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Pesquisa : A02.165.308.410.500 [Categoria DeCS]
Referências encontradas : 119 [refinar]
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  1 / 119 MEDLINE  
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PMID:29390319
Autor:Wang Y; Yi XD; Li CD
Endereço:Department of Orthopedics, Peking University First Hospital, Beijing, China.
Título:The influence of artificial nucleus pulposus replacement on stress distribution in the cartilaginous endplate in a 3-dimensional finite element model of the lumbar intervertebral disc.
Fonte:Medicine (Baltimore); 96(50):e9149, 2017 Dec.
ISSN:1536-5964
País de publicação:United States
Idioma:eng
Resumo:OBJECTIVE: This study aimed to investigate the effects involved with the artificial nucleus pulposus (NP) replacement on stress distribution of the cartilaginous endplate (CEP) in a 3-dimensional lumbar intervertebral disc (IVD) model using a finite element (FE) analysis. METHODS: A healthy male volunteer was recruited for the purposes of the study and a spiral computed tomography scan was subsequently conducted to obtain the data information in relation to the L4/5 motion segment. An FE model of the L4/5 motion segment constructed, on the basis of which degenerative IVD, IVD with NP removal, and IVD with NP replacement were in turn built. The stress distribution of the CEP and bulging of IVD were estimated using various motion states, including axial loading, forward flexion, backward extension, left axial rotation, and right axial rotation. RESULTS: Under different motion states, the vertebral stress was higher in the degenerative IVD, the IVD with NP removal, and the IVD with NP replacement, in comparison to that of the normal IVD. Furthermore, a higher vertebral stress was detected in the degenerative IVD than the IVD with NP removal and the IVD with NP replacement. An even distribution of vertebral stress was observed in the IVD model with an artificial NP replacement, while the vertebral stress and bulging displacement were lower than after NP removal. Our findings provided confirmation that stress of the CEP was consistent with the vertebral stress. CONCLUSION: This study provided evidence suggesting that NP replacement, vertebral stress, and bulging displacement are lower than that of degenerative IVD and IVD with NP removal under different motion states.
Tipo de publicação: JOURNAL ARTICLE


  2 / 119 MEDLINE  
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PMID:29222149
Autor:Annette W; Posporis C
Endereço:Neurology and Neurosurgery Service, Pride Veterinary Centre, Derby, UK.
Título:Compressive hydrated nucleus pulposus extrusion: is surgery necessary?
Fonte:Vet Rec; 181(23):622-624, 2017 12.
ISSN:2042-7670
País de publicação:England
Idioma:eng
Tipo de publicação: JOURNAL ARTICLE; COMMENT


  3 / 119 MEDLINE  
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PMID:29192043
Autor:Beltran E
Endereço:Department of Clinical Science & Services, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire AL9 7TA, UK.
Título:Acute hydrated non-compressive nucleus pulposus extrusion: what do we know so far?
Fonte:Vet Rec; 181(22):591-593, 2017 12.
ISSN:2042-7670
País de publicação:England
Idioma:eng
Tipo de publicação: JOURNAL ARTICLE; COMMENT


  4 / 119 MEDLINE  
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PMID:28964544
Autor:De Decker S; Fenn J
Endereço:Department of Clinical Science and Services, Royal Veterinary College, University of London, Hatfield, Hertfordshire, UK. Electronic address: sdedecker@rvc.ac.uk.
Título:Acute Herniation of Nondegenerate Nucleus Pulposus: Acute Noncompressive Nucleus Pulposus Extrusion and Compressive Hydrated Nucleus Pulposus Extrusion.
Fonte:Vet Clin North Am Small Anim Pract; 48(1):95-109, 2018 Jan.
ISSN:1878-1306
País de publicação:United States
Idioma:eng
Resumo:Acute herniation of nondegenerate nucleus pulposus material is an important and relative common cause of acute spinal cord dysfunction in dogs. Two types of herniation of nondegenerate or hydrated nucleus pulposus have been recognized: acute noncompressive nucleus pulposus extrusion (ANNPE) and acute compressive hydrated nucleus pulposus extrusion (HNPE). Spinal cord contusion plays an important role in the pathophysiology of both conditions. Sustained spinal cord compression is not present in ANNPE, whereas varying degrees of compression are present in HNPE. Although affected animals often present with severe neurologic signs, good outcomes can be achieved with appropriate treatment.
Tipo de publicação: JOURNAL ARTICLE; REVIEW


