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
What is important about dermatomyotome location?
Each dermatomyotome retains its own segmental innervation from its origin
26
Intermediate mesoderm
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.
27
Cephalocaudal Folding
Rapid head and tail growth causes the embryo to curl toward the ventral surface
28
Lateral Folding
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
29
What cavities are formed from extraembyonic celoem?
intraembryonic cavity Thoracic and abdomainal cavity
30
Lateral Plate Mesoderm
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
31
In which location lateral plate mesoderm does not split?
Head
32
Endoderm Derivatives
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
33
Pharmacology definition
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.
34
Pharmacology subcategories
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.
35
Pharmacy definition
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.
36
Drug names
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.
37
Who is responsible for regulating laws regarding drugs? How?
FDA Right to regulate, recall, and safety aleart
38
Drug Discovery Map
39
Initially Drug Discovery Process
(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
40
Investigational New Drug (IND)
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
41
Phases in human testing
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
42
Items that need to be completed in order to receive license for a new drug.
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
43
GLP
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.
44
Why G proteins are important?
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
45
How many transmembrane folds are in GPCRs?
7
46
How G-protein is activated?
Signal molecule binds to GPCR Alpha subunit is phosphorylated It dissociates from beta-gamma complex
47
Types of GPCRs
48
Functions cAMP, cGMP, and Ca2+
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)
49
How does Vibrio cholerae affects intestinal cells?
Locks GPCRs in active state
50
How does Pertussis toxin (*Bordetella pertussis*) affects respiratory cells?
Inactivates Gi protein leading to cAMP overproduction Produces uncontrollable, violent coughing
51
Downstream effect of Gi
Alpha -- inhibits adenylyl cyclase Beta/Gamma -- Opens potassium channels
52
Downstreams of Gs
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)
53
Which G receptors is involved in fight or flight in muscle?
Gs
54
Downstream of Gq
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
55
How Ca++ is kept low in cell?
Exchangers Ca++ pump Ca++ binding Ca++ import to mitochondria Ca++ pump to ER
56
How cystolic calcium is changed?
Nerve terminal: Ca++ bidns to voltage-gated Ca++ channels Cell: ligand binds, signal to release Ca++ from ER
57
Downstream of Golf
alpha activates adenylyl cyclase cyclic AMP causes Na+ channels to open
58
Downstream of Gt
Light -\> Activate rhodopsin -\> Gt -\> PDE -\> less cGMP Na+ channels close; so now the rod cell is hyperpolarized
59
How GPCR can be desensitized?
GPCR kinease phosphrylates GPCR Arrestin binds to these phosphate
60
How many times does tryosine kinease passes through a membrane?
1
61
How is secondary messenger is connected with fight or flight response?
(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
5 classes of RTK
63
Subfamilies of RTKs
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
PDGF receptor (RTK)
Signaling proteins with SH2 domains bind to PO4-Y docking sites on an activated
65
Insulin and IGF-1 receptor (RTK)
Have phosphorylated docking stations that bind proteins
66
Ras Superfamily
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
Activation and inactivation of Ras
68
What can happen when tyrosine kinease receptors are phsophrylated?
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
SH2 domain binds to
Tyrosine-(P)
70
SH3 domain binds to
Poly proline regions
71
What protein provides crucial link between receptor Tyr kineases and the downstream signaling cascades?
Monomeric Ras
72
How Ras is activated?
RTK is activated Adaptor proteins binds with SH2 to RTK and SH3 to Ras-GEF Ras is activated
73
Downstream effects of RAS
RAS -\> MAP KKK (Raf) -\> MAP KK (Mek) -\> MAP K (Erk) MAP K can be phsoporylated both on theorenine and tyrosine leading to specificity
74
What binds to PH domain?
Phsophatidylinositol (PI) that can be altered by phosporylation (PIP2 and PIP3 by PI3 kinase)
75
PI3 kinase signaling pathway: B cell activation
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
PI3 kinase and Akt promote cell survival
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
Receptor is
–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
Receptor Theory The Hill-Langmuir Equation
(eq) D + R \<--\> DR -\>\> Effect rate of reaction is proportional to the product of the concentration of the reactant
79
Hill-Langmuir Equation
D+R\<-\>DR
80
Saturation Binding Isotherm
81
Scatchard plot
82
Concentration/Dose-Response Curves Linear vs. SemiLog
83
efficacy / Intrinsic activity
the relative maximal response caused by a drug in a tissue preparation
84
Potency
how much of a ligand is needed to cause a measured change
85
Types of receptors
Channel G-protein RTK Intracellular receptor
86
How attenuation can occur?
Refractoriness Desensitization Down regulation Tachyphylaxis Supersensitivity
87
Quantal Dose-Response
Describe population rather than single individual responses to drugs all-or-none death, pregnancy, cure, pain releif
88
Graded Concentration-Response Curves
Inifinite number of intermediate states vessel dialtion, blood pressure change, heart rate change
89
Types of antagonism
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
Competitive Antagonists vs. Non-Competitive Antagonists
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
Spare receptors
Pool of availible receptors exceeds the nubmer required for a full response
92
Drug desensitization types
Recepotor mediated: loss of receptor function (fast); reduction of number of recetors (slow) Non-Receptor Mediated: reduction of signalling, reduction of drug concentration
93
Full agonist Partial agonist Inactive compound Inverse agonist
94
Sites of hematopoesis
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
Where lymphocytes become immunocompetent?
