“That would be the end of our industry”

[Hilljackoutlaw]

Once you understand how vast and flat the boreal forest is up there you may change your view about the difficulty. My uncle had a fishing resort near Itasca State Park in Minnesota. The boreal forest there is similar. The only breakup of the landscape is the lakes.

I understand the vastness...my point is how hard is it to wake up at 5AM and look at the map and pick what bait pile to go sit by? That's not real tough. It's not like these guides are understanding the terrain and finding hidden funnels or saddles or dried up creek beds or depressions that the deer are using to travel from place to place. They just throw out bails of alfalfa in areas where deer are and go sit by them. Here is my $2000 sign me up and after I harvest one here is a $500 tip for great guide work.
It's also incredibly tough hunting whitetail deer in the adirondacks of NY but nobody is baiting over there, but guys and gals are still getting it done.

 

[Hilljackoutlaw]

I'm sure there is much more to it than that. Like tracking, gutting, skinning, etc... but the actual guiding part seems like the easy part. And I understand why you would fight against something that is gonna stop you from being provided easy money. But they aren't getting any sympathy from me.

 

[RockinU]

As someone who has guided for years in a state that baits, I can tell you that there is way more to it than that. I know it would seem like that's all that's involved, makes sense...but I've seen lots of people set up feeders or bait piles that get little to no traffic, or the wrong traffic, or traffic at the wrong time, etc. There is an element of reading terrain, understanding where the animals are, when they are there, where they are going to go, and how they are going to get there.

I know everyone has watched on TV as a feeder goes off on an over populated ranch in Texas, and deer come running out of the woods, and there's 30 or 40 to choose from, and that's a real thing, I've seen it. But on a ranch with good habitat, and a population that is suitable for that habitat, I've seen poorly placed feeders with big piles of corn under them untouched by anything other than birds and raccoons.

 

[thusby]

"Hold on I got a veterinarian on the other line"

*Hangs up on wildlife biologist*

"Yeah, hey doc, cancel the baiting, got it"

 

[Hunting Wife]

CWD is an organism called a Prion. These prions are composed of abnormal proteins. Prions are transmitted to normal proteins. Prions are not composed of nucleic acids like viruses making them a unique organism. However recent science suggests that prions can only be transmitted by attaching to a DNA or RNA strand.

Don’t even know where to start...

First, I would be curious to see a link to the research about prions only transmitting by attachment to DNA. First I’ve heard of such a thing.

Second, in an effort to be accurate about this - a prion is not an organism. It is not alive. It is simply a protein, made up of amino acids and synthesized by cells in the body as all proteins are. This is what DNA does...codes for the proteins that make us up. There are countless normal versions of prion proteins produced by your body every day. You are right in that prions are not made of nucleic acids, but neither are viruses, though viruses do contain some DNA or RNA genetic material. Prions do not-they are just a product of a nucleic acid sequence.

Proteins acquire some of their properties by their physical shape. Infectious disease causing prions like the one that causes CWD have a normal amino acid sequence, but an abnormal 3D shape. These abnormal prions are not “transmitted” to other proteins per se...they bind to normal proteins and induce them to fold into the same abnormal shape. This is how CWD amplifies, in a nutshell.

I don’t know a single biologist who would look at you with a straight face and claim continued baiting is a good idea in light of CWD. So I find it darkly comical how so many people argue for “science based management”, yet go through extreme mental gyrations to construct conspiracy theories when the science says anything other than what they personally want to hear.

 

[Gila]

I'm sure there is much more to it than that. Like tracking, gutting, skinning, etc... but the actual guiding part seems like the easy part. And I understand why you would fight against something that is gonna stop you from being provided easy money. But they aren't getting any sympathy from me.

Having a narrow small food plot with an apartment on stilts in the middle of it, using a rifle on a bench rest is ok? But baiting in the middle of a 100 sq mile flat forest is not ok?

 

[thusby]

"Scientists" teamed with "Activists" is definitely a cause for consternation. The question isn't whether CWD can spread through baiting. We know it does. The question is whether you can bait at an acceptable level that isn't going to cause a mass die-off. A lot of rural Canadian communities are very dependent on seasonal American sportsman showing up.

I personally hunt over bait in northwest Wisconsin (2 gallons/day) legally and we have had CWD in our state longer than most have. The CWD prevalence has not increased in my county over the past 20 years either.

 

[RockinU]

Don’t even know where to start...

First, I would be curious to see a link to the research about prions only transmitting by attachment to DNA. First I’ve heard of such a thing.

