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Block 1 > Week 3 Random > Flashcards

Week 3 Random Flashcards

1
Q

Where does the implantation usually occurs?

A

Posterior-Superior side of uterus

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2
Q

When is the implantation complete?

A

11-12 day because of the plug

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3
Q

What is the organ system that becomes functional by the 8th week?

A

Cardiovascular

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4
Q

When does the embryo has the shape of a human?

A

Week 8

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5
Q

What are phases in embryonic development?

A

growth (mitosis; cell division)

morphogenesis (making structures like heart, liver)

differentiation (maturation of physiological processes)

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6
Q

What are derivatives of ectoderm?

A

Neuroectoderm that gives rise to all CSN and PSN

Epidermis

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7
Q

What induces neurulation?

A

Precordal plate and notochord

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8
Q

What is neurulation? Describe steps

A

Folding creates neural tube

  1. BMP4 blocked -> prechordal plate and notochord induces neural plate
  2. neural plate forms neural tube
  3. fusion from cranial to caudal
  4. neuphores close cranial 25 caudal 27
  5. neural crest formation
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9
Q

What is neuropores?

A

The openings after neurulation (posterior and anterior)

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10
Q

What is neural plate converted after it rolls?

A

Neural tube

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11
Q

BMP4

A

BMP4 is blocked allowing induction of neural plate by notochord and prechordal plate

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12
Q

Direction of fusion of neural tube

A

Cranial to caudal

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13
Q

When does cranial neuropore and caudal neuropore close?

A

cranial neuropore closes day 25 caudal neuropore closes day 27

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14
Q

What is forming besides neural tube during neurulation?

A

Neural crest

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15
Q

Neural Crest Cells:

Where do they come from?

Where do they migrate?

What do they become?

A

from neural folds migrate to mesenchyme form PNS and a lot more:

Connective tissue and bones of the face

Cranial nerve ganglia

C cells of the thryoid gland

Conotruncal septum in the heart

Odontoblasts

Dermins in the face and neck

Spinal (dorsal root) ganglia

Sympathetic chain and preaortic ganglia

Prarasympathetic ganglia of the gastrointestinal tract

Adrenal medulla

Schwann cells

Glial cells

Arachnoid and pia matter

Melanocytes

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16
Q

Define Mesenchyme

A

It is connective tissue of mesoderm.

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17
Q

What is epidermal covering?

A

Derivative of ectoderm

epidermis, sweat glands, sebaceous glands, mammary, glands, hair, nails, cornea, anterior pituitary, enamel, internal ear, lens of the eye

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18
Q

What are subdivisions of ectoderm?

A

Neuroectoderm: CNS, PNS

Ectoderm: epidermis, sweat glands, sebaceous glands, mammary glands, hair, nails, cornea, anterior pituitary, enamel, internal ear, lens of the eye

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19
Q

Name mesoderm parts

A

Axial

Paraxial

Intermediate

Lateral

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20
Q

Axial mesoderm

A

Forms notochord cranial

Limited by prechordal plate caudal and caudal eminence

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21
Q

Paraxial mesoder

A

Somitomeres

in head: somitomeres1-7 + neural plate -> neuromeres -> wonderful thing

in body: somitomeres -> somites

* 3/day can be used as a clock

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22
Q

Which direction do somites grow?

A

Cranial to caudal

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23
Q

Types of somites

A

sclerotome cells migrate medially to form bones (vertebrae, ribs, some base of the skull)

dermomyotome dermatome cells migrate under ectoderm to form connective tissue of the skin – dermis myotome cells migrate to form skeletal muscle

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24
Q

What do somites pull with them?

A

The innvervations of spinal cord

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25
Q

What is important about dermatomyotome location?

A

Each dermatomyotome retains its own segmental innervation from its origin

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26
Q

Intermediate mesoderm

A

Forms most organs (CT, smooth muscle and epithelial linings) in both the urinary and genital systems.

