How you can use these notes:

Write them again and again- every day & memorise them.
Write out/ Print in A4 and stick on your wall- read before sleep. Print out as A5 flashcards and revise from them. All of the above because youre serious about that grade.

PHOTOSYNTHESIS

6CO2 + 6H2O C6H12O6 + 6O2

Definition: Using energy from sunlight to split apart the strong bonds in water molecules. Storing the hydrogen in a fuel (glucose) by combining it with CO2 and releasing oxygen gas to the atmosphere as a waste product.

Light- dependant reactions (in the thylakoid membrane) [Produces ATP and reduced NADP]
Energy from sunlight raises two electrons in chlorophyll to a higher energy level. The electrons passed through the electron transport chain combine with H+ and the coenzyme NADP to make reduced NADP. The two electrons pass through carrier proteins in the electron transport chain. They gain and lose energy through a series of oxidation and reduction reactions. Electrons from photolysis of water replace those emitted by the chlorophyll molecule (so it is no longer positively charged). Photolysis raises H+ concentration in the thylakoid space. Energy lost by the electrons are used to produce ATP in photophosphorylation (P(i) added to ADP using energy from sunlight.) In the thylakoid space, an enzyme catalyses the photolysis of water into H+ , electrons and O2 (waste product.)

Light- independent reactions (The Calvin Cycle) (in the stroma) [Produces GALP]
CO2 combines with (5C) RuBP (Ribulose Biphosphate). This reaction is catalysed by the enzyme RUBISCO (Ribulose Biphosphate Carboxylase.) This forms an unstable (6C) compound which immediately breaks down into two (3C) compounds called GP (Glycerate 3phosphate.) GP is reduced using the ATP and reduced NADP from L-dependant reactions, regenerating coenzyme NADP. This produces (3C) GALP (Glyceraldehyde 3-phosphate.) 2/12 GALP used to synthesise a (6C) sugarthis is used to make biological molecules e.g. amino acids, lipids, nucleic acids & polysaccharides.

10/12 GALP used to regenerate RuBP to continue the Calvin cycle. The 10 GALP rearrange to form 6 (5C) compounds which are phosphorylated using ATP to form RuBP.

ESTIMATING TIME OF DEATH

Body temperature
Human core body temperature is around 37oc. Immediately after death, the temperature starts to fallin the absence of heat-producing chemical reactions. Core temperature is measured via the rectum or using an abdominal slab.

Rigor mortis
After death muscles totally relax, then stiffen. -After death, the body is starved of oxygen so oxygen-dependant reactions stop. -Respiration is now anaerobic which produces lactate. -Lactic acid decreases the pH of cells which inhibits enzymes so anaerobic respiration stops. -The ATP required for muscle contraction is not available- this causes bonds between muscle proteins to become fixed. -The proteins can no longer move over one another to shorten the muscle- fixing muscles and joints. -Rigor mortis eventually passes off as muscle tissue starts to break down, in the order in which it was formed.

Factors that affect post-mortem cooling

-Body size -Body position -Clothing -Movement of air -Humidity -Temperature -Whether the corpse was immersed in water

Stages of succession
The population of organisms on a corpse changes over time as the body decays. There is a succession of species. The community of species found on the body can give an estimate of T.O.D. by allowing the stage of succession to be determined.

Signs of decomposition
Putrefaction- Greenish colouration of the lower abdomen as a result of a formation on sulphaemglobin. Gas or liquid blisters appear on skin.

Forensic entomology The stage of development of any insect on the corpse, though its lifecycle can help work out
T.O.D. The stage of development of maggots can be considered with reference to the life cycle of a fly- to give estimate of maggot age. Determining age of insects- can estimate when eggs were laid on the body= estimate T.O.D. assuming eggs were laid soon after death. Other factors e.g. toxins will affect results (cocaine will affect development.)

Pathogens enter the body through:

-Cuts on skin -Digestive system via food & drink -Respiratory system via being inhaled -Other mucosal surfaces.

NON- SPECIFIC IMMUNITY

Inflammation at the infection site
Site at which pathogens enter becomes red, swollen, warm and painful. Immune system cells recognise foreign antigens and release molecules that trigger inflammation. -Molecules cause vasodilation around site. -Increases blood flow to site> molecules increase permeability of blood vessels> lots of blood cells, these destroy the pathogen.

But the body has BARRIERS to infection

- Skin: physical barrier. However, if the skin is damaged, pathogens can enter the blood stream. Blood clots to prevent this but pathogens may enter before clotting. - Stomach acid: Pathogens in your food & drink will mostly be killed by stomach acid. Those that survive pass into intestines, invade the gut wall and cause disease. - Gut and skin flora: The intestines and skin are covered with billions of harmless microbes. These compete with pathogens for nutrients and space, keeping their numbers down. - Lysozyme: Enzyme present in secretions produced by mucosal surfaces (eyes, mouth, nose.) These kill bacteria by damaging their cell walls> causes cell lysis> causes cell death.

Interferon: anti-viral protein

Cells infected with viruses produce protein interferon's. -These prevent viruses spreading to uninfected cells by: (1) Preventing viral replication by inhibiting production of viral proteins. (2) Activate cells of specific immunity to kill infected cells. (3) Activate other non-specific mechanisms e.g. inflammation.

Phagocytosis: engulfment of pathogens

Phagocytes are found in the blood and tissues, they are the first cells in the body to respond to pathogens. Phagocyte recognises antigen on pathogen as foreign> cytoplasm of phagocyte moves around the pathogen, engulfing it. The pathogen is now in a phagocytic vacuole. -A lysosome (organelle) which contains digestive enzymes, fuses with the phagocytic vacuole and the enzymes break down the pathogen. The pathogen then becomes and Antigen Presenting Cell (APC.)

