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A, Rajendran L (2009) The transcellular spread of cytosolic amyloids, prions, and prionoids. Neuron 64:783–790. doi:10.1016\u002Fj.neuron.2009.12.016\nAngot E, Steiner JA, Lema Tomé CM et al (2012) Alpha-synuclein cell-to-cell transfer and seeding in grafted dopaminergic neurons in vivo. PLoS One 7:e39465. doi:10.1371\u002Fjournal.pone.0039465\nBabcock DT, Ganetzky B (2015) Transcellular spreading of huntingtin aggregates in the Drosophila brain. Proc Natl Acad Sci USA 112:E5427–E5433. doi:10.1073\u002Fpnas.1516217112\nBrundin P, Melki R, Kopito R (2010) Prion-like transmission of protein aggregates in neurodegenerative diseases. Nat Rev Mol Cell Biol 11:301–307. doi:10.1038\u002Fnrm2873\nChow WNV, Luk HW, Chan HYE, Lau K-F (2012) Degradation of mutant huntingtin via the ubiquitin\u002Fproteasome system is modulated by FE65. Biochem J 443:681–689. doi:10.1042\u002FBJ20112175\nCicchetti F, Gould PV, Parent A (1996) Sparing of striatal neurons coexpressing calretinin and substance P (NK1) receptor in Huntington’s disease. Brain Res 19(730):232–237. doi:10.1016\u002F0006-8993(96)00307-1\nCicchetti F, Lacroix S, Cisbani G et al (2014) Mutant huntingtin is present in neuronal grafts in Huntington’s disease patients. Ann Neurol 76:31–42. doi:10.1002\u002Fana.24174\nCisbani G, Cicchetti F (2012) An in vitro perspective on the molecular mechanisms underlying mutant huntingtin protein toxicity. Cell Death Dis 3:e382. doi:10.1038\u002Fcddis.2012.121\nCostanzo M, Abounit S, Marzo L et al (2013) Transfer of polyglutamine aggregates in neuronal cells occurs in tunneling nanotubes. J Cell Sci 126:3678–3685. doi:10.1242\u002Fjcs.126086\nCrook ZR, Housman D (2011) Huntington’s disease: can mice lead the way to treatment? Neuron 69:423–435. doi:10.1016\u002Fj.neuron.2010.12.035\nDanzer KM, Kranich LR, Ruf WP et al (2012) Exosomal cell-to-cell transmission of alpha synuclein oligomers. Mol Neurodegener 7:42. doi:10.1186\u002F1750-1326-7-42\nde Calignon A, Polydoro M, Suarez-Calvet M et al (2012) Propagation of tau pathology in a model of early Alzheimer’s disease. Neuron 73:685–697. doi:10.1016\u002Fj.neuron.2011.11.033\nDesplats P, Lee HJ, Bae EJ et al (2009) Inclusion formation and neuronal cell death through neuron-to-neuron transmission of alpha-synuclein. Proc Natl Acad Sci USA 106:13010–13015. doi:10.1073\u002Fpnas.0903691106\nEllrichmann G, Petrasch-Parwez E, Lee DH et al (2011) Efficacy of fumaric acid esters in the R6\u002F2 and YAC128 models of Huntington’s disease. PLoS One 6(1):e16172. doi:10.1371\u002Fjournal.pone.0016172\nGarden GA, La Spada AR (2012) Intercellular (mis)communication in neurodegenerative disease. Neuron 73:886–901. doi:10.1016\u002Fj.neuron.2012.02.017\nGoedert M, Clavaguera F, Tolnay M (2010) The propagation of prion-like protein inclusions in neurodegenerative diseases. Trends Neurosci 33:317–325. doi:10.1016\u002Fj.tins.2010.04.003\nGrad LI, Yerbury JJ, Turner BJ et al (2014) Intercellular propagated misfolding of wild-type Cu\u002FZn superoxide dismutase occurs via exosome-dependent and -independent mechanisms. Proc Natl Acad Sci USA 111:3620–3625. doi:10.1073\u002Fpnas.1312245111\nGusella JF, Wexler NS, Conneally PM et al (1983) A polymorphic DNA marker genetically linked to Huntington’s disease. Nature 306:234–238. doi:10.1038\u002F306234a0\nHansen C, Angot E, Bergström AL et al (2011) alpha-Synuclein propagates from mouse brain to grafted dopaminergic neurons and seeds aggregation in cultured human cells. J Clin Invest 121:715–725. doi:10.1172\u002FJCI43366\nHerrera F, Tenreiro S, Miller-Fleming L, Outeiro TF (2011) Visualization of cell-to-cell transmission of mutant huntingtin oligomers. PLoS Curr 3:RRN1210. doi:10.1371\u002Fcurrents.RRN1210\nJeon I, Lee N, Li JY et al (2012) Neuronal properties, in vivo effects, and pathology of a Huntington’s disease patient-derived induced pluripotent stem cells. Stem Cells 30:2054–2062. doi:10.1002\u002Fstem.1135\nJucker M, Walker LC (2013) Self-propagation of pathogenic protein aggregates in neurodegenerative diseases. Nature 501:45–51. doi:10.1038\u002Fnature12481\nKordower JH, Chu Y, Hauser RA, Freeman TB, Olanow CW (2008) Lewy body-like pathology in long-term embryonic nigral transplants in Parkinson’s disease. Nat Med 14:504–506. doi:10.1038\u002Fnm1747\nLi JY, Englund E, Holton JL et al (2008) Lewy bodies in grafted neurons in subjects with Parkinson’s disease suggest host-to-graft disease propagation. Nat Med 14:501–503. doi:10.1038\u002Fnm1746\nLin CH, Tallaksen-Greene S, Chien WM et al (2001) Neurological abnormalities in a knock-in mouse model of Huntington’s disease. Hum Mol Genet 10:137–144. doi:10.1093\u002Fhmg\u002F10.2.137\nLuk KC, Kehm V, Carroll J et al (2012) Pathological alpha-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice. Science 338:949–953. doi:10.1126\u002Fscience.1227157\nLuk KC, Kehm VM, Zhang B, O’Brien P, Trojanowski JQ, Lee VM (2012) Intracerebral inoculation of pathological alpha-synuclein initiates a rapidly progressive neurodegenerative alpha-synucleinopathy in mice. J Exp Med 209:975–986. doi:10.1084\u002Fjem.20112457\nMarangoni M, Adalbert R, Janeckova L et al (2014) Age-related axonal swellings precede other neuropathological hallmarks in a knock-in mouse model of Huntington’s disease. Neurobiol Aging 35(10):2382–2393. doi:10.1016\u002Fj.neurobiolaging.2014.04.024\nMenalled L, El-Khodor BF, Patry M et al (2009) Systematic behavioral evaluation of Huntington’s disease transgenic and knock-in mouse models. 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Mov Disord 23:1491–1504. doi:10.1002\u002Fmds.21971\nPouladi MA, Graham RK, Karasinska JM et al (2009) Prevention of depressive behaviour in the YAC128 mouse model of Huntington disease by mutation at residue 586 of huntingtin. Brain 132:919–932. doi:10.1093\u002Fbrain\u002Fawp006\nPrusiner SB, Woerman AL, Mordes DA et al (2015) Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism. Proc Natl Acad Sci USA. doi:10.1073\u002Fpnas.1514475112\nRajendran L, Honsho M, Zahn TR et al (2006) Alzheimer’s disease beta-amyloid peptides are released in association with exosomes. Proc Natl Acad Sci USA 103:11172–11177. doi:10.1073\u002Fpnas.0603838103\nRen P-H, Lauckner JE, Kachirskaia I, Heuser JE, Melki R, Kopito RR (2009) Cytoplasmic penetration and persistent infection of mammalian cells by polyglutamine aggregates. Nat Cell Biol 11:219–225. doi:10.1038\u002Fncb1830\nSoto C (2012) Transmissible proteins: expanding the prion heresy. Cell 149:968–977. doi:10.1016\u002Fj.cell.2012.05.007\nThéry C, Amigorena S, Raposo G, Clayton A (2006) Isolation and characterization of exosomes from cell culture supernatants and biological fluids. Curr Protoc Cell Biol Chapter 3:Unit 3.22. doi:10.1002\u002F0471143030.cb0322s30\nVan Raamsdonk JM, Pearson J, Slow EJ, Hossain SM, Leavitt BR, Hayden MR (2005) Cognitive dysfunction precedes neuropathology and motor abnormalities in the YAC128 mouse model of Huntington’s disease. J Neurosci 25:4169–4180. doi:10.1523\u002FJNEUROSCI.0590-05.2005\nYang W, Dunlap JR, Andrews RB, Wetzel R (2002) Aggregated polyglutamine peptides delivered to nuclei are toxic to mammalian cells. Hum Mol Genet 11:2905–2917. doi:10.1093\u002Fhmg\u002F11.23.2905\nZuccato C, Valenza M, Cattaneo E (2010) Molecular mechanisms and potential therapeutical targets in Huntington’s disease. Physiol Rev 90:905–981. doi:10.1152\u002Fphysrev.00041.2009",{"EN":328},"Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder of the central nervous system (CNS) that is defined by a CAG expansion in exon 1 of the huntingtin gene leading to the production of mutant huntingtin (mHtt). To date, the disease pathophysiology has been thought to be primarily driven by cell-autonomous mechanisms, but, here, we demonstrate that fibroblasts derived from HD patients carrying either 72, 143 and 180 CAG repeats as well as induced pluripotent stem cells (iPSCs) also characterized by 143 CAG repeats can transmit protein aggregates to genetically unrelated and healthy host tissue following implantation into the cerebral ventricles of neonatal mice in a non-cell-autonomous fashion. Transmitted mHtt aggregates gave rise to both motor and cognitive impairments, loss of striatal medium spiny neurons, increased inflammation and gliosis in associated brain regions, thereby recapitulating the behavioural and pathological phenotypes which characterizes HD. In addition, both in vitro work using co-cultures of mouse neural stem cells with 143 CAG fibroblasts and the SH-SY5Y human neuroblastoma cell line as well as in vivo experiments conducted in newborn wild-type mice suggest that exosomes can cargo mHtt between cells triggering the manifestation of HD-related behaviour and pathology. This is the first evidence of human-to-mouse prion-like propagation of mHtt in the mammalian brain; a finding which will help unravel the molecular bases of HD pathology as well as to lead to the development of a whole new range of therapies for neurodegenerative diseases of the CNS.",{"EN":330},"Human-to-mouse prion-like propagation of mutant huntingtin protein",{"VOID":332},"10.1007\u002Fs00401-016-1582-9","PUBLICATION","VERIFIED","Auto 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DF, Salazar H, Maroon JC, Hough LJ (1980) Prolactinsecreting pituitary adenomas: serum and tissue prolactin levels with ultrastructural correlation. Am J Obstet Gynecol 137: 646–652\nBauserman S, Hardman J, Schochet S, Earle KM (1978) Pituitary oncocytoma. Arch Pathol Lab Med 102:456–459\nCapella C, Usellini L, Frigerio B, Buffa R, Fontana P, Solcia E (1979) Argyrophil pituitary tumours showing TSH cells or small granule cells. Virchows Arch [Pathol Anat] 381:295–312\nCravioto H, Fukaya T, Zimmerman EA, Kleinberg DL, Flamm ES (1981) Immunohistochemical and electron microscopic studies of functional and non functional pituitary adenomas including one TSH secreting tumour in a thyrotoxic patient. Acta Neuropathol (Berl) 53:281–292\nDuello TM, Halmi NS (1980) Immunocytochemistry of prolactin-producing human pituitary adenomas. Am J Anat 158:463–469\nFarmer PM (1979) Electron microscopy in the diagnosis of pituitary tumours. Ann Clin Lab Sci 9:275–288\nFelix IA, Horvath E, Kovacs K (1981) Massive Crooke's hyalinisation in corticotroph cell adenomas of the human pituitary. A histological, immunocytological and electron microscopic study of three cases. Acta Neurochir 58:235–243\nFukaya T, Kageyama N, Kuwayama A, Takanohashi M, Okada C, Yoshida J, Osamura Y (1980) Morphofunctional study of pituitary adenomas with acromegaly by immunoperoxidase technique and electron microscopy. Cancer 45:1598–1603\nGirod C, Dubois MP, Trouillas J (1976) Apport de l'immunofluorescence a l'étude cytologiques des adénomes hypophysaires humains. Ann Endocrinol 37:279–280\nHassoun J, Charpin C, Jaquet P, Lissitzky JC, Grisoli F, Toga M (1982) Corticolipotropin immunoreactivity in silent chromophobe adenomas: a light and electron microscopic study. Arch Pathol Lab Med 106:25–30\nHorvath E, Kovacs K (1974) Misplaced exocytosis: distinct ultrastructural feature in some pituitary adenomas. Arch Pathol Lab Med 97:221–224\nHorvath E, Kovacs K (1976) Ultrastructural classification of pituitary adenomas. Can J Neurol Sci 3:9–21\nHorvath E, Kovacs K, Killinger DW, Smyth HS, Platts ME, Singer W (1980a) Silent corticotrophic adenomas of the human pituitary gland: a histologic, immunocytologic and ultrastructural study. Am J Pathol 98:617–638\nHorvath E, Kovacs K, Ryan N, Ezrin C (1980b) Null cell adenomas of the human adenohypophysis. Lab Invest 42:164\nHorvath E, Kovacs K, Singer W, Smyth HS, Killinger DW, Ezrin C, Weiss MH (1981) Acidophil stem cell adenoma of the human pituitary: clinico-pathologic analysis of 15 cases. Cancer 47:761–771\nKameya T, Tsumuraya M, Adachi I, Abe K, Ichikizaki K, Toya S, Demura R (1980) Ultrastructure, immunohistochemistry and hormone release of pituitary adenomas in relation to prolactin production. Virchows Arch [Pathol Anat] 387:31–46\nKornfeld M, Buckman MT, McClellan G (1981) Morphometric analysis of secretory granules and prolactin levels in chromophobe pituitary adenomas. Acta Neuropathol (Berl) 53:1–5\nKovacs K (1977) Morphology of prolactin producing adenomas. Clin Endocrinol (Oxf) [Suppl] 6:715–805\nKovacs K, Horvath E (1973) Pituitary chromophobe adenoma composed of oncocytes. Arch Pathol Lab Med 95:235–239\nKovacs K, Corenblum B, Sirek AM, Penz G, Ezrin C (1976) Localisation of PRL in chromophobe pituitary adenomas. Study of human necropsy material by immunoperoxidase technique. J Clin Pathol 29:250–258\nKovacs K, Horvath E, Ezrin C (1977) Pituitary adenomas. In: Sommers S, Rosen PP (eds) Pathology annual, part II. Appleton-Century-Crofts, New York, pp 341–382\nKovacs K, Horvath E, Bayley T, Hassaram ST, Ezrin C (1978) Silent corticotroph cell adenoma with lysosomal accumulation and crinophagy. Am J Med 64:492–499\nKovacs K, Horvath E, Ryan N, Ezrin C (1980) Null cell adenoma of the human pituitary. Virchows Arch [Pathol Anat] 387:165–174\nLewis PD, Van Noorden S (1974) “Non functioning” pituitary tumours. A light and electron microscopical study. Arch Pathol Lab Med 97:178–182\nMcComb DJ, Kovacs K, Horvath E, Singer W, Killinger DW, Smyth HS, Ezrin C, Weiss MH (1980) Correlative ultrastructural morphometry of human prolactin-producing adenomas. Acta Neurochir 53:217–225\nMartinez AJ, Lee A, Moossy J, Maroon JC (1980) Pituitary adenomas: clinicopathological and immunohistochemical study. Ann Neurol 7:24–36\nMosca L, Buffa R, Castello A (1975) Recherche d'une secretion dans les microadenomes hypophysaire humains. Rev Fr Endocrinol Clin 16:433–443\nNiewenhyzen, Kruseman AC, Bots GT, Lindeman J, Schaberg A (1976) Use of immunohistochemical methods for the identification of human growth hormone producing pituitary adenoma. Cancer 38:1162–1170\nPeillon F, Racadot J, Olivier L, Vila-Porcile E (1980) Microadenomas, structure and function. In: Faglia G, Giovanelli M, MacLeod R (eds) Pituitary microadenomas. Academic Press, London, pp 91–106\nRobert F (1981) Prolactinoma: pathologic aspects. Neurochrurgie [Suppl 1] 27:61–73\nRobert F, Pelletier G, Hardy J (1978) Pituitary adenomas in Cushing's disease. A histologic, ultrastructural and immuno-cytochemical study. Arch Pathol Lab Med 102:448–455\nRyder DR, Horvath E, Kovacs K (1980) Fine structural features of secretion in adenomas of human pituitary gland. Arch Pathol Lab Med 104:518–522\nScanarini M, Mingrino S (1980) Functional classification of pituitary adenomas. Acta Neurochir 52:195–202\nSaeger W (1975) Comparative light microscopic and electron microscopic studies of oncocytic pituitary adenomas. Virchows Arch [Pathol Anat] 369:29–44\nSinger W, Kovacs K, Ryna N, Horvath E (1978) Demonstration of immunoreactive α endorphin in corticotroph cell adenomas of the human pituitary. IRCS Med Sci 6:250\nSloper JJ, Powell TP (1978) Observations on the process of degeneration of the afferent connections of the sensori-motor cortex of the monkey. Neuroscience 3:1031–1044\nTramu G, Beauvillain JC, Mazzuca M, Girard