Liproxstatin‑1 induces cell cycle arrest, apoptosis, and caspase‑3/GSDME‑dependent secondary pyroptosis in K562 cells.

Leukemia is a fatal hematopoietic disorder with a poor prognosis. Drug resistance is inevitable after the long‑term use of chemotherapeutic agents. Liproxstatin‑1, commonly known as a ferroptosis inhibitor, has never been reported to have anticancer effects.

Key immune-related gene ITGB2 as a prognostic signature for acute myeloid leukemia.

Background: The tumor microenvironment (TME) has an essential role in tumorigenesis, progression, and therapeutic response in many cancers. Currently, the role of TME in acute myeloid leukemia (AML) is unclear. This study investigated the correlation between immune-related genes and prognosis in AML patients.

Congenital dysfibrinogenemia caused by γAla327Val mutation: structural abnormality of D region.

Background: : Congenital dysfibrinogenemia (CD) is a coagulation disorder caused by mutations in the fibrinogen genes, which result in abnormal fibrinogen function. However, the precise pathogenesis underlying it remains unclear.

Methods: : In this study, we identified a novel heterozygous mutation in an asymptomatic patient with CD caused by γ Ala327Val mutation.

Analyzing the key gene expression and prognostics values for acute myeloid leukemia.

Background: Acute myeloid leukemia (AML) is one of the first tumor types sequenced at the whole genome level. However, numbers of the mutated genes expression levels, functions, and prognostics values still unclear.

Methods: To most ordinary mutated genes were analyzed via cancer virtual cohort discovery analysis platform (CVCDAP), and further investigated the mutational conversions, variant allele frequencies (VAF), driver genes, and potential druggable mutated genes in AML.

Comprehensively analyze the expression and prognostic role for ten-eleven translocations (TETs) in acute myeloid leukemia.

Background: The ten-eleven translocation (TET) family oxidize 5-methylcytosines (5mCs) and promote the locus-specific reversal of DNA. The role of TETs in acute myeloid leukemia (AML) is mostly unknown.

Methods: TETs mRNA expression levels were analyzed via Gene Expression Profiling Interactive Analysis (GEPIA).

Identification the prognostic value of glutathione peroxidases expression levels in acute myeloid leukemia.

Background: Glutathione peroxidases (GPXs) are an enzyme family with peroxidase activity. Abnormal GPX expression is associated with carcinogenesis. However, the potential role of the GPX gene family in acute myeloid leukemia (AML) remains to be comprehensively examined.

[Significance of Tissue Factor-Bearing Microparticle Procoagulation Activity and Antithrombin Ⅲ Detection in Thalassemia Patients].

Objective: To explore whether the high risk factors possibly leading to hypercoagulative status and thrombosis exist in Thalassemia patients of Guangxi region through detecting plasma tissne factor-bearing microparticles (TFMP), procoagulatima activity, coagulation and anticoagulation function, fibrinolytic function, endothelial function and platelet count.

Methods: The TFMP procoagulation activity was detected by chromogenic saubstract method, the levels of tissue factors (TF), tissue factor pathway inhibitor(TFPI), protein C (PC), protein S (PS), antithrombin Ⅲ(AT-Ⅲ), tissue plasminogen activator (tPA), thrombin-activated fibrinolysis inhibitor (TAFI), soluble E-selectin (sE-sel), intercellular adhesion molecule-1 (ICAM-1) and thrombomodulin (TM) were detected by ELISA in thalassemia group (n=71) and control group (n=20 heathy persons).

Results: Compared with control group, the AT-Ⅲ level decreased in β-thalastemia major group (TM) (P<0.

A novel fibrinogen gamma-chain mutation, p.Cys165Arg, causes disruption of the γ165Cys-Bβ227Cys disulfide bond and ultimately leads to hypofibrinogenemia.

Background: Congenital hypofibrinogenemia is a type of hereditary disease characterized by impaired fibrinogen synthesis and/or secretion induced by mutations in the fibrinogen gene.

Objectives: We investigated the phenotypes, genotypes, and pathogenesis of congenital hypofibrinogenemia in an affected family.

