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MCM > CIS plus other small details > Flashcards

CIS plus other small details Flashcards

1
Q

What is Acute Chest Syndrome Indicated By?

What Symptoms?

A

New pulmonary infiltrate on Chest X ray

-Fever, Chest Pain, Hypoxemia, Wheezing, Cough, Respiratory Distresss

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2
Q

What is Acute Chest Syndrome?

A

Infection( w/ new infiltrates in the lungs on the CXR)

  • Mycoplasma
  • Streptococcus Pneumioniae

Infection due to Thrombosis

embolic phenomena due to fat embolism 20 bone marrow infarction
second most common cause of hospitalization in KIDS

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3
Q

Splenic Sequestration Crisis?

A
  • vaso-occulsion in the spleen secondary to sickle cells
  • splenic pooling of Red cells (marked fall in hemoglobin)
  • elevated reticulocyte count
  • rapidly enlarging spleen
  • Hypovolemic shock
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4
Q

Autosplenectomy makes children susceptible to which encapsulated organism?

A
  • streptococcus pneumoniae
  • Neesieria meningitdis
  • Klebsiella pnemondia
  • Influenzae
  • Salmonella typhi
  • Cryptococcus neoformans
  • pseudomonas aerugionosa
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5
Q

Name the beta globin AA substitution and chromosome involved in sickle cell disease?

A

Glu–> Val
Point, missense mutation

Chromosome 11

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6
Q

Which AA residues on Histone protein tails are the targets of PTMs?

Phosphorylation is the exception?

A

Lysine and Arginine

Serine and threonine

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7
Q

Nucleosome?

Protein + DNA = ?

A

8 histone proteins (octamer)

Chromatin

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8
Q

CGH array

A

comparative genome hybridization

copy # varation

compare to “normal” reference

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9
Q

Histone Deacetylation

A

Represses gene expression

-compact and repressed (beads tight on string)

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10
Q

Histone Acetylation

A

Open and transcriptionally active (beads are wound loosely on strings cause Acetylgroups unwind em)

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11
Q

DNA methylation on which nucleotides?

what effect does it have and what areas are targeted?

can it be passed on to daughter cells?

A

Cytosine and Adenine

Represses Gene (silencing) transcription when it is at promoter region (CpG islands)

Yes, ex) gene imprinting and epigentics

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12
Q

Topoisomerase inhibitor names?

what effects as anti cancer agents?

A

Irinotencan (Type 1 topo)

Etoposide & anthrocyclines (type 2 topo)

block the cell cycle, generate single and double stranded breaks, harm the integrity of the genome which leads to apoptosis and cancer cell death.

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13
Q

 Ionizing radiation (uranium) can cause

A
  • strand breaks

- DNA-protein cross-links (e.g., thymine-tyrosine cross-link).

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14
Q

 Non-ionizing radiation (UV) causes

A

pyrimidine cyclobutane dimers (corrected by photolyase)

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15
Q

what is depurination?

WHat is deanimation?

A

base is broken from the sugar phosphate

where C is changed to U. A to HypoX. G to X

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16
Q

Methylation gone wrong? What enzyme must fix (inefficient)

A
  • Deamination of methyl-C produces T which is now mismatched with G
  • glycolsyalse
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17
Q

Cross linking agents (DNA damge)

A

Nitrogen mustard, cisplatin, mitomycin C,

Carmustine

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18
Q

alkylating agents

A

Dimethyl sulfate (DMS) and MMS

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19
Q

Intercalating agents

A

Thalidomide

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20
Q

BRCA2/breast cancer

DNA repair pathway?

A

Repaired by homologous recombination

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21
Q

Xeroderma Pigmentosum

DNA repair pathway?

A
  • skin cancer, UV sensitivity

- Mismatch repair

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22
Q

Cockayne Syndrome

DNA repair pathway?

A

Transcription coupled repair( normally RNA poly stalls ast lesions and directs repair machinery there)

disease: RNA poly is permenantly stalled at sites of damage

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23
Q

MSH2, MSH6, HNPCC

DNA repair pathway?

