Efficacy of PE-PLIF with a novel ULBD approach for lumbar degeneration diseases: a large-channel endoscopic retrospective study.

PURPOSE: This study aims to assess the effectiveness of Percutaneous Endoscopic Posterior Lumbar Interbody Fusion (PE-PLIF) combined with a novel Unilateral Laminotomy for Bilateral Decompression (ULBD) approach using a large-channel endoscope in treating Lumbar Degenerative Diseases (LDD). METHODS: This retrospective analysis evaluates 41 LDD patients treated with PE-PLIF and ULBD from January 2021 to June 2023. A novel ULBD approach, called 'Non-touch Over-Top' technique, was utilized in this study. We compared preoperative and postoperative metrics such as demographic data, Visual Analogue Scale (VAS) for pain, Oswestry Disability Index (ODI), Japanese Orthopedic Association (JOA) score, surgical details, and radiographic changes. RESULTS: The average follow-up duration was 14.41 ± 2.86 months. Notable improvements were observed postoperatively in VAS scores for back and leg pain (from 5.56 ± 0.20 and 6.95 ± 0.24 to 0.20 ± 0.06 and 0.12 ± 0.05), ODI (from 58.68 ± 0.80% to 8.10 ± 0.49%), and JOA scores (from 9.37 ± 0.37 to 25.07 ± 0.38). Radiographic measurements showed significant improvements in lumbar and segmental lordosis angles, disc height, and spinal canal area. A high fusion rate (97.56% at 6 months, 100% at 12 months) and a low cage subsidence rate (2.44%) were noted. CONCLUSIONS: PE-PLIF combined with the novel ULBD technique via a large-channel endoscope offers significant short-term benefits for LDD management. The procedure effectively expands spinal canal volume, decompresses nerve structures, improves lumbar alignment, and stabilizes the spine. Notably, it improves patients' quality of life and minimizes complications, highlighting its potential as a promising LDD treatment option.

ILC2s: Unraveling the innate immune orchestrators in allergic inflammation.

The prevalence rate of allergic diseases including asthma, atopic rhinitis (AR) and atopic dermatitis (AD) has been significantly increasing in recent decades due to environmental changes and social developments. With the study of innate lymphoid cells, the crucial role played by type 2 innate lymphoid cells (ILC2s) have been progressively unveiled in allergic diseases. ILC2s, which are a subset of innate lymphocytes initiate allergic responses. They respond swiftly during the onset of allergic reactions and produce type 2 cytokines, working in conjunction with T helper type 2 (Th2) cells to induce and sustain type 2 immune responses. The role of ILC2s represents an intriguing frontier in immunology; however, the intricate immune mechanisms of ILC2s in allergic responses remain relatively poorly understood. To gain a comphrehensive understanding of the research progress of ILC2, we summarize recent advances in ILC2s biology in pathologic allergic inflammation to inspire novel approaches for managing allergic diseases.

Involvement and repair of epithelial barrier dysfunction in allergic diseases.

The epithelial barrier serves as a critical defense mechanism separating the human body from the external environment, fulfilling both physical and immune functions. This barrier plays a pivotal role in shielding the body from environmental risk factors such as allergens, pathogens, and pollutants. However, since the 19th century, the escalating threats posed by environmental pollution, global warming, heightened usage of industrial chemical products, and alterations in biodiversity have contributed to a noteworthy surge in allergic disease incidences. Notably, allergic diseases frequently exhibit dysfunction in the epithelial barrier. The proposed epithelial barrier hypothesis introduces a novel avenue for the prevention and treatment of allergic diseases. Despite increased attention to the role of barrier dysfunction in allergic disease development, numerous questions persist regarding the mechanisms underlying the disruption of normal barrier function. Consequently, this review aims to provide a comprehensive overview of the epithelial barrier's role in allergic diseases, encompassing influencing factors, assessment techniques, and repair methodologies. By doing so, it seeks to present innovative strategies for the prevention and treatment of allergic diseases.

The efficacy and safety of ultrasonic bone scalpel for removing retrovertebral osteophytes in anterior cervical discectomy and fusion: A retrospective study.

