The membrane lysophospholipase activity of erythrocytes obtained from Duchenne muscular dystrophy patients was lower than that of erythrocytes from age-matched normal boys. On the other hand, the membrane enzyme activity of erythrocytes from myotonic dystrophy patients was not different from that of their age- and sex-matched controls. Dipyridamole (0.1 mM) and glycerol 3-phosphorylcholine (2 mM) had no significant effect on these enzyme activities. These results suggest that membrane lysophospholipid metabolism may be altered in Duchenne muscular dystrophy but not in myotonic dystrophy.
Theiler's virus (TV)-infected mice were treated with antithymocyte serum (ATS), cyclophosphamide or pepstatin (a protease inhibitor) to determine the effect on demyelination. When ATS and cyclophosphamide were begun at the time of infection there was significantly less demyelination at 2.5-3.5 weeks than in pepstatin or non-treated infected controls. When immunosuppression was continued for 5 weeks, or when it was not started until 5 weeks post-infection, no significant decrease in demyelination was seen compared to controls. The findings indicate that timing of immunosuppression is critical in determining the extent of TV demyelination. Such demyelination may occur by different mechanisms that are active at different times. The "bystander effect' may be important in early demyelination, but late demyelination may be due to other causes, such as oligodendrocyte lytic infection.
Zinc profiles were examined in 68 patients with multiple sclerosis, 62 normal volunteers, and 13 patients with other neurological diseases. Plasma zinc levels were slightly increased in patients with multiple sclerosis and significantly increased in those with other neurological impairments ( p <0.01), compared with control subjects. Albumin‐bound as well as protein‐bound zinc levels were normal in all groups tested. The α 2 macroglobulin‐bound zinc level was significantly lower ( p < 0.01) in patients with multiple sclerosis than in control subjects. Erythrocyte‐bound zinc levels were significantly increased ( p < 0.05) in patients with multiple sclerosis when compared with control subjects. Erythrocyte‐bound zinc was normal in patients with other neurological impairments. Because erythrocyte‐bound zinc levels are relatively independent of daily fluctuations in dietary zinc intake, an increase in these values may suggest alterations in the control mechanisms governing zinc compartmentalization in patients with multiple sclerosis.
HomeStrokeVol. 13, No. 1Sympathetic nerves protect against blood-brain barrier disruption in the spontaneously hypertensive rat. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBSympathetic nerves protect against blood-brain barrier disruption in the spontaneously hypertensive rat. S M Mueller, P J Ertel, D L Felten and J M Overhage S M MuellerS M Mueller , P J ErtelP J Ertel , D L FeltenD L Felten and J M OverhageJ M Overhage Originally published1 Jan 1982https://doi.org/10.1161/01.STR.13.1.83Stroke. 1982;13:83–88 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Ghali M, Marchenko V, Yaşargil M and Ghali G (2020) Structure and function of the perivascular fluid compartment and vertebral venous plexus: Illumining a novel theory on mechanisms underlying the pathogenesis of Alzheimer's, cerebral small vessel, and neurodegenerative diseases, Neurobiology of Disease, 10.1016/j.nbd.2020.105022, 144, (105022), Online publication date: 1-Oct-2020. Kucuk M, Kaya M, Kalayci R, Cimen V, Kudat H, Arican N, Elmas I and Korkut F (2002) Effects of losartan on the blood–brain barrier permeability in long-term nitric oxide blockade-induced hypertensive rats, Life Sciences, 10.1016/S0024-3205(02)01772-1, 71:8, (937-946), Online publication date: 1-Jul-2002. Lincoln J (1995) Innervation of cerebral arteries by nerves containing 5-hydroxytryptamine and noradrenaline, Pharmacology & Therapeutics, 10.1016/0163-7258(95)02017-9, 68:3, (473-501), Online publication date: 1-Jan-1995. Shaver S, Wall K, Wainman D and Gross P (1992) Regional quantitative permeability of