FOXO3-Activated HOTTIP Sequesters miR-615-3p away from COL2A1 to Mitigate Intervertebral Disc Degeneration.

In this study, knockout of FOXO3 was found to impair intervertebral disc maturation and homeostasis in postnatal mice as well as facilitating extracellular matrix degradation. RNA sequencing can uncover disease-related gene expression and investigate disease pathophysiology. High-throughput transcriptome sequencing and experimental validations were used to identify the essential gene and mechanism involved in intervertebral disc degeneration (IDD). Nucleus pulposus (NP) tissue samples were collected from the mice with conditional knockout of FOXO3 (FOXO3 KO) for high-throughput sequencing, followed by screening of differentially expressed lncRNAs and mRNAs. The mRNAs were subjected to GO and KEGG enrichment analyses. Interactions among FOXO3, HOTTIP, miR-615-3p, and COL2A1 were analyzed. NP cells were subjected to a series of mimics, inhibitors, overexpression plasmids, and shRNAs to validate the mechanisms of FOXO3 in controlling HOTTIP/miR-615-3p/COL2A1 in IDD. Mechanistically, FOXO3 transcriptionally activated HOTTIP, facilitated the competitive HOTTIP binding to miR-615-3p, and increased the expression of the miR-615-3p target gene COL2A1. Thus, NP cell proliferation was induced, cell apoptosis was diminished, resulting in delayed development of IDD. Based on these data, the transcription factor FOXO3 may decrease miR-615-3p binding to COL2A1 and up-regulate COL2A1 expression by activating HOTTIP transcription, which in turn inhibits NP cell apoptosis and promotes its proliferation, to prevent the degradation of intervertebral disc matrix and maintain the normal physiological function of intervertebral disc, thereby preventing the occurrence and development of IDD.

PLAGL2 induces nucleus pulposus cell apoptosis via regulating RASSF5 expression and thus accelerates intervertebral disc degeneration.

Excessive apoptosis of nucleus pulposus (NP) cells is the main pathological change in intervertebral disc degeneration (IVDD) progression. Pleomorphic adenoma gene like-2 (PLAGL2) plays a key role in cell apoptosis, however, the effect of PLAGL2 on IVDD has not been clarified yet. In this study, we established mouse IVDD models via the annulus fibrosis needle puncture, TUNEL and safranin O staining were used to verify the successful establishment of IVDD models, and PLAGL2 expression was detected in disc tissues. Then, NP cells isolated from disc tissues were used to construct PLAGL2 knockdown cells. PLAGL2 expression in NP cells was analyzed with qRT-PCR and Western blot. The impact of PLAGL2 on the viability, apoptosis, and mitochondria function of NP cells was evaluated by MTT assay, TUNEL, JC1 staining, and flow cytometry assay. Additionally, the regulatory mechanism of PLAGL2 was further assessed. We found that PLAGL2 was upregulated in IVDD disc tissues and serum deprivation (SD)-stimulated NP cells. PLAGL2 knockdown inhibited apoptosis and mitochondria damage in NP cells. Moreover, knockdown of PLAGL2 downregulated the expression of downstream apoptosis-related factors RASSF5, Nip3, and p73. Mechanically, PLAGL2 transcriptionally activated RASSF5 via binding to its promoter. In general, our findings indicate that PLAGL2 induces apoptosis in NP cells and aggravates IVDD progression. This study provides a promising therapeutic target for IVDD treatment.

Exosomal miR-532-5p from bone marrow mesenchymal stem cells reduce intervertebral disc degeneration by targeting RASSF5.

The transplantation of bone marrow mesenchymal stem cells (BMSCs) has been found to be used as an effective therapy of intervertebral disc degeneration (IDD). However, the underlying mechanisms of BMSCs in the progress of IDD are not fully explained. In this study, we found that exosomes derived from BMSCs (BMSCs-Exos) inhibited the apoptotic rate, extracellular matrix (ECM) degradation, and fibrosis deposition in TNF-α-induced nucleus pulposus cells (NPCs). Importantly, the level of miR-532-5p was observed to be decreased in apoptotic NPCs, but abundant in BMSCs-Exos with TNF-α treatment. The results showed that BMSCs-Exos under TNF-α stimuli exerted better effects on NPCs than BMSCs-Exos, which might be mitigated by the inhibition of miR-532-5p in BMSCs-Exos. The gain-of-function results suggested that the direct overexpression of miR-532-5p in NPCs could inhibit TNF-α-induced increase of apoptotic process, activation of apoptotic proteins, imbalance of anabolism/catabolism levels, and accumulation of collagen I. In addition, RASSF5 was demonstrated to be a target of miR-532-5p. Knockdown of RASSF5 could decrease the apoptotic cells and reduce the activated apoptotic protein levels in TNF-α-induced NPCs. Overall, these data indicate that exosomes from BMSCs may suppress TNF-α-induced apoptosis, ECM degradation, and fibrosis deposition in NPCs through the delivery of miR-532-5p via targeting RASSF5. This work provides a promising therapeutic strategy for the progress of IDD.