** The endoderm provides the remaining epithelial linings of some UG organs.

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27
Q

Cephalocaudal Folding

A

Rapid head and tail growth causes the embryo to curl toward the ventral surface

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28
Q

Lateral Folding

A

endoderm becomes folded into a long narrow tube within the embryo.

mesoderm continues to separate out ectoderm from endoderm.

the ectoderm and amniotic cavity completely encircle the embryo.

the ectoderm forming the outer covering of the embryo

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29
Q

What cavities are formed from extraembyonic celoem?

A

intraembryonic cavity Thoracic and abdomainal cavity

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30
Q

Lateral Plate Mesoderm

A

somatic -> connective tissue and smooth muscle of body wall, bones and cartilage of limbs and limb girdles

splanchnic -> connective tissue and smooth muscle lined organs and ALL tissues of cardiovascular system

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31
Q

In which location lateral plate mesoderm does not split?

A

Head

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32
Q

Endoderm Derivatives

A

forms the epithelial lining of GI tract mesoderm and endoderm induce each other to form specific GI organs epithelial components of several other organs: pharyngeal buds, lung buds, liver, pancreas and gall bladder buds

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33
Q

Pharmacology definition

A

the study of the interactions of chemicals, other than foods, with living systems. It is a science based upon an understanding of organic chemistry, biochemistry, physiology, pathology and microbiology that focuses on the mechanism of action of drugs on living systems.

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34
Q

Pharmacology subcategories

A

Pharmacodynamics: Mechanisms of Drug Action

Pharmacokinetics: Absorption, distribution, metabolism and elimination of drugs.

Therapeutics: The application of pharmacology to the problems of clinical medicine.

Chemotherapy: The use of drugs, which ideally have little effect on the host (patient) but destroy or retard the growth of invading cells and organisms.

Safety Pharmacology: A relatively new discipline that is focuses on the MOA of unwanted effects of drugs in humans during drug product development.

Toxicology: The pharmacology of the harmful effects of poisons, environmental and industrial chemicals and drugs on the human body.

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35
Q

Pharmacy definition

A

The science broadly interested in all aspects of drugs, with two primary emphases: one on the manufacture, compounding, preparation and dispensing of drugs; the other on the therapeutic management of drug treatment of patients; therapeutacist.

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36
Q

Drug names

A

Chemical name: Any typical organic chemical name.

Generic name: The assigned name of a drug, by which it will be known throughout the world no matter how many different companies manufacture it.

Official name: This is the name by which a drug is listed in one of the following official publications: a) U.S. Pharmacopoeia, b) National Formulary, c) U.S. Adopted Names.

Trade name: The name that is given by a particular company that is manufacturing the drug.

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37
Q

Who is responsible for regulating laws regarding drugs? How?

A

FDA

Right to regulate, recall, and safety aleart

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38
Q

Drug Discovery Map

A
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39
Q

Initially Drug Discovery Process

A

(basic lab) Lead identification and optimization: Classical medicinal chemistry, Molecular modeling, Natural product screening, Novel biotechnology, Serendipity

(confirmation in models) Pharmacologic evaluation: In vitro receptor binding, Cell-based assays, Animal disease models

(toxicity) Preliminary assessment of development challenges: Toxicology, Pharmacokinetics, In vitro tests, Exploratory, dose range finding studies, Scale-up potential, Costs of clinical evaluation

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40
Q

Investigational New Drug (IND)

A

Application submitted by a sponsor to study:

Chemical and biological activities
Dosage form specifications for humans
Quality control details
Description of company facilities and personnel
Scientific qualifications of the investigators
Specific details of the protocol to be followed

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41
Q

Phases in human testing

A

Phase 1: 9-18mo 20-100 health = safety; tolerability; administration

Phase 2: 18-24mo 30-40 control & subject = response ; dosage ;

Phase 3: 2-4yr 100-1000+ experimental = clinical benefit ; RCT

Drug is considered safe.

Phase 4: 1-2yr = broader population; compares effectiveness with other drugs

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42
Q

Items that need to be completed in order to receive license for a new drug.

