Topic AO2 AO3
Immunity: Auto-immune disease – antibody response Antibody binds to gangliosides at the
Guillain-Barre is mounted against Campylobacter jejuni, motor neurone terminal and activates the
Syndrome which cross-reacts with glycolipids called classical complement cascade, which
gangliosides on the surface membranes of forms a pore in the membrane, allowing
motor neurones. calcium ions into the axon. Calcium ions
activate the protease enzyme calpain,
which breaks down axon proteins. Nerve
terminals are broken down.
Muscle Antibodies cause damage to nerves in This huge calcium ion influx through the
contraction: GBS by activating the classical complement pore results in an
Guillain-Barre complement cascade. This results in the uncontrolled release of acetylcholine from
Syndrome formation of a pore on the cell all the vesicles in the presynaptic
membranes of peripheral neurones, neurone, creating uncoordinated
particularly the vulnerable presynaptic activation of the muscles. This unchecked
motor nerve terminals of the calcium ion influx also acts as an ‘on’
neuromuscular junction. The pores allow switch for a protease enzyme known as
free movement of ions in and out of the calpain, which digests axon proteins,
axon. Crucially, this include calcium ions, including those of neurofilaments. All of
which are usually tightly regulated by this results in the destruction of the motor
Calcium ion channels. neurone terminals and paralysis of the
muscles they innervate. Understanding of
this helps to develop treatments, which
include inhibitors of the complement
pathway.
Proteins: the Within the cytoplasm there is a Microfilaments – this allows molecules and
cytoskeleton filamentous scaffolding of protein fibres structures to be moved through the
which span the cell in different directions, cytoplasm in an organised way, known as
known as the cytoskeleton cellular trafficking, as well as cytoplasmic
Microfilaments are solid protein threads, streaming and cytokines during cell
containing two actin polymers that division in animal cells
intertwine into a structure that resembles Microtubules – form the spindle threads
a double helix. Their main function that pull homologous chromosomes and
involves movement within the cytoplasm; sister chromatids apart during cell
they act as railway tracks along with division. They are an important
molecules of the motor protein myosin constituent of cilia and flagella and control
can ‘walk’ their beating
Microtubules are follow cylinders Intermediate filaments – provide the
containing tubulin polymers. Like scaffolding that maintains the 3D
microfilaments, microtubules are involved structure of the cell and supports the
in intracellular transport, providing tracks nuclear envelope. Some degenerative
for motor proteins called kinesins and disorders e.g. muscular dystrophy are
dyneins, which move vesicles through the associated with a failure of intermediate
cytoplasm filaments to support cell structure
Receptors: Novichok - a nerve agent – binds Novichok allows too much acetylcholine to
nerve agents irreversibly to the enzyme build up, meaning contractions become
acetylcholinesterase, preventing it from convulsions, causing an extreme and
hydrolysing the neurotransmitter often fatal parasympathetic response.
acetylcholine, which keeps rebinding to Atropine is extracted from Atropine
the to the receptors, making the neurone belladonna; its mechanism of action is to
fire action potentials repeatedly. block a type of acetylcholine receptor
without activating it. This means
acetylcholine cannot bind and initiate
impulses through the parasympathetic
, network. Atropine is an antagonist which
causes the sympathetic nervous system
to dominate. So the symptoms of atropine
poisoning are that of an extreme
sympathetic response; dilated pupils and
blurred vision, dry skin and mouth, rapid
heartbeat and eventually paralysis, coma
and respiratory failure
Responses to Masting – perennial plants show huge Concentrating output (fruit) into
changes in variation in annual food production in occasional mast years leads to lower long-
the internal response to their environment. For run average costs (photosynthate and
and external example, oaks are wind-pollinated. Dry mineral resources). Years with very low
environment: and warm conditions during the flowering fruit production starve populations of fruit-
masting period mean that pollen travels further eating animals such as insects and birds.
and faster. This increases the efficiency of This reduced the size of their populations.
