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Fiber Loss (fiber + loss)
Selected AbstractsStudies on internal and external water treatment at a paper and cardboard factoryJOURNAL OF CHEMICAL TECHNOLOGY & BIOTECHNOLOGY, Issue 5 2003Mamdouh M Nassar Abstract The treatment of effluent from a paper/board factory that produced 280 tons of cardboard and consumed 1200 m3 of water per day was carried out. Wastewater analysis showed that the mill effluent contained 3000 mg dm,3 suspended solids, 1400 mg dm,3 COD (chemical oxygen demand) and 500 mg dm,3 BOD (biochemical oxygen demand). An internal treatment cycle is suggested that involves recirculation of paper-machine wastewater (white-water) and may be accomplished by installing a flotation saveall (fiber recovery) unit. This arrangement reduced fresh water use by about 90%, reduced fiber loss by 80,90%, and increased board production by 13%. An external treatment process for the effluent was assessed by conducting laboratory coagulation tests (alum, ferric chloride, ferrous sulfate, and polyelectrolyte) on the whole mill effluent. Oxidation of the mill effluent using calcium hypochlorite before discharging the effluent to a lagoon offers the benefits of killing the harmful bacteria and reducing the pollution load. Copyright © 2003 Society of Chemical Industry [source] Molecular architecture of myelinated peripheral nerves is supported by calorie restriction with agingAGING CELL, Issue 2 2009Sunitha Rangaraju Summary Peripheral nerves from aged animals exhibit features of degeneration, including marked fiber loss, morphological irregularities in myelinated axons and notable reduction in the expression of myelin proteins. To investigate how protein homeostatic mechanisms change with age within the peripheral nervous system, we isolated Schwann cells from the sciatic nerves of young and old rats. The responsiveness of cells from aged nerves to stress stimuli is weakened, which in part may account for the observed age-associated alterations in glial and axonal proteins in vivo. Although calorie restriction is known to slow the aging process in the central nervous system, its influence on peripheral nerves has not been investigated in detail. To determine if dietary restriction is beneficial for peripheral nerve health and glial function, we studied sciatic nerves from rats of four distinct ages (8, 18, 29 and 38 months) kept on an ad libitum (AL) or a 40% calorie restricted diet. Age-associated reduction in the expression of the major myelin proteins and widening of the nodes of Ranvier are attenuated by the dietary intervention, which is paralleled with the maintenance of a differentiated Schwann cell phenotype. The improvements in nerve architecture with diet restriction, in part, are underlined by sustained expression of protein chaperones and markers of the autophagy,lysosomal pathway. Together, the in vitro and in vivo results suggest that there might be an age-limit by which dietary intervention needs to be initiated to elicit a beneficial response on peripheral nerve health. [source] Microvasculitis In Non-Diabetic Lumbosacral Radiculoplexus Neuropathy (LSRPN): Similarity To The Diabetic Variety (DLSRPN)JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2001Pjb Dyck Diabetic lumbosacral radiculoplexus neuropathy (DLSRPN) has been shown to be due to ischemic injury from microvasculitis. The present study tests whether ischemic injury and microvasculitis are the pathologic cause of non-diabetic lumbosacral radiculoplexus neuropathy (LSRPN), and whether the pathologic alterations are different between LSRPN and DLSRPN. We studied distal cutaneous nerve biopsies of 47 patients with LSRPN and compared findings with those of 14 age-matched healthy controls and 33 DLSRPN patients. In both disease conditions, we found evidence of ischemic injury (multifocal fiber degeneration and loss, perineurial degeneration and scarring, characteristic fiber alterations, neovascularization, and injury neuroma) that we attribute to microvasculitis (mural and perivascular mononuclear inflammation of microvessels, inflammatory separation, fragmentation and destruction of mural smooth muscle, and previous microscopic bleeding [hemosiderin]). Teased nerve fibers in LSRPN showed significantly increased frequencies of axonal degeneration, segmental demyelination, and empty nerve strands. The segmental demyelination appeared to be clustered on fibers with axonal dystrophy. The nerves with abnormal frequencies of demyelination were significantly associated with nerves showing multifocal fiber loss. We reached the following conclusions: 1) LSRPN is a serious condition with much morbidity that mirrors DLSRPN. 2) Ischemic injury from microvasculitis appears to be the cause of LSRPN. 3) Axonal degeneration and segmental demyelination appear to be linked and due to ischemia. 4) The pathologic alterations in LSRPN and DLSRPN are indistinguishable, raising the question whether these 2 conditions have a common underlying mechanism, and whether diabetes mellitus contributes to the pathology or is a risk factor in DLSRPN. 