Submitted by Setor de Tratamento da Informa??o - BC/PUCRS (tede2@pucrs.br) on 2015-10-09T19:45:36Z No. of bitstreams: 1 475655 - Texto Completo.pdf: 1136903 bytes, checksum: 1a2ad879662fb2a0203c2418ab7dc36f (MD5) / Made available in DSpace on 2015-10-09T19:45:36Z (GMT). No. of bitstreams: 1 475655 - Texto Completo.pdf: 1136903 bytes, checksum: 1a2ad879662fb2a0203c2418ab7dc36f (MD5) Previous issue date: 2015-05-15 / Liver fibrosis is a complex disease that is caused by inappropriate tissue repair due to the deposition of connective tissue. When a chronic lesion affects the liver, regenerative response fails and hepatocytes are replaced with abundant extracellular matrix (ECM). The imbalance between production and degradation of ECM will result in the accumulation of proteins that change normal liver architecture, and thus its functionality. The main source of ECM is the activated hepatic stellate cell (HSC). In order, to clarify possible therapeutic approaches to the disease, the this work aimed to evaluate the possible antifibrotic action of Pluchea sagitallis (Lam.) Cabrera on an activated HSC immortalized lineage (GRX). Our results demonstrated that the P. sagittalis aqueous extract at 0.039 and 0.078 mg/mL concentrations was able to reduce cell growth and proliferation. Regarding to oxidative stress evaluation, there was no statistically significant difference between the treated group and the control. Staining with OilRed-O (ORO) showed a statistically significant increase in intracellular lipid content after 5 days of treatment, exerting in vitro effect on the GRX phenotypic change of activated towards the quiescent state. These results were confirmed by colorimetric quantification of lipid content. Regarding the TGF-?1 and collagen production, there were no statistically significant differences observed between the groups. In conclusion, the P. sagittalis aqueous extract reduces the growth and proliferation of GRX cells and induces the reversal of activated towards a quiescent phenotype. There was no decrease in cell proliferation either by necrosis or by apoptosis via activation of the senescence. Thus, our data suggest that the extract showed an antifibrotic effect, possibly by activating phenotype reversal. / A fibrose hep?tica apresenta uma patog?nese complexa causada por reparo tecidual inadequado devido ? deposi??o de tecido conectivo. Quando um dano cr?nico acomete o f?gado, a resposta regenerativa falha e os hepat?citos s?o substitu?dos por matriz extracelular (ECM) excedente. Assim, o desequil?brio entre a degrada??o e a produ??o de ECM acarretar? no ac?mulo dessas prote?nas que alteram a arquitetura normal do f?gado e, consequentemente, sua funcionalidade. A principal fonte de ECM ? a c?lula estrelada hep?tica (HSC) ativada. Sendo assim, na tentativa de elucidar poss?veis abordagens terap?uticas para a doen?a, o objetivo desse trabalho foi avaliar a poss?vel a??o antifibr?tica do extrato aquoso de Pluchea sagitallis (Lam.) Cabrera sobre uma linhagem imortalizada de HSC ativadas (GRX). Nossos resultados demonstraram que as concentra??es de 0,039 e 0,078 mg/mL do extrato aquoso de P. sagitallis foram capazes de diminuir o crescimento e a prolifera??o celular. Quanto ? avalia??o do estresse oxidativo, n?o foi observada diferen?a estatisticamente significativa entre o grupo tratado e controle. A colora??o com oil red (ORO) mostrou aumento significativo do conte?do lip?dico intracelular ap?s 5 dias de tratamento, indicando efeito in vitro sobre a mudan?a fenot?pica em linhagem GRX, do estado ativado para o estado quiescente. Esses resultados foram confirmados pela quantifica??o colorim?trica de lip?dios. Em rela??o ? produ??o de TGF-?1 e col?geno total, n?o foram observadas diferen?as estatisticamente significativas entre os grupos. Concluindo, o extrato aquoso da P. sagittalis diminuiu o crescimento e a prolifera??o das c?lulas GRX e induziu a revers?o do fen?tipo ativado para quiescente. A diminui??o na prolifera??o celular n?o ocorreu nem por necrose nem por ativa??o da apoptose e senesc?ncia. Sendo assim, nossos resultados sugerem que o extrato apresenta um efeito antifibr?tico, possivelmente pela via que ativa a revers?o do fen?tipo.