Second, in an effort to be accurate about this - a prion is not an organism. It is not alive. It is simply a protein, made up of amino acids and synthesized by cells in the body as all proteins are. This is what DNA does...codes for the proteins that make us up. There are countless normal versions of prion proteins produced by your body every day. You are right in that prions are not made of nucleic acids, but neither are viruses, though viruses do contain some DNA or RNA genetic material. Prions do not-they are just a product of a nucleic acid sequence.

Proteins acquire some of their properties by their physical shape. Infectious disease causing prions like the one that causes CWD have a normal amino acid sequence, but an abnormal 3D shape. These abnormal prions are not “transmitted” to other proteins per se...they bind to normal proteins and induce them to fold into the same abnormal shape. This is how CWD amplifies, in a nutshell.

I don’t know a single biologist who would look at you with a straight face and claim continued baiting is a good idea in light of CWD. So I find it darkly comical how so many people argue for “science based management”, yet go through extreme mental gyrations to construct conspiracy theories when the science says anything other than what they personally want to hear.

This is interesting, and while I make meager attempts to educate myself, I'd like to learn more. I think I understand that there is a big difference between frequency dependent distribution, and density dependent distribution, and that it is believed that CWD at a certain point is more frequency dependent, so wouldn't it make sense, if that were the case, to strategically reduce an infected population for a period of time? Or does the prion's persistence in the environment preclude something like that from being efficient? If population reduction were a viable mitigating tool, I could see baiting being a useful aspect of that, but that of course does not relate to the original topic.

 

[Hilljackoutlaw]

Having a narrow small food plot with an apartment on stilts in the middle of it, using a rifle on a bench rest is ok? But baiting in the middle of a 100 sq mile flat forest is not ok?

No I dont think any baiting is ok with the exception of bears maybe, but I dont bear hunt. Were not cavemen who rely on the meat for survival. In life or death situations like that anything goes. But were not in life or death situations it's a hobby and a tradition for 99% of us so it should be fair chase. I dont believe baiting is fair chase. Especially paying someone to bait for you and guide you so you can harvest a trophy. That's ego driven not passion driven.
But to each their own just cause others do it doesn't mean I have to do it or support it. Their adults and can make their own decisions without my help. but like I said no sympathy coming from my end.

 

[Hilljackoutlaw]

Also I dont consider a food plot a bait pile. A food plot takes time, energy, and dedication. A bait pile takes Polaris ranger gas and 12 year old girl muscles to dump a 50 pound bag of food onto the ground. Or maybe the ranger has a dump bed in that case just the mental capacity to pull the dump lever.

 

[warmer]

Don’t even know where to start...

First, I would be curious to see a link to the research about prions only transmitting by attachment to DNA. First I’ve heard of such a thing.

Second, in an effort to be accurate about this - a prion is not an organism. It is not alive. It is simply a protein, made up of amino acids and synthesized by cells in the body as all proteins are. This is what DNA does...codes for the proteins that make us up. There are countless normal versions of prion proteins produced by your body every day. You are right in that prions are not made of nucleic acids, but neither are viruses, though viruses do contain some DNA or RNA genetic material. Prions do not-they are just a product of a nucleic acid sequence.

Proteins acquire some of their properties by their physical shape. Infectious disease causing prions like the one that causes CWD have a normal amino acid sequence, but an abnormal 3D shape. These abnormal prions are not “transmitted” to other proteins per se...they bind to normal proteins and induce them to fold into the same abnormal shape. This is how CWD amplifies, in a nutshell.

I don’t know a single biologist who would look at you with a straight face and claim continued baiting is a good idea in light of CWD. So I find it darkly comical how so many people argue for “science based management”, yet go through extreme mental gyrations to construct conspiracy theories when the science says anything other than what they personally want to hear.

I like this. Don't understand a single word, but I like it.

 

[RockinU]

Also I dont consider a food plot a bait pile. A food plot takes time, energy, and dedication. A bait pile takes Polaris ranger gas and 12 year old girl muscles to dump a 50 pound bag of food onto the ground. Or maybe the ranger has a dump bed in that case just the mental capacity to pull the dump lever.

So it's not the concentrating animals over an unnatural food source that you take issue with, but how much effort is placed into creating the food source?

What if they dump corn in the middle of a food plot?

 

[Hilljackoutlaw]

So we have a farm in PA. Our 85 acres of alfalfa that we plant and bail for cows is considered a food plot cause we have anywhere from 20 to 50 deer in it every night, but I dont consider it unnatural. We also have corn that's harvested is this unnatural?

