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Objectives To verify the utility of triangular extension of a hinge flap in buccal mucosal staged urethroplasty to resolve stomal stenosis after the first stage and ultimately prevent restenosis. Methods A total of 23 patients (triangular extension group) were studied in 2013-2019. In the first stage, buccal mucosa was transplanted, and an extended triangle portion of the mucosa was placed beside the proximal and/or distal stoma that was created when the stricture segment of the urethra was resected. In the second stage, during tubularization of the urethral plate, an incision was made at the stoma to increase the caliber to which the triangular extension was inserted. The procedure was considered successful when a 17-Fr flexible cystoscope passed through the reconstructed urethra at 6 months after the second-stage urethroplasty and no additional surgery or bougie dilation required. The clinical course of the triangular extension group was compared with 24 patients who underwent conventional staged urethroplasty (control group). Results In total, 20 patients from each group underwent second-stage surgery. No patients in the triangular extension group required additional revision surgery because of stomal stenosis after first-stage surgery, whereas five (20%) control patients did. Urethroplasty was successful in 19 patients (95%) in the triangular extension group and in 19 patients (95%) in the control group. Uroflowmetry after the second-stage surgery indicated that the mean maximum urinary flow rate was 21.5 and 15.8 mL/s after triangular extension and the control procedure, respectively (P = 0.027). Conclusions The triangular extension technique reduces the need for revision surgery and prevents postoperative restenosis.

Carotid artery stenosis is elicited by atherosclerosis and is the main cause of cerebral thrombosis. Flow-mediated endothelial vasodilation (FMD) can be measured noninvasively to assess vascular endothelial function related to atherosclerosis. The pulse wave velocity (PWV) is used to evaluate the vascular media involved in atherosclerosis. We investigated the relationship between these measurements in 75 consecutive patients with atherosclerotic cerebral thrombosis. They were assigned to three equal groups based on the severity of carotid artery stenosis on ultrasonograms. Group 1 had no stenosis, group 2 manifested moderate stenosis (

We report on the operation of co-located ${}^{129}$Xe and ${}^{131}$Xe nuclear spin masers with an external feedback scheme, and discuss the use of ${}^{131}$Xe as a comagnetometer in measurements of the ${}^{129}$Xe spin precession frequency. By applying a correction based on the observed change in the ${}^{131}$Xe frequency, the frequency instability due to magnetic field and cell temperature drifts are eliminated by two orders of magnitude. The frequency precision of 6.2 $\mu$Hz is obtained for a 10$^4$ s averaging time, suggesting the possibility of future improvement to $\approx$ 1 nHz by improving the signal-to-noise ratio of the observation., Comment: 8 pages, 5 figures

Objective Current consensus from numerous animal studies has emerged that disturbances at any stage of palatal development can cause cleft palate. However, several clinical cases of uncommon forms of cleft palate that may have resulted from rupture after palatal fusion have been previously reported and treated. This hypothesis of postclosure opening as a cause of cleft palate was reviewed in the literature. Materials and methods We reviewed Japanese and English-language literature describing uncommon forms of cleft palate, which included palatal remnants, perforation, and divided nevi. In addition, a retrospective chart review of over 1300 cleft palate repairs performed by the authors was done. Results There were many reports of palatal remnants and perforations, but no reports of divided nevi on the cleft palate. Our retrospective chart review revealed that 12 cases may have resulted from postclosure opening, with 5 cases due to epithelial remnants on the hard palate, 5 cases of cleft palate with perforation, 1 case of a palatal sinus, and 1 case of a divided nevus over the cleft. Conclusions Epithelial remnants did not seem to be evidence of a postclosure opening event, because they were found in 23–85% of intact palates. However, perforation of the hard palate and a divided nevus on the cleft cannot be explained by embryology, which might indicate postclosure opening as a cause of the cleft. Clinical or animal studies are required to test this hypothesis further.

Although a superficial circumflex iliac artery perforator (SCIP) flap has recently been widely used owing to its various advantages, reports on its use in the pediatric population are limited. A case of a supermicrosurgical reconstruction of a soft tissue defect of the ankle associated with the congenital deficiency of the tibia using a free sensate SCIP flap in a 1-year-old child has been presented. The correction of the valgus deformity of the ankle resulted in a soft tissue defect, which required flap coverage. The lateral cutaneous branch of the intercostal nerve of the flap was coapted with the deep peroneal nerve for sensory recovery. Postoperative course was uneventful and the flap completely survived. The patient was able to ambulate independently at 7 months after surgery. To the best of our knowledge, this is the youngest case of a SCIP flap transfer in literature. This case showed that young age is not a contraindication for SCIP flap transfer. It is believed that the SCIP flap procedure may be a useful option for free flap reconstruction in children.

We demonstrate spin-exchange optical pumping of 129Xe atoms with our newly made laser system. The new laser system was prepared to provide higher laser power required for the stable operation of spin maser oscillations in the 129Xe EDM experiment. We studied the optimum cell temperature and pumping laser power to improve the degree of 129Xe spin polarization. The best performance was achieved at the cell temperature of 100 ◦C with the presently available laser power of 1 W. The results show that a more intense laser is required for further improvement of the spin polarization at higher cell temperatures in our experiment.

