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1

Atorino, Luigia, Laura Silvestri, Mirko Koppen, et al. "Loss of m-AAA protease in mitochondria causes complex I deficiency and increased sensitivity to oxidative stress in hereditary spastic paraplegia." Journal of Cell Biology 163, no. 4 (2003): 777–87. http://dx.doi.org/10.1083/jcb.200304112.

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Mmutations in paraplegin, a putative mitochondrial metallopeptidase of the AAA family, cause an autosomal recessive form of hereditary spastic paraplegia (HSP). Here, we analyze the function of paraplegin at the cellular level and characterize the phenotypic defects of HSP patients' cells lacking this protein. We demonstrate that paraplegin coassembles with a homologous protein, AFG3L2, in the mitochondrial inner membrane. These two proteins form a high molecular mass complex, which we show to be aberrant in HSP fibroblasts. The loss of this complex causes a reduced complex I activity in mitoc
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2

Koppen, Mirko, Metodi D. Metodiev, Giorgio Casari, Elena I. Rugarli, and Thomas Langer. "Variable and Tissue-Specific Subunit Composition of Mitochondrial m-AAA Protease Complexes Linked to Hereditary Spastic Paraplegia." Molecular and Cellular Biology 27, no. 2 (2006): 758–67. http://dx.doi.org/10.1128/mcb.01470-06.

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ABSTRACT The m-AAA protease, an ATP-dependent proteolytic complex in the mitochondrial inner membrane, controls protein quality and regulates ribosome assembly, thus exerting essential housekeeping functions within mitochondria. Mutations in the m-AAA protease subunit paraplegin cause axonal degeneration in hereditary spastic paraplegia (HSP), but the basis for the unexpected tissue specificity is not understood. Paraplegin assembles with homologous Afg3l2 subunits into hetero-oligomeric complexes which can substitute for yeast m-AAA proteases, demonstrating functional conservation. The functi
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3

Akhtar, Ammara, Sobia Nazir Choudhry, Rana Muhammad Mateen, and Mureed Hussain. "Genetics A Comprehensive In Silico Analysis of Deleterious SNPs of Paraplegin Protein Associated with Hereditary Spastic Paraplegia through Mitochondrial Dysfunction." BioScientific Review 2, no. 2 (2020): 1–14. http://dx.doi.org/10.32350/bsr.0202.01.

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Hereditary spastic paraplegia (HSP) is a heterogenous neurological disorder primarily associated with progressive spasticity. Paraplegin is a mitochondrial protein and mutations in this protein can lead to HSP. In this study, in silico analysis was carried out to identify the pathogenic variants of SPG7 (paraplegin protein). To find novel pathogenic mutations, missense and splicing variants were collected from gnomAD database and passed through a detailed and stringent analysis with the help of a variety of bioinformatic tools. The list of mutations was examined and compared in ClinVar. Altoge
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4

Almomen, MM, KA Martens, A. Hanson, L. Korngut, and G. pfeffer. "P.071 Novel mutations in SPG7 identified from patients with late-onset spasticity." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, s2 (2018): S35. http://dx.doi.org/10.1017/cjn.2018.173.

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Background: Hereditary spastic paraplegia (HSP) is a group of genetic diseases that cause progressive degeneration of the corticospinal tract. Historically, this disease was divided into two types:the classic subtype, with leg weakness and hypertonic bladder, and the complicated subtype, with features such as cerebellar ataxia or optic atrophy.Mutations in SPG7 (encoding paraplegin) leads to complicated HSP causing cerebellar ataxia, progressive external ophthalmoplegia in addition to the classical symptoms. AFG3L2 is a binding partner of paraplegin and mutations in AFG3L2 cause a similar synd
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5

Elleuch, N., C. Depienne, A. Benomar, et al. "Mutation analysis of the paraplegin gene (SPG7) in patients with hereditary spastic paraplegia." Neurology 66, no. 5 (2006): 654–59. http://dx.doi.org/10.1212/01.wnl.0000201185.91110.15.

