Since launching on the iPhone X back in 2017, facial recognition has become a staple feature in most smartphones. But while the technology is undeniably handy, it could land you in hot water if you have a smartphone from Honor, Motorola, Nokia, Oppo, Samsung, Vivo, or Xiaomi. Experts from Which? have warned that 19 phones from these popular brands have facial recognition systems that can easily be fooled by 2D photos. Lisa Barber, Tech Editor at Which?, said: 'It's unacceptable that brands are selling phones that can easily be duped using a 2D photo, particularly if they are not making their customers aware of this vulnerability. 'Our findings have really worrying implications for people's security and susceptibility to scams.' Since launching on the iPhone X back in 2017, facial recognition has become a staple feature in most smartphones.

Drug discovery is vitally important for protecting human against disease. Target-based screening is one of the most popular methods to develop new drugs in the past several decades. This method efficiently screens candidate drugs inhibiting target protein in vitro, but it often fails due to inadequate activity of the selected drugs in vivo. Accurate computational methods are needed to bridge this gap. Here, we propose a novel graph multi task deep learning model to identify compounds carrying both target inhibitory and cell active (MATIC) properties. On a carefully curated SARS-CoV-2 dataset, the proposed MATIC model shows advantages comparing with traditional method in screening effective compounds in vivo. Next, we explored the model interpretability and found that the learned features for target inhibition (in vitro) or cell active (in vivo) tasks are different with molecular property correlations and atom functional attentions. Based on these findings, we utilized a monte carlo based reinforcement learning generative model to generate novel multi-property compounds with both in vitro and in vivo efficacy, thus bridging the gap between target-based and cell-based drug discovery.