A

Mistmatch repair

-colon cancer

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24
Q

HDAC keeps genes repressed

what are some ant cancer drugs that affect this?

A

Valproic acid, varinostat

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25
Q

Inhibitors of HAT are showing promise in treatment of several diseases? why

A

HATS activate Genes so the mechanism is probably to inhbit thtis and to keep the genes repressed?

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26
Q

What is the one thing Staudinger kept saying about PTMS (phosphorylation, acetylation. ubiquination, SUMOylation, methylation?

A

All PTMS talk to each other and work together

they do not work in a vaccum(alone)

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27
Q

How are Antibiotics generally used?

A

They target prokaryotic translational machinery

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28
Q

Streptomycin

A

binds to small 30s to disrupt INITITATION

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29
Q

Tetracycline

A

binds to small 30s subunit to disrupt ELONGATION

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30
Q

Clindamycin and Erythromycin(pertussis reatment)

A

bind to the large 50s subunit to, bloacking translocation of the ribosome

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31
Q

Chloramphenicol

A

inhibits peptidyl transferase(ELONGATION), prok and mitochondria

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32
Q

Cycloheximide

A

inhibits peptidyl transferase in eukaryotes

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33
Q

Ricin and Shiga toxin

A

binds to 60S subunit blocking entry of aminoacyl-tRNA to ribosomal complex.

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34
Q

Diphtheria toxin

A

inactivates EF2-GTP and inhibits elongation.

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35
Q

Puromycin

A

ELongation inhibitor in both euk and prok

premature chain relase

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36
Q

Cytoplasmic Pathway

What is needed to go to each of these destinations?

A

Cytosol(no sequence)

mitochondria(N-terminal hydrophobic alpha-helix)(TIM AND TOM)

Nucleus( nuclear localization signals: 4 continuous basic AA residues (arg and lys) (Nuclear Pore)

peroxisome(SKL sequence)

-translation on free ribosome in cytosol

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37
Q

Secretory Pathway

whats needed in first 20 AA to go to this pathway?

what is needed to go to each of these destinations?

A
  • ER targeting sequence to go this pathway((1-2 basic positively charged near N-terminal; Hydrophobic (10-15 AA near C terminus)

Plasma membrane(Stop Transfer Sequence)

excretion from cell (Tryptophan rich domain)
,
ER( ER retention signal–> KDEL)

lysosome(Mannose 6P)

Translation paused on free ribosomes and Signal recognition particle brings ribosome-mrna-peptide complex to ER

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38
Q

I-Cell disease

A

Lyosomal proteins do not make it lysosome because mannose 6p target sequence is defective

  • high plasma levels of lysosome enzymes
  • failure to thrive
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39
Q

Acetylation attaches to what group? and what residue is affected?

A

NH3 (amine) and Lysine

Acetyl coA is donor

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40
Q

Glycosylation attaches what group? and what residue is affected

A

happens in ER lumen
-OH(hydroxyl) or N
Ser or Threonine groups

N or O glyc link

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41
Q

Phosporylation attaches what group? and what residue is affected

A

Ser or Thr or Tyrosine kinase

-OH

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42
Q

Collagen needs what to be fully functional? and what Vitamin helps with that?

A

Vitamin C scurvy

lysyl hydroxylase

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43
Q

 Alzheimer’s disease (β-amyloid): amyloid β

A

 Alzheimer’s disease (β-amyloid): Misfolding/aggregation of Aβ forms plaques in extracellular brain.

Hyperphosphorylation of Tau causes neurofibrillary tangles intracellularly. Can have familial or sporadic forms

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44
Q

 Parkinson’s disease (α-synuclein (AS)):

A

Aggregation of AS proteins deposit as Lewy bodies in dopaminergic neurons in substantia nigra. This causes a reduced availability to dopamine. Both familial and sporadic forms.

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45
Q

 Huntington’s disease (poly-glutamine(CAG) repeat diseases):

A

Mutation in Huntingtin gene results in expansion of CAG triplet repeats → Polyglutamine repeats in abnormal HTT protein. Selective death of cells in basal ganglia cause the symptoms.

