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Study Design: Retrospective study., Objective: To analyze the causes of and factors influencing early recurrence after TELD performed in the treatment of lumbar disc herniation., Methods: We included 285 patients with single-segment lumbar disc herniation treated using transforaminal endoscopy lumbar discectomy TELD from January 2017 to December 2019 at the First Affiliated Hospital of the University of South China. Patients were classified into early recurrence and non-early recurrence groups based on clinical symptoms and MRI reexamination. Imaging data (eg, disc height index (DHI), Pfirrman grades, base width, postoperative annulus-fibrosus tear size, cross-sectional area of the foramen (CSAF), etc.)were analyzed, and multivariate, binomial logistic regression was utilized to determine which factors were associated with early recurrence after TELD., Results: A total of 285 patients completed surgery and clinical follow-up, during which 19 patients relapsed within 6 months postsurgery, for an early recurrence rate of 6.7%. There were statistically significant differences between DHI, Pfirrman grades, base width, postoperative annulus-fibrosus tear size, herniation sites, CSAF and Modic changes between the early recurrence and non-early recurrence groups (P < .05). On multivariate logistic regression,the degree of disc degeneration (OR = .747, P = .037), CSAF (OR = 5.255, P = .006), degree of Modic change (OR = 1.831, P = .018) and base width of the herniation (OR = 4.942, P = .003) were significantly correlated with early recurrence after TELD., Conclusions: Postoperative annulus-fibrosus tear size, DHI, and location of the disc herniation were associated with early recurrence after TELD. Increased base width of the herniation, severe disc degeneration, decreased CSAF and Modic change were risk factors for early recurrence after TELD., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background: Colorectal cancer (CRC) is one of the most prevalent diseases and the second leading cause of death worldwide. However, the relationship between CRC and cerebrovascular-specific mortality (CVSM) remains elusive, and less is known about the influencing factors associated with CVSM in CRC. Here, we aimed to analyze the incidence as well as the risk factors of CVSM in CRC., Methods: Patients with a primary CRC diagnosed between 1973 and 2015 were identified from the Surveillance Epidemiology and End Results database, with follow-up data available until 31 December 2016. Conditional standardized mortality ratios were calculated to compare the incidence of CVSM between CRC patients and the general U.S., Population: Univariate and multivariate survival analyses with a competing risk model were used to interrogate the risk factors for CVSM., Results: A total of 563,298 CRC individuals were included. The CVSM in CRC patients was significantly higher than the general population in all age subgroups. Among the competing causes of death in patients, the cumulative mortality caused by cerebrovascular-specific diseases steadily increased during the study period. While age, surgery, other/unknown race and tumors located at the transverse colon positively influenced CVSM on both univariate and multivariate analyses, male patients and those who had radiotherapy, chemotherapy, a more recent year (2001-2015) of diagnosis, a grade II or III CRC, rectal cancer, or multiple primary or distant tumors experienced a lower risk of CVSM., Interpretation: Our data suggest a potential role for CRC in the incidence of CVSM and also identify several significant predictors of CVSM that may be helpful for risk stratification and the therapeutic optimization of cerebrovascular-specific diseases in CRC patients.

Background: Immunotherapy only achieves efficacy in some cancer patients, and less is known about other immune checkpoint molecules in chordoma. Here, we aimed to determine the expression of PD-L1, HHLA2, B7H3, IDO-1 and Galectin-9 in spinal chordoma and evaluated their association with tumor infiltrating lymphocytes (TILs), clinicopathological characteristics and survival of patients., Methods: Using multiplexed quantitative immunofluorescence (QIF), we simultaneously measured the levels of five different immune checkpoint molecules and major TIL subsets in 92 human spinal chordoma samples., Results: Tumor HHLA2 and PD-L1 were positive in 80.0% and 86.0% of cases, respectively. However, B7H3, IDO-1 and Galectin-9 positivity on tumor cells were only seen in 21.0% of cases, despite all showing predominantly stromal expression. Coexpression of these QIF markers in the tumor compartment was scarcely detected except for PD-L1 and HHLA2, which was observed in 69.6% of cases. While tumoral HHLA2 and stromal B7H3 expressions were associated with an aggressive tumor phenotype, suppressive immune response (specifically including elevated PD-1 + TILs level and decreased CD8 + TIL density) and poor prognosis, stromal levels of PD-L1 and Galectin-9 predicted the opposite outcomes. Importantly, HHLA2 and PD-L1 coexpression on tumor cells independently predicted both worse local recurrence-free survival and overall survival., Conclusion: These data provide a better understanding of the immunosuppressive mechanism in chordoma and may be useful for the development of combination or novel immunotherapy approaches aiming to improve therapeutic efficacy and survival., Competing Interests: Author Y-LC was employed by the company Shenzhen Audaque Data Technology Co., Ltd. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Xia, Huang, Chen, Fu, Tang, Zhang, Li, Lv, Yan, Ouyang, Yao, Wang and Zou.)

