Relevant bibliographies by topics / Injury repair

Academic literature on the topic 'Injury repair'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Injury repair"

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Stenberg, Lena, Derya Burcu Hazer Rosberg, Sho Kohyama, Seigo Suganuma, and Lars B. Dahlin. "Injury-Induced HSP27 Expression in Peripheral Nervous Tissue Is Not Associated with Any Alteration in Axonal Outgrowth after Immediate or Delayed Nerve Repair." International Journal of Molecular Sciences 22, no. 16 (August 11, 2021): 8624. http://dx.doi.org/10.3390/ijms22168624.

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We investigated injury-induced heat shock protein 27 (HSP27) expression and its association to axonal outgrowth after injury and different nerve repair models in healthy Wistar and diabetic Goto-Kakizaki rats. By immunohistochemistry, expression of HSP27 in sciatic nerves and DRG and axonal outgrowth (neurofilaments) in sciatic nerves were analyzed after no, immediate, and delayed (7-day delay) nerve repairs (7- or 14-day follow-up). An increased HSP27 expression in nerves and in DRG at the uninjured side was associated with diabetes. HSP27 expression in nerves and in DRG increased substantially after the nerve injuries, being higher at the site where axons and Schwann cells interacted. Regression analysis indicated a positive influence of immediate nerve repair compared to an unrepaired injury, but a shortly delayed nerve repair had no impact on axonal outgrowth. Diabetes was associated with a decreased axonal outgrowth. The increased expression of HSP27 in sciatic nerve and DRG did not influence axonal outgrowth. Injured sciatic nerves should appropriately be repaired in healthy and diabetic rats, but a short delay does not influence axonal outgrowth. HSP27 expression in sciatic nerve or DRG, despite an increase after nerve injury with or without a repair, is not associated with any alteration in axonal outgrowth.
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Sánchez Piedra, Genaro Miguel, José Adrián Sánchez León, Juan Sebastián Sánchez León, and Marcela Nataly Parra Álvarez. "Lesión y reparación de la vía biliar: Serie de casos desde 1989 hasta 2020." Revista Médica del Hospital José Carrasco Arteaga 14, no. 1 (April 30, 2022): 33–38. http://dx.doi.org/10.14410/2022.14.1.ao.05.

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BACKGROUND: The benign lesion of the bile duct is a complication of difficult diagnosis and treatment; which has increased due to the use of laparoscopic cholecystectomy (LC) in the management of cholecystolithiasis. Rates of 0.2 to 0.4% of bile duct injuries have been reported, becoming a significant cause of mortality at the time of repair. METHODS: This is an observational, descriptive study, a retrospective case series, based on primary sources of information. The universe of the study are the patients who underwent surgery for bile duct injury from 1989 to 2020, in a private clinic in the city of Cuenca-Ecuador. RESULTS: In more than 30 years, 24 bile duct injury repairs were performed, which occurred: 6 during conventional surgery and 18 during laparoscopic surgery. 54.2% of the lesions occurred less than two centimeters from the confluence of the hepatic ducts. 58.4% of lesions were repaired with Roux-en-Y anastomosis. Antibiotic therapy and drainage were administered to 100% of the patients; 45.83% of the drains placed were tubular drains. 70.8% of the patients didn´t have complications after the repair procedure; the complications that occurred are: bilioma, fistulas, stenosis, cholangitis. CONCLUSION: In most patients who had bile duct injury, the injury occurred during laparoscopic surgery. The injury was most often located less than two centimeters from the confluence of the hepatic ducts. The most frequently performed repair procedure was the Roux-en-Y anastomosis. The most frequent complication after repair was cholangitis.
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Sharma, Shobhit, Vishwanath Pratap Singh, and Sudipta Bera. "Brachial artery injury in pediatric patients: review of management and outcome in 29 patients." International Surgery Journal 6, no. 12 (November 26, 2019): 4419. http://dx.doi.org/10.18203/2349-2902.isj20195405.

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Background: The brachial artery is the most frequently injured artery in the upper extremity due to its vulnerability and commonly it is associated with road traffic accidents and occupational injuries. But brachial artery injury in pediatric age group is not very frequent as in adults and commonly associated with supracondylar fracture of humerus. They may present with or without features of ischemia. Prompt diagnosis and treatment is essential for salvage of limb in established ischemia. Obscure presentation of arterial injury poses challenge in early diagnosis and treatment. Repair of the injured artery in these cases is not clearly recommended. We are presenting a series of 29 pediatric brachial artery injuries and their outcome in our institute over the last 5 years.Methods: Twenty nine pediatric patients with brachial artery injury managed in our institute between 2014 to 2018 are assessed retrospectively for operative procedure and outcome.Results: Supracondylar fracture was the most common cause (55.17%). Ischemic and non-ischemic presentation was noted in 41.37% and 69.63% cases respectively. Artery repair was done in 17 (58.62%) cases. Primary repair and interposition vein graft repair was done 8 and 9 cases respectively. Among the 17 repaired artery good functional outcome with Grade 5/5 muscle power noted in 14cases. Amputation was done in two cases.Conclusions: Good functional recovery may be achieved in segmental injury repair with a vein graft. Though in closed injury without ischemic features artery may not be repaired, full functional recovery is possible due to collateral circulations. Obscure presentation detected and repaired early also has a satisfactory result.
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Colantonio, Donald, Anthony Le, Richard Lee, Andres Piscoya, Tobin Eckel, and Alexander Lundy. "Paper 93: Biomechanical Comparison of Tibiotalar Contact Pressures After Syndesmosis Injury With or Without Deltoid Ligament Repair." Orthopaedic Journal of Sports Medicine 10, no. 7_suppl5 (July 1, 2022): 2325967121S0065. http://dx.doi.org/10.1177/2325967121s00656.

