Refer to Exercises 3 and 4. An atmospheric scientist notices that the slope of the least-squares line in the study described in Exercise 4 differs from the one in the study described in Exercise 3. He wishes to test the hypothesis that the effect of humidity on ozone level differs between the two cities. Let βA denote the change in ozone level associated with an increase of 1 percent relative humidity for the city in Exercise 3, and βB denote the corresponding increase for the city in Exercise 4.
a. Express the null hypothesis to be tested in terms of βA and βB.
R-Sq(adj) = 8.9%
b. Let and denote the slopes of the least-squares lines. Assume these slopes are independent. There are 120 observations in each data set. Test the null hypothesis in pan (a). Can you conclude that the effect of humidity differs between the two cities?
MICROBIOLOGY 210 – EXAM 3 STUDY GUIDE • TYPES OF SYMBIOSIS – living together o MUTUALISM – both organisms benefit o COMMENSALISM – one benefits, other is unaffected by the other’s presence o PARASITISM – one benefits, other is harmed • NORMAL MICROBIOTA – microbes that live in and on you normally, and don’t typically cause you any harm (normal flora, indigenous microbiota, etc.). These organisms are found on every body ‘surface’ o Resident: with you most of your life. These guys are moved in permanently o Transient: can’t survive on the body long-‐term. They are outcompeted, killed by the body’s defenses, or unfit chemically or physically to stay • NORMAL MICROBIOTA CAUSING DISEASE – they don’t really do this unless one of these three things happens. When they do so, they are called ‘opportunistic pathogens’ o Unusual site – moved to a place they don’t normally colonize o Immune suppression – your immune system would usually keep the microbes in check, but when it is compromised, they take over the area o Shifts in normal microbiota populations – in the ‘microbial antagonism’ system, the different types of microbes compete for resources and space on your body. When the populations shift, one can become overly abundant • TYPES OF RESERVOIRS – sources of pathogenic infection o Animal: domesticated and wild. The more similar the animal is to us, the more likely we are to be able to catch their diseases o Human: actively diseased and carriers (have no obvious symptoms) o Nonliving: soil, water, or food • CONTACT TRANSMISSION o Direct Contact Transmission: handshake, kiss o Indirect Contact Transmission: drinking after someone, sharing toothbrush o Droplet Transmission: droplets through air (within a meter) like from a sneeze • VEHICLE TRANSMISSION o Airborne Transmission: dust or droplets that travel more than a meter o Waterborne Transmission: streams, public pools o Foodborne Transmission: meat • VECTOR TRANSMISSION o Mechanical Vector Transmission: on the bodies of bugs (when they land on stuff) o Biological Vector Transmission: in blood that bugs transfer (mosquito, tick, etc.) • CONTAMINATION & INFECTION RELATIONSHIP – contamination is the presence of microbes somewhere, while infection is the successful establishment of a pathogen colony. Contamination has to occur for infection to occur, however a contamination can be unharmful (resident microbiota) or fought off by the body’s defenses. When the contamination is not warded off, and a pathogen becomes established, it is infection • PATHOGEN PORTALS – how pathogens get in and out of the body: breaks in the skin, growing on mucous membranes, or passing through the placenta • ADHESION’S ROLE IN INFECTION – microbes used adhesion factors (attachment proteins) to stick to host cells better. Essentially, they have to be able to attach to a host cell in order to infect it. Hosts evolve ways to ‘unstick’ microbes, and microbes evolve new ways to stick to and invade hosts • BIOFILM FACILITATING CONTAMINATION & INFECTION – biofilms are groups of organisms that interact with each other. Biofilm interactions can be symbiotic, and as a group the organisms may be more equipped for contamination and infection • INFECTION – successful invasion of the body by a pathogen • DISEASE – decrease in the host’s fitness due to a pathogenic infection • MORBIDITY – synonym to disease, decrease in health • PATHOGENICITY – ability of a microbe to cause disease. Harmless (normal flora), opportunistic (can cause harm in the wrong place), or pathogenic (causes harm) • VIRULENCE – degree of pathogenicity, or ‘talent’ at causing a disease in a host. A microbe is virulent if it has a characteristic, or multiple characteristics, that are advantageous for invading a host and establishing itself 2 • SYMPTOMS – disease characteristics felt by the infected patient • SIGNS – outward characteristics observed by those