A RuCoBO Nanocomposite for Highly Efficient and Stable Electrocatalytic Seawater Splitting.

Efficient and stable electrocatalysts are critically needed for the development of practical overall seawater splitting. The nanocomposite of RuCoBO has been rationally engineered to be an electrocatalyst that fits these criteria. The study has shown that a calcinated RuCoBO-based nanocomposite (Ru2Co1BO-350) exhibits an extremely high catalytic activity for H2 and O2 production in alkaline seawater (overpotentials of 14 mV for H2 evolution and 219 mV for O2 evolution) as well as a record low cell voltage (1.466 V@10 mA cm-2) and long-term stability (230 h @50 mA cm-2 and @100 mA cm-2) for seawater splitting. The results show that surface reconstruction of Ru2Co1BO-350 occurs during hydrogen evolution reaction and oxygen evolution reaction, which leads to the high activity and stability of the catalyst. The reconstructed surface is highly resistant to Cl- corrosion. The investigation suggests that a new strategy exists for the design of high-performance Ru-based electrocatalysts that resist anodic corrosion during seawater splitting.

Long non-coding RNA in coronary artery disease: the role of PDXDC1-AS1 and SFI1-AS1.

This study investigates the interaction between long non-coding RNAs (lncRNAs) and metabolic risk factors that contribute to coronary artery disease (CAD). A total transcriptome high throughput sequencing study was conducted on peripheral blood mononuclear cells from five patients with CAD and five healthy controls. Validation assay by qRT-PCR was conducted among 270 patients and 47 controls. Finally, to evaluate the lncRNAs' diagnostic value for CAD, the Spearman correlation test and receiver operating characteristic curve (ROC) analysis were utilized. Additionally, univariate and multivariate logistic regression along with crossover analyses were conducted to identify the interaction between lncRNA and environmental risk factors. A total of 2149 of 26,027 lncRNAs identified by RNA sequencing were differentially expressed in CAD patients compared to controls. Validation by qRT-PCR showed significantly different relative expression levels for lncRNAs PDXDC1-AS1, SFI1-AS1, RP13-143G15.3, DAPK1-IT1, PPIE-AS1, and RP11-362A1.1 between the two groups (all P<0.05). The area under the ROC values of PDXDC1-AS1 and SFI1-AS1 is 0.645 (sensitivity=0.443 and specificity=0.920) and 0.629 (sensitivity=0.571 and specificity=0.909), especially. Multivariate logistic regression analyses showed that lncRNAs PDXDC1-AS1 (OR=2.285, 95%CI=1.390-3.754, p=0.001) and SFI1-AS1 (OR=1.163, 95%CI=1.163-2.264, p=0.004) were protective factors against CAD. Under the additive model, cross-over analyses demonstrated significant interactions between lncRNAs PDXDC1-AS1 and smoking in relation to CAD risk (S=3.871, 95%CI=1.140-6.599). PDXDC1-AS1 and SFI1-AS1 were sensitive and specific biomarkers for CAD and exhibited synergistic effects with certain environmental factors. These results highlighted their potential use as CAD diagnostic biomarkers for future research.

Characteristics of circular RNAs expression of peripheral blood mononuclear cells in humans with coronary artery disease.

Circular RNAs (circRNAs) function as promising biomarkers and therapeutic targets for coronary artery disease due to their high stability, covalently closed structure, and potential gene regulation. We aimed to identify the expression profile and role of circular RNAs (circRNAs) in coronary artery disease (CAD). We performed RNA sequence analysis of circRNAs in peripheral blood mononuclear cells of five patients with CAD and five controls. Bioinformatics analyses were adopted to explore biological functions of differentially expressed circRNAs. The miRanda and TargetScan tools were used to predict the microRNA (miRNA)-targeting interactions and to construct a triple network of differentially expressed gene-circRNA-miRNA-mRNA. In total, 13,160 downregulated and 12,905 upregulated circRNAs were identified in CAD. A gene ontology annotation analysis showed that genes in the network were involved in organelle organization, cell cycle, mitotic cycle, and cellular metabolic process. Parental genes of the 10 dysregulated circRNAs were involved in metabolism and protein modification, and these circRNAs might regulate gene expression associated with CAD via miRNA sponges. As potential competing endogenous RNAs (ceRNAs), dysregulated circRNAs may be involved in the pathogenesis of CAD, which provides new insights into the diagnosis and prognosis of coronary artery disease.

