Intervertebral disc degeneration (IVDD) is a major reason for low back pain. Inflammation and oxidative stress are key drivers for initiating and progressing IVDD, triggering extracellular matrix (ECM) degradation and inducing the apoptosis of nucleus pulposus cells. However, effective treatment modalities targeting the harsh and degenerative nature of the intervertebral disc are lacking. Herein, we prepared an advanced multifunctional injectable bimetallic metal-organic framework (MOF)-loaded OHA@PA@Fe@QCS (OPQ) hydrogel (OPQ@MOFs) to alleviate IVDD. The bimetallic MOF nanozymes exhibited potent antioxidant enzyme-like activity, counteracting oxidative stress and normalizing the redox equilibrium. The hydrogel OPQ exhibited injectability, biodegradability, favorable biocompatibility, and antibacterial and hemostatic capabilities, working collectively to synergistically enhance the therapeutic efficacy of MOFs. In vitro studies revealed that OPQ@MOFs can alleviate oxidative stress, decrease inflammatory responses, and prevent abnormal ECM degradation. RNA sequencing revealed that its underlying mechanism was associated with the PPAR gamma signaling pathway. In vivo experiments validated that OPQ@MOFs facilitated ECM regeneration, preserved the morphological and structural integrity of the nucleus pulposus, and alleviated IVDD. Collectively, these results suggest the substantial potential of the bimetallic MOFs-loaded hydrogel in treating IVDD.

The high retear rate post tendon-bone reconstructive surgery is attributed to scar tissue replacing fibrocartilage, which compromises mechanical properties. Macrophages play a pivotal role in this process. Bone marrow mesenchymal stem cells-derived exosome (BMSCs-Exo) have emerged as a promising biological therapeutic approach. However, their role and underlying mechanisms in regulating macrophage polarization and tendon-bone healing require further investigation. Primary macrophages were cultured, and a rat Achilles tendon-calcaneus reconstruction model was established, followed by BMSCs-Exo treatment. Exosome diameter was analyzed by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). Macrophage polarization was assessed via flow cytometry and immunofluorescence. ELISA measured cytokine levels, and immunohistochemistry evaluated molecular expression and distribution. Apoptosis levels were analyzed using TUNEL staining, and HE as well as Safranin O-Fast Green staining were utilized to examine tissue morphology and fibrocartilage regeneration at the tendon-bone junction. Biomechanical testing was used to assess joint stability. Western blot assessed molecular expression, while circRNA-seq was conducted to explore the impact of BMSCs-Exo on circRNA expression profiles in tendon-bone junction macrophages. qRT-PCR quantified circRNA and linear RNA levels, and fluorescence in situ hybridization (FISH) was used to observe circRNA expression and localization. We isolated BMSCs-Exo and discovered its ability to promote macrophage polarization from M1 to M2 both in vitro and in vivo. This polarization was accompanied by a decrease in pro-inflammatory cytokines IL-1β and IL-12, and an increase in anti-inflammatory cytokines TGF-β1 and IL-10. Additionally, BMSCs-Exo significantly enhanced tendon-bone healing, improved the tissue morphology at the tendon-bone junction, increased chondrocyte and fibrocartilage formation, upregulated the expression of collagen I, Aggrecan, and collagen II, improved joint stability. However, macrophage depletion using Clodronate liposomes (CL) effectively inhibited the therapeutic effects of BMSCs-Exo. Mechanistic studies revealed that BMSCs-Exo transfers circRNA1052 to macrophages, driving their polarization from M1 to M2, thereby mitigating early inflammatory responses and enhancing tissue repair during later stages, ultimately facilitating tendon-bone healing. Furthermore, downregulation of circRNA1052 expression attenuated the beneficial effects of BMSCs-Exo. BMSCs-Exo transfer circRNA1052 to macrophages, suppressing their pro-inflammatory phenotype and promoting polarization toward the tissue-repairing M2 phenotype. This process enhances fibrocartilage formation, improves tissue morphology, and accelerates tendon-bone healing.

