Communicable Diseases Flashcards

the scary diseases that ANY of us can contract, and WHY...!

1
Q

What is a pathogen?

A
  • This is a microorganism that can causes diseases in other organisms, acting as the host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Explain the bacteria that causes disease…

A

Undergoes binary fission by means of reproduction, damaging cells through toxins released.
* PROKARYOTES
* Reletivly large, compared to the virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain the fungi that causes disease

A
  • Grows into structures of micellium as main-body structures, that may grow into mushrooms.
  • Produces reproductive hyphae, releases spores in the atmosphere to reproduce across environment
  • Hyphae = releases extracellular digestive enzymes (cellulase) causing additional decay
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain the Viruses that causes disease

A
  • Invade organism cells, using genetic machinery to manufacture more copies of same virus
  • Host cell will burst, cusing cell damage, relasesing many more viruses to invade further cells
  • NON-LIVING, according to M.R.S G.R.E.N

Movement, Respiration, Sensitivity, Growth, Reproduction, Excretion and Nutrition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the Protists that causes disease

A
  • These enter host’s cell, and will feed with the available nutrition to grow and reproduce
  • Normally carried with vectors, and transfered through fluids/contact

e.g Plasmodium via Mosquitoes…….

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does Ring Rot come about?

A
  1. Occurs in PLANTS
  2. Caused by BACTERIA
  3. Ring of decay around vascular tissues in potatoes/tomatoes, alongside leaf wilting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does Tobacco Mosaic Virus come about?

A
  1. Occurs in PLANTS
  2. Caused by VIRUSES
  3. Leaf discolouration in mosaic-like pattern in many plants.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does Blight come about?

A
  1. Occurs in PLANTS
  2. Caused by PROTISTS
  3. Chlorosis and browning of plant tissues in potatoe tubers, alongside leaf wilting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does Black Sigatoka come about?

A
  1. Occurs in PLANTS (bananas mostly)
  2. Caused by FUNGI
  3. causing leafing spots on bananas, significantly reducing yeilds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does Athlete’s Foot come about?

A
  1. Occurs in ANIMALS (human mostly)
  2. Caused by FUNGI
  3. Redness, Itching and flaking of growth between toes in feet.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does Ring Worm come about?

A
  1. Occurs in ANIMALS
  2. Caused by FUNGI
  3. Ring-shaped growth with spores erupting through the skin, causing rashes in mammals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does Influenza come about?

A
  1. Occurs in ANIMALS
  2. Caused by VIRUS
  3. attacking respiratory system, causes muscle pains and headache in humans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does Bacterial Meningitis come about?

A
  1. Occurs in ANIMALS
  2. Caused by BACTERIA
  3. infection of the meninges, being membranes surrounding brain and nerves , may become inflamed/swollen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does HIV come about?

A
  1. Occurs in ANIMALS
  2. Caused by VIRUS
  3. **destroys the immune system by attacking WBCs, compromising immune response ** in humans
  4. Becomes AIDS when developed for a while, becoming much more susceptible to many other diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What makes HIV a more unique virus to many?

A
  1. This is a RETROVIRUS!
  2. Will contain RNA rather than DNA, like a regular virus
  3. Will have enzyme Reverse Transriptase, to convert single stranded RNA genome to DNA when injected into host cell’s machinery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why would Bacteria and Fungi thrive more in vascular tissue, in a plant?

A
  1. Abundant supplyof water (xylem) and sugar+nutrients (phloem)
  2. Will MASSIVLEY aid for optimal growth in these organisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does Malaria come about?

A
  1. A parasite in the bloodstream that can cause headaches and repeating episodes of fever - comas and even DEATH
  2. Protist = Plasmodium Falciparum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does Tuberculosis (TB) come about?

