Hematopoietic Research Articles

Erythropoietin as banned substance in professional sports: effects on maximal aerobic capacity, endurance and detection methods - a review

Introduction and purpose: Erythropoietin (Epo) and its analogs used as performance-enhancing substance and are considered doping and are therefore forbidden in sports, however the scientific evidence behind doping is frequently weak. We aimed to determine the effects erythropoietin on maximal aerobic capacity(VO₂ max), endurence and to present direct detection methods. State of knowledge: Erythropoietin is a glycoprotein cytokine. During cellular hypoxia, Epo is secreted mainly by the kidneys, it stimulates bone marrow production of red blood cells. To compensate for normal red cell turnover, low levels of Epo are constantly secreted in sufficient quantities. In addition to anemia and chronic lung disease, cellular hypoxia can result in elevated levels of Epo. VO₂ max is the peak volume of oxygen that a person can consume during exercise. Essential for breathing, oxygen is inhaled by the lungs and converted into energy, which then fuels human cells and expels carbon dioxide in the exhaled breath. This allows the body to manage more efficiently aerobic workouts that involve a large amount of oxygen intake, such as running, swimming or other cardio exercises. Conclusions: Current data from PubMed indicate a significant relationship between Epo overuse and endurance in professional sports. That is one of the most important reasons to pay attention to the effects of EPO and new detection methods.

Prevalence of anemia and its predictors among patients with chronic kidney disease admitted to a teaching hospital in Ethiopia: A hospital-based cross-sectional study.

Anemia is a common complication of chronic kidney disease (CKD) and is associated with adverse patient outcomes. However, data on the prevalence of anemia in CKD patients is sparse, particularly in resource-limited settings. Therefore, this study aimed to assess the prevalence of anemia and its predictors among patients with CKD admitted to the Jimma medical center, southwest Ethiopia. A hospital-based prospective cross-sectional study was conducted from September 1 to November 30, 2020. All adult patients with CKD aged ≥18 years who fulfilled the inclusion criteria were consecutively recruited into the study. Data were entered into the Epi data manager version 4.4.1 and then exported to SPSS version 22 (IBM Corp., Armonk, NY) for analysis. The predictors of anemia were determined using multivariable logistic regression analysis. Statistical significance was set at P < .05. A total of 150 patients were included in this study. Of these, 64.67% were male, 56.67% had stage 5 CKD, 78% had a CKD duration of less than 1 year, and 74% had proteinuria. Hypertension (40.7%) and diabetes (14.7%) were the common causes of CKD. The prevalence of anemia was 85.33%. Of the patients, 28.67%, 40.67%, and 16% had mild, moderate, and severe anemia, respectively. On multivariate logistic regression, stage 4 CKD (adjusted odds ratio [AOR] 3.2, confidence interval [CI]: 1.78-12.91, P = .025), stage 5 CKD (AOR 4.03, CI: 1.17-13.73, P = .016), and CKD duration of less than 1 year (AOR 3, CI: 1.19-9.11, P = .007) were significantly associated with anemia. The prevalence of anemia among stage 3 to 5 CKD patients was very high. Anemia was significantly associated with the severity and duration of CKD. Therefore, serial follow-up of patients with a long duration and advanced stages of CKD may help prevent anemia and its adverse consequences.

The Role of Red Cell Distribution Width as a Prognostic Marker in Chronic Liver Disease: A Literature Review.

Liver disease is one of the leading public health problems faced by healthcare practitioners regularly. As such, there has been a search for an inexpensive, readily available, non-invasive marker to aid in monitoring and prognosticating hepatic disorders. Recently, red blood cell distribution width (RDW) has been found to be associated with various inflammatory conditions with implications for its use as a potential marker for assessing disease progression and prognosis in multiple conditions. Multiple factors effect red blood cell production whereby a dysfunction in any process can lead to anisocytosis. Furthermore, a chronic inflammatory state leads to increased oxidative stress and produces inflammatory cytokines causing dysregulation and increased intracellular uptake and use of both iron and vitamin B12, which leads to a reduction in erythropoiesis causing an increase in RDW. This literature review reviews in-depth pathophysiology that may lead to an increase in RDW and its potential correlation with chronic liver diseases, including hepatitis B, hepatitis C, hepatitis E, non-alcoholic fatty liver disease, autoimmune hepatitis, primary biliary cirrhosis, and hepatocellular carcinoma. In our review, we examine the use of RDW as a prognostic and predictive marker for hepatic injury and chronic liver disease.