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6

Duvezin-Caubet, Stéphane, Mirko Koppen, Johannes Wagener, et al. "OPA1 Processing Reconstituted in Yeast Depends on the Subunit Composition of the m-AAA Protease in Mitochondria." Molecular Biology of the Cell 18, no. 9 (2007): 3582–90. http://dx.doi.org/10.1091/mbc.e07-02-0164.

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The morphology of mitochondria in mammalian cells is regulated by proteolytic cleavage of OPA1, a dynamin-like GTPase of the mitochondrial inner membrane. The mitochondrial rhomboid protease PARL, and paraplegin, a subunit of the ATP-dependent m-AAA protease, were proposed to be involved in this process. Here, we characterized individual OPA1 isoforms by mass spectrometry, and we reconstituted their processing in yeast to identify proteases involved in OPA1 cleavage. The yeast homologue of OPA1, Mgm1, was processed both by PARL and its yeast homologue Pcp1. Neither of these rhomboid proteases
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7

Gelbard, Harris A. "Synapses and Sisyphus: life without paraplegin." Journal of Clinical Investigation 113, no. 2 (2004): 185–87. http://dx.doi.org/10.1172/jci20783.

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8

Gelbard, H. A. "Synapses and Sisyphus: life without paraplegin." Journal of Clinical Investigation 113, no. 2 (2004): 185–87. http://dx.doi.org/10.1172/jci200420783.

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9

Pirozzi, M. "Intramuscular viral delivery of paraplegin rescues peripheral axonopathy in a model of hereditary spastic paraplegia." Journal of Clinical Investigation 116, no. 1 (2005): 202–8. http://dx.doi.org/10.1172/jci26210.

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10

Pirozzi, Marinella, Angelo Quattrini, Gennaro Andolfi, et al. "Intramuscular viral delivery of paraplegin rescues peripheral axonopathy in a model of hereditary spastic paraplegia." Journal of Clinical Investigation 124, no. 2 (2014): 871. http://dx.doi.org/10.1172/jci75082.

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11

Casari, Giorgio, Maurizio De Fusco, Sonia Ciarmatori, et al. "Spastic Paraplegia and OXPHOS Impairment Caused by Mutations in Paraplegin, a Nuclear-Encoded Mitochondrial Metalloprotease." Cell 93, no. 6 (1998): 973–83. http://dx.doi.org/10.1016/s0092-8674(00)81203-9.

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12

Koppen, Mirko, Florian Bonn, Sarah Ehses, and Thomas Langer. "Autocatalytic Processing of m-AAA Protease Subunits in Mitochondria." Molecular Biology of the Cell 20, no. 19 (2009): 4216–24. http://dx.doi.org/10.1091/mbc.e09-03-0218.

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m-AAA proteases are ATP-dependent proteolytic machines in the inner membrane of mitochondria which are crucial for the maintenance of mitochondrial activities. Conserved nuclear-encoded subunits, termed paraplegin, Afg3l1, and Afg3l2, form various isoenzymes differing in their subunit composition in mammalian mitochondria. Mutations in different m-AAA protease subunits are associated with distinct neuronal disorders in human. However, the biogenesis of m-AAA protease complexes or of individual subunits is only poorly understood. Here, we have examined the processing of nuclear-encoded m-AAA pr
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13

Çopuroğlu, Burak, Ali Ulvi Uca, Ayse Gul Zamani, Mahmut Selman Yıldırım, Mustafa Altaş, and Betül Okur Altındaş. "The role of spastin and paraplegin genes in primary progressive multiple sclerosis." Turkish Journal of Neurology 30, no. 4 (2024): 236–43. https://doi.org/10.55697/tnd.2024.12.

