Takeaki Sato

An attempt at preparation of corrosion-resistant bulk amorphous Ni–Cr–Ta–Mo–P–B alloys

Abstract Preparation of cylindrical amorphous alloys with low contents of three corrosion-resistant elements, chromium, tantalum and molybdenum, were attempted by copper-mold casting. Ni–5Cr–5Ta–3Mo–16P–4B alloy of 1 mm diameter is identified as a single amorphous phase alloy and spontaneously passive in 6 and 12 M HCl, similar to the melt-spun amorphous counterpart, although high resolution TEM observation reveals the presence of nanocrystalline precipitates of about 2 nm diameter. Ni–5Cr–5Ta–5Mo–16P–4B alloy is also amorphous as shown by X-ray diffraction studies but contains nanocrystallites of about 5 nm diameter, the anodic current in 6 M HCl being more than one order of magnitude higher than that of the melt-spun amorphous counterpart. All other copper-mold cast Ni–16P–4B alloys with chromium, tantalum and molybdenum are composed of crystalline precipitates in the amorphous matrix.

Farnesoid X receptor, hepatocyte nuclear factors 1α and 3β are essential for transcriptional activation of the liver-specific organic anion transporter-2 gene

BackgroundWe isolated the human liver-specific organic anion transporter gene, LST-2 (OATP8/SLCO1B3), which is exclusively expressed in the basolateral membrane of the hepatocytes. In this study, we analyzed the transcriptional regulation of the LST-2 gene in hepatocyte-derived cells and the effect of bile acid.MethodsTranscriptional activity of the LST-2 gene was measured using a human LST-2 promoter–luciferase reporter plasmid under various concentrations of bile acids. Electrophoresis mobility shift assays of farnesoid X receptor (FXR), hepatocyte nuclear factor (HNF) 1α, and HNF3β were performed.ResultsLuciferase analysis showed that the 5′-flanking region from −180 to −20 bp is responsible for LST-2 transcriptional activity. By site-directed mutation analysis, it was revealed that the consensus binding sites for FXR, HNF1α, and HNF3β play important roles in the transcriptional activity of the LST-2 gene. By electrophoresis mobility shift assay, we observed specific protein–DNA complexes of FXR, HNF1α, and HNF-3β. Luciferase activity was increased fivefold when chenodeoxycholate or deoxycholate were added. Northern blot analyses revealed that the expression of LST-2 was increased by addition of chenodeoxycholate or deoxycholate in a dose-dependent manner.ConclusionsThis study demonstrated that the transcription of the LST-2 gene is regulated by three transcription factors, FXR, HNF1α, and HNF3β. HNF1α and HNF3β might contribute to its liver-specific expression, and FXR might play a role in its transcriptional activation by bile acids.

Some corrosion characteristics of stainless surface alloys laser processed on a mild steel

Abstract Preparation of corrosion-resistant ferritic and austenitic surface alloys on a mild steel was attempted by laser processing of chromium-plated mild steel and chromium and nickel-plated mild steel. The passivating ability increased with increasing number of laser irradiations due to an improvement of homogeneity of laser-processed surface layer with increasing number of meltings. However, there is an optimal number of irradiations, since further increase in number of laser irradiation meltings lowered both the passivating ability and pitting potential due to a decrease in chromium content in the laser-processed layer by evaporation.

Surface vitrification of Fe-based alloys by laser treatment

Abstract Vitrification of FeSiB, FeCrPC and FeCrMoPC alloy surfaces by CO 2 laser treatment was studied. X-ray diffraction patterns of the specimens were changed by the laser surface treatment in such a way that the main diffraction peaks from the crystalline phases almost disappeared for the FeCrPC and FeCrMoPC alloys. The polarization curves for the laser surface-treated Fe−10Cr−14.5P−9.5C alloy in 1N HCl solution showed one order of magnitude lower passive current density than that of the untreated counterpart. For the FeSiB alloy, the crystalline phases were observed not only at the border of two amorphous phases but also inside the amorphous phase after successive irradiations of pulsated laser beams on the adjacent portions in the surface. In contrast, the majority of the surface on the FeCrPC and FeCrMoPC alloys were vitrified by the laser treatment, although the crystalline phases appeared at some borders between adjacent amorphous phases formed by successive irradiations of pulsated laser beams. The width of the crystalline phases at the borders was about 20 μm for FeCrMoPC alloys irrespective of alloy composition and pulse on-time within the tested range.

Body temperature abnormalities in non-neurological critically ill patients: a review of the literature

Body temperature abnormalities, which occur because of several infectious and non-infectious etiologies, are among the most commonly noted symptoms of critically ill patients. These abnormalities frequently trigger changes in patient management. The purpose of this article was to review the contemporary literature investigating the definition and occurrence of body temperature abnormalities in addition to their impact on illness severity and mortality in critically ill non-neurological patients, particularly in patients with severe sepsis. Reports on the influence of fever on outcomes are inconclusive, and the presence of fever per se may not contribute to increased mortality in critically ill patients. In patients with severe sepsis, the impacts of elevated body temperature and hypothermia on mortality and the severity of physiologic decline are different. Hypothermia is significantly associated with an increased risk of mortality. In contrast, elevated body temperature may not be associated with increased disease severity or risk of mortality. In patients with severe sepsis, the effect of fever and fever control on outcomes requires further research.

