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We hypothesized that chronic WMI is related to a combination of delayed oligodendrocyte (OL) lineage cell death and arrested maturation of preoligodendrocytes (preOLs). We determined whether ex vivo MRI can distinguish distinct microglial and astroglial responses related to WMI progression and arrested preOL differentiation.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods:\u003C\u002Fjats:title>\u003Cjats:p>We employed a preterm fetal sheep model of global cerebral ischemia in which acute WMI results in selective preOL degeneration. We developed novel algorithms to register histopathologically‐defined lesions with contrast‐weighted and diffusion‐weighted high‐field ex vivo MRI data.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results:\u003C\u002Fjats:title>\u003Cjats:p>Despite mild delayed preOL degeneration, preOL density recovered to control levels by 7 days after ischemia and was ∼2 fold greater at 14 days. However, premyelinating OLs were significantly diminished at 7 and 14 days. WMI evolved to mostly gliotic lesions where arrested preOL differentiation was directly proportional to the magnitude of astrogliosis. A reduction in cerebral WM volume was accompanied by four classes of MRI‐defined lesions. Each lesion type displayed unique astroglial and microglial responses that corresponded to distinct forms of necrotic or non‐necrotic injury. High‐field MRI defined 2 novel hypointense signal abnormalities on T\u003Cjats:sub>2\u003C\u002Fjats:sub>‐weighted images that coincided with microscopic necrosis or identified astrogliosis with high sensitivity and specificity.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Interpretation:\u003C\u002Fjats:title>\u003Cjats:p>These studies support the potential of high‐field MRI for early identification of microscopic necrosis and gliosis with preOL maturation arrest, a common form of WMI in preterm survivors. 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many perinatal factors have been linked to adverse neurodevelopmental outcomes in very premature infants, much of the variation in outcome remains unexplained. The impact on brain development of 1 potential factor, exposure to stressors in the neonatal intensive care unit, has not yet been studied in a systematic, prospective manner.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods:\u003C\u002Fjats:title>\u003Cjats:p>In this prospective cohort study of infants born at <30 weeks gestation, nurses were trained in recording procedures and cares. These recordings were used to derive Neonatal Infant Stressor Scale scores, which were employed to measure exposure to stressors. Magnetic resonance imaging (brain metrics, diffusion, and functional magnetic resonance imaging) and neurobehavioral examinations at term equivalent postmenstrual age were used to assess cerebral structure and function. Simple and partial correlations corrected for confounders, including immaturity and severity of illness, were used to explore these relations.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results:\u003C\u002Fjats:title>\u003Cjats:p>Exposure to stressors was highly variable, both between infants and throughout a single infant's hospital course. Exposure to a greater number of stressors was associated with decreased frontal and parietal brain width, altered diffusion measures and functional connectivity in the temporal lobes, and abnormalities in motor behavior on neurobehavioral examination.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Interpretation:\u003C\u002Fjats:title>\u003Cjats:p>Exposure to stressors in the Neonatal Intensive Care Unit is associated with regional alterations in brain structure and function. Further research into interventions that may decrease or mitigate exposure to stressors in the neonatal intensive care unit is warranted. 