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46
Q

 Creutzfeldt-Jakob/Kuru/Mad Cow disease (prion proteins):

A

Misfolded prion proteins. Transmissible (can convert normal proteins to misfolded form), thus belongs to TSE family of diseases

spongy brain.

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47
Q

• Summarize the different types of signaling

A

o Endocrine: Hormone signaling through the blood. Example is epinephrine
o Paracrine: signal diffuses to a neighboring target cell of a different cell type. E.g. testosterone.
o Autocrine: Secrete a signaling molecule which signals themselves. E.g. interleukin-1
o Juxtacrine: Signaling molecule binds to itself, which then bind to a receptor on a target cell. E.g. heparin

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48
Q

• Summarize the types of signaling molecules and their receptors

A

o Lipophilic: Can pass through the plasma membrane. Once bound to intracellular receptors, they act as transcription factors.
—- Hydrophilic: Cannot penetrate the plasma membrane. They have to interact with cell surface receptors ex( GPCR, RTK)

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49
Q

What are the viral, his risk strains of HPV?

A

16 and 18

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50
Q

HPV protein E6 inhibits which protein in cell cycle?

A

p53, E6 has a super high affinity for p53

  • p53 pauses cell cycle, so without it == bad
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51
Q

HPV protein E7 inhibits which protein in cell cycle?

A

Rb, E7 has a super high affinity for Rb

Rb, sequesters E2F, which helps stop cell cycle. With Rb gone, E2F constantly expressed

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52
Q

Southern Blot is?
North Blot is?
Western Blot is?

A

DNA-DNA
DNA-RNA
Protein or antibody measurmenet

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53
Q

PCR advantages

Disadvantages?

A

Adv:-very small amount of DNA template needed, 10^9 fold amplification from trade

Disadv: Need to know the sequence of the flanking DNA for primer design, error prone, amplification of contaminating DNA

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54
Q

qPCR or real time pcr

A

This is used to quantify copy number of a specific gene in two or more samples in real time. This technique also uses a probe which fluoresces only in the presence of a PCR product. This is used to detect levels of an infectious agent, or determine levels of gene expression.

cell cycle number n
X^N power

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55
Q

Norman Human Insulin has Proline at what position, terminus and which chain?

Has Lysine at what?

Lispros reversal of these AA positions resulted in what?

Insulin Aspart had the same results as Lispros, but what was change about the original sequence?

A

28, C Terminus, B chain

29, C terminus, B chain

Insulin that was faster absorbed

Proline at 28 taken out and aspartic acid put in

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56
Q

ELISA looking for what?

Indirect Elisa measures what? what is method?ex?

Sandwhich measures what? what is method? ex?

A

levels of specific antigen or antibody

IE: target is to measure amount of ANTIBODY. Antigen first, antibody of interest, then antibody w/ enzyme attached

ex) diagnosing HIV,

SE: goal is to measure amount of ANTIGEN. Antibody first, then antigen of interest, then antibody w enzyme attached(sandwhich)

ex) Myocardioal Infarction(troponin levels)
ex) pregnancy test

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57
Q

Western Blotting

A

detect levels of a target PROTEIN(ex) HIV antigen)

SDS page(e field and size)
same mechanism as Indirect Elisa

Protein(antigen) first, then primary antibody then secondary with enzyme tag

if patient no HIV infection then nothing on the western blot(using your blood check if antibody there)

ex) confirmation of HIV

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58
Q

Rifampicin is a inhibitor of what?

A

inhibitor of mRNA synthesis (transcription)

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59
Q

Robertsonian Translocation

Can lead to what?

