Shape variety of food can boost its visual appeal.

We investigated whether food shape and its variety within a group affect visual appeal using a four-shaped fast-food chicken product known as Chicken McNuggets®. In Experiment 1, participants rated the visual appeal of each nugget shape both individually and when presented in groups of variously shaped nuggets. The results revealed that the rounder nugget was less visually appealing than those of other shapes.

Clusters in Infant Environmental Factors Influence School-Age Children's Vegetable Preferences in Japan.

It remains unclear how the various environmental factors are combined in practice to influence vegetable preferences in school-aged children. This study aimed to clarify the environmental factors during infancy and their association with vegetable preference in school-aged children. To find clusters of early childhood environmental factors, we conducted a factor analysis on 58 items related to early childhood environmental factors and a k-means cluster analysis using the factors obtained.

Effects of pulmonary exposure to carbon nanotubes on lung and systemic inflammation with coagulatory disturbance induced by lipopolysaccharide in mice.

Despite intensive research as to the pathogenesis of lipopolysaccharide (LPS)-related inflammation with coagulatory disturbance, their exacerbating factors have not been well explored. This study examined the effects of pulmonary exposure to two types of nano-sized materials (carbon nano-tubes: CNT [single-wall: SWCNT, and multi-wall: MWCNT]) on lung inflammation and consequent systemic inflammation with coagulatory disturbance induced by pulmonary exposure to LPS in mice and their cellular mechanisms in vitro. ICR male mice were divided into 6 experimental groups that intra-tracheally received the vehicle, two types of CNT (4 mg/kg), LPS (33 mu g/kg), or LPS plus either type of CNT.

Effects of components derived from diesel exhaust particles on lung physiology related to antigen.

Our previous study has shown that diesel exhaust particles (DEP), main constituents in ambient particulate matters (PM), enhance airway hyperresponsivness in a murine model of allergic asthma (Takano et al., 1998). However, it remains unknown which components in DEP are responsible for the enhancement.

Role of interleukin-6 in toll-like receptor 4 and 2 expressions induced by lipopolysaccharide in the lung.

Our previous study demonstrated that interleukin (IL)-6 is protective against hemorrhagic lung inflammation induced by lipopolysaccharide (LPS) in mice, at least partly, by inhibition of the enhanced expressions of proinflammatory cytokines. The present study elucidated the role of IL-6 in Toll like receptor (TLR) 4 and 2 expressions in the lung during inflammation induced by intraperitoneal administration of LPS (1 mg/kg) using IL-6 null (-/-) mice and wild type (WT) mice. The expressions of mRNA for both TLR4 and 2 in the lung were evaluated 72 hrs after intraperitoneal administration.

Effects of naphthoquinone on airway responsiveness in the presence or absence of antigen in mice.

We have recently demonstrated that naphthoquinone (NQ), one of extractable chemical compounds of diesel exhaust particles (DEP), enhances antigen-related airway inflammation with goblet cell hyperplasia in mice (Inoue et al. in Eur Respir J 209(2):259-267, 2007). Further, NQ has enhanced lung expressions of interleukin (IL)-4 and IL-5.

Effects of diesel exhaust particles on cytokine production by splenocytes stimulated with lipopolysaccharide.

It was previously shown that pulmonary exposure of mice to diesel exhaust particles (DEP) enhances inflammatory conditions induced by allergens or bacterial endotoxin (lipopolysaccharide: LPS) via enhanced local expression of cytokines. However, resolution of the underlying mechanisms, in which DEP exaggerate inflammation, remains uncompleted. Investigation of the actions of DEP on mouse-derived mononuclear cells may provide a clue to the mechanisms, because mononuclear cells produce and release several types of cytokines.

Effects of diesel exhaust on lung inflammation related to bacterial endotoxin in mice.

We have previously shown that intratracheal instillation of diesel exhaust particles enhances lung inflammation and lung expression of proinflammatory cytokines and chemokines related to bacterial endotoxin (lipopolysaccharide) in mice. The present study was designed to elucidate the effects of inhalation of diesel exhaust on lung inflammation related to lipopolysaccharide. ICR mice were exposed for 12 hr to clean air or diesel exhaust at a soot concentration of 0.

Pulmonary exposure to diesel exhaust particles enhances coagulatory disturbance with endothelial damage and systemic inflammation related to lung inflammation.

Pulmonary exposure to diesel exhaust particles (DEP) enhances lung inflammation related to bacterial endotoxin (lipopolysaccharide [LPS]) in mice. Severe lung inflammation can reportedly induce coagulatory abnormalities and systemic inflammation. This study examined the effects of components of DEP on lung inflammation, pulmonary permeability, coagulatory changes, systemic inflammatory response, and lung-to-systemic translocation of LPS in a murine model of lung inflammation.

Effects of airway exposure to nanoparticles on lung inflammation induced by bacterial endotoxin in mice.

Background: Although adverse health effects of particulate matter with a diameter of < 100 nm (nanoparticles) have been proposed, molecular and/or experimental evidence for their facilitation of lung inflammation in vivo is not fully defined.

Objective: In the present study we investigated the effects of nanoparticles on lung inflammation related to bacterial endotoxin [lipopolysaccharide (LPS) ] in mice.

Results: We intratracheally administered vehicle, two sizes (14 nm, 56 nm) of carbon black nanoparticles (4 mg/kg) , LPS (2.

Role of interleukin-6 in fibrinolytic changes induced by lipopolysaccharide in mice.

We have recently demonstrated that interleukin (IL)-6 is protective against coagulatory and hemostatic disturbance and subsequent pulmonary hemorrhage induced by bacterial endotoxin, at least partly, via the inhibition of proinflammatory cytokines and chemokines using IL-6-null [IL-6(-/-)] mice and corresponding wild-type mice. Its role in fibrinolytic systems remains undefined, however. The present study elucidated the role of IL-6 in the activity of alpha(2)-plasmin inhibitor, an inhibitor of fibrinolysis, during inflammation induced by intraperitoneal administration of lipopolysaccharide in IL-6(-/-) and wild-type mice.

