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98 Cards in this Set

  • Front
  • Back

Biotech

tech application of bio knowledge for human purposes

Recombinant DNA

application of cutting, splicing and creating DNA

Genetic engineering

manipulate genetic makeup

restriction enzyme

cut at a specific place

plasmids

(bacterial) amplifies the gene of interest

transgenic

genetic material that is not their own


ex: insulin and HGH (organisms), vitamins (plants),

bGH

bovine growth hormone: faster animal growth

gene pharming

introduce human genes into dairy animals so that the proteins can be expressed in the milk

gene therapy

introducing human genes into human cells to treat/correct disease


-doesn't change the germ cells

gene editing

permanently correct heritable genes

retrovirus

human gene package (inside own DNA and chromosomes)


-embed into a plasmid and then into a liposome




option: ejecting naked DNA

bacteria with CRIPSPR cas9

incorporate viral DNA into their own DNA

CRISPR

clustered regularly interspaced short palindromic repeats

Cas 9

endonuclease with gRNA to find and cut invading DNA

PAM

where to cut, complementary to foreign DNA

sickle cell anemia

altered hemoglobin,


frequent in countries with malaria because it is the only immunity to malaria

Paracrine signals

from one cell to a short distance to the cells nearby (same tissue)


*not through the blood

Juxtacrine signals

the signal (ligand) must be in close contact with the the receptor

exocrine

excreted through ducts and into a surface

endocrine

excreted into the blood

steroid hormone

-slower


-lipid soluble


-looks like cholesterol


-activates gene inside to make proteins

non-steroidal hormone

-faster


-lipid insoluble, binds on receptors


-protein looking


-activates on binding site, cAMP sends a message and the cell activity is altered.

controlled variable


control center


effector

ex: glucose, oxytocin


endocrine gland ex:pancreas


target tissue ex:pancreas

Alpha cells


Beta cells


Delta cells

-increase blood sugar (breakdown of stored glycogen in the liver)


-decrease in blood sugar (storage of fats, conversion of glucose into glycogen)


-inhibits secretion of both

Hypothalamus

for homeostasis, links for N and E systems, makes 2 hormones and monitors pituitary gland

Pituitary Gland

-master gland


- produces 8 hormones

Posterior (posture/back) Gland

-connected to HTH by neuroendocrine cells


-hormones for storage and release (doesnt make its own hormones)


-non-steroidal: oxytocin

Oxytocin

nerves in nipple travel up to the neuroendocrine cells, the release of oxytocin by the posterior pituitary and through blood to the mammary glands
-contractions and milk

Anterior (A is first)

-controlled by HTH


-releases and inhibits hormones


-6 key hormones: Prolactin and GH(2)

Prolactin

Anterior pituitary


stimulates milk and mammaries


-inhibited by dopamine in hypothalamus

GH releasing

hypothalamus

GH inhibiting

from anterior pituitary (somatostatin)

Gigantism


Acromegaly


Dwarfism

1. hyper-secretion in childhood


2. hyper-secretion in adults


3. hypo-secretion

Diabetes

Excess of glucose because cells cannot absorb it

Type 1

5-10%, children


genetics, environmental


not enough insulin, destruction of beta cells

Type 2

90-95%, adults


lifestyle and exercise


resistance to insulin

Cell Cycle

Interphase (18-24hrs)


Mitotic Phase (<1hr)

Interphase

G1, S, G2

G1

primary growth in size, reproducing organelles, dna is chromatin (unravelled)

S

synthesis of DNA for the next division, unwind and replicate

G2

final growth, enough to make two, sister chromatids held by a centromere

Mitotic phase

PMAT and cytokinesis, DNA is condensed and pulled apart

Prophase

everything is condensed into the nucleus

Metaphase

chromosomes start lining up

Anaphase

the chromosomes start to split to different sides

Telophase

the uncoiling of the chromosomes, getting ready for splitting

cytokinese

the cytoplasm starts a cleavage furrow and splits to make 2 daughter cells

Meiosis I

homologous pairs separate making 2 unique daughter cells, reduction division

Meiosis II

haploids into haploid again, 4 unique haploid cells

Checkpoints

G1: restriction checkpoint, size, growth damage? if yes then goes into G0


G2: Cell size and DNA replication


Interphase: chromosome attachent to spindle

Transcription

in nucleus


2 strand DNA into 1 strand mRNA


DNA unwinds (polymerase), RNA nucleotides complement one strand, forms mRNA (with introns and exons)