A
  1. Occurs in ANIMALS
  2. Caused by BACTERIA
  3. Killing cells in the entire body, mainly affecting respiratory systems (lungs…)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give and explain the methods of Direct Transmissions of disease

A
  1. Physical Contact: direct touching involved my ANY means; stopped by Condoms, Disinfectant, Sterilising equipments
  2. Feacal/Oral: Consuming anything with pathogens; stopped by Sewage Treatment, Cooked and Washed meats
  3. Droplets: Pathogens carried in air via drops; stopped by “Catch it - Kill it -Bin it”, tissues when sneezing
  4. Spore Transmission: Fungal/pathogenic spores carried in air; stopped by masks when needed, wash skin after soil contact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give and explain the methods of Indirect Transmissions of disease

A
  1. Vector Transmission: another organism used to gain entry into primary host, without harming this organism; stopped byKilling potential vector organisms, vaccinations, sterilising vectors
  2. Fungal Spores: airborne transission carried in the air; stopped by Condoms, Disinfectant, Sterilising equipments
  3. Leaf Distribution: Infected leaf shedding falls to soil, able to reproduce, and infect other plants ; stopped by Incinerating infected leaves/entire plant before shedding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does Malaria infect an individual?

A
  1. A female anopheles mosquito will suck blood of infected person
  2. Will also pick up gammetes of plasmodiumin the bloodstream
  3. Plasmodium will be nurtured and develop in mosquitotes salivary glands
  4. Another person is bitten
  5. Inside the liver, the parasites invade liver cells and multiply asexually to form more parasites.
  6. After maturing, the liver cells burst, releasing many parasites back into the bloodstream.
  7. The parasites (plasmodium falciparium) then invade erythrocytes, where they continue to multiply and cause the symptoms of malaria.
    and cycle starts over!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are Passive Defences in organsims?

A
  • These are defences in place BEFORE a pathogen infection has taken place, preventing initial entry of said pathogen!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are Active Defences in organisms?

A
  • These are defences in place AFTER a pathogen infection has taken place, preventing internal speading of said pathogen, using ENERGY, and CHEMICALS (mostly….)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a way to remeber Plant Physical Defences?

A
  1. LST CW BC = Lost Cow Back!

