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84 Cards in this Set
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Passage Through Plasma Membrane
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Simple Diffusion
Facilitated Transport Active Transport Secondary Active Transport |
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Simple Diffusion
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-Molecules passively move through membrane
-Dependent on charge/concentration gradient, solubility and size of molecule |
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Facilitated Transport
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-Generally accomplished by carrier proteins
-Expedites an already favorable process (moving molecules in the direction they would go anyways b/c of conc./charge grad |
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Active Transport
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-Accomplishes movement of molecules against their gradients
-Uses ATP directly to accomplish movement -BOTH molecules move against their gradients -Example: Na+/K+ ATPase (sodium/potassium pump) |
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Secondary Active Transport
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-Moves molecules against their concentration gradients
-Uses ATP indirectly by using favorable gradient created by an ATP requiring transporter to drive a second molecule in an unfavorable direction *Symporter- moves one substance WITH its concentration gradient and one against it. Favorable energetics of moving one will drive movement of the other. Substances move in the SAME DIRECTION. *Antiporter- Operates the same way as a symporter only substances move in OPPOSITE DIRECTIONS |
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How Rxns are similar
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ALL change fuel to ATP, GTP, NADH or FADH2
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How Rxns differ
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where they take place in cell
-magnitude of energy extracted -chemical storage form of energy extracted -metabolic regulation |
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Central Dogma of Molecular Biology
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DNA transcribed to RNA translated to Proteins
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Cell Sensing and Signaling Commonalities
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-specificity of signal recognition
-signal amplification/transduction -reversible protein phosphorylation to modify fxn -appropriateness of response(short vs long; graded response proportional to mag of transmission; qualitatively and temporaly appropriate to bio context) -Mech of Control-> +/- feedback, desensitization/resensitization |
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Components of Cell Signaling Systems
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1. Ligand (Primary Messanger)
2. Receptor 3. Second Messanger 4. Effectors |
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Ligand
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-Called ligand because of physical connection/interaction between it and the receptor
-Can be many different things such as odorants, neurotransmitters, hormones etc |
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Receptor
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-Sensor molecule that typically resides at cell surface (in plasma membrane)
-Signals second messenger inside cell -SPECIFIC, typically will only bind/recognize one particular ligand |
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Second Messenger
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-Form in response to receptor activation
-Usually produced from existing chemical precursors or mobilized from intracellular reservoirs -Transduce signal to effector systems (produces biologically meaningful response) -Rapidly metabolized or sequestered back into their reservoirs to terminate or reduce cellular response |
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Effector Systems
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-Involves amplification of signal via phosphorylation cascades (transfer phosphate from ATP to amino acid side chains)
- Changes can be things like increasing or inhibiting enzymatic activity by altering structure, binding affinity, or stability -Allow for finely tuned control -Rapidly reversable by protein phosphatases (enzymes that remove phosphate group). These enzymes can themselves be controlled by phosphorylation |
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Cell Response to Rc-Mediated Signaling Systems
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-can be long or short
-long term changes pattern of gene expression in target cells |
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Changing Patterns of Gene Expression
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Cells can rapidly change phenotype in response to changing external environmental conditions by influencing Transcription Factors
TRANSCRIPTION FACTORS: inside cell -PROMOTE/INHIBIT whether or not RNA polymerase can bind and initiate transcription. -Can be controlled by either: -Intracellular Signalling: ligand activated (Glucocorticoid molecules) -Extracellular signaling: cascades employ intracellular protein kinases or induce mitosis -ES -> changes in patterns of gene expression -> changes in activity of transcription factors-> changes in DNA synth by RNA polymerase Ex: MITOGENS= signaling agents from outside the cell -cause cells to undergo mitosis by activating transcription factors that direct cell to enter/progress through the cell cycle -Increase cyclin D production and block its breakdown |
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Cell Cycle
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Cycle is characterized by phases: G0, G1, S, G2, and M
G1-cells grow in size and accumulate ATP S-Chromosomes are replicated, transcription ceases G2-ATP restored in preparation for distribution of chromosomes and organelles M-When actual process of mitosis occurs |
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What Controls the Cell Cycle?
