic resistance develop?

By following the steps of natural selection…
•   Person has a bacterial infection e.g. food poisoning (antibiotic given to treat it)
-NATURALLY, there is VARIATION within this bacterial population: some are resistant to the antibiotic, some are not (e.g. only 90% may die while the 10% resistant live).
•   This 10% resistant survive + reproduce → pass on this favourable characteristic to their offspring.
•   Over time, population of bacteria becomes resistant to those antibiotics → person can no longer treat this bacterial infection with these (→ new ones must be created as these no longer effective).

Causes:
•   Widespread use of antibiotics increases the chance of this happening
•   Often used for viral disease (cold, flu) which have no effect
•   People often do not take the antibiotics for the whole course (more bacteria survive)                    - person stops antibiotic early (some resistant and some not resistant bacteria alive → GENE TRANSFER - gene of resistance passed to bacterial without it)
•   Food-producing animals are given antibiotics (overexposure to antibiotics on consumption)

Types of antibiotic resistance

1.Inherent (natural)
2.Acquired
*vertical gene transfer
-once resistant genes developed, they are transferred directly to all the bacteria’s offspring during DNA replication (acquired from resistant parent).
*horizontal gene transfer
-resistance transferred via DNA between bacteria of same or even diff species.

Why is it recommended NOT to stop taking the course of antibiotics early (or taking them if have e.g. virus, NOT a bacterial infection)?
•   If a person does this, some non-resistant bacteria that should have died will actually survive → ‘gene transfer’ could occur, with the resistant gene passed on to the bacteria without it → more resistant bacteria than there should be (which reproduce etc).
What are the problems relating to antibiotic resistance?
•   Diseases that COULD be cured may become untreatable → more deaths (especially in third world countries).
•   Some bacterial infections are becoming very difficult to treat e.g. superbugs Golden Staph and TB → having to resort to very expensive, strong antibiotics
New types of antibiotic must be developed to treat the same bacterial infections.

4. Defence against disease

5. The immune response

6. Epidemiological studies

7. Modern Strategies

These topics can be extremely confusing which is why I recommend looking at the notes which have also been uploaded to this website! They are detailed with lots of helpful diagrams and flow charts which will allow you to properly understand all the components, especially for the immune response.

[TheAspiringDoc]

Hi teodora,

Thanks for posting your guide!

I thought it might be of some use if I were to add my* notes (*which I'll admit aren't technically mine as approx. one third is just copied and pasted with a few minor tweaks by yours truly ) on to elaborate on some concepts?



Mitosis

Spoiler

Cell growth stops at this stage and cellular energy is focused on the orderly division into two daughter cells or two daughter nuclei? . A checkpoint in the middle of mitosis (the Metaphase Checkpoint) ensures that the cell is ready to complete cell division.
 
More on Mitosis
 
Mitosis is a part of the cell cycle process by which chromosomes in a cell’s nucleus are separated into two identical sets of chromosomes, each in its own nucleus.
 
The stages of mitosis are: prophase, metaphase, anaphase, and telophase.
 
During mitosis, the chromosomes, which have already duplicated, condense and attach to fibers that pull one copy of each chromosome to opposite sides of the cell. The result is two genetically identical daughter nuclei. The cell may then divide by cytokinesis to produce two daughter cells.
 
Errors can occur during mitosis. One such error is multipolar mitosis, in which the wrong amounts of daughter cells areproduced. Other errors during mitosis can induce apoptosis (programmed cell death) or cause mutations. Certain types of cancer can arise from such mutations.
 
The Phases of Mitosis
 
Prophase
 
The complex of DNA and proteins contained in the nucleus, known as chromatin, condenses in preparation for division. Mitotic spindles also begin to form.
 
Metaphase
 
The cell’s chromosomes align themselves in the middle (or ‘equator’) of the cell.
 
There is a checkpoint between metaphase and anaphase, to ensure that the mitotic spindle has successfully attached to the centromeres of each chromosome, so that sister chromatids can be pulled apart during anaphase.
 
Unsure about the above (metaphase checkpoint)
 
Anaphase
 
Chromosomes split (into sister chromatids) and the sister chromatids move to opposite poles of the cell through a type of cellular “tug of war” in which spindle fibres are like ropes and the centrioles are like “teams”, who are tugging them apart.
 
Telophase
 
The sister chromatids reach opposite poles and the small nuclear vesicles in the cell begin to reform around the group of chromosomes at each end.
 

Proto-Oncogenes (Ras and Myc)

Spoiler

Proto-oncogenes produce protein products that normally enhance cell division or inhibit normal cell death. The mutated forms of these genes are called oncogenes. 
 
Ras
 
Ras refers to a family of related proteins. All Ras proteins are involved in transmitting signals within cells (cellular signal transduction). When Ras is ‘switched on’ by incoming signals, it subsequently switches on other proteins, which ultimately turn on genes which are involved in cell growth, differentiation and survival. As a result, mutations in ras genes can lead to the production of permanently activated Ras proteins. This can cause unintended and overactive signaling inside the cell, even in the absence of incoming signals.
 
Because these signals result in cell growth and division, overactive Ras signaling can ultimately lead to cancer. The three Ras genes in human (H-ras, K-ras, and N-ras) are the most common oncogenes in human cancer; mutations that permanently activate Ras are found in 20% to 25% of all human tumours and up to 90% of certain types of cancer (e.g., pancreatic cancer). For this reason, Ras inhibitors are being studied as a treatment for cancer.
 