= Ligin, Stomata, Tylose, Cellulose, Waxy Cuticle, Bark, CALLOSE,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
How can we describe **CALLOSE** and **TYLOSE?**
1. ***CALLOSE*** = **Large polysaccharide, blocking sieve end-wall plates**, as such polymers will block pathogen = spread decrease! 2. ***TYLOSE*** = **Baloon-Like swelling of toxic chemicals, filling/blocking xylem cavity**, containing Terpenes, also toxic to pathogens
26
What is a way to remeber **Plant Chemical Defences?**
1. **P.A.T.H.O.D.** = **say how it is read** = **Phenols** (tanins that kill insects), **Alkeniods** (caffine, cocaine = bitter taste!), **Terpeniods** (antibacterial oils) , **Hydrolictic** Enzymes (degrading pathogen cell wall), **Defensive** Proteins (inhibiting ion channel transport), **Oxidative** Reagents (highly reactive oxygen molecules damaging pathogens)
27
Another means of ***Active defence***? *(plants...)*
***NECROSIS!*** **Another programmed cell death**, due to *untreatable site of infection* ***Killings infected cells*** = Stoppping pathogen spead through *stopping water/nutrient access to reproduce*
28
Define what is meant by ***parasite***
This is an organism that **lives inside a host organism**, **feeding and using nutrients** from this organism, while **harming this host organism**
29
Suggest reasons for **possible rapid spread of pathogens** (e.g. Fungi)?
1. **Vectors/Infected individuals moving** over a large geographical area 2. **Lack of resistance/Immunity** from the pathogen 3. **Overpopulation/Overcrowding** in a small area 4. Fungal spores / larger distances
30
Why would protsist ***Plasmodium*** use erythrocytes as part of life cycle?
1. To **avoid any foreign recognition** from the immune system 2. To **complete** its life cycle 3. Provides a **source of nutrients** to grow and nourish
31
What *chemical* processes will take place during **Blood Clotting?**
1. **Abrasion to skin** will cause opening to pathogens! 2. ***Exposed Collagen*** will bind to ***platelets***, to release ***12 Clotting Factors + Ca2 ions*** 3. ***Inactive Thrombokinase*** will become ***Active Thrombokinase*** = important enzyme for next step 4. THEN ***Prothrombin*** becomes ***Active Thrombin*** = another enzyme inportant for next step 5. THENN ***Soluable Fibrinogen*** becomes ***Insoluable Fibrin*** = big player in "fish netting" of RBCs. 6. THENNN ***RBCs and Platelets are all trapped in a fat clump***, **drying up** and becoming **solid**....... ## Footnote Thrombin becomes active when certain amino acids are removed from the active site: REALLY COOL!
32
Outline the **Skin's details** on primary defence....
* **Upper Layer = Epidermis Layer**, with layer of **cells underneath** * Most cells are ***Keratinocytes, produced by mitosis from base-layer Multipotent Adult Stem Cells*** * As such cells approach surface, they undergo **Keratinisation** = ***Cytpolasm slowly replaced by Keratin Protien, drying out.....*** * Keratinised **DEAD CELL SURFACE LAYER** becomes very surface of skin! *HENCE, BEING MAIN PRIMARY DEFENCE OF HUMANS!*
33
What makes the skin surface a **good primary defence**
**Keratin-Tough Epidermis**= Keratinocyes provide a very tough outer barrier to pathogens to penetrate **Non-Living cells** = no cyloplasm; no chemical reactions; less susceptible to pathogenic infection on skin!
34
What is an **Enzyme Cascade?**
* An enzymatic cascade is **a sequence of successive activation reactions involving enzymes**, characterized by a **series stemming from an initial stimulus.** * The **product** of each **preceding reaction catalyzes and is consumed in the next reaction**, and so forth......
35
*WHERE* and *WHY* are the **Mucus Membranes** found?
1. Found in: *Ears, Lungs, Genitals and Digestive System* 2. These all have **very thin membranes that means pathogens can enter much more easily**, into the body 3. Hence, at airways, epithelial tissue has ***GOBLET CELLS*** that **secretes the mucus**, to ***TRAP*** said pathogens 4. At epithelial tissue, we also have ***Ciliated cells***, that have ***Cilia***, to **waft bands of mucus away from the lungs!!**
36
How does **Inflammation Response** take place?
* Pathogen enters via **wound site!** * ***Mast Cells*** will **detect and recognise** foreign pathogens invading tissue, releasing ***Histamines*** in response * Histamines will cause ***VASODILATION*** in nearby blood vessels, **causing neutrophils and erythrocytes to leak out** * ***ERYTHROCYTES*** = causes the **redness and swelling**, due to more concentrated in a **smaller** location * ***MACROPHAGES*** = Releases **cytokines** to initiate **tissue repair** | (can be paired with *specific* immune response....)
37
How does the Lymphatic Sytem help with Inflammation?
