RESUMEN

Recovery and reuse of bulk waste wood are particularly challenging because of usage defects and contaminations. Here, we present a robust and efficient strategy for regenerating used wood veneers into high-performance structural materials through micro/nano interface manipulation. Our approach involves using cellulose-based interlayers to bind together two waste wood plates without an external adhesive by partially dissolving and regenerating the interlayer using a solution of ionic liquids and dimethyl sulfoxide. The mechanical properties of the regenerated wood exceed that of natural wood, displaying over a 16 and 20 times increase in transverse tensile strength and modulus, respectively, and 4-6 times improvement in longitudinal tensile strength and modulus. Nanoscale mechanical analyses show that the improvement is possible as a result of several factors, including the robust network structure of the interlayer, the good adhesion at the wood-interlayer interface, the compacted wood structure, and the low stiffness and deformation gradients between the interlayer and the wood structure. The interlayers can be created from waste papers and wood particles by taking advantage of the nanofibrillar structure of cellulose.

RESUMEN

OBJECTIVE: To investigate the role of high-mobility group AT-hook 2 (HMGA2) in osteogenic differentiation of adipose-derived mesenchymal stem cells (ADSCs) and the effect of Hmga2 knockdown for promoting bone defect repair. METHODS: Bioinformatics studies using the GEO database and Rstudio software identified HMGA2 as a key factor in adipogenic-osteogenic differentiation balance of ADSCs. The protein-protein interaction network of HMGA2 in osteogenic differentiation was mapped using String and visualized with Cytoscape to predict the downstream targets of HMGA2. Primary mouse ADSCs (mADSCs) were transfected with Hmga2 siRNA, and the changes in osteogenic differentiation of the cells were evaluated using alkaline phosphatase staining and Alizarin red S staining. The expressions of osteogenic markers Runt-related transcription factor 2 (RUNX2), osteopontin (OPN), and osteocalcein (OCN) in the transfected cells were detected using RT-qPCR and Western blotting. In a mouse model of critical-sized calvarial defects, mADSCs with Hmga2-knockdown were transplanted into the defect, and bone repair was evaluated 6 weeks later using micro-CT scanning and histological staining. RESULTS: GEO database analysis showed that HMGA2 expression was upregulated during adipogenic differentiation of ADSCs. Protein-protein interaction network analysis suggested that the potential HMGA2 targets in osteogenic differentiation of ADSCs included SMAD7, CDH1, CDH2, SNAI1, SMAD9, IGF2BP3, and ALDH1A1. In mADSCs, Hmga2 knockdown significantly upregulated the expressions of RUNX2, OPN, and OCN and increased cellular alkaline phosphatase activity and calcium deposition. In a critical-sized calvarial defect model, transplantation of mADSCs with Hmga2 knockdown significantly promoted new bone formation. CONCLUSION: HMGA2 is a crucial regulator of osteogenic differentiation in ADSCs, and Hmga2 knockdown significantly promotes osteogenic differentiation of ADSCs and accelerates ADSCs-mediated bone defect repair in mice.

Asunto(s)

RESUMEN

Structural imperfections can cause both beneficial and detrimental consequences on the excitonic characteristics of transition metal dichalcogenides (TMDs). Regarding valley selection, structural defects typically promote valley depolarization in monolayer TMDs, but defect healing via an additional growth process can restore valley polarization in vertical heterobilayers (VHs). In this study, we analyzed the valley polarization of center-nucleated and edge-nucleated VHs (WS2/MoS2) grown using a controlled growth process and discovered that defect-related photoluminescence (PL) is strongly suppressed in the center-nucleated VHs due to defect healing. Additionally, we demonstrated that the valley polarization of lower-lying intralayer excitons is more sensitive to the defect density of the sample than to higher-lying intralayer excitons. Despite defect healing in the center-nucleated VHs, the temperature-dependent PL study indicated that valley depolarization of the lower-lying intralayer excitons becomes significant below 100 K because of stronger hybridization of defect states. Also, we conducted a comprehensive study on the excitation intensity dependence to investigate the electron-doping-induced Auger recombination mechanism, which also contributes to valley depolarization of intralayer excitons via regeneration of intervalley trions. Our findings provide valuable insight into the development of VH-based valleytronic devices.

