bio 5/6 markers idk

• Describe the difference between active and passive immunity


  1) Active involves memory cells, passive does not

  2) Active involves production of antibody by plasma/memory cells

  3) Passive involves antibody introduced into body from outside

  4) Active long term, because antibody produced in response to antigen

  5) Passive short term, because (given) antibody is broken down

  6) Active can take time to develop/work, passive fact acting
• Explain the passage of action potential along non-myelinated axons for a nerve impulse.


  1.Stimulus causes Na+ to move in so threshold is reached so Na+ voltage gated channels open.

  2.Depolarisation of axon until action potential is reached.

  3. Na+ passively moves down the axon by repulsion and diffusion.

  4. Threshold is met in adjacent region so Na+ voltage gate channels open in the adjacent region so Na+ enter by facilitated diffusion.

  5. Depolarisation of adjacent region until action potential is reached.
• Passage of action potential along myelinated axons for a nerve impulse- saltatory conduction


  1. Na+ enter at the node of Ranvier by facilitated diffusion through Na+ voltage gate channels.

  2. Axon is depolarised until action potential is reached.

  3. Na+ passively move down the axon by repulsion and diffusion, myelination prevents leakage of ions.

  4. Threshold is met at the next node of Ranvier so Na+ voltage gate channel open so Na+ enter by facilitated diffusion.

  5. Region of axon is depolarised until action potential is reached.
• Explain cholinergic synaptic transmission


  1. Action potential reaches the pre-synaptic knob.

  2. Ca2+ (calcium) voltage gated channels open and Ca2+ move in by facilitated diffusion.

  3. Pre-synaptic vesicles containing the acetylcholine move and fuse with the pre-synaptic membrane.

  4. Acetylcholine are released by exocytosis and diffuse across the synaptic cleft.

  5. Acetylcholine binds to the receptors of Na+ ligand-gated channels on the post synaptic membrane.

  6. Na+ ligand-gated channels open allowing Na+ to diffuse in by facilitated diffusion.

  7. Threshold is reached so Na+ voltage gated channels open allowing Na+ to diffuse in by facilitated diffusion for action potential to be reached.

  8. Acetylcholinesterase breaks down acetylcholine into ethanoic acid and choline- taken by pre-synaptic neurone.

  9. Ethanoic acid and choline regenerated into acetylcholine by ATP.
• Explain neuromuscular junctions


  1. Depolarisation cause Ca2+ voltage gate channels to open in the pre-synaptic knob so Ca2+ enters by facilitated diffusion.

  2. The synaptic vesicles move and fuse with the membrane, acetylcholine is released by exocytosis into junction.

  3. Acetylcholine binds to receptors on the sarcolemma causing Na+ to move in by facilitated diffusion.

  4. Depolarisation spreads along sarcolemma and down t-tubles so Ca2+ voltage gate channels on sarcoplasmic reticulum opens.

  5. Ca2+ released from reticulum by facilitated diffusion causes muscle contraction.

  6. Ca2+ is actively transported back into reticulum/acetylcholinesterase breaks down acetylcholine so muscles relax.
• Myofibril contraction


  1.Myosin heads are not attached to the actin. ADP and Pi bound to myosin head .

  2.If Ca2+ enters the sarcoplasm, they bind to troponin and move tropomyosin.

  3.This exposes the binding sites on actin for myosin to bind for actinomyosin cross bridge to be formed.

  4.ADP and Pi are released, energy from ATP stored in the myosin head is used to bend the myosin head.

  5.The bending of the myosin head pulls actin towards the centre of sarcomere in a rowing action- power stroke.

  6. New molecules of ATP binds to the myosin head so it detaches from the actin and the cross bridges break.

  7. Ca2+ activate ATP hydrolase to hydrolyse ATP into ADP and Pi which provides energy for myosin to move back to its original position (recovery stroke)

  8. If Ca2+ is still present the myosin head can rebind to the actin further down the filament.
• The action of insulin


  1.High blood glucose concentration detected by B cells in Islets of Langerhans.