* Main Role: **Drains away waste fluids** from site of injuries! * Such fluid will drain to nearby **Lymph Nodes**, containing **Lymphocytes** (can have***Lymph Node Swelling*** during sudden ***surge of lymphocyes activity and numbers!!)***
38
What does Lymph Fluid consist of?
* Contains fluid that **CAN NOT be absorbed back into the cappileries!!!** * Consists of *Fats, Protiens, Damaged/Cancerous cells, Pathogens and Lymphocytes*
39
What are some other *secret* primary defences?
1. **TEARS:** Contains enzymes, providing killing of some pathogens in the eyes 2. **WAX:** At ear canal, ca trap entering pathogens 3. **REPRODUCTIVE:** Mucus plug walls in the cervix, also trapping pathogens!
40
Some expulsive forces to remove pathogens by Reflex Actions?
* SNEEZING! * COUGHING! * VOMITING! All are methods to urgently remove disturbances/toxins/irritation inflicted by PATHOGENS!!
41
What are ***Secondary Non-Specific Defences?***
* These are defences that are used when a **pathogen has already entered the bloodstream** * These still remain as **NOT SPECIFIC to antigens**, but forigen pathogens as a **whole...**
42
What are Antigens?
* These are **protiens on plasma membrane** that are **chemical markers for immune system** to recognise if **self or foriegn** cell
43
What are ***Opsonins?*** ## Footnote ***BE SURE TO CHECK THIS LIL BIT OUT!!!!!***
1. These are **protien molecule that attach to antigens on pathogen surface** 2. Type of **UNIVERSAL ANTIBODY** that is **NON-SPECIFIC**, allowing a phagocytic cell to **easily bind, engulf and digest** the pathogen. 3. Hence, are able to bind to a **RANGE of antigens of differing pathogens**, (but not ALL...) ## Footnote ***RELEASED BY PHAGOCYTES!!!!!!!!!!!!!!***
44
What is ***Opsoninisation?***
The act of **Opsonins binding to antigens on the pathogen** surfaces.......
45
What are some activity differences between **Neutrophils** and **Macrophages?**
1. **Macrophages**: Engulfs pathogens, but *not FULLY digesting* Antigens on digested pathogens are **conserevd**, and used for **protien complex on plasma membrane** Becomes ***antigen presenting cell***, presenting antigens for **antibody production in Lymphocytes** 2. **Neutrophils:** *100% killing* , undergoes the good and proper **engulfing and digesting of pathogens**, containing ***lysosomes of hydrolyctic enzymes*** to do so!
46
What are some physical differences between **Neutrophils** and **Macrophages?**
1. **Macrophages**: ***Larger*** in size, lasts for ***3 months***, ***irregular outer membrane shape***, engulfs up to ***100*** pathogens 2. **Neutrophils:** ***Smaller*** in size, ***Multi-Lobed nucleus***, ***smoother outer membrane shape***, lasting for a **few days with consumption of up to 20** pathogens.
47
What is a **Monocyte** and a **Phagosome**?
1. **Monocyte** = This is the **IMMATURE VERSION** of a *Macrophage*, as it travels inactive in the bloodstream (more adolecscent in the life cycle) 2. **Phagosome** = The large vauole/vesicle that *surrounds pathogens* when engulfed
48
How do **Neutrophils** engulf and digest pathogens?
* They contain *many Lysosomes*, that contain **Hydrolyctic Enzymes, that will break down the structure of the pathogen**, destroying it * Waste products will be expelled via *excocytosis*
49
Why does the **macrophages also antigen-presetning cells**, and not *neutrophils*? | and WHY ANTIGEN **PRESENTING**, and not just ANTIGEN....
* This is because **macrophages are larger in size, with a much longer lifespan** than neutrophils *(despite both phagocytes)* * This will mean that they will be **able to carry antigen-presetning much longer, for the lymphocytes to produce antibodies for same antigen!** ## Footnote If a sole antigen, macrophage will be recognised by **immune response as foreign**, and will be **attacked**, and we do NOT want thia to happen
50
4 Main ways Phagocytes are adapted to their function!
1. ***Well Developed Cytoskeleton*** = Easily **changes shape to engulf and digest pathogens** + important **lysosome transportation** network 2. ***Many mitochondria*** = ATP **releases energy** for cell movements + endo/exocytosis 3. ***Multi-LObed Nucleus (neutrophils specific)*** = Able to **squeeze through cell layers in tissue** to reach infected locations 4. ***Many Ribossomes*** = Efficient **protiensynthesis to make lysozyme enzymes + antigen-presenting!**
51
Where are the phagocytes made??
**IN THE BONE MARROW!!!!**
52
What are Hydrolyctic Enzymes?
Enzymes using **water molecules to break down most chemical bonds** in *biological* structues (ester/peptide/Hydrogen....)
53
Describe how a Neutrophil can undergo phagocytosis!
