Objective To observe the effects of ligustrazine intra-articular injection on cartilage degeneration in OA.To estimate and discuss the vistas of clinical application with ligustrazine intraarticular injection.(Methods)26 New Zealand white rabbits were randomly divided into 4 groups,2 rabbits in normal group,8 rabbits in model,control and experimental group,respectively.OA animal model was established in rabbits by the way of fixing right posterior knee joint with plaster cast in strecthing state in model,control and experimental group.(0.3mL) ligustrazine intra-articular injection was carried out once a week in experimental group.(0.3mL) dexamethasone in the same way was made in control group.At 6 week and 9 weeks later,optic and electron microscopic examinations were conducted to observe the pathological changes of articular cartilage of the knee of these animals.Results There was a significant difference in Mankin scale between experimental group and 3 other groups((P0.05)),and between these 2 groups the electro microscopic observation was similar.Conclusion Intra-articular injection of ligustrazine can alleviate degeneration and promote self-reparation of articular cartilage.Method of intra-articular injection of cortisocteroid has no reparation effect on OA cartilage(degeneration).

ObjectiveTo guide fluid management and evaluate the clinical index through monitoring extravascular lung water index(EVLWI) of patients with pulmonary contusion.MethodsThirtyone severe chest trauma patients with pulmonary contusion were selected,performed with central venous catheterization or femoral artery catheterization,and connected to pulse index continuous cardiac output (PICCO).EVLWI after pulmonary contusion were measured by using thermal dilution.The intake and output of patients were recorded in detail,fluid intake was controlled,furosemide was prescribed,and the changes and correlations of oxygenation index,EVLWI and liquid balance difference at different time points were evaluated.ResultsEVLWI after pulmonary contusion at 1st to 7th d after hospitalization was respectively (9.25 ±0.71),(8.98 ±0.61),(8.61 ±0.59),(7.75±0.53),(6.64 ±0.49),(6.22±0.36),(5.59 ±0.39) ml/kg.Comparing with 1st d after hospitalization,EVLWI declined from 3rd d (P ＜ 0.05).Oxygenation index at Ist to 7th d after hospitallzation was respectively( 145.76±23.61 ),( 144.19±20.24),( 146.67±19.25 ),(159.33±15.42),(177.38±14.25),(199.33±19.04),(213.71±18.51) mm Hg(1 mm Hg =0.133 kPa).Comparing with 1st d,oxygenation index from 4th to 7th d had significant difference (P ＜ 0.05 ).The fluid volume at 1st d to 7th d were all negative balance,that of 3rd d to 6th d had significant difference comparing with 1st d [(-431.43±121.17),(-601.43±127.09),(-629.52±140.69),(-320.01 ±93.71) ml vs.(-213.81±63.91 ) ml](P ＜ 0.05 ).Oxygenation index and EVLWI had negative correlation(r =-0.824,P＜0.01).Liquid balance difference and the changes of oxygenation index and EVLWI had no correlation.ConclusionEVLWI effectively monitoring after pulmonary contusion can not only evaluate the changes of pulmonary vascular permeability of patients with pulmonary contusion,but also have important significance to guide fluid management.

OBJECTIVE: To explore the genetic pathogenesis of X-linked agammaglobulinemia in two patients for clinical diagnosis and family counseling. METHODS: Data was collected from the patients' family including clinical information, blood immunoglobulin level, as well as classification and subgrouping of B lymphocytes. Gene mutations were screened by whole exome sequencing (WES) through next-generation sequencing (NGS), the result was verified with Sanger sequencing. RESULTS: A BTK c.1627T>C (p.Ser543Pro) variant was found in the pedigree. The phenotype and variant have co-segregated in the pedigree. The variant was not found in population database. The variant has affected in the kinase domain which contained no benign variants and is harmful as predicted through bioinformatic analysis. CONCLUSION BTK c.1627T>C (p.Ser543Pro) is a pathogenic variant contributing to X-linked agammaglobulinemia in this pedigree. Above finding has provided reproduction guidance for this family.
Agammaglobulinaemia Tyrosine Kinase/genetics* ; Agammaglobulinemia/genetics* ; DNA Mutational Analysis ; Genetic Diseases, X-Linked ; Humans ; Mutation ; Pedigree

