Search

Introduction: In the acute phase after a spinal cord injury or disease (SCI/D), various therapeutic assessments and interventions are applied with the goal of restoring structures, preventing complications and preparing the patient as best as possible for further activity and finally participation. The goal was to identify and evaluate the available evidence on assessments and interventions for body functions and structures to prepare adults with acute spinal cord SCI/D for activity and participation during the first 14 days., Methods: A scoping review was conducted. The search was performed on June 19, 2023 using the databases PubMed, PEDro, Cochrane library and Embase. These were screened for studies including patients with acute SCI/D and physiotherapeutic or occupational therapy assessments and interventions. Only studies in English or German published between 2012 and 2023 were included., Results: Twelve publications met the inclusion criteria, namely three systematic reviews, two randomized controlled trials, two observational studies and five clinical practice guidelines. Assessments as the Spinal Cord Independence Measure, as well as exercises such as daily passive mobilization of body structures against contractures were used in the entire population, while others were only applied in subgroups of SCI/D such as the Graded Redefined Assessment of Strength, Sensation and Prehension or functional electrical stimulation with and without additional movements. The methodological quality of the studies found varied greatly from good to very poor., Discussion: Heterogeneity in research design and study population as well as lack of high-quality studies do not cover the standard of clinical management in the acute phase and further comprehensive research is needed., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Irrgang, Himmelhaus, Allek, Debecker, Gemperli, Kynast, von Reumont and Scheel-Sailer.)

The increasing prevalence of diabetes and its accompanying long-term complications, as well as the associated economic burden, calls for a rapid clinical translation of biomedical research to better valid the physiological relevance of the findings from basic research. To meet this condition, the Collaborative Research Center (CRC) 1118 has established the first nationwide diabetes-specific Biomaterialbank (BMB) that permanently preserves solid and liquid specimen retro- and prospectively at the Institute of Pathology and Department of Endocrinology of the University Hospital Heidelberg. The main purpose of this BMB is to collect, preserve, characterize and provide human diabetic specimen to researchers investigating the role of reactive metabolites (RM) as cause of diabetic late complications. In this review we discuss the urgent need to support translational and clinical research projects by making use of diabetic solid and liquid specimen and provide an insight into the organization and general conditions of biobanking procedures which are pivotal to guaranteeing high-quality human biomaterial. In light of diabetes-tailored biobanking, we describe our newly initiated activities and introduce the diverse technology platforms that can be used for the investigation of promising molecular targets pertinent for diabetes. With this article we demonstrate that the preservation of rare specimen is also particularly relevant in the non-neoplastic field and contributes to basic investigation, promotes comprehensive scientific data and fortifies the sustainability for diabetes research. In addition, the increased understanding of how metabolic imbalance triggers diabetes onset and progression and favors diabetic late symptoms might hold some promise for future innovative diagnostic and/ or therapeutic applications, eventually adding to the improvement of patient care., Competing Interests: Conflict of Interest: The authors have no conflict of interest., (© Georg Thieme Verlag KG Stuttgart · New York.)

Engulfment and cell motility 1 (ELMO1) functions as a guanine exchange factor for Rac1 and was recently found to protect endothelial cells from apoptosis. Genome wide association studies suggest that polymorphisms within human elmo1 act as a potential contributing factor for the development of diabetic nephropathy. Yet, the function of ELMO1 with respect to the glomerulus and how this protein contributes to renal pathology was unknown. Thus, this study aimed to identify the role played by ELMO1 in renal development in zebrafish, under hyperglycaemic conditions, and in diabetic nephropathy patients. In zebrafish, hyperglycaemia did not alter renal ELMO1 expression. However, hyperglycaemia leads to pathophysiological and functional alterations within the pronephros, which could be rescued via ELMO1 overexpression. Zebrafish ELMO1 crispants exhibited a renal pathophysiology due to increased apoptosis which could be rescued by the inhibition of apoptosis. In human samples, immunohistochemical staining of ELMO1 in nondiabetic, diabetic and polycystic kidneys localized ELMO1 in glomerular podocytes and in the tubules. However, ELMO1 was not specifically or distinctly regulated under either one of the disease conditions. Collectively, these results highlight ELMO1 as an important factor for glomerular protection and renal cell survival via decreasing apoptosis, especially under diabetic conditions.

Inhibitor-κB kinase ε (IKKε) was only recently identified as an enzyme with high homology to the classical I-κB kinase subunits, IKKα and IKKβ. Despite this similarity, it is mainly discussed as a repressor of viral infections by modulating type I IFNs. However, in vitro studies also showed that IKKε plays a role in the regulation of NF-κB activity, but the distinct mechanisms of IKKε-mediated NF-κB activation are not clear. Given the paramount role of NF-κB in inflammation, we investigated the regulation and function of IKKε in models of inflammatory hyperalgesia in mice. We found that IKKε was abundantly expressed in nociceptive neurons in the spinal cord and in dorsal root ganglia. IKKε mRNA and protein levels rapidly increased in spinal cord and dorsal root ganglia during hind paw inflammation evoked by injection of zymosan or formalin. IKKε knockout mice showed normal nociceptive responses to acute heat or mechanical stimulation. However, in inflammatory pain models, IKKε-deficient mice exhibited a significantly reduced nociceptive behavior in comparison with wild type mice, indicating that IKKε contributed to the development of inflammatory hyperalgesia. Antinociceptive effects were associated with reduced activation of NF-κB and attenuated NF-κB-dependent induction of cyclooxygenase-2, inducible NO synthase, and metalloproteinase-9. In contrast, IRF-3, which is an important IKKε target in viral infections, was not regulated after inflammatory nociceptive stimulation. Therefore, we concluded that IKKε modulates inflammatory nociceptive sensitivity by activation of NF-κB-dependent gene transcription and may be useful as a therapeutic target in the treatment of inflammatory pain.