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HISTOLOGY LAB

QUESTIONS, COMMENTS PLEASE EMAIL

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WC-101

Manhattan, MSG

The Iranian- Firouz Naderi, Ph.D. A NASA Scientist

http://www.searchles.com/links/show/id/323860

Scott's Resources

Hi all,

Just a reminder that we have a (completely optional!) lecture tonight.  Topics I'll try to cover include SNP genotyping (as in, how do they figure out which SNPs you have?), some cloning, and the use of enhancer traps, a technique we briefly discussed in the material on Fbx15.  Again, the lecture is optional, and will not affect your grade.  I will not have the final exams to pass back... if you want your final exam returned, I will pass them back in the second week of the 355 course I run in the summer.  Semester grades should be complete by this Friday.

A few other things...  Some have asked for good sources of information on biology.  I would recommend sciencedaily.com, which does an excellent job of explaining complicated research findings in a comprehensible way.  

I would also suggest a subscription to Science magazine, one of the preeminent science journals in the world.  The magazine provides both original research papers and multiple reviews that are accessible to "non-experts".  

https://pubs.aaas.org/org_membership/new_member_setup.asp

An undergraduate subscription is $75 a year, only $1.50 per weekly issue... less than half the cost of a venti latte at Starbucks.

Finally, if you haven't registered to vote in the fall, it is VERY easy to do... the form, which takes five minutes to complete, is online.

http://www.sos.ca.gov/elections/elections_vr.htm

The only way that issues which are important to you will be addressed is if you VOTE.  Go register!  Do it!  :)

Have a great summer,
-sw

Histology Notes 4/17/08

HISTOLOGY THURSDAY  4/17

Three gland adrenal thyroid and panrcreas

adrenal gland ( suprarenal gland) endocrine gland

two glands in one ( gland in center – medulla) edge-cortext separate endocrine glands

hormones they secrete is very different

Adrenal medulla ( Epinephrine (20%)/NeuroEpi(80%))

alpha and beta receptors ( heart Beta Recetor ( epinephrine) increase H.R. and contractibility

cortex secretes steroids equal amounts in females and males

 

steroids- Mineralocorticoides (aldosterone)→ regulates kidney increase Na reabor and sodium excretion

 

glucocorticoide ( cortisol/ corticosterone)

sex hormones ( all steroids)

different types → androgen( increase sex character)

 

CT capsule outside covering with dots

cortex three zone middle is the largest very verticles

medullary cords

cells of 2/3 of cortex

notice the circulation vessels coming into the surface

figure 20-11

hormones from the cortex pass through the medulla

medullary artery

tropic hormone ( stimulate other hormones-anterior pituitary)

receptors for the ACTH peptide ( surface receptor) signal transduction and the cell makes steroid.

cortisol negatively feed back ( only)

inhibits ACTH

aldosterone →kidney salt sweet in the middle like insulin (cortisol) plasma glucose

androgen as the

figure 20-15

disease s

hyposecretion( ectomy removal) hypophosectomy ( atrophy) smaller

stress → activity of the cortex

 

medulla different kind of cell

no T. M.

Rough ER, Golgi present

secretory granules.

no stored hormones in cortext

tyrosine ( transporter)

hormones

stimulus for releasing hormones( sympapathic) preganglionic cell

cholinergic nerve ending

postganglinic neuron cell by itself

 

THYROID

infront of the treacha

adam’s apple

along the trachea

palate very soft

can be check for cancer- arise in the thyroid often

gland itself when radiated ( radioactive I) can cause cancer

parathyroid( posterior) four bundle of the tissue

very well vascularized

ball of cells- follicles

pars intermedia of the pituitary

entire gland is made up of follicles

Colloid (describe protein)

parafollicular cells along side of the follicles (T3-T4)

para- Calcitonin ( lowers ca2+)

PTH( parathyroid hormone raises plasma calcium)

