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The Middle Picture, Explained
The Middle Picture is dated 10-24-05, but I think that may be transposed. Here is a 10-25-04 talk by Thorpe:
"So here we took Tarvacin and radiolabeled it and we injected it into a rat with a prostate tumor, and it's growing here. Then two days later we scanned the animal and we looked for where the radioactivity was, and the radioactivity is color coded, so where it's red it's intense, where it's yellow it's less intense but still strong, and as you get into green and blue, where it's pale blue and then dark blue, [ ??] but what we can see is the Tarvacin is localized to the prostatic carcinoma in the rats. We can also see this little area[!?] right here, which is Tarvacin floating with the blood flow through the heart and the lungs, so that's normal."
http://www.investorshub.com/boards/read_msg.asp?message_id=4440307
We do have the possibility (see recent Jazz post quoting some language in a patent or patent application) that Bavi has an antibacterial effect, but the only beneficial bacteria I am aware of in the body are in the intestinal tract, which Bavi probably won't reach. And if it does, maybe the yogurt they tell us to eat with our antibiotics to repopulate an intestinal tract 'sterilized' by anitbiotics would also be good with Bavi.
The dead-eyed Republican liars got caught trying to smear Joe Wilson because he was exposing the fact that the Iraq war was based on almost 100% lies. It was never about Wilson, it was an attempt to discredit his message. Now that the special prosecutor has decided, either because he believed him or for some other reason, not to indict the Rove, they're gonna say this proves they were right about Iraq.
Doesn't matter they lied about the aluminum tubes.
Dosen't matter they lied about the mobile labs.
Doesn't matter they lied about WMD.
Doesn't matter Iraq produces less oil and less electricity that it did before April 2003 (except to the oil companies whose other oil is now worth about about $10-12 per barrel more).
Nothing else matters.
Rove didn't get indicted, ergo, Bush was right about Iraq.
You will hear this, I guarantee it.
FWIW, the PR referred both to "activity" and to "initial efficacy."
FWIW, Googling 'Peregrine' now brings us up on the first retrieval page, in eighth position.
I have not seen that before.
This seems relevant, but I do not subscribe.
"Suppression of Antitumor Immunity by IL-10 and TGF-beta -Producing T Cells Infiltrating the Growing Tumor: Influence of Tumor Environment on the Induction of CD4+ and CD8+ Regulatory T Cells"
Article to appear in 7/15 issue of Journal of Immunology
http://www.jimmunol.org/future/177.2.shtml#BRIEFREVIEWS
Well, apparently the clinical subjects weren't bursting out of the clinic immediately and fully cured, doing handsprings down the street to the music of a marching band, but this is good enough for me.
Effects of PS exposure on stimulated neutrophils
"The removal of neutrophils from inflammatory sites is essential for the resolution of inflammation. Surface changes, including phosphatidylserine exposure, label neutrophils for phagocytosis by macrophages.
Here, we demonstrate that [1] externalization of phosphatidylserine and [2] uptake by monocyte-derived macrophages occurred in human neutrophils ingesting Staphylococcus aureus. Both processes were dependent on oxidant production from the neutrophil NADPH oxidase. There was no requirement for myeloperoxidase, and H2O2 was identified as the most likely trigger for PS exposure.
We hypothesize that clearance of stimulated neutrophils would be delayed in chronic granulomatous disease (CGD) neutrophils, which lack a functional NADPH oxidase [and which, therefore, would not externalize PS??-- ed.].
To explore this possibility, heat-killed S. aureus were injected into the peritoneum of CGD and normal mice. Elevated neutrophil numbers were observed in the inflammatory exudate of the CGD animals, consistent with impaired recognition and clearance."
http://www.jleukbio.org/cgi/content/abstract/71/5/775
OK, so stimulated neutrophils expose PS when digesting staph bacteria (maybe others?), and depend on that exposure to get eaten and disposed of along with the staph.
We are agreed, I think, that continued inflammation is a design feature of Bavi's action against the cancer, and I note that this experiment does not support the idea that Bavi prevents the staph from getting eaten in the first instance by the neutrophils, but will Bavi also prolong inflammation resulting from staph and possibly other bacterial infection? If it does, will it be something to worry about? Or will it be yet another benefit?
Interesting in which particular?
Another un-PR'd presentation?
