Dynamics of Liquid Oil that Flows Inside Aqueous Wet Foam.

Wet soap foam spontaneously imbibes liquid oil without defoaming when it is brought into contact. The kinetics behind this recently observed phenomenon was studied experimentally, with focus on the origin of the suction force and on the oil front dynamics. Using an aqueous foam with an air volume fraction slightly greater than the critical value Ï•C, we show that the pumping pressure of oil and/or miscible liquid into the wet foam is attributed to the interfacial distortion of the bubble surfaces. Two distinct regimes along time t were observed in the oil imbibition dynamics. The proceeding oil front evolves with t1/2 dependency in the early imbibition time in accordance with the classical theory of penetration of a porous medium, whereas it departs into t1/3 at late imbibition time. The latter process is attributed to the elongation of an oil branch trapped inside the foam when pumping of the exterior oil has ceased.

Efficacy of the combined use of a mild foaming cleanser and moisturizer for the care of infant skin.

OBJECTIVE: Despite the application of skin care treatments, many infants have skin problems such as dryness and erythema. We proposed a new combination skin care for infants which consisted of a foaming cleanser with lower surfactant activity and moisturizers that contained pseudo-ceramide. SUBJECTS AND METHODS: A total of 50 infants (age: 3-24 months) with insignificant levels of dry skin were enrolled in this usage trial. The parents washed the infants with the test cleanser while bathing and then applied the moisturizer (lotion or cream) containing pseudo-ceramide. Prior to and following the 4-week usage period, visual evaluation of the skin condition was conducted by a dermatologist, in addition to instrumental analysis. RESULTS: Erythema and papule, accompanied by dryness, were commonly observed at week 0. However, by week 4, these symptoms significantly improved; the condition of none of the subjects deteriorated. The number of infants with lower cutaneous barrier function and higher skin pH decreased. The parents of the infants recognized improvements in the skin symptoms and were appreciative of the test materials. CONCLUSION: The combined usage of the foaming cleanser with lower surfactant activity and a moisturizer containing pseudo-ceramide may be effective in maintaining healthy infant skin and ameliorating the skin symptoms.

Inhibition of emotional needs and emotional wellbeing predict disease progression of chronic hepatitis C patients: an 8-year prospective study.

BACKGROUND: The role of psycosocial factors in the disease progression of chronic hepatitis C (CHC) patients remains unclear. The aim of the present study was to prospectively evaluate the prognostic value of behavioral patterns and the quality of life (QOL) of patients with CHC. METHODS: Two hundred and forty Japanese CHC patients (mean age 62.4 years) were assessed for behavioral patterns (Stress Inventory), QOL (Functional Assessment of Chronic Illness Therapy-Spiritual), and known prognostic factors at baseline then followed for a maximum of 8 years for disease progression, defined as either the first diagnosis of hepatocellular carcinoma (HCC) or hepatitis-related death. RESULTS: Forty-nine events occurred during the study period (46 newly diagnosed HCC cases, three hepatitis-related deaths). In a Cox proportional hazard model including known prognostic factors and treatment-related factors as time-dependent variables, behavioral patterns associated with inhibition of emotional needs (hazard ratio (HR): 1.35; 95 % confidence interval (CI): 1.02-1.77; p = 0.036) and QOL, representing emotional wellbeing (HR 0.60; 95 % CI 0.37-0.98; p = 0.041), were each associated with the risk of disease progression. CONCLUSION: Psychosocial factors such as behavioral patterns relevant to the inhibition of emotional needs and emotional wellbeing independently affect the clinical course of patients with CHC.

A Role of Medial Olivocochlear Reflex as a Protection Mechanism from Noise-Induced Hearing Loss Revealed in Short-Practicing Violinists.

