A retrospective study of the mid-term efficacy of full-endoscopic annulus fibrosus suture following lumbar discectomy.

Aims: Full-endoscopic discectomy is associated with a high risk of disc reherniation due to the poor mechanical strength of the annulus fibrosus after scar healing. It is technically difficult to place a full-endoscopic annulus fibrosus suture. We designed an annulus fibrosus suture device that can be used to suture annulus defects under microendoscopy. The present study investigated the safety and feasibility of this technology. Patients and Methods: We retrospectively analyzed the outcomes of patients who underwent surgical treatment for lumbar disc herniation (LDH) from January 2018 to October 2020. We compared 40 patients with LDH treated with full-endoscopic annulus fibrosus suture following lumbar discectomy (LD + AFS group) with 42 patients treated with lumbar discectomy alone (LD group) regarding demographic data, symptoms, and recurrence and reoperation rates. Lumbar MRI and CT were performed 3 and 12 months. A 10-point visual analog scale (VAS) and the Oswestry Disability Index (ODI) was used to evaluate pain and the lumbar spine function. Results: The cohort comprised 82 patients, including 40 patients in the LD + AFS group and 42 in the LD group. All operations were successfully completed without serious complications. Reherniation occurred in no patients in the LD + AFS group and three patients in the LD group. The VAS scores for lumbar and leg pain and ODI score were significantly improved postoperatively (p < 0.05). Conclusion: Compared with conventional lumbar discectomy, full-endoscopic annulus fibrosus suture following full-endoscopic lumbar discectomy is a safe and effective minimally invasive technique that reduces the LDH recurrence rate.

Percutaneous endoscopic lumbar discectomy via the medial foraminal and interlaminar approaches: A comparative study with 2-year follow-up.

Objective: The purpose of this study was to analyze the clinical effect of percutaneous endoscopic medial foraminal discectomy (PEMFD) in the treatment of lumbar disc herniation (LDH). Methods: We retrospectively examined and compared clinical data from 39 single-level LDH patients who underwent PEID and 47 who underwent PEMFD. All the patients were diagnosed with single-level LDH and were treated in Xuzhou Central Hospital for single-segmental lumbar disc herniation between June 2017 and December 2019. Collect and count surgical-related indicators, intraoperative bleeding volume and 24-hour postoperative drainage volume, lower extremity numbness Visual Analogue Scale (VAS), the pain VAS and lumbar Oswestry Disability Index (ODI) scores. Results: Intraoperative bleeding volume and 24-hour postoperative drainage volume were significantly lower in the PEMFD group (p < 0.05). Operation time and length of hospital stay did not significantly differ between the groups. Transient spinal cord injury and surgical site infection did not occur. Recurrence occurred in two patients in each group. Repeat surgery in these patients demonstrated remarkable epidural scarring in the PEID group patients; no scarring was evident in the PEMFD group patients. The numbness VAS score 72 h after surgery and the pain VAS and ODI scores 1 month after surgery significantly differed between groups; however, pain VAS and ODI scores 6, 12, and 24 months after surgery did not. At last follow-up, the modified MacNab criteria outcome did not significantly differ between the groups. Conclusion: PEMFD and PEID have similar short- and medium-term outcomes. However, PEMFD has several advantages: simplicity, lower bleeding volume, and preservation of the LF.

HDAC6 inactivates Runx2 promoter to block osteogenesis of bone marrow stromal cells in age-related bone loss of mice.

