bio processes unit 5

7/29/2019 Bio Processes Unit 5

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Adam Clarke www.brain-freeze.co.uk

Biology Unit 5 Revision Summary

Slow twitch muscle fibres Fast twitch muscle fibres

Red colour rich in oxygen storing myoglobin White less myoglobin therefore less oxygen

storedLong-term maintaining posture/ long-distance

running

Short-term sprinting, eye movement

Aerobic respiration releases energy slowly Anaerobic respiration using glucose from

glycogen

Lots of mitochondria/myoglobin and rich blood

to supply oxygen to muscle

Fewer mitochondria/myoglobin more

myofibrils

Contract slowly Contract quickly

Myoglobin protein that holds oxygen required for muscles

Myofibrils long cylindrical organelles made of proteins specialised for contraction made of units

of sarcomeres

Sarcomeres- made of myosin and actin

Sarcoplasm muscle cells cytoplasm

Sarcolemma cell membrane of muscle fibre cells

Myosin two long polypeptide chains twisted together ending with a globular head that has ADP

and Pi attached to it. make up thick myofilaments

Actin made up of actin monomers has myosin binding sites at regular intervals - make up thin

myofilaments

Tropomyosin wraps around double actin chains, in a relaxed muscle it covers up the myosinbinding sites

Troponinattached regularly along tropomyosin chain

How muscles contract

1) calcium ions bind to troponin molecules changing their shape

2) Troponin molecules pull on the tropomyosin molecules they are attached to.

3) The tropomyosin moves from the myosin binding sites exposing them ready for action.

4) Myosin head binds to the actin forming an actomyosin bridge

5) ATP and inorganic phosphate are released from the myosin head causing the myosin to change

shape with the head bending forward moving the actin filament along the myosin filament

shortening the sarcomere.

6) Free ATP binds to the head causing another shape change in the myosin so the binding of the

head to the actin strand is broken.

7) This alongside the use of calcium ions activates ATPase in the myosin head

8) ATP is hydrolysed releasing energy to return the myosin head to its original position primed with

ADP and Pi, ready for the process to restart.

9) Calcium ions remain in the sarcoplasm and the cycle is repeated. Some are pumped into the

sarcoplasmic reticulum using ATP energy.

10) Troponin and tropomyosin return to their original positions and the contraction is complete, the

muscle fibre becomes relaxed.


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Movement

1) Muscle contraction exerts a pull on a bone

2) When they relax they stop contracting and become capable of being pulled back to their original

shape

3) Muscles are found in pairs

4) One pulls the bone in one direction, the other pulls it back to its original position - working in

opposition to each other as antagonistic pairs

Antagonistic pair muscles work in opposition of one another

Bones matrix of collagen and calcium salts

Cartilage chondrocytes collagen fibrils elastic

Tendons- bundles of collagen fibres connects muscle to bone

Ligaments bone to bone

Joints ball and socket, pivot, saddle, hinge

Control of heartbeat

1)The sinoatrial node (SAN the hearts pacemaker) sends a wave of electrical excitation causing the

atria to contract

2)Excitation spreads to similar tissue called the atrioventricular node.

3)The AVN is excited as a result of the SAN from which the wave of depolarisation passes to the

bundle of His

4)The bundle of His carries the electrical excitation from the AVN down to the Purkyne tissue.

(The Purkyne tissue penetrates through the septum of the heart spreading between and around the

ventricles)

5) As the depolarisation travels through the tissue it sets of the contraction of the ventricles starting

at the bottom and so squeezing blood out of the heart.

Bodily response to exercise

1) Atria fill with blood at start of cardiac cycle with stretch receptors in the muscle walls of the heart

responding to the stretching by sending nerve impulses to the cardiovascular control centre.

2) At the start of a period of exercise more blood than usual returns to the heart because the big

muscle blocks in the legs and arms squeeze more blood along the veins when they work

3)Increased blood flow into the atria causes the receptors to be more stretched than usual making

them send more nerve impulses to the cardiovascular centre of the brain.

4) This consequently sends more nerve impulses along the sympathetic nerve to the SAN causing an

increase in heart rate.

5) An increase in stretching of the heart atrial muscle as blood returns from the body also makes the

muscles contract harder to increase the volume of blood released in every stroke.

6) Baroreceptors found in the sinuses of the carotid arteries in the neck are also important in the

feedback control of the heart rate particularly as exercise ends.

7) An increase in blood pressure of the arteries stretches the baroreceptors which send nerve

impulses to the cardiovascular centre causing the parasympathetic system to slow down the heart

rate and cause a widening of the blood vessels to lower blood pressure.