blood-brain barrier lesions in rats with chronic renal hypertension, Brain Research, 10.1016/0006-8993(92)90747-W, 579:1, (99-106), Online publication date: 1-May-1992. Edmunds M and Walls J (2007) Pathogenesis of Seizures During Recombinant Human Erythropoietin Therapy, Seminars in Dialysis, 10.1111/j.1525-139X.1991.tb00080.x, 4:3, (163-167) Isaacson L, Saffran B and Crutcher K (1990) Intracerebral NGF infusion induces hyperinnervation of cerebral blood vessels, Neurobiology of Aging, 10.1016/0197-4580(90)90062-5, 11:1, (51-55), Online publication date: 1-Jan-1990. Koistinaho J, Wadhwani K and Rapoport S (1989) Increased density of perivascular adrenergic innervation in tibial and vagus nerves of spontaneously hypertensive rats, Journal of Neuroscience Research, 10.1002/jnr.490240312, 24:3, (424-430), Online publication date: 1-Nov-1989. Tsai S, Tew J and Shipley M (1989) Cerebral arterial innervation: II. Development of calcitonin-gene-related peptide and norepinephrine in the rat, The Journal of Comparative Neurology, 10.1002/cne.902790102, 279:1, (1-12), Online publication date: 1-Jan-1989. Dhítal K, Gerli R, Lincoln J, Milner P, Tanganelli P, Weber G, Fruschelli C and Burnstock G (1988) Increased density of perivascular nerves to the major cerebral vessels of the spontaneously hypertensive rat: differential changes in noradrenaline and neuropeptide Y during development, Brain Research, 10.1016/0006-8993(88)90910-9, 444:1, (33-45), Online publication date: 1-Mar-1988. Baumbach G, Dobrin P, Hart M and Heistad D (1988) Mechanics of cerebral arterioles in hypertensive rats., Circulation Research, 62:1, (56-64), Online publication date: 1-Jan-1988. Clostre F (1988) From the Body to the Cellular Membranes: The Different Levels of Pharmacological Action of Ginkgo Biloba Extract Rökan, 10.1007/978-3-642-73686-5_20, (180-198), . Harper S (1987) Antihypertensive drug therapy prevents cerebral microvascular abnormalities in hypertensive rats., Circulation Research, 60:2, (229-237), Online publication date: 1-Feb-1987. Reed W and Anderson R (1986) Effects of rapid blood pressure reduction on cerebral blood flow, American Heart Journal, 10.1016/0002-8703(86)90585-5, 111:1, (226-228), Online publication date: 1-Jan-1986. Aubineau P, Reynier-Rebuffel A, Bouchaud C, Jousseaume O and Seylaz J (1985) Long-term effects of superior cervical ganglionectomy on cortical blood flow of non-anesthetized rabbits in resting and hypertensive conditions, Brain Research, 10.1016/0006-8993(85)90243-4, 338:1, (13-23), Online publication date: 1-Jul-1985. Mueller S and Black W (1985) Sympathetic nerve activity: a link to stroke?, Stroke, 16:1, (73-75), Online publication date: 1-Jan-1985. Reed G and Devous M (1985) Cerebral Blood Flow Autoregulation and Hypertension, The American Journal of the Medical Sciences, 10.1097/00000441-198501000-00007, 289:1, (37-44), Online publication date: 1-Jan-1985. Harper S and Bohlen H (1984) Microvascular adaptation in the cerebral cortex of adult spontaneously hypertensive rats., Hypertension, 6:3, (408-419), Online publication date: 1-May-1984.Mueller S, Muller J and Asdell S (1984) Cerebral hemorrhage associated with phenylpropanolamine in combination with caffeine., Stroke, 15:1, (119-123), Online publication date: 1-Jan-1984. Busija D and Heistad D (1984) Factors involved in the physiological regulation of the cerebral circulation Reviews of Physiology, Biochemistry and Pharmacology, Volume 86, 10.1007/BFb0027696, (161-211), . Spatz M (1984) Attenuated Blood-Brain Barrier Structural Elements of the Nervous System, 10.1007/978-1-4684-4586-2_18, (501-543), . Harrell L, Barlow T and Davis J (1983) Sympathetic sprouting and recovery of a spatial behavior, Experimental Neurology, 10.1016/0014-4886(83)90410-7, 82:2, (379-390), Online publication date: 1-Nov-1983. Igloffstein J and Laas R (1983) Cerebral infarction due to carotid occlusion and carbon monoxide exposure. II. Influence of preganglionic cervical sympathectomy., Journal of Neurology, Neurosurgery & Psychiatry, 10.1136/jnnp.46.8.768, 46:8, (768-773), Online publication date: 