F, Laine E, Christiaens JL, Wemeau JL, Fossati P, Linquette M (1976) Dissociation des résultats obtenus en immunofluorescence avec des antisérums anti ACTH dans 3 cas d'adénome chromophobe sans hypercorticisme. Ann Endocrinol (Paris) 37:55–56\nTramu G, Beauvillain JC, Mazzuca M, Lefebvre J, Fossati P, Christiaens JL (1978) Adénome hypophysaire à cellules α 17–39. ACTH et βMSH sans hypercorticisme. Ann Endocrinol (Paris) 39:51–52\nTrouillas J, Girod C, Lhéritier M, Claustrat B, Dubois MP (1980) Morphological and biochemical relationships in 31 human pituitary adenomas with acromegaly. Virchows Arch [Pathol Anat] 389:127–142\nTrouillas J, Girod C, Sassolas G, Claustrat B, Lhéritier M, Dubois MP, Goutelle A (1981) Human pituitary gonadotropic adenoma: histological, immunocytochemical and ultrastructural and hormonal studies in eight cases. J Pathol 135:315–336\nZimmerman EA, Defendini R, Frantz AG (1974) Prolactin and growth hormone in patients with pituitary adenomas. A correlative study of hormone in tumour and plasma by immunoper-oxidase technique and radio immunoassay. J Clin Endocrinol Metab 38:579",{"EN":651},"An analysis is presented of the immunohistological and ultrastructural features in a series of 118 surgically removed pituitary adenomas all of which were studied immunohistologically using antisera to growth hormone (GH), prolactin (PRL) ACTH, βFSH, βLH and βTSH, and 75 of which were studied ultrastructurally. Results were analysed according to the mode of presentation of patients. Forty-one (35%) of the tumours were from patients with acromegaly or gigantism, ten (9%) from patients with Cushing's syndrome or Nelson's syndrome, 19 (16%) from patients with clinical features associated with hyperprolactinaemia and 48 (40%) from patients with space occupying lesions which appeared clinically to be overtly endocrinologically functionless. By light microscopy, using the immunoperoxidase (PAP) technique, immunoreactive GH was demonstrated in all the tumours from patients with acromegaly or gigantism, immunoreactive ACTH in all tumours from patients with Cushing's syndrome or Nelson's syndrome and immunoreactive PRL in 95% of tumours associated with effects of hyperprolactinaemia. Forty-five percent of the tumours from acromegalic patients contained some PRL-positive cells as well as GH-positive cells. Among the tumours which appeared clinically to be endocrinologically functionless were three tumours (from males) uniformly stained for immunoreactive PRL. Of the remainder, 60% were negative for immunoreactive hormones and 40% contained small numbers of cells which were positive for a variety of immunoreactive hormones. ACTH-cell and PRL-cell tumours had ultrastructural features as described in previous studies. Fifty percent of GH-cell tumours examined at the EM level contained fibrous bodies, while in the remainder these structures were not identified. Tumours with fibrous bodies were more likely to contain PRL as well as GH with immunoperoxidase. All tumours that were endocrinologically functionless and which were examined at the EM level contained secretory granules. Oncocytic change was common in these tumours. No ultrastructural differences were observed between those which contained immunoreactive hormones by light microscopy and those which did not.",{"EN":653},"Pituitary adenomas: Immunohistology and ultrastructural analysis of 118 tumors",{"VOID":655},"10.1007\u002FBF00684914","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00684914",[658,673,690,705],{"id":659,"sortIndex":437,"researcher":20,"roles":660,"affiliations":661,"properties":670},"5019a7f4-9436-49bd-8edc-1b07c70940c0",[342],[662],{"id":20,"sortIndex":21,"affiliation":663,"properties":20},{"id":664,"createTime":665,"updateTime":665,"relativeEntities":666,"slug":20,"properties":667,"entityType":56,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"33b8d23b-5b87-4b30-b60c-0647ff2a706a","2023-12-28T12:15:44.775+00:00",[],{"title":668},{"VI":669},"Dept of Neurosurgery, Radcliffe Infirmary, Oxford, UK",{"title":671},{"VI":672},"C. B. T. 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Adv Neurol 28:197–205\nBoiadjieva S, Hallberg C, Hogstrom M, Busch C (1984) Methods in laboratory investigations. Exclusion of trypan blue from micro-carriers by endothelial cells: an in vitro barrier function test. Lab Invest 50:239–246\nBradford M (1976) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem 72:248–254\nBuege JA, Aust SD (1978) Microsomal lipid peroxidation. Methods Enzymol 52:302–310\nChan PH, Fishman RA (1984) Phospholipid degradation and the early release of polyunsaturated fatty acids in the evolution of brain edema. In: Go KG, Baethmann A (eds) Recent progress in the study and therapy of brain edema. Plenum Press, New York London, pp 193–202\nChan PH, Fishman RA, Caronna J, Schmidley JW, Prioleau G, Lee J (1983) Induction of brain edema following intracerebral injection of arachidonic acid. Ann Neurol 13:625–632\nDobretsov GE, Borschevskaya TA, Petrov VA, Vladimirov YA (1977) The increase of phospholipid bilayer rigidity after lipid peroxidation. FEBS Lett 84:125–128\nFridovich I (1976) Oxygen radicals, hydrogen peroxide and oxygen toxicity. In: Pryor WA (ed) Free radicals in biology. Academic Press, New York London, pp 239–277\nHalliwell B (1987) Oxidants in human disease: some new concepts. FASEB J 1:358–364\nHenning B, Chow CK (1988) Lipid peroxidation and endothelial cell injury: implication in atheroscleosis. Free Radical Biol Med 4:99–106\nHennig B, Shasby MD, Fulton AB, Spector AA (1984) Exposure to free fatty acid increases the transfer of albumin across cultured endothelial monolayers. Arteriosclerosis 4:489–497\nKatz AM, Messineo FC (1981) Lipid-membrane interactions and the pathogenesis of ischemic damage in the myocardium. Circ Res 48:1–16\nKempski O, Spatz M (1987) Blood-brain barrier: in vitro studies of endothelial permeability. In: Cervos-Navarro J, Ferszt R (eds) Stroke and microcirculation. Raven Press, New York, pp 223–227\nKempski O, Villacara A, Spatz M, Dodson RF, Corn C, Merkel N, Bembry J (1987) Cerebromicrovascular endothelial permeability in-vitro studies. Acta Neuropathol (Berl) 74:329–334\nKogure K, Arai H, Abe K, Nakano M (1985) Free radical damage of the brain following ischemia. Prog Brain Res 63:237–259\nKontos HA (1985) Oxygen radicals in cerebral vascular injury. Circ Res 57:508–516\nLentz BR, Barenholz Y, Thompson TE (1976) Fluorescence depolarization studies of phase transition and fluidity in phospholipid bilayers. Biochemistry 15:4529–4537\nMolitoris BA, Kinne R (1987) Ischemia induces surface membrane dysfunction, mechanism of altered Na+-dependent glucose transport. J Clin Invest 80:644–654\nMcCord JM (1987) Oxygen derived radicals: a link between reperfusion injury and inflammation. Fed Proc 46:2402–2406\nRice-Evans C, Hochstein P (1981) Alterations in erythrocyte membrane fluidity by phenylhydrazine-induced peroxidation of lipids. Biochem Biophys Res Commun 100:1537–1542\nShinitzky M, Barenholz Y (1978) Fluidity parameters of lipid regions determined by fluorescence polarization. Biochim Biophys Acta 515:367–394\nSpatz M, Bembry J, Dodson RF, Hervonen H, Murray MR (1980) Endothelial cell cultures derived from isolated cerebral microvessels. Brain Res 191:577–582\nStubbs ChD, Smith AD (1984) The modification of mammalian membrane polyunsaturated fatty acid composition in relation to membrane fluidity and function. Biochim Biophys Acta 779:89–137\nUnterberg A, Wahl M, Hammersen F, Baethmann A (1987) Permeability and