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A three‐compartment model, which incorporates hydrolysis of FDG‐6‐PO\u003Cjats:sub>4\u003C\u002Fjats:sub> to FDG, was developed for the measure of kinetic constants and calculation of LCMRGlc. Our model is an extension of that developed by Sokoloff et al. Although small, hydrolysis of FDG‐6‐PO\u003Cjats:sub>4\u003C\u002Fjats:sub> was found to be significant. A PCT system, the ECAT, was used to determine the rate constants, lumped constant, and stability of the model in human beings. The data indicate that cerebral FDG‐6‐PO\u003Cjats:sub>4\u003C\u002Fjats:sub> in humans increases for about 90 minutes, plateaus, and then slowly decreases. After 10 minutes, cerebral blood FDG activity levels were found to be a minor fraction of tissue activity. Precursor pool turnover rate, distribution volumes, and red blood cell‐plasma concentration ratios were determined. Reproducibility (precision) of LCMRGlc measurements (∼2 cm\u003Cjats:sup>2\u003C\u002Fjats:sup> regions) was ± 5.5% over a 5‐hour period. 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JM, 1977, Cerebral glucose‐6‐phosphatase and the movement of 2‐deoxy‐D‐glucose across cell membranes, J Biol Chem, 252, 7035, 10.1016\u002FS0021-9258(19)66931-0",{"doi":1216},"10.1016\u002FS0021-9258(19)66931-0",{"id":24,"text":1218,"url":24,"identifiers":1219},"10.1172\u002FJCI104452",{"doi":1218},{"id":24,"text":1221,"url":24,"identifiers":1222},"10.1172\u002FJCI103324",{"doi":1221},{"id":24,"text":1224,"url":24,"identifiers":1225},"10.1172\u002FJCI104453",{"doi":1224},{"id":24,"text":1227,"url":24,"identifiers":1228},"10.1042\u002Fbj1280199",{"doi":1227},{"id":24,"text":1230,"url":24,"identifiers":1231},"Betz AL, 1973, Kinetics of unidirection glucose transport in the isolated dog brain, Am J Physiol, 225, 586, 10.1152\u002Fajplegacy.1973.225.3.586",{"doi":1232},"10.1152\u002Fajplegacy.1973.225.3.586",{"id":24,"text":1234,"url":24,"identifiers":1235},"Buschiazzo PM, 1970, Sugar transport across the blood brain barrier, Am J Physiol, 219, 1505, 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The factors responsible for the bio‐distribution of 18F‐2‐deoxy‐2‐fluoro‐D‐glucose (18FDG), J Nucl Med, 19, 1154",{},{"id":24,"text":1254,"url":24,"identifiers":1255},"10.1016\u002FS0021-9258(18)84948-1",{"doi":1254},{"id":24,"text":1257,"url":24,"identifiers":1258},"10.1111\u002Fj.1471-4159.1975.tb04395.x",{"doi":1257},{"id":24,"text":1260,"url":24,"identifiers":1261},"10.1007\u002FBF01478536",{"doi":1260},{"id":24,"text":1263,"url":24,"identifiers":1264},"10.1161\u002F01.RES.43.2.324",{"doi":1263},{"id":24,"text":1266,"url":24,"identifiers":1267},"10.1001\u002Farchneur.1973.00490190056006",{"doi":1266},{"id":24,"text":1269,"url":24,"identifiers":1270},"10.1161\u002F01.STR.5.5.630",{"doi":1269},{"id":24,"text":1272,"url":24,"identifiers":1273},"10.1016\u002F0306-4522(78)90106-9",{"doi":1272},{"id":24,"text":1275,"url":24,"identifiers":1276},"Hers HG, 1957, Le Métabolisme du fructose, 102",{},{"id":24,"text":1278,"url":24,"identifiers":1279},"Hers HG, 1950, Le Systeme phosphatasique: repartition de l'activité glucose‐6‐phosphatasique dans les tissus, Bull Soc Chim Biol, 32, 20",{},{"id":24,"text":1281,"url":24,"identifiers":1282},"10.1097\u002F00004728-197906000-00001",{"doi":1281},{"id":24,"text":1284,"url":24,"identifiers":1285},"HuangSCPhelpsMEHoffmanEJet al: Non invasive determination of local cerebral metabolic rate of glucose in normal man with (F18)2‐fluoro‐2‐deoxyglucose and emission computed tomography: theory and results.Am J Physiol(in press)",{},{"id":24,"text":1287,"url":24,"identifiers":1288},"Ido T, 1978, Labeled 2‐deoxy‐D‐glucose analogs. 