New Science/Tech Site up
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Joined: Nov 2010
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New Science/Tech Site up
Got my science/blog/ journal thing up and revamped tonight. Take a look and tell me what you think and subscribe if you like it.
The Alchemists Corner
The Alchemists Corner
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Joined: May 2009
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From: Houston, Texas
i was all about cellular biology a couple years ago. mitochondria, lysosomes, krebs cycle couldn't get enough of it. somewhere along the way i got more interested in quantum physics and cosmology. black holes, super-massive stars, M-theory are what i have been reading up on lately.
Thread Starter
Joined: Nov 2010
Posts: 1,096
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[/quote]
Awesome! I have a new author to the group who is studying physics at UCSF. Look for some posts on those topics!
Registered User
Joined: May 2009
Posts: 26,916
Likes: 1
From: Houston, Texas
Originally Posted by Benn-O' timestamp='1304315691' post='20527847
[quote name='Fujin' timestamp='1304315234' post='20527834']
[quote name='Benn-O' timestamp='1304315005' post='20527830']
i liked the article on cortical folding. i find the brain so fascinating.
[quote name='Benn-O' timestamp='1304315005' post='20527830']
i liked the article on cortical folding. i find the brain so fascinating.
[/quote]
Awesome! I have a new author to the group who is studying physics at UCSF. Look for some posts on those topics!
[/quote]
cool! i would love to have a better understanding of Quantum entanglement/tunneling. first time i heard it, it was hard not to think of it as magic.
Joined: Mar 2004
Posts: 17,163
Likes: 4
Cool blog!
If you don't mind the plug, you may be interested in some recent work published by the lab I currently work in:
http://www.ncbi.nlm.nih.gov/pubmed/19806203
It is typically thought that the CNS is privileged thanks to the BBB, however, infecting mice with an attenuated form of rabies does allow for immune cells/effector compounds to infiltrate, and the eventual clearing of virus. This is in contrast to the typical outcome of rabies, should you not receive PEP: Death in 99% of cases where the virus reaches the CNS. Over 50,000 people die every year due to rabies.
Here is a figure showing B lymphocytes pumping out IgG antibody from multiple foci in the cerebellum of a mouse infected with the attenuated rabies virus:
I am personally researching whether or not expression of specific chemokines (chemoattractant cytokines) at or near the BBB influence the recruitment of B lymphocytes to the CNS in an attenuated rabies virus infection, and to compare the expression levels of these compounds to expression levels in the wild-type infected mouse. This includes CCR7/CCL19/CCL21, CXCR4/CXCL12, and so on.
We are trying to understand why, and how, during a wild-type rabies infection, CNS tissue remains closed off to immune cells, whereas the attenuated form (attenuated due to slight changes in the rabies surface glycoprotein) does not result in this obstruction, and leads to the elimination of virus from CNS tissue.
This work isn't entirely about rabies, however. If we can figure out the various intricacies involved in:
1) Stimulating an immune response to the CNS
2) Opening the BBB to immune cells/effector functions
3) Clearance of the target
4) Successful exit from CNS
Then we may possibly be able to design successful treatments for brain tumors by utilizing an immune response specifically targeting tumor "antigen"; you get in, stage an attack on the tumor, and get out!
Additionally, it may be that multiple sclerosis is a disease of the BBB, thus allowing immune cells to infiltrate and possibly (if any T cell happens to have receptors matching myelin proteins) leading to autoimmune attack and demyelination of CNS neurons.
Sorry for the ramble, good luck with the blog
If you don't mind the plug, you may be interested in some recent work published by the lab I currently work in:
http://www.ncbi.nlm.nih.gov/pubmed/19806203
It is typically thought that the CNS is privileged thanks to the BBB, however, infecting mice with an attenuated form of rabies does allow for immune cells/effector compounds to infiltrate, and the eventual clearing of virus. This is in contrast to the typical outcome of rabies, should you not receive PEP: Death in 99% of cases where the virus reaches the CNS. Over 50,000 people die every year due to rabies.
Here is a figure showing B lymphocytes pumping out IgG antibody from multiple foci in the cerebellum of a mouse infected with the attenuated rabies virus:
Sections from the cerebella of wild-type mice either uninfected (A and C) or infected with CVS-F3 12 days previously (B and D) were stained for IgG (brown). Photomicrographs taken at low magnification are shown in panels A and B and at higher magnification in C and D.