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Objectives: This study aimed to detect the presence of mutations in the spastin (SPG4) and paraplegin (SPG7) genes in patients with primary progressive multiple sclerosis (PPMS) to determine the role of hereditary spastic paraplegia (HSP) genes on the susceptibility to PPMS, clinical course, and severity and to reveal its potential role on motor pathways leading to spastic paraparesis clinic. Patients and methods: The descriptive study was conducted with 25 patients with PPMS. The patients were divided into two groups: those presenting with (n=16; 8 males, 8 females; mean age: 47.2±8.4 years;
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14

Kim, Mun ki, Hyeon soo Park, Jea hyeon Cho, Gon sup Kim, and Chungkil Won. "Pramipexole protects dopaminergic neurons through paraplegin against 6-hydroxydopamine." NeuroReport 26, no. 2 (2015): 74–80. http://dx.doi.org/10.1097/wnr.0000000000000303.

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15

Brugman, F., H. Scheffer, J. H. J. Wokke, et al. "Paraplegin mutations in sporadic adult-onset upper motor neuron syndromes." Neurology 71, no. 19 (2008): 1500–1505. http://dx.doi.org/10.1212/01.wnl.0000319700.11606.21.

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16

Banfi, Sandro, Maria Teresa Bassi, Grazia Andolfi, et al. "Identification and Characterization of AFG3L2, a Novel Paraplegin-Related Gene." Genomics 59, no. 1 (1999): 51–58. http://dx.doi.org/10.1006/geno.1999.5818.

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17

Coppola, Massimiliano, Alessandro Pizzigoni, Sandro Banfi, Maria Teresa Bassi, Giorgio Casari, and Barbara Incerti. "Identification and Characterization of YME1L1, a Novel Paraplegin-Related Gene." Genomics 66, no. 1 (2000): 48–54. http://dx.doi.org/10.1006/geno.2000.6136.

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18

Liu, Yihui, Jiang Xu, Wanyun Tao, et al. "Exome Sequencing Identifies a Mutation (Y740C) in Spastic Paraplegia 7 Gene Associated with Adult-Onset Primary Lateral Sclerosis in a Chinese Family." European Neurology 81, no. 1-2 (2019): 87–93. http://dx.doi.org/10.1159/000500672.

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Background: Primary lateral sclerosis (PLS) is considered a rare variant of motor neuron disease (MND) characterized by selective upper motor neuron dysfunction leading to limb weakness, spasticity, and even bulbar symptoms. Previous studies have demonstrated that mutations in ALSIN, spastic paraplegia 7 (SPG7), TBK1, ALS2, ERLIN2, and FIG4 are responsible for PLS. Most of them occurred in childhood to young-adult onset patients. The aim of this study was to identify the genetic lesion of patients with adult-onset PLS. Methods: We applied whole-exome sequencing (WES) and MND and ataxia-related
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19

Mancuso, Giuseppe, Esther Barth, Pietro Crivello, and Elena I. Rugarli. "Alternative Splicing of Spg7, a Gene Involved in Hereditary Spastic Paraplegia, Encodes a Variant of Paraplegin Targeted to the Endoplasmic Reticulum." PLoS ONE 7, no. 5 (2012): e36337. http://dx.doi.org/10.1371/journal.pone.0036337.

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20

Finsterer, Josef. "Mitochondrial Parkinsonism due to SPG7/Paraplegin variants with secondary mtDNA depletion." Movement Disorders 34, no. 12 (2019): 1931–32. http://dx.doi.org/10.1002/mds.27905.

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21

McDermott, C. J., R. K. Dayaratne, J. Tomkins, et al. "Paraplegin gene analysis in hereditary spastic paraparesis (HSP) pedigrees in northeast England." Neurology 56, no. 4 (2001): 467–71. http://dx.doi.org/10.1212/wnl.56.4.467.

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22

Bellinvia, Angelo, Luisa Pastò, Claudia Niccolai, et al. "A new paraplegin mutation in a patient with primary progressive multiple sclerosis." Multiple Sclerosis and Related Disorders 44 (September 2020): 102302. http://dx.doi.org/10.1016/j.msard.2020.102302.

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23

Thal, Dietmar, Stephan Züchner, Stephan Gierer та ін. "Abnormal Paraplegin Expression in Swollen Neurites, τ- and α-Synuclein Pathology in a Case of Hereditary Spastic Paraplegia SPG7 with an Ala510Val Mutation". International Journal of Molecular Sciences 16, № 10 (2015): 25050–66. http://dx.doi.org/10.3390/ijms161025050.

