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| 1 | Bacteremia in hemodialysis patients显示文摘Infection is a common complication and is the second leading cause of death in hemodialysis patients. The risk of bacteremia in hemodialysis patients is 26-fold higher than in the general population, and 1/2-3/4 of the causative organisms of bacteremia in hemodialysis patients are Gram-positive bacteria. The ratio of resistant bacteria in hemodialysis patients compared to the general population is unclear. Several reports have indicated that hemodialysis patients have a higher risk of methicillin-resistant Staphylococcus aureus infection. The most common site of infection causing bacteremia is internal prostheses; the use of a hemodialysis catheter is the most important risk factor for bacteremia. Although antibiotic lock of hemodialysis catheters and topical antibiotic ointment can reduce catheter-related blood stream infection(CRBSI), their use should be limited to necessary cases because of the emergence of resistant organisms. Systemic antibiotic administration and catheter removal is recommended for treating CRBSI, although a study indicated the advantages of antibiotic lock and guidewire exchange of catheters over systemic antibiotic therapy. An infection control bundle recommended by the Center for Disease Control and Prevention succeeded in reducing bacteremia in hemodialysis patients with either a catheter or arteriovenous fistula. Appropriate infection control can reduce bacteremia in hemodialysis patients. | Masashi Suzuki Nobuhiko Satoh Motonobu Nakamura Shoko Horita George Seki Kyoji Moriya | 2016 | World Journal of Nephrology2016，5，6： | 14 |
| 2 | Porous Coordination-Polymer Crystals with Gated Channels Specific for Supercritical Gases 显示文摘 | Ryo Kitaura Kenji Seki George Akiyama | 2003 | Angew Chem Int Ed2003，42，4： | 1 |
| 3 | Functional coupling of V-ATPase and CLC-5显示文摘Dent's disease is an X-linked renal tubulopathy characterized by low molecular weight proteinuria,hypercalciuria and progressive renal failure. Disease aetiology is associated with mutations in the CLCN5 gene coding for the electrogenic 2Cl^-/H^+ antiporter chloride channel 5(CLC-5),which is expressed in the apical endosomes of renal proximal tubules with the vacuolar type H^+-ATPase(V-ATPase). Initially identified as a member of the CLC family of Cl- channels,CLC-5 was presumed to provide Cl- shunt into the endosomal lumen to dissipate H^+ accumulation by V-ATPase,thereby facilitating efficient endosomal acidification. However,recent findings showing that CLC-5 is in fact not a Cl-channel but a 2Cl^-/H^+ antiporter challenged this classical shunt model,leading to a renewed and intense debate on its physiological roles. Cl- accumulation via CLC-5 is predicted to play a critical role in endocytosis,as illustrated in mice carrying an artificial Cl- channel mutation E211 A that developed defective endocytosis but normal endosomal acidification. Conversely,a recent functional analysis of a newly identified disease-causing Cl^- channel mutation E211 Q in a patient with typical Dent's disease confirmed the functional coupling between V-ATPase and CLC-5 in endosomal acidification,lending support to the classical shunt model. In this editorial,we will address the current recognition of the physiological role of CLC-5 with a specific focus on the functional coupling of V-ATPase and CLC-5. | Nobuhiko Satoh Masashi Suzuki Motonobu Nakamura Atsushi Suzuki Shoko Horita George Seki Kyoji Moriya | 2017 | World Journal of Nephrology2017，6，1： | 1 |
| 4 | Regulatory roles of nitric oxide and angiotensin Ⅱ on renal tubular transport显示文摘Renal tubules regulate blood pressure and humoral homeostasis.Mediators that play a significant role in regulating the transport of solutes and water include angiotensin Ⅱ(AngⅡ) and nitric oxide(NO).AngⅡ can significantly raise blood pressure via effects on the heart,vasculature,and renal tubules.AngⅡ generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules.Stimulation of renal proximal tubule(PT) transport is thought to be essential for AngⅡ-mediated hypertension.However,AngⅡ has a biphasic effect on in vitro PT transport in mice,rats,and rabbits:stimulation at low concentrations and inhibition at high concentrations.On the other hand,NO is