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Objectives: Recent studies have stressed the important role of the deltoid ligament in maintaining global ankle stability. However, controversy remains around whether deltoid ligament repair is necessary in addition to syndesmotic repair when addressing injuries that disrupt both the syndesmosis and deltoid ligament. The purpose of this study was to measure differences in tibiotalar joint contact pressures and tibio-talar torsional stability in the presence of deltoid ligament injury, syndesmotic injury, and after their respective repairs using a cadaveric model. Our hypotheseis were 1) injury to the syndesmoosis and deltoid would increase contact pressures and decrease torsional stability, 2) repaired injuries would restore biomechanics to near native state, and 3)that there would be similar tibiotalar contact pressures and torsional stability with syndesmosis repair alone compared to syndesmosis and deltoid ligament repair. Methods: Twelve fresh-frozen human cadaveric lower extremity specimens with intact ankle joints were randomized and tested under a series of conditions: 1) intact syndesmosis and deltoid, 2) sectioning of syndesmosis or deltoid, 3) sectioning of both the syndesmosis and deltoid, 4) repair of syndesmosis or deltoid, 5) repair of both the syndesmosis and deltoid. In one group, the syndesmosis was sectioned and repaired first and in the other the deltoid was sectioned and repaired first. The syndesmosis was repaired with a single high-tensile strength suture mechanism (TightRope, Arthrex), and deltoid ligament repairs were performed with a single suture anchor (FiberTak, Arthrex). Specimens were tested under each condition with 800 N axial compression load, followed by cyclic torsional preconditioning of 5 Nm internal tibial torque (i.e., external foot rotation) at a rate of 2.5 Nm/s, and then a single rotation test of 7.5 Nm internal tibial torque at 1 Nm/s under 800 N axial compression load on a servohydraulic mechanical testing system. Contact pressures within the tibiotalar joint were measured with a digitized pressure sensor film (Tekscan, Boston MA), and coronal plane motion about the tibia was measured in angular displacement. Results: There was no significant difference in peak contact pressures between conditions except when the comparing an isolated deltoid ligament injury to a combined deltoid and syndesmosis injury (4.43±1.33MPa vs 2.67±0.45MPa, p=0.038). Total contact area was less following syndesmosis repair in isolation (609.55±312.37mm2) and combined syndesmosis and deltoid repair (598.28±181.47mm2) compared to all other conditions (p<0.001). There was also a decrease in total contact area compared to native state when the deltoid was repaired in isolation (951.51±72.79mm2 vs 888.72±105.74mm2, p=0.027). The mean external rotation angle was greater when the syndesmosis (15.67±5.39°), deltoid (13.21±3.28°), and both injuries combined (16.59±4.01°) compared to native state (8.55±2.02°), however these values did not achieve statistical significance. Additionally, There was no statistically significant difference in external rotation angle between isolated syndesmosis, isolated deltoid, or combined repairs. Conclusions: These findings demonstrate that ankle contact pressures and torsional stability do not differ significantly when a deltoid ligament repair is performed in conjunction with a syndesmosis repair for a purely ligamentous injury. However, the change in contact area following syndesmosis repair may play a role in the development of post-traumatic arthritis. This finding reinforces the importance of striving for an anatomic syndesmotic reduction, and care should be taken not to over-reduce the syndesmosis during repair.
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RAYAN, G. M., S. I. SAID, S. L. CAHILL, and J. DUKE. "Vasoactive Intestinal Peptide and Nerve Regeneration." Journal of Hand Surgery 16, no. 5 (October 1991): 515–18. http://dx.doi.org/10.1016/0266-7681(91)90106-x.

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The role of vasoactive intestinal peptide (V.I.P.) in nerve regeneration was investigated by assessing the changes in immunoreactive V.I.P. levels in rat sciatic nerves following injury and repair. 60 rats were divided into three surgical groups and one control group: In group I (primary repair), sciatic nerves were divided and immediately repaired; in group II (secondary repair), sciatic nerves were divided and repaired two weeks later; in group III (no repair), sciatic nerves were divided and not repaired; and in group IV (controls), sciatic nerves were exposed but not divided. Animals were sacrificed at three days and at weekly intervals. Their sciatic nerves were extracted and assayed for V.I.P. concentrations by a specific radioimmunoassay. The mean V.I.P. concentration varied between 22 and 46 pg./mg. protein in the control nerves and between 60 and 529 pg./mg. protein in all other groups. In the three surgical groups the levels were significantly higher in proximal than in distal stumps. Following nerve injury, there was an increase in V.I.P. concentration in the injured and repaired areas. This increase was greater in injured non-repaired areas and was highest in the first 48 hours, but continued during regeneration. The accumulation of V.I.P. in divided nerves occurred in response to nerve injury.
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Haney, Lauren J., Esther Bae, Mary Jo V. Pugh, Laurel A. Copeland, Chen-Pin Wang, Daniel J. MacCarthy, Megan E. Amuan, and Paula K. Shireman. "Patency of arterial repairs from wartime extremity vascular injuries." Trauma Surgery & Acute Care Open 5, no. 1 (December 2020): e000616. http://dx.doi.org/10.1136/tsaco-2020-000616.

