Identification and mechanism characterization of Streptomyces griseoaurantiacus XQ-29 with biocontrol ability against pepper southern blight caused by Sclerotium rolfsii.

Pepper southern blight, caused by Sclerotium rolfsii, is a devastating soil-borne disease resulting in significant loss to pepper, Capsicum annuum L. production. Here, we isolated an antagonistic bacterial strain XQ-29 with antifungal activity against S. rolfsii from rhizospheric soil of pepper. Combining the morphological and biochemical characteristics with the 16S rDNA sequencing, XQ-29 was identified as Streptomyces griseoaurantiacus. It exhibited an inhibition of 96.83% against S. rolfsii and displayed significant inhibitory effects on Botrytis cinerea, Phytophthora capsica and Rhizoctonia solani. Furthermore, XQ-29 significantly reduced the pepper southern blight by 100% and 70.42% during seedling and growth stages, respectively. The antifungal mechanism involved altering the mycelial morphology, disrupting cell wall and membrane integrity, accompanied by accumulation of reactive oxygen species and lipid peroxidation in S. rolfsii mycelia. Furthermore, XQ-29 promoted growth and stimulated resistance of pepper plants by increasing defense-related enzyme activities and upregulating defense-related genes. Correspondingly, XQ-29 harbors numerous functional biosynthesis gene clusters in its genome, including those for siderophores and melanin production. The metabolic constituents present in the ethyl acetate extracts, which exhibited an EC50 value of 85.48 ± 1.62 µg/mL, were identified using LC-MS. Overall, XQ-29 demonstrates significant potential as a biocontrol agent against southern blight disease.

Pterostilbene suppresses human endometrial cancer cells in vitro by down-regulating miR-663b.

Resveratrol has long been known as an antioxidant and a chemopreventive agent. Similar to resveratrol, pterostilbene (PT) is also a phenolic compound extracted from the Vitis species. However, there are few studies on the antitumor effect of PT. Thus, we investigated the effects of PT on the endometrial cancer (EC) cells in vitro and the related molecular mechanisms. Treatment of EC cell lines HTB-111 and Ishikawa with PT (25-100 µmol/L) dose-dependently suppressed the cell viability and induced apoptosis. Using miR microarrays, we examined the miR expression profile in Ishikawa cells with or without PT, and revealed that miR-663b was the most decreased in PT-treated Ishikawa cells. Furthermore, we predicted and verified that the pro-apoptosis factor BCL2L14 is the direct target of miR-663b. Over-expression of miR-663b and knock-down of BCL2L14 counteracted the suppressing effects of PT on HTB-111 and Ishikawa cells. In addition, we evaluated the miR-663b levels in EC tissues of 51 patients using an in situ hybridization technique. With the median of the score of miR-663b as a cut-off value, these EC patients were divided into two groups, and the patients with high miR-663b expression had significantly poor prognosis.

Selumetinib suppresses cell proliferation, migration and trigger apoptosis, G1 arrest in triple-negative breast cancer cells.

BACKGROUND: Triple-negative breast cancer (TNBC) has aggressive progression with poor prognosis and ineffective treatments. Selumetinib is an allosteric, ATP-noncompetitive inhibitor of MEK1/2, which has benn known as effective antineoplastic drugs for several malignant tumors. We hypothesized that Selumetinib might be potential drug for TNBC and explore the mechanism. METHODS: After treated with Selumetinib, the viability and mobility of HCC1937 and MDA-MB-231 were detected by MTT, tunnel, wound-healing assay, transwell assay and FCM methods. MiR array was used to analysis the change of miRs. We predicted and verified CUL1 is the target of miR-302a using Luciferase reporter assay. We also silenced the CUL1 by siRNA, to clarify whether CUL1 take part in the cell proliferation, migration and regulated its substrate TIMP1 and TRAF2. Moreover, after transfection, the antagomir of miR-302a and CUL1 over-expressed plasmid into HCC1937 and MDA-MB-231 cell accompanied with the Selumetinib treatment, we detected the proliferation and migration again. RESULTS: Selumetinib reduce the proliferation, migration, triggered apoptosis and G1 arrest in TNBC cell lines. In this process, the miR-302a was up-regulated and inhibited the CUL1 expression. The later negatively regulated the TIMP1 and TRAF2. As soon as we knockdown miR-302a and over-expression CUL1 in TNBC cells, the cytotoxicity of Selumetinib was reversed. CONCLUSIONS: MiR-302a targeted regulated the CUL1 expression and mediated the Selumetinib-induced cytotoxicity of triple-negative breast cancer.

