Guillain-barré Syndrome In The Elderly: Clinical, Electrophysiological, Therapeutic And Outcome Features

There are few papers devoted to geriatric Guillain-Barré (GBS) and many related issues remain unanswered. Objective: To describe clinical, electrophysiological and therapeutic features in this age. Method: Clinico-epidemiological data and therapy of GBS patients older than 60 years were reviewed. Hughes scores were used to quantify neurological deficit and define outcome. Results: Among 18 patients (mean age 64.8 years), 9 had evident prodrome and 80% noticed initially sensory-motor deficit. Demyelinating GBS was found in 8 and axonal in 6 subjects. There was one Miller-Fisher and 3 unclassified cases. Plasmapheresis (PFX) was single therapy in 12 patients and intravenous immunoglobulin (IVIg) in 2. Disability scores just before therapy were similar in both groups, so as short and long term outcome. Conclusion: Axonal GBS seems to be more frequent in the elderly and this may have prognostic implications. PFX and IVIg were suitable options, but complications were noticed with PFX. Prospective studies are needed to better understand and manage GBS in the elderly.633 B772775Kuwabara, S., Guillain-Barré syndrome: Epidemiology, pathophysiology and management (2004) Drugs, 64, pp. 597-610Hughes, R.A.C., Rees, J.H., Clinical and epidemiological features of Guillain-Barré syndrome (1997) J Infect Dis, 176 (SUPPL. 2), pp. S92-S98Hartung, H.P., Willison, H.J., Kieseier, B.C., Acute immunoinflammatory neuropathy: Update on Guillain-Barré syndrome (2002) Curr Opin Neurol, 15, pp. 571-577Efficiency of plasma exchange in Guillain-Barré syndrome: Role of replacement fluids (1987) Ann Neurol, 22, pp. 753-761Greenwood, R.J., Newsom Davis, J.M., Hughes, R.A.C., Controlled trial of plasma exchange in acute inflammatory polyradiculoneuropathy (1984) Lancet, 1, pp. 877-879Osterman, P.O., Lundemo, G., Pirskanen, R., Beneficial effects of plasma exchange in acute inflammatory polyradiculoneuropathy (1984) Lancet, 2, pp. 1296-1299Plasmapheresis and acute Guillain-Barré syndrome (1985) Neurology, 35, pp. 1096-1104Plasma exchange in Guillain-Barré syndrome: One-year follow-up (1992) Ann Neurol, 32, pp. 94-97Van Der Meché, F.G.A., Schmitz, P.I.M., A randomized trial comparing intravenous immune globulin and plasma exchange in Guillain-Barré syndrome (1992) N Engl J Med, 326, pp. 1123-1129Randomised trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barré syndrome (1997) Lancet, 349, pp. 225-230Sridharan, G.V., Tallis, R.C., Gautam, P.C., Guillain-Barré syndrome in the elderly: A retrospective comparative study (1993) Gerontology, 39, pp. 170-175Winner, S.J., Evans, J.G., Guillain-Barré syndrome in Oxfordshire: Clinical features in relation to age (1993) Age Ageing, 22, pp. 164-170Yamashita, S., Morinaga, T., Matsumoto, K., Sakamoto, T., Kaku, N., Matsukura, S., Severe Guillain-Barré syndrome in aged patients: The effect of plasmapheresis (1992) Intern Med, 31, pp. 1313-1316Rana, S.S., Rana, S., Intravenous immunoglobulins versus plasmapheresis in older patients with Guillain-Barré syndrome (1999) J Am Geriatr Soc, 47, pp. 1387-1388Asbury, A.K., Cornblath, D.R., Assessment of current diagnostic criteria for Guillain-Barré syndrome (1990) Ann Neurol, 27 (SUPPL.), pp. S21-S24Seneviratne, U., Guillain-Barré syndrome (2000) Postgrad Med J, 76, pp. 774-782Hughes, R.A.C., Newsom-Davis, J.M., Perkin, G.D., Pierce, J.M., Controlled trial of prednisolone in acute polyneuropathy (1978) Lancet, 2, pp. 750-753Rocha, M.S.G., Brucki, S.M.D., Carvalho, A.A.S., Lima, U.W.P., Epidemiologic features of Guillain-Barre syndrome in São Paulo, Brazil (2004) Arq Neuropsiquiatr, 62, pp. 33-37Van Der Meche, F.G., Visser, L.H., Jacobs, B.C., Endtz, H.P., Meulstee, J., Van Doom, P.A., Guillain-Barré syndrome: Multifactorial mechanisms versus defined subgroups (1997) J Infect Dis, 176 (SUPPL. 2), pp. S99-S102Sheth, R.D., Riggs, J.E., Hobbs, G.R., Gutmann, L., Age and Guillain-Barré syndrome severity (1996) Muscle Nerve, 19, pp. 375-377Dias-Tosta, E., Kuckelhaus, C.S., Guillain-Barre syndrome in a population less than 15 years old in Brazil (2002) Arq Neuropsiquiatr, 60, pp. 367-37

