A2 UNIT 5 BIOLOGY REVISION CARDS

3 MAIN TYPES OF MUSCLE:

• CARDIAC MUSCLE: Found in the heart. Striated. Cross connections join the fibres.
• SMOOTH MUSCLE: Controlled by INS. Found in the gut, blood vessels. Contracts/fatigues slowly.
• STRIATED MUSCLE: Attached to the skeleton. Involved in the locomotion. Controlled by VNS. Contracts rapidly. Fatigues quickly.

STRUCTURE OF A MUSCLE:

MUSCLE~> BUNDLE OF MUSCLE FIBRES~>MYOFIBRILS~> CONTRACTIVE UNITS OF SACROMERES~> ACTIN (troponin,tropomyosin) & MYOSIN PROTEINS

2 MAIN TYPES OF MUSCLE FIBRES:

• FAST TWITH: Uses anaerobic respiration. Rapid intense contractions. Rapid build up of lactate. Used at short explosive excercise. Fibres fatigue easily. Low levels of myoglobin. Low levels of mitochondria.
  
• SLOW TWITCH: Uses aerobic respiration. Slower sustained contractions. Can cope with long periods of excercise. Little phospocreatine stored. High levels of myoglobin. High levels of mitochondria.
  

SLIDING FILMENT THEORY

• Calcium ions are released from the sarcoplasmic retuculum.
• Calcium ions bind to troponing on the actin causing it to move with the threads of tropomyosin. (Myosin binding sites are blocked by trotopyosin, this is the reason why myosin heads cannot bind.)
• As the threads move, myosin binding sites are exposed.
• Myosin forms cross bridges with the actin filament.
• Myosin heads release ADP + Pi and changes shape.
• Actin moves towards the centre of the sarcomere.
• ATP produced binds to myosin and causes it to detach form actin.
• ATPase causes ATP hydrolysis.
• Myosin heads return to uprght position, as there is a stimulus to stop the antagonistic muscle contraction.
• Circle starts again.

ANTAGONISTIC MUSCLE PAIRS: muscles can only pull, thus two muscles are required to move a bone to and fro.

LIGAMENT: binds the bines together. Prevents dislocation. Strong and flexible. Can resist too much streching. High in fibrous connective tissues. More elsatic than a tendon.

TENDON: Anchors muscle to bone. high in tesile strenght. Resists streching. Force exerted by the muscle is directly transferred into the movement of bone with minimum loss of energy.

Flexors: muscles providing the flexion (angle between two joints decreases).

Extensors: muscles providing extension (angle between tow joints increases).

KEY HOLE SYRGERY:

• Minimum damage done to the surrounding stuctures.
• Fiber optic tube inserted through a hole made thought the skin.
• A light source and small instruments are fet thought tubes.
• Short reconvery time.
• Less anasthetic needed.
• Cheaper than invasive surgery.
• More patients can be treated.

PROSTHESIS: An aritificial body part used by someone with a disability to enable them to regain some degree of normal function or appearance. These allow return of limb mobility and remove the pain of the deseased joint. Materials used are: plastics, carbon fibles, or new alloys.These allow disabled athelete to compete against able bodiesd atheletes - this is now banned as this gives compatitor an unfair advantage (THIS IS AN ETHICAL ISSUE)

DRUGS IN SPORT: Many performance enhancing drugs are now banned from sport. Arguments for preventing the use of drugs in sport include:

• Many of these substances can cause damage to the athletes health, especially if used over a long period of time. They may causeliver damage and in some cases are thought to have caused the early death of an athlete, often by causing heart attacks.
• Athletes who use drugs may have a competitive advantage over those who do not, making it an unfair competition.

On the other hand some people think they should be allowed:

• It is impossible to detect every performance-enhancing drug that can be used in sport. New drugs are always being tried, and it is difficult for regulators to develop new tests quickly enough to keep up with these developments.
• There is no ban on nutritional supplements such as vitamins - so where do we draw the line between an illegal performance-enhancing drugs and a legal vitamin supplement?