A

Long arms of two acrocentric(very short arm on oneside) chromosomes combined and short arms lost.

can lead to a heritable type of down syndrome

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60
Q

Labile cells

Stable cells

Permanent cells

A

never enter G0 and are constantly dividing to replace cell populations that are continuously lost

those that retain the ability to exit G0 and enter G1 when stimulated by growth factors

Permanent cells stuck in G0

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61
Q

Chronic Myelogenous Leukemia

A

Translocation of chromosome 9 and 22 (genes BCR and ABL together now)

Philadelphia chromosome(BCR-ABL)

Reciprocal translocation

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62
Q

Turner Syndrome

A 
45XO
short
female
infertile, low hairline, 
normal intellgience
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63
Q

Klinefelter syndrome

A

47XXY

  • male
  • varying degrees of cognitive problems
  • small testes
  • tall
  • infertile,
  • can have even more than just two X chromosomes
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64
Q

Trisonomy 21 Downs sydnrome

A
  • occur via nondisJ or robersonian transloc t(14,21)
  • most common because most stable to survive
  • increased risk with maternal age
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65
Q

Genomic Imprinting

A

is essentially Gene silencing

  • through methylation of 5’ region of gene
  • chromatin condensation
  • epigenetic imprints remain at life times
  • in germ cells, epigenetics arereset at each generation during meiosis
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66
Q

How many genes are paternally imprinted?

Maternally?

A

30 genes paternally imprinted( silenced), maternally expressed

70 Genes maternally imprinted(silenced), paternally expressed

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67
Q

Prader Wili Syndrome Deletion in what chromosome # and in what chromosome maternal or Paternal?

A

chromosome 15
Paternal chromosome deletion
-short, hypotomia, obese,

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68
Q

Angelman Syndrome

A

chromosome 15
maternal deletion
Severe intellectual disability

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69
Q

True or False: Individuals with distinct genotypes can have single phenotype

A

True

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70
Q

Pleiotropy

A

individuals with the same genotype can have multiple phenotypes

-environment effects

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71
Q

X linked recessive disease

72
Q

X linked dominant disease

A

Hypopospatemia

73
Q

Autosomal dom disease

A

Polydactyl

74
Q

autosomal recessive disease

75
Q

Penetrance

A

% the gene manifests itself if you have it

ex) retinoblastoma

76
Q

Locus Heterogeneity

A

SIngle disorder, trait, cause dby mutations in genes at different chromosomal loci

77
Q

Hrady-weinberg

A

Not easy to find genotype (not like co dominance)

  • making algorithm based on if we we only know the amount of alleles in the population

assume random mating

78
Q

Mitochondrial (mtDNA)

A
  • circular
  • dsDNA
  • transcription indep of nucleus
  • no introns
  • INHERITED Exclusively through MATERNAL line
  • only daughters pass on to all kids
79
Q

Multifactorial inheritance

A
  • environment factors cause variation
  • combined effects of multiple genes are (POLGYGENIC)
  • follow bell shape curve
80
Q

Multifactorial inheritance: liability distribution

A

Need to pass a threshold of liability to be considered expressing the disease

  • below threshold normal, above effected Ex(3/5 genes defected you are effected but 2/5 not)
  • threshold higher in female, but can be passed on easier to male kids too
81
Q

G1 Phase what is needed?

A

lot of growth and protein production

82
Q

Where are the checkpoints in Cell cycle?

Restriction point?

A

G1, G2, Metaphase

R point is before G1 check point

83
Q

What is the restricting factor in G1 restriction point?

A

Growth factors are limited(2 hours before S phase)

-after pass R point its GF independent

84
Q

G1 check point checks for?

A

DNA damage around same time as R point. Must fix errors

85
Q

G2 check point checks for?

A

Verifying complete genomic duplication, and no errors

86
Q

Metaphase check point?

A

Ensure chromosome attached to mitotic spindle

87
Q

Myc (from the MAPK, pathway) is a transcription factor that does what?

A
  • Increases levels of CDK
  • CDK (w cyclin(partially active) and 1 phosphate group (fully active) phoshphorylates Rb
  • inactivates it and it releases E2F
88
Q

What does Rb do?

what does E2F do?

How is G1 check point bypassed?

