[Latin Name] Amorphophallus konjac

[Plant Source] from China

[Specifications] Glucomannan85%-90%

[Appearance] White or cream-color powder

Plant Part Used:Root

[Particle size] 120 Mesh

[Loss on drying] ≤10.0%

[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

[Introduction]

Konjac is a plant that is found in China, Japan and Indonesia. The plant is part of the genus Amorphophallus. Typically, it thrives in the warmer regions of Asia.

The extract of the Konjac root is referred to as Glucomannan. Glucomannan is a fiber-like substance traditionally used in food recipes, but now it is utilized as an alternative means of weight loss. Along with this benefit, konjac extract contains other benefits for the rest of the body as well.

The main material of the natural konjac gum is fresh konjac, which grow in virgin forest in Hubei area. We use advanced method to distill the KGM, aminophenol, Ca, Fe, Se which are good for health. Konjac is known as“ the seventh nutriment for human”.

Konjac Gum with its special water holiding capacity, stability, emulsibility, thickening property,suspension property and gel propery can especially adopted in food industry.

[Main Function]

1.It could reduce postprandial glycemia, blood cholesterol and blood pressure.

2.It could control appetite and reduce body weight.

3.It could increase insulin sensitivity.
4.It could control insulin resistant syndrome and diabetesII development.
5.It could reduce heart disease.

[Application]

1) Gelatinizer(jelly, pudding, Cheese, soft candy, jam );

2) Stabilizer(meat, beer);

3) Film Former(capsule, preservative)

4) Water-keeping agent( Baked Foodstuff );

5) Thickener (Konjac Noodles, Konjac Stick, Konjac Slice, Konjac Imitating Food stuff);

6) Adherence agent( Surimi );

7) Foam Stabilizer (ice cream, cream, beer)

Characterizing the DNA Damage Response by Cell Tracking Algorithms and Cell Features Classification Using High-Content Time-Lapse Analysis. Walter Georgescu et al (2015), PLoS ONE https://dx.doi.org/10.1371/journal.pone.0129438

Traditionally, the kinetics of DNA repair have been estimated using immunocytochemistry by labeling proteins involved in the DNA damage response (DDR) with fluorescent markers in a fixed cell assay. However, detailed knowledge of DDR dynamics across multiple cell generations cannot be obtained using a limited number of fixed cell time-points. Here we report on the dynamics of 53BP1 radiation induced foci (RIF) across multiple cell generations using live cell imaging of non-malignant human mammary epithelial cells (MCF10A) expressing histone H2B-GFP and the DNA repair protein 53BP1-mCherry. Using automatic extraction of RIF imaging features and linear programming techniques, we were able to characterize detailed RIF kinetics for 24 hours before and 24 hours after exposure to low and high doses of ionizing radiation. High-content-analysis at the single cell level over hundreds of cells allows us to quantify precisely the dose dependence of 53BP1 protein production, RIF nuclear localization and RIF movement after exposure to X-ray. Using elastic registration techniques based on the nuclear pattern of individual cells, we could describe the motion of individual RIF precisely within the nucleus. We show that DNA repair occurs in a limited number of large domains, within which multiple small RIFs form, merge and/or resolve with random motion following normal diffusion law. Large foci formation is shown to be mainly happening through the merging of smaller RIF rather than through growth of an individual focus. We estimate repair domain sizes of 7.5 to 11 µm2 with a maximum number of ~15 domains per MCF10A cell. This work also highlights DDR which are specific to doses larger than 1 Gy such as rapid 53BP1 protein increase in the nucleus and foci diffusion rates that are significantly faster than for spontaneous foci movement. We hypothesize that RIF merging reflects a “stressed” DNA repair process that has been taken outside physiological conditions when too many DSB occur at once. High doses of ionizing radiation lead to RIF merging into repair domains which in turn increases DSB proximity and misrepair. Such finding may therefore be critical to explain the supralinear dose dependence for chromosomal rearrangement and cell death measured after exposure to ionizing radiation.

For more info go to: https://www.marketamerica.com/hismart/topproducts-13009/isotonix-opc3.htm