Made available in DSpace on 2015-04-14T13:35:14Z (GMT). No. of bitstreams: 1 431811.pdf: 3112602 bytes, checksum: 978ebd0c621320bc564a724a51874119 (MD5) Previous issue date: 2011-04-26 / INTRODU??O : A doen?a hep?tica gordurosa n?o alco?lica tem alta preval?ncia em pacientes obesos m?rbidos e ? importante pelo seu potencial evolutivo para cirrose. O objetivo deste trabalho foi avaliar a preval?ncia de fibrose hep?tica em pacientes obesos m?rbidos submetidos ? cirurgia bari?trica e seu comportamento ap?s o emagrecimento. M?TODO : Este estudo ? uma coorte hist?rica que compara bi?psias hep?ticas realizadas no momento da cirurgia bari?trica com bi?psias realizadas ap?s o emagrecimento com rela??o ? fibrose hep?tica. Os achados de fibrose foram comparados com o sexo, a idade, o IMC, o ?ndice APRI, a presen?a de comorbidades, o grau de esteatose e a baloniza??o hepatocit?ria. RESULTADOS : Dos 78 pacientes estudados, 35 pacientes (44,9%) apresentaram fibrose, na bi?psia do transoperat?rio. A m?dia de perda do excesso de peso foi de 82,4%. Ap?s o emagrecimento, 24 pacientes (30,8%) apresentavam fibrose. Dos que tinham fibrose na primeira bi?psia, 45,7% apresentaram regress?o da fibrose, e 54,3% continuavam com fibrose. Dos que n?o tinham fibrose na primeira bi?psia, 88,4% continuaram sem, e 11,6% passaram a apresentar algum grau de fibrose. N?o houve diferen?a estatisticamente significativa entre os pacientes que apresentavam ou n?o fibrose com rela??o ao sexo, ? idade, ao IMC e aos graus de esteatose, tanto no transoperat?rio quanto no p?s-operat?rio. Na bi?psia transoperat?ria, os pacientes com fibrose tinham mais DM2 e dislipidemia. A baloniza??o hepatocit?ria foi a ?nica vari?vel que esteve mais prevalente nos pacientes com fibrose tanto no transoperat?rio (P<0,001) quanto no p?s-operat?rio (P= 0,008). CONCLUS?O : Dos 35 pacientes com fibrose, cerca de metade (45,7%) apresentou regress?o da fibrose, muitos se mantiveram est?veis, e apenas 11,6% apresentaram piora da fibrose ap?s o emagrecimento secund?rio ? cirurgia bari?trica

The Muon Ionisation Cooling Experiment (MICE) has been commissioned to provide the first demonstration of ionisation cooling. MICE will aim to demonstrate that ionisation cooling can be used to reduce of the emittance of a beam of muons to meet the requirements of future particle physics experiments such as the Neutrino Factory, or Muon Collider. As of October 2016, commissioning of Step IV of MICE has been completed which provides an opportune time to make material physics studies on the absorber material. The cooling formula that MICE will use to measure the emittance reduction was reviewed. It is shown that the energy loss term is important when measuring cooling, and an accurate measurement of the energy loss will hence improve the accuracy of the cooling formula. The physics of ionisation cooling is also reviewed. The primary absorber used in the early data taking of MICE Step IV will be a 65mm disk of Lithium Hydride. The energy loss of Lithium Hydride was estimated using the equations of energy loss developed by Bethe. Methods were developed in this thesis to make measurements of the energy loss using data from the MICE trackers, and the timeof- flight data through the cooling channel. The energy loss of muons in monte-carlo simulations measured with the two alternative methods was found to be in agreement, with a measurement by the trackers of 9.02 ± 0.07, and from simulated time-of-flight of 9.32 ± 0.15. The first measurement of energy loss by 200 MeV/c muons was made using time-of-flight data using real muons in the MICE channel of ∆E = 9.23 ± 0.13 MeV, corresponding to a stopping power of Lithium Hydride of dE/dx = 1.42 ± 0.02 MeV g−1 cm2.