  2.Insulin released binds to complementary receptors on target cells so more glucose channel proteins embedded in membrane so permeability to glucose increases.

  3. More glucose absorbed by facilitated diffusion.

  4. More respiration in muscle cells (glycolysis).

  5.Enzymes convert glucose to glycogen in liver cells (glycogenesis).

  6. Enzymes convert glucose to fat in adipose cells.

  7. Blood glucose concentration decreases
• The action glucagon


  1. Low blood glucose concentration detected by A cells in Islets of Langerhans.

  2.Glucagon released binds to complementary receptors on liver cells.

  3. Activates enzymes that converts glycogen into glucose (glycogenolysis) and converts proteins/fats into glucose (gluconeogenesis).

  4. Blood glucose concentration increases.
• Oestrogen stimulating transcription of genes of the development of female character


  1. The DNA binding site is blocked by an inhibitory molecule.

  2. Oestrogen enters the cell by simple diffusion and binds to the oestrogen binding site on the oestrogen receptor.

  3. This changes the tertiary structure of the oestrogen receptor.

  4. So, the inhibitor is released which exposes the DNA binding site.

  5. The complex passes through the nuclear pores and binds to the promoter region on a specific DNA base sequence.

  6. RNA polymerase is stimulated which binds to the promoter region and transcribes the gene
• mRNA translation from target genes can be inhibited by RNAi


  1. DNA is transcribed to form double stranded RNAi which leaves the nucleus.

  2. The double stranded RNAi becomes single stranded as one stand degrades.

  3. RNAi associates with a complex of proteins one of which is RNA hydrolase.

  4. The complex binds to a complementary specific mRNA strand by complementary base pairing.

  5. This can cause either the mRNA to be broken down or prevents the mRNA binding to a ribosome.

  6. Which prevents gene translation.
• Explain how high oestrogen concentrations develop breast cancer


  1. Oestrogen binds to the oestrogen receptor.

  2. The tertiary structure of the oestrogen receptor changes so the DNA binding site is exposed.

  3. The oestrogen receptor binds to the promoter region of the oncogene.

  4. RNA polymerase binds and so oncogene is transcribed and translated for.

  5 The protein is produced which stimulates cell division.

  6. This eventually causes uncontrollable cell division which causes cancer cells to develop.
• DNA probing of whole chromosomes


  1. Create the probe and PCR it.

  2. The probe and the target DNA are denatured- to allow binding.

  3. DNA hybridisation occurs by the probe binding to the complementary DNA.

  4. If the complementary DNA is present, the marker gene will show its presence
• DNA probing of a fragment of DNA using DNA gel electrophoresis


  1. Obtain the DNA and cut into fragments.

  2. Place onto the gel end it will move towards the positive end of the gel as it is negatively charged.

  3. The speed at which the DNA fragments move depends on their size and their charge.

  4. Smaller fragments move further and faster.

  5. Pour the probe and wash away the unbound.

  6. Put X-ray film or U.V light to identify which fragment has the DNA.
• Identifying which alleles of a gene are present


  1. Use restriction endonuclease to prepare the DNA fragments.

  2. Probe should be complementary to region of allele unique to the allele.

  3. Homozygous shows as one band and heterozygous genes show as two alleles.

  4.The shorter allele travels further down the gel electrophoresis.
• Describe what the Lokta-Volterra Model looks like