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Closely regulated Protein complexes:
-Cyclins -Cyclin dependent protein kinases (Cdk): act on protein substrates to activate machinery associated with each step -Both regulated by phosphorylation, Cip,Ink4 and... -Mitogens: control expression of the Cdks of G1, which regulate Cdks of G1 to S transition -CONTROL RATE AND FIDELITY OF CYCLE!! |
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Where can errors occur in the cell cycle?
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Errors can occur in transcription, DNA replication, or chromosome segregation. Mechanisms exist in the cell to accomplish “damage control”. Cells are capable of detecting and repairing errors, or if the damage is beyond repair, they can initiate apoptosis, or controlled lysis (cell death).
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What errors can occur in transcription?
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-problems with timing (genes expressed at an inappropriate time)
-problems with magnitude (transcription occurring either too much or too little in relation to magnitude of stimulus) -problems with fidelity of base pairing (RNA nucleotides are mismatched to its DNA base pair) **RNA POLYMERASE CAN DETECT AND REPAIR MISMATCHES** |
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What if there is a persistant mismatch?
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(RNA polymerase either does not detect or does not repair mismatched DNA/RNA base pair)
-Can result in a silent mutation -does not result in any change to translated protein. Could code for same amino acid regardless of one different base pair or different amino acid that does not affect overall structure or function of protein -Can result in actual mutation -changes translated protein in a way that alters its function usually by changing the structure. Example: changes in a way that alters how the protein folds -Can effect the structural soundness or the lifespan of RNA (persists too long, degrades too early) |
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What happens if genomic DNA is damaged?
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-damage can be detected by specialized nuclear pathways. Sensors transduce the message in a
similar way to how messages are transduced from outside the cell. -Depending on the severity and ease of repair of the damage, consequences can be: -DNA repair -Cell cycle arrest -Transcription -Apoptosis |
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How can DNA be damaged?
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-Several things can cause damage, but the most common are chemical agents such as those used in chemotherapy or physical insult such as ionizing radiaton.
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How is DNA repaired?
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-Protein complex marks off/surrounds damage
-then unwind it, incise the damaged part with an endonuclease (usually only one side of double helix) -Gap filled via DNA synthesis (DNA polymerase) |
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How is damage control accomplished during the cell cycle?
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Cell Cycle “checkpoints”
-Protein kinases are actived -which activate multiple checkpoint enzymes -which activate components that will arrest the cell cycle or parts within it until the insult is repaired via reversible phosphorylation of proteins -Major checkpoints: end of G1, the end of S phase, the end of G2, and at several points during M phase, most notably at the development of the spindle (prophase), development of kinetochore (prometaphase), or metaphase -Development of spindle crucial because it is what directs chromosomes to opposite poles -Development of kinetochore is crucial because it is what “attaches” chromosomes to spindle fibers -Metaphase is crucial because if alignment is off, chromosomes may distribute incorrectly APOPTOSIS if irreparable |
-Checkpoints CAN fail= persistence of mutations and genomic rearrangements -> genetic instability.
-THINK birth defects or development of genetic diseases . CANCER: mutations in proteins of M phase produce failure of that checkpoint -> ANEUPLOIDY Down's syndrome (trisomy 21) and is also a hallmark of cancer cells. |
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What is apoptosis?
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-Regulated or programmed cell death
-Essential for normal animal development and function -Example: all limbs in fetus start off as paddles, apoptosis occurs at specific places to produce fingers and/or toes -Vital in response to serious insults like UV radiation or chemicals that damage DNA -Involves an orderly dismantling of critical cell survival components and pathways, healthy, unaffected parts of cell such as organelles can be recycled -In this way it is DIFFERENT from necrosis. Necrosis is disorderly lysis of cells that triggers an inflammatory response. Necrosis destroys all parts of the cell. |
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How is apoptosis accomplished?
