Hydrothermal Surface-Wave Instability and the Kuramoto-Sivashinsky Equation

We consider a system formed by an infinite viscous liquid layer with a constant horizontal temperature gradient, and a basic nonlinear bulk velocity profile. In the limit of long-wavelength and large nondimensional surface tension, we show that hydrothermal surface-wave instabilities may give rise to disturbances governed by the Kuramoto-Sivashinsky equation. A possible connection to hot-wire experiments is also discussed.Comment: 11 pages, RevTex, no figure

Biology and management of horseweed

"This publication discusses some of the biological characteristics that make horseweed particularly troublesome to control in agronomic crops. Then it provides management strategies, using technologies now available, that will allow growers to control herbicide-resistant horseweed and hopefully slow the spread of glyphosate resistance."--Extension website, viewed October 31, 2022.Reviewed by Kevin Bradley (Division of Plant Sciences), Mark Loux (Ohio State University), Jeff Stachler (Ohio State University), Bill Johnson (Purdue University), Glenn Nice (Purdue University), Vince Davis (Purdue University), Dawn Nordby (University of Illinois)Reviewed 10/22Includes bibliographical reference

Features and Prognosis of Severe Malaria Caused by Plasmodium falciparum, Plasmodium vivax and Mixed Plasmodium Species in Papua New Guinean Children

BACKGROUND: Mortality from severe pediatric falciparum malaria appears low in Oceania but Plasmodium vivax is increasingly recognized as a cause of complications and death. The features and prognosis of mixed Plasmodium species infections are poorly characterized. Detailed prospective studies that include accurate malaria diagnosis and detection of co-morbidities are lacking. METHODS AND FINDINGS: We followed 340 Papua New Guinean (PNG) children with PCR-confirmed severe malaria (77.1% P. falciparum, 7.9% P. vivax, 14.7% P. falciparum/vivax) hospitalized over a 3-year period. Bacterial cultures were performed to identify co-incident sepsis. Clinical management was under national guidelines. Of 262 children with severe falciparum malaria, 30.9%, 24.8% and 23.2% had impaired consciousness, severe anemia, and metabolic acidosis/hyperlactatemia, respectively. Two (0.8%) presented with hypoglycemia, seven (2.7%) were discharged with neurologic impairment, and one child died (0.4%). The 27 severe vivax malaria cases presented with similar phenotypic features to the falciparum malaria cases but respiratory distress was five times more common (P=0.001); one child died (3.7%). The 50 children with P. falciparum/vivax infections shared phenotypic features of mono-species infections, but were more likely to present in deep coma and had the highest mortality (8.0%; P=0.003 vs falciparum malaria). Overall, bacterial cultures were positive in only two non-fatal cases. 83.6% of the children had alpha-thalassemia trait and seven with coma/impaired consciousness had South Asian ovalocytosis (SAO). CONCLUSIONS: The low mortality from severe falciparum malaria in PNG children may reflect protective genetic factors other than alpha-thalassemia trait/SAO, good nutrition, and/or infrequent co-incident sepsis. Severe vivax malaria had similar features but severe P. falciparum/vivax infections were associated with the most severe phenotype and worst prognosis

Characterization and mapping of dwelling types for forest fire prevention

Définition des habitats isolés, diffus et groupés. Méthode de caractérisation et de cartographie de ces types d'habitat dans le contexte de prévention du risque d'incendie. Mise en relation des types d'habitat avec le risque d'incendie. / In a context of forest fire risk , the development of actions concerning wildfire prevention and land management is necessary and essential particularly in wildland urban interfaces (WUI). The term WUI' always includes components such as human presence and wildland vegetation. Both the hazard (probability of fire outbreak, distribution) and the vulnerability of urban areas can be characterized through the spatial organization of houses and vegetation. The first required step is to characterize and map WUI in large areas and at a large scale, which in turn requires qualifying different types of dwellings and mapping them. With this goal in view, the paper presents a brief synthesis of results coming from an exploratory process for the characterization of dwelling types (Lampin et al., 2007), and develops a method based on GIS-geo treatments to characterize different types of dwelling with regard to fire risk. Three types of dwellings were classified: isolated dwellings, scattered dwellings and clustered dwellings, using criteria based on the distance between houses, the size of clusters of houses and housing density, which can be mapped automatically. Within dwelling types, the density value of forest fire ignition changed and was twice as high for isolated dwellings as for clustered dwellings. The spatial organization of dwellings seems to have a real impact on fire occurrence. Thus maps of different dwelling types can be interpreted for use in developing fire fighting strategies or prevention actions concerning end-users such as forest and land planning managers or fire-fighters