BACKGROUND:Postmenopausal osteoporosis (PMOP) necessitates novel therapeutics with defined targets. Rehmannioside D (RD), a bioactive compound from Rehmannia glutinosa, exhibits anti-inflammatory properties, yet its anti-osteoporotic mechanism remains unclear. PURPOSE:This study integrated network pharmacology with experimental validation to elucidate the efficacy and mechanism of RD in suppressing osteoclastogenesis. METHODS:Potential targets were screened via network pharmacology. In vitro, the effects of RD on RANKL-induced osteoclast differentiation and function were assessed in bone marrow-derived macrophages (BMDMs). Target interaction was verified using Cellular Thermal Shift Assay (CETSA), molecular docking, and Co-IP. In vivo, osteoprotective efficacy was evaluated in ovariectomized (OVX) mice. RESULTS:Network analysis highlighted c-Jun and c-Fos as core targets. In vitro, RD significantly inhibited osteoclastogenesis and resorptive function without cytotoxicity. Mechanistically, RD exerted a dual inhibitory effect: It suppressed the activation of MAPK and NF-κB signaling pathways, thereby downregulating NFATc1 expression and inhibiting osteoclast differentiation; Distinctly, RD was identified to interact with and stabilize to c-Jun, sterically hindering its heterodimerization with c-Fos to dismantle the AP-1 complex. This disruption of AP-1 subsequently triggered intrinsic apoptosis, evidenced by an elevated Bax/Bcl-2 ratio and Caspase-3 cleavage. In vivo, RD prevented trabecular bone loss and preserved microarchitecture in OVX mice by reducing osteoclast numbers. CONCLUSION:RD attenuates bone loss via a dual mechanism: it inhibits osteoclast differentiation by suppressing MAPK/NF-κB signaling and simultaneously induces mature osteoclast apoptosis by targeting c-Jun to disrupt the AP-1 complex.

Postoperative fatigue syndrome (POFS) comprises symptoms including fatigue, insomnia, inattention, depression, tension, and anxiety following surgery. These manifestations encompass exhaustion, weakness, malaise, and emotional disturbances, impacting hospital stay duration, quality of life, rehabilitation progress, and work performance. While the etiology of POFS remains complex, recent evidence suggests that external stimuli may induce pro-inflammatory cytokine release, leading to fatigue. Surgical procedures trigger an inflammatory reaction that stimulates the nervous system, generating fatigue symptoms. Both animal and human studies demonstrate that vagus nerve stimulation (VNS) can reduce pro-inflammatory cytokine production by activating the cholinergic anti-inflammatory pathway (CAP). Considering the pivotal role of inflammation in the development of POFS and the vagus nerve's capacity to modulate inflammatory responses, we hypothesize that transcutaneous auricular vagus nerve stimulation (taVNS) holds significant potential for alleviating POFS in elderly patients undergoing colorectal cancer surgery. In this paper, we propose a hypothetical scheme to validate this hypothesis through the application of taVNS in future clinical studies.

BACKGROUND:The quadratus lumborum block at the lateral supra-arcuate ligament (QLB-LSAL) is a recent development in the field of regional anaesthetic techniques, offering several advantages over the traditional quadratus lumborum block. However, most current studies on this topic are single-centre and small-sample studies, which may limit the evaluation of the efficacy and safety of this block method. METHODS:This protocol adopts the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. This evaluation aims to assess the efficacy and safety of QLB-LSAL for postoperative analgesia. The primary outcome is the total consumption of opioid morphine equivalents within 24 h post-surgery. Secondary outcomes comprised numerical rating scale (NRS) pain scores within 24 h postoperatively, Quality of Recovery-15 (QoR-15) scores, patient satisfaction scores, opioid-related side effect incidence and block-related adverse events. This study will only include randomized clinical trials. We will conduct electronic database searches based on the established search strategy. The two review authors will independently screen the literature, extract data and use the Cochrane Risk of Bias 2 tool to assess the risk of bias. We will conduct a meta-analysis on the extracted data and assess the risk of bias for each study. We will also conduct trial sequential analysis, sensitivity analysis and subgroup analysis and assess the overall risk of publication bias. Finally, the GRADE guidelines will be used to assess the certainty of the evidence. DISCUSSION:The latest systematic review methodology will be used to assess the efficacy and safety of QLB-LSAL for the treatment of postoperative pain. The findings are expected to provide valuable insights for clinicians to apply QLB-LSAL in the management of postoperative analgesia.