Efg1 and Cas5 Orchestrate Cell Wall Damage Response to Caspofungin in Candida albicans.

Echinocandins are recommended as the first-line drugs for the treatment of systemic candidiasis. Cas5 is a key transcription factor involved in the response to cell wall damage induced by echinocandins. In this study, through a genetic screen, we identified a second transcription factor, Efg1, that is also crucial for proper transcriptional responses to echinocandins. Like CAS5, deletion of EFG1 confers hypersensitivity to caspofungin. Efg1 is required for the induction of CAS5 in response to caspofungin. However, ectopically expressed CAS5 cannot rescue the growth defect of efg1 mutant in caspofungin-containing medium. Deleting EFG1 in the cas5 mutant exacerbates the cell wall stress upon caspofungin addition and renders caspofungin-resistant Candida albicans responsive to treatment. Genome-wide transcription profiling of efg1/efg1 and cas5/cas5 using transcriptome sequencing (RNA-Seq) indicates that Efg1 and Cas5 coregulate caspofungin-responsive gene expression, but they also independently control induction of some genes. We further show that Efg1 interacts with Cas5 by yeast two-hybrid and in vivo immunoprecipitation in the presence or absence of caspofungin. Importantly, Efg1 and Cas5 bind to some caspofungin-responsive gene promoters to coordinately activate their expression. Thus, we demonstrate that Efg1, together with Cas5, controls the transcriptional response to cell wall stress induced by caspofungin.

Inhibiting Fungal Echinocandin Resistance by Small-Molecule Disruption of Geranylgeranyltransferase Type I Activity.

Echinocandin resistance in Candida is a great concern, as the echinocandin drugs are recommended as first-line therapy for patients with invasive candidiasis. However, therapeutic efforts to thwart echinocandin resistance have been hampered by a lack of fungal specific drug targets. Here, we show that deleting CDC43, the ß subunit of geranylgeranyltransferase type I (GGTase I), confers hypersensitivity to echinocandins, which renders GGTase I a tractable target in combatting echinocandin resistance. The membrane localization of Rho1, which is critical for (1,3)-ß-d-glucan synthase Fks1 activation, is disrupted in the cdc43 mutant, resulting in decreased amounts of glucans in the cell wall, thereby exacerbating the cell wall stress upon caspofungin addition. Guided by this insight, we found that selective chemical inhibition of GGTase I by L-269289 potentiates echinocandin activity and renders echinocandin-resistant Candida albicans responsive to treatment in vitro and in animal models for disseminated infection. Furthermore, L-269289 and echinocandins also act in a synergistic manner for the treatment of Candida tropicalis and Candida parapsilosis Importantly, deletion of CDC43 is lethal in Candida glabrata L-269289 is active on its own to kill C. glabrata, and its fungicidal activity is enhanced when combined with caspofungin. Thus, targeting GGTase I has therapeutic potential to address the clinical challenge of echinocandin-resistant candidiasis.

Cognitive impairment and sleep disturbances after minor ischemic stroke.

PURPOSE: Post-stroke cognitive impairment (PSCI) is common among stroke survivors, although its risk factors are not well understood. Here, we assessed cognitive function in patients within 14 days after minor stroke and investigated the risk factors of PSCI, including sleep-related factors. METHODS: Patients with minor acute ischemic stroke (n = 86) were continuously recruited from November 2015 to October 2016. Demographic and clinical data were collected, and cognitive assessment and polysomnography were performed. Based on their cognitive performance, stroke patients were divided into PSCI and no PSCI groups. Age-, sex-, and education-matched participants (n = 36) were included as a healthy control (HC) group. RESULTS: Stroke patients showed impairments in multiple cognitive domains relative to HC participants (p < 0.01). Among stroke patients, the prevalence of PSCI and obstructive sleep apnea was 81.4 and 74.4%, respectively. Impairments in attention and working memory (87.1%) and executive function (84.3%) were the most common among stroke patients. Compared with no PSCI patients, PSCI patients showed a higher prevalence of obstructive sleep apnea (50.0 vs. 80.0%, p = 0.030) and shorter total sleep time (435.1 ± 104.0 vs. 347.3 ± 98.1 min, p = 0.002). Logistic regression analysis showed that education duration, total sleep time, and lowest SaO2 were independent risk factors for PSCI. CONCLUSIONS: The prevalence of PSCI is high after minor ischemic stroke. In particular, attention and working memory and executive function are most commonly impaired. Although the risk factors for PSCI are numerous, shorter total sleep time and degree of hypoxia at night warrant further attention.

