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Components & Functions Biological Molecules: Carbohydrates, Proteins, Lipids, Vitamins, Nucleic Acids, Water Define Risk Factor & Metabolism Monomers & Polymers: Carbohydrates, Proteins, Nucleic Acids Condensation VS Hydrolysis Reactions C: CHON F: C: energy Store,Supply,Structure P: Structural components, Antibodies, Membrane carrier & pores, Enzymes, Hormones, Growth & Repair L: Hormones, thermal Insulation, Membrane V: act Coenzymes, form Larger molecules (anabolic reactions) NA: Store & Carrier info H2O: Support plants, Solvent, Transport RF: increasing chance of developing a particular disease M: sum total biochemical reactions in cells of organismsanabolic (build small into large-muscle growth, protein synthesis)/catabolic (break down large into small-respiration, digestion) C,P,NA: All anabolic, form similar, smaller molecules Monomer Polymer Carbohydrate Monosaccharide Polysaccharide Amino acids Polypeptide Proteins Nucleotide DNA & RNA Nucleic Acids Bonds Glycosidic Peptide H (between bases) Con: anabolic, H2O released, bond forms, catalysed by enzymes, monomerpolymer H: catabolic, H2O added, bond broken, cbe, polymermonomer Carbohydrates Function: see 1st card^^ St (starch), Su (glucose during respiration),Str (cellulose (plant cell wall), chitin(exoskeleton insects), peptidoglycan(bacteria cell wall)) CHO Sweet, Soluble, Small, form Crystals 5 carbon monosaccharide-pentose sugar, furranose, 5 membered ring structure e.g. Fructose, Ribose, Deoxyribose 6 carbon monosaccharide-hexose sugar, pyrranose, 6 membered ring structure e.g. Glucose, Galactose Same molecular formula, different structural formula Structural Isomer: Define & α & β Glucose Glucose Monosaccharides bond to form… α H β hydroxyl (OH) group of carbon 1 is below the plane of the ring --above— Break down for respiration (Glucose+ O2Co2+H2O+ATP) Animals & Plants cannot break down different arrangement, can’t used respiration Rotated 180˚ Long, straight chains No rotation Coiled (Amylose), Branched (Amylopectin) Starch, Glycogen Page 1 of 24 Cellulose, Micro&Macrofibrils How Glycosidic bond forms Starch VS Glycogen α 1,4 Glycosidic bond form maltose… amylose (coil, spring shape=compact, trap iodine in coils(test turn blue-black) /amylopectin (branched, 1,6 Glycosidic bond)…starch Starch Cellulose β, Micro & Macrofibrils & Structure:Function Glycogen Mix long, straight Amylose Only 1,4 Glycosidic bonds shorter, more (1,4, coil, compact, iodine) & branches branched Amylopectin 1,4 &1,6 (branches) More compact Stored chloroplasts & cells Forms Glycogen granules, found muscle of storage organs- lots starch grains & liver cells Plants Animals α Glucose, energy stores, insoluble, stored don’t affect ψ, chains easily hydrolysed for respiration β glucose Glucose has a no. of OH groups, so H bonds can form. 60-70 βG=Micro fibrils crosslinked H bonds, lots microf=macrof- form cell wall, S:F---S:cell walls made macrof crosslinked with H bonds, F: adds strength & support S:Cellulose plant cell walls when H2O moves in stops bursting becomes turgid, F: support Arrangement of macrof determines how cell grows/changes shape, F:e.g. Guard cells, stomata, inner edge, help open for photosynthesis/ inadvertently transpiration CHON S (cytosteine in R Group) Function: see 1st card^^ S,A,M,E,H, G&R Proteins Acid group Amphoteric (both basic & acidic properties) R group determines characteristics o P need nitrates (DNA) from soil to manufacture aa o Animals need essential aa can’t build from materials taken in, found in meat, vegetarians have soya (Plants have fewer essential aa) o A can’t store aa, toxic, removed deamination in liver, converted to urea & removed in urine aadipeptidepolypeptide(condensation reaction)protein Page 2 of 24 Primary sequence: 2D, aa, aa specific sequence as code for a specific protein & determined by DNA Condensation/hydrolysis reactions are catalysed by enzymes-Hydrolysis of peptide bondsProtease enzymes. E.g. ageing (lose elasticity, older build less collagen (protein))/hormone regulation (need to break down so effects not permanent, any cell targeted by hormones needs enzymes to hydrolyse hormone) Secondary: β pleated sheets & α helix- held H bonds, Tertiary: 3D, globular/fibrous, specific shape, has disulphide bridges (cysteine), ionic bonds(attraction between opposite charges), hydrophobic interactions, H bonds (uneven distribution of e-) Quaternary: more than 1 polypeptide chain, 2 identical/ a no. of different subunits Globular: globe shape, hydrophobic turn in, hydrophilic turn out, make proteins H2O-soluble H2O easily clusters-metabolic role, enzymes, have tertiary & quaternary structure as well Fibrous: regular, repetitive sequence of aa, insoluble, structural role-keratin/collagen, generally only primary & secondary structure Heat protein temp beyond optimum, KE increase, molecules vibrate, break weak bonds, hold tertiary structure, unravel & protein not function, even if cooled will not reform- denatured Haemoglobin Haemoglobin VS Collagen S:F Lipids: Function, Made up of, Fatty Acids Triglyceride VS Phospholipid VS Cholesterol Wide range aa in primary sequence, wound α helix 4 polypeptide chains: 2 α, 2 β Globular-H2O-soluble 4 Haem group (nonprotein, no aa) contain ferrous ions, carries 4 O2 molecules, associates at lungs, disassociates at tissues Collagen 35% primary- glycine CHON 3 polypeptide chains: coil, compact Fibrous-insoluble H bonds between, add strength e.g. artery walls stop blood bursting walls at high pressure e.g. tendons allow bone to move Function see 1st card: H, I, M, So (more e than carbohydrates), St e Dissolve in alcohol not H2O Not polymer, not made up of identical subunits & can’t add more CHO Fat- control fluidity, Unsaturated (HDL, healthy, e.g. Oleic acid, c=c, fewer H bonds, changes shape pushes molecules apart, greater fluidity, lots in plants ) o Saturated (LDL, unhealthy, stearic acid, c-c, lots in animals) Triglyceride 1 glycerol & 3 fatty acids (carboxylic acid & hydrocarbon chain) Energy store Insoluble doesn’t affect ψ Stored fat, protection, insulation joined ester bonds Page 3 of 24 Phospholipid 1 glycerol, 2 fatty acids (hydrophobic tail)& phosphate group (hydrophilic head) Phosphatecarbohydrate, carbohydrate attached to protein= glycolipid, involved cell signalling Cholesterol 4 Carbon based ring structures joined Strengthen, support bilayer Used form steroid hormones H bonding, Role of H2O Chemical Tests Biuret (proteins), Starch (carbohydrates), Ethanol