Pretibial myxoedema: a case report with scanning electron microscopy.

Made available in DSpace on 2018-01-11T23:40:39Z (GMT). No. of bitstreams: 1 Suita17Pretibialmyxoedemaacase1.pdf: 679167 bytes, checksum: 44436932aec60db1830d43527c90b3c4 (MD5) Previous issue date: 2018-01-10bitstream/item/170810/1/Suita-17-Pretibial-myxoedema-a-case-1.pd

Interviewing Peter Gow — Dundee, June 24, 2017

This interview presents an initial dialogue about Peter Gow’s trajectory as an anthropologist, trying to bring to light particularly the fieldwork experiences and events that it had not been possible to commenton and explore in the published material. Its aim is to understand more closely the particular ways in which Peter Gow had come to arrive at the insights and the analyses presented in his brilliant ethnographies with the Yine/Piro people of Amazonia

Macrophage migration inhibitory factor downregulation: a novel mechanism of resistance to anti-angiogenic therapy.

Anti-angiogenic therapies for cancer such as VEGF neutralizing antibody bevacizumab have limited durability. While mechanisms of resistance remain undefined, it is likely that acquired resistance to anti-angiogenic therapy will involve alterations of the tumor microenvironment. We confirmed increased tumor-associated macrophages in bevacizumab-resistant glioblastoma patient specimens and two novel glioblastoma xenograft models of bevacizumab resistance. Microarray analysis suggested downregulated macrophage migration inhibitory factor (MIF) to be the most pertinent mediator of increased macrophages. Bevacizumab-resistant patient glioblastomas and both novel xenograft models of resistance had less MIF than bevacizumab-naive tumors, and harbored more M2/protumoral macrophages that specifically localized to the tumor edge. Xenografts expressing MIF-shRNA grew more rapidly with greater angiogenesis and had macrophages localizing to the tumor edge which were more prevalent and proliferative, and displayed M2 polarization, whereas bevacizumab-resistant xenografts transduced to upregulate MIF exhibited the opposite changes. Bone marrow-derived macrophage were polarized to an M2 phenotype in the presence of condition-media derived from bevacizumab-resistant xenograft-derived cells, while recombinant MIF drove M1 polarization. Media from macrophages exposed to bevacizumab-resistant tumor cell conditioned media increased glioma cell proliferation compared with media from macrophages exposed to bevacizumab-responsive tumor cell media, suggesting that macrophage polarization in bevacizumab-resistant xenografts is the source of their aggressive biology and results from a secreted factor. Two mechanisms of bevacizumab-induced MIF reduction were identified: (1) bevacizumab bound MIF and blocked MIF-induced M1 polarization of macrophages; and (2) VEGF increased glioma MIF production in a VEGFR2-dependent manner, suggesting that bevacizumab-induced VEGF depletion would downregulate MIF. Site-directed biopsies revealed enriched MIF and VEGF at the enhancing edge in bevacizumab-naive patients. This MIF enrichment was lost in bevacizumab-resistant glioblastomas, driving a tumor edge M1-to-M2 transition. Thus, bevacizumab resistance is driven by reduced MIF at the tumor edge causing proliferative expansion of M2 macrophages, which in turn promotes tumor growth