Neutrophils play a major role in the early immune response and are recruited in large numbers into inflamed and infected tissues. By secreting chemoattractants that bind G protein–coupled receptors (GPCRs) on neighboring cells, neutrophils coordinate their behavior as a swarm. Less clear is how this auto-amplifying swarming activity is ultimately turned off. Kienle et al. show that desensitization of these GPCRs by the same chemoattractants by GPCR-kinase 2 (GRK2) is one way in which these swarms are shut down (see the Perspective by Rocha-Gregg and Huttenlocher). Unexpectedly, mice with GRK2-deficient neutrophils showed impaired rather than enhanced bacterial clearance. The heightened scanning ability of GRK2-deficient neutrophils may come at the cost of suboptimal phagocytosis and containment of bacteria. Science , abe7729, this issue p. [eabe7729][1]; see also abj3065, p. [1262][2] ### INTRODUCTION The collective behavior of cells and insects often relies on self-organizing processes. By releasing attractant signals, a few individuals can initiate the accumulation and aggregation of a whole population. Neutrophils, key players in the innate immune response, infiltrate inflamed and infected tissues in large numbers. These cells make use of such positive feedback amplification to find and kill bacteria in tissues. By secreting attractants that act through cell surface–expressed G protein–coupled receptors (GPCRs) on neighboring cells, neutrophils use this form of intercellular communication and coordinate their hunt for pathogens as a swarm. How this swarming response is terminated to avoid uncontrolled neutrophil accumulations and prevent excessive inflammation is currently unknown. ### RATIONALE The stop signals for neutrophil swarming in mammalian tissues have not yet been defined. They may be derived from cells of the surrounding inflammatory environment or from neutrophils themselves. We reasoned that the attractants released by neutrophils may become highly concentrated at sites where these cells cluster in larger numbers. It is well established that high chemoattractant concentrations can attenuate cellular responses by a process termed GPCR desensitization. We hypothesized a self-limiting mechanism for swarming: The local accumulation of the same neutrophil-expressed attractants that amplify swarming during early stages would cause desensitization of their respective GPCRs at later stages of neutrophil clustering. This led us to investigate the role of GPCR desensitization in neutrophil tissue navigation and host defense. ### RESULTS We generated mouse strains whose neutrophils were deficient in GPCR kinases (GRKs), critical enzymes for mediating the GPCR desensitization process. Of the four GRK isoforms tested, in vitro experiments identified GRK2 as the kinase necessary to desensitize GPCRs activated by swarm-released attractants (LTB4 and CXCL2). When neutrophils sense high concentrations of swarm attractants in vitro, GRK2 desensitizes the corresponding receptors to induce migration arrest. Two-photon intravital imaging of injured skin and infected lymph nodes of mice showed that GRK2 and GPCR desensitization play critical roles during neutrophil swarming in physiological tissue. At sites where swarming neutrophils accumulate and self-generate local fields of high swarm attractant concentration, GPCR desensitization was crucial to stop neutrophil migration arrest. Desensitization-resistant neutrophils moved faster and explored larger areas of lymph node tissue infected with the bacterium Pseudomonas aeruginosa . Such behavior suggested more effective bacterial sampling throughout the infected organ. Surprisingly, mice with GRK2-deficient neutrophils showed impaired rather than improved bacterial clearance. This finding could not be explained by altered antibacterial effector functions. In vitro assays for the detailed analysis of swarming behavior and bacterial growth revealed that GPCR desensitization to swarm attractants is required to induce neutrophil arrest for optimal bacterial phagocytosis and containment in swarm clusters. ### CONCLUSION We describe a cell-intrinsic stop mechanism for the self-organization of neutrophil collectives in infected tissues, which is based on sensing the local accumulation of the same cell-secreted attractants that amplify swarming during early stages. GPCR desensitization acts as a negative feedback control mechanism to stop neutrophil migration in swarm aggregates. This navigation mechanism allows neutrophils to self-limit their dynamics within forming swarms and ensures optimal elimination of bacteria. Desensitization to a self-produced activation signal as a principle of self-organization is important for immune host defense against bacteria, and likely informs other categories of collective behavior in cells and insects. ![Figure][3] Self-organization of neutrophil swarms. Top: Swarming neutrophils self-amplify their highly chemotactic recruitment toward sites of tissue injury or bacterial invasion by releasing attractants that act on neighboring neutrophils. Neutrophils are displayed as spheres with migration tracks (right). Bottom: The local accumulation of the same cell-secreted attractants stops neutrophils when they accumulate and form clusters, a process important for the containment of bacteria in infected tissues. Neutrophils communicate with each other to form swarms in infected organs. Coordination of this population response is critical for the elimination of bacteria and fungi. Using transgenic mice, we found that neutrophils have evolved an intrinsic mechanism to self-limit swarming and avoid uncontrolled aggregation during inflammation. G protein–coupled receptor (GPCR) desensitization acts as a negative feedback control to stop migration of neutrophils when they sense high concentrations of self-secreted attractants that initially amplify swarming. Interference with this process allows neutrophils to scan larger tissue areas for microbes. Unexpectedly, this does not benefit bacterial clearance as containment of proliferating bacteria by neutrophil clusters becomes impeded. Our data reveal how autosignaling stops self-organized swarming behavior and how the finely tuned balance of neutrophil chemotaxis and arrest counteracts bacterial escape. [1]: /lookup/doi/10.1126/science.abe7729 [2]: /lookup/doi/10.1126/science.abj3065 [3]: pending:yes

Consider for a moment what it takes to visually identify and describe something to another person. Now imagine that the other person can't see the object or image, so every detail matters. How do you decide what information is important and what's not? You'll need to know exactly what everything is, where it is, what it's doing in relation to other objects, and note other attributes like color or position of objects in the foreground or background. This exercise shows there's no question that translating images into words is a complex task--one humans do so often and innately it seems automatic at times--requiring a wide range of knowledge about many unique things. In order to translate this skill into artificial intelligence (AI), we need to carefully consider and adapt models to the deep relationships between words and objects, the way they interrelate in expected and unexpected ways, and how contexts like environment and pose of an object affect the subtleties of associating and understanding new objects within categories.

