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Protracted bacterial bronchitis (PBB) is an important cause of chronic wet cough.Bacterial infection is the main pathogen of PBB,so antibacterial infection is the main treatment.As the main antibiotic of experiential treatment,Amoxicillin-clavulanate is recommended to be used for at least 2 weeks,usually 4 weeks,and 6 to 8 weeks in part.If the sputum culture or bronchoalveolar lavage fluid is positive,the selection of antibiotic therapy can be according to drug sensitivity test.
ABSTRACT
Protracted bacterial bronchitis (PBB) is one of the most common causes of chronic wet cough in children.Pediatricians have paid more attention to the PBB.Three most commonly identified bacteria are non-typeable Haemophilus influenzae,Streptococcus pneumoniae and Moraxella Mora bacteria.The occurrence of PBB is associated with bacterial biofilm formation in the airway,tracheobronchomalacia,systemic immune function disorder,and environmental pollution.The clinical presentations of PBB are wet cough and wheezing.Pulmonary signs are moist rale and(or) wheezeing.International guidelines recommend the treatment of Amoxicillin and C1 avulanate,the courses are at least two weeks.Domestic scholars have also used traditional Chinese medicine or western medicine therapy for the treatment of PBB.
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Objective To evaluate the effect of sinomenine on apoptosis in renal tubular epithelial cells of rats subjected to renal ischemia-reperfusion (I/R), and the relationship with C-Jun N-terminal kinase (JNK) signaling pathway.Methods Fifty-four male Wistar rats, aged 6-8 weeks, weighing 180-220 g, were randomly divided into 3 groups (n =18 each) using a random number table: sham operation group (group S), I/R group and sinomenine group (group SIN).Renal ischemia was induced by occlusion of the left renal pedicle for 45 min followed by reperfusion, and the right kidney was removed immediately after onset of reperfusion in anesthetized rats in I/R and SIN groups.In group SIN, sinomenine 60 mg/kg was injected intraperitoneally at 30 min before reperfusion, while the equal volume of normal saline was given instead of sinomenine at the same time point in S and I/R groups.Six animals in each group were selected at 0.5, 6 and 24 h of reperfusion, blood samples were collected by cardiac puncture for determination of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations.Immediately after blood sampling, the left kidney was removed for examination of pathological changes in renal tissues (with light microscopes) and for determination of phosphorylated JNK (p-JNK) and caspase-3 expression (by immune-histochemistry) and apoptosis in renal tubular epithelial cells (by TUNEL).The apoptotic rate was calculated.Results Compared with group S, the serum Cr and BUN concentrations were significantly increased, the expression of p-JNK and caspase-3 was up-regulated, and the apoptotic rate was increased in I/R and SIN groups.Compared with group I/R, the serum Cr and BUN concentrations were significantly decreased, the expression of p-JNK and caspase-3 was down-regulated, and the apoptotic rate was decreased in group SIN.The microscopic examination showed that the pathological changes of kidney were significantly attenuated in group SIN compared with group I/R.Conclusion The mechanism by which sinomenine attenuates renal I/R injury is related to inhibited activation of p-JNK signaling pathway and reduced apoptosis in renal tubular epithelial cells of rats.
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Objective To investigate the effect of sinomenine on the levels of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) during renal ischemia-reperfusion (I/R) in rats.Methods Seventy-two healthy male Wistar rats, aged 6-9 weeks, weighing 180-220 g, were randomly assigned into 4 groups (n =18 each) using a random number table: control group (group C), sinomenine group (group SIN), group I/R, and sinomenine+I/R group (group SIN+I/R).The animals were anesthetized with 10％ chloral hydrate 350 mg/kg.The left renal pedicles were clamped with atraumatic microclips for 45 min followed by reperfusion, and the right kidney was removed immediately after onset of reperfusion to establish the model of renal I/R injury.Sinomenine 60 mg/kg was injected intraperitoneally at 30 min before reperfusion in group SIN +I/R, and at the corresponding time point in group SIN.At 6, 8 and 12 h of reperfusion, the blood samples were drawn by cardiac puncture for measurement of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations.The left renal specimens were obtained for examination of pathological changes (with light microscopes) and for determination of the rate of NF-κB-positive cells and iNOS expression in renal tissues (by immunohistochemistry).Results Compared with group C, the concentrations of serum Cr and BUN, and rate of NF-κB-positive cells were significantly increased, and the expression of iNOS was up-regulated in I/R and SIN+I/R groups, and no significant change was found in the parameters mentioned above in group SIN.Compared with group I/R, the concentrations of serum Cr and BUN, and rate of NF-κB-positive cells were significantly decreased, and the expression of iNOS was down-regulated in group SIN+I/R.The microscopic examination showed that the pathological changes of kidney were significantly attenuated in group SIN+I/R compared with group I/R.Conclusion The mechanism by which sinomenine attenuates renal I/R injury is related to inhibited activity of NF-κB and down-regulated expression of iNOS in rats.