vasomotor response of cerebral vessels during exposure to arachidonic acid. Acta Neuropathol (Berl) 73:209–219\nVan Blitterswijk WJ, Van Hoevan RP, Van der Meer BW (1981) Lipid structural order parameters (reciprocal of fluidity) in biomembranes derived from steady state fluorescent measurements. Biochim Biophys Acta 644:323–332\nYamamoto Y, Shima T, Uozumi T, Sogabe T, Yamada K, Kawasaki T (1983) A possible role of lipid peroxidation in cellular damages caused by cerebral ischemia and the protective effect of α-tocopherol administration. Stroke 14:977–982\nYoshida S, Inoh S, Asano T, Sano K, Kubota M, Shimazaki H, Ueta N (1980) Effect of transient ischemia on free fatty acids and phospholipids in the gerbil brain. J Neurosurg 53:323–331",{"EN":766},"The relationship of free arachidonic acid (AA) to cellular permeability, lipid peroxidation and physical state “fluidity” of the membrane was investigated in cultured endothelial cells (EC) dissociated from cerebral microvessels of rats. The results demonstrate that AA can induce a reversible alteration of endothelial permeability to trypan blue albumin (TBA). Exposure of EC to AA increases membrane “fluidity” as measured by fluorescence anisotropy using 1,6-diphenyl-1,3,5 hexatriene as a fluorescent probe. The AA modification of EC membrane “fluidity” is not associated with changes in EC permeability. Addition of AA and H2O2 to the incubation medium of EC leads to persistant alteration of EC permeability which can be prevented by catalase treatment. Both AA and H2O2 induce a greater formation of malondialdehyde, the product of lipid peroxidation, than AA alone. These findings strongly suggest that a release of AA either from the capillary or cellular membrane of the brain under a pathological condition may alone or through a peroxidative process alter the function of blood-brain barrier.",{"EN":768},"Effect of arachidonic acid on cultured cerebromicrovascular endothelium: permeability, lipid peroxidation and membrane “fluidity”",{"VOID":770},"10.1007\u002FBF00687761","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00687761",[773,788,803,815,827],{"id":774,"sortIndex":250,"researcher":20,"roles":775,"affiliations":776,"properties":785},"1908d83b-1b86-466a-8741-2068028c7444",[342],[777],{"id":20,"sortIndex":21,"affiliation":778,"properties":20},{"id":779,"createTime":780,"updateTime":780,"relativeEntities":781,"slug":20,"properties":782,"entityType":56,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"14b718cf-d905-45ac-9e52-5ff2a2df54bc","2024-01-19T17:48:07.476+00:00",[],{"title":783},{"VI":784},"Department of Cell Biology and Environmental Sciences, The University of Texas, Health Center at Tyler, Tyler, USA",{"title":786},{"VI":787},"C. 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Neuron 46:181–189. doi: 10.1016\u002Fj.neuron.2005.04.001",{"doi":1360},"10.1016\u002Fj.neuron.2005.04.001",{"id":1362,"createTime":1363,"updateTime":1364,"relativeEntities":1365,"slug":1366,"properties":1367,"entityType":333,"verifyStatus":334,"verifyTime":1364,"verifyNote":335,"syncStatus":19,"languages":1376,"translateLanguages":20,"viewCount":21,"primaryUrl":1377,"fullTextUrl":20,"authors":1378,"publicationType":603,"publisherRelationship":1420,"citationCount":20,"citationInfo":20,"publishDate":1449,"publishYear":1450,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":1451,"isForceReanalyzing":640},"a7460d1f-8660-4b49-97e2-eb5c483fda43","2024-04-09T11:17:29.334+00:00","2025-01-08T23:59:20.628+00:00",[],"Immunohistochemical-studies-on-cellular-character-of-microtumors-induced-by-ethylnitrosourea-in-the-rat-brain-utilizing-anti-leu-7-and-anti-glial-fibrillary-acidic-protein-antibodies",{"keywords":1368,"abstract":1370,"title":1372,"doi":1374},{"EN":1369},"",{"EN":1371},"To clarify the chronologic changes in the cellular morphology of ENU-induced rat brain tumors, microtumors in the early stage were examined ummunohistochemically in comparison with macrotumors in the advanced stage. The tumor cells composing microtumors were negative for glial fibrillary acidic protein (GFAP), a specific marker of astrocylic cells, and Leu 7, a marker of oligodendrocytes, while cells of macrotumors were positive for either GFAP or Leu 7, showing characteristics of mature glial cells. The results suggested that the small round cells in the early devolopmental stage, generally thought to resemble mature oligodendrocytes, are not differentiated oligodendrocytes or astrocytes.",{"EN":1373},"Immunohistochemical studies on cellular character of microtumors induced by ethylnitrosourea in the rat brain utilizing anti-leu 7 and anti-glial fibrillary acidic protein antibodies",{"VOID":1375},"10.1007\u002FBF00688694",[897],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00688694",[1379,1396,1408],{"id":1380,"sortIndex":21,"researcher":20,"roles":1381,"affiliations":1382,"properties":1393},"b26ccc3c-d644-4a55-bc46-d0c7c4b9161e",[],[1383],{"id":20,"sortIndex":21,"affiliation":1384,"properties":20},{"id":1385,"createTime":1386,"updateTime":1387,"relativeEntities":1388,"slug":1389,"properties":1390,"entityType":56,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"87f86c42-c53a-4d12-90de-f8569b727bfc","2024-04-09T11:17:29.517+00:00","2024-06-18T05:10:49.253+00:00",[],"Dept-of-Pathology-Okayama-University-Medical-School-Okayama-Japan",{"title":1391},{"EN":1392},"Dept. of Pathology, Okayama University Medical School, Okayama, Japan",{"title":1394},{"EN":1395},"T. 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J Public Health (Oxf) 29(3):246–250. doi:10.1093\u002Fpubmed\u002Ffdm028",{"EN":1932},"Neuromuscular disorders (NMD) such as neuropathy or myopathy are rare and often severe inherited disorders, affecting muscle and\u002For nerves with neonatal, childhood or adulthood onset, with considerable burden for the patients, their families and public health systems. Genetic and clinical heterogeneity, unspecific clinical features, unidentified genes and the implication of large and\u002For several genes requiring complementary methods are the main drawbacks in routine molecular diagnosis, leading to increased turnaround time and delay in the molecular validation of the diagnosis. The application of massively parallel sequencing, also called next generation sequencing, as a routine diagnostic strategy could lead to a rapid screening and fast identification of mutations in rare genetic disorders like NMD. This review aims to summarize and to discuss recent advances in the genetic diagnosis of neuromuscular disorders, and more generally monogenic diseases, fostered by massively parallel sequencing. We remind the challenges and benefit of obtaining an accurate genetic diagnosis, introduce the massively parallel sequencing technology and its novel applications in diagnosis of patients, prenatal diagnosis and carrier detection, and discuss the limitations and necessary improvements. Massively parallel sequencing synergizes with clinical and pathological investigations into an integrated diagnosis approach. Clinicians and pathologists are crucial in patient selection and interpretation of data, and persons trained in data management and analysis need to be integrated to the diagnosis pipeline. 