bio biodiversity evolution and disease

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140 Terms

1
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plant passive defences physical

waxy cuticle, cellulose cell wall, stomata, bark, casparian strip

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passive plant defences chemical

toxic compounds e.g catechol, bark resin, enzyme inhibitors like tannins, yeast on leaf surface

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active plant defences

hypersensitivity- rapid death of tissue surrounding infection

reinforced cell walls (callose and lignin deposition)

plasmodesmata narrowing by callose

cytoplasm of nearby cells grows into xylem to make a callose wall

sieve pores of phloem blocked up by callose so sap can’t be transported

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cell signalling in plant defence

when pathogens break down cell walls with cellulase and molecules produced act as signals to cell surface receptors. release phytoalexins

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signalling molecules in plant defence

phytoalexins, salicylic acid, ethylene

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what do phytoalexins do in plant signalling

disrupt pathogen metabolism, delay pathogen reproduction, disrupt bacterial cell surface membranes, stimulate the release of chitinase

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role of salicylic acid in plant signalling

migrates through plant to unaffected areas and activates defence mechanisms that protect the plant against pathogens for a period. long-term protection called systemic acquired resistance

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what does ethylene do in plant signalling

plants secrete it when pathogens are attacking. it vaporises and stimulates other leaves on the plant to react and other plants

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primary non specific animal defences

skin/sebum, expulsive reflexes, mucous membranes, lysozymes, stomach acid

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lysozymes role and where found

break down bacterial cell walls. found in blood, sweat tears, breast milk

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what is commensal bacteria and where is it found

non-pathogenic bacteria found ina nd on humans. E. coli and Candida albicans are common. found in skin, mouth, and intestines.

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why is commensal bacteria good

compete with pathogenic microorganisms for nutrients and space and prevent them from invading host tissue

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second line of defence molecules

phagocytes and antimicrobial proteins

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second line of defence responses

blood clotting, inflammation, wound repair, phagocytosis

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blood clotting cascade overview

platelets trigger a reaction cascade that results in the formation of fibrin which forms a scab

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the inflammatory response charecteristics

redness, swelling, heat, pain, loss of function

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what is inflammation

a local repsonse to infection and tissue damage

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what happens in the inflammatory response

mast cells secrete the cell signalling molecule histamine, which causes vasodilation (increases blood flow through capilliaries) and fluid enters the tissues, creating swelling. some plasma leaves the blood and phagocytes, and cells release cytokines that trigger an immune response in the infected area

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what are cytokines

cell signalling compounds that stimulate inflammation and an immune response. they are proteins

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what are interleukins

a type of cytokine. IL-1 and IL-6 promote inflammation, IL-1 targetting the brain causing drowsiness and fever.

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process of wound repair

scab is formed from blood clotting, stem cells divide by mitosis underneath. blood vessels form, collagen is produced, granulation tissue forms to fill the wound, stem cells move over the new tissue and produce epithelial cells, contractile cells cause wound contraction, unwanted cells die

<p>scab is formed from blood clotting, stem cells divide by mitosis underneath. blood vessels form, collagen is produced, granulation tissue forms to fill the wound, stem cells move over the new tissue and produce epithelial cells, contractile cells cause wound contraction, unwanted cells die</p>
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what is a phagocyte

white blood cells produced in bone marrow.

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phagocyte function

remove dead cells and pathogens. non-specific immune response

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types of phagocyte

neutrophil, macrophage, dendritic cells

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what is phagocytosis

the process of recognising and engulfing cells or particles

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neutrophil definition

short lived phagocytes that act in the body tissues. multilobed nucleus. released in large numbers during infection.

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neutrophil mode of action

attracted to pathogens or cells under attack by chemotaxis. recognise antibody molecules on pathogens and attatch to them. cell surface membrane extends out and around the pathogen, engulfing it and trapping the pathogen in a phagocytic vacuole. endocytosis. lysosome fuses to form phagolysosome, killing and digesting the pathogens, dying themselves.

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what is a sign of dead neutrophils

pus

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what is a macrophage

large long-lived phagocytes.

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where are macrophages produced

bone marrow

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where are neutrophils produced

bone marrow

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what do macrophages mature from

monocytes, developing into macrophages when they leave the blood

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where do macrophages reside

lungs, liver, spleen, kidney, lymph nodes

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macrophages mode of action

initiate the specific immune response. don’t completely destroy pathogens, but take the antigens and become antigen presenting cells, whihc can be recognised by lymphocytes

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what are dendritic cells

large phagocytic cells with lengthy extensions. large surface area.

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where are dendritic cells found

throughout the body

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what is the role of antigen presenting cells

t cell activation to provide a specific immune response

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what can an antigen presenting cell present

the antigens from toxins, foreign cells and ingested pathogens

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what are cytokines

cell signalling proteins produced by mast cells in damaged tissue, which attract white blood cells to the site of damage.