We have epitaxially grown silicon carbide (SiC) films on an aluminum nitride (AlN) layer on Si(100) substrate by ultralow-pressure chemical vapor deposition using monomethylsilane (CH 3 SiH 3 ), and investigated the crystallinity and surface morphology of the grown films. Wurtzite AlN(0001) layers were formed on Si(100) substrate by pulsed laser deposition using an AlN target and a N 2 gas, and then 3C–SiC(111) films were grown on the AlN layers. The growth rates of the 3C–SiC(111) films on the AlN layers were higher than those of 3C–SiC(100) films on the Si substrate. In the case of the SiC growth on the Si substrate, Si outdiffusion from the Si substrate occurred, leading to the formation of voids at the SiC/Si interface. It was found that the formation of the AlN intermediate layer was very effective in preventing the Si outdiffusion during the SiC growth. Concurrently, the crystallinity and surface morphology of the SiC films on the AlN layers were improved by insertion of the AlN layer.

Hepatocellular carcinoma (HCC) is one of the most prevalent human cancers, with a rising incidence worldwide. The molecular mechanisms associated with the development of HCC are complex and include multiple interconnected molecular alterations with mounting evidence indicating an important role of microRNAs (miRNAs) in the pathogenesis of HCC. In humans, the development of HCC is commonly associated with liver cirrhosis. To study fibrosis-associated liver carcinogenesis, we used a mouse model designed to emulate the development of HCC in cirrhotic liver. Specifically, we were interested in evaluating the role of miRNAs in the molecular pathogenesis of liver carcinogenesis in male B6C3F1/J mice treated with N-nitrosodiethylamine (DEN) or carbon tetrachloride (CCl4 ) alone or a combination of DEN and CCl4 and characterized by a differential tumor incidence that increased in the following order: DEN

We search for 129Xe EDM by using an active nuclear spin maser. In this experiment, the amplitude of the maser oscillation signal is one of the most important parameters that eventually determine the frequency precision. The amplitude is proportional to the ratio of the transverse spin relaxation time T 2 to the effective longitudinal spin relaxation time $T_{1}^{\ast }$ . In particular, for a spin maser of 3He (a co-magnetometer) for which $T_{1}^{\ast }$ typically reaches ∼50 h, a long T 2 is needed. T 2 depends on the homogeneity of the magnetic field which is applied with coils in order to keep the spins under precession. In the present report, we discuss on the design and construction of a new coil which provided a root-mean square (rms) field gradient of less than 5.0 μG/cm. The result of the field measurement has shown that the field gradient in the cell fulfills the target condition $\sqrt {\langle {(\nabla B_{z})^{2}} \rangle }

Background It was recently reported that serum interleukin (IL)-17 levels increased in liver fibrosis associated with human alcoholic liver disease. However, the role of IL-17 in liver fibrosis has not yet been elucidated. Therefore, the aim of this study was to evaluate the role of IL-17 on cholestatic liver fibrosis. Materials and methods IL-17A knockout (KO) and wild-type (WT) mice were subjected to bile duct ligation. Animals were sacrificed at designated times, and serum and liver tissues were collected. The mRNA expression of hepatic fibrotic markers was assessed, and distribution of activated hepatic stellate cells (HSCs) was determined by immunohistochemical staining. In an in vitro study, Kupffer cells (KCs) and HSCs were isolated from WT mice. KCs were cultured with IL-17A or IL-17F, and production of tumor necrosis factor α (TNF-α) and transforming growth factor β1 (TGF-β1) was measured. HSCs were cultured with IL-17A or IL-17F, and morphologic changes were assessed by immunohistochemical staining. Results Liver damage observed in the WT mice was significantly improved in the KO mice. Serum TNF-α and TGF-β1 levels were significantly decreased in the KO compared with the WT mice. The hepatic mRNA expression of TNF-α, TGF-β1, and collagen 1α1, which increased in the WT mice, also significantly decreased in the KO mice. Increased hepatic fibrosis in the WT mice was significantly improved in the KO mice. Cytokine production was increased in IL-17A-treated KCs. The most remarkable myofibroblast-like changes were observed in isolated HSCs in the presence of IL-17A. Conclusions IL-17A was involved in the pathogenesis of cholestatic liver fibrosis by activation of both the KCs and HSCs.

Aim The specific purpose of this study was to investigate the role of macrophage colony-stimulating factor (M-CSF) in initiation and progression of hepatocellular carcinoma using M-CSF-deficient mice. Methods M-CSF-deficient (osteopetrotic: op/op) and their littermate (LM) mice were i.p. injected with diethylnitrosamine (DEN) to induce hepatocellular carcinoma. Twenty-eight weeks after DEN administration, the tumor incidence rate and serum M-CSF levels were assessed. Furthermore, distribution of the activated macrophages and the mRNA expression of CD163 and CD204 were evaluated. Moreover, angiogenesis was analyzed in tumors. In another set of experiments, apoptosis and proliferation of the hepatocytes were examined in the acute phase after DEN administration. Isolated hepatic macrophages were cultured with or without M-CSF, and vascular endothelial growth factor (VEGF) production was assessed by enzyme-linked immunoassay. Results Tumor incidence was significantly reduced in the op/op compared with the LM mice. Serum M-CSF levels were increased in the carcinogenesis models of the LM mice. Hepatic macrophages were found only in tumors in the op/op but in both normal liver tissue and tumors in the LM mice. In the op/op group, the mRNA expression of inflammatory cytokines was significantly lower compared with the LM mice. Furthermore, apoptosis was significantly increased in the op/op than the LM mice. Angiogenesis increased in liver tumors from the LM compared with the op/op mice. Production of VEGF was greater in the hepatic macrophages incubated with M-CSF compared with those without M-CSF. Conclusion Thus, M-CSF is involved in the progression of chemically induced hepatocarcinogenesis.

