PocketCare: Tracking the Flu with Mobile Phones using Partial Observations of Proximity and Symptoms

Mobile phones provide a powerful sensing platform that researchers may adopt to understand proximity interactions among people and the diffusion, through these interactions, of diseases, behaviors, and opinions. However, it remains a challenge to track the proximity-based interactions of a whole community and then model the social diffusion of diseases and behaviors starting from the observations of a small fraction of the volunteer population. In this paper, we propose a novel approach that tries to connect together these sparse observations using a model of how individuals interact with each other and how social interactions happen in terms of a sequence of proximity interactions. We apply our approach to track the spreading of flu in the spatial-proximity network of a 3000-people university campus by mobilizing 300 volunteers from this population to monitor nearby mobile phones through Bluetooth scanning and to daily report flu symptoms about and around them. Our aim is to predict the likelihood for an individual to get flu based on how often her/his daily routine intersects with those of the volunteers. Thus, we use the daily routines of the volunteers to build a model of the volunteers as well as of the non-volunteers. Our results show that we can predict flu infection two weeks ahead of time with an average precision from 0.24 to 0.35 depending on the amount of information. This precision is six to nine times higher than with a random guess model. At the population level, we can predict infectious population in a two-week window with an r-squared value of 0.95 (a random-guess model obtains an r-squared value of 0.2). These results point to an innovative approach for tracking individuals who have interacted with people showing symptoms, allowing us to warn those in danger of infection and to inform health researchers about the progression of contact-induced diseases

Annexin A3 is a therapeutic target for CD133+ liver cancer stem cells

This journal suppl. entitled: Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CAFrequent tumor relapse in hepatocellular carcinoma (HCC) has been commonly attributed to the failure to completely eradicate cancer stem cells (CSCs) in the tumor residues by conventional treatments. We have previously reported that the tumor growth of HCC is fuelled, at least in part, by a small subset of CSCs marked by the CD133 surface phenotype. Our present study aims 1) to delineate the molecular mechanism by which CD133+ liver CSCs mediate HCC tumor formation and progression; and 2) to develop a novel diagnostic / prognostic biomarker and targeted therapy for HCC detection and treatment. RNA-Seq profiling was employed to compare the gene expression profiles between sorted CD133+ and CD133- subsets isolated from HCC cell lines ...postprin

Effect of electron correlation on high-order-harmonic generation of helium atoms in intense laser fields: Time-dependent generalized pseudospectral approach in hyperspherical coordinates

This is the published version, also available here: http://dx.doi.org/10.1103/PhysRevA.73.023403.We present a time-dependent generalized pseudospectral (TDGPS) approach in hyperspherical coordinates for fully ab initio nonperturbative treatment of multiphoton dynamics of atomic systems in intense laser fields. The procedure is applied to the investigation of high-order-harmonic generation (HHG) of helium atoms in ultrashort laser pulses at a KrF wavelength of 248.6nm. The six-dimensional coupled hyperspherical-adiabatic-channel equations are discretized and solved efficiently and accurately by means of the TDGPS method. The effects of electron correlation and doubly excited states on HHG are explored in detail. A HHG peak with Fano line profile is identified which can be attributed to a broad resonance of doubly excited states. Comparison of the HHG spectra of the ab initio two-electron and the single-active-electron model calculations is also presented

Printable magnesium ion quasi-solid-state asymmetric supercapacitors for flexible solar-charging integrated units.

Wearable and portable self-powered units have stimulated considerable attention in both the scientific and technological realms. However, their innovative development is still limited by inefficient bulky connections between functional modules, incompatible energy storage systems with poor cycling stability, and real safety concerns. Herein, we demonstrate a flexible solar-charging integrated unit based on the design of printed magnesium ion aqueous asymmetric supercapacitors. This power unit exhibits excellent mechanical robustness, high photo-charging cycling stability (98.7% capacitance retention after 100 cycles), excellent overall energy conversion and storage efficiency (ηoverall = 17.57%), and outstanding input current tolerance. In addition, the Mg ion quasi-solid-state asymmetric supercapacitors show high energy density up to 13.1 mWh cm-3 via pseudocapacitive ion storage as investigated by an operando X-ray diffraction technique. The findings pave a practical route toward the design of future self-powered systems affording favorable safety, long life, and high energy

Dnmt3b ablation impairs fracture repair through upregulation of Notch pathway

We previously established that DNA methyltransferase 3b (Dnmt3b) is the sole Dnmt responsive to fracture repair and that Dnmt3b expression is induced in progenitor cells during fracture repair. In the current study, we confirmed that Dnmt3b ablation in mesenchymal progenitor cells (MPCs) resulted in impaired endochondral ossification, delayed fracture repair, and reduced mechanical strength of the newly formed bone in Prx1-Cre;Dnmt3bf/f (Dnmt3bPrx1) mice. Mechanistically, deletion of Dnmt3b in MPCs led to reduced chondrogenic and osteogenic differentiation in vitro. We further identified Rbpjκ as a downstream target of Dnmt3b in MPCs. In fact, we located 2 Dnmt3b binding sites in the murine proximal Rbpjκ promoter and gene body and confirmed Dnmt3b interaction with the 2 binding sites by ChIP assays. Luciferase assays showed functional utilization of the Dnmt3b binding sites in murine C3H10T1/2 cells. Importantly, we showed that the MPC differentiation defect observed in Dnmt3b deficiency cells was due to the upregulation of Rbpjκ, evident by restored MPC differentiation upon Rbpjκ inhibition. Consistent with in vitro findings, Rbpjκ blockage via dual antiplatelet therapy reversed the differentiation defect and accelerated fracture repair in Dnmt3bPrx1 mice. Collectively, our data suggest that Dnmt3b suppresses Notch signaling during MPC differentiation and is necessary for normal fracture repair