Rapid advances in technology, connectivity and telecommunications are conspiring to make Africa's large, rapidly growing population a valuable asset for the automation revolution. It is imperative that Africa quickly develop agency in data and artificial intelligence and it will be lucrative for investors who support them by financing Africa's telecom and data backbone.Africa must urgently develop cogent digital strategy. This at first seems fanciful, or even superfluous, given the continent's relative lack of more basic development. Indeed, there are myriad other challenges to which most would assign primacy. However, by setting their sights on participating in the ongoing fourth industrial revolution, developing nations in Africa may be able to chart a navigable course to rapidly raising living standards.

Kevin Gray: AI has become part of our daily lives, hasn't it! Dr. Anna Farzindar: I was working on my laptop when my college daughter said "Mom please don't do anything wrong with AI!" Then two days later during our family dinner, my younger freshman high school daughter told a story about a video on social media showing a small home care robot that tricked the owner and lied. She asked me "Mom, aren't you afraid of robots?" These short conversations made me think about how the new generation is a big consumer of technology but, at the same time, they are concerned and worried about the future AI. KG: Getting back to basics, what is AI? AF: From talking to your virtual assistance on smartphone (like SIRI), watching a recommended movie on Netflix, searching on Google, following the suggested Instagram posts, using the sophisticated methods of an auto trading stock market, applying the decision making systems for your loan approval, or (soon) sitting in a self-driving car, AI algorithms are so embedded in our daily life that is hard to imagine living a single day without them!

Existing methods for estimating uncertainty in deep learning tend to require multiple forward passes, making them unsuitable for applications where computational resources are limited. To solve this, we perform probabilistic reasoning over the depth of neural networks. Different depths correspond to subnetworks which share weights and whose predictions are combined via marginalisation, yielding model uncertainty. By exploiting the sequential structure of feed-forward networks, we are able to both evaluate our training objective and make predictions with a single forward pass. We validate our approach on real-world regression and image classification tasks. Our approach provides uncertainty calibration, robustness to dataset shift, and accuracies competitive with more computationally expensive baselines.

Robustly learning in expressive languages with real-world data continues to be a challenging task. Numerous conventional methods appeal to heuristics without any assurances of robustness. While PAC-Semantics offers strong guarantees, learning explicit representations is not tractable even in a propositional setting. However, recent work on so-called "implicit" learning has shown tremendous promise in terms of obtaining polynomial-time results for fragments of first-order logic. In this work, we extend implicit learning in PAC-Semantics to handle noisy data in the form of intervals and threshold uncertainty in the language of linear arithmetic. We prove that our extended framework keeps the existing polynomial-time complexity guarantees. Furthermore, we provide the first empirical investigation of this hitherto purely theoretical framework. Using benchmark problems, we show that our implicit approach to learning optimal linear programming objective constraints significantly outperforms an explicit approach in practice.

If you think that the Sahara is covered only by golden dunes and scorched rocks, you aren't alone. In an area of West Africa 30 times larger than Denmark, an international team, led by University of Copenhagen and NASA researchers, has counted over 1.8 billion trees and shrubs. The 1.3 million km2 area covers the western-most portion of the Sahara Desert, the Sahel and what are known as sub-humid zones of West Africa. "We were very surprised to see that quite a few trees actually grow in the Sahara Desert, because up until now, most people thought that virtually none existed. We counted hundreds of millions of trees in the desert alone. Doing so wouldn't have been possible without this technology. Indeed, I think it marks the beginning of a new scientific era," asserts Assistant Professor Martin Brandt of the University of Copenhagen's Department of Geosciences and Natural Resource Management, lead author of the study's scientific article, now published in Nature.

Amazon SageMaker is now available in the Africa (Cape Town) and Europe (Milan) AWS regions. Amazon SageMaker is a fully managed service that provides every developer and data scientist with the ability to build, train, and deploy machine learning (ML) models quickly. SageMaker removes the heavy lifting from each step of the machine learning process to make it easier to develop high quality models.