DDX10 overexpression predicts worse prognosis in osteosarcoma and its deletion prohibits cell activities modulated by MAPK pathway.

Osteosarcoma (OS) is an invasive cancer in the skeletal system. The molecular mechanism of its etiology and pathogenesis are still not clear, so the effective treatment strategy of OS needs further research. First, we analyzed the expression level and prognostic ability of the RNA helicase DDX10 in OS patients based on the data obtained from GEO database. Next, we used CCK8 to test OS cell viability. Besides, we used wound-healing assay and transwell migration assay to detect cell migration of OS MG63 cell line. And the cell invasion was tested by transwell invasion assay. Moreover, we used QRT-PCR and western blot to analyze the mRNA and protein expression levels. We found that DDX10 was significantly over-expressed in OS patients and elevated level of DDX10 was associated with a poor prognosis. Silencing of DDX10 inhibited proliferation, invasion and migration of MG63 cells in vitro. Down-regulation of DDX10 inhibited MAPK signaling pathway. The expression of p-MEK and p-ERK were also decreased by silencing of DDX10. Therefore, Silencing of DDX10 inhibited proliferation, invasion and migration of MG63 cells, which might be regulated by suppression of MAPK pathway. In conclusion, our results unfold a novel area of studying for understanding how DDX10 functions in OS oncogenic and prognostic significance, accordingly implying a promising therapeutic target for OS treatment.

LINC00969 promotes the degeneration of intervertebral disk by sponging miR-335-3p and regulating NLRP3 inflammasome activation.

Long noncoding RNAs (LncRNAs) may serve as miRNA sponges to regulate the expressions of miRNA target genes. LncRNA LINC00969 has been indicated to be upregulated in intervertebral disk degeneration. However, the regulatory mechanism of LINC00969 in intervertebral disk degeneration progression remains unclear. Differently expressed LINC00969, miR-335-3p, and thioredoxin-interacting protein (TXNIP) were determined in nucleus pulposus (NP) tissues and cells isolated from patients with intervertebral disk degeneration. The interaction between LINC00969, miR-335-3p, and TXNIP was also assessed. In this study, we demonstrated that LINC00969 was highly expressed, whereas miR-335-3p was aberrantly downregulated in NP tissues and cells of intervertebral disk degeneration patients. In addition, our results suggested that LINC00969 enhanced NP cell apoptosis. More importantly, LINC00969 was identified to function as a competitive endogenous RNA (ceRNA) for miR-335-3p to positively regulate TXNIP expression in vitro. Our study provided evidence for the cross-talk between LINC00969, miR-335-3p, and TXNIP, shedding light on the therapy for intervertebral disk degeneration. © 2018 IUBMB Life, 71(5):611-618, 2019.

[Effect and mechanisms of TET on human gastric carcinoma cell line SGC7901 and SGC7901/ADR].

OBJECTIVE: To investigate the effect of tetrandrine (TET) on zinc finger protein 139 (ZNF139) and multidrug resistance (MDR) of human gastric carcinoma cell lines and possible mechanisms. METHODS: Cultured SGC7901 and SGC7901/ADR were treated with TET (0.5, 1.0, 1.5, 2.0, and 2.5 microg/mL), then inhibition rates were measured by MTT assay in vitro. The expressions of ZNF139, MRP-1, MDR1, and GST-pi were detected by RT-PCR. The correlation between ZNF139 and each multidrug resistance factor was analyzed using Spearman correlation analysis, and the coefficient correlation was calculated. RESULTS: The inhibition rate of TET (< or = 2.0 microg/mL) for SGC7901 and SGC7901/ADR was less than 10% with MTT assay. Expressions of ZNF139, MRP-1, MDR1, and GST-pi mRNA were higher in SGC7901/ADR than in SGC7901 (all P < 0.05). The expressions of ZNF139, MRP-1, MDR1, and GST--pi were down-regulated in SGC7901/ADR cells efficiently (all P < 0.01). Positive correlation existed between ZNF139 and MRP-1, ZNF139 and MDR1 before treated by TET in SGC7901/ADR, and this relationship also existed in SGC7901/ADR cells after treated by TET (all P < 0.05). CONCLUSION: TET could achieve MDR reversion in gastric cancer cells by down-regulating the expression of ZNF139, MRP-1, and MDR1.