Given that in apoptosis, intracellular death pathways are evolutionarily conserved, and that in apoptotic cells, exposed PS has some role in attracting phagocytes while suppressing inflammation, I wonder if any mechanism or process has evolved that relies the absence of inflammation, and which, if inflammation is allowed to occur, will change to yield a bad result.
Is this just a restatement of the basis of the concern with the possibility of undesired autoimmunity?
In an attempt to remedy my ignorance, I have discovered the NCBI Bookshelf, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books
The 5th edition of 2001(the current version is the 6th) of Immunobiology by Charles Janeway et al., is available there at
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=imm.TOC&depth=10
This URL gives table of contents, with a search box.
If you enter a topic (the unnumbered entries under the Arabic-numbered entries) in the search box, you will get a hit list, and somewhere in that hit list you will find the book's entire treatment of the topic, including the plates.
Message Board Peculiarity
When someone replies to an original post that is subsequently deleted, and a reader of the reply clicks on the original post number, there is no message that the original post has been deleted-- instead, the system defaults to the next remaining post.
I have seen this cause some cross-chop before, so I thought I'd note it aloud here.
It seems you are right.
The reason I am curious is that I remember some discussion on this board of the various IgGs, and that IgG3 was talked about as having something of an edge over IgG1, IgG2, or IgG4 for our purposes.
Isn't 3G4 an IgG3 mab AND NOT an IgG1?
"A new mouse immunoglobulin G3 monoclonal antibody, 3G4, was raised that binds anionic phospholipids in the presence of serum or ß2-glycoprotein I. The antibody was tested for its ability to localize to tumor vessels and exert antitumor effects in mice."
http://clincancerres.aacrjournals.org/cgi/content/full/11/4/1551
Interesting Article on Cancer Immunity and Immunotherapy
I don't have a subscription to PNAS, but here is the news article about the research:
http://www.latimes.com/news/printedition/la-sci-cancer9may09,0,1982462.story
"White blood cells from mice that are naturally immune to cancer cured tumors in other mice and provided them with lifelong immunity to the disease, researchers reported Monday.
The finding indicates the existence of a biological pathway previously unsuspected in any species. A small team of researchers is working to understand the genetic and immunological basis of the surprising phenomenon.
Preliminary studies hint at the existence of a similar resistance in humans. Researchers hope that harnessing the biological process could lead to a new approach to treating cancer.
"The idea of cells being able to kill tumor cells … is very exciting," said biologist Howard Young of the National Cancer Institute's Center for Cancer Research in Frederick, Md. "But this is a mouse, and there is no guarantee that the same gene will exist in people."
(snip)
Zhen Cui of Wake Forest, whose team published the findings in the Proceedings of the National Academy of Science, said he expected rapid replication of the results because the findings were so clear-cut and easily observed.
"This is a truly remarkable phenomenon … and it really needs confirmation from other institutions," he said.
Cui and his colleagues stumbled on the immune mice by accident in 1999. They were injecting mice with a highly virulent form of cancer cells as part of an ongoing study of the biological mechanisms that cause cancer to spread.
On April 13 of that year, a graduate student told Cui that one of the mice she had injected did not develop a tumor. Assuming the student had simply overlooked the mouse, he told her to do it again. And again.
After a total of five injections — the last equal to 10% of the animal's body weight — the mouse remained free of tumors.
Intrigued, they bred the mouse and found that about half its offspring had the same resistance. The trait bred true through subsequent generations and the team eventually had a colony of about 700 resistant mice. Cross-breeding the mice with other strains transferred the resistance to them as well.
When cancer cells are injected into the mice, their white blood cells surround the tumor cells and rupture them in a process called cytolysis. The same killing process occurs when tumor cells are formed naturally by the action of carcinogens.
As the animals get older, injected cells might form a tumor, but the cancer is cleared in a day or two. The animals live a normal lifespan, about two years.
In the new study, the team took white blood cells from the immune mice — a combination of natural killer cells, macrophages and neutrophils — and injected them into mice already carrying a variety of tumors, some of which were extremely aggressive. In every case, the cancers were destroyed, even if the cells were injected at a point distant from the tumor. Healthy tissues were not affected.
The mice that received the cells, furthermore, were protected from new tumors for the rest of their lives. The researchers have no idea how the immunity continues.
