slide on excitation of skeletal m

Excitation of skeletal muscle contraction
Events occruing after action potential reached the terminal nerve
calcium channel opens
influx of calcium ions
calcium serve as attractant to the vesicles
fusion of vesicles to the neural membrane
release of actylcholine by exocytosis
acetylcholine opens the acetylcholine gated channel
effects of acetylcholine
acetylcholine attaches to the channel
conformational change open the ionic channel
allows Na ions to pass thru the channel
creates an end plate potential
excitation of the skeletal muscle fiber
destruction of acetylcholine
acetylcholinesterase
diffusion out of synaptic cleft
its removal prevents muscle re-excitation
safety factor for the transmission at the nmj
Each impulse at the NMJ is 3-4 times as much end
plate potential needed to stimulate the muscle
fiber - high SAFETY FACTOR

Stimulation greater than 100 times/sec. for several
mins. diminishes the number of vesicles at each
impulse – FATIGUE
drugs that affect transmission at the nmj
A. drugs that stimulate the muscle fiber by
acetylcholine-like action
1. metacholine
2. carbachol
3 nicotine
-difference is they are not destroyed by
acetylcholinesterase
-prolonged action can cause: SPASM
B. drugs that block transmission at the NMJ
curareform drugs – D-tubocurarine

- competes with actylcholine for the receptor sites
- prevents passage of impulse from endplate into the
muscle
C. drugs that stimulate the NMJ by inactivating
acetylcholinesterase
1. neostigmine
2. physostigmine
3. diisopropyl fluorophosphate
- inactivate cholinesterase at the synapses
- accumulation of acetylcholine
- can cause repetitive stimulation of muscle fiber
§ MUSCULAR SPASM
Myasthenia gravis
Paralysis is due to inability of the NMJ to transmit signal
from nerve to muscle fiber
Pathology: antibodies attack the acetylcholine-gated
transport protein
Patient may die of paralysis of respiratory muscles
Treatment:
neostigmine
Allow acetylcholine to accumulate
Excitation contraction coupling
action potential will have to penetrate all the myofibrils
transmission of the action potential from surface to myofibrils
is facilitated by transverse tubules
T tubule action potential cause the sarcoplasmic reticulum to
release calcium ion
Calcium ion then diffuse to the myofibril and binds with
troponin C
calcium pump
Muscular contraction will continue as long as the calcium ions remain high in concentration in sarcoplasmic fluid
Calcium pump -pumps calcium back the sarcoplasmic tubules
Calsequestrin - can bind calcium over 40 times

micropatho

You need to understand the immune system its classification and how it works. Then review your understanding of the hemodynamics of the microcirculation at cellular level. good luck

To live longer, drink and exercise

Drinking is healthy,
exercise is healthy,
and doing a little of both is even healthier,
Danish researchers say

A study done on 12,000+ individuals followed up for 20 years . Moderate drinkers with moderate exercise are 30% better off in their survival than teetotallers.

People who had the lowest risk of dying from any cause were physically active, moderate drinkers while those at highest risk were the physically inactive, heavy drinkers, the study found.

http://uk.reuters.com/article/topNews/idUKL0871640820080109?
feedType=RSS&feedName=topNews

what is moderate drinking, what is moderate and vigorous exercises?
http://www.newsmax.com/health/drinking_exercise_keys/2008/01/09/62932.html

viral infection- a parasitic infestation

This is not sea urchin.

This is Human immunodeficiency virus.Viruses in general unlike bacteria are packages or capsules of genetic material.

They require living hosts — such as people, plants or animals — to multiply and survive.

When a virus enters your body, it invades some of your cells and takes over the cell machinery, redirecting it to produce the virus. The virus may eventually kill the host cells.

Viruses could either be DNA or RNA virus. Once inside the host cell it could insert its viral genome to the host's nucleus and use its nuclear apparatus to reproduce and multiply. The infected cell usually dies because the virus keeps it from performing its normal functions. When it dies, the cell releases new viruses, which go on to infect other cells.

http://www.hhmi.org/biointeractive/animations/infection/inf_frames.htm

fusion of T lymphocyte and HIV mechanism

http://pathmicro.med.sc.edu/weaver/fusion.htm

http://www.dbc.uci.edu/~faculty/wagner/hsvbinding.html

see HIV attacking the T cell in youtube http://www.youtube.com/watch?v=RO8MP3wMvqg&feature=related

I just wonder what happens to the regulatory processes -splicing and proof-reading in the transcriptin process..can anybody help?