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Acute Damage (acute + damage)
Selected AbstractsGenetic dissection reveals two separate pathways for rod and cone regeneration in the teleost retinaDEVELOPMENTAL NEUROBIOLOGY, Issue 5 2008Ann C. Morris Abstract Development of therapies to treat visual system dystrophies resulting from the degeneration of rod and cone photoreceptors may directly benefit from studies of animal models, such as the zebrafish, that display continuous retinal neurogenesis and the capacity for injury-induced regeneration. Previous studies of retinal regeneration in fish have been conducted on adult animals and have relied on methods that cause acute damage to both rods and cones, as well as other retinal cell types. We report here the use of a genetic approach to study progenitor cell responses to photoreceptor degeneration in the larval and adult zebrafish retina. We have compared the responses to selective rod or cone degeneration using, respectively, the XOPS-mCFP transgenic line and zebrafish with a null mutation in the pde6c gene. Notably, rod degeneration induces increased proliferation of progenitors in the outer nuclear layer (ONL) and is not associated with proliferation or reactive gliosis in the inner nuclear layer (INL). Molecular characterization of the rod progenitor cells demonstrated that they are committed to the rod photoreceptor fate while they are still mitotic. In contrast, cone degeneration induces both Müller cell proliferation and reactive gliosis, with little change in proliferation in the ONL. We found that in both lines, proliferative responses to photoreceptor degeneration can be observed as 7 days post fertilization (dpf). These two genetic models therefore offer new opportunities for investigating the molecular mechanisms of selective degeneration and regeneration of rods and cones. © 2008 Wiley Periodicals, Inc. Develop Neurobiol, 2008. [source] Distinct pattern of microglial response, cyclooxygenase-2, and inducible nitric oxide synthase expression in the aged rat brain after excitotoxic damageJOURNAL OF NEUROSCIENCE RESEARCH, Issue 14 2008O. Campuzano Abstract Microglial and inflammatory responses to acute damage in aging are still poorly understood, although the aged brain responds differently to injury, showing poor lesion outcome. In this study, excitotoxicity was induced by intrastriatal injection of N-methyl-D-aspartate in adult (3,4 months) and aged (22,24 months) rats. Cryostat brain sections were processed for the analysis of microglial response by lectin histochemistry and cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS) expression by immunohistochemistry and confocal analysis. Aged injured animals showed more widespread area of microglial response at 12 hr postlesion (hpl) and greater microglia/macrophage density at 3 days postlesion (dpl). However, aged reactive microglia showed prevalence of ramified morphologies and fewer amoeboid/round forms. Aged injured animals presented a diminished area of COX2 expression, but a significantly larger density of COX2+ cells, with higher numbers of COX2+ neurons during the first 24 hpl and COX2+ microglia/macrophages later. In contrast, the amount of COX2+ neutrophils was diminished in the aged. iNOS was more rapidly induced in the aged injured striatum, with higher cell density at 12 hpl, when expression was mainly neuronal. From 1 dpl, both the iNOS+ area and the density of iNOS+ cells were reduced in the aged, with lower numbers of iNOS+ neurons, microglia/macrophages, neutrophils, and astrocytes. In conclusion, excitotoxic damage in aging induces a distinct pattern of microglia/macrophage response and expression of inflammatory enzymes, which may account for the changes in lesion outcome in the aged, and highlight the importance of using aged animals for the study of acute age-related insults. © 2008 Wiley-Liss, Inc. [source] The effect of tibial lengthening using the Ilizarov method on the cartilage and the menisci of the knee jointJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 4 2001Bernd Fink In order to investigate possible acute damage to the knee joint cartilage and the menisci during tibial lengthening, sixteen young beagle dogs underwent 30% lengthening of the right tibia of 2.5 cm by callus distraction at a distraction rate of twice 0.5 mm per day. A further four dogs comprised the control group with fixator and osteotomy but without lengthening. After a distraction period of 25 days half the dogs were killed (group A) while the other half (eight dogs with limb lengthening and two dogs without) were killed after a further period of 25 days (group B). At the end of the study, the menisci were removed together with three cartilage-bone cylinders from both femoral condyles from the weight-bearing zones as well as from the corresponding tibial condyles. Serial sections from the menisci were stained with haematoxylin and eosin (H&E) and Elastica van Gieson. Sections of the cartilage-bone cylinders were stained with H&E and safranin-O. Cartilage thickness was measured and the glycosaminoglycan content of the joint cartilage was determined using microspectrophotometry. None of the histological preparations obtained from the untreated and distracted sides showed any signs of damage to the cartilage or to the menisci. There were no significant differences between cartilage thickness and proteoglycan content of the untreated side and the lengthened side. Thus, tibial lengthening using the Ilizarov method does not appear to cause acute damage to the cartilage of the knee joint or to the menisci. © 2001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Effect of oral glucosamine on cartilage and meniscus in normal and chymopapain-injected knees of young rabbitsARTHRITIS & RHEUMATISM, Issue 9 2002Theodore R. Oegema Jr. Objective To determine if oral glucosamine (GlcN) improves joint biology after acute damage by a protease. Methods The effect of 8 weeks of dietary GlcN (20 or 100 mg/kg/day) on knee joint cartilage was evaluated in 2.2-kg male NZW rabbits with and without damage introduced by intraarticular injection of chymopapain (CP). Cartilage was evaluated histologically and scored according to the Mankin scale. Analyses of total hydroxyproline and glycosaminoglycan (GAG) contents and reverse transcription,polymerase chain reaction (RT-PCR) analysis of selected genes were performed. Results After 8 weeks, there was no effect of GlcN on the GAG content of normal cartilage. Both levels of GlcN treatment significantly increased the sulfated GAG content in the cartilage of the medial femoral condyle in damaged and contralateral knees, but did not change the collagen content. In CP-injected knees, there was still some loss of surface proteoglycan (PG) that was not completely corrected by dietary GlcN. Even after 8 weeks, levels of messenger RNA (mRNA) detected by RT-PCR showed changes indicative of damage and repair, such as elevated type II collagen mRNA, and these levels were not influenced by GlcN treatment. Meniscal GAG content was increased in the contralateral knee of rabbits receiving high-dose GlcN, but was decreased in those receiving no GlcN or low-dose GlcN. Neither diet nor treatment affected the meniscal collagen content. Conclusion These results suggest that oral GlcN treatment might be useful in a situation where GlcN is limiting, such as where there is a rapid replacement of cartilage PG. [source] Permanent alopecia after busulfan chemotherapyBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2005A. Tosti Summary Systemic chemotherapy is a well known cause of reversible hair loss. Busulfan chemotherapy, however, is responsible for a permanent alopecia that usually occurs in bone marrow transplant patients. We report two patients with permanent alopecia due to busulfan chemotherapy. Both patients had a diffuse alopecia characterized by greatly reduced hair density with short, thin hair. The pathology showed reduced follicular density in the absence of fibrosis, suggesting that alopecia may result either from hair follicle stem cell destruction or from acute damage to the keratinocytes of the lower portion of some follicles. 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