Student Presentations Flashcards

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1
Q

what is an endocrine?

A

hormones secreted by glands throughout the entire body thru the blood stream

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2
Q

what are estrogen and androgens responsible for?

A

estrogen = implantation, placentation
androgens = male development, sex characterisitics

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3
Q

what is an endocrine disruptor?

A

something that disrupts normal flow of endocrines
- several things (synthetic & naturally)
- mainly impact endocrine receptors

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4
Q

what is the main endocrine disruptor we talked about? what is it used for?

A

BPA
- synthetic estrogen
- making plastic
- in 90% of people’s urine
- only 20-400 mg can cause effects

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5
Q

what are the three types of trophoblastic cells? describe them

A

CTB (Cytotrophoblasts)= progenitor cell
* STB (Syncytiotrophoblast) = form chorion, secrete hormones
* EVT (Extravillious trophoblast) = anchor placenta to uterus

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6
Q

which receptor is BPA an agonist for? what about antagonist?

A

estrogen ALPHA agonist
estrogen BETA antagonist

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7
Q

describe how BeWo cells were used to see the effects of BPA

A

BeWo cells function very similarly to EVT cells
- adding BPA to BeWo cells decreased implantation by 50%

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8
Q

what is important for regulating endocrine disruptors?

A

Classification
- very difficult and expensive to do
- important to prevent manufacturing of harmful substances

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9
Q

what is metamorphosis?

A

modifications to morphological characteristics of larval tissue to transition an animal to next life stage
- caterpillar to butterfly

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10
Q

what does the thyroid gland do?

A

controls many things in the body including development, homeostasis, and metamorphosis

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11
Q

what converts T4 into T3? why is it converted?

A

deiodinases (removal of an iodine)
- T3 is what binds to receptors (T4 does not)

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12
Q

describe the Atlantic Halibut research

A

looked at muscle and skin tissues of the fish to see if metamorphic changes occurred as a result of T4 to T3 conversion
- looked at the deiodinases
- found that D2 and D3 expression drives metamorphosis

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13
Q

what happened in amphibians when T3 was blocked?

A

no. metamorphosis occurred
- instead of turning into a frog, it turned into a giant tadpole

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14
Q

what are the four clinical features of fetal alcohol syndrome?

A

facial dysmorphology
neurobehavioral disabilities
growth retardation
CNS dysfunction

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15
Q

describe what happens when glial cells are exposed to alcohol prematurely

A

reduces differentiation
- impairs astroglial proliferation, survival, and function
- decreased white matter

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16
Q

describe the Shh experiment with ethanol

A

half injected with ethanol, other half injected with antibody to remove Shh
- showed physical similarities b/w both groups
- PCR was ran to show a decrease in Shh and TF’s when introduced to ethanol
- Shh that uses PATCHED receptor was decreased

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17
Q

what is Marfan Syndrome?

A

dominant genetic disorder that affects connective tissue

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18
Q

what gene in Marfan Syndrome does it mutate? describe what it normally does

A

fibrillin-1 gene (FBN1)
- makes elastic fibers & microfibrils

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19
Q

what is the diagnostic tool used to classify Marfan Syndrome? describe how it works

A

Ghent nosology
- created a chart of symptoms to reference when making a diagnosis
- long limbs, issues with cardiovascular & muscular systems
- aortic valve issues (aneurysms -> weak & widened wall)

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20
Q

describe the experiment to find the mutations that lead to Marfan’s Syndrome

A

isolated and sequenced FBN1
- missing EGF-like domains led to the most severe cases
- result of inframe exon skipping

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21
Q

what is mosaic pleiotropy?

A

gene is independently expressed in many tissues of the body

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22
Q

what two cell types interact to form teeth?

A

mesenchymal & epithelial

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23
Q

what are the 5 stages of tooth development?

A
  1. initiation (6-7 week)
  2. bud (8 week)
  3. cap (9 week)
  4. bell (10-14 week)
  5. maturation
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24
Q

what is occurring during the initiation stage of tooth development? (include genes)

A

forms primary epithelial bands & dental placodes
- Fgf8 activates Pax9 = tooth development
- BMPs block Pax9 in the areas we don’t want teeth

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25
Q

what is occurring during the bud stage of tooth development? (include genes)

A

dental placodes invaginate
- Fgf9 activates MSX1 = epithelial cells move into mesenchymal cells

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26
Q

what is occurring during the cap stage of tooth development? (include genes)

A

unequal rate of division (creates a concave shape)
- Fgf20 produced by enamel knot (epithelial)
- Fgf3 produced by mesenchymal cells

27
Q

what is occurring during the bell stage of tooth development? (include genes)

A

produce dentin and enamel (mineralization)
- triggered by the decrease in Fgf’s

28
Q

what produces dentin and enamel?

A

odontoblasts = dentin
ameloblasts = enamel

29
Q

what is important to know about the enamel knot in relation to rate of cell division?

A

enamel knot does NOT have Fgf receptors
- leads to less growth in this area which creates that concave shape

30
Q

what is LADD syndrome?

A

missing teeth, underdeveloped salivary glands, etc.
- due to a missense mutation in Fgf receptors
- codes for a different amino acid

31
Q

what are the three phases of normal wound healing?

A
  1. inflammation
  2. proliferation
  3. scar remodeling
32
Q

what is different about scar formation in the early embryo?