TAK1 Is Required for Survival of Mouse Fibroblasts Treated with TRAIL, and Does So by NF-κB Dependent Induction of cFLIPL

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known as a “death ligand”—a member of the TNF superfamily that binds to receptors bearing death domains. As well as causing apoptosis of certain types of tumor cells, TRAIL can activate both NF-κB and JNK signalling pathways. To determine the role of TGF-β-Activated Kinase-1 (TAK1) in TRAIL signalling, we analyzed the effects of adding TRAIL to mouse embryonic fibroblasts (MEFs) derived from TAK1 conditional knockout mice. TAK1−/− MEFs were significantly more sensitive to killing by TRAIL than wild-type MEFs, and failed to activate NF-κB or JNK. Overexpression of IKK2-EE, a constitutive activator of NF-κB, protected TAK1−/− MEFs against TRAIL killing, suggesting that TAK1 activation of NF-κB is critical for the viability of cells treated with TRAIL. Consistent with this model, TRAIL failed to induce the survival genes cIAP2 and cFlipL in the absence of TAK1, whereas activation of NF-κB by IKK2-EE restored the levels of both proteins. Moreover, ectopic expression of cFlipL, but not cIAP2, in TAK1−/− MEFs strongly inhibited TRAIL-induced cell death. These results indicate that cells that survive TRAIL treatment may do so by activation of a TAK1–NF-κB pathway that drives expression of cFlipL, and suggest that TAK1 may be a good target for overcoming TRAIL resistance

Water Network Optimization with Wastewater Regeneration Models

The conventional water network synthesis approach greatly simplifies wastewater treatment units by using fixed recoveries, creating a gap for their applicability to industrial processes. This work describes a unifying approach combining various technologies capable of removing all the major types of contaminants through the use of more realistic models. The following improvements are made over the typical superstructure-based water network models. First, unit-specific shortcut models are developed in place of the fixed contaminant removal model to describe contaminant mass transfer in wastewater treatment units. Shortcut wastewater treatment cost functions are also incorporated into the model. In addition, uncertainty in mass load of contaminants is considered to account for the range of operating conditions. Furthermore, the superstructure is modified to accommodate realistic potential structures. We present a modified Lagrangean-based decomposition algorithm in order to solve the resulting nonconvex mixed-integer nonlinear programming (MINLP) problem efficiently. Several examples are presented to illustrate the effectiveness and limitations of the algorithm for obtaining the global optimal solutions.The authors would like to acknowledge financial support from the National Science Foundation for financial support under grant CBET-1437668, the program “Estancias de movilidad en el extranjero “Jose Castillejo” para jóvenes doctores” (JC2011-0051) of the Spanish Ministerio de Educación, and from the University of Alicante (GRE11-19)

Nitrite-derived nitric oxide reduces hypoxia-inducible factor 1α-mediated extracellular vesicle production by endothelial cells