18F‐labeled 2‐deoxy‐2‐fluoro‐D‐glucose, 2‐deoxy‐2‐fluoro‐D‐mannose and 14‐2‐deoxy‐12‐fluoro‐D‐glucose, J Label Compds Radiopharm, 24, 174",{},{"id":24,"text":1290,"url":24,"identifiers":1291},"Ingvar DH, 1965, Regional cerebral blood flow, Acta Neurol Scand [Suppl], 24, 65",{},{"id":24,"text":1293,"url":24,"identifiers":1294},"10.1002\u002Fana.410040402",{"doi":1293},{"id":24,"text":1296,"url":24,"identifiers":1297},"KuhlDEAlaviAHoffmanEJet al: Local cerebral blood volume in head‐injured patients: determination by emission computed tomography of Tc‐99mred cells.J Neurosurg(in press)",{},{"id":24,"text":1299,"url":24,"identifiers":1300},"Kuhl DE, 1977, Medical Radionuclide Imaging, 309",{},{"id":24,"text":1302,"url":24,"identifiers":1303},"10.1097\u002F00004728-197811000-00040",{"doi":1302},{"id":24,"text":1305,"url":24,"identifiers":1306},"Kuhl DE, 1977, Initial clinical experience with 18F‐2‐deoxy‐D‐glucose for determination of local cerebral glucose utilization by emission computed tomography, Acta Neurol Scand, 56, 192",{},{"id":24,"text":1308,"url":24,"identifiers":1309},"10.1161\u002F01.RES.36.5.610",{"doi":1308},{"id":24,"text":1311,"url":24,"identifiers":1312},"10.1111\u002Fj.1471-4159.1977.tb09610.x",{"doi":1311},{"id":24,"text":1314,"url":24,"identifiers":1315},"10.1161\u002F01.CIR.7.5.724",{"doi":1314},{"id":24,"text":1317,"url":24,"identifiers":1318},"Passow H, 1964, The Red Blood Cell, 71",{},{"id":24,"text":1320,"url":24,"identifiers":1321},"Pennell RB, 1964, The Red Blood Cell, 29",{},{"id":24,"text":1323,"url":24,"identifiers":1324},"10.1016\u002FS0001-2998(77)80042-1",{"doi":1323},{"id":24,"text":1326,"url":24,"identifiers":1327},"Phelps ME, 1973, Correlation between PaCO2 and regional cerebral blood volume by x‐ray fluorescence, J Appl Physiol, 35, 274, 10.1152\u002Fjappl.1973.35.2.274",{"doi":1328},"10.1152\u002Fjappl.1973.35.2.274",{"id":24,"text":1330,"url":24,"identifiers":1331},"10.1152\u002Fjappl.1973.35.5.741",{"doi":1330},{"id":24,"text":1333,"url":24,"identifiers":1334},"Phelps ME, 1977, Positron tomography: an “in vivo” autoradiographic approach to measurement of cerebral hemodynamics and metabolism, Acta Neurol Scand, 56, 446",{},{"id":24,"text":1336,"url":24,"identifiers":1337},"Phelps ME, 1978, ECAT: a new computerized tomographic imaging system for positron emitting radiopharmaceuticals, J Nucl Med, 19, 635",{},{"id":24,"text":1339,"url":24,"identifiers":1340},"Phelps ME, 1977, Medical Radionuclide Imaging, 233",{},{"id":24,"text":1342,"url":24,"identifiers":1343},"Phelps ME, 1978, Investigation of (18F)‐2‐fluoro‐2‐deoxyglucose for the measure of myocardial glucose metabolism, J Nucl Med, 19, 1311",{},{"id":24,"text":1345,"url":24,"identifiers":1346},"10.1097\u002F00004728-197811000-00042",{"doi":1345},{"id":24,"text":1348,"url":24,"identifiers":1349},"10.1210\u002Fendo-82-1-1",{"doi":1348},{"id":24,"text":1351,"url":24,"identifiers":1352},"10.3181\u002F00379727-105-26150",{"doi":1351},{"id":24,"text":1354,"url":24,"identifiers":1355},"Raichle ME, 1975, In vivo measurement of brain glucose transport and metabolism employing glucose‐11C, Am J Physiol, 228, 1936, 10.1152\u002Fajplegacy.1975.228.6.1936",{"doi":1356},"10.1152\u002Fajplegacy.1975.228.6.1936",{"id":24,"text":1358,"url":24,"identifiers":1359},"10.1126\u002Fscience.414358",{"doi":1358},{"id":24,"text":1361,"url":24,"identifiers":1362},"Reivich M, 1977, Measurement of local cerebral glucose metabolism in man with 18F‐2‐fluoro‐2‐deoxy‐D‐glucose, Acta Neurol Scand, 56, 192",{},{"id":24,"text":1364,"url":24,"identifiers":1365},"10.1161\u002F01.RES.44.1.127",{"doi":1364},{"id":24,"text":1367,"url":24,"identifiers":1368},"Robinson GD, 1978, F‐18 fluorodeoxyglucose: remote, semi automated production using a compact cyclotron (abstract), J Nucl Med, 19, 701",{},{"id":24,"text":1370,"url":24,"identifiers":1371},"10.1172\u002FJCI102150",{"doi":1370},{"id":24,"text":1373,"url":24,"identifiers":1374},"Smith AL, 1971, Effect of arterial CO2 tension on cerebral blood flow, mean transit time and vascular volume, J Appl Physiol, 31, 701, 10.1152\u002Fjappl.1971.31.5.701",{"doi":1375},"10.1152\u002Fjappl.1971.31.5.701",{"id":24,"text":1377,"url":24,"identifiers":1378},"10.1111\u002Fj.1471-4159.1977.tb10649.x",{"doi":1377},{"id":24,"text":1380,"url":24,"identifiers":1381},"10.1016\u002F0006-8993(76)90011-1",{"doi":1380},{"id":24,"text":1383,"url":24,"identifiers":1384},"10.1097\u002F00000542-197201000-00013",{"doi":1383},{"id":24,"text":1386,"url":24,"identifiers":1387},"Weiner RS, 1955, The use of “arterialized” blood for the