Intron

edited out of the mRNA

Exons

coding sequence for amino acids to be made

translation

cytoplasm


mRNA goes through the ribosome where tRNA brings the corresponding amino acids in the codon (triplet)


Initiation, Elongation Termination



DNA


A


C


G


T

mRNA RNA


U A


G C


C G


A U

Codon start and codon stop

AUG


UGA, UAA, UAG

point mutations

missense: replaced nucleotide = different aa


nonsense: replaced nucleotide = stops aa


silent: replaced nucleotide = same aa

insertion and deletion

insertion: inserts nucleotide, changes sequence that follows


deletion: deleted nucleotide, changes sequence that follows

duplication and translocation

duplication: duplicates a segment of the chromosome


translocation: genetic material is exchanged with non homologous pairs

Enzymes recognize errors

cut out, replace, reconnect




Numerous DNA repair enzymes–Cell cycle phase–The type of DNA damage

Differentiation

based on gene expression


cells divide (16-32cells) and exposed to environment (no grow)


8 cells is where theres beginning of specialization

Cloning I - embryo splitting

splitting the 8 celled zygote to make 8 identical individuals

Cloning II - nuclear trnasfer

somatic (diploid) cell is taken and inserted into an enucleated cell, electric current and then implant egg


identical to the somatic cell donor

Reprogramming influenced cells (epigenetic)

-from environment or development of earlier cells ( which genes are tight or loose)


-open genes needed for development and chemical modification (Histone modification and DNA methylation)

Therapeutic Cloning I

control a cell during differentiation or modify the genome to produce a donatable functioning organ

Embryonic stem cells

produce all cells of the body

Common

Men: PCL


Women: BLC


tissues that rely on hormones

Dangerous

Men:LCP


Women: LBC

Cancer vs normal cells

disease of cell differentiation and division. Normal has an internal clock, hormones, one location and inhibitory signals

1. Hyperplasia

increase in cell division

2.Dysplasia

change in the cell structure

3. Benign (in situ)

one location, can be treated,


4. Malignant (metastatic)

cells that have spread, can form else where, leak into blood and lymph



Tumour

discreet mass of cells from hyperplasia

Sarcoma

rare, in the connective tissue, solid

Leukemias and Lymphomas

in the blood and immune system, 8%

Carcinomas

epithelial tissues, 90%

Sustained proliferative signalling

No rate of cell growth (growth factor independent)

Evade growth suppressors

ignores signals

Activating invasion and metastasis

break away from origin and invade a different area

Replicative immortality

Can replicate

Angiogenesis

nutrition

Resisting cell death

evade apoptosis

Proto-oncogenes

normal


growth, division, adhesion, survival

Oncogenes

mutated


quick growth, division, better survival


fails to respond to inhibitory signals

1. Point mutation

low expressed gene becomes mutated and replicated to be expressed higher

2. Translocation

change of cell makeup, fusion protein accelerates growth

ErbB2

growth factor receptor is mutated, treated with Herceptin

Tumour suppressors

represses cell growth, regulates adhesion and division. If it breaks it can cause cancer

p53

guardian of the genome, it is a tumour suppressor


(beginning of S and G2 phase)

BRCA 1/2

tumour suppressor for DNA repair


(end of S, end of G2 phase

contributing factors (disease)

-bacteria/virus (<15)


-HPV (cervical)


-HEP B/C (liver


-HIV (sarcoma)


-EBV (Hodgkins)


-Helicobacter (gastro)

contributing factors (controlled)

-tobacco (30%)


-alcohol


-radiation (Xray, UV)


-diet and obesity (30%)


red meat: colon, rectum, prostate


alcohol: breast, colon, rectal, liver


salt: stomach


type II: high risk of death

internal factors (4)

-free radicals from metabolism: damage DNA


-antioxidants (A,C,E vit) neutralize free radicals (combat antioxidants)


-errors in DNA replication


-weak immune response

Detection

X rays, MRI, PET


genetic test (BRCA 1/2)


enzyme test

Treatment

surgery


radiation/chemo (cytotoxic) - damages cells


starving: angiogenic


molecular treatment: target onconogens (Herceptin --> ErB2

cancer stem cells

dont divide rapidly


not effectively killed by things that target rapidly dividing cells


renew themselves and rapidly dividing cells

reduce risk

less sun


watch diet and weight


moderate alcohol


dont smoke


screening


know history