Need an expert!

charface

charface

Well-Known Member
farmerfischer said:
Peony.. it will be covered in black ants.. they help open the buds and protect it..
Click to expand...
Thats kind of stuff is amazing.
I was watching bees collect from the thousands of flowers on a bush.

Wondered how they knew how to tell which had been collected.

Then I noticed that after collection each bee flipped a petal and it stayed in that position. It happened so fast it was by luck i noticed.

Now I cant say exactly why they did it
My impression was that they used it as a signal to the others not to waste time on that flower.

I want to record it this year.
Go fuckin viral with the bee nerds
Edit,
And shit!
 
farmerfischer

farmerfischer

Well-Known Member
charface said:
Thats kind of stuff is amazing.
I was watching bees collect from the thousands of flowers on a bush.

Wondered how they knew how to tell which had been collected.

Then I noticed that after collection each bee flipped a petal and it stayed in that position. It happened so fast it was by luck i noticed.

Now I cant say exactly why they did it
My impression was that they used it as a signal to the others not to waste time on that flower.

I want to record it this year.
Go fuckin viral with the bee nerds
Edit,
And shit!
Click to expand...
Could be.. I know they use various pheromones for signalling and shit.. like when to defend..
Ive been thinking about buying some honey bee's.. I have a shit ton of rhododendrons on my property..
 
Singlemalt

Singlemalt

Well-Known Member
farmerfischer said:
Could be.. I know they use various pheromones for signalling and shit.. like when to defend..
Ive been thinking about buying some honey bee's.. I have a shit ton of rhododendrons on my property..
Click to expand...
Careful:
Grayanotoxin
From Wikipedia, the free encyclopedia
Grayanotoxins are a group of closely related neurotoxins named after Leucothoe grayana, a plant native to Japan originally named for 19th century American botanist Asa Gray.[1] Grayanotoxin I (grayanotaxane-3,5,6,10,14,16-hexol 14-acetate) is also known as andromedotoxin, acetylandromedol, rhodotoxin and asebotoxin.[2] Grayanotoxins are produced by Rhododendron species and other plants in the Ericaceae family. Honey made from the pollen and nectar of these plants also contains grayanotoxins and is commonly referred to as mad honey. Consumption of the plant or any of its secondary products, including mad honey, can cause a very rare poisonous reaction called grayanotoxin poisoning, mad honey disease, honey intoxication, or rhododendron poisoning.[3] It is most frequently produced and consumed in regions of Nepal and Turkey as a recreational drug and traditional medicine.[4]

Biological Effects
Prolonged sodium channel activation and cell depolarization leads to overstimulation of the central nervous system. Physical symptoms from grayanotoxin poisoning appear after a dose-dependent latent period of several minutes to approximately three hours. The most common clinical symptoms include various cardiovascular effects, nausea and vomiting, and a change in consciousness. The cardiovascular effects may include hypotension (low blood pressure) and various cardiac rhythm disorders such as sinus bradycardia (slow regular heart rhythm), bradyarrhythmia (slow irregular heart rhythm) and partial or complete atrioventricular block.[5][8]

Other early-onset symptoms may include diplopia and blurred vision, dizziness, hypersalivation, perspiration, weakness and paresthesia in the extremities and around the mouth. In higher doses, symptoms can include loss of coordination, severe and progressive muscular weakness, electrocardiographic changes of bundle branch block and/or ST-segment elevations as seen in ischemic myocardial threat, and nodal rhythm or Wolff-Parkinson-White syndrome.[9]

The primary mediator of this grayanotoxin pathophysiology is the paired vagus nerve (tenth cranial nerve).[5] The vagus nerve is a major component of the parasympathetic nervous system (a branch of the autonomic nervous system) and innervates various organs including the lungs, stomach, kidney and heart. In one study, experimental administration of grayanotoxin to bilaterally vagotomized rats failed to induce bradycardia, a common symptom of grayanotoxin poisoning, supporting the role of vagal stimulation.[10] Vagal stimulation of the myocardium, specifically, is mediated by M2-subtype muscarinic acetylcholine receptors (mAChR).[11] In severe cases of grayanotoxin poisoning, atropine (a non-specific mAChR antagonist) can be used to treat bradycardia and other heart rhythm malfunctions. In addition to correcting rhythm disorders, administration of fluids and vasopressors can also help treat hypotension and mitigate other symptoms.[12]

