Bibliographies thématiques / R Injury

Littérature scientifique sur le sujet « R Injury »

Auteur : Grafiati
Publié le 11 mars 2023

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Articles de revues sur le sujet "R Injury"

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Campbell, Thomas F., Christine Dollaghan, Janine Janosky, Heather Leavy Rusiewicz, Steven L. Small, Frederic Dick, Jennell Vick et P. David Adelson. « Consonant Accuracy After Severe Pediatric Traumatic Brain Injury : A Prospective Cohort Study ». Journal of Speech, Language, and Hearing Research 56, no 3 (juin 2013) : 1023–34. http://dx.doi.org/10.1044/1092-4388(2012/12-0077).

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Purpose The authors sought to describe longitudinal changes in Percentage of Consonants Correct—Revised (PCC–R) after severe pediatric traumatic brain injury (TBI), to compare the odds of normal-range PCC–R in children injured at older and younger ages, and to correlate predictor variables and PCC–R outcomes. Method In 56 children injured between age 1 month and 11 years, PCC–R was calculated over 12 monthly sessions beginning when the child produced ≥ 10 words. At each session, the authors compared odds of normal-range PCC–R in children injured at younger (≤ 60 months) and older (> 60 months) ages. Correlations were calculated between final PCC–R and age at injury, injury mechanism, gender, maternal education, residence, treatment, Glasgow Coma Score, and intact brain volume. Results PCC–Rs varied within and between children. Odds of normal-range PCC–R were significantly higher for the older than for the younger group at all sessions but the first; odds of normal-range PCC–R were 9 to 33 times higher in the older group in sessions 3 to 12. Age at injury was significantly correlated with final PCC–R. Conclusion Over a 12-month period, severe TBI had more adverse effects for children whose ages placed them in the most intensive phase of PCC–R development than for children injured later.
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Kuboki, Satoshi, Nozomu Sakai, Johannes Tschöp, Michael J. Edwards, Alex B. Lentsch et Charles C. Caldwell. « Distinct contributions of CD4+ T cell subsets in hepatic ischemia/reperfusion injury ». American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no 5 (mai 2009) : G1054—G1059. http://dx.doi.org/10.1152/ajpgi.90464.2008.

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Helper T cells are known to mediate hepatic ischemia/reperfusion (I/R) injury. However, the precise mechanisms and subsets of CD4+ T cells that contribute to this injury are still controversial. Therefore, we sought to determine the contributions of different CD4+ T cell subsets during hepatic I/R injury. Wild-type, OT-II, or T cell receptor (TCR)-δ-deficient mice were subjected to 90 min of partial hepatic ischemia followed by 8 h of reperfusion. Additionally, wild-type mice were pretreated with anti-CD1d, -NK1.1, or -IL-2R-α antibodies before I/R injury. OT-II mice had diminished liver injury compared with wild-type mice, implicating that antigen-dependent activation of CD4+ T cells through TCRs is involved in hepatic I/R injury. TCR-δ knockout mice had decreased hepatic neutrophil accumulation, suggesting that γδ T cells regulate neutrophil recruitment. We found that natural killer T (NKT) cells, but not NK cells, contribute to hepatic I/R injury via CD1d-dependent activation of their TCRs, as depletion of NKT cells by anti-CD1d antibody or depletion of both NKT cells and NK cells by anti-NK1.1 attenuated liver injury. Although regulatory T cells (Treg) are known to suppress T cell-dependent inflammation, depletion of Treg cells had little effect on hepatic I/R injury. The data suggest that antigen-dependent activation of CD4+ T cells contributes to hepatic I/R injury. Among the subsets of CD4+ T cells, it appears that γδ T cells contribute to neutrophil recruitment and that NKT cells directly injure the liver. In contrast, NK cells and Treg have little effects on hepatic I/R injury.
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Lu, Ping, Shihui Xiao, Shaoze Chen, Youlin Fu, Peng Zhang, Yaner Yao et Feng Chen. « LncRNA SNHG12 downregulates RAGE to attenuate hypoxia-reoxygenation-induced apoptosis in H9c2 cells ». Bioscience, Biotechnology, and Biochemistry 85, no 4 (3 février 2021) : 866–73. http://dx.doi.org/10.1093/bbb/zbaa090.

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ABSTRACT Ischemia-reperfusion (I/R) injury causes cardiac dysfunction through several mechanisms including the irregular expression of some long noncoding RNA. However, the role of SNHG12 in myocardial I/R injury remains unclear. Here, we found the increase of the SNHG12 level in hypoxia-reoxygenation (H/R)-injured-H9c2 cells. SNHG12 silencing enhanced the apoptosis of H/R-injured H9c2 cells, while SNHG12 overexpression relieved the cardiomyocyte apoptosis induced by H/R stimulation. Additionally, the suppression of SNHG12 significantly boosted the H/R-induced expression and the production of TNF-α, IL-6, and IL-1β, as well as the activation of NF-κB, which were fully reversed after overexpression of SNHG12. Mechanistically, SNHG12 adversely regulated the production of receptor for advanced glycation end products (RAGE) in H/R-stimulated H9c2 cells. Antibody blocking of RAGE alleviated the apoptosis of H/R-injured H9c2 cells. Collectively, we have determined a valuable mechanism by which the high level of SNHG12 contributes to H9c2 cells against H/R injury through the reduction of RAGE expression.
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Miyake, Hiromasa, Katsuyuki Tanabe, Satoshi Tanimura, Yuri Nakashima, Tomoyo Morioka, Kana Masuda, Hitoshi Sugiyama, Yasufumi Sato et Jun Wada. « Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury ». International Journal of Molecular Sciences 21, no 12 (26 juin 2020) : 4545. http://dx.doi.org/10.3390/ijms21124545.

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Acute kidney injury (AKI) has been increasingly recognized as a risk factor for transition to chronic kidney disease. Recent evidence suggests that endothelial damage in peritubular capillaries can accelerate the progression of renal injury. Vasohibin-2 (VASH2) is a novel proangiogenic factor that promotes tumor angiogenesis. However, the pathophysiological roles of VASH2 in kidney diseases remain unknown. In the present study, we examined the effects of VASH2 deficiency on the progression of ischemia–reperfusion (I/R) injury-induced AKI. I/R injury was induced by bilaterally clamping renal pedicles for 25 min in male wild-type (WT) and Vash2 homozygous knockout mice. Twenty-four hours later, I/R injury-induced renal dysfunction and tubular damage were more severe in VASH2-deficient mice than in WT mice, with more prominent neutrophil infiltration and peritubular capillary loss. After induction of I/R injury, VASH2 expression was markedly increased in injured renal tubules. These results suggest that VASH2 expression in renal tubular epithelial cells might be essential for alleviating I/R injury-induced AKI, probably through protecting peritubular capillaries and preventing inflammatory infiltration.
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Edwards, Jessica K. « New antagonist prevents I/R injury ». Nature Reviews Nephrology 11, no 11 (29 septembre 2015) : 631. http://dx.doi.org/10.1038/nrneph.2015.161.

