3 resultados para bandwidth 2.0 GHz to 2.45 GHz

em Brock University, Canada


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The optical cross section of PS I in whole cells of Porphyridium cruentum (UTEX 161), held in either state 1 or state 2, was determined by measuring the change in absorbance at 820nm, an indication of P700+; the X-section of PS2 was determined by measuring the variable fluorescence, (Fv-Fo)/Fo, from PS2. Both cross-sections were 7 determined by fitting Poisson distribution equations to the light saturation curves obtained with single turnover laser flashes which varied in intensity from zero to a level where maximum yield occurred. Flash wavelengths of 574nm, 626nm, and 668nm were used, energy absorbed by PBS, by PBS and chla, and by chla respectively. There were two populations of both PSi and PS2. A fraction of PSi is associated with PBS, and a fraction of PS2 is free from PBS. On the transition S1->S2, only with PBS-absorbed energy (574nm) did the average X-section of PSi increase (27%), and that of PS2 decrease (40%). The fraction of PSi associated with PBS decreased, from 0.65 to 0.35, and the Xsection of this associated PS 1 increased, from 135±65 A2 to 400±300A2. The cross section of PS2 associated with PBS decreased from 150±50 A2 to 85±45 A2, but the fraction of PS2 associated with PBS, approximately 0.75, did not change significantly. The increase in PSi cross section could not be completely accounted for by postulating that several PSi are associated with a single PBS and that in the transition to state2, fewer PSi share the same number of PBS, resulting in a larger X-section. It is postulated that small changes occur in the attachment of PS2 to PBS causing energy to be diverted to the attached PSi. These experiments support neither the mobile-PBS model of state transitions nor that of spillover. From cross section changes there was no evidence of energy transfer from PS2 to PSi with 668nm light. The decrease in PS2 fluorescence which occurred at this wavelength cannot be explained by energy transfer; another explanation must be sought. No explanation was found for an observed decrease in PSi yield at high flash intensities.

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The crystal structure of Cu(PM)2(N03hoH20 (where PM is pyridoxamine, CSHI2N202) has been determined from three dimensional x-ray diffraction data. The crystals are triclinic, space group pI, a = 14.248 (2), b = 8.568 (1), c = 9.319 (1) 1, a = 94.08 (1), e = 89.73 (1), y~~ 99.18 (1)°, z = 2, jl(MoK) = 10.90 em-I, Po = 1.61 g/cm3 and Pc = 1.61 g/em3• The structure a was solved by Patterson techniques from data collected on a Picker 4-circle diffractometer to 26max = 45°. All atoms, including hydrogens, have been located. Anisotropic thermal parameters have been refined for all nonhydrogen atoms. For the 2390 independent reflections with F ? 3cr(F) , R = 0.0408. The results presented here provide the first detailed structural information of a metal complex with PM itself. The copper atoms are located on centres of symmetry and each is chela ted by two PM zwitterions through the amino groups and phenolate oxygen atoms. The zwitterionic form found in this structure involves the loss of a proton from the phenolate group and protonation of the pyridine ring nitrogen atoms. The two independent Cu(PM)2 moieties are symmetrically bridged by a single oxygen atom from one of the nitrate groups. The second nitrate group is not coordinated to the copper atoms but is central to an extensive hydrogen bonding network involving the water molecule and uncoordinated functional groups of PM.