In this study, we present a novel surgical method that utilizes the ultrasonic bone scalpel (UBS) for the removal of large retrovertebral osteophytes in anterior cervical discectomy and fusion (ACDF) and evaluate its safety and efficacy in comparison to the traditional approach of using high-speed drill (HSD). A total of 56 patients who underwent ACDF for retrovertebral osteophytes were selected. We recorded patients' baseline information, operation time, intraoperative blood loss, complications, JOA and VAS scores, and other relevant data. The mean operation time and the mean intraoperative blood loss in the UBS group were less than those in the HSD group (P < 0.05). Although both groups exhibited considerable improvements in JOA and VAS scores following surgery, there was no statistically significant difference between the two groups (P > 0.05). Additionally, no significant disparities were found in bone graft fusion between the two groups at 6- and 12-months postsurgery. Notably, neither group exhibited complications such as dura tear or spinal cord injury. Our study found that the use of UBS reduced operative time, minimized surgical bleeding, and led to clinical outcomes comparable to HSD in ACDF. This technique offers an effective and safe method of removing large retrovertebral osteophytes.

Long non-coding RNA ZMIZ1-AS1 promotes osteosarcoma progression by stabilization of ZMIZ1.

BACKGROUND: Osteosarcomas (OS) are frequent primary sarcomas of the bone in children and adolescents. The long non-coding RNAs (lncRNAs) can affect the progression of many cancers by their sense transcripts. The present study was designed to probe the role of ZMIZ1-AS1 and the downstream pathway in OS progression. METHODS: Cell proliferation, invasion, and migration were detected by colony formation, transwell, and wound healing assays. The binding of SOX2 or MYC protein with ZMIZ1-AS1 promoter was explored by ChIP assay and dual-luciferase reporter assay. Interaction between PTBP1 protein and ZMIZ1-AS1 (or ZMIZ1 mRNA) was detected by RIP assay. RESULTS: SOX2 and MYC are the downstream effectors of the Hippo pathway and transcriptionally activated ZMIZ1-AS1. Compared to the controls, OS tissues and cells contained higher ZMIZ1-AS1 expression. Silencing of ZMIZ1-AS1 repressed OS cell viability, proliferation, migration, and invasion. Our findings further showed that ZMIZ1-AS1 recruits RNA-binding protein PTBP1 to stabilize ZMIZ1 mRNA. PTBP1 or ZMIZ1 overexpression rescues the suppressive effects of silenced ZMIZ1-AS1 on OS cellular processes. Importantly, ZMIZ1-AS1 promotes OS growth in vivo by stabilization of ZMIZ1. CONCLUSIONS: Long non-coding RNA ZMIZ1-AS1 promotes OS progression by stabilization of ZMIZ1. The Hippo pathway is inactivated in osteosarcoma. Transcriptional factors SOX2 and MYC downstream the Hippo pathway induce the upregulation of ZMIZ1-AS1 in osteosarcoma. ZMIZ1-AS1 recruits RNA binding protein PTBP1 that stabilizes ZMIZ1, the sense transcript of ZMIZ1-AS1. ZMIZ1-AS1 promotes osteosarcoma cell viability, proliferation, migration, and invasion by ZMIZ1 in a PTBP1 dependent manner.

Nek2B accelerates the progression of hepatocellular carcinoma through regulating SFRP1 to activate the Wnt/ß-catenin pathway.

PURPOSE: The purpose of this study was to clarify the expression pattern of Nek2B in hepatocellular carcinoma (HCC) and its influence on malignant phenotypes of HCC through regulating SFRP1 and the Wnt/ß-catenin pathway. METHODS: Nek2B levels in 64 paired HCC tissues and adjacent normal ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The correlation between Nek2B level and clinical parameters of HCC patients was analyzed. Regulatory effects of Nek2B and SFRP1 on clonality, proliferation and apoptosis of MHCC97H and Hep3B cells were determined through functional experiments. Western blot was conducted to detect protein levels of SFRP1, ß-catenin, c-myc, cyclinD1 and MMP7 in HCC cells with overexpression or knockdown of Nek2B. At last, rescue experiments were performed to clarify the role of Nek2B/SFRP1 regulatory loop in aggravating the progression of HCC. RESULTS: Nek2B was upregulated in HCC tissues and cells. HCC patients expressing a high level of Nek2B were in more advanced tumor stage and had worse prognosis. Overexpression of Nek2B in MHCC97H cells enhanced clonality, 5-Ethynyl-2'- deoxyuridine (EdU)-positive ratio and suppressed apoptosis. Besides, knockdown of Nek2B in Hep3B cells yielded the opposite results. SFRP1 was downregulated in HCC, and low level of SFRP1 predicted worse prognosis of HCC. Overexpression of Nek2B downregulated SFRP1, but upregulated ß-catenin, c-myc, cyclinD1 and MMP7 in HCC cells. Importantly, Nek2B/SFRP1 regulatory loop was identified to aggravate the progression of HCC. CONCLUSIONS: Nek2B is upregulated in HCC, and closely linked to tumor stage and poor prognosis in HCC patients. Through interaction with SFRP1, Nek2B aggravates the progression of HCC by activating the Wnt/ß-catenin pathway.