Flt3- and Tie2-Cre tracing identifies regeneration in sepsis from multipotent progenitors but not hematopoietic stem cells.

In response to infections and stress, hematopoiesis rapidly enhances blood and immune cell production. The stage within the hematopoietic hierarchy that accounts for this regeneration is unclear under natural conditions invivo. We analyzed by differentiation tracing, using inducible Tie2- or Flt3-driven Cre recombinase, the roles of mouse hematopoietic stem cells (HSCs) and multipotent progenitors (MPPs). During polymicrobial sepsis, HSCs responded transcriptionally and increased their proliferation and cell death, yet HSC differentiation rates remained at steady-state levels. HSC differentiation was also independent from the ablation of various cellular compartments-bleeding, the antibody-mediated ablation of granulocytes or B lymphocytes, and genetic lymphocyte deficiency. By marked contrast, the fate mapping of MPPs in polymicrobial sepsis identified these cells as a major source for accelerated myeloid cell production. The regulation of blood and immune cell homeostasis by progenitors rather than stem cells may ensure a rapid response while preserving the integrity of the HSC population.

Human hematopoietic stem cell vulnerability to ferroptosis.

Hematopoietic stem cells (HSCs) have a number of unique physiologic adaptations that enable lifelong maintenance of blood cell production, including a highly regulated rate of protein synthesis. Yet, the precise vulnerabilities that arise from such adaptations have not been fully characterized. Here, inspired by a bone marrow failure disorder due to the loss of the histone deubiquitinase MYSM1, characterized by selectively disadvantaged HSCs, we show how reduced protein synthesis in HSCs results in increased ferroptosis. HSC maintenance can be fully rescued by blocking ferroptosis, despite no alteration in protein synthesis rates. Importantly, this selective vulnerability to ferroptosis not only underlies HSC loss in MYSM1 deficiency but also characterizes a broader liability of human HSCs. Increasing protein synthesis rates via MYSM1 overexpression makes HSCs less susceptible to ferroptosis, more broadly illustrating the selective vulnerabilities that arise in somatic stem cell populations as a result of physiologic adaptations.

Ghrelin: A Potent Nephro-protective Agent against Nicotine Induced Kidney Damage in Mice

Background: Kidneys are the major organs responsible for elimination of toxic metabolites from the body. Apart from this kidneys play a vital role in maintaining body fluid and electrolyte balance, blood pressure regulation, red blood cells production and vitamin D activation. Aim: To evaluate role of ghrelin in ameliorating nicotine induced kidney damage by estimating renal function test and serum antioxidant enzymes in BALB/c mice. Methodology: It was a Randomized Control Trial. Healthy male BALB/c mice (n=27) were taken from NIH Islamabad and sorted into 3 groups (nine each). Group I was labeled as control group and given intra-peritoneal normal saline for 29 days. Group II was labeled as nicotine group and received intra-peritoneal nicotine for 29 days. Group III was labeled as ghrelin + nicotine and received intra-peritoneal ghrelin on alternate days and nicotine daily for 29 days. On 30th day intra-cardiac sampling was done for estimation of renal function test and serum antioxidant enzyme levels. Data was evaluated by using SPSS version 23. One way ANOVA and post hoc tukey’s test were applied. Results: In group II, nicotine administration led to decrease level of antioxidants enzymes and significant deterioration of renal function test in comparison with group I. In group III, administration of ghrelin along with nicotine prevented the fall in antioxidant enzymes and restored renal function test back to normal. Practical Implication: Ghrelin a newly discovered peptide has shown to have anti-oxidant properties and thus has potential to reduce the onset and progression of different diseases. It can directly remove reactive oxygen species or can increase the levels of anti-oxidant enzymes thus nullifying oxidative damage. Conclusion: It was concluded that ghrelin by virtue of its anti-oxidant properties protects against nicotine induced kidney damage as reflected through restoration of serum antioxidant enzymes and renal function test. Keywords: Ghrelin, Oxidative Stress, Nicotine, Anti-oxidant Enzymes.

