Therapeutic effects and modulatory mechanism of Alpiniae oxyphyllae Fructus in chronic intermittent hypoxia induced enuresis in rats.

OBJECTIVE: The objective of this study was to explore the effect of Alpiniae oxyphyllae Fructus (AOF) on a rat model of chronic intermittent hypoxia (CIH)-induced enuresis. Findings of this study may help identify therapeutic targets in children with nocturnal enuresis (NE). METHODS: Female rats were randomly divided into a control group (saline gavage, 4 weeks of normal air), CIH group (saline gavage, 4 weeks of CIH), and AOF group (AOF gavage, 4 weeks of CIH). The variables measured in this study included water intake, urine output, bladder leak point pressure (BLPP), malondialdehyde (MDA) levels, and superoxide dismutase (SOD) activity. The expression levels of the purinergic P2X3 receptor, muscarinic M3 receptor, and ß3-adrenergic receptor (ß3-AR) in the bladder were also measured. The bladder was subjected to haematoxylin and eosin (HE) and Weigert staining, and histological changes were observed under a light microscope to evaluate the morphological changes in the bladder in each group. RESULTS: Compared with the control group, urine output was increased, and the BLPP was decreased in the CIH group, but AOF administration decreased urine output and increased BLPP. In addition, the serum MDA level increased and the SOD activity decreased in the CIH group compared with the control group. Administration of AOF decreased the MDA level and increased the SOD activity. Additionally, compared with the control group, HE and Weigert staining in the CIH group showed that the bladder detrusor muscle bundles were disordered and loose, some muscle bundles were broken, the content of collagen fibres in the gap was reduced, and the gap was significantly widened. However, following the administration of AOF, the bladder detrusor muscle bundles were neatly arranged, and the content of collagen fibres in the gap was increased. Furthermore, compared with the control group, the purinergic P2X3 receptor and muscarinic M3 receptor were expressed at higher levels, and ß3-AR was expressed at lower levels in the CIH group, but AOF administration decreased the expression of the purinergic P2X3 receptor and muscarinic M3 receptor and increased the expression of the ß3-AR. CONCLUSIONS: AOF improves enuresis by inhibiting oxidative stress and regulating the expression of the purinergic P2X3 receptor, muscarinic M3 receptor, and ß3 adrenergic receptor.

[Streptococcus pneumoniae induces SPLUNC1 and the regulatory effects of resveratrol].

OBJECTIVE: To investigate the host-defense role of short palate, lung, and nasal epithelium clone 1 (SPLUNC1) in Streptococcus pneumoniae (SP) infection and the effect of resveratrol (Res) on SPLUNC1 expression, and to provide new thoughts for the treatment of diseases caused by SP infection. METHODS: According to the multiplicity of infection (MOI), BEAS-2B cells with SP infection were divided into control group, MOI20 SP group, and MOI50 SP group. According to the different concentrations of Res, the BEAS-2B cells with MOI20 SP infection pretreated by Res were divided into 12.5Res+SP group, 25Res+SP group, and 50Res+SP group (the final concentrations of Res were 12.5, 25, and 50 µmol/L, respectively). Cell Counting Kit-8 was used to measure cell activity and determine the optimal concentration and action time of SP and Res. In the formal experiment, the cells were divided into control group, Res group, SP group, and Res+SP group. Real-time PCR and ELISA were used to measure the mRNA and protein expression of SPLUNC1. RESULTS: Over the time of SP infection, cell activity tended to decrease. Compared with the control group and the MOI20 SP group, the MOI50 SP group had a reduction in cell activity. Compared with the MOI20 SP group, the 25Res+SP group had increased cell activity and the 50Res+SP group had reduced cell activity (P<0.05). MOI20 SP bacterial suspension and 25 µmol/L Res were used for the formal experiment. Over the time of SP infection, the mRNA expression of SPLUNC1 in BEAS-2B cells firstly increased and then decreased in the SP group and the Res+SP group (P<0.05). Compared with the SP group, the Res+SP group had significant increases in the mRNA and protein expression of SPLUNC1 at all time points (P<0.05). Compared with the control group, the Res group had no significant changes in the mRNA and protein expression of SPLUNC1 (P>0.05). CONCLUSIONS: SP infection can induce SPLUNC1 expression and the host-defense role of SPLUNC1. Res can upregulate SPLUNC1 expression during the development of infection and enhance cell protection in a concentration- and time-dependent manner.

