[Tullia]

(Original post by Mocking_bird)
So could be

Yeah like the whole... environmental is polygenic and that kinda dealy

Ah, you mean the stuff on discontinuous and continuous variation. I'm with you. I'll see what I can pluck out and put down.

[britash]

I thought the graph would look identical for both diffusion and facilitated diffusion, so how can you tell its facilitated? x

[Tullia]

(Original post by britash)

I thought the graph would look identical for both diffusion and facilitated diffusion, so how can you tell its facilitated? x

No, they would be different.

The evidence supporting facilitated diffusion is the fact that after a certain level of external concentration of substance, the curve levels off. This is the point at where the channel proteins are saturated with molecules.

[Mocking_bird]

(Original post by britash)

I thought the graph would look identical for both diffusion and facilitated diffusion, so how can you tell its facilitated? x

Tullia may come swoop down to correct me again () but i thinkkk.. Nevermind, he just ninja'd me instead

But think of it like the enzyme substrate graph when it plateaus its because the enzymes active sites are saturated.. so relating it to faciliated diffusion, the carrier/channel proteins are saturated so the limiting factor is the time it takes for the molecule to pass through the protein.. whereas normal diffusion wouldnt flatten out.

[Tullia]

(Original post by Mocking_bird)
Tullia may come swoop down to correct me again () but i thinkkk.. Nevermind, he just ninja'd me instead

But think of it like the enzyme substrate graph when it plateaus its because the enzymes active sites are saturated.. so relating it to faciliated diffusion, the carrier/channel proteins are saturated so the limiting factor is the time it takes for the molecule to pass through the protein.. whereas normal diffusion wouldnt flatten out.

You've done it to me in the past.

Very well explained though. We make a pretty good team.

[britash]

(Original post by Mocking_bird)
Tullia may come swoop down to correct me again () but i thinkkk.. Nevermind, he just ninja'd me instead

But think of it like the enzyme substrate graph when it plateaus its because the enzymes active sites are saturated.. so relating it to faciliated diffusion, the carrier/channel proteins are saturated so the limiting factor is the time it takes for the molecule to pass through the protein.. whereas normal diffusion wouldnt flatten out.

(Original post by Tullia)
No, they would be different.

The evidence supporting facilitated diffusion is the fact that after a certain level of external concentration of substance, the curve levels off. This is the point at where the channel proteins are saturated with molecules.

Okay, cool. Thank-you both, that makes more sense now.
I clearly need to read up on all this diffusion/osmosis topic D:!!!! xoxo

[britash]

(Original post by Tullia)
You've done it to me in the past.

Very well explained though. We make a pretty good team.

Do you both know each other? *pokes manchester*??
You both are always on here and are always willing to help! Thank-you! x

[Tullia]

(Original post by britash)
Do you both know each other? *pokes manchester*??
You both are always on here and are always willing to help! Thank-you! x

We do know one another quite well in TSR terms, but we've never met in person. As you say though, we are local to one another in that both live in the Manchester area.

It says you're from the North West, so whereabouts would that be then?

And you're welcome. It helps us as well as it is a kind of revision and if we come across a question we can't answer then we know we need to do some more learning.

[britash]

(Original post by Tullia)
We do know one another quite well in TSR terms, but we've never met in person. As you say though, we are local to one another in that both live in the Manchester area.

It says you're from the North West, so whereabouts would that be then?

And you're welcome. It helps us as well as it is a kind of revision and if we come across a question we can't answer then we know we need to do some more learning.

Manchester ..
Yeah I find it useful I can ask someone who replies quickly.
Plus I find myself learning things if I explain them to some-one else

[thescientist17]

(Original post by britash)
Where are they? I cant find them

I had to search the thread..

Here they are; and I'm not trying to take credit from them! Thanks to The Assassin

[britash]

(Original post by thescientist17)
I had to search the thread..