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Song, Ying, Weihai Liu, Yi Ding, Yanyan Jia, Jinyi Zhao, Fan Wang, Juan Bai et al. « Salvianolic acid A ameliorates renal ischemia/reperfusion injury by activating Akt/mTOR/4EBP1 signaling pathway ». American Journal of Physiology-Renal Physiology 315, no 2 (1 août 2018) : F254—F262. http://dx.doi.org/10.1152/ajprenal.00508.2017.

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Salvianolic acid A (Sal A) has been shown to prevent and treat ischemic cardiovascular, as well as cerebral vascular diseases. However, little is known about Sal A in renal ischemia/reperfusion (I/R) injury. In this study, a renal I/R injury model in rats and a hypoxia/reoxygenation (H/R) model to damage proximal renal tubular cells (HK-2) were used to assess whether Sal A halts the development and progression of renal I/R injury. As compared with vehicle treatment, Sal A significantly attenuated kidney injury after renal I/R injury, accompanied by decreases in plasma creatinine, blood urea nitrogen levels, the number of apoptosis-positive tubular cells, and kidney oxidative stress. Sal A also activated phosphorylated protein kinase B (p-Akt) and phosphorylated-mammalian target of rapamycin (p-mTOR) compared with vehicle-treated I/R injury rats. In H/R-injured HK-2 cells, Sal A can reduce the levels of reactive oxygen species in a dose-related manner. Similar to the results from in vivo experiments, in vitro Sal A also increased the protein expression of phosphorylated-eukaryotic initiation factor 4E binding protein 1 (p-4EBP1) compared with vehicle. Furthermore, the cytoprotective activity of Sal A was inhibited by LY294002 and rapamycin. These findings indicate that Sal A can ameliorate renal I/R injury and promote tubular cell survival partly via the Akt/mTOR/4EBP1pathway. Sal A could be a candidate compound to prevent ischemic tissue damage.
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Hu, Yongjun, Hongwei Pan, Jianqiang Peng, Jin He, Mingxiang Tang, Sulan Yan, Jingjing Rong et al. « Resveratrol inhibits necroptosis by mediating the TNF-α/RIP1/RIP3/MLKL pathway in myocardial hypoxia/reoxygenation injury ». Acta Biochimica et Biophysica Sinica 53, no 4 (4 mars 2021) : 430–37. http://dx.doi.org/10.1093/abbs/gmab012.

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Abstract Resveratrol (RES) protects myocardial cells from hypoxia/reoxygenation (H/R)-caused injury. However, the mechanism of this effect has not been clarified. Thus, in this study, we aimed to determine whether RES attenuates H/R-induced cell necroptosis by inhibiting the tumor necrosis factor-alpha (TNF-α)/receptor-interacting protein kinase 1 (RIP1)/RIP3/mixed-lineage kinase domain-like (MLKL) signaling pathway. Rat myocardial ischemia/reperfusion (I/R) models and H/R-injured cell models were constructed. Our study showed that myocardial H/R injury significantly increased the levels of TNF-α, RIP1, RIP3, and p-MLKL/MLKL by western blot analysis. Cell viability assay and 4,6-dianmidino-2-phenylindole (DAPI)–propidium iodide staining showed that the cell viability was decreased, and necroptosis was increased after myocardial H/R injury. The expressions of TNF-α, RIP1, RIP3, and p-MLKL/MLKL in H/R myocardial cells treated with different concentrations of RES were significantly downregulated. In addition, we also found that the cell viability was increased and necroptosis was decreased in dose-dependent manners when H/R-injured cells were treated with RES. In addition, the enhanced effect of TNF-α on necroptosis in myocardial H/R-injured cells was improved by RES, and the effect of RES was confirmed in vivo in I/R rats. This study also showed that RES suppresses necroptosis in H9c2 cells, which may occur through the inhibition of the TNF-α/RIP1/RIP3/MLKL signaling pathway. Our data suggest that necroptosis is a promising therapeutic target and may be a promising therapeutic target for the treatment of myocardial I/R injury.
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Neely, C. F., et I. M. Keith. « A1 adenosine receptor antagonists block ischemia-reperfusion injury of the lung ». American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no 6 (1 juin 1995) : L1036—L1046. http://dx.doi.org/10.1152/ajplung.1995.268.6.l1036.

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Ischemia-reperfusion (I-R) injury of the lung occurs after lung transplantation, pulmonary thromboembolectomy, or cardiopulmonary bypass. In the heart, adenosine, A1 adenosine receptor agonists, and a brief period of preconditioning ischemia attenuate I-R injury. Moreover, in the lung, thromboxane is released during ischemia and is an important mediator of I-R injury. We previously reported that adenosine produces vasoconstriction in the feline pulmonary vascular bed by acting on A1 receptors to induce the release of thromboxane and that these vasoconstrictor responses are desensitized by low doses of A1 receptor agonists. Because A1 receptor agonists mimic the effect of preconditioning ischemia, we hypothesized, in contrast to previously proposed mechanisms, that small amounts of adenosine released during preconditioning ischemia desensitize A1 receptors. Also, we hypothesized that greater amounts of adenosine are released after longer periods of ischemia, which activate A1 receptors. Thus if desensitization of A1 receptors is the mechanism by which preconditioning attenuates I-R injury of the heart and A1 receptor activation during ischemia plays an important role in I-R injury of the lung, A1 receptor antagonists should provide a protective effect in I-R injury of the lung. In this study, 2 h of ischemia and 2 h of reperfusion of the left lower lobe in intact-chest, spontaneously breathing cats caused lung injury characterized by the presence of neutrophils, macrophages, and RBCs in alveoli and caused alveolar edema, which was blocked in a highly significant manner by the A1 receptor antagonists xanthine amine congener (XAC) and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). An intralobar arterial infusion of XAC (30 min before ischemia) reduced the %injured alveoli (defined as presence of 2 or more inflammatory cells or RBCs, or edematous fluid) from 60 +/- 10 to 7 +/- 2%, which was not significantly different from controls (5 +/- 1%; P < 0.0001). DPCPX (iv) reduced the %injured alveoli to 13 +/- 7% when administered 30 min before ischemia and to 6 +/- 2% when administered after 1 h of reperfusion, not significantly different from controls (P < 0.0001). Preconditioning ischemia (10-min ischemia +10-min reperfusion) also reduced the %injured alveoli after 2 h ischemia and 2 h reperfusion to 23 +/- 13%, almost identical to 2 h ischemia and 1 h reperfusion. These data support the hypothesis that A1 receptor antagonists block I-R injury of the lung. A1 receptor antagonists may be useful in preventing I-R injury after transplant surgery and during surgical procedures associated with I-R injury of the heart, brain, kidney, and spinal cord.
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Sprague, Christy L., Donald Penner et James J. Kells. « Enhancing the margin of selectivity of RPA 201772 inZea mayswith antidotes ». Weed Science 47, no 5 (octobre 1999) : 492–97. http://dx.doi.org/10.1017/s004317450009216x.

