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Copyright of Lettre de Medecine Physique et de Readaptation is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In breast cancers, clinical symptoms of inflammation localised around the tumour at the time of diagnosis have been considered to have poor prognosis significance. In this study, the biological mechanisms responsible for the deleterious action of monocytes in cancer were investigated. The incubation of the breast-cancer-derived MDA-MB231 cells with monocytes resulted in an increase in factors involved in cell invasion (i.e. both cancer cells and monocytes-associated urokinase and Tissue Factor, and PAl-I and MMP-9 secretion). Moreover, the functions of monocytes were also modified. Incubation of monocytes with MDA-MB231 cancer cells resulted in a down-regulation in the secretion of the antiproliferative cytokine Oncostatin M, while the apoptotic factor TNF alpha was dramatically increased. However, MDA-MB231 cancer cells have been shown to be resistant towards the apoptotic action of TNF alpha. These findings demonstrate that incubation of MDA-MB231 cancer cells with monocytes induced a crosstalk, which resulted in an increased expression of factors involved in cancer cell invasiveness and in a modification of monocytes function against cancer cells, while inflammatory effects were increased. [ABSTRACT FROM AUTHOR]

Sodium phenylacetate (NaPa), a non-toxic phenylalanine metabolite, has been shown to induce in vivo and in vitro cytostatic and antiproliferative effects on various cell types. In this work, we analysed the effect of NaPa on the invasiveness of breast cancer cell (MDA-MB-231, MCF-7 and MCF-7 ras). Using the highly invasive breast cancer cell line MDA-MB-231, we demonstrated that an 18-hour incubation with NaPa strongly inhibits the cell invasiveness through Matrigel (86% inhibition at 20 mM of NaPa). As cell invasiveness is greatly influenced by the expression of urokinase (u-PA) and its cell surface receptor (u-PAR) as well as the secretion of matrix metalloproteinases (MMP), we tested the effect of NaPa on these parameters. An 18-hour incubation with NaPa did not modify u-PA expression, either on MDA-MB-231 or on MCF-7 and MCF-7 ras cell lines, and induced a small u-PA decrease after 3 days of treatment of MDA-MB-321 with NaPa. In contrast, an 18 h incubation of MDA-MB-231 increased the expression of u-PAR and the secretion of MMP-9. As u-PAR is a ligand for vitronectin, a composant of the extracellular matrix, these data could explain the increased adhesion of MDA-MB-231 to vitronectin, while cell adhesivity of MCF-7 and MCF-7 ras was unmodified by NaPa treatment. NaPa induced also an increased expression of both Lymphocyte Function-Associated-1 (LFA-1) and Intercellular Adhesion Molecule-1 (ICAM-1), which was obvious from 18 hour incubation with NaPa for the MDA-MB-231 cells, but was delayed (3 days) for MCF-7 and MCF-7 ras. Only neutralizing antibodies against LFA-1 reversed the decreased invasiveness of NaPa-treated cells. Therefore we can conclude that the strong inhibition of MDA-MB-231 invasiveness is not due to a decrease in proteases involved in cell migration (u-PA and MMP) but could be related both to the modification of cell structure and an increased expression of adhesion molecules such as u-PAR and LFA-1. [ABSTRACT FROM AUTHOR]

Study design:Case report.Objectives:To describe a case of suprascapular nerve entrapment (SNE) in a patient with a spinal cord injury (SCI) as a cause of shoulder pain.Setting:Physical Medicine and Rehabilitation Institute, Nancy, France.Report:Six months after the occurrence of acute paraplegia T9 ASIA, a 45-year-old man complained of pain in the posterior and lateral areas of the left shoulder. A clinical assessment found an atrophy of the infraspinatus muscle and a muscular weakness during external shoulder rotation. SNE was suggested as a cause of pain and confirmed by nerve conduction recording. Magnetic resonance imaging excluded any compressive cyst. SNE at the spinoglenoid notch, related to upper limb overuse, was suggested. A gluco-corticoid injection in the proximity of the suprascapular nerve eliminated the pain in a few hours. Two months after the injection, the pain had not reappeared, the infraspinatus muscle atrophy was resolved, and supraspinal nerve conduction was normalized.Conclusion:Shoulder pain is common in individuals with paraplegia, but this is the first time that SNE has been reported as a cause of pain. This micro-traumatic pathology, well known in athletes, is probably under-diagnosed in patients with SCI who overuse their upper limbs for wheelchair propulsion and body transfers. [ABSTRACT FROM AUTHOR]

Study design:Prospective study.Objectives:To determine the mechanisms of body illusions in paraplegia patients as compared with the amputee phantom phenomena.Methods:A vestibular caloric stimulation was performed in 10 consecutive patients with complete section of the spinal cord. Perception of body, before and after stimulation, was classed as illusion of a normal body (lower limbs with normal morphological, postural and kinetic characteristics perceived as before spinal injury), normal phantom (overly vivid perception of all or part of the lower limbs), deformed phantom (perception of all or part of the limbs below the injury level as abnormal in shape, posture, movement or even number), or painful phantom.Results:After vestibular caloric stimulation, nine out of 10 patients stated their perception of body segments below the injury level had changed to normal phantoms or to deformed phantoms (morphological, postural or kinetic changes). Among the four patients who initially had painful limbs, two stated the stimulation greatly relieved their pain.Conclusion:The normal or deformed phantom evoked by vestibular stimulation would result from use of identity data or instantaneous data as is observed in amputees. Cerebral remapping following deafferentation could be the origin of the deformed phantoms. Illusions corresponding to phenomena perceived at the time of the accident corresponding to autobiographical engrammes do not appear to be evoked by vestibular stimulation, as is also the case in amputees.Spinal Cord (2001) 39, 85–87. [ABSTRACT FROM AUTHOR]