1.Potential mechanism of myocardium apoptosis of right ventricle in rat under chronic hypoxia
Xiaohong XU ; Jianxin TAN ; Huajun FENG
Chinese Journal of Pathophysiology 1986;0(01):-
AIM: We used an animal model of chronic hypoxia to mimic right ventricular hypertrophy and try to study the potential mechanism of myocardium apoptosis of right heart in rat under chronic hypoxia.METHODS: Rat hypoxia models were established by exposing the rats to normobaric chronic hypoxia(oxygen levels were maintained at 9.5%-10.5%).Sixty rats were separated into two groups: one exposed to hypoxia and the other serving as control.Ten rats,randomly selected from each group were killed at 14,21,28 d after hypoxia.The apoptosis was determined.The changes of RV weight to left ventricle and interventricular septum weight ratio[RV/(LV+S)],the RV weight to body weight ratio(RV/BW) were also observed.The ?-MHC,bcl-2 and bad mRNA levels in right ventricle were detected by semi-quantitative RT-PCR assays and expression of ?-MHC,Bcl-2 and Bad protein levels were detected by Western blotting.RESULTS: The RV/(LV+S),RV/BW and apoptosis index in chronic hypoxia group were higher than those in normal control group(P0.05).Finally,a decreased bcl-2/bad ratio in chronic hypoxia group was found compared with control group(P
2.Glutamine enriched enteral nutrition for severe traumatic brain injury: a meta-analysis
Hao LU ; Huajun TAN ; Ruoyang FENG ; Qian CHEN ; Hua YAN
Chinese Journal of Trauma 2018;34(10):898-905
Objective To evaluate the efficacy of Glutamine enriched enteral nutrition in the treatment of severe traumatic brain injury (sTBI).Methods PubMed,Cochrane Library,Chinese National Knowledge Infrastructure (CNKI),VIP Database for Chinese Technical Periodicals,and Wanfang databases were searched to identify randomized controlled trials (RCT) on the application of Glutamine enriched enteral nutrition for severe TBI patients from database establishment time to May 2017.Two investigators screened the literature strictly according to the inclusion and exclusion criteria,extracted the data,evaluated the literature quality,and performed meta-analysis using RevMan 5.3 software.The effects of glutamine enhanced enteral nutrition on albumin content,immunoglobulin G (IgG) level,the incidence of diarrhea,incidence of pulmonary infection,blood glucose,Glasgow Coma Scale (GCS),length of hospital stay,and mortality were evaluated.Results A total of 17 articles involving 939 sTBI patients were included,with 512 patients in Glutamine group and 427 controls in control group.There were no significant differences in the length of hospital stay and mortality between the two groups (P > 0.05).Significant differences were found in albumin content (95 % CI 0.19-2.54,Z =2.27,P<0.05),level of IgG (95% CI 0.67-1.80,Z =4.25,P <0.01),incidence of diarrhea (95% CI 0.23-0.57,Z =4.41,P < 0.01),incidence of lung infections (95% CI 0.14-0.56,Z =3.62,P<0.01),blood sugar (95% CI-2.53--0.52,Z=2.98,P<0.01),and the GCS score (95%CI0.50-2.68,Z=1.49,P<0.01) between the two groups.Conclusion Compared with routine enteral nutrition,Glutamine enriched enteral nutrition can increase albumin content and IgG level,reduce the incidence of diarrhea and lung infections,reduce blood sugar,and improve the GCS score,but it cannot shorten hospital stay or reduce mortality.
3.Hereditary hemorrhagic telangiectasia complicated by aortic sinus aneurysm caused by a pathogenic mutation in the ACVRL1 gene: a family survey
Na YAN ; Yan LIU ; Huajun LI ; Yang LI ; Xuanfeng TAN ; Yi YANG ; Liang JIN
Chinese Journal of Dermatology 2022;55(8):716-720
Objective:To investigate clinical and genetic characteristics of a family with hereditary hemorrhagic telangiectasia complicated by aortic sinus aneurysm, and to analyze causative genes.Methods:Clinical data and peripheral blood samples were collected from the proband and her relatives, and genomic DNA was extracted. Causative genes were screened by whole-exome sequencing, and then verified by Sanger sequencing.Results:A heterozygous mutation c.137G>A was identified at position 137 in exon 3 of the ACVRL1 gene in the proband, her daughter, grandson and granddaughter, which led to the substitution of cysteine by tyrosine at amino acid position 46 (p.C46Y) . The mutation was not found in any of the other 5 family members without clinical symptoms.Conclusion:A causative mutation c.137G>A (p.C46Y) in the ACVRL1 gene was identified in the family with hereditary hemorrhagic telangiectasia type 2 complicated by aortic sinus aneurysm, which had not been previously reported in Asian populations.