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Numerous modern technologies are reliant on the low-phase noise and exquisite timing stability of microwave signals. Substantial progress has been made in the field of microwave photonics, whereby low-noise microwave signals are generated by the down-conversion of ultrastable optical references using a frequency comb 1 – 3 . Such systems, however, are constructed with bulk or fibre optics and are difficult to further reduce in size and power consumption. In this work we address this challenge by leveraging advances in integrated photonics to demonstrate low-noise microwave generation via two-point optical frequency division 4 , 5 . Narrow-linewidth self-injection-locked integrated lasers 6 , 7 are stabilized to a miniature Fabry–Pérot cavity 8 , and the frequency gap between the lasers is divided with an efficient dark soliton frequency comb 9 . The stabilized output of the microcomb is photodetected to produce a microwave signal at 20 GHz with phase noise of −96 dBc Hz −1 at 100 Hz offset frequency that decreases to −135 dBc Hz −1 at 10 kHz offset—values that are unprecedented for an integrated photonic system. All photonic components can be heterogeneously integrated on a single chip, providing a significant advance for the application of photonics to high-precision navigation, communication and timing systems. We leverage advances in integrated photonics to generate low-noise microwaves with an optical frequency division architecture that can be low power and chip integrated.

Numerous modern technologies are reliant on the low-phase noise and exquisite timing stability of microwave signals. Substantial progress has been made in the field of microwave photonics, whereby low-noise microwave signals are generated by the down-conversion of ultrastable optical references using a frequency comb13. Such systems, however, are constructed with bulk or fibre optics and are difficult to further reduce in size and power consumption. In this work we address this challenge by leveraging advances in integrated photonics to demonstrate low-noise microwave generation via two-point optical frequency division4,5. Narrow-linewidth self-injection-locked integrated lasers6,7 are stabilized to a miniature Fabry-Perot cavity8, and the frequency gap between the lasers is divided with an efficient dark soliton frequency comb9. The stabilized output of the microcomb is photodetected to produce a microwave signal at 20 GHz with phase noise of-96 dBc Hz1 at 100 Hz offset frequency that decreases to -135 dBc Hz1 at 10 kHz offset-values that are unprecedented for an integrated photonic system. All photonic components can be heterogeneously integrated on a single chip, providing a significant advance for the application of photonics to high-precision navigation, communication and timing systems.

The unique benefits of Fabry-Pérot resonators as frequency-stable reference cavities and as an efficient interface between atoms and photons make them an indispensable resource for emerging photonic technologies. To bring these performance benefits to next-generation communications, computation, and timekeeping systems, it will be necessary to develop strategies to integrate compact Fabry-Pérot resonators with photonic integrated circuits. In this paper, we demonstrate a novel reflection cancellation circuit that utilizes a numerically optimized multi-port polarization-splitting grating coupler to efficiently interface high-finesse Fabry-Pérot resonators with a silicon photonic circuit. This circuit interface produces spatial separation of the incident and reflected waves, as required for on-chip Pound-Drever-Hall frequency locking, while also suppressing unwanted back reflections from the Fabry-Pérot resonator. Using inverse design principles, we design and fabricate a polarization-splitting grating coupler that achieves 55% coupling efficiency. This design realizes an insertion loss of 5.8 dB for the circuit interface and more than 9 dB of back reflection suppression, and we demonstrate the versatility of this system by using it to interface several reflective off-chip devices.

Numerous modern technologies are reliant on the low-phase noise and exquisite timing stability of microwave signals. Substantial progress has been made in the field of microwave photonics, whereby low noise microwave signals are generated by the down-conversion of ultra-stable optical references using a frequency comb. Such systems, however, are constructed with bulk or fiber optics and are difficult to further reduce in size and power consumption. Our work addresses this challenge by leveraging advances in integrated photonics to demonstrate low-noise microwave generation via two-point optical frequency division. Narrow linewidth self-injection locked integrated lasers are stabilized to a miniature Fabry-P\\'{e}rot cavity, and the frequency gap between the lasers is divided with an efficient dark-soliton frequency comb. The stabilized output of the microcomb is photodetected to produce a microwave signal at 20 GHz with phase noise of -96 dBc/Hz at 100 Hz offset frequency that decreases to -135 dBc/Hz at 10 kHz offset--values which are unprecedented for an integrated photonic system. All photonic components can be heterogeneously integrated on a single chip, providing a significant advance for the application of photonics to high-precision navigation, communication and timing systems.