Ginsenoside Rg1 relieves rat intervertebral disc degeneration and inhibits IL-1ß-induced nucleus pulposus cell apoptosis and inflammation via NF-κB signaling pathway.

The study aimed to investigate the effect of ginsenoside Rg1 on intervertebral disc degeneration (IVDD) in rats and IL-1ß-induced nucleus pulposus (NP) cells, and explore its underlying mechanism. Forty IVDD rat models were divided into the IVDD group, low-dose (L-Rg1) group (intraperitoneal injection of 20 mg/kg/d ginsenoside Rg1), medium-dose (M-Rg1) group (intraperitoneal injection of 40 mg/kg/d ginsenoside Rg1), and high-dose (H-Rg1) group (intraperitoneal injection of 80 mg/kg/d ginsenoside Rg1). The pathological change was observed by HE and safranin O-fast green staining. The expression of IL-1ß, IL-6, TNF-α, MMP3, aggrecan, and collagen II was detected. The expression of NF-κB p65 in IVD tissues was detected. Rat NP cells were induced by IL-1ß to simulate IVDD environment and divided into the control group, IL-1ß group, and 20, 50, and 100 µmol/L Rg1 groups. The cell proliferation activity, the apoptosis, and the expression of IL-6, TNF-α, MMP3, aggrecan, collagen II, and NF-κB pathway-related protein were detected. In IVDD rats, ginsenoside Rg1 improved the pathology of IVD tissues; suppressed the expression of IL-1ß, IL-6, TNF-α, aggrecan, and collagen II; and inhibited the expression of p-p65/p65 and nuclear translocation of p65, to alleviate the IVDD progression. In the IL-1ß-induced NP cells, ginsenoside Rg1 also improved the cell proliferation and inhibited the apoptosis and the expression of IL-6, TNF-α, aggrecan, collagen II, p-p65/p65, and IκK in a dose-dependent manner. Ginsenoside Rg1 alleviated IVDD in rats and inhibited apoptosis, inflammatory response, and ECM degradation in IL-1ß-induced NP cells. And Rg1 may exert its effect via inhibiting the activation of NF-κB signaling pathway.

Tumor chemosensitivity is correlated with expression of multidrug resistance associated factors in variously differentiated gastric carcinoma tissues.

BACKGROUND/AIMS: To evaluate the relationship between chemosensitivities in vitro and expressions of multidrug resistance (MDR) associated factors in differentiated gastric carcinomas. METHODOLOGY: Gastric carcinomas tissues of varying degree of differentiation (65 cases) were collected and chemosensitivities to 5-FU, HCPT, PTX, L-OHP, CDDP and eADM were detected by sulphorhodamine B (SRB) assay, and expressions of P-gp, GST-π, Topo IIα, p53, Bcl-2, Bax and Survivin were tested by immunohistochemical staining. RESULTS: Inhibition rates of 5-FU, L-OHP and CDDP for well differentiated tumors were lower than those of poorly differentiated tumors (p<0.05). Expressions of P-gp, Bcl-2 and Survivin were higher in well differentiated than in poorly differentiated carcinomas (p<0.05); while expression of Topo IIα in well differentiated carcinomas was lower than in poorly differentiated carcinomas (p<0.05). The expression of MDR factors was different between well and poorly differentiated carcinomas. CONCLUSIONS: Different MDR characteristics were exhibited in well and poorly differentiated gastric carcinomas, which may be caused by different expressed MDR associated factors in these tissues.

Clinical Efficacy of Bilateral Decompression Using Biportal Endoscopic Versus Minimally Invasive Transforaminal Lumbar Interbody Fusion for the Treatment of Lumbar Degenerative Diseases.

