Senile scleral plaques imaged with enhanced depth optical coherence tomography

PURPOSE Senile scleral plaques (SSP) are sharply demarcated greyish areas located just anterior to the insertions of the horizontal rectus muscles and thus are frequently encountered during transscleral intravitreal injections. The aim of this study was to characterize SSP using enhanced depth imaging spectral domain anterior segment optical coherence tomography (OCT) in a cohort of patients attending intravitreal injection clinics. METHODS Prospective cross-sectional study of 380 patients attending the clinic for intravitreal injections at the Department of Ophthalmology at the Bern University Hospital. Thirty-two patients with SSP were identified and the anatomical features were assessed using anterior segment OCT. RESULTS In our patient cohort, we found a SSP prevalence of 8.2%. Senile scleral plaques were easily identifiable using anterior segment OCT and were found at the insertion sites of the horizontal recti muscles. The mean horizontal diameter was 2.2 mm (±760 μm SD), the mean vertical diameter was 3.3 mm (±144 μm SD), and the average surface area was 5.3 mm(2) (±0.4 mm(2) SD). The mean senile scleral plaque thickness was 0.6 mm (±149 μm SD). The mean distance from the limbus was 2.24 mm for nasally located SSP and 3.22 mm for temporally located SSP. CONCLUSION SSP are frequently encountered during intravitreal injections as they are located just anterior to the insertion sites of the horizontal recti muscles. Because the scleral stroma is rarefied and due to calcifications within SSP, these areas should be avoided when performing multiple intravitreal injections as this may result in rupture of the sclera.

Predicting Psychotherapy Dropouts: A Multilevel Approach

The role of therapeutic processes in predicting premature termination of psychotherapy has been a particular focus of recent research. The purpose of this study was to contrast outpatients who completed therapy and those who dropped out with respect to their self-reported in-session experiences of self-esteem, mastery, clarification and the therapeutic alliance. The 296 patients with mixed disorders were treated with an integrative form of cognitive–behavioural therapy without pre-determined time limit (M = 20.2 sessions). Multilevel analyses indicated that patients who did not completetreatment reported, on average, lower levels of self-esteem, mastery and clarification and lower ratings of their therapeutic alliance in treatment in contrast to patients who completed therapy. Patient-reported change in self-esteem experiences over the course of treatment turned out to be the strongest predictor of dropout from psychotherapy or successful completion. When dropout occurred before the average treatment length was reached, patients reported fewer clarifying experiences as early as the first session and their ratings of the therapeutic alliance were characterized by an absence of positive development. Both of these aspects seem to be involved in patients' decisions to leave treatment early. The findings underscore the importance of the therapeutic process in understanding the mechanisms behind treatment dropout. Copyright © 2014 John Wiley & Sons, Ltd.

Ellis-van Creveld Syndrome in Grey Alpine Cattle: Morphologic, Immunophenotypic, and Molecular Characterization

Ellis-van Creveld (EvC) syndrome is a human autosomal recessive disorder caused by a mutation in either the EVC or EVC2 gene, and presents with short limbs, polydactyly, and ectodermal and heart defects. The aim of this study was to understand the pathologic basis by which deletions in the EVC2 gene lead to chondrodysplastic dwarfism and to describe the morphologic, immunohistochemical, and molecular hallmarks of EvC syndrome in cattle. Five Grey Alpine calves, with a known mutation in the EVC2 gene, were autopsied. Immunohistochemistry was performed on bone using antibodies to collagen II, collagen X, sonic hedgehog, fibroblast growth factor 2, and Ki67. Reverse transcription polymerase chain reaction was performed to analyze EVC1 and EVC2 gene expression. Autopsy revealed long bones that were severely reduced in length, as well as genital and heart defects. Collagen II was detected in control calves in the resting, proliferative, and hypertrophic zones and in the primary and secondary spongiosa, with a loss of labeling in the resting zone of 2 dwarfs. Collagen X was expressed in hypertrophic zone in the controls but was absent in the EvC cases. In affected calves and controls, sonic hedgehog labeled hypertrophic chondrocytes and primary and secondary spongiosa similarly. FGF2 was expressed in chondrocytes of all growth plate zones in the control calves but was lost in most EvC cases. The Ki67 index was lower in cases compared with controls. EVC and EVC2 transcripts were detected. Our data suggest that EvC syndrome of Grey Alpine cattle is a disorder of chondrocyte differentiation, with accelerated differentiation and premature hypertrophy of chondrocytes, and could be a spontaneous model for the equivalent human disease.