Background Postmenopausal Osteoporosis (PMOP) is an estrogen-deficiency disorder that leads to impaired bone remodeling and a higher incidence of fractures. Liquiritin, a flavonoid from Glycyrrhiza uralensis, has documented bioactivities but previously unexplored potential for PMOP treatment. Purpose To investigate liquiritin's therapeutic effects on PMOP and its underlying mechanisms, constituting the first comprehensive investigation of its role in osteoclasts regulation and apoptosis induction within PMOP pathophysiology. Methods Network pharmacology was employed to predict potential targets of Liquiritin in PMOP. The CCK-8 assay assessed its effect on bone marrow-derived macrophages (BMDMs) viability. RANKL was used to induce BMDMs differentiation into mature osteoclasts. TRAcP and F-actin staining detected osteoclasts formation; bone resorption assays evaluated functionality. Western blotting and immunofluorescence were applied to evaluate osteoclasts-related proteins, MAPK/NF-κB pathway activity, and apoptosis. Notably, molecular docking predicted Liquiritin’s binding to PPARγ, validated by CETSA. An OVX-induced PMOP mouse model was constructed in vivo; bone microarchitecture and osteoclasts activity were evaluated using micro-CT, H&E, and TRAcP staining. Results Liquiritin suppressed osteoclasts formation and bone resorption in vitroand mitigated bone loss in vivo by downregulating osteoclasts-specific genes, inhibiting MAPK/NF-κB pathways, and most importantly, inducing PPARγ-mediated apoptosis—a novel mechanistic insight not previously reported. Conclusion Liquiritin exerts anti-osteoporotic effects by targeting Osteoclastogenesis, inducing apoptosis, and inhibiting bone resorption via PPARγ activation, highlighting its novel therapeutic potential for PMOP treatment.

Mitochondria orchestrate the production of new mitochondria and the removal of damaged ones to dynamically maintain mitochondrial homeostasis through constant biogenesis and clearance mechanisms. Mitochondrial quality control particularly relies on mitophagy, defined as selective autophagy with mitochondria-targeting specificity. Most ROS are derived from mitochondria, and the physiological concentration of mitochondrial ROS (mtROS) is no longer considered a useless by-product, as it has been proven to participate in immune and autophagy pathway regulation. However, excessive mtROS appears to be a pathogenic factor in several diseases, including acute lung injury (ALI). The interplay between mitophagy and mtROS is complex and closely related to ALI. Here, we review the pathways of mitophagy, the intricate relationship between mitophagy and mtROS, the role of mtROS in the pathogenesis of ALI, and their effects and related progression in ALI induced by different conditions.

