Boron carbide thin film surface characterization after graphitic carbon removal using low-pressure oxygen gas RF plasma.

B 4 C-coated thin film mirrors are used in high brilliance synchrotron and x-ray free electron laser beamlines due to their low absorption coefficient and high thermal stability. As in the case of gold, platinum, and other thin film mirrors, B 4 C-coated mirrors also are affected due to synchrotron radiation-induced carbon contaminations in beamlines. In the present study, a graphitic carbon (C) layer deposited on top of boron carbide (B x C) thin film surface is removed by five successive oxygen radio frequency (RF) plasma exposures (RF power, 10 W; O 2 flow, 30 sccm; exposure time, 10 min each). Before and after the carbon layer removal, structural and compositional properties of the B x C/C bilayer are characterized by soft x-ray reflectivity, x-ray photoelectron spectroscopy, grazing angle x-ray diffraction, and Raman spectroscopy techniques. Characterization results reveal that in the first four exposures the carbon layer thickness decreases continuously without affecting the B x C layer properties; however, in the fifth exposure, the carbon layer is completely removed along with a partial etching of the B x C layer too.

Study of interface reaction in a B4C/Cr mirror at elevated temperature using soft X-ray reflectivity.

Boron carbide is a prominent material for high-brilliance synchrotron optics as it remains stable up to very high temperatures. The present study shows a significant change taking place at 550°C in the buried interface region formed between the Cr adhesive layer and the native oxide layer present on the silicon substrate. An in situ annealing study is carried out at the Indus-1 Reflectivity beamline from room temperature to 550°C (100°C steps). The studied sample is a mirror-like boron carbide thin film of 400 Šthickness deposited with an adhesive layer of 20 ŠCr on a silicon substrate. The corresponding changes in the film structure are recorded using angle-dependent soft X-ray reflectivity measurements carried out in the region of the boron K-edge after each annealing temperature. Analyses performed using the Parratt recursive formalism reveal that the top boron carbide layer remains intact but interface reactions take place in the buried Cr-SiO2 region. After 300°C the Cr layer diffuses towards the substrate. At higher temperatures of 500°C and 550°C the Cr reacts with the native oxide layer and tends to form a low-density compound of chromium oxysilicide (CrSiOx). Depth profiling of Si and Cr distributions obtained from secondary ion mass spectroscopy measurements corroborate the layer model obtained from the soft X-ray reflectivity analyses. Details of the interface reaction taking place near the substrate region of boron carbide/Cr sample are discussed.

Potential role of NK cells in the pathogenesis of inflammatory bowel disease.

NK cells are a major component of the innate immune system and play an important role in the tissue inflammation associated with autoimmune diseases such as inflammatory bowel disease (IBD). NK cells are unique in bearing both stimulatory and inhibitory receptors specific for MHC class I molecules, and their function is regulated by a series of inhibiting or activating signals. The delicate balance between activation and inhibition that decides NK cell final action provides an opportunity for their possible modulatory effect on specific therapeutic settings. Intestinal NK cells are phenotypically distinct from their counterparts in the blood and resemble "helper" NK cells, which have potentially important functions both in promoting antipathogen responses and in the maintenance of intestinal epithelial homeostasis. NK cell activities have been found to be significantly below normal levels in both remissive and active stages of IBD patients. However, some proinflammatory cytokines (e.g., IL-15, IL-21, and IL-23) could potently induce NK cell activation to secret high levels of proinflammatory cytokines (e.g., IFN-γ and TNF) and promote the cytolytic activities against the target cells. This paper provides the characteristics of intestinal NK cells and their potential role in the pathogenesis of IBD.

Explicit analytical tuning rules for digital PID controllers via the magnitude optimum criterion.

Analytical tuning rules for digital PID type-I controllers are presented regardless of the process complexity. This explicit solution allows control engineers 1) to make an accurate examination of the effect of the controller's sampling time to the control loop's performance both in the time and frequency domain 2) to decide when the control has to be I, PI and when the derivative, D, term has to be added or omitted 3) apply this control action to a series of stable benchmark processes regardless of their complexity. The former advantages are considered critical in industry applications, since 1) most of the times the choice of the digital controller's sampling time is based on heuristics and past criteria, 2) there is little a-priori knowledge of the controlled process making the choice of the type of the controller a trial and error exercise 3) model parameters change often depending on the control loop's operating point making in this way, the problem of retuning the controller's parameter a much challenging issue. Basis of the proposed control law is the principle of the PID tuning via the Magnitude Optimum criterion. The final control law involves the controller's sampling time Ts within the explicit solution of the controller's parameters. Finally, the potential of the proposed method is justified by comparing its performance with the conventional PID tuning when controlling the same process. Further investigation regarding the choice of the controller's sampling time Ts is also presented and useful conclusions for control engineers are derived.

