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5658. Proving that lim xua f 1x2 3 L Use the following

Calculus: Early Transcendentals | 2nd Edition | ISBN: 9780321947345 | Authors: William L. Briggs ISBN: 9780321947345 167

Solution for problem 56 Chapter 2.7

Calculus: Early Transcendentals | 2nd Edition

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Calculus: Early Transcendentals | 2nd Edition | ISBN: 9780321947345 | Authors: William L. Briggs

Calculus: Early Transcendentals | 2nd Edition

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Problem 56

5658. Proving that lim xua f 1x2 3 L Use the following definition for the nonexistence of a limit. Assume f is defined for all values of x near a, except possibly at a. We write lim xSa f 1x2 L if for some e 7 0, there is no value of d 7 0 satisfying the condition f 1x2 - L 6 e whenever 0 6 x - a 6 d. For the following function, note that lim xS2 f 1x2 _ 3. Find all values of e 7 0 for which the preceding condition for nonexistence is satisfied. 1 2 3 4 x 6 1 2 3 4 5 y 0 y _ f (x)

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Clemson University Spring 2016 Immune System PowerPoint Slide 1: Immune System • Immune system doesn’t have numerous organs working together but instead it has functions working together that bring about an immune response • Immune System can: -­‐ Prevent the entry of pathogens into the body -­‐ Prevent the spread of pathogens throughout the body by keeping the pathogenic problem to one area + killing it if there was a breech • Pathogen: A disease causing agent • Antigen: Foreign thing that the body wants to get rid of it enters the body (Can include pathogens) Slide 2: Immune Systems: Nonspecific Immune System • AKA innate immune system • Part of the immune system that attacks anything foreign • Consists of external body membranes and can include inflammatory response • Inflammatory Response: -­‐ Ex: Cut on the body o The inflammatory response is activated since the membrane of the skin was cut and some substances were able to enter through the breech o Inflammatory response works to try to keep the foreign substances localized to that area so that they don’t spread to the rest of the body -­‐ Ex: Mosquito Bite: o Can see where the inflammatory response keeps the foreign substance localized Slide 3: Immune Systems: Specific Immune System • AKA adaptive immune system • Individual cells respond to certain and specific foreign substances • Includes B and T lymphocytes • Ex: There are B lymphocytes that only respond to Staphylococcus Slide 4: Superficial Nonspecific Defenses: Skin • Unbroken epidermis is a great barrier to antigens/pathogens • Epidermal tissue does not have a blood supply à Means that the skin is made up of squamous epithelium that is mostly dead • Have protein layers stacked up on top of each other = barrier Slide 5: Superficiual Nonspecific Defenses: Mucous Membranes • A mucosal lining can be found on all internal body cavities that is composed of epithelial tissue and also creates a physical barrier • Mucous membranes also secrete mucous that act like a trap so that any foreign substances inside the body can be stuck in the cavities of the mucous membranes • Mucous secretions create an acidic environment à Foreign cells can be destroyed by the acids • Production of protein digesting enzymes that are able to break down foreign substances with a protein coat • Some mucous membranes can produce lysozymes: Enzymes in lysosomes that are able to break apart foreign substances (Can be found in tears, saliva, etc. *Overall: Skin and mucous membranes function to keep foreign substances out of the body, but the barriers can be breeched so there is a need for additional nonspecific mechanisms Slide 6: Internal Nonspecific Defenses: Phagocytes • Phagocytosis: Phagocytic cells surround something that is foreign by extending their cytoplasm and bring it inside a vacuole to destroy it • Free phagocytes: Found in circulation • Fixed phagocytes: Found in the lymph organs that hang out in the reticular cells • Phagocytes: a) Macrophages: -­‐ Derived from monocytes that escaped from circulation through diapedesis b) Neutrophils: -­‐ Continuously in circulation in the blood stream -­‐ Become phagocytic when they bind to a foreign cell c) Eosinophils: -­‐ Continuously in circulation in the blood