Objective To investigate whether free heme released in hemolysis could directly damage hepatocytes and disrupt liver function. Methods The mice model of hemolytic transfusion reaction was established, and ALT, AST and other biochemical indexes were detected to analyze the liver function. In vitro, the LO2 cells were stimulated with different concentrations of lysed supernatant of red blood cells and heme respectively. Then the levels of ALT and AST were detected to analyze the liver function. Cell viability was observed by flow cytometry, and cell morphology and skeleton structure were observed by immunofluorescence. Results Abnormal liver function was observed on the mice model of hemolytic transfusion reaction. The results of in vitro experiments showed that LO2 cell viability decreased and the proportion of dead cells increased along with the incremental concentration of free heme. The biochemical indexes such as ALT and AST were aggravated significantly. And free heme could directly destroy the cytoskeleton of LO2 cells. Conclusion Free heme can directly destroy the cell structure of hepatocytes, inhibit cell vitality, induce cell death and abnormal liver function. The degree of damage is positively correlated with the concentration of free heme.

Objective To investigate the effects of platelets with different storage days and quantities on the proliferation of liver cancer cells. Methods Twelve type O platelet braids were collected from Nanning Central Blood Station and sent to the First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine. According to the storage days, they were divided into fresh PLT group and old PLT group, of which the fresh PLT group was platelets stored for 1 day. In the old PLT group, platelets stored for 4 days were used. The two groups of platelets were co-cultured with human liver cancer cell Huh-7. The confluence degree of Huh-7 cells in each group within 48 hours was observed by scratch test, and the invasion ability of Huh-7 cells in each group within 24 hours was observed by transwell test. Results The results of scratch test showed that the proliferation ability of Huh-7 cells was significantly enhanced after co-culture with platelets. When the same amount of PLT was added, old PLT could promote the proliferation of Huh-7 cells more strongly. When PLT with the same storage days was added, PLT with a higher number generally showed a relatively stronger ability to stimulate cell proliferation. The results of transwell experiment were similar to the results of scratch. When the number of PLT was the same, the number of Huh-7 cells invaded by old PLT group was more than that of fresh PLT group, and the difference was statistically significant (P<0.05). The more PLT was added into Huh-7 cells, the more invasive cells occurred in the fresh PLT group and the old PLT group, and the difference was statistically significant (P<0.05). Conclusion The ability of platelets to promote cell proliferation and invasion is positively correlated with the storage time of platelets and the number of platelets. The application rules of platelet products need to be analyzed according to the specific clinical conditions. In the treatment of patients with neoplastic diseases, the application of old platelets should be avoided as far as possible, and the transfusion of platelets should be minimized when platelets have to be used, so as to achieve the purpose of slowing down the proliferation and metastasis of tumor cells.

The treatment of chronic non-healing wounds remain challenging in terms of complexity. Although platelet rich plasma (PRP) therapy has been widely proven effective, the traditional method of in vitro activation of PRP leads to the rapid release of all growth factors. Due to the separation of colloid and supernatant after activation, the factor-rich supernatant is easy to flow and lose, and it is difficult to form a stable structure, which affects its therapeutic effect. To overcome this problem, researchers in recent years have explored hydrogels as carriers for PRP to improve the shortcomings of traditional PRP treatment. This article reviews the latest research on hydrogel-loaded PRP for the treatment of chronic non-healing wounds and provides a reference for optimal treatment.

Anemia leads to increased perioperative blood transfusion rate and blood transfusion volume, prolonged hospital stay in coronary artery bypass grafting patients, and is also an independent risk factor for postoperative complications and mortality.Patient blood management is a patient-centered, systematic, evidence-based approach to improve patient outcomes through the diagnosis and treatment of perioperative anemia and the protection of autologous blood.This paper reviews the research progress in the prevention and treatment of perioperative anemia in patients with coronary artery bypass grafting, which hopely improves the treatment plan and clinical outcome of patients with anemia after coronary artery bypass grafting.