 

[Hilljackoutlaw]

Like I said to each their own...if someone wants to dump a bag of feed on the ground in deer country and hunt over it more power to them. I'm not gonna do it and I'm not gonna support it tho.
There is obviously a difference of opinion on this matter and that's fine. Some people prefer the easy way some people dont.

 

[RockinU]

So we have a farm in PA. Our 85 acres of alfalfa that we plant and bail for cows is considered a food plot cause we have anywhere from 20 to 50 deer in it every night, but I dont consider it unnatural. We also have corn that's harvested is this unnatural?

I'm not trying to change your mind, and I agree with you that within the constraints of the law, it's each to their own...but would that alfalfa be there if you didn't plant it, and cultivate it? Would there be 20-50 deer in that field if it weren't there? Doesn't seem natural to me. I get that the alfalfa wasn't put there in order to attract the deer, where a feeder is, but in the final result it's a distinction without a difference.

For what it's worth, guiding whitetail hunters in Texas where I've done plenty of feeder hunting is what led me to western hunting. I've always enjoyed spot and stalk, and rattling for deer way more than sitting. Being active is just more fun for me.

 

[Gila]

Don’t even know where to start...

First, I would be curious to see a link to the research about prions only transmitting by attachment to DNA. First I’ve heard of such a thing.

Second, in an effort to be accurate about this - a prion is not an organism. It is not alive. It is simply a protein, made up of amino acids and synthesized by cells in the body as all proteins are. This is what DNA does...codes for the proteins that make us up. There are countless normal versions of prion proteins produced by your body every day. You are right in that prions are not made of nucleic acids, but neither are viruses, though viruses do contain some DNA or RNA genetic material. Prions do not-they are just a product of a nucleic acid sequence.

Proteins acquire some of their properties by their physical shape. Infectious disease causing prions like the one that causes CWD have a normal amino acid sequence, but an abnormal 3D shape. These abnormal prions are not “transmitted” to other proteins per se...they bind to normal proteins and induce them to fold into the same abnormal shape. This is how CWD amplifies, in a nutshell.

I don’t know a single biologist who would look at you with a straight face and claim continued baiting is a good idea in light of CWD. So I find it darkly comical how so many people argue for “science based management”, yet go through extreme mental gyrations to construct conspiracy theories when the science says anything other than what they personally want to hear.

I don't find your reply to be entirely accurate but I am not a biologist or medical expert that is qualified to argue those points. The research is there to postulate that it fits the classic definition of an organism:

"Prion proteins can act as infectious agents, spreading disease when transmitted to another organism"

"The concept that transmissible spongiform encephalopathies (TSEs) are caused only by proteins has changed the traditional paradigm that disease transmission is due solely to an agent that carries genetic information. The central hypothesis for prion diseases proposes that the conversion of a cellular prion protein (PrPC) into a misfolded, β-sheet-rich isoform (PrPSc) accounts for the development of (TSE). There is substantial evidence that the infectious material consists chiefly of a protein, PrPSc, with no genomic coding material, unlike a virus particle, which has both. However, prions seem to have other partners that chaperone their activities in converting the PrPC into the disease-causing isoform. Nucleic acids (NAs) and glycosaminoglycans (GAGs) are the most probable accomplices of prion conversion. Here, we review the recent experimental approaches that have been employed to characterize the interaction of prion proteins with nucleic acids and glycosaminoglycans. A PrP recognizes many nucleic acids and GAGs with high affinities, and this seems to be related to a pathophysiological role for this interaction. A PrP binds nucleic acids and GAGs with structural selectivity, and some PrP:NA complexes can become proteinase K-resistant, undergoing amyloid oligomerization and conversion to a β-sheet-rich structure. These results are consistent with the hypothesis that endogenous polyanions (such as NAs and GAGs) may accelerate the rate of prion disease progression by acting as scaffolds or lattices that mediate the interaction between PrPC and PrPSc molecules. In addition to a still-possible hypothesis that nucleic acids and GAGs, especially those from the host, may modulate the conversion, the recent structural characterization of the complexes has raised the possibility of developing new diagnostic and therapeutic strategies."

