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The objective of the present study was to investigate the effect of transoral endoscopic adenoidectomy on peripheral blood T lymphocyte subsets in pediatric patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and its treatment strategy. Ninety-eight pediatric patients with adenoidal hypertrophy associated with OSAHS admitted to the Department of Otolaryngology, Xuzhou Children's Hospital were selected. After admission, patients received perfected 24 h polysomnogram monitoring, routine blood examination, fasting blood biochemistry examination, T-lymphocyte subset count, 24 h ambulatory blood pressure monitoring, and nasopharyngeal computed tomography. After patients were diagnosed with adenoidal hypertrophy associated with OSAHS, they underwent transoral endoscopic adenoidectomy with a power microdebrider. Patients were evaluated at 3-, 6- and 12-week follow-up visits. The CD3+, CD4+, and CD8+ T-cell counts, CD4+/CD8+ T lymphocyte ratio, and changes of 24 h ambulatory blood pressure before and after surgery were recorded. After the 6-week follow-up visit, the mean CD4+ T lymphocyte count in patients was increased significantly compared with that before surgery, the CD4+/CD8+ T lymphocyte ratio increased gradually, and the differences were statistically significant (P<0.05). The frequency of nocturnal awakening of patients was decreased significantly after surgery and the duration of nocturnal sleep was extended significantly (P<0.05). Through analysis of the preoperative and postoperative clinical data of pediatric patients, the CD4+/CD8+ T lymphocyte ratio was negatively correlated with mean arterial pressure (MAP) (r=-1.06, P=0.003). In conclusion, adenoidectomy can significantly decrease the MAP in pediatric patients with OSAHS and increase the duration of nocturnal sleep. The peripheral blood CD4+/CD8+ T lymphocyte ratio in pediatric patients was significantly negatively correlated with MAP. [ABSTRACT FROM AUTHOR]

Chondrocytes are specialized cells that form cartilage tissue, and are able to respond to their osmotic environment and exercise important roles in endochondral ossification via undergoing proliferation, hypertrophy and apoptosis. The transient receptor melastatin potential 7 (TRPM7) cation channel can modulate the intracellular and extracellular levels of Ca2+ and Mg2+, and therefore the cellular osmotic environment. However, the molecular pathways involved in TRPM7‑mediated signal transduction have yet to be elucidated. In the present study, the expression and functionality of TRPM7 were investigated during chondrocyte proliferation and hypertrophy. The ATDC5 mouse cell line was employed and cellular viability was evaluated using the MTT assay, whereas hypertrophy was monitored via evaluating the expression of chondrogenic marker genes and the activity of alkaline phosphatase (ALP). Gene expression of TRPM7 appeared slightly upregulated during the proliferative stages of chondrocyte development, and significantly upregulated during the hypertrophic stages, suggesting the importance of Ca2+/Mg2+homeostasis for chondrocyte growth. Low extracellular Ca2+/Mg2+levels significantly reduced the expression of type X collagen, Indian hedgehog homolog (Ihh) and matrix metalloproteinase (MMP)‑13 genes, as well as ALP activity; however, cell viability remained unaffected. Conversely, the gene expression levels of TRPM7 appeared upregulated in ATDC5 cells under low extracellular Ca2+ or Mg2+ conditions. Silencing TRPM7 expression during the chondrocyte differentiation period also reduced type X collagen, Ihh and MMP‑13 gene expression, and ALP activity. Furthermore, the phosphatidylinositol‑4,5‑bisphosphate 3‑kinase (PI3K)‑Akt signaling pathway was activated following TRPM7 overexpression, and inhibited following TRPM7 silencing. Notably, the actions of TRPM7 on chondrocyte hypertrophy were abolished through the inhibition of PI3K‑Akt signaling. The present results suggested that TRPM7 may be involved in Ca2+/Mg2+homeostasis during chondrocyte hypertrophy, and contribute to endochondral ossification via interacting with the PI3K‑Akt signaling pathway. [ABSTRACT FROM AUTHOR]

Rhinitis is a common global disorder that impacts on the quality of life of the sufferer and caregivers. Treatment for pediatric rhinitis is empirical and does not include a detailed history of the allergy triggers or allergy testing. Thus, allergen avoidance advice is not tailored to the child's sensitivities, which may result in adenoid hypertrophy. However, infant onset rhinitis, especially its relationship with respiratory viruses, remains to be further clarified. Rhinitis basically involves inflammation of the upper nasal lining, presenting typically with symptoms of runny nose (rhinorrhea), nasal blockage, and/or sneezing. While not typically fatal, it does impose significant health, psychological, and monetary burden to its sufferers, and is thus considered a global health problem. Previous findings showed that immunotherapy had significant clinical efficacy in children with allergic rhinitis. The present review article aims to highlight recent perspectives pertaining to the rhinitis risk factors especially in pediatric patients. [ABSTRACT FROM AUTHOR]

Fowlicidins are a group of cathelicidin antimicrobial peptides that were initially identified in chickens. Fowlicidin-2, which is composed of 31 amino acids, is widely expressed in the majority of tissues in chickens and has an important role in innate immunity. In the present study, a recombinant expression system for fowlicidin-2 was successfully constructed using Pichia pastoris X-33 and the expression vector pPICZα-A. Under the optimized fermentation conditions, 85.6 mg fowlicidin-2 with >95% purity was obtained from 1 liter culture medium following purification by ion exchange chromatography and reversed phase high performance liquid chromatography. The recombinant fowlicidin-2 exhibited broad spectrum antimicrobial activity and had a minimum inhibitory concentration ranging from 1 to 4 μM. Furthermore, recombinant fowlicidin-2 exhibited hemolytic activity, promoting 50% human erythrocyte hemolysis in the concentration range of 128-256 μM, and anticancer activity, resulting in the death of 50% of A375 human malignant melanoma cells in the concentration range of 2-4 μM. The results of the present study suggest that recombinant fowlicidin-2 may be a promising candidate for therapeutic applications. [ABSTRACT FROM AUTHOR]

The aim of the present study was to determine the in vitro susceptibility of wild-type and mutant clinical isolates of Chlamydia (C.) trachomatis strains to erythromycin, azithromycin and josamycin, and to identify the resistance-conferring 23S ribosomal (r)RNA mutations in the isolates. The wild-type resistant isolates were defined as those with minimum inhibitory concentration values above the tissue concentration of the antibiotic in the urogenital system. Furthermore, all resistant C. trachomatis isolates were exposed to sub-inhibitory concentrations of macrolides, and 13 resistant mutants were selected following serial passages. Among the 8 wild-type isolates that were resistant to erythromycin, 3 isolates had a mutation at T2611C in the 23S rRNA gene while the others did not show any 23S rRNA mutations. The selected mutant isolates showed a 4- to 16-fold reduction in in vitro sensitivities. With regard to the mutant strains, the T2611C mutation was found in 10 isolates, A2057G mutation in 6 isolates, and A2059G mutation in 1 isolate. Thus, the macrolide-resistant isolates of the wild-type strain had different mutations from those selected by exposure to sub-inhibitory concentrations of macrolides. Also, since 23S rRNA mutations were not identi- fied in certain isolates, it was considered that other molecular mechanisms may also be responsible for the macrolide resistance of C. trachomatis. [ABSTRACT FROM AUTHOR]