determination of arterial O2 and CO2 tensions, J Thorac Surg, 30, 683, 10.1016\u002FS0096-5588(20)30592-4",{"doi":1388},"10.1016\u002FS0096-5588(20)30592-4",{"id":24,"text":1390,"url":24,"identifiers":1391},"Yudilevich DL, 1971, Blood‐brain transfer of glucose and other molecules measured by lipid indicator dilution, Am J Physiol, 220, 841, 10.1152\u002Fajplegacy.1971.220.3.841",{"doi":1392},"10.1152\u002Fajplegacy.1971.220.3.841",{"id":1394,"createTime":1395,"updateTime":1396,"relativeEntities":1397,"slug":1398,"properties":1399,"entityType":119,"verifyStatus":120,"verifyTime":1414,"verifyNote":121,"languages":1415,"translateLanguages":24,"viewCount":25,"primaryUrl":1416,"fullTextUrl":24,"authors":1417,"publicationType":365,"publisherRelationship":1532,"citationCount":1581,"citationInfo":1582,"publishDate":1586,"publishYear":1583,"citationAnalyzeStatus":23,"lastCitationAnalyze":1587,"indexDatabases":1588,"openAccess":24,"references":1589,"isForceReanalyzing":613},"1f45b680-715c-4b4d-815d-99ea485d1e98","2024-10-06T20:52:54.492+00:00","2026-07-22T07:54:53.834+00:00",[],"Sustained-neocortical-neurogenesis-after-neonatal-hypoxic-ischemic-injury",{"mag":1400,"gsPaper":1402,"openalex":1404,"abstract":1406,"title":1408,"pm":1410,"doi":1412},{"VOID":1401},"2108828244",{"VOID":1403},"[\"8786987263931458493\"]",{"VOID":1405},"W2108828244",{"EN":1407},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\u003Cjats:title>Objective\u003C\u002Fjats:title>\u003Cjats:p>Neocortical neurons are sensitive to hypoxic‐ischemic (H‐I) injuries at term and their demise contributes to neurological disorders. Here we tested the hypothesis that the subventricular zone of the immature brain regenerates neocortical neurons, and that this response is sustained.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>Systemic injections of 5‐bromo‐2′‐deoxyuridine (BrdU) and intraventricular injections of replication‐deficient retroviruses were used to label newly born cells, and confocal microscopy after immunofluorescence was used to phenotype the new cells from several days to several months after perinatal H‐I in the postnatal day 6 rat. Quantitative polymerase chain reaction was used to evaluate chemoattractants, growth factors, and receptors.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Robust production of new neocortical neurons after perinatal H‐I occurs. These new neurons are descendants of the subventricular zone, and they colonize the cell‐sparse columns produced by the injury to the neocortex. These columns are populated by reactive astrocytes and microglia. Surprisingly, this neuronogenesis is sustained for months. Molecular analyses demonstrated increased neocortical production of insulin‐like growth factor‐1 and monocyte chemoattractant factor‐1 (but statistically insignificant production of erythropoietin, brain‐derived neurotrophic factor, glial‐derived neurotrophic factor, and transforming growth factor‐α).\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Interpretation\u003C\u002Fjats:title>\u003Cjats:p>The young nervous system has long been known to possess a greater capacity to recover from injury than the adult system. Our data indicate that H‐I injury in the neonatal brain initiates an enduring regenerative response from the subventricular zone. These data suggest that additional mechanisms than those previously surmised contribute to the remarkable ability of the immature brain to recover from injury. Ann Neurol 2007\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":1409},"Sustained neocortical neurogenesis after neonatal hypoxic\u002Fischemic injury",{"VOID":1411},"17286251",{"VOID":1413},"10.1002\u002Fana.21068","2024-10-06T20:52:54.491+00:00",[123],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fana.21068",[1418,1439,1458,1473,1492,1507],{"id":1419,"sortIndex":25,"researcher":24,"roles":1420,"affiliations":1421,"properties":1430,"displayName":1434,"givenName":24,"familyName":24},"90705140-feb7-4e6a-8bae-88df51d0d01b",[],[1422],{"id":1423,"sortIndex":25,"affiliation":1424,"properties":24},"782f5952-f2d6-4596-983a-c041243df083",{"id":1423,"createTime":24,"updateTime":24,"relativeEntities":1425,"slug":24,"properties":1426,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1429,"statistic":24},[],{"title":1427},{"EN":1428},"Department