A

To obtain license for a new drug:

Completed results of Phase I, II and III

Long term toxicity studies on animals

Effects on fertility and reproduction and young animals

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43
Q

GLP

A

Good laboratory practices

Are regulatory guidelines followed by a validated laboratory to ensure each and every step of the study/experiment is validated. So that every step performed in a study/experiment can be precisely and accurately repeated.

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44
Q

Why G proteins are important?

A

these membrane proteins represent more than half the current drug targets and a market of tens of billions of dollars annually

all tisues, organs, and cells express GPCRs

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45
Q

How many transmembrane folds are in GPCRs?

A

7

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46
Q

How G-protein is activated?

A

Signal molecule binds to GPCR

Alpha subunit is phosphorylated

It dissociates from beta-gamma complex

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47
Q

Types of GPCRs

A
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48
Q

Functions cAMP, cGMP, and Ca2+

A

2nd messenger

(cAMP): Binds to PKA (Gs); Activates Na+ channels in olfactory neurons (Golf)

(Ca++): Binds to PKC (Gq)

(cGMP): Opens Na+ channels in rod cells (Gt)

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49
Q

How does Vibrio cholerae affects intestinal cells?

A

Locks GPCRs in active state

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50
Q

How does Pertussis toxin (Bordetella pertussis) affects respiratory cells?

A

Inactivates Gi protein leading to cAMP overproduction

Produces uncontrollable, violent coughing

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51
Q

Downstream effect of Gi

A

Alpha – inhibits adenylyl cyclase

Beta/Gamma – Opens potassium channels

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52
Q

Downstreams of Gs

A

Gs.

alpha – Activates adenylyl cyclase

cAMP binds to regulatory units of PKA

activated PKA activates CREB causing CREB binding protein (CPB) to cyclic AMP response element (CRE)

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53
Q

Which G receptors is involved in fight or flight in muscle?

A

Gs

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54
Q

Downstream of Gq

A

alpha – Activates phsopholipase C

Breaks down PI(4,5)-biphosphate to inositol 1,4,5 (IP3) and diacylglycerol

IP3 opens calcium channels in ER

Calcium and diacylglycerol activates protein kinease C

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55
Q

How Ca++ is kept low in cell?

A

Exchangers

Ca++ pump

Ca++ binding

Ca++ import to mitochondria

Ca++ pump to ER

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56
Q

How cystolic calcium is changed?

A

Nerve terminal: Ca++ bidns to voltage-gated Ca++ channels

Cell: ligand binds, signal to release Ca++ from ER

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57
Q

Downstream of Golf

A

alpha activates adenylyl cyclase

cyclic AMP causes Na+ channels to open

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58
Q

Downstream of Gt

A

Light -> Activate rhodopsin -> Gt -> PDE -> less cGMP

Na+ channels close; so now the rod cell is hyperpolarized

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59
Q

How GPCR can be desensitized?

A

GPCR kinease phosphrylates GPCR

Arrestin binds to these phosphate

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60
Q

How many times does tryosine kinease passes through a membrane?

A

1

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61
Q

How is secondary messenger is connected with fight or flight response?

A

(Downstream of Gs)

cAMP activates PKA

PKA phosphorylates and activates glycogen phosphorylase that adds phosphate to glycogen and leads to breakdown of it to glucose-6P

PKA phosphorylates and inactivates glycogen syntahse by

62
Q

5 classes of RTK

A
63
Q

Subfamilies of RTKs

A

Epidermal growth factor -> EGF receptors

Insulin -> Insulin redcetpor

Insulin-like growth factors (IGF1 and IGF2) -> IGF receptor-1

Nerve Growth Factor (NGF) -> Trk A

Platelet derived growth factors -> PDGF receptors

Macrophage-colony-stimulating factors (MCSF) -> FGF receptors

Vascular endothelail growth factor (VEGF) -> VEGF receptors

64
Q

PDGF receptor (RTK)

A

Signaling proteins with SH2 domains bind to PO4-Y docking sites on an activated

65
Q

Insulin and IGF-1 receptor (RTK)

A

Have phosphorylated docking stations that bind proteins

66
Q

Ras Superfamily

A

Ras (relay signals from RTKs)

Rho (Relay signals from surface to cystoskeleton)

ARF (formation of protein vessicles)

Rab (regulate intracellular traffic)

Ran (regulates mitotic spindle)

67
Q

Activation and inactivation of Ras

A
68
Q

What can happen when tyrosine kinease receptors are phsophrylated?