IL-25 downregulates Th1/Th17 immune response in an IL-10-dependent manner in inflammatory bowel disease.

BACKGROUND: Interleukin 25 (IL-25) is involved in the initiation of T helper cell (Th)2-mediated immunopathologies. In this study, we investigated the expression of IL-25 in inflammatory bowel disease (IBD) and its role in the induction of CD4 T-cell differentiation. METHODS: Expression of IL-25 in inflamed mucosa of patients with IBD was determined by quantitative real-time polymerase chain reaction, immunohistochemistry, and enzyme-linked immunosorbent assay. The correlation of IL-25 expression with endoscopic disease activities and C-reactive protein was evaluated. Peripheral blood and lamina propria CD4 T cells were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies in the presence of IL-25. Transcription factors and cytokines were determined with real-time polymerase chain reaction, flow cytometry, and enzyme-linked immunosorbent assay. RESULTS: IL-25 was significantly decreased in the sera and inflamed mucosa of patients with active IBD compared with controls. It was upregulated in the sera of patients with Crohn's disease after treatment with infliximab. The levels of IL-25 in inflamed mucosa and sera were inversely correlated with endoscopic disease activities and C-reactive protein, respectively, in IBD. IL-25 could markedly inhibit IBD CD4 T cells to produce tumor necrosis factor, interferon γ, and IL-17A but promote IL-10 secretion. It suppressed the differentiation of IBD CD4 T cells into Th1 and Th17 cells but did not interfere with Th2 cell differentiation. Importantly, blockade of IL-10 secretion by IBD CD4 T cells markedly attenuated the inhibitory role of IL-25 in modulating both Th1 and Th17 immune responses. CONCLUSIONS: IL-25 is markedly decreased in IBD and inhibits IBD CD4 T-cell activation and differentiation into Th1/Th17 cells in an IL-10-dependent manner, suggesting that it may be a potential therapeutic agent for IBD.

Comparative evaluation of intragastric bile acids and hepatobiliary scintigraphy in the diagnosis of duodenogastric reflux.

AIM: To assess the diagnostic value of a combination of intragastric bile acids and hepatobiliary scintigraphy in the detection of duodenogastric reflux (DGR). METHODS: The study contained 99 patients with DGR and 70 healthy volunteers who made up the control group. The diagnosis was based on the combination of several objective arguments: a long history of gastric symptoms (i.e., nausea, epigastric pain, and/or bilious vomiting) poorly responsive to medical treatment, gastroesophageal reflux symptoms unresponsive to proton-pump inhibitors, gastritis on upper gastrointestinal (GI) endoscopy and/or at histology, presence of a bilious gastric lake at > 1 upper GI endoscopy, pathologic 24-h intragastric bile monitoring with the Bilitec device. Gastric juice was aspirated in the GI endoscopy and total bile acid (TBA), total bilirubin (TBIL) and direct bilirubin (DBIL) were tested in the clinical laboratory. Continuous data of gastric juice were compared between each group using the independent-samples Mann-Whitney U-test and their relationship was analysed by Spearman's rank correlation test and Fisher's linear discriminant analysis. Histopathology of DGR patients and 23 patients with chronic atrophic gastritis was compared by clinical pathologists. Using the Independent-samples Mann-Whitney U-test, DGR index (DGRi) was calculated in 28 patients of DGR group and 19 persons of control group who were subjected to hepatobiliary scintigraphy. Receiver operating characteristic curve was made to determine the sensitivity and specificity of these two methods in the diagnosis of DGR. RESULTS: The group of patients with DGR showed a statistically higher prevalence of epigastric pain in comparison with control group. There was no significant difference between the histology of gastric mucosa with atrophic gastritis and duodenogastric reflux. The bile acid levels of DGR patients were significantly higher than the control values (Z: TBA: -8.916, DBIL: -3.914, TBIL: -6.197, all P < 0.001). Two of three in the DGR group have a significantly associated with each other (r: TBA/DBIL: 0.362, TBA/TBIL: 0.470, DBIL/TBIL: 0.737, all P < 0.001). The Fisher's discriminant function is followed: Con: Y = 0.002TBA + 0.048DBIL + 0.032TBIL - 0.986; Reflux: Y = 0.012TBA + 0.076DBIL + 0.089TBIL - 2.614. Eighty-four point zero five percent of original grouped cases were correctly classified by this method. With respect to the DGR group, DGRi were higher than those in the control group with statistically significant differences (Z = -5.224, P < 0.001). Twenty eight patients (59.6%) were deemed to be duodenogastric reflux positive by endoscopy, as compared to 37 patients (78.7%) by hepatobiliary scintigraphy. CONCLUSION: The integrated use of intragastric bile acid examination and scintigraphy can greatly improve the sensitivity and specificity of the diagnosis of DGR.