Sirolimus induces apoptosis and reverses multidrug resistance in human osteosarcoma cells in vitro via increasing microRNA-34b expression.

AIM: Multi-drug resistance poses a critical bottleneck in chemotherapy. Given the up-regulation of mTOR pathway in many chemoresistant cancers, we examined whether sirolimus (rapamycin), a first generation mTOR inhibitor, might induce human osteosarcoma (OS) cell apoptosis and increase the sensitivity of OS cells to anticancer drugs in vitro. METHODS: Human OS cell line MG63/ADM was treated with sirolimus alone or in combination with doxorubicin (ADM), gemcitabine (GEM) or methotrexate (MTX). Cell proliferation and apoptosis were detected using CCK-8 assay and flow cytometry, respectively. MiRNAs in the cells were analyzed with miRNA microarray. The targets of miR-34b were determined based on TargetScan analysis and luciferase reporter assays. The expression of relevant mRNA and proteins was measured using qRT-PCR and Western blotting. MiR-34, PAK1 and ABCB1 levels in 40 tissue samples of OS patients were analyzed using qRT-PCR and in situ hybridization assays. RESULTS: Sirolimus (1-100 nmol/L) dose-dependently suppressed the cell proliferation (IC50=23.97 nmol/L) and induced apoptosis. Sirolimus (10 nmol/L) significantly sensitized the cells to anticancer drugs, leading to decreased IC50 values of ADM, GEM and MTX (from 25.48, 621.41 and 21.72 µmol/L to 4.93, 73.92 and 6.77 µmol/L, respectively). Treatment of with sirolimus increased miR-34b levels by a factor of 7.5 in the cells. Upregulation of miR-34b also induced apoptosis and increased the sensitivity of the cells to the anticancer drugs, whereas transfection with miR-34b-AMO, an inhibitor of miR-34b, reversed the anti-proliferation effect of sirolimus. Two key regulators of cell cycle, apoptosis and multiple drug resistance, PAK1 and ABCB1, were demonstrated to be the direct targets of miR-34b. In 40 tissue samples of OS patients, significantly higher miR-34 ISH score and lower PAK5 and ABCB1 scores were detected in the chemo-sensitive group. CONCLUSION: Sirolimus increases the sensitivity of human OS cells to anticancer drugs in vitro by up-regulating miR-34b interacting with PAK1 and ABCB1. A low miR-34 level is an indicator of poor prognosis in OS patients.

Studies on dynamic motion compensation and positioning accuracy on star tracker.

Error from motion is the dominant restriction on the improvement of dynamic performance on a star tracker. As a remarkable motion error, the degree of nonuniformity of the star image velocity field on the detector is studied, and thus a general model for the moving star spot is built. To minimize velocity nonuniformity, a novel general method is proposed to derive the proper motion compensation and location accuracy in cases of both uniform velocity and acceleration. Using this method, a theoretic analysis on the accuracy of time-delayed integration and similar techniques, which are thought of as state-of-the-art approaches to reduce error from motion, is conducted. The simulations and experimental results validate the proposed method. Our method shows a more steady performance than the dynamic binning algorithm. The positional error could be neglected when the smear length is far less than 3.464 times the scale of star spot, which suggests accuracy can be maintained by changing frame-integration time inverse proportional to the velocity on the focal plane. It also shows that the acceleration effect must be compensated to achieve accuracy close to the Cramér-Rao lower bound.