"This is the first report of a novel [treatment] mechanism," said Dr. Andrew Raubitschek, a cancer immunologist at the City of Hope National Medical Center in Duarte. "The two most dramatic things are: one, that the response itself is outstanding, and two, the fact that they looked at a variety of different cell lines and found the activity was there for all of them."
The fact that the immunity can be transferred between mice indicates that the phenomenon is more than a simple aberration in one strain of mice and gives hope that such manipulations can lead to a therapy for humans.
"This deserves intensive follow-up," said Dr. Richard Miller of the University of Michigan Medical School. Cui's papers "are technically sound, carefully controlled and well thought out. But whenever there is a result this surprising, it's always important to have others confirm it."
Cui and his colleagues believe that the resistance results from a mutation in a single gene and are attempting to find it, but that has proved frustrating. The primary problem is that while the gene mutation may be in one location in one family of mice, it may occur on a different chromosome in another family.
(snip)
Cui's team developed a test-tube assay to determine whether mice were immune without injecting them with tumor cells. In the test, white blood cells from the animal are mixed with tumor cells. If the animal is immune, the white cells surround the tumor cells in a characteristic rosette pattern.
Cui said the team had tested cells from humans in the same fashion and had observed the same phenomenon.
"Some people never get cancer," said Young of the National Cancer Institute. "That may mean they have an active gene and are inherently more resistant to cancer. That is not at all inconceivable."
The approach used in mice would most likely not be applicable in humans, Willingham said. The need to match cell types to avoid rejection would make using living cells extremely difficult, and there would also be the issue of viruses and other potential contaminants.
But if scientists can understand the mechanism, he added, they can manipulate it with drugs to spark a similar immune response in the patient's own cells.
Despite the obvious promise of the approach, Young urged caution.
"People have been killing tumors in mice for 30 years, and only some of those techniques have led to human therapy…. Because they don't know anything about the gene yet, the application to human therapy remains a big question mark."
AVII is getting killed today.
These results did not appear to satisfy the fans.
http://biz.yahoo.com/bw/060510/20060510005293.html
"The second phase of the trial has been designed to assess the safety, tolerability, pharmacokinetics (PK) and viral and clinical response to treatment with AVI's proprietary NEUGENE® antisense compound, AVI-4065, among HCV patients.
AVI-4065 exhibited favorable safety and tolerability profiles in all patients treated thus far, with no serious drug-related adverse events or tolerability issues observed during treatment or follow-up. Based on the relatively long elimination half-life of AVI-4065 and its mechanism of action, an irreversible binding to the viral genome preventing viral protein synthesis, a slow, steady liver loading with test drug was expected in patients with high levels of viral target in the liver. This correspondingly predicts a slow, steady decrease in viral load over the drug-loading period.
The PK analysis in patients treated thus far was consistent with this prediction; there was a significant decrease in the concentration of drug in the plasma (Cmax) in HCV patients compared with the normal subjects in the initial phase of the trial. This was consistent with an increased elimination of drug found in the urine, most likely bound to the virus in the HCV-infected patients. In addition, there was a significant correlation between viral titer at day one and the extent of reduction in Cmax, further supporting this mechanism of elimination. These observations demonstrate a significant and direct pharmacodynamic response to HCV infection.
Viral responses have been assessed in only a few patients out to the 28th day of the study. During the 14 days of treatment, three of five patients evaluated had an initial decrease in viral load, whereas two of five exhibited little initial change in viral titer. The mean viral titers of all patients tested thus far showed a slight decrease (0.30 log reduction) both during and after treatment, with no rebound effect observed out to 28 days. These are very preliminary results in a small number of patients, and active enrollment and evaluation is ongoing, with formal results expected around the end of the year.
'Based on the PK and mechanism-of-action of our drug, we expected a slow, steady accumulation of drug in the liver with a corresponding decrease in viral load,' said Dr. Iversen. 'The maximal tissue concentration of drug would be reached in three to five half-lives, or approximately 33 to 55 days. This indicates that an extension of treatment duration is required to reach maximum drug concentration and reduction of viral load in the liver. These preliminary results are consistent with that and very encouraging for ongoing drug development. Extending the treatment period would be expected to further reduce viral load in responding patients and may ultimately decrease viral load in those patients who are not early responders.'"
I hope we can do better.
Re Jazz's work: You can click on his name and get all his posts.
This link to the patent appl works:
http://appft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FP...
"PPHM does not dare to publish these"
They have said tey will publish them. What is the matter with you that you have to distort like this?