RESUMEN

Proteasome activator subunit 3 (PA28γ) is a member of the proteasome activator family, which mainly regulates the degradation and stability of proteins. Studies have shown that it plays crucial roles in lipid formation, stemness maintenance, and blood vessel formation. However, few studies have clarified the association between PA28γ and bone diseases. Herein, we identified PA28γ as a previously unknown regulator of bone homeostasis that coordinates bone formation and lipid accumulation. PA28γ-knockout mice presented with the characteristics of low bone mass and accumulation of lipids. Suppressed expression of PA28γ restrained the osteogenic differentiation and enhanced the adipogenic differentiation of bone marrow stromal cells (BMSCs). Overexpression of PA28γ promoted osteogenic differentiation and inhibited adipogenic differentiation of BMSCs. Mechanistically, PA28γ interacted with Wnt5α, and the two interactors appeared to be positively correlated. PA28γ mainly activated the downstream Wnt/ß-catenin signaling pathway, which affects BMSCs differentiation homeostasis. Deletion of Wnt5α significantly delayed the promotion of osteogenic differentiation and partially alleviated the inhibitory effect of adipogenic differentiation of BMSCs in the PA28γ-overexpressing group. Furthermore, we demonstrated that PA28γ-knockout mice had an inhibited rate of bone healing in a drill-hole femoral bone defect model in vivo. Therefore, our results confirm the effects of PA28γ on bone formation and bone defect repair, indicating that PA28γ mainly interacts with Wnt5α to activate the Wnt/ß-catenin signaling pathway regulating BMSCs differentiation homeostasis. Our results reveal the function of PA28γ in bone diseases and provide a new theoretical basis for expanding the treatment of bone diseases.

Asunto(s)

RESUMEN

Perovskite quantum dots (PQDs) have emerged as one of the most promising candidates for next-generation solar cells owing to its remarkable optoelectronic properties and solution processability. However, the optoelectronic properties of PQDs suffer from severe degradation in storage due to the dynamically binding ligands, predominantly affecting photovoltaic applications. Herein, an in situ defect healing treatment (DHT) is reported to effectively rejuvenate aged PQDs. Systematically, experimental studies and theoretical calculations are performed to fundamentally understand the causes leading to the recovered optoelectronic properties of aged PQDs. The results reveal that the I3 - anions produced from tetra-n-octylammonium iodide and iodine could strongly anchor on the surface matrix defects of aged PQDs, substantially diminishing the nonradiative recombination of photogenerated charge carriers. Meanwhile, an DHT could also renovate the morphology of aged PQDs and thus improve the stacking orientation of PQD solids, substantially ameliorating charge carrier transport within PQD solids. Consequently, by using a DHT, the PQD solar cell (PQDSC) yields a high efficiency of up to 15.88%, which is comparable with the PQDSCs fabricated using fresh PQDs. Meanwhile, the stability of PQDSCs fabricated using the rejuvenated PQDs is also largely improved.

RESUMEN

The development of patient-specific bone scaffolds that can expedite bone regeneration has been gaining increased attention, especially for critical-sized bone defects or fractures. Precise adaptation of the scaffold to the region of implantation and reduced surgery times are also crucial at clinical scales. To this end, bioactive fluorcanasite glass-ceramic microparticulates were incorporated within a biocompatible photocurable resin matrix following which the biocomposite resin precursor was 3D-printed with digital light processing method to develop the bone scaffold. The printing parameters were optimized based on spot curing investigation, particle size data, and UV-visible spectrophotometry. In vitro cell culture with MG-63 osteosarcoma cell lines and pH study within simulated body fluid demonstrated a noncytotoxic response of the scaffold samples. Further, the in vivo bone regeneration ability of the 3D-printed biocomposite bone scaffolds was investigated by implantation of the scaffold samples in the rabbit femur bone defect model. Enhanced angiogenesis, osteoblastic, and osteoclastic activities were observed at the bone-scaffold interface, while examining through fluorochrome labelling, histology, radiography, field emission scanning electron microscopy, and x-ray microcomputed tomography. Overall, the results demonstrated that the 3D-printed biocomposite bone scaffolds have promising potential for bone loss rehabilitation.