Mature B cells and mesenchymal stem cells control emergency myelopoiesis.

Systemic inflammation halts lymphopoiesis and prioritizes myeloid cell production. How blood cell production switches from homeostasis to emergency myelopoiesis is incompletely understood. Here, we show that lymphotoxin-β receptor (LTβR) signaling in combination with TNF and IL-1 receptor signaling in bone marrow mesenchymal stem cells (MSCs) down-regulates Il7 expression to shut down lymphopoiesis during systemic inflammation. LTβR signaling in MSCs also promoted CCL2 production during systemic inflammation. Pharmacological or genetic blocking of LTβR signaling in MSCs partially enabled lymphopoiesis and reduced monocyte numbers in the spleen during systemic inflammation, which correlated with reduced survival during systemic bacterial and viral infections. Interestingly, lymphotoxin-α1β2 delivered by B-lineage cells, and specifically by mature B cells, contributed to promote Il7 down-regulation and reduce MSC lymphopoietic activity. Our studies revealed an unexpected role of LTβR signaling in MSCs and identified recirculating mature B cells as an important regulator of emergency myelopoiesis.

Responses to Hypoxia: How Fructose Metabolism and Hypoxia-Inducible Factor-1a Pathways Converge in Health and Disease.

Oxygen is critical for the high output of energy (adenosine triphosphate) generated by oxidative phosphorylation in the mitochondria, and when oxygen delivery is impaired due to systemic hypoxia, impaired or reduced delivery of red blood cells, or from local ischemia, survival processes are activated. One major mechanism is the activation of hypoxia-inducible factors (HIFs) that act to reduce oxygen needs by blocking mitochondrial function and stimulating glucose uptake and glycolysis while also stimulating red blood cell production and local angiogenesis. Recently, endogenous fructose production with uric acid generation has also been shown to occur in hypoxic and ischemic tissues where it also appears to drive the same functions, and indeed, there is evidence that many of hypoxia-inducible factors effects may be mediated by the stimulation of fructose production and metabolism. Unfortunately, while being acutely protective, these same systems in overdrive lead to chronic inflammation and disease and may also be involved in the development of metabolic syndrome and related disease. The benefit of SGLT2 inhibitors may act in part by reducing the delivery of glucose with the stimulation of fructose formation, thereby allowing a conversion from the glycolytic metabolism to one involving mitochondrial metabolism. The use of hypoxia-inducible factor stabilizers is expected to aid the treatment of anemia but, in the long-term, could potentially lead to worsening cardiovascular and metabolic outcomes. We suggest more studies are needed on the use of these agents.

Pre-analytical conditions influencing analysis of folate in dried plasma microsamples

IntroductionDetermination of folate insufficiency is of considerable interest given its importance in fetal development and red blood cell formation; however, access to blood tests may be limited due to the requirement for phlebotomy as well as controlled temperature shipping of blood specimens to laboratories for testing due to the inherent instability of folate and its vitamers. MethodsAn LC-MS/MS test was developed and validated for the measurement of 5-methyltetrahydrofolate (5MTHF) in dried plasma specimens collected from fingerstick blood using a laminar flow blood separation device, as well as liquid venous plasma for comparison. Two pre-analytical factors investigated influencing the measurement of 5MTHF in dried plasma were hemolysis of the fingerstick blood during collection and storage/shipment of the dried plasma. ResultsAlthough observed infrequently, hemolysis >10 % resulted in elevated 5MTHF measurements, but hemolysis >1 % resulted in elevated chloride measurements, which were necessary to normalize 5MTHF measurements for variation in volume of dried plasma specimens. Stability of 5MTHF was improved in dried plasma relative to liquid plasma at ambient temperatures, but not sufficiently to allow for uncontrolled temperature shipping despite controlling for humidity and light exposure. Shipping studies emulating ISTA procedure 7D were conducted with a reusable cold packaging solution. The packaging failed to stabilize 5MTHF in dried plasma specimens during a 2-day summer shipping evaluation, but did provide sufficient temperature control to stabilize 5MTHF during the overnight shipping evaluation. ConclusionOur studies provide boundary conditions with respect to hemolysis, storage, and shipping for successful analysis of 5MTHF from dried plasma specimens.