A novel method to produce spin-aligned rare-isotope (RI) beam has been developed, that is the two-step projectile fragmentation method with a technique of dispersion matching. The present method was verified in an experiment at the RIKEN RIBF, where an RI beam of 32Al with spin alignment of 8(1) % was successfully produced from a primary beam of 48Ca, with 33Al as an intermediate nucleus. Figure of merit of the present method was found to be improved by a factor larger than 50 compared with a conventional method employing single-step projectile fragmentation. ispartof: pages:47-51 ispartof: Hyperfine Interactions vol:220 issue:1 pages:47-51 ispartof: 4th Joint International Conference on Hyperfine Interactions / International Symposium on Nuclear Quadrupole Interactions (HFI/NQI) location:Beijing, China date:10 Sep - 14 Sep 2012 status: published

The present status of an active spin maser which is being developed for an experimental search for 129Xe atomic electric dipole moment (EDM) is presented. In order to realize the long term stability of maser frequency, systematic effects for the spin maser operation were investigated. The correlations in the maser frequency with the solenoid current, the environmental field and the cell temperature were found. With the solenoid current and environmental field being stabilized and the cell temperature lowered, a frequency precision of 7.9 nHz has been achieved for the maser operation.

A 129Xe nuclear spin oscillator with an artificial feedback was constructed, and detailed studies were conducted on its performance, focusing on the frequency stability. As a result, the major sources of drift of the precession frequency in the present spin oscillator setup were identified to be drifts of a solenoid current and an environmental magnetic field. By introducing stabilization systems for the current and the environmental field, which yielded improvements by one order of magnitude on the solenoid current and by a factor of three on the environmental field, a frequency precision of 7.9 nHz was obtained for a one-shot measurement of 3 × 104 s duration. We found, however, that the Allan deviation leveled off at around 30 μHz, indicating a strong need for the precision monitor of the experimental conditions represented by magnetometry. The frequency stability of the spin oscillator is discussed in relation to an experimental search for an electric dipole moment of the 129Xe atom.

Objective The purpose of this study was to investigate whether inhibition of Kupffer cells (KCs) affects the expression of high mobility group box 1 (HMGB1) and mortality in septic peritonitis. The role of the spleen in septic peritonitis was also investigated. Methods Rats were given liposome-entrapped dichloromethylene diphosphonate (lipo-MDP) to eliminate KCs or non-entrapped liposome (lipo) before cecal ligation and puncture (CLP), and serum HMGB1 levels and mortality were assessed after CLP. Furthermore, KCs and tissue macrophages were isolated, and production of HMGB1 was investigated. Effects of splenectomy on serum HMGB1 levels and mortality were also investigated after CLP. Results Elimination of the Kupffer cells by lipo-MDP increased serum HMGB1 concentrations and mortality significantly. Furthermore, HMGB1 expression in both the periportal area of the liver and the spleen was greater in the lipo-MDP group than the lipo group. On the other hand, splenectomy blunted serum HMGB1 levels and improved mortality after CLP. The HMGB1 expression was greater in the spleen compared with the liver after CLP. Furthermore, production of HMGB1 was greatest in splenic macrophages in vitro . The number of ED3-positive cells increased significantly in non-splenectomized animals but not in splenectomized animals after CLP. In the lipo-MDP treated groups, the number of ED3-positive macrophages also increased in the liver from non-splenectomized animals but not in the splenectomized animals after CLP. Conclusions The liver and the spleen play key roles in host defense during septic peritonitis. Migrating macrophages into the liver are, in part, derived from the spleen after CLP.

We have constructed a 129Xe nuclear spin oscillator which executes a self-sustained oscillation through an external feedback loop with optical detection of nuclear spin. The oscillator is capable of operating at frequencies much lower than the conventional nuclear spin maser. A method for efficient optical detection of spin has been developed and applied to the nuclear spin oscillator, and the frequency characteristics of the oscillator at low frequencies has been investigated. The spin oscillator was operated at frequencies 2.5–36 Hz. The frequency performance of the oscillator is discussed in relation to a planned search for an atomic electric dipole moment taking advantage of the present oscillator scheme.

Background Interleukin (IL)-17A is a proinflammatory cytokine and plays an important role in neutrophil recruitment. We investigate the role of IL-17A in a mouse polymicrobial sepsis model. Materials and Methods IL-17A knockout mice (KO) and wild-type (WT) mice were subjected the cecal ligation and puncture (CLP). Survival was assessed for the following 7 d after the CLP operation, and histopathologic findings were evaluated 12 h after CLP. Bacterial outgrowth in blood was assessed by blood culture 12 h after CLP. After CLP, expression of inflammatory mediators in serum was assessed by enzyme-linked immunosorbent assay (ELISA). Furthermore, expression of FOXP3 and IL-17A in the spleen was assessed by immunohistochemical staining and flow cytometry. Results Mortality was increased in KO mice compared with WT mice after CLP. Furthermore, bacterial outgrowth in blood and serum high mobility group box 1 (HMGB1) levels were also significantly greater in KO mice than WT mice. The expression of FOXP3 in the spleen was significantly greater in KO mice than WT mice. Conclusion IL-17A play pivotal role in host defense during septic peritonitis.