of Neurology and Neurosciences, UMDNJ-New Jersey Medical School, New Jersey Institute of Technology, Newark, NJ 07103, USA.",[],{"orcid":1431,"title":1433,"gsAuthor":1435,"openalex":1437},{"VOID":1432},"https:\u002F\u002Forcid.org\u002F0000-0003-2447-6540",{"EN":1434},"Zhengang Yang",{"VOID":1436},"[\"UlrvVXQAAAAJ\"]",{"VOID":1438},"A5036867426",{"id":1440,"sortIndex":147,"researcher":24,"roles":1441,"affiliations":1442,"properties":1451,"displayName":1453,"givenName":24,"familyName":24},"6e8555fc-40c9-4522-aacc-f0635fa8f62d",[],[1443],{"id":1444,"sortIndex":25,"affiliation":1445,"properties":24},"06d53cff-dbaa-4781-98df-ad139738a1b6",{"id":1444,"createTime":24,"updateTime":24,"relativeEntities":1446,"slug":24,"properties":1447,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1450,"statistic":24},[],{"title":1448},{"EN":1449},"Department of Neurology and Neurosciences, UMDNJ–New Jersey Medical School, New Jersey Institute of Technology, Newark, NJ",[],{"title":1452,"gsAuthor":1454,"openalex":1456},{"EN":1453},"Matthew Covey",{"VOID":1455},"[\"gYCugSgAAAAJ\"]",{"VOID":1457},"A5029038731",{"id":1459,"sortIndex":165,"researcher":24,"roles":1460,"affiliations":1461,"properties":1468,"displayName":1470,"givenName":24,"familyName":24},"b4aaedf0-bd51-4150-b4bb-05f0551cf8b5",[],[1462],{"id":1444,"sortIndex":25,"affiliation":1463,"properties":24},{"id":1444,"createTime":24,"updateTime":24,"relativeEntities":1464,"slug":24,"properties":1465,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1467,"statistic":24},[],{"title":1466},{"EN":1449},[],{"title":1469,"openalex":1471},{"EN":1470},"Claudine L. 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Failure to assess the verbal score in intubated patients and the inability to test brainstem reflexes are shortcomings. We devised a new coma score, the FOUR (Full Outline of UnResponsiveness) score. It consists of four components (eye, motor, brainstem, and respiration), and each component has a maximal score of 4. We prospectively studied the FOUR score in 120 intensive care unit patients and compared it with the GCS score using neuroscience nurses, neurology residents, and neurointensivists. We found that the interrater reliability was excellent with the FOUR score (κ\u003Cjats:sub>w\u003C\u002Fjats:sub> = 0.82) and good to excellent for physician rater pairs. The agreement among raters was similar with the GCS (κ\u003Cjats:sub>w\u003C\u002Fjats:sub> = 0.82). Patients with the lowest GCS score could be further distinguished using the FOUR score. We conclude that the agreement among raters was good to excellent. 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We have established linkage between the disease phenotype “lubag” and DNA markers which span the Xp11.22‐Xq21.3 region by using a large Filipino family with 8 affected men in three generations. These DNA markers define an interval of about 20 centimorgans in the pericentromeric region of the X chromosome as the most likely site of the disease locus XDPD (X‐linked dystonia‐parkinsonism). XDPD has a maximum multipoint log likelihood ratio score (Z\u003Cjats:sub>max\u003C\u002Fjats:sub>) of about 4.6 over the interval from Xq12 to Xq21.31 (DXS159‐DXYS1X). The co‐occurrence of dystonia and parkinsonism in lubag and in other known disorders suggests there may be a common pathogenetic mechanism. 