Development of a Triphenylmethyl Alkylation Pre-Column Derivatization Method for HPLC Quantitative Analysis of Chemically Unstable Halogenated Compounds.

The primary limitations of the quantitative analysis of thermally labile halogenated compounds by traditional gas chromatography (GC) are the inadequacy of identifying the insufficiently volatile impurity (often with a high boiling point) and the difficulty in obtaining a standard substance with a reliable standardized assay. Taking the 4-(Chloromethyl)-5-methyl-1,3-dioxol-2-one (DMDO-Cl, 1) as an example, we reported a triphenylmethanamino-derivatization method to overcome the challenges of the assay determination of such species. During the quantification of 1, the presence of GC-undetectable polymeric impurity 10 poses a critical challenge in assessing the material quality. Moreover, the standard substance of 1 is not available on the market due to its inherent instability during storage and handling, further complicating the quantitative analysis. In this work, a precolumn HPLC-UV derivatization method based on triphenylmethanamino-alkylation was developed to quantitatively analyze 1. The resulting derivative 2 exhibits excellent crystallinity and superior physical and chemical stability and possesses effective chromophores for UV detection. The conversion from analyte 1 to derivative 2 demonstrates desirable reactivity and purity, facilitating quantitative analysis using the external standard method. The chemical derivatization-chromatographic detection method was optimized and validated, demonstrating its high specificity, good linearity, precision, accuracy, and stability. This method offers a valuable alternative to the general quantitative NMR (qNMR) detection technique, which exhibits reduced specificity in the presence of increased levels of impurities in compound 1.

MCP-1 controls IL-17-promoted monocyte migration and M1 polarization in osteoarthritis.

Osteoarthritis (OA) is a low-grade inflammatory joint illness in which monocytes migrate and infiltrate synovial tissue, differentiating into the pro-inflammatory M1 macrophage phenotype. IL-17 is a proinflammatory mediator principally generated by Th17 cells, which is elevated in OA patients; nevertheless, investigators have yet to elucidate the function of IL-17 in M1 polarization during OA development. Our analysis of clinical tissues and results from the open online dataset discovered that the level of M1 macrophage markers is elevated in human OA tissue samples than in normal tissue. High-throughput screening demonstrated that MCP-1 is a potential candidate factor after IL-17 treatment in OA synovial fibroblasts (OASFs). Immunohistochemistry data revealed that the level of MCP-1 is higher in humans and mice with OA than in normal tissues. IL-17 stimulation facilitates MCP-1-dependent macrophage polarization to the M1 phenotype. It also appears that IL-17 enhances MCP-1 synthesis in human OASFs, enhancing monocyte migration via the JAK and STAT3 signaling cascades. Our findings indicate the IL-17/MCP-1 axis as a novel strategy for the remedy of OA.

Deployment Protection for Interference of 5G Base Stations with Aeronautical Radio Altimeters.

In this manuscript, we present a novel deployment protection method aimed at safeguarding aeronautical radio altimeters (RAs) from interference caused by fifth-generation (5G) telecommunication base stations (BSs). Our methodology involves an integrated interference model for defining prohibited zones and utilizes power control and angle shutoff methods to mitigate interference. First, to ensure reliable protection, we define both horizontal and vertical prohibited zones and investigate their variations to immunize RA against 5G interference. Second, we validate the effectiveness of the model in various operational scenarios, analyzing the influence of factors such as base station types, antenna parameters, flight altitude, and aircraft attitudes to cover a wide range of real-world scenarios. Third, to mitigate interference, we propose and analyze the power control and angle shutoff methods through simulation for the RMa prohibited zone. Our results demonstrate the efficacy of the deployment protection method in safeguarding RAs from 5G interference, providing guidance for interference protection during civil aviation operations and base station deployment near airports.

Navigation-Assisted One-Staged Posterior Spinal Fusion Using Pedicle Screw Instrumentation in Adolescent Idiopathic Scoliosis-A Case Series.

