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A mid-infrared (MIR) focusing grating coupler (FGC) with a single circular arc element (CAE) in the front of the gratings based on a germanium-on-silicon (Ge-on-Si) platform is designed and demonstrated. It can be used equivalently to a traditional FGC with all-focusing gratings. By optimizing the structural parameters of the CAE, the combination of a tapered linear grating and the CAE can improve the coupling efficiency to 8.61%, which is twice as large as that of the traditional MIR grating couplers. To the best of our knowledge, it is the highest coupling efficiency in a full-etch grating coupler based on Ge-on-Si. Moreover, the proposed grating coupler can be used for refractive index (RI) sensing, and the maximum sensitivity is 980.7 nm/RIU when the RI changes from 1 to 1.04. By comparing with traditional grating couplers requiring secondary etching, the proposed full-etch grating coupler structure can reduce the complexity of fabrication and can provide a prospective platform for MIR photonic integration and photonic biosensor detection.

Accumulating evidence has demonstrated that N6-methyladenosine (m6A) plays important roles in many major diseases, including atherosclerosis (AS). In the present study, we aimed to explore the transcriptomic m6A landscape of endothelial function-associated genes and identify potential regulators in AS progression.The GEO data (GSE142386) from MeRIP-seq in human umbilical vein endothelial cells (HUVECs) with METTL3 knocked down or not were analyzed. RNA-seq was performed to identify differences in gene expression. Gene ontology (GO) functional and Kyoto encyclopedia of genes and genomes (KEGG) pathway analyses were conducted to evaluate the potential functions of the differentially expressed genes. MeRIP-qPCR was used to measure the m6A and mRNA levels of the top 8 downregulated genes, and NPC1L1 was selected as the candidate gene. Oxidized low-density lipoprotein (ox-LDL) was used to stimulate HUVECs, and METTL3 or NPC1L1 was silenced in ox-LDL-treated cells. And Transwell, ELISA, and cell apoptosis assays were performed to assess cell functional injury. ApoE-/- mice were fed with high-fat diet for 8 weeks to establish an AS model, and adenovirus-mediated NPC1L1 shRNA or NC shRNA was injected into the mice through the tail vein. Mouse aortic tissue damage and plaque deposition were evaluated by HE, Oil Red O, and TUNEL staining.One hundred and ninety-four hypermethylated m6A peaks and 222 hypomethylated peaks were detected in response to knockdown of METTL3. Genes with altered m6A peaks were significantly involved in the histone modification, enzyme activity, and formation of multiple complexes and were predominantly enriched in the MAPK pathway. NPC1L1 was a most significantly downregulated transcript in response to knockdown of METTL3. Moreover, knockdown of NPC1L1 or de-m6A (METTL3 knockdown)-mediated downregulation of NPC1L1 could improve ox-LDL-induced dysfunction of HUVECs in vitro and high-fat diet-induced atherosclerotic plaque in vivo, which was associated with the inactivation of the MAPK pathway.METTL3-mediated NPC1L1 mRNA hypermethylation facilitates AS progression by regulating the MAPK pathway, and NPC1L1 may be a novel target for the treatment of AS.

To overcome the inherent defect of centralized data processing in cloud computing, the mobile edge computing (MEC) brings data storage and computing capacities, to the edge closer to end users. However, the uneven distribution of access vehicles, as well the volume of computing data, cause the workload diversity among various mobile edge computing servers (MECSs). In this paper, we propose a hierarchical model with quality of service (QoS)-aware and power-aware resource management for the cooperative edge-computing-based intelligent vehicular network (CEC-IoV), and the system latency and energy efficiency at MECSs are respectively optimized. Specifically, considering the changing response times versus MECSs' workloads, the Minimum Latency with Migration Loads (MLML) scheme is developed for workload balance among multiple MECSs. By selecting the appropriate response time threshold and migration loads from overloading MECSs to idle MECSs simultaneously, the load-balancing problem can be efficiently solved for multiple MECSs with unbalanced workloads. On the other hand, through performing workload redistribution and dynamic reconfiguration of virtual machines (VMs) instantiated onto the parallel computing platform at one MECS, the energy-efficiency can be also optimized while guaranteeing the QoS requirement on the processing delay. With the latency constraint, the power minimization problem is formulated to be a convex one, and the semi-closed forms for optimal solutions of VMs' workloads and processing rates are provided using KKT conditions. Compared with the performance obtained by benchmark schemes, numerical results exhibit that our resource management schemes gain lower system latency and higher energy efficiency.

