The optical density (OD) of EBT3 radiochromic films (Ashland Specialty Ingredients, Bridgewater, NJ, USA) exposed to absorbed doses to water up to D  =  20 Gy in magnetic fields of B  =  0.35 and 1.42 T was measured in the three colour channels of an Epson Expression 10000XL flatbed scanner. A 7 cm wide water phantom with fixed film holder was placed between the pole shoes of a constant-current electromagnet with variable field strength and was irradiated by a 6 MV photon beam whose axis was directed at right angles with the field lines. The doses at the film position at water depth 5 cm were measured with a calibrated ionization chamber when the magnet was switched off and were converted to the doses in presence of the magnetic field via the monitor units and by a Monte Carlo-calculated correction accounting for the slight change of the depth dose curves in magnetic fields. In the presence of the 0.35 and 1.42 T fields small negative changes of the OD values at given absorbed doses to water occurred and just significantly exceeded the uncertainty margin given by the stochastic and the uncorrected systematic deviations. This change can be described by a  +2.1% change of the dose values needed to produce a given optical density in the presence of a 1.42 T field. The thereby modified OD versus D function remained unchanged irrespective of whether the original short film side-the preference direction of the monomer crystals of the film-was directed parallel or orthogonal to the magnetic field. The 'orientation effect', the difference between the optical densities measured in the 'portrait' or 'landscape' film positions on the scanner bed caused by the reflection of polarised light in the scanner's mirror system, remained unaltered after EBT3 film exposure in magnetic fields. An independent optical bench investigation of EBT3 films exposed to doses of 10 and 20 Gy at 0.35 and 1.42 T showed that the direction of the electric vector of polarised light experiencing the largest transmission through EBT3 films remained unaltered after film exposure in the magnetic fields. The observed small modification of the OD versus D curve of the radiochromic film EBT3 in the range up to 20 Gy and 1.42 T, hardly exceeding the experimental uncertainty margin, numerically confirms other recent studies on EBT3 film. A stronger magnetic field effect had been observed with the previous product EBT2 exposed to Co gamma radiation at 0.35 T.

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The well-known field-size dependent overresponse in small-field photon-beam dosimetry of solid-state detectors equipped with very thin sensitive volumes, such as the PTW microDiamond, cannot be caused by the photon and electron interactions within these sensitive layers because they are only a few micrometers thick. The alternative explanation is that their overresponse is caused by the combination of two effects, the modification of the secondary electron fluence profile (i) by a field size too small to warrant lateral secondary electron equilibrium and (ii) by the density-dependent electron ranges in the structural detector materials placed in front of or backing the sensitive layer. The present study aims at the numerical demonstration and visualization of this combined mechanism. The lateral fluence profiles of the secondary electrons hitting a 1 µm thick scoring layer were Monte-Carlo simulated by modelling their generation and transport in the upstream or downstream adjacent layers of thickness 0.6 mm and densities from 0.0012 to 3 g cm, whose atomic composition was constantly kept water-like. The scoring layer/adjacent layer sandwich was placed in an infinite water phantom irradiated by circular Co, 6 MV and 15 MV photon beams with diameters from 3 to 40 mm. The interpretation starts from the ideal case of lateral secondary electron equilibrium, where the Fano theorem excludes any density effect. If the field size is then reduced, electron tracks potentially originating from source points outside the field border will then be numerically 'cut away'. This geometrical effect reduces the secondary electron fluence at the field center, but the magnitude of this reduction also varies with the density-dependent electron ranges in the adjacent layers. This combined mechanism, which strongly depends on the photon spectrum, explains the field size and material density effect on the response of detectors with very thin sensitive layers used in small-field photon-beam dosimetry.

