Berührungslose Schweißdetektion an Fahrzeuginsassen für die Automatisierung der Klimasteuerung

Die vorliegende Arbeit beschäftigt sich mit der berührungslosen Schweißdetektion im Fahrzeug als Bestandteil der automatisierten Klimasteuerung. Für die Erkennung von Schweiß wird eine Wärmebildkamera herangezogen, da austretender Schweiß durch Entzug der Verdampfungswärme die Haut abkühlt und daher auf dem Wärmebild zu sehen ist. Die Ergebnisse basieren auf verschiedenen Studien, in denen 20 Probanden ein sportliches Training absolvieren mussten, um ins Schwitzen zu kommen. Dabei wurde in regelmäßigen Abständen nach dem Schweißstatus gefragt und der Kopfbereich im Wärmebild aufgenommen. Für die Auswertung wurde der Stirnbereich auf dem Wärmebild explorativ untersucht, da dieser meistens nicht von Haaren oder Kleidung bedeckt ist. Der Stirnbereich wurde dann für verschiedene Schweißzustände betrachtet und die Temperaturdifferenz zwischen maximaler und minimaler Temperatur, sowie die festgestellte Fleckigkeit anhand einer räumlichen Frequenzanalyse analysiert. Die Ergebnisse zeigen, dass anhand der 2D-Fouriertransformation, mit anschließender Bildung des radialen Mittelwerts aus dem Powerspektrum, die beste Unterscheidung zwischen einem schwitzenden und nicht schwitzenden Insassen gemacht werden können. Speziell bei der Betrachtung eines Pixelbereichs von 21 Pixel x 21 Pixel auf der Stirn konnte mithilfe der Signalentdeckungstheorie eine Treffer-Rate von 95 % unter 5 % falschen Alarmen festgestellt werden. Das bedeutet, dass es möglich ist, anhand eines Wärmebilds der Stirn das Schwitzen bei einem Insassen im Fahrzeug mit einer Sicherheit von 95 % zu erkennen

Unified description of the dc conductivity of monolayer and bilayer graphene at finite densities based on resonant scatterers

We show that a coherent picture of the dc conductivity of monolayer and bilayer graphene at finite electronic densities emerges upon considering that strong short-range potentials are the main source of scattering in these two systems. The origin of the strong short-range potentials may lie in adsorbed hydrocarbons at the surface of graphene. The equivalence among results based on the partial-wave description of scattering, the Lippmann-Schwinger equation, and the T-matrix approach is established. Scattering due to resonant impurities close to the neutrality point is investigated via a numerical computation of the Kubo formula using a kernel polynomial method. We find that relevant adsorbate species originate impurity bands in monolayer and bilayer graphene close to the Dirac point. In the midgap region, a plateau of minimum conductivity of about $e^2/h$ (per layer) is induced by the resonant disorder. In bilayer graphene, a large adsorbate concentration can develop an energy gap between midgap and high-energy states. As a consequence, the conductivity plateau is supressed near the edges and a "conductivity gap" takes place. Finally, a scattering formalism for electrons in biased bilayer graphene, taking into account the degeneracy of the spectrum, is developed and the dc conductivity of that system is studied.Comment: 25 pages, 13 figures. published version: appendixes improved, references added, abstract and title slightly changed, plus other minor revision

Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta

During the resolution of acute inflammation, macrophages undergo reprogramming from pro-inflammatory, to anti-inflammatory/reparative, and eventually to pro-resolving macrophages. Galectin-1 (Gal-1) is a bona fide pro-resolving lectin while interferon β (IFN-β) was recently shown to facilitate macrophage reprogramming and resolution of inflammation. In this study, we found Gal-1null mice exhibit a hyperinflammatory phenotype during the resolution of zymosan A-induced peritonitis but not during the early inflammatory response. This phenotype was characterized by reduced macrophage numbers, increased secretion of pro-inflammatory cytokines, such as interleukin-12 (IL-12), and reduced secretion of anti-inflammatory cytokines, such as interleukin-10 (IL-10). In addition, we found a delayed expression of the pro-resolving enzyme 12/15-lipoxygenase in macrophages and heightened levels of the inflammatory protease proteinase-3 (PR3) in peritoneal fluids from Gal-1null mice. Moreover, we observed sex-dependent differences in the inflammatory profile of Gal-1null mice. Notably, we found that IFN-β levels were reduced in resolution-phase exudates from Gal-1null mice. Administration of IFN-β in vivo or ex vivo treatment was able to rescue, at least in part, the hyperinflammatory profile of Gal-1null mice. In particular, IFN-β recovered a subset of F4/80+GR-1+ macrophages, restored IL-12 and IL-10 secretion from macrophages to WT values and diminished abnormal peritoneal PR3 levels in Gal-1null mice. In conclusion, our results revealed a new Gal-1-IFN-β axis that facilitates the resolution of inflammation and might restrain uncontrolled inflammatory disorders.Fil: Yaseen, Hiba. University of Haifa; IsraelFil: Butenko, Sergei. University of Haifa; IsraelFil: Polishuk Zotkin, Irina. University of Haifa; IsraelFil: Schif Zuck, Sagie. University of Haifa; IsraelFil: Pérez Sáez, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Ariel, Amiram. University of Haifa; Israe

Two consecutive phase II studies of oxaliplatin (L-OHP) for treatment of patients with advanced colorectal carcinoma who were resistant to previous treatment with fluoropyrimidines

Background Oxaliplatin (L-OHP) is a platinum complex that possesses activity against human and murine cells in vitro and in vivo, including colorectal carcinoma-derived cell lines, and cells that have been selected for resistance to cisplatin. We report two consecutive phase H trials of L-OHP for treatment of patients with advanced colorectal carcinoma. Patients and methods: Fifty-eight patients were entered in study I, and 51 patients in study II. All of the patients had tumor progression when they were treated, prior to their enrolment, with a fluoropyrimidine-containing regimen. In both trials treatment consisted of L-OHP, 130 mg/m2 by i.v. infusion for two hours; the treatment was repeated every 21 days. Results Response to therapy: Study I: Fifty-five patients were assessed for response. The response rate was 11% (95% CI, 0.03-0.19). Study II: All 51 patients were assessed for response. The response rate was 10% (95% CI, 0.017-0.18). The overall response rate for the 106 evaluated patients was 10% (95% CI, 0.046-0.16). Times to disease progression in responders were 4, 4, 4.5+, 5, 5, 6, 6, 6, 6+, 9, and 13 months. The dose-limiting toxic effect was sensory peripheral neuropathy. The incidence of severe peripheral neuropathy grades was: Study I: grade 3, 23% of patients, and grade 4, 8% of patients. Study II: grade 3, 14% of patients, and grade 4, 4% of patients. Severe neuropathy had a favorable course in all of the patients who had long-term neurologic follow-up. Diarrhea and myeloid impairment were minor. Conclusion L-OHP produced modest, but definite antitumor activity in patients with advanced colorectal carcinoma who were previously resistant to chemotherapy including fluoropyrirnidines. Toxicity is within acceptable limits of tolerance at the dose and schedule of oxaliplatin used in this tria

The complex TIE between macrophages and angiogenesis

Macrophages are primarily known as phagocytic immune cells, but they also play a role in diverse processes, such as morphogenesis, homeostasis and regeneration. In this review, we discuss the influence of macrophages on angiogenesis, the process of new blood vessel formation from the pre-existing vasculature. Macrophages play crucial roles at each step of the angiogenic cascade, starting from new blood vessel sprouting to the remodelling of the vascular plexus and vessel maturation. Macrophages form promising targets for both pro- and anti-angiogenic treatments. However, to target macrophages, we will first need to understand the mechanisms that control the functional plasticity of macrophages during each of the steps of the angiogenic cascade. Here, we review recent insights in this topic. Special attention will be given to the TIE2-expressing macrophage (TEM), which is a subtype of highly angiogenic macrophages that is able to influence angiogenesis via the angiopoietin-TIE pathway