Intrapulmonale Ruptur eines Aortenaneurysmas

Aneurysmen der thorakalen Aorta führen in der Regel über eine intraperikardiale (Herzbeuteltamponade) oder intrapleurale Ruptur (inneres Verbluten) zum Tod. Außerordentlich selten sind intrapulmonale Rupturen von thorakalen Aortenaneurysmen, die über eine Hämoptyse symptomatisch werden und über eine Blutaspiration letal verlaufen können. Berichtet wird über den Fall eines 40-jährigen Mannes, bei dem nach thorakalen Schmerzen an den Vortagen plötzlich eine Hämoptyse auftrat. Während der diagnostischen Abklärung der Blutungsquelle verstarb er unvorhergesehen. Todesursache war die primäre intrapulmonale, final intrapleurale Ruptur eines thorakalen Aortenaneurysmas an der Stelle einer operativ korrigierten Aortenisthmusstenose.

Fatal steamer accident; blunt force injuries and drowning in post-mortem MSCT and MRI.

Steamer accidents, through contact with the bucket wheel, are very seldom today. No publication of such a kind of fatal accident could be found in literature. We present the case of a fatal steamer accident, in which the findings of a blunt traumatization of a person by the ship was completely documented by post-mortem combined multi-slice computed tomography (MSCT) and magnetic resonance imaging (MRI) examinations. A rupture of the aorta was detected using both radiological methods without use of radiopaque material. Radiological examination revealed a comminuted fracture of the thorax vertebrae at the same level as the aortic rupture. Injuries of the soft tissues of the back, caused by the bucket wheel of the steamer, were also diagnosed. In addition to the signs of blunt force trauma the findings of drowning such as an over inflation of the lungs, fluid in the stomach and duodenum were revealed. Furthermore, algological analysis detected diatoms in the lung tissue and blood from the left heart. Therefore, the cause of death was considered being a combination of fatal hemorrhage, caused by the aortic rupture, and drowning. We conclude that virtual autopsy using combined post-mortem MSCT and MRI is a useful tool for documentation, visualisation and analysis of the findings of blunt force trauma and drowning with a large potential in forensic medicine.

Mitochondrial impairments contribute to Spinocerebellar ataxia type 1 progression and can be ameliorated by the mitochondria-targeted antioxidant MitoQ

Spinocerebellar ataxia type 1 (SCA1), due to an unstable polyglutamine expansion within the ubiquitously expressed Ataxin-1 protein, leads to the premature degeneration of Purkinje cells (PCs), decreasing motor coordination and causing death within 10-15 years of diagnosis. Currently, there are no therapies available to slow down disease progression. As secondary cellular impairments contributing to SCA1 progression are poorly understood, here, we focused on identifying those processes by performing a PC specific proteome profiling of Sca1154Q/2Q mice at a symptomatic stage. Mass spectrometry analysis revealed prominent alterations in mitochondrial proteins. Immunohistochemical and serial block-face scanning electron microscopy analyses confirmed that PCs underwent age-dependent alterations in mitochondrial morphology. Moreover, colorimetric assays demonstrated impairment of the electron transport chain complexes (ETC) and decrease in ATPase activity. Subsequently, we examined whether the mitochondria-targeted antioxidant MitoQ could restore mitochondrial dysfunction and prevent SCA1-associated pathology in Sca1154Q/2Q mice. MitoQ treatment both presymptomatically and when symptoms were evident ameliorated mitochondrial morphology and restored the activities of the ETC complexes. Notably, MitoQ slowed down the appearance of SCA1-linked neuropathology such as lack of motor coordination as well as preventing oxidative stress-induced DNA / RNA damage and PC loss. Our work identifies a central role for mitochondria in PC degeneration in SCA1 and provides evidence for the supportive use of mitochondria-targeted therapeutics in slowing down disease progression.

