Photoinduced Formation of Peroxide Ions on La2O3 and Nd2O3 under O2: Effects of Excitation Wavelength and Crystal Structure.

Photoinduced formation of peroxide ions on La2O3 and Nd2O3 under O2 was studied by in-situ microprobe Raman spectroscopy with attention focused on the effect of excitation wavelength and crystal structure on the O2(2-) formation. It was found that photoexcitations at 633, 532, 514, and 325 nm can induce O2(2-) formation over La2O3 at 450 °C. By contrast, photoexcitation at 785 nm does not cause formation of O2(2-) up to 500 °C. Photoexcitation at 325 nm can induce O2(2-) formation on cubic Nd2O3 at 25 °C, but cannot induce O2(2-) formation on hexagonal Nd2O3 up to 200 °C. The significant difference in the behavior of O2(2-) formation over the Nd2O3 samples of the two structures can be related to the difference in the capacity to adsorb O2. Since the number of oxygen vacancies in cubic Nd2O3 is larger than that in the hexagonal one, the former has a higher capacity than the latter to adsorb O2. As a result, cubic Nd2O3 is more favorable to the reaction of O2 with O(2-) to generate O2(2-). The structural similarity between cubic Nd2O3 and Nd2O2(O2) may be another factor in favor of peroxide formation.

[Long-term efficacy of Dermatophagoides pteronyssinus immunotherapy in patients with allergic rhinitis: a 3-year prospective study].

OBJECTIVE: To evaluate the long-term efficacy of subcutaneous immunotherapy with Dermatophagoides pteronyssinus (DerP) in patients with allergic rhinitis. METHODS: Ninety-two patients with allergic rhinitis to DerP were randomly allocated to receive either specific immunotherapy (n = 46) or medical treatment (n = 46). Symptom and medication scores and skin response to Derp were assessed to evaluate the clinical efficacy in the baseline and after three years treatment. DerP-specific IgE and IgG4 were measured. RESULTS: After three years treatment, the immunotherapy group showed sustained reductions in symptom scores (before treatment 9.20 [7.50;11.13], after treatment 3.32 [2.49;5.12], Z = -5.13, P < 0.05), medication scores (before treatment 0.72 [0.47;0.83], after treatment 0.31 [0.28;0.45], Z = -5.78, P < 0.05) and specific skin response to Derp (t = 6.37, P < 0.05) when compared with control group. There were no differences in the level of serum specific IgE before and after three-year treatment (before treatment 16.32 [4.34;38.65] kU/L, after treatment 15.85 [4.93;46.27] kU/L, Z = -0.84, P > 0.05), but the level of serum specific IgG4 increased significantly after one year treatment in immunotherapy group (before treatment 486 [319;1439] AU/L, after treatment 8387 [7732;16 634] AU/L, Z = -2.81, P < 0.05). After three-year treatment, 7.5% (3/40) of patients had asthma in immunotherapy group compared to 27.8% (10/36) in the control group (χ(2) = 5.50, P < 0.05), and 15.0% of the initially DerP nonsensitized patients in immunotherapy group had developed new sensitization compared to 47.2% in the control group (χ(2) = 9.32, P < 0.05). CONCLUSION: Three years immunotherapy improves allergic rhinitis symptoms, increases the level of serum specific IgG4, reduces the development of asthma and new sensitization.

[Association of single nucleotide polymorphisms of GATA3 with allergic rhinitis phenotypes in Chinese].

OBJECTIVE: To evaluate the association between single nucleotide polymorphisms (SNP) of GATA3 and Chinese with allergic rhinitis. METHODS: This study included 109 patients with allergic rhinitis and 112 healthy control people. SNP of two loci with restriction fragment length polymorphism was detected, rs1269486 at promoter region and rs2229360 located 92 bp downstream of STOP codon. Total IgE and specific IgE of Der p and Der f with different genotypes of the two loci were compared. RESULTS: There was SNP at both loci of rs1269486 and rs2229360. The genotypes of rs1269486 were GG, GA and AA, and the genotypes of rs2229360 were CC, CT and TT. The frequency of genotype GG and allele G in patient group was significantly higher than that in control group (chi2 = 13.75, P <0.01; chi2 = 12.91, P <0.01), and the frequency of genotype GA and allele A in patient group was significantly lower than that in control group (chi2 = 11.90, P <0.01; chi2 =12.91, P <0.01). There were no significant differences between patient group and control group for the frequencies of genotypes and alleles at rs2229360 (P > 0.05). The haplotype frequency of GC in patient group was significantly higher than that in control group (chi2 = 114.59, P < 0.01), and the haplotype frequency of AC in patient group was significantly lower than that in control group (chi2 = 87.52, P <0.01). There was no significant difference of the levels of serum total IgE and specific IgE to Der p and Der f with the genotypes at the two loci (P >0.05). CONCLUSIONS: The SNP at rs1269486 of GATA3 is associated with allergic rhinitis in Chinese.