INTRODUCTION: Ventricular septal defect (VSD) is a mechanical complication of acute myocardial infarction (MI) with a very high mortality, despite advances in surgical and circulatory support. The tremendous hemodynamic disturbance and the severely fragile myocardium render surgical repair a great challenge. The optimal time of surgical repair with or without circulatory support is still controversial. OBJECTIVE The aim of this study is to review our experience with early surgical repair of post-MI VSD in a single major cardiac institution in China. METHODS From January 2013 to October 2020, 9consecutive patients presented to our emergency department with a diagnosis of post-MI VSD. Among them, 8 were male, and the mean age was 58 ± 7years. The mean VSD size was 22.5 ± 5.7 mm. In all patients, an intra-aortic balloon pump (IABP)was inserted immediately after admission to cardiac surgery service. All patients were operated within one week of the rupture (range of surgery time 1 to 9 days post-VSR, mean 3.3 ± 2.9 days, and 4 within 24 hours. In 5 cases, the VSD was located superiorly, and 4 cases in the posterior septum. RESULTS The overall 30-day mortality was 11% (1/9). All patients underwent urgent percutaneous coronary intervention (PCI), and 5 additional coronary artery bypass grafting (CABG) during VSD repair. There was no death in all 5 patients with anterior septal perforation. One patient with posterior septal perforation died in the operating room due to bleeding from the ventriculotomy site. Three survived patients were diagnosed witha small residual defect and mild left to right shunt post-repair. However, no further intervention was required, and patients remained asymptomatic (NYHA class II in 1 and III in 2). CONCLUSION In our experience, early surgical repair of post-MI VSD and concomitant coronary revascularization after hemodynamic stabilization and proper rescucitationcan beachieved with favorable survival and earlyoutcomes.

High-grade serous ovarian cancer (HGSOC) is an aggressive disease that is largely resistant to today's immunotherapies. Here, we aimed to investigate the prognostic significance of CTLA4, PD-1, and T-cell activation status in HGSOC.Using a publicly accessed microarray dataset including 260 HGSOC samples, we calculated Kaplan-Meier survival curves for overall survival (OS), evaluated associations with multivariate Cox regression models to evaluate the associations, and summarized using a hazard ratio (HR). The correlations between PD-1 gene expression and that of other genes were calculated by Pearson correlation.Multivariate survival analyses showed that high PD-1 expression but not CTLA4 was associated with longer OS (HR = 0.69; 95% confidence interval [CI] = 0.52-0.91; p = 0.01), and that higher T-cell activation score was associated with better outcome (HR = 0.74; 95% confidence interval [CI] = 0.58-0.95; p = 0.02). The top three PD-1 highly correlated genes were SIRPG (r = 0.90, p 2E-16), FASL (r = 0.89, p 2E-16), and CD8a (r = 0.87, p 2E-16). HGSOC patients' OS is positively associated T-cell activation score and PD-1 expression but not CTLA4.T cell activation score may serve as a candidate for personalized immunotherapy in HGSOC. The application of anti-PD-1 therapy to HGSOC should be cautious.

Unmanned aerial vehicles (UAV) are widely applied for service provisioning in many domains such as topographic mapping and traffic monitoring. These applications are complicated with huge computational resources and extremely low latency requirements. However, the moderate computational capability and limited energy restrict the local data processing for the UAV. Fortunately, this impediment may be mitigated by utilizing wireless power transfer (WPT), and employing the multi-access edge computing (MEC) paradigm for offloading demanding computational tasks from the UAV via wireless communications. Particularly, the offloaded information may become compromising by the eavesdropper (Eve) when UAVs offload the computational tasks to MEC servers. To address this issue, a UAV-MEC system (UMEC) with energy harvesting is studied, where the full-duplex protocol is considered to realize simultaneously receiving confidential data from the UAV and broadcasting the control instructions. It is worth noting that, in our proposed scheme, these control instructions also serve as the artificial interference to confuse the Eve. To improve the energy efficiency for offloading, the computational communication resource allocation is optimized to minimize the energy-consumption for UAV with the consumed and harvested energy. Specially, the worst case secrecy offloading rate and computation-latency constraint are considered, to further enhance the reliability and security of the proposed system. Since the objective optimization problem is non-convex, we convert it into a convex one by analytical means. The semi-closed form expressions of the offloading time, offloading data size and transmit power are respectively derived. Moreover, the conditions of non-offloading, partial, and full offloading are also discussed from a physical perspective. With the specific conditions of activating abovementioned three offloading options, numerical results verify the performance of our proposed offloading strategy in various scenarios, and show the superiority of our offloading strategy with existing works in terms of the offloading capacity and energy efficiency.

