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Microscopic Evidence (microscopic + evidence)
Selected AbstractsCover Picture: Microscopic Evidence for Spatially Inhomogeneous Charge Trapping in Pentacene (Adv. Mater.ADVANCED MATERIALS, Issue 11 200511/2005) Abstract Trapped charge has been observed in polycrystalline pentacene films by electric force microscopy in work reported by Muller and Marohn on p.,1410. The cover shows an optical fiber watching the motion of a metal-coated cantilever hovering over a polycrystalline pentacene film. The film occupies the 6.5,,,m gap in a working field-effect transistor. Trapped charge (dark blue and black areas in the pentacene) appears as large patches randomly distributed throughout the device, implying that long-lived traps in polycrystalline pentacene are not correlated with grain boundaries. [source] Microscopic Evidence of the Metalation of a Free-Base Porphyrin Monolayer with IronCHEMPHYSCHEM, Issue 2 2007Florian Buchner Microscopic evidence of the in situ complexation of Fe-porphyrins is presented. The figure shows the sub-molecular resolved scanning tunneling microscopy images which document the metalation of 2H-TPP (central cavity; TPP: tetraphenylporphyrin) with evaporated iron (protrusions are identified as Fe-TPP). This promising technique enables future surface science investigations of clean iron porphyrin films under ultrahigh vacuum conditions. [source] Evaluation of gastric toxicity of indomethacin acid, salt form and complexed forms with hydroxypropyl-,-cyclodextrin on Wistar rats: histopathologic analysisFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2009A.C. Ribeiro-Rama Abstract Indomethacin (IM) is a non-steroidal anti-inflammatory drug which inhibits prostaglandin biosynthesis. It is practically insoluble in water and has the capacity to induce gastric injury. Hydroxypropyl-,-cyclodextrin (HP-,-CD) is an alkylated derivative of ,-CD with the capacity to form inclusion complexes with suitable molecules. IM is considered to form partial inclusion complexes with HP-,-CD by enclosure of the p -chlorobenzoic part of the molecule in the cyclodextrin channel, reducing the adverse effects. The aim of this paper is to evaluate the gastric damage induced by the IM inclusion complex prepared by freeze-drying and spray-drying. A total of 135 Wistar rats weighing 224.4 ± 62.5 g were put into 10 groups. They were allowed free access to water but were maintained fasted for 18 h before the first administration until the end of the experiment. IM acid-form, IM trihydrated-sodium-salt and IM-HP-,-CD spray and freeze-dried, at normal and toxic doses, were administered through gastric cannula once/day for 3 days. Seventy-two hours after the first administration, the animals were sacrificed and the stomachs collected and prepared for morphological study by using the haematoxylin-eosin technique. Lesion indexes (rated 0/4) were developed and the type of injury was scored according to the severity of damage and the incidence of microscopic evidence of harm. Microscopic assessment demonstrated levels of injury with index one on 10,25%. The type of complexation method had different incidence but the same degree. The results show that IM inclusion complexation protects against gastric injury, reducing the incidence and the maximum degree of severity from 4 to 1, with a better performance of the spray-dried complex. [source] The development of cutaneous lesions during follow-up of patients with primary neuritic leprosyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 3 2005Sujai Suneetha PhD Background, Primary neuritic leprosy (PNL) is a rare form of leprosy where the characteristic skin lesions are absent. Investigations of apparently normal skin from the areas of sensory change have revealed microscopic evidence of nerve involvement. Clinical studies have found that a proportion of patients develop visible skin lesions during follow-up. The aim of the study was to perform a clinical and histological analysis of PNL patients who developed visible skin lesions during treatment and follow-up, to gain insight into the pathogenesis of the disease. Methods, Twenty-nine individuals in a series of 182 PNL patients developed visible skin lesions during follow-up. Analysis of the number, location, histology and time of onset of the new skin lesions in relation to the type and regularity of the treatment regimen were noted. A biopsy from the new skin lesion when available was compared with the nerve biopsy findings at the time of initial diagnosis. Results, Thirty-eight per cent of patients developed a single patch and 28% developed two patches. Over three-quarters of these were on the lower limb (47%) or the upper limb (29%). Sixty-two per cent of patients developed the lesions within 2 years of the onset of symptoms. Patients on regular treatment developed patches earlier than those on irregular treatment or no treatment. A skin biopsy from the new patch revealed borderline tuberculoid leprosy histology in 47% of the patients. Conclusions, The findings suggest that leprosy primarily affects the nerve and that a neuritic phase precedes the development of visible cutaneous lesions. [source] A novel model for the interpretation of small-angle scattering experiments of self-affine structuresJOURNAL OF APPLIED CRYSTALLOGRAPHY, Issue 1 2010Gerald J. Schneider A novel theory is presented which allows, for the first time, the analytical description of small-angle scattering experiments on anisotropic shaped clusters of nanoparticles. Experimentally, silica-filled rubber which is deformed is used as an example. The silica can be