p21-activated kinase 7 is an oncogene in human osteosarcoma.

p21-activated kinase 7 (PAK7), also named as PAK5, is a member of Rac/Cdc42-associated Ser/Thr protein kinases. It is overexpressed in some types of cancer such as colorectal and pancreatic cancers. However, the expression status and biological function of PAK7 in osteosarcoma are still ambiguous. To evaluate the expression levels of PAK7 in osteosarcoma tissues and cell lines, immunohistochemistry was used. To investigate the role of PAK7 in cell proliferation, apoptosis and tumorigenicity in vitro and vivo, a recombinant lentivirus expressing PAK7 short hairpin RNA (Lv-shPAK7) was developed and transfected into Saos-2 cells. The silencing effect of PAK7 was confirmed by quantitative real-time PCR (qRT-PCR) and Western blot technique. PAK7 was overexpressed in osteosarcoma tissue and cell line. By knocking-down of PAK7, the proliferation and colony formation of Saos-2 cells were inhibited and apoptosis enhanced significantly. The in vivo tumorigenic ability in xenograft model of Saos-2 cells was also notably inhibited when PAK7 was knocked down. Our results imply that PAK7 promotes cell proliferation and tumorigenesis and may be an attractive candidate for the therapeutic target of osteosarcoma.

Oral nano-formulations for endocrine therapy of endometrioid adenocarcinomas.

Endometrial cancer is one of the three major malignant tumors of the reproductive system that threaten women's lives and health. The incidence of this disease is on the rise globally. Most cases of endometrial cancer comprise endometrioid adenocarcinomas, whose treatment is challenged by factors such as their high recurrence rate and the need to preserve fertility among young patients. Thus, oral endocrine therapy has become the main treatment modality. The main drugs used in oral endocrine therapy are progestins, selective estrogen receptor antagonists, and aromatase inhibitors. However, their clinical use is hindered by their low solubility and low oral utilization. The rapid development of nanotechnology allows the combination of these drugs with oral nano-formulations to create a good carrier. Such nanocarriers, including nanospheres, nanocapsules, and micelles can protect the drug against clearance and increase the site specificity of drug delivery. This paper reviews the pathogenesis of endometrioid endometrial cancer (EEC) and oral nano-formulations for endocrine therapy.

Overall survival benefits for irinotecan-containing regimens as first-line treatment for advanced gastric cancer: an updated meta-analysis of ten randomized controlled trials.

The standard treatment for patients with advanced gastric cancer (AGC) is still debated, and the available data on the benefit of irinotecan-containing regimen as first-line treatment for those patients are controversial. We performed a systematic review and meta-analysis of randomized controlled trials to determine the survival benefits of irinotecan-containing regimens in this setting. A total of 1,837 patients from ten trials were included in the analysis. Our results showed that irinotecan-containing regimens significantly improved overall survival [OS: hazard ratio (HR) 0.86, 95% CI = 0.78-0.94, p = 0.002] and progression-free survival [HR = 0.82, 95% CI = 0.69-0.97, p = 0.026); however, the improvement of time to failure (HR = 0.90; 95% CI = 0.77-1.04, p = 0.15), 1-year survival rate [1-year SR: relative risk (RR) 1.10, 95% CI = 0.97-1.24, p = 0.13] and overall response rate (RR = 1.16, 95% CI = 0.91-1.49, p = 0.24] were nonsignificant. Equivalent frequencies of toxicities were found between the two groups excluding more Grade 3 or 4 fatigue (p = 0.001) in irinotecan-containing regimens. This updated meta-analysis provided strong evidence for a survival benefit of irinotecan-containing regimen as first-line treatment for AGC. A clear advantage of irinotecan-containing over nonirinotecan-containing regimen had not been established. These results should help to inform decisions about patient management and design of future trials.

