Syftet med denna studie är att undersöka, diskutera och problematisera i vilken utsträckning läroböcker i religionskunskap framställer substantiell och funktionell religionsförståelse om de fem världsreligionerna judendom, kristendom, islam, hinduism och buddhism. I tidigare forskning har kvalitativa undersökningar genomförts i stor utsträckning för att analysera hur religioner, såsom kristendom och islam, framställs i läroböcker. Det har även tidigare undersökts om läroböcker i religionskunskap beskriver de fem världsreligionerna som idéer eller människor och om perspektiven lära om och lära från religion förmedlas i läromedel. I denna studie tillämpas en kvantitativ innehållsanalys för att undersöka vilket meningserbjudande som text och bild förmedlar. Materialet som ligger till grund för studien är fyra läroböcker avsedda för religionskunskap i årskurs 4–6. Analysen har genomförts med hjälp av två kodnings-scheman, ett för bild och ett för text. Dessa scheman har konstruerats utifrån definitioner av substantiell och funktionell religionsförståelse, där den första handlar om vad religion är och den andra om vad religion gör. Dessutom har Ninian Smarts sju dimensioner av religion använts och förgrenats för att generera studiens kodningsscheman. Vidare har en komparativ analys även tillämpats för att undersöka meningserbjudandets kongruens mellan bild och bildtext. Resultatet i denna studie visar att substantiell religionsförståelse dominerar i alla läroböckers skriftliga text. Vad gäller läroböckernas bilder får funktionell religionsförståelse ett mer likställt utrymme än vad det får i text. I två av studiens fyra läroböcker återfinns funktionell förståelse även i störst utsträckning bland bilder. Resultatet visar även att meningserbjudandet som förmedlas i läroböckernas bild och bildtext har högre överrensstämmelse än avvikelse, vilket innebär att bilder i större utsträckning inkluderar bildtext som förmedlar samma religions-förståelse. Slutsatsen är att det finns ett behov av större balans mellan belysta religionsförståelser, men att det är naturligt att skriftlig text förmedlar substantiell förståelse för att behålla ett objektivt förhållningssätt, medan bilder erhåller större funktionell religionsförståelse då läromedelsförfattarna rimligtvis vill illustrera individer som religionen berör.

A Radioterapia em arco modulado volumétrico (VMAT) é uma das modalidades mais avançadas em teleterapia para o tratamento de câncer. Os diversos avanços tecnológicos, bem como a evolução das técnicas de tratamento tornaram o VMAT como uma das modalidades de estado da arte para o tratamento de alguns cânceres. Parte deste avanço é creditada à melhoria na acurácia e na prescrição de dose absorvida recomendada ao paciente ao longo dos anos. Este avanço permite que atualmente seja possível realizar os cálculos dosimétricos, por meio de sistemas de planejamento computadorizado, considerando as heterogeneidades dos pacientes, tais como: tecidos e órgãos com composições diferentes da água (meio de referência em radioterapia), contorno do paciente individualizado e o movimento dos tumores com a respiração. Tais avanços demandam o controle de qualidade destas ferramentas, com objetivo de assegurar que todo o processo de tratamento seja satisfatório e acurado. A comunidade dispõe poucos sistemas experimentais capazes de avaliar, considerando os níveis de incerteza, se os sistemas de planejamento computadorizados são aptos a considerar a movimentação dos alvos nos tratamentos com VMAT. Neste trabalho serão apresentados os resultados obtidos empregando um objeto simulador Fricke Xylenol Gel, com capacidade de mensurar as diferenças introduzidas pela movimentação, utilizando Imagem por Ressonância Magnética - MRI e comparando qualitativamente e quantitativamente os resultados. São discutidas as principais etapas de desenvolvimento deste objeto simulador, seus resultados experimentais, conclusões. / Volumetric Modulated Arc Therapy (VMAT) is one of the methods most commonly used in teletherapy to treat cancer. The various technological advances and the evolution of treatment techniques made the VMAT as one of the state of the art methods for the treatment of some cancers. Part of this improvement is credited to improvements in accuracy and prescription dose absorbed recommended to the patient over the years. This advance allows currently is possible to perform dosimetric calculations by means of the computerized planning system, considering the heterogeneity of patients, such as tissues and organs with different water compositions medium (reference radiation), and individual patient contour the movement of tumors breathing. Such advances require quality control of these tools, in order to ensure that the entire treatment process is satisfactory and accurate. Up to now, the community lacks an experimental system capable of evaluating, considering the uncertainty levels if the computerized planning systems are able to consider the movement of targets in the treatments with VMAT. In this paper, will be presented the results obtained with the phantom Fricke Xylenol Gel, capable of measuring the differences introduced by movement using the Magnetic Resonance Image - MRI and compared qualitatively and quantitatively. The main stages of the phantom development, their experimental results, conclusions and comparisons with other systems are discussed.