Background Dysbiosis of the gut microbiome is involved in the pathogenesis of various diseases, but the contribution of gut microbes to the progression of chronic obstructive pulmonary disease (COPD) is still poorly understood. Methods We carried out 16S rRNA gene sequencing and short-chain fatty acid analyses in stool samples from a cohort of 73 healthy controls, 67 patients with COPD of GOLD stages I and II severity, and 32 patients with COPD of GOLD stages III and IV severity. Fecal microbiota from the three groups were then inoculated into recipient mice for a total of 14 times in 28 days to induce pulmonary changes. Furthermore, fecal microbiota from the three groups were inoculated into mice exposed to smoke from biomass fuel to induce COPD-like changes. Results We observed that the gut microbiome of COPD patients varied from that of healthy controls and was characterized by a distinct overall microbial diversity and composition, a Prevotella -dominated gut enterotype and lower levels of short-chain fatty acids. After 28 days of fecal transplantation from COPD patients, recipient mice exhibited elevated lung inflammation. Moreover, when mice were under both fecal transplantation and biomass fuel smoke exposure for a total of 20 weeks, accelerated declines in lung function, severe emphysematous changes, airway remodeling and mucus hypersecretion were observed. Conclusion These data demonstrate that altered gut microbiota in COPD patients is associated with disease progression in mice model.

Moiré superlattices in van der Waals materials have emerged as a promising platform for studying the correlated states in condensed matter physics. These correlated states have substantial effects on the emission coherence, an important parameter for quantum light applications. However, the effect of correlated states on the excitonic emission coherence is largely unexplored. Here, we show that the coherence of moiré interlayer exciton emission in tungsten diselenide (WSe 2 )/molybdenum disulfide (MoS 2 ) heterobilayers is sensitive to the correlated insulating states in this material. We demonstrate that the emission linewidth of interlayer exciton shows a dip at a particular power range, which we attributed to the excitonic (bosonic) interaction. Moreover, such linewidth minima also appear in the doping dependence of the photoluminescence spectrum at the integer electronic filling factor, f el = 1, demonstrating the effect of the electronic (fermionic) correlated insulating state on the interlayer exciton emission coherence. Our results demonstrate the richness of exciton-exciton and exciton-electron interactions in moiré semiconductors and pave the way for engineering emission coherence by controlling such interactions. The interaction between correlated states and the excitonic emission coherence in van der Waals moiré systems remains largely unexplored. Here, the authors report evidence of enhanced interlayer exciton emission coherence in twisted WSe 2 /MoS 2 heterobilayers, attributed to exciton-exciton and exciton-electron interactions.

Background Schizophrenia (SZ) is a severe mental illness that significantly impairs patients' quality of life and cognitive functioning. Objective This study investigates the role of nitric oxide (NO) in SZ pathogenesis by examining its induction of neuronal pyroptosis and its correlation with cognitive impairment. We aimed to identify potential therapeutic targets by analyzing the expression of pyroptosis-related genes (NLRP3, Caspase-1, GSDMD), inflammatory factors (IL-1β, IL-18), and SZ susceptibility genes (CUX2, DTNBP1). Methods (1) SH-SY5Y cells were treated with sodium nitroprusside (NO donor) at varying concentrations. Cell viability, NO levels, and gene expression were assessed using Cell Counting Kit-8(CCK-8), Griess reagent, and qPCR assays. (2) Clinical analysis included 58 SZ patients and 62 healthy controls. Cognitive function was evaluated using RBANS, and NO levels and gene expression were measured in blood samples. Results (1) NO treatment reduced SH-SY5Y cell viability and altered the expression of pyroptosis-related and susceptibility genes, and the IC 50 value of sodium nitroprusside on SH-SY5Y cells was 1.4 mM. (2) SZ patients exhibited elevated NO levels, reduced cognitive scores, and dysregulated gene expression compared to controls. NLRP3 and IL-18 were strongly associated with cognitive impairment. Conclusion NO serves an essential role in the pathological mechanisms of schizophrenia by inducing neuronal pyroptosis, potentially through the key factor NLRP3. Additionally, NLRP3 and IL-18 are strongly linked with cognitive impairment in schizophrenia.