Objective Marvelous advancements have been made in cancer therapies to improve clinical outcomes over last few years. However, therapeutic resistance has always been a major difficulty in cancer therapy, with extremely complicated mechanisms remain elusive. N6-methyladenosine (m6A) RNA modification, a hotspot in epigenetics, has gained growing attention as a potential determinant of therapeutic resistance. As the most prevalent RNA modification, m6A is involved in every links of RNA metabolism, including RNA splicing, nuclear export, translation and stability. Three kinds of regulators, methyltransferase (writer), demethylase (eraser) and RNA binding proteins (reader), together orchestrate the dynamic and reversible process of m6A modification. Herein, we primarily reviewed the regulatory mechanisms of m6A in therapeutic resistance, including chemotherapy and targeted therapy. Then we discussed the clinical potential of m6A modification to overcome resistance and optimize cancer therapy. Additionally, we proposed prospects of m6A modification for future research.

Objective To investigate the mechanism by which evodiamine alleviates blood transfusion related acute lung injury (TRALI) in rats by regulating high mobility group protein Bl (HMGB1)/ toll like receptor 4 (TLR4)/nuclear transcription factor-κB (NF-κB) signaling pathway. Methods A total of 72 SD rats were randomly divided into the model group, low-dose evodiamine group, high-dose evodiamine group, no load group, high-dose evodiamine+HMGB1 overexpression group, and control group with 12 rats in each. Except for the control group, the TRALI model was prepared by intraperitoneal injection of lipopolysaccharide (LPS) combined with infusion of human plasma. After that, we analyzed the lung function indexes such as inspiratory resistance (Ri), minute ventilation (MV) and peak expiratory flow (PEF). Then, in each group we examined the lung wet-dry ratio of rats and the pathological changes of lung tissue by hematoxylin-eosin (HE) staining; the platelet and neutrophil aggregation in lung tissue by immunofluorescence staining; the total number of cells and the percentage of neutrophils in bronchoalveolar lavage fluid (BALF); the levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in BALF and serum by enzyme-linked immunosorbent assay (ELISA); as well as the expression of HMGB1/TLR4/NF-κB signaling pathway-related proteins in lung tissue by western blotting. Results Compared with the model group, the pulmonary function indexes MV and PEF in low-dose evodiamine group and high-dose evodiamine group were increased (P<0.05), while Ri, lung wet-dry ratio, lung histopathological score, platelet-neutrophil optical density in lung tissue, total number of cells in BALF, percentage of neutrophils, levels of pro-inflammatory factors TNF-α and IL-1β in BALF and serum, HMGB1 and TLR4 protein expression in lung tissue and p-NF-κB p65/NF-κB p65 were all decreased (P<0.05). Overexpression of HMGB1 attenuated the improvement of lung function by evodiamine in TRALI rats. Conclusion Evodiamine may inhibit the inflammation in TRALI rats by inhibiting the activation of HMGB1/TLR4/NF-κB signaling, thereby reducing its acute lung injury, and repairing its lung function.

Preoperative Advanced Autologous Apheresis (AAA) is a new type of preoperative autologous blood donation. In recent years, this technology has been introduced in many hospitals across the country. However, there has yet to be a consensus or technical standard for its implementation process and quality control. To address this, the Chinese Blood Transfusion Association Clinical Transfusion Management Committee organized experts from related fields nationwide to extensively and deeply discuss the technical principles, entry requirements, indications, contraindications, operational key points, adverse reaction prevention and treatment, and blood quality evaluation and disposition of preoperative Advanced Autologous Apheresis, and jointly formulated this consensus. The aim is to better manage autologous blood for patients and to provide a basis for medical staff to implement preoperative Advanced Autologous Apheresis more safely and standardized.