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Objective To evaluate the effects of sinomenine on the expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) during renal ischemia-reperfusion (I/ R) in rats.Methods Fifty-four male Wistar rats, weighing 180-220 g, were randomly divided into 3 groups (n=18 each) using a random number table: sham operation group (group S) , group I/R and sinomenine group (group SIN).Renal I/R was induced by clamping the left renal pedicle for 45 min followed by reperfusion in I/R and SIN groups.In group S, the bilateral renal pedicels were only exposed.Sinomenine 60 mg/kg was intraperitoneally injected at 30 min before reperfusion in group SIN, while the equal volume of normal saline was given in group S and group I/R.At 6, 12 and 24 h (T1-3) of reperfusion, 6 rats from each group were chosen, and blood samples were drawn from the hearts for determination of the serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations.The animals were then sacrificed, and the left kidney was removed and embedded into a paraffin block for determination of the expression of HIF-1α and VEGF in the renal tissues (by immuno-histochemistry).Results Compared with group S, the serum Cr and BUN concentrations were significantly increased at T1-3 , and the expression of HIF-1α was significantly up-regulated at T2,3 in group I/R and group SIN, and the expression of VEGF was significantly upregulated at T2,3in group I/R, and at T1-3 in group SIN.Compared with group I/R, the serum Cr concentration at T1-3 and serum BUN concentration at T2,3 were significantly decreased and the expression of HIF-1α at T2,3and VEGF at T1-3was significantly up-regulated in group SIN.Conclusion The mechanism by which sinomenine attenuates renal I/R injury is related to up-regulation of the expression of HIF-1α and VEGF in the renal tissues of rats.
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Objective To evaluate the effect of lappaconitine on renal ischemia-reperfusion (I/R) injury in mice.Methods Thirty-six male Wistar rats,weighing 180-220 g,were randomly divided into 3 groups (n=12 each) using a random number table:sham operation group (group S),group I/R and lappaconitine group (group LA).Renal I/R was induced by occlusion of the left renal pedicle for 45 min with atraumatic microclips followed by reperfusion,and the right kidney was removed after atraumatic microclips were released.At 30 min before reperfusion,lappaconitine 4 mg/kg was injected intraperitoneally in group LA,and normal saline 2 ml was given in S and I/R groups.In group S,the left renal pedicle was only isolated.At 5 and 24 h of reperfusion,blood samples were taken from the inferior vena cava for determination of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations,and kidney specimens were obtained for histopathologic examination (with light microscope) and for determination of the expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2) in renal tissues (by immunohistochemistry).Results Compared with group S,the serum Cr and BUN concentrations were significantly increased,and the expression of COX-2 and MMP-2 in renal tissues was up-regulated at 5 and 24 h of reperfusion in I/R and LA groups.Compared with group I/R,the serum Cr and BUN concentrations were significantly decreased,the expression of COX-2 and MMP-2 in renal tissues was down-regulated at 5 and 24 h of reperfusion and histopathologic changes were reduced in group LA.Conclusion Lappaconitine can attenuate renal I/R injury through inhibiting the expression of COX-2 and MMP-2 in rats.
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Objective To study the role of Anopheles anthropophagus in malaria transmission and transmission threshold so as to provide basis for vector surveillance and malaria control strategy. Methods Parasitological and entomological methods were used in the investigation at 5 villages of Xinyang City, Henan Province. Results From July to August, 1999, 74 febrile cases (10^9% of the total population) were examined. Among them 50 were infected, the incidence in the population of surveyed spots was 7^4%. Active detection was made in another randomly selected two villages and found that the parasite rate in the inhabitants was 2^0%, and the positive rate of IFA was 8^4%. Only vivax malaria was detected. An.anthropophagus and An.sinensis were collected, with An.anthropophagus as the predominant one in human dwellings. The estimated man\|biting rate and the human blood index were 4^9388 and 0^7858 respectively. The vectorial capacity of An. anthropophagus was 5^5296. The critical man\|biting rate of An.anthropophagus was 0^2407 as calculated by the formula (ma=-rlnP/abP\+n) according to Macdonald′s model.The local man\|biting rate was 20 times higher than that of the critical man\|biting rate. Conclusion The results demonstrated that An.anthropophagus is the principal vector in malaria transmission in the area. The findings imply that the critical man\|biting rate is of practicable importance in vector surveillance.