A

-sequesters E2F(in active form)

  • E2F is transcription factor that drives cell from G1 to S b
  • it does this by increasing the gene for making G1 cyclins(Cyclin E) and S phase cyclin (Cyclin A)
  • both stimulate CDK even more making Rb even more hyperphosphorylated and inactive. This drives Cell into S phase where Cyclin A is used
89
Q

Cyclin Dependent Kinase(CDK)

How is CDK partially and full active?

A
  • are inactive without cyclin
  • Cyclin-CDK complex drives phosphoration of specific substrates
  • Cyclin-CDK comples only partially active
    -to be fully active needs CDK-activating Kinase( CAK) to phosphorylate the T loop(cave site)
    (opening up active site fully)
90
Q

Inhibitors of CDK? How they work?

A

P27(CKI protein)–> inactivates Cyclin-CDK-P complex by binding to it. making a p27-cyclin-CDK-P complex

P27 in G1 to S transition

Wee1 Kinase–> phosphorylates the roof site of Cyclin-CDK complex (2 phosphates)

91
Q

Cyclin D what phase and point?

A

Resctrition point
G1
CDK 4 and 6

92
Q

Cyclin E what phase and point?

Cyclin A?

B?

A

G1/S
G1 checkpoint

S phase and Mitosis

Mitosis

93
Q

Anaphase promoting complex( APC/C) or cyclosome

how does it work?

A
  • Ubiquitin Ligase Family member
  • APC/C activated by binding to CDC20(activating subunit)
  • active form poly-ubiquinates its substrate (S and M cyclin complexes)
  • cyclins degraded by proteasome
  • absence of Cyclins inactivates CDKs
  • Repression of Cell cycle
94
Q

What keeps p53 inactive/degraded?

95
Q

p53(guardian of genome) is a transcription factor, how is it activated what does it do?

A
  • activated by DNA damage(PK) (not broken down)
  • p53 is stabilized/activated by phosphorylation
  • activation of P53 leads to increase in transcription p21(CKI) and causes cell cycle arrest
96
Q

p21

A

is a CKI that binds to cyclin-CDK2 complexes causing them to be inactive

  • this means no phosphorylation of Rb
  • which means Rb is active and sequesters E2F and pauses cell cycle
97
Q

Caspases

A
  • -inactive precursor (zymogen)
  • need proteolytic cleavage
  • when cleaved form heterodimer
98
Q

Initiator Caspases?

Executioner Caspase?

A

Caspase 8 and 9 are initiators of the caspase
cascade

  • Caspase 3 is executioner (destroys target– this is apoptosis)
99
Q

BCL-2 are anti or pro apoptotic?

A

BCL2 family are anti-apoptotic

100
Q

Intrinsic Apoptosis

what protein is mainly involved?

what is released that activates the rest of the cascade?

A
  • DNA damage stimuli
  • inactive BAX proteins in mitochondrial membrane aggregate in response to signal
  • Cytochrome C
101
Q

Cytochrome C release from mitochondria activates what protein?

what is formed? and what does this product activate?

A

APAF1 combined with cytochrome C and makes an Apoptosome( many ATP used)

Apoptosome cleaves procaspase 9 which becomes caspase 9

102
Q

Caspase 8 from which pathway?

Caspase 9 from which pathway?

at what point do they become one pathway? whats the final step that’s in common?

A

8–> extrinsic

9–> intrinsic

both of them cleave procaspases 3, 6, 7

to become caspase 3 which is an executioner that executes apoptosis

103
Q

Gain of function mutation?

what are some proto oncogenes?

A
  • point mutation, deletion, gene amplication, or translocation
  • increased expression of protein products
  • expression of altered protein (oncoprotein) that does not respond to normal signals
  • GFs and TFs and there receptors
  • signal transducers
104
Q

HER2 receptor(RTK) could become and oncogene from two different ways what are they?

A
  • Simple Gene amplification

- Point mutation from valine to Glutamine

105
Q

HER2 point mutation what is changed? and what is the new name of this oncogene?