Risk of venous thromboembolic events associated with VEGFR-TKIs: a systematic review and meta-analysis.

Vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) have been widely used in advanced cancers. Concerns have arisen regarding the risk of venous thromboembolism with the use of these drugs. Currently, the contribution of VEGFR-TKIs to venous thromboembolism is still unknown. We performed a meta-analysis to determine the incidence and relative risk (RR) of venous thromboembolism events (VTEs) associated with these agents. Eligible studies included phase II and III prospective trials evaluating US Food and Drug Administration approved VEGFR-TKIs (pazopanib, sunitinib, sorafenib and vandetanib), and data on VTEs were available. Overall incidence rates, RR and 95% confidence intervals (CI) were calculated employing fixed- or random-effects models depending on the heterogeneity of included trials. A total of 14 studies (4,430 patients) were selected for this meta-analysis. The incidence of VTEs related to VEGFR-TKIs was 3% (95%CI: 1.7-5.1%), and there was no statistically significant increase in the risk of VTEs for VEGFR-TKIs versus controls in overall population (RR0.912, 95%CI: 0.617-1.348, p = 0.643). On subgroup analysis, no significant increase in the risk of VTEs was found among different VEGFR-TKIs or tumor types. No evidence of publication bias was observed. The use of VEGFR-TKIs does not significantly increase the risk of VTEs, the risk of VTEs in patients with cancer is driven predominantly by tumor types, host factors and concomitant usage of anticancer agents. These results would provide important information for clinicians who use VEGFR-TKIs to treat patients with solid cancer.

Incidence and risk of hypertension with vandetanib in cancer patients: a systematic review and meta-analysis of clinical trials.

AIM: To perform a systematic review and meta-analysis of published clinical trials to determine incidence rate and overall risk of hypertension with vandetanib in cancer patients. METHODS: A comprehensive literature search for studies published up to March 2012 was performed. Summary incidence rates, relative risk (RR), and 95% confidence intervals (CI) were calculated employing fixed- or random-effects models depending on the heterogeneity of the included trials. RESULTS: A total of 11 trials with 3154 patients were included for the meta-analysis. The summary incidences of all-grade and high-grade hypertension in patients with cancer were 24.2% [95% confidence interval (CI), 18.1-30.2%] and 6.4% (95% CI, 3.3-9.5%), respectively. Subgroup analysis demonstrated that the pooled incidences of all-grade and high-grade hypertension were 21.8% [95% CI, 15-30.5%] and 7.6% (95% CI, 2.8-18.8%), respectively, among non-small-cell lung cancer (NSCLC) patients, and 32.1% (95% CI: 27.3-37.3%) and 8.8% (5.9%-12.9%), respectively, among MTC patients, and 15.4 (95% CI: 3.2-33.7%) and 3.4% (95% CI: 1%-11.1%) respectively, among non-MTC/NSCLC tumors patients. Furthermore, vandetanib was associated with a significant increased risk of all-grade hypertension (RR 5.1, 95% CI: 3.76-6.92, P = 0.000) and high-grade hypertension (RR 8.06, 95% CI: 3.41-19.04, P = 0.000) in comparison with controls. CONCLUSIONS: There is a significant risk of developing hypertension in cancer patients receiving vandetanib. Appropriate monitoring and treatment is strongly recommended to prevent cardiovascular complications.

Pirarubicin inhibits multidrug-resistant osteosarcoma cell proliferation through induction of G2/M phase cell cycle arrest.

