ABSTRACT
Authenticity verification is a very important aspect of medical device registration quality management system verification of medical device. How to verify the authenticity of samples is a problem worth discussing. This study analyzes the methods of authenticity verification from the aspects of product retention sample, registration inspection report, traceability of records, hardware facilities and equipment. In order to provide reference for relevant supervisors and inspectors in the verification of registration quality management system.
ABSTRACT
Objective To systematic evaluate the efficacy of paricalcitol on estimated glomerular filtration rate (eGFR) and proteinuria in non-dialysis chronic kidney disease (CKD) patients.Methods According to the collaborative search strategy,PubMed,the clinical control test database of Cochrane Library,Embase,Chinese Wanfang database,CNKI,VIP database (form the date of database establishment to March 2014) were searched.Published and unpublished literature,abstracts in academic meetings (ASN,WCN,CSN) were also searched by hand.The randomized controlled trials (RCTs) about the efficacy paricalcitol on eGFR and proteinuria in non-dialysis CKD patients were selected.Review Manager Software 5.2 was used for statistical analysis.Results Seven RCTs with a total of 834 patients were included (508 in experimental group,326 in placebo group).No statistical difference of the efficacy on eGFR[SMD=-0.10,95％ CI:(-0.28-0.07),P=0.26] between lower dose paricalcitol (＜ 2 μg/d) group and placebo group,while higher dose (2 μg/d) group reduced eGFR significantly [SMD=-0.45,95％ CI:(-0.63--0.27),P ＜ 0.01].Compared with placebo,paricalcitol reduced proteinuria significantly [OR(95％C1):2.09(1.52-2.58),P ＜ 0.01],and there was no difference between different dose groups [OR(95％CI):1.09(0.62-1.91),P=0.77].Lower dose group [OR(95％C1):0.93(0.57-1.52),P=0.76] and higher dose group [OR(95％ CI):2.08(0.70-6.18),P=0.19] did not significantly increase the risk of adverse events.Conclusions Lower dose paricalcitol (＜ 2 μg/d)has no effect on eGFR in non-dialysis CKD patients meanwhile reduces proteinuria.The higher dose (2μg/d) may reduce eGFR without farther reduction in proteinuria.
ABSTRACT
Objective To investigate the expression of JNK2 in hyperoxic lung injury ,and explore the protective effect of sub-stance P (SP) on hyperoxic lung injury and its mechanism .Methods Sixteen SD rats were divided into four groups with 4 rats in each group :room-air and f 9 g/L saline group (group A) ,room-air and SP group (group B) ,hyperoxia injury group and f 9 g/L sa-line group (group C) ,hyperoxia injury group and SP group (group D) .Rats ingroup B and D were injected with SP 1 × 10-6 mol · L -1 · kg -1 · d-1 intraperitoneally ,group A and group C were injected with an equal volume of 9 g/L saline .The animals were sac-rificed after 14 days of experiment .Lung pathology was examined with light microscopy ,lung wet/dry (W/D) ratio and the level of SP and PCNA and TUNEL in lung were evaluated .The Superoxide dismutase (SOD) ,malondialdehyde (MDA) and glutathione (GSH) level were assayed respectively in lung tissue .The quanlity of JNK2 protein was detected by Western blot analysis .Results Compared with group A ,the high oxygen groups all had different degrees of lung injury ,,while the lung pathological pictures in group D was improved significantly compared with group C .Western blot showed that level of JNK2 in group C was obviously higher than that of group A ;After the intervention ,level of JNK2 in group D was lower than that of group C .The lung W/D retio , TUNEL and PCNA expression and distribution SOD ,MDA and GSH was consistent with the trends of JNK2 protein expression . Conclusion High oxygen stress can activate damage lung tissue JNK 2 activity ;SP protection mechanism of high oxygen lung injury may be induced by cutting high oxygen activation of JNK 2 to inhibit oxidative damage .