CATABOLISM: breaking down reactions.

ANABOLISM: building up reactions.

HYDROLASE: enzyme that catalyses the breakdown of a compound by combination of a substrate with water.

OXIDOREDUCTASE: enzyme that catalyses oxidation and reduction reactions.

DEHYDROGENASE: enzyme that catalyses the trasfer of hydrogen ions from one coumpound to another.

GLYCOLYSIS (In the cytoplasm) :

• A glucose molecule is phosphorylated, as two ATP's donate phosphate to it.
• This produces a hexose bisphosphate molecule, which splits into 2 triose phosphates.
• Each triose phosphate is converted to a pyruvate molecule. This involves the removal of hydrogen, which are taken up by a coenzyme called NAD. This produces reduced NAD. During this step the phosphate groups from the triose phosphates are added to ADP to make ATP.
• Overall two molecules of ATP are used and four are made during glycolysis of one glucose molecule, make a net gain of 2 ATP's per glucose.

THE LINK REACTION (in the matrix):

• If oxygen is available, the pyruvate moves into the matrix of mitochondrion, where the link reaction and the Krebs cycle take place. During these processes, the glucose is completely oxidised.
• Pyruvate gets decarboxylated, then dehydrogenated.
• Carbon dioxide is gine off. This carbon dioxide diffuses out of the mitochondrion and out of the cell. Hydrogen is also removed from the pyruvate, and is picked up by NAD, producing reduced NAD.
• Pyruvate is converted into a two carbon compound. This immediately combines with coenzyme A to produce acetyl coenzyme A, that is in charge of carrying the C acetyl groups to the KREBS CYCLE.

KREBS CYCLE (in the matrix):

Acetyl coenzyme A has two carbon atoms. It combines with a four-carbon compound to produce a six carbon compound. This is gradually converted to the four carbon compound again through a series of enzyme-controlled steps.

During this process, more carbon dioxide is released and diffuses out o the mitochondrion and out of the cell. More hydrogens are released and picked up by the NAD and another coenzyme called FAD. This produces reduced NAD and reduced FAD. ATP is also produced.

Roles of the krebs cycle: To provide elctrons for oxidative phoporylation to produce more ATP. Thus a source of energy.

OXIDATIVE PHOSPORYLATION:

• The hydrogens picked up by NAD and FAD are now split into electrons and protons. The electrons are passed along the electron transport chain, on the inner membrane of the mitochondria.
• As they move along the chain they give off energy. This energy is used to actively transport hydrogen ions from the matrix of the mitochondrion, across the inner membrane and into the space between the inner and outer membrane. This builds up a high concentration of hydrogen ions in this space.
• The hydrogen ions are allowed to diffuse back into the matrix through special channel proteins that work as ATPases. The movement of the hydrogen ions through the ATPases provides energy to cause ADP and Pi to combine to make ATP.
• The active transport and subsequent diffusion of the hydrogen ions across the inner membrane of the mitochondrial membrane is known as chemiosmosis.
• At the end of the chain the elections reunite with protons. They combine with oxygen to produce water. This is why oxygen is required for aerobic respiration, if the supply of oxygen stops then the Krebs cycle stops.

ANAEROBIC RESPIRATION:

• If oxygen is not available the Krebs cycle and the link reaction come to a halt. However glycolysis can still continue as long as the pyruvate made can be removed and the reduced NAD can be converted back to NAD. In animals this is done by converting the pyruvate to lactate. 

