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Recently, researchers from McGill University in England found that the main chemical components of salt - sodium , is a major neurotransmitter receptor specificity "switch." The receptor is known as kainate (kainate-receptor), which is associated with a number of diseases such as epilepsy and neuropathic pain . Related study published in the "Nature Structural & molecular BioLogy"

The balance of kainate receptor activity is the key to maintaining the normal brain functions. Under conditions such as epilepsy, kainate activity is considered to be excessive. Thus, the drugs that closed the activity of kainate are expected beneficial . The researchers said that, over past decades, the assumed brain receptor "switches" are considered to locate in the neurotransmitter binding site. Now scientists have discovered a completely separate sites, the sodium combined with a single atom , controlling kainate receptors on and off.

Sodium switch is special for kainate receptor , indicating aimed to stimulate the current switch drugs are not functional in others parts of the brain . Researchers believed that : Now that we have known how to stimulate kainate receptor, then it should be possible to design drugs to turn off the receptors. Researchers are trying to use computer simulation to predict how sodium affects the kainate receptors.

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Recently, mycologist Paul Stamets demonstrated the benefits of a kind of fungus called agarikon , which grows on forest trees in North America and Europe . Researcher reported the ability of the fungus to anti-bacteria and fungi , at the same time they also claimed that we should protect the original forest trees so that this antibacterial fungus can always go on.

Agarikon fungi growth on a tree, similar to a big hornet's nest, historical records Native American people have grated this fungi , considering it as a drug to treat many disease . Even the ancient Greeks knew pharmaceutical properties of this fungus, which indicating that in ancient times , people had used this agarikon fungi to defend a series of disease . In this study, researchers in cooperation with the University of Illinois to study medicinal properties of agarikon . And they proved that agarikons sre used as a resistance of Mycobacterium tuberculosis , it has certain activity . And at same time , this fungi also can reduce the inflammation, which may also be used to combat bacteria, virus infection.

With deep study, the researchers also found that agarikon also can help against vaccinia, swine flu and avian flu ; In some cases, agarikon is more effective than conventional therapies . But there are no evidence to confirm that agarikon has no side effects on human body .The researchers noted that their mission is not just discovery the agarikon , but they also want to look for other natural medicines which contribute to human health,in view of this point , the researchers hope we will not destroy the ecosystem , in particular some trees. Finally, the discovery of the agarikon could allow scientists to conduct more deep studies to conduct clinical experiment to help treat human diseases.

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Cancer cells are escaping experts , now the scientists from University of California, Moores Cancer Center have revealed their secret. Research shows that a key protein promotes tumor growth, contributing to help cancer cells break through the organization captivity. After the formation of the tumor cells , it would be limited by the surrounding tissue, only to enter into the blood or lymphatic vessels, can it be transferred to other parts. Studies have shown that the growth factor VEGF may help cancer cells release the connection between the vessel wall endothelial cells, allowing cancer cells to squeeze blood as well as spread to other tissues through the metastatic .

This effect of VEGF is associated with the phosphorylation of protein VEC,which is a protein can closely linked to the endothelial cell. VEC phosphorylation will cause the dissociation of the whole complex, forming voids in endothelial cells. The researchers noted that focal adhesion kinase FAK is critical in the process of described above, VEGF will make FAK accumulating in the cell junction. Researchers tested on two group of mice , these two groups of mice were suffering from breast cancer and ovarian cancer. They treated these mice with FAK inhibitor , finding that in tumor-associated blood vessels, FAK inhibitor prevented the phosphorylation of VEC tyrosine 658. Subsequently, they introduced into mutation into the mouse endothelial cells FAK to inactivate the FAK as well as the injection of VEGF, and the research indicated that VEC tyrosine 658 was phosphorylated for the contrast mice .

Researchers released tumor cells of the VEGF and mixed with endothelial cells in vitro. These tumor cells firstly adhered to the endothelial cell layer, and then pass therethrough. Research shows that when FAK in endothelial cells is inactivated, tumor cells still can adhere to the endothelial cell layer, but they can not cross this barrier. Moreover, if a mutation in the endothelial cells of VEC can not lead to the phosphorylation, it is difficult to tumor cells through the cell layer.

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Recently, the University of California, San Francisco (UCSF) Diabetes Research Center conducted a new study and found that a enzyme called EHMT with a higher level in brown fat tissues is a essential ingredient of cDM16 transcription compound to control the fate of brown fat cells . This study provides a new mechanism of obesity research .

The losing of EHMT1 in brown fat cells lead to the missing of characteristics of brown fat , which induce muscle differentiation by demethylation of Histone 3 Lys 9 controlled by muscle selective gene.In contrast, EHMT1 expression by making protein PRDM16 become stable to open up heat gene program in brown fat cells . The removing of EHMT1 from the fat will reduce the adaptive heat generation which mediated by BAT, resulting in obesity and insulin resistance.

This research indicated that enzyme EHMT1 master the “fate” of brown fat cells to against obesity and related disease , which also provides a new clue to research and develop effective drugs to defend obesity . Enzyme EHMT1 plays an important role in controlling brown fat cells , which also contribute to kill brown fat cells to inhibit obesity . This new research bring new hope for patients with obesity and some related disease such as diabetes and some others metabolic diseases .

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Myosin myosins are a class of molecular motors in eukaryotic cells, playing an important role in cell movement and transport , such as myosin II plays an important role in muscle contraction and cell division process; myosin protein VIIa (MYO7A) in cells in the body is responsible for the transport of molecules, it is particularly important for the function of the hair cells of human hearing and eye development; myosin X can help to establish a connection between the neurons in development and others neurons

Researchers from Hong Kong University of Science and Technology have discovered a myosin X is different from the past cognition, antiparallel coiled - curled dimer structure, the researchers believed that this dimerization may be able to helpmyosin X walking in a single and multi-beam actin filaments. The study found the movement of unconventional myosin in actin filaments usually needs protein dimer . While about myosin dimer, a widely accepted mechanism is that it expand towards to motor lever arm domains through the terminal carboxyl group of amino acid residues , forming a parallel coiled - Curl dimer.

The researchers found that myosin X predicts to appear a curl - in the area of curl , it forms a high stable and antiparallel coiled -anti-CC . If by a single point mutation, or with a parallel coiled coil having a similar length to replace anti-CC , it will interrupt the anti-CC. And in further experiments, the researchers found that anti-CC as well as the single α-helical domain of myosin X can connect each other by semi-rigid screw connector . All of the research results suggested that dimerization directed by anti-CC may help contribute to the myosin X walking on single and multi-beam actin filaments

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