Posts Tagged ‘settings’

Brain-computer interface lets ALS patient communicate with her family

An ALS patient who received a brain implant at University Medical Center Utrecht (UMCU) in the Netherlands has reportedly become the first person with the neurodegenerative condition to use this technology to communicate with family, friends, and caregivers in her own home. The feat, detailed this week in the New England Journal of Medicine, is […]

The post Brain-computer interface lets ALS patient communicate with her family appeared first on Redorbit.

Control of mitochondrial function and cell growth by the atypical cadherin Fat1

Mitochondrial products such as ATP, reactive oxygen species, and aspartate are key regulators of cellular metabolism and growth. Abnormal mitochondrial function compromises integrated growth-related processes such as development and tissue repair, as well as homeostatic mechanisms that counteract ageing and neurodegeneration, cardiovascular disease, and cancer. Physiologic mechanisms that control mitochondrial activity in such settings remain incompletely understood. Here we show that the atypical Fat1 cadherin acts as a molecular ‘brake’ on mitochondrial respiration that regulates vascular smooth muscle cell (SMC) proliferation after arterial injury. Fragments of Fat1 accumulate in SMC mitochondria, and the Fat1 intracellular domain interacts with multiple mitochondrial proteins, including critical factors associated with the inner mitochondrial membrane. SMCs lacking Fat1 (Fat1KO) grow faster, consume more oxygen for ATP production, and contain more aspartate. Notably, expression in Fat1KO cells of a modified Fat1 intracellular domain that localizes exclusively to mitochondria largely normalizes oxygen consumption, and the growth advantage of these cells can be suppressed by inhibition of mitochondrial respiration, which suggest that a Fat1-mediated growth control mechanism is intrinsic to mitochondria. Consistent with this idea, Fat1 species associate with multiple respiratory complexes, and Fat1 deletion both increases the activity of complexes I and II and promotes the formation of complex-I-containing supercomplexes. In vivo, Fat1 is expressed in injured human and mouse arteries, and inactivation of SMC Fat1 in mice potentiates the response to vascular damage, with markedly increased medial hyperplasia and neointimal growth, and evidence of higher SMC mitochondrial respiration. These studies suggest that Fat1 controls mitochondrial activity to restrain cell growth during the reparative, proliferative state induced by vascular injury. Given recent reports linking Fat1 to cancer, abnormal kidney and muscle development, and neuropsychiatric disease, this Fat1 function may have importance in other settings of altered cell growth and metabolism.

Academy of Social Sciences Names 83 New Fellows

The Academy of Social Sciences has conferred the award of fellow on 83 leading social scientists, including such luminaries as Lord Stern, Nudge Unit founder David Halpern and Madeleine Atkins of HEFCE.

The post Academy of Social Sciences Names 83 New Fellows appeared first on Social Science Space.

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