[Benign infantile convulsions associated with mild gastroenteritis: a clinical analysis and follow-up study].

OBJECTIVE: To study the clinical features and prognosis of benign infantile convulsions associated with mild gastroenteritis (BICE). METHODS: A retrospective analysis was performed for the clinical data of 436 children with BICE, and among these children, 206 were followed up for 1.5 to 7 years. Some parents were invited to complete the Weiss Functional Defect Scale to evaluate the long-term social function. RESULTS: The peak age of onset of BICE was 13-24 months, and BICE had a higher prevalence rate in September to February of the following year. Convulsions mainly manifested as generalized tonic-clonic seizures, which often occurred within 24 hours after disease onset and lasted for less than 5 minutes each time. Sometimes they occurred in clusters. During the follow-up of 206 children, only one had epileptiform discharge, and the other children had normal electroencephalographic results. The parents of all the 206 children thought their children had normal intelligence and had no marked changes in character. Based on the Weiss Functional Defect Scale completed by the parents of some BICE children, there was no significant difference in the long-term social function between BICE children and healthy children matched by age and sex. CONCLUSIONS: BICE mainly occurs in children aged 1-2 years, with the manifestation of transient generalized seizures in most children and cluster seizures in some children. BICE seldom progresses to epilepsy and has good prognosis.

Obesity in children with different risk factors for obstructive sleep apnea: a community-based study.

This study investigated the association between obesity and obstructive sleep apnea (OSA) in preschool and school-age children. Parents of obese and randomly chosen normal weight children completed a questionnaire on sleep-related symptoms, demography, family, and medical history. All subjects were invited to undergo polysomnography (PSG). OSA cases were defined as obstructive apnea hypopnea index (OAHI) ≥1. A total of 5930 children were studied with 9.5% obese (11.9% boys/6.1% girls), 205/2680 preschool and 360/3250 school children. There were 1030 children (535 obese/495 normal weight) who underwent PSG. OSA was higher in obese children and obese school children had higher OAHI, arousal index, and shorter total sleep time. However, there was no positive correlation between OSA and body mass index (BMI). The main risk factors for OSA in preschool children were adenotonsillar hypertrophy and recurrent respiratory tract infection. The main cause for OSA in school children was a history of parental snoring and obesity. Mallampati scores and sleep-related symptoms were found to be associated with OSA in both preschool and school children. CONCLUSION: We demonstrated differential risk factors for OSA in obese children, which suggest that a different mechanism may be involved in OSA development in preschool and school-age children. WHAT IS KNOWN: Various risk factors have been reported in obese children with OSA owing to the different age and different study design. Obese children have a higher prevalence and severity of obstructive sleep apnea (OSA). OSA risk factors in obese children are affected by different ages and study designs. WHAT IS NEW: A differential prevalence and risk factors for obese preschool and school-age children with OSA has been demonstrated.

[Lower respiratory tract infection caused by influenza virus A and influenza virus B in Wenzhou, China: a clinical analysis of 366 children].

OBJECTIVE: To compare the epidemiological and clinical features of lower respiratory tract infection (LRTI) caused by influenza virus A (IVA) and influenza virus B (IVB) in children. METHODS: The clinical data of 366 children with LRTI caused by influenza virus (IV), who were hospitalized in Yuying Children′s Hospital of Wenzhou Medical University between 2010 and 2014, were analyzed retrospectively, and there were 272 cases caused by IVA and 94 cases caused by IVB. RESULTS: IV was mainly prevalent from December to March of the next year, with the predominance of IVA. There were small peaks of IVA prevalence in July or September every other year, and IVB was prevalent from December to March of the next year every other year. The children with LRTI caused by IVA alone had a significantly higher white blood cell (WBC) count and significantly higher percentages of children with increased WBC, abnormal serum sodium, and abnormal serum potassium than those caused by IVB alone (P<0.05). However, there were no significant differences in age, sex, underlying diseases, clinical manifestations, and co-infection rate with bacteria or atypical pathogens between the two groups (P>0.05). The rate of co-infection with respiratory syncytial virus (RSV) was significantly higher in the IVB group than in the IVA group (P<0.01). CONCLUSIONS: IVA is prevalent in winter and spring every year and has small peaks in summer every other year, while IVB is prevalent in winter and spring every other year. Compared with IVB, IVA causes more cases of increased WBC and electrolyte disturbance. The children infected with IVB are more likely to be co-infected with RSV. The children with LRTI caused by IVA and IVB have similar clinical manifestations.

