He Cell Structure Membrane systems and organelles ~ plasma. membrane: contro what enters / aves cell (nuclear pores] = nucleus + _ surrounded "nuclear envelope - contain “ehromesemes"- long molecule of DIVA - ‘nucleolus. sie g ribeseme precluction ~ code on part of DIVA ~ ribosomes: _ RIVA + protein - free in eytoplam + attached te RER - RER: _ enclose small_spaces “cisternae” ribosomes prota sycthess — Clinking amine_acick ) meve into asternae — <——I > break inte membrene- bound vesicles — Golgi apparatus Gyi body: modifies protein C+ corbohydrale group: ) — break away —> cell surface imembrane > secreted vic exceyfosis ~ Smooth ER: — more flattened esternae. ~ involve On synthesis + transport of steroids + lipids break doun fexins chonokia: _ site ot respirotien ATP producecl ~ 2 membranes Cinner 1s folded. — enstae ) > Aysosomes: _ little packages of hydrolyhe Colgestive) enaymes - broken off fom Colgi apparatus digest: ~ food taken inte cell ~ Boeteria fells faken in by phagocyloss ~ break dlewn unwanted /damaged organelles -Ceniioles: — nwerehabules form spindle churing animal call cliw'sion. -Chloroplast: — envelepe gq & membranes ~ background matertal Csrema) contains. patrect membranes Cthylakolds) > stacks Grana) which contains shlerophyll FOS$ ~ May conlain starch grains flows Vet cyeplecm betwen calls pA v pb lesrodaFrokenyotie. » Exkoryctic calls ; us Frokoryotic._cellg ~ much smaller 1-5 pm diameter -_ 9 membrane ~ bound. nucleus / other mem brane - keunel organelles — plasma membrane onl i genetic material noked in cytoplasm — organelles ribosomes, ribosome presi —— ~cell membrane Eukaycte calls auclecid DNA > deuble membrone- bound nuclet's separates genehe mater! from other organelles ~ endlerrembrane system: different membrane ~bourc! organelles that mansport meacterialy arounol > energy pradueing organelles: mitechonokra, ehlerepkast > metabolism / energy cenversion the ell Prokarychic | Bic jotic — cel animal plant - call membrane, G) | Go) : G) 4 ne call wall | @) peptclegiyeom | C-) | cotfeclose | r nucleus tenvebpe ‘Coen c+) | ( chromosomes | bacteria! chremotemk - several. linecur \ “y circular DINA ghisi DNA mekeules XS s - plesrnicl |. + histenes sitlcabaalints c+) a) ogteplasmn ribosomes. | ¥CS 60m 308 220m | armies | C-) wa | ee] Vruses non -callular structures -mocle. of protein and nuclere accel @NA f RNA). Are- Provide energy fer ony energy = eensuming _activhyA. Biological Nlolecules Corbohyorates xT Lipids sor gi CH, 0, Ls energy scurce Cstoreh +glycegen) —>stered! S structuralsmerterialCeellulos¢.) Monosaccharides . gluccse , fructese, galactose - often has ring form simple sugar A- glucose. P- glucose CHCH CH,CH Oe = = ol Sones Noe eM 4 cH Dissccharides - cleuble sugar ~ sucrese <2 menol] = joined — by maltese = .gluccse: + glucose glycosidic _benals lactose = "+ galactose sucrose = * 4) fructose eendensation reactions + _2 mene covalently ycined - 1,0 fermed 2 AW giycesiic SS mo enol hycholysis reaction «disc split > A mene by breaking J ~ oc meleoule of HC a octlel suereas —s HO eg sucrose glucese + fluctese Gren-redlucing sugar zest ) form * menomer: identcal molecules that can be jomed —- polymers polymer: long chein of joined monomers macromolecule + Jorge biolagreal molecules 8 polysaccharide: eemplex sugar=regpiration = storage molecule et eee if + source of C “Polysaccharide — a produce. other 4. Storage ps ata Starch 10k - AOk 8b ~FOh amy lose amylepecten Amylose a orn ~ very long chain ucth 4-4 links > ehein coils > spiral scheld in shope by H bonds. behween gluct units Amylopectin: © oO es highly “branched! - shert side chains: 30 'gluecse nn = ab -30 unrh with 4-6 linkages aleng. the chain Glycogen - d-glucose moleculer + glycesrdre bonds -mestly (4 Inks; sen 4-6 links — branches ~ bench can by hydrolysed + enzymes = sterecl o — mena > respirochion. ~ branch s 7 hydlrelysis rate 2. Structural - Gilulose @- glucese, IH links - adj acent molecules = upude down «straight chain Cspot) - H bonds beheeen chains —> Strong micro brils = _ell_wall doesn't break easily when abcerb MO 2 diffoult to. cligest glee srdve /<— MOOD CHO COOO COO POROD sh peeebs- CHO oe Jinseluble in H.0 Liprols 2 ‘yglycercle + phospholipid 4. Triglyceride - 4 glycercl + 3. forty acid Garwsd by ester bonds eo » energy storage in plants’ “animals, fungi @. mammak ~ build up under skin — adipose ssuc: Bry * contain oil dropleb b ic. energy store in seeclt oO + insulate body ~ cotyledens Guntlower seeck) E +p = % bucyancy endosperm Caster beans) V aquetie mammals + pretective layer around organs Ckidney) + hermenes 2. Phespholipicl -1 glyercl + 2 fatty aad NA + 4 phosphate group pean ier hyctrephebre > bilayer —> cell membrane PRoteins COCH- carboxy | | Peptide bondl group | = condensation : _S : A amine acrds ___, dipeptide ‘ NIEC-Ie + pepticle bend HO. { ie aul ~ hydrolysis — rR) ee eh | dipeprde amine accds Ss Re group Chrecik peptide bond by eS ae using a molecule gd H,0) neutro:| a v es i corde on J eromeitie _ AMES aaPrimary Structure < sequence cf omune aciels in the chain Secondary Structure: chains ferm: . & helices - PF pleateol sheet. = held by H bends — stobilty fer shape secondary structure feld up to ferm a precise Tertiary Structure ~ disulphrole _benels 30 structure Ferces* ~ HH benoly - fone bendy ~ von der Waals’ Aydrephebre interactions Quaternary Structure: The assccration of alifferent pelypsptide. chain: - H bends: . form between wurde. variety of R= groups