Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
It already does, exosomes.. eom
You're out over your skies in regards to "blockbuster".
Although I'm impressed with patients willingness to biopsy, the markers were not what I was looking for. They would have been better served to parallel preclinical revelations.
Good effort, less than blockbuster result..
All the best,
John
Keep_Trying,
Don't go leaving for 6 years like I did :)
Hope all is well,
John
Thanks CP, great information and wouldn't expect anything less from you..
All the best,
John
Researchers Discover Proteins That Block Both HIV And Ebola Virus Release
August 26, 2014 | by Justine Alford
In an unexpected twist, a family of proteins that have been found to promote HIV-1 entry into cells also potently block viral release. Interestingly, these proteins were also found to inhibit the release of other viruses, including Ebola virus. These intriguing new findings provide us with novel insights into both viral infection and the development of AIDS, which could ultimately lead to new antiviral strategies. The study has been published in Proceedings of the National Academy of Sciences.
Viruses are unable to replicate by themselves and thus must hijack a host cell’s machinery in order to do so. To get inside host cells, HIV, or human immunodeficiency virus, needs to bind to receptors found on target cells. This triggers a series of events that ultimately lead to viral entry; once inside, HIV converts the cell into a factory for making more viruses.
Recent studies have identified a family of proteins, called TIM proteins, which play critical roles in facilitating the entry of various viruses including Ebola, West Nile and dengue viruses. Intriguingly, University of Missouri researchers have now discovered that these proteins not only promote HIV-1 entry into host cells, but they also prevent viral release.
For the study, scientists investigated the interactions between HIV-1 and TIM proteins using various molecular, biochemical and microscopic techniques. They found that as HIV-1 begins to bud from, or escape, the host cell, TIM proteins become incorporated into the virions and tether the particles to the cellular membrane. This is mediated through interactions with a lipid called phosphatidylserine (PS) that is found both on the cell membrane and the outside of the virus particles. Usually, PS is expressed on the inside of the cell, but viral infection causes it to flip to the outside, meaning that both PS and TIM are now present on the cell and viral surface. TIM and PS then bind to one another as HIV-1 attempts to escape from the cell, causing the particles to be retained at the cell surface.
Interestingly, the team also discovered that TIM proteins inhibited the release of other viruses including a mouse virus belonging to the same family as HIV (murine leukemia virus), and also Ebola virus.
While these discoveries extend our understanding of viral infection, lead researcher Shan-Lu Liu points out that it is not clear at this stage whether HIV’s interaction with TIM proteins is a positive or negative factor. “However, this discovery furthers our ultimate goal of understanding the biology of TIM-family proteins and potentially developing applications for future antivirus therapies,” he says.
http://www.iflscience.com/health-and-medicine/researchers-discover-proteins-block-both-hiv-and-ebola-virus-release
Remember Crestor (statin drug) + Bavituximab for Ebola? Well maybe statin for Ebola is gaining traction. ABC News seems to think so..
By Rachael RettnerPublished October 15, 2014
Statins should be considered as a possible treatment for Ebola, some researchers argue.
In addition to their ability to lower cholesterol levels, statins have anti-inflammatory effects, and may be able to fight the out-of-control immune-system response in Ebola patients that damages the body, said Dr. David Fedson, a retired professor and vaccine expert in France who wrote an editorial on the topic in the Sept. 30 issue of The Journal of Infectious Diseases.
www.foxnews.com/health/2014/10/15/could-statins-treat-ebola/
Single cell viruses hijack host cells and replicate in the cytoplasm of the infected cell. Ebola therefore would have the potential for virulency.
As it exist now the Ebola virus cannot recombine, and you are correct in that..
All the best,
John
I've posted about Antigenic drift and viral recombination here, but without comment. Seems some research is late in my thinking..
"Ebola Outbreak Boosts Odds of Mutation Helping It Spread"
"What happens to MDSCs that are/were present? They disappear? Waste?"
The elimination process would be the same immunologic manifest for all cells including MDSC's. The word to use here would be "Immunoediting" or "Immunosurveillance". MDSC's are not immune to this process, IMO..
