Efficient synchronous retrieval of OAM modes and AT strength using multi-task neural networks.

Encoding information using OAM beams as carriers greatly alleviates the capacity crisis in communication systems. When transmitted through the atmospheric channel, OAM beams are influenced by the random fluctuations in the refractive index caused by atmospheric turbulence, resulting in phase distortion and intensity dispersion of the beams, leading to severe signal interference. Due to the high randomness of atmospheric turbulence, it is essential for OAM mode recognition methods to have good stability to ensure communication quality. We establish an equivalence relationship between the continuous dynamics system and the network unit RUEM, ensuring its stability through theoretical derivation and numerical experiments. We propose a multitask neural network model, OATNN, embedded with RUEM to achieve efficient simultaneous recognition of turbulence intensity in atmospheric turbulence environments and OAM modes in free-space optical communication systems. Numerical experimental results show that under four turbulence intensity levels, the network achieves a recognition accuracy of 99.37%, and for ten modes, the recognition accuracy is 99.05%. Additionally, we explore the performance of this network in a 2000m channel transmission scenario.

Molecular Engineering of Plasma Membrane and Mitochondria Dual-Targeted NIR-II AIE Photosensitizer Evoking Synergetic Pyroptosis and Apoptosis.

Phototherapy provides a noninvasive and spatiotemporal controllable paradigm to inhibit the evasion of the programmed cell death (PCD) of tumors. However, conventional photosensitizers (PSs) often induce a single PCD process, resulting in insufficient photodamage and severely impeding their application scopes. In this study, molecular engineering is conducted by adjusting electron donors to develop an aggregation-induced NIR-II emissive PS (DPITQ) for plasma membrane and mitochondria dual-targeted tumor therapy by evoking synergetic pyroptosis and apoptosis. DPITQ displays boosted type I and II reactive oxygen species generation as well as a high photothermal conversion efficacy (43%) after laser irradiation of 635 nm. The excellent biocompatibility and appropriate lipophilicity help the DPITQ to specifically anchor in the plasma membrane and mitochondria of cancer cells. Furthermore, the photosensitized DPITQ can disrupt the intact plasma membrane and cause mitochondrial dysfunction, ultimately causing concurrent pyroptosis and apoptosis to suppress cancer cell proliferation even under hypoxia. It is noteworthy that the DPITQ nanoparticles (NPs) present clear NIR-II fluorescence imaging capability on the venous vessels of nude mice. Notably, the DPITQ NPs exert efficient NIR-II fluorescence imaging-guided phototherapy both in multicellular tumor spheroids and in vivo, causing maximum destruction to tumors but minimum adverse effects to normal tissue.

Efficient NIR-II Type-I AIE Photosensitizer for Mitochondria-Targeted Photodynamic Therapy through Synergistic Apoptosis-Ferroptosis.

Hypoxia, the hallmark of malignant tumors, has been recognized as a major obstacle for photodynamic therapy (PDT). Precisely targeting cancer cells in intricate biological scenarios by a hypoxia-resistant photosensitizer (PS) is the cornerstone to conquer the inevitable tumor recurrence and metastasis. Herein, we describe an organic NIR-II PS (TPEQM-DMA) possessing potent type-I phototherapeutic efficacy to overcome the intrinsic pitfalls of PDT in combating hypoxic tumors. TPEQM-DMA exhibited prominent NIR-II emission (>1000 nm) with an aggregation-induced emission feature and efficiently produced superoxide anion and hydroxyl radical in the aggregate state under white light irradiation exclusively through a low-O2-dependent type-I photochemical process. The suitable cationic nature assisted TPEQM-DMA to accumulate in cancerous mitochondria. Meanwhile, the PDT of TPEQM-DMA impaired the cellular redox homeostasis, led to the mitochondrial dysfunction, and raised the level of lethal peroxidized lipids, which induced cellular apoptosis and ferroptosis. This synergistic cell death modality enabled TPEQM-DMA to suppress the growth of cancer cells, multicellular tumor spheroids, and tumors. To improve the pharmacological properties of TPEQM-DMA, TPEQM-DMA nanoparticles were prepared by encapsulation of polymer. In vivo experiments proved the appealing NIR-II fluorescence imaging-guided PDT effect of TPEQM-DMA nanoparticles for tumors.

High-Performance Near-Infrared Aggregation-Induced Emission Luminogen with Mitophagy Regulating Capability for Multimodal Cancer Theranostics.