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recently, all approved multiple sclerosis (MS) disease treatments were administered parenterally. Oral fingolimod was approved in September 2010 by the US Food and Drug Administration to reduce relapses and disability progression in relapsing forms of MS. In the clinical trials that led to approval, fingolimod reduced not only acute relapses and magnetic resonance imaging lesion activity but also disability progression and brain volume loss, suggesting preservation of tissue. Fingolimod's mechanism of action in MS is not known with certainty. Its active form, fingolimod‐phosphate (fingolimod‐P), is a sphingosine 1‐phosphate receptor (S1PR) modulator that inhibits egress of lymphocytes from lymph nodes and their recirculation, potentially reducing trafficking of pathogenic cells into the central nervous system (CNS). Fingolimod also readily penetrates the CNS, and fingolimod‐P formed in situ may have direct effects on neural cells. Fingolimod potently inhibits the MS animal model, experimental autoimmune encephalomyelitis, but is ineffective in mice with selective deficiency of the S1P\u003Cjats:sub>1\u003C\u002Fjats:sub> S1PR subtype on astrocytes despite normal expression in the immune compartment. These findings suggest that S1PR modulation by fingolimod in both the immune system and CNS, producing a combination of beneficial anti‐inflammatory and possibly neuroprotective\u002Freparative effects, may contribute to its efficacy in MS. In clinical trials, fingolimod was generally safe and well tolerated. Its interaction with S1PRs in a variety of tissues largely accounts for the reported adverse effects, which were seen more frequently with doses 2.5 to 10× the approved 0.5mg dose. Fingolimod's unique mechanism of action distinguishes it from all other currently approved MS therapies. 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Accessed March 23 2011.",{},{"id":24,"text":2973,"url":24,"identifiers":2974},"10.1016\u002Fj.coph.2006.09.008",{"doi":2973},{"id":24,"text":2976,"url":24,"identifiers":2977},"10.1177\u002F002215540205000507",{"doi":2976},{"id":24,"text":2979,"url":24,"identifiers":2980},"10.1042\u002Fbj3550189",{"doi":2979},{"id":24,"text":2982,"url":24,"identifiers":2983},"10.1111\u002Fj.1600-6143.2005.00754.x",{"doi":2982},{"id":24,"text":2985,"url":24,"identifiers":2986},"10.1124\u002Fjpet.103.062828",{"doi":2985},{"id":24,"text":2988,"url":24,"identifiers":2989},"Gergely P, 2009, Phase I study with the selective S1P1\u002FS1P5 receptor modulator BAF312 indicates that S1P1 rather than S1P3 mediates transient heart rate reduction in humans (P437), Mult Scler, 15, S125",{},{"id":24,"text":2991,"url":24,"identifiers":2992},"10.1177\u002F0091270006289853",{"doi":2991},{"id":24,"text":2994,"url":24,"identifiers":2995},"DiMarco JP, 2010, First‐dose effect of fingolimod: pooled safety data from two phase 3 studies (TRANSFORMS and FREEDOMS) (P830), Mult Scler, 16, S290",{},{"id":24,"text":2997,"url":24,"identifiers":2998},"10.1172\u002FJCI10905",{"doi":2997},{"id":24,"text":3000,"url":24,"identifiers":3001},"10.1016\u002Fj.prostaglandins.2004.01.006",{"doi":3000},{"id":24,"text":3003,"url":24,"identifiers":3004},"10.4049\u002Fjimmunol.175.11.7151",{"doi":3003},{"id":24,"text":3006,"url":24,"identifiers":3007},"10.1111\u002Fj.1600-6143.2004.00476.x",{"doi":3006},{"id":24,"text":3009,"url":24,"identifiers":3010},"10.1002\u002Fjcb.20088",{"doi":3009},{"id":24,"text":3012,"url":24,"identifiers":3013},"10.1016\u002Fj.coph.2005.12.004",{"doi":3012},{"id":24,"text":3015,"url":24,"identifiers":3016},"10.1038\u002Fnrd2356",{"doi":3015},{"id":24,"text":3018,"url":24,"identifiers":3019},"10.1016\u002FS0014-2999(03)01731-X",{"doi":3018},{"id":24,"text":3021,"url":24,"identifiers":3022},"10.1038\u002Fnri1650",{"doi":3021},{"id":24,"text":3024,"url":24,"identifiers":3025},"10.1161\u002F01.RES.0000164321.91452.00",{"doi":3024},{"id":24,"text":2745,"url":24,"identifiers":3027},{"doi":2745},{"id":24,"text":3029,"url":24,"identifiers":3030},"10.1186\u002F1465-9921-6-48",{"doi":3029},{"id":24,"text":3032,"url":24,"identifiers":3033},"10.1124\u002Fjpet.106.110718",{"doi":3032},{"id":24,"text":3035,"url":24,"identifiers":3036},"10.1165\u002Frcmb.2006-0383OC",{"doi":3035},{"id":24,"text":3038,"url":24,"identifiers":3039},"10.4049\u002Fjimmunol.164.11.5761",{"doi":3038},{"id":24,"text":3041,"url":24,"identifiers":3042},"Schmouder R, 2010, Effects of fingolimod on antibody response