Thesis (M.Tech.: Chiropractic), Durban Institute of Technology, 2003. / Low back pain is one of the largest known causes of disability in western society. The purpose of this study was to evaluate the relative effectiveness of combined spinal manipulation and interferential current therapy versus combined oral meloxicam and interferential current therapy in the treatment of acute mechanical low back pain. / M

O controle da dor na ortodontia é necessário, pois a movimentação dos elementos dentais por forças específicas causa uma reação inflamatória no periodonto e consequente sensação dolorosa. O controle do processo inflamatório pode alterar a movimentação ortodôntica pela diminuição da irrigação sanguínea do periodonto. Este trabalho prospectivo, duplo-cego randomizado, estudou o efeito do tenoxicam na analgesia preemptiva e na movimentação ortodôntica de caninos superiores. Foram avaliados 36 pacientes submetidos a retrações ortodônticas bilaterais de dentes caninos superiores. Cada lado foi tratado em 3 momentos distintos, totalizando 216 ativações de retração, realizadas altenando-se os lados. O paciente foi seu próprio controle. As retrações foram divididas em três grupos de 24 pacientes cada. No grupo A, foi realizada a retração administrando-se o tenoxicam via oral para controle da dor, quarenta e cinco minutos antes do procedimento e imediatamente após o mesmo houve a administração do placebo. No grupo B, o placebo foi administrado quarenta e cinco minutos antes do procedimento e o tenoxicam imediatamente após o término do mesmo, e no Grupo C os pacientes receberam o placebo tanto antes quanto depois da retração. Esses procedimentos se repetiram em intervalos de 15 dias, totalizando 90 dias de tratamento por paciente. Os pacientes puderam utilizar como resgate o analgésico dipirona sempre que fosse necessário. Questionários contendo a escala analógica visual (EAV), a descritiva de dor (EDD) e uma tabela para controle do consumo de analgésico resgate foram fornecidos após cada procedimento. As movimentações foram executadas pela técnica de Roth (arco reto) com forças padronizadas por um dinamômetro e molas de níquel titânio (NiTi). A quantidade de movimentação foi avaliada por meio de medidas lineares aferidas com um paquímetro. O tenoxicam não influenciou a movimentação dos dentes, uma vez que os resultados obtidos mostraram que a quantidade de movimentação não foi estatisticamente diferente entre os 3 grupos. Os pacientes que receberam o tenoxicam tiveram melhor controle da dor que os pacientes controle, não sendo evidenciado efeito preemptivo neste modelo de dor. Os resultados permitiram concluir que o tenoxicam não demonstrou influência na movimentação ortodôntica de retração de caninos, proporcionando um bom controle de dor ao longo das ativações / Pain control is need in orthodontics because the tooth movements caused by specific forces lead to an inflammatory reaction in the periodontium and a consequent painful sensation. Controlling the inflammatory process may change the orthodontic movement through diminishing the blood irrigation of the periodontium. This doubleblind randomized prospective study investigated the effect of preemptive analgesia using tenoxicam and its influence on upper canine orthodontic movement. Thirty-six patients who underwent bilateral orthodontic retraction of the upper canines were evaluated. Each side was treated on three different occasions, thus totaling 216 retraction activations, which were implemented with alternation between the sides. The patients were themselves the controls. The retractions were divided into three groups of 24 patients each. In group A, the retraction was implemented with tenoxicam administered orally to control the pain intensity, fourty five minutes before the procedure, placebo was then administered immediately after the procedure. In group B, placebo was administered 45 minutes before the procedure and tenoxicam immediately afterwards. In group C, placebo was administered both before and after the procedure. These procedures were repeated at 15-day intervals, thus totaling 90 days of treatment per patient. The patients were allowed to use dipyrone as rescue medication whenever necessary. Questionnaires containing a visual analog scale, a descriptive pain scale and a table for monitoring the rescue medication intake were supplied to the patients after each procedure. The movements were implemented using the Roth technique (straight arch), with forces standardized using a dynamometer and nickel-titanium springs. The amount of movement was evaluated by means of linear measurements using a pachymeter. The tenoxicam did not influence the teeth movement, since the obtained results shown that the amounts of movement did not differ statistically between the three groups. The patients medicated with tenoxicam achieved better pain control than did the patients in the control group, but no preemptive effect was shown in this pain model. The results allow to conclusion that the tenoxicam did not show any influence on the orthodontic movement of canine retraction and it provided good pain control over the course of the activations