stream -­‐ Attack internal parasitic worms Slide 7: Internal Nonspecific Defenses: Mast Cells • Mast cells are somewhat phagocytic but are different than phagocytes in the way they find the foreign substance and bring it inside the mast cell • Have specific receptors that are non-­‐specific à Means that mast cells can bind to a number of different things that then digest the bound components and kill them • Mostly bind to bacteria Slide 8: Internal Nonspecific Defenses: Natural Killer Cells • Natural killer cells are a class of lymphocytes (In addition to the T and B lymphocytes) that circulate in the blood stream so that when they encounter anything abnormal, they automatically kill it • Lyse foreign substances and not phagocytize them • Attack cancerous cells or cells infected by a virus • Cancerous cells are abnormal cells • Virus within a cell: Parts of the virus appear on the surface of the body cell so that it looks weird à Therefore, natural killer cells attack any cell that does not look normal Slide 9: Internal Nonspecific Defenses: Inflammation • Inflammation is the result of the dilation of capillaries that become larger and porous • 4 Symptoms of Inflammation: a) Redness: -­‐ Capillaries are dilated so more blood is able to rush to the site of damage -­‐ Blood pigment is red so because there is more blood, the area will appear more red b) Swelling: -­‐ When the capillaries dilate, they become more permeable -­‐ Fluids leak out of the bloodstream and accumulate as a result to create swelling c) Heat: -­‐ Blood is warmer than the rest of the body -­‐ Therefore, when blood accumulates in one spot à That location will feel much warmer than the rest of the body d) Pain: -­‐ As fluid accumulates at the site of inflammation, it causes pressure that activates pain receptors • Purpose of inflammation: By delivering more blood to the site of damage, more most mast cells, natural killer cells, phagocytic cells, etc. can be delivered to fight off foreign substances in a non-­‐specific fashion + keeps the foreign substances from leaving that location Slide 10: Internal Nonspecific Defenses: Antimicrobial Proteins • Antimicrobial Protein: Attack microorganisms by destroying them or interfering with their reproduction (Like with viruses) • Interferon: -­‐ Antimicrobial protein secreted by a cell infected by a virus in order to signal neighboring cells to induce changes to protect themselves form the virus -­‐ Disrupts viral replication in neighboring cells so that they can’t reproduce • Complement System: -­‐ Involves more than 20 different proteins that function in complement -­‐ Blood proteins that circulate in the blood -­‐ If they become activated, complement system (proteins) promote inflammation -­‐ Some complement proteins can cause lysis to occur Slide 11: Internal Nonspecific Defenses: Fever • Fever: Elevation of body temperature à Systemic response • Interferes with replication of foreign cells Slide 12: Phagocytic Mechanism (Phagocytosis) • Phagocyte recognizes pathogen’s carbohydrate surface markers -­‐ Phagocytes are able to differentiate between body cells and pathogens because “Self” markers on body cells are MHC (Major histocompatibility complex) and pathogens do not have the MHC self marker • *(Phagocytes located in the body and in interstitial space and lymphatic organs are not active until they encounter a foreign cell) • Opsonization: -­‐ Enhances the recognition of a foreign cell -­‐ Antibodies that attach to the foreign cell are able to flag it and make it easier to be found and destroyed • Adherence: Phagocytic cells attach to the foreign cell by sending out cytoplasmic extensions that adhere to the pathogen • After adherence to the pathogen, the phagocyte brings the foreign cell into its own body in vacuole à Phagocyte + pathogen inside = phagosome • Phagosome combines with lysosomes (Carry lysozymes) to forms a phagolysosome so that the lysozymes break down the pathogen • Lysozymes can be aided by respiratory burst (Additional chemicals) in breaking down pathogen • Breakdown products: -­‐ Residual bodies still contained within the phagosome that are expelled out of the phagocyte and filtered through the blood and lymph to be expelled as waste Slide 13: Natural Killer Mechanism • Natural killer cells detect body cells that have become cancerous or infected through