Previous studies have indicated that extended exposure to a high level of sound might increase the risk of hearing loss among professional symphony orchestra musicians. One of the major problems associated with musicians' hearing loss is difficulty in estimating its risk simply on the basis of the physical amount of exposure, i.e. the exposure level and duration. The aim of this study was to examine whether the measurement of the medial olivocochlear reflex (MOCR), which is assumed to protect the cochlear from acoustic damage, could enable us to assess the risk of hearing loss among musicians. To test this, we compared the MOCR strength and the hearing deterioration caused by one-hour instrument practice. The participants in the study were music university students who are majoring in the violin, whose left ear is exposed to intense violin sounds (broadband sounds containing a significant number of high-frequency components) during their regular instrument practice. Audiogram and click-evoked otoacoustic emissions (CEOAEs) were measured before and after a one-hour violin practice. There was a larger exposure to the left ear than to the right ear, and we observed a left-ear specific temporary threshold shift (TTS) after the violin practice. Left-ear CEOAEs decreased proportionally to the TTS. The exposure level, however, could not entirely explain the inter-individual variation in the TTS and the decrease in CEOAE. On the other hand, the MOCR strength could predict the size of the TTS and CEOAE decrease. Our findings imply that, among other factors, the MOCR is a promising measure for assessing the risk of hearing loss among musicians.

Liquid oil that flows in spaces of aqueous foam without defoaming.

A very interesting phenomenon has been observed in which foam formed from an aqueous fatty acid potassium salt solution spontaneously absorbs liquid oil immediately upon contact without defoaming. Although this phenomenon initially appeared to be based on capillary action, it was clarified that the liquid oil that flows in foam film did not wet the air/water interface. In this study, it is discussed why aqueous foam can spontaneously soak up liquid oil without defoaming using equilibrium surface tension, dynamic oil/water interfacial tension, and image analysis techniques. The penetration of oil was attributed both to the dynamic decrease in the surface tension at the oil/water interface and to Laplace pressure, depending on the curvature of the plateau border. Therefore, the foam does not absorb the oil, but the oil spontaneously penetrates the foam. This interesting behavior can be expected to be applied to aqueous detergents for liquid oil removal.

The hepatic vagus nerve attenuates Fas-induced apoptosis in the mouse liver via alpha7 nicotinic acetylcholine receptor.

BACKGROUND & AIMS: Although accumulating evidence has recently shown that the efferent vagus nerve attenuates systemic inflammation, it remains unclear whether or not the vagus nerve can affect Fas-induced liver apoptosis. We investigated the effect of the vagus nerve by using a selective hepatic vagotomy. METHODS: We assessed the mortality and apoptosis in Fas-induced fulminant hepatitis in sham-operated and vagotomized male C57BL/6 mice. To determine how the nerve influences hepatocyte apoptosis, hepatitis was preceded by pretreatment with nicotine; PNU-282987, an alpha7 nicotinic acetylcholine receptor (AChR) agonist; liposome-encapsulated dichloromethylene diphosphonate (lipo-Cl(2)MDP), a macrophage eliminator; and Mn (III) tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP), an oxidative inhibitor. RESULTS: Mortality in the vagotomized mice was significantly higher than that in the sham-operated mice following intravenous administration with the anti-Fas antibody Jo-2. This result was also supported by the data from both terminal deoxynucleotidyl-transferase mediated dUTP nick-end labeling and caspase-3 assay, in which vagotomized livers showed a significant elevation in the number of apoptotic hepatocytes and increased caspase-3 activity following Jo-2 treatment compared with the sham-operated livers. Supplementation with nicotine and PNU-282987 dose dependently inhibited this detrimental effect of the vagotomy. Moreover, the vagotomy-triggered exacerbation of Fas-induced hepatitis was completely blocked by lipo-Cl(2)MDP. Similarly, pretreatment with MnTBAP also completely suppressed the vagotomy-triggered exacerbation. CONCLUSIONS: The hepatic vagus nerve appears to play an important role in attenuating Fas-induced hepatocyte apoptosis through alpha7 nicotinic AChR, perhaps by causing the Kupffer cells to reduce their generation of an excessive amount of reactive oxygen species.