Kajian Naratif: Praktik Konsumsi Jenis Makanan Untuk Peningkatan Kadar Hemoglobin Pada Remaja Putri

Anemia is a condition where the red blood cells are below the normal category. The incidence of adolescent girls anemia in 2012 in Indonesia was 75.9%. One way to overcome the incidence of anemia by consuming foods that contain high iron and other nutrients. The purpose of the study was to determine the types of food that could be consumed by adolescent girls in order to increase Hb levels. The research method is literature review. Search articles using Google Scholar and ResearchGate with the keywords (“Hemoglobin Increase” and “Adolescent Girls”). Synthesis of the results using a matrix of summary articles, identification and comparison of themes. The results showed that there was an effect of certain types of food on increasing Hb levels, namely in the form of juices (kurlapa juice, SF+red guava juice, beetroot juice, green bean juice) and other foods (rice flakes+jaggery, dates, eggs, laddu yeast+ Moringa leaf powder + Fe tablets, Moringa leaf powder, tolo bean sticks). Green bean juice is most effective because it contains substances for the formation of red blood cells. The provision of green bean juice which is relatively cheap and easy to manufacture can be widely given to young women.

Novel Finding of Urinary Erythropoietin as an Early Biomarker of Cisplatin-Induced Nephrotoxicity.

Cisplatin is a chemotherapeutic drug used to treat a great variety of solid tumors. Its dose is commonly limited by its nephrotoxicity, manifested as acute kidney injury (AKI). Erythropoietin (Epo) is a glycoprotein hormone that regulates the production of red blood cells. This study was performed to evaluate the presence of endogenous Epo in male Wistar rat urine and to analyse changes in urinary Epo levels in response to cisplatin- induced AKI. Dose-dependent studies and time-dependent experiments were performed to evaluate changes in urea nitrogen and creatinine in plasma as well as Epo, neutrophil gelatinase-associated lipocalin (NGAL), alkaline phosphatase (AP) activity, creatinine and total proteins in urine at 2days post-dosing. Rats received 2, 5 or 10mg/kg b.w., i.p. of cisplatin. At 5mg/kg b.w., i.p. cisplatin, significant increases in urinary Epo were detected. Significant increases in urea nitrogen and creatinine in plasma, NGAL, AP, proteins, and Epo were observed in urine from rats that received 10mg/kg b.w., i.p. of cisplatin. In the time-dependent experiments, rats were injected with a dose of 5mg/kg b.w., i.p. of cisplatin, and sampling occurred 2, 4, and 14 days post-dosing. In these animals, there were significant increases in urea nitrogen and creatinine in plasma and total proteins, AP activity, Epo, and NGAL in urine on day 4. Urinary Epo was also detected on day 2. Taken together, these findings provide weight of evidence for urinary Epo as a promising early biomarker of cisplatin-induced AKI in male rats.

An efficient EGWO algorithm as feature selection for B-ALL diagnoses and its subtypes classification using peripheral blood smear images

Acute lymphoblastic leukemia (ALL) is the most serious type of leukemia that develops because it causes an abnormal increase in the production of immature white blood cells in the bone marrow. ALL spreads rapidly in children's bodies and leads to their death. The main objective of this paper is to introduce an enhanced methodology based on the k-means clustering algorithm for classifying all subtypes of ALL. Image preprocessing is the first step of the proposed methodology. For obtaining the images' descriptive features, feature extraction is the second step that has been used. To select the most vital features that can characterize the histology of the blood cells, Enhanced Grey Wolf Optimization (EGWO) algorithm has been used in the third step. Hence, EGWO will start to select the search agents based on certain criteria as the best cluster center by using the k-means clustering algorithm. Several supervised classifiers as Random Forest (RF), K Nearest Neighbors (KNN), Support Vector Machine (SVM), and Naïve Bayes (NB) have been compared. The proposed methodology achieves a high degree of accuracy of99.22%,precision of99%,and sensitivity of99%.A comparative study has been established in order to verify the effectiveness of the proposed methodology.

