Detection of respiratory pathogens and clinical features in 225 children with acute exacerbation of bronchial asthma / 中国当代儿科杂志

OBJECTIVE@#To investigate the respiratory pathogens and clinical features in children with acute exacerbation of bronchial asthma.@*METHODS@#Nasopharyngeal swabs were collected from 225 children with acute exacerbation of bronchial asthma, aged <14 years, who attended the outpatient service or were hospitalized from August 2017 to August 2019. Quantitative real-time PCR was used to detect 12 pathogens, i.e., respiratory syncytial virus (RSV), human rhinovirus (HRV), influenza virus A (IFVA), influenza virus B (IFVB), parainfluenza virus types 1-3 (PIV1-3), human metapneumovirus (HMPV), adenovirus (ADV), Bordetella pertussis (BP), Chlamydia pneumoniae (CP), and Mycoplasma pneumoniae (MP).@*RESULTS@#The overall detection rate of virus was 46.2% (104/225), and 7 kinds of viruses were detected, i.e., HRV (19.6%, 44/225), ADV (16.0%, 36/225), IFVB (5.8%, 13/225), RSV (4.9%, 11/225), IFVA (3.6%, 8/225), PIV3 (1.8%, 4/225), and HMPV (0.4%, 1/225). Of all pathogens, BP had the highest detection rate of 28.4% (64/225), and the detection rates of MP and CP were 16.4% (37/225) and 0.4% (1/225), respectively. The mild exacerbation group had a higher detection rate of BP than the severe exacerbation group (P<0.05), while the severe exacerbation group had significantly higher detection rates of RSV and MP than the mild exacerbation group (P<0.05). There were significant differences in the proportion of children with paroxysmal cough, spasmodic cough, fever, lung rales and abnormal lung imaging findings among the simple BP infection, simple virus infection and simple MP infection groups (P<0.05).@*CONCLUSIONS@#BP, HRV, and MP are common respiratory pathogens detected in children with acute exacerbation of bronchial asthma, and respiratory virus infection is an important pathogen of acute exacerbation of asthma in children. Acute exacerbation of asthma caused by different pathogens has different clinical features and severities.

Design, synthesis and antitumor activities of novel E-substituted 2,3-diaryl propenoic acyloxy phosphonate derivatives / 药学学报

According to the super-position principle of the reinforcement of biological activities, a series of novel E-substituted 2, 3-diaryl propenoic acyloxy phosphonate derivatives were designed and synthesized. And the structures of the target compounds were confirmed by IR, 1H NMR, 13C NMR and elemental analysis. Furthermore, the cytotoxicities of all compounds on A-549, SGC-7901 and EC-109 in vitro were evaluated by MTT assay, and some of them showed good antitumor activity. Among the active compounds, especially, the IC50 value of compound 3e was (12.7 ± 1.9) μmol x L(-1) against A-549 cells, similar to cisplatin [IC50 = (8.0 ± 1.5) μmol x L(-1)], compounds 3g and 3k had better inhibition effect on EC-109 cells growth, with the IC50 values of (9.5 ± 1.8) μmol x L(-1) and (11.5 ± 0.9) μmol x L(-1) respectively, and compounds 3i and 3k exhibited good cytotoxic property on A-549, SGC-7901 and EC-109, which were worth further investigation.

Relation between GLu-R and the protective effect of hypothermia on oxygen and glucose deprivation injury in hippocampal slice or rat / 中国应用生理学杂志

<p><b>AIM</b>To investigate the relation between Glu-R and the protective effect of hypothermia on oxygen and glucose deprivation (OGD) injury in hippocampal slices of rat.</p><p><b>METHODS</b>(1) We had established OGD injury model in rat hippocampal slices. The changes of orthodromic population spike(OPS) during OGD and after administration of hypothermia (32 degrees C, 25 degrees C) were observed. (2) We had established Glu excitatory toxicity injury model in rat hippocampal slices. The changes of OPS after exposure to Glu and the effect of hypothermia (32 degrees C, 25 degrees C) against the Glu excitatory toxicity injury were observed. The non-NMDA receptor-mediated excitatory postsynaptic potentials (EPSP) in the CA1 area were recorded via adding the GABA-R specific agonists bicuculline (BMI) and NMDAR agonists D-(-)-2-Amino-5-phosphonopentanoic Acid (AP5) in normal artificial cerebrospinal fluid (nACSF), the NMDA receptor-mediated EPSP were recorded via adding the BMI and non-NMDA-R agonists 6,7-Dinitroquinoxaline-2, 3(1H,4H)-dione(CNQX) in nACSF. The variety of the changes of OPS during OGD14min in nACSF groups and added BMI compounded AP5 or BMI compounded CNQX ACSF groups were observed after administration of 25 degrees C hypothermia 28 min. (3) The changes of ultrastructure of CA1 area after OGD 1 h and the effect of hypothermia (25 degrees C) on it were observed.</p><p><b>RESULTS</b>(1) OPS reduced and abolished quickly during OGD14min, and the recovery amplitude of OPS was very low after reoxygenation/glucose 1 h. While the time of OPS abolishing significantly elongated and the recovery of OPS was higher in hypothermia (32 degrees, 25 degrees C) groups. The effect in groups 25 degrees C was more significant than those in groups 32 degrees C. (2) In control groups, Glu (2 mmol/L, 14 min) decreased the amplitude of OPS, after the end of Glu exposure the recovery amplitude of OPS was very low. After administration of hypothermia (32 degrees C, 25 degrees C), the recovery amplitude and rate of OPS were significantly higher than those in the control groups, while the antagonism on Glu excitatory toxicity injury in H 25 degrees C was more significant than those in H 32 degrees C. The changes of OPS during OGD 14 min were no distinct difference in nACSF groups and added BMI (50 micromol/L) compounded AP5(20 micromol/L) or BMI (50 micromol/L) compounded CNQX (100 micromol/L) ACSF groups. The protection of hypothermia (25 degrees C) could not be cancelled by added AP5 compounded BMI or BMI compounded CNQX in nACSF. (3) After OGD (14 min) 1 h, the nuclear membrane of pyramidal cells in CA1 area was irregular, nucleus were homogenized, the organelle in the cytoplasm was degenerate, even more to necrosis or loss, mitochondrion swelled, ridge was vacuoles. In H 25 degrees C the nuclear membrane was regular, mitochondrion swelled only lightly. Small chromatin gathered to edge.</p><p><b>CONCLUSION</b>Hypothermia shows the protective effects of against OGD injury in hippocampal slices. The mechanism is related to the antagonism of Glu excitor toxicity and maintenance the ATP level in cells, and the antagonism perhaps is mediated by NMDA-R and non-NMDA-R.</p>