TRPS1 and YAP1 Regulate Cell Proliferation and Drug Resistance of Osteosarcoma via Competitively Binding to the Target of circTADA2A - miR-129-5p.

INTRODUCTION: The yes-associated protein (YAP) and trichorhinophalangeal syndrome 1 (TRPS1) have been reported to account for the pathogenesis of cancers and may play an important role in osteosarcoma (OS). This study intended to investigate the modulatory effect and relationship of TRPS1 and YAP1 in OS cells. METHODS: The expression difference of YAP1 and TRPS1 in OS cells was measured. Then, the effect of circTADA2A silence on YAP1 and TRPS1 expression as well as OS proliferation and drug resistance was estimated. RESULTS: TRPS1 and YAP1 were upregulated in OS cell lines, and TRPS1 and YAP1 were highly expressed in MG63 and U2OS cells, respectively. The cell proliferation of MG63 was lower than that of U2OS, but the opposite result was observed in the presence of cisplatin (DDP). CircTADA2A was upregulated while miR-129-5p was downregulated in MG63 and U2OS cells compared. Besides, circTADA2A knockdown inhibited cell proliferation and reduced DDP resistance in both MG63 and U2OS. MiR-129-5p was increased but TRPS1 and YAP1 were decreased by circTADA2A knockdown. Meanwhile, circTADA2A knockdown reduced TRPS1 protein expression but enhanced phosphorylated (p)-YAP1. In xenograft OS tumor mice, circTADA2A knockdown inhibited tumor growth in the absence or presence of DDP. Finally, miR-129-5p could bind to circTADA2A, TRPS1 and YAPS. DISCUSSION: CircRNA TADA2A could target miR-129-5p, which was competitively bound by TRPS1 and YAP1, thereby regulating OS cell proliferation and drug resistance.

Lateral wall osteotomy combined with embedded biodegradable implants for displaced intra-articular calcaneal fractures.

BACKGROUND: The extensile lateral approach (ELA) has been widely used to treat displaced intra-articular calcaneal fractures (DIACFs) and remains the gold standard procedure. Orthopedic surgeons are extremely concerned of the high rate of wound complications. This study intended to report a new surgical technique of the lateral wall osteotomy combined with an embedded biodegradable implant for treating DIACFs and assess clinical and radiological results. METHODS: From May 2013 to December 2015, a total of 17 patients with 19 calcaneal fractures underwent surgical treatment using our new technique. Radiographic images, computed tomography (CT) scans, and magnetic resonance (MR) images of the operative limb were obtained to assess fracture healing and biodegradable implant degradation. American Orthopaedic Foot and Ankle Society (AOFAS) ankle/hindfoot score at the last follow-up was obtained to assess functional result for all cases. Böhler's and Gissane's angles, width, and height of the injured calcaneus were analyzed using preoperative and last follow-up radiographic images. RESULTS: All radiological parameters were significantly improved at the last follow-up, with an increase of 15.58°, 8.38°, and 7.65 mm in Böhler's angle, Gissane's angle, and calcaneal height, respectively, and a decrease of 2.51 mm in calcaneal width (p < 0.05). Mean AOFAS score at the last follow-up was 84.37 ± 9.98, with 9, 6, and 4 feet, having excellent, good, and fair rates, respectively. None had nonunion, delayed union, or malunion after a mean follow-up of 34.69 ± 5.22 months. One superficial infection occurred 6 days post-surgery. CONCLUSIONS: Osteotomy of the lateral wall of the calcaneus allows tension-free suturing and avoids damage to penetrating branches of the lateral calcaneal artery (LCA). Biodegradable implants are easy to reshape and do not require surgical removal. However, they should be limited to Sander's type II and III fractures only. LEVEL OF EVIDENCE: Level IV, case series without controls.

Tankyrase1 antisense oligodeoxynucleotides suppress the proliferation, migration and invasion through Hippo/YAP pathway in human osteosarcoma cells.