Here they are; and I'm not trying to take credit from them! Thanks to The Assassin

Ah thank-you. I found them a while ago, but thanks anyway.
Just to let you know, there's a mistake on the first point about a triglyceride.. it doesnt have a phosphate molecules, but the notes he wrote said that it does!!! xx

[Ganep001]

Any ideas on the potential 6 marker?

[Tullia]

Variation

Organisms differ from one another.

Differences between species is called interspecific variation.

Differences between individuals in the same species is called intraspecific variation.

Intraspecific variation is due to differences in genetic make up and/or the effects of their environment.

Phenotype- an organism's total physical appearance, constitution and behaviour.

Genotype- an organism's genetic make up (i.e. the alleles an organism possesses).

Sources of variation

Genetic variation (variation in genotypes) may be passed on to the next generation so it is the most important type of variation in evolutionary terms. It arises by:

• Mutations- the ultimate source of all genetic variation. A mutation is a change in the DNA base sequence of an individual that may produce a new form of a gene (a new allele).
• Reshuffling of alleles during sexual reproduction by: events in meiosis (crossing over and random segregation) and random fertilisation.

Environmental variation is acquired during the lifetime of the individual and cannot be passed on to the offspring. Most characteristics are affected in some way by the environment. The greater the environmental influence the less distinct the phenotypic groups become, i.e. the variation becomes more continuous.

Genetic- e.g. blood group
Environmental- e.g. dialect
Combination of both- e.g. intellect

Patterns of variation in populations

Variation in a population may be continuous or discontinuous.

Discontinuous variation occurs when an individual can have one of a narrow range of phenotypes / can fall into a narrow range of categories. It usually occurs in characteristics that are controlled by single genes where there is little environmental influence.

[insert image with distinct bar chart and distinct peaks]

Discontinuous characteristics are rare in humans and other animals, but are more common in plants. Some examples are human blood group, detached ear lobes, flower colour, seed colour, etc. These characteristics are very useful for geneticists because they give clear-cut results.

Continuous variation occurs when an individual can have one of a range of phenotypes which tend to be quantitative, with overlaps between categories. It usually occurs when a characteristic is controlled by several genes (it is polygenic) or where there is a lot of environmental influence.

[insert image with non-distinct bar chart and non-distinct peaks]

Continuous characteristics are very common in humans and other animals. Some examples are height, hair colour, heart rate, muscle efficiency, intelligence, growth rate, rate of photosynthesis, etc.

Sometimes you can see the effect of both variations. For example, the histogram of height of humans can be bimodal (i.e. two peaks). This is because the two sexes (a discontinuous characteristic) each have their own normal distribution of height (a continuous characteristic).

[insert image with bimodal peak]


I can't be bothered searching for any images just now, but might add them later. Although, this is just some write up for people to tweak for their own use and so you can always add them yourselves which is why I've given descriptions of what they should be.

M_B, do you think sampling would be helpful? It does link in with variation as it is how you analyse and interpret data relating to these variations. Let me know.

[britash]

Has anyone got any notes on chapters 13 or 16? x

[Tullia]

(Original post by britash)
Has anyone got any notes on chapters 13 or 16? x

What topics are they? I'm happy to help and so not being funny, but it would allow me to help you.

[britash]

(Original post by Tullia)
What topics are they? I'm happy to help and so not being funny, but it would allow me to help you.

Thanks:
On 13, The whole Blood Vessels section really.
I've got your notes you wrote yesterday on cohesion tension theory and root pressure ones, which are useful
On 16, the antibiotic resistance, how it causes mutation, that whole little topic really.

My teacher just told us to research the anitibiotic resistance for the MRSA and TB, so naturally, noones notes are correct :/
Thanks x

[Tullia]

(Original post by britash)
Thanks:
On 13, The whole Blood Vessels section really.
I've got your notes you wrote yesterday on cohesion tension theory and root pressure ones, which are useful
On 16, the antibiotic resistance, how it causes mutation, that whole little topic really.

My teacher just told us to research the anitibiotic resistance for the MRSA and TB, so naturally, noones notes are correct :/
Thanks x

OK, well I'll do Chapter 16 (antibiotics) now and then perhaps do Chapter 13 (blood vessels) later on.

