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Now, pill that can explode cancer cellsResearchers have discovered that a substance called Vacquinol-1 that makes cells from glioblastoma, the most aggressive type of brain tumour, literally explode.

Researchers at Karolinska Institute and colleagues at Uppsala University have discovered an entirely new mechanism to kill tumour cells in glioblastoma. Researchers in an initial stage have exposed tumour cells to a wide range of molecules. If the cancer cells died, the molecule was considered of interest for further studies, which initially applied to over 200 kinds of molecules.Following extensive studies, a single molecule has been identified as being of particular interest.  It was found that the molecule gave the cancer cells an uncontrolled vacuolisation, a process in which the cell carries substances from outside the cell into its interior. This carrying process is made via the vacuoles, which can roughly be described as blisters or bags consisting of cell membranes.

When cancer cells were filled with a large amount of vacuoles, cell membranes collapsed and the cell simply exploded and necrotised. Researchers made mice that had human glioblastoma cells transplanted ingest the substance for five days. The average survival was about 30 days for the control group that did not receive the substance and those received the substance were still alive after 80 days.
New treatment could halt progression of dementiaResearchers have discovered a way to potentially halt the progression of dementia caused by accumulation of a protein known as tau.Normally, tau protein is involved in microtubule formation, which acts as a brain cell’s transportation system for carrying nutrients in and waste out. In the absence of tau protein, brain cells become dysfunctional and eventually die. In many forms of dementia, such as Alzheimer’s disease and chronic traumatic encephalopathy caused by multiple concussions, the tau protein starts behaving badly and instead of performing its normal cellular functions, it begins accumulating and interfering with cell-to-cell communications.

Without the ability of brain cells to receive signals, they become severely dysfunctional and if enough of them die in a given area of the brain, the result is cognitive impairment, which means difficulty in planning tasks and remembering things. This accumulation of tau results in the formation of tau oligomers (oligo- meaning “many”), the toxic form of tau protein.Scientists believe that if you can get rid of this toxic oligomeric tau protein, you can potentially stop the spread of tau-related dementia. The trick is to remove the toxic oligomeric tau without also removing the normal, functional tau protein.

Researchers have demonstrated that treatment with their tau oligomer-specific monoclonal antibody, called TOMA, in experiments involving a rodent model of tauopathy (tau-related dementia) improved locomotor function and performance on memory tests. The TOMA antibody sticks to the oligomeric tau so it can no longer interfere with cell-to-cell communication, but leaves the native tau protein intact.
How muscle physiology affects leannessResearchers have found that aerobic capacity is a major predictor of daily physical activity level among humans and laboratory animals.Researchers compared female rats with high aerobic capacity and low aerobic capacity to investigate how muscle physiology affects leanness.

Though the rats in each group were similar in weight and lean body mass, the rats with a high aerobic capacity were consistently more active than the low capacity rats. While all the rats had similar energy expenditures when at rest, big differences occurred during mild exercise. The researchers found the muscles of rats with lean genes demonstrated “poor fuel economy,” meaning that they burned more calories.

This may be due to more lean rats having higher levels of proteins that support energy expenditure and lower levels of proteins that encourage energy conservation or an increased sympathetic nervous system role in powering the muscles of lean rats.

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