Plasma transfusion is clinically used to replenish clotting factors and correct coagulopathy, playing an important role in the treatment of massive hemorrhage. Universal plasma and low titer group O whole blood can improve the timeliness and accessibility of urgent transfusions in patients with major bleeding. The strategy of ABO non-identical plasma transfusion, in the form of active and passive transfusion, has been extensively adopted in clinical practice. Active transfusion mainly includes group AB and A plasma; passive transfusion, on the other hand, involves the transfusion of low titer group O whole blood and ABO non-identical platelets. However, hemolysis and circulating immune complex formation are recognized to be the risks associated with transfusion of ABO non-identical plasma. Together, the risk-benefit trade-off with transfusion of non-ABO identical plasma deserves more attention and further exploration.

Cellular immunotherapies, new complementary therapies for tumor patients, are aimed at malignant tumors with low ability of autoimmune cells, including T cell-based chimeric antigen receptor T cell (CAR-T) therapy, tumor infiltrating lymphocytes (TILs) therapy, NK cell-based chimeric antigen receptor NK cell (CAR-NK) therapy, and autologous cell immunotherapy (CIK), as well as infusion therapies based on other immune cells such as mononuclear phagocytes like dendritic cells and macrophages. Among them, nature killer cells (NK cells), important to the body's natural immunity, matter greatly in anti-tumor, antiviral infection and immune regulation. Like T cells, it can be engineered to target tumor treatment, and can also be transfused with allogeneic NK cells, making up for the shortcomings of limited T cell source and allogeneic immune rejection. No evidence shows that patients tansfused with allogeneic NK cells may develop severe Graft Versus Host Disease (GVHD). NK cells not only expand the types of cells used in cellular immunotherapy, but also provide a broad application prospect for the formation of low-cost cellular immunotherapy products. However, there are still problems such as unstable quality of NK cells and lack of unified quality standards in the preparation process. Although some NK cell immunotherapy products have been approved by the Food and Drug Administration (FDA) or the National Medical Products Administration (NMPA), there is still no clear and publicly available standardized production system for NK cell immunotherapy products. Starting from the unique immunomodulatory mechanism of NK cells, this paper summarizes the therapeutic strategies applied by researchers in the treatment of malignant tumors in recent years and the latest progress of preclinical studies and clinical trials, and finally focuses on the research progress of in vitro expansion methods and maintenance of active function of NK cells, indicating that NK cells promise to be a unified quality of cellular immunotherapy products.

Objective To investigate the antiplatelet effect of tanshinone ⅡA (Tan IIA) and its inhibition effect of the interaction between human platelets and HCT116 cells of colon cancer. Method Whole blood or platelets of healthy volunteers were treated with different concentrations of Tan ⅡA (10, 20, 40 μmol/L), and inhibition rate of platelet aggregation triggered with Adenosine diphosphate (ADP) and arachidonic acid (arachidonic acid) were detected by TEG. The expression rates of CD62P and PAC-1 in platelets were detected by flow cytometry, the adhesion test was used to detect the adhesion of platelets to HCT116 cells after Tan ⅡA treatment, and the effect of platelets on the migration ability of HCT116 cells after Tan ⅡA treatment was tested by scratch test. Results The TEG results showed that Tan ⅡA inhibited ADP and AA-induced platelet aggregation in a concentration-dependent manner (P<0.01), low concentration Tan ⅡA treatment can obtain higher ADP inhibition rate, which is (73.48±19.63) %, high concentration Tan ⅡA treatment can obtain higher AA inhibition rate, which is (78.20±18.58) %. Flow cytometry detection showed that Tan IIA inhibited thrombin or ADP-induced expression of CD62P and PAC-1 on platelet surface in a concentration-dependent manner (P<0.05). Adhesion test results confirmed that Tan ⅡA could significantly inhibit the adhesion between thrombin or ADP-activated platelets and HCT116 cells, and the inhibition ability was positively correlated with Tan ⅡA concentration. The results of scratch test showed that activated platelets could promote the migration of HCT116 cells, and treatment of platelets with low concentration (10 μmol/L) Tan ⅡA could significantly inhibit promotion of platelet to the migration of tumor cells. Conclusion Tan IIA can inhibit the interaction between platelets and tumor cells by inhibiting platelet aggregation and activation.

