Improvement of Varian a-Si EPID dosimetry measurements using a lead-shielded support-arm

Dosimetry measurements with Varian amorphous silicon electronic portal imaging devices (a-Si EPIDs) are affected by the backscattered radiation from the EPID support arm. In this study, the nonuniform backscatter from an E-type support arm was reduced by fixing a thick (12.2 × 10.5 × 0.5 cm³) piece of lead on top of the arm, and the remaining backscatter was modeled and included in an existing dose prediction algorithm. The applied backscatter kernel was the average of kernels on different regions of the EPID over the arm. The lead-shielded arm reduced the nonuniform backscatter component by about 50% for field sizes ranging from 3 × 3 to 30 × 30 cm² and the field symmetry improved for medium to large fields up to 3%. Gamma evaluation of the measured and modeled doses (2%, 2-mm criteria) showed that using the lead-shielded arm in the model increased the number of points with Gamma index <1 by 5.7% and decreased the mean Gamma by 0.201. Even using the lead alone (no modeling) could increase the number of points with Gamma index <1 by 4.7% and decrease the mean Gamma by 0.153. This is a simple and easy method to decrease the nonuniform arm backscatter and improve the accuracy of dosimetry measurements with the existing EPIDs used for clinical applications.     

Effects of berberine on β-secretase activity in a rabbit model of Alzheimer's disease

Introduction

Relevant aspects of Alzheimer''s disease (AD) can be modeled by aluminium-maltolate injection into specific regions of the brain. The possible role of berberine chloride (BC) as an anti-inflammatory agent in the brain has been previously addressed.

Material and methods

Rabbits were divided into control (C), untreated lesion (L) and BC-treated + lesion (L + BC) groups. Animals in L + BC received BC (50 mg/ kg) orally 1 day after surgery and daily for 2 weeks. The lesion was induced by injection of 100 µl of either vehicle or water containing 25 mM aluminium-maltol into intraventricular fissure. Weight loss, ataxia, paralysis and tremor were monitored. For histopathology, Bielschowsky silver and H&E staining were employed. β-Secretase activity in hippocampus was finally assessed.

Results

All L animals died on days 12-15 after lesion. Seven to 10 days after lesion, abnormal symptoms as well as cachexia were seen in over 90% of cases. L rabbits lost an average of 0.5 kg which was significant on days 10 and 12 (p < 0.05); this was not completely prevented by BC. Up to day 15, all L animals had lost their lives (p < 0.001). BC treatment protected the hippocampus from degeneration, altered the behavior and decreased the activity of β-site amyloid precursor protein cleaving enzyme-1 (BACE-1).

Conclusions

Considering the findings in regard to physiological abilities, histological changes and BACE-1 activity in hippocampus changes, it is concluded that BC treatment could be an effective therapy in restoring Al maltol-induced behavioral derangements in the rabbit model of AD.     

Quantitative CEST and MT at 1.5T for monitoring treatment response in glioblastoma: early and late tumor progression during chemoradiation

Journal of Neuro-Oncology - Quantitative MRI (qMRI) was performed using a 1.5T protocol that includes a novel chemical exchange saturation transfer/magnetization transfer (CEST/MT) approach. The...     

Antigen-independent signalosome of CARMA1, PKCθ, and TNF receptor-associated factor 2 (TRAF2) determines NF-κB signaling in T cells

NF-κB activation is essential for T-cell responses, and costimulatory molecules in the TNF receptor (TNFR) superfamily are viewed as a major source of this signal. Although the TNFR family recruits TNFR-associated factor (TRAF) molecules leading to IKKα/β/γ activation, it is not clear whether simple binding of TRAFs explains why they are such strong activators of NF-κB and so important for T-cell immunity. We now show that one TNFR family member, OX40 (CD134), after ligation by OX40L, assembles a unique complex that not only contains TRAF2, RIP, and IKKα/β/γ but also CARMA1, MALT1, BCL10, and PKC, molecules previously shown to regulate NF-κB activation through the T-cell receptor (TCR). The OX40 signalosome is formed in membrane microdomains irrespective of TCR engagement, and strongly promotes NF-κB activation only if CARMA1 and PKC are recruited. This NF-κB signal allows effector/memory T cells to survive when antigen is no longer available. Thus, by recruiting TCR-related intracellular molecules into the TRAF2 complex, OX40 provides the T cell with a high level of NF-κB activity needed for longevity.     

Treatment of peroneal tendon dislocation and coexisting medial and lateral ligamentous laxity in the ankle joint

Purpose  

Acute dislocation of the peroneal tendon is caused by massive combined flexion-torsion trauma supported by preexisting ligamentous laxity of the ankle joint.