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BIO270 MIDTERM OCT 2012 – Study Notes Lec 1 – 5 Lec 1: Basic Physiological Principles 1. HISTORY OF PHYSIOLOGY Definition: Study of how the parts of the animals work together / integrate  Unity (common ancestor) within the diversity Physiologists  Hippocrates: OBSERVATION, documentation of what he saw Observational  Aristotle: rela b/w structure < -- > function - Non-experimental ---------------------------------------------------------------------------------------------------------------------------------------------------- st  Claudius Galenus “Galen” : “founder of physiology”, 1 systematic experimental physiologist Experimental  Designed experiments to figure out functions of the body  Brain involved in ctrl-ing speech: cut group of nerves  pigs don’t squeal  Kidneys involved in urine formation: tied ureter together  kidney don’t eject urine  Ibn al-Nafis: anatomy of heart & lung st st  Andreas Vesalius: 1 human anatomy textbook, 1 to show that Galen made errors  William Harvey: discovered “closed circulation”  Scientific Method 1. [Bacon] Inductive Method: “anatomy knowledge”: use what you see to make predictions about other stuff 2. [DesCartes] Hypothetico-Deductive Method: “physiological knowledge” : formulate falsifiable hypothesis  Boerhaave & von Haller: INTEGRATED physiology : bodily func’ are a combo of chem & physical processes  Schleiden & Schwann: cell theory  Claude Bernard: Milieu interieur – living organisms maintained an internal envt distinct from external 1. Walter Cannon : Homeostasis  Diversity 1. Scholander: comparative physiology 2. Prosser: brain – central pattern generators : grps of nerves ctrl activities like breathing 3. Knut Schmidt-Nielsen: animals in harsh envt  Camel’s nose recaptures moisture from exhaled air; their RBC are oval & manoeuvre thru arteries easily 4. Bartholomew: Ecological physiology ; animals < -- > envt 5. Hochachka: Adapt. Biochem: molecules involved in surviving in harsh envt 2. STUDY OF PHYSIOLOGY Biological Level of Organization  Levels: cell/molecular  systems (organs interaction)  organismal  ecological (animal envt)  integrative (multiple levels)  Reductionism: understand a system by studying it in its parts  Emergence: properties in a system are due to interactions; hard to understand by isolating ea. part Processes that Cause Physiological Variation  Developmental Physiology: structure/func change from embryo  death  Envt al physiology: animals use physiological responses to overcome envt challenges o E.g.: whale stay underwater for long time: ↑ Hb = store 2 until needed o E.g. #2: penguins in cold climate: ↓ SA:V = ↓ heat dissipation  Evolutionary physiology: traits arise from N.S. Ultimate Goals of Research  Pure physiology: just knowledge, no GOAL  Applied Physiology: o Medical Physiology: cure disease o Comparative physiology: why can some animals do what others can’t?  August-Krogh Principle: model-species exist for every organism we want to study o E.g.: Squid: long axons easily seen & compared to humans 3. UNIFYING THEMES IN PHYSIOLGOY Physics & Chemistry  Physical properties  structure & function o E.g.: what a bone can do is determined by the molecular components of the bone forming cells  Chm laws: Heat affects rate of rxn  Elec laws: membrane potential  Allometric Scaling: o Graph: Metabolic rate vs. body mass o Take home msg: Physiological parameters do not change proportionally to body size (m = 0.74) ; there are constraints such as the SA:V ratio  E.g.: Heat PRODUCTION varies w/ body mass; but Heat LOSS varies w/ SA. [multiple constraints to physiological parameters] Physiological Regulation  Conformers: change body acc. to envt  Regulators: maintain constant body cond’ns regardless of envt o Homeostasis: body initiates a response to bring back to ↓ change  -ve feedback (↓ stimulus, bring to set pt) w/ antagonistic controls [ON 1 side, OFF the other]  Benefit: keeps body stable, prevent envt dmg to physiology  Cost: expensive Phenotype, Genotype, Envt  Phenotype: genotype + ENVT  phenotype  physiology/behavior  ↑ repro  evolution  Phenotypic Plasticity: ∆ phenotype in response to envt ∆ o Irreversible : Polyphenism : developmental plasticity  E.g.: preds prod. karimone: benefits daphnia which develops helmet in its presence o Reversible : Acclimation / Acclimatization : slow gradual change to cope w/ envt (altitude/temp) Physiology & Evolution  Proximate Cause: HOW did this characteristic develop (e.g.: what genes determined this?)  