Child ; Contraindications ; Humans ; Immunotherapy ; adverse effects ; Rhinitis, Allergic, Perennial ; therapy

Child ; Humans ; Immunoglobulin E ; blood ; Rhinitis, Allergic, Perennial ; diagnosis ; Skin Tests

Bronchoalveolar Lavage ; Child ; Child, Preschool ; Female ; Humans ; Male ; Pneumonia, Mycoplasma ; therapy ; Pulmonary Atelectasis ; therapy

Administration, Inhalation ; Humans ; Respiratory Therapy

Otolaryngology

Objective: To explore the effect of suberoylanilide hydroxamic acid (SAHA) improving cardiac hypertrophy via inhibiting histone deacetylases (HDAC) in experimental mice and to provide a new idea for prevention and treatment of cardiac hypertrophy. Methods: Cardiac hypertrophy mice model was established by thoracic aorta ligation. A total of 60 Kunming mice were randomly divided into 4 groups: Normal control group, Sham operation group, Cardiac hypertrophy (CH) group and CH+SAHA group. There were 6 mice used in each group. Myocardial cell morphology was observed by HE staining, cardiac function was assessed by echocardiography, mRNA and protein expressions of HDAC5 (the isoform of HDAC) and β-MHC were examined by RT-PCR and Western blot analysis. Results: The mice in CH group had myocardial cell hypertrophy, disordered arrangement and hyperchromatic nucleus. Compared with Sham operation group, CH group showed decreased left ventricular end diastolic diameter (LVEDD), left ventricular end diastolic volume (LVEDV) and increased thickness of inter-ventricular septum (IVS), allP<0.05; CH group presented elevated mRNA and protein expressions of HDAC5 and β-MHC,P<0.05. SAHA obviously decreased HDAC5 expression, down regulated cardiac hypertrophy related β-MHC gene expression, improved cardiac function and hypertrophy, all P<0.05. Conclusion: HDAC were involved in myocardial hypertrophy; SAHA could inhibit HDAC expression and therefore,improved myocardial hypertrophy in experimental mice.

[ ABSTRACT] AIM: To investigate the regulatory mechanism of histone acetylation on cardiac hypertrophy in -duced by phenylephrine , and to provide a new idea for preventing and curing hypertrophic cardiomyopathy .METHODS:Phenylephrine was given by continuous subcutaneous injection for modeling cardiac hypertrophy in C 57BL/6 mice.The le-vel of histone H3 lysine 27 acetylation (H3K27ac) in the promoter of cardiac nuclear transcription factor GATA4 and the mRNA expression of GATA4 were identified by chromatin immunoprecipitation (ChIP) and real-time PCR, respectively. Meanwhile, the protein expression of histone H3K27ac, atrial natriuretic peptide (ANP) and α-myosin heavy chain (α-MHC) was determined by Western blot .Cardiac hypertrophy in the mice was observed by HE staining and echocardio-graphy.RESULTS:The results of Western blot showed that the level of histone H 3K27ac in phenylephrine group was sig-nificantly increased compared with normal saline group (P<0.05), and ChIP-qPCR data showed that the level of histone H3K27ac in the promoter of GATA4 was increased significantly in the same samples (P<0.05).The expression levels of GATA4 mRNA and ANP protein in phenylephrine group were apparently increased compared with normal saline group ( P<0.05).However, histone acetylase inhibitor anacardic acid attenuated histone H 3K27 hyperacetylation induced by pheny-lephrine, and downregulated the over-expression of GATA4 and ANP in the heart of the mice (P<0.05).HE staining and echocardiography data showed that phenylephrine apparently increased left ventricular posterior wall thickness and de -creased left ventricular end-systolic diameter and left ventricular end-diastolic diameter , while anacardic acid also reversed these indexes that mentioned above and attenuated cardiac hypertrophy induced by phenylephrine in the mice .CONCLU-SION:Histone acetylation modification imbalance is involved in cardiac hypertrophy induced by phenylephrine , and the histone acetylase inhibitor anacardic acid decreases histone hyperacetylation induced by phenylephrine and attenuates car -diac hypertrophy in the mice .

Objective To investigate if the anticancer prescription Fuzhengyiaitang in combination with progestogen matching chems can have better clinical effects than progestogen alone.Methods Collecting 60 patients and grouped into two randomly.One group named the experimental group and the other is named the control.The experimental group is given Fuzhengyiaitang and progestogen and the control ine is given the progestogen alone.The clinical effects are investigated.Results The experimental group had better clinical effects than the other one and the results had statistical significance.The experimental group are stronger,had better immunal functions and less side effects.Conclusion Fuzhengyiaitang and progestogen match cbems Can have better clinical effects in treating the stage I's operation.

OBJECTIVE To evaluate the association between the results of skin prick test (SPT) of dust mites and serum specific IgE (S-IgE). METHODS A total of 170 patients with allergic rhinitis received SPT and detection of S-IgE of Der p and Der f. The positive rates and grades of S-IgE to different diameters of skin reaction or skin index (SI) were compared. RESULTS The positive rates and grades of S-IgE showed significant differences among different diameters of skin reaction or skin index (SI) patients. The positive rates and grades of S-IgE increased significantly according to the diameters of skin reaction or SI. CONCLUSION There is a significant association between SPT of dust mites and S-IgE.

Objective:To investigate the effects of Helicobacter pylori on NLRP3 inflammasomes activation in THP-1 ( human monocytic cell line) -derived macrophages and evaluate the role of ROS.Methods:H.pylori strain SS1 was co-cultured with the THP-1-derived macrophages at a multiplicity of infection (MOI) of 1∶100 based on trial results with different MOIs (ratios of THP-1 cells to bacteria ranging from 1∶25 to 1∶200).The co-culture supernatants and THP-1 cells were collected at various time points (3 h,6 h,12 h,24 h) and cytokine production was quantitated using ELISA analysis.The generation of intracellular ROS was detected by FCM,and the mRNA transcript levels of NLRP3 and caspase-1 were measured by Real-time PCR.Western blot was employed to analyze the expression of active caspase-1 subunit ( p10).Then we observed the inhibitory effects of NAC and siRNA specific for NLRP3 on the ex-pression of NLRP3 inflammasome-related components and the secretion of cytokines induced by H.pylori.Results:We found that H.pylori SS1 induced IL-1βand IL-18 production in human acute monocytic leukemia cell line THP-1 in a time-and dose-dependent manner.We further showed that H.pylori could induce the mRNA expressions of NLRP3 and caspase-1 in THP-1 cells.Moreover, release of IL-1βand IL-18 from H.pylori-infected THP-1 cells was suppressed by the ROS scavenger NAC,which was an agent known to inhibit NLRP3 inflammasome formation.NAC administration also resulted in a significant decrease in the level of H.pylori-induced caspase-1 protein expression in THP-1 cells.Additionally,secretion of IL-1βand IL-18 in response to H.pylori infection was remarkably reduced by NLRP3-siRNA.Conclusion:The induction of IL-1βand IL-18 secretion by H.pylori strain SS1 in THP-1 cells could be mediated through activation of NLRP3 inflammasome via ROS signaling pathway, which may be involved in the host innate immune defence and the pathogenesis of the bacteria.