BACKGROUND: Senile osteoporosis can cause bone fragility and increased risk for fractures and has been one of the most prevalent and severe diseases affecting the elderly population worldwidely. The underlying mechanisms are currently intensive areas of investigation. In age-related bone loss, decreased bone formation overweighs increased bone resorption. The molecular mechanisms underlying defective bone formation in age-related bone loss are not completely understood. In particular, the specific role of histone acetylation in age-related bone loss has not been examined thoroughly. METHODS: We employed 6- and 18-month-old mice to investigate the mechanisms of defective bone formation in age-related bone loss. Bone marrow stromal cells (BMSCs) were induced to undergo in vitro osteogenic differentiation. Chromatin immunoprecipitation (ChIP) was used to investigate the binding of histone deacetylases (HDACs) on Runx2 promoter in BMSCs. Luciferase reporter and transient transfection assay were employed to study Runx2 gene expression modulation by HDAC and androgen receptor (AR). siRNA and HDAC6 inhibitor, Tubastatin A, were used to inhibit HDAC6 in vitro. And systemic administration of Tubastatin A was used to block HDAC6 in vivo. RESULTS: Age-related trabecular bone loss was observed in 18-month-old mice compared with 6-month-old mice. In vitro osteogenic differentiation potential of BMSCs from 18-month-old mice was weaker than 6-month-old mice, in which there was Runx2 expression inactivation in BMSCs of 18-month-old mice compared with 6-month-old mice, which was attributable to HDAC6-mediated histone hypoacetylation in Runx2 promoter. There was competitive binding of HDAC6 and AR on Runx2 promoter to modulate Runx2 expression in BMSCs. More importantly, through siRNA- or specific inhibitor-mediated HDAC6 inhibition, we could activate Runx2 expression, rescue in vitro osteogenesis potential of BMSCs, and alleviate in vivo age-related bone loss of mice. CONCLUSION: HDAC6 accumulation and histone hypoacetylation on Runx2 promoter contributed to the attenuation of in vitro osteogenic differentiation potential of BMSCs from aged mice. Through HDAC6 inhibition, we could activate Runx2 expression and osteogenic differentiation potential of BMSCs from aged mice and alleviate the age-related bone loss of aged mice. Our study will benefit not only for understanding the age-related bone loss, but also for finding new therapies to treat senile osteoporosis.

RANKL expression of primary osteoblasts is enhanced by an IL-17-mediated JAK2/STAT3 pathway through autophagy suppression.

Objective: Interleukin-17 (IL-17), produced by T helper (Th)-17 cells, is a potent regulator of bone homeostasis. Osteoblasts are key cells that orchestrate inflammatory bone destruction and bone remodeling. This study examines the effect of different concentrations of IL-17 on osteogenesis and receptor activator of nuclear factor-kappa B ligand (RANKL) expression of primary osteoblasts.Methods: First, the growth of primary osteoblasts was evaluated. Second, we assessed the effects of IL-17 on the level of autophagy and the related Janus activated kinase 2 (JAK2) and downstream signal transducer and activator of transcription 3 (STAT3) signaling pathway. Next, osteogenic activity in different concentrations of IL-17 was tested. Finally, the specific JAK2/STAT3 signaling pathway inhibitor AG490 and autophagy inhibitor 3-MA were used to investigate the involvement of this pathway and autophagy in IL-17-induced regulation of RANKL expression.Results: Initially, we found that IL-17 treatment promoted growth of osteoblasts in a time- and dose-dependent manner. Next, we showed that low levels of IL-17 promoted autophagy activity, whereas the opposite was observed at high levels of IL-17. Moreover, high levels of IL-17 activated the JAK2/STAT3 signaling pathway, although this effect was reversed by upregulation of autophagy. Furthermore, our findings indicated that high concentrations of IL-17 promoted the differentiation, calcification, and RANKL expression of murine osteoblasts via activation of the JAK2/STAT3 pathway. Importantly, downregulation of autophagy at high IL-17 concentrations further enhanced RANKL expression via suppressing the JAK2/STAT3 cascade.Conclusion: Overall, our findings demonstrate, for the first time, that IL-17 modulates RANKL expression of osteoblasts through an autophagy-JAK2-STAT3 signaling pathway, thus affecting bone metabolism.

Wnt signaling: An attractive target for periodontitis treatment.

Periodontitis is the most common chronic inflammatory disease, and a leading cause of tooth loss. Characterized by resorption of alveolar process and destruction of periodontal ligaments, periodontitis can impact not only periodontal tissues but also systemic diseases, such as diabetes, cardiovascular diseases, and respiratory infections. Currently, it is a hotspot to manage destruction and gain regeneration of periodontal tissues. Increasing evidence indicates that the Wnt signaling plays an important role in homeostasis of periodontal tissues, functions of periodontal derived cells, and progression of periodontitis. Its molecule expressions were abnormal in periodontitis. As such, modulators targeting the Wnt signaling may be an adjuvant therapy for periodontitis treatment. This review elucidates the role of Wnt signaling and its molecules, with a view to develop a potential application of drugs targeting the Wnt signaling for periodontitis treatment.

