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Morphological Damage (morphological + damage)
Selected AbstractsVascular endothelium: the battlefield of dengue virusesFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2008Atanu Basu Abstract Increased vascular permeability without morphological damage to the capillary endothelium is the cardinal feature of dengue haemorrhagic fever (DHF)/dengue shock syndrome (DSS). Extensive plasma leakage in various tissue spaces and serous cavities of the body, including the pleural, pericardial and peritoneal cavities in patients with DHF, may result in profound shock. Among various mechanisms that have been considered include immune complex disease, T-cell-mediated, antibodies cross-reacting with vascular endothelium, enhancing antibodies, complement and its products, various soluble mediators including cytokines, selection of virulent strains and virus virulence, but the most favoured are enhancing antibodies and memory T cells in a secondary infection resulting in cytokine tsunami. Whatever the mechanism, it ultimately targets vascular endothelium (making it a battlefield) leading to severe dengue disease. Extensive recent work has been done in vitro on endothelial cell monolayer models to understand the pathophysiology of vascular endothelium during dengue virus (DV) infection that may be translated to help understand the pathogenesis of DHF/DSS. The present review provides a broad overview of the effects of DV infection and the associated host responses contributing towards alterations in vascular endothelial cell physiology and damage that may be responsible for the DHF/DSS. [source] Significance of determining the point of reperfusion failure in experimental torsion of testisINTERNATIONAL JOURNAL OF UROLOGY, Issue 1 2005ELIJAH O KEHINDE Abstract Background:, Experimental studies of the use of free radical scavengers in ischemic/reperfusion (I/R) injury following detorsion of the torted testis have yielded conflicting results due to differences in the period of ischemia used. The authors studied I/R injury in the rabbit model, to define the point beyond which there is reperfusion failure. Methods:, Ischemia/reperfusion injury of the testis was created in 3,6-month-old male New Zealand white rabbits by cross-clamping the left spermatic cord for periods of ischemia lasting 0, 15, 30, 60, 90, 120 and 180 min. There were eight animals per experimental group. The right testis served as internal control. Both testes were harvested after 24 h of reperfusion in four animals and after 3 months in the remaining four animals for each group. Testicular malondialdehyde (MDA), a measure of free radical damage, was determined by using the thiobarbituric acid reaction on testicular homogenates. Johnsen score was used to assess morphological damage caused by the ischemia. Results:, After 24 h of reperfusion, the mean testicular MDA in the control right testes at 0, 15, 30, 60, 90, 120 and 180 min was 2.1, 2.5, 2.9, 2.4, 2.1 and 1.9 nmol/mg protein, respectively. The mean left testicular MDA at corresponding ischemic periods was 1.6, 2.0, 3.9, 10.0, 4.4, 6.1 and 1.0 nmol/mg protein, respectively. The maximum left testicular MDA was at 60 min (10.0 nmol/mg protein), following which the level dropped significantly to 1.0 nmol/mg protein at 180 min. At 3 months, the mean Johnsen scores for left testes subjected to 0, 60, 120 and 180 min ischemia were 9.4, 8.8, 2.3, 3.5, respectively. Conclusion:, The results suggest that following ischemia of up to 60 min in the rabbit testis, adequate reperfusion is possible, but ischemia lasting beyond 60 min results in inadequate reperfusion leading to irreversible damage. Thus, in experiments for assessing the effect of antioxidants on I/R injury of the testis in rabbits, periods up to 60 min of ischemia should be regarded as optimum to observe an effect. [source] DOES THE CYTOSKELETON OF INTESTINAL EPITHHELIAL CELLS FUNCTION AS A CELLULAR ALARM TO IDENTIFY THE E. COLI INFECTIONJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2001Zhe Li Intestinal epithelial cells play an important role in regulating host immunity in response to intestinal infection. Pathogenic bacteria (EPEC and EHEC) cause profound cytoskeletal rearrangement in intestinal epithelial cells during attachment or invasion. Rearrangement of cytoskeletal proteins could be a signal to up-regulate host defence response. Aims, To determine the role of actin cytoskeleton and microtubles in IL-8 mRNA response to E. coli infection. Methods, T84 cell monolayers in 6-well plates were infected with HB101, EPEC and EHEC (105 CFU/well) and compared with uninfected control at 3, 6 and 12 h post infection. Control and infected monolayers were treated with nocodazole (Noc, microtubule disrupter, 30 mm), taxol (Tax, microtubule stabiliser, 10 mm), cytochalasin D (CytoD, actin depolymeriser, 100 nm) and Jasplakinolide (Jasp, actin polymeriser, stabilise actin filaments, 1 mm) and studied 6 h post infection. IL-8 gene expression was measured by semiquantitative RT,PCR in control and uninfected monolayers with and without drug treatment and IL8 protein secretion by ELISA. The morphology of F-actin and ,-tubulin was examined by FITC-phaloidin staining (FAS), immunohistochemistry and confocal microscopy. Results, IL-8 mRNA and IL-8 were increased by infection with all bacterial strains at 3 and 6 h but both IL-8 mRNA and IL-8 in EHEC and EPEC infection were decreased compared with control and HB101 at 12 h. Disruption of microfilaments by Noc increased IL-8 (2.7 fold) while preservation of microfilaments by Tax inhibited IL8 response (0.5 fold) to HB101 infection only. CytoD decreased (0.1,0.5 fold) IL8 expression at all time points in all infections while stabilising actin by Jasp markedly increased the IL8 response (2,6 fold) in control, HB101, EHEC and EPEC at 3 and 6 h. CytoD inhibited Noc-induced IL8 gene expression. Confocal microscopy demonstrated that CytoD and Noc caused major morphological damage to the actin and ,-tubulin by 6 h. Similar changes were also observed in EPEC and EHEC infection at 12 h but not HB101. Jasp preserved actin stress filaments in both