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The antidotes dichlormid, MON-4660, CGA-154281, R-29148, and MON-13900 were tested in the greenhouse to protectZea maysL. (corn) against RPA 201772 injury. High rates of RPA 201772 injured four Z.mayshybrids > 30%. R-29148 and MON-13900 were the most effective of the five antidotes evaluated. R-29148 applied at rates ⩾ 45 g ha−1provided excellent protection against RPA 201772 injury and also prevented injury toZ. maysfrom diketonitrile, the active metabolite of RPA 201772. In laboratory studies, R-29148 did not alter absorption of14C-RPA 201772 from soil; however, R-29148 significantly enhanced the rate of RPA 201772 metabolism and inactivation inZ. mays.The mixed function oxidase inhibitor piperonyl butoxide (PBO) increased RPA 201772 injury on all hybrids. These results demonstrate thatZ. maystolerance to RPA 201772 can be enhanced with the use of antidotes such as R-29148 and MON-13900, that R-29148 protectsZ. maysfrom RPA 201772 and diketonitrile by the enhancement of metabolism, and that oxidative reactions may be involved in the metabolism of RPA 201772 inZ. mays.
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Meng, X., M. Wei, D. Wang, X. Qu, K. Zhang, N. Zhang et Xinjian Li. « The protective effect of hesperidin against renal ischemia-reperfusion injury involves the TLR-4/NF-κB/iNOS pathway in rats ». Physiology International 107, no 1 (mars 2020) : 82–91. http://dx.doi.org/10.1556/2060.2020.00003.

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AbstractRenal injury is reported to have a high mortality rate. Additionally, there are several limitations to current conventional treatments that are used to manage it. This study evaluated the protective effect of hesperidin against ischemia/reperfusion (I/R)-induced kidney injury in rats. Renal injury was induced by generating I/R in kidney tissues. Rats were then treated with hesperidin at a dose of 10 or 20 mg/kg intravenously 1 day after surgery for a period of 14 days. The effect of hesperidin on renal function, serum mediators of inflammation, and levels of oxidative stress in renal tissues were observed in rat kidney tissues after I/R-induced kidney injury. Moreover, protein expression and mRNA expression in kidney tissues were determined using Western blotting and RT-PCR. Hematoxylin and eosin (H&E) staining was done for histopathological observation of kidney tissues. The data suggest that the levels of blood urea nitrogen (BUN) and creatinine in the serum of hesperidin-treated rats were lower than in the I/R group. Treatment with hesperidin also ameliorated the altered level of inflammatory mediators and oxidative stress in I/R-induced renal-injured rats. The expression of p-IκBα, caspase-3, NF-κB p65, Toll-like receptor 4 (TLR-4) protein, TLR-4 mRNA, and inducible nitric oxide synthase (iNOS) was significantly reduced in the renal tissues of hesperidin-treated rats. Histopathological findings also revealed that treatment with hesperidin attenuated the renal injury in I/R kidney-injured rats. In conclusion, our results suggest that hesperidin protects against renal injury induced by I/R by involving TLR-4/NF-κB/iNOS signaling.
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Thèses sur le sujet "R Injury"

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Mitchell, Margaret. « Recovery from personal injury ». Thesis, University of Glasgow, 1991. http://theses.gla.ac.uk/40922/.

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Clasper, Jonathan C. « Mortality and orthopaedic injury following military trauma ». Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8964/.

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This thesis details my contribution to the literature on military surgery, based on both front-line surgical experiences as well as research carried out on causes of death and disability, particularly in relation to limb injuries, the most common site of wounding in conflict. Injury analysis (6 papers). Injury prevention/mitigation (5 papers). Management (8 papers). Outcome (13 papers). Education (9 papers).
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Foster, Mark Anthony. « Steroids and immunity from injury through to rehabilitation ». Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6686/.

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There are over one million deaths from road traffic collisions. In Afghanistan, there have been 2005 UK battle injuries over 10 years. Advances in military trauma care have improved survival, resulting in more severely injured individuals entering the trauma care pathway. Improved understanding of immunoendocrine changes after severe trauma may facilitate novel interventions to improve outcomes. We prospectively recruited 102 severely injured patients at the QEH Birmingham; 52 military and 50 civilian patients with a mean Injury Severity Score of 27.2±13.9. Blood and 24-hr urine were collected at baseline (injury < 24h) and at regular intervals from while in hospital and at 3,4, and 6 months. Results demonstrated a reduced neutrophil function following a surge of DAMPs and cytokines that were released into the circulation. Both DHEA and DHEAS were significantly down-regulated (p < 0.0001). Serum testosterone was initially completely suppressed (p < 0.0001) but normalised after week 4. Protein and muscle loss followed a U-shaped curve; catabolism began to recovery 4-6 weeks following injury. In conclusion, the acute response to severe injury comprises increased glucocorticoid activation and down-regulation of adrenal and gonadal androgens. Delineation of whether the endocrine changes are beneficial or adverse will determine the potential for future intervention studies.
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Philp, Fraser Derek. « Validating models of injury risk prediction in football players ». Thesis, Keele University, 2018. http://eprints.keele.ac.uk/4993/.

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Association football (soccer) is a popular sport and there is a high risk of injury for participants. Within the context of professional clubs, the risk of injury is also associated with the risk of financial costs. Therefore, injury reduction processes are considered important, and previous studies have sought to identify and model injury risk factors. Although formal screening tests e.g. The Functional Movement Screen (FMS) and monitoring procedures e.g. Union of European Football Associations (UEFA) have been developed for modelling and predicting injuries, the processes in current use, lack precision or clinical usefulness. The aims of this thesis were therefore to explore why existing methods of screening, measuring and modelling are not effective in predicting injuries. In order achieve this the following things were done; Literature review to evaluate the UEFA screening process and advocated variables, Validation of the FMS, the most commonly used exercise screening test, against a 3D photogrammetric system (Vicon (©Vicon Motion Systems Ltd)) Injury modelling on a pre-established database designed in accordance with the UEFA guidelines The literature review confirmed that the established database was compliant with the UEFA screening guidelines. The most commonly used screening measure (FMS) for injury risk was found to be an invalid measure and therefore removed from the modelling process. The models developed were unable to prospectively model injuries accurately (R = 0.23), and the primary problem was a large number of false positives i.e. those predicted as having risk of injury not sustaining injury. Reasons for poor model performance could be attributed to inappropriate screening methods, inadequate datasets or inadequate modelling methods for rare events. Future work should focus on addressing the limitations in the existing UEFA screening framework and simultaneously develop better methods of rare event modelling from small datasets.
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McKinlay, William W. « Psychosocial outcome and family burden after traumatic brain injury ». Thesis, University of Glasgow, 1996. http://theses.gla.ac.uk/4831/.

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The persistence of psychosocial symptoms after severe head injury has been identified as one of the main long-term difficulties facing such patients and their families. Not only have such problems proved persistent, they have been found to present particular problems for community re-entry including return to work. They have been associated in particular with stress on carers and also with disruption of family activities and health. Given that so many survivors of severe head injury rely on their families for long-term support, this topic has attracted increasing attention. The present study described the psychosocial problems after severe head injury and their relationship to various "burdens" on carers and the wider family based on a group of 54 patients studied at 3, 6, and 12 months post-injury. Replication and extension of some findings is made through study of a multi-centre internationally collected group of 562 survivors of severe head injury. Thepersistence of psychosocial problems is noted alongside their differing relationships to various aspects of "burden". Aspects of burden, and especially of social isolation, present challenges especially for those working in rehabilitation and community re-entry programmes
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Khalid, Usman. « The role of microRNAs and ischaemic preconditioning in kidney ischaemia reperfusion injury ». Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/95843/.