who observe the patient • SYNDROMES – group of signs and symptoms that are characteristic of a disease • STAGES OF INFECTIOUS DISEASE o Incubation – no signs or symptoms o Prodromal Period – microbe is growing at a faster rate, first signs and symptoms o Illness – peak of microbe presence, feeling the worst o Decline – immune system is decreasing bacterial load, still feel bad o Convalescence – getting back to normal, eradicating pathogen • VIRULENCE FACTORS: help make a microbe virulent, a better pathogen o microbial extracellular enzymes – secreted by pathogen to help maintain infection and invade host cells (coagulase, kinases, collagenase, etc.) o toxins – harms tissues and triggers harmful immune responses (exotoxins destroy host cells, while endotoxin stimulates detrimental immune responses) o adhesion factors – allows to adhere to host cells o antiphagocytic factors – evades detection by immune system (capsule) • INCIDENCE – number of new disease cases at the same time in an area • PREVALENCE – number of cases, new and already existing at the same time in an area • ENDEMIC – constant number of cases in an area • SPORADIC – here and there the disease pops up • EPIDEMIC – large number of cases occurs all at once in an area • PANDEMIC – large number of cases occurs all at once across several continents • HEALTHCARE ASSOCIATED INFECTIONS: DEVLEOPMENT – Hospitals and doctors’ offices are full of infected people, as well as immunocompromised people so it is not uncommon for diseases to be swapped or acquired there. Nosocomial diseases are acquired in the healthcare facility, while a superinfection is an escalation of a person’s preexisting infection due to inhibition of some resident microbiota o EXOGENOUS HAI – pathogen acquired from the health environment o ENDOGENOUS HAI – arises from opportunistic normal microbiota o LATROGENIC HAI – infection from medical procedure 3 CHAPTER 15 • FIRST LINE OF DEFENSE – external (skin and mucous membranes) • SECOND LINE OF DEFENSE – internal, nonspecific blood borne chemicals and killing of invaders in general • THIRD LINE OF DEFENSE – specifically targeting unique species of pathogens • SKIN: WHY IT IS GOOD AT ITS JOB – lots of layers of dead, tightly packed cells. Sheds and microbes fall off with it. Very salty from sweat, inhibits growth of lots of microbes • MUCOUS MEMBRANES – you have these guys in all of the body cavity openings. Think your nose, throat, lungs, genitals, eyes • MUCOUS MEMBRANES: WHY THEY ARE GOOD AT THEIR JOB TOO – tightly packed living cells that continually shed as well. Covered in sticky mucus to trap microbes. Lysozyme is found there as well to prevent microbe growth • LACRIMAL APPARATUS – produce and drain away the tears that cover your eye. Tears have lysozyme, and when you blink it spreads tears across your eye, and washes the surface of the eye with new ones. The old tears flow into the nasal mucus line and are swallowed with the other old stuff from the mucous membrane surface • NORMAL MICROBIOTA – outcompete potential pathogens by taking up space and nutrients, changing the pH of the environment with byproducts, and symbiotically providing the body with nutrients that support a healthy immune system • PEPTIDES – also called defensins. On skin, mucous membranes, and neutrophils • BLOOD ON DEFENSE o PLASMA – sequester iron from microbes. Proteins include complement and antibodies, necessary for specific defense o LEUKOCYTES – granulocytes and agranulocytes • PHAGOCYTOSIS – Chemotaxis, Adherence, Ingestion, Maturation, Killing, Elimination • INTERFERONS – proteins released by the host to inhibit viral infection spread. Type 1 is the kind that warns neighboring cells that a ‘martyr’ cell has been infected • COMPLEMENT – Classical pathway (antibody activated), Alternate pathway (pathogenic products activate), or Lectin pathway (microbial polysaccharides activate) 4 • INFLAMMATION IS A GOOD THING – this is a response to tissue damage. It is the dilation and increased permeability of blood vessels. Phagocytes migrate to clear the area and the tissue is repaired before the swelling, redness, heat, and pain subsides • FEVER IS A GOOD THING – pyrogens make the hypothalamus increase the body’s core temperature. Blood vessels in the peripheral parts of the body contract and cause chills. When pyrogens decrease the hypothalamus will reset you start to sweat and go back to normal metabolic rate CHAPTER 16 • ADAPTIVE IMMUNITY FAST 5 – specificity, inducibility, clonality, self, and memory • WHITE BLOOD CELL TYPES IN ADAPTIVE IMMUNITY – B cells (arise and mature in red bone marrow), and T cells (arise in red bone marrow and mature in thymus) • ADAPTIVE IMMUNITY DIVISIONS– Lymphatic system (physical