following steady‐state dosing in healthy volunteers: a 4‐week randomised, placebo‐controlled study (P412), Mult Scler, 16, S135",{},{"id":24,"text":3044,"url":24,"identifiers":3045},"Novartis. FTY720 in patients with primary progressive multiple sclerosis (INFORMS). ClinicalTrials.gov Identifier: NCT00731692. Available at:http:\u002F\u002Fclinicaltrials.gov\u002Fct2\u002Fshow\u002FNCT00731692. Accessed March 23 2011.",{},{"id":24,"text":3047,"url":24,"identifiers":3048},"Khatri B, 2010, 24‐month efficacy and safety from the TRANSFORMS extension study of oral fingolimod (FTY720) in patients with relapsing‐remitting multiple sclerosis(P03.125), Neurology, 74, A239",{},{"id":24,"text":3050,"url":24,"identifiers":3051},"Calabresi PA, 2010, Oral fingolimod (FTY720) in relapsing‐remitting multiple sclerosis: baseline patient demographics and disease characteristics from a 2‐year phase III trial (FREEDOMS II) (P05.038), Neurology, 74, A416",{},{"id":24,"text":3053,"url":24,"identifiers":3054},"Novartis. Efficacy and safety of fingolimod (FTY720) in patients with relapsing‐remitting multiple sclerosis (FREEDOMS II). ClinicalTrials.gov Identifier: NCT00355134. Available at:http:\u002F\u002Fclinicaltrials.gov\u002Fct2\u002Fshow\u002FNCT00355134. Accessed March 23 2011.",{},{"id":24,"text":3056,"url":24,"identifiers":3057},"Novartis and Mitsubishi Tanabe Pharma. Efficacy and safety of FTY720 in patients with relapsing multiple sclerosis (MS). ClinicalTrials.gov Identifier: NCT00537082. Available at:http:\u002F\u002Fclinicaltrials.gov\u002Fct2\u002Fshow\u002FNCT00537082. Accessed March 23 2011.",{},{"id":24,"text":3059,"url":24,"identifiers":3060},"10.1371\u002Fjournal.pone.0004112",{"doi":3059},{"id":24,"text":3062,"url":24,"identifiers":3063},"10.1016\u002Fj.bbrc.2007.02.043",{"doi":3062},{"id":24,"text":3065,"url":24,"identifiers":3066},"10.1111\u002Fj.1471-4159.2005.03451.x",{"doi":3065},{"id":3068,"createTime":3069,"updateTime":3070,"relativeEntities":3071,"slug":3072,"properties":3073,"entityType":119,"verifyStatus":120,"verifyTime":3069,"verifyNote":121,"languages":3090,"translateLanguages":24,"viewCount":25,"primaryUrl":3091,"fullTextUrl":24,"authors":3092,"publicationType":365,"publisherRelationship":3180,"citationCount":3229,"citationInfo":3230,"publishDate":3234,"publishYear":3231,"citationAnalyzeStatus":3235,"lastCitationAnalyze":3236,"indexDatabases":3237,"openAccess":24,"references":3238,"isForceReanalyzing":613},"195940db-8a50-4d88-80d1-64e32a37c911","2024-09-12T00:52:14.300+00:00","2026-02-24T09:10:49.307+00:00",[],"A-novel-recessive-i-Nefl-i-mutation-causes-a-severe-early-onset-axonal-neuropathy",{"mag":3074,"gsPaper":3076,"pmc":3078,"openalex":3080,"abstract":3082,"title":3084,"pm":3086,"doi":3088},{"VOID":3075},"2036943768",{"VOID":3077},"[]",{"VOID":3079},"4439312",{"VOID":3081},"W2036943768",{"EN":3083},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\u003Cjats:title>Objective\u003C\u002Fjats:title>\u003Cjats:p>To report the first cases of a homozygous recessive mutation in \u003Cjats:italic>NEFL\u003C\u002Fjats:italic>, the gene that encodes the light subunit of neurofilaments.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>Clinical and electrophysiologic data were evaluated, and a sural nerve biopsy from one affected child was examined by immunohistochemistry and electron microscopy. The ability of the mutant protein to form filaments was characterized in an established cell culture system.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Four of five siblings developed of a severe, progressive neuropathy beginning in early childhood. Serial nerve conduction studies showed progressively reduced amplitudes with age and pronounced slowing at all ages. Visual‐evoked responses were slowed in three children, indicating that central nervous system axons were subclinically involved. All four affected children were homozygous for a nonsense mutation at glutamate 210 (E210X) in the \u003Cjats:italic>NEFL\u003C\u002Fjats:italic> gene; both parents were heterozygous carriers. A sural nerve biopsy from an affected patient showed markedly reduced numbers of myelinated axons; the remaining myelinated axons were small and lacked intermediate filaments. The E210X mutant protein did not form an intermediate filament network and did not interfere with the filament formation by wild‐type human light subunit of neurofilaments in SW‐13 vim\u003Cjats:sup>−\u003C\u002Fjats:sup> cells.