Creating carbon footprint calculating tool for plastic packaging products

The environmental challenges of plastic packaging industry have increased remarkably along with climate change debate. The interest to study carbon footprints of packaging has increased in packaging industry to find out the real climate change impacts of packaging. In this thesis the greenhouse gas discharges of plastic packaging during their life cycle is examined. The carbon footprint is calculated for food packaging manufactured from plastic laminate. The structure of the laminate is low density polyethylene (PE-LD) and oriented polypropylene (OPP), which have been joined together with laminating adhesive. The purpose is to find out the possibilities to create a carbon footprint calculating tool for plastic packaging and its usability in a plastic packaging manufacturing company. As a carbon footprint calculating method PAS 2050 standard has been used. In the calculations direct and indirect greenhouse gas discharges as well as avoided discharges are considered. Avoided discharges are born for example in packaging waste utilization as energy. The results of the calculations have been used to create a simple calculating tool to be used for similar laminate structures. Although the utilization of the calculating tool is limited to one manufacturing plant because the primary activity data is dependent of geographical location and for example the discharges of used energy in the plant. The results give an approximation of the climate change potential caused by the laminate. It is although noticed that calculations do not include all environmental impacts of plastic packaging´s life cycle.

The Integrin Tail: A Tale of Cell Motility and Division

Integrin transmembrane receptor functions are regulated by adaptor molecules binding to their alpha and beta subunit intracellular domains, or tails, thus affecting integrin traffic and adhesion during e.g. cell motility. Interestingly, many cellular proteins function in both cell motility and cell division, thus raising the possibility that integrins might be involved in regulating the cell cycle. A thorough understanding of cell division is essential in cell biology and in human malignancies. It is well established that failures to complete cell cycle can give rise to genetically unstable cells with tumorigenic properties. Transformed cells promote the disruption of intercellular adhesions such as tight junctions, and this correlates with the onset of cell motility, invasion and unfavorable prognosis in cancer. In this study, we analyzed integrin regulation, mediated by adaptor binding to the  subunit tail, during cell motility and cell division. We revealed a novel molecular mechanism by which Rab21, through association with the integrin alpha subunits, drives integrin endosomal traffic during mitotic phases. In addition, we found indications for this finding in vivo, as RAB21 gene deletions were mapped in ovarian and prostate cancer samples. Importantly, the multinucleated phenotype of cultured ovarian cancer cells could be reverted by Rab21 overexpression. In this thesis work, we also show how the tight junction protein ZO-1 unexpectedly interacts with the 5 integrin cytoplasmic domain in the lamellipodia to promote cell motility and at the cleavage furrow to support separation of the daughter cells. The alpha5-ZO-1 complex formation was dependent on PKC which regulates ZO-1 phosphorylation and its subcellular localization. In addition, by an in situ detection method, we showed that a subset of metastatic human lung cancers expressed the alpha5beta-ZO-1 complex. Taken together, we were able to identify new molecular pathways that regulate integrin functions in an alpha tail-mediated fashion. These findings firmly suggest that genetic alterations in integrin traffic may lead to progression of tumorigenesis as a result of failed cell division. Also, the interplay of integrins and ZO-1 in forming spatially regulated adhesive structures broadens our view of crosstalk between pathways and distinct adhesive structures that can be involved in cancer cell biology.