Thyroid diseases ( graves disease) well known hyperthyroidism autoimmune disease- auto anti-bodies stimulating the thyroid gland as if they were pitatary hormone ( TSH)

more T3 and T4 increase in follicular growth

 

Pathology ( Hashimoto’s thyroditis autoimmune hypothyroidism

follicle rising in the tissue massive inflammation of thyroids

synthesis- follicular cells colloid is on top

starting is amino acids (fig20-27)

hormone exocytose in the

thyroglobulin

when the cel

cleavage of  the large protein

puts them together T3 and T4(four iodides tyrosine)

parathyroid glands

laryngeal nerve (thyroid cancer)

prevention of phonation( speaking)

brown deposit of sec reaction calcitonin positive (parafollicular cells)

 

PANCREAS

B cells insulin

A cell glucogon

USMLE step 1

Provided by Foad N.

More Histology

Click here for more histology 

provided by Paul L.

Email Problems

There has been problems with current email address for the blog. it is now updated and ready to go. please email any questions you have. 

Seminar-Cancer Biology

More O-CHEM help

www.chemhelper.com

www.chemistry.msu.edu

chemistry2.csudh.edu/rpendarvis/index.html

more Genetics

OFFICE HOUR:

Monogenic diseases

polygenic what would they look like in the pedigree

two genes homework

example of two traits in the pedigree

three point crosses

three genes map them for drosiphila

coeffinient of map units

interference strength

centromere inhibit cross over opposite of centromere

no chi square

•            centromere inhibit cross over

inhibit crossing over between them – closer together

Dna preventing from the normal amount of crossover

distinction between the physical map and the genetic map

not always the same

how mayn letter between these letter

how much cross over happened in these genes

use the genetic map to imply the physical map

over 50 physical map units

70 ph apart how much recombination( 50%)

50 or greater independent

physically linkend but not genetically linked

certain part of chromosomes more than you expect

some DNA doesn’t cross over that much

 

each human is couple of physical map

chromosome 1 2 3 800 map units

 

prions tertiary form

sporatic CJD

primary – 

seconday X alpha sheet

tertiary huge difference in the structure

 

FFI all of the above ( same gene PRNP human gene) specific mutant allele

 

varient / seconday and tertiary

 

sporatic goes to abnomal without environmental

 

enviromental factors

 

CDC

 

Genetics?!

I have been asked to put up some of the Genetic notes we are covering for the midterm next week. It could also be a good review for those Taking any kind of admission test.

Genetics Monday 4/7/08

cancer

second to heart diease

differences who get cancers

breast cancer local tumor-

distant tumors- single location rate goes down

liver cancer—> dead

metastesize

genetics differences between cancers

melanoma-

darker skin is protective against mutagen.

cancer strikes when older

Gene- Restinoblastoma cancer of the eye

how do get cancer?

two hit model for cancer prevention genes

diploid we have to copies

inheritance of the bad copy

mutant for being RB much more chance to get the cancer

only one mutation to lead you no functional copies of RB

nondisjunction

two copies identical

mitotic recombination

simple point mutation

only one functional copy

one mutation to get rid of the functional copy of the RB

gene conversiotn when chromosome- recombination

cross over

single stranded tail of one of the chromosomes

two overhanding strands of tails

one of them invades the double stranded blue chromosesm

replaces the second strand of blue chromosomes

 

end result: cross over one green one red hamlet

DNA mismatch

hybrid molecule

randomly picks

gene conversion three copies of little a allele

gene conversion

mitotic recombination uses the mechanism

section 6.5

mismatch repair

RB Minus homozygous

can proliferate and become the tumor cell

cancer cells character

six specific

almost all cancer cells

sustained angiogenecis- tumor forms induce blood vessel growth need o2 inducing blood vessel growth

Evading apoptosis- if picking up too many mutation- cell suicide cancer

self sufficen in growth signal- produce their own growth signal or become efficient