Ho Toi Sze Joyce. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 65-74). / Abstracts in English and Chinese. / Acknowledgement --- p.ii / Contents --- p.iii / Abstract --- p.viii / List of Abbreviations --- p.xvii / List of Tables --- p.xix / List of Figures --- p.xx / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- The role of Non-steroidal anti-inflammatory drugs (NSAIDs) --- p.1 / Chapter 1.2 --- NSAID-induced gastrointestinal (GI) toxicity --- p.1 / Chapter 1.2.1 --- Pathogenesis of NSAID-induced GI toxicity --- p.2 / Chapter 1.2.2 --- GI symptoms --- p.4 / Chapter 1.2.3 --- GI ulcers --- p.4 / Chapter 1.2.4 --- GI complications --- p.5 / Chapter 1.2.5 --- Risk factor for GI complications --- p.6 / Chapter 1.2.6 --- Ulcerogenicity of different NSAIDs in upper GI events --- p.6 / Chapter 1.3 --- Prevention of NSAID-induced GI toxicity --- p.7 / Chapter 1.3.1 --- H2-receptor antagonists --- p.8 / Chapter 1.3.2 --- Misoprostol --- p.8 / Chapter 1.3.3 --- Proton Pump Inhibitor (PPI) --- p.9 / Chapter 1.3.4 --- Selective COX-2 Inhibitors --- p.10 / Chapter 1.3.4.1 --- GI safety of selective COX-2 inhibitors --- p.11 / Chapter 1.3.4.1.1 --- Gastrointestinal outcomes research of rofecoxib --- p.13 / Chapter 1.3.4.1.2 --- Celecoxib Long term Arthritis Safety Study --- p.14 / Chapter 1.3.4.2 --- Cardiovascular toxicity of NSAIDs --- p.15 / Chapter 1.3.4.2.1 --- Cardiovascular toxicity of non-selective NSAIDs --- p.15 / Chapter 1.3.4.2.2 --- Cardiovascular toxicity of selective COX-2 inhibitors --- p.16 / Chapter 1.4 --- Guidelines on the management of osteoarthritis (OA) and rheumatoid arthritis (RA) --- p.21 / Chapter 1.4.1 --- American College of Rheumatology (ACR) Subcommittee --- p.22 / Chapter 1.4.2 --- National Institute for Clinical Excellence (NICE) --- p.23 / Chapter 1.4.3 --- Hong Kong Hospital Authority (HA) --- p.23 / Chapter 1.5 --- Cost of illness of upper GI events in the setting of an emergency room of a regional hospital in Hong Kong and cost analysis of selective COX-2 inhibitor with non-selective NSAID plus gastroprotective agent --- p.24 / Chapter 1.6 --- Objectives --- p.25 / Chapter Chapter 2 --- Cost of illness of upper GI events in the setting of an emergency room of a regional hospital in Hong Kong --- p.26 / Chapter 2.1 --- Methods --- p.28 / Chapter 2.1.1 --- Study site --- p.28 / Chapter 2.1.2 --- Cohort participants --- p.28 / Chapter 2.1.3 --- Resource data collection --- p.29 / Chapter 2.1.4 --- Cost data --- p.30 / Chapter 2.1.5 --- Statistical Methods --- p.31 / Chapter 2.1.6 --- Study perspective --- p.31 / Chapter 2.2 --- Results --- p.31 / Chapter 2.2.1 --- Demographic data --- p.31 / Chapter 2.2.2 --- Total direct medical cost of upper GI complaints in UCH --- p.33 / Chapter 2.3 --- Discussion --- p.35 / Chapter 2.3.1 --- Total direct medical cost of upper GI events --- p.35 / Chapter 2.3.2 --- Cost of upper GI events associated with NSAID usage --- p.38 / Chapter 2.3.3 --- Low dose aspirin on NSAID-induced GI toxicity --- p.38 / Chapter 2.3.4 --- Limitation --- p.39 / Chapter 2.3.5 --- Future study --- p.41 / Chapter 2.4 --- Conclusion --- p.41 / Chapter Chapter 3 --- Cost analysis of selective COX-2 inhibitor versus non-selective NSAID with gastroprotective agent --- p.43 / Chapter 3.1 --- Methods --- p.46 / Chapter 3.1.1 --- Local randomized clinical trial --- p.46 / Chapter 3.1.1.1 --- Study population --- p.46 / Chapter 3.1.1.2 --- Cost data --- p.47 / Chapter 3.1.1.3 --- Statistical Methods --- p.48 / Chapter 3.1.1.4 --- Sensitivity analysis --- p.49 / Chapter 3.1.2 --- Large randomized clinical trial --- p.49 / Chapter 3.1.2.1 --- Study population --- p.49 / Chapter 3.1.2.2 --- Cost data --- p.50 / Chapter 3.2 --- Results --- p.50 / Chapter 3.2.1 --- Local randomized clinical trial --- p.51 / Chapter 3.2.1.1 --- Demographic data --- p.51 / Chapter 3.2.1.2 --- Cost analysis --- p.52 / Chapter 3.2.1.3 --- Sensitivity analysis --- p.53 / Chapter 3.2.2 --- Large randomized clinical trial --- p.54 / Chapter 3.2.2.1 --- Demographic data --- p.54 / Chapter 3.2.2.2 --- Cost analysis --- p.55 / Chapter 3.3 --- Discussion --- p.55 / Chapter 3.3.1 --- Cost analysis --- p.55 / Chapter 3.3.2 --- Sensitivity analysis --- p.59 / Chapter 3.3.3 --- Low dose aspirin on NSAID-induced GI toxicity --- p.59 / Chapter 3.3.4 --- Limitation --- p.60 / Chapter 3.4 --- Future study --- p.62 / Chapter 3.5 --- Conclusion --- p.62 / Chapter Chapter 4 --- Conclusion --- p.63 / Chapter Chapter 5 --- Reference --- p.65 / Appendix Data collection form --- p.75