Patients/methods: The proband had a risk of bleeding; therefore, conventional coagulation screening was performed for the proband and her family members.

Alterations of anticoagulant proteins and soluble endothelial protein C receptor in thalassemia patients of Chinese origin.

Background: Thalassemia is characterized by a hypercoagulable state in which the protein C (PC) pathway controls thrombosis. We investigated changes in PC, protein S (PS), antithrombin III (AT III) and soluble endothelial protein C receptor (sEPCR) in thalassemia.

Methods: A group of 129 patients with β-thalassemia major (β-TM), β-thalassemia intermedia (β-TI), α-thalassemia intermedia (α-TI) and combined α-/β-thalassemia (α + β-thal) were compared with 32 gender- and age-matched controls.

[Clinical Significance of Detecting Tissue Factor and Tissue Factor Pathway Inhibitor in Thalassemia Patients].

Objective: To investigate the changes of E-selectin, thrombin-antithrombin complex（TAT）, prothrombin fragment 1+2（F1+2）, tissue factor（TF）and tissue factor pathway inhibitor（TFPI）before and one year after splenectomy in thalassemia patients.

Methods: A total of 30 thalassemia patients undergoing electric laparoscopic splenectomy and 30 normal controls（NC） were enrolled in the study．Plasma levels of E-selectin, TAT, F1+2, TF and TFPI were detected by enzyme-linked immuno sorbent assay（ELISA）.

Results: One year after splenectomy，the plasma concentrations of E-selectin, TAT, F1+2, TF, TFPI were significantly higher than those in both preoperative and NC groups．Levels of E-selectin, TAT, F1+2 before splenectomy were significantly higher than those in NC groups.

Abnormal fibrinogen with an Aα 16Arg → Cys substitution is associated with multiple cerebral infarctions.

We found a heterozygous dysfibrinogenemia caused by a substitution of AαArg16Cys. The proband suffered multiple cerebral infarctions. Routine coagulation tests revealed a prolonged thrombin time.

Management of dysfibrinogenemia in pregnancy: A case report.

Background: Dysfibrinogenemia is a rare coagulation disorder caused by mutations in the fibrinogen gene that results in abnormal fibrinogen function. Dysfibrinogenemia has a wide spectrum of clinical manifestations including asymptomatic(55%), hemorrhage (25%), and thrombosis (20%).

Methods: We reported a 30-year-old woman with 35 weeks gestation.

Combined use of Clauss and prothrombin time-derived methods for determining fibrinogen concentrations: Screening for congenital dysfibrinogenemia.

Background: In this study, the significance of fibrinogen concentration assessed by a combination of Clauss and prothrombin time (PT)-derived methods for screening for congenital dysfibrinogenemia were investigated, and the screening efficiency of fibrinogen PT-derived/Clauss ratio on congenital dysfibrinogenemia was analyzed.

Methods: We compared fibrinogen concentrations determined by the Clauss, PT-derived, and enzyme-linked immunosorbent assay (ELISA) methods in 73 patients with congenital dysfibrinogenemia and 81 normal controls. Receiver operating characteristic (ROC) curves were utilized to evaluate the efficacy of fibrinogen PT-derived/Clauss ratio in screening for congenital dysfibrinogenemia.

[Research Advance of Microparticles in Hypercoagulation of Hemolytic Anemia-Review].

Microparticles (MP) are small membrane vesicles released from many different cell types in response to cellular activation or apoptosis, which have the procoagulant effect. Hemolytic anemia(HA) is a type of anemia that have a short life expectancy of red blood cells due to the destruction which exceed the hematopoietic compensatory capacity of bone marrow. Sickle cell anemia(SCD), thalassemia and paroxysmal nocturnal hemoglobinuria(PNH) are all characterized by hypercoagulation and thromboembolism (TE).

Over-expression of miR-196b-5p is significantly associated with the progression of myelodysplastic syndrome.

Myelodysplastic syndrome (MDS) is a clonal stem cell disorder characterized by ineffective hematopoiesis with a high risk of transformation to acute myeloid leukemia (AML). miRNAs function as tumor suppressors and oncogenes in various cancers and regulate the differentiation potential of hematopoietic stem and progenitor cells (HSPCs). It has been suggested that miRNAs may play an important role in progression of MDS.