Autophagy was involved in tumor necrosis factor-α-inhibited osteogenic differentiation of murine calvarial osteoblasts through Wnt/ß-catenin pathway.

Periodontitis is an inflammatory disease with a high incidence characterized by irreversible destruction of alveolar bone. This study aimed to investigate the effect of tumor necrosis factor-α (TNF-α) on osteogenic differentiation and its molecular mechanism. TNF-α inhibited osteogenic differentiation as revealed by the lower accumulation of osteoblastic genes like runt-related transcription factor (Runx2), alkaline phosphatase (ALP), osteoprotegerin (OPG), and osteocalcin (OCN). Moreover, TNF-α down-regulated the expressions of LC3II, ATG7, and beclin 1 (BECN1); suggesting that autophagy was inhibited during the process of osteogenic differentiation. Consistently, Wnt/ß-catenin signaling pathway members such as low-density lipoprotein receptor-related protein 5 (LRP5), ß-catenin, and phosphorylated-ß-catenin (p-ß-catenin) were reduced by TNF-α. Furthermore, the inhibitory effect of TNF-α on osteogenic differentiation and the Wnt/ß-catenin signaling pathway could be abated by autophagy inducers but exacerbated by autophagy inhibitors. The most intriguing finding of all was that TNF-α inhibited osteoblastic differentiation and the Wnt/ß-catenin signaling pathway by down-regulating autophagy, and autophagy positively regulated the Wnt/ß-catenin pathway and thus influenced osteoblastic differentiation. Our study provides a theoretical basis for autophagy-inducer therapy for the alveolar bone loss caused by periodontitis.

Autophagy negative-regulating Wnt signaling enhanced inflammatory osteoclastogenesis from Pre-OCs in vitro.

Periodontitis thereby the alveolar bone loss induced by inflammation, is a wide-spread phenomenon around the world. It is an ongoing challenge faced by clinicians worldwide. This study aimed to identify the effects of lipopolysaccharide (LPS) on osteoclasts (OCs) differentiation in vitro and to investigate its molecular mechanism. For bone marrow derived macrophages (considered as Pro-OCs), LPS impaired their differentiation into OCs in a dose-dependent manner. In contrast, it promoted Pre-OCs (referred to receptor activator of nuclear factor-κB ligand (RANKL) pretreated Pro-OCs) and differentiated to OCs with increased maximum diameter, quantity, the covering area and the fusion index in vitro. It also facilitated OCs proliferation, bone resorption and OCs related genes expression. Furthermore, it was revealed that LPS enhanced OCs genesis from Pre-OCs via activating autophagy pathway consequently elevated the accumulation of TRAP, Cts K and NFATC1, specific genes of OCs. The members of Wnt signaling were expressed as at lower states during the LPS induced OCs formation, but they could be rescued in the presence of autophagy inhibitor. The most promising observation was the direct interaction of LC3B and Dvl2, indicating that the crosstalk between above pathways existed in OCs. Taken together, we consider that LPS activates autophagy which negatively regulates Wnt signaling via autophagic degradation of Dvl2 is significant for osteoclastogenesis from Pre-OCs in vitro. Our study sheds light on the fact that autophagy inhibitors will become a new, potentially applicable therapeutic option in the treatment of periodontal bone loss.

Crystal-Like Glassy Structure in Sc-Doped BiSbTe Ensuring Excellent Speed and Power Efficiency in Phase Change Memory.