double : v Disulphide: between Q sulfur atoms of amins acd S=S Ceysteine molecules) Tenie bend: between R -groups containing amine + eorboay! groups Toppewtely ehavged Hydrephebre interactions - betveen R- groups eshich are non-polar. Chyerephobre) =I ely peptide chains yom fe form a profein ~ con be inveled with acldlitenal jnerganic _camponent \+ Prosthetic Group Haemoglobin. - globular protein > Ba +26 pelypeptcle chouns + 4 presthehe Hasm groups - carry ©, \t tertiary structure —> soluble + chains + hydrephile R groups :cutsrde — form +H pberds with 4G ceil so that x hydrephebic * * insice molecule. + haem group — eombine with C2 ve Fe’* > 4 hoe group <> 0, molecule + shope of Hb + pick up + rekase g O, (Sem : after 4 ©, molecule hax combined with a haem grow) molecuk CHANGES SHAPE —> easrer fer 6, to combine with remaining 5 heam groups eesupperé + elewticity Chuman skin, bones, tenctons ) Collagen - fibrous protein w IOCE exch - 3 pelypeptce cheinrs“wouncl croundl each other Gn he! ces) = structure strength ft ~ HH bend behveen chavs > wthstand pressure = collagen molecules wrapped around each other — Collagen Fibrils —> Collagen Fibres 4 molecule size —> inschible + & stranded moleade high tensile strength. + glyeine Cevery 3'ominc coc) — compactness « lysine — > formation of fibres later H- bond = attracticn behveer 57 onc §~ port ef rarghbouring H,O molecceler = Solvent properties Char dipcles) i molecules /@ eharges / can be seporated inte rons — clissolvable — transpert substances. ghicese, O,, ion: clssclve reactant — enable metabolic reactions - 7 specific heat capacity fot of energy neck! to break H bonols and 7 t° — cceans, lakes CH,C) doesnt chonge 1° os easily Car ar) - latent: heat gf voporisation lets energy neeckd for 1,0 to ehange state — abserb Jott of heat from — surroundings a { — sweating | cooling = franspirecion effecteee Bee 5 glebular proteins oe catalyses metabale rece tions Chrologrcal catalyst ) emymes funetion inside Cintrecellalar) ancl cutsole Cextacellular ) calls Mode of action a - active. si: crea whrch emnyme = substrorte subshrate binds te en2yme complex octve wt + R= groups cf amine acids. form tem porary bends & substrate ae — pulls shope — product octivationt > celieahie..adaiy leaegy t ene need fer substrate —> product x. heating 3 — th 2 atalyst emymes dae. > It : cataly - distort shape of substrate when it binds at en2yme’s achve site — _— Leck -and- key hypothesis CFmil Fisher, me) -Ispeerfierty i shapes must be ComPLEMBNTARY bo Specific &D shapes = fit exactly Trducecl- At hypothesis - shapes ere net complementary - in presence of substrate, active site contnuclly reshapes’ by iB interactions & substraa — fit completely - enryme rs flexible —> moldan Se diploid cell: one that possesses two complete sets of chromosomes - an haploid cell: cne that possesses ene complete set ct chromosomes -1 meiosis —? reduction division: number of chromosemes reduced! number ot chromosomes woulcl double each generatron - Tt net out oS ~ Evidence for effects of smoking on health 940) gemete geome - Epidemiclogrcal ewclence + lerge 4 A involved — researchers lock fer correlation behveen smoking cind be porticular diseases — > shece wether or not there + cewict + physiclegical ewiclence oO casual relabenship. - Experimental evidence cut centrolled experiments GI > carrying + ZV: smokes? + DV aspect of _physiclogy using cells growun. in tissue culture. — exposure te chemicals feund inter. >. damage DNA Preventing and treating CHD D risk > inheriting alleles Igenes ~ net sufficient exercise - diet: sat fat +cholestercl - chesity = smoking + Coronary bypass + piece of blood vessel from ancther body —> sewn — > provcle alternative route for, part of exygencted blood from aorta te heart musele + Heart transplant > long term eption £5 A just ‘clied 5 similar tissue type ~ recipient: dake immune suppressant drugs reject trangplant rest_ot life immune systern may ! Prevention: lifestyle choicesCAPR asa Om EN AO aD, AER TEN The need for transport systems = Unicllular omansms — diffusion alone + deesnt take long fer substonces te diffuse fren membrane to cantre cf all, wee versa + large SA: V rate Mulbeellular orgpnisns + centre tec for cuvay from surface small SA: V ratio + Tonsport systems tec. leng te diffuse. cory substances + ® SA cf some ports of beoly by mass flow thin, tlet leaves highly folded gas exchange surface Planis- roles of nitrate and magnesium fons 6 NO, ~~ amine accds - muckeotides = erganic bases ~ coemymes ~ proteins ~ chlerephyll bs deficreney: _ pacr grousth ier? - old baves tum yellow, die premocturely Ng** — chlerephyll molecules have Mg tem in stricture enter ~ emtymes hove Hg™! at active site eg ATPose.tosses between _ plant, and Primary consumers ab al rts ore ecrten a eaten ore _oligestible. =—seme_energy less’ 0s heat within the consumer's. digestive system + Less energy available at each successive trophic level — > food chains normally howe 4-S links © beyonc! ffi crert energy © energy lest te environment as heat (a) Nitrogen cycle N=N strong trple covalent > unreactive. Nitrogen fixing Jation +: convert Ny into ergonic molecules - lightning: Pt providing Tenergy : N, +C, > nitregen omdes - Haber process: produce NH3 ,momufactue ferhlisers ~ nitregen- fixing bacteria . produce NHy* cons, 4 Rhizebium in rect nodules ot legumincus plants Nitrificection eee _irogenase - nitrifying bacteria oxidise cmmoneoc — nitrate sens + Nitrosomonas + NH” — NO, nitrite: ions + Nitrobocter + NC,” — NO, nitrate ions NC, taken up by plant rects Decay and ammonification Animals excrete nitregen -containing esmpcunds eg. Ney, urea Pode decomposing bacteriq break cua protein molecules > rekkose Ny and NHy* into soil Denitrification ~ Bacterio. geh energy by converting mtrate icons to nitrogen gas —> returns to. otmesphere « Rhischiann ~nitrogenase ~ cendlitiens hyckogen svpply + AIP og 1_onaerabic envEcolog (a) - habitat + the place” Shere an organism , pepulatien or community lives s niche: tha role o an ergonism in om ecosystem - population: all organisms of same species present in the same plow ,oat the same time - can interbreed with each ether = community: all living, organisms , q all species, that are found im @ particular ecosystem ot a particular time = ecosystem + all living organiams of all species living components thet ) ceand..ell non che) feund dogether in a elefined avec interoet wth each cihar (b) Food chains and food webs — interrelationships pathway which energy is. transferred from one organism between many fecel_chouns te another c 19 nsfer > heterctreph: on organism neacling o supply of organic mekcules os sts 1 Corben — scurce. focd in 5 ch hy producers ~ auictreph: on organism thet can trop an inorganic carton scurce (Co, ) usng energy from Light or from. chemicals "g id 7 = organisme that obtarns : = eats ; cle evs er chemesynthe ~ trophic judnky Position at which an erganr Ce) Fhergy losses along focal ehcun sm feeds in a food chain efficiency doh Ps10.2. Antibiotics = & drug that — stops/ kills growth of bacteria < - without harming cell of infected person /organism E > interfere with bacterum’s growth » metabolism 7 + bacterial wall synthesis, protein synthesis + call surface membrane furetion 4 enzyme action Antibiotics does not affect viruses: - viruses don't hove cells ; replicate insicle host cell — antibiotic destroy host all —> ontiproductive Roieillin bacterial! Ss peptidoglycan ‘cell walls helcl O—K together by crosslinks ~ penicillin prevents synthesis of crosslinks. Cinhibits enzyme that build cresslinks ) o@ago e 0006 New brocterial grows —* secretes ‘autolysin’ — create Acles in cell wall — bacteria stretch to form new cresslinks #0 = penicillin prevents links ferming — walls get weak - bacteria live in watery environment cS Burst! — osmosis — burst under pressure tho Antibiotic resistance => cocles. for protein > bacteria gains are that protects them from anbbiches 4. Mutation 1 on existing gene changes spontanccusly — nuciecticle sequence 4 slightly altered protein hth etteredeR eee TTA Vertical — transmission | Horizontal transmission - parent to oll spring Om HO =. + bacterra have one eepy —- genes on plasmids © ot each gene (part — transferred between bacterium & single DNA. bep) Mutant of different species gene. immediate effect eg. resistonee in_nen-pathegen _ bactericx - asexual repreducticn posse tc pathogenic _boctericr binary fission 2. Selection resistonce. spreads quickly = Where lets of antibichies ore usec , ameng different species of bacteria & plasmicls carcying resistance genes fer several fs 49 g different antbichcs —> multiple resistance Consequences of antibiotic resistance bacteria _ causes infections after surgen HRSA \ resistant to mang ontibrotres C+‘ last resort’) g spreacling quickly Treatment of antibiotic resistance. have differently ~ behaw iy > search fer new anhbichcs —— 4 ~ slightly ehange chamical structure of antibichice ‘Semi synthetic Reduce crsk = use antibrohes minimally > complete course antibiohes — kill al! bacteria in becky - reduce countries selling antibictes withast prescriptions - fest bacten'c for effectiveness Cin lab) of antibrahe before expasing bacteria 6 selective pressure.Factors affecting rate gf enryme - catalysed reactions Bets -t°R = KET = FP successful coiliscons = T rote - ot optimum 1% = mowimum rate - abeve thié , H- bends helding molecule breaks > chenge tertiory shucture of emyme Clenctwation ) — ochie sik defermed — ¥ binding - s/e complexes formed 2. pH Fe OD cede 5 mecsure of concantraten of H jens lewpH Caerctic) high pH Colkoline) < tec mony CH —_octive site Outside normal pH © chonge 3D shape J enzyme + active site 3. Emyme concentration substroie Demeyme —> limibing foetor: emyme cone Temyme conc = T collisions » T emyme/substrate complexes A. Substrate concertration T= 1 collisions - T e/s complexes 5. Tnhibitor concentration slows dewn rote which emyme vwoorks Competitive inhibitors Noncompetitive inhibitors ~similar shape te substrate = ctoches to enzyme somevuhere > prevent bincting Shit teas other thar. the active site i> Vels complexes 7 changes shape of actrve site enzyme cleesnt ecitalyse reaction — e/S complexes cant form > no producti fermecl 4 no catalysis substrate Lipa eS emyrng4.Cell membrane * transport 4.1. Fluid mosaic membranes ta | from aloe: proteins arranged mosaic pattern phesphelprd + protein can move about by diffusion glyco - ~ pretein 0 GG oc micalle SEES e is Cd000 =e : Ho eg maa oe phospholipid hyclicphobic tar/s _ biloyer hyolio philic heads S-glyeclipiol —~ corbehy cote port Phas pholiprols > Fluicl <== P_unsedurostect teuls more © shorter 2 Fleaicl ’ ( ~ permeaible: small molecules — Cnen- potir) 2 é > impermeable large melecules / ens 4 2 eg < sugars, amine aciols, proteins Cholesterol - maintons fluidity of membrane } supe scaler prevenis clese packing cf tails ae - increases mechanical! stability prevents