Class notes

Biomedical Sciences 2 lecture notes

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Course
Biomedical Sciences 2

Institution
The University Of Edinburgh (ED)

Topics:Cell communication, Body fluids, Synaptic transmission in the CNS, Chemical synaptic transmission, Nervous system, Data Analysis, Reproductive system , Respiratory system, Endocrine system

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Uploaded on May 15, 2022
Number of pages 78
Written in 2021/2022
Type Class notes
Professor(s) N/a
Contains All classes

bms2
biomedical sciences 2
biomedical science
bms
biomedical science 2
bms2 notes
bms2 lecture notes
bms2 summary notes

Institution
The University of Edinburgh (ED)
Education Unknown
Course
Biomedical Sciences 2

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Biomedical sciences 2 complete lecture summaries

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1. Class notes - Biomedical sciences 2 lecture notes
2. Class notes - Biomedical sciences 2 lecture notes (semester 2)
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BMSZ (semi)

2021/2022

,Principles
cell
of
communication

,CELL Lt +2
COMMUNICATION

L1

How do cells communicate ?

1) Gap junctions
soluble signals
for
↳ small

Allows communication without membrane
needing to
negotiate with plasma
↳ .

2) Free diffusion
↳
for hydrophobic molecules

3) Pumps / transporters / ion channels / vesicle fusion/fission / indirect
↳
far hydrophilic molecules

How are
signals released ?
1) Exocytosis (constitutive evoked release) or

↳
proteins, peptides, aa
,
nucleotides

2) Channels r
transporters ¢ or
e)
↓ ↓
↳ ions passive gated

3) Free diffusion (c)
↳ steroids,
gases

Forms
of signalling
PARACRINE

AUTOCRINE

SYNAPTIC signals highly concentrated @ synapse receptors
low-aqim.ly
→
are : .
are

ENDOCRINE →
signals get diluted @ blood : -

receptors are
high-affinity
GASEOUS (can bypass plasma mem .
+ receptors to activate enzymes directly inside )
cell

, L2

4 major types of receptors
v.
fast IONOTROPIC -

flow of ions across membranes down
dveousiongr .
A membrane potential
nicotinic Alk R
e)
.

fast METABOTROPIC / G- PROTEIN -
LINKED -

generate new
signals inside cell
(2ⁿᵈ messengers) regulate activity of
muscarinic Ach R ↓ ↓ membrane-bound
eg
a

tht
.

7- transmembrane a P 8
opioid R 3 subunits :
, ,
" """
target protein
domain structure
/\/ -

(enzyme channels
""
to receptor
to membrane
config or ion
+

to
-
GDP
a④
Upon ar
:
GTP attached instead 1) activation a subunit
of
-

2) release /8 subunits to target protein
g p
termination hydrolysis of
signalling by a-subunit
ATP GDP
of
: →

=

fast KINASE
modify existing molecules to
generate signals (are enzymes usually) + can also control
-

new

gene transcription
autophosphorylation ↓
ligand binding FÑÑÑaÉ
mum
themselves enzyme activity
is inside the cell

creates additional interaction sites

for more recruitment o
phosphorylation

amplify their
signal via a series
of phosphorylation reactions

termination of phosphatases
signalling
:

=

ligand binding
required for can bind

NUCLEAR/
DNA
binding
without
ligand
↓ ↓
slow STEROID -

change expression of genes ( in
cytosol or in nucleus
)

steroid hormones,
thyroid hormones , retinoids ,
✓ it -
D
( aka meat, hyE signals) freely diffuse
membrane → bind to intracellular receptors this activation
regulates transcription of genes
across →
directly
activated within 30min
1° response =
specific genes
other activated
2° response genes
=

, Same have tors
divergent effects
signal can :

↓
their location have different
is
affinities
hey to the
physiological for ligands
response

L3
Difference in
fingerprints between identical twins . : one
piece of anatomy cannot be

determined
by a
b¥nt

kidney intermediate
mesenchyme
L >

embryonic origin metanephwgenic mesenchyme urelewc bud
:
+

↓ ↓ [branching]
nephron collecting duct
how this
branching
is

controlled ?
test this L
by looking for Hypothesis :
cells around UB

pins AND
mathers that ⇐ (mesenchymal cells) secrete

are in the
right place for this a
signalling substance
UB

I

④ UB grind to
express net & MM to express INF } Ret / ADNF
signalling
↓
antibody binding
to GDNF to
test to / GDNF
Ret
by interrupting
→
the prevent its binding
neay for branching regulation
see
if
is
signal to net

+
beads
agarose
soaked in
test to see
if Ret/ a DNF is
Ñt for branching regulation by introducing an ectopic signal
→
daooenentats
(replace ADNF)

and
placing
r

them in close

proximity to a v

early tube .