                                                              GLUCOSE ~> 2PYRUVATE + 4H+ ~> 2LACTATE

• Lactate causes the Ph of the cells fall which will inhibit the enzymes that catalyse glycolysis. Substrate will no longer bind to the enzyme active sites.
• The lactate that is produced (usually in muscles) diffuses into the blood and is carried in solution in the blood plasma to the liver. Here, liver cells convert it back to pyruvate.
• This requires oxygen, so extra oxygen required after exercise has finished, this is known as the oxygen debt. 
• When the exercise is finished and the oxygen is available again, some of the pyruvate in the liver cells is oxidised through the link reaction, the Krebs cycle and the electron transport chain. Some of the pyruvate is reconverted to glucose in the liver cells and this may be released into the blood or converted into glycogen and stored.

INSTANT ENERGY SUPPY:

CREATINE PHOSPHATE (STORED IN MUSCLES) + ADP ~> CREATINE + ATP

The heart is myogenic - this means it contracts and relaxes automatically without the need for EXTERNAL stimulation from nerves. Depolarisation is brought about.

• SINOATRIAL NODE (SAN): In the wall of the right atrium there is a patch of muscle tissue. This has an intrinsic rate of contraction a little higher than that of the reat of the heart muscle. Initiates depolarisation.
  
•  ATRIAL SYSTOLE: As the cells of the SAN contract, they send out a wave of depolarisation along the wall of the left and right atria, causing them to contract.
  
• VENTRICULAR SYSTOLE: When the wave of depolarisation reaches the atrioventricular node (AVN) in the septum it is delayed briefly. It then continues down the septum between the ventricles, along fibres called the bundle of His and then up through the ventricle walls. This causes the ventricle to contract.
• AVN valves close and prevent flow to atria. Semilunar valves get oppened by pressure. Blood is forced into the arteries.
  
• DIIASTOLE: There is then a short delay before the next wave of depolarisation is generated in the SAN. Semilunar valves close.

ELECTROCARDIOGRAM: An ECG is a visual recording of the electrical changes in the body due to the changes of the heart beat cycle, it can show abnormal heart activity that has caused arrythmia. It shows a repeated pattern/trace. Electrodes called elads pick up the changes from variuos locations over the body on the skin. Skin is first cleaned alcohol to remove any grease to improve the conduction of electrodes.

Being able to go for long periods of strenuous exercise depends on maintaining a constant supply of ATP, and this depends on aerobic capacity: ability to take in/transport/use oxygen. Exercise involves the contraction of muscle. Muscles obtain energy from ATP which is produced by respiration. Exercise therefore requires increased rate of respiration in muscles which requires more oxygen. This is achieved through:

•  increasing cardiac output
• faster and deeper rate of breathing,which increases the rate at which oxygen enters the blood in the lungs and carbon dioxide leaves it.
• faster and stronger heart beat, which increases the rate at which blood moves through the blood vessels, delivering oxygen to muscle tissues nd removing carbon dioxide and lactate from them.

CARDIAC OUTPUT: the the volume of blood leaving the left ventricle with each beat multiplied by the number of beats per minute. Cardiac output depends on the volume of blood ejected from the left ventricle (the stroke volume) and the heart rate:                               Cardiac output (CO) = stroke volume (SV) x heart rate (HR)

STROKE VOLUME: Is the volume of blood pumped out of the left ventricle each time the ventricle contracts. How much blood the heart pumps out with each contraction is determined by how much blood is filling the heart, this is the volume of blood returning to the heart from the body. During exercise there is greater muscle contraction so more blood returns to the heart this is called venous return. In diastole during exercise the heart fills with a larger volume of blood. The heart muscle is stretched to a greater extent, this increases stroke volume and cardiac output.

Variations in the heart rate is provided though the neurogenic control by the cardiovascular control centre, located in the medula oblongata. Heart is controlled by the cardiovascular control centre sending signals though nerves forming part of the ANS. The two nerves are sympathetic (accelerator) and parasympathetic (deccelerator).

Cardiovascular control centre detects accumulation of: CO2. Reduction of O2. Increase in temperature. Lactate. Mechanical activity in the muscles and joints that is firt dected by sensory receptors then sent along to CCC.

