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  • 1
    Electronic Resource
    Electronic Resource
    A neutrophil elastase inhibitor (ONO-5046) reduces neurologic damage after spinal cord injury in rats (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In view of a cytoprotective effect of elastase inhibitor on chemokine-mediated tissue injury, we examined the neuroprotective effect of ONO-5046, a specific inhibitor of neutrophil elastase, in rats with spinal cord injury. Standardized spinal cord compression markedly increased cytokine-induced neutrophil chemo-attractant (CINC)-1 mRNA and protein. Their increases correlated with neurologic severity of injured rats. Immunohistochemically, CINC-1 protein was detected sequentially in vascular endothelial cells at 4 h, in perivascular neutrophils at 8 h, and in neutrophils infiltrating into cord substance at 12 h. Pretreatment with ONO-5046 (50 mg/kg) markedly ameliorated motor disturbance in injured rats, and reduced CINC-1 protein and mRNA expression. ONO-5046 also significantly reduced the increase of neutrophil accumulation or infiltration estimated by myeloperoxidase activity, and the extent of vascular permeability by Evans blue extravasation in the injured cord segment in comparison to control animals receiving vehicle. These results suggest that CINC-1 contributed to inflammation in rat spinal cord injury and ONO-5046 attenuated neurologic damage partly by blocking CINC-1 production of the chemoattractant, preventing neutrophil activation and vascular endothelial cell injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00488.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mesoscopic transport in Si metal-oxide-semiconductor field-effect transistors with a dual-gate structure (1994)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 76 (1994), S. 5561-5566 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: This article studies the mesoscopic transport of electrically controllable inversion layers of Si metal-oxide-semiconductor field-effect transistors that use a dual-gate structure. We have developed two kinds of devices: a quasi-one-dimensional device (1D-FET) and a Coulomb blockade device (CB-FET). In both devices, the field effect is used to change the channel structure by introducing potential barriers in the narrow inversion channel. The 1D-FET changes a long diffusive quantum wire into a short ballistic one. Strong oscillations in differential conductance, even negative differential conductance, have been observed at 4.2 K, indicating enhanced modulation of electron mobility by intersubband scattering suppression. The CB-FET, on the other hand, transforms a simple quantum wire into a coupled quantum-dot array. A clear change in transport properties is observed with changes in the barrier height at low temperatures. The experimental results are consistent with the theory of one-dimensional subbands and the Coulomb blockade of single-electron tunneling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.357159
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  • 3
    Electronic Resource
    Electronic Resource
    Coulomb blockade in the inversion layer of a Si metal-oxide-semiconductor field-effect transistor with a dual-gate structure (1994)
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 64 (1994), S. 586-588 
    Details
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We have studied the transport properties of artificially squeezable inversion layers in a Si metal-oxide-semiconductor field-effect-transistor with a dual-gate structure. Increasing the potential barrier height with constant intervals along the one-dimensional channel gradually transforms a simple quantum wire into coupled quantum dots. The clear change in transport properties has been observed by changing the tunnel barrier height at low temperatures. The experimental results are discussed in terms of one-dimensional subbands and the Coulomb blockade of single-electron tunneling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.111085
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  • 4
    Electronic Resource
    Electronic Resource
    Role of rBAT Gene Products in Cystinuria (1996)
    Oxford, UK : Blackwell Publishing Ltd
    International journal of urology 3 (1996), S. 0 
    Details
    ISSN: 1442-2042
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To investigate whether rBAT gene products function as a crystine transporter component or as a transport activator, we microinjected several C–terminal deletion mutants of rBAT cRNA into Xenopus oocytes, and measured transport activity for arginine, leucine and cystine in the presence and absence of sodium. Wild type rBAT significantly stimulated the uptake of all 3 amino acids 10–20 fold compared to control mutants. On the other hand, no mutant, except a Δ511–685 mutant, stimulated the uptake of these amino acids. However, the Δ511–685 mutant significantly increased the uptake of arginine. In the presence of sodium, the Δ511–685 mutant also increased the uptake of leucine. The Δ511–685 mutant did not stimulate crystine uptake in the presence and absence of sodium. Furthermore, inhibition of L–arginine uptake by L–homoserine was seen only in the presence of sodium. These results suggest that mutant rBAT stimulates the endogenous amino acid transport system y+ in oocytes. Finally, rBAT gene products, as the primary cause of cystinuria, may function as activators of the amino acid transport system in renal brush border membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1442-2042.1996.tb00354.x
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  • 5
    Electronic Resource
    Electronic Resource
    Molecular and cellular regulation of renal phosphate transporters in X-linked hypophosphatemia (1998)
    Springer
    Clinical and experimental nephrology 2 (1998), S. 178-182 
    Details
    ISSN: 1437-7799