Orientador: Eduardo de Moraes Gregores. / Dissertação (mestrado) - Universidade Federal do ABC. Programa de Pós-Graduação em Física, 2012.

Choi, Siu Cheong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 132-148). / Abstracts in English and Chinese. / Acknowledgement --- p.i / Abstract --- p.ii / Abbreviation --- p.v / List of Figures --- p.viii / List of Tables --- p.xii / Table of Content --- p.xiii / Chapter Chapter 1: --- General Introduction / Chapter 1.1 --- Introduction --- p.1 / Chapter 1.1.1 --- Treatment resistance in cancer --- p.1 / Chapter 1.1.1.1 --- Surgery --- p.2 / Chapter 1.1.1.2 --- Chemotherapy --- p.3 / Chapter 1.1.1.3 --- Radiotherapy --- p.3 / Chapter 1.1.1.4 --- Hormonal therapy --- p.4 / Chapter 1.1.2 --- Hypoxia/reoxygenation and its correlation with treatment resistance --- p.5 / Chapter 1.1.3 --- Aim of the study --- p.6 / Chapter Chapter 2: --- The drug sensitivity in HepG2 cells and A431 cells / Chapter 2.1 --- Introduction --- p.8 / Chapter 2.1.1 --- Treatment of cancer --- p.8 / Chapter 2.1.2 --- Drug resistance --- p.9 / Chapter 2.2 --- Materials and Methods --- p.10 / Chapter 2.2.1 --- Cell culture --- p.10 / Chapter 2.2.2 --- Drugs --- p.10 / Chapter 2.2.3 --- MTT assay --- p.11 / Chapter 2.3 --- Results --- p.12 / Chapter 2.3.1 --- The drugs to which G10HR and G20HR cells were more resistant --- p.12 / Chapter 2.3.2 --- "The drugs of which GP, G10HR and G20HR cells have similar response" --- p.12 / Chapter 2.3.3 --- The drugs to which A10HR and A20HR cells were more resistant --- p.17 / Chapter 2.3.4 --- The drugs to which A10HR and/or A20HR cells were more sensitive --- p.17 / Chapter 2.3.5 --- "The drugs which AP, A10HR and A20HR cells have similar response" --- p.18 / Chapter 2.4 --- Discussion --- p.24 / Chapter 2.4.1 --- Camptothecin and 10-hydroxy camptothecin --- p.27 / Chapter 2.4.2 --- Etoposide --- p.30 / Chapter 2.4.3 --- Hydrogen peroxide --- p.32 / Chapter 2.4.4 --- Interferons --- p.32 / Chapter 2.4.4.1 --- Interferon alpha --- p.33 / Chapter 2.4.4.2 --- Interferon gamma --- p.34 / Chapter 2.4.5 --- Methotrexate --- p.35 / Chapter 2.4.6 --- Vincristine --- p.36 / Chapter Chapter 3: --- The resistance mechanism of doxorubicin in A431 cells / Chapter 3.1 --- Introduction --- p.38 / Chapter 3.1.1 --- Chemotherapeutic resistance --- p.38 / Chapter 3.1.2 --- Tumor hypoxia --- p.39 / Chapter 3.1.3 --- Structure and function of doxorubicin --- p.39 / Chapter 3.1.4 --- Clinical use of doxorubicin --- p.40 / Chapter 3.1.5 --- Mechanisms of doxorubicin resistance --- p.41 / Chapter 3.1.6 --- Structure and function of P-glycoprotein --- p.42 / Chapter 3.1.7 --- Drug resistance contributed by P-glycoprotein and the solution --- p.43 / Chapter 3.1.8 --- Epigenetic modulation of mdr1 --- p.45 / Chapter 3.2 --- Materials and Methods --- p.47 / Chapter 3.2.1 --- Cell culture --- p.47 / Chapter 3.2.2 --- MTT assay --- p.47 / Chapter 3.2.3 --- Reverse transcription polymerase chain reaction (RT-PCR) --- p.47 / Chapter 3.2.4 --- Western blot analysis --- p.48 / Chapter 3.2.5 --- Doxorubicin efflux assay --- p.50 / Chapter 3.2.6 --- Drug sensitivity of A431 cells treated with verapamil --- p.50 / Chapter 3.2.7 --- Treatment with DNA methyltransferase inhibitor --- p.51 / Chapter 3.2.8 --- Drug sensitivity of A431 cells treated with 5-Aza-dC --- p.51 / Chapter 3.2.9 --- Methylation-specific PCR (MSP) --- p.51 / Chapter 3.2.10 --- Bisulfite genomic DNA sequencing --- p.52 / Chapter 3.3 --- Results --- p.54 / Chapter 3.3.1 --- Drug sensitivity of A431 cells to doxorubicin --- p.54 / Chapter 3.3.2 --- Expression profile of mdrl and P-glycoprotein in A431 cells --- p.54 / Chapter 3.3.3 --- Dox efflux-pump activity in A431 cells --- p.57 / Chapter 3.3.4 --- Drug sensitivity of A431 cells in the presence of verapamil --- p.59 / Chapter 3.3.5 --- Expression profile of mdrl in A431 cells in the presence of 5- Aza-dC --- p.59 / Chapter 3.3.6 --- Drug sensitivity of A431 cells in the presence of 5-Aza-dC --- p.62 / Chapter 3.3.7 --- Methylation status of mdrl promoter region --- p.64 / Chapter 3.3.8 --- Bisulfite genomic DNA sequencing of the mdrl promoter --- p.64 / Chapter 3.4 --- Discussion --- p.67 / Chapter Chapter 4: --- The resistance mechanism of cisplatin in HepG2 cells / Chapter 4.1 --- Introduction --- p.70 / Chapter 4.1.1 --- Tumor hypoxia and chemotherapeutic resistance --- p.70 / Chapter 4.1.2 --- Cisplatin and its action mechanism --- p.71 / Chapter 4.1.3 --- Mechanisms of cisplatin resistance --- p.74 / Chapter 4.1.4 --- Mismatch repair genes --- p.79 / Chapter 4.1.5 --- Epigenome and drug resistance in cancer --- p.80 / Chapter 4.2 --- Materials and Methods --- p.84 / Chapter 4.2.1 --- Cell culture --- p.84 / Chapter 4.2.2 --- MTT assay --- p.84 / Chapter 4.2.3 --- Reverse transcription polymerase chain reaction (RT-PCR) --- p.84 / Chapter 4.2.4 --- Oligonucleotide transfection --- p.85 / Chapter 4.2.5 --- Treatment with DNA methyltransferase inhibitor --- p.86 / Chapter 4.2.6 --- Drug sensitivity of HepG2 cells treated with 5-Aza-dC --- p.87 / Chapter 4.2.7 --- Treatment with histone deacetylase inhibitor --- p.87 / Chapter 4.2.8 --- Drug sensitivity of HepG2 cells treated with TSA --- p.87 / Chapter 4.3 --- Results --- p.89 / Chapter 4.3.1 --- Drug sensitivity of HepG2 cells to cisplatin --- p.89 / Chapter 4.3.2 --- Expression profile of the MMR genes in HepG2 cells --- p.89 / Chapter 4.3.3 --- Drug sensitivity of HepG2 cells to cisplatin after the knock- down of PMS2 --- p.91 / Chapter 4.3.4 --- Expression profile of MMR genes in the presence of 5-Aza-dC --- p.95 / Chapter 4.3.5 --- Drug sensitivity of HepG2 cells to cisplatin after the addition of 5-Aza-dC --- p.95 / Chapter 4.3.6 --- Expression profile of MMR genes in the presence of trichostatin A --- p.98 / Chapter 4.3.7 --- Sensitivity of HepG2 cells to cisplatin after the addition of trichostatin A --- p.98 / Chapter 4.4 --- Discussion --- p.101 / Chapter Chapter 5: --- The role of PMS2 in cisplatin-induced apoptosis / Chapter 5.1 --- Introduction --- p.105 / Chapter 5.1.1 --- Apoptosis --- p.105 / Chapter 5.1.2 --- Extrinsic pathway of apoptosis --- p.106 / Chapter 5.1.3 --- Intrinsic pathway of apoptosis --- p.106 / Chapter 5.1.4 --- Cisplatin-induced apoptosis --- p.107 / Chapter 5.1.5 --- MMR and apoptosis --- p.109 / Chapter 5.2 --- Materials