Integrative eQTL-based analyses reveal the biology of breast cancer risk loci.

Germline determinants of gene expression in tumors are infrequently studied due to the complexity of transcript regulation caused by somatically acquired alterations. We performed expression quantitative trait locus (eQTL)-based analyses using the multi-level information provided in The Cancer Genome Atlas (TCGA). Of the factors we measured, cis-acting eQTLs accounted for 1.2% of the total variation of tumor gene expression, while somatic copy-number alteration and CpG methylation accounted for 7.3% and 3.3%, respectively. eQTL analyses of 15 previously reported breast cancer risk loci resulted in the discovery of three variants that are significantly associated with transcript levels (false discovery rate [FDR] < 0.1). Our trans-based analysis identified an additional three risk loci to act through ESR1, MYC, and KLF4. These findings provide a more comprehensive picture of gene expression determinants in breast cancer as well as insights into the underlying biology of breast cancer risk loci.

Epigenome-augmented eQTL-hotspots reveal genome-wide transcriptional programs in 36 human tissues.

Expression quantitative trait loci (eQTLs) are used to inform the mechanisms of transcriptional regulation in eukaryotic cells. However, the specificity of genome-wide eQTL identification is limited by stringent control for false discoveries. Here, we described a method based on the non-homogeneous Poisson process to identify 125 489 regions with highly frequent, multiple eQTL associations, or 'eQTL-hotspots', from the public database of 59 human tissues or cell types. We stratified the eQTL-hotspots into two classes with their distinct sequence and epigenomic characteristics. Based on these classifications, we developed a machine-learning model, E-SpotFinder, for augmented discovery of tissue- or cell-type-specific eQTL-hotspots. We applied this model to 36 tissues or cell types. Using augmented eQTL-hotspots, we recovered 655 402 eSNPs and reconstructed a comprehensive regulatory network of 2 725 380 cis-interactions among eQTL-hotspots. We further identified 52 012 modules representing transcriptional programs with unique functional backgrounds. In summary, our study provided a framework of epigenome-augmented eQTL analysis and thereby constructed comprehensive genome-wide networks of cis-regulations across diverse human tissues or cell types.

The dysfunction of CD8+ T cells triggered by endometriotic stromal cells promotes the immune survival of endometriosis.

Endometriosis is defined as an oestrogen-dependent and inflammatory gynaecological disease of which the pathogenesis remains unclear. This study aimed to investigate the cellular heterogeneity and reveal the effect of CD8+ T cells on the progress of endometriosis. Three ovarian endometriosis patients were collected, and single-cell RNA sequencing (scRNA-seq) progressed and delineated the cellular landscape of endometriosis containing five cell clusters. The endometrial cells (EMCs) were the major component, of which the mesenchymal cells were preponderant and characterized with increased inflammation and oestrogen synthesis in endometriosis. The proportion of T cells, mainly CD8+ T cells rather than CD4+, was reduced in endometriotic lesions, and the cytokines and cytotoxicity of ectopic T cells were depressed. CD8+ T cells depressed the proliferation of ESCs through inhibiting CDK1/CCNB1 pathway to arrest the cell cycle and triggered inflammation through activating STAT1 pathway. Correspondingly, the coculture with ESCs resulted in the dysfunction of CD8+ T cells through upregulating STAT1/PDCD1 pathway and glycolysis-promoted metabolism reprogramming. The endometriotic lesions were larger in nude mouse models with T-cell deficiency than the normal mouse models. The inhibition of T cells via CD90.2 or CD8A antibody increased the endometriotic lesions in mouse models, and the supplement of T cells to nude mouse models diminished the lesion sizes. In conclusion, this study revealed the global cellular variation of endometriosis among which the cellular count and physiology of EMCs and T cells were significantly changed. The depressed cytotoxicity and aberrant metabolism of CD8+ T cells were induced by ESCs with the activation of STAT1/PDCD1 pathway resulting in immune survival to promote endometriosis.

