Lung distension belongs to chronic obstructive pulmonary disease (COPD) in modern medicine.In recent years,its disease incidence and mortality have increased year by year.Supported by the traditional Chinese medicine (TCM) standardization of the State Administration of TCM project-TCM preventive treatment practice guidelines-prevention of lung distension recrudescence,the first draft of the TCM Preventive Treatment Practice Guideline on Prevention of Lung Distension Recrudescence was formulated on the basis of preventive treatment theory,evidences from both ancient and modern literatures,and through the Delphi method as well as expert consensus conference.And then,peer review comments were collected,which laid the foundation for the further improvement of this guideline.This guideline was aimed to achieve the industry consensus,to improve the quality of life (QoL) in patients of the stable period,to reduce the economic burden of patients,as well as to improve both the theoretical connotation and practical value of preventive treatment in TCM.

Objective To investigate the adiponectin levels in non-obese first-degree relatives (FDR)of type 2 diabetic subjects and its relation to insulin sensitivity and the intima-media thickness of the common carotid artery (IMT) during 5-year follow-up. Methods Fifty-three FDR subjects and 37 control subjects who were free of type 2 diabetes were enrolled. Plasma adipenectin, lipid profile, blood glucose, fasting insulin, and blood pressure were determined at baseline and after 5-year follow-up. IMT and endothelial-dependent vasodilation (EDVD) were measured by high-resolution B-mode ultrasound imaging. Homeostasis model assessment was used to evaluate insulin resistance (HOMA-IR)and β-cell function (HOMA-β). 29 FDR subjects and 20 control subjects completed the follow-up. Results Comparing with the control, plasma adiponectin levels in non-obese FDR subjects were lower at baseline [(10.06±5.79)vs (14.43±7.91) mg/L, P< 0.05]. Plasma adiponectin were decreased 24.0% in non-obese FDR and 36.7% in control duning 5 year follow-up (both P<0.05). Adiponectin levels were negatively correlated with waist-to-hip ratio (r = -0. 397), fasting blood glucose (r = -0. 373), IMT (r = -0. 372), and HOMA-IR (r=-0. 40)in the non-obese FDR. After adjusting other relevant risk factors,adiponectin was associated with age, high-density lipoprotein-cholesterol, and IMT in multiple regression analyses in non-obese FDR group. In the control group, a similar analysis revealed that low-density lipoprotein-cholesterol and IMT explained 25% of the variability in the adiponectin concentration. Conclusion Plasma adiponectin levels were decreased after 5 years in both non-obese FDR and control subjects. Decreased adiponectin level may be related to IMT increment.

Objective To investigate low density lipoprotein receptor (LDLR)gene mutation in familial hypercholesterolemia (FH) patients. Methods The proband was given clinical diagnosis of homozygous FH based on marked features and blood lipid tests results. After apoB100R3500Q mutation was excluded, the promoter region and all of the 18 exons of LDLR gene were amplified by touch-downpolymerase chain reaction (PCR). The PCR products were analyzed by single-strand conformationalpolymorphism (SSCP). The PCR products with abnormal single strands were sequenced directly. Thesecondary structures of the mutational and wild type proteins were analyzed and compared byANTHEPROT5.0, and then the tertiary structures of the mutant and wild type LDLR were predicted atSWISS MODEL homepage online. Results A homozygous mutation A606T at exon 13 of the patients wasfound by SSCP and confirmed by DNA sequencing. GOR Ⅰ method in ANTHEPROT5.0 indicates that therandom coils and turns would replace some helixes at the mutation site. The online prediction from theSWISS MODEL homepage indicates the backbone structure of the mutant LDLR has no difference from thewild type one. Conclusion The results suggest the A606T mutation of LDLR gene is the cause of the FH inthis pedigree.