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-Two pathways
1. Extrinsic: apoptotic signal comes from cell-surface receptors 2. Intrinsic or mitochondrial: signals received intracellularly (cytochrome C released from damaged mitochondria) -Both pathways: -caspases break down cytoskeletal proteins and DNA repair enzymes -DNAses cleave the DNA in the nucleus -These systems are not foolproof!! |
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What are the features of apoptosis?
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MORPHOLOGICAL:
-Chromatin condensation -cell shrinkage - membrane blebbing BIOCHEMICAL: -DNA fragmentation -protein cleavage at specific locations -increased mitochondrial membrane permeability -appearance of phosphatidylserine on the cell surface |
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What are some important properties of muscles?
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Contractility- ability of muscle to shorten and generate force
Excitability- capacity of muscle ot respond to a stimulus Extensibility- muscle can be stretched to its normal resting place and beyond to a limited degree Elasticity- Ability of muscle to recoil and return to its original resting length |
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What helps give muscle its elasticity?
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-Tendons : pulled tight, exhibit passive tension
-Surrounding connective tissue |
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Series Elastic Component
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The muscle and tendon act as a series elastic component
-The tendons attached to the muscle constitute the majority of the series elastic component. Since the muscle and tendon are in a straight line, they are a SERIES elastic component. When the musculotendinous unit is stretched, as in eccentric muscle action, the SEC acts as a spring and is lengthened. |
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Parallel Elastic Component
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The parallel elastic component
-The sarcolemma and connective tissue act as a PARALLEL elastic component because they run parallel to the muscle fibers. The PEC provides passive resting tension when the muscle is at resting length. Thus the muscle can to an extent resist lengthening. |
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Types of Muscle
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1. Skeletal
-Attached to bones -Multiple nuclei that are peripherally located just beneath the plasma membrane (sarcolemma). Cells can also be described as multinucleated syncitium. Cells are also LARGE, about 0.1mm in diameter and up to several cm in length -Tissues are striated and are involved in voluntary motion as well as some involuntary (reflexes) 2. Smooth -Walls of hollow organs like blood vessels, eyes, glands, skin etc -Single nucleus that is centrally located -Are NOT striated, involved in in involuntary motion, gap junctions are present in visceral smooth muscle 3. Cardiac Only in the heart -Single nucleus that is centrally located -Has striations and intercalated disks, involved in involuntary motion |
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What is the gross structure of skeletal muscle?
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Entire muscle is surrounded by the epimysium
-Muscles are broken down into bundles called fascicles, each fascicle is surrounded by a membrane called the perimysium -Fascicles are further broken down into individual muscle fibers (individual muscle cells) which are surrounded by a membrane called the endomysium. -Muscles are attached to bones via tendons. An aponeurosis is a broad, flat, sheet-like tendon. |
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Muscle Terms:
-Origin -Insertion -Belly -Synergists -Prime Mover -Agonist/Antagonist -Fixators |
-Origin or head: end of muscle that is attached to the more stationary of the two bones it
connects -Insertion: Other end of the muscle, attached to the bone with the greatest movement -Belly: Largest portion of muscle between origin and insertion -Synergists: Separate muscles that work in concert to cause a movement. -Example: latissimus dorsi and deep pectorals both draw the forelimb caudally -Prime mover: Plays the major role in accomplishing the movement. -Agonist/Antagonist: muscles that produce opposite actions -Example: triceps and biceps (one flexes while the other extends) -Fixators: Muscles that stabilize the joint that is crossed by the prime mover. They serve to fix the joint in a given position during the movement of other joints. |
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What are the 4 muscle Functions?
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1. Flexor: accomplishes flexion or the bending of a joint or limb
2. Extensor: accomplishes extension or the straightening of a joint or limb 3. Adductor: accomplishes adduction or drawing the limb toward the medial axis of the body 4. Abductor: accomplishes abduction or drawing the limb away from the medial axis of the body |
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What are the two types of fiber architecture in skeletal muscle?
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1. Parallel: fibers run parallel to the longitudinal axis
-Example: rectus abdominus, transverse superficial pectoral 2. Pennate: Fibers run at an angle to the longitudinal axis -Example: rectus femoris *When pennate muscles contract, the overall shortening of the muscle is less than in muscles with longitudinally arranged fibers, however a greater degree of tension is possible |
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Why do muscles have abundant nerve and BV supplies?