EZ, I am sorry but I don't understand how your reply to my post has anything whatsoever to do with my post.
What is it in my post that you call "another Annexin?"
My question was, "If it turns out that PS-receptors on macrophages are not necessarily involved in the phagocytosis of apoptotic cells, does that mean anything for us?"
Does it matter to us if the PS receptor on the macrophages should turn out not to be strictly necessary for phagocytosis of apoptotic cells? Our virtue, as I understand it, is in blocking immunosuppression incident to phagocytosis of apoptotic cells, thereby allowing inflammation to occur, bringing more macrophages to the site. We are content, are we not, with their course-of-nature performance once they are on-site?
What do we make of this? Full text at http://jbiol.com/content/3/4/15
"Our studies demonstrate that Ptdsr is not a primary receptor for the uptake of apoptotic cells. Investigation of apoptotic cell clearance in vivo in Ptdsr -/- embryos conclusively showed that removal of apoptotic cells is not compromised by ablation of Ptdsr function. Comparative analysis of ten different tissues and organs in Ptdsr+/+ and Ptdsr -/- animals at several stages of embryonic development and in neonates failed to identify impaired uptake of apoptotic cells at any time during development. Furthermore, phagocytosis assays in vitro demonstrated a completely normal uptake of apoptotic cells by Ptdsr -/- macrophages, with some knockout macrophages showing loads even higher than wild-type of engulfed dead cells. These results are contrary to the expected role of Ptdsr in apoptotic cell clearance and to the reported findings of Li et al. [31] and Kunisaki et al. [32], as well as to a study done with a phosphatidylserine receptor null allele in C. elegans [45]."
"As the New Year rolled around, shares were priced at 90 cents. The price as of last Friday was $1.54, roughly a 98 percent gain, not too shabby."
71%, not 98%. What happened to numeracy?
Slightly OT, but did anyone catch the 4-9-06 NYT article about how Rodman & Renshaw treated their Halozyme analyst?
It's now (already!) behind the NYT pay-per-view wall, but IMO R&R came off looking pretty sleazy.
UPDATE: I found this.
http://www.spdrindex.com/eqsnaps/index.cfm?story=newsStory&symbol=XLY&fk=11285&newsID=29...
(begin excerpts)April 10, 2006 (FinancialWire) Analyst Matthew Murray was fired by Rodman & Renshaw (OTC: RRSHQ) after he refused to change a downgrade on Halozyme Therapeutics (AMEX: HTI), and Rodman & Renshaw never published the analyst's report, according to Gretchen Morgenson of the New York Times (NYSE:NYT) in yet another devastating revelation about apparent continued research conflicts at some investment banks despite the $1.4 billioin global research settlement of just over three years ago.
* * *
The firing came after the analyst asked to be removed from the company's coverage because he believed his name on the previous report violated his professional requirement that he sign that the report's findings were "solely his own," saying those were "no longer" his view.
An aim of the $1.4 billion research settlement, you may recall, was to protect analysts from pressure by investment bankers or employees in other parts of their firms to write favorably about the companies they followed," noted Morgenson. "But according to Mr. Murray, that kind of pressure is exactly what he experienced."
She said Murray began recommending Halozyme last September, when the stock was at $1.86. "He assigned a price target of $2.88 to it. In mid-December, Halozyme raised about $17.5 million from the public in a stock offering managed by S. G. Cowen & Company, Rodman & Renshaw and Roth Capital Partners. The price was $1.75 a share; buyers of the deal cannot sell their stock until mid-June.
"All was quiet in January, but by mid-February, the stock was moving. It rose to $2; later that month it was $2.45. On Friday, Feb. 24, the stock hit $2.80, on no apparent news, Mr. Murray said. Because it was nearing his price target and the company's fundamentals had not changed, he prepared his downgrade report."
Murray reportedly talked to Halozyme's CFO, listed as David A. Ramsay, and confirmed there were no new developments and then discussed his rating change with the four members of Rodman's investment policy committee.
The next day, a Saturday, Morgenson said he received an e-mail message from Michael G. King Jr., the research director at Rodman, suggesting that he maintain his rating on Halozyme by raising his price target.
"If you'd like some help regarding how to finesse the price target on HTI your conversation should be had with me," Mr. King wrote, referring to the company, in the e-mail message that Murray provided a copy of to The New York Times.
