Abstract: Blood cells are subjected to various mechanical forces; including pressure, flow, shear force, gravity, and forces acting against them with varying stiffness (eg. blood vessel wall). Scientists have discovered that these forces have profound effects on cellular growth, differentiation, secretion of cytokines, cell death, and migration. These processes are called mechanotransduction, a conversion of mechanical forces to biochemical signals. In this article the author reviews biophysical forces that affect biological functions of blood cells and their responses in normal physiology and pathophysiology. Although input (forces) and output (cellular responses) have been well studied by utilizing recently developed various force-generating devices, the molecular mechanism of mechanotransudction is still a mystery. This is because reconstructing molecular interaction in the presence of mechanical forces in vitro is highly challenging and until now the molecular dynamics involved in structural changes caused by these forces are largely unknown. Nevertheless, the author has reviewed a few examples of potential structural effects on the molecular mechanism of mechanotransduction.
Abstract: Platelet transfusion, as the primary treatment for severely low platelet count (thrombocytopenia) or disorders of platelet function, is used extensively in patients with blood system diseases or active hemorrhaging. In recent decades platelet related researches in China have steadily increased. In the clinical application of platelet transfusion, there are large differences between the treatment’s effects on different patients. Immune or nonimmune factors, such as platelet-specific antibodies, platelet gene analysis and matches, and auxiliary treatment, may affect the curative effect, and even result in ineffective platelet transfusion. Platelets used in clinical therapy include platelets made from whole blood and hemapheresis platelets, and the latter is the main application type used in China. Both preparation and preservation methods can affect the quality of platelets and influence the therapeutic effect. Researches on the molecular basis or the curative effect of platelet transfusion are increasing, such as the relationship between platelet-activating factors, tissue factors, thrombopoietin, membrane glycoprotein and platelet activation, and their influence on the curative effect of platelet transfusion, the inhibition of antiplatelet therapy in platelet activation, and platelet signal transduction pathways and their significance in the curative effect of platelet transfusion. This article aims to review the research progress on the curative effect of platelet transfusion and its molecular mechanisms.
Abstract: This study aimed to investigate the frequency of unexpected antibodies and evaluate the cumulative incidence of additional unexpected antibodies in Beijing. From January 1, 2011 to December 31, 2014, blood samples from 2,095 patients from 98 medical institutes in Beijing were sent to the Beijing Red Cross Blood Center for antibody identification. Of the unexpected antibodies, 29.5% were autoantibodies and 70.5% were alloantibodies. Anti-E was the most prevalent form of allo-antibodies (n = 445), accounting for 52.9% of the Rh system, followed by anti-M (76.6% of the MNS system) and then 142 cases of anti-C,e, 128 cases of anti-E,c, and 113 cases of anti-Lea. The cumulative incidences of additional antibodies were 0.55% (after the first transfusion), 1.82% (second time), 2.33% (fourth time), 3.07% (firth time), and 4.24% (seventh time). Antibody against the Rh system was the most prevalent, followed by antibodies against MNS, Lewis, Kidd, P1, and Duffy.
Abstract: The aim of this study was to provide an overview of massive transfusion in Chinese hospitals, identify the important indications for massive transfusion and corrective therapies based on clinical evidences and supporting experimental studies, and propose guidelines for the management of massive transfusion. This multi-region, multi-center retrospective study involved a Massive Blood Transfusion Coordination Group composed of 50 clinical experts specializing in blood transfusion, cardiac surgery, anesthesiology, obstetrics, general surgery, and medical statistics from 20 tertiary general hospitals across five regions in China. Data were collected for all patients, who received ≥ 10 U red blood cell transfusion within 24 hours in the participating hospitals from January 1 2009 to December 31 2010, including patient’s demographics, pre-, peri-, and post-operative clinical characteristics, laboratory test results before, during, and after transfusion, and patient mortality at post-transfusion and discharge. We also designed an in vitro hemodilution model to investigate the changes of blood coagulation indices during massive transfusion and the correction of coagulopathy through supplement blood components under different hemodilutions. The experimental data in combination with the clinical evidences were used to determine the optimal proportion and timing for blood component supplementation during massive transfusion. Based on the findings from the present study, together with an extensive review of domestic and international transfusion-related literature and consensus feedback from the 50 experts, we drafted the guidelines on massive blood transfusion that may help Chinese hospitals to develop standardized protocols for massive blood transfusion.
Abstract: Anti-E alloantibody has been one of the most frequently detected clinically significant alloantibodies in previous studies. Red blood cell (RBC) transfusion is unique in its common intravenous introduction of foreign E antigen and provides a valuable opportunity to study the human immunologic response to intravenous foreign E antigen. Patients exposed to foreign E antigen while receiving RBC transfusions are at risk of forming anti-E alloantibody. Valid estimates of anti-E alloimmunization risk are clinically important, but the forming mechanism of anti-E alloimmunization remains unclear. Here, we screened 516 inpatients at risk of exposure to foreign E antigen while receiving RBC transfusions and monitored the development of anti-E alloantibody for up to two years after left hospital. However, only 2 cases of anti-E alloimmunization were identified in this study. Patients who received RBC transfusion had a very high risk of exposure to foreign E antigen, but the anti-E alloantibody production incidence was very low and few anti-E alloantibodies were produced within 3 to 6 months after RBC transfusion in this study. Further research would contribute to our knowledge of the anti-E alloimmunization mechanism and prevent anti-E development, which would be significantly useful in clinical for transfusions, obstetric management, and the evaluation and management of transfusion reactions in laboratory and institutional resources and cost reduction in healthcare system.