Effects of nano particles on cytokine expression in murine lung in the absence or presence of allergen.

Particulate matter (PM) can exacerbate allergic airway diseases. Health effects of PM with a diameter of less than 100 nm, called nano particles, have been focused. We have recently demonstrated that carbon nano particles (14, 56 nm) exaggerate allergic airway inflammation in mice.

Role of metallothionein in coagulatory disturbance and systemic inflammation induced by lipopolysaccharide in mice.

Although metallothionein (MT) can be induced by inflammatory mediators, its roles in coagulatory disturbance during inflammation are poorly defined. We determined whether MT protects against coagulatory and fibrinolytic disturbance and systemic inflammation induced by intraperitoneal administration of lipopolysaccharide (LPS) in MT-I/II null (-/-) and wild-type (WT) mice. As compared with WT mice, MT (-/-) mice revealed significant prolongation of prothrombin and activated partial thromboplastin time, a significant increase in the levels of fibrinogen and fibrinogen/fibrin degradation products, and a significant decrease in activated protein C, after LPS treatment.

Antioxidative role of urinary trypsin inhibitor in acute lung injury induced by lipopolysaccharide.

We have previously demonstrated the protective role of urinary trypsin inhibitor (UTI) against acute inflammatory lung injury induced by lipopolysaccharide (LPS) using UTI-deficient (-/-) mice and corresponding wild-type (WT) mice. The protection was mediated, at least partly, through inhibition of the enhanced local expression of proinflammatory cytokines, chemokines, and intercellular adhesion molecule-1. In the present study, we addressed whether UTI regulates oxidative stress generated by LPS challenge in the lung.

Effects of nano particles on antigen-related airway inflammation in mice.

Background: Particulate matter (PM) can exacerbate allergic airway diseases. Although health effects of PM with a diameter of less than 100 nm have been focused, few studies have elucidated the correlation between the sizes of particles and aggravation of allergic diseases. We investigated the effects of nano particles with a diameter of 14 nm or 56 nm on antigen-related airway inflammation.

Effects of 15-deoxy-delta(12,14)-prostaglandin J2 on nuclear localization of GATA-3 in the murine lung in the presence of lipopolysaccharide.

15-Deoxy-delta(12, 14)-prostaglandin J2 (15d-PG J2) is a regulator of a nuclear transcriptional factor, peroxisome proliferator-activated receptor (PPAR)-gamma. A previous study has demonstrated that 15d-PG J2 enhanced acute lung injury induced by lipopolysaccharide (LPS) in mice. 15d-PG J2 induced mucin-producing cells in the bronchial epithelium, especially in the presence of LPS.

Protective role of urinary trypsin inhibitor in acute lung injury induced by lipopolysaccharide.

Urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used as a drug for patients with acute inflammatory disorders such as disseminated intravascular coagulation, shock, and pancreatitis. However, direct contribution of UTI to inflammatory diseases has not been established. The present study analyzed acute inflammatory lung injury induced by lipopolysaccharide (LPS) in UTI-deficient (-/-) mice and corresponding wild-type (WT) mice.

Cytoprotection by interleukin-6 against liver injury induced by lipopolysaccharide.

The role of interleukin (IL)-6 in inflammatory injury remains controversial. The present study elucidated the role of IL-6 in liver damage during severe inflammation induced by intraperitoneal administration of lipopolysaccharide (LPS; 1 mg/kg) using IL-6 null (-/-) mice and corresponding wild-type (WT) mice. Histological study showed that LPS treatment caused more severe liver injury with centrilobular vacuolation of hepatocytes and neutrophilic infiltration in the liver of IL-6 (-/-) mice; in contrast, neutrophilic infiltration and mild vacuolar change of hepatocytes were found in the liver of LPS-treated WT mice.

Role of metallothionein in antigen-related airway inflammation.

Metallothionein (MT) is a protein that can be induced by inflammatory mediators and participates in cytoprotection. However, its role in antigen-related inflammation remains to be established. We determined whether intrinsic MT protects against antigen-related airway inflammation induced by ovalbumin (OVA) in MT-I/II null (MT [-/-]) mice and in corresponding wild-type (WT) mice.

Urinary trypsin inhibitor protects against systemic inflammation induced by lipopolysaccharide.

Urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used as a drug for patients with acute inflammatory disorders such as disseminated intravascular coagulation, shock, and pancreatitis in Japan. Recent studies have demonstrated that serine protease inhibitors may play an anti-inflammatory role beyond merely an inhibitory action on neutrophil elastase at the site of inflammation at least in vitro. To clarify the direct contributions of UTI to inflammatory condition in vivo, we analyzed its roles in experimental systemic inflammatory response induced by intraperitoneal administration of lipopolysaccharide (LPS) using UTI deficient (-/-) mice and corresponding wild-type (WT) mice.

Protective role of interleukin-6 in coagulatory and hemostatic disturbance induced by lipopolysaccharide in mice.

Although the role of interleukin (IL)-6 in inflammatory diseases has been previously examined, its role in hemostasis, fibrinolysis, and coagulation during inflammation remains to be established. The present study elucidated the role of IL-6 in hemostatic and coagulatory changes during severe inflammation induced by intraperitoneal administration of lipopolysaccharide (LPS: 1 mg/kg) using IL-6 null (-/-) mice. After LPS challenge, IL-6 (-/-) mice revealed significant prolongation of prothrombin time and activated partial thromboplastin time and a significant decrease in platelet counts as compared with wild type mice.