Fractional time differential equations as a singular limit of the Kobayashi-Warren-Carter system

This paper is concerned with a singular limit of the Kobayashi-Warren-Carter system, a phase field system modelling the evolutions of structures of grains. Under a suitable scaling, the limit system is formally derived when the interface thickness parameter tends to zero. Different from many other problems, it turns out that the limit system is a system involving fractional time derivatives, although the original system is a simple gradient flow. A rigorous derivation is given when the problem is reduced to a gradient flow of a single-well Modica-Mortola functional in a one-dimensional setting.Comment: 24 page

High SDF-1 Expression in HIV-1 Carriers Does Not Correlate with CD8+T-Cell-Mediated Suppression of Viral Replication

AbstractStromal cell-derived factor 1 (SDF-1) inhibits T-cell tropic (T-tropic) HIV-1 infectionin vitro. In this study, we examined the regulatory role of SDF-1 on HIV-1 replication in peripheral blood mononuclear cells (PBMC) of HIV-infected individuals. We found that the amount of SDF-1 mRNA in freshly isolated PBMC of HIV-1 carriers was higher than in healthy donors. Moreover, PBMC from some asymptomatic carriers (ACs) exhibited high levels of SDF-1 mRNA expression. The level of SDF-1 expression in PBMC did not correlate with the magnitude of CD8+T cell-mediated suppression of HIV-1 among ACs. SDF-1 inhibited HIV-1 replication at the viral entry step, whereas a single-cycle HIV-1 infection system showed that the major part of the CD8+T-cell-mediated suppression occurs after intracellular penetration of the virus. Our results suggest that SDF-1 acts as a suppressor of virus replication in a CD8+T-cell-independent mechanism in HIV-infected individuals

Gas Embolism Caused by Portal Vein Gas: Case Report and Literature Review

Introduction: We describe a case of pulmonary gas embolism caused by portal vein gas (PVG) observed using echocardiography. Echography revealed gas flowing through the hepatic vein, inferior vena cava, right atrium, and right ventricle, as well as pulmonary hypertension. The patient was diagnosed as having pulmonary gas embolism caused by PVG. Objective: We consider PVG routes to pulmonary circulation, diagnosis of gas embolism caused by PVG, and treatment of gas embolism caused by PVG.Methods: We reviewed reports of eight cases of gas embolism caused by PVG and compared these cases to cases of gas embolism without PVG. Results: Mortality of gas embolism caused by PVG was 67%, positive blood culture was observed in six cases, and pulmonary edema was seen in three cases. PVG initially excites microbubble formation, which causes tissue damage in the liver and liver abscess. A large volume of PVG causes portal obstruction. As a result, portal hypertension, a portosystemic shunt or gastrointestinal congestion can occur. PVG can travel to the systemic vein through the liver or portosystemic shunt without anomaly and cause pulmonary gas embolism, followed by arterial embolism. In this environment, sepsis easily occurs. Echocardiography is useful for diagnosis of gas embolism caused by PVG, but the gas can be seen intermittently. The view of pulmonary edema is important for pulmonary gas embolism caused by PVG. Conclusion: It is important to treat the underlying disease, but PVG must be considered and treated as the gas embolism’s source

Effect of AZD1480 in an epidermal growth factor receptor-driven lung cancer model