OBJECTIVE: The study purpose was to compare unilateral biportal endoscopic lumbar interbody fusion (ULIF) with minimally invasive transforaminal lumbar interbody fusion (MIS-TLIF) for the treatment of lumbar degenerative diseases in terms of surgical trauma and short-to medium-term postoperative results. METHODS: Forty-nine patients with lumbar degenerative diseases (25 underwent ULIF, 24 underwent MIS-TLIF) who were treated between May 2019 and October 2021, were included in this retrospective analysis. We compared the 2 groups' blood loss, serum C-reactive protein (CRP), visual analog scale (VAS) scores for low back and leg pain, and the Oswestry Disability Index (ODI) score and slip percentage (SP). The modified Macnab score was obtained at the last follow-up. RESULTS: On the postoperative day, the CRP levels (P < 0.05) were considerably lower in the ULIF group than those in the MIS-TLIF group. In addition, the ULIF group had significantly decreased intraoperative blood loss (P = 0.00) and postoperative blood loss (P = 0.00). After surgery, there was significant improvement in both groups in the VAS scores for low back and leg pain and in the ODI scores (P < 0.05). Two weeks after surgery, the ODI and VAS scores for low back pain of the ULIF group were considerably lower than those of the MIS-TLIF group (P < 0.05). The excellent and good rates of the Macnab criteria between the 2 groups were not significantly different at the last follow-up (P = 0.95). CONCLUSIONS: The ULIF technique can effectively treat short-segment lumbar degenerative diseases and is a feasible alternative to the traditional minimally invasive surgery.

Study on synergistic pyrolysis and kinetics of mixed plastics based on spent fluid-catalytic-cracking catalyst.

At present, disposable plastic products such as plastic packaging are very common in our daily life. These products are extremely easy to cause serious damage to the soil and marine environment due to their short design and service life, difficulties in degradation, or long degradation cycles. Thermochemical method (pyrolysis or catalytic pyrolysis) is an efficient and environmentally friendly way to treat plastic waste. In order to further reduce the energy consumption of plastic pyrolysis and improve the recycling rate of spent fluid catalytic cracking (FCC) catalysts, we adopt the "waste-to-waste" approach to apply the spent FCC catalysts as catalysts in the catalytic pyrolysis of plastics, exploring the pyrolysis characteristics, kinetic parameters, and synergistic effects between different typical plastics (polypropylene, low-density polyethylene, polystyrene). The experimental results show that the spent FCC catalysts used in the catalytic pyrolysis of plastics are beneficial to reduce the overall pyrolysis temperature and activation energy, in which the maximum weight loss temperature decreases by about 12 â„ƒ and the activation energy decreases by about 13%. The activity of spent FCC catalysts is improved after modification by microwave and ultrasonic, which further improve the catalytic efficiency and reduce the energy consumption of pyrolysis. The co-pyrolysis of mixed plastics is dominated by positive synergistic effect, which is conducive to improving the thermal degradation rate and shortening the pyrolysis time. This study provides relevant theoretical support for the resource application of spent FCC catalysts and "waste-to-waste" treatment of plastic waste.

[Comparative study on effectiveness of percutaneous endoscopic and Wiltse-approach transforaminal lumbar interbody fusion in the treatment of lumbar spondylolisthesis].