BackgroundOsteosarcoma is the most prevalent malignant bone tumour with a poor prognosis. Shikonin (SHK) is derived from the traditional Chinese medicine Lithospermum that has been extensively studied for its notable anti-tumour effects, including for osteosarcoma. However, its application has certain limitations. Valproic acid (VPA) is a histone deacetylase inhibitor (HDACI) that has recently been employed as an adjunctive therapeutic agent that allows chromatin to assume a more relaxed state, thereby enhancing anti-tumour efficacy.PurposeThis study was aimed to investigate the synergistic anti-tumour efficacy of SHK in combination with VPA and elucidate its underlying mechanism.Methods/Study designCCK-8 assays were utilized to calculate the combination index. Additional assays, including colony formation, acridine orange/ethidium bromide double fluorescent staining, and flow cytometry, were employed to evaluate the effects on osteosarcoma cells. Wound healing and transwell assays were utilized to assess cell mobility. RNA sequencing, PCR, and Western blot analyses were conducted to uncover the underlying mechanism. Rescue experiments were performed to validate the mechanism of apoptotic induction. The impact of SHK and VPA combination treatment on primary osteosarcoma cells was also assessed. Finally, in vivo experiments were conducted to validate its anti-tumour effects and mechanism.ResultsThe combination of SHK and VPA synergistically inhibited the proliferation and migration of osteosarcoma cells in vitro and induced apoptosis in these cells. Through a comprehensive analysis involving RNA sequencing, PCR, Western blot, and rescue experiments, we have substantiated our hypothesis that the combination of SHK and VPA induced apoptosis via the ROS-EGR1-Bax axis. Importantly, our in vivo experiments corroborated these findings, demonstrating the potential of the SHK and VPA combination as a promising therapeutic approach for osteosarcoma.ConclusionThe combination of SHK and VPA exerted an anti-tumour effect by inducing apoptosis through the ROS-EGR1-Bax pathway. Repurposing the old drug VPA demonstrated its effectiveness as an adjunctive therapeutic agent for SHK, enhancing its anti-tumour efficacy and revealing its potential value. Furthermore, our study expanded the application of natural compounds in the anti-tumour field and overcame some of their limitations through combination therapy. Finally, we enhanced the understanding of the mechanistic pathways linking reactive oxygen species (ROS) accumulation and apoptosis in osteosarcoma cells. Additionally, we elucidated the role of EGR1 in osteosarcoma cells, offering novel strategies and concepts for the treatment of osteosarcoma.

Larotaxel (LTX) and SB-T-1214 (SBT), two new synthetic experimental toxoids, have shown broad-spectrum antitumor activity, especially against tumors that are resistant to other drugs. However, their poor solubility, membrane permeability, and first-pass effect limits their use in oral administration. We designed and synthesized two long-chain triglyceride-mimic prodrugs of LTX (LTXSSTG) and SBT (SBTSSTG), which are bridged by disulfide bonds and efficiently incorporated them into Self-nanoemulsifying drug delivery system (SNEDDS). These prodrugs can bypass hepatic metabolism by entering the blood through intestinal lymphatic transport, following a similar oral absorption pathway to dietary lipids. It was found that LTXSSTG and SBTSSTG significantly improved oral bioavailability (about 4.5-fold for LTX and 3.4-fold for SBT) compared to their solution forms. Moreover, with LTXSSTG and SBTSSTG incorporating reduction stimulus-responsive spacer were much more effective in suppressing tumor growth in vivo with eliminated adverse effects than solution form. To sum up, this strategy provides a new avenue to enhance oral delivery of new toxoids.

Background: Craniocerebral interventional surgery is a common and essential treatment for cerebrovascular diseases. Despite continuous progress in interventional diagnosis and treatment technology, there is no effective method to alleviate contrast-induced kidney injuries. In this retrospective cohort study, we investigated the effect of the concurrent use of Dexmedetomidine (DEX) during the perioperative period on the renal function of patients following craniocerebral interventional surgery. Methods: We identified 228 cases of patients underwent craniocerebral interventional surgery from January 2018 to March 2022. Patients who used DEX during general anesthesia were in the DEX group (DEX group) or that did not use dexmedetomidine as the control group (CON group). The markers of kidney injury were recorded before and within 48 h after surgery. Results: Compared with CON group, the urea nitrogen (BUN) of the DEX group decreased significantly on the first day and the second day after surgery (p < 0.05). The serum cystatin-C and the blood urea nitrogen/creatinine ratio (BUN/Cr) was significantly lower than that in CON group on the second day (p < 0.05). The urine output in the DEX group increased significantly, and the mean arterial pressure (MAP) was higher than the CON group (p < 0.01). There was no difference in postoperative complications, ICU stay time and hospitalization time between the two groups. Conclusion: The combined use of dexmedetomidine in general anesthesia for craniocerebral interventional surgery can reduce BUN levels within 48 h after surgery, significantly increase intraoperative urine volume, maintain intraoperative circulation stability.