High-mobility group box 1 (HMGB1) acts as an early mediator of inflammation and organ damage in hepatic ischemia-reperfusion (I/R) injury. Glycyrrhizin is a natural anti-inflammatory and antiviral triterpene in clinical use. The purpose of this study was to investigate the effect of glycyrrhizin on liver injury caused by I/R and production of HMGB1 by Kupffer cells in rats. In the first test period, rats were given saline or glycyrrhizin 20 min before segmental hepatic warm I/R. Serum alanine aminotransferase and HMGB1 levels and hepatic histopathological findings were evaluated after I/R. Furthermore, expression of HMGB1 in the liver was assessed by immunohistochemical staining after I/R. Kupffer cells were isolated by collagenase digestion and differential centrifugation, and production of HMGB1 was assessed. In another set of experiments, the effect of inhibition of Kupffer cells by injection of liposome-entrapped dichloromethylene diphosphonate (lipo-MDP) on liver injury and expression of HMGB1 were investigated after I/R. Liver injury was prevented in the glycyrrhizin group compared with the control group. Furthermore, serum HMGB1 levels were also significantly blunted in the glycyrrhizin group compared with the control group. Cells expressing HMGB1 were detected in the hepatic sinusoid by immunohistochemistry and recognized morphologically as Kupffer cells. Furthermore, the expression of HMGB1 was reduced in the glycyrrhizin group compared with the control group. Production of HMGB1 was reduced in Kupffer cells isolated from the glycyrrhizin group compared with the control group. It is noteworthy that treatment with lipo-MDP significantly blunted serum HMGB1 levels and prevented liver injury after I/R. These results suggest that glycyrrhizin has the therapeutic potential to prevent warm I/R-induced injury during hepato-biliary surgery.

Frequency characteristics of a 129 Xe nuclear spin maser was studied, which is under development at Tokyo Institute of Technology for the search for a permanent electric dipole moment in diamagnetic 129 Xe atom. Drifts in the solenoid current and cell temperature were found to be the most influential factors on the maser frequency. From correlation coefficient analysis, there seem to exist other origins of frequency fluctuation, such as phase drifts in the maser oscillation. In order to improve the stability of the maser frequency, the intensity of the pumping laser required to fully polarize 129 Xe nuclei was evaluated. Construction of a polarization assessment system for 129 Xe gas cells and development of a new scheme of current stabilization are also remarked.

The development of a nuclear spin oscillator system, namely a spin maser with an external feedback, for use in the search for 129Xe atomic EDM is presented. By introducing a new current source for the B0 field solenoid, drifts in the maser frequency were remarkably suppressed. This in turn clearly brought out the correlation between the maser frequency and the environmental field. Correcting for the effect of the environmental field, the frequency precision of 5 nHz in the measurement time of 45,000 s was attained. Origins of the remaining drifts in the maser frequency are now under investigation.

It was reported from this laboratory that Kupffer cells (KCs) were activated in patients infected with HCV. Since dendritic cells, monocytes, and macrophages were activated by stimulation with HCV-related proteins, the specific aim of this study was to investigate the role of HCV-related proteins in activation of KCs, the signal pathway of activation of KCs mediated by Toll-like receptor (TLR) 4, and the influence of HCV infection on function of KCs. Kupffer cells isolated from non-cancerous surgical specimen were co-cultured with HCV-related proteins (Core, NS3, NS4, and NS5), and production of cytokines (TNF-α, IL-1β, and IL-10) and hydrogen peroxide were assessed. Furthermore, effects of neutralization antibodies against the TLR2, TLR3, or TLR4, and cytochalasin B on the production TNF-α by KCs were investigated. Kupffer cells produced markedly a proinflammatory cytokine TNF-α by stimulation with all HCV-related proteins studied, and values were as same as production by KCs stimulated with LPS. Importantly, this production in the case of NS3 was significantly blunted by about 60% by neutralization antibodies against the TLR4, but not cytochalasin B. Production of TNF-α by isolated KCs stimulated with LPS was significantly greater in the HCV-infected livers than the HCV/HBV-negative livers. These results indicated that HCV-related proteins may cause prolonged activation of KCs in the HCV-infected liver, leading to accumulation of inflammatory cytokines that contribute to DNA damage and carcinogenesis. Furthermore, function of KCs was difference between patients infected with and without HCV infection.

Alcohol-induced liver injury (ALI) has been associated with, among other molecular changes, abnormal hepatic methionine metabolism, resulting in decreased levels of S-adenosylmethionine (SAM). Dietary methyl donor supplements such as SAM and betaine mitigate ALI in animal models; however, the mechanisms of protection remain elusive. It has been suggested that methyl donors may act via attenuation of alcohol-induced oxidative stress. We hypothesized that the protective action of methyl donors is mediated by an effect on the oxidative metabolism of alcohol in the liver. Male C57BL/6J mice were administered a control high-fat diet or diet enriched in methyl donors with or without alcohol for 4 weeks using the enteral alcohol feeding model. As expected, attenuation of ALI and an increase in reduced glutathione:oxidized glutathione ratio were achieved with methyl donor supplementation. Interestingly, methyl donors led to a 35% increase in blood alcohol elimination rate, and while there was no effect on alcohol metabolism in the stomach, a profound effect on liver alcohol metabolism was observed. The catalase-dependent pathway of alcohol metabolism was induced, yet the increase in CYP2E1 activity by alcohol was blunted, which may be mitigating production of oxidants. Additional factors contributing to the protective effects of methyl donors in ALI were increased activity of low- and high-K(m) aldehyde dehydrogenases leading to lower hepatic acetaldehyde, maintenance of the efficient mitochondrial energy metabolism, and promotion of peroxisomal beta-oxidation. Profound changes in alcohol metabolism represent additional important mechanism of the protective effect of methyl donors in ALI.