We are trying to understand why, and how, during a wild-type rabies infection, CNS tissue remains closed off to immune cells, whereas the attenuated form (attenuated due to slight changes in the rabies surface glycoprotein) does not result in this obstruction, and leads to the elimination of virus from CNS tissue.
This work isn't entirely about rabies, however. If we can figure out the various intricacies involved in:
1) Stimulating an immune response to the CNS
2) Opening the BBB to immune cells/effector functions
3) Clearance of the target
4) Successful exit from CNS
Then we may possibly be able to design successful treatments for brain tumors by utilizing an immune response specifically targeting tumor "antigen"; you get in, stage an attack on the tumor, and get out!
Additionally, it may be that multiple sclerosis is a disease of the BBB, thus allowing immune cells to infiltrate and possibly (if any T cell happens to have receptors matching myelin proteins) leading to autoimmune attack and demyelination of CNS neurons.
Sorry for the ramble, good luck with the blog
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Thread Starter
Joined: Nov 2010
Posts: 1,096
Likes: 2
Cool blog!
If you don't mind the plug, you may be interested in some recent work published by the lab I currently work in:
http://www.ncbi.nlm.nih.gov/pubmed/19806203
It is typically thought that the CNS is privileged thanks to the BBB, however, infecting mice with an attenuated form of rabies does allow for immune cells/effector compounds to infiltrate, and the eventual clearing of virus. This is in contrast to the typical outcome of rabies, should you not receive PEP: Death in 99% of cases where the virus reaches the CNS. Over 50,000 people die every year due to rabies.
Here is a figure showing B lymphocytes pumping out IgG antibody from multiple foci in the cerebellum of a mouse infected with the attenuated rabies virus:
I am personally researching whether or not expression of specific chemokines (chemoattractant cytokines) at or near the BBB influence the recruitment of B lymphocytes to the CNS in an attenuated rabies virus infection, and to compare the expression levels of these compounds to expression levels in the wild-type infected mouse. This includes CCR7/CCL19/CCL21, CXCR4/CXCL12, and so on.
We are trying to understand why, and how, during a wild-type rabies infection, CNS tissue remains closed off to immune cells, whereas the attenuated form (attenuated due to slight changes in the rabies surface glycoprotein) does not result in this obstruction, and leads to the elimination of virus from CNS tissue.
This work isn't entirely about rabies, however. If we can figure out the various intricacies involved in:
1) Stimulating an immune response to the CNS
2) Opening the BBB to immune cells/effector functions
3) Clearance of the target
4) Successful exit from CNS
Then we may possibly be able to design successful treatments for brain tumors by utilizing an immune response specifically targeting tumor "antigen"; you get in, stage an attack on the tumor, and get out!
Additionally, it may be that multiple sclerosis is a disease of the BBB, thus allowing immune cells to infiltrate and possibly (if any T cell happens to have receptors matching myelin proteins) leading to autoimmune attack and demyelination of CNS neurons.
Sorry for the ramble, good luck with the blog
If you don't mind the plug, you may be interested in some recent work published by the lab I currently work in:
http://www.ncbi.nlm.nih.gov/pubmed/19806203
It is typically thought that the CNS is privileged thanks to the BBB, however, infecting mice with an attenuated form of rabies does allow for immune cells/effector compounds to infiltrate, and the eventual clearing of virus. This is in contrast to the typical outcome of rabies, should you not receive PEP: Death in 99% of cases where the virus reaches the CNS. Over 50,000 people die every year due to rabies.
Here is a figure showing B lymphocytes pumping out IgG antibody from multiple foci in the cerebellum of a mouse infected with the attenuated rabies virus:
Sections from the cerebella of wild-type mice either uninfected (A and C) or infected with CVS-F3 12 days previously (B and D) were stained for IgG (brown). Photomicrographs taken at low magnification are shown in panels A and B and at higher magnification in C and D.
We are trying to understand why, and how, during a wild-type rabies infection, CNS tissue remains closed off to immune cells, whereas the attenuated form (attenuated due to slight changes in the rabies surface glycoprotein) does not result in this obstruction, and leads to the elimination of virus from CNS tissue.
This work isn't entirely about rabies, however. If we can figure out the various intricacies involved in:
1) Stimulating an immune response to the CNS
2) Opening the BBB to immune cells/effector functions
3) Clearance of the target
4) Successful exit from CNS
Then we may possibly be able to design successful treatments for brain tumors by utilizing an immune response specifically targeting tumor "antigen"; you get in, stage an attack on the tumor, and get out!
