Current Issue : January - March Volume : 2017 Issue Number : 1 Articles : 7 Articles
Background: The success of cochlear implantation may be further improved by minimizing implantation trauma. The\nphysical trauma of implantation and subsequent immunological sequelae can affect residual hearing and the viability\nof the spiral ganglion. An ideal electrode should therefore decrease post-implantation trauma and provide support to\nthe residual spiral ganglion population. Combining a flexible electrode with cells producing and releasing protective\nfactors could present a potential means to achieve this. Mononuclear cells obtained from bone marrow (BM-MNC)\nconsist of mesenchymal and hematopoietic progenitor cells. They possess the innate capacity to induce repair of\ntraumatized tissue and to modulate immunological reactions.\nMethods: Human bone marrow was obtained from the patients that received treatment with biohybrid electrodes.\nAutologous mononuclear cells were isolated from bone marrow (BM-MNC) by centrifugation using the Regenlabââ??¢\nTHT-centrifugation tubes. Isolated BM-MNC were characterised using flow cytometry. In addition, the release of\ncytokines was analysed and their biological effect tested on spiral ganglion neurons isolated from neonatal rats. Fibrin\nadhesive (Tissealââ??¢) was used for the coating of silicone-based cochlear implant electrode arrays for human use in order\nto generate biohybrid electrodes. Toxicity of the fibrin adhesive and influence on insertion, as well on the cell coating,\nwas investigated. Furthermore, biohybrid electrodes were implanted in three patients.\nResults: Human BM-MNC release cytokines, chemokines, and growth factors that exert anti-inflammatory and\nneuroprotective effects. Using fibrin adhesive as a carrier for BM-MNC, a simple and effective cell coating procedure for\ncochlear implant electrodes was developed that can be utilised on-site in the operating room for the generation of\nbiohybrid electrodes for intracochlear cell-based drug delivery. A safety study demonstrated the feasibility of autologous\nprogenitor cell transplantation in humans as an adjuvant to cochlear implantation for neurosensory restoration.\nConclusion: This is the first report of the use of autologous cell transplantation to the human inner ear. Due to the\nsimplicity of this procedure, we hope to initiate its widespread utilization in various fields...
Background: Graft-versus-host disease (GVHD) after liver and kidney transplantation has high mortality and causes\ndiagnostic challenges. This study aims to describe the cytokine and human leukocyte antigen (HLA) profile in the\nGVHD after liver and kidney transplantation.\nMethods: A high-throughput detection kit was applied and altogether 18 different cytokines were tested simultaneously.\nGVHD patients included 23 post-liver transplantation patients; 22 post-renal transplantation patients; The\ncontrol patients include 22 hepatocellular carcinoma (HCC) patients without transplantation and 20 healthy controls.\nTheir HLA characters were compared.\nResults: The full spectrum of cytokines was present. The inflammatory markers were activated significantly in liver\ntransplantation. The level of inflammatory markers in liver transplantation was higher than that in renal transplantation,\nHCC or healthy controls. GVHD was associated with the HLA characters; HLA characters are involved in liver\nGVHD occurrence and act as risk factors.\nConclusion: Our findings confirmed that the inflammatory cytokines play a pathogenic role in GVHD and can be\nused as early diagnostic markers. The HLA mismatch acts as a risk factor in liver transplantation to predict GVHD\noccurrence....
Changes in distribution policies have increased median MELD at transplant with recipients requiring increasing intensive care\nperioperatively. We aimed to evaluate association of preoperative variables with postoperative respiratory failure (PRF)/increased\nintensive care unit length of stay (ICU LOS)/short-term survival in a high MELD cohort undergoing liver transplant (LT).\nRetrospective analysis identified cases of PRF and increased ICU LOS with recipient, donor, and surgical variables examined.\nVariables were entered into regression with end points of PRF and ICU LOS > 3 days. 164 recipients were examined: 41 (25.0%)\nexperienced PRF and 74 (45.1%) prolonged ICULOS. Significant predictors of PRF with univariate analysis: BMI > 30, pretransplant\nMELD, preoperative respiratory failure, LVEF < 50%, FVC < 80%, intraoperative transfusion > 6 units, warm ischemic time >\n4 minutes, and cold ischemic time > 240 minutes. On multivariate analysis, only pretransplant MELD predicted PRF (OR 1.14,\n...
Background: Following recent approval of pirfenidone and nintedanib for idiopathic pulmonary fibrosis (IPF),\nquestions arise about the use of these antifibrotics in patients awaiting lung transplantation (LTx).\nMethods: Safety and efficacy of antifibrotic drugs in IPF patients undergoing LTx were investigated in a single-centre\nretrospective cohort analysis.\nResults: A total of nine patients, receiving antifibrotic therapy for 419 Ã?± 315 days until subsequent LTx, were included. No\nmajor side effects were noted. Significant weight loss occurred during antifibrotic treatment (p = 0.0062). FVC tended to\nstabilize after 12 weeks of treatment in most patients. A moderate decline in FVC, TLC and DLCO was noted during the\nwhole pretransplant time period of antifibrotic therapy. Functional exercise capacity and lung allocation score remained\nunchanged. No post-operative thoracic wound healing problems, nor severe early anastomotic airway complications\nwere attributable to prior antifibrotic treatment. None of the patients developed chronic lung allograft dysfunction after a\nmedian follow-up of 19.8 (11.2ââ?¬â??26.5) months; and post-transplant survival was 100% after 1 year and 80% after 2 years.\nConclusions: Antifibrotic drugs can probably be safely administered in IPF patients, possibly attenuating disease\nprogression over time, while awaiting LTx....
