Blood transfusion is a fundamental and life-saving procedure where the consequence of errors can be fatal. Nurses’ knowledge plays an essential role in ensuring quality and safety in blood transfusion. The objective of this study was to assess blood transfusion-associated knowledge of tertiary hospital nurses on the east coast of Malaysia. This was a cross-sectional study with 200 registered nurses involved in blood transfusion procedures at Hospital Universiti Sains Malaysia. The knowledge of the nurses was evaluated by using the routine blood transfusion knowledge questionnaire based on five parts, and <50%, 50–74%, or ≥75% of the knowledge was considered as poor, moderate, or high, respectively. Based on the scoring system, the overall knowledge of blood transfusion among Malaysian nurses (33.2 ± 8.4 years) was estimated to be 54.9 ± 7.6%. In individual items, the scoring was 81.0%, 45.4%, 49.2%, 63.0%, and 90.0% in knowledge prior to blood transfusion, on pre-transfusion, on post-transfusion, on complications, and on transfusion policy, respectively. The findings of this study indicated that most of the nurses’ overall knowledge of blood transfusion was at a moderate level; therefore, training courses and continuous medical education are warranted to improve knowledge and skills of the nurses to ensure good practices of blood transfusion.

Multiple myeloma (MM) is an exceptionally complicated and heterogeneous disease that is caused by the abnormal proliferation of malignant monoclonal plasma cells initiated in the bone marrow. In disease progression, a multistep process including differentiation, proliferation, and invasion is involved. Despite great improvement in treatment outcomes in recent years due to the substantial discovery of novel therapeutic drugs, MM is still regarded as an incurable disease. Patients with MM are afflicted by confronting remission periods accompanied by relapse or progression outcomes, which inevitably progress to the refractory stage. In this regard, MM may need new medications or modifications in therapeutic strategies to overcome resistance. A variety of genetic abnormalities (e.g., point mutations, translocations, and deletions) and epigenetic changes (e.g., DNA methylation, histone modification, and non-coding RNA) contribute to the pathogenesis and development of MM. Here, we review the significant roles of epigenetic mechanisms in the development and progression of MM. We also highlight epigenetic pathways as potential novel treatment avenues for MM, including their interplay, use of epigenetic inhibitors, and major involvement in immuno-oncology.

Venous thromboembolism (VTE), which encompasses deep venous thrombosis (DVT) and pulmonary embolism (PE), is a major public health concern due to its high incidences of morbidity and mortality. Patients who have experienced trauma with prolonged immobilization are at an increased risk of developing VTE. Plasma D-dimer levels have been known to be elevated in trauma patients, and they were closely correlated with the number of fractures. In other words, plasma D-dimer levels cannot be used as the only indicator of VTE in trauma cases. Given the limitations, further study is needed to explore other potential biomarkers for diagnosing VTE. To date, various established and novel VTE biomarkers have been studied in terms of their potential for predicting VTE, diagnostic performance, and improving clinical therapy for VTE. Therefore, this review aims to provide information regarding classic and essential haemostasis (including prothrombin time (PT), activated partial thromboplastin time (aPTT), D-dimer, fibrinogen, thrombin generation, protein C, protein S, antithrombin, tissue factor pathway inhibitor, and platelet count) and inflammatory biomarkers (C-reactive protein, erythrocyte sedimentation rate, and soluble P-selectin) as potential diagnostic biomarkers that can predict the risk of VTE development among trauma patients with prolonged immobilization. Thus, further advancement in risk stratification using these biomarkers would allow for a better diagnosis of patients with VTE, especially in areas with limited resources.