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BackgroundExtremity vascular injury (EVI) causes significant disability in Veterans of the Afghanistan/Iraq conflicts. Advancements in acute trauma care improved survival and decreased amputations. The study of wartime EVI has relied on successful limb salvage as a surrogate for vascular repair. We used imaging studies as a specific measure of arterial repair durability.MethodsService members with EVI were identified using the Department of Defense Trauma Registry and validated by chart abstraction. Inclusion criteria for the arterial patency subgroup included an initial repair attempt with subsequent imaging reports (duplex ultrasound, CT angiography, and angiogram) documenting initial patency.ResultsThe cohort of 527 included 140 Veterans with available imaging studies for 143 arterial repairs; median follow-up from injury time to last available imaging study was 19 months (Q1–Q3: 3–58; range: 1–175). Injury mechanism was predominantly explosions (52%) and gunshot wounds (42%). Of the 143 arterial repairs, 81% were vein grafts. Eight repairs were occluded, replaced or included in extremity amputations. One upper extremity and three transtibial late amputations were performed for chronic pain and poor function averaging 27 months (SD: 4; range: 24–32). Kaplan-Meier analysis estimated patency rates of 99%, 97%, 95%, 91% and 91% at 3, 6, 12, 24, and 36 months, respectively, with similar results for upper and lower extremity repairs. Explosive and gunshot wound injury mechanisms had similar patency rates and upper extremity injuries repaired with vein grafts had increased patency.ConclusionsArterial repair mid-term patency in combat-related extremity injuries is excellent based on imaging studies for 143 repairs. Assertive attempts at acute limb salvage and vascular repair are justified with decisions for amputation versus limb salvage based on the overall condition of the patient and degree of concomitant nerve, orthopedic and soft tissue injuries rather than the presence of arterial injuries.Level of evidenceTherapeutic/care management, level IV.
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Rayhan, Md Ferdous, Mazharul Rezwan, and Md Mohoshin Sarker. "Evaluation of the result of early repair of open tendo achilles injury." MOJ Orthopedics & Rheumatology 14, no. 1 (February 28, 2022): 24–27. http://dx.doi.org/10.15406/mojor.2022.14.00572.

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Introduction: Toilet pan injury or accidental cut injury which causes open tendo achilles injury is very much common in our country. The Achilles tendon injury is very difficult to treat, sometimes it creates a disabling condition due to calf muscle contracture, wound infection or skin necrosis. Therefore even in immediate repair of fresh injury will need reconstruction. So early repair of Tendo-Achilles injury after meticulous surgical toileting give best result. Objective: Assessments of result in primary repair of open Tendo-Achilles injury and evaluate the outcomes. To calculate the percentage of results of early repair of open TendoAchilles injury. Assess the rate of infections, skin necrosis, and failure of healing in primary repair. Material & methods: Thirty patients who had acute open Tendo-Achilles injury were studied. Variable level of open acute Tendo-Achilles injury were treated at Sher-E-Bangla Medical College Hospital, Barishl in the period from July 2018 to June 2020. After thorough surgical toileting cut tendon was repaired end to end by modified Kessler method. Plaster cast was given for immobilization & broad spectrum antibiotic given for two to three weeks. Result: Final outcome measured according to Juhana Leppilahti modified scoring scale. Thirty patients with Tendo-Achilles injury were studied. Fifteen cases result were excellent, eleven cases good, two case fair and two cases poor. Conclusion: In early repair of open Tendo-Achilles injury need short period of post operative inactivity. It will help to return a Tendo-Achilles injured patient to his normal work early as well as reduce burden of hospital cost and his family. Early repair of open Tendo-Achilles injury within 12 hours is effective procedure for patients as for surgeon
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Lundy, Alexander, Donald Colantonio, Anthony Le, Richard C. Lee, Andres S. Piscoya, Erik Holm, and Tobin T. Eckel. "Biomechanical Changes in the Ankle Joint after Syndesmosis and Deltoid Injury and Subsequent Repair in a Cadaveric Model." Foot & Ankle Orthopaedics 7, no. 4 (October 2022): 2473011421S0076. http://dx.doi.org/10.1177/2473011421s00760.

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Category: Ankle; Trauma Introduction/Purpose: Recent studies have stressed the important role of the deltoid ligament in maintaining global ankle stability. However, controversy remains around whether deltoid ligament repair is necessary in addition to syndesmotic repair when addressing injuries to both. The purpose of this study was to measure differences in tibiotalar joint contact pressures and tibiotalar contact area in the presence of deltoid ligament injury, syndesmotic injury, and after their respective repairs using a cadaveric model. Our hypotheses were 1) injury to the syndesmosis and deltoid would increase contact pressures and decrease contact area, 2) repaired injuries would restore biomechanics to near native state, and 3) that there would be similar tibiotalar contact pressures and contact area with syndesmosis repair alone compared to syndesmosis and deltoid ligament repair. Methods: Twelve human cadaveric lower extremities were randomized and tested under a series of conditions: 1) native, 2) sectioning of syndesmosis or deltoid, 3) sectioning of both the syndesmosis and deltoid, 4) repair of syndesmosis or deltoid, 5) repair of both. In one group, the syndesmosis was sectioned and repaired first and in the other the deltoid was sectioned and repaired first. The syndesmosis was repaired with a single high-tensile strength suture mechanism and deltoid ligament repairs were performed with a single suture anchor. Specimens were tested under each condition with an axial compressive and torsional load. Contact pressures and area within the ankle were measured with a digitized pressure sensor (Tekscan, Boston MA). Changes in contact pressure and area were compared with two-way repeated measure analysis of variance and significant findings were tested with post-hoc pairwise comparisons of estimated marginal means with Bonferroni-adjusted p-values for multiple comparisons (α = 0.05). Results: The highest mean contact pressure was seen when the deltoid was injured, but the syndesmosis was still intact (4.43 +/- 1.328 mPa) compared to mean contact pressure of 3.142 +/-0.511 mPa in the native condition. The lowest mean contact pressure was seen when the deltoid was repaired, but the syndesmosis was still disrupted (3.068 +/- 0.477). However, these differences in mean contact pressures did not differ significantly with pairwise comparison. Total contact area was significantly less following syndesmosis repair in isolation when compared to the native condition (609.55+-312.37mm2 vs 903.854mm2 p=0.0183). When the syndesmosis was repaired, irrespective of the state of the deltoid, the distribution of contact pressures shifted from the medial half of the joint to the lateral half of the joint in all but one specimen. Conversely, after deltoid ligament repair the distribution of pressure remain concentrated in the medial half of the joint, like the native state. Conclusion: We did not find a significant difference in overall mean ankle contact pressures between the various tested conditions. However, there can be a significant decrease in the joint contact area and a shift in the distribution of contact pressures within the joint after syndesmosis repair that was not seen after deltoid repair. In fact, with a deltoid repair alone, the distribution of contact pressures and the joint contact area did not differ significantly from the native state. These changes in contact area and distribution of pressures may affect long-term clinical and radiographic outcomes.
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Eriksson, Karl, Erik Rönnblad, Bjorn Barenius, and Bjorn Engstrom. "Meniscal Sutures are Superior to Bioabsorbable Arrows: Results After 918 Consecutive Meniscal Repairs in a Dual Center Analysis." Orthopaedic Journal of Sports Medicine 5, no. 5_suppl5 (May 1, 2017): 2325967117S0019. http://dx.doi.org/10.1177/2325967117s00197.