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Successful kidney transplantation transforms outcome for patients with end stage kidney disease. Delayed graft function (DGF) following Ischaemia Reperfusion Injury (IRI) is a major problem, is hard to predict or monitor, and preventative or therapeutic strategies are lacking. Ischaemic Preconditioning (IPC) may limit IRI, but results are variable and potential mechanisms are not well defined. The aims of this thesis were to study the role of microRNAs, which are post-transcriptional regulators of gene expression vital in many physiological and pathophysiological processes, in the context of IRI, IPC and DGF. An in vivo model of IRI and IPC was developed, and histological, biochemical and mRNA kidney injury marker analyses were undertaken. MicroRNAs were then profiled using both Next Generation Sequencing (NGS) and hybridisation arrays, and changes in selected microRNAs confirmed by RTqPCR. Histology scores, serum creatinine and expression of kidney injury markers were significantly reduced in IPC compared with IRI. Microarray and NGS analysis identified a highly reproducible IRI signature, which was attenuated by IPC. Subsequently, microRNAs were profiled using Taqman Low Density Array (TLDA) and validated by RT-qPCR, from urine samples of kidney transplant patients with and without DGF. A DGF microRNA profile was uncovered, with overlap to the results from the IRI model. These data have identified a microRNA signature of IRI that was attenuated by IPC, which also improved outcome. Urinary microRNAs also showed a promising capability to predict DGF in human kidney transplantation. MicroRNAs thus show significant promise as biomarkers and potential therapeutic targets in this context.
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Yu, Zanzhe. « Local and systemic endothelial injury in renal failure treated with peritoneal dialysis ». Thesis, Keele University, 2013. http://eprints.keele.ac.uk/1828/.

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Excess fluid and waste products of metabolism, as well as protein, are removed from the peritoneal cavity in Peritoneal Dialysis (PD). Increased peritoneal protein clearance (Pcl) is associated with a greater risk of mortality. It is not clear whether this association reflects systemic endothelial injury or local peritoneal capillary damage and inflammation, or both. To investigate this problem a series of analyses were undertaken in different incident, prevalent and longitudinal patient cohorts. Transcapillary escape rate of albumin (TERalb) was measured to determine systemic capillary permeability. Luminex assays combined with principle component analysis were applied to measure endothelial biomarker patterns. It was demonstrated that: (1) Pcl is a function of both local peritoneal inflammation, membrane area (PSTR) and comorbidity (especially cardiovascular) but only its association with the latter predicted survival. (2) There is a progressive uncoupling of the Pcl, (indicative of large pore pathway) and PSTR (effectively the small pore area) with time on PD. (3) Isolated small pore ultrafiltration (due to icodextrin) decreases with prolonged time on PD and is also uncoupled from the increase in peritoneal membrane area. (4) The systemic endothelial barrier function is decreased in PD patients, especially diabetics, but not associated with hypoalbuminaemia which is linked to systemic inflammation. (5) Hydration status is related to plasma albumin concentration but not endothelial dysfunction as measured by soluble biomarkers. Pcl is a function of both local peritoneal factors, e.g. inflammation and progressive fibrosis, and systemic patient characteristics, e.g. age and comorbidity. The influence of comorbidity is complex depending on type, associated patterns of endothelial injury and causes of associated hypoalbuminaemia. The importance of plasma colloidal pressure in determining fluid status was emphasized. Strategies to improve fluid distribution should focus on reducing peritoneal protein loss and increasing albumin synthesis rather than blocking systemic vascular leak.
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Low, Emma Louise. « Dissecting transforming growth factor-beta signalling pathways in the context of acute vascular injury ». Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30703/.