AIM: Pirarubicin (THP) is recently found to be effective in treating patients with advanced, relapsed or recurrent high-grade osteosarcoma. In this study, the effects of THP on the multidrug-resistant (MDR) osteosarcoma cells were assessed, and the underlying mechanisms for the disruption of cell cycle kinetics by THP were explored. METHODS: Human osteosarcoma cell line MG63 and human MDR osteosarcoma cell line MG63/DOX were tested. The cytotoxicity of drugs was examined using a cell proliferation assay with the Cell Counting Kit-8 (CCK-8). The distribution of cells across the cell cycle was determined with flow cytometry. The expression of cell cycle-regulated genes cyclin B1 and Cdc2 (CDK1), and the phosphorylated Cdc2 and Cdc25C was examined using Western blot analyses. RESULTS: MG63/DOX cells were highly resistant to doxorubicin (ADM) and gemcitabine (GEM), but were sensitive or lowly resistant to THP, methotrexate (MTX) and cisplatin (DDP). Treatment of MG63/DOX cells with THP (200-1000 ng/mL) inhibited the cell proliferation in time- and concentration-dependent manners. THP (50-500 ng/mL) induced MG63/DOX cell cycle arrest at the G(2)/M phase in time- and concentration-dependent manners. Furthermore, the treatment of MG63/DOX cells with THP (200-1000 ng/mL) downregulated cyclin B1 expression, and decreased the phosphorylated Cdc2 at Thr(161). Conversely, the treatment increased the phosphorylated Cdc2 at Thr(14)/Tyr(15) and Cdc25C at Ser(216), which led to a decrease in Cdc2-cyclin B1 activity. CONCLUSION: The cytotoxicity of THP to MG63/DOX cells may be in part due to its ability to arrest cell cycle progression at the G(2)/M phase, which supports the use of THP for managing patients with MDR osteosarcoma.

Galangin promotes cell apoptosis through suppression of H19 expression in hepatocellular carcinoma cells.

BACKGROUND: Galangin has been extensively studied as the antitumor agent in various cancers. However, the effect of galangin in hepatocellular carcinoma (HCC) remains elusive. METHODS: Using RNA sequencing, the differential expression of lncRNA in human HCC cell line with highly metastatic potential (MHCC97H) cells treated with galangin was investigated. Furthermore, H19 expression pattern was also determined in MHCC97H cells following treatment with galangin. In addition, knockdown and overexpression of H19 was performed to analyze the effect of the expression pattern of H19 on cell apoptosis, cell cycle, migration, and invasion in HCC cells. Moreover, the in vivo effect of galangin on tumor development was also determined in nude mice. In order to analyze loss expression of H19 in vivo, clustered regularly interspaced short palindromic repeats/Cas9 (CRISPR/Cas9) was used. RESULTS: Total of 50 lncRNAs were significantly differentially expressed in MHCC97H cells treated with galangin. Besides, the expression of H19 was markedly reduced following treatment with galangin in MHCC97H cells. Compared to the Control group, the galangin-treated group inhibited cell migration and invasion. Knockdown of H19 expression showed increased cell apoptosis and decreased invasion. In addition, RNA-seq data also identified 161 mRNA which was significantly differentially expressed following treatment with galangin. To further determine the underlying mechanism, p53 protein was analyzed. Notably, the results indicated that knockdown of H19 and miR675 induced the expression of p53, eventually promoting cell apoptosis in MHCC97H cells. These results indicated that galangin promoted cell apoptosis through reduced the expression of H19 and miR675 in MHCC97H cells. The in vivo result showed that compared to the Con, tumor growth was remarkably suppressed with loss expression of H19. CONCLUSION: Our data suggested that galangin has a crucial role in hepatocarcinogenesis through regulating the expression pattern of H19.

Incidence and Risk Factors of the Caudal Screw Loosening after Pelvic Fixation for Adult Spinal Deformity: A Systematic Review and Meta-analysis