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Objectives: It has been long known that removal of the meniscus can lead to degenerative changes, and preserving surgery rather than meniscal resection is likely to have better long-term outcomes. Success rates after meniscal repair ranges from 60- 95%, but with most studies having small number of patients. The purpose of this study was to review all meniscal repairs, and potential predictors for failure, during a 12-year period. Methods: A dual center retrospective analysis was performed on two consecutive cohorts of meniscal repairs, during the period 1999-2011 and 1999-2010 respectively. Data from surgical protocols and follow up charts were reviewed including type of tear, location, associated injury to the knee, and surgery. Study endpoint was failure of repair, which was defined as a need for reoperation and secondary partial or total meniscal resection, within 3 years. Kaplan-Meier was used to assess repair device survival. Results were expressed as hazard ratios (HR) with 95% confidence intervals (CI) and were adjusted for confounding factors using cox regression. results: 954 meniscal repairs were performed on 918 patients (n = 536 males [58%] and 382 females [42%]) with a mean age of 23 years (12-60). 64% underwent medial meniscal repair and 36% underwent lateral meniscal repair. 4% were repaired both medially and laterally. 75% of the repairs were performed using meniscal sutures (predominantly Fast-Fix), and 25% of the meniscal tears were repaired using bioabsorbable arrows (Biofix). The median time from injury to surgery was 23 days (0-360). The reoperation rate in the whole cohort was 29%. 35% of the medial meniscal repairs failed and 17% failures were noted on the lateral side. Repair with bioabsorbable arrows on the medial meniscus resulted in reoperation in 44% of the cases, whereas the reoperation rate for meniscal sutures was 32% on the medial side. On the lateral side 18% failures were noticed when using arrows, and 17% when sutures were used. 62% of the patients had a simultaneous anterior cruciate ligament (ACL) injury. When medial meniscal repair was preformed with simultaneous ACL-reconstruction 26% of the meniscal repairs failed, when no simultaneous ACL- reconstruction was performed 37% of the meniscal repairs failed and with no associated ACL-injury 41% of the meniscal repairs failed. Analyzing failure in a multivariate cox regression, adjusted according to age, gender, meniscus, ACL-pathology and days- to-surgery, revealed a higher failure rate for medial meniscal repairs (HR 3.006 [2.074-4.355; p = 0.000). Bioabsorbable arrows had significantly more failures than meniscal sutures (HR 1.656 [1.207-2.273]; p = 0.002). With reference to no ACL injury, meniscal repairs performed with a simultaneous ACL-reconstruction resulted in less failure than when no simultaneous ACL-reconstruction was performed (HR 0.605 [0.413-0.885]; p = 0.010). Conclusion: The failure rate was significantly higher on the medial side, especially when using Biofix-arrows. Patients who underwent a simultaneous ACL-reconstruction had a significantly better healing than conservatively treated ACL-ruptures, and patients with no ACL-injury. Age and days-to-surgery were not significant factors for failure.
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Roman, William, Helena Pinheiro, Mafalda R. Pimentel, Jessica Segalés, Luis M. Oliveira, Esther García-Domínguez, Mari Carmen Gómez-Cabrera, Antonio L. Serrano, Edgar R. Gomes, and Pura Muñoz-Cánoves. "Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction." Science 374, no. 6565 (October 15, 2021): 355–59. http://dx.doi.org/10.1126/science.abe5620.

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Muscle repair without stem cells Skeletal muscle is a mechanical organ that endures cellular damage after contraction. Lesions caused by external injury can be repaired by muscle stem cells, which fuse with injured cells or create entirely new myofibers. Roman et al . describe a cell-autonomous repair process that is independent of muscle stem cells (see the Perspective by McNally and Demonbreun). After localized damage, myonuclei migrate to injury sites and locally deliver messenger RNA for cellular reconstruction. This myofiber self-repair represents a model for understanding the restoration of muscle architecture in health and disease. —BAP
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Dissertations / Theses on the topic "Injury repair"

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Oryan, Ahmad. "Experimental tendon injury and repair." Thesis, University of Bristol, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260544.

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Henderson, Neil C. "Molecular mechanisms of hepatic injury and repair." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/1554.

