6

Question 1

what are introns

Answer 1

non coding blocks in DNA

Question 2

what are short tandem repeats

Answer 2

within introns short DNA sequences are repeated many times- 2 to 50 base pairs- can be repeated multiple times
The same STRs occur at the same loci on both chromosomes of a homologous pair- no. of times repeated can be different
2 individuals highly unlikely to have same combo of STRs

Question 3

obtaining DNA- DNA smapling

Answer 3

tissue obtained for DNA to be extracyted- fragments of diff lengths made by cutting DNA
tissue sample physically broken down in a buffer solution that includes salts and detergents to disrupt the cel membrane- DNA separated from rest of cell debris by filtering or centrifuging
protease enzymes are incubated with the suspension to remove proteins and then cod ethanol is added to precipitate out the DNA

Question 4

creating fragments

Answer 4

treat DNA with restriction enzymes- cut DNA at specific base sequences

Question 5

polymerase chain reaction

Answer 5

DNA copied numerous of times- replicate specific regions- ampifiedA reaction mixture is set up by mixing the DNA sample, primers (short DNA sequences complementary to the DNA adjacent to the STR)- these are marked by fluorescent tags, free nucleotides and DNA polymerase which is the enzyme involved in creang new DNA strands.The mixture is then heated to 95 degrees to break the hydrogen bonds and to separate the two strands for around 30 secondsThe mixture is then cooled to a temperature between 50-65 degrees depending on the type of primers used, so that they can bind to the strands, this takes around 20 secondsTemperature is increased to about 70 degrees as this is the temperature DNA polymerase works at. DNA polymerase lines up free DNA nucleotides on template strands to create a copy of the sample . The mixture is le for at least one minute for the sample to be amplified. The cycle can then be repeated many mes and gives rise to an amount of DNA sufficient to create a DNA profile.new copies of DNA fragments are formed so one cycle completed- repeated with 4 template strands- number of strands x2 each cycle

Question 6

seperating the fragments - gel electroporesis

Answer 6

1. Fragments of DNA are cut with restricon endonuclease enzymes (either side of satellites).
   load electrophoresis tank using a micropipette w/ DNA fragments of a set value in well at the negative end of agarose gel get covered in buffer solution- maintains optimum ph
2. These fragments are placed in wells in agarose gels and dyed with ethidium bromide so they fluoresce under UV light. A current is then applied to the gel. DNA is negave hence moves towards the anode. Fragments of different sizes move at different speeds, according to mass so ‘bands’ appear.
3. A nylon or nitrocellulose filter is placed on top of the plate - the dry, absorbent material draws soluon containing DNA fragments to the filter. The fragments appear as ‘blots’.
4. Gene probes (complementary sequences labeled with fluorescent or radioacve markers) are added and bind with the DNA in a process known as hybridistaion.
5. ‘Blots’ compared and number of satellites visualised. Repeated sequences of DNA in introns are referred to as mini/microsatellites depending on their size. The more closely related two people/species are, the more similar the repeats are

Question 7

uses of DNA profiling

Answer 7

since DNA is inherited, similarities will be present on DNA of reatives- used to avoid inbreddin, identify relatiobns and identify DNA

Question 8

body temp- time of death

Answer 8

human core body temp approx 37
when person dies body starts to cool due to absence of heat prosuing exothermic chem reactions such as respiration
used to estimate death during 1st 24 hours post mortem
meaused through rectum or abdomina stab
cooling of body foowa aigmoid curve
initial temp plateau normally lasts 30-60 mins
dependent on- body size, position, clothing, air movement, humidity, temp of surroundings

Question 9

rigor mortis

Answer 9

after death muscle cells become deprived of o2 and o2 dependent reactions stop. Respiration in the cells becomes anaerobic and produces lactic acid. The pH of cells falls inhibiting enzymes and thus inhibiting anaerobic respiration. muscles begin to siffen as ATP is used up, calcium ions build up in the muscle cells and they become fixed in a state of contraction. Proteins can non longer move over one another to shorten the muscle-fixing muscle and joints. This is called rigor mortis, and the extent of rigor mortis can be used to determine time of death. completed at around 6-9hours after death, the siffness only lasts around 36 hours, so limited in use in determining time of death.
passes off as muscle tissue starts to breakdown