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8) The reverse process occurs when exercise starts as the blood vessels dilate with adrenaline

causing the blood pressure to fall

9) The stretching of the baroreceptors is reduced and when they dont stimulate the cardiovascular

control centre it immediately sends signals along the sympathetic nerve to stimulate the heart rate

and increase blood pressure again.

Control and regulation of breathing

1) Inhalation occurs when impulses from the respiratory centre (medulla) travel along sympathetic

nerves causing the intercostal muscles and the diaphragm to contract.

2)As the lungs inflate, stretch receptors in the walls of the bronchi send nerve impulses increasingly

rapidly to the respiratory centre.

3)These impulses eventually inhibit the respiratory centre and stop stimulating the breathing

muscles.

4) Breathing in stops and with the relaxation of the muscles, exhalation occurs.

Homeostasismaintenance of a steady internal state in the body regardless of changes in the

internal or external conditions

Negative feedback systema change is conditions is registered by receptors and results in effectors

stimulated to restore equilibrium

Positive feedbackeffectors work to increase the effect which has triggered the response

Cardiac volumevolume of blood pumped in each heartbeat

Cardiac outputcardiac volume x heart rate

Sympathetic nervous systemexcitatory speeds up heart rate

Parasympathetic inhibitory slows heart rate

Baroreceptor sensors sensitive to pressure

Components of lung volume

Ventilation rate = tidal volume x frequency of respiration

Control and regulation of breathing

1) The respiratory centre (in the medulla of the hindbrain) sends impulses along sympathetic nerves

causing the intercostal muscles and diaphragm to contract.

2) As the lungs inflate stretch receptors in the walls of the bronchi send nerve impulses to the

respiratory centre

3) Eventually the nerve impulses inhibit the respiratory centre causing it to stop stimulating

breathing muscles.

4) As breathing in stops, the muscles relax and exhalation starts.


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Homeostasis and breathing

1) Chemoreceptors sensitive to the level of carbon dioxide send impulses back to the main

respiratory centre when carbon dioxide levels rise.

2) Impulses are then sent out to the breathing muscles so the breathing rate changes to remove the

extra carbon dioxide.

3) The chemical sensors and the stretch receptors of the muscles and lungs act on the respiratory

centre to maintain the increase in ventilation until exercise is complete.

Temperature limits

Low critical temperature this is the point at which thermoregulatory mechanisms are no longer

sufficient in conserving heat.

Low lethal temperature- individual dies due to low temperature

High critical temperature thermoregulation can no longer keep temperatures down - faster

metabolic rate with increase in temperature continues the increase in metabolic rate.

Mechanisms to increase temperature Mechanisms to decrease temperature

Vasoconstriction = arterioles constrict less

blood to surface less heat loss

Vasodilation arterioles near surface of skin

dilate more blood flows so heat can be lost

More Subcutaneous fat Less subcutaneous fat

Shivering involuntary muscle contraction Sweating high specific heat capacity of water

allows absorption of heat

Increased metabolism more respiration more

heat released

Lowered metabolism

Control of core blood temperature

1) Hypothalamus contains temperature receptors to detect changes in temperature of the blood

flowing through it

2) At higher temperatures a heat loss centre is activated sending impulses along motor nerves to

effectors that increase blood flow and sweating/ lower metabolic rates.

3) If the temperature drops the heat gain centre reacts sending nerve impulses to the skin for

vasoconstriction / for involuntary muscles contractions (shivering) and increased metabolism.

Heart rate

ECG - Electrocardiograph

P wavedepolarisation of the SAN / related tissue in the atrium

QRS complexspread of excitation through the ventricles

T wave- rapid repolarisation of the Purkyne tissue in the ventricles

Arrhythmianormal electrical activity of the heart is disrupted and the rhythm of the contraction

of the muscles will change.

Ischaemicrestriction in blood supply

Atrial fibrillationatria beating too fast and ineffectively


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Tachycardiaheart beats too fast

Ventricular fibrillationventricles lose rhythm contract erratically and weakly little blood is

pumped into the arteries fall in blood pressure heart attack / body brain starved of blood

Defibrillatorlarge electric shock to normalise abnormal heart rhythm

Osteoarthritis

1) Cartilage roughens and erodes

2) Bone ends thicken and the synovial membrane makes more fluid joint swells and the joint

capsule thickens too.

3) The whole joint becomes swollen and painful

4) The cartilage wears away completely until the bone ends touch5)The bone ends wear away changing the shape of the joint causing severe pain

Anabolic steroids

1) Steroids pass through the cell surface membrane

2) In the cell they bind with receptor molecules

3) The complex formed acts as a transcription factor

4) the complex binds to the DNA and switches on particular genes linked to protein synthesis.