Patients exposed to low doses of grayanotoxin typically recover within a few hours. In more severe cases, symptoms may persist for 24 hours or longer and may require medical treatment (as described above). Despite the risk cardiac problems, grayanotoxin poisoning is rarely fatal in humans.[12]


https://en.wikipedia.org/wiki/Grayanotoxin
 
farmerfischer

farmerfischer

Well-Known Member
Singlemalt said:
Careful:
Grayanotoxin
From Wikipedia, the free encyclopedia
Grayanotoxins are a group of closely related neurotoxins named after Leucothoe grayana, a plant native to Japan originally named for 19th century American botanist Asa Gray.[1] Grayanotoxin I (grayanotaxane-3,5,6,10,14,16-hexol 14-acetate) is also known as andromedotoxin, acetylandromedol, rhodotoxin and asebotoxin.[2] Grayanotoxins are produced by Rhododendron species and other plants in the Ericaceae family. Honey made from the pollen and nectar of these plants also contains grayanotoxins and is commonly referred to as mad honey. Consumption of the plant or any of its secondary products, including mad honey, can cause a very rare poisonous reaction called grayanotoxin poisoning, mad honey disease, honey intoxication, or rhododendron poisoning.[3] It is most frequently produced and consumed in regions of Nepal and Turkey as a recreational drug and traditional medicine.[4]

Biological Effects
Prolonged sodium channel activation and cell depolarization leads to overstimulation of the central nervous system. Physical symptoms from grayanotoxin poisoning appear after a dose-dependent latent period of several minutes to approximately three hours. The most common clinical symptoms include various cardiovascular effects, nausea and vomiting, and a change in consciousness. The cardiovascular effects may include hypotension (low blood pressure) and various cardiac rhythm disorders such as sinus bradycardia (slow regular heart rhythm), bradyarrhythmia (slow irregular heart rhythm) and partial or complete atrioventricular block.[5][8]

Other early-onset symptoms may include diplopia and blurred vision, dizziness, hypersalivation, perspiration, weakness and paresthesia in the extremities and around the mouth. In higher doses, symptoms can include loss of coordination, severe and progressive muscular weakness, electrocardiographic changes of bundle branch block and/or ST-segment elevations as seen in ischemic myocardial threat, and nodal rhythm or Wolff-Parkinson-White syndrome.[9]

The primary mediator of this grayanotoxin pathophysiology is the paired vagus nerve (tenth cranial nerve).[5] The vagus nerve is a major component of the parasympathetic nervous system (a branch of the autonomic nervous system) and innervates various organs including the lungs, stomach, kidney and heart. In one study, experimental administration of grayanotoxin to bilaterally vagotomized rats failed to induce bradycardia, a common symptom of grayanotoxin poisoning, supporting the role of vagal stimulation.[10] Vagal stimulation of the myocardium, specifically, is mediated by M2-subtype muscarinic acetylcholine receptors (mAChR).[11] In severe cases of grayanotoxin poisoning, atropine (a non-specific mAChR antagonist) can be used to treat bradycardia and other heart rhythm malfunctions. In addition to correcting rhythm disorders, administration of fluids and vasopressors can also help treat hypotension and mitigate other symptoms.[12]

Patients exposed to low doses of grayanotoxin typically recover within a few hours. In more severe cases, symptoms may persist for 24 hours or longer and may require medical treatment (as described above). Despite the risk cardiac problems, grayanotoxin poisoning is rarely fatal in humans.[12]


https://en.wikipedia.org/wiki/Grayanotoxin
Click to expand...
Thanks malt.. I knew this already.. but I appreciate the looking out..
 
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