EMF Blocking and EMF Shielding
No matter if you live in an apartment or house or just need to ensure that your house is free from EMFs, there are a number options to limit your exposure. block emf of the easiest is to restrict your use of electronic devices. https://k12.instructure.com/eportfolios/372604/Home/Information_about_Emf_Blocking_Radiation_2 can also turn to EMF blocker paint to block EMF radiation from reaching your home. Another method to protect your home from EMF radiations is to install a RF shielding canopy. It is a type made of net that has EMF shielding. It's used to prevent EMFs from entering a space. Another option is to have your house equipped with an electrical enclosure. These enclosures are known as Faraday cages.
A number of studies have proven that the non-ionizing RF EMF can cause antiproliferative effects in HCC cells. The mechanism of AM RF EMF's anticancer activity in vitro is thought to result from the deregulation the cancer stem cell. This could explain the long-term responses seen in some patients with advanced HCC. However, the mechanism behind AM EMF's impact on patients with cancer is not clear.
Effects from AM electromagnetic fields (RFEM) on HCC tumor growth in vivo were studied in mice. The tumours were divided into 3 groups. First, the group that was unaffected to RF EMF. Second group members were exposed to RF EMF at frequencies similar to the one used by humans. Third group members were exposed RF EMF with HCC-specific modulation frequencies. The impact of HCCMF on tumors was compared to that of RCF. The results revealed that cancers treated with HCCMF showed significant shrinkage. However, tumours treated with RCF showed no evidence of tumour shrinkage.
The mechanism behind tumour-specific AM RF EMF might be based on the fact that tumour cells require Cav3*2 voltage calcium channels for proliferation and down-regulation. AM RF EMF's antiproliferative effects upon HCC cells is caused by CACNA1H the protein that mediates tumour-specific Ca2+ influx. Look at more info indicate that CACNA1H could have more broader implications for treatment and diagnosis of many cancers.
The tumours of the control group were not exposed to RF EMF, and were fed a normal mouse diet. The tumours in those in the HCCMF group were treated with Huh7 cells after they were 5 to 7 weeks old. The tumors were then killed in cases of excessive burden.
The tumors of the three groups also showed distinct growth curves. The tumors treated with HCCMF had a significant reduction in size of the tumor after eight weeks. However, the tumors that were treated using RCF showed no shrinkage. The difference was substantial. The tumors treated by RCF showed necrosis, which is common in tumors that have been that are exposed to RCF. There is a possibility that the necrosis is caused by an absence of oxygen in larger tumours.
In sum, the results show an AM-RF EMF is a powerful source of anticancer activity in vitro and in vivo. Numerous studies have demonstrated that AM RF EMF produces measurable reduction in tumours within HCC patients. There is a possibility that AM RF EMF triggers these effects due to CACNA1H which is a protein involved in tissue-specific Ca2+ influx. Additionally, AM RF EMF may cause a lasting impact on the growth of HCC tumors in vivo.