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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.

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.

Background The mechanisms responsible for the development of allergic rhinitis(AR) are not fully understood. The present study was designed to explore the possible roles of carbon monoxide(CO) on the pathogenesis of AR. Methods AR guinea pig model was established by nasal ovalbumin sensitization. Twenty-four AR guinea pigs were divided into four groups, 6 in each: Saline control group, AR sensitized group, Hemin treated group, and Zinc protoporphyrin (ZnPP) treated group. The frequency of sneezing and nose rubbing was recorded. Leukocyte infiltration in nasal lavage fluid, serum IgE level and plasma CO were measured. Expression of heme oxygenase-1 (HO-1) mRNA in nasal mucosa was determined by real time RT-PCR, and expression of HO-1 protein was detected by immunohistochemistry. Results The frequency of sneezing and nose rubbing, leukocyte infiltration, serum IgE, plasma CO, and HO-1 mRNA levels in sensitized guinea pigs were higher than those of control (P < 0.05). Except for serum IgE level, all above parameters were even higher (P < 0.05) when treated with Hemin, a heme oxygenase-1 inducer; but significantly decreased (P < 0.05) when treated with ZnPP, a heme oxygenase inhibitor. Immunohistochemical results showed that positive staining of HO-1 was present in the lamina of mucosa of sensitized guinea pigs, and there was an increase of HO-1 immunoreactivity with Hemin administration (P < 0.05) and a decrease with ZnPP treatment. Conclusion The endogenous CO may take part in the inflammation process of AR and is positively correlated with expression of HO-1 in nasal mucosa. Endogenous CO plays a significant role in the pathogenesis of AR.