lack of “Self” (MHC) markers or by the presence of certain sugars • Key that natural killer cells detect problems with body cells and NOT foreign cells • Adherence of a natural killer cell to an abnormal body cell activates the natural killer cell to release perforins (proteins) that lead to a cytotoxic T cell process (Both cT and natural killer cells use the same key mechanism— discussed later) à natural killer cells bore holes into the plasma membrane to disrupt the cell and cause it to become fractured • Channels in the plasma membrane of the target cells result to allow the formation of holes in the nuclear membrane as well so that the nucleus disintegrates Slide 14: Inflammatory Mechanism • Macrophages have toll-­‐like receptors that are non-­‐specific on their surfaces that recognize pathogens • When the toll-­‐like receptors bind to the pathogen, cytokines are released • Cytokines promote inflammation à signaling capillaries to dilate • Cytokines also attract white blood cells wherever they are produced (Exhibit positive chemotaxis) • Activation of the toll-­‐like receptors on a macrophage causes other cells in the same area to release other chemicals that are inflammatory mediators such as histamines, prostaglandins, or any sort of chemical with a localized change or effect • Cytokines signal blood vessels in the injured area to dilate and increase permeability à hyperemia: Excessive blood • Increased permeability allows the plasma to leave the capillary and move into the interstitial space à Exudate (Fluid and clotting factors containing antibodies that have left circulation and that accumulate at the site where the capillary is most permeable) • When exudate accumulates this leads to swelling, which is also known as edema • Edema functions and effects: -­‐ Helps to dilute the foreign substances à more exposure for the immune system to be more efficient in detecting the foreign substances -­‐ Brings oxygen and nutrients to activate other substances like enzymes -­‐ Carries clotting proteins to plug breaks in a barrier with a clot Slide 15: Results of Inflammation • Injured cells release leukocytosis-­‐inducing factors à Cause neutrophils to be released from the red bone marrow • Leukocytosis: Higher than normal numbers of neutrophils in the blood Slide 16: Results of Inflammation • Loss of fluids slows blood flow locally • Flow of fluids leaking out of the bloodstream à low blood pressure à ultimately slows down blood flow Slide 17: Results of inflammation • Neutrophils are able to accumulate at the site of damage due to the slow blood flow • Some neutrophils will be grabbed and held near the site of damage due to endothelial cells from inside the wall of a capillary secreting selectin • Margination: The process of holding neutrophils at the wall of a capillary near the site of damage • Neutrophils held on the cell wall of capillaries near the site of damage will then diapedese and escape the capillaries • Neutrophils are phagocytic cells that attack foreign substances Slide 18: Results of Inflammation • Inflammatory chemicals (Includes selectins and mediator chemicals) act as chemotactic agents that mostly attract neutrophils to an area of damage • Once neutrophils have escaped the walls of the capillaries, monocytes follow out (Diapedese) of the capillaries as well and become macrophages • Macrophages have more lysosomes (Full of enzymes that break substances apart) Slide 19: Interferon Mechanism • Cells infected by a virus release interferons (IFN) • Interferons diffuse into neighboring cells that causes them to synthesize PKR protein that interferes with viral replication through prevention of use of the host cell’s machinery • Interferons also activate macrophages and natural killer cells Slide 20: Complement System Mechanism I • Antibodies bind to antigens/pathogens (Opsonization has occurred) -­‐ Antibodies binding to specific antigens is part of a specific immune response that can invoke a non-­‐specific action (Here the complement proteins) • Complement proteins bind to antibody-­‐pathogen complexes • Lysis, phagocytosis, and inflammation result • Complement proteins circulate in the plasma portion of the blood and wait to be called to action Slide 21: Complement System Mechanism II • Complement proteins bind directly to the polysaccharide molecules on the antigen/pathogen (Skip antibody attachment step) • Lysis, phagocytosis, and inflammation result Slide 22: Fever Mechanism • Leukocytes and macrophages exposed to pathogens secrete pyrogens • Pyrogens signal the hypothalamus to elevate body temperature • By increasing whole body temperature, the availability of iron and zinc is reduced which are important components that bacteria used to divide à Bacteria eliminated as a result since they aren’t able to divide • Pyrogens also elevate metabolic activity à One way of producing the necessary heat -­‐ Heat is produced from shivering when you feel cold even though the body temperature can be at 102+ degrees F -­‐ Then fever breaks Slide 23: Antigen • French • Any substance that promotes an immune response (Anything foreign) Slide 24: Antigenic Properties • Antigens demonstrate immunogenicity • Reactivity: -­‐ Markers on the surface of cells are able to interact with antibodies or lymphocytes -­‐ Antigens promote interactions with immune cells due to their reactive components (Antigenic determinants) • Antigenic determinants: Reactive parts of a an antigen that gives it immunogenicity Slide 25: Major Histocompatibility Complex • Body cells have genetically determined markers on their surface = “self” antigens that are also known as MHC markers • MHC markers are not immunogenic to us (Not reactive/immune system wouldn’t attack them) • Our own MHC markers would be immunogenic to other individuals except for those with identical twins Slide 26: Characteristics of Specific Immunity • AKA adaptive immunity • Pathogen specific • Specific immunity is not immediately active à When specific immune cells come in contact with the specific antigen, there is a delay before the specific immune cells become fully active • Systemic with specific immune cells circulating the body all the time scanning for specific pathogens • Provides memory: The activation of specific immune cells will cause the production of more of those cells that will then interact with the antigen faster the next time it encounters it (Time lag is shortened as well) Slide 27: Pathways: Humoral • Humoral: Fluid • Specific immune cells interact with antigens that are free floating (Found in the blood stream and circulating the body) • Humoral pathway is an antibody-­‐mediated pathway since antibodies detect the free floating pathogens (Uses B lymphocytes) • Antigens + antigenic determinants on the surface of an antigen along with the antibodies are specific • Antibodies do NOT kill the specific antigen directly à It is marked so that another immune cell can kill it, such as complement proteins or phagocytic cells • In general, a specific immune response is able to activate a non-­‐specific immune response • Main point: Humoral pathway marks antigens for destruction Slide 28: Pathways: Cell-­‐Mediated • Pathway where one of our body cells has become infected so the T lymphocytes will attack and kill the infected body cell • This process is similar to that of the natural killer cells, except that the natural killer cells attack anything à Each T lymphocyte in the cell-­‐mediated pathway can only bind to a certain type of infectious agent • Main point: Cell-­‐mediated pathway kills infectious agents directly by cell lysis Slide 29: Lymphocyte Production • Humoral: B lymphocytes • Cell-­‐mediated: T lymphocytes • All lymphocytes are produced by stem cells in the red bone marrow • Immature lymphocytes are virtually identical until they mature • Immature lymphocytes migrate to the bone marrow or thymus (Primary lymph organs) to become immunocompetent (Point where receptors are required to interact with a specific antigen and its antigenic determinants) Slide 30: Lymphocyte Production • T lymphocytes: Immunocompetent in the thymus Slide 31: Lymphocyte Production • B lymphocytes: Immunocompetent in the bone marrow **Immunocompetent T and B lymphocytes still have to remain in secondary lymph organs (Spleen, lymph nodes, etc.) until they mature and even when they are mature, they are not fully functional until they bind to an antigen Slide 32: Lymphocyte Production: Recap • Produced by stem cells in red bone marrow • T cells become immunocompetent in thymus • B cells become immunocompetent in bone marrow • Immunocompetent cells mature in secondary lymphoid organs Slide 33: Lymphocyte Production: Recap • Not