Electron Divergence of Cuδ- and Pdδ+ in Cu3Pd Alloy-Based Heterojunctions Boosts Concerted C≡C Bond Binding and the Volmer Step for Alkynol Semihydrogenation.

Electrocatalytic semihydrogenation of alkynols presents a sustainable alternative to conventional thermal methodologies for the high-value production of alkenols. The design of efficient catalysts with superior catalytic and energy efficiency for semihydrogenation poses a significant challenge. Here, we present the application of an electron-divergent Cu3Pd alloy-based heterojunction in promoting the electrocatalytic semihydrogenation of alkynols to alkenols using water as the proton source. The tunable electron divergence of Cuδ- and Pdδ+, modulated by rectifying contact with nitrogen-rich carbons, enables the concerted binding of active H species from the Volmer step of water dissociation and the C≡C bond of alkynols on Pdδ+ sites. Simultaneously, the pronounced electron divergence of Cu3Pd facilitates the universal adsorption of OH species from the Volmer step and alkynols on the Cuδ- sites. The electron-divergent dual-center substantially boosts water dissociation and inhibition of completing hydrogen evolution to give a turnover frequency of 2412 h-1, outperforming the reported electrocatalysts' value of 7.3. Moreover, the continuous production of alkenols at industrial-related current density (-200 mA cm-2) over the efficient and durable Cu3Pd-based electrolyzer could achieve a cathodic energy efficiency of 45 mol kW·h-1, 1.7 times the bench-marked reactors, promising great potential for sustainable industrial synthesis.

Dual Starvations Induce Pyroptosis for Orthotopic Pancreatic Cancer Therapy through Simultaneous Deprivation of Glucose and Glutamine.

Pancreatic cancer is a highly fatal disease, and existing treatment methods are ineffective, so it is urgent to develop new effective treatment strategies. The high dependence of pancreatic cancer cells on glucose and glutamine suggests that disrupting this dependency could serve as an alternative strategy for pancreatic cancer therapy. We identified the vital genes glucose transporter 1 (GLUT1) and alanine-serine-cysteine transporter 2 (ASCT2) through bioinformatics analysis, which regulate glucose and glutamine metabolism in pancreatic cancer, respectively. Human serum albumin nanoparticles (HSA NPs) for delivery of GLUT1 and ASCT2 inhibitors, BAY-876/V-9302@HSA NPs, were prepared by a self-assembly process. This nanodrug inhibits glucose and glutamine uptake of pancreatic cancer cells through the released BAY-876 and V-9302, leading to nutrition deprivation and oxidative stress. The inhibition of glutamine leads to the inhibition of the synthesis of the glutathione, which further aggravates oxidative stress. Both of them lead to a significant increase in reactive oxygen species, activating caspase 1 and GSDMD and finally inducing pyroptosis. This study provides a new effective strategy for orthotopic pancreatic cancer treatment by dual starvation-induced pyroptosis. The study for screening metabolic targets using bioinformatics analysis followed by constructing nanodrugs loaded with inhibitors will inspire future targeted metabolic therapy for pancreatic cancer.

CDSKNNXMBD: a novel clustering framework for large-scale single-cell data based on a stable graph structure.