"In a return e-mail message, Mr. Murray said he was not interested in finessing the price target. He did, however, agree to meet on Monday, Feb. 27, with the chief financial officer from Halozyme to assess its fundamentals once more. Rodman was about to be host for a series of meetings for Halozyme with the firm's clients. While many meetings like this are related to a securities offering, this one was not.
"Halozyme shares hit $3 that day. Having confirmed his previous investment thesis in his meeting with the C.F.O., Mr. Murray submitted his downgrade report. Mr. King, citing what he called the 'abysmal' quality of the writing in the report, advised the analyst that the report could not go out. Mr. Murray asked to convene a meeting with the investment policy committee, to no avail. No report has been published."
Murray then asked William A. Iommi, Rodman's head of compliance, to remove his name from the coverage due to his belief he could no longer certify the report available to the public reflected his opinion.
On March 2, Iommi told Rodman's employees that Murray was "leaving" its research department, and 12 days later he was fired.
The Times noted that from March 2005, when Murray joined the firm, the First Call ranking for the firm's biotech research climbed from 17th to third and he was the top-ranked analyst at the firm.
* * *
Murray has apparently left the profession and has applied to join the National Guard.(end excerpts)
Halozyme (HTI), a company with whom we do business, closed today at $2.76.
Thanks. BTW, I am not a physician or a Ph.D., it is an old musical alias.
Sorry, that isn't me, I have never posted on that bd under any alias. I'd love to see the messages you are talking about.
"somebody tell me why I'm not able to ignore certain posters?"
Try it again, in my (free membership) case, the phrase "Ignore This Poster" changes instantly to "Unignore This Poster." You just missed it, perhaps.
I just did to a well-known basher from another board who has started to post here, and it worked just dandy.
Your "48 minutes" evidently came from this article at your URL, and not from the PPHM article.
(quote)Hepatitis C: Serum Viral Levels Recur Rapidly After Liver Transplant
http://www.xagena.it/
--- --- --- --- --- --- --- --- --- ---
"In most patients," the authors report," HCV RNA levels decreased rapidly during and after transplantation and subsequently began to increase – reaching above pre-transplant levels in all but one patient – within a few days of the procedure." They found that when the diseased liver was removed, virus levels dropped with an average half-life of 48 minutes. After the new liver was implanted, they found that virus levels continued to drop for up to 23 hours, then began to rise, doubling every 2 days.(end quote)
http://www.hcvadvocate.org/news%5CnewsRev%5C2006/NewsRev-142.html
Your tone leaves something to be desired. There should have been a "please" in there, especially as it looks like you have never been to the company's website. You have to register, and I checked just now to confirm it is still alive.
http://www.peregrineinc.com/content.php?mi=MzI=&appAction=--PRINT&Id=MTIyOTMyNQ==&ir_nv=
You're welcome.
Or does the 44-day "median survival time" of the 8 Tarv+radiation rats include the three with complete regressions tumors, arbitrarily assigned a number of days for statistical purposes?
"The authors conclude that the anti-tumor effect of the Tarvacin equivalent antibody plus irradiation was equivalent to what would have been expected if 99.99% of brain cancer cells had been destroyed."
It would be great if we knew that Tarv+radiation killed 99.99% of cancerous cells, but because it appears not to be an actual observed number, I am wondering what they meant by the 99.99% figure. It was not an observed number, so was it a calculated number, based on known measures of the disease's invasiveness in rats, and the fate the 8-member Tarv+radiation group (the three rats with "complete regressions" and the five rats with a 44-day median survival time)?
I'm guessing that in humans, the disease does not progress as fast as it does in mice, so a comparable increase in mean survival time might be significantly more than 17 or 26 days.
Meanwhile, AVII has some more news:
http://biz.yahoo.com/bw/060330/20060330005252.html
I am curious about how B2GP1 manages to help the phagocyte see the PS exposed on the viral envelope or on the plasma membrane of the apopoptotic cell. Schroit, et al. [2005] say that in nature, the binding between B2GP1 monomer and the exposed PS is weak, but have some interesting remarks that may explain a stronger binding, and may also hint at what is happening with Tarvacin. Apologies if this was posted earlier, I cannot search this thread.
http://www.biochemj.org/bj/386/0271/bj3860271.htm
Numbers in brackets are citations to other articles.
