No abstract

Nemonoxacin 500 mg once daily for 7-10 days is as effective and safe as levofloxacin for treating adult CAP patients in terms of clinical cure rates, microbiological success rates, and safety profile. ClinicalTrials.gov identifier: NCT01529476.

Either 500 mg or 750 mg of oral nemonoxacin taken once daily for 7-10 days demonstrated high clinical and bacteriological success rates in Chinese adult patients with CAP. Nemonoxacin at 500 mg once daily for 7-10 days is recommended for future Phase III clinical trials. ClinicalTrials.gov identifier: NCT01537250.

The subepithelial fibrosis component of airway remodeling in asthma is mediated through induction of transforming growth factor-beta1 (TGF-beta1) expression with consequent activation of myofibroblasts to produce extracellular matrix proteins. The number of myofibroblasts is increased in the asthmatic airway and is significantly correlated with the thickness of lamina reticularis. However, much is still unknown regarding the origin of bronchial myofibroblasts. Emerging evidence suggests that myofibroblasts can derive from epithelial cells by an epithelial-to-mesenchymal transition (EMT). In this study we investigated whether TGF-beta1 could induce bronchial epithelial EMT in the human bronchial epithelial cell. Cultured human bronchial epithelial cells, 16HBE-14o, were stimulated with 10 ng/ml TGF-beta1. Morphologic changes were observed and stress fiber by actin reorganization was detected by indirect immunostaining. The expression of alpha-SMA (alpha-smooth muscle actin) and the epithelial cell marker E-cadherin were detected in those 16HBE-14o cells after TGF-beta1 stimulation for 72 h, using immunostaining and RT-PCR. The contents of collagen I were determined by radioimmunoassay, and the levels of endogenous TGF-beta1 were measured with ELISA. Human bronchial epithelial cells stimulated with TGF-beta1 were converted from a "cobblestone" epithelial structure into an elongated fibroblast-like shape. Incubation of human bronchial epithelial cells with TGF-beta1 induced de novo expression of alpha-SMA, increased formation of stress fiber by F-actin reorganization, and loss of epithelial marker E-cadherin. Moreover, a significant increase in the levels of collagen I and endogenous TGF-beta1 released from bronchial epithelial cells stimulated with TGF-beta1 were observed. These results suggested that human bronchial epithelial cells, under stimulation of TGF-beta1, underwent transdifferentiation into myofibroblasts.

ObjectiveWhile individuals with insomnia consistently complain of cognitive impairment, previous studies on the effect of insomnia on objective measures of cognitive function have obtained ambiguous results. The relationship between daytime sleepiness and cognitive manifestations in insomnia patients is not clear.MethodsThirty-six primary insomnia patients (PIPs) and 26 good sleep controls (GSCs) with age and gender matched manner were included in the study. Participants underwent an overnight polysomnography followed by a multiple sleep latency test (MSLT) and an examination of the attention network test (ANT). ANT reflected three attentional networks including alerting, orienting and executive control. According to whether accompanied with excessive daytime sleepiness (EDS), the insomnia group were subdivided into PIPs with EDS (n = 12, score on MSLT<10 min) and PIPs without EDS (n = 24, score on MSLT≥10 min).ResultsPIPs only performed worse on executive control function than GSCs in ANT. PIPs with EDS had longer overall reaction time (RT) related to PIPs without EDS. Further analyses with Pearson correlation analysis showed a significant negative correlation between the overall RT and MSLT latency in insomniacs (r = −0.444, p<0.01), whereas no such correlation was found in controls.ConclusionsResults suggest that PIPs do show executive control function deficits compared with GSCs. Daytime sleepiness in terms of MSLT latency was associated with poor cognitive manifestations in patients with insomnia.