by Hon-wing Tsui. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1988. / Bibliography: leaves 151-203.

by Shik Yuen Lo. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 102-124). / Abstract / List of Illustrations / List of Tables / Acknowledgements / Chapter 1. --- Introduction --- p.1 / Chapter 2. --- Literature Review / Chapter 2.1 --- Anatomy of the Human Nasopharynx --- p.4 / Chapter 2.2 --- Histology of the Human Nasopharynx --- p.6 / Chapter 2.3 --- Intra-epithelial Lesions of the Nasopharyngeal Epithelium --- p.10 / Chapter A. --- Hyperplasia / Chapter B. --- Metaplasia / Chapter C. --- Koilocytes / Chapter D. --- Nasopharyngeal intra-epithelial neoplasia / Chapter 2.4 --- Nasopharyngeal Carcinoma --- p.19 / Chapter A. --- Histopathological classification of NPG / Chapter B. --- Epidemiology / Chapter C. --- Etiological factors / Chapter 2.5 --- Epstein-Barr Virus and Nasopharyngeal Carcinoma --- p.27 / Chapter A. --- Serological / Chapter B. --- EBV genome in NPC / Chapter C. --- EBV encoded latent gene products / Chapter 2.6 --- Cancer Genes in Nasopharyngeal Carcinoma --- p.28 / Chapter A. --- "Tumours suppressor Gene, p53" / Chapter B. --- "Oncogenes, c-myc, ras and bcl-2" / Chapter 2.7 --- Immunohistochemical methods --- p.33 / Chapter A. --- Avidin-Biotin Complex method (ABC) / Chapter B. --- Alkaline phosphotase Anti-alkaline phosphotase method (APAAP) / Chapter C. --- Unmasking of antigens / Chapter 2.8 --- Techniques in ISH --- p.40 / Chapter 3. --- Material and Methods --- p.42 / Chapter 3.1 --- Tissue Samples --- p.42 / Chapter A. --- "Samples for ras, c-myc and p53 studies" / Chapter B. --- Samples for LMP-1 study / Chapter C. --- Samples for bcl-2 study / Chapter D. --- Samples for EBER-RNAs study / Chapter 3.2 --- Monoclonal Antibodies --- p.47 / Chapter 3.3 --- Tissue Processing --- p.49 / Chapter A. --- Tissue processing for formalin fixed tissue / Chapter B. --- Tissue processing for frozen section / Chapter 3.4 --- IHC Techniques --- p.50 / Chapter A. --- Pretreatment of Laboratory Wares / Chapter B. --- Determination of optimum dilution and incubation time for p53antibody / Chapter C. --- Determination of optimum dilution and incubation time for bcl-2 and LMP-1 antibodies / Chapter D. --- Determination of optimum dilution and incubation time for c-myc and ras / Chapter E. --- "Detection of p53, c-myc and ras by ABC method" / Chapter F. --- Detection of bcl-2 and LMP-1 by APAAP method / Chapter 3.6 --- ISH --- p.57 / Chapter A. --- Pretreatment of laboratory wares / Chapter B. --- FITC conjugated EBER oligonucleotide probe / Chapter C. --- Determination of PK dilution for paraffin section / Chapter D. --- Determination of PK dilution for frozen section / Chapter E. --- Determination of the choice of fixative for frozen section / Chapter F. --- Detection of EBER-RNAs by ISH method / Chapter 3.7 --- Statistical analysis --- p.62 / Chapter A. --- p53 / Chapter B. --- c-myc and ras / Chapter 4. --- Results --- p.63 / Chapter A. --- ras / Chapter B. --- c-myc / Chapter C. --- p53 / Chapter D. --- LMP-1 / Chapter E. --- Bcl-2 / Chapter F. --- EBER-RNAs / Chapter 5. --- Discussion --- p.86 / Chapter 6. --- Conclusion and Summary --- p.97 / Appendix --- p.99 / Reference --- p.102

by Suet-ching Leung. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1989. / Bibliography: leaves 170-198.