  5 / 119 MEDLINE  
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PMID:28942283
Autor:Lin H; Ma X; Wang BC; Zhao L; Liu JX; Pu FF; Hu YQ; Hu HZ; Shao ZW
Endereço:Department of Orthopedic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China.
Título:Edaravone ameliorates compression-induced damage in rat nucleus pulposus cells.
Fonte:Life Sci; 189:76-83, 2017 Nov 15.
ISSN:1879-0631
País de publicação:Netherlands
Idioma:eng
Resumo:AIMS: Edaravone is a strong free radical scavenger most used for treating acute ischemic stroke. In this study we investigated the protective effects and underlying mechanisms of edaravone on compression-induced damage in rat nucleus pulposus (NP) cells. MATERIALS AND METHODS: Cell viability was determined using MTT assay methods. NP cell apoptosis was measured by Hoechst 33,258 staining and Annexin V/PI double staining. Intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and intracellular calcium ([Ca ] ) were determined by fluorescent probes DCFH-DA, JC-1 and Fluo-3/AM, respectively. Apoptosis-related proteins (cleaved caspase-3, cytosolic cytochrome c, Bax and Bcl-2) and extracellular matrix proteins (aggrecan and collagen II) were analyzed by western blot. KEY FINDINGS: Edaravone attenuated the compression-induced decrease in viability of NP cells in a dose-dependent manner. 33,258 and Annexin V/PI double staining showed that edaravone protected NP cells from compression-induced apoptosis. Further studies confirmed that edaravone protected NP cells against compression-induced mitochondrial pathway of apoptosis by inhibiting overproduction of ROS, collapse of MMP and overload of [Ca ] . In addition, edaravone promoted the expression of aggrecan and collagen II in compression-treated NP cells. SIGNIFICANCE: These results strongly indicate that edaravone ameliorates compression-induced damage in rat nucleus pulposus cells. Edaravone could be a potential new drug for treatment of IDD.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Aggrecans); 0 (Collagen Type II); 0 (Free Radical Scavengers); 0 (Reactive Oxygen Species); S798V6YJRP (phenylmethylpyrazolone); T3CHA1B51H (Antipyrine)


  6 / 119 MEDLINE  
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PMID:28887038
Autor:Zhang B; Xu L; Zhuo N; Shen J
Endereço:Department of Orthopaedic Surgery, The People's Hospital of Zhengzhou, No.33 Huanghe Rd, Zhengzhou, Henan Province, 450003, China.
Título:Resveratrol protects against mitochondrial dysfunction through autophagy activation in human nucleus pulposus cells.
Fonte:Biochem Biophys Res Commun; 493(1):373-381, 2017 Nov 04.
ISSN:1090-2104
País de publicação:United States
Idioma:eng
Resumo:Intervertebral disc degeneration (IVDD) is closely related with aging, whereas mitochondrial damage is a common feature of aging that results in cell apoptosis. Resveratrol (RES) is a natural antioxidant that protects against mitochondrial dysfunction in various cells. This study aimed to investigate the protective role of RES against mitochondrial dysfunction and human nucleus pulposus cell (NPC) apoptosis. We found that mitochondrial dysfunction and NPC apoptosis could be induced under oxidative stress by 100 µmol/l of H O . However, RES tended to attenuate the H O -mediated cytotoxicity. Therefore, autophagic state was evaluated in NPCs to further reveal the underlying mechanism. Results showed that RES reversed the impaired autophagy induced by H O , and this increased autophagic flux was confirmed by the addition of bafilomycin A1. Moreover, pretreatment with 3-methyladenine showed that the potential mechanism of RES to prevent deteriorating mitochondrial function and cell apoptosis was related to autophagy activation. Furthermore, MRI and histological detection were employed to provide more solid evidence that RES injection in an IVDD rabbit model effectively retards the degenerative process of the intervertebral discs in vivo. In summary, these results suggested that RES could alleviate mitochondrial dysfunction and cell apoptosis under oxidative stress and may delay the progression of disc degeneration, whose mechanism is associated with an advantageous role of autophagy induced by RES.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antioxidants); 0 (Stilbenes); Q369O8926L (resveratrol)


