Welchen Einfluss haben Skapula stabilisierende Übungen bei Patientinnen und Patienten mit einem Subakromialen Impingement Syndrom bezüglich Schmerz, Beweglichkeit und Kraft?

Darstellung des Themas: Das Subakromiale Impingement Syndrom (SIS) ist das meist gesehene Schmerzsyndrom an den Schultergelenken. Oft ist die glenohumerale Schulterbeweglichkeit schmerzhaft eingeschränkt. Die Skapula stabilisierende Muskulatur bildet zusammen mit der Rotatorenmanschette die Basis für ein gut funktionierendes Glenohumeralgelenk. Das Beüben der Muskulatur der Skapula wird in der Praxis oft vernachlässigt. Zielsetzung: Ziel dieser Arbeit war, die Wichtigkeit von Übungen der Skapula führenden Muskulatur, bei Menschen mit einem SIS zu untersuchen. Dies erfolgte mithilfe der Verlaufsparameter Schmerz, Beweglichkeit und Kraft. Methode: Vier randomisiert, kontrollierte Studien (RCT) wurden aus den Datenbanken Medline, Pubmed, Cinahl und Google Scholar anhand vordefinierter Kriterien extrahiert. Die Qualitätsprüfung erfolgte anhand der PEDro Skala sowie mithilfe des EMED Rasters. Relevante Ergebnisse: Skapula stabilisierende Übungen zeigen einen positiven Effekt bezüglich der subjektiven Verlaufsparameter Schmerz und der gesundheitsabhängigen Lebensqualität. Ebenfalls konnte die glenohumerale Beweglichkeit in Innen- und Aussenrotation sowie die Kraft der Mm. trapezius und serratus anterior Signifikanz generieren. Schlussfolgerung: Anhand der Studienresultate können keine genauen Angaben zur Art der Skapula stabilisierenden Übungen und deren Dosierung gemacht werden. Fest steht einzig, dass das Training täglich erfolgen, sowie auf jedes Individuum einzeln angepasst werden sollte

Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells

Background: Dental follicle cells (DFCs) are dental stem cells and interesting options for regenerative therapies in dentistry. However, DFCs acquire replicative senescence in long-term cultures, but little is known about molecular processes. In previous studies, we observed that DFC cell lines become senescent at different rates. We hypothesized that short telomere length and increased DNA damage with genomic instability correlate with the accelerated induction of cellular senescence. Results: For this study we compared DFC cell lines that became senescent at different rates (DFC_F: strong senescent phenotype; DFC_S: weak senescent phenotype). The telomeres of DFC_F were shorter than those of the telomeres of DFC_S prior senescence. Interestingly, telomere lengths of both cell lines were nearly unchanged after induction of senescence. Gene expression analyses with genes associated with DNA damage before and after the induction of cellular senescence revealed that almost all genes in DFCs_F were down-regulated while the gene expression in DFC_S was almost constitutive. Moreover, number of aneuploid DFC_F were significantly higher after induction of cellular senescence. Conclusion: Our results supported our initial hypothesis that telomere length and genomic instability correlate with the accelerated induction of cellular senescence in DFC_F

Evaluation of Current Studies to Elucidate Processes in Dental Follicle Cells Driving Osteogenic Differentiation

When research on osteogenic differentiation in dental follicle cells (DFCs) began, projects focused on bone morphogenetic protein (BMP) signaling. The BMP pathway induces the transcription factor DLX3, whichh in turn induces the BMP signaling pathway via a positive feedback mechanism. However, this BMP2/DLX3 signaling pathway only seems to support the early phase of osteogenic differentiation, since simultaneous induction of BMP2 or DLX3 does not further promote differentiation. Recent data showed that inhibition of classical protein kinase C (PKCs) supports the mineralization of DFCs and that osteogenic differentiation is sensitive to changes in signaling pathways, such as protein kinase B (PKB), also known as AKT. Small changes in the lipidome seem to confirm the participation of AKT and PKC in osteogenic differentiation. In addition, metabolic processes, such as fatty acid biosynthesis, oxidative phosphorylation, or glycolysis, are essential for the osteogenic differentiation of DFCs. This review article attempts not only to bring the various factors into a coherent picture of osteogenic differentiation in DFCs, but also to relate them to recent developments in other types of osteogenic progenitor cells