Antibiotics

Antibiotics are chemicals produced by or derived from microorganisms (e.g. bacteria and fungi), that kill or prevent the growth of other microorganisms.

Antibiotics only work on bacterial cells.

Bacteriostatic - inhibits the growth of bacteria.
Bacteriocidal - kills bacteria.

How do antibiotics work?

Since the introduction of penicillin, a variety of other classes of antibiotics have been discovered and each class of antibiotics has its own mode action.

• Penicillin: belongs to a class of antibiotics called B-lactams; this class of drugs interferes with peptidoglycan (murin) cell wall structure. These eventually weaken the cell walls and the cells burst (lysis).

Key point to note is that they cause cell walls to burst.

• Tetracycline: broad spectrum antibiotics that disable bacteria by interfering with the cells ability to make proteins. This prevents the bacteria growing.

Key point to note is that they prevent protein synthesis.

• Quinolone: this class of antiobiotics interferes with the bacterial cells ability to copy its DNA; something that must be done before a cell can divide and multiply. The DNA of human cells is packaged differently, so its replication is not disabled by quinolones.

Key point to note is that they prevent DNA replication.

Development of antibiotic resistance

Antibiotic resistance is a natural phenomenon. Variation in antibiotic resistance is due to variation in certain genes carried by the bacteria. These genes for resistance to antibiotics are usually found on the plasmid.

What is a plasmid?

A plasmid is a small loop of circular DNA (separate from linear DNA).

Explanation as to how gene mutation can give rise to genetic variation.

Gene mutation causes a difference in the sequence of amino acids, which will code for different proteins. Different enzymes will be produced.

When an antibiotic is used, bacteria that can resist that antibiotic have a greater chance of survival than those that are susceptible. Susceptible bacteria are killed or inhibited by an antibiotic, resulting in a selective pressure for the survival of resistant strains of bacteria. When you take an antibiotic the least resistant bacteria die first. In this way resistant forms of the bacteria are selected. As a result of this, resistance will accumulate in the bacterial population and the antibiotic will eventually stop working.

How does antibiotic resistance spread?

Genetically, antibiotic resistance spreads through bacterial populations both vertically, when new generations inherit antibiotic resistant genes, and horizontally, when bacteria share or exchange sections of genetic material with other bacteria. Horizontal gene transmission can even occur between different bacterial species. Environmentally, antibiotic resistance spreads as bacteria themselves move from place to place; bacteria can travel via aeroplanes, water and wind. People can pass the resistant bacteria to others; for example, by coughing or contact with unwashed hands.

Vertical gene transmission

The plasmid carrying the antibiotic gene is replicated when the cell divides. All subsequent generations will carry the resistant plasmid.

Horizontal gene transmission

The process of conjugation via pilus allows plasmids to be replicated and transferred to a different bacterial cell.

[Tullia]

What is tuberculosis (TB)?

Tuberculosis (TB) is a disease caused by germs that are spread from person to person through the air (droplet infection). TB usually affects the lungs, but it can also affect other parts of the body, such as the brain, the kidneys, or the spine. In most cases, TB is treatable; however, persons with TB can die if they do not get proper treatment.

What is multi drug resistant tuberculosis (MDR TB)?

Multi drug resistant TB (MDR TB) is TB that is resistant to at least two of the best anti-TB drugs, isoniazid and rifampicin. These drugs are considered first-line drugs and are used to treat all persons with TB disease.

What is extensively drug resistant tuberculosis (XDR TB)?

Extensively drug resistant TB (XDR TB) is a relatively rare type of MDR TB. XDR TB is defined as TB which is resistant to isoniazid and rifampicin, plus resistant to any fluoroquinolone and at least one of three injectable second-line drugs (i.e. amikacin)

Because XDR TB is resistant to first-line and second-line drugs, patients are left with treatment options that are much less effective.

