OBJECTIVE: Discussion of lung function changes in patients with allergic rhinitis and its clinical significance. METHOD: Using UNICAP100 allergen detector testing 64 patients of allergic rhinitis without asthma symptoms, testing the value of serum total IgE and using immunofluorescence methods for testing inhalation allergen, simultaneously checking the pulmonary function and bronchial provocation. Checking the lung function of 64 patients with non-symptoms of allergic rhinitis in other departments (control group), lung function were compared into two groups of patients. RESULT: In the allergic rhinitis group, 37 patients had abnormal lung function (57.81%), 8 cases in them had obstructive pulmonary ventilation, 12 cases had small airway dysfunction, 31 cases had increased airway resistance respectively. In the control group 15 patients (23.44%) had pulmonary function abnormalities, 2 cases had obstructive pulmonary ventilation, 4 cases had small airway dysfunction, 11 cases had increased airway resistance respectively. Changes in lung function compared in the two groups was statistically significant (P < 0.05). Allergic rhinitis patients with abnormal lung function bronchial provocation test positive rate was significantly higher than the normal lung function in patients with allergic rhinitis, there had statistically significant difference between the two groups (P < 0.05). CONCLUSION After checking the lung function of non-asthmatic symptom patients with allergic rhinitis, we could find abnormal lung function patients of allergic rhinitis and do bronchial provocation test in them, there has important clinical significance of early detection and treatment the patients of allergic rhinitis with bronchial asthma.
Adult ; Bronchial Hyperreactivity ; physiopathology ; Case-Control Studies ; Female ; Humans ; Male ; Nasal Septum ; abnormalities ; Peak Expiratory Flow Rate ; Respiratory Function Tests ; Rhinitis, Allergic, Perennial ; physiopathology

Parkinson's disease (PD) is a kind of common degenerative diseases of the nervous system. Levodopa replacement therapy is the most important clinical treatment method. However, long-term use can lead to the occurrence of dyskinesia and seriously affect the quality of life of patients. The current treatment methods for PD dyskinesia include drug therapy and non-drug therapy; most patients with dyskinesia can got improvement well by adjusting the dosage of drugs, changing the methods of administration, combination medication, or surgical treatments. Based on this, this article reviews the latest research on the treatment of PD dyskinesia to further help clinical colleagues effectively treat PD dyskinesia.

To study the effect of miR-340-5p on the proliferation of laryngeal cancer Hep2 cells and explore its intrinsic molecular mechanism, so as to screen potential biomarkers and targets for the diagnosis and treatment of laryngeal cancer. The expression of miR-340-5p in laryngeal cancer tissues, paracancerous tissues, laryngeal cancer cell lines Hep2 and normal bronchial HBE cell lines was quantitatively analyzed by qRT-PCR; The double luciferase reporter vector was constructed to verify whether STAT3 was a potential target gene of microRNA-340-5p; The miR-340-5p mimics/inhibitor was transfected into Hep2 cells by liposome and verified by qRT-PCR; The CCK-8 method and Annexin V/PI method were used to analyze the proliferation and apoptosis of transfected cells; and Western Blot was used to detect the expression of STAT3 and Wnt/β-catenin pathway-related proteins after transfection. The results of qRT-PCR showed that the level of miR-340-5p in laryngeal cancer tissues and Hep2 cells was significantly lower than that in adjacent tissues and HBE cells, and the expression of miR-340-5p was significantly increased or decreased after overexpression or inhibition; Luciferase activity showed that miR-340-5p directly interacted with target gene STAT3 3'-UTR and negatively regulated its expression; Cell proliferation and apoptosis analysis showed that up-regulation of microRNA-340-5p could significantly inhibit the proliferation and induce apoptosis of Hep2 cells in vitro, and vice versa; Western Blot results showed that the levels of STAT3 and β-catenin, c-Myc, TCF-4, CyclinD1 and ROCK1 in Hep2 cells were significantly lower than those in the control group after over-expression of miR-340-5p, and vice versa. The expression of miR-340-5p is abnormally low in laryngeal cancer tissues and Hep2 cells. It can be used as a potential biological target for diagnosis and treatment of laryngeal cancer by targeting STAT3 gene to negatively regulate Wnt/β-catenin signaling pathway.

Objective: To study the effect of miR-340-5p on the proliferation of laryngeal cancer Hep2 cells and explore its intrinsic molecular mechanism, so as to screen potential biomarkers and targets for the diagnosis and treatment of laryngeal cancer. Method: The expression of miR-340-5p in laryngeal cancer tissues, paracancerous tissues, laryngeal cancer cell lines Hep2 and normal bronchial HBE cell lines was quantitatively analyzed by qRT-PCR; The double luciferase reporter vector was constructed to verify whether STAT3 was a potential target gene of microRNA-340-5p; The miR-340-5p mimics/inhibitor was transfected into Hep2 cells by liposome and verified by qRT-PCR; The CCK-8 method and Annexin V/PI method were used to analyze the proliferation and apoptosis of transfected cells; and Western Blot was used to detect the expression of STAT3 and Wnt/β-catenin pathway-related proteins after transfection. Result: The results of qRT-PCR showed that the level of miR-340-5p in laryngeal cancer tissues and Hep2 cells was significantly lower than that in adjacent tissues and HBE cells, and the expression of miR-340-5p was significantly increased or decreased after overexpression or inhibition; Luciferase activity showed that miR-340-5p directly interacted with target gene STAT3 3'-UTR and negatively regulated its expression; Cell proliferation and apoptosis analysis showed that up-regulation of microRNA-340-5p could significantly inhibit the proliferation and induce apoptosis of Hep2 cells in vitro, and vice versa; Western Blot results showed that the levels of STAT3 and β-catenin, c-Myc, TCF-4, CyclinD1 and ROCK1 in Hep2 cells were significantly lower than those in the control group after over-expression of miR-340-5p, and vice versa. Conclusion The expression of miR-340-5p is abnormally low in laryngeal cancer tissues and Hep2 cells. It can be used as a potential biological target for diagnosis and treatment of laryngeal cancer by targeting STAT3 gene to negatively regulate Wnt/β-catenin signaling pathway.