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M., Amsterdam, D., Brooks, S., Schneck, L., Volk, B. W.: Transformed cells from fetal Tay-Sachs disease (TSD) induced by Simian virus 40 (SV40). J. Neuropath. Exp. Neurol.36, 590 (1977)\nAdachi, M., Schneck, L., Volk, B. W.: Ultrastructural studies of eight cases of fetal Tay-Sachs disease. Lab. Invest.30, 102–112 (1974)\nAdachi, M., Schneck, L., Volk, B. W.: Neurotoxic effects of chlorphentermine on rats. In: Neurotoxicology Vol. 1 (eds. L. Roizin, H. Shiraki and N. Grčević), p. 497 New York: Raven Press 1977\nAdachi, M., Torii, J., Amsterdam, D., Brooks, S., Schneck, L., Volk, B. W.: Tissue culture from fetal Tay-Sachs disease. J. Neuropath. Exp. Neurol.31, 208 (1972)\nAdachi, M., Torii, J., Karvounis, P. C., Volk, B. W.: Alterations of astrocytic organelles in various lipidoses and allied diseases. Acta neuropath. (Berl.)18, 74–83 (1971)\nAdachi, M., Torii, J., Schneck, L., Volk, B. W.: The fine structure of fetal Tay-Sachs disease. Arch. Path.91, 48–54 (1971)\nAdachi, M., Torii, J., Schneck, L., Volk, B. W.: Fine structure of early Tay-Sachs disease. In: Sphingolipids, sphingolipidoses and allied disorders (eds. B. W. Volk and S. M. Aronson), p. 1. New York: Plenum Press 1972\nAdachi, M., Tsai, C.-Y., Greenbaum, M., Mask, B., Volk, B. W.: Ultrastructure and biochemical studies of rat CNS and viscera after subcutaneous injection of chlorphentermine. In: Current trends in sphingolipidoses and allied disorders (eds. B. W. Volk and L. Schneck), p. 429 New York: Plenum Press 1976\nAdachi, M., Tsai, C.-Y., Hoffman, L. M., Schneck, L., Volk, B. W.: The central nervous system, liver, and spleen of FM mice. Arch. Path.97, 232–238 (1974)\nAdachi, M., Tsai, C.-Y., Wellmann, K. F., Volk, B. W.: Ultrastructural alterations of liver, lung, pancreas and CNS of mice induced by chlorphentermine. Fed. Proc.33, 607 (1974)\nAdachi, M., Volk, B. W.: Pathology. In: The gangliosidoses (eds. B. W. Volk and L. Schneck), p. 125. New York: Plenum Press 1975\nAdachi, M., Volk, B. W.: Methodology: Histochemistry. In: The gangliosidoses (eds. B. W. Volk and L. Schneck), p. 249. New York: Plenum Press 1975\nAdachi, M., Volk, B. W.: Gaucher's disease in mice induced by conduritol-B-epoxide. Arch. Path.101, 255–259 (1977)\nAdachi, M., Volk, B. W., Schneck, L.: Animal model of human disease. Niemann-Pick disease type C. Am. J. Path.85, 229–231 (1976)\nAdachi, M., Volk, B. W., Schneck, L., Relkin, R.: Ultrastructural alterations of endocrine glands in Tay-Sachs disease. Am. J. Clin. Path.57, 557–561 (1972)\nAdachi, M., Volk, B. W., Schneck, L., Torrii, J.: Fine structure of the myenteric plexus in various lipidoses. Arch. Path.87, 228–241 (1969)\nAdachi, M., Wallace, B. J., Schneck, L., Volk, B. W.: Fine structure of central nervous system in early infantile Gaucher's disease. Arch. Path.83, 513–526 (1967)\nAndrews, J. M., Cancilla, P. A.: Cytoplasmic inclusions in human globoid cell leukodystrophy. Arch. Path.89, 53–55 (1970)\nArgyrakis, A., Pilz, H., Goebel, H. H., Müller, D.: Ultrastructural findings of peripheral nerve in a preclinical case of adult metachromatic leukodystrophy. J. Neuropath. Exp. Neurol.36, 693–711 (1977)\nAronson, S. M.: Epidemiology. In: Tay-Sachs disease (ed. B. W. Volk), p. 118 New York: Grune & Stratton 1964\nAronson, S. M.: Epidemiology. In: The gangliosidoses (eds. B. W. Volk and L. Schneck), p. 159. New York: Plenum Press 1975\nAronson, S. M., Aronson, B. E., Volk, B. W.: A genetic profile of infantile amaurotic family idiocy: statistical evaluation of one hundred thirty-one patients. J. Dis. Child.98, 50–65 (1959)\nAronson, S. M., Valsamis, M. P., Volk, B. W.:Infantile amaurotic idiocy. Occurrence, genetic considerations and pathophysiology in the non-Jewish infant. Pediat.26, 229–242 (1960)\nAronson, S. M., Volk, B. W.: Genetic and demographic considerations concerning Tay-Sachs disease. In: Cerebral sphingolipidoses (eds. S. M. Aronson and B. W. Volk), p. 375. 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A GM1-Étude a propos d'un cas diagnostique du vivant due malade. Ann. Pediat. (Paris)51, 165–184 (1968)\nSharp, H. L., Desnick, R. J.: Sandhoff's disease: Diagnosis and evaluation by precutaneous liver biopsy. Gastroenterol.60, 752 (1971)\nShaw, C. M., Carlson, C. B.: Crystalline structures in globoid-epithelioid cells: An electron microscopic study of globoid leukodystrophy (Krabbe's disease). J. Neuropath. Exp. Neurol.29, 306–319 (1970)\nSinger, J. D., Cotlier, E., Krimmer, R.: Hexosaminidase A in tears and salive for rapid identification of Tay-Sachs disease and its carriers. Lancet2, 1116 (1973)\nSuzuki, K.: Ultrastructural study of experimental globoid cells. Lab. Invest.23, 612–619 (1970)\nSuzuki, K., Chen, G. C.: Brain ceramide hexosides in Tay-Sachs disease and generalized gangliosidosis (GM1-gangliosidosis). J. Lipid Res.8, 105–113 (1967)\nSuzuki, K., Grover, W. D.: Krabbe's leukodystrophy (globoid cell leukodystrophy): An ultrastructural study. Arch. Neurol.22, 385–396 (1970)\nSuzuki, K., Suzuki, K., Chen, G. C.: Isolation and chemical characterization of metachromatic granules from a brain with metachromatic leukodystrophy. J. Neuropath. Exp. Neurol.26, 537–550 (1967)\nSuzuki, K., Suzuki, K., Chen, G. C.: GM1-Gangliosidosis (generalized gangliosidosis) morphology and chemical pathology. Path. Europ.3, 389–408 (1968)\nSuzuki, K., Suzuki, K., Rapin, I., Suzuki, Y., Ishii, N.: Juvenile GM2-gangliosidosis: Clinical variant of Tay-Sachs disease or a new disease. Neurol. (Minncap.)20, 190–203 (1970)\nSuzuki, K., Suzuki, Y.: Globoid cell leucodystrophy (Krabbe's disease) deficiency of galactocerebroside beta-galactosidase. Proc. Nat. Acad. Sci. USA66, 302–309 (1970)\nSuzuki, K., Tanaka, H., Suzuki, K.: Studies on the pathogenesis of Krabbe's leukodystrophy: Cellular reaction of the brain to exogenous galactosylsphingosin, monogalactosyl diglyceride, and lactosylceramide. In: Current trends in sphingolipidoses and allied disorders (eds. B. W. Volk and L. Schneck), p. 99. New York: Plenum Press 1976\nSuzuki, Y., Jacob, J. C., Suzuki, K., Kutty, K. M., Suzuki, K.: GM2-gangliosidosis with total hexosaminidase deficiency. Neurol. (Minneap.)21, 313–328 (1971)\nSvennerholm, L.: Chromatographic separation of human brain gangliosides. J. Neurochem.10, 613–623 (1963)\nSvennerholm, L.: Some aspects of the biochemical changes in leucodystrophy. In: Brain lipids and lipoproteins, and the leucodystrophies (eds. J. Folch-Pi and H. Bauer), p. 104. Amsterdam: Elsevier 1963\nSweeley, C. C., Klionsky, B.: Fabry's disease: classification as a sphingolipidosis and partial characterization of a novel glycolipid. J. Biol. Chem.238, 3148–3150 (1963)\nSweeley, C. C., Klionsky, B.: Glycolipid lipidosis: Fabry's disease, In: The metabolic basis of inherited disease (eds. J. B. Stanbury, J. B. Wyngaarden, and D. S. Fredrickson), p. 618. New York: McGraw-Hill 1966\nSweeley, C. C., Klionsky, B., Krivit, W., Desnick, R.: Fabry's disease: Glycosphingolipid lipidosis. In: The metabolic basis of inherited disease (eds. J. B. Stanbury, J. B. Wyngaarden and D. S. Fredrickson), p. 663. New York: McGraw Hill 1972\nTakebayahi, S., v. Bassewitz, D. B., Themann, H.: Feinstrukturelle Veränderungen der Niere bei generalisierter Gangliosidose GM1. Virchows Arch. B.5, 301–313 (1970)\nTanaka, J., Garcia, J. H., Max, S. R., Vioriz, J. E., Kamijyo, Y., McLaren, N. K., Cornblath, M., Brady, R. O.: Cerebral sponginess and GM3 gangliosidosis. J. Neuropath. Exp. Neurol.34, 249–262 (1975)\nTay, W.: Symmetric changes in the region of the yellow spot in each eye of an infant. Trans. Ophthal. Soc. U. K.1, 55–57 (1881)\nTerry, R. D., Weiss, M.: Studies on Tay-Sachs disease. II Ultrastructure of the cerebrum. J. Neuropath. Exp. Neurol.22, 18–55 (1963)\nThemann, H., Dickmann, L., v. Bassewitz, D. B.: Die Feinstruktur der menschlichen Leber bei Generalisierter Gangliosidose GM1. Beitr. path. Anat. allg. Path.140, 194–211 (1970)\nThomas, P. K., King, R. H., Kocen, R. S., Brett, E. M.: Comparative ultrastructural observations on peripheral nerve abnormalities in the late infantile, juvenile and late onset forms of metachromatic leukodystrophy. Acta neuropath. (Berl.)39, 237–245 (1977)\nVanier, M.