Nanostructured silicon via metal assisted catalyzed etch (MACE): chemistry fundamentals and pattern engineering.

There are a range of different methods to generate a nanostructured surface on silicon (Si) but the most cost effective and optically interesting is the metal assisted wet chemical etching (MACE) (Koynov et al 2006 Appl. Phys. Lett. 88 203107). MACE of Si is a controllable, room-temperature wet-chemical technique that uses a thin layer of metal to etch the surface of Si, leaving behind various nano- and micro-scale surface features or 'black silicon'. MACE-fabricated nanowires (NWs) provide improved antireflection and light trapping functionality (Toor et al 2016 Nanoscale 8 15448-66) compared with the traditional 'iso-texturing' (Campbell and Green 1987 J. Appl. Phys. 62 243-9). The resulting lower reflection and improved light trapping can lead to higher short circuit currents in NW solar cells (Toor et al 2011 Appl. Phys. Lett. 99 103501). In addition, NW cells can have higher fill factors and voltages than traditionally processed cells, thus leading to increased solar cell efficiencies (Cabrera et al 2013 IEEE J. Photovolt. 3 102-7). MACE NW processing also has synergy with next generation Si solar cell designs, such as thin epitaxial-Si and passivated emitter rear contact (Toor et al 2016 Nanoscale 8 15448-66). While several companies have begun manufacturing black Si, and many more are researching these techniques, much of the work has not been published in traditional journals and is publicly available only through conference proceedings and patent publications, which makes learning the field challenging. There have been three specialized review articles published recently on certain aspects of MACE or black Si, but do not present a full review that would benefit the industry (Liu et al 2014 Energy Environ. Sci. 7 3223-63; Yusufoglu et al 2015 IEEE J. Photovolt. 5 320-8; Huang et al 2011 Adv. Mater. 23 285-308). In this feature article, we review the chemistry of MACE and explore how changing parameters in the wet etch process effects the resulting texture on the Si surface. Then we review efforts to increase the uniformity and reproducibility of the MACE process, which is critical for commercializing the black Si technology.

HTB50-2 Inhibits Growth and Migration of Triple-negative Breast Cancer via FOSL2/FOXC1 Signaling Axis and Subsequent Ferroptosis.

BACKGROUND: The manipulation of ferroptosis in cancer cells is a possible therapeutic technique that has been investigated for use in the treatment of cancer. Consequently, ferroptosis-inducing medications have recently received increased interest in cancer therapy. In this research, we assessed the anticancer efficacy of 14ß-hydroxy- 3ß-(ß-D-Glucopyranosyloxy)-5α-bufa-20,22-dienolide (HTB50-2), a natural product derived from the plant Helleborus thibetanus Franch, in Triple-Negative Breast Cancer (TNBC). Moreover, we also studied its potential mechanisms. METHODS: The biological effects of HTB50-2 in a series of breast cancer cell lines were analyzed using sulforhodamine B (SRB) and other methods. The migration ability was analyzed using three methods: wound healing assay, transwell assay, and Western blot. Meanwhile, the potential therapeutic value of HTB50-2 was evaluated in BALB/c mice by orthotopic transplantation. Transcriptome sequencing was conducted to explore the FOS-like antigen 2 (FOSL2) gene, and its role in ferroptosis was verified by Western blot and immunohistochemistry. The association of FOSL2 and ferroptosis-related genes was analyzed using NetworkAnalyst databases, and a TF-Gene interaction network was constructed. RESULTS: Ferroptosis was found to be induced in TNBC cells by HTB50-2. Furthermore, HTB50-2 inhibited tumor development by inducing ferroptosis in TNBC in vivo. Mechanistically, we demonstrated that a transcription factor FOSL2 mediated ferroptosis by HTB50-2. Additionally, it was found that Forkhead box C1 (FOXC1) was regulated by FOSL2 and correlated with ferroptosis. CONCLUSION: Our data suggest that HTB50-2 exerts its anti-cancer properties by ferroptosis via FOSL2/FOXC1 signaling pathway. Hence, HTB50-2 has an important application potential in the treatment of TNBC.

