Mean Time Between Failure of Ring Arbiter with Requests Differing in Incidences

In asynchronous arbiters, failures may happen, caused by metastable operations. The purpose of this study is to derive a formula to estimate such failures in a ring arbiter as mean time between failures (MTBF), under the condition that incidences of requests issued in all devices are different from each other. The operation of the arbiter is formularized by a markov chain. This chain is used to decide the probability at which each of possible failures contributes to MTBF. The sum of such probabilities gives the MTBF which can be represented as a sum of a finite number of terms. As an example, MTBF of a ring arbiter composed of 3 cells is shown

2001-GT-0083 DEVELOPMENT OF DRY LOW-NOX COMBUSTOR FOR 300 KW CLASS GAS TURBINE APPLIED TO CO-GENERATION SYSTEMS

ABSTRACT A 300 kWe class gas turbine which has a two-shaft and simple-cycle has been developed to apply to co-generation systems. The gas turbine engine is operated in the range of about 30% partial load to 100% load. The gas turbine combustor requires a wide range of stable operations and low NOx characteristics. A double staged lean premixed combustor, which has a primary combustion duct made of Si 3 N 4 ceramics, was developed to meet NOx regulations of less than 80 ppm (corrected at 0% oxygen). The gas turbine with the combustor has demonstrated superior low-emission performance of around 40 ppm (corrected at 0% oxygen) of NOx, and more than 99.5% of combustion efficiency between 30% and 100% of engine load. Endurance testing has demonstrated stable high combustion performance over 3,000 hours in spite of a wide compressor inlet air temperature (CIT) range of 5 to 35 degree C.. While increasing the gas generator turbine speed, the flow rate of primary fuel was controlled to hold a constant equivalence ratio of around 0.5 in the CIT range of more than 15 C. The output power was also decreased while increasing the CIT, in order to keep a constant temperature at the turbine inlet. The NOx decreases in the CIT range of more than 15 C. On the other hand, the NOx increases in the CIT range of less than 15 C when the output power was kept a constant maximum power. As a result, NOx emission has a peak value of about 40 ppm at 15 C

Predicting the Prognosis of Swallowing Function in Stroke Patients with Dysphagia Using the Videofluoroscopic Dysphagia Scale

The aim of the present study was to evaluate the correlation between parameters of the videofluoroscopic dysphagia scale (VDS) and the outcome of dysphagia to determine the usefulness of the VDS in patients admitted to convalescent rehabilitation wards. Patients (n = 23) with stroke-related dysphagia admitted to our rehabilitation hospital between April 2007 and March 2009. Medical records and videofluoroscopy findings on admission to hospital were reviewed retrospectively and the VDS score was calculated by adding individual VDS parameters. Subjects were divided into two groups: those who were able to ingest orally without tube feeding before discharge (Group 1) and those who still needed tube feeding on discharge (Group 2). The VDS scores were compared between the two groups. There were no significant differences in any individual parameter on the VDS between the two groups. However, the total VDS score was significantly lower in Group 1 patients (p < 0.05), as was the time from stroke onset to admission to our hospital (p < 0.05). There were no significant differences in any other parameters evaluated. The findings of the present study suggest that the total VDS score may be useful in predicting the prognosis of stroke-related dysphagia

Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction

In autoimmune arthritis, traditionally classified as a T helper (Th) type 1 disease, the activation of T cells results in bone destruction mediated by osteoclasts, but how T cells enhance osteoclastogenesis despite the anti-osteoclastogenic effect of interferon (IFN)-γ remains to be elucidated. Here, we examine the effect of various Th cell subsets on osteoclastogenesis and identify Th17, a specialized inflammatory subset, as an osteoclastogenic Th cell subset that links T cell activation and bone resorption. The interleukin (IL)-23–IL-17 axis, rather than the IL-12–IFN-γ axis, is critical not only for the onset phase, but also for the bone destruction phase of autoimmune arthritis. Thus, Th17 is a powerful therapeutic target for the bone destruction associated with T cell activation

Restoration of E-cadherin expression by selective Cox-2 inhibition and the clinical relevance of the epithelial-to-mesenchymal transition in head and neck squamous cell carcinoma