parts of adaptive immune system), Antigens (molecules that trigger adaptive immune response), antibodies, and chemical signs • LYMPH FLOW VS BLOOD FLOW o Lymph – organs are red bone marrow, thymus, nodes, spleen, tonsils and MALT. One-‐way system that takes lymph to concentration of lymphocytes o Blood – more circulatory, brings nutrients through vessels and removes wastes • RED BONE MARROW – primary lymphoid organ. Origin of both B and T cells. B cells mature in this marrow • THYMUS – primary lymphoid organ. Where T cells mature • LYMPH NODES – filter lymph • SPLEEN – filters blood and removes harmful substances from the blood • TONSILS – secondary lymphoid organ • MALT – contains most of the body’s lymphocytes. Parts include appendix, vagina, bladder, mammary glands, and Peyer’s patches in small intestine • ANTIGENS – recognized as foreign. Stimulates attack. 3D shape, epitope, is the antigenic determinant, or what is recognized as not self. Complex molecules are more easily recognized as foreign, so they are better antigens 5 • EXOGENOUS ANTIGEN – part of a microbe that had not invaded a cell before being presented on the cell exterior. Many of these are bacterial. Viruses can be exo or endo • ENDOGENOUS ANTIGEN – part of a microbe that was inside the cell before being presented on the cell exterior • AUTOANTIGEN – markers on our own cells that help the body identify itself • THYMUS & T CELLS – T cells mature under the Thymus’s influence. The T cell is mature after 500,000ish copies of a T-‐cell receptor (TCR) has been replicated and imbedded in the membrane of the individual cell • T CELL RECEPTORS – each T cell has a different shaped TCR. They only recognize a certain epitope, and only epitopes on an MHC presenting protein • MHC I – found in all cells’ membranes except red blood cells because they don’t have nucleus. These present endogenous antigens • MHC II – found in antigen presenting cells, so only cells that are able to ‘hunt’ a microbe, digest it, and present the pieces. These present exogenous antigens • TYPES OF T CELLS o Cytotoxic T Lymphocyte – kills infected or abnormal cells o Helper T Lymphocyte – helps regulate B cell activity and cytotoxic T cells by providing necessary signals and growth factors (Th1 with T cells, Th2 with B) o Regulatory T Lymphocyte – represses adaptive immune response to prevent autoimmune action • CLONAL DELETION – this helps avoid immune action against the self. In their ‘training,’ the B and T cells are exposed to autoantigens, and the ones that react are destroyed. That way, the only cells left are the ones that will react with foreign things, not self • B CELL SPECIFICTY – each B cell’s receptors are unique to that cell. Every B cell has 500,00 of the same receptor on it, but there are at least 10 different B cells in your body, all with a different specific BCR • IMMUNOGLOBULIN MOLECULE – act against the epitope that ‘fit’ into the B cell • 5 ANTIBODY CLASSES -‐ IgM, IgG, IgA, IgE, IgD • IMMUNE SYSTEM CYTOKINES – soluble proteins that are intercellular messages 6 • TYPES OF ACQUIRED IMMUNITY o Naturally Acquired Active Immunity – body responds to antigens that it acquired organically, like when a kid gets chicken pox from another kid at school o Naturally Acquired Passive Immunity-‐ antibodies are transferred from mother to offspring through the placenta or breastfeeding o Artificially Acquired Active Immunity – a vaccine containing antigens for the body to respond to itself o Artificially Acquired Passive Immunity – a vaccine containing antibodies for the body to acquire and put into practice when the time comes MAKE SURE TO LOOK AT THAT CHART SHE EMAILED US WITH THE ABOVE CHAPTER Email me if you need it, and I will try my best to get it to you in a timely manner email@example.com CHAPTER 17 • VACCINATION HISTORY – in response to smallpox epidemics, 12 century Chinese variolation, Edward Jenner created vaccination. Nobody knew how or why, just that these worked. By late 1900s, vaccines led to eradication of smallpox. Hopeful future for worldwide eradication of polio, measles, mumps, and rubella • VACCINE TYPES – Attenuated, Inactivated, Toxoid, Combination, Recombinant Gene • VACCINES IN CONTACT IMMUNITY – being vaccinated means you are less likely to become diseased, even in contact with a reservoir or another infected person • VACCINES IN HERD IMMUNITY – by protecting yourself from infection, you are protecting everyone who comes in contact with you from becoming infected • ACTIVE IMMUNIZATION – giving patient antigens for their immune system to learn how to deal with so the response will be quicker at a ‘real’ exposure • PASSIVE IMMUNOTHERAPY – giving patient antibodies that are already formed 7