Adoptive cellular therapy is a promising strategy for cancer treatment. However, the effectiveness of this therapy is limited by its intricate and immunosuppressive tumor microenvironment. In this study, a targeted therapeutic strategy for macrophage loading of drugs is presented to enhance anti-tumor efficacy of macrophages. K7M2-target peptide (KTP) is used to modify macrophages to enhance their affinity for tumors. Pexidartinib-loaded ZIF-8 nanoparticles (P@ZIF-8) are loaded into macrophages to synergistically alleviate the immunosuppressive tumor microenvironment synergistically. Thus, the M1 macrophages decorated with KTP carried P@ZIF-8 and are named P@ZIF/M1-KTP. The tumor volumes in the P@ZIF/M1-KTP group are significantly smaller than those in the other groups, indicating that P@ZIF/M1-KTP exhibited enhanced anti-tumor efficacy. Mechanistically, an increased ratio of CD4+ T cells and a decreased ratio of MDSCs in the tumor tissues after treatment with P@ZIF/M1-KTP indicated that it can alleviate the immunosuppressive tumor microenvironment. RNA-seq further confirms the enhanced immune cell function. Consequently, P@ZIF/M1-KTP has great potential as a novel adoptive cellular therapeutic strategy for tumors.

Osteoporosis is a systemic bone metabolic disorder that plagues the health and quality of life of the elderly. Autophagy plays an important role in bone formation while maintaining the homeostasis of the body. Trehalose is a mTOR-independent autophagy inducer, but to the best of our knowledge, there is no rat model of postmenopausal osteoporosis. The present study found that trehalose can delay postmenopausal osteoporosis in rats, which may be achieved by inducing and enhancing AKT/transcription factor EB pathway-dependent autophagy flow. The specific mechanism of its occurrence needs to be further studied. Trehalose-containing drugs are promising for delaying postmenopausal osteoporosis. Hematoxylin and eosin (H&E) staining, western blotting, micro computerized tomography (CT) scanning and Transmission electron microscopy were used to investigate the role of trehalose in postmenopausal osteoporosis rat model at protein, cell and histology aspects. According to the H&E staining results, the bone trabecular histological structure of the trehalose group was superior to that of the model group. The Micro CT scanning indicated the imaging structure of bone trabeculae in the trehalose group was superior to than that in the model group. Western blotting indicated the activation of autophagic flow in trehalose group, the autophagy degree of the trehalose group is greater than that of the model group; Transmission electron microscopy indicated the autophagy degree of the Trehalose group was greater than that of the model group under electron microscopy. Trehalose can delay postmenopausal osteoporosis in rats, which may be achieved by inducing and enhancing Akt/TFEB pathway-dependent autophagy flow.

The imbalance of bone homeostasis is the root cause of osteoporosis. However current therapeutic approaches mainly focus on either anabolic or catabolic pathways, which often fail to turn the imbalanced bone metabolism around. Herein we reported that a SIRT-1 agonist mediated molecular therapeutic strategy to reverse the imbalance in bone homeostasis by simultaneously regulating osteogenesis and osteoclastogenesis via locally sustained release of SRT2104 from mineral coated acellular matrix microparticles. Immobilization of SRT2104 on mineral coating (MAM/SRT) harnessing their electrostatic interactions resulted in sustained release of SIRT-1 agonist for over 30 days. MAM/SRT not only enhanced osteogenic differentiation and mineralization, but also attenuated the formation and function of excessive osteoclasts via integrating multiple vital upstream signals (β-catenin, FoxOs, Runx2, NFATc1, etc.) in vitro. Osteoporosis animal model also validated that it accelerated osteoporotic bone healing and improved osseointegration of the surrounding bone. Overall, our work proposes a promising strategy to treat osteoporotic bone defects by reversing the imbalance in bone homeostasis using designated small molecule drug delivery systems.