Insensitivity to anti- growth signal- uncontrolled have to ignore the signal

tissue invation and metastatis- cells can move on and mestastize

limitless replicative potential- when chrom replicated- shorter- too short → apoptosis

cancer cell bypass

how cancer cell avoid to shut cell of that proliferate

what about stem cell- many more division

growth factor recepters- ligands- downstream will get activated.

cancer cell can pick up mutation

ligand independent factors

GFR mutation

Autocrine signaling self sufficient for growth signals

insensitive to anti growth signals

contact inhibition- stop dividing when contacting cell closely.

ignore apoptotic signals

loss of cell adhesion free from tumor to go to other places. Junctions have to be lost- you can go to metastesize.

ability of the cell to divide forever.

everytime cell divided

Telomerate-TERT functional unit- adds DNA to the ends of chromosomes after replication- so you can compensate- telomere sequence.

tert is only on germ line (active)

cancer cells – turn on the enzyme that should not be on

limitless replicational potential

abornomal production

how does telomerase do this trick

protein and nucleic acid that it carries- bind to the end of the chromosomes

cell has gone through the dna replication

DNA POLYMERESES

Uses RNA template

To bind to the end \

uses the temp to fil the strand of DNA

hopp farther down

Does it put the right sequence- it’s the right sequence

no multiple telomerase

Linear chromosomes which al the genes are in the middle of the chromomes

not disrupting the genes

how cells die – shorttend the DNA into the gene

structure of the telomerase

only cell in the body cell germ line and any cancer cells

angiogenesis- six characteristics

induce the formation of more blood vessels. Produce blood vessles

signal that promote angiogenes

VEGF recepter epithial cells that produce positive signal

induces the endothilal cell to produces blood vessels

DLL4 negative signal

prevent blood vessel growth blood vessel formation

balance Between DDL4 and VEGF that bring actual blood vessel growth

where does the signals come out?

Tumor cell also has the transmembrane

localize DLL4 signaling

Form blood vessles in the direction you need

lot of drugs againt angiogenesis

entirely body reforming making

total angionesis

blood supply to tomor and also other places in the body

VEGF stops all angiogenesis

PIGF – placental and tumor cells

next big question

six charachteristics

order of the mutations

does It have to have the mutation?

mutaiton that can happened later for tumor become fully capable

no specific order of mutation that can

cell divisiton picks up mutation

cell contiues to replicate

1st 2nd 3rd and forth

point- aquiring increase the rate at which the cell prolifereate

early mutation make the cell divide to much to make the cell incapable of

more cell proliferation necessary for the cancer

liver cancers have different histology

color cancer

one cell picks of mutation APC gene slightly changed morphology

third mutation

P53

Invasive carcinoma

Loss of p53

pick up mutation when loosing the chromosomes

tumor cell from HENritetta Lacks

HELA cells

some of the biopsy- peti dish with nutrients

cancer cells pick up mutation could grow in dish when they have food

cervical cancer cells

1st cancer then live in the dish

used for biomedical research

how do translation, cell cycle and polyvaxyly

Biomedical ethics

jhu.edu

normal karyote for the cell

spectral karyotype

each chromosome different color

two greens

Cancer is not just gene mutation

genomic stablitly – massive

Cancer genes are not just mutated

unstable genome and cell mutation we will study

all chromosomes are stained- all karyote

all different number of copies

bladder cancer        

 

 

 

Genetic workshop

3 point cross

pen vs ept

mutation

Robertsonian translocation

Mitochondrian

Prions

Sup35

RB

Gene conversion

Cancer

Penetrance/ expressivity

Low penetrance

Autosomal or sex linked dominant or recessive

Mitochondirail inheritance

Sons don’t pass it down along

What are the type of mutations,:

Neomorph

Anti

Hypo hyper

Haploinssuficeint

Null

Gene shorter links hypermorph shorter legs

Look at what the gene does

Null non functional

Phenocopy- xzavior same phenotype as the genetic disease but not caused x indivdual genetics

Multfactorial- breast cancer

BROC1 and 2 cancer prevention genes only for breast cancer

Balanced and unbalanced robersonian translocation

High penetrance 100% everyone would have it.

