The Efficacy of Pyogenic Cavity Aerobic Therapy with Negative Pressure Drainage in the Treatment of Deep Neck Space Infections.

OBJECTIVE: To determine the effectiveness of pyogenic cavity aerobic therapy with negative pressure drainage in the treatment of deep neck space infections (DNSI). METHODS: The study was a prospective, observational analysis of 36 cases of DNSI at a tertiary care center. The patients were divided into two groups according to the treatment method. Group A was treated with pyogenic cavity aerobic therapy with negative pressure drainage and included 13 patients (6 males and 7 females), while group B was treated with traditional incision debridement drainage and included 23 patients (12 males and 11 females). The average hospitalization days and doctors' workload (ie, average days of postoperative dressing changes) were analyzed and compared between the two groups. RESULTS: The mean hospitalization days in the traditional dressing group were 26.74 ± 3.39 days, while the average days of postoperative dressing change were 25.91 ± 3.43 days. In contrast, the averages for hospitalization days and days of postoperative dressing changes in the pyogenic cavity aerobic therapy plus negative pressure drainage were 11.08 ± 2.11 and 3.69 ± 0.21 days, respectively. All 36 patients were cured. Compared with the group B, group A had a shorter hospital stays and lower doctor workloads (P < 0.001). CONCLUSION: Pyogenic cavity aerobic therapy is an effective and simple method for changing dressings after DNSI. This therapy, when combined with negative pressure drainage, shortens hospitalization days and days that require a dressing change. This has reduced the workload of clinical doctors and pain experienced by patients. This therapy also has a high degree of safety and a very satisfactory curative effect.

Effect of PM2.5 on MicroRNA Expression and Function in Nasal Mucosa of Rats With Allergic Rhinitis.

BACKGROUND: Particulate matter 2.5 (PM2.5) refers to particulate matter with aerodynamic equivalent diameter less than or equal to 2.5 µm, which is an important component of air pollution. PM2.5 aggravates allergic rhinitis (AR) and promotes AR nasal mucosa inflammation. Therefore, the influence of PM2.5 inhalation exposure on microRNA (miRNA) expression profiles and function in the nasal mucosa of AR rats was investigated. METHODS: Female Sprague Dawley rats were distributed randomly to 2 groups: AR model PM2.5 exposure group (ARE group) and AR model PM2.5-unexposed control group (ARC group). The rats of ARE group were made to inhale PM2.5 at a concentration of 200 µg/m3, 3 h/day, for 30 days. miRNA expression profiles of the nasal mucosa from both groups were determined using an miRNA gene chip and were verified by quantitative real-time PCR (qRT-PCR). Gene function enrichment analysis was performed using bioinformatics analysis. RESULTS: The ARE group revealed 20 significantly differentially expressed miRNAs, including 4 upregulated and 16 downregulated miRNAs (fold change > 1.5 or < 0.66, P < .05). Of these, 9 selected miRNAs were verified by qRT-PCR, and the results of 8 miRNAs were in accordance with the miRNA gene chip results, with highly positive correlation (r = .8583, P = .0031). Numerous target genes of differentially expressed miRNAs were functionally enriched in high-affinity immunoglobulin E receptor signaling, ErbB signaling, mucin O-glycans biosynthesis, transforming growth factor ß signaling, mitogen-activated protein kinase signal transduction, phosphatidylinositol signaling, mucopolysaccharide biosynthesis, mammalian target of rapamycin signaling, T cell receptor signaling, Wnt signaling, chemokine signal transduction, and natural killer cell-mediated cytotoxicity pathways. CONCLUSIONS: PM2.5 causes significant changes in miRNA expression in the nasal mucosa of AR rats. miRNA plays an important role in regulating PM2.5 effects in AR rat biological behavior and mucosal inflammation. This study provides a theoretical basis for the prevention and treatment of AR from the effects of environmental pollution on the gene regulation mechanism.

Effects of PM2.5 on mucus secretion and tissue remodeling in a rabbit model of chronic rhinosinusitis.