A Microfiber Mach-Zehnder interferometer (MMZI) based on tapered seven-core fiber (SCF) for curvature measurement has been reported and demonstrated. The tapered SCF promoted the light coupling efficiency from the single-mode fiber (SMF) to the SCF, which results in the transmission spectrum with a low loss and high extinction ratio. In the process of curvature measurement, the sensitivity can reach up to 174.02957 nm/m−1, which is the highest curvature sensitivity in the MZI with SCF as best as we have known. Furthermore, the maximum temperature sensitivity is 0.00956 nm/°C when the temperature changes from 30 °C to 140 °C. It shows that this sensor is naturally insensitive to temperature, which has a good performance in avoiding the cross-sensitivity effect between the temperature and curvature.

Cultured primary neurons are a well-established model for the study of neuronal function. Conventional stable isotope labeling with amino acids in cell culture (SILAC) requires nearly complete metabolic labeling of proteins and therefore is difficult to apply to cultured primary neurons, which do not divide in culture. In a multiplex SILAC strategy, two different sets of heavy amino acids are used for labeling cells for the different experimental conditions. This allows for straightforward SILAC quantitation using partially labeled cells because the two cell populations are always equally labeled. When combined with bioorthogonal noncanonical amino acid tagging (BONCAT), it allows for comparative proteomic analysis of de novo protein synthesis. Here we describe protocols that utilize the multiplex SILAC labeling strategy for primary cultured neurons to study steady-state and nascent proteomes.

Enterococcus faecalis is a normal commensal of the human gastrointestinal tract (GIT). However, upon disruption of gut homeostasis, this nonmotile bacterium can egress from its natural niche and spread to distal organs. While this translocation process can lead to life-threatening systemic infections, the underlying mechanisms remain largely unexplored. Our prior work showed that E. faecalis migration across diverse surfaces requires the formation of matrix-covered multicellular aggregates and the synthesis of exopolysaccharides, but how enterococcal cells are reprogrammed during this process is unknown. Whether surface penetration endows E. faecalis with adaptive advantages is also uncertain. Here, we report that surface penetration promotes the generation of a metabolically and phenotypically distinct E. faecalis population with an enhanced capacity to endure various forms of extracellular stress. Surface-invading enterococci demonstrated major ultrastructural alterations in their cell envelope characterized by increased membrane glycolipid content. These changes were accompanied by marked induction of specific transcriptional programs enhancing cell envelope biogenesis and glycolipid metabolism. Notably, the surface-invading population demonstrated superior tolerance to membrane-damaging antimicrobials, including daptomycin and β-defensins produced by epithelial cells. Genetic mutations impairing glycolipid biosynthesis sensitized E. faecalis to envelope stressors and reduced the ability of this bacterium to penetrate semisolid surfaces and translocate through human intestinal epithelial cell monolayers. Our study reveals that surface penetration induces distinct transcriptional, metabolic, and ultrastructural changes that equip E. faecalis with enhanced capacity to resist external stressors and thrive in its surrounding environment.

SUMMARYThe phosphoinositide 3-kinase, p110α, is an essential mediator of insulin signaling and glucose homeostasis. We systematically interrogated the human serine, threonine, and tyrosine kinome to search for novel regulators of p110α and found that the Hippo kinases phosphorylate and completely inhibit its activity. This inhibitory state corresponds to a conformational change of a membrane binding domain on p110α, which impairs its ability to engage membranes. In human primary hepatocytes, cancer cell lines, and rodent tissues, activation of the Hippo kinases, MST1/2, using forskolin or epinephrine is associated with phosphorylation and inhibition of p110α, impairment of downstream insulin signaling, and suppression of glycolysis and glycogen synthesis. These changes are abrogated when MST1/2 are genetically deleted or inhibited with small molecules. Our study reveals a novel inhibitory pathway of PI3K signaling and a previously unappreciated link between epinephrine and insulin signaling.