and Methods --- p.111 / Chapter 5.2.1 --- Cell culture --- p.111 / Chapter 5.2.2 --- Flow cytometric analysis of apoptosis --- p.111 / Chapter 5.2.3 --- Oligonucleotide transfection --- p.111 / Chapter 5.2.4 --- Western blot analysis --- p.111 / Chapter 5.2.5 --- Drug and antibodies --- p.112 / Chapter 5.3 --- Results --- p.113 / Chapter 5.3.1 --- Cisplatin induced apoptosis --- p.113 / Chapter 5.3.2 --- Knockdown of PMS2 by siRNA --- p.113 / Chapter 5.3.3 --- Cisplatin-induced apoptosis involved caspases --- p.115 / Chapter 5.3.4 --- Protein expressions of anti-apoptotic genes --- p.119 / Chapter 5.3.5 --- Protein expressions of pro-apoptotic genes --- p.119 / Chapter 5.3.6 --- Protein expressions of apoptotic proteins after knockdown of PMS2 --- p.122 / Chapter 5.4 --- Discussion --- p.124 / Chapter Chapter 6: --- General discussion and conclusion / Chapter 6.1 --- Diverse sensitivity for hypoxia/reoxygenation treated cells to anticancer drugs --- p.128 / Chapter 6.2 --- Resistance mechanism of doxorubicin in A10HR and A20HR cells --- p.129 / Chapter 6.3 --- Resistance mechanism of cisplatin in G10HR and G20HR cells --- p.129 / Chapter 6.4 --- The role of PMS2 as a direct signaling molecule and the alteration of apoptotic proteins in cisplatin-induced apoptosis --- p.130 / Chapter 6.5 --- Future work --- p.131 / References --- p.132

癌症復發往往伴隨著耐藥性和轉移率的增加。目前我們仍未完全瞭解確切的腫瘤逃脫機制。皮下無水酒精注射（PEI）已經被用於治療肝細胞癌（HCC）幾十年，而PEI治療後的癌症復發仍然是該方法的一個主要限制。最近有許多證據表明癌細胞能夠逆轉化學誘導的細胞凋亡過程而得以存活，這有可能是其中一個導致癌細胞復發的原因。這篇論文的重點在於研究肝癌細胞HepG2經歷乙醇誘導凋亡事件後存活下來的後果。 / 這個研究首先證實肝癌細胞 HepG2能從乙醇誘導凋亡事件後存活下來。然後我們對存活下來的肝癌細胞HepG2進行增殖率，耐藥性，運動性以及侵襲性的研究。結果表明，存活下來的HepG2有46%的乙醇耐藥性和84%的高運動性。然後爲了發現存活下來的HepG2是否對其他臨床常用藥物也同樣具有耐藥性，4種臨床常用藥物包括阿黴素，紫杉醇，順鉑，5-氟尿嘧啶（5Fu）均被用於測試。有趣的是，存活下來的HepG2對5-氟尿嘧啶變得更加敏感，平均敏感性下降了58.2%。 / 總的來說，我們的研究結果表明肝癌細胞可從乙醇誘導凋亡事件中恢復過來。此外，存活下來的細胞變得更具有耐藥性和侵入性。這種恢復過程可能是導致癌症復發的原因之一。出乎意料的是，雖然所有存活下來的細胞對乙醇具耐受性，但是它們對於5-氟尿嘧啶均變得更加敏感。這些結果表明，乙醇和5-氟尿嘧啶的聯合治療可能有助於提高PEI治療效果從而預防肝癌癌症復發。 / Cancer relapse, associated with increased drug resistance and higher rate of metastasis, often occurs after chemotherapy. The cancer escape mechanisms are still incompletely understood. Percutaneous ethanol injection (PEI) has been used for treating hepatocellular carcinoma (HCC) for decades, but the recurrence after PEI treatment remains a major limitation. Recently there are mounting evidences showing that cancer cells could survive from chemical-induced apoptosis, suggesting a potential route through which cancer relapse may occur. This thesis focuses on the consequences of the recovery of HepG2 cells from ethanol-induced apoptotic event. / This study verified that HepG2 cells could recover from ethanol-induced apoptosis. Proliferation rate, drug resistance, motility and invasiveness were investigated in recovered HepG2 cells. On average, the recovered HepG2 cell clones were found to be 46% more resistant to ethanol and 84% higher in motility than the parental cell clones. And then four commonly used clinical drugs were assayed to determine whether the recovered cell clones were also resistant to other clinical drugs, including doxorubicin, docetaxel, cisplatin and 5-fluorouracil (5-Fu). Interestingly, the