Introduction Extracellular vesicles (EVs) are small, spherical particles enclosed by a phospholipid bilayer (∼30–1000 nm) released from multiple cell types, and have been shown to have pathophysiological roles in a plethora of disease states. The transcription factor hypoxia-inducible factor-1 (HIF-1) allows for adaptation of cellular physiology in hypoxia and may permit the enhanced release of EVs under such conditions. Nitric oxide (NO) plays a pivotal role in vascular homeostasis, and can modulate the cellular response to hypoxia by preventing HIF-1 accumulation. We aimed to selectively target HIF-1 via sodium nitrite (NaNO2) addition, and examine the effect on endothelial EV, size, concentration and function, and delineate the role of HIF-1 in EV biogenesis. Methods Endothelial (HECV) cells were exposed to hypoxic conditions (1% O2, 24 h) and compared to endothelial cells exposed to normoxia (21% O2) with and without the presence of sodium nitrite (NaNO2) (30 μM). Allopurinol (100 μM), an inhibitor of xanthine oxidoreductase, was added both alone and in combination with NaNO2 to cells exposed to hypoxia. EV and cell preparations were quantified by nanoparticle tracking analysis and confirmed by electron microscopy. Western blotting and siRNA were used to confirm the role of HIF-1α and HIF-2α in EV biogenesis. Flow cytometry and time-resolved fluorescence were used to assess the surface and intravesicular protein content. Results Endothelial (HECV) cells exposed to hypoxia (1% O2) produced higher levels of EVs compared to cells exposed to normoxia. This increase was confirmed using the hypoxia-mimetic agent desferrioxamine. Treatment of cells with sodium nitrite (NaNO2) reduced the hypoxic enhancement of EV production. Treatment of cells with the xanthine oxidoreductase inhibitor allopurinol, in addition to NaNO2 attenuated the NaNO2-attributed suppression of hypoxia-mediated EV release. Transfection of cells with HIF-1α siRNA, but not HIF-2α siRNA, prior to hypoxic exposure prevented the enhancement of EV release. Conclusion These data provide evidence that hypoxia enhances the release of EVs in endothelial cells, and that this is mediated by HIF-1α, but not HIF-2α. Furthermore, the reduction of NO2− to NO via xanthine oxidoreductase during hypoxia appears to inhibit HIF-1α-mediated EV production

NIK Stabilization in Osteoclasts Results in Osteoporosis and Enhanced Inflammatory Osteolysis

Maintenance of healthy bone requires the balanced activities of osteoclasts (OCs), which resorb bone, and osteoblasts, which build bone. Disproportionate action of OCs is responsible for the bone loss associated with postmenopausal osteoporosis and rheumatoid arthritis. NF-κB inducing kinase (NIK) controls activation of the alternative NF-κB pathway, a critical pathway for OC differentiation. Under basal conditions, TRAF3-mediated NIK degradation prevents downstream signaling, and disruption of the NIK:TRAF3 interaction stabilizes NIK leading to constitutive activation of the alternative NF-κB pathway.Using transgenic mice with OC-lineage expression of NIK lacking its TRAF3 binding domain (NT3), we now find that alternative NF-κB activation enhances not only OC differentiation but also OC function. Activating NT3 with either lysozyme M Cre or cathepsinK Cre causes high turnover osteoporosis with increased activity of OCs and osteoblasts. In vitro, NT3-expressing precursors form OCs more quickly and at lower doses of RANKL. When cultured on bone, they exhibit larger actin rings and increased resorptive activity. OC-specific NT3 transgenic mice also have an exaggerated osteolytic response to the serum transfer model of arthritis.Constitutive activation of NIK drives enhanced osteoclastogenesis and bone resorption, both in basal conditions and in response to inflammatory stimuli

An In Vitro Model of the Glomerular Capillary Wall Using Electrospun Collagen Nanofibres in a Bioartificial Composite Basement Membrane

The filtering unit of the kidney, the glomerulus, contains capillaries whose walls function as a biological sieve, the glomerular filtration barrier. This comprises layers of two specialised cells, glomerular endothelial cells (GEnC) and podocytes, separated by a basement membrane. Glomerular filtration barrier function, and dysfunction in disease, remains incompletely understood, partly due to difficulties in studying the relevant cell types in vitro. We have addressed this by generation of unique conditionally immortalised human GEnC and podocytes. However, because the glomerular filtration barrier functions as a whole, it is necessary to develop three dimensional co-culture models to maximise the benefit of the availability of these cells. Here we have developed the first two tri-layer models of the glomerular capillary wall. The first is based on tissue culture inserts and provides evidence of cell-cell interaction via soluble mediators. In the second model the synthetic support of the tissue culture insert is replaced with a novel composite bioartificial membrane. This consists of a nanofibre membrane containing collagen I, electrospun directly onto a micro-photoelectroformed fine nickel supporting mesh. GEnC and podocytes grew in monolayers on either side of the insert support or the novel membrane to form a tri-layer model recapitulating the human glomerular capillary in vitro. These models will advance the study of both the physiology of normal glomerular filtration and of its disruption in glomerular disease