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Coronary artery bypass grafting (CABG) is a mainstay in the treatment of coronary heart disease (CHD), a leading cause of premature death in the UK. However, fewer than 60 % of saphenous vein grafts remain patent in the long-term due to the formation of a hyperplastic, occlusive neointima within the grafted vessel. Excessive vascular smooth muscle cell (VSMC) proliferation, migration and extracellular matrix (ECM) synthesis are key events in the pathogenesis of vein graft intimal hyperplasia (IH), and subsequent necrotic core formation and intraplaque haemorrhage further accelerate the process of vein graft failure by forming unstable atherosclerotic lesions. Early IH therefore represents an important target for therapeutic interventions aimed at improving clinical outcomes after CABG. The pleiotropic cytokine transforming growth factor-beta (TGFβ) is highly expressed in restenotic vessels from CHD patients and is acutely upregulated following vein graft implantation in large and small animal models of vein graft disease. To date, most studies investigating the role of TGFβ in IH have used global approaches to target TGFβ, or have focused on the canonical activin receptor-like kinase 5 (ALK5), Smad2/3-mediated pathway. However, TGFβ elicits a diverse range of cellular responses by activating several distinct signalling pathways, and in certain cell types can also signal via ALK1, activating a separate set of receptor-regulated Smad proteins (R-Smads; Smad1/5) that can antagonise ALK5 signalling. Importantly, the role of ALK1 in the pathogenesis of vein graft IH remains unclear and studies have yet to conclusively show whether TGFβ is able to signal via ALK1 in VSMCs. Moreover, in vivo studies indicate that the three mammalian TGFβ isoforms have discrete biological functions, especially during wound healing, a process similar to IH involving cell migration, proliferation and ECM formation. Therefore, the principal aim of this thesis was to dissect the roles of ALK5- and ALK1-mediated signalling in VSMCs during vein graft IH. In addition, this thesis aimed to evaluate whether TGFβ1, TGFβ2 and TGFβ3 differentially regulate VSMC behaviour in the context of vein graft IH. Initially, the expression of the TGFβ isoforms, ALK receptors and R-Smads in VSMCs during the development of IH was evaluated in both small and large animal models of arterial injury and vein graft disease. IHC analysis of wire-injured mouse carotid arteries 14 days post-injury revealed that TGFβ1, TGFβ3, ALK5 and ALK1 were expressed in αSMA+ intimal and medial VSMCs. Interestingly, while nuclear localisation of phosphorylated Smad2/3 (pSmad2/3) within αSMA+ VSMCs was observed in both non-injured and injured vessels, nuclear pSmad1/5 was only detected within VSMCs following vascular injury. IHC analysis of TGFβ signalling components in diseased pre-implantation human saphenous vein (HSV) with pre-existing IH showed that TGFβ1, TGFβ3, TβRII (TGFβ type II receptor), ALK5 and ALK1 were expressed in αSMA+ VSMCs within both the intima and media. Importantly, dual staining for TβRII and ALK5 or ALK1 showed strong co-localisation between ALK5/ALK1 and TβRII. Both pSmad2/3 and pSmad1/5 were localised to the nuclei of intimal αSMA+ VSMCs, suggesting that both ALK5 and ALK1 signalling pathways may be active in these cells. Confocal microscopy analysis of three failed vein graft specimens obtained from patients undergoing cardiac transplantation revealed abundant nuclear-localised pSmad2/3 and pSmad1/5 in αSMA+ intimal VSMCs. These data suggest that both the ALK5 and ALK1 pathways may be activated in VSMCs during the development of IH. Having localised TGFβ1, TGFβ3, TβRII, ALK5, ALK1, pSmad2/3 and pSmad1/5 to intimal vein graft SMCs, subsequent mechanistic characterisation of TGFβ signalling via ALK5/ALK1 was performed in SMC outgrowth cultures from pre-implantation HSV segments from CABG patients (HSVSMC). Affinity labelling and crosslinking studies using 125I-TGFβ1 revealed binding of TGFβ1 to ALK5, ALK1 and TβRII, as well as the accessory receptors endoglin and betaglycan in HSVSMC. qRT-PCR confirmed the expression of these receptors at the RNA level, while immunoblotting revealed that treatment with all three TGFβ isoforms could induce a rapid increase in pSmad2 as well as pSmad1/5. Immunocytochemistry demonstrated the nuclear localisation of both pSmad2/3 and pSmad1/5 signalling complexes following stimulation of HSVSMC with TGFβ1, while qRT-PCR evaluation of ALK5 and ALK1 target genes (SERPINE1 and ID1, respectively) confirmed the transcriptional activation of both ALK signalling pathways by all three TGFβ isoforms. Importantly, pharmacological inhibition of ALK5 or ALK1 (using SB525334 or K02288, respectively) or siRNA-mediated knockdown of ALK5 or ALK1 in TGFβ-stimulated HSVSMC, reduced the expression of pSmad2 and pSmad1/5, respectively, confirming that TGFβ can bind to and signal through both ALK5 and ALK1 in HSVSMC. Functional assays performed in HSVSMCs indicated that TGFβ1, TGFβ2 and TGFβ3 regulate VSMC proliferation and migration in a similar manner in vitro. To gain insight into how the ALK5 and ALK1 TGFβ signalling pathways regulate VSMC proliferation, migration and apoptosis, functional assays were performed in HSVSMC treated with TGFβ1 ± SB525334 or K02288. Pharmacological inhibition of ALK5 or ALK1 did not significantly alter HSVSMC proliferation in response to TGFβ1. Interestingly, TGFβ1-mediated HSVSMC migration was significantly attenuated in the presence of ALK1 small molecule inhibitor, K02288, whereas inhibition of ALK5 signalling by SB525334 had no significant effect on HSVSMC migration. TGFβ1 protected from hydrogen peroxide-induced HSVSMC apoptosis and inhibition of ALK5 or ALK1 signalling reversed this effect. These studies indicate that TGFβ signalling via ALK5 and ALK1 differentially regulates HSVSMC migration, but not proliferation or apoptosis. Data output from the Human TGFβ/BMP RT2 Profiler PCR Arrays suggested that several TGFβ signalling pathway genes were differentially expressed following rTGFβ treatment in HSVSMCs, whereby some TGFβ isoform-specific effects on gene expression were observed. However, following validation, no TGFβ isoform-specific effects on gene expression were detected. Whole genome expression profiling of migrating HSVSMCs treated with TGFβ1 ± SB525334 or K02288 was performed in order to compare the gene expression profiles directly regulated by ALK5 and ALK1. In total, the expression of 3,235 genes was modulated by TGFβ1 treatment compared with non-stimulated HSVSMCs, approximately half of which appeared to be co-ordinately dysregulated following ALK5 and ALK1 inhibition. Two groups of putative ALK5- and ALK1-specific transcriptional targets were chosen for more detailed evaluation and validation. qRT-PCR validation in HSVSMC confirmed fibroblast growth factor 2 (FGF2) and Mal, T-cell differentiation protein like (MALL) as ALK5-specific target genes, and fatty acid desaturase 1 (FADS1), H1 histone family member 0 (H1F0) and scavenger receptor class A member 3 (SCARA3) as ALK1-specific target genes. Together, this data indicates that TGFβ regulates HSVSMC behaviour during the pathogenesis of vein graft IH by activating distinct, ALK receptor-specific transcriptional networks. Overall, the findings from this thesis indicate that the ALK1/Smad1/5 TGFβ signalling pathway is activated following vascular injury and induces specific transcriptional changes to promote VSMC migration. Moreover, these studies indicate that TGFβ1, TGFβ2 and TGFβ3 regulate VSMC behaviour in a similar manner in vitro and all isoforms appear to have equivalent effects on the induction of established ALK5 and ALK1 target genes. Together, these findings highlight the potential of targeting non-canonical TGFβ signalling pathways in the setting of vein graft failure.
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Nesargikar, Prabhu. « Role of leukocytes, complement system and endothelium in rat renal ischaemia-reperfusion injury ». Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/85582/.

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Introduction: Renal Ischaemia-Reperfusion injury (IRI) is a complex mechanism involving the interplay between endothelium, leukocytes and the complement system. To evaluate the role of these three key mediators, a rat model was used to evaluate changes seen in renal IRI. Two interventional agents: Anti-Thymocyte Globulin (ATG) and Soluble Complement Receptor-1 (sCR1) were used to modulate leukocyte and complement response in this IRI model with a view to assess, and define IRI mechanism. Methods: The Ischaemia-Reperfusion (IR) model involved unilateral left renal ischemia (n=10) for 40 minutes, followed by 48 hours of reperfusion. ATG (n=8), ATG Isotype (n=8) and sCR1(n=8) were given IV prior to the laparotomy followed by IR model. The sham group (n=6) served as controls. Blood CD3 lymphocyte counts and CH50 complement assay were used to check efficacy of ATG and sCR1 respectively. The kidneys retrieved at 48 hours were analysed for histology, immunohistochemistry and RT-qPCR studies. Results: The IR group showed significant injury compared to the sham group. ATG treatment offered significant histological protection mainly via decreased leukocyte infiltrate and endothelial protection compared to the IR and Isotype controls. CH50 assay showed complete ablation of complement activity at the time of reperfusion, with return to normality at 24 hours. sCR1 treatment conferred protection from IRI predominantly via suppression of the complement cascade (C3, C9), reduced leukocyte infiltrates and V endothelial protection. RT-qPCR showed down-regulation of injury molecules – KIM-1 and NGAL in both the intervention groups. Conclusion: Modulation of leukocytes and complement system using single dose ATG and sCR1 led to significant endothelial protection, resulting in amelioration of renal ischaemia-reperfusion injury. The complement system was ablated at the time of reperfusion and was reconstituted by 24 hours, thus indicating that suppression of complement system during the phase of IR provides an avenue for mitigating IRI.
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Al-Mousawi, Abdul-Majeed M. « A study of warm-up and injury in hamstring muscles ». Thesis, University of Glasgow, 2005. http://theses.gla.ac.uk/6899/.