BACKGROUND: Accurate and efficient cell grouping is essential for analyzing single-cell transcriptome sequencing (scRNA-seq) data. However, the existing clustering techniques often struggle to provide timely and accurate cell type groupings when dealing with datasets with large-scale or imbalanced cell types. Therefore, there is a need for improved methods that can handle the increasing size of scRNA-seq datasets while maintaining high accuracy and efficiency. METHODS: We propose CDSKNNXMBD (Community Detection based on a Stable K-Nearest Neighbor Graph Structure), a novel single-cell clustering framework integrating partition clustering algorithm and community detection algorithm, which achieves accurate and fast cell type grouping by finding a stable graph structure. RESULTS: We evaluated the effectiveness of our approach by analyzing 15 tissues from the human fetal atlas. Compared to existing methods, CDSKNN effectively counteracts the high imbalance in single-cell data, enabling effective clustering. Furthermore, we conducted comparisons across multiple single-cell datasets from different studies and sequencing techniques. CDSKNN is of high applicability and robustness, and capable of balancing the complexities of across diverse types of data. Most importantly, CDSKNN exhibits higher operational efficiency on datasets at the million-cell scale, requiring an average of only 6.33 min for clustering 1.46 million single cells, saving 33.3% to 99% of running time compared to those of existing methods. CONCLUSIONS: The CDSKNN is a flexible, resilient, and promising clustering tool that is particularly suitable for clustering imbalanced data and demonstrates high efficiency on large-scale scRNA-seq datasets.

Verteporfin regulates corneal neovascularization through inhibition of YAP protein activation.

Corneal neovascularization (CNV) is a vision-threatening disease that is becoming a growing public health concern. While Yes-associated protein (YAP) plays a critical role in neovascular disease and allow for the sprouting angiogenesis. Verteporfin (VP) is a classical inhibitor of the YAP-TEAD complex, which is used for clinical treatment of neovascular macular degeneration through photodynamic therapy. The purpose of this study is to explore the effect of verteporfin (VP) on the inhibition of CNV and its potential mechanism. Rat CNV model were established by suturing in the central cornea and randomly divided into three groups (control, CNV and VP group). Neovascularization was observed by slit lamp to extend along the corneal limbus to the suture line. RNA-sequencing was used to reveal the related pathways on the CNV and the results revealed the vasculature development process and genes related with angiogenesis in CNV. In CNV group, we detected the nuclear translocation of YAP and the expression of CD31 in corneal neovascular endothelial cells through immunofluorescence. After the application of VP, the proliferation, migration and the tube formation of HUVECs were significantly inhibited. Furthermore, VP showed the CNV inhibition by tail vein injection without photoactivation. Then we found that the expression of phosphorylated YAP significantly decreased, and its downstream target protein connective tissue growth factor (CTGF) increased in the CNV group, while the expression was just opposite in other groups. Besides, both the expression of vascular endothelial growth factor receptor 2 (VEGFR2) and cofilin significantly increased in CNV group, and decreased after VP treatment. Therefore, we conclude that Verteporfin could significantly inhibited the CNV without photoactivation by regulating the activation of YAP.

Unveiling the potent effect of vitamin D: harnessing Nrf2/HO-1 signaling pathways as molecular targets to alleviate urban particulate matter-induced asthma inflammation.

