Surfactant coated FePt nanoparticles were characterized using Fourier transform infrared spectroscopy (FTIR). The FTIR spectra indicate that there is a conversion of the alkyl chain of the surfactant from the oleyl form (cis-9-octadecenyl) to the elaidyl form (trans-9-octadecenyl) during the synthesis of the FePt nanoparticles. This is revealed by the presence of several vibrational absorption bands in the region of the olefinic CH stretching modes. The appearance of infrared absorption bands due to olefinic CH stretching is due to the presence of Fe in the nanoparticles. The FTIR spectrum of platinum nanoparticles does not reveal the presence of olefinic CH modes. The concentration of Fe in the FePt nanoparticles influences the intensity of the olefinic CH stretching modes. The high intensity of these olefinic CH modes in nanoparticles with high Fe concentration indicates that Fe acts as a catalyst for cis to trans conversion and may lead to dehydrogentation of the alkyl chains.

Ordered self-assembled monolayers of FePt nanoparticles have been studied for the first time on fluorinated carbon thin film substrates. High resolution scanning electron microscopy of the resulting films showed homogenous hexagonally closed packed monolayers of FePt ordered over length scales of several millimeters. The annealing of self-assembled monolayers of FePt nanoparticles at 600 degrees C for 30 min showed significantly less sintering than on other types of substrates and the hexagonal ordering of the self-assembled monolayers was preserved during the annealing step. This is a significant step towards development of a viable patterned media for high density data storage. (c) 2006 Elsevier B.V. All rights reserved.

OBJECTIVES To describe the clinical and neuroradiological features of basilar impression in patients with osteogenesis imperfecta type IV. METHODS Four patients with basilar impression were ascertained in a population study of osteogenesis imperfecta. All four had detailed clinical and neuroradiological examination with both CT and MRI of the craniocervical junction andposterior fossa structures. RESULTS All four showed significant compression of the posterior fossa structures and surgical decompression was performed with relief of symptoms. CONCLUSION Symptoms of cough headache and trigeminal neuralgia occurring in patients with osteogenesis imperfecta are indications for detailed clinical and neuroradiological investigation to document basilar impression.

British Journal of HaematologyVolume 79, Issue 3 p. 521-523 FATAL PERIPHERAL NEUROPATHY ASSOCIATED WITH AXONAL DEGENERATION AFTER HIGH-DOSE CYTOSINE ARABINOSIDE IN ACUTE LEUKAEMIA M. Paul, M. Paul Department of Haematology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorD. Joshua, D. Joshua Department of Haematology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorN. Rahme, N. Rahme Department of Haematology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorJ. Pollard, J. Pollard Department of Neurology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorJ. Ell, J. Ell Department of Neurology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorJ. Gibson, J. Gibson Department of Haematology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorD. Bonnet, D. Bonnet Hopital Gaston Bourret, Noumea, New CaledoniaSearch for more papers by this author M. Paul, M. Paul Department of Haematology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorD. Joshua, D. Joshua Department of Haematology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorN. Rahme, N. Rahme Department of Haematology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorJ. Pollard, J. Pollard Department of Neurology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorJ. Ell, J. Ell Department of Neurology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorJ. Gibson, J. Gibson Department of Haematology, Royal Prince Alfred Hospital, Sydney, AustraliaSearch for more papers by this authorD. Bonnet, D. Bonnet Hopital Gaston Bourret, Noumea, New CaledoniaSearch for more papers by this author First published: November 1991 https://doi.org/10.1111/j.1365-2141.1991.tb08067.xCitations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat REFERENCES Bayard, L., Powell, R. L., Capizzi, E., Lyerly, S. & Cooper, M. R. (1986) Peripheral neuropathy after high-dose cytosine arabinoside, daunorubicin, and asparaginase consolidation for acute nonlymphocyte leukemia. Journal of Clinical Oncology, 4, 95–97. PubMedWeb of Science®Google Scholar Borgeat, A., De Muralt, B. & Stalder, M. (1986) Peripheral neuropathy associated with high-dose Ara-C therapy. Cancer, 58, 852–854. 10.1002/1097-0142(19860815)58:4<852::AID-CNCR2820580408>3.0.CO;2-I CASPubMedWeb of Science®Google Scholar Capizzi, R. L., Yan, J. -L., Cheng, E., Bjornsson, T., Sahasrabudhe, D., Tan, R. S. & Cheng Y. -C. (1983) Alteration of the pharmacokinetics of high-dose Ara-C by its metabolite, high Ara-U in patients with acute leukemia. Journal of Clinical Oncology, 1, 763. 10.1200/JCO.1983.1.12.763 CASPubMedWeb of Science®Google Scholar Johnson, N. T., Crawford, S. W. & Sargur, M. (1987) Acute acquired demyelinating polyneuropathy with respiratory failure following high-dose systemic cytosine arabinoside and marrow transplantation. Bone Marrow Transplantation, 2, 203–207. PubMedGoogle Scholar Lopex, J. A. & Nassif, E. et al (1984) Acute cerebellar toxicity after high-dose cytarabine associated with CNS accumulation of its metabolite, uracil arabinoside. Cancer Treatment Reports, 68, 1309. PubMedWeb of Science®Google Scholar Nevill, T. J., Benstead, T. J., McCormick, C. W. & Hayne, O. A. (1989) Horner's syndrome and demyelinating peripheral neuropathy caused by high-dose cytosine arabinoside. American Journal of Hematology, 32, 314–315. 10.1002/ajh.2830320414 CASPubMedWeb of Science®Google Scholar Citing Literature Volume79, Issue3November 1991Pages 521-523 ReferencesRelatedInformation

Ten patients with an accepted diagnosis of Friedreich's ataxia have been examined neuro-otologically, and oculomotor, vestibular and auditory function assessed. Brainstem auditory evoked potentials (BAEPs) were also recorded. A high incidence of various eye movement disorders was noted. Some of these were indicative of cerebellar dysfunction. Reduced vestibular function and impaired hearing were common to most of the patients. BAEPs were also abnormal in the majority; reasons underlying these abnormalities are discussed. Neuro-otologically, the patients did not constitute an homogeneous group. The findings cast doubt upon the accuracy and validity of the currently accepted criteria for the diagnosis and classification of the spinocerebellar degenerations.

The effects of the "vestibular sedative" drug Flunarizine upon the oculomotor functions of pursuit and voluntary saccades and upon the vestibular response (to rotational stimuli) were assessed in twenty volunteer subjects. The study was then extended to three patients with chronic imbalance of central origin who had reported a beneficial symptomatic response to the drug. Three of the volunteer subjects were found to have a directional preponderance (presumed to arise from peripheral dysfunction). In the remaining seventeen normal subjects Flunarizine was found to reduce the amplitudes of fast phases of vestibular nystagmus. The directional preponderance in the other three subjects was redressed through production of fast phases which were of lower and more uniform amplitude. In the patients, in addition to a reduction in fast phase amplitude, there was a reduction or abolition of after nystagmus. In no case was any reduction in slow phase velocity observed. Pursuit and voluntary saccades were unaffected by the drug. It was concluded, on the basis that the fast phases of nystagmus are centrally generated, that Flunarizine has a central action rather than a depressant effect upon the vestibular end organ. In view of known oculomotor physiology and pharmacology it is proposed that vestibular sedatives act by depression of Type II vestibular neurons, and modification of the functional relationships between the vestibular nuclei, the perihypoglossal nuclei and the flocculus of the cerebellum. A trial of vestibular active drug is indicated particularly in patients in whom asymmetry of the vestibular response and/or abnormal after nystagmus is demonstrated.