Novel Players in the Integrin Signaling Orchestra: TCPTP and MDGI

Metastases are the major cause of cancer deaths. Tumor cell dissemination from the primary tumor utilizes dysregulated cellular adhesion and upregulated proteolytic degradation of the extracellular matrix for progeny formation in distant organs. Integrins are transmembrane adhesive receptors mediating cellcell and cellmatrix interactions that are crucial for regulating cell migration, invasion, proliferation, and survival. Consequently, increased integrin activity is associated with augmented migration and invasion capacity in several cancer types. Heterodimeric integrins consist of an alpha - and beta-subunit that are held together in a bent conformation when the receptor is inactive, but extension and separation of subdomains is observed during receptor activation. Either inside-out or outside-in activation of receptors is possible through the intracellular molecule binding to an integrin cytoplasmic domain or extracellular ligand association with an integrin ectodomain, respectively. Several regulatory binding partners have been characterized for integrin cytoplasmic beta-domains, but the regulators interacting with the cytoplasmic alpha-domains have remained elusive. In this study, we performed yeast two-hybrid screens to identify novel binding partners for the cytoplasmic integrin alpha-domains. Further examination of two plausible candidates revealed a significant coregulatory role of an integrin alpha-subunit for cellular signaling processes. T-cell protein tyrosine phosphatase (TCPTP) showed a specific interaction with the cytoplasmic tail of integrin alpha1. This association stimulated TCPTP phosphatase activity, leading to negative regulation of epidermal growth factor receptor (EGFR) signaling and diminished anchorage-independent growth. Another candidate, mammary-derived growth inhibitor (MDGI), exhibited binding to several different integrin cytoplasmic alpha-tails through a conserved GFFKR sequence. MDGI overexpression in breast cancer cells altered EGFR trafficking and caused a remarkable accumulation of EGFR in the cytoplasm. We further demonstrated in vivo that MDGI expression induced a novel form of anti-EGFR therapy resistance. Moreover, MDGI binding to α-tails retained integrin in an inactive conformation attenuating integrin-mediated adhesion, migration, and invasion. In agreement with these results, sustained MDGI expression in breast cancer patients correlated with an increased 10-year distant disease-free survival. Taken together, the integrin signaling network is far from a complete view and future work will doubtless broaden our understanding further.

Influence of Heat Treatment on Strength Properties of Finger-jointed Components

The purpose for the thesis was to study the thermo treatment of finger-jointed wood. The thesis concentrated on examining the tensile and bending strength of finger-jointed and thermo treated wood. The aim was to find out how different treatment temperature levels and adhesives influence the strength of wood that has been finger-jointed before heat treatment. Secondary objectives were to examine the influence of the treatment time at one temperature, determine differences in the strength between the joints in heartwood and sapwood, examine the visual appearance of the finger joints after the treatment and establish possibilities to reach a characteristic strength level corresponding to C14. Only minor differences in strength properties were measured between the finger-jointed wood treatments II and III. A greater difference was shown between these two treatment temperatures I, which lead to reduced strength. The average strength of joints glued with adhesive 2 was higher after treatments II and III compared to those glued with the adhesive 1. At the treatment temperature I, the adhesive 1 strength properties were at the same level compared to the adhesive 2 or better. There were not any significant differences.

Antimicrobial Resistance in Campylobacter jejuni and Campylobacter coli

Antimicrobial Resistance in Campylobacter jejuni and Campylobacter coli Campylobacters are a common cause of bacterial gastroenteritis worldwide, with Campylobacter jejuni and C. coli being the most common species isolated in human infections. If antimicrobial treatment is required, the drugs of choice at the moment are the macrolides and fluoroquinolones. In this thesis, the in vitro resistance profiles of the C. jejuni and C. coli strains were evaluated with emphasis on multidrug resistance. The aim was also to evaluate the different resistance mechanisms against the macrolides. Further, the disk diffusion method was compared to agar dilution method and its repeatability was evaluated, since it has been widely used for the susceptibility testing of campylobacters. The results of the present study showed that resistance to the fluoroquinolones is common in strains isolated from Finnish patients, but resistance to the macrolides is still rare. Multidrug resistance was associated with resistance to both ciprofloxacin and erythromycin. Among the available per oral drugs, least resistance was observed to coamoxiclav There was no resistance to the carbapenems. Sitafloxacin and tigecycline were in vitro highly effective towards Campylobacter species. A point mutation A2059G of the 23S rRNA gene was the main mechanism behind the macrolide resistance, whereas the efflux pumps did not seem to play an important role when a strain had A2059G mutation. A five amino acids insertion, which has not been described previously, in the ribosomal protein L22 of one highly-resistant C. jejuni strain without mutation in the 23S rRNA gene was also detected. Concerning the disk diffusion method, there was variation in the repeatability In conclusion, macrolides still appear to be the first-choice alternative for suspected Campylobacter enteritis. The in vitro susceptibilities found suggest that co-amoxiclav might be a candidate for clinical trials on campylobacteriosis, but in life-threatening situations, a carbapenem may be the drug of choice. More studies are needed on whether the disk diffusion test method could be improved or whether all susceptibilities of campylobacters should be done using a MIC based method.