BACKGROUND: Asthma is the most common allergic disease characterized by an inflammatory response in the airways. Mechanismly, urban particulate matter (PM) is the most widely air pollutant associated with increased asthma morbidity and airway inflammation. Current research found that vitamin D is an essential vitamin with anti-inflammatory, antioxidant and other medical efficacy. Inadequate or deficient vitamin D often leads to the pathogenesis and stability of asthma. NGF exacerbates airway inflammation in asthma by promoting smooth muscle cell proliferation and inducing the Th2 immune response. Activation of the Nrf2/HO-1 signaling pathway can exert a protective effect on the inflammatory response in bronchial asthma. However, the specific mechanism of this pathway in PM-involved asthmatic airway smooth muscle cells remains unclear. METHODS: Mice were sensitized and challenged with Ovalbumin (OVA) to establish an asthma model. They were then exposed to either PM, vitamin D or a combination of both, and inflammatory responses were observed. Including, acetylcholine stimulation at different concentrations measured airway hyperresponsiveness in mice. Bronchoalveolar lavage fluid (BALF) and serum were collected for TNF-α, IL-1ß, IL-6, and Nerve growth factor (NGF) analysis. Additionally, lung tissues underwent histopathological examination to observe alveolar structure and inflammatory cell infiltration. Specific ELISA kits were utilized to determine the levels of the inflammatory factors TNF-α, IL-1ß, IL-6, and Nerve growth factor (NGF). Nrf2/HO-1 signaling pathways were examined by western blot analysis. Meanwhile, we constructed a cell system with low HO-1 expression by lentiviral transfection of airway smooth muscle cells. The changes of Nrf2, HO-1, and NGF were observed after the treatment of OVA, PM, and Vit D were given. RESULTS: The in vivo results showed that vitamin D significantly alleviated pathological changes in lung tissue of PM-exposed mice models. Mechanismly, vitamin D decreased substantial inflammatory cell infiltration in lung tissue, as well as the number of inflammatory cells in BALF. Furthermore, vitamin D reduced the heightened inflammatory factors including of TNF-α, IL-1ß, IL-6, and NGF caused by PM exposure, and triggered the activity of nucleus Nrf2 and HO-1 in PM-exposed asthmatic mice. Notably, knockdown HO-1 weakens the Vitamin D- mediated inhibition to pollution toxicity in asthma. Importantly, in vitro experiments on OVA-stimulated mice airway smooth muscle cells, the results showed that OVA and PM, respectively, reduced Nrf2/HO-1 and increased NGF's expression, while vitamin D reversed the process. And in the HO-1 knockdown cell line of Lenti-si-HO-1 ASMCs, OVA and PM reduced Nrf2's expression, while HO-1 and NGF's expression were unchanged. CONCLUSIONS: The above results demastrate that vitamin D downregulated the inflammatory response and the expression of NGF by regulating the Nrf2/HO-1 signaling pathways in airway smooth muscle cells, thereby showing potent anti-inflammatory activity in asthma.

From bits to green: Unraveling the digital economy's influence on natural resource efficiency.

This study explores the impact of the digital economy (DE) on natural resource efficiency (NRE) across 275 Chinese cities between 2011 and 2021. Through a comprehensive empirical analysis, we find that the DE significantly positively affects NRE. A key moderating factor in this relationship is green technological innovation (GTI), focusing on the quality rather than the quantity of green technology. Our study also uncovers regional variations of moderating effect. Additionally, we identify several mechanisms through which the DE contributes to enhanced NRE, including the transformation of industrial structure and improvements in green total factor productivity. A detailed heterogeneity analysis shows that the DE's impact on NRE varies according to city-specific factors such as natural resource endowment, city size, environmental regulations, and administrative levels. These findings provide a more nuanced understanding of how the DE influences NRE at the urban level, contributing to the broader discourse on sustainable development in the digital age. Our research offers policy recommendations and potential pathways for cities to leverage the DE for greater natural resource efficiency.

Circular RNA 0001789 sponges miR-140-3p and regulates PAK2 to promote the progression of gastric cancer.

BACKGROUND: Gastric cancer (GC) is the third-leading cause of cancer-associated mortalities globally. The deregulation of circular RNAs (circRNAs) and microRNAs (miRNAs or miRs) is widely implicated in the pathogenesis and progression of different cancer types. METHODS: The expression profiling of circRNAs in GC is required to identify crucial circRNAs as biomarkers or therapeutic targets. In the present study, a published circRNA microarray dataset was used to identify differentially expressed circRNAs between GC tissues and normal gastric mucosa tissues. Reverse transcription-quantitative PCR was performed to validate the expression of circ_0001789. Fisher's exact test, receiver operating characteristic curve and Kaplan-Meier plots were employed to analyze the clinical significance of circ_0001789. The miRNA targets of circ_0001789 were predicted using an online database, and their functional interaction was further confirmed by RNA pull-down, RNA immunoprecipitation and dual luciferase reporter assays. Transwell assays were conducted to investigate the biological functions of circ_0001789, miR-140-3p and p21 activated kinase 2 (PAK2) in the migration and invasion of GC cells. A xenograft mouse model was established to validate the role of circ_0001789 in the tumorigenesis of GC cells. RESULTS: circ_0001789 was identified as a highly expressed circRNA in GC tissues versus normal gastric mucosa tissues. Silencing circ_0001789 attenuated the malignancy of GC cells, and exosomal circ_0001789 was sufficient to regulate the malignant phenotype of GC cells. miR-140-3p was further identified as a downstream target of circ_0001789, which showed a negative correlation with circ_0001789 expression in GC tissues. Overexpression of miR-140-3p suppressed cell migration, invasion and epithelial-mesenchymal transition in GC cells. PAK2 was identified as the target of miR-140-3 to mediate the malignant phenotype of GC cells. CONCLUSION: The present data suggested that the upregulation of circ_0001789 was associated with the progression of GC and with poor prognosis in patients with GC, and that miR-140-3p/PAK2 served as the downstream axis to mediate the oncogenic effect of circ_0001789.