1-Aug-1983. Mueller S, Ertel P, Felten D and Overhage J (1983) The chronic influence of sympathetic nerves on cerebral vessels is age-related., Stroke, 14:2, (286-289), Online publication date: 1-Mar-1983.Mueller S and Ertel P (1983) Association between sympathetic nerve activity and cerebrovascular protection in young spontaneously hypertensive rats., Stroke, 14:1, (88-92), Online publication date: 1-Jan-1983. January 1982Vol 13, Issue 1 Advertisement Article InformationMetrics Copyright © 1982 by American Heart Associationhttps://doi.org/10.1161/01.STR.13.1.83 Originally publishedJanuary 1, 1982 PDF download Advertisement
The two main electrophysiological abnormalities seen in the first two weeks of the acute Guillain-Barré syndrome (GBS) were conduction block and, in some patients, low maximum M response amplitudes. In this study period, maximum motor and sensory conduction velocities were often in the normal range and temporal dispersion was relatively less common. The conduction block was generalized in its distribution in some peripheral nerves, while in others the block was predominantly proximal or distal in location. Conduction abnormalities in excess of those proximal or distal to it were frequent at common sites of entrapment. Very low M response amplitudes early in the course of the disease correlated well with the subsequent development and frequency of denervation in the muscle(s) and unfavourable clinical recovery. We conclude that conduction block is the main cause of the acute paralysis and sensory loss in the GBS. Axonal degeneration contributes variably to the acute disorder, but is the main cause of lasting disability.
A 2‐week‐old boy had profound generalized weakness, hypotonia, hyporeflexia, macroglossia, and severe lactic acidosis. The infant improved spontaneously: he held his head at 4 1/2 months, rolled over at 7 months, and walked by 16 months. At 33 month of age, he had mild proximal weakness. Macroglossia disappeared by age 4 months. Blood lactic acid declined steadily and was normal by 14 months of age. Histochemical and ultrastructural studies of muscle biopsy specimens obtained at 1 and 7 months of age showed excessive mitochondria, lipid, and glycogen; a third biopsy at age 36 months showed only atrophy of scattered fibers. Cytochrome c oxidase stain was positive in fewer than 5% of fibers in the first biopsy, in approximately 60% of fibers in the second biopsy, and in all fibers in the third biopsy. Biochemical analysis showed an isolated defect of cytochrome c oxidase activity, which was only 8% of the lowest control level in the first biopsy; the activity increased to 47% in the second biopsy and was higher than normal in the third. In contrast to that in the fatal infantile form of cytochrome c oxidase deficiency, the enzyme defect in this condition is reversible. The biochemical basis for this difference remains to be explained.
Proton nuclear magnetic resonance (NMR) images depict the distribution and concentration of mobile protons modified by the relaxation times T1 and T2. Using the steady-state-free-precession (SSFP) technique, serial coronal images were obtained sequentially over time in laboratory animals with experimental ischemic infarction. Image changes were evident as early as 2 hours after carotid artery ligation, and corresponded to areas of ischemic infarction noted pathologically. Resulting SSFP images in experimental stroke are contrasted to inversion-recovery NMR images in an illustrative patient with established cerebral infarction. Bulk T1 and T2 measurements were made in vitro in three groups of gerbils: normal, those with clinical evidence of infarction, and those clinically normal after carotid ligature. Infarcted hemispheres had significantly prolonged T1 and T2 (1.47 +/- .12 sec, 76.0 +/- 9.0 msec, respectively) when compared to the contralateral hemisphere (T1 = 1.28 +/- .05 sec, T2 = 58.7 +/- 3.9 msec) or to the other two groups. These data suggest that changes in NMR parameters occur and can be detected by NMR imaging as early as two hours after carotid artery ligation.
