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Background and Aim: Tick-borne pathogens such as Babesia canis, Hepatozoon canis, and Ehrlichia canis can cause serious disease in canines. Each blood parasite can be associated with different hematological characteristics in infected dogs. Identification of hematological alterations during routine laboratory screening of blood samples from dogs displaying clinical signs is essential for diagnosing blood parasitic infections. This study aimed to evaluate parasitic infections and hematological alterations in blood samples of infected dogs in Southern Thailand. Materials and Methods: A total of 474 blood samples were collected from dogs presented at the Veterinary Teaching Hospital of the Prince of Songkla University between 2016 and 2019. An automatic hematology analyzer was used to establish hematological values; peripheral blood films were screened for blood parasites and their detection was associated with hematological alterations to determine the odds ratio (OR). Results: This study found that E. canis (n=127) was the most common blood parasite infecting dogs in southern Thailand, followed by H. canis (n=100) and B. canis (n=24). Hematological alterations caused by Ehrlichia infections included anemia, thrombocytopenia, monocytosis, and eosinophilia (OR=14.64, 17.63, 20.34, and 13.43, respectively; p<0.01). The blood samples of Hepatozoon-infected dogs were characterized by anemia, thrombocytopenia, leukocytosis, neutrophilia, and monocytosis (OR=6.35, 3.16, 12.80, 11.11, and 17.37, respectively; p<0.01). Anemia, thrombocytopenia, eosinopenia, and lymphopenia (OR=10.09, 33.00, 20.02, and 66.47 respectively; p<0.01) were associated with B. canis-infected dogs. Conclusion: These data support the fact that hematological abnormalities are a hallmark for the identification of tick-borne infections. The hematological values, hereby reported, can be used as a guideline for the clinical diagnosis of canine blood parasitic infections in Southern Thailand.

BRCA1 is a tumor suppressor gene. Its translated product has an important function in transcriptional activation and DNA repair pathways. Damaged BRCA1 due to cisplatin treatment may lead to loss of such functions. To address a potential drug target of BRCA1 for cisplatin treatment, we investigated the biophysical characterization and functional consequences of the 3'-terminal region of human BRCA1 after in vitro platination with cisplatin. To analyze the base/sequence specificity of cisplatin damage, the measurement for sensitivity of cisplatin-treated BRCA1 to restriction enzymes (EcoO109I and PvuII) and sequence gel analysis was conducted. The results suggested that the platination favorably occurred at the d(GpG) and the d(GpC) sites. An increase in drug concentrations resulted in increased interstrand crosslinks at the d(GpC) site. Cisplatin affected the transition temperature of the BRCA1 gene fragment in a biphasic fashion. DSC thermogram of DNA adducts was shifted to a lower transition temperature at lower cisplatin concentration. However, at higher drug concentration, the thermogram peaked at a slightly higher transition temperature with predominantly increased heat specific capacity. Reduction in cellular DNA repair of cisplatin-damaged plasmid DNA, using host cell reactivation assay, was a consequence of an increase in platination levels on the reporter gene. The GAL4-fused BRCA1 slightly enhanced the transcription of the reporter gene in the absence of GAL4 binding site. The transcriptional transactivation activity of cisplatin-modified BRCA1, when tested in "one-hybrid GAL4 transcriptional assay," was inversely proportional to cisplatin doses. Furthermore, the transcriptional transactivation activity was dramatically diminished in the presence of a second expression vector containing multiple cisplatin-damaged sites. The data provide the first evidence for direct interaction of cisplatin with BRCA1 and raise the possibility of BRCA1 as a therapeutic target for platinum drug-based chemotherapy.