cells breaking + bursting ees HG oat pessing through oa: eps pelea Sees eas Ire re naieee)Glycolipids « glycoproteins’ > carbehycrete chains —> sugor coating "glycocalyx > cell surface receptor molecules <— hircs 4. signalling recepters recognize hormones + neurcfansmitters — coordinate activities of animal cells e.g: insulin receptors @ pver , muscle cells 2. evel endocytosis 3. cell - adhesion ~ antigens cell markers —*_cell- ce/| recogni ten Proteins glyce proteins bind o& — treinsport proteins extoeellkar signalling mckeule channel = tensoluct message. intc carrier = enaymes | egecrta lyse Ayolrolysis [eas intracelldar signalling mot cule changes call behewiour gd disaccharides eS : 4.2. Movement of substances inte and out of alls Deter rier BEN inom mehr oth molecules Jiens of a substance from a regen of No — de. ~ steepness. ef cone gradient Colif in conc) aa fc ee Sat more oli fhesion nature molecules fiens + _lorger —> Jd nod 1 KE woter —> = non =pobr YW soluble in phespholipicl to’ smellFacilitated diffusion ~~ No’. Cl” = movement of specific molecules - dewen e.graalrent - aid g channel + carrrer proteins - ne energy usec . Cpassive) - channel proteins + carrier proteins + specific + Open up werter - Filled + allow diffusion cress membran é for large polar melecules pores across al + molecule attach fe preten membrane. = change shope Cw vi) — enty Jexit Ee — delivered ae Not c> K through. membrane a) y Osmosis. : net movement g water molecules £...] through a Faille: permeable membrane dilute solution /_H, i ‘ concemboted elution sugar RAC plant 4 la el tl burst turgid : animal cells We We flacerd * pice ean flacerd: Wer © Cne p cn call walls) vacucle SHRINKS as — mere water w pulled out = cell membrane peels ara —?_ PLASMOLYSED ‘from cell wall > bype'tenic — seluben: weak _soluchon ~ hypertonie — seluhion. strong soludion ~ isotenre solron + equili rumacs eee rE Active transport the uptake af molecules / ions against a cone. gradient using energy from _respireition vic corrrer preteins ~ energy usec! te change protein’ shape ATP — ABP +R Bulk xansport - endecytesrs ancl exocytosis fer macromolecules feo large fer manspert proteins transported in membrane bound vesicles 4. Eneleeg tosis + engulfing materials by the surface @ phagecytosis = “call eating” ‘> sclidl material — — vesicle —> fuse @ lyseseme — empty enzymes > preducts absorbed by eytepasm, eg WRC, amoeba © pinceytesis: "ceil drinking” +— Irqurd materrel 229. in Humon £q9 cells 2. Exe cy tosis materrals release from call through fusren. of a membrane bound vesicle with call membrane . = material surrounded by membrane — vesicle = meves te plasma membrane, breciks cpen ~ fuses with membrane expelling waste, secreting substances proteins hormones= The Viitotic Cell Cycle DNA _ structure ' DNA molecule packeged inte a thread: like structure “CHRENOSOMES ” & coiled around "HISTONE" proteins +— support shucture . a & chromatid cre g the 3 Ee - identical strand of DNA. that - makes. the chromosome. region of repetrtive nucleotide sequences at each end of a chromotd - protects the end from dketerrorating / fusion with neighbouring chromosomes - shortens curing centromere ~ joins 2 chromaticls together yh region winch fibres attach to during cell olivision eal olvision » hislenes gene regulation = centibute to >order length of DNA in cells ellular oging + dliseases Mitosis. - division of the ‘NUCLEUS’ Significance : - production ef genehically identical cells: keeps #of chromoscr constant + genehe stability in daughter cells —> linear heredity » = growth: a single call civics repeatedly —> ail ceils - repr of tissue, call replacement: of damaged /worn cut cells = asexual repreducticn: identical eff spring 4. Interphase atalaeat % * G1- phose + cells “moniter” environment — Vv signals — synthesize RIVA + proteins —> induce grousth + S-phase: DNA replication © chramcsome 1 2 DNA + antomere + Ga- phase: calls grow, prepare fer mitosrs : = organelles Cratcehondria + chlereplasts) replicateda. Mitotic phase Cu-phase) @. Mrtosrs _ nuckelus breaks down Frophase : ~ chromosomes condense ~ centrroles duplicate — opposite poles Paoferm — spindle fibres - nuckar envelope breaks down Metaphase: - chromosomes line up along equater of cell - uhrematd of ech end Lies on either side ~ spindle fibres attach te cartromere Anaphase: - spindle fibres contract - sister chromatid pulls to opposite poles of the cell Telophase: - separaticn of chromatids is complete - spindle fibres olisintegrate - _ chrematid + ehromoseme > nuclear envelope referms crouncl each group of chromosomes cit its poles 6. Oytokénesis > cinches + divicles at the waust —. genetically icentica! laughter cells jem cells — unclifferentiated biological cells that can differentiote into specialized cells embryonic stem cells > cet as repair system adult E bmvtosis: 4 daugher all stays ar stem cell, f ol fferentiates eats Ie vision, ‘7 1 stem cell pool’ = genes thet control cell diviston mutate = all divide cver — irregular mass of cells + malignant tumour: break off — form tumeurs elsewhere & supplied with blecd+ lymph vessels — ametestosis 7 eoreinagens «- UV light fensing rediction Secondery tumour bX rey tor in je bacco smoke [cher virus infect ere ditary preclispesiticn6. Nucleic acids »Fotein synthesis Structure and replication of DNA ae ee nitrogen containing — base phosphate group penne. pyr ine ane > adenine CA) thymine. 