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A para-substituted bis(3-aminopropyl)hexaisobutyl-polyhedral oligomeric silsesquioxane (POSS) was successfully synthesized via a selective corner-opening reaction of 3-aminopropylheptaisobutyl-POSS and a subsequent corner-capping reaction. The selectivity of the corner-opening reaction was studied by density functional theory calculations. Polymerization of the POSS monomer with pyromellitic dianhydride resulted in a yellow, self-standing film.

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A para-substituted bisvinylhexaisobutyl-T8 caged monomer was successfully synthesized via a selective corner-opening reaction of the vinylheptaisobutyl-T8 cage and a subsequent corner-capping reaction.

SummaryIt has been unclear how acute hypoxia at moderate altitude affects stroke volume (SV), an index of cardiac function, during exercise. The present study was conducted to reveal whether acute normobaric hypoxia might alter SV during exercise.Nine healthy male subjects performed maximal exercise testing under normobaric normoxic, and normobaric hypoxic conditions (O 2 : 14.4%) in a randomized order. A novel thoracic impedance method was used to continuously measure SV and cardiac output (CO) during exercise.Acute hypoxia decreased maximal work rate (hypoxia; 247 ± 6 [SE] versus normoxia; 267 ± 8 W, P < 0.005) and VO 2 max (hypoxia; 2761 ± 99 versus normoxia; 3039 ± 133 mL/min, P < 0.005). Under hypoxic conditions, SV and CO at maximal exercise decreased (SV: hypoxia; 145 ± 11 versus normoxia; 163 ± 11 mL, P < 0.05, CO: hypoxia; 26.7 ± 2.1 versus normoxia; 30.2 ± 1.8 L/min, P < 0.05). In acute hypoxia, SV during submaximal exercise at identical work rate decreased. Furthermore, in hypoxia, 4 of 9 subjects attained their highest SV at maximal exercise, while in normoxia, 8 of 9 subjects did.Acute normobaric hypoxia attenuated the increment of SV and CO during exercise, and SV reached a plateau earlier under hypoxia than in normoxia. Cardiac function during exercise at this level of acute normobaric hypoxia might be attenuated. (Int Heart J 2010; 51: 170-175) Key words: Normobaric hypoxia, Cardiac output, Oxygen uptake, Exercise testing D uring ascent to a moderate to high altitude, individuals are exposed to progressive decreases in atmospheric pressure that lead to a reduction in inspired, alveolar, and arterial oxygen pressures. Training at moderate altitude (corresponding to 2000 -3000 m) is associated with relatively severe hypoxemia during submaximal and maximal exercise, 1) and acute hypoxia of this level decreases VO 2 max as well as exercise capacity.2-4) Thus, hypoxia at moderate altitude limits training intensity, which leads to relative deconditioning in elite athletes, although endurance athletes often use hypoxic training to improve sea-level performance. 5) Because VO 2 is the product of cardiac output (CO) and the arterio-venous oxygen content difference (C(a-v)O 2 ), a decrease in VO 2 max at maximal exercise may be due to a decrease of either factor, or both.Acute hypoxia may induce abnormalities in cardiac function and redistribution of CO not only at rest but also during exercise. In an animal study, CO at rest increased during acute severe hypoxia (FiO 2 10% and 5%), and blood flow to all organs increased except for the skin and muscle.6) In humans under acute hypoxia, heart rate (HR) and CO increase while systemic vascular resistance decreases. 7)Echocardiography also reveals altered mitral flow patterns, suggestive of mild LV diastolic dysfunction.8) Subacute hypoxia (FiO 2 12%, simulating an altitude of approximately 4000 m) induced mild diastolic dysfunction in young healthy individuals. 9)Stroke volume (SV) increases as the work rate increases at low to moderate intensity exercise, ...

We prepared two types of polyimides containing T8 cages in the main chains by polymerization of para-substituted bis(3-aminopropyl)hexaisobutyl-substituted T8 cage, and studied their mechanical, thermal, and optical properties.

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We aimed to determine the responses of salivary secretory immunoglobulin A (SIgA) and the incidence of upper respiratory tract infections (URTI) symptoms among elite speed skaters during an actual competition period. The subjects were 8 international-class elite speed skaters. Saliva samples were obtained 3, 2, and 1 days before the race, the day of the race, and 1 day after the race. Salivary secretory immunoglobulin A concentration was measured by enzyme immunoassay, and SIgA secretion rate was calculated. A visual analogue scale was used to subjectively assess fatigue and tension. Daily URTI symptoms were recorded by using a questionnaire. There was no statistically significant difference in the saliva flow rate (p = 0.69), SIgA concentration (p = 0.07), and subjective fatigue (p = 0.07) during the competition period. The SIgA secretion rate recorded for the day of the race was significantly high compared with that of 3 and 2 days before and 1 day after the race (p < 0.05). The subjective tension recorded on the race day was significantly high compared with that for 3, 2, and 1 days before the race (p < 0.05). Two subjects exhibited URTI symptoms after the race. These findings suggest that salivary SIgA in elite speed skaters increased after a tapering period and that an actual high-intensity speed skating race decreased salivary SIgA in elite speed skaters. These data also suggest that the incidence of URTI symptoms might be related to the SIgA level. Coaches may need to take precautions after competitions to minimize their athletes' contact with cold viruses and adjust training load for a few days after competition to improve the decreased mucosal immune function.