Question 10

decompisition

Answer 10

tissues start to breakdown due to actions of enzymes- auotlysis- body’s own enzymes from digestive tract and ysosomes breakdown cells, bacteria from gut and gaseous system rapidly invade the tissues after death, reading enzymes that result in decomposition - loss of o2 in tissues favours the growth of anaerobic bacteria
greenish decolouration of skin of lower abdomen- formation of sulfhaemoglobin in the blood- spread across rest of the body- reddish green to purple-black colour
gas or liquid blisters on skin- body swell or becomes boated- co2, methane, etc- as tissues further decompose gas released and body deflates
nornmal temp decolouration occurws 36-72 hours and gas formation after a weka
affected by environmental conditions such as temp- lower temps means lower rate of decompostion

Question 11

micro-organims

Answer 11

act to continue carbon cycle, enzymes secreted by mico-organims to break down dead organic matter, small molecules used for respiration, respiration released co2 and ch4 back into environment

Question 12

forensic etomology

Answer 12

is the study of insects to determine the time of death. Each species of insects has a specific life cycle. Determining the age of insects present enables theti me of death to be determined
records location and conditions of body- take smaplles of any insects near or on or under body
temp of air, body, ground and maggot mass are recorded
flies appear after a few hours, other insects colonies later, tod also determiemned by stage of ife cycle insects are in

Question 13

succession of the corpse

Answer 13

as the body decays, the species colonising the body change. Therefore, analysis of the community of species present can be used to determine time of death.immediately after death body suitable for bacteriaas tissues decompose, conditions most suitable for flies and larvaeas larvae feed conditions become suitable for beetles as body dries arvae leave and beetles decompose dry tissueswhen tissue gone conditions are not suitable for most organisms affected by location, seaons, weather, size of body

Question 14

viruses

Answer 14

consist of a strand of nucleic acid (DNA or RNA) enclosed with a protein coat- viral DNA can be single or double stranded
lack some internal structures required for growth and reproduction- have to enter the cells of organisms they infect and use the host’s metabolic system, to make more viruses
when a hijack of host cell occurs , the biochem is disrupted, after reproducing inside the host cell, new virus particles may bud fro, the cell surface or burst out the cell- lysis- may cause enzymes of other chemo released to damage neighbouring cells- causes the disease symptoms produced by the virus infection
no plasma membrane, cytoplasm or ribosomes- use mechanisms in host cell for protein synthesis
some viruses have an envelope taken from the host’s cell surface membrane-lipids and proteins
viral envelope also has glycoproteins from virus itself- antigens
envelope helps virus attach to cell and penetrate surface membrane
protei coat around rna/dna called capsia
some carry protein in capsid

Question 15

purpose of DNA primers

Answer 15

specific base sequence
bind to complementary bases of the DNA being amplified
therefore provide a site for DNA polymerase to bind

Question 16

why fragments may be at different positions

Answer 16

the base sequence of the alleles are different
the dan restriction enzymes cuts at a specific site/base sequence- this sequence would be only present in one of the alleles- different in each
this would produce different sized fragments- diff positions

Question 17

investigation to determine the optimum no. of cycle for per to take place

Answer 17

sample of DNA, primers, free nucleotides and DNA polymerase95 degrees to break hydrogen bonds55 degrees to allow primers to bond to either ends of the dna70 degrees for free nucleotides to bond to DNA- DNA polymeraserepeat but change the no. of cyclesuse gel electrophoresis to see quantity of DNA produced choose smallest no. of cycle that produces an observable band

Question 18

how to study forensic entomology

Answer 18

standardisation of body- e.g pig- same size, breed, mass, age, sex
control environmental factors- temperature monitored as effects type of insects
record the presence of different species of insect hourly

Question 19

changes in body after 1 week death

Answer 19

body temp falls- room temp
rigor mortis
breakdown of cells by enzymes in body- autolysis
Putrefaction, discolouration, bloating

Question 20

effects of temperature on decomposition

Answer 20

increase in temperature increases the rate of decomposition
increases enzyme activity- more kinetic energy- increased frequency of collisions between enzyme and substrate
increase in temperature increases growth rate of decomposers

Question 21

why increasing temp within dead body benefits

Answer 21

increases enzyme activity for larvae
high temp denatures enzymes of other species
this increases food availability by reducing competion
increases decomposition

Question 22

decomposition of plants

Answer 22

decomposers- fungi/bacteria- release enzymes
monomers/glucose/amino acids in plants- soluble and dissolve
some soluble molecules soak into the ground and taken up by other organisms nims like worms
glucose used for respiration by decomposers- releases co2
water loss