Background: miR-584-5p is a critical regulator in the progression of multiple cancers. However, its specific role and downstream targets in osteosarcoma are unclear. This research aimed to investigate the roles and underlying mechanisms of miR-769-5p and hippo pathway in osteosarcoma cells. Materials and Methods: RT-qPCR, CCK-8 and EdU and colony formation, wound-healing and transwell chamber, flow cytometry, and Western blot assay detected the expression of miR-584-5p and CTGF, cell proliferation, migration, invasion apoptosis and protein expression. Result: Their study illuminated that miR-584-5p overexpression repressed osteosarcoma cell migration/invasion and proliferation and facilitated apoptosis. Mechanistically, miR-584-5p targets negatively regulated connective tissue growth factor (CTGF). miR-584-5p inhibited osteosarcoma cell metastasis by regulating CTGF. In addition, miR-584-5p inactivated Hippo pathway through CTGF in osteosarcoma. Conclusion: miR-584-5p inhibits osteosarcoma cell proliferation, migration, and invasion and promotes apoptosis by targeting CTGF, indicating that miR-584-5p acts as a promising diagnostic and predictive biomarker for osteosarcoma.

Osteosarcoma has a relatively high incidence rate among primary malignant tumors, and the survival rate is low. Clinically, surgical resection and chemotherapy are mainly used, which are difficult to utilize to treat metastatic or recurrent osteosarcoma. The combination of chemotherapy and immuno-therapy can achieve a better tumor treatment effect. M1 macrophages (M1 Mo) can kill tumor cells and have tumor-targeting and phagocytosis ability, which are an ideal tool for tumor-targeted drug delivery. However, as carriers, living cells have the disadvantages of uncontrollable size, poor tissue permeability, and poor stability. In this study, the M1 macrophage membrane (M1M) was used as the carrier and loaded with MMP-2 (matrix metalloproteinase-2)-sensitive drug-loaded liposomes (GL) to prepare a complex nanovesicle drug delivery system M1M (GL/DOX/TPI-1), with a tumor active targeting function, for combined chemical and immune therapy from doxorubicin (DOX) and tyrosine phosphatase inhibitor 1 (TPI-1). The complex nanovesicles not only retain the tumor-targeting ability from the M1 macrophage membrane but also have the advantages of controllable size, responsive drug release, and high stability. The results of in vivo efficacy test show that the drug delivery system realizes active targeted enrichment in osteosarcoma tissue. Under the response of MMP-2, the internally encapsulated antitumor drugs DOX and TPI-1 from the system are released. This drug delivery system combined with chemical and immune treatment can effectively achieve the aim of the treatment of osteosarcoma.

Post-fracture osteolysis of the pubic bone is a rare entity characterized by destructive changes in the pubic bone. We report a case of a 70-year-old woman who presented with a four-month history of left-sided groin pain radiating to the left hip. The radiographs showed osteolysis of the left superior pubic ramus, mimicking a malignant lesion. Histological examination showed no evidence of malignancy. After eight weeks of conservative treatment, the pain was significantly relieved. Post-fracture osteolysis may simulate malignancy; physicians should be aware of that to avoid unnecessary invasive procedures.