recovered clones became 58.2% more sensitive to 5-fluorouracil on average. / In conclusion, our findings showed that HepG2 cells can recover from ethanol-induced apoptotic event. In addition, some cell clones recovered from apoptosis became more resistant to ethanol and some became more invasive. Such recovery might be one of the reasons causing cancer recurrence. Unexpectedly, although the recovered cell clones were more resistant to ethanol, they became more sensitive to 5-Fu treatment. These results indicated that ethanol-5-Fu combined treatment might be useful in enhancing the PEI treatment and preventing HCC cancer recurrence. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Wang, Shanshan. / Thesis (Ph.D.) Chinese University of Hong Kong, 2014. / Includes bibliographical references (leaves 115-130). / Abstracts also in Chinese.

The discovery of a charged Higgs boson (H+) would be an unambiguous sign of physics beyond the Standard Model. This thesis describes preparations for the H+ search with the ATLAS experiment at the Large Hadron Collider at CERN. The H+ discovery potential is evaluated, and tools for H+ searches are developed and refined. The H+→τν decay mode has been known as the most promising H+ discovery channel. Within this thesis, first studies of this channel with realistic detector simulation, trigger simulation and consideration of all dominant systematic uncertainties have been performed. Although, as shown by these studies, the discovery sensitivity is significantly degraded compared to studies using a parametrized detector simulation, this channel remains the most powerful ATLAS H+ discovery mode. Future searches will rely on multivariate analysis techniques like the Iterative Discriminant Analysis (IDA) method. First studies indicate that a significant sensitivity increase can be achieved compared to studies based on sequential cuts. The largest uncertainty in H+ searches is the expected $t\bar{t}$ background contribution. It is shown that numbers obtained from simulated events could be off by a factor of two, decreasing the discovery sensitivity dramatically. In this thesis, the Embedding Method for data-driven background estimation is presented. By replacing the muon signature in $t\bar{t}$ events with a simulated τ, events which allow an estimation of the background contribution at the 10% level are obtained. The ATLAS τ identification focuses on comparably clean environments like Z and W decays. To optimize the performance in high-multiplicity events like H+→τν, tau leptons are studied in $t\bar{t}$ and pile-up events. Variables which do not show discrimination power in high-multiplicity events are identified, and in some cases similar, more powerful variables are found. This allows to recover some of the performance loss and to increase the robustness of the τ identification. For the analysis of large amounts of data produced by the ATLAS detector, seamless interoperability of the various Grid flavors is required. This thesis introduces translators to overcome differences in the information system between a number of Grid projects,and highlights important areas for future standardization.