The specific purpose of this study was to investigate the effects of medium-chain triglycerides (MCTs) on intestinal cell proliferation and mucous secretion of the small intestine in the rat.Rats were fed chow diet and given MCTs or the same weight of corn oil (5 g/kg per day) by gavage daily for 2 weeks, and then tissue samples of the small intestines were harvested. Leptin concentration in the small intestine was measured. Cell proliferation and apoptosis in the small intestine was determined by immunohistochemistry. Diamine oxidase (DAO) activity was measured by colorimetric assay.In rats fed only chow diet (normal rats), the number of goblet cells per villi was 14.2 +/- 0.75 in the jejunum and 15.2 +/- 1.12 in the ileum. The number of goblet cells increased significantly in rats given MCTs compared with rats given corn oil or normal rats. Ki-67-positive cells were detected on the entire villi and the crypts in the small intestine. Furthermore, the proliferative index and the apoptotic index were also significantly greater in rats given MCTs than rats given corn oil or normal rats. Moreover, DAO activity and leptin concentration in the small intestine were significantly greater in rats given MCTs than rats given corn oil or normal rats.MCTs enhance cell proliferation of the intestinal epithelium and mucous secretion from goblet cells in the small intestine. These effects may protect the gut in patients suffering from inflammatory bowel disease or enterogenous infection.

A 62-year-old woman presented with a symptomatic arachnoid cyst of the right occipital convexity manifesting as visual disturbances and headache. She underwent craniotomy with membranectomy and fenestration to the subarachnoid space. Postoperatively, her complaints disappeared and brain magnetic resonance (MR) imaging showed cyst shrinkage. During the first 1 year after surgery, she made a good recovery without clinical symptoms or cyst enlargement. However, she complained of visual disturbances after 6 years. Brain MR imaging revealed cyst enlargement and Goldmann perimetry detected left lower quadrantanopia. The diagnosis was recurrent arachnoid cyst. A second surgical procedure was performed including membranectomy for histological examination of the cyst membrane, and an Ommaya reservoir was inserted into the cyst cavity to prevent further cyst enlargement. The histological findings were compatible with arachnoid cyst, similar to the results seen at the first surgery. She was discharged 3 weeks after the second operation with no complications, and follow up continues as an outpatient. Patients with symptomatic arachnoid cysts typically have good progress after surgery, but the present case shows that follow up should continue for at least 6 years after surgery, even if cyst volume reduction was initially favorable.

Background Elimination of Kupffer cells (KCs) exacerbated acute lung injury and mortality by inhibiting serum interleukin (IL)-10 levels in a rat peritonitis model. Since infiltrating inflammatory cells play a pivotal role in organ injury, the specific purpose of this study was to determine whether elimination of the KC and systemic IL-10 affect the expression of inflammatory mediators and the number of infiltrating inflammatory cells in the lung in the peritonitis model. Materials and methods Rats were given saline or gadolinium chloride (GdCl3), a KC toxicant, 24 h before cecal ligation and puncture (CLP). Tissue and serum samples were harvested after CLP, and the expression of inflammatory mediators was investigated. In another set of experiments, anti-rat IL-10 antibodies (anti-IL-10 Abs) were injected immediately after CLP to investigate the effects of immunoneutralization of endogenous IL-10. Results Serum levels of proinflammatory cytokines and chemokines were significantly greater in the GdCl3 group than the control group after CLP. Furthermore, expression inflammatory mediators, as well as the number of infiltrating inflammatory cells in the lung were significantly greater in the GdCl3 group than the control group. Alternatively, serum levels of inflammatory cytokines and chemokines, and the number of infiltrating inflammatory cells into the lung also increased significantly in rats treated with anti-IL-10 Abs compared with IgG after CLP. Conclusions Thus, depletion of KCs and neutralization of IL-10 increased the expression of chemokines and the number of infiltrating inflammatory cells in the lung, leading to exacerbated acute lung injury in sepsis.

High-temperature oxidation behavior of Ni-20Cr alloys with small amounts of rare earth elements (Y, Lu) was studied in oxygen for 18ks at 1473K, by mass gain measurements, observation of surface appearance,X-ray diffraction (XRD) and scanning electron microscopy (SEM). The mass gains of the Ni-20Cr alloys with rare earth elements decreased with increasing Y and Lu up to 0.5%. The outermost continuous scale on Ni-20Cr alloy consists of NiO which is a planar morphology. On the other hand, the scale on Ni-20Cr-0.5Y (Lu) alloys consists of Cr2O3 which is a fine granular morphology.

Although a superficial circumflex iliac artery perforator (SCIP) flap has recently been widely used owing to its various advantages, reports on its use in the pediatric population are limited. A case of a supermicrosurgical reconstruction of a soft tissue defect of the ankle associated with the congenital deficiency of the tibia using a free sensate SCIP flap in a 1-year-old child has been presented. The correction of the valgus deformity of the ankle resulted in a soft tissue defect, which required flap coverage. The lateral cutaneous branch of the intercostal nerve of the flap was coapted with the deep peroneal nerve for sensory recovery. Postoperative course was uneventful and the flap completely survived. The patient was able to ambulate independently at 7 months after surgery. To the best of our knowledge, this is the youngest case of a SCIP flap transfer in literature. This case showed that young age is not a contraindication for SCIP flap transfer. It is believed that the SCIP flap procedure may be a useful option for free flap reconstruction in children.

Hepatocellular carcinoma (HCC) is one of the most prevalent human cancers, with a rising incidence worldwide. The molecular mechanisms associated with the development of HCC are complex and include multiple interconnected molecular alterations with mounting evidence indicating an important role of microRNAs (miRNAs) in the pathogenesis of HCC. In humans, the development of HCC is commonly associated with liver cirrhosis. To study fibrosis-associated liver carcinogenesis, we used a mouse model designed to emulate the development of HCC in cirrhotic liver. Specifically, we were interested in evaluating the role of miRNAs in the molecular pathogenesis of liver carcinogenesis in male B6C3F1/J mice treated with N-nitrosodiethylamine (DEN) or carbon tetrachloride (CCl4 ) alone or a combination of DEN and CCl4 and characterized by a differential tumor incidence that increased in the following order: DENCCl4DEN+CCl4 . Treatment with DEN alone had negligible effect on hepatic miRNA expression. In contrast, treatment with either CCl4 alone or a combination of DEN and CCl4 resulted in major changes in miRNA expression. The analysis of miRNA profiles demonstrated an involvement of dysregulated miRNAs in major processes associated with the development of liver tumors, including inflammation, fibrosis, and stem cell activation. Importantly, the greatest incidence of liver tumors in mice treated with DEN+CCl4 was accompanied by a distinct over-expression of miRNAs suggesting that miRNA alterations may be responsible, at least in part, for the high tumor incidence.