Emulsion & Grease Spot (lipids), Reducing & Non-Reducing Sugars Uneven distribution of e- creates electrostatic attraction H bonds continuously making & breaking, allow movement High specific heat capacity great amount of energy to raise temp 1kg of H2O by 1˚c, lots of energy for H bonds to break, difficult turn (Lg) evaporating uses lots energy, heat to 100˚c before boils. reason why temp lakes stable even when dramatic changes in temp. takes lots energy for a small variations temp, doesn’t heat up/cool quicklyacts thermal buffer (s-ice) temp falls, H2O less movement, less KE, less vibrations, H bonds form don’t break as easily, forms semi-crystalline shape, less dense than (L), free to move, spread out whereas (s) H2O pushed apart by H bonds. Cools density increases until 4˚c then density lowers ice forms on surface, insulates below, organism survive winter, don’t freeze, allows H2O to circulate cohesive-sticks to each other creates high surface tension charged will dissolve, - & + charges interact with H2O, H2O clusters around charged part, dissolves See sheet Quantitative: quantities/amounts have changed e.g. carry out Benedict’s test on each conc, filter liquid from precipitate, more reducing sugar, more precipitate, place liquid in curvette, measure absorbance of liquid using colorimeter (measures how much light can pass through), more cu sulphate used up, more precipitate form, less light transmitted, after each reading, zero colorimeter reset with water, 100% transmission, make calibration curve plot conc (x axis) against absorbance (y) Qualitative: observation, e.g. colour IV Independent & Dependent Variable, Control, Reliability, Precise DV Reaction rate (y) Lines are DV IV (x axis) Variable/Limiting Factor, measure no. time intervals IV: Factor investigated, know values, set up by investigator, must be accurate & precise so DV are valid C DV: Factor measured each change of IV, don’t know values 1 Variable measured, rest kept constant Control: test to show observed results due to IV no other factor Reliability: confidence data obtained again repeated. E.g. repeat x3, identify anomalous results, take a mean Valid: data is reliable & answers original question e.g. control conc substrate, pH, temp Accuracy: value close to true value, e.g. more intermediate values, narrower range Page 4 of 24 DNA All DNA acts as info store RNA 3 forms: messenger RNA (template coding strand, moves out nuclear pore, attaches to ribosome, contains genetic information-protein synthesis), transfer RNA (brings aa to ribosome in correct order to form polypeptides, interprets code genetic info on mRNA into aa, specific sequence peptide bonds form giving rise to primary & thus… secondary, tertiary, quaternary structure can form, clover shape), ribosomal RNA (forms structure of ribosome, 2 subunits, assembly site aaproteins) Pentose ribose sugar Replicates in Interphase Pentose deoxyribose sugar Adenine=Uracil, Guanine (3 Nitrogenous organic bases: hydrogen bonds) Cytosine Adenine=Thymin RNA bases can be e, Guanine (3 complementary to DNA bases hydrogen bonds) Cytosine Double stranded, Single stranded antiparallel5’Prime end to 3’Prime end on left & 3-5’ on right Hold coded info to build organism, sugar-phosphate backbone 1. 2. 3. 4. 5. Semiconservative Replication DNA Structure: Function Enzymes Key Terms DNA helicase unwinds & unravels double helix, breaking H bonds between complementary base pairs. Each strand of parent DNA acts as a template. Free nucleotides attracted & align with exposed bases, bind to complementary base pairs, H bonds form A=T, C (3 H bonds) G. DNA Polymerase forms bonds between nucleotides to complete sugar-phosphate backbone Produces 2 DNA molecules genetically identical, 1 strand from each from original, parent DNA & 1 strand from each from new, daughter DNA. Info store-protein synthesis, info to build organism Long- so lots of info stored Bases complementary- info can be replicated Double helix- stability Weak H bonds- easy unzip Globular-H2O Soluble (see pg3) Complementary & Specific shape Reaction catalysed enzymes: need 1 specific enzymeGlycosidic, ester, peptide. More than 1 enzymerespiration, photosynthesis Acts as a Catalyst- speeds up a reaction by lowering the activation energy (amount energy required for reaction to proceed), not used up, unchanged after reaction 3D/Tertiary shape Activity can be effected by: temp, pH, (anything that affects no. of collisions which form ES complexes & shape of active site) E.g. lactase breaks down lactoseα Glucose + Galactose Page 5 of 24 Define Heterotroph bread, amylase. Branching hyphae penetrate bread, secrete digestive enzymes & absorb soluble products, o Enzymes digest carbohydrates (Amylase breaks down starchmaltose. maltase (disaccharide) breaks down maltoseα Glucose & α Glucose---- lactase. Lactose αGlucose & Galactose, sucrose, break down sucrose αGlucose & Fructose) o Proteins (protease. Break down paa) o Lipids (lipase. Break down to glycerol & hydrocarbon fatty acid chain) Intracellular & Extracellular Enzyme Action Lock & Key Heterotrophs-organisms obtain nutrients by consuming others Intrac: enzymes catalyse inside cell. E.g. defence in phagocytosis/ DNA replication DNA polymerase Extrac: enzymes catalyse outside cell e.g. mould digests Induced Fit LK: enzymes, proteins specific tertiary shape due to sequence of aa in primary structure, specific active site, only bind to one type of specific, complementary shaped substrate, IF: enzyme changes shape, due to flexibility/ charges on R groups of aa in active site, opposite charges attract, active site fit closely/widens slightly to allow larger substrate (e.g. competitive inhibitors) form E-S complex, change in enzyme shape add strain to substrate, reaction occurs more easily E-P complex forms, product different shape to active site moves away, enzyme returns to original shape & catalyses another reaction Limiting Factors affect enzyme activity: Temp, pH, Enzyme & Substrate conc Only models: simple representation of the process or showing people how it works IF more likely, supported by more evidence, more evidence fits more closely (than lock & key) 1 Variable measured, rest kept constant T: (use a water bath with controlled thermostat to control) higher, more KE, bonds vibrate more & greater strain, molecules move faster, enzyme & substrate moving faster a greater no. & more successful collisions with enzyme active site, more E-S complexes form, more EP complexes form, more products, higher rate of reaction, optimum, max rate