[Effects of asthma and inhaled corticosteroids in children on the final adult height: a systemic review and Meta analysis].

OBJECTIVE: To evaluate the effects of asthma and inhaled corticosteroids (ICS) in children on the final adult height. METHODS: A search was performed to collect studies evaluating the relationship between asthma and ICS in children and the final adult height in PubMed, BCI, EMbase, Web of Science, CNKI and Wanfang databases, then a systemic review and Meta analysis were conducted. RESULTS: Six studies evaluating the relationship between childhood asthma and the final adult height were enrolled. Three of them indicated that the final adult height was not influenced by childhood asthma. Two of them suggested a mild effect, and the effect was correlated with severity of childhood asthma. One of them indicated that a lower final adult height related to childhhod asthma was found only in black females without a high school education. Four studies evaluating the relationship between ICS and the final adult height were included. Compared with the non-ICS treatment group, healthy control group and the target height, ICS treatment had no effects on the final adult height. CONCLUSIONS: Childhood asthma does not or only mildly decrease the final adult height. ICS treatment does not significantly affect the final adult height.

Role of SIRT1 in Streptococcus pneumoniae-induced human ß-defensin-2 and interleukin-8 expression in A549 cell.

Streptococcus pneumoniae is an important pathogen of pneumonia in human. Human alveolar epithelium acts as an effective barrier and is an active participant in host defense against invasion of bacterial by production of various mediators. Sirtuin 1 (SIRT1), the prototypic class III histone deacetylase, is involved in the molecular control of lifespans and immune responses. This study aimed at examining the role of SIRT1 in mediating S. pneumoniae-induced human ß-defensin-2 (hBD2) and interleukin-8(IL-8) expression in the alveolar epithelial cell line A549 and the underlying mechanisms involved. A549 cells were infected with S. pneumoniae for indicated times. Exposure of A549 cells to S. pneumoniae increased the expressions of SIRT1 protein, hBD2 and IL-8 mRNA, and protein. The SIRT1 activator resveratrol enhanced S. pneumoniae-induced gene expression of hBD2 but decreased IL-8 mRNA levels. Blockade of SIRT1 activity by the SIRT1 inhibitors nicotinamide reduced S. pneumoniae-induced hBD2 mRNA expression but increased its stimulatory effects on IL-8 mRNA. S. pneumoniae-induced activation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK). SIRT1 expression was attenuated by selective inhibitors of ERK and p38 MAPK. The hBD2 mRNA production was decreased by pretreatment with p38 MAPK inhibitor but not with ERK inhibitor, whereas the IL-8 mRNA expression was controlled by phosphorylation of ERK. These results suggest that SIRT1 mediates the induction of hBD2 and IL-8 gene expression levels in A549 cell by S. pneumoniae. SIRT1 may play a key role in host immune and defense response in A549.

[Coordinated regulation of PI3K and Notch signal pathways in the activation and proliferation of CD4(+)T lymphocytes in asthma mice].