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In this thesis I examined molecular mechanisms involved in acute and chronic liver injury, and also studied basic pathways mediating tumour promotion. Acute hepatic failure secondary to paracetamol poisoning is associated with high mortality. C-jun (NH2) terminal kinase (JNK) is a member of the mitogen activated protein kinase family and is a key intracellular signaling molecule involved in the control of cell fate. Paracetamol induced hepatic JNK activation in both human and murine paracetamol hepatotoxicity, and in a murine model preceded the onset of hepatocyte death. JNK inhibition in vivo (using two JNK inhibitors with different mechanisms of action) markedly reduced mortality in murine paracetamol hepatotoxicity. In addition, delayed administration of JNK inhibitor was more effective than N-acetylcysteine following paracetamol poisoning in mice. JNK inhibition was not protective in acute carbon tetrachloride or anti-Fas antibody mediated hepatic injury, suggesting specificity for the role of JNK in paracetamol hepatotoxicity. Furthermore, disruption of the JNK1 or JNK2 genes did not protect against paracetamol-induced hepatic damage. Pharmacological JNK inhibition had no effect on paracetamol metabolism, but markedly inhibited hepatic TNF-alpha production following paracetamol poisoning. These data demonstrate a central role for JNK in the pathogenesis of paracetamol induced liver failure, thereby identifying JNK as an important therapeutic target in the treatment of paracetamol hepatotoxicity. Liver fibrosis with loss of tissue architecture and subsequent hepatic failure represents a massive healthcare burden worldwide. Expression of Galectin-3 (a beta-galactoside binding animal lectin) is upregulated in established human fibrotic liver disease, during the development of experimental liver fibrosis and is temporally and spatially related to the induction and resolution of experimental hepatic fibrosis. Disruption of the gene encoding Galectin-3 blocks transdifferentiation of precursors to myofibroblasts in vitro and in vivo, markedly attenuating hepatic scarring in a murine model of liver fibrosis. Inhibition of Galectin-3 expression by siRNA in primary murine and human hepatic stellate cells significantly reduced myofibroblast activation and procollagen(I) expression. The reduction in hepatic fibrosis observed in the Galectin-3-/- mouse occurred despite equivalent liver injury and inflammation, and similar tissue expression of TGF-beta. TGF-beta failed to transactivate Galectin-3-/- hepatic stellate cells, in contrast with wild type hepatic stellate cells. However TGF-beta stimulated signaling via Smad-2 and 3 was equivalent in both Galectin-3-/- and wild type hepatic stellate cells indicating that Galectin-3 is required for TGF-beta mediated myofibroblast activation and matrix production. This supports a novel and important mechanistic role for Galectin-3 in the regulation of myofibroblast activation and consequent liver fibrosis. Finally, in vivo siRNA knockdown of Galectin-3 inhibited myofibroblast activation following hepatic injury and may therefore provide a novel therapeutic approach to the prevention and treatment of liver fibrosis. CD98hc (a ligand for Galectin-3) constitutively and specifically associates with beta1 integrins and is highly expressed on the surface of human tumour cells irrespective of the tissue of origin. CD98hc promotes both anchorage- and serum-independent growth. Using chimeras of CD98hc and the type II membrane protein CD69 demonstrated that the transmembrane domain of CD98hc is necessary and sufficient for integrin association in cells. Furthermore, CD98hc/β1 integrin association is required for focal adhesion kinase-dependent phosphoinositol 3-hydroxykinase activation and cellular transformation. Amino acids 82-87 in the putative cytoplasmic/transmembrane region appear to be critical for the oncogenic potential of CD98hc and provide a novel mechanism for tumour promotion by integrins.
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Fitton, Anthony Robert. "Muscle recovery following peripheral nerve injury and repair." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418071.

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Assinck, Peggy Lee. "Myelinating cells in repair of spinal cord injury." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/62788.

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Hiebert, Paul Ryan. "Granzyme B in skin aging, injury and repair." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44226.

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Glass, B. J. L. "The role of connexins in tissue injury repair." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1443464/.

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Skin integrity is essential for sustaining life and it is important to understand the processes involved in its maintenance and repair. There are several key stages involved in wound healing that rely on the complex communication through gap junctions and their connexins to ensure the resolution of the wound. Gap junctions are expressed in all cells linked with tissue repair and provide a regulated pathway linking the cytoplasm of neighbouring cells and allowing signals to pass freely between the two. In the skin there are three key connexins (Connexins 26, 30 and 43) that undergo dynamic changes and regulate the stages of wound closure. To date, extensive research has shown that inhibiting Cx43 expression can achieve significant improvements in wound repair. Synthetic connexin mimetic peptide Gap27 which possess a conserved homology to the second extracellular loop of Cx43 is now being considered as a candidate to improve the rate of wound repair. At low concentrations Gap27 has been shown to block hemichannels but can target gap junctional intercellular communication at higher concentrations and for longer incubation periods. By using Gap27 as a tool, this thesis explores the importance of connexins, hemichannels and gap junctions in tissue injury and repair. I have dissected out the relative contributions of connexins and their involvement with hemichannels and gap junctions in wound repair while investigating if and how Gap27 reduces other connexins. Further work using in vitro wound healing models has shown how Gap27 can enhance the rate of wound healing in early stages. In the second half of this thesis I continue to use Gap27 to investigate the connexin based communication involved in the spread of cell death and damage during ischemia reperfusion injury in vitro and in vivo. The potential therapeutic implications of the wound healing properties of Gap27 are exciting, novel and promising.
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Watson, Tim. "The bioelectric correlates of musculoskeletal injury and repair." Thesis, University of Surrey, 1994. http://epubs.surrey.ac.uk/843861/.

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There is a need for outcome measurement tools which are able to provide accurate and reliable information regarding the efficiency and efficacy of therapeutic intervention of soft tissue injury e.g. ligament tear. Electrical activity within the body tissues has been shown to be influenced by the tissue state, and following injury, bioelectric changes have been demonstrated for example in bone healing and nerve regeneration. This project considers the relationship between the electrical potentials recorded from the skin surface and clinical recovery following a soft tissue lesion. The measurement of the skin potential is not new but the application and approach used is novel in that a non invasive differential skin surface potential is used instead of the traditional and invasive transcutaneous potential. The differential potential was initially investigated in non injured subjects in order to gain an understanding of its character and behaviour. Simultaneous monitoring of environmental, physiological and psychological factors enabled evaluation of their influence on the generation mechanisms. In order to carry out the work, specialist instrumentation was designed and computer software developed. Injured subjects were recruited during two test series and the results compared with those obtained from the non-injured subjects. Differences in potential profiles were marked on occasions. However a significant percentage of injured subjects presented a profile which was very similar to the non injured subject potentials. The failure to demonstrate consistent differences between potentials from the groups may reflect the lability of tissue potentials or that their behaviour is not purely related to local tissue state. Psychological factors were shown to exert influences on the potentials and differences in environmental and physiological conditions may also be responsible for the variations seen. The refinement of the test apparatus and protocol which is discussed may facilitate more discriminative data collection.
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Simon, Crystal Michelle. "Investigation of plasma membrane compromise and citicoline-mediated repair after spinal cord injury repair." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/28276.

