A new paper published in the journal Proceedings of the Royal Society B indicates the dangers of living in an "eternal summer." The authors are from a team of researchers at the University of Aberdeen in the U.K. They think that we may be working against health related bodily systems which have evolved during hundreds of thousands of years to protect us from dangers in each unique season. Artificially changing the environment we live in, such as living in central heating environment, may be responsible for this.
Humans are sensitive to seasonal variations, as has been known for scientists—it is in our genes, about a quarter of them by recent estimates. We simulate summer conditions and go on to live in heated homes filled with light and heat when winter comes, doesn't it have any impacts on our bodies? It is still an unsolved mystery. The researchers evolved in this paper believe that there is an impact, which is not good.
According to the researchers, our bodies have been programmed to adapt regularly to seasonal changes. Important genes have evolved to the nudge the production of proteins, normally would be responsible for helping guard against ailments like the flu. If we stay in relatively high temperature, which seems to fool our body into thinking that they will be in summer all the time, it will make us more vulnerable. They also point out that modern people are protecting themselves artificially against global warming. When the temperature grows higher, we tend to keep the thermostat at the level we like. However, it could be dangerous, for we don't know what the real condition outside is when we are in the environment created as we like. It leads to disconnect between the reality and us.
The study provides many kinds of scenarios surrounding seasonal disruption, stressing out what the researchers believe are key areas of concern—all from a variety of viewpoints which include an overall environmental perspective, one focused on agricultural and others focused on anthropological, veterinary or biomedical standpoints—with each circling around the de-synchronization of our internal biology and the real environment outside of our virtual existences. Each topic can be an area of study and they can be put together to form the basis of a framework for trans-disciplinary research, which can finally unlock the secret of the impact of humans living in artificial environments, according to the researchers.
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2015年10月14日星期三
A team finds the first sensor mechanism of detecting electric fields
Many animals have the ability to sense and react to electric fields. Living human cells will move along an electric field for wound healing. But how do they sense the electric fields? A research team led by Min Zhao at the UC Davis Institute for Regenerative Cures now has found the first "sensor mechanism" that allows a living cell to detect an electric field. Their work is published in the journal Nature Communications on Oct. 9.
These researchers believed that there were several types of sensing mechanisms, and none of them were known. Now they provide experimental evidence to suggest a mechanism which has not been even hypothesized before. It is a two-molecule sensing mechanism.
Zhao and his colleagues have been studying these "electric senses" in cells from both larger animals and in the soil-dwelling amoeba Dictyostelium. By knocking out some genes in Dictyostelium, they previously identified some of the genes and proteins that allow the amoeba to move in a certain direction when exposed to an electric field.
In the new research a human cell line, they found that two elements, a protein called Kir4.2 which is made by gene KCNJ15, and molecules within the cell called polyamines, were needed for signaling to occur. Kir4.2 is a potassium channel. It forms a pore through the cell membrane that allows potassium ions to enter the cell. Such ion channels are often involved in transmitting signals into cells. Polyamines are molecules within the cell that carry a positive charge.
During the researche, they found that when the cells were in an electric field, the positively-charged polyamines tend to accumulate at the side of the cell near the negative electrode. The polyamines bind to the Kir4.2 potassium channel, and regulate its activity.
Zhao said that haven't got definitive evidence of how "switching" of the potassium channel by polyamines translates into directional movement by the cell. But the exploration of the sixth sense will never stop.
Read more:http://www.cusabio.com/catalog-9-1.html
These researchers believed that there were several types of sensing mechanisms, and none of them were known. Now they provide experimental evidence to suggest a mechanism which has not been even hypothesized before. It is a two-molecule sensing mechanism.
Zhao and his colleagues have been studying these "electric senses" in cells from both larger animals and in the soil-dwelling amoeba Dictyostelium. By knocking out some genes in Dictyostelium, they previously identified some of the genes and proteins that allow the amoeba to move in a certain direction when exposed to an electric field.
In the new research a human cell line, they found that two elements, a protein called Kir4.2 which is made by gene KCNJ15, and molecules within the cell called polyamines, were needed for signaling to occur. Kir4.2 is a potassium channel. It forms a pore through the cell membrane that allows potassium ions to enter the cell. Such ion channels are often involved in transmitting signals into cells. Polyamines are molecules within the cell that carry a positive charge.
During the researche, they found that when the cells were in an electric field, the positively-charged polyamines tend to accumulate at the side of the cell near the negative electrode. The polyamines bind to the Kir4.2 potassium channel, and regulate its activity.
Zhao said that haven't got definitive evidence of how "switching" of the potassium channel by polyamines translates into directional movement by the cell. But the exploration of the sixth sense will never stop.
Read more:http://www.cusabio.com/catalog-9-1.html
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