Background: Percutaneous endoscopic lumbar discectomy (PELD) has been widely used, before which foraminoplasty is necessary to widen the foramen for subsequent procedures. However, the learning curve of this technology is high, as the use of traditional reamers requires repeated intraoperative fluoroscopy. We sought to compare the clinical outcomes by using the visualized and traditional reamers in PELD foraminoplasty for the treatment of lumbar disc herniation., Methods: Eighty patients with lumbar disc herniation who were treated with PELD between 1 January 2017 and 1 January 2019 were retrospectively reviewed. The patients were randomly divided into 2 groups (40 patients in the Visualized Bone Reamer group) and (40 patients in the Traditional Bone Reamer group). Intraoperative fluoroscopy time, cannulation introduction time, visual analog scale, and Macnab criteria score were compared between the 2 groups., Results: The mean follow-up durations were 17.41 ± 1.47 and 18.37 ± 1.69 months in the visualized and traditional groups, respectively. The average cannulation introduction time and intraoperative fluoroscopy times in the visualized group is significantly lower than those in traditional group (29.20 ± 3.31 vs. 39.85 ± 3.98 minutes, P < 0.001; and 12.30 ± 2.38 vs. 20.65 ±3.51 seconds, P < 0.001, respectively). One patient in the traditional group required reoperation, and no complications occurred in the visualized group. There were no severe durotomies or vascular or visceral injuries., Conclusions: Full-endoscopic foraminoplasty using a visualized reamer is safe and effective and can decrease intraoperative fluoroscopy time in PELD., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Previous studies have suggested that interleukin (IL)-17A is a key factor that contributes to intervertebral disc degeneration (IDD), whereas autophagy has been shown to be a protective mechanism in IDD. However, the relationship between IL-17A and autophagy in IDD remains to be fully elucidated. This study sought to evaluate the association between IL-17 and autophagy and the potential mechanism through which IL-17A affects autophagy in IDD., Methods: Intervertebral disc specimens were collected from 10 patients with lumbar disc herniation. Human degenerated nucleus pulposus (NP) cells were cultured in the presence or absence of IL-17A treatment. Western blot and monodansylcadaverine staining were used to measure autophagy levels in human degenerated NP cells. Subsequently, phosphatidylinositol 3-kinase (PI3K)/Akt/Bcl-2 pathway inhibitors were used to reveal the potential mechanism., Results: IL-17A treatment inhibited the autophagic activity in human NP cells in a time- and dose-dependent manner. Moreover, monodansylcadaverine staining showed that cells treated with IL-17A had significantly fewer changes in their autophagic vacuoles compared with control-treated cells. After IL-17A treatment, expression levels of PI3K, p-Akt, and Bcl-2 in NP cells were significantly increased. Further assays with PI3K/Akt/Bcl-2 inhibitors revealed that IL-17A suppressed autophagy in NP cells by activating the PI3K/Akt/Bcl-2 signaling pathway., Conclusions: These data suggest that IL-17A promotes IDD by inhibiting autophagy through activation of the PI3K/Akt/Bcl-2 signaling pathway and may offer new insights for targeted therapy of this disease., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: Published data have suggested a critical role for microRNA (miRNA) expression in chordoma progression. However, most of these studies focus on single miRNA and no multi-miRNA prognostic signature has been currently established for chordoma. In this study, we sought to develop and validate a 6-miRNA risk score (miRscore) model for survival prediction., Methods: Medline, Embase, and Google scholar searches (from inception to July 20, 2018) were conducted to identify candidate miRNAs with prognostic value as per predefined criteria. Quantitative RT-PCR was used to measure miRNA levels in 114 spinal chordoma (54 in the training and 60 in the validation cohort) and 20 control specimens. Subsequently, the miRscore was built based on miRNAs data., Results: Literature searches identified six prognostic miRNAs (miR-574-3p, miR-1237-3p, miR-140-3p, miR-1, miR-155, and miR-1290) with differential expression in tumor tissues. Bioinformatical analysis revealed an important regulatory role for miR-574-3p/EGFR signaling in chordoma and showed that the target genes of these prognostic miRNAs were mainly enriched in transcription regulation, protein binding and cancer-related pathways. In both cohorts, the miRscore was associated with surrounding muscle invasion by tumor and/or other aggressive features. The miRscore model well predicted local recurrence-free survival and overall survival, which remained after adjusting for other relevant covariates. Further time-dependent receiver operating characteristics analysis in the two cohorts found that the miRscore classifier had stronger prognostic power than known clinical predictors and improved the ability of Enneking staging to predict outcomes. Importantly, recursive-partitioning analysis of both samples combined separated patients into four prognostically distinct risk subgroups for recurrence and survival (both P < 0.001)., Conclusions: These data suggest the miRscore as a useful prognostic stratification tool in spinal chordoma and may represent an important step toward future personalized treatment of patients., (Copyright © 2020 Huang, Yan, Wang, Ouyang, Li, Zhang, Wang, Wang, Lv, Li and Zou.)