by Ka-chun Yiu. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1989. / Bibliography: leaves 162-192.

Ng Dean Yew, Dennis. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 85-98). / Abstract --- p.i / Acknowledgments --- p.iii / Table of contents --- p.iv / List of figures --- p.vii / List of tables --- p.ix / List of abbreviation --- p.x / Chapter Chapter 1 --- Introduction / Chapter 1.1. --- History --- p.1 / Chapter 1.2. --- Classification and structure of Epstein-Barr Virus --- p.2 / Chapter 1.3. --- Genomic organization of EBV --- p.3 / Chapter 1.4. --- Replication cycle of EBV --- p.5 / Chapter 1.5. --- EBV latent and lytic cycle proteins --- p.6 / Chapter 1.6. --- Clinical diseases associated with EBV Infection --- p.11 / Chapter 1.7. --- Association of EBV and NPC --- p.13 / Chapter 1.8. --- EBV serological markers in the diagnosis of NPC --- p.13 / Chapter 1.9. --- Sources of EBV-specific DNase --- p.15 / Chapter 1.10. --- Characteristics of Epstein-Barr virus alkaline DNase --- p.15 / Chapter 1.11. --- Aim of the project --- p.18 / Chapter Chapter 2 --- Materials & Methods / Chapter 2.1. --- Molecular cloning --- p.19 / Chapter 2.1.1. --- Cell culture --- p.19 / Chapter 2.1.2. --- mRNA purification --- p.19 / Chapter 2.1.3. --- First strand cDNA synthesis --- p.21 / Chapter 2.1.4. --- Polymerase chain reaction (PCR) of cDNA --- p.21 / Chapter 2.1.5. --- Purification of PCR product after gel electrophoresis --- p.22 / Chapter 2.1.6. --- Ligation of PCR amplified DNase gene into pUC18 Sma/BAP vector --- p.23 / Chapter 2.1.7. --- Transformation by electroporation --- p.24 / Chapter 2.1.7.1. --- Cell preparation --- p.24 / Chapter 2.1.7.2. --- Electroporation procedure --- p.25 / Chapter 2.2. --- Extraction ofplasmid DNA --- p.28 / Chapter 2.2.1. --- Boiling preparation --- p.28 / Chapter 2.2.2. --- Plasmid digestion --- p.29 / Chapter 2.3. --- Large-scale purification ofplasmid --- p.29 / Chapter 2.4. --- Small-scale purification ofplasmid --- p.32 / Chapter 2.5. --- DNA sequencing --- p.33 / Chapter 2.5.1. --- Annealing of primer to template DNA --- p.33 / Chapter 2.5.2. --- Labelling reaction --- p.34 / Chapter 2.5.3. --- Sequencing termination reaction --- p.35 / Chapter 2.5.4. --- Prepartion of sequencing gel --- p.36 / Chapter 2.5.5. --- Autoradiography of sequencing gel --- p.38 / Chapter 2.6. --- Epitope mapping --- p.39 / Chapter 2.6.1. --- Processing of EBV- specific DNase peptides --- p.39 / Chapter Chapter 3 --- Results / Chapter 3.1. --- Molecular cloning --- p.41 / Chapter 3.1.1. --- Cell culture --- p.41 / Chapter 3.1.2. --- mRNA purification --- p.42 / Chapter 3.1.3. --- PCR amplification --- p.42 / Chapter 3. 