The massive connectivity and information exchange in the Internet of Things (IoT) pose great challenges to the bandwidth efficiency. To overcome this issue, this article investigates a cooperative full-duplex device-to-device system with nonorthogonal multiple access (NOMA) and partial decode-and-forward (P-DF). In the proposed system, the base station simultaneously transmits signals to all receiving nodes. Two kinds of scenes are considered depending on the locations of the users, where the cases with and without an eavesdropper are respectively studied. According to the P-DF protocol, three kinds of relay forwarding strategies are studied, where only the correctly decoded symbol will be forwarded to the user equipments to avoid performance loss. For the full-duplex relay, it is allowed to forward its own signal by superposing the partial correctly decoded symbol from the previous phase to other users, to further improve the spectral efficiency. Closed-form expressions of the ergodic sum rate, outage probability and secrecy rate are derived. Simulation results verify the analytical results especially in the high signal-to-noise ratio region, and show the superiority of our proposed P-DF-NOMA scheme in terms of outage probability performance.

A vehicular ad hoc network (VANET) is a mobile ad hoc network composed of communication between vehicles, between vehicles and roadside units, and between vehicles and pedestrians, in order to achieve traffic safety and entertainment services. The design of the routing protocol is very important for the realization of the service function of VANET. Local optimum and network congestion problems are restraints of traditional geographic routing protocols for VANET. In this paper, a software-defined network (SDN) based unicast routing scheme in an urban traffic environment is proposed, which uses Dijkstra’s algorithm to find a global optimal anchor path. The RSU neighbor discovery protocol is proposed, through which each RSU can discover its neighbor RSUs, and then each RSU periodically sends ant packets to its neighbor RSUs, evaluates the communication connection quality of each street segment according to the statistical data of the ant packets received, and sends the evaluation value to the SDN server in time. The SDN server has the connection quality evaluation values of all street segments in the global scope, from which an optimal anchor path can be calculated. The simulation results show that the proposed scheme has better packet delivery ratio than other related schemes.

The demanding computing capacity of emerging vehicular applications has emerged as a challenge in Internet of vehicles (IoVs). Multi-access edge computing (MEC) can significantly enhance computing capability and prolong battery life of vehicles through offloading computation-intensive tasks for edge computing. Considering the impact of vehicles’ mobility on communication quality, this paper provides an energy-efficient computation offloading scheme for vehicular edge computing networks (VECN). An energy-efficiency cost (EEC) minimization problem is formulated to make a tradeoff between latency and energy consumption, for completing computational tasks in an effective manner. Since that multiple variables and time-varying channel conditions make the formulated problem difficult to solve, we transform the original non-convex problem into a two-level optimization problem and develop an iterative distributed algorithm to obtain an optimal solution. Numerical results verify the convergence and superiority of the proposed algorithm.

Low-dose carbon monoxide (CO) is under investigation in clinical trials to treat non-cancerous diseases and has an excellent safety profile. Due to early detection and cancer awareness, an increasing number of cancer patients are diagnosed at early stages, when potentially curative surgical resection can be done. However, many patients ultimately experience recurrence. Here, we evaluate the therapeutic effect of CO on metastatic cancer progression. We show that 250 ppm CO inhibits the migration of multiple types of cancer cell lines, including breast, pancreatic, colon, prostate, liver, and lung cancer and reduces the ability to adhere to fibronectin. We demonstrate that in mouse models, 250 ppm inhaled CO inhibits lung metastasis of breast cancer and liver metastasis of pancreatic cancer. Moreover, low-dose CO suppresses recurrence and increases survival after surgical removal of primary pancreatic cancer in mice. Mechanistically, low-dose CO blocks transcription of heme importers, leading to diminished intracellular heme levels and a heme-regulated enzyme, cytochrome P4501B1 (CYP1B1). Either supplementing heme or overexpressing CYP1B1 reverses the anti-migration effect of low-dose CO. Taken together, low-dose CO therapy inhibits cell migration, reduces adhesion to fibronectin, prevents disseminated cancer cells from expanding into gross metastases, and improves survival in pre-clinical mouse models of metastasis.

With the evolution of the technologies for IoV to be intelligent and interconnected, V2X communication technology serves as a core technology for information interaction among intelligent connected vehicles, and an important technology to realize environment sensing for future autonomous driving. In order to provide wireless communication services with ultra-low delay, ultra-high reliability and ultra-large bandwidth, this article proposes architectures of 5G-V2X communication networks by exploiting the technologies of 5G new radio (NR), network slicing, and deviceto- device communications. We discuss their principles and key features, and foresee the challenges, opportunities, and future research trends. The applications of related technologies of the software defined network (SND) and multi-access edge computing (MEC) are also introduced. Finally, the technologies of information security and privacy protection are identified to support the diverse services and applications in the future 5G-V2X networks.