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24

McDermott, Christopher J., Dewi Roberts, Janine Tomkins, Kate M. Bushby, and Pamela J. Shaw. "Spastin and paraplegin gene analysis in selected cases of motor neurone disease (MND)." Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders 4, no. 2 (2003): 96–99. http://dx.doi.org/10.1080/14660820310012718.

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25

Karlberg, Tobias, Susanne van den Berg, Martin Hammarström, et al. "Crystal Structure of the ATPase Domain of the Human AAA+ Protein Paraplegin/SPG7." PLoS ONE 4, no. 10 (2009): e6975. http://dx.doi.org/10.1371/journal.pone.0006975.

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26

De la Casa‐Fages, Beatriz, Gorka Fernández‐Eulate, Josep Gamez, et al. "Reply to: “Mitochondrial Parkinsonism due to SPG7/Paraplegin variants with secondary mtDNA depletion”." Movement Disorders 34, no. 12 (2019): 1932–33. http://dx.doi.org/10.1002/mds.27899.

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27

Wecht, Jill M., Ronald E. De Meersman, Joseph P. Weir, Ann M. Spungen, and William A. Bauman. "Cardiac homeostasis is independent of calf venous compliance in subjects with paraplegia." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (2003): H2393—H2399. http://dx.doi.org/10.1152/ajpheart.01115.2002.

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The purpose of this study was to examine cardiac hemodynamics during acute head-up tilt (HUT) and calf venous function during acute head-down tilt (HDT) in subjects with paraplegia compared with sedentary nondisabled controls. Nineteen paraplegic males (below T6) and nine age-, height-, and weight-matched control subjects participated. Heart rate, stroke volume, and cardiac output were assessed using the noninvasive acetylene uptake method. Venous vascular function of the calf was assessed using venous occlusion plethysmography. After supine measurements were collected, the table was moved to
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28

Rodenbaugh, David W., Heidi L. Collins, Dustin G. Nowacek, and Stephen E. DiCarlo. "Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 6 (2003): H2605—H2613. http://dx.doi.org/10.1152/ajpheart.00319.2003.

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Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias. To test this hypothesis, intact ( n = 10) and paraplegic ( n = 6) male Wistar rats were chronically instrumented to measure atrioventricular
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29

Ashry, Ahmed, Ayman Tarek Mahmoud, and Mohamed Gabr. "Delayed recovery from paraplegia following resections of thoracic meningiomas." Surgical Neurology International 11 (October 2, 2020): 321. http://dx.doi.org/10.25259/sni_575_2020.

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Background: In this retrospective study, we evaluated the patterns of postoperative recovery for patients who were initially paraplegic before the excision of thoracic spine meningiomas. We also determined how the various prognostic factors impacted outcomes. Methods: Twenty patients with paraplegia underwent surgical excision of thoracic spine meningiomas at 2016– 2019. Patients’ demographics, clinical, radiological data, operative details, histopathology, and postoperative complications were recorded; patients were reassessed at 6 months and 1 year postoperatively. Results: Fourteen patients
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30

Elegbe, Oloruntoba, Mirdhu Wickremaratchi, and Martyn Hinchcliffe. "The Patient with Acute Paraplegia: A Problem-Based Review." Acute Medicine Journal 10, no. 1 (2011): 40–44. http://dx.doi.org/10.52964/amja.0462.

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Acute paraplegia is an emergency requiring immediate assessment by the acute medical team because of the need to rule out compressive lesions of the cord for which intervention may preserve neurological function and limit persistent disability. In addition acute paraplegia could be complicated by life-threatening problems. These require prompt recognition and treatment to prevent further deterioration. The following clinical scenario, based on a real case of acute paraplegia seen by the authors is aimed at providing a problem-based approach to the management of patients presenting with acute p
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31

Lujan, Heidi L., Ying Chen, and Stephen E. DiCarlo. "Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemia-induced ventricular tachycardia in conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 5 (2009): H1364—H1372. http://dx.doi.org/10.1152/ajpheart.01286.2008.