5) The RNA produced is affected changing the type and numbers of proteins and subsequently the

enzymes produced.

Erythropoietin

1) The erythropoietin peptide hormone binds to a receptor in the cell surface membrane

2) The membrane bound complex activates a second messenger in the cell cytoplasm

3) A protein kinase cascade is triggered.

4) Different proteins are activated until final product

5) This enters the nucleus and acts as a transcription factor switching on the genes linked to protein

synthesis of the enzymes required for the production of more red blood cells.

Hormones can switch on genes

1) Proteins called transcription factors in cells control the transcription of genes

2) These bind to DNA sites near the start of the genes and increase (activator) /decrease (repressor)

the rate of transcription

3) Hormones can bind to transcription factors to change body temperature

4) At cold temperatures thyroxine is released which binds to the thyroid hormone receptor causing it

to act as activator.

5) The transcription rate increases to produce more protein which increases the metabolic rate to

increase body temperature


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Ethical issues regarding performance-enhancing drugs

For AgainstAthletes have the right to make their own

decision

Some are illegal

Drug-free sport isnt fair anyway different

athletes have access to various training facilities,

coaches, equipment.

Some may gain an advantage by taking drugs

not through hard work or training

Athletes that want to compete at high levels may

only be able to using performance enhancing

drugs

Serious health risks blood pressure and heart

problems

Some may not be fully informed about the risks


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Sensitivity in plants

Meristemareas of cell division and elongation which occur behind the tip of a root or shoot

Red light (580 to 660nm)

stimulates germinationFar red light (700-730nm)inhibits germination

Phytochrome plant photoreceptor blue-green pigment that reacts with different types of light

Pr - absorbs red light (leads to flowering)

Pfrabsorbs far red light (in this form the plant is germinating, growth of internodes are inhibited as

etiolation is not necessary)

(Pfr to Pr in dark)

When one form absorbs light it converts reversibly into the other form.

Photoperiods

Long-day plantsbuild up of Pfr during daylight hours stimulates flowering

Short-day plantslack of Pfr stimulates flowering

Tropism plant growth in response to an environmental cue

Phototropism growth of plant in response to light

Positive tropismgrowth towards the stimulus e.g. shoots grow towards the light

Negative tropismgrowth away from stimulus roots grow away from light

Geotropism

growth of plant in response to gravity shoots negatively geotropic / roots positivelygeotropic.

Auxinsgrowth factor that stimulates growth of shoots by cell wall elongation.

Unilateral lightlight affecting plant from one side

Indoleacetic acid auxin in tips of shoots that controls tropisms causing uneven growth

Phototropism IAA moves to shaded parts to increase growth towards light


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Myelin sheathfatty layer around nerve fibre made of Schwann cells repeatedly wrapped around

themselves.

Nodes of ranviergaps between the Schwann cells

Axonfibres that carry impulses away from nerve cell body

Dendrons fibres that carry impulses towards the cell body

Action potential

1) Stimulusexcitation of the neurone cell membrane causing sodium ion channels to open

making it permeable to sodium with ions diffusing into the neurone down the electrochemical

gradient making the inside of the neurone less negative.

2) Depolarisationif potential reaches the threshold of -55mv, more sodium channels open with

ions diffusing into the neurone.

3) Repolarisationwhen potential difference is +30mv, sodium channels close and potassium

channels open with the membrane being more permeable to potassium ions leading them to diffuse

out of the neurone causing the neurone to progress towards resting potential.

4) Hyperpolarisation potassium ion channels are slow to close so too many potassium ions diffuse

out of the neurone with the potential difference becoming more negative than the resting potential

at -70mV.

5) Resting potential ion channels are reset with the sodium-potassium pump returning the

membrane to its resting potential until the membrane is excited by another stimulus.

There is a refractory period during which ion channels cant be opened acting as a time delay

between one action potential and the next, ensuring that action potentials are unidirectional and

pass along as discrete impulses.


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Synapses

1) The arrival of an impulse at a synaptic knob increases the permeability of the presynaptic

membrane to calcium ions as calcium ion channels open up.

2) Calcium ions then move into the synaptic knob down their concentration gradient.

The effect of an influx of calcium ions is to cause the synaptic vesicles which contain a transmitter

substance or neurotransmitter to move to the presynaptic membrane.

3) Each vesicle contains around 3000 neurotransmitters. Some vesicles fuse with the presynaptic

membrane releasing transmitter substance into the synaptic cleft.

4) The molecules diffuse across the gap and become attached to specific protein receptor sites on

the post-synaptic membrane.