In this paper, a partial de-code-and-forward (P-DF) cooperative relaying network (CRN) with non-orthogonal multiple access (P-DF-CRN-NOMA) for maritime space communications is proposed. Without loss of generality, three kinds of relay forwarding protocols are studied to characterize the superiority of the proposed P-DF-CRN-NOMA scheme, where, after receptions from the coastal base station (BS), the island relay forwards the successful decoded symbols to the ship user to avoid the performance loss provided by the high decoding requirement in decode-and-forward (DF). To further improve the system performance, as well as for a fairness comparison, the maximum ratio combining (MRC) is utilized at the ship user. Specifically, to present the impact of the channel qualities, the scenarios of the weak and strong links that from the source to destination (S-D) are both considered. The closed-form expressions for the outage probability of the P-DF-CRN-NOMA are derived considering the three proposed forwarding cases. Qualitative numerical results corroborating our theoretical analysis, especially for the high signal-to-noise ratio (SNR), show that the proposed P-DF-CRN-NOMA scheme significantly improves the outage probability performance in comparison to the conventional CRN-NOMA schemes. Furthermore, for an increased S-D link, the corresponding outage probability performance will be also better for all the cases.

Three thiadiazole derivatives with different substituent groups, 2-(benzylthio)-5-methyl-1,3,4-thiadiazole(BMT), 2-(benzylthio)-5-(butylthio)-1,3,4-thiadiazole(BBT), and 5-(benzylthio)-1,3,4-thiadiazole-2-thiol(BTT), were synthesized and studied as the corrosion inhibitors for N80 carbon steel in CO2-saturated oilfield produced water. It is found that the synthesized thiadiazole derivatives could effectively inhibit the corrosion of N80 carbon steel by chemisorption. The corrosion inhibition performance of the organic compounds is in the order: BTT > BBT > BMT. The theoretical calculations indicate that the tautomeric transformation from thiol-BTT to thione-BTT may be responsible for the high inhibition performance of BTT.

Dihydronicotinamide riboside (NRH) has been suggested to act as a precursor for the synthesis of NAD+, but the biochemical pathway converting it has been unknown. Here, we show that NRH can be converted into NAD+ via a salvage pathway in which adenosine kinase (ADK, also known as AK) acts as an NRH kinase. Using isotope-labelling approaches, we demonstrate that NRH is fully incorporated into NAD+, with NMNH acting as an intermediate. We further show that AK is enriched in fractions from cell lysates with NRH kinase activity, and that AK can convert NRH into NAD+. In cultured cells and mouse liver, pharmacological or genetic inhibition of AK blocks formation of reduced nicotinamide mononucleotide (NMNH) and inhibits NRH-stimulated NAD+ biosynthesis. Finally, we confirm the presence of endogenous NRH in the liver with metabolomics. Our findings establish NRH as a natural precursor of NAD+ and reveal a new route for NAD+ biosynthesis via an NRH salvage pathway involving AK.

Background Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers, especially in China. Its 5-year survival rate remains very low. Lysosomal associated membrane proteins (LAMPs), including LAMP1 and LAMP2, are major protein components of the lysosome, which also plays an important role in tumor evolution. Our previous studies have confirmed that LAMP1 and LAMP2 play an important role in the evolution and prognosis of ESCC. To further explore their roles in ESCC, we compared the roles of LAMP1 and LAMP2 in predicting the prognosis of ESCC. Methods Five hundred and seventy-nine ESCC patients were enrolled in this study. The clinical information, address and telephone number of patients were collected from the medical records. Results The 3-year survival rate was 51.91% (231/445), and 5-year survival rate was 34.58% (83/240). Kaplan-Meier survival curves indicated that the higher the expression level of LAMP1, the worse the prognosis of patients, compared with LAMP2 (P

As an important part of future 5G wireless networks, a vehicular network demands safety, reliability and connectivity. In this context, networking survivability is usually considered an important metric to evaluate network performance. In this paper, we propose a survivability model for vehicle communication networking based on dual cluster heads, wherein a backup cluster head (CH) will be activated if the primary CH fails, thereby effectively enhancing the network lifetime. Additionally, we introduce a software rejuvenation strategy for the prime CH to further improve the survivability of the entire network. Using the Probabilistic Symbolic Model Checker (PRISM), we verify and discuss the proposed survivability model via numerical simulations. The results show that network survivability can be effectively improved by introducing an additional CH and further enhanced by adopting the software rejuvenation technique.