Ultimate Cause: WHY – did this trait provide evolutionary advantage? (e.g.: did long neck allow more leaves eaten?)  Adaptation: must be change over evolutionary time (many generations)  Evolution: o Variation exist o Traits heritable o Traits ↑ fitness o Relative fitness depends on envt : having the enzyme’s only useful when envt stressor present, otherwise its energetically costly to make  Genetic Drift: differences DID NOT arise due to adaptation; BY CHANCE allele freq is diff due to forest fires (e.g.) Lec 2: Biochemical Basis of Physiology 1. ENERGY  Thermodynamics st o 1 Law: Conservation of Energy: energy can be converted; but total amt in universe is constant o 2 Law: Entropy : universe is random  Living organisms DELAY entropy by inhibiting natural processes that leads to its breakdown & taking from envt (break down glu) to maintain self  Energy: radiant, mechanical & electrical (potential & kinetic), thermal, chemical (stored in bonds) o Transfer : heat is lost @ every transfer (food web)  Gradient : o Chemical Gradient: diff in [] across membrane + o Elec-chem Gradient: diff in DISTRIBUTION of CHARGED molecules across membrane (more + out, more Na out)  Thermal Energy: o Enthalpy: avg. thermal energy of molecules  Exergonic: release nrg: – ∆G®  Endergonic : absorb nrg: + ∆G® o Transition State: chm rxns reversible, @ this pt: can go back to substrate OR to product o ↑ temperature: more molecules reach E A ↑ rate of rxn, ↑ likelihood of endergonic (it req more nrg) 2. CHEMICAL BONDS  Covalent: STRONG; sharing elec – b/w molecules w/ unpaired elec – o Functional grps are covalently bonded o Bond energy: ↑ bond nrg = strong bond; amt nrg needed to break/form bond  Non-covalent: WEAK: structure/func = organize molecules into 3D shapes o Van der walls: transient dipole; by CHANCE more e- on 1 side of atom; when extremely close to another molecule, it Mutual attraction influence charge dist’n on a neighbouring molecule ↑ temp = weaker o H-Bonds: asymmetric sharing of e- b/w H & O/N/F [O more elec-negative] o Ionic: ATTRACTION, NOT TRANSFER b/w anion & cation Mutual aversion2to HoO Hydrophobic : molecules have mutual aversion to water; H:C equal e- sharing ↑ temp = STRONGER 3. WATER  ↑Temp : molecules have more nrg to break surface tension [BOIL] ↓Temp : molecules stabilized w/ added H-bonds [FREEZE]  Ice: less dense than water; more H-bonds spread further apart Water: most dense at 4•C o Stable: ↑ Melting pt, ↑ Boiling pt, ↑ Heat of Vaporization – when we sweat, molecules that evap takes heat energy with them, cooling skin surface  Solutes affect Colligative Properties: properties of water that depend on NUMBER of solute particles (not size/charge) o ↓ Freezing Pt : inhibit H-Bond formation Vapor Pressure: not as many H2O molecules can evap and exert pressure back on liquid o ↑Boiling Pt: less SA for molecules to exit Osmotic Pressure: forces more H2O to move in  Osmotic Pressure: “associated w/ pure diff in] b/w 1 part & another”  chemistry related o PENETRATING AND non-penetrating o ↑ osmolarity: hyperosmotic (draw H2O twds self better) ↓ “ : hyposmotic (lose H2O to another part)  Tonicity: “assoc. w/ the effect of a solution on cell volume “ o Only non-penetrating o Cells shrink: in hypertonic solution Cells swell: in hypotonic solution  Rate of diffusion: Fick equation: o Explanation :2R-D , ↑ w/ diffusion coeff, ↑w/ diffusion Area, ↑ w. size of [ ]gradient, ↓w/ thickness of membrane  T ∝ X : 1 mm membrane  3 hr. diffusion time 4. ROLE OF ENZYMES IN METABOLISM  Enzymes: makes rxns faster w/o being consumed; DOES NOT change G; active @ ↓ [ ] o Specificity: enzymes target specific rxns; just ↑ing temp would ↑ rate of every rxn o Evolutionary Adaptation: Km = [solute] @ enzymes ½ max rate - ↑km = ↓affinity for substrate Km increase w/ increasing temperature - Animals @ ↑ temperatures evolved variation in enzyme structure allows km to be conserved in their natural cond’ ns  Regulation of enzymes: Competitive Inhibition - Inhibitor can block active site but can ↑amount of substrate to get the same lvl of enzyme activity - Therefore, won’t affect Vmax o Allosteric Activation - activator bind on diff site , ∆ shape - activator decrease the amt of substrate needed by (↑ing affinity )to get a ↑ lvl of enzyme activity - Affect Km + Vmax o Covalent Activation (phosphorylation) - ∆ shape of enzyme to work @ optimal speed - Affect Km + Vmax o 5. BIOMOLECULES  Proteins o Structure :  1 : peptide bonds b/w a.a  2 : H-bond ONLY w/ consitutents of the backbone rd  3 : H-bond b/w R-GROUPS [can be protein if this prot only has 1 subunit] o Molecular Chaperones: helps proteins fold; binds to heat-shocked/denatured protein & help fold  Carbohydrates o Glycosylation: alters macromolecule, protect it from degradation o Polysaccharide: store energy / structural molecule: chitin / hyaluronate  Lipids o Metabolism:  FA Syn: Fatty Acid Synthase; FA Breakdown: B – oxidation  Storage: lipogenesis/esterification into triglycerides ; Unstorage : Lipase back into FA o Ketones: LIVER – FA (acetyl-coA)  Ketones delivered to BRAIN – Ketones  acetyl-coA for usage [brain can’t metab FA] o Phospholipids: phosphoglycerides in lipid bilayer sphingolipids in mylin sheath o Steriods: 4C rings 6. INTEGRATION OF METABOLIC PATHWAYS  Energy Storage: o 1) Oxidoreductase: enzymes that transfer reducing equivalents (high nrg e bound to carrier) b/w reduced (high nrg) and oxidized (low nrg) molescules o 2) High energy bonds: ATP, NADH, Acetyl – CoA Glucose Syn [GLUCONEOGENESIS] Glucose Breakdown [GLYCOLYSIS] - Pyruvate carboxylase ON: nrg↑ - Hexokinase ON: nrg ↓ - Fruc- 1,6 – bisphosphatase OFF: nrg ↓ - Phosphofructokinase - Pyruvate Kinase OFF: nrg ↑  Allosteric regulation of ↑ nrg indicies -NADH - Glu ---> 2ATP + 2pyruvate + 2NADH enzymes involved in both -ATP pathways -Acetyl-CoA cytoplasm Oxidation (in presence of O2) Oxidation (in absence of O2) PDH (pyruvate dehydrogenase) LDH + - Pyruvate ---> acetyl-CoA + NADH - Pyruvate + NADH -----> NAD + Lactate Redox Shuttles x2 *** anoxic tolerant animals make less toxic products / - NADH ------> NAD+ store glycogen / reduce metab  avoid lactate Mitochondria Fatty-Acids FAcyl-CoA Synthase Lipogenesis FAS FA F-Acyl-CoA B-oxidation Triglycerides Acetyl-CoA Palmitate Acetyl-CoA Lipase  Bottom line: BOTH glycolysis & B-oxidation makes acetyl-CoA Mitochondria TCA/ Krebs Cycle Oxidative Phosphorylation - Oxidize acetyl-CoA 1. ETC [oxidation] - Reducing equivalents (NADH) pass e- thru complexes - Reducing equivalents produced during cycle - 4e + 4H used to reduce O 2--- > H2O o NADH x 3 [oxidation of reducing equivalents] o FADH 2 - H+ Pump: complex I, III, IV  create Proton Motive Force 2. ATP Synthesis [phosphorylation] - F1F0 ATPase: Energy from ∆p used to + P to ADP  FUTILE cycles minimized by high nrg indicies  NADH  Acetyl –CoA - Produce ATP  ATP  Oxidation & phosphorylation-couProduce ATPred dependence on ∆p 7. MEMBRANE & TRANSPORT a. MEMBRANE  Profile of Lipid Bilayer o Phosphoglycerides: structural func’n o Spingolipids/Glycolipids: neural cells; electrical properties + communication o Cholesterol: H-philic & H-phobic regions  ENHANCE fluidity: disrupt FA tail interactions  DECREASE PERMEABILITY: fills gaps, prevents small molecules crossing o Lipid Rafts: ↑in glycolipid &cholesterol  Thick portion w/ longer FA tails & longer TM protein domains  Rigid : good for signalling  Fluidity o Temp: cold temp causes ↑of van der walls  rigid packing  Adaptation: if live in the cold, animals choose unsaturated : kink -- > keeps membrane fluid  Membrane Protein: Integral & Peripheral Membrane Proteins ( weak assoc w membrane, interact w/ integral or glycolipids ) b. TRANSPORT Passive Transport Active Transport Diffusion Facilitated Transport 1 o 2 o Solute Mvmt HIGH  LOW LOW  HIGH Energy Yes Yes (indirectly) / - Energy: provided by ATP hydrolysis Transport