OBJECTIVE: To explore whether the signal pathways of phosphoinositide 3-kinase (PI3K) and Notch can realize coordinated regulation on the activation and proliferation of CD4(+)T lymphocytes. METHODS: Male BALB/c mice were randomly divided into control and asthma groups. Then the murine model of asthma was established by the method of ovalbumin (OVA) challenge. The CD4(+)T lymphocytes were isolated by magnetic activated cell sorter (MACS) and then activated with phytohaemagglutinin (PHA) (10 µg/ml) and IL-2 (1000 U/ml) for 6 h. Those cells were then divided into Group A: without any treatment; Group B: treatment with PI3K inhibitor (LY294002); Group C: treatment with Notch inhibitor (gamma-secretase inhibitor, DAPT); Group D: treatment with PI3K inhibitor and Notch inhibitor. The protein and transcription levels of Cyclin A, Cyclin D1 and P27(kip1) of CD4(+)T lymphocytes were assessed by flow cytometry and reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: The results of flow cytometry showed that the purity of MACS-isolated CD4(+)T lymphocytes was 90.0% ± 5.2% and the survival rate 94.8% ± 3.2%. The protein (28.0% ± 3.5%, 14.9% ± 3.4%) and mRNA levels (0.55 ± 0.16, 1.38 ± 0.42) of Cyclin A and Cyclin D1 in CD4(+)T lymphocytes of asthma group were significantly higher than those of the control group (13.4% ± 3.5%, 7.7% ± 1.8% and 0.32 ± 0.10, 0.92 ± 0.37) (P = 0.002, 0.036 and P = 0.007, 0.042). The protein and mRNA levels (23.3% ± 3.9% and 0.16 ± 0.03) of P27(kip1) of asthma group were significantly lower than those of control group (37.5% ± 5.8% and 0.32 ± 0.03, P = 0.006 and P = 0.000). The protein and mRNA levels of Cyclin D1 in groups A, B, C and D-treated CD4(+)T lymphocytes were 12.2% ± 3.7%, 7.3% ± 3.0%, 8.1% ± 2.3%, 4.2% ± 1.7% and 1.71 ± 0.44, 1.07 ± 0.31, 1.21 ± 0.32 and 0.62 ± 0.20 respectively; groups B, C and D decreased markedly compared with group A (all P < 0.01) while group D decreased significantly compared with groups B and C (all P < 0.05). The protein levels of P27(kip1) in groups A, B, C and D were 22.9% ± 3.0%, 31.6% ± 5.3%, 28.4% ± 5.6% and 44.6% ± 2.8% respectively; group B was significantly higher than that of group A (P = 0.016) while group D was significantly higher than those of groups A, B and C (P = 0.003, 0.004, 0.000). Meanwhile P27(kip1) mRNA levels in each group were 0.16 ± 0.07, 0.36 ± 0.09, 0.63 ± 0.08 and 0.99 ± 0.21 respectively; groups B, C and D were much higher than that of group A (P = 0.016, 0.000, 0.000) while group D was significantly higher than those of groups B and C (P = 0.000, 0.023). The protein and mRNA levels of CylinA showed no statistical significance among different experimental groups (all P > 0.05). CONCLUSION: The signal pathways of PI3K and Notch may coordinately up-regulate the expression of positive regulatory factor cylinD1 and down-regulation the expression of negative regulatory factor P27(kip1) of CD4(+)T lymphocytes.

[Application of continuous thoracic close drainage using central venous catheter in the treatment of tuberculous pleurisy in children].

OBJECTIVE: To study the clinical effect of continuous thoracic close drainage using central venous catheter instead of repeated thoracocentesis in the treatment of tuberculous pleurisy in children. METHODS: Thirty-nine children with tuberculous pleurisy, who received continuous thoracic close drainage using central venous catheter in addition to conventional antituberculous chemotherapy, were used as the observation group and 42 children with tuberculous pleurisy who underwent repeated thoracocentesis in addition to conventional antituberculous chemotherapy served as the control group. The two groups were compared in terms of time to pleural effusion absorption, improvement in pleural thickening, length of hospital stay, and puncture-related expenses. RESULTS: Compared with the control group, the observation group had significantly faster pleural effusion absorption (8 ± 4 d vs 12 ± 6 d; P < 0.01), significantly more improvement in pleural thickening (1.50 ± 0.25 mm vs 3.10 ± 0.30 mm; P < 0.05), a significantly shorter length of hospital stay (11 ± 3 d vs 18 ± 6 d; P < 0.01), and significantly lower puncture-related expenses (269 ± 24 yuan vs 475 ± 50 yuan; P < 0.05), as well as alleviated pain. CONCLUSIONS: Continuous thoracic close drainage using central venous catheter is superior to repeated thoracocentesis in the treatment of tuberculous pleurisy in children, and it holds promise for clinical application in pediatric patients.

[Clinical characteristics of children with Streptococcus pneumoniae septicemia and drug sensitivity of Streptococcus pneumoniae].