Low penetrance : 3 or 4.

Meiotic nondisj in 1 or 2

Anaphase 1 and 2 and know the number of chromosome

Monosomy and trisomy and look at the diagram

Down syndrome

Retinoblastome CML chronic myologenis leukemia

No viability too much of 14 or too little of 14

Mitochondrial diseases

Cardiac muscle lots of mitochondria more atp is needed

Any tissue that requires mitochondria

Inheritance in yeast

Heterplasmic some good some bad

Retinablastome multifactorial

Gene conversion

Mismatch big a A

Invasion of single stranded DNA into double stranded DNA

Holiday junction

Tertiary possible every cell division

Gene conversion

Exceptional female white

She had three six chromosomes

Number of X

1 x male

3x female

XYY dead

XXY exceptional female

Two while eyes XW x XWy

No XXY

No XX

78 c

88 B

106 A

PRIONS- Transmissible spongiform

protein based system

how proteins strucuture formed

1st primary structure

3r structure folder

how protein folds

intermediate lower energy-> folded lowest energy

intermediate final structure stable conformation stable not  final

can interchange with the intermediate

prions- diff kind based on the proteins gnene PRNP

wildtype C structure

second structure that is stable but no biologically active

alpha hecices into beta plated sheet ( orginal more alpha helices)

what is happeing with prion shaped proein?

PRPSC abnormal shape good +bad ---> bad shaped

SC abnormal

PRNP- prions are normal

in human is callye PRNP

abnormal can cause disease, getting rid of PRPC

Kuru epidemiology

women were effected

incubation period

******* no nuclide acid in the aget virus RNA genone

enzyme that disovler

conclude infections protein

cruetzelf jakon disease

@@@@@@@@@@@@@

prions resistance to protease- to get rid of misfolder protein

most protease activity ( mostly resistant)

sporatic

acquired – envirinment

familia

varient- eating food contaminated with prions

CJD- Cruetzfield jakob diseasel

different infection- propagation- and disease properties

heterozygous- different allele (2) rate dramaylly slowed down

human prion progien is compsed of 253 amino acids. There are two common allele which inserts valine or methionine at postion 129

Beiing heterozygous

M and V allele

differner race of people

mouse prions

IE not internet explore

Insuff

hamster- hamster E

hamster – mouse IE

Hamter- mouse that makes the hamster prions- E

trans mouse- mouse IE

--->E

mouse – hamster IE

mouse mouse E

Mouse – mouse trans IE

trans mouse – hamster IE

mouse trans ( hamster gene ) and got prions can pass to another mouse

prions are very noninfections across species barrier

but environment of prions

history where it was formd? Org? can effect prion shape.

multiple misfolded, disease causing conformations

familia fatal insominia FFI

PRNP gene allele misfolded prion gene

thalamus FFI attacks thalamus

FFI single mutation in Amino acid 178

chronic wasting diease

CWD in deer infectionous

yeast

sup35

truncated adenine systnths enzyme made

non sense suppression eveyatal substition o f an amino acid

Sup 35 yeast prion gene – prion like confirmation and aggregate= cant act at stop codon.

Molecular for aggression of the prions

 structure for the shape when the prions are aggerateion of htat protein

 cannont function when it aggeratge

what was the point>?

point to prove proein folding problem

misfolded protein

adenine biosysyteh.

sub35 fuction- recognize the non sense in the middle of the gen ewe get the trunked version whcihc is red

induce the prions shape of the j

prion with yeast. Sub35 no longer function when

adenine biosynthesis gene.

white non function sup35

GnHCL cause protein folidng aloow refolding

guanine hydrochloride

unfold all the prions and let them refold majority

precurser build up when you make the truncated enzyme.

5mM G