Current Guidelines for Obesity Prevention in Childhood and Adolescence

Objective: Current guidelines for prevention of obesity in childhood and adolescence are discussed. Methods: A literature search was performed in Medline via PubMed, and appropriate studies were analyzed. Results: Programs to prevent childhood obesity have so far remained mainly school-based and effects have been limited. Analyses by age group show that prevention programs have the best results in younger children (Conclusion: Behavior-oriented prevention programs showed only limited long-term effects. Certain groups at risk for the development of obesity are not reached effectively by current programs. Although universally valid conclusions cannot be drawn given the heterogeneity of available studies, clearly combining behavior-based programs with community-based prevention to counteract an ‘obesogenic environment' is crucial for sustainable success of future obesity prevention programs

High endogenous expression of parathyroid hormone-related protein (PTHrP) supports osteogenic differentiation in human dental follicle cells

Dental follicle cells (DFCs) are progenitor cells for mineralizing cells such as alveolar osteoblasts, but little is known about the mechanisms of the differentiation. Interestingly, different cell lines sometimes have different potentials to differentiate into mineralizing cells. In this study, we compared two different DFC lines, with one cell line (DFC_B) showing a high alkaline phosphatase (ALP) activity in long-term cultures with standard medium and a reliable mineralizing potential. However, the other cell line DFC_A shows low ALP activity in standard medium and almost no mineralization. Known osteogenic markers such as RUNX2 were similarly expressed in both cell lines. However, the proosteogenic signaling pathway of the bone morphogenetic protein (BMP) is induced in DFC_B, and the parathyroid hormone-related protein (PTHrP), which is involved in tooth root development, was also expressed more strongly. Previous studies have shown that the secreted PTHrP negatively regulate the transition from pre-osteoblastic progenitors to osteoblasts, but we showed that an inhibition of PTHrP gene expression reduced the ALP activity and the BMP-signaling pathway. In addition, endogenously expressed PTHrP is located in the cell nucleus. In contrast, supplementation of PTHrP or an inhibitor for the PTHrP receptor did not affect the ALP activity of DFC_B. In conclusion, our data suggest that a high endogenous expression of PTHrP in DFCs supports the induction of osteogenic differentiation via an intracrine mode

WNT5A supports viability of senescent human dental follicle cells

The osteogenic differentiation of dental follicle cells (DFCs) is inhibited by the onset of cellular senescence, but the cause for this is largely unknown. Recently it was shown that WNT5a, which is an inductor of the non-canonical WNT pathway, stimulates both cellular senescence and osteogenic differentiation of different cell types. In this study, we investigated the role of WNT5a for viability and osteogenic differentiation in human DFCs after the induction of cellular senescence. DFCs were cultivated until the induction of cellular senescence. The induction of cellular senescence was confirmed by -galactosidase staining, estimation of population doubling time, and slightly telomere length shortening. After induction of cellular senescence, the expression of WNT5A and the potential to induce the osteogenic differentiation decreased. Inhibition of WNT5A by specific siRNAs had significant effect on the viability of DFCs. Cell proliferation was reduced, whereas both cellular senescence and cell death were increased in DFCs. However, an inhibition of WNT5A did only slightly effect the osteogenic differentiation of DFCs. Our results suggest that WNT5A supports viability during both cell proliferation and osteogenic differentiation of DFCs

Flightless-I governs cell fate by recruiting the SUMO isopeptidase SENP3 to distinct HOX genes

Background: Despite recent studies on the role of ubiquitin-related SUMO modifier in cell fate decisions, our understanding on precise molecular mechanisms of these processes is limited. Previously, we established that the SUMO isopeptidase SENP3 regulates chromatin assembly of the MLL1/2 histone methyltransferase complex at distinct HOX genes, including the osteogenic master regulator DLX3. A comprehensive mechanism that regulates SENP3 transcriptional function was not understood. Results: Here, we identified flightless-I homolog (FLII), a member of the gelsolin family of actin-remodeling proteins, as a novel regulator of SENP3. We demonstrate that FLII is associated with SENP3 and the MLL1/2 complex. We further show that FLII determines SENP3 recruitment and MLL1/2 complex assembly on the DLX3 gene. Consequently, FLII is indispensible for H3K4 methylation and proper loading of active RNA polymerase II at this gene locus. Most importantly, FLII-mediated SENP3 regulation governs osteogenic differentiation of human mesenchymal stem cells. Conclusion: Altogether, these data reveal a crucial functional interconnection of FLII with the sumoylation machinery that converges on epigenetic regulation and cell fate determination