Asunto(s)

RESUMEN

Fragile and expensive transparent conductive oxide anodes and noble metal cathodes in typical perovskite photovoltaic devices pose unavoidable issues, i.e., poor flexibility and high material cost, making it inaccessible to commercial application. Here, we report an ultrasimple indium tin oxide (ITO)-free and HTL-free all-carbon-electrode flexible perovskite solar cell (AC-F-PSC) with an architecture of PEN/carbon/SnO2/perovskite/carbon which contains an anode made of a carbon-based integrator (CNT-GR) comprising carbon nanotubes and low-dose graphene, and a cathode made of the commonly used conductive carbon. The CNT-GR anode exhibits low sheet resistance, high light transmittance, and superior flexibility beyond ITO. Density functional theory calculations reveal that O atoms from GR anchored onto the interwoven CNT network have strong covalent binding capacity with bond-deficient Sn ions, inhibiting the formation of oxygen vacancies in SnO2. Such a binding effect induces a significant reduction of the conduction band minimum of SnO2, yielding favorable energy level alignment for carrier transport at the SnO2/perovskite interface. Also, a heat-pressing approach as a tiny trick is used to fill the gaps at the perovskite/carbon cathode interface. The resulting AC-F-PSC device attains an efficiency of 13.14%, which is a record value among reported carbon-electrode F-PSCs, with superior mechanical flexibility, i.e., ∼71% of initial efficiency after bending 4000 cycles at 4 mm bending radius. This PSC based on an ultrasimple all-carbon-electrode offers a promising route for robust and cost-effective flexible photovoltaic devices.

RESUMEN

The forging-healing of the internal porosity defects affects the tensile, impact and fatigue properties of heavy forgings. In the present work, the effect of deformation process on the microstructure in the joint area as well as the tensile strength, impact toughness and fatigue strength was studied experimentally. It is shown that the tensile strength is restored once the porosity defects were healed, and the impact toughness is recovered when the flat grain band is eliminated. The fatigue strength can be restored if a uniform grain structure can be achieved in both the joint area and the matrix, whereafter precipitate become the key factor affecting the fatigue strength. A complete healing of the porosity defects, a uniform grain structure in the joint area and the matrix, and a fully controlled precipitate are essential to guarantee the mechanical properties and in-service performance of the heavy forgings.

RESUMEN

OBJECTIVE: The purpose of this study was to compare the effects of the selective serotonin reuptake inhibitor (SSRI) fluoxetine and the serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine on bone defect healing. MATERIALS AND METHODS: Wistar rats were randomly divided into three groups of eight animals each. The first received 0.1 ml/kg sterile saline solution, the second 5 mg/kg fluoxetine, and the third 5 mg/kg venlafaxine, daily by gastric gavage over 7 weeks. At week 3 of drug therapy, 5-mm diameter calvarial defects were created in the parietal bone of all of the animals. All rats were euthanized four weeks after surgery, micro-CT analysis and histomorphometric analysis were carried out to evaluate the following parameters: Bone volume fraction (BV/TV), bone surface (BS), bone surface density (BS/BV; bone surface/bone volume, 1/mm), trabecular number (Tb. N), trabecular thickness (Tb. Th), areas of new bone structure (positive areas), areas of mature bone structure (negative areas). RESULTS: Micro-CT analysis showed the presence of similar levels of bone formation within the defect site in all three groups (p>0.05). Histomorphometric analysis revealed the presence of bone-forming cells at the defect periphery, with less activity indicating bone formation at the center. No statistically significant difference was observed between the groups (p>0.05). CONCLUSION: Based on the findings of this study, it can be said that the use of both antidepressants hasn't any effect on bone defect healing.