Celecoxib is a COX-2 selective non-steroidal anti-inflammatory drug which has been shown to inhibit growth and induce apoptosis in various cancer cell lines. Using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and an apoptosis detection kit, we demonstrated that celecoxib was able to induce growth inhibition and apoptosis in a dose-dependent manner in 3 NPC cell lines: HK-1, Hone-1, and C666-1. Afterwards, a proteomic approach was used to study the underlying mechanisms involved in celecoxib-mediated effects on two COX-2 positive NPC cell lines (HK-1 and C666-1). Results showed that a total of 18 protein spots were differentially expressed in the HK-1 and C666-1 cells. On the other hand, we also compared the proteomic expression profile between an NPC cell line (C666-1) and a normal nasopharynx cell line (NP69) in order to study whether those differentially expressed proteins after celecoxib treatment were also involved in NPC carcinogenesis. Proteomics results with confirmation using Western blotting discovered that HSP27 phosphorylated of serine 82 (HSP27-pSer82) protein was up-regulated in C666-1 cells when compared with that in NP69 cells. After treatment with celecoxib, expression of HSP27-pSer82 protein was down-regulated in both HK-1 and C666-1 cells. These findings suggest that down-regulation of HSP27-pSer82 protein expression may have mediated the growth-inhibitory effects of celecoxib in HK-1 and C666-1 cells. Finally, other differential expressed proteins identified from proteomics with confirmation by immunocytochemical staining in the 2 NPC cell lines and 40 NPC patient specimens showed that down-regulation of annexin 2 and beta2-tubulin may be important in NPC formation. / COX-2 over-expression has been found in various cancers such as colorectal cancer, liver cancer and lung cancer. In vivo studies have shown that mice overexpressing COX-2 developed breast cancer whereas COX-2 knockout mice had reduced rates of cancer formation in the intestines and skin. In the present study, COX-2 expression in NPC patient biopsies was examined and correlated with the clinicopathological data of the patients. Immunocytochemical staining showed that COX-2 protein was over-expressed in 84.6% (66/78) of non-metastatic NPC patients and was associated with an advanced nodal stage (P<0.05). All these data support an important role for COX-2 in NPC pathogenesis. / In summary, this study is the first to identify HSP27-pSer82 protein as a potential target of celecoxib in NPC cells. Detailed investigations of the functional role of molecular targets identified in this study would improve our understanding of the chemotherapeutic effects of celecoxib and, in the long run, may lead to a more effective chemotherapeutic treatment to this common cancer. / Nasopharyngeal carcinoma (NPC) is prevalent in southern China. Although early stage patients have a high rate of cure with radiotherapy alone, the prognosis for those with stage III or IV disease remains poor due to subsequent development of distant metastases. Therefore there is an urgent need to develop novel biologic agents to improve treatment outcomes. / Chan, Ming Lok. / Adviser: Anthony T.C. Chan. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3418. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 141-171). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

