• Created by: HASNAAN
  • Created on: 08-06-09 13:41


Found on all humans and unique to each individual. (Even identicle twins)

Ridges on fingers, palms and soles of feat.

Caused by folding of the epidermal layer of the skin.

Vary in length and width and branch.

Join together to form ridges and furrows.

Impressions left by sweat and oils on surface of skin.

Oils screated from sebaceous glands.

None of these glands on palms or fingers but are easily transferred to them.

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Detection of fingerprints.

Visualised using fine aluminium powder. (magnets and magnetic powder also used.)

Ninhydrin used to develope prints on absorbent surfaces.

Reacts with amino acid to produce purple coloured impressions.

Four main types of print...




4) lOOP.

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Dental Records

Dental records are used when person is unidentifiable.

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DNA fingerprinting.

AKA Gentic fingerprinting and dna profiling.

Relies on everyones DNA is unique. (except twins)

Introns. Dna which dows not code for protiens.

Mini satellites - Contains 20-50 base pairs. Can be repeated from 50 to several hundered times.

Micro-satellites - usually contain 2-4 base pairs. Can be repeated between 5 - 15 times.

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How is a DNA fingerprint made.

1) Double stranded DNA cut using restriction enzyme into fragments of double stranded DNA.

2) Fragments seperatd using Gel electropheresis.

3) Blotted onto nylon membrane Use alkali as buffer to separte strands

4) Placed in asealed bag with DNA probe

5) Single srtrandfed Probe binds to comploimentary Fragments sequences.

6) Detected using ...

6.i)X-ray film for radioactive probes.

6.ii)Laser and detector used for flourecent probes.

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Polymerase chain reaction.

1) Cells treated with dtergent to break up cells and release DNA. (DNA aded to test tube)

2) DNA polymerase, DNA primers with flourecen markers and neucleotides added to reaction tube.

3) DNA separates into two strands. (95 'C)

4) DNA polymerases attach.

5) Nucleotides added to extend DNA from primer. (70'C)

6) The satelite and adjacent DNA replicated. (70'C)

7) Primers attach to satelite. (55'C)

8) DNA strands seperate. (95'C)

9) Primer attach to each satellite sequence.

10) DNA ploymerases attach and replication occurs from each primer.

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DNA fingerprinting uses

1) Identification purposes.

2) Setteling paterninty disputes.

3) Looking at variation and evolutionary relationships between organisms.

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Determining the time of death.

Changes occuring after death can be used to determine time of death.

1) Temprature. Useful in identifying time of death in first 24 hiurs.

2) Degree of rigor Mortis.

3) State of decomposition.

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Factors effecting post mortem cooling

1) body size.

2) Body position.

3) Clothing.

4) air movement.

5) Humidity.

6) immersed in water will cool quicker.

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Rigor mortis.


1) After death, muscles become starved of oxygen and oxygen dependent reaction stop.

2) Respiration in cells becomes anaerobic lactic acid produce.

3) pH of cells falls, inhibiting enzymes and thus respiration.

4) ATP needed for muscle contraction no longer produced.

5) Muscles and jointys become fixed.

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Tissues start to break down due to action of enzymes.

enzymes from digestive track and lysosomes break down cell. (AUTOLYSIS).

Bacteria from the gut and gas exchange system invade tissues releasing enzymes for decomposition.

Temprature affects rate of decomposition. warmth speeds up decomposition.

Injuries and open wounds allow bacteria in aiding decomposition.

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Difference betweeen bacteria and viruses. (Bacteri


no nucleus

lack membrane bound organelles.

do not produce spindel dduring nuclear division.

Reproduce asexually through binary fission.

Cause food poisoning, cholera.

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Difference betweeen bacteria and viruses. (virus.)

Strand of nucleic acid (RNA or DNA) enclosed in protien coat.

Viral DNA can be single or double stranded.

Some enveloped by hosts cell ssurface membrane.

Have glycoprotiens (antigens.)

Cause Flu, measels, chicken pox and cold sores.

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Virus replication.

1) Virus attaches to host cell

2) Inserts nucleic acid.

3) Viral nucleic acids replicate

4) Viral protien coats synthesised.

5) New virus particles formed.

6) Virus partivcles released due to cell lysis.

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Transmission of TB

Carried by droplets and can be released into air when sneezing talking or coughing.

People then inhale these droplets and can become infected. (droplet Infection)

Poor diet and poor health can increase risk of developing disease.

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Bodies response to infection.

1) Specific immune response

2) Non specific response.

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Immune response. (Non - specific.)

1) Immediate.

2) Lysosymes.

3) Inflamation.

4) Phagocytosis.

5) Antimicrobial proteins.

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Immune response (specific.)

1) Delayed.

2) B cells produce antibodies.

3) T cells.

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Lysosyme in tears.

Kills bacteria by breaking down cell wall.

found in saliva and nasal secretions.

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1) Cut enbles microbes to enter.

2) Blood clot seals wound.

3) Histamine released.

4) arterioles dilate increasing blood flow to sight.

5) Capillaries become more permeable.

6) Plasma fluid, white blood cells and anti bodies leak into tissue. (oedeama)

7) Microbes attacked by white blood cells.

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Phagocytes - white blood cell which engulf and destroy foriegn matter.

1) Neutrophils - engulf and destroy bacteria. 80,000,000. more during infection.

2) Monocytes - Turn into macrophage once in tissues. Engulf and destroy foriegn matter.

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1) Bacteria engulfed by neutrophiul or macrophage.

2) Enclosed in acuole.