Abnormal trophoblast self-renewal and differentiation during early gestation is the major cause of miscarriage, yet the underlying regulatory mechanisms remain elusive. Here, we show that trophoblast specific deletion of Kat8 , a MYST family histone acetyltransferase, leads to extraembryonic ectoderm abnormalities and embryonic lethality. Employing RNA-seq and CUT&Tag analyses on trophoblast stem cells (TSCs), we further discover that KAT8 regulates the transcriptional activation of the trophoblast stemness marker, CDX2, via acetylating H4K16. Remarkably, CDX2 overexpression partially rescues the defects arising from Kat8 knockout. Moreover, increasing H4K16ac via using deacetylase SIRT1 inhibitor, EX527, restores CDX2 levels and promoted placental development. Clinical analysis shows reduced KAT8, CDX2 and H4K16ac expression are associated with recurrent pregnancy loss (RPL). Trophoblast organoids derived from these patients exhibit impaired TSC self-renewal and growth, which are significantly ameliorated with EX527 treatment. These findings suggest the therapeutic potential of targeting the KAT8-H4K16ac-CDX2 axis for mitigating RPL, shedding light on early gestational abnormalities. Embryo implantation failure is a leading cause of miscarriage, though the mechanisms underlying trophoblast defects are not well understood. Here they show that the histone acetyltransferase KAT8 is essential for proper activation of the trophoblast stemness gene CDX2, and that placental development can be partially rescued by inhibiting histone deacetylase activity.

Electron correlation plays an essential role in the macroscopic quantum phenomena in the moiré heterostructure, such as antiferromagnetism and correlated insulating phases. Unlike the phenomena where the interaction involves only electrons in one layer, the interaction of distinct phases in two or more layers represents a new horizon forward, such as the one in the Kondo lattice model. Here, using interlayer excitons as a probe, we show that the interlayer interactions in heterobilayers of tungsten diselenide and molybdenum disulfide (WSe2/MoS2) can be electrically switched on and off, resulting in a layer-dependent correlated phase diagram, including single-layer, layer-selective, excitonic-insulator and layer-hybridized regions. We demonstrate that these correlated phases affect the interlayer exciton non-radiative decay pathways. These results reveal the role of strong correlation on interlayer exciton dynamics and pave the way for studying the layer-resolved strong correlation behaviour in moiré heterostructures.The authors demonstrate electrical on/off switching of interlayer interactions in tungsten diselenide/molybdenum disulfide heterobilayers, the phase diagram of which contains layer-dependent correlated regions that reveal the role of strong correlations in interlayer exciton dynamics.

Head and neck squamous cell carcinoma (HNSCC) is currently one of the most common malignancies with a poor prognosis worldwide. Meanwhile, small ubiquitin-like modifier (SUMO) specific peptidase 1 (SENP1) was associated with ferroptosis. However, the specific functions and underlying mechanisms of action of SENP1 in ferroptosis and tumor progression of HNSCC remain to be established. The findings of the present study implicated a novel ferroptosis pathway in the initiation and progression of HNSCC, providing new functional targets to guide future therapy. In the present study, The Cancer Genome Atlas database was employed to establish a gene model related to ferroptosis and verified SENP1 as a key gene via transcriptome sequencing. Expression of SENP1 in HNSCC tissue and CAL-27 cells was detected based on reverse transcription-quantitative PCR and western blot analysis. Proliferation and migration abilities of cells were determined using Cell Counting Kit-8, wound healing and Transwell experiments. Expression levels of iron, glutathione (GSH) and lipid peroxidation end-product malondialdehyde (MDA) under conditions of silencing of SENP1 with shRNA lentivirus were assayed. Additionally, the relationship between SENP1 and long-chain acyl-coenzyme A synthase 4 (ACSL4) was validated with the aid of immunoblotting and co-immunoprecipitation (co-IP). Finally, the influence of shSENP1 on the expression of key ferroptosis proteins, glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11, was evaluated via western blotting. It was revealed that SENP1 was significantly overexpressed in HNSCC and associated with low patient survival. Silencing of SENP1 led to significant suppression of cell proliferation, migration and invasion, increase in the contents of iron ions and MDA and decline in GSH levels in HNSCC cells, thereby enhancing ferroptosis and inhibiting disease progression. Conversely, overexpression of SENP1 suppressed ferroptosis and promoted progression of HNSCC. Co-IP and western blot analyses revealed a SUMOylation link between SENP1 and ACSL4. SENP1 reduced the stability of ACSL4 protein through deSUMOylation, leading to inhibition of ferroptosis. SENP1 silencing further inhibited the expression of the key iron death protein, GPX4, to regulate ferroptosis. Taken together, SENP1 deficiency promoted ferroptosis and inhibited tumor progression through reduction of SUMOylation of ACSL4 in HNSCC. The collective results of the present study supported the utility of SENP1 as an effective predictive biomarker for targeted treatment of HNSCC.