Whipple's Disease With Neurological Manifestations: Case Report

Whipple's disease (WD) is an uncommon multisystem condition caused by the bacillus Tropheryma whipplei. Central nervous system involvement is a classical feature of the disease observed in 20 to 40% of the patients. We report the case of a 62 yeards old man with WD that developed neurological manifestations during its course, and discuss the most usual signs and symptoms focusing on recent diagnostic criteria and novel treatment regimens.622 A342346Whipple, G.H., A hitherto undescribed disease characterized anatomically by deposits of fat and fatty acids in the intestinal and mesenteric lymphatic tissues (1907) Johns Hopkins Hosp Bull, 18, pp. 382-391Marth, T., Raoult, D., Whipple's disease (2003) Lancet, 36, pp. 239-246Gerard, A., Sarrot-Reynauld, F., Liozon, E., Neurologic presentation of Whipple disease: Report of 12 cases and review of the literature (2002) Medicine (Baltimore), 81, pp. 443-457Brown, A.P., Lane, J.C., Murayama, S., Vollmer, D.G., Whipple's disease presenting with isolated neurological symptoms: Case report (1990) J Neurosurg, 73, pp. 623-627Bostwick, D.G., Bensch, K.G., Burke, J.S., Whipple's disease presenting as aortic insufficiency (1981) N Engl J Med, 305, pp. 995-998Raoult, D., A febrile, blood culture-negative endocarditis (1999) Ann Intern Med, 131, pp. 144-146Chan, R.Y., Yannuzzi, L.A., Foster, C.S., Ocular Whipple's disease: Earlier definitive diagnosis (2001) Ophthalmology, 108, pp. 2225-2231Louis, E.D., Lynch, T., Kaufmann, P., Fahn, S., Odel, J., Diagnostic guidelines in central nervous system Whipple's disease (1996) Ann Neurol, 40, pp. 561-568Sieracki, J.C., Whipple's disease: Observations on systemic involvement (1958) Amer Med Asso Arch Pathol, 66, pp. 464-467Anderson, M., Neurology of Whipple's disease (2000) J Neurol Neurosurg Psychiatry, 68, pp. 2-5De Coene, B., Gilliard, C., Indekeu, P., Whipple's disease confined to the central nervous system (1996) Neuroradiology, 38, pp. 325-327Verhagen, W.I.M., Huygen, P.L.M., Dalman, J.E., Schuurmans, M.M.J., Whipple's disease and the central nervous system: A case report and a review of the literature (1996) Clin Neurol Neurosurg, 98, pp. 299-304Feldman, M., Hendler, R.S., Morrison, E.B., Acute meningoencephalitis after withdrawal of antibiotics in Whipple's disease (1980) Ann Intern Med, 93, pp. 709-711Schwartz, M.A., Selhorst, J.B., Ochs, A.L., Oculomasticatory myorhythmia: A unique movement disorder occurring in Whipple's disease (1986) Ann Neurol, 20, pp. 677-683Manzel, K., Tranel, D., Cooper, G., Cognitive and behavioral abnormalities in a case of central nervous system Whipple disease (2000) Arch Neurol, 57, pp. 399-403Halperin, J.J., Landis, D.M., Kleinman, G.M., Whipple's disease of the nervous system (1982) Neurology, 32, pp. 612-617Feurle, G.E., Volk, B., Waldherr, R., Cerebral Whipple's disease with negative jejunal histology (1979) N Engl J Med, 300, pp. 907-908Madoule, P., Ciaudio-Lacroix, C., Halimi, P., Osteoarticular lesions in Whipple's disease, a propos of a destructive form and review of the literature (1985) J Radiol, 66, pp. 345-350Brändle, M., Ammann, P., Spinas, G.A., Relapsing Whipple's disease presenting with hypopituitarism (1999) Clin Endocrinol, 50, pp. 399-403Topper, R., Gartung, C., Block, F., Neurologic complications in inflammatory bowel diseases (2002) Nervenarzt, 73, pp. 489-499Clarke, C.E., Falope, Z.F., Abdelhadi, H.A., Cervical myelopathy caused by Whipple's disease (1998) Neurology, 50, pp. 1505-1506Ramzan, N.N., Loftus, E., Burgart, L.J., Diagnosis and monitoring of Whipple disease by polymerase chain reaction (1997) Ann Intern Med, 126, pp. 520-527Von Herbay, A., Ditton, H.J., Scuhmacher, F., Whipple's disease: Staging and monitoring by cytology and polymerase chain reaction analysis of cerebrospinal fluid (1997) Gastroenterology, 113, pp. 434-441Kremer, S., Besson, G., Bonaz, B., Pasquier, B., Le Bas, J.F., Grand, S., Diffuse lesions in the CNS revealed by MR imaging in a case of Whipple disease (2001) Am J Neuroradiol, 22, pp. 493-495Romanul, F.C., Radvany, J., Rosales, R.K., Whipple's disease confined to the brain: A case studied clinically and pathologically (1977) J Neurol Neurosurg Psychiatry, 40, pp. 901-909Thompson, D.G., Leidingham, J.M., Howard, A.J., Brown, C.L., Meningitis in Whipple's disease (1978) BMJ, 2, pp. 14-15Feurle, G.E., Marth, T., An evaluation of antimicrobial treatment for Whipple's disease: Tetracycline versus trimethoprim-sulfamethoxazole (1994) Dig Dis Sci, 39, pp. 1642-1648Misbah, S.A., Mapstone, N.P., Whipple's disease revisited (2000) J Clin Pathol, 53, pp. 750-755Schnider, P.J., Reisinger, E.C., Berger, T., Krejs, G.J., Auff, E., Treatment guidelines in central nervous system Whipple's disease (1997) Ann Neurol, 41, pp. 561-56