Beyond Xiaomi and Realme, one Chinese smartphone brand that has seen amazing growth in India is Vivo which will double down on its efforts to develop Artificial Intelligence (AI)-enabled 5G devices in 2020 to match the fast-paced lifestyle of consumers, a top company executive said on Wednesday. The brand took a big leap with capturing 17 per cent market share – its highest-ever -- in the third quarter (July-September period) this year. It is now third in the India smartphone market – after Xiaomi and Samsung – and according to Nipun Marya, Director Brand Strategy, Vivo India, the brand has recorded its highest-ever market share of 23 per cent for the month of October (according to German market research firm GfK). "Yes! 2019 has been a good year for Vivo in India. Our endeavour is to constantly give industry-first innovations to our customers, continually expand our distribution footprint, and announce more investments as part of our commitment to the India market," Marya told IANS in an interview.

Beyond Xiaomi and Realme, one Chinese smartphone brand that has seen amazing growth in India is Vivo which will double down on its efforts to develop Artificial Intelligence (AI)-enabled 5G devices in 2020 to match the fast-paced lifestyle of consumers, a top company executive said on Wednesday. The brand took a big leap with capturing 17 percent market share - its highest-ever -- in the third quarter (July-September period) this year. It is now third in the India smartphone market - after Xiaomi and Samsung - and according to Nipun Marya, Director Brand Strategy, Vivo India, the brand has recorded its highest-ever market share of 23 percent for the month of October (according to German market research firm GfK). "Yes! 2019 has been a good year for Vivo in India. Our endeavour is to constantly give industry-first innovations to our customers, continually expand our distribution footprint, and announce more investments as part of our commitment to the India market," Marya told IANS in an interview.

Ever wonder how neuroscientists are able to monitor and study what happens inside a living brain in action? One of the challenges in neuroscience is observing the activity of neurons intact in brain tissue that is taking place in a living organism--in vivo. One approach, two-photon calcium imaging, is a method developed circa 1990. In mammalian neurons, calcium is an intracellular messenger. This imaging approach involves the loading of calcium ions (Ca2) indicator dyes in the desired brain region for neuronal monitoring and a two-photon laser scanning microscope for visualization.

Adaptive behaviors ranging from self-assembly to self-healing showcase the ability of such systems to sense and adapt to dynamic environments based on signaling between living cells. This signaling takes on many forms--biochemical, mechanical, and electrical--and uncovering it has become as much the purview of regenerative medicine as of fundamental biology. We cannot reverse-engineer native tissues if we do not understand the fundamental design rules and principles that govern their assembly from the bottom up (1). Movement is fundamental to many living systems and driven primarily by skeletal muscle in human bodies. Disease or damage that limits the functionality of skeletal muscle severely affects human health, mobility, and quality of life.

Where were you when we defeated the robots? If you missed yesterday's Starcraft II stream, we'll fill you in on the details of DeepMind's latest gaming exploits. Also, MoviePass is ready to try unlimited tickets again, and we've got another new phone with (almost) no ports. Rise and fly, humans.DeepMind AI AlphaStar goes 10-1 against top'StarCraft II' pros After laying waste to the best Go players in the world, DeepMind has moved on to computer games. Its AI agent, named AlphaStar, managed to pick up 10 wins against StarCraft II pros TLO and MaNa in two separate five-game series that took place back in December.

Chinese phone maker Vivo has announced its own 3D sensing technology that could rival Apple's Face ID facial recognition feature. Vivo claims that its technology will have 10 times more sensor points than Apple's solution. "Vivo's TOF 3D Sensing Technology features industry-leading performance in depth of information captured with its 300,000 sensor points, which is 10 times the number of existing Structured Light Technology. This raises the bar by enabling 3D mapping at up to three meters from the phone while having a smaller baseline than Structured Light," Vivo said in a press release. "TOF 3D Sensing Technology is also simpler and smaller in structure and allows for more flexibility when embedded in a smartphone. This will enable much broader application of this technology than was previously possible."