- **Chemicals released** by pathogens as well as chemicals released by the body cells under attack **attract neurtophills via chemotaxis** to the site where the pathogen are located - Neutrophills **move towards pathogens**, Which **may have antibodies attached** to their surface antigens - Neutrophills have **receptor molecules** on their surface that recognise antibody molecule and attatch to them - Once attached to the **pathogen the cell surface membrane of the neurtophill extends out engulfing the pathogen** and trapping the pathogen with a phagosome - This part of the process is known as ***endocytosis*** - The neutrophill releases digestive enzymes into the vacuole, **becoming phagolysosome to occur** - These **enzymes destroy the pathogens structure** - After killing and digesting the pathogens the neutrophill die (eventually)
54
What is a **Lymphocyte?**
* This is a *WBC* with **a round, whole nucleus, found mostly in the lymphatic nodes/vessels** * Undergoes **SPECIFIC IMMUNE RESPONSE**, capable of recognising **specific antigens**!
55
What are **Cytokines?**
1. These are **cell-signalling chemicals heavily involved in immune response** (but *not quite* hormones) 2. Use to signall **to other WBCs, to carry out certain immune responses**
56
What are the **different types of Cytokines**?
1. ***Monokines:*** *Released by macrophages*, **attracting neutrophils to stimulate B lymphocytes to differentiate and relase specific antibodies** 2. ***Interleukins:*** *Released by T Cells and macrophages* Stimulates **clonal expansion and differentiation of B lymphocytes** 3. ***Interferons:*** **Inhibiting virus replication**, by stimulating **T Killer Cell activity**!
57
What is **Clonal Expansion?**
This is a method of **mitosis** to **rapidly produce lymphocytes in a shorter** given time period
58
What are B lymphocytes Plasma+Memory Cells?
* ***B PLASMA CELLS:*** These will **produce the specific, complamentary antibodies via exocytosis**, at very very large quantities * ***B MEMORY CELLS:*** Cells that remain in the bloodstream for a **very long period, providing immunity from encountered pathogens and a much faster secondary immune response**
59
How would **B Lymphocytes respond to antigen exposure?**
1. B lymphocytes **encounters anitgen via pathogen or macrophage antigen-presenting cell** 2. *Interleukins* released from T Cells and macrophages will cause **CLONAL EXPANSION**. 3. *Monokines* released from macrophages will cause **CELL DIFFERENTIATION**, into ***plasma and memory cells*** 4. Plasma cells die in days due to *ATP energy all used for mass-producing antibodies*, while Memory cells *remain for YEARS!* ## Footnote ***CLONAL EXPANSION = PROLIFERATION!! (hit a 4 if u forget.....)***
60
What are ***T*** **Helper+Killer+Memory+Regulator** cells
1. ***T Helper Cells:*** *Secretes cytokines to stimulate colonal expansion and differentiation* of **B** Cells 2. ***T Killer Cells:*** *Destroys cells infected with viruses, by injecting H2O2*, causing cell lysis (killing away *cell+virus*) 3. ***T Memory Cells:*** Remains *in the blood, casugin a much faster secondary response upon second encounter*!
61
What do T Regulator Cells even do?
* They are **responsible for shutting down immune activity** following removal of pathogen * Preventing ***AUTOIMMUNITY!***
62
**Mention and state** why do we need the ***3 lines of Defences***?
These are ***PRIMARY NON-SPECIFIC, SECONDARY NON-SPECIFIC AND SPECIFIC DEFENCES*** 1. = **Prevents initial pathogen entry** into body/bloodstream 2. = **Short-Term response that can remove pathogen**, but ***NOT*** lead to *longer-term immunity* 3. = Immune response that ***remains SPECIFIC to PARTICULAR ANTIGEN***, leading to *life-long immunity* via *B Memory Cells*!
63
What is a **immunoglobin?**
* Complex protiens **produced by B Plasma Cells**, released in response to an *infection!* * *Antibodies* can be classified as immunoglobins!
64
How can we describe the **structure of an Antibody?**
1. Consists of *Light polypeptide* (top region) and *Heavy polypeptide chains* (lower region) 4. ***CONSTANT REGION***: Universal region for *overall body of the antibody* and providing *easy binding site for phagocytes*! 5. ***VARIABLE REGION***: Has *specific shape to anigen*, different for *ALL antibodies*, and will bind to the antigen 6. ***HINGE REGION***: Region that allows *antibody flexibility, can bind to more than one antigen per antibody*! 7. ***DISULFIDE BRIDGES***: *Holding polpeptides together* in antibody
65
What are the **main types** of Antibodies?
1. ***Opsonins***: Binds to pathogen antigens;binding sites for phagocytic cells, allowing easly phagocytosis! 2. ***Agglutinins***: Each antibody has *2 binding sites*; will use each "arm" to bind to 2 pathogens each, *clumping together* (easily engulfednd digested) > **agglutination!!** 3. ***Antitoxins***: will bind to *toxic chemicals with antibodies produced by pathogens*, cancelling out toxic effect in the body!
66
What are Primary and Secondary responses?