Antigens:
Protein or polysaccharide markers found on the surface of all cells- helps to identify them e.g. as self cells or foreign cells. APCs show antigens on the surface membranes to activate other immune cells. Macrophages are a type of phagocyte (White Blood Cell) that can become an APC (Antigen Presenting Cell) after engulfing a pathogen.

Antibodies:
Plasma cells make antibodies to a specific antigen. Antibodies then bind to antigens on the surface of pathogens to produce lots of antigen- antibody complexes. The variable regions form antigen binding sites that are complementary to the shape of the antigen. Hinge regions allow flexibility when an antigen binds. Disulphide bridges hold polypeptide chains together.

What antibodies do: Antigen-antibody complex:

Antigen 1) Agglutinating pathogens- each antibody can bind to two pathogens and make them clump together so phagocytes can engulf many pathogens at once. 2) Neutralising toxins- antibodies bind to toxins produced by pathogens, forming antibody-toxin complexes which get engulfed. 3) Prevents pathogens binding to human cells- by blocking the cell surface receptors that pathogens need to bind to host cells. This happens when the antigen-antibody complex is made. This means that these pathogens cannot affect human cells.

Light chain

Variable region

Constant regions Hinge protein

Heavy chain

T-CELLS: activated by phagocytes

-Surface is covered in receptors. -Receptors bind to antigens presented by phagocytes. -Each T-cell has different receptors so each T-cell will bind to a different complementary antigen. The binding activates the T-cell so it divides into two different types with different functions: - T-helper cell: releases substances to activate T-killer cells, macrophages and B-cells. - T-killer cell: attaches to antigens on an APC and kills the cell. - T-memory cell: divides into the correct type of T-cell to kill the cell presenting the non-self antigen.

B-CELLS: activated by T-helper cells

-Surface is covered in antibodies. -Each antibody binds to an antigen on the surface of a pathogen, forming an antigen-antibody complex. -Each B-cell has a different type of antibody on its surface so it will bind to a different complementary antigen. This binding, and chemicals released by T-helper cells (cytokines) activates the B-cell so that it divides by mitosis into: -B effector cells/plasma cells: secrete the correct antibody to the pathogens antigen. -B memory cells: can later divide into plasma cells. Memory cells remain in the body for months/years- giving the person IMMUNITY to that pathogen.

Role of T-killer cells

Bacterium infects the host cell which becomes an APC. The complementary receptors on a T-killer cell bind to the APC. This, as well as chemicals (cytokines) released by T-helper cells activates the T-killer cell so that it divides and differentiates into (a) Clones of T-killer memory cells and (b) Clones of active T-killer cells. The active T-killer cells bind to the APC and secrete chemicals which cause pores to form on the APC, leading to cell lysis and cell death.

B-cell clonal selection:

Bacterium has antigens on its surface. Antigens bind to complementary antibodies on the surface of the B-cell. The B-cell becomes an APC. A T-helper cell with complementary receptors binds to the APC and release protein cytokines which activate the B-cell. The B-cell divides and differentiates into (a) B- memory cells and (b) B-effector cells. The B-effector cells further differentiate into plasma cells which release the antigen-specific antibodies. Antibodies bind to antigens on pathogens, making them easily identifiable for destruction.

Activation of T-helper cells:

Bacterium is covered in antigens. Macrophages engulf the bacterium, becoming APCs (Antigen-Presenting Cells.) Thelper cells with complementary CD4 receptors binds to the APC. This binding activates the T-helper cell so it divides and differentiates into (a) Clones of T-helper memory cells and (b) Clones of active T-helper cells.

HIV & AIDS

-The Human Immunodeficiency Virus causes AIDS. -The virus infects and destroys immune system cells. -AIDS is a condition where the immune system deteriorates and eventually fails. People with HIV are classed as having AIDS when symptoms of their failing immune system starts to appear. -AIDS sufferers generally develop opportunistic infections- which would not cause serious problems to someone with a healthy immune system. -The length of time between infection with HIV and development of AIDS varies but is usually 8-10 years. The disease then progresses through a series of symptoms: Initial symptoms: Minor infections of mucus membranes and recurring respiratory infections-caused by lower than normal number of immune system cells. Progression: Number of immune system cells further decreases. More serious infections e.g. Chronic diarrhoea, severe bacterial infections, Tuberculosis. Later stages: Very low immune system cell count at this point. Suffers a RANGE of serious infections e.g. Toxoplasmosis of the brain, Candidiasis of the respiratory system. It is the serious infection that kills the person, not the HIV itself.

TB (Tuberculosis)
-Mycobacterium Tuberculosis causes TB- a lung disease. -The bacterium infects phagocytes in the lungs. -Most people dont develop TB straight away- their immune system seals off the infected phagocytes in the lung in structures called tubercules. -The bacteria is dormant inside the tubercules and the person shows no obvious symptoms. -The bacteria can become reactivated, overcoming the immune system and causing TB. This is more likely in people with weakened immune systems e.g. AIDS sufferers. -The length of time between infection with the bacteria and the development of TB varies- from weeks to years. -TB then progresses through a series of symptoms. Initial symptoms: fever, general weakness, severe coughing- caused by inflammation of lungs. Progression: TB progression damages the lungs. If its left untreated, it can cause respiratory failure which can cause death. -Also, TB can spread from the lungs to other parts of the body e.g. the brain and kidneys. If this is left untreated, it can cause organ failure and can lead to death.