Early-life psychological stress exacerbates adult mouse asthma via the hypothalamus-pituitary-adrenal axis.

RATIONALE: Despite accumulating evidence that psychological stress has a short-lasting detrimental effect on asthma, little is known about the way stress in childhood predisposes to adult asthma. OBJECTIVES: Using a communication box, we investigated the long-lasting effect of early psychological and physical stress on adult asthma in mice. METHODS: Male BALB/c mice were exposed to either psychological stress or physical stress three times (every other day) during their fourth week of life. The mice were sensitized to ovalbumin at 8 and 10 weeks, and an ovalbumin airway challenge was conducted at the age of 11 weeks. RESULTS: Twenty-four hours after ovalbumin challenge, both psychological and physical stress-exposed mice exhibited a significant acceleration in the number of total mononuclear cells and eosinophils and airway hyperresponsiveness compared with control mice. No differences in serum anti-OVA-specific immunoglobulin E levels were found between stress-exposed and control animals after antigen sensitization. In the psychological stress group, but not in the physical stress group, an elevation of the serum corticosterone levels during ovalbumin challenge was significantly attenuated in comparison with the control group. Moreover, pretreatment with RU-486, a glucocorticoid receptor antagonist, before ovalbumin challenge completely inhibited a psychological stress-induced exacerbation of asthma. However, pretreatment with GR-82334, a neurokinin-1 receptor antagonist, failed to affect physical stress-induced augmentation of airway inflammation. CONCLUSION: Early psychological and physical stresses aggravated adult asthma via hyporesponsiveness of the hypothalamic-pituitary-adrenal axis during antigen challenge and via a pathway(s) distinct from the hypothalamic-pituitary-adrenal axis or neurokinin-1 receptors.

Social disruption stress exacerbates alpha-galactosylceramide-induced hepatitis in mice.

OBJECTIVE: Psychosocial stress has been suggested as a possible aggravating factor in liver diseases, however, the underlying mechanism has yet to be clarified. Recently, our research revealed that electric foot-shock stress aggravated NK1.1 Ag(+) T cell-dependent alpha-galactosylceramide (alpha-GalCer)-induced hepatitis in mice via a mechanism mediated by endogenous glucocorticoids. In this study, we examined whether or not such aggravation could be applied to a psychosocially stressful situation, e.g. social disruption stress. METHODS: Male wild-type C57BL/6 (B6) or B6 hepatitis virus type B surface antigen transgenic (HBs-tg) mice, a hepatitis B virus carrier mouse model, were exposed 3 times in 1 week to social disruption stress in which an 8-month-old aggressive male intruder was placed into their home cage (5 mice per group) for 2 h. Twelve hours after the final exposure to the stress, the wild-type and HBs-tg mice were intravenously injected with alpha-GalCer. RESULTS: The stress-exposed wild-type mice exhibited significantly reduced thymus weight loss compared with the control animals. Moreover, this stress regimen led to a significant increase in serum alanine aminotransferase levels in both the wild-type and the HBs-tg mice, although the increase in the HBs-tg mice was higher than that in the wild-type mice. CONCLUSION: These findings demonstrated that, similar to electric foot-shock stress, social disruption stress exacerbated alpha-GalCer-induced hepatitis.

Postnatal microbial colonization programs the hypothalamic-pituitary-adrenal system for stress response in mice.