OBJECTIVE: To compare the effectiveness of percutaneous endoscopic transforaminal lumbar interbody fusion (PE-TLIF) and Wiltse-approach TLIF (W-TLIF) in the treatment of lumbar spondylolisthesis. METHODS: The clinical data of 47 patients with lumbar spondylolisthesis who met the selection criteria between July 2018 and June 2019 were retrospectively analyzed, in which 21 patients were treated with PE-TLIF (PE-TLIF group) and 26 patients were treated with W-TLIF (W-TLIF group). There was no significant difference between the two groups in age, gender, disease duration, level of spondylolisthesis vertebrae, spondylolisthesis degree, spondylolisthesis type, and preoperative visual analogue scale (VAS) score of low back pain and leg pain, lumbar Japanese Orthopaedic Association (JOA) score, and the disc height (DH), segmental lordosis (SL), and Taillard index (TI) of the operated vertebrae ( P>0.05). The operation time, intraoperative blood loss, postoperative drainage, postoperative bedridden time, and complications were compared between the two groups. The VAS score and JOA score were used to evaluate the improvement of pain and function. At last follow-up, DH, SL, and TI of operated vertebrae were measured by X-ray films, and lumbar CT was performed to evaluate the interbody fusion. RESULTS: Compared with W-TLIF group, the operation time in PE-TLIF group was significantly longer, but the intraoperative blood loss and postoperative drainage were significantly less, and the postoperative bedridden time was significantly shorter ( P<0.05). There were 2 cases of transient lower limb radiating pain in PE-TLIF group and 1 case of superficial incision infection in W-TLIF group. There was no significant difference in the incidence of complications (9.5% vs. 3.8%) between the two groups ( χ 2=0.037, P=0.848). The patients in both groups were followed up 12-24 months, with an average of 17.3 months in PE-TLIF group and 17.7 months in W-TLIF group. The VAS scores of low back pain and leg pain, and the JOA scores of the two groups significantly improved at each time point after operation when compared with those before operation ( P<0.05). Compared with W-TLIF group, the VAS scores of low back pain in PE-TLIF group significantly lower at 3 days and 3 months after operation ( P<0.05), and the JOA score of PE-TLIF group was significantly higher at 3 months after operation ( P<0.05), and there was no significant difference in each score at any other time point between the two groups ( P>0.05). At last follow-up, the DH, SL, and TI of operated vertebrae of the two groups significantly improved when compared with those before operation ( P<0.05), and there was no significant difference in the differences of each parameter between the two groups ( P>0.05). According to Suk's standard, the fusion rates of PE-TLIF group and W-TLIF group were 90.5% (19/21) and 92.3% (24/26), respectively, with no significant difference ( χ 2=0.000, P=1.000). At last follow-up, there was no case of Cage sunk into the adjacent vertebral body, or dislodgement of Cage anteriorly or posteriorly in both groups. CONCLUSION: PE-TLIF and W-TLIF are both effective in the treatment of grade Ⅰ and Ⅱ lumbar spondylolisthesis. Although the operation time is prolonged, PE-TLIF has less intraoperative blood loss and postoperative drainage, shorter postoperative bedridden time, and can get more obvious short-term improvement of low back pain and function.

p300 arrests intervertebral disc degeneration by regulating the FOXO3/Sirt1/Wnt/ß-catenin axis.

The transcription factor p300 is reportedly involved in age-associated human diseases, including intervertebral disc degeneration (IDD). In this study, we investigate the potential role and pathophysiological mechanism of p300 in IDD. Clinical tissue samples were collected from patients with lumbar disc herniation (LDH), in which the expression of p300, forkhead box O3 (FOXO3), and sirtuin 1 (Sirt1) was determined. Nucleus pulposus cells (NPCs) isolated from clinical degenerative intervertebral disc (IVD) tissues were introduced with oe-p300, oe-FOXO3, Wnt/ß-catenin agonist 1, C646 (p300/CBP inhibitor), or si-p300 to explore the functional role of p300 in IDD and to characterize the relationship between p300 and the FOXO3/Sirt1/Wnt/ß-catenin pathway. Also, we established a rat IDD model by inducing needle puncture injuries in the caudal IVDs for further verification of p300 functional role. We found that p300 was downregulated in the clinical tissues and NPCs of IDD. Overexpression of p300 promoted the proliferation and autophagy of NPCs while inhibiting cell apoptosis, which was associated with FOXO3 upregulation. p300 could increase the expression of FOXO3 by binding to the Sirt1 promoter, and thus, contributed to inactivation of the Wnt/ß-catenin pathway. In vivo results further displayed that p300 slowed down the progression of IDD by disrupting the Wnt/ß-catenin pathway through the FOXO3/Sirt1 axis. Taken together, we suggest that p300 can act to suppress IDD via a FOXO3-dependent mechanism, highlighting a potential novel target for treatment of IDD.

[Application of CFP short-stem prosthesis in the treatment of osteonecrosis of the femoral head].

OBJECTIVE: To investigate the clinical outcome for the treatment of osteonecrosis of the femoral head (ONFH) in advanced stage by a short-stem prosthesis preserving femoral neck in total hip arthroplasty (THA). METHODS: From June 2008 to December 2009, 9 hips in 8 patients with advanced stage of ONFH were treated by a short-stem preserving femoral neck in THA. The mean age was 24.1 years (range: 20 - 36). There were 3 patients (3 hips) with alcohol-induced ONFH and 5 patients (6 hips) with steroid-induced ONFH. According to the classification of Association Research Circulation Osseous (ARCO), 7 hips were in stage III-C and 2 hips in stage IV respectively. The clinical outcomes were evaluated according to the Harris evaluation score and radiographic analysis. RESULTS: All patients were followed up for a mean duration of 18.1 months (range: 12 - 30). The mean Harris hip score improved from preoperative (42.8 ± 8.6) points to (92.8 ± 6.1) points at the time of final follow-up. The outcomes were excellent in 7 hips and better in 2 hips. Neither osteolysis of mortar and femur nor loose component was found from radiological films. The pain of all hips disappeared and no complications occurred. CONCLUSION: The short-term clinical outcome is satisfactory for treating young patients with advanced stage of ONFH by a short-stem prosthesis preserving femoral neck in THA.