Adrenaline is a hormone which has a direct effect on the sinoatrial node. The cardiac output is increased by increasing the strengh of contraction or by increasing the number of beats per min. Just before and during excercise:

• Adrenaline is secreted from the adrenal glands stimulating the SAN to increase its rate of contraction.
• Action potentials are sent along the motor neurone from the cardiovascular control centre in the brain, to the SAN. The neurone releases noradrenaline when it reaches the SAN, causing the SAN to increase its rate of contraction. This may happen if there is too much carbon dioxide in the blood. This decreases the pH of the blood which stimulates the cardiac centre to generate a higher frequency of action potentials in the sympathetic nerve.
• When oxygen concentration falls in muscles, the walls of blood vessels secrete nitric oxide. This makes muscles relax so arterioles dilate and carry more blood. This increases the rate at which blood is returned to the right atrium of the heart.
  

DURING NORMAL BREATHING: rhythmic patterns of nerve impulses are sent from the ventilation centre in the medulla oblongata in the brain to the muscles in the diaphragm which respond by contracting rhythmically.

• INHALATION: Ventilation centre send nerve impulses to the external intercostal muscles and the diaphragm. Both of these sets of muscles contract causing inhalation.
  
•  EXHALATION: During lung inflation, strech receptors in brocheoles are stimulated to send inhibitory imulses back to the ventilation centre. This allows muscles to relax as inhalations stops. Exhalation is caused by elastic recoil of lungs and gravity.
  

DURING EXCERCISE: CO2 concentration increases and dissoves in blood plasma.Carbonic acid is made which dissociates into H+ and HCO3- ions. As concnetraiton of H+ ions rises the blood ph decreases. Chemoreceptors in ventilation centre sense a fall in pH. Impulses are sent to other parts of VC. Impulses from VC are sent to stimulate the muscles involved in breathing.

CHANGES IN PH: Carbon dioxide concentration is also sensed by receptors in a patch of tissue in the wall of the aorta, called the aortic body. Another set of chemoreceptors in the walls of the carotid arteries, called carotid bodies, sense concnetraiton, as well as carbon dioxide concnetration in blood.

Nerve impulses are sent from the aortic body and carotid bodies to the ventilation centre, and this then sends impulses to the breathing muscles, causing them to contract harder and faster. This increases the rate and depth of breathing.

HOMEOSTASIS: Maintenance of stable internal envoronment, within a narrow limit of the optimum conditions needed for the cells to function properly. It is achieved by maintaining stable conditions in the blood, ph, water popential, temperature, CO2 and glucose concentrations.

NEGATIVE FEEDIBACK: Each controlled condition has a norm value. Receptors detect deviation from the NORM, by sending impulses to a control mechanism which can turn on/ off effectors to regulate the norm.

Respiration produces heat, so does muscle contraction. During vigorous exercise, considerable quantities of heat are generated in muscles and this causes the temperature of the blood to rise. It's important that core temperature remains constant, around 37.8C as if it rises much above this then enzyme molecules become denatured, and normal metabolic reactions can't take place and cells may be damaged.

A change in core temperature is detected by thermoreceptors in the hypothalamus in the brain. The hypothalamus receives inputs from temperature receptors in the skin. 

• As themperature falls arterioles constrict so less heat is lost.
• Sweat glands secrete little or no sweat.
• Erector muscles contract pulling hairs up on end. This traps a later of insulating air next to the skin.
• Certain muscles contract and relax rapidly (shivering), generating extra heat which increases blood temperature.

• Temperature rise is detected by the receptors.
• This allows them to sned an impulse to the hypothalamus.
• This stimulates the sweat glands to secrete sweat. Sweat flows up the sweat ducts onto the surface of the skin, where the water in it evaporates. Heat is therefore lost though evepaoration of water.
• Arteoles vasodilate. Arterioles delivering blood to the skin dilate so a greater volume of blood flows into the surface capillaries. This allows heat to be lost by radiation from the blood through the skin surface.
• Heat gained = Heat lost.
• This is negative feedback which acts to to bring the condition back to normal.
• The heat loss centre also inhibits the hair erector muscles (to relax to let hairs lie flat so they don't trap a layer of insulating air), liver (to decrease the metabolic rate) and skeletal muscles (to relax).

