I would suggest keeping it do-able as well.
Your research question should come first anyhow.
I would suggest keeping it do-able as well.
Your research question should come first anyhow.
1. Set up a total of 240 colonies split into 6 different apiaries. All of the colonies in an apiary should be one cell size
How do you account for dfferences in yards? One yard can do poorly while 2 miles down the road another of equal strength initially can do great.
5 As colonies die out, replace them with walk away splits
But that's a managment plan that will effect the varroa populations. If they die out, should they even be replaced?
DarJones, I'd sign off on that. But it's probably bigger than necessary and it's easily involved enough to be somebody's Ph. D. project. It would be a full time job for two or more people. I kinda like Barry's idea. How feasible would it be for each of two dozen or more beekeepers to set aside ten hives to follow the exact same procedure qualified under the categories you suggest? The queens could be provided from common sources. The results could be agglomerated and I believe they would be more valid because they're being collected from a broader variety of locations.
A thought occurred to me a little while ago. The biggest thing this whole discussion proves is that the anecdotal evidence given is contradictory in every possible direction, including within the stories of some individuals.
I know it isn't "done that way", but I've always thought a research team from a university ought to send one student out to a SCer and simply study, take data, observe, etc. and verify that the beekeeper is successful not treating. Then, based on that data, decided what a study should look like and have at it, with existing hives.
If you have evidence to back up your accusation, I recommend you post it to support this claim. Otherwise, I'd like to see this statement retracted. Such an accusation is extremely inflammatory and downright libelous to anyone involved in peer-reviewed research (as the authors of the papers are).The authors withheld the real findings, and substituted plausible ones, because they would conflict with another major project. -WLC
"If you have evidence to back up your accusation, I recommend you post it to support this claim. Otherwise, I'd like to see this statement retracted."
It happens all the time.
The authors consulted with Gillespie about QW33 who would have told them that it contained the famous R2 insertion site and that polyadenylation was a hallmark of retrotransposition.
So, they certainly did withhold the information because of another project. The Beeologic/Monsanto project.
A project that was launched because of the discovery of immunity by retrotransposition/RNAi in the Honeybee.
Unless of course, you think that they're simply incompetent and have no business doing genomics research.
I could live with that.
That site is a hotspot for Honeybee molecular immunity, and it is also a critical marker for those interested in proving the efficacy of treatment free beekeeping and the use of small cell/natural comb.
Or, would you prefer to relegate these folks to counting mites and dead colonies instead?
Last edited by WLC; 11-21-2011 at 04:30 AM.
But that's not a finding of the research conducted in these papers. It could possibly be a note in the discussion at the end of one or more of the papers, but it's not a finding.The authors consulted with Gillespie about QW33 who would have told them that it contained the famous R2 insertion site and that polyadenylation was a hallmark of retrotransposition. -WLC
You claimed they withheld the real results of their results (the results of the data collected in the field) and replaced those results with "more plausible" results. You've accused them of falsifying data, in essence, or of deliberately modifying their data to fit with a hypothesis that they prefer.
Such things may actually run concurrent with the findings of these papers. Immunity this way would be to viruses vectored by Varroa mites. These studies found that smaller cell sizes do not reduce mites numbers in hives. Very simple finding. An explanation for why so-called small-cell hives might continue to survive despite mite numbers being just as high as in so-called large-cell hives might rely on just such transpositional immunity. That still doesn't change the numbers of these studies and goes beyond the scope of the projects in these papers.A project that was launched because of the discovery of immunity by retrotransposition/RNAi in the Honeybee. -WLC
Kieck, so basically what you're saying is:
I can understand your confusion.
I have to toss a monkey wrench into WLC's tub. You obviously have a hobbyhorse to ride re RNA transposition. Unfortunately, it meets reality head on in the varroa mite. If RNA transposition were part of the equation with honeybees, then rationally you would have colonies that could acquire immunity to the viral assault. That would leave the mites to deal with. If unchecked, the mite load in the colony would spiral out of control until there were more mites than bees. Then it would climb higher still until each bee was inundated in mites. Just when do you think the bees start to die? If RNA transposition were a cure all, then feral colonies would now be immune to just about everything. Why aren't they immune to AFB? EFB? Sacbrood? BPV? IAPV? add as many others as you like.
At one time, Penicillin was considered a wonder drug. Just take a little and it would cure what ails you. Today we know that the efficacy of penicillin is limited and that all subsequently developed antibiotics are similarly limited. You can bet that RNA transposition will also be limited.
DarJones - 45 years, 10 colonies (max 40), sideliner, treatment free since 2005, 11 frame broodnest, small cell
You need a proxy for mite virulence.
Something that you can measure simply or in greater depth using the same marker.
I'll avoid getting into the backstory, but measuring the proxy will avoid false positives, that you can get when using standard methods for measuring virus loads (AKA-virulence)and pathogens, by using a single primer pair that measures the status of the Honeybee's molecular immunity.
It can answer the fundamental question of how small cell (and treatment free beekeeping) can positively affect the Honeybee's immunity.
There are already more than enough studies that miss the mark.
It's time to aim for the heart of the matter with a 'robust' and flexible methodology.
Last edited by WLC; 11-21-2011 at 03:27 PM.
Yes, the part you quoted was done, but what I went on to say was not, AFAIK. Did Berry spend a couple of years observing Bill's bees before the study? Did she verify how the bees were dealing with Varroa? If she found the varroa level in his hives to be no different than her LC bees, why do a study on mite loads? Commonsense would say there is something else at work and the study should have been done on another aspect. I know of no published statements by her that say "going into this study, the mite counts in Bill's hives were such and such over a two year period.
I drew you in and didn't even try!
The entire idea of following the colonies for x number of years is purposeless. They set out to determine if, as was commonly reported, small cell reduces varroa mite loads. Under the conditions they had...it did not. Six months, ten years, it doesn't matter. The trial was designed to eliminate as many variables as possible. It did a pretty good job. No real world testing can eliminate everything. The longer a trial goes on, the more variables enter in. The small cell folks complained about all kinds of ‘faulty trial’ conditions. Then the Florida group with Jerry Hayes and Amanda Ellis eliminated many of those. Then the Seeley group eliminated more.
The research folks spent valuable time, energy and money studying the small cell proponents’ main argument. Small cell failed that test. Now those same small cell folks want these researchers to perform countless, extended trials for every imaginable combination of variables that they can dream up. It ain’t gonna happen. The honey bee research community is strapped for funding…..always has been…and now even more so. They aren’t going to invest more in pure speculation.
If anyone has a pet theory and can finance or conduct their own trial, then that is what they need to do.
Is it time to actually discuss the studies yet? That does seem to be the topic of the thread.The small cell folks complained about all kinds of ‘faulty trial’ conditions. Then the Florida group with Jerry Hayes and Amanda Ellis eliminated many of those. Then the Seeley group eliminated more.
Is it your contention that the Seeley study is the most refined of the studies, and that the results/claims are robust and defendable? Have you read the study?
Do you mean this one?
Did any of the studies cited in Seeley measure virus levels or immunity in the Honeybees in any way, shape, or form? Or, did they simply count mites/dead colonies?
Last edited by WLC; 11-23-2011 at 02:37 PM.
Thanks WLC, I've been looking for that one. Let the discussion on the studies begin.