5) Both LSRPN and DLSRPN are potentially treatable conditions. [source] Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: New insights into pathophysiology and treatmentMUSCLE AND NERVE, Issue 4 2002P. James B. Dyck MD Abstract Diabetic lumbosacral radiculoplexus neuropathy (DLRPN) (also called diabetic amyotrophy) is a well-recognized subacute, painful, asymmetric lower-limb neuropathy that is associated with weight loss and type II diabetes mellitus. Nondiabetic lumbosacral radiculoplexus neuropathy (LRPN) has received less attention. Comparison of large cohorts with DLRPN and LRPN demonstrated that age at onset, course, type and distribution of symptoms and impairments, laboratory findings, and outcomes are similar. Both conditions are lumbosacral radiculoplexus neuropathies that are associated with weight loss and begin focally with pain but that evolve into widespread, bilateral paralytic disorders. Although both are monophasic illnesses, patients have prolonged morbidity from pain and weakness, and many patients become wheelchair-dependent. Although motor-predominant, there is unequivocal evidence that autonomic and sensory nerves are also involved. Cutaneous nerves from patients with DLRPN and LRPN show pathological evidence of ischemic injury (multifocal fiber loss, perineurial thickening and degeneration, neovascularization, microfasciculation, and swollen axons with accumulated organelles) and microvasculitis (mural and perivascular inflammation, separation and fragmentation of mural smooth muscle layers of microvessels and hemosiderin-laden macrophages). Controlled trials with immune-modulating therapies in DLRPN are in progress, and preliminary data suggest that such therapy may be beneficial in LRPN. It is likely that DLRPN and LRPN are immune-mediated neuropathies that should be separated from chronic inflammatory demyelinating polyneuropathy and from systemic necrotizing vasculitis. © 2002 Wiley Periodicals, Inc. Muscle Nerve 25: 000,000, 2002 [source] Disrupted myelin and axon loss in the anterior commissure of the aged rhesus monkeyTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2003Julie H. Sandell Abstract This study assesses the effects of age on the composition of the anterior commissure of the rhesus monkey. The anterior commissures of nine young (5,10 years), five middle-aged (15,20 years), and eight old (25,35 years) monkeys were examined by light and electron microscopy. In all, 90,95% of the nerve fibers in the anterior commissure are myelinated. With age, the structure of the myelin sheaths of some nerve fibers is altered. Some of the axons also show signs of degeneration and this leads to a loss of nerve fibers. Thus, in young and the middle-aged monkeys the mean number of myelinated nerve fibers in the anterior commissure is 2.2 × 106, while in the old monkeys the mean is 1.2 × 106. Increasing age is correlated with a reduction in the number of myelinated nerve fibers in the anterior commissure, an increase in the frequency of structural alterations in myelin sheaths, and an increase in the frequency of occurrence of degenerating axons. However, the number of myelinated nerve fibers is the only variable that correlates with cognition: in monkeys 5,20 years of age the fewer the number of nerve fibers the poorer the cognitive performance, as measured by our Cognitive Impairment Index (CII). The most common neuroglial cells in the anterior commissure are oligodendrocytes. They account for 86% of all neuroglial cell profiles, while astrocytes account for 9%, and microglial cells for 5% of profiles. There is no apparent change with age in the total numbers of neuroglial cells, although as they age each of the neuroglial cell types acquires some inclusions in their cytoplasm. The data, together with those from previous studies, support the concept that in aging there is a ubiquitous loss of myelinated nerve fibers from the brain and that fiber loss is preceded by alterations in the structure of many of the myelin sheaths. J. Comp. Neurol. 466:14,30, 2003. © 2003 Wiley-Liss, Inc. [source] Sural nerve biopsy may predict future nerve dysfunctionACTA NEUROLOGICA SCANDINAVICA, Issue 1 2009S. Thrainsdottir Objective,,, Sural nerve pathology in peripheral neuropathy shows correlation with clinical findings and neurophysiological tests. The aim was to investigate progression of nerve dysfunction over time in relation to a baseline nerve biopsy. Methods,,, Baseline myelinated nerve fiber density (MNFD) was assessed in sural nerve biopsies from 10 men with type 2 diabetes, 10 with impaired and 10 with normal glucose tolerance. Nerve conduction and quantitative perception thresholds were estimated at baseline and follow-up (7,10 years later). Results,,, Subjects with low MNFD (,,4700 fibers/mm2) showed decline of peroneal amplitude (P < 0.02) and conduction velocity (P < 0.04), as well as median nerve sensory amplitude (P < 0.05) and motor conduction velocity (P < 0.04) from baseline to follow-up. In linear regression analyses, diabetes influenced decline of nerve conduction. MNFD correlated negatively with body mass index (r = ,0.469; P < 0.02). Conclusion,,, Low MNFD may predict progression of neurophysiological dysfunction and links obesity to myelinated nerve fiber loss. [source] | |||||||||||||