Notice: Trying to access array offset on value of type null in /srv/pobeda.altspu.ru/wp-content/plugins/wp-recall/functions/frontend.php on line 698
If you reside in an apartment or a house or simply would like to keep your home free from EMFs There are a variety options to limit your exposure. One of the easiest is to restrict your electronic device use. You could also consider EMF block paint to stop EMF radiation from entering your house. Another easy way to protect your house against EMF radiations is to install an RF shielding canopy. This is a cloth of net that has EMF shielding. It’s used to stop EMFs from entering a space. Another option is to have your home equipped with an enclosure that is conductive. These devices are called Faraday cages.
Several studies have shown how the emf blockers that is not ionized has antiproliferative properties in HCC cells. The mechanism behind AM RF EMF’s anticancer activity in vitro is believed to be based on the downregulation of cancer stem cells. This may account for the long-term responses seen in patients with advanced HCC. But, the reason for AM EMF’s impact on cancer patients is not yet clear.
Effects of AM electromagnetic fields (RFEM) on HCC tumor growth in vivo were studied in mice. The tumours were classified into 3 groups. The first group was not exposed to RF EMF. Second group members were exposed RF EMF at frequencies similar to that of humans. In the third, they were subjected RF EMF with HCC-specific modulation frequencies. The impact of HCCMF on the tumours was compared to that of RCF. The results showed that the cancers treated with HCCMF were significantly shrinking. However, the tumours treated with RCF didn’t show evidence of shrinkage of the tumor.
The mechanism behind tumour-specific AM RF EMF may be based on the fact that tumour cells require Cav3*2 voltage calcium channels for their proliferation and down-regulation. AM RF EMF’s ability to inhibit proliferation on HCC cells is caused by CACNA1H which is a protein that regulates the Ca2+ influx specific to tumors. The findings suggest that CACNA1H could have wider implications for treatment and diagnosis of various cancers.
The tumours in those in the group that were unaffected to RF EMF, and were fed a standard mouse diet. The tumours in the HCCMF group were injected with Huh7 cells when they were 5 to 7 weeks old. The tumors were then killed when they showed excessive burden.
The tumours in the three groups also displayed distinct growth curves. The tumors treated with HCCMF showed a significant decrease in tumour size after 8 weeks. However, the tumors that were treated using RCF showed no shrinkage. The difference was highly significant. The tumours treated with RCF showed necrosis that is common in tumors that have been that are exposed to RCF. There is a possibility that the necrosis was due to the lack of oxygen in the larger tumours.
In conclusion, the findings indicate that AM RF EMF exhibits anti-cancer properties in vitro as well as in live. Several studies have shown it is true that AM RF EMF produces measurable reduction in tumours in HCC patients. The possibility is that the AM EMF triggers these effects through CACNA1H which is a protein involved in tissue-specific Ca2+ influx. Furthermore, AM RF EMF may exert a sustained effect on the growth of HCC tumours in the vivo.