pollen transfer between flowers, so large When a subsequent mast year arrives, the
acorn crops in the autumn tend to follow number of fruits produced overwhelms the
warm and dry springs capacity of the remaining animals to eat
them all. Consequently, some fruits
survive, so that the seeds they contain
germinate the next year. This strategy of
starving and satiating fruit predators – the
predator satiation hypothesis – holds the
key to successful reproduction; there is no
point producing energy-packed fruits if
only the animals get to benefit from them
Responses to Wound healing can be considered a Immune cells encourage the secretion of
changes in homeostatic process because it restores matrix molecules synthesised within cells
the internal your internal environment to its to rapidly repair damaged tissue. The ECM
and external undamaged state. Following a cut, provides both structural integrity and a
environment: damage to collagen causes the release of foundation for immune cell migration and
wound- soluble factors to encourage adhesion via receptors across the matrix
healing inflammation, by promoting migration of to the injury site to mediate wound
immune cells to the area of damage. This closure
in turn initiates healing
Control of Matrix metalloproteinases (MMPs) are During asthma, the ratio of TIMPs : MMPs
processes: enzymes capable of degrading is often disrupted, suggesting that this
the components of the ECM (the non-cellular ratio may promote disease pathogenesis.
extracellular component of all tissues and organs in the During asthma, changes to the
matrix body). MMPs can therefore change how organisation and composition of the ECM
cells attach to the ECM and can release in the airway underpins thickening of the
ECM fragments into the surrounding bronchial wall and reduction of airway
tissue. This can in turn activate immune diameter. This worsens disease severity
signalling. MMPs can become uncontrolled and reduces lung function. Numbers of
and over-expressed, resulting in increased fibroblasts and myofibroblasts increase,
breakdown of the ECM. It is important that which contributes to the thickening of the
there is another level of ECM regulation to bronchi and subsequent disease severity.
prevent this. A family of proteins called This makes MMPs a future potential target
tissue inhibitors of metalloproteinases for asthma therapy
(TIMPs) can bind MMPs and inhibit MMPs
activity.
Homeostasis: In placental mammals (endotherms), heat Optimum temperature for enzymes and
thermogenes is generated by shivering thermogenesis prevents denaturation
is and the and non-shivering thermogenesis. During
Immunity: Auto-immune disease – antibody response Antibody binds to gangliosides at the
Guillain-Barre is mounted against Campylobacter jejuni, motor neurone terminal and activates the
Syndrome which cross-reacts with glycolipids called classical complement cascade, which
gangliosides on the surface membranes of forms a pore in the membrane, allowing
motor neurones. calcium ions into the axon. Calcium ions
activate the protease enzyme calpain,
which breaks down axon proteins. Nerve
terminals are broken down.
Muscle Antibodies cause damage to nerves in This huge calcium ion influx through the
contraction: GBS by activating the classical complement pore results in an
Guillain-Barre complement cascade. This results in the uncontrolled release of acetylcholine from
Syndrome formation of a pore on the cell all the vesicles in the presynaptic
membranes of peripheral neurones, neurone, creating uncoordinated
particularly the vulnerable presynaptic activation of the muscles. This unchecked
motor nerve terminals of the calcium ion influx also acts as an ‘on’
neuromuscular junction. The pores allow switch for a protease enzyme known as
free movement of ions in and out of the calpain, which digests axon proteins,
axon. Crucially, this include calcium ions, including those of neurofilaments. All of
which are usually tightly regulated by this results in the destruction of the motor
Calcium ion channels. neurone terminals and paralysis of the
muscles they innervate. Understanding of
this helps to develop treatments, which
include inhibitors of the complement
pathway.
