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STUDY DESIGN: A retrospective study. BACKGROUND: Conventional cage-plate construct (CCP) was widely used in anterior cervical discectomy and fusion (ACDF), but the rigid fixation limits the motion of fused segments. Self-locking stand-alone cage (SSC) was an alternative for ACDF procedures and showed several superiorities. However, the effect of hybrid fixation in 3-level ACDF remains unknown. OBJECTIVE: To assess the clinical and radiological outcomes of hybrid fixation with SSC and CCP against conventional CCP in 3-level ACDF. METHOD: A retrospective review of patients who underwent 3-level ACDF at Renji Hospital between January 2018 and December 2019 was performed. Eighty-three patients met the inclusion and exclusion criteria and were stratified into 2 groups based on the fixation methods. The clinical outcomes, functional outcomes, and radiological parameters were collected and analyzed. RESULTS: No significant difference was observed between the two groups in the mean age, sex, body mass index, hospital stay, and duration of follow-up. The postoperative C2-7 Cobb angle in the CCP group was significantly greater than that in the hybrid group. The rate of cervical proximal junctional kyphosis (CPJK) in the hybrid group was significantly lower than that in the CCP group. The CCP group suffered significantly higher rates of adjacent segment degeneration (ASD) than the hybrid group at 2 years postoperatively. Moreover, the incidence of postoperative dysphagia was lower in the hybrid group. No significant differences were observed in JOA and NDI scores between the two groups. CONCLUSION: The hybrid fixation achieved comparable clinical outcomes against CCP fixation, indicating that hybrid fixation is an alternative procedure in 3-level ACDF.
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OBJECTIVE: R6G-ddATP was used as a dideoxy fluorescence substrate to establish the single base end extension (SNaPShot)-gel fluorescence method for the rapid detection of the genotypes of three high-risk human papillomaviruses (HR-HPV) ( HPV18, HPV33 and HPV35) genotypes. METHODS: HPV quality control products were used as as samples, and R6G-ddATP dideoxy fluorescence reagent was used as substrate. Firstly, HPV was amplified by using universal primers to obtain the first round of amplified products, which were purified and used as templates for subsequent SNaPShot reactions. Then, specific one-step extension primers were used to perform SNaPShot reaction to generate R6G-fluorescence-labeled DNA extension products. The product was subjected to agarose gel electrophoresis, the results of which were observed under a Gel Imager, and the HPV genotyping was done with different one-step extension primers. Each sample was tested three times and the results were compared with DNA sequencing results. RESULTS: The preferred annealing temperature for SNaPShot reaction is 55 â. Three HPV genotypes were examined by R6G-ddATP/SNaPShot gel fluorescence assay under optimal conditions, and the results were consistent with DNA sequencing results. CONCLUSION: The R6G-ddATP/SNaPShot-gel fluorescence method for the micro-detection methods of three HR-HPV genotypes was successfully established and can be used for rapid detection of HPV genotypes.
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Alphapapillomavirus , Papillomaviridae , Infecciones por Papillomavirus , ADN Viral/genética , Nucleótidos de Desoxiadenina , Didesoxinucleótidos , Genotipo , Humanos , Papillomaviridae/genética , Reacción en Cadena de la PolimerasaRESUMEN
OBJECTIVE: Cervical angina is an underrecognized type of noncardiac chest pain and its mechanism of pain remains obscure. The objective of the current study was to investigate the clinical outcomes of different surgical strategies for patients with cervical angina and to analyze the potential pathogenesis of Luschka's joint osteophyte. METHODS: From February 2013 to March 2018, a prospective study on cervical angina was performed in our hospital. All patients who were diagnosed with both noncardiac chest pain and cervical pathology were identified. During admission, they consulted with a cardiologist and underwent strict cardiac workups to exclude true angina pectoris. The included 41 patients were randomly divided into two groups according to different surgical strategies of whether or not to remove Luschka's joint osteophyte during anterior cervical decompression surgery: the osteophyte resection (OR group) and the nonresection (NR group). RESULTS: The OR group consisted of 21 patients (8 men and 13 women) with a mean age of 54.7 years (range, 41-65 years). The NR group was composed of 20 patients (9 men and 11 women) with an average age of 56.3 years (range, 43-68 years). Before surgery, the mean duration of symptoms was 6.1 months (range, 4-20 months). The Luschka's joint osteophytes were located at C6 -C7 (19 cases, 46.3%), C5 -C6 (17 cases, 41.5%), and C4 -C5 (4 cases, 12.2%). Their average area was 34.85 mm2 and the average length were 5.09 mm. No statistically significant differences in demographic characteristics were detected between the two groups (P > 0.05). After operation, there were significant improvements in the Japanese Orthopedic Association score and the Neck Disability Index score in both groups (P < 0.05). However, the visual analogue scale score for chest pain in the OR group was statistically lower than that in the NR group (1.4 ± 1.0 vs 2.1 ± 1.6, P < 0.05). In the OR group, the results of cervical spine surgery were excellent in 18 patients (85.7%), and fair in 3 patients (14.3%). In the NR group, there were 10 patients (50.0%) with excellent results, 9 patients with fair results (45.0%), and 1 patient with poor results (5.0%). Notably, there were statistically significant differences between the two groups (χ2 = 6.265, P = 0.044). The average follow-up was 31 months (24-52 months). CONCLUSION: Anterior cervical decompression surgery with resection of Luschka's joint osteophyte can effectively reduce cervical angina symptom and improve the patient's quality of life. In addition to nerve root compression, Luschka's joint osteophyte may be another pathogenic factor in cervical angina.