Question 23

how are dan profiles compared

Answer 23

total no. of bands
position of bands
size/width of bands

Question 24

b. chem defences- non specific

Answer 24

lysozyme- enzymes that breakdown granum-prositive cell walls- found in naval secretions
sebum-oily substance from sebaceous glands that forms a protective layer over skin- contains unsaturated fatty acids which inhibit growth of certain phagogenic bacteria and fungi
ph low- skin ph 3-5 cuased by lactic acid and fatty acid
perspiration- produced by sweat glands- contains lyzozymes and acids

Question 25

antigens

Answer 25

any molecule the body recognisesas not being of its self cell surfacemolecules made up of glycoproteins+lipids capable of triggering an immune repsonse

Question 26

inflammation

Answer 26

helps to destroyinvading microbes- triggered by tissue damage- if destruction is not possible, to limit effects by confining the pathogens and its products + repair and replace damage of pathogensvasodilation of arterioles triggered by chems released by damaged cells: histamine, kinins, prostaglandins and leukotrieneshistamine also causes permeability of capillaries to increasephagocyte migration and margination: margination is the process in which phagocytes stick to lining of BV. Diapedeses (emigration): phagocyte squeeze between endothelia cells of bv and enter surrounding tissue- causing swellingphagocytes are attracted to site of infection through chemotaxisphagocytes destroy microbes, as well as dead and damaged host cellstissue repair: dead and damaged cells are replaced

Question 27

phagocytosis

Answer 27

chemtaxis: phage them attracted to site of infection- released by bacteria and damaged cellsadherence: phags plasma membrane attaches to surface of pathogen or foreign materials- can be inhibited by capsules or M proteinOpsonisation- coating process with opsonins that facilitates attraction opsonins includes antibodies and complement proteiningestion: plasma membrane of phagocytes extends projections (pseudopods) which engulf the microbe- microbe engulfed in a sac called phagosomedigestion: inside the cell- phagosome fuses with lysomosme to form phagosome lysosomal enzymes kill most bacteria within 30 mins and includelysosomes- destroy cell wall peptidoglycan lipase and protease RNAses and DNAdesafter digestion, residual body with indigestible materials is discharged

Question 28

what is phagocytosis carried out by

Answer 28

neutrophils- predominate early in the infectionwandering macrophages- originate from monocytes that leave blood and enter infected tissue and develop into phagocyte cells- leave BV through gaps in endothelia cellsfixed macrophages- located in liver, nervous system, lungs, lymph nodes, bone marrow and serval other tissues

Question 29

antimicrobial protiens

Answer 29

most non specfic defences are aimed at invading bacteria interferon- aginst viruses, some bacteria and protozoamicrobe infected cells produce this protein and it diffuses to the surrounding cells where it prevents the microbes from multiplyig inhibits microbe protein synthesis limits the formation of new microbe particles

Question 30

symptoms of TB

Answer 30

initial infection consists of fever , general weakness , a severe coughing progression leads to lung damage , causing respiratory failure if untreated can also spread to other parts of the body , e-g- brain ✗ Kidneys to cause organ failure if untreated, it may lead to death

Question 31

evasion mechanisms

Answer 31

during phagocytosis immune response , bacteria produces substances preventing lysosome fusion w/ phagocytic vacuole , so bacteria aren't broken down I can multiply undetected in phagocytes disrupt antigen presentation in certs so they are never marked as infected . so immune system never recognises or kills infected phagocytes .

Question 32

B cells

Answer 32

B lymphocytes produced in bone marrow each B cells one specific type of antigen receptor on its surface- activated when its receptor binds to an antigen with complementary shape- multiply to form a large clone of effector cells which differentiate into plasma cells or memory cells which secrete antibodies b effector cells once activated B cells secrete antibodies - bind to the antigens on the microbe cell surface membrane- acts as labels allowing phagocytes to recognise and destroy cells each antigen on microbe will bind and activate diff B cells

Question 33

antibodies

Answer 33

4 polypeptide chains (2 heavy 2 light) with a variable & constant region variable regions form antigen binding sites (complementary to a particular antibody) and differ between antibodies hinge region allows flexibility whilst antibody binds constant regions allow binding to receptors on immune system cells e-g. phagocytes & is the same in all antibodies disulfide bridges hold polypeptide chain together

Question 34

antibodies purpose

Answer 34

1 . Agglutinating pathogens is the process of binding 2 pathogens at the same time so that they clump ↳ allows phagocytes to bind to large clumps a phagocytose many pathogens at the same time 2 .Neutralising toxins : antibodies may bind to toxins produced by pathogens to prevent toxins affecting human cells (neutralisation) before toxin antibody complex is phagocytosed 3- Preventing pathogen binding : antibodies block pathogen cell surface receptors to prevent binding to host cells , so pathogen cannot bind to or infect host cells