Experimental approaches to the interaction of the prion protein with nucleic acids and glycosaminoglycans: Modulators of the pathogenic conversion

The concept that transmissible spongiform encephalopathies (TSEs) are caused only by proteins has changed the traditional paradigm that disease transm…

www.sciencedirect.com

 

[RockinU]

I don't find your reply to be entirely accurate but I am not a biologist or medical expert that is qualified to argue those points. The research is there to postulate that it fits the classic definition of an organism:

"Prion proteins can act as infectious agents, spreading disease when transmitted to another organism"

"The concept that transmissible spongiform encephalopathies (TSEs) are caused only by proteins has changed the traditional paradigm that disease transmission is due solely to an agent that carries genetic information. The central hypothesis for prion diseases proposes that the conversion of a cellular prion protein (PrPC) into a misfolded, β-sheet-rich isoform (PrPSc) accounts for the development of (TSE). There is substantial evidence that the infectious material consists chiefly of a protein, PrPSc, with no genomic coding material, unlike a virus particle, which has both. However, prions seem to have other partners that chaperone their activities in converting the PrPC into the disease-causing isoform. Nucleic acids (NAs) and glycosaminoglycans (GAGs) are the most probable accomplices of prion conversion. Here, we review the recent experimental approaches that have been employed to characterize the interaction of prion proteins with nucleic acids and glycosaminoglycans. A PrP recognizes many nucleic acids and GAGs with high affinities, and this seems to be related to a pathophysiological role for this interaction. A PrP binds nucleic acids and GAGs with structural selectivity, and some PrP:NA complexes can become proteinase K-resistant, undergoing amyloid oligomerization and conversion to a β-sheet-rich structure. These results are consistent with the hypothesis that endogenous polyanions (such as NAs and GAGs) may accelerate the rate of prion disease progression by acting as scaffolds or lattices that mediate the interaction between PrPC and PrPSc molecules. In addition to a still-possible hypothesis that nucleic acids and GAGs, especially those from the host, may modulate the conversion, the recent structural characterization of the complexes has raised the possibility of developing new diagnostic and therapeutic strategies."

Experimental approaches to the interaction of the prion protein with nucleic acids and glycosaminoglycans: Modulators of the pathogenic conversion

The concept that transmissible spongiform encephalopathies (TSEs) are caused only by proteins has changed the traditional paradigm that disease transm…

www.sciencedirect.com

The prion is the agent of infection from one organism to another...it's not the organism, it's a protein.

 

[thusby]

From a purist perspective, the agricultural practices are creating higher deer population and density. The guy dumping a bail of alfalfa is creating seasonally greater density but not necessarily population. I think I just talked myself into banning farming.

 

[Gila]

I like this. Don't understand a single word, but I like it.

What it really means is that the scientists and medical experts still don't know jack sheet about CWD

 

[RockinU]

I don't find your reply to be entirely accurate but I am not a biologist or medical expert that is qualified to argue those points. The research is there to postulate that it fits the classic definition of an organism:

"Prion proteins can act as infectious agents, spreading disease when transmitted to another organism"

"The concept that transmissible spongiform encephalopathies (TSEs) are caused only by proteins has changed the traditional paradigm that disease transmission is due solely to an agent that carries genetic information. The central hypothesis for prion diseases proposes that the conversion of a cellular prion protein (PrPC) into a misfolded, β-sheet-rich isoform (PrPSc) accounts for the development of (TSE). There is substantial evidence that the infectious material consists chiefly of a protein, PrPSc, with no genomic coding material, unlike a virus particle, which has both. However, prions seem to have other partners that chaperone their activities in converting the PrPC into the disease-causing isoform. Nucleic acids (NAs) and glycosaminoglycans (GAGs) are the most probable accomplices of prion conversion. Here, we review the recent experimental approaches that have been employed to characterize the interaction of prion proteins with nucleic acids and glycosaminoglycans. A PrP recognizes many nucleic acids and GAGs with high affinities, and this seems to be related to a pathophysiological role for this interaction. A PrP binds nucleic acids and GAGs with structural selectivity, and some PrP:NA complexes can become proteinase K-resistant, undergoing amyloid oligomerization and conversion to a β-sheet-rich structure. These results are consistent with the hypothesis that endogenous polyanions (such as NAs and GAGs) may accelerate the rate of prion disease progression by acting as scaffolds or lattices that mediate the interaction between PrPC and PrPSc molecules. In addition to a still-possible hypothesis that nucleic acids and GAGs, especially those from the host, may modulate the conversion, the recent structural characterization of the complexes has raised the possibility of developing new diagnostic and therapeutic strategies."

Experimental approaches to the interaction of the prion protein with nucleic acids and glycosaminoglycans: Modulators of the pathogenic conversion

The concept that transmissible spongiform encephalopathies (TSEs) are caused only by proteins has changed the traditional paradigm that disease transm…

www.sciencedirect.com

Also, your quote confirms her assertion that prions are not transmitting by attachment to dna.