The possibility that Kupffer cells (KCs) play key beneficial and deleterious roles in multiple organ injury in sepsis has been discussed. The role of KCs in lung injury in a rat peritonitis model was investigated. Specifically, the involvement of interleukin (IL)-10, which has anti-inflammatory effects, was examined. Rats were given saline or gadolinium chloride (GdCl3), a KC toxicant, 24 h before cecal ligation and puncture (CLP). Survival was assessed for 7 days after CLP. The liver, lung, and serum were harvested, and the expression of cytokines was assessed. Macrophages were isolated from each organ after CLP, and the mRNA expression of inflammatory mediators was assessed. GdCl3 treatment increased lung injury and mortality. Plasma endotoxin levels were significantly greater, whereas serum IL-10 levels were lower in the GdCl3 than in the control group after CLP. IL-10 levels were significantly greater in the aorta than the hepatic vein. The mRNA expression of IL-10 was less in KCs from the GdCl3 than the control group. In the liver, the expression of IL-10 increased rapidly and continuously, up to 9 h in the control group, but values were significantly lower in the GdCl3 group. Rabbit anti-rat IL-10 antibodies were injected just after CLP to investigate the effects of immunoneutralization of endogenously produced IL-10. In the antibody-treated group, lung injury and mortality increased compared with animals treated with rabbit immunoglobulin G. Taken together, these results indicate that KCs play a protective role in lung injury in sepsis by production of IL-10.

The purpose of this study was to investigate the regulation of lung macrophages (Μϕs) by Kupffer cells (KCs) in lung injury caused by endotoxemia. Phenotypic differences in tissue Μϕs were also investigated. Μϕs were isolated from gadolinium chloride (GdCl 3 )- or saline-treated rats 2 h after saline or lipopolysaccharide (LPS) administration. Furthermore, rats were given GdCl 3 24 h prior to LPS administration, and survival rate was assessed for 24 h. Moreover, lung edema was assessed 9 h after LPS injection. Expression of inflammatory mediators was measured in the liver and lung. KCs were divided into three subpopulations based on size and phagocytosis. The expression of TNF-α and MIP-2 was greater in the small KCs and lung Μϕs, while the expression of IL-6, IL-10, and MCP-1 was greater in the large and intermediate KCs. GdCl 3 eliminated ED2-positive large KCs and did not have any effect on the lung Μϕs. The number of ED1-positive KCs increased significantly in both organs after LPS challenge and was reduced by GdCl 3 . The population of ED2-positive KCs did not change following LPS administration. GdCl 3 completely prevented increases in lung microvascular permeability and mortality after LPS infusion. After LPS administration, expression of TNF-α and IL-6 increased rapidly and then decreased gradually in both organs. GdCl 3 inhibited these increases in the liver significantly and enhanced the expression of MCP-1 and IL-10 in the lung 9 h after LPS administration. Thus, the heterogeneous response of KCs to endotoxin leads to production of certain cytokines and chemokines that affect lung function.

An experimental search for an electric dipole moment in the diamagnetic atom 129 Xe is in progress through the precision measurement of spin precession frequency using an active nuclear spin maser. A 3 He comagnetometer has been incorporated into the active spin maser system in order to cancel out the long-term drifts in the external magnetic field. Also, a double-cell geometry has been adopted in order to suppress the frequency shifts due to interaction with polarized Rb atoms. The first EDM measurement with the 129 Xe active spin maser and the 3 He comagnetometer has been conducted.

We aim to measure the electric dipole moment (EDM) of a diamagnetic atom 129Xe using an optical-detection nuclear spin maser technique. The relation of EDM in a diamagnetic atom to nuclear Schiff moment and fundamental sources generating it is discussed, and the present status for the development of our experimental setup is presented.

This paper proposes a Bayesian approach for automatic music transcription of polyphonic MIDI signals based on generative modeling of onset occurrences of musical notes. Automatic music transcription involves two subproblems that are interdependent of each other: rhythm recognition and tempo estimation. When we listen to music, we are able to recognize its rhythm and tempo (or beat location) fairly easily even though there is ambiguity in determining the individual note values and tempo. This may be made possible through our empirical knowledge about rhythm patterns and tempo variations that possibly occur in music. To automate the process of recognizing the rhythm and tempo of music, we propose modeling the generative process of a MIDI signal of polyphonic music by combining the sub-process by which a musically natural tempo curve is generated and the sub-process by which a set of note onset positions is generated based on a 2-dimensional rhythm tree structure representation of music, and develop a parameter inference algorithm for the proposed model. We show some of the transcription results obtained with the present method.