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-Muscles require large amounts of glucose and oxygen in order to generate enough ATP to do their jobs. Maintaining and using a muscle cell is very expensive energetically. ATP is required both to accomplish contraction and maintain intracellular proteins and structures.
-Muscles also require a lot of innervation because each muscle fiber needs its own synapse in order to contract. This synapse is called the neuromuscular junction. |
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How do muscle cells develop?
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-Precursor cells called myoblasts that contain only one nucleus and no contractile proteins, fuse into structures called myotubes. Once they reach this stage of development they differentiate into their definitive form by developing specialized structures such as myofibrils (contractile proteins) and sarcoplasmic reticulum (specialized calcium storage organelle) and transverse or T tubules (infoldings of plasma membrane).
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What composes the contractile unit of muscle fibers?
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-Within each muscle fiber are units called sarcomeres, these are the fundamental contraction unit. The sarcomere is further subdivided into regions
-The Z-line: where thin actin filaments are anchored, the length of a single sarcomere is from Z-line to Z-line -The M-line: the midpoint of the sarcomere, located in the center of the H-zone -The H-Zone or H-Band: the distance between the ends of the thin filaments. -The I band: the distance between the ends of thick filaments -The A band: length of thick filaments -Within each sarcomere are specialized structures called myofilaments. These filaments, actin (the thin filaments) and myosin (thick filaments) are what actually accomplish contraction via their interaction |
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What composes myofilaments?
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ACTIN : G actin molecules form a double coil
-then wrapped by a strand of tropomyosin -troponin subunit attaches to tropomyosin at regular intervals MYOSIN: myosin molecules arranged in coiled alpha-helices -heavy chains and light chains -myosin head groups in heavy chains at both ends -central portion (located in the H-zone)=bare zone **limits the degree of contraction |
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What other components are vital to the structure and action of myofilaments?
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There are 3 important cytoskeletal components
1. Titin (BIG protein complex) -runs from M-line along the thick filaments all the way to the Z-line -Anchors thick filaments to Z-line -Maintains alignment of thick and thin filaments -Prevents sarcomere from being pulled apart during muscle stretching 2. Nebulin -Acts as a template for the formation of the thin filament -Stabilizes thin actin filaments 3. alpha-actinin -Attaches actin to Z-line |
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How do muscles contract?
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*Muscles contract via the sliding filament theory, whereby shortening is accomplished via the interactions between actin filaments and myosin heads. When this occurs the sarcomere shortens in length; A bands remain the same (length of thick filaments does not change), I bands shorten (the distance between the ends of thick filaments gets shorter), and the H band also shortens (distance between the ends of thin filaments get shorter)
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What is the step mechanism of contraction?
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**. Ca 2+ bind to troponin -> tropomyosin moves away from myosin binding sites on actin
1.Rigor Configuration: Attachment is the initial stage of the contraction cycle, in which the myosin head is tightly bound to the actin molecule of the thin filament (rigor mortis occurs b/c w/o ATP, myosin never relaxes) 2. Release is the 2nd stage of the cycle in which myosin head uncouples from actin due to ATP binding 3. Bending: myosin hydrolyzes ATP->ADP+Pi, head advances in relation to actin (relaxed state w/ cocked head) 4. Force Generation: myosin releases Pi as binds to actin, Pi releases-> myosin returning to unbent conformation = power stroke. Actin moves towards M-line. ADP is lost 5. Reattachment: Myosin binds tightly to new actin molecule |
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Transmission of AP
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1. Membrane potential generated by Na+ and K+
2. Na+ channels open in response to neuronal signal, Na+ rushes into axon -> depolarization that continues AP 3. Na+ channels inactivate (prevents AP from going backward) 4. K+ channels open-> hyperpolarization 5. Na+/K+ ATPase restablishes resting MP |
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Excitation-Contraction Coupling
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1. Somatic motor neuron releases ACh at neuromuscular junction
2. Net entry of Na+ through ACh of receptor-channels in motor-end plate initiates a muscle action potential (End Plate Potential) 3. AP travels along sarcolemma and T-tubules 4. DHP Rc allows extracellular Ca++ to enter and opens RyR Ca2+ release channels in sarcoplasmic reticulum 5. Ca++ enters cytoplasm 6. Ca ++ binds to troponin, allowing actin-myosin binding 7. Myosin executes power stroke 8. Actin filament slides towards M Line |
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SERCA
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Once the contraction is completed, mechanisms exist to remove calcium from the sarcomere and return it to the sarcoplasmic reticulum. The main player in this is the sarcoplasmic reticulum calcium ATPase (SERCA). This pump uses ATP to drive calcium against its gradient back into the SR. Once calcium dissipates, tropomyosin returns to its resting configuration; covering the binding sites for myosin heads.
