Cardiovascular complications are a major concern in thalassemia patients, primarily driven by endothelial dysfunction. This systematic review and meta-analysis evaluated endothelial biomarkers as indicators of cardiovascular disease risk in thalassemia. A systematic search of PubMed, Scopus, and Embase identified 41 studies comparing biomarkers in thalassemia patients and healthy individuals. The biomarkers analyzed included ICAM-1, VCAM-1, E-selectin, P-selectin, von Willebrand factor (vWF), endothelial microparticles (EMPs), nitric oxide (NO), nitric oxide synthase (NOS), asymmetric dimethylarginine (ADMA), and endothelin-1 (ET-1). Using random effects modeling, pooled standardized mean differences (SMDs) and 95% confidence intervals (CIs) were calculated. The results showed significantly elevated levels of ICAM-1 (SMD 2.15, 95% CI: 1.09–3.22), VCAM-1 (SMD 2.50, 95% CI: 1.35–3.66), E-selectin (SMD 1.21, 95% CI: 0.92–1.50), P-selectin (SMD 1.62, 95% CI: 0.83–2.42), and ET-1 (SMD 1.23, 95% CI: 0.03–2.42) in thalassemia patients. However, NO, ADMA, and vWF showed no significant differences. No studies on NOS were identified, while only one study found significantly elevated EMPs in thalassemia patients. This review highlights ICAM-1, VCAM-1, E-selectin, P-selectin, and ET-1 as key biomarkers for cardiovascular complications in thalassemia. Further research on EMPs and NOS is essential to enhance the understanding of endothelial dysfunction in this population.

Toxoplasmosis is a significant parasitic zoonosis caused by Toxoplasma gondii. Among livestock animals, small ruminants, especially sheep and goats, are the most infected. This infection is a leading cause of abortion, resulting in considerable economic losses for goat breeders. The present study aimed to assess the prevalence of T. gondii infection in goats in northern Thailand, with an emphasis on its potential zoonotic transmission to humans. Polymerase chain reaction (PCR) targeting the T. gondii dihydrofolate reductase-thymidylate synthase (Tgdhfr-ts) gene was employed for molecular detection. This represents the first report of T. gondii molecular detection in blood samples from small ruminants in Thailand by PCR. A total of 176 meat goat blood samples were analyzed, yielding an 8.52% (15/176) positivity rate for T. gondii DNA. The selected DNA sequences from the positive T. gondii DNA displayed a high degree of nucleotide sequence homology with the reference Tgdhfr-ts sequence. Phylogenetic analysis revealed a single clade alongside other T. gondii strains, showing no differentiation based on genotype. This study contributes to the understanding of T. gondii epidemiology and provides a foundation for future strategies to control and manage T. gondii transmission in livestock populations.

Iron overload is a major pathological feature of β-thalassemia and a key driver of hepatic injury through oxidative stress and mitochondrial dysfunction. This study investigated the molecular effects of iron overload on liver mitochondria and evaluated the therapeutic potential of a deferiprone–resveratrol hybrid (DFP-RVT) in a β-thalassemia mouse model. Proteomic analysis was performed on liver tissues from baseline control, iron-overloaded, and DFP-RVT-treated mice to identify differentially expressed proteins and affected pathways. Iron overload resulted in marked downregulation of mitochondrial proteins, particularly components of oxidative phosphorylation and iron–sulfur cluster-associated pathways, including frataxin. In contrast, DFP-RVT treatment restored the expression of multiple mitochondrial proteins involved in respiratory chain function and energy metabolism. Comparative proteomic profiling revealed opposing regulation patterns between iron-overloaded and DFP-RVT-treated groups, indicating recovery of mitochondrial integrity following iron chelation therapy. These findings suggest that iron-induced hepatic injury in β-thalassemia is closely linked to mitochondrial protein dysregulation and that DFP-RVT may mitigate this process by restoring mitochondrial protein expression and iron homeostasis. This study provides mechanistic insight into iron-mediated mitochondrial dysfunction and supports the therapeutic potential of DFP-RVT for iron overload-associated liver injury.

Hemoglobin H/Constant Spring (Hb H/CS) disease represents a form of non-deletional Hb H disease characterized by chronic hemolytic anemia that ranges from moderate to severe and may lead to transfusion-dependent thalassemia. To study the underlying mechanisms of this disease, we conducted an analysis of erythropoiesis and gene expression in erythroid progenitor cells derived from CD34+ hematopoietic stem/progenitor cells from patients with Hb H/CS disease and normal controls. Twelve patients with Hb H/CS disease and five normal controls were enrolled. Peripheral blood samples were collected to isolate CD34+ hematopoietic stem/progenitor cells for the analysis of cell proliferation and differentiation. Six samples from patients with Hb H/CS disease and three controls were subsequently studied for gene expression by next generation sequencing analysis. Erythroid progenitor cells derived from patients with Hb H/CS disease exhibited a trend towards increased rates of erythroid proliferation and decreased cell viability compared to those from controls. Moreover, erythroid progenitor cells derived from patients with Hb H/CS disease demonstrated delayed terminal differentiation. Gene expression profiling revealed elevated levels of genes encoding molecular chaperones, including the heat shock protein genes (HSPs) and the chaperonin containing TCP-1 subunit genes (CCTs) in the Hb H/CS disease group. In summary, erythroid progenitor cells derived from patients with Hb H/CS disease exhibit a trend towards heightened erythroid proliferation, diminished cell viability, and delayed terminal differentiation. Additionally, the increased expression of genes encoding molecular chaperones was observed, providing information on potential underlying pathophysiological mechanisms.