Topic 6 Flashcards

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1
Q

time of death of a mammal can be determined by.. extent of …

A

Extent of decomposition- standard pattern of decay-enzymes of the gut break down the wall of th gut and then the surrounding area. As cells die, they release enzymes which break down tissues; the discolouration of the skin, gas formation combined with information surrounding environmental conditions allow the time of death to be estimated.

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2
Q

the time of death of a mammal can be determined by .. forensic…

A

Forensic entomology- study of insects to determine time of death. Study the age of insect larvae on the body allows the time the eggs were laid to be determined; an estimate of time of death can be made; there is a succession of species of insects on the body; the species present when the body is found allows the stage of succession to be determined. The type of species can help identify the location of death.

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3
Q

the time of death of a mammal can be determined by… body …

A

temperature. The body temp decreases after death (as exothermic metabolic reactions stop). Only in the first 24 hours, until body reached the temp of the surroundings. This will also depend on the sixze of the body, covering (e.g. clothes) and weather conditions.

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4
Q

time of death os a mammal can be determined by … extent of ..

A

Muscle contraction or rigor mortis. After death, muscles stiffen and become fixed within 6-9 hours of death because ATP is used up, calcium ions build up in muscle cells and are unable to recover to relaxed position. This wears off after 36 hours (as enzymes destroy muscle tissue)

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5
Q

decomposition allows nutrients to be…

A

recycled

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6
Q

microorganisms are crucial to …

A

decomposition.

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7
Q

introns are ..

A

non-coding regions of DNA

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8
Q

exons..

A

are coding regions of DNA

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9
Q

The introns consist of many repeating base sequences known as … in sections known as …

A

short-tandem repeats in sections known as satellites.

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10
Q

the polymerase chain reaction:

A

allows tiny samples of DNA to be amplified so that they can be used in DNA profiling.

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11
Q

what is required for PCR:

A
  • DNA primers, which are short sequences of DNA complementary to the DNA adjacent to the STR.
  • DNA sample
  • free nucleotides
  • DNA polymerase
  • A cycle of temperature changes results in huge numbers of the DNA fragments being produced.
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12
Q

steps for PCR:

A
  1. 90-95 degrees C for 30 seconds- DNA strand seperates
  2. 50-60 degrees C for 20 seconds- primers bind to DNA strands
  3. 72 degrees C for at least a minute- DNA polymerase builds up complementary strands of DNA
  4. Steps 1-3 are repeated 20-40 times
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13
Q

DNA is slightly …. charged, therefore, moves towarsds the …

A

negatively, anode.

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14
Q

gel electrophoresis:

A
  • seperates DNA fragments of different lengths.
  • In this process, the DNA is cut into fragments with restriction endonucleases.
  • the result is an electrophotogram which is a DNA profile
  • the technique is used to look at how closely related individual plants and animals are, and help to determine evolutionary relationships.
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15
Q

process of gel electrophoresis:

A
  1. Double stranded DNA and restriction endonucleases- DNA is cut into fragments
  2. Fragments of double stranded DNA are loaded into the wells of an agrose gel tank and dyed with ethidium bromide so they fluoresce under UV light- The negatively charged DNA moves to towards the positive electrode when a current is applied to the gel.
  3. Fragments of different sizes move at different speeds (smaller ones move faster and further), according to mass, so distanced bands appear.
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16
Q

southern blotting in gel electrophoresis:

A
  1. A nylon or nitrocellulose filter is placed on top of the plate- the dry absorbant material draws solution containing DNA fragments to the filter. The fragments appear as ‘blots’.
  2. Gene probes (complementary single stranded sequences labelled with fluorescent of radioactive markers) are added and bind with the DNA in a process known as hybridisation.
  3. Blots are compared and the number of satellites is visualised.
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17
Q

Differences between bacteria and viruses:

A
  1. bacteria has a cell surface membrane, cytoplasm, cell wall, ribosomes, plasmids and sometimes mesosomes, flagellum and pilli and viruses has no cell wall, membrane, cytoplasm or organelles.
  2. The nucleic acids of viruses are contained in a protein coat and bacteria’s nucleic acids are not.
  3. Bacteria has a circular strand of DNA whereas viruses have linear DNA/RNA
  4. Bacteria can live independently/ are living- viruses require a host living organism and are non-living themselves
  5. Bacteria are a lot bigger
  6. bacteria often have a mucus- based outer capsule whereas viruses may have the puter membrane of host cell surface membrane.
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18
Q
  • Mycobacterium tuberculosis is carried in …
A

droplets when someone coughs or sneezes

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19
Q

what is the main organ affected by TB?