of reaction (40-50˚c)Temp goes beyond optimum, too high weak bonds break, hold tertiary structure, unravel & protein not function, even if cooled will not reform, can’t be restored- denatured. pH: (Maintain use buffer solutions, e.g. optimum= pH 7) Higher conc H+, more acidic, lower pH. Significant increase/decrease pH away from the optimum, alter tertiary structure & thus active site, held in place by no. of bonds (H+, ionic) rely on charges to form. Lower pH, more H+, attract – charges on α helix, replace H bonds, change structure, active site changes shape, specific & complementary substrate can no longer fit, new bonds interfere binding substrate, few E-S & E-P complexes, rate reaction slows/reduced. Only denatures if extreme pH changes. E.g. pepsin, in stomach optimum pH2, trypsin, small intestine pH7. Temp&pH Enzyme conc: (accurately measured volume, in living tissue measure mass, must ensure all tissue has same no. of enzyme molecules) if EC variable (thing that changes) then fixed SC. More enzymes, greater no. available active sites, more ES & EP complexes, more products, higher rate of reaction. Further increase in EC, not enough substrates, limits rate, flattens (at max rate) Substrate & Enzyme conc Substrate conc: (accurately measure volume/mass, have to ensure same no. of substrates) if SC variable (thing that changes (in excess)) then fixed EC. More substrates, more freq collisions…. Further increase, meet max rate reaction, all available enzyme active sites will be full, rate flatten can’t increase further, limits rate Page 6 of 24 A B Initial Rate Competitive & Non-Competitive Inhibitors Inhibitor-slows the rate by affecting the enzyme Comp: similar, complementary, tertiary structure to active site, form E-I complexes, no product forms, inhibitor doesn’t break up, prevents substrate enters directly competes for active site, E-S & E-P complexes reduced, rate slows. Amount inhibition depends on conc substrate & inhibitor, Higher substrates, inhibitor less effect, substrate more likely to collide with active site e.g. Penicillin- permanent, (bind effectively denatured) Statins- reversible (when remove inhibitor, enzyme unaffected) Non c: don’t compete, inhibitor binds away from active site, distorts tertiary structure, changes specific shape of active site, substrate not complementary, doesn’t fit, less E-S &E-P complexes form, rate decreases. High conc of inhibitor, reaction slows, rate reduced, substrate can’t collide different shape e.g. Potassium Cyanide- Permanent Cofactor -some enzymes only catalyse if certain non- Cofactors (+ Inorganic ion cofactors) & Coenzymes (Prosthetic group) Metabolic Poisons Initial Rate- max possible rate it’s when enzyme & substrate first mixed together. Reaction proceeds, products formed, substrate broken down & used up, less available, less freq & less successful (product gets in way) collisions, rate slows, flattens Always be a limiting factor (reason why plateaus)- could be temp, pH, enzyme/substrate conc When describing the graph, describe each region Rate of Reaction=1/time Compare DV compare initial rates, take several reading & plot on graph IV (x axis), DV (lines/y axis), take tangent at steepest portion=initial rate protein groups present (not involved in reaction, just have to be present), only bind for short time either same time/just before substrate binds o Inorganic ion cofactors- e.g. amylase breaks down starchmaltose only if Cl- present Coenzyme- involved in reaction & change as a result, recycled, link metabolic pathways that need to take place in sequence (1st enzyme product becomes 2nd enzyme’s substrate…final enzyme’s product is 1st enzyme’s substrate/non comp inhibitor so end product doesn’t build up) o Prosthetic group- co e, permanent part of enzyme Inhibit/Over activate enzymes Potassium Cyanide-non comp, permanent inhibitor-inhibits cell respiration in enzyme, cytochrome oxidase in mitochondria, decreases respiration so less O2 & ATP produced organism only anaerobic respiration so build up lactic acid in blood. Untreated, unconsciouscomadeath 2hrs Page 7 of 24 Biosensor Drugs work inhibiting enzyme activity (Viruses, (Penicillin) Bacteria, Antibiotics, Cystic Fibrosis BS: Uses enzyme reactions to detect presence of substances, if present enzyme reactions take place to break down, reduce amount Virus- treatment use protease inhibitors, prevent virus replicating, stops virus build new virus coats- comp inhibitor Bacteria- treat Penicillin, competes substrate used in cell walls & inhibits enzyme forms crosslinks, add strength, penicillin binds instead, walls weak & fall apart, bacteria can’t replicate Antibiotics- inhibit growth of microorganisms cause bacterial infections Cystic Fibrosis- digestive enzymes in pancreas blocked, can’t digest, treat: enzyme, acid resistant coat not denatured in stomach 1. Natural Selection 2. Genetic Variation/ Random mutations 3. Resistant/ Survival of fittestmust be a selection pressure e.g. antibiotics, climate, enviro 4. Those best adapted (selective advantage) survive, passing on alleles (selective advantage) to offspring 5. Allele only confers resistance/survival to that particular selection pressure in that specific conc/temp/pH etc. 6. Happens for many generations, selective advantage passed on, helping o to survive Resistance Define Balance Diet BD: all nutrients required for health in appropriate proportions C:St,Su,Str e.g. bread, sugar–P:Str,A,M,E,H,G&R e.g. eggs, meat--V: C, L, H20/Fat soluble--H2O: Su, So,T 60% body (See pg1, card 1) Mi: Inorganic, Essential— Fibres: Indigestible, Essential—F/L: M, Energy e.g. Nutrients: Function & e.g. (Carbohydrates, Proteins, Vitamins, H2O, Minerals, Fibre, Fats/Lipids) 57% carbohydrates, 30% fats, 13% proteins Level of Activity More active, need more ^^ nutrients If increase in weight, eating too many energy containing foods (carbohydrates, fats, proteins) vice versa for decrease in weight. Energy Intake=Outake, no weight put on or lost O: 20%+ heavier than recommended weight for height, BMI 30+, important dietary factor lead to Cancer, CVD, Type 2 Diabetes Malnutrition- unbalanced diet-obesity/defiency BMI= dairy, oil Define Obesity Define Malnutrition BMI Page 8 of 24 𝑀𝑎𝑠𝑠 𝑖𝑛 𝑘𝑔 (ℎ𝑒𝑖𝑔ℎ𝑡 𝑖𝑛 𝑚)2 Coronary Heart Disease Hypertension Fats/Lipids, Cholesterol & Lipoproteins Humans depend on plats for food Make food production efficient Result fatty deposits by atherosclerosis, increase friction (no longer smooth endothelium), energy lost going over deposits, encourage more deposition, narrows