Inactivation of Escherichia coli and bacteriophage T4 by high levels of dissolved CO2

Little information is available regarding the effectiveness of water disinfection by CO₂ at low pressure. The aim of this study was to evaluate the use of high levels of dissolved CO₂ at 0.3–0.6 MPa for the inactivation of microorganisms. Bacteriophage T4 was chosen as the model virus and Escherichia coli was selected as the representative bacterium. The results of the study showed a highly effective log inactivation of E. coli and bacteriophage T4 at low and medium initial concentrations by high levels of dissolved CO₂ at 0.3 MPa with a treatment time of 20 min. When the pressure was increased to 0.6 MPa, inactivation of both microorganisms at high initial concentrations was improved to different extents. Neither pressurized air nor O₂ effectively inactivated both E. coli and bacteriophage T4. The pH was not a key factor affecting the inactivation process by this method. The results of scanning electron microscopy of E. coli and transmission electron microscopy of bacteriophage T4 suggested that “CO₂ uptake at high pressure and bursting of cells by depressurization” were the main reasons for lethal effect on microorganisms. This technology has potential for application in the disinfection of water, wastewater, and liquid food in the future.     

Corneal damage and lacrimal gland dysfunction in a smoking rat model

Smoking is a serious public health problem around the world and causes many diseases such as chronic obstructive pulmonary disease, lung cancer, and some eye diseases. Cytochrome P450s (CYPs) are xenobiotic-metabolizing enzymes and are distributed in the corneas, protecting the ocular surface against chemical compounds in the environment. Although CYPs are principally detoxification enzymes, CYP1A1 and CYP2A6 are known to participate in the induction of lung cancer by smoking. We studied the participation of CYPs in corneal dysfunction caused by exposure to mainstream cigarette smoke (MCS) in a smoking rat model. Six-week-old male Sprague-Dawley rats were exposed to MCS. Exposure to MCS caused corneal damage and lacrimal gland dysfunction. Immunohistochemical analysis revealed that CYP1A1 expression was upregulated in the corneal epithelium and ducts of the lacrimal glands, accompanied by an increase in production of reactive oxygen species (ROS). An increase in 8-hydroxy-2'-deoxyguanosine, which is a marker of oxidative DNA damage, was detected only in areas where CYP1A1 was expressed, whereas the level of hexanoyl-lysine adduct, which is an initial marker of oxidative damage of phospholipids, did not increase. Exposure to MCS damaged the corneas and lacrimal glands probably through DNA oxidation by ROS produced by CYP1A1. Although the influence of other components in MCS remains unclear, CYPs, especially CYP1A1, probably participate in corneal damage and lacrimal gland dysfunction induced by smoking.     

Up-regulation of ceramide glucosyltransferase during the differentiation of U937 cells

The phorbol ester tetradecanoylphorbol acetate (TPA) induces promyelocytic leukaemia cells to differentiate to macrophage-like cells in vitro. During the course of this differentiation, the cells adhere to the bottom of the culture dish, a process that requires an increase in cell surface glycosphingolipids (GSLs). We examined the cellular content of glucosylceramide (GlcCer), the simplest of the GSLs, in a TPA-treated leukaemia cell line, U937. Following TPA treatment, we observed a 3.5-fold increase in GlcCer levels that was caused by enhanced activity of ceramide glucosyltransferase (GlcT-1), which catalyses ceramide glycosylation. Furthermore, in TPA-treated cell GlcT-1 amounts were increased at both the mRNA and protein levels. We also found decreased activity of lactosylceramide synthase in TPA-treated cells, which could also contribute to the increase in cellular GlcCer content.     

Effectiveness of a red-visor cap for preventing light-induced melatonin suppression during simulated night work

Bright light at night improves the alertness of night workers. Melatonin suppression induced by light at night is, however, reported to be a possible risk factor for breast cancer. Short-wavelength light has a strong impact on melatonin suppression. A red-visor cap can cut the short-wavelength light from the upper visual field selectively with no adverse effects on visibility. The purpose of this study was to investigate the effects of a red-visor cap on light-induced melatonin suppression, performance, and sleepiness at night. Eleven healthy young male adults (mean age: 21.2±0.9 yr) volunteered to participate in this study. On the first day, the subjects spent time in dim light (<15 lx) from 20:00 to 03:00 to measure baseline data of nocturnal salivary melatonin concentration. On the second day, the subjects were exposed to light for four hours from 23:00 to 03:00 with a nonvisor cap (500 lx), red-visor cap (approx. 160 lx) and blue-visor cap (approx. 160 lx). Subjective sleepiness and performance of a psychomotor vigilance task (PVT) were also measured on the second day. Compared to salivary melatonin concentration under dim light, the decrease in melatonin concentration was significant in a nonvisor cap condition but was not significant in a red-visor cap condition. The percentages of melatonin suppression in the nonvisor cap and red-visor cap conditions at 4 hours after exposure to light were 52.6±22.4% and 7.7±3.3%, respectively. The red-visor cap had no adverse effect on performance of the PVT, brightness and visual comfort, though it tended to increase subjective sleepiness. These results suggest that a red-visor cap is effective in preventing melatonin suppression with no adverse effects on vigilance performance, brightness and visibility.     