A

Dimerize and autophosphorylate

Phosophates provide docking stations

Phosphates near kinease domain increases the kinease activity

Sometimes docking proteins might mediate signal (e.g. IRS-1)

69
Q

SH2 domain binds to

A

Tyrosine-(P)

70
Q

SH3 domain binds to

A

Poly proline regions

71
Q

What protein provides crucial link between receptor Tyr kineases and the downstream signaling cascades?

A

Monomeric Ras

72
Q

How Ras is activated?

A

RTK is activated

Adaptor proteins binds with SH2 to RTK and SH3 to Ras-GEF

Ras is activated

73
Q

Downstream effects of RAS

A

RAS -> MAP KKK (Raf) -> MAP KK (Mek) -> MAP K (Erk)

MAP K can be phsoporylated both on theorenine and tyrosine leading to specificity

74
Q

What binds to PH domain?

A

Phsophatidylinositol (PI) that can be altered by phosporylation (PIP2 and PIP3 by PI3 kinase)

75
Q

PI3 kinase signaling pathway: B cell activation

A

B cell receptor causes PI(4,5) to be phosphorylated to PI(3,4,5)

PI(3,4,5) binds to BTK that binds and activated PLC-gamma
PLC-gamma cleaves PI(3,4) to diacylglycerol and IP3

Clonal expansion

76
Q

PI3 kinase and Akt promote cell survival

A

PI(3,4,5)P3 activates PDK1

PDK1 and mTOR phosphorylates Atk

Atk dissociates from PI(3,4,5)P3 and inactivates Bad

Bad release apoptosis inhibitorty protein=

77
Q

Receptor is

A

–A protein that binds a neurotransmitter/modulator

–A protein that binds a small molecule

–A protein that binds another protein

–A nucleic acid that binds a protein

–A macromolecule that binds a drug

–A macromolecule that binds a toxicant

78
Q

Receptor Theory

The Hill-Langmuir Equation

A

(eq) D + R <–> DR ->> Effect

rate of reaction is proportional to the product of the concentration of the reactant

79
Q

Hill-Langmuir Equation

A

D+R<->DR

80
Q

Saturation Binding Isotherm

A
81
Q

Scatchard plot

A
82
Q

Concentration/Dose-Response Curves

Linear vs. SemiLog

A
83
Q

efficacy / Intrinsic activity

A

the relative maximal response caused by a drug in a tissue preparation

84
Q

Potency

A

how much of a ligand is needed to cause a measured change

85
Q

Types of receptors

A

Channel

G-protein

RTK

Intracellular receptor

86
Q

How attenuation can occur?

A

Refractoriness

Desensitization

 Down regulation

Tachyphylaxis

Supersensitivity

87
Q

Quantal Dose-Response

A

Describe population rather than single individual responses to drugs

all-or-none

death, pregnancy, cure, pain releif

88
Q

Graded Concentration-Response Curves

A

Inifinite number of intermediate states

vessel dialtion, blood pressure change, heart rate change

89
Q

Types of antagonism

A

Chemical: interaction of two drugs in solution such that the effect of active drug is lost

Physiological: Interaction of two drugs with opposing physiological actions

Pharmacological: Blockade of the action of a drug-receptor interaction by another compound

90
Q

Competitive Antagonists vs. Non-Competitive Antagonists

A

Competitive Antagonists

  • bind to same site on receptor as agonists
  • inhibition can be overcome by increasing agonist concentration (reversible)
  • primarily affect agonist potency
  • clinically useful

Non-Competitive Antagonists

  • bind covalently to same site as agonist (irreversible) or to a site distinct from that of agonist (irreversible or reversible)
  • inhibition cannot be overcome by increasing agonist concentration
  • primarily affect efficacy
  • limited clinical use
91
Q

