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  • 1
    Keywords: Medical genetics ; Medicine ; Biochemistry ; Neurosciences ; Gene Function ; Molecular Medicine ; Protein Science ; Neurosciences ; Springer eBooks
    Description / Table of Contents: Chapter 1. Molecular and Functional Properties of Progranulin -- Chapter 2. Progranulin as a biomarker for neurodegenerative diseases -- Chapter 3. PGRN and FTLD -- Chapter 4. PGRN and neurodegenerative diseases other than FTLD -- Chapter 5. Progranulin Regulations of Lysosomal Homeostasis and its Involvement in Neurodegenerative Diseases -- Chapter 6. Molecular and Functional Properties of Progranulin -- Chapter 7. PGRN and neuroinflammation -- Chapter 8. Neural Stem/Progenitor Cells and Progranulin -- Chapter 9. Generation and phenotyping of progranulin-deficient mice -- Chapter 10. Pleiotropic protective effects of progranulin in the treatment of ischemic stroke -- Chapter 11. New therapeutic approaches against ocular diseases
    Abstract: This book presents the latest knowledge on the roles of progranulin (PGRN) in normal physiology and pathology and explores the emerging significance of PGRN as a therapeutic target and biomarker in various CNS disorders, including frontotemporal lobe degeneration and other neurodegenerative diseases. Following initial recognition of the importance of PGRN in sexual differentiation of the developing brain and adult neurogenesis, it was subsequently discovered that PGRN acts as a chaperone of lysosomal enzymes and plays a crucial role in maintaining cellular protein homeostasis. It has also been found that sex steroids modulate the expression of PGRN and its trophic effects in the developing CNS and that PGRN directly or indirectly influences neural stem and progenitor cells. Against this background, deeper understanding of the molecular and functional properties of PGRN would provide fresh impetus for the development of mechanism-based therapeutic approaches for multiple disorders. Medications targeting the recovery of lysosomal function appear to hold particular promise in patients with neurodegenerative diseases resulting from PGRN insufficiency. In examining multiple aspects of this fascinating field, the book will be of high value for researchers and graduate students
    Pages: VII, 183 p. 37 illus., 13 illus. in color. : online resource.
    ISBN: 9789811361869
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  • 2
    ISSN: 1432-0533
    Keywords: Secretory meningioma ; Rosette ; Moyamoya vessel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case of secretory meningioma with numerous meningothelial rosettes is reported. A 66-year-old man with moyamoya disease gradually developed skull deformity, and underwent surgery for the skull tumor overlying the hemisphere. Histological examination disclosed numerous meningothelial rosettes quite similar to those induced by subarachnoid injection of epinephrine and pseudopsammoma bodies described by Kepes. This may be the first case of meningioma associated with numerous rosette formations.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In the present study we examined the effects of a new Ca2+ channel blocker (lomerizine), an antimigraine drug, on cerebral cortical blood flow (CBF) in anaesthetized rats (laser Doppler flowmetry) and on vertebral blood flow in anaesthetized beagle dogs (electromagnetic flowmeter).2. Lomerizine (1.25–10 mg/kg, p.o.) dose-dependently increased CBF in rats without affecting blood pressure (BP) or heart rate (HR).3. The plasma concentration of lomerizine (free base) in anaesthetized rats at 30 and 60 min after the initial administration of 5 mg/kg, p.o., times at which there was a significant increase in CBF, was similar to that reported in healthy subjects receiving lomerizine at 10 mg (2 × 5 mg)/day, p.o., a dose that significantly reduces the frequency and mean duration of headache attacks.4. Flunarizine (10 mg/kg, p.o.) did not increase CBF significantly. Flunarizine (20 mg/kg, p.o.) did not increase CBF, but did decrease BP 30–120 min after its administration.5. Lomerizine (2.5 and 5 mg/kg, intraduodenally) dose- dependently increased vertebral blood flow in dogs without significantly changing BP or HR. With 10 mg/kg intraduodenal lomerazine, vertebral blood flow remained elevated from 20 to 240 min after administration and BP was decreased from 20 to 120 min.6. Thus, lomerizine had a greater effect on CBF than on BP and HR and, therefore, it may be clinically effective in con-ditions associated with circulatory disturbances in the brain, such as migraine, without producing systemic effects (e.g. hypotension) generally seen with other Ca2+ channel blockers.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Cortical spreading depression (CSD) was induced by direct current stimulation of the lateral frontal cortex in awake and freely moving rats.2. Regional cerebral blood flow (rCBF) was continuously measured by a laser Doppler flowmeter using an acrylic cup which was chronically fixed on the surface of the cerebral cortex. Under the resting condition rCBF remained constant throughout the observation period and showed a high reproducibility.3. rCBF increased to approximately 190% of control values during 1-3 min after CSD, and decreased to approximately 80% of control values, before returning to normal values 60 min after CSD.4. These results are consistent with those found in anesthetized animals. This is the first study which has continuously monitored cortical hypoperfusion after CSD in awake and freely moving rats. The model is a useful system for studying migraine with aura.