Abstract: The aim of study is to use erythrocyte ABO genotyping to assist serological typing in the identification of suspected ABO subtypes. Nine samples with discrepancies in ABO serological forward and reverse typing were subjected to ABO 6–7 exon sequencing, and their respective results were cisAB01O1, Bw12O2, Ael05B, Bel03O1, Ael05O1, B(A)04O1, B(A)02O1, and two cases of O1O2 weak antibody for the reverse typing test. The ABO genotyping and serological ABO forward and reverse typing were combined for subtype identification. In the results of ABO genotyping, cisAB and B(A)04 are only found B gene in genotyping, thus the presence of A subtype B was excluded. The samples with a weak antibody for serological O type in reverse typing were tested ABO genotyping to exclude subtype A or B. We summarized a combination of ABO genotyping and serological typing can be used for identification of suspected ABO blood groups.
Abstract: The study was designed to evaluate the molecular and serological features of a newborn with severe hemolytic disease of the newborn (HDN) caused by anti-Jk3, and to further rich our understanding of Kidd subgroup genetics using pedigree analysis which is the first analysis of a Jk null phenotype in China and the first report of severe HDN caused by anti-Jk3. A female baby presented with hyperbilirubinemia (36 μmol/L) on the day of birth. Antibody screening tests using blood samples from the patient and her family indicated that the mother’s plasma contained alloantibodies against high frequency antigens and the results of direct Coombs test were all negative. Kidd phenotypes were Jk(a-b-), Jk(a-b+), and Jk(a-b+) in the mother, father, and baby, respectively. Kidd genotype was determined by PCR amplification of a single nucleotide polymorphism (838) and all family members were Jk(a-b+). Kidd gene exons 4 to 11 were sequenced to identify potential mutations.Sequencing analysis revealed that c.838 G>A and intron c.3 -78 G>A homozygosity occurred in all family members along with homozygosity and heterozygosity for c.IVS5-1G>A in the mother and newborn, respectively. In conclusion, serological and genetic analyses confirmed that the Jk(a-b-) phenotype was caused by homozygous IVS5-1G>A mutation of the Kidd gene. This result is consistent with that of a previous report and presents a useful diagnostic tool to identify HDN caused by anti-Jk3. A further study is required to identify the effect of intron 3 -78 G>A mutation on phenotype.
Abstract: The aim of this study was to confirm the concordance between the ABO phenotype and genotype in 34 patients undergoing renal transplant before 2010 in Sir Run Run Shaw Hospital. The ABO genotyping kit and column agglutination test (CAT) were used to examine the ABO type, and ABO subgroup was checked by sequence analysis of ABO exons 6 and 7. We found that the genotypes of serological A, AB, O, and B patients were A1A1 in 3 patients and A1O1 in 5 patients, A1B, O1O2 in 1 patient and O1O1 in 11 patients, and BB in 6 patients and BO1 in 6 patients, respectively. However, one patient, who was originally reported as serological B in the 2010 medical record and CAT showed Asub B in 2016 and sequence analysis of ABO exons 6 and 7 demonstrated B(A)04/O1.[not clear] The ABO column agglutination testing combined with genotyping may provide additional value in pre-renal transplantation laboratory examinations, and it may be safe to transplant a B/O1 kidney to a B(A)04/O1 recipient since the transplantation has been success for 6 years.
Abstract: This study was designed to identify the rare type ABO blood groups, B(A) 02, from Eastern China. Three samples with discordant serological results during routine blood type identification and four samples from one sample’ family were selected. All of them were detected by serological method. The exon 6 and 7 of the ABO genes were amplified by PCR and sequenced. They were typed as AsubB by serology and as BO by genotype. In AsubB samples, nt 700C>G mutation was detected in B gene, which was previously defined as B(A)02 alleles. In these seven samples, six showed B(A)02/O01 and one showed B(A)02/O02.B(A)02 allele was found to be more common in this study than B(A)04 which is considered to be more frequent than B(A)02. The careful identification of rare blood types is important for the safety of clinical blood transfusion.
Abstract: Ingestion of Amanita phalloides, a deadly wild mushroom, can cause multi-organic injury. The value of therapeutic plasma exchange (TPE) in treating mushroom poisoning was controversial, especially for those patients at the later stage. We reported three cases of acute liver injury, coagulopathy, and hepatic encephalopathy secondary to mushroom poisoning at the later stage. Therapeutic plasma exchange (TPE) session was repeated 2~5 times depending on the patients’ conditions. Pathological plasma ranging from 1600 to 1800 mL was exchanged for each session with fresh frozen plasma and normal saline based on the patients’ body weight. Patients’ liver function, coagulation function, and clinical symptoms were immediately improved upon TPE treatment. TPE is a reliable therapy for patients with acute liver injury, coagulopathy, and hepatic encephalopathy secondary to mushroom poisoning at the later stage of poisoning.