YF343, A Novel Histone Deacetylase Inhibitor, Combined with CQ to Inhibit- Autophagy, Contributes to Increased Apoptosis in Triple- Negative Breast Cancer.

BACKGROUND: Compounds that target tumor epigenetic events are likely to constitute a prominent strategy for anticancer treatment. Histone deacetylase inhibitors (HDACis) have been developed as prospective candidates in anticancer drug development, and currently, many of them are under clinical investigation. We assessed the anticancer efficacy of a now hydroxamate-based HDACi, YF-343, in triple-negative breast cancer development and studied its potential mechanisms. METHODS: YF-343 was estimated as a novel HDACi by the HDACi drug screening kit. The biological effects of YF-343 in a panel of breast cancer cell lines were analyzed by Western blot and flow cytometry. YF-343 exhibited notable cytotoxicity, promoted apoptosis, and induced cell cycle arrest. Furthermore, it also induced autophagy, which plays a pro-survival role in breast cancer cells. RESULTS: The combination of YF-343 with an autophagy inhibitor chloroquine (CQ) significantly suppressed breast tumor progression as compared to the YF-343 treatment alone both in vitro and in vivo. Mechanistically, the molecular mechanism of YF-343 on autophagy was elucidated by gene chip expression profiles, qPCR analysis, luciferase reporter gene assay, chromatin immunoprecipitation assays, immunohistochemical analysis, and other methods. E2F7, a transcription factor, promoted the expression of ATG2A via binding to the ATG2A promoter region and then induced autophagy in triple-negative breast cancer cells treated with YF-343. CONCLUSION: Our studies have illustrated the mechanisms for potential action of YF-343 on tumor growth in breast cancer models with pro-survival autophagy. The combination therapy of YF-343 and CQ maybe a promising strategy for breast cancer therapy.

Sensitive and Specific Detection of Estrogens Featuring Doped Silicon Nanowire Arrays.

Estrogens and estrogen-mimicking compounds in the aquatic environment are known to cause negative impacts to both ecosystems and human health. In this initial proof-of-principle study, we developed a novel vertically oriented silicon nanowire (vSiNW) array-based biosensor for low-cost, highly sensitive and selective detection of estrogens. The vSiNW arrays were formed using an inexpensive and scalable metal-assisted chemical etching (MACE) process. A vSiNW array-based p-n junction diode (vSiNW-diode) transducer design for the biosensor was used and functionalized via 3-aminopropyltriethoxysilane (APTES)-based silane chemistry to bond estrogen receptor-alpha (ER-α) to the surface of the vSiNWs. Following receptor conjugation, the biosensors were exposed to increasing concentrations of estradiol (E2), resulting in a well-calibrated sensor response (R 2 ≥ 0.84, 1-100 ng/mL concentration range). Fluorescence measurements quantified the distribution of estrogen receptors across the vSiNW array compared to planar Si, indicating an average of 7 times higher receptor presence on the vSiNW array surface. We tested the biosensor's target selectivity by comparing it to another estrogen (estrone [E1]) and an androgen (testosterone), where we measured a high positive electrical biosensor response after E1 exposure and a minimal response after testosterone. The regeneration capacity of the biosensor was tested following three successive rinses with phosphate buffer solution (PBS) between hormone exposure. Traditional horizontally oriented Si NW field effect transistor (hSiNW-FET)-based biosensors report electrical current changes at the nanoampere (nA) level that require bulky and expensive measurement equipment making them unsuitable for field measurements, whereas the reported vSiNW-diode biosensor exhibits current changes in the microampere (µA) range, demonstrating up to 100-fold electrical signal amplification, thus enabling sensor signal measurement using inexpensive electronics. The highly sensitive and specific vSiNW-diode biosensor developed here will enable the creation of low-cost, portable, field-deployable biosensors that can detect estrogenic compounds in waterways in real-time.

Transforming Growth Factor-ß Receptor III is a Potential Regulator of Ischemia-Induced Cardiomyocyte Apoptosis.

