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Permanent Damage (permanent + damage)
Selected AbstractsNew concepts in bilirubin encephalopathyEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2003J. D. Ostrow Abstract Revised concepts of bilirubin encephalopathy have been revealed by studies of bilirubin toxicity in cultured CNS cells and in congenitally jaundiced Gunn rats. Bilirubin neurotoxicity is related to the unbound (free) fraction of unconjugated bilirubin (Bf), of which the dominant species at physiological pH is the protonated diacid, which can passively diffuse across cell membranes. As the binding affinity of plasma albumin for bilirubin decreases strikingly as albumin concentration increases, previously reported Bf values were underestimated. Newer diagnostic tests can detect reversible neurotoxicity before permanent damage occurs from precipitation of bilirubin (kernicterus). Early toxicity can occur at Bf only modestly above aqueous saturation and affects astrocytes and neurons, causing mitochondrial damage, resulting in impaired energy metabolism and apoptosis, plus cell-membrane perturbation, which causes enzyme leakage and hampers transport of neurotransmitters. The concentrations of unbound bilirubin in the cerebro-spinal fluid and CNS cells are probably limited mainly by active export of bilirubin back into plasma, mediated by ABC transporters present in the brain capillary endothelium and choroid plexus epithelium. Intracellular bilirubin levels may be diminished also by oxidation, conjugation and binding to cytosolic proteins. These new concepts may explain the varied susceptibility of neonates to develop encephalopathy at any given plasma bilirubin level and the selective distribution of CNS lesions in bilirubin encephalopathy. They also can suggest better strategies for predicting, preventing and treating this syndrome. [source] Interactions between land use, habitat use, and population increase in greater snow geese: what are the consequences for natural wetlands?GLOBAL CHANGE BIOLOGY, Issue 6 2005Gilles Gauthier Abstract The North American greater snow goose population has increased dramatically during the last 40 years. We evaluated whether refuge creation, changes in land use on the wintering and staging grounds, and climate warming have contributed to this expansion by affecting the distribution, habitat use, body condition, and migration phenology of birds. We also reviewed the effects of the increasing population on marshes on the wintering grounds, along the migratory routes and on the tundra in summer. Refuges established before 1970 may have contributed to the initial demographic increase. The most important change, however, was the switch from a diet entirely based on marsh plants in spring and winter (rhizomes of Scirpus/Spartina) to one dominated by crops (corn/young grass shoots) during the 1970s and 1980s. Geese now winter further north along the US Atlantic coast, leading to reduced hunting mortality. Their migratory routes now include portions of southwestern Québec where corn production has increased exponentially. Since the mid-1960s, average temperatures have increased by 1,2.4°C throughout the geographic range of geese, which may have contributed to the northward shift in wintering range and an earlier migration in spring. Access to spilled corn in spring improved fat reserves upon departure for the Arctic and may have contributed to a high fecundity. The population increase has led to intense grazing of natural wetlands used by geese although these habitats are still largely undamaged. The foraging in fields allowed the population to exceed limits imposed by natural marshes in winter and spring, but also prevented permanent damage because of their overgrazing. [source] Stress and hippocampal plasticity: implications for the pathophysiology of affective disordersHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue S1 2001Bruce S. McEwen Abstract The hippocampal formation, a structure involved in declarative, spatial and contextual memory, is a particularly sensitive and vulnerable brain region to stress and stress hormones. The hippocampus shows a considerable degree of structural plasticity in the adult brain. Stress suppresses neurogenesis of dentate gyrus granule neurons, and repeated stress causes atrophy of dendrites in the CA3 region. In addition, ovarian steroids regulate synapse formation during the estrous cycle of female rats. All three forms of structural remodeling of the hippocampus are mediated by hormones working in concert with excitatory amino acids (EAA) and N -methyl- D -aspartate (NMDA) receptors. EAA and NMDA receptors are also involved in neuronal death that is caused in pyramidal neurons by seizures and by ischemia and prolonged psychosocial stress. In the human hippocampus, magnetic resonance imaging studies have shown that there is a selective atrophy in recurrent depressive illness, accompanied by deficits in memory performance. Hippocampal atrophy may be a feature of affective disorders that is not treated by all medications. From a therapeutic standpoint, it is essential to distinguish between permanent damage and reversible atrophy in order to develop treatment strategies to either prevent or reverse deficits. In addition, remodeling of brain cells may occur in other brain regions. Possible treatments are discussed. Copyright © 2001 John Wiley & Sons, Ltd. [source] Relative longevity and field metabolic rate in birdsJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 5 2008A. P. MØLLER Abstract Metabolism is a defining feature of all living organisms, with the metabolic process resulting in the production of free radicals that can cause permanent damage to DNA and other molecules. Surprisingly, birds, bats and other organisms with high metabolic rates have some of the slowest rates of senescence begging the question whether species with high metabolic rates also have evolved mechanisms to cope