Large particulate allergens can elicit mast cell-mediated anaphylaxis without exit from blood vessels as efficiently as do small soluble allergens.

Anaphylaxis is a rapid-onset, life-threatening allergic reaction in that IgE, mast cells and histamine are commonly involved. It can be experimentally induced in IgE-sensitized animals by intravenous injection of corresponding allergens, and the sign of anaphylactic reaction can be detected within minutes after allergen challenge. However, it remains puzzling why the anaphylactic reaction can be initiated in vivo so quickly, considering that allergens are delivered into the blood circulation while mast cells reside within peripheral tissues but not in the blood circulation. To address this issue, we compared two different forms of the same allergen, small soluble and large particulate ones, in their ability to induce anaphylaxis in IgE-sensitized mice. In contrast to our expectation, particulate allergens could induce anaphylaxis as quickly and efficiently as did soluble allergens, even though they remained inside of blood vessels. In vivo imaging analysis suggested the direct interaction of intravascular particulate allergens and perivascular mast cells across the capillary wall. Taken together with previous report that perivascular mast cells can capture IgE in the blood circulation by extending cell processes across the vessel wall, our findings imply that blood-circulating allergens, regardless of their size, can stimulate mast cells without exit from blood vessels, by means of cross-linking IgE on mast cell processes inserted into the vessel lumen, and hence initiate anaphylactic reaction so quickly.

Morphine-induced changes of adenylate and guanylate cyclase in locus ceruleus, periaqueductal gray, and substantia nigra in rats.

OBJECTIVES: To observe the changes of adenylate cyclase (AC) and guanylate cyclase (GC) in the cerebral regions including the locus ceruleus, periaqueductal gray, and substantia nigra in rats that were physiologically dependent on morphine. We also investigated the relationship of enzymatic changes in these cerebral regions to the mechanism of morphine dependence. METHODS: A morphine-dependent rat model was established and withdrawal symptoms evaluated. Enzyme histochemistry was used to detect the variations of AC and GC in cerebral regions. RESULTS: Compared to controls, AC and GC significantly increased in morphine-dependent groups. Comparisons of four different morphine-dependent groups also showed AC and GC significantly differed at weeks 1, 2, 4, and 8. CONCLUSIONS: Results found that the content of AC and GC increased in these cerebral regions in rats that demonstrated morphine dependence and appeared to be closely linked to increases in AC and GC activity.

Characterization and cysteine sensing performance of nanocomposites based on up-conversion excitation host and rhodamine-derived probes.

Optical sensing for cysteine (Cys) recognition is an interesting topic due to Cys biological participation. In this paper, two rhodamine-based chemosensors were designed for Cys optical sensing. For chemosensor photostability improvement, up-conversion nanocrystals were synthesized and used as excitation host. These nanocrystals were modified with a phase transfer reagent α-cyclodextrin (α-CD) to improve their compatibility with chemosensors. An efficient energy transfer from these nanocrystals to chemosensors under 980nm radiation was observed and confirmed by spectral match analysis, energy transfer radius calculation and emission decay lifetime comparison. A direct bonding mechanism between Cys and chemosensors with bonding stoichiometry of 1:1 was established by Job's plot experiment. Given the presence of Cys, chemosensor emission was increased, showing emission turn on effect. These two chemosensors showed good selectivity, improved photostability and linear sensing response towards Cys.

Erythromycin combined with corticosteroid reduced inflammation and modified trauma-induced tracheal stenosis in a rabbit model.

BACKGROUND: Patients with endotracheal intubation or tracheostomy are subject to benign tracheal stenosis (TS), for which current therapies are unsatisfactory. We conducted a preliminary investigation of drugs and drug combinations for the prevention and treatment of TS in a rabbit model. METHODS: Fifty-four rabbits were apportioned into nine groups according to treatment: sham-operated control; untreated TS model; amikacin; budesonide; erythromycin; penicillin; amikacin + budesonide; erythromycin + budesonide; and penicillin + budesonide. TS was induced by abrasion during surgery. The drugs were applied for 7 days before and 10 days after the surgery. Rabbits were killed on the eleventh day. Tracheal specimens were processed for determining alterations in the thicknesses of tracheal epithelium and lamina propria via hematoxylin and eosin. The tracheal mRNA (assessed by real-time quantitative polymerase chain reaction) expressions of the following fibrotic-related factors were determined: transforming growth factor-ß1 (TGF- ß1), collagen type I (COL1A1), collagen type III (COL3A1), and interleukin-17 (IL-17). The protein levels of TGF-ß1, COL1A1, and COL3A1 were determined through immunohistochemistry and integrated optical densities. RESULTS: Compared with all other groups, the untreated TS model had significantly thicker tracheal epithelium and lamina propria, and higher mRNA and protein levels of all targeted fibrotic factors. The mRNA and protein levels of the targeted fibrotic factors in all the drug-treated groups were lower than those of the untreated TS model, and differences were most significant in the erythromycin + budesonide group. CONCLUSIONS: Erythromycin combined with budesonide may reduce inflammation and modify fibrosis progression in TS after tracheal injury.