Wookie, I would suggest that you read up on something called, "Cell potency". This will set you straight and give you a good handle on MDSC's.
All the best,
John
Not from that article, but more proof in antips' functionality to take away the keys that viruses use to drive. In this case, the keys to unlock the vehicle in which they (viruses) enter to drive.
"phosphatidylserine mediated virus entry-enhancing receptors"
Author information
1Department of Microbiology, University of Iowa, Iowa City, Iowa, USA.
2Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.
3SugarCone Biotech LLC, Holliston, Massachusetts, USA.
4Department of Microbiology, University of Iowa, Iowa City, Iowa, USA wendy-maury@uiowa.edu.
Abstract
T-cell immunoglobulin and mucin domain 1 (TIM-1) and other TIM family members were recently identified as phosphatidylserine (PtdSer)-mediated virus entry-enhancing receptors (PVEERs). These proteins enhance entry of Ebola virus (EBOV) and other viruses by binding PtdSer on the viral envelope, concentrating virus on the cell surface, and promoting subsequent internalization. The PtdSer-binding activity of the immunoglobulin-like variable (IgV) domain is essential for both virus binding and internalization by TIM-1. However, TIM-3, whose IgV domain also binds PtdSer, does not effectively enhance virus entry, indicating that other domains of TIM proteins are functionally important. Here, we investigate the domains supporting enhancement of enveloped virus entry, thereby defining the features necessary for a functional PVEER. Using a variety of chimeras and deletion mutants, we found that in addition to a functional PtdSer-binding domain PVEERs require a stalk domain of sufficient length, containing sequences that promote an extended structure. Neither the cytoplasmic nor the transmembrane domain of TIM-1 is essential for enhancing virus entry, provided the protein is still plasma membrane bound. Based on these defined characteristics, we generated a mimic lacking TIM sequences and composed of annexin V, the mucin-like domain of a-dystroglycan, and a glycophosphatidylinositol anchor that functioned as a PVEER to enhance transduction of virions displaying Ebola, Chikungunya, Ross River, or Sindbis virus glycoproteins. This identification of the key features necessary for PtdSer-mediated enhancement of virus entry provides a basis for more effective recognition of unknown PVEERs.
IMPORTANCE:
T-cell immunoglobulin and mucin domain 1 (TIM-1) and other TIM family members are recently identified phosphatidylserine (PtdSer)-mediated virus entry-enhancing receptors (PVEERs). These proteins enhance virus entry by binding the phospholipid, PtdSer, present on the viral membrane. While it is known that the PtdSer binding is essential for the PVEER function of TIM-1, TIM-3 shares this binding activity but does not enhance virus entry. No comprehensive studies have been done to characterize the other domains of TIM-1. In this study, using a variety of chimeric proteins and deletion mutants, we define the features necessary for a functional PVEER. With these features in mind, we generated a TIM-1 mimic using functionally similar domains from other proteins. This mimic, like TIM-1, effectively enhanced transduction. These studies provide insight into the key features necessary for PVEERs and will allow for more effective identification of unknown PVEERs.
Copyright © 2014, American Society for Microbiology. All Rights Reserved.
PMID: 24696470 [PubMed - indexed for MEDLINE] PMCID: PMC4054341 [Available on 2014/12/1]
Share on FacebookShare on TwitterShare on Google+
http://www.ncbi.nlm.nih.gov/pubmed/24696470
All the best,
John
Anti Ebola cocktail of Crestor and Bavituximab would potentially take away the "keys" to the "vehicle" of which the virus uses to drive.
Needs to be studied, NOW, IMO.
All the best,
John
The patent portfolio flood gates will open with Bavituximab approval, and King will be rewarded. A standard of care vaccine that turns all the glitter to gold, and you wonder why some are threatened?
Waiting on the new MOA, and unlocking cross-presentation. Will the real Bavituximab please stand up..
The FDA will be rewarded too, IMO
All the best,
John
I reiterate Bavituximab is the first true cancer vaccine, IMO
How? By unlocking cross-presentation, IMO.