1. ***PRIMARY***: This is the *first encounter* with pathogen, where *plasma cells first start producing the specific antibodies* for specific pathogen **(SLOWER RESPONSE ,FEWER ANTIBODIES PRODUCED)** 2. ***SECONDARY***: This is the *second encounter* with same pathogen, but *B and T memory cells* with recognise pathogens, stimulating *cytokines to plasma cels to produce many* antibodies **(RAPID RESPONSE, HUGE AMOUNT OF ANTIBODIES)**
67
What is vaccination?
* A method of stimulating an immune response to achieve immunity!
68
What can be contained in vaccines?
1. **Whole, live microorganisms** with similar antigens (copox vs smallpox) 2. **Weakened versions** of the pathogens 3. **Dead version** of pathogen 4. **Antigens only** only! 5. **Harmless version** of toxin!
69
How can vaccines prevent disease spread?
* ***Herd Vaccination:*** almost all population are given vaccine, where disease spread to non-immune hosts is very unlikey *(herd immunity acheived)* * ***Ring Vaccination:*** Vaccinating people, mostly towns, villages and homes, in the IMMIDIATE VICINITY of new cases or possible occurences of infection with pathogen (Smallpox...)
70
How can we combat an **ever-mutating virus** like influenza?
1. **High-mutation rate: constant change of virus antigens** 2. In order to decrease chance to develop a pandemic of particular strain, most vulnerable people are vaccinated (65+, respiratory issues, weak immune systems)
71
What are 4 types of immunity achieved? | What are
1. ***Natural*** = Acheived through natural, biological processes *(Natural body infection/Placenta and Breastfeeding in newborns)* 2. ***Artificial*** = Acheived through medical interventions *(Dead-Pathogen Vaccination/Antibody antigens)* 3. ***Active*** = immune system activated and making own antibodies 4. ***Passive*** = antibodies made supplied by another source
72
Why some diseases have **vaccines over others??**
1. Humans being the **main host** 2. Pathogen **mutates** *very* slow 3. Easy to identify **symptoms** 4. Pathogen **not concelased in other cell** in life cycle!
72
Why do we need **to research for new medicines**
* New diseases *emerging* always * *Non-effective* treatments of some disease * Antibiotics *less* effective!
73
Main sources of finding **new medicines?**
1. **Accidental findings** = Penicillin discovery 2. **Traditional, herbal medicine** = Poppy Seeds for morphine 3. **Observing Wildlife** = Elephant+Parrot clay eating for toxin treatment 4. **Using plant sources** = Foxgloves = *Digitalis* and Willow tree = *Aspirin*
74
Why should we *sustainably farm* rainforests?
1. **As plants are used for medicine**, we must ensure to **not allow species to be extinct, by removing them!** 2. Species are potential sources for new medicines!
75
What are personalised medicines?
* Where ***we sequence the genes of specific individuals***, and use them to ***create specific, tailored medicine treatment*** to the same patient!!
76
How has the *Human Genome Project* helped with *personalised medicine?*
* Access to a full genetic sequence can help **identify faulty genes in individual, that may give rise to certain diseases!**
77
What is ***Synthetic Biology?***
This is the ***production of new molecules that mimic natural processes***, or the ***use of natural molecules to produce new biological systems***, that ***DO NOT EXIST IN NATURE!!!!***
78
Examples of *Synthetic Biology* taking place!
* *Tomatoes* with ***anthocyanin*** pigment, being ***antioxidants against CHD*** * *Goldent Rice*, a GM Crop, producing ***beta-carotene***, used to produce ***vitamin A to combat blindless*** in children
79
How antibiotics kill bacteria? | and ***SOMETIMES WILL NOT!***
* They are ***chemicals that inhibits the growth of the bacteria***, allowing them to be managed and killed via immune response! * BUT, antibiotic resistance is a real deal, so must **COMPLETE COURSES** and **PRESCRIBE WHEN NECESSARY** to reduce this!
80
Describe the shape of *Primary Response curve*!
1. ***Lag time*** = time needed for *clonal selection and expansion of B Lymphocytes* 2. ***Rise*** = *B Plasma cells rapidly divide,* producing *specific antibodies* to pathies 3. ***Fall*** = Plasma cells *eventually die*, and infection *is overcome* 4. ***Rapid Increase+Shorter timespan*** = *B memory cells remain in blood*, giving ***faster secondary response***
81
Why no symptoms felt in upon second infection in *Primary Response curve?*
* **Second immune response is much faster**, with much larger quantity of antibodies produced!
82
How do vaccines lead into Memory Cells?
1. Vaccines **inject antigens**, where **APC presents to T helper cells** 2. **Antigen will bind to T Helper**, releases **cytokines** 3. **B Lymphocytes for clonal selection and expansion**, forming **B memory cells after differnetiation!!**