Resumo: Os metabólitos do AA exercem um reconhecido papel na patogênese da doença periodontal. O objetivo deste trabalho foi avaliar o efeito do celecoxib, um inibidor seletivo da enzima cicloxigenase-2 (COX-2), sobre o desenvolvimento de doença periodontal induzida por ligadura em ratos. Após a colocação de ligadura de algodão ao redor dos primeiros molares inferiores direitos, 180 ratos Holtzman foram aleatoriamente subdivididos em 3 grupos experimentais com 60 animais cada, os quais receberam diariamente dose oral de celecoxib 10 mg ou 20 mg/ kg de peso corporal (grupos Ce1 e Ce2, respectivamente) ou, dose oral de 10ml/kg de NaCl a 0,9% (grupo Controle). Aos 3, 5, 10, 18 e 30 dias após o início do experimento, 12 animais de cada grupo experimental foram sacrificados. O tratamento com celecoxib, em ambas as concentrações, reduziu significantemente (p<0.05) a perda óssea alveolar radiográfica aos 5 dias e, diminuiu a intensidade da reabsorção óssea, observada histologicamente, aos 30 dias. Ainda, o celecoxib atrasou o início e, diminui a magnitude, do processo inflamatório agudo. Estes resultados demonstram que a inibição seletiva da COX-2 com o celecoxib, pode interferir com a resposta do tecido periodontal frente à presença de ligadura em ratos. / Abstract: Arachidonic acid metabolites have a recognized role in the pathogenesis of periodontal disease. The purpose of this study was to evaluate the effect of a selective cyclooxygenase-2 (COX-2) inhibitor, celecoxib, on the progression of periodontal disease in a ligature-induced periodontitis model in rats. After ligature placement in the mandibular right first molars, 180, 6-week-old Holtzman rats were ramdomly assigned to one of the following groups of treatment that consisted in a daily oral dose of 10mg/kg body weight of celecoxib (Ce1), 20mg/kg body weight of celecoxib (Ce2) or 10ml/kg of 0,9%NaCl (Control). At 3, 5, 10, 18 and 30 days later, 12 animals of each group were sacrificed. Treatment with celecoxib significantly (p < 0.05) decreased the radiographic bone loss at 5 days of experiment and, decreased the bone loss activity, histologically observed at 30 days. In addition, celecoxib was shown to delay the onset and to suppress the magnitude of the acute inflammatory process. These results show that selective cyclooxygenase-2 (COX-2) inhibition with celecoxib, can interfer with the periodontal tissue response to ligature placement in rats. / Orientador: Luís Carlos Spolidorio / Coorientador: Elcio Marcantonio Junior / Banca: Joni Augusto Cirelli / Banca: Maria Angela Naval Machado / Mestre

No description available.