7) s : uracil Cu)? NA guanine.) cytosine CC) La ( pentese. sugar * ATP Cadenosine triphosphate) - nucle tide molecule doesnt. > cr me energy .corrier ir eovelent ‘Hydrogen S, ~ Single stranded bor bends E - folded ch e up itself Significance. of base pairing = 2 stands, cppesité = ensure mistakes are net macle directions > double | when copying/ fransenibing BINA helix ent porallel Hydrogen bends -H bends betveen | ~ held adjacent sections tegether | complementary, | complementary hase hese pariring pairs Semi - conservative repli cation > H-bonds between stronds broken —"un2ips”, separates 2 strands - nucketides free in solution hump tnte exposed ene > Bem 4 ~ bends Complementary base pair) - DNA polymerase links phosphate ancl deexyribese groups of adj cicent nuclectidesFectein synthesis * polypeptice is ceded fer by a gene t genes a. length cl DNA that codes for o pentoular protein/ polypeptide + gene mutation» change in sequence of nuclecticles that may resull in altered polypeptide Transcription: DNA template strand censtruct a strand of mRNA = DNA unripped , H bends befveen bases broken > exposing the bases ~ Free RNA ruclecticles ia nucleus form net H~beridls wuith expesedt termplal = RNA ruc linked together —rmRNA molecule (PNA polynierase ) se « Feern. promoter te. terminator region: i a Translation: = mRNA. breaks away from DNA, moves from nucleus — cytep! crens —- atfoch onto ribosome = RNAi cytoplasm Clwvisted: clover leo shope >. 2 anticodon erposec!) = amino acid defermine by anticadion base sequence-siie for otach omino ocd ~ rRNA ard complementary tRIVA H-bonds form between bases ‘enticsdor - amwne acids carried by2adjacent tRNAs Linked by peptide band > continue until step codon. —> chain breaks. awoy Sickle cell oncemia - © polypeptide Ho * : Hb> Glutamic acid Veine base substi tution GAG (ene Fes hycke philic hydro phobic. . 9 tb more soluble Hb less solubleF. Tran sport in. _ plants ; F-1. Structure. of tronsport tissues Transverse section - root a i, = rect hair AeA phloem eombiunr J ae Transverse section- stem vascular bundle sel_renchyma lugrifed fibresSatie EE ES dee Re eee 1. SP Pe, ES aa ae le ae a ee 4 — S54 } ee = i} ~ |_ tengitidine! section ~ lem vessel r ereway | vessel ———> _ dead cells element - impermeable all walls - transport woter + minerals Wergane eg to leaves) substancer thick walls, ~ upward flow thickened ~ Lignin tissue contains fibres Zong) ticiral section ~ phloem vessel 7 es sect soc saith perforations —» pores | companion cel pester nermal plant call structure seivé | | - 2 * mitochondria + ribosomes ) element |_| sl — metabolically very active | = plosmecksmate. pass through | cell wails. | seive= tube element be this Laills “ne nucleus, ~ permeable call wills tonoplast 5 ribesemes tronspert food! (<1.c1o%« = small cyfeplasm Source. _—> ~ bwing cells > flew TY7.4. Transport mechanisms Movement of 4,0 in plaris trom scil —>_ roet hair vio esmasrs ? woter potential —> 4 water potential trom wef —> atmesphere: via olffusion Ctranspiration) ? woter petenhal —> 4 water petenhal from xylem across leaf opeplast ~ — symplast Cohesion + water melecules ottracted| je each other by Ht bending Adhesion: —* “shiek te callulose call wall H,C lost through stomata via transpiration ore gi lew pressure within plant Lrension ) 7 +40 mere from high low pressure Lechesion] helps +0 move against gravity Mass flow: 4 © meleculs mere together, up xylem vessels Apoplast porhwoy * substance maes fiom call - fo -cell through call usal) Symplast pathway: subsiance maves from all to all via _plasmedesmater Casparian strip * a thick, i waterproof, waxy band of suberin a that is formed! ir. the endockrmis’s ell well, — barrier —> water -can’t Reet heur: pass. : mineral rons 420 meves through cytcplasm of = endeckrmal cells — give plant contre) active transport over what token up by inorganic tens pass Inte xylem vesselssunten stomata, PT humidity) dh tfusron = leet heirs trop domp Q very thick waxy cuticle / 1 evaporation trem. upper epidermis air close is surface smaller kaves — SA 1 transpiration - close stamata <—_ rolling up leaves during doy > tap humid air next Viloss H30 } to stomata — beva <— succulent kaves > stems store HO Shallow, extensive rect system ebserb 4,0 from rain + development qf sdavenchyma prevent from co {lexpsing amine ace} the. SFanspert of assimilates Ce g.: sucrose) through a plant jin phloem tissue Translocation requires metallic energ y > flerd sugar source: produce sugar (leat) suger sink store, consume sugar roots, tebert) ts Scurces produce sugar water pctential actively i ; loackel inte seive tube ements — f cone 3. t,O enters ste, ts @ sclutes we esmesi§ meves inte area with f conc. gclutes Inflow of weter = turgor pressure 1 AC + sugar eves sugar sink. 5. Sugar sink uses _ sugarTranspiration - the tors of weiter vapeur fiom o plant to its enwerment, by olffiasion deun e uciter potentio! gredtient » most transpiration dakes place through the stomata in the baves, SEX out e 6 fou a 9€ -11 neceh. CC, corcequence el gets exchange fr_photesyrihesig_—2 Foctors: = humidity * steeper grewent - wind speed _ 1°: more KE supplied te vopour particles = light intensity : stomata dey — open ai night — close phetesynthesr, , gas exchange i recice_unecessory woter _kss - very dry condlrhens+ — groclrent too. steep — plant compromises + closing stomata fe prevent leaves eying <Tpctennad gradient on Sut, J \ {protien | (pee pueny? a AT? — App + % REP R hot \| OOS Nochvel tranebovtl! Rare cay, Ht 