Background: Heart transplantation is an uncommon treatment for unresectable and non-metastatic primary\ncardiac sarcomas, and the role of it is unclear. This study aims to offer a survival analysis of it.\nMethods: This study consists of 6 patients from our institution and 40 patients identified in a literature search who\nunderwent heart transplantation for non-metastatic primary cardiac sarcomas. Seven patients with unresectable\ncardiac angiosarcoma who received palliative therapies at our institution were included for comparison. All the\nclinicopathologic data were collected, retrospectively reviewed and statistically analyzed.\nResults: Among the 46 patients receiving heart transplantation for primary cardiac sarcomas, the overall median\nsurvival was 16 months (2ââ?¬â??112 months). The most common histologic type receiving heart transplantation was\nangiosarcoma. Its median survival time after heart transplantation (n = 14) was much less than that of other\nhistologic types (n = 31) (9 vs 36 months; P = 0.002), which means it was not different from the median survival of\n8 months for patients (n = 7) receiving palliative therapies (P = 0.768). The patients with grade 2 cardiac sarcomas\n(n = 5) survived much longer after heart transplantations than patients with grade 3 tumors (n = 15) (mean\nsurvival: 85 vs 18 months; P = 0.006). Neoadjuvant or adjuvant chemotherapy didnââ?¬â?¢t provide survival benefits after\nheart transplantation.\nConclusions: Cardiac angiosarcoma seems to be not the proper indication of heart transplantation. The role of\nheart transplantation in other histologic subtypes still remains undefined. Lower grade and less aggressive\nhistologic subtypes benefit more from heart transplantation....
Background: Non-invasive goal directed fluid therapy during deceased donor renal transplant\n(CRT) may reduce the incidence of delayed graft function. Plethysmograph Variability Index (PVI)\nhas been shown to predict fluid responsiveness during surgery. This pilot study evaluated the feasibility\nof goal directed fluid administration protocol based upon PVI studying the incidence of\ndelayed graft function (DGF) in renal transplant recipients. Methods: Twenty patients underwent\nprimary CRT. The Control group received intravenous fluid (IVF) at a calculated constant rate. The\nTreatment group received a baseline IVF infusion throughout the surgery. PVI values greater than\n13% were treated with 250 ml boluses of IVF. Primary end point was DGF; total IVF administration\nand urinary biomarker NGAL levels were secondary endpoints. Results: Treatment group at every\ntime point received significantly less IVF. There was no significant difference in incidence of DGF\nbetween the groups. 2 patients in the Control group and 6 in the Treatment group developed DGF.\nNGAL was not associated with the group assignment or total IVF given (p < 0.2). Conclusions: The\neffectiveness of goal directed fluid therapy with non-invasive dynamic parameters has not been\nvalidated in renal transplant surgery and larger prospective studies are needed to determine its\nutility in renal transplantation....
Background: The role of DNA methylation in the regulation of the anti-donor-directed immune response after\norgan transplantation is unknown. Here, we studied the methylation of two mediators of the immune response: the\npro-inflammatory cytokine interferon Ã?³ (IFNÃ?³) and the inhibitory receptor programmed death 1 (PD1) in naÃ?¯ve and\nmemory CD8+ T cell subsets in kidney transplant recipients receiving immunosuppressive medication. Both\nrecipients experiencing an episode of acute allograft rejection (rejectors) as well as recipients without rejection\n(non-rejectors) were included.\nResults: CpGs in the promoter regions of both IFNÃ?³ and PD1 were significantly (p < 0.001) higher methylated in the\nnaÃ?¯ve CD8+ T cells compared to the memory T cell subsets. The methylation status of both IFNÃ?³ and PD1 inversely\ncorrelated with the percentage of IFNÃ?³ or PD1-producing cells. Before transplantation, the methylation status of both\nIFNÃ?³ and PD1 was not significantly different from healthy donors. At 3 months after transplantation, irrespective of\nrejection and subsequent anti-rejection therapy, the IFNy methylation was significantly higher in the differentiated\neffector memory CD45RA+ (EMRA) CD8+ T cells (p = 0.01) whereas the PD1 methylation was significantly higher in all\nmemory CD8+ T cell subsets (CD27+ memory; p = 0.02: CD27âË?â?? memory; p = 0.02: EMRA; p = 0.002). Comparing the\nincrease in methylation in the first 3 months after transplantation between rejectors and non-rejectors demonstrated a\nsignificantly more prominent increase in the PD1 methylation in the CD27âË?â?? memory CD8+ T cells in rejectors (increase\nin rejectors 14%, increase in non-rejectors 1.9%, p = 0.04). The increase in DNA methylation in the other memory CD8+\nT cells was not significantly different between rejectors and non-rejectors. At 12 months after transplantation, the\nmethylation of both IFNÃ?³ and PD1 returned to baseline levels.\nConclusions: The DNA methylation of both IFNÃ?³ and PD1 increases the first 3 months after transplantation in memory\nCD8+ T cells in kidney transplant recipients. This increase was irrespective of a rejection episode indicating that general\nfactors of the kidney transplantation procedure, including the use of immunosuppressive medication, contribute to\nthese variations in DNA methylation....
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