Indigenous microbiota have several beneficial effects on host physiological functions; however, little is known about whether or not postnatal microbial colonization can affect the development of brain plasticity and a subsequent physiological system response. To test the idea that such microbes may affect the development of neural systems that govern the endocrine response to stress, we investigated hypothalamic-pituitary-adrenal (HPA) reaction to stress by comparing germfree (GF), specific pathogen free (SPF) and gnotobiotic mice. Plasma ACTH and corticosterone elevation in response to restraint stress was substantially higher in GF mice than in SPF mice, but not in response to stimulation with ether. Moreover, GF mice also exhibited reduced brain-derived neurotrophic factor expression levels in the cortex and hippocampus relative to SPF mice. The exaggerated HPA stress response by GF mice was reversed by reconstitution with Bifidobacterium infantis. In contrast, monoassociation with enteropathogenic Escherichia coli, but not with its mutant strain devoid of the translocated intimin receptor gene, enhanced the response to stress. Importantly, the enhanced HPA response of GF mice was partly corrected by reconstitution with SPF faeces at an early stage, but not by any reconstitution exerted at a later stage, which therefore indicates that exposure to microbes at an early developmental stage is required for the HPA system to become fully susceptible to inhibitory neural regulation. These results suggest that commensal microbiota can affect the postnatal development of the HPA stress response in mice.

Electric foot shock stress-induced exacerbation of alpha-galactosylceramide-triggered apoptosis in mouse liver.

Recently, liver natural killer T (NKT) cells, which are specifically stimulated by alpha-galactosylceramide (alpha-GalCer), were found to play a critical role in intrahepatic immunity to several infections and certain hepatic disorders. However, the role of psychophysical stress on NKT cell-dependent liver injury induced by alpha-GalCer still remains to be elucidated. In this study, we employed inescapable electric foot shock as the mode of psychophysical stress and evaluated its effect on alpha-GalCer-induced hepatitis. Pre-exposure of 12 hours of foot shock stress before alpha-GalCer administration significantly enhanced alpha-GalCer-triggered increase in serum alanine aminotransferase levels, followed by increases in both liver caspase-3 activity and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive hepatocytes, thus indicating that the liver NKT cell-dependent apoptotic response was exacerbated by stress. Foot shock stress also significantly increased both the number of liver NKT cells and Fas expression levels on hepatocytes. Pretreatment with RU-486, a glucocorticoid (GC) receptor antagonist, completely reversed such stress-induced enhancement of the alpha-GalCer-triggered serum alanine aminotransferase and hepatocyte Fas antigen responses. In contrast, such a reversal effect was not found in the mice pretreated with naloxone, a micro-opioid receptor antagonist, which thus suggests that an elevation of endogenous GCs, but not beta-endorphin, as responsible for such stress-induced aggravation in mouse hepatitis models. In conclusion, foot shock stress-induced elevation of endogenous GCs exacerbates alpha-GalCer-initiated hepatic apoptosis through the expansion of liver NKT cells and the up-regulation of hepatocyte Fas antigen.

Endogenous glucocorticoids inhibit scratching behavior induced by the administration of compound 48/80 in mice.

In this study, we investigated the effects of endogenous glucocorticoids on the compound 48/80 (a condensation product of N-methyl-p-methoxyphenethylamine with formaldehyde)-induced mouse scratching behavior using either RU-486 (mifepristone), a glucocorticoid receptor antagonist, or a surgical resection of the adrenal glands. Subcutaneous injection of compound 48/80 induced not only a corticosterone elevation in the plasma but also an enhanced expression of corticotropin releasing hormone (CRH) mRNA in the paraventricular nucleus, which thus suggests that hypothalamic-pituitary-adrenal axis is activated by the compound 48/80-induced cutaneous reaction. Inhibition of such an endogenous glucocorticoid activity by RU-486 significantly increased the degree of scratching behavior at not only the early-phase (<60 min) but also the late-phase (>60 min) time course after the injection of compound 48/80. Since the elevation of the histamine levels in the plasma in the RU-486-treated mice was no longer found in late-phase scratching behavior, these results thus indicate that histamine is a dominant mediator responsible for early-phase scratching behavior, while different mediators other than histamine may be also involved in the induction of late-phase scratching behavior. Moreover, surgical removal of adrenal glands also significantly increased the compound 48/80-induced scratching behavior without affecting anxiety and locomotor parameters, indicating that endogenous glucocorticoids exert their anti-pururitogenic effects independently of changes in behavioral performance. In conclusion, endogenous glucocorticoid activity was found to suppress the compound 48/80-induced scratching behavior in mice.