Ras proteins function as molecular switches that control intracellular signaling networks. Ras-regulated signal pathways control such processes as actin cytoskeletal integrity, proliferation, differentiation, cell adhesion, apoptosis, and cell migration. Ras and ras-related proteins are often deregulated in cancers, leading to increased invasion and metastasis, and decreased apoptosis DOESN’T THAT MAKE RAS A TUMOUR SUPPRESSOR GENE?
 
Myc
c-Myc is a regulator gene that codes for a transcription factor.  The protein encoded by this gene plays a role in cell cycle progression, apoptosis and cellular transformation.
 
Myc mutated in many cancers in a way such that it is persistently expressed. This leads to the unregulated expression of many genes, some of which are involved in cell proliferation, and results in the formation of cancer.
 
A common human chromosomal translocation involving Myc is critical to the development of most cases of Burkitt Lymphoma. Malfunctions in Myc have also been found in carcinoma of the cervix, colon, breast lung and stomach. Myc is thus viewed as a promising target for anti-cancer drugs.           
 
Myc activation results in numerous biological effects. The first to be discovered was its capability to drive cell proliferation (by upgrading cyclins and down regulating p21), but it also plays a very important role in regulating cell growth (by upregulating ribosomal RNA and proteins), apoptosis (by downregulating Bcl-2), differentiation, and stem cell self-renewal. Myc is a very strong proto-oncogene and it is very often found to be upregulated in many types of cancers. Myc overexpression stimulates gene amplification, presumably through DNA over-replication.
 
A major effect of Myc is B cell proliferation.                                                                                                                                                                                                                                                                                                   

Tumour Suppressor Genes (p53 and APC)

Spoiler

A tumour suppressor gene, or an anti-oncogene, is a type of gene that makes a protein called a tumour suppressor protein that helps control cell growth and protects a cell from one step on the path to cancer. Mutations in the DNA of this gene that cause a loss or reduction in its function can lead to cancer, usually in combination with other genetic changes.
 
Makes proteins that normally prevent cell division or cause cell death.
 
p53
 
p53 is a tumour suppressor protein and transcription factor that is altered in many forms of cancer. The gene tumour suppressor gene TP53 codes for p53. p53 has been described as "the guardian of the genome” because of its role in conserving stability by preventing genome mutation. The gene is the most frequently mutated gene (>50%) in human cancer, indicating that the TP53 gene plays a crucial role in preventing cancer formation
If a person inherits only one functional copy of the TP53 gene from their parents, they are predisposed (liable) to cancer and usually develop several independent tumours in a variety of tissues in early adulthood. This condition is rare, and is known as Li-Fraumeni syndrome. However, mutations in p53 are found in most tumour types, and so contribute to the complex network of molecular events leading to tumour formation.
In the cell, the p53 (transcription factor) protein binds to DNA, which in turn activates the production of a protein called p21 that interacts with a cell division-stimulating protein (cdk2). When p21 is complexed with cdk2 the cell cannot pass through to the next stage of cell division. Mutant p53 can no longer bind DNA in an effective way, and as a consequence the p21 protein is not made available to act as the 'stop signal ' for cell division. Thus cells divide uncontrollably, and form tumours.
In other words, p21 blocks the activity of a cyclin-dependent kinase that is required to proceed through G1. This ‘block’ allows time for the cells to repair the DNA before it is replicated. If the DNA damage is so extensive that it cannot be repaired, p53 triggers the cell to commit suicide. (IS THIS NECROSIS OR APOPTOSIS??)
The amount of information that exists on all aspects of p53s normal function and mutant expression in human cancers is now vast, reflecting its key role in the pathogenesis of human cancers. It is clear that p53 is just one component of a network of events that culminate in tumourformation.
 
 
 
APC
 
APC, or Adenomatous Polyposis Coli, is a tumour suppressor protein that is encoded by the tumour suppressor gene APC. Mutations in both copies of the APC gene can lead to familial adenomatous polyposis of the colon (FPC). The protein made by the APC gene plays a critical role in several cellular processes that determine whether a cell may develop into a tumour. The APC protein helps control how often a cell divides, how it attaches to other cells within a tissue, or whether a cell moves within or away from a tissue. This protein also helps ensure that the chromosome number in cells produced through cell division is correct. The APC protein accomplishes these tasks mainly through association with other proteins, especially those involved in cell attachment and signaling.
 
The APC protein is a negative regulator (meaning that it decreases the concentrations of) that controls Beta-catenin concentrations and interacts with E-cadherin, which are involved in cell adhesion.
 
E-cadherin, or epithelial cadherin, is a tumour suppressor gene that is involved in the cellular adhesion within a tissue. If E-cadherin loses function or expression, cancer cells acquire the capability of metastasis.
 
Beta-catenin is a protein that in humans is encoded by the CTNNB1 gene. Beta catenin regulates the coordination of cell-cell adhesion and gene transcription.
 

[nibblez16]

Do we need to know about Macfarlane Burnets contribution?

[stephanieazzopardi]

Do we need to know about Macfarlane Burnets contribution?

Hi nibblez16,

The only information you would need to know, is what is in the title for section number 5 for SFBH: MacFarlane Burnet’s work in the middle of the twentieth century contributed to a better understanding of the immune response and the effectiveness of immunisation programs

They may ask you to assess his contribution based on your understanding of the content in section 5.  but it's not a syllabus dot point so I wouldn't worry about it too much. 

[Skidous]

If there are any more questions please direct them towards the question thread