Additionally, it may be that multiple sclerosis is a disease of the BBB, thus allowing immune cells to infiltrate and possibly (if any T cell happens to have receptors matching myelin proteins) leading to autoimmune attack and demyelination of CNS neurons.
Sorry for the ramble, good luck with the blog
Registered User
Joined: May 2006
Posts: 7,659
Likes: 3
From: Braselton, GA
Originally Posted by C U AT 9K' timestamp='1304345180' post='20528505
Cool blog!
If you don't mind the plug, you may be interested in some recent work published by the lab I currently work in:
http://www.ncbi.nlm.nih.gov/pubmed/19806203
It is typically thought that the CNS is privileged thanks to the BBB, however, infecting mice with an attenuated form of rabies does allow for immune cells/effector compounds to infiltrate, and the eventual clearing of virus. This is in contrast to the typical outcome of rabies, should you not receive PEP: Death in 99% of cases where the virus reaches the CNS. Over 50,000 people die every year due to rabies.
Here is a figure showing B lymphocytes pumping out IgG antibody from multiple foci in the cerebellum of a mouse infected with the attenuated rabies virus:
I am personally researching whether or not expression of specific chemokines (chemoattractant cytokines) at or near the BBB influence the recruitment of B lymphocytes to the CNS in an attenuated rabies virus infection, and to compare the expression levels of these compounds to expression levels in the wild-type infected mouse. This includes CCR7/CCL19/CCL21, CXCR4/CXCL12, and so on.
We are trying to understand why, and how, during a wild-type rabies infection, CNS tissue remains closed off to immune cells, whereas the attenuated form (attenuated due to slight changes in the rabies surface glycoprotein) does not result in this obstruction, and leads to the elimination of virus from CNS tissue.
This work isn't entirely about rabies, however. If we can figure out the various intricacies involved in:
1) Stimulating an immune response to the CNS
2) Opening the BBB to immune cells/effector functions
3) Clearance of the target
4) Successful exit from CNS
Then we may possibly be able to design successful treatments for brain tumors by utilizing an immune response specifically targeting tumor "antigen"; you get in, stage an attack on the tumor, and get out!
Additionally, it may be that multiple sclerosis is a disease of the BBB, thus allowing immune cells to infiltrate and possibly (if any T cell happens to have receptors matching myelin proteins) leading to autoimmune attack and demyelination of CNS neurons.
Sorry for the ramble, good luck with the blog
If you don't mind the plug, you may be interested in some recent work published by the lab I currently work in:
http://www.ncbi.nlm.nih.gov/pubmed/19806203
It is typically thought that the CNS is privileged thanks to the BBB, however, infecting mice with an attenuated form of rabies does allow for immune cells/effector compounds to infiltrate, and the eventual clearing of virus. This is in contrast to the typical outcome of rabies, should you not receive PEP: Death in 99% of cases where the virus reaches the CNS. Over 50,000 people die every year due to rabies.
Here is a figure showing B lymphocytes pumping out IgG antibody from multiple foci in the cerebellum of a mouse infected with the attenuated rabies virus:
Sections from the cerebella of wild-type mice either uninfected (A and C) or infected with CVS-F3 12 days previously (B and D) were stained for IgG (brown). Photomicrographs taken at low magnification are shown in panels A and B and at higher magnification in C and D.
We are trying to understand why, and how, during a wild-type rabies infection, CNS tissue remains closed off to immune cells, whereas the attenuated form (attenuated due to slight changes in the rabies surface glycoprotein) does not result in this obstruction, and leads to the elimination of virus from CNS tissue.
This work isn't entirely about rabies, however. If we can figure out the various intricacies involved in:
1) Stimulating an immune response to the CNS
2) Opening the BBB to immune cells/effector functions
3) Clearance of the target
4) Successful exit from CNS
Then we may possibly be able to design successful treatments for brain tumors by utilizing an immune response specifically targeting tumor "antigen"; you get in, stage an attack on the tumor, and get out!
Additionally, it may be that multiple sclerosis is a disease of the BBB, thus allowing immune cells to infiltrate and possibly (if any T cell happens to have receptors matching myelin proteins) leading to autoimmune attack and demyelination of CNS neurons.
Sorry for the ramble, good luck with the blog
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