4. WY lew pe high pe through preten pum)> Sactive transpert> ATP) 5 ap 4 P. <4 Through, ec -Mansperter pretern , no move cut — inside cell GUTSIDE CELL low sucrose cone, ® 4 Aas OOO (es Fenser G Got 1 i protein, Ht Pilea Iu } Oe oe 1M ae | Oo oOo ® ral gradient eae ee hegh sucrose cone INSIDE CELL %. Through ce ~tansporter protein , loo sucrose eone —> hrgh cone- Sucrose leacled inte seive tebes active transport > > © used - H* jens pumped cut ef companion cell \ . = A comier protein carries H4 and sucrese tens a ~ suerese. conried against cone. groclrent3. Transport in mammals : i 8./. The circulatory system Mommolian cireulatory system is + — elosecl - ckuble circulation syste ~ consisting of a heort, blood vese , Blocd veins arteries connective tissue fibrous tissue simocth muscle elastre fibres encle the lium, - carry few-pressure blood ihvek , elastic walls to expand and reco:l when high bock te the heart pressure loccl pulses through | - thin muscular walls, tte elastre tissue cory bleed cuvay from heart small lumen: high pressure - lorge lumen: reduce frrehen that may slew dewn bleed! steacly pressure qf movement oscillations - valves : prevent beckficw cf bleod = muscle in wall controls blood | -[ blood in veins js mevecl by flow: eontract skeletal muscle centracten ] eapillories - link arterres. and veins - ne muscle , elashe tissue = lunes srsait CRBC sire.) - 1 cell. thick walls Agee. — minimise diffusren olrstance, rapid exchange ,behveen flood aind bedy cells ~ - wail en gop = — plasma leaks cut ~ small. dkometer = TSA: V =. short diffusion. distance endethelium > reduce aif ol nutients, hermenes waste productsLae AEN EE RES No. ror Bere ec ‘ Re po heed /neck mates Iga nee upper / fere Se | » red blood cal - flattened discs _ Z cee ¥ venwiele nae - he te ter ” ae a ver eee hepatic pertol vein 2 cdl see. an, Vee stemoch «4 ae — biconcave __ hs se Tiel fale malas *— coe ae = granules in eytep smfT Hb > 10, — Bloocl_eompanents - red blood cell- no nuclus + mitechondrra — 1 SA = ct white blocd cell - defend bedy against infecten / disease L= , lymphocyte ;recegnie wr boc ferergn —> antibodies destroy unucint ect cells; flexible shape + phageeyte ~ platelets: fragment of larger cells - help bleod elottng — form plug —> @ bleeding - re nucleus Tissue flwol «lymph. > plasma tak from pny gaps in © capillary — fill spaws behveen body cells —> tissue flurd molecules can't get large through Calbumin - protein ) bathes hedy cells » glucose, urea affuse, 2 \O SS iymphotre o- eS e = tf OOO | a; behveen blood plasma + cells capilovy = some. fluicl moverchack into. capillaries inte lymphahe vessel, — lymph Feature - |. Blood | issue paul | Lymph cells rbc, whe, platelets some whe lymphocyte pretens |normones - hormones - few proteins | plasma on _ secreted! pretein glucose more fete nene, less samiNo cera ” less 3 OQ. H pian AL Bs less more more CeHoemaglobin x 0, transport dissociation curve = Hb quaternary structure Centre) 4 polypepticle chains , hoem group vs : | ~ hoem group: 4 Fe?* ton be combine. with Oz £ ~ ecne Cp = partral pressure pC, a hinds B pCa y all Hb combined wrth Cz x 3 | Ue pees Se eS a m4 (kPa) partial pressure OG, Beer unlead Effect g pH- Bchr effect caused HhO, te dissociate uth O, = an aerele envirenment preRne O, fe Hstet od Sally PH = lorge Vk satiation > presence q CO, +f cone H* Jong H* clisplaces ©) from HbO) Ht +HbC,— > HHb +6) haemoglobonre ciel Hb meps up free H” to maintain acidity —> _ buffer peek CO, transport 85h CO, — +Hccy — office : Hb + CO, — corbaminchasmog|lobin hy CD = re carbone anhydrase catalyses OG, HO Gt, Conair HOOT ett, > bleed plawma -5k @, dessclve in blood plasma ~Seme cliffuse inte RAC completely jcombine with amine grou>acrta ~ Oo helkw organ surrounded by a ceuble membrane Cpericardium ) ~ space befveen Q membranes ore fille with wotery fluid " 8.2. The heart E-upehe == tw vena cava 4 ‘\ g —S > prevent freticr puleaernany 2 eal when heart bec veins x4 ff conf pulmenory right efium Ce orterty “4 ' | es \ | a Left ventricle CA chambers) cerenery arteries right Sa ventricle TeX. inferior = vena cava . Tnternal structure. * a museular septum diwcls heart into a right + left half * 4 chambers + smooth dining » pericardium exyg enated blood = mitral yolve Coicuspid) Ey + lett side sright “ :de* valve % + walls mode of cardiac muscles, + ventricle walls: threker f& preduce more pressure + left ventricle theeker preduce encugh pressure tricuspid 2 fo move bleed qround body. 4,0: serniluner volves otic ventricular volves — 3,4n sy stele! contraction deastele : relaxation volves: shut: prevent ficws/ beck flow The Cardiac Cycle - atrial systole: _ atria — ventrreles ; AV valves ~ pressure from this contraction is toeak ~ semi-lunar valves closed - ventricular — ventricles wall muscles confraet systole pressure in ventricles > ofy ia —> AV valves shut ‘actfles = blood forced cut of oerta + pulmenary artery ; si valve ~ diastole + - wall muscles of otra + ventreles relax ~ pressure in ventricles V , sl valves close than in the arterres > bleed from veins flew infe atria Tnitiation » control of the cardiac eycle * Cavdiiac muscles are myogenic - contract / relax automaticaly. witheut stimulation by nerves , by electrical impulses passing through cardiac muscle tissue > SAN: ~small pateh of muscle tissue in right ofan wel = myogenre sineedtrral = celk in SAN contract ~4= night to left ofriunt node atral systcle action potential reach AVN ~ patch of