A

Valine to Gln
- NEU

its always active cause always dimerized even without ligand

106
Q

Tumor Supressor Genes

A
  • Repress cell cycle Progression
  • promote apoptosis
  • couple DNA damge to cell cycle
  • DNA repair proteins (BRCA)
    ex) P53, Rb
107
Q

Loss of function in tumor repressor genes

A
  • have to lose both copies
108
Q

Hall marks of Cell cancer

A
  1. self sufficiency in growth
  2. Evading growth repressors
  3. activating invasion and metastasis
  4. enabiling replicative immortality
  5. Inducible angiogenesis
  6. Resisting Cell death
  7. deregulating cellur energetics
  8. avoding immune desctruction
  9. tumor-promoting inflammation
  10. Genome instability/mutation
109
Q

Herceptin is an anti cancer inhibitor of what?

what type of cancer

A

HER 2 and its oncogene counter part NEU

Breast cancer

110
Q

Gleevec anticancer agent that inhibits?

treatment in what?

A

BCR-ABL fusion protein

treatment in

Chronic myelogenous leukemia

111
Q

viral oncogenesis

A

Viral genome injects its DNA into a healthy cell and the viral DNA is taken up near a proto-oncogene. The virus then hijacks the cell and transcribes the viral genome. Since there is little error correcting in transcription, the proto-oncogene mutates into an oncogene.

112
Q

alkylating agents

A

block dna rep

113
Q

cytoxic agents

A

intercalate to inhibit DNA synth

114
Q

Antimetabolites

A

inhibit enzymes of DNA synth

115
Q

Albumin does what

A

Source of major colloid osmotic pressure ( on vessel walls)

-carrier proteins

116
Q

Hereditary spherocytosis

A

Ad mutation

  • affects ankyrin complex (band 3 and 4.2)
  • leads to detachment of membrane and peel off
  • makes spherical RBCs
117
Q

Hereditary elliptocytosis

A

AD mutation

  • Spectrin-spectrin bonds and band 4.1
  • membrane fails to rebound and progressively elongates
  • ellpitcal RBC
118
Q

Neutrophils

A
  • multilobed
  • acute inflammation and tissue injury
  • secrete enzymes
  • Puss?
  • bind to foreign bacteria
119
Q

Eosnophils

A
  • bi lobed
  • pink
  • histaminASE (NOT ACTUAL HISTAMINE THATS BASOPHIL)
  • remove antigen-antibody complex
  • attack PARASITES
120
Q

Basophil

A
  • very visible granules hard to see nucleus
  • Purple
  • anaphalaxis
  • realse HISTAMINE
  • vasoactivators??
121
Q

Lymphocytes

A
  • Big nucleus covering all of cell
  • These are the main functional cells of the immune system
  • not terminally differentiate(will make T and B lymphocytes)
122
Q

Monocytes

A
  • heart, kidney shape nucleus
  • small granules
  • phagocytic system
  • macrophages of connective tissue,
  • can leave blood supply
123
Q

o T cells

A

differentiate in the thymus; long life span and are involved in cell-mediated immunity.

124
Q

o B cells

A

Form and differentiate in the bone marrow; transform into plasma cells → secrete Antibodies

125
Q

o Diapedesis

A

when neutrophils leave the circulation and migrate to their site of action in tissues. This is controlled by cell adhesion molecules that interact with ligands on endothelial cells. They can be further directed to injury site via chemotaxis.

126
Q

Thrombocytes(platelets)

Thrombocytosis

A
  • hemostasis- control of bleeding
  • Platelets release serotonin which is a potent vasoconstrictor causing smooth muscle contraction in order to reduce blood flow at injury site
  • they release ADP and thromboxane A2 which increase aggregation of platelets to form the primary hemostatic plug

-These platelets provide a surface for conversion of soluble fibrinogen → fibrin, causing fibrin to form a mesh over the initial plug entrapping platelets. This is causing the formation of the secondary hemostatic plug.

127
Q

Nuclear Lamina made from?