Spare receptors

A

Pool of availible receptors exceeds the nubmer required for a full response

92
Q

Drug desensitization types

A

Recepotor mediated: loss of receptor function (fast); reduction of number of recetors (slow)

Non-Receptor Mediated: reduction of signalling, reduction of drug concentration

93
Q

Full agonist

Partial agonist

Inactive compound

Inverse agonist

A
94
Q

Sites of hematopoesis

A

Yolk Sac (Mesoblastic phase 2wk) +RBCs

Liver (Hepatic phase 6wk) +WBCs

Spleen (Splenic phase (2nd tri)

Bone Marrow (Myeloid phase 2nd tri)

Sternum, ribs and vertebra (Fatty replacement in long bones 20 yrs)

* Anemia can cause hematopoesis in spleen

95
Q

Where lymphocytes become immunocompetent?

A

T = Thymus

B = Bone Marrow

96
Q

Pluripotent vs. Progenitor vs. Precursor

A

Pluripotent - capable of differentiating into different types of cells

Progenitor cell - unipotent (committed to a particular cell line), and capable of self-renewal

Precursor cell - immature unipotent cell, not capable of self-renewal

97
Q

Stromal cells in bone marrow

A

fibroblasts, macrophages, adipocytes, osteoblasts, osteoclasts, endothelial cells, hematopoetic supportive stroma, osteocyte

98
Q

Formed elements

A

Blood

99
Q

Two blood cell lines

A

Myeloid & Lymphoid

100
Q

BFU

CFU

CSF

A

BFU=blast forming unit

CFU=colony forming unit

CSF=colony stimulating factor

101
Q

Erythropoesis

A

Epo secreted by Kideny

Both BFU-E and CFU-E are stimulated by epo to divide

CFU-E’s when stimulated mature into RBC precursors

Progenitor cells form spherical cluster around macrophages known as “nurse cells”

Macrophages phagocytize extruded red cell nuclei

Reticulocytes that are released into circulation mature in the blood stream

102
Q

Granulocytopoiesis

A

CFU for each cell line give rise to blasts
CFUs are stimulated to proliferate and differentiate by CSFs and other cytokines (chemical cell signals)

Granulocytes mature in the bone marrow in the hemopoietic cords

In cases of need such as infection the bone marrow will respond by releasing almost mature neutrophils(bands or stabs) into the circulation

Neutrophils will marginate to the inner wall of the blood vessels and quickly release when needed-allowing for a quick response in injury, inflammation

103
Q

Monocytopoiesis

A

Also arise from CFUs, when mature enter circulation for a short time until migrating into tissue to become macrophage

104
Q

Platelet formation

A

CFU>megakaryoblast>megakaryocyte 40-100 uM

Single multilobed nucleus can give appearance of being multinucleated

Located next to sinusoids in bone marrow and break off bits of cytoplasm into the circulation that break up into platelets

105
Q

Lymphocytopoeisis

A

Lymphocytes are derived from CFU-Ly stem cells>B or T CFU progenitors
B cells develop and become immunocompetent in the bone marrow

T cells develop in the bone marrow and become immunocompetent in the thymus

106
Q

Examination of bone marrow

A

Bone marrow: aspirate (cellular detail)
biopsy: (structure and ratios of cell populations)

Blood: peripheral smear obtained from a venous blood sample

107
Q

Structure of bone marrow

A

bony trabeculae

Stromal cells provide a supportive framework for islands of blood cells called hematopoietic cords to develop
Vascular channels provide nutrients and are where new blood cells enter circulation

Over time hemopoietic cords replaced with adipocytes

108
Q

RBCs charactersitics

A

no nucleus

no organelles

carbonic anhydrase

salmon pink biconcave discs
lipid bilayer supported by lattice of spectrin and actin

Carbohydrate chains on the membrane surface are the A and B antigens

Rh complex set

Increased surface area for gas exchange

7um

109
Q

Monocytes function

A

Monocytes circulate for a day or two and then enter tissue through postcapillary venules and become macrophages
Phagocytosis of cellular debris bacterial antigen presentation to lymphocytes