lumen, restricts blood flow, if lumen becomes blocked starve cells of O2 & nutrients required to survive, cells die. Blocks coronary artery, starve heart O2. E.g. excess salt, decrease ψ of blood, more H2O moves into blood plasma, (increase blood pressure= hypertension) Fats: Sat (c-c, unhealthy),Unsat (see page 3) Cholesterol: Sa f, in cell/skin membrane, insoluble in H2O Lipoproteins transport fats & cholesterol around body, made up of lipids, cholesterol, proteins. Don’t eat but diet effects conc of them. In Blood, taken up cells correct receptors (on plasma membrane) HDL LDL Healthy Unhealthy Carry cholesterol from tissues Carry c liver to back to liver tissues Produced by uns fats Sa f At Liver used to make bile Decreases cholesterol (Sa f, Increases cholesterol LDL) levels in blood, reduces in blood, less able to amount deposited in artery walls removed, more to be by atherosclerosis deposited Basis of food chain, Omnivores- directly eat plants/indirectly eat herbivorous animals P: Use pesticides/insecticides-reduce loss plants by pests/disease-----Use fertilisers-increase fertility of crops & thus size of yield A: Increase productivity, rate of growth & resistance to disease (selective breeding/artificial selection) 1. 2. Selective Breeding/Artificial Selection Genetic Variation/ Random mutations Resistant/ Survival of fittestmust be a selection pressure e.g. climate, enviro 3. Those best adapted (selective advantage) survive. 4. Isolation: Humans select offspring showing the specific characteristics/ selective advantage to breed 5. Inbreeding: When they breed, they pass on alleles (selective advantage) to offspring 6. Allele only confers resistance/survival to that particular selection pressure in that specific conc/temp/pH etc. 7. Happens for many generations, selective advantage passed on, helping organisms to survive & increase growth rate/yield/ productivity. (don’t use words already in question, no marks) Animals In Viro Fertilisation, surrogate mother place (fertilised egg) embryo into uterus Artificial insemination Plants Prevent cross pollination, reduce gene pool, reduce genetic diversity, maintains carefully selective bred traits, by cutting off stamens Test if plant has desirable characteristics e.g. want it to be salt tolerant, test in soil with high salt conc. E.g. low pH etc. Marker Assisted Selection: section DNA used as marker to identify desirable characteristic, selection begin young age when Page 9 of 24 DNA checked Microorganisms-Penicillin on bread, extracellular enzyme action, enzymes catalyse outside cell, mould digests bread, amylase. Branching hyphae penetrate bread, secrete digestive enzymes & absorb soluble products/nutrients, Salmonella, Food Spoilage & Methods to prevent Prevent FS o Pickling- low pH, high acidity, denature enzymes prevent it from breaking down food o Dry, Salting & Coat in Sugar- dehydrates, H2O leaves by osmosis o Cook- high temp denature enzymes prevent it Example of how Microorganisms can make food + + + + Define Health, Disease, Parasite, Pathogen Cause Disease o o o o from breaking down food Prevent further contamination- canning (heated & sealed, denatured & can’t enter), vacuum wrapping (no air, microbes can’t respire aerobically) E.g. Alcohol & Bread- yeast, anaerobic, release CO2 causes rise Quorn: microorganism, single cell protein, made from edible fungus, meat substitute + No - Conditions grow in fats/cholesterol are also ideal for pathogens- take care No animal welfare prevent infection of to consider wrong organism Production can - Different taste other increase/decrease proteins with demand Grows on waste, - People don’t want to econ viable eat things grown on waste H: state mental, physical & social wellbeing D: departure from good health caused by malfunction of mind/body Par: organism lives on (external p- head louse)/in (internal p- tapeworm) another living thing, causes harm to host which lead secondary infections allow other o to invade Pat: organism causes disease Protoctista (Kingdom) enter host & feed contents as grows, e.g. Causive Agent: Malaria, Plasmodium feeds on RBC contents Prokaryote (Kingdom) Bacteria reproduce rapidly, cause damage to cells. E.g. CA: Mycobacterium Tuberculosis/ M. Bovis Fungi (Kingdom) e.g. Ringworm lives in skin sends out reproductive hyphae grow surface of skin release spores Virus- invade cells takes over organelles, nucleus, cause cells manufacture more virus, host cell bursts releases virus Page 10 of 24 Cause & Transmission & Global Impact of TB Cause Transmission Mycobacterium Bovis/ Tuberculosis Droplet Infection from infected- coughing, sneezing etc. Infected when inhale droplets Contract milk/meat of cattle Effects Lungs More likely if… Close contact over prolonged period Poor ventilation, diet, health Homeless Worldwide Many inactive/controlled immune system Global Impact Cause & Transmission & Global Impact of Malaria Cause Parasite: Transmission Spread Vector female anopheles Plasmodium mosquito falciparum/ 1. If host already has malaria, suck parasite vivax gametes into stomach 2. Gametes fuse, Zygote develops in stomach 3. Infective stages formed (spread disease), move to mosquito’s salivary glands 4. Mosquito bites another, injects saliva as anticoagulant, reduce blood clotting 5. Salivary glands contain infective stages 6. In host, salivary glands enter liver, where they multiply before passing into blood again 7. In blood enter RBCs, gametes are produced Malarial parasites live RBC of host feed Haemoglobin Global Impact Limited where vector female anopheles mosquito can survive Cause 1. HIV (human Cause & Transmission & Global Impact of immunodeficiency virus) infective agent: causes AIDS (Acquired Immune Deficiency Syndrome) opportunistic infections 3. 