Image based Wheel Detection using Random Forest Classification

The aim of this master thesis is to detect and recognise wheels in images by means of image analysis. This could later on serve as a foundation for a safer vehicle counting and classification method than those currently in use that requires personnel to cross the lanes on installation. The general layout of the classification system consists of five stages: multi-scale transformation, window extractor, pre-processing, classification and cluster analysis. In order to obtain the training and testing data for evaluation and construction of the system, images that illustrate moving cars on a road are acquired. From these, several positive and negative windows are extracted that visualizes wheels and non-wheels. For the classification stage, the learning algorithm used is Random Forest. Moreover, with the Random Forest as the foundation, two different concepts were introduced to further improve the predictions. These are referred to as bootstrap configuration and cascading classification. The results are evaluated be means of Receiver Operating Characteristics and contingency tables. In this master thesis, the final system produces a satisfying result based on the false positive rate and true positive rate. For future development, the amount of examples in the training data could be increased in order to gain more knowledge in the teaching of the classifier. Furthermore, an optimization of the program could lead to faster execution time, which is a requirement if this system is to operate in real-time. To conclude, the system produces a satisfying result for wheel detection that can be used as a foundation when constructing a general system for vehicle counting and classification

Regionalization : a new step in companies internationalization process?

Bakgrund: Det sista steget i Uppsala-skolans etableringskedja innebär att företagen flyttar betydande delar av verksamheten utomlands, men är det verkligen det sista steget? Sedan en tid tillbaka har alltfler företag valt att regionalisera sin internationella verksamhet, vilket innebär att olika nationella verksamheter samordnas och att en regional organisation skapas över nationsgränserna. Hur tar sig en regionalisering i uttryck och kan regionalisering ses som ett nytt steg i företags internationaliseringsprocess? S yfte: Utifrån en studie av företags regionalisering syftar uppsatsen till att bidra med kunskap om företags internationalisering genom att undersöka om regionalisering är ett nytt steg i företags internationaliseringsprocess. Genomförande: För att kunna uppfylla vårt syfte har vi genomfört 12 stycken intervjuer med representanter på åtta multinationella företag som har en regionaliserad Nordenverksamhet. Resultat: Utifrån våra teoretiskt förankrade kriterier för regionalisering har vi kunnat konstatera att samtliga fallföretag kan karaktäriseras som regionaliserade då de; har en geografisk samordning över nationsgränserna genom integration av ländernas verksamhetsområden, har ett gemensamt huvudkontor med en övergripande regionledning, tillämpar både en global och lokal internationaliseringsstrategi, tar vara på kompetenser inom regionen, effektiviserar och rationaliserar sin regionala verksamhet genom att ta hänsyn till var olika verksamhetsfunktioner skall skötas. Vidare har vi kommit fram till att regionalisering kan ses som ett nytt steg i Uppsala-skolans etableringsprocess med utgångspunkt i våra uppsatta kriterier för ett nytt steg. Vi anser således att en regionalisering bidrar med tillräckligt omfattande förändringar av organisationsstrukturen för att det skall kunna klassificeras som ett nytt steg i företags internationaliseringsprocess

Är skolans mål möjliga att nå för alla? : Hinder och förutsättningar för elevers måluppfyllelse i kärnämnen ur ett lärarperspektiv