110
Q

Neutrophils function

A

Neutrophils migrate through post capillary venules to phagocytize and destroy bacteria
(this also kills the neutrophill)
Have membrane receptors for antibodies

Release substances involved in the inflammatory response

pus is an accumulation of dead leukocytes, bacteria, extracellular fluid

111
Q

Eosinophil function

A

Binding substances released by other inflammatory cells
Release substances to inactivate histamine and other inflammatory mediators

Destroy parasites

112
Q

Basophil function

A

Release granule contents that cause allergic reaction
Histamine>>leaky vessels, vasodilation, bronchial smooth muscle contraction

Interesting hypothesis not pertinent to this session: these cells may have a some point provided protection against certain kinds of venom (verbal opinion from an allergist)

113
Q

Platelets function

A

Damaged endothelial cells release substances promoting vasoconstriction and clotting including von Willebrand factor (vWF)
Platelets adhere to exposed collagen in basement membrane enhanced by vWF

Platelets are activated to degranulate and adhere to one another

platelets aggregated into a thrombus or clot

114
Q

What 2 factors play a role in mRNA stability and degradation?

A

Poly-A-tail and G-cap

eIF4G is connected to Poly-A-tail

eIF4E is conntected to 5’ cap

115
Q

Deadenylation nuclease (DAN)

A

) associates with the 5’ cap of the mRNA and then shortens the poly-A tail in the 3’ to 5’ direction

116
Q

Ribosome structure

A

80S

60S (2.8Mb) = 5S+28S+5.8S + 49 proteins

40S (1.4Mb) = 18S + 33 Proteins

117
Q

Translation initiation

A

eIF2-GTP associates with amnioacyl-tRNA and small ribosomal subunit

eIF4E/eIF4G comes with mRNA

ATP is hydrolized and complex searches for Kozak

Large subunit binds GTP is hydrolized

118
Q

EF-Tu

EF-G

A

eEF-1

eEF-2

119
Q

Post translational control

A

Proteolysis (non-reversible)

Folding

Adding functional groups

Structural changes

Processing

Removal of start methionine

120
Q

What are some hormone-induced cell responses that are mediated by cAMP?

A
121
Q

What is the difference between fertilization and gestation age

A

Fertilization age (embryology) counter after fertilization (38 weeks)

Gestational or Menstrual Age (OBGYN) counter after LNMP (40 weeks)

122
Q

Characteristics of Autosomal Dominant Inheritance

A

Recurrence 50%

Vertical transmission pattern

Equal males and females (usually)

Father to son is possible

123
Q

Autosomal Dominant

Heterozygote frequency

A

2q

124
Q

Autosomal Dominant

Familial Hypercholesterolemia

Related vs. nonrelated unaffected

A

Cannot determine related untested

Assume aa for unrelated untested

100% Cholesterol penetrance

Not 100% Cardiovascular disease penetrance

125
Q

Autosomal Dominant

Homozygous Recessive Assumption of uneralted individual

A

For the purpose of calculating recurrence risk asume that unrelated individuals are unaffected unless disease frequency is >1/20

126
Q

Characteristics of Autosomal Recessive Inheritance

A

Recurrence 25%

Horizontal transmission pattern

Equal males and females (usually)

Father to son is possible, consanguinity is seen

127
Q

Autosomal Recessive

Disease frequency

Carrier frequency

A

Disease frequency q^2

Carrier frequency 2q

128
Q

Autosomal Recessive

2/3 rule

A

Applies only when you know there is a possibility of homozygous

affected offspring, but the individual is not affected.