Prolidase Deficiency Causes Spontaneous T Cell Activation and Lupus-like Autoimmunity.

Prolidase deficiency (PD) is a multisystem disorder caused by mutations in the PEPD gene, which encodes a ubiquitously expressed metallopeptidase essential for the hydrolysis of dipeptides containing C-terminal proline or hydroxyproline. PD typically presents in childhood with developmental delay, skin ulcers, recurrent infections, and, in some patients, autoimmune features that can mimic systemic lupus erythematosus. The basis for the autoimmune association is uncertain, but might be due to self-antigen exposure with tissue damage, or indirectly driven by chronic infection and microbial burden. In this study, we address the question of causation and show that Pepd-null mice have increased antinuclear autoantibodies and raised serum IgA, accompanied by kidney immune complex deposition, consistent with a systemic lupus erythematosus-like disease. These features are associated with an accumulation of CD4 and CD8 effector T cells in the spleen and liver. Pepd deficiency leads to spontaneous T cell activation and proliferation into the effector subset, which is cell intrinsic and independent of Ag receptor specificity or antigenic stimulation. However, an increase in KLRG1+ effector CD8 cells is not observed in mixed chimeras, in which the autoimmune phenotype is also absent. Our findings link autoimmune susceptibility in PD to spontaneous T cell dysfunction, likely to be acting in combination with immune activators that lie outside the hemopoietic system but result from the abnormal metabolism or loss of nonenzymatic prolidase function. This knowledge provides insight into the role of prolidase in the maintenance of self-tolerance and highlights the importance of treatment to control T cell activation.

A Customized Efficient Deep Learning Model for the Diagnosis of Acute Leukemia Cells Based on Lymphocyte and Monocyte Images

The production of blood cells is affected by leukemia, a type of bone marrow cancer or blood cancer. Deoxyribonucleic acid (DNA) is related to immature cells, particularly white cells, and is damaged in various ways in this disease. When a radiologist is involved in diagnosing acute leukemia cells, the diagnosis is time consuming and needs to provide better accuracy. For this purpose, many types of research have been conducted for the automatic diagnosis of acute leukemia. However, these studies have low detection speed and accuracy. Machine learning and artificial intelligence techniques are now playing an essential role in medical sciences, particularly in detecting and classifying leukemic cells. These methods assist doctors in detecting diseases earlier, reducing their workload and the possibility of errors. This research aims to design a deep learning model with a customized architecture for detecting acute leukemia using images of lymphocytes and monocytes. This study presents a novel dataset containing images of Acute Lymphoblastic Leukemia (ALL) and Acute Myeloid Leukemia (AML). The new dataset has been created with the assistance of various experts to help the scientific community in its efforts to incorporate machine learning techniques into medical research. Increasing the scale of the dataset is achieved with a Generative Adversarial Network (GAN). The proposed CNN model based on the Tversky loss function includes six convolution layers, four dense layers, and a Softmax activation function for the classification of acute leukemia images. The proposed model achieved a 99% accuracy rate in diagnosing acute leukemia types, including ALL and AML. Compared to previous research, the proposed network provides a promising performance in terms of speed and accuracy; and based on the results, the proposed model can be used to assist doctors and specialists in practical applications.

Knowledge, Practice, and Factors Affecting Sunlight Exposure of Infants Among Mothers at Governmental Health Facilities in Dessie Town, Ethiopia, 2021.