The purpose of this study was to assess the factors affecting caudal screw loosening after spinopelvic fixation for adult patients with spinal deformity. This meta-analysis calculated the weighted mean difference (WMD) and odds ratio (OR) using Review Manager ver. 5.3 (RevMan; Cochrane, London, UK). The loosening group was older than the control group (WMD, 2.17; 95% confidence interval [CI], 0.48–3.87; p=0.01). The S2 alar-iliac (S2AI) could prevent the caudal screw from loosening (OR, 0.43; 95% CI, 0.20–0.94; p=0.03). However, gender distribution (p=0.36), the number of fusion segments (p=0.24), rod breakage (p=0.97), T-score (p=0.10), and proximal junctional kyphosis (p=0.75) demonstrated no difference. Preoperatively, only pelvic incidence (PI) in the loosening group was higher (WMD, 5.08; 95% CI, 2.71–7.45; p<0.01), while thoracic kyphosis (p=0.09), lumbar lordosis (LL) (p=0.69), pelvic tilt (PT) (p=0.31), pelvic incidence minus lumbar lordosis (PI–LL) (p=0.35), sagittal vertical axis (SVA) (p=0.27), and T1 pelvic angle (TPA) demonstrated no difference (p=0.10). PI–LL (WMD, 6.05; 95% CI, 0.96–11.14; p=0.02), PT (WMD, 4.12; 95% CI, 0.99–7.26; p=0.01), TPA (WMD, 4.72; 95% CI, 2.35–7.09; p<0.01), and SVA (WMD, 13.35; 95% CI, 2.83–3.87; p=0.001) were higher in the screw loosening group immediately postoperatively. However, TK (p=0.24) and LL (p=0.44) demonstrated no difference. TPA (WMD, 8.38; 95% CI, 3.30–13.47; p<0.01), PT (WMD, 6.01; 95% CI, 1.47–10.55; p=0.01), and SVA (WMD, 23.13; 95% CI, 12.06–34.21; p<0.01) were higher in the screw loosening group at the final follow-up. However, PI–LL (p=0.17) demonstrated no significant difference. Elderly individuals were more susceptible to the caudal screw loosening, and the S2AI screw might better reduce the caudal screw loosening rate than the iliac screws. The lumbar lordosis and sagittal alignment should be reconstructed properly to prevent the caudal screw from loosening. Measures to block sagittal alignment deterioration could also prevent the caudal screw from loosening.

Progress of Microsatellite (GT/CA)n Repeat Polymorphisms in Non-small Cell Lung Cancer / 肿瘤防治研究

Non-small cell lung cancer (NSCLC) is the most important histological type of lung cancer. This disease affects a large number of patients, and the prognosis of advanced patients is poor. Although great progress has been achieved for existing treatment methods, challenges still exist. Cancer is a genetic disease, and its occurrence is accompanied by substantial genomic-sequence instability. (GT/CA)n repeat sequence is a common microsatellite sequence serving as transcriptional function-related regions, DNA-methylation modification sites, and other functional sites. Its polymorphism is closely related to the expression of EGFR, HO-1, and HIF-1α in NSCLC patients. (GT/CA)n repeat sequence is the breakthrough point to explore the molecular mechanism of NSCLC occurrence and development, develop molecular markers for diagnosis and prognosis and epigenetics research. This paper summarizes the studies on (GT/CA)n repeat polymorphisms in NSCLC with the aim of providing references for relevant NSCLC research.

The c.91C>T mutation in DNAJB2 gene associated distal hereditary motor neuropathy and early-onset Parkinson′s disease: a family report / 中华神经科杂志

A family carrying a homozygous variant of DNAJB2 gene C.91C>T (p.His31Tyr) with distal hereditary motor neuropathy (dHMN) associated with early-onset Parkinson′s disease was reported. The patient presented with distal limb weakness and atrophy at the early stage of the disease, and developed Parkinson′s symptoms more than 10 years later. Neuroelectrophysiological examination suggested motor and sensory axonal involvement. This mutation site had not been reported and was considered to be a neogenic mutagenicity of dHMN, excluding other mutations that can cause early-onset Parkinson′s disease.