OBJECTIVE：To st udy preventive effect and mec hanism of ginsenoside Rg 1 on focal cerebral ischemia-reperfusion injury（CIRI）model rats. METHODS ：Totally 78 SD rats were randomly divided into sham operation group ，model group ， butylphthalide control group （positive control ，10 mL/kg），ginsenoside Rg 1 low-dose，medium-dose and high-dose groups （10， 20，40 mg/kg），with 13 rats in each group. Administration groups were give relevant medicine intraperitoneally ，sham operation group and model group were given constant volume of normal saline intraperitoneally ，once a day ，for consecutive 7 d. After medication，except for the sham operation group ，focal CIRI model was induced by middle cerebral artery occlusion （MCAO） method in other groups. After modeling ，neurological deficit scoring was performed according to the modified neurological difict scoring standard ； TTC staining was used to detected the percentage of cerebral infarction of rats ；the cerebral water content was measured by dry/wet weight method ；serum contents of IL- 1β and IL-6 were detected by ELISA ；the protein expressions of p-p 38 MAPK and p-NF-κB p65 in cerebral tissue were determined by immunohistochemistry and Western blotting assay. RESULTS ： Compared with sham operation ，neurological deficits score ，percentage of cerebral infarction and cerebral water content ，serum contents of IL- 1β and IL-6，positive expression numbers of cells and protein expressions of p-p 38 MAPK and p-NF-κB p65 in cerebral tissue were increased significantly in model group （P＜0.05 or P＜0.01）. Compared with model group ，above index levels of administration groups were all decreased significantly （P＜0.05 or P＜0.01），and the effect of ginsenoside Rg 1 had a dose-dependent trend ；there was no significant difference of all above indexes between ginsenoside Rg 1 middle-dose，high-dose groups and butylphthalide control group （P＞0.05）. CONCLUSIONS ：Ginsenoside Rg 1 has a certain preventive effect on focal CIRI model rats ，the mechanism of which may be associated with down-regulating the protein expression of p-p 38 MAPK and p-NF-κB p65，inhibiting the release of inflammatory factors such as IL- 1β and IL-6.

BACKGROUND: The aim of this study is to systematically evaluate the efficacy and adverse effects of Lobaplatin and Cisplatin in the treatment of malignant pleural effusion. METHODS: The databases of Medline (PubMed), Embase, Web of Science, Cochrane, Wanfang, CNKI and VIP were retrieved so as to search the studies about the randomized controlled clinical trials (RCT) that compared the Lobaplatin and Cisplatin for malignant pleural effusion. The main outcome indicators include objective response rate, complete response, partial response, nephrotoxicity, chest pain, gastrointestinal reaction, myelosuppression, fever response and hepatotoxicity. Relative risk was used as the effect size, which was expressed as 95% confidence interval. The meta-analysis was performed using Stata 14.0 statistical software. RESULTS: A total of 12 RCTs and 720 MPE patients were included. The results showed that the ORR (RR=1.27, 95%CI: 1.15-1.40, P<0.001), CR (RR=1.39, 95%CI: 1.09-1.78, P=0.007), PR (RR=1.21, 95%CI: 1.02-1.42, P=0.026) in LBP thoracic perfusion chemotherapy were significantly higher than those in DDP thoracic perfusion chemotherapy. The incidence of nephrotoxicity (RR=0.31, 95%CI: 0.13-0.71, P=0.005) and gastrointestinal reactions (RR=0.44, 95%CI: 0.31-0.62, P<0.001) in the LBP group were significantly lower than those in DDP group. CONCLUSIONS Compared with DDP pleural perfusion chemotherapy, the ORR, CR and PR of LBP pleural perfusion chemotherapy for MPE are significantly better than DDP, and its nephrotoxicity and gastrointestinal reactions are remarkably lower than DDP.
Antineoplastic Agents ; adverse effects ; therapeutic use ; Cisplatin ; adverse effects ; therapeutic use ; Cyclobutanes ; adverse effects ; therapeutic use ; Humans ; Organoplatinum Compounds ; adverse effects ; therapeutic use ; Pleural Effusion, Malignant ; drug therapy ; Randomized Controlled Trials as Topic