RESUMEN

Defects on graphene over a micrometer in size were selectively blocked using polyvinyl alcohol through the formation of hydrogen bonding with defects. Because this hydrophilic PVA does not prefer to be located on the hydrophobic graphene surface, PVA selectively filled hydrophilic defects on graphene after the process of deposition through the solution. The mechanism of the selective deposition via hydrophilic-hydrophilic interactions was also supported by scanning tunneling microscopy and atomic force microscopy analysis of selective deposition of hydrophobic alkanes on hydrophobic graphene surface and observation of PVA initial growth at defect edges.

RESUMEN

Overcoming throughput challenges in current graphene defect healing processes, such as conventional thermal annealing, is crucial for realizing post-silicon device fabrication. Herein, a new time- and energy-efficient method for defect healing in graphene is reported, utilizing polymer-assisted rapid thermal annealing (RTA). In this method, a nitrogen-rich, polymeric "nanobandage" is coated directly onto graphene and processed via RTA at 800 °C for 15 s. During this process, the polymer matrix is cleanly degraded, while nitrogen released from the nanobandage can diffuse into graphene, forming nitrogen-doped healed graphene. To study the influence of pre-existing defects on graphene healing, lattice defects are purposefully introduced via electron beam irradiation and investigated by Raman microscopy. X-ray photoelectron spectroscopy reveals successful healing of graphene, observing a maximum doping level of 3 atomic nitrogen % in nanobandage-treated samples from a baseline of 0-1 atomic % in non-nanobandage treated samples. Electrical transport measurements further indicate that the nanobandage treatment recovers the conductivity of scanning electron microscope-treated defective graphene at ≈85%. The reported polymer-assisted RTA defect healing method shows promise for healing other 2D materials with other dopants by simply changing the chemistry of the polymeric nanobandage.

RESUMEN

The treatment of large bone defects represents a major clinical challenge. 3D printed scaffolds appear as a promising strategy to support bone defect regeneration. The 3D design of such scaffolds impacts the healing path and thus defect regeneration potential. Among others, scaffold architecture has been shown to influence the healing outcome. Gyroid architecture, characterized by a zero mean surface curvature, has been discussed as a promising scaffold design for bone regeneration. However, whether gyroid scaffolds are favourable for bone regeneration in large bone defects over traditional strut-like architecture scaffolds remains unknown. Therefore, the aim of this study was to investigate whether gyroid scaffolds present advantages over more traditional strut-like scaffolds in terms of their bone regeneration potential. Validated bone defect regeneration principles were applied in an in silico modeling approach that allows to predict bone formation in defect regeneration. Towards this aim, the mechano-biological bone regeneration principles were adapted to allow simulating bone regeneration within both gyroid and strut-like scaffolds. We found that the large surface curvatures of the gyroid scaffold led to a slower tissue formation dynamic and conclusively reduced bone regeneration. The initial claim, that an overall reduced zero mean surface curvature would enhance bone formation, could not be confirmed. The here presented approach illustrates the potential of in silico tools to evaluate in pre-clinical studies scaffold designs and eventually lead to optimized architectures of 3D printed implants for bone regeneration.