fully functional until bound with antigen Slide 34: Antigen-­‐Presenting Cells • Engulfs pathogen and presents its fragments as antigens Slide 35: Cell-­‐Mediated Immune Response • Review: -­‐ 1 line of defense (Non-­‐specific): Protective barrier -­‐ 2 line of defense (Non-­‐specific): Keeping the antigen in one spot + attempting to eliminate it rd -­‐ 3 line of defense (Specific): Specific approach where the specific immune system tries to target invaders and kill them -­‐ 4 line of defense (Specific): After body cells have become infected, the immune system has to attack its own altered body cells and lyse them • Non-­‐specific immune system keeps working even though it may not initially solve the pathogenic problem Slide 36: Antigen Challenge • Antigen challenge: First encounter between a specific naïve immunocompetent lymphocyte and antigen • Review: -­‐ Lymphocytes are produced in red bone marrow à lymphocyte à primary lymphoid organ (Bone marrow or thymus) à Immucompetency achieved -­‐ Cells producing proteins due to genes are expressed on the surface of the cell that become the receptors specific for their specific antigens • Immunocompent lymphocyte: Can interact with specific antigens but won’t yet • Naïve competent cell: Ready to interact with specific antigen but hasn’t yet Slide 37: Primary Humoral Response • Antigens in the humoral pathway are free floating in the fluids in the plasma and lymph • Antigens bind with surface receptors on naïve immunocompetent B lymphocytes • When the specific antigen and immunocompent B lymphocyte connect à B lymphocyte becomes active and the clonal sectional process is stimulated • Clonal Selection: When the cell grow and multiplies to produce clones of that particular lymphocyte with identical receptors for that specific antigen • Most clones produce and become plasma cells that produce antibodies (Mark specific antigen for destruction) • Some clones instead of producing plasma cells and therefore antibodies are stored/remain as memory cells that wait to respond to another of the same infection in the future (Secondary humoral response) • Primary Humoral Response: The very first encounter between a naïve immunocompetent lymphocyte and its specific antigen Slide 38: Secondary Humoral Response • Refers to any subsequent exposure • Same mechanism as primary humoral response but is much more rapid and produces a lot more antibodies (Higher titer-­‐ concentration of antibodies) that last longer (For months) • Figure: a) Primary humoral response to antigen X: Takes about 7-­‐10 days for us to reach maximum titer (maximum number of antibodies) that lasts for about 4-­‐5 days that then declines -­‐ AKA primary response characteristics include, lag, limited antibody production and short duration b) Secondary humoral response to antigen X: More rapid, more antibodies produced (higher titer) and last longer c) Exposure to antigen Y is shown along with secondary exposure to antigen X so that primary humoral response is induced again for antigen Y Slide 39: Sources of Humoral Immunity • Refers to how to get antibodies present in the body for humoral responses • Active Immunity: -­‐ Our own system makes the antibodies due to a full-­‐blown antigen being present -­‐ AKA: Antigen activate B lymphocytes to produce plasma to produce antibodies • Passive Immunity: -­‐ Obtaining antibodies from a source other than our own bodies -­‐ AKA: Antibodies were produced somewhere else • Natural and artificial immunity • Combinations: a) Natural Active Immunity: -­‐ Similar to active immunity in that we had to have been infected by a full-­‐ blown pathogen to induce production of antibodies by our own body b) Natural Passive Immunity: -­‐ Ex: Antibodies are produced by the mother that pass across the placenta and are given to the baby -­‐ Ex: Antibodies produced by the mother that are passed to the baby through breast milk c) Artificial Active Immunity: -­‐ Immunizations are where an attenuated (weakened) antigen is injected so that it won’t make you sick but it still activates an immune response so that the body can make its own antibodies d) Artificial Passive Immunity: -­‐ Vaccines are where antibodies (Called immunoglobulins here) are injected into another body -­‐ Antibodies have been made to fight off infections for you Slide 40: Antibody Structure • Antibodies