with damage induced by metabolism. To test whether species with the highest metabolic rates also lived the longest I determined the relationship between relative longevity (maximum lifespan), after adjusting for annual adult survival rate, body mass and sampling effort, and mass-specific field metabolic rate (FMR) in 35 species of birds. There was a strongly positive relationship between relative longevity and FMR, consistent with the hypothesis. This conclusion was robust to statistical control for effects of potentially confounding variables such as age at first reproduction, latitude and migration distance, and similarity in phenotype among species because of common phylogenetic descent. Therefore, species of birds with high metabolic rates senesce more slowly than species with low metabolic rates. [source] Targeted Cytotoxic Analogue of Luteinizing Hormone-Releasing Hormone (LH-RH) Only Transiently Decreases the Gene Expression of Pituitary Receptors for LH-RHJOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2002M. Kovacs Abstract A cytotoxic analogue of LH-RH, AN-207, consisting of 2-pyrrolinodoxorubicin (AN-201) linked to carrier [D-Lys6]LH-RH, was developed for targeted therapy of cancers expressing LH-RH-receptors. To determine its possible side-effects on the pituitary gland, we investigated the gene expression of pituitary LH-RH-receptors and LH secretion in ovariectomized female and normal male rats after treatment with the maximum tolerated dose of AN-207. The effect of AN-207 on the gene expression of the pituitary GH-RH-receptors and GH secretion was also assessed in male rats. Five hours after a single i.v. injection of AN-207 at 175 nmol/kg, there was a 39,51% decrease in mRNA expression for the pituitary LH-RH-receptors in male and female rats. The carrier, at an equimolar dose, caused a similar reduction (37,39%), whereas the cytotoxic radical AN-201, at an equitoxic dose (110 nmol/kg), produced only a 12,24% decrease (NS) in the mRNA expression of LH-RH-receptors. AN-207 and the carrier analogue induced a comparable 90,100-fold increase in serum LH concentrations in male rats, and the same 12-fold elevation in OVX rats at 5 h. Seven days after treatment with AN-207, the mRNA levels for the LH-RH receptors and the serum LH concentration were back to normal in both sexes. AN-207, the carrier, and AN-201 had no significant effect on the expression of mRNA for GH-RH-receptors in the pituitary. In vitro, a continuous perfusion of pituitary cells with 10 nM AN-207 did not affect the hormone-releasing function of the targeted LH cells or the nontargeted GH cells. Our results demonstrate that cytotoxic LH-RH analogue AN-207, at the maximum tolerated dose causes only a transient decrease in the gene expression of the pituitary LH-RH receptors, and the levels of mRNA for LH-RH receptor fully recover within 7 days. Moreover, the carrier hormone moiety, and not the cytotoxic radical in AN-207 is responsible for this transient suppression. Our findings suggest that the therapy with cytotoxic LH-RH analogues will not inflict permanent damage to pituitary function. [source] Electrophysiological Changes In Diabetic Neuropathy: From Subclinical Alterations To Disabling AbnormalitiesJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000M. Baba Clinical spectrum of diabetic neuropathy is variable; it may be asymptomatic, but once established, it becomes irreversible and disabling. Some investigators suggested that earliest change in diabetic nerve function is alteration in axonal excitability due to alterations in ion conductance of axon membrane, although these functional changes of ion channels necessarily cause permanent damage or degeneration of nerve fibers. Among various parameter of nerve conduction study in diabetics, prolonged F-wave latency in the peroneal and tibial nerve seems the commonest abnormality in asymptomatic patients. Decrease in amplitude of compound sensory action potential of sural nerve is another earlier abnormality, which is, then, accompanied by a fall in motor amplitude of peroneal and tibial nerves in advanced patients. In disabled patients no motor response is often elicited in the legs. Previous electrophysiological studies could not make clear if central axons were involved or not in diabetic neuropathy. Recently, our group has demonstrated that somatosensory central conduction from the spinal cord to the sensory cortex is delayed in diabetics as well as in the peripheral conduction, which might be partly responsible for the irreversible clinical presentation of diabetic neuropathy. [source] The use of vein grafts in the repair of the inferior alveolar nerve following surgeryAUSTRALIAN DENTAL JOURNAL, Issue 2 2010RHB Jones Abstract Damage to the branches of the trigeminal nerve can occur as a result of a variety of causes. The most common damage to all divisions of this nerve occurs as a result of facial trauma. Unfortunately, iatrogenic damage to the inferior alveolar branch of the mandibular division of the trigeminal nerve is common because of its anatomical position within the mandible and its closeness to the teeth, particularly the third molar. It has been reported there is an incidence of approximately 0.5% of permanent damage to the inferior alveolar nerve following third molar removal. Extraction of other teeth within the mandible carries a lower incidence of permanent damage. However, damage can still occur in the premolar area, where the nerve exits the mandible via the mental foramen. Dental implants are a relatively new but increasing cause of damage to this nerve, particularly if the preoperative planning is inadequate. CT scanning is important for planning the placement of implants if this damage is to be reduced. Primary repair of the damaged nerve will offer the best chance of recovery. However, if there is a gap, and the nerve ends cannot be approximated without tension, a graft is required. Traditionally, nerve grafts have