Question 35

cloning B cells

Answer 35

Complementary receptors on the surface of B cells bind to non-self antigens and become antigen presenting cells (APC) in the same way macrophages do. Antigen presenting b cells bind with active, cloned T helper cells that are presenting the same antigen. Once attached the T helper cells release chemo called cytokines which stimulate division and differentiation of the B cells produce B effector cells and B memory cells

Question 36

T helper cells

Answer 36

mature in thymus gland one specific type of antigen on their surface- only binds to one complementary antigen when activated stimulate the B cells to divide and become cells capable of producing antibodies when a piece of biological material is engulfed by a macrophage, protein fragments from the material become attached to proteins in the cells- added to macrophages cells surface membrane- non self antigens alert immune system of foreign antigens in body- APCs Helper cell with complementary receptors, CD4, bind to surface of antigen printing cell, once activated divide to produce clone of active T HELPER cell and a clone of Memory cell

Question 37

T killer cells

Answer 37

if a pathogen infects a body cell, a fragment of the antigen is presented on the cell surface membrane- T killer cells with complementary receptors bind to antigen presenting body cell- divide to form active clone- stimulated by cytokines from T helper cells T killer cells release enzymes that create pores in the membrane of infected cells - enables ions and water to flow into infected cell which swells and burns the cell- lysis- pathogens within cell released- once out of cell can be labelled by antibodies from b cells as targets for destruction by macrophages

Question 38

secondary immune response

Answer 38

immune system responds much faster- involves memory cells - Bm can differentiate immediately tp produce plasma cells and release antibodies- Greta production of antibodies and response last longer

Question 39

TB

Answer 39

unsanitary conditions linked to poverty and cramped living conditions help spread of infection bacterial infection- mycobacterium tuberculosis - infection- spread through air- droplets inhaled into the lungs and taken up by phagocytes- initiates phagocytosis whilst preventing enzymes that destroy bacteria- stays in phagosome ↳ infected phagocytes are sealed in tubercles by immune system , so bacteria become dormant and infected person shows no obvious symptoms dormant bacteria eventually become reactivated & overcome immune system, which is more likely in people w/ weakened immune system, e-g. AIDS sufferers

Question 40

primary stage

Answer 40

causes an inflammatory response - macrophages engulf bacteria- mass of tissue known as a granuloma forms- in TB. these tissue masses are anaerobic and have dead bacteria and macrophages in the middle- called tubercles

Question 41

bacteria invades immune system

Answer 41

bacteria taken up by phagocytes but once inside resit killing mechanisms bacteria have thick waxy cell walls, making them v difficult to breakdown-can lie dormant for years- remain within tubercules no signs or symptoms as immune system controls infection survive and breed in macrophages- can suppress T cells

Question 42

Active Tb

Answer 42

if immune system cannot contain the disease when it 1st arrives in lungs- too great a no. of bacteria reasons for lowered activity of immune systemold age or too youngmalnutrition and poor living conditions AIDS

Question 43

respiratory TB

Answer 43

bacteria multiply rapidly in the lungs destroy lung tissue create holes or cavities reduces SA, decreasing rate of gas exchange- cells starve from o2 and build up. of co2

Question 44

role of fever

Answer 44

inflammatory response- fever causing subs released from neutrophils and macrophages- chemo affect hypothalamus and alter the set point for core body temp to a higher temp enhances immune function and phagocytosis bacteria and viruses may reproduce more slowly in high temperatures- TB stop reproducing at temps above 42 however above 40 enzymes increasingly denatured

Question 45

glandular TB

Answer 45

bones, lymph nodes and central nervous system symptoms include enlarged lymph glands

Question 46

skin and blood tests

Answer 46

small amount of tuberculin injected under the skin and forearm ps= inflamed area of skin - tb antigens present false neg if person has latent tb false pos if had vaccine

Question 47

identification of bacteria

Answer 47

sample of sputum coughed up by patient is taken and cultured

Question 48

chest xray

Answer 48

to discover extent of damage and disease in lungs

Question 49

HIV

Answer 49

infection occurs when comes in contact of mucosal surfaces replicate inside T helper cellsattachment protein attaches to receptor molecule on the cell membrane of a T helper cell- gp120 (HIV) onto CD4 receptorsenvelope surrounding virus fuses with T helper cell membrane, enabling RNA of virus to enetr cellcapsid is released into cell where it uncoats to release genetic material reverse transcriptase is used to make a complementary strand of DNA from viral RNA templatedouble strand is made & integrated to human DNA by integrase host cell enzymes are used to make viral proteins from viral DNA from human DNA viral proteins are assembled into new viruses , which bud from the cell to infect others