are complex proteins à Made up of 4 subunits • Also called immunoglobulins or gamma globulins • 2 identical light chains: Variable region à Have antigen binding sites to determine what antigen the antibody will bind to • 2 identical heavy chains: Constant region à Same in each antibody and dictates how an antigen will be destroyed • Some constant regions will bind complement proteins that will lyse cells and kill them, attract phagocytic cells, or simply mark the antigen for destruction (Ex: By phagocytosis with a dendritic cell or macrophage) Slide 41: Classes of Antibodies: IgD, IgG, and IgE • Most antibodies are single units with light (short) chains that bind the antigen and heavy (long) chains that destroy the antigen • IgD: -­‐ Receptor on the surface of a B lymphocyte -­‐ Is incorporated into the B lymphocyte to make it immunocompetent • IgG: -­‐ Most abundant of all antibodies -­‐ Main antibody present in the late portion of the primary and secondary response -­‐ There is a longer lag time in the production of IgG than others because they have to get to the end of the responses before circulating in the plasma to fight off antigens -­‐ Can invoke passive immunity by crossing the placenta -­‐ Bind to specific antigen and use complement proteins and otherwise exhibit phagocytosis (On the heavy chains) • IgE: -­‐ Don’t have many IgE -­‐ Increase seen with individuals with allergies -­‐ Can bind to mast cells that have engulfed a foreign substance and tells basophils to release histamine granules -­‐ Overalll: IgE cause the production of histames that causes IgE to replicate • IgG:IgE à IgE should be far more numerous, but if there isn’t much for the immune system to do, the IgE will respond to allergens • In order to control allergies, suppression of IgE leads to suppression of histamine response Slide 42: Classes of Antibodies: IgA • IgA: -­‐ Dimer: 2 units (monomers) are attached together à Have 4 receptor sites (Instead of the usual 2) on the variable region and constant region -­‐ Tend to accumulate in mucous and other body secretions -­‐ Binding to their specific antigens prevents the antigens from attaching to epithelial cells Slide 43: Classes of Antibodies: IgM • IgM: -­‐ Pentamer: 5 monomers are attached together à Have 10 receptor sites -­‐ First antibody secreted by plasma cells during a primary immune response to help prevent the spread of the foreign substance (IgG are produced later in the response and have more of these than IgM) -­‐ Can be used in a diagnostic test to see if an individual has had a recent infection or an older infection -­‐ Readily fixes and activates complement -­‐ Promotes agglutination: o Agglutination: Antigens bound to IgM clump together and are isolated in one spot so that non-­‐specific cells (Ex: Natural killer and phagocytic cells) are drawn towards that area Slide 44: Antibody Functions • Formation of antigen-­‐antibody complex à Mark antigens for destruction through variable site • Provides site for binding of complement proteins through the constant region -­‐ Complement protein fixation à Secretion of perforins that cause lysis of cells (Or due to another cytolytic chemical) • Blocks sites on pathogens so they won’t be able to bind to other cells in the bodyà Neutralization process in neutralizing the antigen so it won’t attack our bodies (Ex: IgA function) • Cause clumping of antigen-­‐containing cells that allows greater phagocytosis efficiency in keeping the antigens in one spot à Sometimes they can still be traveling throughout the body • Cause clumping of soluble antigen molecules: It’s even better to precipitate out the antigens so they don’t have to travel as much à Again, taking the soluble antigen molecules out of solution helps so that phagocytes can have better access to the antigens Slide 45: Monoclonal Antibodies • Commercially produced antibodies • Process: -­‐ Infect another organism -­‐ Organism produces antibodies -­‐ Collect blood serum or plasma -­‐ Extract antibodies to be used for vaccines, research, cancer treatment, etc. Slide 46: Cell-­‐Mediated Immune Response • Part of B lymphocytes functions to attract phagocytes to infected body cells in addition to trying to eliminate free floating antigens in the humoral response • Cell-­‐mediated response has to do with an infected body cells à A naive immunocompetent T cell