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This project is the first to investigate blood perfusion in the human hamstrings during isometric exercise with a near infrared spectroscopy (NIRS). A Kin Com dynamometer has been used to fix the knee positions and to measure torques during contractions. Both the NIRS optodes and the electromyography (EMG) electrodes were attached to the skin over the hamstrings. Previous studies used a NIRS to measure muscle blood flow in the forearm, quadriceps and calf muscles. The changes in haemoglobin concentrations were calculated using Spike 2 software. A total of 46 male volunteers participated in the four series of experiments described in this thesis. The following overall conclusions can be drawn: perfusion decreases in the hamstrings during contractions and then returns to normal levels after a period of time, changing the limb position at which the contractions are made does not affect the perfusion, warm-up exercises increase in blood perfusion for 8 minutes at 30 and 40% of MVC. The perfusion did not significantly change during an episode of DOMS or in the injured and non-injured limbs. These conclusions show the importance of warm-up before sports activities but not necessarily avoid injury. It can be concluded that there is no association between such conditions with hamstring injuries. The maintained perfusion at different conditions is a positive finding as the perfusion is not restricted indicating good delivery of oxygen despite muscle injury.
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Livres sur le sujet "R Injury"

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Pike, Jeffrey A. Neck Injury The Use of X-Rays, CTs, and MRIs to Study Crash-Related Injury Mechanisms. Warrendale, PA : SAE International, 2002. http://dx.doi.org/10.4271/r-268.

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Malia, Kit B. Brainwave-R : Cognitive strategies and techniques for brain injury rehabilitation. Austin, Tex : PRO-ED, 2002.

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University of Kentucky. Behavioral Research Aspects of Safety and Health Working Group et United States. Bureau of Mines, dir. Marvin R. Letcher exercise : Instructor's copy. Lexington, Ky : Behavioral Research Aspects of Safety and Health Group, Institute for Mining and Minerals Research, University of Kentucky, 1987.

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Evans, Phillip C. Erythropoietically-mediated neuroprotective effects of r-Hu-EPO following mechanically induced brain injury in female rats. Sudbury, Ont : Laurentian University, 2005.

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Securing Protections for the Injured from Limitations on Liability Act : Report together with additional views (to accompany H. R. 5503) (including committee cost estimate). Washington, D.C : U.S. G.P.O., 2010.

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Smith, Joann, et Michael Dow. Nurse Florence(R), What Is a Traumatic Brain Injury ? Lulu Press, Inc., 2022.

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Smith, Joann, et Michael Dow. Nurse Florence(R), What Is a Traumatic Brain Injury ? Lulu Press, Inc., 2022.

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Fink, Mitchell P. Ischaemia-reperfusion injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0308.

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Ischaemia/reperfusion (I/R) injury contributes to the pathogenesis of many common clinical conditions, including stroke, myocardial damage after percutaneous intervention for acute coronary artery occlusion, primary graft dysfunction after solid organ transplantation. The mechanisms that are responsible for I/R injury remain incompletely understood, but damage caused by reactive oxygen species (ROS) and reactive nitrogen species clearly is important. A number of therapeutic approaches, such as administration of ROS scavengers, are effective in animal models of I/R injury, but for the most part, translation of these findings into strategies that can clearly benefit patients has yet to be achieved.
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Pike, Jeffrey A. Neck Injury : The Use of X-Rays, CT's, and MRI's to Study Crash-Related Injury Mechanisms [R-268]. Society of Automotive Engineers Inc, 2002.

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Maddocks, Gini. R&R : Rescue and Relief for Computer Users and Those at Risk of Repetitive Motion Injury (RMI). Good Natured Publishing, 2003.

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Chapitres de livres sur le sujet "R Injury"

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James, Mark. « Player Violence and Compensation for Injury : R v Barnes [2005] 1 Cr App Rep 507 ». Dans ASSER International Sports Law Series, 323–36. The Hague, The Netherlands : T. M. C. Asser Press, 2013. http://dx.doi.org/10.1007/978-90-6704-909-2_20.

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Young, Lindon H., Aisha Phillipson, Didi Omiyi, Norrell Atkinson, Manoj Jivani, Jovan Adams, Ellen E. Peterman, Philip Taormina, Richard J. Brue et Margaret Harvey. « Protein Kinase C Isoform (PKC) Peptide Activator/Inhibitors Exert Cardioprotective Effects in Polymorphonuclear Leukocyte (PMN)-induced Ischemia/Reperfusion (I/R) Injury ». Dans Understanding Biology Using Peptides, 457–58. New York, NY : Springer New York, 2006. http://dx.doi.org/10.1007/978-0-387-26575-9_194.

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Mehan, Neal D., Matthew A. Bank, Jamie S. Ullman et Raj K. Narayan. « Multiple Surgical Teams in the O. R. at Once—Priority of Effort and Who Takes the Lead ? » Dans Neurotrauma Management for the Severely Injured Polytrauma Patient, 141–46. Cham : Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-40208-6_15.

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« M eth ods to R educe Ischem ia /R eperfusion In ju ry — PICSO ». Dans Ischemia-Reperfusion Injury in Cardiac Surgery, 112–18. CRC Press, 2000. http://dx.doi.org/10.1201/9781498712842-13.

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« TED R. MILLER Assessing the Burden of Injury : Progress and Pitfalls ». Dans Injury Prevention and Control, 61–82. CRC Press, 2000. http://dx.doi.org/10.1201/9781482268348-13.

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Teratani, Takumi, Eiji Kobayashi et Lauren Brasile. « Stem Cells Approach to I/R Injury ». Dans Regenerative Medicine Applications in Organ Transplantation, 945–52. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-398523-1.00068-9.

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« A poptosis in Ischem ia— R eperfusion I n ju ry ». Dans Ischemia-Reperfusion Injury in Cardiac Surgery, 54–61. CRC Press, 2000. http://dx.doi.org/10.1201/9781498712842-6.

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« . The C ellu lar Basis o f Im m ed ia te L ethal R eperfusion In ju ry ». Dans Ischemia-Reperfusion Injury in Cardiac Surgery, 41–53. CRC Press, 2000. http://dx.doi.org/10.1201/9781498712842-5.

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« IGF-1/IGF-R Signaling in Traumatic Brain Injury : Impact on Cell Survival, Neurogenesis, and Behavioral Outcome ». Dans Brain Neurotrauma, 90–107. CRC Press, 2015. http://dx.doi.org/10.1201/b18126-14.

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Jungraithmayr, Wolfgang. « Receptor Blockade of CD26/DPP4 as a Therapeutic Strategy Against I/R Injury and Lymphocytic Inflammation and its Clinical Implications ». Dans Immunity and Inflammation in Health and Disease, 127–32. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-805417-8.00010-x.

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Actes de conférences sur le sujet "R Injury"

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Uspuriene, Aiste Barbora, et Matas Simanavičius. « Competencies of Health Educators for Sports Injury Prevention ». Dans International Scientific and Practical Conference. TSNS Interaktiv Plus, 2020. http://dx.doi.org/10.21661/r-541400.