129
Q

Test to detect Cystic Fibrosis

A

Sweat chloride test

Measures Cl- concentration

130
Q

OCA1

A

tyrosine-negative albinism

autosomal recessive

131
Q

Characteristics of X-linked recessive inheritance

A

Female carriers

Males are hemizygous

No male to male transmissions

More males affected

132
Q

Examples of X-linked recessive inheritance

A

Hemophilia (1/10000) – clotting factor VIII (A) or IX (B)

Duchenne Muscular Dystrophy – (1/3500) dystrophin complex (die before reproduction age)

G6PD Deficiency – (1/10) [female carriers 1/5] Glucose-6-phosphate dehydrogenase low activity leading to anemia (by breakdown of cells) symptoms are observed after drug treatment (oxidative stress)

133
Q

Haldane Principle:

A

in a population with a stable disease frequency

rate of spontaneous new mutation = rate of loss of alleles

134
Q

Examples of X-linked dominant inheritance

A

hypophosphatemic rickets

135
Q

Characteristics of X-linked dominant inheritance

No skipped generations

Twice as many females affected

No male to male transmission

A
136
Q

Sex-influenced traits

A

pertaining to an autosomal genetic trait, such as pattern baldness or gout, that is expressed in both homozygotes and heterozygotes in one sex butonly homozygotes in the other sex.

137
Q

Exmaples of sex-influenced trait

A

Baldness (X-linked = androgen receptor , autosomal dominant sex-influenced = csome 20)

androgenic alopecia (AGA)

In men with reduced androgen levels (i.e. testicular injury), no baldness seen until treated with androgens

In females with elevated androgen levels (i.e. adrenal tumors), hair loss observed

138
Q

DNA extractio

A

Lyse cells, digest proteins and RNAs

Bind DNA (- charged) to + charged magnetic beads (low pH)

Wash beads containing DNA to remove contaminants (cell debris, membranes, proteins, RNAs)
Elute DNA from neutralized beads (high pH)

(Silica-based)

139
Q

Gender typing

A

AMELX (Amelogenin)

gene is present on X and Y chromosomes but different introns

140
Q

STRs vs. SNPs

A

SNPs used when DNA is degraded

SNP are less variable (paternal testing)

141
Q

Epigenetic processes

A
  1. Regulation of histone modification and heterochromatin formation.
  2. DNA methylation
  3. Genomic imprinting DNMT-1 transfer patterns of methylations to a newly synthesized DNA after DNA replication
  4. Gene silencing
  5. X-chromosome inactivation
142
Q

Antibiotics acting on Replication

A

Acyclovir:

Modified by viral thymidine kinease to become acyclo-GMP; it truncates DNA replication because it lacks 3’ OH

Actinomycin D

is an antibiotic anticancer drug that inhibits Pol

143
Q

Antibiotics acting on Translation

A

BACTERIA ONLY

Tetracycline (blocks A site)

Streptomycin (prevents initiation to elongation)

Chloramphenicol (blocks peptidyl transferase)

Erythromycin (binds exit and prevent elongation)

BOTH BAC AND EUK

Puromycin (premature release of chain)

EUKARYOTES

Cycloheximide (blocks translocation)

Aniomycin (blocks peptidyl transferase)

144
Q

Antibiotics acting on Transcription

A

BACTERIA

Rifamycin (binds to RNA Pol and prevent initiation)

BOTH BAC AND EUK

Actinomycin D (binds to DNA prevent movement of RNA Pol)

EUKARYOTES

a-Amanitin (bind to RNA Pol II)

145
Q

4 sites on ribosome

A

E

P

A

mRNA binding

146
Q

How does aminoacyl-tRNA synthetase ensures that right amino acid is connected to right tRNA?

A
147
Q

What is Kozak sequence?

A

A/G-X-X-AUG-G

148
Q

Hsp60

A

Molecular chaperone

149
Q

Hemophilia

A

(1/10,000)

(A; B is 1/10 as common); clotting factors VIII (A) and IX (B).

150
Q

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

A

African populations (10% of African American men)

X-linked recessive

An acute but self limiting anemia secondary to intravascular breakdown of red blood cells (hemolysis).

Hemolysis occurs in response to oxidative damage to the RBC.

Symptoms observed after treatment with certain drugs (anti-malarials or antibiotics), or after other stresses (infection).

Red blood cells lack a nucleus and ribosomes and cannot make G6PD after they are formed, so supply is limited. G6PD regenerates NADPH which regenerates reduced glutathione which protects cells from oxidative stress.

Block 1 (25 decks)

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