A

the lungs

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20
Q

the first infection may be ….

A

assymptomatic but tubercles form in lungs due to inflammatory response

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21
Q

some bacteria may … inside the tubercles due to their ….. coat. They lie …/…. but can become …. again

A

survive due to their thick waxy coat. They lie dormant/ latent but can become active again.

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22
Q

symptoms of TB:

A

cough, coughing blood, weight loss, appetite loss and fever

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23
Q

in some cases, the bacteria invade … and the ….

A

glands (lymphatic system) and the central nervous system (CNS) leading to death.

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24
Q

HIV is in the ….. and can be transmitted by a …

A

blood, semen, vaginal secretions and can be transmitted by needle sharing, unprotected sex, direct blood/ body fluid transfer through cuts or from mother to foetus.

25
Q

initial symptoms of HIV:

A

fever, headaches, tiredness, swollen glands or sometimes assymptomatic

26
Q

After a 3-12 weeks of having HIV,

A

HIV antibodies appear in the blood, and the patient is now HIV positive.

27
Q

After years of having HIV,

A

the infection leads to AIDS allowing opportunistic infections to be fatal.

28
Q

An example of an opportunistic infection due to HIV…

A
  • HIV destroys T helper cells. This means bacterial cells such as TB are not destroyed by the immune system and so they proliferate and lead to TB.
29
Q

preventing entry of pathogens: the first line of defense.

A
  1. eyes- tears contain the lysozyme enzyme with digests microbes (breaks the peptidoglycan cell wall)
  2. respiritory tract- contains mucus which traps bacteria. The mucus is swallowed and microbes are destrpoyed by the HCl in the stomcach.
  3. gastrointestinal tract- acid in the stomach and gut flora. These compete with pathogens for food and space. Our bacteria also excrete lactic acid which deters pathogens.
  4. Skin and skin flora- pathogens can only enter breaks through the skin. Skin has microbes which out-compete other pathogens. Sebum is an oily fluid which is made by the skin and also kills microbes.
30
Q

non-specific responses- the second line of defense: I…

A

Inflammation- damaged white cells release histamines that cause arterioles to dilate and capillaries to become more permeable; blood flow to the area increases and plasma, white blood cells and antibodies leak out into tissues, where they attack the pathogen (swelling= oedema). Fever- increases temperature so that the rate of our enzyme driven reactions increases but the reproduction rate of the pathogen decreases.

31
Q

non-specific responses- the second line of defense: l…

A

lysozyme action- an enzyme found in tears, sweat and the nose, destroys bacteria by breaking down the bacterial peptidoglycan cell walls

32
Q

non-specific responses- the second line of defense: inter…

A
  • a chemical released from infected cells, which prevents viral replication
33
Q

non-specific responses: the second line of defense: p…

A

Phagocytosis: white blood cells engulf, digest and destroy bacteria and other foreign material. The foreign material is enclosed in a vesicle, into which the cell secretes digestive enzymes from lysosomes, which destroy the bacteria; these phagocytes include neutrophils and monocytes (which become macrophages), these cells are also involves with the specific immune response.

34
Q

specific immunity- the humoral response: T helper activation:

A
  1. Bacterium is engulfed by macrophage.
  2. Antigens are displayed on the surface of the macrophage on MHCs (major histocompatability complexes). The macrophage becomes an APC (antigen presenting cell)
  3. the phagocyte presents the antigen to the T helper cell, where it binds with CD4 receptors (on T-helper cell)
  4. The T-helper cell is activated and divides by mitosis to form t memory cells and active T helper clones
35
Q

specific immunity: the humoral response- effector stage:

A
  1. B cells with a complementary receptor bind to the antigen on a bacterium, becoming an APC
  2. An activated T helper cell eith a complementary receptor protein to the antigens binds to the B cell APC. It produces cytokines
  3. Cytokines stimulate the B cell to divide by mitosis and form B memory cells and B effector cells
  4. B effector cells differentiate and divide by mitosis into plasma cells
  5. Plasma cells synthesise antibodies
36
Q

how do antibodies destroy the pathogen?