BACKGROUND: Myocardial infarction (MI) is often accompanied by cardiomyocyte apoptosis, which decreases heart function and leads to an increased risk of heart failure. The aim of this study was to examine the effects of transforming growth factor-ß receptor III (TGFßR3) on cardiomyocyte apoptosis during MI. METHODS AND RESULTS: An MI mouse model was established by left anterior descending coronary artery ligation. Cell viability, apoptosis, TGFßR3, and mitogen-activated protein kinase signaling were assessed by methylthiazolyldiphenyl-tetrazolium bromide assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, immunofluorescence, electron microscopy, and Western blotting. Our results demonstrated that TGFßR3 expression in the border region of the heart was dynamically changed during MI. After stimulation with H2O2, TGFßR3 overexpression in cardiomyocytes led to increased cell apoptosis and activation of p38 signaling, whereas TGFßR3 knockdown had the opposite effect. ERK1/2 and JNK1/2 signaling was not altered by TGFßR3 modulation, and p38 inhibitor (SB203580) reduced the effect of TGFßR3 on apoptosis, suggesting that p38 has a nonredundant function in activating apoptosis. Consistent with the in vitro observations, cardiac TGFßR3 transgenic mice showed augmented cardiomyocyte apoptosis, enlarged infarct size, increased injury, and enhanced p38 signaling upon MI. Conversely, cardiac loss of function of TGFßR3 by adeno-associated viral vector serotype 9-TGFßR3 short hairpin RNA attenuated the effects of MI in mice. CONCLUSIONS: TGFßR3 promotes apoptosis of cardiomyocytes via a p38 pathway-associated mechanism, and loss of TGFßR3 reduces MI injury, which suggests that TGFßR3 may serve as a novel therapeutic target for MI.

Metal assisted catalyzed etched (MACE) black Si: optics and device physics.

Metal-assisted catalyzed etching (MACE) of silicon (Si) is a controllable, room-temperature wet-chemical technique that uses a thin layer of metal to etch the surface of Si, leaving behind various nano- and micro-scale surface features, including nanowires (NWs), that can be tuned to achieve various useful engineering goals, in particular with respect to Si solar cells. In this review, we introduce the science and technology of MACE from the literature, and provide an in-depth analysis of MACE to enhance Si solar cells, including the outlook for commercial applications of this technology.

Efficient target strategies for contagion in scale-free networks.

Organizations or individuals often have an incentive to target a certain number of agents to launch a contagion process effectively and efficiently, for example, sampling consumers in the diffusion of new products. We present an effective strategy for contagion in scale-free networks. The proposed strategy, hub strategy, calls for targeting mostly the highly connected nodes. The biased level implemented in this strategy characterizes its ability to identify hub nodes. We demonstrate that hub strategy can improve the contagion effects evidently. We find that biased level increases first with heterogeneity level of contagion network but decreases with that after a certain value, and decreases with initial adopter rate all the time. Moreover, degree correlations in contagion networks may reduce biased level.

Bone marrow mesenchymal stem cell transplantation retards the natural senescence of rat hearts.

Bone marrow mesenchymal stem cells (BMSCs) have been shown to offer a wide variety of cellular functions including the protective effects on damaged hearts. Here we investigated the antiaging properties of BMSCs and the underlying mechanism in a cellular model of cardiomyocyte senescence and a rat model of aging hearts. Neonatal rat ventricular cells (NRVCs) and BMSCs were cocultured in the same dish with a semipermeable membrane to separate the two populations. Monocultured NRVCs displayed the senescence-associated phenotypes, characterized by an increase in the number of ß-galactosidase-positive cells and decreases in the degradation and disappearance of cellular organelles in a time-dependent manner. The levels of reactive oxygen species and malondialdehyde were elevated, whereas the activities of antioxidant enzymes superoxide dismutase and glutathione peroxidase were decreased, along with upregulation of p53, p21(Cip1/Waf1), and p16(INK4a) in the aging cardiomyocytes. These deleterious alterations were abrogated in aging NRVCs cocultured with BMSCs. Qualitatively, the same senescent phenotypes were consistently observed in aging rat hearts. Notably, BMSC transplantation significantly prevented these detrimental alterations and improved the impaired cardiac function in the aging rats. In summary, BMSCs possess strong antisenescence action on the aging NRVCs and hearts and can improve cardiac function after transplantation in aging rats. The present study, therefore, provides an alternative approach for the treatment of heart failure in the elderly population.