[Effect of Pranlukast on tissue remodeling in experimental guinea pig allergic rhinitis model].

OBJECTIVE: To explore the impact of Pranlukast in nasal mucosal remodeling in experimental allergic rhinitis. METHODS: Fourteen male guinea pigs were randomly divided into 3 groups: control group, ovalbumin (OVA) group and OVA + Pranlukast group. In the OVA group and OVA + Pranlukast group, OVA sensitized Hartley guinea pigs were exposured intranasally to OVA for a total of 12 weeks, the OVA + Pranlukast group received additional Pranlukast treatment from the second week to the 12th week. Paraffin embedded sections were stained with hematoxylin and eosin (HE), alcian blue-periodic acid-Schiff (AB-PAS), and Masson's Trichrome (MT). Infiltrating eosinophils, the number of goblet cells in the surface epithelium and gland cells in subepithelial nasal septal mucosa were counted. The damage of epithelium in nasal septum and extracellular matrix of nasal septal mucosa and conchae were determined. RESULTS: Compared with the control, the prolonged OVA exposure protocol caused significant pathological changes in the nasal mucosa, which included eosinophils infiltration into epithelium and submucosa (106.90 +/- 13.66), significant goblet hyperplasia (22.05 +/- 5.81/mm), epithelial damage (intact epithelium: 47.25% +/- 7.67%) and deposition of extracellular matrix. These changes were significantly inhibited by Pranlukast, in which group, there were few eosinophils(8.95 +/- 2.32) , few goblet cells (5.73 +/- 1.07/mm), and relative intact epithelium (intact epithelium: 83.15% +/- 8.05%), and no significant ECM deposition. CONCLUSIONS: Early Pranlukast intervention could inhibit nasal mucosal remodeling in allergic rhinitis.

[Nasal mucosa remodeling in guinea pig model of allergic rhinitis].

OBJECTIVE: To explore the feature of nasal mucosa remodeling in experimental allergic rhinitis. METHODS: Twenty-four male Hartley guinea pigs (4 weeks, 250 -300 g) were randomly divided into four groups (control group and allergen exposure groups 1 - 3), each group had 6 guinea pigs. Allergen exposure animals were sensitized by intraperitoneal (ip) injection of ovalbumin (OVA). Sensitized guinea pigs were subjected to either brief or prolonged exposure to allergen. Both brief exposure group (allergen exposure groups) and prolonged exposure group (allergen exposure group 2 and 3) received a daily intranasal challenge with 5% OVA in 0.9% saline from Day 22 to Day 28, the prolonged exposure group (allergen exposure group 2 and 3) followed by twice weekly exposure to 5% OVA intranasal for an additional 8 and 12 weeks respectively. Control animals were given saline only. At 24 h after the last intranasal challenge, the guinea pigs were killed and the heads of the animals were removed and fixed in 10% neutral buffered formalin for 24 hours, then decalcified in 5% trichloroacetic acid for 10 days. The tissue blocks were embedded in paraffin. The paraffin sections 3 microm thick were stained with hematoxylin and eosin (HE), alcian blue (pH, 2. 6)-periodic acid-Schiff (AB-PAS), and Masson's Trichrome (MT). The infiltrating eosinophils in nasal mucosa were examined, AB-PAS-positive cells in the surface epithelium in nasal septal mucosa were counted. The percentage area of MT stained extracellular matrix in septal mucosa and conchae and damage of epithelium were determined by an image analyzer. RESULTS: The control group only presented a few eosinophils. Significant eosinophil infiltration was observed in the sensitized groups. Compared with control group (intact epithelium 87.7% +/- 11.1%), there was no significant epithelial damage in 1 week exposure group. Significant epithelial damage were observed in 8 and 12 weeks groups (intact epithelium 36.7% +/- 16.9%, 37.9% +/- 12.9%, respectively). An increase in AB-PAS-positive cells was observed in the mucosa of nasal septum in the prolonged allergen exposure groups, but not in the brief allergic inflammation group in comparison with the control. The brief OVA exposure group did not show increased collagen fibrils within the mucosa of nasal septum and conchae. In contrast, after prolonged OVA exposure an increase in matrix was observed. Furthermore, in both the nasal septum and conchae, significant increasing of ECM deposition was found in a further prolonged exposure for 12 weeks compared to 8 weeks. CONCLUSIONS: Epithelial damage, goblet cells hyperplasia and extracellular matrix deposition were observed as the features of remodeling in this guinea pig model of allergic rhinitis.