Mathieu D.,Center Hospitalier et University |
Ratzenhofer-Komenda B.,Medical University of Graz |
Kot J.,Medical University of Gdansk
Diving and Hyperbaric Medicine
Many of the accepted indications for hyperbaric oxygen treatment (HBOT) may occur in critically ill patients. HBOT itself may cause a number of physiological changes which may further compromise the patient’s state. Guidelines on the management of critically ill patients in a hyperbaric facility have been founded on the conclusions of the 2007 European Committee for Hyperbaric Medicine (ECHM) meeting. With regard to patient management, HBOT should be included in the overall care of ICU patients only after a risk/benefit assessment related to the specifics of both the hyperbaric centre and the patient’s clinical condition and should not delay or interrupt their overall management. Neither patient monitoring nor treatment should be altered or stopped due to HBOT, and any HBOT effects must be strictly evaluated and appropriately mitigated. With regard to the hyperbaric facility itself, the hyperbaric chamber should be specifically designed for ICU patients and should be fully equipped to allow continuation of patient monitoring and treatment. The hyperbaric chamber ideally should be located in, or around the immediate vicinity of the ICU, and be run by a sufficiently large and well-trained team of physicians, nurses, chamber operators and technicians. All devices to be introduced into the chamber should be evaluated, tested and acknowledged as safe for use in a hyperbaric environment and all procedures (standard and emergency) should be tested and written before being implemented. © 2016, South Pacific Underwater Medicine Society. All rights reserved. Source
Hu C.,University of Birmingham |
Wei W.,University of Birmingham |
Chen X.,University of Birmingham |
Chen X.,Guangdong Medical College |
And 15 more authors.
Previous studies have reported that the tumour cells of nasopharyngeal carcinoma (NPC) exhibit recurrent chromosome abnormalities. These genetic changes are broadly assumed to lead to changes in gene expression which are important for the pathogenesis of this tumour. However, this assumption has yet to be formally tested at a global level. Therefore a genome wide analysis of chromosome copy number and gene expression was performed in tumour cells micro-dissected from the same NPC biopsies. Cellular tumour suppressor and tumour-promoting genes (TSG, TPG) and Epstein-Barr Virus (EBV)-encoded oncogenes were examined. The EBV-encoded genome maintenance protein EBNA1, along with the putative oncogenes LMP1, LMP2 and BARF1 were expressed in the majority of NPCs that were analysed. Significant downregulation of expression in an average of 76 cellular TSGs per tumour was found, whilst a per-tumour average of 88 significantly upregulated, TPGs occurred. The expression of around 60% of putative TPGs and TSGs was both up-and down-regulated in different types of cancer, suggesting that the simplistic classification of genes as TSGs or TPGs may not be entirely appropriate and that the concept of context-dependent onco-suppressors may be more extensive than previously recognised. No significant enrichment of TPGs within regions of frequent genomic gain was seen but TSGs were significantly enriched within regions of frequent genomic loss. It is suggested that loss of the FHIT gene may be a driver of NPC tumourigenesis. Notwithstanding the association of TSGs with regions of genomic loss, on a gene by gene basis and excepting homozygous deletions and high-level amplification, there is very little correlation between chromosomal copy number aberrations and expression levels of TSGs and TPGs in NPC. © 2012 Hu et al. Source
Ryckewaert A.,Center Hospitalier et University |
Allain-Launay E.,University of Nantes |
Moreau A.,University of Nantes |
Blancho G.,University of Nantes |
And 3 more authors.
Bortezomib has appeared recently as a potential active treatment for acute AMR for few years. We reported a patient who received two courses of bortezomib for the treatment of an acute AMR associated with de novo HLA DSA that occurred 18 months after renal transplantation because of non-compliance. Graft biopsy revealed features of acute humoral rejection with plasmocyte infiltration and C4d staining. Bortezomib was associated with corticosteroid pulses, IVIgs, and PP. Despite this rapid management, the patient lost his graft and carried on dialysis. Bortezomib therapy in addition to current therapy of AMR is not always effective in the treatment for late acute AMR in renal transplantation. We discuss on the place of such a treatment and other therapeutic strategies in this indication. © 2013 John Wiley & Sons A/S. Source
Aubert O.,University of Paris Descartes |
Aouba A.,University of Paris Descartes |
Deshayes S.,Institute Jean Godinot |
Georgin-Lavialle S.,University of Paris Descartes |
And 2 more authors.
Joint Bone Spine
Erdheim-Chester disease is a rare non-langerhans cell histiocytosis characterized by infiltration of foamy CD68-positive but CD1a-negative macrophages and fibro-inflammatory lesions as retroperitoneal, periureteral areas or bones. Interferon-α therapy has been used as treatment but it had variable efficiency and limited tolerance. More recently, a recombinant form of interleukin-1 receptor antagonist (anakinra) was used with success but no skeletal radiological improvement was recorded. We report here a case of interleukin-1 receptor antagonist in the treatment of refractory bones infiltration in Erdheim-Chester disease. After 1 year of treatment, the positron emission tomography-computed tomography showed an outstanding response of the skeletal involvement with clearly lower and smaller hypermetabolism images. © 2012 Société française de rhumatologie. Source
Le Rhun E.,Breast Unit |
Le Rhun E.,Center Hospitalier et University |
Tu Q.,Nancy University Hospital Center |
Tu Q.,University of Lorraine |
And 11 more authors.
Melanoma is the most frequent solid tumor associated with leptomeningeal metastasis (LM). The usual diagnostic tools, that is, cytomorphological assessment of cerebro-spinal fluid (CSF) and gadolinium-enhanced MRI of the entire neuraxis both lack effectiveness. The CellSearch® Veridex technology for the detection of circulating tumor cells (CTC) in blood was designed for the follow-up and prognosis of breast, prostate, colorectal, and lung cancer, which express EpCAM markers. We have previously adapted this technology to detect malignant cells in the CSF of breast cancer LM. Our objective here was to check if this technology would also allow the detection and the enumeration of CTC in the CSF of melanoma patients presenting with LM although melanoma does not express EpCAM markers. On the occasion of the intrathecal treatment of LM in 2 melanoma patients, 5 mL of CSF and 7.5 mL of blood were collected on CellSave® Preservative Tubes and analyzed within 3 days after CSF sampling using a melanoma-dedicated kit. The CellSearch® Veridex technology was then adapted to direct enrichment, enumeration, and visualization of melanoma cells in the CSF. CD146+, HMW-MAA+, CD34-, and CD45- cells with typical morphology could be observed and enumerated sequentially with reproducible results, corresponding to CSF melanoma cells (CSFMC). In contrast to the current gold standard cytomorphological analysis, this new approach allowed a precise quantification of CSFMC in all samples concomitantly analyzed. This methodology, established on a limited volume of sample and allowing delayed processing, could prove of great interest in the diagnosis and follow-up of melanoma patients with LM. © 2013 Springer Science+Business Media New York. Source