This mechanism of temperature regulation is an example of a negative feedback mechanism.

In negative feedback, a receptor detects a change in the normal state of a system. If it detects an increase, it triggers events which bring about a decrease. If it detects a decrease, it triggers events which bring about an increase. The change is then detected by the receptor, which once again acts accordingly. The process is ongoing.

There is a slight time lag between the sensor detecting a change and the effectors responding, therefore in temperature regulation for example, the core temperature does rise and fall a little. However it rarely fluctuates far from the norm, this is called dynamic equilibrium. 

LONG TERM TEMPERATURE REGULATION:

If a person spends a few days in a very cold environment, the hypothalamus releases more of the hormone TRH, which stimulate the anterior pituitary gland to secrete TSH. This stimulates the thyroid gland to secrete more thyroxine. 

Thyroxine travels in the blood to it's target cells where it diffuses through the cell surface membrane and into the nucleus. Here it switches on several genes which are responsible for encoding respiratory enzymes, especially cytochrome oxidase and ATPase. It also causes more mitochondria to be produced. This increases the rate of aerobic respiration in cells, generating more heat.

• Peptide hormones are protein chains, they are charged molucules thus they cannot pass through the cell membrane. Instead they bind to a receptor on a cell membrane, activating a second messanger.
• Second messager brings about chemical changes within the cell affecting gene transcription. 
• Hormone receptor complex fuctions as a transcription factor.

1. Thyroxine affects protein synthesis in a cell by binding to transcription factors in the nucleus of a cell. The activated transcription factors bind to a specific region of DNA and change the ability of RNA polymerase to attach to the DNA and catalyse the production of a complementary strand of mRNA from that gene.

2. This may increase the transcription of a particular gene, called up-regulating, or it may decrease transcription, called down-regulating. Most steroid hormones, such as oestrogen and testosterone, act in this way.

3. Transcription factors may bind with a large number of different areas of DNA, so they can switch many genes on or off. Thyroxine, for example, is known to affect the expression of at least 20 genes.

Regular exercise increases fitness:

• It decreases the risk of obesity as it increases metabolic rate during exercise. There is often a temporary increase for some time after the exercise has finished. 
• Type 2 diabetes is caused by a decrease in the sensitivity of live and muscle cells to insulin. This means that high blood glucose levels are not returned to normals as fast as they should be. this can damage cells in all parts of the body.
• Coronary heart disease (CHD) is more likely to develop in people who do not exercise.

However people who exercise too much run the risk of causing damage to the body:

• Joints may become abnormally worn.
• There is evidence that very strenuous exercise taken over long periods of time can cause the immune system to become less effective.

Reflex Arcs:

1.   Receptors detect a stimulus and generate a nerve impulse

.2.   Sensory neurones conduct a nerve impulse to the CNS along a sensory pathway.

 3.   Sensory neurones enter the spinal cord through the dorsal route.

4.   Sensory neurone forms a synapse with a relay neurone in the CNS.

5.   Relay neurone forms a synapse with a motor neurone that leaves the spinal cord through the ventral route.

6.   Motor neurone carries impulses to an effector which produces a response.

Resting Potential

1.   Na+/K+ pump creates concentration gradients across the membrane.

2.   K+ diffuse out of the cell down the K+ gradient, making the outside of the membrane positive and the inside negative.

3.   The electrical gradient will pull K+ back into the cell.

4.   At -70mV potential difference, the two counteract each other and there is no net movement of K+.

Action Potential

1.   At resting potential, membrane is polarised.

2.   Depolarisation: Voltage-dependant Na+ channels open, Na+ flows into axon, depolarising the membrane. Voltage becomes less negative and reaches -40mv.