Background and Objectives: Adolescent idiopathic scoliosis (AIS) is a prevalent three-dimensional spinal disorder, with a multifactorial pathogenesis, including genetics and environmental aspects. Treatment options include non-surgical and surgical treatment. Surgical interventions demonstrate positive outcomes in terms of deformity correction, pain relief, and improvements of the cardiac and pulmonary function. Surgical complications, including excessive blood loss and neurologic deficits, are reported in 2.27-12% of cases. Navigation-assisted techniques, such as the O-arm system, have been a recent focus with enhanced precision. This study aims to evaluate the results and complications of one-stage posterior instrumentation fusion in AIS patients assisted by O-arm navigation. Materials and Methods: This retrospective study assesses 55 patients with AIS (12-28 years) who underwent one-stage posterior instrumentation correction supported by O-arm navigation from June 2016 to August 2023. We examined radiological surgical outcomes (initial correction rate, loss of correction rate, last follow-up correction rate) and complications as major outcomes. The characteristics of the patients, intraoperative blood loss, operation time, number of fusion levels, and screw density were documented. Results: Of 73 patients, 55 met the inclusion criteria. The average age was 16.67 years, with a predominance of females (78.2%). The surgical outcomes demonstrated substantial initial correction (58.88%) and sustained positive radiological impact at the last follow-up (56.56%). Perioperative complications, including major and minor, occurred in 18.18% of the cases. Two patients experienced a major complication. Blood loss (509.46 mL) and operation time (402.13 min) were comparable to the literature ranges. Trend analysis indicated improvements in operation time and blood loss over the study period. Conclusions: O-arm navigation-assisted one-stage posterior instrumentation proves reliable for AIS corrective surgery, achieving significant and sustained positive radiological outcomes, lower correction loss, reduced intraoperative blood loss, and absence of implant-related complications. Despite the challenges, our study demonstrates the efficacy and maturation of this surgical approach.

Assessing Neurologic Complications in Thoracic Three-Column Osteotomy: A Clinical Application of a Novel MRI-Based Classification Approach.

STUDY DESIGN: Retrospective comparative study. OBJECTIVE: To investigate the occurrence of neurologic complications in patients undergoing thoracic three-column osteotomy (3CO) utilizing an MRI-based classification that assesses spinal cord shape and the presence of cerebrospinal fluid (CSF) at the curve apex, and evaluate its prognostic capacity for postoperative neurologic deficits. SUMMARY OF BACKGROUND DATA: Recent advancements in correction techniques have improved outcomes for severe spinal deformity patients undergoing 3CO. A novel MRI-based spinal cord classification system was introduced, but its validation and association with postoperative complications remain unexplored. MATERIALS AND METHODS: Between September 2012 and September 2018, a retrospective analysis was conducted on 158 adult patients with spinal deformities undergoing 3CO. Radiographic parameters were measured. T2-weighted axial MRI was employed to describe spinal cord morphology at the apex. Intraoperative neurophysiologic monitoring (INOM) alerts were recorded, and preoperative and postoperative neurologic functions were assessed using the Frankel score. Categorical data were compared using the Chi-Square or Fisher's exact test. The paired t-test was utilized to assess the mean difference between pre- and postoperative measurements, while the one-way ANOVA and independent t-test were employed for comparative analyses among the different spinal cord types. RESULTS: Patients were categorized into three groups: type 1, type 2, and type 3, consisting of 12, 85, and 61 patients. Patients with type 3 morphology exhibited larger Cobb angles of the main curve (P<.001). This disparity persisted both postoperatively and during follow-up (P<.05). IONM alerts were triggered in 32 patients (20.3%), with a distribution of one case in type 1, six cases in type 2, and 22 cases in type 3 morphologies (P<.001). New neurologic deficits were observed in 15 patients (9.5%), with one, three, and 11 cases in type 1, 2, and 3 morphologies, respectively. CONCLUSIONS: Patients with type 3 morphology exhibited greater spinal deformity severity, higher likelihood of preoperative neurologic deficits, and an elevated risk of postoperative neurologic complications. This underscores the utility of the classification as a tool for predicting postoperative neurologic complications in patients undergoing thoracic 3CO. LEVEL OF EVIDENCE: Level IV.

Contamination status, partitioning behavior, ecological risks assessment of legacy and emerging per- and polyfluoroalkyl substances in a typical heavily polluted semi-enclosed bay, China.