A

Intermediate filaments

128
Q

Progeria disease

A
  • messed up nuclear lamina
129
Q

Taxol

A
  • binds at stabilizes Microtubules
  • prevents depolymerization
  • beneficial in cancer to stop mitosis
130
Q

Colcine,colcemid

Vinblastine, vincristine

A

binds the tubulin DIMERS and prevents there poly

131
Q

Actin Filaments (F- actin aka filamentous actin)

A
  • made up of G-actin monomer(twisted together)

- all cell types, unstable , essential for movment

132
Q

Phalloidin (toxic mushrrom)

A

Binds and stabilizes actin FILAMENTS( F-actin) not monomors

-prevent depolymerization

133
Q

Cytochalasin

Latrunculin

A

C: caps filament plus ends(no depoly)

L: binds actin monomers preventing poly

134
Q

Collagen is the main structural protein in?

A
  • extra cellular matrix and ECM/connective tissue
135
Q

Collage formation?

A
  • heterotrimer
  • triple helix formation is done in the ER lumen by hydroxylation and glycosylation
  • comes out to ECM via vesicle as ProCollagen
  • it is then cleaved and self assembly into fibrils and then fibers
136
Q

Scurvy
what enzyme?
what vitamin?

A
  • Strength of Collagen is lost
  • Prolyl Hydroxylase cofactor is Ascorbate( Vit C)
  • wounds reopen, loss of teeth, pale skin
137
Q

Anchoring Junction

A

Junctions from cell-cell, cell-BM, or cell-ECM. Important to recognize that it is interacting with cytoskeletal filaments.

138
Q

Occluding Junction

A

Help maintain cell polarity and prevent movement from things between cells or out of cells.

139
Q

Channel forming Junction

A

Allows for the movement of cellular components between cells.

140
Q

Signal relaying junction

A

Example is a neuronal junction.

141
Q

Cadherins

A

Ca2+ dep

  • important in junction formation b/n cells
  • Homophilic interaction
  • interacts with cytoskeleton (actin)
142
Q

E cadherin stands for?
N Cadherin stands for?

classical or atypical?

A

Epithelial cadherin

Neural Cadherin

Classical (type 1)

143
Q

VE cadherin stands for?
LI cadherin

classical or atypical?

A

Vascular-ENDOthelial

Liver- Intestine

atypical

144
Q

EMT in transitional bladder cancer? what results in increase metatstic potential?

A

E-cadherin way down

N cadherine way up

145
Q

Ig super family

A
  • immune cell interaction
  • hetero or homophilic
  • involved in recognition, binding or adhesion
  • calcium dep
146
Q

Selectins

A
  • calc dep
  • binds to EC carbohydrates
  • important role in host defense mechanism
  • increased during inflammatory response
  • WBC markers are ligands for selectin
  • Low-affinity of selectins for leukocyte allow “ROLLING” slowing down of leuk cyte
147
Q

Integrin

A
  • couple EC to cytoskeleton
  • can activate signaling pathways
  • cell cell interactions via B2 FAMILY!!! integrins on leukocytes allow for adhesion and diapedesis
  • higher affinity for ligands then selectin causes WBC to STOP!
148
Q

Stem cell basic characteristics

A

not terminally differentiated, can divide without limit (due to telomerase), undergo slow division.

149
Q

Cord blood is what type of potency?

A

multipotent

Hemopoietic
stem cells

150
Q

Founder stem cells

A

cells capable of clonally dividing and giving rise to a large number of cells. Each tissue is given a fixed number of founder cell populations. They are programmed to have a fixed number of divisions. These cells define the size of large final structures.

151
Q

Transit amplifying cell

A

These are not stem cells. These cells divide frequently, and transit from a cell with stem cell characteristics to a differentiated cell. These leave the basal layer and incorporate into the layers above. They are finite (programmed to only have a limited number of divisions). These cells are committed.

152
Q

o Multipotent

o Pluripotent:
o Totipotent

A

: ability to give rise to different cell types of a given lineage (e.g. adult stem cells).
Ability to give rise to all cells of an embryo and subsequently, adult tissues (e.g. embryonic stem cells).
: Ability to give rise to all cells of an organism, including embryonic and extraembryonic tissues (e.g. a zygote is totipotent).