Zinc binding to lambda phage DNA studied by voltammetric techniques

A interação do zinco com o DNA do fago lambda foi investigada utilizando a voltametria de pulso diferencial e a voltametria cíclica. Os métodos baseiam-se no monitoramento direto da corrente de redução e oxidação do zinco na ausência e na presença do DNA viral. Curvas de titulação do Zn2+ com o DNA do fago lambda foram obtidas nos intervalos de concentração 3,57 x 10-12 a 3,92 x 10-11 mol L-1 e 6,97 x 10-12 a 5,56 x 10-11 mol L-1. Estes dados foram utilizados para o cálculo da constante de dissociação do complexo e da estequiometria. O mecanismo da reação foi estudado utilizando a voltametria cíclica. Curvas do tipo I (corrente de oxidação do zinco) versus v½ (raiz quadrada da velocidade de varredura) mostraram que o processo oxidação-redução do zinco deixa de ser difusional na presença do DNA do fago lambda.Binding of zinc to lambda phage DNA was investigated by differential pulse voltammetry and cyclic voltammetry. These methods rely on the direct monitoring of reduction and oxidation current of zinc in the absence and presence of this virion DNA. Titration graphs of Zn2+ with DNA were obtained in the concentration ranges from 3.57 x 10-12 to 3.92 x 10-11 mol L-1 and 6.97 x 10-12 to 5.56 x 10-11 mol L-1. These data were used to calculate the dissociation constant of the complex and the stoichiometry. The mechanism of this reaction was studied by cyclic voltammetry through curves I (oxidation current of Zn2+) versus v½ (square root of scan rate). These curves showed that the oxidation-reduction process of Zn2+ was not controlled by diffusion in the presence of lambda phage DNA

Calcified Abdominal Pregnancy With Eighteen Years Of Evolution: Case Report.

CONTEXT: The lithopedion (calcified abdominal pregnancy) is a rare phenomenon and there are less than 300 cases reported in the medical literature. CASE REPORT: In this case, a 40 year-old patient had had her only pregnancy 18 years earlier, without medical assistance since then. She came to our hospital with pain and tumoral mass of approximately 20 centimeters in diameter. Complementary examinations (abdominal X-ray, ultrasonography and computerized tomography) demonstrated an extra-uterine abdominal 31-week pregnancy with calcification areas. Exploratory laparotomy was performed, with extirpation of a well-conserved fetus with partially calcified ovular membranes.118619219

No entropy enigmas for N=4 dyons

We explain why multi-centered black hole configurations where at least one of the centers is a large black hole do not contribute to the indexed degeneracies in theories with N=4 supersymmetry. This is a consequence of the fact that such configurations, although supersymmetric, belong to long supermultiplets. As a result, there is no entropy enigma in N=4 theories, unlike in N=2 theories.Comment: 14 page