Fluorescent Probes with Multiple Binding Sites for the Discrimination of Cys, Hcy, and GSH.

Biothiols such as cysteine (Cys), homocysteine (Hcy), and glutathione (GSH) play crucial roles in maintaining redox homeostasis in biological systems. This Minireview summarizes the most significant current challenges in the field of thiol-reactive probes for biomedical research and diagnostics, emphasizing the needs and opportunities that have been under-investigated by chemists in the selective probe and sensor field. Progress on multiple binding site probes to distinguish Cys, Hcy, and GSH is highlighted as a creative new direction in the field that can enable simultaneous, accurate ratiometric monitoring. New probe design strategies and researcher priorities can better help address current challenges, including the monitoring of disease states such as autism and chronic diseases involving oxidative stress that are characterized by divergent levels of GSH, Cys, and Hcy.

Alteration of brainstem raphe measured by transcranial sonography in depression patients with or without Parkinson's disease.

The purpose of our study was to assess the alteration of the brainstem raphe (BR) on transcranial sonography (TCS) in depression patients with or without Parkinson's disease (PD) and to explore whether the different changes of BR could reflect an increasing impairment of raphe structures. TCS was performed in patients with PD, depression with PD, depression only, and controls. Using the red nucleus as an internal standard, the BR was rated semi-quantitatively from grades 1-4 with grades 1-3 determined as abnormal. The rate of abnormal BR (≤grade 3) was found to be only 10 % in patients with PD (4/40) and 5 % in control patients (2/40). The rate of abnormal raphe was significantly higher (p < 0.05) in patients with both depression and PD (85 %, 34/40) or patients with depression only (87.5 %, 35/40). TCS of the raphe in most patients with mild depression scored grade 3, while those with moderate depression scored grade 2-3, and those with severe depression scored grade 1. The different BR echogenicity score reflected an increasing impairment of raphe structures in depression patients with or without PD (p < 0.05). TCS provides a good tool for assessing depression, more severe depressive symptoms were associated with different aspects in TCS studies.

Retinal nerve fiber layer thinning: a window into rapid eye movement sleep behavior disorders in Parkinson's disease.

PURPOSE: Retinal nerve fiber layer (RNFL) thinning occurs in Parkinson's disease (PD) and other neurodegenerative diseases. Idiopathic RBD (iRBD) is a well-established prodromal hallmark of synucleinopathies and occurs secondary to many neurodegenerative diseases, including PD. The aim of this study is to determine whether or not retinal structures are altered with the onset of rapid eye movement (REM) sleep behavior disorders (RBD). METHODS: In all, a total of 63 patients with PD, 14 patients with idiopathic RBD, and 26 sex- and age-matched healthy controls were enrolled and underwent optical coherence tomography measurements (HD-OCT (Zeiss) ) for the average and every quadrant of RNFL thickness. The REM Sleep Behavior Disorder Screening Questionnaire (RBDSQ) was used to classify PD patients with clinically probable RBD (PD + pRBD) or without probable RBD (PD - pRBD). Patients with iRBD were identified by polysomnography. RESULTS: For patients with RBD (idiopathic or secondary to PD), we found a significant decrease in RNFL thickness compared with groups without RBD (PD - pRBD and healthy controls) (all p < 0.05). Average RNFL thickness in patients with iRBD is significantly thinner than in healthy controls (p < 0.05). In PD, the average RNFL thickness was dramatically thinner in the PD + pRBD group than the PD - pRBD group (p < 0.005). Compared with healthy controls, RNFL thickness was slightly thinner in the drug-naive PD group but not the PD group with drug treatment. Multiple linear regression analysis showed that RBDSQ score was negatively associated with average and inferior RNFL variation in PD (all p < 0.005). CONCLUSIONS: The findings show that RNFL was slightly but significantly thinner in idiopathic RBD. In PD, RNFL thickness may vary depending on the presence of RBD.

Parkinson's disease patients with pain suffer from more severe non-motor symptoms.