153
Q

Pluripotent cell TFs

GFs

Induced pluripotent stem cells(iPS)

A

-Nanog, Oct4, Sox2, FoxD3
-Cripto, GDF3
could be a common molecular blue print of gene expression in pluripotent cells

If you could get these Tfs to be active in humans adult stem cells
you can exhibit ES cell like properties (pluripotency)

–VERY HIGH POTENTIAL FOR terAtoMA

154
Q

Adult stem cells

A
  • respond to growth and repair
  • found in tissues
  • strictly imposed molecular restraint on genes
155
Q

Mesenchymal stem cells : found in ? and form what?

A

Bone marrow

connective tissues,

156
Q

Somatic cell nuclear transfer

A
  • somatic cell fusion with egg cell(must remove egg cell nucleus first)
  • extract inner cell mass of blastocyte

and culture pluripotent cell

  • very unethical(clones)
  • DOLLY THE LAMB
  • very inefficient( need 100s of oocytes)
  • less teratoma potential
157
Q

Erythropoeisis stages?

A

Hemocytoblast–> proerythroblast–> early erythroblast–> late erythrblast–>Normoblast–> reticulocyte–> RBC

158
Q

All chains of hemoglobin derived from what two chromosomes?

159
Q

Hydroxyurea

A

used to induce HbF, in hobes to cure sickle cell disease.Since HbF uses gamma chain instead of Beta chain (beta is the problem)

-toxic

160
Q

HbF doesn’t bind well to 2.3BPG therefore

A

has highher affinity for oxygen

161
Q

Normal body iron?

Heriditary Hemochromatosis?

162
Q

Hepcidin activation

A

Transferrin receptor releases Hfe when Transferin comes in/

  • Hfe goes to TfR2 where it is internalized and stimulates Hepcidin production
163
Q

What does Hepcidin do?

A

-it binds ferroporin and causes internalization of it.
ferro porin then destroyed by proteolysis
LOWERS iron absorption when [Iron} is HIGH

164
Q

Folic Acid is absorbed in what part of intestine?

How much folic acid does liver store? and how long last?

A

Jejunum

5-10 mg, 3-6 months

165
Q

Once folic acid absorbed by intestine it is reduced to its methyl THF form(primary form circulating in blood). why is this a problem and what u need to fix?

A

Cant convert toanything else

Folate trap

Need b12 cobalamin

166
Q

B12 absorption

A
  • dietary b12 binds to R binder (stomach)
  • Intrinsic factor made by parietal cells
  • proteases(pancreas) degrade R-binder
  • Intrinsic factor binds to Cobalamin in duodenum and carries it to the ileum where the receptors bring it into the blood(receptor mediated endocytosis of IF-cobalamin)
167
Q

Cobalamin travels through blood as what form

A

Transcobolamin

168
Q

Pernicious Anemia

A

-megaloblastic macrocytic anemia from lack of intrinsic factor (needed for absoroption)

169
Q

What is to find out the cause of B12 deficiency?

A

Schilling Test part one:

if labeled cobalamin not present in urine than (pernicious anemia) gotta do part two
Should see cobalamin in urine regularlry

170
Q

Schilling Test part 2

(

A

again need oral dose of labeled B12 this time add Intrinsic factor

  • if radioactive b12 present in urine then lack of intrinsic factor is reason for pernicious anemia
171
Q

Biosynthesis of Heme in?

A

liver and erythroid cells

172
Q

Heme Degradation

A

Retiuculo endothelial

173
Q

Porphyria cutanea Tarda (PCT)

A
  • uroPorhyrinogen decarboxylase

both hepatic and erythropoietic

174
Q

Acute intermittent Poryphyria

A

PBG deaminase
hepatic
-4 rings put togehter

175
Q

Congenital Erythropoetic poryhyria

A

Uropporghyingen 3 cosynthase

build up of uropor 1

  • red teeth, red urine, skin photosensitivity
176
Q

Variegate poryhria

A

Celebrity
King George 3
uro p 9 oxidade

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