OBJECTIVE: To study the clinical characteristics of children who suffered from Streptococcus pneumoniae (SP) septicemia and the drug sensitivity of SP strains. METHODS: A retrospective analysis was performed on the clinical data of 25 children with SP septicemia between January 2009 and December 2012. RESULTS: Of the 25 cases, 16 (64%) were aged under 2 years, 5 (20%) were aged 2-5 years, and 4 (16%) were aged over 5 years. Fourteen cases (56%) were complicated by infection of other organs, and 5 cases (20%) had underlying chronic diseases. Fever was the most common clinical manifestation, and the majority presented with remittent fever. Eight patients with pneumonia or pyothorax had pulmonary symptoms. Five patients with purulent meningitis had neurological symptoms, five cases had hepatosplenomegaly and two cases had septic shock. Nineteen cases (76%, 19/25) had significantly elevated white blood cell (WBC) counts, twenty-one cases (84%, 21/25) had significantly elevated serum C-reactive protein (CRP) levels, and eight cases (50%, 8/16) had significantly elevated serum procalcitonin (PCT) levels. The drug sensitivity analysis showed that invasive SP had high resistance rates to penicillin (96%), clindamycin hydrochloride (88%) and erythromycin (84%), and it was completely sensitive to imipenem, vancomycin, levofloxacin and linezolid. The multi-drug resistance rate of invasive SP was up to 88%. Twenty-three cases (92%) were cured or improved after active treatment. CONCLUSIONS: SP septicemia is commonly seen in children aged under 2 years. The most common clinical manifestation is fever, accompanied by elevated WBC count, CRP level and PCT level, and it is usually complicated by pulmonary or brain infection. Resistance to multiple antibiotics is very common in SP strains, so it is important to properly use antibiotics according to drug sensitivity test results. Patients who receive active treatment have a good clinical outcome.

Urotensin upregulates transforming growth factor-ß1 expression of asthma airway through ERK-dependent pathway.

Airway smooth muscle cells (ASMCs) play a key role in the process of asthma airway remodeling. Urotensin II (UII) and transforming growth factor (TGF)-ß are potent mitogens for ASMCs proliferation. The study was aimed to determine whether UII-upregulated TGF-ß-mediated ASMCs proliferation and extracellular signal-regulated kinase (ERK) was required for such an effect. OVA-sensitized rats were challenged to induce asthma. Lung morphology and airway dynamic parameters were monitored. ASMCs from control and asthma rats were purified for the measurement of UII and TGF-ß1 expression. In vitro experiments were conducted to determine the direct effect of UII on TGF-ß1 expression by ASMCs. Finally, U0126, an ERK inhibitor was used to examine the role of ERK pathway in UII mediated TGF-ß1 upregulation. We found that both UII and TGF-ß1 were upregulated in asthma lung tissues. In vitro study on ASMCs further revealed that UII may render its effect on ASMCs cells through the upregulation of TGF-ß1. Data also supported the conclusion that ERK pathway was required, but not sufficient in UII-induced TGF-ß1 upregulation. The current study provides new evidence that UII is involved in the TGF-ß mediated mitogenic effect on ASMCs. UII, at least partially, uses ERK pathway to render such effect.

[Effects of dexamethasone on 15-lipoxygenase expression in lungs of asthmatic rats].

OBJECTIVE: 15-lipoxygenase (15-LO) is a prooxidant enzyme which is expressed in asthmatic lungs leading to formation of pro- and anti-inflammatory mediators. Gene expression profiling studies show the association between 15-LO and allergic asthma. This study was designed to observe the expression of 15-LO in lungs of asthmatic rats and examine the effects of dexamethasone on 15-lipoxygenase expression. METHODS: Twenty-seven male Sprague-Dawley (SD) rats were randomly divided into three groups: control, asthma and dexamethasone (DXM) intervention. An asthma model was prepared by sensitization and challenging with ovalbumin. The production of 15-LO in lung tissue homogenates was measured using ELISA.The expression of 15-LO mRNA in lungs was determined by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The levels of 15-LO mRNA and protein in the asthma group (0.51 ± 0.14 and 2080 ± 73 µg/mL, respectively) were lower than those in the control group (0.76 ± 0.15 and 2472 ± 106 µg/mL, respectively; P<0.01). DXM intervention increased significantly the levels of 15-LO mRNA and protein (1.02 ± 0.34 and 2562 ± 218 µg/mL) compared with the asthma group (P<0.01). CONCLUSIONS: The production of 15-LO in lung tissues is reduced in asthmatic rats. DXM can increase the expression of 15-LO in lung tissues and thus might provide anti-inflammatory effects in asthmatic rats.