A

-agglutination (clumping them together- making it a bigger target to engulf)
- oppsonisation- recognising and targeting pathogens (flagging them)
- lysis
- precipitation (soluble toxins are made insoluble)
- neutralisation (neutralising harmful toxins)

37
Q

The cell mediated response:
when a pathogen invades a host cell…

A
  1. Host displays antigens- APC formed
  2. T-killer cell with complementary receptor proetins binds to APC
  3. Cytokines secreted by active T helper cells stimulate the T killer cell to divide by mitosis
  4. T killer cell divides to form active T killer cells and T memory cells (which remain in the body to provide immunity)
  5. Active T killer cells bind to APCs and secrete granzymes and perforins which cause pores to form in the cell membrane
    6, The infected cell lyses and dies
38
Q

B lymphocytes (B cells) are produced and mature in …

A

the bone marrow.

39
Q

T lymphocytes (T cells) are produced and mature..

A
  • produced in the bone marrow, mature in the thymus gland
  • T killer cells destroy body cells the have foreign proteins on their surface
  • T helper cells stimulate all specific responses.
40
Q

clonal selection in immunity:

A

activation of only the cells that recognise the antigen

41
Q

clonal expansion in immunity:

A

the proliferation of the cells needed so that there are very large numbers

42
Q

one gene can give rise to ..

A

more than one protein through post-transciptional changes to messenger RNA (mRNA)

43
Q

mRNA splicing:

A
  1. the nRNA made in the nucleus is pre-mRNA
  2. Non-coding regions, called introns, are removed by spliceosomes
  3. The coding regions (exons) are then spliced together to form the mRNA
  4. The exons can be spliced in different combinations to give different mRNAs and thus different proteins.
44
Q

antibody structure:

A
  • they have a specific region and a variable region
  • the have di-sulfide bridges that hold the polypeptide chains together.
45
Q

secondary immune response:

A
  • memory cells produced after first exposure to an antigen (the primary response) allow a faster and greater response to the future exposure (secondary response) so fewer symptoms occur.
46
Q

benefits of the secondary immune response:

A
  • much shorter lag period as more of the specific lymphocytes are in circulation
  • more rapid production of effector cells
  • much greater production of antibodies and T killer cells.
47
Q

how is immunity developed: natural and active:

A

normal response to foreign antigen (specific immune response)

48
Q

how is immunity developed: natural and passive

A
  • antibodies cross the placenta to protecxt the baby while its immune system still develops; breast milk, especially colostrum also contains antiboies
49
Q

how is immunity developed: artificial and active

A
  • vaccines use inactive antigens from pathogens in a harmless form to cause a primary response; reinfection will then cause a secondary response
50
Q

how is immunity developed: artificial and passive

A
  • an antiserum contains antibodies, usually from the blood of animals, following exposure to an antigen; injecting these antibodies will neutralise the antigen, but will not provide long term protection.
51
Q

herd immunity:

A

enough people have been vaccinated to make transmission of a disease very unlikely

52
Q

antibiotics are used to

A

fight infection by killing the bacteria and stopping their growth

53
Q

bacteriocidal antibiotics:

A
  • kill bacteria by destroying their cell wall, causing them to burst
54
Q

bacteriostatic antibiotics:

A

inhibit the growth of bacteria by stopping protein synthesis and the production of nucleic acids so that the bacteria doesn’t survive and grow

55
Q

some bacteria can become … to antibiotics as a result of ….

A

resistant to antibiotics as a result of natural selection.

56
Q

The bacteria that are not killed by the antibiotic possess a …

A
  • selective advantage- resistance which enables them to survive and reproduce. Therefore the allel for antibiotic resistance is passed onto their offspring thus creating a resistant strain.
  • Moreover, there is an ongoing evolutionary race between organisms and pathogens as pathogens evolve adaptations which enable them to survive and reproduce
57
Q

Hospitals have developed various ways of controlling the spread of antibiotic resistant infections:

A
  • new patients are screened at arrival, isolated and treated if they are infected to prevent the spread of bacteria between patients
  • antibiotics are only used when needed and their course is completed to ensure that all the bacteria is destroyed, to minimise the selection pressure on bacteria to prevent resistant strains from forming
  • all staff must follow the code of practice which includes strict hygiene regimes such as washing hands which alcohol based antibacterial gels + wearing suitable clothing which minimises the transmission of resistant bacteria (e.g. no jewelry).
58
Q

post -transciptional modification of mRNA: what does it do and how does it work?

A

RNA splicing enables eukaryotes to produce more proteins than they have genes. RNA splicing enables more than one protein to be produced from one gene.
1. a gene is transcribed which results in pre-mRNA (the transcript of a whole gene)
2. All introns and some exons are removed
3. the remaining genes are joined back up by enzyme complexes called splicosomes. The same exons can be joined in a variety of combinations to produce several versions of a mature functional RNA.