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Plastic bronchitis (PB) constitutes a life-threatening pulmonary disorder, predominantly attributed to Mycoplasma pneumoniae (MP) infection. The pathogenic mechanisms involved remain largely unexplored, leading to the absence of reliable approaches for early diagnosis and clear treatment. Thus, the present investigation aimed to develop an MP-induced mouse model of PB, thereby enhancing our understanding of this complex condition. In the first stage, healthy BALB/c mice were utilized to investigate the optimal methods for establishing PB. This involved the application of nebulization (15–20 min) and intratracheal administration (6–50 μL) with 2-chloroethyl ethyl sulfide (CEES) concentrations ranging from 4.5% to 7.5%. Subsequently, the MP model was induced by administering an MP solution (2 mL/kg/day, 108 CFU/50 μL) via the intranasal route for a duration of five consecutive days. Ultimately, suitable techniques were employed to induce plastic bronchitis in the MP model. Pathological changes in lung tissue were analyzed, and immunohistochemistry was employed to ascertain the expression levels of vascular endothelial growth factor receptor 3 (VEGFR-3) and the PI3K/AKT/mTOR signaling pathway. The administration of 4.5% CEES via a 6 µL trachea was the optimal approach to establishing a PB model. This method primarily induced neutrophilic inflammation and fibrinous exudate. The MP-infected group manifested symptoms indicative of respiratory infection, including erect hair, oral and nasal secretions, and a decrease in body weight. Furthermore, the pathological score of the MP+CEES group surpassed that of the groups treated with MP or CEES independently. Notably, the MP+CEES group demonstrated significant activation of the VEGFR-3 and PI3K/AKT/mTOR signaling pathways, implying a substantial involvement of lymphatic vessel impairment in this pathology. This study successfully established a mouse model of PB induced by MP using a two-step method. Lymphatic vessel impairment is a pivotal element in the pathogenetic mechanisms underlying this disease entity. This accomplishment will aid in further research into treatment methods for patients with PB caused by MP. [ABSTRACT FROM AUTHOR]

Objective: To investigate the development, distribution and GLUT-1 expression of infantile hemangioma and to discuss the early surgical intervention for better results and avoiding severe complication., Methods: The lesion site of each case was recorded and analyzed by SPSS V13.0 to study the distribution. The operation was guided by the principle of plastic surgery to remove the hemangioma. The GLUT-1 expression was detected by immunohistochemical technique in all the resected samples., Results: All the results were satisfactory. The GLUT-1 expression was positive in all the cases. The incidences in different sites were significantly different (P < 0.05). 71.7% of the hemangiomas were located at upper and lower lip, periorbital region and facial midline. It indicates that hemangioma is not randomly distributed. Most of them were located at the fusion of facial prominences during embryological development., Conclusions: Infantile facial hemangioma maybe originated from endothelial progenitor cells of placenta which migrate and implant on the fusion of facial prominences. Early surgical intervention is one of the best choice for infantile facial hemangioma.

Background & Objective: Polymorphisms of human leukocyte antigen (HLA) gene play an important role in the development of cervical cancer. This study was to screen single nucleotide polymorphisms (SNPs) of HLA-DQA1 gene involved in susceptibility of cervical cancer by a bioinformatics approach, and analyze their correlations to abnormal gene functions., Methods: SNPs of HLA-DQA1 were screened from a public database dbSNP by SNPper software, and relevant FASTA subsequences were also obtained from dbSNP. PARSESNP software was used to analyze cSNPs., Results: Two SNPs, rs9272693 and rs9272703, which may induce mis-sense mutation, were identified in codon region of HLA-DQA1 gene. A PSSM difference>10 was used to predict deleterious mutation., Conclusions: SNPper software in combination with PARSESNP software could be used to analyze SNPs of HLA-DQA1 gene and select the variants in a conserved region, and it provides an evaluation criterion. But the results need to be verified in cervical cancer patients and control populations.