15 December 2008
Immunity From Mom
Studies lead by teams from BYU, Harvard, and Stanford found the molecule CCR10 to be an important player in the ability to pass along immunity from the mother to the baby via breast feeding. This study was done in mice and they found that mice that lack this CCR10 molecule had 70 times fewer cells that produce antibodies in the mammary gland.
In essence, the mechanism underlying breast feeding as a means to pass along immunity to our infant is more complicated than I thought. Without the CCR10 molecule, good breast feeding practice wouldn't be any good in providing IgA protection.
References:
Breast Milk Molecule Gives Mom's Immunity to Baby -http://www.nlm.nih.gov/medlineplus/news/fullstory_70850.html
Breast-feeding, infant formulas, and the immune system -
http://www.ncbi.nlm.nih.gov
13 December 2008
miRNA regulates immune system
Seminars in Cancer Biology
Volume 18, Issue 2, April 2008, Pages 131-140
Postgenetic Oncology - MicroRNA and Cell Proliferation
12 December 2008
Bird Flu
Since we've talked about vaccines in class, I wonder how much Baxter would help out if people in this area are vaccinated with it? I don't know if these countries (people within these countries) are able to afford this vaccine.
References:
http://www.who.int/en/
The Varicella-Autoantibody Syndrome
The study groups consisted of 52 children without acute varicella virus exposure and 43 patients with varicella (VZV) exposure. The second group was further broken down into 17 children with thromboembolism (blood clots) or purpura fulminans and VZV and 26 with uncomplicated VZV exposure. There were significant differences between the group without VZV exposure and the group with VZV exposure. Those exposed to VZV frequently developed a lupus anticoagulant (measured by dilute Russel Viper Venom Time dRVVT) and several other antibodies to phospholipids regardless of whether they had uncomplicated exposure or if they developed thromboembolism. Although there was no difference between the two groups when it came to antibodies made in the acute phase, the difference came in duration of antibodies and their effect on Protein S. Those that developed a thromboembolism or purpura fulminans had significantly lower Protein S levels and significantly higher levels of antibodies to Proteins S.
The interesting question that I brought from this paper is: what the difference is between these two groups of children? They both are producing a cross-reactive antibody to VZV and Protein S, but only a small portion develop low levels of Protein S and high levels of antibodies which lead to thromboembolism. Could this be a problem with T cell regulation in these patients? If not, what is different with these patients?
Pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?otool=uchsclib&term=the%20varicella-autoantibody%20syndrome&cmd=search&db=pubmed
11 December 2008
DVT - Deep Vein Thrombosis
That week my dad was diagnosed with a DVT - Deep Vein Thrombosis in his leg. He had been active and couldn't figure out why. He hadn't been on a long flight or anything similar that month. We were very concerned about a Pulmonary Embolism. Yes, the dislodged clot could travel to the lungs!! (capillaries) This is what killed young reporter, David Bloom, in Iraq.
Well, a couple of months earlier, my dad was recovering from eye surgery. He was told to stay on the couch until his detached retina healed. His doctor did mention that my dad should, however, get up every 30 minutes or so to "get the blood moving." This was great advice, but it wasn't quite enough exercise to prevent a DVT. (My dad's blood test was normal and he was on a low dose aspirin regimen before this.)
I just want to express how important exercise is --even when we are cramming for a test or finishing a long experiment. Anyone up for running the stairs at lunch break?
http://en.wikipedia.org/wiki/Deep_vein_thrombosis
10 December 2008
Fake Blood Real Stokes
Since one of the functions of inflammation is to increase blood flow, do you think supplying all this O2 can curtail some or any of the swelling and the potentially harmful effects of an inflammed brain?? Does the property of increased Oxygen delivery decrease the length of time it takes to bring down swelling, in effect speeding up the healing process? I think this chemical is lacking in anti-inflammatory properties and that O2 delivery just might be the only, yet important, characteristic, would you agree? Comments?
http://www.thescizone.com/news/articles/1481/1/Synthetic-Blood-Announces-Oxycyte-Development-Strategy/1.html
http://hamptonroads.com/2008/03/type-artificial-blood-may-be-key-surviving-brain-injury
Inflammatory Bowel Disease and the Hygiene Hypothesis
Anyway, I think the University of Iowa study is right on. Thanks Dr. Cohen for telling us!