Protein Yes Yes Yes Types: Types: 1. Pump : set up gradient 1. Ion channels 1. P-type: pump ions 2. Carrier: to move molecule - small & gated pores 2. F & V-type: H+ - voltage, ligand, mechano-3. ABC: large organic Examples: gated molecules - Antiport: molecules move in opp. dir / 2. Porins - eg. Na+ moves in, drive Ca+ out - larger molecules - Symport: move in same dir 3. Permease - e.g. Na+ move in, drive Cl- in - like enzymes: can be saturated - conf ∆ move things across Solute Small & Nonpolar Ion & Hydrophilic * hydrophobic means you need transporter * low  high means you need energy C. MEMBRANE POTENTIAL  Carriers : Electroneutral carriers: exchange uncharged/ equal # of particles w. same charge Electrogenic carriers: unequal transfer of charge (e.g.: 3Na+ out, 2K+ in)  Membrane Potential o Purpose: energy for membrane transport & cell signaling (axons) o Resting membrane potential: uncharged, more K+ inside, more Na+ outside (-ve inner membrane) o Depolarization: Na+ channels open, Na+ enters , inside more +ve o Hyperpolarization: K+ channels open, K+ leaves, inside more –ve 7. CELL STRUCTURES  Mitochondria o MATRIX: TCA cycle enzymes INNER MEMBRANE: oxidative phosphorylation enzymes o Organisation: exists individually or in mitochondrial reticulum ( lots on muscle fibers work together to contract) o Syn Regulation: respond to nrg needs: genes from DNA & mtDNA  Cytoskeleton o Microfilaments: ACTIN (muscles)  Motor protein: myosin o Microtubules : TUBULIN (large)  Motor proteins: dynein & kinesin o Intermediate Filaments: skin/nails  Endomembrane System o Goal: bring proteins made by the ER/ RER to the cell membrane  ER & Golgi : ribosomes makes proteins, enters ER, packaged by Golgi  Vesicles : carried to compartments by motor proteins moving on cytoskeleton (don’t just float)  Extracellular Matrix o Def: cement b/w cells that’s connected to cell cytoskeleton by integrin o Breakdown: cells breakdown ECM to migrate thru tissues ; e.g.: blood vessels penetrate thru ECM o Examples: chitin = insect cytoskeleton; calcium carbonate = shell, collagen + Ca Phosphate = bone 8. PHYSIOLOGICAL GENETICS &GENOMICS  Nucleic Acid o DNA o Histones  COMPACTION = Chromatin: DNA compressed into chromatin by binding to +ve lysine of histone which attracts –ve charge of phosphate groups  DNA compact to fit into nucleus  UNWINDING = Acetylation: neutralize +ve lysine; affinity for DNA lost  DNA unwinds for transcription  Protection: of DNA from dmg = radiation o Organisation  Genome  Chromosome  Genes (specific sequence for transcription  Exons (coding) / Introns (not exactly junk, have some func’n)  Centromere: most compact center region  Telomere: repetitive buffer added by telomerase [unstoppable in cancer]  Transcription o Acetylation: DNA unwraps o Regulators: must form translation initiation complex at promoter TATA box  Transcriptional modification o 1 o mRNA transcript : (1) Introns removed, (2) Poly-A tail added to 3’ (3) 5’ cap o Transported: to cytoplasm o Regulation: RNase  endonuclease, exonuclease  Translation: o Location: many ribosomes @ a time on RER can translate o Regulation: specifically / NON-specifically by phosphorylation, elongation fctrs, inhibitors etc  Proteins o Protein Degradation  Bad prot = tagged by ubiquitin, degraded by proteasome  all 3 molecules recycled o Protein Isoforms : non-lethal copy; material for evolu’n  Variation in protein structure  Alternative splicing, alleles (2 parents diff copies of allele), whole genome duplications (randomly)  Homologous Recombination  Unequal Crossover  Progeny w/ extra copy: gets extra material; MAY OR MAY NOT be lethal/beneficial  Progeny w/ less: dies  Mobile elements (TRANSPOSONS)  Transposase cut transposon out which sometimes catches other genes which gets transferred along with the transposon to give another allele an extra copy. Lec 6: Reproduction 1. OVERVIEW OF REPRODUCTION  History o Eukaryotes: first organism that sexually reproduced  Development o Formation of gonads (sex organs) which produce gametes (gametogenesis) 2. SEX DETERMINATION By Genotype By Environment By Asexual Reproduction Mammals: Temperature