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BackgroundSevere deep neck space infection is rare and critical.The objective is to deepen the understanding of severe deep neck space infection and improve the level of clinical diagnosis and treatment. Case presentationA retrospective analysis of the diagnosis and treatment of 5 cases of serious deep neck infections admitted to our department. The 5 patients were all diagnosed by cervical CT and surgical exploration. 3 patients with diabetes, 2 patients with diabetic ketoacidosis, 3 patients with mediastinal infection; 3 patients underwent tracheotomy and 2 patients with tracheal intubation; All patients were treated by neck incision, drainage, dressing change and targeted antibiotics. Conclusions Severe deep neck infections are prone to occur in patients with diabetes and other systemic basic diseases. Early diagnosis, timely neck incision exploration, drainage to maintain airway patency and targeted antibiotic treatment are the keys to diagnosis and treatment.

The gamma radiation induced catalytic degradation of p-nitrophenol (PNP) in the presence of titanium dioxide (TiO2) nanoparticles in aqueous solution was investigated. The initial concentration of PNP solution was 50 mg/L, and the additional TiO2 doses were 0, 0.5, 1.0, and 2.0 g/L. The experimental results indicated that the PNP decomposition kinetics conformed to the modified pseudo-first order reaction equation under all applied conditions. When the TiO2 dose was in the range of 0–2.0 g/L, the effect of additional TiO2 on PNP decomposition rate was not obvious because PNP could be removed quite well by irradiation even in the absence of TiO2 nanoparticles; however, the removal of total organic carbon (TOC) and total nitrogen (TN) was significantly accelerated in the presence of TiO2 nanoparticles, the TOC removal efficiency increased from about 16% to 42%, and therefore the mineralization of PNP could be enhanced by TiO2 nanoparticles. The inorganic nitrogen products were quantitatively measured to estimate the decomposition degree of PNP. The major aromatic intermediates, as well as carboxylic acids were identified by LCMS and IC. Possible reactions involved in radiation induced catalytic decomposition of PNP in aqueous solutions were proposed.

Background Allergic rhinitis (AR) is a common disease characterized by chronic inflammation of the nasal mucosa, but we have not fully understood the mechanism responsible for the development of AR. MicroRNAs (miRNAs) are short endogenous noncoding RNAs regulating protein translation through a mechanism known as RNA interference. To understand the molecular mechanisms of miRNA involved in the pathogenesis of AR, expressed miRNAs in AR were investigated through genomewide microarray analysis. Methods Mammalian miRNA microarrays containing whole human mature and precursor miRNA sequences were used for analyzing eight samples of nasal mucosa of AR and eight samples of nonallergic patients. Quantitative reverse transcriptase–polymerase chain reaction (RT-PCR) of some different expressed miRNAs was used to confirm the array results. Results The miRNA microarray chip analysis identified 421 miRNAs differentially expressed in the nasal mucosa of AR, and a total of 9 miRNAs were identified in the AR group with twofold change compared with control samples (p < 0.05). These included up-regulated miRNAs, hsa-hsa-miR-7, and hsa-miRPlus-E1194, and down-regulated miRNAs, hsa-miR-498, hsa-miR-187, hsa-miR-874, hsa-miR-143, hsa-miR-886–3p, hsa-miR-224, and hsa-miR-767–5p. RT-PCR results also confirmed that part of differentially expressed miRNAs as hsa-miR-224, hsa-miR-187, and hsa-miR-143 were down-regulated in AR. Conclusion The report indicated that many miRNA expressions were altered in AR and differentially expressed miRNAs appear to be involved in the development of AR. The study of miRNAs may lead to a better understanding about the roles of identified miRNAs in the pathogenesis of AR; this would be considered in future therapeutic strategies.

The objective of this study is to evaluate the effect of exhaled CO (eCO) on the development of asthma and allergic rhinitis (AR) by means of reviewing published literature. The literatures published between January 1997 and December 2008 from the US National Library of Medicine (NLM) Database were obtained according to inclusion criteria. Meta-analysis of randomized controlled trials (RCTs) was performed. CO levels of asthma and AR patients were compared with that of normal controls. HO-1(heme oxygenase-1) expression and effect of corticosteroids on eCO levels were also analyzed. Fifteen studies concerning asthma and four studies concerning AR were included in this analysis. Heterogeneity from different studies was evident (P < 0.0001), so a random-effects model was preferred. The meta-analysis revealed that asthmatic patients had significantly higher levels of eCO compared to normal controls. There was significant difference between asthma and control groups in terms of eCO (combined weighted mean difference (WMD) 1.33 (95% confidence interval 0.72 to 1.95), P < 0.0001), and no significant difference between AR and control (combined WMD 0.93 (95% confidence interval −0.54 to 2.40), P = 0.22). HO-1 expression were also reviewed, asthma group produced greater expression of HO-1 than control group with significant difference (combined standardized mean difference (SMD) 2.98 (95% confidence interval 1.13 to 4.84), P = 0.002). After corticosteroid therapy, significantly different levels of eCO were produced after corticosteroid therapy than did asthma group (combined WMD −1.23 (95% confidence interval −2.43 to −0.03), P = 0.04). The analysis reveals that eCO levels were significantly raised in asthma and it may attribute to high expression of HO-1, but there were no significantly high eCO levels between AR and control groups. Due to sensitivity to corticosteroid inhibition, eCO may be used as a practical marker to detect and monitor exacerbation of asthma.