Non-motor symptoms, including pain, depression, sleep disorder, and olfactory dysfunction, occur frequently in patients with Parkinson's disease (PD), even before the onset of motor symptoms. Although studies have examined the correlation between pain and depression or sleep disorder in PD, few studies have investigated the correlation between pain and a range of other non-motor symptoms of PD. PD patients (n = 142) with or without pain were included in the study. PD severity was evaluated with the Unified Parkinson's Disease Rating Scale (UPDRS) and the Hoehn and Yahr (H/Y) staging scale. Pain severity was analyzed with the Visual Analog Scale. The Hamilton Rating Scale for Depression (HRSD; 24 items), Montreal Cognitive Assessment Beijing Version (MoCA), and non-motor questionnaire (NMSQT) measured symptoms of depression, cognitive function, and non-motor symptoms. The incidence of pain was 47.9% in patients with PD, most of whom had moderate pain levels. Patients with pain showed higher HRSD, UPDRS, H/Y, and NMSQT scores and lower MoCA scores compared to those of patients without pain. HRSD and NMSQT scores were closely related with pain (P < 0.001). Non-motor symptoms were more prominent in patients with pain compared to that of controls and PD patients without pain.

The Model Study of Phase-Transitional Magnetic-Driven Micromotors for Sealing Gastric Perforation via Mg-Based Micropower Traction.

Gastric perforation refers to the complete rupture of the gastric wall, leading to the extravasation of gastric contents into the thoracic cavity or peritoneum. Without timely intervention, the expulsion of gastric contents may culminate in profound discomfort, exacerbating the inflammatory process and potentially triggering perilous sepsis. In clinical practice, surgical suturing or endoscopic closure procedures are commonly employed. Magnetic-driven microswarms have also been employed for sealing gastrointestinal perforation. However, surgical intervention entails significant risk of bleeding, while endoscopic closure poses risks of inadequate closure and the need for subsequent removal of closure clips. Moreover, the efficacy of microswarms is limited as they merely adhere to the perforated area, and their sealing effect diminishes upon removal of the magnetic field. Herein, we present a Fe&Mg@Lard-Paraffin micromotor (LPM) constructed from a mixture of lard and paraffin coated with magnesium (Mg) microspheres and iron (Fe) nanospheres for sutureless sealing gastric perforations. Under the control of a rotating magnetic field, this micromotor demonstrates precise control over its movement on gastric mucosal folds and accurately targets the gastric perforation area. The phase transition induced by the high-frequency magnetothermal effect causes the micromotor composed of a mixed oil phase of lard and paraffin to change from a solid to a liquid phase. The coated Mg microspheres are subsequently exposed to the acidic gastric acid environment to produce a magnesium protonation reaction, which in turn generates hydrogen (H2) bubble recoil. Through a Mg-based micropower traction, part of the oil phase could be pushed into the gastric perforation, and it would then solidify to seal the gastric perforation area. Experimental results show that this can achieve long-term (>2 h) gastric perforation sealing. This innovative approach holds potential for improving outcomes in gastric perforation management.

Olfactory three needle regulates the proliferation of olfactory bulb neural stem cells and ameliorates brain injury after subarachnoid hemorrhage by regulating Wnt/ß-catenin signaling.

Background: Subarachnoid hemorrhage (SAH) is a serious cerebrovascular emergency. The incidence of SAH and hazard ratio of death increase with age. Objective: In this study, we aimed to observe the effects and potential mechanisms of olfactory three needle (OTN) on cognitive impairment, neuronal activity, and neural stem cell differentiation in SAH rats. Methods: Sprague-Dawley (SD) rats were randomly divided into five groups: Sham, SAH group, SAH + Nimodipine (NMP) group, and SAH + OTN group. The rats in the SAH + OTN group received the OTN electroacupuncture treatment. For treatment with recombinant DKK1 (a Wnt/ß-catenin inhibitor), mice were injected with DKK1. Results: Our results found that OTN improved cognitive impairment and hippocampal neuron damage in SAH rats. Furthermore, OTN promoted the proliferation of neural stem cells in SAH rats. Mechanistically, OTN activated Wnt/ß-catenin signaling in SAH rats, as indicated by the increased expression levels of Wnt1, ß-Catenin, LMNB1, and p-GSK-3ß. DKK1 reversed the improvement effect of OTN on cognitive impairment and neuronal damage in SAH rats. Meanwhile, DKK1 blocked the promoting effect of OTN on the proliferation of NSCs in SAH rats. Conclusions: OTN electroacupuncture may be an effective therapeutic strategy for SAH.

A N-doped carbon substrate makes the Ru-Co alloy an efficient electrocatalyst for pH-universal seawater splitting.

Designing electrocatalysts for seawater splitting remains challenging. A Ru-Co alloy supported by an N-doped carbon substrate catalyst has been designed using etching and a low-temperature treatment method. Studies show that the superior performance of this catalyst is related to the hollow-structured N-doped carbon frame and surface reconstruction of the Ru-Co alloy.