BACKGROUND: According to epidemiologic studies, fine particulate matter (particulate matter ≤2.5 µm, PM2.5) is closely associated with increases in the incidence and severity of chronic rhinosinusitis (CRS). However, the role of PM2.5 in the pathophysiology of CRS remains largely unknown. In this study, we investigated the effects of PM2.5 on nasal cilia, tissue remodeling, and mucus hypersecretion in a rabbit model of CRS. METHODS: CRS rabbits were exposed to ambient PM2.5 via a PM2.5 inhalation exposure system. The degree of ciliary damage was evaluated using scanning electron microscopy (SEM). Histopathologic changes were determined using periodic acid-Schiff (PAS) staining of goblet cells and Masson trichrome (MT) staining for collagen in the nasal mucosa. MUC5AC expression was assessed by immunohistochemistry. RESULTS: PM2.5 exposure substantially aggravated ciliary disruption in rabbits with CRS. PM2.5 also significantly increased goblet cell hyperplasia and collagen deposition, as reflected by PAS and MT staining. The nasal mucosa of CRS rabbits displayed markedly elevated MUC5AC expression after PM2.5 exposure. CONCLUSION: Increases in ciliary disruption, nasal remodeling, and mucus hypersecretion may be the pathophysiologic mechanisms underlying the PM2.5-induced aggravation of CRS.

Chinese Society of Allergy Guidelines for Diagnosis and Treatment of Allergic Rhinitis.

Allergic rhinitis (AR) is a global health problem that causes major illnesses and disabilities worldwide. Epidemiologic studies have demonstrated that the prevalence of AR has increased progressively over the last few decades in more developed countries and currently affects up to 40% of the population worldwide. Likewise, a rising trend of AR has also been observed over the last 2-3 decades in developing countries including China, with the prevalence of AR varying widely in these countries. A survey of self-reported AR over a 6-year period in the general Chinese adult population reported that the standardized prevalence of adult AR increased from 11.1% in 2005 to 17.6% in 2011. An increasing number of Journal Articles and imporclinical trials on the epidemiology, pathophysiologic mechanisms, diagnosis, management and comorbidities of AR in Chinese subjects have been published in international peer-reviewed journals over the past 2 decades, and substantially added to our understanding of this disease as a global problem. Although guidelines for the diagnosis and treatment of AR in Chinese subjects have also been published, they have not been translated into English and therefore not generally accessible for reference to non-Chinese speaking international medical communities. Moreover, methods for the diagnosis and treatment of AR in China have not been standardized entirely and some patients are still treated according to regional preferences. Thus, the present guidelines have been developed by the Chinese Society of Allergy to be accessible to both national and international medical communities involved in the management of AR patients. These guidelines have been prepared in line with existing international guidelines to provide evidence-based recommendations for the diagnosis and management of AR in China.

Nasal epithelial barrier disruption by particulate matter ≤2.5 µm via tight junction protein degradation.

Upper airway diseases including sinonasal disorders may be caused by exposure to fine particulate matter (≤2.5 µm; PM2.5), as proven by epidemiological studies. PM2.5 is a complex entity whose chemical constituents and physicochemical properties are not confined to a single, independent "particle" but which in this study means a distinctive environmental "toxin." The mechanism whereby PM2.5 induces nasal epithelial barrier dysfunction leading to sinonasal pathology remains unknown. In the present study, human nasal epithelial cells were exposed to non-cytotoxic doses of PM2.5 to examine how PM2.5 affects the nasal epithelial barrier. Tight junction (TJ) integrity and function were assessed by transepithelial electric resistance and paracellular permeability. The expression levels of TJ proteins such as zona occludens-1, occludin and claudin-1 were assessed by immunofluorescence staining and western blot. PM2.5 exposure induced epithelial barrier dysfunction as reflected by increased paracellular permeability and decreased transepithelial electric resistance. TJ proteins zona occludens-1, occludin and claudin-1 were found to be downregulated. Pretreatment with N-acetyl-l-cysteine alleviated PM2.5-mediated reactive oxygen species generation in RPMI 2650 cells, further preventing barrier dysfunction and attenuating the degradation of TJ proteins. These results suggest that PM2.5 induces nasal epithelial barrier disruption via oxidative stress, and N-acetyl-l-cysteine counteracts this PM2.5-mediated effect. Thus, nasal epithelial barrier disruption caused by PM2.5, which leads to sinonasal disease, may be prevented or treated through the inhibition of reactive oxygen species.

T-helper type 1-T-helper type 2 shift and nasal remodeling after fine particulate matter exposure in a rat model of allergic rhinitis.