1.4 --- DNA purification of PCR product --- p.42 / Chapter 3.1.5. --- Molecular cloning of PCR amplified DNase gene into pUC18 SmaI/BAP vector --- p.44 / Chapter 3.1.6. --- Transformation by electroporation --- p.46 / Chapter 3.1.7. --- Extraction of plasmid DNA --- p.48 / Chapter 3.1.7.1. --- Boiling preparation --- p.48 / Chapter 3.1.8. --- Plasmid digestion --- p.51 / Chapter 3.2. --- DNA sequencing --- p.51 / Chapter 3.2.1. --- Comparison of B95-8 EBV-speicific DNase gene with gene sequence of EBV in GeneBank --- p.50 / Chapter 3.2.2. --- Comparison of 5' end of Raji & B95-8 EBV derived EBV-specific DNase gene --- p.57 / Chapter 3.2.3. --- Comparison of the 3'end of the Raji and B95-8 denved EBV-specific DNase gene --- p.63 / Chapter 3.2.4. --- Amino acid sequence homology between B95-8 & Raji EBV-specific DNase --- p.64 / Chapter 3.2.5. --- Amino acid sequence comparison between the 3' end of the B95-8 EBV DNase protein with that of the Raji EBV DNase protein --- p.62 / Chapter 3.3. --- Epitope mapping --- p.67 / Chapter 3.3.1. --- Amino acid key --- p.67 / Chapter 3.3.2. --- Amino acid sequence of peptides --- p.73 / Chapter 3.3.2. --- O.D. readings at 492nm of five histologically proven NPC sera --- p.74 / Chapter Chapter 4 --- Discussions / Chapter 4.1. --- Overall strategy --- p.75 / Chapter 4 2 --- Significance of EBV-specific DNase as marker for NPC --- p.76 / Chapter 4.3. --- Characterization of EBV-specific DNase --- p.76 / Chapter 4.4. --- Molecular cloning of PCR amplified gene into PUC18 SmaI/BAP vector --- p.77 / Chapter 4.4.1. --- Cell culture --- p.77 / Chapter 4.4.2. --- PCR amplification --- p.73 / Chapter 4.4.3. --- "Blunting,kinasing and ligation of EBV-specific DNase cDNA into pUC18 vector" --- p.78 / Chapter 4.4 .4 --- .Transformation by electroporation --- p.80 / Chapter 4.4.5. --- Restriction enzyme digestion of pUC18/EBV-DNase plasmid … --- p.81 / Chapter 4.5. --- DNA sequencing --- p.81 / Chapter 4.6. --- Epitope mapping --- p.83 / Reference --- p.85

by Liu Chun Ki, Kevin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 126-142). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.ii / Table of contents --- p.iii / List of figures --- p.viii / List of tables --- p.x / List of abbreviations --- p.xi / Chapter Chapter 1 --- Introduction Epstein-Barr Virus / Chapter 1.1 --- History --- p.1 / Chapter 1.2 --- Classification --- p.2 / Chapter 1.3 --- Virus and genome structure --- p.3 / Chapter 1.4 --- Epidemiology --- p.6 / Chapter 1.4.1 --- Prevalence of infection --- p.6 / Chapter 1.4.2 --- Modes of transmission --- p.7 / Chapter 1.5 --- Pathogenesis of EBV --- p.7 / Chapter 1.5.1 --- "Adsorption, penetration and dissemination" --- p.7 / Chapter 1.5.2 --- Lytic infection cycle --- p.8 / Chapter 1.5.3 --- Latent infection cycle --- p.9 / Chapter 1.5.4 --- Functions of the EBV-specific proteins associated with latent infection cycle proteins --- p.10 / Chapter 1.5.4.1 --- EBNA1 --- p.10 / Chapter 1.5.4.2 --- EBNA2 --- p.11 / Chapter 1.5.4.3 --- "EBNA 3A, 3B and 3C" --- p.11 / Chapter 1.5.4.4 --- EBNA LP --- p.12 / Chapter 1.5.4.5 --- LMP1 --- p.13 / Chapter 1.5.4.6 --- Characteristics of EBV LMP 2 gene --- p.14 / Chapter 1.5.4.7 --- Functions of LMP 2A --- p.15 / Chapter 1.5.4.8 --- Functions of LMP 2B --- p.18 / Chapter 1.6 --- Clinical significance of EBV --- p.20 / Chapter 1.6.1 --- Infectious mononucleosis (IM) --- p.20 / Chapter 1.6.2 --- Burkitt's lymphoma (BL) --- p.20 / Chapter 1.6.3 --- Nasopharyngeal carcinoma (NPC) --- p.21 / Chapter 1.6.4 --- Hodgkin's lymphoma (HL) --- p.21 / Chapter 1.7 --- Immune response to EBV infection --- p.22 / Chapter 1.7.1 --- Humoral immune response --- p.22 / Chapter 1.7.2 --- Cellular immune response --- p.22 / Chapter 1.8 --- Diagnosis of EBV infection --- p.26 / Chapter 1.9 --- Treatment and prevention --- p.27 / Chapter 1.10 --- Nasopharygneal Carcinoma (NPC) --- p.28 / Chapter 1.10.1 --- Epidemiology --- p.28 / Chapter 1.10.2 --- Etiology --- p.28 / Chapter 1.10.2.1 --- Environmental factor associated with NPC --- p.30 / Chapter 1.10.2.2 --- Genetic factors associated with NPC --- p.31 / Chapter 1.10.2.3 --- Association of NPC and EBV --- p.31 / Chapter 1.10.3 --- Diagnosis ofNPC --- p.32 / Chapter 1.10.4 --- Treatment --- p.33 / Chapter 1.11 --- Objective of the project --- p.34 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- EBV-containing cell cultures --- p.35 / Chapter 2.2 --- Extraction of total RNA --- p.36 / Chapter 2.2.1 --- Cell lysis --- p.36 / Chapter 2.2.2 --- Protein digestion --- p.36 / Chapter 2.2.3 --- DNA digestion --- p.37 / Chapter 2.2.4 --- Elution of total RNA --- p.37 / Chapter 2.2.5 --- Purity and electrophoresis analysis of total RNA --- p.38 / Chapter 2.3 --- First strand cDNA synthesis --- p.38 / Chapter 2.4 --- PCR amplification of LMP 2 cDNA --- p.39 / Chapter 2.5 --- Isolation of the PCR amplified LMP 2 cDNA --- p.40 / Chapter 2.6 --- Purification of the PCR amplified LMP 2 cDNA --- p.41 / Chapter 2.7 --- Confirmation of the PCR amplified cDNA --- p.42 / Chapter 2.7.1 --- Nested PCR --- p.42 / Chapter 2.7.2 --- Restriction enzyme digestion --- p.44 / Chapter 2.8 --- Ligation of insert LMP 2 cDNA with vector --- p.45 / Chapter 2.9 --- Transformation of competent cells JM109 --- p.45 / Chapter 2.10 --- Screening of the recombinant clones --- p.47 / Chapter 2.11 --- Small scale purification of plasmid DNA --- p.47 / Chapter 2.12 --- Determination of the size of the insert DNA --- p.48 / Chapter 2.13 --- DNA sequencing --- p.48 / Chapter 2.13.1 --- The cycle sequencing reaction --- p.48 / Chapter 2.13.2 --- Preparation of the acrylamide gel and TBE buffer --- p.51 / Chapter 2.13.3 --- Running conditions of the electrophoresis --- p.52 / Chapter 2.13.4 --- "Processing, editing and exporting the sequences" --- p.52 / Chapter 2.14 --- Data analysis --- p.53 / Chapter 2.14.1 --- Sequence analysis --- p.53 / Chapter 2.14.2 --- Amino acid analysis --- p.53 / Chapter 2.14.3 --- Protein secondary structure analysis --- p.53 / Chapter 2.14.4 --- Hydrophobicity analysis --- p.54 / Chapter 2.14.5 --- Isoelectric point analysis --- p.54 / Chapter Chapter 3 --- Results / Chapter 3.1 --- Cell Cultures --- p.55 / Chapter 3.2 --- Extraction of total RNA --- p.56 / Chapter 3.3 --- PCR amplification --- p.61 / Chapter 