61. |
- Andreasen, F M, et al.
(författare)
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Long-term survival of fragment bonding in the treatment of fractured crowns: a multicenter clinical study.
- 1995
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Ingår i: Quintessence international (Berlin, Germany : 1985). - 0033-6572. ; 26:10, s. 669-81
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Tidskriftsartikel (refereegranskat)abstract
- In three Scandinavian dental facilities, a series of 334 permanent incisors with fractures of the crown or crown and root was treated by reattachment of the fragment with a resin composite. Two centers (Oslo and Stockholm) employed acid etching of enamel alone for fragment bonding (n = 146), while the third center (Copenhagen) used a combination of enamel etching and dentinal bonding (n = 188). Although the final retention rate of fragment bonding was similar in the two groups, it took the dentinal bonding group almost three times as long to drop to 50% fragment retention. This difference could be attributed to greater bonding strength in the dentinal bonding group, greater risk of second injury in the younger acid-etching group, or difficulty in maintaining a dry operative field in the younger age group. The good fragment retention, acceptable esthetics, and pulpal vitality observed in the present series indicate that reattachment of the coronal fragment is a realistic alternative to placement of conventional resin-composite restorations.
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66. |
- Andreasson, M., et al.
(författare)
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Altered CSF levels of monoamines in hereditary spastic paraparesis 10 A case series
- 2019
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Ingår i: Neurology-Genetics. - : Ovid Technologies (Wolters Kluwer Health). - 2376-7839. ; 5:4
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Tidskriftsartikel (refereegranskat)abstract
- Objective To perform a comprehensive clinical characterization and biochemical CSF profile analyses in 2 Swedish families with hereditary spastic paraparesis (HSP) 10 (SPG10) caused by 2 different mutations in the neuronal kinesin heavy chain gene (KIF5A). Methods Structured clinical assessment, genetic studies, and neuroradiologic and electrophysiological evaluations were performed in 4 patients from 2 families with SPG10. Additional CSF analysis was conducted in 3 patients with regard to levels of neurodegenerative markers and monoamine metabolism. Results All patients exhibited a complex form of HSP with a mild to moderate concurrent axonal polyneuropathy. The heterozygous missense mutations c.767A>G and c.967C>T in KIF5A were found. Wide intrafamilial phenotype variability was evident in both families. CSF analysis demonstrated a mild elevation of neurofilament light (NFL) chain in the patient with longest disease duration. Unexpectedly, all patients exhibited increased levels of the dopamine metabolite, homovanillic acid, whereas decreased levels of the noradrenergic metabolite, 3-methoxy-4-hydroxyphenylglycol, were found in 2 of 3 patients. Conclusions We report on CSF abnormalities in SPG10, demonstrating that NFL elevation is not a mandatory finding but may appear after long-standing disease. Impaired transportation of synaptic proteins may be a possible explanation for the increased dopaminergic turnover and noradrenergic deficiency identified. The reasons for these selective abnormalities, unrelated to obvious clinical features, remain to be explained. Our findings need further confirmation in larger cohorts of patients harboring KIF5A mutations.
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