3.Analysis on iron metabolism indicators in children with various genotypes of thalassemia
International Journal of Laboratory Medicine 2015;(20):2947-2949
Objective To study the value of iron metabolism indicatorsin thalassemia .Methods 218 cases of thalassemia ,57 ca‐ses of iron deficiency anemia (IDA) children and 70 healthy children(control group) were enrolled in the study ,and serum iron (SI) ,total iron binding capacity(TIBC) ,transferrin(Tf) ,serum ferritin (SF) were detected for them .Results β‐thalassemia double heterozygous(β0 ) or homozygous group :SI levels were significantly higher than the other groups(P<0 .05) ,while TIBC ,Tf levels were significantly lower than the other groups(P<0 .05);α‐thalassemia group (static α‐thalassemia ,standard α‐thalassemia):SI , TIBC levels compared with control group showed no significant difference(P>0 .05) ,but Tf level was higher than control group(P<0 .05);hemoglobin H disease group:when TIBC ,Tf levels compared with the control group ,the difference was statistically signif‐icant(P<0 .05) ,when SI compared with the control group ,the difference was not statistically significant(P>0 .05) .Conclusion Compared with Tf ,SI and TIBC are better indicators for monitoring iron loading in children with thalassemia .The increased SI level and decreased TIBC level are two indicators for the diagnosis of β0 thalassemia in children with cellule anaemia .
4.Interaction of GSTM1, GSTT1 Polymorphism and Air Pollution in Asthma
Journal of Environment and Health 1993;0(01):-
0.05). In stratified studies, risk of asthma in individuals with null genotype of GSTM1 is 2.667 times of that with wild genotype after exposure to light air pollution. Risk of asthma in individuals living in heavy air pollution area is 2.125 time of that in light pollution area for all wild genotype of GSTM1 individuals, but without statistical significance. Conclusion It was not found that the relationship between GSTM1, GSTT1 polymorphism and asthma. Synergism of genotype of GSTM1, GSTT1 and air pollution was not also seen in this study.
6.Roles of macrophages in intracranial aneurysm
Weilin RONG ; Xi XIAO ; Meihua LI
International Journal of Cerebrovascular Diseases 2016;24(3):279-283
Inflammation plays a key role in the formation of intracranial aneurysm. At present, the pathophysiological processes of intracranial aneurysms are mainly caused by both hemodynamic abnormalities and inflammation. Studies have shown that the inflammatory cels in the intracranial aneurysm wal are mainly mononuclear macrophages, and can secrete various effector molecules, weakening and destroying the structures of the vessel wal . Therefore, the research of the roles of differences played in different subtypes of macrophages and their effector molecules in the pathophysiological processes of intracranial aneurysms wil provide clues for exploring the pathogenesis of intracranial aneurysms and effective targeted therapy.
7.Changes of S-100B Protein in Umbilical Cord Blood of Asphyxial Neonates with Hypoxic-Ischemic Encephalopathy and Its Clinical Significance
Journal of Applied Clinical Pediatrics 2006;0(14):-
Objective To study clinical significance of S-100B protein in umbilical cord blood of asphyxial neonates with hypoxic-ischemic encephalopathy(HIE).Methods Forty-three cases of healthy infants were regarded as control group(group 1).Sixty cases of asphyxial neonates were divided into two groups(44 cases without HIE as group 2;another 16 cases with HIE as group 3).S-100B protein levels in umbilical cord blood of three groups were measured with enzyme-linked immunosorbent assay retrospectively. Results Levels of S-100B protein in group 1,group 2 and group 3 were(1.055?0.356) ?g/L,(1.572?0.533) ?g/L and(2.394?(0.943) ?g/L,) respectively.S-100B protein levels in umbilical cord blood of group 2 and group 3 were significantly higher than that of group 1(t=2.306,7.991 P
8.Expression of Growth Arrest and DNA Damage Inducible Gene 45 ? during Preadipocyte Differentiation and Regulative Role of Tumor Necrosis Factor-Alpha