The contaminant status, spatial distribution, partitioning behavior, and ecological risks of 26 legacy and emerging perfluoroalkyl and polyfluoroalkyl substances (PFASs) in Laizhou Bay, China were investigated. The concentrations of ∑PFASs in surface and bottom seawater ranged from 37.2 to 222 ng/L and from 34.2 to 305 ng/L with an average of 116 ± 62.7 and 138 ± 93.8 ng/L, respectively. There were no significant differences in the average concentrations between the surface and bottom seawater (P > 0.05). Perfluorooctanoic acid (PFOA) and short-chain PFASs dominated the composition of PFASs in seawater. The concentrations of ∑PFASs in sediments ranged from 0.997 to 7.21 ng/g dry weight (dw), dominated by perfluorobutane sulfonate (PFBS), perfluorobutanoic acid (PFBA), and long-chain PFASs. The emerging alternatives of perfluoro-1-butane-sulfonamide (FBSA) and 6:2 fluorotelomer sulfonic acid (6:2 FTSA) were detected for the first time in Laizhou Bay. The ∑PFASs in seawater in the southwest of the bay were higher than those in the northeast of the bay. The ∑PFASs in sediments in the northeast sea area were higher than those in the inner area of the bay. Log Kd and log Koc values increased with increasing carbon chain length for PFASs compounds. Ecological risk assessments indicated a low ecological risk associated with HFPO-DA but a moderate risk associated with PFOA contamination in Laizhou Bay. Positive matrix factorization (PMF) analysis revealed that fluoropolymer manufacturing, metal plating plants, and textile treatments were identified as major sources contributing to PFASs contamination.

S-adenosylmethionine attenuates angiotensin II-induced aortic dissection formation by inhibiting vascular smooth muscle cell phenotypic switch and autophagy.

It is well known that aortic dissection (AD) is a very aggressive class of vascular diseases. S-adenosylmethionine (SAM) is an autophagy inhibitor with anti-inflammatory and anti-oxidative stress effects; however, the role of SAM in AD is unknown. In this study, we constructed an animal model of AD using subcutaneous minipump continuous infusion of AngII-induced ApoE-/-mice and a cytopathic model using AngII-induced primary vascular smooth muscle cells (VSMCs) to investigate the possible role of SAM in AD. The results showed that mice in the AngII + SAM group had significantly lower AD incidence, significantly prolonged survival, and reduced vascular elastic fiber disruption compared with mice in the AngII group. In addition, SAM significantly inhibited autophagy in vivo and in vitro. Meanwhile, SAM also inhibited the cellular phenotypic switch, mainly by up regulating the expression levels of contractile marker proteins [α-smooth muscle actin (α-SMA) and smooth muscle 22α (SM22α)] and down regulating the expression levels of synthetic marker proteins [osteoblast protein (OPN), matrix metalloproteinase-2 (MMP2), and matrix metalloproteinase-9 (MMP9)]. Molecularly, SAM inhibited AD formation mainly by activating the PI3K/AKT/mTOR signaling pathway. Using a PI3K inhibitor (LY294002) significantly reversed the protective effect of SAM in AngII-induced mice and VSMCs.Our study demonstrates the protective effect of SAM on mice under AngII-induced AD for the first time. SAM prevented AD formation mainly by inhibiting cellular phenotypic switch and autophagy, and activation of the PI3K/AKT/mTOR signaling pathway is a possible molecular mechanism. Thus, SAM may be a novel strategy for the treatment of AD.

Microglial FoxO3a deficiency ameliorates ferroptosis-induced brain injury of intracerebral haemorrhage via regulating autophagy and heme oxygenase-1.