5) This opens sodium ion channels in the membrane and there is an influx of sodium ions into the

fibre causing a change in the potential difference across the membrane and an excitatory post-

synaptic potential to be set up.

6) With sufficient EPSPs the positive charge in the post-synaptic cell exceeds the threshold level andan action potential is set up which then travels on along the post-synaptic neurone.

7) The neurotransmitter can also have the opposite effect if different ion channels open in the

membrane allowing inwards movement of negative ions causing the inside to be more negative than

the normal resting potential.

8) An inhibitory post-synaptic potential results which makes it less likely that an action potential will

occur in the post-synaptic fibre.

The ISPs play a part in the way we hear patterns of sound

Once a neurotransmitter has had an effect it is destroyed by enzymes in the synaptic cleft so thatthe receptors on the post-synaptic membrane are emptied and can react to a subsequent impulse.

Nervous system communication

Sensory neurones - transmit electrical impulses from receptors to the CNS

Relay neurons - transmit electrical impulses between sensory neurons and motor neurons

Motor neurones - transmit electrical impulses from CNS to effectors

e.g.

Dim light > light receptors detect lack of light > CNS processes info > radial muscles in the iris are

stimulated by motor neurones > radial muscles contract to dilate your pupils making them bigger

Stimulus > Receptors > CNS > effectors > response


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Hormonal system communication

Gland - is a group of cells specialised to secrete a hormone e.g. pancreas secretes insulin

Hormones chemical messengers proteins/peptides or steroids

Glands can be stimulated by change in concentration or by electrical impulses, working by diffusing

directly into blood taken around the body to diffuse and bind to specific receptors on the

membranes of target cells causing a response in them.

e.g.

Low blood glucose concentration > receptors on pancreas cells detect low blood glucose

concentration > pancreases releases hormone glucagon into the blood > target cells in the liver

detect glucagon and convert glycogen into glucose > glucose is released into blood so glucose

concentration increases

Computerised tomographyThese use x-ray radiation to produce cross-sectional images of the brain

Denser structures in the brain absorb more radiation than the less dense structures and so show up

with a lighter colour on screen.

Brain structure major structures

Brain function- can see loss of function alongside diseased/damaged part of brain

Medical diagnosis damaged/diseased part of brain e.g. stroke blood has different density so

shows up lighter colour where blood from damaged blood vessels can be seen and loss of function

determined.

MRI

These use strong magnetic fields and radio waves to produce cross-section images of the brain

Investigating structure more detail difference between normal and abnormal parts

Function damaged parts loss of function- find relationship

Medical diagnosis show damaged or diseased areas of brain tumour cells show up different to

magnetic field than healthy cells find location and size and determine what functions are affected

FMRI

Shows brain activity more oxygenated blood in active areas (to supply neurons with glucose andoxygen). Molecules with oxygenated blood respond differently to a magnetic field than

deoxygenated blood. More active areas of the brain can be identified on an fMRI scan.

Investigating structure detailed structure similar to MRI

Brain function function carried out whilst person is in the scanner part of the brain involved will be

more active

Medical diagnosis show damaged and diseased areas as well as conditions caused by abnormal

activity in the brain where structural cause isn't obvious.


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Receptors 1) Light enters the eye through the pupil where the amount of light that enters is

controlled by the muscle of the iris.

2) Light rays are focused by on the retina lining the inside of the eye by the lens

3) It is the retina that contains photoreceptor cells that detect light

4) In the retina the fovea is an area where lots of photoreceptors are contained

5) When light hits the photoreceptors they bleach the light-sensitive pigments causing a chemical

change.

6) A nerve impulse is triggered along a bipolar neurone (which connects photoreceptors to the optic

nerve) consequently taking impulses to the brain.

Rods (peripheral parts of retina) - only give information in black and white sensitive to low light/

movement

Cones (in fovea) give information in colour red-sensitive, green-sensitive and blue-sensitive which

are stimulated in different proportions so different colours are seen involving the pigment iodopsin.

Rods contain a light-sensitive pigment called rhodopsin which is made of retinal and opsin.

When it is dark the rods are not stimulated: 1) sodium ions are pumped out of the cell using active

transport but sodium ions diffuse back in to the cell through open sodium channels.

2) The inside of the cell is only slightly negative compared to the outside so the cell membrane is

said to be depolarised, triggering the release of neurotransmitters.

3) These neurotransmitters inhibit the bipolar neurone so it cant fire an action potential therefore

no information goes to the brain.

The process when the rods are stimulated by light.