Considering its low affinity under physiological conditions, we conclude that binding of monomeric b2GPI to PS-exposing cell membranes in vivo is negligible. It is possible, though, that any in vivo function requiring high-affinity binding of b2GPI could be fulfilled by multivalent b2GPI–cell interactions. Indeed, multimeric structures of b2GPI, either artificial [50] or present in plasma [51,52], will bind even in the absence of antibodies to plasma membranes containing surface-exposed PS. The relatively high-affinity binding in the presence of antibody can be considered to mimic the multimeric form of the protein. Alternatively, multivalency may be accommodated by multiple b2GPI–cell-surface interactions [7,53] or by adaptor proteins that enhance the association of b2GPI with PS. Conceivably, binding of b2GPI to phagocytes via interaction with a non-lipid-binding domain of the protein could enhance its affinity for PS-expressing cells through clustering of accessible lipid-binding domains of b2GPI on the surface of the macrophage, enabling multiple interactions with PS-exposing membranes of apoptotic cells. In summary, we have quantitatively characterized the binding of b2GPI and prothrombin to PS-exposing platelets. The results demonstrate that, under physiological conditions, the binding of b2GPI to such platelets is of low affinity. This finding stresses the importance of multimeric complexes in the functioning of b2GPI in cellular interactions.
King's remarks are not very clear. I take from them that IV Tarvacin may or may not ever be effective against H5n1 flu.
To the extent that avian flu is a whole-body flu, IV delivery might be necessary in addition to or even effective instead of pulmonary delivery.
"Monto [2004] added that, while this mutated strain [of H5n1] is susceptible to Relenza, there is no guarantee that Relenza will be effective against the avian flu, because Relenza is not designed to treat a systemic infection such as the avian flu. If, when the virus transfers from humans to humans, it stops being a systemic infection, then Relenza might be a realistic option," he said. "If it does not and we see an increased resistance to oseltamivir, then we've got a problem on our hands." (emphasis added)
http://www.caromont.org/blank.cfm?print=yes&id=381&action=detail&ref=11899
In the case of Relenza, at least, it looks like very little of the inhaled drug escapes the lungs to travel systemically, i.e., via the bloodstream, to other parts fo the body. A 1999 report (not talking about H5n1): "This may be attributed to the low systemic bioavailability of zanamivir, which is given by oral inhalation, direct to the primary site of viral replication [for ordinary flu]. The potential advantages of this include a reduced risk of drug-drug interactions, other nontarget organ toxicities (e.g. brain) and drug clearance issues from both kidney and liver."
http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=10514019&....
GSK is apparently working on an injectable form of Relenza in response to the bird flu threat: "Relenza, . . . has limited usefulness because it is administered as a nasal spray. It cannot be used by people who have trouble breathing, which occurs if it is severe flu. Its manufacturer, the British company GlaxoSmithKline, said it would be two years before they could produce an injectable form."
http://www.guardian.co.uk/birdflu/story/0,14207,1673215,00.html
I don't know whether H5n1 replicates in the intestinal tract of humans, as it has been shown to do in birds and cats, but if the virus replicates significantly there, pulmonary delivery alone might not work.
Katie, I may not be understanding your statement, "Tarvacin's only method of administration is intravaneously, it's common knowledge this type of administration is not effective against any type of flu."
If you mean that there is no IV flu treatment, these might interest you:
"This study demonstrates that intravenously administered zanamivir is distributed to the respiratory mucosa and is protective against infection and illness following experimental human influenza A virus inoculation."
http://aac.asm.org/cgi/content/abstract/43/7/1616
and:
"However, a limited number of healthy volunteers who were administered high doses of intravenous zanamivir tolerated systemic levels of zanamivir that were substantially higher than those resulting from administration of zanamivir by oral inhalation at the recommended dose."
http://www.cdc.gov/mmwr/preview/mmwrhtml/rr54e713a1.htm
If I have misunderstood, please enlighten me.
R-M
Thanks, I didn't even think of that.
NewYork, I looked at the cover page for this board, and reviewed the last 100 posts, and couldn't find what significant event will be marked at the "close of the 27th."
Could you enlighten me, please?
TIA.
R-M
TechnicalWin, do you (technically) consider $1.35 a buyable dip? $1.30?
That is interesting, and it may explain why I gain weight when all I eat is carrots and celery, LOL.
FWIW, adenoviruses (including AD-36) have no envelope.