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Write out/ Print in A4 and stick on your wall- read before sleep.

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All of the above because you’re 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 The two electrons pass through carrier Energy lost by the electrons are used
raises two electrons in proteins in the electron transport chain. They to produce ATP in
chlorophyll to a higher gain and lose energy through a series of photophosphorylation (P(i) added to
energy level. oxidation and reduction reactions. ADP using energy from sunlight.)

The electrons passed through
the electron transport chain
combine with H+ and the
coenzyme NADP to make
reduced NADP.
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.
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 This forms an unstable (6C) GP is reduced using the ATP and
(Ribulose Biphosphate). This compound which immediately reduced NADP from L-dependant
reaction is catalysed by the breaks down into two (3C) reactions, regenerating coenzyme NADP.
enzyme RUBISCO (Ribulose compounds called GP (Glycerate 3- This produces (3C) GALP
Biphosphate Carboxylase.) phosphate.) (Glyceraldehyde 3-phosphate.)

10/12 GALP  used to regenerate RuBP to continue the Calvin 2/12 GALP  used to synthesise a (6C) sugar-
cycle. The 10 GALP rearrange to form 6 (5C) compounds which this is used to make biological molecules e.g.
are phosphorylated using ATP to form RuBP. amino acids, lipids, nucleic acids &
polysaccharides.
 ESTIMATING TIME OF DEATH
Body temperature Rigor mortis
Human core body temperature is around 37oc. After death muscles totally relax, then stiffen.
Immediately after death, the temperature starts to fall- -After death, the body is starved of oxygen so oxygen-dependant
in the absence of heat-producing chemical reactions. reactions stop.
Core temperature is measured via the rectum or using -Respiration is now anaerobic which produces lactate.
an abdominal slab. -Lactic acid decreases the pH of cells which inhibits enzymes so
anaerobic respiration stops.
Factors that affect post-mortem cooling -The ATP required for muscle contraction is not available- this
-Body size -Body position causes bonds between muscle proteins to become fixed.
-Clothing -Movement of air -The proteins can no longer move over one another to shorten
-Humidity -Temperature the muscle- fixing muscles and joints.
-Whether the corpse was immersed in water -Rigor mortis eventually passes off as muscle tissue starts to
break down, in the order in which it was formed.

Stages of succession
The population of organisms on a corpse changes over
Signs of decomposition
time as the body decays. There is a succession of
Putrefaction- Greenish colouration of the lower abdomen as a
species. The community of species found on the body
result of a formation on sulphaemglobin. Gas or liquid blisters
can give an estimate of T.O.D. by allowing the stage of
appear on skin.
succession to be determined.

Forensic entomology – The stage of development of any insect on the corpse, though it’s 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.
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.
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.
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: Antibodies:

Protein or polysaccharide markers found on the surface
of all cells- helps to identify them e.g. as self cells or
foreign cells.
APC’s 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.
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: 1) Agglutinating pathogens- each antibody can bind to two

Antigen 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
Variable
Light engulfed.
region
chain 3) Prevents pathogens binding to human cells- by blocking
the cell surface receptors that pathogens need to bind to
Constant host cells. This happens when the antigen-antibody
regions complex is made. This means that these pathogens cannot
Hinge
affect human cells.
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.
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.
Activation of T-helper cells:
Bacterium is covered in antigens. Macrophages engulf the
bacterium, becoming APC’s (Antigen-Presenting Cells.) T-
helper 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.
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 it’s 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 pathogen’s 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.
B-cell clonal selection:
Bacterium has antigens on it’s 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.
 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 don’t 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 it’s 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.