[Effects of lentinan on interleukin-1ß-induced transdifferentiation of human embryonic lung fibroblasts to myofibroblasts].

OBJECTIVE: To study the effects of interleukin-1ß (IL-1ß) on transdifferentiation of human embryonic lung fibroblasts to myofibroblasts and the effects of lentinan on the transdifferentiation. METHODS: The human embryonic lung fibroblasts were cultured in vitro, and fibroblasts were treated with different concentrations of IL-1ß and lentinan. The proliferation activity of the human embryonic lung fibroblasts was evaluated by the Cell Counting Kit-8 (CCK-8). The expression of α-smooth muscle actin (α-SMA) protein was measured by immunocytochemistry. The levels of fibronectin (FN), typeⅠcollagen (ColⅠ) and α-SMA mRNA were detected by RT-PCR. RESULTS: Compared with the untreated control group, the absorbance value of cell proliferation, α-SMA protein levels, FN, ColⅠand α-SMA mRNA expression were significantly up-regulated after different concentrations of IL-1ß (0.1, 1, 10 ng/mL) treatment for 48 hrs (P<0.01). Lentinan treatment inhibited up-regulation of the cell proliferation activity, α-SMA protein levels, FN, ColⅠand α-SMA mRNA expression induced by IL-1ß in a dose-independent manner (P<0.01). CONCLUSIONS: Lentinan can suppress human embryonic lung fibroblast proliferation, fibroblast-myofibroblast transdifferentiation and extra cellular matrix synthesis induced by IL-1ß.

[The role of phosphorylation of c-Jun NH2-terminal kinase in airway remodeling of asthmatic rats and the effect of glucocorticoids].

OBJECTIVE: To study the role of phosphorylation of c-Jun NH2-terminal kinase (JNK) in asthmatic airway remodeling and to explore the effect of glucocorticoids on IL-1beta, JNK and airway remodeling. METHODS: Forty-eight 4 - 6 week old male SD rats were randomly divided into 4 groups with 12 rats in each group: the control group, the asthma group, the budesonide (BUD) group, and the dexamethasone (DXM) group. The asthma airway remodeling models were made by intra-peritoneal injection of ovalbumin (OVA) on days 1 and 8 and inhalation of OVA every other day for 12 weeks since day 15. The BUD group underwent inhalation of BUD 30 min before every inhalation; the DXM group received intra-peritoneal injection of DXM 30 min before every inhalation; while the control group received normal saline instead of OVA. The histopathology and ultrastructural changes of pulmonary tissues were observed by light microscope and transmission electron microscope (TEM). The total bronchial wall thickness (Wat) and the airway smooth muscle thickness (Wam) were measured by image analysis system. The concentrations of IL-1beta in serum and BALF were tested by sandwich ELISA. The protein expressions of P-JNK and P-c-Jun were detected by immunohistochemistry technique. Lung tissue extracts were analyzed for phosphorylation of JNK by Western blot. Linear correlation analysis was used to evaluate correlations between Wat and P-JNK protein (mA), Wam and P-JNK protein (mA), P-JNK protein (mA) and levels of IL-1beta in serum, P-JNK protein (mA) and levels of IL-1beta in BALF. RESULTS: In the asthma group, HE-staining showed inflammatory cell infiltration around bronchi and mucous gland hyperplasia. TEM examination showed airway smooth muscle and collagen fiber proliferation, and widening of intercellular distance. The Wat and Wam of the asthma group were significantly higher than those of the control group, while the thickness of airway wall in the glucocorticoid intervention groups became significantly decreased. The concentrations of IL-1beta in serum and BALF of the asthma group [(81 +/- 4) ng/L, (331 +/- 15) ng/L] were significantly higher than those of the control group [(53 +/- 6) ng/L, (130 +/- 9) ng/L] (t = -8.62 and t = -24.10, both P < 0.01). Mean absorbance values (by immunohistochemistry) of P-JNK and P-c-Jun in the asthma group were significantly higher than those of the control group, and the mean absorbance values of P-JNK and P-c-Jun in the BUD and DXM groups were significantly lower than those of the asthma group, but higher than those of the control group (F = 223.59 and F = 76.53, both P < 0.01). Absorbance (by Western blot) of P-JNK in the control, asthma, BUD, and DXM groups were (1.00 +/- 0.00), (1.66 +/- 0.16), (1.18 +/- 0.12), and (1.29 +/- 0.14), respectively; that of the asthma group was significantly higher than that of the control group, while absorbance of P-JNK in the BUD and the DXM groups were significantly lower than that of the asthma group, but higher than that of the control group (F = 17.84, P < 0.05). Strong positive correlations were found between Wat or Wam and P-JNK (mA) (r = 0.700 and r = 0.769, P < 0.01, respectively, n = 48). Strong positive correlations were also found between P-JNK (mA) and concentration of IL-1beta in serum or BALF (r = 0.689 and r = 0.805, P < 0.01, respectively, n = 48). CONCLUSION: Phosphorylation of JNK is closely related to asthma airway remodeling. Glucocorticoids can inhibit phosphorylation of JNK, one mechanism of which may be down-regulation of IL-beta expression.