3.   Repolarisation: Voltage-dependant Na+ channels close, voltage-dependant K+ channels open, K+ions leave the axon repolarising the membrane.

4.   Hyperpolarisation: The membrane is hyperpolarised, asd the potential difference overshoots. Voltage-dependant K+ channels close, K+ diffuse back into the axon to restore the resting potential (refractory period).

 PROPAGATION OF AN IMPULSE ALONG AN AXON (IN NON MYELINATED CELL)

1. At resting potential there is +ve charge on the outside of the membrane and -ive charge on the inside, with higher sodium ion concentration outside and high potassium ion concentration inside.
2. When stimulated, voltage-dependent sodium ion channels open, and sodium ions flow into the axon, depolarising the membrane. Localised electric currents are generated in the membrane. Sodium ions move to the adjacent polarised (resting) region causing a change in the electrical charge (potential difference) across this part of the membrane.
3. The change in potential difference in the membrane adjacent to the first action potential initiates a second action potential. At the site of the first action potential the voltage-dependent sodium ion channels close and voltage-dependent potassium ion channels open. Potassium ions leave the axon, repolarising the membrane. The membrane becomes hyperpolarised.
4. A third action potential is initiated by the second. In this way local electric currents cause the nerve impulse to move along the axon. At the site of the first action potential, potassium ions diffuse back into the axon, restoring the resting potential.

IN MYELINATED CELLS: Action potential propagates faster and more efficiently. The electrical signal jumps from one node of ranvier to the other. (Node of ranvier is the only area that can be depolarised/repolarised).

Functioning of a Synapse

1. An action potential arrives.
2. The membrane depolarises. Calcium channels open. Calcium ions enter the membrane.
3. Calcium ions cause synaptic vesicles containing neurotransmitter to fuse with the presynaptic membrane.
4. Neurotransmitter is released into the synaptic cleft.
5. Neurotransmitter binds with receptors on the postsynaptic membrane.
   
6. Sodium channels open for the ions to flow through the channels.
7. The membrane depolarises and initiates an action potential.
8. When released the neurotransmitter will be taken back up across the presynaptic membrane (whole or after being broken down), or it can diffuse away and be broken down.

SUMMATION:

Spatial summation: Impulses from several different neurones produce an action potential in post synaptic neurone.              Temporal summation: Several impulses in one neurone produce an action potential in post synaptic neurone.

INHIBITORY SYNSPSES: Block the transmission of impulses. Makes the generation of a nerve impulse in the post synaptic membrane less likely by making neurotransmitters open Cl- ion channels to move into the cell and hyperpolarise the membrane.

Visual Transduction: In the dark

1. Na+ diffuse in through open cation channels.
2. Na+ move down the concentration gradient.
3. Na+ is actively pumped out.
4. Membrane slightly depolarised -40mV.
5. Inhibitory neurotransmitter is released and binds to bipolar cell, preventing it depolarising.

Visual Transduction: In the light

1. Rhodopsin is broken down.
2. Na+ channels closed.
3. Na+ actively pumped out.
4. Membrane hyperpolarised.
5. No neurotransmitter is released.
6. Cation channels in bipolar cell open and membrane becomes depolarised, generating an action potential in the neurone of the optic nerve.

A phytochrome molecule consists of a protein component bonded to a non-protein light-absorbing pigment molecule.The five phytochromes differ in their protein component. The non-protein component exists in two forms which are different isomers:

• Pr - phytochrome red; absorbs red light
• Pfr - phytochrome far-red; absorbs far-red light

These two isomers are photoreversible but plants synthesise phytochromes in the Pr form. Absorption of red light converts Pr into Pft, absorption of far red light converts Pfr back into Pr. In sunlight Pr is converted into Pfr and Pfr is converted into Pr. The former reaction dominates in sunlight because more red than far-red light is absorbed. Therefore Pfr accumulates in the light. And in the dark any Pfr present is slowly converted to Pr

Phytochromes and Greening

1. Light activates Phytochrome.
2. Activates proteins in signal pathway.
3. Activate transcription factors.
4. Transcription.
5. Translation.
6. Greening proteins.