1) Light energy causes rhodopsin to break apart into retinal and opsin in a process called bleaching

(where light energy changes cis-retinal into trans-retinal) causing the sodium ion channels to close.

2) Sodium ions are actively transported out of the cell so they cant diffuse back in.

3) Sodium ions build up on the outside of the cell making the inside of the membrane

hyperpolarised.

4) In this state it stops releasing neurotransmitters meaning that theres no inhibition of the bipolar

neurone.

5) The bipolar neurone is no longer inhibited causing it to depolarise. If the change in potential

difference reaches the threshold with an action potential transmitted to the brain via optic nerve.

Pupil reflex

1) Light enters the eye

2) the brighter the light the more action potentials travel along neurones in the optic nerve to the

brain

3) This is detected by a control centre in the midbrain

4) The impulses then travel along two neurones into further control centres where they synapse

with branches of the parasympathetic cranial nerve (the oculomotor) which transmits impulses to

the iris

5) These stimulate the effects i.e. the muscles of the iris with the circular muscles contracting andthe radial muscles relaxing so the pupil constricts.


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Visual Cortex development

This is an area of the cerebral cortex which is used to receive and process visual information.

Neurones in the visual cortex receive information from either your left or right eye.

Neurones are grouped together in columns called ocular dominance columns with the right eye

receiving information from the right ocular dominance / left eye from left ocular dominance

columns.

The columns are the same size and are arranged in alternating pattern across the visual cortex.

Study investigating how the visual cortex develops (Hubel and Wiesel)

They used cats and monkeys to study the electrical activity of the neurones in the visual cortex.

They found that the left ocular dominance columns were stimulated when an animal used its left eye

/ the right ocular dominance columns are stimulated when an animal uses its right eye.

The experiment involved very young kittens:1) One eye was stitched

2) Their eye was kept like this for several months

3) When the eye was unstitched, that eye was blind.

4) The ocular dominance columns for the stitched up eye were also a lot smaller than normal /

ocular dominance columns larger than normal

5) The ocular dominance columns for the open eye had expanded to take over the other columns

that werent being stimulated neurones in the visual cortex are said to have switched dominance.

6) This experiment was repeated in adult cats where it was found that they had not gone blind in the

stitched eye and that their ocular dominance columns remained the same.

7) This demonstrates how we have a critical window in which the visual cortex must develop during

infancy, because if prevented from growing then, it does not do so later in life. Additionally where

children have a cataract and are unable to develop their visual cortex they will be blind however

adults with cataracts can recover their sight.

Habituation

1) Use a stimulus to elicit a response from an organism

2) Time how long it takes to withdraw from the response

3) Evoke the response as regular intervals and record how long it takes to withdraw

4) If habituation has taken place with withdrawal time should decrease at each interval

5) If a novel stimulus is used, the response should increase the time taken to withdraw its response.


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Ethics of using animals in medical research

For Against

Some animals share a lot of similarities tohumans and have lead to breakthroughs

Difficult to generalise results from animals

Animals are looked after - painkillers /

anaesthetics used

Pain and distress can be caused in animals

Cell cultures and computer models arent a true

representation of how cells may react animals

are the only way to study behaviour

Computer models/ cultures of human cells can

be used as safer alternatives

We have a greater right to life than other

animals

Animals right activitists say that animals have the

right not to be experimented on

L-Dopa

Because dopamine cant cross the blood-brain barrier a precursor to it is used, which allows the

sythnesis of more dopamine in the substantia nigra.

MDMA

Ecstasy blocks the serotonin reuptake transport system so synapses are completely flooded with

serotonin which cant be returned to the presynaptic knob. Alternatively the drug may make the

transport system release all the serotonin from the presynaptic knob into the synapse affecting the

post-synaptic membrane by flooding the brain with impulses.

Genetically modified microorganisms

1) Isolate and cut out required gene2) Place gene into plasmid vector using DNA ligase

3) Place plasmid into host bacterial cell

4) Downstream processing- use bioreactor to remove human insulin for use

Genetically modified plants

1) Insert required gene into bacterium plasmid

2) Infect plant with modified bacteria so the gene becomes part of the plant chromosome.

3) Tumour develops in the plant with cells containing gene tumour cells are cultured with new

plants grown containing the new genes.

Ethics of using genetic modification

For Against

Technology may be used only for wealthy Genetic modification violates rights of organism

GM Crops higher yield / more nutrition

reduce famine

Transmission of genetic material crossover

with wild organisms

Pest resistant save money Safety of genetically modified food

Use GMO to make enzymes

GM bacteria human insulin

Vaccines in plant tissue environment already

suitable

Cheaper drugs more available

bio processes unit 5

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