Evaluating wearable multimodal sensor insoles for motion-pattern measurements in stroke rehabilitation - A pilot study.

The majority of stroke patients experience deficits in motoric functions, especially in gait and mobility. They need rehabilitation to regain walking independence, which is a major goal of rehabilitation after stroke. To document and assess the rehabilitation progress, instrumented motion analysis and clinical assessments are commonly used. In a clinical pilot study the applicability of an instrumented insole system in stroke rehabilitation is evaluated. Motion parameter of 35 stroke patients were gathered with the system while completing 90 s level walking and Timed Up & Go test at the beginning and end of four weeks inpatient rehabilitation. For level walking the motion parameter were gathered with the clinical reference system simultaneously. The mean stride time for level walking decreased from 1.20 s to 1.16 s (clinical system), or from 1.19 s to 1.12 s (insole system), respectively. Focusing on individual comparison of each patient's progress, 9 gait parameters are extracted for level walking, 6 sub-phases of Timed Up & Go test are detected and analyzed, as well as progress of Center of Pressure in the sub-phases is examined. Although the overall data show wide distribution, the system proofed to be applicable in clinical stroke rehabilitation routine. As the system is location-independent, and has the advantage of assessing additional parameters of the Timed Up & Go test, it is additionally suitable for integration in a tele-or home rehabilitation system.

A Framework for (Tele-) Monitoring of the Rehabilitation Progress in Stroke Patients: eHealth 2015 Special Issue.

BACKGROUND: Preservation of mobility in conjunction with an independent life style is one of the major goals of rehabilitation after stroke. OBJECTIVES: The Rehab@Home framework shall support the continuation of rehabilitation at home. METHODS: The framework consists of instrumented insoles, connected wirelessly to a 3G ready tablet PC, a server, and a web-interface for medical experts. The rehabilitation progress is estimated via automated analysis of movement data from standardized assessment tests which are designed according to the needs of stroke patients and executed via the tablet PC application. RESULTS: The Rehab@Home framework's implementation is finished and ready for the field trial (at five patients' homes). Initial testing of the automated evaluation of the standardized mobility tests shows reproducible results. CONCLUSIONS: Therefore it is assumed that the Rehab@Home framework is applicable as monitoring tool for the gait rehabilitation progress in stroke patients.

The putative role of cell adhesion molecules in endometriosis: can we learn from tumour metastasis?

Endometriosis, one of the most frequent diseases in gynaecology, is a considerable threat to the physical, psychological and social integrity of women. The etiology and pathogenesis of this important disease, defined as the ectopic location of endometrium-like glandular epithelium and stroma outside the uterine cavity, is poorly understood. Clinical observations and in vitro experiments imply that endometriotic cells are invasive and able to metastasize. Analogous to tumour metastasis, it is likely that cell adhesion molecules are central for the invasion and metastasis of endometriotic cells. Investigation of these molecules in endometriosis should increase our understanding of the molecular mechanisms involved in the pathogenesis of this disease.

Tracing cellular and molecular mechanisms involved in endometriosis.

The aetiology and pathogenesis of endometriosis, defined as the presence of endometrium-like tissue outside the uterine cavity, is largely unknown. In this paper we present and discuss possibilities to study the putative pathogenic properties of endometriotic cells in vitro. The current focus of our investigations is on the invasive phenotype of the disease, assuming that this might contribute to the pathogenesis of endometriosis. So far, we have shown that: (i) cytokeratin-positive and E-cadherin-negative endometriotic cells have an invasive phenotype in a collagen invasion assay in vitro similar to metastatic carcinoma cells; (ii) the invasiveness of endometriotic but not of eutopic endometrial cells can be stimulated by a heat-stable protein present in peritoneal fluid; and (iii) the endometriotic cell line EEC145T, which we established, may be a useful tool for the identification of gene products which are, positively or negatively, invasion-related. Finally, our studies suggest that the invasive phenotype in endometriosis shares aspects with tumour metastasis, but might also have unique mechanisms.

Nonmalignant epithelial cells, potentially invasive in human endometriosis, lack the tumor suppressor molecule E-cadherin.

Endometriosis is one of the most frequent diseases in gynecology. It is a histologically defined nonmalignant disease in which endometrium-like tissue is found outside the uterus (for example, peritoneum, gut, or lung). The pathogenesis of endometriosis is unknown, but invasive mechanisms have been implicated in the development of the disease. Indeed, primary cells from human endometriotic biopsies but not from human endometrial biopsies are invasive in an in vitro collagen invasion assay. In this study, these in vitro invasive endometriotic cells were found to be nonmalignant epithelial cells lacking E-cadherin, which acts as an invasion suppressor molecule in carcinomas. Immunocytochemistry showed that the E-cadherin-negative epithelial cell type was increased in sections of endometriosis tissue as compared with sections of eutopic endometrium. On the basis of these data we propose that the E-cadherin-negative invasive endometriotic cells seen in vitro represent the cell population that migrates to ectopic (extrauterine) locations and thus causes endometriosis in vivo. Accordingly, the loss of E-cadherin expression is postulated to constitute a crucial mechanism in the pathogenesis of endometriosis.

Properties of a Wolinella succinogenes mutant lacking periplasmic sulfide dehydrogenase (Sud).

A delta sud deletion mutant of Wolinella succinogenes that lacked the periplasmic sulfide dehydrogenase (Sud) was constructed using homologous recombination. The mutant grew with sulfide and fumarate, indicating that Sud was not a component of the electron transport chain that catalyzed fumarate respiration with sulfide as an electron donor. Likewise, growth with formate and either polysulfide or sulfur was not affected by the deletion. Removal of Sud from wild-type W. succinogenes by spheroplast formation did not decrease the activity of electron transport to polysulfide. The delta psr deletion mutant that lacks polysulfide reductase (Psr) grew by fumarate respiration with sulfide as an electron donor, indicating that Psr is not required for this activity.

Invasiveness of endometriotic cells in vitro.

The pathogenesis of endometriosis is not known. The currently favoured theory is that viable endometrial cells, shed from the endometrium into the pelvic cavity by retrograde menstruation, reattach and invade other tissues. We used a collagen gel invasion assay to assess invasive potential of endometriotic cells. The invasion indices of cells from peritoneal endometriotic lesions and a metastatic bladder carcinoma cell line (EJ28) were similar (2.2-15.6 vs 8.4-11.6) whereas cells from normal endometrium and non-metastatic carcinoma cells (RT112) were non-invasive (indices < 1). Invasiveness of endometriotic cells might contribute to the pathogenesis of endometriosis.