Background: Hypoxia promotes cancer progression. Hypoxia-inducible factor-1a (HIF-1a) has been reported to enhance tumor invasion and metastasis via activating downstream genes, such as matrix metalloproteinases (MMPs). The purpose of this study was to explore the probable roles of HIF-1a and MMP13 in the invasion and metastasis of ovarian cancer under hypoxic conditions. Material/Methods: The expression of HIF-1a and MMP13 protein were detected with immunohistochemistry staining in ovarian cancer tissues, metastatic lesions, and normal fallopian tissues. Ovarian cancer A2780 cells were cultured under normoxic condition and hypoxic condition. mRNA and protein expression of HIF-1a and MMP13 were detected by RT-PCR and Western blot analysis. The effects of siRNA against HIF-1a on MMP13 expression were examined by RT-PCR and Western blot analysis. Transwell invasion assays were performed to test the invasive ability of A2780 cells. Results: Immunohistochemistry staining showed significantly higher expression of HIF-1a and MMP13 protein in ovarian cancer tissues and metastatic lesions than in normal fallopian tissues. HIF-1a and MMP13 expression were closely related. After exposure to hypoxia, mRNA and protein levels of HIF-1a and MMP13 were upregulated. siRNA effectively inhibited HIF-1a expression and MMP13 expression. The number of invading A2780 cells decreased after HIF-1a was silenced. Conclusions: This study suggests that HIF-1a promotes ovarian cancer cell invasion through a MMP13 mechanism. It might be an effective strategy targeting HIF-1a-MMP13 to inhibit invasion and metastasis of ovarian cancer.

Tiron functions as an effective antioxidant alleviating the intracellular reactive oxygen species (ROS) or the acute toxic metal overload. Previous studies have shown that cardiac myocyte apoptosis can be effectively inhibited by tiron administration in streptozotocin (STZ)-induced diabetic rats, primary neonatal rat cardiomyocytes (NRVMs), and H9c2 embryonic rat cardiomyocytes. However, the underlying signalling mechanism is ill-defined. In the present study, we found that tiron supplementation significantly inhibited apoptosis of high glucose (HG)-treated NRVMs and the left ventricular cardiomyocytes from STZ-diabetic rat, accompanied with a reduction of osteopontin (OPN) levels as well as an inhibition of PKCδ phosphorylation. OPN knockdown protected NRVMs against HG-induced cell apoptosis. In addition, genetic inhibition of PKCδ mitigated HG-stimulated enhancement of intracellular OPN levels in NRVMs. These findings indicate that ROS-mediated activation of PKCδ upregulated OPN expression, leading to cardiac myocyte apoptosis. Interfering with ROS/PKCδ pathway by antioxidants such as tiron provides an optional therapeutic strategy for treatment and prevention of apoptosis-related cardiovascular diseases including diabetic cardiomyopathy.

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Fibrin has been widely used in wound healing. However, its benefit for spinal cord injury (SCI) is limited. In this study, we investigated the impact of fibrin scaffolds containing ectomesenchymal stem cells (EMSCs) on histological and behavioral recovery after SCI and compared it with fibrin alone. To achieve this, EMSCs derived from adult rat nasal respiratory mucosa were cultured, characterized and transfected with green fluorescent protein adenovirus before transplantation. Then, Sprague-Dawley host rats were randomly assigned into four groups: the control group (laminectomy); the SCI group (laminectomy and transection of spinal cords); the fibrin group (fibrin was transplanted immediately after SCI), and the fibrin cell (FC) group (fibrin scaffolds containing EMSCs were transplanted after SCI). Three days after the operation, a TUNEL assay indicated less apoptotic cells in the FC group than in the fibrin group. Two weeks after SCI, fluorescence staining demonstrated not only the survival and migration of EMSCs into the lesion sites, but also a higher number of nerve fibers in the FC group than in the fibrin group. Histological examination including immunohistochemistry and transmission electron microscopy 12 weeks after the operation showed more nerve fibers and a thicker myelin sheath in the FC group compared to the fibrin group. Western blotting confirmed these morphological results. Consistent with the histological results, Basso, Beattie and Bresnahan locomotor scores of the FC group were higher than those of the fibrin group. These results suggest that fibrin scaffolds containing EMSCs can improve the behavioral and histological recovery after SCI better than fibrin alone.

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