Osteosarcoma is the most common malignant tumor of bone with a high potential for metastasis and poor prognosis. This study intends to explore the effect of tankyrase1 (TANK1) in the development of osteosarcoma cells and the underlying mechanism. The osteosarcoma cell line MG-63 cells were cultured and transfected with tankyrase1 antisense oligodeoxynucleotides (TANK1-ASODN). Cell proliferation was detected with CCK-8 and immunofluorescence. Cell migration and invasion were examined by wound healing assay and Transwell assay, respectively. Reverse transcription-quantitative polymerase chain reaction was performed to detect the mRNA level of TANK1 and western blot was conducted to detect relative protein expression during the research. As a result, we demonstrated that TANK1 was upregulated in osteosarcoma. The TANK1-ASODN inhibited MG-63 cell proliferation, migration and invasion. The progress of epithelial-mesenchymal transition (EMT) was also suppressed in TANK1-ASODN transfected MG-63 cells compared to control group. Besides, the TANK1-ASODN activated and modulated the Hippo/YAP signaling which might be the pathway that TANK1 depended on. Overall, our finding supported that TANK1-ASODN slowed down the progress of osteosarcoma by suppressing cell proliferation, migration, invasion and EMT through Hippo/YAP pathway.

PYGB siRNA inhibits the cell proliferation of human osteosarcoma cell lines.

Osteosarcoma is the most common malignant bone carcinoma that primarily occurs between childhood to adolescence. It was suggested by recent research that the Brain type glycogen phosphorylase (PYGB) gene may serve an important role in various types of cancer. In the present study, the PYGB gene was knocked down in order to evaluate the cell viability, invasion and migration of the human osteosarcoma cell lines MG63 and HOS. The expression levels of PYGB in osteosarcoma and bone cyst tissue samples, as well as in the osteosarcoma cell lines were identified using reverse transcription­quantitative polymerase chain reaction and western blot assay. Subsequently, a Cell Counting kit 8 assay was employed to evaluate cell proliferation. Cell apoptosis rate and cell cycle distribution were measured by flow cytometry. In addition, cell invasion and migration were evaluated through a Transwell assay. The expression levels of the cell apoptosis and tumor metastasis associated proteins B­cell lymphoma 2 (Bcl­2), Bcl­2­associated X protein, E­cadherin, Twist, matrix metalloproteinase (MMP)­9 and MMP2 were measured via western blotting. PYGB exhibited a higher expression level in the osteosarcoma tissue samples, particularly in the human osteosarcoma cell lines MG63 and HOS. Knockdown of PYGB resulted in a decline in cell proliferation, invasion and migration, which was coupled with induced cell apoptosis and cell cycle arrest in MG63 and HOS cells. Furthermore, alterations in the expression of apoptosis and metastasis associated proteins indicated that small interfering (si)PYGB may have regulated cell viability by targeting the Bcl/Caspase and cyclin dependent kinase (CDK)­1 signaling pathway. In conclusion, PYGB siRNA exerted an inhibitory effect on the cell viability of the human osteosarcoma cells MG63 and HOS by blocking the Caspase/Bcl and CDK1 signaling pathway, highlighting novel potential therapeutic methods for treating osteosarcoma.

Dose-dependence of PTH-related peptide-1 on the osteogenic induction of MC3T3-E1 cells in vitro.

Parathyroid hormone (PTH), an 84-amino acid peptide, is an endocrine hormone that is secreted by parathyroid glands. PTH performs important functions in calcium regulation and bone remodeling. The PTH (1-34) named teriparatide, a 34-amino acid peptide derived from the N-terminus of PTH, conserves most of the functions of PTH, specifically the osteogenic capability. However, teriparatide is only used by injection and exhibits short duration. In addition, this PTH could not thoroughly expose active sites. In this study, a novel PTH-related peptide (designated PTHrP-1) derived from the N-terminus of PTH was added into the complete medium at different concentrations of PTHrP-1 (0, 50, 100, and 200 ng/mL) to induce the MC3T3-E1 cells. PTHrP-1 was detected by high-performance liquid chromatography and matrix-assisted laser desorption/ionization-time-of-flight mass spectroscopy. Cell morphology, cell proliferation, alkaline phosphatase (ALP), and ALP activity, osteocalcin concentration, and collagen type I (Col-I), osteopontin (OPN), and osteocalcin (OCN) mRNA expression by RT-PCR and protein expression by western blotting were observed and detected. The purity of the PTHrP-1 was 95.14%, and the PTHrP-1 can induce MC3T3-E1 cells into osteoblasts, thus improving ALP activity and OCN concentration, and increasing Col-I, OPN, and OCN mRNA expression and protein expression in MC3T3-E1 cell cultures. The PTHrP-1 proved to be an ideal active peptide. In addition, the osteogenic ability of PTHrP-1 at 200 and 100 ng/mL concentrations was not significantly different but significantly higher than 50 and 0 ng/mL groups. Results indicate that PTHrP-1 is a kind of active peptides that exhibits good biocompatibility with MC3T3-E1 cells and could improve cell proliferation and osteogenic differentiation. Moreover, PTHrP-1, at the preferable concentration of 100 ng/mL, could effectively promote MC3T3-E1 cells into osteoblasts.