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  • 1
    Electronic Resource
    Electronic Resource
    The Simian Virus 40 Large T Antigen Does Not Inhibit Translation of the 14-kDa Myelin Basic Protein mRNA in Reticulocyte Lysates or in Transfected Cells (1995)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 64 (1995), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Viral T antigens are transcription factors that have been suspected of inhibiting expression of the myelin basic protein (MBP) mRNA at the translational level in vitro and in vivo. The effect of simian virus 40 (SV40) large T antigen (T-ag) was examined on the translation of the 14-kDa MBP mRNA in reticulocyte lysates and on MBP expression after transfection into cells that express SV40 T-ag. SV40 T-ag did not inhibit translation of 14-kDa MBP cRNAs in cell-free translations even at 30 µM (∼600 µg/ml) T-ag. Permanent transfection of COS-1 cells (which endogenously express SV40 T-ag) with the 14-kDa MBP cDNA resulted in the expression of the 14-kDa MBP as determined by western blot analysis. Permanent transfection of N20.1 cells, an oligodendrocyte line immortalized with a temperature-sensitive SV40 T-ag, with the 14-kDa MBP cDNA construct also resulted in the expression of the 14-kDa MBP under conditions in which the cells expressed functional SV40 T-ag. These results indicate that SV40 T-ag does not prevent expression of the MBP gene at the translational level and that in those immortalized oligodendrocyte lines that express MBP mRNA, but not MBP protein, some factor other than the SV40 large T-ag is responsible for the posttranscriptional regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1995.64020928.x
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  • 2
    Electronic Resource
    Electronic Resource
    The expression of Na+/K+-ATPase β-subunit cRNA injected into Xenopus oocytes is affected by coinjection with α-subunit cRNA (1995)
    Springer
    The journal of membrane biology 148 (1995), S. 51-56 
    Details
    ISSN: 1432-1424
    Keywords: Na+/K+ ; ATPase ; cDNA expression ; Subunit assembly ; Xenopus oocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The cRNA for Torpedo californica Na+/K+-ATPase β-subunit (cRNAβ) was injected into Xenopus oocytes alone or with the cRNA for the Na+/K+-ATPase α-subunit (cRNAα). When cRNAβ was injected alone, the amount of the β-subunit that accumulated in oocytes increased with increasing amounts of injected cRNAβ. When cRNAβ and cRNAα were injected simultaneously, less β-subunit accumulated than when cRNAβ was injected alone, whereas the Na+/K+-ATPase activity increased markedly. The decrease in the accumulation of the β-subunit was dose-dependent upon the cRNAα. The mutant β-subunit unable to assemble with the α-subunit accumulated in oocytes independently of cRNAα, suggesting that post-translational control mechanisms may serve to reduce the accumulation of the β-subunit.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00234155
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  • 3
    Electronic Resource
    Electronic Resource
    Role of cytochrome P450 in hepatotoxicity induced by di- and tributyltin compounds in mice (1995)
    Springer
    Archives of toxicology 69 (1995), S. 655-658 
    Details
    ISSN: 1432-0738
    Keywords: Key words Butyltin compounds ; Cytochrome P450 ; Hepatotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The role of cytochrome P450 in the induction of hepatotoxicity by butyltin compounds such as tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) was investigated in vivo. The pretreatment of mice with SKF-525A, which decreased hepatic levels of cytochrome P450, suppressed TBTC-induced hepatotoxicity, as estimated by serum ornithine carbamyl transferase activity, whereas pretreatment with phenobarbital (PB), which increased the levels of cytochrome P450, enhanced the hepatotoxicity of TBTC. In the case of DBTC, PB pretreatment enhanced hepatotoxicity, while SKF-525A had no effect. Under these experimental conditions only PB pretreatment was found to increase hepatic levels of tin in mice treated with TBTC. These results suggest that hepatic metabolism of butyltin compounds by cytochrome P450 is more closely related to the induction of hepatotoxicity by TBTC than by DBTC. The active tin compounds formed during hepatic metabolism, which are responsible for induction of hepatotoxicity, will be discussed
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050228
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  • 4
    Electronic Resource
    Electronic Resource
    Familial amyloid polyneuropathy associated with transthyretin Gly42 mutation: a quantitative light and electron microscopic study of the peripheral nervous system (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 516-525 
    Details
    ISSN: 1432-0533