Proteins: the Within the cytoplasm there is a Microfilaments – this allows molecules and
cytoskeleton filamentous scaffolding of protein fibres structures to be moved through the
which span the cell in different directions, cytoplasm in an organised way, known as
known as the cytoskeleton cellular trafficking, as well as cytoplasmic
Microfilaments are solid protein threads, streaming and cytokines during cell
containing two actin polymers that division in animal cells
intertwine into a structure that resembles Microtubules – form the spindle threads
a double helix. Their main function that pull homologous chromosomes and
involves movement within the cytoplasm; sister chromatids apart during cell
they act as railway tracks along with division. They are an important
molecules of the motor protein myosin constituent of cilia and flagella and control
can ‘walk’ their beating
Microtubules are follow cylinders Intermediate filaments – provide the
containing tubulin polymers. Like scaffolding that maintains the 3D
microfilaments, microtubules are involved structure of the cell and supports the
in intracellular transport, providing tracks nuclear envelope. Some degenerative
for motor proteins called kinesins and disorders e.g. muscular dystrophy are
dyneins, which move vesicles through the associated with a failure of intermediate
cytoplasm filaments to support cell structure
Receptors: Novichok - a nerve agent – binds Novichok allows too much acetylcholine to
nerve agents irreversibly to the enzyme build up, meaning contractions become
acetylcholinesterase, preventing it from convulsions, causing an extreme and
hydrolysing the neurotransmitter often fatal parasympathetic response.
acetylcholine, which keeps rebinding to Atropine is extracted from Atropine
the to the receptors, making the neurone belladonna; its mechanism of action is to
fire action potentials repeatedly. block a type of acetylcholine receptor
without activating it. This means
acetylcholine cannot bind and initiate
impulses through the parasympathetic
, network. Atropine is an antagonist which
causes the sympathetic nervous system
to dominate. So the symptoms of atropine
poisoning are that of an extreme
sympathetic response; dilated pupils and
blurred vision, dry skin and mouth, rapid
heartbeat and eventually paralysis, coma
and respiratory failure
Responses to Masting – perennial plants show huge Concentrating output (fruit) into
changes in variation in annual food production in occasional mast years leads to lower long-
the internal response to their environment. For run average costs (photosynthate and
and external example, oaks are wind-pollinated. Dry mineral resources). Years with very low
environment: and warm conditions during the flowering fruit production starve populations of fruit-
masting period mean that pollen travels further eating animals such as insects and birds.
and faster. This increases the efficiency of This reduced the size of their populations.
pollen transfer between flowers, so large When a subsequent mast year arrives, the
acorn crops in the autumn tend to follow number of fruits produced overwhelms the
warm and dry springs capacity of the remaining animals to eat
them all. Consequently, some fruits
survive, so that the seeds they contain
germinate the next year. This strategy of
starving and satiating fruit predators – the
predator satiation hypothesis – holds the
key to successful reproduction; there is no
point producing energy-packed fruits if
only the animals get to benefit from them
Responses to Wound healing can be considered a Immune cells encourage the secretion of
changes in homeostatic process because it restores matrix molecules synthesised within cells
the internal your internal environment to its to rapidly repair damaged tissue. The ECM
and external undamaged state. Following a cut, provides both structural integrity and a
environment: damage to collagen causes the release of foundation for immune cell migration and
wound- soluble factors to encourage adhesion via receptors across the matrix
healing inflammation, by promoting migration of to the injury site to mediate wound
immune cells to the area of damage. This closure
in turn initiates healing
Control of Matrix metalloproteinases (MMPs) are During asthma, the ratio of TIMPs : MMPs
processes: enzymes capable of degrading is often disrupted, suggesting that this
the components of the ECM (the non-cellular ratio may promote disease pathogenesis.
extracellular component of all tissues and organs in the During asthma, changes to the
matrix body). MMPs can therefore change how organisation and composition of the ECM
cells attach to the ECM and can release in the airway underpins thickening of the
ECM fragments into the surrounding bronchial wall and reduction of airway
tissue. This can in turn activate immune diameter. This worsens disease severity
signalling. MMPs can become uncontrolled and reduces lung function. Numbers of
and over-expressed, resulting in increased fibroblasts and myofibroblasts increase,
breakdown of the ECM. It is important that which contributes to the thickening of the
there is another level of ECM regulation to bronchi and subsequent disease severity.
prevent this. A family of proteins called This makes MMPs a future potential target
tissue inhibitors of metalloproteinases for asthma therapy
(TIMPs) can bind MMPs and inhibit MMPs
activity.
Homeostasis: In placental mammals (endotherms), heat Optimum temperature for enzymes and
thermogenes is generated by shivering thermogenesis prevents denaturation
is and the and non-shivering thermogenesis. During