alls, lecated in septum = delays excitation waves atrioventricular node, — > 7 sweep chun septum along fibres of PURKYNE Tissue and up ventricle calls Ls contract —? venticular systole - shert delay before rext wove of action potentials = OD muscles relax clrastole- Gas exchange “A Smoking 9.1. The gas exchange system tee ae bronchiole = respiratory, Z bronchicle alveclay duct alveoli ovr sacs ronchus Bronchicle pleural faphragm membranes, irregular Trachea carh lagegt C-shaped rings ation ee sgl ~ cartilage | ¢ walls of tracheq + bronchi. + prevents tubes collapsing when air pressure inside 1s low iegular blocks ~ ciliated epithelium + single 1ayer of cells with ela — sweeps mucus cle, + becleria upwords te mouth preven? dust 7. ~ goblet cells, in eiicded! epithelium + secrete mucus: tops dust particles + bacteria = smecth muscle + controet slowly for long pericds + Contreclhs —> reduce diameter of tubes elastic fibres: » walls of all tuber + alveot + inepraticn: fibres stretch — alveoli + aurwoy expands expiration recoil WV, expel air Gas, exchange between cir, alveoli’, blood Aic in alvectus; * ©, cone Blood in. ¥CCx cone copillarres C, diffuses trom alvecl’ — blood In capillarres through — thin. walls qf alveclus 4 capillary CO, diffuses trem bleed in capriiarres —> alveoli’. Diffusion grecient maintained = at breadhing movementS : infate CO: — fcone 0, /N cone CC, m alvech blood Flow past alveolus: - brings deO; bleod, camies orvoy ©, becTor: mixtire of compounds » 9. 2. Smokin black sticky, setiles on Etfects on gas exchange system the lining of the curway Lung _cancer Careinegens react with DNA in epithelial cell — mutation — multiply uncentelably —> tumour . Cancer spreads fom bronchial epithelium, enters lymphatic tissues’ —5 metastasis = symptoms: coug! f - detect cancer Chronre Obstructive Fulmonary Disease C.coPb) 4. Chronic Bronchitis Tar stimulotes goblet cells and muceus glands to produce f mucus — inhibits cleaning action of cilia .—> mucus builds up — block smaller bronchicles Patho gens clevelep in mucus —> causes infections in bronchioles Unings are inflamed. smoct muscles in brenchieles thicken lumen narrows ol. Emphysema ~ Trfecticn in lungs > phagocytes leave bleed to line the airways Fuse enayme' elastase’ do break down elastin in wall of alveoli ) - Bronchioles collapse during exahalation — fir wopped in alvecl’ —> alvecl bursts — in alveck’ — VSA fer gas exchange VQ, getting hlocd large spacesPewee ey Sheet term effects of nicobne ACB ieh cardio vascular . sytten Niecting - stmulates: nervors system: reduce artencle rameter + release adrenaline from adrenal glands cextiemetier | = Vrate, blocd pressure *, reduce blood supply to hands, feet - increase risk of blood elotting CO: - diffuses ceress walls of alvecti inte the bleed in the. lungs — diffuse inte RBC, cembines with Hb — corkexyhaemaglebin Cstable ] — Hb J fully exygenated > 4 9-IGh Cy tomsported to Y murcle > strain, especially ducing exercise - damage lining of arteries Smeking —> Atherosclerosis + thickening ond less of elasbel ty in. forty material walls of arteries atheroma: build-up ef plaques Ceholestercl + fibres) in blood vessel wall — rough surface lining — stimulates formation, of bleed clots L thrombus —> process: thrombosis ~ bleed elect breaks away , gets stuck im_a narrow vessel. prevents bleed passing + cells $C, > die +. @ brevn: STROKE less gq elestrerty in artery /ortencle * ? vessel bursts shen high pressure bleed passes ema CHD: Atherosclerosis in cerenary = angina _pector's arteries ~ heart attack : myocardial infarction) + port of muscle starved of sage — des > heart fetlure blockage of main corenary ortery ™ gradual damage of hecwt muscle410. Infectious Disease 40.4. Infectious diseases + disease’ an illness/dlisorder of the bedy/mind that leads to poor health; each disease is associated with a set of symptoms a - infectious: cated by pathogen (bacteria, fingis proto vires - nen- infectious + lung cancer ( long-term degenerative disease) cance = Sickle cell ancemia Cinherited / genetic disease) Disease, Pathogen cholera vibrio cholerae *¢ malaric plasmodium p Hiv / AIDS. human. immune deficrency dis: TUS tuberculosis Hycobocterium tuberculosts becterfum M. bovis measles Mor billivirus vir simul pox Varricla virus Cholera ~ transmission: _ contaminated food + water - bacteria breed in small intestine —* secrete joxins reduces ability of epithelium in intestine te absorb salts ond weter into blood — lest in foeces — diarrhoea - prevention « - crouded, impoverished conditions no_vaceint - treat sewoge effectively - chon water supply , good hygiene feod prep Halario - transmission: insect vector: PF Ancpheles mosquito saliva - prevention + V population of mosquitees '> liver, RBC, brain epic, sub- = femeving seurces. of ioter Jd) tro pic_regiers = relcasing loge numbers f 1 high - sleeping under nets (repre, sub *repic regions) = prophylacte drugs . prevent posite but some Plosmediuim has. become cesistantTubereulesi's CT) = transmission: _ airborne. droplets CH.tdberculosis) - undercooked meat , unpasteurized milk — Cu.bovs) lungs » lymph nedes., bones, guts M9 crewder = prevention - 1m _peer “living conclitions malnutrition = vaccination + BCG infection of HIV. ~ drug therapy - antibiotics. However: + Motub > resistance to most antihiohes used + bacteria reproduces inside hedy cells 7 harder reach + drugs meed to be. token over a leng time period HIV / AIDS ~ transmissions semen / vaginal