Aim:  To evaluate the ability of high‐energy ultraviolet A (UVA) light‐emitting diode (LED) to inactivate bacteria in water and investigate the inactivating mechanism of UVA irradiation. Methods and Results:  We developed a new disinfection device equipped with high‐energy UVA‐LED. Inactivation of bacteria was determined by colony‐forming assay. Vibrio parahaemolyticus, enteropathogenic Escherichia coli, Staphylococcus aureus and Escherichia coli DH5α were reduced by greater than 5‐log10 stages within 75 min at 315 J cm−2 of UVA. Salmonella enteritidis was reduced greater than 4‐log10 stages within 160 min at 672 J cm−2 of UVA. The formation of 8‐hydroxy‐2′‐deoxyguanosine in UVA‐LED irradiated bacteria was 2·6‐fold higher than that of UVC‐irradiated bacteria at the same inactivation level. Addition of mannitol, a scavenger of hydroxyl radicals (OH˙), or catalase, an enzyme scavenging hydrogen peroxide (H2O2) to bacterial suspensions significantly suppressed disinfection effect of UVA‐LED. Conclusion:  This disinfection system has enough ability to inactivate bacteria and OH˙ and H2O2 participates in the disinfection mechanism of UVA irradiation. Significance and Impact of the Study:  We newly developed UVA irradiation system and found that UVA alone was able to disinfect the water efficiently. This will become a useful disinfection system.

Ultraviolet (UV) irradiation is an effective disinfection method. In sterilization equipment, a low-pressure mercury lamp emitting an effective germicidal UVC (254 nm) is used as the light source. However, the lamp, which contains mercury, must be disposed of at the end of its lifetime or following damage due to physical shock or vibration. We investigated the suitability of an ultraviolet light-emitting diode at an output wavelength of 365 nm (UVA-LED) as a sterilization device, comparing with the other wavelength irradiation such as 254 nm (a low-pressure mercury lam) and 405 nm (LED). We used a commercially available UVA-LED that emitted light at the shortest wavelength and at the highest output energy. The new sterilization system using the UVA-LED was able to inactivate bacteria, such as Escherichia coli DH5 alpha, Enteropathogenic E. coli, Vibrio parahaemolyticus, Staphylococcus aureus, and Salmonella enterica serovar Enteritidis. The inactivations of the bacteria were dependent on the accumulation of UVA irradiation. Taking advantage of the safety and compact size of LED devices, we expect that the UVA-LED sterilization device can be developed as a new type of water sterilization device.

Ouabain-insensitive, furosemide-sensitive Rb+ influx (JRb) into HeLa cells was examined as functions of the extracellular Rb+, Na+ and Cl- concentrations. Rate equations and kinetic parameters, including the apparent maximum JRb, the apparent values of Km for the three ions and the apparent Ki for K+, were derived. Results suggested that one unit molecule of this transport system has one Na+, one K+ and two Cl- sites with different affinities, one of the Cl- sites related with binding of Na+, and the other with binding of K+(Rb+). A 1:1 stoichiometry was demonstrated between ouabain-insensitive, furosemide-sensitive influxes of 22Na+ and Rb+, and a 1:2 stoichiometry between those of Rb+ and 36Cl-. The influx of either one of these ions was inhibited in the absence of any one of the other two ions. Monovalent anions such as nitrate, acetate, thiocyanate and lactate as substitutes for Cl- inhibited ouabain-insensitive Rb+ influx, whereas sulfamate and probably also gluconate did not inhibit JRb. From the present results, a general model and a specialized cotransport model were proposed: In HeLa cells, one Na+ and one Cl- bind concurrently to their sites and then one K+(Rb+) and another Cl- bind concurrently. After completion of ion bindings Na+, K+(Rb+) and Cl- in a ratio of 1:1:2 show synchronous transmembrane movements.

The effect of exposure to extremely low frequency-electromagnetic field (ELF-EMF: 3 mT, 60 Hz) on differentiation of mouse osteoblast-like MC3T3-E1 cells was examined together with addition of insulin-like growth factor I (IGF-I). As a marker of the differentiation, the cellular collagen content was determined by the absorbance of Sirius red-stained cells measured at the wavelength of 510-520 nm with an imaging microspectroscopy. Exposure to ELF-EMF increased significantly the collagen in the cells. Treatment with PD98059, an inhibitor of extracellular signal-regulated kinase 1/2 (ERK1/2) activation, reduced the collagen in all of the cells examined on control, IGF-I addition and ELF-EMF exposure, however, PD98059 did not prevent the increase in the collagen caused by ELF-EMF exposure, and IGF-I also increased the collagen in the presence of the inhibitor. When phosphatidylinositol 3-kinase (PI3K) pathway was inhibited by LY294002, the increase in collagen induced by ELF-EMF exposure was accelerated, however, the increase in collagen observed by IGF-I addition was suppressed. Treatment with SB203580, an inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), suppressed the increase in the collagen induced by ELF-EMF exposure, whereas IGF-I addition increased the collagen in the presence of the inhibitor. These results suggested that collagen synthesis stimulated by ELF-EMF exposure was carried out by the participation of p38 MAPK pathway, and that PI3K pathway may have the role to suppress the collagen synthesis induced by ELF-EMF exposure, and that the suppression of the PI3K pathway may allow the acceleration of the collagen synthesis.

Cerebral blood volume flow and flow velocity have been reported to increase during dynamic exercise, but whether the two increase in parallel and whether both increases occur as functions of exercise intensity remain unsettled. In this study, blood flow velocity in the common carotid artery was measured using the Doppler ultrasound method in eight healthy male students during graded treadmill exercise. The exercise consisted of stepwise progressive increases and decreases in exercise intensity. The peak intensity corresponded to approximately 85% of maximal oxygen consumption. During this exercise, the heart rate (fc), mean blood pressure (BP) in the brachial artery and mean blood flow velocity (vcc) in the common carotid artery increased as functions of exercise intensity. At the peak exercise intensity, fc, BP and vcc increased by 134.5%, 20.5% and 51.8% over the control levels before exercise (P < 0.01), respectively. The resistance index (RI) and pulsatility index (PI) were determined from the velocity profile and were expected to reflect the distal cerebral blood flow resistance. The RI and PI increased during the graded exercise, but tended to decrease at the highest levels of exercise intensity. As vcc increased with increases in exercise intensity it would be expected that cerebral blood flow would also increase at these higher intensities. It is also suggested that blood flow velocity in the cerebral artery does not proportionately reflect the cerebral blood flow during dynamic exercise, since the cerebral blood flow resistance changes.