Dependent Sex Determination (TDS) 1. Cloning [less common]  Hetero M (XY); Homo F (XX)  Temp: ↓/↑/extreme/moderate temps - m  m ; f  f Birds determine sex of offspring - colony of same ones produced like corals (altho corals can prod sexually as  Hetero F (ZW); Homo M (ZZ) - pivotal temp: ratio at which 1f:1m Honeybee produced well)  Can CONTROL # m/f  Hormone: supplements TDS; estradiole: 2. Parthogenesis (virgin birth) [common]  Fertilized = diploid f testosterone ratio (vary depending on - only female reproduce; males only beg/end of season) determines # f:m made when cond’ns bad [daphnia] Unfertilized = haploid m produced as well ** Automictic Parthenogenesis: 2 polar body fertilizes ovum a. Thelytoky: homogametic f  f b. Arrhenotoky: heterogametic f  m - 3. REPRODUCTIVE HORMONES  Steroid Hormones 1. Progesterone = precursor from cholesterol made in gonad OR adrenal glands 2. Androgens  Androstenedione  testosterone = ctrl male reproduction 3. Cytochrome P450 Aromatase converts Androgens  Estrogens 4. Estrogens  Estrone Estradiole = ctrls female reproduction  Steroid Hormone Ctrl Pathway 1. Hypothalamus: release GnRH (Gonadotropin releasing hormone) 2. which stimulates Anterior Pituitary: release FSH & LH (**primates: Chorionic Gonadotropin in pregnancy) 3. which stimutes Gonads : release steroid hormones  Insects o 2 hormones ctrl reproductive development 1. Prothoracic gland: release Ecdysone that stimulates ecdysis (breaking out of cuticle) 2. Corpus allatum: release Juvenile Hormone (JH) that stimulates making larval cuticle & preventing pupation; when JH ↓, stop making cuticle and become adult butterfly 4. OOGENESIS  Modes of reproduction Ovipary Vivipary Ovovivipary - Not born live - Both born LIVE - Since can be external fertilization, - Nutrient provided by mother - Nutrient from yolk ovum expelled to grow on outside to a baby  Oogenesis o Meiosis  Asymmetrical division of 2 polar bodies before one mature ovum (haploid) is produced  2ndmeiotic division (polar body productions) are delayed until puberty o Ova Production & ovulation  Follicle has granulose cells that secrete nutrients to Zona pellucida (ECM) which passes it to oocyte. Entire follicle surrounded by Theca (membrane) which produce/release androgens, passes it to granulose cells, which has aromatse to produce estrodiole.  In invertabrates: instead of granulose cells, nurse cells (oocyte that didn’t develop into) give nutrients to oocyte  Folliculogenesis = all but 1 follicule degenerates, this follicule bursts to release ovum, ovum swept by fimbriae into fallopian tubes ; if fertilized at this time, muscle contractions push it to implantation.  Vitellogenesis: Yolk production o Except placental animals, yolk (lipids & proteins) needed to supply nutrients o Production  When hormones released (JH/estrogen), brain release : vitellogenic fctrs, stimulates fat body/liver to release vitellogenin, stimulates oocyte to MAKE : vitellin.  Chorion surrounds insect egg o Before implantation, follicle cells make chorion that surrounds ovum. o Purpose: Allows egg to be strong & withstand terrestrial conditions; strong enuf to not disintegrate, but still allows sperm to penetrate through a micropyle tunnel & allow gas exchange.  Egg structure in water vs. on land Aquatic Animals Terrestrial Placental / Marsupial Viscous coating Hard Shell No shell - fertilization external - fertilization must be internal -Development into baby is internal -eggs always need water - embryo enclosed in amnion (cushion that provides favorable envt to grow. - Amniote egg: (1) Amnion: stores fluids and protect embryo (2) Allantois : outward gut that stores waste (3) Yolk : store nutrients (4) Chorion: most outer layer for protection & gas exchange 5. SPERMATOGENESIS  In Seminiferous Tubules  Leydig Cells: when LH stimulates it, it secretes testosterone  Sertoli Cells: when FSH & testosterone stimulates it, it regulate spermatogenesis  Androgen Binding Protein: Binds the testosterone produced by leydig cells and keeps it into tubule so that sperms can develop.  