Chimpanzees get more selective over who they associate themselves with as they age, new research reveals. In a study spanning two decades in a Ugandan national park, US experts observed social interactions among 21 wild male chimps, ranging in age from 15 to 58 years. Both chimps and humans prefer to be around the company of old friends and spend less time among new faces, the experts conclude. Ageing male chimps have more mutual and positive friendships than younger chimps, who have more one-sided, antagonistic relationships. Chimps also showed a shift from negative interactions to more positive ones as they reached their twilight years, 'like humans looking for some peace and quiet'.

The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs can be more susceptible to infectious diseases. Furthermore, the autoantibody system dampens IFN response to prevent damage from pathogen-induced inflammation. Two studies now examine the likelihood that genetics affects the risk of severe coronavirus disease 2019 (COVID-19) through components of this system (see the Perspective by Beck and Aksentijevich). Q. Zhang et al. used a candidate gene approach and identified patients with severe COVID-19 who have mutations in genes involved in the regulation of type I and III IFN immunity. They found enrichment of these genes in patients and conclude that genetics may determine the clinical course of the infection. Bastard et al. identified individuals with high titers of neutralizing autoantibodies against type I IFN-α2 and IFN-ω in about 10% of patients with severe COVID-19 pneumonia. These autoantibodies were not found either in infected people who were asymptomatic or had milder phenotype or in healthy individuals. Together, these studies identify a means by which individuals at highest risk of life-threatening COVID-19 can be identified. Science , this issue p. [eabd4570][1], p. [eabd4585][2]; see also p. [404][3] ### INTRODUCTION Clinical outcomes of human severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection range from silent infection to lethal coronavirus disease 2019 (COVID-19). Epidemiological studies have identified three risk factors for severe disease: being male, being elderly, and having other medical conditions. However, interindividual clinical variability remains huge in each demographic category. Discovering the root cause and detailed molecular, cellular, and tissue- and body-level mechanisms underlying life-threatening COVID-19 is of the utmost biological and medical importance. ### RATIONALE We established the COVID Human Genetic Effort ([www.covidhge.com][4]) to test the general hypothesis that life-threatening COVID-19 in some or most patients may be caused by monogenic inborn errors of immunity to SARS-CoV-2 with incomplete or complete penetrance. We sequenced the exome or genome of 659 patients of various ancestries with life-threatening COVID-19 pneumonia and 534 subjects with asymptomatic or benign infection. We tested the specific hypothesis that inborn errors of Toll-like receptor 3 (TLR3)– and interferon regulatory factor 7 (IRF7)–dependent type I interferon (IFN) immunity that underlie life-threatening influenza pneumonia also underlie life-threatening COVID-19 pneumonia. We considered three loci identified as mutated in patients with life-threatening influenza: TLR3 , IRF7 , and IRF9 . We also considered 10 loci mutated in patients with other viral illnesses but directly connected to the three core genes conferring influenza susceptibility: TICAM1/TRIF , UNC93B1 , TRAF3 , TBK1 , IRF3 , and NEMO/IKBKG from the TLR3-dependent type I IFN induction pathway, and IFNAR1 , IFNAR2 , STAT1 , and STAT2 from the IRF7- and IRF9-dependent type I IFN amplification pathway. Finally, we considered various modes of inheritance at these 13 loci. ### RESULTS We found an enrichment in variants predicted to be loss-of-function (pLOF), with a minor allele frequency <0.001, at the 13 candidate loci in the 659 patients with life-threatening COVID-19 pneumonia relative to the 534 subjects with asymptomatic or benign infection ( P = 0.01). Experimental tests for all 118 rare nonsynonymous variants (including both pLOF and other variants) of these 13 genes found in patients with critical disease identified 23 patients (3.5%), aged 17 to 77 years, carrying 24 deleterious variants of eight genes. These variants underlie autosomal-recessive (AR) deficiencies ( IRF7 and IFNAR1 ) and autosomal-dominant (AD) deficiencies ( TLR3 , UNC93B1 , TICAM1 , TBK1 , IRF3 , IRF7 , IFNAR1 , and IFNAR2 ) in four and 19 patients, respectively. These patients had never been hospitalized for other life-threatening viral illness. Plasmacytoid dendritic cells from IRF7-deficient patients produced no type I IFN on infection with SARS-CoV-2, and TLR3−/−, TLR3+/−, IRF7−/−, and IFNAR1−/− fibroblasts were susceptible to SARS-CoV-2 infection in vitro. ### CONCLUSION At least 3.5% of patients with life-threatening COVID-19 pneumonia had known (AR IRF7 and IFNAR1 deficiencies or AD TLR3, TICAM1, TBK1, and IRF3 deficiencies) or new (AD UNC93B1, IRF7, IFNAR1, and IFNAR2 deficiencies) genetic defects at eight of the 13 candidate loci involved in the TLR3- and IRF7-dependent induction and amplification of type I IFNs. This discovery reveals essential roles for both the double-stranded RNA sensor TLR3 and type I IFN cell-intrinsic immunity in the control of SARS-CoV-2 infection. Type I IFN administration may be of therapeutic benefit in selected patients, at least early in the course of SARS-CoV-2 infection. ![Figure][5] Inborn errors of TLR3- and IRF7-dependent type I IFN production and amplification underlie life-threatening COVID-19 pneumonia. Molecules in red are encoded by core genes, deleterious variants of which underlie critical influenza pneumonia with incomplete penetrance, and deleterious variants of genes encoding biochemically related molecules in blue underlie other viral illnesses. Molecules represented in bold are encoded by genes with variants that also underlie critical COVID-19 pneumonia. Clinical outcome upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ranges from silent infection to lethal coronavirus disease 2019 (COVID-19). We have found an enrichment in rare variants predicted to be loss-of-function (LOF) at the 13 human loci known to govern Toll-like receptor 3 (TLR3)– and interferon regulatory factor 7 (IRF7)–dependent type I interferon (IFN) immunity to influenza virus in 659 patients with life-threatening COVID-19 pneumonia relative to 534 subjects with asymptomatic or benign infection. By testing these and other rare variants at these 13 loci, we experimentally defined LOF variants underlying autosomal-recessive or autosomal-dominant deficiencies in 23 patients (3.5%) 17 to 77 years of age. We show that human fibroblasts with mutations affecting this circuit are vulnerable to SARS-CoV-2. Inborn errors of TLR3- and IRF7-dependent type I IFN immunity can underlie life-threatening COVID-19 pneumonia in patients with no prior severe infection. [1]: /lookup/doi/10.1126/science.abd4570 [2]: /lookup/doi/10.1126/science.abd4585 [3]: /lookup/doi/10.1126/science.abe7591 [4]: https://www.covidhge.com [5]: pending:yes