(1) Background: Alpha (α)-thalassaemia is a genetic disorder that affects 5% of the world population. Deletional or nondeletional mutations of one or both HBA1 and HBA2 on chromosome 16 will result in reduced production of α-globin chains, a component of haemoglobin (Hb) that is required for the formation of red blood cells (RBCs). This study aimed to determine the prevalence, haematological and molecular characterisations of α-thalassaemia. (2) Method: The parameters were based on full blood count, high-performance liquid chromatography and capillary electrophoresis. The molecular analysis involved gap-polymerase chain reaction (PCR), multiplex amplification refractory mutation system-PCR, multiplex ligation-dependent probe amplification and Sanger sequencing. (3) Results: With a total cohort of 131 patients, the prevalence of α-thalassaemia was 48.9%, leaving the remaining 51.1% with potentially undetected α gene mutations. The following genotypes were detected: -α^3.7/αα (15.4%), -α^4.2/αα (3.7%), --^SEA/αα (7.4%), α^CSα/αα (10.3%), α^Adanaα/αα (0.7%), α^{Quong Szeα}/αα (1.5%), -α^3.7/-α^3.7 (0.7%), α^CSα/α^CSα (0.7%), -α^4.2/α^CSα (0.7%), –^SEA/α^CSα (1.5%), –^SEA/α^{Quong Sze}α (0.7%), -α^3.7/α^Adanaα (0.7%), --^SEA/-α^3.7 (2.2%) and α^CSα/α^Adanaα (0.7%). Indicators such as Hb (p = 0.022), mean corpuscular volume (p = 0.009), mean corpuscular haemoglobin (p = 0.017), RBC (p = 0.038) and haematocrit (p = 0.058) showed significant changes among patients with deletional mutations, but not between patients with nondeletional mutations. (4) Conclusions: A wide range of haematological parameters was observed among patients, including those with the same genotype. Thus, a combination of molecular technologies and haematological parameters is necessary for the accurate detection of α-globin chain mutations.

Testing for ABO incompatibility between a potential blood donor and recipient is the cornerstone of pretransfusion testing. Occasionally, weak agglutination reactions occur due to low expression of A and B antigens on the surface of red blood cells. This can lead to inconsistencies in blood group typing, as seen in a case where a patient’s forward and reverse typing showed discrepancies. Following a comprehensive analytical assessment, the patient was identified as having a distinctive variant of blood group A, belonging to the less common subgroups—A ₃ , A _end , A _x , A _m , A _y , and A _el . Herein, we present 3 case series of ABO subgroups identified through extended ABO blood grouping procedures.

Thalassemia is a significant health burden in Malaysia. This report presents a retrospective analysis of nationwide diagnostic data compiled over seven years, investigating β-thalassemia spectrum in 731 referred family trios. Genomic analysis used gap-PCR, ARMS-PCR, MLPA, Sanger sequencing, and exome sequencing to validate rare CNVs. We identified 468 at-risk couples, with 440 children inherited biallelic mutations. Heterogeneous mutations were recorded among Peninsular Malaysian children with 43 β-, four δ-, 11 α-thalassemia and variant types, and five α-globin duplications. Among children in Sabah, 15 β-, one δ-, and two α-thalassemia and variants, and one α-globin duplications were recorded. Sarawak exhibited lowest heterogeneity. In Peninsular Malaysia, β ^E was most prevalent among Malays, followed by IVS 1–5 (G > C), β ^Malay , and IVS 1–1 (G > T). IVS 2–654 (C > T) and − 28 (A > G) were observed only among Chinese individuals in this referred cohort, while Cd 41/42 -TTCT was common to both ethnicities. β ^E /β-thalassemia was the most frequent disease with 188 cases. In Sabah, homozygous β ^Filipino was the most frequent genotype across multiple ethnicities, with 35.2% (31/88) of these cases exhibiting concomitant -α ^3.7 . Overall, 15.2% (111/731) of children with HBB mutations had concomitant α-thalassemia, and 10 had α-triplications. These findings highlight the necessity of HBA genotyping for accurate genetic counseling. We present two novel mutation, codon 122 (TTC > TGC) mutation (HBB:c.368 T > G; p.Phe123Cys) named β ^{Tanah Merah} , and α-globin cluster duplication, ααα ⁹¹ (NC_000016.10:g.87820_179080dup). This comprehensive dataset is essential for improving molecular diagnostics and optimizing DNA analysis workflows in highly heterogeneous populations.