BACKGROUND: The epithelial-to-mesenchymal transition (EMT) accompanied by the downregulation of E-cadherin has been thought to promote metastasis. Cyclooxygenase-2 (Cox-2) is presumed to contribute to cancer progression through its multifaceted function, and recently its inverse relationship with E-cadherin was suggested. The aim of the present study was to investigate whether selective Cox-2 inhibitors restore the expression of E-cadherin in head and neck squamous cell carcinoma (HNSCC) cells, and to examine the possible correlations of the expression levels of EMT-related molecules with clinicopathological factors in HNSCC. METHODS: We used quantitative real-time PCR to examine the effects of three selective Cox-2 inhibitors, i.e., celecoxib, NS-398, and SC-791 on the gene expressions of E-cadherin (CDH-1) and its transcriptional repressors (SIP1, Snail, Twist) in the human HNSCC cell lines HSC-2 and HSC-4. To evaluate the changes in E-cadherin expression on the cell surface, we used a flowcytometer and immunofluorescent staining in addition to Western blotting. We evaluated and statistically analyzed the clinicopathological factors and mRNA expressions of Cox-2, CDH-1 and its repressors in surgical specimens of 40 patients with tongue squamous cell carcinoma (TSCC). RESULTS: The selective Cox-2 inhibitors upregulated the E-cadherin expression on the cell surface of the HNSCC cells through the downregulation of its transcriptional repressors. The extent of this effect depended on the baseline expression levels of both E-cadherin and Cox-2 in each cell line. A univariate analysis showed that higher Cox-2 mRNA expression (p = 0.037), lower CDH-1 mRNA expression (p = 0.020), and advanced T-classification (p = 0.036) were significantly correlated with lymph node metastasis in TSCC. A multivariate logistic regression revealed that lower CDH-1 mRNA expression was the independent risk factor affecting lymph node metastasis (p = 0.041). CONCLUSIONS: These findings suggest that the appropriately selective administration of certain Cox-2 inhibitors may have an anti-metastatic effect through suppression of the EMT by restoring E-cadherin expression. In addition, the downregulation of CDH-1 resulting from the EMT may be closely involved in lymph node metastasis in TSCC

NK cells control tumor-promoting function of neutrophils in mice

Although NK cells are recognized as direct antitumor effectors, the ability of NK cells to control cancer-associated inflammation, which facilitates tumor progression, remains unknown. In this study, we demonstrate that NK cells control tumor-promoting inflammation through functional modification of neutrophils. NK cells control the tumor-promoting function of neutrophils through an IFNgamma-dependent mechanism. Tumor progression in an NK cell-depleted host is diminished when the IL17A-neutrophil axis is absent. In NK cell-depleted mice, neutrophils acquire a tumor-promoting phenotype, characterized by up-regulation of VEGF-A expression, which promotes tumor growth and angiogenesis. A VEGFR inhibitor which preferentially suppressed tumor growth in NK cell-depleted mice was dependent on neutrophils. Furthermore, the systemic neutropenia caused by an anti-metabolite treatment showed an anti-cancer effect only in mice lacking NK cells. Thus, NK cells likely control the tumor-promoting and angiogenic function of neutrophils

Role of Epiligament in Ligamentum Flavum Hypertrophy in Patients with Lumbar Spinal Canal Stenosis : a Pilot Study

Ligamentum flavum (LF) hypertrophy is one of the main factors of lumbar spinal canal stenosis (LSCS). The primary object of this study is to clarify the existence of epiligament in the LF and its role in hypertrophy, and to develop an LF hypertrophy animal model. A cadaveric spine from a 30-year-old man was used to investigate the existence of epiligament in LF. Five LF samples from LSCS patients were obtained to evaluate hypertrophied LF. To create a rat model, we destabilized the lumbar spine. Each LF was sagittally cut for histological evaluation. The epiligament was clearly evident in normal LF specimens, which stained pink on Elastica van Gieson and green on Masson Trichrome. Onelayer was observed on the dural side and another on the dorsal side of the LF. LSCS patients had an enlarged dorsal epiligament, at around 30 times that of the regular thin epiligament on the dural side. The destabilized rat model showed an enlarged dorsal epiligament, with a mean thickness 8-fold that of the control. LF hypertrophy may be due to enlargement of the dorsal epiligament. Mechanical loading of the LF is an important factor for inducing hypertrophy in the rat model