4. HIV / AIDS 2. Takes control when entered T cells: viral DNA, inserted in host DNA, viral RNA produced & codes for viral proteins Transmission Physical Contact Virus enters, remains inactive (HIV Positive) Active-attacks & destroys T helper cells (WBCs help to prevent infection, ability to resist infection is reduced, unable to defend) vulnerable Contract range of opportunistic infections Effect of these diseases that kills T: Use unsterilized surgical equipment Exchange body fluids(blood-toblood contact) Sharing hypodermic needles From Mother to Baby during breastfeeding Global Impact Worldwide Page 11 of 24 Key terms They determine: o o o o Incidence (no. new cases in pop per year) Prevalence (no. people with the disease at a given time) Mortality (no. who die from disease each yr) Morbidity (no. people with disease as a proportion of pop) o Identify countries at greatest risk, age range at risk With info ^^ health organisations can: target research find cures major diseases, target advertisement raise awareness LEDCs tend poorer health- poverty, poor hygiene & nutrition, less educated Immune Response: Primary>>> Immune Response: Secondary Pandemic (worldwide epidemic), Endemic (always present in pop), Epidemic (spreading rapidly large no. over large area) Epidermiology- study of distribution of disease in pop, calculate average risk of a person in a certain pop developing a disease & factors influence spread Pathogens: transmitted, when reach host need pass through primary defences (attempt prevent pathogens entering & causing harm to host), inside pass through secondary defences/immune response Primary (non-specific) Skin- act as a physical barrier, prevent entry of microorganisms Mucous Membrane- certain substances need to enter/ exit, leaves body exposed to infection. e.g. gut, ears, nose--epithelial layer of goblet cells, secrete mucus & trap pathogens & cilia, removes pathogens, moves synchronised pattern wafts mucus up trachea, swallowed down oesophagus to stomach, high acidity, low pH, kills pathogens Other- eyes protected antibodies in tear fluid, kills bacteria Phagocytes Neutrophils Macrophages Multi-lobed nucleus Larger Manufacture bone marrow Manufacture bone marrow Travel in blood move out into TF Travel in blood as monocytes, settle organs & Short lived develop into macrophages Involved specific response 1. Phagocytes engulf & destroy. Pathogen enters, Infected cells release histamine, attracts recognised as ‘foreign’ by antigens on outer neutrophils plasma membrane, (own cells have antigens Histamine makes capillaries more leaky, more recognised as ‘self’ & don’t produce a response) fluid leaves capillaries into TF into lymphatic 2. Phagocytes have receptors on plasma system leads pathogens towards fixed membrane attach to antibodies bind antigens on macrophages in lymph nodes pathogen. 3. Once phagocyte bound pathogen, envelop pathogen by infolding membrane, form a phagosome (vacuole). Lysosomes fuse phagosome, release hydrolytic enzymes, digest pathogen. End products, harmless, absorbed into cytoplasm. Immune Response- activation of lymphocytes in blood& production of antibodies to fight disease Page 12 of 24 Antigen: stimulate immune response Antibody/Immunoglobulin: proteins identify & neutralise antigens Define Antigen & Antibody Complementary shape to particular antigen, immune system manufacture 1 antibody for every antigen Structure of Antibody Agglutination & Neutralisation 2 light + 2 heavy chains= 4 polypeptide chains held by disulphide bridges Constant Regionsame on all, so antibodies can attach to receptors on plasma membrane of phagocytes in phagocytosis Hinge Region-flexibility, allows branches move further apart & bind more than 1 antigen A: large antibody binds many antigens, too large to enter host, many specific variable regions N: attach antigen, cover pathogen binding site, prevent binding & entering to host cell P: Infecting agent (pathogen) enters, stimulates immune response, immune system produces antibodies, few days find correct lymphocyte (clonal selection) & divide& replicate (clonal expansion) to sufficient levels to combat infection successfully S: Antibodies don’t stay in blood. If same pathogen invades again, memory cells recognise it, response starts earlier, greater quantity & more rapid production of antibodies, rises to sufficient level faster Immune Response: Primary & Secondary Variable Region- specific aa sequence, complementary & specific shape so only specific antigens can bind Page 13 of 24 Communication between cells to coordinate a response, involves glycolipids & glycoproteins, release cytokines (signal), target cell detects signal, signal+ receptor bind, complementary shape. B+T lymphocytes receptors on plasma membrane complementary to specific foreign antigens, antigen detected, lymphocytes activated, e.g. stimulate production antibodies/phagocytosis etc. Identification: pathogen has foreign antigens on its plasma membrane, act as markers, signal pathogen is foreign T & B cells have antibodies attached to plasma membrane, complementary to only one type of antigen. o Clonal selection- select specific T/B cell by antigen presenting cells (macrophages fixed in lymph node, act as phagocytes engulf & digest, separate antigens & incorporate in plasma membrane of macrophage=antigen presenting cell, function: find lymphocytes neutralise particular antigen)/T helper cells (role: release cytokines (signals) & interleukins, stimulate B cells to divide & stimulate phagocytosis and plasma cells which produce antibodies). o Clonal expansion- T & B cells divide by mitosis, increasing no. of lymphocytes, all with identical receptors/variable regions in their antibodies attached. Cell Signalling Structure & Mode of action of T & B Lymphocytes o Communication using Cytokines (signals) o e.g. macrophages release monokines: attract neutrophils by chemotaxis &--- stimulate B cells to differentiate & release antibodies o T, B cells & macrophages release interleukins, stimulate proliferation & differentiation of B & T cells (B cells differentiate & grow in Bone Marrow, T cells grow in Bone Marrow & differentiate in Thymus Gland) T cells- cell mediated immunity, grow bone marrow & matures thymus gland B cells-humoral immunity, grow & matures bone marrow T Cells B Cells T cells differentiate: B cells differentiate: Form plasma cells T helper cells produce antibodies T killer cells-recognise complementary to & destroy infected cells antigen by apoptosis, can’t spread the infection. T & B memory cells-remain in ., ready to respond in future if the same pathogen with same antigens, provides immunological memory. Invades again-memory cells recognise antigen, produce clone, form B plasma cells (produce antibodies against antigen), destroy before symptoms appear, form T helper/killer/more memory cells Instructions: cytokines (signals) released act as instructions to target cells, bind to receptor on plasma membrane, triggers response, release 2nd messenger inside cell triggers further response. When cells send distress signals: pathogens enter & infect cells, causes damage to pathogen (lysosomes in cell attempt break down) & body cells (pathogen remain on plasma membrane of body cell- act distress signal & marker show cell is infected See sheet Page 