XDR TB is of special concern for persons with HIV infection or other conditions that can weaken the immune system. These persons are more likely to develop TB disease once they are infected, and also have a higher risk of death once they develop TB.

How is TB spread?

Drug-susceptible TB and MDR TB are spread the same way. TB germs are put into the air when a person with TB disease of the lungs or throat coughs, sneezes, or sings. These germs can float in the air for several hours, depending on the environment. Persons who breathe in the air containing these TB germs can become infected.

TB is not spread by:

• shaking someones hand
• sharing food or drink
• touching bed linens or toilet seats
• sharing toothbrushes
• kissing

How does drug resistance happen?

Resistance to anti-TB drugs can occur when these drugs are misused or mismanaged. Examples include when patients do not complete their full course of treatment; when healthcare providers prescribe the wrong treatment, the wrong dose, or length of time for taking the drugs; when the supply of drugs is not always available; or when the drugs are of poor quality.

Who is at risk for getting MDR TB?

Drug resistance is more common in people who:

• do not take their TB medicine regularly
• do not take all of their TB medicine as told by their doctor or nurse
• develop active TB disease again, after having taken TB medicine in the past
• come from areas of the world where drug-resistant TB is common
• have spent time with someone known to have drug-resistant TB disease

---

What is MRSA?

Staphylococcus aureus is a common bacterium (germ). It lives on the skin or in the nose of 20-40% of people without causing any problems. These people are described as being 'colonised' with staphylococcus aureus.

Occasionally these germs cause skin infections such as boils, abscesses, and spots, especially if the skin has been scratched.

Staphylocci (and many other bacteria) will sometimes get into the bloodstream and travel to the internal parts of the body to cause serious infections. This is more likely to occur if the person is already unwell or debilitated or have a poor immune system, or if they had an invasive investigation or operation in hospital.

Meticillin is an antibiotic which is closely related to flucloxacillin, the antibiotic most commonly prescribed for 'skin infections'.

Meticillin resistant staphylococcus aureus describes a variety of staphylococcus aureus that has become resistant to treatment with some antibiotics inlcuding penicillins, methicillin and flucloxacillin, and subsequently there are a limited number of antibiotics which can be used to treat the germ if it causes an infection.

MRSA can also live harmlessly on the skin and in the nose and is no more virulent and therefore no more harmful than ordinary staphylococcus aureus. MRSA is not a risk to healthy people in the community.

If a person is 'colonised' with MRSA and has no signs of infection, no treatment is required. If the person has an infection caused by MRSA their doctor will prescribe antibiotics which the organism is sensitive to.

How is MRSA identified?

If an infection is suspected an appropriate sample or wound swab should be sent to the microbiology laboratory for testing. If staphylococcus aureus is detected further test are done to see which antibiotics the bacteria is sensitive to.

Some hospitals now test all healthy people prior to them having major surgery to identify whether they are 'colonised' with MRSA. This is known as MRSA screening. If MRSA is identified, the surgeon will arrange for the patient to undergo a programme of skin washes and nasal ointments to try and clear the MRSA prior to their surgery.

How is MRSA spread?

Staphylocci are spread from person to person, usually by direct skin contact. Equipment which has not been properly cleaned between being used on different people may also be a reservoir of the organisms.

Preventing the spread of MRSA is by thorough regular hand washing. As MRSA has been shown to survive in dust, thorough cleaning of the environment is important. Hospital visitors do not generally need to wear protective clothing but they must wash and dry their hands thoroughly after contact.

[Mocking_bird]

(Original post by Tullia)
x

Saved and printed, thanks
Sampling would be helpful i think, but like i said last time, only if you get time

[Tullia]

(Original post by Mocking_bird)
Saved and printed, thanks
Sampling would be helpful i think, but like i said last time, only if you get time

I've got a couple of requests for other topics, but I'll get onto doing it later on probably.

What do you think of what I've wrote so far regarding antibiotics? I mean in terms of content, and not necessarily my terrible layout and English.

Oh, and how did the BIOL2 mock go? Was it the Jan '12 paper?