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Midthoracic spinal cord injury is associated with ventricular arrhythmias that are mediated, in part, by enhanced cardiac sympathetic activity. Furthermore, it is well known that sympathetic neurons have a lifelong requirement for nerve growth factor (NGF). NGF is a neurotrophin that supports the survival and differentiation of sympathetic neurons and enhances target innervation. Therefore, we tested the hypothesis that paraplegia is associated with an increased cardiac NGF content, sympathetic tonus, and susceptibility to ischemia-induced ventricular tachyarrhythmias. Intact and paraplegic (6
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32

Coarelli, Giulia, Rebecca Schule, Bart P. C. van de Warrenburg, et al. "Loss of paraplegin drives spasticity rather than ataxia in a cohort of 241 patients with SPG7." Neurology 92, no. 23 (2019): e2679-e2690. http://dx.doi.org/10.1212/wnl.0000000000007606.

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ObjectiveWe took advantage of a large multinational recruitment to delineate genotype-phenotype correlations in a large, trans-European multicenter cohort of patients with spastic paraplegia gene 7 (SPG7).MethodsWe analyzed clinical and genetic data from 241 patients with SPG7, integrating neurologic follow-up data. One case was examined neuropathologically.ResultsPatients with SPG7 had a mean age of 35.5 ± 14.3 years (n = 233) at onset and presented with spasticity (n = 89), ataxia (n = 74), or both (n = 45). At the first visit, patients with a longer disease duration (>20 years, n = 62) s
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33

Ferreirinha, Fatima, Angelo Quattrini, Marinella Pirozzi, et al. "Axonal degeneration in paraplegin-deficient mice is associated with abnormal mitochondria and impairment of axonal transport." Journal of Clinical Investigation 113, no. 2 (2004): 231–42. http://dx.doi.org/10.1172/jci200420138.

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34

Richter, Uwe, Kah Ying Ng, Fumi Suomi, et al. "Mitochondrial stress response triggered by defects in protein synthesis quality control." Life Science Alliance 2, no. 1 (2019): e201800219. http://dx.doi.org/10.26508/lsa.201800219.

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Mitochondria have a compartmentalized gene expression system dedicated to the synthesis of membrane proteins essential for oxidative phosphorylation. Responsive quality control mechanisms are needed to ensure that aberrant protein synthesis does not disrupt mitochondrial function. Pathogenic mutations that impede the function of the mitochondrial matrix quality control protease complex composed of AFG3L2 and paraplegin cause a multifaceted clinical syndrome. At the cell and molecular level, defects to this quality control complex are defined by impairment to mitochondrial form and function. He
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35

Lin, Xiang, Hui-Zhen Su, En-Lin Dong, et al. "Stop-gain mutations in UBAP1 cause pure autosomal-dominant spastic paraplegia." Brain 142, no. 8 (2019): 2238–52. http://dx.doi.org/10.1093/brain/awz158.

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Abstract Hereditary spastic paraplegias refer to a heterogeneous group of neurodegenerative disorders resulting from degeneration of the corticospinal tract. Clinical characterization of patients with hereditary spastic paraplegias represents progressive spasticity, exaggerated reflexes and muscular weakness. Here, to expand on the increasingly broad pools of previously unknown hereditary spastic paraplegia causative genes and subtypes, we performed whole exome sequencing for six affected and two unaffected individuals from two unrelated Chinese families with an autosomal dominant hereditary s
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36

Giacomini, Leonardo, Roger Neves Mathias, Andrei Fernandes Joaquim, Mateus Dal Fabbro, Enrico Ghizoni, and Helder Tedeschi. "Is there a right time for surgery in paraplegic patients secondary to non traumatic spinal cord compression?" Einstein (São Paulo) 10, no. 4 (2012): 508–11. http://dx.doi.org/10.1590/s1679-45082012000400020.