Human being needs sunlight for physical and mental well-being. Sunlight helps the body to produce vitamin D, an important vitamin for skeletal development, immune function, and blood cell formation. So, the community should be counseled to get sufficient sun exposure and vitamin D supplementation to uphold the serum 25 (OH) D levels. This study designed to assess the mothers' knowledge, practice, and factors affecting the sunlight exposure of their infants. A facility-based cross-sectional study was conducted at governmental health facilities in Dessie Town, 2021. A total of 398 mothers were interviewed using semi structured questionnaires. Data were entered into the EPI data version 3.1 and analyzed using SPSS 23. Binary and multivariate logistic regression analyses were also performed. In multivariate analysis, a significant association was considered at P-value of <.05. Response rate was 98.9%. About 76.6% and 58.9% of the mothers had poor knowledge and poor practice regarding sunlight exposure of infants respectively. Mothers' occupation (aOR = 0.124, 95% CI = 0.042, 0.365), mothers' source of information (aOR = 18.604, 95% CI = 7.564, 45.75), and attitude (aOR = 2.773, 95% CI = 1.474, 5.215) had showed a significant association with mothers' knowledge. On the other hand, mothers' age (aOR = 3.191, 95% CI = 1.334, 7.633), mothers occupation (aOR = 4.226, 95% CI = 2.321, 7.694), and baby age (aOR = 1.989, 95% CI = 1.260, 3.140) had a significant association with their practice about sunlight exposure of infants. Mothers' knowledge and practice of sunlight exposure of infants are poor in Dessie Town. Hence measures should be taken to increase and improve mothers' responsiveness of sunlight exposure of infants.

In vitro production of red blood cells for future transfusion medicine

Large-scale in vitro red blood cell (RBC) production has been attempted in recent years. Potential cell sources for RBC production include hematopoietic stem/progenitor cells, pluripotent stem cells, and immortalized erythroid progenitor cell lines, which can induce enucleated RBCs with characteristics such as oxygen-carrying capacity and deformability. A phase I clinical study of cultured RBCs produced from hematopoietic stem/progenitor cells has revealed a similar in vivo half-life between cultured and native RBCs. Thus, the application of cultured RBCs in blood transfusion is gradually advancing. However, a single transfusion requires a large number of cells, unlike other cell therapies. Therefore, developing a method to mass-produce RBCs from a small culture volume at a low cost is important in the future. This review summarizes the current status and prospects concerning in vitro RBC production using each cell source, which can improve future transfusion medicine.

Metabolism in Hematopoiesis and Its Malignancy.

Hematopoietic stem cells (HSCs) are multipotent stem cells that can self-renew and generate all blood cells of different lineages. The system is under tight control in order to maintain a precise equilibrium of the HSC pool and the effective production of mature blood cells to support various biological activities. Cell metabolism can regulate different molecular activities, such as epigenetic modification and cell cycle regulation, and subsequently affects the function and maintenance of HSC. Upon malignant transformation, oncogenic drivers in malignant hematopoietic cells can remodel the metabolic pathways for supporting the oncogenic growth. The dysregulation of metabolism results in oncogene addiction, implying the development of malignancy-specific metabolism-targeted therapy. In this chapter, we will discuss the significance of different metabolic pathways in hematopoiesis, specifically, the distinctive metabolic dependency in hematopoietic malignancies and potential metabolic therapy.

Sickle Cell Disease and Thromboembolism: New Insights on the Pathophysiology, Diagnosis, and Treatment.

Sickle cell disease (SCD) is a genetic hemoglobinopathy caused by the abnormal hemoglobin S (HbS) in red blood cells. As a result of its deoxygenation and polymerization, the properties and formation of red blood cells become altered, which ultimately leads to the development of SCD. Chronic inflammatory processes produced by hemolytic and vaso-occlusive episodes, define SCD clearly. These processes result in various effects, including organ damage and increased mortality in people suffering from the disease. Thromboembolism, a potentially fatal disease, is common in patients with sickle cell disease. Despite the known association between hypercoagulability and SCD, thromboembolism is often overlooked as a major complication of SCD. However, thromboembolism affects nearly one-quarter of adult patients and appears to be a risk factor for death in SCD. It has been well documented that in SCD, hemostatic alterations and thrombotic events are associated with endothelium and leukocyte activation. In SCD, inflammatory pathways play an important role in the activation of coagulation and the generation of platelet activation. Although among other mechanisms, it also involves the activation of tissue factors, the expression of adhesion molecules, and the stimulation of innate immune responses. So, mouse model studies may provide novel mechanistic pathways. These studies on mice models are yet to be applied to humans which will lead to the development of clinical lab treatments and therapeutic drugs. Additionally, SCD is a condition that responds favorably to biological treatments like gene therapy. SCD patients now have more potentially curative alternatives with recent developments in hematopoietic stem cell (HSC) transplantation and gene therapy platforms, including Lentiglobin vectors. In the present review, a discussion of the pathophysiology and thromboinflammation of sickle cell disease, along with its global burden in terms of both diagnosis and treatment, is presented.