3.4 --- Isolation of PCR amplified LMP 2 cDNA --- p.62 / Chapter 3.5 --- Confirmation of the PCR amplified cDNA --- p.66 / Chapter 3.5.1 --- Nested PCR --- p.66 / Chapter 3.5.2 --- Restriction enzyme digestion --- p.71 / Chapter 3.6 --- Transformation and screening --- p.77 / Chapter 3.7 --- Extraction of plasmid DNA and its digestion with restriction enzyme --- p.78 / Chapter 3.8 --- DNA sequencing --- p.83 / Chapter 3.8.1 --- DNA sequence comparison --- p.84 / Chapter 3.9 --- Amino acid sequence homology --- p.89 / Chapter 3.9.1 --- Amino acid sequence comparison --- p.90 / Chapter 3.10 --- Hydrophobicity analysis --- p.92 / Chapter 3.10.1 --- Comparison of hydrophobicity of B95-8 derived LMP2 with GeneBank --- p.93 / Chapter 3.10.2 --- Comparison of hydrophobicity of CB 14022-derived LMP2 with GeneBank --- p.95 / Chapter 3.10.3 --- Comparison of hydrophobicity of Raji-derived LMP2 with GeneBank --- p.97 / Chapter 3.11 --- Protein secondary structure analysis --- p.100 / Chapter 3.11.1 --- Comparison of secondary structure of B95-8-derived LMP2 with GeneBank --- p.100 / Chapter 3.11.2 --- Comparison of secondary structure of CB 14022-derived LMP2 with GeneBank --- p.100 / Chapter 3.11.3 --- Comparison of secondary structure of Raji-derived LMP2 with GeneBank --- p.101 / Chapter 3.12 --- Isoelectric point analysis --- p.103 / Chapter Chapter 4 --- Discussions / Chapter 4.1 --- Overall strategy for the cloning and sequencing of EBV LMP 2 gene --- p.106 / Chapter 4.2 --- Implications of the results obtained in sequencing --- p.107 / Chapter 4.3 --- Results interpretation --- p.108 / Chapter 4.3.1 --- Cell culture --- p.108 / Chapter 4.3.2 --- Extraction of total RNA --- p.108 / Chapter 4.3.3 --- PCR amplification --- p.109 / Chapter 4.3.4 --- Confirmation of the PCR amplified cDNAs using nested PCR --- p.109 / Chapter 4.3.5 --- Confirmation of the PCR amplified cDNAs using restriction enzyme digestion --- p.110 / Chapter 4.3.6 --- Ligation of EBV LMP 2 cDNA to pGEM-T Easy Vector --- p.111 / Chapter 4.3.7 --- Transformation and screening --- p.114 / Chapter 4.3.8 --- Extraction of plasmid DNA and digestion with restriction enzyme --- p.115 / Chapter 4.4 --- DNA sequencing and sequence homology --- p.116 / Chapter 4.5 --- Amino acid sequence homology --- p.117 / Chapter 4.6 --- Hydrophobicity analysis --- p.119 / Chapter 4.7 --- Protein secondary structure analysis --- p.120 / Chapter 4.8 --- Isoelectric point analysis --- p.122 / Chapter 4.9 --- Summary of results --- p.122 / Chapter 4.10 --- Conclusions --- p.124 / References --- p.126

