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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.

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.

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.

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.

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.

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.

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.

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.