Microglial HO-1 regulates iron metabolism in the brain. Intracerebral haemorrhage (ICH) shares features of ferroptosis and necroptosis; hemin is an oxidized product of haemoglobin from lysed red blood cells, leading to secondary injury. However, little is known about the underlying molecular mechanisms attributable to secondary injury by hemin or ICH. In this study, we first show that FoxO3a was highly co-located with neurons and microglia but not astrocytes area of ICH model mice. Hemin activated FoxO3a/ATG-mediated autophagy and HO-1 signalling resulting in ferroptosis in vitro and in a mice model of brain haemorrhage. Accordingly, autophagy inhibitor Baf-A1 or HO-1 inhibitor ZnPP protected against hemin-induced ferroptosis. Hemin promoted ferroptosis of neuronal cells via FoxO3a/ATG-mediated autophagy and HO-1 signalling pathway. Knock-down of FoxO3a inhibited autophagy and prevented hemin-induced ferroptosis dependent of HO-1 signalling. We first showed that hemin stimulated microglial FoxO3a/HO-1 expression and enhanced the microglial polarisation towards the M1 phenotype, while knockdown of microglial FoxO3a inhibited pro-inflammatory cytokine production in microglia. Furthermore, the microglia activation in the striatum showed significant along with a high expression level of FoxO3a in the ICH mice. We found that conditional knockout of FoxO3a in microglia in mice alleviated neurological deficits and microglia activation as well as ferroptosis-induced striatum injury in the autologous blood-induced ICH model. We demonstrate, for the first time, that FoxO3a/ATG-mediated autophagy and HO-1 play an important role in microglial activation and ferroptosis-induced striatum injury of ICH, identifying a new therapeutic avenue for the treatment of ICH.

How sintering temperature affects the electrochemical performance of ultra-high nickel (Ni > 0.9) cathode material.

The burgeoning demand for electric vehicles with extended driving ranges has propelled ongoing development efforts for ultra-high nickel (Ni > 0.9) cathode materials. Despite significant ongoing research focused on Ni-rich cathode materials, a more comprehensive foundational understanding of ultra-high nickel cathode materials is essential. In our research, we employed LiNi0.94Co0.06O2 as a model ultra-high nickel cathode material to systematically delve into the interplay between sintering temperature, structural features, and electrochemical behavior. Within a sintering temperature spectrum of 660-720 °C, we discerned that specimens produced at diminished temperatures manifest a reduced initial discharge capacity yet excel in cycling endurance. In stark contrast, their counterparts produced at augmented temperatures behave inversely. Identifying a singular sintering temperature that achieves equilibrium between initial discharge capacity and cycling performance proves elusive. Through X-ray diffraction and high-resolution transmission electron microscopy, it became evident that samples synthesized at lower temperatures exhibit pronounced lithium-nickel mixing and develop a thicker NiO layer on the surface, leading to compromised initial discharge performance and capacity. Utilizing focused ion beam scanning electron microscopy, differential capacity analysis, and in-situ X-ray diffraction, we confirm that samples synthesized at lower temperatures possess smaller particle sizes, enabling them to withstand volumetric expansion stress during cycling, resulting in enhanced cycling performance. In the realm of ultra-high nickel cathode materials, elevating the sintering temperature is a conduit to superior initial discharge efficiency and capacity. Yet, the imperative of preserving diminutive particle dimensions, as a stratagem to bolster cycling performance, stands out as a pivotal research frontier.

Mitochondrion-targeted carboxymethyl chitosan hybrid nanoparticles loaded with Coenzyme Q10 protect cardiac grafts against cold ischaemia‒reperfusion injury in heart transplantation.