Prognostic factors of chondroblastic osteosarcoma and nomogram development for prediction: A population-based, STROBE-compliant study.

ABSTRACT: The present study aimed to develop nomograms to predict survival in patients with chondroblastic osteosarcoma (COS).An analysis was conducted of 320 cases of COS collected from the surveillance, epidemiology, and end results (SEER) database between 2004 and 2015. Independent prognostic factors were screened using univariate and multivariate Cox analyses. Subsequently, nomograms were established to predict the patients' cancer-specific survival (CSS) and overall survival (OS) rates. The prediction accuracy and discriminative ability of the nomograms were examined using calibration curves and the concordance index (C-index).As revealed in the univariate and multivariate Cox regression analysis, age, tumor size, the primary site, the presence of metastasis, a history of having undergone surgery, and a history of having received radiotherapy were found to be independent prognostic factors associated with survival in patients with COS (all P < .05). Furthermore, age >39 years, the presence of distant metastasis, no history of having undergone any surgery, and tumor size >103 mm were found to be associated with poor prognosis in patients, while the primary site of the mandible and no history of having undergone radiotherapy showed associations with a more favorable prognosis in patients. Next, nomograms were constructed to predict the OS and CSS in patients with COS.We constructed nomograms that can provide accurate survival predictions in patients with chondroblastic osteosarcoma. These nomograms can help surgeons customize the treatment strategies for patients with chondroblastic osteosarcoma.

Clinical therapeutic effects of combined methotrexate and other chemotherapeutic agents in treating children and young patients with osteosarcoma: A protocol for systematic review and meta-analysis.

BACKGROUND: Osteosarcoma is one of the most common primary bone tumour in children and young patients, and the third most common among adults. Its main treatment option is currently based on neoadjuvant or adjuvant chemoradiotherapy along with the lesion's surgical resection. The current study's primary aim is to examine the clinical therapeutic impacts of combined methotrexate, along with other chemotherapeutic agents to treat children and young adults suffering from osteosarcoma. METHODS: We will perform a comprehensive literature search in English database (PubMed, EMBASE, Cochran Library CINAHL, and PsycINFO) and Chinese database (Chinese National Knowledge Infrastructure, VIP information database, Chinese Biomedical Database, and WanFang Database) with no language restriction from their inception to the search date. Additionally, two independent authors will screen the works of literature obtained from these databases, obtain information, and examine the risks of data included for the studies' bias. Furthermore, we intend to employ the Q statistics as well as I2 statistics to calculate heterogeneity among each study's analysis. Accordingly, we will utilize the funnel plots and Egger test to assess the possibility of publication bias where relevant. RESULTS: The current study aims to provide significant information regarding the clinical therapeutic impacts of combines methotrexate along with other chemotherapeutic agents to treat children and young adults suffering from osteosarcoma. CONCLUSIONS: The present study will generate compelling evidence of combined methotrexate as well as other chemotherapeutic agents for osteosarcoma among children and young adults. Also, it will provide clinical practice suggestions. ETHICS AND DISSEMINATION: The study is founded upon published data. Therefore, there is no requirement for ethics approval. OSF REGISTRATION NUMBER: March 26, 2021.osf.io/a23rc. (https://osf.io/a23rc/).

[Comparison of the effectiveness of oblique lumbar interbody fusion and posterior lumbar interbody fusion for treatment of Cage dislodgement after lumbar surgery].