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Thesis (M. S.)--Biomedical Engineering, Georgia Institute of Technology, 2008.
Committee Chair: LaPlaca, Michelle; Committee Member: Backus, Deborah; Committee Member: Bellamkonda, Ravi; Committee Member: Lee, Robert; Committee Member: Prausnitz, Mark.
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Clarke, L. "Endothelial injury and repair in vasculitis of the young." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/17421/.

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The vasculitides are a wide spectrum of disorders which are characterised by vascular inflammation. Endothelial injury can occur as a consequence of inappropriate inflammation and is central to the pathogenesis of these varied diseases. This thesis documents the development of assays for detection of novel biomarkers of endothelial injury and/or activation and subsequent reparative responses in children with primary systemic vasculitis. It focuses in particular on circulating endothelial cells, cellular microparticles, growth factors involved in angiogenesis/vasculogenesis and endothelial progenitor cells. Circulating endothelial cells are mature endothelial cells which have become detached from the vessel wall and represent a highly damaged vasculature and were found to be significantly higher in children with active primary systemic vasculitis compared to healthy child controls and patients in remission. Microparticles are released from activated cells, including the endothelium and leukocytes. In this study endothelial and monocyte derived microparticles were found to be elevated during active vasculitis. Growth factors released in response to endothelial injury regulate reparative responses, of which endothelial progenitor cells may play a key role. In this study, patients at disease onset prior to treatment were found to have significantly higher levels of growth factors and endothelial progenitor cells, which decreased with remission inducing therapy. Overall this thesis has investigated the changes in these interlinked biomarkers of injury and repair during active disease, remission and disease flare.
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Lee, Sena. "ATP and its receptors in nerve injury and repair." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8668.

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Unlike the peripheral nervous system (PNS), adult neurons in the central nervous system (CNS) have limited regenerative capacity after injury. One interesting phenomenon observed nearly four decades ago was that lesion of a peripheral nerve can significantly enhance the regenerative capacity of the central axons of the corresponding dorsal root ganglion (DRG) neurons, termed a ‘conditioning lesion’, but the underlying mechanism is still not fully understood. Since ATP is released after nerve injury and extracellular ATP has a broad range of biological activities, we postulated that ATP might be the injury signalling molecule that triggers the regenerative machinery in the injured neurons. If that were the case, injection of ATP into a peripheral nerve should be able to mimic the effect of a conditioning lesion. To test this theory, we injected ATP into a peripheral (sciatic) nerve after a dorsal column transection and found that ATP injection did promote the regeneration of injured axons into the lesion cavity. We also found that ATP injection activated transcription factor STAT3 and increased the expression of growth associated protein 43 (GAP43) in the corresponding DRG neurons. ATP injection increased the concentrations of ciliary neurotrophic factor and interleukin-6 in sciatic nerve and DRG. These results indicate that intraneural injection of ATP can mimic conditioning lesion to a certain degree. Most interestingly, we found that a second injection of ATP one week after the first one markedly boosted the effects of the first injection as many more axons grew into or across the lesion compared with double saline injection or ATP plus saline injection. Double ATP injection is also more effective in sustaining the expression of phospho- STAT3 and GAP43. Immunohistochemical analysis showed ATP injection caused little Wallerian degeneration at the injection site. Behavioural tests showed no long-term adverse effects to the injected sciatic nerve. In order to explore the underlying mechanism of ATP induced elevation of the regeneration state of DRG neurons and look for more potent purinoceptor agonists to stimulate axonal regeneration, we first tried to identify the expression of purinoceptor subtypes in sciatic nerves using quantitative PCR and immunohistochemistry. We found that mRNAs for all the four P1 and fourteen P2 purinoceptor subtypes were expressed in the sciatic nerve, DRG or dissociated Schwann cells at various levels. Immunohistochemical analysis showed that purinoceptor subtypes are expressed by different types of cells. Due to the expression of nearly all purinoceptor subtypes in the sciatic nerve, it will be a big challenge to identify the receptor subtype(s) responsible for ATP induced axonal regeneration. We have set up a compartmented co-culture system to test various agonists/antagonists of purinoceptors. Taken together, we have shown that intraneural ATP injection can mimic conditioning lesion in promoting sensory axonal regeneration. Identification of the receptor subtype(s) and other molecules involved in the enhanced regeneration capacity of injured neurons may lead to the development of therapeutic agents to effectively promote the axonal regeneration of both peripheral and central neurons.
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Books on the topic "Injury repair"

1

Lundborg, Göran. Nerve injury and repair. Edinburgh: Churchill Livingstone, 1988.

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Knee ligaments: Injury & repair. St. Louis: Mosby, 1993.

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Collision sports: Injury and repair. Oxford: Butterworth-Heinemann, 1998.

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Schnapp, Lynn M., and Carol Feghali-Bostwick, eds. Acute Lung Injury and Repair. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-46527-2.

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M, Gressner A., Heinrich P. C, and Matern S, eds. Cytokines in liver injury and repair. Dordrecht: Kluwer Academic, 2002.

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1949-, Lee R. C., Despa Florin, Hamann Kimm Jon, and New York Academy of Sciences., eds. Cell injury: Mechanisms, responses, and repair. New York, N.Y: New York Academy of Sciences, 2005.

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1939-, Daniel Dale M., Akeson Wayne H. 1928-, and O'Connor John J. 1934-, eds. Knee ligaments: Structure, function, injury, and repair. New York: Raven Press, 1990.

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Brock, Rita Nakashima. Soul repair: Recovering from moral injury after war. Boston: Beacon Press, 2012.