Phase change memory (PCM) is regarded as a promising technology for storage-class memory and neuromorphic computing, owing to the excellent performances in operation speed, data retention, endurance, and controllable crystallization dynamics, whereas the high power consumption of PCM remains to be a short-board characteristic that limits its extensive applications. Here, Sc-doped Bi0.5Sb1.5Te3 has been proposed for high-speed and low-power PCM applications. An operation speed of 6 ns and a threshold current of 0.7 mA have been achieved in 190 nm Sc0.23Bi0.5Sb1.5Te3 PCM, which consumes lower power than GeSbTe and ScSbTe PCM. A good endurance of 5 × 105 has been achieved, which is attributed to the small volume change of 4% during phase change and a good homogeneity phase in the crystalline state. The structure of amorphous Sc0.23Bi0.5Sb1.5Te3 has been characterized by experimental and theoretical methods, showing the existence of a large amount of crystal-like structural factions, which can efficiently minimize the atomic movements required for crystallization and subsequently improve the operation speed and power efficiency. The low diffusivity of Sc and Bi at room temperature and the rapidly increased diffusivity of Bi at elevated temperatures are fundamental for the high data retention of 94 °C and the fast crystallization in Sc0.23Bi0.5Sb1.5Te3. The combination of high atomic mobility and minimized atomic movements during crystallization ensures the high speed and low power consumption of Sc0.23Bi0.5Sb1.5Te3 PCM, which can promote its application to energy-efficient systems, that is, AI chips and wearable electronics.

Interleukin­17A facilitates osteoclast differentiation and bone resorption via activation of autophagy in mouse bone marrow macrophages.

Interleukin 17A (IL­17A) exerts pleiotropic effects on periodontitis, partially through enhancement of alveolar bone loss. Osteoclasts are the main culprits that absorb alveolar bone. However, studies describing the correlation between IL­17A and osteoclasts are not conclusive. Previously, autophagy was revealed to be involved in osteoclast differentiation and bone resorption. However, the role of autophagy in IL­17A­mediated osteoclast formation is yet to be clarified. In the present study, bone marrow macrophages (BMMs) were treated with or without IL­17A. 3­Methyladenine (3­MA) was applied to inhibit autophagy. Osteoclast formation was detected by tartrate­resistant acid phosphatase (TRAP) staining, immunofluorescence, and scanning electron microscope. The effects of IL­17A on osteoclast­specific genes and autophagy­related genes during osteoclast differentiation were examined by real­time quantitative polymerase chain reaction and western blot analysis. Autophagosomes were observed by transmission electron microscope. Hematoxylin and eosin (H&E), and TRAP staining was adopted to assess alveolar bone destruction and the number of osteoclasts, respectively in a rat periodontitis model. Consequently, IL­17A stimulated osteoclast differentiation and bone resorption of BMMs accompanied by an increase in the mRNA expression of osteoclast­specific genes. Furthermore, IL­17A increased the levels of autophagy­related genes and proteins, and inhibition of autophagy with 3­MA attenuated the IL­17A­mediated osteoclastogenesis. In addition, there was an increase in the number of osteoclasts and alveolar bone resorption with IL­17A treatment in the periodontitis rat model. Collectively, these findings indicated that IL­17A facilitated osteoclast differentiation and bone resorption in vitro and in vivo, which may contribute to the understanding of the molecular basis of IL­17A in alveolar bone destruction and provide insight on the clinical therapeutic targets for periodontitis.

Electrical switching properties and structural characteristics of GeSe-GeTe films.

Germanium chalcogenides, especially GeSe and GeTe alloys, have recently gained popularity because of their Ovonic threshold (volatile) and memory (non-volatile) switching properties, with great potential for electric storage applications. Materials designed in a pseudo-binary way may possess superior properties in their phase transition, e.g. GeTe-Sb2Te3 materials, and bring about revolutionary advances in optical storage. However, to date, the electrical switching behaviors of films of pseudo-binary GeSe-GeTe have not yet been studied, and neither have the structural characteristics. Herein, we present both the thermally and electrically induced switching behaviors of GeSe-GeTe film, as well as the structural evolution due to composition tuning. The crystallization temperature of GeSe-GeTe films increases with GeSe content quite sensitively. An atom-resolved picture of the GeSe-GeTe alloy with a state-of-the-art atomic mapping technology has been presented, where a randomly mixed arrangement of Se and Te atoms is determined unambiguously in Ge50Se13Te34 with a GeTe-like rhombohedral structure. The local structural motifs in GeSe-GeTe, more specifically, sixfold coordinated octahedra with a distinguished degree of Peierls distortion and geometric variety, are essential to understand its electric properties. GeSe-GeTe alloy, Ge50Se13Te34, based memory cells have been fabricated, showing a fast memory switching behavior and excellent retention of 10 years at 208 °C.