3) Lysosomes fuse with vacuole. release digestive enzymes to break down foriegn material.

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Lymphatic system.

1) Tissue fluid drains into lymphatic vessels.

2) Lympth flow along lympth vessels, through lympth nodes, and back into blood via thoracic ducts.

3) Macrophages and lymphocytes activated when pathogens are present and can be destroyed.

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Provides no specific response against viruses.

inhibits viral protien synthesis and therefore multiplication.

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Specific immunity

Lymphocytes - B and T Involved in antibody production.

Gather in large numbers at sight of infection.

Held in strategically positioned lymphoid tissue.

Two main types -

B lymphocytes - respon to antigens by secreting antibodies.

Specialised type of protein molecule - immunoglobulins.

Antibodies bind to antigens and upon detection are destroyed by phagocytes.

Produced in bone marrow.

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T lymphocytes.

Produced in bone marrow but mature in thymus glands.

Two types of T cells.

1) T helper cells - Stimulate B cells to divide and produce antibodies. Enhance activity of phagocytes.

2) T killer cells - Destroy pathogen infected cells. But also can destro transplanted tissue leading to problems with rejection.

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Primary immune response. (Activation of T cells.)

1) Bacterium Engulfed by macrophage.

2) Macrophage becomes an antigen presenting molecule by presenting antigens on the major hist-compatibility complexes.

3) APC binds to T- Helper cell.

4) T-helper cell activated and divides.

5) Clones of T helper and T memory cells produced.

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Primary Immune response. (Clonal selection.)

B Cells bind to antigens and become antigen presenting molecules.

Active T - Helper cells Presenting same antigen bind to antigen presenting B cells.

T-cells release cytokines which stimulate division and differentiation of B-cells.

B effector cells - These Differentiate to produce plasma cells which release antibodies intyo blood and lymph.

B- Memory cells - Live longer preparing an invidual for effective response if the pathogen invaddes again.

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Role of T-Killer cells.

1) Bacterium infects host cell.

2) Host celol become APC.

3) T-Killer cells with complimetay receptor bind to presented antigen.

4) Divide to form clones of T killer cells. (stimulated by cytokines)

5) Host cll destroyed as enzymes released by T-Killer cells create pores in cell membrane.

6) Host cell swells due addition of water nd other ions and cell lysis takes place.

7) Pathogens released from host can be destroyed by macrophages.

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Secondary immune response.

If same pathogen infects again immune response much quicker.

Involves memory cells and takes only 2-7 days.

B memory cells immediately differentiate into plasma cells and aniti-bodies are produced.

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Response to TB (1st Phase).

Two phases of TB

1st phase can last for several months and have no symptoms.

TB evokes inflammatory response from hosts immune system.

Macrophages engulf the bacteria.

Anaerobic granuloma formed with dead bacteria and macrophages in centre.

Infection controlled and affected area heals.

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Bacteria evade immune system.

TB can survive inside Macrophages as it is difficult to break down due to its thicj waxy cell wall.

Lays dormant inside macrophage and are released when patients immune systemis weakened and can supress T- Cells and .

This reduces amount of antibodies and therefore attack by by T - Killer cells.

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Active tuberclosis (2nd Phase)

Can be a result of uncontainable amount of bacteria entering at 1st phase.

Or more often previously contained TB becomes active due weakeening of immune system


1) Coughing - Patient may cough up blood.

2) Shortness of Breath.

3) Loss of appetite and wieght loss.

4) Fever and extreme fatigue.

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Role of fever.

Chemicals released by macrophages and neutrophils affect hypothalamus and alter set point.

efectors act to warm up the body to new set point. (40.5 'C)

Raised temprature enhances immune function and phagocytosis.

Bacteria and viriuses may reproduce more slowly at higher tempratures.

TB is temprature sensitive and will stop reproducing at tempratures higher than 42 'C

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Negative feedback

Deviation form the norm results in the action of effectors bringing conditions back to the norm.

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HIV Invasion, replication, lysis.

1) HIV surface protien binds to to cell receptors. (GP120 to CD4 receptors.)

2) Virus envelope fuse with cell surface membrane and enters host.

1) Viral reverse transcriptase makes DNA copy of the RNA.

2) DNA intergrated into hosts cells by enzyme intergrase.

3) DNA transcribed and translated to produce new viral protiens.

Destruction of T- Helper cell.

1) New viruses bud out of cell taking enveloping cell surface membrane with them.

2) Cell lysis occurs.

3) T - killer cells also attack infected t - helper cells, Reduction in T - helper cells prevent proper functioning of Macrophages, T and B cells.

4) This leads to immune system becoming deficient.

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3 Phases of the HIV (ACUTE PHASE)


  • HIV antibodies appear in blood after 3-12 weeks.
  • Symptoms - fever, sweats, headache, headache, sore throat, swollen lymph nodes.
  • Rapid replication and loss of T-Helper cells.
  • t-killer cells destroy infected T-Helper cells. Reducing rate of replication buut does not totally eliminate it completely.
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3 Phases of the HIV (chronic Phase.)


  • May be no symptoms as replication is kept in check. Fu's and cold may be common and last longer.
  • Dormant diseases like TB and shingles can reactivate.
  • Can last for upto 20 years in fit young people.
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3 Phases of the HIV (disease phase.)


  • Decline on T-Helper cells lead to onbset of AIDS.
  • Opportunistic infections take advantage of the weakened immune system.
  • Opportunistic infections include pneumonia and TB.
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Bactericidal - antibiotics which destroy bacteria.

Bacteriostatic - antibiotics which prevent replication, immune system can destroy pathogen

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