Multiple-Rod Constructs in Adult Spinal Deformity Surgery: A Systematic Review and Meta-Analysis

The purpose of this research was to compare the therapeutic efficacy of multiple-rod constructs vis-a-vis 2-rod constructs in the treatment of adult spinal deformity. A systematic review and meta-analysis were performed to determine whether the multiple-rod construct outperformed the 2-rod construct. We initially retrieved 357 papers, but only 12 were chosen for further meta-analysis. The rod breakage rates in the multiple-rod and the 2-rod groups were 10.66% and 29.87%, respectively. The multiple-rod construct inhibited rod breakage (odds ratio [OR], 0.28; 95% confidence interval [CI], 0.19–0.41; p<0.001), pseudarthrosis (OR, 0.30; 95% CI, 0.18–0.50; p<0.001) and rod fracture at the osteotomy site (OR, 0.34; 95% CI, 0.13–0.89; p=0.03). Furthermore, the multiple-rod construct reduces the risk of revision surgery (OR, 0.38; 95% CI, 0.20–0.73; p=0.04) as well as the revision risk of pseudarthrosis/rod fracture in the multiple- rod group (OR, 0.31; 95% CI, 0.18–0.52; p<0.001), but increases the risk of caudal screw loosening (OR, 4.99; 95% CI, 1.87–13.30; p=0.001). There was no statistically significant difference in proximal junctional kyphosis (PJK) parameters (p=0.85), cerebrospinal fluid leakage (p=0.09), wound infection (p =0.71), age at surgery (p=0.62), gender distribution (p=0.93), body mass index (p =0.86), smoking status (p=0.05), hospital stay (p=0.09), osteoporosis (p=0.95), CoCr rod material (p=0.15), bone morphogenetic protein-2 (p=0.58), L5/S1 interbody fusion (p=0.07), high-grade osteotomies (p=0.07), the number of fusion levels (p=0.11), operation time (p=0.30), and blood loss volume (p=0.34). Regarding radiographic parameters, only preoperative sagittal vertical axis was found to be higher (weight means difference [WMD], 25.60; 95% CI, 15.43–35.77; p<0.001) in the multiple-rod group. There was no difference in preoperative Oswestry Disability Index (ODI) (WMD, −3.32; 95% CI, −7.38 to 0.73; p=0.11), but the multiple-rod group had a lower ODI at follow-up (WMD, −7.71; 95% CI, −11.62 to −3.86; p<0.001). Multiple-rod constructs could prevent rod breakage and pseudarthrosis while also lowering the revision rate, resulting in a better clinical outcome than the 2-rod construct. Nonetheless, due consideration should be given to PJK and screw loosening in multiple-rod constructs, possibly due to the increased stiffness caused by the multiple-rod structure.

Correlation between spinous process deviation and lumbar disc herniation in young patients / 中国骨伤

OBJECTIVE@#To explore the relationship between spinous process deviation and lumbar disc herniation in young patients.@*METHODS@#From March 2015 to January 2022, 30 treated young (under the age of 30) patients with lumbar disc herniation were included as the young group. In addition 30 middle-aged patients (quinquagenarian group) with lumbar disc herniation and 30 patients with non-degenerative spinal diseases (young non-degenerative group) were selected as control groups. The angle of the spinous process deviation was measured on CT and statistically analyzed by various groups. All the data were measured twice and the average value was taken and recorded.@*RESULTS@#The average angle of spinous process deviation in the degenerative lumbar vertebra of young patients were (3.89±3.77) degrees, similar to the (3.72±2.98) degrees of quinquagenarian patients(P=0.851). The average angle of s spinous process deviation young non-degenerative group were (2.20±2.28) degrees, significantly less than young group(P=0.040). The spinous process deviation angle of the superior vertebral of the degenerative lumbar in the young group was (4.10±3.44) degrees, which similar to the (3.47±2.87) degrees in the quinquagenarian group (P=0.447). A total of 19 young patients had the opposite deviation direction of the spinous process of the degenerative lumbar vertebra and upper vertebra, while only 7 quinquagenarian patients had this condition(P=0.02). The type of lumbar disc herniation in young patients had no significant relationship with the direction of spinous process deflection of the degenerative or upper lumbar vertebra (P>0.05).@*CONCLUSION@#Spinous process deviation is a risk factor of young lumbar disc herniation patients. If the deviation directions of adjacent lumbar spinous processes are opposite, it will increase the incidence of lumbar disc herniation in young patients. There was no significant correlation between the type of disc herniation and the deviation direction of the spinous process of the degenerative or upper lumbar vertebra. People with such anatomical variation can strengthen the stability of spine and prevent lumbar disc herniation through reasonable exercise.

