Respiratory tract infection is very common in children. Viruses play a critical role in childhood respiratory infection. Recently, there are several newly discovered viruses which have been investigated widely.Here we tried to introduce the epidemiology and clinical research of human metapneumovirus,SARS-coronavirus,coronavirus-NL63,coronavirus-HKU1 ,human Boca virus,KI-polyomavirus and WU-polyomavirus.

Objective To investigate the effects of PDGF-D/PDGFR-β signaling on interstitial collagen hyperplasia and fibroplasia of myocardium following cardiopulmonary resuscitation (CPR)in rats.Methods A total of 90 male Sprague-Dawley (SD) rats were randomly (random number) assigned into 5 groups:sham,control,Imatinib,Ad-GFP and Ad-PDGFR groups.Each group was further subdivided into post-resuscitation (PR) 4 h and PR 72 h groups.The ventricular fibrillation cardiopulmonary resuscitation (CPR) model was used.Cardiac collagen volume fraction (CVF) was measured with Sirius red staining.Platelet derived growth factor D (PDGF-D) was detected by enzyme-linked immunosorbent assay (ELISA).Collagen Ⅰ,α smooth muscle actin (α-SMA),vimentin and PDGF receptor β (PDGFRβ) were detected by Western blot.The data were analyzed by a two-way ANOVA and Bonferroni test.P ＜0.05 was considered statistically significant.Results (1) At PR 72 h,the CVF value in the control group was significantly higher than that in the sham group [(11.24 ± 0.31) vs (1.65 ± 0.19),t =10.81,P ＜0.05] and in the Ad-PDGFR group significantly higher than that in Ad-GFP group [(25.60 ±4.09) vs (10.73 ± 2.42),t =16.77,P ＜0.05],respectively.Compared to the control group,the level of CVF in the Imatinib group significantly decreased [(5.11 ± 0.29)vs (11.24 ± 0.31),t =3.892,P ＜0.05].(2) At PR 4 h,compared with the sham group,the expression of serum PDGF-D was greatly increased in the control,Imatinib,Ad-GFP and Ad-PDGFR groups (all P＜0.05).At PR 72 h,serum PDGF-D was continuously significantly higher in the Ad-PDGFR group when compared with the sham group [(296.46± 30.82) pg/mL vs (93.74 ± 5.43) pg/mL,t =7.755,P ＜0.05].(3) At PR 72 h,the expression of Collagen I,α-SMA,Vimentin and PDGFR-β in the control and Ad-PDGFR groups were significantly increased than those in the sham and Ad-GFP groups,respectively (all P＜0.05).However,compared with the control group,Imatinib significantly decreased the expressions of the above proteins (all P＜0.05).Conclusions The interstitial collagen hyperplasia and fibroplasia of myocardium at 72 h following CPR in rats might be related to the increased levels of PDGF-D in serum and PDGFR-β in myocardium.

Objective To investigate the mechanism of cerebral protection by treatment of butylphthalide (NBP) and its effect to mitochondria in a porcine model of cardiac arrest (CA) after cardiopulmonary resuscitation (CPR). Methods Healthy Wuzhishan pigs weighting (30±2) kg were divide into three groups randomly(random number): The sham group (n=6), the control group (n=12) and the NBP group (n=12). Operation was performed in the sham group. Cardiac arrest of ventricular fibrillation was induced by programed electrical stimulation in the control and NBP group. After CPR, asynchronous defibrillation of 150J was performed to achieve the restoration of spontaneous circulation. NBP was injected at the rate of 2.5 mg?kg-1 in the NBP group. Hemodynamics were recorded at baseline, 1 hr, 2 hr, 3 hr and 4 hr after CPR. The number of injured neurons, apoptosis index and evaluation of mitochondrial injury were calculated under light and electrical microscope respectively. Mitochondria were separated by differential centrifugation. Mitochondrial respiratory function was measured with oxygen consumption of R3 and R4, respiratory control rate (RCR), ADP/oxygen. Mitochondrial permeability transition pore (MPTP) open was tested by colorimetric. Results After CPR, the mean artery pressure, coronary perfusion pressure and cardiac output decreased significantly, whereas no significant differences were found between the control and NBPgroup (P>0.05). Significant cerebral injury was found after CPR. The number of injured neurons, apoptosis index and evaluation of mitochondrial injury were improved significantly by the NBP treatment (P<0.05). Compared with the sham group, oxygen consumption of R3 and R4, R3/R4 and ADP/O decreased significantly in the cerebral frontal cortex mitochondria of the control group (P<0.01), whereas they were increased in the NBP group (P<0.01). MPTP increased in the control group, which could be improved by the NBP treatment. Conclusions NBP can improve the neurologic outcome after CPR and decrease the apoptosis of neurons by improving the respiratory function of mitochondria and inhibiting the MPTPopening.