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Angina de Pecho/etiología , Vértebras Cervicales/cirugía , Descompresión Quirúrgica/métodos , Osteofito/cirugía , Radiculopatía/cirugía , Adulto , Anciano , Evaluación de la Discapacidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Osteofito/complicaciones , Dimensión del Dolor , Estudios Prospectivos , Calidad de Vida , Radiculopatía/complicacionesRESUMEN
Osteoarthritis (OA) is a common clinical degenerative disease characterized by the destruction of articular cartilage, which has an increasing impact on people's lives and social economy. The pathogenesis of OA is complex and unclear, and there is no effective way to block its progress. The study of the pathogenesis of OA is the prerequisite for the early diagnosis and effective treatment of OA. To define the pathogenesis of OA, this review considers the pathological mechanism of OA that involves microRNA, lncRNA, and exosomes. More and more evidence shows that microRNA, lncRNA, and exosomes are closely related to OA. MicroRNA inhibits the target gene by binding to the 3'- untranslated region of the targets. LncRNA usually competes with microRNA to regulate the expression level of downstream genes, while exosomes, as a carrier of intercellular information transfer, transmit the biological information of mother cells to target cells, and the effect of exosomes secreted by different cells on OA are different. In this review, we emphasized that different microRNA, lncRNA, and exosomes have different regulatory effects on chondrocyte proliferation and apoptosis, extracellular matrix degradation and inflammation. Besides, we classified and analyzed these molecules according to their effects on the progress of OA. Based on the analysis of the reported literature, this review reveals some pathogenesis of OA, and emphasizes that microRNA, lncRNA, and exosomes have great potential to assist early diagnosis and effective treatment of OA.
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Exosomas/metabolismo , MicroARNs/metabolismo , Osteoartritis/metabolismo , Osteoartritis/patología , ARN Largo no Codificante/metabolismo , Progresión de la Enfermedad , HumanosRESUMEN
OBJECTIVE: To evaluate the antitumor capability and to investigate the underlying molecular mechanism of paclitaxel. METHODS: First, cck-8 and apoptosis assays were used to determine survival and apoptotic effects of HS 737.T cells under treatment of paclitaxel. Next, RNA-seq and bioinformatics were used to determine the differentially expressed genes and to analyze the pathway involved. Quantitative real-time polymerase chain reaction was used to verify the accuracy of some differentially expressed genes (DEG). ClueGO was used to decode and visualize functionally grouped GO terms of differentially expressed genes, and to map the DEG protein-protein interactions (PPI) network. Western blotting was used to check the expression of target genes, the cleavage of Caspase-3 and PARP1, and the phosphorylation level of p53. Finally, transcriptomics, bioinformatics, and RNAi were used to estimate the antitumor capability and to identify the underlying mechanisms of paclitaxel in GCTB. RESULTS: Our data revealed that paclitaxel had significant time-dependent effects on the viability and induced apoptosis of HS 737.T cells. RNA-seq and bioinformatics analysis showed that apoptosis, death receptor signaling pathway, TNF signaling pathway, and TP53 regulated transcription of cell death genes pathway were closely associated with paclitaxel in the treatment of GCTB. Western bolt results revealed that paclitaxel induced cleavage of Caspase-3 and PARP1, and increased the phosphorylation level of p53 in HS 737.T cells. RNAi results showed that the expression level of TP53INP1 was significantly decreased in HS737.T cells (the decrease was more than 70%). In addition, we found that the inhibitory ratios of paclitaxel on HS737.T cells deficient in TP53INP1 were less than in HS737.T cells with empty vector (19.88 and 40.60%, respectively). Hence, our data revealed that TP53INP1 regulated paclitaxel-driven apoptosis in HS737.T cells. CONCLUSION: Paclitaxel can significantly repress cell proliferation and induce apoptosis of HS 737.T cells through activating Caspase-3, PARP1, p53, and TP53INP1. Paclitaxel may be an effective drug in the management of GCTB.