RESUMEN

Introduction Cystic lesions of the jaws and the impacted teeth are two of the most common cases that require surgical intervention in oral and maxillofacial surgery; however, surgeons also frequently use a traditional technique that involves the removal of the buccal bone plate. This study was conducted to compare the clinical and radiologic outcomes of the bone lid technique and the traditional technique. Methods This randomized controlled trial included 20 patients who were randomly divided into two groups (n = 10 each): the T group, in which the lesions were accessed using the traditional technique with classical rotating instruments, and the BL group, in which the lesions were accessed with the bone lid technique performed using a piezoelectric device, with repositioning of the buccal bone plate. Operative time, pain, edema, inferior alveolar nerve injury, and bone defect healing were measured during clinical and radiological follow-ups at 24 h, 72 h, one week, one month, and six months after the surgery. Results Normal soft tissue and bone healing were observed in all cases except one case in the BL group. The T group had a shorter mean operative time than the BL group. In terms of pain, edema, and inferior alveolar nerve injury, the groups did not differ statistically significantly. The percentage of bone defect healing was significantly greater in the BL group than in the T group after six months of follow-up. Conclusion The bone lid technique performed using a piezoelectric device was effective and safe for managing lesions in the posterior mandibular region and was not associated with increased postoperative complications. The disadvantages of this technique include a longer operative time and the need for fixation tools in some cases. In contrast, this technique outperforms the traditional technique in terms of reducing bone loss and improving the healing of bone defects.

RESUMEN

The increasing population and industrial development are responsible for environmental pollution. Among toxic chemicals, polycyclic aromatic hydrocarbons (PAHs) are highly carcinogenic contaminants resulting from the incomplete combustion of organic materials. Two-dimensional materials, such as transition metal dichalcogenides (TMDCs), are ideal sensory scaffolds, combining high surface-to-volume ratio with physical and chemical properties that are strongly susceptible to environmental changes. TMDCs can be integrated in field-effect transistors (FETs), which can operate as high-performance chemical detectors of (non)covalent interaction with small molecules. Here, we have developed MoS2-based FETs as platforms for PAHs sensing, relying on the affinity of the planar polyaromatic molecules for the basal plane of MoS2 and the structural defects in its lattice. X-ray photoelectron spectroscopy analysis, photoluminescence measurements, and transfer characteristics showed a notable reduction in the defectiveness of MoS2 and a p-type doping upon exposure to PAHs solutions, with a magnitude determined by the correlation between the ionization energies (EI) of the PAH and that of MoS2. Naphthalene, endowed with the higher EI among the studied PAHs, exhibited the highest output. We observed a log-log correlation between MoS2 doping and naphthalene concentration in water in a wide range (10-9-10-6 M), as well as a reversible response to the analyte. Naphthalene concentrations as low as 0.128 ppb were detected, being below the limits imposed by health regulations for drinking water. Furthermore, our MoS2 devices can reversibly detect vapors of naphthalene with both an electrical and optical readout, confirming that our architecture could operate as a dual sensing platform.

RESUMEN

Nitrogen (N) doping is an effective strategy for improving the solar-driven photocatalytic performance of anatase TiO2, but controllable methods for nitrogen-rich doping and associated defect engineering are highly desired. In this work, N-rich doped anatase TiO2 nanoparticles (4.2 at%) were successfully prepared via high-temperature nitridation based on thermally stable H3PO4-modified TiO2. Subsequently, the associated deep-energy-level defects such as oxygen vacancies and Ti3+ were successfully healed by smart photo-Fenton oxidation treatment. Under visible-light irradiation, the healed N-doped TiO2 exhibited a ~2-times higher activity of gas-phase acetaldehyde degradation than the non-treated one and even better than standard P25 TiO2 under UV-visible-light irradiation. The exceptional performance is attributed to the extended spectral response range from N-rich doping, the enhanced charge separation from hole capturing by N-doped species, and the healed defect levels with the proper thermodynamic ability for facilitating O2 reduction, depending on the results of ∙O2- radicals and defect measurement by electron spin resonance, X-ray photoelectron spectroscopy, atmosphere-controlled surface photovoltage spectra, etc. This work provides an easy and efficient strategy for the preparation of high-performance solar-driven TiO2 photocatalysts.

