No description available.

This research is concerned specifically with the growth of two selected algae found surviving in chlorinated water in outdoor swimming pools. Unialgal cultures were used to determine the free chlorine residuals that these algae were able to tolerate.

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

published_or_final_version / Pharmacology / Doctoral / Doctor of Philosophy

published_or_final_version / Pharmacology / Master / Master of Philosophy

Lactic acid, which induces pH depression, leads to ATP efflux from muscle to extracellular space: it was reported that CFTR was involved in this process. However, the mechanism by which lactic acid activated CFTR and brought about the ATP release is still unknown. This study was performed to investigate (1) what channels may be involved or even conduct ATP release, and (2) how lactic acid activated CFTR. Expression of the possible channels that may conduct ATP release in L6 cells was investigated using RT-PCR: ClC-2, ClC-3, ClC-7, CACC, VDAC, connexin 40, connexin 43 and pannexin 3 were expressed in L6. Incubation of cultured L6 cells with lactic acid (10 mM) increased the extracellular ATP from 0.6 ± 0.06 to 1.1 ± 0.09 nM (P ? 0.05), indicating that lactic acid stimulated ATP efflux in vitro. The non-specific chloride channel inhibitor, DIDS, failed to abolish the lactic-acid-induced ATP release, suggesting that DIDS-sensitive chloride channels were not involved in the ATP efflux. Among the non-specific inhibitors of connexin channels, gadolinium inhibited acidosis-induced ATP efflux, but carbenoxolone failed to inhibit it, and so the role of connexins remains uncertain. The specific inhibitor of CFTR, CFTRinh-172, and the non-specific open-channel blocker of CFTR, glibenclamide, both abolished the acidosis-induced ATP release, but another specific inhibitor of CFTR, GlyH-101, which blocks CFTR from the external side, failed to abolish the ATP release, suggesting that acidosis-induced ATP is dependent on CFTR-activation, but does not involve ATP moving through the CFTR chloride channel. We hypothesize that, at low pH, the Na+/H+ exchanger (NHX) extruded H+ out of the cell and the resulting intracellular Na+ was transported out by Ca2+/Na+ exchanger (NCX); the localized increase in Ca2+ activated adenyl cyclase (AC), thus elevating intracellular cAMP; cAMP-activated-PKA then phosphorylated CFTR, which regulated an ATP release channel. KT-5720, an inhibitor of PKA, abolished the acidosis-induced ATP release, and forskolin, an agent that elevates cAMP, stimulated it, suggesting that the cAMP/PKA pathway was involved. The specific inhibitor of NCX, SN-6 and KB-R7943, both abolished the acidosis-induced ATP release, supporting a role for NCX in mediating this process. However, amiloride, the non-specific inhibitor of NHX failed to abolish ATP efflux. The whole cell Cl- currents were studied in L6 cells: lactic acid increased the whole cell currents from 2.33 ± 0.10 to 3.54 ± 0.34 nA (P ? 0.05), and this lactic-acid-induced increase in Cl- current could be inhibited by CFTRinh-172, suggesting that the CFTR Cl- channel was opened at low pH. Moreover, forskolin increased whole cell Cl- currents, which supported a role for the cAMP/PKA pathway in the lactic-acid-induced increase in CFTR current. These data confirm that CFTR is involved in the lactic-acid-induced ATP release from L6 cells. The roles of the NCX and cAMP/PKA pathway in activating CFTR at low pH are supported, but further studies are required to determine whether the NHX is involved in CFTR activation and whether connexins participate in ATP release. / published_or_final_version / Physiology / Master / Master of Philosophy

published_or_final_version / Pharmacology / Doctoral / Doctor of Philosophy

Twenty-one male subjects volunteered to participate in this study of the effects of an u1tramarathon run under competitive conditions. Selected anthropometric measurements were made before and after the race. Blood samples were taken before, and within 10 min. of completing the race. Haematocrit and cortisol concentrations were analysed from each sample. Three ratings of perceived exertion (RPE) - local, central and overall, were obtained at two-hourly intervals throughout the race. The shortened form of the Eysenck Personality Inventory (EPI) was administered before the race. The Profile of Mood States (POMS) test was completed both before and immediately after the race. The average running intensity was estimated to be about 32% VO₂max which would not have caused major lactate accumulation. Repetitive compressive forces as a result of heel-strike resulted in intervertebral disc fluid loss. This resulted in a significant (p<0.05) decrease in stature after the race. Mobilization of glycogen, trig1ycerides and protein for metabolism as well as fluid loss via sweat resulted in significantly decreased body mass after the race. Plasma volume and serum cortisol concentrations were significantly increased after the race compared to pre-race baseline levels. Local RPE responses were dominant throughout the entire race, followed by overall RPE. Running 160 km had an effect on mood state. "Depression", "fatigue" and "confusion" (profile of Mood states) were all significantly increased compared to pre-race scores. Sleep deprivation as a result of running through the night was probably an important contributing factor. The anthropometric profile of the ultramarathon runners in this sample was more like that of the general population than elite marathon runners from the literature. The ultramarathon runners were more extroverted than elite marathon runners, but exhibited a similar Profile of Mood state before the race. The stressor - running 160 km - resulted in a 'strain response'. This was evident in the decreased stature and mass, and increased serum cortisol, "depression", "confusion" and above all "fatigue".