Red phosphorus in its two-dimensional limit: novel clathrates with varying band gaps and superior chemical stabilities.

First-principles calculations within density functional theory reveal the preferred structures of red phosphorus in the two-dimensional (2D) limit to be porous with intriguing structural, electronic, and chemical properties. These few-atomic-layer structures are stabilized as novel 2D clathrates with tunable pore sizes and varying semiconducting band gaps, labelled as V-Hex, P-Monoclinic, P-Hex, and V-Tetr in descending energetic stabilities. The cohesive energies of the 2D clathrates are all substantially higher than that of white phosphorus. More strikingly, the V-Hex structure is energetically as stable as black phosphorene, but possesses distinctly superior chemical stability when exposed to O2 due to the presence of a much higher activation barrier against chemisorption. We also exploit the salient properties of these 2D clathrates for their important application potentials, including serving as effective elemental photocatalysts for visible-light-driven water splitting, and as a new class of sieves for molecular separation and DNA sequencing.

Reducing the stochasticity of crystal nucleation to enable subnanosecond memory writing.

Operation speed is a key challenge in phase-change random-access memory (PCRAM) technology, especially for achieving subnanosecond high-speed cache memory. Commercialized PCRAM products are limited by the tens of nanoseconds writing speed, originating from the stochastic crystal nucleation during the crystallization of amorphous germanium antimony telluride (Ge2Sb2Te5). Here, we demonstrate an alloying strategy to speed up the crystallization kinetics. The scandium antimony telluride (Sc0.2Sb2Te3) compound that we designed allows a writing speed of only 700 picoseconds without preprogramming in a large conventional PCRAM device. This ultrafast crystallization stems from the reduced stochasticity of nucleation through geometrically matched and robust scandium telluride (ScTe) chemical bonds that stabilize crystal precursors in the amorphous state. Controlling nucleation through alloy design paves the way for the development of cache-type PCRAM technology to boost the working efficiency of computing systems.

Pilose antler peptide potentiates osteoblast differentiation and inhibits osteoclastogenesis via manipulating the NF-κB pathway.

Bones are inflexible yet ever-changing metabolic organs, and bone homeostasis is maintained through two delicately regulated processes: bone construction and bone reabsorption. An imbalance in bone metabolism is linked to most orthopedic diseases, including osteoporosis and rheumatoid arthritis. Importantly, tumor necrosis factor-α (TNF-α) blocks osteoblast differentiation and stimulates osteoclast formation, resulting in delayed deposition of new bone and accelerated bone resorption, especially in rheumatoid arthritis patients with inflammatory conditions. Pilose antler peptide (PAP) isolated and purified from deer antlers has been shown to have beneficial effects on chronic inflammation. In the present study, we studied the impact of PAP on osteoblast differentiation and evaluated the regulatory mechanism, with particular emphasis on the effect of PAP on TNF-α-mediated NF-κB signaling. Mouse primary osteoblast cells were activated with bone morphogenetic protein-2 (BMP-2) for osteoblast differentiation. A significant stimulatory effect of PAP in osteoblastogenesis was observed using ALP activity and Alizarin Red S staining assays. Meanwhile, PAP significantly rescued TNF-α-induced impairment of osteoblast formation as well as mineralization. Furthermore, we found a similar trend upon analyzing osteoblast-specific gene expression. PAP significantly rescued TNF-α-mediated decrease in expression of osteoblast-specific genes. A molecular mechanism assay indicated that PAP significantly inhibited TNF-α-mediated stimulation of NF-κB signaling activity, as well as nuclear translocation of its subunit p65. Moreover, over-expression of p65 reversed the stimulatory effects of PAP on osteoblast differentiation. Furthermore, we also identified that PAP dose dependently inhibit osteoclastogenesis, and this effect might be achieved via suppressing NF-κB activity. In summary, this study shows that PAP promotes osteoblast differentiation and blocks TNF-α-mediated suppression of osteoblastogenesis in vitro via the NF-κB/p65 pathway, as well as inhibits osteoclastsogenesis in vitro. Therefore, PAP, a novel drug with both antiresorptive and osteoanabolic activity, shows therapeutic potential as an alternative treatment for osteolytic diseases, including rheumatoid arthritis and osteoporosis.