BACKGROUND: Heart transplantation (HT) has been approved as an optimal therapeutic regimen for patients with terminal-stage cardiac failure. However, cold ischaemia‒reperfusion (I/R) injury remains an unavoidable and outstanding challenge, which is a major factor in early graft dysfunction and an obstacle to long-term survival in HT. Cold I/R injury induces cardiac graft injury by promoting mitochondrial dysfunction and augmenting free radical production and inflammatory responses. We therefore designed a mitochondrion-targeted nanocarrier loaded with Coenzyme Q10 (CoQ10) (CoQ10@TNPs) for treatment of cold I/R injury after cardiac graft in a murine heterotopic cardiac transplantation model. METHODS: Hybrid nanoparticles composed of CaCO3/CaP/biotinylated-carboxymethylchitosan (CaCO3/CaP/BCMC) were synthesized using the coprecipitation method, and the mitochondria-targeting tetrapeptide SS31 was incorporated onto the surface of the hybrid nanoparticles through biotin-avidin interactions. Transmission electron microscopy (TEM) and dynamic light scattering (DLS) analysis were used for characterisation. In vitro, the hypoxia-reoxygenation model of H9c2 cells was employed to replicate in vivo cold I/R injury and treated with CoQ10@TNPs. The impact of CoQ10@TNPs on H9c2 cell injury was assessed by analysis of oxidative damage and apoptosis. In vivo, donor hearts (DHs) were perfused with preservation solution containing CoQ10@TNPs and stored in vitro at 4 °C for 12 h. The DHs were heterotopically transplanted and analysed for graft function, oxidative damage, apoptosis, and inflammatory markers 1 day post-transplantation. RESULTS: CoQ10@TNPs were successfully synthesized and delivered CoQ10 to the mitochondria of the cold ischaemic myocardium. In vitro experiments demonstrated that CoQ10@TNPs was taken up by H9c2 cells at 4 °C and localized within the mitochondria, thus ameliorating oxidative stress damage and mitochondrial injury in cold I/R injury. In vivo experiments showed that CoQ10@TNPs accumulated in DH tissue at 4 °C, localized within the mitochondria during cold storage and improved cardiac graft function by attenuating mitochondrial oxidative injury and inflammation. CONCLUSIONS: CoQ10@TNPs can precisely deliver CoQ10 to the mitochondria of cold I/R-injured cardiomyocytes to effectively eliminate mitochondrial reactive oxygen species (mtROS), thus reducing oxidative injury and inflammatory reactions in cold I/R-injured graft tissues and finally improving heart graft function. Thus, CoQ10@TNPs offer an effective approach for safeguarding cardiac grafts against extended periods of cold ischaemia, emphasizing the therapeutic potential in mitigating cold I/R injury during HT. These findings present an opportunity to enhance existing results following HT and broaden the range of viable grafts for transplantation.

Novel drug delivery strategies for antidepressant active ingredients from natural medicinal plants: the state of the art.

Depression is a severe mental disorder among public health issues. Researchers in the field of mental health and clinical psychiatrists have long been faced with difficulties in slow treatment cycles, high recurrence rates, and lagging efficacy. These obstacles have forced us to seek more advanced and effective treatments. Research has shown that novel drug delivery strategies for natural medicinal plants can effectively improve the utilization efficiency of the active molecules in these plants and therefore improve their efficacy. Currently, with the development of treatment technologies and the constant updating of novel drug delivery strategies, the addition of natural medicinal antidepressant therapy has given new significance to the study of depression treatment against the background of novel drug delivery systems. Based on this, this review comprehensively evaluates and analyses the research progress in novel drug delivery systems, including nanodrug delivery technology, in intervention research strategies for neurological diseases from the perspective of natural medicines for depression treatment. This provided a new theoretical foundation for the development and application of novel drug delivery strategies and drug delivery technologies in basic and clinical drug research fields.

Understanding the Plasmonic Effect of Enhanced Photodegradation with Au Nanoparticle Decorated ZnO Nanosheet Arrays under Visible Light Irradiation.

Plasmonic-enhanced photocatalysis using visible light is considered a promising strategy for pollution photodegradation. However, there is still a lack of comprehensive and quantitative understanding of the underlying mechanisms and interactions involved. In this study, we employed a two-step process to fabricate arrays of ZnO nanosheets decorated with Au nanoparticles (Au-ZnO NS). Various characterization techniques were used to examine the morphological, structural, and chemical properties of the fabricated Au-ZnO NS array. Furthermore, we systematically investigated the photocatalytic degradation of methyl orange under visible light irradiation using Au-ZnO NS arrays prepared with varying numbers of photochemical reduction cycles. The results indicated that as the number of photochemical reduction cycles increased, the photodegradation efficiency initially increased but subsequently decreased. Under visible light irradiation, the Au-ZnO NS array obtained via four cycles of photochemical reduction exhibits the highest photocatalytic degradation rate of methyl orange 0.00926 min-1, which is six times higher than that of the ZnO NS array. To gain a better understanding of the plasmonic effect on photodegradation performance, we utilized electromagnetic simulations to quantitatively investigate the enhancement of electric fields in the Au-ZnO NS array. The simulations clearly presented the nonlinear dependencies of electric field intensity on the distribution of Au nanoparticles and the wavelength of radiation light, leading to a nonlinear enhancement of hot electron injection and eventual plasmonic photodegradation. The simulated model, corresponding to four cycles of photochemical reduction, exhibits the highest electric field intensity at 550 nm, which can be attributed to its strong plasmonic effect. This work provides mechanistic insights into plasmonic photocatalysts for utilizing visible light and represents a promising strategy for the rational design of high-performance visible light photocatalysts.