The construction of intelligent near-infrared (NIR) fluorophores for high specificity to cancer cells and application in multiple therapeutic modalities is crucial for precise cancer diagnostic and therapy. In this study, an aggregation-induced emission-active NIR fluorophore (TACQ) with mitophagy-modulating activity was synthesized and developed for mitochondrial targeting multimodal cancer theranostics. The strengthened push-pull interaction extended the emission of TACQ into the NIR-II region (>1000 nm). Further, the rotor structure and twisted molecular conformation enables nanoaggregates of TACQ to balance the radiative and nonradiative decays to simultaneously exhibit bright NIR emission, high photothermal conversion efficiency (55%), and efficient generation of reactive oxygen species. The lipocationic property of TACQ allows it to selectively accumulate in the mitochondria of cancer cells. TACQ can induce mitophagy and block mitophagic flux facilitating cancer cell apoptosis. Both in vitro and in vivo evaluations revealed that TACQ is an efficient theranostic agent for NIR fluorescence and photothermal imaging-guided synergistic chemo-photothermal and photodynamic therapy.

The application of individualized abutment-crown integrated provisional restoration in optimizing the peri-implant soft tissue contour in the esthetic zone.

OBJECTIVE: This article introduced a modified method to fabricate an individualized abutment-crown integrated provisional restoration for single-tooth implant restoration in the esthetic zone, which created a satisfactory peri-implant soft tissue architecture. CLINICAL CONSIDERATIONS: Three months after the implant placement, the individualized abutment-crown integrated provisional restoration was designed and fabricated in the laboratory, by referring to the profile of natural contra-lateral tooth digitally, and seated on the implant afterwards. The peri-implant soft tissue architecture was evaluated and the Pink Esthetic Score (PES) was recorded. The provisional restoration stayed on the implant for 3 months until the individualized definitive ceramic abutment and crown were fixed on the implant. CONCLUSIONS: This protocol provided an alternative solution for shaping the peri-implant soft tissue morphology in the esthetic zone by using an individualized abutment-crown integrated provisional restoration and showed promising effect on the esthetics of anterior single-tooth implant restoration. CLINICAL SIGNIFICANCE: The individualized abutment-crown integrated provisional restoration whose emergence profile mirroring that of the natural contra-lateral tooth, was designed with the help of computer-aided design-manufacture (CAD/CAM). It may help shaping the peri-implant soft tissue in the esthetic zone with merits of saving amount of hand labor of technicians as well as clinicians, and reducing the visits of patients.

Suppressing ROS generation by apocynin inhibited cyclic stretch-induced inflammatory reaction in HPDLCs via a caspase-1 dependent pathway.

It has been reported that cyclic stretch could induce inflammatory reaction in human periodontal ligament cells (HPDLCs). Though reactive oxygen species (ROS) has been reported to be involved in pathogen-induced periodontal inflammatory reaction, its role in the force-related periodontal diseases has not been well clarified. This study inspected the role of ROS in the cyclic stretch-induced inflammatory reaction in HPDLCs and studied the inhibitory effect of antioxidant apocynin on this inflammatory reaction. Results confirmed that cyclic stretch induced inflammatory reaction and production of ROS in HPDLCs. This inflammatory reaction was inhibited by apocynin through blocking the production of ROS. The cyclic stretch also induced the expression of caspase-1 and NLRP3 inflammasome, which could also be inhibited by apocynin. Moreover, the cyclic stretch-induced inflammatory reaction was inhibited by caspase-1 inhibitor. Collectively, it is the first time that increased intracellular ROS was proved to play as an intermediate signal in the cyclic stretch-induced inflammatory reaction in HPDLCs, via a caspase-1-dependent pathway. The inhibitory effect of apocynin on the cyclic stretch-induced inflammatory reaction in HPDLCs shows the potential of antioxidants in the treatment of force-related periodontal inflammatory diseases.

Efficient photosensitizers with aggregation-induced emission characteristics for lysosome- and Gram-positive bacteria-targeted photodynamic therapy.

Two efficient photosensitizers (PSs) with aggregation-induced emission characteristics were designed and synthesized for specific lysosome-targeted photodynamic therapy (PDT). Both PSs efficiently discriminated Gram-positive bacteria from Gram-negative bacteria and killed Gram-positive bacteria through the PDT effect.

Controllable Coumarin-Based NIR Fluorophores: Selective Subcellular Imaging, Cell Membrane Potential Indication, and Enhanced Photodynamic Therapy.

Fluorescent materials with advanced functionalities provide powerful tools to visualize subcellular microstructures and monitor subcellular dynamic functions, which significantly boost our understanding of complex biological phenomena and manipulation of biological behaviors. However, realization of diverse biological applications from a single molecular backbone is still a challenging endeavor. In this contribution, a series of coumarin-based cationic fluorophores (Cou-n, n = 1-4) with near-infrared emission (675 nm) and large Stokes shifts (110 nm) have been developed. Considering their excellent biocompatibilities and alkyl chain-dependent lipophilicities, Cou-1 and Cou-3 could selectively and ultrafast (<30 s) stain the cell plasma membrane and mitochondria in a washing-free manner, respectively. Meanwhile, Cou-1 could sensitively respond to the change of the plasma membrane potential, which enabled Cou-1 to successfully indicate the cell passage number. Taking advantage of specific mitochondria targeting as well as efficient singlet oxygen generation, Cou-3 exhibited enhanced photodynamic therapy (PDT) effect for tumor inhibition in vivo. In addition, the suitable lipophilicity of Cou-3 aided it in selectively imaging Gram-positive bacteria and efficiently killing bacteria by the PDT process.