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Gabriella, Lettini, ed. Soul repair: Recovering from moral injury after war. Boston: Beacon Press, 2012.

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1922-, Chrétien Jacques, and Dusser Daniel 1951-, eds. Environmental impact on the airways: From injury to repair. New York: M. Dekker, 1996.

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Book chapters on the topic "Injury repair"

1

Schaper, Jutta, S. Hein, C. M. Heinrichs, and D. Weihrauch. "Myocardial Injury and Repair." In Myocardial Response to Acute Injury, 1–16. London: Macmillan Education UK, 1992. http://dx.doi.org/10.1007/978-1-349-12522-7_1.

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Aronsen, Elizabeth L., and John M. Shannon. "Epithelial Injury and Repair." In ARDS Acute Respiratory Distress in Adults, 197–213. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-3430-7_12.

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Hendrich, Christian, Norbert Schütze, Thomas Barthel, Ulrich Nöth, and Jochen Eulert. "Cartilage Injury and Repair." In Cartilage Surgery and Future Perspectives, 9–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19008-7_2.

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Eagleton, Matthew J. "Spinal Cord Injury Prevention and Management." In Endovascular Aortic Repair, 709–19. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-15192-2_47.

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Brittberg, Mats. "Cell-Based Cartilage Repair." In Cartilage Injury of the Knee, 219–31. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78051-7_19.

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Hevesi, Mario, Bradley M. Kruckeberg, Aaron J. Krych, and Daniel B. F. Saris. "Emerging Cartilage Repair Options." In Cartilage Injury of the Knee, 283–88. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78051-7_24.

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Kon, Elizaveta, Daniele Altomare, Andrea Dorotei, Berardo Di Matteo, and Maurilio Marcacci. "Scaffolds for Cartilage Repair." In Cartilage Injury of the Knee, 243–52. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-78051-7_21.

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Czaja, Mark J. "Liver regeneration following hepatic injury." In Liver Growth and Repair, 28–49. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4932-7_2.

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Trippel, Stephen B., and Henry J. Mankin. "Articular Cartilage Injury and Repair." In Traumatic Disorders of the Knee, 19–36. New York, NY: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4612-4310-6_3.

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Weber, Renata V., Andrew Yee, Michael M. Bottros, and Susan E. Mackinnon. "Nerve injury, repair and reconstruction." In Plastic and reconstructive surgery, 777–96. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118655412.ch56.

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Conference papers on the topic "Injury repair"

1

Zikan, M., O. Dubova, V. Student, P. Koliba, and T. Brtnicky. "792 Vessel injury and repair." In ESGO 2021 Congress. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/ijgc-2021-esgo.280.

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Shiomi, T., B. Mercer, P. Bodine, and J. D'Armiento. "SFRP1 Regulates Tissue Injury and Repair." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1974.

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Bachan, P., HJ Kim, and DH Ingbar. "Alveolar Epithelial Repair Following Acute Lung Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4996.

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Aggarwal, S., I. Ahmad, S. Gu, H. Paiste, M. N. Gillespie, and S. Matalon. "Mitochondrial DNA Repair Ameliorates Inhalation Lung Injury." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1020.

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Lee, Y.-S., C. Ezebuiroh, C. Collins, and T. L. Arinzeh. "An electroactive conduit for spinal cord injury repair." In 2009 IEEE 35th Annual Northeast Bioengineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/nebc.2009.4967725.

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Guo, R., J. Liang, T. Xie, N. Liu, PW Noble, and D. Jiang. "Regulation of MicroRNA during Lung Injury and Repair." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1901.

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Yalcinkaya, C., and GI Aytok. "1083 Laparoscopic repair of external iliac vein injury." In ESGO 2021 Congress. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/ijgc-2021-esgo.287.

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Musah, Sadiatu, Connie Schlueter, Jing Chen, and Gary Hoyle. "Repair Of Tracheal Epithelium After Chlorine-Induced Injury." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6327.

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Curley, Gerard F., Maya Contreras, Brendan Higgins, Daniel O'Toole, Cecelia O'Kane, and John Laffey. "Time Course Of Lung Injury, Inflammation, Repair And Fibrosis Following Ventilator Induced Lung Injury." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1670.

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Hefernan, John. "Genzyme Tissue Repair." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2500.

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Abstract Genzyme Tissue Repair (GTR) is a leading developer of cell therapies for the treatment of knee injuries and severe burns. GTR has pioneered the field of autologous cell therapy, in which a patient’s own cells are used to replace those that have been lost to injury or disease. With two major products on the market, GTR continues to be one of the leading companies in the field of tissue engineering. This portion of the presentation will focus on the process controls and specifications to produce these two products detailed below.
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Reports on the topic "Injury repair"

1

Bazan, Nicolas G. Neural Responses to Injury: Prevention, Protection, and Repair. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada373634.

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Bazan, Nicolas G. Neural Responses to Injury: Prevention, Protection, and Repair. Neurochemical Protection of the Brain, Neural Plasticity and Repair. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada373622.

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Peterson, Daniel. Research Recruiting Endogenous Tissue Stem Cells to Repair Injury and Degeneration. Office of Scientific and Technical Information (OSTI), October 2014. http://dx.doi.org/10.2172/1160139.

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Zeng, Jing, Qing Liu, Zhengfang Lei, Zhe Sun, and Yang Wang. Evaluation of Integrated Neuromuscular Training on the Recovery of Joint Injury: A Meta-Analysis and Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0136.

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Review question / Objective: This study will provide new evidence for the effect of integrated neuromuscular training on the recovery of joint injury. Information sources: According to the PICOS principle, the third and fourth authors of this paper searched PsycINFO, Science direct, PubMed, Eric, Willey, China Knowledge Network (CNKI) Academic Journal Online Publishing General Library and China Knowledge Network (CNKI) excellent doctoral thesis full-text database by computer to collect relevant research on the impact of INT on joint injury repair. The time limit of injury retrieval is from the establishment of the database to December 2021.
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Cao, Siyang, Yihao Wei, Tiantian Qi, Peng Liu, Yingqi Chen, Fei Yu, Hui Zeng, and Jian Weng. Stem cell therapy for peripheral nerve injury: An up-to-date meta-analysis of 55 preclinical researches. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0083.