modelled by solid spheres which form clusters. The experiments demonstrate that the clusters become anisotropic as a result of the deformation whereas the spheres are not affected. A comparison of the newly derived model function and the experiments provides, for the first time, microscopic evidence of the inhomogeneous deformation of clusters in the rubbery matrix. [source] Pulmonary responses and recovery following single and repeated inhalation exposure of rats to polymeric methylene diphenyl diisocyanate aerosolsJOURNAL OF APPLIED TOXICOLOGY, Issue 6 2002Joanne D. Kilgour Abstract Acute and repeated inhalation exposures (for 28 days) to polymeric methylene diphenyl diisocyanate (PMDI) were performed in rats. Investigations were made at the end of exposures and after 3, 10 and 30 days of recovery following single acute exposures and after 30 days of recovery following 28 days of exposure. Acute exposures to 10, 30 or 100 mg m,3 PMDI produced clinical signs in all animals that were consistent with exposure to irritant aerosols. An exposure concentration-related body weight loss and increase in lung weight were seen post-exposure, with complete recovery by day 8. The time course of changes in the lung over the initial days following exposure consisted of a pattern of initial toxicity, rapid and heavy influx of inflammatory cells and soluble markers of inflammation and cell damage, increased lung surfactant, a subsequent recovery and epithelial proliferative phase and, finally, a return to the normal status quo of the lung. During these stages there was evidence for perturbation of lung surfactant homeostasis, demonstrated by increased amounts of crystalline surfactant and increased number and size of lamellar bodies within type II alveolar cells. Repeated exposure over 28 days to the less toxic concentrations of 1, 4 or 10 mg m,3 PMDI produced no clinical signs or body weight changes, but an increase in lung weight was seen in animals exposed to 10 mg m,3, which resolved following the 30-day recovery period. Other effects seen were again consistent with exposure to irritant aerosols, but were less severe than those seen in the acute study. Analysis of bronchoalveolar lavage fluid revealed similar changes to those seen in the acute study. At both 10 and 4 mg m,3 PMDI increased numbers of ,foamy' macrophages in lung lavage cell pellet correlated with the increased phospholipid content of the pellet. Changes in lung lavage parameters and electron microscopic evidence again suggested perturbations in surfactant homeostasis. Histologically, bronchiolitis and thickening of the central acinar regions was seen at 10 and 4 mg m,3, reflecting changes in cell proliferation in the terminal bronchioles and centro-acinar regions. Almost all effects seen had recovered by day 30 post-exposure. Both acute and subacute studies demonstrate rapid recovery of effects in the lung following exposure to PMDI, with no progression of these effects even at concentrations higher than those shown to produce tumours in a chronic study. These findings add weight to the hypothesis that pulmonary tumours seen following chronic exposure to PMDI are most likely due to a combination of the chronic irritant effects of repeated exposure, coupled with the presence of insoluble polyureas formed by polymerization of PMDI (found in studies reported here and previous chronic studies), and therefore acute or short-term exposures to PMDI are likely to be of little concern for long-term pulmonary health. Copyright © 2002 John Wiley & Sons, Ltd. [source] Expression of human tissue factor under the control of the mouse tissue factor promoter mediates normal hemostasis in knock-in miceJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2 2008L. A. SNYDER Summary.,Background:,Tissue factor (TF) is expressed widely at the subluminal surface of blood vessels and serves as the primary cellular initiator of the extrinsic pathway of blood coagulation. Lack of TF in mice resulted in lethality in utero, but human TF (huTF) expressed at low levels from a human minigene rescued null mice from prenatal death. Although these low-TF expressing transgenic mice developed to term, they had a significantly shorter life span and exhibited hemorrhage and fibrosis in the heart. Methods:,Human TF knock-in (TFKI) mice were generated by replacing the first two exons of the mouse (murine) TF (muTF) gene with the huTF complete coding sequence, thus placing it under the control of the endogenous muTF promoter. Results:,Expression of huTF in the TFKI mice was similar to muTF in wild-type (wt) mice. The TFKI mice showed no microscopic evidence of spontaneous hemorrhage in the heart, nor cardiac fibrosis at up to 18 months of age. Immunohistochemistry showed that huTF was expressed in cells surrounding blood vessels in TFKI mice. Coagulation activity of brain homogenates from TFKI mice was comparable with that from wt brain. Cardiac hemorrhage similar to that of the low-TF transgenic mice occurred in the TFKI mice when huTF was blocked by a neutralizing anti-huTF monoclonal antibody. Conclusion:,We generated a transgenic mouse line that expresses huTF under the control of the endogenous muTF promoter at physiological levels. Our results suggest that huTF can fully reconstitute the murine coagulation system and mediate normal hemostasis. [source] Diameter of the Cochlear Nerve in Endolymphatic Hydrops: Implications for the Etiology of Hearing Loss in Ménière's Disease,THE LARYNGOSCOPE, Issue 9 2005Cliff A. Megerian MD Abstract Objective/Hypothesis: Endolymphatic hydrops (ELH) is an important histopathological hallmark of Ménière's disease. Experimental