Intervertebral disc degeneration (IDD) is the most common cause leading to low back pain, a highly prevalent, costly and crippling condition worldwide. Overexpression of miR-21 has been shown to promote proliferation of nucleus pulposus (NP) cells. However, it remains unclear whether miR-21 can promote the degradation of type II collagen (Col II) and aggrecan, two main extracellular matrix components within the disc. Here, the miRNA microassay assay identified 29 differentially expressed miRNAs in NP tissues from IDD patients compared with healthy controls. Following qRT-PCR validation, miR-21 expression was significantly upregulated in degenerated NP tissues, and showed a positive correlation with disc degeneration grade. Through gain-of-function and loss-of-function studies in human NP cells, miR-21 was shown to inhibit autophagy and then upregulate the expression of matrix metalloproteinase (MMP)-3 and MMP-9, leading to increased degradation of Col II and aggrecan. Mechanistically, phosphatase and tensin homolog (PTEN) was identified as a direct target of miR-21, and activated PTEN/ Akt/mammalian target of rapamycin (mTOR) signaling pathway was involved in miR-21-induced autophagy inhibition and Col II and aggrecan breakdown. Taken together, these results suggest that miR-21 contributes to Col II and aggrecan catabolism by inhibiting autophagy via the PTEN/Akt/mTOR signaling pathway in human NP cells., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Multilevel cervical reconstruction and fusion after cervical tuberculosis has always been a challenge. The current implantation materials for cervical fusion, including titanium mesh, cage, and plate are limited by its inferior biological mechanical characteristics and the properties of the metallic material. This has led to the increased risk of recurrent infection after surgery. In addition, the unique nature of tuberculosis infection results in the low rate of cervical fusion and high risk of recurrence. This case report presents 1 patient who suffered from long segmental cervical tuberculosis and had reconstruction surgery using a vascularized fibula graft. The patient had successful graft incorporation 3 months postsurgery and was followed-up for 30 months. In this review, we detail the advantages of using vascularized fibular grafts and compare it with other types of grafts., (Copyright © 2017 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.)