been used for this purpose but other conduits have also been used, including vein grafts. This article demonstrates the use of vein grafts in the reconstruction of the inferior dental branch of the mandibular division of the trigeminal nerve following injury, in this case due to difficulty in third molar removal, following sagittal split osteotomy and during the removal of a benign tumour from the mandible. In the five cases presented, this technique has demonstrated good success, with an acceptable return of function occurring in most patients. [source] Post-polio syndrome: epidemiologic and prognostic aspects in BrazilACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009M. T. R. P. Conde Objectives,,, To describe the clinical and epidemiological aspects of post-polio syndrome (PPS) and identify predictors of its severity. Materials and methods,,, 132 patients with PPS were selected at the Neuromuscular Disease Outpatient Clinic of the Federal University of São Paulo. Descriptive analysis was carried out and predictors of PPS severe forms were investigated using an unconditional logistic regression. Results,,, The average age at onset was 39.4 years. The most common symptoms were fatigue (87.1%), muscle pain (82.4%) and joint pain (72.0%); 50.4% of the cases were severe. The following were associated with PPS severity: a ,4-year period of neurological recovery (OR 2.8), permanent damage in two limbs (OR 3.6) and residence at the time of acute polio in a city with more advanced medical assistance (OR 2.5). Conclusions,,, Health professionals should carefully evaluate polio survivors for PPS and be aware of the implications of muscle overuse in the neurological recovery period. [source] Serious complications of cosmetic NewColorIris implantationACTA OPHTHALMOLOGICA, Issue 6 2010Justin E. Anderson Acta Ophthalmol. 2010: 88: 700,704 Abstract. Purpose:, This case report describes serious postoperative complications and markedly elevated intraocular pressure (IOP) associated with the NewColorIris cosmetic implant. Methods:, We report an interventional case series of two patients who suffered multiple complications after NewColorIris implantation carried out in Panama. Assessment included visual acuity, photography, endothelial cell count and anterior segment optical coherence tomography (OCT) when possible. Results:, Both patients presented with endothelial cell loss, uveitis, pigment dispersion and elevated IOP. Anterior segment OCT demonstrated irregularities in the position and configuration of the implants within the anterior chamber with resultant areas of implant,iris and implant,endothelial contact. One patient had acute postoperative hyphaema that resolved with anterior chamber tissue plasminogen activator injection. Both patients required explantation OU, one eye has required trabeculectomy, and one eye with bullous keratopathy is being evaluated for Descemet's stripping endothelial keratoplasty. Conclusions:, Implantation of the NewColorIris cosmetic implant can lead to serious complications including hyphaema, uncontrolled IOP, severe endothelial cell loss, bullous keratopathy and anterior uveitis. Explantation may lead to improvement, but permanent damage to the trabecular meshwork and corneal endothelium persists. [source] Mycobacterial infection in a series of 1261 renal transplant recipientsCLINICAL MICROBIOLOGY AND INFECTION, Issue 6 2003J. A. Queipo Objective To describe the incidence and clinical characteristics of mycobacterial infection in renal transplant recipients. Methods We retrospectively analyzed the cases of mycobacterial infection in a series of 1261 renal transplants carried out in our Unit of Renal Transplantation from 1980 to 2000. Demographic parameters and clinical antecedents such as age, cause of end-stage renal disease, time of follow-up of the graft, previous renal function and type of immunosuppression were considered. Moreover, the clinical onset, diagnostic tools, treatment policy and evolution were studied. The pathogenesis of the different types of mycobacteria isolated was also analyzed. Diagnosis was made with the Ziehl,Neelsen staining method. Culture was performed by the conventional Löwenstein,Jensen method and the Bactec-460 radiometric method. Results We found mycobacterial infection in 27 patients (2.1%), due to Mycobacterium tuberculosis in 20 cases, M. kansasii in five patients, and M. fortuitum in two patients. The mean elapsed time from the renal transplant was 20.5 months; the infection appeared in 18 patients during the first eight months after transplantation. The clinical onset was pulmonary infection in 17 cases (12 M. tuberculosis and five M. kansasii); five had urinary symptoms (three M. tuberculosis and two M. fortuitum); three cases of M. tuberculosis infection had abdominal symptoms; another one began with a perineal tuberculous abscess; the rest of the patients were asymptomatic. The types of specimen on which microbiological identification was carried out were, in decreasing order: sputum and/or bronchial washing/pleural aspiration, urine, feces, gastric and peritoneal fluids, bone marrow and blood. The first-line drug isoniazid had the highest resistance index in the susceptibility test. Clinical dissemination was observed in eight patients, four of whom died. Another three patients had a significant impairment in renal function, and in one of these patients an allograft nephrectomy was necessary due to a severe septic syndrome. Conclusions Mycobacterial infection, mainly by M. tuberculosis, has an important impact on kidney transplant recipients, particularly during the first year after surgery. Diagnosis often presents some difficulties, and a delay in treatment represents a determinant factor for the evolution, with a risk of death or permanent damage in renal function. Therefore, early diagnosis is mandatory. When the Mantoux reaction is positive, antituberculous prophylaxis seems advisable. [source] | |||||||||||||