Intelligence Advanced Research Projects Activity (IARPA), the intelligence community’s research arm, will soon launch two programs designed to detect fake fingerprints and develop devices to collect fingerprint data without the aid of a human operator, according to a report by GCN.
The Odin program, which is scheduled to begin with four prime developers in early March, will develop detection technologies that can spot presentation attacks on biometric devices that attempt to spoof physical biometric samples, said Chris Boehnen, senior program manager at IARPA.
Boehnen said that prosthetic fingers, fake fingerprints made with wood glue and other tactics can dupe current fingerprint sensors.
Is Synbio the next big thing? Hmmm; depends. If we’re talking about ensuring that we have a solid foundation/ infrastructure (including platforms; etc.) on QC 1st then with the existing evolution and maturity of the fundamentals around Synbio as a 1st step; then accelerating the further maturity of Synbio into creating super humans and singularity? My answer is yes. If we’re not even considering that we need QC and just focused on Synbio only; my answer is No as QC will be required as a foundation for things like real Humanoid AI, cell circuited humans/ super humans, etc.
Why we might soon be buying silk, wood, and more fabricated out of genetic code.
Could we eventually see a day where we have cell circuitry nanobot pill that eliminates hunger and obesity as replacement to gastric bypasses? Maybe.
The human body responds to starving conditions, such as famine, to promote the chance of survival. It reduces energy expenditure by stopping heat production and promotes feeding behavior. These “hunger responses” are activated by the feeling of hunger in the stomach and are controlled by neuropeptide Y (NPY) signals released by neurons in the hypothalamus. However, how NPY signaling in the hypothalamus elicits the hunger responses has remained unknown.
Sympathetic motor neurons in the medulla oblongata are responsible for heat production by brown adipose tissue (BAT). Researchers centered at Nagoya University have now tested whether the heat-producing neurons respond to the same hypothalamic NPY signals that control hunger responses. They injected NPY into the hypothalamus of rats and tested the effect on heat production. Under normal conditions, blocking inhibitory GABAergic receptors or stimulating excitatory glutamatergic receptors in the sympathetic motor neurons induced heat production in BAT. After NPY injection, stimulating glutamatergic receptors did not produce heat, but inhibiting GABAergic receptors did. The study was recently reported in Cell Metabolism.
Retrograde and anterograde tracing with fluorescent dyes revealed which brain region provided the inhibitory GABAergic inputs to heat-producing motor neurons.
Clearing out senescent cells could lead to better fitness and health as we age.
From around age forty we start to lose muscle mass due to various aging processes, one of these processes is the accumulation of senescent cells. Senescent cells are simply cells that have become damaged or have reached their maximum number of divisions. Normally these cells are shut down by a kind of self destruct program inside the cell, ready to be disposed of by the immune system.
However as the immune system ages, it stops clearing house properly, leaving many of these senescent cells in place. This would not be such a big deal, but senescent cells actually send out toxic inflammatory signals that block tissue regeneration. This includes the compromised formation and repair of muscle tissue[1–2]. Some researchers suggest that removing senescent cells could potentially lead to better performance and extending peak, allowing you to enjoy sports and remain competitive for longer.
There have been some interesting results on cardiovascular health and performance seen in pre-clinical studies so far. In tests aged mice had significantly improved vascular health when treated, compared to control mice left to age normally[3–4]. Perhaps even more exciting is the discovery that this therapy can also make an impact on heart disease. So reducing senescent cells could be a route to better cardiovascular health and improved fitness as we get older[5].
What does the New Year have in store for #CRISPR? This blog presents 5 CRISPR-enabled breakthroughs to look for in 2017. (Partner content via Synthego)
Today scientists at the Institute for Research in Biomedicine (IRB Barcelona) present a study in Cell (“The in vivo architecture of the exocyst provides structural basis for exocytosis”) where they have been able to observe protein nanomachines (also called protein complexes)—the structures responsible for performing cell functions—for the first time in living cells and in 3D. This work has been done in collaboration with researchers at the University of Geneva in Switzerland and the Centro Andaluz de Biología del Desarrollo in Seville.
On the left, in vivo image of nanomachines using current microscopy techniques; on the right, the new method allows 3D observation of nanomachines in vivo and provides 25-fold improvement in precision (O. Gallego, IRB Barcelona)
