Talk:2009 Group 8 Project

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--Mark Hill 13:43, 19 March 2009 (EST) Adjusted your title format and moved your microscopy information to the discussion page (here). Note, only single square bracket for external links.

microscopy services offered at SOMS UNSW: [1]

--Bridget Josephs 20:01, 29 March 2009 (EST)Hi all just posting a timeline of the necrosis process that we can start working from:

--Leone Chare 14:15, 1 April 2009 (EST) Thanks Bridget! Since our group meeting today fell through lol, we decided it was probably best to post on to this discussion board what proteins we're interested in doing for our individual projects and also which parts of the group project we're keen to do. But we can discuss this more tomorrow during the lab.

--Gurkiran Flora 21:25, 1 April 2009 (EST)I found some really interesting information about Ischemia and how it leads to necrosis... Bridget touched on this too. It is Necrosis caused by hypoxia resulting from local deprivation of blood supply. There is also some nice brief information on necrosis on this site,M1

--Leone Chare 22:45, 12 April 2009 (EST) I found this textbook which is a tad old, but I found it to be pretty comprehensive in explaining the fundamental differences between apoptosis and necrosis. It has some good stuff on cellular mechanisms affected by necrosis and there are also some good references we could use. It's called Cell Death and Diseases of the Nervous System By Vassilis E. Koliatsos, Rajiv R. Ratan - you can just paste that into google and there's a preview version on googlebooks.

--Mark Hill 23:44, 12 April 2009 (EST) Good to see your group working on your project. Time line is a good start. You now need some images of necrotic cells (EM or light) and some details about the process itself.

--Leone Chare 13:33, 1 May 2009 (EST) Here’s a simplified overview of the causes of necrosis (feel free to correct)—thought it may be useful for organising the research into easy to understand sections. The first part is the simplified overview and each subsequent section goes into more detail. (the numbers correspond to the ones in the general overview)

General overview

  • 1) stimulus
  • 2) stress
  • 3) activation of first messengers
  • 4) activation of second messengers
  • 5) release of killers
  • 6) necrotic cell death

Lack of oxygen and/or glucose

  • 1) lack of oxygen and/or glucose
  • 2) acute energy depletion
  • 3) resting potential of neurons collapse
  • 4) glutamate release at synaptic clefts
  • 5) excitation of neurons
  • 6) necrotic cell death

The calpain/cathepsin pathway

  • 1) exposure to ROS (reactive oxygen species—usually caused by ischemia etc.)
  • 2) oxidative stress
  • 3) increase in intracellular Ca2+
  • 4) calpain activation -- eventually leads to cytoplasm collapse
  • 5) lysosome membrane damage -- leads to cathepsins release
  • 6) necrotic cell death

Chronology of the pathologic process of necrosis

· Necrotic insult initiating the irreversible cell death eg - ischemic injury - chemical (toxic) injury

In general:

Macroscopic (visible) level:

0-24hrs: necrotic tissue undergoes a colour change and becomes firm (note however that this does not include necrotic tissue within the brain)
2-3 days: a border demarcated by an inflammatory response can be observed. A fibrinous exudate may additionally be observed
> 1week: healing by fibrosis begins to take place: observe a grey/white periphery zone
After several months: fibrous scar

Microscopic level:

Observation of an acute inflammatory infiltrate in the effected tissue (vasodilation of blood vessels, neutrophils predominating in early stages and later replaced by macrophages, edema etc)
2-3 days: vascular granulation
1 week: fibrous granulation tissue
Months: fibrosis

· Consequence: death of the affected tissue. Sometimes this can result in the death and loss of function of an entire organ

Necrosis is classified as Type III cell death--Bridget Josephs 12:55, 30 April 2009 (EST)