I present the results of a search for pair production of scalar top quarks (~t1) in an R-parity violating supersymmetric scenario using 322 pb_1 of pp collisions at ps = 1.96 TeV collected by the upgraded Collider Detector at Fermilab. I assume each ~t1 decays into a tau lepton and a b quark, with branching ratio B, and search for final states containing either an electron or a muon from a leptonic tau decay, a hadronically decaying tau lepton, and two or more jets. Two candidate events pass my final selection criteria, consistent with the expectation from standard model processes. I present upper limits on the cross section times branching ratio squared (~t1~t1)B2 as a function of the stop mass m(~t1). Assuming B = 1, I set a 95% confidence level limit m(~t1) > 153 GeV=c2. These limits are also fully applicable to the case of a pair produced third generation scalar leptoquark that decays into a tau lepton and a b quark.

An ecosystem always involves some implicit relations between habitat environment and inhabitants, whose reciprocal links can not be identified easily. Three sets of ecological monitoring data were analyzed in this study, including coral reef, algae (Thalassia hemprichii Aschers) in Kenting National Park, and Formosan landlocked salmon (Oncorhynchus masou formosanus) in the basin of Chichiawan Stream. Two data-oriented analysis techniques, which are Habitat Evaluation Procedure (HEP) and Group Method of Data Handling (GMDH), were applied to retrieve the embedded patterns from these data sets. Eventually, for each data set, a forecasting model based on the technique of combined forecasting were developed, which is to integrate the results from HEP and GMDH, for improving the overall modeling precision. The results of this study show that the data-oriented analyses, such as HEP and GMDH, are useful for finding valid information from the ecological data. Furthermore, the combined forecasting technique can really improve the performance of model prediction even for the ecological research. In order to acquire the most important habitat environmental factors affecting the inhabitants, this study also performed sensitivity analysis of the models. The contributions of this study are to identify effective knowledge for future ecological research and to provide reasonable suggestions for formulating conservation strategy.

This paper presents an outline of the generation of mass for the massive Standard Model particles (fermions, $W^\pm$, $Z^0$) through electroweak symmetry breaking via the Higgs mechanism, and how the Higgs boson emerges from this framework. A Monte Carlo study was done on the decay $H\rightarrow\tau\tau$, with one leptonically and one hadronically decaying tau, with two different production channels for the $H$, gluon-gluon fusion (gg) and vector boson fusion (VBF), at $\sqrt s = 7\tev$ with a Higgs mass $m_H = 120\gev$. The kinematics of these two production channels were compared and it was found that the transverse momentum of muons produced in VBF were higher on average than those produced in gg. This differance was greater in muons originating from the leptonically decaying tau in the Higgs decay, than those produced by other processes in the underlying event. In the latter, however, the difference was still noticable. Jets were slightly more abundant in VBF than in gg, and were in VBF more distributed along the beam axis. The separation in pseudorapidity between the two jets with highest transverse momentum was found to be greater in VBF than in gg. An attempt to reconstruct the Higgs mass using Monte Carlo data run through a simulation of the ATLAS detector was done. The estimator used was the transverse mass of the system consisting of the visible part of the hadronically decaying tau, the lepton from the leptonically decaying tau and the total missing transvese energy. In gg the mean of the transvese mass distribution was found to be $89.26\gev$ with a root mean square uncertainty (RMS) of $23.86\gev$. In VBF the mean was found to be $85.57\gev$ with RMS $27.08\gev$.