[Products Name]  Propolis block, pure propolis, raw propolis

[Specification]  Propolis content 90%,95%

[Gerneral feature]

1. Low antibiotics

2. Low PAHs, can approve to 76/769/EEC/German:LMBG;

3.Organic certified by ECOCERT, according to EOS & NOP organic standard;

4.Pure natural propolis;

5.High content of flavones;

6.Low temperature extracted, retain high activity of all nutritions;

[Packaging]
1. 1kg/aluminum foil bag, 20kgs/carton.

[How to get it]

First, we collect raw propolis from beehives, then extract by low temperature with ethanol. Filter and concentrate, we get the pure propolis block at 90% to 95%.

[Introduction]

Propolis comes from the substance like natural resin, which is collected by the bees from exudates of plants branches and bud the chemical substances of Propolis are found to be various, such as beeswax, resin, incense lipids, aromatic oil, fat-soluble oils, pollen and other organic matter. Studies have shown that the source of propolis resin in material has three types: bees collected plants secreted fluid, secretion in vivo metabolism of bee, and involvement in the process of forming the material.

We can supply Propolis Extract with food-grade and medicine-grade .The raw materiall is came from non-polluting food grade propolis .Propolis extract was made of high-grade propolis. It maintains the propolis effective ingredients during the procedure of extraction under constant low temperature , taking off the useless substances and sterilization.

[Function]

Propolis is a natural product processed by bees mixed with glutinous and its secretion.

Propolis contains more than 20 kinds of useful flavonoids, rich vitamins, enzymes, amino acids and other microelements, etc. Propolis is called “purple gold” owing to its valued nutrients.

Propolis can remove free radical, lower blood sugar and blood fat, soften blood vessels, improve micro-circulation, enhance immunity, anti-bacteria and anti-cancer.

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.

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