Histopathology of the Chimpanzee Ear

Four female and two male chimpanzees were secured in various positions on a Daisy Decelerator and subjected to forces ranging from 54 to 180 G. It was found that forces in excess of 54 G may rupture the tympanic membranes and cause subepithelial hemorrhages in the middle ear. The majority of cases showed proteinaceous material, with or without cells in the petrous air spaces. When exposed to forces above 119 G, there was engorgement and often rupture of the pericarotid venous plexus. When supine, distortion of both superior and posterior semicircular canals was found. With forces in excess of 54 G, the cupulae of the cristae ampullaris were either elevated or destroyed. The hair processes were also often broken off. The otolithic membranes, especially of the maculae utriculi were also elevated or otherwise distorted and the saccule was often partially collapsed. In several instances, there was an overabundance of a proteinaceous substance in the lumina of the vestibular apparatus and in the cochlear ducts with their associated scalae. In half the cases, the cochlear duct was narrowed by the depression of the vestibular membrane. Although there seems to be considerable individual variation in ability to withstand these forces, neither age, sex nor weight appear to directly influence the results. The possible sources for the materials found both in the air cells and labyrinth are discussed

Single electron response and energy resolution of a Micromegas detector

Micro-Pattern Gaseous Detectors (MPGDs) such as Micromegas or GEM are used in particle physics experiments for their capabilities in particle tracking at high rates. Their excellent position resolutions are well known but their energy characteristics have been less studied. The energy resolution is mainly affected by the ionisation processes and detector gain fluctuations. This paper presents a method to separetely measure those two contributions to the energy resolution of a Micromegas detector. The method relies on the injection of a controlled number of electrons. The Micromegas has a 1.6-mm drift zone and a 160-$\mu$m amplification gap. It is operated in Ne 95%-iC$\mathrm{_4}$H$\mathrm{_{10}}$ 5% at atmospheric pressure. The electrons are generated by non-linear photoelectric emission issued from the photons of a pulsed 337-nm wavelength laser coupled to a focusing system. The single electron response has been measured at different gains (3.7 10$\mathrm{^4}$, 5.0 10$\mathrm{^4}$ and 7.0 10$\mathrm{^4}$) and is fitted with a good agreement by a Polya distribution. From those fits, a relative gain variance of 0.31$\pm$0.02 is deduced. The setup has also been characterised at several voltages by fitting the energy resolution measured as a function of the number of primary electrons, ranging from 5 up to 210. A maximum value of the Fano factor (0.37) has been estimated for a 5.9 keV X-rays interacting in the Ne 95%-iC$\mathrm{_4}$H$\mathrm{_{10}}$ 5% gas mixture.Comment: Preprint submitted to Nuclear Instrumentation and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment; Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment in press (2009

Interferon-α resistance in renal carcinoma cells is associated with defective induction of signal transducer and activator of transcription 1 which can be restored by a supernatant of phorbol 12-myristate 13-acetate stimulated peripheral blood mononuclear cells

Therapy of selected human malignancies with interferon-α is widely accepted but often complicated by the emergence of interferon-α resistance. Interferon is a pleiotropic cytokine with antiproliferative, antitumour, antiviral and immunmodulatory effect; it signals through the Jak-STAT signal transduction pathway where signal transducer and activator of transcription 1 plays an important role. Here we report both, a lack of signal transducer and activator of transcription induction in interferon-α resistant renal cell carcinoma cells and signal transducer and activator of transcription 1 reinduction of phorbol 12-myristate 13-acetate-stimulated peripheral blood mononuclear cells supernatant. Preliminary experiments on the identification of the molecules that reinducing signal transducers and activators of transcription 1 indicate that interferon-γ may be the responsible candidate cytokine, but several others may be involved as well. This work provides the basis for therapeutic strategies directed at the molecular modulation of interferon-α resistance in human neoplasms

Incongruence in number–luminance congruency effects

Congruency tasks have provided support for an amodal magnitude system for magnitudes that have a “spatial” character, but conflicting results have been obtained for magnitudes that do not (e.g., luminance). In this study, we extricated the factors that underlie these number–luminance congruency effects and tested alternative explanations: (unsigned) luminance contrast and saliency. When luminance had to be compared under specific task conditions, we revealed, for the first time, a true influence of number on luminance judgments: Darker stimuli were consistently associated with numerically larger stimuli. However, when number had to be compared, luminance contrast, not luminance, influenced number judgments. Apparently, associations exist between number and luminance, as well as luminance contrast, of which the latter is probably stronger. Therefore, similar tasks, comprising exactly the same stimuli, can lead to distinct interference effects

Modulation of SOCS protein expression influences the interferon responsiveness of human melanoma cells

<p>Abstract</p> <p>Background</p> <p>Endogenously produced interferons can regulate the growth of melanoma cells and are administered exogenously as therapeutic agents to patients with advanced cancer. We investigated the role of negative regulators of interferon signaling known as suppressors of cytokine signaling (SOCS) in mediating interferon-resistance in human melanoma cells.</p> <p>Methods</p> <p>Basal and interferon-alpha (IFN-α) or interferon-gamma (IFN-γ)-induced expression of SOCS1 and SOCS3 proteins was evaluated by immunoblot analysis in a panel of n = 10 metastatic human melanoma cell lines, in human embryonic melanocytes (HEM), and radial or vertical growth phase melanoma cells. Over-expression of SOCS1 and SOCS3 proteins in melanoma cells was achieved using the PINCO retroviral vector, while siRNA were used to inhibit SOCS1 and SOCS3 expression. Tyr⁷⁰¹-phosphorylated STAT1 (P-STAT1) was measured by intracellular flow cytometry and IFN-stimulated gene expression was measured by Real Time PCR.</p> <p>Results</p> <p>SOCS1 and SOCS3 proteins were expressed at basal levels in melanocytes and in all melanoma cell lines examined. Expression of the SOCS1 and SOCS3 proteins was also enhanced following stimulation of a subset of cell lines with IFN-α or IFN-γ. Over-expression of SOCS proteins in melanoma cell lines led to significant inhibition of Tyr⁷⁰¹-phosphorylated STAT1 (P-STAT1) and gene expression following stimulation with IFN-α (IFIT2, OAS-1, ISG-15) or IFN-γ (IRF1). Conversely, siRNA inhibition of SOCS1 and SOCS3 expression in melanoma cells enhanced their responsiveness to interferon stimulation.</p> <p>Conclusions</p> <p>These data demonstrate that SOCS proteins are expressed in human melanoma cell lines and their modulation can influence the responsiveness of melanoma cells to IFN-α and IFN-γ.</p