Methodological considerations for aging research: Introduction to a symposium and methodological commentary

This article introduces a set of papers which illustrate the application or multivariate techniques to problems in aging research. Multivariate research strategies raise new issues in the choice of sample size that are discussed. The papers reviewed in this introduction are concerned with factorial invariance, the measurement of change, and various regression techniques useful in modeling developmental data.     

miRNA与肺纤维化的研究新进展

MicroRNA(miRNA)是一类非编码小RNA,长度仅22个核苷酸左右,在基因转录后水平调节靶基因表达,参与调控机体各种生理进程,包括细胞增殖、分化、凋亡等.最新研究发现,一些miRNA与肺纤维化发生、发展密切相关,在此综述了这一方面的研究进展,以进一步认识肺纤维化的发生机制.     

Dyspnoea at 6-min walk test in idiopathic pulmonary fibrosis: comparison with COPD

The characteristics of dyspnoea in idiopathic pulmonary fibrosis (IPF) during a 6-min walk test are not clear. This study was designed to evaluate dyspnoea and desaturation during the 6-min walk test in IPF in comparison with that in chronic obstructive pulmonary disease (COPD), which is one of the most studied chronic lung diseases. The 41 consecutive patients with IPF included in this study were assessed by a 6-min walk test and concurrent measures of disease severity. Forty-one age-matched and resting PaO(2) value-matched COPD patients who had undertaken the test during the same period were selected as the control. Only O(2) saturation at the end of the test was an independent predictor of dyspnoea in IPF (r(2)=0.27, P=0.0005), whereas forced expiratory volume in 1s (FEV(1)) was the only predictor in COPD (r(2)=0.16, P=0.0096). Desaturation was significantly more severe in IPF (83.6+/-9.1% in IPF versus 88.0+/-5.9% in COPD, P<0.001). In contrast, dyspnoea assessed with the Borg scale was significantly more severe in COPD (3.6+/-2.1 in IPF versus 4.6+/-1.9 in COPD, P<0.05). O(2) saturation is an independent predictor of dyspnoea at the end of a 6-min walk test in IPF. In comparison with COPD, desaturation is more severe, although dyspnoea is milder.     

Hepatitis C and pulmonary fibrosis: Hepatitis C and pulmonary fibrosis

Background

Hepatitis C virus (HCV) is a hepatotropic and lymphotropic virus that causes hepatic and extrahepatic disease. Emerging clinical data suggest that chronic HCV infection can lead to many direct and indirect effects on the lung.

Objectives

This article discusses evidence on the relationship between HCV infection and pulmonary fibrosis to increase knowledge on this topic among clinicians and scientists and highlights the need for further study.

Methods

We searched the MEDLINE, ISI WEB OF KNOWLEDGE, OVID, ELSEVIER, and MDCONSULT databases and top respiratory journals, such as the American Journal of Respiratory and Critical Care, Chest, and Thorax for articles in English using the following keywords: hepatitis C, HCV infection, IPF, pulmonary fibrosis, and interstitial pneumonitis. We reviewed the reference lists of all identified studies.

Results

The evidence for a pathogenetic link between pulmonary fibrosis and HCV is: the higher frequency of HCV markers in IPF patients, an increase in lymphocyte and neutrophil numbers in bronchoalveolar lavage of chronic HCV infection patients, and the development of IPF in HCV-related chronic hepatitis that is treated with interferon. There is a discrepancy between studies on the frequency of HCV in IPF patients, which might be attributed to geographical differences of in the prevalence of HCV infection, selection bias in choosing the control group, and the HCV genome.

Conclusions

BAL studies in HCV infection are associated with increased counts of lymphocytes and neutrophils in BAL fluid. These studies show that HCV infection is associated with nonspecific pulmonary inflammatory reactions that are not compatible with IPF but that it can lead to pulmonary fibrosis. The other factor is interferon therapy. Interstitial pneumonia and sarcoidosis are well-documented complications of IFN therapy. More extensive cohort studies should be conducted to confirm an actual causal relationship between HCV infection and pulmonary fibrosis.