Effect of Hand and Foot Massage Therapy on Psychological Factors and EEG Activity in Elderly People Requiring Long-Term Care: A Randomized Cross-Over Study.

Massage therapy is widely used as a complementary therapy in the elderly. Here, we investigate the effect of hand and foot massage therapy on psychological factors and electroencephalographic (EEG) activity in elderly people requiring long-term care. We included 12 elderly people requiring long-term care, who were randomly divided into two groups (A and B). Group A received hand massage and group B received foot massage, both for 15 min each. After 1 week, group A received foot massage and group B received hand massage, both for 15 min each. We assessed emotions and mood states with a Likert scale after each massage and resting-state EEG activity was measured before and after each massage. Our results showed that both hand and foot massage led to a high degree of pleasant, relaxed, and refreshed feelings. Moreover, resting-state alpha activity significantly increased in the left insular cortex after hand massage (p < 0.05), and in the right and left posterior cingulate cortex after foot massage (p < 0.05). This study suggests that hand and foot massage therapy modulate psychological factors and EEG activity in elderly people requiring long-term care.

Airborne Asian sand dust enhances murine lung eosinophilia.

There is no experimental study demonstrating the effects of airborne Asian sand dust (AASD) on allergic lung eosinophilia. The organic substances adsorbed onto AASD collected from the atmosphere of Iki-island in Japan were excluded by heat treatment at 360°C for 30 min. The effects of AASD or heated-AASD (H-AASD) towards allergic lung inflammation were compared in murine lungs to investigate the role of organic substances. ICR mice were administrated with the two kinds of AASD and/or ovalbumin (OVA) intratracheally four times at 2-week intervals. AASD and H-AASD enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. AASD and H-AASD synergistically increased Th2 cytokines-interleukin-13 (IL-13), eosinophil-relevant cytokine and chemokine, such as IL-5, and monocyte chemotactic protein-3 (MCP-3) induced by OVA in whole lung lavage fluid. The enhancing effects were much greater in AASD than in H-AASD. AASD induced adjuvant effects on OVA-specific immunoglobulin E (IgE) and IgG1 production. In an in vitro study using RAW264.7 cells, AASD increased the expression of Toll-like receptors 2 (TLR2) mRNA, but not TLR4 mRNA. AASD increased mRNA expression of NALP3, ASC, and IL-1ß compared with the control. H-AASD caused no expression of either mRNA. These results suggest that the aggravated lung eosinophilia in AASD is due to activation of a Th2-associated immune response and that the activation of TLR2 and NALP3 inflammasome by microbial materials could be participating in this phenomenon.

Urban particulate matter in Beijing, China, enhances allergen-induced murine lung eosinophilia.

It has been reported that ambient particulate matter (PM) in some large cities, such as Beijing, China, causes adverse respiratory health effects. However, there is currently no experimental report on the relationship between bronchial asthma and urban PM (UPM) in northeast Asia. In this study, the microbial and chemical substances adsorbed onto UPM collected in Beijing were excluded by heat-treatment at 360 degrees C for 30 min. The effects of UPM or heated UPM (H-UPM) toward allergic lung inflammation were compared in murine lungs to investigate the role of organic substances. ICR mice were administrated intratracheally with the two kinds of UPM and/or ovalbumin (OVA) 4 times at 2-week intervals. UPM and H-UPM enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. UPM and H-UPM synergistically increased Th-2 cytokines--interleukin (IL)-4 and IL-13, eosinophil-relevant cytokines and chemokines, such as IL-5 and monocyte chemotactic protein-3 (MCP-3), induced by OVA in bronchoalveolar lavage fluid (BALF). The enhancing effects were much greater in UPM than in H-UPM. UPM induced adjuvant effects on specific immunoglobulin E (IgE) and IgG1 production by OVA. In an in vitro study using RAW264.7 cells, UPM increased the expression of Toll-like receptor 2 (TLR2) mRNA, but not TLR4 mRNA. H-UPM caused no expression of both TLR mRNAs. These results suggest that the aggravated lung eosinophilia in UPM was due to activation of a Th2-associated immune response via the activation of TLR2 by microbial materials. Chemical materials of air pollutant origin contained in UPM, and inorganic components (elemental carbon, mineral elements) in H-UPM, could also cause the aggravation.

Characterization of NIES CRM No. 23 Tea Leaves II for the determination of multielements.

A candidate environmental certified reference material (CRM) for the determination of multielements in tea leaves and materials of similar matrix, NIES CRM No. 23 Tea Leaves II, has been developed and characterized by the National Institute for Environmental Studies (NIES), Japan. The origin of the material was tea leaves, which were ground, sieved through a 106-microm mesh, homogenized, and then subdivided into amber glass bottles. The results of homogeneity and stability tests indicated that the material was sufficiently homogeneous and stable for use as a reference material. The property values of the material were statistically determined based on chemical analyses by a network of laboratories using a wide range of methods. Sixteen laboratories participated in the characterization, and nine certified values and five reference values were obtained. These property values of the candidate CRM, which are expressed as mass fractions, were close to the median and/or mean values of the mass fractions of elements in various tea products. The candidate CRM is appropriate for use in analytical quality control and in the evaluation of methods used in the analysis of tea and materials of similar matrix.