Aggregation-Induced Emission Luminogens with the Capability of Wide Color Tuning, Mitochondrial and Bacterial Imaging, and Photodynamic Anticancer and Antibacterial Therapy.

Recently, luminogens with the aggregation-induced emission characteristic (AIEgens) have received much attention in the field of bioimaging and therapeutic applications. However, the development of AIEgens that are derived from the simple core skeleton with emission color tuning for imaging and therapy is still a formidable challenge. To address this constraint, we present a series of cationic AIEgens based on cyanopyridinium salts (CP1-CP5). The AIEgens can be facilely prepared by varying the aromatic electron donor while fixing the cyanopyridinium group as the electron acceptor within a single benzene ring. The obtained AIEgens possess wide color tunability, large Stokes shifts, and bright emission in the condensed state. Due to their good biocompatibility and cationic nature, these AIEgens can be utilized for multiple-color imaging of intracellular mitochondria as well as Gram-negative and Gram-positive bacteria. Importantly, these AIEgens exhibit remarkable structure-dependent singlet-oxygen generation ability under white light illumination (25 mW cm-2), and CP4 was optimized to serve as an excellent photosensitizer for photodynamic anticancer and antibacterial therapy.

Interaction between caspase-3 and caspase-5 in the stretch-induced programmed cell death in the human periodontal ligament cells.

In our previous studies, programmed cell death (PCD) was induced in human periodontal ligament (PDL) cells, through activation of caspase-3 and upregulation of CASP5 gene (encoding caspase-5 protein), in response to mechanical stretch loading. The aim of this study is to explore the relationship between the inflammatory caspase, caspase-5, and the apoptotic executioner protein, caspase-3, in human PDL cells. Here, we found that cyclic stretching upregulated the activity and the protein expression level of caspase-3 and -5 and the addition of the caspase-3 inhibitor or caspase-5 inhibitor significantly inhibited the stretch-induced PCD. Meanwhile, the inhibition of caspase-5 inhibited the activation of caspase-3 and vice versa. The result of coimmunoprecipitation also demonstrated that the expression of caspase-3 was immunoprecipitated with caspase-5. Thus, our study revealed that the in vitro application of cyclic stretching induced PCD by activation of caspase-3 and -5 in human PDL cells, and these two caspases could interact with each other after mechanical stretch loading. The study may facilitate further studies on the mechanism of stretch-induced PCD and help us understand the force-related periodontal homeostasis and remodeling better.

Gasdermin-d Played a Critical Role in the Cyclic Stretch-Induced Inflammatory Reaction in Human Periodontal Ligament Cells.

It has been shown that cyclic stretch could induce inflammatory response such as pyroptosis and the release of IL-1ß in human periodontal ligament cells, through activating inflammasome and related caspases. Though gasdermin-d (GSDMD) has been reported to be present in some inflammatory diseases and function as a crucial executioner of pyroptosis, the role of GSDMD in the stretch-induced inflammatory response in human periodontal ligament cells (HPDLCs) has not been well clarified. In this study, it was found that GSDMD was activated by cyclic stretch, and its activation affected the pyroptotic rate in HPDLCs, leading to the maturation and secretion of IL-1ß and IL-18 ultimately. In addition, GSDMD was found to be regulated by caspase-1 directly. Nevertheless, the exact relationship between inflammasomes and GSDMD in the stretch-induced inflammatory response still needs to be further elucidated.

Evaluation of Outcomes of Dental Implants Inserted by Flapless or Flapped Procedure: A Meta-Analysis.

PURPOSE: The purpose of this meta-analysis was to evaluate the failure risk and marginal bone loss of dental implants inserted by flapless or flapped procedure. MATERIALS AND METHODS: Studies were identified by searching PubMed, Web of Knowledge, and the Cochrane Library within 10 years, along with a hand search of the reference lists of the retrieved articles. RESULTS: A total of 2717 articles were filtered after the searching strategy, and 31 studies were finally selected. Failure rate of dental implants was statistically affected by different insertion procedures (flapless or flapped) with a risk ratio (RR) of 1.70 (95% confidence interval [CI]: 1.13-2.55; P = 0.01; heterogeneity: I = 0.0%; P heterogeneity = 0.97). Subgroup analysis indicated that in the situation of immediate/early loading, the flapless procedure showed a higher risk of implant failure comparing with flapped procedure (RR = 2.24; 95% CI: 1.05-4.78; P = 0.04; heterogeneity: I = 0.0%; P heterogeneity = 0.91). Mean difference of marginal bone loss between the flapless group and the flapped group was -0.10 mm (95% CI: -0.18 to -0.02; P = 0.02; heterogeneity: I = 82%; P heterogeneity = 0.00). CONCLUSIONS: This meta-analysis revealed that flapless procedure may increase the failure risk of the dental implants, especially in the situation of immediate/early loading. Nevertheless, flapless procedure showed a superiority in preserving bone tissues.