Silicon-on-insulator-based adiabatic splitter with simultaneous tapering of velocity and coupling.

We propose and experimentally demonstrate a 2×2 3 dB adiabatic splitter based on silicon-on-insulator technology, with simultaneous tapering of the phase velocity and coupling. The advantages of the proposed splitter are indicated by analyzing the effective index evolution of the system modes and comparing them with the simulated performances. The experimental results are in good agreement with the simulations. Over the 100 nm wavelength range measured, the output uniformity is better than 0.2 dB. A low and flat excess loss of about 0.3 dB per splitter is obtained, with a variation below 0.2 dB.

Application and interpretation of current autophagy inhibitors and activators.

Autophagy is the major intracellular degradation system, by which cytoplasmic materials are delivered to and degraded in the lysosome. As a quality control mechanism for cytoplasmic proteins and organelles, autophagy plays important roles in a variety of human diseases, including neurodegenerative diseases, cancer, cardiovascular disease, diabetes and infectious and inflammatory diseases. The discovery of ATG genes and the dissection of the signaling pathways involved in regulating autophagy have greatly enriched our knowledge on the occurrence and development of this lysosomal degradation pathway. In addition to its role in degradation, autophagy may also promote a type of programmed cell death that is different from apoptosis, termed type II programmed cell death. Owing to the dual roles of autophagy in cell death and the specificity of diseases, the exact mechanisms of autophagy in various diseases require more investigation. The application of autophagy inhibitors and activators will help us understand the regulation of autophagy in human diseases, and provide insight into the use of autophagy-targeted drugs. In this review, we summarize the latest research on autophagy inhibitors and activators and discuss the possibility of their application in human disease therapy.

[Clinical characteristics in Parkinson's disease patients with cognitive impairment and effects of cognitive impairment on sleep].

OBJECTIVE: To analyze the clinical characteristics, correlation factors and clinical heterogeneities in Parkinson's disease (PD) patients with cognitive impairment and identify whether cognitive impairment could influence the aspect of sleep. METHODS: A total of 130 PD outpatients and inpatients of sleep center at our hospital were eligible for participation. According to Montreal cognitive assessment (MOCA), they were divided into cognitive normal group (MOCA ≥ 26) (n = 51) and cognitive impairment group (MOCA < 26) (n = 79). Their clinical characteristics were mainly evaluated by unified Parkinson's disease rating scale (UPDRS) , Hoehn-Yahr (H-Y) stage, Hamilton depression scale (HAMD-24 item) and Epworth sleepiness scale (ESS). And all of them underwent video-polysomnography (PSG). RESULTS: The proportion of cognitive impairment (MOCA < 26) was 60.76%. Compared to those without cognitive impairment, the PD patients with cognitive impairment had significantly higher score of HAMD (10 ± 7 vs 7 ± 4), increased incidence of hallucinations (40.50% vs 19.60%) and REM behavior disorders (RBD) (63.29% vs 39.21%), significantly higher H-Y stage [2.5(2.0-3.0) vs 2.0 (2.0-2.5)] , United Kingdom Parkinson Disease Society (UPDRS) part III (22 ± 10 vs 19 ± 10) and levodopa-equivalent daily dose (LED) (511 ± 302vs 380 ± 272) (all P < 0.05). However, no significant differences existed in the subscores of MOCA between PD patients with different sides of onset and motor subtypes of onset (all P > 0.05). Non-conditional Logistic regression analysis showed that PD duration, score of HAMD and H-Y stage were the major influencing factors of cognition. On PSG, significantly decreased sleep efficiency (57% ± 21% vs 66% ± 17%), higher percentage of non-REM sleep stage 1 (NREMS1) (37% ± 21% vs 27% ± 13%), lower percentage of NREMS2 (40% ± 17% vs 46% ± 13%) and REM sleep (39% ± 28% vs 54% ± 36%) were found for PD patients with cognitive impairment (all P < 0.05). CONCLUSION: The PD patients with cognitive impairment have more severe disease and partial nonmotor symptoms. And the severity of disease and depression is closely associated with cognitive impairment. Cognitive impairment may also affect sleep to cause decreased sleep efficiency and severe sleep structure disorder.

Water activating fresh NiMo foam for enhanced urea electrolysis.

