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The radiobiology was characterized by in vivo irradiation of rat liver, dog liver, and dog brain. The animals were killed at varying intervals of time, and histological examinations were performed. Rats and dogs that were killed weeks to months after liver irradiation tended to have sharply demarcated lesions. Liver enzyme levels, measured serially in the dogs, did not give evidence of chronic inflammation.

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The study involved a group of 88 consecutively studied patients with clinical and radiological evidence of idiopathic NPH, for whom a frontal brain biopsy was obtained. For 79 patients, hydrodynamic criteria of NPH were fulfilled and a ventriculoperitoneal shunt was performed. The dosimetry was characterized by two independent methods: thermoluminescent dosimeters and radiochromic film.

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We previously showed in vivo that coding-end processing is specific for each coding end, suggesting that specific motifs in a coding-end sequence influence nucleotide deletion and P-region formation. In this study, we created a panel of recombination substrates containing actual immunoglobulin and T-cell receptor coding-end sequences and dissected the role of each motif by comparing its processing pattern with those of variants containing minimal nucleotide changes from the original sequence.

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Furthermore, possible correlations between white matter lesion scores, ventricular width, and age were investigated. Normal-pressure hydrocephalus (NPH) is a potentially treatable syndrome with abnormal cerebrospinal fluid dynamics. Meningeal fibrosis and/or obliteration of the subarachnoid space has been suggested as the pathoanatomic basis. The purpose of the present study was to investigate whether meningeal fibrosis causes increased resistance to cerebrospinal fluid outflow (R(out)) and/or increased B-wave activity and whether pathological changes in the brain parenchyma after brain compliance, causing increased B-wave activity.

Eight patients reported excellent pain relief, and four patients described good results. SCS is an effective treatment for the pain of RSD, including recurrent pain after ablative sympathectomy. The low morbidity of this procedure and its efficacy in patients with refractory pain related to RSD suggest that SCS is superior to ablative sympathectomy in the management of RSD.

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Our results demonstrate the determinant role of specific sequence motifs on coding-end processing and also the importance of the context in which they are found. We propose that each coding-end sequence dictates a unique hairpin structure, the result of a particular energy conformation between nucleotides organizing the loop and the stem, and that the interplay between this structure and specific sequence motifs influences the frequency and location of nicks which open the coding-end hairpin. These findings indicate that the sequences of the coding ends determine their own processing and have a profound impact on the development of the primary B- and T-cell repertoires.

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The results suggest that leptomeningeal fibrosis is not the only pathoanatomic basis of increased R(out) and/or B-wave activity in patients with NPH and that various degenerative changes in the parenchyma may be responsible for the altered cerebrospinal fluid dynamics characteristic of NPH. The purpose of this study was to determine the efficacy of spinal cord stimulation (SCS) in patients with symptoms of reflex sympathetic dystrophy (RSD), a disabling clinical condition with significant consequences of morbidity and loss of productivity.

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