Tensor linear regression is an important and useful tool for analyzing tensor data. To deal with high dimensionality, CANDECOMP/PARAFAC (CP) low-rank constraints are often imposed on the coefficient tensor parameter in the (penalized) $M$-estimation. However, we show that the corresponding optimization may not be attainable, and when this happens, the estimator is not well-defined. This is closely related to a phenomenon, called CP degeneracy, in low-rank tensor approximation problems. In this article, we provide useful results of CP degeneracy in tensor regression problems. In addition, we provide a general penalized strategy as a solution to overcome CP degeneracy. The asymptotic properties of the resulting estimation are also studied. Numerical experiments are conducted to illustrate our findings.

Directional data consist of observations distributed on a (hyper)sphere, and appear in many applied fields, such as astronomy, ecology, and environmental science. This paper studies both statistical and computational problems of kernel smoothing for directional data. We generalize the classical mean shift algorithm to directional data, which allows us to identify local modes of the directional kernel density estimator (KDE). The statistical convergence rates of the directional KDE and its derivatives are derived, and the problem of mode estimation is examined. We also prove the ascending property of our directional mean shift algorithm and investigate a general problem of gradient ascent on the unit hypersphere. To demonstrate the applicability of our proposed algorithm, we evaluate it as a mode clustering method on both simulated and real-world datasets.