Objective To detect the Rh antigens C, c, E, e in hematopoietic stem cell transplantation (HSCT) patients with blood diseases and donors before and after transplantation, and analyze the time and process of the conversion of Rh blood type from recipients to donor Rh antigens C, c, E, e. Methods Anticoagulant blood samples were collected from patients and donors before and after transplantation for detection of antigen transformation by using microcolumn agglutination card, ABO and Rh antigen conversion time were analyzed and compared. Results Excluding the effects of red blood cell transfusions, the average time length of 58 HSCT patients was 57.81±8.99 days that Rh antigens C, c, E, e completely transformed from recipient to donor after transplantation. Patient age and hematological classification showed impact on the time of Rh antigens conversion, while the gender, ABO blood group compatibility, as well as transplant mode showed no influence on the Rh antigen conversion time. Donor's red blood cells appeared in some patients as early as 3rd week after transplantation, mixed chimerism of donor and patient was detected from the 4th week, and the Rh blood group antigens were found to be completely transformed from the 7th to the 10th week. In addition, both Rh and ABO blood group antigen transition time in 25 HSCT patients those Rh and ABO blood type between patients and donors were different were analyzed, and the Rh transition time was shorter than ABO, and its difference was statistically significant. Conclusion Regular typing of Rh blood group antigen is necessary for patients after HSCT transplantation, and these Rh antigens are indicators to judge transplantation treatment effect, and they also show a significance of guiding transfusion of Rh blood group compatible red blood cells in HSCT patients after transplantation.

Objective To study the inhibitory effect of ginkgolide B (GB) on platelet activation as well as on the interaction between platelets and colorectal cancer HCT-116 cells. Methods Whole blood or platelets were treated with different concentrations of GB (5, 15, 30 μmol/L). Thromboelastogram (TEG) , then platelet Adenosine diphosphate was detected . The inhibitory rate of ADP and arachidonic acid (AA) pathway was detected by flow cytometry. The effects of GB on the expression of CD62P and PAC-1 after thrombin and ADP-activated platelets were detected. The effect of GB on the cell migration of platelets and HCT-116 cells after 24 and 48 h interaction was observed by cell scratch test, and the effect of GB on the adhesion of platelets to HCT-116 cells was observed by cell adhesion test. Results (1) TEG test results showed that with the increase of GB concentration, AA inhibition rates increased significantly in dose-dependent manner (P<0.001), the difference was statistically significant compared with the control group (P<0.001); The inhibition rate of ADP in the drug group was significantly increased compared with the control group in a dose-dependent manner (P<0.001), the differences were statistically significant (P<0.001). (2) Flow cytometry showed that after thrombin and ADP activated platelets, the positive rates of CD62P and PAC-1 in the drug group decreased with the increase of drug concentration in a dose-dependent manner (P<0.001), the positive rate of PAC-1 in 5 µmol/L group with thrombin activation pathway was lower than that in control group, and the difference was not statistically significant (P<0.05), the positive rate of CD62P in 5 µmol/L group, the positive rate of PAC-1 in 5µmol/L and 15µmol/L groups of ADP-activated pathway drugs was lower than that of control group, and the difference was not statistically significant (P<0.05), and there were statistically significant differences between the remaining concentration groups and the control group (P<0.01). (3) Scratch test results showed that 24 and 48 h cell mobility in different concentration groups was lower than that in thrombin group and ADP group, respectively, and the difference was statistically significant (P<0.01), cell mobility at 24 and 48 h in 15µmol/L group was significantly lower than that in 5 µmol/L group, and the difference was statistically significant (P<0.05), the mobility of 30 µmol/L group was lower than that of 15 µmol/L group, but the difference was not statistically significant (P<0.05). (4) The adhesion test results showed that activated platelets could enhance the adhesion between them and tumor cells, but the adhesion rate of all groups in the drug group was lower than that in the positive group, and the adhesion rate decreased with the increase of drug concentration. Conclusion GB can inhibit platelet activation through AA pathway and ADP pathway, and then inhibit the adhesion of platelets to HCT-116 tumor cells and promote the migration of tumor cells.