  7 / 119 MEDLINE  
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PMID:28793234
Autor:Liu W; Xia P; Feng J; Kang L; Huang M; Wang K; Song Y; Li S; Wu X; Yang S; Yang C
Endereço:Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China; Department of Orthopaedics, First Hospital of Wuhan, Wuhan 430022, China.
Título:MicroRNA-132 upregulation promotes matrix degradation in intervertebral disc degeneration.
Fonte:Exp Cell Res; 359(1):39-49, 2017 Oct 01.
ISSN:1090-2422
País de publicação:United States
Idioma:eng
Resumo:MicroRNAs (miRNAs) have been shown to be involved in the pathogenesis of intervertebral disc degeneration (IDD). This experiment was designed to study the expression and role of the miRNA, miR-132, in IDD. MiR-132 expression in human nucleus pulposus (NP) tissue was assessed by quantitative real-time PCR. The methylation status of the miR-132 was assessed with methylation-specific PCR and bisulfite sequencing PCR. The regulation of growth differentiation factor5 (GDF5) expression by miR-132 was evaluated by luciferase reporter assay. Moreover, we investigated the function of miR-132 on IDD in vivo using a classic needle-punctured rat tail model. These results showed that miR-132 expression was upregulated during IDD and this upregulation was associated with hypomethylation of its promoter. MiR-132 overexpression led to increased expression of ECM catabolic factors, including MMP13 and ADAMTS4, in NP cells while levels of anabolic proteins, such as type II collagen and aggrecan, were diminished. GDF5 was identified as a direct target of negative regulation by miR-132. MAPK/ERK signaling was also found to be associated with miR-132-induced ECM degradation. In addition, we showed that miR-132 inhibition effectively attenuated NP ECM degradation in IDD in vivo. Our findings demonstrated that miR-132 promotes ECM degradation by human NP cells by direct targeting of GDF5. Hence, miR-132 represents a potential therapeutic target in the treatment of IDD.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (GDF5 protein, human); 0 (Growth Differentiation Factor 5); 0 (MIRN132 microRNA, human); 0 (MIRN132 microRNA, rat); 0 (MicroRNAs)


  8 / 119 MEDLINE  
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PMID:28784693
Autor:Mari L; Behr S; Shea A; Dominguez E; Johnson PJ; Ekiri A; De Risio L
Endereço:Department of Neurology/Neurosurgery, Centre for Small Animal Studies, Animal Health Trust, Newmarket, Suffolk, UK.
Título:Outcome comparison in dogs with a presumptive diagnosis of thoracolumbar fibrocartilaginous embolic myelopathy and acute non-compressive nucleus pulposus extrusion.
Fonte:Vet Rec; 181(11):293, 2017 Sep 16.
ISSN:2042-7670
País de publicação:England
Idioma:eng
Resumo:Dogs with fibrocartilaginous embolic myelopathy (FCEM) or acute non-compressive nucleus pulposus extrusion (ANNPE) are reported to have a fair prognosis; however, persistent motor/autonomic deficits are possible. Specific MRI patterns have been suggested to differentiate these diseases although never been validated with histopathology in large studies. The aim of this retrospective study was to evaluate if these MRI patterns are associated with different clinical outcomes in dogs with peracute non-progressive T3-L3 myelopathy. Two hundred and one dogs were included. Outcome data were obtained via medical records and telephone questionnaires. MRIs were blindly reviewed by three board-certified observers, obtaining substantial to almost perfect interobserver agreement on diagnoses (κ=0.635-0.828). Presumptive ANNPE and FCEM were diagnosed in 157 and 44 dogs , respectively. Ambulatory function was regained in 99 per cent of cases, with persistent motor deficits in 83.6 per cent and 92.5 per cent of dogs with presumptive ANNPE and FCEM, respectively. The presumptive diagnosis was not associated with motor function recovery, recovery times or urinary continence. Faecal incontinence was five times more likely in dogs with presumptive ANNPE (23 per cent) compared with presumptive FCEM (7.5 per cent).Distinguishing between MRI patterns of presumptive ANNPE or FCEM in dogs with peracute non-progressive T3-L3 myelopathy may help predict the risk of developing faecal incontinence.
Tipo de publicação: JOURNAL ARTICLE