BACKGROUND: Exposure to fine particulate matter (particulate matter ≤2.5 µm [PM2.5]) increases the risk of allergic rhinitis (AR), but the underlying mechanisms remains unclear. Thus, we investigated the roles of T-helper (Th)1-Th2 cytokines and nasal remodeling after ambient PM2.5 exposure in a rat model of AR. METHODS: Female Sprague-Dawley rats were randomized into six groups: a negative control group, a group of healthy rats exposed to 3000 µg/m3 PM2.5, an ovalbumin (OVA) induced AR model, and three PM2.5-exacerbated AR groups exposed to three different concentrations (200, 1000, and 3000 µg/m3) of PM2.5 for 30 days via inhalation. Nasal symptoms, levels of Th1-Th2 cytokines, the degree of eosinophilia in nasal lavage fluid (NLF), and the messenger RNA (mRNA) expressions of transcription factors GATA-3 and T-bet in the nasal mucosa were measured in each individual rat. Hyperplasia of globet cells and collagen deposition were examined by histology. RESULTS: PM2.5 significantly increased the number of sneezes and nasal rubs in rats with AR. PM2.5 also significantly decreased interferon gamma and increased interleukin (IL) 4 and IL-13 expressions as well as the number of eosinophils in NLF. The mRNA expression of GATA-3 in the nasal mucosa of rats with AR was upregulated by PM2.5, whereas T-bet was significantly downregulated. Statistically significant differences in OVA-specific serum immunoglobulin E, goblet cell hyperplasia, collagen deposition, and transforming growth factor beta 1 levels were observed between the PM2.5-exacerbated AR groups and the AR model group. CONCLUSION: Analysis of our data indicated that an increase in the immune response with Th2 polarization and the development of nasal remodeling may be the immunotoxic mechanisms behind the exacerbation of AR after exposure to PM2.5.

PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats.

Exposure to PM2.5 (particulate matter ≤2.5 µm) increases the risk of nasal lesions, but the underlying mechanisms, especially the mechanisms leading to mitochondrial damage, are still unclear. Thus, we investigated the in vivo effects of PM2.5 exposure on the inflammatory response, oxidative stress, the enzyme activities of Na⁺K⁺-ATPase and Ca2+-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. Exposure to PM2.5 occurred through inhalation of a PM2.5 solution aerosol. The results show that the PM2.5 exposure induced increased levels of malondialdehyde (MDA) and levels of proinflammatory mediators, including interleukin 6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). These changes were accompanied by decreases in the activities of total superoxide dismutase (T-SOD), Na⁺K⁺-ATPase, and Ca2+-ATPase in rat nasal mucosa. PM2.5 significantly affected the expression of specific mitochondrial fission/fusion genes (OPA1, Mfn1, Fis1, and Drp1) in nasal mucosa. These changes were accompanied by abnormal alterations of mitochondrial structures, including mitochondrial swelling, cristae disorder, and even fission resulting from higher doses of PM2.5. Our data shows that oxidative damage, inflammatory response, and mitochondrial dysfunction may be the toxic mechanisms that cause nasal lesions after exposure to PM2.5.

Human papillomavirus infection and the malignant transformation of sinonasal inverted papilloma: A meta-analysis.

A growing number of molecular epidemiological studies have been conducted to evaluate the association between human papillomavirus (HPV) infection and the malignancy of sinonasal inverted papilloma (SNIP). However, the results remain inconclusive. Here, a meta-analysis was conducted to quantitatively assess this association. Case-control studies investigating SNIP tissues for presence of HPV DNA were identified. The odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by the Mantel-Haenszel method. An assessment of publication bias and sensitivity analysis were also performed. We calculated a pooled OR of 2.16 (95% CI=1.46-3.21, P<0.001) without statistically significant heterogeneity or publication bias. Stratification by HPV type showed a stronger association for patients with high-risk HPV (hrHPV) types, HPV-16, HPV-18, and HPV-16/18 infection (OR=8.8 [95% CI: 4.73-16.38], 8.04 [95% CI: 3.34-19.39], 18.57 [95% CI: 4.56-75.70], and 26.24 [4.35-158.47], respectively). When only using PCR studies, pooled ORs for patients with hrHPV, HPV-16, and HPV18 infection still reached statistical significance. However, Egger's test reflected significant publication bias in the HPV-16 sub-analysis (P=0.06), and the adjusted OR was no longer statistically significant (OR=1.65, 95%CI: 0.58-4.63). These results suggest that HPV infection, especially hrHPV (HPV-18), is significantly associated with malignant SNIP.