Target therapy for highly heterogeneous cancers represents a major clinical challenge due to the lack of recurrent therapeutic targets identified in these tumors. Herein, the authors report a tumor-customized targeting photothermal therapy (PTT) strategy for highly heterogeneous cancers, by which 2D supramolecular self-assembled nanodiscs are modified with tumor-specific binding peptides identified by phage display techniques. Taking osteosarcoma (OS) as a model heterogeneous cancer, an OS targeting peptide (OTP) is first selected after biopanning and is demonstrated to successfully bind to this heterogeneous cancer cells/tissues. Successful conjugation of OTP to heptamethine cyanine (Cy7)-based 2D nanodiscs Cy7-TCF (2-dicyanomethylene-3-cyano-4,5,5-trimethyl-2,5-dihydrofuran,TCF) enables the 2D nanodiscs to specifically target the heterogeneous tumor. Notably, a single dose injection of this targeted nanodisc (T-ND) not only effectively induces enhanced photothermal tumor ablation under near-infrared light, but also exhibits sevenfold increase of tumor retention time (more than 24 days) compared to generic nanomedicine. Thus, the authors' findings suggest that the combination of phage display-based affinity peptides selection and 2D supramolecular nanodiscs leads to the development of a platform technology for highly heterogeneous cancers precise therapy, offering specific tumor targeting, ultralong tumor retention, and precise PTT.

Photothermal Therapy In article number 2200179, Xuesheng Jiang, Xiaohua Yu, Zhaoming Ye, and co-workers introduce a strategy of precise photothermal therapy for highly heterogenous cancers by a tumor-customized 2D supramolecular nanodisc (T-ND). By modifying Cy7-TCF crystal with phage display derived tumor-customized binding peptides, T-ND shows excellent photothermal efficacy to ablate the tumor and achieves ultralong retention time of more than 24 days in the “off-target” tumor site.

Background The anatomic and biomechanical aspects of the L5-S1 level present unique operative challenges compared with the L4-L5 level. We aim to explore the clinical outcomes and radiographic measurements of L4-L5 patients compared with L5-S1 patients after undergoing Percutaneous Endoscopic Transforaminal Discectomy with Foraminoplasty (PETDF). Methods A total of 84 patients who underwent PETDF for LDH treatment between January 2017 and June 2020 were included in this study. Preoperative, perioperative, demographic data, clinical and radiographic outcomes were compared between patients with L4-L5 involvement and patients with L5-S1 involvement. Results There were no significant differences between the two groups in terms of Age, Gender, Follow-up time, the postoperative questionnaire results (Visual Analog Scale [leg], VAS [lower back], and Oswestry Disability Index) or the Excellence and Good Rate and Recurrence Rate. There was no significant difference in the mean preoperative to postoperative change in Intervertebral Space Height (ISH), Intervertebral Space Angle (ISA), Lumbar Lordosis, Foraminal Area (FA) of Operating Side and FA of Contralateral Side between the 2 groups. The mean VAS of Leg Pain, VAS of Lower Back Pain and ODI postoperative scores were significantly improved over the preoperative scores in each of the two groups and the ISH, ISA, FA of Operating Side and FA of Contralateral Side postoperative were significant difference form preoperative Conclusion PETDF is an effective and safe treatment approach for lumbar disc herniation in both L4/L5 and L5/S1 level. Although it may increase lumbar ISA and result in low CFA (contralateral foraminal area) and ISH.

Long non-coding RNAs refer to transcripts over 200 nt in length that lack the ability to encode proteins, which occupy the majority of the genome and play a crucial role in the occurrence and development of human diseases, especially cancers. SBF2-AS1, a newly identified long non-coding RNA, has been verified to be highly expressed in diversiform cancers, and is involved in processes promoting tumorigenesis, tumor progression and tumor metastasis. Moreover, upregulation of SBF2-AS1 expression was significantly related to disadvantageous clinicopathologic characteristics and indicated poor prognosis. In this review, we comprehensively summarize the up-to-date knowledge of the detailed mechanisms and underlying functions of SBF2-AS1 in diverse cancer types, highlighting the potential of SBF2-AS1 as a diagnostic and prognostic biomarker and even a therapeutic target.