The aim of this study was to investigate and identify the relationship between urinary cysteinyl leukotriene E(4) levels and clinical response to antileukotriene treatment in patients with asthma. Forty-eight patients with stable mild to moderate asthma were treated with montelukast in a four-week trail. Asthmatic symptom score, beta(2)-agonist usage, percentage of eosinophil, total serum IgE concentration, forced expiratory volume in the first second (FEV(1)), peak expiratory flow rate (PEFR), and urinary leukotriene E(4) (uLTE(4)) were measured before and after treatment. Clinical response was assessed by the improvement of asthma symptom scores, beta(2)-agonist usage, and FEV(1). Responders were defined as patients who had to fit the following three criteria: a reduction of more than 20% in mean symptom score; a reduction of more than 20% in beta(2)-agonist usage, and a mean improvement of FEV(1) of more than 10% from baseline value. Others were classified as nonresponders. Logistic analysis was used to access the various clinical factors correlated with the clinical response. There were 25 responders and 23 nonresponders. The mean uLTE(4) level from the responders was higher than that from the nonresponders (224.5 +/- 34.4 vs. 175.3 +/- 37.1 pg/mg creatinine, p < 0.05). There was a significant correlation between the clinical response and the uLTE(4) level but not demographic features, percentage of eosinophils, serum IgE concentration, or spirometry (p > 0.05). Subjects with a uLTE(4) level of >/= 200 pg/mg creatinine were 3.5 times more likely to respond to montelukast than those with less than 200 pg/mg creatinine (95% confidence interval [CI] = 1.7-15.8). The uLTE(4) level is closely correlated with antileukotriene treatment. uLTE(4) is a good biomarker for selecting this drug to treat asthma.

The aim of this study was to investigate the effects of Astragaloside IV (AS) on cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD). Our results showed that AS alleviated CS-induced pathological injury in lung tissue. AS also increased superoxide dismutase (SOD) and reduced the level of malondialdehyde (MDA) in serum and lung. AS also reduced cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in serum and lung. More, AS significantly reduced the protein expression of JAK3/STAT3/NF-κB pathway in CS-induced mice. In vitro, cigarette smoke extract (CSE) stimulation exposed to normal human bronchial epithelial (HBE) cells. Results further confirmed that AS significantly inhibited the protein levels of JAK3/STAT3/NF-κB pathway in CSE-induced HBE. Our result showed that AS might effectively ameliorate COPD via JAK3/STAT3/NF-κB pathway.

Background/Aims: The endothelial nitric oxide synthase (eNOS) gene has been enlisted by previous research as a candidate gene of preeclampsia predisposition. This study investigates the specific roles of 3 polymorphisms of the eNOS gene in a population of Chinese origin from mainland China. Methods: We studied the association of 3 commonly studied polymorphisms of the eNOS gene, namely 4b/a, T-786C and Glu298Asp, in a case-controlled sample of 220 patients diagnosed with preeclampsia and 200 healthy controls. The association between eNOS polymorphisms and preeclampsia was evaluated by performing genotyping for the eNOS variants and calculating odds ratios (OR) and 95% confidence intervals. The plasma nitrite concentration in participants was determined to examine how 3 eNOS polymorphisms affect plasma nitric oxide (NO) concentrations in pregnant women. Results: The frequencies of both the variant 298Asp allele and eNOS 4a allele were significantly lower in preeclamptic women than in the control group and had a significantly lower OR. The variant 298Asp allele and eNOS 4a are strongly associated with higher plasma NO concentrations in pregnant women. Conclusions: Polymorphisms in the eNOS gene may be protective against preeclampsia in a Chinese population, and this protective effect may be associated with NO formation in plasma in pregnant women.