[Latin Name] Cinnamomun camphcra

[Plant Source] It is extracted from Ginkgo Biloba Leaf.

[Specifications]

1, Ginkgo Biloba Extract 24/6

Total Ginkgo flavone glycosides 24%

Total terpene lactones 6%

2, Ginkgo Biloba Extract 24/6

Total Ginkgo flavone glycosides 24%

Total terpene lactones 6%

Ginkgolic acid 5ppm

3,CP2005

Total Ginkgo flavone glycosides 24%

Quercatin: kaemperol 0.8–1.5

Total terpene lactones 6%

Ginkgolic acid <5ppm

4.Germany Standard

Total Ginkgo Flavone Glycosides 22.0%-27%

Total Terpene Lactones 5.0%-7.0%

Bilobalides 2.6%-3.2%

Ginkgolic acid <1ppm

5.Water-Soluble Ginkgo Biloba Extract 24/6

Water Solubility: 5g Ginkgo Biloba Extract will be dissolved completely in 100g water

Total Ginkgo Flavone Glycosides 24.0%

Total Terpene Lactones 6.0%

Ginkgolic acid <5.0ppm

[Appearance] Light yellow fine powder

[Particle size] 80 Mesh

[Loss on drying] £ 5.0%

[Heavy Metal] £10PPM

[Extract solvents] Ethanol

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

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

[Function]

Expanding blood vessel, resisting insufficient blood and oxygen deficit, increasing blood flow, improving cerebral arteries and distal

blood flow. Promoting cerebral circulation metabolism, improving memory function, resisting depression, resisting lipidic overoxidation,

protecting liver damage.

In clinic, curing high blood pressure, hyperlipoidemia, coronary heart disease, angina pectoris, arterial sclerosis, cerebral embolism,

senile dementia, primary and periodic dropsy, acute drumming in the ears, epicophosis, a variety of body function in disorder, dizziness

and so on.

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The Classical pathway of activation of the complement system is a group of blood proteins that mediate the specific antibody response. The main activators of the Classical Pathway are antigen-antibody complexes.
It is triggered by antigen-bound antibody molecules. (The only antibodies capable of binding are two units of IgG or one IgM, although IgM is more effective at activating complement. IgG4 cannot bind, but the other three IgG types can.) It is the binding of Fc region to the C1 component that initiates this pathway. The classical pathway can also be triggered by binding of C1 to some types of structures on the target microbe. Also, it can be triggered by C-Reactive Protein binding to microbic polysaccharides such as phosphocholine.[
This initial enzyme, C1, is a complex formed through a calcium-dependent association between two reversibly interacting subunits, C1q and C1 (C1qr2s2). Approximately 70% of C1 is at all times present in this complex form. C1 occurs in serum as a proenzyme that tends to undergo autoactivation but is strictly controlled by C1-inhibitor (C1-In or C1 esterase). Upon the binding of C1 to immune complexes by virtue of the affinity of C1q for immunoglobulins (to be specific, IgM and IgG), the controlling action of C1-In is overcome, and C1q effects activation of C1r2s2.

C1q possesses no intrinsic catalytic activity, but, when any of several activators bind to the C1q subcomponent of C1, the homologous C1r and C1s subcomponents are converted into catalytically active species, namely C1r* and C1s*, triggering the first step of the classical pathway of complement activation.

Thus, on binding to immune complexes through C1q, the subunits of C1 become firmly associated and autoactivation commences even in the presence of the Cl-In. Source of the article published in description is Wikipedia. I am sharing their material. Copyright by original content developers of Wikipedia.
Link- https://en.wikipedia.org/wiki/Main_Page