data from human temporal bones as well as animal models of the disorder have generally failed to determine the mechanism by which ELH or related pathology causes hearing loss. Hair cell and spiral ganglion cell counts in both human and animal case studies have not, for the most part, shown severe enough deterioration to explain associated severe sensorineural hearing loss. However a limited number of detailed ultrastructural studies have demonstrated significant reductions in dendritic innervation densities, raising the possibility that neurotoxicity plays an important role in the pathology of Ménière's disease (MD) as well as experimental endolymphatic hydrops (ELH). This study tests the hypothesis that neurotoxicity is an important primary mediator of injury to the hydropic ear and is reflected in measurable deterioration of the cochlear nerve in the animal model of ELH. This study also explores the previously presented hypothesis that cochlear injury in ELH is mediated through the actions of nitric oxide (NO) by evaluating whether hearing loss or various measures of cochlear damage can be ameliorated by administration of an agent that limits excess production of NO. Study Design: Part one of the project involves the surgical induction of endolymphatic hydrops and correlation of long term hearing loss with histological parameters of ELH severity as well as cochlear nerve and eighth cranial nerve diameter measurements. In part two, aminoguanidine is administered orally to a separate set of hydropic animals in an attempt to limit cochlear injury presumably mediated by NO. Methods: Guinea pigs are subjected to surgical induction of unilateral endolymphatic hydrops after establishing baseline ABR thresholds at 2, 4, 8, 16, and 32 kHz. Threshold shifts are established prior to sacrifice at 4 to 6 months and temporal bones processed for light microscopy. Measurements of cochlear nerve and eighth cranial nerve maximal diameters as well as average maximal diameters are carried out and correlated to hearing loss and a semi-quantitative measure of hydrops severity. The identical experiments are carried out in animals treated with aminoguanidine, an inhibitor of inducible nitric oxide synthase. Results: The mean maximal diameter (n = 14) of the hydropic cochlear nerve was significantly reduced (432.14 ± 43.18 vs. 479.28 ± 49.22 microns, P = .0025) as compared to the control nerve. This was also seen in measures of the eighth cranial nerve (855.71 ± 108.82 vs. 929 ± 81.53 microns, P = 0.0003). Correlation studies failed to show correlation between hydrops severity and a cochlear nerve deterioration index (r = -0.0614, P = .8348). Similarly, hearing loss severity failed to correlate with cochlear nerve deterioration (r = 0.1300, P = .6577). There was a significant correlation between hearing loss and hydrops severity (r = 0.6148, P = .0193). Aminoguanidine treated animals (n = 5) also sustained nerve deterioration to the same degree as non-treated animals and there appeared to be no protective effect (at the dosage administered) against ELH related hearing loss, hydrops formation, or nerve deterioration. Conclusion: ELH results in significant deterioration of cochlear nerve and eighth cranial nerve maximal diameters in the guinea pig model. These findings are in accord with previous studies which detected ultrastructural evidence of dendritic damage and indicate that neural injury is of sufficient severity to result in light microscopic evidence of cochlear nerve and eighth cranial nerve deterioration. These data support the concept that the principle pathological insult in ELH is a form of neurotoxicity, especially in light of previous studies which indicate relative preservation of hair cells at similar points in time. The lack of correlation between the severity of hydrops and nerve deterioration suggests that nerve deterioration is independent of hydrops severity. [source] What is the best approach to an apparently nonmetastatic adrenocortical carcinoma?CLINICAL ENDOCRINOLOGY, Issue 5 2010Martin Fassnacht Summary In suspected nonmetastatic adrenocortical carcinoma (ACC) a careful preoperative diagnostic work up is needed including comprehensive endocrine analysis as recommended by the European Network for the Study of Adrenal Tumors (http://www.ENSAT.org/ACC.htm). Staging prior surgery, in particular chest CT, is indispensable to exclude distant metastases. Open surgery is still the recommended approach in ACC. However, in localized non-invasive ACC with a diameter <10 cm laparoscopic adrenalectomy by an expert surgeon is probably similarly effective and safe. As many patients will suffer from tumor recurrence after seemingly complete removal of ACC, adjuvant treatment based on the individual risk status is recommended. Key factors for risk assessment are tumor stage, resection status and the proliferation marker Ki67. All patients considered at high risk for recurrence should receive adjuvant mitotane for a minimum of 2 years aiming at a drug level of 14,20 mg/l. In selected patients (e.g. R1 resection) we recommend additional radiotherapy of the tumor bed. Patients with a low/intermediate risk for recurrence should be included in the Adiuvo trial comparing adjuvant mitotane with observation only (http://www.adiuvo-trial.org). In low/intermediate risk patients who cannot be included in this trial observation only can be justified in cases with a tumor diameter of <8 cm and no microscopic evidence for invasion of blood vessels or tumor capsule. In all patients a structured follow-up for 10 years is strongly recommended. 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