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According to the analysis of literature, it can be stated in, that there is a lower risk of experiencing sports injury during training, working with such health educators who has higher education in sports science. It is also can be stated that there are few studies which would determine the education of health educators, the quality of training and sports injuries suffered by clients and their frequency during the conducted trainings (Waryasz, Daniels, Gil, Suric, & Eberson, 2016). Research aim – to determine competencies of health educators for sports injury prevention.
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Uspuriene, Aiste Barbora, et Vilius Iurgelaitis. « Competences of physical education teachers in the sports injuries prevention ». Dans International Research-to-practice conference. TSNS Interaktiv Plus, 2019. http://dx.doi.org/10.21661/r-508096.

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School is a place where children spend most of their time. Thus, it is particularly important to ensure that it has a healthy and safe learning environment. Quite often, children experience injuries during physical education classes. Considering to the problem of children injuries in physical education classes, it is important to examine their prevalence, to analyze the causes of injury in physical education classes to prevent or reduce them. There is still a lack of research on the competence of physical education teachers in the prevention of sports injuries. Research aim – to identify the competences of physical education teachers for the sports injuries prevention. Using the questionnaire survey we investigated that physical education teachers pay attention to the warm-up and correct exercise in the physical education lesson. Students are rarely injured in the lessons of these physical education teachers. The research showed that competencies of surveyed physical education teachers are high.
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Ozaki, Masaaki, Yoshifumi Nishida et Tatsuhiro Yamanaka. « 503 Prioritizing injury situation to be prevented based on AI-Aided Situational R-Map ». Dans 14th World Conference on Injury Prevention and Safety Promotion (Safety 2022) abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/injuryprev-2022-safety2022.229.

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Ondrasik, Regina, Qian Chen, Katelyn Navitsky, William Chau, Issachar Devine, On S. Lau, Tyler Galbreath, Robert Barsotti et Lindon H. Young. « Cardioprotective Effects of Mitochondrial-Targeted Antioxidants in Myocardial Ischemia/Reperfusion (I/R) Injury ». Dans The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.064.

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Uspuriene, Aiste Barbora, et Vaida Zhiglite. « Signs and Types of Sports Injuries in Sports Clubs ». Dans International Scientific and Practical Conference. TSNS Interaktiv Plus, 2021. http://dx.doi.org/10.21661/r-553239.

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One of the most important factors influencing the quality of sports club services is the competencies of the hired staff. It is also emphasized that special attention must be paid to the competencies of coaches in the field of injury prevention. Research aim – to analyze the literature and to reveal expression and type of sports injuries in sports clubs.
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Hernandes Júnior, Paulo Roberto, Juliana de Souza Rosa, Patrick de Abreu Cunha Lopes, Bárbara Tisse da Silva, Heloá Santos Faria da Silva, Tiago Veiga Gomes, Giovanna de Camargo Innocencio et Jhoney Francieis Feitosa. « Overview of the conservative treatment of light grain cranioencephalic traumatism in the state of São Paulo ». Dans XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.115.

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Background: The traumatic brain injury is one of the main causes of mortality and disability in the world. Objectives: To analyze the current panorama of conservative treatment procedures for mild traumatic brain injury performed in the State of São Paulo and correlate with the current epidemiology. Methods: Literature review and observational, descriptive and transversal data collect on conservative treatment of mild grade traumatic brain injury, available at DATASUS from January 2008 to December 2020 and articles from Scielo, Lilacs and PubMed. Results: There were 150,743 hospitalizations for the conservative treatment of mild traumatic brain injury, being considered of medium complexity. They represent a total expenditure of R$ 64,098,819.38, with 2010 being the year with the highest number of hospitalizations (14,153) and 2011 being the year with the highest amount spent during the period (R$ 5,522,391.52). Of the total procedures, 1,744 are elective and 112,805 are urgent. In the public sector, 53,820 were carried out and 45,050 in the private sector. The total mortality rate was 1.60, corresponding to 2,413 deaths, with 2008 being the year with the highest mortality rate, 2.20 and 2016 had the lowest rate, 1.18. The mortality rate for elective procedures was 1.89 compared to 1.71 for urgent procedures, whereas in the public sector it was 1.73 compared to 1.58 for the private sector. The average total hospital stay was 2.4 days, with an average cost of R$ 425.22. Conclusion: The conservative treatment of traumatic brain injury has a low hospital stay and average cost.
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Hernandes Júnior, Paulo Roberto, Juliana de Souza Rosa, Patrick de Abreu Cunha Lopes, Bárbara Tisse da Silva, Heloá Santos Faria da Silva, Tiago Veiga Gomes, Tiago Veiga Gomes, Giovanna de Camargo Innocencio et Jhoney Francieis Feitosa. « Overview of the conservative treatment of light grain cranioencephalic traumatism in the state of São Paulo ». Dans XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.728.

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Background: The traumatic brain injury is one of the main causes of mortality and disability in the world. Objectives: To analyze the current panorama of conservative treatment procedures for mild traumatic brain injury performed in the State of São Paulo and correlate with the current epidemiology. Methods: Literature review and observational, descriptive and transversal data collect on conservative treatment of mild grade traumatic brain injury, available at DATASUS from January 2008 to December 2020 and articles from Scielo, Lilacs and PubMed. Results: There were 150,743 hospitalizations for the conservative treatment of mild traumatic brain injury, being considered of medium complexity. They represent a total expenditure of R$ 64,098,819.38, with 2010 being the year with the highest number of hospitalizations (14,153) and 2011 being the year with the highest amount spent during the period (R$ 5,522,391.52). Of the total procedures, 1,744 are elective and 112,805 are urgent. In the public sector, 53,820 were carried out and 45,050 in the private sector. The total mortality rate was 1.60, corresponding to 2,413 deaths, with 2008 being the year with the highest mortality rate, 2.20 and 2016 had the lowest rate, 1.18. The mortality rate for elective procedures was 1.89 compared to 1.71 for urgent procedures, whereas in the public sector it was 1.73 compared to 1.58 for the private sector. The average total hospital stay was 2.4 days, with an average cost of R$ 425.22. Conclusion: The conservative treatment of traumatic brain injury has a low hospital stay and average cost.
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Van de Water, A., R. Xhonneux et F. De Clerck. « ANTI-THROMBOTIC EFFECT IN CANINE CORONARY ARTERIES OF A COMBINED TXA2 synthetase/TXA2-prostaglandin ENDOPEROXIDE RECEPTOR INHIBITOR (R 68070) ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643463.