Here is the publication:
Helminths and harmony
http://gut.bmj.com/cgi/content/full/53/1/7
09 December 2008
Protecting virus
An article I read a while back discusses a novel method of controlling flu virus infection using a protecting virus. The concept was developed for influenza type A and involves a genetically modified version of the virus that has an 80% deletion on one of the 8 RNA strands. This deletion renders the virus harmless and interferes with the ability to reproduce once inside a cell. When it is joined by another normal influenza virus, the protecting virus replicates much faster than the normal influenza virus thereby crowding it out resulting in a slowed rate of progression. This delay allows the immune system time to develop and mount an immune response.
The implications of such a cascade are that any strain of influenza that you encounter will become it's own vaccine by giving the body time to recognize the virus and develop an effective response. Thus, protection is conferred against unforeseen strains and mutations that vaccines have a lesser ability to deal with. This is especially desirable for a virus that mutates often leaving vaccines that cannot protect against all variations. In addition, by using a live infection, you are creating a better immune response than by using peptides of the viral products alone. Current research shows that protection from infection happens immediately upon administration and can even be given 24 hrs after exposure while maintaining effectiveness.
Some experiments have been done to show that by putting the protecting virus in drinking water of animals they have gained protection from various strains of influenza. From our discussions in class regarding H5N1 and the jump from birds to humans, could this be useful to impact the spread of avian flu within bird populations? Because of the protecting virus' ability to act as a vaccine to highly mutable viruses, could this be a tool to use against other infections?
This pioneering research was done by Nigel Dimmock at the
Emerging viruses in transplantation
HHV-6 is another common virus and is latent in ~90% of adults in immune, salivary and bronchial epithelial cells. Immunocompromised individuals reactivate with replication in CD4+ cells further suppressing the patient immune response ultimately leading to high mortality rates of up to 58%. Once detected as an active infection, antivirals have been seen to be effective treatments. Mumps and measles have a slightly different approach to deal with in immunocompromised patients as there are no specific antiviral treatments. It is recommended to vaccinate for example, stem cell transplant patients 2 years after the transplant. However, this leaves a small gap in time where people are susceptible with high attack rates and associated high mortality rates. The evaluation of viral infection, diagnosis and treatment continue in this paper but all remain serious threats and deserve attention as they can be major factor in increasing the longevity of transplant patients.
Emerging Viruses in Transplantation: There Is More to Infection After Transplant Than CMV and EBV.
Transplantation. 86(10):1327-1339, November 27, 2008.
Fischer, Staci A.
Chemokine microbicides
Both analogues tested show equivalent potency against viral replication as compared to PSC-RANTES invitro and in macaque challenge models. They achieve this in the same manner as PSC-RANTES by inhibiting the CCR5 receptor availability to the virus. One analogue causes the CCR5 receptor to sequester intracellularly but the other analogue doesn’t utilize this method and a mechanism was not described here. In the absence of a vaccine, the meaning of this very exciting discovery is enhanced due to the need of other avenues to slow the spread of virus. At the lecture, a recent study was also presented that statistically, we could treat out way out of this epidemic by affecting the spread of the disease. This is clearly a step in that direction while research to develop vaccines continue.
Cerini, Fabrice *; Landay, Alan PhD + ; Gichinga, Carolyne + ; Lederman, Michael M MD ++ ; Flyckt, Rebecca MD [S] ; Starks, David MD [S] ; Offord, Robin E PhD || ; Le Gal, Francois PhD [P]; Hartley, Oliver PhD * , Chemokine Analogues Show Suitable Stability for Development as Microbicides. J Aquir Defic Syndr. 2008;49;472-476.