is going to bind with one of the antigen infected body cells that does not have a normal MHC “self” marker • T lymphocyte with the specific receptor will bind to that infected cell (AKA T cell has bound to an antigen presenting cell) • Next, a second binding has to occur where the other arm has to bind to something else to release costimulatory signals that help activate T lymphocytes • Key: After the T lymphocyte has bound to the infected cell with one arm and the binding of something to the other arm has occurred to allow the release of costimulatory cells, the T lymphocyte has then been activated -­‐ This is different than B lymphocytes where when a B lymphocytes attaches to an antigen it is activated • Activated T cell will go through clonal selection to produce more T lymphocytes with receptors for that specific antigen + some clones will remain as memory cells for future encounters of the same infection • *T lymphocytes do NOT produce antibodies but they attack altered body cells Slide 47: T Cells • There is more than one type of T cell • CD4 and CD8 cells differentiation is due to differences of markers (glycoproteins) on the surfaces of these T cells that ultimately affect what antigens they can bind to Slide 48: T Cell Activators • CD4 Cells: T4 Cells à Helper T cells • CD8 Cells: T Cells à Cytotoxic T cells/Killer T cells 8 • Differences between the 2 T cells: Antigens they’ll attach to and what activates them • Two classes of altered MHC “self” markers on body cells that activate T cells: a) Class I MHC Protein-­‐Linked Antigens: CD8 -­‐ Endogenous (Produced by the body) -­‐ Antigen part comes from the body itself -­‐ A virus affects a body cell that has MHC + part of virus (antigen) present on the surface -­‐ Cancerous cells included -­‐ All body cells can produce MHC except for red blood cells -­‐ Any body cell that is infected will put antigen on surface of cell -­‐ T 8 (CD8) or cytotoxic cells interact with class I MHC b) Class II MHC Protein-­‐Linked Antigens: CD4 -­‐ Exogenous (Antigen part is produced outside of the body and is foreign) -­‐ Found on phagocytic cells that engulf bacteria -­‐ T 4 (CD4) or helper T cells interact with class II MHC Slide 49: Antigen Binding • T cell antigen receptors bind to antigen-­‐MHC complex Slide 50: Co-­‐stimulators • Then there has to be a second step where there binding to other receptors on APC (Antigen presenting cells) that causes the production of costimulatory signals such as cytokines and interleukins • Each costimulatory signal promotes a different response that either facilitates or disables activation • T lymphocyte is activated after antigen binding and constimulatory signal release Slide 51: Cell-­‐Mediated Immune Response • T cell binds with antigen infected body cell • Co-­‐stimulatory signals are present • T cell is activated • Clones are produced • Some clones become memory cells Slide 52: Types of T Cells: Cytotoxic T Cells • Cytoxic T cell = CD8 cell • Directly attacks and kills cells with Class I MHC • Therefore, once the CD8 cell attaches to the specific antigen and the costimulatory signals are present, the infected body cell is lysed and broken up Slide 53: Types of T Cells: Helper T Cells • Helper T Cells = CD4 cells that bind to Class II MHC (Phagocytic cell engulfed something foreign) • One the helper T cells have attached to the antigen and the co-­‐stimulatory signals are released, the helper T cell is activated • Activated helper T cells activate CD8 (cytotoxic) T cells and B cells • B cells are released as a result and attach to the foreign antigens directly • CD8 cells are recruited to kill the exogenously infected cells (Class II MHC) • Overall: Helper T cells (CD4) link the B and cytotoxic (CD8) T cell sides à Regulatory cells that regulate the activity of other cells Slide 54: Types of T Cells: Suppressor T Cells • One T cells are activated à Clonal selection and clones are continued to be produced until suppressor T cells shut them off • Cytokines produced by costimulatory signals or lysis chemicals produced by T lymphocytes activate suppressor T cells that produce other chemicals to stop clonal selection to ultimately stop the immune response • In general: Suppressor T cells are activated by chemicals that activated the T cells to begin with or the chemicals produced by T cells that are released