Tuulivoimalan staattoripakan puristusrakenteen kehittäminen

Diplomityössä tutkittiin voidaanko tuulivoimalan generaattorin staattoripakan puristamisessa hyödyntää komposiittista rakenneratkaisua. Tyypillisesti generaattorissa staattorin teräslevyt puristetaan erilaisilla teräsrakenteilla toisiaan vasten. Tavoitteena oli selvittää, voidaanko puristavan komposiittirakenteen osana hyödyntää liimaliitosta tai laminoitua liitosta. Tarkoitus oli etsiä rakenteeseen soveltuva liima ja liimaliitoksen arvot tai laminoitu rakenne ja sille soveltuvat materiaalit ja suoritustapa. Työssä on perehdytty erilaisiin tuulivoimalatyyppeihin, sekä niissä käytettäviin kesto- ja vierasmagnetoituihin generaattorityyppeihin. Tämän lisäksi on tarkasteltu niissä käytettävien staattorien valmistusvaihtoehtoja ja syitä miksi niissä olevat teräslevyt on puristettava toisiaan vasten. Samalla on luotu katsaus nykyisin käytössä oleviin rakenteisiin, joilla puristus voidaan toteuttaa. Liimauksesta on käsitelty perusteoriaa, sekä seikkoja jotka vaikuttavat liimaliitoksen kestoon. Työssä tutkittavaan liitokseen soveltuvien liimojen ominaisuuksia on käsitelty. Myös laminoituun liitokseen jo aiemmin kovettuneeseen komposiittiin on perehdytty. Tutkittavaan rakenteeseen soveltuvia hartsi- ja lasikuitutyyppejä on esitelty. Komposiittien mekaaniseen liittämiseen on lyhyesti perehdytty. Työssä suoritettiin useita vetokokeita, joilla selvitettiin puristusrakenteen tutkimista varten valmistettujen koekappaleiden suurin vetokuormankesto. Vetokokeiden perusteella voitiin valita soveltuvin rakenne staattorin puristamiseksi.

Runkopaperin imukyvyn optimointi

Diplomityön tarkoituksena oli optimoida laminaatin valmistuksessa käytettävän runkopaperin imukyky niin, että pienemmällä hartsimäärällä saavutetaan vähintään jo olemassa olevat impregointi- ja laminaatin ominaisuudet tai että nykyisellä hartsimäärällä saadaan nopeampi imeytyminen läpi paperirakenteen. Kirjallisuusosassa etsittiin ja selvitettiin erilaisten tekijöiden tai toimintatapojen vaikutukset, joilla voitaisiin muokata paperin imukyky halutulle tasolle. Kirjallisuudesta löydetyistä tekijöistä ja menetelmistä valittiin kokeelliseen osaan tutkittavaksi potentiaalisimmat sekä toteutuskelpoisimmat tavat. Diplomityön kokeellinen osuus koostui kahdesta osasta. Ensimmäisessä vaiheessa kirjallisuudesta löydettyjä menettelyjä testattiin laboratoriomittakaavassa erilaisilla esikokeilla. Työn toisessa vaiheessa suoritettiin pilotpaperikoneella koeajo, jossa tutkittiin tarkemmin esikokeiden menetelmiä, jotka olivat antaneet lupaavia tuloksia. Lisäksi tutkittiin menetelmiä, joita ei esikokeissa kokeiltu, mutta jotka olivat teoreettisesti kiinnostavia. Tulosten perusteella paperin hartsinottokykyä pystyttiin madaltamaan nestemäisen AKD-liiman sekä erään kemikaalin avulla. Hartsin imeytymisnopeutta paperiin pystyttiin kasvattamaan kuidun entsymaattisella käsittelyllä, lämpösarveistamalla sekä käyttämällä erästä pinta-aktiivista ainetta.