RESUMEN

Large bone defects represent a clinical challenge for which the implantation of scaffolds appears as a promising strategy. However, their use in clinical routine is limited, in part due to a lack of understanding of how scaffolds should be designed to support regeneration. Here, we use the power of computer modeling to investigate mechano-biological principles behind scaffold-guided bone regeneration and the influence of scaffold design on the regeneration process. Computer model predictions are compared to experimental data of large bone defect regeneration in sheep. We identified two main key players in scaffold-guided regeneration: (1) the scaffold surface guidance of cellular migration and tissue formation processes and (2) the stimulation of progenitor cell activity by the scaffold material composition. In addition, lower scaffold surface-area-to-volume ratio was found to be beneficial for bone regeneration due to enhanced cellular migration. To a lesser extent, a reduced scaffold Young's modulus favored bone formation. STATEMENT OF SIGNIFICANCE: 3D-printed scaffolds offer promising treatment strategies for large bone defects but their broader clinical use requires a more thorough understanding of their interaction with the bone regeneration process. The predictions of our in silico model compared to two experimental set-ups highlighted the importance of (1) the scaffold surface guidance of cellular migration and tissue formation processes and (2) the scaffold material stimulation of progenitor cell activity. In addition, the model was used to investigate the effect on the bone regeneration process of (1) the scaffold surface-area-to-volume ratio, with lower ratios favoring more bone growth, and (2) the scaffold material properties, with stiffer scaffold materials yielding a lower bone growth.

Asunto(s)

RESUMEN

BACKGROUND: Periosteum plays a significant role in bone formation and regeneration by storing progenitor cells, and also acts as a source of local growth factors and a scaffold for recruiting cells and other growth factors. Recently, tissue-engineered periosteum has been studied extensively and shown to be important for osteogenesis and chondrogenesis. Using biomimetic methods for artificial periosteum synthesis, membranous tissues with similar function and structure to native periosteum are produced that significantly improve the efficacy of bone grafting and scaffold engineering, and can serve as direct replacements for native periosteum. Many problems involving bone defects can be solved by preparation of idealized periosteum from materials with different properties using various techniques. METHODS: This review summarizes the significance of periosteum for osteogenesis and chondrogenesis from the aspects of periosteum tissue structure, osteogenesis performance, clinical application, and development of periosteum tissue engineering. The advantages and disadvantages of different tissue engineering methods are also summarized. RESULTS: The fast-developing field of periosteum tissue engineering is aimed toward synthesis of bionic periosteum that can ensure or accelerate the repair of bone defects. Artificial periosteum materials can be similar to natural periosteum in both structure and function, and have good therapeutic potential. Induction of periosteum tissue regeneration and bone regeneration by biomimetic periosteum is the ideal process for bone repair. CONCLUSIONS: Periosteum is essential for bone formation and regeneration, and it is indispensable in bone repair. Achieving personalized structure and composition in the construction of tissue engineering periosteum is in accordance with the design concept of both universality and emphasis on individual differences and ensures the combination of commonness and individuality, which are expected to meet the clinical needs of bone repair more effectively. THE TRANSLATIONAL POTENTIAL OF THIS ARTICLE: To better understand the role of periosteum in bone repair, clarify the present research situation of periosteum and tissue engineering periosteum, and determine the development and optimization direction of tissue engineering periosteum in the future. It is hoped that periosteum tissue engineering will play a greater role in meeting the clinical needs of bone repair in the future, and makes it possible to achieve optimization of bone tissue therapy.