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Paraplegia is a well-defined state of complete motor deficit in lower limbs, regardless of sensory involvement. The cause of paraplegia usually guides treatment, however, some controversies remain about the time and benefits for spinal cord decompression in nontraumatic paraplegic patients, especially after 48 hours of the onset of paraplegia. The objective of this study was to evaluate the benefits of spinal cord decompression in such patients. We describe three patients with paraplegia secondary to non-traumatic spinal cord compression without sensory deficits, and who were surgically treate
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37

Chavhan, Dinesh G., Amita A. Mehta, and Sarasawti Iyer. "Study of the availability of home modifications in paraplegics." International Journal Of Community Medicine And Public Health 11, no. 8 (2024): 3069–72. http://dx.doi.org/10.18203/2394-6040.ijcmph20242165.

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Background: Paraplegia is loss of motor strength, sensations and bowel bladder function below the level of injury due to spinal cord damage. Spinal cord injury is medically managed along with rehabilitation which includes muscle strengthening, and mobility in a wheelchair with proper training and home modification. The paraplegic population is the most demoted section of our society and is confronted with barriers to accessibility, health facilities, educational opportunities, and skill development. Accessibility is very important for the paraplegic population and lack of accessibility may aff
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Shin, Sanghoon, Jinyoung Park, Juntaek Hong, and Jung Hyun Park. "Improved gait speed in spastic paraplegia: a new modality." BMJ Supportive & Palliative Care 10, no. 4 (2019): e41-e41. http://dx.doi.org/10.1136/bmjspcare-2018-001738.

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ObjectivesThe gait disturbance in spastic paraplegic patients lowers the gait speed, increases fall risk and eventually lower the quality of life. This study aims to investigate the effect of electrical twitch obtaining intramuscular stimulation (ETOIMS) on spastic paraplegic patients’ gait speed and pattern.MethodsA prospective short-term cohort study was designed in the outpatient clinic of the department of rehabilitation in a tertiary hospital. Patients with spastic paraplegia (N=5) were participated, including spinal cord tumour (N=2), cervical myelitis (N=1), hereditary spastic paraplegi
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Craig, H. Lichtblau, Scott Raffa, Kaveh Assadi, Christopher Warburton, Gabrielle Meli, and Allyson Gorman. "Need for Appropriate Amount and Level of Care in Paraplegics Patients." International Journal of Physical Medicine & Rehabilitation 12, no. 2 (2024): 4. https://doi.org/10.35248/2329-9096.24.12.721.

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Paraplegic patients suffer physical and emotional disability and are at heightened risk for comorbidities and potentially life-threatening complications. The economic costs associated that paraplegics face are significant and vary depending on factors such as level of disability and presence of chronic pain and/or depression. Providing the right amount and level of care is critical for optimizing health and life expectancy and minimizing suffering in paraplegic patients
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Guspara, Winta Adhitia. "Exploring Somaesthetic Design and Phenomenology in Understanding Paraplegic Mobility." International Journal of Creative Multimedia 5, no. 2 (2024): 55–63. http://dx.doi.org/10.33093/ijcm.2024.5.2.4.

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This study explores how somaesthetic design and phenomenological approaches can offer insights into the mobility experiences of individuals with paraplegia. By examining how design, technology, and symbols intersect with the challenges faced by paraplegic individuals, the study presents an alternative perspective on disability that emphasizes user experience, independence, and freedom of mobility. The paper discusses the role of design in shaping assistive devices and considers the implications for user-centered design practices. While the scope is primarily focused on the experiences of parap
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41

Dreyer, Hans C., Erin L. Glynn, Heidi L. Lujan, Christopher S. Fry, Stephen E. DiCarlo, and Blake B. Rasmussen. "Chronic paraplegia-induced muscle atrophy downregulates the mTOR/S6K1 signaling pathway." Journal of Applied Physiology 104, no. 1 (2008): 27–33. http://dx.doi.org/10.1152/japplphysiol.00736.2007.