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Introduction: The prevalence of coronary artery disease (CAD) is ever increasing in western industrialized societies. An individuals overall risk for CAD may be quantified by integrating a number of factors including, but not limited to, cardiorespiratory fitness, body composition, blood lipid profile and blood pressure. It might be expected that interventions aimed at improving any or all of these independent factors might improve an individual 's overall risk. To this end, the influence of standard endurance type exercise on cardiorespiratory fitness, body composition, blood lipids and blood pressure, and by extension the reduction of coronary risk factors, is well documented. On the other hand, interval training (IT) has been shown to provide an extremely powerful stimulus for improving indices of cardiorespiratory function but the influence of this training type on coronary risk factors is unknown. Moreover, the vast majority of studies investigating the effects of IT on fitness have used laboratory type training protocols. As a result of this, the influence of participation in interval-type recreational sports on cardiorespiratory fitness and coronary risk factors is unknown. Aims: The aim of the present study was to evaluate the effectiveness of recreational ball hockey, a sport associated with interval-type activity patterns, on indices of aerobic function and coronary risk factors in sedentary men in the approximate age range of 30 - 60 years. Individual risk factors were compiled into an overall coronary risk factor score using the Framingham Point Scale (FPS). Methods: Twenty-four sedentary males (age range 30 - 60) participated in the study. Subject activity level was assessed apriori using questionnaire responses. All subjects (experimental and control) were assessed to have been inactive and sedentary prior to participation in the study. The experimental group (43 ± 3 years; 90 ± 3 kg) (n = 11) participated in one season of recreational ball hockey (our surrogate for IT). Member of this group played a total of 16 games during an 11 week span. During this time, the control group (43 ± 2 years; 89 ± 2 kg) (n = 11) performed no training and continued with their sedentary lifestyle. Prior to and following the ball hockey season, experimental and control subjects were tested for the following variables: 1) cardiorespiratory fitness (as V02 Max) 2) blood lipid profile 3) body composition 5) waist to hip ratio 6) blood glucose levels and 7) blood pressure. Subject V02 Max was assessed using the Rockport submaximal walking test on an indoor track. To assess body composition we determined body mass ratio (BMI), % body fat, % lean body mass and waist to hip ratio. The blood lipid profile included high density lipoprotein, low density lipoprotein and total cholesterol levels; in addition, the ratio of total cholesterol to high density was calculated. Blood triglycerides were also assessed. All data were analyzed using independent t - tests and all data are expressed as mean ± standard error. Statistical significance was accepted at p :S 0.05. Results: Pre-test values for all variables were similar between the experimental and control group. Moreover, although the intervention used in this study was associated with changes in some variables for subjects in the experimental group, subjects in the control group did not exhibit any changes over the same time period. BODY COMPOSITION: The % body fat of experimental subjects decreased by 4.6 ± 0.5%, from 28.1 ± 2.6 to 26.9 ± 2.5 % while that of the control group was unchanged at 22.7 ± 1.4 and 22.2 ± 1.3 %. However, lean body mass of experimental and control subjects did not change at 64.3 ± 1.3 versus 66.1 ± 1.3 kg and 65.5 ± 0.8 versus 64.7 ± 0.8 kg, respectively. In terms of body mass index and waist to hip ratio, neither the experimental nor the control group showed any significant change. Respective values for the waist to hip ratio and body mass index (pre and post) were as follows: 1 ± 0.1 vs 0.9 ± 0.1 (experimental) and 0.9 ± 0.1 versus 0.9 ± 0.1 (controls) while for BMI they were 29 ± 1.4 versus 29 ± 1.2 (experimental) and 26 ± 0.7 vs. 26 ± 0.7 (controls). CARDIORESPIRATORY FITNESS: In the experimental group, predicted values for absolute V02 Max increased by 10 ± 3% (i.e. 3.3 ± 0.1 to 3.6 ± 0.1 liters min -1 while that of control subjects did not change (3.4 ± 0.2 and 3.4 ± 0.2 liters min-I). In terms of relative values for V02 Max, the experimental group increased by 11 ± 2% (37 ± 1.4 to 41 ± 1.4 ml kg-l min-I) while that of control subjects did not change (41 ± 1.4 and 40 ± 1.4 ml kg-l min-I). BLOOD LIPIDS: Compared to pre-test values, post-test values for HDL were decreased by 14 ± 5 % in the experiment group (from 52.4 ± 4.4 to 45.2 ± 4.3 mg dl-l) while HDL data for the control group was unchanged (49.7 ± 3.6 and 48.3 ± 4.1 mg dl-l, respectively. On the other hand, LDL levels did not change for either the experimental or control group (110.2 ± 10.4 versus 112.3 ± 7.1 mg dl-1 and 106.1 ± 11.3 versus 127 ± 15.1 mg dl-1, respectively). Further, total cholesterol did not change in either the experimental or control group (181.3 ± 8.7 mg dl-1 versus 178.7± 4.9 mg dl-l) and 190.7 ± 12.2 versus 197.1 ± 16.1 mg dl-1, respectively). Similarly, the ratio of TC/HDL did not change for either the experimental or control group (3.8 ± 0.4 versus 4.5 ± 0.5 and 4 ± 0.4 versus 4.2 ± 0.4, respectively). Blood triglyceride levels were also not altered in either the experimental or control group (100.3 ± 19.6 versus 114.8 ± 15.3 mg dl-1 and 140 ± 23.5 versus 137.3 ± 17.9 mg dl-l, respectively). BLOOD GLUCOSE: Fasted blood glucose levels did not change in either the experimental or control group. Pre- and post-values for experimental and control groups were 92.5 ± 4.8 versus 93.3 ± 4.3 mg dl-l and 92.3 ± 11.3 versus 93.2 ± 2.6 mg dl-1 , respectively. BLOOD PRESSURE: No aspect of blood pressure was altered in either the experimental or control group. For example, pre- and post-test systolic blood pressures were 131 ± 2 versus 129 ± 2 mmHg (experimental) and 123 ± 2 and 125 ± 2 mmHg (controls), respectively. Pre- and post-test diastolic blood pressures were 84 ± 2 and 83 ± 2 mmHg (experimental) and 81 ± 1 versus 82 ± 1 mmHg, respectively. Similarly, calculated pulse pressure was not altered in the experimental or control as pre- and post-test values were 47 ± 1 versus 47 ± 2 mmlHg and 42 ± 2 versus 43 ± 2 mmHg, respectively. FRAMINGHAM POINT SCORE: The concerted changes reported above produced an increased risk in the Framingham Point Score for the subjects in the experimental group. For example, the pre- and post-test FPS increased from 1.4 ± 0.9 to 2.7 ± 0.7. On the other hand, pre- and post-test scores for the control group were 1.8 ± 1 versus 1.8 ± 0.9. Conclusions: Our data confirms previous studies showing that interval-type exercise is a useful intervention for increasing aerobic fitness. Moreover, the increase in V02 Max we found in response to limited participation in ball hockey (i.e. 16 games) suggests that recreational sport may help reduce this aspect of coronary risk in previously sedentary individual. On the other hand, our results showing little or no positive change in body composition, blood lipids or blood pressures suggest that one season of recreational sport in not in of itself a powerful enough stimulus to reduce the overall risk of coronary artery disease. In light of this, it is recommended that, in addition to participation in recreational sport, the performance of regular physical activity is used as an adjunct to provide a more powerful overall stimulus for decreasing coronary risk factors. LIMITATIONS: The increase in the FPS we found for the experimental group, indicative of an increased risk for coronary disease, was largely due to the large decrease in HDL we observed after compared to above one season of ball hockey. In light of the fact that cardiorespiratory fitness was increased and % body fat was decreased, as well as the fact that other parameters such as blood pressure showed positive (but non statistically significant) trends, the possibility that the decrease in HDL showed by our data was anomalous should be considered. FUTURE DIRECTIONS: The results of this study suggesting that recreational sport may be a potentially useful intervention in the reduction of CAD require to be corroborated by future studies specifically employing 1) more rigorous assessment of fitness and fitness change and 2) more prolonged or frequent participants.