T3 inhibits the calcification of vascular smooth muscle cells and the potential mechanism.

OBJECTIVE: This study aimed to investigate the potential molecular mechanism underlying the T3 induced vascular calcification and phenotype transformation of vascular smooth muscle cells (VSMCs). METHODS: Rat thoracic aortic smooth muscle cells (A7r5) were cultured in vitro and randomly assigned into normal control group, calcification group, T3 group and inhibitor group. RESULTS: When compared with normal control group, the osteocalcin content, ALP activity, Osterix and Runx2 mRNA expression and OPN protein expression increased significantly (P<0.01), and the protein expression of SMα and SM22α reduced dramatically in A7r5 cells of calcification group (P<0.01). After T3 treatment, the osteocalcin content and ALP activity reduced markedly, mRNA expression of Osterix and Runx2 and OPN protein expression reduced significantly. However, MMI (inhibitor of T3) was able to block the above effects of T3. When compared with calcification group, Osterix and Runx2 mRNA expression and OPN protein expression increased markedly (P<0.01). In addition, the protein expression of ERK1/2, p-ERK, Akt and p-Akt increased significantly in calcification group. In the presence of integrin αvß3/ERK blocker (PD98059) and/or PI3K/Akt antagonist (LY294002), T3 was still able to inhibit the calcification, and this effect was similar to that after treatment with inhibitors alone. Moreover, LY294002 had a better inhibitory effect as compared to PD98059. CONCLUSION: T3 may act on PI3K/Akt signaling pathway to inhibit the phenotype transformation of VSMC, which then suppresses the calcium/phosphate induced calcification of rat VSMCs. Thus, T3 is an endogenous molecule that can protect the blood vessels against calcification.

Identification, structure and function of a novel tetraspaninhomologue from Spirometra erinaceieuropaei.

OBJECTIVE: To identify a full length c DNA sequence of a novel tetraspanin (TSP) homologue from Spirometra erinaceieuropaei and to predict the structure and function of its encoding protein using bioinformatics methods. METHODS: Using the NCBI, EMBI, Expasy and other online sites, the open reading frame (ORF), conserved domain, physical and chemical parameters, signal peptide, transmembrane domain, epitope, topological structures of the protein sequences were predicted. And Vector NTI software was used for multiple sequence alignment and phylogenetic tree construction. RESULTS: The target sequence was 1132 bp length with a 681 bpbiggest ORF encoding 226 amino acids protein with typical TSP conserved domain. It was confirmed as full length c DNA of TSP16 from Spirometra erinaceieuropaei and named as SeTSP16 (GenBank accession number: JF728872). The predicted molecular weight and isoelectric point of the deduced protein were 24 750.5 Da and 7.88 Da, respectively. Compared with TSP16s from Schistosoma japonicum and Schistosoma mansoni, it showed similarity of 59% and 59%, respectively. SeTSP16 contained four transmembrane domains (TM1-4), intracellular N and C-termini, one short small extracellular loop and one large extracellular loop. Four major epitopes that were significant different from the corresponding epitope regions of TSP16 from Schistosoma mansoni and Schistosoma japonicum were predicted. CONCLUSIONS: The full length c DNA sequences of SeTSP16 are identified. It encodes a transmembrane protein which might be an ideal diagnosis antigen and target molecule for antiparasitic drugs.

Enhanced biodecolorization of azo dyes by electropolymerization-immobilized redox mediator.

The biodecolorization rate of azo dyes can be improved by the addition of some soluble quinoid redox mediators, but continuous dosing and discharge of these mediators will result in the secondary contamination due to their recalcitrant trait. In this study, the effect of anthraquinone-2,6-disulfonate (AQDS) bound into polypyrrole (PPy) on activated carbon felt (ACF) on anaerobic biodecolorization of azo dyes was investigated and compared with that immobilized on platinum (Pt). The results showed that in the presence of AQDS/PPy/ACF, the biodecolorization efficiency of azo dye RR15 reached over 80% at the optimal pH 7 in 8h and kept stable during successive 10 times repeated experiments. In contrast, in the presence of AQDS/PPy/Pt biodecolorization efficiency of RR15 was less than 60% under the above conditions, and the PPy doped by AQDS desquamated from the substrate material Pt at the third biodecolorization experiment. In addition, in the presence of AQDS/PPy/ACF biodecolorization efficiencies of 5 reactive dyes, 4 acid dyes and 2 direct dyes increased more than 3-fold than that without AQDS. This indicates that electropolymerization-immobilized AQDS (AQDS/PPy/ACF) has potential applications in accelerating the anaerobic biodecolorization of azo dyes.