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Ribosomal S6 kinase 1 (S6K1) is a downstream component of the mammalian target of rapamycin (mTOR) signaling pathway and plays a regulatory role in translation initiation, protein synthesis, and muscle hypertrophy. AMP-activated protein kinase (AMPK) is a cellular energy sensor, a negative regulator of mTOR, and an inhibitor of protein synthesis. The purpose of this study was to determine whether the hypertrophy/cell growth-associated mTOR pathway was downregulated during muscle atrophy associated with chronic paraplegia. Soleus muscle was collected from male Sprague-Dawley rats 10 wk followin
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42

Mussa, S., S. Kakar, and G. Bentley. "Total Hip Arthroplasty for Late Hip Dislocation in Paraplegia." HIP International 12, no. 3 (2002): 338–41. http://dx.doi.org/10.1177/112070000201200310.

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Late hip dislocation is uncommon, particularly in the context of paraplegia. We report a case in which total hip arthroplasty with a semi-constrained acetabular component was a successful treatment for this condition. A review of the literature revealed that this method of treatment had not been previously described in paraplegics. For patients with late hip dislocation in spastic paraplegia, total hip arthroplasty with a semi-constrained acetabular component, combined with adequate adductor release and obturator neurectomy is recommended.
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43

Azevedo, ERFBM, KC Alonso, and A. Cliquet. "Body composition assessment by bioelectrical impedance analysis and body mass index in individuals with chronic spinal cord injury." Journal of Electrical Bioimpedance 7, no. 1 (2019): 2–5. http://dx.doi.org/10.5617/jeb.2421.

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Abstract Purpose: To assess body composition and obesity in individuals with spinal cord injury (SCI) who practice and do not practice physical activity using body mass index (BMI) and bioelectrical impedance analysis (BIA). Methods: 39 patients with SCI went through BIA evaluation and BMI was assessed. Patients were divided into four groups according to injury level (paraplegia or tetraplegia) and physical activity achievement (active or inactive). Results: 22 individuals with paraplegia (7 active and 15 inactive) and 17 with tetraplegia (5 active and 12 inactive) were evaluated. BMI, fat per
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44

Yoo, Kyung Y., JongUn Lee, Hak S. Kim, and Woong M. Im. "Hemodynamic and Catecholamine Responses to Laryngoscopy and Tracheal Intubation in Patients with Complete Spinal Cord Injuries." Anesthesiology 95, no. 3 (2001): 647–51. http://dx.doi.org/10.1097/00000542-200109000-00017.

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Background Endotracheal intubation in patients undergoing general anesthesia often causes hypertension and tachycardia, which may be altered when the efferent sympathetic fiber to the cardiovascular system is interrupted. The aim of the current study was to investigate the effects of different levels of spinal cord injury on the cardiovascular responses to intubation. Methods Fifty-four patients with traumatic complete cord injuries requiring tracheal intubation were grouped into quadriplegics (above C7; n = 22), high paraplegics (T1-T4, n = 8), and low paraplegics (below T5, n = 24) according
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Morita, Tomoyo, and Eiichi Naito. "Facilitation of Hand Proprioceptive Processing in Paraplegic Individuals with Long-Term Wheelchair Sports Training." Brain Sciences 12, no. 10 (2022): 1295. http://dx.doi.org/10.3390/brainsci12101295.

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Previous studies have revealed drastic changes in motor processing in individuals with congenital or acquired limb deficiencies and dysfunction. However, little is known about whether their brains also exhibit characteristic proprioceptive processing. Using functional magnetic resonance imaging, we examined the brain activity characteristics of four individuals with congenital or acquired paraplegia (paraplegic group) who underwent long-term wheelchair sports training, when they passively experienced a right-hand movement (passive task) and when they actively performed a right-hand motor task
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Olmez, Akgun, and Haluk Topaloglu. "HEREDITARY SPASTIC PARAPLEGIA: PATHOGENESIS AND PATHOPHYSIOLOGY." National Journal of Neurology 1, no. 05 (2014): 10–22. http://dx.doi.org/10.61788/njn.v1i14.01.