    Keywords: Familial amyloid polyneuropathy ; Transthyretin ; Ultrastructure ; Lectin histochemistry ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We performed extensive quantitative analyses of the peripheral nervous system (PNS) of two siblings with familial amyloid polyneuropathy (FAP) caused by a transthyretin (TTR) Gly42 mutation. Pronounced amyloid deposition was found in the sympathetic ganglia (SyG), dorsal root ganglia (DRG) and throughout the length of the peripheral nerve fibers with some accentuation in the more proximal portion. There was severe neuronal loss in the SyG and DRG together with nerve fiber depletion in the nerve trunk, while only a small amount of amyloid deposition with mild fiber loss was seen in the spinal roots. Sprouts of regenerating axons were very scanty even in the spinal nerves or roots. A teased fiber study mainly showed demyelinating fibers, but axonal degeneration was also present throughout peripheral nerves. An electron microscopic study showed fine amyloid fibrils in direct contact with the axoplasmic membrane of demyelinated axons and destruction of axons in some areas. Amyloid deposition within the PNS in this type of FAP resembled that in type I FAP (TTR Met30). However, direct axonal damage by amyloid fibrils appeared to be more prominent in our cases than in type I FAP. Lectin histochemistry using Ulex europaeus agglutinin I demonstrated preferential depletion of small neurons in the DRG and their primary afferent fibers in the spinal dorsal horn. Primary axonal degeneration and ganglionopathy due to amyloid deposition appear to be the pathogenetic mechanisms for peripheral neuropathy in this type of FAP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294814
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  • 5
    Electronic Resource
    Electronic Resource
    Familial amyloid polyneuropathy associated with transthyretin Gly42 mutation: a quantitative light and electron microscopic study of the peripheral nervous system (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 516-525 
    Details
    ISSN: 1432-0533
    Keywords: Key words Familial amyloid polyneuropathy ; Transthyretin ; Ultrastructure ; Lectin histochemistry ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We performed extensive quantitative analyses of the peripheral nervous system (PNS) of two siblings with familial amyloid polyneuropathy (FAP) caused by a transthyretin (TTR) Gly42 mutation. Pronounced amyloid deposition was found in the sympathetic ganglia (SyG), dorsal root ganglia (DRG) and throughout the length of the peripheral nerve fibers with some accentuation in the more proximal portion. There was severe neuronal loss in the SyG and DRG together with nerve fiber depletion in the nerve trunk, while only a small amount of amyloid deposition with mild fiber loss was seen in the spinal roots. Sprouts of regenerating axons were very scanty even in the spinal nerves or roots. A teased fiber study mainly showed demyelinating fibers, but axonal degeneration was also present throughout peripheral nerves. An electron microscopic study showed fine amyloid fibrils in direct contact with the axoplasmic membrane of demyelinated axons and destruction of axons in some areas. Amyloid deposition within the PNS in this type of FAP resembled that in type I FAP (TTR Met30). However, direct axonal damage by amyloid fibrils appeared to be more prominent in our cases than in type I FAP. Lectin histochemistry using Ulex europaeus agglutinin I demonstrated preferential depletion of small neurons in the DRG and their primary afferent fibers in the spinal dorsal horn. Primary axonal degeneration and ganglionopathy due to amyloid deposition appear to be the pathogenetic mechanisms for peripheral neuropathy in this type of FAP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294814
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  • 6
    Electronic Resource
    Electronic Resource
    Clinical evaluation of gastric fundic gland polyps without familial polyposis coli (1995)
    Springer
    Abdominal imaging 20 (1995), S. 101-105 
    Details
    ISSN: 1432-0509
    Keywords: Stomach, polyposis ; Stomach, fundic gland polyp ; Stomach, cystic hamartomatous polyp ; X-ray examination, endoscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Assessments were made of 63 cases of fundic gland polyposis (FGP) unassociated with adenomatosis coli. These cases were evaluated by radiological examination over 2 years follow-up. All polyps were pathologically confirmed by endoscopic biopsies. Methods: Most cases were asymptomatic when diagnosed during mass radiological surveys of the upper gastrointestinal tract. The majority of patients ranged in age from 40–60 years, and the polyps numbered fewer than 20 in 55 cases (87.3%). Polyps were detected in the fundic glands using the congo red test and by biopsies. Results: All serum gastrin values were within the normal range. During the course of this study, the polyps of 13 cases (20.6%) increased and those of three cases (4.8%) decreased or resolved completely. Conclusion: From these findings it is considered that FGP are observed in stomachs with less atrophy, and that polyps follow courses in which they increase, decrease, disappear, along with atrophy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00201512
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