CEREBRUM:

FRONTAL LOBE: learning, reasoning, memory.
OCCIPITAL LOBE: receinves sensory input from the eyes.
PARIETAL LOBE: cognition, sensations, speech.
TEMPORAL LOBE: hearing, sound recognition.

CEREBELLUM: coordinate movement, balance, posture.                                                                                                      MEDULLA OBLONGATA: controls heart rate, blood pressure, breathing, involuntary actions: saliva secretion.            HYPOTHALAMUS: thermoregulatory centre, cts as an endocrine gland secreting hormanes - in control of the pituitary gland. BRAIN IMAGING:  CT scans: narrow beam X-rays rotated around the patient. The rays are attenuated according to the density of tissue, to produce a 3D image from wihch different tissues are distinguished. The X-rays can cause mutations. Artefacts may be detected. MRI scans: Magnetic field and radio waves are used to detect soft tissues. Hydrogen atoms in water are monitored as the direction and frequency of the hydrogen nuclei spin is changed, when on e magnetic field is superimposed on another one. The energy absorbed from the radio waves by the hydrogen nuclei  is released. This energy is detected producing 3D image. Procedure produces loud noises as patient sats still, it is non invasive but expensive. fMRI scans: Magnetic field and radio waves are used. Monitors increased neural activity when blood flow increases - so does oxyhaemoglobin. Deoxyhaemoglobin absorbs the radio waves, so areas with oxyhaemoglin will light up, in the brains cross sectional images. Images are collected continually whiles the subject alternates between resting and carrying out tasks. Clear images are produced, it is non invasive, it is loud.

HABITUATION: simple type of learning. Involves the loss of response to a repeated stimulus which fails to provide any form of reinforcement.

1. With repeated stimulation, Ca+ channels become less responsive so less Ca²⁺ crosses the presynaptic membrane.
2. Less neurotransmitter is released into the synaptic cleft.
3. There is less depolarisation of the postsynaptic membrane so no action potential is triggered in the motor neurone.

1. Isolated human gene, modified if necessary.
2. Plasmid, circular piece of nucleic acid able to pass between cells.
3. Extracted plasmid is cut with restriction enzyme.
4. Human gene spliced into plasmid.
5. Modified plasmid put back into bacterial cells.
6. Cells multiply in fermenter.
7. Produce human insulin.
8. Insulin protein extracted and purified.
9. Bacterial cells destroyed.

1. Plasmid carrying the desired gene and an antibiotic resistance gene (marker gene) is used.
2. DNA gun or insertion of a new gene of virus DNA used to incorporate genes into the plant DNA of some cells.
3. Incubation in growth medium with antibiotic.
4. Only cells with the new genes survive.
5. Micropropagation: Cells grow in sterile culture medium containing sucrose, amino acids, inorganic ions and plant growth substances.
6. Plant growth substances stimulate root and shoot growth.
7. Transgenic plant: All new cells contain the new genes.
8. Plantlets separated and grown into full size plants.

FACTORS THAT AFFECT GRMINATION:

• Temperature (use a water bath to control this factor)
• Oxygen concnetration
• Water

• Syringe with the three way tap is used to return monometer levels back to normal.
• KOH solution absorbs CO2 from the air inside the apparatus.
• Volume of oxygen that is used up is calculated by measuring the volume of gas needed for the syringe to return the levels to the original values.
• CONTROL SET UP: Run an identical setup with a dummy organism with the same volume, that way any changfes in pressure or temperature can be observed.

Tidal volume and vital capacity can be measured using a SPIROMETER.

EXPERIMENT STEPS:

1. Person breathes through tube that is attached to a chamer filled with oxygen that has a movable lid.

2. Pen attached to the lid moves as the breathing commences. pen writes on a rotating drum creating a spirmeter trace.

3.Sodalime is kept inside the chamber to absorb the CO2.