-T., Svennerholm, L.: Chemical pathology of Krabbe's disease: The occurrnece of psychosine and other neutral sphingoglycolipids. In: Current trend in sphingolipidoses and allied disorders (eds. B. W. Volk and L. Schneck), p. 115. New York: Plenum Press 1976\nVolk, B. W.: Pathologic anatomy. In: Tay-Sachs disease (ed. B. W. Volk), p. 36. New York: Grune and Stratton 1964\nVolk, B. W., Adachi, M.: Diffuse cerebral sclerosis-Krabbe type. In: Handbook of clinical neurology. Vol. 10. Leucodystrophies and polydystrophies (eds. P. J. Vinken and G. W. Bruyn), p. 67. Amsterdam: North-Holland 1970\nVolk, B. W., Adachi, M., Schneck, L., Saifer, A., Kleinberg, W.: G5-ganglioside variant of systemic late infantile lipidosis. Arch. Path.87, 393–403 (1969)\nVolk, B. W., Wallace, B. J.: The liver in lipidosis. An electron microscopic and histochemical study. Am. J. Path.49, 203–225 (1966)\nWallace, B. J., Schneck, L., Kaplan, H., Volk, B. W.: Fine structure of the cerebellum in children with lipidoses. Arch. Path.80, 466–486 (1965)\nWallace, B. J., Volk, B. W., Schneck, L., Kaplan, H.: Fine structural localization of two hydrolytic enzymes in the cerebellum of children with lipidoses. J. Neuropath. Exp. Neurol.25, 76–96 (1966)\nWascowitz, B.: Niemann-Pick disease. Am. J. Dis. Child.42, 356–365 (1931)\nWebster, H., de F.: Schwann cell alterations in metachromatic leukodystrophy: Preliminary phase and electron microscopic observations. J. Neuropath. Exp. Neurol.21, 534–554 (1962)\nWeissmann, G., Cohen, C., Hoffstein, S.: The correction, in vitro, of lysosomal enzyme deficiencies by means of immunoglobulin coated liposomes. In: Current trends of sphingolipidoses and allied disorders (eds. B. W. Volk and L. Schneck), p. 509. New York: Plenum press 1976\nWenger, D. A., Barth, G., Githens, J. H.: Nine cases of sphingomyelin lipidosis, a new variant in Spanish-American children. Am. J. Dis. Child.131, 955–961 (1977)\nWenger, D. A., Sattler, M., Clark, C., Tanaka, H., Suzuki, K., Dawson, G.: Lactosyl ceramidosis: Normal activity for two lacytosyl ceramide beta-galactosidase. Science188, 1312–1314 (1975)\nWenger, D. A., Sattler, M., Hiatt, W.: Globoid cell leukodystrophy: Deficiency of lactosyl ceramide beta-galactosidase. Proc. Nat. Acad. Sci.71, 854–857 (1974)\nWenger, D. A., Sattler, M., Markey, S. P.: Deficiency of monogalactosyl diglyceride beta-galactosidase activity in Krabbe's disease. Biochem. Biophys. Res. Commun.53, 680–685 (1973)\nWolfe, L. S., Callahan, J., Fawcett, J. S., Andermann, F., Scriver, C.: GM1 gangliosidosis without chondrodystrophy of visceromegaly; beta-galactosidase deficiency with gangliosidosis and the excessive excretion of a keratan sulfate. Neurol. (Minneap.)20, 23–44 (1970)\nWood, S., MacDougall, B. G.: Juvenile Sandhoff disease: Some properties of the residual hexosaminidase in cultured fibroblasts. Am. J. Hum. Genet.28, 489–495 (1976)\nYajima, K., Fletcher, T. F., Suzuki, K.: Sub-plasmalemmal linear density: A common structure in globoid cells and mesenchymal cells. Acta neuropath. (Berl.)39, 195–200 (1977)\nYajima, K., Fletcher, T. F., Suzuki, K.: Canine globoid cell leukodystrophy. Part. 1. Further ultrastructural study of the typical lesion. J. Neurol. Sci.33, 179–197 (1977)\nYoung, E. P., Ellis, R. B., Lake, B. D., Patrick, A.: Tay-Sachs disease and related disorders. Fractionation of brain N-acetyl-beta-hexosaminidase. FEBS letter9, 1–4 (1970)\nYunis, E. J., Lee, R. E.: The ultrastructure of globoid (krabbe) leukodystrophy. Lab. Invest.21, 415–519 (1969)\nYunis, E. J., Lee, R. E.: The morphologic similarities of human and canine globoid leukodystrophy. Am. J. Path.85, 99–114 (1976)",{"EN":2082},"Progress in investigations of sphingolipidoses",{"VOID":2084},"10.1007\u002FBF00684994","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00684994",[2087,2102,2118],{"id":2088,"sortIndex":21,"researcher":20,"roles":2089,"affiliations":2090,"properties":2099},"6fda29ea-9e05-4bba-8514-74af4351322d",[342],[2091],{"id":20,"sortIndex":21,"affiliation":2092,"properties":20},{"id":2093,"createTime":2094,"updateTime":2094,"relativeEntities":2095,"slug":20,"properties":2096,"entityType":56,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"83a0cacc-f4c5-4ea2-a3fd-7479b7e68604","2024-01-17T16:48:57.627+00:00",[],{"title":2097},{"VI":2098},"Departments of Pathology and Neurology, Downstate Medical Center, State University of New York, Brooklyn",{"title":2100},{"VI":2101},"M. 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Differences between malignant tumours and other disorders were of special interest with respect to the question of the possible existence of a remote effect of cancer on skeletal muscle. The number of central nuclei within muscle fibre cross sections was considered as the most simple parameter for myopathic reaction. Atrophic fibre changes were examined quantitatively by measurement of the orthogonal fibre diameters and calculating the variation of fibre size. In addition, a semi-quantitative histological evaluation of the muscles was performed. While tumour cases did not show a significant difference from the remainder with respect to myopathic changes, they did display a significant difference with regard to scattered and small-group fibre atrophy. The reasons for the muscular changes are discussed. From the present investigation the changes seem to be due chiefly to metabolic impairment and wasting. No signs for a specific carcinotoxic effect on skeletal muscles could be demonstrated.",{"EN":2179},"Quantitative analysis of voluntary muscles from routine autopsy material, with special reference to the problem of remote carcinomatous changes (“Neuromyopathy”)",{"VOID":2181},"10.1007\u002FBF00685009",{"VOID":2183},"[\"11581747713022277593\"]","2024-05-01T09:51:08.856+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00685009",[2187],{"id":2188,"sortIndex":21,"researcher":20,"roles":2189,"affiliations":2190,"properties":2199},"bd5aa44c-3122-45b8-ae94-cfe5cf9eb2f7",[342],[2191],{"id":20,"sortIndex":21,"affiliation":2192,"properties":20},{"id":2193,"createTime":2194,"updateTime":2194,"relativeEntities":2195,"slug":20,"properties":2196,"entityType":56,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"e36ec6ea-90df-433c-8d29-57aeff043159","2023-12-27T23:50:24.808+00:00",[],{"title":2197},{"VI":2198},"Institute of Neuropathology, University of Heidelberg, Heidelberg 1, German Federal Republic",{"title":2200},{"VI":2201},"Horst