Fibrinogen is a coagulation protein with the highest concentration in the blood circulation. During the treatment of massive traumatic hemorrhage, more and more evidence showed that fibrinogen played a key role not only as the main hemostatic component, but also as a regulator in inflammatory immunity and the anti-microbial infection. This article provides a brief overview of the multiple function of fibrinogen in the treatment of massive traumatic hemorrhage from the prospective of its influence on the early and late mortality, aiming to provide more theoretical supports to the early and sufficient fibrinogen replacement.

Objective To compare the effect of double filtration plasmapheresis (DFPP) and plasma exchange (PE) on blood type antibody removal before ABO-incompatible kidney transplantation (ABOi-KT). Method Clinical data and antibody titers before and after each treatment of 36 recipients treated with DFPP and 27 recipients treated with PE before ABOi-KT from February 2021 to December 2023 in the First Affiliated Hospital of Zhengzhou University were collected and analysed. Results 98 and 82 times of treatment were performed in DFPP and PE group, respectively. The titers of blood type antibodies after DFPP and PE treatment were significantly lower than those before treatment (P<0.05). Both DFPP and PE showed good removal effect on high titer antibodies, and the removal effect of DFPP on IgG anti-A, IgG anti-B and IgM anti-B antibodies in group of titer ≥32 was better than that in group of titer ≤16 (P<0.05). The removal effect of PE on IgM anti-A and IgM anti-B antibodies in group of titer ≥32 was better than that in group of titer ≤16 (P<0.05). Overall, DFPP and PE showed no significant difference in the removal effect on different types of antibodies. However, both DFPP and PE showed a better removal effect on IgM antibodies in group of titer ≥32 compared with group of titer ≤16 (P<0.05), and the effect of PE was more obvious. The removal effect on anti-A antibodies in PE group was better than that in DFPP group. This advantage was mainly manifested as follows: PE had a better removal effect on IgG anti-A antibody than DFPP in group of titer ≤16 (P<0.05); PE had a better removal effect on IgM anti-A antibody than DFPP in group of titer ≥32 (P<0.05). There was no significant difference between the two methods in the removal effect on the other blood group antibodies (P>0.05). Conclusion Both DFPP and PE can significantly reduce the titer of blood type antibodies, and the two methods have a better removal effect on high titer antibodies. There was no significant difference between the two methods in the removal of antibodies of other blood groups, except that the removal efficiency of low titer IgG anti-A and high titer IgM anti-A antibodies by PE was better than that by DFPP.

Objective The purpose of this study was to explore the mechanism of Sema7a protein promoting the adhesion between endothelial cells and megakaryocytes. Methods Human umbilical vascular endothelial cells (HUVECs) and megakaryocyte line MEG01 were used to simulate the adhesion of pulmonary vessels and megakaryocytes in vitro. Immunofluorescence, flow cytometry, 4D Label free and other biological techniques were used to detect the adhesion between endothelial cells and megakaryocytes, the amount of Sema7a binding to HUVECs, and the changes of protein expression and biological information in HUVECs. Immunofluorescence was used to detect the expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in HUVECs. Results The adhesion between MEG01 and HUVECs was promoted after Sema7a binding to HUVECs, with the MAPK signal pathway been activated, and molecules ICAM-1 and VCMA-1 of HUVECs been up-regulated. Conclusion Sema7a promoted the adhesion between megakaryocytes MEG01 and endothelial cells HUVECs by up-regulating the expression of molecules ICAM-1 and VCMA-1 in HUVECs.