Inhibin: inhibits FSH secretion (-ve feedback; even enough sertoli cells stimulated, don’t want more)  Sperm Life Cycle  Birth in Seminiferous Tubules: sperm has no fluids/cytoplasm, abundant mitochondria, condensed DNA, can’t swim  Storage & Maturation: when pushed into epididymis for storage & maturation, sperm gains swim abilities  Ejaculation: (1) vas deferens has smooth muscle + cilia in that push it (2) Fluids addition: [a] Seminal Vesicles: add alkaline fluid to neutralize acidic uterus [b] prostate: secretes nutrients/citrate [c] Bulbourethral gland : add lubricating mucus  Ejaculation Control  Signal Tranduction: AP cause Nitric Oxide release; activates Guanylate Cyclase  cGMP  PKG (1) Inhibit Ca+ release (2) Inhibit Sliding Filaments  ↓ contractions, ↑ dilation of arteries leading to penis, ↑ blood flow/ ↓ venous rtrn = ERECTION  Copulatory Organs  Non-true penis: (eg Hemipene) a pathway for sperm to transfer into female  True Penis: direct extension of male gonad that transfers sperm  Os Penis / Baculum : bone in penis, sperm release w/o erection 6. FEMALE REPRODUCIVE SYSTEM  Ovulation Cycle  A) Late follicular phase: rise in estrogen now stimulates GnRH (FSH & LH) relase  Estrogen especially causes LH surge , which cause granulosa cells to secrete oocyte growth fctrs o Also cause endometrium to thicken to prepare for implantation  Rise in FSH  causes follicles to burst and release ovum o Formation of left over corpus luteum = secretes progesterone & estrogen  uterine wall thicken for implantation  B) Luteal Phase: Corpous Luteum: secretes progesterone --------> might disintegrate unless rescued  Unsuccessful cycle / success cycle? o No Fertilization : NO implanation  no placenta  no chorionic gonadintropin to rescue corpous luteum; progesterone↓, wall sheds o Fertilization: YES implanation  placenta release CG which rescues corpous luteum; continues to release progesterone & estrogen until placenta matures to become main source of progestrone/estrogen.  Endometrium Lining: - Follicular = (1) Proliferative Phase: [by estrogen] lining thickens - Luteal = (2) Secretory Phase: [by estrogen & progesterone?] that secretes reg fctrs on wall to prepare for implanation  Placenta  Trophoblast: outer most cells of blastula, invade endometrium to form placenta (cells of both mom & child)  Early in preg: placenta secretes CG that cause Corpous Luteum to keep making prog & estrog Later in preg: placenta itself makes prog & estrog  Gestation Period  Short: Altricial Species = Have many badly developed babies  Long: Precocial Species = Have less more developed babies  Parturition (birth)  Myometrium: uterine muscles that push out baby (estrogen promotes contraction, progesterone inhibits contraction)  Hormonal Changes:  Progesterone ↓ to let contractions  Prostaglandin + Oxytocin ↑ = estrogen increase [ ] of their receptors  uterine contractions  Milk Production  Milk PREPARATION: ↑ Estrogen from placenta induces anterior pituitary to release prolactin.  Prolactin = prepares the mammary gland machinery FOR milk production when preg is expected  Milk PRODUCTION  When baby actually comes out: placenta is lost & estrogen + progesterone ↓  Milk SECRETION  Process: (1) exocytosis brings out lactose, casein, lipids to the milk duct lumen (2) transcytosis brings blood proteins from capillary to the lumen  Types of Milk 1. Early secretions: Colostrum = for protecting baby /immune system : Vit A, D, growth fctrs 2. Late “ : for energy : lipids, lactose ,casein Lec 7 & 8: Muscles I 1. CYTOSKELETON & MOTOR PROTEINS  Microtubules o Monomers are dimers: a-tubulin – b-tubulin; (both bound GTP, when dimerized, b-tubulin hydrolyze GTPGDP) o Anchored : (1) MTOC @ “-“ center of cell (2) Integral Protein @ “+” cell membrane o Assembly  Monomers dimerize: a-tubulin GTP intact; b-tubulin hydrolyze GTPGDP  Roll: Protofilament  sheet  Microtubule (13 protofilaments)  Asymmetrical Growth: faster @ + end o Dynamics (length) affected by:  [Tubulin] : “+” end has ↓er c (pt b/w growth & shrinkage) than “—“ end  @ any [tubulin], + end more likely to grow, - end more likely to shrink  Treadmilling range: length is maintained ;
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