    Keywords: kidney ; phosphate ; hypophosphatemia ; mutation ; vitamin D ; transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion Recent investigations of X-linked hypophosphatemia support the concept that the kidney is intrinsically normal in this disorder, and that the characteristic phosphaturia is caused by a humoral factor. The mechanisms involved in the pathophysiology of X-linked hypophosphatemia, Hyp, and oncogenic hypophosphatemic osteomalacia are complex and are the results of mutations in a putative zinc metalloprotease. Inactivation inPHEX gene function initiates a series of events that result in severe perturbations in renal Pi transport and metabolism of vitamin D. There are a number of possible working models that could explain the experimental observations. However, our studies clearly show that a humoral factor (phosphatonin) inhibits the transcription of the type II Na+/Pi cotransporter gene (Fig. 4). Phosphatonin may be a key modulator of phosphate homeostasis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02480555
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  • 6
    Electronic Resource
    Electronic Resource
    Effect of dietary phosphate on Na+-dependent phosphate cotransporters function and expression in the rat kidney (1998)
    Springer
    Clinical and experimental nephrology 2 (1998), S. 109-116 
    Details
    ISSN: 1437-7799
    Keywords: Na+-phosphate cotransporter ; dietary phosphate ; kidney ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background Three types (typeI, II, andIII) of sodium-dependent phosphate cotransporters have recently been isolated and shown to be expressed in the mammalian kidney. Understanding of the functional roles and regulation of each transporter is still fragmented, however. Methods We analyzed the functional roles of each transporter by using antisense oligonucleotides in theXenopus oocytes expression system, and by localization in the proximal tubules of rat kidney using immunohistochemistry. Results Phosphate uptake in brush border membranes was increased by about 2 times in rats fed a low-phosphate, as compared with a high-phosphate, diet. Expression of typeI, II, andIII transporter mRNAs was observed in renal poly(A)+RNA, isolated from the rats fed a low-phosphate diet. Phosphate uptake increased about 2.5-fold inXenopus oocytes injected with the poly(A)+RNA, compared with those given RNA from rats fed a high-phosphate diet. Hybrid depletion of the typeII sodium-dependent phosphate transporter (NaPi-2), but not of the typeI (rNaPi-1) or typeIII transporters (PiT-1 and PiT-2), significantly decreased phosphate transport activity in oocytes injected with the poly(A)+RNA from each experimental group rat kidney. In rats fed the lowphosphate diet, NaPi-2 immunoreactivity increased markedly in the brush border membranes of renal proximal tubular cells, whereas rNaPi-1 protein was not changed. Conclusion This study suggests that the typeII transporter functions mainly as a sodium-dependent phosphate cotransporter, and is regulated by dietary phosphate in the rat kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02479931
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  • 7
    Electronic Resource
    Electronic Resource
    Dietary regulation of renal phosphate transporters in hypophosphatemic mice (1998)
    Springer
    Journal of bone and mineral metabolism 16 (1998), S. 234-240 
    Details
    ISSN: 1435-5604
    Keywords: Key words: hypophosphatemia ; Na-dependent phosphate cotransporter ; kidney ; mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: X-linked hypophosphatemic rickets (XLH) is known to impair renal adaptive response to Pi restriction. We investigated the effects of dietary Pi on the synthesis of renal sodium-dependent inorganic phosphate (Na/Pi) cotransporters (Npt1 and NaPi-7) in X-linked hypophosphatemic mice (Hyp). The NaPi-7 mRNA level in Hyp mice was reduced to 50% of that of normal mice while the Npt1 mRNA level was unchanged. After feeding a low-Pi diet, the amounts of NaPi-7 protein and mRNA were markedly increased in both normal and Hyp mice. In contrast, after feeding a high-Pi diet, the levels of protein and mRNA were largely decreased in both mice. Immunohistochemical analysis indicated that NaPi-7 staining was largely enhanced in the apical membrane of renal proximal tubular cells in the normal and Hyp mice fed the low-Pi diet. In contrast, NaPi-7 staining was decreased in both groups of rats fed the high-Pi diet. Npt1 immunoreactivity was detected in the apical membrane of proximal convoluted and straight tubular cells in Hyp and normal mice, and was unchanged regardless of dietary Pi manipulation in both mice. Thus, dietary regulation for the synthesis of the two cotransporters is not impaired in Hyp mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007740050050
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  • 8
    Electronic Resource
    Electronic Resource
    Genetic heterogeneity of histidinemia detected by screening newborn infants in Japan (1985)
    Springer
    Journal of human genetics 30 (1985), S. 287-295 
    Details
    ISSN: 1435-232X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Eleven patients with histidinemia, detected by screening new-born infants, were tentatively classified into two groups on the basis of their skin histidase activity: those with activity of less than 10% (group 1), and those with activity of about 20% (group 2) of the normal value. One of the patients in group 2 had two histidinemic siblings who were also classified into group 2. The skin histidase of the two histidinemic siblings were found to have altered kinetic properties. The skin histidase activities of the 22 parents of the histidinemic patients in groups 1 and 2 ranged from 26 to 82% and from 45 to 79%, respectively, of the average control value. All the 16 parents of the eight patients in group 1 and the six parents of the three probands of group 2 could be distinguished from the patients in groups 1 and 2, respectively, by their skin histidase activity as well as fasting level of serum histidine. In addition, 20 of 22 parents could be distinguished from normal controls by their skin histidase activity. However, two fathers of patients in groups 1 and 2 seemed to be normal, although the mothers were presumably heterozygous carriers. These results suggest that there is genetic heterogeneity in histidinemia detected by screening newborn infants in Japan. The results also suggest that some cases of histidinemia exhibit different mode of inheritance, although most of histidinemia is autosomal recessive.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907966
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