Question 50

HIV to AIDS

Answer 50

Deteriorating and eventually fails immune system -classed as AIDS when symptoms of immune system failure appear , or T helper cell count drops. sufferers may develop opportunistic infections, where normally weak infections have a serious effect on an immune system infected with HIV initial symptoms include minor infections of mucous membranes , e.g- ears , nose ✗ genitals) and recurring respiratory infections , caused by a decreased T helper cell count ↳ progression of AIDS causes further drop of T helper cell count , leaving patients vulnerable to more serious infections, e-g. chronic diarrhoea ,bacterial infections, & TB in later stages , patients have very few T helper cells & suffer from a range of serious infections, e. g- brain toxoplasmosis & respiratory system candidiasis , which may kill them. -Survival time with AIDS varies depending on existing infections , strain of HIV , & healthcare

Question 51

Evasion mechs

Answer 51

° Kills immune system it infects , reducing overall no . of immune system cells in body. further reducing the chance of detection / triggering of immune response ◦high rate of mutation in genes coding for antigen proteins, forming new strains (antigenic variation) . so memory cells will no longer recognise the strain with a different antigen , so a immune response response must occur with each new strain , increasing cell infection rate °disrupts antigen presentation in infected cells , so APC cannot be formed a immune system cannot recognise a kill infected cells.

Question 52

HIV structure

Question 53

acute phase

Answer 53

HIV antibodies appear in the blood after 3-12 weeksinfect person may experience symptoms such as a fever, sweats headache, sore throat and swollen lymph nodesrapid replication of virus and loss of T helper cells after a few weeks, infected T helper cells are recognised by T killer cells, which start to destroy them- reduces the rate of virus replication but does not eliminate it

Question 54

chronic phase

Answer 54

virus continues to reproduce, but the no. are kept in check by the immune systemmay be no symptoms during this phase, but there can be an increasing tendency to suffer colds or infections which are slow to go away dormant diseases like TB and shingles can reactivate can last for many years- 20 or more

Question 55

disease phase

Answer 55

increased no. of viruses in circulation and declining no. of T helper cells indicates the onset of AIDS- decrease in the no. of T helper cells leaves the immune system vulnerable to other diseasesopportunistic infections- include AIDS and pneumonia

Question 56

skin

Answer 56

keratin in outer layer effective in stopping the entry of microorganismsskin flora- microbes- live on skin surface- harmless and prevent colonisation by other bacteria- well adapted to environment ton skin- other bacteria not suited to salty conditions so are outcompeted in their nicheee

Question 57

mucous membranes

Answer 57

line airways and gut providing easier routes into body- posit conditions favourable for bacteria growth- mucus secretion from goblets traps microbes and other particles and the carried up the throat where it is swallowed

Question 58

stomach acid

Answer 58

ph less than 2- kills bacteria

Question 59

gut flora

Answer 59

out compete pathogens in the gut for food

Question 60

active immunity

Answer 60

production of antibodies long term protection , but takes time to develop Natural : immunity obtained after catching a disease Artificial: immunity obtained after vaccination w/ harmless dose of antigens

Question 61

passive immunity

Answer 61

immunity gained from being given antibodies produced by a diff. Organism so you never produce any Short term but immediate protection Natural : baby becomes immune from antibodies mother through placenta/breast milk Artificial : immunity gained after injection W antibodies

Question 62

gaining immunity

Answer 62

-initial primary response (nonspecific then specific) is slow due to lack of B cells available to form antigen specific antibodyafter production of sufficient antibodies , infection is overcome after exposure T ✗ B certs produce memory cells which remain in the body↳ T memory cell remember the specific antigen and will recognises it it exposure occurs again↳ B memory cells remember specific antibodies needed to bind to the antigenpresence of B/ T memory cells give immunity as body can respond quickly to a 2nd infection, so it same pathogen reinfect , the body produces a quicker a stronger 2° immune response↳ T memory cells divide into helper / killer cells & B memory cells divide into plasma certs to produce antibody

Question 63

what's in vaccination

Answer 63

attenuated viruskilled bacteriatoxin altered to be harmlessfragment of antigen bearing pathogen

Question 64

vaccination

Answer 64

as B cells divide during infection , person suffers from diseasevaccines have only antigens without pathogen , so memory cells can be produced w/o getting symptomsvaccines may contain various antigens to protect against different strains (antigenic variation)vaccines may also contain mRNA coding for antigens ot pathogen , providing instruction for antigen or stimulating an immune response and creating an immunity