A method to produce spin-aligned rare isotope (RI) beams has been developed, where a scheme of twostep projectile fragmentation to produce the RI of interest with high spin alignment and a technique of momentum-dispersion matching are combined. Effectiveness of the present method was demonstrated in an experiment at the RIKEN RIBF, where an RI beam of 32Al with spin alignment of 8(1)% was successfully produced from a primary beam of 48Ca, via an intermediate RI of 33Al. Figure of merit of the present method was found to be more than 50 times greater than that of the conventional method employing single-step projectile fragmentation. ispartof: Nuclear Instruments & Methods in Physics Research B vol:317 pages:769-773 ispartof: location:JAPAN, RIKEN Nishina Ctr Accelerator Based Sci, Matsue status: published

We have deposited nitrogen-doped diamond-like carbon (N-DLC) films by plasma-enhanced chemical vapor deposition using CH4, N2, and Ar, and investigated the effects of N doping on the structure and the electrical, mechanical, and optical properties of the N-DLC films. We fabricated undoped DLC/p-type Si and N-DLC/p-type Si heterojunctions and examined the current–voltage characteristics of the heterojunctions. When the N2 flow ratio was increased from 0 to 3.64%, the resistivity markedly decreased from the order of 105 Ω·cm to that of 10−2 Ω·cm and the internal stress also decreased. The resistivity gradually increased with increasing N2 flow ratio from 3.64 to 13.6%, and then it decreased at a N2 flow ratio of 13.6%. These behaviors can be explained in terms of the clustering of sp2 carbons and the formation of sp3C–N, sp2C=N, sp1C≡N, and C–H n bonds. The rectification ratio of the heterojunction using the N-DLC film prepared at 3.64% was 35.8 at ±0.5 V.

AIM To investigate the role of macrophage colony-stimulating factor (M-CSF) in patients with hepatocellular carcinoma (HCC) after surgery. METHODS Expression of M-CSF, distribution of M2 macrophages (MΦs), and angiogenesis were assessed in the liver, including tumors and peritumoral liver tissues. The prognostic power of these factors was assessed. Mouse isolated hepatic MΦs or monocytes were cultured with media containing M-CSF. The concentration of vascular endothelial growth factor (VEGF) in media was assessed. Furthermore, the role of the M-CSF-matured hepatic MΦs on proliferation of the vascular endothelial cell (VEC) was investigated. RESULTS A strong correlation between the expressions of M-CSF and CD163 was observed in the peritumoral area. Also, groups with high density of M-CSF, CD163 or CD31 showed a significantly shorter time to recurrence (TTR) than low density groups. Multivariate analysis revealed the expression of M-CSF or hepatic M2MΦs in the peritumoral area as the most crucial factor responsible for shorter TTR. Moreover, the expression of M-CSF and hepatic M2MΦs in the peritumoral area had better predictable power of overall survival. Values of VEGF in culture media were significantly greater in the hepatic MΦs compared with the monocytes. Proliferation of the VEC was greatest in the cells co-cultured with hepatic MΦs when M-CSF was present in media. CONCLUSION M-CSF increases hepatocarcinogenesis, most likely by enhancing an angiogenic factor derived from hepatic MΦ and could be a useful target for therapy against HCC.

The specific purpose of this study was to investigate the role of macrophage colony-stimulating factor (M-CSF) in initiation and progression of hepatocellular carcinoma using M-CSF-deficient mice.M-CSF-deficient (osteopetrotic: op/op) and their littermate (LM) mice were i.p. injected with diethylnitrosamine (DEN) to induce hepatocellular carcinoma. Twenty-eight weeks after DEN administration, the tumor incidence rate and serum M-CSF levels were assessed. Furthermore, distribution of the activated macrophages and the mRNA expression of CD163 and CD204 were evaluated. Moreover, angiogenesis was analyzed in tumors. In another set of experiments, apoptosis and proliferation of the hepatocytes were examined in the acute phase after DEN administration. Isolated hepatic macrophages were cultured with or without M-CSF, and vascular endothelial growth factor (VEGF) production was assessed by enzyme-linked immunoassay.Tumor incidence was significantly reduced in the op/op compared with the LM mice. Serum M-CSF levels were increased in the carcinogenesis models of the LM mice. Hepatic macrophages were found only in tumors in the op/op but in both normal liver tissue and tumors in the LM mice. In the op/op group, the mRNA expression of inflammatory cytokines was significantly lower compared with the LM mice. Furthermore, apoptosis was significantly increased in the op/op than the LM mice. Angiogenesis increased in liver tumors from the LM compared with the op/op mice. Production of VEGF was greater in the hepatic macrophages incubated with M-CSF compared with those without M-CSF.Thus, M-CSF is involved in the progression of chemically induced hepatocarcinogenesis.

Background Liver regeneration after partial hepatectomy (PH) is regulated by tumor necrosis factor (TNF)-α derived from the Kupffer cell. Furthermore, it was reported from our laboratory that interleukin (IL)-17A enhances the production of TNF-α by the Kupffer cell, suggesting that IL-17A may play a role in liver regeneration. Objective The purpose was to determine the role of IL-17A and the spleen in liver regeneration after PH. Methods Two mouse models including the wild-type (WT) mice or the IL-17A knockout (KO) mice underwent PH. Animals were killed at the designated time points; liver tissues were harvested for further investigation. Proliferation of hepatocytes was evaluated. Furthermore, the messenger RNA and protein expression of TNF-α and IL-6 were measured in the liver. In another set of experiments, the two animal models underwent splenectomy before PH. In an in vitro study, CD4-positive lymphocytes in the spleen were isolated from mice, and the number of IL-17A–positive cells was investigated. Results Liver regeneration was significantly impaired in the KO mice compared with the WT mice. This was associated with suppression of cell proliferation assessed by cell proliferation markers in the KO mice. In the WT mice that underwent splenectomy, liver regeneration was significantly delayed compared with animals without splenectomy. In contrast, splenectomy did not affect liver regeneration in the KO mice. IL-17A–positive lymphocytes increased significantly in the spleen in the WT mice after PH. Conclusions These results indicate that IL-17A derived from CD4-positive lymphocytes in the spleen is a key regulator in liver regeneration after PH.