A

no scar formation
- scar formation correlates with hair follicle development
- does not need amniotic fluid to do healing

33
Q

what are the two Wnt pathways? which one is used for early embryo wound healing?

A

Canonical = scar formation, can’t make new skin cells
Non-canonical = NO SCAR, plasticity for re-epithelialization

34
Q

describe the experiment with grafting human fetal skin onto mice

A

cutaneous (in skin) = scar tissue
subcutaneous (under skin) = no scar
- proved that subcutaneous is less physiologically active

35
Q

what Wnt is responsible for blocking the canonical pathway to allow for the non-canonical pathway to be active? describe what promotes this

A

Wnt5a
- Wnt 5a promotes EMT (epithelial mesodermal transition) to activate mesenchymal cells to divide and close the wound through contraction of the skin

36
Q

what week of development is the most susceptible to ethanol? what stage of development does this correlate with?

A

3rd week of development
- gastrulation
- embryonic stage

37
Q

what three main types of cells are impacted by ethanol exposure in the neuro, cardio, and ocular regions?

A

Neuro = cranial neural crest cells
Cardio = heart progenitor cells
Ocular = retina

38
Q

what structure in the brain has the most damaging effects when exposed to ethanol? when does this structure form?

A

Corpus Callosum
- 6-7th week

39
Q

what is the difference between Symmetric and Asymmetric effects for FAS?

A

Symmetric = 1st & 2nd trimester, defects of whole fetus

Asymmetric = 3rd trimester, normal head, underdeveloped abdomen

40
Q

what chemical mechanism does alcohol effect?

A

one-carbon metabolism
- methylation of DNA & histones

41
Q

describe the miRNA experiment for FAS

A

miRNA’s are needed for stem cell renewal & blocking transcription of a gene (regulates proteins produced)
- when a fetus is exposed to alc, these miRNAs were overexpressed
- decreased osteogenic differentiation (production of bone stem cells)

42
Q

what was the one miRNA that was decreased in the FAS experiment?

A

miR-206-3p

43
Q

what is a orofacial cleft?

A

lip & roof of mouth doesn’t join and creates a facial abnormality

44
Q

what are the three types of orofacial clefts? describe the difference b/w them

A

unilateral = one side of lip, MOST COMMON
bilateral = both sides of lip
isolated = cleft palate w/o lip deformity

45
Q

what is the difference between nonsyndromic and syndromic? what is an example of a syndromic disease that involved a cleft lip

A

nonsyndromic = isolated defect
syndromic = defect seen with other abnormalities
- Patau Syndrome (hernia, cardio defects, renal issues)

46
Q

what weeks of development does the cleft lip form?

A

4th-12th week
- fusion occurs anterior to posterior

47
Q

describe the experiment looking at the effect of specific genes on cleft lips (list the three genes they studied). Which gene was the main gene found to have an effect?

A

epithelium and connective tissue was collected from a nonsyndromic patient
- looked at expression of Pax7, Pax9, and RYK in a normal vs effect patient
- Pax7 was found to be the MAIN gene involved with cleft lip

48
Q

what does Pax7 do for cleft development?

A

craniofacial development
- neural crest cells
- MAIN GENE!!!!!

49
Q

what does Pax9 do for cleft development?

A

RNA polymerase that regulates protein expression
- dependent on cleft type

50
Q

what does RYK do for cleft development?

A

ectoderm development
- formation of craniofacial regions

51
Q

what does the amygdala do? where in the brain is it found?

A

limbic system, temporal lobe
- involved in senses, behavior, learning, memory
- processing emotion, interpreting social cues

52
Q

describe the experiment focusing on how maltreatment can effect the brain (mention the gene they looked at but don’t describe it)

A

go/no-go task
- humans were placed in an MRI scanner and shown threatening images
- mice were well taken care of, and then placed into a cage with bright lighs, no odor, and boring (threatening)
- they then measured the c-Fos expression in the amygdala

53
Q

what does the c-Fos gene do? what function did it have on the amygdala?

A

cell proliferation and cell differentiation
- correlated with anxiety
- turns a short-term stimuli into a long-term response

54
Q

what is fragile X syndrome?

A

X-linked recessive disorder that causes intellectual disability
- creates large ears, hyper-extensible joints
- due to the mutation of the promoter of FMR1 gene

55
Q

what is situs solitus?

A

normal symmetry of organs

56
Q

what is situs inversus?

A

inverted symmetry of organs
- asymptomatic

57
Q

what is situs ambiguous?

A

inverted symmetry of organs
- severe medical issues

58
Q

when in development, does the L/R axis form in chicks (stage & developmental stage)? what structure is the most important for determining this

A

stage 5 -> gastrulation
- Hensen’s Node!

59
Q

what main molecule is responsible for activating Pitx2 on the left side?

A

Nodal

60
Q

what organ does Pitx2 form? which side is this on?

A

right side of lung

61
Q

what are the two TF’s that are activated by Pitx2? (list them, don’t describe)

A

Foxh1
Nkx2

62
Q

describe how Pitx2 TFs are regulated

A

ASE enhancer regulates the binding of Pitx2 to Foxh1 & Nkx2

63
Q

what are the functions of Foxh1 and Nkx2?

A

Foxh1 = target of nodal signaling, initiates asymmetry
Nkx2 = late-stage expression of Pitx2

64
Q

what is the Nodal Flow Hypothesis

A

cilia tilt toward the LEFT side to move nodal & extracellular fluid
- breaks up symmetry in early embryo