BACKGROUND: Myelodysplastic syndromes (MDS) are clonal hematopoietic diseases of the elderly characterized by chronic cytopenias, ineffective and dysplastic haematopoiesis, recurrent genetic abnormalities and increased risk of progression to acute myeloid leukemia. A challenge of routine laboratory Complete Blood Counts (CBC) is to correctly identify MDS patients while simultaneously avoiding excess smear reviews. To optimize smear review, the latest generations of hematology analyzers provide new cell population data (CPD) parameters with an increased ability to screen MDS, among which the previously described MDS-CBC Score, based on Absolute Neutrophil Count (ANC), structural neutrophil dispersion (Ne-WX) and mean corpuscular volume (MCV). Ne-WX is increased in the presence of hypogranulated/degranulated neutrophils, a hallmark of dysplasia in the context of MDS or chronic myelomonocytic leukemia. Ne-WX and MCV are CPD derived from leukocytes and red blood cells, therefore the MDS-CBC score does not include any platelet-derived CPD. We asked whether this score could be improved by adding the immature platelet fraction (IPF), a CPD used as a surrogate marker of dysplastic thrombopoiesis.
METHODS: Here, we studied a cohort of more than 500 individuals with cytopenias, including 168 MDS patients. In a first step, we used Breiman\'s random forests algorithm, a machine-learning approach, to identify the most relevant parameters for MDS prediction. We then designed Classification And Regression Trees (CART) to evaluate, using resampling, the effect of model tuning parameters on performance and choose the \"optimal\" model across these parameters.
RESULTS: Using random forests algorithm, we identified Ne-WX and IPF as the strongest discriminatory predictors, explaining 37 and 33% of diagnoses respectively. To obtain \"simplified\" trees, which could be easily implemented into laboratory middlewares, we designed CART combining MDS-CBC score and IPF. Optimal results were obtained using a MDS-CBC score threshold equal to 0.23, and an IPF threshold equal to 3%.
CONCLUSIONS: We propose an extended MDS-CBC score, including CPD from the three myeloid lineages, to improve MDS diagnosis on routine laboratory CBCs and optimize smear reviews.

Canine babesiosis is a tick-borne disease caused by apicomplexan intraerythrocytic hemoprotozoan parasites. It is caused by the small (Babesia gibsoni, B. conradae, and B. vulpes) and large (B. vogeli, B. canis, and B. rossi) Babesia groups. As per the recent reports, the most prominent Babesia species encountered in the Kerala state are the small Babesia, B. gibsoni followed by the large Babesia, B. vogeli. The latter is regarded as mildly pathogenic, causing subclinical or mild disease; however severe complications like systemic inflammatory response syndrome, multiple organ dysfunction syndrome, etc. have also been reported. The information on the status of hematological alterations in naturally infected dogs with large Babesia is lacking, particularly from the state of Kerala. The present study involves a retrospective study of clinical cases of large Babesia infection in dogs. The complete haematological profile from well-documented laboratory records of 4039 dogs suspected for babesiosis presented to District Veterinary Centre, Kannur during the period from December 2018 to October 2020 was analyzed for the study. Natural infections were recorded in 35 (0.87%) dogs based on the presence of intraerythrocytic piroplasm of large Babesia spp. by light microscopic examination of Giemsa-stained blood smears. The most consistent features observed were mild to moderate regenerative, normocytic and normochromic anemia, lowered to normal neutrophil count and thrombocytopenia. In comparison to hemolytic anemia, thrombocytopenia was the most frequent clinicopathological finding in the study with an increased presence of large activated platelets or macro-platelets.

The genetic causes of congenital hypothyroidism due to thyroid dysgenesis (TD) remain largely unknown. We identified three novel TUBB1 gene mutations that co-segregated with TD in three distinct families leading to 1.1% of TUBB1 mutations in TD study cohort. TUBB1 (Tubulin, Beta 1 Class VI) encodes for a member of the β-tubulin protein family. TUBB1 gene is expressed in the developing and adult thyroid in humans and mice. All three TUBB1 mutations lead to non-functional α/β-tubulin dimers that cannot be incorporated into microtubules. In mice, Tubb1 knock-out disrupted microtubule integrity by preventing β1-tubulin incorporation and impaired thyroid migration and thyroid hormone secretion. In addition, TUBB1 mutations caused the formation of macroplatelets and hyperaggregation of human platelets after stimulation by low doses of agonists. Our data highlight unexpected roles for β1-tubulin in thyroid development and in platelet physiology. Finally, these findings expand the spectrum of the rare paediatric diseases related to mutations in tubulin-coding genes and provide new insights into the genetic background and mechanisms involved in congenital hypothyroidism and thyroid dysgenesis.

OBJECTIVE: To characterize platelet indices at time of diagnosis of septic peritonitis in dogs and to assess the relationship between platelet parameter data and survival to discharge in dogs treated surgically.
METHODS: Retrospective, observational, descriptive pilot study from 2009 to 2014.
METHODS: University teaching hospital.
METHODS: Forty-eight dogs diagnosed with septic peritonitis were included in this study. Thirty-six dogs had surgical source control. Blood samples from 46 healthy control dogs were used for reference interval (RI) generation.
METHODS: None.
RESULTS: Dogs with septic peritonitis had significantly increased mean values for mean platelet volume (MPV), plateletcrit (PCT), and platelet distribution width (PDW) with increased proportions of dogs having values above the RI compared to healthy dogs. A significantly increased proportion of dogs with septic peritonitis had platelet counts above (12.5%) and below (8.3%) the RI, with no significant difference in mean platelet count compared to healthy dogs. No significant differences in the mean platelet count, MPV, PCT, or PDW were found between survivors and nonsurvivors in dogs with surgical source control; however, dogs with MPV values above the RI had significantly increased mortality compared to dogs within the RI (P = 0.025). Values outside the RI for other platelet parameters were not associated with significant differences in mortality.
CONCLUSIONS: Dogs with septic peritonitis have increased frequency of thrombocytosis and thrombocytopenia with increased MPV, PCT, and PDW. An increased MPV may be a useful indicator of increased risk of mortality in dogs treated surgically.