4. Total volume of O2 gas decreases over time- this is due to the air being breathed out as a mixture of CO2 and O2 gas each breath.

5. Spirometer has to be calibrated to work out the volume of air that is being breathed that causes the equivalent movement of the trace.

                                  RATE OF O2 CONSUMPTION = DECREASE IN VOLUME / TIME FOR THE FALL

                                               VENTILATION = TIDAL VOLUME x BREATHING RATE

Conjunctiva - protects the cornea

cornea - bends light

lens - focuses light on retina

iris - controls amount of light entering the eye

sclera - protective layer

blind spot - no light-sensitive cells where optic nerve leaves the eye

yellow spot (fovea) - most sensitive part of the retina located in the macula the central area of the retina

retina - contains light-sensitive cells

vitreous humour - transparent jelly

choroid - black layer prevents internal reflection of light

ciliary muscle - alters thickness of lens for focusing

Dopamine is a neurotransmitter secreted by neurones in the basal ganglia, located in part of the midbrain. These neurones normally release dopamine in the motor cortex.

Parkinson's patient motor cortex receives less dopamine thus there is a loss of control of muscular movement.

The main symptoms of the disease are:

• stiffness of muscles
• tremor of the muscles
• slowness of movement
• poor balance
• walking problems
• depression
• difficulties with speech and breathing

Treatment: L-DOPA: it is a dopamine precursor, in the brain it gets turned into dopamine. This is effective because it can cross the blood brain barrier, where as dopamine can't. L-dopa allow to make as much dopamine as possible. DOPAMINE AGONIST: bind to dopamine receptors and mimic the effect of dopamine. MAOB INHIBITOR: inhibits monoamine oxidase enzyme that breaks down dopamine in the brain synapse, therefore it reduces the destruction of the rest of the dopamine made. GENE THERAPY AND STEM CELL THERAPY ARE THE NEW TREATMENTS.

• Neurones that secrete serotonin are stimulated in the brain stem. a lack of serotonin has been linked to depression.
• Their axons extend to the cortex, the cerebellum and the spinal cord, targetinga a huge area of the brain.
• Depression is a multifactorial condition; several genes my be involved but so my environmental factors.
• A gene called 5-HTT is known to influence our susceptibility to depression, people with the 'short' version of the 5-HTT gene are more likely to develop depression after a stressful life event.
• When someone is depressed, fewer never impulses than normal are transmitted about the brain, which may cause low levels of neurotransmitters to be produced.
• Serotonin binding sites are more numerous than normal when depressed to make up for the low levels of the molecule.

Drug treatment:

SSRI: the drugs inhibit the reuptake of serotonin from synaptic clefts.

PROZAC: Maintains a higher level of serotonin. Increases the rate of nerve impulses in serotonin pathway.

• The effect of ecstasy: effects thinking, mood and memory and can also cause anxiety and altered perceptions. Its most desirable effect is that it provides feelings of emotional warmth and empathy. Short-term effects include changes in behaviour and brain chemistry, sweating, dry mouth, increased heart rate, fatigue, muscle spasms and hypothermia.

   There are five different stages in synaptic transmission that can be affected by drugs: neurotransmitter synthesis and storage, neurotransmitter release, neurotransmitter-receptor binding, neurotransmitter reuptake, neurotransmitter breakdown.

Ecstasy increases the concentration of serotonin in the synaptic cleft

• It does this by binding to molecules in the presynaptic membrane that are responsible for transporting the serotonin back into the cytoplasm.
• This prevents serotonin removal from the synaptic cleft.
• The drug may also cause the transporting molecules to work in reverse, further increasing the amount of serotonin outside the cell.
• These higher levels of serotonin bring about the mood changes.
• There is growing evidence of long-term effects including insomnia, depression and other psychological problems.