Premature Osteoblast Clustering by Enamel Matrix Proteins Induces Osteoblast Differentiation through Up-Regulation of Connexin 43 and N-Cadherin

In recent years, enamel matrix derivative (EMD) has garnered much interest in the dental field for its apparent bioactivity that stimulates regeneration of periodontal tissues including periodontal ligament, cementum and alveolar bone. Despite its widespread use, the underlying cellular mechanisms remain unclear and an understanding of its biological interactions could identify new strategies for tissue engineering. Previous in vitro research has demonstrated that EMD promotes premature osteoblast clustering at early time points. The aim of the present study was to evaluate the influence of cell clustering on vital osteoblast cell-cell communication and adhesion molecules, connexin 43 (cx43) and N-cadherin (N-cad) as assessed by immunofluorescence imaging, real-time PCR and Western blot analysis. In addition, differentiation markers of osteoblasts were quantified using alkaline phosphatase, osteocalcin and von Kossa staining. EMD significantly increased the expression of connexin 43 and N-cadherin at early time points ranging from 2 to 5 days. Protein expression was localized to cell membranes when compared to control groups. Alkaline phosphatase activity was also significantly increased on EMD-coated samples at 3, 5 and 7 days post seeding. Interestingly, higher activity was localized to cell cluster regions. There was a 3 fold increase in osteocalcin and bone sialoprotein mRNA levels for osteoblasts cultured on EMD-coated culture dishes. Moreover, EMD significantly increased extracellular mineral deposition in cell clusters as assessed through von Kossa staining at 5, 7, 10 and 14 days post seeding. We conclude that EMD up-regulates the expression of vital osteoblast cell-cell communication and adhesion molecules, which enhances the differentiation and mineralization activity of osteoblasts. These findings provide further support for the clinical evidence that EMD increases the speed and quality of new bone formation in vivo.

Effect of two different bioabsorbable collagen membranes on guided bone regeneration: a comparative histomorphometric study in the dog mandible

BACKGROUND: This study compared bone regeneration following guided bone regeneration with two bioabsorbable collagen membranes in saddle-type bone defects in dog mandibles. METHODS: Three standardized defects were created, filled with bone chips and deproteinized bovine bone mineral (DBBM), and covered by three different methods: control = no membrane; test 1 = collagen membrane; and test 2 = cross-linked collagen membrane (CCM). Each side of the mandible was allocated to one of two healing periods (8 or 16 weeks). The histomorphometric analysis assessed the percentage of bone, soft tissue, and DBBM in the regenerate; the absolute area in square millimeters of the bone regenerate; and the distance in millimeters from the bottom of the defect to the highest point of the regenerate. RESULTS: In the 8-week healing group, two dehiscences occurred with CCM. After 8 weeks, all treatment modalities showed no significant differences in the percentage of bone regenerate. After 16 weeks, the percentage of bone had increased for all treatment modalities without significant differences. For all groups, the defect fill height increased between weeks 8 and 16. The CCM group showed a statistically significant (P = 0.0202) increase over time and the highest value of all treatment modalities after 16 weeks of healing, CONCLUSIONS: The CCM showed a limited beneficial effect on bone regeneration in membrane-protected defects in dog mandibles when healing was uneventful. The observed premature membrane exposures resulted in severely compromised amounts of bone regenerate. This increased complication rate with CCM requires a more detailed preclinical and clinical examination before any clinical recommendations can be made.