A New Adaptive Hungarian Mating Scheme in Genetic Algorithms

In genetic algorithms, selection or mating scheme is one of the important operations. In this paper, we suggest an adaptive mating scheme using previously suggested Hungarian mating schemes. Hungarian mating schemes consist of maximizing the sum of mating distances, minimizing the sum, and random matching. We propose an algorithm to elect one of these Hungarian mating schemes. Every mated pair of solutions has to vote for the next generation mating scheme. The distance between parents and the distance between parent and offspring are considered when they vote. Well-known combinatorial optimization problems, the traveling salesperson problem, and the graph bisection problem are used for the test bed of our method. Our adaptive strategy showed better results than not only pure and previous hybrid schemes but also existing distance-based mating schemes

Cigarette Smoking Triggers Colitis by IFN-γ+ CD4+ T Cells

The increased incidence of Crohn’s disease in smokers has been recently reported, suggesting a strong association of cigarette smoke (CS) with colitis. However, the mechanism of the action of CS on colitis has not yet been explored. Here, we demonstrate that CS exposure is sufficient to induce colitis in mice. Interestingly, the colitis is mainly mediated by Th1, but not Th17, responses. CD4+ T-cell depletion or T-bet/IFN-γ deficiency protects against the development of colitis induced by CS. Additionally, IFN-γ-producing CD4+ T cells play a substantial role in CS-induced colitis. The adoptive transfer (AT) of effector T cells from CS-exposed WT mice into colitis-prone mice caused these mice to develop colitis, while the AT of effector T cells from IFN-γ knock-out mice did not. These findings have implications for broadening our understanding of CS-induced pathology and for the development of novel therapeutic strategies to treat Crohn’s disease

Highly Sensitive, Stretchable Pressure Sensor Using Blue Laser Annealed CNTs

A piezoresistive sensor is an essential component of wearable electronics that can detect resistance changes when pressure is applied. In general, microstructures of sensing layers have been adopted as an effective approach to enhance piezoresistive performance. However, the mold-casted microstructures typically have quite a thick layer with dozens of microscales. In this paper, a carbon microstructure is formed by blue laser annealing (BLA) on a carbon nanotube (CNT) layer, which changes the surface morphology of CNTs into carbonaceous protrusions and increases its thickness more than four times compared to the as-deposited layer. Then, the pressure sensor is fabricated using a spin-coating of styrene–ethylene–butylene–styrene (SEBS) elastomer on the BLA CNTs layer. A 1.32 µm-thick pressure sensor exhibits a high sensitivity of 6.87 × 105 kPa−1, a wide sensing range of 278 Pa~40 kPa and a fast response/recovery time of 20 ms, respectively. The stability of the pressure sensor is demonstrated by the repeated loading and unloading of 20 kPa for 4000 cycles. The stretchable pressure sensor was also demonstrated using lateral CNT electrodes on SEBS surface, exhibiting stable pressure performance, with up to 20% stretching

2µm band coherent transmission of Nyquist WDM 16-QAM signal by on-chip spectral translation

We propose and demonstrate the first low-latency 2-μm-band coherent NWDM transmission by on-chip spectral translation of 4×32-Gbaud 16-QAM signals with 33-GHz spacing. 318.25 Gbit/s net-rate is achieved with error-free performance after 1.15-km hollow-core fiber transmission

2-µm-band coherent transmission of Nyquist-WDM 16-QAM signal by on-chip spectral translation

We propose and demonstrate the first low-latency 2-µm-band coherent N-WDM transmission by on-chip spectral translation of 4×32-Gbaud 16-QAM signals with 33-GHz spacing. 318.25 Gbit/s net-rate is achieved with error-free performance after 1.15km hollow-core fiber transmission

Super-broadband on-chip continuous spectral translation unlocking coherent optical communications beyond conventional telecom bands

Today’s optical communication systems are fast approaching their capacity limits in the conventional telecom bands. Opening up new wavelength bands is becoming an appealing solution to the capacity crunch. However, this ordinarily requires the development of optical transceivers for any new wavelength band, which is time-consuming and expensive. Here, we present an on-chip continuous spectral translation method that leverages existing commercial transceivers to unlock the vast and currently unused potential new wavelength bands. The spectral translators are continuous-wave laser pumped aluminum gallium arsenide on insulator (AlGaAsOI) nanowaveguides that provide a continuous conversion bandwidth over an octave. We demonstrate coherent transmission in the 2-μm band using well-developed conventional C-band transmitters and coherent receivers, as an example of the potential of the spectral translators that could also unlock communications at other wavelength bands. We demonstrate 318.25-Gbit s−1 Nyquist wavelength-division multiplexed coherent transmission over a 1.15-km hollow-core fibre using this approach. Our demonstration paves the way for transmitting, detecting, and processing signals at wavelength bands beyond the capability of today’s devices

Interrupting specific hydrogen bonds between ELF3 and MED23 as an alternative drug resistance-free strategy for HER2-overexpressing cancers

Introduction: HER2 overexpression induces cancer aggression and frequent recurrences in many solid tumors. Because HER2 overproduction is generally followed by gene amplification, inhibition of protein–protein interaction (PPI) between transcriptional factor ELF3 and its coactivator MED23 has been considered an effective but challenging strategy. Objectives: This study aimed to determine the hotspot of ELF3-MED23 PPI and further specify the essential residues and their key interactions in the hotspot which are controllable by small molecules with significant anticancer activity. Methods: Intensive biological evaluation methods including SEAP, fluorescence polarization, LC-MS/MS-based quantitative, biosensor, GST-pull down assays, and in silico structural analysis were performed to determine hotspot of ELF3-MED23 PPI and to elicit YK1, a novel small molecule PPI inhibitor. The effects of YK1 on possible PPIs of MED23 and the efficacy of trastuzumab were assessed using cell culture and tumor xenograft mouse models. Results: ELF3-MED23 PPI was found to be specifically dependent on H-bondings between D400, H449 of MED23 and W138, I140 of ELF3 for upregulating HER2 gene transcription. Employing YK1, we confirmed that interruption on these H-bondings significantly attenuated the HER2-mediated oncogenic signaling cascades and exhibited significant in vitro and in vivo anticancer activity against HER2-overexpressing breast and gastric cancers even in their trastuzumab refractory clones. Conclusion: Our approach to develop specific ELF3-MED23 PPI inhibitor without interfering other PPIs of MED23 can finally lead to successful development of a drug resistance-free compound to interrogate HER2 biology in diverse conditions of cancers overexpressing HER2