A novel mutation in the fibrinogen Aα chain (Gly13Arg, fibrinogen Nanning) causes congenital dysfibrinogenemia associated with defective peptide A release.

Dysfibrinogenemia is characterized by blood coagulation dysfunction induced by an abnormal molecular structure of fibrinogen. Here, we describe a new case. A 32-year-old female was suspected of having dysfibrinogenemia during routine laboratory screening, based on her decreased functional fibrinogen level, normal fibrinogen antigen level, and prolonged thrombin time.

[Expression of miR-550a-5p in Myelodysplastic Syndrome and Its Prediction of Target Genes].

Objective: To investigate the expression of miR-550a-5p in bone marrow of patients with myelodysplastic syndrome (MDS), and to predict its target genes and function by bioinformatics analyses, so as to provide the evidence to furthre explore the role of miR-550a-5p and its target genes in pathogenesis of MDS.

Methods: Real-time PCR was used to detect the expression of miR-550a-5p in 54 MDS patients, 16 acute myeloid leukemia transformed from MDS (sfAML) and 19 healthy controls, and the correlation between the expression of miR-550a-5p and clinical pathologic characteristics of MDS, including chromosome, percentage of marrow blasts, absolute neutrophil count, platelet count and hemoglobin levels were analyzed. The sequence of miR-550 was searched in miRBase database.

Three cases of congenital dysfibrinogenemia in unrelated Chinese families: heterozygous missense mutation in fibrinogen alpha chain Argl6His.

Congenital dysfibrinogenemia (CD) is a qualitative fibrinogen disorder caused by an abnormal fibrinogen molecule structure, leading to dysfunctional blood coagulation. This study describes 3 cases of dysfibrinogenemia identified in the unrelated Chinese pedigrees.Routine coagulation screening tests were performed on the probands and their families.

Analysis of the genetic variants associated with recurrent thromboembolism in a patient with hemoglobin H disease following splenectomy: A case report.

Reports of recurrent thromboembolism in thalassemia, particularly in hemoglobin H (HbH) disease associated with congenital thrombophilic mutations, are scarce. However, several mutations were detected in a 22-year-old woman with HbH disease. The patient experienced the first thrombotic event at the age of 20 years and had four recurrent thromboses in a short time interval, despite receiving anticoagulant treatment.

[Advances in Pathogenesis and Related Clinical Research of Thromboembolism in Patients with Thalassemia after Splenectomy].

Thalassemia is the most common human hereditary hemolytic anemia. Due to splenomegaly and hypersp-lenism, splenectomy can be used as a means of treatment for thalassemia. Various complications following splenectomy, however, especially thromboembolic complications are remarkable.

[Analysis of a family with congenital dysfibrinogenemia caused by an Arg275His mutation in the gamma chain of fibrinogen].

Objective: To explore the clinical phenotype of a family affected with congenital dysfibrinogenemia and potential mutations underlying the disease.

Methods: Coagulation testing and hepatorenal function testing were conducted on 18 individuals from three generations. Plasma fibrinogen was extracted and analyzed with SDS-PAGE electrophoresis.

Fas-670A>G polymorphism is not associated with an increased risk of acute myeloid leukemia development.

The association between the increased risk of acute myeloid leukemia (AML) and Fas promoter polymorphisms has been reported previously; however, the results are inconclusive. The present study performed one case-control study to investigate the association, and a total of 98 AML patients and 2,014 healthy controls were genotyped. The data showed that the distribution of Fas-670AA, GA and GG genotypes among the AML patients were not significantly different from those of the healthy controls, all P>0.

Dysfibrinogenemia in a patient undergoing artificial abortion after misdiagnosis and review of the literature.

Background: Dysfibrinogenemia is characterized by dysfunction induced by an abnormal fibrinogen molecule structure that results in blood coagulation dysfunction. The clinical manifestations are diverse. Dysfibrinogenemia is misdiagnosed or miss diagnosis in the absence of an appropriate laboratory examination.