Will discuss after disclosure and new MOA..
All the best,
John
Bidrite had the best response, and he's correct.
If you were in a clinical trial and suspected that you were receiving placebo, would you withdraw?
Yes, that's a serious question.
All the best,
John
31 members planned not assigned? Point me in the right direction if I'm wrong. TIA.
All the best,
John
Three letter word
BOD
I guess you can call it a loophole, because I said I was done complaining about management. Now what does Patriot Scientific have to do with current management? Nothing, IMO.
King, Shan, Garnick and other day to day officers are not the ones sucking the wind out Peregrine's sails, IMO.
The problem is the man behind the curtain, ask the Tin Man and friends.
All the best,
John
Patriot Scientific..LOL Gravy Train x 2
Given the chance, i would have Dr Thorpe's platform to market, and do so like stockholders worked for Google, IMO.
I'm here till the end, but have already written off this money, and made more to replace it, without even missing it. With that said it's looking like we're another Patriot, IMO..
Many here deserve Google type of treatment as employees and owners of Peregrine stock.
All the best,
John
In Lincoln NE I know there are only two reputable clinical research facilities.
Both nothing. No sunrise IMO.
http://net.unmc.edu/ctsearch/index_unmc.php
http://www.chihealthstelizabeth.com/cancer-clinical-trials
And for good measure if you want to find Sunrise in Nebraska, then surely it's here.. NOT
Nebraska Cancer Research Center
http://www.aboutmvcc.org/clinical-trial
In my opinion anyway..
All the best,
John
CP, in your opinion how many patients are currently being dosed in Sunrise?
Are you suggesting "none", as I have recently, and if so why?
As much as I love the science, I'm wondering if a "delayed" PR is in our future?
I am certain that it's not a worldwide conspiracy to jumble the websites where Sunrise is enrolling, in an attempt to thwart Bavituximab, as I'm sure some will propose.
Is it incompetence?. Deliberate from management, as a way to keep the low price "options" "gravy train" going a little longer. Greed?
I'm lost at what your suggesting, but have seen it all in 11 + years, and would like an explanation from Peregrine. We should all demand an explanation, considering the past debacle, and sabotage.
All the best,
John
In my opinion, Bavituximab is the first true cancer vaccine.
Totally different from cervical cancer vaccine (HPV virus)
All the best,
John
I'm done complaining about management.
They've given Dr Thorpe's research a chance, and that's more than fair to him and the science.
I'm done being influenced from other notable posters here. I know what I know and that's all I need to know. I've got an idea of what Dr Thorpe envisioned and believe its legitimate.
After 11 years I'm not losing sleep over money lost or gained here. I just know we have a chance in Phase 3 NLCLC. How many other Phase 3 NSCLC trials can you say that about? How many other small cap biotechs can you say that about?
It's not perfect and it's frustrating at times, especially after 11 years, but at least we have a chance.
I'm in all, and all the best,
John
The share price tells you what you're worth. Just like in football, "you're only as good as what your record is"
Our record is $1.52 and $272MM
Saying the SP doesn't matter is like saying size doesn't matter :)
I've been told otherwise.. LOL
All the best,
John
Joe Shan's word or CP's links?
It seems that Peregrine is sitting on their thumbs (AGAIN).
Regenerative medicine?
Well I read your earlier post, and wanted to bring up the fountain of youth theory, but didn't because I've already made my point with that.
However, since you bring it up again I'll respond.
First and formost I would say that manipulating phosphatidylserine has broad potential in bone tissue engineering. This was basically discovered by happenstance during ERK inhibitor research. If you want to know, read up on ERK signalling pathway and PS..
I wouldn't say this was my initial thought process in regards to Bavituximab and regenerative medicine, but it's definetely an outlier.
Regarding your link and the future of medicine, I'll say that it's old news and much of it is focused on telomere manipulation, or stem cell therapy.. I'm sure you remember Michael D. West and Geron a few tears ago?
All the best,
John