Simvastatin alleviates cardiac fibrosis induced by infarction via up-regulation of TGF-ß receptor III expression.

BACKGROUND AND PURPOSE: Statins decrease heart disease risk, but their mechanisms are not completely understood. We examined the role of the TGF-ß receptor III (TGFBR3) in the inhibition of cardiac fibrosis by simvastatin. EXPERIMENTAL APPROACH: Myocardial infarction (MI) was induced by ligation of the left anterior descending coronary artery in mice given simvastatin orally for 7 days. Cardiac fibrosis was measured by Masson staining and electron microscopy. Heart function was evaluated by echocardiography. Signalling through TGFBR3, ERK1/2, JNK and p38 pathways was measured using Western blotting. Collagen content and cell viability were measured in cultures of neonatal mouse cardiac fibroblasts (NMCFs). Interactions between TGFBR3 and the scaffolding protein, GAIP-interacting protein C-terminus (GIPC) were detected using co-immunoprecipitation (co-IP). In vivo, hearts were injected with lentivirus carrying shRNA for TGFBR3. KEY RESULTS: Simvastatin prevented fibrosis following MI, improved heart ultrastructure and function, up-regulated TGFBR3 and decreased ERK1/2 and JNK phosphorylation. Simvastatin up-regulated TGFBR3 in NMCFs, whereas silencing TGFBR3 reversed inhibitory effects of simvastatin on cell proliferation and collagen production. Simvastatin inhibited ERK1/2 and JNK signalling while silencing TGFBR3 opposed this effect. Co-IP demonstrated TGFBR3 binding to GIPC. Overexpressing TGFBR3 inhibited ERK1/2 and JNK signalling which was abolished by knock-down of GIPC. In vivo, suppression of cardiac TGFBR3 abolished anti-fibrotic effects, improvement of cardiac function and changes in related proteins after simvastatin. CONCLUSIONS AND IMPLICATIONS: TGFBR3 mediated the decreased cardiac fibrosis, collagen deposition and fibroblast activity, induced by simvastatin, following MI. These effects involved GIPC inhibition of the ERK1/2/JNK pathway.

Volatility, irregularity, and predictable degree of accumulative return series.

Recently it was shown that financial time series are not completely random process but exhibit long-term or short-term dependences, which offer promises for predictability. However, we do not clearly understand the potential relationship between serial structure and predictability. This paper proposed a framework to magnify the correlations and regularities contained in financial time series through constructing accumulative return series. This method can help us distinguish the real world financial time series from random-walk process effectively by examining the change patterns of volatility, Hurst exponent, and approximate entropy. Furthermore, we have found that the predictable degree increases continually with the increasing length of accumulative return. Our results suggest that financial time series are predictable to some extent and approximate entropy is a good indicator to characterize the predictable degree of financial time series if we take the influence of their volatility into account.

Fairness emergence from zero-intelligence agents.

Fairness plays a key role in explaining the emergence and maintenance of cooperation. Opponent-oriented social utility models were often proposed to explain the origins of fairness preferences in which agents take into account not only their own outcomes but are also concerned with the outcomes of their opponents. Here, we propose a payoff-oriented mechanism in which agents update their beliefs only based on the payoff signals of the previous ultimatum game, regardless of the behaviors and outcomes of the opponents themselves. Employing adaptive ultimatum game, we show that (1) fairness behaviors can emerge out even under such minimalist assumptions, provided that agents are capable of responding to their payoff signals, (2) the average game payoff per agent per round decreases with the increasing discrepancy rate between the average giving rate and the average asking rate, and (3) the belief update process will lead to 50%-50% fair split provided that there is no mutation in the evolutionary dynamics.