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The effects of R 68070 an oxime-alkane carboxylic acid derivative combining specific thromboxane A2 (TXA2) synthetase inhibition with TXA2/prostaglandin endoperoxide receptor blockade in one molecule, on thrombus formation in a coronary artery following electrically-induced endothelial injury and on its myocardial repercussions were examined in dogs. In an open-chest model in anaesthetized dogs, a stainless steel electrode was inserted into the left anterior descending coronary artery (LAD) distally (+ 1 cm) from an electromagnetic flow probe. ECG and heart rate were derived from limb leads. Serum TXB2 levels were measured by RIA on venous spontaneously coagulated blood (1 h, 37°C). Endothelial cell injury in the LAD coronary artery was induced by the application of an anodal current of 300 μA during 30 min; after an additional 60 min observation period, the thrombus wet weight was determined.In comparison with solvent treatment (n = 8), R 68070 (1.25 mg/kg I.V. 10 min before electrical stimulation, n = 7), significantly reduced the thrombus mass (solvent : 43 mg; R 68070 : 18 mg median value, p < 0.05), the incidence of ECG changes indicative for myocardial ischemia (fibrillation : solvent 1/8; R 68070 0/7; arrhythmias : solvent 3/8; R 68070 2/7; ST changes : solvent 7/8; R 68070 1/7, p < 0.05) and the decrease in coronary blood flow after electrical stimulation (solvent : from 13 to 6.5 ml/min; R 68070 : from 13 to 11 ml/min median values, p < 0.05). Serum TXB2 levels were reduced by 92 % at 100 min after the injection of the active compound (median value, n = 7).Heart rate and coronary blood flow measured before the induction of the endothelial injury were not modified by R 68070.The present study thus demostrates that R 68070 exerts a potent anti-thrombotic effect in canine coronary arteries. The relative contributions to this effect of TXA2 synthetase inhibition and of TXA2/prostaglandin endoperoxide receptor blockade exerted by the compound are being investigated.
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Devine, Issachar, Qian Chen, Regina Ondrasik, William Chau, Katelyn Navitsky, On Say Lau, Christopher W. Parker et al. « Cardioprotective Effects of Cell Permeable NADPH Oxidase Inhibitors in Myocardial Ischemia/Reperfusion (I/R) Injury ». Dans The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.00142.

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Zheng, Nigel, Hongsheng Wang et Koco Eaton. « Ulnar Collateral Ligament and Elbow Joint Loading During Throwing ». Dans ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80699.

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Ulnar collateral ligament (UCL) rupture is one of the most common throwing arm injuries for throwing athletes. Reconstructive surgery known as Tommy John surgery is often performed to restore joint stability [1]. According to the 2002 Major League Baseball Disability Analysis, almost 70% of players on the disabled list are pitchers and throwing arm related injuries account for 53% of all disabled list placements. To reach a high ball speed, pitchers cock, or excessively externally rotate their pitching arm to or near an extreme ROM of 180° [2]. The shoulder is then immediately internally rotated at over 7000°/s after the leading foot contact. The excessive external rotation ROM and astonishing internal rotation velocity are thought to contribute to throwing arm injury [3]. Repeated exposure to the large valgus torque may cause excessive laxity and catastrophic rupture of UCL [2]. A recent study showed that uninjured pitchers with higher elbow valgus torque exhibited UCL thickening whereas uninjured pitchers with lower elbow valgus torque did not have such adaptation in UCL appearance [4]. It is believed that microtear and catastrophic rupture of UCL are related to higher elbow valgus torque [2]. However, it is not clear how the conditions of the UCL are related to the elbow valgus torque during throwing. Therefore, it is our interest to investigate risk factors to throwing arm injuries. In this study, we investigated the elbow joint loading during throwing among subjects without UCL injury at the time of testing and after testing, with UCL reconstruction (UCL-R) at the time of testing, and UCL reconstruction after testing (PUCL-R). It was hypothesized that there was no significant differences in elbow joint loading between subjects with UCL-R, PUCL-R and uninjured groups. Findings from this may improve our understanding of UCL injury and assist us to identify risk factors for UCL injury.
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Rapports d'organisations sur le sujet "R Injury"

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Hochman, Ayala, Thomas Nash III et Pamela Padgett. Physiological and Biochemical Characterization of the Effects of Oxidant Air Pollutants, Ozone and Gas-phase Nitric Acid, on Plants and Lichens for their Use as Early Warning Biomonitors of these Air Pollutants. United States Department of Agriculture, janvier 2011. http://dx.doi.org/10.32747/2011.7697115.bard.

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Introduction. Ozone and related oxidants are regarded as the most important phytotoxic air pollutant in many parts of the western world. A previously unrecognized component of smog, nitric acid, may have even greater deleterious effects on plants either by itself or by augmenting ozone injury. The effects of ozone on plants are well characterized with respect to structural and physiological changes, but very little is known about the biochemical changes in plants and lichens exposed to ozone and/or HNO3. Objectives.To compare and contrast the responses of crop plants and lichens to dry deposition of HNO3 and O3., separately, and combined in order to assess our working hypothesis that lichens respond to air pollution faster than plants. Lichens are most suitable for use as biomonitors because they offer a live-organism-based system that does not require maintenance and can be attached to any site, without the need for man-made technical support systems. Original Immediate aims To expose the tobacco (Nicotiana tabacum L.) cultivar Bel-W3 that is ozone supersensitive and the ozone sensitive red kidney bean (Phaseolusvulgaris) and the lichen Ramalinamenziesii to controlled HNO3 and O3 fumigations and combined and to follow the resulting structural, physiological and biochemical changes, with special reference to reactive oxygen species related parameters. Revised. Due to technical problems and time limitations we studied the lichen Ramalinamenziesii and two cultivar of tobacco: Bel-W3 that is ozone supersensitive and a resistant cultivar, which were exposed to HNO3 and O3 alone (not combined). Methodology. Plants and lichens were exposed in fumigation experiments to HNO3 and O3, in constantly stirred tank reactors and the resulting structural, physiological and biochemical changes were analyzed. Results. Lichens. Exposure of Ramalinamenziesiito HNO3 resulted in cell membrane damage that was evident by 14 days and continues to worsen by 28 days. Chlorophyll, photosynthesis and respiration all declined significantly in HNO3 treatments, with the toxic effects increasing with dosage. In contrast, O3 fumigations of R. menziesii showed no significant negative effects with no differences in the above response variables between high, moderate and low levels of fumigations. There was a gradual decrease in catalase activity with increased levels of HNO3. The activity of glutathione reductase dropped to 20% in thalli exposed to low HNO3 but increased with its increase. Glucose 6-phosphate dehydrogenase activity increase by 20% with low levels of the pollutants but decreased with its increase. Tobacco. After 3 weeks of exposure of the sensitive tobacco cultivar to ozone there were visible symptoms of toxicity, but no danmage was evident in the tolerant cultivar. Neither cultivar showed any visible symptoms after exposure to HNO3.In tobacco fumigated with O3, there was a significant decrease in maximum photosynthetic CO2 assimilation and stomatal conductance at high levels of the pollutant, while changes in mesophyll conductance were not significant. However, under HNO3 fumigation there was a significant increase in mesophyll conductance at low and high HNO3 levels while changes in maximum photosynthetic CO2 assimilation and stomatal conductance were not significant. We could not detect any activity of the antioxidant enzymes in the fumigated tobacco leaves. This is in spite of the fact that we were able to assay the enzymes in tobacco leaves grown in Israel. Conclusions. This project generated novel data, and potentially applicable to agriculture, on the differential response of lichens and tobacco to HNO3 and O3 pollutants. However, due to experimental problems and time limitation discussed in the body of the report, our data do not justify yet application for a full, 4-year grant. We hope that in the future we shall conduct more experiments related to our objectives, which will serve as a basis for a larger scale project to explore the possibility of using lichens and/or plants for biomonitoring of ozone and nitric acid air pollution.
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