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What are the five types of muscle contractions?
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1. Twitch-the response of skeletal muscle to a single stimulation (action potential)
2. Summation-an increase in the frequency with which a muscle is stimulated increases the strength of contraction. With rapid stimulation (so rapid that a muscle does not completely relax between successive stimulations), a muscle fiber is re-stimulated while there is still some contractile activity. As a result, there is a 'summation' of the contractile force. In addition, with rapid stimulation there isn't enough time between successive stimulations to remove all the calcium from the sarcoplasm. So, with several stimulations in rapid succession, calcium levels in the sarcoplasm increase. More calcium means more active cross-bridges and, therefore, a stronger contraction. 3. Tetany-A smooth, sustained contraction that occurs when a muscle fiber is stimulated so rapidly that it does not relax AT ALL between stimuli. 4. Isotonic-Tension or force generated by the muscle is greater than the weight of the load and the muscle shortens 5. Isometric-Weight of load is greater than the tension or force generated by the muscle and the muscle does not shorten. |
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How can the magnitude of force produced in a whole muscle contraction be controlled?
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1. Number of motor units
2. Rate of stimulation (summation of twitches) 3. Starting length of individual muscle fibers. [Fibers generate greatest force when they at or near resting lengths. Muscles already shortened,have less actin/myosin interaction=smaller force. If stretched beyond resting length, actin and myosin will be pulled too far apart to interact with each other and create a contraction.] 4. Density/number of thick and thin filaments within fiber 5. ELASTIC RECOIL: If a muscle is stretched slightly beyond its resting length (not so far that there is no opportunity for myosin/actin interaction) the active force generated by the contracting fibers will combine with the passive force of the tendon shortening. 6. Stretch reflexes: involuntary; safeguard against muscle or tendon injury. When stretched to a certain length,reflex tells the muscle to contract. Increases the magnitude of the contractile signal being delivered to the muscle (voluntary plus reflex signals). |
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What are the 3 different types of muscle fibers?
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**Muscle fibers are classified based on their myosin ATP-ase activity and the type of fuel they use**
1. Slow-oxidative 2. Fast-oxidative 3. Fast-glycolytic SLOW or type 1 fibers have low myosin ATP-ase activity and thus a lower shortening velocity, they fatigue more slowly than fast fibers. FAST or type 2 fibers have high myosin ATP-ase activity and thus a high shortening velocity, they fatigue rapidly. OXIDATIVE fibers contain numerous mitochondria and have a high capacity for oxidative phosphorylation. Their ATP production is dependent upon blood delivered oxygen and fuel. They contain myoglobin, an iron and oxygen binding protein that is related to hemoglobin. Myoglobin increases the rate of oxygen capture in the fiber. GLYCOLYTIC fibers in contrast have few mitochondria. They do however have a high concentration of glycolytic enzymes and glycogen (the storage form of glucose). This is their main source of fuel. They are larger and contain more myofilaments and can therefore develop a stronger contraction with more tension. They fatigue rapidly. |
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What are the effects of exercise on skeletal muscle?
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-Increased contractile activity->increase in muscle size (more myofibrils are made) and in capacity for ATP production.