Luistonestojärjestelmän ja elektronisen tasauspyörästön testaus ja implementointi hybridityökoneympäristöön

Työssä toteutettiin C-kielellä luistonestojärjestelmä ja elektroninen tasauspyörästö Simulinkmallien pohjalta hybridityökoneeseen. Hybridityökoneen sähkökäytöt mahdollistavat tarkan vääntömomentin säädön, joka mahdollistaa työssä kuvatun kaltaisen järjestelmän toteuttamisen. Toteutettua järjestelmää simuloitiin MeVEA Oy:n ajoneuvomallinnukseen kehitetyssä simulaattorissa. Lisäksi järjestelmästä kehitettiin Visedo Oy:n sähkökäyttösimulaattoriin sopiva versio, jota testattiin Visedon sähkökäyttöjä simuloivan ohjelman kanssa. Simulointituloksien mukaan luistonesto estää vetäviä pyöriä luistamasta liukkaalla alustalla eikä toisaalta vähennä aiheetta kuljettajan asettamaa vääntömomenttia. Myös sähköinen tasauspyörästö toimi kuten oli suunniteltu. Työssä kehitetty luistonesto tarvitsee toimiakseen tiedon ajoneuvon kokonaismassasta, joten työssä kehitettiin myös tapa ajoneuvon massan estimoimiseksi ajoneuvon kiihdyttäessä. Massan estimointia testattiin pitävällä ja liukkaalla alustalla. Massan estimointi toimi simulaattoriympäristössä hyvällä tarkkuudella.

Leukocyte trafficking: a special focus on VAP-1 and CLEVER-1

It is crucial that lymphocytes patrol the body against foreign intruders and that leukocytes invade inflamed tissues to ameliorate the infection or injury. The adhesion molecules in leukocytes and endothelial cells play an essential role in the immune response by directing the traffic of leukocytes. However, the same molecules that guide leukocyte traffic under physiological conditions are also involved in pathological situations, when an overly excessive or harmful inflammatory response leads to tissue destruction and organ dysfunction or tumor growth. Vascular adhesion protein-1 (VAP-1) and Common lymphatic endothelial and vascular endothelial receptor-1 (CLEVER-1) are endothelial molecules that participate in the adhesion of leukocytes to the endothelia. This study was designed to elucidate, using different inflammation models, the role of VAP-1 and CLEVER-1 in leukocyte migration to the inflamed tissue, and to evaluate the use of antibodies against these molecules as an anti-adhesive therapy. Also, the role of CLEVER-1 during tumorigenesis was studied. Blocking the function of VAP-1 with antibodies significantly decreased the accumulation of leukocytes in the inflamed tissue. Targeting CLEVER-1 prevented cell migration via lymphatic vessels, as well as leukocyte traffic during inflammation. Following the anti-CLEVER-1 antibody treatment the number of immune regulating leukocytes in tumors was reduced, which led to a decrease in tumor growth. However, the normal immune response towards immunization or bacterial infection was not compromised. Thus, VAP-1 and CLEVER-1 are both potential targets for antiinflammatory therapies for preventing the harmful accumulation of leukocytes in inflamed areas. Targeting CLEVER-1 may also inhibit tumor growth by reducing immunosuppressive leukocytes in tumors