Cyclic stretch-induced the cytoskeleton rearrangement and gene expression of cytoskeletal regulators in human periodontal ligament cells.

OBJECTIVE: This study aimed to explore the mechanism of the stretch-induced cell realignment and cytoskeletal rearrangement by identifying several mechanoresponsive genes related to cytoskeletal regulators in human PDL cells. MATERIAL AND METHODS: After the cells were stretched by 1, 10 and 20% strains for 0.5, 1, 2, 4, 6, 12 or 24 h, the changes of the morphology and content of microfilaments were recorded and calculated. Meanwhile, the expression of 84 key genes encoding cytoskeletal regulators after 6 and 24 h stretches with 20% strain was detected by using real-time PCR array. Western blot was applied to identify the protein expression level of several cytoskeletal regulators encoded by these differentially expressed genes. RESULTS: The confocal fluorescent staining results confirmed that stretch-induced realignment of cells and rearrangement of microfilaments. Among the 84 genes screened, one gene was up-regulated while two genes were down-regulated after 6 h stretch. Meanwhile, three genes were up-regulated while two genes were down-regulated after 24 h stretch. These genes displaying differential expression included genes regulating polymerization/depolymerization of microfilaments (CDC42EP2, FNBP1L, NCK2, PIKFYVE, WASL), polymerization/depolymerization of microtubules (STMN1), interacting between microfilaments and microtubules (MACF1), as well as a phosphatase (PPP1R12B). Among the proteins encoded by these genes, the protein expression level of Cdc42 effector protein-2 (encoded by CDC42EP2) and Stathmin-1 (encoded by STMN1) was down-regulated, while the protein expression level of N-WASP (encoded by WASL) was up-regulated. CONCLUSION: The present study confirmed the cyclic stretch-induced cellular realignment and rearrangement of microfilaments in the human PDL cells and indicated several force-sensitive genes with regard to cytoskeletal regulators.

Caspase-8 and Caspase-9 Functioned Differently at Different Stages of the Cyclic Stretch-Induced Apoptosis in Human Periodontal Ligament Cells.

BACKGROUND: Human periodontal ligament (PDL) cells underwent apoptosis after mechanical stretch loading. However, the exact signalling pathway remains unknown. This study aimed to elucidate how the apoptotic caspases functioned in the cyclic stretch-induced apoptosis in human PDL cells. MATERIALS AND METHODS: In the present study, 20% cyclic stretch was selected to load the cells for 6 or 24 h. The following parameters were analyzed: apoptotic rates, the protein levels of caspase-3, -7, -8 and -9 and the activities of caspase-8 and -9. Subsequently, the influences of caspase-8 and caspase-9 inhibitors on the apoptotic rate and the protein level of the activated caspase-3 were assessed as well. RESULTS: The apoptotic rates increased in response to cyclic stretch, but the cells entered different apoptotic stages after 6 and 24 h stretches. Caspase-3, -7, -8 and -9 were all activated after stretch loading. The stretch-induced apoptosis and the protein level of the activated caspase-3 were inhibited after inhibiting both caspase-8 and caspase-9 in both 6 and 24 h stretched cells and after inhibiting caspase-9 in 24 h stretched cells. CONCLUSION: Caspase-8 and -9 functioned differently at different apoptotic stages in human PDL cells after cyclic stretch.

Activation of NLRP1 and NLRP3 inflammasomes contributed to cyclic stretch-induced pyroptosis and release of IL-1ß in human periodontal ligament cells.

Inflammasomes have been reported to be present in periodontal inflammatory tissue, but the exact role of inflammasomes in periodontal inflammatory reactions especially those related to mechanical stimulations has not been clarified. In this study, it was shown that cyclic stretch activated the nucleotide-binding oligomerization domain-like receptor containing pyrin domain 1 and 3 (NLRP1 and NLRP3) inflammasomes and induced the release of IL-1ß and pyroptosis via a caspase-1-related mechanism in human periodontal ligament cells (HPDLCs). This study firstly demonstrated that activation of NLRP inflammasomes contributed to the stretch-induced inflammatory response in HPDLCs. As inflammasomes have been reported to be involved in both programmed cell death and inflammation, further studies are required to elucidate the exact roles and signaling pathway of inflammasomes in stretch-induced periodontal inflammation.