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Interpretation\u003C\u002Fjats:title>\u003Cjats:p>This is the first demonstration of a recessive \u003Cjats:italic>NEFL\u003C\u002Fjats:italic> mutation, which appears to cause a simple loss of function, resulting in a severe, early‐onset axonal neuropathy with unique features. These results confirm that neurofilaments are the main determinant of axonal caliber and conduction velocity, and demonstrate for the first time that neurofilaments are required for the maintenance of myelinated peripheral nervous system axons. Ann Neurol 2009;66:759–770\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":3085},"A novel recessive \u003Ci>Nefl\u003C\u002Fi> mutation causes a severe, early‐onset axonal neuropathy",{"VOID":3087},"20039262",{"VOID":3089},"10.1002\u002Fana.21728",[123],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fana.21728",[3093,3112,3131,3146,3163],{"id":3094,"sortIndex":25,"researcher":24,"roles":3095,"affiliations":3096,"properties":3105,"displayName":3109,"givenName":24,"familyName":24},"6672e864-df73-43cb-a337-d1c52178c0ad",[],[3097],{"id":3098,"sortIndex":25,"affiliation":3099,"properties":24},"1156f784-9c63-4449-97e6-4f9b8839fef4",{"id":3098,"createTime":24,"updateTime":24,"relativeEntities":3100,"slug":24,"properties":3101,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3104,"statistic":24},[],{"title":3102},{"EN":3103},"Section of Neurology, St. Christopher's Hospital for Children, Drexel University College of Medicine, Philadelphia, PA 19134, USA.",[],{"orcid":3106,"title":3108,"openalex":3110},{"VOID":3107},"https:\u002F\u002Forcid.org\u002F0000-0002-5243-5546",{"EN":3109},"Sabrina W. 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immunoglobulin (IVIg) is the first choice treatment for Guillain‐Barré syndrome (GBS). All patients initially receive the same arbitrary dose of 2g per kg body weight. Not all patients, however, show a good recovery after this standard dose. IVIg clearance may depend on disease severity and vary between individuals, implying that this dose is suboptimal for some patients. In this study, we determined whether the pharmacokinetics of IVIg is related to outcome in GBS.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>We included 174 GBS patients who had previously participated in 2 randomized clinical trials. At entry, all patients were unable to walk unaided and received a standard dose of IVIg. Total IgG levels in serum samples obtained immediately before and 2 weeks after the start of IVIg administration were determined by turbidimetry and related to clinical outcome at 6 months.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>The increase in serum IgG (ΔIgG) 2 weeks after IVIg treatment varied considerably between patients (mean, 7.8g\u002FL; standard deviation, 5.6g\u002FL). Patients with a low ΔIgG recovered significantly more slowly, and fewer reached the ability to walk unaided at 6 months (log‐rank \u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.001). In multivariate analysis adjusted for other known prognostic factors, a low ΔIgG was independently associated with poor outcome (\u003Cjats:italic>p\u003C\u002Fjats:italic> = 0.022).\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Interpretation\u003C\u002Fjats:title>\u003Cjats:p>After a standard dose of IVIg treatment, GBS patients show a large variation in pharmacokinetics, which is related to clinical outcome. This may indicate that patients with a small increase in serum IgG level may benefit from a higher dosage or second course of IVIg. 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