  1. Prey population increases because there are not many predators to eat the prey.

  2. The predator population increases because there is plenty of prey to eat- more survive and reproduce.

  3. Prey population decreases because there are lots of predators eating the prey.

  4. Predator population decreases because not as many prey, so less food so more intraspecific competion.

  5. Cycle repeats over...years
• In Vitro cloning referred to as the Polymerase chain reaction (PCR)


  1. Mix together DNA nucleotides, DNA polymerase and primers and the section of DNA you want to amplify.

  2. Heat DNA to 95 degrees so that the hydrogen bonds break, and the strands separate.

  3. Lower temperature to 55 so the primers anneal to the specific sequence by complementary base pairing.

  4. The DNA nucleotides attach to the strands by complementary base pairing.

  5. Heat to 72 degrees so DNA replication takes place and the taq DNA polymerase joins the nucleotides together.

  6. Repeats the cycle many times.
• What does exercising do to effect heart rate


  1. Reduces blood pH as more CO2 dissolves which is detected by chemoreceptors in the carotid artery and arch of aorta.

  2. Cardioaccelaratory centre stimulated, cardioinhibitory centre inhibited.

  3. Frequency of impulses through sympathetic nerve increases and decreases through parasympthetic nerve to SAN.

  4. More noradrenaline to SAN

  5. Higher frequency of impulses across atria to AVN and then to ventricles.

  6. Increase in heart rate.
• What does less exercise do to effect heart rate


  1. increases blood pH which is detected by chemoreceptors in the carotid artery and arch of aorta.

  2. Cardioaccelatory centre inhibited, cardioinhibitory centre stimulated.

  3. Frequency of impulses through parasympathetic nerve increases and decreases through sympthetic nerve to SAN.

  4. More acetylcholine to SAN.

  5. Lower frequency of impulses across atria to AVN and then to ventricles.

  6. Decrease in heart rate.
• Explain ultrafiltration


  1. Afferent arteriole is wider than efferent arteriole creating high hydrostatic pressure.

  2. Small molecules like glucose, water and urea are forced out of the blood through the endothelium fenestrations.

  3. Molecules are then forced through the basement membranes and then through the gaps between the podocytes.

  4. Molecules then enter the lumen of Bowman's capsule forming glomerular filtrate.

  5. Large proteins remain in the blood.
• Explain the reabsorption of glucose and water by a proximal convoluted tubule


  1. 3Na+ is actively transported out of the epithelial cell on the PCT and 2k+ are transported through Na/K+ pump.

  2. Na+ concentration decreases in the epithelial cell.

  3. Co-transport protein brings Na+ and glucose in by active transport.

  4. Glucose travels out by facilitated diffusion down concentration gradient through symport protein.
• How does the loop of Henle maintain a gradient of Na+


  1. Na+ and Cl- are actively transported out of the ascending limb into the tissue fluid of the medulla.

  2. Some of the ions from the tissue fluid enter the descending limb by facilitated diffusion.

  3. Water moves out of descending limb by osmosis through aquaporins but not from ascending as it is impermeable.

  4. Concentration of Na+ increases down the descending limb and moves out of the bottom limb by facilitated diffusion.

  5. Deeper into medulla(Na+) increases so water potential of filtrate is always less negative than the tissue fluid its next to.

  6. Osmosis can occur across whole length of collecting duct as water potential gradient is maintained.

  7. Water moves out of collecting duct into the tissue fluid and then into vasa recta capillaries.
• Explain counter-current multiplier


  1. Na+ moves out of ascending limb and water moves out of descending so water potential in descending limb decreases slowly.

  2. Process repeats down descending limb due to counter current between the ascending and descending limb
• Explain what happens with the production of ADH when there is lack of water (opposite thing will happen when there is too much)


  1. Produced by the hypothalamus that secretes ADH into the posterior pituitary gland where it is stored.

  2. Osmoreceptor detects change in water potential

  3. Lack of water triggers hypothalamus to increase frequency of impulses secreted to thirst centre of the brain and specialised nerve cells in the posterior pituitary gland causing more ADH to be released into the blood.

  4. ADH binds to receptors on the CD/DCT causing vesicles to fuse with the membrane so more aquaporins are embedded.

  5. So less urine production
• Generation action potential


  1. Resting potential

  2. Generator potential

  3. Depolarisation

  4. Action potential

  5. Repolarisation

  6. Hyperpolarisation

  7. Resting potential
• oxygen consumption/strength of stimulus graph


  1. Straight as stimulus below threshold so no action potential- Na+/K+ pump still active and using ATP.

  2. Frequency of action potentials increases, Na+/K+ pump works faster, requires ATP so greater aerobic respiration rate.

  3. Above certain strength, number of action potentials does not increase further due to refractory period