generally thought to inhibit renal tubular transport.In PTs,NO seems to be involved in the inhibitory effect of AngⅡ.A recent study reports a surprising finding:AngⅡ has a monophasic stimulatory effect on human PT transport.Detailed analysis of signalling mechanisms indicates that in contrast to other species,the human NO/guanosine3',5'-cyclic monophosphate/extracellular signal-regulated kinase pathway seems to mediate this effect of AngⅡ on PT transport.In this review we will discuss recent progress in understanding the effects of AngⅡ and NO on renal tubular transport. | Shoko Horita Motonobu Nakamura Ayumi Shirai Osamu Yamazaki Nobuhiko Satoh Masashi Suzuki George Seki | 2014 | World Journal of Nephrology2014，3，4： | 1 |
| 5 | Role of renal proximal tubule transport in thiazolidinedioneinduced volume expansion显示文摘Thiazolidinediones(TZDs), pharmacological activators of peroxisome-proliferator-activated receptors γ(PPARγ), significantly improve insulin resistance and lower plasma glucose concentrations. However, the use of TZDs is associated with plasma volume expansion, the mechanism of which has been a matter of controversy. Originally, PPARγ-mediated enhanced transcription of the epithelial Na channel(ENaC) γ subunit was thought to play a central role in TZD-induced volume expansion. However, later studies suggested that the activation of ENaC alone could not explain TZD-induced volume expansion. We have recently shown that TZDs rapidly stimulate sodium-coupled bicarbonate absorption from renal proximal tubule(PT) in vitro and in vivo. TZD-induced transport stimulation was dependent on PPARγ/Src/EGFR/ERK, and observed in rat, rabbit and human. However, this stimulation was not observed in mouse PTs where Src/EGFR is constitutively activated. Analysis in mouse embryonic fibroblast cells confirmed the existence of PPARγ/Src-dependent non-genomic signaling, which requires the ligand binding ability but not the transcriptional activity of PPARγ. The TZD-induced enhancement of association between PPARγ and Src supports an obligatory role for Src in this signaling. These results support the view that TZD-induced volume expansion is multifactorial. In addition to the PPARγ-dependent enhanced expression of the sodium transport system(s) in distal nephrons, the PPARγ-dependent non-genomic stimulation of renal proximal transport may be also involved in TZD-induced volume expansion. | George Seki Yoko Endo Masashi Suzuki Hideomi Yamada Shoko Horita Toshiro Fujita | 2012 | World Journal of Nephrology2012，1，5： | 0 |
| 6 | Species differences in regulation of renal proximal tubule transport by certain molecules显示文摘Renal proximal tubules(PTs) play important roles in the regulation of acid/base, plasma volume and blood pressure. Recent studies suggest that there are substantial species differences in the regulation of PT transport. For example, thiazolidinediones(TZDs) are widely used for the treatment of type 2 diabetes mellitus, but the use of TZDs is associated with fluid overload. In addition to the transcriptional enhancement of sodium transport in distal nephrons, TZDs rapidly stimulate PT sodium transport via a non-genomic mechanism depending on peroxisome proliferator activated receptor g/Src/epidermal growth factor receptor(EGFR)/MEK/ERK. In mouse PTs, however, TZDs fail to stimulate PT transport probably due to constitutive activation of Src/EGFR/ERK pathway. This unique activation of Src/ERK may also affect the effect of high concentrations of insulin on mouse PT transport. On the other hand, the effect of angiotensin Ⅱ(Ang Ⅱ) on PT transport is known to be biphasic in rabbits, rats, and mice. However, Ang Ⅱ induces a concentration-dependent, monophasic transport stimulation in human PTs. The contrasting responses to nitric oxide/guanosine 3',5'-cyclic monophosphate pathway may largely explain these different effects of Ang Ⅱ on PT transport. In this review, we focus on the recent findings on the species differences in the regulation of PT transport, which may help understand the species-specific mechanisms underlying edema formation and/or hypertension occurrence. | George Seki Motonobu Nakamura Masashi Suzuki Nobuhiko Satoh Shoko Horita | 2015 | World Journal of Nephrology2015，4，2： | 0 |
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