Haematopoietic Stem Cell Transplantation in Thalassaemia Major: A Narrative Review

Thalassaemia constitutes an especially prevalent human monogenic illness caused by a lack of synthesis of the α- or β-globin chains. The clinical impact of β-thalassaemia is worse since it consists of the same pair gene configuration, thalassaemia major, causing significant health discouragement and loss of life due to life threateningly insufficient haemoglobin (Hb) levels. Only a few nations have successfully reduced the prevalence of β-thalassaemia major, even though comprehensive screening, group counselling, pre-natal detection and public education can all be used. Since over ½ century ago, the fundamental elements of treatment for thalassaemia major have been iron chelation and hypertransfusion. The globin chain that makes up the adult Hb molecule is missing or synthesised at a reduced rate in β-thalassemia. The aberrant buildup of the α-globin chain and faulty formation of red blood cells (RBCs) leading to RBC haemolysis are the outcomes of this genetic abnormality. Since allogeneic haematopoietic stem cell transplantation (Allo-HSCT) has been a well-established gene replacement therapy for individuals with thalassaemia major for several years, it has had very successful outcomes for patients with access to it. Over the past 20 years, the consequences for more susceptible patients have also steadily improved, leading to 80%–90% longer-term life expectancy amongst this group of patients. However, providing Allo-HSCT as a treatment for these patients globally presents numerous difficulties. Replacing genes in autologous HSCs employing viral vectors has been possible in recent years.

Lightweight EfficientNetB3 Model Based on Depthwise Separable Convolutions for Enhancing Classification of Leukemia White Blood Cell Images

Acute lymphoblastic leukemia (ALL) occurs when undeveloped lymphocytes are grown excessively in the bone marrow due to the formation of many immature white blood cells (WBC) in the bone marrow to destroy the healthy cell, which may lead to death. White blood cells are part of the immune system fighting against germs. A timely and accurate cancer diagnosis is important for effective treatment to improve survival rates. Since the image of acute lymphoblastic leukemia cells (cancer cells) under the microscope is complicated to recognize the difference between ALL cancer cells and normal cells. In order to reduce the severity of this disease, it is necessary to classify immature cells at an early stage. In recent years, different classification models have been introduced based on machine learning (ML) and deep learning (DL) algorithms, but they need to be improved. This work enhances the diagnosis of ALL with a computer-aided system that yields accurate results by using deep learning techniques. This research proposed a lightweight DL-assisted robust model based on EfficientNet-B3 using depthwise separable convolutions for classifying acute lymphoblastic leukemia and normal cells in the white blood cell images dataset. The main objective of the proposed lightweight EfficientNet-B3 is to utilize less trainable parameters to enhance the performance and efficiency of the classification of leukemia. Furthermore, two publicly available datasets are considered to evaluate the effectiveness and generalization of the proposed lightweight EfficientNet-B3. In addition, different measures are employed to evaluate the effectiveness and efficiency of the proposed classifier for the accurate and reliable classification of leukaemia cells. In addition, a detailed analysis is given to evaluate and compare the performance and efficiency of the proposed with existing pre-trained and ensemble DL classifiers. Based on experimental results, it is investigated that the proposed model for image classification achieves better performance and outperforms the existing benchmark DL and other ensemble classifiers. Moreover, our finding suggests that the proposed lightweight EfficientNet-B3 model is reliable and generalized to facilitate clinical research and practitioners for leukemia detection.