-LOW intensity exercise: OXIDATIVE fibers inc number of mitochondria and capillaries. -HIGH intensity exercise: GLYCOLYTIC fibers inc diameter via synthesis of actin/myosin filaments and inc production of glycolytic enzymes. **More nuclei are required to support protein expression and maintain an appropriate ratio of cell volume to nuclei density. -Muscle cells don't have high capacity for cell division -SATELLITE CELLS (progenitor cells) located between sarcolemma and basement membrane; proliferate in response to the mechanical stress of exercise; micro-tears may attract SCs; DONATE NUCLEI **Fiber types thought to interconvert** **Muscle fatigue is associated with depletion of ATP within the fiber as well as loss of efficiency in calcium storage and release** |
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What are the effects of inactivity on skeletal muscle?
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-Skeletal muscle= energetically expensive to build and maintain
-When muscles are in disuse cells will degrade contractile proteins in the cell -> Muscle Atrophy -Depressed protein synthesis -Transient is GOOD: Proteins broken down provide the body with free amino acids for protein synthesis in vital organs and energy via direct oxidation or gluconeogenesis. -Sustained=BAD: muscle atrophy or wasting affects breathing and overall ability of the body to recover from stress or illness -> increased morbidity and mortality. **Regardless of activity, some muscle fibers are lost with age** |
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Characteristics of Skeletal Muscle in athletes
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**Skeletal muscle is highly developed and adapted to athletic potential. Skeletal muscle makes up over 50% of total body weight, and uses about 78% of cardiac output at VO2max.**
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What is a diagnostic tool used to assess skeletal muscle damage?
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-Measure serum levels of the muscle enzymes creatine kinase (CK) and Aspartate aminotransferase (AST).
-When muscle cells are damaged, these enzymes that are normally present in high concentrations within intact muscle cells leak into the bloodstream and become elevated in the serum. -CK will peak first, around 6-12 hours post injury (acute enzyme). CK concentration also will return to normal more quickly (around 24 hours) provided there is no further damage. -AST peaks around 24 hours, and can take days to weeks to return to normal concentration. **because of these properties, measuring the enzyme levels can help determine both the timing and extent of injury.** |
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Tendon structure and Function
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-The smallest unit in a tendon is a tropocollagen fiber. These fibers are organized into microfibrils. Microfibrils are organized into subfibrils, which are then organized into fibrils. Fibrils are organized into fascicles, and multiple fascicles make up a tendon.
-The tendon contains a lot of extracellular matrix with sparse fibroblasts (cells that make tendon components) -Extracellular matrix contains mainly collagen and proteoglycans -Clinical injury or rupture occurs either when there are problems with the fibroblasts themselves or the rate of damage is too fast for the cell/matrix to keep up with repair. Usually inadequate response leads first to subclinical injury and then to clinical injury/rupture. **Structure is extremely important because tendons must deal with a tremendous amount of force, the energy stored during the stretch of the tendon is released upon shortening** -Tendons perform differently based on the load applied. -When stretch first occurs the TOE REGION which has a “crimp” or area of fiber overlap will stretch easily as the crimp straightens out. -When more load is applied the tendon enters the linear phase of reversible elongation. -As more load is applied the tendon will eventually reach the yield point. The yield point is the point of tendon failure and results in irreversible damage. |
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Collagen Structure
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-The primary structure is very specific amino acids. Every 3rd amino acid in a collagen molecule is glycine (makes up 33% of molecule). This is important because some of the other amino acids (such as proline, hydroxyproline) are very large and the small glycine amino acid allows folding into its secondary, tertiary, and quaternary structures.
-The tertiary structure consists of 3 chains wound into a triple helix. -Quaternary structure is molecules arranged parallel to each other along lines of tension. They are then cross linked by intermolecular cross links that help impart strength to the tendon. Also the way they are stacked allows for the most molecules per square mm possible. |
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Collagen Formation
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1. triple helix is originally formed as pro-collagen inside the cell.