\u27Normalizing\u27 the malignant phenotype of luminal breast cancer cells via alpha(v)beta(3)-integrin

Reestablishing tissue organization of breast cancer cells into acini was previously shown to override their malignant phenotype. In our study, we demonstrate that alpha(v)beta(3) integrin (Int-αvβ3), previously shown to play a role in cancer progression, promoted differentiation and growth arrest of organoids derived from luminal A breast cancer cells grown in their relevant three-dimensional microenvironment. These organoids differentiated into normal-like acini resembling a benign stage of breast tissue. Likewise, we demonstrate that Int-αvβ3 is selectively expressed in the epithelium of the benign stage of breast tissues, and is lost during the early stages of luminal A breast cancer progression. Notably, the organoids’ reversion into normal-like acini was mediated by cancer luminal progenitor-like cells expressing both EpCAM$^{high}$CD49f$^{low}$CD24$^{+}$ and Int-αvβ3. Furthermore, downregulation of Notch4 expression and downstream signaling was shown to mediate Int-αvβ3-induced reversion. Intriguingly, when luminal A breast cancer cells expressing Int-αvβ3 were injected into a humanized mouse model, differentiated tumors developed when compared with that generated by control cells. Hence, our data suggest that promoting differentiation of luminal A breast cancer cells by signaling emanating from Int-αvβ3 can potentially promote ‘normalization’ of their malignant phenotype and may prevent the malignant cells from progressing

Targeting the Monocyte–Macrophage Lineage in Solid Organ Transplantation

textabstractThere is an unmet clinical need for immunotherapeutic strategies that specifically target the active immune cells participating in the process of rejection after solid organ transplantation. The monocyte-macrophage cell lineage is increasingly recognized as a major player in acute and chronic allograft immunopathology. The dominant presence of cells of this lineage in rejecting allograft tissue is associated with worse graft function and survival. Monocytes and macrophages contribute to alloimmunity via diverse pathways: antigen processing and presentation, costimulation, pro-inflammatory cytokine production, and tissue repair. Cross talk with other recipient immune competent cells and donor endothelial cells leads to amplification of inflammation and a cytolytic response in the graft. Surprisingly, little is known about therapeutic manipulation of the function of cells of the monocyte-macrophage lineage in transplantation by immunosuppressive agents. Although not primarily designed to target monocyte-macrophage lineage cells, multiple categories of currently prescribed immunosuppressive drugs, such as mycophenolate mofetil, mammalian target of rapamycin inhibitors, and calcineurin inhibitors, do have limited inhibitory effects. These effects include diminishing the degree of cytokine production, thereby blocking costimulation and inhibiting the migration of monocytes to the site of rejection. Outside the field of transplantation, some clinical studies have shown that the monoclonal antibodies canakinumab, tocilizumab, and infliximab are effective in inhibiting monocyte functions. Indirect effects have also been shown for simvastatin, a lipid lowering drug, and bromodomain and extra-terminal motif inhibitors that reduce the cytokine production by monocytes-macrophages in patients with diabetes mellitus and rheumatoid arthritis. To date, detailed knowledge concerning the origin, the developmental requirements, and functions of diverse specialized monocyte-macrophage subsets justifies research for therapeutic manipulation. Here, we will discuss the effects of currently prescribed immunosuppressive drugs on monocyte/macrophage features and the future challenges

Resolution of inflammation: a new therapeutic frontier

Dysregulated inflammation is a central pathological process in diverse disease states. Traditionally, therapeutic approaches have sought to modulate the pro- or anti-inflammatory limbs of inflammation, with mixed success. However, insight into the pathways by which inflammation is resolved has highlighted novel opportunities to pharmacologically manipulate these processes — a strategy that might represent a complementary (and perhaps even superior) therapeutic approach. This Review discusses the state of the art in the biology of resolution of inflammation, highlighting the opportunities and challenges for translational research in this field