[Changes in urotensin-II expression in airway remodelling in asthmatic rats].

OBJECTIVE: To study the role of urotension-II in serum and bronchoalveolar lavage fluid (BALF) in the process of airway remodelling in asthmatic rats. METHODS: Thirty-two male Sprague-Dawley (SD) rats were randomly divided into normal control and 2-week, 4-week and 8-week asthmatic groups (OVA inhalation of 2, 4 and 8 weeks respectively). Rats were sensitized and challenged by OVA to establish a model of asthma. The bronchial wall thickness and the airway smooth muscle thickness were measured by image analysis system. The urotension-II contents in serum and BALF were determined using ELISA. RESULTS: The bronchial wall thickness and the airway smooth muscle thickness in the three asthmatic groups significantly increased compared with those in the normal control group (P<0.01). The urotension-II contents in serum and BALF in the three asthmatic groups also increased significantly compared with those in the normal control group (P<0.01). The urotension-II contents in serum and BALF in the 8-week asthmatic group were the highest, followed by the 4-week and the 2-week asthmatic groups (P<0.01). BALF urotension-II contents were positively correlated with the bronchial wall thickness and the airway smooth muscle thickness as well as serum U-II contents in the four groups. CONCLUSIONS: The urotension-II contents in serum and BALF in the process of airway remodeling increase in asthmatic rats. The changes in serum and BALF urotension-II contents may be associated with airway remodeling in asthmatic rats.

[Expression of Rock2 and TGF-ß1 mRNA and glucocorticoid intervention in asthmatic rats].

OBJECTIVE: To study the roles of rhoassociated coiled coil forming protein kinase 2 (Rock2) and transforming growth factor-ß1 (TGF-ß1) mRNA in acute asthma and the effect of glucocorticoid intervention on the Rock2 and TGF-ß1 mRNA expression in rats. METHODS: Forty-eight male rats were randomly divided into 4 groups (n=12 each): asthma, control, dexamethasone treated (DXM) and budesonide treated (BUD). Rat model of asthma was prepared by the ovalbumin (OVA) challenge. The animals were sacrificed 24 hrs after the last challenge. The total cell number and differentiation cell number were counted in bronchoalveolar lavage fluid (BALF). The protein expression of Rock2 was ascertained by immunohistochemistry and the mRNA expression of TGF-ß1 was ascertained by hybridization in situ. RESULTS: The pathological changes in the BUD and the DXM groups were alleviated when compared with the asthma group. The total cell number and the percentage of eosinophil (EOS), polymorphonuclear leukocytes (PMN) and lymphocytes (Lym) in BALF in the asthma group were significantly higher than those in the control group (P<0.01). The percentage of macrophage (Mф) in the asthma group was significantly lower than that in the control group (P<0.01). The total cell number and the percentage of EOS and Lym in BALF in the DXM and the BUD groups decreased, while the percentage of Mф increased significantly compared with those in the asthma group (P<0.01). The Rock2 and TGF-ß1 mRNA expression in lung tissues in the asthma group increased significantly compared with those in the control, BUD and DXM groups, while there were no significant differences in the Rock2 expression and TGF-ß1 mRNA expression between the DXM or BUD group and the control group. CONCLUSIONS: The expression of Rock2 and TGF-ß1 mRNA in lung tissues is increased in rats with acute asthma. Glucocorticoids can significantly decrease the expression of Rock2 and TGF-ß1 in lung tissues, thus alleviates airway inflammation.

