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‘Good sleep’ essential for brain health

Researchers have found that one night of sleep depravity can cause morning blood concentrations of molecules NSE and S-100B to increase in healthy young men.

These molecules are typically found in the brain. Thus, their rise in blood after sleep loss may indicate that a lack of snoozing might be conducive to a loss of brain tissue.

The study involved fifteen normal-weight men, and in one condition they were sleep-deprived for one night, while in the other condition they slept for approximately 8 hours.

Sleep researcher Christian Benedict at the Department of Neuroscience, Uppsala University, who lead the study, said that they observed that a night of total sleep loss was followed by increased blood concentrations of NSE and S-100B.

He said that these molecules typically rise in blood under conditions of brain damage, asserting that their results indicate that a lack of sleep may promote neurodegenerative processes.
New potential cure for melanomas on horizon

Researchers have identified two novel BRAF fusions in melanomas previously considered to be negative for molecular targets, and that melanomas with these fusions were found to be potentially sensitive to anticancer drugs called MEK inhibitors.

According to Dr Jeffrey A. Sosman, professor of medicine at Vanderbilt-Ingram Cancer Center in Nashville, Tennessee, said that after performing a sophisticated analysis called targeted next-generation sequencing, it appears that about 8 percent of pan-negative melanomas have BRAF fusions.

In a pan-negative melanoma sample from one of their patients, Drs. Sosman and William Pao, M.D., Ph.D., a 2009 Stand Up To Cancer Innovative Research Grant recipient, and their colleagues identified a fusion between two genes, PAPSS1 and BRAF, which they called PAPSS1-BRAF.

They then evaluated melanomas from an additional 51 patients, 24 of which were pan-negative. In one of these 24 pan-negative samples, they identified a second novel BRAF fusion, called TRIM24-BRAF.

The investigators found that both BRAF fusions activated a pathway in the cancer cells called the MAPK signaling pathway. They then treated these fusion-bearing cells either with the BRAF inhibitor vemurafenib or with trametinib, a drug that inhibits a protein in the MAPK signaling pathway called MEK.
Chemotherapy could be more effective for pancreatic cancer

Researchers believe that they have found an effective strategy to make chemotherapy treatment more effective for pancreatic cancer patients.

The research found pancreatic cancer cells may have their own specialised energy supply that maintains calcium levels and keeps cancer cells alive. Maintaining a low concentration of calcium within cells is vital to their survival and this is achieved by calcium pumps on the plasma membrane.

This calcium pump, known as PMCA, is fuelled using ATP – the key energy currency for many cellular processes.

Scientists used cells taken from human tumours and looked at the effect of blocking each of these two energy sources in turn.

Their study showed that blocking mitochondrial metabolism had no effect. However, when they blocked glycolysis, they saw a reduced supply of ATP which inhibited the calcium pump, resulting in a toxic calcium overload and ultimately cell death.

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