OBJECTIVE: To compare the clinical and radiological effectiveness of oblique lumbar interbody fusion (OLIF) and posterior lumbar interbody fusion (PLIF) in the treatment of Cage dislodgement after lumbar surgery. METHODS: The clinical data of 40 patients who underwent revision surgery due to Cage dislodgement after lumbar surgery betweem April 2013 and March 2017 were retrospectively analyzed. Among them, 18 patients underwent OLIF (OLIF group) and 22 patients underwent PLIF (PLIF group) for revision. There was no significant difference between the two groups in age, gender, body mass index, intervals between primary surgery and revision surgery, number of primary fused levels, disc spaces of Cage dislodgement, and visual analogue scale (VAS) scores of low back pain and leg pain, Oswestry disability index (ODI), the segmental lordosis (SL) and disc height (DH) of the disc space of Cage dislodgement, and the lumbar lordosis (LL) before revision ( P>0.05). The operation time, intraoperative blood loss, hospital stay, and complications of the two groups were recorded and compared. The VAS scores of low back pain and leg pain were evaluated at 3 days, 3, 6, and 12 months after operation, and the ODI scores were evaluated at 3, 6, and 12 months after operation. The SL and DH of the disc space of Cage dislodgement and LL were measured at 12 months after operation and compared with those before operation. CT examination was performed at 12 months after operation, and the fusion of the disc space implanted with new Cage was judged by Bridwell grading standard. RESULTS: The intraoperative blood loss in the OLIF group was significantly less than that in the PLIF group ( t=-12.425, P=0.000); there was no significant difference between the two groups in the operation time and hospital stay ( P>0.05). Both groups were followed up 12-30 months, with an average of 18 months. In the OLIF group, 2 patients (11.1%) had thigh numbness and 1 patient (5.6%) had hip flexor weakness after operation; 2 patients (9.1%) in the PLIF group had intraoperative dural sac tear. The other patients' incisions healed by first intention without early postoperative complications. There was no significant difference in the incidence of complications between the two groups ( χ 2=0.519, P=0.642). The VAS scores of low back pain and leg pain, and the ODI score of the two groups at each time point after operation were significantly improved when compared with those before operation ( P<0.05); there was no significant difference between the two groups at each time point after operation ( P>0.05). At 12 months after operation, SL, LL, and DH in the two groups were significantly increased when compared with preoperative ones ( P<0.05); SL and DH in the OLIF group were significantly improved when compared with those in the PLIF group ( P<0.05), and there was no significant difference in LL between the two groups ( P>0.05). CT examination at 12 months after operation showed that all the operated disc spaces achieved bony fusion. According to the Bridwell grading standard, 12 cases were grade Ⅰ and 6 cases were grade Ⅱ in the OLIF group, and 13 cases were grade Ⅰ and 9 cases were grade Ⅱ in the PLIF group; there was no significant difference between the two groups ( Z=-0.486, P=0.627). During follow-up, neither re-displacement or sinking of Cage, nor loosening or fracture of internal fixation occurred. CONCLUSION: OLIF and PLIF can achieve similar effectiveness in the treatment of Cage dislodgement after lumbar surgery. OLIF can further reduce intraoperative blood loss and restore the SL and DH of the disc space of Cage dislodgement better.

Effect of Ginsenoside Rg1 on the intervertebral disc degeneration rats and the degenerative pulposus cells and its mechanism.

OBJECTIVE: To explore the effect of ginsenoside Rg1 on intervertebral disc degeneration (IVDD) in vivo and in vitro and its mechanism. METHODS: 60 rats were underwent surgery to construct rat models of IVDD and divided in the sham group, model group and gradient G-Rg1 groups (10 mg/kg/d, 20 mg/kg/d and 40 mg/kg/d).The change of histology was observed by HE staining, the water content and the expression of ß-catenin in IVD were detected. Rat nucleus pulposus cells(NPCs) were isolated from IVDD rats and divided in D-NPCs group, and gradient G-Rg1 groups(20 µg/ml, 50 µg/ml and 100 µg/ml).The cell proliferation activity, cell apoptosis rate,the expression of proteins related to ECM and Wnt/ß-catenin were detected respectively, Finally the agonist of Wnt/ß-catenin pathway LiCl was used for reversed experiments. RESULTS: In vivo, G-Rg1 treatment could improve the structural disorganization, low water content, NPCs number and aggrecan and collagenⅡ expression in IVD and down-regulate the expression of ß-catenin. In vitro NPCs, G-Rg1 treatment could improve the low cell proliferation, high apoptosis rate and low expression of aggrecan and collagenⅡ in degenerative NPCs in a dose-dependent manner.G-Rg1 treatment could down-regulate the expression of proteins related to ß-catenin signal and LiCl could reverse the increase of cell proliferation and ECM synthesis, decrease of apoptosis of degenerative NPCs induced by G-Rg1. CONCLUSION: G-Rg1 could promote ECM synthesis of degenerative NPCs and inhibiting its apoptosis, improve the IVDD via inhibiting the Wnt/ß-catenin pathway.

Application of positive behavior management in patients after breast cancer surgery.