2. pro-peptides attached to it inhibit the full collagen fibril from being assembled inside the cell itself. 3. Self assembly is energetically favorable, and the fibril would be too large to export from the cell. 4. Pro-collagen is secreted outside the cell -> pro-peptides are cleaved-> pro-collagen is converted to tropocollagen 5.Self assembly |
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Proteoglycans
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-They regulate water content, provide lubrication and spacing between collagen fibers, and acts to “cushion” the joints. When a force is applied and the tendon is shortened, all of the water held by the proteoglycans is squeezed out. When the tendon straightens back out, the water moves back to the proteoglycans. As such they act as mini shock absorbers for the tendon/joint.
-There are two regions of the tendon: -Tensile region -Contains small amounts of small sized proteoglycans -Compressive region -Contains large amounts (3x as many as tensile region) of large sized proteoglycans and looks more like cartilage because of this. |
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Tendon Response to Injury
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3 stages of repair
1. Inflammatory phase: vascular and cellular 2. Repair phase: fibroblast proliferation 3. Remodeling phase **Goal is normal architecture BUT not achievable with natural healing. Injured tendon never fully returns to normal, re-injury is common** **Tendons and muscles are the support system of the body-injuries such as tendon laceration, fibrotic myopathy (fibrosis or scar tissue forms in the injured muscle), or muscle rupture=serious impairments in mobility** |
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Common Injuries of Muscles and Tendons
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-lacerations of the 3 tendons that support the fetlock of a horse
-Laceration of just the Superficial Digital Flexor Tendon will cause the fetlock to drop, of both the SDFT and Deep DFT will cause that in addition to the toe being off the ground, and a laceration of both tendons plus the suspensory ligament will result in the fetlock completely on the ground with the toe off the ground. -The external appearance of the fetlock can clue you in as to the nature of the injury! -Fibrosis of the semitendinosis muscle in the horse causes a characteristic gait change -Peroneus tertius muscle rupture in ruminants -Muscle is part of the pelvic limb stay apparatus. When ruptured, the animal can flex the stifle and extend the hock at the same time, and the stability of the entire limb is compromised. -Ruptured gastrocnemius muscle in the horse -Entire hock will drop to ground |
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Homeostasis
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Operation of intrinsic mechanisms in biol systems to maintain internal conditions within tolerable limits in the face of changing internal or external conditions.
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Negative Feedback Systems
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Typically contain sensors (monitor environment), integrators (compare monitored parameter to set point), and effectors (execute appropriate functions to return internal conditions to setpoint or acceptable range)
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Positive Feedback Systems
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Serve to amplify/accelerate responses as opposed to limit them.
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Structural Levels
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Organism>Organs>Tissues>Cells. All levels exhibit specialization, redundancies, communication, energy/information management, and ability to repair damage to varying degrees.
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Protein
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-Monomer= alpha amino acids
-Polymer= proteins, polypeptides. Linked by peptide bonds (formed w/H2O as byproduct) -Linear (primary) structure of polypeptides determined by mRNA -Higher order structure (secondary, tertiary, quaternary) determined by folding of chains, aggregation of multiple units *After polymerization, proteins are subject to further modification on amino acid side chains. Ex: addition of lipids -Many functions: structural, mechanical, catalysts/enzymes, chemical messengers, sensors, fuel, source of chemical energy. |
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Nucleic Acids
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-Monomer= nucleotide
-Polymer= nucleic acids. Linked by phosphodiester bonds. -Many functions: Structural (ribosomal RNA, small nuclear RNA), catalytic/regulatory (small interfering RNA). *NucleoSIDE= nitrogenous base coupled to ribose *NucleoTIDE= nucleoside coupled to phosphate(s). Ex: ATP |
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Lipids
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-Monomer/polymer= lipids are the only exception to the monomer/polymer rule. Lipid base
units are not considered monomers. -Functions: solubility barrier, membrane, structural, chemical messengers. *Have low water solubility-important for function as membrane! *Fatty acids have one end that is water soluble and then a long non-soluble chain. Ex: phospholipids (fatty acid group with phosphate group). MAJOR MEMBRANE COMPONENT. Backbone is glycerol, fatty acid chain end is hydrophobic, polar head group end is hydrophilic. |
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Carbohydrates
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-Monomer= monosaccharides (sugars)
-Polymer= di, oligo, or polysaccharides. Linked by glycosidic bonds. -Functions: Energy storage (glycogen), Fuel (glucose), structure (glycoproteins), cellular recognition (blood group antigens). |
