ABSTRACT
【Objective】 To investigate the frequency of platelet antibodies in voluntary blood donors and patients in Zhongshan, Guangdong Province, and to study the specificity and cross-matching of platelet antibodies. 【Methods】 Platelet antibodies of blood donors and patients were screened by solid-phase immunoadsorption (SPIA), rechecked by flow cytometry (FCM), and antibody specificity was identified by PakPlus enzyme immunoassay, and platelet cross-matching was simulated by SPIA. 【Results】 A total of 1 049 blood donor samples and 598 patient samples were tested, with 6 (0.57%) and 49 (8.19%) samples positive for SPIA,respectively(P<0.05); In SPIA positive samples, the positive concordance rate of FCM in blood donors and patients was 100% vs 95%, and that of enzyme immunoassay was 100% vs 88%. Among the initial screening positive samples of blood donors, 5 were anti-HLA Ⅰ antibodies, accounting for 83%, and 1 was anti CD36 antibody, accounting for 17%, with an incidence rate of 0.10%. Among the 14 samples of enzyme immunoassay positive patients, 2 were anti-GP Ⅱb/Ⅲa, 1 was anti-GP Ⅱa/Ⅱa, 8 were anti HLA Ⅰ, and 3 were mixed antibodies (HLA Ⅰ, GP Ⅱb/Ⅲa, GP Ⅰa/Ⅱa). According to the types of antibodies, HLA Ⅰ antibodies were the most common, accounting for 65% (11/17), followed by HPA related anti GP, accounting for 35% (6/17). The majority of patients had a platelet antibody positive typing rate below 30%, accounting for 71.4% (10/14). 【Conclusions】 The positive rate of platelet antibody of patients in Zhongshan area is significantly higher than that of voluntary blood donors, and most of them are anti-HLA Ⅰ and anti-GP, and the incidence of anti-CD36 is extremely low. Therefore, it is necessary to establish a known platelet antigen donor bank, and at the same time, carry out platelet antibody testing and matching of patients, which is helpful to solve the issue of platelet transfusion refractoriness.
ABSTRACT
【Objective】 To research the genetic polymorphism of HPA 1-6/10/15/21 in platelet donors in Zhongshan area, and establish a gene bank of platelet donors with HPA locus. 【Methods】 The HPA 1-6/10/15/21 system genotyping was performed by Real time fluorescent PCR combined with TaqMan probe technology on 192 platelet donors in Zhongshan area, and the genotype frequency and gene frequency were calculated. 【Results】 Only HPA-aa genotype was found within HPA-4/10, and no allele HPA-b had been detected. The majority of HPA-1, 2, 5, 6 and 21 genotypes were aa. HPA-3 and HPA-15 showed high heterozygosity, with genotype frequency of 0.307 3, 0.494 8 and 0.197 9 for HPA- 3aa, HPA-3ab and HPA-3bb, while 0.270 8, 0.505 2 and, 0.224 0 for HPA -15aa, HPA-15ab and HPA-15bb, respectively. 【Conclusion】 The distribution characteristics of HPA 1-6 /10/15/21 of platelet donors in Zhongshan shows regional differences compared with similar researches from other regions. The establishment of HPA gene bank is helpful to avoid alloimmunization caused by incompatible platelet transfusion.
ABSTRACT
【Objective】 To investigate the frequency of CD36 deletion and gene mutation in voluntary blood donors of Zhongshan city, and to explore the possibility of establishing local CD36 negative platelet donor bank. 【Methods】 Platelet CD36 antigen was detected by ELISA in 1 654 voluntary blood donors.Some of the negative samples were confirmed by flow cytometry, and genotyping was also performed. 【Results】 Platelet CD36 antigen was negative in 27 cases, accounting for 1.6% (27/1654), among which 1.6% (18/1149) were males and 1.8% (9/505) were females.No significant difference was noticed between males and females in CD36 antigen deletion cases (P>0.05). Fifteen CD36 negative samples were randomly selected, genotyped and sequenced, with type I deletion in 1 case[ 6.7% (1/15)], type Ⅱ deletion in 14 cases[ 93.3% (14/15)], and gene mutation in exon 3-14 detected in 8 cases. 【Conclusion】 The frequency of platelet CD36 antigen deletion in Zhongshan is comparable to that in other southern regions of China.The establishment of CD36 negative platelet donor bank is conductive to improve the effectiveness of platelet transfusion.
ABSTRACT
OBJECTIVE： To study the effects of Tiaopi huxin prescription （TPHXP） on the atherosclerosis （AS） of ApoE－/－ mice， and to investigate its mechanism. METHODS： Forty male ApoE－/－ mice were divided into blank group， model group， simvastatin group （positive control， 5 mg/kg） and TPHXP low-dose and high-dose groups （50， 150 mg/kg）， with 8 mice in each group. Except that blank group was given common diet， other groups were given high-lipid diet to induce AS model. After modeling， administration groups were given relevant medicine intragastrically， and blank group and model group were given constant volume of normal saline intragastrically， once a day， for consecutive 12 weeks. After last medication， the serum levels of TC， TG， LDL-C and HDL-C were determined by spectrophotometry. The serum level of NO was detected by nitrate reduction method. The serum levels of IL-6 and VCAM-1 were determined by ELISA. After separating thoracic aorta， HE staining was used to observe the formation of plaque in the thoracic aorta of mice in each group， and the corrected plaque area was calculated. Western blotting was conducted to determine the expression of NF-κB p65， Cav-1 and eNOS. RESULTS： Compared with blank group， the serum levels of TC， TG， LDL-C， IL-6 and VCAM-1 were increased significantly in model group， while the levels of HDL-C and NO were decreased significantly （P＜0.01）. The plaque of thoracic aorta was obvious and the corrected plaque area were increased significantly （P＜0.01）. The relative expression of NF-κB p65 and Cav-1 were increased significantly， while the relative expression of eNOS was decreased significantly （P＜0.01）. Compared with model group， the serum levels of TC， TG and LDL-C in administration groups， the serum levels of IL-6 and VCAM-1 in simvastatin group and TPHXP high-dose group were decreased significantly， while the serum levels of HDL-C and NO were increased significantly in administration groups （P＜0.05 or P＜0.01）. In administration groups， the plaques of thoracic aorta were reduced and the corrected plaque area was decreased significantly （P＜0.05 or P＜0.01）； the relative expression of NF-κB p65 and Cav-1 were decreased significantly， while the relative expression of eNOS was increased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： TPHXP can regulate the level of blood lipid， decrease the level of inflammatory factors and inhibit the formation of AS plaque， the mechanism of which may be associated with inhibiting Cav-1/NF-κB pathway.