Vikten av utbildning och livslångt lärande är betydelsefulla faktorer för att den ekonomiska tillväxten i vårt land ska stimuleras, för att välfärden ska kunna tryggas och för att motverka ytterligare samhällsklyftor. Statistik från Skolverket visar på en konstant andel, ca 10 % de senaste fem åren, av elever i årskurs 9 som inte är behöriga att söka till gymnasiet. Det beror på att de inte har uppnått kursplanemålen för att få godkänt i kärnämnena svenska, matematik och engelska. Detta är bakgrunden till att vi har valt att redogöra för och belysa lärares utsagor och resonemang kring hinder och förutsättningar för elevers måluppfyllelse i kärnämnena. I denna kvalitativa studie har vi använt oss av intervjuer som teknik. Vi har intervjuat sex lärare, på fem olika skolor i en mellanstor kommun i sydvästra Sverige. Studien är uppdelad på tre nivåer, organisations-, grupp- och individnivå. På organisationsnivå handlar det bland annat om skolpolitik, skolans ledning och skolans styrdokument. På gruppnivå handlar det om klassen/gruppen och arbetslaget och på individnivå handlar det om den enskilde eleven och den enskilde läraren. Resultatet indikerar på att lärarnas resonemang till stor del kom att kretsa kring lärarens egen roll för elevers måluppfyllelse. Ytterligare framkom det att styrdokumenten spelar en betydande roll, på grund av att de lämnar stort tolkningsutrymme. Andra faktorer som resultatet visar på är att elever inte är tillräckligt motiverade för skolarbete och därigenom måluppfyllelse. Det finns elever som har låg begåvning och det finns elever med utländsk bakgrund som kommer in sent i det svenska skolsystemet. De kan därför få svårigheter att uppnå målen. Vår slutsats är därför; nej skolans mål är inte möjliga att nå för alla elever!The importance of education and lifelong learning are essential factors to ensure and stimulate economic growth in our country, to secure welfare and counteract polarisation of social classes. During the last five years statistics from the Swedish Board of Education shows a constant number of approximately 10 % of the students in year 9 who have not qualified for upper secondary education. This is because they have not attained the goals of the syllabus which require a pass in the core subjects of Swedish, mathematics and English. This fact is the reason for our investigation in which we illustrate teachers’ assertions and lines of arguments concerning impediments and preconditions for attaining the goals of the core subjects. In this qualitative study we have used interviews as our main approach. We have interviewed six teachers at five different schools in a medium size municipality in the south-west of Sweden. The study is divided into three levels, organization, group and individual level. On the organization level the key issues are school policy, school administration and the steering documents of the school. On the group level the key issues are the class/group and the working team and on the individual level the study focuses on the individual pupil/student and the individual teacher. The result indicates that the teachers’ lines of arguments were focused on his/her own role of importance for the pupils’/students’ attainments of the goals. Furthermore it appeared that the steering documents play an important part because they can be interpreted in many ways. Other factors shown in the study are that pupils/students are not motivated enough to do schoolwork and thereby reach the goals. There are pupils/students who are less talented and others who have a different cultural background and get enrolled in the Swedish school system late. They might therefore have difficulties attaining the goals. Thus our conclusion is; no it is not possible for every pupil/student to attain the goals of school! We use both the words pupil and student because we sometimes mean the younger children (pupils) but also the older ones (students)

Angiopoietin-2 Inhibition of Thrombomodulin-Mediated Anticoagulation : A Novel Mechanism That May Contribute to Hypercoagulation in Critically Ill COVID-19 Patients

Hypercoagulation and endothelial dysfunction play central roles in severe forms of COVID-19 infections, but the molecular mechanisms involved are unclear. Increased plasma levels of the inflammatory cytokine and TIE2 receptor antagonist Angiopoietin-2 were reported in severely ill COVID-19 patients. In vitro experiments suggest that Angiopoietin-2 bind and inhibits thrombomodulin. Thrombomodulin is expressed on the luminal surface of endothelial cells where it is an important member of the intrinsic anticoagulant pathway through activation of protein C. Using clinical data, mouse models, and in vitro assays, we tested if Angiopoietin-2 plays a causal role in COVID-19-associated hypercoagulation through direct inhibition of thrombin/thrombomodulin-mediated physiological anticoagulation. Angiopoietin-2 was measured in 61 patients at admission, and after 10 days in the 40 patients remaining in the ICU. We found that Angiopoietin-2 levels were increased in COVID-19 patients in correlation with disease severity, hypercoagulation, and mortality. In support of a direct effect of Angiopoietin-2 on coagulation, we found that injected Angiopoietin-2 in mice associated to thrombomodulin and resulted in a shortened tail bleeding time, decreased circulating levels of activated protein C, and increased plasma thrombin/antithrombin complexes. Conversely, bleeding time was increased in endothelial-specific Angiopoietin-2 knockout mice, while knockout of Tie2 had no effect on tail bleeding. Using in vitro assays, we found that Angiopoietin-2 inhibited thrombomodulin-mediated anticoagulation and protein C activation in human donor plasma. Our data suggest a novel in vivo mechanism for Angiopoietin-2 in COVID-19-associated hypercoagulation, implicating that Angiopoietin-2 inhibitors may be effective in the treatment of hypercoagulation in severe COVID-19 infection

How the Innate Immune System of the Blood Contributes to Systemic Pathology in COVID-19-Induced ARDS and Provides Potential Targets for Treatment