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Bunazosin hydrochloride is a potent and selective α1-adrenoceptor antagonist that has been clinically used both as a systemic antihypertensive as well as an ocular hypotensive drug. In a number of studies, we have examined some effects of bunazosin hydrochloride that might indicate its potential as an anti-glaucoma drug. In normal rabbit eyes, topically instilled bunazosin hydrochloride reached the posterior retina by local penetration at concentrations sufficient to attenuate the phenylephrine- or endothelin-1 (ET-1)-induced constriction of retinal arteries. Furthermore, bunazosin hydrochloride improved the impairment of optic nerve head (ONH) blood flow, the prolongation of visual-evoked potentials (VEP) implicit time, the enlargement of the optic disk cup, and the decrease in the number of retinal ganglion cell layer cells induced by repeated injections of ET-1 in rabbits. Topically instilled bunazosin hydrochloride improved the reductions in ONH capillary blood flow and VEP amplitude induced in rabbit eyes by nitric oxide synthase inhibition. In rat primary retinal cultures, bunazosin hydrochloride reduced glutamate-induced neuronal cell death, presumably through a Na+ channel blocking effect. In healthy humans, topically instilled bunazosin hydrochloride reportedly increases blood velocity in the ONH, retina and choroid, without significantly altering either blood pressure or heart rate. These results indicate that bunazosin hydrochloride exerts both an improvement effect within the ocular circulation and a direct neuroprotective effect. Hence, bunazosin hydrochloride may be useful as a therapeutic drug against ischemic retinal diseases (such as glaucoma and retinal vascular occlusive diseases) that are associated with disturbances of the ocular circulation.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    CNS drug reviews 1 (1995), S. 0 
    ISSN: 1527-3458
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Glaucoma is defined as an optic neuropathy with characteristic changes in the optic nerve head and ultimate loss of visual field. Previous studies have suggested that (a) mechanical damage due to raised intraocular pressure and (b) a compromised tissue circulation in the optic nerve head play significant roles in the development of glaucomatous damage in the optic nerve head. Recently, we found that lomerizine, a new Ca2+ channel blocker, increased ocular circulation and protected neuronal cells against retinal neurotoxicity both in vitro and in vivo with minimal cardiovascular side effects. We examined the effect of lomerizine on the ocular circulation and compared it with those of other Ca2+ channel blockers in normal rabbits and in rabbits with an endothelin-1-disturbed circulation in the optic nerve head. In anesthetized rabbits, lomerizine and the other Ca2+ channel blockers increased the ocular circulation and also inhibited the hypoperfusion induced in optic nerve head tissue by an intravitreous injection of endothelin-1. Whereas the other Ca2+ channel blockers produced changes in blood pressure and heart rate, the effects of lomerizine on these parameters were slight. In healthy humans, lomerizine increased blood velocity in the optic nerve head, without significantly altering blood pressure or heart rate. Moreover, lomerizine reduced retinal damage in rats both in vitro and in vivo, presumably through a Ca2+ channel blocking effect via an action that may involve a direct protection of retinal neurons as well as an improvement in the ocular circulation. These results indicate that lomerizine may be useful as a therapeutic drug against ischemic retinal diseases (such as glaucoma and retinal vascular occlusive diseases) that involve a disturbance of the ocular circulation.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0878
    Keywords: Retrograde tracing ; Immunocytochemistry ; Vascular innervation ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The origin of nerve fibers to the superficial temporal artery of the rat was studied by retrograde tracing with the fluorescent dye True Blue (TB). Application of TB to the rat superficial temporal artery labeled perikarya in the superior cervical ganglion, the otic ganglion, the sphenopalatine ganglion, the jugular-nodose ganglionic complex, and the trigeminal ganglion. The labeled perikarya were located in ipsilateral ganglia; a few neuronal somata were, in addition, seen in contralateral ganglia. Judging from the number of labeled nerve cell bodies the majority of fibers contributing to the perivascular innervation originate from the superior cervical, sphenopalatine and trigeminal ganglia. A moderate labeling was seen in the otic ganglion, whereas only few perikarya were labeled in the jugular-nodose ganglionic complex. Furthermore, TB-labeled perikarya were examined for the presence of neuropeptides. In the superior cervical ganglion, all TB-labeled nerve cell bodies contained neuropeptide Y. In the sphenopalatine and otic ganglia, the majority of the labeled perikarya were endowed with vasoactive intestinal polypeptide. In the trigeminal ganglion, the majority of the TB-labeled nerve cell bodies displayed calcitonin gene-related peptide, while a small population of the TB-labeled neuronal elements contained, in addition, substance P. In conclusion, these findings indicate that the majority of peptide-containing nerve fibers to the superficial temporal artery originate in ipsilateral cranial ganglia; a few fibers, however, may originate in contralateral ganglia.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1437-2320
    Keywords: Cerebral circulation ; perivascular innervation ; subarachnoid hemorrhage ; vasospasm
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The authors describe the perivascular innervation of cerebral circulation. The different nerve fiber systems can be classified as follows: 1. Sympathetic (noradrenaline, neuropeptide Y), 2. Parasympathetic (acetylcholine, vasoactive intestinal peptide/peptide histidine isoleucine (methionine), 3. Sensory (tachykinins, calcitonin gene-related peptide). Each of these systems is outlined by their basic anatomical and physiological facts. Then, the etiology of cerebral vasospasm after subarachnoid hemorrhage is discussed in relation to the cerebrovascular innervation.
    Type of Medium: Electronic Resource
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