Moiré enhanced charge density wave state in twisted 1T-TiTe2/1T-TiSe2 heterostructures.

Nanoscale periodic moiré patterns, for example those formed at the interface of a twisted bilayer of two-dimensional materials, provide opportunities for engineering the electronic properties of van der Waals heterostructures1-11. In this work, we synthesized the epitaxial heterostructure of 1T-TiTe2/1T-TiSe2 with various twist angles using molecular beam epitaxy and investigated the moiré pattern induced/enhanced charge density wave (CDW) states with scanning tunnelling microscopy. When the twist angle is near zero degrees, 2 × 2 CDW domains are formed in 1T-TiTe2, separated by 1 × 1 normal state domains, and trapped in the moiré pattern. The formation of the moiré-trapped CDW state is ascribed to the local strain variation due to atomic reconstruction. Furthermore, this CDW state persists at room temperature, suggesting its potential for future CDW-based applications. Such moiré-trapped CDW patterns were not observed at larger twist angles. Our study paves the way for constructing metallic twist van der Waals bilayers and tuning many-body effects via moiré engineering.

High-speed mid-infrared graphene electro-optical modulator based on suspended germanium slot waveguides.

The mid-infrared (MIR) region is attracting increasing interest for on-chip synchronous detection and free-space optical (FSO) communications. For such applications, a high-performance electro-optical modulator is a crucial component. In this regard, we propose and investigate a graphene-based electro-absorption modulator (EAM) and microring modulator (MRM) using the suspended germanium waveguide platform. The modulators are designed for the second atmospheric window (8 to 12 µm). The incorporation of double-layer graphene on the suspended slot waveguide structure allows for the significant enhancement of light-graphene interaction, theoretically achieving a 3-dB bandwidth as high as 78 GHz. The EAM shows a calculated modulation depth of 0.022-0.045 dB/µm for the whole operation wavelength range. The MRM exhibits a calculated extinction ratio as high as 68.9 dB and a modulation efficiency of 0.59 V·cm around 9 µm. These modulators hold promise for constructing high-speed FSO communication and on-chip spectroscopic detection systems in the MIR atmospheric window.

Silicon MMI-based power splitter for multi-band operation at the 1.55 and 2†µm wave bands.

Multimode interference (MMI)-based power splitters are fundamental building blocks for integrated photonic devices consisting of an interferometer structure. In order to forestall the 'capacity crunch' in optical communications, integrated devices capable of operating in multiple spectral bands (e.g., the conventional telecom window and the emerging 2 µm wave band) have been proposed and are attracting increasing interest. Here, we demonstrate for the first time, to the best of our knowledge, the realization of a dual-band MMI-based 3 dB power splitter operating at the 1.55 and 2 µm wave bands. The fabricated power splitter exhibits low excess losses of 0.21 dB and 0.32 dB with 1 dB bandwidths for 1500-1600 nm and 1979-2050 nm, respectively.