Asian sand dust aggravates allergic rhinitis in guinea pigs induced by Japanese cedar pollen.

Asian sand dust (ASD) contains microbial materials, sulfate (SO(4)(2-)), and nitrate (NO(3)(-)), and is derived from air pollutants in East China. ASD reportedly causes adverse respiratory health effects; a case in point is aggravated allergen-associated experimental lung eosinophilia. Guinea pigs were administered normal saline (control), ASD (0.3 mg/animal), ASD (0.6 mg/animal), Japanese cedar pollen (JCP) (0.2 mg/kg body weight), JCP + ASD (0.3 mg/animal), or JCP + ASD (0.6 mg/animal), into their nasal cavities at seven weekly intervals. The number of sneezes, amount of nasal secretions, and nasal obstructing response were measured as indices of nasal responses. Total immunoglobulin E (IgE) antibodies in serum and the number of eosinophils, histamine, and arachidonic acid metabolites in nasal cavity lavage fluids (NCLF) were also measured. ASD enhanced the JCP-associated nasal obstructing response, but not the number of sneezes or amount of nasal secretions. ASD enhanced JCP-associated cysteinyl leukotrienes (C(4), D(4), E(4)) and histamine production in NCLF. ASD augmented the number of eosinophils in NCLF and total IgE in serum induced by JCP. ASD enhanced eosinophil recruitment in the nasal mucosa, and goblet cell proliferation in the nasal epithelium induced by JCP. These results suggest that ASD enhances the nasal allergic reaction induced by repeated JCP administration in guinea pigs.

Effects of asian sand dust, Arizona sand dust, amorphous silica and aluminum oxide on allergic inflammation in the murine lung.

The aggravating effects of Asian sand dust (SD) and related minerals on the allergic inflammation were examined in the murine lungs. The toxic materials adsorbed onto Asian SD, Arizona SD were inactivated by heat-treatment. ICR mice were administered mineral samples (0.1 mg/mouse) and/or ovalbumin (OVA) (1 microg/mouse) - normal saline (control), Asian SD, Arizona SD, SiO2, Al2O3, OVA, OVA + Asian SD, OVA + Arizona SD, OVA + SiO2, and OVA + Al2O3 - intratracheally four times at two-week intervals. All samples tested enhanced eosinophil recruitment induced by ovalbumin in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. Arizona SD alone caused a slight increase of neutrophils in bronchoalveolar lavage fluids along with pro-inflammatory mediators, such as keratinocyte chemoattractant, but Asian SD alone or Al2O3 alone showed no effect. The test particles, except Al2O3, synergistically increased the numbers of eosinophils in BALF induced by ovalbumin. In particular, Arizona SD and SiO2 synergistically increased the eosinophil relevant cytokine and chemokine, such as IL-5 and monocyte chemotactic protein (MCP)-3. The aggravating effects of the samples were dependent on the SiO2 content. All samples tested also induced the adjuvant effects to specific IgG1 production by OVA. These results suggest that the aggravated allergic inflammation by mineral dusts may be due to the mineral elements (mainly SiO2). The enhancement by Arizona SD may be mediated, at least partially, by the increased expression of IL-5 and MCP-3 and also by the modulated expression of IL-5 and MCP-3.

Asian sand dust enhances ovalbumin-induced eosinophil recruitment in the alveoli and airway of mice.

Asian sand dust (ASD) containing sulfate (SO4(2-)) reportedly causes adverse respiratory health effects but there is no experimental study showing the effect of ASD toward allergic respiratory diseases. The effects of ASD and ASD plus SO4(2-) toward allergic lung inflammation induced by ovalbumin (OVA) were investigated in this study. ICR mice were administered intratracheally with saline; ASD alone (sample from Shapotou desert); and ASD plus SO4(2-) (ASD-SO4); OVA+ASD; OVA+ASD-SO4. ASD or ASD-SO4 alone caused mild nutrophilic inflammation in the bronchi and alveoli. ASD and ASD-SO4 increased pro-inflammatory mediators, such as Keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-1 alpha, in bronchoalveolar lavage fluids (BALF). ASD and ASD-SO4 enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. However, a further increase of eosinophils by addition of SO4(2-) was not observed. The two sand dusts synergistically increased interleukin-5 (IL-5) and monocyte chemotactic protein-1 (MCP-1), which were associated with OVA, in BALF. However, the increased levels of IL-5 were lower in the OVA+ASD-SO4 group than in the OVA+ASD group. ASD caused the adjuvant effects to specific-IgG1 production by OVA, but not to specific-IgE. These results suggest that the enhancement of eosinophil recruitment in the lung is mediated by synergistically increased IL-5 and MCP-1. IgG1 antibodies may play an important role in the enhancement of allergic reaction caused by OVA and sand dust. However, extra sulfate may not contribute to an increase of eosinophils.