Question 65

1 and 2 immune response

Answer 65

- 1 response occurs slowly as immune response finds correct antigen ( 1st slow bump) -After 10 response T memory cells remain and store antigen needed , B memory cells store antibody needed -At 2nd infection , 2° response occurs a memory cells are activated quickly (larger and quicker bump ) -B memory cells differentiate into plasma cells , & fight off infection much quicker

Question 66

reverse transcriptase inhibitors

Answer 66

prevent viral RNA from making DNA for integration into host's genome

Question 67

protease inhibitors

Answer 67

inhibit protease that catalyses the cutting of larger proteins into small polypeptides for use of contraction of new viruses

Question 68

antibiotics

Answer 68

bactericidal- antibiotics that destroy bacteria bacteriostatic antibiotics prevent the multiplication of bacteria - host immune system destroys bacteria inhibit bacteria CELL WALL synthesis- weak wall formation leading to lysisdisruption of cell membrane, causing changes in permeability that lead to cell lysisinhibition of nucleic acid synthesis, replication and transcription- prevents cell division and/or synthesis of enzymesinhibition of protein synthesis inhibition of specific enzymes found in bacteria cell

Question 69

conjugation

Answer 69

plasmid carrying gene for antibiotic resistance transfers one if its strand between bacteria

Question 70

why bacteria become resistance

Answer 70

reproduce quciklylarge populationsgene mutations- enzymes thatch destroy bacteria or resistant

Question 71

healthcare associated infections (HCAIs)

Answer 71

infections caught when a patient is at hospital, transmitted by poor hygiene - not washing hands, lack of disinfectant + unconfined cough, occurs in hospital due to weakened immune system

Question 72

prevention of HCAIs

Answer 72

antibiotics only used when the patient has defiantly been diagnosed with suffering from a bacterial infectionpatients should complete their treatment even when feeling better, all bacteria destoryedinfection control should be used in hospitals to prevent spreading of bacteria rotate the use of different antibiotics

Question 73

infection control practices by doctors

Answer 73

hand washing stations doctors not to wear ties/long sleaves testing patients for the presence of antibiotic resistant bacteria before admission isolation of infected paitents disinfectant of beds and stations- washing of beds

Question 74

bactericidal

Answer 74

destroys bacteria

Question 75

bacteriostatic

Answer 75

prevents multiplication of bacteria, host's immune system will destroy bacteria

Question 76

combat antimicrobial resistance

Answer 76

speedy development of new antibioticstrack resistance data nationwiderestrict antimicrobial usedirect observed dosinguse of narrow spectrum antibiotics use of antimicrobial cocktails

Question 77

classifying on basis of mechanism of action

Answer 77

cell wall synthesis inhibitors DNA synthesis inhibitors RNA synthesis inhibitors protein synthesis inhibitors mycolic acid synthesis inhibitors tolic acid synthesis inhibitors

Question 78

classifying on basis of spectrum of activity

Answer 78

broad spectrum antibioticsshort spectrum antibiotics

Question 79

classifying on basis of mode of action

Answer 79

bactericidalbacteriostatic

Question 80

how destruction of T helper cells causes symptoms of AIDs

Answer 80

reduced production of cytokine which stimulates the differentiation of B cells. effector B cells produce antibodies, without them there will be a reduction in antibodies. This increases the risk of opportunistic infections as antibodies aid in the process of phagocytosis

Question 81

flora on skin and gut prevention of pathogenic multiplication

Answer 81

better adapted to the conditionsoutcompete pathogens bacteria in gut secrete chems which help destroy pathogens

Question 82

role of interferon

Answer 82

protein that inhibits viral replication inside cells, the greater amount of interferon the fewer virus particles produced produced by infected cells

Question 83

differences in DNA of bacteria and viruses

Answer 83

bacteria have DNA whilst viruses have DNA or RNA bacteria have circular genetic material whilst viruses have linearbacteria have plasmids whilst viruses do not

Question 84

characteristics of an antibody

Answer 84

glycoprotein 4 polypeptide chains- disulphide bridge antigen binding site antibodies have a similar constant regionproduced by plasma cells opsonization, lysis, immobilization, agglutination

Question 85

why people wont know if they have HIV

Answer 85

does not always produce symptoms provirus latency/ virus is dormant tests needed to detect HIV, those would not test if they didn't have symptoms or suspect they have HIV symptoms common to other diseases