The increased expression of IL-23 in inflammatory bowel disease promotes intraepithelial and lamina propria lymphocyte inflammatory responses and cytotoxicity.

This study analyzed IL-23p19 expression in inflamed mucosa of IBD and the role in the induction of IEL and NK cell activation as well as Th17 cell differentiation. Expression of IL-23p19 was performed by immunohistochemistry and quantitative real-time PCR. Expression of IL-23R was assessed by flow cytometry. Cytolytic activities of IEL and NK cells by IL-23 were determined by a standard (51)Cr-release assay. Cytokine levels were analyzed by ELISA and quantitative real-time PCR. Expression of IL-23p19 was increased significantly in inflamed mucosa of CD compared with that in UC and healthy controls. Double-staining confirmed that IL-23p19(+) cells were mainly CD68(+) macrophages/DCs. IL-23R(+) cells were increased significantly in PB- and LP-CD4(+) and -CD8(+) T and NK cells. IL-23 markedly promoted IBD IEL and NK cell activation and cytotoxicity and triggered IBD PB- and LP-T cells to secrete significantly higher levels of IFN-γ, TNF, IL-2, and IL-17A compared with controls. Importantly, IL-23 promoted IBD PB- or LP-CD4(+) T cells to differentiate into Th17 cells, characterized by increased expression of IL-17A and RORC. Anti-TNF treatment could markedly reduce IL-23 expression and Th17 cell infiltration in inflamed mucosa of CD patients. These data indicate that IL-23 is highly expressed in inflamed mucosa of IBD and plays an important role in the induction of IEL, NK, and T cell activation, proinflammatory cytokine secretion, and Th17 cell differentiation. Targeted therapy directed against IL-23p19 may have a therapeutic role in treatment of IBD.

Palm fatty acid biodiesel: process optimization and study of reaction kinetics.

The relatively high cost of refined oils render the resulting fuels unable to compete with petroleum derived fuel. In this study, biodiesel is prepared from palm fatty acid (PFA) which is a by-product of palm oil refinery. The process conditions were optimized for production of palm fatty acid methyl esters. A maximum conversion of 94.4% was obtained using two step trans-esterification with 1:10 molar ratio of oil to methanol at 65°C. Sulfuric acid and Sodium hydroxide were used as acid and base catalyst respectively. The composition of fatty acid methyl esters (FAME) obtained was similar to that of palm oil. The biodiesel produced met the established specifications of biodiesel of American Society for Testing and Materials (ASTM). The kinetics of the trans-esterification reaction was also studied and the data reveals that the reaction is of first order in fatty acid and methanol (MeOH) and over all the reaction is of second order.

Current strategies for the treatment of ulcerative colitis.

Ulcerative colitis (UC) is a chronic, relapsing and debilitating idiopathic inflammation of the gastrointestinal tract. Dysregulation of the mucosal immune response toward commensal bacterial flora together with genetic and environmental factors plays an important role in the pathogenesis. Refractory UC refers to disease that does not respond to or responds poorly to the many drugs used to treat the disease. The aim of medical treatment is to induce and maintain clinical remission. The most commonly used drugs, including mesalazine, azathioprine, 6-mercaptopurine, cyclosporine, and more recently anti-tumor necrosis factor (TNF) monoclonal antibody (e.g., infliximab), are chosen to suppress the immune system in intestinal mucosa. Additionally, colectomy may be required if medical treatments are unsuccessful or if complications develop. Some of the recent patent related to the field also discuss in this review article.

Potential role of Th17 cells in the pathogenesis of inflammatory bowel disease.

The etiopathology of inflammatory bowel disease (IBD) remains elusive. Accumulating evidence suggests that the abnormality of innate and adaptive immunity responses plays an important role in intestinal inflammation. IBD including Crohn's disease (CD) and ulcerative colitis (UC) is a chronic inflammatory disease of the gastrointestinal tract, which is implicated in an inappropriate and overactive mucosal immune response to luminal flora. Traditionally, CD is regarded as a Th1-mediated inflammatory disorder while UC is regarded as a Th2-like disease. Recently, Th17 cells were identified as a new subset of T helper cells unrelated to Th1 or Th2 cells, and several cytokines [e.g. interleukin (IL)-21, IL-23] are involved in regulating their activation and differentiation. They not only play an important role in host defense against extracellular pathogens, but are also associated with the development of autoimmunity and inflammatory response such as IBD. The identification of Th17 cells helps us to explain some of the anomalies seen in the Th1/Th2 axis and has broadened our understanding of the immunopathological effects of Th17 cells in the development of IBD.