Made available in DSpace on 2014-06-11T19:26:40Z (GMT). No. of bitstreams: 0 Previous issue date: 2012-02-28Bitstream added on 2014-06-13T20:54:58Z : No. of bitstreams: 1 macedo_ac_me_botfca.pdf: 374862 bytes, checksum: cdd44a701a245c0b3d70c50804f7e207 (MD5) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Os fungicidas até pouco tempo eram usados exclusivamente para o controle de doença, no entanto observações de efeitos fisiológicos trouxeram um novo conceito para o uso desses produtos. As estrobilurinas possuem efeitos fisiológicos positivos no rendimento das culturas, devido ao aumento da fotossíntese líquida e melhor balanço hormonal. Já o boscalida complementa a ação desses fungicidas, aplicado alternadamente ou em conjunto. O presente trabalho teve como objetivo avaliar o efeito da aplicação de piraclostrobina, azoxistrobina e boscalida em plantas de melão rendilhado (Cucumis melo var. reticulatus), em condições de ambiente protegido, visando seus efeitos fisiológicos no metabolismo e desenvolvimento da planta, bem como no aumento da produção e qualidade dos frutos. O experimento foi conduzido em área experimental da Faculdade de Ciências Agronômicas da Universidade Estadual Paulista, Campus de Botucatu-SP em ambiente protegido. O delineamento experimental foi em blocos ao acaso com cinco tratamentos: uma testemunha e quatro aplicações de fungicidas: azoxistrobina 60g ha-1, boscalida 75g ha-1, piraclostrobina 50 g ha-1, boscalida (37,5g ha-1) + piraclostrobina (25 g ha-1), aplicados 14 dias após o transplante, a intervalo de 7 dias, via foliar. O efeito dos tratamentos foi avaliado através das observações das seguintes características: trocas gasosas, eficiência do uso da água, índice SPAD na folha, atividade das enzimas nitrato redutase, peroxidase, catalase e superóxido dismutase (SOD) e na pós colheita dos frutos de melão rendilhado. Em função dos resultados obtidos, pode-se concluir que os fungicidas testados apresentam efeitos fisiológicos positivos na cultura do melão rendilhado. As plantas tratadas com boscalida obtiveram um incremento positivo na taxa de assimilação de CO2 além... / The fungicides were until recently used exclusively for disease control, however observations of physiological effects brought a new concept to the use of these products. The strobilurins have positive physiological effects on crop yields, due to increased net photosynthesis and better hormonal balance. On the other hand, boscalida complements the action of these fungicides, applied alternately or together. This study aimed on evaluating the effect of pyraclostrobin, azoxystrobin and boscalida in plants of net melon (Cucumis melo var. Reticulatus) under conditions of protected environment, aiming its physiological effects on metabolism and plant development, as well as increased production and fruit quality. The experiment was conducted in the experimental area of the College of Agricultural Sciences, Universidade Estadual Paulista, Campus of Botucatu in a protected environment. The experimental design was randomized blocks with five fungicide treatments: control, 60 g azoxystrobin ha-1, 75 g ha-1 boscalid, pyraclostrobin 50 g ha-1, boscalid (37.5 g ha-1) + pyraclostrobin (25 g ha -1), applied on the leaves, 14 days after transplantation in an interval of 7 days. The treatment effect was evaluated by the following observations: gas exchange, water use efficiency, chlorophyll index, activity of the enzymes nitrate reductase, peroxidase, catalase and superoxide dismutase (SOD) and post-harvest of the fruits of net melon. According to the results obtained, it could be concluded that the fungicide that were tested have positive physiological effects on the culture of net melon. Plants treated with boscalida had a positive increase in the rate of CO2 assimilation and also a positive influence on the chlorophyll content of the leaves. The fruits from these plants had greater mass apart from higher content of soluble... (Complete abstract click electronic access below)