, by experimental
same

/ processes
Other discovered that communicate to UB where /when it should
signals elongate
:

"

BMP2
"
-

keep out

BMP 7
" "

go straight
-

BMP4
"

TGF,
"

elongate
-

,

~

How do branches not
tangle ?
(horrid )
i

hypothesised Self loathing
'

Égqg
-
: -
model :
UB secretes a substance whose cone .
directs

branching direction
(towards least [horrid])

Experimental model :
culture
kidneys aimed at one another before adding various test
drugs
I
BE found to be a
¥sne signal (made
from
U
B)

How do MM to waste cells ?
cells sense when MM condensates are
large enough to
fam a nephron or not be too large

↳ sÉsmgsystemw) Wnt
a
quorum -

Quorum →
4 autocrine
signal within
sensing
=

no MET

÷÷÷÷É;É÷
MM that
nurse : propagates
✗ -1 -

mass wntl,
mesenchymal aggregation
•

÷÷%%%
o o

7
•
; I
,

f
°

@nt 4] threshold reached
o
o
°
•
if
¥É¥¥ :
o o o o
o > > Control
8. % go
.
°
o
renal vesicle RV) starts to
(
differentiate into nephron .

°
J o
o

+
> Li
¥1
•

; .
too
gew Lit =
illusion
of Ñ[Wnt4]
cells

Emergence the presence
of properties
at
system level that not present at component level
-
-
are

(Eg branching tree not present in cells but
)
emerged during developing organ

,L4

Drug
a chemical that produces
biological effect when given to
living organism
~
a a

}
→ structure must be know

→
FDA definition
not a nutrient

Medicine contains its components
drugs as one
of

Drug action is selective +
specific
↳ absolute however
specificity is never

(drugs often interact with +9 protein targets side
effects)
-
k -
i receptors
LIGAND t RECEPTOR LIGAND / RECEPTOR COMPLEX
^
k +1

¥%
Equilibrium constant (k ) ,
=

quantifiable measure
of affinity measured
by ftp.?y?-
K
☒É
'

n
aˢˢʳiaHcnrate_
-

KD =

KI
=

dissociation rate
(lug )
scale

÷:;H
• that
receptors

k☐ =

KD 50% og receptors occupied
ligand
=
conc .
at which are

The
higher ligand (
the K →
the the the
smaller
, affinity of as
@my]
less is required
to
occupy
50% q receptors )
Beland.pe#eptor-cupan-oy-ofoeot-
Most
frequently it is the effect to a of
"
a
drug (Aao Nist)
that is
quantified and not
Cigand]
↳ "

guinea pig
-
ileum
,
receptors in
gut practical .

, drug Che
The effect to administration
of
a
functional response) is
usually
not
directly proportional
to receptor
occupancy
responses of the
aha same
occupancy
evokes
different drug .

eg .

Due to this :
the [agonist] at 50% response ≠ K,

The effective dose at which response =
50% of Max . (ED )
so
is nevertheless useful as it allows

comparison of the potency of duooerent drugs .

Efficacy ~
the
ability of agonist
to
an elicit an
effect once bound to receptor

Drug A efficacy Drug B
>

Antagonists
have
affinity and
zeweqgicacy (only agonists have
efficacy)
^ competitive reversible
antagonist

[
,

response

competitive , irreversible antagonist
.y

Allosteric modulators receptor fue
alters action
of agonist by binding to an site neutral
ve

accessory
-
-
on -
or
,

(
allosteric
modulation
no
effect in absence of
agonist

, NiiÑeptc
1) ligand-gated ion channel
(agonist binding allows rotation
of pore
-

lining region →
opening gate

Has 2
binding sites

both with
rely charged Glu Asp aa residues → interact with +ve trim
ethyl ammonium components
-
- +

Ach
of .

-

have polar residues → coordinate rest
of molecule these interactions
form basis of
affinity
not identical however
affinity
-
→ As in

Muscarinic Ach receptor

2) a protein -

coupled
its
binding site
is v.
different from (1) but still has high aqginity
-

D-mytargets #targets)
# RECEPTORS

- 10N CHANNELS (blockers
↓
or allosteric
modulators
local
ey anaesthetics

°Ñ ENZYMES (inhibitors , false sybstrates or
pro
-

drugs)
\
abnormal inactive -→ active
produce
reaction product

☒= TRANSPORTERS (inhibitors or
false substrates
(for non -

lipid hydrophilic )
, \
leads to accumulation

of
abnormal compound

, Body
Fluids

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