Direct observation of titanium-centered octahedra in titanium-antimony-tellurium phase-change material.

Phase-change memory based on Ti0.4Sb2Te3 material has one order of magnitude faster Set speed and as low as one-fifth of the Reset energy compared with the conventional Ge2Sb2Te5 based device. However, the phase-transition mechanism of the Ti0.4Sb2Te3 material remains inconclusive due to the lack of direct experimental evidence. Here we report a direct atom-by-atom chemical identification of titanium-centered octahedra in crystalline Ti0.4Sb2Te3 material with a state-of-the-art atomic mapping technology. Further, by using soft X-ray absorption spectroscopy and density function theory simulations, we identify in amorphous Ti0.4Sb2Te3 the titanium atoms preferably maintain the octahedral configuration. Our work may pave the way to more thorough understanding and tailoring of the nature of the Ti-Sb-Te material, for promoting the development of dynamic random access memory-like phase-change memory as an emerging storage-class memory to reform current memory hierarchy.

Understanding the crystallization behavior of as-deposited Ti-Sb-Te alloys through real-time radial distribution functions.

Phase change materials, successfully used in optical data-storage and non-volatile electronic memory, are well-known for their ultrafast crystallization speed. However, the fundamental understanding of their crystallization behavior, especially the nucleation process, is limited by present experimental techniques. Here, real-time radial distribution functions (RDFs), derived from the selected area electron diffractions, are employed as structural probes to comprehensively study both nucleation and subsequent growth stages of Ti-doped Sb2Te3 (TST) materials in the electron-irradiation crystallization process. It can be found that the incorporation of Ti atoms in Sb2Te3 forms wrong bonds such as Ti-Te, Ti-Sb, breaks the originally ordered atomic arrangement and diminishes the initial nucleus size of the as-deposited films, which results in better thermal stability. But these nuclei hardly grow until their sizes exceed a critical value, and then a rapid growth period starts. This means that an extended nucleation time is required to form the supercritical nuclei of TST alloys with higher concentration. Also, the increasing formation of four-membered rings, which served as nucleation sites, after doping excessive Ti is responsible for the change of the crystallization behavior from growth-dominated to nucleation-dominated.

Ti-Sb-Te alloy: a candidate for fast and long-life phase-change memory.

Phase-change memory (PCM) has great potential for numerous attractive applications on the premise of its high-device performances, which still need to be improved by employing a material with good overall phase-change properties. In respect to fast speed and high endurance, the Ti-Sb-Te alloy seems to be a promising candidate. Here, Ti-doped Sb2Te3 (TST) materials with different Ti concentrations have been systematically studied with the goal of finding the most suitable composition for PCM applications. The thermal stability of TST is improved dramatically with increasing Ti content. The small density change of T0.32Sb2Te3 (2.24%), further reduced to 1.37% for T0.56Sb2Te3, would greatly avoid the voids generated at phase-change layer/electrode interface in a PCM device. Meanwhile, the exponentially diminished grain size (from ∼200 nm to ∼12 nm), resulting from doping more and more Ti, enhances the adhesion between phase-change film and substrate. Tests of TST-based PCM cells have demonstrated a fast switching rate of ∼10 ns. Furthermore, because of the lower thermal conductivities of TST materials, compared with Sb2Te3-based PCM cells, T0.32Sb2Te3-based ones exhibit lower required pulse voltages for Reset operation, which largely decreases by ∼50% for T0.43Sb2Te3-based ones. Nevertheless, the operation voltages for T0.56Sb2Te3-based cells dramatically increase, which may be due to the phase separation after doping excessive Ti. Finally, considering the decreased resistance ratio, TixSb2Te3 alloy with x around 0.43 is proved to be a highly promising candidate for fast and long-life PCM applications.

Aluminum-centered tetrahedron-octahedron transition in advancing Al-Sb-Te phase change properties.