Most SARS-CoV-2 infected patients experience influenza-like symptoms of low or moderate severity. But, already in 2020 early during the pandemic it became obvious that many patients had a high incidence of thrombotic complications, which prompted treatment with high doses of low-molecular-weight heparin (LMWH; typically 150-300IU/kg) to prevent thrombosis. In some patients, the disease aggravated after approximately 10 days and turned into a full-blown acute respiratory distress syndrome (ARDS)-like pulmonary inflammation with endothelialitis, thrombosis and vascular angiogenesis, which often lead to intensive care treatment with ventilator support. This stage of the disease is characterized by dysregulation of cytokines and chemokines, in particular with high IL-6 levels, and also by reduced oxygen saturation, high risk of thrombosis, and signs of severe pulmonary damage with ground glass opacities. The direct link between SARS-CoV-2 and the COVID-19-associated lung injury is not clear. Indirect evidence speaks in favor of a thromboinflammatory reaction, which may be initiated by the virus itself and by infected damaged and/or apoptotic cells. We and others have demonstrated that life-threatening COVID-19 ARDS is associated with a strong activation of the intravascular innate immune system (IIIS). In support of this notion is that activation of the complement and kallikrein/kinin (KK) systems predict survival, the necessity for usage of mechanical ventilation, acute kidney injury and, in the case of MBL, also coagulation system activation with thromboembolism. The general properties of the IIIS can easily be translated into mechanisms of COVID-19 pathophysiology. The prognostic value of complement and KKsystem biomarkers demonstrate that pharmaceuticals, which are licensed or have passed the phase I trial stage are promising candidate drugs for treatment of COVID-19. Examples of such compounds include complement inhibitors AMY-101 and eculizumab (targeting C3 and C5, respectively) as well as kallikrein inhibitors ecallantide and lanadelumab and the bradykinin receptor (BKR) 2 antagonist icatibant. In this conceptual review we discuss the activation, crosstalk and the therapeutic options that are available for regulation of the IIIS

How the Innate Immune System of the Blood Contributes to Systemic Pathology in COVID-19-Induced ARDS and Provides Potential Targets for Treatment

Most SARS-CoV-2 infected patients experience influenza-like symptoms of low or moderate severity. But, already in 2020 early during the pandemic it became obvious that many patients had a high incidence of thrombotic complications, which prompted treatment with high doses of low-molecular-weight heparin (LMWH; typically 150-300IU/kg) to prevent thrombosis. In some patients, the disease aggravated after approximately 10 days and turned into a full-blown acute respiratory distress syndrome (ARDS)-like pulmonary inflammation with endothelialitis, thrombosis and vascular angiogenesis, which often lead to intensive care treatment with ventilator support. This stage of the disease is characterized by dysregulation of cytokines and chemokines, in particular with high IL-6 levels, and also by reduced oxygen saturation, high risk of thrombosis, and signs of severe pulmonary damage with ground glass opacities. The direct link between SARS-CoV-2 and the COVID-19-associated lung injury is not clear. Indirect evidence speaks in favor of a thromboinflammatory reaction, which may be initiated by the virus itself and by infected damaged and/or apoptotic cells. We and others have demonstrated that life-threatening COVID-19 ARDS is associated with a strong activation of the intravascular innate immune system (IIIS). In support of this notion is that activation of the complement and kallikrein/kinin (KK) systems predict survival, the necessity for usage of mechanical ventilation, acute kidney injury and, in the case of MBL, also coagulation system activation with thromboembolism. The general properties of the IIIS can easily be translated into mechanisms of COVID-19 pathophysiology. The prognostic value of complement and KKsystem biomarkers demonstrate that pharmaceuticals, which are licensed or have passed the phase I trial stage are promising candidate drugs for treatment of COVID-19. Examples of such compounds include complement inhibitors AMY-101 and eculizumab (targeting C3 and C5, respectively) as well as kallikrein inhibitors ecallantide and lanadelumab and the bradykinin receptor (BKR) 2 antagonist icatibant. In this conceptual review we discuss the activation, crosstalk and the therapeutic options that are available for regulation of the IIIS

The Outcome of Critically Ill COVID-19 Patients Is Linked to Thromboinflammation Dominated by the Kallikrein/Kinin System

An important manifestation of severe COVID-19 is the ARDS-like lung injury that is associated with vascular endothelialitis, thrombosis, and angiogenesis. The intravascular innate immune system (IIIS), including the complement, contact, coagulation, and fibrinolysis systems, which is crucial for recognizing and eliminating microorganisms and debris in the body, is likely to be involved in the pathogenesis of COVID-19 ARDS. Biomarkers for IIIS activation were studied in the first 66 patients with COVID-19 admitted to the ICU in Uppsala University Hospital, both cross-sectionally on day 1 and in 19 patients longitudinally for up to a month, in a prospective study. IIIS analyses were compared with biochemical parameters and clinical outcome and survival. Blood cascade systems activation leading to an overreactive conjunct thromboinflammation was demonstrated, reflected in consumption of individual cascade system components, e.g., FXII, prekallikrein, and high molecular weight kininogen and in increased levels of activation products, e.g., C4d, C3a, C3d,g, sC5b-9, TAT, and D-dimer. Strong associations were found between the blood cascade systems and organ damage, illness severity scores, and survival. We show that critically ill COVID-19 patients display a conjunct activation of the IIIS that is linked to organ damage of the lung, heart, kidneys, and death. We present evidence that the complement and in particular the kallikrein/kinin system is strongly activated and that both systems are prognostic markers of the outcome of the patients suggesting their role in driving the inflammation. Already licensed kallikrein/kinin inhibitors are potential drugs for treatment of critically ill patients with COVID-19