Intervertebral disc degeneration (IDD) is thought to be the most common cause of low back pain. Dysregulation of microRNAs (miRNAs) is involved in the development of IDD. The aim of this study was to explore the influence of miR-210 on type II collagen (Col II) and aggrecan expression and possible mechanisms in human degenerated nucleus pulposus (NP) cells. Our results showed that miR-210 levels were significantly increased in degenerated NP tissues compared with healthy controls, and positively correlated with disc degeneration grade. By gain-of-function and loss-of-function studies in human degenerated NP cells, miR-210 was shown to inhibit autophagy and then upregulate MMP-3 and MMP-13 expression, leading to increased degradation of Col II and aggrecan. Autophagy-related gene 7 (ATG7) was identified as a direct target of miR-210. Knockdown of ATG7 by small interfering RNA (siRNA) abrogated the effects of miR-210 inhibitor on MMP-3, MMP-13, Col II and aggrecan expression. Taken together, these results suggest that miR-210 inhibits autophagy via silencing of ATG7, leading to increased Col II and aggrecan degradation in human degenerated NP cells., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)

Intervertebral disc degeneration (IDD) is thought to be the primary cause of low back pain, a severe public health problem worldwide. Current therapy for IDD aims to alleviate the symptoms and does not target the underlying pathological alternations within the disc. Activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway protects against IDD, which is attributed to increase of ECM content, prevention of cell apoptosis, facilitation of cell proliferation, induction or prevention of cell autophagy, alleviation of oxidative damage, and adaptation of hypoxic microenvironment. In the current review, we summarize recent progression on activation and negative regulation of the PI3K/Akt signaling pathway, and highlight its impact on IDD. Targeting this pathway could become an attractive therapeutic strategy for IDD in the near future., Competing Interests: CONFLICTS OF INTEREST The authors have declared no conflicts of interest.

In the title compound, C(15)H(12)O(4)·H(2)O, the two benzene rings are not coplanar, making a dihedral angle of 7.24 (16)°. An intra-molecular hy-droxy-carbonyl O-H⋯O hydrogen bond occurs. In the crystal, four inter-molecular O-H⋯O hydrogen bonds involving the hy-droxy residues, the carbonyl group and the water mol-ecule lead to the formation of a three-dimensional network. The supra-molecular structure is further stabilized by weak C-H⋯O inter-actions.

Objective: To investigate the effect of metallothionein (MT) on rifampicin (RFP)-induced hepatotoxicity and the possible mechanisms., Methods: Male MT- I / II null (MT-/-) and wild type (MT+/+) mice were randomly divided into 4 groups, respectively, and were orally administered RFP (50, 100 or 200 mg/kg) or equal volumes of solvent daily for 15 consecutive days. Levels of plasma alanine aminotransferase (ALT), alkaline phosphatase (ALP) and direct bilirubin (DB) were determined. Liver indexes were calculated and liver histopathologic changes were examined by hematoxylin and eosin (HE) staining. The content of glutathione (GSH) as well as the activities of glutathione peroxydase (GPx) and glutathione reductases (GR) were measured in the liver homogenates., Results: RFP treatment induced significant increases in plasma ALT, AST and DB, as well as liver index. Significant histopathologic changes which were charactered as fatty degeneration in liver were noteced. Moreover, augmentations of GSH content and GR activity and attenuation of GPx activity were observed. More severe hepatic injuries in MT-/- mice were observed as compared to MT+/+ mice, which were evidenced by higher liver/body weight ratio and GR activity, lower GSH content and GPx activity, and more serious fatty degeneration., Conclusion: RFP-induced hepatotoxicity was associated with cholestasis and oxidative damage. MT -/- mice were more susceptible than MT +/+ mice to RFP-induced hepatotoxicity and the enhanced hepatotoxicity involves increased oxidative stress.

Eleven BALB/c mouse strains of Beijing, Shanghai, Shenyang, Haerbin, Guangzhou, Chongqing and Changchun were monitored in order to assure the genetic quality of inbred BALB/c mouse strains in China and to estimate the credibility of microsatllite markers. Fourteen microsatellites loci on different chromosomes were investigated by PCR analysis. It showed that all these microsatellites DNA loci displayed single allelic gene band in mouse strains of Beijing, Shanghai and Haerbin. But the mice came from Shenyang, Guangzhou, Chongqing and Changchun had polymorphisms or heterozygosis, among which the Shenyang and Changchun strains showed polymorphisms and heterozygosis at two separate loci. Four loci showed polymorphisms or heterozygosis in one of the Guangzhou mouse strains. The Chongqing strains showed polymorphisms and heterozygosis at seven loci, including the D10Mit180 locus as compared with the Shanghai strains.