29 research outputs found
A rare case of complete C2–C3 dislocation with mild neurological symptoms
The authors report a rare case of complete C2–C3 dislocation with unexpectedly mild neurological symptoms in a 57 year old man involved in a motor vehicle accident, who had previously undergone posterior laminectomy from C3 through C7. A retrospective chart analysis and a thorough radiographic review were performed. X-rays and CT of the cervical spine demonstrated a complete dislocation at the C2–C3 level. Computed tomographic angiography revealed disruption of both vertebral arteries; however, blood flow was evident in the basilar artery. After radiologically guided placement in cervical traction with tongs that reduced the subluxation by approximately 50% the patient had spontaneous eye opening and was able to follow commands. A two-stage 360(o) stabilization and fusion was performed and the patient was finally discharged 24 days after admission with his neurological status essentially unchanged. In conclusion, our patient presented with surprisingly mild neurological symptoms. The previously performed laminectomy could have both predisposed to injury as well as protected his spinal cord from potentially fatal trauma
The role of TG2 in regulating S100A4-mediated mammary tumour cell migration
The importance of S100A4, a Ca2+-binding protein, in mediating tumour cell migration, both intracellularly and extracellularly, is well documented. Tissue transglutaminase (TG2) a Ca2+-dependent protein crosslinking enzyme, has also been shown to enhance cell migration. Here by using the well characterised non-metastatic rat mammary R37 cells (transfected with empty vector) and highly metastatic KP1 cells (R37 cells transfected with S100A4), we demonstrate that inhibition of TG2 either by TG2 inhibitors or transfection of cells with TG2 shRNA block S100A4-accelerated cell migration in the KP1cells and in R37 cells treated with exogenous S100A4. Cell migration was also blocked by the treatment with the non-cell permeabilizing TG2 inhibitor R294, in the human breast cancer cell line MDA-MB-231 (Clone 16, which has a high level of TG2 expression). Inhibition was paralleled by a decrease in S100A4 polymer formation. co-immunoprecipitation and Far Western blotting assays and cross-linking assays showed not only the direct interaction between TG2 and S100A4, but also confirmed S100A4 as a substrate for TG2. Using specific functional blocking antibodies, a targeting peptide and a recombinant protein as a competitive treatment, we revealed the involvement of syndecan-4 and a5ß1 integrin co-signalling pathways linked by activation of PKCa in this TG2 and S100A4-mediated cell migration. We propose a mechanism for TG2-regulated S100A4-related mediated cell migration, which is dependent on TG2 crosslinking
Epigenetic regulation of S100 protein expression
S100 proteins are small, calcium-binding proteins whose genes are localized in a cluster on human chromosome 1. Through their ability to interact with various protein partners in a calcium-dependent manner, the S100 proteins exert their influence on many vital cellular processes such as cell cycle, cytoskeleton activity and cell motility, differentiation, etc. The characteristic feature of S100 proteins is their cell-specific expression, which is frequently up- or downregulated in various pathological states, including cancer. Changes in S100 protein expression are usually characteristic for a given type of cancer and are therefore often considered as markers of a malignant state. Recent results indicate that changes in S100 protein expression may depend on the extent of DNA methylation in the S100 gene regulatory regions. The range of epigenetic changes occurring within the S100 gene cluster has not been defined. This article reviews published data on the involvement of epigenetic factors in the control of S100 protein expression in development and cancer
Fabric dependence of wave propagation in anisotropic porous media
Current diagnosis of bone loss and osteoporosis is based on the measurement of the Bone Mineral Density (BMD) or the apparent mass density. Unfortunately, in most clinical ultrasound densitometers: 1) measurements are often performed in a single anatomical direction, 2) only the first wave arriving to the ultrasound probe is characterized, and 3) the analysis of bone status is based on empirical relationships between measurable quantities such as Speed of Sound (SOS) and Broadband Ultrasound Attenuation (BUA) and the density of the porous medium. However, the existence of a second wave in cancellous bone has been reported, which is an unequivocal signature of poroelastic media, as predicted by Biot’s poroelastic wave propagation theory. In this paper the governing equations for wave motion in the linear theory of anisotropic poroelastic materials are developed and extended to include the dependence of the constitutive relations upon fabric - a quantitative stereological measure of the degree of structural anisotropy in the pore architecture of a porous medium. This fabric-dependent anisotropic poroelastic approach is a theoretical framework to describe the microarchitectural-dependent relationship between measurable wave properties and the elastic constants of trabecular bone, and thus represents an alternative for bone quality assessment beyond BMD alone
Prognostic Factors in Patients Hospitalized for Heart Failure
Each year, there are over one million hospitalizations for heart failure in the United States, with a similar number in Western Europe. Although these patients respond to initial therapies, they have very high short and intermediate term (2-6 months) mortality and readmission rates, while the healthcare system incurs substantial costs. Several risk prediction models that can accurately identify high-risk patients have been developed using data from clinical trials, large registries or administrative databases. Use of multi-variable risk models at the time of hospital admission or discharge offers better risk stratification and should be encouraged, as it allows for appropriate allocation of existing resources and development of clinical trials testing new treatment strategies for patients admitted with heart failure