Group IIIA elements, Al, Ga, or In, etc., doped Sb-Te materials have proven good phase change properties, especially the superior data retention ability over popular Ge2Sb2Te5, while their phase transition mechanisms are rarely investigated. In this paper, aiming at the phase transition of Al-Sb-Te materials, we reveal a dominant rule of local structure changes around the Al atoms based on ab initio simulations and nuclear magnetic resonance evidences. By comparing the local chemical environments around Al atoms in respective amorphous and crystalline Al-Sb-Te phases, we believe that Al-centered motifs undergo reversible tetrahedron-octahedron reconfigurations in phase transition process. Such Al-centered local structure rearrangements significantly enhance thermal stability of amorphous phase compared to that of undoped Sb-Te materials, and facilitate a low-energy amorphization due to the weak links among Al-centered and Sb-centered octahedrons. Our studies may provide a useful reference to further understand the underlying physics and optimize performances of all IIIA metal doped Sb-Te phase change materials, prompting the development of NOR/NAND Flash-like phase change memory technology.

Understanding phase-change behaviors of carbon-doped Ge2Sb2Te5 for phase-change memory application.

Phase-change materials are highly promising for next-generation nonvolatile data storage technology. The pronounced effects of C doping on structural and electrical phase-change behaviors of Ge2Sb2Te5 material are investigated at the atomic level by combining experiments and ab initio molecular dynamics. C dopants are found to fundamentally affect the amorphous structure of Ge2Sb2Te5 by altering the local environments of Ge-Te tetrahedral units with stable C-C chains. The incorporated C increases the amorphous stability due to the enhanced covalent nature of the material with larger tetrahedral Ge sites. The four-membered rings with alternating atoms are reduced greatly with carbon addition, leading to sluggish phase transition and confined crystal grains. The lower RESET power is presented in the PCM cells with carbon-doped material, benefiting from its high resistivity and low thermal conductivity.

One order of magnitude faster phase change at reduced power in Ti-Sb-Te.

To date, slow Set operation speed and high Reset operation power remain to be important limitations for substituting dynamic random access memory by phase change memory. Here, we demonstrate phase change memory cell based on Ti0.4Sb2Te3 alloy, showing one order of magnitude faster Set operation speed and as low as one-fifth Reset operation power, compared with Ge2Sb2Te5-based phase change memory cell at the same size. The enhancements may be rooted in the common presence of titanium-centred octahedral motifs in both amorphous and crystalline Ti0.4Sb2Te3 phases. The essentially unchanged local structures around the titanium atoms may be responsible for the significantly improved performance, as these structures could act as nucleation centres to facilitate a swift, low-energy order-disorder transition for the rest of the Sb-centred octahedrons. Our study may provide an alternative to the development of high-speed, low-power dynamic random access memory-like phase change memory technology.

Role of the nano amorphous interface in the crystallization of Sb2Te3 towards non-volatile phase change memory: insights from first principles.

The nano amorphous interface is important as it controls the phase transition for data storage. Yet, atomic scale insights into such kinds of systems are still rare. By first-principles calculations, we obtain the atomic interface between amorphous Si and amorphous Sb2Te3, which prevails in the series of Si-Sb-Te phase change materials. This interface model reproduces the experiment-consistent phenomena, i.e. the amorphous stability of Sb2Te3, which defines the data retention in phase change memory, and is greatly enhanced by the nano interface. More importantly, this method offers a direct platform to explore the intrinsic mechanism to understand the material function: (1) by steric effects through the atomic "channel" of the amorphous interface, the arrangement of the Te network is significantly distorted and is separated from the p-orbital bond angle in the conventional phase-change material; and (2) through the electronic "channel" of the amorphous interface, high localized electrons in the form of a lone pair are "projected" to Sb2Te3 from amorphous Si by a proximity effect. These factors set an effective barrier for crystallization and improve the amorphous stability, and thus data retention. The present research and scheme sheds new light on the engineering and manipulation of other key amorphous interfaces, such as Si3N4/Ge2Sb2Te5 and C/Sb2Te3, through first-principles calculations towards non-volatile phase change memory.