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Cell Similarities
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All cells:
-contain entire genome -attain final phenotype by process of differentiation (gain defining characteristics but generally lose ability to differentiate into other cell types (multipotency) and ability to proliferate indefinitely (features of stem cells)) WAYS IN WHICH ALL CELLS ARE THE SAME 1. Need to generate/utilize energy 2. Need to interact in a meaningful way with noncellular components of surrounding environment such as connective tissue or extracellular matrix 3. Sense and respond to environment |
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Cell Differences
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1. Function/size/shape/polarity/tissue adherence/responsiveness to specific stimuli
2. Capacity to replicate by mitosis 3. Lifespan 4. Information retrieval/response to extracellular signals (tailored to differentiated function) |
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Nucleus
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-Contains chromatin and apparatus for DNA replication/transcription
-Highly organized by cytoskeletal proteins -Surrounded by membrane with pores (around 10um)--->nuclear envelope -Envelope is continuous with RER |
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Mitochondria
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Major site of energy metabolism--->Krebs cycle, oxidative phosphorylation (generates ATP)
-Has some of its own DNA -Receives products from glycolysis in cytoplasm to fuel TCA/ETC |
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Ribosomes
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-Site of protein synthesis--->translation of mRNA into proteins
-Either free polyribosomes in cytoplasm attached to mRNA (encodes intracellular proteins) - or attached to RER (synthesize proteins for plasma membrane/cell surface or secretion) ( First peptides synthesized will signal where the protein will go). |
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Endoplasmic Reticulum
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Two types, rough and smooth. Rough is studded with ribosomes and is the site of protein synthesis. Smooth is where the vesicles carrying newly synthesized proteins from the RER are budded off.
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Golgi Apparatus
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-Site of protein storage, modification, export
-Receives vesicles from ER containing proteins for export or insertion into PM -Provides site for addition of carb chains and other modifications or multi-subunit protein assembly -Vesicles FROM golgi apparatus convey proteins to destination (exocytosis) -Movement of vesicles is highly regulated and requires ATP |
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Lysosomes
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-Site of degradation of internal and ingested material
-Plays a role in normal biomolecule and organelle turnover and defense against infection -Fuses with vesicles created by endo or phagocytosis and degrades contents |
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Plasma Membrane
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-Defines cell boundary
-Consists of phospholipid bilayer with proteins associated. Lipids are organized with polar (hydrophilic) ends facing aqueous compartments inside/outside cell and hydrophobic ends facing each other on interior of membrane -Forms solubility/permeability barrier and insulated barrier to create reservoirs of potential energy in the form of ion gradients, concentration gradients, osmotic gradients etc. -Site of receptor proteins (sensors) to monitor external environment or regulate activites inside/outside cell -Mechanisms exist for selective entry and exit of molecules/particles |
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Neurotransmission
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accomplished by the action potential, a rapid, sequential re-distribution of ions down their concentration gradients that locally depolarizes the membrane along the length of cell
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Ion Channels
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: membrane-bound proteins that act as extremely fast channels for ion movement across excitable membranes;
-gating:opening/closing of ion channel pores in response to an electrical or chem signal -selective permeability: each class of ion channel is selective in their permeability to one or more ions |
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Resting Membrane Potential
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Motoneuron: -70mV
Muscle: -90 mV Depends on relative conc. of major ions on each side of PM and permeability of membrane to each |
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Motor unit
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a motor neuron plus all the muscle fibers to which it connects
In vivo,all fibers have an axon terminal |
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Innervation Ratio
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# of muscle fibers per motor neuron. INC # of motor units to INC control
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Length-Tension Relationship
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Force exerted depends on the number of myosin heads pulling together at the same time
A bell-shaped curve, tension generated varies with length |
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Major areas of Energy Consumption in Skeletal Muscle
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-Cross-bridge recycling
-Pumping of calcium, other ions -Synthesis of Contractile Proteins |
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