14of 24 Vaccination: Define, Natural, Artificial, Passive, Active, Ring, Herd Passive (produced not manufactured??, immunity without activation of lymphocytes, short-lived) Active (activate immune system, lymphocytes produced, longlasting) New sources of medicine & HIV Deliberate exposure to antigenic material, actives immune system to make immune response& provide immunity Artificial (deliberate exposure to antigen/antibody) Immunity provided by injection of antibodies made by another individual (tetanus injection ) Immunity provided by antibodies made in immune system as result of vaccination. Deliberate exposure to antigenic material that is harmless (dead/attenuate weakened, harmless version) activates immune system treats as real disease, produces antibodies & memory cells (TB & Influenza) Ring V: new case reported, vaccination all in immediate vicinity-e.g. used control livestock disease Herd V: provide immunity all pop at risk- e.g. vaccination programmes New strains form by mutations, existing vaccinations have little/no effect, especially viruses (Influenza-strain changes/mutates every year, different antigens, antibody produced needs match antigen) New drugs needed: antibiotics less effective as microorganisms evolve, random mutations, new drugs act as selection pressure & new diseases are emerging HIV- if receptors on plasma membrane blocked, pathogen can’t enter & cause harm to host. Isolate & look at aa sequence, use modelling determine shape of receptor, produce drug identical shape, no major side effects Smoking Short & Long Term Effects Natural (gained immunity through exposure during normal life) Antibodies provided via placenta, baby immune to disease Mother’s immune to Immunity provided by antibodies made in immune system as result of infection Suffer once then immune (chicken pox) Short: o Tar settles lining airways, increases diffusion pathway, narrows bronchioles, reduces elasticity, causes allergic reaction-smooth muscle contracts, narrows lumen, constricts airways Long: o Lead COPD (Chronic Obstructive Pulmonary Disease) o Damage lining airways by constant cough, o Page 15 of 24 replaced scar tissue, reflex to remove scar tissue, damage thicker (increases diffusion pathway, narrows lumen, airways restricted) Elasticity reduced alveoli &bronchioles, exhale don’t recoil, bronchioles collapse, decreases SA, traps air, pressure increases, alveoli burst Lung Cancer: Symptoms S: Continual coughing, chest pain, shortness of breath Entrance to bronchi, smoke hits fork in airway, deposits tar contains carcinogen compounds in smoke. Tar destroys cilia can’t remove, longer time in contact with epithelial cells, enter nucleus of epithelial cells in lung tissue, effect DNA controls cell division, causes mutation-uncontrollable cell division, forms tumour &… Emphysema (COPD): Symptoms & … Chronic Bronchitis (COPD): Symptoms & … Smoke contains: Atherosclerosis Thrombosis CHD Stroke & Symptoms S: tired, breathing shallow & rapid, harder exhale, loss elastin Phagocytes invade secrete enzyme ,elastin destroyed, alveoli fail to recoil ; constriction of bronchioles, forced expiration, causes alveoli to burst , reduces SA S: Cough mucus, Lung irritation Inflammation airways, Tar destroys cilia, mucus not removed & over-active goblet cells, build-up of mucus leads to bronchitis Tar (see page 15) CO (enters RBCs, combines haemoglobin, more readily than O2 form carboxyhaemoglobin, reduces O2 carrying capacity, less O2 associate, less disassociates at respiring tissues, less O2 for respiration, less ATP produced &energy released, strain on heart, has to increase heart rate to pump sufficient O2 to tissues, damage artery lining) Nicotine (addictive--makes platelets sticky, increase chance blood clots/thrombosis,--mimics transmitter substances at synapses between nerves, makes nervous system more sensitive, smoker more alert) Deposition under endothelium, in artery wall CO & high blood pressure damages endo, repaired by (WBCs) phagocytes, encourages growth smooth muscle & deposition fatty substances (e.g. LDLs, unhealthy,(see page 9) & cholesterol (LDLs transport)). Deposits/Atheromas. Atheromas build up under endo-, breaks through endo- forms plaque (sticks out in lumen), less flexible& rougher, narrows lumen, reduces blood flow. Increase chance blood clot (thrombus) caused by: plaque increases friction, blood slows & deposits further when flowing over plaque &---nicotine makes platelets stickier. Blood clot/thrombus block artery. Clot can break free, travel until blocks artery, stops blood flow. S:hard to exercise, shortness of breath Coronary artery supplies Cardiac muscle with O2, high pressure, lumen narrowed plaques, reduces blood flow, less O2 for respiration, (increase heart rate, pump faster get sufficient O2) lead CHD: Angina (chest pain), Myocardial Infarction (S: severe pain chest & arms, death of part of heart muscle, caused thrombus), Heart Failure (can’t sustain pumping action- blockage coronary artery). S: numbness, trouble walking & seeing Multifactorial- No single factor causes it Death part of brain tissue- loss blood flow to part of brain. Cause: blood clot (thrombus), haemorrhage (artery bursts) Page 16 of 24 CVD Problem Risk Factors increase/decrease CVD & Less of a Problem in LEDCs Types of Risk & Define Correlation, Cause • • • • Key Terms Importance Biodiversity Discrepancies in Biodiversity Estimates • • • • • • Expensive treat, long term drugs/surgery Multifactorial- links unclear Increase risk: Age (older, more time build-up fatty deposits-atherosclerosis), Gender (Men more likely under 50yrs) Less problem LEDCs: different lifestyle, lower life expectancy, higher chance developing other diseases Perceived- different due to factors: – Personal experiences – Media representation – Lack of info Actual- supported by scientific research Correlation is link/relationship between two patterns. Cause: The reason why something happens. Species Diversity-measure of biodiversity of a particular area. Species- group of organisms-share common morphological, physiological and behavioural characteristics, can interbreed to produce fertile offspring. Habitat- range of physical, biological and environmental factors within which a species can survive. Variety of life- the range of living organisms in an area Ecosystem: All the living and non-living components in a specific area and their interactions. Biodiversity- measure how varied an ecosystem is. It can be measured in terms of genes, species or habitats. Catalogue of Life-catalogue