This thesis studies non-simple Jacobians and non-simple abelian varieties. The moti- vation of the study is a construction which gives a distinguished genus 4 curve in the linear system of a (1, 3)-polarised surface. The main theorem characterises such curves as hyperelliptic genus 4 curves whose Jacobian contains a (1, 3)-polarised surface. This leads to investigating the locus of non-simple principally polarised abelian g- folds. The main theorem of this part shows that the irreducible components of this locus are Is~, defined as the locus of principally polarised g-folds having an abelian subvariety with induced polarisation of type d. = (d1, ... , dk), where k ≤ g/2 Moreover, there are theorems which characterise the Jacobians of curves that are etale double covers or double covers branched in two points. There is also a detailed computation showing that, for p > 1 an odd number, the hyperelliptic locus meets IS4(l,p) transversely in the Siegel upper half space

The pathogenesis of heart failure (HF) involves compensatory left ventricular hypertrophy. Reactive oxygen species (ROS) are elevated in HF and mediate myocardial hypertrophy. ROS also mediate formation of lipid peroxidation byproducts, yet little is known about their role in promoting hypertrophy. One lipid peroxidation byproduct, 4-hydroxy-trans-2-nonenal (HNE) is a reactive aldehyde that forms covalent adducts on proteins. HNE levels are also elevated in HF and may mediate hypertrophy via HNE-adduct formation. LKB1 - a tumor suppressor protein - regulates cellular growth through activation of the downstream kinase AMPK. Activation of AMPK suppresses functions that consume ATP and simultaneously activates processes to generate energy. The LKB1 protein is inhibited by oxidants, but whether this results in myocardial hypertrophy is unclear. I hypothesized that HNE can directly promote cardiac hypertrophy via the modification of LKB1. In HEK293T cells I observed that HNE adducts inhibit activity of LKB1 through direct oxidative modification. Mutation of LKB1 Lys-96 or Lys-97 resulted in less HNE-LKB1 adduct formation. Mutation of LKB1 Lys-97 prevented the inhibitory effect of HNE, suggesting that HNE-adduction at this residue is sufficient to inhibit LKB1. In cardiomyocytes HNE inhibited both LKB1 and AMPK, increased phosphorylation of mTOR, p70S6K, and S6K, and increased protein synthesis. HNE also activated Erk1/2, which contributed to S6K activation but was not required for cellular growth. Hypertrophic S6K activation was dependent on mTOR. Mice fed a high-fat high-sucrose (HFHS) diet have myocardial hypertrophy that can be prevented by antioxidants. Hearts of HFHS mice have HNE-LKB1 adducts, inhibited LKB1 activity, yet no change in AMPK activation. Mice lacking aldehyde dehydrogenase 2 (ALDH2), an enzyme involved in HNE detoxification, have increased myocardial hypertrophy when fed HFHS diet yet have increased LKB1 activity. In summary HNE directly causes hypertrophy in cardiomyocytes. This occurs through inhibition of LKB1 and in part through Erk1/2 activation. In HFHS-fed mice HNE-LKB1 adduct formation is associated with decreased LKB1 activity. Impairing detoxification of reactive aldehydes in the ALDH2-KO mice is sufficient to increase myocardial hypertrophy, but this appears to be independent of LKB1. This study demonstrates a novel mechanism of cardiac hypertrophy caused by reactive aldehydes.