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- Hereditary spastic paraplegias constitute a larger group of disorders than expected. - Autosomal dominant types are mainly composed of SPAST, Atlastin (SPG3A) and REEP1 mutations. Genetic testing is suggested mainly for these genes. - The most common autosomal recessive type is SPG11, hereditary spastic paraplegia with thin corpus callosum, but SPG15 shares the same clinical features with SPG11. Genetic testing should be done for both if thin corpus callosum is present in patients. - How different genes with many different biological functions, including axonal transport, mitochondrial funct
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Srivastava, Sudhir, Aditya Raj, Rishi Agarwal, Sunil Bhosale, and Nandan Marathe. "Management dilemma of tuberculous paraplegia in pregnancy – A case report and review of literature." Surgical Neurology International 11 (December 29, 2020): 470. http://dx.doi.org/10.25259/sni_772_2020.

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Background: Tuberculosis (TB)/tuberculous spondylodiscitis of the spine causing paraplegia in the 2nd trimester of pregnancy is rare and poses significant management dilemmas. Pregnancy, a relatively immunocompromised state with high hormonal levels, may prompt rapid TB destruction of a vertebral body resulting in an acute/ profound neurological deficit. Here, a pregnant paraplegic mother was diagnosed with spondylodiscitis that warranted immediate decompression/fusion to achieve neurological recovery. Case Description: A 26-year-old female was 23 weeks pregnant when she presented with an acut
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Ehses, Sarah, Ines Raschke, Giuseppe Mancuso, et al. "Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1." Journal of Cell Biology 187, no. 7 (2009): 1023–36. http://dx.doi.org/10.1083/jcb.200906084.

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Mitochondrial fusion depends on the dynamin-like guanosine triphosphatase OPA1, whose activity is controlled by proteolytic cleavage. Dysfunction of mitochondria induces OPA1 processing and results in mitochondrial fragmentation, allowing the selective removal of damaged mitochondria. In this study, we demonstrate that two classes of metallopeptidases regulate OPA1 cleavage in the mitochondrial inner membrane: isoenzymes of the adenosine triphosphate (ATP)–dependent matrix AAA (ATPase associated with diverse cellular activities [m-AAA]) protease, variable assemblies of the conserved subunits p
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Silva, Gelson Aguiar da, Juliana Neves da Costa, and Thelma Leite de Araujo. "Cuidado de enfermagem ao portador de paraplegia à luz do modelo de adaptação de Roy." Revista de Enfermagem UFPE on line 3, no. 3 (2009): 656. http://dx.doi.org/10.5205/reuol.149-181-1-rv.0303200929.

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ABSTRACT Objective: to analyze the nursing care adequacy to the paraplegic carrier based on the Model of Adaptation of Roy. Method: case study, qualitative character carried through with a traumatic paraplegic carrier, in phase of medullar shock, in public institution in Fortaleza city, Ceará, Brazil, from October to November 2007. It’s used the process of nursing proposed by Roy, who understands in: behaviors evaluation, stimulus evaluation, nursing diagnosis, goals establishment, interventions and evaluation. Results: it had been identified alterations in the physiological mode, the presence
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Mesquita Junior, Nelson, Flavia Natalia Marques Kingerski, Giovana Liz Marioto, Fabio Alex Fonseca Viegas, Suzelaine Fidelis da Silva Mesquita, and Sonia Perreto. "Prevalence of deep vein thrombosis in patients with paraplegia caused by traumas." Jornal Vascular Brasileiro 12, no. 4 (2013): 271–77. http://dx.doi.org/10.1590/jvb.2013.051.

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BACKGROUND: Deep vein thrombosis is a common disease among people who are immobilized. Immobility is inherent to paraplegia and leads to venous stasis, which is one of the factors covered by Virchow's triad describing its development. Trauma is the primary cause of paraplegia and is currently increasing at a rate of 4% per year. OBJECTIVE: To determine the prevalence of deep vein thrombosis in paraplegic patients whose paraplegia was caused by traumas, using color Doppler ultrasonography for diagnosis. METHODS: This was a cross-sectional observational study of 30 trauma-induced paraplegia pati
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