Multi-band all-silicon TM-pass polarizer based on one-dimensional photonic crystals nanohole array.

We propose an on-chip transverse magnetic (TM)-pass polarizer utilizing one-dimensional photonic crystals for multi-band operation. The TE0 modes in the 1550/2000nm wave band are suppressed by carefully selecting the pitch lengths of the nanoholes, leveraging the bandgap of the nanohole array. Conversely, the TM0 modes remain almost unaffected. The TM-pass polarizer employs a single-etched design on a standard 220 nm SOI platform and has a compact length of ∼ 17.9 µm. The simulated bandwidths (BWs) for polarization extinction ratios (PERs) > 20 dB and > 25 dB are about 210 nm and 195 nm for the 1550 nm wave band, and 265 nm and 240 nm for the 2000nm wave band. Moreover, the insertion losses (ILs) are ∼ 0.5/0.3 dB at wavelengths of 1550/2000nm, respectively. For the fabricated device, the measured BWs for PER > 20 dB and > 25 dB are evaluated to be larger than 100 nm for both 1550/2000nm wave bands. The measured ILs are 1/0.8 dB at wavelengths of 1550/2000nm. This straightforward and compatible design opens possibilities for the development of practical multi-band silicon photonic integrated circuits.

Iron Vacancy Tunable Superconductor-Insulator Transition in FeSe/SrTiO_{3} Monolayer.

The Fe_{4}Se_{5} with a sqrt[5]×sqrt[5] Fe vacancy order is suggested to be a Mott insulator and the parent state of bulk FeSe superconductor. The iron vacancy ordered state has been considered as a Mott insulator and the parent compound of bulk FeSe-based superconductors. However, for the superconducting FeSe/SrTiO_{3} monolayer (FeSe/STO) with an interface-enhanced high transition temperature (T_{c}), the electronic evolution from its Fe vacancy ordered parent phase to the superconducting state, has not been explored due to the challenge to realize an Fe vacancy order in the FeSe/STO monolayer, even though important to the understanding of superconductivity mechanism. In this study, we developed a new method to generate Fe vacancies within the FeSe/STO monolayer in a tunable fashion, with the assistance of atomic hydrogen. As a consequence, an insulating sqrt[5]×sqrt[5] Fe vacancy ordered monolayer is realized as the parent state. By using scanning tunneling microscopy and scanning tunneling spectroscopy, the spectral evolution from superconductivity to insulator is fully characterized. Surprisingly, a prominent spectral weight transfer occurs, thus implying a strong electron correlation effect. Moreover, the Fe vacancy induced insulating gap exhibits no Mott gap-like features. This work provides new insights in understanding the high-T_{c} superconductivity in FeSe/STO monolayer.

The Use of Iron-Doped Anatase TiO2 Nanofibers for Enhanced Photocatalytic Fenton-like Reaction to Degrade Tylosin.

The removal of antibiotics from wastewater to prevent their environmental accumulation is significant for human health and ecosystems. Herein, iron (Fe)-atom-doped anatase TiO2 nanofibers (Fe-TNs) were manufactured for the photocatalytic Fenton-like decomposition of tylosin (TYL) under LED illumination. Compared with the pristine TiO2 nanofibers (TNs), the optimized Fe-TNs exhibited improved visible-light-driven photocatalytic Fenton-like activity with a TYL degradation efficiency of 98.5% within 4 h. The effective TYL degradation could be attributed to the expanded optical light absorption and accelerated separation and migration of photogenerated electrons and holes after the introduction of Fe. The photogenerated electrons were highly conducive to the generation of active SO4•- radicals as they facilitated Fe(III)/Fe(II) cycles, and to oxidizing TYL. Moreover, the holes could be involved in TYL degradation. Thus, a significant enhancement in TYL degradation could be achieved. This research verifies the use of iron-doped anatase nanofibers as an effective method to synthesize novel photocatalytic Fenton-like catalysts through surface engineering for wastewater remediation.