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Review question / Objective: It has been the gold standard for decades to reconstruct a large peripheral nerve injury with a nerve autograft, and this remains true today as well. In addition to nerve autografts, biological conduits and vessels can also be applied. A fair amount of studies have examined the benefits of adding stem cells to the lumen of a nerve conduit. The aim of this meta-analysis was to summarize animal experiments related to the utilization of stem cells as a luminal additive when rebuilding a peripheral nerve injury using nerve grafts. Eligibility criteria: The inclusion criteria were as following: 1.Reconstruction of peripheral nerve injury; 2.Complete nerve transection with gap defect created; 3.Animal in-vivo models; 4.Experimental comparisons between nerve conduits containing and not containing one type of stem cell; 5.Functional testing and electrophysiology evaluations are performed. The exclusion criteria were as following: 1.Repair of central nervous system; 2.Nerve repair is accomplished by end-to-end anastomosis; 3.Animal models of entrapment injuries, frostbite, traction injuries and electric injuries; 4.Nerve conduits made from autologous epineurium; 5.Clinical trials, reviews, letters, conference papers, meta-analyses or commentaries; 6.Same studies have been published in different journals under the same or a different title.
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Hoke, Ahmet, and Hai-Quan Mao. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada613645.

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Hoke, Ahmet, and Hai-Quan Mao. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada581474.

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Christe, Kari. Use of GDNF-Releasing Nanofiber Nerve Guide Conduits for the Repair of Conus Medullaris/Cauda Equina Injury in the Nonhuman Primate. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599060.

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Goeckeritz, Joel, Nathan Schank, Ryan L Wood, Beverly L Roeder, and Alonzo D Cook. Use of Urinary Bladder Matrix Conduits in a Rat Model of Sciatic Nerve Regeneration after Nerve Transection Injury. Science Repository, December 2022. http://dx.doi.org/10.31487/j.rgm.2022.03.01.

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Previous research has demonstrated the use of single-channel porcine-derived urinary bladder matrix (UBM) conduits in segmental-loss, peripheral nerve repairs as comparable to criterion-standard nerve autografts. This study aimed to replicate and expand upon this research with additional novel UBM conduits and coupled therapies. Fifty-four Wistar Albino rats were divided into 6 groups, and each underwent a surgical neurectomy to remove a 7-millimeter section of the sciatic nerve. Bridging of this nerve gap and treatment for each group was as follows: i) reverse autograft—the segmented nerve was reversed 180 degrees and used to reconnect the proximal and distal nerve stumps; ii) the nerve gap was bridged via a silicone conduit; iii) a single-channel UBM conduit; iv) a multi-channel UBM conduit; v) a single-channel UBM conduit identical to group 3 coupled with fortnightly transcutaneous electrical nerve stimulation (TENS); vi) or, a multi-channel UBM conduit identical to group 4 coupled with fortnightly TENS. The extent of nerve recovery was assessed by behavioural parameters: foot fault asymmetry scoring measured weekly for six weeks; electrophysiological parameters: compound muscle action potential (CMAP) amplitudes, measured at weeks 0 and 6; and morphological parameters: total fascicle areas, myelinated fiber counts, fiber densities, and fiber sizes measured at week 6. All the above parameters demonstrated recovery of the test groups (3-6) as being either comparable or less than that of reverse autograft, but none were shown to outperform reverse autograft. As such, UBM conduits may yet prove to be an effective treatment to repair relatively short segmental peripheral nerve injuries, but further research is required to demonstrate greater efficacy over nerve autografts.
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Goeckeritz, Joel, Nathan Schank, Ryan L Wood, Beverly L Roeder, and Alonzo D Cook. Use of Urinary Bladder Matrix Conduits in a Rat Model of Sciatic Nerve Regeneration after Nerve Transection Injury. Science Repository, December 2022. http://dx.doi.org/10.31487/j.rgm.2022.03.01.sup.

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Previous research has demonstrated the use of single-channel porcine-derived urinary bladder matrix (UBM) conduits in segmental-loss, peripheral nerve repairs as comparable to criterion-standard nerve autografts. This study aimed to replicate and expand upon this research with additional novel UBM conduits and coupled therapies. Fifty-four Wistar Albino rats were divided into 6 groups, and each underwent a surgical neurectomy to remove a 7-millimeter section of the sciatic nerve. Bridging of this nerve gap and treatment for each group was as follows: i) reverse autograft—the segmented nerve was reversed 180 degrees and used to reconnect the proximal and distal nerve stumps; ii) the nerve gap was bridged via a silicone conduit; iii) a single-channel UBM conduit; iv) a multi-channel UBM conduit; v) a single-channel UBM conduit identical to group 3 coupled with fortnightly transcutaneous electrical nerve stimulation (TENS); vi) or, a multi-channel UBM conduit identical to group 4 coupled with fortnightly TENS. The extent of nerve recovery was assessed by behavioural parameters: foot fault asymmetry scoring measured weekly for six weeks; electrophysiological parameters: compound muscle action potential (CMAP) amplitudes, measured at weeks 0 and 6; and morphological parameters: total fascicle areas, myelinated fiber counts, fiber densities, and fiber sizes measured at week 6. All the above parameters demonstrated recovery of the test groups (3-6) as being either comparable or less than that of reverse autograft, but none were shown to outperform reverse autograft. As such, UBM conduits may yet prove to be an effective treatment to repair relatively short segmental peripheral nerve injuries, but further research is required to demonstrate greater efficacy over nerve autografts.
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