BACKGROUND: As a radical treatment, breast cancer surgery has a positive psychological impact on most patients. However, some patients do not have a clear understanding of the disease, which requires a more scientific and comprehensive consideration during clinical intervention and are based on cognition. The positive behavior management model is based on this kind of background-derived new interventions, which can better serve the clinical rehabilitation process of patients. The positive behavior management model based on cognitive architecture is a new type of intervention derived from this background, which can better serve the clinical rehabilitation process of patients. AIM: To analyze the influence of a positive behavior management model based on cognitive framework on the degree of hope and self-efficacy of patients with breast cancer surgery. METHODS: Eighty-four patients with breast cancer who underwent surgical treatment in our hospital from August 2016 to December 2018 were included in the study. The patients were divided into the experimental group (n = 42) and control group (n = 42) by random number table grouping. The control group received traditional nursing intervention, while the experimental group received a positive behavior management model based on cognitive framework based on the traditional intervention of the control group. General Self-efficacy Scale, Herth Hope Scale, Self-Rating Anxiety Scale, Self-Rating Depression Scale and Cancer Patient Specific Scale were used to evaluate the two groups before and 1 wk after intervention. RESULTS: After the intervention, self-efficacy and hope level of the experimental group were significantly higher than those of the control group (P < 0.05). The Self-Rating Anxiety Scale and Self-Rating Depression Scale scores in the experimental group were significantly lower than those in the control group (P < 0.05). There was no significant difference in the quality of life scores between the two groups before intervention (P > 0.05). The quality of life scores in all aspects in the experimental group after intervention were significantly higher than those in the control group (P < 0.05). CONCLUSION: The positive behavior management model based on cognitive framework applied to patients with breast cancer surgery improved hope for treatment and self-efficacy, reduced negative emotion, and improved quality of life.

Trans-upper-sternal approach to the cervicothoracic junction.

UNLABELLED: From August 1999 to February 2006, 11 patients with cervicothoracic lesions (eight males, three females; age range, 17-77 years) were surgically treated using the trans-upper-sternal approach. Combined cervicothoracic incision and upper sternotomy facilitated exposure for tumor resection, partial or subtotal removal of the involved vertebrae, and spinal cord decompression. The spinal column then was stabilized. Neurologic status was assessed using the Frankel classification. Followup for a minimum of 10 months (mean, 31 months; range, 10-56 months) revealed one patient had a chyle leak (50 mL) 1 day after surgery, which resolved after 2 days of drainage. One patient had a transient vocal cord paresis, which recovered within 3 months of surgery. All the patients had improved neurologic function. No nonunions or instrument-related complications developed. Stability of the vertebral column was maintained during followup in all patients. The trans-upper-sternal approach can provide excellent exposure for reconstruction of the cervicothoracic junction. Special care must be taken to avoid injury to the recurrent laryngeal nerve and the thoracic duct. LEVEL OF EVIDENCE: Level IV, therapeutic study. See the Guidelines for Authors for a complete description of levels of evidence.

Downregulation of annexin A7 decreases proliferation, migration, and invasion of gastric cancer cells by reducing matrix metalloproteinase 1 and 9 expression.

High annexin A7 expression is a potential indicator of lymphatic metastasis and poor prognosis in patients with gastric cancer (GC). The mechanism underlying the effects of annexin A7 on GC cells remains unclear. In patients with GC, primary adenocarcinoma tissues had higher annexin A7 expression than adjacent non-cancerous tissues (P < 0.05). Among three human GC cell lines with high, moderate, and low levels of differentiation, respectively, the cell line with the lowest level of differentiation displayed the highest level of annexin A7 expression. We transfected cells of the human GC cell line BGC823 with short interfering RNAs (siRNAs) targeting annexin A7 and investigated the effects on signaling pathways related to cancer progression by quantitative real-time PCR and western blot. The silencing of endogenous annexin A7 suppressed the proliferation, migration, and invasion abilities of the BGC823 cells. In the cells treated with annexin A7 siRNA, the expression of p16, p21, and p27 was significantly upregulated while that of proliferating cell nuclear antigen (PCNA), cyclin A, cyclin D1, cyclin E1, matrix metalloproteinase-2 (MMP-2), MMP-9, and intercellular cell-adhesion molecule-1 (ICAM-1) was significantly downregulated compared with that in control cells. Our results suggest that the downregulation of endogenous annexin A7 inhibits GC cell proliferation, migration, and invasion by impacting cell cycle regulators and the expression of MMP-1, MMP-2, and ICAM-1. Targeting annexin A7 may represent a valuable strategy for the diagnosis and clinical treatment of GC.