P. Schmitt",{"url":2185,"publisher":2203,"properties":2231},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2204,"slug":10,"properties":2205,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":2209,"manageAffiliations":2210,"indexDatabases":2211,"url":20,"thumbnailPath":20,"statistic":2226,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":2206,"eissn":2207,"title":2208},{"VOID":13},{"VOID":15},{"EN":17},[],[],[2212,2219],{"id":93,"indexDatabase":2213,"url":106,"indexYears":107,"academicFieldIds":2218,"indexDatabaseRanking":112},{"id":95,"createTime":96,"updateTime":97,"relativeEntities":2214,"label":2215,"description":2216,"key":103,"publicationTags":2217,"standard":20},[],{"EN":100,"VI":100},{"EN":100,"VI":102},[105],[109,110,111],{"id":72,"indexDatabase":2220,"url":87,"indexYears":20,"academicFieldIds":2225,"indexDatabaseRanking":20},{"id":74,"createTime":75,"updateTime":76,"relativeEntities":2221,"label":2222,"description":2223,"key":83,"publicationTags":2224,"standard":20},[],{"EN":79,"VI":79},{"VI":81,"EN":82},[85,86],[89,90,91],{"impactFactor":21,"impactFactorByYear":2227,"i10Index":129,"i10IndexLast5Year":130,"totalPublication":131,"totalPublicationByYear":2228,"totalCitation":189,"totalCitationByYear":2229,"totalCitationPerPublication":251,"totalCitationPerPublicationByYear":2230,"hindexLast5Year":313,"hindex":313},{"1979":115,"2011":116,"2012":117,"2013":118,"2014":119,"2015":120,"2016":121,"2017":122,"2018":123,"2019":124,"2020":125,"2021":126,"2022":127,"2023":128},{"1961":133,"1962":134,"1963":135,"1964":136,"1965":137,"1966":138,"1967":139,"1968":140,"1969":141,"1970":142,"1971":143,"1972":144,"1973":145,"1974":146,"1975":147,"1976":148,"1977":149,"1978":150,"1979":151,"1980":152,"1981":153,"1982":154,"1983":155,"1984":156,"1985":157,"1986":158,"1987":159,"1988":160,"1989":161,"1990":162,"1991":155,"1992":163,"1993":164,"1994":162,"1995":165,"1996":166,"1997":167,"1998":168,"1999":161,"2000":169,"2001":170,"2002":171,"2003":172,"2004":173,"2005":174,"2006":175,"2007":176,"2008":177,"2009":178,"2010":145,"2011":179,"2012":146,"2013":180,"2014":181,"2015":182,"2016":150,"2017":183,"2018":184,"2019":185,"2020":186,"2021":187,"2022":146,"2023":188,"2024":138},{"1961":130,"1962":133,"1963":191,"1964":192,"1965":193,"1966":194,"1967":195,"1968":196,"1969":197,"1970":181,"1971":198,"1972":199,"1973":200,"1974":201,"1975":202,"1976":203,"1977":204,"1978":205,"1979":206,"1980":207,"1981":208,"1982":209,"1983":210,"1984":211,"1985":212,"1986":209,"1987":213,"1988":214,"1989":215,"1990":216,"1991":217,"1992":218,"1993":219,"1994":220,"1995":221,"1996":222,"1997":223,"1998":224,"1999":225,"2000":226,"2001":227,"2002":228,"2003":229,"2004":230,"2005":231,"2006":232,"2007":233,"2008":234,"2009":235,"2010":236,"2011":237,"2012":238,"2013":239,"2014":240,"2015":241,"2016":242,"2017":243,"2018":244,"2019":245,"2020":246,"2021":247,"2022":248,"2023":249,"2024":250},{"1961":253,"1962":254,"1963":255,"1964":256,"1965":257,"1966":126,"1967":258,"1968":259,"1969":260,"1970":261,"1971":257,"1972":262,"1973":263,"1974":264,"1975":265,"1976":266,"1977":267,"1978":268,"1979":269,"1980":270,"1981":271,"1982":272,"1983":273,"1984":274,"1985":275,"1986":276,"1987":277,"1988":278,"1989":279,"1990":280,"1991":281,"1992":282,"1993":283,"1994":284,"1995":283,"1996":285,"1997":286,"1998":287,"1999":288,"2000":289,"2001":290,"2002":291,"2003":292,"2004":293,"2005":294,"2006":295,"2007":296,"2008":297,"2009":298,"2010":299,"2011":300,"2012":301,"2013":302,"2014":303,"2015":304,"2016":305,"2017":306,"2018":307,"2019":308,"2020":309,"2021":310,"2022":311,"2023":312,"2024":116},{"volume":2232,"pages":2233},{"VOID":2164},{"VOID":2234},"143-152",{"total":494,"publishYear":2168,"statisticByYear":2236},{"1979":437,"1982":250,"1985":261,"1986":437,"1990":437,"2013":437},[2238,2241,2247,2250,2253,2256,2259,2262,2265,2271,2274,2277,2280,2283,2286,2289,2292,2295,2298,2301,2304,2307,2310,2313,2316,2319,2322,2325,2328,2331,2337,2340,2343,2346,2352,2355,2361,2364,2367,2370,2373,2376,2379,2382,2385,2388,2391,2394,2397,2400,2403,2406,2409,2412,2415,2418,2421,2424,2427,2430,2433,2436,2439,2442,2445,2448,2451,2454,2460,2463,2466,2469,2472,2475,2481,2484,2487,2490,2493,2496,2499,2502,2505,2508,2511,2514,2517,2520,2523,2526,2529,2532,2535,2538,2544],{"id":20,"text":2239,"url":20,"identifiers":2240},"Adams, R. 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N.Y.45, 1069 (1942)",{"doi":2246},{"id":2242,"text":2257,"url":2244,"identifiers":2258},"Bischoff, A.: Ultrastructural pathology of the peripheral nervous system in early diabetes. In: R. A. Camerini-Davalos, H. S. Cole (Eds.) Vascular and Neurologic Changes in Early Diabetes, pp. 441–449, New York: Academic Press 1973",{"doi":2246},{"id":2242,"text":2260,"url":2244,"identifiers":2261},"Bradley, W. G.: Disorders of peripheral nerves. Oxford-London-Edinburgh: Blackwell 1974",{"doi":2246},{"id":20,"text":2263,"url":20,"identifiers":2264},"Brain, R., Henson, R. A.: Neurological syndromes associated with carcinoma. The carcinomatous neuromyopathy. Lancet2, 971 (1958)",{},{"id":2266,"text":2267,"url":2268,"identifiers":2269},"d9b599b0-87c1-4eee-9805-b7aa6ec65440","Brown, M. J., Martin, J. R., Asbury, A. K.: Painful diabetic neuropathy. Arch. Neurol. (Chic.)33, 164 (1976)","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0891842208000128",{"doi":2270},"10.1016\u002Fj.cpm.2008.02.004",{"id":2242,"text":2272,"url":2244,"identifiers":2273},"Brownell, B., Hughes, J. T.: Degeneration of muscle in association with carcinoma of the bronchus. J. Neurol., Neurosurg., Psychiat.38, 363 (1975)",{"doi":2246},{"id":20,"text":2275,"url":20,"identifiers":2276},"Bylund, A.-C., Bjurö, T., Cederblad, G., Holm, J., Lundholm, K., Sjörström, M., Ängquist, K. A., Schertén, T.: Physical training in man: skeletal muscle metabolism in relation to muscle morphology and running ability. Eur. J. appl. Physiol.36, 151 (1977)",{},{"id":2242,"text":2278,"url":2244,"identifiers":2279},"Chopra, J. S., Sawhney, B. B., Chakravorty, R. N.: Pathology and time relationship of peripheral nerve changes in experimental diabetes. J. Neurol. Sci.32, 53 (1977)",{"doi":2246},{"id":2242,"text":2281,"url":2244,"identifiers":2282},"Clawson, B. J., Noble, J. F., Lufkin, N. H.: Nodular inflammatory and degenerative lesions of muscles from 450 autopsies. Arch. Path.43, 479 (1947)",{"doi":2246},{"id":20,"text":2284,"url":20,"identifiers":2285},"Coërs, C.: Sur quelques types cliniques et histologiques de polymyosites. Rev. Belg. Path. Med. Exp.25, 369 (1956)",{},{"id":20,"text":2287,"url":20,"identifiers":2288},"Systemic effects of tumors with special reference to the nervous system. In: L. Brain, F. H. Norris (Eds.) The remote effects of cancer on the nervous system. New York-London: Grune and Stratton 1965",{},{"id":20,"text":2290,"url":20,"identifiers":2291},"Croft, P. B., Wilkinson, M.: Carcinomatous neuromyopathy. Its incidence in patients with carcinoma of the lung and carcinoma of the breast. Lancet1, 184 (1963)",{},{"id":20,"text":2293,"url":20,"identifiers":2294},"Croft, P. B., Wilkinson, M.: The incidence of carcinomatous neuromyopathy with special reference to carcinoma of the lung and the breast. In: W. R. Brain, F. H. Norris (Eds.) The remote effects of cancer on the nervous system, pp. 44–54. New York-London: Grune and Stratton 1965a",{},{"id":20,"text":2296,"url":20,"identifiers":2297},"Croft, P. B., Wilkinson, M.: The incidence of carcinomatous neuromyopathy in patients with various types of carcinoma. Brain88, 427 (1965b)",{},{"id":20,"text":2299,"url":20,"identifiers":2300},"Croft, P. B., Henson, R. A., Urich, H.: Sensory neuropathy with bronchial carcinomas: a study of four cases showing serological abnormalities. Brain88, 501 (1965c)",{},{"id":20,"text":2302,"url":20,"identifiers":2303},"Croft, P. B., Urich, H., Wilkinson, M.: Peripheral neuropathy of sensorymotor type associated with malignant disease. Brain90, 31 (1967)",{},{"id":20,"text":2305,"url":20,"identifiers":2306},"Currie, S., Henson, R. A., Morgan, H. G., Poole, A. J.: The incidence of the non-metastatic neurological syndromes of obscure origin in the reticuloses. Brain93, 269 (1970)",{},{"id":20,"text":2308,"url":20,"identifiers":2309},"Currie, S., Henson, R. A.: Neurological syndromes in the reticuloses. Brain94, 307 (1971)",{},{"id":20,"text":2311,"url":20,"identifiers":2312},"Dayan, A. D., Croft, P. B., Wilkinson, M.: Association of carcinomatous neuropathy with different histological types of carcinoma of the lung. Brain88, 427 (1965)",{},{"id":20,"text":2314,"url":20,"identifiers":2315},"Denny-Brown, D.: Primary sensory neuropathy with muscular changes associated with carcinoma. J. Neurol. Neurosurg. Psychiat.11, 73 (1948)",{},{"id":2242,"text":2317,"url":2244,"identifiers":2318},"Denny-Brown, D.: The nature of polymyositis and related muscular diseases. Trans. Stud. Coll. Physens. Philad.28, 14 (1960)",{"doi":2246},{"id":20,"text":2320,"url":20,"identifiers":2321},"Eaton, L. M., Lambert, E. H.: Electromyographic and electrical stimulation of nerves in diseases of motor unit. Observation on myasthenic syndrome associated with malignant tumors. J. Amer. med. Ass.63, 1117 (1957)",{},{"id":20,"text":2323,"url":20,"identifiers":2324},"Edström, L., Kugelberg, E.: Histochemical composition, distribution of fibres and fatiguability of single motor units. J. Neurol. Neurosurg. Psychiat.31, 424 (1968)",{},{"id":20,"text":2326,"url":20,"identifiers":2327},"Engel, W. K.: Histochemistry of neuromuscular disease—significance of muscle fiber types. “Neuromuscular” diseases. Proc. VIII. Int. Congr. Neurology, Vienna 1965. Amsterdam: Excerpta Medica 1965",{},{"id":20,"text":2329,"url":20,"identifiers":2330},"Engel, W. K., Brooke, M. H., Nelson, P. G.: Histochemical studies of denervated or tenotomized cat muscle: Illustrating difficulties in relating experimental animal conditions to human neuromuscular diseases. Ann N.Y. Acad. Sci.138, 160 (1966)",{},{"id":2332,"text":2333,"url":2334,"identifiers":2335},"dff10d44-cc8a-4851-b75b-fe6d68e9dcdb","Engel, W. K., Hawley, R. J.: Focal lesions of muscle in peripheral vascular disease. J. Neurol.215, 161 (1977)","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00312474",{"doi":2336},"10.1007\u002FBF00312474",{"id":2242,"text":2338,"url":2244,"identifiers":2339},"Erbslöh, F.: Die entzündlichen Erkrankungen der Skeletmuskulatur. Verh. dtsch. Ges. inn. Med.71, 207 (1965)",{"doi":2246},{"id":20,"text":2341,"url":20,"identifiers":2342},"Erbslöh, F.: Die Muskelentzündungen. Internist13, 88 (1972)",{},{"id":20,"text":2344,"url":20,"identifiers":2345},"Erbslöh, F.: Muskelkrankheiten. In: G. Bodechtel (Ed.) Differentialdiagnose neurologischer Krankheitsbilder, pp. 815–910, 3. Aufl. Stuttgart: Thieme 1974",{},{"id":2347,"text":2348,"url":2349,"identifiers":2350},"faf9cf54-006f-401a-9cd0-84536df7892e","Fusjisawa, K.: Some observations on the skeletal musculature of aged rat. J. Neurol. Sci.22, 353 (1974)","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002F0022510X75901707",{"doi":2351},"10.1016\u002F0022-510x(75)90170-7",{"id":20,"text":2353,"url":20,"identifiers":2354},"Furtado, D.: The paracancerous neuropathies (french) Rev. Oto-, Neuro-, Ophthal.32, 364 (1960)",{},{"id":2356,"text":2357,"url":2358,"identifiers":2359},"86dee0e2-375a-48da-8b38-fa324eec6a8a","Garland, H.: Diabetic amyotrophy. Brit. med. J.2, 1287 (1955)","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002F000293436390086X",{"doi":2360},"10.1016\u002F0002-9343(63)90086-x",{"id":20,"text":2362,"url":20,"identifiers":2363},"Goerttler, Kl.: Risiken und Nebenwirkungen zytotoxischer Therapie. Diagnostik10, 367 (1977)",{},{"id":2242,"text":2365,"url":2244,"identifiers":2366},"Greenfield, J. G., Shy, G. M., Alvord, E. E., Berg, L.: An atlas of muscle pathology in neuromuscular diseases. Edinburgh-London: Livingstone 1957",{"doi":2246},{"id":2242,"text":2368,"url":2244,"identifiers":2369},"Heffner, R. R., Jr.: Myopathy of embolic origin in patients with carcinoma. Neurology (Minneap.)21, 840 (1971)",{"doi":2246},{"id":2242,"text":2371,"url":2244,"identifiers":2372},"Henson, R. A.: Non-metastatic neurological manifestations of malignant disease. In: D. Williams (Ed.) Modern Trends in Neurology, 5, 209. London: Butterworth 1970",{"doi":2246},{"id":20,"text":2374,"url":20,"identifiers":2375},"Henson, R. A.: Neuromuscular disorders associated with malignant disease, 3rd Ed. Edinburgh-London-New York: Churchill Livingstone 1974",{},{"id":2242,"text":2377,"url":2244,"identifiers":2378},"Henson, R. A., Urich, H.: Peripheral neuropathy associated with malignant disease. In: P. J. Vinken, G. W. Bruyn (Eds.) Handbook of Clinical Neurology, Vol. 8, pp. 131–148. Amsterdam: North Holland 1970",{"doi":2246},{"id":20,"text":2380,"url":20,"identifiers":2381},"Henson, R. A., Russel, D. S., Wilkinson, M.: Carcinomatous neuromyopathy. A clinical and pathological study. Brain77, 82 (1954)",{},{"id":20,"text":2383,"url":20,"identifiers":2384},"Hildebrand, J., Coërs, C.: Neuromuscular function in patients with malignant tumours. Brain90, 67 (1967)",{},{"id":20,"text":2386,"url":20,"identifiers":2387},"Hill, K., Ernst, J.: Einzelthsernekrosen in der Skelettmuskulatur. Verh. dtsch. Ges. Path.58, 656 (Autoref.) (1974)",{},{"id":20,"text":2389,"url":20,"identifiers":2390},"Hutchinson, E. C., Leonard, B. J., Maudsley, C., Yates, P. O.: Neurological complications of the reticuloses. Brain81, 75 (1958)",{},{"id":2242,"text":2392,"url":2244,"identifiers":2393},"Jacobsen, J., Lundbaek, K.: Neuropathy in experimental diabetes—An animal model. Brit. med. J.2, 278 (1976)",{"doi":2246},{"id":2242,"text":2395,"url":2244,"identifiers":2396},"Jennekens, F. G. J., Tomlinson, B. E., Walton, J. N.: Histochemical aspects of five limb muscles in old age. An autopsy study. J. 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Med.31, 389 (1897)",{},{"id":2242,"text":2413,"url":2244,"identifiers":2414},"Mancall, E. L., Rosales, R. K.: Necrotizing myelopathy associated with visceral carcinoma. Brain87, 639 (1964)",{"doi":2246},{"id":2242,"text":2416,"url":2244,"identifiers":2417},"McCombs, R. P., MacMahon, H. E.: Dermatomyositis associated with metastasizing bronchogenic carcinoma. Med. Clin. N. Amer.31, 1148 (1947)",{"doi":2246},{"id":20,"text":2419,"url":20,"identifiers":2420},"Medsger, T. A., Robinson, H., Masi, A. T.: Factors affecting survivorship in polymyositis. Arthritis Rheum.14, 249 (1971)",{},{"id":20,"text":2422,"url":20,"identifiers":2423},"Moody, J. F.: Electrophysiological investigations into the neurological complications of carcinoma. Brain88, 1023 (1965)",{},{"id":2242,"text":2425,"url":2244,"identifiers":2426},"Moore, M. J., Rebeiz, J. J., Hoden, M., Adams, R. D.: Biometric analysis of normal skeletal muscle. Acta neuropath. 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Arch. Psychiat.18, 487 (1887)",{"doi":2246},{"id":20,"text":2443,"url":20,"identifiers":2444},"Oppenheim, H.: Über Hirnsymptome bei Carcinomatose ohne nachweisbare Veränderungen im Gehirn. Charité-Ann.13, 335 (1888)",{},{"id":2242,"text":2446,"url":2244,"identifiers":2447},"Papanicolaou, G. N., Falk, E. A.: General muscular hypertrophy induced by androgenic hormone. Science87, 238 (1938)",{"doi":2246},{"id":2242,"text":2449,"url":2244,"identifiers":2450},"Pearson, C. M.: The incidence and type of pathologic alterations observed in muscles in a routine autopsy survey. Neurology (Minneap.)9, 757 (1959)",{"doi":2246},{"id":2242,"text":2452,"url":2244,"identifiers":2453},"Rebeiz, J. J., Moore, M. J., Holden, E. M., Adams, R. D.: Variations in muscle status with age and systemic diseases. Acta neuropath. (Berl.)22, 127 (1972)",{"doi":2246},{"id":2455,"text":2456,"url":2457,"identifiers":2458},"30f87065-c82b-4316-b1f7-4ff5d3ee5705","Reisner, H.: Paraneoplastische neurologische Syndrome. 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