Journal of Applied Clinical Pediatrics 2006;0(17):-
Objective To investigate the changes of growth arrest and DNA damage inducible gene ?(GADD45?)expression during 3T3-L1 preadipocyte differentiation and analyze the regulative role of tumor necrosis factor-alpha(TNF-?) on GADD45? gene expression in matured 3T3-L1 adipocytes.Methods 3T3-L1 preadipocytes were cultured in vitro and differentiated into the matured adipocytes.TNF-? in different concentrations(0.1,1.0,10.0 ?g/L) was added into the culture medium of fully differentiated adipocytes(day 10) for various times(0.5,2,6,12,24 h).The levels of GADD45? gene mRNA expression were evaluated by reverse transcription polymerase chain reaction(RT-PCR).Results With the 3T3-L1 preadipocytes being differentiated into the matured adipocytes,the level of GADD45? gene mRNA expression was downregulated and reached the lower level in fully differentiated adipocytes.There was a significant difference between any 2 detected phases in the levels of GADD45? gene mRNA expression(P0.05).Treatment of day 10(3T3-L1) adipocytes with TNF-? of different concentrations resulted in a significant increase in the level of GADD45? gene mRNA expression.The induction effect of TNF? on GADD45? gene mRNA expression generally tended to be reinforced with the elongation of time course.Conclusions GADD45? gene may be involved in adipocyte differentiation and adipogenesis.TNF-? can upregulate the mRNA expression of GADD45? gene in matured adipocytes.The induction effect of TNF-? on GADD45? gene expression is generally(time-)correlated.
10.Erythromycin for improving enteral nutrition tolerance in adult critical patients: a systematic review and Meta-analysis
Rong LUAN ; Huilin TANG ; Suodi ZHAI ; Xi ZHU
Chinese Critical Care Medicine 2014;26(6):425-430
Objective To systematically review the efficacy and safety of erythromycin on enteral nutrition (EN) tolerance in adult critical care patients.Methods Databases including PubMed,EMbase,the Cochrane Library,CNKI and Wangfang data were retrieved up to June,2013 to collect the randomized controlled trial (RCT) concerning erythromycin in improving EN tolerance or increasing the successful rate of postpyloric EN tube as compared with other treatments.Two reviewers independently screened the literature,extracted the data,and assessed the quality of methodology.Then Meta-analysis was performed using RevMan 5.2 software.Results A total of 16 RCTs were included.Ten RCTs involving 668 patients were included for evaluating erythromycin in improving EN tolerance.Six RCTs involving 353 patients were included for evaluating erythromycin to increase the successful rate of postpyloric EN tube.The result of Meta-analysis showed that compared with placebo,erythromycin could significantly improve the successful rate of postpyloric EN tube placement [relative risk (RR) =1.82,95% confidence interval (95%CI) 1.40-2.37,P<0.000 01],while there was no significant difference between erythromycin and metoclopramide (RR=1.04,95% CI 0.79-1.36,P=0.799).In patients who needed early EN,compared with placebo or blank control,erythromycin had higher successful gastric feeding rate over 5 days (RR =1.89,95% CI 1.19-3.00,P=0.007).In patients who failed EN,compared with metoclopramide,erythromycin could significantly increase the successful gastric EN rate for 24 hours (RR=1.30,95%CI 1.02-1.66,P=0.03),72 hours (RR=1.57,95%CI 1.15-2.14,P=0.005) and 144 hours (RR=2.04,95%CI 1.23-3.37,P=0.006).The median time of EN intolerance was postponed in erythromycin group than that in metoclopramide group.Adverse reactions were reported in 5 studies.There was no statistic difference except for the higher diarrhea rate in the combination treatment group compared with erythromycin group.Conclnsions Postpyloric EN tube placement rate can be improved by erythromycin,which could be a choice of substitute for bedside intubation without fluoroscopy or endoscopic assistance.Based on the evidence,we recommended that intravenous erythromycin in a small dose of approximately 3 mg/kg weight as an option for EN intolerance in critical patients.