Objective: STAT3 plays a vital role in inducing and maintaining a pro-carcinogenic inflammatory microenvironment and is reported to be a critical mediator of the oncogenic effects of EGFR mutations. STAT3 activation is mediated through JAK family kinases. We investigated the effect of the JAK1/2 inhibitor AZD1480 on lung tumors induced by an activating EGFR mutation. Materials and methods: Three EGFR tyrosine kinase inhibitor-resistant cell lines (RPC-9, PC-9/Van-R and PC-9/ER3) established from PC-9 harboring an EGFR exon19 deletion mutation were used. Growth inhibition was measured using an MIT assay. Effects of AZD1480 were also evaluated in the xenograft model and in the EGFR transgenic mice model. Protein expressions were assessed by immunoblotting and immunohistochemistry. Group differences were compared using Student's t-test. To evaluate the efficacy of AZD1480 on survival, AZD1480 or vehicle was administered orally from 7 weeks of age of the transgenic mice. Overall survival curves were calculated using the Kaplan-Meier method. Results: The sensitivities of resistant and parent cells to AZD1480 were similar in vitro. AZD1480 (30 or 50 mg/kg/day, per os) reduced angiogenesis and revealed significant tumor regression in a mouse xenograft model: Subsequently, the transgenic mice were treated with AZD1480 (30 mg/kg/day) or vehicle alone. The numbers of lung tumors (long axis exceeding 1 mm) in the AZD1480-treated group and control group were 0.37 +/- 0.18 and 2.25 +/- 0.53 (p <0.001), respectively. AZD1480 treatment suppressed pSTAT3, pJAK1, pJAK2 and angiogenesis. The median survival time in the AZD1480-treated group (217 days) was significantly greater than that in the control group (106 days) (log-rank test, p <0.0001). Conclusion: AZD1480 may be effective against lung tumors driven by an activating EGER mutation

Log N - Log S Relations and Spectral Properties of Sources from the ASCA Large Sky Survey --- their Implications for the Origin of the Cosmic X-ray Background (CXB)

We carried out the first wide-area unbiased survey with the ASCA satellite in the 0.7-10 keV band around a north Galactic-pole region covering a continuous area of 7 square degrees (Large Sky Survey; LSS). To make the best use of ASCA capability, we developed a new source-detection method where the complicated detector responses are fully taken into account. Applying this method to the entire LSS data independently in the total (0.7-7 keV), hard (2-10 keV), and soft (0.7-2 keV) band, we detected 107 sources altogether with sensitivity limits of 6 x 10E-14 (0.7-7 keV), 1 x 10E-13 (2-10 keV), and 2 x 10E-14 erg sE-1 cmE-2 (0.7-2 keV), respectively. A complete list of the detected sources is presented. Based on detailed studies by Monte Carlo simulations, we evaluated effects of the source confusion and accurately derived Log N - Log S relation in each survey band. The Log N - Log S relation in the hard band is located on the extrapolation from the GINGA and HEAO1 results with the Euclidean slope of -3/2, while that in the soft band is consistent with the results by ROSAT. At these flux limits, 30 (+/- 3) percent of the CXB in the 0.7-7 keV band and 23 (+/- 3) percent in the 2-10 keV band have been resolved into discrete sources. The average spectrum of faint sources detected in the total band shows a photon index of 1.63 +/- 0.07 in the 0.7-10 keV range, consistent with the comparison of source counts between the hard and the soft energy band. Those detected in the hard band show a photon index of 1.49 +/- 0.10 in the 2-10 keV range. These spectral properties suggest that contribution of sources with hard energy spectra become significant at a flux of 10E-13 erg sE-1 cmE-2 (2-10 keV). The most plausible candidates are type-II AGNs, as indicated by on-going optical identifications.Comment: 28 pages, 11 figures, to appear in ApJ 518, 1999; figure 1 replaced, minor errors in text correcte

Scalar chiral ground states of spin ladders with four-spin exchanges

We show that scalar chiral order can be induced by four-spin exchanges in the two-leg spin ladder, using the spin-chirality duality transformation and matrix-product ansatz. Scalar-chiral-ordered states are found to be exact ground states in a family of spin ladder models. In this scalar chiral phase, there is a finite energy gap above the doubly degenerate ground states and a $Z_2 \times Z_2 \times Z_2$ symmetry is fully broken. It is also shown that the SU(4)-symmetric model, which is self-dual under the duality transformation, is on a multicritical point surrounded by the staggered dimer phase, the staggered scalar chiral phase, and the gapless phase.Comment: 8 pages, 2 figures, to appear in Phys. Rev.