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what are opsonins

chemicals that bind to and tag foreign cells, making them easily recognisable to phagocytes

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what is a phagosome

a vesicle that forms within a phagocyte

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what is a lysosome

vesicles that contain enzymes capable of breaking down biological polymers

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what cells are involved in the cellular response

T cells (helper, killer, cytotoxic, regulatory, memory)

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where do t cell mature

the thymus gland

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where to b cells mature

the bone marrow

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where do t lymphocytes orginate from

bone marrow

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what happens when t cells mature

gain specific cell surface receptors called t cell receptors, which have a similar structure to antibodies

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t cell role in immune response

complementary t cells binds to antigen presenting cell, and divide by mitosis to produce clones, which differentiate into t helper and t killers

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what is a t helper cell

a t cell that release interleukins that increase phagocyte activity and activate b cells

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what is a t killer cell

search for antigen presenting cekks and attatch to the antigens and secrete toxic substances to kill infected cells and the pathogen inside. secrete perforins

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what is a perforin

a glycoprotein responsible for pore formation in cell membranes

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what is a t memory cell

a t cell that remains in the blood after infection ready to be activated for clonal selection if there is reinfection

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what is clonal selection

specific b or t lymphocytes containin receptors complementary to a particular antigen are selected and activated

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what is clonal expansion

the process of rapid cell division resulting in the multiplication of genetically identical cell clones from a single parent cell

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where are b lymphocytes found

the whole body, concentrated in the lymph nodes and spleen

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what produces the humoral response

b lymphocytes

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b cell activation

b cells with complementary antibody receptors bind to antigen presenting cells. clonal selection. also binds with interleukins and t helper cells

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clonal expansion in b cells

activated b cells divide by mitosis to produce clones. some differentiate to plasma cells and some memory cells

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plasma cell

a type of b cell that mass produces antibodies. short lived

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primary immune response

response to a newly encountered antiged. time dela weaker and more short lived

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secondary immune response

response to a previously encountered antigen. stronger more long lasting

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what happens in the primary immune response

clonal selection and expansion of specific t and b cells, synthesis of antibodies

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how long doe sthe primary immmune response take to produce antibodies

10-17 days

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why is the seocndary immune resposne quicker

more memory cells present to be selected than the original clone than before so more antibodies can be quickly produced

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what do b memory cells divide into

plasma cells and more memory cells

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types of t memory cells

memory helper t cells, memory killer t cells

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what are antibodies

globular glycoproproteins called immunoglobulins

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what structure do antibodies have

quaternary. y shape. two heavy polypeptide chains disulfide bonded to two light polypeptide chains. constant and variable region

<p>quaternary. y shape. two heavy polypeptide chains disulfide bonded to two light polypeptide chains. constant and variable region</p>
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how many types of mammalian antibody are there

5

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what is the constant region of an antibody for

binding to b cells

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what is the variable region of an antibody for

binding to specific antigens to form antigen-antibody complex

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what is the hinge region of an antibody

gives felxibility to the antibody and allows antigen bindign sites at different angles

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antibodies function

destroy pathogens directly or by activating other immune cells. anti-toxins, opsonins, agglutinins

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antibodies as antitoxins

bidning to toxins produced by pathogens neutralising them

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antibodies as opsonins

attatch to pathogens, making them easily identifiable to phagocytes. called opsonisation

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antibodies as agglutinins

cause pathogens with antigen antibody complexes to clump together. called agglutination. makes phagocytosis easier

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antibodies deactivating pathogens

attatch to bacteria flagella making them less active. phagocytosis easier

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antibodies stimulating cell lysis

work with complement protein to cause holes in cell wall and lysis

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active natural immunity and example

immune system naturally exposed to pathogen and produces antibodies against it. eg catching a cold

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active artificial immunity example

vaccination

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active immunity

antigen enters the body triggering a specific immune response

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passive immunity

antibodies not produced by infected person

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passive natural immmunity example

antibodies passed from mother to child through breastmilk

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passive artificial immunity example

injection of antibodies or tetannus antitoxin

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what is an autoimmune disease

the immune system attacks one or more self-antigens. targeted towards a single organ or the entire body

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rheumatoid arthritis

autoimmune disease that solely affects the joints. begins int eh fingers and hands, spreading to shoulders and elsewhere.

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rheumatoid arthritis symptoms

muscle spasms, inflamed tendons, lethargy, constant joint pain

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causes of autoimmune disease

not fully understood. inheritable

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herd immunity

indirect protection from an infectious disease when a population is immune through vaccination or previous infection

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ring vaccination

when a person gets an infection, those in close contact are vaccinated against it

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what could a vaccine contain

dead or inactivated pathogens, attenuated pathogen strains, harmless version of toxin, isolated antigens, genetically engineered antigens

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what is an attenuated pathogen

a weakened version

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why are booster vaccines given

to provide longer lasting immunity as memory cells do not last forever

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who has weak immmune systems

babies elderly immunocompromised

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antigenic variability

some pathogens have rapidly mutating antigens so a vaccine against one strain may not recognise the antigens from another strain

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what are antibiotics

drugs that kill or inhibit bacterial growth

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ways that antibiotics can affect bacteria

preventing the synthesis of dna, proteins, or bacterial cell walls

disrupting proteins activity int he cell membrane or enzyme action

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why don’t antibiotics work on viruses

viruses don’t have cell structure so antibiotics cannot target metabolic reactions. also viruses are inside host cells

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what is antibiotic resistance

what occurs when the use of antibiotics leads to resistant strains in bacteria due to mutations

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how does antibiotic resistance occur

natural selection. variation in a population, antibiotic used and resistant survive, go on to reproduce and offspring have resistance too