Linears stability boundary for simulated oscillatory flow phenomena in vertical condensing flows

Papers presented to the 11th International Conference on Heat Transfer, Fluid Mechanics and Thermodynamics, South Africa, 20-23 July 2015.In an earlier paper the results of a simulation of unstable flow phenomena in vertical condensing flows were presented. The horizontal condensing flow model was extended to include gravitational effects. The simulation of the non-linear model revealed existence of limit-cycle type of oscillations of large amplitude, including possibilities of flow reversals, as were observed on horizontal flows. The simulations also revealed that the gravitational effects have an attenuating effect on the oscillatory behavior in downward flows, and an enhancing effect on the upward flows. Matlab/Simulink tools were used for the system simulations. In the present paper the non-linear model was linearized, leading to an identification of the stable and unstable domains of operation for vertical condensing flows in both upward and downward flow directions. The stability boundary for the horizontal condensing flows lies in between the stability boundaries for vertical flows. The downward condensing flow is more stable and has a narrower unstable region than the horizontal flow. By comparison the vertical condensing upward flow is more unstable than both horizontal and downward flows. These observations are in correspondence with those of the non-linear model. A linear stability criterion including effects of gravity for vertical flows, that is an extension of such a criterion for horizontal flows, is presented.am201

Ideal Spin Filters: Theoretical Study of Electron Transmission Through Ordered and Disordered Interfaces Between Ferromagnetic Metals and Semiconductors

It is predicted that certain atomically ordered interfaces between some ferromagnetic metals (F) and semiconductors (S) should act as ideal spin filters that transmit electrons only from the majority spin bands or only from the minority spin bands of the F to the S at the Fermi energy, even for F with both majority and minority bands at the Fermi level. Criteria for determining which combinations of F, S and interface should be ideal spin filters are formulated. The criteria depend only on the bulk band structures of the S and F and on the translational symmetries of the S, F and interface. Several examples of systems that meet these criteria to a high degree of precision are identified. Disordered interfaces between F and S are also studied and it is found that intermixing between the S and F can result in interfaces with spin anti-filtering properties, the transmitted electrons being much less spin polarized than those in the ferromagnetic metal at the Fermi energy. A patent application based on this work has been commenced by Simon Fraser University.Comment: RevTeX, 12 pages, 5 figure

Transformation of SOX9(+) cells by Pten deletion synergizes with steatotic liver injury to drive development of hepatocellular and cholangiocarcinoma

SOX9 (Sex-determining region Y Box 9) is a well-characterized transcription factor that is a marker for progenitor cells in various tissues. In the liver, cells delineated by SOX9 are responsible for regenerating liver parenchyma when cell proliferation is impaired following chronic injury. However, whether these SOX9(+) cells play a role in liver carcinogenesis has not been fully understood, although high SOX9 expression has been linked to poor survival outcome in liver cancer patients. To address this question, we developed a liver cancer mouse model (Pten(loxP/loxP); Sox9-Cre(ERT+); R26R(YFP)) where tumor suppressor Pten (phosphatase and tensin homolog deleted on chromosome ten) is deleted in SOX9(+) cells following tamoxifen injection. In this paper, we employ lineage-tracing to demonstrate the tumorigenicity potential of the Pten(-), SOX9(+) cells. We show that these cells are capable of giving rise to mixed-lineage tumors that manifest features of both hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (CCA). Our results suggest that PTEN loss induces the transformation of SOX9(+) cells. We further show that to activate these transformed SOX9(+) cells, the presence of liver injury is crucial. Liver injury, induced by hepatotoxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) or high-fat diet (HFD), substantially increases tumor incidence and accelerates liver carcinogenesis from SOX9(+) cells in Pten null mice but not in control mice. We further examine the mechanisms underlying tumor formation in this model to show that concurrent with the induction of niche signal (i.e., Wnt signaling), liver injury significantly stimulates the expansion of tumor-initiating cells (TICs). Together, these data show that (1) SOX9(+) cells have the potential to become TICs following the primary transformation (i.e. Pten deletion) and that (2) liver injury is necessary for promoting the activation and proliferation of transformed SOX9(+) cells, resulting in the genesis of mixed-lineage liver tumors

Loss of pten and activation of kras synergistically induce formation of intraductal papillary mucinous neoplasia from pancreatic ductal cells in mice

BACKGROUND & AIMS: Intraductal papillary mucinous neoplasias (IPMNs) are precancerous cystic lesions that can develop into pancreatic ductal adenocarcinomas (PDACs). These large macroscopic lesions are frequently detected during medical imaging, but it is unclear how they form or progress to PDAC. We aimed to identify cells that form IPMNs and mutations that promote IPMN development and progression. METHODS: We generated mice with disruption of Pten specifically in ductal cells (Sox9CreER(T2);Pten(flox/flox);R26R(YFP) or Pten(ΔDuct/ΔDuct) mice) and used Pten(ΔDuct/+) and Pten(+/+) mice as controls. We also generated Kras(G12D);Pten(ΔDuct/ΔDuct) and Kras(G12D);Pten(ΔDuct/+) mice. Pancreata were collected when mice were 28 weeks to 14.5 months old and analyzed by histology, immunohistochemistry, and electron microscopy. We performed multiplexed droplet digital polymerase chain reaction to detect spontaneous Kras mutations in Pten(ΔDuct/ΔDuct) mice and study the effects of Ras pathway activation on initiation and progression of IPMNs. We obtained 2 pancreatic sections from a patient with an invasive pancreatobiliary IPMN and analyzed the regions with and without the invasive IPMN (control tissue) by immunohistochemistry. RESULTS: Mice with ductal cell-specific disruption of Pten but not control mice developed sporadic, macroscopic, intraductal papillary lesions with histologic and molecular features of human IPMNs. Pten(ΔDuct/ΔDuct) mice developed IPMNs of several subtypes. In Pten(ΔDuct/ΔDuct) mice, 31.5% of IPMNs became invasive; invasion was associated with spontaneous mutations in Kras. Kras(G12D);Pten(ΔDuct/ΔDuct) mice all developed invasive IPMNs within 1 month. In Kras(G12D);Pten(ΔDuct/+) mice, 70% developed IPMN, predominately of the pancreatobiliary subtype, and 63.3% developed PDAC. In all models, IPMNs and PDAC expressed the duct-specific lineage tracing marker yellow fluorescent protein. In immunohistochemical analyses, we found that the invasive human pancreatobiliary IPMN tissue had lower levels of PTEN and increased levels of phosphorylated (activated) ERK compared with healthy pancreatic tissue. CONCLUSIONS: In analyses of mice with ductal cell-specific disruption of Pten, with or without activated Kras, we found evidence for a ductal cell origin of IPMNs. We also showed that PTEN loss and activated Kras have synergistic effects in promoting development of IPMN and progression to PDAC