Abstract- Botryodiplodia sp. AUMC 9468 was isolated in pure culture from canker on Ficus benjamina, on side of Ibraheemia bank stream at Assiut governorate, Egypt. The analysis of growth condition suggested the trees were stressed induced by light, nutrient and medium factors. This report is the first for Botryodiplodia canker on F. benjamina in Egypt. The pathogenicity test were resulted on that the fungus was introduced with the trees, penetrated through bark wounds, and incubated under conditions stressful to the well-being of the tree.

Keywords- Canker,Ficus benjamina, Botryodiplodia.

With the integration of cloud computing, smart phones enormously improved in processing power, storage, communication efficiency, and reliability. The technical architecture of Cloud strongly supports the efficient delivery of services in mobile environment. Whereas the mobile cloud users can access all the resources as a service dynamically in elastic mode. Accessing Digital Intellectual Property as a Service (DIPaaS) on flexible economic basis is a major interest among the mobile users. DIP is the piece of work of human intellectual in digital form such as eBook, software program, e-painting, movie, song, computer game, and etc. The DIP services complex in nature, involves creator, manufacturer, distributor, licensing agencies, and service providers. However, the service limitations exist, shall be overcome with an understanding approach to Service Level Agreement (SLA). DIP applications consume a large of local resources and could not be implemented on standalone mobile phones. Therefore, we realize increasing demand for an efficient service-model which satisfies the mobile cloud users at large. We proposed the first service-model includes both technical and service architecture to encourage the stakeholders for DIP access in mobile cloud environment. Eventually we present an efficient access to Digital Intellectual Property as a Service in Mobile Cloud Environment (DIPaaSMCE).

OBJECTIVE. In a clinical setting, lipoma can sometime show low signal intensity on susceptibility-weighted imaging (SWI) mimicking hemorrhage. The purpose of this study was to evaluate the fat-water interface chemical-shift artifacts between SWI and T2*-weighted imaging with a phantom study and evaluate SWI in lipoma cases.

MATERIALS AND METHODS. SWI, magnitude, high-pass filtered phase, and T2*-weighted imaging of a lard-water phantom were evaluated in the in-phase, out-of phase, and standard partially out-of-phase TE settings used for clinical 3-T SWI (19.7, 20.9, and 20.0 ms, respectively) to identify the most prominent fat-water interface low signal. SWI of five cases of CNS lipoma were retrospectively evaluated by two neuroradiologists.

RESULTS. TE at 19.7 ms (in-phase) showed the minimum fat-water interface low signal in the phase-encoding direction on magnitude, high-pass filtered phase, and SWI. TE at 20.9 ms (out-of-phase) showed the maximum fat-water interface in the phase-encoding direction on magnitude, high-pass filtered phase, and SWI. TE at 20.0 ms (partially out-of-phase) showed more fat-water interface low signal on SWI than on T2*-weighted imaging, especially in the phase-encoding direction. All lipomas in the five patients showed high signal intensity with surrounding peripheral dark rim on SWI.

CONCLUSION. Fat-water interface is more prominent on the standard TE setting used for clinical SWI (20.0 ms) than that of T2*-weighted imaging and shows a characteristic surrounding peripheral low-signal-intensity rim in lipoma. Knowing the fat-water appearance on SWI is important to avoid misinterpreting intracranial lipomas as hemorrhages.

The objective of the current study was to investigate the effect of vanadium (V(5+)) on Cyp1 expression and activity in C57BL/6 mice liver and isolated hepatocytes. For this purpose, C57BL6 mice were injected intraperitoneally with V(5+) (5 mg/kg) in the absence and presence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (15 μg/kg) for 6 and 24 h. Furthermore, isolated hepatocytes from C57BL6 mice were treated with V(5+) (5, 10, and 20 μM) in the absence and presence of TCDD (1 nM) for 3, 6, 12, and 24 h. In vivo, V(5+) alone did not significantly alter Cyp1a1, Cyp1a2, or Cyp1b1 mRNA, protein, or catalytic activity levels. Upon co-exposure to V(5+) and TCDD, V(5+) significantly potentiated the TCDD-mediated induction of the Cyp1a1, Cyp1a2, and Cyp1b1 mRNA, protein, and catalytic activity levels at 24 h. In vitro, V(5+) decreased the TCDD-mediated induction of Cyp1a1 mRNA, protein, and catalytic activity levels. Furthermore, V(5+) significantly inhibited the TCDD-induced AhR-dependent luciferase activity. V(5+) also increased serum hemoglobin (Hb) levels in animals treated for 24 h. Upon treatment of isolated hepatocytes with Hb alone or in the presence of TCDD, there was an increase in the AhR-dependent luciferase activity. When isolated hepatocytes were treated for 2 h with V(5+) in the presence of TCDD, followed by replacement of the medium with new medium containing Hb, there was further potentiation to the TCDD-mediated effect. The present study demonstrates that there is a differential modulation of Cyp1a1 by V(5+) in C57BL/6 mice livers and isolated hepatocytes and demonstrates Hb as an in vivo specific modulator.