Peroxisome proliferator-activated receptor α activates cyclooxygenase-2 gene transcription through bile acid transport in human colorectal cancer cell lines

BackgroundEvidence is accumulating that bile acids are involved in colon cancer development, but their molecular mechanisms remain unexplored. Bile acid has been reported to be associated with induction of the cyclooxygenase-2 (COX-2) gene. Because the human liver-specific organic anion transporter-2 (LST-2/OATP8/OATP1B3) is expressed in gastrointestinal cancers and might transport bile acids to the intracellular space, we studied the molecular mechanisms by which bile acids induce the transcription of COX-2, and the role of LST-2 in colonic cell lines.MethodsTranscriptional activity of COX-2 was measured using a human COX-2 promoter-luciferase assay under various concentrations of bile acids. Electrophoresis mobility shift assays (EMSAs) for peroxisome proliferators-activated receptor (PPAR) α and cyclic AMP responsive element (CRE) were performed.ResultsThe COX-2 promoter was induced by lithocholic acid (LCA), deoxycholic acid (DCA), and chenodeoxycholic acid (CDCA). Deletion and site-directed mutation analyses showed that CRE is the responsive element for LCA. An adenovirus expression system revealed that LST-2 is responsible for induction of COX-2. By EMSA using oligonucleotides of CRE, we observed formation of a specific protein-DNA complex, which was inhibited by a specific antibody against PPARα and CRE. A PPARα-specific agonist induced transcription of COX-2.ConclusionThese results indicate that COX-2 is transcriptionally activated by the addition of LCA, CDCA, and DCA and that LST-2 plays an important role by transporting bile acid to the intracellular space. Moreover, LCA-dependent COX-2 gene activation consists of a transcriptional complex including PPARα and CRE-binding protein. Thus, this induction of COX-2 may participate in carcinogenesis and progression of colorectal cancer cells.

Amorphous FeCrMo13P7C alloys unsusceptible to hydrogen embrittlement in deaerated solutions of different pH

Abstract Bending tests were performed to clarify the effect of chromium and molybdenum contents of amorphous FeCrMo13P7C alloys on the susceptibility to hydrogen embrittlement in deaerated solutions of different pH at 40°C. Some alloys suffered hydrogen embrittlement in deaerated 1 M HCl, 1 M NaCl and deionized water. The addition of sufficient sound amounts of both the elements improved the corrosion resistance and resulted in immunity to the embrittlement due to spontaneous passivation. The increase in pH also decreased the susceptibility to hydrogen embrittlement.

Lactate, a useful marker for disease mortality and severity but an unreliable marker of tissue hypoxia/hypoperfusion in critically ill patients

Early aggressive hemodynamic resuscitation using elevated plasma lactate as a marker is an essential component of managing critically ill patients. Therefore, measurement of blood lactate is recommended to stratify patients based on the need for fluid resuscitation and the risks of multiple organ dysfunction syndrome and death. Hyperlactatemia is common among critically ill patients, and lactate levels and their trend may be reliable markers of illness severity and mortality. Although hyperlactatemia has been widely recognized as a marker of tissue hypoxia/hypoperfusion, it can also result from increased or accelerated aerobic glycolysis during the stress response. Additionally, lactate may represent an important energy source for patients in critical condition. Despite its inherent complexity, the current simplified view of hyperlactatemia is that it reflects the presence of global tissue hypoxia/hypoperfusion with anaerobic glycolysis. This review of hyperlactatemia in critically ill patients focuses on its pathophysiological aspects and recent clinical approaches. Hyperlactatemia in critically ill patients must be considered to be related to tissue hypoxia/hypoperfusion. Therefore, appropriate hemodynamic resuscitation is required to correct the pathological condition immediately. However, hyperlactatemia can also result from aerobic glycolysis, unrelated to tissue dysoxia, which is unlikely to respond to increases in systemic oxygen delivery. Because hyperlactatemia may be simultaneously related to, and unrelated to, tissue hypoxia, physicians should recognize that resuscitation to normalize plasma lactate levels could be over‐resuscitation and may worsen the physiological status. Lactate is a reliable indicator of sepsis severity and a marker of resuscitation; however, it is an unreliable marker of tissue hypoxia/hypoperfusion.

Relationship between nitrogen loss and blood urea nitrogen concentrations in patients requiring continuous renal replacement therapy

It is well known that continuous renal replacement therapy (CRRT) produces some amount of nitrogen loss, but there are few tools that are easily applied to measure it. This study aimed to evaluate nitrogen loss using blood urea nitrogen (BUN) measurement in patients receiving CRRT.

A Case Report of Guillain-Barre Syndrome Induced by Transcatheter Chemoembolization after Percutaneous Transhepatic Portal Embolization Analyzed by Cytokines

経皮的経肝門脈枝塞栓術 (以下, PTPE) は, 主に, 肝細胞癌や肝門部胆管癌, 胆嚢癌などの肝胆道系悪性腫瘍に対する拡大肝切除術術前処置としてもはや疑いの無いところであるが, その反面合併症などが少なからず存在し, 今回PTPEおよび肝動脈化学塞栓療法 (TACE) 施行後にギランバレー症候群を発症した症例を経験したので報告する. 症例は68歳の男性, 慢性肝炎 (C型) で経過観察中, 拡大右葉切除予定でPTPE施行するも肝機能不良にて手術施行せずTACE施行. その後, 感冒様症状を呈した後, ギラン-バレー症候群を発症した. この症例を詳細に検討した結果, IL-6の過剰な反応が見られ, 何らかの免疫反応異常の可能性が示唆された.PTPEおよびTACE施行後に肝梗塞が生じた場合, の侵襲の大きさから予期せぬ合併症が生ずることがあり, PTPE後のTACEは適応を選び慎重に行う必要があると考えられる.