Boosting Mass Exchange between Pd/NC and MoC/NC Dual Junctions via Electron Exchange for Cascade CO2 Fixation.

Merging existing catalysts together as a cascade catalyst may achieve "one-pot" synthesis of complex but functional molecules by simplifying multistep reactions, which is the blueprint of sustainable chemistry with low pollutant emission and consumption of energy and materials only when the smooth mass exchange between different catalysts is ensured. Effective strategies to facilitate the mass exchange between different active centers, which may dominate the final activity of various cascade catalysts, have not been reached until now, even though charged interfaces due to work function driven electron exchange have been widely observed. Here, we successfully constructed mass (reactants and intermediates) exchange paths between Pd/N-doped carbon and MoC/N-doped carbon induced by interfacial electron exchange to trigger the mild and cascade methylation of amines using CO2 and H2. Theoretical and experimental results have demonstrated that the mass exchange between electron-rich MoC and electron-deficient Pd could prominently improve the production of N,N-dimethyl tertiary amine, which results in a remarkably high turnover frequency value under mild conditions, outperforming the state-of-the-art catalysts in the literature by a factor of 5.9.

Facilitating Hot Electron Injection from Graphene to Semiconductor by Rectifying Contact for Vis-NIR-Driven H2 O2 Production.

Solar-driven production of hydrogen peroxide (H2 O2 ), as an important industrial chemical oxidant with an extensive range of applications, from oxygen reduction is a sustainable alternative to mainstream anthraquinone oxidation and direct hydrogenation of dioxygen methods. The efficiency of solar to hydrogen peroxide over semiconductor-based photocatalysts is still largely limited by the narrow light absorption to visible light. Here, the authors proposed and demonstrate the proof-of-concept application of light-generated hot electrons in a graphene/semiconductor (exemplified with widely used TiO2 ) dyad to largely extend visible light spectra up to 800 nm for efficient H2 O2 production. The well-designed graphene/semiconductor heterojunction has a rectifying interface with a zero barrier for the hot electron injection, largely boosting excited hot electrons with an average lifetime of ≈0.5 ps into charge carriers with a long fluorescent lifetime (4.0 ns) for subsequent H2 O2 production. The optimized dyadic photocatalyst can provide an H2 O2 yield of 0.67 mm g-1  h-1 under visible light irradiation (λ ≥ 400 nm), which is 20 times of the state-of-the-art noble-metal-free titanium oxide-based photocatalyst, and even achieves an H2 O2 yield of 0.14 mm g-1  h-1 upon photoexcitation by near-infrared-region light (≈800 nm).

Silicon photonic flat-top WDM (de)multiplexer based on cascaded Mach-Zehnder interferometers for the 2†µm wavelength band: publisher's note.

This publisher's note contains a correction to [Opt. Express30, 28232 (2022)10.1364/OE.467473].

Silicon photonic flat-top WDM (de)multiplexer based on cascaded Mach-Zehnder interferometers for the 2 µm wavelength band.

The 2 µm wavelength band has proven to be a promising candidate for the next communication window. Wavelength-division multiplexing (WDM) transmission at 2 µm can greatly increase the capacity of optical communication systems. Here, we experimentally demonstrate a high-performance silicon photonic flat-top 8-channel WDM (de)multiplexer based on cascaded Mach-Zehnder interferometers for the 2 µm wavelength band. A three-stage-coupler scheme is utilized to provide passbands and reduce channel crosstalk, and 11 thermo-optic phase shifters have allowed active compensation of waveguide phase errors. The fabricated device shows low insertion loss (< 0.9 dB), channel crosstalk (< 20.6 dB) and 1-dB bandwidth of 2.3 nm for operating wavelength ranging from 1955nm to 1985nm. The demonstrated (de)multiplexer could potentially be used for WDM optical data communication in the 2 µm spectral band.