RESUMEN

The applications of any ultrathin semiconductor device are inseparable from high-quality metal-semiconductor contacts with designed Schottky barriers. Building van der Waals (vdWs) contacts of 2D semiconductors represents an advanced strategy of lowering the Schottky barrier height by reducing interface states, but will finally fail at the theoretical minimum barrier due to the inevitable energy difference between the semiconductor electron affinity and the metal work function. Here, an effective molecule optimization strategy is reported to upgrade the general vdWs contacts, achieving near-zero Schottky barriers and creating high-performance electronic devices. The molecule treatment can induce the defect healing effect in p-type semiconductors and further enhance the hole density, leading to an effectively thinned Schottky barrier width and improved carrier interface transmission efficiency. With an ultrathin Schottky barrier width of ≈2.17 nm and outstanding contact resistance of ≈9 kΩ µm in the optimized Au/WSe2 contacts, an ultrahigh field-effect mobility of ≈148 cm2  V-1 s-1 in chemical vapor deposition grown WSe2 flakes is achieved. Unlike conventional chemical treatments, this molecule upgradation strategy leaves no residue and displays a high-temperature stability at >200 °C. Furthermore, the Schottky barrier optimization is generalized to other metal-semiconductor contacts, including 1T-PtSe2 /WSe2 , 1T'-MoTe2 /WSe2 , 2H-NbS2 /WSe2 , and Au/PdSe2 , defining a simple, universal, and scalable method to minimize contact resistance.

RESUMEN

Critical-sized bone defects are critical healing conditions that, if left untreated, often lead to non-unions. To reduce the risk, critical-sized bone defects are often treated with recombinant human BMP-2. Although enhanced bone tissue formation is observed when BMP-2 is administered locally to the defect, spatial and temporal distribution of callus tissue often differs from that found during regular bone healing or in defects treated differently. How this altered tissue patterning due to BMP-2 treatment is linked to mechano-biological principles at the cellular scale remains largely unknown. In this study, the mechano-biological regulation of BMP-2-treated critical-sized bone defect healing was investigated using a multiphysics multiscale in silico approach. Finite element and agent-based modeling techniques were combined to simulate healing within a critical-sized bone defect (5 mm) in a rat femur. Computer model predictions were compared to in vivo microCT data outcome of bone tissue patterning at 2, 4, and 6 weeks postoperation. In vivo, BMP-2 treatment led to complete healing through periosteal bone bridging already after 2 weeks postoperation. Computer model simulations showed that the BMP-2 specific tissue patterning can be explained by the migration of mesenchymal stromal cells to regions with a specific concentration of BMP-2 (chemotaxis). This study shows how computational modeling can help us to further understand the mechanisms behind treatment effects on compromised healing conditions as well as to optimize future treatment strategies.

Asunto(s)

RESUMEN

Atomically thin 2D materials provide an opportunity to investigate the atomic-scale details of defects introduced by particle irradiation. Once the atomic configuration of defects and their spatial distribution are revealed, the details of the mesoscopic phenomena can be unveiled. In this work, we created atomically small defects by controlled irradiation of gallium ions with doses ranging from 4.94 × 1012 to 4.00 × 1014 ions/cm2 on monolayer molybdenum disulfide (MoS2) crystals. The optical signatures of defects, such as the evolution of defect-activated LA-bands and a broadening of the first-order (E' and A'1) modes, can be studied by Raman spectroscopy. High-resolution scanning transmission electron microscopy (HR-STEM) analysis revealed that most defects are vacancies of few-molybdenum atoms with surrounding sulfur atoms (VxMo+yS) at a low ion dose. When increasing the ion dose, the atomic vacancies merge and form nanometer-sized holes. Utilizing HR-STEM and image analysis, we propose the estimation of the finite crystal length (Lfc) via the careful quantification of 0D defects in 2D systems through the formula Lfc = 4.41/ηion, where ηion corresponds to the ion dose. Combining HR-STEM and Raman spectroscopy, the formula to calculate Lfc from Raman features, I(LA)/I(A'1) = 5.09/Lfc2, is obtained. We have also demonstrated an effective route to healing the ion irradiation-induced atomic vacancies by annealing defective MoS2 in a hydrogen disulfide (H2S) atmosphere. The H2S annealing improved the crystal quality of MoS2 with Lfc greater than the calculated size of the A exciton wave function, which leads to a partial recovery of the photoluminescence signal after its quenching by ion irradiation.