Chitosan nanoparticles encapsulated with BEZ235 prevent acute rejection in mouse heart transplantation.

Acute rejection may manifest following heart transplantation, despite the implementation of relatively well-established immunosuppression protocols. The significance of the mTOR signaling pathway in rejection is widely acknowledged. BEZ235, a second-generation mTOR inhibitor with dual inhibitory effects on PI3K and mTOR, holds promise for clinical applications. This study developed a nanodelivery system, BEZ235@NP, to facilitate the intracellular delivery of BEZ235, which enhances efficacy and reduces adverse effects by improving the poor solubility of BEZ235. In the complete MHCII-mismatched model, BEZ235@NP significantly prolonged cardiac allografts survival compared to free BEZ235, which was attributed to more effective suppression of effector T cell activation and promotion of greater expansion of Tregs. These nanoparticles demonstrated excellent biosafety and exhibited no short-term biotoxicity upon investigation. To elucidate the mechanism, primary T cells were isolated from the spleen and it was observed that BEZ235@NP treatment resulted in the arrest of these cells in the G0/G1 phase. As indicated by Western blot analysis, BEZ235@NP substantially reduced mTOR phosphorylation. This, in turn, suppressed downstream pathways and ultimately exerted an anti-proliferative and anti-activating effect on cells. Furthermore, it was observed that inhibition of the mTOR pathway stimulated T-cell autophagy. In conclusion, the strategy of intracellular delivery of BEZ235 presents promising applications for the treatment of acute rejection.

Reexamining the Causes and Effects of Cholesterol Deposition in the Brains of Patients with Alzheimer's Disease.

Alzheimer's disease (AD) is a degenerative disease of the central nervous system. Numerous studies have shown that imbalances in cholesterol homeostasis in the brains of AD patients precede the onset of clinical symptoms. In addition, cholesterol deposition has been observed in the brains of AD patients even though peripheral cholesterol does not enter the brain through the blood‒brain barrier (BBB). Studies have demonstrated that cholesterol metabolism in the brain is associated with many pathological conditions, such as amyloid beta (Aß) production, Tau protein phosphorylation, oxidative stress, and inflammation. In 2022, some scholars put forward a new hypothesis of AD: the disease involves lipid invasion and its exacerbation of the abnormal metabolism of cholesterol in the brain. In this review, by discussing the latest research progress, the causes and effects of cholesterol retention in the brains of AD patients are analyzed and discussed. Additionally, the possible mechanism through which AD may be improved by targeting cholesterol is described. Finally, we propose that improving the impairments in cholesterol removal observed in the brains of AD patients, instead of further reducing the already impaired cholesterol synthesis in the brain, may be the key to preventing cholesterol deposition and improving the corresponding pathological symptoms.

Trends and treatments of pelvic and acetabular fractures in Taiwan: facing an aging society.

Pelvic-acetabular fractures lead to high mortality in elders and their association between different groups is not known. Our results indicate that older age with pelvic-acetabular fracture was significantly associated with mortality. This finding may help planning and allocating healthcare resources, risk stratification, and optimizing the treatment of pelvic fractures. PURPOSE: Pelvic or acetabular fractures are among main outcomes of low-energy trauma such as falls, especially in older adults. They represent approximately 3-8% of all fractures and are associated with a high mortality rate ranging from 4 to 28%. This study is aimed at comparing the incidence and trends of hip fractures and pelvic-acetabular fractures in the Taiwanese general population, gender differences in adults aged over 65 years, and mortality risk between pelvic or acetabular fractures and hip fractures and surgery trends in patients with these fractures. METHODS: A retrospective study was conducted extracting data from the National Health Insurance Research Database of patients diagnosed with hip fracture and pelvic acetabular fracture between 2000 and 2018. RESULTS: Older age with pelvic-acetabular fracture was significantly associated with increased mortality. No significant differences were found in comorbidities between the two fracture groups. Results provide clear epidemiological evidence for trends in pelvic-acetabular fractures in Taiwan and demonstrate the need for better strategies to manage these fractures and comorbidities, particularly in older adults. CONCLUSION: Findings of this study may aid in planning and allocating healthcare resources, risk stratification, and optimizing the treatment of pelvic fractures among older adults in Taiwan.