Question 86

bacterial resistance

Answer 86

• Use of antibiotics is a selection pressure allowing evolution of antibiotic-resistance • Antibiotics kill/stop growth of all non-resistant bacteria • Only bacteria with a mechanism of resistance will survive and reproduce • Examples of mechanisms which have evolved – destruction of antibiotic/ decrease antibiotic uptake/ activation of transport mechanism/ modification of target site • Bacteria have single DNA molecule so any mutation is expressed • Conjugation/ exchange of plasmids allows mutations to pass between bacteria • Each antibiotic has a specific target in the bacterial cell, so resistant mechanism specific for that bacteria and that antibiotic • Discussion of hospital practices to reduce development of resistance and why they are effective – hygiene / screening and isolation of patients / management of antibiotic use

Question 87

how to prevent HAICs

Answer 87

hand wash (stations) (1) • (doctors / nurses) not to wear { ties / watches / long sleeves } (1) • testing patients for the presence of antibiotic resistant bacteria before admission / {isolation / quarantine} of infected patients (1) • increased washing of bedding / disinfection of { beds / surfaces } (1) ALLOW antibacterial / antiseptic /alcohol gel / hand sanitisers

Question 88

why TB not destroyed by immune system

Answer 88

• the bacteria are inside {macrophages /phagocytes} (1) • this bacterium has a (thick) waxy cell wall (1) • lysosomes cannot fuse with phagocytic vacuole /bacteria not destroyed by enzymes (1) • bacteria within tubercles (cannot be destroyed) (1)

Question 89

clinical trials vaccine

Answer 89

• (small groups of) healthy volunteers are given the vaccine to test for side effects (1) • (healthy volunteers) tested for presence of antibodies to the virus (following vaccination) (1) • a group of people at risk of contracting the disease is given the vaccine (1) • the number of people who develop the viral disease (following vaccination) are monitored (1)

Question 90

chi square test

Answer 90

determines whether there is a significant difference between the observed and expected results in an experiment It is important to formulate a null hypothesis - this states that there is no significant difference between the observed and expected results The critical value is read from a table of critical values and depends on the probability level used and the degrees of freedom-Biologists generally use a probability level of 0.05 or 5 % degrees of freedom = number of classes - 1

Question 91

t tests (unpaird)

Answer 91

The unpaired t-test (or just t-test, and also known as the Student’s t-test) tests for differences between two sets of independent data. The unpaired t-test tests the null hypothesis that there is no difference between the means of the two sets Calculate the degrees of freedom: dof = (n1 – 1) + (n2 – 1)

Question 92

null hypothesis

Answer 92

A hypothesis which states that there is no significant difference between two sets of data, and any difference observed is due to chance. no difference from test group and control groups if you're testing the effect of light intensity on photosynthesis rate: Null hypothesis: "Light intensity has no effect on the rate of photosynthesis." If you're testing two groups, like antibiotic effectiveness: Null hypothesis: "There is no significant difference in the zones of inhibition produced by antibiotic A and antibiotic B."

Question 93

paired t test

Answer 93

In some experimental designs the data are matched, or paired. This can happen when we look at the same locations at different times, or in a “before and after” experiment. In this case we can use a more powerful version of the t-test called the paired t-test, which looks at the differences between each pair. The paired t-test tests the null hypothesis that the mean of the paired differences is zero, in other words that there is no difference between the two groups. Note that this is a different test from the unpaired t-test, so it has a slightly different null hypothesis.- The mean of the paired differences is zero calcuate differences and then claculate mean of those differences

Question 94

correlation coefficent

Answer 94

Sometimes we are looking for a correlation between two sets of numeric data (e.g. if this goes up does that go up?). The Spearman rank correlation coefficient (rs) gives the strength of a correlation, on a scale of –1 to +1 –1 is a perfect negative correlation (as x goes up y goes down)  +1 is a perfect positive correlation (as x goes up y goes up)  0 is no correlation at all The Spearman rank correlation coefficient tests the null hypothesis that there is no correlation between the two sets We rank the data in the first column (fathers’ heights), writing the ranks in a new column. We start with the biggest value (so 1.80m is ranked 1) and then the second biggest and so on. There is a tie for the next tallest height (1.77m), so we give them both the mean of their ranks (2.5 instead of 2 and 3). The next rank is 4. There is a tie for the shortest height too We rank the data in the second column (sons’ heights) in exactly the same way, writing the ranks in a new column. We can rank the data in either direction (highest to lowest or lowest to highest), so long as we do the same for both columns For each row we then calculate the difference in each of the paired ranks and square it, writing that value in a new column We add up the squared differences (sum of D 2) in this column and write the sum at thebottom of the column. 7. We can now put all the values into the formula to calculate rs: if probability less then the 0.05 value reject the null hypotesis

Question 95

standard deviation

Answer 95

The standard deviation (s) measures the dispersion of the raw data around the mean. The standard deviation is calculated from all the replicate data, so is more representative than the range. The larger the standard deviation the larger the spread of the data about the mean, so the less reliable the sample mean.