Effect of 3D-printed nano-β-tricalcium phosphate in repairing seawater-soaked tibial defects in rabbits / 中华创伤杂志

Objective:To explore the repairing effects of 3D-printed nano-β-tricalcium phosphate (β-TCP) scaffolds loaded with vancomycin and bone morphogenetic protein-2 (BMP-2) for seawater -soaked tibial bone defects in rabbits. Methods:A total of 27 male New Zealand White rabbits were assigned to the normal group using a random number table method, with each group consisting of 9 rabbits. The rabbit tibial bone defect model was created using the osteotomy surgical method. Eight hours after operation, the wounds in the control group and seawater group were immersed in seawater for 2 hours, and those in the normal group were not immersed. After an observation period of 5-7 days, no significant redness or purulent discharge was observed in the wound appearance, then debridement was performed followed by corresponding implantations: the control group with gelatin sponges loaded with vancomycin and BMP-2, and the other two groups with 3D-printed nano-β-TCP scaffolds loaded with vancomycin and BMP-2. After filling the bone defects with the respective materials, all groups underwent layer-by-layer suturing of the wound, followed by disinfection with iodine and injection of gentamicin to prevent infection. The affected limbs were then immobilized using a plaster cast. The affected limbs were imaged using anteroposterior X-ray at 4, 8 and 16 weeks after operation, and the repair effects were evaluated using the Lane-Sandhu X-ray scoring system. At 16 weeks after operation, the bone defect tissues were collected for HE staining to observe bone tissue growth.Results:At 4 weeks after operation, the Lane-Sandhu X-ray score in the control group was significantly lower than that in the normal group [(2.8±1.1)points vs. (1.1±0.9)points] ( P<0.05), and that in the seawater group [(2.2±1.0)points] was not significantly different from those in the other two groups (all P>0.05). At 8 weeks after operation, the seawater group [(6.1±0.9)points] and the control group [(2.8±1.0)points] exhibited lower Lane-Sandhu X-ray score compared to the normal group [(8.2±1.0)points] (all P<0.05), and the seawater group showed a higher score compared to the control group ( P<0.05). At 16 weeks after operation, the control group [(3.8±1.0)points] exhibited a lower Lane-Sandhu X-ray score compared to the normal group [(10.0±1.3)points] and the seawater group [(9.3±1.2)points] (all P<0.05), while no significant difference was noted between the latter two ( P>0.05). At 16 weeks after operation, histological observations revealed varying degrees of bone tissue formation in three groups, with the normal group showing the best bone defect repair effect, followed by the seawater group. Conclusion:The 3D-printed nano-β-TCP scaffolds loaded with vancomycin and BMP-2 are effective for the treatment of seawater -soaked bone defects, which can promote bone tissue repair.

Recent advance in anti-neurexin-3α antibody-associated encephalitis / 中华神经医学杂志

Neurexin-3α, discovered in 2016, is a new type of autoimmune encephalitis antibody. Anti-neurexin-3α antibody-associated encephalitis is generally associated with prodromal symptoms or mood changes, having main clinical manifestations as seizures, memory disorders, confusion or loss of consciousness, central ventilation insufficiency, abnormal behavior, and speech disorders. This paper reviews the relevant research progress at home and abroad about pathogenesis, diagnosis and differential diagnosis, treatment and prognosis of anti-neurexin-3α antibody-associated encephalitis, so as to expand the understanding of clinicians for this disease.