Complete Intradural Interbody Cage Migration in Lumbar Spine Surgery: A Case Report and Literature Review.

Background: Spinal fusion is a common surgery, in which vertebrae are fused to restore spinal stability and eliminate pain during movement. The use of an interbody cage facilitates spinal fusion. However, complete cage migration into the dura matter rarely occurs and can be challenging to manage. Case Presentation: A 44-year-old man presented at our spine center with a history of incomplete paraplegia and cauda equina syndrome that had lasted for 2 years and 4 months. This condition developed after he underwent six lumbar spine surgeries to address lower back pain and right-sided sciatica. A structural allograft kidney-shaped cage was found completely within the dura at the level of the L3 vertebra. Durotomy, cage retrieval, and pedicle screw fixation from the L2 to L4 vertebrae were performed. Numbness in both lower limbs markedly decreased within several days of the operation. After four months following the progressive physical therapy, the patient could partially control both urination and defecation. Five months postoperatively, he could stand with slight assistance. Conclusions: Complete intradural cage migration is a rare and serious complication. To the best of our knowledge, this is the first reported case with such a condition in the literature. Even if treatment is delayed, surgical intervention may salvage the remaining neurologic function and may even lead to partial recovery.

Glut10 restrains neointima formation by promoting SMCs mtDNA demethylation and improving mitochondrial function.

Neointimal hyperplasia is a major clinical complication of coronary artery bypass graft and percutaneous coronary intervention. Smooth muscle cells (SMCs) play a vital roles in neointimal hyperplasia development and undergo complex phenotype switching. Previous studies have linked glucose transporter member 10(Glut10) to the phenotypic transformation of SMCs. In this research, we reported that Glut10 helps maintain the contractile phenotype of SMCs. The Glut10-TET2/3 signaling axis can arrest neointimal hyperplasia progression by improving mitochondrial function via promotion of mtDNA demethylation in SMCs. Glut10 is significantly downregulated in both human and mouse restenotic arteries. Global Glut10 deletion or SMC-specific Glut10 ablation in the carotid artery of mice accelerated neointimal hyperplasia, while Glut10 overexpression in the carotid artery triggered the opposite effects. All of these changes were accompanied by a significant increase in vascular SMCs migration and proliferation. Mechanistically, Glut10 is expressed primarily in the mitochondria after platelet-derived growth factor-BB (PDGF-BB) treatment. Glut10 ablation induced a reduction in ascorbic acid (VitC) concentrations in mitochondria and mitochondrial DNA (mtDNA) hypermethylation by decreasing the activity and expression of the Ten-eleven translocation (TET) protein family. We also observed that Glut10 deficiency aggravated mitochondrial dysfunction and decreased the adenosinetriphosphate (ATP) content and the oxygen consumption rate, which also caused SMCs to switch their phenotype from contractile to synthetic phenotype. Furthermore, mitochondria-specific TET family inhibition partially reversed these effects. These results suggested that Glut10 helps maintain the contractile phenotype of SMCs. The Glut10-TET2/3 signaling axis can arrest neointimal hyperplasia progression by improving mitochondrial function via the promotion of mtDNA demethylation in SMCs.

Morphological Control of Supported ZnO Nanosheet Arrays and Their Application in Photodegradation of Organic Pollutants.