Question 96

how infflamation and immune res[onse cause damge to tissues

Answer 96

{chemical mediators / histamine} released (1) increasing blood flow / increasing capillary permeability / causing oedema (1) {increasing number of / activating / recruiting} white blood cells (in the area of inflammation) (1) (stimulating) the release of (catabolic) enzymes / increasing phagocytosis (of damaged tissue) (1)

Question 97

how evasion mechanisms help pathens become drug resistant

Answer 97

(accumulation of) mutations resulting in change in target recognised by host (1) transfer of genetic material coding for resistance genes (1)- transfer of plasmids

Question 98

skin flora

Answer 98

(skin flora) {prevents /reduces } colonisation by other microbes (1)  make environment hostile for other microbes (1)  outcompetes other microbes

Question 99

similarities + doffernecex of HIV and bacteria

Answer 99

Similarities  both contain { genetic material / RNA } (1)  both have a phospholipid bilayer (1) Differences  (only) bacteria have { cytoplasm / ribosomes / pili / slime capsule / flagellum /cell wall / cell membrane / plasmid } (1)  (only) HIV has { capsid / protein coat / GP 120 } (1)

Question 100

how inhibiting enzymes prevents hiv infection

Answer 100

1. idea that drugs would prevent viral replication ; 2. idea that T (helper) {cells / lymphocytes} will not be { killed / burst / destroyed}(by virus particles leaving cell) ; 3. idea of {inhibition / eq} of reverse transcriptase ; 4. idea that (viral) DNA could not be made; 5. from the (viral) RNA ; 6. idea of {inhibition / eq} of integrase ; 7. idea that (viral) DNA cannot integrate into (host) {DNA / genome} / eq ;

Question 101

how bacteria in food may not cause infection

Answer 101

reference to enzymes {killing / destroying / eq} (microorganisms) ;- enzymes in slava 2. reference to {stomach acid / hydrochloric acid / HCl} {killing / destroying / eq} (microorganisms) ; 3. reference to lack of oxygen affecting (microorganisms) ; 4. idea of competition by gut flora with (microorganisms) ; 5. idea that insufficient numbers of (microorganisms) (to cause food poisoning) ; 6. idea that the (microorganisms) may not be {pathogenic/ harmful / cause food poisoning} ; 7. reference to (immediate) vomiting to remove (microorganisms)

Question 102

how viruses assmeble in host cell

Answer 102

reference to synthesis of RNA ; 2. using host cell {enzymes / named enzyme / (RNA) nucleotides} ; 3. reference to synthesis of (viral) proteins ; 4. using host cell {enzymes / named enzyme / amino acids / ribosomes / tRNA / ATP} ; 5. reference to assembly of {viruses / particles} (inside cells) ;

Question 103

how pollen is not decomposed in peat bogs

Answer 103

the pollen is not breken down due {lack of / very slow} decomposition as there is a lack of {microorganisms / bacteria / fungi / named decomposer} (involved in decomposition) / eq ; meaning there was a lower production of enzymes by decompsoers involved in the process of breaking down organic materials Low levels of decomposers due to low pH conditions which {reduces enzyme activity / kills microorganisms /eq} ; As well as this theri is low oxygen which affects respiration (of microorganisms)- bacteria cannot produce enzymes to breakdown pollen ;

Question 104

hwo b cells become APCS

Answer 104

BCR on b ceels binf to specific antigen internalises itnecalises BCR-antigen complex and then incorporates it into cell mebrane become APC

Question 105

cpac 15

Answer 105

aspetic technices serial dilution to find minimum ihibitory concentrations- adding distilled water to antibiotics Use a sterile pipette or spreader to apply the bacterial suspension evenly across the surface of a sterile nutrient agar plate Flame the forceps until red hot and allow to cool. Use the sterile forceps to pick up an antibiotic disc. Lift the lid of the agar plate just enough to insert the disc. Place the disc firmly but gently onto the surface of the agar. Repeat for each antibiotic, spacing them evenly apart. Seal the lid of the petri dish with two strips of sellotape (do not tape all the way around — this prevents anaerobic conditions). Label the base of the plate with the name of each antibiotic next to its position. Incubate the plate upside down at 30°C for 24 hours.