[Latin Name]  Ribes nigrum

[Specification] Anthocyanosides≥25.0%

[Appearance] Purple black fine powder

Plant Part Used: Fruit

[Particle size] 80Mesh

[Loss on drying] ≤5.0%

[Heavy Metal] ≤10PPM

[Storage] Store in cool & dry area, keep away from the direct light and heat.

[Shelf life] 24 Months

[Package] Packed in paper-drums and two plastic-bags inside.

[Net weight] 25kgs/drum

[What is Black currant?]

The black currant bush is a 6-foot tall perennial that entered the world somewhere in the regions that include northern Asia and central and northern Europe. Its flowers display five reddish-green to brownish petals. The celebrated black currant fruit is a glossy-skinned berry that carries several seeds laden with marvelous nutritional and curative treasures. An established bush can produce ten pounds of fruit per season

[Benefits]

1. Vision help my eyesight

2. Urinary Tract Health

3. Ageing & Brain Function.

4. Natural Brain Boost

5. Digestion & Fighting Cancer

6. Reducing Erectile Dysfunction

Preheat oven to 350 F.

1) Clean the pulp off the pumpkin seeds (or squash seeds), and dry with paper towels.

2) If desired, toss with a little olive or other oil. You only need enough to barely coat, otherwise, they will be greasy.

3) Add salt and any kind of seasoning you want – garlic powder, Cajon seasoning, dried chile powder, or whatever sounds good to you! “Try using a light oil and sprinkling a little cinnamon on the pan and the surface. You can add cane or brown sugar to make a sweet crunchy desert!”

4) Cover a baking sheet with foil and spread the seeds out in one layer.

5) Bake for 3-5 minutes, until seeds just start to color and smell really nice.

Sometimes I use a longer but safer method of using a lower temperature. If you roast the seeds at 250 degrees F., you don’t have to watch them as carefully. It takes about 45 -60 minutes.

Nutritional information: Pumpkin seeds are packed with nutrition,
5 grams of usable carb and 2 grams of fiber for 1/4 cup.

“Equine Polysaccharide Storage Myopathy” is an inheritable glycogen storage disease of horses that causes exertional rhabdomyolysis. It is most commonly associated with heavy horse breeds and the American Quarter Horse. While incurable, PSSM can be managed with appropriate diet and exercise. There are currently 2 subtypes, known as Type 1 PSSM and Type 2 PSSM.

Glycogen is a molecular polymer of glucose used to store energy, and is important for maintaining glucose hemostasis in the blood, as well as for providing energy for skeletal muscle and cardiac muscle contraction. Molecules of glucose are linked into linear chains by α-1,4-glycosidic bonds. Additionally, branches of glucose are formed off of the chain by α-1,6-glycosidic bonds. 2 molecules of glucose are joined into an α-1,4-glycosidic bonds by an enzyme known as glycogen synthase. This bond may be broken by amylase when the body wishes to break down glycogen into glucose for energy. Glycogen branching enzyme is responsible for the required α-1,6-glycosidic bonds needed to start a branch off of these linear chains.

Any disruption to this system results in a glycogen storage disease. There are currently 3 subcategories of glycogen storage diseases in horses: Type 1 Polysaccharide Storage Myopathy, Glycogen Branching Enzyme Deficiency , and Type 2 Polysaccharide Storage Myopathy.

Type 1 PSSM is caused by an autosomal dominant genetic mutation known as GSY1. This mutation causes an up-regulation of glycogen synthase, and high levels of glycogen synthase relative to glycogen branching enzyme . This altered ratio of glycogen synthase to GBE results in glycogen molecules with long chains and few branches, making these molecules somewhat amylase resistant. The GSY1 mutation is associated with altered glucose metabolism , as well as accumulation of high levels of glycogen and abnormal polysaccharide in the muscles of the horse. Additionally, some horses have been shown to have insulin sensitivity, which improves glucose uptake by muscle cells and contributes to excessive glycogen storage that is already elevated secondary to the GSY1 mutation.

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