Supported nanostructured photocatalysis is considered to be a sustainable and promising method for water pollution photodegradation applications due to its fascinating features, including a high surface area, stability against aggregation, and easy handling and recovery. However, the preparation and morphological control of the supported nanostructured photocatalyst remains a challenge. Herein, a one-step hydrothermal method is proposed to fabricate the supported vertically aligned ZnO nanosheet arrays based on aluminum foil. The morphologically controlled growth of the supported ZnO nanosheet arrays on a large scale was achieved, and the effects of hydrothermal temperature on morphologic, structural, optical, and photocatalytic properties were observed. The results reveal that the surface area and thickness of the nanosheet increase simultaneously with the increase in the hydrothermal temperature. The increase in the surface area enhances the photocatalytic activity by providing more active sites, while the increase in the thickness reduces the charge transfer and thus decreases the photocatalytic activity. The influence competition between the area increasing and thickness increasing of the ZnO nanosheet results in the nonlinear dependence between photocatalytic activity and hydrothermal temperature. By optimizing the hydrothermal growth temperature, as fabricated and supported ZnO nanosheet arrays grown at 110 °C have struck a balance between the increase in surface area and thickness, it exhibits efficient photodegradation, facile fabrication, high recyclability, and improved durability. The RhB photodegradation efficiency of optimized and grown ZnO nanosheet arrays increased by more than four times that of the unoptimized structure. With 10 cm2 of as-fabricated ZnO nanosheet arrays, the degradation ratio of 10 mg/L MO, MB, OFL, and NOR was 85%, 51%, 58%, and 71% under UV irradiation (365 nm, 20 mW/cm2) for 60 min. All the target pollutant solutions were almost completely degraded under UV irradiation for 180 min. This work offers a facile way for the fabrication and morphological control of the supported nanostructured photocatalyst with excellent photodegradation properties and has significant implications in the practical application of the supported nanostructured photocatalyst for water pollution photodegradation.

Research progress on the circRNA­mediated regulation of tumor angiogenesis through ceRNA mechanisms (Review).

Tumors are one of the most common fatal diseases worldwide and pose a severe threat to human health. Effective tumor prevention and treatment strategies are persistent challenges in the medical community. Angiogenesis plays a critical role in and is the basis for tumor development and metastasis. Circular RNAs (circRNAs) are novel single­stranded covalently closed RNA molecules that are widely expressed in tumors due to their structural specificity and conservation. circRNAs affect angiogenesis by functioning as microRNA sponges to regulate vascular endothelial growth factor­related pathways, thereby participating in various stages of tumor growth, invasion and proliferation. The present review summarizes the involvement of circRNAs in the regulation of tumor angiogenesis through competing endogenous RNA mechanisms, with a particular focus on the regulatory role of circRNAs in tumor angiogenesis in various systems. It is considered that circRNAs have great potential for use as tumor diagnostic markers and anti­angiogenic therapies, and are thus worthy of further research and exploration.

Lymph-Node-Targeted Drug Delivery for Effective Immunomodulation to Prolong the Long-Term Survival After Heart Transplantation.

The chronic rejection responses and side effects of the systematic administration of immunosuppressants are the main obstacles to heart allograft and patient survival. The development of xenotransplantation also urgently requires more efficient immune regulation strategies. Herein, it is demonstrated that lymph-node (LN)-targeted drug delivery can realize LN-specific immunomodulation with attenuated immune suppression on distant peripheral immune organs to effectively prolong long-term survival after heart transplantation in a chronic murine heart transplantation model. A chemokine C-C motif ligand 21 (CCL21) specific aptamer for LN targeting is decorated onto the surface of the hybrid nanoparticular delivery vector mainly composed of CaCO3 /CaP/heparin. The targeting delivery system can dramatically enhance accumulation of the loaded immunosuppressant, fingolimod hydrochloride (FTY720), in draining lymph nodes (dLNs) for inducing powerful immune suppression. By promoting the generation of endogenous regulatory T cells (Tregs ) and decreasing the proportion of effector T cells (Teffs ) in dLNs after heart transplantation, the LN-targeting strategy can effectively regulate local immune responses instead of systemic immunity, which reduces the incidence of long-term complications. This study provides an efficient strategy to improve the survival rate after organ transplantation by precise and localized immunoregulation with minimized side effects of immunosuppression.