Recently, production of hydrogen (H2) through the urea oxidation reaction (UOR) and hydrogen evolution reaction (HER) has acquired great attention because it is more environmentally friendly and energy-saving. Herein, an approach of water activation was developed for in situ growth of NiMo LDH nanosheet arrays on NiMo foam without using any binder or pressurizing or heating steps. The obtained NiMo foam electrodes showed exceptional catalytic activity and durability for both the UOR and HER. This work offers a new standpoint on designing electrodes with high activation for efficient and sustainable hydrogen production coupled with urea organic oxidation.

Aspartoacylase suppresses prostate cancer progression by blocking LYN activation.

BACKGROUND: Globally, despite prostate cancer (PCa) representing second most prevalent malignancy in male, the precise molecular mechanisms implicated in its pathogenesis remain unclear. Consequently, elucidating the key molecular regulators that govern disease progression could substantially contribute to the establishment of novel therapeutic strategies, ultimately advancing the management of PCa. METHODS: A total of 49 PCa tissues and 43 adjacent normal tissues were collected from January 2017 to December 2021 at Zhongnan Hospital of Wuhan University. The advanced transcriptomic methodologies were employed to identify differentially expressed mRNAs in PCa. The expression of aspartoacylase (ASPA) in PCa was thoroughly evaluated using quantitative real-time PCR and Western blotting techniques. To elucidate the inhibitory role of ASPA in PCa cell proliferation and metastasis, a comprehensive set of in vitro and in vivo assays were conducted, including orthotopic and tumor-bearing mouse models (n = 8 for each group). A combination of experimental approaches, such as Western blotting, luciferase assays, immunoprecipitation assays, mass spectrometry, glutathione S-transferase pull-down experiments, and rescue studies, were employed to investigate the underlying molecular mechanisms of ASPA's action in PCa. The Student's t-test was employed to assess the statistical significance between two distinct groups, while one-way analysis of variance was utilized for comparisons involving more than two groups. A two-sided P value of less than 0.05 was deemed to indicate statistical significance. RESULTS: ASPA was identified as a novel inhibitor of PCa progression. The expression of ASPA was found to be significantly down-regulated in PCa tissue samples, and its decreased expression was independently associated with patients' prognosis (HR = 0.60, 95% CI 0.40-0.92, P = 0.018). Our experiments demonstrated that modulation of ASPA activity, either through gain- or loss-of-function, led to the suppression or enhancement of PCa cell proliferation, migration, and invasion, respectively. The inhibitory role of ASPA in PCa was further confirmed using orthotopic and tumor-bearing mouse models. Mechanistically, ASPA was shown to directly interact with the LYN and inhibit the phosphorylation of LYN as well as its downstream targets, JNK1/2 and C-Jun, in both PCa cells and mouse models, in an enzyme-independent manner. Importantly, the inhibition of LYN activation by bafetinib abrogated the promoting effect of ASPA knockdown on PCa progression in both in vitro and in vivo models. Moreover, we observed an inverse relationship between ASPA expression and LYN activity in clinical PCa samples, suggesting a potential regulatory role of ASPA in modulating LYN signaling. CONCLUSION: Our findings provide novel insights into the tumor-suppressive function of ASPA in PCa and highlight its potential as a prognostic biomarker and therapeutic target for the management of this malignancy.

25 Gbit/s silicon microring modulator based on misalignment-tolerant interleaved PN junctions.

A high-speed depletion-mode silicon-based microring modulator with interleaved PN junctions optimized for high modulation efficiency and large alignment tolerance is demonstrated. It is fabricated using standard 0.18 µm complementary metal-oxide-semiconductor processes and provides low V(π)L(π)s of 0.68 V·cm to 1.64 V·cm with a moderate doping concentration of 2 × 10(17) cm(-3). The measured modulation efficiency decreases by only 12.4% under ± 150 nm alignment errors. 25 Gbit/s non-return-zero modulation with a 4.5 dB extinction ratio is experimentally realized at a peak-to-peak driving voltage of 2 V, demonstrating the excellent performance of the novel doping profile.

High-speed silicon modulator based on cascaded microring resonators.

A high-speed silicon modulator based on cascaded double microring resonators is demonstrated in this paper. The proposed modulator experimentally achieved 40 Gbit/s modulation with an extinction ratio of 3.9 dB. Enhancement of the modulator achieves with an ultra-high optical bandwidth of 0.41 nm, corresponding to 51 GHz, was accomplished by using cascaded double ring structure. The described modulator can provides an ultra-high-speed optical modulation with a further improvement in electrical bandwidth of the device.