Recently we demonstrated the ability of mercuric chloride (Hg(2+)) in human hepatoma HepG2 cells to significantly decrease the TCDD-mediated induction of Cytochrome P450 1A1 (CYP1A1) mRNA, protein, and catalytic activity levels. In this study we investigated the effect of methylmercury (MeHg) on CYP1A1 in HepG2 cells. For this purpose, cells were co-exposed to MeHg and TCDD and the expression of CYP1A1 mRNA, protein, and catalytic activity levels were determined. Our results showed that MeHg did not alter the TCDD-mediated induction of CYP1A1 mRNA, or protein levels; however it was able to significantly decrease CYP1A1 catalytic activity levels in a concentration-dependent manner. Importantly, this inhibition was specific to CYP1A1and was not radiated to other aryl hydrocarbon receptor (AhR)-regulated genes, as MeHg induced NAD(P)H:quinone oxidoreductase 1 mRNA and protein levels. Mechanistically, the inhibitory effect of MeHg on the induction of CYP1A1 coincided with an increase in heme oxygenase-1 (HO-1) mRNA levels. Furthermore, the inhibition of HO-1 activity, by tin mesoporphyrin, caused a complete restoration of MeHg-mediated inhibition of CYP1A1 activity, induced by TCDD. In addition, transfection of HepG2 cells with siRNA targeting the human HO-1 gene reversed the MeHg-mediated inhibition of TCDD-induced CYP1A1. In conclusion, this study demonstrated that MeHg inhibited the TCDD-mediated induction of CYP1A1 through a posttranslational mechanism and confirms the role of HO-1 in a MeHg-mediated effect.

We read with interest the article entitled “Detection of Intratumoral Calcification in Oligodendrogliomas by Susceptibility-Weighted MR Imaging” and would like to comment on the appearance of calcification on the high-pass-filtered phase images.

The authors reported that the paramagnetic (authors wrote “diamagnetic”) hemorrhagic component of the tumor would cause a negative phase shift and appear as dark signal on the high-pass-filtered phase images, while the diamagnetic (authors wrote “paramagnetic”) intratumoral calcifications would cause an opposite positive phase shift and appear as bright signal on the high-pass-filtered phase images. This description is true, but only in the case of right-handed MR imaging systems, while in left-handed MR imaging systems, the complete opposite signal would be seen: Paramagnetic substances would appear bright, while diamagnetic substances would appear dark.

In Figs 2D and 3D of the above-mentioned article, the high-pass-filtered phase images are those of a left-handed MR imaging system, evident by the bright signal of the veins (paramagnetic deoxyhemoglobin).

The article showed that high-pass-filtered phase images can depict intratumoral calcification in oligodendrogliomas better than conventional MR images; this finding has been reported before. Understanding the contrast appearance of high-pass-filtered phase images on left-handed versus right-handed MR imaging systems would make distinguishing diamagnetic calcification from paramagnetic hemorrhage a much easier task and prevent any possible confusion.

Heavy metals, typified by arsenite (As(III)), have been implicated in altering the carcinogenicity of aryl hydrocarbon receptor (AhR) ligands, typified by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), by modulating the induction of the Cyp1a1 enzyme, but the mechanism remains unresolved. In this study, the effects of As(III) on Cyp1a1 expression and activity were investigated in C57BL/6 mouse livers and isolated hepatocytes. For this purpose, C57BL/6 mice were injected intraperitoneally with As(III) (12.5 mg/kg) in the absence and presence of TCDD (15 μg/kg) for 6 and 24 h. Furthermore, isolated hepatocytes from C57BL/6 mice were treated with As(III) (1, 5, and 10 μM) in the absence and presence of TCDD (1 nM) for 3, 6, 12, and 24 h. At the in vivo level, As(III) decreased the TCDD-mediated induction of Cyp1a1 mRNA at 6h while potentiating its mRNA, protein, and catalytic activity levels at 24 h. At the in vitro level, As(III) decreased the TCDD-mediated induction of Cyp1a1 mRNA in a concentration- and time-dependent manner. Moreover, As(III) decreased the TCDD-mediated induction of Cyp1a1 protein and catalytic activity levels at 24 h. Interestingly, As(III) increased the serum hemoglobin (Hb) levels in animals treated for 24 h. Upon treatment of isolated hepatocytes with Hb alone, there was an increase in the nuclear accumulation of AhR and AhR-dependent luciferase activity. Furthermore, Hb potentiated the TCDD-induced AhR-dependent luciferase activity. Importantly, when isolated hepatocytes were treated for 5h with As(III) in the presence of TCDD and the medium was then replaced with new medium containing Hb, there was potentiation of the TCDD-mediated effect. Taken together, these results demonstrate for the first time that there is a differential modulation of the TCDD-mediated induction of Cyp1a1 by As(III) in C57BL/6 mouse livers and isolated hepatocytes. Thus, this study implicates Hb as an in vivo-specific modulator.

The paper attempt a closer investigation to re-interpret the role of CSR in limiting the extreme practices in earnings management (EM), using evidence from large UK companies.