  9 / 119 MEDLINE  
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PMID:28756222
Autor:Chen J; Jia YS; Liu GZ; Sun Q; Zhang F; Ma S; Wang YJ
Endereço:Department of Orthopedics, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China.
Título:Role of LncRNA TUG1 in intervertebral disc degeneration and nucleus pulposus cells via regulating Wnt/ß-catenin signaling pathway.
Fonte:Biochem Biophys Res Commun; 491(3):668-674, 2017 Sep 23.
ISSN:1090-2104
País de publicação:United States
Idioma:eng
Resumo:OBJECTIVE: To investigate the role of TUG1 in intervertebral disc degeneration (IDD) and human nucleus pulposus cells (NPCs) via regulating Wnt/ß-catenin pathway. METHODS: The study collected nucleus pulposus (NP) tissue samples from 30 patients with lumbar disc herniation (LDH) (Case group) and 18 patients with lumbar spine trauma (Control group). NPCs induced by TNF-α in vitro were divided into Blank, Vector, TUG1, TUG1-siRNA, XAV-939, TUG1 + XAV-939 groups. qRT-PCR was used to detect the expression of TUG1 and ECM-related genes, Western blot to determine the expression of Wnt/ß-catenin pathway and apoptosis-related proteins, and ELISA to measure the expression of ECM-related proteins. The apoptosis was detected by TUNEL and Annexin V-FITC/PI double-staining. The proliferation and senescence were tested by CCK-8 and SA-ß-gal staining respectively. RESULTS: TUG1 was upregulated in patients with IDD, which was positively related to Wnt and ß-catenin. Besides, TUG1, Wnt1 and ß-catenin were greatly increased in the NPCs after TNF-α induction. Compared with the Blank group, TUG1-siRNA and XAV-939 can appreciably down-regulate the expressions of Wnt1, ß-catenin, Caspase-3, Bax, MMP3 and ADAMTS5, up-regulate the expression of Bcl-2, Aggrecan and COL2A1, inhibit the apoptosis and senescence, and promote cell proliferation; however, the TUG1 group had the completely opposite results. CONCLUSION: Silencing TUG1 may not only protect human NPCs from TNF-α-induced apoptosis and senescence, but also promote cell proliferation by blocking Wnt/ß-catenin pathway, which provides a theoretical basis for the clinical treatment of IDD.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (RNA, Long Noncoding); 0 (TUG1 long noncoding RNA, human)


  10 / 119 MEDLINE  
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PMID:28709868
Autor:Xiong X; Dai L; Liang W; Zhang J; Qin S; Cao W; Ye D; Liang P; Liu Z
Endereço:Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Medical College, Jinan University, China.
Título:Protective effect of p53 on the viability of intervertebral disc nucleus pulposus cells under low glucose condition.
Fonte:Biochem Biophys Res Commun; 490(4):1414-1419, 2017 Sep 02.
ISSN:1090-2104
País de publicação:United States
Idioma:eng
Resumo:P53 is a famous cancer suppressor and plays key roles in metabolism. Intervertebral disc (IVD) is the largest avascular cartilaginous structure in humans and its degeneration is a common cause of spine diseases initiated from damaged nucleus pulposus (NP) cells. The potential cause of disc degeneration has been attributed to aging, genetic factors, mechanical factors and nutrition. In this study, we found that p53 decreased and leaked to the cytoplasm in NP cells as the glucose level decreases, in contrast to cancer cells in which p53 increases and concentrates to the nuclei. Comparing with in p53 knockdown NP cells, relative high p53 expression in normal control NP cells inhibited autophagy and the pentose phosphate pathway. Furthermore, the expression of Sox 9 and type II collagen were higher in p53 normal control than p53 knockdown NP cells. Based on these results, we believe that relative high p53 facilitates NP cell viability and integrity.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Collagen Type II); 0 (RNA, Small Interfering); 0 (SOX9 Transcription Factor); 0 (SOX9 protein, human); 0 (Tumor Suppressor Protein p53); IY9XDZ35W2 (Glucose)



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