The cell cycle regulator protein P16 and the cellular senescence of dental follicle cells

Cellular senescence is a restricting factor for regenerative therapies with somatic stem cells. We showed previously that the onset of cellular senescence inhibits the osteogenic differentiation in stem cells of the dental follicle (DFCs), although the mechanism remains elusive. Two different pathways are involved in the induction of the cellular senescence, which are driven either by the cell cycle protein P21 or by the cell cycle protein P16. In this study, we investigated the expression of cell cycle proteins in DFCs after the induction of cellular senescence. The induction of cellular senescence was proved by an increased expression of beta-galactosidase and an increased population doubling time after a prolonged cell culture. Cellular senescence regulated the expression of cell cycle proteins. The expression of cell cycle protein P16 was up-regulated, which correlates with the induction of cellular senescence markers in DFCs. However, the expression of cyclin-dependent kinases (CDK)2 and 4 and the expression of the cell cycle protein P21 were successively decreased in DFCs. In conclusion, our data suggest that a P16-dependent pathway drives the induction of cellular senescence in DFCs

p53 inhibits the osteogenic differentiation but does not induce senescence in human dental follicle cells

Replicative senescence causes a reduced osteogenic differentiation potential of senescent dental follicle cells (DFCs). The transcription factor p53 is often involved in the induction of cellular senescence, but little is known about its role in DFCs. This study examined for the first time the role of p53 compared to its pro-proliferative antagonist E2F-1 in terms of osteogenic differentiation potential and induction of senescence. Protein expression of E2F-1 decreased during cell aging, while p53 was expressed constitutively. Gene silencing of E2F1 (E2F-1) inhibited the proliferation rate of DFCs and increased the induction of cellular senescence. The induction of cellular senescence is regulated independently of the gene expression of TP53 (p53), since its gene expression depends on the expression of E2F1. Moreover, gene silencing of TP53 induced E2F1 gene expression and increased cell proliferation, but did not affect the rate of induction of cellular senescence. TP53 knockdown further induced the alkaline phosphatase and mineralization in DFCs. However, the simultaneous silencing of TP53 and E2F1 did not inhibit the inductive effect of TP53 knockdown on osteogenic differentiation, indicating that this effect is independent of E2F-1. In summary, our results suggest that p53 inhibits osteogenic differentiation and cell proliferation in senescent DFCs, but is not significantly involved in senescence induction

Characterizing death acceptance among patients with cancer

Objective: Death acceptance may indicate positive adaptation in cancer patients. Little is known about what characterizes patients with different levels of death acceptance or its impact on psychological distress. We aimed to broaden the understanding of death acceptance by exploring associated demographic, medical, and psychological characteristics. Methods: At baseline, we studied 307 mixed cancer patients attending the University Cancer Center Hamburg and a specialized lung cancer center (age M = 59.6, 69% female, 69% advanced cancer). At 1-year follow-up, 153 patients participated. We assessed death acceptance using the validated Life Attitude Profile–Revised. Patients further completed the Memorial Symptom Assessment Scale, the Demoralization Scale, the Patient Health Questionnaire, and the Generalized Anxiety Disorder Questionnaire. Statistical analyses included multinomial and hierarchical regression analyses. Results: At baseline, mean death acceptance was 4.33 (standard deviation [SD] = 1.3, range 1-7). There was no change to follow-up (P = 0.26). When all variables were entered simultaneously, patients who experienced high death acceptance were more likely to be older (odds ratio [OR] = 1.04; 95% confidence interval [CI], 1.01-1.07), male (OR = 3.59; 95% CI, 1.35-9.56), widowed (OR = 3.24; 95% CI, 1.01-10.41), and diagnosed with stage IV (OR = 2.44; 95% CI, 1.27-4.71). They were less likely to be diagnosed with lung cancer (OR = 0.20; 95% CI, 0.07-0.58), and their death acceptance was lower with every month since diagnosis (OR = 0.99; 95% CI, 0.98-0.99). High death acceptance predicted lower demoralization and anxiety at follow-up but not depression. Conclusions: High death acceptance was adaptive. It predicted lower existential distress and anxiety after 1 year. Advanced cancer did not preclude death acceptance, supporting the exploration of death-related concerns in psychosocial interventions