Abstract not available

Asthma is a chronic inflammatory disease of the airways. Using a murine model which replicates many characteristic features of human asthma, this study evaluated the effects of treatment with anti-inflammatory drugs on the lesions of chronic asthma, and investigated potential underlying molecular mechanisms. Treatment with dexamethasone, a glucocorticoid, was compared with roflumilast, a novel phosphodiesterase-4 (PDE4) inhibitor. BALB/c mice sensitised to ovalbumin were challenged with a low mass concentration of aerosolised antigen for 30 min/day, 3 days/week for 6 weeks. In weeks 5 and 6, groups of animals were treated with either dexamethasone or roflumilast. Assessment included changes in acute-on-chronic inflammation, structural remodelling of the airways and airway hyper-responsiveness to a bronchoconstrictor stimulus. These were correlated with the expression of pro-inflammatory cytokines and growth factors. Compared to vehicle-treated control animals, dexamethasone- and roflumilast-treated mice exhibited reduced accumulation of intra-epithelial eosinophils and chronic inflammatory cells, including CD3+ T-lymphocytes in the airways. Similarly, both drugs inhibited subepithelial fibrosis and airway epithelial thickening, although only dexamethasone inhibited goblet cell hyperplasia/metaplasia. Airway hyper-reactivity was not diminished by either drug. Both treatments suppressed production of Th2 cytokines by ovalbumin-restimulated peribronchial lymph node cells. In selectively dissected airway tissue from vehicletreated animals, increased expression of mRNA for several pro-inflammatory cytokines (TNF-α, GM-CSF, IL-6) and cytokines characteristic of Th1 (IFN-γ), Th2 (IL-5, IL-13)and Th17 (IL-17A) cells was demonstrated using real-time PCR. Enhanced expression of growth factors (TGF-β1 and FGF-2) was also demonstrated in airway epithelium isolated by laser capture microdissection. Interestingly, whereas treatment with dexamethasone significantly inhibited expression of mRNA for all of the inflammationrelated cytokines examined, roflumilast inhibited only IL-17A, TNF-α, GM-CSF and IL-6. Both drugs inhibited mRNA expression of growth factors by epithelial cells. Because roflumilast was as effective as dexamethasone in suppressing inflammation and most changes of remodelling, the selective suppression of IL-17A, TNF-α, GM-CSF and IL-6 suggests that these mediators, or the cells that produce them, may have critical roles in pathogenesis. Furthermore, they may be particularly appropriate therapeutic targets in chronic asthma.

Bibliography: leaves 161-204 / xv, 204 leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (M.D.)--University of Adelaide, Dept. of Medicine and Pathology, 1985

Placental vessels and the umbilical circulatory network function to carry oxygen and nutrients to the fetus. It is at this level that placental lesions such as villitis, obliterative vasculopathy, and thrombotic vasculopathy have been observed in association with fetal inflammatory response syndrome (FIRS) and cerebral palsy. We used human umbilical vein endothelial cells (HUVECs) as a model to study the regulation of inflammation and thrombosis in fetal vessels by microbial products. In this thesis we measured interleukin-8 (IL-8) and tissue factor (TF) expression by HUVECs treated with lipopolysaccharide (LPS), poly (I:C) (PIC), and peptidoglycan (PG). Our results show a profound induction of IL-8 by PIC, a TLR-3 ligand. We also show a moderate induction of tissue factor expression in PIC-treated HUVECs. These results show that HUVECs are exquisitely sensitive to PIC and suggests an important role for viral infection in umbilical vessel inflammation. We additionally treated HUVECs with dexamethasone (DEX), an anti-inflammatory steroid, and melatonin (MT), a pineal gland product with immunomodulatory and anti-oxidant properties. DEX reduced the level of both IL-8 and TF expression in PIC-treated cells. MT, however, further enhanced IL-8 expression in PIC-treated cells. Our results indicate a potential role for glucocorticoid therapy in reducing placental vessel inflammation and thrombosis. Thus, intervention with GC in pregnancies with FIRS may reduce the severity of placental lesions associated with cerebral palsy.