EPEC and EHEC. Conclusions, Disruption of microtubules and exogenous rearrangement of actin by pathogenic organism may be primary stimuli to up-regulate proinflammatory cytokine gene expression. Preservation of actin filaments is required for this response and may be necessary for signal transduction to the nucleus. [source] Odorants as cell-type specific activators of a heat shock response in the rat olfactory mucosaTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2001Virginian McMillan Carr Abstract Heat shock, or stress, proteins (HSPs) are induced in response to conditions that cause protein denaturation. Activation of cellular stress responses as a protective and survival mechanism is often associated with chemical exposure. One interface between the body and the external environment and chemical or biological agents therein is the olfactory epithelium (OE). To determine whether environmental odorants affect OE HSP expression, rats were exposed to a variety of odorants added to the cage bedding. Odorant exposure led to transient, selective induction of HSP70, HSC70, HSP25, and ubiquitin immunoreactivities (IRs) in supporting cells and subepithelial Bowman's gland acinar cells, two OE non-neuronal cell populations involved with inhalant biotransformation, detoxification, and maintenance of overall OE integrity. Responses exhibited odor specificity and dose dependency. HSP70 and HSC70 IRs occurred throughout the apical region of supporting cells; ubiquitin IR was confined to a supranuclear cone-shaped region. Electron microscopic examination confirmed these observations and, additionally, revealed odor-induced formation of dense vesicular arrays in the cone-like regions. HSP25 IR occurred throughout the entire supporting cell cytoplasm. In contrast to classical stress responses, in which the entire array of stress proteins is induced, no increases in HSP40 and HSP90 IRs were observed. Extended exposure to higher odorant doses caused prolonged activation of the same HSP subset in the non-neuronal cells and severe morphological damage in both supporting cells and olfactory receptor neurons (ORNs), suggesting that non-neuronal cytoprotective stress response mechanisms had been overwhelmed and could no longer adequately maintain OE integrity. Significantly, ORNs showed no stress responses in any of our studies. These findings suggest a novel role for these HSPs in olfaction and, in turn, possible involvement in other normal neurophysiological processes. J. Comp. Neurol. 432:425,439, 2001. © 2001 Wiley-Liss, Inc. [source] In Vivo Assessment of a New Method of Pulsatile Perfusion Based on a Centrifugal PumpARTIFICIAL ORGANS, Issue 2 2010Jesús Herreros Abstract The aim of this study was to assess platelet dysfunction and damage to organs after extracorporeal circulation using a pump based on a new method that adds a pulsatile flow to the continuous flow provided by a centrifugal pump. The continuous component of the total flow (2,3 L/min) is created by a Bio-Pump centrifugal pump, while the pulsatile component is created by the pulsating of an inner membrane pneumatically controlled by an intra-aortic counterpulsation balloon console (systolic volume of 37.5 mL in an asynchronous way with a frequency of 60 bpm). Six pigs were subjected to a partial cardiopulmonary bypass lasting 180 min and were sacrificed 60 min after extracorporeal circulation was suspended. The hematological study included the measurement of hematocrit, hemoglobin, leukocytes, and platelet function. The new pump did not significantly alter either platelet count or platelet function. In contrast, hematocrit and hemoglobin were significantly reduced during extracorporeal circulation (approximately 5% P = 0.011, and 2 g/dL P = 0.01, respectively). The leukocyte count during extracorporeal circulation showed a tendency to decrease, but this was not significant. In general, the short-term use of the new pump (4 h) did not cause any serious morphological damage to the heart, lung, kidney, or liver. The results suggest that the hemodynamic performance of the new pump is similar to a conventional centrifugal pump and could therefore be appropriate for use in extracorporeal circulation. [source] Morphological study of acute zonal occult outer retinopathy (AZOOR) by multiplanar optical coherence tomographyACTA OPHTHALMOLOGICA, Issue 4 2009Yoshiko Takai Abstract. Purpose:, We set out to determine whether morphological retinal changes occur in patients with acute zonal occult outer retinopathy (AZOOR). Methods:, Five patients diagnosed with AZOOR were studied. They included two men and three women, with an age range of 23,51 years. Symptoms and findings were retrospectively and prospectively collected. The three-dimensional multiplanar optical coherence tomography (OCT) Ophthalmoscope® was used to examine the morphology of the retina in patients who were examined between April 2000 to December 2004. Standardized full-field electroretinograms (ERGs) and multifocal ERGs (mfERGs) were recorded. Results:, All the patients reported an acute onset of visual disturbances including a decrease of central vision and photopsia. The a- and b-waves of full-field ERGs were decreased, and the mfERGs in the central area were reduced. Ophthalmoscopic examination showed no obvious fundus abnormalities. OCT Ophthalmoscopic® images of a cross-sectional plane revealed hyporeflection at the level of the photoreceptor layer in the macular region in three of five patients, and presence of one or two layers in which the inner/outer segment junction of the photoreceptor layer was absent in the other two patients. En-face, constant depth C-scans, which present the image parallel to the retina, revealed an abnormal, patchy hyper-reflection in the affected eyes of two patients and in the non-affected eye in one of these two patients. Conclusions:, The changes in OCT Ophthalmoscope® B-scan images indicate morphological damage to the photoreceptors, which probably accounts for the functional alterations. The alterations in the C-scan image in the normal fellow eye of one patient suggest that morphological changes may precede symptomatic changes. [source] |