[Results of skin prick test in 908 children with asthma].

OBJECTIVE: To report the results of skin prick test in 908 children with asthma in order to provide references for treatment of asthma. METHODS: Skin prick test was performed using ALK-Abell's inhaled prick reagents and the German Merck company's food prick reagents. Histamine was used for positive control, and normal saline, for negative control. RESULTS: Skin prick test showed positive in 703 cases (77.4%). The positive rates of inhaled and food allergens were 76.9% and 37.1%, respectively. Dermatophagoides culinae and house dust mite were two common inhaled allergens (72.4% and 74.7% respectively). Shrimp was the most common food allergen (22.9%), followed by tuna (7.3%) and mussels (6.7%). The strongest response of skin prick test was usually caused by dermatophagoides culinae (64.0%) and house dust mite (66.4%), followed by mould 1 (7.1%). The positive rate of inhaled and food allergens increased with increasing age (p<0.05). CONCLUSIONS: The positive rate of skin prick test in the 908 children with asthma was higher. These results of this study may be useful in an epidemiological survey and specific immunotherapy of asthma.

Current perspectives on the correlation of nocturnal enuresis with obstructive sleep apnea in children.

BACKGROUND: Obstructive sleep apnea (OSA) and nocturnal enuresis (NE) are common clinical problems in children. OSA and NE are thought to be interrelated, but the exact pathophysiological mechanisms are not yet clear. This review aims to explain the possible pathogenesis of NE in children with OSA. DATE SOURCES: We have retrieved all relevant original articles from Database that have been published so far, including the prevalence studies of NE and OSA in children, sleep characteristic studies that use polysomnography (PSG) to focus on children with NE, and studies on the relationship between OSA and NE. RESULTS: Clinical studies have revealed that the risk of NE in children with OSA was increased compared with that of their healthy peers. This increased risk may be associated with sleep disorders, bladder instability, detrusor overactivity, nocturnal polyuria, endocrine and metabolic disorders, and inflammation. CONCLUSIONS: Cardiopulmonary and renal reflex-induced neuroendocrine disorder may play an important role in the mechanism of NE in children with OSA, but this remains to be confirmed by animal studies. Other causes such as oxidative stress and inflammatory responses need to be further researched.

TNF-α increases Staphylococcus aureus-induced death of human alveolar epithelial cell line A549 associated with RIP3-mediated necroptosis.

AIM: To explore the role of tumor necrosis factor-alpha (TNF-α) on Staphylococcus aureus-induced necroptosis in alveolar epithelial cells. MAIN METHODS: The A549 alveolar epithelial cell line was pretreated with small interfering RNA (siRNA) against receptor interacting protein-3 (RIP3) and then stimulated by S. aureus, where some cells were pretreated with TNF-α or TNF-α with anti-TNF-α antibody simultaneously. A549 cell death was assessed using lactate dehydrogenase (LDH) leakage and flow cytometry analyses. The protein expressions of RIP1, RIP3, cleaved caspase-1, and cleaved caspase-8 were analyzed by western blot. KEY FINDINGS: S. aureus-induced LDH release was increased significantly by TNF-α. In addition, flow cytometry showed that TNF-α increased A549 cell apoptosis and necrosis in S. aureus-infected cell cultures. Levels of RIP3 and cleaved caspase-1 protein in A549 cells infected with S. aureus increased at 12 h post-infection, as shown by western blot. Significant additional increases in RIP3 expression were observed following the addition of TNF-α. Decreasing RIP3 levels by siRNA significantly suppressed the release of LDH induced by TNF-α and S. aureus. RIP3 siRNA also significantly suppressed A549 cell necrosis induced by S. aureus and TNF-α at 6 and 12 h post-infection as shown by flow cytometry analysis. SIGNIFICANCE: TNF-α enhances the damage of S. aureus on lung epithelial cells, and its mechanism is associated with RIP3 mediated necroptosis.