Alcohol abuse continues to be a major social and clinical problem as excessive drinking is regarded to be a major risk factor for morbidity, disability and death globally1. Liver is a major, but not the only, target organ for alcohol-induced injury and a statistically significant relationship between per capita consumption of alcohol and mortality from liver cirrhosis, one of the major alcohol-related disease diagnoses, exists in all countries with published data2. Alcoholic liver disease represents a spectrum of clinical illnesses that range from fatty liver to hepatitis, fibrosis, cirrhosis and cancer3. Not all alcohol abusers develop alcoholic liver disease, especially pathology more severe than steatosis4, and the contribution of genetic and other risk factors for disease development and the mechanisms by which it occurs remain unclear1. The major pathways of alcohol’s adverse effect on the liver is through de-regulation of the metabolism, immune system response and oxidative stress5,6. Both “candidate gene” and “genome-wide association” approaches have been used to study gene-environment interactions that may exacerbate the risk of liver damage and promote clinically-evident disease1. Many of the candidate gene-based epidemiology studies suggested that polymorphisms in genes for alcohol (e.g., ADH and ALDH, etc.) and folate metabolism (e.g., MTHFR), as well as oxidative stress (e.g., MNSOD) and immune response (e.g., CD14, tumor necrosis factor α), are likely to be genetic modifiers of alcohol-related diseases7. The strongest evidence, confirmed in large meta-analyses of the data, exists for a role of polymorphisms in ADH1B and ALDH2 in alcohol-related cancer risk8. Recent advances in genotyping technologies and their embrace by clinicians are likely to bring additional information through the genome-wide association studies on large human cohorts. For example, a polymorphism in patatin-like phospholipase domain containing 3 gene, the product of which is involved in energy homeostasis, has been identified as strongly associated with the severity of both non-alcoholic fatty liver disease9 and alcohol-related cirrhosis10. This study evaluated key molecular events postulated to play a role in alcoholic liver injury: ER stress, lipid and one-carbon metabolism. Specifically, we tested a hypothesis that a panel of genetically diverse mouse strains may be used to examine the role of one carbon metabolism in the mechanism of inter-individual variability in alcoholic liver injury. The rationale for the focus of this study is the key role that one-carbon metabolism plays in susceptibility to liver steatosis, alcoholic liver injury and carcinogenesis11-13.

We report on the spectroscopic quadrupole moment measurement of the 7/2(1)(-) isomeric state in S-43(16)27 [E* = 320.5(5) keV, T-1/2 = 415(3) ns], using the time dependent perturbed angular distribution technique at the RIKEN RIBF facility. Our value, vertical bar Q(s) vertical bar = 23(3) efm(2), is larger than that expected for a single-particle state. Shell model calculations using the modern SDPF-U interaction for this mass region reproduce remarkably well the measured vertical bar Q(s) vertical bar, and show that non-negligible correlations drive the isomeric state away from a purely spherical shape.

The degree of freedom of spin in quantum systems serves as an unparalleled laboratory where intriguing quantum physical properties can be observed, and the ability to control spin is a powerful tool in physics research. We propose a novel method for controlling spin in a system of rare isotopes which takes advantage of the mechanism of the projectile fragmentation reaction combined with the momentum-dispersion matching technique. The present method was verified in an experiment at the RIKEN RI Beam Factory, in which a degree of alignment of 8% was achieved for the spin of a rare isotope Al-32. The figure of merit for the present method was found to be greater than that of the conventional method by a factor of more than 50., Comment: 18 pages, 5 figures

International audience; To produce a radioactive-isotope (RI) beam with high spin alignment, we have developed a novel method, the two-step projectile-fragmentation (PF) method, that employs momentum-dispersion matching. An on-line experiment to produce 32Al from 48Ca via 33Al was performed at RIKEN RI Beam Factory. In the experiment, we succeeded in producing approximately 8% spin alignment in an RI beam of 32Al. In this paper, we focus on evaluating the magnitude of spin alignment realized in one-nucleon removal from 33Al

Recent evidence suggests that IL-17A regulates neutrophil-dependent organ injury. Accordingly, the purpose of this study was to determine the role of IL-17A in neutrophil recruitment after ischemia–reperfusion (I/R) and in subsequent liver injury. Two mouse models including wild-type and IL-17A knockout mice were evaluated for I/R injury. The medial largest lobe of the liver was clamped for 90 min. In another set of experiments, recombinant mouse (rm)IL-17A homodimer or rmIL-17A/F heterodimer were administered to knockout mice before I/R, and liver injury was investigated. Isolated Kupffer cells were incubated with rmIL-17A or rmIL-17F, and production of TNF-α was measured. Studies evaluating the extent of liver injury as measured by serum transaminase levels demonstrated similar levels in the acute phase (6 h) in these two models. In contrast, in the subacute phase (20 h) after I/R, both serum transaminase levels and percent of hepatic necrosis were significantly reduced in the knockout mice compared with the wild-type mice. This reduction in liver injury seen in the knockout mice was associated with suppression of chemokine and adhesion molecule expression and reduction in infiltration of neutrophils into the liver. Administration of rmIL-17A homodimer, but not IL-17A/F heterodimer, increased liver injury in the subacute phase of I/R in KO mice. TNF-α production by isolated Kupffer cells increased significantly in the cells incubated with rmIL-17A compared with rmIL-17F. These results indicate that IL-17A is a key regulator in initiating neutrophil-induced inflammatory responses and hepatic injury in the subacute phase after reperfusion.