T = Thymus B = Bone Marrow
96
Pluripotent vs. Progenitor vs. Precursor
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
Stromal cells in bone marrow
fibroblasts, macrophages, adipocytes, osteoblasts, osteoclasts, endothelial cells, hematopoetic supportive stroma, osteocyte
98
Formed elements
Blood
99
Two blood cell lines
Myeloid & Lymphoid
100
BFU CFU CSF
BFU=blast forming unit CFU=colony forming unit CSF=colony stimulating factor
101
Erythropoesis
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
Granulocytopoiesis
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
Monocytopoiesis
Also arise from CFUs, when mature enter circulation for a short time until migrating into tissue to become macrophage
104
Platelet formation
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
Lymphocytopoeisis
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
Examination of bone marrow
Bone marrow: aspirate (cellular detail) biopsy: (structure and ratios of cell populations) Blood: peripheral smear obtained from a venous blood sample
107
Structure of bone marrow
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
RBCs charactersitics
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
Monocytes function
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
Neutrophils function
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
Eosinophil function
Binding substances released by other inflammatory cells Release substances to inactivate histamine and other inflammatory mediators Destroy parasites
112
Basophil function
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
Platelets function
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
What 2 factors play a role in mRNA stability and degradation?
Poly-A-tail and G-cap eIF4G is connected to Poly-A-tail eIF4E is conntected to 5' cap
115
Deadenylation nuclease (DAN)
) associates with the 5’ cap of the mRNA and then shortens the poly-A tail in the 3’ to 5’ direction
116
Ribosome structure
80S 60S (2.8Mb) = 5S+28S+5.8S + 49 proteins 40S (1.4Mb) = 18S + 33 Proteins
117
Translation initiation
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
EF-Tu EF-G
eEF-1 eEF-2
119
Post translational control
Proteolysis (non-reversible) Folding Adding functional groups Structural changes Processing Removal of start methionine
120
What are some hormone-induced cell responses that are mediated by cAMP?
121
What is the difference between fertilization and gestation age
Fertilization age (embryology) counter after fertilization (38 weeks) Gestational or Menstrual Age (OBGYN) counter after LNMP (40 weeks)
122
Characteristics of Autosomal Dominant Inheritance
Recurrence 50% Vertical transmission pattern Equal males and females (usually) Father to son is possible
123
Autosomal Dominant Heterozygote frequency
2q
124
Autosomal Dominant Familial Hypercholesterolemia Related vs. nonrelated unaffected
Cannot determine related untested Assume aa for unrelated untested 100% Cholesterol penetrance Not 100% Cardiovascular disease penetrance
125
Autosomal Dominant Homozygous Recessive Assumption of uneralted individual
For the purpose of calculating recurrence risk asume that unrelated individuals are unaffected unless disease frequency is \>1/20
126
Characteristics of Autosomal Recessive Inheritance
Recurrence 25% Horizontal transmission pattern Equal males and females (usually) Father to son is possible, consanguinity is seen
127
Autosomal Recessive Disease frequency Carrier frequency
Disease frequency q^2 Carrier frequency 2q
128
Autosomal Recessive 2/3 rule
Applies only when you know there is a possibility of homozygous ## Footnote affected offspring, but the individual is not affected.
129
Test to detect Cystic Fibrosis
Sweat chloride test Measures Cl- concentration
130
OCA1
tyrosine-negative albinism autosomal recessive
131
Characteristics of X-linked recessive inheritance
Female carriers Males are hemizygous No male to male transmissions More males affected
132
Examples of X-linked recessive inheritance
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
Haldane Principle:
in a population with a stable disease frequency rate of spontaneous new mutation = rate of loss of alleles
134
Examples of X-linked dominant inheritance
hypophosphatemic rickets
135
Characteristics of X-linked dominant inheritance No skipped generations Twice as many females affected No male to male transmission
136
Sex-influenced traits
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
Exmaples of sex-influenced trait
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
DNA extractio
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
Gender typing
AMELX (Amelogenin) gene is present on X and Y chromosomes but different introns
140
STRs vs. SNPs
SNPs used when DNA is degraded SNP are less variable (paternal testing)
141
Epigenetic processes
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
Antibiotics acting on Replication
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
Antibiotics acting on Translation
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
Antibiotics acting on Transcription
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
4 sites on ribosome
E P A mRNA binding
146
How does aminoacyl-tRNA synthetase ensures that right amino acid is connected to right tRNA?
147
What is Kozak sequence?
A/G-X-X-AUG-G
148
Hsp60
Molecular chaperone
149
Hemophilia
(1/10,000) (A; B is 1/10 as common); clotting factors VIII (A) and IX (B).
150
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
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.