fluscls during sexual interccurse - infected blecd: contaminated hypedermic needles - mother— fetus via plaanta, — child vin breast milk T helper lyrnphoeytes , macrophages , brain cells * worldwide + Z sub-Sahoran Afrrea, SEA Ceconomic reasons) ~ prevention: — screen blood transfusion - sterile hypodermic needles —> disposed after = unknewn HIV stehis —% abstenance - codoms - drugs | %®X infected with HIV > cleveloping ADS Measles —> highly infectious ~ transmission: ainholing cir-berne meishure droplets > prevention. ~ vaccination: @& dosesLmmunity Phogseytes —? produced in bone. marrow 4. Neutrophil 2. Macrophages > 60k gf whe ~ menecytes in blecdl ~ potrol - long livecl > squeeze threugh walls - initiate immune response J copillanes - cut up antigens and display ~ short _tivedl Tham for lymphocytes. te ~ releasd in large numbers recegnie during infections ~ ergone lungs, liver, spleen, kidney * Phogooytosrs ~ During infection. 4 pathogen, attacked alls release histamine = attract neutrophils Cehemetans) towards antibody ccreredt antigen Creapicr proteins on cell surface recognise sentibecles ) ™ ailtach , engulf Gndecyles's) inte phagscytic vacucle — digestive enrymes secreted by lysosomes (isin , kill, ingestion) Lymphocytes. Rethogens invade —> macrophage: antigen presentation ~ B cells arth complamantory surface receplers with antigen — selectecl te respond Lclenal selection ] clone of cells divide by mites's Felenal expansion | —-_ a Plasma cells Memory cells. & = preduce antibody molecules = long lived fer several yecns quickly ~ seconclary response. —> divrole quickly ~ Short lived ~ davelep > more plasma. + mamery cells podheg € ipemiune. - When nelper T- calls achvated > secrete. hormones C cytokines) + stimulate B celle to olivide, develop > plasma calls > secrete ant’ bodies. + : macrophages te carry cub phagocytosi\ more vigerously ease killer T-eolls divale (mitosis), differentiate by producing. vecucle full q texinsKillec T-cells search Rr presented antigens by imecec! cil - recegnae antigens —> attach to surface of infected cell > secrete tcxic substances H,O, > kill booly cally + pathogen Ant bodies hinge regicn: flexibility when bincling ath : > ointigen \ X [fe voriable region) antig en binding site : kegnt Sf specific fo a portiewlor clone ¢ B-cells that polypephole. \| it 1s secreted fem + ankigen on OH ut ehoin of suger molecceles Vo heavy + Ant bedies : glycoproteins cated polypeptide. chaune immunaglobins secictecl by plasma cal’s Vaccination sae he 4 ee Active immunity Passive ” - Tmmuns response. = No immune response ~ Permanent protection = Temperary protection ~ Antigens encountered - Aatigens net enceunterecl - Memory calls produced — - Msmery cell net produced - Antibodies present in. >t weeks before antibodies are, blocd _immedtiotely present: tn_bloed Actifierel | Injection f live or Tnjechon cf antibodies attenuated pathegen er _anbteains. 2: Notural | Tinfection Antibodies fem. a mether | i breast milk = acres plocanta + Veccination: help develop immunity by imitating an. infection Colors. net couse iilness). Develop seme immune. respense as ic o real infection —> feng. term immunity - ortificral active immunity < = immune respense_ortificially activated by injecting _ antigens 4 or_token_oredly e.g. fer pelioSmoilpox = sucessful = vaccine heghly effective, = ring vaccination: vaccinate _pecple orouncl_ infectec!_incividluctl - virus dees not mutate. = virus did not infect animals - easier io break tremsm’ on_cycle . diet - peer 2 [F bing. conditions ~ several doses required ~espectally children wth weak _immune_systeng virus very effective. > need fo vaccinate _lorge lk ¢} pepulertion 1 Chere immunity ] Measles - UNsuccess ful _- beesler yorccine TB ~__UNsuccessfal = bacterium = Lives insicte, booly calls ~ greuwn resistang to antbrotcs _ = BCC vaceinetien. only gives partexl immunity ~ eukeryctic — not affected by & or T cells Chelera- UNsuccessfd = bacterium lives andl reproduces in smodl intestine, outsicle becly — ee — herd te reach by lymphocytes ond ont belies inject bs MYacane does not reach intestine —> inetective _ oral vaccines mere effective. ponB= lymphocytes ~ medure in bene marrow > genes fer antibodies change —> code for different antibodies — diivicle tc make cells that produce some antibodies E clene] z= anti bedly remain on cell surface membrane as gijeoprotei recepters T= _lymphooytes ~ cell surface receptors ‘ T cell receptors’ similar to antibodies — specific te one antigen CT all is octivated cc entigen) f 'g Len macro phage cell bod cdecl by antigen enhigen ev € response: Taalls > mitosis, clonal selechion, clenal expansion Memon hilpec TS, precdicilieseme_nectve.quikly suring killer T secondary response Antibodies ~ stick bacteria together -—> bacteria cannet divide & eosier for phagocytes te clesivoy ~ neutralise toxins preduced by pathogens ~ prevent bacteria sticking to body tissues - bind 46 viruses — prevent them from infecting celleCorben. dioxide transport ~ 35h Bohr effect (CO, diffuses tom respiring cells —> blood plarma —> A&C = in RBC cytoplasm: carbene anhydrewse peso ihabee a eke. HiCO s carbonic acd tHe Wee. - hydregen carbonate ion RBC, inte bleed @* Ly dithise cut ABS platma eo eared gelutien Ab tH oy ane hacmogiobenic acict \ bout tter) case O,, mep ub H* Chi - 5h: CO, dissolve into bleed plasma ~ (Ole CO, diffuse into RBC Ls combines directly with Hb = cor ba minchaemog!abin (at terminal omme greup - Nt.)