Dietary deficiency of essential amino acids rapidly induces cessation of the rat estrous cycle

Reproductive functions are regulated by the sophisticated coordination between the neuronal and endocrine systems and are sustained by a proper nutritional environment. Female reproductive function is vulnerable to effects from dietary restrictions, suggesting a transient adaptation that prioritizes individual survival over reproduction until a possible future opportunity for satiation. This adaptation could also partially explain the existence of amenorrhea in women with anorexia nervosa. Because amino acid nutritional conditions other than caloric restriction uniquely alters amino acid metabolism and affect the hormonal levels of organisms, we hypothesized that the supply of essential amino acids in the diet plays a pivotal role in the maintenance of the female reproductive system. To test this hypothesis, we examined ovulatory cyclicity in female rats under diets that were deficient in threonine, lysine, tryptophan, methionine or valine. Ovulatory cyclicity was monitored by daily cytological evaluations of vaginal smears. After continuous feeding of the deficient diet, a persistent diestrus or anovulatory state was induced most quickly by the valine-deficient diet and most slowly by the lysine-deficient diet. A decline in the systemic insulin-like growth factor 1 level was associated with a dietary amino acid deficiency. Furthermore, a paired group of rats that were fed an isocaloric diet with balanced amino acids maintained normal estrous cyclicity. These disturbances of the estrous cycle by amino acid deficiency were quickly reversed by the consumption of a normal diet. The continuous anovulatory state in this study is not attributable to a decrease in caloric intake but to an imbalance in the dietary amino acid composition. With a shortage of well-balanced amino acid sources, reproduction becomes risky for both the mother and the fetus. It could be viewed as an adaptation to the diet, diverting resources away from reproduction and reallocating them to survival until well-balanced amino acid sources are found.     

P301S mutant human tau transgenic mice manifest early symptoms of human tauopathies with dementia and altered sensorimotor gating

Tauopathies are neurodegenerative disorders characterized by the accumulation of abnormal tau protein leading to cognitive and/or motor dysfunction. To understand the relationship between tau pathology and behavioral impairments, we comprehensively assessed behavioral abnormalities in a mouse tauopathy model expressing the human P301S mutant tau protein in the early stage of disease to detect its initial neurological manifestations. Behavioral abnormalities, shown by open field test, elevated plus-maze test, hot plate test, Y-maze test, Barnes maze test, Morris water maze test, and/or contextual fear conditioning test, recapitulated the neurological deficits of human tauopathies with dementia. Furthermore, we discovered that prepulse inhibition (PPI), a marker of sensorimotor gating, was enhanced in these animals concomitantly with initial neuropathological changes in associated brain regions. This finding provides evidence that our tauopathy mouse model displays neurofunctional abnormalities in prodromal stages of disease, since enhancement of PPI is characteristic of amnestic mild cognitive impairment, a transitional stage between normal aging and dementia such as Alzheimer's disease (AD), in contrast with attenuated PPI in AD patients. Therefore, assessment of sensorimotor gating could be used to detect the earliest manifestations of tauopathies exemplified by prodromal AD, in which abnormal tau protein may play critical roles in the onset of neuronal dysfunctions.     

Costs of parturition and rearing in female sika deer (Cervus nippon)

The costs of parturition and lactation of female sika deer on Kinkazan Island (9.6 km(2) in size), northern Japan, which live at a high density (about 50 deer/km(2)), were evaluated by comparison of body weights of 481 females measured during a 15 year study (1993-2008). Weight data were chosen from only females that did not give birth in the preceding year. The mean body weight of females that did not give birth ("yelds") was significantly lower (P < 0.001) than that of females who gave birth ("milks"); yelds' body weight was 93.1% and 83.5% that of milks in the preceding and parturition years, respectively. The yelds increased in body weight by the following March by 8.2% (P < 0.001), whereas milks did not. Among the milks, those whose fawns survived until the following May ("rearing milks") lost body weight by 14.9% (P < 0.001). Milks who lost fawns within a week after birth ("early fawn-less milks") did not lose body weight (P = 0.583), while those whose fawns died after the first autumn but died before May ("late fawn-less milks") lost body weight by 19.9% (P < 0.001). These results indicate that sika deer females do not enter estrus unless they are heavy enough, and that both parturition and rearing are costly for sika deer mothers living in high-density conditions.