of all known species Many species not yet discovered could be potential life-saving drugs or miracle foods Intrinsic value Ensures ability of organisms to adapt to environmental change Many species becoming endangered or are becoming extinct Large areas not yet explored Continuing evolution and speciation Page 17 of 24 Random Sampling How Random Samples Taken Study small part of habitat & assume representative of whole habitat, should count all individuals-not practical e.g. single celled organism impossible Random no. generator table/computer plot coordinates Need to give accurate measure of no. species & relative abundance Small plants too numerous measure % ground cover Sample- study how human activities effect enviro so reduce impact Plants Animals • Quadrat, Transect • Sweep Netting (Interrupted/Continuous • Trees-white sheet Belt Transect) SR: no. species present in habitat. Doesn’t take into account no. individuals in each species. No. different types species not individuals, qualitative SE: measure abundance (%) of individuals in each species, quantitative 𝑛 2 (𝑆𝑖𝑚𝑝𝑠𝑜𝑛𝑠 𝐼𝑛𝑑𝑒𝑥 𝑜𝑓 𝐷𝑖𝑣𝑒𝑟𝑠𝑖𝑡𝑦)𝐷 = 1 − [𝛴 × [ ] ] 𝑁 n= total no. individuals N=total no. all individuals of all species Σ=Sum of… Species Richness & Evenness Simpsons Index of Diversity Define: Classification, Phylogeny & Taxonomy • • Difference between Taxonomy & Classification • • Relationship Phylogeny & Classification Difference between Phylogenetic System & Hierarchy Recent Common Ancestor C- process of sorting living things into groups. Study similarities between species. Classify based on phylogeny, taxonomy, T- study principles of classification & differences between species e.g. physical. P- study of evolutionary relationships between organisms. (e.g. Human&Gorillas-shared common ancestor) How closely related. P studies evolutionary relationship, C groups organisms based on common ancestors, based on evolutionary relationship/phylogeny P: evolutionary relationships, arranged in groups H: based on shared characteristics (Hierarchylarge groups spilt into smaller groups) Recent common ancestor, more closely related, short evolutionary distance, closer on evolutionary tree-basis for natural classification Page 18 of 24 Outline characteristics of 5 kingdoms Prokaryotes Kingdom: Prokaryota/ Monera e.g. salmonella, e.coli circular DNA (naked, not associated histone protein) no mbo smaller ribosomes (70S, 18nm) Free Living Autotrophic & Heterotrophic nutrition Cell WallPeptidoglycan Protoctista K: Protoctista e.g. Amoeba, Euglena Single celled+ multicellular Both plant/ animal features Fungi Plants K:Fungi E.g. Rhucor Multinucleate Cause decay of organic matter Animals K: Plantae E.g. Moss, Roses Multicellular K:Animalia E.g. Mammals, Fish Multicellular Eukaryote- MBO, larger ribosomes (80S, 22nm), linear chromosomes associated histone proteins Autotrophic & Heterotrophic nutrition Cell WallSometimes Heterotrophic nutrition Autotrophic nutrition Heterotrophic nutrition Cell Wall: Chitin Cell Wall: Cellulose No Autotrophic- Gain nutrients from photosynthesis Heterotrophic- Gain nutrients by digesting and absorbing organic matter Domain Kingdom Phylum Class Order Family Genus Species Taxonomic Hierarchy Compare & Contrast Domain 3 D- Bacteria (Eub-), Archaea (Archaeab), Eukaryote 5 K- Prok, Protoctista, Fungi, Plants, Animals Down- more diverse, fewer similarities Different Same Structural o Bacteria has: different cell membrane structuresometimes-flagella, o Different internal structure-different enzymes o No histone proteins bound to DNA o Different mechanism DNA replication (Binary Fission) Archae share Euk: o Similar enzymes building RNA o Similar mechanisms for DNA replication (mitosis) Reason for Classification Define Binomial system of nomenclature & Dichotomous Key Common name doesn’t work Dear King Philip Came Ordered Fat Greasy Sausages Page 19 of 24 see relationships easier to identify convenience BSN: 2 names identify each species. Latin. GENUS (CAPITAL) species (lower case). printed text italics, written underlined DK: series questions 2 alternative answers help identify specimen Same common name used different species in other parts world Different common name, different countries Translation languages give different name Latin-universal lang CC is protein needed for respiration. All living respire, few exceptions, therefore all organisms have cc, not identical all species. CC is protein made aa, compare from 2 different species: greater similarity, closer related. Not identical due to (variation) mutations (random changes in the nucleotide bases). The aa for proteins are initially coded for from genes on DNA, then transfers info to mRNA in the nucleus etc... Therefore DNA bases & genes must be very similar to then code for similar aa & similar protein, cc. Genes are made up of a sequence of nucleotide bases. D: more similar nucleotide bases, more closely related Classify organisms Compare: Cytochrome C/ DNA Sequence Define variation Differences between individuals caused by DNA/Environment Variation within species- skin colour, eye colour Variation between species- used to separate members of 1 species from another- wings, backbone Continuous Difference between continuous& discontinuous variation Causes of Variation Page 20 of 24 Range of intermediate values between 2 extremes Quantitative Most individuals close to mean No. individuals at extremes is low e.g. length of stalk, height humans Discontinuous 2+ distinct categories Qualitative No intermediate values Members species evenly distributed between different forms/ more 1 type than other e.g. Human blood groups: A or B or AB or O, Gender-F/M/H, Genetic: genes inherited, define characteristics, combination alleles unique (unless identical twin). Share similarities other species never exactly same. Environmental: diet:overfed=obese, sunlightskin=tan, enviro affects direction + amount of growth, stunted, malnourished Define Adaptation Behavioural, Physiological, Anatomical, Xerophytic Adaptations of Organisms Speciation Adaptation- enhances survival and long term reproductive success. B: behaviour enhances survival- earthworm touches& withdraws P: correct functioning of cell processes-yeast respire sugars an&aerobically to release energy, depending how much O2 in enviro A: structure enhances survival- bacteria- flagella for movement X: + B: roll leaves reduces water loss traps moist air less steep water vapour potential gradient, less SA exposed, + P: mechanism plant opens/closes stomata, photosynthesis + A: long roots reach H2O deep underground Speciation/Evolution 1. Through Natural Selection 2. Genetic Variation/ Random mutations 3. Resistant/ Survival of fittestmust be a selection pressure e.g. climate, enviro (diseases, availability of food) 4. Those best adapted (selective advantage) survive, passing on alleles (selective advantage) to offspring 5. Allele only confers resistance/survival to that particular selection pressure in that specific conc/temp/pH etc. 6. Happens for many generations, selective advantage passed on, helping organisms to survive. Over time small variations arise, if aid survival, change. Eventually 1 group of organisms belonging to 1 species could give rise to another species-speciation. New species, must have reproductive barrier so different can’t interbreed with original species evolved from to produce fertile offspring, Reproductive Barrier causes Speciation Evidence Supports Evolution Gaps in Fossil Record Geographical separation. Different groups same species on different islands unlikely interbreed. Speciation-Allopatric speciation Biochemical change prevents fertilisation due to behavioural changes- courtship dance not recognised/gamete incompatibility:sexual organs not compatible can’t mate. Sympatric s Biological molecules-certain molecules found in most. 1 species gives rise to another, both likely to have same biological molecules. Evidence for all species coming from 1 original ancestor. CC & DNA sequence(see pg 19) 2 closely related species, recently evolved as separate species, similar biological molecules.-speciation Gaps in records: only hardest part survives, many living things don’t have hard parts-no fossil. Only form certain conditions. Damaged/destroyed by movements rock. Page 21 of 24 Selection Pressure Conc pesticides in food chain. Insect resistant survives then Predator eats lots of insecticide, large conc, predator eaten, conc increases up food chain reaches humans. Antibiotics strong selection pressure, kills most of bacteria. Small no. resistant, rarely completely unaffected, more resistant than most. Most b killed, feel better, stop antibiotic course, resistant survive and reproduce more resistant. Overuse+ incorrect use- strains b resistant nearly all antibiotics in use. Prescribe multiple antibodies reduce chances of bacteria surviving. Reasons for Conservation of animal and plant species: Economical, Ecological, Ethical & Aesthetic Reasons Climate Change Impacts on Biodiversity, Agricultural & Diseases Important conserve Biodiversity Human activities cause harm indirectly/ directly other species thus loss biodiversity & extinction e.g. loss bd: monoculture,(reduces variation, diversity, lead extinction) habitat destruction: deforestation, (reduces pop, decreases variation, decreases ability to evolve) Econ: regulation atmos (photosynthesis) +climate, (without O2 unable breath) Ecol: answers technical problems (best aerodynamic shape in H2O) Eth: loss habitat+biodiversity prevents things living where they should Aes: patients recover quicker stress+injury exposed natural enviro C: Species already lost genetic variation won’t be able to adapt & evolve to changing temp etc. Forced move, whole ecosystems forced migrate- problem for national parks, protected species move as climate unsuitable, more vulnerable to extinction-hunting etc. A: Climate change increase CO2 effect photosynthesis, temp increase growing rates, increase evaporation rates more precip. Domesticated plants & animals at risk, selectively bred to provide best yield in specific conditions, as conditions change unable adapt & evolve D: crops grown new areas, encounter new diseases & pests, not be resistant. Higher temp, longer growing season, longer for pests to increase. Page 22 of 24 Wild plants & animals hold answers to climate change, thousands of years to evolve & adapt to enviro problems In Situ- Define, Advantage & Disadvantages Ex Situ- Define, Advantage & Disadvantages Conserving species in normal enviro, minimise human impact & protect natural enviro e.g. conservation parks + Conserved natural enviro + Permanently protects biodiversity & representative examples of ecosystem + Facilitates scientific research - People continue to hunt protected animals for food - Tourists feed/leave litter - Illegal harvesting timber etc. Repopulation-increase biodiversity e.g. recreating wildlife habitats Conserving endangered species by activities taking place outside natural enviro e.g. zoos, botanical gardens, seed banks (level moisture affects storage) + + + - Protected predators Health maintained Sufficient food Space limited, limit no. individuals, limits genetic diversity, reduces variation, gene pool restricted, may be less able to adapt to changing conditions, affect if breed successfully - Reproduction successful, still have to survive reintroduction- find food, survive predators Modern techniques- preserve genetic material- e.g. artificial insemination, sperm freezing, carry out research on domestic species similar to target species effective & save rare, endangered individuals from experimental work Conservation Plants +&- - + + + Plants- bred asexually, only need 1 In life cycle have dormant stage-seed, produce large no. (large supply for research) & can be collected in wild without much disturbance - - Bred asexually will be genetically identical, reduce genetic variation Seeds of same species from different areas will be genetically different, may not succeed. C I T E S (Convention on International Trade in Endangered Species of Wild Fauna and Flora) CITES & CBD Aims: Regulates & monitors international trade in selected species plants & animals o Less endangered may be traded subject to permit o Ensure trade of wild plants for commercial purposes prohibited Difficult-where demand, attempts to smuggle C B D Convention on Biological Diversity Aims: conserve biodiversity o Appropriate shared access to genetic resources & sharing scientific knowledge & tech + Import genetic material, save time, cheaper, less distress to rare animals Page 23 of 24 EIA Environmental Impact Assessment-assess enviro impact of development, can lead to improvements in planning & design International Level: avoid/minimise adverse effects on biodiversity of area & ensure potential enviro consequences taken into account Local Level consider- size of development, enviro sensitivity, types of impact expected 3 stages: developer complies enviro statement, publicised, authority takes into account when making planning decision Page 24 of 24