In this paper, a cooperative, non-orthogonal multiple access (NOMA)-based internet of vehicles (IoV) network is proposed, which is assisted by a reconfigurable intelligent surface (RIS) to enhance signal transmission. Due to the intelligent control of RISs, the channel condition of our proposed IoV system is more diversified compared to conventional NOMA–RIS schemes, and thus two power allocation schemes are considered to tackle this issue, providing better channel gain to transmit signals. In this proposed scheme, power allocation schemes are discussed for a diverse number of reflecting elements, and a number of elements are obtained serving users near or far. To further improve system capacity and guarantee quality of service (QoS), we derive the number of elements to guarantee the same transmission data sum-rate under different channel qualities. Numerical and simulation results verify the correctness as well as superiority of our proposed scheme.

Objective Casein kinase 2 a1 (CSNK2A1) has been shown to be involved in tumorigenesis by enhancing several oncogenic signaling pathways in various cancers. However, the function and mechanism of CSNK2A1 in gastric cancer remain unclear, and this study aimed to elucidate the role of CSNK2A1 in gastric cancer. Methods CSNK2A1 expression was assessed by Western blot and qPCR in four gastric cancer (GC) cell lines and one normal gastric epithelial cell line. Stable cancer cell lines with CSNK2A1 gene overexpression or knockdown were established to investigate the function and mechanism of CSNK2A1 in GC cells. Results CSNK2A1 expression was higher in GC cells than in normal gastric epithelial cells. Stable overexpression of CSNK2A1 in SNU216 cells significantly increased cellular proliferation, invasion, and migration. Silencing CSNK2A1 expression in SGC-790 cells effectively inhibited its oncogenic function. We further verified that epithelial-mesenchymal transition (EMT) was affected by CSNK2A1 and that CSNK2A1 promotes GC cell invasion through the PI3K-Akt-mTOR signaling pathway. Conclusion Our findings suggested that CSNK2A1 plays important oncogenic roles in GC invasion via EMT and the PI3K-Akt-mTOR signaling pathway and that CSNK2A1 may serve as a novel prognostic and/or therapeutic target in GC.

Aurora kinase A (AURKA) has emerged as a drug target for glioblastoma (GBM). However, resistance to therapy remains a critical issue. By integration of transcriptome, chromatin immunoprecipitation sequencing (CHIP-seq), Assay for Transposase-Accessible Chromatin sequencing (ATAC-seq), proteomic and metabolite screening followed by carbon tracing and extracellular flux analyses we show that genetic and pharmacological AURKA inhibition elicits metabolic reprogramming mediated by inhibition of MYC targets and concomitant activation of Peroxisome Proliferator Activated Receptor Alpha (PPARA) signaling. While glycolysis is suppressed by AURKA inhibition, we note an increase in the oxygen consumption rate fueled by enhanced fatty acid oxidation (FAO), which was accompanied by an increase of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α). Combining AURKA inhibitors with inhibitors of FAO extends overall survival in orthotopic GBM PDX models. Taken together, these data suggest that simultaneous targeting of oxidative metabolism and AURKAi might be a potential novel therapy against recalcitrant malignancies., Glioblastoma patients are treated with Aurora kinase A (AURKA) inhibitors but resistance can occur. Here, the authors show that AURKA inhibition induces metabolic reprogramming, which leads to increased mitochondrial activity and inhibition of oxidative metabolism sensitizes glioblastoma cells to AURKA inhibition.

A tunable triple dissipative solitons (DSs) mode-locked laser without a spectral filter in the all-normal dispersion (ANDi) system is reported and demonstrated. The nonlinear polarization evolution (NPE) acted as an artificial bandwidth filter for formatting the pulses with multiple DSs hysteresis phenomenon and adjusting the output wavelength with tuning. The spectral range can be adjusted from 1036.24 to 1043.44 nm, and the temporal distances between adjacent pulses are all equal to 33.9 ns. With the pump power of 560 mW, the highest output energy of the triple DSs is 48.8 nJ at a repetition rate of 2.541 MHz. Besides, the mode-locking states were stabilized during the wavelength tuning process.