02657nas a2200241   4500008004100000022001400041245005700055210005600112260009200168300001200260490000800272520186700280653000802147653002402155653002002179653003502199653001002234653000802244100002502252700002402277700002602301856008802327       2005                        eng d  a1042-015000aSurface disorder in c-Si induced by swift heavy ions0 aSurface disorder in cSi induced by swift heavy ions  a4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLANDbTAYLOR & FRANCIS LTDcJUN  a207-2180 v1603 a<p>The disorders induced in crystalline silicon (c-Si) through the process of electronic energy loss in the swift heavy ion irradiation were investigated. A number of silicon &lt;100&gt; samples were irradiated with 65 MeV oxygen ions at different fluences, 1x10(13) to 1.5x10(14) ions/cm(2), and characterized by the Raman spectroscopy, the optical reflectivity, the X-ray reflectivity, the atomic force microscopy (AFM) and the X-ray diffraction (XRD) techniques. The intensity, redshift, phonon coherence length and asymmetric broadening associated with the Raman peaks reveal that stressed and disordered lattice zones are produced in the surface region of the irradiated silicon. The average crystallite size, obtained by analyzing Raman spectrum with the phonon confinement model, was very large in the virgin silicon but decreased to &lt;100 nm dimension in the ion irradiated silicon. The results of the X-ray reflectivity, AFM and optical reflectivity of 200-700 nm radiation indicate that the roughness of the silicon surface has enhanced substantially after ion irradiation. The diffusion of oxygen in silicon surface during ion irradiation is evident from the oscillation in the X-ray reflectivity spectrum and the sharp decrease in the reflectivity of 200-400 nm radiation. The rise in temperature, estimated from the heat spike model, was high enough to melt the local silicon surface. The results of XRD indicate that lattice defects have been induced and a new plane &lt;211&gt; has been formed in the silicon &lt;100&gt; after ion irradiation. The results of the present study show that the energy deposited in crystalline silicon through the process of electronic energy loss similar to 0.944 keV/nm per ion is sufficient to induce disorders of appreciable magnitude in the silicon surface even at a fluence of similar to 10(13) ions/cm(2).</p>10aAFM10acrystalline silicon10aion irradiation10aoptical and X-ray reflectivity10aRaman10aXRD1 aBogle, Kashinath, A.1 aGokhale, Suresh, P.1 aBhoraskar, Vasant, N.  uhttps://library.ncl.res.in/content/surface-disorder-c-si-induced-swift-heavy-ions-002686nas a2200265   4500008004100000022001400041245012000055210006900175260007200244300001200316490000700328520175700335653000802092653001702100653002402117653001302141100002102154700002202175700001802197700002102215700002002236700001902256700001602275856012902291       2008                        eng d  a0022-074400aImaging the interaction between dengue 2 virus and human blood platelets using atomic force and electron microscopy0 aImaging the interaction between dengue 2 virus and human blood p  aGREAT CLARENDON ST, OXFORD OX2 6DP, ENGLANDbOXFORD UNIV PRESScJUN  a113-1180 v573 a<p>Thrombocytopenia is frequently associated with dengue virus infection. Host factors such as anti-platelet immunopathogenic processes have been implicated in the origin of dengue-associated thrombocytopenia but the role of dengue virus in directly interacting with platelets and altering their hemostatic property remains incompletely understood. In the present study, we examined the effect of dengue 2 virus on the morphology and physiological activation profile of normal human platelets using atomic force microscopy, electron microscopy and flowcytometry. Platelets obtained from healthy donors were exposed to a cell culture-adapted 10(4) LD(50) dengue 2 virus isolate in vitro and the subsequent effect on morphology and activation biology studied. Our results show that dengue 2 virus exposure at doses comparable to natural viremic states in human infections can activate platelets with an increase in P-selectin expression and fibrinogen-binding property. Atomic force, scanning and transmission electron microscopy also showed typical activation-related morphological changes such as altered platelet membrane architecture, degranulation, presence of filopodia and dilatation of the open canalicular system in the dengue 2 virus-exposed platelets but not in the controls. Importantly, Japanese encephalitis virus exposure at the same dose did not activate platelets or show any morphological changes. Our findings suggest that dengue 2 virus may directly interact with and activate platelets - an event that might be important in the origin of dengue-associated thrombocytopenia. Detailed molecular characterization of this effect might provide key knowledge toward better prophylaxis of the hemostatic complications of dengue disease.</p>10aAFM10adengue virus10aElectron microscopy10aplatelet1 aGhosh, Kanjaksha1 aGangodkar, Shobha1 aJain, Preksha1 aShetty, Shrimati1 aRamjee, Sandhya1 aPoddar, Pankaj1 aBasu, Atanu  uhttps://library.ncl.res.in/content/imaging-interaction-between-dengue-2-virus-and-human-blood-platelets-using-atomic-force-0