in the process of the antigen they are trying to kill Slide 55: Primary Immune Response Summary Slide 56: Immune Disorders • Immunodeficiency: -­‐ Any condition that causes the immune cells to behave abnormally -­‐ Could be insufficient production of immune cells -­‐ Could be that there are enough immune cells that aren’t doing their proper function • Autoimmune Diseases: -­‐ When the immune system attacks its own body cells (Can’t distinguish MHC “self” markers vs. the antigen markers) • Hypersensitivities: -­‐ When the immune system responds to stimuli that wouldn’t normally activate the immune system (Harmless cells that are antigenic) -­‐ Ex: Allergies caused by allergens (antigens) Slide 57: Immunodeficiencies • Congenital Immunodeficiency: -­‐ Genetic, inborn, from birth -­‐ Ex: SCIDS (Severe Combined Immunodeficiency Syndrome) à Fails to produce enough T and B lymphocytes so that even the smallest infection can be detrimental Slide 58: Immunodeficiencies • Acquired: -­‐ Ex: AIDS (Acquired Immunodeficiency Sydrome) à HIV virus causes AIDS by destroying helpter T cells o It’s subsequent infection that kills a person with HIV since there are no helper T cells available to get rid of the infection Slide 59: Autoimmune Diseases • Multiple Sclerosis: -­‐ Destroys the myelin of the white matter in the brain and spinal cord -­‐ Lose conductivity and can’t send electrical signals à Loss in muscle control and movement Slide 60: Autoimmune Diseases • Myasthenia Gravis: -­‐ Immune cells attack neuromuscular junction in skeletal muscle -­‐ Impairs communication between nerves and skeletal muscles -­‐ Ex: Loss of control of eye muscles as seen in picture Slide 61: Autoimmune Diseases • Grave’s Disease: -­‐ Immune system attacks the thyroid gland so that it produces excessive amounts of thyroxine -­‐ Bulging eyeballs is one symptom Slide 62: Autoimmune Diseases • Juvenile Diabetes: -­‐ Type I Diabetes -­‐ Immune system attacks the pancreatic cells that produce insulin -­‐ Results in insufficient insulin production Slide 63: Autoimmune Diseases • Lupus: -­‐ Immune system attacks the kidneys, heart, and lungs -­‐ Skin lesions association to where someone looks like they have been bitten by a dog or wolf -­‐ Butterfly rash = distinguishing characteristic Slide 64: Autoimmune Diseases • Rheumatoid arthritis: -­‐ Immune cells attack the synovial membranes -­‐ Joints destroyed à rheumatoid arthritis Slide 65: Hypersensitivities: Immediate • Immediate (Acute) à Anaphylaxis -­‐ Response to allergen occurs within contact • Anaphylaxis: -­‐ Systemic release of histamine that causes systemic vasodilation à incredible drop in blood pressure -­‐ Often fatal • EpiPen: -­‐ Someone is told to carry this after there has been a warning in an initial episode where the person’s body responds to something and loses the ability to breathe, drop in blood pressure, etc. -­‐ Epinephrine is contained in the EpiPen and causes vasoconstriction so the vasodilation is reversed temporarily (Must get to the hospital still as soon as possible) Slide 66: Hypersensitivities: Subacute • Subacute: -­‐ Response to an allergen occurs a few hours after the initial contact • Transfusion reaction: -­‐ When the wrong blood type is injected in another individuals body à The body starts to reject the blood Slide 67: Hypersensitivities: Delayed • Delayed: -­‐ Response occurs 1-­‐3 days after contact with the allergen • Poison ivy reaction Slide 68: Transplants • Autograft: -­‐ Transplant from one part to another part of the same body -­‐ Only works in some cases -­‐ Transplant won’t be rejected • Isograft: -­‐ Transplant from an identical twin since twins have identical MHC markers on body cells -­‐ Transplant won’t be rejected • Allograft: -­‐ Key to look for closeness in relatedness in relatives (Can include strangers though too) -­‐ The closer the MHC markers on body cells are, the less likely of a rejection -­‐ There is still possibility of a rejection due to donor cells being foreign cells to acceptor • Xenograft: -­‐ Transplant from a different species -­‐ Ex: Pig heart valves

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Textbook: Calculus: Early Transcendentals
Edition: 2
Author: William L. Briggs
ISBN: 9780321947345

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5658. Proving that lim xua f 1x2 3 L Use the following